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Sexual Precocity in a 16-Month-Old
$ X( t) j0 T9 I' x  g! qBoy Induced by Indirect Topical* J) W" Y, q# C" E, B
Exposure to Testosterone
- q2 K( K3 H/ n) N9 P, B" _Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2+ i- s7 F# _# e% ]" B
and Kenneth R. Rettig, MD1# [- q3 g5 m2 j; o" v: N
Clinical Pediatrics
& [+ M! H" m9 L1 a! P4 nVolume 46 Number 6
3 `$ m. u4 A9 Y: \& s3 {) A$ AJuly 2007 540-543# M7 |# @! L1 V) h2 b2 O
© 2007 Sage Publications9 T1 _1 i+ S5 x
10.1177/0009922806296651" G+ W0 C6 ?! j
http://clp.sagepub.com9 c9 l$ x/ n9 b+ |$ e1 p  Q
hosted at
4 O3 o0 Q$ E5 W, fhttp://online.sagepub.com5 [, Z5 u# V0 b& B
Precocious puberty in boys, central or peripheral,
% K$ L! `& h* \( cis a significant concern for physicians. Central* b. R" r# U5 H
precocious puberty (CPP), which is mediated& f( U) N3 ?0 V5 j# w; V- ]
through the hypothalamic pituitary gonadal axis, has; S' ~) V, m9 V, Z
a higher incidence of organic central nervous system5 l6 h+ M; x# N  D5 c/ A
lesions in boys.1,2 Virilization in boys, as manifested/ q. I0 r! P. ^' k, @. b2 f) a' q
by enlargement of the penis, development of pubic0 M; ?( z( ?8 }8 S
hair, and facial acne without enlargement of testi-0 `7 g3 b$ w% }, J5 \- D1 u- d3 Q
cles, suggests peripheral or pseudopuberty.1-3 We
6 ^7 }3 F; D2 g: @- v0 _: O  t( lreport a 16-month-old boy who presented with the
7 f1 T$ G% _9 d+ w+ G: F7 r0 W  Cenlargement of the phallus and pubic hair develop-
9 H6 l9 Q4 D4 |: a) C9 I& ]6 Dment without testicular enlargement, which was due
6 g( o% ]. K5 [# g1 p2 {' J( h2 ~to the unintentional exposure to androgen gel used by
8 W% E( v0 k3 k3 g8 lthe father. The family initially concealed this infor-7 p+ Z5 a5 {+ b% b  o# v- I
mation, resulting in an extensive work-up for this& F: C* W1 B( e* r% _. T. _
child. Given the widespread and easy availability of+ O# t7 A; z& \) v$ h
testosterone gel and cream, we believe this is proba-
4 t0 M1 T, X6 X5 ebly more common than the rare case report in the& x- x: N$ v' E7 _, G$ D2 Y
literature.4
- w; \/ h' @" o( \' V/ tPatient Report+ L9 y( ?# O7 i' R
A 16-month-old white child was referred to the
% h# }; K; o( P  B4 ~; P- i4 v, hendocrine clinic by his pediatrician with the concern1 L7 Y; F  x/ I' z, |5 `( @" G* Z# |
of early sexual development. His mother noticed
, P1 n4 @: M, y! Rlight colored pubic hair development when he was
+ n& ]# R4 E* C9 M( ]6 H8 `" rFrom the 1Division of Pediatric Endocrinology, 2University of
5 P0 y' i/ u4 j6 l  ?* H+ {South Alabama Medical Center, Mobile, Alabama.+ k. T- P2 Q  Y2 t, h$ Q6 z
Address correspondence to: Samar K. Bhowmick, MD, FACE,
9 m8 _2 C3 F1 F- k4 UProfessor of Pediatrics, University of South Alabama, College of% F+ P! Z1 S* ^9 ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) s' U0 C4 m# p/ O( Se-mail: [email protected]." c. h) T; E/ v0 N& a( f- Q
about 6 to 7 months old, which progressively became& H$ e: Z1 L2 s5 w, c
darker. She was also concerned about the enlarge-
( P4 {# `3 n' s6 Nment of his penis and frequent erections. The child
7 B9 b& U7 i- a* bwas the product of a full-term normal delivery, with' u8 C1 I# K% _2 Z! o4 I9 `' e) n( v
a birth weight of 7 lb 14 oz, and birth length of
1 P; t% p9 l7 c/ w$ L0 n9 b20 inches. He was breast-fed throughout the first year$ R* V: G4 Q0 p# o9 C5 c+ E" q4 I
of life and was still receiving breast milk along with
+ v. {' s9 {% |4 M( m7 Ysolid food. He had no hospitalizations or surgery,* |7 }5 ^( A# \4 m" P; o5 a; ?3 [
and his psychosocial and psychomotor development3 k3 \1 O7 y& a- s
was age appropriate.
0 V  T4 e' \2 f& C5 t( K/ M. [The family history was remarkable for the father," P* n0 \& z2 P" g( j6 t: l( S
who was diagnosed with hypothyroidism at age 16," o5 d7 I8 i6 i  Q; z3 _( p
which was treated with thyroxine. The father’s) _8 ^# P" m! Y8 G0 S. p* G# g
height was 6 feet, and he went through a somewhat
' x& S0 c# d6 }# w8 R/ Dearly puberty and had stopped growing by age 14.
" Q6 w3 |) c  T" a7 K; C5 @8 CThe father denied taking any other medication. The
' V* C1 O" e- S( y6 F6 mchild’s mother was in good health. Her menarche
/ i4 o7 U. q( l7 _& S  _2 L% Bwas at 11 years of age, and her height was at 5 feet7 y- I4 x  {/ y. q) L9 t( c3 T
5 inches. There was no other family history of pre-
7 f! S  e( M/ P; _cocious sexual development in the first-degree rela-
% r" l) y2 G* Z' @( ftives. There were no siblings.
0 J- N6 g& L# Y( B2 dPhysical Examination
) y1 x' X7 P6 n' m# jThe physical examination revealed a very active,
# V) l2 j8 `9 C+ Z+ Aplayful, and healthy boy. The vital signs documented) N" g; ^" E8 H9 x/ b2 u3 d
a blood pressure of 85/50 mm Hg, his length was  H. H2 j/ E. p  n/ Z/ H5 z
90 cm (>97th percentile), and his weight was 14.4 kg5 o: L8 ?: ^2 M# s
(also >97th percentile). The observed yearly growth* h7 T1 {1 ?. n
velocity was 30 cm (12 inches). The examination of& b% x: d; K' V- X
the neck revealed no thyroid enlargement.' S2 U# ]  L3 O7 K5 z8 a+ I8 C
The genitourinary examination was remarkable for
/ D+ W% L9 C4 c. k6 g2 L; }" p0 ienlargement of the penis, with a stretched length of
3 {1 i8 c) l0 D7 ~; ?7 w8 cm and a width of 2 cm. The glans penis was very well0 {8 m1 L8 ^& G$ E1 B2 Q- t; o6 H5 N: x, }
developed. The pubic hair was Tanner II, mostly around
" r( M1 x8 Y% j$ M8 n" [5405 P" b  r# |- `; @4 U% z( b# v
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, [( W! q1 U7 {) u5 U
the base of the phallus and was dark and curled. The
0 i1 `9 s. {( v2 ]/ c, ktesticular volume was prepubertal at 2 mL each.
% g- A( @  q  n; Y' |4 yThe skin was moist and smooth and somewhat
( f6 Y6 }2 C9 ?9 w7 @oily. No axillary hair was noted. There were no8 I! b4 m8 e  h% r) Q* {2 _
abnormal skin pigmentations or café-au-lait spots.
: l' h) |: ?2 h4 J. M: _Neurologic evaluation showed deep tendon reflex 2+
5 f1 R& T" _8 B" d" i. l7 }; Vbilateral and symmetrical. There was no suggestion, Z: G' z  ?3 b6 X* L% |
of papilledema.
' C) L' ~2 Y, _7 B8 mLaboratory Evaluation& a  Y6 I; c! u. n
The bone age was consistent with 28 months by
3 d1 p8 O; `- Q- M8 g$ Ausing the standard of Greulich and Pyle at a chrono-
+ u- T# S- p. K0 q; N0 x# }# \logic age of 16 months (advanced).5 Chromosomal% \6 V; J# t0 @1 [
karyotype was 46XY. The thyroid function test
6 }7 z5 g' x' T: hshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
: Z- u! ~2 Y* t8 ~lating hormone level was 1.3 µIU/mL (both normal).
: ?8 o6 Z: q, `7 W4 P) ^9 z/ D( NThe concentrations of serum electrolytes, blood
  F1 A8 d: k3 n$ i/ z, R! Jurea nitrogen, creatinine, and calcium all were# S9 A/ s5 ^1 s5 H$ d
within normal range for his age. The concentration
* o) l2 U/ g" u8 y6 |5 }" Bof serum 17-hydroxyprogesterone was 16 ng/dL3 T% x# P% n  Q7 x
(normal, 3 to 90 ng/dL), androstenedione was 20
& [  d# C% z+ tng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 J+ Z8 T- U( k) D  |' G& n8 B+ uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
! k0 F! e- ]9 odesoxycorticosterone was 4.3 ng/dL (normal, 7 to; |/ Y6 n7 H+ l- o/ ?
49ng/dL), 11-desoxycortisol (specific compound S)* B9 w  y3 O- a4 l6 r
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 @$ R7 P/ E% h1 ctisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total! E' U, i% @' V8 Z/ _$ N
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ b: P( o% B' _1 h5 T5 \
and β-human chorionic gonadotropin was less than
$ c# L' r/ j, t* c* P5 mIU/mL (normal <5 mIU/mL). Serum follicular
  h, u9 [! `* P$ Q9 J) ?# Xstimulating hormone and leuteinizing hormone& y- ]. a$ o7 G6 o& H
concentrations were less than 0.05 mIU/mL7 v. a" h( o' o9 ~9 H' F
(prepubertal).
7 k' J! L  R3 r: k/ R- z1 w3 V, b; nThe parents were notified about the laboratory( ?6 \) T5 x' m" Z6 G) h( i' ]
results and were informed that all of the tests were
* v' g$ [7 [( `/ y4 C% ynormal except the testosterone level was high. The' W6 q+ Y; Z& }5 T" H( J( ]5 k
follow-up visit was arranged within a few weeks to
* ^7 P6 H+ x: M- D, M$ `obtain testicular and abdominal sonograms; how-! w4 j9 p7 @' z+ ]9 p
ever, the family did not return for 4 months.
8 ]* s- ?  G8 s: p; }6 q0 P* TPhysical examination at this time revealed that the+ z0 Z& M( v3 g) }% ~8 |& X
child had grown 2.5 cm in 4 months and had gained
; l7 U: z; Z8 h, u* W2 kg of weight. Physical examination remained1 g9 A' Z/ N# Z: _2 |% j
unchanged. Surprisingly, the pubic hair almost com-% P+ ]6 k+ g  ?7 d# i- m
pletely disappeared except for a few vellous hairs at; t% s% q, B/ b8 d
the base of the phallus. Testicular volume was still 2
' `# R3 x; T9 ?( G+ v. j  WmL, and the size of the penis remained unchanged.7 ?1 y2 V8 ~9 u( _
The mother also said that the boy was no longer hav-
' t6 j, V% I+ t. Ling frequent erections.5 O2 _  u1 O4 e: p
Both parents were again questioned about use of- w* \# a6 [+ q/ s
any ointment/creams that they may have applied to
5 @5 H- o+ e4 w$ z5 k+ a0 Q4 bthe child’s skin. This time the father admitted the
( ~7 e2 Y9 @8 w) m- QTopical Testosterone Exposure / Bhowmick et al 541% k5 U) i2 x$ o: B
use of testosterone gel twice daily that he was apply-6 I4 H5 z5 k- c; \, e/ Y; o
ing over his own shoulders, chest, and back area for
, s& t, B" i; oa year. The father also revealed he was embarrassed
; y* r5 x5 R% C% S& n5 Qto disclose that he was using a testosterone gel pre-. P3 o% p& c' n# k  E; B1 Y' [
scribed by his family physician for decreased libido- S( Y+ h! W6 D
secondary to depression.
" Y  s* h# f. h- w! q6 e0 `3 fThe child slept in the same bed with parents.
2 }# O& q+ o+ O# D7 t- IThe father would hug the baby and hold him on his
" K/ k; D% ^- z4 M& W& Pchest for a considerable period of time, causing sig-
; O$ |+ U: F. mnificant bare skin contact between baby and father.
6 F; K+ X- ]; [" ~( {0 F  _The father also admitted that after the phone call,% I5 ?9 p! g2 R; o) ?
when he learned the testosterone level in the baby) N# s, s% \4 ?* G
was high, he then read the product information. h, B/ @4 i! q- l+ g
packet and concluded that it was most likely the rea-* V: W" V4 F/ p! z
son for the child’s virilization. At that time, they
0 ^- V: O) }  ~3 F" kdecided to put the baby in a separate bed, and the: B- a" G+ Q& e) c. o5 l2 y: T
father was not hugging him with bare skin and had+ t  S1 {1 b% H/ c9 y& O: b( X6 E
been using protective clothing. A repeat testosterone
) X" x% v6 i: {5 S, |6 D& @test was ordered, but the family did not go to the
' ]1 t2 k7 W$ g  klaboratory to obtain the test.
0 v  n$ f: y; _" @* wDiscussion
+ D$ c/ M2 G0 y9 \3 X+ UPrecocious puberty in boys is defined as secondary( y6 h- c) |$ [2 j
sexual development before 9 years of age.1,4
7 n1 S- i  A- B2 N- \% d+ ]# Z2 @Precocious puberty is termed as central (true) when- ]+ g8 U) @- V" S/ [
it is caused by the premature activation of hypo-
' x" Q$ ]& l) @/ Dthalamic pituitary gonadal axis. CPP is more com-
% y4 U' ]4 t2 f3 r& ]$ smon in girls than in boys.1,3 Most boys with CPP
6 M) v& T2 d5 z# U% e& Amay have a central nervous system lesion that is& |# N4 F& g/ X$ a
responsible for the early activation of the hypothal-$ x2 G' @' b% D) r9 O1 z( y
amic pituitary gonadal axis.1-3 Thus, greater empha-; J0 D$ i1 A/ o: _) j
sis has been given to neuroradiologic imaging in7 o  ~8 \! r8 Q$ s7 p2 }
boys with precocious puberty. In addition to viril-3 s' W+ v8 ]" G3 @$ G+ X0 P( k
ization, the clinical hallmark of CPP is the symmet-' {0 a, S8 y# l, P. g) V9 j
rical testicular growth secondary to stimulation by- Z+ M/ X3 o' }' ?; g9 D, |* M6 e
gonadotropins.1,35 L' R0 A. C* X3 D* C1 z8 Y2 p# P
Gonadotropin-independent peripheral preco-
3 t) y/ ~4 O! {& F$ [- z& u/ Ocious puberty in boys also results from inappropriate$ `& P7 Y* E! e& }
androgenic stimulation from either endogenous or+ [# [$ B9 x: t) A
exogenous sources, nonpituitary gonadotropin stim-
5 \3 E/ ]* h" G+ K/ z( x- Rulation, and rare activating mutations.3 Virilizing9 R; d! _3 R+ g% v9 |2 ?; H! v" L
congenital adrenal hyperplasia producing excessive! ~9 x* Z& v) r4 y' M5 O
adrenal androgens is a common cause of precocious( z  c% P3 f, }* w
puberty in boys.3,4
. K0 v7 \& T+ sThe most common form of congenital adrenal
9 Z  q" B; c7 Y7 R/ k% X/ @hyperplasia is the 21-hydroxylase enzyme deficiency.: q* |: z7 W9 w! G9 ?* Z
The 11-β hydroxylase deficiency may also result in
( {  E( ?- o# O3 R7 ]; x; zexcessive adrenal androgen production, and rarely,
" V/ W8 q1 I# Fan adrenal tumor may also cause adrenal androgen
  K* {! v4 [7 q/ d8 O1 m* z( texcess.1,3
1 h$ L8 p( K0 w$ v5 l& fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 Z% {7 s1 `3 B* d$ |542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 T, ]6 x( y/ d/ }% `( ^! ]
A unique entity of male-limited gonadotropin-6 z0 E3 z, T, O& k0 w3 b& g
independent precocious puberty, which is also known$ P, I* `) z! R$ _, i
as testotoxicosis, may cause precocious puberty at a
$ N2 z# K8 u) z4 `* Z+ C( Tvery young age. The physical findings in these boys
- b/ U' {# I3 K/ F8 g! Dwith this disorder are full pubertal development,* Q! Q* R0 Q  J
including bilateral testicular growth, similar to boys
1 F, {! L6 K  D% c* I: `with CPP. The gonadotropin levels in this disorder* z/ F: C: N0 P/ S" I4 @
are suppressed to prepubertal levels and do not show  Y7 T. H: I2 b& X
pubertal response of gonadotropin after gonadotropin-
  g# v! Y9 T, r7 s1 X0 greleasing hormone stimulation. This is a sex-linked
" D: @1 }, Q" n( X( Z5 M1 Y2 @& {autosomal dominant disorder that affects only2 Q" C/ w) S+ n$ B
males; therefore, other male members of the family' B- `+ P, l0 z( d0 f3 @
may have similar precocious puberty.3
1 {5 d, T1 \3 s# IIn our patient, physical examination was incon-4 ^, {2 ?5 ?; Y
sistent with true precocious puberty since his testi-" C3 |, C+ j; r" l- B
cles were prepubertal in size. However, testotoxicosis
9 i9 q; H" _7 y8 |was in the differential diagnosis because his father
( s; \* D# D  Estarted puberty somewhat early, and occasionally,9 C5 `4 y* T3 \9 F
testicular enlargement is not that evident in the
2 m# u2 T2 }2 G3 x0 Ybeginning of this process.1 In the absence of a neg-
) c$ u; g8 n* ^1 c8 F8 Yative initial history of androgen exposure, our5 l; E8 N. \1 y6 n  _
biggest concern was virilizing adrenal hyperplasia,
: n% K  P/ Y% b! i9 @either 21-hydroxylase deficiency or 11-β hydroxylase
2 D$ |9 b. e% l& `) ], o  I  ^deficiency. Those diagnoses were excluded by find-
4 O4 a) o# W0 s* D7 Ring the normal level of adrenal steroids.9 j% t& `2 i+ p
The diagnosis of exogenous androgens was strongly
4 `1 n+ n7 @3 ~suspected in a follow-up visit after 4 months because
" n1 h4 \& o8 k1 r9 o7 V$ m$ T" hthe physical examination revealed the complete disap-& S& q8 s3 O: c
pearance of pubic hair, normal growth velocity, and) L2 n; @6 o) [/ O7 o
decreased erections. The father admitted using a testos-4 x' [6 q$ A. j0 S) t
terone gel, which he concealed at first visit. He was
! ^6 |; m" A; }using it rather frequently, twice a day. The Physicians’! c# G) _! P1 Q8 U4 v2 V
Desk Reference, or package insert of this product, gel or
- Y/ t% f' R, `2 C/ Ccream, cautions about dermal testosterone transfer to
: L6 R* b6 L: O3 ^! S, q) ?3 j9 V9 Xunprotected females through direct skin exposure." ~2 d& i9 W9 m6 n+ Z2 ?" A6 W
Serum testosterone level was found to be 2 times the5 a, _5 |" X3 j" Z0 O8 `
baseline value in those females who were exposed to
# B; H4 `9 B1 H/ E" g( Zeven 15 minutes of direct skin contact with their male
! B. H) o2 ~* G) spartners.6 However, when a shirt covered the applica-
8 K9 k" q* U  @5 `tion site, this testosterone transfer was prevented.
4 J! h# c( q* T5 v; fOur patient’s testosterone level was 60 ng/mL,7 m7 h: {2 |& C6 u5 H9 I" R2 s+ b
which was clearly high. Some studies suggest that* n" g# `; m3 ^8 r- y3 z- u
dermal conversion of testosterone to dihydrotestos-/ U! @+ T6 ]; I7 {% N) x- f$ p
terone, which is a more potent metabolite, is more
5 A  A( h2 B. M0 E9 a  jactive in young children exposed to testosterone* W  C. n, k% z4 G0 U4 I
exogenously7; however, we did not measure a dihy-4 B9 }% b; U1 C/ V+ p
drotestosterone level in our patient. In addition to
: @  O0 w! L8 a% L# U( nvirilization, exposure to exogenous testosterone in
: [6 O% m# M( \9 t/ ichildren results in an increase in growth velocity and. w, ?- R* U( O+ R4 w
advanced bone age, as seen in our patient.
: t& L; r$ n5 p" i/ }" w! g0 ]The long-term effect of androgen exposure during4 i1 `# ]3 Z2 Y2 d
early childhood on pubertal development and final
% z0 ]% d( ]& u* i1 a% b+ {adult height are not fully known and always remain  V3 E* ^( h# g5 }' a* @9 q( |
a concern. Children treated with short-term testos-
2 g2 @( q- f; t, mterone injection or topical androgen may exhibit some
. r) @# m5 k, b- m3 J4 G6 Aacceleration of the skeletal maturation; however, after
$ I4 g  B* Y$ d4 m# A- |cessation of treatment, the rate of bone maturation
6 R8 d6 ?* U; B/ R( F. B& O6 hdecelerates and gradually returns to normal.8,9
4 |) a, c$ d7 Q* X$ Z) C! zThere are conflicting reports and controversy
* T7 m" y6 s  ~9 Sover the effect of early androgen exposure on adult
! ~- |) ^6 Y" Z+ npenile length.10,11 Some reports suggest subnormal
6 q5 f! x2 ^0 a; k( U8 uadult penile length, apparently because of downreg-
5 U; k5 o0 R* V5 T- Mulation of androgen receptor number.10,12 However,1 k1 Y. @' G- y- `, s
Sutherland et al13 did not find a correlation between
  D- i& y' s# h% d8 j2 nchildhood testosterone exposure and reduced adult! n: P2 D+ P2 h) Y  s% X, i
penile length in clinical studies.
; t3 c2 P2 K$ V( Q: e+ x/ `Nonetheless, we do not believe our patient is
1 G2 [2 v: Y4 X$ [, ~9 L" y3 R$ sgoing to experience any of the untoward effects from
" a# Z6 H8 }) A1 ?1 c6 G: R! itestosterone exposure as mentioned earlier because
: a$ r; ^1 f/ o* m" r: p: X) Rthe exposure was not for a prolonged period of time./ j& W( U3 {, ~9 o
Although the bone age was advanced at the time of1 u2 \* }, d+ P+ U2 E$ Q
diagnosis, the child had a normal growth velocity at
8 W) I' q7 f# kthe follow-up visit. It is hoped that his final adult
. G* y- W; ?, Q3 ]( yheight will not be affected.
6 H7 B5 L7 Q3 H$ {7 }" [Although rarely reported, the widespread avail-
5 ^) J; a1 e9 Y2 sability of androgen products in our society may
; K! c8 B; S5 c$ v, ^  oindeed cause more virilization in male or female+ ?0 @; N( u5 B$ J1 F
children than one would realize. Exposure to andro-
. D' v0 v* n- kgen products must be considered and specific ques-
  z1 y; d4 b* L* J* E6 ~$ L8 `5 F+ d6 Otioning about the use of a testosterone product or
9 T& D& n% e% y* [  v+ Pgel should be asked of the family members during
' i: t) y! }$ Mthe evaluation of any children who present with vir-; J  b5 s3 ^/ ]/ c4 i1 x
ilization or peripheral precocious puberty. The diag-
9 i$ ]8 j. P+ y8 L$ Y8 \nosis can be established by just a few tests and by
5 t$ T$ V( m* u3 N4 yappropriate history. The inability to obtain such a
6 N, C5 Z( ^( y; H8 W2 o) s) r4 khistory, or failure to ask the specific questions, may( f# L" U/ N& {1 |. u4 d
result in extensive, unnecessary, and expensive
! U# Q7 |- l- ~5 D$ oinvestigation. The primary care physician should be6 ^6 S' ^1 Q8 N" ?: T
aware of this fact, because most of these children
2 T# C8 i' n" Nmay initially present in their practice. The Physicians’
/ ]) Q0 }) k3 l- d! z/ @$ s9 TDesk Reference and package insert should also put a0 i# a. Q* K  t$ Y( K  T( W
warning about the virilizing effect on a male or
% N! l3 b2 F0 k1 v& }; i, l0 X  L) D$ _female child who might come in contact with some-; M: O) j. c. S2 {& b8 K
one using any of these products.1 }8 E1 t% |1 L1 I' V3 u
References
  {* a+ K8 B* O! y& Q6 V+ ]1. Styne DM. The testes: disorder of sexual differentiation
" f1 P! U. o& b" q5 A5 ^6 pand puberty in the male. In: Sperling MA, ed. Pediatric2 h# Z$ }7 |6 E; ~
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 i7 D2 a/ p: a" t
2002: 565-628./ g" E6 Y* T. ^: W) b4 [  ?$ ~3 b
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- J  ]; E6 G$ t
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
. B# _4 s5 E3 I5 ?$ vBoy Induced by Indirect Topical
8 ~1 R& _2 b' w" ]2 m$ r# B& }, tExposure to Testosterone- ?+ L: {- m! }
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 f' b# P) b  }0 ^8 {& Y1 }# @7 V
and Kenneth R. Rettig, MD1
: A" c9 f0 ]% f% ?- ?Clinical Pediatrics
6 U# x' j0 k1 w/ n. V$ ?Volume 46 Number 6# K! ?' y  c# N4 K3 x6 L
July 2007 540-543
1 o  i9 l0 Q! u8 G© 2007 Sage Publications
) S" e4 j) W+ x( }: y  H; o10.1177/0009922806296651
) f  |! l7 ~) x8 Rhttp://clp.sagepub.com
5 n& Q4 u* f$ ?: w) ?hosted at
2 e8 H4 d" f* H; n- S" [& o; U& xhttp://online.sagepub.com. |: c- |  {' j( O& I
Precocious puberty in boys, central or peripheral,
% z. ]8 ~# O; b8 z: O9 O! z$ [is a significant concern for physicians. Central* D5 v0 W" N* T( I- b  i1 v& F
precocious puberty (CPP), which is mediated9 O- E: R/ [  q* Q1 L
through the hypothalamic pituitary gonadal axis, has1 S9 u$ e! i3 _0 d' u9 ^" B5 |
a higher incidence of organic central nervous system
9 M0 ]+ J) _- E* W/ Alesions in boys.1,2 Virilization in boys, as manifested
( B  c+ p) |) d2 @0 dby enlargement of the penis, development of pubic
4 q% Q4 r  o* ], qhair, and facial acne without enlargement of testi-; x; u' a* W3 _4 D
cles, suggests peripheral or pseudopuberty.1-3 We  E, g+ o2 r2 P3 p: m1 d
report a 16-month-old boy who presented with the. k: s0 V0 E1 s" `
enlargement of the phallus and pubic hair develop-: U; M" W: H3 e, _/ ]3 S
ment without testicular enlargement, which was due
: ~! p3 p, S9 P5 v! m; uto the unintentional exposure to androgen gel used by
& z' o9 U6 M7 b/ v$ x. j8 Dthe father. The family initially concealed this infor-/ x# l- [+ J9 t9 T
mation, resulting in an extensive work-up for this
3 O; j2 h0 T0 Z$ I" hchild. Given the widespread and easy availability of& X1 A  F- n  J6 f( e4 O; R" d
testosterone gel and cream, we believe this is proba-" @1 J7 `7 k# n. {% i3 x
bly more common than the rare case report in the
, Q+ F6 \% H. r; \- M  _literature.4
' g/ X6 b. D' R/ q9 y1 f  |Patient Report. @9 ^3 x) h* D6 F$ @9 J' g6 l* W
A 16-month-old white child was referred to the
) s; O2 o! h# cendocrine clinic by his pediatrician with the concern# Z1 |# m$ G6 \* J
of early sexual development. His mother noticed
# i2 m0 h6 F2 Elight colored pubic hair development when he was
1 t4 k! Y* G8 E; J( r+ qFrom the 1Division of Pediatric Endocrinology, 2University of
0 t% r4 R# i1 G/ z- ^% B! }9 pSouth Alabama Medical Center, Mobile, Alabama.
! g4 ?! T6 `+ ?5 t; U- [) uAddress correspondence to: Samar K. Bhowmick, MD, FACE,0 R3 j& z, Y. |$ a
Professor of Pediatrics, University of South Alabama, College of
9 ~; a3 T+ b7 K0 W; fMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ J9 ?6 ~* A/ i  a$ J5 _' v9 ue-mail: [email protected].
0 n: l) Y3 O, T# a5 zabout 6 to 7 months old, which progressively became0 t' O* {! H$ X1 ~
darker. She was also concerned about the enlarge-
+ L6 @5 h, {: @. @3 e8 n6 }ment of his penis and frequent erections. The child
! V; U! x0 J! U9 U( f! cwas the product of a full-term normal delivery, with2 _) J# l' g0 d4 B: I' ]4 z
a birth weight of 7 lb 14 oz, and birth length of
5 c8 k- L) m: q8 E# m. y20 inches. He was breast-fed throughout the first year
) x6 A2 Q1 b6 N7 f6 j, p6 _8 b4 zof life and was still receiving breast milk along with# E; ^2 ~! K5 W2 S8 c9 w5 b3 l# I
solid food. He had no hospitalizations or surgery,
. t. S8 z" B& x9 y4 d- G; }/ Hand his psychosocial and psychomotor development
; W8 P6 l5 ?: L% G5 Z: Nwas age appropriate.. v/ L3 h- c4 B* C, |
The family history was remarkable for the father,
  u$ h. f& W$ E" y$ ?( Dwho was diagnosed with hypothyroidism at age 16,7 m6 X4 ?4 b6 N$ L. ~' z- d5 R% H9 Y2 \
which was treated with thyroxine. The father’s8 \  U9 j; ]" k) c+ y- }4 h- v) z
height was 6 feet, and he went through a somewhat- J* L) K- D8 y9 C, F+ w! s- Q
early puberty and had stopped growing by age 14.) @- j$ W$ D' m0 A0 U
The father denied taking any other medication. The3 T6 H9 {6 Y& t, T) G' p
child’s mother was in good health. Her menarche
3 d/ w) ]: }( Cwas at 11 years of age, and her height was at 5 feet+ t% o8 ]9 m$ b/ A' q
5 inches. There was no other family history of pre-
- @7 }0 O& o% H3 \% r9 T8 @cocious sexual development in the first-degree rela-  Q0 f* K# I% V4 `. _+ h* d
tives. There were no siblings.- V/ j( @8 X$ I+ D# h3 L
Physical Examination
7 Q8 w; r: R5 sThe physical examination revealed a very active,
" p2 }+ k: k( ~: Q" v5 @. s5 K$ Z" Kplayful, and healthy boy. The vital signs documented+ |# R, ?2 J7 m& t5 o
a blood pressure of 85/50 mm Hg, his length was
( O" W2 M/ |5 c( l6 b' C90 cm (>97th percentile), and his weight was 14.4 kg' F2 r* F( \* u8 _( C, }" s8 Y6 s
(also >97th percentile). The observed yearly growth* w( c9 t- S9 K2 J: p# A
velocity was 30 cm (12 inches). The examination of
7 n- u  U: f( B$ _2 i- B- ~/ Dthe neck revealed no thyroid enlargement./ w1 m" j: I3 ?0 p" o" U/ x
The genitourinary examination was remarkable for: A. F; H4 ]0 x4 g0 i7 j6 G/ `
enlargement of the penis, with a stretched length of
% o2 ]1 l# y4 A* @; l8 cm and a width of 2 cm. The glans penis was very well4 i3 C/ Y( X; W( J+ w8 T
developed. The pubic hair was Tanner II, mostly around
7 i0 G9 C+ R# l! X& Y5401 O5 G( p7 d, q6 ~" w
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the base of the phallus and was dark and curled. The6 d4 J% i5 O) ?' J3 V& P! I
testicular volume was prepubertal at 2 mL each.! Q$ e' `! i$ ?! S9 J
The skin was moist and smooth and somewhat  N$ t# z$ o4 D9 T% P) x
oily. No axillary hair was noted. There were no
- ^& S7 R/ x: i% s/ Habnormal skin pigmentations or café-au-lait spots.
1 B8 t- w/ w+ a2 dNeurologic evaluation showed deep tendon reflex 2+' Y! h: t9 |6 q' J0 S1 I. m
bilateral and symmetrical. There was no suggestion8 \! U2 y, k; p3 U5 t
of papilledema.
2 Q1 {/ v" z% }2 jLaboratory Evaluation6 t2 `( [( h! `" Y" t
The bone age was consistent with 28 months by
0 a% x# s) a( P; c5 j$ [using the standard of Greulich and Pyle at a chrono-# {3 L' v1 ?: N/ ^4 W
logic age of 16 months (advanced).5 Chromosomal
/ D# U3 t. w) H! ^karyotype was 46XY. The thyroid function test
* ]5 N2 f( d5 c# K5 @) Cshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ W  s' `$ i6 p7 b5 G, y! f* ?' Rlating hormone level was 1.3 µIU/mL (both normal)." v# m4 O& z9 [
The concentrations of serum electrolytes, blood! O5 p' C& t! l/ L  O
urea nitrogen, creatinine, and calcium all were
: _  T" B8 c0 V8 ^/ vwithin normal range for his age. The concentration
( A# N/ b0 P! u. f/ ?of serum 17-hydroxyprogesterone was 16 ng/dL
5 I2 U6 m; g2 H7 V" I3 `- n2 D8 B(normal, 3 to 90 ng/dL), androstenedione was 206 ]3 {) K# s# W9 K+ N/ H8 _- `
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( e9 O6 ^0 d0 }* v
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
: l! {9 }4 c7 ^9 a5 w% b+ adesoxycorticosterone was 4.3 ng/dL (normal, 7 to* x$ j/ E' f) K
49ng/dL), 11-desoxycortisol (specific compound S)
: V# g$ V: N0 \( f. ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
- g4 }7 T; O: Btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 e1 d9 c" l7 A0 ^; n5 S( etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; m8 z( f6 w' Z) a5 Y3 q& j, Kand β-human chorionic gonadotropin was less than- V% S; T5 A% n
5 mIU/mL (normal <5 mIU/mL). Serum follicular( ~# E, X) \* t& q( ?; q
stimulating hormone and leuteinizing hormone
% _: [5 S3 a3 F0 q$ e7 {$ r7 iconcentrations were less than 0.05 mIU/mL
! n, r! L/ j6 x6 V; V* R7 ?(prepubertal).' t( J. x+ l* T: ^: M
The parents were notified about the laboratory
& ^* w. Q8 [! S1 {  wresults and were informed that all of the tests were' Y- S4 c, c( s' T4 @3 E
normal except the testosterone level was high. The
- f8 c3 J* x& s. T7 P7 @follow-up visit was arranged within a few weeks to
7 Y8 G+ U. C* o% I9 P3 l7 n* Robtain testicular and abdominal sonograms; how-
5 x5 W0 f/ @: m7 Dever, the family did not return for 4 months.* O6 ?$ ]: B6 x: u* r
Physical examination at this time revealed that the9 ~; ]9 J- Q: o1 p: E3 V/ T  Y
child had grown 2.5 cm in 4 months and had gained7 h8 h0 v; c, C4 y+ ?. u
2 kg of weight. Physical examination remained
, s. q+ ?7 D2 ~8 p* b) S0 c' yunchanged. Surprisingly, the pubic hair almost com-5 b# u, X& x2 m! |; O
pletely disappeared except for a few vellous hairs at5 W2 n( r# c" o) o; g
the base of the phallus. Testicular volume was still 2
" g4 t$ i2 v4 J5 i- KmL, and the size of the penis remained unchanged.
6 v% H, M) S% S( qThe mother also said that the boy was no longer hav-
+ V# P8 W* k+ Xing frequent erections.
) p5 [) ^5 P% d8 SBoth parents were again questioned about use of
" Y* z, R8 p) t- ?5 j. @% tany ointment/creams that they may have applied to
! P* S& T1 W0 a8 h( t! q( ^3 athe child’s skin. This time the father admitted the
+ n) n/ R7 R' {6 o4 MTopical Testosterone Exposure / Bhowmick et al 541- ~5 k( J, o1 ~& Q, G
use of testosterone gel twice daily that he was apply-
" _! Y# O' b! u) ^  ging over his own shoulders, chest, and back area for. z; E4 [% Q  Z7 j& Z, Z
a year. The father also revealed he was embarrassed5 @/ t( T* @- [
to disclose that he was using a testosterone gel pre-0 w8 b1 z, }1 ~0 w$ `5 h
scribed by his family physician for decreased libido9 F+ g, o9 E# z8 N# L
secondary to depression.
$ m. i4 r, D1 W0 {1 hThe child slept in the same bed with parents.% B1 x5 U! C- l' B8 z3 E
The father would hug the baby and hold him on his
2 f, n& i( K1 c4 Xchest for a considerable period of time, causing sig-
# f9 H2 w9 x. E. I4 m8 ^3 Vnificant bare skin contact between baby and father.
. ?- o* n, E  V* [- S. VThe father also admitted that after the phone call,
& x' j/ w  F7 Nwhen he learned the testosterone level in the baby
8 ]6 U# s. y# H* O  w6 Xwas high, he then read the product information3 O" `" T, {$ V6 G2 n& o
packet and concluded that it was most likely the rea-3 F9 X. |* |1 w" A# E1 [  y, V
son for the child’s virilization. At that time, they8 r" [% S* h6 c9 N! F
decided to put the baby in a separate bed, and the
* g- T& a( b% b9 s' m( c+ \/ Gfather was not hugging him with bare skin and had2 i- h5 l7 h: i* a+ p* {
been using protective clothing. A repeat testosterone0 e8 s4 S; l/ z2 Y) H
test was ordered, but the family did not go to the
1 j8 F( V5 y7 O2 ?1 I8 Jlaboratory to obtain the test.
+ ?$ Y! ?/ Z7 u0 i  o: C& ?Discussion3 O8 D$ l7 g. h5 x- X
Precocious puberty in boys is defined as secondary
1 z, q" s: i- F$ Hsexual development before 9 years of age.1,4
. Y; u( o  x- z: g+ v& m" XPrecocious puberty is termed as central (true) when6 V# ^; p7 G8 Z3 A/ D6 j- H( Y6 U
it is caused by the premature activation of hypo-; a6 D8 Z/ |: V, F( E
thalamic pituitary gonadal axis. CPP is more com-9 q; B- ]% [& m) e. ^9 A
mon in girls than in boys.1,3 Most boys with CPP
8 ~: m& Z* I# m( L1 c7 z  E/ o$ mmay have a central nervous system lesion that is
( v. R/ q2 z1 U9 c$ i5 q, l8 zresponsible for the early activation of the hypothal-
8 o/ P  T; r1 Y, d. o4 Samic pituitary gonadal axis.1-3 Thus, greater empha-
0 \/ g; \2 s, }$ I3 }+ Gsis has been given to neuroradiologic imaging in# k& g! s" S! z
boys with precocious puberty. In addition to viril-/ a3 {- p5 ?8 a6 Q8 h
ization, the clinical hallmark of CPP is the symmet-* w3 N+ \$ @6 s: \! K8 Y
rical testicular growth secondary to stimulation by; K4 ?( u& T0 \* O6 b  k- @8 G
gonadotropins.1,3
& k; [/ c- z7 {$ C4 g, rGonadotropin-independent peripheral preco-- C, O: d% _$ z
cious puberty in boys also results from inappropriate
' Z) x+ E: k' Pandrogenic stimulation from either endogenous or
- ]7 ^7 Z% {* jexogenous sources, nonpituitary gonadotropin stim-
# U# ?1 n: C" Q: mulation, and rare activating mutations.3 Virilizing: k1 M9 r' H: K9 P9 s% Y$ q
congenital adrenal hyperplasia producing excessive/ c& n" T/ |  U' K3 [: U
adrenal androgens is a common cause of precocious
# v9 _  g8 K8 f# Q3 Vpuberty in boys.3,4
/ z2 ]( o0 M: A4 D" u6 M: @' _  hThe most common form of congenital adrenal
1 J" H1 p2 c0 J9 g+ [& bhyperplasia is the 21-hydroxylase enzyme deficiency.5 X2 t- `/ ]& I& }2 l! h- ?# L6 E: d
The 11-β hydroxylase deficiency may also result in+ Q' l5 c. W" M% r3 v& d
excessive adrenal androgen production, and rarely,
  `& ~/ b6 x9 q* I! t7 e7 kan adrenal tumor may also cause adrenal androgen
$ M8 j" j4 @" C% i. bexcess.1,3$ e- B- p+ ^) [8 U9 f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% t0 f) z! E, F( y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' J) G# S/ l) Q9 u) ~
A unique entity of male-limited gonadotropin-' y  Q# ~5 @% ?& Q; Q
independent precocious puberty, which is also known
+ ^# F6 H7 `1 T5 Y9 E6 ras testotoxicosis, may cause precocious puberty at a3 e$ q  p" A) N4 u2 i% H
very young age. The physical findings in these boys
/ X8 [" c6 \" P$ m3 h. Ewith this disorder are full pubertal development,
0 F$ u& n& ?4 S3 W& p2 kincluding bilateral testicular growth, similar to boys
* q2 w& c$ [  G+ q+ A# y; hwith CPP. The gonadotropin levels in this disorder
2 Y7 ^8 c! Y8 N, Z1 v9 p2 K+ p: v8 xare suppressed to prepubertal levels and do not show: n- e* N0 Q9 b
pubertal response of gonadotropin after gonadotropin-$ i0 ]: D+ G4 i5 v: A
releasing hormone stimulation. This is a sex-linked
8 W+ K0 l9 ?  O! o# J4 K' ?8 Z" [autosomal dominant disorder that affects only
. m2 l6 z9 h. m1 K  Y4 N% W( omales; therefore, other male members of the family
$ [- @3 H8 Q/ z' x5 H. C) cmay have similar precocious puberty.3* X, t4 W' Z9 S) ?1 Z# v; I
In our patient, physical examination was incon-
. i& x( {/ u7 `% zsistent with true precocious puberty since his testi-
$ f" u% v* ?1 \2 {cles were prepubertal in size. However, testotoxicosis
2 ~6 f/ S( ~, F$ R3 F% gwas in the differential diagnosis because his father3 c3 A+ _/ D' m, R8 Y( q) e" a
started puberty somewhat early, and occasionally,
5 h6 l) |) s, o2 q( O) mtesticular enlargement is not that evident in the& r* P  h9 ~& B
beginning of this process.1 In the absence of a neg-/ ]8 m9 S$ L; D* o/ Z/ S6 }
ative initial history of androgen exposure, our
! K$ L9 i9 j, [. O) F, H0 gbiggest concern was virilizing adrenal hyperplasia,
) \% L; j. G& @9 _either 21-hydroxylase deficiency or 11-β hydroxylase  c' {, d2 A' e1 @' k, |
deficiency. Those diagnoses were excluded by find-$ r! H5 F- n/ }
ing the normal level of adrenal steroids.
$ l, j" }& |" R/ B5 c7 aThe diagnosis of exogenous androgens was strongly  I1 N/ n4 F$ ~9 K% w* P' D7 K
suspected in a follow-up visit after 4 months because
1 k# R, x- ?& m( b$ ythe physical examination revealed the complete disap-
) A8 p# o" h& b8 Y; P, T- W3 l/ r" gpearance of pubic hair, normal growth velocity, and, _  x1 n) J% @$ q0 ]* c
decreased erections. The father admitted using a testos-
2 z8 K- H5 C9 r1 aterone gel, which he concealed at first visit. He was; o; M; U' T# `, W+ a8 U
using it rather frequently, twice a day. The Physicians’  b' n; y! P  r, i
Desk Reference, or package insert of this product, gel or
( c! R6 F4 o5 i  h3 h& Y; `cream, cautions about dermal testosterone transfer to+ ^) \0 v& K' w
unprotected females through direct skin exposure.
4 Z( j# l( `6 U8 v3 `6 \Serum testosterone level was found to be 2 times the/ w9 M6 y6 H! Y3 d8 e: R) {
baseline value in those females who were exposed to2 U4 H6 Q6 {. c
even 15 minutes of direct skin contact with their male
% k# p; t4 W" Spartners.6 However, when a shirt covered the applica-
& P5 r- G; `/ R$ @9 W4 ition site, this testosterone transfer was prevented.
; B1 `9 v! k: vOur patient’s testosterone level was 60 ng/mL,& e% d( \5 i2 N2 z# m6 c% i1 W; C
which was clearly high. Some studies suggest that
# @8 X6 Q) Q( o8 `8 }8 ?3 Cdermal conversion of testosterone to dihydrotestos-5 [8 j8 K/ `$ w- J
terone, which is a more potent metabolite, is more. N' i' m1 ]1 a% U! t# U( a: `
active in young children exposed to testosterone9 l! x# H; v! T; u! |
exogenously7; however, we did not measure a dihy-
" e/ _2 q/ ^" D: {& c. b# v. @6 Fdrotestosterone level in our patient. In addition to  ~9 L/ N& `( o/ w" u
virilization, exposure to exogenous testosterone in0 A' m; M) A( D2 x0 }. z
children results in an increase in growth velocity and7 U$ I: w: E# q- t2 `2 Y  q
advanced bone age, as seen in our patient.. S* v! A6 C/ g+ H
The long-term effect of androgen exposure during
% j- ^0 J- c/ I' X. dearly childhood on pubertal development and final
. w1 f( U2 m* |! Q0 Z/ O! sadult height are not fully known and always remain1 T8 Z3 L( y, m/ N3 L' w
a concern. Children treated with short-term testos-
9 z* F' Q$ k, o/ D# kterone injection or topical androgen may exhibit some
: K) C: v, [9 R* g0 ]acceleration of the skeletal maturation; however, after  ]7 e7 }, K0 d* H  c) p
cessation of treatment, the rate of bone maturation
6 A& q( [2 d) X4 B6 M+ M6 ldecelerates and gradually returns to normal.8,97 m6 J% j9 `4 e4 {
There are conflicting reports and controversy4 [% j) N: W6 y" H
over the effect of early androgen exposure on adult" b9 H6 }4 _7 v7 B6 A7 m1 E) \
penile length.10,11 Some reports suggest subnormal
- I/ M1 y0 G! F, ^2 uadult penile length, apparently because of downreg-. Y9 \# j. N8 J& H6 M
ulation of androgen receptor number.10,12 However,5 E3 i6 E0 H" @# P  `
Sutherland et al13 did not find a correlation between. I' Q  g* M* a( [+ ]: M$ x
childhood testosterone exposure and reduced adult9 N! M8 t7 h/ H+ B5 @
penile length in clinical studies.; e$ b6 h" v, a5 ^2 u1 v  K% A% _
Nonetheless, we do not believe our patient is
8 w7 q1 B5 d- s- Jgoing to experience any of the untoward effects from
# D* \7 v  {8 z/ j8 Dtestosterone exposure as mentioned earlier because
- O% E) ?3 w) V# e4 Q1 t. rthe exposure was not for a prolonged period of time.& c9 Z1 b" o2 g8 V% |  e
Although the bone age was advanced at the time of3 r8 B' ?' {9 S% Y
diagnosis, the child had a normal growth velocity at& {& X, j6 D* [' o& B
the follow-up visit. It is hoped that his final adult$ `# E6 d# @6 p; x* L* S
height will not be affected.# T0 h' O- c% R$ F+ i+ @* @: T
Although rarely reported, the widespread avail-
$ n7 P( I0 z* K, sability of androgen products in our society may
4 g; o/ f. [# i3 n2 _indeed cause more virilization in male or female
) G; ?8 c+ V* M9 a1 Zchildren than one would realize. Exposure to andro-; {/ k/ ^: i  l% p3 P6 b* S+ S
gen products must be considered and specific ques-
4 g" `& C. h' ktioning about the use of a testosterone product or
/ }9 s* b: _- p) d! b7 P8 I! sgel should be asked of the family members during8 Q2 Z& ?+ X9 B( I* l* w' |: C
the evaluation of any children who present with vir-& Q/ J1 L9 B, ]6 o/ b& J
ilization or peripheral precocious puberty. The diag-
/ O: R! X& F& R2 x: rnosis can be established by just a few tests and by
% |3 b, j) T; d6 S% Lappropriate history. The inability to obtain such a
% |# x$ o5 {$ Chistory, or failure to ask the specific questions, may+ ?( M" V. B$ K; _! Z* ?* h
result in extensive, unnecessary, and expensive1 Q1 J  M4 p9 \% I! }2 b3 t# s8 \9 P2 V
investigation. The primary care physician should be9 P) w9 i8 p# S, P( N$ Y
aware of this fact, because most of these children
& s: x. G4 {( P4 O7 i! G5 _may initially present in their practice. The Physicians’* o. Z& D, p6 B2 E, J+ n* F* D% i
Desk Reference and package insert should also put a) C2 I2 i+ x* A8 M* G0 x) v
warning about the virilizing effect on a male or
) c6 x) f$ o( A2 T" W( P6 K$ bfemale child who might come in contact with some-8 v, ^& m; i& V% _8 k/ |& k
one using any of these products.3 m' a" |4 u5 E0 F( V: T, q  S
References- A" {4 p0 F5 P8 h% p' P. v
1. Styne DM. The testes: disorder of sexual differentiation3 w# z! I' ?7 Z
and puberty in the male. In: Sperling MA, ed. Pediatric& Y0 ~1 W7 m9 Z( ]2 Z' v
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 G3 F  c% w5 u$ B  o5 Z2002: 565-628.
( n2 \! u5 f8 [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 b! Y$ X7 u1 `0 E+ ^# k: ?
puberty in children with tumours of the suprasellar pineal
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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!

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發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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!
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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

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發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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4个什么样的?
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發表於 2025-1-19 02:41:05 | 顯示全部樓層
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精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!

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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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