Intentional Use of Testosterone by a Father to Stimulate Penis Growth in an Infant

Introduction

With the increased use of various forms of testosterone in adult males, its potential misuse can adversely affect children. Accidental exposure to topical forms of testosterone has been well documented to stimulate untimely androgen-stimulated changes among children of both sexes, resulting in findings consistent with precocious puberty among boys and excessive virilization among girls. The reported occurrences appear to be a consequence of careless use of this hormone.^1-7

In this instance, we report a case of intentional, albeit nonmalicious, use of depot testosterone by a father in an attempt to treat a concealed or hidden penis in an infant.

Case Report

An 11-month-old male, previously healthy baby presented to the endocrine clinic for evaluation of increased penile length and pubic hair growth, which were noted by an urologist evaluating foreskin adhesions. Both parents attended the appointment and reported increased penis size 2 months previously and pubic hair development 1 month ago. Frequent, prolonged erections were also noted but no body odor or acne. His father related his previous concern about his son’s penis size and appearance for the first several months of life. Initially, the patient’s penis was entirely below the skin surface and could not be seen without depression of the suprapubic fat pad (concealed penis). History also included a notable increase in appetite and flushed skin in the genital area, but no increase in the linear growth or weight gain was appreciated. Family history of early puberty was negative. Past medical history was remarkable for the child being a conceived by in vitro fertilization secondary to paternal partial hypogonadism. Of note, his father had been receiving depot testosterone therapy for low testosterone, prescribed for complaints of tiredness and decreased libido. Following a term delivery, normal genitalia was documented, and a routine circumcision was performed. The father did not deny administering testosterone injection(s) to his child.

On physical exam, the infant’s length was 78.6 cm (90th percentile), and weight was 13.1 kg (>97th percentile). His build was stocky, and testes were prepubertal (2 mL bilaterally). Tanner stage 3 pubic hair and a midpubertal-sized penis in both length (9 cm) and diameter (2.25 cm) were appreciated along with ruddy genital skin. Skin exam showed no café-au-lait macules or acne.

Laboratory values were as follows: serum testosterone, 145 ng/dL (normal <10 ng/dL, 5.0 nmol/L); luteinizing hormone, 0.013 mIU/mL (normal 0.02-7 mIU/mL); follicle-stimulating hormone, 0.3 mIU/mL (normal 1-12 mIU/mL); 17-hydroxyprogesterone, 38 ng/dL (normal 0-50 ng/dL, 1.14 nmol/L); androstenedione, 16 ng/dL (normal <69 ng/dL, 559 nmol/L); dehydroepiandrosterone, 4 µg/dL (normal 10-60 µg/dL, 10.9 nmol/L); and β–human chorionic gonadotropin, 0.7 mIU/mL (normal <3.0 mIU/mL).

Based on the laboratory results, central precocious puberty, congenital adrenal hyperplasia, and an adrenal or testicular tumor were excluded. Potential diagnoses were gonadotropin-independent precocious puberty and exogenous testosterone exposure. These results were discussed with the parents. Then, 1 month later, the patient had grown 4 cm, Tanner stage 3 pubic hair had been shaved, his nonstretched penile length was 6 cm, and testes remained 2 mL bilaterally. A bone age X ray yielded a value of 18 months, and the testosterone level was 93 ng/dL; it was 68 ng/dL when repeated 6 weeks later. At 16 months of age, his length was at the 90th percentile, pubic hair had regressed, stretched penile length was 5.5 cm, and testosterone level was <10 ng/dL.

Discussion

When a child presents with virilization during childhood, a potential diagnosis is simple virilizing congenital adrenal hyperplasia; if elevated testosterone and low gonadotropins are found, the differential diagnosis also includes luteinizing hormone–receptor defect (male-limited gonadotropin-independent precocious puberty), an androgen secreting tumor, McCune-Albright syndrome, or exposure to exogenous androgen.

Although previous reports of signs of puberty in boys or virilization in girls during early childhood caused by testosterone contact exist, these were all ascribed to accidental exposure.^1,2 This is the first case in which the exposure was apparently intentional, so as to cause penis growth and increase visibility. Although the father’s action cannot be condoned, this raises the question of whether increased androgen stimulation during infancy and the testosterone secreted during the infant phase of increased hypothalamic-pituitary-testicular activity, peaking between 6 weeks and 3 months, have any impact on adult penis size. There is no clear evidence that increasing testosterone levels during infancy has any impact on eventual penis size, although it appears, based on animal studies8 and from evidence among humans, that normal penis size at birth depends on normal testosterone exposure during fetal life, with adult size being the result of multiple factors involved in the fetal “masculinzation programming window.” The infant did not have diminished size at birth, although his father was concerned about the penis being concealed. Although the infant in this case had a penis of midpubertal size during infancy, it is expected that his adult penis size will not be changed.

The concealed penis is a normal variant, an entity different from a buried or trapped penis9 and is the result of skin attaching to the distal portion of the shaft, just below the glans. In a buried penis, skin extends along the shaft, requiring corrective surgery.

Hence, in any situation with concern about penis size, parental education is key. In this case, perhaps counseling the father would have avoided the scenario.