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Parathyroid
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What is a parathyroid gland and when is it a problem
Last reviewed: October 4, 2026
Summary
The parathyroid glands are four small glands in the neck that control the level of calcium in the blood by releasing parathyroid hormone (PTH). The most common parathyroid problem is primary hyperparathyroidism, in which one or more glands make too much PTH and the blood calcium rises. It affects about 1 in 100 adults and is most common in women after menopause [1, 2]. Most people are diagnosed through routine blood work before they have obvious symptoms, but the condition can still thin the bones and cause kidney stones over time [3, 4].
Surgery to remove the overactive gland or glands (parathyroidectomy) is the only cure. In experienced hands it cures about 97% to 98% of patients, and serious complications are uncommon [5, 6]. International guidelines recommend surgery for anyone with symptoms and for people without symptoms who meet specific criteria. For mild disease, a 10-year randomized trial found that careful observation was a safe option for many patients, although surgery protected bone density [4, 7, 8].
The sections below explain how the glands work, the types of parathyroid disease, low parathyroid function after neck surgery, how hyperparathyroidism is evaluated and when surgery is recommended, and how surgeons find glands that are in unusual places. A numbered reference list is at the end of the page. Where the evidence is limited or mixed, the page says so.
Introduction: what the parathyroid glands do
A parathyroid gland is a tiny cluster of cells, usually about the size of a grain of rice, that produces parathyroid hormone. Most people have four, two on each side, sitting on or near the back of the thyroid gland. Despite the shared name and location, the parathyroid glands have a completely different job from the thyroid. In a pooled analysis of 26 studies and more than 7,000 people, about 81% had exactly four glands; the rest had fewer or more [9].
The glands form early in fetal development from structures in the neck called pharyngeal pouches. The upper (superior) glands come from the fourth pouch and travel only a short distance. The lower (inferior) glands come from the third pouch together with the thymus and travel down into the neck with it, which is why a lower gland is sometimes found low in the neck, in the thymus, or in the upper chest [10].
Calcium in the blood must stay within a narrow range for nerves, muscles, the heart and many other organs to work normally. The parathyroid glands sense the blood calcium level directly. When calcium drops, they release more PTH. PTH raises calcium in three ways: it releases calcium from bone, it tells the kidneys to hold on to calcium and let go of phosphate, and it tells the kidneys to activate vitamin D, which in turn increases calcium absorption from food [11, 3]. When calcium is high, healthy glands turn PTH production down and the calcium level falls back toward normal. Only a small amount of healthy parathyroid tissue, roughly half of one normal gland, is needed to keep calcium normal.
A few terms are used throughout this page. Hypercalcemia means a high blood calcium level. An adenoma is a benign (non-cancerous) growth of a single gland. Multigland disease means more than one gland is overactive. Parathyroidectomy is the operation to remove an overactive gland. Localization refers to imaging tests used before surgery to find which gland is overactive.
Types of hyperparathyroidism
Hyperparathyroidism means too much PTH. The cause, and whether surgery helps, depends on whether the problem starts in the glands themselves or is the glands' response to a problem elsewhere in the body.
Primary hyperparathyroidism
When one or more parathyroid glands become a tumor that makes excess PTH and no longer turns off when calcium is high, this is called primary hyperparathyroidism. It is the most common cause of a high calcium level in people who are otherwise well. About 1 in 100 adults has it, rising to about 2 in 100 among postmenopausal women [1]. In the United States, new cases are diagnosed in about 66 per 100,000 women and 25 per 100,000 men each year [2].
The underlying cause is usually one of the following [11, 3, 12]:
A single adenoma, in about 80% to 85% of patients. Removing that one gland cures the disease.
Multigland disease, in about 10% to 20%. This includes enlargement of all four glands (hyperplasia) and two separate adenomas (double adenoma).
Parathyroid carcinoma, which is rare, accounting for about 1% of cases or fewer.
How it shows up. Because calcium is measured on routine blood panels, most people are now diagnosed before they have classic symptoms. When the disease does cause problems, the main ones are [3, 2]:
Kidney stones, and less often calcium deposits in the kidneys (nephrocalcinosis) or reduced kidney function.
Bone loss and fractures. Calcium drawn from the skeleton over years thins the bones, especially the outer (cortical) bone of the forearm and hip, leading to osteopenia, osteoporosis and fractures.
Nonspecific symptoms such as fatigue, low mood, poor concentration, memory complaints, joint and muscle aches, thirst, constipation and abdominal discomfort. These are common in people with hyperparathyroidism, but they are also common in the general population, so it is hard to prove which are caused by the calcium level and which will improve after surgery.
Even people with no symptoms can have silent changes such as reduced bone density, high urine calcium or stones seen only on imaging. This is why the evaluation described below includes bone density testing and kidney imaging [4].
Normocalcemic primary hyperparathyroidism is a milder form in which PTH is persistently high but blood calcium stays normal, after other causes of a high PTH (especially low vitamin D and kidney disease) have been ruled out. Some, but not all, of these patients go on to develop high calcium. Its natural history is less well understood than the classic form, and decisions about surgery are made case by case [4, 6].
Hereditary hyperparathyroidism
About 10% of people with primary hyperparathyroidism have an inherited form [13]. The best known are multiple endocrine neoplasia type 1 (MEN1, caused by changes in the MEN1 gene), multiple endocrine neoplasia type 2A (MEN2A, RET gene) and the hyperparathyroidism-jaw tumor syndrome (CDC73 gene). Inherited disease more often involves several glands and is more likely to come back after surgery. In a National Institutes of Health series of patients who had a family history of hyperparathyroidism, 60% carried a disease-causing gene change. Age 45 or younger, male sex and multigland disease each made a positive genetic test more likely, and the cure rate after a first operation was lower in the familial group (89% compared with 96%) [13]. Genetic testing is generally considered for people diagnosed young, those with multigland disease or parathyroid carcinoma, and those with a family history of hyperparathyroidism or related tumors [4].
Secondary hyperparathyroidism
Secondary hyperparathyroidism is a normal response of healthy glands to a low calcium signal. The most common causes are chronic kidney disease, in which the kidneys cannot activate vitamin D or clear phosphate, and vitamin D deficiency. Like a muscle getting exercised, all of the glands enlarge and make more PTH to hold the calcium level up, but they are still doing their job correctly, so the blood calcium is normal or low rather than high. The first treatment is to correct the underlying problem: vitamin D replacement, and in kidney disease, phosphate control, active vitamin D and medicines called calcimimetics (such as cinacalcet) that lower PTH. Kidney guidelines suggest parathyroidectomy for severe secondary hyperparathyroidism that does not respond to medical treatment [14].
Tertiary hyperparathyroidism
Tertiary hyperparathyroidism develops after a long period of secondary hyperparathyroidism, most often in people with kidney failure. The glands become self-driven and keep making too much PTH even after the original problem is fixed, typically after a successful kidney transplant, and the calcium becomes high. Persistent hyperparathyroidism has been found in up to 80% of patients during the first year after kidney transplantation and is associated with fractures and with poorer kidney graft and patient outcomes [15]. In a meta-analysis of transplant recipients, parathyroidectomy lowered PTH and calcium more than calcimimetic medicine, with no difference in kidney graft function [16].
Primary and tertiary hyperparathyroidism are diseases treatable with parathyroid surgery, whereas secondary hyperparathyroidism is mainly a problem of the kidneys or vitamin D and is treated medically first.
Parathyroid carcinoma
Parathyroid carcinoma is one of the rarest endocrine cancers. It tends to cause much higher calcium and PTH levels than a benign adenoma, often with bone pain, muscle weakness, kidney problems and sometimes a firm lump in the neck. There is no single blood test or scan that reliably separates it from a benign adenoma before surgery, so the diagnosis is usually made by pathologic examination of the removed gland. When cancer is suspected, the recommended operation is removal of the tumor in one piece (en bloc) with clear margins, often with the neighboring thyroid lobe. The cancer can come back in up to half of patients, but it usually grows slowly, and 10-year survival is about 60% to 70%. When it is fatal, the cause is more often uncontrollable high calcium than the tumor itself [12, 17].
hypoparathyroidism
Having too little parathyroid hormone is hypoparathyroidism. Without enough PTH the blood calcium falls, which can cause tingling around the mouth and in the fingers, muscle cramps, and in more severe cases muscle spasms. About 75% of hypoparathyroidism follows neck surgery, mainly thyroid surgery, and the remainder comes from autoimmune, genetic and other causes [18].
Temporary and permanent hypoparathyroidism after surgery
The parathyroid glands are delicate and have a very small blood supply, so they are easily "stunned" when surgery is done on or near them. Low calcium in the first days after surgery is common and usually temporary. In a review of 115 studies of thyroidectomy, the median rate of temporary low calcium was 27%, and the median rate of permanent low calcium was 1% [19]. Hypoparathyroidism is considered permanent (chronic) when it still requires treatment more than 12 months after surgery [18]. Risk is higher when fewer than two healthy glands are seen and preserved during the operation, after reoperation for bleeding, with Graves' disease and with larger goiters [19].
After parathyroid surgery, the remaining normal glands have often been suppressed by the high calcium and may take days to weeks to wake up. Temporary low calcium is less common after a focused operation on one gland (about 2%) than after an exploration of all four glands (about 14%) [5]. Permanent hypoparathyroidism after surgery for primary hyperparathyroidism is rare unless all glands have been removed or have lost their blood supply. People with severe, long-standing disease and significant bone loss can develop hungry bone syndrome, in which the healing skeleton rapidly takes up calcium after the overactive gland is removed. This can cause a prolonged drop in calcium that needs close monitoring and calcium and vitamin D treatment [6].
Treatment
The 2022 international guidelines on hypoparathyroidism recommend conventional therapy, which is calcium supplements and active vitamin D (calcitriol), as the first treatment. The goal is to keep the blood calcium in the low-normal range, which relieves symptoms while limiting calcium loss in the urine and the risk of kidney stones and kidney damage. When conventional therapy does not control calcium well, causes side effects, or requires a large pill burden, the guidelines suggest considering parathyroid hormone replacement [18].
The newest option is palopegteriparatide, a long-acting form of PTH given as a once-daily injection. In the PaTHway randomized trial of 84 adults with chronic hypoparathyroidism, 79% of patients on palopegteriparatide reached normal calcium without needing active vitamin D or more than a small amount of calcium, compared with 5% on placebo. Quality-of-life and symptom scores improved, and 24-hour urine calcium returned to normal on average [20]. The trial lasted 26 weeks with longer extension data, so experience over many years is still limited.
evaluation of hyperparathyroidism
Making the diagnosis
Primary hyperparathyroidism is diagnosed with blood and urine tests, not with scans. The typical pattern is a high blood calcium together with a PTH level that is high or "inappropriately normal" (a PTH that should have been turned off by the high calcium but was not) [6, 4]. Most cases are first noticed on routine blood work. Others are found during an evaluation for kidney stones or bone loss, or when an enlarged gland is seen by chance on imaging done for another reason.
The evaluation recommended by the Fifth International Workshop on primary hyperparathyroidism (2022) and the American Association of Endocrine Surgeons (AAES, 2016) usually includes [4, 6]:
Blood calcium (often repeated), PTH measured at the same time, phosphate, creatinine (kidney function) and 25-hydroxyvitamin D.
A 24-hour urine collection for calcium and creatinine.
Bone density testing (DXA) of the spine, hip and forearm, and in some patients spine imaging to look for silent vertebral fractures.
Kidney imaging (ultrasound or CT) to look for stones or calcium deposits.
Ruling out familial hypocalciuric hypercalcemia
An inherited condition called Familial Hypocalciuric Hypercalcemia (FHH) can look like primary hyperparathyroidism on blood tests. In FHH, the body's calcium "set point" is higher than normal in the person and in their blood relatives. FHH is harmless in most people and does not improve with surgery, so it must be ruled out first. A clue is a family member who had unsuccessful parathyroid surgery. The 24-hour urine calcium is used to calculate a calcium-to-creatinine clearance ratio, which is usually below 0.01 in FHH and above 0.02 in primary hyperparathyroidism [4]. The test is helpful but imperfect: in one study of 198 patients, the ratio correctly flagged only about 64% of the patients who turned out to have FHH [21]. When results are borderline or the family history is suggestive, genetic testing for FHH can settle the question.
Who should have surgery
Parathyroidectomy is recommended for everyone with symptoms or complications of the disease, such as kidney stones or fractures. For people without symptoms, the Fifth International Workshop recommends surgery if any of the following is present [4, 22]:
Blood calcium more than 1.0 mg/dL above the upper limit of normal.
Bone density T-score of -2.5 or lower at the spine, hip or forearm, or a vertebral fracture seen on imaging.
Creatinine clearance (kidney function) below 60 mL/min.
24-hour urine calcium above 250 mg in women or 300 mg in men, or other markers of high stone risk.
Kidney stones or kidney calcium deposits seen on imaging.
Age under 50.
The AAES guidelines are similar but go somewhat further. They state that surgery is appropriate for people who meet these criteria and can also be offered to patients who do not, including those with neurocognitive or psychiatric symptoms that may be related to the disease, because surgery is the only cure and is more cost-effective than long-term monitoring [6]. The evidence for these broader reasons is weaker than for the bone and kidney criteria [23].
Surgery compared with observation
For people with mild disease who do not meet the criteria above, the choice between surgery and monitoring has been tested in randomized trials, the strongest kind of study.
The Scandinavian (SIPH) trial randomly assigned 191 patients with mild primary hyperparathyroidism to surgery or observation. Over 10 years and an extended follow-up, deaths and major health events (heart and vascular events, stroke, cancer, fractures and kidney stones) were similar in the two groups [7]. Surgery did improve bone density compared with observation, most clearly at the spine and hip, but this did not translate into fewer fractures during the study [8]. On quality-of-life questionnaires, the surgery group scored better on vitality after 10 years, but the differences between groups were small and of uncertain importance [24].
Pooled randomized trials. A meta-analysis that combined the SIPH trial with earlier randomized trials from the United States and Italy [25, 26, 27] found that surgery raised bone density by about 3.5% at the spine and hip and lowered calcium, but did not show a difference in fractures, kidney stones or most quality-of-life measures [28]. A 2023 Cochrane review of eight trials found that surgery cured 99% of patients and observation cured none, and judged the evidence on longer-term outcomes to be uncertain [1].
Large observational studies. Among more than 210,000 Medicare patients with primary hyperparathyroidism, those who had parathyroidectomy had about 22% fewer fractures over the following years than those who were observed, a benefit seen across age groups and in those who did not meet surgical guidelines [29]. Studies like this can be biased by who is chosen for surgery, but they follow far more people for longer than the randomized trials.
Taken together, the evidence shows that surgery reliably cures the disease and protects bone density, and that careful monitoring is a reasonable choice for many people with mild disease, especially older patients or those with higher surgical risk. People who choose monitoring are usually followed with yearly calcium and kidney tests and bone density scans every one to two years, and surgery is recommended if they come to meet a criterion [4].
How people feel after surgery
Many patients report better energy, mood, sleep and concentration after a successful operation. In a systematic review of 31 studies that followed patients for at least a year, 27 found a significant and lasting improvement in quality of life after parathyroidectomy [30]. A study using objective cognitive tests found measurable improvement in thinking after surgery [31]. The randomized trials have shown smaller and less consistent effects on these symptoms [24, 28], so improvement in how a person feels is likely but cannot be promised.
Variable anatomic location of parathyroid glands
From: Anatomy, Head and Neck, Parathyroid, Ectopic Glands
StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2023 Jan-.
Typically, there are four parathyroid glands, with two situated on each side of the thyroid gland. However, it is worth noting that the anatomic location of parathyroid glands can vary among individuals. In some cases, these glands may be found in ectopic or abnormal locations, such as in the thymus, within the thyroid gland itself, or even in the chest or mediastinum. Ectopic parathyroid glands can present challenges in their identification and surgical treatment due to their atypical positions. Therefore, a combination of pre-operative localizing studies and the surgeon's awareness of the variable anatomic locations of parathyroid glands help minimize the risk of not finding a parathyroid gland.
How often glands are in unusual places
In the pooled analysis of more than 7,000 patients, about 16% of all parathyroid glands were in an ectopic location: about 12% elsewhere in the neck and about 4% in the chest (mediastinum) [9]. Some people also have a fifth or sixth (supernumerary) gland. In a series of 202 patients whose overactive gland was ectopic, the most common sites were [32]:
The thymus, in the lower neck or upper chest (38%).
Behind or beside the esophagus (31%).
Inside the thyroid gland (18%).
Less common sites, including deeper in the chest and high in the neck near the jaw (an "undescended" gland).
Finding the overactive gland before surgery
Once the diagnosis is made from blood tests, imaging is used to find the overactive gland and plan the operation. Imaging is not used to decide whether a person has the disease, and a negative scan does not mean surgery should be avoided [6]. The main tests are:
Ultrasound of the neck, which also checks the thyroid. Pooled sensitivity (the share of overactive glands found) is about 76% [33].
Sestamibi scan, a nuclear medicine scan, usually combined with a CT as SPECT-CT. Pooled sensitivity is about 79% [33]. It is better than ultrasound at finding glands in the chest and behind the esophagus [32].
4D-CT, a CT scan taken at several time points after contrast injection, which shows the rapid uptake and washout typical of an adenoma. Pooled sensitivity is about 85% in more recent studies, and it is often used when ultrasound and sestamibi do not agree [34, 33].
Fluorocholine PET-CT, the newest test. In a meta-analysis it found about 92% of patients' overactive glands and outperformed 4D-CT when the two were compared directly [34]. In one study of 144 patients it identified 148 of 149 abnormal glands [35]. Availability is still limited in many areas.
Focused surgery or four-gland exploration
When imaging clearly points to one gland, the surgeon can do a focused (minimally invasive) parathyroidectomy through a small incision, removing only that gland. Otherwise, or when the findings during surgery suggest more than one abnormal gland, the surgeon does a bilateral neck exploration, examining all four glands. Both approaches work well. In a meta-analysis of 88 studies, cure rates were 97% for focused surgery and 98% for bilateral exploration. Focused surgery had lower rates of temporary low calcium (2.3% compared with 14%) and of nerve injury affecting the voice (0.3% compared with 0.9%) [5]. A Cochrane review of five randomized trials found success rates of 97% and 99% at six months, with about half as many complications after focused surgery, while noting that the evidence was of low certainty [36].
Measuring PTH during surgery
PTH has a half-life of only a few minutes, so the surgeon can measure it in the operating room to confirm that all overactive tissue has been removed. The most widely used rule (the Miami criterion) looks for a drop of more than 50% from the highest level 10 minutes after the gland is removed. If the level does not fall enough, the surgeon looks for another abnormal gland. A network meta-analysis of 72 studies and more than 19,000 patients found that the Miami criterion was the most accurate of the commonly used rules, and that checking the level again at 15 minutes or later improved accuracy further [37].
Cure, recurrence and complications
Cure. About 97% to 98% of patients are cured by the first operation [5]. Failure is most often due to multigland disease or a gland in an unusual location.
Recurrence. High calcium can return years later. In a community-based cohort followed over five decades, 9% had persistent high calcium after surgery and 14% had a recurrence at a median of about 12 years, although many of these episodes were mild, temporary or due to other causes such as medications [38]. Long-term calcium checks are therefore reasonable after surgery.
Complications. Serious complications are uncommon. They include injury to the recurrent laryngeal nerve, which moves the vocal cord (see the voice page), temporary or rarely permanent low calcium, and bleeding [5].
Surgeon experience. A European Society of Endocrine Surgeons review found that parathyroid surgery done in low-volume settings has more failures, complications and reoperations. It recommended at least 15 parathyroidectomies a year, and more than 40 for difficult cases such as glands that cannot be localized, inherited disease and reoperations [39]. This evidence comes from observational studies rather than randomized trials.
Additional links
• Video explaining parathyroid surgery.
• Parathyroid diseases information on the American Head and Neck Society website.
• Parathyroid surgery and treatment on this site.
• Related Learning Center pages: thyroid, general tumor information, neck, and voice.
Summary
Primary hyperparathyroidism is common, usually mild, and most often found on routine blood tests. It is diagnosed with blood and urine tests, after ruling out the harmless inherited mimic FHH. Most cases are caused by a single benign adenoma. Surgery is the only cure, succeeds in about 97% to 98% of patients when done by an experienced surgeon, and is recommended for people with symptoms and for those who meet international criteria based on calcium level, bone density, kidney findings and age. For mild disease, randomized trials show that observation is a safe choice for many people over a decade, while surgery improves bone density. Imaging helps the surgeon find the overactive gland, including glands in unusual places, and PTH measured during surgery confirms the cure. Low calcium after neck surgery is common and usually temporary, and new hormone replacement treatment is available for the uncommon patient whose low parathyroid function becomes permanent.
References
Pappachan JM, Lahart IM, Viswanath AK, et al. Parathyroidectomy for adults with primary hyperparathyroidism. Cochrane Database Syst Rev. 2023;3(3):CD013035. doi:10.1002/14651858.CD013035.pub2
Zhu CY, Sturgeon C, Yeh MW. Diagnosis and Management of Primary Hyperparathyroidism. JAMA. 2020;323(12):1186-1187. doi:10.1001/jama.2020.0538
Insogna KL. Primary Hyperparathyroidism. N Engl J Med. 2018;379(11):1050-1059. doi:10.1056/NEJMcp1714213
Bilezikian JP, Khan AA, Silverberg SJ, et al. Evaluation and Management of Primary Hyperparathyroidism: Summary Statement and Guidelines from the Fifth International Workshop. J Bone Miner Res. 2022;37(11):2293-2314. doi:10.1002/jbmr.4677
Singh Ospina NM, Rodriguez-Gutierrez R, Maraka S, et al. Outcomes of Parathyroidectomy in Patients with Primary Hyperparathyroidism: A Systematic Review and Meta-analysis. World J Surg. 2016;40(10):2359-77. doi:10.1007/s00268-016-3514-1
Wilhelm SM, Wang TS, Ruan DT, et al. The American Association of Endocrine Surgeons Guidelines for Definitive Management of Primary Hyperparathyroidism. JAMA Surg. 2016;151(10):959-968. doi:10.1001/jamasurg.2016.2310
Pretorius M, Lundstam K, Heck A, et al. Mortality and Morbidity in Mild Primary Hyperparathyroidism: Results From a 10-Year Prospective Randomized Controlled Trial of Parathyroidectomy Versus Observation. Ann Intern Med. 2022;175(6):812-819. doi:10.7326/M21-4416
Lundstam K, Pretorius M, Bollerslev J, et al. Positive Effect of Parathyroidectomy Compared to Observation on BMD in a Randomized Controlled Trial of Mild Primary Hyperparathyroidism. J Bone Miner Res. 2023;38(3):372-380. doi:10.1002/jbmr.4763
Taterra D, Wong LM, Vikse J, et al. The prevalence and anatomy of parathyroid glands: a meta-analysis with implications for parathyroid surgery. Langenbecks Arch Surg. 2019;404(1):63-70. doi:10.1007/s00423-019-01751-8
Kameda Y. Cellular and molecular mechanisms of the organogenesis and development, and function of the mammalian parathyroid gland. Cell Tissue Res. 2023;393(3):425-442. doi:10.1007/s00441-023-03785-3
Bilezikian JP, Bandeira L, Khan A, et al. Hyperparathyroidism. Lancet. 2018;391(10116):168-178. doi:10.1016/S0140-6736(17)31430-7
Rodrigo JP, Hernandez-Prera JC, Randolph GW, et al. Parathyroid cancer: An update. Cancer Treat Rev. 2020;86:102012. doi:10.1016/j.ctrv.2020.102012
El Lakis M, Nockel P, Gaitanidis A, et al. Probability of Positive Genetic Testing Results in Patients with Family History of Primary Hyperparathyroidism. J Am Coll Surg. 2018;226(5):933-938. doi:10.1016/j.jamcollsurg.2018.01.007
Ketteler M, Block GA, Evenepoel P, et al. Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder: Synopsis of the Kidney Disease: Improving Global Outcomes 2017 Clinical Practice Guideline Update. Ann Intern Med. 2018;168(6):422-430. doi:10.7326/M17-2640
Cianciolo G, Tondolo F, Barbuto S, et al. A roadmap to parathyroidectomy for kidney transplant candidates. Clin Kidney J. 2022;15(8):1459-1474. doi:10.1093/ckj/sfac050
Koimtzis G, Stefanopoulos L, Geropoulos G, et al. Calcimimetics or parathyroidectomy for kidney transplant recipients: is there still a question? a systematic review, meta-analysis and trial sequential analysis. Endocrine. 2025;88(3):671-681. doi:10.1007/s12020-025-04189-9
Roser P, Leca BM, Coelho C, et al. Diagnosis and management of parathyroid carcinoma: a state-of-the-art review. Endocr Relat Cancer. 2023;30(4). doi:10.1530/ERC-22-0287
Khan AA, Guyatt G, Ali DS, et al. Management of Hypoparathyroidism. J Bone Miner Res. 2022;37(12):2663-2677. doi:10.1002/jbmr.4716
Edafe O, Antakia R, Laskar N, et al. Systematic review and meta-analysis of predictors of post-thyroidectomy hypocalcaemia. Br J Surg. 2014;101(4):307-20. doi:10.1002/bjs.9384
Khan AA, Rubin MR, Schwarz P, et al. Efficacy and Safety of Parathyroid Hormone Replacement With TransCon PTH in Hypoparathyroidism: 26-Week Results From the Phase 3 PaTHway Trial. J Bone Miner Res. 2023;38(1):14-25. doi:10.1002/jbmr.4726
Bhangu JS, Selberherr A, Brammen L, et al. Efficacy of calcium excretion and calcium/creatinine clearance ratio in the differential diagnosis of familial hypocalciuric hypercalcemia and primary hyperparathyroidism. Head Neck. 2019;41(5):1372-1378. doi:10.1002/hed.25568
Walker MD, Shane E. Hypercalcemia: A Review. JAMA. 2022;328(16):1624-1636. doi:10.1001/jama.2022.18331
Campbell MJ. The Definitive Management of Primary Hyperparathyroidism: Who Needs an Operation? JAMA. 2017;317(11):1167-1168. doi:10.1001/jama.2017.1620
Pretorius M, Lundstam K, Hellström M, et al. Effects of Parathyroidectomy on Quality of Life: 10 Years of Data From a Prospective Randomized Controlled Trial on Primary Hyperparathyroidism (the SIPH-Study). J Bone Miner Res. 2021;36(1):3-11. doi:10.1002/jbmr.4199
Rao DS, Phillips ER, Divine GW, et al. Randomized controlled clinical trial of surgery versus no surgery in patients with mild asymptomatic primary hyperparathyroidism. J Clin Endocrinol Metab. 2004;89(11):5415-22. doi:10.1210/jc.2004-0028
Ambrogini E, Cetani F, Cianferotti L, et al. Surgery or surveillance for mild asymptomatic primary hyperparathyroidism: a prospective, randomized clinical trial. J Clin Endocrinol Metab. 2007;92(8):3114-21. doi:10.1210/jc.2007-0219
Bollerslev J, Jansson S, Mollerup CL, et al. Medical observation, compared with parathyroidectomy, for asymptomatic primary hyperparathyroidism: a prospective, randomized trial. J Clin Endocrinol Metab. 2007;92(5):1687-92. doi:10.1210/jc.2006-1836
Anagnostis P, Vaitsi K, Veneti S, et al. Efficacy of parathyroidectomy compared with active surveillance in patients with mild asymptomatic primary hyperparathyroidism: a systematic review and meta-analysis of randomized-controlled studies. J Endocrinol Invest. 2021;44(6):1127-1137. doi:10.1007/s40618-020-01447-7
Seib CD, Meng T, Suh I, et al. Risk of Fracture Among Older Adults With Primary Hyperparathyroidism Receiving Parathyroidectomy vs Nonoperative Management. JAMA Intern Med. 2022;182(1):10-18. doi:10.1001/jamainternmed.2021.6437
Livschitz J, Yen TWF, Evans DB, et al. Long-term Quality of Life After Parathyroidectomy for Primary Hyperparathyroidism: A Systematic Review. JAMA Surg. 2022;157(11):1051. doi:10.1001/jamasurg.2022.4249
Lightle WR, Zheng F, Makris KI, et al. Objectively measured cognitive dysfunction in patients with primary hyperparathyroidism improves after parathyroidectomy. Surgery. 2024;175(1):161-165. doi:10.1016/j.surg.2023.07.045
Roy M, Mazeh H, Chen H, et al. Incidence and localization of ectopic parathyroid adenomas in previously unexplored patients. World J Surg. 2013;37(1):102-6. doi:10.1007/s00268-012-1773-z
Cheung K, Wang TS, Farrokhyar F, et al. A meta-analysis of preoperative localization techniques for patients with primary hyperparathyroidism. Ann Surg Oncol. 2012;19(2):577-83. doi:10.1245/s10434-011-1870-5
Patel DD, Bhattacharjee S, Pandey AK, et al. Comparison of 4D computed tomography and F-18 fluorocholine PET for localisation of parathyroid lesions in primary hyperparathyroidism: A systematic review and meta-analysis. Clin Endocrinol (Oxf). 2023;99(3):262-271. doi:10.1111/cen.14875
Boudousq V, Guignard N, Gilly O, et al. Diagnostic Performance of Cervical Ultrasound, (99m)Tc-Sestamibi Scintigraphy, and Contrast-Enhanced (18)F-Fluorocholine PET in Primary Hyperparathyroidism. J Nucl Med. 2022;63(7):1081-1086. doi:10.2967/jnumed.121.261900
Ahmadieh H, Kreidieh O, Akl EA, et al. Minimally invasive parathyroidectomy guided by intraoperative parathyroid hormone monitoring (IOPTH) and preoperative imaging versus bilateral neck exploration for primary hyperparathyroidism in adults. Cochrane Database Syst Rev. 2020;10(10):CD010787. doi:10.1002/14651858.CD010787.pub2
Staibano P, Au M, Zhang H, et al. Intraoperative Parathyroid Hormone Monitoring Criteria in Primary Hyperparathyroidism: A Network Meta-Analysis of Diagnostic Test Accuracy. JAMA Otolaryngol Head Neck Surg. 2025;151(3):190-200. doi:10.1001/jamaoto.2024.4453
Szabo Yamashita T, Mirande M, Huang CT, et al. Persistence and Recurrence of Hypercalcemia After Parathyroidectomy Over 5 Decades (1965-2010) in a Community-based Cohort. Ann Surg. 2023;278(2):e309-e313. doi:10.1097/SLA.0000000000005688
Iacobone M, Scerrino G, Palazzo FF. Parathyroid surgery: an evidence-based volume-outcomes analysis : European Society of Endocrine Surgeons (ESES) positional statement. Langenbecks Arch Surg. 2019;404(8):919-927. doi:10.1007/s00423-019-01823-9
Learning Center Main Index:
Throat:
swallowing, tonsils and adenoids, obstructive sleep apnea, voice, oral lesions and mucositis
Aesthetics:
skin regimen, injectables {neuromodulators (e.g., Botox), hyaluronic acid fillers (e.g., Juvederm), and others}, rhinoplasty, chin, facelift, neck lift, and brow lift, blepharoplasty (eyelid surgery), skin resurfacing, scar treatment
Tumors (benign and malignant/cancerous):
general tumor information, thyroid, parathyroid, skin, neck, lymphatics, oropharynx, larynx (voice box), salivary gland, nose and sinus, inverted papilloma, oral cavity (mouth and lips), nasopharynx, hypopharynx, radiation therapy, chemotherapy and immunotherapy, gastric feeding tube, central line
Nose and Sinus:
rhinoplasty (functional and cosmetic), sinusitis, breathing
Ear:
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