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Sexual Precocity in a 16-Month-Old
4 l7 a9 G/ V5 F+ a* X* p# EBoy Induced by Indirect Topical7 _+ }5 m- y$ V
Exposure to Testosterone
( }4 @" |$ {/ A! x) F5 k% }1 W* VSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
* \* a  E+ k. }5 \and Kenneth R. Rettig, MD13 k: h0 g! C9 X
Clinical Pediatrics( W# A1 I- j& O6 s9 {
Volume 46 Number 69 i" r) G5 J1 `" T: C2 F
July 2007 540-543
  y, t) Y( J4 v  I& w. j9 ]© 2007 Sage Publications
! ]3 Y) d7 X; Q( ^4 i10.1177/0009922806296651& `4 e* y$ u$ d0 d0 p
http://clp.sagepub.com
2 }* k# M- h% w5 Z9 U. Ehosted at
) W7 z* p2 u! f: q& @* Xhttp://online.sagepub.com# _6 v5 G* f: e8 y9 O3 Q% L
Precocious puberty in boys, central or peripheral,. y7 b, R- P+ p. C/ P' [' N) b! n
is a significant concern for physicians. Central9 M* U) }9 {! X( _
precocious puberty (CPP), which is mediated
- y8 V# j$ D3 ?6 V  A# B' p9 e! zthrough the hypothalamic pituitary gonadal axis, has
8 p5 @$ x+ |/ o5 i% I; N0 ea higher incidence of organic central nervous system
0 A  \0 Y' j1 v! ^6 _lesions in boys.1,2 Virilization in boys, as manifested
4 w: y1 ?/ s( A* A9 K) _/ Dby enlargement of the penis, development of pubic
  e. U# A7 Q% G5 Thair, and facial acne without enlargement of testi-0 q& t; {: m* Q: ?
cles, suggests peripheral or pseudopuberty.1-3 We
0 e' u) r# b+ Areport a 16-month-old boy who presented with the5 F+ D6 ?( I! ~2 k
enlargement of the phallus and pubic hair develop-7 I; |) ]+ Z' G! o9 _- }
ment without testicular enlargement, which was due
* W) s8 D/ \9 Y, \4 X: Rto the unintentional exposure to androgen gel used by
0 [( d7 C# {, w3 j9 Q6 A8 _& Z" lthe father. The family initially concealed this infor-. R% P' G* y/ X5 g( i7 ]; f5 T
mation, resulting in an extensive work-up for this
( h. r7 L- g3 gchild. Given the widespread and easy availability of8 v. z: M& y  C) s% T
testosterone gel and cream, we believe this is proba-
( @- {9 v( d8 A  f# U) Gbly more common than the rare case report in the
) L# d' J" i4 K8 U3 jliterature.4
! b) n$ U+ U' c8 Q9 _5 R4 z1 e, bPatient Report5 V% k  I+ l5 h( s. W- q" X6 F9 P5 s3 E
A 16-month-old white child was referred to the# W0 `: G. a0 e' }* u+ U8 Q
endocrine clinic by his pediatrician with the concern* `" u- f, M) H: s$ @! |
of early sexual development. His mother noticed8 I+ [7 `# B! K
light colored pubic hair development when he was
6 V( E2 L; Q# i+ l) N0 P4 s; MFrom the 1Division of Pediatric Endocrinology, 2University of
$ Q( H0 a8 i; J3 w: y" p' Z6 }South Alabama Medical Center, Mobile, Alabama.2 S' d3 t5 c/ {$ i' O3 S
Address correspondence to: Samar K. Bhowmick, MD, FACE,
. Z' u0 V* d# a; Q, QProfessor of Pediatrics, University of South Alabama, College of5 T& A7 L2 P" s9 t8 O
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
* Y9 W) A7 S6 xe-mail: [email protected].
7 R' ^, Y, {) ~& B" O1 a4 d7 K! F9 tabout 6 to 7 months old, which progressively became# p% U- g6 u% D
darker. She was also concerned about the enlarge-
7 J0 j. L: }+ U3 K# L  xment of his penis and frequent erections. The child; \4 b% m/ w0 ~$ q. E
was the product of a full-term normal delivery, with
3 p7 y5 C# W  d/ |' j* ^, Ma birth weight of 7 lb 14 oz, and birth length of
% r# }4 U; y! H% m, e$ x20 inches. He was breast-fed throughout the first year
4 J3 I9 j, O" k, Xof life and was still receiving breast milk along with
' _/ q- Q" F9 B* i" |' F) G% Bsolid food. He had no hospitalizations or surgery,
0 c/ m5 t" p( b, ?3 |& aand his psychosocial and psychomotor development
$ E' k7 i& R# q9 Rwas age appropriate.
: }  J$ @. Q5 D) LThe family history was remarkable for the father,
4 R3 f; k0 z+ M/ L) g5 i# iwho was diagnosed with hypothyroidism at age 16,5 i6 a0 l$ c3 D6 H0 r
which was treated with thyroxine. The father’s
9 n" N7 I( k% ]. jheight was 6 feet, and he went through a somewhat7 P/ M, o% j" @9 ]
early puberty and had stopped growing by age 14.
6 |/ q& Q( W; Z7 {5 d7 CThe father denied taking any other medication. The. q2 r8 z: w; a  r! f' Y3 Y
child’s mother was in good health. Her menarche
8 J. M& U- t$ L! {3 n- |was at 11 years of age, and her height was at 5 feet/ w$ u5 M6 j) ?2 q3 @: f, \8 g
5 inches. There was no other family history of pre-- }& f! ]* J* ?+ |0 I5 R$ o3 U+ F1 Z
cocious sexual development in the first-degree rela-. w4 t9 g  F1 C
tives. There were no siblings.
! U8 x, Q4 o; R- i! [( L6 S2 DPhysical Examination  l8 R) U& t- V
The physical examination revealed a very active,
& U& S8 p- j9 R5 x' `1 eplayful, and healthy boy. The vital signs documented4 e) X$ S: |% y, }  V% R
a blood pressure of 85/50 mm Hg, his length was
8 G, h7 ~" ?; ?3 ?90 cm (>97th percentile), and his weight was 14.4 kg) }, K6 [/ X; H( i, W0 q" W
(also >97th percentile). The observed yearly growth
" _- e. T& ^  R7 j  U" Fvelocity was 30 cm (12 inches). The examination of' @4 i4 H$ Q# Z, b  I
the neck revealed no thyroid enlargement.
* N, H$ I0 B, ?, A0 x0 SThe genitourinary examination was remarkable for" M& `# v7 _0 J$ P& y
enlargement of the penis, with a stretched length of
+ _' _) V' b$ R+ \8 cm and a width of 2 cm. The glans penis was very well2 s" n8 \  _2 F- M5 [
developed. The pubic hair was Tanner II, mostly around& \# r% s) a1 k1 K/ K+ K& `( H2 x
540! o" H$ S5 R$ D$ O0 h! k* x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ {. @, c; t) V* Uthe base of the phallus and was dark and curled. The
/ E  [, a9 N, otesticular volume was prepubertal at 2 mL each.
7 E4 V" f+ h6 M( Z+ @The skin was moist and smooth and somewhat
( N  M4 s* Q5 h8 S3 P6 ], ]. _oily. No axillary hair was noted. There were no4 f% R5 Y' s, e
abnormal skin pigmentations or café-au-lait spots.
4 k: y0 y1 x: m3 R6 e6 LNeurologic evaluation showed deep tendon reflex 2+' q4 v" [( c6 W0 ^4 Z2 G& Q5 J
bilateral and symmetrical. There was no suggestion9 Q  ^6 a. G# o) G0 f
of papilledema.
- j2 q; ~8 L8 I# L  o! _Laboratory Evaluation
% f8 s4 {3 I& E9 V6 Q' T! Q& O4 ?The bone age was consistent with 28 months by8 X  E4 b) e0 @  p) l' z8 ~9 Z
using the standard of Greulich and Pyle at a chrono-. r  T% V, v% ]) R& t
logic age of 16 months (advanced).5 Chromosomal) U6 R& s4 O7 Q, j4 ~
karyotype was 46XY. The thyroid function test
' B, R& q. \! F9 W1 l6 y7 {6 J# tshowed a free T4 of 1.69 ng/dL, and thyroid stimu-# X1 i7 J) k" K4 n# D+ c* T
lating hormone level was 1.3 µIU/mL (both normal).
" q# I5 K7 a2 a' p" d1 AThe concentrations of serum electrolytes, blood
* v2 ~6 u2 ]2 T- i5 i3 c" c# Rurea nitrogen, creatinine, and calcium all were/ N2 L" W6 h  v, X) D
within normal range for his age. The concentration; S$ a! k9 t( v* N, p/ o
of serum 17-hydroxyprogesterone was 16 ng/dL
7 `5 h, [4 U1 \1 w- z% Q( K(normal, 3 to 90 ng/dL), androstenedione was 20
8 Z! W4 R" M# I" j' G. }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& F# m! u, M6 o8 V
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
& F* E% b4 n: {) ~0 g: Q4 l# Idesoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 A- U0 l' V% Z) {49ng/dL), 11-desoxycortisol (specific compound S)
- |7 J( o/ _: c  _0 O: `5 }was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 N5 B5 {* B  p% K: C
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total  y' [4 P  p& U
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 j' N1 r; l5 U0 t6 c5 `- m3 Aand β-human chorionic gonadotropin was less than
( R# ]0 |" x2 q# |# N5 mIU/mL (normal <5 mIU/mL). Serum follicular& }8 F( x- y1 E
stimulating hormone and leuteinizing hormone
/ O- r! A2 [& C; ~% G9 Lconcentrations were less than 0.05 mIU/mL
& c& I& ?3 A1 e- {. e9 i! S; p(prepubertal).2 n% K. d& C! K1 |+ D7 V2 k
The parents were notified about the laboratory
  }2 H4 g: L' ~$ @$ h0 d& h8 yresults and were informed that all of the tests were0 ]8 d5 C1 l  h) E( E
normal except the testosterone level was high. The) c4 N" u5 S4 v$ f. X% P. {
follow-up visit was arranged within a few weeks to
; X1 z+ Z# }) u' Uobtain testicular and abdominal sonograms; how-
/ ?& T" A0 B+ R: s& d! l. Rever, the family did not return for 4 months.
# ~. k, {$ N" ?Physical examination at this time revealed that the
; X1 L& S" h1 u. V3 E! q2 Kchild had grown 2.5 cm in 4 months and had gained
( F2 M* ~, r6 C: W% W9 x2 kg of weight. Physical examination remained  _7 Q2 p2 B3 Y+ ~4 d% ]
unchanged. Surprisingly, the pubic hair almost com-
1 S2 w# L6 W: I- F' y5 {1 Epletely disappeared except for a few vellous hairs at
: @9 A  O7 h) J- J( @the base of the phallus. Testicular volume was still 2
+ a# q* o. V; T/ GmL, and the size of the penis remained unchanged.! Y0 X9 K5 t$ ]- o3 P6 b
The mother also said that the boy was no longer hav-0 r& J! l/ W/ U( x4 a8 z* I5 H, L
ing frequent erections.4 ~/ f7 G$ r' D! ]+ _5 R
Both parents were again questioned about use of2 n9 e6 l' K* D( m, |/ P
any ointment/creams that they may have applied to
6 E4 U9 G6 c' U2 C6 {1 uthe child’s skin. This time the father admitted the+ j2 b2 F! K, _9 p  a; Z
Topical Testosterone Exposure / Bhowmick et al 541
% u) {5 N- L( _9 Tuse of testosterone gel twice daily that he was apply-
$ B3 `7 ?# \7 n2 Ning over his own shoulders, chest, and back area for
6 _2 J1 y3 X( Q* Qa year. The father also revealed he was embarrassed9 d% u3 m* F7 w# w% y- _! W
to disclose that he was using a testosterone gel pre-
& k: N# s. l6 G# tscribed by his family physician for decreased libido6 r8 ?' |/ c4 L, j
secondary to depression.
& ]. n  o4 M. X8 J/ ?! y! JThe child slept in the same bed with parents.) t: E! T, N$ f& g9 @1 H# k3 [/ u; x9 e
The father would hug the baby and hold him on his
5 |9 C' O1 H( ]3 h9 b2 V* j9 O8 qchest for a considerable period of time, causing sig-
9 z( b" g; s- e* P, gnificant bare skin contact between baby and father.
+ {. ]9 |( ~* R! E% p; r6 @1 _& @The father also admitted that after the phone call,& k" J. V8 q/ P, O( ^( p7 Y
when he learned the testosterone level in the baby
: B( }9 ]2 R6 _; [was high, he then read the product information
" v$ ?7 e) ?, C; ?packet and concluded that it was most likely the rea-
1 ?) s' O- G9 q* g2 kson for the child’s virilization. At that time, they7 v: ]  ]: N. K9 ]/ e/ E9 U" x
decided to put the baby in a separate bed, and the
+ `" y! F" G) f5 A( V: \( ?father was not hugging him with bare skin and had
/ `7 k, d, N1 @# @% Z1 abeen using protective clothing. A repeat testosterone
3 h7 K+ B% L  k7 Htest was ordered, but the family did not go to the
# X& g7 c, b# S; o+ i& klaboratory to obtain the test.4 }0 I! F% }) X6 ]& L6 C  R
Discussion: ~) g6 R8 x2 q' v" Q; m
Precocious puberty in boys is defined as secondary* D3 F% |2 j) v0 @, N" ]+ f3 h
sexual development before 9 years of age.1,4# A6 X/ L) d3 z5 P- [1 X
Precocious puberty is termed as central (true) when
! l& M& K" A2 I* x/ @8 r3 sit is caused by the premature activation of hypo-) f1 [/ U9 G! S+ M8 F
thalamic pituitary gonadal axis. CPP is more com-
" {! \' k2 h0 q% Z' l/ [$ p4 X) \mon in girls than in boys.1,3 Most boys with CPP! y5 s/ ]% L. J7 {' a, o- a0 e
may have a central nervous system lesion that is$ r# L/ V, f6 [1 g7 y7 E
responsible for the early activation of the hypothal-1 G6 V, p8 a9 H* [" U
amic pituitary gonadal axis.1-3 Thus, greater empha-
: w% o8 F2 h+ b3 p, _7 [sis has been given to neuroradiologic imaging in9 ~7 p! {! t: m
boys with precocious puberty. In addition to viril-- u: B1 @* G0 {8 z
ization, the clinical hallmark of CPP is the symmet-
$ @9 I, u9 K. C  Arical testicular growth secondary to stimulation by& X; U3 Y" j' W5 M
gonadotropins.1,31 y2 ~! U( H. P7 C
Gonadotropin-independent peripheral preco-" c, I% F* z# X8 [* C
cious puberty in boys also results from inappropriate7 A2 g& ]* _( N4 M+ a* \
androgenic stimulation from either endogenous or
1 |+ p7 ~: {6 D6 C. g9 Uexogenous sources, nonpituitary gonadotropin stim-$ B8 G3 i2 M4 _) o  O
ulation, and rare activating mutations.3 Virilizing9 T/ W0 I3 ]% }& a9 J
congenital adrenal hyperplasia producing excessive
& P/ C  @$ z$ u& J8 padrenal androgens is a common cause of precocious
6 {! `9 V% w5 L7 K- w9 k/ Bpuberty in boys.3,4
0 X" H8 n0 r* v8 A% ^3 kThe most common form of congenital adrenal, k' P  ?$ G" \0 v
hyperplasia is the 21-hydroxylase enzyme deficiency.* w0 g9 B5 Q: n  Q  R1 j" e
The 11-β hydroxylase deficiency may also result in" c9 e7 v9 g" J/ N8 I
excessive adrenal androgen production, and rarely,  X' j) b6 Z' Y* M' b9 y" |) n
an adrenal tumor may also cause adrenal androgen
% l) r3 K' q, _4 h3 O/ uexcess.1,3
( x* |0 Y. G2 Wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 u7 |/ [& o! n" o& _; L3 O* E+ H
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ ?+ @; f7 V! i! a1 O$ _' WA unique entity of male-limited gonadotropin-
/ E  ]) j5 N+ C2 e6 v! X. a) Tindependent precocious puberty, which is also known
( \- G5 E! J! D+ L* I. sas testotoxicosis, may cause precocious puberty at a/ m8 d$ F, e. D9 s& y8 h/ @5 a) i
very young age. The physical findings in these boys- E. K2 t% U; Z+ p  k
with this disorder are full pubertal development,- @6 b* s& {0 e% j3 v! |7 G
including bilateral testicular growth, similar to boys1 E9 c4 @2 h' X" O
with CPP. The gonadotropin levels in this disorder
! B+ T$ _3 ~. bare suppressed to prepubertal levels and do not show1 K, f. u0 R1 L2 `+ w+ ?! I
pubertal response of gonadotropin after gonadotropin-
5 ^$ T6 n1 P: f& W. Creleasing hormone stimulation. This is a sex-linked
1 s4 t5 b) S* }- U/ kautosomal dominant disorder that affects only
1 Y. p. @: h8 H* f7 A. cmales; therefore, other male members of the family
% |* W. _* f; D2 t5 Jmay have similar precocious puberty.3
& H4 {/ ~5 \. _4 iIn our patient, physical examination was incon-
1 v# q$ s' c# Y; K7 W( s5 Gsistent with true precocious puberty since his testi-
9 ]7 v1 s4 f( w+ C- }$ wcles were prepubertal in size. However, testotoxicosis3 `) l( o8 X1 v
was in the differential diagnosis because his father
9 R7 }8 h5 O/ m, Zstarted puberty somewhat early, and occasionally,
0 N9 z' a4 B& [8 x& }  btesticular enlargement is not that evident in the
  _8 B/ ?/ b% [& u1 p) t2 {3 h) i- Rbeginning of this process.1 In the absence of a neg-3 B9 V! ~/ |9 U  t5 [
ative initial history of androgen exposure, our
, P9 V2 e2 A6 y7 Y1 x' Pbiggest concern was virilizing adrenal hyperplasia,
" e5 t8 i0 `3 a& E) V# geither 21-hydroxylase deficiency or 11-β hydroxylase" R, U( g" Q( _8 t$ @/ E
deficiency. Those diagnoses were excluded by find-, m2 [& S5 W" c& |
ing the normal level of adrenal steroids.+ S, ]% m: P: _! F) N
The diagnosis of exogenous androgens was strongly5 x( [9 m- }% k- H7 K% ~$ `
suspected in a follow-up visit after 4 months because
2 f* r" `) E* m4 x2 d! \# Z+ Gthe physical examination revealed the complete disap-1 G) D" u  D1 v' J' D
pearance of pubic hair, normal growth velocity, and% Z  J) J; j" o4 X
decreased erections. The father admitted using a testos-6 R# Z3 Q2 U5 z8 }+ m5 u  m
terone gel, which he concealed at first visit. He was( q  f2 ]1 _% l/ B
using it rather frequently, twice a day. The Physicians’
  A) T: u% \) k4 m% p1 q" C# S" G! s' jDesk Reference, or package insert of this product, gel or
: u' M7 Y( P7 I! y& s8 F8 E' Zcream, cautions about dermal testosterone transfer to
5 `' Y8 m" @6 F, v! Wunprotected females through direct skin exposure.9 Q; v0 t) [  u" L2 U# v
Serum testosterone level was found to be 2 times the
/ ~2 p, y/ f4 j* [% F. tbaseline value in those females who were exposed to( d* j4 E0 m0 K% }" u
even 15 minutes of direct skin contact with their male* V+ B6 f2 R, q/ a& g! a7 T3 E
partners.6 However, when a shirt covered the applica-/ x$ K' Z  `* c( m7 A! }- m
tion site, this testosterone transfer was prevented.2 i" b! a: w3 X3 Q% ]1 s, |7 D: N
Our patient’s testosterone level was 60 ng/mL,) ~/ [3 p0 s4 |% }( E6 l
which was clearly high. Some studies suggest that; f0 [9 b+ e/ q4 I' w
dermal conversion of testosterone to dihydrotestos-
1 R& p# M1 {; t, U9 tterone, which is a more potent metabolite, is more% L# I1 M9 I% `* B# Z+ u* c* F  u) w
active in young children exposed to testosterone! _5 t& h$ u/ {
exogenously7; however, we did not measure a dihy-
' L# _0 G- x- Z' f7 }# {; ?drotestosterone level in our patient. In addition to% K1 O6 W2 n7 f# `
virilization, exposure to exogenous testosterone in
0 y9 G* N& R/ \7 T5 `! Dchildren results in an increase in growth velocity and* l- C; f; R. Z; ?
advanced bone age, as seen in our patient.: i; t* L" @: O' b$ F; o
The long-term effect of androgen exposure during3 e! |, E$ Z. ^! f9 o* @: X# o) J
early childhood on pubertal development and final' p( X* v+ ]7 B
adult height are not fully known and always remain4 L0 H3 c) f' t: F9 I' V
a concern. Children treated with short-term testos-3 b) }' H2 d* W8 K& O
terone injection or topical androgen may exhibit some
) u% f$ V- Z% P2 b: uacceleration of the skeletal maturation; however, after
6 ~% ^  v# ]5 v( m/ _cessation of treatment, the rate of bone maturation
& y. y2 C& o# {$ t. Y0 Q7 a% D% qdecelerates and gradually returns to normal.8,9+ y8 B2 t' Z2 {: E8 c- b! \
There are conflicting reports and controversy
, c3 z$ n! a6 q$ h8 Cover the effect of early androgen exposure on adult6 o" Q6 L5 j# B% q# `2 m  f
penile length.10,11 Some reports suggest subnormal
% w2 _/ d" n  @/ V$ A3 y7 P  Uadult penile length, apparently because of downreg-
4 \4 z) p3 [8 z4 T0 u0 C8 r& b  ?1 qulation of androgen receptor number.10,12 However,! t( L7 L5 @1 b5 _& s( M
Sutherland et al13 did not find a correlation between
* i/ H4 ^8 e9 W! S/ Q! N% Q- W- J! c" ~childhood testosterone exposure and reduced adult
; a3 E/ f4 c# Z  ?8 ?penile length in clinical studies.* L$ C. L; V8 h; {( n
Nonetheless, we do not believe our patient is3 r) M! i/ G0 c
going to experience any of the untoward effects from, S/ W. _# U5 H1 Z. E2 t
testosterone exposure as mentioned earlier because0 j6 V" s& B2 [$ G4 ]8 b
the exposure was not for a prolonged period of time.# _. R2 i: \0 @, t4 f$ A
Although the bone age was advanced at the time of
4 L3 n# [/ w9 b( {$ Udiagnosis, the child had a normal growth velocity at
" Q. x% C2 w3 h: }1 |4 Sthe follow-up visit. It is hoped that his final adult
6 P5 V" X6 Y5 k, N5 X6 v8 }height will not be affected.) ]6 P2 g- y  B( x9 i5 @+ z2 T
Although rarely reported, the widespread avail-+ W* L! Y, R" O) o; {% h
ability of androgen products in our society may
; ]5 ~5 b+ e3 n2 C/ }9 o7 d9 lindeed cause more virilization in male or female
/ A# m% Y# h  Y! @children than one would realize. Exposure to andro-
* H6 j* ], ~: }, Lgen products must be considered and specific ques-  A  m- E4 a$ h9 a
tioning about the use of a testosterone product or
0 U! b' D) S) G% _3 Vgel should be asked of the family members during
5 U/ p. j9 W9 p( D% I9 ethe evaluation of any children who present with vir-+ f3 m7 i& g: D* Z9 Z
ilization or peripheral precocious puberty. The diag-
" b, ?+ i' u( P: K6 W  `nosis can be established by just a few tests and by
5 ?! f$ S) N: Q# `/ t( iappropriate history. The inability to obtain such a2 \; C" S3 j& M- |: E* e& `. |- N4 U
history, or failure to ask the specific questions, may$ m% G: r$ [1 ~# l( i! ?2 \
result in extensive, unnecessary, and expensive, z# V' I2 c8 Q! q7 f
investigation. The primary care physician should be' P# v* G, H) H8 r+ f
aware of this fact, because most of these children
: ?( I& q0 w8 R$ k$ pmay initially present in their practice. The Physicians’8 V5 d6 I6 T" P
Desk Reference and package insert should also put a
, s4 E  N4 @. a6 k3 D" Q4 k& }, hwarning about the virilizing effect on a male or
5 y% i% Y! C/ ifemale child who might come in contact with some-5 C) H8 z  {* ~! ?
one using any of these products.
4 x4 L9 l0 k& J9 B- W# JReferences) g: x; u& t/ ?6 f7 {/ Q2 X7 R
1. Styne DM. The testes: disorder of sexual differentiation
( s1 ^9 n+ U9 k' a" i* ~and puberty in the male. In: Sperling MA, ed. Pediatric
. V: S# a0 T" X& u6 }/ a$ yEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;; f6 R/ D  s) a) @; o
2002: 565-628.
9 x: m- U+ r. h7 B8 d6 r4 Z# H2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% O; P; b! }. w% L
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
/ j& C% K. D9 e2 nBoy Induced by Indirect Topical
+ t& I* @9 w, h5 \Exposure to Testosterone. {3 S, H  O4 H- d# L6 ]1 G: o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: l% e( Z. C- h) z) {and Kenneth R. Rettig, MD14 ~" \! j. w1 V6 P7 n
Clinical Pediatrics
% f3 I: ^% t# DVolume 46 Number 6  a7 y( J4 _0 K
July 2007 540-5433 y' n5 K$ o& o' y3 E7 @4 r
© 2007 Sage Publications2 ^5 K% e. ]. c4 P3 v7 `( m
10.1177/0009922806296651
& e# l# n) [, ohttp://clp.sagepub.com, @% c$ M  G  q) i3 L8 @
hosted at2 C) R6 q% v. M# V
http://online.sagepub.com
" ]# o  s( g3 p/ E- Z7 x* W# hPrecocious puberty in boys, central or peripheral," ]! X. t: P$ a, R; e7 G' |
is a significant concern for physicians. Central
, t. Y" Y$ G8 R9 L7 kprecocious puberty (CPP), which is mediated
" v$ r7 {5 c$ zthrough the hypothalamic pituitary gonadal axis, has8 b' e) X* U5 P
a higher incidence of organic central nervous system
/ F. U1 Z. q( b$ \  Tlesions in boys.1,2 Virilization in boys, as manifested
( i5 T9 \( D- t. M' Qby enlargement of the penis, development of pubic
. E2 X  V) T  r1 Z" ohair, and facial acne without enlargement of testi-" R/ _8 e( s1 R  {6 D# H
cles, suggests peripheral or pseudopuberty.1-3 We: z9 V/ {6 m  X
report a 16-month-old boy who presented with the8 m% h9 L" v6 b# I( w2 ?
enlargement of the phallus and pubic hair develop-
$ A( v+ z+ d0 b, e4 [ment without testicular enlargement, which was due) q7 d7 U4 _2 ~5 F2 M9 \# }% y0 a
to the unintentional exposure to androgen gel used by" ?' `$ e( ~$ U# W0 J
the father. The family initially concealed this infor-- f* ]4 j, y  G' S% [0 M! b
mation, resulting in an extensive work-up for this
& E2 U3 x! y* R- `child. Given the widespread and easy availability of9 z; n, G: M' V0 ?; ~% N
testosterone gel and cream, we believe this is proba-
4 @% ?' B& J2 V' J$ T: T5 ?bly more common than the rare case report in the: b4 u) f# t( ~5 h- e1 o( o
literature.4
" z8 x; {* \1 Z8 s$ n6 q7 NPatient Report- t1 X( |* f, d6 f
A 16-month-old white child was referred to the; K! y5 C+ D$ q
endocrine clinic by his pediatrician with the concern3 |, m9 S  `" p: l3 G6 N( T8 l
of early sexual development. His mother noticed
6 `' r: e( \% H0 Slight colored pubic hair development when he was( S" c1 J6 n- o  L; y3 @0 F, P7 L
From the 1Division of Pediatric Endocrinology, 2University of
) Y4 k) A! A& aSouth Alabama Medical Center, Mobile, Alabama.
9 ]3 R- N  j. c4 i# x$ `4 H, NAddress correspondence to: Samar K. Bhowmick, MD, FACE,
$ K, N8 t) g/ a: b8 WProfessor of Pediatrics, University of South Alabama, College of
. A9 @" _* z: y- mMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# V$ O! F5 D- m0 h+ b& me-mail: [email protected].
; T- Y2 o4 i) Y0 t( X8 q. Habout 6 to 7 months old, which progressively became
3 q! W# B2 ~" Udarker. She was also concerned about the enlarge-0 y1 B. R, K, N# l6 ?
ment of his penis and frequent erections. The child
" C! [8 h. G" k% U5 awas the product of a full-term normal delivery, with0 L  c7 C2 B- r* S; ^5 G* B
a birth weight of 7 lb 14 oz, and birth length of- A1 y- g3 F& a/ ]; j1 C
20 inches. He was breast-fed throughout the first year: a7 i7 H" S6 Y# H
of life and was still receiving breast milk along with
$ K* v4 S& k0 p+ Lsolid food. He had no hospitalizations or surgery,
. [2 q9 ~/ ~* O6 M% A8 k4 p( {* nand his psychosocial and psychomotor development
1 \+ C! E, w* K4 d  Pwas age appropriate.: _7 V% B$ p) X6 i
The family history was remarkable for the father,
" w6 d- c$ X% e/ wwho was diagnosed with hypothyroidism at age 16,
$ y: k4 o4 x2 h8 F0 T4 k* Q, }which was treated with thyroxine. The father’s
) ?* y! p0 l$ ~6 f/ j6 _- fheight was 6 feet, and he went through a somewhat
( m9 L/ W# `" @( S" D0 _early puberty and had stopped growing by age 14.
/ [- C9 o4 ]/ i3 p' f4 H2 @, SThe father denied taking any other medication. The
: F' P3 w0 l1 W" e  ~/ D* L9 `child’s mother was in good health. Her menarche
+ o; `  _1 v* h; R' H" x' |was at 11 years of age, and her height was at 5 feet0 x1 j, R' t  C/ {
5 inches. There was no other family history of pre-+ h1 \9 Y( B& F5 \  q9 ^# G9 y0 o) t, N
cocious sexual development in the first-degree rela-: m7 P5 T% Z( e6 n
tives. There were no siblings.
+ J. m5 g* T- X: C! T: z8 DPhysical Examination
) a4 k9 Y' ^/ y( E) \The physical examination revealed a very active,8 \& F: P" P3 r' G3 ?# T2 U
playful, and healthy boy. The vital signs documented# Y6 X$ ?. G7 u4 @9 s
a blood pressure of 85/50 mm Hg, his length was1 E: w4 `$ D* K. Y& K, `0 A( w) e
90 cm (>97th percentile), and his weight was 14.4 kg
/ ^( m: L8 |/ o5 q$ S(also >97th percentile). The observed yearly growth
/ x0 b( o3 ?( @' F- o1 vvelocity was 30 cm (12 inches). The examination of6 F) W6 J7 I( i) l" r+ K1 A8 g
the neck revealed no thyroid enlargement.
# `* h( {  ^9 p# T/ L( y- `The genitourinary examination was remarkable for/ d: H: s! _" p( u
enlargement of the penis, with a stretched length of" r6 R0 B) O! N4 p1 M2 g0 [/ C+ v
8 cm and a width of 2 cm. The glans penis was very well6 Y0 p! f# ?# A& r4 a4 R! k2 B
developed. The pubic hair was Tanner II, mostly around% n: r  P2 f1 C6 B6 p* \+ A- w
540# u7 `7 F' a3 |$ h2 i
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; l( i4 h2 D9 K6 }: [/ Q
the base of the phallus and was dark and curled. The: J2 ?' V+ U( i4 Y9 D3 n% F
testicular volume was prepubertal at 2 mL each.( @( V- x6 Y) r; e! I% z! c. k
The skin was moist and smooth and somewhat
' g0 s. i; U  E" V3 g% ~- xoily. No axillary hair was noted. There were no& S# s6 z, |% {3 a* L' `
abnormal skin pigmentations or café-au-lait spots.' M1 C1 J  X5 i8 \/ i( r
Neurologic evaluation showed deep tendon reflex 2+
! |- \: e. Y, ?( V3 |bilateral and symmetrical. There was no suggestion
; e. N) M0 @* u! W" B# T# Q' f4 Dof papilledema.
! Z; q# _0 T- yLaboratory Evaluation
" ~7 B) ~6 ~) F% p& u8 L7 z0 qThe bone age was consistent with 28 months by
& P- }# q" y, S, {using the standard of Greulich and Pyle at a chrono-
" J" \% y8 ~9 xlogic age of 16 months (advanced).5 Chromosomal/ Y  q0 q7 n: q% q2 k
karyotype was 46XY. The thyroid function test
( m% w. e6 N& C5 u9 _showed a free T4 of 1.69 ng/dL, and thyroid stimu-7 C* A/ S) y% k7 i& C
lating hormone level was 1.3 µIU/mL (both normal).
* S; l. `) x5 g. |The concentrations of serum electrolytes, blood( U9 z7 ~/ \2 ?! t+ M
urea nitrogen, creatinine, and calcium all were+ D% ~8 s6 Y3 o, |" ^% b# C; ~
within normal range for his age. The concentration
# t: G& {' I) O6 W, {of serum 17-hydroxyprogesterone was 16 ng/dL* {2 m: \( W0 n3 n, I
(normal, 3 to 90 ng/dL), androstenedione was 208 L$ |; l% k, v) q' K: j
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  X# q2 |; B  R3 ~
terone was 38 ng/dL (normal, 50 to 760 ng/dL)," r/ f! `4 x% e1 g0 U
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
# H' L. ^& B0 w/ z49ng/dL), 11-desoxycortisol (specific compound S)( g5 B7 _$ ?% q3 r* s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 |) D3 |6 z' m) Z: s" ]5 [# e: [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- u4 X# a- V# `& w- _
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) ?3 B9 T% W5 W, A! K" rand β-human chorionic gonadotropin was less than
) F' G  I3 Y' ~, X( o- r/ m5 mIU/mL (normal <5 mIU/mL). Serum follicular
7 x3 ^/ d# T$ Lstimulating hormone and leuteinizing hormone
4 f4 a8 m8 d, B  Q4 A5 Rconcentrations were less than 0.05 mIU/mL; r' c6 H! o% W+ U8 f
(prepubertal).) M3 V! \# E' B2 T) w% p
The parents were notified about the laboratory
, x0 ^% q+ m2 {+ s* `; J# W" T# Sresults and were informed that all of the tests were
# V. Q/ Y, m# k& s9 bnormal except the testosterone level was high. The
( K  E7 E2 |6 H. i; j8 ~follow-up visit was arranged within a few weeks to
# S0 j- @3 r: w4 F4 kobtain testicular and abdominal sonograms; how-8 j7 A9 Y7 n6 j* q* i. E/ q, I
ever, the family did not return for 4 months.
% |& J" j! x5 s6 L/ k5 qPhysical examination at this time revealed that the+ J4 P( ]8 V0 `7 K% W9 F
child had grown 2.5 cm in 4 months and had gained
5 [7 D$ J7 y& y6 u' x9 i2 kg of weight. Physical examination remained
5 @  w, l- h5 K1 X+ Q8 R8 K3 g6 Tunchanged. Surprisingly, the pubic hair almost com-
/ I$ r' N7 s1 G( Y$ Dpletely disappeared except for a few vellous hairs at7 J$ `; G% O7 v9 Q+ ?, g- m$ c
the base of the phallus. Testicular volume was still 2$ D. z2 P+ e  d; B( ~
mL, and the size of the penis remained unchanged.
4 d7 x$ k+ Q3 [3 x  o' [The mother also said that the boy was no longer hav-
! g! O/ j: [9 ]9 |$ P& Xing frequent erections.
" |1 p3 ^6 d2 L: O- e. U' j/ aBoth parents were again questioned about use of
6 K9 I/ V" M/ ]. b0 K& Dany ointment/creams that they may have applied to
7 ?, j4 ^  c1 @the child’s skin. This time the father admitted the
+ P% Q7 T8 N4 A, h5 z8 l* J: N0 iTopical Testosterone Exposure / Bhowmick et al 541/ h: J, n+ D* |: B
use of testosterone gel twice daily that he was apply-2 E9 Q2 \2 m( x) U7 T# x' b
ing over his own shoulders, chest, and back area for$ Q) h9 {4 [' s6 ?* o$ d: \! L. w9 n
a year. The father also revealed he was embarrassed  U1 C" C' T# }' v3 r$ a7 |8 v* w
to disclose that he was using a testosterone gel pre-, d" s$ D$ C. ?; V
scribed by his family physician for decreased libido$ W( e6 E. `: a9 c* X
secondary to depression.
- _: g+ z( e! _The child slept in the same bed with parents.
! S& j% y* I4 d, r5 }3 k7 W9 WThe father would hug the baby and hold him on his: K& }+ N& ?: X9 r2 i
chest for a considerable period of time, causing sig-
! `( N  c, d9 N/ W3 A, |4 Nnificant bare skin contact between baby and father.
1 x! N7 Z/ {' i* R7 WThe father also admitted that after the phone call,1 W& I0 c) S0 o  [7 w8 ^
when he learned the testosterone level in the baby
8 {3 Y8 i: _1 k2 Z; bwas high, he then read the product information) m$ P' u2 J- _% ]. |8 E
packet and concluded that it was most likely the rea-  `- x4 B& e2 u5 y. }* e# T. N- X
son for the child’s virilization. At that time, they2 Q3 `8 U2 Z1 G/ M
decided to put the baby in a separate bed, and the+ X, h0 |' N& [2 S, g7 C/ P4 r
father was not hugging him with bare skin and had
* j  u, I& p& ]% Zbeen using protective clothing. A repeat testosterone
! g' ?& d5 B5 H( d6 htest was ordered, but the family did not go to the6 X) Y; W0 _" b
laboratory to obtain the test.
8 H7 N7 }% v& I; q# KDiscussion
* j& c$ V7 c6 V# Y% t/ k8 RPrecocious puberty in boys is defined as secondary
  ]6 A$ z# W( u1 I  xsexual development before 9 years of age.1,4
9 m, G/ _; S) J' W: _! bPrecocious puberty is termed as central (true) when
& O& B2 p( ?, f0 K! S  A8 g8 bit is caused by the premature activation of hypo-0 e! ~$ N% `( t4 r, c- Q0 d) S( {
thalamic pituitary gonadal axis. CPP is more com-
8 Q1 b. d5 V; G6 J4 S  kmon in girls than in boys.1,3 Most boys with CPP
- i* q- d- e. Smay have a central nervous system lesion that is
- O1 v8 j; l) A* @6 O% B1 K7 Oresponsible for the early activation of the hypothal-3 J, W2 n4 _, n/ i% z, R
amic pituitary gonadal axis.1-3 Thus, greater empha-7 q9 a5 f( `& {
sis has been given to neuroradiologic imaging in, v6 I( H/ V5 T/ w& N* ]+ P
boys with precocious puberty. In addition to viril-$ Z+ P8 n8 y0 w! O/ e% {- g  V
ization, the clinical hallmark of CPP is the symmet-
2 @/ m) T0 J+ f' j; j9 N) F% |rical testicular growth secondary to stimulation by
* Q" ]) \$ R; f9 a% fgonadotropins.1,3
& P2 D0 B/ K$ ^% SGonadotropin-independent peripheral preco-: m- w7 T8 K( A4 y6 W' \& x8 L: s
cious puberty in boys also results from inappropriate4 P- t5 H+ P0 h5 K+ J! S: `4 h
androgenic stimulation from either endogenous or6 q( J2 F8 R; |8 P6 c
exogenous sources, nonpituitary gonadotropin stim-
) P$ D3 x% B! F+ @- }" dulation, and rare activating mutations.3 Virilizing2 a7 d0 R. V4 o9 e+ c
congenital adrenal hyperplasia producing excessive
# j8 l. n3 f' M1 xadrenal androgens is a common cause of precocious' l; B$ u7 L& t: Z: r# u
puberty in boys.3,4: O5 y  K, W2 ^0 \
The most common form of congenital adrenal: f0 [  @7 ]# Y2 S9 B
hyperplasia is the 21-hydroxylase enzyme deficiency.- \2 M/ C1 A3 c* m1 `
The 11-β hydroxylase deficiency may also result in
. O$ h) ~9 {0 ~) yexcessive adrenal androgen production, and rarely,# ]: s* w+ T* `, K+ S
an adrenal tumor may also cause adrenal androgen$ u  F# o% J9 L) D  D  ]
excess.1,3
9 ]! l5 X& l& _/ U; u! Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' P* d- M3 N! L
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ p1 @. K# P# b! K  YA unique entity of male-limited gonadotropin-
$ Z6 M( D9 b. _/ cindependent precocious puberty, which is also known
( O4 m% V. ]0 vas testotoxicosis, may cause precocious puberty at a" Z5 o* @3 L3 ?; c# Q( A2 p+ R+ M. b
very young age. The physical findings in these boys0 \0 J6 Z7 R: Q$ _) M) |9 I4 E1 Z1 ?
with this disorder are full pubertal development," R% j: L8 E) K! s* f  b7 E) {, z
including bilateral testicular growth, similar to boys
1 H0 e& ^# f: `( Mwith CPP. The gonadotropin levels in this disorder# O% q, w6 D6 z; U5 A0 t0 N
are suppressed to prepubertal levels and do not show( {! W! J% \6 }  K" R
pubertal response of gonadotropin after gonadotropin-
4 C0 H7 `7 ~; p1 p( P1 breleasing hormone stimulation. This is a sex-linked; o; b! b2 \9 w1 W
autosomal dominant disorder that affects only% Z5 V9 \# U- p: m( o
males; therefore, other male members of the family
4 g) ~2 }3 D* _  {may have similar precocious puberty.3" e7 E, z" ]( x$ r7 _/ {
In our patient, physical examination was incon-
: V1 ~; X" X; Q5 I/ J1 p3 ~$ S7 h( `sistent with true precocious puberty since his testi-+ ]7 Y- H: j, S. f" F
cles were prepubertal in size. However, testotoxicosis" f" M1 o$ G# \
was in the differential diagnosis because his father. X  S' |! a  a8 x1 q
started puberty somewhat early, and occasionally,3 `5 U  q3 a! E7 ?+ F+ z. ?
testicular enlargement is not that evident in the' `" E. E. w  t" Z" D# D7 L8 M
beginning of this process.1 In the absence of a neg-
0 r3 |! ^- ^6 o' N* }1 ]! Native initial history of androgen exposure, our
( e; f2 Z: C5 F1 |6 m1 F, obiggest concern was virilizing adrenal hyperplasia,% r: P- \1 g7 M+ d. l' q
either 21-hydroxylase deficiency or 11-β hydroxylase
* n7 Y2 |* w; Ydeficiency. Those diagnoses were excluded by find-! m9 |- {* |2 U
ing the normal level of adrenal steroids.) P, Y" k6 y( v: }# z
The diagnosis of exogenous androgens was strongly
2 a# }% ~- X' @5 {  nsuspected in a follow-up visit after 4 months because8 F- ^5 }" r! E
the physical examination revealed the complete disap-
# c' m$ k$ J  N0 {pearance of pubic hair, normal growth velocity, and/ N- d1 J4 n- F9 ~9 Y* v6 p
decreased erections. The father admitted using a testos-, W. q  d3 d1 |* Z! U
terone gel, which he concealed at first visit. He was
7 r/ J/ f8 H( A+ ]using it rather frequently, twice a day. The Physicians’- G, w  V+ Q! @: N/ P  y
Desk Reference, or package insert of this product, gel or
9 K1 C3 a3 z0 Pcream, cautions about dermal testosterone transfer to
6 o* w! K; l) _4 A, punprotected females through direct skin exposure.: J# T5 T6 T& A9 b- c: t' m/ ^
Serum testosterone level was found to be 2 times the
3 }, F- Q, E$ {+ Y  abaseline value in those females who were exposed to$ T9 f1 e1 ]* x% D; E
even 15 minutes of direct skin contact with their male
6 q. s- T3 ?& p* S% {# H8 ?partners.6 However, when a shirt covered the applica-
) L; C; E5 E1 jtion site, this testosterone transfer was prevented.; Y) Q8 f$ [' N8 b4 [$ s. z
Our patient’s testosterone level was 60 ng/mL,
3 ?) R9 g8 M+ T& E% D, q+ W$ M# I, Zwhich was clearly high. Some studies suggest that
5 I9 s8 {% ?4 w' G  fdermal conversion of testosterone to dihydrotestos-, r4 q: O5 U6 \) f
terone, which is a more potent metabolite, is more
& [- q7 L3 i, j. B( _active in young children exposed to testosterone
5 e% y2 m: m" q1 v& C2 Sexogenously7; however, we did not measure a dihy-" a  P! s, _5 S  O9 x- e* {0 k
drotestosterone level in our patient. In addition to$ ~. n; G; v( J4 ]/ f$ d8 K, a
virilization, exposure to exogenous testosterone in! ]4 k8 y3 p9 `* f: U. `( j  Z) ~
children results in an increase in growth velocity and
% {( x0 w# I" G+ }) B* |/ s+ P( cadvanced bone age, as seen in our patient.
- ]4 M. A4 d. G+ T* v3 f1 uThe long-term effect of androgen exposure during& A: N; [9 g% X  a$ T
early childhood on pubertal development and final
* s* [+ m2 E2 g* v9 Vadult height are not fully known and always remain7 C9 b4 Z, r) I$ x. S- W
a concern. Children treated with short-term testos-
; W4 T! L; r  }5 l' M1 fterone injection or topical androgen may exhibit some  i- A4 M  U) W7 a5 ]4 {
acceleration of the skeletal maturation; however, after+ d$ N' C0 @3 r" T5 l2 C
cessation of treatment, the rate of bone maturation
2 g9 }7 D- ]1 y7 M% u! g0 Pdecelerates and gradually returns to normal.8,97 B) |: ?' Y* B8 ]: @. X
There are conflicting reports and controversy7 }5 _8 L4 i$ v
over the effect of early androgen exposure on adult% K4 }1 a" M* b; h" R
penile length.10,11 Some reports suggest subnormal
( V8 Z- ]4 H! Jadult penile length, apparently because of downreg-: k3 W: S9 n/ t5 U. J( I
ulation of androgen receptor number.10,12 However,
7 V2 ~! T8 P, b; G. `4 RSutherland et al13 did not find a correlation between3 b! c0 |& T8 _  |) _$ _2 V
childhood testosterone exposure and reduced adult. a1 A5 y4 v3 F' V0 O2 s
penile length in clinical studies.
' `, a" D  n- N9 H1 q( W7 fNonetheless, we do not believe our patient is
: K# K7 F" o* S$ A+ Q/ Qgoing to experience any of the untoward effects from+ o" \+ |% S6 K! b1 _$ w5 K
testosterone exposure as mentioned earlier because
% L' S" O2 Y4 z7 F1 e- z9 Cthe exposure was not for a prolonged period of time./ X) ~/ u0 }. U, p1 Y: M! E
Although the bone age was advanced at the time of
* d7 }# ]% b* |2 b- Mdiagnosis, the child had a normal growth velocity at
) s; ^. l+ }3 D& Hthe follow-up visit. It is hoped that his final adult
' k( L4 D- U7 c/ L- P9 D1 Cheight will not be affected.1 D, P: R: H+ R1 Q/ N, s6 R0 M. ~/ A
Although rarely reported, the widespread avail-
( a( M3 L3 _7 F! c: pability of androgen products in our society may* b1 x' d5 U$ m& x/ I- _( V
indeed cause more virilization in male or female
5 R$ b0 A4 ]% nchildren than one would realize. Exposure to andro-/ ~  f9 b$ @" s
gen products must be considered and specific ques-8 M# }9 _4 O0 k/ r5 ^; Y4 [
tioning about the use of a testosterone product or
0 u! w+ l, N: Q% b, ~! Mgel should be asked of the family members during
3 f# T' v6 y. D/ {the evaluation of any children who present with vir-' u( H5 ?$ ^+ X& @
ilization or peripheral precocious puberty. The diag-
/ _4 u- _3 E3 x& |nosis can be established by just a few tests and by2 c: t' R& B. G3 j
appropriate history. The inability to obtain such a6 S  f7 i- L2 `# }) C3 M( t' k
history, or failure to ask the specific questions, may
, t9 Z6 {' H! d/ [$ c6 tresult in extensive, unnecessary, and expensive8 {3 i2 y" v4 X1 g# J; r* I
investigation. The primary care physician should be
& ~& m3 y" L7 g- qaware of this fact, because most of these children0 }4 ], X. s4 b& P
may initially present in their practice. The Physicians’, ^  e" O1 e3 T3 J5 k- }0 m) M, i
Desk Reference and package insert should also put a# d% H# a5 k/ [9 f# U+ b
warning about the virilizing effect on a male or" I6 ?! T/ e5 [0 Q3 p) `
female child who might come in contact with some-' v2 n9 K/ B* ]! t! t% M
one using any of these products.* i7 K2 d0 c1 A; q$ {# x
References# z* k# @; P/ b6 M4 z3 D5 T' x5 G
1. Styne DM. The testes: disorder of sexual differentiation- W# j# D0 }2 f* Q$ L3 E" a
and puberty in the male. In: Sperling MA, ed. Pediatric
$ E# Z; R& W! v, f+ E( GEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ _. R/ R4 U0 [/ w! {# a/ f2002: 565-628.5 ~" o" W+ X/ t
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. r7 i. c% J# h8 F" V  x% m0 hpuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
3 m& B1 ]& H: f5 E$ o  Q) d
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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