Tag: 1991

Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome

Abstract:

OBJECTIVE: To determine the presence of enteroviral sequences in muscle of patients with the postviral fatigue syndrome.

DESIGN: Detection of sequences with the polymerase chain reaction in a well defined group of patients with the syndrome and controls over the same period.

SETTING: Institute of Neurological Sciences, Glasgow.

SUBJECTS: 60 consecutive patients admitted to the institute with the postviral fatigue syndrome who had undergone extensive investigation to exclude other conditions. 41 controls from the same catchment area without evidence of fatigue, all undergoing routine surgery.

MAIN OUTCOME MEASURES: Routine investigations, serological screen for antibodies to a range of viruses, and presence of enteroviral RNA sequences in muscle biopsy specimens.

RESULTS: 15 (25%) patients and 10 (24.4%) controls had important serological findings. 12 patients had neutralising antibody titres of greater than or equal to 256 to coxsackieviruses B1-5 (six positive for enteroviral RNA sequences, six negative); three were positive for Epstein-Barr virus specific IgM (two positive, one negative). Six controls had similar neutralising antibody titres to coxsackieviruses (all negative); one was positive for Epstein-Barr virus specific IgM (negative); and three had titres of complement fixing antibody greater than or equal to 256 to cytomegalovirus (all negative). Overall, significantly more patients than controls had enteroviral RNA sequences in muscle (32/60, 53% v 6/41, 15%; odds ratio 6.7, 95% confidence interval 2.4 to 18.2). This was not correlated with duration of disease, patient and age, or to raised titres of antibodies to coxsackieviruses B1-5.

CONCLUSIONS: Persistent enteroviral infection of muscle may occur in some patients with postviral fatigue syndrome and may have an aetiological role.

Comment in: Postviral fatigue syndrome. [BMJ. 1991]

 

Source: Gow JW, Behan WM, Clements GB, Woodall C, Riding M, Behan PO. Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome. BMJ. 1991 Mar 23;302(6778):692-6. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1669122/ (Full article)

 

Coxsackie B virus and postviral fatigue syndrome

Comment on: Antibody to Coxsackie B virus in diagnosing postviral fatigue syndrome. [BMJ. 1991]

 

SIR,-Dr N A Miller and colleagues highlight the difficulty of associating a virus (coxsackie B virus) with a disease (postviral fatigue syndrome) when the virus in question is common in the general population.’ In a recent serological survey of the family members of children with insulin dependent diabetes mellitus we also found a high prevalence of IgM antibody specific to enterovirus: 14% of children with recently diagnosed insulin dependent diabetes mellitus, 8% of unaffected siblings, and 18% of parents had the antibody at the time of entry into the study. Serum samples were collected between 1985 and 1987. These seroprevalence figures are higher than those reported among control populations in earlier studies in the United Kingdom-5 5% in children during 19822 and 3-5% in adults during 1979-80.3 Because the assay used in these studies was the same as that used by Dr Miller and colleagues this indicates that enterovirus was endemic during 1985-7, which covers the period of the study of Dr Miller and colleagues.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1675464/pdf/bmj00117-0062c.pdf

 

Source: Muir P, Nicholson F, Banatvala JE, Bingley PJ. Coxsackie B virus and postviral fatigue syndrome. BMJ. 1991 Mar 16;302(6777):658-9. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1675464/

 

A personal encounter with a mystery illness

Abstract:

I urge all practitioners to accept that ‘chronic fatigue’ patients have genuine symptoms. This disease can cause depression, but for most patients it is not caused by depression. I acknowledge that a depressed patient can develop the chronic fatigue syndrome in the same way that they can contract any other disease. If you are unable to diagnose a patient with these symptoms please refer them to a centre specialising in this devastating and poorly understood disease.

 

Source: Lopis R. A personal encounter with a mystery illness. Aust Fam Physician. 1991 Mar;20(3):316-7.  http://www.ncbi.nlm.nih.gov/pubmed/2039419

 

A practical approach to chronic fatigue syndrome

Abstract:

Chronic fatigue may have several physical causes, but a psychiatric condition is often involved. A substantial minority of patients are not diagnosed by conventional tests and do not respond to antidepressant therapy. These patients should be referred for psychiatric opinion or observed for new developments. Extensive virologic testing and unorthodox treatment approaches have no scientific basis at present. Claims of dramatic new diagnostic tests or therapy should be treated with caution because of the long history of unsuccessful attempts to categorize chronic fatigue into one diagnosis and the strong placebo effect shown in controlled trials.

 

Source: Hayden SP. A practical approach to chronic fatigue syndrome. Cleve Clin J Med. 1991 Mar-Apr;58(2):116-20. http://www.ncbi.nlm.nih.gov/pubmed/2025913

 

Myalgic encephalomyelitis

Comment in: Myalgic encephalomyelitis. [J R Soc Med. 1991]

Comment on: Myalgic encephalomyelitis: an alternative theory. [J R Soc Med. 1990]

 

I am pleased that Dr Wilson (August 1990 JRSM, p481) has paid me the compliment of giving my article on the vexed topic of ‘myalgic encephalomyelitis’ (April 1989 JRSM, p 215) serious attention, and echoes our call’ for a ‘new approach’ to the problem, based on an absence of prejudice and a sound clinical and social history. He also notes the parallels between neurasthenia and ‘ME’, although the former was not, as he writes, first described in 18842. However, I only wish I could follow the rest of his arguments so clearly:

Dr Wilson states that I failed to realize that ‘about 100%’ of patients have an allergic diathesis and an allergic family history. I was indeed unaware of this remarkable finding. Unfortunately, I have been unable to trace the two sources cited for this observation, one an American paperback, the other a society newsletter. Similarly, I am afraid that neither I nor any of my colleagues have ever met anyone suffering from ‘Alternate Multiple Personality’. Perhaps this was because I was again unaware of the relevant literature. However, in my defence I would not otherwise have known that the two references quoted, namely Dr Wilson’s paper on allergic disease, multiple personality and dowsing, and his paper on possession and multiple personality, are actually about chronic fatigue syndrome. Similarly, I would not have known that an article in the Christian Parapsychologist called ‘Deliverance and dowsing’ is on the psychopathology of allergy and ME, nor that information on treatment of ME would be published in a series of titles beginning with ‘Current theological perspectives on possession. It is becoming harder to keep up with the relevant literature.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1293160/pdf/jrsocmed00126-0074c.pdf

 

See the article “Myalgic encephalomyelitis: an alternative theory.” in volume 83 on page 481.

See letter “Myalgic encephalomyelitis.” on page 633.

See the reply “The author replies” on page 183a.

 

Source: Wessely S. Myalgic encephalomyelitis. J R Soc Med. 1991 Mar;84(3):182-3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1293160/

 

Nurse, is it ME? Understanding myalgic encephalomyelitis

Abstract:

Ignored or dismissed for years, myalgic encephalomyelitis (ME) is now recognised as a genuine illness, and sufferers are recommended strict rest until the symptoms of the virus subside. Public understanding of ME is still uncertain, and nurses are ideally placed to provide practical information and support.

 

Source: Dale S. Nurse, is it ME? Understanding myalgic encephalomyelitis. Prof Nurse. 1991 Mar;6(6):339-40. http://www.ncbi.nlm.nih.gov/pubmed/2000430

 

A comprehensive immunological analysis in chronic fatigue syndrome

Abstract:

A detailed analysis of cell-mediated and antibody-mediated immunity was performed in 20 CDC-defined patients with chronic fatigue syndrome (CFS) and 20 age- and sex-matched healthy controls.

CD3+, CD4+, CD8+, and CD20+ lymphocytes were comparable in two groups. Natural killer cells as defined by CD16, CD56 and CD57 antigens were significantly reduced in CFS. A significant increase in the proportions of CD4+ ICAM 1+ T cells was observed in CFS. Monocytes from CFS displayed increased density (as determined by mean fluorescence channel numbers) of intercellular adhesion molecule 1 (ICAM-1) and lymphocyte function associated antigen 1 (LFA-1), but showed decreased enhancing response to recombinant interferon-gamma in vitro.

The lymphocyte DNA synthesis in response to phytohaemoglobulin (PHA), Concanavalin A (Con A) and pokeweed mitogen (PWM) was normal but the response to soluble antigens was significantly reduced. Serum IgM, IgG, IgA, and IgG subclasses were normal. In vivo specific antibody response to pneumococcus vaccine was depressed in CFS.

Forty percent of patients showed titres of anti-human herpes virus 6 (anti-HHV-6) antibody higher than that in the controls (greater than or equal to 1/80). These data suggest immunological dysfunction in patients with chronic fatigue syndrome. The significance of these observations is discussed.

 

Source: Gupta S, Vayuvegula B. A comprehensive immunological analysis in chronic fatigue syndrome. Scand J Immunol. 1991 Mar;33(3):319-27. http://www.ncbi.nlm.nih.gov/pubmed/1849315

 

Changes in natural killer cell phenotype in patients with post-viral fatigue syndrome

Abstract:

We analysed peripheral blood CD56+ natural killer (NK) cell subsets in 23 carefully characterized patients with post-viral fatigue syndrome (PFS), compared with 19 healthy controls, using fluorochrome-conjugated, specific monoclonal antibodies and the FACScan.

We found significantly increased percentages of CD56+, and especially CD56bright+ NK cells in PFS patients. We also found significantly increased percentages of CD56+ high affinity interleukin-2 (IL-2) receptor (CD25)+ and CD56+ transferrin receptor (CD71+) subsets of cells, most of which also stained brightly for CD56.

Also, we found an increased percentage of CD56+ CD3+ cells, many of which stained brightly for CD56, although there was no increase in the percentage of CD56- CD3+ T cells in these patients. These observations, in conjunction with very low percentage of CD56- CD25+ cells, suggest that there is a preferential involvement of this minor subset of CD56+ CD3+ T cells in PFS.

Finally, a decreased percentage of CD56+ Fc gamma receptor (CD16)+ NK cells was identified, which suggests a reduced capacity of antibody-dependent cellular cytotoxicity in PFS patients. Subsets of CD56+ NK cells co-expressing CD2, CD4 or CD8 did not show any significant difference between PFS patients and healthy controls.

These phenotypic changes provide laboratory evidence of immunological abnormalities in this syndrome, and, we suggest, may be consistent with persistent viral infection.

 

Source: Morrison LJ, Behan WH, Behan PO. Changes in natural killer cell phenotype in patients with post-viral fatigue syndrome. Clin Exp Immunol. 1991 Mar;83(3):441-6. http://www.ncbi.nlm.nih.gov/pubmed/1706238

You can read the full article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1535328/

 

Chronic fatigue syndrome: I. Epstein-Barr virus immune response and molecular epidemiology

Abstract:

Patients with chronic fatigue syndrome were compared to healthy seropositive control subjects in an open study and a case-control study analyzing spontaneous transformation rates of peripheral blood lymphocytes, EBV viral genome characteristics as determined by DNA restriction fragment polymorphisms, and antibody production by Western blot analysis.

Thirty percent of patients versus 8% of control subjects underwent spontaneous transformation in the two studies. Viral genome patterns were overall similar to one another, with polymorphisms frequently present in BamHI B’, K, H, and Y fragments. Only one line was found with the EBNA-2B genotype.

Nineteen lines were found to contain viral DNA in the linear form suggesting active lytic replication. Western blot studies suggested that ill subjects made antibodies to lytic proteins more frequently than did healthy control subjects. Lack of control of EBV outgrowth in vitro is correlated with antibody evidence of active infection in vivo in some patients with chronic fatigue syndrome.

 

Source: Jones JF, Streib J, Baker S, Herberger M. Chronic fatigue syndrome: I. Epstein-Barr virus immune response and molecular epidemiology. J Med Virol. 1991 Mar;33(3):151-8. http://www.ncbi.nlm.nih.gov/pubmed/1679118

 

Cognitive behaviour therapy in chronic fatigue syndrome

Abstract:

Fifty patients fulfilling operational criteria for the chronic fatigue syndrome (CFS), and who had been ill for a mean of five years, were offered cognitive behaviour therapy in an open trial. Those fulfilling operational criteria for depressive illness were also offered tricyclic antidepressants. The rationale was that a distinction be drawn between factors that precipitate the illness and those that perpetuate it.

Among the latter are cognitive factors such as the belief that physical symptoms always imply tissue damage, and behavioural factors such as persistent avoidance of activities associated with an increase in symptoms. Therapy led to substantial improvements in overall disability, fatigue, somatic and psychiatric symptoms. The principal problems encountered were a high refusal rate and difficulties in treating affective disorders. Outcome depended more on the strength of the initial attribution of symptoms to exclusively physical causes, and was not influenced by length of illness.

These results suggest that current views on both treatment and prognosis in CFS are unnecessarily pessimistic. It is also suggested that advice currently offered to chronic patients, to avoid physical and mental activity, is counterproductive.

 

Source: Butler S, Chalder T, Ron M, Wessely S. Cognitive behaviour therapy in chronic fatigue syndrome. J Neurol Neurosurg Psychiatry. 1991 Feb;54(2):153-8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1014351/