title: A pilot study on hypothalamo-pituitary-adrenocortical axis in primary hyperparathyroidism.
abstract: OBJECTIVE
  Parathormone (PTH) and calcium, both have been shown to stimulate adrenal steroidogenesis in animal models and in vitro experiments. This is attributed to structural similarity between 15-25 amino acid region of the parathyroid hormone (PTH) and 1-11 amino acid region of adrenocorticotropin (ACTH). However, there are no in vivo human data regarding the effect of PTHcalcium axis on adrenocortical function.
  
  
  METHODS
  Ten patients with primary hyperparathyroidism underwent evaluation for cortisol dynamics including 0800 h and 2000 h plasma cortisol on day 1, cortisol response to insulin induced hypoglycaemia (IIH) on day 2, and 1 mg overnight dexamethasone suppression test (ONDST) on day 4. Serum aldosterone was also measured at 0800 h in fasting state on salt ad libitum for three days. These parameters were repeated 3 months after curative parathyroidectomy.
  
  
  RESULTS
  Basal plasma cortisol level at 0800 h and 2000 h were within upper normal range and loss of circadian rhythm in cortisol secretion was observed in half and forty per cent of patients had nonsuppressibility with ONDST. The defined peak cortisol response to insulin induced hypoglycaemia (>550 nmol/l) was achieved in all and nearly one third of patients had exaggerated response (>2000 nmol/l). After curative parathyroidectomy, the abnormalities in circadian rhythm and non-suppressibility with ONDST continued to prevail in 40 per cent of patients. The peak cortisol response to IIH showed a decrement but remained higher than normal. No correlation was observed between circulating parathyroid hormone and calcium with cortisol levels. Serum aldosterone was in upper normal range pre - and postoperatively, though it decreased postoperatively, but it could not attain a statistical significance (p = 0.5).
  
  
  CONCLUSIONS
  Abnormalities in hypothalamo-pituitary-adrenocortical axis in primary hyperparathyroidism do occur, however these are inconsistent and do not recover in majority of patients even after 3 months of curative parathyroidectomy.
authors: Department of Endocrinology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
authors: Rajesh
authors: R
authors: Rajput
authors: Anil
authors: A
authors: Bhansali
authors: Sanjay Kumar
authors: SK
authors: Bhadada
authors: Arunanshu
authors: A
authors: Behera
authors: B R
authors: BR
authors: Mittal
authors: Ravinder
authors: R
authors: Sialy
authors: N
authors: N
authors: Khandelwal
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000450:Aldosterone / Q000097:blood; D000818:Animals; D003907:Dexamethasone / Q000378:metabolism; D005260:Female; D005938:Glucocorticoids / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D049950:Hyperparathyroidism, Primary / Q000503:physiopathology* / Q000601:surgery; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology* / Q000503:physiopathology; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000235:genetics / Q000378:metabolism; D010865:Pilot Projects; D010913:Pituitary-Adrenal System / Q000502:physiology* / Q000503:physiopathology; D055815:Young Adult
chemical_list: D005938:Glucocorticoids; D010281:Parathyroid Hormone; D000450:Aldosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone