title: Hypokalaemia during insulin-induced hypoglycaemia in hypopituitary adults with and without growth hormone deficiency.
abstract: OBJECTIVE
  We have investigated plasma potassium changes during insulin-induced hypoglycaemia (IIH) in adult patients with growth hormone deficiency (GHD) who have low total body potassium and may also have a vulnerable myocardium due to an increased prevalence of atherosclerosis.
  
  
  METHODS
  Hypoglycaemia was induced through the administration of intravenous soluble insulin (0.1 U/Kg, i.v.).
  
  
  METHODS
  23 consecutive adult patients undergoing routine biochemical evaluation for hypopituitarism.
  
  
  METHODS
  GH, cortisol glucose, sodium and potassium levels were measured at 0, 30, 60, 90 and 120 min after insulin administration. Pituitary function was also assessed through measurement of TSH, thyroid hormones, LH/FSH, testosterone and 17-oestradiol. IGF-I concentrations were also analysed.
  
  
  RESULTS
  All patients achieved adequate hypoglycaemia (nadir glucose < 2 mmol/l). 15 patients had GHD (peak GH < 10 mU/l) either in isolation or as part of a spectrum of pituitary hormone deficiencies. The remaining 8 patients had normal pituitary function. Plasma potassium concentrations (mean +/- SEM) fell from 3.8 +/- 0.3 mmol/l (normals) and 3.8 +/- 0.2 mmol/l (GHDs) to nadir concentrations of 3.0 +/- 0.2 mmol/l and 3.1 +/- 0.3 mmol/l, respectively (P < 0.005). Overt hypokalaemia (< 3.5 mmol/l) occurred in 13/15 GHDs and all normals. There were no significant differences between the groups.
  
  
  CONCLUSIONS
  Insulin-induced hypoglycaemia causes similar degrees of significant hypokalaemia in patients with normal pituitary function and in those with GH deficiency, either alone or in combination with other pituitary hormone deficiencies. Therefore, insulin-induced hypoglycaemia does not appear to be associated with any greater risk of hypokalaemia in hypopituitary adults with GHD compared to those with normal anterior pituitary function.
authors.affiliation: Department of Medicine, University of Wales College of Medicine, Cardiff, UK.
authors.forename: J S
authors.initials: JS
authors.lastname: Davies
authors.forename: N P
authors.initials: NP
authors.lastname: Hinds
authors.forename: E M
authors.initials: EM
authors.lastname: Millward
authors.forename: I
authors.initials: I
authors.lastname: McDowell
authors.forename: M F
authors.initials: MF
authors.lastname: Scanlon
mesh_terms: D000328:Adult; D002318:Cardiovascular Diseases / Q000209:etiology; D005260:Female; D013006:Growth Hormone / Q000097:blood / Q000172:deficiency*; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D007008:Hypokalemia / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D007018:Hypopituitarism / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D007031:Hypothalamus / Q000503:physiopathology; D007328:Insulin / Q000009:adverse effects; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010901:Pituitary Function Tests; D012307:Risk Factors; D012964:Sodium / Q000097:blood
chemical_list: D007328:Insulin; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D012964:Sodium; D006854:Hydrocortisone