1995 – Page 2 – American ME and CFS Society

Chronic active Epstein-Barr virus infection in children in Japan

Abstract:

The patients with chronic active Epstein-Barr virus infection (CAEBV) in childhood in Japan are described. Among 39 registered cases, 20 patients were males and 19 were females. Unlike the X-linked lymphoproliferative syndrome, there was no hereditary background.

The incidence of hypersensitivity to mosquito bites was high (31.3%) as a past history. Most patients exhibited hepatomegaly (92.3%), splenomegaly (87.2%) and fever (84.6%). The incidence of absent anti-EB virus nuclear antigen titres was unexpectedly low (17.1%). Lymphoreticular disorders and cardiovascular diseases were major complications.

Twenty-four (61.5%) patients died 6 months to 8 years after the onset, mainly of hepatic failure (eight cases), cardiac failure (five cases), virus-associated haemophagocytic syndrome (three cases) and haematological malignancies (two cases). This study reveals the CAEBV in Japan has several clinical features and should be informative for the pathogenesis of EB virus.

Source: Ishihara S, Okada S, Wakiguchi H, Kurashige T, Morishima T, Kawa-Ha K. Chronic active Epstein-Barr virus infection in children in Japan. Acta Paediatr. 1995 Nov;84(11):1271-5. http://www.ncbi.nlm.nih.gov/pubmed/8580625

Brainstem perfusion is impaired in chronic fatigue syndrome

Abstract:

We looked for brain perfusion abnormalities in patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). An initial pilot study revealed widespread reduction of regional brain perfusion in 24 ME/CFS patients, compared with 24 normal volunteers. Hypoperfusion of the brainstem (0.72 +/- 0.05 vs. 0.80 +/- 0.04, p < 0.0001) was marked and constant. We then tested whether perfusion to the brainstem in ME/CFS patients differs from that in normals, patients with major depression, and others with epilepsy.

Data from a total of 146 subjects were included in the present study: 40 normal volunteers, 67 patients with ME/CFS (24 in the pilot study, 16 with no psychiatric disorders, 13 with ME/CFS and depression, 14 with ME/CFS and other psychiatric disorders), 10 epileptics, 20 young depressed patients and 9 elderly depressed individuals.

Brain perfusion ratios were calculated using 99Tcm-hexamethylpropylene amine oxime (99Tcm-HMPAO) and single-photon emission tomography (SPET) with a dedicated three-detector gamma camera computer/system (GE Neurocam).

Brain-stem hypoperfusion was confirmed in all ME/CFS patients. Furthermore, the 16 ME/CFS patients with no psychiatric disorders and the initial 24 patients in the pilot study showed significantly lower brainstem perfusion (0.71 +/- 0.03) than did depressed patients (0.77 +/- 0.03; ANOVA, p < 0.0001).

Patients with ME/CFS have a generalized reduction of brain perfusion, with a particular pattern of hypoperfusion of the brainstem.

Comment in: Brainstem hypoperfusion in CFS. [QJM. 1996]

Source: Costa DC, Tannock C, Brostoff J. Brainstem perfusion is impaired in chronic fatigue syndrome. QJM. 1995 Nov;88(11):767-73. http://www.ncbi.nlm.nih.gov/pubmed/8542261

Outcome and prognosis of patients with chronic fatigue vs chronic fatigue syndrome

Abstract:

BACKGROUND: There are few data on the natural history and prognosis of persons with chronic fatigue (CF) or CF syndrome (CFS). Therefore, we compared functional outcomes in patients with each condition and tested the validity of various prognostic indicators.

METHODS: Four hundred forty-five (89%) of 498 consecutive referral patients were surveyed an average of 1.5 years after an initial evaluation. Data from the initial evaluation were used to predict outcomes.

RESULTS: Sixty-four percent of all patients reported improvement, but only 2% reported complete resolution of symptoms. Patients initially diagnosed as having CFS reported greater symptom severity and lower level of functioning at follow-up than did patients with CF. Major depression predicted unemployment in the CF group. Older age, longer duration of illness, and a lifetime history of dysthymia predicted less improvement in the CF group. Current dysthymia predicted less improvement for the CFS group.

CONCLUSIONS: The case definition of CFS according to the Centers for Disease Control and Prevention identifies chronically fatigued patients with poorer prognosis. In a tertiary care setting, recovery from CF or CFS is rare, but improvement is common. Prognostic indicators vary for the two groups, but the coexistence of dysthymia suggests poorer outcomes generally.

Source: Bombardier CH, Buchwald D. Outcome and prognosis of patients with chronic fatigue vs chronic fatigue syndrome. Arch Intern Med. 1995 Oct 23;155(19):2105-10. http://www.ncbi.nlm.nih.gov/pubmed/7575071

Illness behaviour in the chronic fatigue syndrome and multiple sclerosis. Disentangling common characteristics is not so easy

Comment on: “Abnormal” illness behaviour in chronic fatigue syndrome and multiple sclerosis. [BMJ. 1995]

EDITOR,-Over the past few years I have seen a growing number of patients with the chronic fatigue syndrome who have been told by psychiatrists and psychologists that abnormal illness behaviour and psychosocial factors are the main factors perpetuating their disability. Few patients have accepted or believed this explanation; neither have I. The ME Association now has evidence that the fashionable theory of abnormal illness behaviour linked to somatisation is being used by several agencies as a convenient excuse for turning down applications for financial benefits or for putting pressure on vulnerable patients to undergo speculative “rehabilitation” programmes, which they may be reluctant to participate in.

Although Peter Trigwell and colleagues conclude that patients with the chronic fatigue syndrome and multiple sclerosis have virtually identical patterns of illness behaviour without any form of shared aetiology, their study suggests that the two conditions may have more in common than just central fatigue and uncertainty about long term prognosis.’ When DeLuca et al examined patients with the chronic fatigue syndrome, patients with multiple sclerosis, and healthy controls using a paced auditory serial addition test (a method of assessing processing of complex auditory information) they found that both groups of patients scored significantly below the controls, indicating similar difficulties with tasks that require simultaneous processing of cognitive information.2

You can read the full comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2551397/pdf/bmj00615-0064a.pdf

Source: Shepherd C. Illness behaviour in the chronic fatigue syndrome and multiple sclerosis. Disentangling common characteristics is not so easy. BMJ. 1995 Oct 21;311(7012):1093. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2551397/pdf/bmj00615-0064a.pdf

Illness behaviour in the chronic fatigue syndrome and multiple sclerosis. Choice of multiple sclerosis as comparison condition was inappropriate

Comment on: “Abnormal” illness behaviour in chronic fatigue syndrome and multiple sclerosis. [BMJ. 1995]

EDITOR,-Peter Trigwell and colleagues compared patients with the chronic fatigue syndrome with patients with multiple sclerosis and report similar responses on Pilowsky’s illness behaviour questionnaire.’ There is accumulating evidence that the chronic fatigue syndrome is a functional disorder, with psychological, social, and physical factors implicated in its cause, whereas in multiple sclerosis the primary cause is physical. Wood et al compared patients with the chronic fatigue syndrome with patients with various muscle diseases and found a threefold increase in psychiatric diagnoses in the group with the chronic fatigue syndrome.2 Wessely et al describe an important prospective cohort study and conclude that common infections play little part in causing the chronic fatigue syndrome but that both previous psychological disorder and previous fatigue are associated with its development.3

We agree with Trigwell and colleagues that illness behaviour is highly relevant to the chronic fatigue syndrome, but we share their reservations about the particular method of assessing this. We also suggest that the choice of multiple sclerosis as a comparison condition was inappropriate. Multiple sclerosis, in contrast to muscle diseases, follows a relapsing and remitting course, often manifests sensory (subjective) rather than motor (objective) signs, and might therefore lead to illness behaviour that is abnormal, albeit for different reasons from those that might apply in the chronic fatigue syndrome.

You can read the full comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2551396/pdf/bmj00615-0063c.pdf

Source: Campion PD, Dowrick CF, Edwards RH. Illness behaviour in the chronic fatigue syndrome and multiple sclerosis. Choice of multiple sclerosis as comparison condition was inappropriate. BMJ. 1995 Oct 21;311(7012):1092-3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2551396/pdf/bmj00615-0063c.pdf

High incidence of antibodies to 5-hydroxytryptamine, gangliosides and phospholipids in patients with chronic fatigue and fibromyalgia syndrome and their relatives: evidence for a clinical entity of both disorders

Abstract:

The fibromyalgia syndrome (FMS) is one of the most frequent rheumatic disorders showing a wide spectrum of different symptoms. An association with the chronic fatigue syndrome (CFS) has been discussed. Recently, a defined autoantibody pattern consisting of antibodies to serotonin (5-hydroxytryptamine, 5-HT), gangliosides and phospholipids was found in about 70% of the patients with FMS. We were therefore interested in seeing whether patients with CFS express similar humoral immunoreactivity.

Sera from 42 CFS patients were analysed by ELISA for these antibodies, and the results were compared with those previously observed in 100 FMS patients. 73% of the FMS and 62% of the CFS patients had antibodies to serotonin, and 71% or 43% to gangliosides, respectively. Antibodies to phospholipids could be detected in 54% of the FMS and 38% of the CFS patients. 49% of FMS and 17% of the CFS patients had all three antibodies in parallel, 70% and 55%, respectively had at least two of these antibody types. 21% of FMS and 29% of CFS patients were completely negative for these antibodies. Antibodies to 5-HT were closely related with FMS/CFS while antibodies to gangliosides and phospholipids could also be detected in other disorders.

The observation that family members of CFS and FMS patients also had these antibodies represents an argument in favour of a genetic predisposition. These data support the concept that FMS and CFS may belong to the same clinical entity and may manifest themselves as ‘psycho-neuro-endocrinological autoimmune diseases’.

Source: Klein R, Berg PA. High incidence of antibodies to 5-hydroxytryptamine, gangliosides and phospholipids in patients with chronic fatigue and fibromyalgia syndrome and their relatives: evidence for a clinical entity of both disorders. Eur J Med Res. 1995 Oct 16;1(1):21-6. http://www.ncbi.nlm.nih.gov/pubmed/9392689

Patients with a self diagnosis of myalgic encephalomyelitis

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

EDITOR,-S J Hurel and colleagues should have checked their facts more thoroughly before making such a generalised attack on the content of literature produced by the two support groups for patients with myalgic encephalomyelitis (ME).

The ME Association does not believe that candida albicans is involved in the pathogenesis of the condition. Our booklet Guidelines for the Care of Patients states that “no reliable scientific evidence has ever been published to support such a link” and that “consequently, anti-candida regimes involving highly restricted diets, probiotics and antifungal drugs cannot be recommended.”2 Equally, we repeatedly warn our members about the serious dangers of colonic cleansing (particularly in relation to the risk of unhygienic operators transferring gastrointestinal pathogens) and advise extreme caution when consulting herbalists or buying over the counter herbal remedies. If we really were producing literature that contained pseudoscientific nonsense and advocated dubious forms of alternative therapy I doubt whether the Department of Health would be providing funding to expand the work of our information department.

Had the authors checked with our booklet they would have found that we are not in favour of self diagnosis and strongly recommend consideration of nearly 50 physical and psychological conditions that can present with chronic fatigue as the principal clinical feature. In this context pituitary tumours are specifically mentioned as we are aware of at least two other cases similar to that reported by Hurel and colleagues in which misdiagnosis occurred. Furthermore, our literature emphasises that “significant or progressive weight loss is not a normal feature of ME, and where it occurs alternative explanations (eg hormonal) should always be excluded.”

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2550999/pdf/bmj00614-0065a.pdf

Source: Shepherd C. Patients with a self diagnosis of myalgic encephalomyelitis. BMJ. 1995 Oct 14;311(7011):1021. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2550999/pdf/bmj00614-0065a.pdf (Full comment)

Chronic fatigue syndrome–a review of the literature

Abstract:

Chronic fatigue syndrome is a clinical condition characterized by abnormal fatigue, subfebrile body temperature, sore throat, lymphadenopathy, arthralgia, myalgia and neuropsychiatric symptoms. Typically, the syndrome develops after a flu-like illness and is markedly exacerbated by exercise. The etiology is unknown and there is no single diagnostic test. The patients may have cognitive dysfunction, immunological and endocrinological abnormalities and abnormal mitochondria. Magnetic resonance imaging scans may show increased uptake of signals in the brain, and single photon emission computerized tomography reveals regional hypoperfusion of the brain. The author discusses similarities and distinctions between the syndrome and depression.

Source: Hamre HJ. Chronic fatigue syndrome–a review of the literature. Tidsskr Nor Laegeforen. 1995 Oct 10;115(24):3042-5. [Article in Norwegian] http://www.ncbi.nlm.nih.gov/pubmed/7570537

Postviral fatigue syndrome

Abstract:

The post-viral fatigue syndrome occurs sporadically and in local outbreaks (Los Angeles, Akureyri, Royal Free Hospital). The clinical picture is marked by long-lasting muscular fatigue directly following an acute infection. Other conditions associated with pronounced fatigue must be excluded. The diagnostic criteria set up by Centers for Disease Control (CDC) are the ones most commonly used. Aetiology and pathogenesis are unknown. Coxsackie B-virus seems to be associated with some cases at least. Immunological and endocrinological aberration, morphological changes in mitochondria and reduced cerebral blood perfusion have been demonstrated in some patients. There is no specific therapy. It is important for the patient that the symptoms be accepted by the doctor and society in general.

Comment in: [Chronic fatigue syndrome]. [Tidsskr Nor Laegeforen. 1995]

Source: Haukenes G, Aarli JA. Postviral fatigue syndrome. Tidsskr Nor Laegeforen. 1995 Oct 10;115(24):3017-22. [Article in Norwegian] http://www.ncbi.nlm.nih.gov/pubmed/7570529