Skin morphological changes in growth hormone deficiency and acromegaly

Objective: To evaluate the histomorphology of skin and its appendages, espe cially eccrine sweat glands, in patients with GH disorders, because reduced sweating ability in patients with growth hormone deficiency (GHD) is assoc iated with increased risk of hyperthermia under stressed conditions. Design and Methods: A skin biopsy was obtained from 17 patients with GHD tr eated with GH, five patients with untreated GHD. 10 patients with active ac romegaly and 13 healthy controls. Results: The sweat secretion rate (SSR) was significantly decreased in both the untreated (median 41 mg/30 min, range 9-79 mg/30 min) and the GH-treat ed (median 98 mg/30 min, range 28-147 mg/30 min) patients with GHD compared with that in controls (median 119 mg/30 min, range 90-189 mg/30 min; P = 0 .001 and 0.01 respectively). Epidermal thickness was significantly decrease d in both untreated (median 39 mum, range 28-55 mum) and GH-treated patient s with GHD (median 53 mum, range 37-100 mum), compared with that in control s (median 66 mum, range 40-111 mum; P < 0.02). A statistically non-signific ant tendency towards thinner epidermis (median 59 <mu>m, range 33-83 mum) w as recorded in acromegalic patients (P = 0.08) compared with controls. Ther e was no significant difference in the area of the sebaceous glands in the biopsies between the three groups and the controls. The area of eccrine swe at gland glomeruli was significantly decreased in the untreated patients wi th GHD (median 16407 mum(2), range 12758-43976 mum(2)) compared with that i n controls (median 29446 mum(2), range 13511-128661 mum(2); P = 0.03), but there was no significant difference between the GH-treated patients with GH D and controls. Conclusions: We conclude that GH, either directly or via IGF-I, may have bo th a structural and a functional effect on human skin and its appendages, a nd that patients with GHD have histomorphological changes in skin compared with controls. Importantly, these changes are not fully reversed despite lo ng-term and adequate GH treatment in patients with childhood onset GHD.