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Sexual Precocity in a 16-Month-Old
9 T. u& C, S: `( i( zBoy Induced by Indirect Topical/ G& H# D& ^7 j) o4 A: H# Y8 i
Exposure to Testosterone9 U+ v$ I/ X, p1 v0 ^9 {2 E2 N
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 Q6 v3 Z9 v6 G6 i8 ]: a
and Kenneth R. Rettig, MD1" ?" O1 n$ c! a. q% p6 ^2 x$ s6 q# T
Clinical Pediatrics
5 f5 J8 ?' d6 u: dVolume 46 Number 6& R+ N" A6 p. _
July 2007 540-543
: D% c; \/ v9 G# K# N) Y. O© 2007 Sage Publications
+ O7 c! c; A- p6 S10.1177/0009922806296651' |0 Z/ [; ^1 p
http://clp.sagepub.com) N0 S, q9 D/ ?! W
hosted at
. Y2 F$ y0 }9 _. \# N, x! Xhttp://online.sagepub.com
  F- R, u& M/ d7 U% U5 ]- r% V6 YPrecocious puberty in boys, central or peripheral,
5 [( F3 G, ~, m- nis a significant concern for physicians. Central- P9 r) `5 @6 s
precocious puberty (CPP), which is mediated6 F# }' C5 C* I- f
through the hypothalamic pituitary gonadal axis, has
6 H. d$ V8 }2 t# K9 E  La higher incidence of organic central nervous system/ k/ i0 f6 Z9 ]. m  A
lesions in boys.1,2 Virilization in boys, as manifested
5 I7 L+ W0 j  [& D) `' |* _by enlargement of the penis, development of pubic- V: v; U4 C2 ~- W) z: ~
hair, and facial acne without enlargement of testi-
. S: G/ k, G+ R0 g% ?( r' ?7 W! Gcles, suggests peripheral or pseudopuberty.1-3 We6 |  b( F9 M. o( I, O
report a 16-month-old boy who presented with the3 T9 g2 X) s: h: A
enlargement of the phallus and pubic hair develop-9 Q  D, \# h" j; ]
ment without testicular enlargement, which was due. r# m& k# n5 ?* f' H5 c9 f" q
to the unintentional exposure to androgen gel used by
% G7 j+ ]% n6 Athe father. The family initially concealed this infor-
! o7 \% I& Y/ Z  Mmation, resulting in an extensive work-up for this
# U2 T& g6 m6 G) S6 }child. Given the widespread and easy availability of. k+ c+ z2 {2 I# y5 a$ g. Q! s# O
testosterone gel and cream, we believe this is proba-
! _/ Y9 o# s. x8 x) Ibly more common than the rare case report in the* I( s- n  T& h/ b
literature.4; h0 A8 W% V& Y* q7 V4 ^+ c
Patient Report; z/ p: |' s) b  D% c) u( A
A 16-month-old white child was referred to the, Y& F; j- Q9 B2 L# t3 ?& v( k  Z
endocrine clinic by his pediatrician with the concern
6 q9 o% ^9 P* u  k$ |; [* u( oof early sexual development. His mother noticed$ Q1 V4 ~" s4 Q
light colored pubic hair development when he was6 z% k: J$ s1 j: r+ x
From the 1Division of Pediatric Endocrinology, 2University of
5 T0 Q$ J& ^1 n% O) mSouth Alabama Medical Center, Mobile, Alabama.) l9 u' W3 {+ t9 B" P
Address correspondence to: Samar K. Bhowmick, MD, FACE,& ^& E. l; d8 a$ z2 h& R+ ~
Professor of Pediatrics, University of South Alabama, College of' _! v5 @, g, y! X# N0 C7 a
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; e. {0 S' O  u/ @; P
e-mail: [email protected].
5 O- N: p0 ?3 H2 K0 y; y$ m6 qabout 6 to 7 months old, which progressively became
5 K& B( S' l1 ?( T2 |# `" Cdarker. She was also concerned about the enlarge-( ]. f  p% U/ Q
ment of his penis and frequent erections. The child. ]3 ~" T& ^! K5 F" h& p
was the product of a full-term normal delivery, with
( d# w$ j) j2 {& b* da birth weight of 7 lb 14 oz, and birth length of
* J) e$ a+ H& `, y20 inches. He was breast-fed throughout the first year
% p6 A8 U& u0 g1 i' w7 V. Mof life and was still receiving breast milk along with
, x! b$ N2 t, L8 s; ssolid food. He had no hospitalizations or surgery,
6 h( J% l; O, u0 o7 W6 M7 mand his psychosocial and psychomotor development; o) |# U8 K+ ?$ u; e
was age appropriate." U3 ]* s! \5 [; g; H
The family history was remarkable for the father,
* }( `. Q+ J; Y$ Z6 N/ p) mwho was diagnosed with hypothyroidism at age 16,# U4 `1 E# j9 ~1 a. n6 b" A/ P6 T2 e
which was treated with thyroxine. The father’s
2 F, F; \) s# \; [8 b9 y+ {% x# fheight was 6 feet, and he went through a somewhat
  i% v. c' k' p% i1 Fearly puberty and had stopped growing by age 14.& D* |5 m) H. v* D4 S8 ]( K* v
The father denied taking any other medication. The
6 l: f3 L7 d. W0 b4 y9 T/ B3 v4 m9 Bchild’s mother was in good health. Her menarche! B; C1 L9 h0 ?* {" V
was at 11 years of age, and her height was at 5 feet
3 \; {+ z' [8 ~6 V5 B7 C5 inches. There was no other family history of pre-) g$ \* q$ B* I4 [* E
cocious sexual development in the first-degree rela-8 U" a' h" `' s. A+ h1 I
tives. There were no siblings.% t! Z' K5 @% y8 K9 [$ D' y- N8 U5 r
Physical Examination9 v* F: ~- e# D9 b: g" C
The physical examination revealed a very active,7 y( O1 O; U- l  }$ e$ u
playful, and healthy boy. The vital signs documented
6 @( U+ X2 M& K6 Va blood pressure of 85/50 mm Hg, his length was
1 L5 K- J5 e% a4 t) O& m$ n  R" U90 cm (>97th percentile), and his weight was 14.4 kg
3 h) o5 I/ i& Y' g/ d: V(also >97th percentile). The observed yearly growth
3 S3 v8 Q/ v3 n4 r8 r# t% |velocity was 30 cm (12 inches). The examination of
. [6 w( X1 G5 z+ l8 Uthe neck revealed no thyroid enlargement.* O+ [8 J- e! {) q8 b+ _1 U
The genitourinary examination was remarkable for, U: ]) f& l7 K# O# p2 J8 m, B5 H
enlargement of the penis, with a stretched length of
$ D* D6 N1 y1 t7 U, q8 cm and a width of 2 cm. The glans penis was very well
" G  F% a& p  D6 c; i7 Vdeveloped. The pubic hair was Tanner II, mostly around) P- v0 q; A6 n% x
540
% G" y, ?" u9 D) C% m/ B( m$ kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! j. \2 k0 i1 |
the base of the phallus and was dark and curled. The
6 V- ]" R0 f) x' d3 x/ Ytesticular volume was prepubertal at 2 mL each.. M$ C' i; F0 J) k7 l3 l7 G2 ?
The skin was moist and smooth and somewhat% }4 z8 j: o/ y, Z) ]' a
oily. No axillary hair was noted. There were no
3 O0 `1 _; B& [: Babnormal skin pigmentations or café-au-lait spots.
) K; |- `% i; G* F6 v! C3 ]) bNeurologic evaluation showed deep tendon reflex 2+$ W  {" w4 y+ u+ y. f% J
bilateral and symmetrical. There was no suggestion
& H+ F$ L0 E1 ^  K) O4 yof papilledema./ I0 r/ ~* L1 U9 `5 \; i
Laboratory Evaluation( K, ~/ E0 v: y- ]! i
The bone age was consistent with 28 months by: n: I" r9 x5 M$ E% y
using the standard of Greulich and Pyle at a chrono-
+ W: y; s( |2 j; ~" d  E7 Tlogic age of 16 months (advanced).5 Chromosomal
0 P; X4 z$ i4 F! l/ Q0 ]% skaryotype was 46XY. The thyroid function test+ \# K* u) @* F% P
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
: A( X& s0 ^2 H- e# s: d. H  |. s% Plating hormone level was 1.3 µIU/mL (both normal).* w" F6 c6 v' H) ^
The concentrations of serum electrolytes, blood" E2 I3 X4 `" O, ^7 L' Y5 h
urea nitrogen, creatinine, and calcium all were
9 [( h8 f5 N1 y& o7 Ywithin normal range for his age. The concentration2 Z. h/ ^5 ~; {* P6 W1 w
of serum 17-hydroxyprogesterone was 16 ng/dL% y# E. }! d- {& r6 V+ b
(normal, 3 to 90 ng/dL), androstenedione was 20; N8 }5 V7 s* w% K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( J: M8 Y5 x$ o
terone was 38 ng/dL (normal, 50 to 760 ng/dL),$ s( }/ m. U  z9 o4 k+ d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
% U0 V7 x( H( A4 n7 Q4 ]49ng/dL), 11-desoxycortisol (specific compound S)0 V' d1 z/ g' x8 W% @5 X, s+ g% ^5 C
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) d$ q# h4 u$ k# s/ q; d9 J5 D
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ I2 Y4 f% n9 n4 @4 j
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 U2 I( Y; F+ ]4 K$ z
and β-human chorionic gonadotropin was less than0 M% l! e: g, c7 D
5 mIU/mL (normal <5 mIU/mL). Serum follicular
- _5 b8 \+ p. }( q2 g7 Kstimulating hormone and leuteinizing hormone7 Z  j* p' y5 k' m
concentrations were less than 0.05 mIU/mL; p. F" w+ N4 ^
(prepubertal).
* Z% h% Z: H- zThe parents were notified about the laboratory/ d4 q( j; r2 J# g& H
results and were informed that all of the tests were
; e, T# s1 Q; Onormal except the testosterone level was high. The2 `; t+ M9 b3 }0 w2 Y9 l! k5 r4 w8 Q/ Y, |
follow-up visit was arranged within a few weeks to
, P, ~0 D# z: G1 n7 s4 o) t# q7 U% bobtain testicular and abdominal sonograms; how-1 d4 t; z" r1 {* o$ W9 p2 b% O
ever, the family did not return for 4 months.
: _) ^/ {/ S1 ]$ }) i9 U5 Z  X, tPhysical examination at this time revealed that the
* z! ~4 L# n4 G1 O* echild had grown 2.5 cm in 4 months and had gained5 _: P$ M3 I+ P$ @
2 kg of weight. Physical examination remained9 A: j6 `) o! r' }( @
unchanged. Surprisingly, the pubic hair almost com-
1 H1 J" @7 [2 G* D; b, Gpletely disappeared except for a few vellous hairs at
4 M" G1 L* C6 I$ Ithe base of the phallus. Testicular volume was still 2
$ O9 K9 Z! |4 h$ ]& [" i; R) o% ]mL, and the size of the penis remained unchanged.# X4 b; Q$ F5 a, @7 ?1 f8 o
The mother also said that the boy was no longer hav-( o( P1 [/ u, ?" s% H
ing frequent erections.
  V6 o0 A1 g4 S+ GBoth parents were again questioned about use of
- y. c( |, s" ?4 g  Sany ointment/creams that they may have applied to
1 g6 I$ a- [$ |- f) _4 |the child’s skin. This time the father admitted the3 Z( `+ a. d! V% f) X" o
Topical Testosterone Exposure / Bhowmick et al 541
" t2 i6 e" G3 g8 t" N" ]use of testosterone gel twice daily that he was apply-
7 a4 Y1 z& {/ H% ]5 x3 Oing over his own shoulders, chest, and back area for
6 E7 k& P8 F, {" ^) Q8 c  g/ [a year. The father also revealed he was embarrassed
# v4 F) W) q7 ?8 Oto disclose that he was using a testosterone gel pre-% i2 f9 t  ]! P+ g: Q9 X. F8 y
scribed by his family physician for decreased libido
3 ~8 Y1 t0 n4 A/ E! a" O; Qsecondary to depression.& C3 O  b2 R8 d$ ]/ ^* C6 B
The child slept in the same bed with parents.
. z6 Q0 F" X7 d* @- rThe father would hug the baby and hold him on his; t4 \" F7 g- c0 }& ]9 V* L+ G* F
chest for a considerable period of time, causing sig-2 l: [: K5 E5 T# z' {) V
nificant bare skin contact between baby and father.  \% y! i' u: _% U0 B' B4 c
The father also admitted that after the phone call,
! }, ^2 L0 ~8 c" n4 V. V! W* zwhen he learned the testosterone level in the baby
0 G6 c% {8 Y# P. }( F" S. U# V+ c) ?0 pwas high, he then read the product information5 M: M6 X% Z6 _2 P) h
packet and concluded that it was most likely the rea-
* \0 _) R  L. R( F9 p/ v# u6 d2 pson for the child’s virilization. At that time, they
# a! L- ^, R2 A7 P1 o2 m+ l+ p  Jdecided to put the baby in a separate bed, and the
/ L7 M$ o/ o4 Afather was not hugging him with bare skin and had( ^# E! w+ N7 Z4 q% m8 r
been using protective clothing. A repeat testosterone
( z2 q& S2 L+ \$ F* o1 b6 q! Etest was ordered, but the family did not go to the( S) n3 x# Z: e0 M& Y4 y
laboratory to obtain the test.& W2 h& T" F- `
Discussion
7 R+ `) H6 O. }0 n7 t. |+ DPrecocious puberty in boys is defined as secondary
2 |' y1 x  z7 Qsexual development before 9 years of age.1,4
5 W* }# Q0 U( r/ XPrecocious puberty is termed as central (true) when
8 K7 G. N+ N% cit is caused by the premature activation of hypo-
. C9 T! _* E8 W$ T7 U. @thalamic pituitary gonadal axis. CPP is more com-
2 l9 O0 f- c% d. T- Nmon in girls than in boys.1,3 Most boys with CPP2 f; T0 m) p' G
may have a central nervous system lesion that is
) N% ~2 f5 q5 p! F6 C5 dresponsible for the early activation of the hypothal-0 G$ Z# s3 p) P
amic pituitary gonadal axis.1-3 Thus, greater empha-
. O7 h+ K# E- _9 E3 l4 A0 ~/ ^sis has been given to neuroradiologic imaging in
+ u! Q) \! G" g" F! q) hboys with precocious puberty. In addition to viril-2 V' b$ N# v% P5 L4 R
ization, the clinical hallmark of CPP is the symmet-. r) x+ q) U8 b& m
rical testicular growth secondary to stimulation by: h7 R3 n- e. n) T6 |
gonadotropins.1,36 H1 K+ s4 o% R: S8 D
Gonadotropin-independent peripheral preco-
( b4 ^! d4 _) D$ qcious puberty in boys also results from inappropriate
3 ]% y7 m( |3 o: ^. Pandrogenic stimulation from either endogenous or) U) J4 _$ P4 h2 @- v
exogenous sources, nonpituitary gonadotropin stim-
5 o  x' ]5 I' {3 H0 w" h2 ], `ulation, and rare activating mutations.3 Virilizing, q& ?- u2 L: d4 B, V+ X
congenital adrenal hyperplasia producing excessive
) u$ U7 \1 c4 r: j+ @: F' }/ tadrenal androgens is a common cause of precocious
: a' W- c, K. x% c: zpuberty in boys.3,44 T# c) |) o2 N! m9 ^2 r1 H" _
The most common form of congenital adrenal1 p* C; @! g) p9 l% o. ~- t
hyperplasia is the 21-hydroxylase enzyme deficiency.
8 K$ D; V- E- U5 {' h* YThe 11-β hydroxylase deficiency may also result in, }; [2 Y6 O! e' `: L
excessive adrenal androgen production, and rarely,/ Y; a  I( ?( }# Z
an adrenal tumor may also cause adrenal androgen1 e1 \' q2 k8 [' k8 ^
excess.1,31 D$ h& V( W7 A8 s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 U" a7 f: W/ w1 n% G542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' f# ]0 V3 Q$ m) w* RA unique entity of male-limited gonadotropin-# m+ b, e, x- _2 i0 v
independent precocious puberty, which is also known+ L# U6 J0 q! e2 R8 G9 L
as testotoxicosis, may cause precocious puberty at a; t7 B7 d) M* }8 j
very young age. The physical findings in these boys
7 e6 o0 i# Z* y3 Cwith this disorder are full pubertal development,
; _# e2 g) `" d. c5 k+ ^including bilateral testicular growth, similar to boys% J7 }5 D! N3 f
with CPP. The gonadotropin levels in this disorder$ H3 i( P0 I8 ^( Z; D6 k
are suppressed to prepubertal levels and do not show
7 W$ F7 m" ]. gpubertal response of gonadotropin after gonadotropin-
. v% b& d+ b1 s( R4 ^/ {- Ereleasing hormone stimulation. This is a sex-linked5 n3 A  V! y1 I2 H( y
autosomal dominant disorder that affects only
. I" j2 A/ x* Y, [" I2 nmales; therefore, other male members of the family9 {8 U4 t; D& H
may have similar precocious puberty.36 L4 f+ h/ ~" P% \
In our patient, physical examination was incon-0 r1 A: A* B* K4 q
sistent with true precocious puberty since his testi-- H+ D. ~2 |7 r3 z, q* B
cles were prepubertal in size. However, testotoxicosis- w! U, @6 U  k# V& L) F
was in the differential diagnosis because his father1 r* i/ n4 \/ S9 Y* q( ^
started puberty somewhat early, and occasionally,9 q7 \2 z2 Z# V7 I
testicular enlargement is not that evident in the
+ a% A0 j& X+ f, `beginning of this process.1 In the absence of a neg-$ s4 [8 r2 o' R- v, h
ative initial history of androgen exposure, our4 e  v  p4 I5 K1 f3 ]' q/ S
biggest concern was virilizing adrenal hyperplasia,
" G% b) a  T" c# F, ^either 21-hydroxylase deficiency or 11-β hydroxylase
- u: k4 f2 J+ H. p5 H; r* p/ `! ndeficiency. Those diagnoses were excluded by find-
# U( v* |; i) c( C; king the normal level of adrenal steroids.
: P6 e5 G( y1 L0 ~) N+ Y- C4 MThe diagnosis of exogenous androgens was strongly
. L3 b( G: y6 S* N4 F$ u" \& ]7 fsuspected in a follow-up visit after 4 months because% I: C$ F- {& Y2 e9 F" F3 [9 k0 F
the physical examination revealed the complete disap-5 y( a; f( F1 y
pearance of pubic hair, normal growth velocity, and; ~7 T% v* V7 }: J. r+ u: ]* _( H
decreased erections. The father admitted using a testos-% p0 Z1 {1 J! G) q% \& l1 i' H9 M
terone gel, which he concealed at first visit. He was
9 C6 W+ g0 u0 F; E/ L" g- _using it rather frequently, twice a day. The Physicians’
+ E) c/ ^8 ?' m0 ^Desk Reference, or package insert of this product, gel or
  k# N- e; K/ m6 }( W- d: Ocream, cautions about dermal testosterone transfer to: `7 U; Z, J/ g( @7 @  p2 Y
unprotected females through direct skin exposure.
  U5 z- u8 ?& s4 B+ vSerum testosterone level was found to be 2 times the
% w; [/ q8 f% z$ J1 J% i- l5 ^baseline value in those females who were exposed to
. T( J) V' {& \4 [# Leven 15 minutes of direct skin contact with their male) M, @' M. b0 Y8 a  r" B3 `) x
partners.6 However, when a shirt covered the applica-& B7 v: t/ L3 j5 L  M/ B
tion site, this testosterone transfer was prevented.6 I7 K. ]$ y% M  s+ Q2 v5 d
Our patient’s testosterone level was 60 ng/mL,
( G9 Y2 e  a* w& \) f: P5 e. |5 Ywhich was clearly high. Some studies suggest that
( u* p( W6 k) K- jdermal conversion of testosterone to dihydrotestos-
" q; U' M2 W+ k% P6 lterone, which is a more potent metabolite, is more
% K: t+ t1 A2 n2 C% B1 `active in young children exposed to testosterone1 B8 L  b1 E( G$ g# l4 D
exogenously7; however, we did not measure a dihy-
& P+ v2 b% q" n5 \7 `9 Udrotestosterone level in our patient. In addition to+ u# T/ }7 W) T5 q" u
virilization, exposure to exogenous testosterone in" ?/ ~' N7 S; v0 _+ @) N
children results in an increase in growth velocity and9 q) c/ \' R" C0 L! a) i
advanced bone age, as seen in our patient.2 V, y, w: a+ r) D% x
The long-term effect of androgen exposure during
6 P9 h% T' |. ~* o% {1 {early childhood on pubertal development and final
5 d2 W7 t) K" q1 e, W8 Zadult height are not fully known and always remain: q+ r& z. a- A/ S) k. N0 ?- S0 H
a concern. Children treated with short-term testos-
1 B- t) R9 |$ [; s& R5 yterone injection or topical androgen may exhibit some# m' o4 H1 i" e: L: A& n
acceleration of the skeletal maturation; however, after% V( P# h; z6 P/ i. [
cessation of treatment, the rate of bone maturation+ M! E6 V8 F  U' J
decelerates and gradually returns to normal.8,9
3 [. l, i# r% q" IThere are conflicting reports and controversy/ O  v+ L% R7 \( l( [
over the effect of early androgen exposure on adult% F% }) T3 h7 N2 N; k2 I4 U" n, N
penile length.10,11 Some reports suggest subnormal  s6 {) k. I: B. o3 t( b% |
adult penile length, apparently because of downreg-
, q& y& k' v( Y4 B3 a" Bulation of androgen receptor number.10,12 However,5 z7 g$ q& n, l$ \  j8 I
Sutherland et al13 did not find a correlation between- |+ |+ X3 J, O& |
childhood testosterone exposure and reduced adult" S% r$ }' F# K7 B0 X/ z4 _2 D
penile length in clinical studies.6 g: g# L  F# S6 G# m( g
Nonetheless, we do not believe our patient is
& ^3 S! q* k+ e* @( Ugoing to experience any of the untoward effects from
4 W( X6 I. k7 G8 m/ K# ~5 xtestosterone exposure as mentioned earlier because
5 `' e! L8 m2 o2 H" |# sthe exposure was not for a prolonged period of time.
: j8 g4 e8 i# z2 CAlthough the bone age was advanced at the time of
6 }0 y. U, W' p- k, udiagnosis, the child had a normal growth velocity at
( `' q* W; k5 g  N$ xthe follow-up visit. It is hoped that his final adult
4 ?2 z% Q2 ^$ b( }) J* Cheight will not be affected., T% Y' Z1 q$ x: `/ j  x) Q7 h4 s
Although rarely reported, the widespread avail-# v7 D! x! ^0 C4 u7 w
ability of androgen products in our society may
# x% E, @8 Y/ Z1 V( C" _9 `indeed cause more virilization in male or female
6 a$ w6 v$ Q5 X" j5 Xchildren than one would realize. Exposure to andro-
0 C: ^- S" z3 c% \! Xgen products must be considered and specific ques-* [, Y) O: u. q/ O9 k0 l7 ^
tioning about the use of a testosterone product or( f' ], n) _# E3 P! L) T5 X
gel should be asked of the family members during: _+ ]/ l% z6 M" n
the evaluation of any children who present with vir-- k- D8 ]5 H. `& k, S1 Z8 ^& R
ilization or peripheral precocious puberty. The diag-6 R) ^! L4 D: V. Z  p
nosis can be established by just a few tests and by  ?) i) m, `1 s! m& }
appropriate history. The inability to obtain such a! p4 Y/ U  h4 T2 D8 z* m% j
history, or failure to ask the specific questions, may3 Q# {  E1 Z$ }, h7 X. {9 m
result in extensive, unnecessary, and expensive/ E$ b* E. c, @) W* r* \; O, e
investigation. The primary care physician should be
+ |' x& [$ p* s: X% J  O6 \aware of this fact, because most of these children% w0 j# E0 c1 [2 x9 Z
may initially present in their practice. The Physicians’# F2 r. t) I8 S2 V" R- K
Desk Reference and package insert should also put a3 c9 d; f2 N9 H- X5 c  z
warning about the virilizing effect on a male or
1 E1 ?+ n8 O; e$ _$ W) Gfemale child who might come in contact with some-1 d- h8 k4 T/ _( L, K3 x. J! W. D! z8 \
one using any of these products.+ D2 z/ [: c- d  h  J
References7 _, I8 i7 N, y7 Z- C
1. Styne DM. The testes: disorder of sexual differentiation4 \3 h9 X8 G8 V4 x
and puberty in the male. In: Sperling MA, ed. Pediatric% F, q) `, p" S# r& ~
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;0 u) P4 W/ z; j: n, n
2002: 565-628." u/ q% U- z( P
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious5 P8 P$ W4 C' m; x( V' `
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
5 `6 L" N7 s6 U  MBoy Induced by Indirect Topical% S  e  d0 u- X
Exposure to Testosterone
0 ?- M1 X8 b( O2 e/ A( c) B- {Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2" ]( [$ z& l" }- `% n$ I' D
and Kenneth R. Rettig, MD1
6 w- Z. p7 a) ^# d" [, QClinical Pediatrics+ }. ?7 t& X, b- V
Volume 46 Number 6& G8 D9 ~7 A0 M* r( K
July 2007 540-5433 @! B/ n" T! ]5 W: e
© 2007 Sage Publications
) S+ k$ Y" t. q5 q- {10.1177/0009922806296651' [" J& o! ~: J- Z9 V4 J: X/ t
http://clp.sagepub.com' q% T, V- _' ?  k6 R! e
hosted at. B7 o: W% u, M! \5 S3 P
http://online.sagepub.com. B! E) p, t. Z. L; N) J
Precocious puberty in boys, central or peripheral,
. C) X9 y" w& R' `# j0 B" u% t) iis a significant concern for physicians. Central0 F3 x8 w( X9 ^  p" u1 S! O
precocious puberty (CPP), which is mediated; T# x* s- B  g% w* e: {& Q& c% p
through the hypothalamic pituitary gonadal axis, has6 n! }( v2 k5 j/ c
a higher incidence of organic central nervous system
3 l! l/ q( y: G# t9 wlesions in boys.1,2 Virilization in boys, as manifested  T3 d2 w. @  h1 l' K0 Z( o
by enlargement of the penis, development of pubic
9 N% J/ O1 i( I$ x& t6 L2 {. Qhair, and facial acne without enlargement of testi-
4 ^) f2 h9 }  h! @cles, suggests peripheral or pseudopuberty.1-3 We. A3 e( o, a# V0 f/ Q
report a 16-month-old boy who presented with the
8 G! t5 E. Z$ f  v' K0 D/ nenlargement of the phallus and pubic hair develop-* ?2 \5 }+ h7 C$ C7 H+ H' g
ment without testicular enlargement, which was due
* f7 Z, M6 W% a& Q4 Bto the unintentional exposure to androgen gel used by
& s- [- y$ Q% vthe father. The family initially concealed this infor-
  ?8 H9 q% Y8 I8 Q; t. ^mation, resulting in an extensive work-up for this- _$ R: V. y- t) z$ a. n( [) F: n
child. Given the widespread and easy availability of0 u. I: z$ m* I' U
testosterone gel and cream, we believe this is proba-
1 ]. k; a+ N! y% Wbly more common than the rare case report in the, s% v2 ?( O4 g- ?- ~
literature.4' }* ?. ~5 V# z2 P' c
Patient Report
0 x% E: K/ j! N+ u. pA 16-month-old white child was referred to the% W. T& V% Z" t% i1 q6 B
endocrine clinic by his pediatrician with the concern
. c: f' R. I  Tof early sexual development. His mother noticed  C# X) q& F4 ~+ c# G
light colored pubic hair development when he was1 Z0 Q/ C" B( \. b* O/ n: v
From the 1Division of Pediatric Endocrinology, 2University of# \5 i% x! ]; f; c( k
South Alabama Medical Center, Mobile, Alabama.
5 Y3 D8 {& N& S* v+ ~! k) g8 \' W5 JAddress correspondence to: Samar K. Bhowmick, MD, FACE,& a2 a7 G  f. f' W5 R/ v# k5 B
Professor of Pediatrics, University of South Alabama, College of% l' p1 Z+ X5 b! U5 p( y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ G  G" O3 v7 m5 e' A/ S" N' T: l
e-mail: [email protected].9 y- X: b' q3 i% S* w) S. r, p; A
about 6 to 7 months old, which progressively became
9 `, c# |: c1 h: g5 y! z' U: ^5 _darker. She was also concerned about the enlarge-
: u9 U3 Y; Y1 B! B' Dment of his penis and frequent erections. The child
' d0 m+ H/ ~3 P/ F$ vwas the product of a full-term normal delivery, with
2 w7 h* S% P# Ca birth weight of 7 lb 14 oz, and birth length of
& L2 y5 z# U6 V6 p20 inches. He was breast-fed throughout the first year
8 ~' N$ Z% i, X% Jof life and was still receiving breast milk along with- X! j7 `' v( U
solid food. He had no hospitalizations or surgery,/ f6 ?) O/ b: Y6 r
and his psychosocial and psychomotor development9 o1 A: X& v4 |
was age appropriate.
+ j- {9 q6 A4 H1 t- _# }& }& pThe family history was remarkable for the father,5 P1 v3 I' e9 U7 _  N9 [
who was diagnosed with hypothyroidism at age 16,- _$ Y! H9 g; r0 `
which was treated with thyroxine. The father’s
* b* j1 D8 H; w% [  yheight was 6 feet, and he went through a somewhat) d# ^! ^; k  c, g6 t$ W9 I7 W3 C
early puberty and had stopped growing by age 14.
' \. G+ P: D3 L" ~! h7 pThe father denied taking any other medication. The
0 Q% q% `+ `# f) e) D3 fchild’s mother was in good health. Her menarche: }8 j& U5 P+ m6 f5 s* Q, G# T
was at 11 years of age, and her height was at 5 feet
" |1 H  f6 K4 c8 A2 u5 inches. There was no other family history of pre-
. k2 W9 D3 X7 e. v# X; Xcocious sexual development in the first-degree rela-
  j1 O1 x: T* O3 I1 D. W/ qtives. There were no siblings.
+ p! _8 Q4 Q3 s7 _) a/ b) _) {7 nPhysical Examination
  k) Z. ^  y0 ]+ u4 d' Z0 pThe physical examination revealed a very active,+ A' a' c# }( F+ v% a% F: l
playful, and healthy boy. The vital signs documented: y/ Q9 y# g9 g( c; I; j
a blood pressure of 85/50 mm Hg, his length was
' D, D; T2 D8 }$ |9 r- I! R2 R  q' R90 cm (>97th percentile), and his weight was 14.4 kg
4 S6 ?+ l! R- [* ?1 X0 A(also >97th percentile). The observed yearly growth
4 I& ?+ L' a+ Q: f( M: x' Ovelocity was 30 cm (12 inches). The examination of7 p! H* P7 ?* V( G0 Q# p0 U
the neck revealed no thyroid enlargement.
% q! b; o# Y8 Z: uThe genitourinary examination was remarkable for
# W" z$ M; P5 S& b: Q# A; Benlargement of the penis, with a stretched length of
& X) {8 `9 e3 o1 u' A: K: H( Y! m8 cm and a width of 2 cm. The glans penis was very well
; F; q7 _! J0 p* W) @) bdeveloped. The pubic hair was Tanner II, mostly around
$ ^; j3 H; J+ ]) p) z$ A540
5 N0 t5 h. ~0 l& Y- oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 }4 z+ q9 f/ j: A; r' y% Y  F9 Y
the base of the phallus and was dark and curled. The
# I/ b# D( V5 [- e, [0 h) |7 U+ itesticular volume was prepubertal at 2 mL each.: n/ O6 |7 Q. D1 t  v' ?
The skin was moist and smooth and somewhat
8 D5 t8 D/ T) _# X' goily. No axillary hair was noted. There were no* I3 c. l- ^* I; X( M9 ~
abnormal skin pigmentations or café-au-lait spots.
  o( i' E: Y' J1 G/ a: m; C$ [Neurologic evaluation showed deep tendon reflex 2+* r" P6 ~$ E2 |# h" ]& k
bilateral and symmetrical. There was no suggestion
) h3 S( \  ^6 T9 `of papilledema.' Q+ V! ]1 l" C2 p! t8 m# q3 _3 K
Laboratory Evaluation
, y" @+ `% U, G+ K% Y. QThe bone age was consistent with 28 months by4 P' ~! I$ B3 Q# I1 w
using the standard of Greulich and Pyle at a chrono-
7 f- x$ z- u) J( V) f+ H  Blogic age of 16 months (advanced).5 Chromosomal
: [0 f3 ^! Q3 I: w! \" Akaryotype was 46XY. The thyroid function test
, ?$ x4 f# B( i" m8 Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
: B' b& U  Y# I7 wlating hormone level was 1.3 µIU/mL (both normal).
# S9 r$ m& e: P" R0 p( ]The concentrations of serum electrolytes, blood
$ Q3 X* c9 W! [# i+ Z: }urea nitrogen, creatinine, and calcium all were! P( z8 p% y6 W
within normal range for his age. The concentration; P3 W+ _! D* V( R
of serum 17-hydroxyprogesterone was 16 ng/dL
4 z4 G2 t' i9 M) q% i(normal, 3 to 90 ng/dL), androstenedione was 20, c# Z, Q# `# ]) Y: b8 g
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
# s' C2 O6 t4 p$ T/ G& W$ |terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 j. i0 ?) {! P# w* e6 ?* m
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 `& m  S% P' D+ T+ X- {% d
49ng/dL), 11-desoxycortisol (specific compound S)# J5 y3 H( U' v) d6 h% ^
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; x7 `. {/ e0 [& i1 K  g1 }* u1 Mtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 ]8 J7 |* b+ ytestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  G# X) [- t% |and β-human chorionic gonadotropin was less than! s) V; ?* ^/ c( Y' m# R
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  L( b+ N% ?& w; z* z2 [stimulating hormone and leuteinizing hormone0 i/ [$ d& p2 e5 A7 V& n
concentrations were less than 0.05 mIU/mL
; A' g) C0 P" ?: d(prepubertal).+ L+ ?5 f# h- ]! h0 s- k
The parents were notified about the laboratory
+ y' u9 G) k% W7 f" t" b. H# gresults and were informed that all of the tests were
, i  V5 x7 T4 x4 `1 qnormal except the testosterone level was high. The
9 q9 H4 a& A" `0 ^follow-up visit was arranged within a few weeks to% {5 T" U1 E$ f0 q- T) y' G" h
obtain testicular and abdominal sonograms; how-
7 Z" j/ F4 k1 {+ `' ^" |7 lever, the family did not return for 4 months.
  T1 a1 K8 V6 l% L" T( Y! VPhysical examination at this time revealed that the- ^- [- F2 O7 f
child had grown 2.5 cm in 4 months and had gained
( g7 I  V) B' R( K& ]( m8 ]9 a" A2 kg of weight. Physical examination remained
! D) v$ |. P- }5 qunchanged. Surprisingly, the pubic hair almost com-+ H/ I# E; o# q9 @" y2 }4 @6 A) {5 O  k
pletely disappeared except for a few vellous hairs at
' f4 N" r3 Z6 ~5 b( B2 X* ?# _the base of the phallus. Testicular volume was still 2. t0 a+ ~6 H( {" x$ J
mL, and the size of the penis remained unchanged.: A0 K9 e; ?# t% C; w
The mother also said that the boy was no longer hav-
9 G& w9 [* |1 jing frequent erections.& k; d" [) f- r5 i
Both parents were again questioned about use of
8 g: a7 K5 q4 y7 A8 r* J/ Aany ointment/creams that they may have applied to) U- _- Q! [% k2 l& E. d; c8 w
the child’s skin. This time the father admitted the0 |) e# {' h9 c+ b8 Q* W
Topical Testosterone Exposure / Bhowmick et al 541  P9 [2 V; P/ o  z& J! B! I
use of testosterone gel twice daily that he was apply-
# n9 Z5 o1 F- @7 N. Z  ding over his own shoulders, chest, and back area for
" Z7 k, U9 t* Ja year. The father also revealed he was embarrassed7 I7 p7 d/ L% ?" E+ C2 Z
to disclose that he was using a testosterone gel pre-
. D+ |3 p- D2 k, H% W3 U/ O& `scribed by his family physician for decreased libido
1 f6 I5 b6 x0 J3 T+ D2 [. bsecondary to depression.: p! i  a$ y4 l/ w- e
The child slept in the same bed with parents.
; D5 f. i8 Y/ U, N9 n& zThe father would hug the baby and hold him on his
4 J/ c7 U0 L1 J# Z- J; S2 W- ~4 s" tchest for a considerable period of time, causing sig-( _+ _8 j+ K6 l9 g
nificant bare skin contact between baby and father.+ U* E- G& W0 z9 J( ?
The father also admitted that after the phone call,
9 e* F2 O: U! ?# j! }7 u. I4 Pwhen he learned the testosterone level in the baby$ D6 P; w  R4 |+ t% K. U
was high, he then read the product information
" s& O! Z$ h5 e& h5 B. [1 upacket and concluded that it was most likely the rea-
3 a) G/ z7 F- @son for the child’s virilization. At that time, they
- O, c! t: V# r0 b  w6 f: W* Jdecided to put the baby in a separate bed, and the
2 |1 f' ]; q+ tfather was not hugging him with bare skin and had$ i( s  W3 r, x; X
been using protective clothing. A repeat testosterone
; ^0 y* L; q3 |) ptest was ordered, but the family did not go to the! Y6 E( i. A$ H& k/ X3 ~( R
laboratory to obtain the test.
" {$ \+ M( X. L7 u9 f: O- p6 R) ZDiscussion
% V& K) G) @1 \; ]3 j0 P, G( y; l0 HPrecocious puberty in boys is defined as secondary& J) @! S+ k( l
sexual development before 9 years of age.1,4
' ?' _0 L( j# g& V+ N( NPrecocious puberty is termed as central (true) when
& D/ X5 d3 r' |it is caused by the premature activation of hypo-
3 r# a8 W2 f( b. L1 ?2 ]* m$ othalamic pituitary gonadal axis. CPP is more com-; F4 }  X& ?3 }- G2 l. D( L
mon in girls than in boys.1,3 Most boys with CPP
& x+ `3 S. D! J5 q: hmay have a central nervous system lesion that is
/ @4 z9 U. P1 G5 v3 P6 `responsible for the early activation of the hypothal-* u# n1 E& B) u0 y4 n
amic pituitary gonadal axis.1-3 Thus, greater empha-9 O9 m4 Y9 T9 i- H
sis has been given to neuroradiologic imaging in# `' W5 g5 K  r" D  z
boys with precocious puberty. In addition to viril-
5 v6 _* d% I5 x: hization, the clinical hallmark of CPP is the symmet-$ Z  ^6 i7 |& O6 v" W" Q3 \0 n
rical testicular growth secondary to stimulation by
1 T7 X/ A1 Y% C) \gonadotropins.1,3( R  X/ F; B) M
Gonadotropin-independent peripheral preco-3 R* s! \8 `" [
cious puberty in boys also results from inappropriate' ^" o, K8 {' S* x" b1 C& J
androgenic stimulation from either endogenous or
# {3 f% D" a- J  Fexogenous sources, nonpituitary gonadotropin stim-
& G7 [, R. m* R3 p) Qulation, and rare activating mutations.3 Virilizing9 k: c4 ]' g% b  ]: p4 F' \
congenital adrenal hyperplasia producing excessive
/ {9 @% n9 s' g+ O$ ^adrenal androgens is a common cause of precocious. |+ N6 s& ]3 P, w* N# q
puberty in boys.3,4
: c4 G" B" [9 j. D8 `0 gThe most common form of congenital adrenal) k* [$ k6 }( v4 {% z5 L6 R
hyperplasia is the 21-hydroxylase enzyme deficiency.
3 j/ F9 ?/ ?' {. o, }  B* iThe 11-β hydroxylase deficiency may also result in
: L! b) O* {* l) D% O% t* ^/ Oexcessive adrenal androgen production, and rarely,
! W) }7 a+ L" }9 d' \5 ]$ ^an adrenal tumor may also cause adrenal androgen( W4 c+ g, m& P! j* B7 \1 g
excess.1,3
( r& m/ }* Y3 _, {' Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 h8 Z7 t5 X, R: \  D! b
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# h" Z& S8 O: h. ^5 O% [/ Q, p
A unique entity of male-limited gonadotropin-, a! l- D) p  P# \! u: @% S6 _. d7 {
independent precocious puberty, which is also known
& d: ?, R8 C; }3 C7 V/ Vas testotoxicosis, may cause precocious puberty at a
% u! ~6 J9 q! t" b( P& wvery young age. The physical findings in these boys) P9 J+ H; `+ k
with this disorder are full pubertal development,. S6 x: p+ V# @1 K: r
including bilateral testicular growth, similar to boys
0 e$ r7 Z2 w2 K/ ~with CPP. The gonadotropin levels in this disorder
) `% ?+ L& {" J/ x( z3 Sare suppressed to prepubertal levels and do not show
4 f/ l$ T0 m) K" T  h/ y: \! Vpubertal response of gonadotropin after gonadotropin-
$ h/ [- _) y! @) ?, {: `  _& Ireleasing hormone stimulation. This is a sex-linked, ~- U) U: P" H$ T: \2 @# c
autosomal dominant disorder that affects only
, L/ v% c. E% N) a- R" ymales; therefore, other male members of the family- J) b' O( Z0 i& j
may have similar precocious puberty.3
5 B: T% [+ G7 z6 K( P- E- B  h. o0 BIn our patient, physical examination was incon-
: _0 N5 p* z: ~sistent with true precocious puberty since his testi-
/ j9 a* b. `2 |% Icles were prepubertal in size. However, testotoxicosis
8 P0 d8 b' Y3 D1 v4 ^2 H5 B, u& t6 Ewas in the differential diagnosis because his father
+ p- X4 x: O# t' B& Jstarted puberty somewhat early, and occasionally,
" r4 n6 d; ^; _9 ?1 [9 b* }testicular enlargement is not that evident in the
7 k2 w/ c* M1 z7 P9 `/ S6 W0 Ebeginning of this process.1 In the absence of a neg-' R) k: {% x: w, Z: [9 W$ k
ative initial history of androgen exposure, our
: b( ?1 G' m) V2 G! V- ibiggest concern was virilizing adrenal hyperplasia,
% r  O( |6 F) z+ N- n2 g8 l2 Ueither 21-hydroxylase deficiency or 11-β hydroxylase, j5 ^4 q' b$ V) l
deficiency. Those diagnoses were excluded by find-
8 V4 ^0 K- w. Eing the normal level of adrenal steroids.
( [. G3 _$ R! ZThe diagnosis of exogenous androgens was strongly( G' n6 n5 R6 t
suspected in a follow-up visit after 4 months because8 f  v( Z6 X# @
the physical examination revealed the complete disap-6 _: i% @7 _" m/ [8 X9 d" u8 O
pearance of pubic hair, normal growth velocity, and
# t: l: y3 J- m+ I- R. udecreased erections. The father admitted using a testos-; L) `! L# I/ N4 V
terone gel, which he concealed at first visit. He was5 n' y+ x/ j- i8 L! n) c
using it rather frequently, twice a day. The Physicians’: L  |- S, a$ Z0 f; _
Desk Reference, or package insert of this product, gel or1 K$ M6 N# D9 ?3 ~, n5 M/ k
cream, cautions about dermal testosterone transfer to
- y, ]( N6 }9 C% k! qunprotected females through direct skin exposure.8 a2 R8 g, Y, {( r
Serum testosterone level was found to be 2 times the
9 Q7 ?7 b/ d2 ]  ?5 X2 fbaseline value in those females who were exposed to% X2 {8 ~+ X% A7 E) @* d: V% ?) O% c
even 15 minutes of direct skin contact with their male$ x/ W2 x. L3 v9 c7 b& u8 ~
partners.6 However, when a shirt covered the applica-2 K  v, C3 Z5 x
tion site, this testosterone transfer was prevented.# p3 m1 e* ^' ~1 C4 W1 ?$ b/ S
Our patient’s testosterone level was 60 ng/mL,5 A7 e# r0 \: M" S
which was clearly high. Some studies suggest that
0 Z) _$ y) _! y; Y" wdermal conversion of testosterone to dihydrotestos-
5 f* X! S& k2 e9 G$ L2 F/ Zterone, which is a more potent metabolite, is more
6 G0 _4 k6 k" D, xactive in young children exposed to testosterone
0 k3 |: K2 r! H. z$ w- t9 E8 Lexogenously7; however, we did not measure a dihy-& r8 ^) i9 _7 K0 N; T  |2 _
drotestosterone level in our patient. In addition to! l! Z! e3 r8 x, W- E9 N
virilization, exposure to exogenous testosterone in! ~- p) z6 y# S3 \% i4 A
children results in an increase in growth velocity and' O) H) @' L' D
advanced bone age, as seen in our patient.
0 c4 p; L4 l; F0 H' M+ {* v/ G8 sThe long-term effect of androgen exposure during
8 f" M1 b' N' Qearly childhood on pubertal development and final/ P: g( U# ]- X
adult height are not fully known and always remain
8 F/ K) f/ _  ?* ^: Na concern. Children treated with short-term testos-. K3 G3 c8 ]* ^5 R$ J+ ^
terone injection or topical androgen may exhibit some7 r. l  U3 ~7 e# J* A
acceleration of the skeletal maturation; however, after- F! l" M0 x1 V$ I+ _+ N
cessation of treatment, the rate of bone maturation( I7 q. n9 i, k; l' t: u
decelerates and gradually returns to normal.8,9
8 d( A9 Y. n) w' j8 y( {' @There are conflicting reports and controversy& T4 o3 O  u' i: D( e8 e5 ]
over the effect of early androgen exposure on adult& [- s" M, \+ h/ [
penile length.10,11 Some reports suggest subnormal
+ v3 A! J8 P5 V1 c7 m5 Badult penile length, apparently because of downreg-
2 j( q, _7 p/ w+ j! v& Y9 O, julation of androgen receptor number.10,12 However,1 _- V. Z' a$ n8 d# L3 c& m, b
Sutherland et al13 did not find a correlation between+ I+ T1 q2 {* G4 R5 i* _  N1 v7 c
childhood testosterone exposure and reduced adult
5 u# C1 a  R9 t6 Y" {* Kpenile length in clinical studies.+ `# z* `, V. t) z6 ]1 @2 [: ?/ l
Nonetheless, we do not believe our patient is
5 X- Z. C7 }$ [- m4 x6 a5 G3 S' c) e4 mgoing to experience any of the untoward effects from
9 B+ r* ~6 W7 `! O+ Y' Otestosterone exposure as mentioned earlier because
' W% }' T) D) o$ xthe exposure was not for a prolonged period of time.  D/ E- ~8 `/ Z" ?9 e! [% v
Although the bone age was advanced at the time of
4 t, z  u: B  u5 v: ]diagnosis, the child had a normal growth velocity at
6 n0 @8 g" C0 j* @9 `  Zthe follow-up visit. It is hoped that his final adult4 Z' s' V- |1 c+ l- T- q
height will not be affected.
" o* P3 g% U7 O$ SAlthough rarely reported, the widespread avail-* \! Z2 r0 n7 o! W
ability of androgen products in our society may3 @# d+ r% c$ x
indeed cause more virilization in male or female( ~& O7 s6 P& K
children than one would realize. Exposure to andro-
, ?( Z1 J; `: r4 e! Fgen products must be considered and specific ques-$ s1 v. k* a2 V) Z4 x3 Q& M1 m6 h
tioning about the use of a testosterone product or
4 Q* J( ~$ O+ [+ J% i# R- agel should be asked of the family members during
- F" G- b; Q# m8 F( }the evaluation of any children who present with vir-
& I* a2 M& X4 _- R6 p- e6 \6 ?ilization or peripheral precocious puberty. The diag-
3 t/ j5 p" f# l) ]6 ]& gnosis can be established by just a few tests and by
4 @* t4 I( a- Q( x7 Happropriate history. The inability to obtain such a
4 s- Z: o3 l7 n7 V- N0 u" ]history, or failure to ask the specific questions, may
+ ~. Q  X) }! t4 iresult in extensive, unnecessary, and expensive' h7 W6 V' ^% B$ j% [, X
investigation. The primary care physician should be2 ?) M+ d' ~0 V1 a" m: p2 p
aware of this fact, because most of these children& R" G. M7 B4 L8 l/ K, t' s/ Z) g2 L
may initially present in their practice. The Physicians’
( x. P+ d; G3 t4 y$ y: J. ^3 SDesk Reference and package insert should also put a
- S, W  r) M* h% cwarning about the virilizing effect on a male or) `3 x- H) [& t$ e* }( f3 P
female child who might come in contact with some-
  x- {1 `# @& a5 R. _one using any of these products.
5 [- l' }+ k( MReferences# l/ [7 t7 R( M" S5 b4 Q5 M
1. Styne DM. The testes: disorder of sexual differentiation6 C/ Y/ M; P6 {% X- Q3 M
and puberty in the male. In: Sperling MA, ed. Pediatric
6 p2 w+ }; h% m1 I8 j1 A: G' HEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
# d* L' z0 O7 \2 g4 \. d. R2002: 565-628.* B6 x7 H+ |* Y  a0 K' q. x
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 w, ]( y8 N8 A- l6 upuberty 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

" @# _* ]. a2 H- z3 [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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