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2017 Authors Author Address Title Publication 2017 Authors Author Title Publication Abstract address [No authors listed] RE: "MULTI-SITE CLINICAL Am J Epidemiol. 2017 ASSESSMENT OF MYALGIC Jul 1;186(1) :129. ENCEPHALOMYELITIS/CHRONIC FATIGUE SYNDROME (MCAM) : DESIGN AND IMPLEMENTATION OF A PROSPECTIVE/RETROSPECTIVE ROLLING COHORT STUDY". [No authors listed] Correction for Naviaux et al., Proc Natl Acad Sci U Erratum for Proc Natl Acad Sci U S A. 2016 Sep 13;113(37) :E5472- Metabolic features of chronic S A. 2017 May 80. fatigue syndrome. 2;114(18) :E3749. ABDULLA J(15) , Torpy Research Chronic Fatigue Syndrome. In: De Groot LJ(1) , et Chronic fatigue syndrome (CFS) is a common, enigmatic medical BDJ(16) . Professor, Cell al. editors. Endotext condition comprising mental and physical fatigue, diagnosed after and Molecular [Internet]. South exclusion of possible medical causes. The prominence of post- Biology, Dartmouth (MA) : exertional exacerbation of fatigue is highlighted by the recently College of the MDText.com, Inc.; suggested re-naming as Syndrome of Exertional Intolerance Disease Environment 2000-. 2017 Apr 20. (SEID) . Diagnosis is syndromic. No clinical test can confirm the and Life presence of CFS. Treatment is supportive with no specific therapy Sciences, shown to be reproducibly effective. There are several categories of University of hypotheses regarding CFS aetiology including infections, immune, Rhode Island, mitochondrial, neurobehavioural or stress system (HPA axis and Kingston, RI sympathetic nervous system) disorders. Recently, fatigue disorders have been popularly referred to as “adrenal fatigue.― Although CFS and the syndromically related fibromyalgia have been shown to have lower HPA axis function especially reduced cortisol, when analysed compared to controls in aggregate, and in some cases excessive sympathetic nervous system usually sympathoneural system responses, these findings overlap with controls and such testing is not diagnostic. Moreover, augmentation of cortisol levels with glucocorticoids has not been shown to be clinically useful. The stress system abnormalities may represent epiphenomena of the disease process rather than pathogenic abnormalities of importance to the symptomatology. Recent studies have pointed to new pathological associations and small treatment trials exist which hold some promise but require replication Ablin JN(1) . Institute of [CENTRALIZED PAIN AND Harefuah. 2017 INTRODUCTION: Fibromyalgia is a syndrome characterized by Rheumatology FIBROMYALGIA: WHAT DO WE Dec;156(12) :762- chronic widespread musculoskeletal pain, tenderness, fatigue and , Tel Aviv MEAN WHEN WE SAY "IT'S ALL 766. associated symptoms which include cognitive difficulties, abdominal Sourasky IN YOUR HEAD"?][Article in symptoms etc. A leading paradigm regarding the pathogenesis of Medical Hebrew] fibromyalgia (and similar functional disorders) focuses on the Center and Tel concept of central sensitization. This concept describes a situation in Aviv which there is an increased sensitivity of the central nervous system University. to the processing and transmission of pain, leading to the development of clinical phenomena such as allodynia and hyperalgesia. Various lines of evidence have contributed to the development of the central sensitization paradigm. A decrease in the capacity of the nervous system to perform descending pain inhibition is one aspect of this paradigm. Increased windup and long term potentiation are additional phenomena. An increase in the CSF- level of pain-facilitating neurotransmitters, coupled with a decrease in pain inhibitory transmitters, has also been described. Novel mechanisms such as microglia cell activation are under investigation. Certain clinical characteristics may alert the clinician to the possibility that a patient is suffering from centralized pain (i.e. fibromyalgia or related syndromes) . Multiple sites of pain are typical, as well as a long history of pain- related complaints in the same patients. Disturbed sleep, fatigue and dyscognition are typical. Various triggers such as physical trauma, infection and stress are often reported and tenderness is demonstrable on physical examination. Functional imaging of the central nervous system, including techniques such as fMRI, proton magnetic resonance spectroscopy and resting connectivity analysis, are improving our understanding regarding the neural mechanism underlying central sensitization. Afrin LB(1) , Self S(2) , Division of Characterization of Mast Cell Am J Med Sci. 2017 BACKGROUND: Mast cell activation syndrome (MCAS) , a recently Menk J(3) , Lazarchick Hematology, Activation Syndrome. Mar;353(3) :207-215. recognized nonneoplastic mast cell disease driving chronic J(2) . Oncology and multisystem inflammation and allergy, appears prevalent and thus Transplantatio important. We report the first systematic characterization of a large n, University MCAS population. METHOD: Demographics, comorbidities, of Minnesota symptoms, family histories, physical examination and laboratory (UMN) , findings were reviewed in 298 retrospective and 115 prospective Minneapolis, patients with MCAS. Blood samples from prospective subjects were Minnesota. examined by flow cytometry for clonal mast cell disease and tested Electronic for cytokines potentially driving the monocytosis frequent in MCAS. address: RESULTS: Demographically, white females dominated. Median ages [email protected] at symptom onset and diagnosis were 9 and 49 years, respectively du. (2) (range: 0-88 and 16-92, respectively) and median time from Department symptom onset to diagnosis was 30 years (range: 1-85) . Median of Pathology numbers of comorbidities, symptoms, and family medical issues and were 11, 20, and 4, respectively (range: 1-66, 2-84, and 0-33, Laboratory respectively) . Gastroesophageal reflux, fatigue and Medicine, dermatographism were the most common comorbidity, symptom Medical and examination finding. Abnormalities in routine laboratories were University of common and diverse but typically modest. The most useful South diagnostic markers were heparin, prostaglandin D2, histamine and Carolina, chromogranin A. Flow cytometric and cytokine assessments were Charleston, unhelpful. CONCLUSIONS: Our study highlights MCAS׳s morbidity South burden and challenging heterogeneity. Recognition is important Carolina. (3) given good survival and treatment prospects. Clinical and Translational Science Institute (CTSI) , University of Minnesota, Minneapolis, Minnesota. Agardy S(1) . ME/CFS Chronic fatigue syndrome J Health Psychol. Petrie and Weinman urge chronic fatigue syndrome patients to patient. patients have no reason to 2017 move on from their beliefs about their illness and accept the findings Member of accept the PACE trial results: Aug;22(9) :1206- of thePACE trial. This is unreasonable in view of the failure of PACE emerge Response to Keith J Petrie and 1208. to achieve evidence of recovery through cognitive behaviour therapy Australia, John Weinman. and graded exercise therapy in either self-reports or the objective patient measure of the 6-minute walking test. Contrary to their suggestion, advocacy the Institute of Medicine describes chronic fatigue syndrome not as group, psychological but as a serious, chronic, systemic disease, with post- Australia. exertional malaise as its main feature which inhibits exercise. Linking debate about PACE with intimidation of researchers is unjustifiable and damaging to patients. Agger JL(1) , The Research Imipramine versus placebo for Lancet Psychiatry. BACKGROUND: Functional somatic syndromes, including chronic Schröder A(2) , Clinic for multiple functional somatic 2017 May;4(5) :378- fatigue syndrome or irritable bowel syndrome, often co-exist. Gormsen LK(3) , Functional syndromes (STreSS-3) : a 388. Treatment guidelines supported by high quality evidence exist for Jensen JS(2) , Jensen Disorders and double-blind, randomised most functional somatic syndromes, but are lacking for multiple TS(4) , Fink PK(2) . Psychosomati study. comorbid functional somatic syndromes. We aimed to assess the cs, Aarhus effect of the tricyclic antidepressant, imipramine, in patients with University multiple functional somatic syndromes defined by the criteria for Hospital, multiorgan bodily distress syndrome, a unifying diagnosis that Noerrebrogad encompasses most functional somatic syndromes and somatoform e, Aarhus, disorders. METHODS: In this single-centre, double-blind, randomised Denmark. trial done in a Danish university hospital setting, participants were Electronic patients consecutively referred (age 20-50 years) fulfilling criteria for address: multiorgan bodily distress syndrome with no concurrent comorbid johanne.agger depression or anxiety disorder. Participants were randomly assigned @aarhus.rm.d (1:1) to receive either 10 weeks of low-dose imipramine or placebo k. (2) The (oral daily doses of 25-75 mg) . The hospital pharmacy handled Research randomisation (computer-generated) and masking, providing Clinic for sequentially numbered packs of study drug that were given serially Functional to the participants. All others involved were masked to allocation. Disorders and Primary outcome was patient-rated overall health improvement on a Psychosomati 5-point clinical global improvement scale. Improvement was defined cs, Aarhus as patients responding "better" or "much better" as opposed to University "unchanged" and "worse" or "much worse" when rating their overall Hospital, health status after 10 weeks of minimum 25 mg study drug. Analyses Noerrebrogad included
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