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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old2 p& b  j* f0 d- I- ~* p* z
Boy Induced by Indirect Topical
3 |! P0 F; K7 b! Y  S( g6 rExposure to Testosterone
) Y8 |* x4 g8 X1 Q2 `Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 R6 ~8 @9 k9 L1 H
and Kenneth R. Rettig, MD10 k! r$ f+ Y$ q2 D' B5 f; l" w1 i
Clinical Pediatrics
) L+ I: \) g- J& QVolume 46 Number 6  G' h# j% Q2 x1 ~: P
July 2007 540-5432 n9 ]8 l7 C4 n/ F7 c: J
© 2007 Sage Publications
; x% l% Z( V1 c# O9 F, P0 x  }. M10.1177/00099228062966515 b7 a* n* \6 ^! w: r+ m; j
http://clp.sagepub.com/ T6 x( S. z; Z' i, d8 S7 Y1 A
hosted at
- X  l4 L0 @+ V/ k  i- |+ G0 Khttp://online.sagepub.com
7 G/ C4 v: \  t$ {) d/ x4 SPrecocious puberty in boys, central or peripheral,8 r, n. ]/ R7 j1 Q* \6 l9 @
is a significant concern for physicians. Central
  l" _7 D5 n/ O3 l7 G& Zprecocious puberty (CPP), which is mediated. k+ s+ L+ j% d6 l
through the hypothalamic pituitary gonadal axis, has( @4 v; @- n4 A# }5 X4 p3 G
a higher incidence of organic central nervous system
* ?0 b, S" V+ R8 ]" d, dlesions in boys.1,2 Virilization in boys, as manifested) ?' ]' X! Z2 o6 I
by enlargement of the penis, development of pubic" @& [/ Q) w+ q! e. ?
hair, and facial acne without enlargement of testi-: o; y% v' p% h  k* @, ~, R. A. D
cles, suggests peripheral or pseudopuberty.1-3 We7 ^; g$ ]/ _6 s1 R$ S
report a 16-month-old boy who presented with the
" ]7 ^7 ?/ Q& S, ~8 \" {+ Fenlargement of the phallus and pubic hair develop-
) B* P- W2 ~/ ^$ i4 m& h% ~ment without testicular enlargement, which was due
/ l7 L; s2 [- |% u* V3 tto the unintentional exposure to androgen gel used by
3 C' g7 A" F  L5 i; K& Bthe father. The family initially concealed this infor-1 R- [  C: C' o/ x: J& M
mation, resulting in an extensive work-up for this7 p% c% r% W& K! B+ Z. b
child. Given the widespread and easy availability of
5 l: a5 V/ I% ?. stestosterone gel and cream, we believe this is proba-
' T5 I% B/ A/ \9 S2 Kbly more common than the rare case report in the4 h6 P  N) j) X$ a
literature.4) r9 I1 d* ^* `
Patient Report
! O& U% \) T+ I0 [( @9 DA 16-month-old white child was referred to the" P; R( h3 c8 |5 h2 Z- ]
endocrine clinic by his pediatrician with the concern7 n8 ]) G% }9 {4 V3 [) y
of early sexual development. His mother noticed7 s1 K! @2 [$ m+ N( G! ~! w
light colored pubic hair development when he was
) M& r) }6 D+ K; v4 D4 B! Y& IFrom the 1Division of Pediatric Endocrinology, 2University of/ r$ D) ]) f- P& v% H" @( B' S
South Alabama Medical Center, Mobile, Alabama.8 J% ~$ U5 O. O4 ?9 D: `
Address correspondence to: Samar K. Bhowmick, MD, FACE,
0 N8 V9 P9 H/ h5 lProfessor of Pediatrics, University of South Alabama, College of0 `* |4 Y% L1 }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 H. @, J7 ^" _( S
e-mail: [email protected].
# {$ G. N+ v. l& V! Y& Habout 6 to 7 months old, which progressively became0 u3 }3 C% U/ [
darker. She was also concerned about the enlarge-
4 q1 _* P: B. O& B, Cment of his penis and frequent erections. The child
4 Z% M- X' D( c$ xwas the product of a full-term normal delivery, with( B$ {/ Z9 i! {$ |5 E1 q
a birth weight of 7 lb 14 oz, and birth length of
# _* ?: {5 f1 a- r+ q20 inches. He was breast-fed throughout the first year; X2 V+ f* B+ E" v4 o. }4 z+ ~
of life and was still receiving breast milk along with
% N* N, T/ E  s) p' `- [: Hsolid food. He had no hospitalizations or surgery,
* U3 V% I% h# h& j9 [6 u9 Dand his psychosocial and psychomotor development
) [5 Q  l2 K7 l, o! z3 |! cwas age appropriate.. q% Q1 L" X" F( l7 r
The family history was remarkable for the father,- `1 e. E, c6 \0 f/ O  s
who was diagnosed with hypothyroidism at age 16,2 t( k) y( Y$ w# K9 w
which was treated with thyroxine. The father’s
2 e3 e2 r0 ]5 T: i3 ]' U( R) zheight was 6 feet, and he went through a somewhat
- Q( Q" z+ ~: K. cearly puberty and had stopped growing by age 14.
/ Z9 X9 X: K& Z  E0 s! T; f- \9 h" jThe father denied taking any other medication. The
( L! }9 a# x2 S1 |) E( [child’s mother was in good health. Her menarche3 ^2 }+ ?* w3 X# x: Y0 Q% O
was at 11 years of age, and her height was at 5 feet9 d4 o5 q. D9 \& p8 ]
5 inches. There was no other family history of pre-
, G( T/ c- u" B2 B5 D0 Jcocious sexual development in the first-degree rela-9 ?6 q0 B& q1 N; c# _) r
tives. There were no siblings.
8 a' l7 y" z9 E: p" |! j1 v% u4 fPhysical Examination6 v7 {: `& Q, S
The physical examination revealed a very active,8 _1 k- D' E6 g, e' F7 q, u: O
playful, and healthy boy. The vital signs documented
- v: R" n* K. o" @/ `" @7 v: G+ V+ Ia blood pressure of 85/50 mm Hg, his length was
$ z& V  |3 d* |) v& J5 E3 N1 Q1 M90 cm (>97th percentile), and his weight was 14.4 kg" O3 U% ^) w; x) h
(also >97th percentile). The observed yearly growth; q2 X# s  S- `3 l6 T
velocity was 30 cm (12 inches). The examination of
8 [5 _. y/ g3 y% [" _- kthe neck revealed no thyroid enlargement.1 f* v( W: G: I1 ^8 U  Y: u0 a% }) S
The genitourinary examination was remarkable for
: k% `7 T% m3 r* n! _/ ^8 wenlargement of the penis, with a stretched length of
5 q0 M' U! H& |$ W8 cm and a width of 2 cm. The glans penis was very well# @( g0 j7 ?* T6 K' ~
developed. The pubic hair was Tanner II, mostly around
$ D& l) f8 \( G% h9 Z540
% _0 ^7 W! a2 L7 V- `" A; d4 gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 y% D  S3 ?( L# g8 ~9 N: mthe base of the phallus and was dark and curled. The9 q$ f% ]; u# N
testicular volume was prepubertal at 2 mL each.
* T" K: z  j5 H" E) zThe skin was moist and smooth and somewhat+ I- x  x6 G9 U& y9 K
oily. No axillary hair was noted. There were no
  e2 m/ j; v$ E3 V) m) iabnormal skin pigmentations or café-au-lait spots.
% Y3 z* {, \0 h" wNeurologic evaluation showed deep tendon reflex 2+* B1 j, x, X9 Y) w  n
bilateral and symmetrical. There was no suggestion) a+ }3 c9 [2 M) |1 Q# K
of papilledema.- A6 d1 ~$ l& H5 t
Laboratory Evaluation
' S- V9 [' f" d( t3 lThe bone age was consistent with 28 months by. W; J' g0 N3 T( l
using the standard of Greulich and Pyle at a chrono-
9 o. b+ H9 G! b) m! a% m4 jlogic age of 16 months (advanced).5 Chromosomal
$ y* F; I. L5 D" Ikaryotype was 46XY. The thyroid function test9 C4 k- c1 q3 r, @: G: z
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
# d; O' B. E: e8 w" Q9 Ylating hormone level was 1.3 µIU/mL (both normal).% H& o) v1 ]" Z/ M' r
The concentrations of serum electrolytes, blood
  \  W- w1 x) H2 _8 L6 N+ Gurea nitrogen, creatinine, and calcium all were
. r/ ?* N" u- C* E8 S. Wwithin normal range for his age. The concentration
- p- }- \# I* Y) A: d" O7 U" D# N+ ]" wof serum 17-hydroxyprogesterone was 16 ng/dL
+ B; T$ b7 B6 m; w5 j9 O(normal, 3 to 90 ng/dL), androstenedione was 20
. e: D" f0 J# J' ?0 E2 h6 v; Sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: `+ m* A3 @" b- y
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* {' S7 [% Y% \$ `9 [% m. {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
; w2 {5 `" Z2 c7 U49ng/dL), 11-desoxycortisol (specific compound S)- V; d! r+ F" k1 Z& @
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-6 g0 o1 c5 l3 l
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
  F  m, [: k( z- ~3 J0 y' I/ W% [testosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 m5 H& i9 i6 a4 r( {" U7 P6 a9 Y
and β-human chorionic gonadotropin was less than
% y/ B# ^- C- P! @& l5 mIU/mL (normal <5 mIU/mL). Serum follicular
! K& T. \6 w5 e# Sstimulating hormone and leuteinizing hormone
2 w# v4 w8 g* {concentrations were less than 0.05 mIU/mL
; ?2 L: G7 \8 M- y; z(prepubertal).6 S" v2 r" I( ~) ]
The parents were notified about the laboratory
' b: E$ i" a1 _. f. n7 tresults and were informed that all of the tests were, b! \+ F( z/ t3 W7 |
normal except the testosterone level was high. The, T3 ]% Q3 Q8 g, |6 c( [2 i6 A
follow-up visit was arranged within a few weeks to) F( `! K' N6 _' z: a
obtain testicular and abdominal sonograms; how-
* `% C. {4 A' ~$ D. s* pever, the family did not return for 4 months.1 e( k0 R& D) _5 f* H
Physical examination at this time revealed that the" Y7 R6 x1 n; v1 H
child had grown 2.5 cm in 4 months and had gained
! N- o+ h( F% ]! ]5 u, P  S2 kg of weight. Physical examination remained
. O0 |" r1 C9 j6 ?unchanged. Surprisingly, the pubic hair almost com-
% k- F$ V4 U. b3 S1 Kpletely disappeared except for a few vellous hairs at& F5 F& Y2 P& c% h
the base of the phallus. Testicular volume was still 2
! q$ w! r1 ^% P' y$ b9 L/ LmL, and the size of the penis remained unchanged.
- P9 u2 V( q" i3 u2 @+ z; IThe mother also said that the boy was no longer hav-, x" n1 C9 |3 t& _, E
ing frequent erections.
5 U* `) J+ O$ \" `5 ?; F9 J8 p" QBoth parents were again questioned about use of: }0 ?* }* e7 [: z
any ointment/creams that they may have applied to4 q% n* V9 G- E3 X2 P" T( }. c) J
the child’s skin. This time the father admitted the& v* o+ T/ F# y& _+ r
Topical Testosterone Exposure / Bhowmick et al 541
& h) f* {+ y: F- Nuse of testosterone gel twice daily that he was apply-4 ^! p7 @6 L- ?6 z* V
ing over his own shoulders, chest, and back area for
  Z* M5 g+ I: C; z% ^  c' m8 m' z) ra year. The father also revealed he was embarrassed
1 q: ]5 Z% ^. C, Cto disclose that he was using a testosterone gel pre-
" W; b" t% Z. O) M- J* {* |scribed by his family physician for decreased libido: [% [7 j  U- ~0 }4 V& R0 P
secondary to depression.7 X9 E; q! h% u4 O! H
The child slept in the same bed with parents.
* J1 {- k1 C, F% lThe father would hug the baby and hold him on his& s# k( A' ]' P; O
chest for a considerable period of time, causing sig-
- e/ z* e; a1 n) L) _2 Rnificant bare skin contact between baby and father.
2 |  [2 M5 k" D: H% R$ YThe father also admitted that after the phone call,
' F' B, x) ]* uwhen he learned the testosterone level in the baby
& _; ?4 m" v& [$ bwas high, he then read the product information
2 P. s5 O# D! Spacket and concluded that it was most likely the rea-. B# N2 H5 j' r1 K9 m& m
son for the child’s virilization. At that time, they
2 y: z7 c; l. P0 }: ndecided to put the baby in a separate bed, and the
# ?7 U3 o0 }/ T7 M* |. k  ^1 ]father was not hugging him with bare skin and had  R! P% V+ C, G4 J  \
been using protective clothing. A repeat testosterone) l  d" W' f6 f8 t% }# o/ i- v& I
test was ordered, but the family did not go to the5 w" O$ V3 B/ s, y7 |5 Z
laboratory to obtain the test.
3 N& z1 O4 ?4 P; ]$ vDiscussion
5 F2 W2 y5 f# RPrecocious puberty in boys is defined as secondary( Y1 q. N" Q  O0 f9 B
sexual development before 9 years of age.1,4
% r3 ~' V# Q+ A- m* |# |; TPrecocious puberty is termed as central (true) when4 r4 i* l* X" x3 w
it is caused by the premature activation of hypo-, f7 ?: T5 u3 H$ j
thalamic pituitary gonadal axis. CPP is more com-# J2 j# q/ k) U5 K8 A
mon in girls than in boys.1,3 Most boys with CPP
# n6 x8 ~% A- F0 ]$ i( H3 Cmay have a central nervous system lesion that is
: C7 ^6 }; N4 P0 z9 Lresponsible for the early activation of the hypothal-6 ]% u6 f# |' g" n5 a
amic pituitary gonadal axis.1-3 Thus, greater empha-! F5 c2 [8 {" Y8 `$ p% K
sis has been given to neuroradiologic imaging in
1 P9 u, c5 l( q& ?5 }) K# oboys with precocious puberty. In addition to viril-% ^$ A/ K+ R) C! Y% M' |/ e. Z
ization, the clinical hallmark of CPP is the symmet-# ~. q8 n$ l0 W/ Z9 z( s7 D6 A
rical testicular growth secondary to stimulation by
$ |7 u) o% b" l# q: l" xgonadotropins.1,3
2 q; |7 u, G3 R  {! XGonadotropin-independent peripheral preco-2 U6 {# |1 Y& I! i* L* f3 W
cious puberty in boys also results from inappropriate
# b  G& @! X/ N2 {androgenic stimulation from either endogenous or( \# t5 q4 y! U$ t& ~; ?/ t. ]  j9 z- u
exogenous sources, nonpituitary gonadotropin stim-
" k* N% V' d+ l( b. Zulation, and rare activating mutations.3 Virilizing
' I# n! J9 V  r6 Scongenital adrenal hyperplasia producing excessive1 o4 C3 e* x% i  a  d
adrenal androgens is a common cause of precocious$ f2 v3 O2 e: H
puberty in boys.3,4" r- ~" `4 P, u& E7 q$ c
The most common form of congenital adrenal% T* c3 E& \# R) @, d2 T+ T& o
hyperplasia is the 21-hydroxylase enzyme deficiency.
0 |0 W0 w, ~) |3 w: oThe 11-β hydroxylase deficiency may also result in# s0 ^, v5 \7 z: c0 {
excessive adrenal androgen production, and rarely,# C6 [# z* G5 m+ o/ `) H3 U
an adrenal tumor may also cause adrenal androgen
# o' b" |5 t; r( B5 P: Iexcess.1,3
! g6 [5 A  F: g% |) B8 I; Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, |- _5 r2 ?( N1 N& E
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& Q* Z& i9 U" @) b( s5 M* u
A unique entity of male-limited gonadotropin-
2 ?7 T: R% W+ ^9 }1 Qindependent precocious puberty, which is also known* P' `8 s+ c4 C$ U% W! m$ `
as testotoxicosis, may cause precocious puberty at a
6 H( r. U9 x' M4 W. A0 Uvery young age. The physical findings in these boys
+ h  W5 j9 K- }! J& p/ d$ Mwith this disorder are full pubertal development,
: q7 V) f2 G5 m9 o; `! Nincluding bilateral testicular growth, similar to boys
# ]: f6 f) O7 L" j1 |6 Nwith CPP. The gonadotropin levels in this disorder. L; P8 _5 o( _! z
are suppressed to prepubertal levels and do not show
2 w& G% A; S. c0 Q+ `. Mpubertal response of gonadotropin after gonadotropin-
8 P5 [2 W8 N+ v' P' ?releasing hormone stimulation. This is a sex-linked
) `0 X6 x8 G$ z4 K/ D- M. X  W+ M" tautosomal dominant disorder that affects only
- u! B& G8 C& J! [males; therefore, other male members of the family
, F( X) m0 D; |4 fmay have similar precocious puberty.3, ?: P/ v( U' \
In our patient, physical examination was incon-
/ Y/ J. K6 S0 K- D6 \# `sistent with true precocious puberty since his testi-! Z' v7 @2 k) W
cles were prepubertal in size. However, testotoxicosis
$ Y# Y7 j: p( K. ^3 F) J7 h  M! Lwas in the differential diagnosis because his father
7 X! v# J( U! Istarted puberty somewhat early, and occasionally,
3 k. \1 J5 u  t4 q7 V) K- Btesticular enlargement is not that evident in the
* g4 |6 g8 Q. g7 p- ^beginning of this process.1 In the absence of a neg-
* C# r4 \: |5 Wative initial history of androgen exposure, our
4 _  B' e( J" ]: ]# ~* Hbiggest concern was virilizing adrenal hyperplasia,
+ g* E9 E) `7 ^3 t( heither 21-hydroxylase deficiency or 11-β hydroxylase
/ L1 h0 `: C# ideficiency. Those diagnoses were excluded by find-* J% N& j' D; V. A
ing the normal level of adrenal steroids.
; y: U% Q% A" K7 U' c1 MThe diagnosis of exogenous androgens was strongly+ C" X* S, c  U% O2 M
suspected in a follow-up visit after 4 months because- p! j# Y% y: }; y3 u* G" G! P4 r
the physical examination revealed the complete disap-
$ }: S6 K3 h% v7 i/ C! h& _pearance of pubic hair, normal growth velocity, and; o; o( k+ N% S) @4 }; b
decreased erections. The father admitted using a testos-
  C+ P0 F( G& I' K- Lterone gel, which he concealed at first visit. He was
1 g5 w$ n" ^3 [# ^! J% D/ w# m; eusing it rather frequently, twice a day. The Physicians’
% S; f) R2 s& P# ?Desk Reference, or package insert of this product, gel or
1 ^, p+ a& M7 w& g1 a0 Jcream, cautions about dermal testosterone transfer to, u# L0 R- A0 K# [% w
unprotected females through direct skin exposure.
3 W; q( W; U3 d: w; L! LSerum testosterone level was found to be 2 times the$ h* r: t$ J' Q  t4 H1 K2 `
baseline value in those females who were exposed to
/ S2 ]8 `* |; `even 15 minutes of direct skin contact with their male- D/ w7 n  P& n* K" L" s) x! a
partners.6 However, when a shirt covered the applica-, X2 J' O9 d; X
tion site, this testosterone transfer was prevented.
0 d' E2 f) u. G; |- \  }Our patient’s testosterone level was 60 ng/mL,$ P7 z4 Z2 _6 ?& _3 B
which was clearly high. Some studies suggest that
5 P& y1 S) f  Kdermal conversion of testosterone to dihydrotestos-
  Y8 T+ K9 b( }6 h; a( Hterone, which is a more potent metabolite, is more
. R4 e5 |, |, i- L5 W2 pactive in young children exposed to testosterone5 r% B/ G0 e$ J! [
exogenously7; however, we did not measure a dihy-
# ?3 ?2 }1 q/ }$ D0 {' Ydrotestosterone level in our patient. In addition to! Y) p/ N) g/ u( X! e9 G3 q
virilization, exposure to exogenous testosterone in
+ e: P- t7 T6 }4 I/ p$ i; Rchildren results in an increase in growth velocity and
5 p0 l0 p; [, }+ h/ r6 Cadvanced bone age, as seen in our patient.: o" G: u" }* p( l8 e
The long-term effect of androgen exposure during
9 |" q# F( ~. e+ Yearly childhood on pubertal development and final8 k# G, v/ C. q8 \& u
adult height are not fully known and always remain
3 O% G6 W% X! `" z% t1 c9 y8 U  D: ?a concern. Children treated with short-term testos-/ m0 B# v, \0 Q( i) r5 B
terone injection or topical androgen may exhibit some
7 t! d. Y$ @0 f  D% [acceleration of the skeletal maturation; however, after8 ^& X/ W; X8 a
cessation of treatment, the rate of bone maturation$ I! L& ]+ ]& }! Q
decelerates and gradually returns to normal.8,9
, h& D" i5 E1 u; e1 o' a" QThere are conflicting reports and controversy0 ^& @5 E) U! m7 P3 S; N0 l( P) N
over the effect of early androgen exposure on adult
1 I/ n8 @+ r7 d+ Bpenile length.10,11 Some reports suggest subnormal
5 @, H6 a1 _& dadult penile length, apparently because of downreg-
8 Y  G% U; j  p6 X& q* r% s* lulation of androgen receptor number.10,12 However,$ f, g1 R0 L( r, O4 M$ `7 G
Sutherland et al13 did not find a correlation between9 h# n2 a8 `2 i- C
childhood testosterone exposure and reduced adult' h4 N- m" k8 k: Y
penile length in clinical studies.
% D( K1 v4 X4 @! NNonetheless, we do not believe our patient is$ v  e: b/ S/ M8 ?, `1 a% e  f
going to experience any of the untoward effects from$ g& ^, g) s3 m* |+ v  u; u4 y
testosterone exposure as mentioned earlier because
' H3 P% d3 v7 W9 a( h% G! Ythe exposure was not for a prolonged period of time.; X% ~( |/ X9 {; q( V/ o( Y* b  `  P1 u
Although the bone age was advanced at the time of3 ]3 ]) f1 C- Z! \" z/ _; s
diagnosis, the child had a normal growth velocity at* B# Z) p1 Z# e! h+ i
the follow-up visit. It is hoped that his final adult
& O% Y* x' k! x! k; r5 q( uheight will not be affected.' C& y: b/ J2 Y! z' p( L2 V9 s
Although rarely reported, the widespread avail-
% G" i/ o5 p/ [. K1 Wability of androgen products in our society may
! s: g5 b, ]% z, Oindeed cause more virilization in male or female
7 ^3 J, S9 A8 N% M" hchildren than one would realize. Exposure to andro-1 |( j+ h. D" A2 U/ Q. p% x2 c
gen products must be considered and specific ques-
4 v) V, Y4 J4 o  q$ N2 M) ktioning about the use of a testosterone product or  h/ [+ ]8 p- o/ J. G  p
gel should be asked of the family members during$ C$ G; I. j3 R, D
the evaluation of any children who present with vir-% A: l; x: {1 J+ v# N/ y6 O5 _
ilization or peripheral precocious puberty. The diag-
/ {; C/ p- c7 f; {4 }" Q$ Z/ N) P( nnosis can be established by just a few tests and by
1 f1 L, L% y. B( @appropriate history. The inability to obtain such a3 N3 [  M, H1 c( Y# |& J/ ^
history, or failure to ask the specific questions, may# n- C/ g7 k* S; T* x& |% Z6 e5 X
result in extensive, unnecessary, and expensive
; `: D% w) O( sinvestigation. The primary care physician should be
) h1 K8 c3 L- raware of this fact, because most of these children
$ Y5 P# n3 X1 Z# p% ~may initially present in their practice. The Physicians’1 n. \2 d+ U6 _
Desk Reference and package insert should also put a# J% N4 R& q0 T( }
warning about the virilizing effect on a male or
8 v0 \! h* l8 Q& A+ y( d4 o- kfemale child who might come in contact with some-$ \1 v* g9 h: }: {0 `$ t- G- G
one using any of these products.9 [1 D! r, Y$ H! {! t/ U3 C
References1 ]9 K9 }/ j! E
1. Styne DM. The testes: disorder of sexual differentiation
; S. L/ _$ G5 f. W  kand puberty in the male. In: Sperling MA, ed. Pediatric# Y$ C5 [( j1 T- W% D
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- m/ y( H8 j: W5 F  F* |) w
2002: 565-628.
# s( [! D$ E8 a+ {2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! p: N/ h2 \' ]puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
6 p, y$ g3 M* l0 e" YBoy Induced by Indirect Topical
6 v" T$ D. `* _% qExposure to Testosterone
/ T0 V3 `  E" HSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& Z* b  b& [* n0 J+ t" L' `7 Land Kenneth R. Rettig, MD1
* O+ w: ?4 l# Q* ^Clinical Pediatrics; J1 d* A5 k) C# O5 Q+ `& v
Volume 46 Number 6* m: \1 F# a! Z  }" k$ F
July 2007 540-5439 v1 Q9 ~* p% k; J1 [
© 2007 Sage Publications% q1 C% a% P* U( x5 t6 z9 G: z8 H
10.1177/0009922806296651
# X% n( c9 p6 t2 q- u! ~http://clp.sagepub.com/ Q1 _; ?& k2 K. R
hosted at
  n# T2 o, C$ K% _- Phttp://online.sagepub.com8 s3 k; W; L- Z
Precocious puberty in boys, central or peripheral,
' F7 l: ~8 `& E% U0 d3 cis a significant concern for physicians. Central
+ d) c$ |* k5 oprecocious puberty (CPP), which is mediated
. `1 [5 a# m5 w. |; {% E1 hthrough the hypothalamic pituitary gonadal axis, has
1 Z0 Y. U% J: D3 J; Q% ca higher incidence of organic central nervous system; N( f6 X3 H% J- D' h! \. j
lesions in boys.1,2 Virilization in boys, as manifested
+ N2 |, n' t5 R6 V; @1 hby enlargement of the penis, development of pubic
/ D- @0 z8 o# {+ }8 t, @. A( |hair, and facial acne without enlargement of testi-3 h- v: O- O' r( p8 J4 X( E
cles, suggests peripheral or pseudopuberty.1-3 We
+ c& E0 l9 a, {' Z- G" Yreport a 16-month-old boy who presented with the6 |# _, d; i" l( u4 H9 l5 x7 t
enlargement of the phallus and pubic hair develop-1 K: `" I* _! B0 V! w+ F2 I9 x
ment without testicular enlargement, which was due6 y1 k. u5 m- H+ t# d1 ^% j$ R' L, U
to the unintentional exposure to androgen gel used by: U6 M0 N1 [1 l) p. @
the father. The family initially concealed this infor-. s$ m8 L1 b' b
mation, resulting in an extensive work-up for this8 ^2 ?# l) p8 A5 W' n, e) ^0 n+ Y- H
child. Given the widespread and easy availability of
, [2 _& o$ a& ~  ztestosterone gel and cream, we believe this is proba-
4 o& i4 Z: z/ d, d% a, Z  Cbly more common than the rare case report in the
* z8 M) F7 y# [9 N" J; uliterature.4
- \8 V5 n$ e5 O% e1 X; SPatient Report
8 z" ?2 H3 S6 A. dA 16-month-old white child was referred to the
+ ^% B# T, @: k5 O" b  |( n3 Y% D! P. dendocrine clinic by his pediatrician with the concern
; a+ d5 C! C( n+ o/ zof early sexual development. His mother noticed
. R2 G* }' [( `7 K8 d" V" Plight colored pubic hair development when he was8 Z7 w5 G* G& B! H3 u$ p( \3 ]
From the 1Division of Pediatric Endocrinology, 2University of
4 d4 S, A% F/ a/ G9 e" H8 m) xSouth Alabama Medical Center, Mobile, Alabama.: V9 o5 }# P5 f& b& C1 H
Address correspondence to: Samar K. Bhowmick, MD, FACE,
( m1 N1 A; A7 i) V5 GProfessor of Pediatrics, University of South Alabama, College of
1 ~# F& e& |3 i- r" A( ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! e# A7 b( {+ z! W
e-mail: [email protected].
/ r6 k6 c* \) f9 s, F: Zabout 6 to 7 months old, which progressively became
3 o* S4 I! O$ o/ U& ]4 Z( B3 Edarker. She was also concerned about the enlarge-
3 A) r3 M# e' ~ment of his penis and frequent erections. The child
9 E, E) C; M# v( wwas the product of a full-term normal delivery, with* s- [+ a  `/ S4 o8 |; q9 w
a birth weight of 7 lb 14 oz, and birth length of
8 m" g$ g+ ]+ }& h7 D20 inches. He was breast-fed throughout the first year$ T4 f2 f& t: o' K8 s3 Y
of life and was still receiving breast milk along with5 u0 K, I7 h3 c3 `
solid food. He had no hospitalizations or surgery,3 f6 x2 P% n. |! N) j2 `
and his psychosocial and psychomotor development. z  G* F5 `: T- \
was age appropriate.
0 n8 e" H) K( W( C+ ~* TThe family history was remarkable for the father,! B+ l; _5 A# d+ X" ]! y
who was diagnosed with hypothyroidism at age 16,
- H( H% D1 i5 _4 @# T( G' E+ {which was treated with thyroxine. The father’s8 m) f3 d- l) k4 a, v! u
height was 6 feet, and he went through a somewhat. P  ^9 H5 d/ A) C" I0 X* E
early puberty and had stopped growing by age 14.9 R9 u' c. C- `, H0 r( [) N% b
The father denied taking any other medication. The* d# v2 `: s2 x  w: a4 c
child’s mother was in good health. Her menarche  \" t% C: I2 B
was at 11 years of age, and her height was at 5 feet5 J  h8 c  k3 ~6 ]/ E- I2 @" A8 N
5 inches. There was no other family history of pre-
1 _+ u, [  m9 wcocious sexual development in the first-degree rela-
; _5 X0 X$ ^/ F  T3 ~; w7 ctives. There were no siblings.% |+ k3 y6 h  Q
Physical Examination
# g2 k# \' N2 W# c& jThe physical examination revealed a very active,
$ t! [/ m& y$ z; a- }playful, and healthy boy. The vital signs documented, G# p- J/ q4 u! ~
a blood pressure of 85/50 mm Hg, his length was4 v' z/ F- X8 N- f7 R
90 cm (>97th percentile), and his weight was 14.4 kg; Z1 [  [' D5 m
(also >97th percentile). The observed yearly growth
" u/ X( |' ?2 _; J. s8 z% K8 Nvelocity was 30 cm (12 inches). The examination of
& p6 V, Q0 w$ R7 J6 I* s8 Mthe neck revealed no thyroid enlargement.# F  w$ K# T; a/ X2 P
The genitourinary examination was remarkable for
8 c2 q! x3 T: zenlargement of the penis, with a stretched length of5 b/ W  r+ }3 Y! T- k( S
8 cm and a width of 2 cm. The glans penis was very well2 \" B( I* w9 L& p+ ?, G
developed. The pubic hair was Tanner II, mostly around! S5 U2 ]$ k$ X
540
& _3 m! u. n( l% i1 x) N1 Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- S) ]0 u/ C1 Sthe base of the phallus and was dark and curled. The! @, }* L% x* l% y7 X/ h8 A
testicular volume was prepubertal at 2 mL each.6 m; B' l* j, L  Y9 z( T
The skin was moist and smooth and somewhat  ]6 T4 O* t3 a
oily. No axillary hair was noted. There were no" C- V' U) @0 M! o6 d! U( u
abnormal skin pigmentations or café-au-lait spots.
4 o# @& d/ G. T" X% ]9 vNeurologic evaluation showed deep tendon reflex 2+
/ \$ y4 i  @; {$ j) I+ v1 T) N( Tbilateral and symmetrical. There was no suggestion) R$ L: n9 A$ E( q) r
of papilledema.
5 l3 b0 i; }0 a$ P7 `Laboratory Evaluation
: y# n, s* p; q2 hThe bone age was consistent with 28 months by$ a4 Z$ ^, _( ~# l1 \1 B
using the standard of Greulich and Pyle at a chrono-
' O; a" ?, X& E- I1 i6 zlogic age of 16 months (advanced).5 Chromosomal
  W+ J( O, y7 Fkaryotype was 46XY. The thyroid function test
2 g$ B  [* o, m4 v7 l0 Q/ K. C' Z; sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-) Q& h* x! p" g6 f
lating hormone level was 1.3 µIU/mL (both normal).
5 F+ ^9 M6 A7 ?- c0 u. ?The concentrations of serum electrolytes, blood' P& Z/ ?( `' ]- @& B  Q
urea nitrogen, creatinine, and calcium all were/ X8 f& C/ }& o. J! ]/ s7 U
within normal range for his age. The concentration
/ q* \0 |. [) z! Nof serum 17-hydroxyprogesterone was 16 ng/dL
1 M8 ^1 L; I9 M- f& C6 U6 E(normal, 3 to 90 ng/dL), androstenedione was 20
  a! Y$ ]5 z% ]/ s* Cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 f4 w" T; G' u# ]) [% u0 @+ P6 Tterone was 38 ng/dL (normal, 50 to 760 ng/dL),8 |2 e( k- O2 t! \4 s* a
desoxycorticosterone was 4.3 ng/dL (normal, 7 to' R* F( x+ m; c- x8 o- D5 D" O( _
49ng/dL), 11-desoxycortisol (specific compound S)/ ~5 j- ?. U  R6 M7 J) z8 x
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. H3 z& J" p3 K$ N: ?  s
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total3 U  O; i  Z. [
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 \+ ^( f& {& g8 n0 n0 B6 Z. Kand β-human chorionic gonadotropin was less than% J# h! d/ Y- v1 }3 Z) Q
5 mIU/mL (normal <5 mIU/mL). Serum follicular
. ?" c$ z9 i/ S$ V3 i( Bstimulating hormone and leuteinizing hormone; i4 q! m" }# Q( A- G
concentrations were less than 0.05 mIU/mL0 w# i: R3 \2 Y! _& H
(prepubertal).8 e& L9 w# I8 q+ @$ R
The parents were notified about the laboratory
0 d& m& A# c/ [' Xresults and were informed that all of the tests were
1 ^% F7 X) q% o: H5 Qnormal except the testosterone level was high. The: ^# F1 G' q6 G# {3 G$ e
follow-up visit was arranged within a few weeks to% ?( d' |3 F7 n8 w7 Z
obtain testicular and abdominal sonograms; how-, a. {6 w, ?  t) Z# {$ Z2 w
ever, the family did not return for 4 months.
7 T0 g( a8 Q+ z- lPhysical examination at this time revealed that the7 x' S8 ~) f: M, c
child had grown 2.5 cm in 4 months and had gained
$ d0 F. B% Z; e2 kg of weight. Physical examination remained
0 z% x9 o7 H$ e& H( k4 Tunchanged. Surprisingly, the pubic hair almost com-$ O9 o2 V  X' \0 f
pletely disappeared except for a few vellous hairs at
+ n  ?; T! B  \the base of the phallus. Testicular volume was still 2
6 N: g! n; P* S2 W8 V3 x/ R8 ^mL, and the size of the penis remained unchanged.
0 _/ t( E: G) [9 gThe mother also said that the boy was no longer hav-
& X" y+ u2 A% C8 {- Uing frequent erections.
, s; b# P  o( ~& Y: bBoth parents were again questioned about use of
0 c0 ?$ }2 L' j; u  F' ~any ointment/creams that they may have applied to+ e2 B5 h* s; [' r: ?  J0 f: M9 K- \
the child’s skin. This time the father admitted the
- [8 B% P# Z: a; [8 G. UTopical Testosterone Exposure / Bhowmick et al 5411 A# {$ `5 `& v8 Q
use of testosterone gel twice daily that he was apply-! z# D' X, G: u) F
ing over his own shoulders, chest, and back area for
, {: c' J6 U/ i: R: ~  y2 Ga year. The father also revealed he was embarrassed
/ V/ `2 `# k. c, {- a! M3 wto disclose that he was using a testosterone gel pre-
! |5 w/ r" @3 d' K. ]scribed by his family physician for decreased libido, D3 I( x( _$ g% q  c6 r) U
secondary to depression.4 {% M: m' [# o6 G& c* u
The child slept in the same bed with parents.' @2 ?( ^; }# y* N  L9 _# k
The father would hug the baby and hold him on his- I) a+ _2 P, r! s
chest for a considerable period of time, causing sig-
  @. s& k# |' p$ m8 S  Inificant bare skin contact between baby and father.
5 d( w% p9 P! ]; a. o4 y! q- uThe father also admitted that after the phone call,
$ b- ^+ f6 ~  F5 p! iwhen he learned the testosterone level in the baby
, ~8 q7 j! c0 G% t5 iwas high, he then read the product information
: b( `6 F; M9 m/ h% Z! }- c+ cpacket and concluded that it was most likely the rea-
) a! z7 X8 d8 ?, a+ A7 V5 O% yson for the child’s virilization. At that time, they
# b$ L9 ~, h# l; P" ]) ^* wdecided to put the baby in a separate bed, and the
5 w4 ]- Q4 Y# t0 |( f5 Zfather was not hugging him with bare skin and had% h3 p, w" u4 K6 U9 z: N5 P- P/ W
been using protective clothing. A repeat testosterone
) V7 b0 m3 L" k" m* y0 L+ G; Itest was ordered, but the family did not go to the
# C( ~! m+ e% j$ \) A" b) d2 R3 Tlaboratory to obtain the test.; Y7 U* S! i: e
Discussion! n( c* q4 C& t3 p1 j
Precocious puberty in boys is defined as secondary! g* `# ?7 f- i
sexual development before 9 years of age.1,4
0 Z. B" G2 X& J  N' l  m, b, WPrecocious puberty is termed as central (true) when
9 F" t& u' a2 ^' h2 rit is caused by the premature activation of hypo-! O7 }! Z8 ^2 p6 r6 K- N
thalamic pituitary gonadal axis. CPP is more com-/ I9 n7 W& h5 i1 ~3 B8 B* s7 S
mon in girls than in boys.1,3 Most boys with CPP
2 b" @; z0 T5 i+ ?+ W6 |+ |+ ~may have a central nervous system lesion that is
" ^4 n: H7 a9 Q* K8 i. p4 Y* oresponsible for the early activation of the hypothal-
" t6 A2 S+ S) }4 ^" Camic pituitary gonadal axis.1-3 Thus, greater empha-
6 O; F) f. b; n) nsis has been given to neuroradiologic imaging in0 {3 E' q! B/ i& u* r& _0 V
boys with precocious puberty. In addition to viril-3 {, o: {1 q, U6 F4 l7 M* h( O" _
ization, the clinical hallmark of CPP is the symmet-
4 Q7 r( L" `3 ^- A1 W0 }rical testicular growth secondary to stimulation by
# u8 `2 x% ?  p% Pgonadotropins.1,33 ^% Z/ G# o0 ]& P7 k, `& [) F# }
Gonadotropin-independent peripheral preco-8 b1 o( I1 {6 v
cious puberty in boys also results from inappropriate0 I4 Y/ h8 l) G3 M1 @
androgenic stimulation from either endogenous or* u5 G8 y2 m' {+ J
exogenous sources, nonpituitary gonadotropin stim-
& g5 U& e  ^: K0 F9 a2 Tulation, and rare activating mutations.3 Virilizing
8 H% [& Y4 p( ^+ N. T/ C/ Tcongenital adrenal hyperplasia producing excessive
- m2 D0 |2 L: Q1 |" u3 o6 j5 o2 m3 Yadrenal androgens is a common cause of precocious
. Z3 u* A; D6 S/ Q! ^- Cpuberty in boys.3,4  @  V6 k" u3 Q+ H
The most common form of congenital adrenal
: F4 U3 Y. P# C6 w) S) o5 T# shyperplasia is the 21-hydroxylase enzyme deficiency.* I& e6 ^! V' E5 `
The 11-β hydroxylase deficiency may also result in5 {( P% e& n1 V0 Y' b
excessive adrenal androgen production, and rarely,
0 }" \' W) W. D# c' U1 _; `an adrenal tumor may also cause adrenal androgen+ L" p" ^; `! `9 G! Z2 j: |
excess.1,3
1 @" k0 n- X* N. d9 b" P9 fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& r1 G/ n6 X: Y/ A: |/ s; ^( c4 `7 ?
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% C1 ?4 k& l% B1 K, I6 p, KA unique entity of male-limited gonadotropin-) \9 E- O% S5 t7 {! p: C7 }
independent precocious puberty, which is also known
- Q3 y! D3 ]) K, h+ b- h" nas testotoxicosis, may cause precocious puberty at a& R* k2 y9 v% [0 m  [$ k
very young age. The physical findings in these boys9 k, }/ H) W1 e$ d4 c; J
with this disorder are full pubertal development,5 d  P4 V4 n' \1 X3 x* A
including bilateral testicular growth, similar to boys
+ n, U. {; K6 ?) Nwith CPP. The gonadotropin levels in this disorder
+ }/ h/ a' g3 U& V! ~/ N( e8 y# Hare suppressed to prepubertal levels and do not show
+ ?: G; D' y. a  w* Q" epubertal response of gonadotropin after gonadotropin-
: K8 g1 v, T. c! n) xreleasing hormone stimulation. This is a sex-linked5 _8 l  L# ~: ~( ]
autosomal dominant disorder that affects only
& ]" V6 C0 S4 t, i) O7 o# lmales; therefore, other male members of the family" `$ U/ H  J* F. u& C: l0 l4 W4 r) }
may have similar precocious puberty.3
2 [3 ~1 R; |% t- FIn our patient, physical examination was incon-; m- R( K) E) D' j; p
sistent with true precocious puberty since his testi-: w& i2 {& H* f7 L$ ?1 Y0 D* K
cles were prepubertal in size. However, testotoxicosis/ r, W8 ?. H  S$ R( I
was in the differential diagnosis because his father
. V! b0 g' M/ m9 Fstarted puberty somewhat early, and occasionally,
3 z* ]% v: m' i1 Y( T5 \testicular enlargement is not that evident in the2 r! A3 j8 J. P
beginning of this process.1 In the absence of a neg-
4 `) Z6 n, G7 \. c+ n) v- Tative initial history of androgen exposure, our
4 X- v" s/ y! F0 ^8 ~! Y1 Gbiggest concern was virilizing adrenal hyperplasia,' T% Y% r: c8 B+ S2 ^
either 21-hydroxylase deficiency or 11-β hydroxylase
( Z" a0 L2 h' h- Ndeficiency. Those diagnoses were excluded by find-
. W* e- Z& K* eing the normal level of adrenal steroids.  K3 x6 Y! R0 s
The diagnosis of exogenous androgens was strongly
, I5 y5 f3 v) k7 A3 Msuspected in a follow-up visit after 4 months because
! G5 e- B3 L( l2 X* f% Q! Dthe physical examination revealed the complete disap-
, q6 {& X" _+ D: }7 A5 Wpearance of pubic hair, normal growth velocity, and
4 _- l/ y6 ~4 @% Ydecreased erections. The father admitted using a testos-
; I8 M6 H# y$ _. ~2 n% Mterone gel, which he concealed at first visit. He was% K) y" D! u8 b6 X( h
using it rather frequently, twice a day. The Physicians’
5 \$ x6 Y6 h1 L  h$ QDesk Reference, or package insert of this product, gel or+ {9 k5 e( [2 c- V. E, f  X
cream, cautions about dermal testosterone transfer to
* ?2 H  k: z# A9 n/ p2 M- \4 runprotected females through direct skin exposure.
. R# B6 R- w6 O8 j3 n. G, {Serum testosterone level was found to be 2 times the
, i4 Z6 Y" h: C0 p' R1 J9 S4 L, fbaseline value in those females who were exposed to1 O" d1 A& N" E
even 15 minutes of direct skin contact with their male
6 Q3 N4 q# E: V* z5 i- [partners.6 However, when a shirt covered the applica-1 b" m+ R1 P, M1 c0 Q
tion site, this testosterone transfer was prevented.
3 a6 ], y" y% f8 i+ \Our patient’s testosterone level was 60 ng/mL,
* w, J9 V0 O; N  qwhich was clearly high. Some studies suggest that
0 [2 u! x# A, T/ z, a5 rdermal conversion of testosterone to dihydrotestos-0 A* n9 t% L- S3 z2 D5 y* ]
terone, which is a more potent metabolite, is more
' @) r( b9 N3 {# T0 A) {8 wactive in young children exposed to testosterone2 _; [0 W3 j" S' t
exogenously7; however, we did not measure a dihy-* V. e! j% d7 q0 F  m$ J% a$ r
drotestosterone level in our patient. In addition to# x- W) F8 ]( g/ b0 C: W; y; y
virilization, exposure to exogenous testosterone in
' y' \. z4 f2 ^children results in an increase in growth velocity and+ p! @% {2 B6 H* Z2 a
advanced bone age, as seen in our patient.
2 r3 j4 N  Q( v) aThe long-term effect of androgen exposure during
' u/ `& T, R/ l( M/ zearly childhood on pubertal development and final& v& L! ?7 b# `. O
adult height are not fully known and always remain% L3 `1 N$ o8 V" X0 e
a concern. Children treated with short-term testos-
% ~4 }4 y; L0 p  e; {) `# U. W2 G* ^terone injection or topical androgen may exhibit some
6 r- a) ?# |8 f" Uacceleration of the skeletal maturation; however, after  U" @0 w6 C" _  G' C0 S4 f0 J
cessation of treatment, the rate of bone maturation" p7 s! p: v$ i! S
decelerates and gradually returns to normal.8,9
* o8 m( d- v; u/ U$ @: oThere are conflicting reports and controversy
1 r: R7 f. R- c% _- `over the effect of early androgen exposure on adult# B! {( @: S$ Z& s/ d( r( m
penile length.10,11 Some reports suggest subnormal
: ^# w* N/ w$ Y4 C- B, Cadult penile length, apparently because of downreg-
) [. m8 x6 Y( o# [: Kulation of androgen receptor number.10,12 However,/ ^2 g9 W- p1 D
Sutherland et al13 did not find a correlation between7 M4 i3 I0 R1 ]1 W
childhood testosterone exposure and reduced adult
2 ~* e2 @. T- ?, G* rpenile length in clinical studies./ n/ _5 `9 T' [+ d
Nonetheless, we do not believe our patient is$ I. }# _9 d  b; ^
going to experience any of the untoward effects from" C$ D4 L/ c# S3 a
testosterone exposure as mentioned earlier because% G0 {+ s8 V% w) R( Q  o
the exposure was not for a prolonged period of time.
- N' y3 U1 F. K6 w% C  _$ M! T# z" ]Although the bone age was advanced at the time of& g4 o. @! G1 B# g5 t9 c. w! N
diagnosis, the child had a normal growth velocity at6 j' X" b$ \! [, g  {4 g
the follow-up visit. It is hoped that his final adult& `/ g; `0 u7 h' d# R
height will not be affected.
/ S. Z& y+ e$ ~9 t0 C, mAlthough rarely reported, the widespread avail-8 r0 I3 a5 D9 q* [8 }
ability of androgen products in our society may2 F6 u( k3 o; b$ q' p2 D
indeed cause more virilization in male or female
' i, I9 H7 i) F& p! t, t& Wchildren than one would realize. Exposure to andro-& o" l0 c5 Y4 E. v2 ~! P
gen products must be considered and specific ques-8 {/ y7 z% z! v, l8 O2 A" M) w
tioning about the use of a testosterone product or
3 J( X! X8 H/ x/ q' G$ ugel should be asked of the family members during1 w9 w6 W/ W- O8 @8 J
the evaluation of any children who present with vir-
: P4 h7 k. y# v; Lilization or peripheral precocious puberty. The diag-4 |2 v4 _% u0 }; Y" Z
nosis can be established by just a few tests and by8 {- H! _) `2 |! C' ]! S( |
appropriate history. The inability to obtain such a. n; A3 e& l! K( {" j
history, or failure to ask the specific questions, may; ^3 @8 U$ A8 M, A0 \$ x) Y
result in extensive, unnecessary, and expensive  @7 y' g# W3 e7 ?# o  K
investigation. The primary care physician should be
# V+ r8 W6 t( B5 h$ L" raware of this fact, because most of these children& D3 R8 M8 |4 ?1 |! q- s! J% V
may initially present in their practice. The Physicians’
, e8 w. W- U/ f: Y- y4 f, zDesk Reference and package insert should also put a* C. q5 a0 p$ ?2 ]0 W
warning about the virilizing effect on a male or' L& o9 i0 g0 |. [3 M
female child who might come in contact with some-
! u% P7 h1 V- e) G, y# f+ Hone using any of these products.
- d4 j. ]$ p; m1 O7 M( VReferences
; o5 F; ]0 E# I& M% t' j1. Styne DM. The testes: disorder of sexual differentiation
4 d- p8 U# q4 |: F8 Eand puberty in the male. In: Sperling MA, ed. Pediatric
: z. A# n% ^& h8 ^  `$ A: m, rEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;; q( [# q4 [9 o5 E+ Z1 e
2002: 565-628.
+ y& ?  e4 c- p0 H0 Q2 ^. x9 q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 b8 Z4 u* c* s1 S1 W
puberty 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
0 {4 X; v) `. r
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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