title: Hypothalamic-pituitary insufficiency following infectious diseases of the central nervous system.
abstract: OBJECTIVE
  Hypothalamic-pituitary insufficiency may have diverse causes. The aim of this study was to determine the incidence of hypothalamic-pituitary insufficiency in patients with previous infectious diseases of the central nervous system (CNS) of different etiologies and mild-to-moderate clinical course.
  
  
  METHODS
  Patient series. Basal and stimulated (insulin tolerance test) pituitary function testing was performed in 19 patients with previous neuroborreliosis, encephalitis, or meningitis following an interval of between 10 and 56 months (mean 26.1+/-13.1 months) after the acute event.
  
  
  RESULTS
  Four patients (21%; two males, two females) showed an isolated corticotropic insufficiency (peak cortisol <181.25 microg/l during the insulin tolerance test). Two patients (11%, males) showed borderline gonadotropic insufficiency (basal testosterone between 2.4 and 3.0 microg/l). No patient had somatotropic or thyrotropic insufficiency or evidence for diabetes insipidus; all had prolactin concentrations within the reference range.
  
  
  CONCLUSIONS
  Hypothalamic-pituitary dysfunction and especially isolated corticotropic insufficiency may develop in a relevant proportion of patients after infectious diseases of the CNS.
authors.affiliation: Division of Endocrinology and Diabetology, Philipps University Hospital, Baldingerstrasse, D-35033 Marburg, Germany. stscha@med.uni-marburg.de <stscha@med.uni-marburg.de>
authors.forename: S
authors.initials: S
authors.lastname: Schaefer
authors.forename: N
authors.initials: N
authors.lastname: Boegershausen
authors.forename: S
authors.initials: S
authors.lastname: Meyer
authors.forename: D
authors.initials: D
authors.lastname: Ivan
authors.forename: K
authors.initials: K
authors.lastname: Schepelmann
authors.forename: P H
authors.initials: PH
authors.lastname: Kann
mesh_terms: D000309:Adrenal Insufficiency / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000328:Adult; D000368:Aged; D015992:Body Mass Index; D002493:Central Nervous System Diseases / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D003141:Communicable Diseases / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D004958:Estradiol / Q000378:metabolism; D005260:Female; D005640:Follicle Stimulating Hormone / Q000378:metabolism; D013006:Growth Hormone / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D007018:Hypopituitarism / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism / Q000473:pathology; D007328:Insulin / Q000378:metabolism; D007986:Luteinizing Hormone / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010913:Pituitary-Adrenal System / Q000378:metabolism / Q000473:pathology; D011374:Progesterone / Q000378:metabolism; D011388:Prolactin / Q000378:metabolism; D013739:Testosterone / Q000378:metabolism; D013972:Thyrotropin / Q000378:metabolism; D013974:Thyroxine / Q000378:metabolism
chemical_list: D007328:Insulin; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D013006:Growth Hormone; D013974:Thyroxine; D006854:Hydrocortisone