Three diagnostic criteria for polycystic ovary

Three diagnostic criteria for polycystic ovary

Polycystic ovary is a common gynecological disease nowadays. After it occurs, many female friends will be very worried about their physical condition, always afraid that it will cause more complications, and most patients are not diagnosed, so they cannot rashly use some drugs to treat it. There are also many ways to determine polycystic ovary, and generally you need to go to the hospital for a detailed gynecological examination.

1. Cushing's syndrome: hyperfunction of the adrenal cortex caused by various reasons. Typical manifestations include moon face, buffalo hump, centripetal obesity, purple skin striae, hirsutism, acne, hypertension, osteoporosis, impaired glucose tolerance, skin pigmentation, and often accompanied by virilization. Laboratory tests showed that the normal circadian rhythm of plasma cortisol was lost and urinary free cortisol was increased. The overnight low-dose dexamethasone suppression test is a simple method to screen for this disease. If cortisol decreases by 50% (<195nmol/L) after medication, Cushing's syndrome can be ruled out. If cortisol is >390nmol/L and there are no factors that cause false positives, it may be Cushing's syndrome.

2. Congenital adrenal hyperplasia (CAH): an autosomal recessive genetic disease. The most common are congenital 21-hydroxylase and 11β-hydroxylase deficiencies. Such patients cannot synthesize glucocorticoids, the pituitary ACTH loses inhibition, and the adrenal cortex hyperplasia causes the accumulation of pre-enzyme metabolites - 17α-hydroxyprogesterone, 17α-hydroxypregnenolone and their metabolite pregnentriol, and increased androgen secretion. The patient's chromosomes are 46, XX, the gonads are ovaries, and the internal reproductive organs are uterus and fallopian tubes. However, due to the effect of excessive androgen, the external genitalia and secondary sexual characteristics have varying degrees of masculinization. Because the fetus has been affected by excessive androgen, abnormal genital development has already occurred at birth.

A small number of patients have late-onset adrenal hyperplasia, and clinical manifestations are often delayed until after puberty, which may manifest as slowly progressive hirsutism, infrequent menstruation, and no obvious genital deformities. Laboratory tests show elevated serum T and A levels (T>2.8nmol/L, A>9.5nmol/L), serum cortisol levels are mostly normal, and 17α-hydroxyprogesterone is elevated (>9.1nmol/L). However, the basal level of 17α-hydroxyprogesterone in late-onset patients may be within the normal range, but its level is significantly higher than normal after the ACTH stimulation test, which is of greatest diagnostic value.

3. Ovarian masculinizing tumors: These tumors include testicular blastoma, ovarian hilar cell tumor, lipid cell tumor, granulosa cell tumor and theca cell tumor.

Benign cystic teratoma. It usually occurs between the ages of 30 and 50. The patient had normal menstruation and fertility before the onset of the disease, but after the onset of the disease, he developed obvious masculinization, amenorrhea and infertility. Laboratory tests show elevated androgen levels, mainly T and A (T>7nmol/L, A>21nmol/L), and the androgen secretion of most tumors is neither regulated by ACTH nor gonadotropin. B-ultrasound is a better way to examine this disease, and CT or MRI can also assist in diagnosis.

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