Category: Etiology

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/

 

Abnormalities of sleep in patients with the chronic fatigue syndrome

Abstract:

OBJECTIVE: To determine whether patients with the chronic fatigue syndrome have abnormalities of sleep which may contribute to daytime fatigue.

DESIGN: A case-control study of the sleep of patients with the chronic fatigue syndrome and that of healthy volunteers.

SETTING: An infectious disease outpatient clinic and subjects’ homes.

SUBJECTS: 12 patients who met research criteria for the chronic fatigue syndrome but not for major depressive disorder and 12 healthy controls matched for age, sex, and weight.

MAIN OUTCOME MEASURES: Subjective reports of sleep from patients’ diaries and measurement of sleep patterns by polysomnography. Subjects’ anxiety, depression, and functional impairment were assessed by interview.

RESULTS: Patients with the chronic fatigue syndrome spent more time in bed than controls (544 min v 465 min, p < 0.001) but slept less efficiently (90% v 96%, p < 0.05) and spent more time awake after initially going to sleep (31.9 min v 16.6 min, p < 0.05). Seven patients with the chronic fatigue syndrome had a sleep disorder (four had difficulty maintaining sleep, one had difficulty getting to sleep, one had difficulty in both initiating and maintaining sleep, and one had hypersomnia) compared with none of the controls (p = 0.003). Those with sleep disorders showed greater functional impairment than the remaining five patients (score on general health survey 50.4% v 70.4%, p < 0.05), but their psychiatric scores were not significantly different.

CONCLUSIONS: Most patients with the chronic fatigue syndrome had sleep disorders, which are likely to contribute to daytime fatigue. Sleep disorders may be important in the aetiology of the syndrome.

 

Source: Morriss R, Sharpe M, Sharpley AL, Cowen PJ, Hawton K, Morris J. Abnormalities of sleep in patients with the chronic fatigue syndrome. BMJ. 1993 May 1;306(6886):1161-4. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1677618/ (Full article)

 

Inability of retroviral tests to identify persons with chronic fatigue syndrome, 1992

Abstract:

Chronic fatigue syndrome (CFS) is characterized by prolonged, debilitating fatigue. Although the cause of CFS unknown, CDC and researchers in other organizations have been investigating whether infection with a previously unidentified retrovirus might be an etiologic factor. Based on reports suggesting that retroviral infection with a human T-lymphotropic virus type 2 (HTLV-II)-like retrovirus or a spumavirus might be associated with CFS, some research and commercial laboratories developed assays to test specimens from persons with CFS. Even though the hypothesized association between infection with retroviruses and CFS has not been confirmed, these tests are used commonly to evaluate patients with CFS. This report summarizes the findings of a controlled, blinded study conducted in 1992 to determine whether three retroviral tests can distinguish serologically between patients with CFS (i.e., case-patients) and healthy controls.

 

Source: Centers for Disease Control and Prevention (CDC). Inability of retroviral tests to identify persons with chronic fatigue syndrome, 1992. MMWR Morb Mortal Wkly Rep. 1993 Mar 19;42(10):183, 189-90. http://www.ncbi.nlm.nih.gov/pubmed/8446093

 

Chronic fatigue and chronic fatigue syndrome: clinical epidemiology and aetiological classification

Abstract:

To determine the medical and psychiatric diagnoses that have an aetiological role in chronic fatigue we conducted a prospective study of 405 (65% women) patients who presented for evaluation with this chief complaint to an academic medical centre.

The average age was 38.1 years and the average duration of fatigue at entry in the study was 6.9 years. All patients were given comprehensive physical and laboratory evaluations and were administered a highly structured psychiatric interview. Psychiatric diagnoses explaining the chronic fatigue were identified in 74% of patients and physical disorders were diagnosed in 7% of patients.

The most common psychiatric conditions in this series were major depression, diagnosed in 58% of patients, panic disorder, diagnosed in 14% of patients, and somatization disorder, diagnosed in 10% of patients. Primary sleep disorders, diagnosed in 2% patients, and chronic infections, confirmed in 1.6% patients, explained the majority of cases whose chronic fatigue was attributed to a physical disorder.

Thirty per cent of patients met the criteria used to define the chronic fatigue syndrome (CFS). Compared with age- and gender-matched control subjects with chronic fatigue, CFS patients had a similarly high prevalence of current psychiatric disorders (78% versus 82%), but were significantly more likely to have somatization disorder (28% versus 5%) and to attribute their illness to a viral infection (70% versus 33%).

We conclude that most patients with a chief complaint of chronic fatigue, including those exhibiting the features of CFS, suffer from standard mood, anxiety and/or somatoform disorders. Careful research is still needed to determine whether CFS is a distinct entity or a variant of these psychiatric illness.

 

Source: Manu P, Lane TJ, Matthews DA. Chronic fatigue and chronic fatigue syndrome: clinical epidemiology and aetiological classification. Ciba Found Symp. 1993;173:23-31; discussion 31-42. http://www.ncbi.nlm.nih.gov/pubmed/8491100

 

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