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Biomedical subjects

J W Hollifield

Publications and source records attributed to J W Hollifield.

At least 73 records · Page 4Linked to original sources
PubMed1976

Differentiation between malignant and benign solitary thyroid nodules by fluorescent scanning.

A quantitative fluorescent technique has been developed for making in vivo iodine content determinations of the total thyroid gland or of selected parts. In solitary thyroid nodules "cold" to radionuclide studies, the ratio of iodine content in the nodule to that in a corresponding area of the contralateral lobe has proven to be a good indicator of malignancy. In a preliminary study of 42 surgical patients, an iodine content ratio (ICR) below 0.60 (chosen a posteriori) proved to be an excellent indication of malignancy with a sensitivity of 100%, a specificity (predictive value) of 79%, and an overall accuracy of 90%. Further definitive studies are needed to verify these preliminary observations.

Diagnosis, Differential↗
PubMed1976

Prostaglandins are overproduced by the kidneys and mediate hyperreninemia in Bartter's syndrome.

In summary, the cardinal features of the syndrome of renal juxtaglomerular hyperplasia include overproduction of plasma renin activity, elevation of plasma angiotensin II concentration, elevation of aldosterone secretion and of plasma aldosterone concentration, hypokalemic alkalosis, and a resistance of arterioles to the pressor action of angiotensin II and norepinephrine. In the present studies, elevation of urinary PGE2 but not of PGF2alpha has been demonstrated. Inhibition of prostaglandin synthetase with indomethacin or ibuprofen has been shown to decrease plasma renin activity, and plasma aldosterone concentration and secretion rate, leading to a positive potassium balance and restoration of normal plasma potassium. The inhibitors decreased and glomerular filtration rate, and induced sodium retention. The results indicate that overproduction of PGE by the kidneys is a cardinal feature, but not necessary the primary one, in the pathogenesis of this syndrome.

Adolescent↗
PubMed1976

Prazosin.

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Humans↗
PubMed1975

Evidence for a new mineralocorticoid in patients with low-renin essential hypertension.

Patients with low-renin essential hypertension have certain features consistent with excessive mineralocorticoid activity. Because known mineralocorticoids are normal in the majority of low-renin essential hypertension patients, an unknown mineralocorticoid was sought in the urine of such patients. Urine extracts from patients with low-renin essential hypertension were assayed for mineralocorticoid activity in adrenalectomized rats and found to contain more such activity than could be accounted for by the known mineralocorticoids in the extracts. The factor responsible for the unexplained mineralocorticoid activity was purfied and then identified by mass spectral analysis as 16beta-hydroxydehydroepiandrosterone (16beta-OH-DHEA). Synthetic 16beta-OH-DHEA was found to have a mineralocorticoid potency one-fortieth that of aldosterone in the rat bioassay. The mineralocorticoid effects of both the urine extracts and the synthetic steroid were blocked in the rat by spironolactone, a mineralocorticoid antagonist. A specific assay for 16beta-OH-DHEA was developed, and its level in the urine was found to be elevated in patients with low-renin essential hypertension.

Adrenalectomy↗
PubMed1975

Renin-secreting clear cell carcinoma of the kidney.

A young woman with mild to moderate hypertension and normal PRA, serum potassium levels, and urinary aldosterone excretion rate was found to have a renal tumor by selective renal arteriogram. Renal vein renin activity indicated an increased production of renin from the kidney containing the tumor. At surgery, a clear cell carcinoma of the kidney was found that contained renin activity in excess of the surrounding kidney tissue. The renin activity appeared identical to human kidney renin. Previous renin-producing tumors have been associated with severe hypertension, elevated plasma renin activity, hypokalemia, and elevated urinary aldosterone excretion. This case should call attention to the renin-secreting tumor as a cause of even mild hypertension.

Adenocarcinoma↗