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is a significant concern for physicians. Central% R! x& }6 g$ b9 ]
precocious puberty (CPP), which is mediated: j4 x3 o% X, R5 E7 O
through the hypothalamic pituitary gonadal axis, has
0 I7 Q1 H8 G5 _( N" O+ |" i0 S! Ea higher incidence of organic central nervous system
1 X4 ~: c( t6 G O/ {lesions in boys.1,2 Virilization in boys, as manifested
7 K; t5 D( r6 V$ `by enlargement of the penis, development of pubic; H L1 f$ m0 I) N* Q- Z& {
hair, and facial acne without enlargement of testi-# H5 O8 ]) {7 o0 F6 c5 L
cles, suggests peripheral or pseudopuberty.1-3 We! w8 l% G) W2 E. u6 p E
report a 16-month-old boy who presented with the
, N9 ]$ ^. n8 R5 uenlargement of the phallus and pubic hair develop-
1 n- Z( w0 E- j5 Q/ y0 f0 K6 Y6 gment without testicular enlargement, which was due
; H7 u" o( {+ E. C zto the unintentional exposure to androgen gel used by
4 R. c- H3 g L, g1 {, wthe father. The family initially concealed this infor-
# i! j3 H6 X( \- s2 pmation, resulting in an extensive work-up for this% r1 b% \+ v' _9 y3 D1 A/ f; D
child. Given the widespread and easy availability of
) x+ A4 u( f: a$ wtestosterone gel and cream, we believe this is proba-% j4 \9 j% \6 |, Z. M
bly more common than the rare case report in the
6 y b# ^5 ]: u% D. ]0 Oliterature.46 r L+ G, \6 v% Z
Patient Report
. T) G: U( e6 U3 U9 W+ v$ AA 16-month-old white child was referred to the
" [ G4 `* I$ J. ]3 |* h5 C# Vendocrine clinic by his pediatrician with the concern" R- {. L) n, I. ~3 |. X3 D% ^ `/ d
of early sexual development. His mother noticed. S+ _$ R; M# e, F8 s4 @
light colored pubic hair development when he was
! |1 y& a8 D. P% l4 o$ `: ^, t& Q) CFrom the 1Division of Pediatric Endocrinology, 2University of
E% v1 x8 E8 k% \& TSouth Alabama Medical Center, Mobile, Alabama.9 Y3 C& Y" K9 R% p/ W: `- ]6 {7 r
Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 q' g( G1 z3 @: W- D. U6 QProfessor of Pediatrics, University of South Alabama, College of3 ^) G( h! Y9 e( p. w! T3 b8 e1 m
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
, @ ]9 c% S* |5 J$ x3 He-mail: [email protected].: q- A* K/ y3 F+ _* s1 R- x
about 6 to 7 months old, which progressively became
& N" p( D- g( h, T5 J3 Odarker. She was also concerned about the enlarge-: z" Y/ Q; @7 a# O2 t$ r
ment of his penis and frequent erections. The child4 G z* o% C/ g9 P# H
was the product of a full-term normal delivery, with
- D/ V+ I& K/ [0 ra birth weight of 7 lb 14 oz, and birth length of
2 m F; V* M# C# A: A3 k1 p* S20 inches. He was breast-fed throughout the first year/ G7 P% D' q) G+ n) e; K
of life and was still receiving breast milk along with" u% c O: t1 j5 c; p+ {
solid food. He had no hospitalizations or surgery,0 a( C# `& Q4 r& } H) P! r' o
and his psychosocial and psychomotor development
" c2 t7 \0 c8 ?& k: Cwas age appropriate.% g% A8 \' K% }) k( U7 d: i
The family history was remarkable for the father,: Q8 I5 f; `2 T4 q; O9 f
who was diagnosed with hypothyroidism at age 16,+ t3 `1 Q( u4 ]8 I$ ^
which was treated with thyroxine. The father’s
8 n2 Z" s) g, N: O& {9 ^height was 6 feet, and he went through a somewhat
+ v$ M9 I4 Q% Hearly puberty and had stopped growing by age 14.
0 Z# N+ i2 a' |5 d4 w7 O5 HThe father denied taking any other medication. The6 ~6 B6 o8 N& a- i H
child’s mother was in good health. Her menarche) L3 _7 l! X: ^0 I) T
was at 11 years of age, and her height was at 5 feet
) F* [! h7 D) a# ]5 inches. There was no other family history of pre-- E( T! Q: ` D' z7 U
cocious sexual development in the first-degree rela-
7 G* p5 q9 w8 E- c6 \1 m* H" J# t! `tives. There were no siblings.
. e- f+ G4 y; G5 xPhysical Examination3 i8 g- |- i; Y2 f# }
The physical examination revealed a very active,; H) E! T- ?- Z+ w# O0 I7 f) c
playful, and healthy boy. The vital signs documented+ u! e* b' z) L$ |. w
a blood pressure of 85/50 mm Hg, his length was
5 k7 I" X. I3 v7 g90 cm (>97th percentile), and his weight was 14.4 kg) h8 V6 J6 S1 |! ^
(also >97th percentile). The observed yearly growth( M' d4 |6 O$ {( z6 L* \
velocity was 30 cm (12 inches). The examination of
2 T, X- m; i, y8 v" S3 {. sthe neck revealed no thyroid enlargement.
2 O; M. e& B! T( a" i4 bThe genitourinary examination was remarkable for
1 f! b! b$ T! `' I2 o: j' p: K+ r. j# menlargement of the penis, with a stretched length of7 J( p2 b; x+ }" _) A
8 cm and a width of 2 cm. The glans penis was very well: e) k5 Z0 R6 e2 a: y ?% U* T
developed. The pubic hair was Tanner II, mostly around- \* U7 c# Z5 E, {: `6 i- e
5408 g+ R* v: v& J) V! ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; c* |6 x7 ^- K3 f! t/ Cthe base of the phallus and was dark and curled. The
( o. {7 g4 Y! k: T9 ?5 ~& S% rtesticular volume was prepubertal at 2 mL each.
9 S& [5 s( m: N3 W2 A/ KThe skin was moist and smooth and somewhat+ u u2 v' l7 E$ Q& K
oily. No axillary hair was noted. There were no
# o4 u7 H" S" h8 j! wabnormal skin pigmentations or café-au-lait spots.1 o* ~5 \" Q7 w
Neurologic evaluation showed deep tendon reflex 2+
7 F& C1 L1 o k8 u0 v2 h3 }7 Ybilateral and symmetrical. There was no suggestion
2 b4 }+ N, J; P2 `3 N' d0 dof papilledema.
2 i) \8 o$ H& i" L; lLaboratory Evaluation2 B7 z v2 ^6 F; A
The bone age was consistent with 28 months by
# _8 @5 E' o% }using the standard of Greulich and Pyle at a chrono-$ c% O6 c( C A
logic age of 16 months (advanced).5 Chromosomal
6 a e/ G1 N$ @1 k5 D, [karyotype was 46XY. The thyroid function test
" T( D6 m+ O- x' r. Y; E+ kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-+ o4 ]( Y9 t' ~: {) E, V+ Y j8 o' E
lating hormone level was 1.3 µIU/mL (both normal).# D+ o4 I6 P7 s3 ?+ G! p
The concentrations of serum electrolytes, blood
) N3 B, X* S3 G2 iurea nitrogen, creatinine, and calcium all were
$ G- { G' D2 ywithin normal range for his age. The concentration; g) K, @$ a: u# w) b0 w6 y4 m4 W
of serum 17-hydroxyprogesterone was 16 ng/dL
/ ~ G. f7 P( d6 c(normal, 3 to 90 ng/dL), androstenedione was 20
2 t8 [2 V* F9 d- ~ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 E0 e2 L1 D2 g: p% P& r# lterone was 38 ng/dL (normal, 50 to 760 ng/dL),/ `/ g7 J" u. c8 e/ B) W# x
desoxycorticosterone was 4.3 ng/dL (normal, 7 to e O; O7 ? K8 S$ N4 T2 d4 @
49ng/dL), 11-desoxycortisol (specific compound S)0 A) A( U1 Y2 {, Z3 J- v8 Y W
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-& E# X3 N2 V$ N8 |5 }5 I% P8 s6 Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 x! y0 {* s" gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; z0 j8 A! c1 I: cand β-human chorionic gonadotropin was less than
4 W1 R l: G7 ]) d$ W1 L0 y5 mIU/mL (normal <5 mIU/mL). Serum follicular, a# A9 [: O0 G
stimulating hormone and leuteinizing hormone
4 [) d! {; Y+ U# N4 o% Z$ Vconcentrations were less than 0.05 mIU/mL, ?6 b( m, a% b5 o4 ]
(prepubertal).
- q* A! M9 c" ?The parents were notified about the laboratory
* _, @8 V+ Y% c1 Bresults and were informed that all of the tests were
; t9 f9 n, ~. {normal except the testosterone level was high. The
; ~2 s) g/ z% c" Y' m- S" xfollow-up visit was arranged within a few weeks to r4 X# q: G: X! q9 b
obtain testicular and abdominal sonograms; how-
y/ b5 G5 {: U' F+ uever, the family did not return for 4 months.8 l7 p; o6 L# g; T; x& O3 E
Physical examination at this time revealed that the3 w0 F* L3 x: l1 Q
child had grown 2.5 cm in 4 months and had gained( [- `, d: J* T' v% G
2 kg of weight. Physical examination remained0 S: g$ H) I/ N$ @. p
unchanged. Surprisingly, the pubic hair almost com-& |: {3 ]/ O6 n! @4 {$ M1 E$ y8 S8 f8 O
pletely disappeared except for a few vellous hairs at, @6 _% p) S" c. _- t3 s. V
the base of the phallus. Testicular volume was still 2' W$ D- _, m3 `$ H/ p1 V
mL, and the size of the penis remained unchanged.
* q+ ^" i) J2 O" uThe mother also said that the boy was no longer hav-. c9 q/ K: s: F# h
ing frequent erections.. P7 m) P0 R" k' }
Both parents were again questioned about use of
' Q, ?6 x5 h. S; F: vany ointment/creams that they may have applied to# L' ^' P! g( b" r& b. N7 M
the child’s skin. This time the father admitted the" x t L) G8 k* `
Topical Testosterone Exposure / Bhowmick et al 541
2 z3 m( C. e7 d- X5 d& guse of testosterone gel twice daily that he was apply-* c& [4 R' r2 f- ?4 r- H* A6 S
ing over his own shoulders, chest, and back area for' L8 }) ~$ j6 d+ H
a year. The father also revealed he was embarrassed
- |& t4 ^- K- X6 Y% H) a. g, f. ^to disclose that he was using a testosterone gel pre-1 b) p( v7 O/ ^4 h) w
scribed by his family physician for decreased libido' I$ ]. R) T/ w) _, S/ p
secondary to depression.- O/ P! p" f3 }1 U- d
The child slept in the same bed with parents., a/ @, e- G9 ~9 S" M" s" _
The father would hug the baby and hold him on his: a) H4 R8 Q0 v' h2 M
chest for a considerable period of time, causing sig-& _; r6 J, H. p' X7 H! Y$ c
nificant bare skin contact between baby and father.4 o, z. K5 P8 u) c! y* [) ]( n
The father also admitted that after the phone call,
8 C2 E. D! y1 O% B, \ F, gwhen he learned the testosterone level in the baby# r0 W4 m/ X- V5 g1 J' r% B& @" j
was high, he then read the product information
2 k" o# I) p Y( Spacket and concluded that it was most likely the rea-
( g, ?0 i! r ^3 P: I- Eson for the child’s virilization. At that time, they3 B% N3 s$ J# M" I
decided to put the baby in a separate bed, and the2 A0 W) b" j# \" ]: k g3 @
father was not hugging him with bare skin and had# h3 |& _3 o' E/ O
been using protective clothing. A repeat testosterone; H& e2 V: p ?+ y& [. W- |* b
test was ordered, but the family did not go to the' {; O0 [4 T. C5 x# Q
laboratory to obtain the test.
3 k4 J4 T7 ?( U) d2 E7 j% wDiscussion
9 J) ^" j) p8 k2 L; oPrecocious puberty in boys is defined as secondary
5 V2 w) }; v- p3 V3 M/ Ysexual development before 9 years of age.1,4( n$ L' K1 ?5 r/ X
Precocious puberty is termed as central (true) when
H3 U4 q8 {7 T( iit is caused by the premature activation of hypo-% H0 p) l, ~* ^) q& e \3 G
thalamic pituitary gonadal axis. CPP is more com-
5 M2 d3 m; y: _mon in girls than in boys.1,3 Most boys with CPP2 I5 Z1 w% i( ~/ V
may have a central nervous system lesion that is n- R* D9 @1 q2 ?# `" J
responsible for the early activation of the hypothal-
8 t. I" s' M% y+ `8 K* ?amic pituitary gonadal axis.1-3 Thus, greater empha-
1 s6 y N9 J0 Bsis has been given to neuroradiologic imaging in3 x5 n# M8 ~8 U1 l
boys with precocious puberty. In addition to viril-
3 e5 p/ V; _/ X" xization, the clinical hallmark of CPP is the symmet-
1 Q) J G6 ^" c5 Irical testicular growth secondary to stimulation by
: W( R1 x: L I* dgonadotropins.1,3
- k& [/ J( S0 e2 z' b9 @7 sGonadotropin-independent peripheral preco- [- q5 ?2 x- Y1 Z* v
cious puberty in boys also results from inappropriate, ^5 p* _0 U1 _; O% c9 y: Z
androgenic stimulation from either endogenous or& f3 p9 B8 q( D+ z4 [
exogenous sources, nonpituitary gonadotropin stim-
% \1 o3 |' s( s- r; sulation, and rare activating mutations.3 Virilizing U2 i5 v4 _' J: L1 Y
congenital adrenal hyperplasia producing excessive {3 I( x/ X. ~8 N( M
adrenal androgens is a common cause of precocious
0 f9 p1 i( _0 k3 s9 V6 c4 B3 K- }puberty in boys.3,4( ~) @# z# E5 \# s7 I
The most common form of congenital adrenal
* o) b/ @' i9 J3 `) P- o( ohyperplasia is the 21-hydroxylase enzyme deficiency.4 |- I2 W$ ]: f% z" K0 p) R* H
The 11-β hydroxylase deficiency may also result in
5 V {% w2 R' x) f$ T3 Mexcessive adrenal androgen production, and rarely,/ `, B2 z; H m2 y; M: [7 {5 I
an adrenal tumor may also cause adrenal androgen
/ X( p* G' c- p- l3 H6 h2 Hexcess.1,3
) @3 e" I- ^) }; ?+ \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& n4 W X% t6 Z5 [8 [ M7 n7 L/ f
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! w1 l1 u T" t
A unique entity of male-limited gonadotropin-6 g6 L ~0 Z2 W, e
independent precocious puberty, which is also known
9 F3 P8 i4 f4 W0 C2 Q9 T, @' ras testotoxicosis, may cause precocious puberty at a( L9 w `7 u& c6 P6 b& h; U
very young age. The physical findings in these boys
1 E: |7 F' k. u0 C# c, T1 Rwith this disorder are full pubertal development,
0 }. s# V. B- R# `3 D$ Z0 Xincluding bilateral testicular growth, similar to boys- g$ X/ f7 g0 d
with CPP. The gonadotropin levels in this disorder7 a$ d) f* a; t+ ^4 e3 O3 m
are suppressed to prepubertal levels and do not show7 C, t; Z. F4 r' J) q5 y
pubertal response of gonadotropin after gonadotropin-2 U" @7 p; u# L2 X+ f1 m
releasing hormone stimulation. This is a sex-linked2 K+ @* j9 K, K* ^& _5 h
autosomal dominant disorder that affects only# u9 h" r2 ~9 Q8 E
males; therefore, other male members of the family) N! i# u3 E4 k4 v! K! P9 ~
may have similar precocious puberty.3
2 I! Z. p6 W9 f1 [6 w' CIn our patient, physical examination was incon-4 c v8 M: M) J" l; I; y" n/ J) m
sistent with true precocious puberty since his testi-7 T& N3 ~. G; k1 O6 s2 R3 S% P9 _
cles were prepubertal in size. However, testotoxicosis9 v1 Z% L7 {7 |
was in the differential diagnosis because his father
; @* i3 Z7 e( T6 _6 t0 W+ sstarted puberty somewhat early, and occasionally,2 y# |1 T" a- j) w" L
testicular enlargement is not that evident in the) Q- D3 a! H3 o" N
beginning of this process.1 In the absence of a neg-
2 T. D6 U! r4 B H5 N1 @- K$ sative initial history of androgen exposure, our
( n7 V2 `: c% M, D/ I% {biggest concern was virilizing adrenal hyperplasia,' _' Q2 G. K& }, T9 _% H0 W
either 21-hydroxylase deficiency or 11-β hydroxylase
' \+ r* R: v8 [% ^& Hdeficiency. Those diagnoses were excluded by find-3 |9 T" ]$ ?; [5 d0 E7 {
ing the normal level of adrenal steroids.- s9 t2 x7 i, w8 Y9 T8 E( ~ b
The diagnosis of exogenous androgens was strongly
3 w: S) f; G, I( |suspected in a follow-up visit after 4 months because
, } N( x' F$ L+ l& M3 i# f8 zthe physical examination revealed the complete disap-
: j: U/ o+ f8 ` i, H$ o1 opearance of pubic hair, normal growth velocity, and) b3 l4 [" c A; v h/ F0 C; q3 x
decreased erections. The father admitted using a testos-
1 \+ t0 l6 f, c4 `terone gel, which he concealed at first visit. He was
# e' W6 q5 I A& L# j- zusing it rather frequently, twice a day. The Physicians’9 V V) C8 k5 Y& h T+ `9 y
Desk Reference, or package insert of this product, gel or# L, |9 r2 s% g8 z) ~. }
cream, cautions about dermal testosterone transfer to$ \: h$ ?( O0 V; [2 i W0 N+ L
unprotected females through direct skin exposure.) ^& I0 P9 N( ^- R" Q3 n4 y
Serum testosterone level was found to be 2 times the
* q* l- z3 L/ `6 wbaseline value in those females who were exposed to
) Z+ b4 u) D' n# d9 K H4 ceven 15 minutes of direct skin contact with their male/ z3 l5 D0 j$ t; o1 j2 B
partners.6 However, when a shirt covered the applica-: a. `9 B( J( |: N' @# K, C. ]2 k
tion site, this testosterone transfer was prevented.
( [ o6 S$ n$ t$ I2 z1 tOur patient’s testosterone level was 60 ng/mL,
& a2 J. p) _: f/ kwhich was clearly high. Some studies suggest that
, k. x3 r% {" \* ]dermal conversion of testosterone to dihydrotestos-
% h$ d$ ]+ R" Y* e& W/ m: v* {terone, which is a more potent metabolite, is more2 Z" c0 E% R# b, r Z. B
active in young children exposed to testosterone
/ U- L7 T# s( @exogenously7; however, we did not measure a dihy-
2 @. H: ~9 L6 o) I1 `" ^, Z0 w: C8 Gdrotestosterone level in our patient. In addition to
% p; _( r0 x2 }6 ]virilization, exposure to exogenous testosterone in
$ I$ p1 z2 D# B7 W/ Q. Wchildren results in an increase in growth velocity and# S: f" ~% s0 H/ Q+ ]4 g( u
advanced bone age, as seen in our patient.
/ B5 o2 m" l5 A& ]The long-term effect of androgen exposure during( E U: w8 o$ r$ ~' I' C
early childhood on pubertal development and final
& u' |9 A7 l4 s' {. ~adult height are not fully known and always remain# K+ L/ p1 J/ h* c2 m: v
a concern. Children treated with short-term testos-1 }3 K( `% S) Y, @
terone injection or topical androgen may exhibit some. `- j, Q3 y9 \4 o& a$ J
acceleration of the skeletal maturation; however, after$ B) R% d6 ]3 K! x& c
cessation of treatment, the rate of bone maturation
8 k3 _* m. g' Fdecelerates and gradually returns to normal.8,9
% y" b) X+ v" D# ]There are conflicting reports and controversy, {2 `7 G o1 O$ y4 Y% t2 c5 W, e
over the effect of early androgen exposure on adult6 D9 t/ y+ i) L' Y3 ?6 s7 ?! _
penile length.10,11 Some reports suggest subnormal# {3 o% V0 i$ k. n( H
adult penile length, apparently because of downreg-$ O7 W4 X( y7 d+ j
ulation of androgen receptor number.10,12 However,6 _% c/ p6 l( `- i. @
Sutherland et al13 did not find a correlation between9 A0 X8 Z& ?4 _
childhood testosterone exposure and reduced adult3 |$ r8 _8 |" p; a
penile length in clinical studies.
/ ^/ q4 \5 f# B7 {2 o8 L0 VNonetheless, we do not believe our patient is4 [, I+ u5 B7 o' E/ T
going to experience any of the untoward effects from
7 B4 R+ X. C, }, x! \1 J; ~6 Xtestosterone exposure as mentioned earlier because( ?" P" J0 p) b" X
the exposure was not for a prolonged period of time.' V4 `4 ?8 {8 ^5 _
Although the bone age was advanced at the time of
: g3 M( g6 E( J3 |. _; c: ]diagnosis, the child had a normal growth velocity at$ ^; L7 r, ?2 g; X' }9 C7 ]
the follow-up visit. It is hoped that his final adult! T/ S1 H+ z0 M3 x: N+ J0 C- N
height will not be affected., l y5 d* w2 \) Z
Although rarely reported, the widespread avail-+ x' Y5 H3 {4 [; t) P1 Y
ability of androgen products in our society may0 q- I- c9 j& Q
indeed cause more virilization in male or female
8 h* V7 a7 V( E) q) u' }: bchildren than one would realize. Exposure to andro-. C' M- F0 Y" O- _; D/ |- `
gen products must be considered and specific ques-( b+ m) @* T: i* k7 n1 j# ^
tioning about the use of a testosterone product or% D* T1 Q. i" N5 g- m
gel should be asked of the family members during
3 T$ M6 f! a' L7 s& B" g# Jthe evaluation of any children who present with vir-
9 {2 \( d9 G: Pilization or peripheral precocious puberty. The diag-3 i* h! A! ~ }# ~
nosis can be established by just a few tests and by% f1 x( M! ^6 y) q
appropriate history. The inability to obtain such a
0 L& g5 Q! S. H- i0 w) X( J8 hhistory, or failure to ask the specific questions, may1 B ]7 s+ y6 x! O- u; \6 @
result in extensive, unnecessary, and expensive' |0 b1 c8 y. V. [
investigation. The primary care physician should be/ t) ]0 J- [" K) l9 g- \
aware of this fact, because most of these children$ g1 m# w4 r' t
may initially present in their practice. The Physicians’( t' W1 z/ p( H, y/ |, G# R& l4 w
Desk Reference and package insert should also put a% o* |( e) b }
warning about the virilizing effect on a male or
& Y, h! q' j% H4 R, q5 ]. o" [! Vfemale child who might come in contact with some-
; j! K0 N3 w. u8 I4 Q: q$ L, Rone using any of these products.7 S, m) h" f. z5 f
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2002: 565-628.
2 }; o( t( a" [1 x2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
]9 T2 ]% ?6 A4 m; [. @9 c: xpuberty in children with tumours of the suprasellar pineal0 h/ v- V4 W1 g$ ^! M( e8 s
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areas: organic central precocious puberty. Acta Paediatr.
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+ K# G$ F6 S2 G( A/ R3. Lee PA. Puberty and its disorders. In: Lifshitz F, ed., w, S( S" A& _9 ^
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; J8 u7 }( w2 C n4. Yu YM, Punyasavatsu N, Elder D, D’Ercole AJ. Sexual/ I3 I9 {! \& ]
development in a two-year-old boy induced by topical" R5 y# b% Y; q6 Q: b( g& K9 O& D+ U5 N
exposure to testosterone. Pediatrics. 1999;104:e23.
" F; G9 b$ G# z& j `( ~3 V5. Greulich WW, Pyle SI, eds. Radiographic Atlas of5 K& c( ~) j* S l+ T& f( [
Skeletal Development of the Hand and Wrist. 2nd ed.% v/ q4 l4 D$ U( A$ ^
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6. Physicians’ Desk Reference. Androgel 1% testosterone,+ W5 y- O! x; e, _3 p9 k, a
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0 \4 I" ^9 l$ E( k; v# B. j( CEconomics Company, Inc; 2004:3239-3241.
5 Y' t8 @* Y+ S3 o5 V2 R* w0 u9 l9 w7. Klugo RC, Cerny JC. Response of micropenis to topical
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