title: Tuberculous Addison's disease: lack of normalization of adrenocortical function after anti-tuberculous chemotherapy.
abstract: OBJECTIVE
  Tuberculosis of the adrenal glands is a common cause of Addison's disease in developing countries. We conducted a study to determine if treatment of such patients with modern anti-tuberculous chemotherapy would lead to an improvement in plasma cortisol and aldosterone levels.
  
  
  METHODS
  Prospective study.
  
  
  METHODS
  5 patients with Addison's disease secondary to tuberculosis.
  
  
  METHODS
  Basal and ACTH stimulated plasma cortisol and aldosterone levels were measured prior to instituting anti-tuberculous chemotherapy, as well as one month after its conclusion. Four patients were again studied over the next 2-5 years.
  
  
  RESULTS
  Peak plasma cortisol levels prior to treatment were markedly reduced (range, < 14-110 mumol/l). There was no improvement one month (< 14-143 mumol/l) or 2-5 years (< 14-69 mumol/l) after completing anti-tuberculous chemotherapy. Peak plasma aldosterone at diagnosis was < 56-210 pmol/l; it was undetectable in 4 patients. No improvement was observed one month (< 56-210 pmol/l), or 2-5 years (< 56-389 pmol/l) after stopping anti-tuberculous chemotherapy. Plasma aldosterone levels at both these time points were far lower than those in control subjects (median 736 pmol/l, 560-1512 pmol/l; p < 0.01). One patient had an increase in peak aldosterone from < 56 pmol/l to 389 pmol/l, though peak cortisol actually declined in this subject (from 110 mumol/l to 69 mumol/l).
  
  
  CONCLUSIONS
  Treatment of tuberculous Addison's disease with anti-tuberculous chemotherapy does not lead to normalization of ACTH stimulated plasma cortisol or aldosterone levels during the 2-5 year period of study. However, prolonged follow up with regular adrenal function tests is warranted in all such patients.
authors.affiliation: Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.
authors.forename: E
authors.initials: E
authors.lastname: Bhatia
authors.forename: S K
authors.initials: SK
authors.lastname: Jain
authors.forename: R K
authors.initials: RK
authors.lastname: Gupta
authors.forename: R
authors.initials: R
authors.lastname: Pandey
mesh_terms: D000224:Addison Disease / Q000097:blood / Q000503:physiopathology*; D000302:Adrenal Cortex / Q000503:physiopathology*; D000304:Adrenal Cortex Function Tests; D000307:Adrenal Gland Diseases / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology; D000324:Adrenocorticotropic Hormone; D000328:Adult; D000450:Aldosterone / Q000097:blood; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D000995:Antitubercular Agents / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005438:Fludrocortisone / Q000627:therapeutic use; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007538:Isoniazid / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D011239:Prednisolone / Q000627:therapeutic use; D011446:Prospective Studies; D011718:Pyrazinamide / Q000627:therapeutic use; D012293:Rifampin / Q000627:therapeutic use; D014383:Tuberculosis, Endocrine / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D000893:Anti-Inflammatory Agents; D000995:Antitubercular Agents; D011718:Pyrazinamide; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D011239:Prednisolone; D005438:Fludrocortisone; D007538:Isoniazid; D012293:Rifampin; D006854:Hydrocortisone