Hypertestosteroneemia
Introduction
Introduction During the follicular phase of the normal menstrual cycle, the serum testosterone concentration averages 0.43 ng/ml, and the upper limit is 0.68 ng/ml. If it exceeds 0.7 ng/ml (=2.44 nmol/L), it is hyperandrogenemia, also known as high testosterone. Blood. It is a common gynecological endocrine disease. [Clinical manifestations] More common are menstrual changes such as menstrual thinning, amenorrhea or dysfunctional uterine bleeding, no ovulation, infertility. Some have masculine changes, such as hairy, enlarged throat, and low pitch. Some obesity, hemorrhoids, breast dysplasia, poor uterine development, ovarian enlargement, a few cases of clitoris hypertrophy.
Cause
Cause
Approximately 34% of patients with polycystic ovary syndrome, followed by adrenal hyperfunction hyperthyroidism accounted for 29%, a few found in follicular hyperplasia and adrenal hyperplasia; about 28% of unknown sources. It has recently been reported that hyperinsulinemia can stimulate the ovary to secrete large amounts of androgen into hypertestosterone. Its etiology is complex, and a series of reproductive system development and dysfunction can occur in the clinic. Polycystic ovary syndrome is the most important cause of hyperandrogenism in women. Almost all patients with polycystic ovary syndrome have elevated androgen, or decreased androgen-binding protein, increased free androgen, and enhanced activity.
Examine
an examination
Related inspection
Obstetric B super follicle stimulating hormone (FSH) testosterone
1. According to clinical manifestations, especially menstrual thinning, amenorrhea or dysfunctional uterine bleeding, plus some masculine performance should consider the possibility of this disease. The diagnosis is based on an increase in blood testosterone of >7.0 ng/m1 or >2.44 nmol/L.
2. In order to identify the lesion from the ovary or adrenal cortex, ACTH stimulation test can be used: intramuscular injection of ACTH 20mg, urine and 17-hydroxyl steroid excretion in 24 hours before and after injection. If the excretion after injection is significantly increased, the adrenal cortical function is abnormal; if there is no significant change in excretion before and after injection, the lesion is in the ovary.
3. B-ultrasound can measure the ratio of ovarian size to uterine size. If the ovary is larger than 1/4 of the uterus, it can be considered as polycystic ovary.
4. Clomiphene treatment test: continuous administration of clomiphene for 3 cycles, if the ovulation is mostly polycystic ovary, such as no ovulation in 3 cycles, it can be considered as follicular hyperplasia.
5. Intraperitoneal wall angiography, the size and shape of the adrenal gland can be examined to distinguish adrenal hyperplasia or hyperfunction.
6. On the 9th day of the menstrual cycle, follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), estradiol (E2) and testosterone (T) were measured by radioimmunoassay or enzyme labeling. LH is high, LH/FSH ratio is high, and T is high.
7. Exclude adrenal cortical tumors and ovarian tumors.
Diagnosis
Differential diagnosis
Differential diagnosis of high testosteroneemia:
First, ovarian masculinizing tumors: including support for a stromal cell tumor, portal cell tumor, lipoblastoma, myxoma, adrenal residual tumor, lutocytoma, teratoma and metastatic cancer. In addition to the above-mentioned dystrophic blastoma, other tumors are mostly unilaterally growing solid tumors, and the androgen secretion is autonomic, masculine symptoms are obvious, and often accompanied by ascites and metastases.
Second, adrenal diseases: including congenital adrenal hyperplasia, adenoma and adenocarcinoma. The latter two mainly secrete androstenedione and DHEA, which are also autonomously secreted, not promoted by ACTH and inhibited by dexamethasone. Congenital adrenal hyperplasia, 21 hydroxylase deficiency, typical vulvar-genitourinary sinus malformation with dysplasia.
Third, thyroid disease: including hyperthyroidism and hypothyroidism. At the time of hyperthyroidism, T3, T4, and SHBG increased, and the androgen clearance rate decreased, which caused the increase of plasma testosterone to cause masculinization and menstrual disorders. When hypothyroidism occurs, the conversion of androgens to estrogen increases to cause anovulation.
Fourth, hereditary hirsutism: a family history, only simple hairy without PCOS symptoms and signs. Fertility is normal.
V. Ovarian follicular cell hyperplasia: The gonadotropin secretion is normal, the ovary does not increase, but the follicular cells are nest (island) hyperplasia, and the plasma androgen is elevated significantly, with severe masculinization. Not sensitive to chlorophenolamine treatment.
Sixth, insulin anti-allergic syndrome and melanin acanthoma: an adiponectin receptor-deficient disease (A / B type), can appear similar to PCOS symptoms and signs. Its prominent features are hyperinsulinemia and melanoma of the neck and palate.
Seven, hyperprolactinemia: amenorrhea, galactorrhea, infertility, PRL and DHEAS increased, masculine symptoms are not obvious, ovarian normal.
According to clinical manifestations, especially menstrual thinning, amenorrhea or dysfunctional uterine bleeding, plus some masculinity characteristics should consider the possibility of this disease. The diagnosis is based on an increase in blood testosterone >0.7 ng/ml or >2.44 nmol/L. Others, such as B-ultrasound, clomiphene test and other auxiliary examinations can assist in diagnosis.
