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Sexual Precocity in a 16-Month-Old
) g4 R# [# z# U8 r9 r. fBoy Induced by Indirect Topical
/ x# c7 J: `. i: \' `% k; f! {/ _, {Exposure to Testosterone
3 T( N) e1 ~8 L/ ~) s! C9 L& r% {: JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. q' H6 Q8 L; X  D
and Kenneth R. Rettig, MD1
: n1 n/ Y+ p9 S' b7 LClinical Pediatrics
/ ~1 f- i1 k$ Z% r6 ]9 y6 ]5 w0 I# wVolume 46 Number 6
! b2 C+ T% b- f# wJuly 2007 540-543
0 J0 M1 T) X1 ]; n/ ]2 l' Z5 n© 2007 Sage Publications$ h, t( r7 k2 N$ C
10.1177/0009922806296651$ {8 j2 T2 Y% B
http://clp.sagepub.com
6 S/ o& ]% l) A7 H; Chosted at
) w, W$ e4 C/ d# ~8 Fhttp://online.sagepub.com& W( U3 t- K! ~9 K# X7 S! i4 e
Precocious puberty in boys, central or peripheral,# {% u( |8 s6 D. O
is a significant concern for physicians. Central
, T1 R+ _5 D" `) _precocious puberty (CPP), which is mediated
0 W9 W' Z+ D' u7 M7 j8 f. Jthrough the hypothalamic pituitary gonadal axis, has1 Q' x  ?# u% w+ D
a higher incidence of organic central nervous system
4 L+ x# `$ B! d& tlesions in boys.1,2 Virilization in boys, as manifested; K# i" Y  v$ v; _2 r) ]; T: G5 I
by enlargement of the penis, development of pubic
4 r+ z9 a! i; g0 S! {* Phair, and facial acne without enlargement of testi-) T( b/ B2 P* P3 F
cles, suggests peripheral or pseudopuberty.1-3 We* e: I' X7 b5 Z! r
report a 16-month-old boy who presented with the
+ b- w. P: \* w5 Fenlargement of the phallus and pubic hair develop-
% u0 H" h* y& D8 hment without testicular enlargement, which was due! J3 c; F7 Z% V0 p  k
to the unintentional exposure to androgen gel used by2 [, L) A, ]% @2 Z" O
the father. The family initially concealed this infor-7 _" Y) w6 k0 [5 P! y: \: {* Z
mation, resulting in an extensive work-up for this! B& F1 B! I( K& ?) y
child. Given the widespread and easy availability of
. C/ a; l9 f4 d( L* {5 stestosterone gel and cream, we believe this is proba-$ V% r3 V5 \+ A! d  {$ l
bly more common than the rare case report in the8 P  v3 x% d' R
literature.4
2 r* _8 R2 N. J4 ZPatient Report$ ~' ?. }. C/ p$ G# I' I9 r9 O9 {
A 16-month-old white child was referred to the
2 W1 y/ m0 ~% cendocrine clinic by his pediatrician with the concern
' [2 b' x" [5 G/ D/ ^' Eof early sexual development. His mother noticed, t; S% U! j, x4 g4 r$ |
light colored pubic hair development when he was
5 _6 t' B7 h! h; E& kFrom the 1Division of Pediatric Endocrinology, 2University of
0 b$ r8 P( L" Y  d1 u8 n2 QSouth Alabama Medical Center, Mobile, Alabama.
# ^" W" p+ g& k6 @; d) ZAddress correspondence to: Samar K. Bhowmick, MD, FACE,3 x1 m; |1 H* C+ e4 Y" {
Professor of Pediatrics, University of South Alabama, College of
/ _. p3 a6 D& M, R2 s4 {1 Q; E& oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 }! K* C# ^% h$ Ae-mail: [email protected].
3 A# t, C# U3 ^+ |* Zabout 6 to 7 months old, which progressively became0 ^! ?1 @4 j, c5 m
darker. She was also concerned about the enlarge-
$ x( [/ t1 d7 A. \+ i" h# x, t% gment of his penis and frequent erections. The child
" I9 w9 L' V" z! I3 ~was the product of a full-term normal delivery, with
* {6 g& J# A% {2 _9 @* q; W4 La birth weight of 7 lb 14 oz, and birth length of
' R6 u5 u* M& h20 inches. He was breast-fed throughout the first year
" k9 j5 b+ N' f% X4 v! Z/ z0 I0 Bof life and was still receiving breast milk along with
. ~& v/ Q; {( K) o' ?& x; Xsolid food. He had no hospitalizations or surgery,8 q% P/ Z6 }8 I
and his psychosocial and psychomotor development) x1 j9 T6 I: N* V2 ^0 G
was age appropriate." D0 o6 g. O6 Q! U9 `* R% ]
The family history was remarkable for the father,  u  [2 t* E7 q* ~# d) q0 {8 V
who was diagnosed with hypothyroidism at age 16,
; y  {" h3 ~7 x# Iwhich was treated with thyroxine. The father’s2 \; v/ N+ ?9 |( h$ R0 t3 c' S
height was 6 feet, and he went through a somewhat3 H7 J& Y" C, f5 u9 B$ v& }1 ]
early puberty and had stopped growing by age 14.
' c: \( a/ p$ S! T; k; c2 x: eThe father denied taking any other medication. The4 F; x  s2 ^$ B% _+ s! O' O
child’s mother was in good health. Her menarche
; u( y! Y( A- N- \8 cwas at 11 years of age, and her height was at 5 feet1 L# L9 Z8 Q; V# N7 ~% s+ n
5 inches. There was no other family history of pre-  q# D) h- }& O/ K" U6 z6 C
cocious sexual development in the first-degree rela-, a  `$ q0 I4 F
tives. There were no siblings.
8 c9 Q: R: d  N2 D5 X$ RPhysical Examination
. t" q4 g# O, N/ m# z5 R# dThe physical examination revealed a very active,
1 t1 I2 }% A% p1 i- z" o# b4 [) [5 yplayful, and healthy boy. The vital signs documented
) w# {: e, Z& P! p* n  ^( r& Sa blood pressure of 85/50 mm Hg, his length was
2 S! d6 r9 |! L8 j8 U90 cm (>97th percentile), and his weight was 14.4 kg
$ a  [' i3 O6 H  g+ d8 J  Z: |(also >97th percentile). The observed yearly growth. l" o* F% u1 R, F
velocity was 30 cm (12 inches). The examination of3 z- N+ a" w( m; C, ~
the neck revealed no thyroid enlargement.
9 F% ^& t0 G6 E5 J9 l: E3 GThe genitourinary examination was remarkable for5 H- J2 a1 c3 d' S
enlargement of the penis, with a stretched length of
# P9 F* w( K2 b2 c7 b& @0 D8 cm and a width of 2 cm. The glans penis was very well
/ b' O$ L2 l: T' y/ t3 Fdeveloped. The pubic hair was Tanner II, mostly around3 t% n' ~$ U& Z  }
540
* C  u9 m, A- l0 |2 N  J3 Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, K' z6 Q# Y  L. w4 {the base of the phallus and was dark and curled. The
$ \4 v. v2 z, [0 e: I% Dtesticular volume was prepubertal at 2 mL each.$ R+ p8 d9 I# U& q! t, w4 y; w
The skin was moist and smooth and somewhat0 b3 B$ ^6 ]& L
oily. No axillary hair was noted. There were no
  C4 A& i& p# Q# X; N4 y  Dabnormal skin pigmentations or café-au-lait spots.8 X1 {6 T4 H0 _1 \
Neurologic evaluation showed deep tendon reflex 2+. Z2 {9 W. u% M1 R
bilateral and symmetrical. There was no suggestion5 Q( D( L( s# B
of papilledema.
/ v+ F! q0 ]  JLaboratory Evaluation  _5 _" q! |! m3 _
The bone age was consistent with 28 months by
7 J! H5 y  S6 Pusing the standard of Greulich and Pyle at a chrono-) x3 b) b6 k! K: R8 G
logic age of 16 months (advanced).5 Chromosomal
, G0 n$ E4 z4 jkaryotype was 46XY. The thyroid function test
4 J4 q/ r5 c1 g# H7 }! ]) r  d1 z" ^showed a free T4 of 1.69 ng/dL, and thyroid stimu-
! a8 w) H7 ]6 z+ Zlating hormone level was 1.3 µIU/mL (both normal)./ x( O) \6 J! r+ m
The concentrations of serum electrolytes, blood
, z, H. N; f" \6 i! Purea nitrogen, creatinine, and calcium all were
: U1 e9 |" j% B  H8 o4 Jwithin normal range for his age. The concentration
$ Q$ [1 E# z/ v( h. D7 Wof serum 17-hydroxyprogesterone was 16 ng/dL
( O) y- A% _9 t/ p6 T+ x. ^' E# a  u(normal, 3 to 90 ng/dL), androstenedione was 20
; y) j6 ?) Z' I' y2 bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ I4 c) [: b" u( V: J% Y( N, dterone was 38 ng/dL (normal, 50 to 760 ng/dL),) T* X) \+ F% {. t6 ?! O
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ y- r$ Z9 [& x( `3 L- s( p49ng/dL), 11-desoxycortisol (specific compound S)5 f( j! `8 o2 i
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 o; y3 A7 b* Q( `tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) y- l. U6 Q' o, E
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, r& |$ Q  Z3 s9 S1 ]5 W7 ^; [and β-human chorionic gonadotropin was less than
  U( p# X' O+ G! ~+ u1 r6 d$ H5 mIU/mL (normal <5 mIU/mL). Serum follicular$ Q# r5 L7 x" P+ _
stimulating hormone and leuteinizing hormone
) S, p& Z. q8 [* a7 ^3 m! Q+ J$ _concentrations were less than 0.05 mIU/mL' J5 U. S# M- O9 K& Z1 x
(prepubertal).
/ ~) G- _, c6 ^, i, AThe parents were notified about the laboratory
: R5 A, J0 s' u4 N: f  a6 v) m2 Nresults and were informed that all of the tests were+ ~- c& M5 y$ i2 d# B: ?
normal except the testosterone level was high. The
' h7 C! Y* w& P  K( R# Jfollow-up visit was arranged within a few weeks to% {; ?6 L/ |; {4 q* M
obtain testicular and abdominal sonograms; how-+ P; F2 T; G3 E# ]7 D. f4 m
ever, the family did not return for 4 months.
$ D% d  }. w: b3 b" `& ^& R: u; UPhysical examination at this time revealed that the
4 d6 [" e3 G  @7 ]3 a) ~child had grown 2.5 cm in 4 months and had gained
, o7 s; q$ O8 |& g6 o, ^/ \2 kg of weight. Physical examination remained
" ~) X+ |) g* ?unchanged. Surprisingly, the pubic hair almost com-$ {# |9 R. N9 A9 Q3 z/ {
pletely disappeared except for a few vellous hairs at
+ F* q8 e" v# `8 C/ |% [1 A5 Y# Ethe base of the phallus. Testicular volume was still 2$ ^) D: E( }, G" p, G
mL, and the size of the penis remained unchanged.5 Z$ Z! g$ n6 p
The mother also said that the boy was no longer hav-) g1 q% N9 [* ~( \/ L/ f
ing frequent erections., x& u- Y) ~  I( o
Both parents were again questioned about use of
. }" g" d( E" H4 k( K3 Many ointment/creams that they may have applied to! s8 W. o" c- Z* [* y
the child’s skin. This time the father admitted the$ }6 N7 m( |+ o! s
Topical Testosterone Exposure / Bhowmick et al 541
6 Q- o+ K* U7 }5 \4 fuse of testosterone gel twice daily that he was apply-' [8 S" I% M- J. e9 ^. T
ing over his own shoulders, chest, and back area for
5 h2 e0 K! c: Z0 r& Y4 Fa year. The father also revealed he was embarrassed
0 W9 Y! A0 }5 M+ W+ Zto disclose that he was using a testosterone gel pre-
5 B  o2 F; K  Y! q, Rscribed by his family physician for decreased libido
6 e' x1 [/ L1 ?( {8 n3 {secondary to depression.
, o7 ], `7 }: R  h: U. k. O$ dThe child slept in the same bed with parents.' q5 z6 U0 L6 b6 x" G0 z. ^
The father would hug the baby and hold him on his  \: C1 D0 R0 y
chest for a considerable period of time, causing sig-
0 q2 ~% U0 T0 N  m) B$ Mnificant bare skin contact between baby and father.
5 o1 @' T( X. ]: `. OThe father also admitted that after the phone call,
! C9 ^) l" C2 b0 i' ^# E$ d3 m0 ?( h( Rwhen he learned the testosterone level in the baby- ?; p( b5 E, @4 @7 A
was high, he then read the product information
2 F/ `7 J3 d* `8 ?$ k0 s/ ]packet and concluded that it was most likely the rea-
* J: a. @% X" c8 _3 X# v& z0 cson for the child’s virilization. At that time, they0 e0 L. m  I" ~' o6 b) f5 b1 }
decided to put the baby in a separate bed, and the8 @; N' h- W0 _7 I7 G
father was not hugging him with bare skin and had) o. x- l/ [0 K7 h
been using protective clothing. A repeat testosterone4 A$ G: x. o" ?( b0 v& @
test was ordered, but the family did not go to the% r/ \! W; {( G; r; p3 g
laboratory to obtain the test.8 @. ]' N7 ~& O4 M6 I
Discussion
3 i8 d( M6 P0 x( y4 k  D" {Precocious puberty in boys is defined as secondary
, P- X7 O. A: \' Y/ c1 Ksexual development before 9 years of age.1,49 e$ ~5 s" o9 M, L
Precocious puberty is termed as central (true) when" |" b& [& y* f
it is caused by the premature activation of hypo-
! {4 n" l4 [8 @4 j7 o4 |7 rthalamic pituitary gonadal axis. CPP is more com-" q/ P% O' A2 U% r( H1 u
mon in girls than in boys.1,3 Most boys with CPP
+ t9 r" A  K+ v" j" ]- D; c' U- ~may have a central nervous system lesion that is
4 J' }9 G7 N$ ]+ \# W1 y) O3 kresponsible for the early activation of the hypothal-
' }, g. E: j. V8 S# @" N# \amic pituitary gonadal axis.1-3 Thus, greater empha-
1 J1 ]4 X- r' o$ F, qsis has been given to neuroradiologic imaging in
/ c8 o4 t& n, }boys with precocious puberty. In addition to viril-
  h7 j" s) ^* I9 L" pization, the clinical hallmark of CPP is the symmet-
1 T9 _) D( ?( [% Brical testicular growth secondary to stimulation by
) T$ O3 ^9 U! ggonadotropins.1,3
! e+ U7 v# U% J4 G! uGonadotropin-independent peripheral preco-5 q4 X4 {6 E; n6 P! T$ d! _0 `
cious puberty in boys also results from inappropriate
2 c, `) H9 L/ |; A6 handrogenic stimulation from either endogenous or% ]( i+ u& U, X
exogenous sources, nonpituitary gonadotropin stim-4 V* e$ V8 ]% b$ o. O' h  V$ B
ulation, and rare activating mutations.3 Virilizing
- ~8 Q9 P! `6 o7 G# [" r6 m; u! hcongenital adrenal hyperplasia producing excessive
. l& f+ w- |  T' E/ ]8 nadrenal androgens is a common cause of precocious
8 n& ?# P" a5 C% ipuberty in boys.3,4
( \0 V, N4 g$ o- U2 k& x$ QThe most common form of congenital adrenal3 u2 j4 N# O5 R$ s% {1 ?0 u
hyperplasia is the 21-hydroxylase enzyme deficiency.$ K6 V2 ]/ }5 e" K& U. r
The 11-β hydroxylase deficiency may also result in% Z7 y; D% g2 j' i
excessive adrenal androgen production, and rarely,
  ]3 l+ V8 j. ~6 s/ Pan adrenal tumor may also cause adrenal androgen1 l5 L/ c8 x8 p" g4 T( X- {
excess.1,3$ U& M) o# h8 m! e% k  ^, a7 a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 ]7 g% q6 j, B: x  i% z0 \  V* i
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: {# |  [3 |- _
A unique entity of male-limited gonadotropin-! L6 B7 l3 F: B4 e- d
independent precocious puberty, which is also known  o( }( W3 A( p7 I& B( M  `  C
as testotoxicosis, may cause precocious puberty at a
( K/ U; q' X1 K6 }/ p5 Rvery young age. The physical findings in these boys
" i9 D+ d: O( \/ v" r7 k6 Awith this disorder are full pubertal development,
( }  V3 a3 f3 r; ]  Vincluding bilateral testicular growth, similar to boys6 z5 z7 T% D( b0 B0 a9 a: \: t: x
with CPP. The gonadotropin levels in this disorder
, q$ W5 Q; X1 V2 Bare suppressed to prepubertal levels and do not show& ~/ x4 U  N  @$ A2 w. ~
pubertal response of gonadotropin after gonadotropin-2 K; l# Q9 t! p% J% I
releasing hormone stimulation. This is a sex-linked1 y; x" A+ L0 e# Q8 u
autosomal dominant disorder that affects only
1 Z: N% A. v; i' X) Rmales; therefore, other male members of the family) m) U' ^7 x* |* ]1 q; V& n
may have similar precocious puberty.31 d+ b) h0 j5 I+ u
In our patient, physical examination was incon-
! e$ O' |. _6 S( p! l' g" r, _$ _- wsistent with true precocious puberty since his testi-
( x' [( B5 c3 I( t& f5 M5 ecles were prepubertal in size. However, testotoxicosis
2 x! o* q/ s/ Uwas in the differential diagnosis because his father' f4 b$ r9 Y$ ]# e: i1 g8 ?# ~7 `6 t
started puberty somewhat early, and occasionally,
; z+ V, J# N( Jtesticular enlargement is not that evident in the
% l/ s5 Q$ B. G9 U& ibeginning of this process.1 In the absence of a neg-
, m0 `8 K3 ]9 ?0 a/ p8 [ative initial history of androgen exposure, our
- A$ a  g! y. v) obiggest concern was virilizing adrenal hyperplasia,* s; z8 ?% A. ?8 E! _9 \
either 21-hydroxylase deficiency or 11-β hydroxylase8 a6 H$ \# H$ `3 ?/ p5 t: |
deficiency. Those diagnoses were excluded by find-
% v0 n1 i5 N! }. jing the normal level of adrenal steroids.
6 |# {  i/ v, u# k# hThe diagnosis of exogenous androgens was strongly
4 f2 p# I+ Q$ I5 f# tsuspected in a follow-up visit after 4 months because+ \4 r2 U6 z8 ]+ m: @. A4 @* U; F5 Y
the physical examination revealed the complete disap-
/ l8 B1 k+ N1 Qpearance of pubic hair, normal growth velocity, and& n+ v2 P! ?: C6 u0 u9 A9 \
decreased erections. The father admitted using a testos-
6 v" \1 a7 \; l& E' z" Y0 {. Xterone gel, which he concealed at first visit. He was
6 u' B/ {) w6 x$ \) Q+ e% Pusing it rather frequently, twice a day. The Physicians’
/ @5 ?: x8 P+ C3 O5 VDesk Reference, or package insert of this product, gel or
# ?: J; E, m& Qcream, cautions about dermal testosterone transfer to+ c$ s1 D, E' g* w
unprotected females through direct skin exposure.4 |( Q; B+ F/ Q  K
Serum testosterone level was found to be 2 times the
9 X% V5 _9 j* e0 \% ^0 G& ubaseline value in those females who were exposed to
3 f/ s# i/ i! i7 j8 r7 e1 Aeven 15 minutes of direct skin contact with their male
7 h% |# p; o& ^  Z4 r9 bpartners.6 However, when a shirt covered the applica-
3 q* d2 `7 T9 c' D4 y3 q/ Ation site, this testosterone transfer was prevented.
" T8 O+ x4 D; v( z0 fOur patient’s testosterone level was 60 ng/mL,
/ U" ]+ h+ V, b, l8 @. w9 Hwhich was clearly high. Some studies suggest that! [" r( N0 s4 O) _# t
dermal conversion of testosterone to dihydrotestos-
4 L/ ?! ?/ I" C. \# mterone, which is a more potent metabolite, is more
. C+ K, T* Y: p1 c; C3 Vactive in young children exposed to testosterone. [3 }+ X& \8 J7 V$ R
exogenously7; however, we did not measure a dihy-
% M# Y  D5 f  J! q6 l% odrotestosterone level in our patient. In addition to
2 [9 P! q! V' H; @9 k+ T, |; Rvirilization, exposure to exogenous testosterone in
7 C7 b! f. w- J( ^: H8 z5 A/ Fchildren results in an increase in growth velocity and
. W7 K% B" r$ ?' k) Z1 b' [advanced bone age, as seen in our patient.5 K" z1 i% j' K5 ], d. P
The long-term effect of androgen exposure during
( V' w/ r3 n4 S1 }) [9 `early childhood on pubertal development and final: }: C) b$ [6 n( J! L0 Q4 R4 c9 n$ d
adult height are not fully known and always remain; C3 C/ L& q3 z' r& Z& e+ A
a concern. Children treated with short-term testos-* S: ~% G; A1 q! X- M
terone injection or topical androgen may exhibit some
7 _3 F8 X7 Q$ d: ^( |acceleration of the skeletal maturation; however, after/ K9 ~1 ]: t7 H, }& e5 V
cessation of treatment, the rate of bone maturation
! Z  ~6 ^8 f: Z3 hdecelerates and gradually returns to normal.8,9" g; Q) f4 _2 n5 e* e- X9 o" ~6 T
There are conflicting reports and controversy
% s, E5 I0 F# o6 d3 iover the effect of early androgen exposure on adult3 y) t9 ^' G- P. \# X$ D: v: e8 q
penile length.10,11 Some reports suggest subnormal1 X+ D0 x0 `6 l; ^+ C" N; g9 S
adult penile length, apparently because of downreg-( a: S2 M" S  ]( H& k, T2 B
ulation of androgen receptor number.10,12 However,
/ d) `6 K! ~) i7 Z9 `$ J! TSutherland et al13 did not find a correlation between2 _  \5 G& B$ A9 F
childhood testosterone exposure and reduced adult6 e" v1 k: ~+ k( e  b$ v
penile length in clinical studies.
! \. _2 _& C# a3 iNonetheless, we do not believe our patient is
( E  u8 o+ |( j9 x; h' o8 S2 N" Kgoing to experience any of the untoward effects from
6 y) `" J0 B& qtestosterone exposure as mentioned earlier because
/ c+ O; O( R/ z2 H$ j, o. `the exposure was not for a prolonged period of time.
. \) n3 n; ~; rAlthough the bone age was advanced at the time of& L! Z  s2 d& K' F! E# A9 ~
diagnosis, the child had a normal growth velocity at
3 o9 b6 B' _1 gthe follow-up visit. It is hoped that his final adult
3 f& F" u5 `% G: ~( }; z$ mheight will not be affected.
1 d) i! ^( ^7 C" w# v4 ]Although rarely reported, the widespread avail-
- J4 O( U6 Z0 q3 B2 K& fability of androgen products in our society may6 M+ u; Q& `2 l8 V. Y' c3 A) \: H
indeed cause more virilization in male or female
+ L9 S& b* {" D1 c. rchildren than one would realize. Exposure to andro-+ D& J' E9 F! w. H- ?* ]. y
gen products must be considered and specific ques-# t2 c# O; H! y& K5 s! @, X0 I3 g
tioning about the use of a testosterone product or  [6 H: m# h( t! Z
gel should be asked of the family members during
1 A- O! t5 e, i/ E, R7 dthe evaluation of any children who present with vir-. U( r4 X+ B1 D, G
ilization or peripheral precocious puberty. The diag-# W/ m" Z" w; ~
nosis can be established by just a few tests and by1 L! O5 |. ]: \' P2 U+ F6 o
appropriate history. The inability to obtain such a( x% N" a9 U) ^. [0 o
history, or failure to ask the specific questions, may1 e; ?7 p  E5 @* r
result in extensive, unnecessary, and expensive4 a9 r* O( w" y
investigation. The primary care physician should be6 c8 k: D+ B/ N2 c' v
aware of this fact, because most of these children
! H' Y9 w) A; r0 Rmay initially present in their practice. The Physicians’% Q8 \# O. f9 A+ i" e$ T3 g
Desk Reference and package insert should also put a8 l8 E# l% C4 b; \. ?
warning about the virilizing effect on a male or
* e: i' Z) T+ \2 M6 Mfemale child who might come in contact with some-
% o" r0 ~: p. f/ hone using any of these products.: B4 V4 d. M) v6 b. T, _4 y- l
References: ~- o+ U( @4 y; X
1. Styne DM. The testes: disorder of sexual differentiation
0 A; }% |- ~. ^) t  jand puberty in the male. In: Sperling MA, ed. Pediatric3 _, f( P0 [+ v# F- R
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 o2 F) O/ E$ V' c) A" i5 G  ?
2002: 565-628.6 l( m/ ^( |2 x! l% C' _7 Y1 i) v- I
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 K3 p% w; Q" W% ?8 {2 U3 spuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
( r; L9 |" M) G3 l- g, Z/ r3 V1 i) SBoy Induced by Indirect Topical8 z( u. P# B, `: V6 ]
Exposure to Testosterone$ a5 f/ d! ]. v2 X
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' J/ D  D- |- c* M
and Kenneth R. Rettig, MD1
9 f# O4 }5 U; HClinical Pediatrics
3 N/ p$ c* X; R0 r* `% V3 wVolume 46 Number 6
9 j4 I! F4 v% ZJuly 2007 540-5435 S" x( k! u" @9 @8 q. ?
© 2007 Sage Publications9 z+ Z5 u9 X9 d7 Q: y2 V
10.1177/00099228062966510 u# G* R! F  b! H( w% M" D( J2 b
http://clp.sagepub.com3 ~0 I  _. c$ N
hosted at& K. @0 B! m# Z- u* ^6 \7 U
http://online.sagepub.com
8 @0 D7 Q8 n8 j) e0 ~, xPrecocious puberty in boys, central or peripheral,/ l2 A; Q+ V% {. ^' |
is a significant concern for physicians. Central
0 D! t8 t- T, B4 |- ^" t3 Jprecocious puberty (CPP), which is mediated) J2 \4 Q2 E) o9 j6 T, c6 l
through the hypothalamic pituitary gonadal axis, has
1 M& T! `) t/ k8 y% za higher incidence of organic central nervous system1 h4 m) ^9 C) l$ u2 e
lesions in boys.1,2 Virilization in boys, as manifested
7 d+ X! s1 ]$ z# g: |) _- ^- i1 U6 ^by enlargement of the penis, development of pubic" F$ r+ p. @" l: N- ]  \
hair, and facial acne without enlargement of testi-
- O, C: m9 I* b$ b  B5 F, v! `cles, suggests peripheral or pseudopuberty.1-3 We
/ x5 N$ g+ t6 |/ B: qreport a 16-month-old boy who presented with the
% N- F0 i1 d; v) g7 O6 K+ M2 Senlargement of the phallus and pubic hair develop-
4 [! `6 M' ^, k/ [5 V& P6 A8 q" K/ Yment without testicular enlargement, which was due
, E6 P  [1 q* g, Bto the unintentional exposure to androgen gel used by/ O7 ?9 D+ z4 N3 t: B; Y9 j& @0 j
the father. The family initially concealed this infor-
7 C2 g) C- O& |3 Mmation, resulting in an extensive work-up for this
1 S+ p: |/ g1 q( Q" j  L, t& F0 q4 Xchild. Given the widespread and easy availability of4 q% D. D# ^  b+ _: T/ e5 g! ]
testosterone gel and cream, we believe this is proba-) l8 z1 L' }0 P. n+ q7 {
bly more common than the rare case report in the
2 d0 g; A+ h* U2 d2 Kliterature.4
& o- [7 a- s* U' ^# g9 i2 U; w2 NPatient Report
$ ~3 b+ q( A% d" k6 OA 16-month-old white child was referred to the: f* N* d) c8 r) C6 J
endocrine clinic by his pediatrician with the concern
) o. b$ a3 M) j  G8 K$ l! @6 h# ?of early sexual development. His mother noticed
: Y8 H$ @9 p* D9 U. J2 c0 [light colored pubic hair development when he was: P- X: \6 |1 c( b* a: e
From the 1Division of Pediatric Endocrinology, 2University of
7 [8 ~8 c. n0 J3 D. ~South Alabama Medical Center, Mobile, Alabama.5 v1 Y& W0 F0 Z/ L
Address correspondence to: Samar K. Bhowmick, MD, FACE,8 k& o2 b' w5 {9 @: [
Professor of Pediatrics, University of South Alabama, College of
9 E+ T5 S2 L5 j2 p0 LMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( D; Q+ ^" w- g, t. _e-mail: [email protected].# w- ]' O# d% Y1 ^
about 6 to 7 months old, which progressively became
! S, |6 u2 _7 k: \/ vdarker. She was also concerned about the enlarge-% k5 F& F* L5 m$ _, N4 T% h
ment of his penis and frequent erections. The child$ O9 Z5 ?" a% v/ R
was the product of a full-term normal delivery, with
$ S4 F. R, V  @$ J) S7 c! F8 [9 @a birth weight of 7 lb 14 oz, and birth length of3 x' c7 r1 ]! t* n+ c
20 inches. He was breast-fed throughout the first year
# G6 a2 E; I* t$ M5 o' j- Jof life and was still receiving breast milk along with
# d& H3 H) R7 rsolid food. He had no hospitalizations or surgery,8 q% D: Y) ?0 z  L3 Y
and his psychosocial and psychomotor development
6 [! m- R: e) p2 a6 a2 J0 }. F8 `was age appropriate.5 e( Y7 q( v! d1 @& X  E: r
The family history was remarkable for the father,
' m/ @0 E; Y+ ewho was diagnosed with hypothyroidism at age 16,
  X0 t8 W5 J' i( t/ Y1 j8 Iwhich was treated with thyroxine. The father’s, {! P" {8 z, o& n. G) L+ g
height was 6 feet, and he went through a somewhat+ S" _( w% U* y* U$ U) T( k7 ^
early puberty and had stopped growing by age 14.: i+ g- n# j9 c2 d! {0 V$ n
The father denied taking any other medication. The- y. T0 g* ]7 ?9 q7 s1 Z
child’s mother was in good health. Her menarche
+ ~. \/ W# W; x3 Owas at 11 years of age, and her height was at 5 feet! N! H, P' e) N' F8 U$ e
5 inches. There was no other family history of pre-" \) c2 ?3 c6 U. P+ v+ s
cocious sexual development in the first-degree rela-
; p1 E! s6 B$ itives. There were no siblings.
" i9 f# ~) `/ ^7 q% V5 J+ P/ RPhysical Examination
0 V( z- [, L) K) T8 TThe physical examination revealed a very active,! l  M" {2 Y. m0 k* l, k1 _) Y
playful, and healthy boy. The vital signs documented% N% Y6 }' l) Q- g
a blood pressure of 85/50 mm Hg, his length was
. k9 o1 E; L" w+ o" i90 cm (>97th percentile), and his weight was 14.4 kg
9 w, k5 G# z  ?5 X% l: L& E- t(also >97th percentile). The observed yearly growth
8 e" M$ F9 y: Lvelocity was 30 cm (12 inches). The examination of! m1 d  B; B/ ?2 [( o5 i+ d$ m
the neck revealed no thyroid enlargement.7 R" x/ l5 b6 \: C5 R' O
The genitourinary examination was remarkable for
. U  X7 u+ F. @' ?enlargement of the penis, with a stretched length of
, s+ H/ K& O! M' s- R6 a* B  D8 cm and a width of 2 cm. The glans penis was very well# s: m2 q  o' T- j
developed. The pubic hair was Tanner II, mostly around
$ P2 B# |3 X9 i  x# l& r5405 \. W5 e, P3 t. ?! @0 w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 t. Z0 Z9 B5 u* k; Z2 fthe base of the phallus and was dark and curled. The
7 l: s9 }1 L" u# d; A) q/ jtesticular volume was prepubertal at 2 mL each.. L9 g' v, j" K8 \
The skin was moist and smooth and somewhat- Z  g, b5 s; R" H  \$ |6 ~' t
oily. No axillary hair was noted. There were no# y; P& O& c9 |2 x
abnormal skin pigmentations or café-au-lait spots.8 {) y6 J9 u! V2 N( G
Neurologic evaluation showed deep tendon reflex 2+- @% @3 ?$ U" K5 O0 o1 e2 \5 b
bilateral and symmetrical. There was no suggestion9 o* |* P$ }. `$ v
of papilledema.( x  _$ H; r& l
Laboratory Evaluation% H; x( z- a+ V  @- i: Z; H
The bone age was consistent with 28 months by
& j4 o7 ^) t/ q1 t8 Z/ i& h6 zusing the standard of Greulich and Pyle at a chrono-
- e2 e5 W% O- D# }4 Q. elogic age of 16 months (advanced).5 Chromosomal& M- |& Z# v4 \7 \
karyotype was 46XY. The thyroid function test
) d) e; a3 t2 s# k7 m" _showed a free T4 of 1.69 ng/dL, and thyroid stimu-2 s# b3 o* q" B9 r2 N* ?
lating hormone level was 1.3 µIU/mL (both normal).- U+ B/ G1 e5 v1 I& g4 Q/ `
The concentrations of serum electrolytes, blood
- S5 R3 \+ o& L+ b/ z# vurea nitrogen, creatinine, and calcium all were% H3 M+ S2 u+ g) ?2 U; C
within normal range for his age. The concentration
$ I& R. O8 A! l* gof serum 17-hydroxyprogesterone was 16 ng/dL1 y4 _/ z3 U0 o9 [6 l
(normal, 3 to 90 ng/dL), androstenedione was 20
1 ^  G! ]5 u9 x  H6 hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 ~; G' n) \7 j5 Q8 t& ?8 C5 {( _; \terone was 38 ng/dL (normal, 50 to 760 ng/dL),& I# i" K8 L& b; B- x; ^
desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 M; U$ K7 E: m
49ng/dL), 11-desoxycortisol (specific compound S)
: j# u, m7 z! R1 @0 Qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
( ~& ^9 a- ]* ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' @6 f) y6 \" A3 s2 S
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! M6 b" Y, Z3 N( Nand β-human chorionic gonadotropin was less than
" P) H+ V0 ~. K' n  k8 E5 mIU/mL (normal <5 mIU/mL). Serum follicular6 j8 \, U( O7 I2 Y! V
stimulating hormone and leuteinizing hormone. E; M- z7 D- \! @) M6 w
concentrations were less than 0.05 mIU/mL
8 m  d8 o- c/ a# ~% e: e(prepubertal).
2 o% l2 w+ A# @6 gThe parents were notified about the laboratory
# S/ V. F+ S9 T5 Zresults and were informed that all of the tests were
/ g3 A: u8 r" g- E9 c, a. Inormal except the testosterone level was high. The
6 n! @4 c6 i+ ?0 \follow-up visit was arranged within a few weeks to
$ |% U4 E. l7 ~6 fobtain testicular and abdominal sonograms; how-
9 c0 h, Z/ z9 x& Zever, the family did not return for 4 months.' A, _9 [9 l0 A' W5 _* P
Physical examination at this time revealed that the
8 E8 I8 x/ c- o4 {; O) F. Qchild had grown 2.5 cm in 4 months and had gained0 m: u% L  \0 O
2 kg of weight. Physical examination remained
3 V5 T5 z1 |; T0 R, Ounchanged. Surprisingly, the pubic hair almost com-
5 l, G6 {$ X3 r9 `" y5 Mpletely disappeared except for a few vellous hairs at
; N4 ]/ T7 c) T: B, |8 O! P. c) \the base of the phallus. Testicular volume was still 2
! M. L# x/ l1 ZmL, and the size of the penis remained unchanged.
, u( |2 F' Y/ s4 w6 yThe mother also said that the boy was no longer hav-
# R/ [8 v: H* m6 x* j* \- cing frequent erections.
9 E3 f9 M! r& x3 l6 eBoth parents were again questioned about use of
: p0 k7 T/ w$ S0 R( A" ?9 G+ Wany ointment/creams that they may have applied to
3 s! f6 `' h$ z( rthe child’s skin. This time the father admitted the
9 Z( l9 E0 m- |% `; t% u& }2 F  h9 x/ TTopical Testosterone Exposure / Bhowmick et al 5411 P. H: q3 K! _7 r) d
use of testosterone gel twice daily that he was apply-
* \; C; ]- `1 ^, j  \$ O1 D% ping over his own shoulders, chest, and back area for
; ^% C( {$ u8 T, m* A4 za year. The father also revealed he was embarrassed& z: x: J) j  Z6 {4 d, y
to disclose that he was using a testosterone gel pre-
3 z/ d# a% ?, s; Nscribed by his family physician for decreased libido1 E& [6 a; N( Y6 ]# g( n' D
secondary to depression.
3 H# M" G- p1 z0 YThe child slept in the same bed with parents.7 K/ l' C3 w$ E
The father would hug the baby and hold him on his& i! h& [; Z# f
chest for a considerable period of time, causing sig-4 C! u/ G/ w3 l( @4 {$ W& T, \
nificant bare skin contact between baby and father.& \7 X& Q6 I% A
The father also admitted that after the phone call,
0 h9 T7 ~# {; D: ]& t/ Qwhen he learned the testosterone level in the baby% g9 h7 H9 y4 Z1 A/ d, H1 T
was high, he then read the product information
3 W: V) k  m/ [: P3 upacket and concluded that it was most likely the rea-: Y7 D1 G- q- U9 Y4 j$ u- B) A
son for the child’s virilization. At that time, they
1 z( T' Z, T& C7 z# B. C3 bdecided to put the baby in a separate bed, and the- p# Q( |# B6 R. ?( Y
father was not hugging him with bare skin and had; ~  ^. V$ `- k* v
been using protective clothing. A repeat testosterone6 U$ e7 I% U+ K+ a$ l# Y1 y# t
test was ordered, but the family did not go to the9 E2 O7 y4 _( c  C: G0 C+ o
laboratory to obtain the test.
  ^# Q0 I9 T' I6 p2 o+ {; IDiscussion' c) d4 m& Z4 [* R7 Q  [4 L
Precocious puberty in boys is defined as secondary
& I0 ~4 }% b" |6 C2 qsexual development before 9 years of age.1,4* }! w( X' ~4 w5 i' w
Precocious puberty is termed as central (true) when# G- Y; i2 M- W! I5 v- x: E
it is caused by the premature activation of hypo-/ g0 j' {* t+ l- E3 ?
thalamic pituitary gonadal axis. CPP is more com-
/ {, k+ _5 z5 i# Smon in girls than in boys.1,3 Most boys with CPP5 v% T9 M3 `' y* r+ x$ [
may have a central nervous system lesion that is  c5 }5 e- F/ g' T* V) y# |
responsible for the early activation of the hypothal-( o5 ~( K1 T& N+ e
amic pituitary gonadal axis.1-3 Thus, greater empha-) ~6 ^2 u: U! r! D+ {6 D( ]6 a, X* P
sis has been given to neuroradiologic imaging in
5 ]& ^# o: J# {boys with precocious puberty. In addition to viril-6 F- c" u% X9 y  {# _
ization, the clinical hallmark of CPP is the symmet-" o3 U* x4 z' i/ @; k$ P4 [
rical testicular growth secondary to stimulation by# p" R7 L" R7 H; S+ [) ]2 R, `
gonadotropins.1,37 w8 U- n# Q* E0 G
Gonadotropin-independent peripheral preco-
' ^! J2 ]1 N1 F1 G; _; E; scious puberty in boys also results from inappropriate
  `& _: h% Q. I3 @1 Jandrogenic stimulation from either endogenous or
1 G. P2 ]6 G3 [1 B# Uexogenous sources, nonpituitary gonadotropin stim-8 y6 i, w+ Q( x: o; G7 Y
ulation, and rare activating mutations.3 Virilizing
; V. b5 {  Q8 l3 W; ocongenital adrenal hyperplasia producing excessive5 I7 I' e$ _9 I7 P
adrenal androgens is a common cause of precocious4 h7 G0 F. z+ I( A/ X6 h: X# x5 U1 ?, S
puberty in boys.3,4
& z# l  F% m  I* G7 N9 lThe most common form of congenital adrenal7 S3 K9 E; t  t8 b
hyperplasia is the 21-hydroxylase enzyme deficiency.
0 w8 n# S3 Z6 o# |The 11-β hydroxylase deficiency may also result in, e9 t$ X3 C6 O# W0 J1 f
excessive adrenal androgen production, and rarely,* q* w: r4 ^( e
an adrenal tumor may also cause adrenal androgen, j! a' q; }. m+ M+ q0 F3 z
excess.1,3$ T. {1 u9 J8 C  u4 k7 x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; W' R3 P! y5 S) T542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* D( j, R) Y: T2 {0 x% c- a( X4 f
A unique entity of male-limited gonadotropin-# m9 j9 Z! J$ x& e1 ?
independent precocious puberty, which is also known
2 [; k! [" B- S* z) _1 G3 O7 O  oas testotoxicosis, may cause precocious puberty at a) H  n7 m' T. F, X$ v8 n9 u3 N2 Q
very young age. The physical findings in these boys; q% |4 v2 Z- b1 t+ M! V( U1 s
with this disorder are full pubertal development,
7 _: i7 s+ i: O4 m' qincluding bilateral testicular growth, similar to boys
8 a# _" L' f& V4 I" gwith CPP. The gonadotropin levels in this disorder' Y1 B+ W% }% k$ i) k5 p
are suppressed to prepubertal levels and do not show
* Q% H/ K6 C, {9 Cpubertal response of gonadotropin after gonadotropin-
% p# o* m4 ?. i- B. preleasing hormone stimulation. This is a sex-linked
  a. o$ d5 N4 l0 Aautosomal dominant disorder that affects only5 ]) z" H. q1 R6 h+ Z
males; therefore, other male members of the family
) m. h' D) X) Pmay have similar precocious puberty.3
' R0 m3 X: E( F  t/ p( e& D& w/ PIn our patient, physical examination was incon-
$ ~+ ]+ z, J5 H" Bsistent with true precocious puberty since his testi-
) d( ^6 Q. O( F1 y  Q. s* c2 fcles were prepubertal in size. However, testotoxicosis- g3 }  m& c- x5 J5 ~' W! ^
was in the differential diagnosis because his father
/ T! T% `3 V9 g0 @1 N4 nstarted puberty somewhat early, and occasionally,
' v/ }- F* ]5 R5 itesticular enlargement is not that evident in the  ^/ _- b5 g7 x5 O
beginning of this process.1 In the absence of a neg-* z, c( I9 {& u: Q% {, F- |" L3 d
ative initial history of androgen exposure, our
( f$ _$ |$ o* x  A, A" Nbiggest concern was virilizing adrenal hyperplasia,
, o; {% \  J# `+ L' i- geither 21-hydroxylase deficiency or 11-β hydroxylase6 R7 O9 }, ?: f4 _: ^, `
deficiency. Those diagnoses were excluded by find-& S0 W; o4 V: X1 c& t, w
ing the normal level of adrenal steroids.: ~" A' L1 i* L% Y9 b  F
The diagnosis of exogenous androgens was strongly" \: ^7 D8 p( E0 v+ D( ~0 x
suspected in a follow-up visit after 4 months because
. v/ a% t0 Y8 _1 O- I# {the physical examination revealed the complete disap-7 |' F  h* e  Y$ ^- a# g
pearance of pubic hair, normal growth velocity, and' x: Q% v1 q2 L, @4 Y) u7 N
decreased erections. The father admitted using a testos-% Z1 L! c0 d+ O7 i6 n+ u
terone gel, which he concealed at first visit. He was
. e/ Y: z) q0 I* Zusing it rather frequently, twice a day. The Physicians’  K( f7 q# V- O5 q8 T- I# a4 T
Desk Reference, or package insert of this product, gel or1 B8 u) Z. B7 r8 {
cream, cautions about dermal testosterone transfer to
( u6 ^/ x( L# ?9 U0 d# I3 ~unprotected females through direct skin exposure.
% i1 I6 q' d- tSerum testosterone level was found to be 2 times the
9 p) m) s: J2 dbaseline value in those females who were exposed to
5 d' A5 I% o- T! V. j$ _, qeven 15 minutes of direct skin contact with their male1 [% l9 t0 e- ~7 v( M( T, ]
partners.6 However, when a shirt covered the applica-
3 p0 d1 a2 ?9 P! c" @tion site, this testosterone transfer was prevented.  a+ O+ ]. }4 |$ L
Our patient’s testosterone level was 60 ng/mL,
5 O# B6 ~" e, }! r3 Gwhich was clearly high. Some studies suggest that( @) i1 @5 C& X. q/ F
dermal conversion of testosterone to dihydrotestos-/ g- t) z8 J6 k: m- D
terone, which is a more potent metabolite, is more8 T8 k! A- I9 u
active in young children exposed to testosterone
4 n7 `+ M: [8 ^exogenously7; however, we did not measure a dihy-
. i  j! Q2 P) f9 Bdrotestosterone level in our patient. In addition to
% m+ D$ _+ y, Z( q# Ivirilization, exposure to exogenous testosterone in
9 K" ]& L5 h9 V5 Vchildren results in an increase in growth velocity and
4 g" ~4 k& _: Q( [* C9 fadvanced bone age, as seen in our patient.
1 |5 t: R8 X% J/ x7 C. ]  tThe long-term effect of androgen exposure during* l3 c6 M* e# Q% M
early childhood on pubertal development and final2 `) }; |6 \( q* Q* ]/ I+ a2 Z
adult height are not fully known and always remain% R' X% a! k- Y$ e6 j
a concern. Children treated with short-term testos-
6 G7 c4 M9 w6 G: p5 P* O( l: fterone injection or topical androgen may exhibit some
/ t" F! e! C5 |* R  Z/ Eacceleration of the skeletal maturation; however, after, `# s! M2 h* P2 O  Q# f. f; j" R
cessation of treatment, the rate of bone maturation( {4 F4 ~& B3 |+ n
decelerates and gradually returns to normal.8,9
2 ?/ ]! h& [& d; @: MThere are conflicting reports and controversy1 Y. o( q+ q  Q' V& K5 I; c4 F& ~3 ^
over the effect of early androgen exposure on adult
8 k4 d+ f* \) {8 A1 g) `: i5 B3 ?# @penile length.10,11 Some reports suggest subnormal
0 Z6 y8 `) [  P* Fadult penile length, apparently because of downreg-1 a1 N0 I! r; X' N
ulation of androgen receptor number.10,12 However,
/ i7 `1 m# M6 a" q4 bSutherland et al13 did not find a correlation between
8 r2 O: H, S: o5 }' cchildhood testosterone exposure and reduced adult$ B  V, |( m" d( N# X
penile length in clinical studies., j* |8 d+ m1 E' f: ?( R. F
Nonetheless, we do not believe our patient is
8 u$ p9 k/ _' W& ]& _5 e* V; Y- y* `; ?going to experience any of the untoward effects from( @7 K) [0 B5 c) _
testosterone exposure as mentioned earlier because
8 Z0 [8 \, ]& R5 F" _2 s9 ithe exposure was not for a prolonged period of time.
1 ]8 H1 w  j5 Q- h, tAlthough the bone age was advanced at the time of: X' ]# n$ d, q
diagnosis, the child had a normal growth velocity at
- o: r. s) ]6 z0 gthe follow-up visit. It is hoped that his final adult' M4 V& O1 c8 T8 o, x5 b
height will not be affected.  a# J, n  ^' z
Although rarely reported, the widespread avail-
. e; r% L5 c1 \$ ?$ ^$ `ability of androgen products in our society may; s( `+ h8 P1 r% h
indeed cause more virilization in male or female
* T% u) P& m! g8 h# i/ Lchildren than one would realize. Exposure to andro-
) [3 J+ c( P( O5 X' @3 U( R9 |& Wgen products must be considered and specific ques-4 R3 h! W3 E3 w1 d
tioning about the use of a testosterone product or2 R3 Z) a5 Y0 q# t! E: ?
gel should be asked of the family members during
; k8 t. k# V$ [  W" M  |the evaluation of any children who present with vir-
8 \! W5 C$ Y5 Q8 V, _  oilization or peripheral precocious puberty. The diag-% w( |& M! x% b1 ^; c: q
nosis can be established by just a few tests and by
1 o! H: \& l8 i4 iappropriate history. The inability to obtain such a9 a0 ]6 Y+ e( E& n+ {
history, or failure to ask the specific questions, may# Z: J4 Q: v& B1 u. f1 Y) o
result in extensive, unnecessary, and expensive, V) E( A2 n% {5 \# ]4 ^! F
investigation. The primary care physician should be6 e( q1 _5 E" l* U$ n9 F5 A* j( `
aware of this fact, because most of these children: M. i0 Z0 v7 V0 X1 l0 c; l6 x
may initially present in their practice. The Physicians’6 L% h, |9 @& }! U. ?) g0 _- T0 G
Desk Reference and package insert should also put a$ e: k4 B* m6 d6 ~
warning about the virilizing effect on a male or: P1 {' p) T$ F6 \
female child who might come in contact with some-5 W: w0 c2 O1 `8 T/ T% `
one using any of these products.
' ]  J8 T3 w" k9 ~4 cReferences
4 o, h+ o: b/ J* R1. Styne DM. The testes: disorder of sexual differentiation& Y) X8 R3 T" D
and puberty in the male. In: Sperling MA, ed. Pediatric
" K7 [* Q7 L6 r$ }: q% O5 aEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- n* ]6 _, Q! C2002: 565-628.
) N6 Z$ }) Z8 C$ g2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 x. W; O1 ?6 `3 Epuberty in children with tumours of the suprasellar pineal
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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

  U5 f: V  l+ P4 T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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