Desmopressin Tablets

Central Diabetes Insipidus (CDI) is a rare endocrine disorder caused by dysfunction of the hypothalamic-neurohypophyseal axis, leading to insufficient or absent secretion of Arginine Vasopressin (AVP), which subsequently reduces renal water reabsorption. Its core clinical manifestations include extreme thirst, polyuria, and hypotonic urine, which severely impair daily life and quality of life.
As a synthetic AVP analogue, Desmopressin Tablets have become a first-line drug for the clinical treatment of central diabetes insipidus due to their convenient oral administration, precise dosing, and high safety profile. They effectively replace endogenous AVP, correct water metabolism disorders, and help patients return to a normal daily life.

The active ingredient of the product is desmopressin acetate, a polypeptide drug obtained through structural modification of natural arginine vasopressin. Its mechanism of action is highly consistent with endogenous AVP, but it has stronger antidiuretic activity and weaker vasoconstrictive side effects, making it more suitable for long-term clinical use.
The core pathological mechanism of central diabetes insipidus is damage to the neurons of the supraoptic and paraventricular nuclei of the hypothalamus, leading to insufficient synthesis or secretion of AVP. This reduces water permeability in the distal renal tubules and collecting ducts, which cannot effectively reabsorb water from the primary urine, resulting in the excretion of large volumes of hypotonic urine and symptoms such as polyuria and polydipsia.

As a synthetic analogue of AVP, it specifically binds to the V2 receptors on the epithelial cells of the renal collecting ducts, activates adenylate cyclase, and promotes increased intracellular cyclic adenosine monophosphate (cAMP) production. This in turn drives the translocation of aquaporin-2 (AQP2) to the luminal membrane of the collecting duct epithelial cells, enhancing renal water reabsorption, reducing urine output, increasing urine osmolality, and lowering plasma osmolality. In this way, it effectively relieves the core symptoms of extreme thirst and polyuria in patients with central diabetes insipidus.
Compared with natural AVP, the antidiuretic-to-pressor ratio of it is approximately 2000–3000 times higher. Its antidiuretic effect lasts longer, reaching 8–12 hours, and it has almost no significant vasoconstrictive or blood pressure-elevating side effects, providing superior safety and supporting long-term regular use.

Desmopressin Tablets demonstrate clear clinical efficacy in the treatment of central diabetes insipidus, effectively improving core symptoms, restoring water metabolic balance, and enhancing quality of life. Efficacy is evaluated based on clinical symptom improvement, laboratory parameter recovery, and long-term prognosis.

For clinical symptom improvement:A distinct antidiuretic effect appears in most patients within 1–1.5 hours after administration. 24-hour urine output is significantly reduced, extreme thirst and polydipsia are relieved, nocturnal frequency is decreased, and sleep quality improves. A multicenter, open-label dose-titration study showed that in 20 CDI patients aged 6–75 years switched from nasal the product to oral the product, mean 24-hour urine volume remained unchanged, and urine osmolality, hourly voiding rate, and specific gravity remained within normal ranges, indicating similar antidiuretic efficacy and better patient acceptance of the oral formulation.

For laboratory parameter recovery:Urine osmolality increases markedly, plasma osmolality gradually normalizes (normal: 280–310 mOsm/kg·H₂O), and serum sodium remains within the normal range (135–145 mmol/L), effectively correcting water dysregulation. A long-term study of 46 CDI patients treated for 12–44 months showed no loss of efficacy or detectable serum antibodies to it, confirming stable long-term efficacy and no significant drug resistance.

For long-term prognosis:Regular use effectively prevents complications such as dehydration and electrolyte disturbances, reduces the risk of coma and shock due to severe dehydration, and restores normal daily function. Compared with nasal sprays and injections, the product avoid nasal irritation and injection pain, are portable, and greatly improve adherence, especially for long-term home-based patients.

The most critical adverse reactions to monitor are water retention and hyponatremia. Insufficient fluid restriction or excessive dosing may cause fluid accumulation, leading to hyponatremia, presenting as headache, vomiting, confusion, seizures, and, in severe cases, life-threatening conditions.
For asymptomatic hyponatremia:Immediate temporary discontinuation, strict fluid restriction, and close monitoring of serum sodium are required.
For symptomatic hyponatremia:In addition to stopping the drug and restricting fluids, intravenous isotonic sodium chloride solution should be administered to correct electrolyte imbalance.

In cases of severe seizures or impaired consciousness:Diuretics (e.g., furosemide) should be added to promote water excretion and relieve symptoms.
Rare adverse reactions include skin allergy and mood disturbances. If allergic reactions (rash, laryngeal edema) occur, the drug should be discontinued immediately and anti-allergic treatment initiated.