Primary aldosteronism, referred to as proaldosteronism, is caused by excessive secretion of aldosterone in the body and typically presents with hypertension, high aldosterone, low blood sodium, low blood renin, alkalosis, and muscle weakness or periodic paralysis. The clinical condition is characterized by aldosterone-secreting adrenal tumors and primary adrenocortical hyperplasia, as well as proaldosteronism, which is not in the adrenal glands and needs to be differentiated. 1, etiology 1, adrenocortical adenoma is the most common, accounting for about 80% of primary aldosteronism, with a single adrenal tumor is more common, aldosterone with a small tumor volume, most less than 3cm in diameter, some only O.3 ~ 0.6cm, the average diameter of 1.8cm, the weight of most 3 ~ 5g. 2, idiopathic aldosteronism, its pathogenesis may be caused by some adrenal extra-adrenal excitatory aldosterone secretion of factors. factor. The disease is sensitive to angiotensin. In the standing position, renin activity and aldosterone secretion are elevated. It is thought to be a component of the multiple clinical types of essential hypertension. 3, primary adrenocortical hyperplasia is rare, and its endocrine biochemical measurements resemble cortical adenoma, and resection of one adrenal gland or subtotal adrenalectomy is effective. 4.Adrenal adenocarcinoma secreting aldosterone is often larger than 3 cm in diameter and the envelope is often infiltrated, because the cancer cells can also secrete glucocorticoids and sex hormones, and the corresponding clinical manifestations can occur. The etiology of glucocorticoid-inhibitable proaldosteronism is unknown, but it may be related to the deficiency of 17α isoenzyme, and there is a family history of high blood aldosterone and similar proaldosteronism. The diagnosis can be confirmed by taking dexamethasone 2 mg once daily and normalizing the patient’s blood potassium, blood pressure and aldosterone secretion after 3 weeks. This disease should not be operated, but need to take dexamethasone for life. Ectopic aldosterone-secreting tumors are extremely rare, and only a few reports of renal and ovarian cancers have been found. These tumors have the function of aldosterone secretion, but do not respond to ACTH and angiotensin. Diagnosis of primary aldosteronism Clinical manifestations 1. blood pressure, mainly elevated diastolic blood pressure, normal blood pressure in primary aldosteronism is extremely rare. 2, drinking, irritable thirst, polyuria, predominantly nocturia. 3, weakness, or even periodic paralysis, first involving the limbs, and in severe cases, flaccid paralysis, and affect breathing and swallowing. Laboratory tests Protoaldosteronism is due to excessive secretion of aldosterone in the body, hydronephrosis, increased renal excretion of potassium, excessive volume of body fluids, while inhibiting the renin angiotensin system, etc., causing the body → series of changes. Laboratory tests should pay attention to the following aspects: 1, low blood potassium, high blood sodium. 2, poisoning, blood CO2. 2, poisoning, blood CO2. binding capacity is normally high or higher than normal. 3, increased potassium excretion, more than 25-30 mmol/ L in 24 hours. 4, and urinary aldosterone levels are elevated. 5. Decreased plasma renin activity, often unresponsive to provocation tests, but the assay is not specific for proaldosteronism, as 25% of hypertensive patients have renin suppression. Special tests 1. spironolactone (Anserine) test spironolactone is a synthetic competitive antagonist of aldosterone. The usual dosage of spironolactone is 80-100mg orally three times a day for 2-3 weeks. In patients with proaldosteronism, blood pressure decreases, muscle weakness improves, urinary potassium decreases, urinary sodium increases, blood potassium rises to normal range, blood Na decreases, CO2 binding capacity decreases, and urinary pH becomes acidic. 2. For those with atypical clinical symptoms and laboratory findings, selective diagnostic tests can be performed to identify the cause. (1) Postural test, the secretion of renin and aldosterone is increased in the standing position in idiopathic aldosteronism. (2) Sodium-potassium balance test, which is only indicated when there is difficulty in diagnosis. Patients with proaldosteronism show a negative potassium balance and sodium balance on a generalized diet; in the case of a hyponatremic diet, the blood potassium is elevated and urinary sodium excretion is reduced. The diagnosis of localization of imaging 1. B ultrasound is often difficult to detect adrenal tumors <1 cm in diameter. 2. CT can show adenomas of 0.8-1 cm in diameter and is the first choice. Adenomas are mostly unilateral. Adenocarcinoma is usually >3cm in diameter with indistinct margins and infiltrative manifestations. Adrenocortical hyperplasia may show bilateral adrenal enlargement or nodular changes. the detection rate of CT for aldosterone homologous tumors over 1 cm in diameter is over 90%. MRI has a lower detection rate than CT for adrenal tumors and is generally not used. 4. 131I-19-iodine-cholesterol adrenal nuclide imaging is useful for differentiating adenoma, cancer and hyperplasia. If one side of the adrenal gland shows radioactive concentration area, it suggests the possibility of aldosterone tumor on that side; if both sides are shown, it suggests the possibility of bilateral hyperplasia or bilateral adenoma. Third, the treatment of primary aldosteronism According to the different etiology of primary aldosteronism, choose the appropriate treatment. Aldosterone with tumor preferred surgical excision can cure adrenal cortical hyperplasia caused by aldosteronism, – generally do not favor surgical treatment. The indications for pharmacological treatment include: preoperative preparation, idiopathic adrenocortical hyperplasia, refusal of surgery or contraindication to surgery, unresectable cortical adenocarcinoma, and glucocorticoid-controlled proto-awakening disease. Drug treatment includes: (1) Spironolactone (Ativan, daily dose 120-480mg, blood pressure and blood He can be normalized after 2-4 weeks of administration. After the symptoms are controlled, the dose can be gradually reduced to 20mg three times a day. As a preoperative preparation, the risk of surgery can be reduced. (2) Aminopyralid (Amiloride), a long-acting potent potassium retention diuretic, has a mechanism of action with the potency to directly inhibit the secretion of aldosterone at a dose of 5mg per dose, orally three times daily. (3) Phenytoin, a potassium retention diuretic, is not an aldosterone competitive antagonist. It acts on the distal tubule and inhibits sodium reabsorption. The dosage is 50-100mg orally three times a day. (4) Other drugs, such as angiotensin-converting enzyme inhibitors captopril and ramipril, and calcium channel blocker nifedipine, are often used in combination with potassium-retaining diuretics or spironolactone, and blood potassium and blood pressure can be normalized quickly. 2. Preoperative treatment Preoperative preparation, including oral spironolactone, to control hypertension and correct hypokalemia; adopt a low sodium and high potassium diet. Surgery should be performed only after hypertension, hypokalemia and alkalosis are corrected. For single unilateral adrenal adenoma, the tumor can be removed with the ipsilateral adrenal gland; for primary adrenal cortical hyperplasia, subtotal resection or total resection of one adrenal gland; for characteristic prolonged awakening disease, adrenal surgery is often ineffective and drug therapy can be used; for adrenocortical adenocarcinoma, an ectopic aldosterone-secreting tumor, radical surgery should be performed. In recent years, laparoscopic technology has advanced and adrenocortical adenoma can be operated laparoscopically.