----- Mensaje reenviado ---- De: matteo sergi <sergimatteo@...> Para: Sin respuesta <notify-dg-lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com> Enviado: sábado, 21 de junio, 2008 22:12:58 Asunto: Re: [Lyme-E] Resumen nº 1106
Hola a todos,
lo siento JuanCarlos, no sabemos como se llama el medico de la Rioja, pero seguramente se pondrá en contacto con nosotros ya que ha pedido el historial de Raquel para estudiar el caso. Esta tarde ha llamado la doctora de Raquel para hablar de las niñas y entre otras cosas piensa que no es un caso congenito si no una casualidad y que las tres se han enfermado en mometos diferentes. Personalmente creo de no haber oido una tonteria mas grande, y tambien piensa que hasta que no tengan mas sintomas no es el caso de tratarlas. ¡Alucinante!
Espero que el pediatra,en el que confío mucho, no ponga problemas en tratarlas....os contaré las novedades.
un saludo, Matteo
----- Mensaje original ---- De: "lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com" <lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com> Para: lyme_y_otras_zoonosis_cronicas_espanol@yahoogroups.com Enviado: sábado, 21 de junio, 2008 15:49:50 Asunto: [Lyme-E] Resumen nº 1106
Sería posible saber el nombre del especialista de la rioja aunque sea al correo privado, aunque me imagino que médico puede ser. Necesito un nuevo médico pues el de ahora me lleva poniendo muchas pegas
Hola a todos, perdonarme la larga ausencia, pero he seguido leyendo todos los mensajes que me han parecidos muy interesantes. Tengo muchas cosas que contar, buena y menos buenas, de todos modos muy importantes. en primer lugar raquel sigue sin un diagnostico definitivo porque los dos ultimos analisis han
resultados negativos, pero la doctora que la sigue, que por cierto es muy profesional, ha decidido según el consejo de un especialista de LA Rioja, de darle doxiciclina indefinitamente en ciclos de tres meses. Hasta que sea necesario. tiene mejorías con empeoramientos, pero la doctora dice que es una reacción normal. Mas adelante os esplicaré con exactitumbre todas las sintomatologia que tiene. Otra noticia muy importante que quiero compartir es que hemos hecho la prueba a nuestras hijas d 2 y 6 años y han resultado ambas positivas. La enfermedad de Lyme contrariamente a lo que dichen los medicos es congenita!! Estamos ahora a la espera de hablar el jueves con su pediatra del Niño Jesús de Madrid para conocer el tratamiento que quiera ponerles. seguiré pasando informaciónes y detalles. un saludo a todos. Matteo.
----- Mensaje reenviado ---- De: matteo sergi <sergimatteo@...> Para: mpmcrono@... Enviado: viernes, 20 de junio, 2008 23:39:20 Asunto: Re: LYME
Hola Montse, y hola a todos,
Compartimos perfectamente tu angustia, de echo al resultar Raquel negativa en las ultimas dos analiticas, pensavamos que resultasen negativas tambien las niñas, pero contrariamente el resultado fue muy claro, positivo.
Montse, de momento, no te puedo dar más información porqué el pediatra de las niñas sigue de baja por enfermedad y todavia no hemos podido hablar con el, y no nos han dado copias de los resultados. Lo asombroso es que el medico sustituto nos dice que no hay prisa, y que hay que esperar las evoluciones. La semana proxima esperemos ver al medico y que nos diga que tratamiento les va a poner (por una parte deseamos un tratamiento yá y por otro nos asusta un poco todas las reacciones que puedan tener las niñas.
Los sintomas que hemos podido observar en ellas son hiperactividad, irritabilidad, nerviosismo, ansia, falta de concentración (en la mayor),unas picaduras raras que le aparecen periodicamente, perdida de memoria a corto plazo, fobias, miedos, pesadillas, sueño interrumpido,dermatitis, dolores articulares repentinos que desaparecen solos y rapidamente, fotofobia (la pequeña), fonofobia, problemas bucales, alteración intestinal, vaginitis frequentes, y podria seguir mucho más. No se si te puede ser de alguna utilidad pero una cosa muy importante que hizo Raquel y que yo desvaluava fué ir apuntando diariamente todas las cosas raras que les ocurrian, desde hace años.
Otra cosa que hemos visto bastante interesante, como prueba del deterioro cognitivo por la infección es el electroencefalograma, que no quisieron hacer a Raquel hasta hace poco, y que reveló unas alteración de las ondas theta en la parte temporal del cerebro, que esplicaria los deja vú, y las visiones recurrentes que tenía sobre accidentes o cosas muy feas, pero sin llegar a ser alucinaciones verdaderas.
Por ultimo queria decir que hace casi un año , antes de empezar el tratamiento de ceftriaxona,Raquel tomó durante unos dias la uncaria tormentosa, provocandole un empeoramiento muy fuerte. Eso creemos que depende del hecho de que tomó la garra de gato normal que se compra en herboristeria y no la garra de gato Toa Free.
Espero que la proxima mail sea aun mas especifica, mientras tanto deseo a todos lo mejor.
Creo que el resultado de nuestras hijas abre una puerta mas frente a esta enfermedad, de la cual habrá mucho que hablar.
un saludo a todos Matteo.
----- Mensaje original ---- De: montserrat pérez martínez <mpmcrono@...> Para: sergimatteo@... Enviado: viernes, 20 de junio, 2008 18:42:34 Asunto: LYME
Hola, Sergi.
Soy Montse, del foro del Lyme. Yo también llevo algún tiempo sin escribir nada, porque no he tenido internet hasta hoy desde hace 3 meses, que no me funcionaba. Pero he ido leyendo los mensajes del grupo cuando he tenido a mano internet de algún familiar.
Verás te escribo a nivel personal porque yo también tengo dos hijos y los tuve ya enferma de Lyme (aunque sin saber el diagnóstico), uno tiene 12 años y el otro 7, al mayor le hice la analitica para anticuerpos, que dió negativo, lo cuál no me dice nada, ya que yo también soy seronegativa para anticuerpos. Me gustaría saber qué tipo de analítica les han practicado y si vosotros habíais notado algún síntoma en vuestros hijos. Los míos están sanos, aunque a veces, no sé si algunos "sintomillas", podrían ser cosa del Lyme.
Muchas gracias por ayudarme y espero que tu mujer siga mejorando, aunque sea poco a poco. Saludos.
Montse Pérez.
Enviado desde Correo Yahoo! La bandeja de entrada más inteligente.
Enviado desde Correo Yahoo! La bandeja de entrada más inteligente.
Enviado desde Correo Yahoo! La bandeja de entrada más inteligente.
perdonarme la larga ausencia, pero he seguido leyendo todos los mensajes que me han parecidos muy interesantes.
Tengo muchas cosas que contar, buena y menos buenas, de todos modos muy importantes.
en primer lugar raquel sigue sin un diagnostico definitivo porque los dos ultimos analisis han resultados negativos, pero la doctora que la sigue, que por cierto es muy profesional, ha decidido según el consejo de un especialista de LA Rioja, de darle doxiciclina indefinitamente en ciclos de tres meses. Hasta que sea necesario.
tiene mejorías con empeoramientos, pero la doctora dice que es una reacción normal.
Mas adelante os esplicaré con exactitumbre todas las sintomatologia que tiene.
Otra noticia muy importante que quiero compartir es que hemos hecho la prueba a nuestras hijas d 2 y 6 años y han resultado ambas positivas. La enfermedad de Lyme contrariamente a lo que dichen los medicos es congenita!!
Estamos ahora a la espera de hablar el jueves con su pediatra del Niño Jesús de Madrid para conocer el tratamiento que quiera ponerles.
seguiré pasando informaciónes y detalles.
un saludo a todos. Matteo.
Enviado desde Correo Yahoo! La bandeja de entrada más inteligente.
Las buenas noticias son realmente fantásticas, si realmente un especialista del centro de referencia nacional para el Lyme en La Rioja, recomienda un tratamiento indefinido con antibióticos, eso es de lo mejor para nosotros.
En cuanto a las malas lo lamento profundamente, y me imagino la angustia por lo que estaréis pasando. A mi hija de 7 años le han picado dos garrapatas y las dos veces la han tratado con claritromicina porque la Doxi produce una coloración permanente de los dientes si se administra antes de los 8 años. A mí me hubiera gustado darle también Amoxi o alguna cefalosporina.
No sabía que los médicos dudasen de la transmisión materno fetal de la borreliosis, pense que eso estaba fuera de toda duda. Si lo necesitas tengo algún artículo sobre ello. No dudes en pedírmelo.
perdonarme la larga ausencia, pero he seguido leyendo todos los mensajes que me han parecidos muy interesantes.
Tengo muchas cosas que contar, buena y menos buenas, de todos modos muy importantes.
en primer lugar raquel sigue sin un diagnostico definitivo porque los dos ultimos analisis han resultados negativos, pero la doctora que la sigue, que por cierto es muy profesional, ha decidido según el consejo de un especialista de LA Rioja, de darle doxiciclina indefinitamente en ciclos de tres meses. Hasta que sea necesario.
tiene mejorías con empeoramientos, pero la doctora dice que es una reacción normal.
Mas adelante os esplicaré con exactitumbre todas las sintomatologia que tiene.
Otra noticia muy importante que quiero compartir es que hemos hecho la prueba a nuestras hijas d 2 y 6 años y han resultado ambas positivas. La enfermedad de Lyme contrariamente a lo que dichen los medicos es congenita!!
Estamos ahora a la espera de hablar el jueves con su pediatra del Niño Jesús de Madrid para conocer el tratamiento que quiera ponerles.
seguiré pasando informaciónes y detalles.
un saludo a todos. Matteo.
Enviado desde Correo Yahoo! La bandeja de entrada más inteligente.
Abstract: DESCRIPTION (provided by applicant): Lyme disease, caused by the spirochete Borrelia burgdorferi, is the most common tick-borne infection in the United States with more than 20,000 cases reported annually since 2002. Of the available strategies to prevent Lyme disease, only vaccination with a recombinant outer surface protein A and antibiotic chemoprophylaxis of Ixodes scapularis tick bites with single-dose doxycycline have been shown to decrease the incidence of human cases. However, the Lyme vaccine is no longer marketed. In June 2003, authorities from the United States Public Health Services at the Centers for Disease Control and Prevention suggested that single-dose doxycycline be considered as an option for the prevention of Lyme disease after an I. scapularis tick bite (Hayes EB, Piesman J. How can we prevent Lyme disease. N Engl J Med 2003 June 12:348:2424-30). A practical limitation of using doxycycline is that the drug is not available over-the-counter; an antibiotic prescription is required and the medication must be obtained within 72 hours of tick removal for the treatment to be effective. In addition, doxycycline is only recommended for patients bitten by I. scapularis ticks that are engorged with blood, an assessment that requires skill and can only be done if the tick has been saved and is relatively intact. Further, doxycycline is contraindicated in young children and pregnant or lactating women. A variety of topical antimicrobials are in wide general usage for treatment of common conditions. These preparations are well accepted and safe. An animal study demonstrated that application of certain topical antimicrobial preparations was highly efficacious in preventing disseminated Borrelia burgdorferi infection after a tick bite, but unfortunately this study did not test antibiotic formulations approved for use on humans. The purpose of the current proposal is to investigate the efficacy of a topical antibiotic preparation suitable for use in humans in a mouse model. If successful, these studies would have highly relevant public health implications and should result in future human trials to test the efficacy and safety of topical antimicrobial therapy in patients at risk for Lyme disease after an Ixodes scapularis tick bite.
Public Health Relevance: This Public Health Relevance is not available.
Thesaurus Terms:
There are no thesaurus terms on file for this project.
Institution:
NEW YORK MEDICAL COLLEGE
ADMINISTRATION BUILDING
VALHALLA, NY 10595
Fiscal Year:
2007
Department:
MEDICINE
Project Start:
01-SEP-2006
Project End:
31-AUG-2008
ICD:
NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
Abstract: DESCRIPTION (provided by applicant): Lyme disease, caused by the spirochete Borrelia burgdorferi, is the most common tick-borne infection in the United States with more than 20,000 cases reported annually since 2002. Of the available strategies to prevent Lyme disease, only vaccination with a recombinant outer surface protein A and antibiotic chemoprophylaxis of Ixodes scapularis tick bites with single-dose doxycycline have been shown to decrease the incidence of human cases. However, the Lyme vaccine is no longer marketed. In June 2003, authorities from the United States Public Health Services at the Centers for Disease Control and Prevention suggested that single-dose doxycycline be considered as an option for the prevention of Lyme disease after an I. scapularis tick bite (Hayes EB, Piesman J. How can we prevent Lyme disease. N Engl J Med 2003 June 12:348:2424-30). A practical limitation of using doxycycline is that the drug is not available over-the-counter; an antibiotic prescription is required and the medication must be obtained within 72 hours of tick removal for the treatment to be effective. In addition, doxycycline is only recommended for patients bitten by I. scapularis ticks that are engorged with blood, an assessment that requires skill and can only be done if the tick has been saved and is relatively intact. Further, doxycycline is contraindicated in young children and pregnant or lactating women. A variety of topical antimicrobials are in wide general usage for treatment of common conditions. These preparations are well accepted and safe. An animal study demonstrated that application of certain topical antimicrobial preparations was highly efficacious in preventing disseminated Borrelia burgdorferi infection after a tick bite, but unfortunately this study did not test antibiotic formulations approved for use on humans. The purpose of the current proposal is to investigate the efficacy of a topical antibiotic preparation suitable for use in humans in a mouse model. If successful, these studies would have highly relevant public health implications and should result in future human trials to test the efficacy and safety of topical antimicrobial therapy in patients at risk for Lyme disease after an Ixodes scapularis tick bite.
Public Health Relevance: This Public Health Relevance is not available.
Thesaurus Terms:
There are no thesaurus terms on file for this project.
Institution:
NEW YORK MEDICAL COLLEGE
ADMINISTRATION BUILDING
VALHALLA, NY 10595
Fiscal Year:
2007
Department:
MEDICINE
Project Start:
01-SEP-2006
Project End:
31-AUG-2008
ICD:
NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
perdonarme la larga ausencia, pero he seguido leyendo todos los mensajes que me han parecidos muy interesantes.
Tengo muchas cosas que contar, buena y menos buenas, de todos modos muy importantes.
en primer lugar raquel sigue sin un diagnostico definitivo porque los dos ultimos analisis han resultados negativos, pero la doctora que la sigue, que por cierto es muy profesional, ha decidido según el consejo de un especialista de LA Rioja, de darle doxiciclina indefinitamente en ciclos de tres meses. Hasta que sea necesario.
tiene mejorías con empeoramientos, pero la doctora dice que es una reacción normal.
Mas adelante os esplicaré con exactitumbre todas las sintomatologia que tiene.
Otra noticia muy importante que quiero compartir es que hemos hecho la prueba a nuestras hijas d 2 y 6 años y han resultado ambas positivas. La enfermedad de Lyme contrariamente a lo que dichen los medicos es congenita!!
Estamos ahora a la espera de hablar el jueves con su pediatra del Niño Jesús de Madrid para conocer el tratamiento que quiera ponerles.
seguiré pasando informaciónes y detalles.
un saludo a todos. Matteo.
Enviado desde Correo Yahoo! La bandeja de entrada más inteligente.
Lyme disease : a diagnostic and treatment dilemma : hearing before the Committee on Labor and Human Resources, United States Senate, One Hundred Third Congress, first session, on examining the adequacy of current diagnostic measures and research activities in the prevention and treatment of lyme disease, August 5, 1993 (1993)
Author: United States. Congress. Senate. Committee on Labor and Human Resources Digitizing Sponsor: Kahle/Austin Foundation and Omidyar Network
[Non-text portions of this message have been removed]
One moves to the suburbs to afford one’s family a better, healthier life. So thought science journalist (and DISCOVER editor) Pamela Weintraub when she, her husband, and their two sons left New York City for the woods of Chappaqua in Westchester County, New York. Instead, what would ensue was a blight—upon their home, their lives, their sanity. The culprit: Lyme disease, a too-often misdiagnosed, mistreated, and misunderstood illness. Cure Unknown details one family’s courageous efforts to be diagnosed and treated in the face of heated controversy over the nature of their disease. Weintraub deftly weaves top-notch research and reporting on this malevolent infection, caused by the bite of a common deer tick, with the personal narrative of a family’s encounters with ignorance and bias while fighting a tenacious, disabling illness. The result is a compelling read that is also important journalism. With an estimated 200,000 new cases each year, the Lyme disease epidemic deserves our attention, and Cure Unknown is poised to become the definitive guide to understanding this illness.
Voy a ver con mi médico que voy a ver dentro de algunos dias, hablaré con él, y si no es posible veré con una farmacia on-line (que esta en los EEUU) y que envia primaquina a Inglaterra donde tengo amigos.
Que opinais del uso de primaquina para matar a las formas hepaticas de la babesia? Hace tanto tiempo que tomo todas las otras cosas que matan a las formas eritrocitarias, pero el momento cuando paro el tratamiento vuelven los sintomas. Ya me canzé de estar siempre tomando todas las ....quinas y todas las arte.....s, funcionan pero parece que tendré que tomarlas mi vida entiera!
Subject: Re: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Gracias, en Francia se necesita una autorisacion especial, y solo es para gente que tienen malaria.
Se la vienden en varias farmacias on-line pero a) no estoy segura de sus productos o b) no quieren enviar nada a Francia porque siempre tienen problemas cuandoquieren importar cualquier cosa a Francia.
Subject: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut.. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot.. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation.. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner.. Each patient must be treated individually.
Subject: Re: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Gracias, en Francia se necesita una autorisacion especial, y solo es para gente que tienen malaria.
Se la vienden en varias farmacias on-line pero a) no estoy segura de sus productos o b) no quieren enviar nada a Francia porque siempre tienen problemas cuandoquieren importar cualquier cosa a Francia.
Subject: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut.. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot.. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation.. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner.. Each patient must be treated individually.
Gracias, en Francia se necesita una autorisacion especial, y solo es para gente que tienen malaria.
Se la vienden en varias farmacias on-line pero a) no estoy segura de sus productos o b) no quieren enviar nada a Francia porque siempre tienen problemas cuandoquieren importar cualquier cosa a Francia.
Subject: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut.. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot.. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation.. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner.. Each patient must be treated individually.
Lyme Disease Spread by Ticks Now Drug Resistant Published 05.06.2008, 09.01 (updated 05.06.2008, 10.08)
It's long been known that ticks spread lyme disease. Research now, however, shows that bacteria from ticks can be immune to antibiotics. Thousands of lyme disease cases are reported in Finland each year.
Researchers say the lyme disease bloodsucking ticks spread, can also conceal itself in the body. This means that people who have already been treated for the disease can start showing symptoms of the malady again.
Professor Matti Viljanen at the University of Turku says in mice, lyme disease can stay hidden away in joint tissue.
These findings in mice mean new, more effective treatment methods can be developed -- such as combining different antibiotics.
"A vaccine for lyme disease is in the works, and could become available in four to five years," says Seppo Meri a professor at the University of Helsinki.
High, grassy areas are a favourite breeding ground for ticks. Researchers say that the lyme disease these blood sucking pests spread, is also good at concealing itself in the body. This means that people who have already been treated for the disease can start showing symptoms of the malady again.
Professor Matti Viljanen at the University of Turku says in mice, lyme disease can stay hidden away in joint tissue.
These findings in mice mean new, more effective treatment methods can be developed -- such as combining different antibiotics.
Seppo Meri a professor at the University of Helsinki says a vaccine for lyme disease is in the works, and could become available in four to five years.
Long Sleeves a Key Precaution
When it comes to guarding against the louse, vigilant inspections of both one's skin and clothing are key. Pets should also not be let into bed in summertime. Ticks for example love to nestle dog fur.
The good news is that lyme disease doesn't spread all too easily to humans. For lyme disease to set in, the tick must be attached to the skin for at least 24 hours. In fact, only one bite out of fifty results in the disease spreading, says Meri.
A few thousand cases of lyme disease are reported in Finland each year -- in the majority of these cases antibiotics do the trick, especially if proper treatment is sought early on.
Cutting-Edge Research in the Fight Against Lyme Disease National Non-Profit Funds Innovative Research
New York, New York (June 4, 2008) – Turn the Corner Foundation (TTC) has announced its 2008 grant recipients. These cutting-edge research projects will have a monumental impact in regard to treatment and diagnosis of Lyme disease. All grant recipients' research will support research, education, awareness and innovative treatments for Lyme disease and other tick-borne diseases, which is TTC's mission.
Under Our Skin This film is the first feature-length documentary that reveals the untold story of Lyme disease. Under Our Skin investigates the shocking human, medical, and political dimensions of this disease. TTC has entered into this strategic partnership because this film has the potential to reach hundreds of thousands of people and it will further TTC's vision of education and awareness of the physical, emotional, and social effects of Lyme disease.
Cheryl Koopman, Ph.D. Stanford University in Stanford, CA This research project will focus on treatment studies for various classes of Lyme patients. It is unique because it includes subjects who have a clinical diagnosis of Lyme disease but have tested negative using standard criteria. These types of patients are often excluded from Lyme disease research. This study will determine if these types of patients require treatment approaches different from today's conventions.
This research is critical because Lyme disease is notorious for false negatives, resulting in patients that are told they do not need treatment. In reality, these patients are sick and deserve a treatment approach tailored to their needs.
Eva Sapi, Ph.D. University of New Haven in West Haven, CT One study aims to identify whether or not deer ticks carry nematodes (microscopic worms) in order to develop more focused treatment for patients infected by tick bites. The second study explores Borrelia burgdorferi, the bacterial agent of Lyme disease, is capable of forming a complex covering called biofilm and if this biofilm increases its resistance to antibiotic treatment.
Alan MacDonald, M.D. St. Catherine of Siena Medical Center in Smithtown, NY This study will explore if a Borrelia burgdorferi infection is the cause of neurodegenerative diseases, such as Alzheimer's disease. It will also seek to discover the role of biofilms in Borrelia infections.
Raphael B. Stricker, M.D. San Francisco, CA This study focuses on reviewing the effectiveness of IV antibiotic treatment for Lyme disease. In studying various doses given at different intervals, doctors will be able to determine the best course of treatment for patients requiring antibiotics. This study is one of the first analyses of the safety and efficacy of true long-term IV antibiotic therapy for neurologic Lyme disease.
Lyme Literacy Programs for Doctors and Patients National TTC also allocates funds for public relations efforts, support groups and educational conferences focused on Lyme disease, projects that increase awareness and further education of this devastating disease. TTC is proud to continue the Physicians Training Program, which provides medical practitioners the opportunity to study with a Lyme-literate health care professional. Through this experience, participants develop the skills necessary to properly diagnose and treat Lyme disease. The Lyme Educational Awareness Development Series (LEADS) was created by TTC to enable community members to host their own educational event on Lyme disease and raise money for a cause that has meaning to them.
Turn the Corner Foundation is a not-for-profit public charity recognized by the IRS under 501 (c) (3). If you are interested in learning more about TTC or applying for a grant, please email your request to info@turnthecorner.org. If you would like to make a donation to TTC to ensure continued funding to these programs, please visit our website at http://www.turnthecorner.org/.
Subject: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut.. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner.. Each patient must be treated individually.
No tan mal como he sido, sino que no consiguo tomar el tini "Miguel fashion". I take it more like "on demand" aproximamente una semana cada mes. Y siempre tengo el dolor de cabeza del infierno cada dia 4.
Ahora tomo doxy 200 y roxy 300 y tambien tomo muchas cosas naturales Ginkgo, extracto de semillas de pomelos (dos cosas que no podia soportar antes), tomo un monton de cosas segun Wheldon/Stratton de cpn. Tomo NAC, ALA, fish oil, tocotrienols, CoQ10, multivits etc
hace un año que ne me hé tenido ni un resfriado. Pienso que no me acuerdo haber pasado un invierno sin tener algo viral.
Ah, si tambien tomo 0,75mg de levothyrox.
Hoy hablé con the international Pharmacy and they don't sell to America, and in Europe they only send to the UK and to Switzerland. Tienen muchas cosas.
Subject: Re: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Debe ser por las lluvias y el aumento de la humedad ambiental (esto ya parece Asturias), pero aunque he sufrido una caida importante del INR muy por debajo de mi margen de seguridad, no he tenido ningún problema. Parece ser que con el tini estoy bien protegido como ya sospechaba, cosa que por cierto el anticoagulante no conseguía.
Lo que me está dando ahora cada 4 días son ciáticas, pero por lo demás sigo bastante bien. ¿Y tú que tal?
pero no sé si me la recibiria sin problemas aqui en Françia. Jacques esta an los EEUU ahora mismo pero vuelve dentro de 3 dias, va a ser demasiado tarde para que la manden a su hotel. Quiero probar Primaquina desde hace muy largo tiempo para ver si puedo parar el lariam definitivamente.
Lo de la heparina sublingual lo lei en CFSFMExperimental, la persona usa la misma heparina que la que se inyectaba previamente.
Como estas, Miguel?
Mi dolor de cabeza ya paso (era un dolor del dia 4 del tini)
Subject: Re: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hola Nelly,
Lo he mirado en el vademecun y no aparece ningún producto con primaquina, así que seguro que no está disponible en las Farmacias españolas.
A mí los primeros meses de inyectarme heparina me hicieron un gran efecto, mi hematóloga me dijo que nunca se había encontrado con ningún otro paciente con tan buena disposición a pincharse en la tripa ¿Donde estaría esa heparina sublingual cuando me hacía falta? Sin embargo más recientemente cuando he tenido que volver a inyectarmela no he sentido ninguna mejoría en absoluto.
Subject: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut.. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot.. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation.. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner.. Each patient must be treated individually.
Debe ser por las lluvias y el aumento de la humedad ambiental (esto ya parece Asturias), pero aunque he sufrido una caida importante del INR muy por debajo de mi margen de seguridad, no he tenido ningún problema. Parece ser que con el tini estoy bien protegido como ya sospechaba, cosa que por cierto el anticoagulante no conseguía.
Lo que me está dando ahora cada 4 días son ciáticas, pero por lo demás sigo bastante bien. ¿Y tú que tal?
pero no sé si me la recibiria sin problemas aqui en Françia. Jacques esta an los EEUU ahora mismo pero vuelve dentro de 3 dias, va a ser demasiado tarde para que la manden a su hotel. Quiero probar Primaquina desde hace muy largo tiempo para ver si puedo parar el lariam definitivamente.
Lo de la heparina sublingual lo lei en CFSFMExperimental, la persona usa la misma heparina que la que se inyectaba previamente.
Como estas, Miguel?
Mi dolor de cabeza ya paso (era un dolor del dia 4 del tini)
Subject: Re: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hola Nelly,
Lo he mirado en el vademecun y no aparece ningún producto con primaquina, así que seguro que no está disponible en las Farmacias españolas.
A mí los primeros meses de inyectarme heparina me hicieron un gran efecto, mi hematóloga me dijo que nunca se había encontrado con ningún otro paciente con tan buena disposición a pincharse en la tripa ¿Donde estaría esa heparina sublingual cuando me hacía falta? Sin embargo más recientemente cuando he tenido que volver a inyectarmela no he sentido ninguna mejoría en absoluto.
Subject: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut.. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot.. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation.. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner.. Each patient must be treated individually.
pero no sé si me la recibiria sin problemas aqui en Françia. Jacques esta an los EEUU ahora mismo pero vuelve dentro de 3 dias, va a ser demasiado tarde para que la manden a su hotel. Quiero probar Primaquina desde hace muy largo tiempo para ver si puedo parar el lariam definitivamente.
Lo de la heparina sublingual lo lei en CFSFMExperimental, la persona usa la misma heparina que la que se inyectaba previamente.
Como estas, Miguel?
Mi dolor de cabeza ya paso (era un dolor del dia 4 del tini)
Subject: Re: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hola Nelly,
Lo he mirado en el vademecun y no aparece ningún producto con primaquina, así que seguro que no está disponible en las Farmacias españolas.
A mí los primeros meses de inyectarme heparina me hicieron un gran efecto, mi hematóloga me dijo que nunca se había encontrado con ningún otro paciente con tan buena disposición a pincharse en la tripa ¿Donde estaría esa heparina sublingual cuando me hacía falta? Sin embargo más recientemente cuando he tenido que volver a inyectarmela no he sentido ninguna mejoría en absoluto.
Subject: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut.. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot.. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation.. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner.. Each patient must be treated individually.
The widely held perception is that Lyme disease is a minor, nagging illness that is easily treated and cured with 14 to 30 days of antibiotics. When an individual complains of persistent illness, they are often told that the symptoms are psychosomatic or are caused by an autoimmune condition for which there is no cure. Transmission is deemed to occur solely by the bite of a tick infected with a spirochete bacteria called Borrelia burgdorferi, which is spread by deer, birds, and rodents. The conventional view holds that the disease is isolated to rural regions of the northeastern United States.
And yet others are calling Lyme disease a countrywide epidemic of major proportions, which is accruing billions of dollars in medical costs, long-term disability expenses, and lost wages. They insist that this debilitating disease has destroyed lives and in some cases has been fatal; a disease that one prominent Lyme physician called "more scary than a terrorist attack" in that it is so difficult to detect and so debilitating. They question why so many physicians are dismissing Lyme patients, denying them treatment, and accusing them of contributing to "Lyme hysteria." Those on this side of this issue claim there is substantial information supporting the existence of chronic infection in long-term sufferers. They believe that the controversy is not just medical, but rather one driven by insurance companies and politics.
Many wonder why the Center of Disease Control (CDC)-by its own admission-systematically underreports Lyme disease and contradicts aggressive treatment. According to the CDC, Lyme borreliosis is the number one vector-borne disease in the country. Statistics from the CDC indicate that there were over 23,000 cases reported in 2005. However, they acknowledge major underreporting, perhaps 10 times higher than their official estimate. In other words, there are almost 250,000 new cases a year and 2 million people in the United States suffering from chronic Lyme disease. Based on the discrepancy between their own clinical findings and that of the CDC, many researchers theorize that Lyme disease rates may be up to 100 times higher than the official CDC numbers. Although Lyme disease occurs predominantly in the northeast, cases have been documented in every state, with a large number of new infections occurring along the West Coast. To further complicate matters, the ticks that transmit Lyme also carry other bacteria, and these co-infections appear to be as complex as Lyme-and as difficult to diagnose and treat.
Animal studies have shown that in less than a week, the Lyme spirochete can deeply embed itself inside tendons, muscles, tissues, the heart, and the brain. The spirochetes can travel through blood-vessel walls and connective tissue. Complicating diagnosis, the symptoms of Lyme disease are many and can vary from one person to the next. The spirochete that causes Lyme appears to target the central nervous system. Flu-like symptoms, including fever, aches and pains, and extreme fatigue are common.
Rheumatological symptoms such as achy joints and inflammation can arise and seem also to be neuropathic in origin. Symptoms also include debilitating headaches, confusion, severe mood changes, hallucinations, paranoia, paralysis and, cognitive dysfunction resulting from encephalopathy. In some cases, what has been thought to be a severe psychiatric disorder has later turned out to be Lyme. Cardiac problems and even heart blocks have been documented. Indeed, Lyme disease and its complications have resulted in death and miscarriages in a number of cases.
There is general agreement that most cases are mild to moderate if treated promptly. But therein lies a problem. As of yet, there are no reliable tests for Lyme disease. Fewer than 50% of patients diagnosed with Lyme ever find the offending tick or telltale bull's eye rash. Available blood tests yield a high percentage of false negatives due to the crafty nature of the spirochete, which is able to change into a dormant, undetectable cyst form, or hide within white blood cells, the very cells that are supposed to destroy invading bacteria. Further, new research shows that the bacteria are able to exchange genetic material with one another and change the outer proteins of its cell walls, allowing the organisms to mutate and effectively hide from targeted human antibodies. The situation is complicated by the fact that there are over 300 strains of the bacteria that cause Lyme disease, and the test kits used by most labs don't detect all of these varieties. This results in thousands of false negative Lyme tests, delaying the treatment of many infected patients.
Lyme disease has been called the new "great imitator" because of its ability to mimic other diseases. Patients are routinely told they might have multiple sclerosis, Lou Gehrig's disease, fibromyalgia, systemic Lupus, Alzheimer's, chronic fatigue syndrome or rheumatoid arthritis. According to one physician, there is not one diagnostic feature of Lyme disease, except for the rash, that is different from any of these other conditions.
The illness can become so debilitating that previously healthy individuals cannot get out of bed and are confined to wheelchairs. Unable to work and faced with rising medical bills, many find themselves bankrupt. They become isolated, depressed, and even suicidal. While the spirochete itself is said to create depressive symptoms by invading brain cells, the toxins they emit if and when they do die-off also have been shown to trigger depression and suicidal tendencies. In many cases the psychological toll of Lyme is as devastating as the physical toll.
Children are particularly susceptible to Lyme disease by virtue of the amount of time they spend outdoors, and because of their still-growing immune systems. Often, when the cognitive symptoms manifest themselves, affected children are misdiagnosed by parents, physicians, and teachers as having learning disabilities, anxieties or behavioral problems. Some become so sick they cannot attend school or participate in sports, resulting in tremendous social and emotional costs.
There are also controversies surrounding the transmission of Lyme disease. All would agree that the blacklegged tick and the Western blacklegged tick are the primary vectors of the disease. These small ticks, no bigger than a poppy seed in their larval and nymphal stages, feed by piercing the skin of a host with their mouthparts and releasing the bacteria into the bloodstream. Some studies suggest that other insects may also transmit Lyme. Many believe that human-to-human contact is contributing to this epidemic. One physician's caseload includes hundreds of children whom he believes were infected while in utero or while breastfeeding. Lyme disease may be transmittable via blood transfusions, and sexual transmission has not been ruled out.
Though physicians in Europe described a Lyme-like disease as early as the mid-nineteenth century, many wonder why the disease has spread so rapidly in the U.S. since the late 1970's. One widely supported explanation is linked to the proliferation of deer, the adult tick's preferred host. In what were once farmlands, reforestation and residential developments are bringing the deer closer to humans. A single deer can carry hundreds of female ticks, each which can lay as many as 3,000 eggs. At the same time, there are few if any natural predators to cull the deer, and hunting is prohibited in many residential areas.
While it is the story of an elusive microorganism, Lyme disease is ultimately a human story. What do the untold numbers of ill patients do, after having journeyed from doctor to doctor, been misdiagnosed or told to see a psychiatrist? Often, they end up seeing one of the approximately 15 "Lyme literate" doctors in the country. These doctors spend an enormous amount of time with their patients and rely more on symptoms rather than test results to make a Lyme diagnosis. And though they acknowledge that there are risks to administering antibiotics, they believe that the physical, cognitive, and functional consequences of untreated Lyme disease warrant the risk. They claim that that those physicians who deny their patients treatment are being medically negligent. They point out that the spirochete that causes Lyme disease is in the same family as the bacteria that causes syphilis and is known to be able to hide out and then reappear, causing severe neurological illness. They explain that the immune evasion strategy of B. burgdorferi is reminiscent of mycobacterial infections such as tuberculosis or leprosy, diseases where months, not days, of antibiotics are required for a cure.
The academic physicians on the other side of the controversy claim that their evidence-based research shows that long-term antibiotics provide no more relief to chronically ill patients than placebos. They recommend that patients with persistent symptoms be given antidepressants, steroids, or pain medication to treat individual symptoms. What's more, they feel that over-prescribing antibiotics might lead to the growth of more drug-resistant strains of bacteria, an omnipresent concern in this era of bioterror threats and global epidemics.
The Lyme-literate physicians dispute the findings of the academics' pivotal chronic Lyme study (commonly referred to as "the Klempner study"). They say that their clinical experiences contradict the conclusions of this study, crying foul at the experimental design, subject selection, and conclusions of Klempner's research.
By prescribing long-term antibiotic treatment, the Lyme-literate physicians open themselves up to a political and medical firestorm. Because published Lyme treatment guidelines recommend only 14 to 30 days of antibiotics, many of these physicians have been dropped by insurance providers and have come under investigation from state licensing boards for prescribing too many antibiotics. Many believe that the insurance companies are trying to put these doctors out of business to reduce the high cost of treating chronic Lyme patients. Some call this "medical McCarthy-ism," as the insurance companies hire their own medical consultants to review patient files and reverse Lyme diagnoses without ever directly examining patients. One could certainly wonder, are the medical boards protecting the medical insurance industry or the patients they are supposed to be serving? And what happens to the patients whose treating doctors are no longer willing to do so? As the political battles rage on, all too often patients are left in a void, without medical insurance or doctors to address their physical and mental decline.
The politics of the Lyme controversy have led some to governmental action. In Rhode Island, a law was passed this past summer that mandates coverage for long-term antibiotics for the treatment of Lyme when ordered by a physician. In New York, where a disproportionate number of Lyme doctors have been investigated and prosecuted by the state medical board, a bill intended to address this was just vetoed by the governor. And New York, Massachusetts, and Connecticut have held recently held public hearings on the controversy. At the federal level, there has been outrage at the limited funding and attention this disease has received from both the NIH and CDC, and questions loom as to what motivates this apparent negligence. On the other side, mainstream Lyme experts decry what they see as mass hysteria and possible hypochondriasis, with false positives churned out by a few suspect laboratories. All the while, Lyme sufferers watch the disease sweep the country by stealth, threatening the nation's health and safety, and affecting untold lives. UNDER OUR SKIN exposes these lives, their struggles, and the tiny, relentless bug under their skin.
Lo he mirado en el vademecun y no aparece ningún producto con primaquina, así que seguro que no está disponible en las Farmacias españolas.
A mí los primeros meses de inyectarme heparina me hicieron un gran efecto, mi hematóloga me dijo que nunca se había encontrado con ningún otro paciente con tan buena disposición a pincharse en la tripa ¿Donde estaría esa heparina sublingual cuando me hacía falta? Sin embargo más recientemente cuando he tenido que volver a inyectarmela no he sentido ninguna mejoría en absoluto.
Subject: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut.. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner.. Each patient must be treated individually.
Subject: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut.. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner.. Each patient must be treated individually.
Subject: [Lyme-E] Hypercoagulation and chronic disease (Lyme)
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut.. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner. Each patient must be treated individually.
Hypercoagulation means thickened blood. Research from the late 1990s reveals that many patients with chronic disease may have an underlying coagulation defect contributing to their symptoms. While few doctors are familiar with this condition, understanding the theory behind it can help explain many symptoms. Treatment based on this theory can lead to improvement and even recovery.
David Berg of Hemex Laboratories has been studying the hypercoagulation often found in patients with chronic disease. This list currently includes CFS/FMS, myofascial pain syndrome, osteonecrosis of the jaw, fetal loss, multiple sclerosis, Crohn�s disease, Sjogren's syndrome, IBS, Lyme disease, autism, gulf war illness and ADD.
Thick blood is the result of fibrin being deposited in the small blood vessels. Fibrin formation is the last step in the clotting process that stops bleeding when blood vessels are cut. Normally, long strands of fibrin weave a mesh around platelets and blood cells to form a clot that plugs the break in the wall of a vessel.
A very complex series of reactions activates the clotting process. The release of thrombin ultimately results in the production of a substance called soluble fibrin monomer (SFM). SFM is a sticky protein that increases blood viscosity (thickness) and results in the deposit of fibrin on the endothelial cells lining the blood vessels. Normally, a single burst of thrombin would generate a large amount of SFM that would produce strands of "cross linked" fibrin, resulting in an actual clot. However, in CFS/FMS and other chronic conditions, continuous generation of low levels of thrombin can occur. The result is hypercoagulation.
There are at least three possible causes or contributing factors:
Virii, bacteria, mycoplasmas, and/or parasites activate certain antibodies in the immune system that trigger the production of thrombin, generate SFM and result in fibrin deposits. Genetic coagulation defects can lead to hypercoagulation. White people are susceptible to this and black people have a resistance to it. Chemical exposure can result in changes that trigger the coagulation process. The results of this thickened blood are: When fibrin coats the walls of the capillaries, nutrient and oxygen delivery to muscle, nerve, bone and organ tissue is compromised. The fibrin coating the capillaries and producing thick blood can make virii and bacteria less accessible to treatment. Thicker blood is harder to pump. By depriving the gut of proper nourishment, hypercoagulation may be a major factor in IBS. If the bowel is deprived of blood, cells will die too rapidly. The endothelial cells lining the capillaries are the source of heparans, the body's natural blood thinners. When fibrin coats these cells, the heparans cannot be released, reducing the body's ability to dissolve the fibrin. Hypercoagulation can be detected by Hemex Laboratories' ISAC (Immune System Activation of Coagulation) test panel. Five substances are measured, and abnormal results on any two are considered a positive test result. A standard coagulation work up usually will not detect any abnormalities, since it only assesses the risk of actual clotting. The ISAC panel is 10 to 20 times more sensitive, as well as being more expensive.
In a 1998 study, heparin was given to 7 FMS and 9 CFS patients suffering from hypercoagulation. Of the 7 FMS patients, 1 reported some, 3 moderate, and 3 significant improvement. Of the 9 CFS patients, 4 reported moderate and 5 significant improvement.
Since then, David Berg has learned that the best chance of success involves treating both the hypercoagulation and the underlying pathogen(s). Ideally, a blood thinner such as heparin is prescribed one month before beginning antibiotics for bacteria (for example mycoplasma or chlamydia pneumonia) and/or transfer factor for viruses (such as HHV6, CMV and EBV). The heparin is continued throughout, and then slightly beyond, the course of anti-microbial treatment. It dissolves the fibrin, making the virus and/or bacteria more vulnerable, thus improving the treatment's effectiveness.
CFS/FMS patients who have been ill for more than ten years may show only one abnormality - or possibly none - on the ISAC test. A trial of heparin, however, especially if accompanied by antibiotics or transfer factor, may change that. Berg suspects that once a pathogen has a large area of fibrin deposits in which to settle, the less active it needs to be. It may therefore stop triggering the coagulation process. As the heparin removes the fibrin and allows a more effective attack against the pathogens, they reactivate and/or become more active, once again triggering the coagulation process. Most patients have more abnormalities on the ISAC test one month into treatment than on their initial test, indicating progress. They often must pass through a time of increased illness when the infection is temporarily activated.
The treatment of this condition is not easy or inexpensive. It requires a doctor who is familiar with the theory, comfortable with the lab testing and willing to individualize treatment.
Hypercoagulation (Thickened Blood) can lead to: Immunity Chronic Fatigue / Fibromyalgia Syndrome Studies show that 79-92% of CFS/FMS patients have a hypercoagulation defect.
Infections Lyme Disease
Mental Autism
Recommendations and treatments for Hypercoagulation (Thickened Blood): Animal-based Heparin Heparin or another anticoagulant may be used as the primary blood thinner. Each patient must be treated individually.
June 9, 2008 -- A virulent strain of Lyme disease germ is spreading in the U.S. and in Europe, a new study shows.
It's not a new strain of Borrelia burgdorferi, the spirochete or spiral-shaped bacterium that causes Lyme disease. In fact, it was one of the first strains ever identified -- found in the cerebrospinal fluid of a patient with severe Lyme meningitis.
But now Wei-Gang Qiu, PhD, Benjamin Luft, MD, and colleagues find that the particularly nasty ospC type A strain appears to be the most common of the 20 or so B. burgdorferi strains found in the U.S. The spread of this virulent strain, they suggest, could be part of the reason for the increase in Lyme disease cases seen over the past two decades.
"OspC type A is the type most widely distributed in the U.S. -- and, as others have shown, this is the most virulent strain," Qiu, an assistant professor at New York's Hunter College, tells WebMD. "If this is widespread, it is not good. You don't want to see this thing increase."
Luft, professor of medicine and former chief of infectious diseases at SUNY Stony Brook, says the spread of the ospC type A strain may explain part of the U.S. Lyme disease epidemic.
"Perhaps part of the Lyme disease story is not that B. burgdorferi just emerged in the 1970s, but that this group of strains that cause more disease became more dominant in our environment," Luft tells WebMD. "So instead of people getting infected with less virulent strains, they got infected with a more virulent strain and got more disease."
Qiu and Luft note that the rise of a more virulent Lyme spirochete isn't the whole story. People get the infection from the bite of a deer tick. As suburbs encroach on rural areas, and as more homes are built near forests, more people are at risk of tick bites. Increased exposure to ticks accounts for most of the increase in Lyme disease.
Qiu and colleagues found that the ospC type A strain is the most widespread strain in the U.S. It's also widespread in Europe. That was a surprise, as Lyme disease spirochetes in Europe are spread by different ticks and harbored by different animal hosts than in the U.S.
"What is surprising is these ospC type A strains in the U.S. and in Europe are genetically almost identical," Qiu says. "So this type is quite unusual in its ability to colonize new habitats. ... This is very strong evidence for this type having a very broad ecological niche in terms of the species that can carry it."
"This means it went from one continent to another continent relatively recently," adds Luft. "And it means that, as Europe and U.S. have very different ecosystems, this strain is highly adaptable to new environments. ... This makes it a formidable foe -- and it causes significant disease."
It's not clear whether this bad Lyme germ traveled from North America to Europe or vice versa. And it's not clear when this happened, although it seems to have occurred in the last 200 years, possibly when a tick-infested bird crossed the Atlantic.
It's likely, Qiu says, that this strain will continue to become more prominent in areas where Lyme disease is established.
CDC medical epidemiologist Kevin Griffith, MD, MPH, says that while Lyme disease has been reported in nearly every state, 10 mostly Northeastern states account for 92% of cases.
Although the 20,000 cases reported to the CDC in 2006 were fewer than the 23,000 cases reported in 2005, Griffith says the true number of cases is probably larger.
"There is probably a true increase in the number of cases," Griffith tells WebMD.
The good news, he says, is that there's been a drop in the most severe, late-stage manifestations of Lyme disease. He attributes this to doctors identifying the disease -- and beginning treatment -- sooner now than in the earlier years of the epidemic.
Qiu and colleagues report their findings in the July issue of the CDC's Emerging Infectious Diseases.
While some doctors treat Lyme disease, others hide behind "there is no chronic beast," even though the documentation "in their own" publications show there is latent and chronic disease. Yet, they deny its existence.
Why has it become so controversial?
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IDSA, et al – Con$cience=Scientific Fraud
by Dottie L. Heffron
While some doctors treat Lyme disease, others hide behind “there is no chronic beast,” even though the documentation “in their own” publications show there is latent and chronic disease.Yet, they deny its existence.
Why has it become so controversial?
Allen Steere, of Tufts University who has been said to discover Lyme disease, wanted to keep the grant funding in Rheumatology, redefining the disease as only a LATE arthritis in a knee.
There have been millions of dollars in grant monies and donations raised to continue research. Together with others they spun a web of fraud and deceit about the disease at the CDC’s Dearborn, MI, Conference in 1994.
It is very important for all of us to understand what transpired at the Dearborn Conference.Labs from across the U.S. were invited to this conference participate in the proceeding to assess Allen Steeres’ new proposal where Lyme would no longer be considered a Relapsing Fever organism (diagnosed by sequential Western blots to look for new and expanding IgM antibodies, which was Steeres’ first proposal),but should only be diagnosed serologically as a late autoimmune arthritis in a knee.
We wonder how could anyone use this criteria to assess vaccines outcomes - a test that only detects 15% of all cases?That clearly means 85% of all cases of vaccine failure will not be detected.
Mr. Wormser is assessing Allen Steeres’ IgG recommendation for the CDC to adopt, and that it was no good, yet it was adopted by the CDC anyway. Just who approved this standard, even though none of the laboratories agreed?
For Gary Wormser to report in the IDSA Guidelines that one has to have a positive test for Lyme means he has published scientific fraud. Similarly, the CDC says their testing for Lyme is “valid,” when it is hardly valid, if only 15% of the cases of Lyme are identified by the Steere IgG panel.
Imugen or Phil Molloy’s lab reported only 14% tested positive to the Steere criteria, which means 86% of all cases were missed.
The Lutheran Hospital in LaCrosse, Wisconsin said Steere’s proposal was 22%. This is it missed detecting 78% of all the known cases of Lyme.
The University of Connecticut’s Lawrence Zemel was referring to Lyme as comparable to juvenile rheumatoid arthritis. He recommended adding band 50 for all childrens’ blots.
The Roche Lab stated 28% were positive for 5 of 10 Steere IgG bands.
While Wadsworth had some different scoring system, it did not report on the accuracy of the Steere method.
MarDx Labs recommended adding bands 31 and 34, but were given CDC positive arthritis positive blood to falsely quality their test strips. Theirs were used in both vaccine trials.
The CDC Atlanta talked about mice, not humans. The mouse criteria were 2 out of 3 from OspC, 16 kD, 17.9 kD.
By showing the data at The Dearborn Conference it should make the reader understand the deceit and fraud that has been committed against mankind. It is not only inexcusable but so evil in its intent to destroy so many lives. One could only wonder if at one time they were good upstanding men and women, or just always driven by money, greed and power, not caring who they have hurt or destroyed in their wake.
Yale, Alan Barbour (a CDC officer) et al, are the owners of many patents on Lyme, and other methods of detection here in the U.S and abroad. Yale owns a patent for a scientifically valid Lyme test, but will not let anyone use it.
How can someone own a patent on a disease or method of detecting a disease? This is truly a conflict of interest. The very same people who are defining the diseases hold patents to make profits off of the sick by the selling of test kits. Why would they want us to get better when they can make more money off the sick and ailing?
The Blumenthal antitrust has opened the eyes of many. Some activists have been put into place by higher echelons to divide the Lyme community and keep them occupied with other trivial matters. Bills were written to fail by some activist groups to keep the diversion alive. Keeping the minion active doing trivial things is a tactic used by governments worldwide.In the antitrust, it simply asked the IDSA to disclose their organizational paperwork.
For two years, it went unanswered. Instead of disclosing their financial and vested interests, the IDSA chose to revamp their staunch 2006 guidelines. If they stood fast beside their own guidelines, why redo them? If they had nothing to protect, then why did they not just simply disclose this information? Even though they have not had one omission of guilt spring from their camp, revamping the guidelines says it all.
Now it is very well known, the scientific fraud and intent to do harm they have deployed on us.
As victims of their abuse, we can now seek retribution.
Barcelona- On May 21, 2008, after a year and a half of hard work, the Catalan CFS/ME and FMS associations reached their first big victory: a Parlamentary Resolution voted by unanimity to organize health services for people with these illnesses. This unanimous vote was only possible because the associations had gathered in 2007 almost 140,000 signatures as part of a Legislative Initiative (for which only 50,000 signatures were necessary).
The process has been a very hard one with, not only the signature gathering, but countless meetings with politicians, associations and organizations, writing documents, educating, press work, etc.
The negotiations with the goverment have been very, very rough, nasty and intense until the last minute. They were not going to accept the demands as a law but we managed to get them all accepted as a Resolution. A law would have been more binding but it would never have passed. This Parlamentary Resolution has the advantage of having been voted unanimously by all parlamentarians and with full press coverage (live on television on real time), which will make it harder for the goverment to back down.
It was an exciting day: the Legislative Promoting Commission (half a dozen of us from various CFS/ME and FMS associations who were leading this initiative) was in the Parlament and we presented our demands. That was followed by presentations by all the parlamentary groups and then the vote. And a standing ovation. Outside the Parlament Building there were almost a thousand people, mostly women with CFS/ME or FMS with sings, singing, cheering and celebrating.
These are the main points that the Resolution covers:
- The setting up 11 CFS/ME-FMS especialized units with three of them being research units also (right now there is one that is operating but it has a 3 year waiting list)
- These units will have multidisciplinary teams (internal medicine, rheumatology, neurology, etc and even pediatricians)
- Waiting lists cannot be longer than 90 days to access a unit (a big change from 3 years)
- Doctors will be trained about CFS/ME-FMS (international specialists will probably have to be invited for this)
- Medical inspectors will be trained on these illnesses
- The follow-up of the setting up of these services will be done by a joint committee in which patients' associations will be represented
Needless to say that the Catalan Minister of Health, Marina Geli, is not so happy about having to carry this out and she said so on the goverment's home page the same day it was voted in Parlament (this would require a long explanation about Catalonia, Spain, and many anthropological concepts...).
So, the associations are not taking a break nor taking the time to celebrate this victory because we know we cannot afford to slack. We have to keep a good watch on what the goverment is doing and not doing. So, we are back at work doing the following:
- Educating patients and their associations to all be watch-dogs and to report on the implementation of this resolution in their area: we are teaching people how to file proper complaints that can be used in a legal case if need be.
- Making sure that all patients know the content of the Resolution. To make this easier, we have written a song with all the main points to the tune of "Yes We Can" (thank you, Obama), so that people can remember it.
- Working with a law firm, Collectiu Ronda, to do a proper and constant follow-up and to gather evidence in case the resolution is not carried out properly. In that case, the law firm will do a colective law suit against the goverment.
- Going back to the press about how we are still on the "war path" until we make sure this Resolution is respected and carried out.
This last year and a half has been decisive for the CFS/ME-FMS movement in Catalonia:
- The associations have joined forces
- 140,000 people have been educated one by one, by our 150 signature gatherers
- Parlament has spent much time talking and arguing about the issue of services for CFS/ME-FMS (one parlamentarian told us that they had never talked so much about any issue before)
- The Catalan Health Deparment has been challenged like never before by civil society and they now know that we are a force to be reckoned with
- There has been an enormous rise in consciousness amongst people with CFS/ME-FMS in Catalonia
- We are a lot less invisible now!
- And we are on our way to getting proper health care services (although much work is still to be done).
We have had a lot of help and support from people, associations and experts in other countries and so to all of you we want to say a big GRACIAS!
You can see some of the photographs of May 21st on this web:
This is a private venue rental not sponsored by the Alamo Drafthouse, but tickets are available to the general public.
It's bigger than AIDS, West Nile Virus and Avian Flu combined, yet most physicians don't recognize it or are afraid to report it. Insurance companies pay experts to say it's all in your head. And the mainstream medical establishment won't want you to see this film.
One of the most misunderstood and controversial illnesses in the history of medicine, Lyme disease is among the fastest growing infectious diseases in the United States. Yet each year tens of thousands go undiagnosed or misdiagnosed with such conditions as fibromyalgia, chronic fatigue and even autism, MS and Alzheimer's. This groundbreaking documentary investigates the human, medical and political dimensions of Lyme disease, an emerging epidemic destroying countless numbers of lives. Following the stories of patients and physicians as they battle for their lives and livelihoods, the film brings into focus a haunting picture and its inabilty to cope with a growing terror under our skin.
Learn more about the film at the www.underourskin.com.
Learn more about the fight against Lyme disease at www.turnthecorner.org
Doors open at 12:00PM, screening to follow.
Admission is $10.
Kid Policy: All Ages will be allowed at all screenings of this show.
Screenings (click on a show time to buy tickets): . Saturday, July 26, 2008 . 12:00p
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