Review covering the pathophysiology of GHRH-GH-IGF1 axis dysregulation in HIV and AIDS, explaining the two distinct mechanisms of GH abnormality: suppressed pulsatile GH secretion driving lipodystrophy in HAART-treated patients (via increased somatostatin tone, reduced ghrelin, insulin resistance) versus GH deficiency in AIDS wasting syndrome, and how tesamorelin targets the HAART-associated mechanism. Provides the endocrine basis for tesamorelin's indication. Establishes the distinct pathophysiological mechanisms underlying GH axis dysfunction in HIV-treated versus untreated/wasting patients—explaining why tesamorelin's GHRH-based approach selectively restores physiological GH pulsatility appropriate for HIV lipodystrophy while not risking growth stimulation relevant to AIDS wasting.
Jain, Shobhit; Desai, Ninad; Bhangoo, Amrit