Addison’s disease, also known as primary chronic hyperaldosteronism, is a disease caused by inadequate secretion of adrenocortical hormones due to bilateral adrenocortical atrophy, severe infections such as tuberculosis, or severe destruction caused by tumors, mostly due to tuberculosis that destroys the adrenal cortex or the removal of large parts or all of the adrenal cortex bilaterally. It can also be secondary to inadequate secretion of CRH by the hypothalamus and ACTH by the pituitary gland, but is more common in those caused by the adrenal glands themselves. In addition, autoimmune diseases and severe trauma can also destroy or atrophy the adrenal cortex; the rest are amyloidosis, tumors, syphilis, fungi, and thrombosis, which can also destroy the adrenal cortex and affect its function. The disease is often insidious, and the first symptoms are gastrointestinal symptoms of unknown origin, such as loss of appetite, abdominal pain and diarrhea. Normal gastrointestinal motility is probably related to adrenocortical function to some extent, but the relationship between the two is still unknown. In addition to gastrointestinal symptoms, the disease may present with debilitating weakness, weight loss, hyperpigmentation, and decreased blood pressure. Patients are mostly middle-aged and young, mostly between the ages of 20 and 50, with an almost equal prevalence in men and women, and more women with unknown causes. The clinical symptoms of cortisol deficiency are: general weakness, weakness and emaciation, pigmentation of skin and mucous membranes, obvious pigmentation of exposed areas of the skin and joint folds, pigmentation of the oral cavity, lips, tongue and cheek mucosa, reduction of pubic hair and axillary hair in women, and hypogonadism in men. In severe cases, it can lead to adrenal crisis, which often occurs in stressful situations such as infection, trauma, surgery, childbirth, overwork, heavy sweating or sudden interruption of treatment. It is characterized by nausea, vomiting, diarrhea, severe dehydration, decreased blood pressure, rapid heart rhythm, weak pulse, often hyperthermia, hypoglycemia, hyponatremia, etc., which can be life-threatening. Laboratory tests show decreased blood sodium, increased blood potassium, blood sodium-potassium ratio less than 30. decreased serum chloride, decreased blood glucose. on x-ray, calcified spots are seen in the adrenal glands. The diagnosis of Addison’s disease mainly relies on the measurement of blood urine cortisol and blood ACTH level. The principles of treatment for this disease are: 1. correction of metabolic disorders in this disease; 2. endocrine replacement therapy; 3. etiological treatment; 4. avoidance of stress and prevention of crises. Since the disease is a chronic process, patients must understand the basic knowledge of prevention and treatment of the disease, and consciously try to avoid stress factors such as excessive fatigue, mental stimulation, cold, heat, infection, injury, etc. They must also avoid sodium and water loss caused by vomiting, diarrhea or sweating. Diet must be rich in sugar, protein and vitamins, more sodium salt and less potassium salt. If the amount of sodium chloride in food is not enough, you can take saline solution, the daily intake is about 10-15g, depending on the needs of each person, to maintain electrolyte balance. Those treated with endocrine therapy still need 3 to 10 g daily. The most basic therapy for this disease requires long-term corticosteroid replacement supplementation in addition to etiological treatment. Currently, corticosteroids (such as cortisone, hydrocortisone, prednisone and prednisolone) and aldosterone hormones (generally various preparations of synthetic 11-desoxycorticosterone) are commonly used for treatment. The doses of various hormones are generally required by the patient, and the doses but must be individualized when applied. After the strict use of endocrine therapy and anti-TB treatment, the patient’s life expectancy is greatly extended and the labor force is significantly restored and can approach normal. Some patients who continue treatment for more than 7 years can have normal pregnancy and childbirth, but care should be taken to prevent adrenal crisis attacks during delivery. The prenatal and postnatal growth and development of the children were completely normal. During the course of treatment, the patient’s resistance is low and is prone to respiratory infections, gastrointestinal disorders and even adrenal crisis attacks, which should be paid attention to. In addition to treatment, more lean meat, milk, eggs and fresh vegetables should be consumed in the diet, and more sodium should be consumed.