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 Successful Surgery in Patients Without Osteoporosis?

Status

UNKNOWN

Phases

Phase 2

Study type

Interventional

Source

ClinicalTrials.gov

Registry ID

NCT00973336

Enrollment

Registered

2009-09-09

Start date

2009-09-30

Completion date

2017-09-30

Last updated

2016-03-16

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Primary Hyperparathyroidism, Bone Metabolism

Keywords

postoperative follow-up

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).

Interventions

DRUGCalcium and vitamin D

1000mg calcium per day 800 IE vitamin D per day

Study design

Allocation

RANDOMIZED

Intervention model

PARALLEL

Primary purpose

TREATMENT

Masking

NONE

Eligibility

Sex/Gender

ALL

Age

18 Years to No maximum

Healthy volunteers

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

Design outcomes

Primary

Measure	Time frame
Parathyroid hormone	1 year

Secondary

Measure	Time frame
BMD of lumbar spine, femoral neck and radius	1 year
Adverse effects calcium or vitamin D	1 year
Other biochemical markers of bone metabolism	1 year

Countries

Austria

Contacts

Primary ContactPhilipp Riss, MD

philipp.riss@meduniwien.ac.at+43140400

Backup ContactBruno Niederle, Professor, MD

chir-endokrin@meduniwien.ac.at+43140400

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026