Journal of Clinical & Experimental Pathology
Open Access

The parathyroid glands are small and barely noticeable, but they are essential to the body's ability to maintain calcium homeostasis. The production of Parathyroid Hormone (PTH), which controls blood calcium levels, is attributed to these four tiny glands, which are usually found on the posterior surface of the thyroid gland. A variety of clinical symptoms can arise from disorders affecting the parathyroid glands, which can cause substantial disruptions in the calcium balance. The parathyroid glands are typically four in number, although variations in their location and number can occur. They are named based on their anatomical position relative to the thyroid gland: Two superior (or upper) parathyroid glands and two inferior (or lower) parathyroid glands. These glands are responsible for secreting Parathyroid Hormone (PTH), a key regulator of calcium and phosphate metabolism. PTH acts primarily on bone, kidney, and intestine to regulate calcium levels in the blood. It stimulates the release of calcium from bone, enhances calcium reabsorption in the kidneys, and promotes the production of activated vitamin D, which facilitates calcium absorption in the intestine. Through these actions, PTH helps maintain serum calcium levels within a narrow physiological range, crucial for various physiological processes, including neuromuscular function, bone health, and cardiac function [1-3].

Primary Hyperparathyroidism disorder occurs due to excessive secretion of PTH from one or more parathyroid glands, typically caused by a benign tumor or hyperplasia of the glands. Primary hyperparathyroidism leads to elevated serum calcium levels (hypercalcemia) and low serum phosphate levels (hypophosphatemia). Patients may present with symptoms such as fatigue, weakness, bone pain, kidney stones, and gastrointestinal disturbances. Long-term untreated hypercalcemia can result in osteoporosis, kidney damage, and cardiovascular complications. Secondary hyperparathyroidism develops as a compensatory response to chronically low serum calcium levels, often seen in conditions such as Chronic Kidney Disease (CKD) or vitamin D deficiency. In this condition, the parathyroid glands become hyperplastic and overproduce PTH in an attempt to maintain normal serum calcium levels. Secondary hyperparathyroidism can lead to bone demineralization, renal osteodystrophy, and cardiovascular complications. Tertiary hyperparathyroidism typically occurs as a complication of long-standing secondary hyperparathyroidism, where the parathyroid glands become autonomously overactive; disregarding the regulatory mechanisms that initially caused their hyperplasia. This condition often develops in patients with advanced CKD who undergo renal transplantation [4,5]. Tertiary hyperparathyroidism is characterized by persistently elevated PTH levels and hypercalcemia, despite successful kidney transplantation. Hypoparathyroidism results from inadequate secretion of PTH, leading to decreased serum calcium levels (hypocalcemia) and increased serum phosphate levels (hyperphosphatemia). This condition can be congenital or acquired, with causes including surgical removal of the parathyroid glands, autoimmune destruction, or genetic disorders such as DiGeorge syndrome. Hypoparathyroidism manifests with symptoms such as muscle cramps, paresthesia, seizures, and cardiac arrhythmias due to neuromuscular irritability and impaired calcium signaling. Diagnosing parathyroid disorders involves a combination of clinical assessment, biochemical tests, and imaging studies [6,7].

Measurement of serum calcium, phosphate, and PTH levels is essential for diagnosing parathyroid disorders. In primary hyperparathyroidism, serum calcium is elevated, while PTH levels are typically elevated or inappropriately normal. Secondary hyperparathyroidism is characterized by elevated PTH levels with either normal or low serum calcium levels. Imaging modalities such as ultrasound, technetium-99 m sestamibi scintigraphy, and more recently, Positron Emission Tomography (PET) scans with radiolabeled tracers, can aid in localizing abnormal parathyroid glands. These imaging techniques help identify the presence of adenomas, hyperplastic glands, or ectopic parathyroid tissue. Dual-Energy X-Ray Absorptiometry (DXA) scans are useful for assessing bone mineral density in patients with primary hyperparathyroidism or hypoparathyroidism, aiding in the diagnosis of osteoporosis or osteopenia. The management of parathyroid disorders depends on the underlying etiology and clinical manifestations. Surgical removal (parathyroidectomy) of the abnormal parathyroid glands is the definitive treatment for primary hyperparathyroidism, particularly in symptomatic patients or those with complications such as nephrolithiasis or osteoporosis. Minimally invasive techniques such as focused parathyroidectomy or intraoperative parathyroid hormone monitoring can help localize and remove the diseased glands with minimal morbidity [8-10].

Pharmacological interventions may include phosphate binders, vitamin D analogs, and calcimimetic agents to control PTH secretion and maintain serum calcium and phosphate levels within the target range. Treatment often involves surgical intervention to remove hyperplastic parathyroid glands, particularly in patients with persistent hypercalcemia and biochemical evidence of autonomous PTH secretion [11].

Management focuses on correcting hypocalcemia and minimizing symptoms while avoiding hypercalcemia and hypercalciuria. This typically involves oral calcium supplementation and active vitamin D analogs to maintain serum calcium levels within the low-normal range and promote intestinal calcium absorption. Close monitoring of serum calcium, phosphate, and urinary calcium excretion is essential to prevent complications such as renal calcifications and nephrolithiasis. A thorough understanding of parathyroid anatomy, physiology, and pathology is crucial for accurate diagnosis and optimal management of these disorders, ultimately improving patient outcomes and quality of life.

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