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Sexual Precocity in a 16-Month-Old
& P# z; f8 x; I. t7 hBoy Induced by Indirect Topical1 ^! ^; ]! h/ j( g
Exposure to Testosterone2 ]( @2 S1 }5 w/ K' I3 Y
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, O3 n9 l4 F. D& I+ d  L6 N
and Kenneth R. Rettig, MD1' M  f$ e; o- h! J& U
Clinical Pediatrics
' L- P- H* Z2 E9 z7 ~Volume 46 Number 6& k3 j% T) V. v5 f
July 2007 540-543! D* C1 f1 f$ K6 j5 {) _3 I
© 2007 Sage Publications; ^8 Y; U1 l: x$ g( d
10.1177/00099228062966512 m6 I5 R" P/ m2 |* g- \; Q3 M  C
http://clp.sagepub.com/ Y1 c" f6 o* K
hosted at4 }# F( |6 s5 E, Y5 \, s# D9 ]. w
http://online.sagepub.com& y. x" q/ f& R+ }" d
Precocious puberty in boys, central or peripheral,( R( Q  y5 y: Z3 e
is a significant concern for physicians. Central: S$ E9 |: h9 o& ]
precocious puberty (CPP), which is mediated
! U9 T6 {& u4 V+ r, g- Ythrough the hypothalamic pituitary gonadal axis, has
& H% z6 v. p3 t. ]  H" W! Ta higher incidence of organic central nervous system
2 D% m" @; S. Y" g/ w1 Q' _lesions in boys.1,2 Virilization in boys, as manifested
; F, ^, K+ m" D; }2 u7 rby enlargement of the penis, development of pubic  u# F) J5 `5 p
hair, and facial acne without enlargement of testi-
8 G* t  [, P4 ocles, suggests peripheral or pseudopuberty.1-3 We, l) J/ |/ b4 w* i" _* C2 i" [
report a 16-month-old boy who presented with the
# {& h4 s! Z  E9 [enlargement of the phallus and pubic hair develop-
8 t/ K) a8 }: T/ {ment without testicular enlargement, which was due
* w! H% \9 ?, u  C7 Xto the unintentional exposure to androgen gel used by7 Z) v6 K5 Q' M" _: ^
the father. The family initially concealed this infor-% C& |  Z2 A& m- ~9 ~
mation, resulting in an extensive work-up for this- D! O; q5 J( E: E: ]  P  E
child. Given the widespread and easy availability of
+ T6 O- u- \; n9 @- v- C1 z+ Dtestosterone gel and cream, we believe this is proba-
# ]) g' E1 v5 B$ F' jbly more common than the rare case report in the
1 T: P; ~9 ?2 U8 \# Hliterature.4
  W& p$ D! I, C& |. }8 LPatient Report9 I7 H. x; M7 c: W. c7 b
A 16-month-old white child was referred to the7 e- D+ i; M) [% Z3 n7 S
endocrine clinic by his pediatrician with the concern
1 }+ r$ B' `3 |of early sexual development. His mother noticed+ @  G$ x3 {7 Z3 g8 S$ Q  a
light colored pubic hair development when he was& D" G6 Q& T1 b: z% M7 A
From the 1Division of Pediatric Endocrinology, 2University of
  q1 ^  T, @* `0 a, \! C, }/ L- bSouth Alabama Medical Center, Mobile, Alabama.
2 z; y3 Y% w1 b- \0 x/ `8 N# vAddress correspondence to: Samar K. Bhowmick, MD, FACE,4 D# G: F+ w0 P; x3 T( |
Professor of Pediatrics, University of South Alabama, College of
4 {: r! P5 Q* Z( E3 Y# CMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
" h) m% g; b0 s8 b" _1 A" Y( k' U  ee-mail: [email protected].
* G; }- y* c; _% Qabout 6 to 7 months old, which progressively became% t" @3 v# Q! \! ~
darker. She was also concerned about the enlarge-
* h" P8 t7 O8 _% P) \5 Mment of his penis and frequent erections. The child
( E& H1 ^; t6 B' ^: i0 ^was the product of a full-term normal delivery, with1 k/ z3 x# {; u
a birth weight of 7 lb 14 oz, and birth length of/ d; k4 s$ s1 T$ d
20 inches. He was breast-fed throughout the first year. b, D9 g4 E  o( k  w1 X
of life and was still receiving breast milk along with
9 e: q3 }/ o  b4 l! T) Nsolid food. He had no hospitalizations or surgery,+ G0 t, e* W' A0 K
and his psychosocial and psychomotor development
% R- N8 {5 e  @  f0 R5 Y- Dwas age appropriate.
9 l# {: k4 C0 ^& v) U% t! z+ K- ]$ YThe family history was remarkable for the father,5 j& R2 l2 h' O* g2 w, K
who was diagnosed with hypothyroidism at age 16,5 K+ q# E) A2 l1 ]' \4 u* \
which was treated with thyroxine. The father’s8 T7 h2 y3 C- o( m  y9 p+ C+ S
height was 6 feet, and he went through a somewhat( q: a% y4 q& p- v4 l
early puberty and had stopped growing by age 14." E/ L9 u6 C- Q  C1 V( K; y
The father denied taking any other medication. The
+ t5 n' k1 H3 m6 x; s( [* `child’s mother was in good health. Her menarche
- ~$ y& x  l/ a! iwas at 11 years of age, and her height was at 5 feet5 V6 N4 G0 u" P  |: T0 s
5 inches. There was no other family history of pre-0 @4 {: G  ~& b$ K9 T( b2 ~
cocious sexual development in the first-degree rela-0 v/ H/ |$ L7 v! R7 w2 m6 `& v
tives. There were no siblings.8 V3 m; r. a. u/ W: b$ F
Physical Examination
( |& a7 L3 r: _0 X$ m  b9 oThe physical examination revealed a very active,
+ j  R% M; ~* J& T# ]% Q" Oplayful, and healthy boy. The vital signs documented& |6 d6 G3 U( V% s- {/ w
a blood pressure of 85/50 mm Hg, his length was8 b6 Y+ W- y# p
90 cm (>97th percentile), and his weight was 14.4 kg
7 m4 Y. F! F( T2 l0 G(also >97th percentile). The observed yearly growth
6 c. F: D; Q% O, T( Z" I1 u9 evelocity was 30 cm (12 inches). The examination of% X( w2 s$ T' ^; j0 f
the neck revealed no thyroid enlargement.- w& F: @$ f' ^# O/ @& B3 p2 S
The genitourinary examination was remarkable for
8 r! A) Y& P( t  P; n# X* \enlargement of the penis, with a stretched length of! a, g! W8 r4 i9 [" Z
8 cm and a width of 2 cm. The glans penis was very well9 s" r# m2 Z$ r# [. n0 {0 C) Z# m
developed. The pubic hair was Tanner II, mostly around
' L& R7 m5 j: K' a540
; a5 z/ J% L4 @; I' xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( g0 B6 ?! N  ^
the base of the phallus and was dark and curled. The
0 z- y' L" i; I5 i) |testicular volume was prepubertal at 2 mL each.2 ^. g3 y8 s2 r8 e+ n
The skin was moist and smooth and somewhat
' _5 t/ n& m( i9 Q9 Q, a/ g5 ?6 zoily. No axillary hair was noted. There were no3 u% n  t8 }2 K( |9 s' |! m, B2 z7 H
abnormal skin pigmentations or café-au-lait spots.
9 Y2 o8 Z" F; g% z3 l* z3 oNeurologic evaluation showed deep tendon reflex 2+
; ~/ \8 i2 o& q0 M) u8 {bilateral and symmetrical. There was no suggestion
: a8 H6 h- A* c1 nof papilledema.
8 \1 k$ ?* {, T4 b0 pLaboratory Evaluation
  L; ?, ?2 k& I0 R) S5 lThe bone age was consistent with 28 months by
3 l4 s+ c: {7 e" ?4 V$ q- @2 c* Yusing the standard of Greulich and Pyle at a chrono-# S" }# r. j" t# m+ y
logic age of 16 months (advanced).5 Chromosomal
$ B$ S9 i- `5 L5 \karyotype was 46XY. The thyroid function test
6 N4 j: \" j8 ~3 W; h5 `showed a free T4 of 1.69 ng/dL, and thyroid stimu-
. u. D9 R, y7 Y+ Alating hormone level was 1.3 µIU/mL (both normal).
% G9 B% g) C; v! m6 @The concentrations of serum electrolytes, blood
( H- ]& ^: J& i9 Z. Y: ~urea nitrogen, creatinine, and calcium all were% [0 `! \. N: a7 [- @
within normal range for his age. The concentration; L" `1 Q7 u  Y! z
of serum 17-hydroxyprogesterone was 16 ng/dL" m: [7 E) m- l- W9 K
(normal, 3 to 90 ng/dL), androstenedione was 20
5 p, G+ `: f' C( }. l' G1 mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; N' f  O* F. h5 `& N
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
) S4 d: L7 R$ P: f1 E2 Y; Xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to; s' w$ V& Q6 X7 w
49ng/dL), 11-desoxycortisol (specific compound S)
$ e' g1 }3 p  M+ z4 D# e1 }was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  V( ]7 i9 z' V+ V) C; a
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total2 X: k* S# h3 x( T  {1 }
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),) I' B  X% G$ S5 z
and β-human chorionic gonadotropin was less than* ?4 f8 w8 M' D
5 mIU/mL (normal <5 mIU/mL). Serum follicular
& T1 E8 \7 u( L  _% Bstimulating hormone and leuteinizing hormone
/ n: [6 x* T) ?& k. q+ u8 F! econcentrations were less than 0.05 mIU/mL6 F7 l" ]* Y' U5 v3 D
(prepubertal).
" i  S  e2 m8 iThe parents were notified about the laboratory
& v7 Z( _. S* Z4 ?results and were informed that all of the tests were
4 y' g6 f0 d) C1 Wnormal except the testosterone level was high. The: B8 j4 E4 B7 G- _) J
follow-up visit was arranged within a few weeks to
8 H  M$ D( q8 z6 Y! H% x3 r7 V, robtain testicular and abdominal sonograms; how-
! g' b3 a& ~0 i# s# m$ W, U& P6 h1 yever, the family did not return for 4 months." a& j- F% D, Y& N3 x! n/ u' J
Physical examination at this time revealed that the
) T: p% Q7 h; ^! s  h( S, echild had grown 2.5 cm in 4 months and had gained" {' c! R4 G; a9 o  n! C5 j& C
2 kg of weight. Physical examination remained, M0 G& R" |% P! j0 l
unchanged. Surprisingly, the pubic hair almost com-* j. C0 c4 K. K" I, ]
pletely disappeared except for a few vellous hairs at4 k& R8 n# z* U* X1 M+ ^, e2 S
the base of the phallus. Testicular volume was still 2
  {& O& ^/ s3 n$ q& h5 zmL, and the size of the penis remained unchanged.7 ^! r& r2 y/ i0 k; u/ m5 w
The mother also said that the boy was no longer hav-
' P  I$ O- s9 hing frequent erections.
% t0 y2 L: _# ZBoth parents were again questioned about use of2 S5 K+ b5 R9 X6 M4 j  G; ~
any ointment/creams that they may have applied to2 C/ }" }$ B) m$ ~1 o
the child’s skin. This time the father admitted the
  ^# U0 g( i6 z( x6 u0 [( tTopical Testosterone Exposure / Bhowmick et al 541" Q$ H# A8 Z9 B- q/ m
use of testosterone gel twice daily that he was apply-
% M4 o2 i) D5 r, r' Z% s7 r( ~3 i' ^ing over his own shoulders, chest, and back area for
* j3 z1 R- A2 N) p  ~* x! Za year. The father also revealed he was embarrassed
7 f: c' H/ ^0 O7 d- z4 B  Lto disclose that he was using a testosterone gel pre-
( X' M6 N4 ]4 i1 kscribed by his family physician for decreased libido
+ o& T8 Y3 h4 L+ Bsecondary to depression.* Q& o" f/ R! C. G
The child slept in the same bed with parents.
: `% j7 \% H' f5 S) Y6 N+ M  W8 `/ u  mThe father would hug the baby and hold him on his
! a" \  A  b* Lchest for a considerable period of time, causing sig-8 c4 E2 C: k' I
nificant bare skin contact between baby and father.4 B1 K% A/ ^" {/ |' n
The father also admitted that after the phone call,
8 R- m% Y" c: ?( |( T) ^% [when he learned the testosterone level in the baby8 A) O8 Z/ U3 W' @
was high, he then read the product information
5 `, i  m) u- v" y: n7 C' X& _& p( opacket and concluded that it was most likely the rea-) g& [" Y( f% z9 ?" A
son for the child’s virilization. At that time, they
- |( u5 y5 U/ r6 H% n! Ddecided to put the baby in a separate bed, and the5 E) B0 M  m0 J$ o. F! l: Q
father was not hugging him with bare skin and had$ v* n  |6 M5 k& o- T
been using protective clothing. A repeat testosterone8 |& _' h+ X% p' M& ^: g
test was ordered, but the family did not go to the
0 {$ O1 Y( k, k9 ?8 \laboratory to obtain the test.- h: [6 L, Q1 e% f  a
Discussion
: L; h- W  I( l$ c3 w! b: O  GPrecocious puberty in boys is defined as secondary
. P! k6 A+ _- p) Q2 t8 ~& csexual development before 9 years of age.1,4
6 \$ J4 o: r5 f, uPrecocious puberty is termed as central (true) when- j! f* a5 n  J4 X
it is caused by the premature activation of hypo-- K  O4 p$ o: r6 n) p9 }4 U- Y
thalamic pituitary gonadal axis. CPP is more com-
0 M% y& |$ B: I3 M) Gmon in girls than in boys.1,3 Most boys with CPP3 j/ |; Y, a. i7 J3 P# S
may have a central nervous system lesion that is
! {1 p% }; _% s  w6 \responsible for the early activation of the hypothal-/ _8 o6 B3 M4 i: A
amic pituitary gonadal axis.1-3 Thus, greater empha-% b0 Q; }2 o. A8 z
sis has been given to neuroradiologic imaging in
+ O3 n- J  E' `$ d8 Qboys with precocious puberty. In addition to viril-
$ _( i" |* ~8 l2 I/ q2 E/ `ization, the clinical hallmark of CPP is the symmet-! c5 G& q9 C' m; G9 X
rical testicular growth secondary to stimulation by
  j1 e5 L. r. i) ?. O$ Y6 Zgonadotropins.1,3
( {+ v& N+ v" ~; f- xGonadotropin-independent peripheral preco-. k" w6 q7 _7 v, y# Z9 ]
cious puberty in boys also results from inappropriate
' e# _6 k+ E: {& T# randrogenic stimulation from either endogenous or" _% L1 b* d9 z% R
exogenous sources, nonpituitary gonadotropin stim-
! C1 ~' I/ x& I% e7 Vulation, and rare activating mutations.3 Virilizing
7 l7 @# W8 G5 M# J( Acongenital adrenal hyperplasia producing excessive
6 S( k2 D( i- V/ ^2 B2 i5 Aadrenal androgens is a common cause of precocious0 G9 B. d+ z8 b# g( l
puberty in boys.3,4
- @) p# U, q! Z8 K8 `1 Z6 c% s0 m8 TThe most common form of congenital adrenal
6 m: l* }) t" Y2 m+ {hyperplasia is the 21-hydroxylase enzyme deficiency.
4 g# w3 a1 I3 A" j5 D1 X2 uThe 11-β hydroxylase deficiency may also result in
- c8 h: W; G2 D6 rexcessive adrenal androgen production, and rarely,8 J+ N' W3 f8 b. E
an adrenal tumor may also cause adrenal androgen
- K! l& M* W0 A) ]excess.1,3
. ]# G6 y6 {) G- ]# s3 `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 D- @* n2 b+ s5 p4 J; L# N0 s
542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 [2 I) ~0 `/ h5 ?) |* a
A unique entity of male-limited gonadotropin-
/ Y6 w- m* x1 p$ f! E. z% M! jindependent precocious puberty, which is also known
" e5 [2 u2 J2 j' A" g% G; ^as testotoxicosis, may cause precocious puberty at a+ C8 q& ]5 J$ b$ N5 y
very young age. The physical findings in these boys
* I" ]& Y# d6 W4 i  Twith this disorder are full pubertal development,
$ J" q- }& o% ]9 \* N; ?including bilateral testicular growth, similar to boys
$ p% Y7 P3 T1 V' ]0 ?with CPP. The gonadotropin levels in this disorder
& F. \) q- f9 Oare suppressed to prepubertal levels and do not show  N/ f! P2 [2 y! R2 K" q
pubertal response of gonadotropin after gonadotropin-
/ }# X9 B! C* z4 p) Greleasing hormone stimulation. This is a sex-linked
6 Z# [; b) {6 U- ^1 `autosomal dominant disorder that affects only
' k; s$ Z$ M0 H+ u4 x" o" \males; therefore, other male members of the family
* i) [4 V) q: a8 P* D1 Imay have similar precocious puberty.3( [+ N( X/ ^' V3 D" A9 s
In our patient, physical examination was incon-
$ m9 e& ~. g4 u' Z1 Rsistent with true precocious puberty since his testi-' V4 Y7 ^3 Q6 x, ]  ~$ h$ J
cles were prepubertal in size. However, testotoxicosis; Z. q$ A7 P" W8 ^+ _. N: Y1 `% ^
was in the differential diagnosis because his father; Q$ g: ?& e1 e# `; s% ?* `) o; N
started puberty somewhat early, and occasionally,
- i* w, K0 b! m" U6 b& ftesticular enlargement is not that evident in the9 N3 R' S# C1 N$ G
beginning of this process.1 In the absence of a neg-& ?1 X+ n0 t  n( h% J) A' j: n
ative initial history of androgen exposure, our. y9 S. J  e7 P& J: g1 ^3 W* ?
biggest concern was virilizing adrenal hyperplasia,
/ e- ?% A8 _) Q* Weither 21-hydroxylase deficiency or 11-β hydroxylase
$ i3 s+ @1 w9 ^) Fdeficiency. Those diagnoses were excluded by find-
$ M+ ]: ?" d. e2 U  King the normal level of adrenal steroids.
$ N# h) d3 Y- f$ r6 nThe diagnosis of exogenous androgens was strongly, w2 F0 Q% d# ~: l0 S
suspected in a follow-up visit after 4 months because
" |. ~6 w& m0 ?  Dthe physical examination revealed the complete disap-8 I" X. ]+ V+ i3 r$ y
pearance of pubic hair, normal growth velocity, and$ a0 ]+ O9 Q0 P5 @1 K
decreased erections. The father admitted using a testos-( C) I& e  K1 `& L  d
terone gel, which he concealed at first visit. He was
% I: ^/ w3 j% k) x+ }! n4 cusing it rather frequently, twice a day. The Physicians’
4 o1 E5 v$ b1 ?- eDesk Reference, or package insert of this product, gel or
; L+ s, `  j" A9 zcream, cautions about dermal testosterone transfer to0 Q" I- {0 z# ~- V9 N$ G" D9 M# b) n
unprotected females through direct skin exposure.
' _8 u' E- B0 `9 gSerum testosterone level was found to be 2 times the
3 s9 q& V" ~( y( Tbaseline value in those females who were exposed to" B7 y7 q7 ~6 [2 B# k8 ]. B
even 15 minutes of direct skin contact with their male
6 u+ X4 I! ~9 i3 y/ Q& B) u" vpartners.6 However, when a shirt covered the applica-
3 ~% e2 f$ ~, y; M/ ltion site, this testosterone transfer was prevented.
; S9 ?0 o- y8 v  C% k$ SOur patient’s testosterone level was 60 ng/mL,
' U$ H! ^- D( |. }5 owhich was clearly high. Some studies suggest that
9 R& h1 l) U* R/ V$ odermal conversion of testosterone to dihydrotestos-. Q- G) n9 n5 s/ y" V
terone, which is a more potent metabolite, is more" m( U4 i4 L1 n5 c( P# Q
active in young children exposed to testosterone
% `* B" B& s+ a7 Iexogenously7; however, we did not measure a dihy-' t# q1 u8 {8 t$ z% E. l% z
drotestosterone level in our patient. In addition to& p! B- ^2 \0 f" d# @& |) J
virilization, exposure to exogenous testosterone in
7 w' |2 `# u. d& ]  b, Mchildren results in an increase in growth velocity and
" ~8 b. c0 p3 j* @6 }3 Dadvanced bone age, as seen in our patient.# [# H; S( g' T  o; W) h, k
The long-term effect of androgen exposure during3 S. V5 r) j, R4 ]# Z7 H1 z- i
early childhood on pubertal development and final
  F. q' h' B2 Y) r" M/ |  c5 T/ Vadult height are not fully known and always remain
: S& x& u1 b0 f8 a2 x' ga concern. Children treated with short-term testos-
! J1 z, y! ?4 c& iterone injection or topical androgen may exhibit some, |) ?2 r3 H+ o1 v
acceleration of the skeletal maturation; however, after" Z" ^1 N3 m9 c
cessation of treatment, the rate of bone maturation
) |, h; j6 \. r- A' r: ]% Ldecelerates and gradually returns to normal.8,9
+ Y; Z2 J8 [+ N- `0 M5 y8 mThere are conflicting reports and controversy3 Q$ t: ]$ f7 z8 c$ ^7 A/ v
over the effect of early androgen exposure on adult
& @% K8 }: e" Hpenile length.10,11 Some reports suggest subnormal0 G( L% X; a" d7 n$ h' u9 `
adult penile length, apparently because of downreg-5 h: o( v; a/ r- {( n' d
ulation of androgen receptor number.10,12 However,( c7 t6 T2 S+ Y4 d- Z5 f* l, p2 F8 @
Sutherland et al13 did not find a correlation between
! M" Z! b) _/ o: G' Z" F1 Uchildhood testosterone exposure and reduced adult3 f. |7 T0 `: U  G# ^! b* R3 }# K
penile length in clinical studies.
- i1 A" d/ o6 t) T- iNonetheless, we do not believe our patient is
! ?- c1 s, i6 Egoing to experience any of the untoward effects from
, }6 C  ]& G, ^% ]testosterone exposure as mentioned earlier because
+ x2 e* Z8 z0 k- f, V9 w1 V, k; n5 |6 m6 Zthe exposure was not for a prolonged period of time.
0 i/ H7 r3 G5 V9 \Although the bone age was advanced at the time of
! T  u4 `2 X# ^$ F1 {+ E( p0 adiagnosis, the child had a normal growth velocity at
2 I+ }! y9 @4 zthe follow-up visit. It is hoped that his final adult4 _* c: g: R8 M2 e& n7 \  c/ Q1 k
height will not be affected.
5 `, b2 E8 H7 {2 ~" tAlthough rarely reported, the widespread avail-3 a5 ?" S0 J+ E, i. `* H' O
ability of androgen products in our society may$ M' u% w& k* b1 A
indeed cause more virilization in male or female3 @9 {0 D% f. p: }2 g' ?
children than one would realize. Exposure to andro-
% b' T8 h6 D7 B% T, t/ v; Wgen products must be considered and specific ques-
! @5 l- P" z1 A% {, xtioning about the use of a testosterone product or  n& B# E9 @4 b" D7 o
gel should be asked of the family members during. z* B1 a: U& k, W( k
the evaluation of any children who present with vir-
# |* n9 \3 z9 {" L% filization or peripheral precocious puberty. The diag-, f! D# E% w/ f! @- v
nosis can be established by just a few tests and by
& Q5 L( a( n( p7 nappropriate history. The inability to obtain such a2 _5 ^% A, n6 K  L1 @6 J
history, or failure to ask the specific questions, may" e" A8 Q# J7 C/ b5 f$ d0 o4 u
result in extensive, unnecessary, and expensive
& s4 H8 Y" `9 K" M) p3 a$ sinvestigation. The primary care physician should be
2 y% q( Q5 q/ M/ Z/ r* C/ ~aware of this fact, because most of these children3 w9 b" R" Q1 w8 |0 o
may initially present in their practice. The Physicians’
% W4 `5 Q3 V) Y: r' WDesk Reference and package insert should also put a
1 y( H) Q# m$ X8 fwarning about the virilizing effect on a male or; l. G3 i% d* v
female child who might come in contact with some-
, E* A' p7 Z$ J) p& Xone using any of these products.# U- n6 `# I! J  @7 B* R
References
1 V' A& o( N, b2 N8 W1. Styne DM. The testes: disorder of sexual differentiation
; \% Y: ]2 |. B4 a% p, hand puberty in the male. In: Sperling MA, ed. Pediatric4 F7 |1 d; V8 ]$ W# L& R
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 S5 n" ^, H2 z$ ~# V
2002: 565-628.9 i/ F  a$ u; U0 Q3 P& }
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 [  a- ^+ i0 ppuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old+ j% o7 [; |9 y  B1 d; ~" i
Boy Induced by Indirect Topical
7 I. x" Y2 Z% dExposure to Testosterone
7 Q, U% m9 c$ s4 E, @% ySamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& s9 }8 N3 A  A" q8 V
and Kenneth R. Rettig, MD1
! p- k0 Z# y! zClinical Pediatrics
! @$ L  r* Q( @. I) VVolume 46 Number 6
2 M! b  r5 J" G) E8 NJuly 2007 540-543
% Y7 q8 s1 F' m© 2007 Sage Publications
* J! F! D% r: s10.1177/0009922806296651( @2 `, r: k& A: i3 k
http://clp.sagepub.com
0 A0 R* e" ~- {hosted at
" X* O& `  X! k; `http://online.sagepub.com
" R4 Y, `- c6 q8 C! DPrecocious puberty in boys, central or peripheral,, a) c, y  k# m0 \- l
is a significant concern for physicians. Central
8 T' g# R6 b  ~7 ^4 Yprecocious puberty (CPP), which is mediated, k9 G6 c3 s: I+ K5 \! C4 o
through the hypothalamic pituitary gonadal axis, has0 Y  v& Q1 v' F; V5 W" C& \
a higher incidence of organic central nervous system) {* x% P- z! V" n) @% S' @
lesions in boys.1,2 Virilization in boys, as manifested
5 Z5 K9 ~  z5 S& Gby enlargement of the penis, development of pubic, _4 _( D* c+ U' d
hair, and facial acne without enlargement of testi-3 G! y. m" {4 Y/ l- u
cles, suggests peripheral or pseudopuberty.1-3 We
$ u% \# P4 J. C) Yreport a 16-month-old boy who presented with the! l! h) o4 O: v" r+ |! b
enlargement of the phallus and pubic hair develop-3 N9 E- b" G6 l
ment without testicular enlargement, which was due
: u& c5 J/ m* u' z% |to the unintentional exposure to androgen gel used by
! |( b7 L9 o3 v8 o$ f+ C9 S, Q0 dthe father. The family initially concealed this infor-" \3 @7 G- u  v. r" Z% r9 ]7 X0 y
mation, resulting in an extensive work-up for this  |  Q! [' e! a8 \! k* }* Y0 |5 L
child. Given the widespread and easy availability of1 ]0 S% r8 ^1 n  d/ g* }( M- \
testosterone gel and cream, we believe this is proba-
8 m9 E& P/ X. K. F* e0 M4 vbly more common than the rare case report in the
0 e5 a/ |# E/ w% P0 j3 eliterature.4
$ I, n1 [6 e! ?, I. EPatient Report5 I9 @  l- ~: H- P+ M9 z/ G6 D/ O
A 16-month-old white child was referred to the9 D  \( U/ l* N( K1 |# R
endocrine clinic by his pediatrician with the concern
8 w( S3 N, A' C  Eof early sexual development. His mother noticed( [+ l7 G# c1 \' l
light colored pubic hair development when he was5 `- A9 Y+ ]' B( O& G+ k# M
From the 1Division of Pediatric Endocrinology, 2University of  P" m4 x3 p. U& R: |
South Alabama Medical Center, Mobile, Alabama.
! _# L' g) d, S5 g6 ^0 lAddress correspondence to: Samar K. Bhowmick, MD, FACE,: _8 q; |( A/ {: x
Professor of Pediatrics, University of South Alabama, College of; Y3 C; f4 L3 I( T. n5 \
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
" @) J( j" j1 Y) fe-mail: [email protected].
' {, v0 g3 h8 Kabout 6 to 7 months old, which progressively became; W! Z4 W2 l  `
darker. She was also concerned about the enlarge-
8 p" x0 J* r2 K& `" Bment of his penis and frequent erections. The child0 h: Y/ d# o$ \
was the product of a full-term normal delivery, with
8 |" y4 a6 f9 u6 g% k1 Qa birth weight of 7 lb 14 oz, and birth length of
: p+ v, K+ @$ S6 K20 inches. He was breast-fed throughout the first year
; o. [. `5 ?* J0 f3 v0 ?: rof life and was still receiving breast milk along with: x, L- ]* i7 w, Y
solid food. He had no hospitalizations or surgery,& v, z& D5 Z1 r! ?
and his psychosocial and psychomotor development8 k. k" a! b) G' {' Z
was age appropriate.* O2 g( X9 d2 ?7 n4 P; C
The family history was remarkable for the father,
3 k% x7 T" R7 T2 k: G) J9 o- n. x2 Lwho was diagnosed with hypothyroidism at age 16,
7 J( F& W( F0 p  E+ W" }# U+ s; V9 xwhich was treated with thyroxine. The father’s) F9 \4 a1 P# M
height was 6 feet, and he went through a somewhat  \/ g+ G  t/ m+ G2 |
early puberty and had stopped growing by age 14.$ C$ X. z+ a! s. O6 p* r
The father denied taking any other medication. The! ^0 Q4 z/ M6 K) C: y7 k. i  M
child’s mother was in good health. Her menarche0 F' g2 K! ]0 Q& a" z
was at 11 years of age, and her height was at 5 feet% r7 m9 X! T' c' T! _
5 inches. There was no other family history of pre-, y* r# i- Y5 X
cocious sexual development in the first-degree rela-
1 C5 \) C- P/ x/ M8 \5 @! ~9 Dtives. There were no siblings.
. a1 u3 a9 ]" O% rPhysical Examination  F$ T8 a& E2 S4 N% }& \4 R. _
The physical examination revealed a very active,
( ^- r8 r. o( S6 ?' ?playful, and healthy boy. The vital signs documented! G3 \/ J  J4 i0 l, M0 ]  H5 F, n' Q; _; u
a blood pressure of 85/50 mm Hg, his length was
* M+ I6 n) F9 g0 M8 K  _$ |5 I90 cm (>97th percentile), and his weight was 14.4 kg  p* s* q# Y. I
(also >97th percentile). The observed yearly growth  g. b- t- Z& W
velocity was 30 cm (12 inches). The examination of0 ~) j, m6 B; ]  R
the neck revealed no thyroid enlargement.
- _% [3 \: M) f( C& q  E2 C6 GThe genitourinary examination was remarkable for
4 M' W* o$ n! J) ?5 yenlargement of the penis, with a stretched length of
4 `  P; m& h, v8 cm and a width of 2 cm. The glans penis was very well: Y' Q0 }; p# r; B
developed. The pubic hair was Tanner II, mostly around# t+ s" C* l* ]/ d
540# T4 u0 s- i: }: }* a4 ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- d" e/ P8 N' w- j- [. {* ]# Hthe base of the phallus and was dark and curled. The- Y- q) P' D% D; r, Y
testicular volume was prepubertal at 2 mL each., F3 p" z6 }+ L* w, A
The skin was moist and smooth and somewhat1 T. o& m+ b1 H$ c4 L
oily. No axillary hair was noted. There were no  @" p, U5 ]+ x$ z* E: |+ ?
abnormal skin pigmentations or café-au-lait spots.
. I4 d# b9 b6 W% L7 `( K  kNeurologic evaluation showed deep tendon reflex 2+' p0 h) Z' T0 @' B
bilateral and symmetrical. There was no suggestion* C% J3 \; |$ v$ a4 H, M4 x
of papilledema.$ [$ |) u3 i" a' s
Laboratory Evaluation
- Z& i: y3 @) Q4 LThe bone age was consistent with 28 months by# ?! C$ r5 D4 C
using the standard of Greulich and Pyle at a chrono-
, e# K3 E) R7 c* c7 N0 Clogic age of 16 months (advanced).5 Chromosomal
& m* K* I# d6 Xkaryotype was 46XY. The thyroid function test" Z  ^, G* E0 t8 l3 W) a
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
. B" E' s7 J$ z2 n- r) }; t! Zlating hormone level was 1.3 µIU/mL (both normal).
6 B* g  R! V/ B' \; ]. fThe concentrations of serum electrolytes, blood
, Y, [; }; f( A4 P, ?urea nitrogen, creatinine, and calcium all were6 t' ~6 b' l* D  f' B, R
within normal range for his age. The concentration
1 ?2 x* \( p$ yof serum 17-hydroxyprogesterone was 16 ng/dL' t# S* P8 A: k: k$ ^$ W$ L
(normal, 3 to 90 ng/dL), androstenedione was 205 e* w' G( C8 _- V1 R  r
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) }0 L7 [6 h* h/ d
terone was 38 ng/dL (normal, 50 to 760 ng/dL),, r7 e' E9 L3 q% t7 a. P  p) u6 v
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ I5 `* _2 g  H2 p& F49ng/dL), 11-desoxycortisol (specific compound S)
# f- f8 C, G" T& a0 ?was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  y  L. A+ s  i* q9 p$ a
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 X0 |6 M. u% h' Otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),: r. \4 {, ^0 x$ P
and β-human chorionic gonadotropin was less than: J9 H- z3 n8 w8 `2 C
5 mIU/mL (normal <5 mIU/mL). Serum follicular
. a5 h* c( \4 M! `' Wstimulating hormone and leuteinizing hormone; x' Y) |5 T8 Z% {7 N% \9 X1 u) l
concentrations were less than 0.05 mIU/mL
# U# T; Y( N0 W  ?0 \5 R: h(prepubertal).
) j3 f# G. v# `The parents were notified about the laboratory, o4 S# D6 y5 @! U# x7 L
results and were informed that all of the tests were
: h7 ^0 h' w( S- J* Z0 I0 [normal except the testosterone level was high. The
9 Q+ D% A) `0 N' V% c2 @8 m+ D/ yfollow-up visit was arranged within a few weeks to
- [3 U5 r3 e* t$ k7 _8 K& ~5 t- |* Dobtain testicular and abdominal sonograms; how-' f: x* M, \8 X% D
ever, the family did not return for 4 months.7 m) A( c2 I% T- M& z/ t$ J
Physical examination at this time revealed that the9 t( D  U( r- W; B- W) p
child had grown 2.5 cm in 4 months and had gained$ O5 ~( A1 E* l4 ~. F9 q
2 kg of weight. Physical examination remained# Z; O3 ^! E' g: G1 k
unchanged. Surprisingly, the pubic hair almost com-8 _+ }) e! D5 }0 j6 ^9 K
pletely disappeared except for a few vellous hairs at
: Q4 W" ^8 Q1 j! K$ _the base of the phallus. Testicular volume was still 2
! O; ?- K" e: EmL, and the size of the penis remained unchanged.5 h* W% l2 l3 y7 G
The mother also said that the boy was no longer hav-+ |. L' j% x/ y4 i) C
ing frequent erections.
$ N9 }3 `4 a! M+ b1 M4 b/ a- [Both parents were again questioned about use of
& p- T6 M. C0 y1 G: }# D  R; I: Q" B7 |3 hany ointment/creams that they may have applied to
" d- A' L4 O% l* ~0 W5 S5 Wthe child’s skin. This time the father admitted the( V) |. w8 c  A6 p
Topical Testosterone Exposure / Bhowmick et al 541
. r2 ?" I7 R, i4 n) Guse of testosterone gel twice daily that he was apply-* n- c2 S% B: I  O/ r  ?- `4 J9 f
ing over his own shoulders, chest, and back area for1 Z2 S  X% z2 I* W: |/ P" [
a year. The father also revealed he was embarrassed5 d$ C0 m+ a: Z
to disclose that he was using a testosterone gel pre-9 B$ s1 w5 L; @/ U$ f
scribed by his family physician for decreased libido1 g  o; O- F( ~# m* a
secondary to depression.
, _( a/ p. q$ ~2 z5 {The child slept in the same bed with parents.
! x9 R2 w. T" m/ T: \The father would hug the baby and hold him on his
4 _+ D+ N4 N' D  Zchest for a considerable period of time, causing sig-$ D0 P, i5 P2 R, ~& d" I9 T
nificant bare skin contact between baby and father.2 C9 v2 V4 @9 D  S
The father also admitted that after the phone call,
9 [% ]' R9 M% H; J4 j. ywhen he learned the testosterone level in the baby
3 S5 p& C2 ]3 jwas high, he then read the product information2 m* j, R" i. l% k+ T7 d, ]0 V/ p
packet and concluded that it was most likely the rea-
% q' F& V2 Q) s4 z3 }5 z. G* ^3 D' |, uson for the child’s virilization. At that time, they8 y# d0 @$ x8 R0 R, N: p
decided to put the baby in a separate bed, and the
& \5 _4 P+ e7 C; Y1 f6 Tfather was not hugging him with bare skin and had8 a$ \' k6 ]" n1 {
been using protective clothing. A repeat testosterone' d) X3 @; i+ ^* Q( j5 ^
test was ordered, but the family did not go to the
% b1 w$ M0 Z' b; a" Zlaboratory to obtain the test.( G+ R3 d- Y- s8 @) B: J8 ~7 m
Discussion; C: g/ \! Y) G! L. V; h
Precocious puberty in boys is defined as secondary
; c- Q: J; n/ l; ^5 T8 ssexual development before 9 years of age.1,4
( N9 \, V4 z  u$ g% r0 s+ T" uPrecocious puberty is termed as central (true) when( {' n4 J6 }- |6 |+ B
it is caused by the premature activation of hypo-
3 ^0 [% V5 Q6 p# Rthalamic pituitary gonadal axis. CPP is more com-
% r( C; s$ A( Zmon in girls than in boys.1,3 Most boys with CPP
% X4 L: z3 R% lmay have a central nervous system lesion that is
6 j# O: s8 A1 \( R% ^3 r* gresponsible for the early activation of the hypothal-
; {9 T; V: O3 I4 @amic pituitary gonadal axis.1-3 Thus, greater empha-
- f) ?2 f7 ^$ Gsis has been given to neuroradiologic imaging in' ]- [% `9 F, v& @9 i& m/ C' A% q
boys with precocious puberty. In addition to viril-
7 t" @. B0 m( iization, the clinical hallmark of CPP is the symmet-
/ Z8 s% p- V9 H1 vrical testicular growth secondary to stimulation by
) G1 m9 |+ t" F9 e4 Pgonadotropins.1,3
2 z, W1 p; R( R; d! Y- bGonadotropin-independent peripheral preco-8 l! v. Z  n- M9 a8 h7 _
cious puberty in boys also results from inappropriate
" y5 A2 ^* Z7 U+ ]' }* wandrogenic stimulation from either endogenous or  i- Z4 V& c0 [: J2 A6 S# r1 R! n: A
exogenous sources, nonpituitary gonadotropin stim-0 i4 F  y" @6 {0 z- L: S
ulation, and rare activating mutations.3 Virilizing
& M4 \/ _$ Z, W. Fcongenital adrenal hyperplasia producing excessive
1 i5 P# j6 U$ t* d0 Zadrenal androgens is a common cause of precocious
' a2 ?0 m: L  o  H7 Q) [: m1 \$ T& {puberty in boys.3,4
' L3 k+ L! I* L5 W5 oThe most common form of congenital adrenal/ W. p" o$ C+ L- y8 \( C
hyperplasia is the 21-hydroxylase enzyme deficiency." e" i$ X: i, m5 a# a
The 11-β hydroxylase deficiency may also result in
) p  D1 |* B( j& \3 Bexcessive adrenal androgen production, and rarely,; ]7 c% E3 I. G
an adrenal tumor may also cause adrenal androgen
* E8 @+ Y4 y8 Qexcess.1,3
& k0 r( L8 h0 Z; o( z  `+ X+ F; hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  G" i$ ^# ]# W2 y4 I  A
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
1 z& ]* A0 R8 q0 [5 p- c; _, K: r  BA unique entity of male-limited gonadotropin-
6 d- D  U; Z( V  g) P# i; W; v% P+ Mindependent precocious puberty, which is also known
: c( q5 z/ S% B. S6 z1 u7 \as testotoxicosis, may cause precocious puberty at a* h, i; c1 j: U- l, d9 }* m
very young age. The physical findings in these boys& H/ R$ z5 G  l+ N. t8 x# k. z
with this disorder are full pubertal development,9 u9 |, X/ E* x7 Z0 k; r( A
including bilateral testicular growth, similar to boys/ k  |8 K) \' b1 @) d9 c2 r
with CPP. The gonadotropin levels in this disorder: t& S/ d: @2 c9 u
are suppressed to prepubertal levels and do not show
6 A% W5 K/ S# ^1 Mpubertal response of gonadotropin after gonadotropin-7 o% d5 }, b# n& K) [6 U
releasing hormone stimulation. This is a sex-linked
( p1 ]) G: T; rautosomal dominant disorder that affects only
# Y7 q$ i! K' j( fmales; therefore, other male members of the family
- {  J( P2 l  ?  X# j$ M8 d! @may have similar precocious puberty.3
9 l# ~" L$ a, U6 n/ G, GIn our patient, physical examination was incon-% a% J" k4 o& z1 V* ]# u
sistent with true precocious puberty since his testi-
7 ]' o+ y0 v- a8 W( e7 D) ycles were prepubertal in size. However, testotoxicosis
# T; x8 o( N$ m" u. K* |$ jwas in the differential diagnosis because his father
) W* @( l9 ]: f* L5 ustarted puberty somewhat early, and occasionally,
* ?  B. f/ b, wtesticular enlargement is not that evident in the
+ d$ O) X; S* w! X: Tbeginning of this process.1 In the absence of a neg-1 a/ h5 p1 w( H5 N, |2 k
ative initial history of androgen exposure, our8 k& u! [4 [/ X" t) C3 E
biggest concern was virilizing adrenal hyperplasia,5 @0 f' o( I$ U' g3 i& z: E
either 21-hydroxylase deficiency or 11-β hydroxylase
! t! f& z8 a2 l. O6 w) hdeficiency. Those diagnoses were excluded by find-
0 f) h3 p* \6 r; L+ Ling the normal level of adrenal steroids.  E- [) E- ^7 e+ A$ W3 y8 Y6 I1 t% @
The diagnosis of exogenous androgens was strongly% T1 d; r* M( V: s+ Y% E: H) q3 P
suspected in a follow-up visit after 4 months because
" u6 F$ m- G/ w4 V' m( e6 Sthe physical examination revealed the complete disap-+ @, q: l  a1 u, Y$ X
pearance of pubic hair, normal growth velocity, and
1 x1 Z8 w/ o8 a, w- O- J6 Odecreased erections. The father admitted using a testos-/ A# o$ R( C- ?" I/ x+ [0 I; M: [
terone gel, which he concealed at first visit. He was
; ?) `- Q; ^5 Y. I) _& }2 x( Eusing it rather frequently, twice a day. The Physicians’& O. F* k9 g4 R5 K0 H8 L! c" @1 f
Desk Reference, or package insert of this product, gel or
* [! a" e8 ~  m! Pcream, cautions about dermal testosterone transfer to  t4 \$ z2 t5 I4 L
unprotected females through direct skin exposure.
+ M7 s  r# W* p/ r- X5 h9 J# BSerum testosterone level was found to be 2 times the4 T9 ~* N  n( u+ t
baseline value in those females who were exposed to
% A4 F! K' m4 \+ F' K/ G. J+ p2 @even 15 minutes of direct skin contact with their male, K+ q/ w% \# T
partners.6 However, when a shirt covered the applica-
: ?% g1 g" [0 z/ q( |; {tion site, this testosterone transfer was prevented.7 d2 v0 E1 ~: Z
Our patient’s testosterone level was 60 ng/mL,
/ u2 m0 z2 @( q% Lwhich was clearly high. Some studies suggest that7 W7 R1 L' r/ q
dermal conversion of testosterone to dihydrotestos-
# F/ }$ W" V6 Y: S( p; o% q/ hterone, which is a more potent metabolite, is more) Q0 p- P  U4 `) S- ^3 B' r. ~2 r
active in young children exposed to testosterone. ?: g! ?7 Z9 q/ i" a5 K
exogenously7; however, we did not measure a dihy-; _  H/ U3 P, a$ L
drotestosterone level in our patient. In addition to
. P8 B/ [: H0 u! f# [6 Avirilization, exposure to exogenous testosterone in8 |+ ~0 T. Y% U/ M  `
children results in an increase in growth velocity and
9 B$ `2 p- L# u) b' N6 Yadvanced bone age, as seen in our patient.# x3 N; J$ M4 C+ ~7 W" ]/ S" f9 j
The long-term effect of androgen exposure during
) M- ?2 O6 ~' z2 v* q, wearly childhood on pubertal development and final- Z& c0 S5 |. K9 F
adult height are not fully known and always remain
; ~; X$ y7 f& ba concern. Children treated with short-term testos-/ Z! L$ X3 N" {, S
terone injection or topical androgen may exhibit some  D. X* @* G8 U
acceleration of the skeletal maturation; however, after
7 W. B1 D0 p5 Q) w8 Rcessation of treatment, the rate of bone maturation1 Q0 F( g  Q& N2 k9 x+ t9 q
decelerates and gradually returns to normal.8,9- H/ `/ U5 p/ ~6 o& Z7 X: c% g
There are conflicting reports and controversy
, }9 j, b2 i# V5 D& u6 Iover the effect of early androgen exposure on adult
, q! R5 S% ~3 J7 Q9 tpenile length.10,11 Some reports suggest subnormal
! L2 [1 D" v7 a4 D9 m0 eadult penile length, apparently because of downreg-
% K$ }* q! B0 H8 b* Culation of androgen receptor number.10,12 However,
" G7 `' z" u* jSutherland et al13 did not find a correlation between4 Z1 q2 K: \5 W
childhood testosterone exposure and reduced adult# w$ ]) G" r& f- I9 |  f# I) q% m) _7 [1 L
penile length in clinical studies.# r/ d" m7 S3 O5 V" D- [/ _! }
Nonetheless, we do not believe our patient is6 u, w; ^" V& g: E
going to experience any of the untoward effects from# n' K* w. ?8 p% ~( [* S
testosterone exposure as mentioned earlier because
( O* t$ O$ A* Q" n2 H/ Sthe exposure was not for a prolonged period of time.. Y% d- C/ D9 F2 N9 I$ v
Although the bone age was advanced at the time of- Y; P+ S# g& [8 g& m% o
diagnosis, the child had a normal growth velocity at$ b+ ]" x" |: W% A7 F
the follow-up visit. It is hoped that his final adult
5 c2 M0 m3 }+ i* R' p/ X, Hheight will not be affected.
1 ^, {& x7 K5 `: @Although rarely reported, the widespread avail-
5 A% S% e  a& |$ ~7 ]0 _) f  k8 mability of androgen products in our society may
. r7 Q: o! E' r* V. xindeed cause more virilization in male or female8 p9 C, c+ r8 n4 `1 v$ f
children than one would realize. Exposure to andro-. B: i, F8 {% ^* d
gen products must be considered and specific ques-4 ~, ^" K6 k8 P( T3 z0 ~
tioning about the use of a testosterone product or
8 e- ?- o' U2 V7 j+ [: k: L+ kgel should be asked of the family members during
( U1 O* h6 I6 x; I% lthe evaluation of any children who present with vir-
5 }) W# M: J# X+ Eilization or peripheral precocious puberty. The diag-
/ V* w: q! Y, f; O5 P3 D! K5 [, f: g) l' Anosis can be established by just a few tests and by. V+ r2 L' i1 `0 A" L+ Z1 U
appropriate history. The inability to obtain such a
9 i9 N2 j/ \$ c5 j1 r- \: H3 K( h6 ehistory, or failure to ask the specific questions, may9 P; ^" p- {% }4 R: N8 I2 I, K
result in extensive, unnecessary, and expensive0 R) b" v  }5 |" {) u
investigation. The primary care physician should be
& J+ C4 o! K1 x6 S4 B+ Z+ vaware of this fact, because most of these children$ H4 b; J- l+ s1 i2 w, q
may initially present in their practice. The Physicians’' P7 q" G5 M8 u% `  ~" a  i
Desk Reference and package insert should also put a
" e! P$ R) E. D" x4 }$ x& Jwarning about the virilizing effect on a male or
9 V0 A1 C& u2 J) }( Ffemale child who might come in contact with some-7 L8 i( Q( T- a2 s" f6 ^  D  `" Z- [% F
one using any of these products.
/ S; j" j) Z2 t9 O4 d3 n" DReferences( H6 k5 M: u% \+ F3 ?5 \! J- L
1. Styne DM. The testes: disorder of sexual differentiation
# r5 ?- `8 I2 ]' ~) Rand puberty in the male. In: Sperling MA, ed. Pediatric/ l- e4 E' U7 }4 ~
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. m" s) O5 }* t. u2002: 565-628.
; ?0 s" Y! a; j8 [  K9 g+ x1 x. s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% K, L/ Q4 U3 g
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
  r. o5 Z- O/ G9 Z
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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