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Background: Labial adhesions, a frequent gynecological condition in prepubertal girls, occur when the labia minora adhere along the midline. The prevailing hypothesis about their etiology suggests that labial adhesion may occur when the delicate and non-estrogenized labia minora undergo an inflammatory response, triggered by exposure to an irritant environment. Therefore, conservative treatment involves the application of topical estrogen or betamethasone cream. The role of androgens has not been considered yet in the pathophysiology or therapy of this condition. However, some studies have shown that androgen receptors are prevalent in the labia minora and vulvar vestibule., Case Summary: We present the case of a 29-month-old girl with symptomatic labial adhesions. She was first ineffectively treated with topical estriol, and then she was treated with a galenic cream containing both estriol and testosterone with complete recovery and without side-effects., Conclusions: Both androgens and estrogens play a significant role in maintaining the physiological trophic state of the vulva and vagina, even during childhood. Topical estriol+testosterone could be considered an alternative treatment for prepubertal labial adhesions refractory to standard topical therapy.

Overweight and obesity during pregnancy have been associated with increased birth weight, childhood obesity, and noncommunicable diseases in the offspring, leading to a vicious transgenerational perpetuating of metabolic derangements. Key components in intrauterine developmental programming still remain to be identified. Obesity involves chronic low-grade systemic inflammation that, in addition to physiological adaptations to pregnancy, may potentially expand to the placental interface and lead to intrauterine derangements with a threshold effect. Animal models, where maternal inflammation is mimicked by single injections with lipopolysaccharide (LPS) resembling the obesity-induced immune profile, showed increased adiposity and impaired metabolic homeostasis in the offspring, similar to the phenotype observed after exposure to maternal obesity. Cytokine levels might be specifically important for the metabolic imprinting, as cytokines are transferable from maternal to fetal circulation and have the capability to modulate placental nutrient transfer. Maternal inflammation may induce metabolic reprogramming at several levels, starting from the periconceptional period with effects on the oocyte going through early stages of embryonic and placental development. Given the potential to reduce inflammation through inexpensive, widely available therapies, examinations of the impact of chronic inflammation on reproductive and pregnancy outcomes, as well as preventive interventions, are now needed.