A 79-year-old female patient with hepatitis C virus-related liver cirrhosis was diagnosed as having hepatocellular carcinoma (HCC) with a diameter of 2.0 cm. She refused therapy for HCC. Nine months after the diagnosis, she developed dermatomyositis when the HCC enlarged to a diameter of 6.0 cm. She underwent therapy for dermatomyositis, and then transcatheter arterial chemoembolization for HCC. Although the manifestations of dermatomyositis improved and entire tumor necrosis was achieved, she died of pneumonia 2 mo after the treatment of HCC. HCC and/or chronic hepatitis C virus infection might be involved in the pathogenesis of dermatomyositis.

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Antithyroglobulin (anti-Tg) antibodies cytophilic for human monocytes were detected in the serum of 30 of 45 patients with Hashimoto's thyroiditis using the passive rosette technique. These antibodies conferred on normal monocytes the ability to form rosettes with Tg-coated erythrocyres (E-Tg) in vitro. The percentage of E-Tg rosette-forming monocytes was correlated with serum anti-Tg antibody titers measured by tanned sheep red cell hemagglutination. Most serum cytophilic activities were recovered in the immunoglobulin G fraction and were not affected by heating to 56 C for 30 min or ultracentrifugation at 105,000 X g for 60 min. Passive E-Tg rosette formation by monocytes was immunologically specific and was inhibited by the addition of small amounts of free Tg into the medium but was not inhibited by the addition of normal human serum. The anti-Tg antibody-armed monocytes became cytotoxic against Tg-coated chicken erythrocytes and lysed target erythrocytes by an extracellular mechanism. It was suggested that monocytes might be armed by cytophilic antibodies in vivo, since monocytes of patients with Hashimoto's thyroiditis showed increased E-Tg binding (rosette formation) relative to monocytes from control subjects. These findings support the possible pathogenetic involvement of monocytes in human autoimmune thyroiditis.

Blood mononuclear cells bearing Fc receptors for immunoglobulin G were measured in patients with thyroid disorders as the percentage of EA rosette-forming cells (% EA-RFC). Levels were normal in patients with untreated Graves' hyperthyroidism, Graves' ophthalmopathy, and Hashimoto's thyroiditis. On the other hand, the % EA-RFC was increased in eight of nine patients with subacute thyroiditis (SAT) tested during the acute phase, returning to normal during recovery. Levels were normal in all five patients with "silent" thyroiditis tested. The majority of the Fc receptor-bearing cells in SAT patients was shown to be phagocytic. There was no evidence for increased killer cell or suppressor cell activity, functions which reside in Fc receptor-bearing mononuclear cell populations, in SAT patients. There was no close correlation between the % EA-RFC and parameters of thyroid damage (erythrocyte sedimentation rate and serum T4 levels) or thyroid antibody titers. While an increase in the % EA-RFC in SAT patients may represent a nonspecific response to a viral inflammation of the thyroid gland, the abnormalities may be markers of a more specific immunological response to thyroid antigen release. Abnormalities of blood mononuclear cell numbers in Graves' hyperthyroidism and SAT are reviewed.