Bin-Abbas B, Conte F A, Grumbach M M, Kaplan S L
Department of Pediatrics, School of Medicine, University of California San Francisco, USA.
J Pediatr. 1999 May;134(5):579-83. doi: 10.1016/s0022-3476(99)70244-1.
Micropenis is commonly due to fetal testosterone deficiency. The clinical management of this form of micropenis has been contentious, with disagreement about the capacity of testosterone treatment to induce a functionally adequate adult penis. As a consequence, some clinicians recommend sex reversal of affected male infants. We studied 8 male subjects with micropenis secondary to congenital pituitary gonadotropin deficiency from infancy or childhood to maturity (ages 18 to 27 years). Four patients were treated with testosterone before 2 years of age (group I) and four between age 6 and 13 years (group II). At presentation, the mean penile length in group I was 1.1 cm (-4 SD; range, 0.5 to 1.5 cm) and in group II it was 2.7 cm (-3.4 SD; range, 1.5 to 3.5 cm). All patients received one or more courses of 3 intramuscular injections of testosterone enanthate (25 or 50 mg) at 4-week intervals in infancy or childhood. At the age of puberty the dose was gradually increased to 200 mg monthly and later to an adult replacement regimen. As adults, both group I and II had attained a mean final penile length of 10.3 cm 2.7 cm with a range of 8 to 14 cm (mean adult stretched penile length for Caucasians is 12.4 2.7 cm). Six of 8 men were sexually active, and all reported normal male gender identity and psychosocial behavior. We conclude that 1 or 2 short courses of testosterone therapy in infancy and childhood augment penile size into the normal range for age in boys with micropenis secondary to fetal testosterone deficiency; replacement therapy at the age of puberty results in an adult size penis within 2 SD of the mean. We found no clinical, psychologic, or physiologic indications to support conversion of affected male infants to girls. Further, the results of this study do not support the notion, derived from data in the rat, that testosterone treatment in infancy or childhood impairs penile growth in adolescence and compromises adult penile length.
小阴茎通常是由于胎儿期睾酮缺乏所致。这种类型小阴茎的临床管理一直存在争议，对于睾酮治疗能否诱导出功能足够的成年阴茎存在分歧。因此，一些临床医生建议对受影响的男婴进行性别转换。我们研究了8名因先天性垂体促性腺激素缺乏导致小阴茎的男性受试者，从婴儿期或儿童期直至成年期（年龄18至27岁）。4例患者在2岁前接受睾酮治疗（第一组），4例在6至13岁之间接受治疗（第二组）。就诊时，第一组的平均阴茎长度为1.1厘米（-4标准差；范围为0.5至1.5厘米），第二组为2.7厘米（-3.4标准差；范围为1.5至3.5厘米）。所有患者在婴儿期或儿童期接受了一个或多个疗程的睾酮庚酸酯（25或50毫克）肌肉注射，每4周注射一次，共3次。青春期时剂量逐渐增加至每月200毫克，随后采用成人替代方案。成年后，第一组和第二组的最终平均阴茎长度均达到10.3厘米±2.7厘米，范围为8至14厘米（白种成年人的平均伸展阴茎长度为12.4±2.7厘米）。8名男性中有6人性活跃，所有患者均报告有正常的男性性别认同和社会心理行为。我们得出结论，婴儿期和儿童期进行1或2个短疗程的睾酮治疗可使因胎儿期睾酮缺乏导致小阴茎男孩的阴茎尺寸增大到该年龄的正常范围；青春期进行替代治疗可使阴茎尺寸在成年时达到平均水平的2个标准差范围内。我们未发现支持将受影响男婴转换为女孩的临床、心理或生理指征。此外，本研究结果不支持源于大鼠数据的观点，即婴儿期或儿童期的睾酮治疗会损害青春期阴茎生长并影响成年阴茎长度。
