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Sexual Precocity in a 16-Month-Old
* P5 w- J! L9 b6 S% `* w0 Q8 `Boy Induced by Indirect Topical
5 X: z+ o/ h1 y5 `& f" NExposure to Testosterone) U- L9 Y/ A' U7 e- W7 T8 R
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 l( q6 k* B7 b/ K
and Kenneth R. Rettig, MD1" a! A$ }1 O" {4 o+ R0 N( |
Clinical Pediatrics
$ L( R7 k( z4 d- b4 h6 P9 SVolume 46 Number 6. Z5 g9 \8 Z; w& r) _
July 2007 540-543
" C0 `; X+ f- W1 H" y) \© 2007 Sage Publications1 M' i4 j2 C( X/ Q) f* e- ]
10.1177/0009922806296651; `( b4 \7 j7 k9 w! M
http://clp.sagepub.com- t" ^: V) u8 U3 n
hosted at
( n( T7 R+ q& N3 C( hhttp://online.sagepub.com
( [9 `3 `+ x; K$ X9 KPrecocious puberty in boys, central or peripheral,
: I$ H2 ?2 c# \: v. ]is a significant concern for physicians. Central3 Y" {6 h( E6 m6 z5 W
precocious puberty (CPP), which is mediated" s" y6 }: y% s; Y) q# O. e7 w$ E
through the hypothalamic pituitary gonadal axis, has2 t3 U( r$ v! H1 g% N, }$ c9 T2 e) N
a higher incidence of organic central nervous system+ y3 }. W$ g$ K; p3 a3 F
lesions in boys.1,2 Virilization in boys, as manifested
9 f0 T) R; z( X3 k* N4 Hby enlargement of the penis, development of pubic+ P: u  J, v! x0 r- H2 _% u' F$ Y
hair, and facial acne without enlargement of testi-
/ O" u9 \, H. ~0 w3 j- O* z( dcles, suggests peripheral or pseudopuberty.1-3 We
5 {! A) Z9 f, |7 I) ], [% X5 Z& Zreport a 16-month-old boy who presented with the" N+ l: y+ g( u
enlargement of the phallus and pubic hair develop-
, q! W3 H* q4 a; S6 |( ement without testicular enlargement, which was due
( ]/ `, r1 F3 x. N1 X4 cto the unintentional exposure to androgen gel used by* }: p; n9 H! n9 N  T
the father. The family initially concealed this infor-
" P; N- O. b$ \) @. ?! H. D; R' Mmation, resulting in an extensive work-up for this& A) Q. r1 a. u8 j. F
child. Given the widespread and easy availability of
, _1 y( I' I4 ?6 T. x6 @testosterone gel and cream, we believe this is proba-1 P1 ~# _, b) Y' V& @6 p9 |- @
bly more common than the rare case report in the
. C3 [' P( I0 h+ Pliterature.4
: J+ Z4 i# m, V1 t) SPatient Report/ r6 G8 h: I  O. z& @
A 16-month-old white child was referred to the
, }( I( ]2 m8 T1 H& k; R8 O" Tendocrine clinic by his pediatrician with the concern
7 I# r" F. |# C- Cof early sexual development. His mother noticed0 W+ q4 }7 p0 e% ]8 p1 I
light colored pubic hair development when he was* S8 P. j3 j( X: h8 B7 }9 D/ t
From the 1Division of Pediatric Endocrinology, 2University of
7 V& @8 p# F6 f; RSouth Alabama Medical Center, Mobile, Alabama.
  i+ r  M0 k* CAddress correspondence to: Samar K. Bhowmick, MD, FACE,
# ?0 E* h& a; G. @- \: ]9 TProfessor of Pediatrics, University of South Alabama, College of
; @* o1 W" Y- j5 F) ~Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) t1 m( L# @/ P  k) G/ h; O& n: Pe-mail: [email protected].
( B, B6 X0 ?; U) S* K& f3 ~  sabout 6 to 7 months old, which progressively became
1 `! ]! Q. |: \! c; _. zdarker. She was also concerned about the enlarge-
0 n0 B, |. H- Q0 B& g* pment of his penis and frequent erections. The child+ @6 a! _+ f1 R' }  H
was the product of a full-term normal delivery, with) r, r) `* W6 U8 l6 B* P' p
a birth weight of 7 lb 14 oz, and birth length of. ^8 Q' J* d2 u# R4 @/ A, }! C
20 inches. He was breast-fed throughout the first year
9 @( c# h+ U: z- eof life and was still receiving breast milk along with; n, z6 W& {0 y
solid food. He had no hospitalizations or surgery,% e1 X- S8 o+ }4 j9 U( J0 H
and his psychosocial and psychomotor development
* P( T/ {5 s  M! }& Q" ]2 Xwas age appropriate.- @+ a" a/ O# `" F; b! m
The family history was remarkable for the father,
6 W* K+ A% W( Swho was diagnosed with hypothyroidism at age 16,
1 j3 |. I* R7 }' ?0 d# d4 N5 h/ z3 ^which was treated with thyroxine. The father’s$ B( s' M1 e; M, [9 t8 r8 V5 M& [
height was 6 feet, and he went through a somewhat
3 s  T& a3 m$ `% `early puberty and had stopped growing by age 14.
' A+ b' ~$ D1 }8 k# ?The father denied taking any other medication. The
1 r$ v6 H: O/ V' m9 {- ]) zchild’s mother was in good health. Her menarche' |9 e3 l5 i1 u2 P% p/ u
was at 11 years of age, and her height was at 5 feet3 A3 l" m5 f7 j. \3 G% H+ F
5 inches. There was no other family history of pre-
9 Q, e' C. Z5 d7 M; bcocious sexual development in the first-degree rela-
7 L, n3 a3 n7 ~* U9 stives. There were no siblings.5 [8 I8 B, s1 [$ K& I1 |7 _
Physical Examination
% }$ s$ k5 K# G0 @* GThe physical examination revealed a very active,/ l0 {0 `! N  @, L. s* @9 K
playful, and healthy boy. The vital signs documented/ W5 A5 D8 g. [) _% f8 c- e
a blood pressure of 85/50 mm Hg, his length was& `9 x3 B0 Z4 z  R7 G  ^8 W
90 cm (>97th percentile), and his weight was 14.4 kg" n1 C' E# _" f. K3 R: b0 K* |
(also >97th percentile). The observed yearly growth
8 q9 m0 y7 L4 i$ S2 {% D, H$ wvelocity was 30 cm (12 inches). The examination of
8 s2 y$ Q5 A5 Mthe neck revealed no thyroid enlargement.- l) K5 k3 \* H
The genitourinary examination was remarkable for
/ K; A# e9 c$ P/ i3 jenlargement of the penis, with a stretched length of4 X# ?/ G. N8 O" V9 ~2 D1 t8 P2 t
8 cm and a width of 2 cm. The glans penis was very well$ i" E; x" j: Y% M$ i0 i* S/ |$ I; v& R
developed. The pubic hair was Tanner II, mostly around
. y* {1 W8 P5 G540) g8 H* S" q6 w0 ^: I- N) c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; S( k# f8 Y9 d% d6 Q: n. n# p' z
the base of the phallus and was dark and curled. The1 l; K! I& S& G% D$ L: B) n2 o
testicular volume was prepubertal at 2 mL each.0 i3 S$ Q/ z2 j2 O; v" j
The skin was moist and smooth and somewhat9 t7 M4 S$ v: Q; Y. D
oily. No axillary hair was noted. There were no
: d+ t; v3 `. s% D: k) d* g( C; gabnormal skin pigmentations or café-au-lait spots.3 h- d- C: H' o7 R0 R6 }3 _
Neurologic evaluation showed deep tendon reflex 2+3 ]: a" J7 R. L
bilateral and symmetrical. There was no suggestion
$ u# b: }' c# {: ^5 V0 tof papilledema.
( R/ r. p3 x1 _# \; T/ i  qLaboratory Evaluation
4 H, o. I% W0 `2 l$ U. y; \! fThe bone age was consistent with 28 months by5 e6 o$ S* L0 B. X& R- Z) a4 l
using the standard of Greulich and Pyle at a chrono-
* M" {" L* R8 T, d* ylogic age of 16 months (advanced).5 Chromosomal
7 Z2 U3 n* F) l0 D2 Y6 j: u- T1 Tkaryotype was 46XY. The thyroid function test; O% k4 I. D+ x# N6 [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-# g( h1 C" a- R! {
lating hormone level was 1.3 µIU/mL (both normal).. b6 n  B& x5 `3 d( ?: I
The concentrations of serum electrolytes, blood0 z* V# k9 t* o% l3 d# n
urea nitrogen, creatinine, and calcium all were
7 l2 |& d4 {0 J* Bwithin normal range for his age. The concentration( m( n' f' y' y9 y0 Q$ D7 N. `
of serum 17-hydroxyprogesterone was 16 ng/dL# U. t  C+ {" n6 L( T
(normal, 3 to 90 ng/dL), androstenedione was 20
, v& U# e+ J% s& R) ]( c/ p; Ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
2 j  g5 s) x/ u1 C+ e! P: @terone was 38 ng/dL (normal, 50 to 760 ng/dL),; n2 D5 j; h7 I
desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 @* B8 L1 G; }( L: U' S
49ng/dL), 11-desoxycortisol (specific compound S); w8 S4 D' W# x. i
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
- q) n% T) m" B) z$ x; ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: [: y* a: V+ e& t* j# W
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ i- D* d5 A) t. _7 L# X& m
and β-human chorionic gonadotropin was less than
# f! I, C- q$ o! R0 t/ ]5 mIU/mL (normal <5 mIU/mL). Serum follicular
5 }" f" k: l, ostimulating hormone and leuteinizing hormone
. g/ t1 X5 v3 Z6 H2 \) p* Nconcentrations were less than 0.05 mIU/mL6 D: N/ I2 I+ ^# t  v; J- V) N
(prepubertal).3 o) W8 i9 Q, N! I2 g( f. M% A8 v* w1 n
The parents were notified about the laboratory
" ^9 [$ y% S6 n; x. E& Rresults and were informed that all of the tests were/ @4 e5 x8 Y" W: B/ k
normal except the testosterone level was high. The
# |8 a* R7 I+ N1 w( Z( lfollow-up visit was arranged within a few weeks to5 P4 X5 |' E/ e- Z: [, S1 c$ }  ^
obtain testicular and abdominal sonograms; how-
6 w2 [( g6 v& P' Qever, the family did not return for 4 months.
& m1 z. X& I8 |: P/ _+ L9 G0 vPhysical examination at this time revealed that the7 t; ^& U! t$ I- J$ ?* R
child had grown 2.5 cm in 4 months and had gained
- s) y4 W& o# o& v2 kg of weight. Physical examination remained
, X) \% K5 z% ?; |unchanged. Surprisingly, the pubic hair almost com-
- X( Q8 Q4 S6 z$ ^# rpletely disappeared except for a few vellous hairs at
% S! m1 x' ?5 D* h$ T& e( K: ~+ M* [the base of the phallus. Testicular volume was still 22 R/ U7 P/ m7 t8 E( q& t( A( O
mL, and the size of the penis remained unchanged.
# b1 U' t' ]  c) Q; wThe mother also said that the boy was no longer hav-6 }3 c/ d- i( B) H( a9 H
ing frequent erections.
: ]6 ^/ |% F& W2 S, m1 N% UBoth parents were again questioned about use of
% c  Q5 x. k9 k" @  r* ?  wany ointment/creams that they may have applied to9 v) I$ ~- o0 G; U) h0 t) y0 E
the child’s skin. This time the father admitted the; C, W; N( K. Z. D/ s( m" T
Topical Testosterone Exposure / Bhowmick et al 541
8 q% Y  i/ c* }  U: a; ]9 S' {5 Luse of testosterone gel twice daily that he was apply-
9 r( Q2 k% \3 M7 y2 k, N; z) ?ing over his own shoulders, chest, and back area for1 V- D) ?; s( D$ D( ?
a year. The father also revealed he was embarrassed9 Z2 E; E# g; b2 C! m
to disclose that he was using a testosterone gel pre-9 l. e' ]+ x8 h! ]7 G; c2 P
scribed by his family physician for decreased libido; o) {3 ]3 e) s7 J7 B
secondary to depression.
' ?4 F5 ]8 n2 m7 K/ JThe child slept in the same bed with parents.
& ~, Z# J. \$ z! ]! ?7 k& Z  gThe father would hug the baby and hold him on his
+ h1 e  R' w' Y" \chest for a considerable period of time, causing sig-
1 p( _$ O4 |; z; [. xnificant bare skin contact between baby and father.
4 G1 r* R( w! f4 Z# kThe father also admitted that after the phone call,% X( A7 J  u/ X' Z5 a$ n
when he learned the testosterone level in the baby
3 C1 P" @# z6 U7 D3 p4 |0 x- x- O4 `was high, he then read the product information
3 t4 Z" i, V: Y4 _  k. K; wpacket and concluded that it was most likely the rea-
8 y$ h. a2 U/ k9 k7 Fson for the child’s virilization. At that time, they3 r% b: V* T% l: V% H
decided to put the baby in a separate bed, and the
" c) q& }0 h$ D! _0 |) hfather was not hugging him with bare skin and had
1 X9 Q: @, x9 [. ^: ?been using protective clothing. A repeat testosterone% y4 V) {8 m+ |
test was ordered, but the family did not go to the
  ?% r5 [7 S6 u$ Olaboratory to obtain the test.
4 l+ G4 Y6 ^! {. i+ ZDiscussion
! x# X# v4 ?( _' g% O0 m4 lPrecocious puberty in boys is defined as secondary
* G- K- x2 I/ s  p# I" Zsexual development before 9 years of age.1,40 x2 S7 k% R4 b! {4 l' [* @
Precocious puberty is termed as central (true) when
: a+ |& D) o% P. Z; sit is caused by the premature activation of hypo-/ ~, s/ \3 ^7 U5 b1 ?" K! \' U$ P
thalamic pituitary gonadal axis. CPP is more com-
4 V" x0 T) ]; @# }, y' g' Imon in girls than in boys.1,3 Most boys with CPP
  E' {! ?* Y: O6 B* s* |may have a central nervous system lesion that is
  g# b+ I) _4 Bresponsible for the early activation of the hypothal-
: O& Y" q7 T. C8 o8 O* |amic pituitary gonadal axis.1-3 Thus, greater empha-
5 _' V/ |+ t- f" M. msis has been given to neuroradiologic imaging in
! w5 A6 ^# q" w6 v$ ^2 iboys with precocious puberty. In addition to viril-
7 a, H4 e0 t( ^% o- }% ]ization, the clinical hallmark of CPP is the symmet-
' `! m* j9 i5 s6 [rical testicular growth secondary to stimulation by
7 }7 o* Z: I* g  H; t8 [gonadotropins.1,3' ~4 E1 ~) e! C( u
Gonadotropin-independent peripheral preco-8 E6 o; O3 i8 z$ S' ~8 k
cious puberty in boys also results from inappropriate
8 O+ A3 E& i# \androgenic stimulation from either endogenous or
0 o0 f0 Z9 e, l! Wexogenous sources, nonpituitary gonadotropin stim-
+ x5 q5 h7 P; k0 d% t( [ulation, and rare activating mutations.3 Virilizing
/ I1 V% v$ V' y& A* ycongenital adrenal hyperplasia producing excessive
6 ]# H/ ~' K# @adrenal androgens is a common cause of precocious4 U. ?8 _/ P0 s2 d- h4 x# R2 X
puberty in boys.3,4
4 D, Y9 |$ Y* D* n$ ?& x  @The most common form of congenital adrenal
# S( R- w& m4 X# U' y) phyperplasia is the 21-hydroxylase enzyme deficiency.( B; F( Q$ e6 @6 l0 C; f
The 11-β hydroxylase deficiency may also result in
. p, C8 E8 H! ]/ w3 ]1 d8 dexcessive adrenal androgen production, and rarely,
! x+ g3 m5 x8 [1 h+ ]7 Can adrenal tumor may also cause adrenal androgen
" b$ }8 `- r& `excess.1,3+ G; S7 {8 Z4 S# V" _3 H9 g2 K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" a  r# h5 j( @% a* g2 _4 Y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 l4 O8 u3 h* mA unique entity of male-limited gonadotropin-
8 e$ G, i& j2 S4 t0 S6 gindependent precocious puberty, which is also known8 n( F8 z5 Z: P7 z0 A. P
as testotoxicosis, may cause precocious puberty at a
7 ]+ Y& A# `- u/ Qvery young age. The physical findings in these boys
+ _- N4 i8 y) {/ r6 m6 n& \6 u0 Zwith this disorder are full pubertal development,
7 r/ y2 u6 P) c, Z+ W+ ~1 xincluding bilateral testicular growth, similar to boys$ |8 A1 w$ E$ s/ ~& k  S/ ^5 E& k% m
with CPP. The gonadotropin levels in this disorder3 r) O3 |. u& Q! ?# n# P1 n4 J
are suppressed to prepubertal levels and do not show
) A7 e# M8 K2 p% h* H* U8 Vpubertal response of gonadotropin after gonadotropin-
. y, F4 B! `: v+ Z+ Nreleasing hormone stimulation. This is a sex-linked; d- x9 l& J% [% d1 n! n
autosomal dominant disorder that affects only9 r/ m% `5 d' o4 s; Y8 ~$ ?- W
males; therefore, other male members of the family$ r$ j$ f6 ?% _; C
may have similar precocious puberty.3
5 p) h: B1 |7 R5 f8 ~In our patient, physical examination was incon-& e; n$ E9 U' [0 W5 u% t
sistent with true precocious puberty since his testi-: H0 s3 L0 k+ s% a
cles were prepubertal in size. However, testotoxicosis
9 c) x7 i1 s0 q) M, o3 ^5 x3 Ewas in the differential diagnosis because his father7 h$ a7 H6 L1 U/ T! e- I9 H
started puberty somewhat early, and occasionally,, Y" O, ^  n+ T, @! v
testicular enlargement is not that evident in the
7 N& s0 P% L8 L) g9 y$ y. vbeginning of this process.1 In the absence of a neg-, Z- o& B, w7 \& i: E
ative initial history of androgen exposure, our9 J$ H8 K5 A9 ]8 ~  ]6 X. c
biggest concern was virilizing adrenal hyperplasia,
, [$ Y$ ~. N$ k2 J3 a/ K+ N& neither 21-hydroxylase deficiency or 11-β hydroxylase
" |* g+ d* g5 x, t4 D, J: E4 ?deficiency. Those diagnoses were excluded by find-' C$ _6 I9 ~- \1 y" N5 ~2 g, w$ f
ing the normal level of adrenal steroids.. e; i9 ]2 |) m( [+ ~9 q. @( ]
The diagnosis of exogenous androgens was strongly  |6 c$ X# P- j: B, y, W% N. v
suspected in a follow-up visit after 4 months because! c8 A0 @; O( `% C6 C
the physical examination revealed the complete disap-  C1 v2 L! m2 z/ ^+ ^
pearance of pubic hair, normal growth velocity, and
" v- S( e: t8 k3 g! a8 i" I' p& P  ?decreased erections. The father admitted using a testos-, {  d3 a* A3 {  C1 u; e$ y
terone gel, which he concealed at first visit. He was
1 I# V* U% ?. ]using it rather frequently, twice a day. The Physicians’
- |, ]5 ~  w" w, `Desk Reference, or package insert of this product, gel or4 y% c+ L1 |3 l; M) S" ^
cream, cautions about dermal testosterone transfer to
4 P$ F  Y( u+ m) p! t& f# Aunprotected females through direct skin exposure./ I# V2 {2 |% L/ ^
Serum testosterone level was found to be 2 times the0 d; m- |2 k* @% U; E5 [$ r$ q+ s
baseline value in those females who were exposed to
/ M. u$ X/ ?3 K8 D# A, ?even 15 minutes of direct skin contact with their male
. f5 \7 j/ x8 s# V$ ?  W+ t# }" H: X. Spartners.6 However, when a shirt covered the applica-
1 N4 |7 `6 O8 B: Vtion site, this testosterone transfer was prevented.
9 @3 Y) a' p; x5 HOur patient’s testosterone level was 60 ng/mL,
( s3 M- J1 b" iwhich was clearly high. Some studies suggest that
9 C' k, W6 F5 G  h1 @dermal conversion of testosterone to dihydrotestos-" B, V1 b: o7 |& K' i
terone, which is a more potent metabolite, is more
) q7 H9 ?* q; ~! B0 S$ l7 lactive in young children exposed to testosterone
$ v7 n4 s# _) W* G& q6 t) w+ Hexogenously7; however, we did not measure a dihy-
! R  |, Y! p/ z+ o0 c) j; R1 Bdrotestosterone level in our patient. In addition to
) P0 c) @: b6 q  K3 lvirilization, exposure to exogenous testosterone in8 ?3 l/ ~- N; U4 ^2 d( y
children results in an increase in growth velocity and- _& V5 i' F) I0 U
advanced bone age, as seen in our patient.
0 l' L4 K* j8 I5 q) YThe long-term effect of androgen exposure during, f; {( b3 f6 w; K
early childhood on pubertal development and final* A+ F( E9 k7 l7 F( j& H
adult height are not fully known and always remain
* T# q( B" H  j) Y# p0 ma concern. Children treated with short-term testos-
8 k  j  `4 j6 rterone injection or topical androgen may exhibit some
1 b/ Q7 c, q" ?: `6 B4 Eacceleration of the skeletal maturation; however, after. l& q4 j. Z8 s
cessation of treatment, the rate of bone maturation, w# q( L8 Y* Z5 b! }$ V" X- z
decelerates and gradually returns to normal.8,9
: b$ s# `7 ^4 f3 B) X& aThere are conflicting reports and controversy
# v9 s; M7 o  O# t% G4 P5 gover the effect of early androgen exposure on adult% F! Y6 @/ a) L5 X( [; O
penile length.10,11 Some reports suggest subnormal0 Z. I8 {/ [4 M
adult penile length, apparently because of downreg-
/ M1 U2 x2 m" i0 J4 N" l+ qulation of androgen receptor number.10,12 However,0 ~- d$ ^7 X' b9 ]: `6 h/ I
Sutherland et al13 did not find a correlation between
' P0 B, O" q1 `5 }childhood testosterone exposure and reduced adult
* @# v2 v3 f7 d7 G3 Y  \8 ppenile length in clinical studies.
: ~1 x! J2 N+ f' Y+ Z% ~1 VNonetheless, we do not believe our patient is
4 S4 \! i2 R/ D& l, Cgoing to experience any of the untoward effects from' R" ^6 }( v! P$ M1 Z
testosterone exposure as mentioned earlier because
$ O6 x  B) }/ ~1 b8 jthe exposure was not for a prolonged period of time.
" W) d' r+ i7 B5 f$ r! Q- kAlthough the bone age was advanced at the time of
, W+ ]$ k8 p& R0 J- X* u2 tdiagnosis, the child had a normal growth velocity at/ r( u: p1 Q3 @& [
the follow-up visit. It is hoped that his final adult
6 D4 U; \- M6 s4 gheight will not be affected." y. V1 u* f  `( i7 r5 j! p' F
Although rarely reported, the widespread avail-
+ V( z. p7 N5 Z1 ?8 u( {; Rability of androgen products in our society may
3 h2 g" o, c3 ]; Sindeed cause more virilization in male or female7 c, F" z9 k+ ~% S
children than one would realize. Exposure to andro-
) s! p9 E# ^0 K/ a0 v) sgen products must be considered and specific ques-
# W/ E9 c+ F7 |# M1 h7 _' a+ itioning about the use of a testosterone product or
7 N2 {6 j  f0 q' f9 ygel should be asked of the family members during
1 N; v: h% M8 o& i& X# W  _' Uthe evaluation of any children who present with vir-
! _( @1 \& g; j0 q" }* [ilization or peripheral precocious puberty. The diag-9 l% ?! h9 H# f! m& Y& v
nosis can be established by just a few tests and by! @0 s4 w2 z) g
appropriate history. The inability to obtain such a
4 c3 \1 ?. |* W# y, g6 Ghistory, or failure to ask the specific questions, may
, f4 X1 h3 L3 N) @8 r7 P7 bresult in extensive, unnecessary, and expensive
3 {& x1 f6 l( dinvestigation. The primary care physician should be
0 M; s% e" j) s$ ]7 S2 n7 h: Saware of this fact, because most of these children: u5 [/ }- N9 W. s' ~. G( ~
may initially present in their practice. The Physicians’
  F! {+ Z' J5 I' p6 ~Desk Reference and package insert should also put a2 d! Q& O  i1 h( ^
warning about the virilizing effect on a male or
' I# T4 y1 I3 k  S% \female child who might come in contact with some-3 g- O; b. b4 a
one using any of these products.
  h( Z/ P* V! h1 B/ q; Z8 uReferences* s) X& I* X& U8 I5 o& E7 h2 _
1. Styne DM. The testes: disorder of sexual differentiation, O6 T4 B, Z. W, k% ^7 a$ t! C
and puberty in the male. In: Sperling MA, ed. Pediatric) g6 n% m# P. s$ O& i
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 v1 m+ L0 k, h5 i8 {! w2002: 565-628.4 |$ g: l) D1 a$ ]. w
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 r: U8 w( \9 r; V
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old" W/ d$ V5 n" f8 J& M! a% R
Boy Induced by Indirect Topical
/ ^$ Q  Q+ G0 q! X, q0 n7 x' oExposure to Testosterone7 @0 i6 a# ^; f
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
- Q5 h; {5 q( @. A! ^2 Nand Kenneth R. Rettig, MD1
& P2 q; `# I) Q/ S8 P! mClinical Pediatrics
) c( b: h9 [8 o' s( @Volume 46 Number 6
! e5 t! J& C2 s% x$ }4 TJuly 2007 540-543" E$ N- ]5 r6 [5 F1 P) z* u
© 2007 Sage Publications
. p) c8 v( Z- S10.1177/0009922806296651  L3 ^/ ~3 I$ T& k  S
http://clp.sagepub.com" V6 N! s$ ?6 I2 n
hosted at
8 f/ K! V2 R# g. Yhttp://online.sagepub.com# L$ |: N. P! v' M
Precocious puberty in boys, central or peripheral,& D: j6 O: C* J' o) Q
is a significant concern for physicians. Central6 p$ ^1 }$ O/ R/ d: j
precocious puberty (CPP), which is mediated  T3 J# J- h; }6 w7 }
through the hypothalamic pituitary gonadal axis, has) w- G( q- S8 M4 \8 p) t6 ]. ?# w2 _' l
a higher incidence of organic central nervous system  `' ^, G1 z: X$ ~. x
lesions in boys.1,2 Virilization in boys, as manifested( d5 u, |  U# P% d" Y3 b
by enlargement of the penis, development of pubic5 q& d( K& j, u
hair, and facial acne without enlargement of testi-: X2 M: L2 S- ^3 D
cles, suggests peripheral or pseudopuberty.1-3 We
- C0 D8 ?6 F5 _, W/ j; K% Vreport a 16-month-old boy who presented with the
* ]; V! G8 _- `0 |enlargement of the phallus and pubic hair develop-9 R0 S" D# V5 U" f) Y% k
ment without testicular enlargement, which was due6 p. v& {: X; G% G
to the unintentional exposure to androgen gel used by
' {1 B  w3 v/ L& D6 `2 H6 Nthe father. The family initially concealed this infor-1 _9 P* I) S: Y4 f. v" K
mation, resulting in an extensive work-up for this
, y$ c- M) l- _5 pchild. Given the widespread and easy availability of( P& ~7 m1 w7 }' C& r1 d# k  r
testosterone gel and cream, we believe this is proba-
$ m& Q, H9 `  u1 D( ?0 Y' Jbly more common than the rare case report in the
) k4 j! `$ C+ p# E9 Aliterature.4
- M+ m1 G/ P: QPatient Report
, P# T+ v& c- N5 O' UA 16-month-old white child was referred to the
/ O# [' y- r! @. L8 B2 Hendocrine clinic by his pediatrician with the concern
1 R* F% q$ q5 ^of early sexual development. His mother noticed
1 z6 P/ e9 m  X0 u$ L8 glight colored pubic hair development when he was
9 A- E/ D9 x2 z& e  ]From the 1Division of Pediatric Endocrinology, 2University of
. d3 M5 R3 H" E' }- K, p8 uSouth Alabama Medical Center, Mobile, Alabama.
9 k% h1 H# X3 F7 h% NAddress correspondence to: Samar K. Bhowmick, MD, FACE,! U8 g  V- v0 O3 I
Professor of Pediatrics, University of South Alabama, College of0 V& X! K7 j$ ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 ~: ~) |: x$ I* s/ Q7 ~
e-mail: [email protected].$ u4 E* W' }0 B) N
about 6 to 7 months old, which progressively became# f4 O4 C8 G8 K: u; \# h) \
darker. She was also concerned about the enlarge-( I" ^* G6 ]6 u
ment of his penis and frequent erections. The child& b7 ]+ c* S! s: _$ I2 `
was the product of a full-term normal delivery, with0 O5 ]# d6 z! P
a birth weight of 7 lb 14 oz, and birth length of  \/ H( q- t) ~- I2 k5 P, Z/ U: c
20 inches. He was breast-fed throughout the first year
" @% C7 g, p+ q% e8 x9 Iof life and was still receiving breast milk along with& a- J+ e8 Y; n% `% ~
solid food. He had no hospitalizations or surgery,
$ o& v3 L# C/ G7 Sand his psychosocial and psychomotor development
1 j6 Q; l  R$ X' v1 }  W4 Mwas age appropriate.; Z7 i! e9 k! P; i9 @! Z* E
The family history was remarkable for the father,
  E4 [8 S/ {5 w& O1 G4 Dwho was diagnosed with hypothyroidism at age 16,
: [! K: _) k' e5 t# \which was treated with thyroxine. The father’s7 Z' n; H# C% L5 L+ M
height was 6 feet, and he went through a somewhat
- `; B8 ^$ k; \& x) d5 searly puberty and had stopped growing by age 14.
& f/ \: V6 I2 d4 u: YThe father denied taking any other medication. The( Z) M$ A$ i- _) t  |# ^) X0 X$ J% K
child’s mother was in good health. Her menarche' }8 |, {/ M7 n9 d3 C
was at 11 years of age, and her height was at 5 feet0 O! N5 s$ u' J/ \' m
5 inches. There was no other family history of pre-) P+ O7 H5 P' B
cocious sexual development in the first-degree rela-
: d! I$ Z$ Q5 F  n0 L9 G9 X5 |tives. There were no siblings.
% X% T* N* y- k" ~6 X, HPhysical Examination
( A# o5 c# c/ Z6 J$ ?/ TThe physical examination revealed a very active,, y& H8 ?3 ?0 z1 v1 u1 b
playful, and healthy boy. The vital signs documented. Z1 W0 O/ [" v
a blood pressure of 85/50 mm Hg, his length was# o8 O; d0 H2 f3 c  m
90 cm (>97th percentile), and his weight was 14.4 kg+ E3 p6 n, R+ t$ d9 _
(also >97th percentile). The observed yearly growth
% x' K8 H% y6 \) zvelocity was 30 cm (12 inches). The examination of
$ X4 l# G* u( ^; S8 y  Mthe neck revealed no thyroid enlargement.
' Y! M& `& ]4 o- EThe genitourinary examination was remarkable for) O2 r! E  W: s/ l$ X
enlargement of the penis, with a stretched length of7 W/ M" w# o4 v
8 cm and a width of 2 cm. The glans penis was very well
7 M: l- f8 Q/ L/ |$ Y' ^' }developed. The pubic hair was Tanner II, mostly around4 D- l% U0 w5 r2 M4 D5 r  H# h
5405 U1 Y- ~- n$ x& L
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( X; j+ o; n9 |( V8 W
the base of the phallus and was dark and curled. The! ~: e4 P1 z# |9 \, I+ o
testicular volume was prepubertal at 2 mL each.
* Q! u/ O' ]) O8 N# k- Y1 eThe skin was moist and smooth and somewhat# ]" f% j& O) d5 p1 c, D
oily. No axillary hair was noted. There were no. p+ R& W; r! r, }
abnormal skin pigmentations or café-au-lait spots.8 U. P' {! s5 R6 m4 T0 }# }7 y2 j; p2 \
Neurologic evaluation showed deep tendon reflex 2+
+ x- H0 p1 Z( z/ cbilateral and symmetrical. There was no suggestion
! o. J% r" r3 E" o9 _  v% `of papilledema., c4 ?$ \# x+ x; _& J: Q2 o
Laboratory Evaluation
  N% M4 R! \1 S0 j( ~) o/ T4 [The bone age was consistent with 28 months by9 f" M; s' ], e4 ]+ i9 O
using the standard of Greulich and Pyle at a chrono-
0 m; G/ J" }, B- {3 ?0 C& Blogic age of 16 months (advanced).5 Chromosomal
2 E% m% _/ J9 h0 |9 n( okaryotype was 46XY. The thyroid function test
' ^  L( ~, r$ b1 D/ N  p6 z3 Tshowed a free T4 of 1.69 ng/dL, and thyroid stimu-: u  ?0 b" T/ T7 l+ K- |6 e
lating hormone level was 1.3 µIU/mL (both normal).
4 t$ Z- _3 E2 A$ vThe concentrations of serum electrolytes, blood3 n7 h3 p. s+ C2 b3 h1 ?
urea nitrogen, creatinine, and calcium all were
+ c8 R; w2 ^" a, Z3 Y, |within normal range for his age. The concentration
% h2 c6 P' o4 B9 K) v! d5 z; Tof serum 17-hydroxyprogesterone was 16 ng/dL
+ b( b, i2 E: T8 {& n0 C(normal, 3 to 90 ng/dL), androstenedione was 20" X9 g1 T  T+ P& I& Z9 ^, L
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
* r( _% @! `9 ?& Y# sterone was 38 ng/dL (normal, 50 to 760 ng/dL),; f2 C. H2 N& X3 [
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
3 W, E% W' J, _# P) P* j/ \49ng/dL), 11-desoxycortisol (specific compound S)
& U' O3 j4 e5 Y8 }7 l. }2 ~+ l2 twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 o! P; S2 P/ P' q* Stisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 C* v" g# \" b9 S0 J
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 p2 q2 [) F5 X8 d
and β-human chorionic gonadotropin was less than7 h; F$ C% M" o$ l# A! k
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 H( |2 j& t2 E4 c$ g* o: C2 sstimulating hormone and leuteinizing hormone. |2 p8 d+ p% t1 \
concentrations were less than 0.05 mIU/mL4 t' J5 G1 B3 z4 ^7 t* m
(prepubertal).
; S7 n" K% S8 D! rThe parents were notified about the laboratory/ j* `( N! z1 g! a2 z; J2 U
results and were informed that all of the tests were
" g* F' |  l0 Q, B. {  z4 h  Ynormal except the testosterone level was high. The8 W' @5 S8 v+ V, V* v$ F
follow-up visit was arranged within a few weeks to8 D6 h- P, h( P! R+ \/ O' B+ E. J$ J
obtain testicular and abdominal sonograms; how-
' X+ n6 g; G3 H% X- w1 T" Xever, the family did not return for 4 months.5 a* t6 [, p, w1 M
Physical examination at this time revealed that the4 G" s& e4 c. \6 L. \
child had grown 2.5 cm in 4 months and had gained5 I, t: ]+ M  p5 A& a+ j
2 kg of weight. Physical examination remained
9 _- D) r: X# Cunchanged. Surprisingly, the pubic hair almost com-. r: @. V' }( W. v) v
pletely disappeared except for a few vellous hairs at
8 p7 V7 h! M9 Y, Sthe base of the phallus. Testicular volume was still 2- ?. \2 o* S' C
mL, and the size of the penis remained unchanged.
3 y0 l$ n5 E0 U+ U! oThe mother also said that the boy was no longer hav-
8 N- q$ j  D1 Ying frequent erections.
% i) s2 B; Y- j9 [" pBoth parents were again questioned about use of
; z0 E/ a# `; d" _any ointment/creams that they may have applied to
2 X  {, d# C0 Q% Wthe child’s skin. This time the father admitted the
+ m. K  t. h1 x1 TTopical Testosterone Exposure / Bhowmick et al 541
# _9 Z7 \# i# y1 t: |$ huse of testosterone gel twice daily that he was apply-$ }) v2 o6 M6 U" B/ h8 \' Z8 F
ing over his own shoulders, chest, and back area for% l7 e2 Z7 ~- v& K$ D+ k7 K$ w
a year. The father also revealed he was embarrassed# Q6 K) d/ }  S4 b; C% T0 q
to disclose that he was using a testosterone gel pre-/ `) z7 m) I6 y
scribed by his family physician for decreased libido
4 H  A$ i2 s/ e+ F9 W' p8 i- rsecondary to depression.% c; U- F( C9 I1 E+ d: u! n3 J5 E
The child slept in the same bed with parents.6 {- U2 q9 u4 w4 H
The father would hug the baby and hold him on his
9 k+ b# J; p" F2 q! vchest for a considerable period of time, causing sig-  W! P' s( U1 D$ e" J5 G
nificant bare skin contact between baby and father.
% Z. _; e- C5 R, {# aThe father also admitted that after the phone call,. R1 M, W! z6 t" h: s
when he learned the testosterone level in the baby( Q; c" W* M: V. c- S
was high, he then read the product information
) h1 z, S- o" _packet and concluded that it was most likely the rea-& t/ {) W, t7 ]+ ]
son for the child’s virilization. At that time, they; \: ]' _) a8 f! R/ V7 M
decided to put the baby in a separate bed, and the2 E* b8 ?; p5 S% B0 Y; E
father was not hugging him with bare skin and had/ y/ E  r8 T4 k# P. `
been using protective clothing. A repeat testosterone
' W( [8 [3 m; i, Atest was ordered, but the family did not go to the- n+ Z7 D: w2 I" I0 Z! k; I
laboratory to obtain the test.
6 F2 I+ ^* t8 t! j# n& T3 L5 c! `Discussion  C' Z1 @  z/ A/ l- P
Precocious puberty in boys is defined as secondary6 M: b( {$ S4 }6 \: s
sexual development before 9 years of age.1,4# _! Q9 K: o- p4 f7 Y
Precocious puberty is termed as central (true) when9 D4 j2 w/ D( U- W& q5 J- W
it is caused by the premature activation of hypo-) L1 h7 X7 S3 m# N
thalamic pituitary gonadal axis. CPP is more com-
4 B8 G. o7 R- @4 z- R' Umon in girls than in boys.1,3 Most boys with CPP
( q' ~1 W. x4 q. l. v8 I1 n( y, r: hmay have a central nervous system lesion that is3 \: v4 c0 w3 q
responsible for the early activation of the hypothal-5 E* s/ T" J2 [* F6 R
amic pituitary gonadal axis.1-3 Thus, greater empha-
% f) o$ n9 Z) V, V8 nsis has been given to neuroradiologic imaging in
4 {. v: B3 P7 x6 H+ Z, ]boys with precocious puberty. In addition to viril-
4 r% N/ E4 Q' k) jization, the clinical hallmark of CPP is the symmet-( \! V4 E' B5 F$ ]/ d/ e( U' @) c
rical testicular growth secondary to stimulation by5 E) H2 g& d! @1 D2 g; }
gonadotropins.1,3
2 e  j8 ^- j# E: F9 jGonadotropin-independent peripheral preco-! W, w. r: _, z" B" a9 E
cious puberty in boys also results from inappropriate
/ j/ m- [- K2 i' F: Fandrogenic stimulation from either endogenous or. a1 A. o6 {+ N) a: D' A
exogenous sources, nonpituitary gonadotropin stim-8 T: ~$ e# t( J( @5 q2 u/ _* P
ulation, and rare activating mutations.3 Virilizing# K! p5 O  U, U$ s0 p1 P
congenital adrenal hyperplasia producing excessive
% p: ^5 {* x2 s8 z% T- s( x  radrenal androgens is a common cause of precocious3 ?! j6 j# g# ~& W$ w1 T, F% a$ @
puberty in boys.3,4
$ {; ^# ]0 E+ c: W; o. XThe most common form of congenital adrenal8 }- z  {: E- I3 d# }3 n6 ?
hyperplasia is the 21-hydroxylase enzyme deficiency.+ K1 f, K* O, b+ H3 q
The 11-β hydroxylase deficiency may also result in
0 L- M$ e/ e: e' Y" q8 X- ^excessive adrenal androgen production, and rarely,
( a+ A, u; i. _  Xan adrenal tumor may also cause adrenal androgen
5 }) U* H' M& T& {. }4 B" wexcess.1,3
2 n& \! p/ N& @4 V) ~. j  fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 I" U  e2 F* }4 \542 Clinical Pediatrics / Vol. 46, No. 6, July 2007, u8 B- E% E4 y; m
A unique entity of male-limited gonadotropin-
9 r( M+ b2 S+ }4 Z. [$ i. {independent precocious puberty, which is also known9 h2 w" g4 Y; }
as testotoxicosis, may cause precocious puberty at a6 s3 Q% k4 @( L6 f
very young age. The physical findings in these boys
- O: H6 `2 k4 z1 I- jwith this disorder are full pubertal development,
1 y& V: K* P) r, Q+ N  P3 s; o  Zincluding bilateral testicular growth, similar to boys
4 L1 C( L! \+ M' ?; c- Zwith CPP. The gonadotropin levels in this disorder8 p/ J, J: G9 |5 J1 h+ x! X
are suppressed to prepubertal levels and do not show1 H. U3 M% X: j" a3 ]- m( X4 e, ?
pubertal response of gonadotropin after gonadotropin-2 h6 `6 a5 J+ M! s
releasing hormone stimulation. This is a sex-linked7 _8 x) M5 ^4 }5 {$ Q9 Q6 l' Q  y
autosomal dominant disorder that affects only' [7 V' P/ l, p; z
males; therefore, other male members of the family& |( x3 Q- W  j7 o
may have similar precocious puberty.3: T) q- f! `/ ?; X' J
In our patient, physical examination was incon-* w9 [# N% a& l6 S" O+ `2 i& h
sistent with true precocious puberty since his testi-( v! c" Y7 L9 |
cles were prepubertal in size. However, testotoxicosis
$ k" @; m% G. i( |' p, O$ cwas in the differential diagnosis because his father
; S1 t! ?" \, G; P: cstarted puberty somewhat early, and occasionally,
# P. B" x4 F4 j3 p+ O' `testicular enlargement is not that evident in the
6 p3 U* B. J, ]) {9 U/ ?# Wbeginning of this process.1 In the absence of a neg-6 _+ F/ L- s: U
ative initial history of androgen exposure, our- l- s5 C* A4 {2 L1 T; }# ~8 x
biggest concern was virilizing adrenal hyperplasia,7 G8 L) S8 k* a/ L% _' Y2 {4 _
either 21-hydroxylase deficiency or 11-β hydroxylase! p, Y4 Z+ Q" m
deficiency. Those diagnoses were excluded by find-# w% q/ }7 C7 k* I
ing the normal level of adrenal steroids.% ~  q/ \' Q; g  a: g
The diagnosis of exogenous androgens was strongly9 `. d+ S! d+ v: L
suspected in a follow-up visit after 4 months because
! k$ ]* ^& U  [: C5 R& W- _the physical examination revealed the complete disap-1 \' ^' G! u; ]
pearance of pubic hair, normal growth velocity, and" }; p5 `* ?/ K: ]. s
decreased erections. The father admitted using a testos-; g. [: b5 f, E$ [) d2 P
terone gel, which he concealed at first visit. He was5 p+ O" B# z9 Q* M/ A+ R
using it rather frequently, twice a day. The Physicians’& C) s' V/ `3 p7 ~! v& S# [2 }
Desk Reference, or package insert of this product, gel or2 T* F% q8 d# s$ f
cream, cautions about dermal testosterone transfer to
+ ]. U0 L5 N7 p, H) c/ V/ Nunprotected females through direct skin exposure.: T3 g' d/ g% c
Serum testosterone level was found to be 2 times the
. X# R$ @% ]1 h" u  b1 lbaseline value in those females who were exposed to
& @( D6 j% k8 X' m7 v* zeven 15 minutes of direct skin contact with their male; d6 R) N2 c3 ]( l
partners.6 However, when a shirt covered the applica-
% S0 ]( _0 C" E1 W9 Qtion site, this testosterone transfer was prevented.
6 K2 X' c7 u. KOur patient’s testosterone level was 60 ng/mL,
. r/ S( X% b: |* q' S3 y/ M" U" Kwhich was clearly high. Some studies suggest that
% s4 B  u- E9 ?* g  ]7 _# z& Ldermal conversion of testosterone to dihydrotestos-. A& l% f) S. T4 O. ^0 X
terone, which is a more potent metabolite, is more
$ U( d/ \$ O, y5 s0 z; A/ wactive in young children exposed to testosterone. ~% ?! z- E- P8 `! s! ~8 m
exogenously7; however, we did not measure a dihy-
! S: Q' P+ F  ]drotestosterone level in our patient. In addition to
; U0 q' j9 R# ?" w' @virilization, exposure to exogenous testosterone in
% m$ V8 n% {! o3 [, U9 Schildren results in an increase in growth velocity and
- x4 j' B( @$ M  q4 f. w6 n# Padvanced bone age, as seen in our patient.
7 j6 \6 g0 N4 A; FThe long-term effect of androgen exposure during
7 V! b" L! c, w& y& searly childhood on pubertal development and final
. k$ d0 a7 S$ o& Vadult height are not fully known and always remain
" L9 w. B- V; p9 z( p, t2 La concern. Children treated with short-term testos-
+ P, f0 c' M. T( O. N1 p! q0 k7 Dterone injection or topical androgen may exhibit some! K6 R' V* G9 A' a
acceleration of the skeletal maturation; however, after& O9 R- n" o" ?9 ]- J' w
cessation of treatment, the rate of bone maturation
5 i4 H- u! q- ?) I  m& h2 idecelerates and gradually returns to normal.8,9/ C: B7 d6 {# g5 j: c8 e
There are conflicting reports and controversy
. o. g. [" B6 P3 q1 k/ cover the effect of early androgen exposure on adult8 D2 m" g- d- _
penile length.10,11 Some reports suggest subnormal9 J+ O0 h% X6 C- R& w' j: X
adult penile length, apparently because of downreg-  A# d  _& Z; N' c- o6 q
ulation of androgen receptor number.10,12 However,) M$ O! x( B: t  R/ V& b, _% K( {
Sutherland et al13 did not find a correlation between, M( T! {& P9 q& d
childhood testosterone exposure and reduced adult: X% _0 T( w# q; w/ j$ l7 `
penile length in clinical studies.4 b# W& ?1 P1 I9 r
Nonetheless, we do not believe our patient is
! J2 g) f7 o2 l9 P0 p8 l  K( Egoing to experience any of the untoward effects from
4 {/ ]) y0 D8 U* p7 Gtestosterone exposure as mentioned earlier because
  u0 q( J% X1 @' zthe exposure was not for a prolonged period of time.3 y5 r1 W( T( ]# u( }
Although the bone age was advanced at the time of
/ B* u( j2 f# M5 R0 F  z( [diagnosis, the child had a normal growth velocity at
* H0 z3 x% C$ L( ^# n" Lthe follow-up visit. It is hoped that his final adult# t0 f0 g7 T  y+ K
height will not be affected." ^6 R8 G0 B5 U  I5 |! s; C( j
Although rarely reported, the widespread avail-( X. b  a: Q$ ~) z$ w( Q  b6 l
ability of androgen products in our society may
. z8 a9 k) w* a3 q6 N0 yindeed cause more virilization in male or female( m$ L& U4 k* K+ p
children than one would realize. Exposure to andro-. J, B, x/ j: M7 L5 [3 f0 P
gen products must be considered and specific ques-$ b# B8 Q; L- x2 w8 C# t
tioning about the use of a testosterone product or
0 s& Z0 x- i: p2 R( x6 G( _* ?gel should be asked of the family members during! E4 e6 p1 \! f2 k: A
the evaluation of any children who present with vir-
0 X8 d1 X+ v& i; \ilization or peripheral precocious puberty. The diag-1 t8 `4 e' `+ \8 F, a, {% x3 T
nosis can be established by just a few tests and by  Q. h$ }2 d9 H) T
appropriate history. The inability to obtain such a
4 X+ D0 h# L& ?( zhistory, or failure to ask the specific questions, may
0 Z  J  B; _% J; U$ E4 c7 mresult in extensive, unnecessary, and expensive/ ^2 P) X' Z9 z
investigation. The primary care physician should be
2 c3 d. v, ^2 paware of this fact, because most of these children' ~3 x! A* b5 V
may initially present in their practice. The Physicians’
3 U  I( a& H' I) lDesk Reference and package insert should also put a
/ u) B; r. H! S: R# uwarning about the virilizing effect on a male or$ I0 R! S) J: i) D
female child who might come in contact with some-
# a8 R4 ?8 o; done using any of these products.
0 A3 A3 ]2 i( l" L1 J9 H3 A# HReferences
1 q# E' `/ l% S& @4 e% @1. Styne DM. The testes: disorder of sexual differentiation
, W. e5 G8 r6 @5 V) y8 U0 _and puberty in the male. In: Sperling MA, ed. Pediatric
8 J% p/ G- @; _, t' E% }4 AEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' f; w+ B4 O; B3 }2 X% H. Q, G: O2002: 565-628.
& i; d$ e0 @; ~/ l0 g3 F- N2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
5 ]" R0 K8 j0 v7 z! T. r+ fpuberty 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
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
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
' a- ]+ G5 Q8 @& V* ^
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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