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Handbook of Clinical Gender Medicine


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      Maternal or Exogenous Sources of Androgens

      Other sources of masculinization with resultant ambiguous genitalia are androgenic stimulation of the fetus in utero from nonfetal sources. Fetal virilization occurs during a critical period between weeks 8 and 13 of gestation and results in labioscrotal fusion and urogenital sinus formation. Female embryos have the same androgen receptor system in the urogenital tract as male embryos; therefore, administration of androgens at the appropriate time during embryogenesis may cause profound masculinization. Internal genitalia are not masculinized and wolffian duct remnants are normal.

      Although CAH is the most common cause of masculinization in the female fetus, masculinization as a consequence of a maternal hormone-producing tumor is becoming a more frequently recognized clinical entity (luteoma of pregnancy, granulosa tumor, arrhenoblastoma, hilar cell tumor, lipoid cell tumor, masculinizing ovarian stromal cell tumor). Other masculinizing tumors which are maternal sources of androgens inducing virilization include: Krukenberg tumor, adrenocortical carcinoma, adrenal myelolipoma, ganglioneuroma, choriocarcinoma, testosterone-secreting adrenal adenoma, and placental site trophoblastic tumor. Bilaterality and multinodularity are more common in luteomas than in these other tumors. Polycystic ovary syndrome and massive ovarian edema are also described as a sporadic cause of virilization during pregnancy.

      Maternal ingestion of androgens, progestagens, and drugs such as danazol, stilboestrol, and 1-9-nortestosterone (for threatened abortion) may cause labial posterior fusion, clitoromegaly, and more pronounced virilization. Ingestion of the off-label ‘appetite stimulant’ cyproheptadine and methandienone (a derivative of testosterone) has been cited as a source of fetal virilization. Maternal application of topical preparations, and exposures noted to induce virilization of the female fetus include: cutaneous androgen preparations, methandrostenolone-containing cream for eczema, and exposure to the fungicide vinclozolin. Only 65% of masculinized mothers deliver masculinized female infants. Protective mechanisms such as active placental aromatization of androgens into estrogens, maternal metabolism of androgens, increases in androgen-binding proteins (SBP and SHBG) under the influence of placental estrogens, and the protective buffering effect of the high concentrations of estrogens found in fetal blood might be responsible for the protection of the fetus against masculinization.

      Undervirilized Males

      Genetic Causes

      Hormonal Failures

      Placental Dysfunction

      The Mother

      The Environment