Parkhon's Syndrome

Excessive vasopressin production (ADH) may be adequate (occur as a result of a physiological reaction of the posterior pituitary in response to appropriate stimuli) and inadequate. Adequate hypersecretion of vasopressin (in response to blood loss , diuretics , hypovolemia , hypotension , etc.) has no independent clinical significance and is aimed at maintaining water-salt homeostasis in case of its disorders ^[4] .

Parhon's syndrome ( diabetes insipidus diabetes ) is characterized by hyponatremia , blood plasma hyposmolarity and excretion of sufficiently concentrated urine (urine osmolarity usually exceeds 300 mOsm / kg). The syndrome may be due to excessive unregulated secretion of ADH (independent of osmotic and non-osmotic stimuli) or an increase in the action of ADH on the cells of the distal nephron . An increased level of ADH was observed in 95% of patients with hyponatremia ^[5] (the most common cause of hyponatremia).

Syndrome of inadequate production of vasopressin may be due to the pathology of the neurohypophysis or be ectopic ^[4] .

Reasons contributing to the development of Parkhon's syndrome ^[5] :

• tumors, especially small cell lung cancer ;
• non-tumor lung diseases: pneumonia , tuberculosis , bronchial asthma , pneumothorax , cavity or abscess , breathing under constant positive pressure, pleural empyema , cystic fibrosis ;
• any lesions of the central nervous system , including volumetric processes, infections, injuries, vascular and metabolic disorders;
• some drugs can cause the syndrome by stimulating the secretion of ADH or enhancing its effect on the collecting tubules.

Hyponatremia with ADH hypersecretion syndrome is caused by an increase in extracellular fluid volume and is highly dependent on water intake - with normal or reduced fluid intake, even very intense secretion of vasopressin does not lead to hyponatremia. On the other hand, increased fluid intake against the background of the most insignificant violation of the regulation mechanism of vasopressin secretion or the regulation mechanism of urine concentration can cause an inadequate ADH secretion syndrome. In most patients, ADH or ADH-like peptides are constantly secreted, despite the hypoosmolarity of extracellular fluid ^[5] .

Permanent secretion of ADH or an increase in the sensitivity of kidney cells to the action of ADH causes a delay in fluid intake, hyponatremia, and a slight increase in extracellular fluid volume, which inhibits the absorption of sodium in the proximal renal tubules and leads to natriuresis. In addition, an increase in bcc stimulates the secretion of atrial natriuretic hormone , which also promotes natriuresis. In case of severe hyponatremia, diluted urine may be released. The excretion of uric acid is enhanced - hypouricemia develops, often observed with ADH hypersecretion syndrome ^[5] .

It is characterized by hyponatremia , hypoosmolarity of blood plasma and the removal of sufficiently concentrated urine (osmolarity of urine> 300 mOsm / kg). The leading symptoms are water intoxication, the severity of which depends on the degree and rate of development of hyponatremia and hyperhydration. The concentration of ADH in the blood plasma exceeds the level that normally corresponds to the measured plasma osmolality. Adrenal and thyroid function is not impaired, often hypouricemia is detected ^[2] .

Patients complain of poor urination against the background of the usual drinking regimen and weight gain. In this case, peripheral edema, as a rule, is absent or insignificant due to the loss of sodium . A significant decrease in the concentration of sodium in blood plasma (up to 125 mmol / L or lower) leads to the development of symptoms of water intoxication: lethargy, headache , anorexia , nausea , vomiting , depression , sleep disturbance or drowsiness, muscle weakness, muscle cramps, cramps . A further decrease in sodium concentration (below 120 mmol / L) and plasma osmolarity below 250 mOsmol / L leads to confusion, disorientation, psychosis , doubt , convulsions , a decrease in body temperature , loss of consciousness, coma - these symptoms indicate the development of cerebral edema . The degree of hyponatremia does not always correlate with clinical symptoms - the severity of the condition largely depends on the speed and intensity of the increase in hypoosmolarity in the cerebral fluid ^[3] .

It is based on clinical symptoms (oliguria with a high specific gravity of urine, weight gain, lack of thirst, the presence of symptoms of intoxication) and the detection of hyponatremia in the patient (below 130 mmol / l) and plasma hypoosmolarity (below 275 mOsmol / l), while urine osmolarity exceeds osmolarity of blood plasma. Nevertheless, it is necessary to exclude the causes that can cause similar biochemical disorders (taking diuretics , prolonged vomiting and diarrhea , severe burns , acute pancreatitis , cardiovascular failure , nephrotic syndrome , cirrhosis ). Determining the level of vasopressin in blood plasma has no independent diagnostic value - it is much more accessible and informative to conduct a sample with a water load (intake for 20-30 minutes of water based on 20 ml / kg body weight). Normally, a patient in a lying position, for 4-5 hours, allocates up to 80% of the volume of fluid drunk, and with Parkhon's syndrome, not more than 40% of the volume of fluid consumed ^[3] . The adrenal and thyroid function is not impaired, often defined hypouricemia ^[5] .

The diagnosis of Parkhon's syndrome is verified by the presence of hyponatremia against the background of urine output with a low specific gravity. In this case, pathology should be excluded ^[5] :

• thyroid gland ;
• adrenal glands ;
• liver
• heart
• kidney and
• hypovolemia .

The basis of the treatment of the syndrome is the relief of symptoms of the underlying disease, complicated by the development of Parkhon's syndrome ^[3] .

There are acute hyponatremia (or an exacerbation of chronic) and asymptomatic chronic hyponatremia. The goal of treatment is the normalization of plasma osmolality and the elimination of hyperhydration. Therapeutic tactics depend on the rate of increase of hyponatremia (acute or chronic), the concentration of sodium in the blood plasma and the patient's condition ^[5] .

The amount of fluid entering the body should be limited and not exceed 500-1000 ml per day. With the rapid introduction of saline, impaired consciousness or convulsions may develop. The medications that may be causing this syndrome (opiates, non-steroidal anti-inflammatory drugs, barbiturates, cyclophosphamide, antidepressants, antipsychotic drugs, carbamazepine, chloropropramide, clofibrate) should be discontinued. You can give diuretics (loop diuretics). Uncontrolled administration of saline can only further reduce serum sodium! In Europe, a group of drugs, vaptans, was developed as a new tool for the special treatment of this syndrome. Since August 2009, tolvaptan has been approved for treatment as the first vasopressin antagonist. It is used orally, blocks the action of vasopressin in the kidney and helps to eliminate fluid from the body, free of electrolytes.

• Adenohypophysis hormones
• Diabetes insipidus