Hyperparathyroidism is a condition that occurs as a result of the parathyroid glands secreting too much parathormone. When the parathormone level in the blood increases, the blood calcium level also increases with the effect of the parathormone. Increased blood calcium level can cause serious life-threatening conditions.

What is hyperparathyroidism?

Hyperparathyroidism is a condition that occurs as a result of the parathyroid glands secreting too much parathormone. When the parathormone level in the blood increases, the blood calcium level also increases with the effect of the parathormone. Increased blood calcium level can cause serious life-threatening conditions.

The average parathormone level ranges from 10 to 65 pg/ml. If a person’s parathormone level rises above this range, it can be said to be hyperparathyroidism.

In patients with hyperparathyroidism, symptoms of depression, frequent tiredness, excessive desire to drink water, frequent urination, feeling sick and weak, muscle weakness, frequent constipation, abdominal pain, confusion and loss of concentration can be seen. If hyperparathyroidism progresses, symptoms of hypercalcemia may be added to the picture. In this case, symptoms such as vomiting, dehydration, muscle spasms, confusion, bone and joint pain, arrhythmia and hypertension can be seen.



In chronic conditions of hyperparathyroidism, conditions such as osteoporosis, kidney stones, stomach ulcers and pancreatitis may also develop in patients with the effect of hypercalcemia. In more advanced or rapidly developing cases, life-threatening conditions such as kidney failure, loss of consciousness or coma may occur.

Hyperparathyroidism can develop in 3 ways:

  • Primary hyperparathyroidism; Caused by the parathyroid gland itself
  • Secondary hyperparathyroidism; It is an increase in parathormone levels as a result of decreased blood calcium levels due to other diseases in the body while the parathyroid glands are normal.
  • Tertiary hyperparathyroidism; Secondary hyperparathyroidism behaves like primary hyperparathyroidism due to conditions that develop after a long time. It is often associated with kidney failure.

Primary hyperparathyroidism

The parathyroid glands are four small endocrine organs in the neck, behind the thyroid glands. These glands secrete parathormone. Parathormone is the most important hormone in maintaining the balance of calcium, vitamin D and phosphorus in the body.



Primary hyperparathyroidism is an increase in the rate of spontaneous parathormone secretion by the parathyroid glands for different reasons. This irregularity can be detected by measuring the blood calcium level.

The average parathormone level ranges from 10 to 65 pg/ml. If a person’s parathormone level rises above this range, it can be said to be hyperparathyroidism.

The most common causes of primary hyperparathyroidism are:

  • Parathyroid gland adenomas
  • Parathyroid hyperplasia
  • Parathyroid carcinoma
  • Multiple adenomas

There are three cell types in the parathyroid glands: chief cells, clear cells, and oxyphil cells. Parathyroid gland adenomas are mostly adenomas formed by chief cells. Adenoma is the state of the tissue growing to the size it should not be and changing its histological structure. They usually occur randomly and in one piece.

Parathyroid hyperplasia is a condition in which growths or abnormalities are seen in all four organ parts. Sometimes, only one part of the growth can be seen.



Parathyroid carcinoma is rare but presents with severe hypercalcemia and palpable neck mass. Parathyroid gland cancers can be limited to the parathyroid glands only, or they can be detected as metastases to the liver, lungs or distant sites.

Primary hyperparathyroidism may occur due to benign parathyroid tumors, which are frequently seen in the group of autosomal dominant endocrine diseases called Multiple Endocrine Neoplasia.

Primary hyperparathyroidism is caused by diseases of such parathyroid gland itself. In primary hyperparathyroidism, the blood parathormone level increases and indirectly the blood calcium level also increases.

Primary parathyroidism may sometimes not cause clinical symptoms in patients. Sometimes it can only be found in laboratory tests. Sometimes it can be detected during the investigation of kidney stones. Symptoms of hypercalcemia resulting from hyperparathyroidism may occur. These patients often have kidney stones and bone destruction called osteopenia. In fact, common infections or kidney failure are added to calcium phostat or calcium oxalate kidney stones.

In advanced diseases, increased bone loss due to increased parathormone level, osteoporosis and easily broken bones can be encountered.

Most patients with primary hyperparathyroidism have no symptoms. Therefore, these patients should be followed up regularly. Rarely, musculoskeletal disorders that require surgery may also be seen in these patients. Some patients may experience weakness, fatigue, weight loss, anemia, loss of appetite or itching. In some patients, in advanced cases, depression, impaired concentration, memory disorders, neuropathy in peripheral nerves and muscle weakness may also be seen. In addition, some patients may experience symptoms such as eye keratopathy, cardiac arrhythmia or hypertension, excessive urination, excessive drinking, bone pain, gout, ulcers, pancreatitis, constipation, nausea or vomiting.



The diagnosis of primary hyperparathyroidism can be made by simultaneous study of blood calcium and parathormone levels.

Secondary hyperparathyroidism

The parathyroid glands are four small endocrine organs in the neck, behind the thyroid glands. These glands secrete parathormone. Parathormone is the most important hormone in maintaining the balance of calcium, vitamin D and phosphorus in the body.

The average parathormone level ranges from 10 to 65 pg/ml. If a person’s parathormone level rises above this range, it can be said to be hyperparathyroidism.

Secondary hyperparathyroidism is a condition characterized by widespread enlargement of the parathyroid glands and an increase in blood parathormone levels due to any disorder or disease other than the parathyroid gland. Severe calcium and vitamin D deficiency states, decreased production of vitamin D, decreased intestinal calcium absorption, resistance to parathormone in the bones, and increased renal phosphate excretion can be seen.

Blood calcium levels may be normal or lower in patients with secondary hyperparathyroidism. In patients with normal kidney function, blood phosphate levels are also low. Despite the increase in the level of parathormone in the blood, the lack of this effect on the bones and even the destruction of the bones can be seen due to chronic deficiency of vitamin D and calcium. For these reasons, calcium excretion from the kidneys is very low in these patients.

Normocalcemic hyperparathyroidism

The parathyroid glands are four small endocrine organs located in the neck, behind the thyroid glands. Parathyroid glands secrete parathormone. Parathormone maintains the balance by keeping the calcium level in the blood within a very narrow range. When the level of calcium in the blood drops, the secretion of parathormone increases, raising the blood calcium. When the blood calcium level rises, the parathormone level in the blood drops quickly.

In some patients, although the calcium level in the blood is high, parathormone levels may not decrease. This condition is called normocalcemic hyperparathyroidism. There are two types of normocalcemic hyperparathyroidism:

  • Normocalcemic primary hyperparathyroidism
  • Normocalcemic secondary hyperparathyroidism

Normocalcemic primary hyperparathyroidism

Elevated parathormone levels in these patients appear to be the result of autonomic hypersecretion of one or more parathyroid glands, with serum calcium measured at least twice over a six-month period, and consistently within the normal range. Most of these patients go undiagnosed for years because their blood calcium levels are normal or higher than normal, although parathormone levels are above normal. Before the diagnosis of normocalcemic primary hyperparathyroidism, secondary causes should be investigated in detail.



Normocalcemic primary hyperparathyroidism may result from any adenoma or hyperplasia of the parathyroid glands.

Normocalcemic primary hyperparathyroidism may be an early form of classical hyperparathyroidism. Most of the patients are asymptomatic. In most of the patients, severe bone loss or nephrolithiasis may develop in the later stages.

Usually the patient clinic is as follows:

  • For secondary hyperparathyroidism, at least two separate corrected or ionized calcium levels at least six months apart in the presence of persistently elevated PTH in the absence of any cause
  • 25(OH) Vitamin D should be 30 ng/ml or higher.
  • GFR should be >60 ml/min.
  • Increased serum calcium/phosphate ratio

Normocalcemic secondary hyperparathyroidism

In these patients, high parathormone in the blood is a reaction to low calcium stimulus caused by various reasons. Parathyroid hormone stays high as long as the low calcium warning continues and returns to normal as soon as it is removed. Patients with secondary hyperparathyroidism typically develop hyperplasia of all four parathyroid glands. Normocalcemic secondary hyperparathyroidism can be cured by removing the problem causing low blood calcium.

Possible causes of normocalcemic secondary hyperparathyroidism:
  • Vitamin D deficiency
  • Kidney failure (most common cause)
  • Intestinal malabsorption syndromes
  • Bariatric surgery
  • Long-term low dietary calcium intake
  • Renal calcium leak
  • Idiopathic hypercalciuria
  • Anticonvulsants
  • Bisphosphonates
  • Celiac disease
  • Denosumab
  • Diuretics (thiazides)
  • Lithium

Although secondary hyperparathyroidism is frequently seen in patients with end-stage renal disease, serum phosphorus is also elevated.

 

 


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