Antibodies to adeno-pituitary cell surface antigen (PCSA) were studied in 40 untreated children with idiopathic growth hormone (GH) deficiency to elucidate the role of autoimmune disorders in the pathogenesis of GH deficiency. Antibodies to rat PCSA were assayed by ELISA. PCSA was detected in 15% of patients with GH deficiency, in contrast to that in healthy children and children with autoimmune thyroid diseases. The authors consider that in some cases GH deficiency may be caused by autoimmune hypophysitis. A family study revealed PCSA in 25% of mothers of patients with GH deficiency. In a population of healthy women PCSA was detected in 5.7% cases. Hence, a hereditary background of autoimmune abnormality cannot be completely ruled out.
Eighty patients with multinodular colloidal euthyroid goiter were examined. Thyrotropin-releasing hormone (TRH) test was carried out in 22 patients and 7 healthy women. The results of the test indicate a clear-cut tendency to reduction of hypophyseal TTH reserve in patients with multinodular euthyroid goiter with enlarged thyroid. In other words, clinical diagnosis of an euthyroid condition in the examinees appears to be groundless, particularly in patients with stage IV multinodular euthyroid goiter who may be referred to latent hyperthyrosis group on the basis of TRH test results. Three types of STH reaction were revealed by TRH test in these patients. The authors put forward a hypothesis on STH contribution as a growth factor to the pathogenesis of multinodular colloid euthyroid goiter.
The significance and mechanisms of action of different antithyroid antibodies in diffuse toxic goiter (Graves' disease) and chronic lymphocytic thyroiditis (Hashimoto’s disease) arc analyzed. Antibodies immediately decreasing the level of cAMP in isolated thyrocytes were revealed in the sera of adolescents with juvenile struma, often resulting from lymphocytic thyroiditis. Complement-fixing cytotoxic antibodies are heterogeneous in patients with Graves' diseases and Hashimoto's thyroiditis. Thyrocytes from the tissue of diffuse toxic goiter are resistant to the cytolytic effect of such antibodies from patients with Graves' diseases but not from patients with Hashimoto's thyroiditis. The causes and mechanisms of development of resistance of thyrocytes from diffuse toxic goiter to antibody-dependent complement-mediated cytotoxicity of sera from patients with Graves' disease and the possibility of using this phenomenon as a differential diagnostic test are discussed.
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