Antidiuretic hormone therapy

Vasopressin and its derivatives are used in die treatment of diabetes insipidus, a disease resulting from die failure of the pituitary to secrete vasopressin or from surgical removal of die pituitary. Diabetes insipidus is characterized by marked increase in urination (as much as 10 L in 24 hours) and excessive tiiirst by inadequate secretion of die antidiuretic hormone or vasopressin. Treatment with vasopressin therapy replaces die hormone in the body and restores normal urination and thirst Vasopressin may also be used for die prevention and treatment of postoperative abdominal distention and to dispel gas interfering with abdominal roentgenography. 

Oxcarbazepine Hyponatremia (serum sodium concentrations less than 125 mEq/L) has been reported and occurs more frequently during the first 3 months of therapy serum sodium concentrations should be monitored in patients receiving drugs that lower serum sodium concentrations (e.g., diuretics or drugs that cause inappropriate antidiuretic hormone secretion) or in patients with symptoms of hyponatremia (e.g., confusion, headache, lethargy, and malaise). Hypersensitivity reactions have occurred in approximately 25-30% of patients with a history of carbamazepine hypersensitivity and requires immediate discontinuation. 

Primary therapy is based on disease severity and type of hemorrhage.7 Most patients with mild to moderate disease and a minor bleeding episode can be treated with l-desamino-8-D-arginine vasopressin [desmopressin acetate (DDAVP)], a synthetic analog of the antidiuretic hormone vasopressin. DDAVP causes release of von Willebrand factor (vWF) and factor VIII from endogenous storage sites. This formulation increases plasma factor VIII levels by three- to fivefold within 30 minutes. The recommended dose is 0.3 mcg/kg intravenously (in 50 mL normal saline infused over 15 to 30 minutes) or subcutaneously or 300 meg intranasally via concentrated nasal spray every 12 hours. Peak effect with intranasal administration occurs 60 to 90 minutes after administration, which is somewhat later than with intravenous administration. Desmopressin infusion may be administered daily for up to 2 to 3 days. Tachyphylaxis, an attenuated response with repeated administration, may occur after several doses.8... 

Li+ also inhibits several hormone-stimulated adenylate cyclases which, in some cases, appear to be related to side effects of Li+ therapy. For instance, Li+ inhibits the hydro-osmotic action of vasopressin, the antidiuretic hormone which increases water resorption in the kidney [136]. This effect is associated with polyuria, a relatively harmless side effect sometimes experienced with Li+ treatment, which arises from the inability of the kidney to concentrate urine. Li+ has been shown to inhibit vasopressin-stimulated adenylate cyclase activity in renal epithelial cells. Additionally, Li+ is reported to enhance the vasopressin-induced synthesis of prostaglandin E2 (PGE2) in vitro in kidney. PGE2 inhibits adenylate cyclase activity by stimulation of Gj, and, therefore, this effect may contribute to the Li+-induced polyuria. 

Aslam MK, Gnaim C, Kutnick J, Kowal RC, McGuire DK. Syndrome of inappropriate antidiuretic hormone secretion induced by amiodarone therapy. Pacing Clin Electrophysiol 2004 27(6 Pt l) 831-2. 

Cutting HO. Inappropriate secretion of antidiuretic hormone secondary to vincristine therapy. Am J Med 1971 51(2) 269-71. 

Garrett CA, Simpson TA Jr. Syndrome of inappropriate antidiuretic hormone associated with vinorelbine therapy. Ann Pharmacother 1998 32(12) 1306-9. 

After several months of continuous therapy with lithium, diabetes insipidus and goiter may develop. The kidney tubules then become insensitive to the action of antidiuretic hormone, and its administration is ineffective. Either a dose reduction or discontinuation of the lithium corrects this side effect without leaving any residual pathology. In the... 

In laboratory animals, papillary necrosis due to non-narcotic analgesic has been extremely difficult to produce. However, papillary necrosis has been demonstrated following administration of 2-bromoethylamine 2-bromoethylamine has been used to demonstrate the role of urinary concentrating mechanisms in the etiology of 2-bromoethylamine-induced papillary necrosis. Maneuvers that produce large volumes of dilute urine, such as diuretic therapy, lack of antidiuretic hormone (Brattleboro rats), or volume expansion with 5% glucose, prevent papillary necrosis due to... 

Zullino D, Brauchli S, Horvath A, Baumann P. Inappropriate antidiuretic hormone secretion and rhabdo-myolysis associated with citalopram. Therapie 2000 55(5) 651-2. 

Desmopressin replacement therapy is the first choice. Thiazide diuretics (and chlortalidone) also have paradoxical antidiuretic effect in diabetes insipidus. That this is not due to sodium depletion is suggested by the fact that the nondiuretic thiazide, diazoxide (see Index), also has this effect. It is probable that changes in the proximal renal tubule result in increased reabsorption and in delivery of less sodium and water to the distal tubule, but the mechanism remains incompletely elucidated. Some cases of the nephrogenic form, which is not helped by antidiuretic hormone, may be benefited by a thiazide. 

DeRubertis FR, Michelis MF, Beck N, Davis BB. Complications of diuretic therapy severe alkalosis and syndrome resembling inappropriate secretion of antidiuretic hormone. Metabolism 1970 19(9) 709-19. 

The biochemical parameters of the patients are also affected by antimonial therapy. Marsden et al. [21] observed evidences of arthritis and raised transaminases with tender hepatomegaly when a long course (20 mg/kg of Sb for 85 days) was given to a nonresponding patient with mucosal leishmaniasis. The renal toxicity of Sb also influences the antidiuretic hormone (ADH) function and cell respiration [8]. A transient increase in the levels of alanine aminotransferase, lactate dehydrogenase, aspartate aminotransferase, triglycerides, creatine phosphokinase and alkaline phosphatase has also been observed in patients receiving pentostam at a dose of 10 mg/kg for 10 days [8]. 

I Adverse Effects. Side effects (see Table 54—6) of carbamazepine may fluctuate daily, paralleling the rise and decline of serum concentrations. The side-effect profile also may follow a circadian rhythm. Neurosensory side effects (e.g., diplopia, blurred vision, nystagmus, ataxia, unsteadiness, dizziness, and headache) are the most common, occurring in 35% to 50% of patients. These side effects are more common during initiation of therapy and may dissipate with continued treatment. Patients have variable threshold concentrations for the occurrence of CNS side effects. If the carbamazepine serum concentration is kept below the individual threshold, the CNS side effects can be minimized. Dosage manipulation, including the use of the controlled- or sustained-release preparations, should be tried before the patient is considered to be intolerant of carbamazepine. Carbamazepine may induce a hyponatremic hyposmolar condition that is similar to the syndrome of inappropriate antidiuretic hormone secretion. The incidence may increase with age. Periodic determinations of serum sodium concentration are recommended, especially in the elderly." ... 

Antidiuretic hormone - replacement therapy in diabetes insipidus... 

DRUGS USED IN THE THERAPY OF SYNDROME OF INAPPROPRIATE SECRETION OF ANTIDiURETIC HORMONE (SIADH)... 

Alonso Navarro H, Sdnz-Aiz A, Izquierdo L, Jimenez Jim6nez FJ. Syndrome of inappropriate antidiuretic hormone secretion possibly associated with amantadine therapy in Parkinson disease. Clin Neuropharmacol 2009 32(3) 167-8. 

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