|Specialty||General surgery, Endocrine surgery|
Parathyroidectomy is the surgical removal of one or more of the (usually) four parathyroid glands. This procedure is used to remove an adenoma or hyperplasia of these glands when they are producing excessive parathyroid hormone (PTH): hyperparathyroidism. The glands are usually four in number and located adjacent to the posterior surface of the thyroid gland, but their exact location is variable. When an elevated PTH level is found, a sestamibi scan or an ultrasound may be performed in order to confirm the presence and location of abnormal parathyroid tissue.
The main indication for parathyroidectomy is primary hyperparathyroidism, a condition in which one or more of the parathyroid glands produce excessive parathyroid hormone. Not all cases of primary hyperparathyroidism require surgery, but it is recommended if the condition causes significant symptoms or if it affects the kidneys (nephrocalcinosis) or bone health (osteoporosis), and also in people under 50 even if they do not have symptoms.  It is not always possible to anticipate if a parathyroid tumor is malignant (i.e. capable of invading other tissues or spreading elsewhere). Any suspicion of parathyroid carcinoma is therefore also an indication for surgery. 
Parathyroidectomy may also be required in secondary hyperparathyroidism. This situation arises mainly in people with severe chronic kidney disease in which the parathyroid glands are overactive to compensate for the low calcium and vitamin D levels often present in CKD. In many cases, the parathyroid hormone production improves when these abnormalities are treated with medication. A small proportion, however, have persistently raised hormone levels six months after treatment has started, thought to be autonomous production of hormone by the glands and loss of feedback mechanisms. In this situation surgical parathyroidectomy may be required, especially if calcium and phosphate levels remain elevated, there is calcium deposition in the wall of blood vessels (calciphylaxis in severe cases) or there is worsening bone disease. In people on dialysis, parathyroidectomy can improve their survival. It does appear that the procedure may be underused. 
The operation requires a general anesthetic (unconscious and pain free) or a local anesthetic (pain free). The surgeon makes an incision around an inch long in the neck just under the larynx (Adam's apple), and locates the offending parathyroid glands. Preoperative testing using sestamibi scanning can help identify the location of glands. It can also be used to limit the extent of surgical exploration when used in conjunction with intraoperative PTH hormone monitoring.  The particular problem or disease process will determine how many of the parathyroid glands are removed. Some parathyroid tissue must be left in place to help prevent hypoparathyroidism.
Recovery after the operation tends to be swift. The PTH level is back to normal within 10–15 minutes, and can be confirmed by intraoperative rapid assessment during the operation. However, the remaining parathyroid glands may take hours to several weeks to return to their normal functioning levels (as they may have become dormant). Calcium supplements are therefore often required to prevent symptoms of hypocalcemia and to restore lost bone mass. 
The patient is placed in a semi-Fowler position and the neck is extended. An abbreviated Kocher incision is made and the platysma muscle is dissected horizontally. The strap muscles are released off of the thyroid gland. Then the thyroid gland is mobilized and the parathyroid arterial blood supply is suture ligated. The entire parathyroid adenoma is identified and dissected out. Intraoperative PTH monitoring can begin at this time and will show falling PTH levels if the entire adenoma has been resected. 
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While mild hypocalcemia is common after partial parathyroidectomy, some people experience persistently prolonged low calcium levels. This is called hungry bone syndrome. Despite the reactivation of unresected parathyroid glands producing normal to elevated levels of PTH, serum calcium continues to be low. The balance between calcium influx and efflux within the bone continues to be disrupted, favoring the former. The bone is said to be "hungry" as it consumes minerals without regard to PTH; calcium, magnesium, and phosphate continue to be deposited into the bones, resulting in hypocalcemia, hypomagnesemia, and hypophosphatemia. Prolonged calcium supplementation may be required. Hungry bone syndrome is particularly common in people who are on long-term regular dialysis.  
Parathyroid glands are small endocrine glands in the neck of humans and other tetrapods. Humans usually have four parathyroid glands, located on the back of the thyroid gland in variable locations. The parathyroid gland produces and secretes parathyroid hormone in response to a low blood calcium, which plays a key role in regulating the amount of calcium in the blood and within the bones.
Parathyroid hormone (PTH), also called parathormone or parathyrin, is a peptide hormone secreted by the parathyroid glands that regulates the serum calcium concentration through its effects on bone, kidney, and intestine.
Hypercalcemia, also spelled hypercalcaemia, is a high calcium (Ca2+) level in the blood serum. The normal range is 2.1–2.6 mmol/L (8.8–10.7 mg/dL, 4.3–5.2 mEq/L), with levels greater than 2.6 mmol/L defined as hypercalcemia. Those with a mild increase that has developed slowly typically have no symptoms. In those with greater levels or rapid onset, symptoms may include abdominal pain, bone pain, confusion, depression, weakness, kidney stones or an abnormal heart rhythm including cardiac arrest.
Disorders of calcium metabolism occur when the body has too little or too much calcium. The serum level of calcium is closely regulated within a fairly limited range in the human body. In a healthy physiology, extracellular calcium levels are maintained within a tight range through the actions of parathyroid hormone, vitamin D and the calcium sensing receptor. Disorders in calcium metabolism can lead to hypocalcemia, decreased plasma levels of calcium or hypercalcemia, elevated plasma calcium levels.
Parathyroid chief cells are one of the two cell types of the parathyroid glands, along with oxyphil cells. The chief cells are much more prevalent in the parathyroid gland than the oxyphil cells. It is perceived that oxyphil cells may be derived from chief cells at puberty, as they are not present at birth like chief cells.
Hypoparathyroidism is decreased function of the parathyroid glands with underproduction of parathyroid hormone (PTH). This can lead to low levels of calcium in the blood, often causing cramping and twitching of muscles or tetany, and several other symptoms. It is a very rare disease. The condition can be inherited, but it is also encountered after thyroid or parathyroid gland surgery, and it can be caused by immune system-related damage as well as a number of rarer causes. The diagnosis is made with blood tests, and other investigations such as genetic testing depending on the results. The primary treatment of hypoparathyroidism is calcium and vitamin D supplementation. Calcium replacement or vitamin D can ameliorate the symptoms but can increase the risk of kidney stones and chronic kidney disease. Additionally, medications such as recombinant human parathyroid hormone or teriparatide may be given by injection to replace the missing hormone.
Hyperparathyroidism is an increase in parathyroid hormone (PTH) levels in the blood. This occurs from a disorder either within the parathyroid glands or as response to external stimuli. Symptoms of hyperparathyroidism are caused by inappropriately normal or elevated blood calcium leaving the bones and flowing into the blood stream in response to increased production of parathyroid hormone. In healthy people, when blood calcium levels are high, parathyroid hormone levels should be low. With long-standing hyperparathyroidism, the most common symptom is kidney stones. Other symptoms may include bone pain, weakness, depression, confusion, and increased urination. Both primary and secondary may result in osteoporosis.
Endocrine surgery is a surgical sub-speciality focusing on surgery of the endocrine glands, including the thyroid gland, the parathyroid glands, the adrenal glands, glands of the endocrine pancreas, and some neuroendocrine glands.
Cinacalcet, sold under the brand name Sensipar among others, is a medication used to treat tertiary hyperparathyroidism, parathyroid carcinoma, and primary hyperparathyroidism.
Primary hyperparathyroidism is a medical condition where the parathyroid gland produce excess amounts of parathyroid hormone (PTH). The symptoms of the condition relate to the resulting elevated serum calcium (hypercalcemia), which can cause digestive symptoms, kidney stones, psychiatric abnormalities, and bone disease.
Multiple endocrine neoplasia type 1 (MEN-1) is one of a group of disorders, the multiple endocrine neoplasias, that affect the endocrine system through development of neoplastic lesions in pituitary, parathyroid gland and pancreas. Individuals suffering from this disorder are prone to developing multiple endocrine and nonendocrine tumors. It was first described by Paul Wermer in 1954.
Osteitis fibrosa cystica is a skeletal disorder resulting in a loss of bone mass, a weakening of the bones as their calcified supporting structures are replaced with fibrous tissue, and the formation of cyst-like brown tumors in and around the bone. Osteitis fibrosis cystica (OFC), also known as osteitis fibrosa, osteodystrophia fibrosa, and von Recklinghausen's disease of bone, is caused by hyperparathyroidism, which is a surplus of parathyroid hormone from over-active parathyroid glands. This surplus stimulates the activity of osteoclasts, cells that break down bone, in a process known as osteoclastic bone resorption. The hyperparathyroidism can be triggered by a parathyroid adenoma, hereditary factors, parathyroid carcinoma, or renal osteodystrophy. Osteoclastic bone resorption releases minerals, including calcium, from the bone into the bloodstream, causing both elevated blood calcium levels, and the structural changes which weaken the bone. The symptoms of the disease are the consequences of both the general softening of the bones and the excess calcium in the blood, and include bone fractures, kidney stones, nausea, moth-eaten appearance in the bones, appetite loss, and weight loss.
Secondary hyperparathyroidism is the medical condition of excessive secretion of parathyroid hormone (PTH) by the parathyroid glands in response to hypocalcemia, with resultant hyperplasia of these glands. This disorder is primarily seen in patients with chronic kidney failure. It is sometimes abbreviated "SHPT" in medical literature.
Tertiary hyperparathyroidism is a condition involving the overproduction of the hormone, parathyroid hormone, produced by the parathyroid glands. The parathyroid glands are involved in monitoring and regulating blood calcium levels and respond by either producing or ceasing to produce parathyroid hormone. Anatomically, these glands are located in the neck, para-lateral to the thyroid gland, which does not have any influence in the production of parathyroid hormone. Parathyroid hormone is released by the parathyroid glands in response to low blood calcium circulation. Persistent low levels of circulating calcium are thought to be the catalyst in the progressive development of adenoma, in the parathyroid glands resulting in primary hyperparathyroidism. While primary hyperparathyroidism is the most common form of this condition, secondary and tertiary are thought to result due to chronic kidney disease (CKD). Estimates of CKD prevalence in the global community range from 11 to 13% which translate to a large portion of the global population at risk of developing tertiary hyperparathyroidism. Tertiary hyperparathyroidism was first described in the late 1960s and had been misdiagnosed as primary prior to this. Unlike primary hyperparathyroidism, the tertiary form presents as a progressive stage of resolved secondary hyperparathyroidism with biochemical hallmarks that include elevated calcium ion levels in the blood, hypercalcemia, along with autonomous production of parathyroid hormone and adenoma in all four parathyroid glands. Upon diagnosis treatment of tertiary hyperparathyroidism usually leads to a surgical intervention.
Endocrine diseases are disorders of the endocrine system. The branch of medicine associated with endocrine disorders is known as endocrinology.
A parathyroid adenoma is a benign tumor of the parathyroid gland. It generally causes hyperparathyroidism; there are very few reports of parathyroid adenomas that were not associated with hyperparathyroidism.
Parathyroid carcinoma is a rare cancer resulting in parathyroid adenoma to carcinoma progression. It forms in tissues of one or more of the parathyroid glands.
Many conditions are associated with disorders of the function of the parathyroid gland. Some disorders may be purely anatomical resulting in an enlarged gland which will raise concern. Such benign disorders, such as parathyroid cyst, are not discussed here. Parathyroid diseases can be divided into those causing hyperparathyroidism, and those causing hypoparathyroidism.
A calcimimetic is a pharmaceutical drug that mimics the action of calcium on tissues, by allosteric activation of the calcium-sensing receptor that is expressed in various human organ tissues. Calcimimetics are used to treat secondary hyperparathyroidism (SHPT).
A sestamibi parathyroid scan is a procedure in nuclear medicine which is performed to localize parathyroid adenoma, which causes Hyperparathyroidism. Adequate localization of parathyroid adenoma allows the surgeon to use a minimally invasive surgical approach.