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The serum PBI concentration and the maximal thyroxine binding capacity for TBG and TBPA were determined in 100 adolescents. The subjects were classified according to sex and degree of sexual maturity. PBI was determined by an autoanalyzer method: Maximal thyroxine binding capacity for TBG fell with increasing maturation in males while TBPA capacity rose in both sexes. The slight changes in serum PBI noted with increasing sexual maturity correlated directly with the slight changes in TBG binding capacity; no correlation between PBI and TBPA binding capacity was observed as maturity progressed.

We have previously shown that growth hormone (GH) can be extracted from the pituitaries of embalmed bodies. In the present work, we have studied the effects in man of GH from the embalmed sources. The metabolic effects of GH from embalmed and non-embalmed sources were compared, using 2 preparations which were equal in biologic activity, and the response to a single injection in 14 normal adult males was found to be similar both quantitatively and qualitatively. Metabolic balance studies were carried out on 2 children with pituitary dwarfism and the response to GH from embalmed sources was similar to that seen with other active preparations of human GH. No untoward effects were observed during either the single or multiple injection studies. It is concluded that GH from embalmed sources is suitable for treatment of human subjects.

Three patients with atypical, intermittent tetany of recent origin, hypocalcaemia, hypocalciuria and normal serum inorganic phosphorus concentration are described. Two patients were postoperative from thyroidectomy by more than 20 years and one had recently experienced metastatic malignant invasion of the thyroid area. A variety of studies showed that these patients were neither normal nor typically hypoparathyroid in the laboratory. Two hypotheses, each with some support are: 1. that the patients were not totally aparathyreotic, and 2. that, while aparathyreotic, they had adapted to the abnormal state by some mechanism operative in the absence of parathyroid hormone.

Laboratory experiments show that effective control of stem eelworms, removed from plant debris, can be obtained by fumigation under conditions which do not reduce either the germination of seed or the yield of lucerne grown from seed similarly fumigated. A practical fumigation of six tons of seed under a gas-proof sheet is described.

A family with autoimmune thyroid disease (Hashimoto's type) involving at least 3 members in 2 generations is described. In addition, abnormalities of serum immunoglobulins were identified in 2 of 3 generations studied. The possible pathogenetic role of at least one of these immunoglobulins is discussed. Congenital thyroid suppression (partially reversible) was present in all 6 offspring (third generation) of one member with autoimmune thyroiditis. The mechanism of this suppression is not apparent.

The effect of 5,5′-diphenylhydantoin on thyroxine metabolism was examined in five normal volunteers. Intravenous injection of radiothyroxine was followed by a 10-12 day control and subsequent 9-14 day treatment periods. During oral administration of diphenylhydantoin, plasma thyroxine concentration decreased to about 80% of its pretreatment level and the plasma radiothyroxine disappearance rate increased a maximum of 20% over control estimates. These changes were a result of increases in both urinary and fecal excretion of radioisotope. A minimum plasma thyroxine was apparent after 10-12 days of diphenylhydantoin administration. In two of the subjects, treatment was sufficiently prolonged to achieve this new steady state. In these subjects, the decrease in total body thyroxine was balanced by the increase in the fractional turnover rate. As a result, absolute thyroxine degradation during diphenylhydantoin administration was unchanged from the pretreatment values. Plasma ultrafiltration was used to estimate the free thyroxine fraction at regular intervals during the control and treatment periods. During diphenylhydantoin treatment, there was little or no change in this fraction and therefore, absolute free thyroxine decreased. Thyroxine-binding globulin and thyroxine-binding prealbumin capacities remained constant. These results indicate that thyroxine degradation can proceed at a normal rate in subjects receiving diphenylhydantoin despite decreases in plasma free thyroxine concentration. If free thyroxine is the only portion of the hormone available for cellular utilization, then free thyroxine clearance must be increased in these subjects. This increase in clearance could represent either a direct stimulation of peripheral thyroxine metabolism by diphenylhydantoin, or it could reflect the response of intrinsic regulatory systems to a diphenylhydantoin-mediated displacement of thyroxine from thyroxine-binding globulin. Whatever the mechanism for this effect, a decreased free thyroxine value in patients receiving diphenylhydantoin may not imply hypothyroidism.

Metastic pulmonary calcification (MPC) developed in a patient with primary hyperparathyroidism. Renal function was only minimally impaired (creatine clearance of 65 ml/min) the day prior to appearance of the lung infiltrate, but deteriorated (creatinine clearance of 14 ml/min) concomitantly with the appearance of MPC. Lung imaging with 99mTc bone-scanning agents helps differentiate MPC from other problems with similar clinical and roentgenographic findings, thus allowing prompt therapy.

In an attemp- to clarify the clinical importance of glucose intolerance associated with acute thyrotoxicosis, 22 patients had evaluations performed for glucose tolerance while thyrotoxic and at mean follow-up times of 8.8 months and 11.6 years after adequate antithyroid treatment. High incidences of glucose intolerance at long-term follow-up (32%) and of histories suggestive of diabetic diathesis (43%) support the hypothesis that there is an inherited relationship between diabetes mellitus and thyrotoxicosis and suggest that initial testing of all thyrotoxic patients for glucose intolerance is advisable. In addition, all thyrotoxic patients displaying diabetic glucose intolerance after a return to the euthyroid state should be considered to have permanent diabetes mellitus until proved otherwise.

Hypercalcemia occurs in approximately one of every five patients with thyrotoxicosis, and one of seven patients with hypercalcemia and thyrotoxicosis will have hyperparathyroidism as the cause of the serum calcium elevation. While there are no clinical features which permit easy identification of patients with hyperparathyroidism and thyrotoxicosis, determination of serum parathyroid hormone levels may help. Parathyroid hormone levels may be normal or suppressed if hypercalcemia is due to hyperthyroidism alone, and an elevated parathyroid hormone level suggest coexisting hyperparathyroidism.

A number of reports have suggested the wider use of Iodine-123 as the ideal radioisotope of iodine because of its theoretical advantages. A short Half-life of 13,3 h, a primary gamma photon of 159 keV of high abundance and absence of beta particle emission result in a dose reduction variously estimated at 30–100 fold over commonly used Iodine-131. In addition, the low energy 159 keV gamma and a lesser abundant 28 keV X-ray offer promise of improved imaging resolution utilizing low energy high resolution collimators.