Ectopic antidiuretic secretion syndrome in the elderly

Introduction of ectopic anti-urea secretion syndrome in the elderly The secretory hormone secreted by tumor cells is called ectopic endocrine, and ectopic anti-urea secretion syndrome (SIADH) is one of the important complications of cancer patients. Mainly manifested as low blood sodium with urine concentration. Ectopic ADH can promote the reabsorption of water by the renal tubules, and thus, imbalance of water and sodium metabolism, water retention and hyponatremia (dilute low sodium) occur. basic knowledge The proportion of illness: 0.008% Susceptible people: the elderly Mode of infection: non-infectious Complications: coma, brain edema, cerebral palsy

The cause of ectopic anti-urea secretion syndrome in the elderly

Genetics (30%):

Cell differentiation is influenced and regulated by specific proteins and enzymes synthesized by RNA, and RNA is regulated by genes on DNA, such as regulatory genes, manipulated genes and structural genes. Under pathological conditions, some malignant tumor cells are depressurized. , that is, the regulation of gene or operator gene removal repression, which can not produce active peptides and hormones can be produced under abnormal conditions, thereby causing the secretion of ectopic hormones and its clinical manifestations, such as ectopic ACTH syndrome is clinically A common disease is currently considered to have three pathological types of small cell lung cancer, carcinoid and pheochromocytoma. Among them, the incidence of ectopic ACTH syndrome caused by small cell lung cancer is the highest, accounting for more than half of the onset. How the tumor suppressor gene and oncogene play a role in the regulation of ACTH secretion remains to be understood, and the relationship between the expression of other ectopic POMC genes and the inhibition of POMC peptide secretion and clinical manifestations needs to be further understood.

Embryonic tissue ectopic (30%):

Secretory Hormone Theory (ie, APUD Cell Theory) The tumor line that produces ectopic hormones is from the APUD cell system, and APUD cells belong to neuroendocrine cells. In 1968, Pearse proposed that the APUD cell line originated from the embryonic ectodermal neural crest. Later distributed in endocrine glands and organ tissues, such as the anterior pituitary, thyroid, thymus, pancreas, lung, gastrointestinal biliary tract, liver, adrenal gland, gonads and ganglia, etc., tumors from APUD cells, called APUDOMA, It can secrete more than 30 kinds of peptide hormones and biogenic amines, such as these cells can secrete ACTH, MSH, CT, ADH, 5-HT, insulin, gastrin, glucagon, secretin, ortho-benzene. Diphenolamine, PRL, TSH, GH, PTH, renin, gonadotropin and erythropoietin, APUD cytology can not fully explain ectopic endocrine phenomenon, it is likely to be related to other cellular genetic defects and abnormalities, or Immune genetics are related.

Synthesis of abnormal proteins (30%):

This is related to genetic theory, which regulates genes that produce certain abnormal proteins and peptides. Specific proteins such as histones act as suppressors, and non-histone proteins that manipulate genes act on histones, removing depressors, and mRNAs through tRNA. The transcription of rRNA gradually produces various specific proteins and enzymes, and has hormone-like effects such as osteoclast activating factor and growth factor.

Prevention of ectopic anti-urea secretion syndrome in the elderly

Treats primary diseases, improves symptoms, strengthens nutrition and supports therapy.

Complications of ectopic anti-urea secretion syndrome in the elderly Complications coma cerebral edema cerebral palsy

The main complications are medullary paralysis, coma, cerebral edema, and cerebral palsy.

Symptoms of ectopic anti-urea secretion syndrome in the elderly Common symptoms Lack of cortisol deficiency coma hyperosmolar urine nausea weight gain fatigue hyponatremia water toxic water retention

Due to water retention, extracellular fluid increases and hyponatremia, ie, dilute hyponatremia, water intoxication and low sodium cause neurological disorders, fatigue, anorexia, nausea, vomiting, weight gain, fatigue, myalgia, headache, etc. Sodium below 115mmol / L can cause confusion, epilepsy, coma, severe hyponatremia can cause brain edema, and occasionally can cause death.

Non-tumor and tumor patients with low blood sodium may have common causes: such as liver disease, heart failure, kidney disease, electrolyte imbalance, lack of cortisol, etc. Therefore, the hyponatremia caused by these causes should be distinguished from SIADH, during the examination, Pay attention to the estimation of liquid volume, serum and urine electrolytes, and osmotic pressure. SIADH has high urinary sodium concentration, low plasma osmotic pressure, but high levels of ADH in the blood. Other causes of hyponatremia in the case of low plasma osmotic pressure. The secretion of ADH in the adrenal gland is inhibited, and the level of ADH in the blood is lowered. In short, the diagnosis of SIADH must be excluded from renal insufficiency or ADH release caused by non-osmotic stimulation.

Conditions for diagnosing SIADH:

1 plasma osmotic pressure is low, usually less than 280mmol / L.

2 urine osmotic pressure is higher than plasma osmotic pressure, usually > 500mmol / L.

3 In the absence of diuretics, urine sodium is greater than 20mmol / L.

Examination of ectopic anti-urea secretion syndrome in the elderly

1. Plasma osmotic pressure decreases with decreasing blood sodium (<270 mOsm/L).

2. When the blood sodium is lower than 125mmol/L, the urine sodium is more than 20mmol/L, up to 80mmol/L or more, and the urine osmotic pressure is increased.

3. Serum chloride and BUN are slightly reduced, and ADH determination is generally not required.

4. Urinary aldosterone is reduced.

Water load ADH inhibition test: a large amount of drinking water in a short period of time (20ml/kg drinking water in half an hour), normal people due to decreased release of ADH, should urinate in large quantities, 80% of drinking water can be discharged within 5h, urine osmotic pressure Can be less than 100mOsm / L (below plasma osmotic pressure), while SIADH patients have less than 40% of urine output, urine osmotic pressure is greater than plasma osmotic pressure, this test has a certain risk, should be selectively carried out (blood sodium >125mmol / L, and no obvious symptoms).

CT scans and MRI examinations can present lesions.

Diagnosis and differentiation of ectopic anti-urea secretion syndrome in the elderly

Diagnostic criteria

The main basis for diagnosis is:

1 About the history of primary disease or medication.

2 hyponatremia, low plasma osmotic pressure.

3 increased urinary sodium (generally 30mmol / L or more), hypertonic urine (urinary osmosis > 100mOsm / L).

4 Water load ADH activity is not inhibited.

Differential diagnosis

1. Ascites caused by other causes of low blood sodium differential congestive heart failure and cirrhosis decompensation, in addition to the primary disease performance, low urine sodium, high urinary aldosterone, edema, or ascites, The liver is swollen.

2. Chronic nephritis can also appear hyperosmolar due to the reduction of GFR, but with azotemia.

3. Loss of water in the gastrointestinal tract, there may be an effective circulation of blood volume reduction, hypotension, dehydration is hypotonic, and with azotemia.

4. Chronic adrenal insufficiency and loss of sodium nephritis, hyponatremia and hyperuric sodium may also occur, but often have insufficient blood volume and hypotension. Selective laboratory tests may further assist in the diagnosis.

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