Hereditary hemorrhagic telangiectasia (HHT) often requires transfusion and has major ill-effects. The recent literature reports successful highdose estrogen treatment of epistaxis caused by HHT. To investigate this, biopsy specimens taken from areas clinically involved with telangiectasia in four patients were evaluated for estrogen-and progesteronebinding receptors. Specimens from two women (ages 34 and 38) were positive for both estrogen and progesterone receptors in ranges observed in breast carcinoma specimens. Specimens from two men (ages 34 and 78) were positive only for progesterone receptors at lower but clearly detectable levels of activity. Nasal mucosa specimens from control patients -2 male and 4 female -yielded no detectable levels of estrogen or progesterone receptors. Because of the side effects of high-dose estrogen (especially in males), we have initiated systemic progesterone therapy with both megestrol acetate and medroxyprogesterone acetate. Marked diminution in epistaxis incidence and severity was observed in three patients after initial systemic progesterone treatment. All treated patients have been maintained with good epistaxis control for over 1 year. (OTOLARYNGOL HEAD NECK SURG 92:564. 1984.)
SUMMARY Twenty-six patients being evaluated for renovascular hypertension were studied to assess the diagnostic value of enhancing the differential between renal venous renins (PRA) by a single 25 mg oral dose of converting enzyme inhibitor (CEI, captopril). Antihypertensive medications were not discontinued prior to the study, and renal venous effluent was sampled before and 30 minutes after CEI. Eight patients without stenosis who did not have surgery had post-CEI ratios of less than 3.0. The other 18 patients had operative intervention, with 14 subsequently having improved blood pressure control. Of these 14, seven patients with unilateral stenosis, four patients with bilateral stenosis, and one patient without overt stenosis but with other evidence of reduced renal blood flow had 30-minute PRA ratios of 3.0 or greater. Five of these 14 patients had prestimulation ratios of less than 1.5 and might not be considered operative candidates by conventional criteria. Four other patients unimproved by surgery had post-CEI ratios of less than 3.0 despite a baseline ratio of greater than 1.5 in two of four. Only two patients with post-CEI ratios of less than 3.0 were improved with surgery. We conclude that a 30-minute post-CEI renal venous ratio of 3.0 or greater enhances the probability that patients with renovascular disease, and hypertension will respond to surgical intervention with improved blood pressure control. (Hypertension 5: 615-622, 1983) KEY WORDS • captopril • converting enzyme inhibitor plasma renin activity • renovascular hypertension R ENOVASCULAR hypertension constitutes less than 5% of hypertensive diseases; yet the potential for successful treatment with surgical intervention, percutaneous dilation, or specific medical management places a premium on accurate diagnosis. Unfortunately, the discovery of renal artery stenosis by angiography does not prove a functional relationship between the vascular lesion and the hypertension.1 ' 2 To clarify the functional role of the stenotic lesion, a ratio of renal venous plasma renin activity (PRA) of 1.5 or greater has been generally accepted as indicative of physiologically significant renal artery stenosis.3 " 7 On occasion this ratio is less than 1.5, yet surgical intervention results in significant improvement in the blood pressure.
The influence of short term, high dose glucocorticoids on pancreatic polypeptide (PP), GH, and PRL responses to insulin-induced hypoglycemia was studied in normal young men. Subjects underwent insulin tolerance tests before (ITTb) and on the fifth day (ITT 5 ) of treatment with prednisone (25 mg orally twice daily) and again 2 (ITT 7 ) and 5 (ITT, 0 ) days after termination of prednisone therapy. Eleven subjects completed ITTH, ITT 7) and ITT 10 . Five of these underwent ITT S . Despite the more pronounced hypoglycemia associated with the higher insulin dose used during prednisone treatment, PP responses were significantly diminished. Basal PP was reduced from 92.7 ± 13 to 38.6 ± 5.7 pg/ml (P < 0.05) at the time of ITT 5 and returned to pretreatment values at the time of ITT7. The peak pretreatment PP concentration of 1328 ± 203 pg/ml was reduced to 584 ± 118 (P < 0.05) during ITT 5 , and after discontinuation of prednisone returned progressively to pretreatment values. A more marked suppression was evident from comparison of the areas under the response curves. The control response of 64,926 ± 10,805 pg-min/ml was reduced to 18,782 ± 3,811 pg-min/ml on the fifth day of prednisone therapy (P < 0.01), returning to .the control values subsequently. GH and PRL responses were suppressed during ITT 5 , and, as observed with PP, the responsiveness of both pituitary hormones to insulin had returned to baseline by ITT 7 . The ITT h GH peak of 61.4 ± 6.5 ng/ml was reduced to 19.2 ± 6.2 (P < 0.01), and the PRL peak of 21.9 ± 4.2 ng/ml was reduced to 5.5 ± 2.6 (P < 0.05) at ITT 5 , with a return by ITT7 to 56.9 ± 6.9 and 25.6 ± 5.4 ng/ml, respectively. Fasting PRL was suppressed from 9.35 ± 1.18 to 3.8 ± 0.77 ng/ml (P < 0.01). We conclude that short term, high dose glucocorticoid treatment suppresses basal and stimulated PP secretion, basal PRL, and stimulated PRL and GH secretion. These suppressive effects are evanescent, since secretory responses normalize within 48 h of cessation of prednisone therapy. (J Clin EndocrinolMetab 50: 298, 1980)
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