From Clinical Infectious Diseases. Epub 13 February 2013.
http://www.ncbi.nlm.nih.gov/pubmed/23408682
Human endogenous retrovirus-k18 superantigen expression and human herpesvirus-6 and human herpesvirus-7 viral loads in chronic fatigue patients.
Oakes B, Hoagland-Henefield M, Komaroff AL, Erickson JL, Huber BT.
Graduate Program in Pharmacology and Experimental Therapeutics, Sackler School of Graduate Biomedical Sciences, Tufts University.
Abstract
BACKGROUND
Chronic fatigue syndrome (CFS) is a complex, heterogeneous disease characterized by debilitating fatigue that is not improved with bed rest and worsens after physical activity or mental exertion. Despite extensive research into a cause of CFS, no definitive etiology has been determined; however, a large percentage of CFS patients note an acute infectious event that triggers their fatigue.
METHODS
Blood and saliva were collected from 39 CFS cases and 9 healthy control subjects. Peripheral blood mononuclear cells (PBMCs) were tested for human endogenous retrovirus-K18 (HERV-K18) env transcripts using a TaqMan quantitative polymerase chain reaction (qPCR). In addition, viral copy number of human herpesvirus-6 (HHV-6) and human herpesvirus-7 (HHV-7) were measured in both saliva and PBMCs using TaqMan qPCRs. Transcript levels and viral copy number were compared to patient CFS symptom severity.
RESULTS
HERV-K18 env transcripts were not significantly different between healthy control subjects and CFS patients. Also, HERV-K18 env transcripts did not correlate with HHV-6 viral copy number or HHV-7 viral copy number in either PBMCs or saliva. HHV-6 viral copy number and HHV-7 viral copy number in both PBMCs and saliva were not significantly different between healthy control subjects and CFS patients. HERV-K18 env transcripts, HHV-6 viral copy number, and HHV-7 viral copy number did not correlate with CFS symptom severity.
CONCLUSIONS
We fail to demonstrate a difference in HERV-K18 env transcripts, HHV-6 viral copy number, and HHV-7 viral copy number between CFS patients and healthy controls. Our data do not support the hypothesis of reactivation of HHV-6 or HHV-7 in CFS.
Hypofuse = Pituitary
(from: 15th European Congress of Endocrinology, Copenhagen, Denmark.
27 April 2013 – 01 May 2013. European Society of Endocrinology)
Endocrine Abstracts (2013)
Morphologial and functional abnormalities of the hypofyse in patients with diagnose of CFS or fibromyalgia. An example of misdiagnosis by Belgian chronic fatigue centres
Francis Coucke, Heidi Lammens, Laurens Coucke & Anne-Birgitte Vogter
METARES, Sint Gillis Was, Belgium.
Abstract
AIM
In consultation, we check a lot of patients who present with diagnose of FM (fibromyalgia) and chronic fatigue syndrome (CFS). Most of these patients have a underlying diagnosis that causes chronic pain or fatigue. These causes are pathologies not easily detected.
Endocrine failure is one of the candidates, with hypofyse dysfunction as a possible candidate.
METHODS
During 1 year: from October 11, 487 patients presented at the consultation we found 47 cases of morphological and functional hypofyse abnormalities. By examining with stress test in patients with clinical complaints and low basal hormones: e.g. low IGF1 or cortisol, combined with morphological abnormalities of the hypofyse.
RESULTS
Forty seven patients with abnormalities of the hypofyse:
• Cystes: 6 cases average age 50.8, all female, mean diameter 5.2 mm
(from 4 to 8 mm). All are ACTH–cortisol deficient and 1 of them is GH
deficient (GHD).
• Adenomas: 31 cases average age: 42 years, 23 female, 8 males, mean
size of 5 mm (from 12 to 3 mm), all are ACTH–cortisol deficient and 11
are also GHD.
• Empty cells: 12 cases: average age: 53, 25 years, 5 males, 7
females, all deficient in ACTH–cortisol and 8 are GHD.
CONCLUSION
Patients with a diagnose of CFS or fibromyalgia should always be checked for underlying chronic diseases. Mostly immunologic but also endocrine diseases can be underlying. E.g. frequently adrenal insufficiency can be detected. A lot of reports document also a low IGF1 and GHD.
Patients with hormone deficiencie should also be checked for other hormone deficiencies. In case of low hypofyse hormones, single or multiple, the hypofyse has to be functionally and morphologically checked. On contrary with the disappointing general therapy of FM or CFS, a good and efficient therapy can be offered to patients by treating the underlying hormonal deficiencies.
From the Journal of Affective Disorders, 10 May 2013.
In myalgic encephalomyelitis/chronic fatigue syndrome, increased autoimmune activity against 5-HT is associated with immuno-inflammatory pathways and bacterial translocation
Michael Maes (a,b,c), Karl Ringel(d), Marta Kubera(e), George Anderson(f), Gerwyn Morris(g), Piotr Galecki(h), Michel Geffard(i)
a) Maes Clinics @ TRIA, Bangkok, Thailand
b) Department of Psychiatry, Chulalongkorn University, Bangkok, Thailand
c) Department of Psychiatry, Deakin University, Geelong, VIC, Australia
d) Immunologischen Laboratorien, Aachen, Germany
e) Department of Experimental Endocrinology, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland
f) CRC, Rm 30, Glasgow, Scotland
g) Tir Na Nog, Pembrey, Llanelli, UK
h) Department of Adult Psychiatry, Medical University of Lódź and Babinski Memorial Hospital, Lódź, Poland
i) Association Institute for Research & Development in Human Pathology and Therapy, Talence, France
Abstract
BACKGROUND
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is accompanied by activation of immuno-inflammatory pathways, increased bacterial translocation and autoimmune responses to serotonin (5-HT). Inflammation is known to damage 5-HT neurons while bacterial translocation may drive autoimmune responses. This study has been carried out to examine the autoimmune responses to 5-HT in ME/CFS in relation to inflammation and bacterial translocation.
METHODS
We examined 5-HT antibodies in 117 patients with ME/CFS (diagnosed according to the centers for disease control and prevention criteria, CDC) as compared with 43 patients suffering from chronic fatigue (CF)but not fulfilling the CDC criteria and 35 normal controls. Plasma interleukin-1 (IL-1), tumor necrosis factor (TNF)α, neopterin and the IgA responses to Gram-negative bacteria were measured. Severity of physio-somatic symptoms was measured using the fibromyalgia and chronic fatigue syndrome rating scale (FF scale).
RESULTS
The incidence of positive autoimmune activity against 5-HT was significantly higher (p<0.001) in ME/CFS (61.5%) than in patients with CF (13.9%) and controls (5.7%). ME/CFS patients with 5-HT autoimmune activity displayed higher TNFα, IL-1 and neopterin and increased IgA responses against LPS of commensal bacteria than those without 5-HT autoimmune activity. Anti-5-HT antibody positivity was significantly associated with increased scores on hyperalgesia, fatigue, neurocognitive and autonomic symptoms, sadness and a flu-like malaise.DISCUSSIONThe results show that, in ME/CFS, increased 5-HT autoimmune activity is associated with activation of immuno-inflammatory pathways and increased bacterial translocation, factors which are known to play a role in the onset of autoimmune reactions. 5-HT autoimmune activity could play a role in the pathophysiology of ME/CFS and the onset of physio-somatic symptoms. These results provide mechanistic support for the notion that ME/CFS is a neuro-immune disorder.
From Griffith University website, 13 May 2013. Story by Louise Durack.
Gold Coast centre gives hope for chronic fatigue syndrome
In good news for people who suffer from chronic fatigue, Griffith University and the Gold Coast Hospital and Health Service (GCHHS) are to give priority to fighting the debilitating condition.
Department of Science, Information Technology, Innovation and the Arts (DSITIA) Director-General Andrew Garner said this would be welcomed by the thousands of Australians suffering from chronic fatigue syndrome (CFS) and the related myalgic encephalomyelitis (ME).
“Chronic Fatigue Syndrome affects around 250,000 Australians. The condition can be crippling, with many people barely able to move, let alone go to work and earn a living,” Mr Garner said.
“To make matters worse, the condition is notoriously difficult to diagnose, meaning that people can go for months without getting the care and attention they require.
“Unfortunately, it also carries a stigma – that there’s nothing wrong with you, especially when your GP can’t find the cause of your condition. But it is real for far too many people.
“Griffith University and the GCHHS recently established the National Centre for Neuroimmunology and Emerging Diseases on the coast, with an emphasis on researchers working with clinicians and patients on effective research outcomes,” he said.
“The new centre, dedicated to research on the interaction between the nervous system and the immune system and led by one of Australia’s foremost authorities on CFS/ME Professor Sonya Marshall-Gradisnik, will give priority to this important research.”
In a two-year study of over 300 people with the disability, Professor Marshall-Gradisnik from Griffith’s School of Medicine found a strong association between the condition and a dysfunctional immune system.
Gold Coast Health Board Chairman Mr Ian Langdon said recent commitments by major funders and benefactors and key government support meant that they could now make this research a priority.
Griffith University’s Pro-Vice Chancellor (Health) Professor Allan Cripps said the development of the research centre was a milestone in an evolving university-health services partnership.
“The National Centre for Neuroimmunology and Emerging Diseases brings to fruition years of research effort culminating in extensive research, academic publications and provides significant insights as to the potential pathology in this disorder,” Professor Cripps said.
“Together we can achieve much more than either entity alone.
“In particular we have already achieved extraordinary success in the immunological area in CFS/ME and expect to have further significan
findings by our research team,” he said.
From ‘My Daily News' website, Australia, 13 May 2013.
SOUTHERN Cross University academics are looking for Chronic Fatigue Syndrome Sufferers to participate in a pilot study to determine the effects of exercise and rest on sufferers.
Dr Suzanne Broadbent and Dr Rosanne Coutts of the School of Health and Human Sciences have received a grant from the JO and JR Wicking Trust and then Mason Foundation to investigate if intermittent or graded exercise improves patient fitness, fatigue and immune function compared to rest.
The study will run for 12 weeks with short exercise sessions three times per week. The exercise will be either low intensity graded exercise or intermittent low intensity exercise with periods of rest.Participants need to have been diagnosed with CFS by a doctor, be aged between 16 to 65, and have their doctor's approval to do some physical activity.
Those interested can contact Natasha Maslen on 02 6626 9585 for further details.
The last two items of the 4 are not abstracts.
The second abstract however provides an objective test for a fatigue cohort which could be tested for HERV-K, unlike the first abstract which only looked in a general fatigue cohort.
“The results show that, in ME/CFS, increased 5-HT autoimmune activity is associated with activation of immuno-inflammatory pathways and increased bacterial translocation, factors which are known to play a role in the onset of autoimmune reactions. 5-HT autoimmune activity could play a role in the pathophysiology of ME/CFS and the onset of physio-somatic symptoms. These results provide mechanistic support for the notion that ME/CFS is a neuro-immune disorder.”
Yes: “ME/CFS is a neuro-immune disorder”.
It couldn’t be clearer, could it? Interestingly, people working in departments of psychiatry have discovered this as well as scientists from other disciplines. What you might call useful interdisciplinary collaboration between international researchers.
Neuropsychiatry isn’t psychiatry.
Yes agree, the Journal of Affective Disorders research findings are v interesting.
Why on earth would the body develop an auto immune reaction to Serotonin? How strange. How very specific. Why serotonin and is there anything else also triggering the autoimmunity?
I wonder how surprised the researchers were by the results and what made them look into it in the first place?!
Is it possible to have a comment from Dr Shepherd/the MEA on this please?
Great to have evidence of neuro immune dysfunction from researchers of ‘affective disorders’. Would be great if this kind of research were followed up. And what on earth would the treatment be if the above were proved to be the case?
I’d like to know the implications of the auto-immune reaction to serotonin and how this might be affected by or cause an effect in somebody stuck on SSRIs because of the depression this disease can so easily cause.
(It’s not as if serotonin is the chemical at the root of depression either. SSRIs are pretty much just ghastly sledgehammers.)