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Biomedical subjects

J H Sunder

Publications and source records attributed to J H Sunder.

At least 19 recordsLinked to original sources

Unresponsiveness to exogenous TSH in obesity.

(1). Assessment of thyroidal and other indices in 275 instances of obesity with body weight excesses up to 200 percent or more of the ideal revealed absent thyroidal I131 uptake responses to TSH in about one out of five patients. Moreover, basal thyroidal I131 uptake of 10 percent or less, prolongation of ankle reflex time, or high levels of serum cholesterol were present in a minority. Also, occasional instances of unduly elevated serum TSH titers were found. Some of the indices deviated from normal more often with the greater excesses of body weight or with increased age. (2). These findings are consonant with a hypothesis that routine thyroidal or related indices are sporadically abnormal in massive obesity almost always without overt hypothyroidism or myxedema, that total unresponsiveness to exogenous TSH is surprisingly frequent, and that such unresponsiveness represents an unexplained endocrine anomaly in association with gross overweight. (3). Our data suggest that some obese persons are not able to respond to exogenous TSH, nor, presumably, to increases of endogenous TSH. This could result in an economy of caloric expenditure and play a contributory role in the genesis or the perpetuation of the obesity.

Achilles Tendon↗

Thyroid hormone-like effects without thyrotoxicosis during one year's therapy with NA-DT3 for hypercholesterolemia.

A thyroid hormone analogue, sodium dextro-triiodothyronine (NaDT3), at a dosage of 1 mg/day for 1 or 2 yr, decreased serum cholesterol levels about 30% in 26 hyperlipidemic adults. There were less sustained decreases in the serum phospholipids, and occasional lowering of the serum triglycerides, but no effects on body weight, blood pressure, or pulse rate. Changes recognized as variable concomitants of spontaneous or induced thyrotoxicosis, such as transient increases in fasting blood glucose, calcium, and globulin, persistent rises in alkaline phosphatase, and nonsustained decreases in hematocrit are consonant with the fact that Na-DT3 exerts about one tenth of the thyroid hormone activity of LT3. These changes, however, appear to represent actions of iodinated amino acids apart from those effects that result in clinical thyrotoxicosis.

Adult↗

Clinical and ultrastructural observations in a kindred with normo-hyperkalaemic periodic paralysis.

Electron microscopic studies of muscle biopsies from clinically unaffected sibs in a family with normo-hyperkalaemic periodic paralysis with variable myotonia have revealed dilatation of the sarcoplasmic reticulum similar to that observed in affected members. This supports the view that such dilatation is not only a significant and likely primary ultrastructural change but that it may precede clinical manifestations and represent an anatomical marker of the genetic trait. Identical dilatation of the sarcoplasmic reticulum was found in the clinically unaffected father of the affected and unaffected grandchildren of the propositus. This raises the possibility that this non-consanguineous member contributed to the genetic trait or its manifestations in the grandchildren of the index patient since similar dilatation of the sarcoplasmic reticulum was not observed in the muscles of healthy control subjects.

Adolescent↗