Syndrome of inappropriate secretion of adg

Syndrome of inappropriate secretion of adg

Syndrome of inappropriate secretion of ADH (SIADH) occurs due to the release of neoosmotically stimulated ADH. May be neurohypophyseal or ectopic. The predominant age is the elderly.


    • Neurohypophyseal
    • CNS diseases. Excessive release of ADH has been shown in patients with epileptic seizures, as well as in patients with TBI, brain tumors and mental illness.
    • Lung diseases. SNADH has been described in tuberculosis and bronchial asthma. The mechanism is believed to be due to stimulation of J-receptors in the pulmonary circulation, which leads to the release of ADH by the pituitary gland.
    • Primary and secondary adrenal insufficiency. Excessive release of ADH occurs due to lack of inhibition of ADH release by glucocorticoids
    • Hypothyroidism
    • Drug-unconditioned SADH
    • Chlorpropamide and clofibrate may increase the release of ADH and increase the susceptibility of the renal tubules to the effects of ADH
    • Thiazide diuretics directly release ADH
    • Psychoactive drugs (eg, phenytoin) increase secretion of ADH by the pituitary gland
    • Idiopathic SNADH (hydropectic syndrome, or Parkhon’s syndrome) is a syndrome of unclear etiology, characterized by increased activity of ADH and manifested by signs of fluid retention in the body (transient change in body weight, edema, periodic oliguria)
    • Ectopic SNADH has been observed in some tumors capable of producing an ADH-like peptide, such as oat cell lung carcinoma or Hodgkin’s disease. Pathogenesis. Excess ADH causes water retention and an increase in extracellular fluid volume, which is compensated by an increase in sodium excretion in the urine. Due to the excessive excretion of sodium in the urine, a clinically significant increase in fluid volume (i.e. edema or arterial hypertension) is not observed. However, due to water retention and sodium loss, hyponatremia develops, a cardinal sign of SIADH. With a reduction in water intake, no such sequence of events is observed, and a drop in serum sodium levels does not occur.

The clinical picture is determined by hyponatremia (p. 254)

Laboratory diagnostics

    • Hyponatremia with low serum osmolarity
    • Daily urinary sodium excretion greater than 20 mEq/L despite low serum sodium; urine osmolarity is higher than serum osmolarity. Other causes of hyponatremia (eg, reduced sodium intake) cause sodium retention in the kidneys, with excretion less than 20 mEq/L per day. Special Studies
    • Chest x-ray to exclude pulmonary pathology
    • MRI of the brain to exclude organic pathology.

Differential Diagnosis

    • Physiological overproduction of ADH during dehydration
    • Adrenal insufficiency
    • Edematous conditions (for example, heart failure, nephrotic syndrome, cirrhosis) occurring with hyponatremia.


    • Restriction of fluid intake to 500-1000 ml every day
    • Correction of hyponatremia (p. 254).

See also Hyponatremia

Reduction. SADH – syndrome of inappropriate secretion of ADH ICD.? 22.2? syndrome of inappropriate secretion of antidiuretic hormone Note. For the first time this syndrome was described in 1933 by Parkhon and associated it with a primary excess of ADH. Subsequently, the term Parhon’s syndrome began to refer to the idiopathic form of SADDH.

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