Parathormone (Parathyroid Hormone, PTH)

Overview and Clinical Significance

Parathyroid Hormone (PTH), also known as parathormone, is a key regulator of calcium homeostasis, influencing bone metabolism, kidney function, and vitamin D activation.

Clinical Significance

  • Calcium & Phosphorus Balance: PTH maintains blood calcium levels by stimulating bone resorption, renal calcium retention, and intestinal calcium absorption.
  • Bone Health & Osteoporosis: Abnormal PTH levels contribute to osteoporosis, fractures, and metabolic bone disorders.
  • Hyperparathyroidism & Hypoparathyroidism:
    • High PTH (Hyperparathyroidism) leads to hypercalcemia, kidney stones, and bone demineralization.
    • Low PTH (Hypoparathyroidism) causes hypocalcemia, muscle spasms, and neurological symptoms.
  • Kidney Function & Vitamin D Activation: PTH enhances renal calcium reabsorption and stimulates vitamin D synthesis, supporting bone mineralization.
  • Diagnostic & Therapeutic Applications: PTH testing helps assess parathyroid disorders, calcium metabolism, and endocrine health.

PTH is a critical hormone in bone health, calcium regulation, and metabolic balance.

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Parathyroid Disorders and Associated Conditions

  • Primary Hyperparathyroidism – Often due to an adenoma or hyperplasia of the parathyroid glands, resulting in excess PTH and hypercalcemia.
  • Secondary Hyperparathyroidism – Commonly seen in chronic kidney disease; when low calcium or vitamin D levels stimulate the parathyroids chronically, PTH increases as a compensatory mechanism.
  • Autoimmune or Post-Infectious Damage – Although less common, autoimmune processes or surgical removal/damage (often following neck surgery) may eventually affect PTH secretion.

Age Considerations

  • ChildrenCongenital disorders (such as DiGeorge syndrome) can lead to hypoparathyroidism rather than excess PTH.
  • Older Adults – Persistent secondary hyperparathyroidism may contribute to bone loss and cardiovascular risks.

Hypoparathyroidism and Associated Effects

  • Causes – Can result from autoimmune destruction, surgical removal (post-thyroidectomy), or congenital defects. Accompanied by hypocalcemia and hyperphosphatemia.

Life-Long Effects

  • Neonates/Young ChildrenLow PTH may impair neuromuscular stability and bone development.
  • Adults – Can lead to symptoms like muscle cramps and tingling.

More Info

Related

Electrolyte and Mineral Markers

This group of markers evaluates essential ion and mineral levels in the blood, each playing a critical role in maintaining physiological balance:

  • Blood Phosphorus: Reflects circulating phosphate levels, crucial for bone health and energy metabolism, influenced by renal excretion and hormonal control.
  • Plasma Potassium: Indicates the concentration of potassium, vital for proper nerve function and muscle contraction.
  • Plasma Sodium: Measures the main extracellular ion responsible for osmotic balance and fluid distribution.
  • Serum Calcium: Reveals calcium levels that support neuromuscular activity, cellular signaling, and bone health.
  • Serum Magnesium: Assesses magnesium status, important for enzymatic reactions and muscle and nerve function.
  • Lithium: Although primarily of therapeutic interest, its circulating levels interact with water and electrolyte balance, mirroring renal handling similar to other electrolytes.

Together, these markers provide a comprehensive view of the body's mineral balance and electrolyte function.

Hormonal Regulators of Electrolytes and Minerals

  • Parathormone (PTH) adjusts calcium and phosphate levels via its influence on bone resorption and kidney reabsorption
  • Antidiuretic Hormone (ADH) modulates water reabsorption in the kidneys to indirectly control plasma sodium levels and overall fluid balance. Together, these markers provide a

Renal Waste Clearance

This is a comprehensive view of kidney performance by evaluating how effectively the organs eliminate metabolic waste and regulate key electrolytes and minerals:

  • Urine Urea:
    Indicates the kidney’s efficiency in excreting urea, a byproduct of protein metabolism.

  • Serum Creatinine & Urine Creatinine:
    Provide essential insights into kidney filtration function by measuring the byproducts of muscle metabolism.

  • Urine Phosphorus:
    Reflects the renal handling of phosphate, linking kidney function to overall mineral and bone metabolism.

  • Urine Potassium:
    Assesses the ability of the kidneys to eliminate potassium, a crucial electrolyte for nerve and muscle function.

  • Serum Ammonia & Urine Ammonia:
    Together, these markers demonstrate how well the kidneys manage and eliminate ammonia, with serum levels reflecting systemic processing and urine levels indicating renal clearance capacity.

These markers collectively detail the kidneys’ proficiency in waste clearance as well as their role in maintaining electrolyte and mineral balance, thereby providing valuable insights into overall renal health.

Hormone Regulators of Renal Waste Clearance

  • Antidiuretic Hormone (ADH): Produced by the pituitary gland, ADH regulates water reabsorption in the kidneys, influencing urine concentration and fluid balance
  • Parathyroid Hormone (PTH): Secreted by the parathyroid glands, PTH modulates calcium and phosphate levels through its effects on bone resorption and renal reabsorption, directly affecting mineral clearance.

All Markers