Hyperparathyroidism • How to recognize the disorder

Author: Dr. Wiebke Kathmann, medical writer
Last updated: June 02, 2021

Hyperparathyroidism is an overactive parathyroid gland. They can be recognized by symptoms such as loss of appetite, weight loss, or constipation. Clarity can be achieved with blood values.

Sudden weight loss can be an indication of an overactive parathyroid gland.
© iStock.com/Rostislav_Sedlacek

A regulatory disorder of the parathyroid glands is called hyperparathyroidism (HPT) or overactive parathyroid glands. The parathyroid glands are four peppercorn-sized hormone-producing glands. In hyperparathyroidism, they produce too much parathyroid hormone, which upsets the calcium balance.

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Symptoms of hyperparathyroidism

In most cases of hyperparathyroidism, a routine blood test will show changes in blood values ​​before symptoms appear.

If the parathyroid gland is mildly overactive, the following symptoms may occur:

If the hyperparathyroidism persists for a long time, bone mass is broken down (osteoporosis), as the parathyroid hormone activates the bone-breaking cells, so that more calcium is released from the bones. Kidney stones can also occur because large amounts of calcium are excreted in the urine. The increased calcium and phosphate concentrations in the blood can also lead to calcification of muscles and blood vessels.

Causes of Hyperparathyroidism

Depending on the cause, one speaks of primary, secondary or tertiary hyperparathyroidism. The primary and tertiary levels are associated with an increase in parathyroid hormone and serum calcium levels. In secondary hyperparathyroidism, only the parathyroid hormone level is increased.

Primary hyperparathyroidism

Primary hyperparathyroidism with increased parathyroid hormone and calcium levels in the blood serum is usually a benign, hormone-producing adenoma of the parathyroid gland. The normal tissue of the parathyroid gland has sensors for the level of calcium in the blood. Parathyroid hormone is only released when they have fallen below the very tightly set target value. It is different with adenoma, here the parathyroid hormone production is no longer based on demand, but takes place continuously. Weak primary hyperparathyroidism can also have genetic causes.

Secondary hyperparathyroidism

In secondary hyperparathyroidism with increased parathyroid hormone but decreased serum calcium levels, a vitamin D deficiency is the cause. This is mostly due to a kidney malfunction.

Tertiary hyperparathyroidism

Tertiary hyperparathyroidism, which is associated with increased parathyroid hormone and serum calcium levels, is caused by a long-standing secondary hyperparathyroidism.

Medicines as further causes

Finally, the overactive parathyroid gland can be caused by medication. For example, the lithium used in the treatment of patients with psychiatric illnesses such as mania or thiazide diuretics prescribed for high blood pressure.

Medical diagnosis of hyperparathyroidism

The diagnosis of an overactive parathyroid gland is primarily made through the detection of an increased level of parathyroid hormone and calcium in the blood. By examining kidney function and vitamin D metabolites, a distinction can be made between primary and secondary hyperparathyroidism. The medical history allows a distinction between primary and tertiary HPT.

In children and adolescents, adenomas are often the cause of primary HPT, which is why an ultrasound examination of the neck and chest area is carried out. Sometimes computed tomography (CT) or MRI may also be needed.

This is how hyperparathyroidism is treated

The treatment of primary hyperparathyroidism consists of an operation (parathyroidectomy) in which the adenoma or the parathyroid glands are removed. If the serum calcium values ​​are only slightly elevated, the blood values ​​for parathyroid hormone and calcium as well as the bone density can be checked regularly.

For patients who cannot or do not want to have an operation, medications that must be taken for life are possible:

  • Drugs that inhibit bone loss, such as bisphosphonates or selective estrogen receptor modulators, which exert an estrogen-like effect on the bones

  • Calcimimetics that bind to the calcium sensing receptor and thus give the signal that the calcium concentration is already high enough. This inhibits the synthesis of parathyroid hormone.

In any case, the patient should be on a low-calcium and vitamin D-rich diet.

Treatment of secondary and tertiary hyperparathyroidism

Secondary hyperparathyroidism is treated by treating the underlying disease, usually chronic kidney disease. The main aim here is to lower the phosphate level with phosphate-binding drugs, so-called phosphate binders, and to supply vitamin D. If this does not lead to success, a therapy attempt with a calcimimetic can be undertaken. Those affected should pay attention to a low-phosphate diet and therefore eat as little meat as possible.

In tertiary hyperparathyroidism, which is caused by a long-lasting secondary hyperparathyroidism and has led to years of overstimulation of the parathyroid glands, the epithelial bodies (parathyroid glands) are surgically removed (parathyroidectomy) and part of an epithelial body is implanted in a muscle can be formed. Alternatively, only part of the epithelial cells can be removed (subtotal parathyroidectomy).

Secondary overactive parathyroid glands can be prevented

Prevention is only possible with secondary hyperparathyroidism or so-called renal osteopathy.

Due to the causal connection with the kidney function, the careful increase of the lowered serum calcium, the lowering of the increased serum phosphate as well as the compensation of the vitamin D deficiency are possible to prevent an overactive parathyroid gland. Care should be taken to ensure that the calcium phosphate product is below 55 mg2/ dl2 remains so that there is no calcium deposits outside the bone.

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