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Biomedical subjects

T H Hsu

Publications and source records attributed to T H Hsu.

At least 73 records · Page 4Linked to original sources
PubMed1978

Thyrotoxicosis in a patient with secondary hypothyroidism.

We have described a patient with panhypopituitarism who developed thyrotoxicosis. There is a widespread belief that pituitary thyrotropin (TSH) is not a pathogenetic factor in most patients with thyrotoxicosis. Due to technical reasons, however, it has been difficult to entirely exclude the role(s) of TSH in the development of thyrotoxicosis. In this report hyperthyroidism appeared in a patient with TSH deficiency proved by the lack of response to TRH administration. This is the first known case in which TRH stimulation demonstrated total abscence of TSH before the onset of thyrotoxicosis. We cannot exclude the possibility that factors of adenohypophyseal origin play some role in the pathogenesis of thyrotoxicosis, but TSH per se does not play a role in the development of Graves' thyrotoxicosis.

Humans↗
PubMed1977

Sudden onset of unilateral third nerve paresis in a patient with Cushing syndrome.

Extraocular muscle pareses in patients with Cushing syndrome are virtually always associated with a greatly enlarged pituitary tumor and with advancement on oculomotor nerves. The present report concerns a patient with a rapidly progressive adrenocorticotropic hormone (ACTH)-dependent hyperadrenocorticism and sudden onset of an unilateral third nerve paresis. The patient had no demonstrable pituitary tumor. After a total adrenalectomy and correction of hyperadrenocortisolism, his third nerve paresis subsided. Ocular paresis may occur in a patient with Cushing syndrome even in the absence of mechanical involvement of ocular nerves by a pituitary tumor.

17-Hydroxycorticosteroids↗
PubMed1977

Breast carcinoma, thyroid carcinoma, and T3 thyrotoxicosis in a male cretin.

A male patient with clinical and radiographic evidence of cretinism was found to have T3 thyrotoxicosis. The cause was thought to be a well-differentiated follicular carcinoma of the thyroid. Although the disease was not documented, the patient probably had long-standing hypothyroidism. Untreated primary thyroid failure accompanied by high serum thyroid stimulating hormone (TSH) may be carcinogenic to the thyroid. The association of thyroid abnormalities and male breast carcinoma is discussed.

Adenocarcinoma↗
PubMed1976

Differential ovarian and adrenal vein catheterization.

Twenty-two hirsute women underwent percutaneous adrenal and ovarian vein catheterization to differentiate and localize excessive hormonal output. All studies were done under fluoroscopic control; catheter placement was verified by venography, and blood samples were withdrawn for hormonal analysis. The right ovarian vein was successfully sampled in 42 per cent of attempts; the left ovarian vein, in 75 per cent; the right adrenal vein, in 56 per cent; and the left adrenal vein, in 100 per cent. Bilateral catheterization did not prove clinically useful. First, anatomic variations in venous size and drainage made catheterization and bilateral sampling difficult. Second, adrenal secretion is both episodic and parallel, necessitating both simultaneous catheterization and serial sampling for adequate diagnosis. The stress of the procedure may provoke increased adrenal output. Third, since ovarian secretion is not parallel, and since increased hormone output has been documented in that ovary containing developing follicles or a corpus luteum, distinguishing ovarian dysfunction proved difficult. Finally, for a time-consuming procedure, patient discomfort cannot be disregarded. This technique has not proved to be a reliable means of determining the site of androgen hypersecretion and thus cannot be recommended in the routine evaluation of female hirsutism.

17-Ketosteroids↗
PubMed1976

Potentiation of the ACTH response to metyrapone by L-dopa in the monkey.

The intravenous injection of L-Dopa (15 mg/kg) to monkeys (Macaca mulatta) failed to alter plasma concentrations of ACTH and of 11-deoxy-cortisol. When cortisol synthesis was blocked with iv metyrapone, potentiation of ACTH secretion by L-Dopa became apparent. Simultaneous injection of L-Dopa and metyrapone resulted in a marked increase in plasma ACTH from 93 +/- 18 pg/ml to 432 +/- 80 pg/ml, whereas plasma 11-deoxycortisol increased from 1.5 +/- 0.2 mug/100 ml to 14.6 +/- 1.0 mug/100 ml 90 min after treatment. Throughout the experiment the rise in ACTH and in 11-deoxycortisol following coadministration of L-Dopa and metyrapone was significantly (P less than 0.01) higher than that produced by metyrapone administration alone. The results suggest that acute administration of L-Dopa in monkeys enhances the response of ACTH to metyrapone. L-Dopa (or one of its metabolites) probably acts upon a noradrenergic or a dopaminergic system located in the hypothalamus to alter the release of hypothalamic corticotropin regulatory factor(s) and thereby enhance the release of ACTH.

Adrenocorticotropic Hormone↗
PubMed1975

Juvenile diabetes mellitus after forty years.

Seventy-three patients with juvenile diabetes mellitus for a mean duration of 42.9 years were retrospectively studied on a multidisciplinary basis. Only three of this group of patients were socially disabled as a result of their long-standing illness. Of all the complications, insulin-induced hypoglycemia was most common. Although diabetic retinopathy was clinically evident in about 75 per cent of patients, only 50 per cent of these seventy-three patients had a significant visual impairment. Nephropathy was apparent in 59 per cent of patients, and neuropathy was demonstrable in half of them. Significant peripheral vascular system impairment was present in 40 per cent and major cardiac complication in 20 percent.

Achievement↗
PubMed1972

Peripheral aromatic L-amino acids decarboxylase inhibitor in Parkinsonism. I. Effect on O-methylated metabolites of L-dopa-2- 14 C.

The effects of MK-486, an inhibitor of peripheral aromatic L-amino acids decarboxylase, on the urinary metabolites derived from orally administered L-Dopa-2-(14)C were studied in three Parkinsonian patients. Treatment with MK-486 before L-Dopa-2-(14)C markedly reduced radioactivity found in catecholamines fraction by 70-80% during 48 hr, but increased 3-O-methyldopa fraction by threefold, as compared with a nonpretreated base line value. Pretreatment with MK-486 for a period of 1 wk resulted in less inhibition of O-methylated amine and acid metabolite fractions than that measured after a single dose of the inhibitor.

Aged↗