Vulvar varicosities in nonpregnant females, either isolated or as a part of the pelvic congestion syndrome, are rare. We present a case of an adolescent girl with morbid obesity with bilateral bluish protrusions on the labia minora, as an incidental finding, that coincided with her excessive weight gain. The adolescent underwent thorough clinical examination, doppler ultrasound, contrast venography and varicography, and magnetic resonance angiography to rule out alternative diagnoses. Imaging results confirmed the presence of large venous lakes. Venous drainage to the internal iliac vein and connections with the long saphenous vein were delineated. Incompetence, dilatation, or reflux of ovarian or internal iliac veins, or their main tributaries, were not noted. Since the adolescent was asymptomatic and other pathologies, such as vascular malformations or hemangiomas were excluded, she was managed conservatively with counseling about lifestyle modification and weight reduction. This is only the third reported case of vulvar venous varicosities in adolescents. Female sex, along with obesity, are known risk factors for varicose vein formation; however, the pathogenesis is not fully understood. Additional research is needed to elucidate the role of excess adipose tissue in the pathophysiology of vulvar varicose veins and to optimize diagnostic workup and management in adolescence.

The aim of this case–control study was to assess the burden of non-alcoholic fatty liver disease (NAFLD) in adolescents with polycystic ovary syndrome (PCOS) and its associations with insulin resistance, hyperandrogenism, and other metabolic characteristics of the syndrome. A total of 87 Caucasian adolescent girls (47 with PCOS and 40 controls), aged 12.3–20.4 years, underwent blood sampling for glucose metabolism, hormonal and lipid profile, gynecological and liver ultrasound, and liver elastography. Indices of insulin resistance, liver steatosis, and liver fibrosis were calculated. NAFLD diagnosed by ultrasound was more prevalent in adolescents with PCOS than controls (22.7% vs. 6.1%, p = 0.046), and was also verified by liver steatosis indices. The latter was not apparent for hepatic fibrosis, as assessed by Fibroscan® and calculated indices. The homeostatic model assessment for insulin resistance (HOMA-IR) was found to predict NAFLD diagnosis by the liver fat score (LFS) index (β = 0.709, p = 0.002). Adolescents with PCOS and high free androgen index (FAI) presented worse NAFLD than those adolescents with PCOS and lower FAI. In addition, adolescents with PCOS and concurrent NAFLD had worse insulin sensitivity indices (HOMA-IR, QUICKI, and glucose to insulin ratio) than adolescents with PCOS alone. Adolescent insulin resistance could be considered a confounder of the association between PCOS and NAFLD.