Aldosterone is an electrolyte-regulating hormone secreted by the globus pallidus of the adrenal cortex. Excessive secretion of this hormone can cause a clinical syndrome, which was first reported by Conn and is referred to as Conn’s syndrome. There are many causes of adrenal hypersecretion of aldosterone, such as primary aldosteronism, which is caused by a lesion in the cortex itself, or secondary aldosteronism, which is caused by an extra-adrenal lesion that stimulates excessive secretion of aldosterone in the cortex. Clinical features Patients with aldosteronism are divided into three groups. Group 1: typical aldosteronoma group (n=95); Group 2: aldosteronoma group in unexpected adrenal tumors (n=21); Group 3: primary hypertension group (n=29). The symptoms and biochemical indices related to metabolic syndrome in each group were detected and analyzed comparatively. The incidence of metabolic syndrome in the three groups was 37.9%, 28.6% and 20.7%, respectively. The blood and urinary aldosterone levels decreased, while plasma renin activity and potassium concentration increased in groups 1, 2 and 3. Systolic and diastolic blood pressures were higher in group 1 than in group 3, and HDL cholesterol was lower than in group 3 (P<0.05). In group 1, group 2 and group 3, 28.4%, 23.8% and 17.2% had elevated waist circumference, respectively; 50.5%, 52.4% and 31.0% had dyslipidemia, respectively; 22.1%, 23.8% and 10.3% had elevated fasting glucose, respectively; and 98.9%, 100% and 100% had hypertension, respectively. Conclusion The incidence of metabolic syndrome is increased in patients with typical aldosterone tumors; aldosterone secretion is only mildly elevated in patients with aldosterone tumors in the adrenal glands, but it also increases the incidence of metabolic syndrome. Clinical manifestations ① Hypertension. It is an early symptom of the disease and is mostly a slowly progressing benign hypertension. The blood pressure level is generally 22.7-24.0/13.0-14.7kPa (170-180/100-110mmHg), and conventional antihypertensive drugs are not effective, but the fundus changes develop slowly. ② Hypokalemia. As a result of large amounts of aldosterone promoting excessive urinary potassium excretion, patients may have muscle weakness, paralysis, flaccidity, and even difficulty in swallowing and breathing, and electrocardiogram showing hypokalemia, sometimes with arrhythmia. Long-term hypokalemia may cause vacuolar degeneration of the distal tubule of the kidney and decrease the concentration function of the kidney. Patients may have thirst, polyuria, increased nocturia and low specific gravity urine. (iii) Alkalosis. Caused by the loss of large amount of intracellular potassium ions and the inward entry of extracellular sodium and hydrogen ions, manifested by the decrease of blood free calcium level, the patient shows symptoms such as numbness of extremities and hand and foot twitching, and the urine is neutral or alkaline. ④Other. Since hypokalemia can inhibit insulin secretion, about half of the patients have hypoglycemic tolerance, and children may have growth retardation due to hypokalemia. Pathology ①Mainly single adenoma (70%-80%). ②Adrenocortical hyperplasia accounts for 20%-30% of patients, of which bilateral hyperplasia is common, also known as idiopathic aldosteronism; the clinical manifestations and biochemical changes of a few hyperplastic patients can be suppressed by small doses of dexamethasone, so it is called adrenocorticotropic hormone (ACTH)-dependent or dexamethasone-suppressible aldosteronism; there is also a unilateral or bilateral hyperplastic patient with biochemical changes similar to adenoma, which is referred to as primary adrenocortical hyperplasia. (iii) Others, such as aldosteronism caused by adenocarcinoma and ovarian tumors that secrete too much aldosterone. It is less common.