Congenital adrenocortical hyperplasia: It is a group of autosomal recessive disorders caused by congenital deficiency of various steroid hormone synthesizing enzymes in the adrenal cortex due to genetic defects, which partially or completely block cortisol synthesis and increase CRH-ACTH compensatory secretion in the hypothalamus-pituitary gland, resulting in adrenocortical hyperplasia. The most common enzyme defect in congenital adrenocortical hyperplasia is 21-hydroxylase deficiency (21-OHD), which accounts for more than 90% of cases, followed by 11-β-hydroxylase deficiency (11β-OHD), 3β-steroid dehydrogenase (3β-HSD) deficiency, 17α-hydroxylase deficiency (17α-OHD), and StAR deficiency. Different types of enzyme deficiencies produce different biochemical changes and clinical manifestations, and early diagnosis and surgical treatment are very important. In particular, 21-hydroxylase and 11-beta-hydroxylase deficiencies, if diagnosed and treated from early embryonic stages, can prevent the emergence of androgenesis and result in normally developing infants. Failure to recognize these deficiencies at birth often results in abundant later developmental abnormalities, and in severe cases of fever, premature death in infancy. In addition to the ACTH-stimulated adrenal hyperplasia, each type of CAH has its own characteristics of presentation. The main manifestations are: salt loss syndrome, androgen excess syndrome (female masculinization and male precocious puberty), hypertension with hypokalemia, and male feminization. Patients with 21-hydroxylase deficiency (21-OHD) suffer from 21-hydroxylase deficiency or reduced activity, failure to convert progesterone and 17-hydroxyprogesterone fatigue into deoxycorticosterone (DOC) and deoxycortisol, reduced cortisol synthesis, feedback increase in ACTH, stimulation of adrenal fasciculus hyperplasia, and increase in intermediate baby metabolites such as progesterone and 17-hydroxyprogesterone, which partially enter the androgen synthesis pathway leading to androgen In severe cases, there can also be salt corticosteroid deficiency, causing salt loss syndrome. 21-OHD can be classified as purely masculine, salt-losing and atypical according to their manifestations. The main manifestations are hyperalgesia of varying degrees and abnormalities in the development of sexual differentiation. Due to the wide spectrum of the disease, the age and degree of symptoms, the severe cases (classic) can be detected at birth with female masculinization/losing salts syndrome: e.g. masculinization of female external genitalia (female pseudohermaphroditism) as well as anorexia, nausea, vomiting, hypoglycemia, hyponatremia, hyperkalemia, metabolic acidosis, pseudohermaphroditism, loss of salts syndrome and hypotension in newborns. In milder cases, the disease is characterized by various degrees of hyperandrogenism, i.e., female masculinization and male precocious puberty. With the growth of age, the symptoms and signs of hyperandrogenism become more obvious and easier to be diagnosed in the middle. Female patients during the growth period may now have early appearance of pubic and axillary hair, acne, mildly accelerated growth, and mild hypertrophy of the clitoris; male children may have accelerated growth and pseudo-precocious puberty (muscular development, early bone age, enlarged penis, but small testicles); female patients during puberty or adulthood may have worse hirsutism , acne, menstrual disorders and infertility. In addition, ACTH is increased and there are different degrees of hyperpigmentation, similar to Addison’s disease, with dark skin all over the body, especially around the skin folds, such as finger joint extensions, axillae, groin and areola. Treatment mainly consists of supplementation with exogenous glucocorticoids and salt corticosteroids, etc., as needed.