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Sexual Precocity in a 16-Month-Old4 y" E! w/ I; }7 A7 ~
Boy Induced by Indirect Topical
# V8 ]' C3 J! |4 m" fExposure to Testosterone
7 ~- o5 Y, j% kSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( r" y- h. i6 g( t# uand Kenneth R. Rettig, MD1
0 y5 }4 A4 a+ n) I+ dClinical Pediatrics
) w7 g& [8 t3 H+ p2 H; T, g& L9 GVolume 46 Number 6! p! R- l  t4 p' I  h, Q& Z
July 2007 540-543
$ A0 G! v2 [: Q3 c) u1 B' O© 2007 Sage Publications
. w4 O0 \7 d5 X: r; F; E$ t7 s10.1177/00099228062966518 T# h( q! G+ \- C9 l( M0 p
http://clp.sagepub.com9 K  T: q! F2 k& G. T
hosted at
+ J4 e7 G; ~( r4 B. hhttp://online.sagepub.com6 O' u, |7 n+ V& _
Precocious puberty in boys, central or peripheral,
" k5 O# V+ \8 x6 F; Y% ^# U/ G, j# Ais a significant concern for physicians. Central% x; Q& T2 @0 n' G, `
precocious puberty (CPP), which is mediated
4 p1 J1 Z  I4 c  Q! S! h6 Y" ithrough the hypothalamic pituitary gonadal axis, has( X6 U1 Y( I7 G1 Q8 v1 o0 y
a higher incidence of organic central nervous system( h  Z& A  P1 ^. R
lesions in boys.1,2 Virilization in boys, as manifested4 ?$ C) i# P7 ]% V( J; |: x
by enlargement of the penis, development of pubic( _3 |, H, t& H$ ~* B8 a
hair, and facial acne without enlargement of testi-# f. j+ ?3 T; p* \' ?
cles, suggests peripheral or pseudopuberty.1-3 We4 i, W) u. v+ ~( e
report a 16-month-old boy who presented with the# T3 x3 j) q' P7 I& l
enlargement of the phallus and pubic hair develop-
! g. ?) t! H- D- x1 ~ment without testicular enlargement, which was due
* [. V! k4 q$ z. g$ C5 V% Ato the unintentional exposure to androgen gel used by
1 l! A7 v" n2 o; W$ u  j3 k1 P: zthe father. The family initially concealed this infor-
1 A+ H7 s5 d8 c8 U! j$ lmation, resulting in an extensive work-up for this3 w$ |+ r9 D5 }/ k) r$ P# D
child. Given the widespread and easy availability of
( G7 U0 i. u" ~& |' \6 itestosterone gel and cream, we believe this is proba-/ t8 x' A. ~! T
bly more common than the rare case report in the8 V" }" n/ P) ]9 L0 n' `" t6 X" e
literature.4; z8 B$ z6 ?0 X" h9 ^  k
Patient Report
  ~' U/ K6 Y. w& jA 16-month-old white child was referred to the
4 ]5 i% X8 ~- y, L: K  l: b0 Dendocrine clinic by his pediatrician with the concern
' f, |( a8 b0 c  F- G7 ~; Sof early sexual development. His mother noticed
1 Q0 j# w7 S, `3 i3 Ulight colored pubic hair development when he was
" W" M) E4 L% W$ B, c$ xFrom the 1Division of Pediatric Endocrinology, 2University of
% R* L# \5 J& D) t. QSouth Alabama Medical Center, Mobile, Alabama.8 p0 V5 L9 n! c# p- {! T
Address correspondence to: Samar K. Bhowmick, MD, FACE,
& Q" N' A/ N4 E# m. V3 q% `Professor of Pediatrics, University of South Alabama, College of
1 K2 B/ W) i% v# YMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 t3 ^7 C( {; @/ m; y
e-mail: [email protected].' ?/ O% f+ {3 z4 }4 F( H0 `
about 6 to 7 months old, which progressively became% V# A$ ~( ?6 t9 A
darker. She was also concerned about the enlarge-2 j% L3 {1 F# v% c8 f
ment of his penis and frequent erections. The child
: M& w( a) A9 T* T+ fwas the product of a full-term normal delivery, with
7 g5 P2 Y+ L( ?) N$ G3 B+ wa birth weight of 7 lb 14 oz, and birth length of
: ?  ^3 ~0 q+ o% D20 inches. He was breast-fed throughout the first year
, }- n( K2 w0 D  j; ~of life and was still receiving breast milk along with
) b2 G. ?, i* L+ v4 A, Hsolid food. He had no hospitalizations or surgery,1 z- k  G$ g5 l8 c! }% S
and his psychosocial and psychomotor development
# A8 m$ j' Q: P- s" ~/ pwas age appropriate.# x' V6 _2 B9 z) ]$ W& _
The family history was remarkable for the father,
, D, c# W: U9 N* L5 C: B8 Twho was diagnosed with hypothyroidism at age 16,4 L/ w5 f3 o6 o$ B+ `  H' n
which was treated with thyroxine. The father’s
. I+ V" h- s$ ?( \height was 6 feet, and he went through a somewhat) j( h' X( G; e! Z9 ]- t3 q: z
early puberty and had stopped growing by age 14./ F" K2 W* x5 z% w3 {
The father denied taking any other medication. The
' o0 a; x9 J+ l0 u/ @child’s mother was in good health. Her menarche& ?% K3 C# r7 c/ i, R
was at 11 years of age, and her height was at 5 feet; Y9 F5 E7 w* Z/ `6 N. e
5 inches. There was no other family history of pre-
8 _) R" X- S4 X# Z% e& icocious sexual development in the first-degree rela-3 w+ H# v5 ^; l- g- Y$ @
tives. There were no siblings.
' h! o4 s! ?7 s7 \9 y' @$ jPhysical Examination
- I0 r3 @  m8 ]# p3 O9 i/ jThe physical examination revealed a very active,
6 {3 ]: M5 i8 K4 R- v5 q( bplayful, and healthy boy. The vital signs documented& V* H  V' J$ J& S
a blood pressure of 85/50 mm Hg, his length was/ y1 N2 H5 E. S, a/ m
90 cm (>97th percentile), and his weight was 14.4 kg
- H2 V1 u" J7 G8 w2 m5 t(also >97th percentile). The observed yearly growth
' y! w% @: `) z% Y8 Svelocity was 30 cm (12 inches). The examination of0 p, [; U! [! ]9 k7 M: z' _1 M
the neck revealed no thyroid enlargement.
- _1 N0 a3 y6 S; ~. z* q3 yThe genitourinary examination was remarkable for  T' C# M/ j2 G6 G- v
enlargement of the penis, with a stretched length of; F! _4 Q( o& b5 o' y& n
8 cm and a width of 2 cm. The glans penis was very well
2 T+ W2 q- z# F; G8 }# kdeveloped. The pubic hair was Tanner II, mostly around
6 e3 H4 R" p0 f540  D. y6 S6 A5 k# r: f9 K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 b* N0 z5 X7 t: h: t0 K0 f0 d$ [the base of the phallus and was dark and curled. The2 I4 P; R9 i# y
testicular volume was prepubertal at 2 mL each.' \- L) ]& r' X* m, F+ m: o
The skin was moist and smooth and somewhat
3 ^4 l$ r+ V* Uoily. No axillary hair was noted. There were no1 v, S  M. u3 Y9 o( w2 v
abnormal skin pigmentations or café-au-lait spots.
7 x# \% a/ {2 \Neurologic evaluation showed deep tendon reflex 2+
8 }/ h1 \! Y" }bilateral and symmetrical. There was no suggestion8 E! c9 t4 x- n0 t2 v7 n1 X  r1 S( l! |
of papilledema.' s, z( I( C* m7 L: f
Laboratory Evaluation
' ?. n4 {: u, a  @) G5 O# xThe bone age was consistent with 28 months by
# O) W2 n: x/ _6 E& rusing the standard of Greulich and Pyle at a chrono-: W% y. r8 U4 W. X) L# e
logic age of 16 months (advanced).5 Chromosomal$ c6 M5 T9 Q  r3 \/ n$ X
karyotype was 46XY. The thyroid function test
& ^5 A- R& d$ q. B1 ]showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ h* d) w+ d. O0 H  K: Wlating hormone level was 1.3 µIU/mL (both normal).
" h" Q. a2 f. v! g) \# EThe concentrations of serum electrolytes, blood( q  L6 L1 q" `( B2 j7 j
urea nitrogen, creatinine, and calcium all were# m( k: p3 }; `
within normal range for his age. The concentration' h2 O' o& E4 m6 w5 x
of serum 17-hydroxyprogesterone was 16 ng/dL$ F" I; ~: W- _: c1 I
(normal, 3 to 90 ng/dL), androstenedione was 200 H( w' Q0 b' U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! C% j* q3 Z* P# mterone was 38 ng/dL (normal, 50 to 760 ng/dL),- V  x9 f  @) \, I/ `% \; ~
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 |! k6 j2 t; H, |# @49ng/dL), 11-desoxycortisol (specific compound S)
. x7 e- c9 g( K) nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 z5 v+ y- R6 h- ]tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 S* x) E" W; o$ k; D% S
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& {( ~! w: a$ }1 O% `. Q) u8 ?7 Gand β-human chorionic gonadotropin was less than, V+ h" ]: z( V6 _& c$ {2 z: }9 J4 J
5 mIU/mL (normal <5 mIU/mL). Serum follicular+ \: y! ~5 O) C5 Q
stimulating hormone and leuteinizing hormone
) I1 W9 h# _% vconcentrations were less than 0.05 mIU/mL
) z7 h! ]/ J  [(prepubertal).* a0 c; I0 R; o$ m9 J8 R5 h
The parents were notified about the laboratory
. n! u2 B1 H( ]) Hresults and were informed that all of the tests were" [$ y! m, n. l
normal except the testosterone level was high. The
: ~! c8 P# C( g) I+ P$ T% ]follow-up visit was arranged within a few weeks to
9 A/ _4 u1 H% f) u) {obtain testicular and abdominal sonograms; how-/ H8 z  k# l! Y3 o% A) X/ E
ever, the family did not return for 4 months.
0 ^, S8 u! Z* n3 E2 _) n$ F0 u+ ^( wPhysical examination at this time revealed that the
1 P! |/ P; G# B6 W0 t0 Tchild had grown 2.5 cm in 4 months and had gained
/ M  |! _) S! i0 {2 kg of weight. Physical examination remained, m" x) {: H  g% R5 Y$ x( D
unchanged. Surprisingly, the pubic hair almost com-
' N. a9 u6 w! L: w& ]. epletely disappeared except for a few vellous hairs at
2 l7 r/ T3 A4 v. c  Sthe base of the phallus. Testicular volume was still 2
" P: Y: e) K) ^9 C- rmL, and the size of the penis remained unchanged.- R, O( L5 S/ @2 D( T! R( L* y4 ^* G; c
The mother also said that the boy was no longer hav-) q! B$ l+ N! M8 b- [, G
ing frequent erections.8 i. w. N1 v$ o3 _5 x1 L& p
Both parents were again questioned about use of( D5 S" u2 C9 f. d' X. l5 }
any ointment/creams that they may have applied to
3 T6 I4 h) H, k2 x0 b* Q" l( K; gthe child’s skin. This time the father admitted the
) s, h/ A4 A! v0 ^Topical Testosterone Exposure / Bhowmick et al 541
3 X/ y, w7 u3 b3 suse of testosterone gel twice daily that he was apply-
$ O% V0 t' t: y6 ?* b0 ding over his own shoulders, chest, and back area for
! L8 p7 o& c0 t5 T, |a year. The father also revealed he was embarrassed
- ?$ y/ ]% e# M$ n% E* ^# oto disclose that he was using a testosterone gel pre-
5 P+ x% t! J& A) b  B) w' F  ]scribed by his family physician for decreased libido
8 ^% w6 H2 H! Xsecondary to depression.0 f# x1 Q4 v& M; Z* ]
The child slept in the same bed with parents.
  O6 ~* k& x3 M( i" e7 n8 QThe father would hug the baby and hold him on his+ ~: j7 f4 g1 w& ~) D" W
chest for a considerable period of time, causing sig-$ C9 v/ @( Y1 {6 [: `
nificant bare skin contact between baby and father.+ Y! |: T8 x. {% H# l  D
The father also admitted that after the phone call,
+ |7 k( l  F, m1 F# bwhen he learned the testosterone level in the baby
* i, @* C/ m  A$ Uwas high, he then read the product information0 s1 Y$ O" F( A* s( A6 i, Y
packet and concluded that it was most likely the rea-# }6 L/ k5 E+ _( X/ g% @
son for the child’s virilization. At that time, they
: ~8 U* u4 _' w3 ndecided to put the baby in a separate bed, and the
3 R% d/ P4 b( ~: X, s3 S  S# Afather was not hugging him with bare skin and had  A0 g7 `7 [7 v& R6 s
been using protective clothing. A repeat testosterone
1 a! ]9 l( d4 g, b( q! utest was ordered, but the family did not go to the
% q7 t+ t. s' B" z/ t; ^9 L# i; R# ~laboratory to obtain the test.
: z  k1 v3 V, iDiscussion  T% A  Z: ^2 O) ]+ E
Precocious puberty in boys is defined as secondary
. i0 }1 k, I7 bsexual development before 9 years of age.1,4, O# ]" h% f$ T3 [  j
Precocious puberty is termed as central (true) when
, o) O  \5 A; Z6 j2 T1 m. Cit is caused by the premature activation of hypo-- [3 \' R7 A/ b+ v: o( E* q" |3 Z
thalamic pituitary gonadal axis. CPP is more com-
! S% e, N" i' Q; f2 omon in girls than in boys.1,3 Most boys with CPP8 M& L9 {7 q: b! ~
may have a central nervous system lesion that is
* x: G& U; ~7 @( N. Cresponsible for the early activation of the hypothal-
8 ]5 A5 @( [# x* H6 W4 V" Xamic pituitary gonadal axis.1-3 Thus, greater empha-( T* D9 s8 }3 S' L9 b: R  D9 ~
sis has been given to neuroradiologic imaging in
- G$ b9 X; r' r' X. eboys with precocious puberty. In addition to viril-
% o0 i* L! c  T) _: Yization, the clinical hallmark of CPP is the symmet-6 n" c; F! _# T! g! |& c: G+ B
rical testicular growth secondary to stimulation by9 W' B3 `6 o; r! D/ i, P$ E! v* j4 h
gonadotropins.1,36 r0 J8 o+ P7 f0 d( {, Y' T5 k
Gonadotropin-independent peripheral preco-
; S6 n4 g: H. F2 r! i$ a+ p" Y, Lcious puberty in boys also results from inappropriate
8 T$ ]4 N* R' T% n- Q$ Sandrogenic stimulation from either endogenous or/ U8 Z, ~3 O) I0 R! Z. X
exogenous sources, nonpituitary gonadotropin stim-
6 q9 J3 f  w$ j; X  ]7 nulation, and rare activating mutations.3 Virilizing
4 K5 ]& E- z' C0 mcongenital adrenal hyperplasia producing excessive; N" u  v" P7 n5 [' D
adrenal androgens is a common cause of precocious0 }" v2 A* R* O) w. q! L) w2 u
puberty in boys.3,4
9 Z7 _/ y! b$ eThe most common form of congenital adrenal
6 N) \3 O& l  w9 O* b! Dhyperplasia is the 21-hydroxylase enzyme deficiency.) {7 x" Z+ r8 {4 B, k
The 11-β hydroxylase deficiency may also result in  e( D6 N/ V* B% w- n/ N; a! {
excessive adrenal androgen production, and rarely,
5 u7 {* H  U! f5 _, ?6 y; can adrenal tumor may also cause adrenal androgen, C; u' q% C4 U  E5 x
excess.1,36 P  `4 Z1 C7 R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ r0 Y( @  o) _- ?
542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 O: g3 O' j+ M
A unique entity of male-limited gonadotropin-
' w# U! D% i; Z! sindependent precocious puberty, which is also known- n5 S/ W! e. v, ]5 m
as testotoxicosis, may cause precocious puberty at a
. L. m% N% o1 Y6 b# S8 @, \; I3 v: ?very young age. The physical findings in these boys
$ |0 J5 _1 [) Q( Q* i! y6 Swith this disorder are full pubertal development,
, W( H' I: o; gincluding bilateral testicular growth, similar to boys  f/ A8 t* N6 Y# k% t
with CPP. The gonadotropin levels in this disorder
/ f: E6 r! L- z- c  z- Iare suppressed to prepubertal levels and do not show4 m  q  l0 v% a: ~
pubertal response of gonadotropin after gonadotropin-- O9 w% d. p' J8 v- ^4 M" h; \
releasing hormone stimulation. This is a sex-linked
, O( L# H4 j8 b- Sautosomal dominant disorder that affects only: I1 p/ \% R1 ^" C
males; therefore, other male members of the family
& D/ Z' _/ u# C% W( imay have similar precocious puberty.3
$ B  e3 Q+ T9 l; QIn our patient, physical examination was incon-* f8 m# m4 e1 e; h" ?- h6 X
sistent with true precocious puberty since his testi-
0 x. J; z2 [0 `4 V# Vcles were prepubertal in size. However, testotoxicosis
* X' o6 ~, z& h6 q5 q* Zwas in the differential diagnosis because his father
% c1 d6 v! N: j( H6 V2 }1 d4 q! jstarted puberty somewhat early, and occasionally,) e3 e- m/ ]$ k% {1 X! o) V
testicular enlargement is not that evident in the  D4 e8 M2 D  ]
beginning of this process.1 In the absence of a neg-
, q) y; z( M8 j( |; G; lative initial history of androgen exposure, our% G, ?% J2 j7 S
biggest concern was virilizing adrenal hyperplasia,% q# }5 Z7 g2 O( L9 v& h5 j  K
either 21-hydroxylase deficiency or 11-β hydroxylase
$ {  ]! m' \6 S  Ldeficiency. Those diagnoses were excluded by find-
$ p& f! |6 M# ]! t$ ting the normal level of adrenal steroids.
: S) z' t: H" S: N/ EThe diagnosis of exogenous androgens was strongly
) }. F, @4 p; K# e, e& [* Osuspected in a follow-up visit after 4 months because
' s3 }, k4 A: O5 b! fthe physical examination revealed the complete disap-
6 \5 W7 f. l" D$ z4 {. d' ]# T( ipearance of pubic hair, normal growth velocity, and$ q; m/ S% z7 H& s2 {/ ^! t
decreased erections. The father admitted using a testos-
1 R, v- w+ D2 z2 C/ mterone gel, which he concealed at first visit. He was  p$ {% a: |7 I) P  P% ^& c
using it rather frequently, twice a day. The Physicians’: q; q3 r2 S  H
Desk Reference, or package insert of this product, gel or. X& M; j" x/ w0 ?& b. _2 C! \  U
cream, cautions about dermal testosterone transfer to
- F+ T3 a) d8 C$ {5 O: a$ T' runprotected females through direct skin exposure.
4 O  m# A, i" ?3 e" G' v/ \% GSerum testosterone level was found to be 2 times the& `+ N+ b  W+ z4 @+ @
baseline value in those females who were exposed to, [0 E: m) {/ p! Y, C5 W9 B
even 15 minutes of direct skin contact with their male
8 J0 b6 B( K) {' |partners.6 However, when a shirt covered the applica-
6 L. n1 O$ i/ o" R/ Ption site, this testosterone transfer was prevented.
, K; l" g6 Z) K9 e$ nOur patient’s testosterone level was 60 ng/mL,
: j, L1 X7 p' z6 Hwhich was clearly high. Some studies suggest that& e* M4 {5 v, x$ P* S9 R
dermal conversion of testosterone to dihydrotestos-
* Y/ @1 O  ?( `8 A' Yterone, which is a more potent metabolite, is more! K: I% n0 t$ J6 S2 h$ r
active in young children exposed to testosterone8 E9 \! ~7 J% i
exogenously7; however, we did not measure a dihy-
9 v( s+ Y/ J; S  Sdrotestosterone level in our patient. In addition to! N' c0 i+ e- q2 y5 e
virilization, exposure to exogenous testosterone in
4 Z2 N/ ^5 o7 ?9 X! f/ tchildren results in an increase in growth velocity and' \% l! ~7 Q$ s+ M) X0 f% ^$ u4 h4 H6 V6 ?
advanced bone age, as seen in our patient.
$ J' c8 g& @& U; I! F( Q: z! {The long-term effect of androgen exposure during9 o1 p- [! d, s' r, v9 E0 P" h
early childhood on pubertal development and final
! h! A5 r' U  k2 r5 z& badult height are not fully known and always remain. o- ~6 D* p, G5 E" r3 e9 H6 u
a concern. Children treated with short-term testos-( E9 G9 R; G% X; i! }" h& N% _: D
terone injection or topical androgen may exhibit some, e8 h1 R8 o) b
acceleration of the skeletal maturation; however, after
2 t  f  j! ^  @& H& Pcessation of treatment, the rate of bone maturation0 w( z" \3 Z% [  v
decelerates and gradually returns to normal.8,9; X' B8 ]7 ~) G+ V
There are conflicting reports and controversy7 g8 a% A1 A# J' E1 B! w
over the effect of early androgen exposure on adult  Q  I: I0 p/ j, w+ ^; j' p
penile length.10,11 Some reports suggest subnormal
2 S0 N! [7 Y4 [. M6 @, hadult penile length, apparently because of downreg-
) o; k$ o7 y  wulation of androgen receptor number.10,12 However,
( a- m- j; o# _8 ~8 CSutherland et al13 did not find a correlation between
# m. |7 o/ ^' }2 ~childhood testosterone exposure and reduced adult
8 S4 f/ N$ m; {! [$ ^7 O! _penile length in clinical studies.* K- X. ]7 [8 A1 ]& Z7 Q
Nonetheless, we do not believe our patient is8 J2 w( E4 }8 H0 D  P( O2 @3 L
going to experience any of the untoward effects from- A" ?. Y( {2 E) _3 K$ f
testosterone exposure as mentioned earlier because4 _5 f2 `1 S, B% h! C+ o
the exposure was not for a prolonged period of time.
$ Z; i# A) m) ?# F/ U1 c; Q4 E/ DAlthough the bone age was advanced at the time of
! _* X2 j5 a$ @# `  f: ^diagnosis, the child had a normal growth velocity at& _# B8 p3 t3 ^' U- ]
the follow-up visit. It is hoped that his final adult
6 v. K$ F7 I) S# q* u) aheight will not be affected.$ T5 ^8 D% D9 q% Z; f0 p1 s* Q+ D
Although rarely reported, the widespread avail-
) Q% }: Z% r  dability of androgen products in our society may5 ~$ |0 ]* E; V( r9 c' S- ]
indeed cause more virilization in male or female! G6 K' ]$ E" S, z4 v; L! ]
children than one would realize. Exposure to andro-
5 [4 W1 m$ x* M3 w0 a+ r, Dgen products must be considered and specific ques-8 ]" \0 O2 a0 W' J1 E$ U/ V; J. J
tioning about the use of a testosterone product or3 M( N$ e, V2 P/ ~- b$ Q
gel should be asked of the family members during
; d1 n! d% o- J3 cthe evaluation of any children who present with vir-6 r8 K. j: T0 _0 X
ilization or peripheral precocious puberty. The diag-0 a$ `, C" M" L
nosis can be established by just a few tests and by
2 H, ~7 V0 g1 x1 Z+ v9 r7 mappropriate history. The inability to obtain such a
7 ]5 @9 S0 E8 Rhistory, or failure to ask the specific questions, may4 q: b) o# u6 j3 w. }
result in extensive, unnecessary, and expensive
! N% F* ?9 ~7 M) s( h5 U1 T  ginvestigation. The primary care physician should be
- [2 Q- ]9 U" o5 Faware of this fact, because most of these children
( e( z8 L$ c9 X3 }8 Wmay initially present in their practice. The Physicians’' O9 F  F# ]- R% H: E1 H
Desk Reference and package insert should also put a
) K' l) m1 f0 S; R; c+ s" twarning about the virilizing effect on a male or
: ]  U- ~0 f8 E1 c3 dfemale child who might come in contact with some-+ e* r+ ~$ l$ L
one using any of these products.. \# B3 a% y4 E& @# Z
References
" \; p# V- v5 J! D' }1. Styne DM. The testes: disorder of sexual differentiation6 T$ l5 i+ n; u* T) y; ~
and puberty in the male. In: Sperling MA, ed. Pediatric
) e  k8 t2 n  O7 a9 Z+ |Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: z! d6 b( V0 ]: E- ^- R! y
2002: 565-628.
% u0 |# V8 B- O. u) w  R/ y5 i2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 r7 k. q  ]1 U1 I! rpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
/ A4 N5 e$ G( d0 RBoy Induced by Indirect Topical: N: J5 |9 n- e( l
Exposure to Testosterone
$ f- R2 G6 m# e! {Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ b% ~! h/ w5 {" x
and Kenneth R. Rettig, MD19 z" ]$ N% u# V8 o+ @
Clinical Pediatrics
6 Z. e/ t+ h0 \) C# vVolume 46 Number 6/ ^8 k4 b. X/ X4 H5 E! A- H' }
July 2007 540-543! R' I/ p  N8 C6 ^- b% i' |8 ^
© 2007 Sage Publications
/ [1 Z5 z1 K- q+ F10.1177/0009922806296651  q& b7 Y+ w8 l% d% ^7 y4 |
http://clp.sagepub.com
& p4 W- j0 j$ w7 f' }9 |! Y- G  A/ zhosted at
/ U. i2 q$ a* Y& f# ^: _: ]0 ahttp://online.sagepub.com
  E; u$ s% N9 h' i; g. B7 GPrecocious puberty in boys, central or peripheral,/ M* M8 @* y9 e2 c( J
is a significant concern for physicians. Central
) t  [' Z) _$ z1 \! tprecocious puberty (CPP), which is mediated6 {, B) \, |( c, z
through the hypothalamic pituitary gonadal axis, has7 }" N# e1 O  m; U9 t
a higher incidence of organic central nervous system
( R2 x) n  l& U# o( W, W% ~  B$ X: x! qlesions in boys.1,2 Virilization in boys, as manifested
' V: [( n1 O$ ~, i. x, h( m8 P$ H/ eby enlargement of the penis, development of pubic4 d% Q5 b( u0 b$ E7 B# A/ N% n$ k
hair, and facial acne without enlargement of testi-
7 q* ?; G& z$ L8 K7 M- Icles, suggests peripheral or pseudopuberty.1-3 We
  p. S2 G! L8 b% Creport a 16-month-old boy who presented with the* X1 b) d5 E1 F0 O3 p! v: m
enlargement of the phallus and pubic hair develop-
1 J  O- l/ a4 F0 Bment without testicular enlargement, which was due
* c+ {. d4 o+ Z8 x$ vto the unintentional exposure to androgen gel used by3 `7 z7 E: x& H/ G/ F, h
the father. The family initially concealed this infor-& _6 J$ x9 j( i0 f' a
mation, resulting in an extensive work-up for this. s& S6 E( n- k2 U0 n
child. Given the widespread and easy availability of
- x( V+ m5 ]) L, w; Gtestosterone gel and cream, we believe this is proba-
3 h: t6 M( V: i# J* E" p0 Ably more common than the rare case report in the% i4 f! I  ~! X+ i; y% @$ j1 D9 u
literature.4
  m1 s, {" i$ w3 LPatient Report
: |/ t, ]6 l( U' n: p/ yA 16-month-old white child was referred to the$ {' @4 s4 `% G- F3 M
endocrine clinic by his pediatrician with the concern
9 D- R; w5 F% Kof early sexual development. His mother noticed4 U1 H4 l7 |* }/ O2 {+ {
light colored pubic hair development when he was2 B1 C+ c3 i9 p9 e9 A: W
From the 1Division of Pediatric Endocrinology, 2University of
; y/ `/ x4 L3 j, z. q" ?South Alabama Medical Center, Mobile, Alabama.9 |* w6 U5 _  [4 q
Address correspondence to: Samar K. Bhowmick, MD, FACE,4 z2 ^+ c: o8 X7 Y* T
Professor of Pediatrics, University of South Alabama, College of
1 `/ ^" h2 R) kMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& w4 ?7 F1 K' d+ Ke-mail: [email protected].
1 [* s5 d/ b) p5 Habout 6 to 7 months old, which progressively became
0 \# J" l* f9 }% Y" S: G  s$ X- Hdarker. She was also concerned about the enlarge-' A! J- K$ y: N) p! ^. D1 u& Y
ment of his penis and frequent erections. The child
. Q; o$ p- R7 f; r1 S# Q/ z7 M7 hwas the product of a full-term normal delivery, with
5 t0 t) I  t0 ?7 q& h2 \- Ka birth weight of 7 lb 14 oz, and birth length of; U$ K# v3 t/ |# s* x* n/ m
20 inches. He was breast-fed throughout the first year+ H) e: }3 p2 W! E/ f8 F: b* {7 S' P
of life and was still receiving breast milk along with) I6 J2 h$ B5 a! G4 \# V' j" O1 |' l
solid food. He had no hospitalizations or surgery,
, F9 D2 f* O! X! x: B5 q: ?" j9 land his psychosocial and psychomotor development
# K  w, v+ ^4 S2 Bwas age appropriate.3 P3 |+ K) `$ A
The family history was remarkable for the father,0 L% u! S) h) l' v" N6 N# e0 |+ G' e. a! E2 l
who was diagnosed with hypothyroidism at age 16,
+ K2 g: a+ H/ W" g& p) ~- twhich was treated with thyroxine. The father’s: t9 o# t: v& x2 E
height was 6 feet, and he went through a somewhat3 [) H" a  d% R7 i& `/ r
early puberty and had stopped growing by age 14.
9 R9 C0 f5 s0 u9 K0 T3 uThe father denied taking any other medication. The
$ e) i( T1 Y6 i7 schild’s mother was in good health. Her menarche
7 Z3 r8 \9 t. n" rwas at 11 years of age, and her height was at 5 feet8 P0 x7 P7 x7 F4 |+ N. R! Q. C5 V
5 inches. There was no other family history of pre-' t2 D( m  ~; K) o! J
cocious sexual development in the first-degree rela-
/ s% T2 ]0 E6 j; Htives. There were no siblings.
, D3 m9 W9 `6 |1 I0 ~Physical Examination
+ E" v. Q9 y1 D5 J) z6 n% tThe physical examination revealed a very active,4 z/ r& B$ V& _4 R* a* T
playful, and healthy boy. The vital signs documented5 V. T# W7 F0 n, D- T9 [7 C$ [8 B
a blood pressure of 85/50 mm Hg, his length was
* Q7 D5 C3 _  N+ `! e90 cm (>97th percentile), and his weight was 14.4 kg
# F3 m' }. H& P/ F$ h- {+ E) ~; n8 {(also >97th percentile). The observed yearly growth
4 L1 k0 ~% c% F" K& B& ?# s# }" u) o+ cvelocity was 30 cm (12 inches). The examination of6 ~: b2 ~8 e9 g0 e- `! f2 Q6 g& B
the neck revealed no thyroid enlargement.
( l7 W, A7 {( `, A3 O1 [The genitourinary examination was remarkable for" q: @% P5 }5 C4 m" g, C# B
enlargement of the penis, with a stretched length of: i5 F  e1 {; `1 u
8 cm and a width of 2 cm. The glans penis was very well* R, l: }# o% [5 |* |6 K2 \3 a) Y, S+ q
developed. The pubic hair was Tanner II, mostly around* L; u% p% G- M- Q+ k: \5 ^3 F
540
$ Y; n" }% c4 C' j' rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# V7 ~- S2 t1 w# R/ F- W; y' g. [+ i
the base of the phallus and was dark and curled. The( ]4 ^7 J, W. l& c( C0 o
testicular volume was prepubertal at 2 mL each.& t' T" R. H; R( x& y
The skin was moist and smooth and somewhat
* F# ~  ?3 |3 X" D( Qoily. No axillary hair was noted. There were no7 [; r8 u0 g" M: A& z$ E8 o
abnormal skin pigmentations or café-au-lait spots.! s8 S8 o5 }# b) `; y* c) ]
Neurologic evaluation showed deep tendon reflex 2+
" Z4 ~* A# w% l, r- u, {& P2 Qbilateral and symmetrical. There was no suggestion
# j; C& u' t5 D: I! A  u$ L0 Vof papilledema.
7 C5 s: Q' q5 r7 L6 K; A/ ~3 G% ELaboratory Evaluation2 @2 B6 p1 o& K. b" @
The bone age was consistent with 28 months by
7 R, u- e9 m8 m7 Q- m. e4 Gusing the standard of Greulich and Pyle at a chrono-
7 K( \/ K+ Q  Y- _logic age of 16 months (advanced).5 Chromosomal) X  d# t9 m# ?: N. }
karyotype was 46XY. The thyroid function test
) {: R* ]+ A6 Rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-2 W! S/ Y( C( T0 o! K" j! B
lating hormone level was 1.3 µIU/mL (both normal).0 J! J3 l0 T& D8 F
The concentrations of serum electrolytes, blood6 ]% v9 u; \  b7 |$ T& V2 P7 ?, t& R
urea nitrogen, creatinine, and calcium all were
0 l7 J5 s2 e" y2 Mwithin normal range for his age. The concentration$ {8 K7 }, Y* \0 i# [
of serum 17-hydroxyprogesterone was 16 ng/dL
+ `+ [4 v; l1 @- }8 h  v( x(normal, 3 to 90 ng/dL), androstenedione was 20  b+ o$ ]( n4 O) Q1 s1 p5 s
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 M) u: T" A) w  M2 A
terone was 38 ng/dL (normal, 50 to 760 ng/dL),( s$ N& A. D( m4 f  l9 o( o
desoxycorticosterone was 4.3 ng/dL (normal, 7 to, N' B7 E1 m) t. P
49ng/dL), 11-desoxycortisol (specific compound S)
9 j0 A6 i5 R) {+ \" E% ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
9 Q. f/ ~2 D7 T7 I+ K3 Jtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( b$ a! O2 Z2 U
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# a; H# J& j' ]! Qand β-human chorionic gonadotropin was less than
/ U9 ~; n/ z; p5 mIU/mL (normal <5 mIU/mL). Serum follicular
' u% G; ?2 a8 R; h! l* I' s, i+ {' m+ Kstimulating hormone and leuteinizing hormone8 s7 v' A0 u# \& L) f9 S+ E
concentrations were less than 0.05 mIU/mL* j; F2 P; n) `5 g
(prepubertal).. \4 E& z  r' r, [6 ^
The parents were notified about the laboratory
/ e8 X) h' G9 ~" V$ f! X' e) Qresults and were informed that all of the tests were5 }+ s9 j9 S3 B* S& K- u9 z
normal except the testosterone level was high. The
7 E7 A0 Z3 N+ Y" }) j# _5 gfollow-up visit was arranged within a few weeks to4 x: W: y/ F3 M) \! i
obtain testicular and abdominal sonograms; how-
' W8 p2 o! \% g2 g" k% g- t& wever, the family did not return for 4 months.- }6 B# a$ S% H& N9 I" v) u
Physical examination at this time revealed that the% p( S, z1 X# w
child had grown 2.5 cm in 4 months and had gained+ m8 q  D! S& P" I9 f
2 kg of weight. Physical examination remained& M2 c* `9 y1 y! q/ r6 x* D7 w0 D
unchanged. Surprisingly, the pubic hair almost com-0 Y' a  T* O6 X: n, `
pletely disappeared except for a few vellous hairs at
. Z! I* g7 `. Z2 u4 D+ ]the base of the phallus. Testicular volume was still 2
! p+ V5 ?8 K2 ~" I8 i3 p- dmL, and the size of the penis remained unchanged.3 q( |" \2 I2 C- A) ?9 [, y$ f
The mother also said that the boy was no longer hav-$ @6 W3 v+ z) K' u
ing frequent erections.! N& S& ~3 k7 ]5 ^  w6 v% Y
Both parents were again questioned about use of, _! r* d/ n$ P% r6 M
any ointment/creams that they may have applied to; G  Z$ J7 u% `
the child’s skin. This time the father admitted the- q, X, a6 _7 b7 k
Topical Testosterone Exposure / Bhowmick et al 5413 h  h& u, J+ g! m
use of testosterone gel twice daily that he was apply-
$ [; L. F; E/ U0 b5 Ning over his own shoulders, chest, and back area for( }" m" g9 z" f- x" ^* f
a year. The father also revealed he was embarrassed' s& k* g* t. r
to disclose that he was using a testosterone gel pre-
- W) @; _% x9 G' f( Jscribed by his family physician for decreased libido1 I5 z3 C- _1 x3 D& m6 e7 T9 d$ a& _
secondary to depression.) S8 h9 y6 H1 d
The child slept in the same bed with parents.
5 g- m. p$ j, X5 QThe father would hug the baby and hold him on his( H5 _0 Z/ g/ `
chest for a considerable period of time, causing sig-- N3 x$ U. Z! V4 T7 D5 ]3 T0 i4 j
nificant bare skin contact between baby and father.6 N, a- O: `; w! J* ^! J' E) z3 _
The father also admitted that after the phone call,
% m( N. A; B& _/ m3 Xwhen he learned the testosterone level in the baby
: S0 b' M% I/ H! i6 dwas high, he then read the product information' X# K% i8 n, }
packet and concluded that it was most likely the rea-/ S& O! B" e" ~" Q% |- K
son for the child’s virilization. At that time, they
1 C6 ~, Z. U3 r3 S0 W, ldecided to put the baby in a separate bed, and the
. V- b5 \% j: q$ `8 W3 N& H. [father was not hugging him with bare skin and had* L' z4 Y% v7 Z5 m
been using protective clothing. A repeat testosterone  z2 l4 b1 p3 G$ L+ ~/ [
test was ordered, but the family did not go to the
) i1 ?* l( U$ E+ Dlaboratory to obtain the test.
/ M3 Q4 ^" _0 I/ R" v, GDiscussion( M; {  r# a( h# f. w$ U' w& R2 O1 a
Precocious puberty in boys is defined as secondary/ e, H7 k; h% K/ y/ H
sexual development before 9 years of age.1,4
& c. h8 ^; i- `, RPrecocious puberty is termed as central (true) when0 F8 ?: v) e; |* i! j! _* T
it is caused by the premature activation of hypo-7 |' o, k# F/ w2 x) E  }/ `
thalamic pituitary gonadal axis. CPP is more com-9 G" B$ r2 g8 h) a5 S# y: j
mon in girls than in boys.1,3 Most boys with CPP
5 ]6 ^; h, t. t; Gmay have a central nervous system lesion that is
; F# v0 @: s1 o/ _responsible for the early activation of the hypothal-
5 |" s2 a4 c( |; ]" B& xamic pituitary gonadal axis.1-3 Thus, greater empha-3 A+ \3 T( D  g: S
sis has been given to neuroradiologic imaging in
, H+ c2 u! ~2 l/ |boys with precocious puberty. In addition to viril-9 ]0 I. s9 p4 F: S$ q
ization, the clinical hallmark of CPP is the symmet-
0 z' o; @) ]( n- E5 e$ xrical testicular growth secondary to stimulation by
* {0 p5 y5 F0 }  L7 K8 P$ a' z2 ugonadotropins.1,3" Y  h6 k; {& l8 R/ B/ O7 i
Gonadotropin-independent peripheral preco-
& P8 Z" u' s, [( L$ e7 w# y& ^" icious puberty in boys also results from inappropriate
$ A- G1 |" W+ Y5 Gandrogenic stimulation from either endogenous or, Y9 K% f# @; G/ L
exogenous sources, nonpituitary gonadotropin stim-# J5 d8 D0 ^3 J3 c2 ?/ \0 Y
ulation, and rare activating mutations.3 Virilizing+ @2 k: ~+ g1 D/ ?( d( z0 j+ [
congenital adrenal hyperplasia producing excessive- A/ j: c  e( A$ G
adrenal androgens is a common cause of precocious9 ^9 d; d1 b/ \# l! k; t' C
puberty in boys.3,4
" ~6 n, G, o/ ?; FThe most common form of congenital adrenal
. j6 u% H& `! S" thyperplasia is the 21-hydroxylase enzyme deficiency.
# D" u* \; |& e( OThe 11-β hydroxylase deficiency may also result in$ I8 N( L! W. L+ x# I
excessive adrenal androgen production, and rarely,
! o' j- k# Q2 H) h, Jan adrenal tumor may also cause adrenal androgen
6 ~) H( D% J5 W  Q! |3 @  p) m4 @excess.1,3. W8 Y0 I! t' ^. V4 X1 V0 `+ i8 P, |: o
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  w$ h5 r7 u; N7 e9 q7 t542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. D( Y. _9 u& e/ L& Y- e2 m; V
A unique entity of male-limited gonadotropin-
) a0 }/ y8 J2 _- k, d" r6 m% nindependent precocious puberty, which is also known- h9 _% g( S' g) ]& k
as testotoxicosis, may cause precocious puberty at a% n  T+ f% W6 T/ O: J
very young age. The physical findings in these boys0 }8 N/ T/ z! j  U' B, R; U
with this disorder are full pubertal development,$ `/ `0 p% T, h$ q3 @9 f
including bilateral testicular growth, similar to boys
& z- T5 w, J$ N3 Qwith CPP. The gonadotropin levels in this disorder' A( A+ T4 P: ^0 q* ]3 g  S. \
are suppressed to prepubertal levels and do not show3 g! M% K0 }" i! ^; I
pubertal response of gonadotropin after gonadotropin-, H2 O3 p+ U+ I7 Q) G, D1 p7 U# g
releasing hormone stimulation. This is a sex-linked
* |3 m& Z# a4 I2 Mautosomal dominant disorder that affects only8 ]7 T  q# |% }/ b9 ^( k3 z
males; therefore, other male members of the family0 }) t0 A6 C( R$ f% u8 F! b
may have similar precocious puberty.3
( v/ e3 }% T9 n+ b0 ~In our patient, physical examination was incon-
3 O- }, ?* e  Qsistent with true precocious puberty since his testi-
5 P& P$ S0 X9 g; ^: [- @# K; o$ ccles were prepubertal in size. However, testotoxicosis- ^" n- U& z0 X" e2 y$ E4 n& N
was in the differential diagnosis because his father
/ x- ]. H: K! ?& V( Mstarted puberty somewhat early, and occasionally,
5 l2 I! L$ x! R! |  w) r6 E: \/ w$ ktesticular enlargement is not that evident in the: Q  i" V9 s4 J1 {- l/ w
beginning of this process.1 In the absence of a neg-/ c/ R+ H- n2 R- |0 r. {8 J( N* {
ative initial history of androgen exposure, our8 V9 g$ P. c: x' J' i
biggest concern was virilizing adrenal hyperplasia,& ~( R! ~9 m3 H! H3 D
either 21-hydroxylase deficiency or 11-β hydroxylase
4 k2 S% e4 d8 W$ p9 D, O" udeficiency. Those diagnoses were excluded by find-- u+ Y4 v' ^8 v
ing the normal level of adrenal steroids.
2 P: H% s: Z# r3 y9 `( rThe diagnosis of exogenous androgens was strongly
3 n& l1 M6 o+ V' D+ |( c7 ^6 I6 M4 Gsuspected in a follow-up visit after 4 months because" Z9 D# @% C" n2 q( O
the physical examination revealed the complete disap-
1 y0 }3 u% ]! d% d+ D$ t5 U1 G! `8 Cpearance of pubic hair, normal growth velocity, and+ H, y- W* f5 ?0 s
decreased erections. The father admitted using a testos-
. b7 b+ O8 R8 `1 Rterone gel, which he concealed at first visit. He was
: `* o7 u1 v* s" H+ Kusing it rather frequently, twice a day. The Physicians’
3 f, Y; @9 i" X5 n6 JDesk Reference, or package insert of this product, gel or
9 D8 H; D& n" d( Hcream, cautions about dermal testosterone transfer to
: v( f$ X2 S8 [$ J# O% H  q* runprotected females through direct skin exposure.) z4 n, Q/ w+ B0 {/ j6 b6 |  [
Serum testosterone level was found to be 2 times the
' b2 ~! v% p  c' p5 bbaseline value in those females who were exposed to
$ o+ a' o2 i2 E$ T% geven 15 minutes of direct skin contact with their male
. N. [! I8 X3 m9 fpartners.6 However, when a shirt covered the applica-7 n, Z1 q( q/ o2 v! {- J
tion site, this testosterone transfer was prevented.4 U' f* t, i# ]/ z  ^* q
Our patient’s testosterone level was 60 ng/mL,- P+ t+ m* I" c! k
which was clearly high. Some studies suggest that( H* y, l( T/ V6 s
dermal conversion of testosterone to dihydrotestos-$ z0 b) O! M$ r+ S% G
terone, which is a more potent metabolite, is more! G* n9 S6 b! [! N$ i% K& N" m* O
active in young children exposed to testosterone
/ a4 k/ e2 T9 H2 M* n( @* i: zexogenously7; however, we did not measure a dihy-
' m8 Z& ?2 u/ A  W* ~! xdrotestosterone level in our patient. In addition to$ {, r0 e  i: E3 A3 L$ f' N  i
virilization, exposure to exogenous testosterone in) Q3 h/ G! c/ O) @! o
children results in an increase in growth velocity and" N( R$ U. ~+ Y6 N) Y
advanced bone age, as seen in our patient.
1 D2 ~4 }' e4 i. IThe long-term effect of androgen exposure during8 S& |# Y; w: l& M6 u
early childhood on pubertal development and final
$ {- f* v, f  ^" V, A8 E7 X; gadult height are not fully known and always remain) J* R; h' c7 B. a! o- C
a concern. Children treated with short-term testos-
5 V0 @  W0 I9 z% y' Eterone injection or topical androgen may exhibit some
9 Z. A- P* [$ D9 ^) T0 d2 \( Nacceleration of the skeletal maturation; however, after
8 V! V% L: L6 K& ?' Acessation of treatment, the rate of bone maturation
( A0 t; s, J5 }3 @0 R) idecelerates and gradually returns to normal.8,9
" O' S+ h2 R# `  r( y1 NThere are conflicting reports and controversy& y& v" L7 j3 _+ }* _
over the effect of early androgen exposure on adult7 t0 q" e0 d# v, Y& q! ]! v7 b
penile length.10,11 Some reports suggest subnormal
$ e: E- v5 Z1 G' qadult penile length, apparently because of downreg-7 _: E0 |- D0 {1 f( [0 S) r
ulation of androgen receptor number.10,12 However,% a$ L) X+ j3 r: r- E1 y' W# a2 [
Sutherland et al13 did not find a correlation between
+ h% Y: R' t5 [3 L' zchildhood testosterone exposure and reduced adult
. _: E5 q# U1 Z2 V3 P% jpenile length in clinical studies.
+ C$ g; G% x) s5 L7 t. XNonetheless, we do not believe our patient is) \5 F( b; |  M8 I
going to experience any of the untoward effects from$ V$ ]3 s* e8 ~& f9 w
testosterone exposure as mentioned earlier because
$ T8 M9 ^; I, X8 C6 o$ hthe exposure was not for a prolonged period of time.
3 `$ H' N. I8 T4 s) q% EAlthough the bone age was advanced at the time of3 ]4 s9 Q$ B0 c2 n5 Y8 P
diagnosis, the child had a normal growth velocity at
( m' k9 ?) o7 |& C/ ^. e& ?the follow-up visit. It is hoped that his final adult
5 [. U" y9 Z( A+ k- y6 n  qheight will not be affected.) |# ~2 n' V" J# X
Although rarely reported, the widespread avail-
' K0 o% S& e" q2 |- ?. t- P% jability of androgen products in our society may
/ E5 U) t8 ?  l+ L+ findeed cause more virilization in male or female
1 J' h5 ~0 O  `8 Tchildren than one would realize. Exposure to andro-
4 p, q$ d  H5 V6 W; S" u. ^) Y+ xgen products must be considered and specific ques-" f; [& @3 A, {7 f, I
tioning about the use of a testosterone product or
0 L5 u: j9 b9 fgel should be asked of the family members during; {: Z# ?0 P% u7 Q5 f
the evaluation of any children who present with vir-* p6 Y1 p2 X4 I  Q' t! g& o  c5 g
ilization or peripheral precocious puberty. The diag-
; N! G- D0 g0 X  B1 y. A) unosis can be established by just a few tests and by
4 g. N' ?8 S! vappropriate history. The inability to obtain such a
$ N/ u% G7 h3 K/ A8 X! c2 fhistory, or failure to ask the specific questions, may
7 q8 R; q* l8 `* Z# j9 ?result in extensive, unnecessary, and expensive
  O& H# q0 R& G* u3 q' P# Oinvestigation. The primary care physician should be
/ z0 H" t1 J; w" e& e. I- e% xaware of this fact, because most of these children
5 M( L+ Y% g1 ^" Zmay initially present in their practice. The Physicians’
$ e  {, {/ j2 O1 C9 }Desk Reference and package insert should also put a4 i, m3 L: ]$ {/ o" l* X3 S' S
warning about the virilizing effect on a male or
, ]# v& C) p2 H" e/ mfemale child who might come in contact with some-
& x5 H9 P' j, r5 h- P* Kone using any of these products.* \9 [* e4 V5 I1 j! i8 q9 _2 [
References
4 `; p/ O* W9 U2 q1 }+ s1. Styne DM. The testes: disorder of sexual differentiation
/ q6 J* L& g  Mand puberty in the male. In: Sperling MA, ed. Pediatric
5 U0 f1 b) h( a; \Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 @, J- ?0 V- E0 I
2002: 565-628.' j1 t; I: t4 _1 n( o
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 i1 }8 J& L1 x7 g
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
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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
- X+ H. ?' I, M7 V4 _* O( G
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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