Citations

Secondary causes of hypertension can affect over 10% of those patients diagnosed with hypertension, and the workup can encompass a wide variety of pathologies. Here we present a case of secondary hypertension found in a young physician who, fortunately, had both of these two entities diagnosed via fortuitous imaging performed for non-diagnostic reasons. This case involves a relatively common cause of secondary hypertension (renovascular) and a more obscure cause (paraganglioma). We outline evidencebased surgical and perioperative management of paragangliomas, as well as the medical management of renovascular hypertension. This case is unique in that it involves both elements of secondary hypertension and presents difficult management decisions.

A newly identified gene fusion defines the vascular cancer epithelioid hemangioendothelioma and encodes a chimeric transcription factor.

To test the postulate that sex difference, sex steroids, and peptidyl secretagogues control GH autofeedback, 11 healthy postmenopausal women and 14 older men were each given 1) a single iv pulse of GH to enforce negative feedback and 2) continuous iv infusion of saline vs. combined GHRH/GHRP-2 to drive feedback escape during pharmacological estradiol (E2; women) or testosterone (T; men) supplementation vs. placebo in a double-blind, prospectively randomized crossover design. By three-way ANCOVA, sex difference, sex hormone treatment, peptide stimulation, and placebo/saline responses (covariate) controlled total (integrated) GH recovery during feedback (each P < 0.001). Both sex steroid milieu ( P = 0.019) and dual-peptide stimulation ( P < 0.001) determined nadir (maximally feedback-suppressed) GH concentrations. E2/T exposure elevated nadir GH concentrations during saline infusion ( P = 0.003), whereas dual-peptide infusion did so independently of T/E2 and sex difference ( P = 0.001). All three of sex difference ( P = 0.001), sex steroid treatment ( P = 0.005), and double-peptide stimulation ( P < 0.001) augmented recovery of peak (maximally feedback-escaped) GH concentrations. Peak GH responses to dual-peptidyl agonists were greater in women than in men ( P = 0.016). E2/T augmented peak GH recovery during saline infusion ( P < 0.001). Approximate entropy analysis corroborated independent effects of sex steroid treatment ( P = 0.012) and peptide infusion ( P < 0.001) on GH regularity. In summary, sex difference, sex steroid supplementation, and combined peptide drive influence nadir, peak, and entropic measurements of GH release under controlled negative feedback. To the degree that the pharmacological sex steroid, GH, and dual-peptide clamps provide prephysiological regulatory insights, these outcomes suggest major determinants of pulsatile GH secretion in the feedback domain.