A disease of the parathyroid glands leads to disturbances in the calcium balance. Because calcium is involved in many processes in the organism, for example, the excitation of muscle and nerve cells, in the construction of our bones and teeth, in blood clotting or cell division, a defect of the epithelial corpuscles causes many symptoms.
Parathyroid hyperfunction – hyperparathyroidism.
In primary or autonomic hyperparathyroidism (pHPT), a benign cell proliferation of the glandular tissue (an adenoma) is most often responsible for the hyperfunction. The tumor also produces parathyroid hormone, resulting in a greatly elevated hormone level. Usually (in 75 percent of those affected) only one epithelial cell is enlarged, occasionally there are two or more. Malignant tumors of the parathyroid glands are very rare.
Consequences
The elevated PTH level increases the calcium level in the blood (hypercalcemia). In most cases, those affected do not notice at first (= asymptomatic hyperparathyroidism); later, numerous symptoms appear. The worst affected are the kidneys: Renal colic with severe pain, kidney stones and calcium deposits develop; in addition, the kidneys function much worse. They excrete urine excessively – you feel much more thirsty.
In the late stages, it also affects the bones. Bone mass decreases (osteoporosis) and rheumatic pain in bones and joints is possible. In addition, psychological changes (for example, depression), gastrointestinal complaints (nausea, vomiting, constipation), weight loss, and cardiac arrhythmias occur. Inflammation of the pancreas and gastric or duodenal ulcers are also common.
Primary hyperparathyroidism also occurs in the very rare hereditary disease MEN syndrome (multiple endocrine neoplasia). In this disorder, other endocrine glands such as the pituitary gland or pancreatic islet cells also exhibit hyperparathyroidism.
Treatment
Most important is surgical removal of the adenoma. If multiple epithelial bodies are enlarged, all but a remnant of circa 100 miligrams are removed. Medications rebalance fluid and electrolyte balance. Calcitonin, bisphosphonate, and glucocorticoids are also administered to limit bone resorption. The general consequences of hypercalcemia usually disappear over the course of a few months. Bone damage, however, takes longer, up to two years, and some even persist permanently.
Incidentally, primary hyperparathyroidism is the third most common endocrine disorder after diabetes mellitus (diabetes) and thyroid disorders. Women are affected twice as often as men, and the peak age is between 40 and 60 years.
Secondary regulatory hyperparathyroidism
Secondary or regulatory hyperparathyroidism (sHPT) results from permanent calcium deficiency in the blood, to which the parathyroid glands respond by increasing PTH production. The reason may be chronic renal failure, in which blood phosphate levels rise while calcium levels fall. This renal secondary hyperparathyroidism occurs, for example, in patients with kidney disease in whom dialysis (blood washing) does not work properly.
In intestinal secondary hyperparathyroidism, our body fails to absorb enough calcium from food. Causes are diseases of the digestive system such as Crohn’s disease, ulcerative colitis, cholestasis, celiac disease or Whipple’s disease, which lead to hypocalcemia.
Consequences
In renal secondary hyperparathyroidism, symptoms are mainly musculoskeletal, i.e., bone and joint pain; fractures are common. In both forms, depending on the underlying disease, other symptoms usually involve the digestive tract, for example, diarrhea, bloody stools, and weight loss. Softening (osteomalacia) and decrease (osteopenia) of bone substance is also possible.
Treatment
In addition to treating the underlying disease, secondary hyperparathyroidism also involves removal of the enlarged epithelial cells. The surgeon either leaves half a parathyroid gland or, in autotransplantation, transplants about 20 pieces of the tissue, each one cubic millimeter in size, into the forearm, where they take over from the parathyroid glands.
