title: Regression of skeletal manifestations of hyperparathyroidism with oral vitamin D.
abstract: BACKGROUND
  Parathyroidectomy is the only effective therapy for osteitis fibrosa cystica in hyperparathyroidism.
  
  
  OBJECTIVE
  The objective of this study was to describe the changes of skeletal and nonskeletal manifestations in a patient with hyperparathyroidism and renal failure after oral vitamin D therapy.
  
  
  METHODS
  This was a descriptive case report.
  
  
  METHODS
  The patient was followed up in a referral center.
  
  
  METHODS
  A 55-yr-old male patient with moderate renal failure was referred for expansile lytic lesions affecting several ribs and the spinous process of T12. His creatinine was 1.8 mg/dl; calcium, 8.9 mg/dl; PTH, 666 pg/ml; and 1,25 dihydroxy-vitamin D, 27 pg/ml. Bone mineral density (BMD) Z-scores by dual-energy x-ray absorptiometry were -4.1 at the spine, -1.7 at the hip, and -4.3 at the forearm.
  
  
  METHODS
  The main outcome measures were the skeletal manifestations of hyperparathyroidism.
  
  
  RESULTS
  At 10 months of therapy, calcium level was 10 mg/d, PTH level declined to 71 pg/ml, and BMD increased by 12% at the spine and 18% at the hip. Computerized tomography (CT) cuts revealed marked regression in the lytic lesions. At 2 yr, BMD increased by an additional 6% at the spine, and there were no further changes in the lytic lesions by CT. The vitamin D receptor genotype using the restriction enzymes Bsm1, Taq1, and Apa1 was Bb, tt, and AA.
  
  
  CONCLUSIONS
  We showed regression of severe skeletal abnormalities of hyperparathyroidism documented by serial CT images in response to oral vitamin D therapy. It is possible that the vitamin D receptor genotype of the patient modulated this response.
authors.affiliation: Calcium Metabolism and Osteoporosis Program, American University of Beirut-Medical Center, Bliss Street, Beirut, Lebanon. aa22@aub.edu.lb
authors.forename: Asma
authors.initials: A
authors.lastname: Arabi
authors.forename: Nabil
authors.initials: N
authors.lastname: Khoury
authors.forename: Laila
authors.initials: L
authors.lastname: Zahed
authors.forename: Adel
authors.initials: A
authors.lastname: Birbari
authors.forename: Ghada
authors.initials: G
authors.lastname: El-Hajj Fuleihan
mesh_terms: D015519:Bone Density; D001847:Bone Diseases / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology*; D002118:Calcium / Q000097:blood / Q000652:urine; D002762:Cholecalciferol / Q000008:administration & dosage; D005838:Genotype; D006801:Humans; D006887:Hydroxycholecalciferols / Q000008:administration & dosage; D006962:Hyperparathyroidism, Secondary / Q000150:complications / Q000188:drug therapy*; D007676:Kidney Failure, Chronic / Q000150:complications; D008297:Male; D008875:Middle Aged; D010002:Osteitis Fibrosa Cystica / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology; D010024:Osteoporosis / Q000175:diagnosis / Q000188:drug therapy / Q000209:etiology; D018167:Receptors, Calcitriol / Q000235:genetics; D013789:Thalassemia / Q000150:complications; D014057:Tomography, X-Ray Computed; D014807:Vitamin D / Q000627:therapeutic use*
chemical_list: D006887:Hydroxycholecalciferols; D018167:Receptors, Calcitriol; D014807:Vitamin D; D002762:Cholecalciferol; D002118:Calcium; C008088:alfacalcidol