Ten-year-old Samantha "Sweet Feet" Gordon isn't just a girl who plays football. She's also the best player in a league full of boys and has become an online sensation. Known for flying past the defense to reach the end zone 35 times while racking up almost 2,000 yards in one season, Sam's YouTube highlight reel made her an overnight sensation. Appearing in her own Super Bowl commercial and on ESPN, Good Morning America, and Cartoon Network, Sam's attitude that girls can do anything, has inspired people across the world, from the U.S. women's soccer team to NFL greats to other kids just like her. She even got her own Wheaties box--the first one to ever feature a female football player. Sam's courage on and off the football field has lead her to greatness, but there were times when it wasn't easy. Readers will hear Sam Gordon's take on her love of football, her rise to fame, and her hopes for the future in this exciting autobiography full of stories and photos that will inspire all kids to go for their dreams.
An autobiography of Samantha "Sweet Feet" Gordon, the 10-year-old football sensation who made international headlines by crushing the competition in a league of boys and gained celebrity status when her football highlights reel reached almost five million views on YouTube in just three days. Simultaneous.
17β-hydroxysteroid dehydrogenase 3 deficiency (17β-HSD3) consists of a defect in the last phase of steroidogenesis, in which androstenedione is converted into testosterone and estrone into estradiol. Patients present female-like or with ambiguous genitalia at birth and most affected males are raised as females. Virilization in subjects with 17β-HSD3 deficiency occurs at the time of puberty and almost half change to be males. Maintenance of the testes in patients raised male is safe and recommended, except when the testes cannot be positioned inside the scrotum. The phenotype of 46,XY disorders of sex development (DSD) owing to 17β-HSD3 deficiency is extremely variable and is clinically indistinguishable from other causes of 46,XY DSD such as partial androgen insensitivity syndrome and 5α-reductase 2 deficiency. Laboratory diagnosis is based on elevated serum levels of androstenedione and estrone and low levels of testosterone and estradiol, resulting in elevated androstenedione:testosterone and estrone:estradiol ratios, indicating an impairment of the conversion of 17-keto into 17-hydroxysteroids. The disorder is due to homozygous or compound heterozygous mutations in the HSD17B3 gene that encodes the 17β-HSD3 isoenzyme. Molecular genetic testing confirms the diagnosis and provides the orientation for genetic counseling. Our proposal in this article is to review the reported and our own cases of 17β-HSD3 deficiency.
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