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Sexual Precocity in a 16-Month-Old
& {; B; Z, Q. q9 o8 i# d9 O  {Boy Induced by Indirect Topical
3 e" \& W, ~- n) XExposure to Testosterone% w) w- [+ F# R) I) B' R
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 X& p9 L6 ?6 Q* A3 R1 j
and Kenneth R. Rettig, MD1
: ^& y* {: f3 YClinical Pediatrics& ~* f, c4 I+ v4 F
Volume 46 Number 6* n, R# ~) q; r& }% W4 l
July 2007 540-543* Q. [* q# D- W1 C* k1 U) N
© 2007 Sage Publications
4 a) t4 r8 v  R; i) H- ~- X. l10.1177/0009922806296651
$ `5 c* W$ U* c8 Yhttp://clp.sagepub.com
' [# t0 x& X* U3 K3 n" P" J4 ghosted at; G0 t: h; Z# r
http://online.sagepub.com( |7 L) s# Z6 x1 e
Precocious puberty in boys, central or peripheral,) |- \2 N, |' v- ?2 [; `& R) x
is a significant concern for physicians. Central0 [+ K, M! V0 Z3 @! y
precocious puberty (CPP), which is mediated
: A  C0 Z+ \" Z% }' r+ \through the hypothalamic pituitary gonadal axis, has
; e- F+ l& e/ D  j& g7 T- B/ sa higher incidence of organic central nervous system
! O- ~, M1 _+ Z. N% Ilesions in boys.1,2 Virilization in boys, as manifested% k( h( \, B7 i& R9 {7 _
by enlargement of the penis, development of pubic" V' z+ V* Q0 ]& G5 f: m
hair, and facial acne without enlargement of testi-- `# L3 P, x1 W9 i/ G; V
cles, suggests peripheral or pseudopuberty.1-3 We! }: X* k9 J! j
report a 16-month-old boy who presented with the$ t5 W: C( Y$ ?' f: v. ^+ ^
enlargement of the phallus and pubic hair develop-! ?: Y$ t3 n7 |; E& c( k" _
ment without testicular enlargement, which was due
5 e# L$ ~3 d1 J# \- I; Cto the unintentional exposure to androgen gel used by
  G) G. g5 V$ l( Dthe father. The family initially concealed this infor-
- r/ [% t9 Q1 J  t% t8 ^mation, resulting in an extensive work-up for this0 s) F6 G% J) m
child. Given the widespread and easy availability of
' q  r/ k8 k7 {; A6 Ntestosterone gel and cream, we believe this is proba-
# r4 p  i# U. W6 T1 g2 @2 h) r, cbly more common than the rare case report in the! |/ m7 G( h+ k
literature.4
* B9 M2 R! ^2 _Patient Report+ q1 [. f: w5 K( A' c) ^* H
A 16-month-old white child was referred to the
- ~" X* |- }  Z2 G; B4 ]8 I% {endocrine clinic by his pediatrician with the concern% |0 m0 d: ^5 W2 `) F8 Z3 s* z9 ]6 ~
of early sexual development. His mother noticed5 ^- e8 s1 H  J6 Q
light colored pubic hair development when he was9 l  g  X, }/ O
From the 1Division of Pediatric Endocrinology, 2University of
3 U0 K7 E6 ]: u9 x/ C% b) p9 tSouth Alabama Medical Center, Mobile, Alabama.! s: V) i) ~/ z* E: H' Z7 ^2 D
Address correspondence to: Samar K. Bhowmick, MD, FACE,
+ D$ |7 J3 w$ v7 _. z! ]Professor of Pediatrics, University of South Alabama, College of
1 z; v( u  H: @6 V( hMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
3 k5 Y+ O4 ^% F& s. h/ a; }e-mail: [email protected].
! j/ U4 L) n8 o& }5 L; Rabout 6 to 7 months old, which progressively became. W+ {2 m0 D* n" g: r! h
darker. She was also concerned about the enlarge-+ ~' R3 J; S9 a: L8 r% o
ment of his penis and frequent erections. The child
0 x" y  j. o+ A5 P" e; l7 zwas the product of a full-term normal delivery, with' Q% |6 v$ `- y6 k( E# i+ C0 l
a birth weight of 7 lb 14 oz, and birth length of9 X' D* I$ J7 `1 P% m; L
20 inches. He was breast-fed throughout the first year, J4 B! H. C! g, L
of life and was still receiving breast milk along with
2 n7 G2 H6 ]& s3 V0 W) o/ b. y' Xsolid food. He had no hospitalizations or surgery,& e; s: k4 f& Y# t+ X- Z: o
and his psychosocial and psychomotor development
6 T  a/ ]9 u  F  p* a* Gwas age appropriate.
8 S* \8 x$ B( N7 pThe family history was remarkable for the father," X0 I) }$ V- h+ J
who was diagnosed with hypothyroidism at age 16,
1 t% W9 d5 l5 O1 m9 N, Y- Awhich was treated with thyroxine. The father’s) ^1 w, K2 M. Z  ]6 U/ _0 U3 h
height was 6 feet, and he went through a somewhat
% {- ]8 ?* H7 I& \7 y* j' Nearly puberty and had stopped growing by age 14.
/ Y; A/ {% _9 h# F* F/ @$ ~) q7 n. V/ kThe father denied taking any other medication. The5 I5 }9 k# u% l$ ?* a
child’s mother was in good health. Her menarche% G5 w9 A* Y" D: T" g" \' A
was at 11 years of age, and her height was at 5 feet
$ j5 e2 P5 R7 t4 u5 inches. There was no other family history of pre-
, P2 c* @2 @$ L7 ^0 G# @& F$ Y7 zcocious sexual development in the first-degree rela-0 s5 z7 b+ u5 g" D& n) x
tives. There were no siblings.# `" z+ ?3 y6 m( R7 u  u1 h
Physical Examination1 K! g2 m* _7 q# E) }$ l
The physical examination revealed a very active,
+ v, T" j) T# i( k0 Q% Vplayful, and healthy boy. The vital signs documented
8 ?, l# I% E( k" R% A0 ?( R  s+ za blood pressure of 85/50 mm Hg, his length was
7 d. w% }9 N2 ~% X1 N) O6 D90 cm (>97th percentile), and his weight was 14.4 kg
* ?8 ^0 r( z) m# T4 A(also >97th percentile). The observed yearly growth2 A! {  p: ~, N" O7 B
velocity was 30 cm (12 inches). The examination of
; b2 F: w- r( G" n, fthe neck revealed no thyroid enlargement.
' w* L$ H* N5 P* Y6 @The genitourinary examination was remarkable for7 R1 ^8 p2 H" F7 M0 o0 i
enlargement of the penis, with a stretched length of1 \2 {- S$ |! L4 l- A
8 cm and a width of 2 cm. The glans penis was very well
: W/ l2 M0 j. O: _; i* e) b) xdeveloped. The pubic hair was Tanner II, mostly around
/ H( E( t, j& w( s( v( N540; t4 _: e7 I3 V9 e! V- L" R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; n8 R% l2 y$ r: Z$ |
the base of the phallus and was dark and curled. The
) U, `9 c4 r5 n7 ftesticular volume was prepubertal at 2 mL each.! R- e; p3 P: q' j4 q( \! y2 y
The skin was moist and smooth and somewhat
: w/ {( Y, X7 qoily. No axillary hair was noted. There were no
! T: l$ }( u4 G# f) }abnormal skin pigmentations or café-au-lait spots.
+ f, H2 T* d& m3 ^5 k7 C+ [Neurologic evaluation showed deep tendon reflex 2+
  T2 Y% H" k3 t* D5 [* G* x0 jbilateral and symmetrical. There was no suggestion9 n# [3 N0 m. K: O
of papilledema.. K* q$ I. u8 W7 d& @+ q4 u, f% i& g
Laboratory Evaluation
& Z8 h. y0 }1 [0 N" NThe bone age was consistent with 28 months by
& D5 {6 c8 y8 [- g- r5 ?0 Q5 Zusing the standard of Greulich and Pyle at a chrono-
! p9 v  O/ s8 l7 U! N' Tlogic age of 16 months (advanced).5 Chromosomal4 ~& ?5 F& q& p( _% b/ p* Z* N
karyotype was 46XY. The thyroid function test
7 o9 Y9 z. X/ }showed a free T4 of 1.69 ng/dL, and thyroid stimu-) l0 ?  \5 `9 t7 s
lating hormone level was 1.3 µIU/mL (both normal)." R% t5 S& L& Y7 C5 p' y: A% {: `
The concentrations of serum electrolytes, blood7 {1 h0 I/ P, Y8 Z4 \; a
urea nitrogen, creatinine, and calcium all were
0 ]2 ^# j& s3 I8 w: s7 l; [3 hwithin normal range for his age. The concentration, N; `) C' g- M+ e
of serum 17-hydroxyprogesterone was 16 ng/dL
. N' c( ^% [) a2 u(normal, 3 to 90 ng/dL), androstenedione was 20
! Q4 p; r4 O( o4 y; z* |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 Y# D4 C4 z* t' @  v; A
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 G2 m: M7 ~) ]+ g( }- Wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to7 u' T, O) |! M# c
49ng/dL), 11-desoxycortisol (specific compound S)" a& v0 L: x$ ]4 w; p- [
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% ]' L# C1 Y0 M( ~% x/ X6 _tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ H, d# T3 }, n( K0 H
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 ~. w$ q5 x' S* w$ c. q* p( A
and β-human chorionic gonadotropin was less than
2 H# h2 N: u- C) c5 mIU/mL (normal <5 mIU/mL). Serum follicular
% y1 z3 f5 |% x9 Estimulating hormone and leuteinizing hormone2 X% t* b2 r: e9 X8 P% s0 \
concentrations were less than 0.05 mIU/mL
: ]! v) t4 c$ F( M, A(prepubertal).
! ?# L) o6 _% j( i1 P! \The parents were notified about the laboratory
6 X+ t; d, T& |! `  T* ]results and were informed that all of the tests were
" h, k$ c, \# n) snormal except the testosterone level was high. The
/ d8 _' h8 U8 Q3 Ofollow-up visit was arranged within a few weeks to) R$ X% h9 V" Z) B
obtain testicular and abdominal sonograms; how-2 x) R9 {9 [2 \
ever, the family did not return for 4 months.# f, p' L4 Y0 h3 P+ [& a
Physical examination at this time revealed that the
0 W9 }2 v! `: m/ K( Tchild had grown 2.5 cm in 4 months and had gained/ Y( e$ W# s: U% r+ t) p3 F
2 kg of weight. Physical examination remained
6 {+ r# ^4 W4 x6 z; o  s' X5 |unchanged. Surprisingly, the pubic hair almost com-" v' C. U, @5 Y0 k% }
pletely disappeared except for a few vellous hairs at2 q$ ]# A5 D! B" n* m
the base of the phallus. Testicular volume was still 2
' S1 h! y3 E1 Q! x" D( A4 D- AmL, and the size of the penis remained unchanged.
# [# F* q, k8 b: k" m$ ZThe mother also said that the boy was no longer hav-; R3 d. A$ C, F; ~( n
ing frequent erections.3 q  l# N$ q1 }" V# W
Both parents were again questioned about use of0 b/ C; i$ q2 I2 w( Z3 G/ M9 U8 B
any ointment/creams that they may have applied to
! X' _. e8 b8 K5 ^9 k* _1 Hthe child’s skin. This time the father admitted the
7 p' I5 c( W, [, O0 S5 ~' iTopical Testosterone Exposure / Bhowmick et al 541, x8 ~/ y: @8 _! e: M$ V
use of testosterone gel twice daily that he was apply-
$ D/ S# j3 b; N+ ]7 qing over his own shoulders, chest, and back area for
: W6 |! p& {9 Y1 u+ n$ ra year. The father also revealed he was embarrassed
) _% U$ a# T( m0 j7 z! {( Gto disclose that he was using a testosterone gel pre-
5 G+ n5 C0 w- X' p* R, h; Pscribed by his family physician for decreased libido; z- J9 q3 A: ^( k: y$ R- ~1 |
secondary to depression.
+ s' F0 l, P8 J5 t' {8 KThe child slept in the same bed with parents.
6 v* _( d$ E. @. I" Z0 l: w  C/ IThe father would hug the baby and hold him on his8 E4 ]; E" v: a+ g9 h* t
chest for a considerable period of time, causing sig-
3 y/ }, {: [1 m0 snificant bare skin contact between baby and father.
1 z* F+ N8 f8 [# z' g2 m( yThe father also admitted that after the phone call,
& D- y. W! ?6 g: J7 Q0 z( Q5 owhen he learned the testosterone level in the baby
$ k! V0 o8 C) a/ s( qwas high, he then read the product information
, R/ D) Z: f0 `- G* c' @9 \packet and concluded that it was most likely the rea-* m6 s4 Z" P. [. t3 `5 c6 j* x( q) p0 Y
son for the child’s virilization. At that time, they: }. Q! y5 T3 ]' h! e# G8 p. v, r8 b8 K
decided to put the baby in a separate bed, and the
  o$ G2 \: K1 Hfather was not hugging him with bare skin and had
5 `+ X4 a) A* E% Ebeen using protective clothing. A repeat testosterone6 f+ K( y+ O1 i7 H  A' h1 L
test was ordered, but the family did not go to the
$ r5 n" d  f6 _( I* Alaboratory to obtain the test.
9 K* c/ M& T# d+ Z! {6 ADiscussion
4 c& T" H6 S0 }7 Z5 p- ^Precocious puberty in boys is defined as secondary; x. E3 U) U4 M7 S  l
sexual development before 9 years of age.1,4
, b9 f7 P5 [, v3 S3 TPrecocious puberty is termed as central (true) when; v+ `0 h" O* g( i. I  |, A( }
it is caused by the premature activation of hypo-
0 W9 a* J: V8 c0 |( f- nthalamic pituitary gonadal axis. CPP is more com-
' h! x/ I+ U. I7 n) E) }mon in girls than in boys.1,3 Most boys with CPP
  @4 P# N4 O1 Q$ x9 G) z, Tmay have a central nervous system lesion that is
3 {& f) `' Q" R- Aresponsible for the early activation of the hypothal-0 n" B! J; T8 g: x4 G
amic pituitary gonadal axis.1-3 Thus, greater empha-" ^# H9 q* T/ c* K$ Z2 _9 F
sis has been given to neuroradiologic imaging in
8 o! s+ q1 k1 pboys with precocious puberty. In addition to viril-- v: L7 ~  V; D+ u6 @
ization, the clinical hallmark of CPP is the symmet-
  q. p5 E0 J* y; N7 Brical testicular growth secondary to stimulation by5 H8 G5 z5 Q9 h) e  R" d* H/ ?
gonadotropins.1,3
  Y! C  _* ^& {  V1 b* }0 A) @Gonadotropin-independent peripheral preco-8 s7 Z3 _( N4 r5 p" }" e5 e
cious puberty in boys also results from inappropriate
& B' E! u1 q1 j( d- Kandrogenic stimulation from either endogenous or
# h$ E3 b+ ~* Z$ _3 cexogenous sources, nonpituitary gonadotropin stim-
3 q6 u; ]0 i1 P- a  sulation, and rare activating mutations.3 Virilizing
7 B$ T' T) O" m/ r1 `/ ^% ]. `1 |congenital adrenal hyperplasia producing excessive
7 z# E" {( N2 e0 B# J) Tadrenal androgens is a common cause of precocious! x2 Q9 Z, L& s) I( J8 ?. N
puberty in boys.3,4
; S/ r% s' S6 S9 k+ e, KThe most common form of congenital adrenal
/ O3 T4 Z0 m. u/ S- _hyperplasia is the 21-hydroxylase enzyme deficiency.
* d) T+ l5 }2 S3 z, PThe 11-β hydroxylase deficiency may also result in
' \  N6 M, t/ J: i& @excessive adrenal androgen production, and rarely,* K$ K& w- ]3 B% j, O$ t' K
an adrenal tumor may also cause adrenal androgen
+ G" S' N# T$ |  `2 oexcess.1,3
; {4 h9 i* `' G. q) t. y/ Sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# n5 M5 \) t9 p8 b3 n1 h
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: l; r( c; I; T& ~. F
A unique entity of male-limited gonadotropin-: n( Z1 j( C9 l. f
independent precocious puberty, which is also known# B9 O2 R# ^" w& p  ~
as testotoxicosis, may cause precocious puberty at a! Q( O% Z( X* P; [' R' F
very young age. The physical findings in these boys# [! ?# z. l  T$ t5 I
with this disorder are full pubertal development,
" r; a! {. S/ e0 |+ {including bilateral testicular growth, similar to boys, J# D( e7 k1 }: v) h! F
with CPP. The gonadotropin levels in this disorder! ~1 z, i$ P! K6 c1 L5 _% \; p
are suppressed to prepubertal levels and do not show1 I  F0 l2 _( A( w$ g# r
pubertal response of gonadotropin after gonadotropin-6 T( x) P3 D% u+ g( O" o7 O$ Q
releasing hormone stimulation. This is a sex-linked
/ c5 \6 B7 R  h$ dautosomal dominant disorder that affects only  G: x: a) x9 J+ S; d8 r
males; therefore, other male members of the family3 G5 n! h$ y8 ^) Y
may have similar precocious puberty.3
2 `) S* C! h, H/ h* h/ |) ]+ _In our patient, physical examination was incon-7 n% M- f/ y* P4 V
sistent with true precocious puberty since his testi-! Z# i6 b  b  W3 ^% k
cles were prepubertal in size. However, testotoxicosis
0 e, w: v/ K% X9 M/ W) n  Twas in the differential diagnosis because his father7 U; W3 u, O/ s1 c& ]' u
started puberty somewhat early, and occasionally,
3 c* c; }$ G! ytesticular enlargement is not that evident in the
+ [( M) c* O9 @- bbeginning of this process.1 In the absence of a neg-# u' {- j, h6 X' U' T
ative initial history of androgen exposure, our; ^7 I' R( m" h( k# M: {
biggest concern was virilizing adrenal hyperplasia,
& Z  `6 r$ Q% |& Ieither 21-hydroxylase deficiency or 11-β hydroxylase4 a1 \; O2 w) b0 F  @: f! B
deficiency. Those diagnoses were excluded by find-
* y2 S( }% [% Ting the normal level of adrenal steroids.) d7 Q! ?" X5 l5 B  q
The diagnosis of exogenous androgens was strongly0 z/ C! t# }% s% K0 D" {  n. H& }
suspected in a follow-up visit after 4 months because
( T9 v! ~9 e# C( Y! @0 Z+ C9 mthe physical examination revealed the complete disap-
: T# e! O2 E/ x: t/ p* q7 }pearance of pubic hair, normal growth velocity, and8 g+ r0 O9 Z( j% B! N' M% t
decreased erections. The father admitted using a testos-
! g0 C9 o7 P' h$ p7 y9 pterone gel, which he concealed at first visit. He was
& t: K, ~9 o+ l9 iusing it rather frequently, twice a day. The Physicians’
8 a& q7 s+ W3 T1 K; KDesk Reference, or package insert of this product, gel or$ `3 A8 H; [, {  ?
cream, cautions about dermal testosterone transfer to. `: d; j' R& S9 A# r- L7 g; q* {
unprotected females through direct skin exposure.
, M" ?+ L2 ^" [& p$ kSerum testosterone level was found to be 2 times the( V8 `/ x/ a- V: Y- C) Y, `! s
baseline value in those females who were exposed to
' ~+ ?8 J* M7 _9 D% `; r" _even 15 minutes of direct skin contact with their male
! a3 N# X$ E0 O- B6 h' W1 C1 E& Zpartners.6 However, when a shirt covered the applica-
9 I' e( s$ |" V+ |( e0 Ttion site, this testosterone transfer was prevented.7 C; e% {. ^8 L" \6 i& w# L
Our patient’s testosterone level was 60 ng/mL,
+ |- ~% u+ E, t2 uwhich was clearly high. Some studies suggest that
" P( f; j2 D8 y) ?: i! cdermal conversion of testosterone to dihydrotestos-
! `2 e5 |0 {; u# ?% D. Dterone, which is a more potent metabolite, is more
0 e/ m! O+ R6 C& O0 k) uactive in young children exposed to testosterone
. J9 y& k* R* f$ ]) D: Z$ ?exogenously7; however, we did not measure a dihy-
( L2 G' `7 d6 ~& t% S& |( z. Sdrotestosterone level in our patient. In addition to
7 `' q0 C& g' @* Z0 q# [3 c8 n; Fvirilization, exposure to exogenous testosterone in$ v4 U* ^1 D# C6 k9 A6 o
children results in an increase in growth velocity and
! I; D4 V( m2 Y) v" y! `advanced bone age, as seen in our patient.8 O+ I+ |4 T& e+ p; O
The long-term effect of androgen exposure during
# C1 m! n- d+ a: ?early childhood on pubertal development and final
7 C0 ^  B2 [' I. O; Hadult height are not fully known and always remain
; F  U7 R) n$ Q5 x+ K- [: M5 {& wa concern. Children treated with short-term testos-+ F9 h0 w1 t8 Q5 B' s
terone injection or topical androgen may exhibit some! M$ o5 p  l- D/ X8 x* X8 P! U  ^. F
acceleration of the skeletal maturation; however, after) d3 [6 }$ x- r# @8 o
cessation of treatment, the rate of bone maturation
1 O+ E+ b8 m$ D; u7 jdecelerates and gradually returns to normal.8,9
" t  \6 A+ S2 {6 bThere are conflicting reports and controversy  R7 O5 O$ x- t) c
over the effect of early androgen exposure on adult
& _6 [* `8 e8 C" |- l# ppenile length.10,11 Some reports suggest subnormal
7 Y0 ^" f) P# c; ?adult penile length, apparently because of downreg-) `2 {3 [3 H- w* o1 Z
ulation of androgen receptor number.10,12 However,  o. m- s- H0 S+ D+ K/ D1 q3 K4 q4 b
Sutherland et al13 did not find a correlation between
8 |7 ^0 ?7 }7 n5 l2 ochildhood testosterone exposure and reduced adult
9 G) {$ d  J$ ~; R6 \2 S. b: Npenile length in clinical studies.
" X' ~! @! j+ [+ jNonetheless, we do not believe our patient is
( Q1 q( y( ]3 L, V3 cgoing to experience any of the untoward effects from' f/ u% ]7 x' d" W9 \0 v) K
testosterone exposure as mentioned earlier because
3 \) U! z* a4 O- b! dthe exposure was not for a prolonged period of time." H7 t# K2 K! z& P; R6 y. A
Although the bone age was advanced at the time of+ d4 ~3 u+ ]* n5 {8 g
diagnosis, the child had a normal growth velocity at
+ g3 Y; P2 x# [# f- _5 jthe follow-up visit. It is hoped that his final adult
4 w. O/ o* h1 x9 W0 a. M9 K( g5 sheight will not be affected.! J; \/ X" T  ^9 o! M
Although rarely reported, the widespread avail-+ R% J( g- H5 z" [$ C  ^
ability of androgen products in our society may- p) u+ Q( c6 c  v0 Y
indeed cause more virilization in male or female) g! R; R9 N- J, n; ^8 U# z
children than one would realize. Exposure to andro-
+ m7 V3 O  O/ A7 R, Tgen products must be considered and specific ques-$ _# Q3 P; K% C2 }9 b$ R
tioning about the use of a testosterone product or$ x5 y# |/ r% U5 m- g
gel should be asked of the family members during) L; n: N0 r. t% F4 M* Y
the evaluation of any children who present with vir-
1 T7 R; Y( }0 y9 f" D  A; Silization or peripheral precocious puberty. The diag-
2 g3 H1 ^, s# y% Cnosis can be established by just a few tests and by
% C3 T+ ?! m" s3 jappropriate history. The inability to obtain such a
6 y1 x( S4 p5 \" G. Q/ B& vhistory, or failure to ask the specific questions, may
' l; f+ _6 c2 z7 x1 M% w0 i. @result in extensive, unnecessary, and expensive' b- R0 q, R* |0 z5 C9 \/ ~
investigation. The primary care physician should be; D! d: z6 J. x
aware of this fact, because most of these children
5 f! n5 w/ |5 b. Mmay initially present in their practice. The Physicians’8 B, a& B" d$ @
Desk Reference and package insert should also put a) I: W% |: s) T  O+ ]; M0 ?
warning about the virilizing effect on a male or0 A# K, T" M, }2 ], s) D& j: g
female child who might come in contact with some-$ w- O# ^! S- @5 u2 Y: E
one using any of these products.
2 c; M+ Q" `6 m/ {References: y& c6 Z: i( u% z% z
1. Styne DM. The testes: disorder of sexual differentiation
2 D9 y! R" j( ^+ Y; oand puberty in the male. In: Sperling MA, ed. Pediatric2 J  T$ K, t) M9 Z# e
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, U" p  O' l( M2002: 565-628.
3 t- `* b- X2 h9 f. ]9 n8 E2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious3 V) c  Y5 E8 D- ]) w5 v
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old+ Z, f' |2 M$ t, M+ [
Boy Induced by Indirect Topical
! c1 n! c1 }! H6 @$ S+ U# VExposure to Testosterone7 k# A# t0 y0 d& y+ j1 F
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 g- ?1 i3 u" W9 j# Q% W
and Kenneth R. Rettig, MD1
& a% T; M1 e9 a" ?  R0 LClinical Pediatrics' e8 B) E% i' q
Volume 46 Number 6. q* l$ |7 X! g' J  b9 W
July 2007 540-543
* ~- h! _  A0 @$ A; D© 2007 Sage Publications
7 T! F7 C+ f1 O$ H4 y! D- j3 r10.1177/0009922806296651% f& d/ \: g8 J6 d) a
http://clp.sagepub.com
7 u. n" q* B  u1 {. H4 [" u3 Ihosted at
4 L" U4 s- }+ v. q3 G% m) thttp://online.sagepub.com2 x" v* J, y5 _* @
Precocious puberty in boys, central or peripheral,
$ g9 H" j! j; g& d3 b7 L. \is a significant concern for physicians. Central
* J8 j: P: |- sprecocious puberty (CPP), which is mediated( Q' L& y) l0 J. P/ c2 F
through the hypothalamic pituitary gonadal axis, has/ P3 H2 B- k( w/ n
a higher incidence of organic central nervous system6 h# ]% r& S7 t* F9 B
lesions in boys.1,2 Virilization in boys, as manifested
% j" I) D( |  x5 R2 f; tby enlargement of the penis, development of pubic0 B& C7 g* }5 \
hair, and facial acne without enlargement of testi-
3 I/ m0 a2 m6 O: acles, suggests peripheral or pseudopuberty.1-3 We! U2 N* i' g. v5 L, d9 l7 ]
report a 16-month-old boy who presented with the
/ h, g7 p! G% r6 penlargement of the phallus and pubic hair develop-; k7 D/ B! W" v9 [
ment without testicular enlargement, which was due
7 e- E5 k, E' o3 z' tto the unintentional exposure to androgen gel used by/ C. [% {" \" k3 w- \
the father. The family initially concealed this infor-: g" I! M) A- Z) e% Q$ V+ n
mation, resulting in an extensive work-up for this
- a3 U) E2 A+ f1 n8 S3 ichild. Given the widespread and easy availability of: j, Z$ \1 L$ D' L5 o# u
testosterone gel and cream, we believe this is proba-
1 Z; O* l7 ?& qbly more common than the rare case report in the
$ `4 `: ^! @. _2 qliterature.4
* e2 H3 Q! Q& ^2 d# ZPatient Report4 J& R! p. M$ Y" H+ b
A 16-month-old white child was referred to the  Z/ {' b! h# ~. X( a) |: ~; C4 U
endocrine clinic by his pediatrician with the concern, L9 p3 N% v8 F! \& j1 D+ [
of early sexual development. His mother noticed
( P# W  g6 x% |5 Y0 G4 clight colored pubic hair development when he was
) G3 d! F) |3 _1 V8 ^( x% cFrom the 1Division of Pediatric Endocrinology, 2University of
# Z! `3 L7 g, P! I  k4 `2 DSouth Alabama Medical Center, Mobile, Alabama.
. V+ u. g% F' s' W! M4 `6 M. g8 }Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 J* b5 |$ P7 j: V6 H" ]Professor of Pediatrics, University of South Alabama, College of3 q( e1 M1 N" r  _2 O7 W
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) G' }4 A' |9 Y5 b  Y  Se-mail: [email protected].
& G( [, ?% C( r6 Z* xabout 6 to 7 months old, which progressively became, `/ k; j/ F6 I; e& ?, E
darker. She was also concerned about the enlarge-
& ~' x  g4 r8 x- Fment of his penis and frequent erections. The child7 f7 M) m" g* E
was the product of a full-term normal delivery, with
6 J- ^* }" d0 d2 o: Qa birth weight of 7 lb 14 oz, and birth length of
% b! {3 I- ~1 X: }! H' e$ e# V1 Z- }20 inches. He was breast-fed throughout the first year9 V- r/ s$ v+ G2 E% M! S: C4 i0 p
of life and was still receiving breast milk along with
* C. e# D4 P+ Q1 g: U  Xsolid food. He had no hospitalizations or surgery,
- x1 w% E; k- x6 `$ E, K( U& sand his psychosocial and psychomotor development4 L2 U1 t2 K1 I1 q3 T1 A  D) O+ C4 r( ]
was age appropriate.
3 r' _# j- @1 h: o8 q8 RThe family history was remarkable for the father,
: t( \8 T5 v, e5 y6 K* swho was diagnosed with hypothyroidism at age 16,
4 B/ b" ^) l+ o% ^& bwhich was treated with thyroxine. The father’s
9 @7 ^; q7 G* Mheight was 6 feet, and he went through a somewhat: w) K) w7 z3 \+ T; {0 r5 Z" l
early puberty and had stopped growing by age 14.  ?' }5 E4 x1 @0 g* M; a+ g: v
The father denied taking any other medication. The
  p( l* _3 f# A" z( d# O2 ]! Ichild’s mother was in good health. Her menarche7 Z/ h) N8 i1 s0 L
was at 11 years of age, and her height was at 5 feet
$ Q9 ~% l8 e9 m5 g7 H5 inches. There was no other family history of pre-- ~2 O! B( A. s9 R! f
cocious sexual development in the first-degree rela-
$ n- g; R3 N0 O, ]) stives. There were no siblings.1 S6 w2 D; T, x# \. [( `3 _: K
Physical Examination
! J: w& ^' O1 g" V6 @# EThe physical examination revealed a very active,
9 y# [6 c  s0 w( @; L) X; N; wplayful, and healthy boy. The vital signs documented
& q  v- r, p4 Pa blood pressure of 85/50 mm Hg, his length was) o' i  @; ?" q
90 cm (>97th percentile), and his weight was 14.4 kg
, S3 b7 {* @- v3 n+ R(also >97th percentile). The observed yearly growth
( X9 |2 _9 `/ {: }velocity was 30 cm (12 inches). The examination of$ w9 d- n) \$ d8 C5 c
the neck revealed no thyroid enlargement.
8 j& u2 H8 @% i/ ~% R# c' wThe genitourinary examination was remarkable for
) l6 b& ]( s. K1 V; Renlargement of the penis, with a stretched length of
. o3 |; }, r) x4 b" @* ^$ f8 cm and a width of 2 cm. The glans penis was very well
% I( H; I6 [0 b4 [2 bdeveloped. The pubic hair was Tanner II, mostly around
& q' v% }& e$ v8 C, q, c( V" g, [540) w4 l8 j% K, ^3 L/ i) H: V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 N6 o& Z5 Y$ h! y5 W/ H. p
the base of the phallus and was dark and curled. The* d6 H9 j3 E  A: r8 f( g
testicular volume was prepubertal at 2 mL each.
! M, m' g& l- z, aThe skin was moist and smooth and somewhat: P  h9 \$ V1 z: R
oily. No axillary hair was noted. There were no
* r0 q& E: ?: Yabnormal skin pigmentations or café-au-lait spots.0 E" p2 @8 E8 m, K9 H& a
Neurologic evaluation showed deep tendon reflex 2+% ]: M4 }8 b4 D4 [& E! z
bilateral and symmetrical. There was no suggestion% m& I4 ^8 z7 D
of papilledema.
" F( V2 t+ g7 ~9 k- A. BLaboratory Evaluation
- f( t. e8 V! u$ _2 BThe bone age was consistent with 28 months by& D0 l2 S* y, h' e. v) M& y
using the standard of Greulich and Pyle at a chrono-) r- y0 L8 A$ D; X6 P, c
logic age of 16 months (advanced).5 Chromosomal/ G1 P$ U6 I5 i/ Z8 P
karyotype was 46XY. The thyroid function test
' ?' e) E8 H! K+ H8 ?$ {showed a free T4 of 1.69 ng/dL, and thyroid stimu-
! O2 u# ?# V- e) X9 I. ^/ M  F1 qlating hormone level was 1.3 µIU/mL (both normal).8 X: J; C, ?# z7 N" K9 ]& Y. p9 }. F
The concentrations of serum electrolytes, blood
) R6 t$ l% a+ M# V. m0 v& Durea nitrogen, creatinine, and calcium all were9 J/ h  G) ~) t0 n3 u
within normal range for his age. The concentration$ a: }8 l. `! A3 y; d- M1 i
of serum 17-hydroxyprogesterone was 16 ng/dL
5 D& ^  h* e- @1 z) S' l# O0 z(normal, 3 to 90 ng/dL), androstenedione was 202 o7 U' u2 b" V: s
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 ?7 O, A7 k* v$ h& m. L  Lterone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 C) L6 l  n! Edesoxycorticosterone was 4.3 ng/dL (normal, 7 to& t4 [; n- _( r7 Q7 e$ y8 O0 s! G
49ng/dL), 11-desoxycortisol (specific compound S)+ w( u+ _) t7 a  X4 _3 h* O; q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 f7 L* G( E3 u. x6 t
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 j( z5 b! j9 ^! h/ j. z$ E) ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* l( L( _& Z9 T0 F( N9 \. D  ^and β-human chorionic gonadotropin was less than( Y% Q" `: P  }* d: e! @
5 mIU/mL (normal <5 mIU/mL). Serum follicular
# t) q, H3 P- k/ Q% Zstimulating hormone and leuteinizing hormone
+ a0 x4 D/ I2 V7 nconcentrations were less than 0.05 mIU/mL# D# P' O1 ?7 @" o
(prepubertal).( z/ G. ?! S. T  x1 ~, ~
The parents were notified about the laboratory# K) @( g3 E+ G
results and were informed that all of the tests were
% o9 d( n- Q5 q1 z( f# X( v) q8 cnormal except the testosterone level was high. The
. ]) p0 [+ E! t7 Mfollow-up visit was arranged within a few weeks to- A. }+ {7 p1 W, _* X
obtain testicular and abdominal sonograms; how-
- Z  o" s# @. J( h' {; V0 {ever, the family did not return for 4 months.
8 b: z: T! C: [5 `6 vPhysical examination at this time revealed that the
0 p- J3 j5 |( B2 V3 R3 o" mchild had grown 2.5 cm in 4 months and had gained
4 B! Z9 @' K( h* \0 B& [2 G2 kg of weight. Physical examination remained1 B" u5 L" c2 ^% E9 H  R8 x
unchanged. Surprisingly, the pubic hair almost com-
) \, E/ `2 _7 W) Spletely disappeared except for a few vellous hairs at
4 D& ^8 L  H! Y6 A1 w9 g3 jthe base of the phallus. Testicular volume was still 21 _. N, s$ k" Z3 r6 V
mL, and the size of the penis remained unchanged.
' q& ]+ e  K, S3 TThe mother also said that the boy was no longer hav-1 |0 ?1 ~- \* [( l
ing frequent erections.
/ B, Y3 z0 ^. Z% U5 D+ \9 r+ LBoth parents were again questioned about use of
0 A2 H. E; [& h- B4 sany ointment/creams that they may have applied to
" D1 A" R8 R! X/ [& {* g& h1 [the child’s skin. This time the father admitted the, r+ C8 u; S1 J; }8 g
Topical Testosterone Exposure / Bhowmick et al 541" A! p9 |7 Y5 W' W  ]7 X
use of testosterone gel twice daily that he was apply-
4 U0 j/ f6 y+ `$ K8 S: hing over his own shoulders, chest, and back area for
0 g$ v, h* ^+ c: X! \: X) ya year. The father also revealed he was embarrassed
- H' e* M2 o& Eto disclose that he was using a testosterone gel pre-
* ^7 ]- k: n" ~5 cscribed by his family physician for decreased libido
9 r8 i' U2 }  W) Ssecondary to depression.! A' T8 [- i( z; i6 a
The child slept in the same bed with parents.
. Y8 I, X  {( T- x! zThe father would hug the baby and hold him on his
* o5 }: t; `) q1 Zchest for a considerable period of time, causing sig-- \0 n, ?+ H6 O3 z
nificant bare skin contact between baby and father.  w7 z$ a; d" f
The father also admitted that after the phone call,% x3 e/ W( }0 @! f, r. _4 L2 x( s
when he learned the testosterone level in the baby
2 R5 b. B! L+ u- w& T* F2 Zwas high, he then read the product information
. L7 D- M: M. i. J( l8 Vpacket and concluded that it was most likely the rea-
- H! g1 H( M6 K0 p3 F& `son for the child’s virilization. At that time, they
: P2 ]" j5 I1 {3 h( ~% m, h* pdecided to put the baby in a separate bed, and the, G6 E$ N- y/ l0 t* ~6 ?7 Q( c
father was not hugging him with bare skin and had
9 U' c) _) A+ Ubeen using protective clothing. A repeat testosterone
; x( d: T( {/ c& W- @test was ordered, but the family did not go to the  [1 T7 g. [0 }8 q9 E
laboratory to obtain the test.) _$ N7 z, P3 M$ E$ e7 Z2 p) }8 E" P
Discussion
% A9 A4 X- F5 c  D$ m, L4 ~& hPrecocious puberty in boys is defined as secondary5 R9 A* m. T" g& b
sexual development before 9 years of age.1,4
# l5 W  V2 ?4 I  A4 @Precocious puberty is termed as central (true) when% `4 v! f! S! ?/ g) z
it is caused by the premature activation of hypo-% y( z( Y/ b2 C! o% j8 g0 l2 g
thalamic pituitary gonadal axis. CPP is more com-+ M: I6 c1 c+ \! x- K
mon in girls than in boys.1,3 Most boys with CPP
: n. l0 ^- N& N4 r# t9 a: B- ^" V- xmay have a central nervous system lesion that is' A- f1 @. |, {. `. u
responsible for the early activation of the hypothal-
" G# H( F4 |7 e" b5 P7 }( qamic pituitary gonadal axis.1-3 Thus, greater empha-( X- R" w# E+ f! Y( T; D
sis has been given to neuroradiologic imaging in7 T3 A/ R1 I5 e7 d  F+ R/ b! s, I
boys with precocious puberty. In addition to viril-
2 A+ G3 M1 }) qization, the clinical hallmark of CPP is the symmet-
! l) F6 [+ z% y9 b# d' U5 r! M+ Prical testicular growth secondary to stimulation by. ~7 c# a9 o! _' x: A$ p
gonadotropins.1,3! d% Y) @+ i; Z! [& h$ T! I8 C, Z
Gonadotropin-independent peripheral preco-
% h! t# g# F% ?  ncious puberty in boys also results from inappropriate
. j6 K" A4 z3 pandrogenic stimulation from either endogenous or; w2 W" e1 s) T4 e* s' Y% d0 O$ k
exogenous sources, nonpituitary gonadotropin stim-' h6 N& I3 O% p: V) k; n
ulation, and rare activating mutations.3 Virilizing
4 c3 x; L3 |* G) Qcongenital adrenal hyperplasia producing excessive" i0 |" n5 G3 N* a+ f: O( s  ?
adrenal androgens is a common cause of precocious
. J. J1 e; v! _( p+ C( C- L% y$ hpuberty in boys.3,4/ }, k7 M7 D5 c- g7 s: G6 L
The most common form of congenital adrenal4 \8 F( e; |: m: l, L* `/ M7 `
hyperplasia is the 21-hydroxylase enzyme deficiency./ I6 r6 ^/ i* f' }
The 11-β hydroxylase deficiency may also result in
  S% y9 D8 A& ]/ ]9 xexcessive adrenal androgen production, and rarely,. T+ ]' E' f3 [8 P
an adrenal tumor may also cause adrenal androgen7 G+ Q8 c  G7 S
excess.1,3
1 Z5 y5 l1 b2 Y! s0 E7 k5 Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, r4 R+ b( h  L1 f" D$ H  e+ ?
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& t0 j" T8 N1 |. [& E( i6 i
A unique entity of male-limited gonadotropin-
8 ]: W! O, V- O; \independent precocious puberty, which is also known- p# {8 L0 V  _) @
as testotoxicosis, may cause precocious puberty at a
% [6 x/ f2 \8 r, a. {) B+ b) {' pvery young age. The physical findings in these boys
* v/ e8 u8 n5 }) s0 T  hwith this disorder are full pubertal development,
2 K! m/ {1 o8 Q$ I2 e) Hincluding bilateral testicular growth, similar to boys
/ [' m% P5 ~2 {+ m- t; \with CPP. The gonadotropin levels in this disorder: t* G, E/ m1 z
are suppressed to prepubertal levels and do not show
1 A0 ?5 H( R& x% w/ l! I2 cpubertal response of gonadotropin after gonadotropin-
# V: H% g4 ]7 E3 v' d! r: S4 q- x6 Jreleasing hormone stimulation. This is a sex-linked
3 D2 q9 Q. L/ F/ _autosomal dominant disorder that affects only- u5 I8 K9 q# Z3 D: v1 D' J3 i8 Q
males; therefore, other male members of the family7 u- Z8 z' \. y" h/ J7 }
may have similar precocious puberty.3; K5 N# c+ e  V" }$ r( m
In our patient, physical examination was incon-
' V/ L3 O4 I& ]. Gsistent with true precocious puberty since his testi-# n$ J2 k1 k. p
cles were prepubertal in size. However, testotoxicosis
* T1 g) U$ M" ~6 E& v; ]- c3 twas in the differential diagnosis because his father$ z9 A0 U& ~* [  ]+ h8 H4 {, B
started puberty somewhat early, and occasionally,
, {8 `  s9 t/ L. dtesticular enlargement is not that evident in the- g& K$ M( \# u
beginning of this process.1 In the absence of a neg-
5 G2 ~2 i) V3 H7 ~& _# W( Y+ g* f' Z3 \, rative initial history of androgen exposure, our" S+ c) l$ ?0 _! Q, m6 x9 Q8 o* o
biggest concern was virilizing adrenal hyperplasia,
+ h8 U3 ^7 b' T9 V! C3 y: meither 21-hydroxylase deficiency or 11-β hydroxylase( }7 l0 z* K/ v. G% |
deficiency. Those diagnoses were excluded by find-
5 q9 b! ~/ d$ G+ {6 S- `ing the normal level of adrenal steroids.
4 l3 Z$ @2 e) K+ lThe diagnosis of exogenous androgens was strongly
& B* }" U' U0 S) n3 {suspected in a follow-up visit after 4 months because
& @9 K1 ~4 R) Gthe physical examination revealed the complete disap-
) V7 K7 e+ R6 t8 Qpearance of pubic hair, normal growth velocity, and. x4 R4 m8 [! b9 w( Z
decreased erections. The father admitted using a testos-
" [1 |5 R* A, `3 J  fterone gel, which he concealed at first visit. He was
/ R# ~: c5 m5 k' U' {% m4 lusing it rather frequently, twice a day. The Physicians’
& g3 h( ~3 l  EDesk Reference, or package insert of this product, gel or
. W8 D* v2 x$ q) c, ccream, cautions about dermal testosterone transfer to6 _; d  M" X1 x- s1 b
unprotected females through direct skin exposure.: A7 K! X+ y" {
Serum testosterone level was found to be 2 times the
8 E$ x# c2 k- i! g% Vbaseline value in those females who were exposed to2 k7 s& S" c' k+ X; @) |
even 15 minutes of direct skin contact with their male1 T* `, P# h6 I; _
partners.6 However, when a shirt covered the applica-
' V3 B3 f8 O3 ~% r  S8 @2 `; Htion site, this testosterone transfer was prevented.
+ g3 r9 e+ T: v/ P; T/ XOur patient’s testosterone level was 60 ng/mL,' y& T/ _# q1 h9 U: _+ b6 Z. r
which was clearly high. Some studies suggest that
6 d9 i( u3 \+ m# ^dermal conversion of testosterone to dihydrotestos-) E* C7 W% A2 w+ m; [
terone, which is a more potent metabolite, is more' E+ f0 \$ ?6 H1 S" B" E
active in young children exposed to testosterone
/ b9 F! H" i- ~8 \; eexogenously7; however, we did not measure a dihy-" i+ T* y: t3 h2 ~. T9 j; g
drotestosterone level in our patient. In addition to
4 d' j+ Z7 A, m2 t. U1 avirilization, exposure to exogenous testosterone in* E/ G& Q' p- n- |3 H4 v* c( J4 j
children results in an increase in growth velocity and: I7 c, x$ K5 D- f& R( X
advanced bone age, as seen in our patient.
9 ^- C$ Y5 {! c# H" i3 M- I$ E) rThe long-term effect of androgen exposure during% [5 I, Y& B; k+ f, S
early childhood on pubertal development and final5 y/ @& I. Q7 K5 y3 Z
adult height are not fully known and always remain8 e' s; y) G( o  u4 [* j
a concern. Children treated with short-term testos-
* c4 j& {% u/ |terone injection or topical androgen may exhibit some# ]# d# m$ `7 w5 `" m! j
acceleration of the skeletal maturation; however, after5 O! B1 j. g5 Q  c; n  v
cessation of treatment, the rate of bone maturation
# ~7 [- D( E/ ^5 y% pdecelerates and gradually returns to normal.8,9% C- u8 {. m2 ~6 [2 C5 _5 N' s- e
There are conflicting reports and controversy
3 y" }9 Z  @8 Y; r" A) u8 [$ A1 Qover the effect of early androgen exposure on adult
* K1 Y, @9 W0 i0 L& |9 P% q8 A% jpenile length.10,11 Some reports suggest subnormal
4 t% t2 Z5 Q6 y% ~adult penile length, apparently because of downreg-
1 w- e; N/ q* v" [2 g# r9 Julation of androgen receptor number.10,12 However,
0 f' j1 B/ R& G. y# N5 ]  }Sutherland et al13 did not find a correlation between
5 x& \; b# D3 J8 W3 W; [0 `( achildhood testosterone exposure and reduced adult: F! A# e4 D$ C0 x6 b! e
penile length in clinical studies.
$ U8 s& I& G& vNonetheless, we do not believe our patient is' d- l& u. ?% c+ r
going to experience any of the untoward effects from
) s4 P$ c1 n& Q3 q5 m/ Dtestosterone exposure as mentioned earlier because
2 I% y1 `, q1 E9 Pthe exposure was not for a prolonged period of time.$ F1 I; a" @0 K0 D  G) S" F
Although the bone age was advanced at the time of
8 r. s* `6 i. Y5 u5 F/ qdiagnosis, the child had a normal growth velocity at
5 c6 [* G9 ^  V* N: ]! ?$ zthe follow-up visit. It is hoped that his final adult% m/ _; E7 S; y
height will not be affected.
& \+ Q5 Q8 r1 U0 K" DAlthough rarely reported, the widespread avail-
; N! i$ s; m4 z' Uability of androgen products in our society may! r' I, W! i2 p
indeed cause more virilization in male or female
; c' [1 a( F( _children than one would realize. Exposure to andro-
. b/ x' K) C" M) Dgen products must be considered and specific ques-8 ?4 O, V( k3 ^3 g
tioning about the use of a testosterone product or- f/ U( d4 Y% ]. K
gel should be asked of the family members during& |" @  \& r( N( @( C. n) x$ Y
the evaluation of any children who present with vir-4 g; s& ]0 l2 ~! `/ ?0 f3 S
ilization or peripheral precocious puberty. The diag-1 ]) z3 u, A) a! d  b
nosis can be established by just a few tests and by0 c6 [* w& F% b! w
appropriate history. The inability to obtain such a
" B; q. {$ g- _  n' v6 \history, or failure to ask the specific questions, may0 G6 G) f/ b9 U1 h/ Q4 I
result in extensive, unnecessary, and expensive
7 J! K' K' K" S9 Xinvestigation. The primary care physician should be
% l7 M: G: w  W& |aware of this fact, because most of these children
5 }8 }, B7 {* g, N/ ?( |0 ]may initially present in their practice. The Physicians’
$ j0 ?8 F3 k# k0 _8 K6 }* `9 GDesk Reference and package insert should also put a
4 M. K# K3 W( R: z* jwarning about the virilizing effect on a male or8 `( Z! y( W5 L+ P# [  i/ w
female child who might come in contact with some-
  w) M' }. p# T8 b/ Kone using any of these products.1 z. M6 Y; U; m/ F! Q% e/ }$ F
References
5 D. o8 u  o7 |1. Styne DM. The testes: disorder of sexual differentiation
$ V: O3 f$ q/ G9 c4 ?6 ]and puberty in the male. In: Sperling MA, ed. Pediatric
6 w7 Q& K5 O: X8 U( ~Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;# ^  J, x  Z9 Y4 ?
2002: 565-628.
2 {- G' W* F% X2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# G% z8 `( k# `
puberty 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
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!
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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

( x0 q7 S5 C" d' o$ I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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