Autoimmunity
Buchwald D, Wener MH, Komaroff AL. Anti-neuronal antibody levels in chronic fatigue syndrome patients with neurologic abnormalities. Arthritis and Rheumatism 1991; 34(11): 1485-6.
Abstract: Anti-neuronal antibody levels in chronic fatigue syndrome patients with neurologic abnormalities.
Cabral DA, Petty RE, Fung M, Malleson PN. Persistent antinuclear antibodies in children without identifiable inflammatory rheumatic or autoimmune disease. Pediatrics 1992; 89; 441-4.
Abstract: One hundred eight children with musculoskeletal pain considered not to be due to an autoimmune or inflammatory disease had an antinuclear antibody (ANA) test performed. Twenty-four of these children were ANA positive on HEp-2 cell substrate at a screening serum dilution of 1:20. A positive ANA test persisted in 21 of 24 of the patients over a mean time period of 38 months (range 1 to 103 months). No sera from any patient at initial evaluation had anti-DNA antibodies by radioimmunoassay or by indirect immunofluorescence on Crithidia luciliae. One patient recently developed elevated anti-DNA (radioimmunoassay) antibodies but still has a negative assay on C luciliae. Four patients had antibodies to core histones by immunoblotting. None had antibodies to Sm, RNP, Ro (SS-A), or La (SS-B) by counterimmunoelectrophoresis. No patient developed an overt inflammatory or autoimmune disease during a mean follow-up period of 61 months (range 13 to 138 months). A child with musculoskeletal pain and a positive test for ANA, but with no clinical evidence at presentation of inflammatory or autoimmune disease, is at low risk of imminently developing such a disease.
Jefferies WM. Mild adrenocortical deficiency, chronic allergies, autoimmune disorders and the chronic fatigue syndrome: a continuation of the cortisone story. Medical Hypotheses 1994; 42(3): 183-189.
Abstract: The possibility that patients with disorders that improve with administration of large, pharmacologic dosages of glucocorticoids, such as chronic allergies and autoimmune disorders, might have mild deficiency of cortisol production or utilization has received little attention. Yet evidence that patients with rheumatoid arthritis improved with small, physiologic dosages of cortisol or cortisone acetate was reported over 25 years ago, and that patients with chronic allergic disorders or unexplained chronic fatigue also improved with administration of such small dosages was reported over 15 years ago, suggesting that these disorders might be associated with mild adrenocortical deficiency. The apparent reasons for the failure of these reports to be confirmed or mentioned in medical textbooks and the facts needed to restore perspective are reviewed, and the need for further studies of the possible relationship of a mild deficiency of the production or utilization of cortisol and possibly other normal adrenocortical hormones to the development of these disorders is discussed.
Plioplys AV. Antimuscle and anti-CNS circulating antibodies in chronic fatigue syndrome. Neurology 1997; 48(6): 1717-19.
Abstract: Chronic fatigue syndrome (CFS) patients suffer from disabling physical and mental fatigue. Circulating autoimmune antibodies may produce symptoms of muscular fatigue by reacting with acetylcholine receptors or calcium binding channels. They can also produce mental status changes by reacting with central nervous system (CNS) antigens. We thoroughly investigated the presence of circulating antimuscle and anti-CNS antibodies in 10 CFS patients and 10 controls. We were unable to detect any pathogenic antibodies.
Von Mikecz A, Konstantinov K, Buchwald DS, Gerace L, Tan EM. High frequency of autoantibodies to insoluble cellular antigens in patients with chronic fatigue syndrome. Arthritis and Rheumatism 1997; 40(2): 295-305.
Abstract: OBJECTIVE: To elucidate the humoral immune response in patients with chronic fatigue syndrome (CFS), by identification and characterization of autoantibodies. METHODS: Initial immunofluorescence histochemistry studies of sera using human HEp-2 cell substrate were followed by antibody class subtyping and colocalization studies with reference antibodies. Association of CFS autoantigens with insoluble cellular components was determined by in situ extraction of soluble components and subsequent immunofluorescence histochemistry studies on the extracted cell substrate. RESULTS: Of 60 CFS patients, 41 (68%) were positive for antinuclear antibodies. Localization of nuclear staining was found at the nuclear envelope (52%), in reticulated speckles (25%), in nucleoli (13%), and in dense fine speckles (5%). Twenty-eight CFS sera (47%) also had antibodies to cytoplasmic antigens. The major cytoplasmic staining pattern was of the intermediate filament type (35%). The observed nuclear envelope pattern of staining co-localized with lamina-associated polypeptide 2 (an integral nuclear membrane protein), the reticulated speckle pattern co-localized with non-small nuclear RNP splicing factor SC-35, and the intermediate filament pattern co-localized with vimentin. The intermediate filament antigen was shown to be vimentin in immunoblotting experiments using recombinant human vimentin, and one of the nuclear envelope antigens was shown previously to be lamin B1. Fifty of the 60 CFS patients (83%) had antibodies to one or another of these antigens, all of which are relatively insoluble cellular antigens, whereas a control group of patients without chronic fatigue had a significantly lower frequency of such antibodies (17%). CONCLUSION: The high frequency of autoantibodies to insoluble cellular antigens in CFS represents a unique feature which might help to distinguish CFS from other rheumatic autoimmune diseases.