title: Reversible adrenocorticotropin deficiency due to probable autoimmune hypophysitis in a woman with postpartum thyroiditis.
abstract: The natural history and pathogenesis of lymphocytic hypophysitis remain poorly understood. We describe a 34-yr-old woman with postpartum thyroiditis and ACTH deficiency, studied at monthly intervals for 18 months after pregnancy. A significant titer of thyroid peroxidase autoantibodies was detected at 16 weeks gestation, and she was recruited into a prospective study of postpartum thyroid function. Four months postpartum she developed mild hyperthyroidism [free T4 (fT4), 27 pmol/L; TSH, less than 0.2 mU/L] and showed a rise in thyroid peroxidase and thyroglobulin autoantibodies. At 9 months postpartum, serum fT4 and fT3 levels were low normal (8.0 and 1.7 pmol/L, respectively), but TSH was not raised (0.4 mU/L). Subsequent investigation showed a low basal plasma cortisol level (28 nmol/L) in association with undetectable ACTH, and subnormal cortisol responses to depot Synacthen (535 nmol/L at 6 h) and hypoglycemia (peak, 145 nmol/L). FSH, LH, GH, and PRL function and computerized tomography of the pituitary were normal. Retrospective analysis of serum samples taken throughout the postpartum year showed developing hypocortisolemia between 3-9 months postpartum. Each sample was also tested for pituitary autoantibodies using a specific indirect immunofluorescent assay; none was detected. The ACTH deficiency recovered spontaneously, with normal cortisol responses to depot Synacthen (greater than 1380 at 6 h) and hypoglycemia (peak, 590) 14 and 18 months postpartum, respectively. This case illustrates that postpartum pituitary deficiencies are potentially reversible. The pattern of pituitary deficit and postpartum thyroiditis supported a diagnosis of autoimmune hypophysitis.
authors.affiliation: Department of Medicine, University Hospital of Wales, Cardiff, United Kingdom.
authors.forename: J S
authors.initials: JS
authors.lastname: Bevan
authors.forename: S
authors.initials: S
authors.lastname: Othman
authors.forename: J H
authors.initials: JH
authors.lastname: Lazarus
authors.forename: A B
authors.initials: AB
authors.lastname: Parkes
authors.forename: R
authors.initials: R
authors.lastname: Hall
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000172:deficiency*; D000328:Adult; D001323:Autoantibodies / Q000032:analysis*; D001327:Autoimmune Diseases / Q000188:drug therapy / Q000503:physiopathology*; D003366:Cosyntropin / Q000627:therapeutic use*; D005260:Female; D005500:Follow-Up Studies; D007987:Gonadotropin-Releasing Hormone; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007453:Iodide Peroxidase / Q000276:immunology*; D010900:Pituitary Diseases / Q000188:drug therapy / Q000276:immunology / Q000503:physiopathology*; D011247:Pregnancy; D011248:Pregnancy Complications / Q000276:immunology* / Q000503:physiopathology; D011644:Puerperal Disorders / Q000276:immunology* / Q000503:physiopathology; D013967:Thyroiditis, Autoimmune / Q000276:immunology / Q000503:physiopathology*; D013972:Thyrotropin / Q000097:blood; D013973:Thyrotropin-Releasing Hormone; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D001323:Autoantibodies; D014284:Triiodothyronine; D003366:Cosyntropin; D007987:Gonadotropin-Releasing Hormone; D013973:Thyrotropin-Releasing Hormone; D000324:Adrenocorticotropic Hormone; D013972:Thyrotropin; D007453:Iodide Peroxidase; D013974:Thyroxine; D006854:Hydrocortisone