Primary Hyperparathyroidism: Does a Systematic Treatment Improve the Calcium and Bone Metabolism After Surgery?

NCT ID: NCT00973336

Last Updated: 2016-03-16

Basic Information

• Recruitment Status: UNKNOWN
• Clinical Phase: PHASE2
• Total Enrollment: 80 participants
• Study Classification: INTERVENTIONAL
• Study Start Date: 2009-09-30
• Study Completion Date: 2017-09-30

Brief Summary

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).

Conditions

Primary Hyperparathyroidism; Bone Metabolism

Study Design

• Allocation Method: RANDOMIZED
• Intervention Model: PARALLEL
• Primary Study Purpose: TREATMENT
• Blinding Strategy: NONE

Study Groups

Calcium and vitamin D

Intervention

Group Type: EXPERIMENTAL

Calcium and vitamin D

Intervention Type: DRUG

1000mg calcium per day 800 IE vitamin D per day

No treatment (control)

Group Type: NO_INTERVENTION

No interventions assigned to this group

Interventions

Calcium and vitamin D

1000mg calcium per day 800 IE vitamin D per day

Intervention Type: DRUG

Eligibility Criteria

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

• Minimum Eligible Age: 18 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: No

Sponsors

Medical University of Vienna

OTHER

Sponsor Role: lead

Responsible Party

Philipp Riss

Assistent Professor

Responsibility Role: PRINCIPAL_INVESTIGATOR

Principal Investigators

Bruno Niederle, Prof., MD

Role: PRINCIPAL_INVESTIGATOR

Medical University of Vienna, Department of Surgery

Locations

Medical University of Vienna

Vienna, , Austria

Site Status: RECRUITING

Countries

Austria

Central Contacts

Philipp Riss, MD

Role: CONTACT

philipp.riss@meduniwien.ac.at

+43140400 ext. 5621

Bruno Niederle, Professor, MD

Role: CONTACT

chir-endokrin@meduniwien.ac.at

+43140400 ext. 6943

Facility Contacts

Philipp Riss, MD

Role: primary

philipp.riss@meduniwien.ac.at

+43140400 ext. 5621

Other Identifiers

PHPT02_2008

Identifier Type: -

Identifier Source: org_study_id