Hypertension in Growth Hormone Excess and Deficiency

Abstract

Cardiovascular and cerebrovascular morbidity and mortality are increased in both acromegaly and adult growth hormone deficiency (GHD), and a significant portion of this elevated risk can be attributed to hypertension. Despite taking into account the effects of derangement of other pituitary hormones that often accompany these conditions and of treatments used for acromegaly or GHD, much appears attributable to the direct and indirect effects of abnormal levels of GH or IGF-I themselves. The hypothesized mechanisms for hypertension have been the subjects of much more study in acromegaly than in GHD; but at present there is no clear consensus on the most important abnormalities underlying hypertension in either condition, nor even on its prevalence, with a wide range of estimates from less than 20% to more than 70% in acromegaly, and 25–30% in GHD. The divergent results arise from differences in the techniques used to measure blood pressure and also the rates of hypertension in the background populations. Mechanisms postulated to underlie hypertension in acromegaly include expansion of plasma volume, direct renal effects, changes in vascular compliance, increased sympathetic tone, and indirect effects due to insulin resistance and to sleep apnea. Hypothesized mechanisms in GHD include endothelial dysfunction and increased vascular stiffness; but several other factors, such as increased sympathetic tone, paradoxically overlap with factors thought to play a role in acromegaly as well. This overlap may signify a U-shaped curve for the effects of GH and IGF-I on blood pressure regulation, with optimum effects within the normal range, but data are currently insufficient to demonstrate this with any certainty. Perhaps the strongest evidence linking acromegaly with abnormal BP is resolution or improvement of hypertension with successful treatment of GH excess.