Chronic fatigue syndrome: influence of histamine, hormones and electrolytes

Abstract:

The chronic fatigue syndrome is poorly understood. We believe the underlying causes in many atopics and women are a persistent infection and hypersensitivity to the immune-suppressive effects of histamine and certain pathogens.

We believe much of the symptomatology can be explained by all four types of hypersensitivity (Gell and Coombs classification) in reaction to a pathogen, electrolyte disturbances which include sometimes permanent changes in cell membranes’ ability to pass electrolytes, sometimes permanent biochemical changes in mitochondrial function, and disturbances of insulin and T3-thyroid hormone functions. We also explain in detail what ‘fatigue’ means for these patients. We present evidence from the medical literature for the plausibility of our hypotheses.

 

Source: Dechene L. Chronic fatigue syndrome: influence of histamine, hormones and electrolytes. Med Hypotheses. 1993 Jan;40(1):55-60. http://www.ncbi.nlm.nih.gov/pubmed/8455468

 

A four-year follow-up study in fibromyalgia. Relationship to chronic fatigue syndrome

Abstract:

The primary objectives of this study were to examine to what extent fibromyalgia patients later on developed presumpted causative somatic diseases and to examine symptoms and muscle strength some years after the diagnosis of fibromyalgia was established. A secondary objective was to describe the overlap between fibromyalgia and chronic fatigue syndrome.

Only in two of 91 the muscle pain was found to be caused by another somatic disease during the median 4 year follow-up period. In one of the 83 attending subjects a somatic disease associated with muscle symptoms was established at the follow-up visit. 60 out of 83 reported increased pain, 8 reported improvement of pain. The 83 subjects showed no significant fall in muscle strength during the follow-up period. The majority reported severe fatigue but only one fifth fulfilled the proposed chronic fatigue syndrome criteria.

 

Source: Nørregaard J, Bülow PM, Prescott E, Jacobsen S, Danneskiold-Samsøe B. A four-year follow-up study in fibromyalgia. Relationship to chronic fatigue syndrome. Scand J Rheumatol. 1993;22(1):35-8. http://www.ncbi.nlm.nih.gov/pubmed/8434245

 

Taking exception to chronic fatigue syndrome prevalence findings by Price, et al.

Comment on: Estimating the prevalence of chronic fatigue syndrome and associated symptoms in the community. [Public Health Rep. 1992]

 

We would like to address some serious methodological issues in the article, “Estimating the Prevalence of Chronic Fatigue Syndrome and Associated Symptoms in the Community,” by Rumi K. Price, et al., published in the September-October issue of Public Health Reports. We believe that because of the deficiencies in the design of this research, the authors’ conclusions are totally illogical and invalid.

In this article, the authors conclude that Chronic Fatigue Syndrome (CFS), as defined by the Centers for Disease Control (CDC) Diagnostic Criteria, might be “quite rare” in the general population, as only 1 of 13,538 individuals studied was deemed to have CFS. The official CDC Diagnostic Criteria, however, were not utilized to diagnose cases of CFS. Instead, the researchers reviewed interview questionnaire data collected between 1981 and 1984 for a purpose unrelated to diagnosing CFS. In fact, the CDC Diagnostic Criteria were not formulated and published until 1988.

You can read the rest of this comment as well as the rely from the authors here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1403345/pdf/pubhealthrep00069-0137c.pdf

 

Source: Robin R, Lipkin DM, Hume GW. Taking exception to chronic fatigue syndrome prevalence findings by Price, et al. Public Health Rep. 1993 Jan-Feb;108(1):135-7. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1403345/

 

Psychotropic treatment of chronic fatigue syndrome and related disorders

Abstract:

BACKGROUND: Chronic fatigue syndrome (CFS) and fibromyalgia frequently are associated with symptoms of major depression. For this reason, antidepressants have been used in treatment of these disorders; however, little direction has been provided into this application in psychopharmacology.

METHOD: First, nine studies were reviewed regarding the relationship of the symptoms of fatigue and depression. Next, 23 reports (12 double-blind studies, 7 open studies, and 4 case reports) were reviewed for the effectiveness of therapy as assessed by global response and improvement of both depression and pain. Studies were differentiated by type of controls, as well as by alleged mechanism of action of the pharmacologic agent.

RESULTS: Disturbances in brain neurochemistry shared by CFS and major depression may serve as a basis for the effectiveness of some antidepressants in CFS. Response to some antidepressants in patients with CFS or fibromyalgia may occur at doses lower than those used in major depression, e.g., amitriptyline 25-75 mg/day. We further found that the more serotonergic treatments (e.g., clomipramine) were more successful in alleviating pain than depression, whereas catecholaminergic agents (e.g., maprotiline, bupropion) seemed particularly effective for symptoms of associated depression.

CONCLUSION: To maximize response of the physiologic and psychological consequences of the disorder, more investigation is needed to replicate the apparent findings that relate the neurochemical impairment underlying CFS and fibromyalgia to the type of antidepressant mechanism.

 

Source: Goodnick PJ, Sandoval R. Psychotropic treatment of chronic fatigue syndrome and related disorders. J Clin Psychiatry. 1993 Jan;54(1):13-20. http://www.ncbi.nlm.nih.gov/pubmed/8428892

 

Central basis of muscle fatigue in chronic fatigue syndrome

Abstract:

We studied whether muscle fatigue, metabolism, or activation are abnormal in the chronic fatigue syndrome (CFS). Subjects performed both an intermittent submaximal and a sustained maximal voluntary isometric exercise protocol of the tibialis anterior muscle.

The extent of fatigue, metabolic response, and changes in both M-wave amplitude and twitch tension during exercise were similar in patients and controls. The response to systemic exercise was also normal in the patients. However, voluntary activation of the tibialis was significantly lower in the patients during maximal sustained exercise.

The results indicate that patients with CFS have (1) normal fatigability and metabolism at both the intracellular and systemic levels, (2) normal muscle membrane function and excitation-contraction coupling, and (3) an inability to fully activate skeletal muscle during intense, sustained exercise. This failure of activation was well in excess of that found in controls, suggesting an important central component of muscle fatigue in CFS.

Comment in: Chronic fatigue syndrome. [Neurology. 1993]

 

Source: Kent-Braun JA, Sharma KR, Weiner MW, Massie B, Miller RG. Central basis of muscle fatigue in chronic fatigue syndrome. Neurology. 1993 Jan;43(1):125-31. http://www.ncbi.nlm.nih.gov/pubmed/8423875

 

Persistence of enterovirus RNA in muscle biopsy samples suggests that some cases of chronic fatigue syndrome result from a previous, inflammatory viral myopathy

Abstract:

Molecular hybridization using an enterovirus group specific probe detected virus RNA in muscle biopsy samples from 25 of 96 cases of inflammatory muscle disease and similarly from 41 of 158 cases of postviral fatigue syndrome (PFS).

Enterovirus RNA was detected in only two of 152 samples of control muscle. The inflammatory myopathy group comprised patients with polymyositis (PM), juvenile dermatomyositis (JDM) or adult dermatomyositis (DM), and all showed the presence of an inflammatory infiltrate and fiber necrosis on histological examination of a muscle biopsy sample.

In contrast, muscle samples from the PFS group were histologically normal except for non-specific changes such as occasional single fiber atrophy. By analogy with enteroviral myocarditis, which can progress to a post-inflammatory disease with persistence of virus in myocardium and disposes to the rapid development of dilated cardiomyopathy, we propose that PFS syndrome may be a sequela of a previous inflammatory viral myopathy.

 

Source: Bowles NE, Bayston TA, Zhang HY, Doyle D, Lane RJ, Cunningham L, Archard LC. Persistence of enterovirus RNA in muscle biopsy samples suggests that some cases of chronic fatigue syndrome result from a previous, inflammatory viral myopathy. J Med. 1993;24(2-3):145-60. http://www.ncbi.nlm.nih.gov/pubmed/8409778

 

Epidemiology of chronic fatigue syndrome: the Centers for Disease Control Study

Abstract:

The US Centers for Disease Control initiated physician-based chronic fatigue syndrome (CFS) surveillance systems in four cities in September 1989 to determine the prevalence, incidence, course and impact of the illness. The participating physicians have referred to our surveillance system 590 patients who were ill during the first two years of surveillance with severe, debilitating, unexplained fatigue for at least the preceding six months.

Referred patients were screened for psychiatric disorders preceding, concurrent with, and subsequent to the onset of their fatigue by specially trained nurses using a modified Diagnostic Interview Schedule. Complete health histories were obtained by interview and review of medical records and a basic panel of standard laboratory diagnostic tests were conducted. Four physicians have independently reviewed the health information of 337 of the patients for classification.

Approximately 26% of patients referred to the surveillance system met the CFS case definition in all regards, 14% lacked one or more of the required eight symptom criteria, 15% were judged to have another possible or known medical illness which could account for the severe fatigue, and the remaining 45% did not meet the case definition because of histories of psychiatric disorders preceding the onset of fatigue.

Minimum prevalence rates for the period 1 September 1989 to 1 September 1991 ranged from 2.0 to 7.3 per 100,000 of the general population across the four study sites and rates based on prorated data ranged from 4.6 to 11.3 per 100,000. More than 80% of the CFS cases were female, most were white, and their average age at onset was approximately 30 years.

 

Source: Gunn WJ, Connell DB, Randall B. Epidemiology of chronic fatigue syndrome: the Centers for Disease Control Study. Ciba Found Symp. 1993;173:83-93; discussion 93-101. http://www.ncbi.nlm.nih.gov/pubmed/8387910

 

Investigation of retroviral involvement in chronic fatigue syndrome

Abstract:

Within the last few years significant efforts have been made to identify objective reliable diagnostic markers from individuals with chronic fatigue syndrome (CFS).

We report the absence of a previously described retroviral marker (HTLV-II gag) in a blinded study of CFS cases. Even with excellent reproducible sensitivities, this marker failed in repeated attempts to distinguish cases from controls. In addition, four other retroviruses (simian T cell leukaemia virus, human spumavirus, bovine leukaemia virus and simian retrovirus) were examined for their presence in these CFS cases and found to be absent.

Our findings suggest that these agents, at least as markers, are non-distinguishing for CFS and that other factors may be confounding the resolution of an aetiology to this syndrome.

 

Source: Folks TM, Heneine W, Khan A, Woods T, Chapman L, Schonberger L. Investigation of retroviral involvement in chronic fatigue syndrome. Ciba Found Symp. 1993;173:160-6; discussion 166-75. http://www.ncbi.nlm.nih.gov/pubmed/8387909

 

Enteroviruses and postviral fatigue syndrome

Abstract:

Postviral fatigue syndrome (PFS) occurs both in epidemics and sporadically. Many of the original epidemics were related to poliomyelitis outbreaks which either preceded or followed them.

The core clinical symptoms are always the same: severe fatigue made worse by exercise, myalgia, night sweats, atypical depression and excessive sleep. The other common symptoms include dysequilibrium disorders and irritable bowel syndrome.

We have detected enteroviral genome sequences in muscle biopsies from cases of PFS, using specific enteroviral oligonucleotide primers in the polymerase chain reaction (PCR). In addition, whole virus particles can be demonstrated in PCR-positive muscle, using solid-phase immuno-electron microscopy.

An increase in the number and size of muscle mitochondria was found in 70% of PFS cases, suggesting an abnormality in metabolic function. Evidence of hypothalamic dysfunction was present, particularly involving 5-hydroxytryptamine metabolism.

A putative model of PFS, based on persistent enteroviral infection in laboratory mice, revealed resolving inflammatory lesions in muscle with, however, a marked increase in the production of certain cytokines in the brain. This model may help to explain the pathogenesis of PFS.

 

Source: Behan PO, Behan WM, Gow JW, Cavanagh H, Gillespie S. Ciba Found Symp. 1993;173:146-54; discussion 154-9. http://www.ncbi.nlm.nih.gov/pubmed/8387908

 

Studies of herpesvirus infection in chronic fatigue syndrome

Abstract:

The relationship of herpesviruses to chronic fatigue syndrome has received considerable attention over the past decade. Data suggesting an association fall into three major categories.

First, among acute precipitants of the syndrome are primary infections with some herpesviruses, most notably Epstein-Barr virus and cytomegalovirus.

Second, a series of studies have detailed elevations of antibodies to most herpesviruses in selected chronic fatigue syndrome populations, with Epstein-Barr virus and human herpes type 6 being the objects of most scrutiny.

Third, one recent study reported a greater ease of recovery of human herpes virus type 6 from chronic fatigue syndrome patients. This review article critically examines the cumulative data regarding an association between one or more herpesviruses and the chronic fatigue syndrome in the context of the known biology and epidemiology of these agents.

In view of these, and additional considerations regarding study methodologies, the conclusion is drawn that herpesviruses are not dominant causes of the chronic fatigue syndrome and may not even be necessary to the perpetuation of the illness, but it is premature to dismiss entirely this latter possibility.

 

Source: Straus SE. Studies of herpesvirus infection in chronic fatigue syndrome. Ciba Found Symp. 1993;173:132-9; discussion 139-45. http://www.ncbi.nlm.nih.gov/pubmed/8387907