title: Pamidronate administration improves the secondary hyperparathyroidism due to "Bone Hunger Syndrome" in a patient with osteoblastic metastases from prostate cancer.
abstract: BACKGROUND
  The so-called Bone Hunger Syndrome is a metabolic derangement that sometimes complicates the natural history of prostate cancer patients with osteoblastic bone metastases. An excessive bone formation leads to calcium entrapment in bone and the subsequent increase of parathyroid hormone (PTH) levels, in response to calcium demand. PTH elevation stimulates the osteoclasts in sites distant from those involving the tumor, leading to osteomalacia.
  
  
  METHODS
  PTH and markers of bone turnover were monitored every 3 weeks, from the start of pamidronate treatment in a prostate cancer patient with progressive disease, to luteinizing hormone releasing hormone analog (LHRH-A) administration, developing hyperparathyroidism, hypophosphatemia, and albumin corrected serum calcium close to the lower limit of normality. Serum bone alkaline phosphatase (BALP), assessed by two different methods: electrophoretic and immunoradiometric, and urinary levels of markers of bone collagen breakdown were also remarkably elevated.
  
  
  RESULTS
  As a consequence of pamidronate infusion (60 mg e.v. every 3 weeks for a total of four times), BALP and PTH decreased consistently, serum calcium and phosphorus returned within the normal range, while markers of collagen resorption showed a significant decrease at the 9th week, preceded by a transient rise.
  
  
  CONCLUSIONS
  This case report indicates that bisphosphonates could inhibit both osteoclast activity. The anti-osteoblastic effect is mainly responsible for the improvement of the pretreatment calcium imbalance of our patient towards hypocalcemia and the consequent hyperparathyroidism.
authors.affiliation: Universitá di Torino, Clinica Medica, Oncologia Medica, Azienda Ospedaliera San Luigi, Orbassano-Torino, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Berruti
authors.forename: P
authors.initials: P
authors.lastname: Sperone
authors.forename: G
authors.initials: G
authors.lastname: Fasolis
authors.forename: M
authors.initials: M
authors.lastname: Torta
authors.forename: D
authors.initials: D
authors.lastname: Fontana
authors.forename: L
authors.initials: L
authors.lastname: Dogliotti
authors.forename: A
authors.initials: A
authors.lastname: Angeli
mesh_terms: D000368:Aged; D000469:Alkaline Phosphatase / Q000032:analysis / Q000097:blood; D001859:Bone Neoplasms / Q000150:complications / Q000503:physiopathology / Q000556:secondary*; D001842:Bone and Bones / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D002118:Calcium / Q000032:analysis / Q000097:blood / Q000378:metabolism; D003094:Collagen / Q000378:metabolism / Q000652:urine; D004164:Diphosphonates / Q000008:administration & dosage / Q000627:therapeutic use*; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000175:diagnosis / Q000188:drug therapy* / Q000209:etiology*; D008297:Male; D008659:Metabolic Diseases / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D018215:Osteoblastoma / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D010147:Pain Measurement; D000077268:Pamidronate; D010281:Parathyroid Hormone / Q000097:blood / Q000378:metabolism; D010758:Phosphorus / Q000097:blood; D017430:Prostate-Specific Antigen / Q000097:blood; D011471:Prostatic Neoplasms / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D013577:Syndrome
chemical_list: D004164:Diphosphonates; D010281:Parathyroid Hormone; D010758:Phosphorus; D003094:Collagen; D000469:Alkaline Phosphatase; D017430:Prostate-Specific Antigen; D000077268:Pamidronate; D002118:Calcium