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. 1984 Nov;59(5):835-9.
doi: 10.1210/jcem-59-5-835.

Protein metabolism in skeletal muscle tissue from hyperthyroid patients after preoperative treatment with antithyroid drug or selective beta-blocking agent. Results from a prospective, randomized study

Protein metabolism in skeletal muscle tissue from hyperthyroid patients after preoperative treatment with antithyroid drug or selective beta-blocking agent. Results from a prospective, randomized study

P O Hasselgren et al. J Clin Endocrinol Metab. 1984 Nov.

Abstract

Protein metabolism in skeletal muscle tissue was studied in three groups of patients undergoing thyroid surgery: group I (n = 8), hyperthyroid patients preoperatively treated with an antithyroid drug and T4; group II (n = 8), hyperthyroid patients preoperatively treated with the beta 1-selective adrenoreceptor blocking agent metoprolol; group III (n = 5), euthyroid patients operated on for nodular goiter or adenoma. The study was prospective and hyperthyroid patients were randomly allocated to one of the two preoperative regimens. During operation a biopsy was taken from the sternohyoid muscle and rates of protein synthesis and degradation were measured in incubated muscle tissue. Clinical improvement was equal in the two groups of hyperthyroid patients during preoperative treatment but serum T3 concentrations remained elevated in patients treated with metoprolol. Thus, these patients were biochemically hyperthyroid at the time of operation. The rate of protein degradation was significantly higher in hyperthyroid patients treated with metoprolol than in patients of groups I and III. A significant positive correlation was found between serum T3 and rate of protein degradation in skeletal muscle. Protein synthesis rates were similar in the three groups of patients. This study demonstrated for the first time increased proteolysis in skeletal muscle tissue from patients with high serum T3 concentrations. The results indicate that changes of skeletal muscle protein metabolism in hyperthyroid patients are not normalized by beta 1-blockade despite the fact that this treatment effectively controlled symptoms and signs of hyperthyroidism.

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