What is hyperparathyroidism?
Hyperparathyroidism is the medical term for overactivity of the parathyroid gland, the four small glands located on the posterior surface of the thyroid gland. Since the parathyroid gland regulates the calcium and phosphate in the body, any abnormal functioning will ultimately impact on these levels of these minerals. In hyperparathyroidism, an excess of parathyroid hormone (PTH) will disrupt the normal levels of calcium and phosphate in the blood, break down bones in the chronic setting and affect intestinal absorption and kidney reabsorption of calcium and phosphate.
Types of Hyperparathyroidism
There are three types of hyperparathyroidism :
- Primary hyperparathyroidism where a mass on parathyroid gland leads to excessive secretion of parathyroid hormone.
- Secondary hyperparathyroidism where the increase in parathyroid hormone secretion is due to declining calcium levels in the blood as a result of some other disease process.
- Tertiary hyperparathyroidism where chronic stimulation of the parathyroid gland, usually by low calcium levels, leads to the formation of a mass which then secretes excessive amounts of PTH. Essentially, tertiary hyperparathyroidism is a primary hyperparathyroidism that arises from secondary hyperparathyroidism.
Causes of an Overactive Parathyroid Gland
Primary hyperparathyroidism is mainly due to a mass on the parathyroid gland. In most cases, this is a benign mass like an adenoma, usually solitary (single) although multiple adenomas are also possible. A single parathyroid adenoma accounts for 90% of the cases of primary hyperparathyroidism. Less commonly, there may be enlargement of the gland due to an increase in the number of cells (hyperplasia), which may be nodular (affecting isolate spots on the gland) or diffuse (affecting the entire gland). The least common cause of primary hyperparathyroidism is parathyroid carcinoma (cancer) which accounts for about 1% of all cases.
Secondary hyperparathyroidism is a consequence of some other disease process that leads to low calcium levels. The most common cause is renal failure, where the body loses calcium in the urine due to the compromised reabsorption process. Other possible causes include malnutrition with a low dietary intake of calcium, malabsorption syndromes and a vitamin D deficiency. High phosphate levels in the blood, associated with chronic renal failure or high dietary intake, may lower calcium levels thereby causing secondary hyperparathyroidism. With the use of drugs like thiazide diuretics, the body may lose calcium which leads to tertiary hyperparathyroidism.
How does hyperparathyroidism occur?
Calcium in the extracellular fluid (blood and tissue spaces) is the main regulator of parathyroid hormone (PTH) secretion. The feedback mechanism that regulates PTH secretion means that high levels of calcium will reduce PTH secretion while low levels of calcium increases PTH secretion.
With primary hyperparathyroidism, the exact cause of an adenoma formation is not known. It appears to be sporadic although certain familial syndromes may indicate a genetic predisposition in a minority of cases. The excess tissue contributes to additional secretion of PTH, above the norm, and the normal regulation by the calcium levels in the blood is lost. PTH is secreted in excess in an uncontrolled manner and causes a rise in calcium levels within the blood and interstitial fluid. The slow phase of PTH secretion also causes the break down of bone and loss of phosphate in the urine.
In secondary hyperparathyroidism, the diseases discussed under causes of hyperparathyroidism contributes to low levels of extracellular calcium. This stimulates the parathyroid gland and PTH is secreted in higher than normal amounts. Overactivity of the parathyroid gland may also cause hypertrophy of the gland as it has to compensate with a greater synthesis and secretion of PTH. Although calcium may not be lost in all the causative diseases, a rise in phosphate can depress calcium levels in the blood which increases PTH secretion. Despite the overactivity of the parathyroid gland, the serum calcium levels usually remains low or close to normal and PTH levels in the blood are high.
Signs and Symptoms of an Overactive Parathyroid Gland
The clinical presentation of primary and secondary hyperparathyroidism may vary due to the differences in pathophysiology.
The clinical presentation of primary hyperparathyroidism is best described as “bones, groans, stones and moans”.
- The effect of high PTH levels on the bones leads to weakening of the bones that easily fracture (osteoporosis), bone and joint pain.
- Abdominal pain often associated with other gastrointestinal disturbances like nausea, vomiting and loss of appetite may also be present.
- There is a predisposition to develop kidney stones due to the high blood calcium levels and higher than normal levels of calcium in the urine (hypercalciuria) and excessive urination (polyuria).
- Patients may also report fatigue, lethargy, depression, inability to concentrate and memory problems.
Since secondary hyperparathyroidism arises moe often in the backdrop of kidney failure without elevated blood calcium levels, the clinical presentation may not always be as obvious for overactvity of the parathyroid gland. Instead the signs and symptoms of renal failure may dominate the clinical picture. There may be some bone pain and a history of bone weakness which is easily fractured. Another less frequently seen feature of secondary hyperparathyroidism is calcification of blood vessels which can lead to ischemic damage to various organs, including the skin.