The sweating apparatus in growth hormone deficiency, following treatment with r-hGH and in acromegaly.
Adult growth hormone deficient patients are known to exhibit reduced sweating and their ability to thermoregulate is diminished. Treatment of these patients with recombinant human growth hormone (r-hGH) is claimed to reverse these abnormalities. We have investigated this claim, as well as the mechanism underlying these altered sweating responses in GH-deficient patients as part of a placebo-controlled study on the effects of 6-12 months r-hGH therapy. Skin biopsies were obtained from these subjects and changes in morphology and innervation parameters for the eccrine sweat glands were examined. These included histochemistry for acetylcholinesterase (AChE) and immunohistochemistry for the neuropeptide vasoactive intestinal polypeptide (VIP) and for PGP9.5, a general neuronal marker. Sweat gland acinar size and periacinar innervation were measured by computerised image analysis. The patients underwent pilocarpine iontophoresis sweat rate tests and their serum insulin-like growth factor 1 (IGF-1) levels were assessed. Since active acromegaly involves excess GH secretion and hyperhidrosis, skin biopsies and sweat tests were also carried out on a group of these patients, as well as on control subjects. We have demonstrated a sweating defect in adult GH-deficiency which is accompanied by a reduction in AChE and VIP levels in the nerve supply to sweat glands. Following r-hGH therapy, an increase in AChE and VIP staining is seen in the sudomotor nerves accompanied by restoration of sweat rates and serum IGF-1 levels. Hence, normalization of sweat gland function includes recovery of sudomotor synapse constituents. A trophic effect of GH on sweat gland epithelium and/or on the associated nerves is proposed, supported by the observation that in acromegaly the size of sweat gland acini and the density of innervation to the sweat glands was greater than in controls.
Hasan
W
W
Department of Endocrinology, Royal Free and University College Medical School, London, UK.
Cowen
T
T
Barnett
P S
PS
Elliot
E
E
Coskeran
P
P
Bouloux
P M
PM
D000110:Acetylcholinesterase / Q000032:analysis; D000172:Acromegaly / Q000473:pathology / Q000503:physiopathology*; D000328:Adult; D000943:Antigens, Differentiation / Q000032:analysis; D001706:Biopsy; D005260:Female; D006130:Growth Disorders / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D013006:Growth Hormone / Q000008:administration & dosage*; D019382:Human Growth Hormone / Q000172:deficiency*; D006801:Humans; D066298:In Vitro Techniques; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007478:Iontophoresis; D008297:Male; D008875:Middle Aged; D018721:Muscarinic Agonists / Q000494:pharmacology; D010862:Pilocarpine / Q000494:pharmacology; D013545:Sweat Glands / Q000294:innervation / Q000473:pathology / Q000502:physiology; D013546:Sweating / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000737:chemistry / Q000201:enzymology / Q000503:physiopathology; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D014446:Tyrosine 3-Monooxygenase / Q000032:analysis; D043222:Ubiquitin Thiolesterase; D014660:Vasoactive Intestinal Peptide / Q000032:analysis
D000943:Antigens, Differentiation; D018721:Muscarinic Agonists; D010862:Pilocarpine; D014284:Triiodothyronine; D019382:Human Growth Hormone; D014660:Vasoactive Intestinal Peptide; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D014446:Tyrosine 3-Monooxygenase; D000110:Acetylcholinesterase; D043222:Ubiquitin Thiolesterase; D013974:Thyroxine