Primary aldosteronism I. Overview Primary aldosteronism is a syndrome characterized by hypertension and hypokalemia due to a lesion in the adrenal cortex that results in excessive secretion of aldosterone, leading to water and sodium retention, increased blood volume, and inhibition of the activity of the renin-angiotensin system. Most of the cases are caused by adrenal aldosterone adenoma, accounting for 65% to 80% of cases, and the tumors are mostly between 1 and 2 cm in diameter. It may also be idiopathic aldosteronism. The progress of laboratory testing and imaging has made the diagnosis and treatment of adrenal gland disease easier and more effective, and the detection rate of patients with incidental tumors has increased significantly. Some foreign scholars have suggested that primary hypertension has become the most common form of secondary hypertension in addition to renal disease, and its incidence can be as high as 15% to 20%. The first choice for surgical treatment of this disease, not suitable for surgery, commonly used in the treatment of the Androstat, while potassium supplementation, plus general antihypertensive drugs. II. Clinical manifestations Regardless of the etiology or type of proaldosteronism, its clinical manifestations are caused by excessive secretion of aldosterone. 1, hypertension: the most common first manifestation, with the course of the disease continues to progress or slightly fluctuate up, but generally a benign passage, blood pressure is about 150-170/90-110mmHg between. Patients have headache, dizziness, malaise, tinnitus, and amblyopia seen in the outpatient internal medicine department. It may appear 2-7 years earlier than hypokalemia. As the disease progresses, blood pressure also rises gradually, and there is often no significant effect on antihypertensive drugs. 2. Hypokalemia: In the early stage of the disease, the blood potassium may be normal or continue to be at the normal low limit, and there are no clinical symptoms of hypokalemia. Since hypokalemia is often below 3 mmol/L, it can lead to the following clinical symptoms: muscle weakness and periodic paralysis: it often occurs suddenly, with numbness and ankylosis at the beginning, followed by a sudden inability to move both lower extremities when waking up in the morning, with reduced or absent reflexes and bilateral symmetry, or even respiratory muscle paralysis in the upper extremities, causing difficulty in breathing and swallowing. The onset of paralysis is related to the degree of decrease in blood potassium. The attacks are more frequent at night and are often triggered by exertion, cold, and the consumption of high-sugar foods. Numbness of extremities and hand-foot convulsions: metabolic alkalosis caused by low potassium leads to numbness of extremities, hand-foot convulsions and muscle spasms. 3, renal manifestations: long-term large loss of potassium, renal tubular concentration function is reduced, causing polyuria, nocturia increased. Excessive aldosterone increases urinary calcium and uric acid excretion, making it easy to develop kidney stones and urinary tract infections, pyelonephritis, and interstitial scar formation. Due to long-term secondary hypertension can lead to renal arteriosclerosis, proteinuria, renal insufficiency. 4. Cardiovascular system: It is easy to cause arrhythmia, ventricular premature contraction or paroxysmal supraventricular tachycardia, and ventricular fibrillation may occur in severe cases. The electrocardiogram is mainly hypokalemic changes, such as prolonged Q-T interval, widened T wave, low flatness or inversion, and obvious U wave. 5. Laboratory tests: (1) Hypokalemia and inappropriate increase in urinary potassium: Most patients with protoaldehyde have blood potassium below 3.5mmol/L, usually between 2-3mmol/L. If blood potassium is <3.5mmol/L and urinary potassium >30mmol/24h, it suggests that the patient has inappropriate increased potassium excretion. (2) Increased and uninhibited aldosterone secretion: Since aldosterone secretion is easily influenced by body position, blood volume and sodium concentration, basal aldosterone levels measured alone have limited diagnostic value for proaldosterone, and an inhibition test is needed to confirm that increased and uninhibited aldosterone secretion has greater diagnostic value. The method often used to inhibit aldosterone secretion is the captopril (mercaptopropionic acid) inhibition test: blood is drawn in the morning in the prone position to measure the aldosterone in blood and the renin activity in plasma, and captopril 25 mg is given orally, and the blood is drawn in the sitting position 2 h later to remeasure the aldosterone and renin activity in blood. Because captopril inhibited angiotensin II production, plasma aldosterone levels were suppressed to below 416 pmol/L (15 ng/dl) in normal subjects or patients with essential hypertension, but not in patients with proaldosteronism. (3) Decreased and unexcited plasma renin activity: Increased aldosterone levels and decreased renin activity are characteristic changes in proaldosteronism. However, renin activity is susceptible to a variety of factors, so a single measurement of basal renin activity or the ratio of plasma aldosterone concentration to plasma renin activity alone is normal, but still insufficient to exclude proaldosteronism, dynamic observation of plasma renin activity changes, commonly used postural stimulation test: 8:00 a.m. fasting lying blood immediately after injection of 40mg of furosemide (0.7mg/kg body weight for those who are obviously wasted, overweight Then let them move in the standing position for 4h and then take blood, and immediately measure plasma renin activity, angiotensin II and aldosterone. If plasma aldosterone is elevated and renin activity is suppressed, it is highly suggestive of proaldosteronism. (1) Ultrasound of adrenal gland: It can detect tumor with diameter >1.3cm or more. However, it is difficult to confirm the diagnosis of small adenomas. (2) CT scan of adrenal gland: It is listed as the first choice in the localization and diagnosis of adrenal lesions. It is also recommended to identify its type, and its correct diagnosis rate is 70%-90%, but some non-functional adrenal accidental tumors should be excluded. The diagnosis is based on two steps: firstly, to clarify whether there is hyperaldosteronism; then to determine its etiological type. Since the results of most tests in the diagnostic process are affected by many drugs and hormones, all drugs must be stopped for more than 2 weeks before the test. 1, hypertension, periodic paralysis, hand and foot twitching, increased nocturia and other clinical manifestations; 2, hypokalemia and inappropriate increased urinary potassium excretion; 3, increased and uninhibited aldosterone secretion; 4, decreased plasma renin activity and unexcited positive postural test. 5, imaging examination with adrenal-related manifestations. The treatment of proaldosteronism depends on the etiology. Adrenal aldosterone adenoma should be treated with early surgery, and most patients can be cured after surgery. Unilateral or subtotal resection of primary adrenocortical hyperplasia is also effective, but the symptoms recur in some patients after surgery, so in recent years, there is a tendency to use more drug therapy. 1.Surgical treatment: In order to ensure the smooth operation, electrolyte disorders and hypokalemic alkalosis should be corrected before surgery to avoid serious arrhythmias. It is advisable to use a low-salt diet and appropriate supplementation of potassium chloride 4-6g/d orally in divided doses, or spironolactone 40-60mg/time, 3-4 times/d. Potassium supplementation is not necessary when spironolactone is used. During the above treatment, blood potassium should be monitored, especially for those with long duration of disease with decompensated renal function, to avoid hyperkalemia. Appropriate supplementation of adrenocorticotropic hormone during the perioperative period. 2.Laparoscopic adrenal adenoma resection: Currently, it is considered suitable for adrenal adenomas <6cm in diameter, and has been widely promoted because it is less traumatic, less physiological interference, less bleeding, no need to cut off the ribs, and safe and effective. 3, drug therapy: where the diagnosis of idiopathic aldosteronism, glucocorticoid suppressible aldosteronism, and surgical treatment of patients with poor results, or patients who do not want to operate or can not tolerate surgery can be used for drug therapy, the following drugs can be used: (1) aldosterone antagonists: spironolactone is the drug of choice for the treatment of primary aldosteronism, the initial dose of 200-400mg/24h, divided into oral doses. Hypokalemia can mostly be corrected quickly, and it takes 4-8 weeks for blood pressure to return to normal. After several months of treatment, the dose can be reduced to 40-60mg/24h. (2) Angiotensin converting enzyme inhibitor: It can reduce the secretion of aldosterone, improve the balance of potassium and lower the blood pressure to normal. Commonly used clinically are captopril, benazepril, etc. Specific usage is the same as the treatment of hypertension. (3) Drugs that inhibit aldosterone synthesis: Aminoglutethimide (aminoglutethimide), which inhibits the synthesis of adrenocorticotropic hormone. The dosage is 0.5~1.5g/d, divided into oral doses. (4) Glucocorticoids: Dexamethasone is effective in patients with glucocorticoid suppressible aldosteronism. Use 0.5~0.75mg/d every night for a long time. If necessary, general antihypertensive drugs can be added. The medication can normalize blood pressure, blood potassium, renin and aldosterone, so that the patient can maintain a normal state for a long time.