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Biomedical subjects

R E Goldsmith

Publications and source records attributed to R E Goldsmith.

At least 19 recordsLinked to original sources
PubMed1992

Subjective age: a test of five hypotheses.

This paper discusses the concept and measurement of subjective age. Five hypotheses are proposed based on earlier studies of subjective age and tested using data from 607 randomly selected adults from five states. The data supported only two of the hypotheses: (1) the agreement between chronological age and subjective age declines steadily throughout the adult decades and (2) people in their 30s are the most likely to see themselves as different, either younger or older, from their chronological age. We conclude that generalizations about subjective age may depend on the subjects providing the data.

Adult↗
PubMed1978

Hypercalcemia in thyrotoxicosis.

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.

Adult↗
PubMed1977

Metastatic pulmonary calcification in primary hyperparathyroidism.

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.

Calcinosis↗
PubMed1976

Familial hyperparathyroidism. Description of a large kindred with physiologic observations and a review of the literature.

Sixty-nine out of a kindred of 100 members covering five generations were examined and studied, and 34 were hypercalcemic. Sixteen subjects were believed, on the basis of laboratory and clinical observations, to have primary hyperparathyroidism. Eight patients were subjected to exhaustive study to identify polyendocrine involvement before neck exploration. No coexisting endocrine abnormalities were found; operation showed multiparathyroid gland involvement in most instances. Measurement of immunoassayable calcitonin and assessment of renal and gut function were carried out in 37 subjects to search out possible causes of "reactive" parathyroid gland hyperfunction. While no such cause-effect relationship was noted for this kindred, 16 of the subjects so tested had serum calcitonin content below the assay limits of sensitivity. What role this apparent lack of calcitonin played in the development of hyperparathyroidism (or vis versa) needs clarification.

Adenoma↗
PubMed1975

Long-term observations of glucose tolerance in thyrotoxic patients.

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.

Adult↗
PubMed1970

The effect of diphenylhydantoin on thyroxine metabolism in man.

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.

Adult↗
PubMed1968

Metabolic effects of human growth hormone in corticosteroid-treated children.

The effects of administered human growth hormone (HGH) were evaluated in dwarfed, prepubertal children who were receiving long-term corticosteroid therapy for a chronic disease. During 11 complete metabolic balance studies, the eight corticosteroid-treated children demonstrated impaired response to large doses of HGH with minimal nitrogen and no phosphorus retention. In contrast, two hypopituitary subjects and two asthmatic children not receiving corticosteroid responded to the same preparations of HGH with nitrogen, potassium, and phosphorus retention. Six corticosteroid-treated children were given large doses of HGH (40-120 mg/wk for 4 to 8 months and showed no improvement in their retarded rate of growth, whereas the hypopituitary subjects showed accelerated growth during administration of 10-15 mg of HGH/wk. It is concluded that dwarfism in steroid-treated children results from corticosteroid-induced antagonism of the effects of HGH at the peripheral tissue level.

Adolescent↗