Primary Hyperparathyroidism: Does a Systematic Treatment Improve the Calcium and Bone Metabolism After Surgery?
Primary Hyperparathyroidism: Does a Systematic Treatment Improve the Calcium and Bone Metabolism After Surgery?
Primary Hyperparathyroidism (pHPT) increases bone turnover and resorption and thus calcium
 efflux out of bone. After successful surgical treatment of pHPT, bone takes up calcium again
 which may result in secondary hyperparathyroidism or even "hungry bone syndrome". Until today
 there are no studies about this problem helping to develop recommendations or guidelines how
 to prevent these symptoms.

 Study hypothesis: Calcium and vitamin D intake after surgery for PHPT protects the bone by
 keeping PTH in the normal range (less secondary, reactive hyperparathyroidism), prevents
 hungry bone- syndrome and improve bone-turnover markers (osteoporosis protection).
Inclusion Criteria:

 -  Postmenopausal women

 -  Male patients

 -  Biochemically proven PHPT, PTX planned

 -  No evidence for osteoporosis

 Exclusion Criteria:

 -  Postoperative hypocalcemia needing substitution with calcium and vitamin D/
 1-25-OH-Vitamin D

 -  Cancer (lung, breast, prostatic, parathyroid cancer and thyroid carcinoma >1cm)

 -  Persisting or recurrent PHPT (postoperative hypercalcemia)

 -  Four-gland hyperplasia

 -  Multiple endocrine neoplasia (MEN) or hereditary PHPT

 -  Familial hypercalciuric hypercalcaemia (Ca/creatinine ratio < 0.01)

 -  Phenylketonuria

 -  Renal impairment (creatinine clearance <30ml/h)

 -  Severe hepatic disorder

 -  Severe systemic disorder

 -  Thyroid dysfunction

 -  Immobilisation

 -  Intake of drugs with potential effects on BMD like glucocorticoids, lithium,
 estrogen-replacement therapy, selective Estrogen-receptor modulators (sERMs),
 bisphosphonates in the last three months

 -  Intake of drugs containing digoxin or digitoxin

 -  Known allergy against any component of the study medication