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Parathyroid hyperactivity

Primary HPT

This disease is characterised by an increase in blood calcium with simultaneously increased or unsuppressed parathyroid hormone (parathormone). Diagnosis is made if this laboratory constellation is present. The next step is to investigate how far the disease has progressed (stage classification). Are kidney stones present, has the patient suffered fractures or are there concomitant diseases such as depression or elevated blood pressure? The bone density is measured. A decision as to whether surgery is indicated is then made. If this is the case, diagnosis is carried out to locate the presumed parathyroid adenoma by means of parathyroid sonography or scintigraphy. Inoperable patients with pHPT can also be treated with drug therapy using Mimpara®.

Secondary HPT

sHPT is characterised by increased parathormone and low normal or reduced serum calcium. The most frequent cause is vitamin D deficiency or renal insufficiency. PTH receptor defects are rarely found in pseudohypoparathyroidism.


This disease is caused by the surgeon during thyroid gland surgery or is congenital. It is characterised by reduced serum calcium and reduced parathormone. Clinically, spasms are presented; if left untreated, Fahr’s disease (basal ganglia calcification) can develop. Osteoporosis does not develop; the bone density is more likely to be high.

The synthetic vitamin D metabolites 1-alfacalcidol or 1,25-dihydroxycholecalciferol are the therapy of choice. This is life-long therapy. Therapy solely with calcium is obsolete.

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