title: Milk-alkali syndrome is a major cause of hypercalcaemia among non-end-stage renal disease (non-ESRD) inpatients.
abstract: OBJECTIVE
  Milk-alkali syndrome, once a common cause of hypercalcaemia, is now considered rare. Our aim was to estimate the prevalence of milk-alkali syndrome among hypercalcaemic, non-end-stage renal disease (non-ESRD) inpatients of a University Hospital and identify patients' and syndrome characteristics.
  
  
  METHODS
  In this retrospective chart review study, we identified patients hospitalized with possible hypercalcaemia between November 1998 and October 2003 by a computer search of admission, discharge and consultation diagnoses. Patients with renal transplantation, stage 5 chronic kidney disease (CKD-5) and those admitted for parathyroidectomy were excluded. The remaining patients' charts were reviewed for confirmation of hypercalcaemia and identification of the cause. In patients with milk-alkali syndrome, additional historical, clinical, laboratory and imaging data were collected.
  
  
  RESULTS
  We identified 125 patients with hypercalcaemia, 11 (8.8%) of whom had milk-alkali syndrome, 42 (33.6%) had malignancy and 37 (29.6%) hyperparathyroidism. Thirty-five patients had severe hypercalcaemia, defined as corrected serum calcium 3.5 mmol/l. Malignancy accounted for 13 of those patients (37.1%) and milk-alkali for nine (25.7%). Conditions prevalent among the milk-alkali inpatients were female gender, hypertension, chronic kidney disease, osteoporosis, upper gastrointestinal diseases, diuretic treatment and vitamin D derivative supplementation. Five of the patients with milk-alkali syndrome were treated with bisphosphonates and all five developed hypocalcaemia, compared to one of the five who received conventional treatment (P = 0.047).
  
  
  CONCLUSIONS
  Milk-alkali was the third leading cause of hypercalcaemia of any degree and the second cause of severe hypercalcaemia among inpatients without ESRD. In milk-alkali syndrome, treatment with bisphosphonates contributes to post-treatment hypocalcaemia.
authors.affiliation: The University of Texas-Houston Medical School, Division of Endocrinology Diabetes and Metabolism, Houston, 77030, USA. picolosnm@hotmail.com
authors.forename: Michalis K
authors.initials: MK
authors.lastname: Picolos
authors.forename: Victor R
authors.initials: VR
authors.lastname: Lavis
authors.forename: Philip R
authors.initials: PR
authors.lastname: Orlander
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002119:Calcium Carbonate / Q000009:adverse effects; D004164:Diphosphonates / Q000009:adverse effects / Q000627:therapeutic use; D004232:Diuretics / Q000627:therapeutic use; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000097:blood / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology*; D007674:Kidney Diseases / Q000097:blood / Q000150:complications* / Q000188:drug therapy; D008274:Magnesium / Q000097:blood; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood; D012189:Retrospective Studies; D017678:Sex Distribution; D017693:Sodium Bicarbonate / Q000009:adverse effects
chemical_list: D004164:Diphosphonates; D004232:Diuretics; D017693:Sodium Bicarbonate; D002119:Calcium Carbonate; D008274:Magnesium; D011188:Potassium