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Sexual Precocity in a 16-Month-Old: B1 J7 U3 O# u5 }5 I$ L  g
Boy Induced by Indirect Topical* [2 C* k5 f7 a
Exposure to Testosterone
& L: }5 L% b* h% j' Y/ X, JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 o  l7 O* n' p# ]2 oand Kenneth R. Rettig, MD1. D3 e: P' K% K7 @. H
Clinical Pediatrics* X" ~8 d) p" m" e: ?/ m
Volume 46 Number 6
$ e% C  K/ X6 s- e  i# j: |July 2007 540-543+ N4 O$ {" C5 d" P
© 2007 Sage Publications
7 P0 z( L6 v; O, F" r1 @# d10.1177/0009922806296651% p' K5 L& E% R
http://clp.sagepub.com
, w" P. U* h6 @8 I" L  F: A( f% chosted at
5 p. W9 r0 f: fhttp://online.sagepub.com* I; n/ N. x6 [! C* _% e8 a! p
Precocious puberty in boys, central or peripheral,
4 t) a7 G$ I9 Y7 ]. jis a significant concern for physicians. Central& q! {7 h1 y% [5 }8 g
precocious puberty (CPP), which is mediated1 _( o% ?9 Z7 b- P- c$ s
through the hypothalamic pituitary gonadal axis, has/ g4 |1 V, t8 R+ w
a higher incidence of organic central nervous system
- x. R  h9 a/ E; Klesions in boys.1,2 Virilization in boys, as manifested4 c& n4 t1 w  [
by enlargement of the penis, development of pubic
8 v( e) I5 B: M( E0 P! t3 zhair, and facial acne without enlargement of testi-7 t& s% x4 p0 T% J$ @) k4 R# h
cles, suggests peripheral or pseudopuberty.1-3 We
8 Z% ?7 T. G+ V" m/ |& v2 e0 dreport a 16-month-old boy who presented with the
+ M" Y6 d- T. ^: O, genlargement of the phallus and pubic hair develop-# i" h4 y' n, O) {& u, a6 h' B
ment without testicular enlargement, which was due; o- v% P4 q2 i  }! u' S
to the unintentional exposure to androgen gel used by' `* A% B; ?- E5 ~$ j! E& W
the father. The family initially concealed this infor-
( z. S' w) c* q8 n( O$ ~2 D4 F8 q0 Nmation, resulting in an extensive work-up for this0 e7 h8 S+ s: F) u1 c
child. Given the widespread and easy availability of6 h3 e/ X: ~8 U0 Y2 F0 R! \3 O
testosterone gel and cream, we believe this is proba-
+ f) [4 u( h0 g) q- B, kbly more common than the rare case report in the  m. M7 [7 F+ h5 Z8 q
literature.4  B2 J7 Z' z: Z- q0 i. R' H. t
Patient Report
9 h* p1 d4 ], k5 q3 J% VA 16-month-old white child was referred to the3 c) c1 r! A. b- r. Q2 ]
endocrine clinic by his pediatrician with the concern8 X, {# Z* c. Z6 n1 q) s
of early sexual development. His mother noticed: Y1 v5 x5 w/ _  k: G
light colored pubic hair development when he was2 G) P( n% x* g1 h: h9 W
From the 1Division of Pediatric Endocrinology, 2University of& v4 g  [4 U9 M8 Z4 @
South Alabama Medical Center, Mobile, Alabama.
1 y4 h% p4 b0 ^  Z0 OAddress correspondence to: Samar K. Bhowmick, MD, FACE,* v6 z/ `" z3 b( i/ Y
Professor of Pediatrics, University of South Alabama, College of
# ?0 p: l0 \/ N7 pMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 u, _) I/ U) d( M* J8 r1 Le-mail: [email protected].
: A; m1 f* Q$ X" Y: K# b: \about 6 to 7 months old, which progressively became- e% g8 P* `2 a% d) `8 b
darker. She was also concerned about the enlarge-, e8 b) l6 ?+ x2 F
ment of his penis and frequent erections. The child
+ n! P+ B; @8 f( kwas the product of a full-term normal delivery, with2 r( y0 b5 M4 Y  L2 A# S
a birth weight of 7 lb 14 oz, and birth length of
: \2 O0 o( t1 C2 R' ?" W8 |2 F4 ]" J20 inches. He was breast-fed throughout the first year
4 Y  G( O4 [/ nof life and was still receiving breast milk along with
' U7 D7 J8 v7 u0 hsolid food. He had no hospitalizations or surgery,
5 X" p% D4 a* B0 M, m& g8 Qand his psychosocial and psychomotor development
0 P+ k! b9 q* z/ M# Z+ P! bwas age appropriate.& M. O" D- j6 L# p# a! X, E* i
The family history was remarkable for the father,* U& Y% D! F  J: {" E( l' o* ]
who was diagnosed with hypothyroidism at age 16,
6 B! y7 g1 u4 A! Q/ Y& ywhich was treated with thyroxine. The father’s
8 J. e9 f% F0 p. n' aheight was 6 feet, and he went through a somewhat
+ f$ w6 R* b+ w3 q+ {early puberty and had stopped growing by age 14.
2 K% g0 k7 w, H# ~' I0 y, k& RThe father denied taking any other medication. The! j  g5 l" d$ Q6 f' f1 t) U
child’s mother was in good health. Her menarche4 w/ J& v# k: v0 J9 `. K" n
was at 11 years of age, and her height was at 5 feet
/ `2 g; n' G3 D! @5 inches. There was no other family history of pre-
- Q! \6 q8 g$ h  `+ }) m6 O* Tcocious sexual development in the first-degree rela-
+ _/ n$ Y% ~% x; N3 d+ ~+ a" L- Xtives. There were no siblings.
# b1 Q  }/ D# PPhysical Examination
5 \8 p& e4 {5 n3 o# x  Q7 b# ]7 bThe physical examination revealed a very active,
6 I9 r0 h2 v/ D" I- P3 eplayful, and healthy boy. The vital signs documented8 O. Q; {& O% t) n" o* f- ^+ z
a blood pressure of 85/50 mm Hg, his length was
$ I# o1 _( Y3 N: k2 E6 u  v90 cm (>97th percentile), and his weight was 14.4 kg
; ~; }" ?5 _+ |: i6 E: M! W4 p" x(also >97th percentile). The observed yearly growth6 V# o# u* i; [
velocity was 30 cm (12 inches). The examination of- p$ h& C6 N5 F% ~- i
the neck revealed no thyroid enlargement.
' E5 p2 ^: g6 OThe genitourinary examination was remarkable for
- ~7 e+ X9 ~3 V- Jenlargement of the penis, with a stretched length of
* T$ ]* i/ `& c2 v! k# [$ J% k, L8 cm and a width of 2 cm. The glans penis was very well! }/ `6 u* V' K" q; D
developed. The pubic hair was Tanner II, mostly around/ e8 C- _: |* U. D
540
, b; v4 i7 O' h+ t" [4 Z5 ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ e, w2 E/ y0 W, c3 ^7 [) gthe base of the phallus and was dark and curled. The
. N+ N" r* l; Itesticular volume was prepubertal at 2 mL each.# Q. H' r1 J9 O; a6 o
The skin was moist and smooth and somewhat/ Z5 q7 E: S4 G9 K7 |) H1 M: g
oily. No axillary hair was noted. There were no: f4 K- V8 t: Y4 y! G5 l
abnormal skin pigmentations or café-au-lait spots., S% B1 v( ^' {/ W# |2 ^+ V
Neurologic evaluation showed deep tendon reflex 2+
2 M. X7 I7 _8 Q( `bilateral and symmetrical. There was no suggestion
. l; L/ O5 n0 c3 wof papilledema.
) ^6 }) [- v  n  K5 V6 E; g7 YLaboratory Evaluation3 P: y. |2 D0 }/ z! A
The bone age was consistent with 28 months by4 M& |. `5 N1 |# z2 s% L
using the standard of Greulich and Pyle at a chrono-
0 k& ^, p; q: h0 R6 z4 r; U4 Ylogic age of 16 months (advanced).5 Chromosomal
1 a- g. \+ e3 ?  g! A8 [karyotype was 46XY. The thyroid function test4 ?! C( T0 ~3 D: `0 N
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
# h+ |- H" n7 q2 f4 vlating hormone level was 1.3 µIU/mL (both normal).: S2 r2 J$ g, ~* r, h
The concentrations of serum electrolytes, blood
; E# X/ \& j9 J) S3 b" ]) h5 u$ i* x7 ?urea nitrogen, creatinine, and calcium all were
0 f; g3 T" X' \# U0 d  K3 t; a: gwithin normal range for his age. The concentration
2 U7 n# I, j5 Kof serum 17-hydroxyprogesterone was 16 ng/dL* r$ O. y' q5 a: @7 B/ j9 t& Y
(normal, 3 to 90 ng/dL), androstenedione was 20
" Y! w/ [3 x& K: C" H5 ~ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ Q: ~+ `4 l$ y3 ^) v+ hterone was 38 ng/dL (normal, 50 to 760 ng/dL),- ^, u2 R+ A2 b6 p* W6 S1 _
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 k8 k4 M; ~3 n7 P49ng/dL), 11-desoxycortisol (specific compound S)
7 x+ W, L# _# k* |$ G$ Cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-6 [6 p+ f! f, Y' Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 J$ _0 J) \3 k* E8 F& jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 E! t- w/ b4 ~3 W/ X
and β-human chorionic gonadotropin was less than
4 n% j; W1 Z0 z; I, d5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 B0 ]5 |  u6 i8 Q: Z( v/ k1 Estimulating hormone and leuteinizing hormone
: C  F, m3 B3 ?% e6 q# Gconcentrations were less than 0.05 mIU/mL
, z" L  R) P* Q  W(prepubertal).* p+ z7 ]. d' q  _5 Z
The parents were notified about the laboratory
1 ]# h* [% C6 x& R- _3 d3 @# qresults and were informed that all of the tests were0 x- y. k. u) b, Q- U5 F
normal except the testosterone level was high. The. O' _8 G! @2 W2 c% W& F. f- A
follow-up visit was arranged within a few weeks to/ }9 c6 q" q' x: h! E- L9 u
obtain testicular and abdominal sonograms; how-* v. P( U; p% k) D0 _  c
ever, the family did not return for 4 months.4 j: N3 b, b6 c
Physical examination at this time revealed that the3 v+ d" C' a9 ^. s$ A5 }
child had grown 2.5 cm in 4 months and had gained
9 W8 r# }; W, @; f/ P0 v; \2 kg of weight. Physical examination remained
( ?* @1 h3 F! l8 ^! r6 h' l' c, {unchanged. Surprisingly, the pubic hair almost com-- I5 J! b( R9 ?+ ?; w0 v* P# r
pletely disappeared except for a few vellous hairs at; {  Z# }% u( I/ e. I1 A1 W
the base of the phallus. Testicular volume was still 2
+ S' c. h- Q8 kmL, and the size of the penis remained unchanged.
$ l; ^$ X: t/ f6 H5 QThe mother also said that the boy was no longer hav-
% N$ X1 i* X  u/ `( Q; uing frequent erections.- I+ @" d: ], t( J! n5 Z5 {' X
Both parents were again questioned about use of1 P9 a2 c! x& z3 S* n: \
any ointment/creams that they may have applied to: y' O2 O5 \3 Y/ B
the child’s skin. This time the father admitted the2 m+ B4 ?9 s& V! [$ Q0 N' U0 X+ Q
Topical Testosterone Exposure / Bhowmick et al 541& g: t' E. z' ^3 w7 r+ \* t
use of testosterone gel twice daily that he was apply-1 y7 @2 g/ ~5 a
ing over his own shoulders, chest, and back area for
4 F0 o3 g) G$ aa year. The father also revealed he was embarrassed3 @4 |9 d: ^' _+ j7 @3 o5 w
to disclose that he was using a testosterone gel pre-
; I5 J3 ?9 l8 h- k" Dscribed by his family physician for decreased libido' s" u0 G  n7 m$ o1 M8 ~
secondary to depression.
! W+ _, D) J& q) x. aThe child slept in the same bed with parents.
( ^5 R2 v6 Y- I; {' q: K) h" wThe father would hug the baby and hold him on his
! O& ?  y# F- z( a3 o3 Bchest for a considerable period of time, causing sig-" Z7 `* z6 ^3 P8 `' q& I3 z
nificant bare skin contact between baby and father.! ~, n0 `/ K; ?3 B- ]! B6 [
The father also admitted that after the phone call,- Z6 i5 M3 m. k2 i, L
when he learned the testosterone level in the baby4 C5 f1 [4 ^# T  o3 g
was high, he then read the product information
; p# f% n! c; R) Z8 ]packet and concluded that it was most likely the rea-  N1 D+ x8 o% h- c8 k  w8 K
son for the child’s virilization. At that time, they7 s$ O1 r0 V1 w) d1 _9 G2 c
decided to put the baby in a separate bed, and the
  _# K: c# O: o2 t& H/ ffather was not hugging him with bare skin and had( S! i* k/ p3 c; z5 l
been using protective clothing. A repeat testosterone
$ N  W/ C2 N2 _) f9 Q1 c1 btest was ordered, but the family did not go to the1 l, O! _9 c$ f7 g! O
laboratory to obtain the test.' a/ P/ @$ ^$ B+ _$ B
Discussion- Q( q+ _. [# m) S$ d6 a/ R
Precocious puberty in boys is defined as secondary8 N8 r4 O- P& S" Z- d  W: x
sexual development before 9 years of age.1,4" f3 L2 Q: Y0 `' s6 B6 Q; R
Precocious puberty is termed as central (true) when: B/ i) s2 u9 p( E( Y
it is caused by the premature activation of hypo-# f/ g1 V. _' U" E
thalamic pituitary gonadal axis. CPP is more com-5 ]5 j# s1 T6 @& p4 A& _
mon in girls than in boys.1,3 Most boys with CPP5 A; c+ m2 k. @5 x5 a
may have a central nervous system lesion that is4 ^0 f; V- ]" l
responsible for the early activation of the hypothal-
, W; }8 Q2 f: [& kamic pituitary gonadal axis.1-3 Thus, greater empha-
4 E7 m( h* L$ m9 W& H8 Rsis has been given to neuroradiologic imaging in
' I! a5 Y1 d' S8 O* h& D% pboys with precocious puberty. In addition to viril-5 T3 |' a2 @2 q; Q3 t
ization, the clinical hallmark of CPP is the symmet-! w8 R. g& F. [. X+ N
rical testicular growth secondary to stimulation by
# f* ~0 A/ x4 g/ q4 W% K" D! s' Tgonadotropins.1,3
" T" Z& J9 @  ?0 p) i1 WGonadotropin-independent peripheral preco-
) d0 u7 \3 U$ E2 n$ S' bcious puberty in boys also results from inappropriate6 E: u' |: {8 |/ O+ ?/ B
androgenic stimulation from either endogenous or6 H' }- m* |  u& M% N0 @1 e1 e
exogenous sources, nonpituitary gonadotropin stim-, J4 g0 C- d* Z8 ]: @5 G. G
ulation, and rare activating mutations.3 Virilizing
, v& h0 X1 [1 N+ r& }  e( Jcongenital adrenal hyperplasia producing excessive
$ j' x) C! W9 Radrenal androgens is a common cause of precocious" i8 J/ l4 V# l0 |# k* u1 J) Z) A" q# p
puberty in boys.3,49 O( k; T+ m% X! a
The most common form of congenital adrenal0 X5 u/ {% J: A$ B
hyperplasia is the 21-hydroxylase enzyme deficiency.
3 C7 `% w9 A6 _& J( `* tThe 11-β hydroxylase deficiency may also result in2 Y/ G6 @* J0 I3 j. {
excessive adrenal androgen production, and rarely,3 ]3 ^7 s: ]8 o' d. R" ~3 B8 m8 y
an adrenal tumor may also cause adrenal androgen
$ J3 d6 q2 a/ n  F% ?excess.1,3
& |* e9 Y- z( l8 {! F/ c/ sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ N2 b8 J- m0 Y8 s9 m3 P542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 f" e; ~$ Z' y  U
A unique entity of male-limited gonadotropin-
! I/ p9 v8 T1 y$ Q3 `independent precocious puberty, which is also known1 m. M9 v: R! u* t6 _) c# i% u
as testotoxicosis, may cause precocious puberty at a
& A- e5 ]) T5 f! _7 D4 L9 S# vvery young age. The physical findings in these boys
6 I& p8 S+ T) m8 jwith this disorder are full pubertal development,
' n  l5 i( ?$ ]# f! R& Sincluding bilateral testicular growth, similar to boys
, X6 Q: d; h; r+ `+ _; vwith CPP. The gonadotropin levels in this disorder
4 z. `9 E2 Z) h" v/ kare suppressed to prepubertal levels and do not show
8 @4 z% l3 P5 q# I, q3 l9 c1 {' [pubertal response of gonadotropin after gonadotropin-
3 ?; |) |, C+ s) U- r- R1 x  ]releasing hormone stimulation. This is a sex-linked
+ i# g' S. v# [( I: M. vautosomal dominant disorder that affects only
4 y5 V6 Q! D9 ~" p0 z2 k# |males; therefore, other male members of the family
6 A* z& [/ O' o: Q7 ]2 Mmay have similar precocious puberty.3  d  z0 M% ~# a2 ^0 z. L+ L/ Z
In our patient, physical examination was incon-
9 d4 g' S1 \4 P" L" t' |- asistent with true precocious puberty since his testi-
1 P2 {' l+ G: x( @( V* i1 lcles were prepubertal in size. However, testotoxicosis+ m5 @. }- _& n! ]* i' P' q' m
was in the differential diagnosis because his father
7 _' B4 N& x9 M" R2 a4 X: \/ c" Dstarted puberty somewhat early, and occasionally,
4 [+ w* t% |$ i( [. ctesticular enlargement is not that evident in the$ {5 K* c( e4 \" _- U
beginning of this process.1 In the absence of a neg-
) p9 Z3 f. ~2 _- g* b$ D0 k( ~- Gative initial history of androgen exposure, our
* I( U8 W* {! P" dbiggest concern was virilizing adrenal hyperplasia,
) {# q" i+ W) j% b7 i8 n% ceither 21-hydroxylase deficiency or 11-β hydroxylase/ y/ `  @1 w! g. t
deficiency. Those diagnoses were excluded by find-  B" [0 K- h* C& P
ing the normal level of adrenal steroids.( E! h/ k  ?9 z# E
The diagnosis of exogenous androgens was strongly
! e$ P) q: r* {* g  B) N# n8 }suspected in a follow-up visit after 4 months because% O/ T( o6 O; Q# t/ e- q. L
the physical examination revealed the complete disap-
3 `4 @  A8 Q2 b# Cpearance of pubic hair, normal growth velocity, and6 ]! b* L2 F2 ]+ R
decreased erections. The father admitted using a testos-+ C1 a& X* `) ^: m
terone gel, which he concealed at first visit. He was3 O1 W* L$ D, _/ B) [
using it rather frequently, twice a day. The Physicians’
: A+ }/ [. q+ v1 XDesk Reference, or package insert of this product, gel or! |9 l5 {+ u0 N
cream, cautions about dermal testosterone transfer to
) c6 ^/ h& @) c! A( f! M& Gunprotected females through direct skin exposure.  U# a: O; X1 H; [. [. b
Serum testosterone level was found to be 2 times the' o. A; n$ O& E8 j
baseline value in those females who were exposed to; S1 b, |0 E( f7 }8 ~. f; _
even 15 minutes of direct skin contact with their male1 L4 p& `! c% u7 s. y1 ?  j; [# V
partners.6 However, when a shirt covered the applica-
3 I  j' T4 l2 k3 Htion site, this testosterone transfer was prevented., A. z% u# h( _! {6 J
Our patient’s testosterone level was 60 ng/mL,
/ W! p. \1 Z9 |# T2 ywhich was clearly high. Some studies suggest that" e' \" j, _0 c: I
dermal conversion of testosterone to dihydrotestos-
+ i. p! l5 g! R8 xterone, which is a more potent metabolite, is more6 L' b/ c& d! X* t, z
active in young children exposed to testosterone
2 Z$ Y- Z- M1 e  J/ N! C+ fexogenously7; however, we did not measure a dihy-$ |! Y' g0 E0 ^4 A, j
drotestosterone level in our patient. In addition to+ p8 ]$ H+ v5 J
virilization, exposure to exogenous testosterone in  }9 Z( l; a* c. l
children results in an increase in growth velocity and% l* E4 A% b3 C
advanced bone age, as seen in our patient.! g7 o/ Z8 m% N1 A, u! _
The long-term effect of androgen exposure during
+ B1 x( W  [% Wearly childhood on pubertal development and final
. m3 d, l) d' \8 g: v2 q7 @adult height are not fully known and always remain5 R+ u# C  x. t1 }7 m9 T
a concern. Children treated with short-term testos-
: C; e! G  N0 m" m  J0 _! H' vterone injection or topical androgen may exhibit some
1 r% p$ ^; U% wacceleration of the skeletal maturation; however, after" Q# y5 A# G  g; Z! ^) i
cessation of treatment, the rate of bone maturation
3 ?0 b* j# I' C" z" [8 ?decelerates and gradually returns to normal.8,9! x" y& a& C# `/ p9 x2 i1 ?
There are conflicting reports and controversy
4 ~/ }" {6 b" p1 m1 N7 C' [) Xover the effect of early androgen exposure on adult
6 y; z- I8 p9 V4 D9 t% a2 ipenile length.10,11 Some reports suggest subnormal% |' n6 z- Z* B( g9 a, n* O
adult penile length, apparently because of downreg-
, k! A: d5 g* r6 p2 B3 tulation of androgen receptor number.10,12 However,
; H% J" [% a! d' E; u6 t) L- oSutherland et al13 did not find a correlation between
! z# |8 `' V0 _" ~: Wchildhood testosterone exposure and reduced adult
9 ]# O- x8 f6 e8 J! s! e# P( rpenile length in clinical studies.6 a: k# [$ I: W3 s6 |
Nonetheless, we do not believe our patient is# @# V3 C% [2 s$ `; ~
going to experience any of the untoward effects from
/ [2 A* `7 E% ytestosterone exposure as mentioned earlier because
, b# Q4 {8 i4 |' G: @the exposure was not for a prolonged period of time.
6 W, T; G# I! G! G7 t  x# NAlthough the bone age was advanced at the time of7 S0 d& W4 x$ F: v6 \& `* K
diagnosis, the child had a normal growth velocity at$ ]# t7 b* N5 ]+ Y
the follow-up visit. It is hoped that his final adult
/ R, }( N: R# b: Wheight will not be affected.
* ]$ z" A1 L, C: F9 ]' dAlthough rarely reported, the widespread avail-7 j2 e$ v( E% Q$ W- ]
ability of androgen products in our society may
& O6 e6 P+ C8 h+ N: \indeed cause more virilization in male or female
. {9 F1 K# i% ]) ]children than one would realize. Exposure to andro-
: p, }# `8 ~8 f! ?2 O% N( kgen products must be considered and specific ques-
: T  d% b  ^# U( s4 E; X6 w# p6 c) K. ytioning about the use of a testosterone product or& f+ {, x$ y1 ]
gel should be asked of the family members during
4 q4 e4 t2 F* ]9 F* b8 zthe evaluation of any children who present with vir-
+ ]8 d" c# C1 K/ V: K* g- uilization or peripheral precocious puberty. The diag-3 q/ e2 {6 G: h5 s$ B
nosis can be established by just a few tests and by
4 w$ H. Z# o' T; ~appropriate history. The inability to obtain such a
: k  g. `+ @0 k7 Xhistory, or failure to ask the specific questions, may) c8 o9 u. |2 ?
result in extensive, unnecessary, and expensive7 W! l$ j. z( h3 U. ?8 L- `
investigation. The primary care physician should be, f( s( r" Z3 {) a
aware of this fact, because most of these children
) C8 a% E. E/ ]" f; K- N& P- jmay initially present in their practice. The Physicians’; H2 @6 i: V  |( m' G1 i4 l
Desk Reference and package insert should also put a0 D9 @  C$ e0 r
warning about the virilizing effect on a male or9 M1 s- V4 U1 Q# V1 \$ N
female child who might come in contact with some-/ @+ H" j/ F0 L0 m
one using any of these products.
9 x2 w6 F" u1 Q4 p5 \" t: H0 G0 ^References& A  i6 Y$ _. k/ b
1. Styne DM. The testes: disorder of sexual differentiation6 G9 k1 m7 t/ R( S& z9 Q
and puberty in the male. In: Sperling MA, ed. Pediatric1 e1 V- K, F/ m* ]2 U. }
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 Y' W% `+ Z7 t# _" z2002: 565-628.8 A: P5 T( \5 T
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" h2 c+ B* k% mpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old! Y5 [' I$ f1 C3 L, Q8 v
Boy Induced by Indirect Topical" {. e7 R2 \: Z# B3 M$ C: ^
Exposure to Testosterone8 [' I/ k, q9 Z- f% F4 w0 V! Q
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% E! j+ C* M* |+ U. h- J+ U
and Kenneth R. Rettig, MD1
" [/ }  Z! Z! @Clinical Pediatrics( O5 }& z$ q9 ~$ D( y1 `
Volume 46 Number 6
8 D% [/ [8 j5 I* r- Y7 x/ p, [5 s# QJuly 2007 540-543
% p+ z, _" _4 _1 V9 O© 2007 Sage Publications8 ^0 H$ U" `! T
10.1177/0009922806296651
+ p$ _. f5 ^4 B: ]$ mhttp://clp.sagepub.com  S7 Q5 Q3 V1 _4 C5 \$ ~, m+ @
hosted at
5 N: ]% \# U, xhttp://online.sagepub.com" W5 B3 ~- ~2 A9 z; C2 b3 ?* m+ e0 A1 ]
Precocious puberty in boys, central or peripheral,
* A. W9 r( E- e; |: I/ Mis a significant concern for physicians. Central- N, y( X* O8 m0 F9 [
precocious puberty (CPP), which is mediated  t; b& ^0 z1 a- G$ S% V
through the hypothalamic pituitary gonadal axis, has
/ K; s7 u0 Y. v; F. Y' }) ?a higher incidence of organic central nervous system0 p& ]; d- D/ R/ L5 z
lesions in boys.1,2 Virilization in boys, as manifested3 u4 Q* l. q) K$ w  O6 J( S( _
by enlargement of the penis, development of pubic$ N2 E9 ~+ l1 M0 J  U
hair, and facial acne without enlargement of testi-& K( Q' ~% Q( E- v; a
cles, suggests peripheral or pseudopuberty.1-3 We$ E* }: k" F$ ]/ \% x# _
report a 16-month-old boy who presented with the
  G3 y$ J7 i3 @& L# \) fenlargement of the phallus and pubic hair develop-
& C5 H6 [; U: c9 ament without testicular enlargement, which was due
- U: h9 y- I9 n" K; Q+ Zto the unintentional exposure to androgen gel used by
; R/ O( i  O* Q8 h! Wthe father. The family initially concealed this infor-" ~; w4 [8 G" c/ C5 f
mation, resulting in an extensive work-up for this
$ T% q9 c8 j2 O. achild. Given the widespread and easy availability of
6 Z8 f! D  M" c3 a2 _. Utestosterone gel and cream, we believe this is proba-
! L4 R+ _. [1 K* Pbly more common than the rare case report in the
( v- R, e) s, A: uliterature.4  L: [$ L2 i! r, H! w3 Q& y
Patient Report
- y; H5 \; K. i" {' C( QA 16-month-old white child was referred to the; t! Z4 d& b% K, A/ n
endocrine clinic by his pediatrician with the concern
* n  |( a0 z- u+ g/ e  _of early sexual development. His mother noticed
: G: E4 X( E- ^2 X% |light colored pubic hair development when he was
7 }) H: u: U  T/ SFrom the 1Division of Pediatric Endocrinology, 2University of
$ T, O3 d: s; `7 D/ SSouth Alabama Medical Center, Mobile, Alabama.
0 s# n, C( d) E: SAddress correspondence to: Samar K. Bhowmick, MD, FACE,
8 ^5 T6 I6 }/ e1 E. bProfessor of Pediatrics, University of South Alabama, College of
! b" C" d& p3 qMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
% e  G: I" A; I6 d! Ae-mail: [email protected].% H$ p* O7 L: E+ x  m
about 6 to 7 months old, which progressively became
& R( u/ W( v% V! h9 A* s% F) ddarker. She was also concerned about the enlarge-( C4 D8 A0 q/ a) G# y% a/ t
ment of his penis and frequent erections. The child
4 k  E" [# I( K1 G0 ]was the product of a full-term normal delivery, with
" s! s  k. O( p+ D1 o- W5 pa birth weight of 7 lb 14 oz, and birth length of
$ M) x( P0 q1 C7 q0 x1 T20 inches. He was breast-fed throughout the first year
8 B4 ?$ C$ w, P' B, \of life and was still receiving breast milk along with
% R$ w$ j$ @: |+ u4 nsolid food. He had no hospitalizations or surgery,
  I- H! K- K8 m+ q! Gand his psychosocial and psychomotor development
; x  I, P0 e1 X3 @) f6 L' a, `, @was age appropriate.% r3 X- V. C7 O. B  x  w
The family history was remarkable for the father,- L1 ]: J0 w5 L1 ]8 W. f
who was diagnosed with hypothyroidism at age 16,
: A: m# y% f( _$ ]4 Ywhich was treated with thyroxine. The father’s
0 F, Y# u& T9 K" Eheight was 6 feet, and he went through a somewhat3 {5 c8 ]" v% R  V5 ~. a/ q  V
early puberty and had stopped growing by age 14.5 P9 [& z. e, I$ t
The father denied taking any other medication. The, I0 M+ |0 ~$ l" ^6 i% T/ |* H3 R
child’s mother was in good health. Her menarche$ Z9 P  c' g2 r! A6 U& S# F) q! l
was at 11 years of age, and her height was at 5 feet" b1 a, j+ M0 [7 _
5 inches. There was no other family history of pre-" d; u% ^  O4 _" Y  U$ v  b
cocious sexual development in the first-degree rela-  _$ Q- C5 E. p$ l. e( \; f5 M
tives. There were no siblings.+ t  l8 c/ Z: r) q
Physical Examination
8 i8 L# k3 B( I9 ^, q, t% k- K4 HThe physical examination revealed a very active,9 p- R/ |" b. ?- g  w2 s6 c7 b
playful, and healthy boy. The vital signs documented+ u# s  Z  ^4 o3 m4 I1 u" ~
a blood pressure of 85/50 mm Hg, his length was' y, Y+ ?& n0 e9 x$ x4 n4 g
90 cm (>97th percentile), and his weight was 14.4 kg
5 D2 h1 c' _3 b' A* W6 ](also >97th percentile). The observed yearly growth  Y; t% Q- W" q+ ?
velocity was 30 cm (12 inches). The examination of
' t  b0 [% l. }+ \5 ~# athe neck revealed no thyroid enlargement., B5 M! \* l/ F6 [  `
The genitourinary examination was remarkable for7 q: ?' Z3 b. n% G) v& ~
enlargement of the penis, with a stretched length of
& `- y" M- E, c- R. _6 ]8 cm and a width of 2 cm. The glans penis was very well
% _( o1 H2 e7 x: f: \developed. The pubic hair was Tanner II, mostly around
* d9 R& D7 S4 ~4 J+ w% n540
8 [" ^$ o3 l. _at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, V9 b# z5 u5 C$ C; ythe base of the phallus and was dark and curled. The& F) U& v6 L. x! [5 _% y
testicular volume was prepubertal at 2 mL each.
3 A1 n' L  y: V2 e/ x4 H0 a4 r& vThe skin was moist and smooth and somewhat
' h0 L- T# _6 @6 u6 j! voily. No axillary hair was noted. There were no
+ G& k* p; y* y, R: o& ]: Nabnormal skin pigmentations or café-au-lait spots.
0 B8 Z9 Q' O5 |# u  W- c# P& KNeurologic evaluation showed deep tendon reflex 2+- `- a: a& L# C2 D0 _) ]9 c
bilateral and symmetrical. There was no suggestion+ `( \0 F" u' g- \
of papilledema.
/ a) L: f; Y2 `& o. @- p: TLaboratory Evaluation
% u- w2 A, u9 m/ B9 ]The bone age was consistent with 28 months by/ K: |% w" S4 h3 z3 @8 l0 r
using the standard of Greulich and Pyle at a chrono-
! O" ]; B2 x2 V2 U9 u. mlogic age of 16 months (advanced).5 Chromosomal
. d5 F2 @" O8 Q7 s, `/ z* rkaryotype was 46XY. The thyroid function test; H& |6 N" j5 v8 Q2 u! q" Z$ y
showed a free T4 of 1.69 ng/dL, and thyroid stimu-$ F1 o' d) \9 P7 h# q; s; z0 x
lating hormone level was 1.3 µIU/mL (both normal).
; D; x$ t/ M: ^" g& k' @The concentrations of serum electrolytes, blood
9 X0 o, y7 B' Q8 o. t$ {% nurea nitrogen, creatinine, and calcium all were' B/ U! p/ M0 P( O
within normal range for his age. The concentration
0 _; A1 T2 ?  d% l, H7 |of serum 17-hydroxyprogesterone was 16 ng/dL
; E- V! J% ?/ ^6 s/ a  y( F2 Z(normal, 3 to 90 ng/dL), androstenedione was 204 `6 o* i6 o' Q& Q1 s
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 }6 V3 |) w) w0 q: P
terone was 38 ng/dL (normal, 50 to 760 ng/dL),! v. O" t7 n$ a( `
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
# G# ~' O) N$ `, c/ g& l1 P49ng/dL), 11-desoxycortisol (specific compound S)$ H3 V) H5 _0 S/ s4 d
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" N, K0 q6 {+ q- D
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) |$ E  ?) ?' l9 ]0 l$ `testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
6 y  s+ b, Z+ x. band β-human chorionic gonadotropin was less than
7 e0 G6 W3 S+ J' T7 ]* b& H  m5 mIU/mL (normal <5 mIU/mL). Serum follicular& g6 w5 C( K9 ?9 |7 s6 m
stimulating hormone and leuteinizing hormone. J# N$ Y' U- h( Y1 P3 _4 r. V
concentrations were less than 0.05 mIU/mL
7 p# x& j# ~* i1 O(prepubertal).
+ O" r; j, Z6 i0 n7 CThe parents were notified about the laboratory- n% R; S6 z, t+ k  I. k# s
results and were informed that all of the tests were0 p* I* R- l# \+ ~
normal except the testosterone level was high. The
3 O, k1 e8 q( x7 Y# F* |follow-up visit was arranged within a few weeks to
- P/ i1 M. Q/ y7 uobtain testicular and abdominal sonograms; how-
& ^* B% j, q2 }. @7 Lever, the family did not return for 4 months.% U. B/ T! R% W2 Q$ G" t( E
Physical examination at this time revealed that the
+ V! `$ S6 g- T& N3 A. _child had grown 2.5 cm in 4 months and had gained
5 {, j, C7 h3 N: L/ |2 kg of weight. Physical examination remained. N$ j2 b2 c- {2 ]
unchanged. Surprisingly, the pubic hair almost com-
" P0 P9 |- c: M; ?; s6 bpletely disappeared except for a few vellous hairs at
& Q% h, H8 y- H- Zthe base of the phallus. Testicular volume was still 2
' p: @7 g5 z) S: g: D' P& D& t2 omL, and the size of the penis remained unchanged.0 E1 l' }4 z7 Y* `9 n
The mother also said that the boy was no longer hav-
* a7 m6 Z, X6 }% o  i, G5 t  ring frequent erections., v+ i; K% C7 D1 H
Both parents were again questioned about use of$ x+ Y' R" |- {
any ointment/creams that they may have applied to
9 c) h7 [& _. U+ F7 ithe child’s skin. This time the father admitted the
$ n4 j$ g# O; K0 F. D7 {% dTopical Testosterone Exposure / Bhowmick et al 541$ j1 \; J3 L9 F4 G2 `' i% O
use of testosterone gel twice daily that he was apply-( U! `) [  a7 I
ing over his own shoulders, chest, and back area for( z8 l! X- c8 ~, Y7 M0 w" W( j
a year. The father also revealed he was embarrassed
- s1 Q$ j  o4 U- }1 R% X9 Z! Zto disclose that he was using a testosterone gel pre-+ v  v$ X" |6 D" g% b# R
scribed by his family physician for decreased libido
8 C% d6 V5 v7 A( e/ M+ n( msecondary to depression.! h2 y) N' ~$ N5 X/ A
The child slept in the same bed with parents.$ i0 F& o. b* h3 C
The father would hug the baby and hold him on his
9 {. V4 I% B/ L/ Kchest for a considerable period of time, causing sig-
% K, g8 a% B) S$ F4 S& s; J2 U0 `nificant bare skin contact between baby and father.) o' e# X0 o& v' p3 s
The father also admitted that after the phone call,
; y4 J7 d: m' K( D4 O7 _5 y7 |when he learned the testosterone level in the baby9 t0 k1 h1 G( i' [0 Q: w
was high, he then read the product information+ `; M% O. Y! N  @# D0 u
packet and concluded that it was most likely the rea-+ Z0 e$ A; U! U5 X6 A1 E
son for the child’s virilization. At that time, they
6 H( {% {: }) a7 C; Cdecided to put the baby in a separate bed, and the, R0 k0 x0 s  }5 _- s' T; n
father was not hugging him with bare skin and had
9 {; w; p7 J" b% K1 \: u1 obeen using protective clothing. A repeat testosterone$ M2 U& v. R) M0 j+ I5 N
test was ordered, but the family did not go to the5 R4 d* }; [. W' g! E
laboratory to obtain the test.
$ R0 P6 J1 F- P6 `Discussion: ]9 C! L( Q3 V" Q9 S
Precocious puberty in boys is defined as secondary" p( |; {2 |: y0 j. q; b
sexual development before 9 years of age.1,41 i: H% {+ }9 |8 U4 Q8 }$ b2 {
Precocious puberty is termed as central (true) when
1 ~8 `1 p/ |# Zit is caused by the premature activation of hypo-
4 C* H3 r) A% A9 C% K! Y( mthalamic pituitary gonadal axis. CPP is more com-1 @5 T4 w* ^& D0 J* s1 A
mon in girls than in boys.1,3 Most boys with CPP
* r8 W6 o, J3 Xmay have a central nervous system lesion that is
7 o% }# y. V+ ~2 }$ oresponsible for the early activation of the hypothal-' V6 @+ v: K' i. W5 l7 u* ?
amic pituitary gonadal axis.1-3 Thus, greater empha-; r$ l2 [: }. B7 }
sis has been given to neuroradiologic imaging in
# l- b  F8 b2 t4 p/ m5 k: eboys with precocious puberty. In addition to viril-
( v( ]$ R8 x8 p& c/ U/ ]7 Bization, the clinical hallmark of CPP is the symmet-
0 [1 ~9 l) Z% J' J$ ~rical testicular growth secondary to stimulation by
# R* i3 v% Z  {4 V8 Y6 i; n9 Pgonadotropins.1,3
1 K0 }& I% k  L" Y1 {Gonadotropin-independent peripheral preco-" s3 W2 F# I/ ?- Z
cious puberty in boys also results from inappropriate& t" w! p% k/ i
androgenic stimulation from either endogenous or
2 b% S4 W# n3 V. Eexogenous sources, nonpituitary gonadotropin stim-
% V9 M/ U! y4 S" g" d1 I* }' o$ julation, and rare activating mutations.3 Virilizing
/ s; \+ c% ~% a5 {congenital adrenal hyperplasia producing excessive0 i! @/ {- N+ N- \4 x
adrenal androgens is a common cause of precocious
5 _7 i# ?: E" qpuberty in boys.3,4
, e- d! b& f6 E5 x7 zThe most common form of congenital adrenal  r  ?, Q6 t7 \
hyperplasia is the 21-hydroxylase enzyme deficiency.- V5 U9 A) T7 m3 G* H
The 11-β hydroxylase deficiency may also result in. r5 M  A4 M' f5 d* |9 g
excessive adrenal androgen production, and rarely,
6 {$ ]' C# w8 o( h+ ]: {% zan adrenal tumor may also cause adrenal androgen0 ^, O5 ^% ^+ G, c% e& G9 y
excess.1,3& R5 b# p. h' E9 ]# v3 e2 F8 A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ f+ _  H: B2 s: b8 |' |542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 A8 p; N& T2 Q4 m) m8 ?
A unique entity of male-limited gonadotropin-
8 r- d4 ?9 j& H% u2 s2 \- Zindependent precocious puberty, which is also known
+ [" D7 s$ R, W7 Qas testotoxicosis, may cause precocious puberty at a
7 ?0 c+ A9 U7 i! L8 v7 V" avery young age. The physical findings in these boys
) v2 p% Y; e- ~* twith this disorder are full pubertal development,
# f6 K% F7 s- k6 E6 X1 d0 Kincluding bilateral testicular growth, similar to boys8 Y9 U4 V& D2 `1 _. G/ S" ^' {
with CPP. The gonadotropin levels in this disorder
; N( a: n! Z. N4 r6 G; X& x! xare suppressed to prepubertal levels and do not show, W. O6 V. X" r4 o+ t7 Q- g( \2 t
pubertal response of gonadotropin after gonadotropin-
- e- e! Z# _; K9 Lreleasing hormone stimulation. This is a sex-linked
2 \0 c1 A- P' M- D8 M; p; [autosomal dominant disorder that affects only+ t' K: i! w2 _/ R3 f- E' v
males; therefore, other male members of the family- P/ \3 Q& `: X' G
may have similar precocious puberty.3
2 G+ f' |5 Y& ?- z7 CIn our patient, physical examination was incon-7 C5 b" A' B, n% l
sistent with true precocious puberty since his testi-
8 r+ F  A8 s2 ?; P' P6 s5 rcles were prepubertal in size. However, testotoxicosis5 g) [4 T1 h& g+ w( K2 c
was in the differential diagnosis because his father
# f5 |( G& u- Z& y" D- J- ^( Jstarted puberty somewhat early, and occasionally,
9 W+ f$ W$ \, ttesticular enlargement is not that evident in the
7 _2 U4 [! b2 ~/ b8 F2 ]beginning of this process.1 In the absence of a neg-
/ M& F& u" C8 F: q1 S+ l! @3 Dative initial history of androgen exposure, our: |3 K: |9 H  z! k( s( `
biggest concern was virilizing adrenal hyperplasia,* K1 r! E; _. [1 q+ V! V
either 21-hydroxylase deficiency or 11-β hydroxylase! O" Y! {: O: Y
deficiency. Those diagnoses were excluded by find-
& W0 z3 m; E$ d: B/ uing the normal level of adrenal steroids.: y6 I: B: E' L5 D9 [
The diagnosis of exogenous androgens was strongly1 R: f5 T& j9 G; }) ^
suspected in a follow-up visit after 4 months because6 n$ `, m. p' d# n7 Z
the physical examination revealed the complete disap-9 q) u6 E# [5 X1 L7 e/ S
pearance of pubic hair, normal growth velocity, and) p9 [+ }* I4 |+ z# A9 b9 i4 q( r
decreased erections. The father admitted using a testos-
9 _8 c! g3 h7 h( k  i4 [9 kterone gel, which he concealed at first visit. He was( y2 R7 U: ~- s
using it rather frequently, twice a day. The Physicians’
- I3 U  u, D8 U" v* R' jDesk Reference, or package insert of this product, gel or
$ d2 z: W8 p/ P6 n1 Xcream, cautions about dermal testosterone transfer to
$ W3 E# Z: o# [9 qunprotected females through direct skin exposure.
# o. ]( m  y; e- Z) @: VSerum testosterone level was found to be 2 times the( {9 l. j) c$ J/ `2 ~  \6 F; X; X3 I
baseline value in those females who were exposed to5 f7 P0 j; i9 S, ?4 T- O' h
even 15 minutes of direct skin contact with their male2 I) c8 O7 k  G4 @# |
partners.6 However, when a shirt covered the applica-
: f* u, H+ Y8 X) y# A" K  ption site, this testosterone transfer was prevented.
) O0 x. J4 B. _) F5 g' Y; e0 [Our patient’s testosterone level was 60 ng/mL,, d2 `5 G5 d' ?3 w  J7 H
which was clearly high. Some studies suggest that* W! B6 ]) l5 S9 G& O
dermal conversion of testosterone to dihydrotestos-
+ n2 [. {' R& c8 W( aterone, which is a more potent metabolite, is more
9 B- a  V& ~' f! i' E( \) ?0 mactive in young children exposed to testosterone* a) z& f8 r' z2 i: K
exogenously7; however, we did not measure a dihy-
* [! f- i3 v- {6 f0 g6 r3 Ldrotestosterone level in our patient. In addition to
% ?; @) U0 G( e0 ?7 z) {# Rvirilization, exposure to exogenous testosterone in/ j1 Y4 C% H9 ?2 A/ ]4 W
children results in an increase in growth velocity and9 Y: g2 m& v- z% h( S+ D/ _/ A
advanced bone age, as seen in our patient.; o( @0 z. C4 ?& N; P- u
The long-term effect of androgen exposure during9 a  v3 Q4 s% z9 A
early childhood on pubertal development and final
# P$ B& P: l# `, ~& P/ Yadult height are not fully known and always remain
1 D0 G4 X3 o' z, N0 t& ?; z* ~- ia concern. Children treated with short-term testos-; u5 [& y! s' G3 K) |; }- }: p
terone injection or topical androgen may exhibit some( h* `" Q5 E7 P- g( n# k0 x9 R# u
acceleration of the skeletal maturation; however, after
% \: x; P6 K% l. g0 j4 X1 mcessation of treatment, the rate of bone maturation
6 d( k; Y  @) q+ |decelerates and gradually returns to normal.8,9
  y0 D9 B, |9 W# A/ GThere are conflicting reports and controversy5 @% s' V+ F3 v+ e5 R' a
over the effect of early androgen exposure on adult
  K. R6 f- w$ R; ?7 Ipenile length.10,11 Some reports suggest subnormal6 w8 {+ C1 Q7 [
adult penile length, apparently because of downreg-
* v$ A" g9 K3 h; R- O: ]5 i% q0 P+ yulation of androgen receptor number.10,12 However,
  F, u9 ?# z! T2 N: CSutherland et al13 did not find a correlation between3 ~# t% e2 ]1 n" F( L
childhood testosterone exposure and reduced adult
& p! C  y9 C5 kpenile length in clinical studies.& ^5 o7 ]9 D. P5 ^! n3 T8 y
Nonetheless, we do not believe our patient is/ p7 j& s' Q& {7 B/ |
going to experience any of the untoward effects from
; S) q- q% q! X4 l, I: z- M$ Ktestosterone exposure as mentioned earlier because
+ D0 b+ I2 d! wthe exposure was not for a prolonged period of time.+ p4 d7 i! p( c
Although the bone age was advanced at the time of) a& t& J2 ^8 K/ d6 ^
diagnosis, the child had a normal growth velocity at
7 ^- E: ~1 N1 z/ ~# t+ e/ q5 H7 ^the follow-up visit. It is hoped that his final adult4 y* }! J" N8 I) F# h: U3 j3 r. }
height will not be affected.! p$ t/ |1 y! h; g2 W. h8 S
Although rarely reported, the widespread avail-4 c9 w4 z6 B( v! _
ability of androgen products in our society may
2 f' E5 J" U8 ]& [* T% Yindeed cause more virilization in male or female, O- w! q5 y, x6 b
children than one would realize. Exposure to andro-
3 r! O- O0 V1 ~: l- ~. r1 Z2 a4 fgen products must be considered and specific ques-+ S" ]4 b; U5 N* L
tioning about the use of a testosterone product or! I$ @: Q& ^; o: L
gel should be asked of the family members during( C$ k1 q% d, Q% V
the evaluation of any children who present with vir-! `: h0 E: Y4 T- s9 ?1 F
ilization or peripheral precocious puberty. The diag-0 ]  x4 L7 e7 x4 {2 u4 y
nosis can be established by just a few tests and by$ ~& h& ^2 R9 ~+ q2 t7 [- V& Z
appropriate history. The inability to obtain such a9 n# l5 G# W, u' r- w! p
history, or failure to ask the specific questions, may" t. F% N8 ~3 D/ p% q) P
result in extensive, unnecessary, and expensive# t% d7 B0 a8 o) L" T
investigation. The primary care physician should be8 K+ q" ]8 L8 `0 z7 U
aware of this fact, because most of these children
$ {7 C' b2 Y6 @& ]( Fmay initially present in their practice. The Physicians’: l2 y  l4 U! M' ?: ?
Desk Reference and package insert should also put a
+ [8 O6 k8 u- T6 ~warning about the virilizing effect on a male or
7 b/ U; E, N. Z1 Y; x& l7 b7 ], Dfemale child who might come in contact with some-: E4 L. y0 `" {. g( E6 M% D
one using any of these products.
$ `$ f1 f* P6 E6 U( KReferences
- e/ R' A7 d- O  R1 C# z1. Styne DM. The testes: disorder of sexual differentiation  C5 l- }* t* V0 _# w! l, Z% x
and puberty in the male. In: Sperling MA, ed. Pediatric
0 U) I& U& v4 ]' vEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! N0 i: G8 C* o9 ^# ?$ D' x0 b
2002: 565-628.7 W; D, v( \4 x. X2 O3 P
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 |) V* k7 `; y# f! x" ~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
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

/ G3 x6 W: W2 r$ F6 k+ o2 x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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