Tag: 1994

Simultaneous measurement of antibodies to Epstein-Barr virus, human herpesvirus 6, herpes simplex virus types 1 and 2, and 14 enteroviruses in chronic fatigue syndrome: is there evidence of activation of a nonspecific polyclonal immune response?

Abstract:

As a test of the hypothesis that elevated titers of viral antibodies in patients with chronic fatigue syndrome (CFS) are due to a nonspecific polyclonal immune response, antibodies to Epstein-Barr virus (EBV), human herpesvirus 6 (HHV-6), and 14 enteroviruses in 20 patients with CFS and 20 age- and gender-matched controls were simultaneously measured.

Similarly, titers of IgG to herpes simplex virus (HSV) types 1 and 2 were measured in 18 of these cases and in the respective controls. IgG to EBV viral capsid antigen (VCA) was present at titers > or = 1:320 in 55% of cases vs. 15% of controls (P = .02).

The geometric mean titers of early antigen antibody to EBV, HHV-6 IgG, and HSV-1 and HSV-2 IgG were not significantly different among cases and controls. Of the 14 enteroviral antibodies tested for, only those to coxsackieviruses B1 and B4 were present at significant titers (> or = 1:8) in cases vs. controls (P = .02 and P = .001, respectively).

Of the cases, 19 (95%) had either an EBV VCA IgG titer > or = 1:320 or a coxsackievirus B1 or B4 antibody titer > or = 1:8, a percentage significantly higher than that of controls (40%; P = .0004). Titers of EBV VCA IgG and coxsackievirus B1 and B4 antibodies were simultaneously elevated in only 20% of cases.

There was no correlation between elevated titers of EBV VCA IgG and IgG to HHV-6, HSV-1, and HSV-2 or antibody to coxsackieviruses B1 and B4 in the cases. The prevalence of reported allergies to medications or other substances was identical in both groups (60%). These findings suggest that in the majority of cases of CFS, elevation of viral antibody titers is not due to a nonspecific polyclonal immune response.

Comment in: Viral antibodies in chronic fatigue syndrome. [Clin Infect Dis. 1995]

 

Source: Manian FA. Simultaneous measurement of antibodies to Epstein-Barr virus, human herpesvirus 6, herpes simplex virus types 1 and 2, and 14 enteroviruses in chronic fatigue syndrome: is there evidence of activation of a nonspecific polyclonal immune response? Clin Infect Dis. 1994 Sep;19(3):448-53. http://www.ncbi.nlm.nih.gov/pubmed/7811864

 

Cognitive functioning in chronic fatigue syndrome and depression: a preliminary comparison

Abstract:

This study used a brief battery of neuropsychological measures to examine the performance of patients with chronic fatigue syndrome (CFS) (N = 16) and patients in a major depressive episode (N = 23). The overall neuropsychological performance of the CFS group was not significantly different from depressed patients, and both groups scored within normal limits on most measures. Variability of neuropsychologic performance was in general unrelated to level of depressive symptoms. The results are discussed in terms of the validity of the cognitive criterion for the CFS diagnosis. Subjective complaints of cognitive dysfunction by CFS patients in light of the lack of objective evidence for the same are considered in terms of a somatic vigilance hypothesis.

 

Source: Schmaling KB, DiClementi JD, Cullum CM, Jones JF. Cognitive functioning in chronic fatigue syndrome and depression: a preliminary comparison. Psychosom Med. 1994 Sep-Oct;56(5):383-8. http://www.ncbi.nlm.nih.gov/pubmed/7809336

 

Chronic fatigue syndrome: a diagnostic challenge for the laboratory

Abstract:

OBJECTIVE: To review the literature and current research about the causes of chronic fatigue syndrome (CFS).

DATA SOURCES: Recent research articles about CFS and data gathered by the author.

STUDY SELECTION: Performed by the author.

DATA EXTRACTION: Performed by the author.

DATA SYNTHESIS: Chronic fatigue syndrome (CFS) is a disease of pain, excessive fatigue after minor exertion, cognitive difficulties, and other symptoms-all occurring in cycles. While its etiology is unclear, CFS is associated with abnormal results of immune system tests. There is no specific marker for the illness. Treatment is symptomatic, and the long-term outlook for recovery is good.

CONCLUSION: A rational, symptomatic approach to treating CFS patients can be made using the model developed at the author’s institution. Research into the causes of CFS must continue.

Source: Lanham RJ. Chronic fatigue syndrome: a diagnostic challenge for the laboratory. Clin Lab Sci. 1994 Sep-Oct;7(5):279-82. http://www.ncbi.nlm.nih.gov/pubmed/10150382

Serum concentrations of 2′,5′-oligoadenylate synthetase, neopterin, and beta-glucan in patients with chronic fatigue syndrome and in patients with major depression

Chronic fatigue syndrome is characterised by debilitating severe fatigue persisting for more than six months. Furthermore, it is associated with physical symptoms, such as mild fever, sore throat, arthralgia, and myalgia, as well as psychological symptoms such as headache, insomnia, depressive state, and neuropsychiatric symptoms. It has often been claimed that the onset of chronic fatigue syndrome follows an infection or infection-like illness; hence a certain microorganism(s) or virus may cause it. Another possible candidate for inducing chronic fatigue syndrome is cellular or humoral immune dysfunction, which has been found in patients with the disease. There is controversy also as to whether or not chronic fatigue syndrome and major depression (mood disorder) represent different entities.

Mild fever, pharyngitis, and lymphadenopathy, which are suggestive of the existence of inflammation, are often associated with chronic fatigue syndrome, but the peripheral leucocyte count, erythrocyte sedimentation rate, and C-reactive protein concentration are usually normal in patients with chronic fatigue syndrome. Hence, it is possible that certain cytokines may produce the symptoms in patients with chronic fatigue syndrome and, possibly, those with major depression. For example, interferon is known to cause fever, fatigue, and psychoneurological abnormalities. We conducted this study to clarify whether or not 2′,5′-oligoadenylate synthetase (2,5-AS), neopterin, adenosine deaminase, endotoxin, or B-glucan participate in the pathogenesis of chronic fatigue syndrome.

You can read the rest of this article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1073106/pdf/jnnpsyc00038-0135b.pdf

 

Source: Matsuda J, Gohchi K, Gotoh N. Serum concentrations of 2′,5′-oligoadenylate synthetase, neopterin, and beta-glucan in patients with chronic fatigue syndrome and in patients with major depression. J Neurol Neurosurg Psychiatry. 1994 Aug;57(8):1015-6. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1073106/

 

Cytomegalovirus-related sequence in an atypical cytopathic virus repeatedly isolated from a patient with chronic fatigue syndrome

Abstract:

An atypical virus, cytopathic for human and animal fibroblasts, was repeatedly cultured from a patient with chronic fatigue syndrome. Viral particles, suggestive of cytomegalovirus (CMV) were seen by electron microscopy. Infected cells did not, however, stain with antisera specific for CMV, herpes, simplex virus, or human herpes-virus-6. Polymerase chain reaction (PCR) assays for these viruses were also negative.

Two distinct products of approximately 1.5 kilobase pairs were amplified from virally infected cells using the human T lymphotropic virus-II tax gene reactive primer, SK44, in low stringency PCR. Sequencing of one of the amplified products showed a region of highly significant partial homology with the UL34 gene of CMV.

The sequence of the other PCR product did not correspond with CMV or any other virus. DNA was extracted from the material pelleted by ultracentrifugation of filtered culture supernatants. It migrated in agarose gels as a single band of approximately 20 kpb. The banded DNA was digested with EcoRI and cloned. A 2.2 kbp plasmid containing the CMV-related sequence identified within the PCR product was recovered.

Sequencing of this plasmid extended the region of partial sequence homology with CMV to include a portion of the UL35 gene of CMV. Initial sequencing of additional plasmids has confirmed the partial relatedness to CMV. The data indicate a novel type of CMV-related “stealth” virus that is able to establish a clinically persistent human infection.

 

Source: Martin WJ, Zeng LC, Ahmed K, Roy M. Cytomegalovirus-related sequence in an atypical cytopathic virus repeatedly isolated from a patient with chronic fatigue syndrome. Am J Pathol. 1994 Aug;145(2):440-51. http://www.ncbi.nlm.nih.gov/pubmed/8053501

 

Psychosocial factors and chronic fatigue syndrome

Abstract:

This study investigated the number and severity of life events, Type A behaviour, coping strategies and social support differences between chronic fatigue and irritable bowel syndrome patients prior to illness and between these groups and healthy controls. Although few differences were found between the groups for life events, a number of interesting results emerged with regard to different aspects of Type A behaviour, various coping strategies and social support. These findings are discussed with respect to existing research in the field.

 

Source: Lewis S, Cooper CL, Bennett D. Psychosocial factors and chronic fatigue syndrome. Psychol Med. 1994 Aug;24(3):661-71. http://www.ncbi.nlm.nih.gov/pubmed/7991748

 

The effect of social adversity on the fatigue syndrome, psychiatric disorders and physical recovery, following glandular fever

Abstract:

Two hundred and fifty patients attending primary care with glandular fever or an upper respiratory tract infection were studied prospectively up to 6 months after onset. Of these patients 228 were interviewed with the Life Events and Difficulties Schedule and the Schedule for Affective Disorders and Schzophrenia, giving Research Diagnostic Criteria for psychiatric disorders.

The experience of severe social adversity (provoking agents) had a significant association with psychiatric disorder at 2 months (odds ratio = 5.3) and 6 months (odds ratio = 5.8) after onset of infection. This association was especially significant for depressive illness (odds ratio = 9.1 at 2 months and 11.9 at 6 months).

In contrast, social adversity had little association with the development of the post-infectious fatigue syndrome, or delayed physical recovery. Social adversity may be an important maintaining factor for psychiatric disorders, especially depressive illness, following acute infections.

 

Source: Bruce-Jones WD, White PD, Thomas JM, Clare AW. The effect of social adversity on the fatigue syndrome, psychiatric disorders and physical recovery, following glandular fever. Psychol Med. 1994 Aug;24(3):651-9. http://www.ncbi.nlm.nih.gov/pubmed/7991747

 

Chronic fatigue syndrome–a controlled cross sectional study

Abstract:

OBJECTIVE: To look for signs of immunodeficiencies and/or longstanding infections underlying chronic fatigue syndrome (CFS).

METHODS: Twenty-one patients fulfilling the Centers for Disease Control criteria for CFS were compared to 21 age and sex matched controls. A number of viral antibodies as well as the following tests evaluating the immune system were studied: autoantibody profile, cell surface markers on isolated blood mononuclear cells, cytokine production, lymphocyte proliferative responses, natural killer cell activity and quantitation of immunoglobulin secreting cells.

RESULTS: Production in vitro of the predominantly T cell derived cytokines interleukin 2 and interferon gamma was significantly higher in patients with CFS compared to the control group. Furthermore, the serum concentrations of IgA and IgE were lower in patients with CFS; however, this difference was caused by a larger number with values of IgA and IgE above the upper limit of the normal range among the controls than among the patients with CFS. All other variables were similar in the 2 groups.

CONCLUSION: A pathogenically significant imbalance of the immune system in patients with CFS cannot be excluded. However, evidence of a causal link between abnormal immunity and CFS was not obtained.

 

Source: Rasmussen AK, Nielsen H, Andersen V, Barington T, Bendtzen K, Hansen MB, Nielsen L, Pedersen BK, Wiik A. J Rheumatol. 1994 Aug;21(8):1527-31. http://www.ncbi.nlm.nih.gov/pubmed/7983659

 

Abnormal left ventricular myocardial dynamics in eleven patients with chronic fatigue syndrome

Abstract:

Eleven patients diagnosed with chronic fatigue syndrome were found to have abnormal left ventricular myocardial dynamics as indicated on MUGA studies. Among the abnormalities noted were abnormal wall motion at rest and stress, dilatation of the left ventricle, and segmental wall motion abnormalities.

 

Source: Dworkin HJ, Lawrie C, Bohdiewicz P, Lerner AM. Clin Nucl Med. 1994 Aug;19(8):675-7. http://www.ncbi.nlm.nih.gov/pubmed/7955743

 

Low grade pyrexia: is it chronic fatigue syndrome?

Abstract:

Eighty seven consecutive patients presenting with prolonged low grade pyrexia (99 degrees-101 +/- F) during 1984-93 were followed up for a mean duration of 2.9 years. Mean age was 37.55 years (SD + 10.16) and 66 (75.8%) were females. Onset of pyrexia was acute in 57 patients and was associated with chilly sensation (42), Fatigue (69), Arthralgias (61), myalgias (55) and several other non specific symptoms. Clinical examination showed paucity of physical signs with 7 patients showing tender lymphadenopathy, 7 showing splenomegaly, 5 hepatomegaly, and 1 phylctenular conjunctivitis. Psychiatric examination was within normal limits. Extensive investigations for any viral or other infection, autoimmune disorder or malignancy were unrewarding. Patients were followed up for an average of 2.9 (2 to 5 years). Thirteen patients had become asymptomatic within one year of onset of symptoms, 38 by two years and 45 by the end of three years. This syndrome may be a variant of chronic fatigue syndrome.

Comment in: Low grade pyrexia: is chronic fatigue syndrome a safe and justified diagnosis? [J Assoc Physicians India. 1995]

 

Source: Anand AC, Kumar R, Rao MK, Dham SK. Low grade pyrexia: is it chronic fatigue syndrome? J Assoc Physicians India. 1994 Aug;42(8):606-8. http://www.ncbi.nlm.nih.gov/pubmed/7868552