- In-Stock Tumor Cell Lines
- Human Orbital Fibroblasts
- Human Microglia
- Human Pulmonary Alveolar Epithelial Cells
- Human Colonic Fibroblasts
- Human Type II Alveolar Epithelial Cells
- Human Valvular Interstitial Cells
- Human Thyroid Epithelial Cells
- C57BL/6 Mouse Dermal Fibroblasts
- Human Alveolar Macrophages
- Human Dermal Fibroblasts, Adult
- Human Lung Fibroblasts, Adult
- Human Retinal Muller Cells
- Human Articular Chondrocytes
- Human Retinal Pigment Epithelial Cells
- Human Pancreatic Islets of Langerhans Cells
- Human Kidney Podocyte Cells
- Human Renal Proximal Tubule Cells
The Role of PTH and Calcium Homeostasis
Parathyroid hormone (PTH) is a critical regulator of calcium balance in the human body. Produced by the parathyroid glands, intact PTH helps maintain stable calcium concentrations by increasing calcium release from bone, enhancing absorption in the intestine, and reducing excretion by the kidneys. When PTH levels become abnormally high, the finely tuned system of calcium regulation is disrupted, leading to hyperparathyroidism—a disorder with systemic skeletal and metabolic consequences.
Hyperparathyroidism and Its Clinical Impact
Hyperparathyroidism is characterized by excessive secretion of PTH, most commonly due to a parathyroid adenoma. This benign tumor accounts for nearly 80–85% of primary hyperparathyroidism cases. Elevated PTH levels cause hypercalcemia, which may present with bone pain, kidney stones, gastrointestinal discomfort, and neurocognitive symptoms. Secondary hyperparathyroidism, in contrast, often arises in patients with chronic kidney disease, where persistent hypocalcemia drives parathyroid overactivity. Accurate measurement of intact PTH levels is therefore essential for diagnosis, disease monitoring, and treatment planning.
Parathyroid Adenoma and Surgical Management
Among treatment strategies, surgical parathyroid removal remains the gold standard for managing parathyroid adenoma. Resection of the affected gland normalizes PTH levels, restores calcium balance, and significantly improves patient outcomes. Advances in imaging and intraoperative PTH monitoring now allow for more precise and minimally invasive parathyroidectomy procedures. Postoperative monitoring of intact PTH and serum calcium is critical to confirm surgical success and prevent recurrence or hypocalcemia.
Research Models for Advancing Hyperparathyroidism Studies
Understanding the molecular mechanisms behind parathyroid adenomas and hyperparathyroidism requires advanced experimental systems. Researchers are investigating the genetic drivers of abnormal PTH secretion, calcium-sensing receptor dysfunction, and tumorigenesis pathways. Reliable in vitro and in vivo models are indispensable for studying parathyroid biology and for developing novel therapies beyond surgery.
AcceGen’s Contribution to Endocrine Research
At AcceGen, we support scientists exploring the complexities of endocrine disorders such as hyperparathyroidism by providing rigorously validated cellular models and molecular tools. AcceGen offers Human Parathyroid Cells (ABC-TC110L) and Human Parathyroid Disease Peripheral Blood Mononuclear Cells (PBMCs), enabling precise study of PTH regulation, calcium signaling, and endocrine tumorigenesis.
Our high-quality products help researchers investigate PTH regulation, calcium signaling pathways, and tumor biology with reproducibility and precision. By integrating AcceGen’s solutions into your workflow, you can accelerate the discovery of new diagnostic biomarkers and potential therapeutic strategies that complement parathyroid removal.
Conclusion: From Bench to Bedside
The study of hyperparathyroidism—from disrupted PTH levels and calcium imbalance to parathyroid adenoma diagnosis and surgical removal—continues to evolve with growing clinical and research insights. With AcceGen’s advanced resources, investigators can deepen their understanding of parathyroid disease and translate discoveries into improved patient care.
Explore AcceGen’s endocrine research portfolio and empower your next breakthrough in parathyroid biology.
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