Background

Parathyroidism refers to disorders involving the parathyroid glands, which are small endocrine glands in the neck, typically behind the thyroid gland. These glands play a crucial role in regulating calcium and phosphorus levels in the body through the secretion of parathyroid hormone (PTH). Parathyroidism can manifest in different ways, primarily as hyperparathyroidism and hypoparathyroidism. 

Hyperparathyroidism: This condition involves the overactivity of one or more parathyroid glands, leading to excessive secretion of parathyroid hormone. Hyperparathyroidism can be categorized as primary, secondary, or tertiary. 

• Primary Hyperparathyroidism: As mentioned earlier, primary hyperparathyroidism is most caused by a benign tumor called a parathyroid adenoma, which results in increased PTH production. Hypercalcemia, which results from this, can have various adverse health effects, such as kidney stones, bone discomfort, and digestive problems. 
• Secondary Hyperparathyroidism: This form usually develops in response to another underlying condition, often chronic kidney disease. When the kidneys cannot effectively regulate calcium and phosphorus levels, the parathyroid glands become overactive to compensate, resulting in bone loss and further complications. 
• Tertiary Hyperparathyroidism: This is an advanced stage of secondary hyperparathyroidism, where the parathyroid glands continue to be overactive even after the underlying condition (like chronic kidney disease) has been treated. This can lead to persistent hypercalcemia. 

Hypoparathyroidism: This condition is characterized by insufficient secretion of parathyroid hormone. It can be caused by damage or surgical removal of the parathyroid glands, autoimmune conditions, or other factors. The low levels of PTH result in decreased calcium levels in the blood (hypocalcemia) and increased phosphorus levels. Symptoms of hypoparathyroidism include muscle cramps, tingling sensations, seizures, and, in severe cases, potentially life-threatening complications. 

Epidemiology

The epidemiology of parathyroidism can vary based on the type and underlying causes: 

• Primary Hyperparathyroidism: This condition is most diagnosed in individuals over 50 and is more common in women. The prevalence increases with age. It is often discovered incidentally through routine blood tests or during evaluations for conditions related to high calcium levels, such as kidney stones or osteoporosis. 
• Secondary Hyperparathyroidism: This type is often associated with chronic kidney disease, particularly in advanced stages. The prevalence of secondary hyperparathyroidism depends on the prevalence of kidney disease in each population. 
• Hypoparathyroidism: This condition is rarer than hyperparathyroidism and can be caused by various factors. It can be congenital (present at birth) or acquired due to surgical procedures involving the thyroid or parathyroid glands. The prevalence of hypoparathyroidism can vary based on the underlying causes. 

Anatomy

Pathophysiology

Primary Hyperparathyroidism: 

• Parathyroid Gland Enlargement (Adenoma or Hyperplasia): In most cases of primary hyperparathyroidism, the disorder is caused by the overactivity of one or more parathyroid glands. This can occur due to the presence of a benign tumor called a parathyroid adenoma or due to hyperplasia (enlargement) of the parathyroid glands. 
• Excessive Parathyroid Hormone (PTH) Production: The enlarged or overactive parathyroid glands produce and release excessive amounts of parathyroid hormone (PTH) into the bloodstream. 
• Dysregulation of Calcium and Phosphorus: PTH plays a central role in regulating calcium and phosphorus levels in the body. It stimulates calcium release from bones, enhances calcium absorption in the intestines, and reduces calcium excretion in the kidneys. However, in primary hyperparathyroidism, excessive PTH leads to increased calcium levels (hypercalcemia) and decreased phosphorus levels in the blood. 
• Effects on Target Organs: Elevated calcium levels can lead to various symptoms and complications. It can result in kidney stones, bone pain, osteoporosis (weakening of bones), gastrointestinal disturbances, and neurological symptoms due to calcium deposition in tissues. 

Secondary Hyperparathyroidism: 

• Underlying Condition (e.g., Chronic Kidney Disease): Secondary hyperparathyroidism occurs due to an underlying condition that disrupts the normal calcium and phosphorus balance in the body.  
• Calcium and Phosphorus Imbalances: In CKD, the kidneys cannot regulate calcium and phosphorus levels. This leads to decreased calcium absorption, increased phosphorus retention, and reduced production of activated vitamin D (calcitriol), which is important for calcium absorption. 
• Stimulation of Parathyroid Glands: The imbalance in calcium and phosphorus levels triggers the parathyroid glands to become overactive and produce more PTH to maintain normal calcium levels. 
• Effects on Bones and Organs: The increased PTH levels stimulate bone resorption (breakdown), releasing calcium from bones. However, this can also contribute to weakened bones over time. Additionally, elevated PTH can negatively affect other organs, including the heart and blood vessels. 

Etiology

Hyperparathyroidism: 

Primary Hyperparathyroidism: 

• Parathyroid Adenoma: The growth of a benign tumour known as a parathyroid adenoma is the most frequent cause of primary hyperparathyroidism.  
• Parathyroid Hyperplasia: In some cases, multiple parathyroid glands may become enlarged and overactive, a condition known as parathyroid hyperplasia. This can also lead to excessive PTH production and hypercalcemia. 

Secondary Hyperparathyroidism: 

• Chronic Kidney Disease (CKD): The most common cause of secondary hyperparathyroidism is chronic kidney disease, particularly in its advanced stages. CKD disrupts the balance of calcium and phosphorus in the body, leading to overactivity of the parathyroid glands as they attempt to regulate these imbalances. 
• Vitamin D Deficiency: Inadequate levels of activated vitamin D (calcitriol) can also contribute to secondary hyperparathyroidism. The parathyroid glands are stimulated to create more PTH when vitamin D levels are low because vitamin D is necessary for calcium absorption. 

Hypoparathyroidism: 

Congenital Hypoparathyroidism: 

• Genetic Mutations: Mutations in genes responsible for the development and function of the parathyroid glands can result in congenital hypoparathyroidism. These mutations can interfere with the proper formation and function of the glands, leading to reduced or absent production of parathyroid hormone (PTH). 
• Autoimmune Disorders: Some cases of congenital hypoparathyroidism are associated with autoimmune disorders that target the parathyroid glands, impairing their function. 

Acquired Hypoparathyroidism: 

• Surgical Removal: Surgical procedures involving the thyroid or parathyroid glands can inadvertently damage or remove the parathyroid glands, leading to acquired hypoparathyroidism. This can occur during thyroidectomy or other neck surgeries. 

• Autoimmune Conditions: Autoimmune disorders such as autoimmune polyendocrine syndrome type 1 (APS-1) and autoimmune polyendocrine syndrome type 2 (APS-2) can cause hypoparathyroidism by attacking and damaging the parathyroid glands. 
• Iatrogenic Causes: Certain medical treatments, such as radiation therapy to the neck area, can damage the parathyroid glands and result in hypoparathyroidism. 

Genetics

Prognostic Factors

Type of Hyperparathyroidism: The type of hyperparathyroidism (primary vs. secondary) can influence prognosis.  

Primary hyperparathyroidism caused by a benign adenoma generally has a better prognosis than secondary hyperparathyroidism associated with chronic kidney disease, where the underlying kidney disease can significantly affect outcomes. 

• Calcium Levels: Higher calcium levels are associated with an increased risk of complications, such as kidney stones, bone loss, and cardiovascular issues. 
• Presence of Symptoms: The presence and severity of symptoms related to hyperparathyroidism, such as bone pain, kidney stones, and digestive issues, can impact prognosis. Timely management of symptoms can improve the quality of life for individuals with hyperparathyroidism. 
• Age and Overall Health: The age and general health of the individual can influence prognosis. The risk of hyperparathyroidism-related consequences may increase in older people or those with prior medical disorders. 
• Surgical Intervention: For primary hyperparathyroidism, surgical removal of the affected parathyroid gland(s) is often recommended in cases with symptoms or complications. Successful surgery can lead to resolution of symptoms and normalization of calcium levels. 

Hypoparathyroidism: 

• Cause of Hypoparathyroidism: The underlying cause of hypoparathyroidism, whether congenital or acquired (e.g., surgical removal of parathyroid glands), can impact prognosis. Congenital cases may require lifelong management, while some acquired cases can be reversible if the underlying cause is treated. 
• Severity of Hypocalcemia: The extent of hypocalcemia (low calcium levels) is a critical prognostic factor. Severe hypocalcemia can lead to muscle spasms, seizures, and other serious complications if not properly managed. 
• Response to Treatment: The ability to manage hypocalcemia effectively with medications and supplements is an important prognostic factor. Regular monitoring and adjustment of treatment regimens can significantly impact long-term outcomes. 
• Quality of Life: Hypoparathyroidism can impact an individual’s quality of life due to the potential for symptoms such as muscle cramps, fatigue, and cognitive issues. Proper treatment can enhance quality of life while decreasing symptom load. 

Clinical History

Primary Hyperparathyroidism: 

• Clinical Presentation: Primary hyperparathyroidism is characterized by excessive parathyroid hormone (PTH) secretion from one or more parathyroid glands. The main feature is hypercalcemia (elevated blood calcium levels), which can lead to various symptoms and complications. 
• Age Group: This condition is more common in older adults and is typically diagnosed in individuals over 50. 

Physical Examination

• Bone Tenderness and Pain: Individuals with primary hyperparathyroidism may experience bone pain and tenderness, especially in the long bones and spine. This could be due to increased calcium release from the bones into the bloodstream. 
• Renal Findings: Kidney stones (nephrolithiasis) are a common complication of hypercalcemia, which can result from hyperparathyroidism. Patients might have symptoms such as flank pain or hematuria (blood in urine) due to the presence of kidney stones. 
• Muscle Weakness and Fatigue: Hypercalcemia can lead to muscle weakness and fatigue. On examination, clinicians might note reduced muscle strength. 
• Neurological Symptoms: Severe hypercalcemia can affect the nervous system and lead to confusion, memory problems, and seizures. These neurological signs should be assessed during examination. 
• Chvostek’s and Trousseau’s Signs: These tests can help identify neuromuscular irritability due to hypocalcemia. Chvostek’s sign involves tapping the facial nerve anteriorly to the ear, resulting in facial twitching. Trousseau’s sign is elicited by inflating a blood pressure cuff on the arm above systolic pressure, leading to carpal spasm. 
• Hypertension: High blood pressure is sometimes associated with primary hyperparathyroidism, but it’s not a consistent finding. 
• Osteopenia or Osteoporosis: Chronic hyperparathyroidism can lead to bone mineral loss and increased risk of fractures over time. This might be evident on physical examination through reduced bone density or signs of osteoporosis. 
• Abdominal Palpation: Abdominal examination might reveal tenderness if there are kidney stones or other hyperparathyroidism-related complications. 

Age group

Associated comorbidity

Primary hyperparathyroidism can occur sporadically or as part of specific genetic syndromes (e.g., multiple endocrine neoplasia type 1 or MEN1). It is more common in individuals with a history of radiation exposure to the head and neck region. There isn’t a specific associated comorbidity, but it can be seen alongside other medical conditions due to its prevalence in older individuals. 

Associated activity

Acuity of presentation

The acuity of presentation varies. Some individuals may be asymptomatic and only have mild hypercalcemia detected incidentally on routine blood tests. Others may experience various symptoms, including fatigue, weakness, bone pain, kidney stones, constipation, frequent urination, and cognitive changes. Severe hypercalcemia can lead to confusion, cardiac arrhythmias, and even coma. 

Hypoparathyroidism: 

• Clinical Presentation: Hypoparathyroidism is characterized by insufficient parathyroid hormone (PTH) production, leading to low levels of calcium in the blood (hypocalcemia) and high levels of phosphorus. 
• Age Group: Hypoparathyroidism can occur at any age but is often diagnosed during childhood or early adulthood. 
• Associated Comorbidities or Activities: Hypoparathyroidism can be caused by surgical removal or damage to the parathyroid glands during thyroid surgery, autoimmune disorders, or genetic conditions like DiGeorge syndrome. It is sometimes associated with autoimmune diseases like Addison’s, type 1 diabetes, and pernicious anemia. 
• Acuity of Presentation: The acuity of the presentation can vary depending on the cause and severity of hypoparathyroidism. Symptoms of hypocalcemia can range from mild (numbness, tingling, muscle cramps) to severe (seizures, muscle spasms, tetany). Chvostek’s and Trousseau’s signs are often positive, indicating increased neuromuscular excitability due to low calcium levels. 

Differential Diagnoses

• Vitamin D Deficiency: Vitamin D deficiency can lead to hypocalcemia and symptoms like parathyroid disorders. This is important to rule out, as vitamin D is essential for proper calcium metabolism. 
• Chronic Kidney Disease: Kidney dysfunction can affect calcium and phosphorus balance, leading to mineral imbalances similar to parathyroid disorders. 
• Multiple Myeloma: This is a type of cancer that affects plasma cells in the bone marrow, often leading to bone pain, fractures, and hypercalcemia due to bone destruction. 
• Sarcoidosis: This inflammatory disease can affect the parathyroid glands, increasing PTH production and hypercalcemia. 
• Familial Hypocalciuric Hypercalcemia (FHH): This genetic condition can mimic primary hyperparathyroidism but is generally benign and does not require surgical intervention. It’s important to differentiate FHH from primary hyperparathyroidism to avoid unnecessary treatment. 
• Thyrotoxicosis (Hyperthyroidism): Excessive thyroid hormone levels can increase bone turnover and calcium release from bones, resulting in hypercalcemia. 
• Medication-induced Hypercalcemia: Certain medications, such as thiazide diuretics and lithium, can cause hypercalcemia by various mechanisms. 
• Malignancies: Some cancers can produce a parathyroid hormone-related protein (PTHrP), leading to hypercalcemia (paraneoplastic syndrome). 
• Hypoparathyroidism: While you’re asking about parathyroidism, it’s important to consider its opposite, hypoparathyroidism, which autoimmune conditions, surgery, or genetic disorders can cause. 
• Granulomatous Disorders: Conditions like tuberculosis and histoplasmosis can lead to granuloma formation in the parathyroid glands, affecting their function. 
• Other Endocrine Disorders: Conditions like adrenal insufficiency (Addison’s disease) or adrenal overactivity (Cushing’s syndrome) can impact calcium metabolism and mimic some symptoms of parathyroid disorders. 
• Gastrointestinal Malabsorption: Disorders like celiac disease or Crohn’s disease can lead to malabsorption of calcium and result in hypocalcemia. 
• Milk-Alkali Syndrome: This can occur due to excessive calcium intake, often in the context of antacid use, leading to hypercalcemia and metabolic alkalosis. 
• Acute Pancreatitis: Severe pancreatitis can lead to calcium binding within the pancreas, causing hypocalcemia. 
• Familial Normocalciuric Hypercalcemia (FHN): This rare condition is characterized by mild hypercalcemia that persists over time without the complications associated with primary hyperparathyroidism. 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

Primary Hyperparathyroidism: 

• Surgical Approach (Parathyroidectomy): The primary treatment for primary hyperparathyroidism caused by a single parathyroid adenoma (the most common cause) is surgical removal of the affected parathyroid gland. Multiple glands may sometimes be affected, requiring more extensive surgery. The aim is to bring calcium levels back to normal and alleviate symptoms. Surgical techniques can vary and may include minimally invasive approaches. 
• Observational Approach: For individuals with mild or asymptomatic hyperparathyroidism and no significant complications, especially in cases where the calcium level is not significantly elevated, a “watchful waiting” approach might be considered. Regular monitoring of calcium and kidney function is essential. 
• Medical Management: In cases where surgery is not recommended or not possible due to underlying health issues, medical management might be considered. This includes managing symptoms and monitoring calcium levels closely. Medications like bisphosphonates or calcimimetics may help control calcium levels and bone health. 

Hypoparathyroidism: 

• Calcium and Vitamin D Supplementation: The mainstay of treatment for hypoparathyroidism is to supplement calcium and vitamin D to maintain the normal blood calcium levels. Calcium carbonate or calcium citrate supplements are commonly used. Vitamin D analogs (calcitriol or alfacalcidol) might also be prescribed to enhance calcium absorption. 
• Active Vitamin D Analogues: In some cases of hypoparathyroidism, when vitamin D metabolism is impaired, active vitamin D analogs may help regulate calcium and phosphorus levels. 
• Adjustment of Medications: Medications that can lower blood calcium levels, such as thiazide diuretics, should be avoided or carefully managed in individuals with hypoparathyroidism. 
• Emerging Treatments: Some newer treatments are being explored, such as recombinant parathyroid hormone (PTH) therapy, which aims to provide the missing hormone to help regulate calcium levels. 
• Lifestyle Management: Individuals with hypoparathyroidism are often educated about managing their condition, including dietary adjustments to optimize calcium intake, monitoring for symptoms of hypocalcemia, and understanding when to seek medical attention. 

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

use-of-a-non-pharmacological-approach-for-treating-parathyroidism

Dietary Modifications: 

For Primary Hyperparathyroidism: 

• Reducing dietary calcium intake might help alleviate some symptoms in cases where hypercalcemia is causing discomfort. However, this should be done under medical supervision, as calcium restriction can lead to complications. 

For Hypoparathyroidism: 

• Increasing dietary calcium intake can help compensate for the lack of parathyroid hormone. Foods rich in calcium include leafy greens, fortified foods, dairy products, and certain types of fish. 
• Maintaining a consistent calcium and vitamin D intake through diet can help stabilize blood calcium levels. 

Lifestyle Changes: 

For Both Types: 

• Regular physical activity and weight-bearing exercises can support bone health and improve overall well-being. 

For Primary Hyperparathyroidism: 

• Staying hydrated and avoiding dehydration can help prevent kidney stone formation, a common complication of hypercalcemia. 

Sun Exposure: 

For Both Types: 

• Adequate sun exposure can help the body produce vitamin D, essential for calcium metabolism. However, this should be balanced with the need to protect the skin from excessive sun exposure. 

Stress Management: 

For Both Types: 

• Managing stress through relaxation techniques, mindfulness, and stress-reduction practices can help mitigate symptoms and improve overall quality of life. 

Nutritional Counselling: 

• Individuals with parathyroid disorders may benefit from working with a registered dietitian specializing in endocrine disorders. They can help tailor dietary recommendations based on the specific needs of the individual. 

Role of Calcimimetics in the treatment of Hyperparathyroidism

Calcimimetics targets the calcium-sensing receptors (CaSR) located on the surface of parathyroid cells. These receptors regulate PTH secretion in response to changes in serum calcium levels. When serum calcium levels are high, the receptors sense it and signal a decrease in PTH secretion. 

Calcimimetics enhances the sensitivity of these receptors to extracellular calcium, effectively tricking the parathyroid glands into thinking that calcium levels are higher than they are. This leads to a reduction in PTH secretion, which subsequently lowers serum calcium levels. 

Role in Primary Hyperparathyroidism: 

• Primary hyperparathyroidism is characterized by excessive secretion of PTH from one or more parathyroid glands, leading to hypercalcemia. 
• Calcimimetics, like cinacalcet, are used in cases of primary hyperparathyroidism, especially when surgery is not immediately indicated or when surgical intervention is not possible or desired by the patient. 
• By reducing PTH secretion, calcimimetics can help lower serum calcium levels, alleviate hypercalcemia-related symptoms, and improve bone health. 

Role in Secondary Hyperparathyroidism and CKD: 

• Calcimimetics is also used in secondary hyperparathyroidism cases in patients with chronic kidney disease (CKD). 
• In CKD, the kidneys may have a reduced ability to regulate calcium and phosphorus levels, leading to elevated PTH levels and mineral imbalances. 
• Calcimimetics can help normalize PTH levels and manage secondary hyperparathyroidism in CKD patients. 

Role of Bisphosphonates in the treatment of Hyperparathyroidism

Primary hyperparathyroidism is characterized by excessive parathyroid hormone (PTH) secretion, leading to elevated calcium levels in the blood (hypercalcemia). 

Bisphosphonates are not used to directly lower PTH levels, which is the primary goal of treating hyperparathyroidism. Instead, they address the consequences of hyperparathyroidism on bone health. 

Hyperparathyroidism can lead to increased bone resorption, resulting in decreased bone density and an increased risk of fractures. 

Bisphosphonates work by inhibiting osteoclast activity, which is responsible for breaking down bone tissue. By reducing bone resorption, bisphosphonates can help improve bone density and reduce the risk of fractures. 

Role of Estrogen or Hormone Replacement Therapy in the treatment of hyperparathyroidism

Primary hyperparathyroidism is characterized by excessive parathyroid hormone (PTH) secretion, leading to elevated calcium levels in the blood (hypercalcemia). 

Postmenopausal women are more commonly affected by primary hyperparathyroidism, which might be related to changes in hormonal status. 

Estrogen, a hormone that declines after menopause, plays a role in maintaining bone health and density. 

In postmenopausal women with primary hyperparathyroidism, estrogen or hormone replacement therapy (HRT) might be considered to address bone loss associated with hypercalcemia and high PTH levels. 

Role of Calcium Supplements in the treatment of Hypoparathyroidism

Calcium supplements are a cornerstone of therapy for this condition. Here’s how calcium supplements are used in the treatment of hypoparathyroidism: 

• Correcting hypocalcemia: Calcium supplements are administered to raise and maintain blood calcium levels within the normal range. This helps alleviate the symptoms of hypocalcemia, which can include muscle cramps, tingling, numbness, and seizures. 
• Preventing Tetany and Seizures: Hypocalcemia can lead to tetany (muscle spasms) and seizures. Calcium supplementation helps prevent these severe complications by maintaining appropriate calcium levels. 
• Supporting Bone Health:Adequate calcium intake is essential for maintaining bone health and preventing the development of osteoporosis and fractures. 
• Types of Calcium Supplements: Calcium supplements can be taken in various forms, including calcium carbonate and calcium citrate. They are available over-the-counter and by prescription. 

Role of Vitamin D analogues in the treatment of Hypoparathyroidism

Enhancing Calcium Absorption: 

• Vitamin D is essential for the absorption of calcium from the intestines. In hypoparathyroidism, where PTH levels are low, the body’s ability to absorb calcium from the diet is compromised. 
• Vitamin D analogs, such as calcitriol (the active form of vitamin D), can enhance the absorption of dietary calcium and help raise blood calcium levels. 

Regulating Calcium and Phosphate Levels: 

• Vitamin D analogs play a role in maintaining the balance between calcium and phosphate levels in the blood. 
• By promoting intestinal calcium absorption and reducing phosphate reabsorption in the kidneys, vitamin D analogs help manage both hypocalcemia and hyperphosphatemia. 

Bone Health: 

• Adequate calcium and phosphate levels are crucial for maintaining bone health and preventing bone-related complications, such as osteoporosis. 
• Vitamin D analogs contribute to bone health by improving calcium availability for bone mineralization. 

Types of Vitamin D Analogues: 

• Different vitamin D analogs are available, including calcitriol (1,25-dihydroxyvitamin D), the active form of vitamin D. 
• In some cases, doctors may prescribe other vitamin D analogs, such as alfacalcidol, which can be converted to calcitriol in the body. 

use-of-intervention-with-a-procedure-in-treating-parathyroidism

Interventional procedures are commonly used to treat parathyroid disorders, particularly in cases of primary hyperparathyroidism where surgical removal of the affected parathyroid gland(s) is required. The primary procedure used to address parathyroid disorders is called parathyroidectomy.  

Parathyroidectomy: 

• Parathyroidectomy is a surgical procedure involving removing one or more parathyroid glands. 
• It is the primary treatment for primary hyperparathyroidism caused by the overproduction of parathyroid hormone (PTH) due to an adenoma (benign tumor) in one of the parathyroid glands. 
• Parathyroidectomy aims to remove the abnormal gland(s) responsible for the excess secretion of PTH, thereby restoring normal calcium levels in the blood. 

• This procedure is performed under general anaesthesia, and different surgical techniques can be used, including traditional open surgery or minimally invasive approaches such as focused parathyroidectomy or video-assisted techniques. 

use-of-phases-in-managing-parathyroidism

The management of parathyroidism typically involves different phases aimed at diagnosing the condition, determining its underlying cause, initiating appropriate treatment, and providing ongoing care. Here are the general phases involved in managing parathyroid: 

Diagnostic Phase: 

In this phase, healthcare providers gather information about the patient’s medical history symptoms and perform diagnostic tests. 

Blood tests measure calcium, parathyroid hormone (PTH), and other relevant markers to assess whether hyperparathyroidism or hypoparathyroidism is present. 

Evaluation and Diagnosis: 

Once diagnostic tests are completed, healthcare providers analyze the results to determine the type of parathyroid disorder (primary, secondary, or tertiary hyperparathyroidism or hypoparathyroidism). 

Imaging studies like ultrasound, sestamibi scans, and potentially more advanced imaging are used to locate abnormal parathyroid glands or tumors. 

Determining Underlying Cause: 

For primary hyperparathyroidism, identifying the underlying cause, such as a parathyroid adenoma or hyperplasia, is essential for treatment planning. 

Identifying the underlying condition (usually kidney disease or vitamin D deficiency) is crucial for secondary hyperparathyroidism. 

Treatment Phase: 

Treatment varies based on the specific type of parathyroid disorder. 

Surgical removal of the affected gland(s) (parathyroidectomy) is often recommended in primary hyperparathyroidism due to an adenoma. 

For secondary hyperparathyroidism, addressing the underlying condition (e.g., kidney disease, vitamin D deficiency) is important to manage parathyroid hormone levels. 

In hypoparathyroidism, treatment includes calcium and vitamin D supplementation to manage low blood calcium levels. 

Surgical Phase: 

Surgical intervention, like parathyroidectomy, is commonly used in cases of primary hyperparathyroidism with significant symptoms or complications. 

This phase includes surgical planning, preoperative evaluations, and postoperative care. 

Postoperative Care: For patients who undergo surgery, postoperative monitoring of calcium and PTH levels is crucial to ensure that levels normalize without complications. 

Medication

Future Trends

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References

The parathyroid glands and vitamin D.ncbi.nlm.nih.gov 

The thyroid gland.ncbi.nlm.nih.gov