Reduced secretion of antidiuretic hormone (ADH) is one of the symptoms of syndrome of inappropriateantidiuretic hormone secretion (SIADH), which refers to the abnormal increase in secretion of endogenous antidiuretic hormone (ADH, i.e., arginine pressor AVP) due to various causes, with plasma ADH concentration at an inappropriately high level relative to body fluid osmolality. This leads to water retention, increased urinary sodium excretion and dilutional hyponatremia, and other related clinical manifestations. I. Etiology and pathogenesis (a) Heterologous ADH secretion: 1. The most common malignant tumor is pulmonary oat cell pain, which is caused by about 80% of SIADH patients. About half of the patients with oat cell carcinoma have increased plasma AVP and impaired water excretion, but not always hyponatremia, and whether SIADH occurs depends on the degree of water load. Other tumors such as pancreatic cancer, lymphosarcoma, Hodgkin’s disease, reticulocytic sarcoma, thymic adenocarcinoma, duodenal cancer, bladder cancer, and prostate cancer. (2) Infectious diseases of the lung pneumonia, tuberculosis, lung abscess, pulmonary aspergillosis can sometimes cause SIADH, probably due to the synthesis and release of AVP from lung tissue; in addition, infected lung tissue can ectopically synthesize and release AVP-like peptides with the same biological properties as AVP. (B) Drugs or diseases leading to excessive release of ADH 1. CNS diseases such as traumatic brain injury, subdural hematoma formation, subarachnoid hemorrhage, cerebral thrombosis, brain abscess, brain atrophy, acute brain infection, tuberculosis or other meningitis can affect hypothalamic-pituitary function, prompting the release of AVP without the control of normal regulatory mechanisms such as osmotic pressure, thus causing SIADH. 2. ADH release or enhance the role of drugs such as chlorosulfonylurea, clofibrate, tricyclic antidepressants (such as aminoglutethimide), general anesthetics, barbiturates and other drugs can stimulate ADH release, chlorosulfonylurea can also increase the activity of ADH. Thiazide diuretics increase water reabsorption from the distal tubule and significantly decrease free water clearance due to their sodium-removal diuresis and resulting decrease in GFR, and also trigger ADH secretion. Anticancer drugs such as vincristine and cyclophosphamide can also stimulate ADH release. (iii) Other stimulation of volume receptors due to sudden decrease in left atrial pressure can reflexively increase ADH secretion, as seen after mitral stenosis separation. SLADH can also be seen in endocrine diseases such as hyperaldosteronism, mucinous edema, and hypopituitarism (due to hypovolemia or impaired renal free water excretion); in a few patients, their SLADH cannot be linked to the above etiology and may There are changes in the sensitivity of renal tubules to ADH. Second, pathophysiology Due to the excessive release of AVP and not controlled by normal regulatory mechanisms, the reabsorption of water by the distal renal tubule and collecting duct increases, urine cannot be diluted, free water cannot be excreted, such as excessive water intake, water retention in the body, extracellular fluid volume expands, blood dilution, and serum sodium concentration and osmolality decrease. At the same time, the intracellular fluid is also in a hypotonic state and the cells swell. When the brain cell function is affected, neurological symptoms may appear. The syndrome does not generally present with edema because when the extracellular fluid volume is expanded to a certain degree, sodium reabsorption by the proximal tubule is inhibited, so that urinary sodium excretion increases and water does not remain in the body in excess. In addition, volume expansion leads to increased release of cardiac natriuretic peptide, which further increases urinary sodium excretion; therefore, sodium metabolism is in negative equilibrium, aggravating hyponatremia and hypotonicity. At the same time, volume expansion, increased glomerular filtration rate, and suppression of aldosterone secretion also increase urinary sodium excretion. Due to the continued secretion of AVP, urine osmolality remains higher than plasma osmolality, although the extracellular fluid is already hypotonic. Type IV: Also known as type D, accounting for about 14% of cases. The body’s ADH secretion mechanism is intact and plasma ADH levels are normal, but the kidney’s sensitivity to ADH is increased. It is also believed that ADH-like substances are present in this type of patient and that it is the ADH-like substances rather than ADH itself that cause the clinical manifestations. Strictly speaking, the term SIADH does not apply to this type because there is no inappropriate secretion of ADH, but it is still customary to classify this type as SIADH.