Parathyroid glands - hyperfunction

A disease of the parathyroid glands leads to disturbances in the calcium balance. Because calcium is involved in many processes in the organism, such as the excitation of muscle and nerve cells, in the build-up of our bones and teeth, in blood clotting or cell division, a defect in the epithelial bodies causes many symptoms.

Parathyroid hyperfunction - hyperparathyroidism

In primary or autonomic hyperparathyroidism (pHPT), benign cell proliferation of the glandular tissue (an adenoma) is most often responsible for hyperfunction. The tumor also produces parathyroid hormone, resulting in a greatly increased hormone level. Most (in 75 percent of those affected) only one epithelial body is enlarged, occasionally there are two or more. Malignant tumors of the parathyroid glands are very rare.


Increased PTH levels increase the calcium content in the blood (hypercalcaemia). Most of the victims do not notice at first (asymptomatic hyperparathyroidism); later, numerous symptoms occur. The kidneys are the worst affected: It causes renal colic with severe pain, kidney stones and calcification, in addition, the kidneys work much worse. You excrete excess urine - you are much more thirsty.

In the late stages, it also hits the bones. The bone mass decreases (osteoporosis) and rheumatic pain in bones and joints are possible. In addition, there are psychological changes (for example, depression), gastrointestinal complaints (nausea, vomiting, constipation), weight loss and cardiac arrhythmias. Also common are inflammations of the pancreas and gastric or duodenal ulcers.

Primary hyperparathyroidism also occurs in the very rare hereditary disease MEN syndrome (multiple endocrine neoplasia). In this disease, other endocrine glands such as the pituitary gland or islet cells of the pancreas have an overfunction.


Most important is the surgical removal of the adenoma. If several epithelial bodies are enlarged, all are removed except for a remainder of about 100 milligrams. Medications bring the fluid and electrolyte balance back into balance. In order to limit the degradation of the bones, calcitonin, bisphosphonate and glucocorticoids are additionally administered. The general consequences of hypercalcemia then usually develop over a few months. However, the bone damage takes longer, up to two years, some even persist permanently.

Incidentally, primary hyperparathyroidism is the third most common endocrine disorder after diabetes mellitus and thyroid disorders. Women are twice as likely to be affected as men, the peak age is between 40 and 60 years.

Secondary hyperparathyroidism

Secondary or regulative hyperparathyroidism (sHPT) is caused by permanent calcium deficiency in the blood, to which the parathyroid glands react by increased PTH production. This may be due to chronic renal failure, in which blood phosphate levels rise while the calcium level decreases. This renal secondary hyperparathyroidism, for example, occurs in patients with kidney disease in whom dialysis (blood washing) does not work properly.

Intestinal secondary hyperparathyroidism does not allow our body to absorb enough calcium from food. Causes include diseases of the digestive system such as Crohn's disease, ulcerative colitis, cholestasis, celiac disease or Whipple's disease, which lead to hypocalcemia.


In renal secondary hyperparathyroidism mainly complaints of the musculoskeletal system occur, ie bone and joint pain, it often leads to bone fractures. In both forms more symptoms depending on the underlying disease usually affect the digestive tract, for example, diarrhea, bloody stool and weight loss. In addition, a softening (osteomalacia) and decrease (osteopenia) of the bone substance is possible.


In addition to the treatment of the underlying disease in secondary hyperparathyroidism also enlarged epithelial bodies are removed. The surgeon either leaves half a parathyroid gland or grafts about 20 cubic millimeters of the tissue into the forearm during an autograft, where they take on the role of the parathyroid glands.

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