A controlled trial of intravenous immunoglobulin G in chronic fatigue syndrome
ABSTRACT Currently, there is no established therapy for chronic fatigue syndrome (CFS), a recently defined illness that has been associated with a variety of immunologic abnormalities. Based on the hypothesis that a chronic viral infection or an immunoregulatory defect is involved in the pathogenesis of CFS, the therapeutic benefit of intravenous immunoglobulin G (IV IgG) was evaluated in a group of patients with CFS. Additionally, serum immunoglobulin concentrations and peripheral blood lymphocyte subset numbers were measured at the outset of the study, and the effect of IV IgG therapy on IgG subclass levels was determined.
Thirty patients with CFS were enrolled in a double-blind, placebo-controlled trial of IV IgG. The treatment regimen consisted of IV IgG (1 g/kg) or intravenous placebo (1% albumin solution) administered every 30 days for 6 months. Participants completed a self-assessment form prior to each of the six treatments, which was used to measure severity of symptoms, functional status, and health perceptions. Patients were also asked to report adverse experiences defined as worsening of symptoms occurring within 48 hours of each treatment.
Twenty-eight patients completed the trial. At baseline, all 28 patients complained of moderate to severe fatigue, and measures of social functioning and health perceptions showed marked impairment. Low levels of IgG1 were found in 12 (42.9%), and 18 (64.3%) had low levels of IgG3. At the end of the study, no significant therapeutic benefit could be detected in terms of symptom amelioration or improvement in functional status, despite restoration of IgG1 levels to a normal range. Major adverse experiences were observed in 20% of both the IV IgG and placebo groups.
The results of this study indicate that IV IgG is unlikely to be of clinical benefit in CFS. In addition to the ongoing need for placebo-controlled trials of candidate therapies for CFS, an expanded research effort is needed to define the etiology and pathogenesis of this disorder.
- SourceAvailable from: Akemi Tomoda
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- "Such symptoms have been attributed to persistent cytokine production (Komaroff, 1988; Komaroff and Buchwald, 1991). To date, there is no clearly effective therapy for this disorder (Miike et al., 2003), but conflicting data from placebo-controlled studies suggest that IVc-globulin may be beneficial (Lloyd et al., 1990; Peterson et al., 1990). This study investigates the immunoactivity depending on the evaluation of cytokine production. "
ABSTRACT: We studied cytokine production in 15 patients with chronic fatigue syndrome (CFS) and 23 controls. CFS patients' peripheral blood mononuclear cells were cultured with lipopolysaccharide or phytohemagglutinin. Enzymatic immunoassay indicated cytokine concentration in culture supernatants. CFS patients showed significantly lower mRNA levels and transforming growth factor-beta1 (TGF-beta1) production. Cytokine dysregulation affects CFS pathogenesis. TGF-beta1 may aid treatment because it affects CFS inflammatory characteristics.Psychiatry Research 04/2005; 134(1):101-4. DOI:10.1016/j.psychres.2005.01.002 · 2.68 Impact Factor
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- "Patarca et al.  and Barker et al.  showed reduced NK activity in CFS patients in contrast with Gold et al.  who demonstrated increased activity. Peterson et al.  found no abnormalities of NK cell structure or function. "
ABSTRACT: Immune dysfunction in patients with chronic fatigue syndrome (CFS) has been widely but inconsistently reported. Traditional reviews of the literature have produced a variety of conclusions. We present the results of the first systematic review of the subject. EMBASE, MEDLINE and PSYCHINFO databases were searched, and leading researchers in the field were contacted. Inclusion criteria were applied, and studies were then divided into groups based on the quality of their methodology. Study results were collated and described. Studies ranged widely in quality. There was an inverse association between study quality and finding low levels of natural killer cells, suggesting that the association may be related to study methodology. On the other hand, reports of abnormalities in T cells and cytokine levels were not related to study quality. The conclusions of this systematic review differ from a recent traditional narrative review of the immunology of CFS. No consistent pattern of immunological abnormalities is identified.Journal of Psychosomatic Research 09/2003; 55(2):79-90. DOI:10.1016/S0022-3999(02)00515-9 · 2.84 Impact Factor
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ABSTRACT: To examine the literature on chronic fatigue syndrome (CFS), especially as it relates to cognitive deficits and exercise, more than 200 articles related to CFS were selected from computer-based research as well as pertinent articles noted in the references of individual articles. All were relevant articles on CFS, although articles in a foreign language were excluded. CFS is a controversial diagnosis of exclusion, but certain subgroups do appear to exist. It may represent multiple diseases or multiple stages of the same disease. Although cognitive deficits are commonly reported, the measured impairments are relatively subtle and are in the area of complex information processing speed, or efficiency. Magnetic resonance imaging, single-photon emission computer tomography, and neuroendocrine studies present preliminary evidence suggestive of the cerebral involvement primarily in the white matter. The weakness and fatigue may be the result of alterations in the central nervous system, not in the peripheral muscles. However, it is hard to separate the documented weakness and endurance deficits from deconditioning. Autonomic symptoms such as orthostatic intolerance and a predisposition to neurally mediated syncope may be explained by cardiovascular deconditioning, a postviral idiopathic autonomic neuropathy, or both. The review points out the need for more carefully designed studies of CFS that focus on the relationship between neuropathology, psychopathology and neuropsychologic functioning. The role of exercise as a stimulus for exacerbation or in treatment needs to be further studied using clear diagnostic criteria as well as control groups that carefully match the activity level.American Journal of Physical Medicine & Rehabilitation 01/1998; 77(2):160-7. · 2.01 Impact Factor