Addison’s disease, also known as chronic hyperaldosteronism, is caused by destruction or dysfunction of the adrenal cortex. The disease was first described by Thomas A. Eddy was first described in 1855 and later named after him. Most of the earlier cases were caused by infections of the adrenal glands, the most common cause being tuberculosis. To this day, adrenal tuberculosis remains an important cause of Addy’s disease in some developing countries or regions, while in developed countries, the most common cause of the disease is non-specific autoimmune destruction. It is caused by the adrenal glands. Pregnancy in combination with Addison’s disease is very rare, with only 50 cases of pregnancy in combination with Addison’s disease reported before 1953, indicating that untreated Addison’s disease is often associated with infertility and many complications even in pregnancy. There were more cases of hyperalgesia in pregnancy only after the availability of prednisone and related drugs. The current diagnosis is often made before pregnancy and maintenance doses of prednisone have been taken. I. Physiology of pregnancy Plasma cortisol rises during normal pregnancy. It is twice as high as normal in early pregnancy and peaks at delivery, about three times as high as in uncomplicated pregnancies. Most of this is due to the rise in cortisol-binding globulin during pregnancy, but free cortisol also rises, as does free cortisol in the urine, while the normal diurnal variation decreases. Plasma renin and aldosterone levels also increase during pregnancy, and urinary 17-hydroxycorticosteroids are reduced. Etiology The disease is primary hyperaldosteronism, an insidious progressive hyperaldosteronism. 70% is due to idiopathic atrophy of the adrenal cortex, with autoimmune adrenal inflammation as its main cause. Clinical symptoms can occur when greater than 90% of the gland is destroyed. A small number of patients develop from destruction of the adrenal glands due to tuberculosis granuloma, flab, amyloidosis, etc. Other rare causes include deep fungal infections, immunodeficiency virus infections, tumors, hemorrhage, and adrenal cerebral white matter dystrophy. Diagnosis (a) Symptoms Fatigue, nausea, vomiting, weight loss, hypotension, and increased skin pigmentation. However, there is also nausea, vomiting, and increased pigmentation in the early stages of normal pregnancy, and there are some difficulties in diagnosis. However, the symptoms of pregnancy Addison’s disease are more serious and persistent, weight loss is more obvious, and it is easy to cause hypoglycemia. (ii) Laboratory tests 1, plasma cortisol levels are low, but may also be within the normal non-pregnancy range. 2.Adrenocorticotropic hormone stimulation test (ACTH test). Take serum basal value, inject ACTH 25U intramuscularly, take serum value after 1h, normal should increase by 2 times, Addy’s disease has low performance. If highly suspected treatment can be given, try to postpone various tests until after delivery to prevent causing fetal abnormalities. Differential diagnosis Differentiate from hypoadrenocorticism caused by ACTH deficiency. Patients with total hypopituitarism or long-term use of adrenocortical steroids and then discontinued are secondary to hyperaldosteronism, not Addison’s disease. Total hypopituitarism can be seen after destruction of pituitary tissue caused by pituitary tumors, granulomas, infections and trauma, and is often accompanied by hypoplasia of other systems, such as hypothyroidism. V. Prognosis Both mother and child can be safe with proper treatment. Hypoglycemia is likely to occur during pregnancy, and there may be an increase in the number of children younger than gestational age. Occasionally, adrenal function of the fetus is suppressed due to the use of prednisone by the mother. Acute adrenal crisis may occur during and after delivery in untreated Addison’s disease. VI. Treatment 1. Adrenocorticotropic hormone supplementation, maintaining 5 mg of prednisone every morning and 2.5 mg at night, may be reduced if edema or hypertension occurs. Hormone supplementation should be slightly lower than non-pregnancy and not higher than non-pregnancy. Monitor closely during pregnancy and postpartum for signs of deficiency or oversupplementation. 2.Corticosteroid supplementation can be increased 2 to 3 times when there are mild manifestations of disease. 3.Adequate corticosteroids should be given at the time of delivery; after delivery or when elective cesarean delivery is decided, give cortisone acetate 100mg, intramuscularly, or hydrocortisone 200mg, divided into one intravenous dose every 6h, and then reduce the previous amount by 50% daily until the original maintenance amount is restored. 4. In acute adrenal crisis, with nausea, vomiting, abdominal pain, fever, hypotension, shock and other symptoms appear, a large amount of fluid and corticosteroid intravenous input should be given for treatment.