A case of chronic fatigue syndrome who showed a beneficial effect by intravenous administration of magnesium sulphate

Abstract:

We have treated a case of chronic fatigue syndrome with atopic diathesis was had suffered general malaise, low grade fever, swelling of the lymph nodes, myalgias and arthralgias for a long time.

A 29-year-old female, who had been treated for atopic dermatitis for 5 years, complained of general malaise in May 1990. She was admitted to the nearest hospital in December 1990 because of low grade fever, swelling of the lymph nodes and an elevation of antinuclear antibody (2520x). She was transferred to our hospital in May 1991.

A diagnosis of collagen disease was not compatible with her condition. In addition to general malaise, fever and lymph node swelling, headache, myalgias, muscle weakness, arthralgias and insomnia were observed, and a diagnosis of chronic fatigue syndrome was made based on the working case definition proposed by Holmes et al.

Although eosinophilia, a high serum level of IgE, and elevation of RAST scores, low NK and ADCC activity, and a reduced level of NK cells in the peripheral blood were detected, serum antibodies to a number of viruses were in the normal range.

Treatments with non-steroid anti-inflammatory drugs, minor tranquilizers and antidepressant drugs were not effective at all. An administration of magnesium sulphate was intravenously performed once a week in order to improve her condition, especially severe general malaise. After about 6-week’s administration of magnesium sulphate, she noticed reduced easy fatigability and an improvement in her impaired daily activities. Finally she was able to leave the hospital in January 1992.(ABSTRACT TRUNCATED AT 250 WORDS)

 

Source: Takahashi H, Imai K, Katanuma A, Sugaya T, Hisano K, Motoya S, Aoki S, Sugiyama T, Yachi. A case of chronic fatigue syndrome who showed a beneficial effect by intravenous administration of magnesium sulphate. Arerugi. 1992 Nov;41(11):1605-10. [Article in Japanese] http://www.ncbi.nlm.nih.gov/pubmed/1492795

 

Bupropion treatment of fluoxetine-resistant chronic fatigue syndrome

Abstract:

Chronic fatigue syndrome (CFS) includes many symptoms of major depression. For this reason, many antidepressants have been used to treat the symptoms of this disorder. Among the more recently released antidepressants are fluoxetine and bupropion.

In this open study, nine CFS patients who either could not tolerate or did not respond to fluoxetine showed significant response when administered 300 mg/day of bupropion for an 8-week period in both rating of HDRS (t = 4.80, p < 0.01) and BDI (t = 2.48, p < 0.05). Furthermore, bupropion improvement in Hamilton Depression Rating Scale correlated significantly with change in plasma homovanillic acid (HVA) (r = 0.96, p < 0.01).

Plasma total methylhydroxyphenolglycol (MHPG) also increased significantly during bupropion treatment (t = 2.37, p = 0.05). Measures of T1 microsomal antibodies also decreased over treatment time; increases in natural killer cell numbers correlated inversely with change in plasma levels of free MHPG (r = -0.88, p < 0.05). Bupropion responders were more likely to have trough blood levels above 30 ng/ml (chi 2 = 3.6, p = 0.05).

 

Source: Goodnick PJ, Sandoval R, Brickman A, Klimas NG. Bupropion treatment of fluoxetine-resistant chronic fatigue syndrome. Biol Psychiatry. 1992 Nov 1;32(9):834-8. http://www.ncbi.nlm.nih.gov/pubmed/1450297

 

Chronic fatigue syndrome–study of 51 cases treated at the Second Tokyo National Hospital

Abstract:

Fifty-one patients with chronic fatigue syndrome (CFS) were studied. Tender points, which are a characteristic clinical feature of fibromyalgia, were found in all but two of the patients at 11.4 points (mean) per patient. IgG antibody titers to EB virus viral capsid antigen were more elevated in the CFS patient group compared to that of the control (p < 0.0015). IgG antibody titers to HHV-6 were not higher in the patient group. NK cell activity was not more decreased in the patient group, whereas, the mean number of NK cells was lower (p < 0.005) in the patient group, when CD57 was used as the NK cell marker. Viral infections and/or disorders in cellular immunity may be important factors in the pathogenesis of CFS.

 

Source: Nishikai M. Chronic fatigue syndrome–study of 51 cases treated at the Second Tokyo National Hospital. Nihon Rinsho. 1992 Nov;50(11):2641-7. [Article in Japanese] http://www.ncbi.nlm.nih.gov/pubmed/1337560

 

Chronic fatigue immune dysfunction syndrome

Abstract:

Chronic fatigue syndrome (CFS) is characterized by unexplained, debilitating fatigue or easy fatigability lasting longer than six months. While a viral basis of infection is proposed to be the cause of CFS, other viral infections do not generally persist after several weeks.

Immunological disorders, including abnormal functions and distributions of T lymphocytes, B lymphocytes, natural killer (NK) cells, and monocyte/macrophages, are described in CFS. NK cells are known to play an important role in host resistance against viral infection as well as in the regulation of the immune systems.

Restoration of NK activity resulted in recovery from CFS. Taken together, immunological abnormalities, especially dysfunction of NK cells, may be involved in CFS.

 

Source: Uchida A. Chronic fatigue immune dysfunction syndrome. Nihon Rinsho. 1992 Nov;50(11):2625-9. [Article in Japanese] http://www.ncbi.nlm.nih.gov/pubmed/1287238

 

Chronic fatigue syndrome: clinical condition associated with immune activation

Abstract:

There is much conflicting immunological and viral data about the causes of chronic fatigue syndrome (CFS); some findings support the notion that CFS may be due to one or more immune disorders that have resulted from exposure to an infectious agent.

In the present study, flow cytometry and several different recognising T, B, and natural killer (NK) cell populations as well as activation and cell adhesion antigens were used to study 147 individuals with CFS.

Compared with healthy controls, a reduced CD8 suppressor cell population and increased activation markers (CD38, HLA-DR) on CD8 cells were found. The differences were significant (p = 0.01) in patient with major symptoms of the disease. These immunological indices were not observed in 80 healthy individuals, in 22 contacts of CFS patients, or in 43 patients with other diseases.

No correlation of these findings in CFS patients with any known human viruses could be detected by serology. The findings suggest that immune activation is associated with many cases of CFS.

 

Source: Landay AL, Jessop C, Lennette ET, Levy JA. Chronic fatigue syndrome: clinical condition associated with . Lancet. 1991 Sep 21;338(8769):707-12. http://www.ncbi.nlm.nih.gov/pubmed/1679864

 

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 herehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1535328/

 

Natural killer cells and the post viral fatigue syndrome

Abstract:

60 patients were referred with a diagnosis of post viral fatigue syndrome (PVFS), but only 50 fulfilled strict criteria for this illness. Many lymphocyte subpopulations were normal, but there was a spectrum of natural killer (NK) cell results: 20/50 (40%) were raised; 8/50 (16%) were low;, 5/50 (10%) were low initially but normal on repeat testing; 17/50 (34%) were normal.

When patients were categorised on their NK cell results, there were significant differences in the two groups with raised or low NK cells compared to the “Not PVFS” group: the CD8 cells were increased (p less than 0.001, p less than 0.02) and the CD4/CD8 ratio was reduced (p less than 0.05) but the CD4 cells were normal.

Clinical data showed that the “Not PVFS” group were older, with less severe illness, less muscle pain and less virological evidence of infection. It is postulated that patients have low NK cells initially and then progress to normal or raised levels dependent on factors such as stress, other infections and behaviour.

 

Source: Ho-Yen DO, Billington RW, Urquhart J. Natural killer cells and the post viral fatigue syndrome. Scand J Infect Dis. 1991;23(6):711-6. http://www.ncbi.nlm.nih.gov/pubmed/1815333

 

Immunologic abnormalities in chronic fatigue syndrome

Abstract:

The chronic fatigue syndrome (CFS), formerly known as chronic Epstein-Barr virus syndrome, is a clinical state of some complexity and uncertain etiology. In order to characterize in a comprehensive manner the status of laboratory markers associated with cellular immune function in patients with this syndrome, 30 patients with clinically defined CFS were studied.

All of the subjects were found to have multiple abnormalities in these markers. The most consistent immunological abnormality detected among these patients, when compared with normal controls, was low natural killer (NK) cell cytotoxicity. The number of NK cells, as defined by reactivity with monoclonal antibody NKH.1 (CD56), was elevated, but the killing of K562 tumor cells per CD56 cell was significantly diminished.

Lymphoproliferative responses after stimulation with phytohemagglutinin and pokeweed mitogen were decreased in most patients when compared with those in normal controls, as was the production of gamma interferon following mitogen stimulation. Lymphocyte phenotypic marker analysis of peripheral blood lymphocytes showed that there were significant differences between patients with CFS and controls.

There was an increase in the percentage of suppressor-cytotoxic T lymphocytes, CD8, and a proportionally larger increase in the number of CD8 cells expressing the class II activation marker. Most patients had an elevated number of CD2 cells which expressed the activation marker CDw26. The numbers of CD4 cells and the helper subset of CD4+CD29+ cells in patients with CFS were not different from those in controls. There was, however, a significant decrease in the suppressor inducer subset of CD4+ CD45RA+ cells. The number of B cells, CD20 and CD21, were elevated, as were the numbers of a subset of B cells which coexpressed CD20 and CD5.

The patterns of immune marker abnormalities observed was compatible with a chronic viral reactivation syndrome.

 

Source: Klimas NG, Salvato FR, Morgan R, Fletcher MA. Immunologic abnormalities in chronic fatigue syndrome. J Clin Microbiol. 1990 Jun;28(6):1403-10. http://www.ncbi.nlm.nih.gov/pubmed/2166084

Note: You can read the full article herehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC267940/

 

The chronic fatigue syndrome: definition, current studies and lessons for fibromyalgia research

Abstract:

Chronic fatigue syndrome (CFS) is characterized by chronic, debilitating fatigue lasting greater than 6 months. Frequent chronic and recurrent findings include fever, pharyngitis, myalgias, adenopathy, arthralgias, difficulties in cognition and disorders of mood. In the majority of patients, the illness starts suddenly with an acute, “flu-like” illness.

The following laboratory abnormalities are seen with some frequency, although none are seen in all patients: lymphocytosis, atypical lymphocytosis, monocytosis, elevation of hepatocellular enzymes, low levels of antinuclear antibodies, varying levels of antithyroid antibodies, partial hypergammaglobulinemia, elevated CD4:CD8 ratio, decreased cytolytic activity of natural killer cells, and low levels of immune complexes. Clinical and serologic studies suggest an association of CFS with all of the human herpesviruses, particularly Epstein-Barr virus (EBV) and the recently discovered human B lymphotropic virus (HBLV) or human herpesvirus 6; neither EBV nor HBLV has yet been shown to play a causal role in the illness.

Preliminary evidence suggests that many of these features of CFS also are seen in patients with fibromyalgia.

 

Source: Komaroff AL, Goldenberg D. The chronic fatigue syndrome: definition, current studies and lessons for fibromyalgia research. J Rheumatol Suppl. 1989 Nov;19:23-7. http://www.ncbi.nlm.nih.gov/pubmed/2691680

 

Phenotypic and functional deficiency of natural killer cells in patients with chronic fatigue syndrome

Abstract:

Natural killer (NK)3 cells are large granular lymphocytes that appear to play a significant role in the host’s defense against viral infection. We performed an extensive phenotypic and functional characterization of NK cells on 41 patients with the chronic fatigue syndrome (CFS), or “chronic active Epstein-Barr virus infection” syndrome, and on 23 age- and sex-matched asymptomatic control subjects in an attempt to further characterize this illness.

These studies demonstrated that a majority of patients with CFS have low numbers of NKH1+T3- lymphocytes, a population that represents the great majority of NK cells in normal individuals. CFS patients had normal numbers of NKH1+T3+ lymphocytes, a population that represents a relatively small fraction of NK cells in normal individuals.

When tested for cytotoxicity against a variety of different target cells, patients with CFS consistently demonstrated low levels of killing. After activation of cytolytic activity with recombinant interleukin 2, patients were able to display increased killing against K562 but most patients remained unable to lyse Epstein-Barr virus-infected B cell targets. Additional cytotoxicity experiments were carried out utilizing anti-T3 monoclonal antibody to block killing by NKH1+T3+ cells.

These experiments indicated that the NK cell that appears to be responsible for much of the functional activity remaining in patients with CFS belongs to the NKH1+T3+ subset, which under normal circumstances represents only approximately 20% of the NK cell population.

 

Source: Caligiuri M, Murray C, Buchwald D, Levine H, Cheney P, Peterson D, Komaroff AL, Ritz J. Phenotypic and functional deficiency of natural killer cells in patients with chronic fatigue syndrome. J Immunol. 1987 Nov 15;139(10):3306-13. http://www.ncbi.nlm.nih.gov/pubmed/2824604