OVERVIEW
Antidiuretic hormone (ADH) hypersecretion syndrome is due to multiple causes of persistent secretion or hyperactive action of endogenous antidiuretic hormone, ADH-like substances, which impairs water excretion, resulting in hyponatremia, water retention, and related clinical manifestations.
Etiology
The most common cause is due to the synthesis and autonomous release of ADH by tumor tissues, which accounts for about 80% of the syndrome, mainly lung oat cell carcinoma, pancreatic cancer, duodenal cancer and lymphoma. Other neuropathies such as pneumonia, tuberculosis and trauma, inflammation and tumor affecting the function of hypothalamus-neuropituitary gland can also cause excessive ADH secretion.
Symptoms
In addition to the manifestations of the original disease, the main manifestations of this syndrome are water retention and hyponatremia, generally the serum sodium is lower than 130mmol/L. When the blood sodium is <120mmol/L, there is weakness, loss of appetite, nausea and vomiting, lethargy, irritability, and even mental disorders, and when the blood sodium is <110mmol/L, there are convulsions, coma and even death.
Hyponatremia, generally low 130mmol/L, but increased urinary sodium, often greater than 20mmol/L. Urinary osmolality is higher than plasma osmolality. No hypovolemic manifestations. Strict restriction of water intake corrects low blood sodium, low plasma osmolality and high urinary sodium. Manifestations of primary disease may be detected.
Examination
Check for blood sodium less than 130 mmol/L and urine sodium usually greater than 30 mmol/L.
Diagnosis
Diagnosis can be made on the basis of history, clinical symptoms and laboratory information.
Differential diagnosis
This syndrome needs to be differentiated from water retention and/or hyponatremia due to renal tubular pathology, hypoadrenocorticism, chronic heart failure, cirrhotic ascites, hypertonic diuretics, and hypothyroidism.
Complications
Convulsions, coma and even death in severe cases.
Treatment
1. Medication
Therapeutically, restriction of water intake is very important for symptom control. In mild and moderate cases, daily water intake should be limited to the sum of unobtrusive loss and urinary excretion (0.8-1.0L), and the symptoms can be improved, body weight can be decreased, serum sodium and osmolality can be increased, and urinary sodium excretion can be decreased. In severe cases, 3% sodium chloride solution should be titrated slowly intravenously at a rate of 1 to 2 ml/kg per hour to gradually elevate blood sodium over several hours, and tachycardia drainage may also be added. Application of anti-ADH drugs, such as tolvaptan tablets can hinder the water reabsorption of ADH into the renal tubules. Lithium salts have a similar effect, but are more toxic.
2. Treatment of etiology
The treatment principle of endocrine disease is to eradicate the cause of the disease or correct the dysfunction and metabolic disorder caused by pathophysiology. The most fundamental treatment for this disease is etiological treatment, and malignant tumors need to be surgically resected, supplemented by radiotherapy and chemotherapy.
Prevention
Many endocrine diseases can be prevented, such as endemic goiter, postpartum anterior pituitary hypopituitarism, adrenal tuberculosis leading to chronic hypoadrenocorticism and thyroid crisis, etc.