Objective. To assess for a correlation between infection and the onset of the giant cell (temporal) arteritis (GCA) syndrome.Methods. A matcheld case-control study design was used. Records of 100 patients with biopsy-proven GCA and 100 patients undergoing corrective surgery for hip fracture who did not have GCA were retrospectively reviewed. Non-GCA patients were sex-matched with GCA patients and were as old or older in age. The review period for GCA patients was up to 4 months before and during the occurrence of symptoms (median 2 months), and for non-GCA patients, it was up to 7 months before hip fracture. The prevalence of infection was compared using matched-pairs odds ratios and their 95% confidence intervals.Results. Infections were 3 times more likely to occur in GCA patients than in non-GCA patients (P < 0.05). Conclusion. A correlation between the occurrence of infection and the onset of GCA is strongly suggested. We speculate that infection may act as a trigger mechanism in the pathogenesis of this syndrome.Giant cell (temporal) arteritis (GCA) has been recognized as an acute inflammatory condition of sudden onset (1) associated with the brisk production of acute-phase reactants, elevated levels of IgG, and

Cell-mediated immunity in rheumatoid arthritis (RA) was assessed by skin testing with 5 common antigens in 84 patients, dinitrochlorobenzene (DNCB) application in 13, and in Vitro phytohemagglutinin (PHA) stimulation of buffy coat cells in 39. Routine skin-test reactions were recorded as the largest diameter of induration present at 48 hours. Controls included normal subjects, family members of patients with rheumatic disorders, and patients with unrelated illnesses. Results revealed two populations of RA patients. Forty-two percent were completely anergic to the 5 antigens and 14% gave a history of herpes zoster. The remainder showed reactivity similar t o that seen in patient controls. Most RA subjects demonstrated normal or only minimally diminished PHA responses. The RA patients had normal inflammatory responses to the initial DNCB application, but immune reactions t o this agent paralleled skin-test reactivity t o the other antigens. The anergic individuals could be separated from the reactive population primarily by the increased duration of disease activity but not by medication taken or the degree of disease activity when tested.In rheumatoid arthritis (RA) the status of skin-test responsiveness and lymphocyte reactivity to phytohemagglutin (PHA) is in question. In some studies patients with kerato-

_A patient with cutaneous anergy and miliary tuberculosis was studied with serial determinations in vivo of skin test responsiveness to natural antigens and to vesicant doses of dinitrochlorbenzene, and in vitro with buffy coat migration inhibition, indirect migration inhibition factor production, and lymphocyte transformation during the acute phase of the disease and during convalescence. During the anergic phase, the patient maintained good lymphocyte transformation to phytohemagglutinin and purified protein derivative of tuberculin and showed strong buffy coat migration inhibition that was partially dependent on autologous serum but not complement; however, indirect migration inhibition factor production to purified protein derivative was not demonstrable. The results suggest that the defect in anergic tuberculosis resides at least partially in the nonimmunologic inflammatory response and that lymphocyte function is at least partially intact.

Women predominate at all ages among patients diagnosed as having primary fibromyalgia. Of 100 patients reviewed, the average age at onset of fibromyalgia was 46. Of 65 patients in whom menopause occurred before diagnosis of fibromyalgia, the average age at menopause was 42, and most of these women had menopause related to surgery and insufficient estrogen therapy. Estrogen deficit is, thus, a prominent promoting factor in the majority of fibromyalgia patients and is likely to have an effect on sleep, mood, and anxiety state. These emotional responses may subsequently be somatized as pain. Therefore, estrogen therapy should be added to the treatment armamentarium for fibromyalgia in selected patients.