Tag: prevalence

Disagreements still exist over the chronic fatigue syndrome

Editor—Although the ME Association welcomes the royal colleges’ unequivocal conclusion that the chronic fatigue syndrome is a genuine and disabling condition,1 we also agree that their report will “engender disagreement on both sides of the Atlantic.”2 We have no problem in accepting that the alternative name for the condition—myalgic encephalomyelitis (ME)—is pathologically incorrect, and this is a matter that we now intend to address. However, labels are important to patients as well as doctors, and support groups throughout the world are unanimous in their view that “chronic fatigue syndrome” is a totally inadequate way of describing the symptomatology and associated disability. The chronic fatigue syndrome may well become a dustbin diagnosis for anyone with chronic fatigue, and a new name that is acceptable to both doctors and patients clearly needs to be found.

You can read the full comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2125625/pdf/9006489.pdf

 

Source: Shepherd C. Disagreements still exist over the chronic fatigue syndrome. BMJ. 1997 Jan 11;314(7074):146. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2125625/pdf/9006489.pdf

 

Epidemiologic advances in chronic fatigue syndrome

Abstract:

Epidemiologic studies of chronic fatigue syndrome (CFS) have been hampered by the absence of a specific diagnostic test, but with increasing interest in this disorder there has been a greater understanding of the risk factors, illness patterns, and other aspects of this multisystem disorder.

Working case definitions have been developed for research purposes but they have continued to change over time and have not always been utilized precisely by various investigators. This has been a major factor in the widely varying estimates of prevalence rates, but two different studies using the same working definition and including a medical work-up have estimated the prevalence to be approximately 200/100,000. Clusters of CFS cases, which appear to be related to earlier reports of “epidemic neuromyasthenia”, have attracted considerable attention and appear to be well documented, although investigated with varying methodology and often with dissimilar case definitions.

Risk factors for cases occurring in clusters and sporadically appear to be similar, the most consistent ones being female gender and the co-existence of some form of stress, either physical or psychological. The prognosis of CFS is difficult to predict, although cases occurring as part of clusters appear to have a better prognosis as a group than sporadic cases, and those with an acute onset have a better prognosis than those with gradual onset.

It is highly unlikely that there is a single agent, infectious or noninfectious, that is responsible for more than a small proportion of CFS cases and, at the present time, the risk factors for developing CFS appear to lie more prominently in the host rather than the environment.

 

Source: Levine PH. Epidemiologic advances in chronic fatigue syndrome. J Psychiatr Res. 1997 Jan-Feb;31(1):7-18. http://www.ncbi.nlm.nih.gov/pubmed/9201643

 

Chronic fatigue syndrome and myalgic encephalomyelitis

Comment on:

Chronic fatigue syndrome. Distinguish between syndromes… [BMJ. 1994]

Chronic fatigue syndrome. Role of psychological factors overemphasised. [BMJ. 1994]

 

Editor,-Our recent editorial on the chronic fatigue syndrome and myalgic encephalomyelitis prompted considerable correspondence,’ which raised issues of case definition, clinical management, and attitudes towards people with psychiatric illnesses. Sadly, many of our critics show that the editor of the BMJ is wrong to state in the “editor’s choice” in the issue of 14 May that “only the naivest medical students think that diseases have some independent, objective reality.” Medical students show greater intellectual sophistication in tackling the classification of ill defined illnesses than many patients and doctors-and particularly medical practitioners with self diagnosed myalgic encephalomyelitis.

Case definition-Ellen M Goudsmit’ and Nick Anderson’ assert that research criteria for the chronic fatigue syndrome fail to distinguish myalgic encephalomyelitis and exaggerate psychiatric associations. The best replicated research finding, however, is that patients suffer substantial emotional morbidity, whether the chronic fatigue syndrome is defined by British or, as patient groups prefer, Australian or American criteria. All three sets of criteria can be used to identify cases on a continuum of fatigue, which includes myalgic encephalomyelitis. We did not cite DO Ho-Yen’s prevalence study as it used an idiosyncratic definition of cases of the ‘chronic fatigue syndrome and surveyed doctors’ diagnoses rather than patients.

You can read the full comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2540769/pdf/bmj00450-0067b.pdf

 

Source: Lawrie SM, Pelosi AJ. Chronic fatigue syndrome and myalgic encephalomyelitis. BMJ. 1994 Jul 23;309(6949):275. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2540769/

 

Biological and molecular characteristics of human herpesvirus 7: in vitro growth optimization and development of a syncytia inhibition test

Abstract:

Two isolates of human herpesvirus 7 (HHV-7) were recovered from phytohemagglutinin-activated peripheral blood mononuclear cells of a patient with chronic fatigue syndrome and of a healthy blood donor. A genetic polymorphism between the two isolates was detected by Southern blot analysis using a novel HHV-7 genomic clone (pVL8) as a probe. We developed optimized conditions for the in vitro propagation of HHV-7 by using enriched populations of activated CD4+ T lymphocytes derived from normal peripheral blood, resulting in the production of high-titered extracellular virus (> 10(6) cell culture infectious doses/ml). Bona fide syncytia formation was documented both in normal CD4+ T lymphocytes and in the Sup-T1 CD4+ T-cell line following infection with high-titered HHV-7. To identify neutralizing antibodies to HHV-7, a syncytia-inhibition test was developed. Variable titers of syncytia-neutralizing antibodies were detected in all the human sera tested, thus confirming the high prevalence of HHV-7 in the human population.

 

Source: Secchiero P, Berneman ZN, Gallo RC, Lusso P. Biological and molecular characteristics of human herpesvirus 7: in vitro growth optimization and development of a syncytia inhibition test. Virology. 1994 Jul;202(1):506-12. http://www.ncbi.nlm.nih.gov/pubmed/8009865

 

Human herpesvirus-7 (HHV-7)

Abstract:

HHV-7 first isolated in 1990 from a healthy individual, is a ubiquitous agent. The second independent isolation of HHV-7 from a chronic fatigue syndrome patient was reported in 1992. The seroepidemiology of HHV-7 suggested that its prevalence rate in the U.S.A. population is > 85%; however, in Japan a low prevalence rate has been reported. HHV-7 can be more readily isolated from the saliva than HHV-6. The primary infection of HHV-7 appears later in life than HHV-6. No disease has been reported that is etiologically linked to HHV-7. HHV-7 is more closely related to HHV-6 and the human cytomegalovirus than other members of the human herpesvirus family.

 

Source: Ablashi DV, Berneman ZN, Kramarsky B, Asano Y, Choudhury S, Pearson GR. Human herpesvirus-7 (HHV-7). In Vivo. 1994 Jul-Aug;8(4):549-54. http://www.ncbi.nlm.nih.gov/pubmed/7893982

 

Human herpesvirus-6 (HHV-6) (short review)

Abstract:

Human Herpesvirus-6 is the etiological agent of Roseola infantum and approximately 12% of heterophile antibody negative infectious mononucleosis. HHV-6 is T-lymphotropic, and readily infects and lyses CD4+ cells. The prevalence rate of HHV-6 in the general population is about 80% (as measured by IFA) with an IgG antibody titer of 1:80. A lower prevalence, however, is observed in some countries.

HHV-6 is reactivated in various malignant and non-malignant diseases as well as in Chronic Fatigue Syndrome and transplant patients. Furthermore, elevated antibody titers were also observed in lymphoproliferative disorders, auto-immune diseases and HIV-1 positive AIDS patients. There appears to be some strain variability in HHV-6 isolates.

The GS isolates of HHV-6 (prototype) was resistant to Acyclovir, Gancyclovir, but its replication was inhibited by Phosphonoacetic acid and Phosphoformic acid. HHV-7 isolated from healthy individuals showed, by restriction analysis, that 6 out of 11 probes derived from two strains of HHV-6, cross-hybridized with DNA fragments, derived from HHV-7.

 

Source: Ablashi DV, Salahuddin SZ, Josephs SF, Balachandran N, Krueger GR, Gallo RC. Human herpesvirus-6 (HHV-6) (short review). In Vivo. 1991 May-Jun;5(3):193-9. http://www.ncbi.nlm.nih.gov/pubmed/1654146