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Sexual Precocity in a 16-Month-Old) D0 Z$ q6 M& Z
Boy Induced by Indirect Topical1 x, F$ a3 u( d0 c( r8 J% M
Exposure to Testosterone
8 @: v' \4 b- u! V# e  oSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
$ A( b8 b: G, p4 qand Kenneth R. Rettig, MD1' }. x" k& @5 o* U
Clinical Pediatrics
) K4 \3 w$ P( p3 g0 n1 DVolume 46 Number 69 T( g5 O: n9 L" n1 _
July 2007 540-543
# {5 i) g& F7 f) S; p$ T2 f© 2007 Sage Publications/ `' ?7 e+ Q8 g% _1 {
10.1177/00099228062966512 _6 M6 ^+ v% X6 O8 l3 x  y
http://clp.sagepub.com% L! Y1 ^# }4 K
hosted at+ _! b, l! a, Y: M0 t
http://online.sagepub.com! X0 h( p. P) I' K8 `! P
Precocious puberty in boys, central or peripheral,
0 g/ q) [# A# e  r" wis a significant concern for physicians. Central
! ^, J  H4 ]) E% u' P3 M% H6 p0 Kprecocious puberty (CPP), which is mediated5 J( ~' T* f$ m9 @3 o
through the hypothalamic pituitary gonadal axis, has( C" K. S! `; m1 }& z  n
a higher incidence of organic central nervous system) ]+ X: z. ]: s; Q/ s/ W! l( ]  }
lesions in boys.1,2 Virilization in boys, as manifested6 |; }5 V/ N. r, c# L. L. [
by enlargement of the penis, development of pubic' U# s) r3 @0 ]. e% e- @
hair, and facial acne without enlargement of testi-3 c* E- G/ d, K( Q
cles, suggests peripheral or pseudopuberty.1-3 We: y" O3 k, G+ [" r2 }& H
report a 16-month-old boy who presented with the% g4 V0 @2 J/ V$ G9 ~2 q
enlargement of the phallus and pubic hair develop-4 ~1 H4 F- X' {% `
ment without testicular enlargement, which was due
! f* Q0 I& J1 E: b, y" f5 Ito the unintentional exposure to androgen gel used by- P" A0 s8 m; [
the father. The family initially concealed this infor-* a: Y# t; ~* u4 y8 C8 i5 F" q
mation, resulting in an extensive work-up for this
( L# _: L9 s6 Z/ U0 Uchild. Given the widespread and easy availability of
1 a, _; D6 C1 ~+ g% w. Htestosterone gel and cream, we believe this is proba-+ ~% j1 g( K) d. Q
bly more common than the rare case report in the- l/ Y+ B* {6 p! M& c$ E0 B, \9 ~
literature.4
0 n& ^' F. Z' X: [Patient Report# b! F+ }5 R, U* s) f: p
A 16-month-old white child was referred to the: Z+ ?; V1 O: j% x  r  R/ Z5 h
endocrine clinic by his pediatrician with the concern0 J5 n' t  H' I
of early sexual development. His mother noticed2 k- k9 L5 G7 b0 l3 R6 L
light colored pubic hair development when he was. z8 `7 _- J; q6 t4 G
From the 1Division of Pediatric Endocrinology, 2University of( g0 i5 f, P' _
South Alabama Medical Center, Mobile, Alabama.! P& r: E/ A: c( x% A$ ^4 `+ ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,3 d9 I0 k6 x5 s2 J+ H* C- w
Professor of Pediatrics, University of South Alabama, College of5 q' ^, _- V3 M7 B/ d# x9 S' N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ a/ m: L- L5 z% Q! B
e-mail: [email protected].* @3 a! E& X6 H3 M1 q0 t/ ]
about 6 to 7 months old, which progressively became* P+ {& C) l: n  w( ]
darker. She was also concerned about the enlarge-
" |% K% l6 H/ t8 C5 @8 Bment of his penis and frequent erections. The child# a! d  N5 Q/ x5 j  c' B: f
was the product of a full-term normal delivery, with
# [+ E% L" [/ Y' Na birth weight of 7 lb 14 oz, and birth length of6 _/ \2 H) x. ?# w* A
20 inches. He was breast-fed throughout the first year
! M# D( k2 N/ s& `of life and was still receiving breast milk along with
6 R. q# [1 j' N: K6 l, qsolid food. He had no hospitalizations or surgery,+ I1 W, ?/ Y2 `6 o, f+ y
and his psychosocial and psychomotor development
! K! b( q: o1 K  k1 Gwas age appropriate./ Y: A/ m) E) ?# y+ V' u' \3 G
The family history was remarkable for the father,
8 p  D3 ?9 c$ _% r4 iwho was diagnosed with hypothyroidism at age 16,
/ @9 X6 N) P" u8 O0 B/ lwhich was treated with thyroxine. The father’s
+ M& @3 p$ j! E, Z. Qheight was 6 feet, and he went through a somewhat3 g* t) g0 J( K1 M1 W
early puberty and had stopped growing by age 14.
; l8 ~# R' L# B$ r  bThe father denied taking any other medication. The
0 e$ v$ _; Y- @child’s mother was in good health. Her menarche) R! Q9 V1 S3 C( a1 G" R
was at 11 years of age, and her height was at 5 feet  h, U& u6 t* I" O* z/ n
5 inches. There was no other family history of pre-/ L' i0 o9 q; e
cocious sexual development in the first-degree rela-
1 g" \$ r1 r3 n8 l( Dtives. There were no siblings.
) V1 `. `+ w; QPhysical Examination
$ h: y  f7 X+ x6 z2 u6 O! N, [The physical examination revealed a very active,
# ^; S' s5 _$ j+ uplayful, and healthy boy. The vital signs documented
1 w( c4 L  u4 M0 o" E9 Q  Va blood pressure of 85/50 mm Hg, his length was9 H6 X9 y7 ?7 \7 _) O# {
90 cm (>97th percentile), and his weight was 14.4 kg  A" O2 ^# d, h+ e" X# G
(also >97th percentile). The observed yearly growth" j: D& K4 W: M# u$ x: A1 ]
velocity was 30 cm (12 inches). The examination of2 L1 D. Y4 W5 q+ S( K, C
the neck revealed no thyroid enlargement.6 [. |. w- U7 ?- z. _! M' U
The genitourinary examination was remarkable for
! }% Q$ G3 m) e7 b  p8 }enlargement of the penis, with a stretched length of
) v/ T0 a2 g( L5 ]- [$ R8 cm and a width of 2 cm. The glans penis was very well
% a, t0 ?1 I' zdeveloped. The pubic hair was Tanner II, mostly around
' K% w' J/ p2 T& ~/ e540% I! y: J1 h" x: b( T0 K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; K! D8 s. V* j( r6 ethe base of the phallus and was dark and curled. The" H+ h! ^; k& y# v
testicular volume was prepubertal at 2 mL each.0 F+ B) Y2 c9 h$ `6 Y7 b; q7 @
The skin was moist and smooth and somewhat0 t9 }% X1 V  z$ C; m# q
oily. No axillary hair was noted. There were no/ U. H  m4 l) U
abnormal skin pigmentations or café-au-lait spots.# E& t3 P# z' M* H; H) w: {* o: m
Neurologic evaluation showed deep tendon reflex 2+' h! W# R& C4 l7 [( w, X. ?
bilateral and symmetrical. There was no suggestion
' N5 M& M0 e! B/ W9 G3 vof papilledema.
# r7 v/ {& {7 e. s8 C  oLaboratory Evaluation
$ ^7 \8 p: C& g, f3 n2 XThe bone age was consistent with 28 months by
; a7 i. r- @" w, L2 }& j0 ?0 b$ Ousing the standard of Greulich and Pyle at a chrono-
1 Q$ O3 E5 f5 k8 L# t: k9 plogic age of 16 months (advanced).5 Chromosomal& e- M$ Q1 e* E* v8 k) M, F1 [
karyotype was 46XY. The thyroid function test3 W3 _" S& L. n0 G+ X; w
showed a free T4 of 1.69 ng/dL, and thyroid stimu-% A+ n( R. y4 u: m* C* w
lating hormone level was 1.3 µIU/mL (both normal).
# J3 R8 Z# M; w; d, ~The concentrations of serum electrolytes, blood
: @  r' ]) q+ i4 O0 \urea nitrogen, creatinine, and calcium all were
9 q% K" ]6 V" }4 L$ \) J: i, \within normal range for his age. The concentration+ [5 |$ _: d  W1 ]
of serum 17-hydroxyprogesterone was 16 ng/dL5 ^2 z8 g; ^* {) w
(normal, 3 to 90 ng/dL), androstenedione was 205 h- T% E/ F, w" u  R
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# g* ?7 L) b0 \9 I3 B, Z) j! O
terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 X4 B3 ]* Q' H
desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 A. l: ?0 g9 v) n% }
49ng/dL), 11-desoxycortisol (specific compound S)
, k! T" W' N- W: w# j  dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' m3 j7 M2 G% v% z# @- Ftisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 J/ {* u2 q& d1 u
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),  j4 f  x+ d$ L6 q) @
and β-human chorionic gonadotropin was less than
7 Z9 E8 r4 a% B' W, B5 mIU/mL (normal <5 mIU/mL). Serum follicular
+ ]- A3 q. w& L. h  f5 z# D: p" Pstimulating hormone and leuteinizing hormone
( J, w) o9 e; O" z, y6 Aconcentrations were less than 0.05 mIU/mL* ^+ B% `& t  k) f; s7 F
(prepubertal).
1 @) I& \5 o( r) e8 s4 g/ MThe parents were notified about the laboratory- O; ?, e# ]9 E& F- \
results and were informed that all of the tests were
2 q& X. f* B% Z8 d( W4 G2 vnormal except the testosterone level was high. The2 g% S5 v9 f2 e" O( S3 }
follow-up visit was arranged within a few weeks to3 W% ~# p+ [. C4 e: o3 _- D* h8 o* j* d5 F
obtain testicular and abdominal sonograms; how-' T' E& g2 K2 E
ever, the family did not return for 4 months.: I' E. N. v& Z6 T8 W1 L
Physical examination at this time revealed that the& @# k0 q8 w/ a! D
child had grown 2.5 cm in 4 months and had gained
6 H" a- |8 W4 ^) [3 ?; e1 {3 ~2 kg of weight. Physical examination remained4 Q5 `$ q! Y0 M
unchanged. Surprisingly, the pubic hair almost com-
+ q) _- n' K/ R) `pletely disappeared except for a few vellous hairs at: E, F* a3 c4 ]% ?/ K- |# J8 T
the base of the phallus. Testicular volume was still 2
0 c3 A; e$ D& h6 ~; E" @mL, and the size of the penis remained unchanged.
1 X5 s) C5 O- vThe mother also said that the boy was no longer hav-
0 K# i1 @0 |$ `( Aing frequent erections.5 G0 Y' X3 |8 L/ {4 ?! G" Z3 c* X4 ]2 U
Both parents were again questioned about use of
' }3 a) E6 s6 v+ m+ v7 |3 ^6 f0 g5 Cany ointment/creams that they may have applied to2 F3 c1 E3 e/ y5 g5 }
the child’s skin. This time the father admitted the
* n* e- B8 e- p2 pTopical Testosterone Exposure / Bhowmick et al 541; |4 J. W. h& g5 A
use of testosterone gel twice daily that he was apply-
& \# F1 e( s- A# ]6 z( ]  Zing over his own shoulders, chest, and back area for
$ W8 h% |1 Q5 F6 q. _% aa year. The father also revealed he was embarrassed6 _* x& Q# d  R  d
to disclose that he was using a testosterone gel pre-
+ j$ A0 Y& F0 a3 s$ [+ M5 Mscribed by his family physician for decreased libido6 ]+ G3 f1 w2 u( r3 ~; q$ v( G/ W! j
secondary to depression.8 N* w0 |9 y- L2 Z$ y4 n& }" X! Z3 V
The child slept in the same bed with parents.
. A2 ?- ^' ?6 T& ]( `' i* FThe father would hug the baby and hold him on his/ y5 c: q- n& `! o# O; y
chest for a considerable period of time, causing sig-
" r0 T' d$ o$ C6 n4 h! i  mnificant bare skin contact between baby and father.
. L0 x; V* f5 KThe father also admitted that after the phone call,
! L; F- Q1 \& M7 r6 h  Vwhen he learned the testosterone level in the baby
: o9 f- q5 e/ l" i, ~. lwas high, he then read the product information: f) ~8 U" Y1 s
packet and concluded that it was most likely the rea-/ p) B0 W  E6 x/ c' }. N, c5 ~& }
son for the child’s virilization. At that time, they
2 Z0 ~( P& e2 {0 _3 B) f/ d# edecided to put the baby in a separate bed, and the' S5 H- g/ C" H, z
father was not hugging him with bare skin and had
9 g' f$ V5 a9 |( P' u: V+ s! Zbeen using protective clothing. A repeat testosterone
' r: Q( y7 U0 w' t( L$ stest was ordered, but the family did not go to the
9 Q* ?2 S/ D5 ilaboratory to obtain the test.
0 v  h, x# _/ N6 WDiscussion
& }9 [+ J8 d; O" x- ?# wPrecocious puberty in boys is defined as secondary1 h. f. \# X/ x, S* q
sexual development before 9 years of age.1,4
& J( J  c$ k) q7 S" b& q% MPrecocious puberty is termed as central (true) when- `. E3 D& q" z2 Q( O
it is caused by the premature activation of hypo-1 [1 ]7 m7 b: ]5 k8 u
thalamic pituitary gonadal axis. CPP is more com-; r" e4 r2 P; r' B& P- x2 m
mon in girls than in boys.1,3 Most boys with CPP
- h, L% `+ B' W! mmay have a central nervous system lesion that is' H+ y* V& Z# {5 t$ M) F1 ^2 B- D
responsible for the early activation of the hypothal-
* d$ A  {8 h4 M. }! y4 I0 Hamic pituitary gonadal axis.1-3 Thus, greater empha-
  V1 `/ ^2 z1 F5 }2 Fsis has been given to neuroradiologic imaging in5 p( v8 g9 f/ _. U5 B: b! R
boys with precocious puberty. In addition to viril-
# G) I1 {% w" i; z6 T3 Dization, the clinical hallmark of CPP is the symmet-
' l/ Q/ h0 H; a* k, _$ hrical testicular growth secondary to stimulation by* r5 T$ a) g( A( A) g8 b
gonadotropins.1,3
- L* Y4 s& g# S1 eGonadotropin-independent peripheral preco-# c6 V5 C6 g0 X# F6 s: Z6 Y
cious puberty in boys also results from inappropriate5 N, S- p' a8 `0 o6 b* C$ i1 N0 k
androgenic stimulation from either endogenous or
- D4 Q2 A/ t* @- [( m8 D; Aexogenous sources, nonpituitary gonadotropin stim-& X0 X# A0 P* f8 M; {
ulation, and rare activating mutations.3 Virilizing4 |2 u+ g1 B3 _  D/ I9 r
congenital adrenal hyperplasia producing excessive1 _9 G  L4 [4 z: G/ O( q% S& M
adrenal androgens is a common cause of precocious7 {4 I# U5 w( M, @1 H% q5 l
puberty in boys.3,4
8 U$ h) T: S9 P; J$ h  {The most common form of congenital adrenal
. j& m+ l# E; Q$ q# C* \hyperplasia is the 21-hydroxylase enzyme deficiency.) _6 O. |& [* {7 B) s* A' T
The 11-β hydroxylase deficiency may also result in
- e' A$ r' Q5 e) l1 w  Hexcessive adrenal androgen production, and rarely,
, K2 ^. s4 s) Wan adrenal tumor may also cause adrenal androgen; \' z' m9 I# V
excess.1,3) j. m7 D4 X% w+ U) J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' @6 ~3 p5 m. y; a542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. w/ i' |2 d  ^. b
A unique entity of male-limited gonadotropin-
6 t/ w+ {8 @  n; {4 }3 eindependent precocious puberty, which is also known
$ l/ }1 ]5 ], y' Pas testotoxicosis, may cause precocious puberty at a
3 x% }% N/ k+ X  u$ N% d9 M) Fvery young age. The physical findings in these boys3 w6 O# R, M% B0 j
with this disorder are full pubertal development,  m  v" g' Q( B% V  D  a
including bilateral testicular growth, similar to boys  [4 Q, ]3 O1 o) Q: Q/ Q
with CPP. The gonadotropin levels in this disorder' d( u7 a2 ?, K
are suppressed to prepubertal levels and do not show
4 V% r& ^  M) v7 j4 Tpubertal response of gonadotropin after gonadotropin-
- k) Y4 _7 k5 J! m0 x  areleasing hormone stimulation. This is a sex-linked
1 n9 o6 E( @* I1 h4 X1 yautosomal dominant disorder that affects only9 m8 u1 }/ U, L4 Y, z3 b# @
males; therefore, other male members of the family% x* [. n% `. C- F" J8 Y5 T0 w
may have similar precocious puberty.39 ]7 h1 |! b) U+ _" U
In our patient, physical examination was incon-. V7 q" Y3 {" ^( P
sistent with true precocious puberty since his testi-
; {* ^5 i- i1 T* I2 ]4 Bcles were prepubertal in size. However, testotoxicosis, ^; U) n! }1 A; E0 v
was in the differential diagnosis because his father% i2 w' E# U0 v( c0 ?+ {
started puberty somewhat early, and occasionally,
" o" C# I# e5 {: T, U7 stesticular enlargement is not that evident in the
1 N: F" @6 L2 w7 t3 lbeginning of this process.1 In the absence of a neg-
1 K6 h2 \& r  x! i8 M4 ]ative initial history of androgen exposure, our
9 |4 Z- x$ N4 u  \9 a0 k3 `, W# Rbiggest concern was virilizing adrenal hyperplasia,
: _! [, u! a5 meither 21-hydroxylase deficiency or 11-β hydroxylase2 l6 R; e4 V% a& G
deficiency. Those diagnoses were excluded by find-: q1 ^# A3 i; c* d6 G
ing the normal level of adrenal steroids.( j" Y9 a& m3 I6 m
The diagnosis of exogenous androgens was strongly' }/ V2 _+ |, h: A9 T
suspected in a follow-up visit after 4 months because4 z0 {& F3 Q+ w. B& P5 q
the physical examination revealed the complete disap-/ ^4 {9 y' ~) Z' E, J
pearance of pubic hair, normal growth velocity, and( z" F0 Y2 n' x) i% j& F) a" T5 q/ A6 h
decreased erections. The father admitted using a testos-
) I4 D& P% a' c+ Z3 r1 [terone gel, which he concealed at first visit. He was8 G  J+ i: |1 k. w5 R9 b3 g
using it rather frequently, twice a day. The Physicians’5 B3 [. f: V- @5 m
Desk Reference, or package insert of this product, gel or
2 @6 {# F* h; N; Y1 acream, cautions about dermal testosterone transfer to
* U+ }9 M4 ~1 N7 t; D- G6 kunprotected females through direct skin exposure.
' M- J' n! A  `4 K& \$ oSerum testosterone level was found to be 2 times the
! r4 c, Q6 n& N" C& ~9 m% P1 D, Lbaseline value in those females who were exposed to
  R  V' ?% G/ r6 K( t2 y; \) N- ~# leven 15 minutes of direct skin contact with their male+ c  H; _+ j0 g5 l0 F0 ?" a8 N
partners.6 However, when a shirt covered the applica-( ?1 L' W  q5 ]" _2 z7 j* H
tion site, this testosterone transfer was prevented.) f4 {- O* C" W8 W2 k
Our patient’s testosterone level was 60 ng/mL,4 F3 @4 v* [& x) O0 I
which was clearly high. Some studies suggest that& n% z  ^* X& a/ `8 i( w4 i
dermal conversion of testosterone to dihydrotestos-5 Z. N& j- i" i, V! ?
terone, which is a more potent metabolite, is more
' N; m/ r9 I: ~8 q' P  Cactive in young children exposed to testosterone
: `7 T' H0 a  O# bexogenously7; however, we did not measure a dihy-
1 `% h9 H$ V. }. O9 Y. Z) Y& zdrotestosterone level in our patient. In addition to2 i1 y3 H+ j5 d5 p# H
virilization, exposure to exogenous testosterone in
, m% s) O  z9 F6 jchildren results in an increase in growth velocity and
( T3 b- o. E# h5 J* M" ?advanced bone age, as seen in our patient.. y' c0 N; x6 ]
The long-term effect of androgen exposure during- x6 `$ b# j1 a' D1 p. d
early childhood on pubertal development and final
# J# H4 p; Z8 a& ~% E4 N  Uadult height are not fully known and always remain/ C4 b2 p: K* G
a concern. Children treated with short-term testos-
5 o! v# F0 {+ Y4 z5 q+ \1 E) {terone injection or topical androgen may exhibit some
/ E% G, R6 `- T, aacceleration of the skeletal maturation; however, after$ r" X; ^6 X* P
cessation of treatment, the rate of bone maturation* z, V% U: X+ k, o3 H$ ^
decelerates and gradually returns to normal.8,91 Q% I' C+ R+ Q
There are conflicting reports and controversy* z  l1 I, r4 |; o& S$ v
over the effect of early androgen exposure on adult
  G/ ~; e( m9 epenile length.10,11 Some reports suggest subnormal
0 U  K& O8 E) }' Z% ~& Xadult penile length, apparently because of downreg-
2 f; {6 D5 H8 _# b3 R" aulation of androgen receptor number.10,12 However,
4 O4 V* t% Q& {, S9 qSutherland et al13 did not find a correlation between
( h: j) `' H+ u1 B& p& w8 Schildhood testosterone exposure and reduced adult
9 `5 f# ^$ Y% L( v' k( o2 ]% D* x0 O2 npenile length in clinical studies.
7 e( ^( K* n8 E  hNonetheless, we do not believe our patient is" p1 k1 l6 R3 o) F
going to experience any of the untoward effects from
5 w7 W8 j% V2 c9 j' d6 ttestosterone exposure as mentioned earlier because( x0 r# ~" D# @
the exposure was not for a prolonged period of time.2 C; d: s# Q, g0 H& A) d
Although the bone age was advanced at the time of/ a4 k$ }" d4 d* f: N. @) g
diagnosis, the child had a normal growth velocity at
7 J! r5 N5 K6 a- g9 rthe follow-up visit. It is hoped that his final adult
% I! j. A0 l  kheight will not be affected.9 G. x$ c* @2 N# I3 h
Although rarely reported, the widespread avail-8 h8 A" f. I( W$ ~& A) m- b
ability of androgen products in our society may" {' o7 O- [6 V7 i9 d
indeed cause more virilization in male or female" m: O: m; E$ O
children than one would realize. Exposure to andro-+ [% g, D5 ~) f+ Z$ n( ^3 J$ J
gen products must be considered and specific ques-. Y- N1 \" x% Z/ E! X
tioning about the use of a testosterone product or$ D, [& E3 ~. H( h
gel should be asked of the family members during
% V! R5 n! t0 O- Mthe evaluation of any children who present with vir-0 ^- }7 K. K4 Q- d7 |
ilization or peripheral precocious puberty. The diag-: m- t* P4 d: R" Q* v2 t( R" c
nosis can be established by just a few tests and by9 R+ f5 N$ B, F" \2 G$ _
appropriate history. The inability to obtain such a
0 m# M7 q. F8 i2 G# }# [history, or failure to ask the specific questions, may! u! V8 {: i' d/ w0 g" j! ?
result in extensive, unnecessary, and expensive
4 a6 q# e, @7 [' b$ Hinvestigation. The primary care physician should be, l4 N) F' T7 j( D) W- d
aware of this fact, because most of these children6 V; }, Q2 E0 H& i9 `- Y0 V& i
may initially present in their practice. The Physicians’
; v7 x7 f7 E# X9 i3 r* @Desk Reference and package insert should also put a9 z# r  J% p' e0 D; f; h! x
warning about the virilizing effect on a male or
; l% p5 ?1 Y$ H2 E' ^6 B% Bfemale child who might come in contact with some-2 [4 ]- c6 f. ?7 E6 Z' S5 b
one using any of these products.
7 _" L  P6 `/ GReferences$ G  @8 r7 E. r: i5 L# I6 Z' n
1. Styne DM. The testes: disorder of sexual differentiation0 o- f, j4 L, H5 o% j
and puberty in the male. In: Sperling MA, ed. Pediatric: M/ I6 n: B( T1 I/ A' l. s1 \
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 b+ W6 h/ z' K3 q9 q* f, ]2002: 565-628." N/ \7 B( [* ]$ y4 G2 [  }
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; k4 b: G- v) N$ ~; J. D; _" P
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
: k. ^1 [8 j: w+ j) h7 gBoy Induced by Indirect Topical
3 D  M& _* Y# f; e4 Q/ {Exposure to Testosterone
5 V+ \# h) K* Z: R/ fSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( g) V; n7 I5 G- }( j# V1 Wand Kenneth R. Rettig, MD1
8 f3 h" z* f' m3 N5 b% N* E8 k3 p/ CClinical Pediatrics
% @& R. C$ C- K$ K& AVolume 46 Number 6
( U, B  [) m) ^$ E6 p' cJuly 2007 540-5433 s" p; C+ B0 t
© 2007 Sage Publications5 i$ w4 `/ s6 _5 {% o4 B3 d
10.1177/0009922806296651
$ j- L1 B7 R# D2 [http://clp.sagepub.com" w. p. c( ^$ O7 `  k& h$ s
hosted at
/ g8 A: W5 R% m1 s* Khttp://online.sagepub.com( z% r0 p6 E1 `
Precocious puberty in boys, central or peripheral,
2 p/ z  t+ k- D2 H, C% B! z% ]is a significant concern for physicians. Central
2 M! F! i7 Y% [) Q# A5 Eprecocious puberty (CPP), which is mediated
# P) S+ f2 }" x4 Y5 P9 pthrough the hypothalamic pituitary gonadal axis, has
5 w7 m0 P  k4 s; r6 O0 f6 I( Qa higher incidence of organic central nervous system
. [; V: o" @$ e: T8 L) Dlesions in boys.1,2 Virilization in boys, as manifested( z1 T8 X' H! d7 @1 Z
by enlargement of the penis, development of pubic) }' C. @+ \; |3 {
hair, and facial acne without enlargement of testi-
0 v7 x4 @1 v9 Z" wcles, suggests peripheral or pseudopuberty.1-3 We- u% y- o+ \: k4 ?3 [
report a 16-month-old boy who presented with the
9 n1 O* h- Z1 @! H8 Jenlargement of the phallus and pubic hair develop-# m% G. M" o8 s1 U6 Q$ L
ment without testicular enlargement, which was due
8 t' x0 C5 e1 yto the unintentional exposure to androgen gel used by
( r* r. W2 C4 Xthe father. The family initially concealed this infor-
- j& E3 G7 _" _6 C  Y% s" gmation, resulting in an extensive work-up for this
! t6 Q! y9 K' hchild. Given the widespread and easy availability of( j! K0 x+ q9 g
testosterone gel and cream, we believe this is proba-: x% t$ P4 g" g) d
bly more common than the rare case report in the
- v) b5 e, ~( f8 }! O, H) p" w6 Rliterature.4
4 d+ S2 ]7 @2 u6 s  A+ IPatient Report' U6 I7 Y6 |. @0 T2 T0 Q, D4 _' ]
A 16-month-old white child was referred to the
1 `" L7 v& `. N& Yendocrine clinic by his pediatrician with the concern
2 f. I3 p% }* H. L8 _7 m; q+ J$ M0 nof early sexual development. His mother noticed
! v. o" N5 {# Flight colored pubic hair development when he was3 ]' Q$ O5 v' P% ]4 Z( b( ~3 _! q
From the 1Division of Pediatric Endocrinology, 2University of" l) D( @9 q# M- }4 Y$ ?# Q- [
South Alabama Medical Center, Mobile, Alabama.* d! a8 k0 |. l1 e$ O
Address correspondence to: Samar K. Bhowmick, MD, FACE,% n* d( S& `$ r# ?8 k; g) @1 h9 C
Professor of Pediatrics, University of South Alabama, College of
" D2 Z* Q2 n3 j. s5 y( Z3 k2 UMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 S; D9 Y0 x6 [, |; r8 b& v) qe-mail: [email protected].
$ B# V2 ~+ B7 Q3 cabout 6 to 7 months old, which progressively became
5 z. R. Y# O. d( R, G* w) qdarker. She was also concerned about the enlarge-% Y* G  u  ~3 e5 y. X8 {4 ~. }1 |
ment of his penis and frequent erections. The child0 }7 d4 @1 {" L& ]3 A
was the product of a full-term normal delivery, with, {4 M, `, x' [8 g& G9 ^4 W
a birth weight of 7 lb 14 oz, and birth length of+ M, a0 X9 a. t! v0 X8 a  c+ `9 L/ n. T
20 inches. He was breast-fed throughout the first year& N+ K; G: ~8 |
of life and was still receiving breast milk along with! `1 O# q& B+ Q
solid food. He had no hospitalizations or surgery,( W0 F  N9 Q3 N+ g* A2 M
and his psychosocial and psychomotor development' b5 E, u/ y2 W  t6 j  h' k4 a
was age appropriate.( a% {' Q3 ^# B* F  R$ [3 V
The family history was remarkable for the father,
6 d8 Z( ]0 u# i" a) K0 ]who was diagnosed with hypothyroidism at age 16,
; f6 ^5 v8 d* xwhich was treated with thyroxine. The father’s: N3 o# L6 U4 Q& ]; r  g  |
height was 6 feet, and he went through a somewhat
9 r8 l+ ~/ E4 n1 V: }$ h4 xearly puberty and had stopped growing by age 14.
% [; ^% z+ o3 s4 ]6 g- n7 UThe father denied taking any other medication. The# y1 S  N7 i$ k' s
child’s mother was in good health. Her menarche% q/ }$ k7 Y- s
was at 11 years of age, and her height was at 5 feet
8 ?, F% k. @* Y+ \, ]) a5 inches. There was no other family history of pre-/ n$ s  Q7 [3 h- J3 e- u
cocious sexual development in the first-degree rela-
7 K( y* u) D  B5 T' x: ctives. There were no siblings.' k. u- T0 a# S
Physical Examination4 j; B4 W6 B; Q% v- b
The physical examination revealed a very active,. Q' O0 K* x% ?- Y7 k, l
playful, and healthy boy. The vital signs documented0 |3 H$ b3 K$ M2 x2 J
a blood pressure of 85/50 mm Hg, his length was
& V- f) J" Y! E' L: ~90 cm (>97th percentile), and his weight was 14.4 kg6 T4 a9 {/ O; d3 Y9 ^2 N
(also >97th percentile). The observed yearly growth
* Y  I) v8 [1 }; i! a$ _. Dvelocity was 30 cm (12 inches). The examination of$ }; l/ G6 \' {; ]
the neck revealed no thyroid enlargement.1 ?! Z0 S* N+ e* |: S, e( e& B( f( z
The genitourinary examination was remarkable for8 M3 x/ }. v, ]4 t
enlargement of the penis, with a stretched length of/ y- F& U8 U8 F: S. S
8 cm and a width of 2 cm. The glans penis was very well
7 S0 m6 ?8 h4 P! {developed. The pubic hair was Tanner II, mostly around" U% j, i8 U$ e- K( {& u
540
9 w! ?$ ~0 p3 `: o* b! h" S- lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 F0 [( a  B# l, b0 j
the base of the phallus and was dark and curled. The7 c' o# k6 j" F5 I; c; q# ^( J  u8 @. k
testicular volume was prepubertal at 2 mL each.% n5 Q4 |1 f. d$ z3 _. I/ d0 ?
The skin was moist and smooth and somewhat. k2 H# C' ^2 V- N5 F1 g
oily. No axillary hair was noted. There were no3 O* l" J+ i' o/ R
abnormal skin pigmentations or café-au-lait spots.
4 Y- t( S6 C$ ?. SNeurologic evaluation showed deep tendon reflex 2+
  @% H/ _( T* Gbilateral and symmetrical. There was no suggestion
- F8 x* n: N9 s( V- z7 H5 Iof papilledema.
+ C+ P, q5 S$ Q: h+ w/ H/ `Laboratory Evaluation2 p; J2 e1 \1 m  y3 j
The bone age was consistent with 28 months by
! m2 X, y. [6 W$ iusing the standard of Greulich and Pyle at a chrono-
. v! N9 j; ?+ j- r1 F2 e, N+ I" @; wlogic age of 16 months (advanced).5 Chromosomal
9 z' H  E3 O. _+ Z1 Z8 A7 a! ?karyotype was 46XY. The thyroid function test
9 U7 L1 m7 j8 Ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-
, z+ }5 _, D6 m% I/ }+ y& t. l3 ?$ Clating hormone level was 1.3 µIU/mL (both normal).
) U: E9 l3 n% v& n0 lThe concentrations of serum electrolytes, blood( W; Z! W, X% b/ q8 @# q) H
urea nitrogen, creatinine, and calcium all were
% Y6 _* y$ n9 \& u4 k& Ywithin normal range for his age. The concentration
. f- m. e1 D; Wof serum 17-hydroxyprogesterone was 16 ng/dL6 V9 K: r3 [# Y+ W+ _6 _
(normal, 3 to 90 ng/dL), androstenedione was 20
+ N* A7 C/ o$ png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ k( Y, p5 u2 T
terone was 38 ng/dL (normal, 50 to 760 ng/dL)," r' C5 e: g+ P
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 j: c* @& M( c% y4 C49ng/dL), 11-desoxycortisol (specific compound S)2 z5 L; B1 B- f5 W5 V
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% j+ a) x5 C. C5 [, g9 y4 j
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* m+ B" L  |7 w; P. Xtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),: {/ a( w( e: D& v. d
and β-human chorionic gonadotropin was less than
7 z8 K' d6 Q/ P/ x5 }# [5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 x1 c7 z4 \& x5 `( Bstimulating hormone and leuteinizing hormone
9 Q" N! g7 Z2 b: X% t8 a" `concentrations were less than 0.05 mIU/mL7 V  L3 g% U- ~
(prepubertal).6 u- ~/ M: ~$ q, D1 V% Z
The parents were notified about the laboratory
$ Y# `9 {5 |( A6 w* u# }( w( N( dresults and were informed that all of the tests were; X( R4 o' ~4 @! L. T) k# G: Q4 |
normal except the testosterone level was high. The
$ U& s9 n7 B; Z: f! U$ Dfollow-up visit was arranged within a few weeks to! \: Z( V2 J' i( e4 {6 [
obtain testicular and abdominal sonograms; how-
0 _% \' R( R/ q* U5 R: C3 p/ Hever, the family did not return for 4 months.! S7 V( U4 I$ D: \, d
Physical examination at this time revealed that the( L5 R) e/ B3 ]& e" b% s
child had grown 2.5 cm in 4 months and had gained- V2 J# O: K& }3 G- o8 ]/ ]
2 kg of weight. Physical examination remained
& Q6 D" |3 A( E' t4 O3 Dunchanged. Surprisingly, the pubic hair almost com-
+ ~: D. [- I; K  ]: ?pletely disappeared except for a few vellous hairs at" l/ G9 p0 W. F7 R& [
the base of the phallus. Testicular volume was still 22 ^5 [7 U, q) q. \1 v' b
mL, and the size of the penis remained unchanged.7 `9 m" i4 [: }  A
The mother also said that the boy was no longer hav-3 h/ M) V. F4 \8 m' z4 f
ing frequent erections.
) a3 t) v1 |( R' k  W3 ]# K* WBoth parents were again questioned about use of
8 g+ k' M0 B) `9 O7 `* j" h5 X1 |/ Gany ointment/creams that they may have applied to. H+ W7 u& `: \9 @
the child’s skin. This time the father admitted the* ^$ [4 s0 c3 n. h% Q
Topical Testosterone Exposure / Bhowmick et al 5419 L) @" v& H* O5 K9 w# J" x! I
use of testosterone gel twice daily that he was apply-
! F1 G. D4 x. S3 i3 }9 Cing over his own shoulders, chest, and back area for+ Z  V  m3 S+ R: D2 ^, C
a year. The father also revealed he was embarrassed
6 R& i9 \% k; _) [to disclose that he was using a testosterone gel pre-
5 ~  @: ]8 L6 s" l* g' l3 B) ]scribed by his family physician for decreased libido
% K  i* C, ^2 }& O; i3 X* R/ `7 p7 Psecondary to depression.
* b1 t7 g8 ]5 W0 h  A/ s' wThe child slept in the same bed with parents.9 C' r2 W/ x$ [& I9 d6 j
The father would hug the baby and hold him on his  v0 ^) q+ m! `6 Y. X* O$ p
chest for a considerable period of time, causing sig-- L3 o, E7 G+ q, ?9 Q5 [' a9 h# e
nificant bare skin contact between baby and father.
0 o% I& v7 `7 }/ o8 g: d. gThe father also admitted that after the phone call,
1 u! O. k4 ]1 c5 Y' {. lwhen he learned the testosterone level in the baby
0 c4 D0 O& d! U, v, U+ {  Lwas high, he then read the product information
. N5 O1 ]! B9 M) w8 @9 \: ~packet and concluded that it was most likely the rea-
' h* y' ^7 {" ^( I3 O+ nson for the child’s virilization. At that time, they
* L4 _% Z5 L; _& [0 V. Vdecided to put the baby in a separate bed, and the! X! Q" }  k0 ^' F; f# t1 o: N
father was not hugging him with bare skin and had$ P& B) p2 Z  Z' ]; s4 a3 z
been using protective clothing. A repeat testosterone
+ W" \; _( C/ L  u, y+ I5 Z$ mtest was ordered, but the family did not go to the7 y. d( D# W' B2 w4 K( O
laboratory to obtain the test.
& l3 |/ d+ }/ K9 N# {  m! a: CDiscussion
3 n5 Q8 e; P6 p& D' l: ~Precocious puberty in boys is defined as secondary
  N. w$ Q, E% m. ]- ~3 ?- L3 ]sexual development before 9 years of age.1,4
3 A# @5 ?* h/ |( J" s/ I. T6 jPrecocious puberty is termed as central (true) when! y: k6 r- {( i1 ^7 g7 e) y
it is caused by the premature activation of hypo-- r8 \; h9 W+ W
thalamic pituitary gonadal axis. CPP is more com-$ @/ I3 o3 |6 K5 P1 ?" s
mon in girls than in boys.1,3 Most boys with CPP6 n* `4 E" ?9 n6 c
may have a central nervous system lesion that is
9 k9 Z7 y! R4 H* i; h6 i& H9 ^! d* m; uresponsible for the early activation of the hypothal-. C( k0 h' @, e* O; e0 X
amic pituitary gonadal axis.1-3 Thus, greater empha-# [& ?, o9 m( R8 u$ l
sis has been given to neuroradiologic imaging in8 E* x2 d# v: H, z3 E
boys with precocious puberty. In addition to viril-
7 h$ t2 v4 I4 p# p* y1 }) R, Xization, the clinical hallmark of CPP is the symmet-+ ?3 E6 _7 h* e( ^, @# J2 v/ v* Y, K
rical testicular growth secondary to stimulation by6 l$ `, K. r3 W3 [
gonadotropins.1,3
" n: f5 l5 Q. T8 E6 kGonadotropin-independent peripheral preco-
' K' g" K! e" t% [4 T- f8 e0 p+ Tcious puberty in boys also results from inappropriate
1 K0 A+ y8 e, T& i* v: Y0 J' gandrogenic stimulation from either endogenous or7 \/ E0 z3 P9 R4 x, m
exogenous sources, nonpituitary gonadotropin stim-
) T" w1 j! X, R  ~. x5 eulation, and rare activating mutations.3 Virilizing
/ f. w6 |6 b! K+ B5 z: Acongenital adrenal hyperplasia producing excessive
) c% j+ q# Z+ {5 `" f4 Radrenal androgens is a common cause of precocious6 f" D% r+ m* B
puberty in boys.3,4& Z9 c, @+ {$ Q8 K" h3 K0 r
The most common form of congenital adrenal- h6 B& k$ j+ v  V4 q. ]5 y0 Z
hyperplasia is the 21-hydroxylase enzyme deficiency.: o2 y: h. ?" R1 k+ ^5 p
The 11-β hydroxylase deficiency may also result in
, e9 ^- o( n. L  Mexcessive adrenal androgen production, and rarely,
# s7 E8 _0 y4 ]3 X+ S% l$ ?; p  can adrenal tumor may also cause adrenal androgen2 N. L# [& P+ f0 Q! b4 m) o! l% c& Y; f
excess.1,3
0 l: A! x5 y% Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* r4 C7 r5 V! u# Y8 p542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
* ^& Q1 N! j% ]( mA unique entity of male-limited gonadotropin-7 S, \* j2 C; J: m: \
independent precocious puberty, which is also known* \8 P' h5 q6 B4 h9 g( R
as testotoxicosis, may cause precocious puberty at a8 o7 B  `$ d" J) ?) P: M
very young age. The physical findings in these boys. c  D7 ?6 d1 K# }5 Y( C
with this disorder are full pubertal development,4 Y4 r4 v$ d1 F+ [9 r) }- A
including bilateral testicular growth, similar to boys
/ S7 S8 w( M9 b6 d2 twith CPP. The gonadotropin levels in this disorder" E3 l4 H. j# S* V' N5 |( t1 g
are suppressed to prepubertal levels and do not show/ V: j* F; p6 e, Z5 M
pubertal response of gonadotropin after gonadotropin-6 I& l  w* n' E( m( F5 p9 I
releasing hormone stimulation. This is a sex-linked
* E1 A1 h) ]& Sautosomal dominant disorder that affects only' J- d& L* J8 C1 t% o' G% O1 a
males; therefore, other male members of the family
' Z' z) `0 F2 U1 P) t- `( N5 lmay have similar precocious puberty.3  C# |* I: S: h1 M2 b" E6 }
In our patient, physical examination was incon-3 D. Q' z+ n# C3 w- T+ Q* V/ T9 b( B
sistent with true precocious puberty since his testi-& U1 O) g  N; c$ V& _
cles were prepubertal in size. However, testotoxicosis
# M: r( I6 l2 @; V+ b" m" V* Zwas in the differential diagnosis because his father1 Q% ?5 l% r6 J( o: J, Y3 x- H  m
started puberty somewhat early, and occasionally,
: s% Q- u' c# b$ a- Ptesticular enlargement is not that evident in the  S) n5 W$ e8 o- s( S
beginning of this process.1 In the absence of a neg-, `5 y& Q3 i5 o+ ?3 G, O, X- |8 x# ^
ative initial history of androgen exposure, our! `: N0 H8 d; p* U. v1 n: h' I4 ^
biggest concern was virilizing adrenal hyperplasia,
( z2 A$ w  d7 B  J/ y. meither 21-hydroxylase deficiency or 11-β hydroxylase, _2 u8 Y7 Z( C) V
deficiency. Those diagnoses were excluded by find-/ i$ H0 L/ U7 k' ]. I5 H
ing the normal level of adrenal steroids.
' O8 l! d& f# O1 P9 UThe diagnosis of exogenous androgens was strongly' S3 T/ U4 r3 [" M0 d0 r, t' @
suspected in a follow-up visit after 4 months because. `( ]4 F* F$ H3 f$ b: {
the physical examination revealed the complete disap-
* E$ n1 ~2 R: L& [pearance of pubic hair, normal growth velocity, and
! ]6 I; T1 V. R5 \% cdecreased erections. The father admitted using a testos-9 O2 ?0 p5 U; K9 S3 ^
terone gel, which he concealed at first visit. He was
0 y/ _* K/ [% ^+ v. xusing it rather frequently, twice a day. The Physicians’
5 b/ O4 a5 j2 A" q, s$ A4 yDesk Reference, or package insert of this product, gel or
% f# b! T+ |/ a1 K% Ncream, cautions about dermal testosterone transfer to
% o( r% [8 v( q/ q* `unprotected females through direct skin exposure.
! `6 H% y* N: M5 M8 L- _, n! V- ESerum testosterone level was found to be 2 times the7 L* f2 X# _3 @' P& H' n4 _
baseline value in those females who were exposed to( a2 x( \/ c+ Y* D4 d5 f
even 15 minutes of direct skin contact with their male. [$ }: J. J1 l2 E5 b
partners.6 However, when a shirt covered the applica-
& h9 D) G' g, v9 H& [2 U1 Htion site, this testosterone transfer was prevented.3 V( a( ?8 u$ E0 S
Our patient’s testosterone level was 60 ng/mL,# L- V! J6 D$ V5 m
which was clearly high. Some studies suggest that
; q( [9 m& o+ S# ?) Q9 @$ L0 Jdermal conversion of testosterone to dihydrotestos-
, h$ e8 p" T5 M1 nterone, which is a more potent metabolite, is more0 i/ g' M) i, Q. b
active in young children exposed to testosterone! t* S6 N; |- e+ @, H  f
exogenously7; however, we did not measure a dihy-
! |$ g% w: t- l5 u' W$ N; pdrotestosterone level in our patient. In addition to0 L6 d3 V/ U4 N* E0 c4 C0 W5 b
virilization, exposure to exogenous testosterone in# d7 M7 ]: E" J5 Q
children results in an increase in growth velocity and
5 U& Q3 w3 M3 ^& F3 D2 i% ?: `advanced bone age, as seen in our patient.
) x2 p2 ~/ r# K# v" Z2 iThe long-term effect of androgen exposure during- j/ L; D5 N8 w
early childhood on pubertal development and final6 ]& ~/ U* e! Q; L
adult height are not fully known and always remain
3 M6 u8 ^& Y8 ?; j  za concern. Children treated with short-term testos-& w* d( H; Z* ^! _/ H) R* H) l' Z
terone injection or topical androgen may exhibit some
5 c- b& |4 [$ B  S) y6 B# racceleration of the skeletal maturation; however, after
, H7 z. D* Z' V" }cessation of treatment, the rate of bone maturation5 i/ r# t2 w6 _
decelerates and gradually returns to normal.8,9
  W% g7 i3 v" e. z9 cThere are conflicting reports and controversy1 Z. B* S$ d& i  [
over the effect of early androgen exposure on adult) w4 I- _8 r# C, K$ \/ i6 B) t
penile length.10,11 Some reports suggest subnormal
% v+ s9 T2 B% g. ?adult penile length, apparently because of downreg-9 w; u) R& e' C+ F
ulation of androgen receptor number.10,12 However,5 x  Y" _$ {- Q, u# c
Sutherland et al13 did not find a correlation between+ C2 D# _* }/ x  p$ N% @
childhood testosterone exposure and reduced adult' v! l3 s' I4 X# g' Q
penile length in clinical studies.
0 r$ ]9 F: P- _: \Nonetheless, we do not believe our patient is: G. y0 R  A1 P+ N; \* e8 _8 S, X2 H
going to experience any of the untoward effects from) k; |* f( o( g9 q
testosterone exposure as mentioned earlier because
. B3 {' r" q5 E& n* M4 \# U& \3 jthe exposure was not for a prolonged period of time.* M( N2 W8 H: T- i0 J
Although the bone age was advanced at the time of+ p5 t8 R/ ^: }  j0 A# K
diagnosis, the child had a normal growth velocity at9 d7 j0 |* R( r+ T. ?1 w
the follow-up visit. It is hoped that his final adult
8 J* V, ]) x/ s+ Uheight will not be affected.( B) W" [) [$ W  ^2 ^- f+ {2 C
Although rarely reported, the widespread avail-7 @2 u/ A9 d' `+ \$ S, U
ability of androgen products in our society may3 S: E7 f" {  e
indeed cause more virilization in male or female4 s. m5 `7 \3 w
children than one would realize. Exposure to andro-
3 M4 {9 @5 `. |8 @gen products must be considered and specific ques-
; T/ o" w% @) s% Y" [: n+ ktioning about the use of a testosterone product or+ a2 q8 t  E' E) I: ?1 B. N
gel should be asked of the family members during
: e0 P/ T3 g3 _9 n; Lthe evaluation of any children who present with vir-) s5 S; d& X  l6 M
ilization or peripheral precocious puberty. The diag-
3 Y! a" \% W) @/ J! i8 \nosis can be established by just a few tests and by3 I7 p2 j. F& t9 T% |9 A
appropriate history. The inability to obtain such a# }) ~& [! R/ U' ]
history, or failure to ask the specific questions, may2 f5 a' `- |# d/ g! v$ u' `$ f0 S- A
result in extensive, unnecessary, and expensive
. {1 i, c8 A$ K( l& w, ]: ?: m3 tinvestigation. The primary care physician should be
& I' D& e! J$ M* p# w: ]5 Vaware of this fact, because most of these children) s# A7 q, T) s; O3 q/ R5 [% N
may initially present in their practice. The Physicians’, z4 r6 {8 X3 K
Desk Reference and package insert should also put a
/ e% `7 N+ @' ~6 n& i1 lwarning about the virilizing effect on a male or
  d2 Y9 D1 ~  I/ m' Cfemale child who might come in contact with some-2 c* I! ]4 ~% D$ R4 M
one using any of these products.
! W, R4 q; a8 z3 z; J0 k' X- Q" u' TReferences
+ I  _" n; T; Y9 \2 A  P& n1. Styne DM. The testes: disorder of sexual differentiation
, Z. j( M3 D$ ]( _2 u8 T$ E! ]and puberty in the male. In: Sperling MA, ed. Pediatric
7 b* P5 ]0 F7 E* R/ k/ GEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;7 p4 h$ y1 \$ F" }/ w1 O' O" ~: G
2002: 565-628.+ M7 a4 u9 D. l4 p) E1 C
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& b; f! L1 [( E
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

% N( g# i$ C( m" c! V7 k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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