Category: Etiology

Chronic intestinal candidiasis as a possible etiological factor in the chronic fatigue syndrome

Abstract:

The chronic candidiasis syndrome, also known as the Candida-related complex, putatively caused by the overgrowth of Candida albicans in the gastrointestinal tract and secondarily in the genital organs, is briefly described.

Patients with this disorder have many of the same symptoms as those with the chronic fatigue syndrome, except for the recurrent flu-like symptoms of the latter disorder. The positive response of a large number of patients with the chronic fatigue syndrome (CFS) to an oral antifungal agent and a diet for intestinal candidiasis has been described by another clinician.

There is evidence that Candida albicans infection of the mucous membranes depresses T cell and natural killer (NK) cell function. Similar abnormalities of immune function are found in the CFS. The function of cytotoxic T cells, T helper cells, and NK cells is important in preventing reactivation of infections from Epstein-Barr virus, cytomegalovirus, and other herpesviruses.

Reactivation of one or more of these viruses could lead to the expression of the flu-like symptoms in the CFS. Yet the immune dysfunction found in this disorder has been considered the primary underlying causal factor.

It is proposed that chronic intestinal candidiasis may be an agent which leads to immune depression in many CFS patients and therefore that it could be a causal factor in CFS.

 

Source: Cater RE 2nd. Chronic intestinal candidiasis as a possible etiological factor in the chronic fatigue syndrome. Med Hypotheses. 1995 Jun;44(6):507-15. http://www.ncbi.nlm.nih.gov/pubmed/7476598

 

Postinfectious fatigue: prospective cohort study in primary care

Abstract:

The idea that chronic fatigue has an infectious origin has become popular, but the main evidence for such an association has come from retrospective case-control studies, which are subject to ascertainment bias. We report a prospective study of the outcome of clinically diagnosed infections in patients presenting to UK general practitioners.

Questionnaires assessing fatigue and psychiatric morbidity were sent to all patients aged 18-45 years in the study practices. The prevalence of chronic fatigue and chronic fatigue syndrome was then ascertained among 1199 people aged 18-45 who presented to the general practitioners with symptomatic infections and in 1167 people who attended the surgeries for other reasons. 84% were followed up at 6 months. 9.9% of cases and 11.7% of controls reported chronic fatigue (odds ratio 1.0 [95% CI 0.6-1.1]). There were no differences in the proportions who met various criteria for chronic fatigue syndrome. No effect of infection was noted when we excluded subjects who reported fatigue or psychological morbidity at the baseline screening.

The strongest independent predictors of postinfectious fatigue were fatigue assessed before presentation with clinical infection (3.0 [1.9-4.7]) and psychological distress before presentation (1.8 [1.2-2.9]) and at presentation with the acute infection (1.8 [1.1-2.8]). There was no effect of sex or social class. Our study shows no evidence that common infective episodes in primary care are related to the onset of chronic fatigue or chronic fatigue syndrome.

Comment in:

Viral illness and chronic fatigue (syndrome). [Lancet. 1995]

Viral illness and chronic fatigue (syndrome) [Lancet. 1995]

Viral illness and chronic fatigue (syndrome). [Lancet. 1995]

Viral illness and chronic fatigue (syndrome) [Lancet. 1995]

Viral illness and chronic fatigue (syndrome). [Lancet. 1995]

 

Source: Wessely S, Chalder T, Hirsch S, Pawlikowska T, Wallace P, Wright DJ. Postinfectious fatigue: prospective cohort study in primary care. Lancet. 1995 May 27;345(8961):1333-8. http://www.ncbi.nlm.nih.gov/pubmed/7752755

 

Epstein-Barr virus (EBV) and the chronic fatigue syndrome: normal virus load in blood and normal immunologic reactivity in the EBV regression assay

Abstract:

The etiology of chronic fatigue syndrome (CFS) is unknown. Some patients have high antibody titers to viral capsid antigen (VCA) and early antigen (EA) of Epstein-Barr virus (EBV), suggesting that reactivation of EBV is involved. We investigated virus load (spontaneous transformation) and immunologic regression of EBV-induced transformation in peripheral blood mononuclear cells (PBMCs) from 10 selected patients with CFS who had high antibody titers to VCA and EA. The outcome was compared with that for nine healthy controls and one patient with severe chronic active EBV infection (SCAEBV). There were no significant differences in viral load between patients and healthy controls. Immunologic regression of in vitro-transformed PBMCs was also equally efficient in patients and controls. The SCAEBV-infected patient and two controls, who were all seronegative for EBV, showed impaired regression. In conclusion, we were unable to demonstrate a role for reactivation of EBV in CFS, even in selected patients with high titers of antibody to VCA and EA of EBV.

 

Source: Swanink CM, van der Meer JW, Vercoulen JH, Bleijenberg G, Fennis JF, Galama JM. Epstein-Barr virus (EBV) and the chronic fatigue syndrome: normal virus load in blood and normal immunologic reactivity in the EBV regression assay. Clin Infect Dis. 1995 May;20(5):1390-2. http://www.ncbi.nlm.nih.gov/pubmed/7620030

 

Chronic fatigue syndrome. 1: Etiology and pathogenesis

Abstract:

Chronic fatigue syndrome (CFS) is a disorder of unknown etiology characterized by debilitating fatigue and other somatic and neuropsychiatric symptoms. A range of heterogeneous clinical and laboratory findings have been reported in patients with CFS. Various theories have been proposed to explain the underlying pathophysiologic processes but none has been proved.

Research findings of immunologic dysfunction and neuroendocrine changes suggest the possible dysregulation of interactions between the nervous system and the immune system. Without a clear understanding of its etiopathogenesis, CFS has no definitive treatment.

Management approaches have been necessarily speculative, and they have evolved separately in a number of medical and nonmedical disciplines. The results of several controlled treatment studies have been inconclusive. An accurate case definition identifying homogeneous subtypes of CFS is needed. The integration of medical and psychologic treatment modalities and the use of both biologic and psychologic markers to evaluate treatment response will enhance future treatment strategies.

 

Source: Farrar DJ, Locke SE, Kantrowitz FG. Chronic fatigue syndrome. 1: Etiology and pathogenesis. Behav Med. 1995 Spring;21(1):5-16. http://www.ncbi.nlm.nih.gov/pubmed/7579775

 

Post-hepatitis syndrome revisited

Abstract:

To examine the role of acute hepatitis A and B infection in the aetiology of chronic fatigue syndrome and psychiatric morbidity we studied 40 patients with acute viral hepatitis A or B consecutively admitted to an infectious diseases unit and studied at least 6 months after recovery.

Liver function tests (LFT) had returned to normal in each case. Forty-seven patients with other infectious diseases, of which 12 were presumed viral, admitted immediately after each hepatitis patient during the same period acted as controls. The main outcome measures were scores on a fatigue and muscle pain questionnaire, general health questionnaire (GHQ-12) and supplementary questions.

The hepatitis cases scored significantly higher fatigue scores, GHQ-12 scores and muscle pain scores. Length of time since recovery from illness, age and sex were not confounding factors. Hepatitis cases were also less energetic, had greater weight change, had altered alcohol tolerance, had less exercise tolerance and felt less fit than the control group and compared with their premorbid state.

Hence fatigue is more common after recovery in patients hospitalized for hepatitis A and B up to 30 months post-infection compared with matched controls hospitalized for other infectious diseases. Hepatitis A and B infection is a risk factor for post-infection fatigue, intermittent fatigue, as well as for psychiatric morbidity.

 

Source: Berelowitz GJ, Burgess AP, Thanabalasingham T, Murray-Lyon IM, Wright DJ. Post-hepatitis syndrome revisited. J Viral Hepat. 1995;2(3):133-8. http://www.ncbi.nlm.nih.gov/pubmed/7493307

 

Stealth viruses as neuropathogens

Abstract:

Neuropsychiatric diseases viewed as multifaceted expression of a dysfunctional brain in which atypical responses are evoked by various sensory inputs. Disease entities have traditionally been classified according to the predominant manifestation ( ) without regard to the overlapping features of many of the diseases (+/-). Thus, mild to moderate pain, mood, cognitive, and neurosomatic symptoms are frequently present in chronic fatigue syndrome (CFS) patients. Fibromyalgia syndrome (FMS) is listed as an example of a predominantly chronic pain syndrome. Affect (mood) disorders include depression (Depress.), anxiety, panic reactions, blunted affect, mania, etc. Schizophrenia (Schizo.) is listed as an example of a major cognitive psychosis. Autism as well as various forms of dementia would be included in this category. Irritable bowel syndrome (IBS) is an example of a neurosomatic disease.

 

Source: Martin WJ. Stealth viruses as neuropathogens. CAP Today. 1994 Oct;8(10):67-70. http://www.ncbi.nlm.nih.gov/pubmed/10150189

 

The etiology and possible treatment of chronic fatigue syndrome/fibromyalgia

Abstract:

It is suggested that chronic fatigue syndrome/fibromyalgia is caused by virus injury to the calcium channels leading to larger quantities than usual of calcium ions entering the striated muscle cells. Should this be true, then treatment with a calcium antagonist (CA) may possibly be of value.

 

Source: Lund-Olesen LH, Lund-Olesen K. The etiology and possible treatment of chronic fatigue syndrome/fibromyalgia. Med Hypotheses. 1994 Jul;43(1):55-8. http://www.ncbi.nlm.nih.gov/pubmed/7968720

 

Professional and popular views of chronic fatigue syndrome

Abstract:

OBJECTIVE: To study the coverage of the chronic fatigue syndrome in the popular and professional press.

DESIGN: Search of all original research papers on the chronic fatigue syndrome published in British journals from 1980 onwards and of professional trade papers, national newspapers, and women’s magazines. Interviews with six medical journalists.

SETTING: British scientific, medical, and popular press.

RESULTS: 37 (49%) articles in research journals did not favour organic causes and 23 (31%) favoured organic causes. By contrast 31 (55%) articles in the medical trade press and 118 (69%) in national newspapers and women’s magazines favoured organic causes.

CONCLUSIONS: Press coverage of chronic fatigue syndrome has amplified and distorted divisions in the research community concerning the chronic fatigue syndrome. Articles in the press concentrate on a simple medical model of illness reinforcing the stigma of psychological illness and dissatisfaction with traditional medical authority.

Comment in:

Chronic fatigue syndrome: prevalence and outcome. [BMJ. 1994]

Patients with a self diagnosis of myalgic encephalomyelitis. [BMJ. 1995]

 

Source: MacLean G, Wessely S. Professional and popular views of chronic fatigue syndrome. BMJ. 1994 Mar 19;308(6931):776-7. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2539637/

You can read the full article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2539637/pdf/bmj00432-0054.pdf

 

Dysregulated expression of tumor necrosis factor in chronic fatigue syndrome: interrelations with cellular sources and patterns of soluble immune mediator expression

Abstract:

Among a group of 70 individuals who met the criteria established by the Centers for Disease Control and Prevention (Atlanta) for chronic fatigue syndrome (CFS), 12%-28% had serum levels exceeding 95% of control values for tumor necrosis factor (TNF) alpha, TNF-beta, interleukin (IL) 1 alpha, IL-2, soluble IL-2 receptor (sIL-2R), or neopterin; overall, 60% of patients had elevated levels of one or more of the nine soluble immune mediators tested.

Nevertheless, only the distributions for circulating levels of TNF-alpha and TNF-beta differed significantly in the two populations. In patients with CFS–but not in controls–serum levels of TNF-alpha, IL-1 alpha, IL-4, and sIL-2R correlated significantly with one another and (in the 10 cases analyzed) with relative amounts (as compared to beta-globin or beta-actin) of the only mRNAs detectable by reverse transcriptase-coupled polymerase chain reaction in peripheral-blood mononuclear cells: TNF-beta, unspliced and spliced; IL-1 beta, lymphocyte fraction; and IL-6 (in order of appearance). These findings point to polycellular activation and may be relevant to the etiology and nosology of CFS.

 

Source: Patarca R, Klimas NG, Lugtendorf S, Antoni M, Fletcher MA. Dysregulated expression of tumor necrosis factor in chronic fatigue syndrome: interrelations with cellular sources and patterns of soluble immune mediator expression. Clin Infect Dis. 1994 Jan;18 Suppl 1:S147-53. http://www.ncbi.nlm.nih.gov/pubmed/8148443

 

Functional hypoglycaemia postulated as cause of chronic fatigue syndrome

Comment on: The chronic fatigue syndrome: what do we know? [BMJ. 1993]

 

Editor,-In discussing the various causes of the chronic fatigue syndrome P K Thomas fails to mention one syndrome-namely, functional hypoglycaemia. We do not believe that such a syndrome exists, but in the Netherlands it has become a popular diagnosis among “alternative doctors,” who claim that chronic fatigue is caused by inappropriately increased postprandial insulin concentrations with subsequent hypoglycaemia. This disease is linked to a so called allergy to endogenous glucose.

It is clear from this description that there is no scientific basis for this syndrome, and this is confirmed in the literature. Unfortunately, doctors and dietitians who recognise this syndrome have burdened their patients with complicated diets, requiring the elimination of all simple carbohydrates. When we asked an alternative doctor why we never see hypoglycaemia in these patients we were told that we do not measure glucose concentrations at the right moment. The diagnosis should be made after a standard oral glucose tolerance test with measurement of glucose concentrations three and five hours after glucose intake. “Overproduction” of insulin is thus shown by reactive hypoglycaemia.

The use of this non-physiological test to diagnose this syndrome has no scientific basis whatsoever. Nevertheless, tens of thousands of patients are treated for this syndrome in the Netherlands.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1678679/pdf/bmj00039-0047a.pdf

 

Source: Heuft L, Bravenboer B, Ziekenhuis C. Functional hypoglycaemia postulated as cause of chronic fatigue syndrome. BMJ. 1993 Sep 18;307(6906):735. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1678679/