title: Evaluation of pituitary function after infectious meningitis in childhood.
abstract: BACKGROUND
  A number of studies of adults have shown that pituitary deficiencies can develop in a considerable proportion of subjects during the acute phase of meningitis or years after the infection has disappeared. The results of the very few studies of the impact of pediatric meningitis on hypothalamic-pituitary function are conflicting.
  
  
  METHODS
  In order to determine the incidence of pituitary dysfunction in children with central nervous system infection, we evaluated pituitary function and anthropometric parameters in 19 children with meningitis of different etiologies (15 males; mean age ± standard deviation [SD] at pituitary evaluation, 5.9 ± 4.0 years; mean time from the acute event ± SD, 18 ± 10 months).
  
  
  RESULTS
  All of the subjects had a normal stature and growth velocity for their age and gender, and none of them was obese. On the basis of Tanner's reference charts, 17 subjects (13 boys and all four girls) were pre-pubertal; two boys were in Tanner stage 2. None of the subjects had central hypothyroidism. All of the patients had normal serum of insulin growth factor (IGF)-I and prolactin. Their sex steroid and gonadotropin levels were concordant with their age and pubertal status. Early morning urine osmolality and serum electrolyte levels showed no signs of diabetes insipidus. All of the patients had normal plasma adrenocorticotropic hormone (ACTH) levels. Peak cortisol responses to the standard dose Synacthen test (SDST) were normal in all cases.
  
  
  CONCLUSIONS
  The results showed that hypopituitarism following infectious meningitis appears to be infrequent in childhood and children's pituitary glands seem to be less vulnerable to damage than those of adults.
authors.forename: Claudia
authors.initials: C
authors.lastname: Giavoli
authors.forename: Claudia
authors.initials: C
authors.lastname: Tagliabue
authors.forename: Eriselda
authors.initials: E
authors.lastname: Profka
authors.forename: Laura
authors.initials: L
authors.lastname: Senatore
authors.forename: Silvia
authors.initials: S
authors.lastname: Bergamaschi
authors.forename: Giulia
authors.initials: G
authors.lastname: Rodari
authors.forename: Anna
authors.initials: A
authors.lastname: Spada
authors.forename: Paolo
authors.initials: P
authors.lastname: Beck-Peccoz
authors.affiliation: Pediatric Highly Intensive Care Unit, Department of Pathophysiology and Transplantation, Università degli Studi di Milano, Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, Via Commenda 9, 20122 Milan, Italy. susanna.esposito@unimi.it.
authors.forename: Susanna
authors.initials: S
authors.lastname: Esposito
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000367:Age Factors; D002493:Central Nervous System Diseases / Q000276:immunology / Q000503:physiopathology*; D002648:Child; D002657:Child Development; D005260:Female; D006801:Humans; D007018:Hypopituitarism / Q000209:etiology / Q000276:immunology / Q000503:physiopathology*; D007030:Hypothalamo-Hypophyseal System / Q000276:immunology / Q000503:physiopathology*; D007558:Italy / Q000453:epidemiology; D008297:Male; D008581:Meningitis / Q000150:complications / Q000276:immunology / Q000503:physiopathology*; D016896:Treatment Outcome
chemical_list: D000324:Adrenocorticotropic Hormone