Milton W. Hamolsky

The Thyroid Gland in Pregnancy

THE purpose of this progress report is to review the present status of knowledge of thyroid-gland function in pregnancy; to discuss recent studies utilizing newer investigative technics to refocus ...

The heart in hypothyroidism

Abstract An attempt has been made to review, from the large body of pertinent data, certain aspects of cardiovascular structure and function in hypothyroidism. Although significant alterations have been defined, the preponderance of the data indicates that myocardial decompensation is only rarely, if ever, a consequence of hypothyroidism. Furthermore, the widely assumed causative role of the hypothyroid state per se in the pathogenesis of atherosclerosis is questioned and the need for a critical re-evaluation defined, particularly in the less severe cases and in patients without attendant complicating factors such as age, hypertension, diabetes, etc. The important role of pericardial effusion in the genesis of certain signs and symptoms is underlined. The meagerness of data relating to significant biochemical effects of hypothyroidism at a cellular or subcellular level is noted. The lack of significant effects of hypothyroidism on the related pulmonary and renal functions is delineated. The induction of hypothyroidism for the therapy of severe angina pectoris or congestive heart failure is reviewed ; the need is underscored for further study of (1) the mechanism of action of lowered thyroid function on these cardiac conditions, (2) the abnormalities of thyroid hormone binding, tissue uptake and turnover in certain euthyroid patients with supraventricular tachycardias, and (3) the therapy of this condition by antithyroid measures.

The Thyroid Hormone-Plasma Protein Complex in Man. I. Differences in Different States of Thyroid Function

The present consensus characterizes thyrotoxicosis,4 a disease of unknown etiology, by the quantitative overproduction and release by the thyroid of excessive amounts of normal thyroid hormone (1-4). According to this concept, the distinctive abnormal signs, symptoms, and laboratory findings of hypermetabolism in patients with diffuse toxic goiter are attributed to the effects of increased amounts of the normal hormone upon peripheral tissue metabolism. Plummer (5), among others, proposed an alternate theory, based chiefly upon clinical observations, which ascribed various manifestations of the disease to the effects of 1) an excess of normal hormone, and 2) a qualitatively abnormal hormone, which he suggested was abnormal because of incomplete iodination. In contrast, he suggested that the abnormality in patients with toxic nodular goiter was due solely to an excess of normal thyroid hormone. Salter and Johnston (6) concluded, on the basis of acetone precipitation of acidified sera, that the plasma thyroid hormone in hyperthyroidism differed from thyroxin added in vitro to normal and hypothyroid sera to levels of protein-bound iodine comparable

EFFECTS OF 2-AMINO-2-HYDROXYMETHYL-1, 3-PROPANEDIOL, p CO2, AND p H ON PLASMA PROTEIN BINDING OF THE THYROID HORMONES*

The problem of the binding and transport of the thyroid hormones-thyroxine and triiodothyronine-by specific plasma proteins has been the subject of recent intensive investigation. For the purpose of this discussion, we first summarize briefly current concepts in this area based on the work of many investigators and reviewed in several recent reports.”’ With this as a framework of reference, we shall present certain of our findings, some of which have already been p ~ b l i s h e d ~ ~ ~ concerning the effects on thyroid hormone binding of Tris buffer, carbon dioxide tension, and PH. Early workers10-12 employed chiefly paper electrophoretic techniques using Veronal buffer at a pH of 8.6. In extensive studies based on this method, it was found that more than 90 per cent of physiological levels of thyroxine (T4) was bound in a highly selective fashion to a trace interalpha globulin protein in plasma, designated the thyroxine-binding protein or TBP. Small amounts of T 4 were also found in the albumin fraction. Triiodothyronine (T3) migrated principally to the same general area, but the binding was much weaker and less selective. Many significant physiological correlations were made, based on such studies. For example, it was found that the percentage of T 4 bound in the T B P area was decreased in thyrotoxicosis and increased in myxedema. It was found further that there was a marked increase in T 4 binding in pregnancy and following estrogen administration, as well as a marked decreased binding in the nephrotic syndrome. The weaker T3 binding in plasma was proposed as a major explanation for its more rapid onset of action and greater potency.