@ iiarjournals.org:
Immunological Similarities between Cancer and Chronic Fatigue Syndrome: The Common Link to Fatigue?
MIRA MEEUS 1 ,2 , WILHELM MISTIAEN 1, LUC LAMBRECHT 3 ,4 and JO NIJS 1 ,2
Author Affiliations
* 1Division of Musculoskeletal Physiotherapy, Department of Health Sciences, Artesis University College Antwerp (AHA), Antwerp
* 2Department of Human Physiology, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel (VUB), Brussel
* 3Private Practice for Internal Medicine, Ghent & Aalst;
* 4CVS Contactgroep, Belgium
* Correspondence to: Jo Nijs, Artesis Hogeschool Antwerpen (AHA), Department of Health Sciences, Division of Musculoskeletal Physiotherapy, Van Aertselaerstraat 31, 2170 Merksem, Belgium. Tel: +32 36418205, e-mail: jo.nijs@vub.ac.be
or jo.nijs@artesis.be
Abstract
Cancer and chronic fatigue syndrome (CFS) are both characterised by fatigue and severe disability. Besides fatigue, certain aspects of immune dysfunctions appear to be present in both illnesses. In this regard, a literature review of overlapping immune dysfunctions in CFS and cancer is provided. Special emphasis is given to the relationship between immune dysfunctions and fatigue.
Abnormalities in ribonuclease (RNase) L and hyperactivation of nuclear factor kappa beta (NF-κB) are present in CFS and in prostate cancer. Malfunctioning of natural killer (NK) cells has long been recognised as an important factor in the development and reoccurrence of cancer, and has been documented repeatedly in CFS patients.
The dysregulation of the RNase L pathway, hyperactive NF-κB leading to disturbed apoptotic mechanisms and oxidative stress or excessive nitric oxide, and low NK activity may play a role in the two diseases and in the physiopathology of the common symptom fatigue. However, in cancer the relation between the immune dysfunctions and fatigue has been poorly studied.
Immunological abnormalities to such as a dysregulated RNase L pathway, hyperactive NF-κB, increased oxidative stress and reduced NK cytotoxicity, among others, are present in both diseases. These anomalies may be part of the physiopathology of some of the common complaints, such as fatigue. Further studies to confirm the hypotheses given here are warranted.
Doctor Speedy and ME in search of medical honesty
Showing posts with label Cancer. Show all posts
Showing posts with label Cancer. Show all posts
Sunday, July 5, 2015
Monday, February 23, 2015
Prof Edward Shorter and the psychic epidemic of ignoring clinical evidence
A phenomenon well familiar to historians of medicine is the psychic epidemic of ignoring clinical evidence by psychiatrists and medical historians, a belief that spreads epidemically, until the evidence become so overwhelming that it becomes clear that these people have been telling porkies for decades, and then their nonsense is forgotten.
In the 20th century, psychiatry fostered such an epidemic with the belief that ego masturbation caused their bank accounts to inflate. Many medical historians and psychiatrists obsessed for years over the thought that their “self-abuse” had pleased their bank managers.
Another epidemic focused on the toxic effects of ignoring clinical evidence on the ovaries. Many male medical historians and male psychiatrists would plead for ovariectomies, on the grounds that their irritated ovaries were blocking clinical evidence which their penis had spotted, to go all the way to their brain. And that this was leading to erectile dysfunction and the inability to have an orgasm.
Once their ovaries were removed, their penis size increased by more than 5 inches. So all these male medical historians and male psychiatrists were pleading their doctors for ovariectomies.
In the late 1980s the belief spread epidemically that reading clinical evidence caused irreversible brain damage, and a number of leading medical historians and psychiatrists wrote books full of advice about eating small meals upside down, with your eyes closed and your brain in hibernation mode, to make sure that clinical evidence would not reach your brain to prevent brain damage.
I realize that these words will fall unreceptively upon some ears, and I regret that some medical historians and psychiatrists, especially from Toronto, may feel slighted by the clinical evidence that is readily available, if only they where willing to turn on their computer and were willing to read biomedical research, for example the fMRI studies from Stanford, or the PET scan study from Japan.
Yet there are larger stakes here. In the way that lives were once ruined with such toxic diagnoses as hysteria, which in this day and age is called MS, millions of lives today are ruined by medical historians and pinocchio psychiatrists who have made a fortune out of ignoring clinical evidence.
Many psychiatrists and medical historians choose their profession so that they didn't have to become productive members of the community. (The IOM report dwelled upon the dangers of severely ill patients being abused by the medical profession.)
Such a waste of human potential is tragic, and if there are lessons that we may draw from the history of medicine, it is that doctors who discover the underlying metabolic problem or cause of such diseases, which medical historians and psychiatrists call psychosomatic, even though they do not have any evidence to back up this claim, will go on to win the Nobel prize for medicine, as the Nobel Prize winner in medicine, Dr Barry Marshall stated a few years ago.
In the 20th century, psychiatry fostered such an epidemic with the belief that ego masturbation caused their bank accounts to inflate. Many medical historians and psychiatrists obsessed for years over the thought that their “self-abuse” had pleased their bank managers.
Another epidemic focused on the toxic effects of ignoring clinical evidence on the ovaries. Many male medical historians and male psychiatrists would plead for ovariectomies, on the grounds that their irritated ovaries were blocking clinical evidence which their penis had spotted, to go all the way to their brain. And that this was leading to erectile dysfunction and the inability to have an orgasm.
Once their ovaries were removed, their penis size increased by more than 5 inches. So all these male medical historians and male psychiatrists were pleading their doctors for ovariectomies.
In the late 1980s the belief spread epidemically that reading clinical evidence caused irreversible brain damage, and a number of leading medical historians and psychiatrists wrote books full of advice about eating small meals upside down, with your eyes closed and your brain in hibernation mode, to make sure that clinical evidence would not reach your brain to prevent brain damage.
I realize that these words will fall unreceptively upon some ears, and I regret that some medical historians and psychiatrists, especially from Toronto, may feel slighted by the clinical evidence that is readily available, if only they where willing to turn on their computer and were willing to read biomedical research, for example the fMRI studies from Stanford, or the PET scan study from Japan.
Yet there are larger stakes here. In the way that lives were once ruined with such toxic diagnoses as hysteria, which in this day and age is called MS, millions of lives today are ruined by medical historians and pinocchio psychiatrists who have made a fortune out of ignoring clinical evidence.
Many psychiatrists and medical historians choose their profession so that they didn't have to become productive members of the community. (The IOM report dwelled upon the dangers of severely ill patients being abused by the medical profession.)
Such a waste of human potential is tragic, and if there are lessons that we may draw from the history of medicine, it is that doctors who discover the underlying metabolic problem or cause of such diseases, which medical historians and psychiatrists call psychosomatic, even though they do not have any evidence to back up this claim, will go on to win the Nobel prize for medicine, as the Nobel Prize winner in medicine, Dr Barry Marshall stated a few years ago.
Tuesday, February 10, 2015
IOM: psychiatrists beliefs are wrong, ME/CFS is a "serious, complex, multisystem disease"
By Miriam E. Tucker, February 10, 2015:
"The illness that has been called "chronic fatigue syndrome" (CFS) in the United States and "myalgic encephalomyelitis" (ME) elsewhere is a "serious, complex, multisystem disease" that physicians need to view as "real" and diagnose, the Institute of Medicine (IOM) says in a new 235-page report."
#########
The etiology is unknown, but evidence of biological disease has been mounting for the last several years.
#########
According to Dr Rowe, "It was a unanimous committee report.... It was interesting for us who are clinicians in the field to see how obvious the direction of the evidence was for those who are scientists, but not specialists in this area." < br >
#########
"the condition's hallmark defining symptom, postexertional malaise, the report proposes a new name be adopted, "systemic exertion intolerance disease (SEID),"
#########
"It's time to stop saying that this is a just figment of people's imagination. This is a real disease, with real physical manifestations that need to be identified and cared for," Committee Chair Ellen Wright Clayton, MD, JD, professor of pediatrics and director of the Center for Biomedical Ethics and Society at Vanderbilt University, Nashville, Tennessee, told"Medscape Medical News".
##########
In particular, the panel found sufficient evidence linking the illness to immune dysfunction, especially diminished natural killer cell function, and infection, particularly Epstein-Barr virus.
#########
She added, "The level of response is much more than would be seen with deconditioning," with reference to the belief voiced by some clinicians that physical abnormalities in these patients are merely a result of their lack of activity. Indeed, Dr Rowe noted, "That argument is untenable with people who have been physically active, some of them athletes, [before becoming ill]. The deconditioning argument is flawed in that respect."
"The illness that has been called "chronic fatigue syndrome" (CFS) in the United States and "myalgic encephalomyelitis" (ME) elsewhere is a "serious, complex, multisystem disease" that physicians need to view as "real" and diagnose, the Institute of Medicine (IOM) says in a new 235-page report."
#########
The etiology is unknown, but evidence of biological disease has been mounting for the last several years.
#########
According to Dr Rowe, "It was a unanimous committee report.... It was interesting for us who are clinicians in the field to see how obvious the direction of the evidence was for those who are scientists, but not specialists in this area." < br >
#########
"the condition's hallmark defining symptom, postexertional malaise, the report proposes a new name be adopted, "systemic exertion intolerance disease (SEID),"
#########
"It's time to stop saying that this is a just figment of people's imagination. This is a real disease, with real physical manifestations that need to be identified and cared for," Committee Chair Ellen Wright Clayton, MD, JD, professor of pediatrics and director of the Center for Biomedical Ethics and Society at Vanderbilt University, Nashville, Tennessee, told"Medscape Medical News".
##########
In particular, the panel found sufficient evidence linking the illness to immune dysfunction, especially diminished natural killer cell function, and infection, particularly Epstein-Barr virus.
#########
She added, "The level of response is much more than would be seen with deconditioning," with reference to the belief voiced by some clinicians that physical abnormalities in these patients are merely a result of their lack of activity. Indeed, Dr Rowe noted, "That argument is untenable with people who have been physically active, some of them athletes, [before becoming ill]. The deconditioning argument is flawed in that respect."
Friday, December 2, 2011
Low-dose interleukin-2 safe and effective in treating immune-mediated diseases
By Todd Neale, Senior Staff Writer, MedPage Today:
Published: November 30, 2011
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Action Points
Low-dose interleukin-2 immunotherapy appears to be safe and effective in treating two immune-mediated diseases, hepatitis C virus (HCV)-induced vasculitis and chronic graft-versus-host disease (GVHD).
Interleukin-2 increased the proportion of regulatory T cells (Tregs) in patients with hepatitis C virus (HCV)-induced vasculitis and in those with chronic graft-versus-host disease.
Low-dose interleukin-2 immunotherapy appears to be safe and effective in treating two immune-mediated diseases, two small, uncontrolled studies showed.
In the first study, David Klatzmann, MD, PhD, of Pierre and Marie Curie University in Paris, and colleagues found that interleukin-2 increased the proportion of regulatory T cells (Tregs) in all 10 patients with hepatitis C virus (HCV)-induced vasculitis and improved symptoms of vasculitis in eight, with few side effects.
In the second study, John Koreth, MBBS, DPhil, of the Dana-Farber Cancer Institute in Boston, and colleagues found that the treatment induced partial responses in about half of patients with chronic graft-versus-host disease (GVHD), with no cases of relapse or progression of the disease.
The results of both studies -- which were reported in the Dec. 1 issue of the New England Journal of Medicine -- "signal a major shift in the therapeutic use of interleukin-2," according to Jeffrey Bluestone, PhD, of the University of California San Francisco.
Overall, the treatment appeared to be safe, but the long-term effects are uncertain, he wrote in an accompanying editorial.
"Thus, these articles and others have provided a path forward for the effective use of interleukin-2 as a regulatory immunotherapy," he concluded. "Future trials involving larger numbers of patients and appropriate control groups are needed to determine the efficacy of not only interleukin-2 therapy but also other approaches to improving Treg numbers and function in autoimmune diseases and GVHD and inhibiting them in cancer."
Klatzmann and colleagues examined whether interleukin-2 could be used to treat patients with vasculitis induced by HCV that does not respond to standard antiviral therapy, rituximab (Rituxan), or both. Interleukin-2 is approved for use as an adjunctive treatment for renal cell carcinoma. It promotes survival and function of Treg cells, which inhibit immune responses.
The study included 10 patients with mixed cryoglobulinemic vasculitis who were not receiving glucocorticoid or immunosuppressant therapy (median age 58.5).
The patients received one course of interleukin-2 at 1.5 million IU per day for five days, followed by three five-day courses of 3 million IU/day at weeks three, six, and nine.
By week nine, there was a significant increase in the proportion of CD4+ T cells that were Tregs -- from 3.6% to 11.8% (P=0.004). That improvement met the primary endpoint of at least a 4% absolute increase.
Nine of the 10 patients also had a reduction in cryoglobulinemia, eight patients saw an improvement in vasculitis, and there was an overall reduction in the expression of genes related to inflammation and oxidative stress.
The treatment appeared to be safe, with no adverse events higher than grade 1 and no significant changes in circulating levels of granulocytes, red cells, or liver enzymes.
In addition, the treatment did not increase the numbers of effector T cells or induce vasculitis flare or increased HCV viremia.
"Further studies are needed to determine whether this intervention could be further modified and whether it would also be effective in the treatment of other inflammatory and autoimmune diseases, such as atherosclerosis or type 1 diabetes," Klatzmann and colleagues concluded.
Koreth and colleagues evaluated interleukin-2 as a treatment option for patients with chronic GVHD, which develops in more than half of patients who have undergone allogeneic hematopoietic stem cell transplantation.
The study included 29 patients (median age 49.5) whose disease did not respond to systemic glucocorticoid therapy.
For eight weeks, patients received daily, low-dose subcutaneous interleukin-2 -- escalating from 300,000 IU per square meter of body-surface area to 1 million IU, then to 3 million IU, if tolerated. The highest dose, however, ...
Published: November 30, 2011
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planner
Action Points
Low-dose interleukin-2 immunotherapy appears to be safe and effective in treating two immune-mediated diseases, hepatitis C virus (HCV)-induced vasculitis and chronic graft-versus-host disease (GVHD).
Interleukin-2 increased the proportion of regulatory T cells (Tregs) in patients with hepatitis C virus (HCV)-induced vasculitis and in those with chronic graft-versus-host disease.
Low-dose interleukin-2 immunotherapy appears to be safe and effective in treating two immune-mediated diseases, two small, uncontrolled studies showed.
In the first study, David Klatzmann, MD, PhD, of Pierre and Marie Curie University in Paris, and colleagues found that interleukin-2 increased the proportion of regulatory T cells (Tregs) in all 10 patients with hepatitis C virus (HCV)-induced vasculitis and improved symptoms of vasculitis in eight, with few side effects.
In the second study, John Koreth, MBBS, DPhil, of the Dana-Farber Cancer Institute in Boston, and colleagues found that the treatment induced partial responses in about half of patients with chronic graft-versus-host disease (GVHD), with no cases of relapse or progression of the disease.
The results of both studies -- which were reported in the Dec. 1 issue of the New England Journal of Medicine -- "signal a major shift in the therapeutic use of interleukin-2," according to Jeffrey Bluestone, PhD, of the University of California San Francisco.
Overall, the treatment appeared to be safe, but the long-term effects are uncertain, he wrote in an accompanying editorial.
"Thus, these articles and others have provided a path forward for the effective use of interleukin-2 as a regulatory immunotherapy," he concluded. "Future trials involving larger numbers of patients and appropriate control groups are needed to determine the efficacy of not only interleukin-2 therapy but also other approaches to improving Treg numbers and function in autoimmune diseases and GVHD and inhibiting them in cancer."
Klatzmann and colleagues examined whether interleukin-2 could be used to treat patients with vasculitis induced by HCV that does not respond to standard antiviral therapy, rituximab (Rituxan), or both. Interleukin-2 is approved for use as an adjunctive treatment for renal cell carcinoma. It promotes survival and function of Treg cells, which inhibit immune responses.
The study included 10 patients with mixed cryoglobulinemic vasculitis who were not receiving glucocorticoid or immunosuppressant therapy (median age 58.5).
The patients received one course of interleukin-2 at 1.5 million IU per day for five days, followed by three five-day courses of 3 million IU/day at weeks three, six, and nine.
By week nine, there was a significant increase in the proportion of CD4+ T cells that were Tregs -- from 3.6% to 11.8% (P=0.004). That improvement met the primary endpoint of at least a 4% absolute increase.
Nine of the 10 patients also had a reduction in cryoglobulinemia, eight patients saw an improvement in vasculitis, and there was an overall reduction in the expression of genes related to inflammation and oxidative stress.
The treatment appeared to be safe, with no adverse events higher than grade 1 and no significant changes in circulating levels of granulocytes, red cells, or liver enzymes.
In addition, the treatment did not increase the numbers of effector T cells or induce vasculitis flare or increased HCV viremia.
"Further studies are needed to determine whether this intervention could be further modified and whether it would also be effective in the treatment of other inflammatory and autoimmune diseases, such as atherosclerosis or type 1 diabetes," Klatzmann and colleagues concluded.
Koreth and colleagues evaluated interleukin-2 as a treatment option for patients with chronic GVHD, which develops in more than half of patients who have undergone allogeneic hematopoietic stem cell transplantation.
The study included 29 patients (median age 49.5) whose disease did not respond to systemic glucocorticoid therapy.
For eight weeks, patients received daily, low-dose subcutaneous interleukin-2 -- escalating from 300,000 IU per square meter of body-surface area to 1 million IU, then to 3 million IU, if tolerated. The highest dose, however, ...
Monday, November 14, 2011
Girl, 13, left in 'waking coma' and sleeps for 23 hours a day after severe reaction to cervical cancer jab
A schoolgirl has been left in a 'waking coma', too tired even to open her eyes, after having a cervical cancer injection. Lucy Hinks, 13, started displaying flu-like symptoms soon after her second, booster, injection in November 2010.
After her third shot, in May this year, Lucy began to experience extreme exhaustion. Her health has deteriorated so badly that for the past seven weeks she has slept for up to 23 hours day. Lucy is also unable to walk or even talk to her devastated family.
Today, her mother Pauline and father Steve, a tyre plant worker, reveal the stress and trauma their family are enduring and their fears that it could be years before she recovers. They now care for Lucy around the clock in what they have describe as a 'living nightmare'.
The couple, from Port Carlisle, Cumbria, are urging parents to find out about the potential side effects of the vaccine, Cervarix. Their warning comes as thousands of year eight pupils prepare to receive the vaccine in schools.
Lucy had her first cervical cancer injection, alongside her classmates, in October last year, a month later she had the second jab of a three injection immunisation. It was then that she started to display flu-like symptoms and joint pain.
Lucy made several visits to her doctor over the Christmas period. It was only after her final HPV injection, in May, that the teenager began to suffer from extreme exhaustion. Read more>>
Wednesday, November 2, 2011
University of Hawaii: theoretical justification for using Rituximab in ME and CFS
Most of the issues raised by Van der Meer and colleagues have been kindly addressed by Prof Jonathan Edwards and Prof Olav Mella.
There is however one thing I would like to add.
Van der Meer and colleagues start off by saying that "The finding of Fluge et al [1] that B lymphocyte depletion the anti-CD20 monoclonal antibody, Rituximab (RTX) has beneficial effects in patients with chronic fatigue syndrome is astonishing, particularly since they do not present any theoretical justification for using RTX."
As we all know, many discoveries in medicine are actually made by accident. We are treating one problem, and by accident, find out that the treatment works for something else. A famous example is the discovery that Viagra didn't work very well for hypertension but works really well for erectile dysfunction. As Prof Mella has described, they were treating a patient with lymphoma with Rituximab and then discovered that it works very well for chronic fatigue syndrome or Myalgic Encephalomyelitis as well. With these sort of accidental findings, the theoretical justification can only be sought afterwards obviously.
People who are familiar with ME or CFS as some want to call it, know that there are almost 5000 research papers showing all sorts of physical abnormalities in this very disabling disease. Most of these abnormalities centre around the mitochondria, immune dysfunction and ongoing viral infections.
A recent study by Yabusaki and colleagues from the University of Hawaii showed that 95% of ME/CFS Patients have Anticardiolipin Antibodies, suggesting that ME/CFS may be an autoimmune condition. And they continued by giving the following theoretical justification for using Rituximab in ME/CFS:
"As a possible autoimmune disease, CFS patients may be treated by suppression of the ACA or by diminishing the antigen CL in serum. Previous studies have shown that treatment with monoclonal antibodies to B cells reduces ACA levels to normal in patients with autoimmune disease, leading to clinical improvements.
Specifically, Rituximab, a chimeric monoclonal CD20 antibody, has been shown to normalize high ACA serum titers of patients with autoimmune systemic lupus erythematosus, rheumatoid arthritis, autoimmune thrombocytopenia, and autoimmune hemolytic anemia.
Rituximab may serve as an effective therapeutic agent for ameliorating the symptoms of CFS." (1).
References:
(1) Y. Hokama, C. Empey Campora, C. Hara, T. Kuribayashi,
D. Le Huynh, and K. Yabusaki, Anticardiolipin Antibodies in the Sera of Patients with Diagnosed
Chronic Fatigue Syndrome, Journal of Clinical Laboratory Analysis 23 : 210–212 (2009)
Competing interests declared: I am a Family Physician or GP as it is called in Australia or the UK. I am also an ME patient unfortunately. Bedbound that is. So at the moment I’m in private practice so to speak.
I have the following conflict of interest: I would like to get better and see that the wasting of public money on CBT (talk therapy for a neurological disease, really helpful) and other silly therapies for ME stops, and will be used in better ways.
Professor Carmen Scheibenbogen: Medical breakthrough in Chronic Fatigue Syndrome
“This is important news, especially for patients in Germany, as the situation that CFS patients encounter here is particularly bad”, she says.
Chronic fatigue syndrome (CFS) is a medical condition that is not well known, although it frequently occurs. It is said that 300.000 people in Germany suffer from it. Its symptoms are mental and physical exhaustion; sleep disorders, permanent fatigue, impaired concentration and memory, joint- and muscle pains, a flu-like sore throat and headaches. The condition worsens after exertions. In a severe clinical course, the patient becomes unable to work and can hardly leave his bed. Owing to its non-specific symptoms, CFS is hard to diagnose, and is often regarded as a mental ailment.
Two thirds of patients improved
A new patient study from Haukeland University Hospital in Bergen, Norway, now verifies that the syndrome involves a physical dysfunction for which there is a promising treatment. In the study, CFS patients were treated with the anti-cancer agent rituximab and observed for twelve months. Rituximab was developed for use in chemotherapy for lymph gland cancer, as it incapacitates B cells in the lymphatic system. Two thirds of the CFS patients reported an improved health condition, whereas only 13 per cent of the patients in the placebo control group reported amelioration. A total of 30 randomly selected patients took part in the study. Neither the patients nor the physicians knew whether treatment took place with rituximab or with a placebo. Haukeland University Hospital is currently preparing a second study on a larger scale.
Professor Carmen Scheibenbogen, Deputy Director of the Institute of Medical Immunology at the Charité University Hospital in Berlin, describes the results of the CFS study as a “breakthrough”: “This is a very important first step. For the first time, a therapeutic study has been conducted with medication that was originally applied to the immune system, and which proved effective for a majority of the patients”, she says. The internist has been head of the Immunodeficiency Outpatient Clinic at Charité University Hospital for four years. Every fourth patient there suffers from chronic fatigue syndrome. Patients who deal with severe infections often come to the Immunodeficiency Outpatient Clinic. “Patients with CFS frequently have more infections,” Scheibenbogen says. “CFS usually starts with an infection. We also find immunodeficiencies more often in patients with CFS. That is why they come to us.”
Physicians do not feel responsibility
Professor Scheibenbogen and her staff at Charité, hold a unique position and have extensive experience and knowledge about CFS. “The situation for CFS patients is disadvantageous compared to other illnesses. In Germany, there are no physicians who feel responsibility for this; if anyone does, they are most likely psychiatrists. There are no centres, at the universities, for example, where the staff has experience with CFS patients and in dealing with the illness. Even in large clinics, there is no consultation for CFS patients. There are no specialists who are well-versed in this topic. What we do here at the Immunodeficiency Outpatient Clinic is an exception.”
“The treatment of many CFS patients is merely symptom-oriented”, says Scheibenbogen. Pains or sleep disorders are treated, nothing more. At her clinic, treatment goes beyond that. “We try to assess the immunodeficiency. We believe that for many patients, a chronic infection triggers these symptoms, and we attempt to treat that infection specifically.”
“We have not seen anything comparable to this”
Haukeland University Hospital’s study also applies to the immune system. The B cells that are attacked by the anti-cancer agent rituximab play an important role in immunoregulation. “Rituximab has many effects”, explains Scheibenbogen. “We know that it temporarily incapacitates a portion of B cells. But we do not know exactly what this means in regard to the cause of chronic fatigue syndrome.” From her point of view, there are two options. “One option would be that it involves an autoimmune disease in which the immune system is triggered by an infection, to which it responds exaggeratedly or wrongly. Autoimmune diseases can be treated by removing the B cells. The other hypothesis is that the Epstein-Barr virus is a frequent trigger of this medical condition. The Epstein-Barr virus specifically affects B cells. If one destroys B cells, the Epstein-Barr virus’ reservoir is also removed. This is the hypothesis that we favour. Even if one cannot clarify the cause of CFS at the moment, it is decisive for patients and their treatment that rituximab is effective.”
Monday, October 31, 2011
Immunological Similarities between Cancer and Chronic Fatigue Syndrome
MIRA MEEUS1,2, WILHELM MISTIAEN1, LUC LAMBRECHT3,4 and JO NIJS1,2:
+ Author Affiliations
1Division of Musculoskeletal Physiotherapy, Department of Health Sciences, Artesis University College Antwerp (AHA), Antwerp
2Department of Human Physiology, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel (VUB), Brussel
3Private Practice for Internal Medicine, Ghent & Aalst;
4CVS Contactgroep, Belgium
Correspondence to: Jo Nijs, Artesis Hogeschool Antwerpen (AHA), Department of Health Sciences, Division of Musculoskeletal Physiotherapy, Van Aertselaerstraat 31, 2170 Merksem, Belgium. Tel: +32 36418205, e-mail: jo.nijs@vub.ac.be or jo.nijs@artesis.be
Abstract
Cancer and chronic fatigue syndrome (CFS) are both characterised by fatigue and severe disability. Besides fatigue, certain aspects of immune dysfunctions appear to be present in both illnesses. In this regard, a literature review of overlapping immune dysfunctions in CFS and cancer is provided. Special emphasis is given to the relationship between immune dysfunctions and fatigue. Abnormalities in ribonuclease (RNase) L and hyperactivation of nuclear factor kappa beta (NF-κB) are present in CFS and in prostate cancer. Malfunctioning of natural killer (NK) cells has long been recognised as an important factor in the development and reoccurrence of cancer, and has been documented repeatedly in CFS patients. The dysregulation of the RNase L pathway, hyperactive NF-κB leading to disturbed apoptotic mechanisms and oxidative stress or excessive nitric oxide, and low NK activity may play a role in the two diseases and in the physiopathology of the common symptom fatigue. However, in cancer the relation between the immune dysfunctions and fatigue has been poorly studied. Immunological abnormalities to such as a dysregulated RNase L pathway, hyperactive NF-κB, increased oxidative stress and reduced NK cytotoxicity, among others, are present in both diseases. These anomalies may be part of the physiopathology of some of the common complaints, such as fatigue. Further studies to confirm the hypotheses given here are warranted.
Thursday, October 27, 2011
Health insurance news - ME could be caused by immune system defect
Posted By Peter Jones on Tue 25th October 2011:
Health insurance customers who are diagnosed with myalgic encephalomyelitis (ME) or Chronic Fatigue Syndrome could be suffering with the illness because of an immune system defect, according to research.
The study, reported in PLoS One, suggested a faulty immune system could be to blame for the illness, as researchers found symptoms in some patients subsided after taking a cancer drug which inhibits the body's defence.
Doctors in Norway were alerted to the possibility of using immune system-inhibiting cancer drugs in 2004 when a patient with both Hodgkin's Lymphoma and ME was given the treatment and her fatigue syndrome improved for five months.
A total of 30 patients with ME were involved in the trial, which showed 67 per cent of the people receiving two doses of Rituximab - a cancer treatment - had their symptoms improve during the process.
Oncology consultant at the Haukeland University Hospital Oystein Fluge told BBC News that two of the patients had no recurrence of the symptoms and it completely changed their life around, while in others there was a varied response.
"I think the fact that patients responded to treatment, improved cognitive function, fatigue and pain makes us believe we're touching one of the central mechanisms," he added.
Dr Charles Shepherd, the UK ME Association's medical adviser said the results are very encouraging for people with the illness as the researchers seem to have confirmed that altering the immune system response could be an effective treatment for at least a small number of patients.
"They help to confirm that there is a significant abnormality in immune system function in this disease. We now need further clinical trials of such anti-cancer agents to see if other research groups can replicate these findings," he added.
According to the news provider, there are around 250,000 people in the UK that suffer from the illness and symptoms include extreme tiredness, problems with memory and concentration, as well as sleep disturbances.
Tuesday, October 25, 2011
Medscape: Cancer Drug Rituximab May Also Treat Chronic Fatigue Syndrome
October 24, 2011 — Researchers in Norway say they've been able to treat symptoms of chronic fatigue syndrome by giving patients a biologic drug that affects the immune system.
The drug, rituximab (Rituxan), works by depleting immune cells called B-cells. It is FDA approved to treat non-Hodgkin's lymphoma, chronic lymphocytic leukemia, rheumatoid arthritis, and two kinds of vasculitis.
For the study, researchers recruited 30 people with chronic fatigue syndrome (CFS). Half got two infusions of rituximab given two weeks apart. The other half got infusions of saline solution as a placebo.
Ten patients in the rituximab group (67%) and two patients in the placebo group (13%) saw at least moderate reductions in fatigue.
In most of the patients, improvements were transient and faded within eight to 44 weeks.
But three patients, two in the rituximab group and one that got the placebo, continue to be symptom free 2 1/2 years after their treatments. Those three patients have all returned to full-time jobs, researchers say.
The study is published in the journal PLoS One.
"Our thought is that in fact CFS is an autoimmune disease in most patients," says study researcher Olav Mella, MD, PhD, an oncologist at Haukeland University Hospital in Bergen, Norway.
Mella and his colleague, Oystein Fluge, MD, PhD, say they accidentally discovered that rituximab might help chronic fatigue syndrome after they used it to treat three patients who suffered from both CFS and non-Hodgkin's lymphoma. All three patients reported significant improvements in fatigue after rituximab infusions. They eventually relapsed and were given more doses of rituximab. All three again had improvements in their CFS, though those eventually faded.
Their cases were reported in BioMedCentral Neurology in 2009.
Is Chronic Fatigue Syndrome an Autoimmune Disease?
Researchers say they aren't sure why the drug is working.
"We cannot know for sure, but what we see is that there's a delay from the rapid B-cell depletion after rituximab treatment to the clinical response. The delay can be from three to perhaps eight months before the response is thought to occur," says Fluge, who is an oncologist and medical physicist at Haukeland Hospital.
B-cells are part of the immune system. They roam the body in relatively small numbers searching for foreign invaders. When a B-cell finds one, it springs into action, becoming an infection-fighting chemical factory.
In some diseases, like leukemia, B-cells may go haywire and cause cancer. In rheumatoid arthritis, B-cells may attack the body's own tissues.
In CFS, however, it's unclear why killing off B-cells might help.
One theory, ...
Monday, October 24, 2011
ME Association's medical adviser: We now need further clinical trials of anti-cancer agents in ME
Dr Charles Shepherd, the UK ME Association's medical adviser, said: "The results of this clinical trial are very encouraging news for people with ME.
"Firstly, they help to confirm that there is a significant abnormality in immune system function in this disease.
"Secondly, they indicate that altering the immune system response in ME could be an effective form of treatment for at least a subset of patients.
"We now need further clinical trials of such anti-cancer agents to see if other research groups can replicate these findings."
Thursday, October 20, 2011
How does Rituximab work ?
Rituximab works by destroying white blood cells that make antibodies. White blood cells are part of the immune system response and ME/CFS studies point to chronic activation of the immune system following an acute infection.
A clear or possible clinical infection preceding CFS onset could be identified in 73% and 67% of the patients in the Rituximab and placebo groups, respectively according to the authors, however, patients with ongoing infections were excluded from the trial.
Like all immune cells, white blood cells are created in the bone marrow. The NIAID reports, that at the heart of the immune system is the ability to distinguish between self and non-self. Immune cells and other cells in the body usually coexist peaceably in a state known as self-tolerance. In abnormal situations (such as an autoimmune disease), the immune system can wrongly identify self as non-self and execute a misdirected immune attack.
A limitation of this study is the lack of predetermined exact definitions of clinical response with respect to duration and extent of improvement. According to the authors, an alternative explanation for the observed clinical improvement from B-cell depletion could be elimination or reduction of B-lymphotrophic viruses such as cytomegalovirus (CMV) or Epstein-Barr virus (EBV).
Two new open-label phase-II studies in Norway (Study 1, Study 2) investigating Rituximab treatment with two infusions two weeks apart (as in the present study) followed by maintenance Rituximab infusions at 3, 6, 10 and 15 months, are being conducted to further explore this treatment principle in CFS (
The anti-cancer drug is also being investigated for treatment of rheumatoid arthritis, lupus/systemic lupus erythematosus, Sjogren’s syndrome multiple sclerosis, and Behcet’s disease.
Read more>>
See also: Cancer drug Rituximab/Rituxan-study in ME/CFS in PLoS ONE: major improvements in all symptoms in 67 % of patients
Friday, October 7, 2011
RIP Mr Apple
A family statement said: "In his public life, Steve was a visionary. In his private life, he cherished his family."
He also had another child Lisa Brennan-Jobs by a previous relationship with Chrisann Brennan. His complex family life means lawyers could struggle to split up his £5.4billion fortune.
The San Francisco-born guru was adopted as an infant after being given up by Syrian Abdulfattah Jandali and Joanne Simpson. It is said they did not want to raise him out of wedlock.
Jobs dropped out of university after just one term and saved money from his first computer job to go on a spiritual retreat to India.
He returned a shaven-headed Buddhist and admitted experimenting with mind-bending drug LSD.
In 2004 he was diagnosed with a rare form of pancreatic cancer. His health deteriorated rapidly in recent years and after two temporary leaves of absence he stepped down as CEO and became Apple chairman
He started the firm in the 1970s in the garage of parents Paul and Clara. Co-founder Steve Wozniak said he will "miss him as much as everyone".
The company went on to develop one of the first commercially successful lines of PCs. Its market value today is $350billion (£227billion). In August it briefly topped Exxon as the world's most valuable company.
Wednesday, October 5, 2011
Dr Snyderman: There is no other explanation for the improvement in my leukemia cell parameters, my cytokine signature and CFS symptoms than a retrovirus responding to anti-retroviral drugs
Michael Snyderman MD said...:
Missing the point and lost opportunities
This quote is for Jason who says it is all about science: “I began comparing Judy Mikovits to Joan of Arc,” Coffin says. “The scientists will burn her at the stake, but her faithful following will have her canonized.”
While we are talking about burning Dr.Mikovits at the stake we should look closer. First focusing on the Western Blot slide is of importance to Jason. As a physician for 40 years I understand disease processes but don’t understand Western Blots or the critical importance of these. I have known Dr. Mikovits for almost 2 years and cannot believe that she would commit fraud. Everyone but postdocs can make mistakes. Dr. Mikovits had nothing to gain as she already knew that she would be fired, even before the Ottawa conference. She was actually fired for “insolence.” She cares about the truth and cares for our suffering.
Jason isn’t alone in missing the point of her presentation. Go back and look at the slides. Look at the graph of my data. There is no explanation for the improvement in my leukemia cell parameters other than a retrovirus responding to anti-retroviral drugs. In addition, my cytokine signature and CFS symptoms improved. Two prominent retrovirologists have tried to explain these results as “selective toxicity” which is ludicrous. At present my blood samples are being analyzed at other laboratories able to do deep sequencing and integration studies.
Let us return to the issue of wasted money. First, remember that this awful disease has disabled millions of people and cost the economy many, many billions of dollars. You are very proud that you participated in research to prove that classical XMRV does not cause CFS. We have known that since Lo and Alter and Dr. Mikovits has been saying that for about a year now. We know XMRV doesn’t cause CFS and cancer but that other retroviruses do. So what have you and other scientists accomplished by spending time (and money) trying to disprove the role of a virus that probably does not exist outside of culture lines? I share Dr. Deckoff-Jones’ frustration. What have you ever done that will lead to diagnosis and treatment of this awful disease?
Michael Snyderman, M.D.
Thursday, September 22, 2011
XMRV / HTLV integrate into precisely the same nucleotides in infected humans and in vitro cell lines
V99, mecfsforums.com:
http://microb230.med.upenn.edu/PDF%20Library/18369476.pdf
Quote
HTLV-1 Integration into Transcriptionally Active Genomic Regions Is Associated with Proviral Expression and with HAM/TSP
Kiran N. Meekings1, Jeremy Leipzig2, Frederic D. Bushman2, Graham P. Taylor3, Charles R. M. Bangham1*
1 Department of Immunology, Wright-Fleming Institute, Imperial College London, London, United Kingdom, 2 Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America, 3 Department of Genitourinary Medicine and Communicable Diseases, Wright-Fleming Institute, Imperial College London, London, United Kingdom
Abstract
Human T-lymphotropic virus type 1 (HTLV-1) causes leukaemia or chronic inflammatory disease in ,5% of infected hosts. The level of proviral expression of HTLV-1 differs significantly among infected people, even at the same proviral load (proportion of infected mononuclear cells in the circulation). A high level of expression of the HTLV-1 provirus is associated with a high proviral load and a high risk of the inflammatory disease of the central nervous system known as HTLV-1- associated myelopathy/tropical spastic paraparesis (HAM/TSP). But the factors that control the rate of HTLV-1 proviral expression remain unknown. Here we show that proviral integration sites of HTLV-1 in vivo are not randomly distributed within the human genome but are associated with transcriptionally active regions. Comparison of proviral integration sites between individuals with high and low levels of proviral expression, and between provirus-expressing and provirus non- expressing cells from within an individual, demonstrated that frequent integration into transcription units was associated with an increased rate of proviral expression. An increased frequency of integration sites in transcription units in individuals with high proviral expression was also associated with the inflammatory disease HAM/TSP. By comparing the distribution of integration sites in human lymphocytes infected in short-term cell culture with those from persistent infection in vivo, we infer the action of two selective forces that shape the distribution of integration sites in vivo: positive selection for cells containing proviral integration sites in transcriptionally active regions of the genome, and negative selection against cells with proviral integration sites within transcription units.
Quote
Supporting Information
Figure S1 HTLV-1 integration in vivo and in vitro is identical at
the nucleotide level. Integration of HTLV-1 in vivo is indistinguishable
from that in vitro at the nucleotide level (in vitro data combined from the
co-culture sites obtained in this report and sites reported byDerse et al
MLVs and HTLV do the same - integrate into the same site!!!!
http://microb230.med.upenn.edu/PDF%20Library/18369476.pdf
Quote
HTLV-1 Integration into Transcriptionally Active Genomic Regions Is Associated with Proviral Expression and with HAM/TSP
Kiran N. Meekings1, Jeremy Leipzig2, Frederic D. Bushman2, Graham P. Taylor3, Charles R. M. Bangham1*
1 Department of Immunology, Wright-Fleming Institute, Imperial College London, London, United Kingdom, 2 Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, United States of America, 3 Department of Genitourinary Medicine and Communicable Diseases, Wright-Fleming Institute, Imperial College London, London, United Kingdom
Abstract
Human T-lymphotropic virus type 1 (HTLV-1) causes leukaemia or chronic inflammatory disease in ,5% of infected hosts. The level of proviral expression of HTLV-1 differs significantly among infected people, even at the same proviral load (proportion of infected mononuclear cells in the circulation). A high level of expression of the HTLV-1 provirus is associated with a high proviral load and a high risk of the inflammatory disease of the central nervous system known as HTLV-1- associated myelopathy/tropical spastic paraparesis (HAM/TSP). But the factors that control the rate of HTLV-1 proviral expression remain unknown. Here we show that proviral integration sites of HTLV-1 in vivo are not randomly distributed within the human genome but are associated with transcriptionally active regions. Comparison of proviral integration sites between individuals with high and low levels of proviral expression, and between provirus-expressing and provirus non- expressing cells from within an individual, demonstrated that frequent integration into transcription units was associated with an increased rate of proviral expression. An increased frequency of integration sites in transcription units in individuals with high proviral expression was also associated with the inflammatory disease HAM/TSP. By comparing the distribution of integration sites in human lymphocytes infected in short-term cell culture with those from persistent infection in vivo, we infer the action of two selective forces that shape the distribution of integration sites in vivo: positive selection for cells containing proviral integration sites in transcriptionally active regions of the genome, and negative selection against cells with proviral integration sites within transcription units.
Quote
Supporting Information
Figure S1 HTLV-1 integration in vivo and in vitro is identical at
the nucleotide level. Integration of HTLV-1 in vivo is indistinguishable
from that in vitro at the nucleotide level (in vitro data combined from the
co-culture sites obtained in this report and sites reported byDerse et al
MLVs and HTLV do the same - integrate into the same site!!!!
Dr Robert H. Silverman: XMRV is contamination
Alice Rusmevichientong1, Jaydip Das Gupta2, Petra S. Elias1, Robert H. Silverman2, and Samson A. Chow1,*:
1 Department of Molecular and Medical Pharmacology, and UCLA AIDS Institute, UCLA School of Medicine, Los Angeles, California 90095 2 Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195 *
Corresponding author. Mailing address: Department of Molecular and Medical Pharmacology, UCLA School of Medicine, CHS 23-133, 605 Charles E. Young Dr. South, Los Angeles, CA 90095, USA. Tel: (310) 825-9600. Fax: (310) 825-6267.
E-mail: schow@mednet.ucla.edu
ABSTRACT We analyzed xenotropic murine leukemia virus-related virus (XMRV) integration site sequences previously identified from human prostate tissues for single nucleotide polymorphisms (SNPs) to discriminate between patient and potential cell line sources of the proviruses. The SNPs of two integration sites were identical to those in cell lines but not the patients, whereas the data on the remaining 12 integration sites were inconclusive. Our results provide direct evidence for contamination during analysis of XMRV integration sites.
See also: XMRV / HTLV integrate into precisely the same nucleotides in infected humans and in vitro cell lines
Friday, September 16, 2011
The brave doctors that risk treating us are ridiculed and scoffed at by their colleagues
Posted by Marzi:
All over the world there are stories of people who suffer with this illness, but because we do not fit in the neat little boxes designed to make doctors feel smart and safe, we are treated like hypochondriacs.
Imagine having HIV before anyone knew what it was. Imagine feeling this rotten wrong thing wrapping tendrils round your system. Imagine going to the hospital, telling them your diagnosis and watching their body language change and their tone lower to condescension. You know it’s biological, you know it is not psychosomatic, you know there is something rotten inside you, but they just look at you dismissively and talk quietly with the nurse about discharging you with some paracetamol.
As you become more outraged at their treatment of you, you are so ill, so tired, in so much pain, you cry and raise your voice in frustration. They nod to you and steal glances with each other, you are only reinforcing their belief it’s all in your head. Can you imagine living like that? Needing help and treatment, yet unable to seek it for fear you will be intentionally misinterpreted and maligned?
That is what it is to have our diagnosis. That is why we say we would rather have Cancer or HIV or other politically incorrect things. Not because we don’t understand the gravity of those illnesses, having experienced what we have we would never doubt nor underestimate the suffering of others. No it is because those illnesses have treatment, awareness, options, research, support, and statistics on survival or death. People look at me incredulously when I say I would rather have most any other life threatening illness. But if you were to walk in my shoes, you would understand.
There is no certainty, but I can fight against that; there is no treatment, but I can pray for one, but to have people treat you like a hypochondriac while you suffer so much quietly against all hope… that is too much. I would rather know the likelihood of my death, than to have to fight not only this insidious illness, but with the very people who have been entrusted with the job of treating me, and yet instead they shake their heads and dismiss my suffering because I refuse to fit into their neat little boxes. And the irony of all ironies, those few brave doctors that risk treating us, specialising in the treatment of our illness, face the same treatment metered out to us by their colleagues. They too are ridiculed and scoffed at. The rare doctor that can think laterally and ... Read more>>
Wednesday, September 7, 2011
Nurse and Admin sacked from ATOS ...
THE NEW REPUBLIC :
Nurse Debbie Carr and admin worker Anthony Treasure are seeing life from the benefit scrounging scum perspective this evening, following their sacking from Atos Healthcare.
The pair were discovered on Facebook calling the sick and disabled “down and outs” and “parasitic wankers”.
The incidents were widely reported in the mainstream press and came shortly before the Government's de-benefitting boot-boys attempted to shut up a bunch of whining cripples by sending them threatening letters.
See also: 3 more assessed "fit for work" by ATOS die
Sunday, September 4, 2011
e-petition: stop unfair re-assessments for disabled people
stop unfair re-assessments for disabled people
Responsible department: Department for Work and Pensions
Stop the unfair and cruel re-assessments via ATOS for disabled people currently on Incapacity Benefit.
ESA is a flawed benefit, and puts terrible pressure and stress on vulnerable people, putting people who cannot work on lesser benefits and applying sanctions.
Source:
http://epetitions.direct.gov.uk/petitions/9834
Sunday, August 14, 2011
Atos doctors could be struck off
Daniel Boffey, policy editor
guardian.co.uk, Saturday 13 August 2011:
Twelve doctors employed by the firm that is paid £100m a year to assess people claiming disability benefit are under investigation by the General Medical Council over allegations of improper conduct.
The doctors, who work for Atos Healthcare, a French-owned company recently criticised by MPs for its practices, face being struck off if they are found not to have put the care of patients first.
The Observer has found that seven of the doctors have been under investigation for more than seven months. The other five were placed under investigation this year following complaints about their conduct.
It is understood that the majority of allegations concern the treatment of vulnerable people when the government's controversial "work capability assessments" were carried out, but the GMC refused to comment on individual cases. The development will add to fears over the pace and radical agenda behind the government's welfare-to-work policy, which led to protests in Westminster in May by thousands of disabled people. It will also raise concerns about ministers' commitment to Atos Healthcare, which was recently granted a three-year extension on its contract.
The government has repeatedly publicised figures showing that the "vast majority" of claimants for employment support allowance (ESA), which has replaced incapacity benefit, are fit for work. But four out of 10 of those who appealed the decision by Atos - whose parent company is run by a former French finance minister, Thierry Breton - to deny them benefits are successful on appeal, a process that costs the taxpayer £50m a year.
Last month Atos, whose staff assess around 11,000 benefit claimants a week, was savaged by the cross-party work and pensions select committee after it found that many people had "not received the level of service from Atos which they can reasonably expect".
MPs further claimed that a combination of the company's conduct and the test itself had prompted "fear and anxiety among vulnerable people".
One GP who attended an Atos recruitment fair told the Observer she feared doctors could become "agents of the state" who were deprofessionalised by involvement in a system that did not make patient care its first concern.
Campaigners for the disabled seized upon the development, claiming the government needed to go back to the drawing board. Richard Hawkes, chief executive of the charity Scope, said: "If the government wants to get disabled people off benefits and into work then it needs to get its assessment right. The test should be the first step on the road to employment. But disabled people's confidence in the work capability assessment is extremely low – and today's news will send it to rock bottom.
"The test is massively flawed. Now it appears that ...
Twelve doctors employed by the firm that is paid £100m a year to assess people claiming disability benefit are under investigation by the General Medical Council over allegations of improper conduct.
The doctors, who work for Atos Healthcare, a French-owned company recently criticised by MPs for its practices, face being struck off if they are found not to have put the care of patients first.
The Observer has found that seven of the doctors have been under investigation for more than seven months. The other five were placed under investigation this year following complaints about their conduct.
It is understood that the majority of allegations concern the treatment of vulnerable people when the government's controversial "work capability assessments" were carried out, but the GMC refused to comment on individual cases. The development will add to fears over the pace and radical agenda behind the government's welfare-to-work policy, which led to protests in Westminster in May by thousands of disabled people. It will also raise concerns about ministers' commitment to Atos Healthcare, which was recently granted a three-year extension on its contract.
The government has repeatedly publicised figures showing that the "vast majority" of claimants for employment support allowance (ESA), which has replaced incapacity benefit, are fit for work. But four out of 10 of those who appealed the decision by Atos - whose parent company is run by a former French finance minister, Thierry Breton - to deny them benefits are successful on appeal, a process that costs the taxpayer £50m a year.
Last month Atos, whose staff assess around 11,000 benefit claimants a week, was savaged by the cross-party work and pensions select committee after it found that many people had "not received the level of service from Atos which they can reasonably expect".
MPs further claimed that a combination of the company's conduct and the test itself had prompted "fear and anxiety among vulnerable people".
One GP who attended an Atos recruitment fair told the Observer she feared doctors could become "agents of the state" who were deprofessionalised by involvement in a system that did not make patient care its first concern.
Campaigners for the disabled seized upon the development, claiming the government needed to go back to the drawing board. Richard Hawkes, chief executive of the charity Scope, said: "If the government wants to get disabled people off benefits and into work then it needs to get its assessment right. The test should be the first step on the road to employment. But disabled people's confidence in the work capability assessment is extremely low – and today's news will send it to rock bottom.
"The test is massively flawed. Now it appears that ...
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