How does hyperparathyroidism cause osteoporosis

KNOWLEDGE- Parathyroid glands

Reactive hyperparathyroidism (rHPT)

The secondary "reactive" hyperparathyroidism occurs as a complication of chronic kidney diseases (severe renal insufficiency, dialysis patients) and long-term bone involvement (= osteomalacia), as a result of long-term hypocalcemia and a compensatory reaction of the parathyroid glands.

This form of secondary hyperparathyroidism predominantly affects patients on chronic hemo- or peritoneal dialysis treatment. It can also only become manifest after a kidney transplant has been carried out.

Depending on the length of time, the greater number of all dialysis patients develop clinically meaningful secondary hyperparathyroidism during treatment. Usually it can be successfully controlled with calcium intake, vitamin D metabolites and a low-phosphate diet. About 5% of all those affected require surgical treatment. Corresponding to the reactive disease, there is always a four-gland involvement with occasionally very different degrees of hyperplasia of the parathyroid glands.

Symptoms

The clinical effects of secondary hyperparathyroidism are manifested in the form of renal osteopathy. It manifests itself primarily through bone pain in various localizations. The deposition of calcium phosphate can lead to extraosseous calcifications in soft tissues, especially in the periarticular tissue, and to increased vascular calcifications. An excruciating itching can be particularly detrimental as a result of calcium phosphate deposits in the skin. At an advanced stage, generalized myopathy can lead to severe mobility impairment.

diagnosis

The tests initially cover the same values ​​as for the primary disease: serum calcium, serum phosphate and parathyroid hormone in the serum. As a rule, there is initially more of a normocalcemia and, as a result of the elimination obstruction, a hyperphosphataemia. Also because of impaired degradation and excretion, an increase in parathyroid hormone in the serum is more common in patients with renal insufficiency. However, if it is more than 10 times the norm, the disease is already severe. In the late stage, hypercalcemia develops with increasing parathyroid hyperplasia and loss of conservative therapeutic effectiveness. The increase in alkaline phosphatase provides an important indication of the destructive bone process. X-rays of the hands show typical subperiosteal resorption zones on the radial sides of the middle phalanges and acroosteolysis. Similar or similar remodeling processes become visible in symptomatic sections of the skeleton and can develop into spontaneous fractures.

The indication for surgery is determined by the subjective and unaffected complaints of bone pain and pruritus, in the presence of spontaneous fractures, severe renal osteopathy proven by bone biopsy or finally by the onset of hypercalcaemia.

therapy

After all medication measures have been exhausted (calcium, vitamin D, calcimimetic - cinacalcet), the operation represents a further treatment option. The following surgical treatment options are available:

  • The subtotal parathyroidectomy with resection of 3 1/2 hyperplastic parathyroid glands and preservation of a partial remnant of at least normal gland size in regular location.
  • Total parathyroidectomy, i.e. complete removal and simultaneous autotransplantation of 20 pieces of parathyroid gland 1x1x3 mm in size into the muscles of a forearm.

To remove "surplus" glands, the fatty tissue behind the breastbone is also removed during each operation (= transcervical thymectomy)

During each operation, parathyroid tissue is frozen using a special procedure (cryopreservation) so that if the remnant of the parathyroid gland or the transplant is underactive, the patient can transplant his or her own parathyroid tissue back (delayed parathyroid autotransplantation).

The first method is based on the assumption that the function of the small remnant of the parathyroid gland remaining in its regular position can be controlled again therapeutically under continued dialysis and that normal regulation begins in any case after the desired and successful kidney transplantation.

The more radical procedure with autotransplantation takes into account the fundamental risk of recurrence and would like to exclude the need for a new neck operation.

The recurrent hyperplasia in the transplant on the forearm can be reduced easily accessible under local anesthesia.

After the operation - regardless of the technique - a sufficiently high calcium and vitamin D supplementation is required, on the one hand until the residual gland or transplant functions reliably and on the other hand because of the severe onset of bone remineralization.