ADH hypersecretion syndrome

Introduction to ADH hypersecretion syndrome Antidiuretic Hormone (ADH) hypersecretion syndrome is caused by a variety of causes of endogenous vasopressin or similar ADH substances, causing water excretion disorders, resulting in hyponatremia, water retention and related Clinical manifestations. It is usually caused by tumor tissue synthesis and autonomous release of ADH, accounting for about 80% of the intrinsic, mainly manifested as water retention and hyponatremia. basic knowledge The proportion of the disease: 0.02%-0.03% (the above is the incidence rate among the middle-aged and elderly people over 50 years old) Susceptible people: good for young men and women Mode of infection: non-infectious Complications: convulsions and convulsions

The cause of excessive secretion of ADH syndrome

The most common cause is the synthesis of tumor tissue and the spontaneous release of ADH, accounting for about 80% of the intrinsic, mainly for lung oat cell cancer, pancreatic cancer, duodenal cancer and lymphoma, etc. Others such as pneumonia, tuberculosis and Trauma, inflammation, tumor and other neuropathy that affect hypothalamic-neuronal pituitary function can also cause excessive secretion of ADH.

ADH hypersecretion syndrome prevention

Many endocrine diseases can be prevented, such as endemic goiter, postpartum pituitary dysfunction, adrenal tuberculosis-induced chronic adrenal insufficiency and thyroid crisis, etc. The principles of treatment of endocrine diseases are mainly to eradicate the cause or correct pathophysiology. Caused by dysfunction and metabolic disorders.

ADH hypersecretory syndrome complications Complications, convulsions and convulsions

There are convulsions, coma and even death when the condition is heavy.

ADH hypersecretion syndrome symptoms common symptoms nausea convulsions hyponatremia appetite loss coma

In addition to the performance of the primary disease, the main manifestations are water retention and hyponatremia, the general serum sodium is less than 130mmol / L, when the blood sodium <120mmol / L, there is weakness, loss of appetite, nausea and vomiting, lethargy, irritability Even mental disorders, when the blood sodium <110mmol / L, convulsions, coma and even death, because the water retention generally does not exceed 3 ~ 4 liters, and part of the water transferred to the cells, it is generally no edema.

1. Hyponatremia, generally 130mmol / L, but increased urinary sodium, often greater than 20mmol / L.

2. Urine osmotic pressure is higher than plasma osmotic pressure.

3. No low blood volume performance.

4. Strictly limit the amount of water to correct low blood sodium, low plasma osmotic pressure and high sodium.

5. The performance of the primary disease can be found.

Examination of ADH hypersecretion syndrome

(1) Serum sodium is generally less than 130 mmo/L.

(2) Plasma osmotic pressure <270mOsm/kgH2O.

(3) The urine osmotic pressure is inappropriately increased, and the urine osmotic pressure is greater than the blood osmotic pressure when the plasma osmotic pressure is decreased.

(4) Increased urinary sodium excretion >20mmol/L.

(5) The carbon dioxide binding force is normal or slightly low, and the serum chloride is low.

(6) Serum urea nitrogen, creatinine, uric acid, and albumin are often reduced.

(7) AVP levels in plasma and urine increased, plasma AVP was greater than 1.5 pg/ml (blood AVP value <0.5-1.5 pg/ml when blood osmotic pressure <280 mOsm/kg H2O).

(8) The thyroid, liver, kidney, heart and adrenal cortex function normally.

Diagnosis and differentiation of ADH hypersecretion syndrome

diagnosis

Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.

Differential diagnosis

Intrinsic needs to be differentiated from renal tubular lesions, adrenal insufficiency, chronic heart failure, cirrhosis ascites, application of hypertonic diuretics, and hypothyroidism caused by water retention and/or hyponatremia.

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