Hyperparathyroidism (HPT) – colloquially called parathyroid hyperfunction – (synonyms: Hyperparathyroidism; HPT; parathyroid hormone excess; parathyroid hormone overproduction; reactive hyperparathyroidism; ICD-10-GM E21.-: Hyperparathyroidism and other parathyroid diseases) describes inadequately high production and secretion (secretion) of the neurotransmitter parathyroid hormone (PTH) from one or more parathyroid glands. In most people, the parathyroid glands (lat. : Glandulae parathyroideae) consist of four organs about the size of a lentil and are located in the neck behind the thyroid gland (lat. Glandula thyreoidea or Glandula thyroidea), below the larynx (larynx). They are also called epithelial corpuscles. Parathyroid hormone is particularly important in the context of calcium metabolism. If the serum calcium level is too low, the parathyroid hormone causes osteoclasts (cells that break down bone) to be activated, thereby mobilizing calcium and phosphate from the bone. Bones are the main storehouse for the mineral calcium. In the presence of vitamin D, parathyroid hormone increases calcium absorption (calcium uptake) in the small intestine and calcium reabsorption (calcium reuptake) in the kidney. These processes increase the serum calcium level (hypercalcemia (calcium excess)). Another effect of parathyroid hormone is stimulation of phosphate excretion in the kidney. Consequently, the serum phosphate concentration decreases (hypophosphatemia (phosphate deficiency)). The physiological antagonist (opponent) of parathyroid hormone is calcitonin, which is produced in the C cells of the thyroid gland. The following forms of hyperparathyroidism are distinguished:
- Primary hyperparathyroidism (pHPT; ICD-10-GM E21.0) – primary disease of the parathyroid glands with increased production of parathyroid hormone and resulting hypercalcemia (calcium excess).
- Secondary hyperparathyroidism, not elsewhere classified (sHPT; ICD-10-GM E21.1); the cause is external to the parathyroid glands and stimulates them to produce more parathyroid hormone
- Renal secondary hyperparathyroidism – underlying renal dysfunction (chronic renal insufficiency (kidney weakness))
- Secondary hyperparathyroidism – with normal renal function.
- Other hyperparathyroidism: tertiary hyperparathyroidism (tHPT; ICD-10-GM E21.2) – develops from long-standing secondary hyperparathyroidism when autonomy of the originally reactive hyperplastic epithelial bodies has occurred
- Hyperparathyroidism, unspecified (ICD-10-GM E21.3 )
Primary hyperparathyroidism is:
- After osteoporosis (bone loss), the most common metabolic disease of the bone,
- After goiter (thyroid enlargement) and diabetes mellitus, the third most common endocrinological disease,
- After tumor-associated hypercalcemia (calcium excess) the most common cause of hypercalcemia (calcium excess).
Triggered primary hyperparathyroidism in the majority of cases by an adenoma (benign tumor). Furthermore, hyperplasia (enlargement) of one or more parathyroid glands (epithelial bodies) can be the cause. Secondary hyperparathyroidism is:
- One of the most common consequences of long-term dialysis treatment required due to renal insufficiency. The longer dialysis continues, the greater the likelihood of developing secondary hyperparathyroidism.
Tertiary hyperparathyroidism describes hypercalcemia (calcium excess) that develops during the course of secondary hyperparathyroidism that has been present for a long time (years/decades). The regulation of secretion of parathyroid hormone by the level of serum calcium is absent. The parathyroid glands autonomously (independently) produce parathyroid hormone. Sex ratio – primary hyperparathyroidism: males to females is 1: 2-3. Frequency peak: the maximum incidence of primary hyperparathyroidism is after the age of 50. The prevalence (disease frequency) for primary hyperparathyroidism is 0.3% (in Germany). The incidence (frequency of new cases) for primary hyperparathyroidism is approximately 1 case per 500-1,000 inhabitants per year (in Germany).Course and prognosis: Hyperparathyroidism leads to increased bone resorption and thus to hypercalcemia (calcium excess). In most cases, the disease is diagnosed incidentally during a routine blood test. The disease is treated, depending on its form, cause and symptoms, by taking medication and/or surgery. Primary hyperparathyroidism is curable if the enlarged epithelial cells are surgically removed in a timely manner. Any organ symptoms that may exist regress after successful parathyroidectomy (removal of pathologically (abnormally) altered parathyroid glands). Bone density also increases again. The course and prognosis of secondary hyperparathyroidism depend on the underlying disease. If chronic renal insufficiency is present, cardiovascular morbidity (incidence of disease) and mortality (number of deaths in a given period, relative to the number in the population concerned) are increased. Therapy for tertiary hyperparathyroidism, analogous to the primary form, is parathyroidectomy.
