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News Article | May 19, 2017
Site: www.eurekalert.org

Jonkoping, Sweden - 19 May 2017: Nearly one-quarter of patients with a mechanical heart valve say it disturbs their sleep, according to research presented today at EuroHeartCare 2017.1 "I will never have silence around me again," said one patient. "For some patients the closing sound of their mechanical heart valve reduces their quality of life, disturbs their sleep, causes them to avoid social situations, and leads to depression and anxiety," said lead author Dr Kjersti Oterhals, a nurse researcher at Haukeland University Hospital in Bergen, Norway. This study investigated how the noise of a mechanical heart valve affected patients' lives, in particular their sleep, and whether there were any differences between women and men. In April 2013 all 1,045 patients who had undergone aortic valve replacement at Haukeland University Hospital between 2000 and 2011 were invited to participate in a postal survey. Of the 908 patients who responded, 245 had received a mechanical valve and were included in the current analysis. Patients were asked if the valve sound was audible to them or others, if they sometimes felt uneasy about the sound, if the sound disturbed them during daytime or during sleep, and whether they wanted to replace the mechanical valve with a soundless prosthetic valve if possible. Patients ranked the noise on a scale of 0 (does not disturb them at all) to 10 (causes maximum stress). The Minimal Insomnia Symptom Scale, which consists of three questions about sleep, was used to give patients a score of 0 to 12 for insomnia. Patients were 60 years old on average and 76% were men. Nearly one-quarter (23%) said the valve sound disturbed them during sleep and 9% said it disturbed them during the day. Some 28% wanted to replace their valve with a soundless prosthetic valve if possible. Over half (51%) said the noise was often or sometimes audible to others, but only 16% said they sometimes felt uneasy about others hearing it. The researchers found that 87% of men and 75% of women said that they were able to hear the closing sound of their mechanical valve. Women were more disturbed by the valve sound than men. Some 53% of the respondents had no insomnia, 31% had subclinical insomnia, and 17% had moderate to severe insomnia. Valve noise perception was the strongest predictor of insomnia, followed by age, and female gender. There was a linear association between insomnia and valve noise perception. And the more patients considered the valve noise a disturbance in daily life, the more insomnia they reported. Dr Oterhals said: "Almost one-fourth of patients said that the sound of their mechanical heart valve makes it difficult for them to sleep. Most of us need a quiet environment when we are going to sleep and these patients found it hard to ignore the noise from the valve." Not all patients are aware before surgery that they may hear their mechanical valve, and while most get used to it, for some it is troublesome for many years. "One female patient said to me, 'I will never have silence around me again' when she realised she would hear the noise 24 hours a day for the rest of her life," said Dr Oterhals. The most common ways patients coped with the noise when trying to sleep were to sleep on their right side which reduced the valve noise, put the duvet around their bodies to isolate the sound, listen to music, and do relaxation exercises. Ear plugs were not effective and made the valve noise louder. Dr Oterhals said: "We are not very proactive about this issue at the moment. It would improve many patients' quality of life if we asked them about valve noise and provided advice to those who find it distressing."

Romi F.,Haukeland University Hospital | Hong Y.,University of Bergen | Gilhus N.E.,Haukeland University Hospital | Gilhus N.E.,University of Bergen
Current Opinion in Immunology | Year: 2017

Myasthenia gravis (MG) is an autoimmune antibody-mediated disease characterized by muscle weakness and fatigability. It is believed that the initial steps triggering humoral immunity in MG take place inside thymic tissue and thymoma. The immune response against one or several epitopes expressed on thymic tissue cells spills over to neuromuscular junction components sharing the same epitope causing humoral autoimmunity and antibody production. The main cause of MG is acetylcholine receptor antibodies. However, many other neuromuscular junction membrane protein targets, intracellular and extracellular proteins are suggested to participate in MG pathophysiology. MG should be divided into subgroups based on clinical presentation and immunology. This includes onset age, clinical characteristics, thymic pathology and antibody profile. The immunological profile of these subgroups is determined by the antibodies present. © 2017

Kreis M.K.F.,Glasgow Caledonian University | Cooke D.J.,Glasgow Caledonian University | Cooke D.J.,University of Bergen | Michie C.,Glasgow Caledonian University | And 2 more authors.
Journal of Personality Disorders | Year: 2012

The Comprehensive Assessment of Psychopathic Personality (CAPP; Cooke, Hart, Logan, & Michie, 2004) is a new personality-based model and clinical assessment of psychopathy. This study was the frst to examine the content validity of the English-language CAPP. Content validation is a crucial part of the development and refnement of any new instrument. Prototypical analysis was used to evaluate the representativeness of CAPP symptoms to the psychopathy construct in adults. Symptoms were rated by international mental health professionals (N = 132). Findings support good content validity of the CAPP, with most symptoms rated as highly representative of psychopathy. Domains relating to interpersonal style were particularly prototypical. Confrmatory factor analyses further suggested that CAPP domains are highly unidimensional. However, some CAPP symptoms may be weaker items in the model and further refnement is needed. © 2012 The Guilford Press.

Hoyersten J.G.,Haukeland University Hospital
Archives of Psychiatry and Psychotherapy | Year: 2015

The medicine of medieval Europe was influenced above all by the Hippocratic and Galenic legacies, conveyed through the medical School of Salerno, albeit also to an extent embedded in demonological and supernatural beliefs and folklore customs. More concrete or extensive clinical descriptions of mental illness are hardly found beyond the anecdotic realm. Between the Viking period (800-1030) and the high Middle Ages (1100-1300) the most vivid and universally available writings and descriptions of mental illness come from fictional literature, more precisely the sagas, written predominantly in Iceland in the native Old Icelandic language during the 13th century. This period was also called the Old Norse renaissance, hallmarked by intense intellectual and literary activity and achievements. The literature of the period has given us a wealth of reports concerning the everyday and social life and mentality, with an eye for peculiarities and abnormalities.

Espehaug B.,Haukeland University Hospital
Tidsskrift for den Norske lægeforening : tidsskrift for praktisk medicin, ny række | Year: 2011

Since information on regional variation in the frequency of primary total hip arthroplasty in Norway is scarce, we studied differences by county and regional health authority throughout the last 20 years. We included 112, 514 primary total hip arthroplasties reported to the Norwegian Arthroplasty Register in the years 1989-2008. Annual gender and age standardized frequencies were calculated, and Poisson regression was used for group comparisons (RR = rate ratio). We observed an increase in hip arthroplasty frequency from 109 operations per 100, 000 inhabitants in the years 1991-1995 to 140 in 2006-2008 (RR = 1.28), and more so for operations performed due to coxarthrosis (RR = 1.46). An increased frequency over time was evident in all five regions and 19 counties. Differences between counties and regions had decreased throughout the study period. In the years 2006-2008, Helse Midt (152 operations) had a statistically significant higher frequency than the other regions except for Helse Sør. The lowest frequencies at county level were found for Finnmark (116 operations) and the highest for Aust-Agder (172). While regional differences have decreased since the early 1990 s, existing differences may in part be due to differing access to surgery, varying indications for surgery, or possibly also genetic or cultural differences.

Vie T.L.,Helse Forde HF Forde Health Trust | Hufthammer K.O.,Haukeland University Hospital | Holmen T.L.,Norwegian University of Science and Technology | Meland E.,University of Bergen | Breidablik H.J.,Helse Forde HF
Social Science and Medicine | Year: 2014

Self-rated health (SRH) is a widely used health indicator predicting morbidity and mortality in a wide range of populations. However, little is known about the stability and biological basis of SRH. The aim of this study was to map the stability of SRH from adolescence to early adulthood, and to examine the relationships between SRH and biological dysregulation, in terms of allostatic load (AL). The AL score comprises the eleven biomarkers systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), cholesterol, high-density lipoprotein cholesterol (HDL), triglycerides, waist-hip ratio (WHR), diabetes risk profile, glucose, C-reactive protein (CRP) and body mass index (BMI). Eleven years prospective data from the Nord-Trøndelag Health Study (HUNT), Norway, were utilised. Baseline data were gathered from 9141 adolescents (mean age 15.9 years) in the Young-HUNT I survey (1995-1997) and follow-up data were gathered from the adult HUNT3 survey (2006-2008). Altogether, 1906 respondents completed both questionnaires and clinical measurements in both studies. Cross-tables for SRH at baseline and follow-up showed that SRH remained unchanged in 57% of the respondents. Only 3% of the respondents changed their ratings by two steps or more on a four-level scale. Further, linear regression analyses adjusted for age and gender revealed that SRH in adolescence predicted AL in young adulthood. Similar patterns were found for most of the individual biomarkers. The consistency found in SRH from adolescence to young adulthood, and its association with AL across time, indicate that routines for dealing with SRH early in life may be a central strategy to prevent morbidity in the adult population. © 2014 Elsevier Ltd.

Thun E.,University of Bergen | Bjorvatn B.,Haukeland University Hospital | Bjorvatn B.,University of Bergen | Flo E.,University of Bergen | And 3 more authors.
Sleep Medicine Reviews | Year: 2015

Sleep deprivation and time of day are both known to influence performance. A growing body of research has focused on how sleep and circadian rhythms impact athletic performance. This review provides a systematic overview of this research. We searched three different databases for articles on these issues and inspected relevant reference lists. In all, 113 articles met our inclusion criteria. The most robust result is that athletic performance seems to be best in the evening around the time when the core body temperature typically is at its peak. Sleep deprivation was negatively associated with performance whereas sleep extension seems to improve performance. The effects of desynchronization of circadian rhythms depend on the local time at which performance occurs. The review includes a discussion of differences regarding types of skills involved as well as methodological issues. © 2014 Elsevier Ltd.

News Article | February 15, 2017
Site: www.newscientist.com

It’s as if a switch has been flicked. Evidence is mounting that chronic fatigue syndrome (CFS) is caused by the body swapping to less efficient ways of generating energy. Also known as ME or myalgic encephalomyelitis, CFS affects some 250,000 people in the UK. The main symptom is persistent physical and mental exhaustion that doesn’t improve with sleep or rest. It often begins after a mild infection, but its causes are unknown. Some have argued that CFS is a psychological condition, and that it is best treated through strategies like cognitive behavioural therapy. But several lines of investigation are now suggesting that the profound and painful lack of energy seen in the condition could in many cases be due to people losing their ability to burn carbohydrate sugars in the normal way to generate cellular energy. Instead, the cells of people with CFS stop making as much energy from sugar as usual, and start relying more on lower-yielding fuels, such as amino acids and fats. This kind of metabolic switch produces lactate, which can cause pain when it accumulates in muscles. Together, this would explain both the shortness of energy, and why even mild exercise can be exhausting and painful. Øystein Fluge of Haukeland University Hospital in Bergen, Norway, and his colleagues studied amino acids in 200 people with CFS, and 102 people without it. The levels of some amino acids in the blood of women with CFS was abnormally low – specifically for the types of amino acid that can be used by the body as an alternative fuel source. These shortfalls were not seen in men with CFS, but that could be because men tend to extract amino acids for energy from their muscles, instead of their blood. And the team saw higher levels of an amino acid that’s a sign of such a process. “It seems that both male and female CFS patients may have the same obstruction in carbohydrate metabolism to energy, but they may try to compensate differently,” says Fluge. Both sexes had high levels of several enzymes known to suppress pyruvate dehydrogenase (PDH), an enzyme vital for moving carbohydrates and sugars into a cell’s mitochondria – a key step for fully exploiting sugar for energy. Fluge thinks PDH is prevented from working in people with CFS, but that it can spontaneously recover. Several studies have now hinted that defects in sugar burning can cause CFS, but there is still uncertainty over how exactly this is disrupted. However, a picture is emerging. Something makes the body switch from burning sugar to a far less efficient way of making energy. “We don’t think it’s just PDH,” says Chris Armstrong at the University of Melbourne in Australia, whose research has also uncovered anomalies in amino acid levels in patients. “Broadly, we think it’s an issue with sugar metabolism in general.” The result is not unlike starvation, says Armstrong. “When people are facing starvation, the body uses amino acids and fatty acids to fuel energy for most cells in the body, to keep glucose levels vital for the brain and muscles as high as possible.” “We think that no single enzyme in metabolism will be the answer to CFS, just as no single enzyme is the ‘cause’ of something like hibernation,” says Robert Naviaux of the University of California at San Diego, who has found depletion of fatty acids in patients suggesting they were diverted as fuel. So what could flick the switch to a different method of metabolism? Fluge’s team thinks that a person’s own immune system may stop PDH from working, possibly triggered by a mild infection. His team has previously shown that wiping out a type of white blood cell called B-cells in CFS patients seems to relieve the condition. These white blood cells make antibodies, and Fluge suspects that some antibodies made to combat infections may also recognise something in PDH and disable it. The team is now conducting a large trial in Norway of the cancer drug rituximab, which destroys the cells that make antibodies, in people with CFS. Results are expected next year. Together, these metabolic approaches are suggesting that CFS has a chemical cause. “It’s definitely a physiological effect that we’re observing, and not psychosomatic, and I’ll put my head on the block on that,” says Armstrong. However, he adds that psychological and brain chemistry factors might be involved in some cases.

News Article | February 15, 2017
Site: www.eurekalert.org

-- Largest imaging study of ADHD to date identifies differences in five regions of the brain, with greatest differences seen in children rather than adults. Attention-deficit hyperactivity disorder (ADHD) is associated with the delayed development of five brain regions and should be considered a brain disorder, according to a study published in The Lancet Psychiatry. The study is the largest to look at the brain volumes of people with ADHD, involving more than 3200 people. The authors say the findings could help improve understanding of the disorder, and might be important in challenging beliefs that ADHD is a label for difficult children or the result of poor parenting. ADHD symptoms include inattention and/or hyperactivity and acting impulsively. The disorder affects more than one in 20 (5.3%) under-18 year olds, and two-thirds of those diagnosed continue to experience symptoms as adults. Previous studies have linked differences in brain volume with the disorder, but small sample sizes mean results have been inconclusive. Areas thought to be involved in ADHD are located in the basal ganglia - a part of the brain that controls emotion, voluntary movement and cognition - and research has previously found that the caudate and putamen regions within the ganglia are smaller in people with ADHD. The new international study measured differences in the brain structure of 1713 people with a diagnosis of ADHD and 1529 people without, all aged between four and 63 years old. All 3242 people had an MRI scan to measure their overall brain volume, and the size of seven regions of the brain that were thought to be linked to ADHD - the pallidum, thalamus, caudate nucleus, putamen, nucleus accumbens, amygdala and hippocampus. The researchers also noted whether those with ADHD had ever taken psychostimulant medication, for example Ritalin. The study found that overall brain volume and five of the regional volumes were smaller in people with ADHD - the caudate nucleus, putamen, nucleus accumbens, amygdala and hippocampus. "These differences are very small - in the range of a few percent - so the unprecedented size of our study was crucial to help identify these. Similar differences in brain volume are also seen in other psychiatric disorders, especially major depressive disorder." said lead author Dr Martine Hoogman, Radboud University Medical Center, Nijmegen, The Netherlands. [1] The differences observed were most prominent in the brains of children with ADHD, but less obvious in adults with the disorder. Based on this, the researchers propose that ADHD is a disorder of the brain, and suggest that delays in the development of several brain regions are characteristic of ADHD. Besides the caudate nucleus and putamen, for which previous studies have already shown links to ADHD, researchers were able to conclusively link the amygdala, nucleus accumbens and hippocampus to ADHD. The researchers hypothesise that the amygdala is associated with ADHD through its role in regulating emotion, and the nucleus accumbens may be associated with the motivation and emotional problems in ADHD via its role in reward processing. The hippocampus' role in the disorder might act through its involvement in motivation and emotion. At the time of their MRI scan, 455 people with ADHD were receiving psychostimulant medication, and looking back further, 637 had had the medication in their lifetime. The different volumes of the five brain regions involved in ADHD were present whether or not people had taken medication, suggesting the differences in brain volumes are not a result of psychostimulants. "The results from our study confirm that people with ADHD have differences in their brain structure and therefore suggest that ADHD is a disorder of the brain," added Dr Hoogman. "We hope that this will help to reduce stigma that ADHD is 'just a label' for difficult children or caused by poor parenting. This is definitely not the case, and we hope that this work will contribute to a better understanding of the disorder." [1] While the study included large numbers of people of all ages, its design means that it cannot determine how ADHD develops throughout life. Therefore, longitudinal studies tracking people with ADHD from childhood to adulthood to see how the brain differences change over time will be an important next step in the research. Writing in a linked Comment Dr Jonathan Posner, Columbia University, USA, said: "[This] is the largest study of its kind and well powered to detect small effect sizes. Large sample sizes are particularly important in the study of ADHD because of the heterogeneity of the disorder both in the biological cause and clinical manifestation... This study represents an important contribution to the field by providing robust evidence to support the notion of ADHD as a brain disorder with substantial effects on the volumes of subcortical nuclei. Future meta-analyses and mega-analyses will need to investigate medication effects as well as the developmental course of volumetric differences in this disorder." The study was funded by the National Institutes of Health. The study is part of the ENIGMA Consortium, where researchers are also studying the structure of the brain in other psychiatric disorders, allowing researchers to define differences and similarities between the disorders. It was conducted by scientists from Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, University of Southern California, University of Groningen, QIMR Berghofer Medical Research Institute, University Medical Center Utrecht, National Human Genome Research Institute, Asociación para la Innovación en Análisis, Gestión y Procesamiento de Datos Científicos y Tecnológicos, University Hospital Aachen, JARA Translational Brain Medicine, Research Center Juelich, Harvard Medical School, The Broad Institute, University of Bergen, Cincinnati Children's Hospital Medical Center, University of California, UC San Diego, University of Tübingen, University of Würzburg, University of Dublin, NYU Langone Medical Center, King's College London, Heidelberg University, Federal University of Rio de Janeiro, University of Zurich, Child Mind Institute, Nathan Kline Institute for Psychiatric Research, Otto-von-Guericke-University, Maastricht University, University Hospital Frankfurt, Haukeland University Hospital, Child and Adolescent Mental Health Center, Beth Israel Deaconess Medical Center, Karakter Child and Adolescent Psychiatry, VU University Amsterdam, Universitat Autònoma de Barcelona, Fundació IMIM, Hospital Universitari Vall d'Hebron, SUNY Upstate Medical University, National Institute of Mental Health. [1] Quote direct from author and cannot be found in the text of the Article. IF YOU WISH TO PROVIDE A LINK FOR YOUR READERS, PLEASE USE THE FOLLOWING, WHICH WILL GO LIVE AT THE TIME THE EMBARGO LIFTS: http://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(17)30049-4/fulltext

News Article | November 9, 2016
Site: www.sciencemag.org

The most anticipated speaker late last month at an international conference devoted to the mysterious malady commonly known as chronic fatigue syndrome (CFS) was not a scientist with a hot new finding—although there was excitement about new research in the air. Rather, it was a National Institutes of Health (NIH) official bearing good news to a community that has long existed on the margins of the biomedical research establishment. Vicky Whittemore, the agency's CFS point person in Bethesda, Maryland, delivered on a promise that NIH Director Francis Collins made last year by announcing that NIH spending for research on the poorly understood disease should rise to roughly $15 million in 2017, doubling the estimated $7.6 million handed out in 2016. What's more, the NIH emissary said to those gathered here, the biomedical agency will in December solicit CFS proposals from outside scientists to establish several collaborative centers for basic and clinical research, and another center to manage their data on the illness. The calls for applications, which will come with dedicated funds from the planned budget increase, are the first of their kind for CFS from the United States's major medical research funder since 2005. "There is a shifting tide at NIH with regard to ME/CFS," Whittemore told the conference, incorporating the term that many with the multisystem illness prefer. (ME stands for "myalgic encephalomyelitis," and the meeting was convened by the International Association for CFS/ME.) Some scientists working on the disease agree. "The fact that there is a budget for it at all means that the agency is taking it seriously. And it's not coming only out of Francis Collins's discretionary fund, but from the individual NIH institutes," says Ian Lipkin, an immunologist at Columbia University, who serves on the Advisory Committee to the Director, Collins's key group of external advisers. Lipkin is also a principal investigator, with Columbia psychiatrist Mady Hornig, on a $766,000 grant from NIH's infectious diseases institute to collect samples from hundreds of patients and controls, looking for biomarkers that could be used to diagnose the disease and searching for clues to its causes. It has been nearly 3 decades since a group of researchers led by the U.S. Centers for Disease Control and Prevention (CDC) coined the term "chronic fatigue syndrome" after an investigation of two outbreaks in the United States. Typified by exhaustion that commonly worsens with physical, mental, or emotional exertion, the condition is also often characterized by short-term memory and concentration problems and profound fatigue that sleep does not relieve. Sufferers may experience widespread muscle and joint pain, immune system problems, headaches, and many other symptoms. The onset of the disease frequently follows an infectious illness. Ever since it was given a name, many researchers and physicians have viewed the malady, which has no Food and Drug Administration–approved treatment and no diagnostic test, as psychosomatic. Then, in 2015, the Institute of Medicine (IOM) dismissed the "misconception" of the disease as psychological in a report informed by a review of more than 9000 articles from 64 years of medical literature. "Remarkably little research funding has been made available to study the etiology, pathophysiology, and effective treatment of this disease, especially given the number of people affected," the authors noted. CDC estimates that ME/CFS affects more than 1 million Americans, a majority of them women. The IOM report "had an unbelievable effect," because it validated patients' experiences—"it told them that they weren't crazy," says geneticist Ronald Davis, who directs the Genome Technology Center at Stanford University in Palo Alto, California, and was one of the report's 15 authors. Davis became a passionate advocate for ME/CFS research and shifted his own studies to the topic after his now 33-year-old son fell ill with ME/CFS in 2008; he is now bedridden. "It also did a lot to NIH and the CDC, who had been ignoring this disease." Not long after the IOM report was published, NIH issued its own written assessment, concluding that research has neglected many of the biological factors behind ME/CFS and urging more basic science aimed at teasing out the mechanisms of the disease. Collins also announced a "strengthening" of the agency's ME/CFS effort. He moved oversight of the research out of the agency's small Office of Research on Women's Health and into the $1.7 billion National Institute of Neurological Disorders and Stroke (NINDS), and launched an intramural study that began enrolling people late last month. Forty patients who have developed the disease within the last 5 years, after an infection, will be run through a battery of exams at the Clinical Center, the NIH's research hospital. The assessments, from exercise stress tests to brain magnetic resonance imaging tests, will probe the biological and clinical characteristics of the disease—for which there is not even a broadly agreed-upon definition. For comparison, the study will also include healthy controls and people who have recovered from Lyme disease, which can cause similar symptoms. Some ME/CFS patients remain skeptical that the NIH moves reflect a genuine commitment to research on the disease. They have criticized what they call the narrow eligibility criteria being used for the Clinical Center study, and they complain that even $15 million scarcely begins to fund the research they say is needed. Critics such as Deborah Waroff, a retired Wall Street energy analyst who fell ill with ME/CFS in 1989, point, for instance, to multiple sclerosis, a similarly chronic, debilitating disease, which affects fewer than half as many Americans, according to one recent estimate. It received about 13 times as much NIH funding in 2016: $98 million. "ME still floats in space, belonging fully to no NIH institute and therefore having de jure claim to no budget," Waroff says. "The disease remains a beggar when it comes to budget." Any goodwill won by Whittemore's appearance in Florida may have evaporated after anger erupted last week when ME/CFS patients learned NIH had invited Edward Shorter, a medical historian at the University of Toronto in Canada, to give a 9 November talk at the agency. Shorter last year called the IOM report affirming the biological basis of ME/CFS "valueless; junk science at its worst." He traces the disease to a 1970s "brew of toxic beliefs about being tired all the time." Walter Koroshetz, the director of NINDS, defended the talk, writing in a letter to ME/CFS patients that "inclusion in the scientific conversation is not an endorsement." In an email to Science, he wrote that Shorter's talk was not "an official ME/CFS lecture. [An] announcement went out to the contrary. That was recalled. End of story." Tangible scientific progress on unraveling ME/CFS might be the best medicine to heal the current divisions. A study published in the Proceedings of the National Academy of Sciences in August found depressed blood levels of scores of metabolites in people with the disease compared with healthy controls, suggesting that the disease may push the body into a low-energy state some have compared with hibernation. Scientists and patients are eagerly waiting for the results of a similar study by Lipkin's team. If replicated, the tantalizing finding could fit with an emerging theory that subpar function by mitochondria, the organelles that provide energy for cells, drives the disease. Hints that the monoclonal antibody rituximab, a drug that destroys antibody-producing B cells, may help some people with ME/CFS have also sparked optimism. ME/CFS patients have a slightly elevated risk of developing B-cell lymphoma, and Norwegian researchers accidentally found that treating a woman who had both conditions with rituximab markedly improved her ME/CFS symptoms. The group went on to do a nonblinded study of the antibody in 29 ME/CFS patients, 18 of whom reported major or moderate improvements in their symptoms. The researchers are now running a larger, double-blind, randomized clinical trial of the drug in 152 patients, planning to evaluate its effectiveness next October. Øystein Fluge, one of the Norwegian trial's leaders and an oncologist at the University of Bergen's Haukeland University Hospital in Norway, remains cautious. "Many places on the internet say this is an autoimmune disease. We haven't said that. We think some features fit, probably, with some autoimmune mechanism. But that's a hypothesis. We aren't sure." Only one thing is sure: After decades of frustration, the mysterious disease remains maddeningly elusive.

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