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Sexual Precocity in a 16-Month-Old/ S, \/ n) K. a  D
Boy Induced by Indirect Topical. I% G: H) C5 n9 i: g; R, B9 f$ l
Exposure to Testosterone
7 x( n" c8 P! p4 q# ~Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; R; e; E# A+ a7 land Kenneth R. Rettig, MD13 |! `# |/ p: P
Clinical Pediatrics
7 t6 c' H" E" Y$ t- j2 A9 CVolume 46 Number 6
% o# R- Z1 v; {2 b0 h8 h. n1 ZJuly 2007 540-543! Q* W% u7 ~: X# D2 p9 ^; Y2 v) U
© 2007 Sage Publications( `2 r! G: a+ X% u
10.1177/0009922806296651. ~" D+ J; _9 G) z5 g" S: m6 a" l
http://clp.sagepub.com# n& u9 [/ `% w3 ?8 \$ x
hosted at
& d: {" M8 I0 P' X  \. \: t: ehttp://online.sagepub.com
& Q, u6 s4 k8 L' s. _Precocious puberty in boys, central or peripheral,$ ]: W8 k- s$ a% q0 c7 b+ F8 E' ?
is a significant concern for physicians. Central& P, j$ f, i7 F. ?
precocious puberty (CPP), which is mediated+ L  \# e5 @$ |4 s8 @8 o/ {* R
through the hypothalamic pituitary gonadal axis, has8 `( T' |/ y3 P+ N
a higher incidence of organic central nervous system
  ~' x4 [1 M. a% ]lesions in boys.1,2 Virilization in boys, as manifested
% y/ S% Y, Z( [. x# |* V- Qby enlargement of the penis, development of pubic0 g; z  p" j0 l( Y9 B
hair, and facial acne without enlargement of testi-
9 r7 @0 s; p. p7 g8 l% K( |# Acles, suggests peripheral or pseudopuberty.1-3 We
. A, z$ o; V# freport a 16-month-old boy who presented with the
0 i8 u" k. o) h/ Senlargement of the phallus and pubic hair develop-. e# e( _5 B. E2 `: K
ment without testicular enlargement, which was due0 u' z' e4 Q! h" A0 j
to the unintentional exposure to androgen gel used by
$ E* j* H3 z, X  M$ f+ T$ pthe father. The family initially concealed this infor-
4 n# D5 o; n$ bmation, resulting in an extensive work-up for this
2 R- ]9 I; M, j9 Q, @) k$ Pchild. Given the widespread and easy availability of
+ a: N( Y7 N3 d1 X& O3 D1 O8 itestosterone gel and cream, we believe this is proba-
! u# c* `7 `2 g/ Hbly more common than the rare case report in the2 C( S. D  A- _! q$ e( \9 M% W
literature.4
7 U- Y4 y' d$ c' lPatient Report+ M6 g  F$ q% l# @/ @: `" g
A 16-month-old white child was referred to the
# z4 w% p& b; S8 S% Wendocrine clinic by his pediatrician with the concern
1 F4 f9 p0 k! i/ ~of early sexual development. His mother noticed
8 x' @/ [; H$ p  T( Xlight colored pubic hair development when he was
2 X% M% w, K6 E$ j6 y5 u; x% X- S2 t1 ZFrom the 1Division of Pediatric Endocrinology, 2University of
0 q$ f1 M! `9 K& C. I% W0 {South Alabama Medical Center, Mobile, Alabama.. c+ \5 X; @! _% L/ K' @
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* d0 I9 y" g. K- t; O2 sProfessor of Pediatrics, University of South Alabama, College of
& f0 f; H5 u6 C& k+ x/ x0 QMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: P  V5 j7 C* n" X/ le-mail: [email protected].4 `# Z) T# Z+ F
about 6 to 7 months old, which progressively became
* U4 X3 o- i" O0 y; Z/ Q1 k5 [darker. She was also concerned about the enlarge-/ X( B. u- S; t1 Z5 }4 `
ment of his penis and frequent erections. The child
; ?" {' X3 r% s0 z- Twas the product of a full-term normal delivery, with1 A. X: U6 B: o5 R" W( P. E
a birth weight of 7 lb 14 oz, and birth length of7 b  u5 `8 R( |1 `7 T0 r
20 inches. He was breast-fed throughout the first year
1 T1 {* D( p" E5 Y% u; qof life and was still receiving breast milk along with
) p& f$ B$ H, A) l/ {, rsolid food. He had no hospitalizations or surgery,
2 ]0 t  s6 R+ S9 h8 b  x" n: l6 a7 Dand his psychosocial and psychomotor development
: n0 Z1 A$ e. C$ Twas age appropriate.5 h7 }% F/ B1 [3 g" J
The family history was remarkable for the father,4 J; Z" N" V/ g3 A# A# Y5 a" E5 k
who was diagnosed with hypothyroidism at age 16,- T7 g  }5 l3 e+ {( Y0 I# J8 g
which was treated with thyroxine. The father’s
+ o* M8 ]3 c& u8 `height was 6 feet, and he went through a somewhat
( P# w$ e' ~/ J. n! |2 j3 gearly puberty and had stopped growing by age 14.
$ ]" C% D$ M2 s5 k4 b  w! XThe father denied taking any other medication. The
8 K8 Z0 U7 l! C& ?: fchild’s mother was in good health. Her menarche
2 D7 O9 A! l, \/ b2 G) Wwas at 11 years of age, and her height was at 5 feet4 }( ]& z, k' R& j
5 inches. There was no other family history of pre-7 r, {; l6 I+ W) m& {( n
cocious sexual development in the first-degree rela-) z* R: {4 C3 c2 f8 L
tives. There were no siblings.
0 p" n) J# q& d& `Physical Examination
1 [7 ?* a) y6 V6 u8 l6 J9 CThe physical examination revealed a very active,
9 j1 m4 o- ?0 \  dplayful, and healthy boy. The vital signs documented
0 F, }  w* E. a# |% Za blood pressure of 85/50 mm Hg, his length was
: r4 F" V) w5 \6 @: `4 d90 cm (>97th percentile), and his weight was 14.4 kg
$ p! ~; t: f  H(also >97th percentile). The observed yearly growth  {" ]0 a1 T; I$ k
velocity was 30 cm (12 inches). The examination of! H5 T- S, r3 ?5 v! g8 e) W, @
the neck revealed no thyroid enlargement.% W$ s0 R3 I) O7 g# F$ A+ i
The genitourinary examination was remarkable for- n& e- n* S& I' s& N
enlargement of the penis, with a stretched length of. _6 S8 R# s) K
8 cm and a width of 2 cm. The glans penis was very well
9 z& }4 H& i; e; Z5 S1 `7 h0 Ndeveloped. The pubic hair was Tanner II, mostly around, d5 ^9 n) N+ t4 j# Y$ \& T
540+ _& {% H3 I" W- b/ H) {, Z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' T" P8 z, F# j' X/ |- ?' `
the base of the phallus and was dark and curled. The
* x: o) Y- Y+ f( Qtesticular volume was prepubertal at 2 mL each.0 ?/ \3 \* J3 B( u. c9 a
The skin was moist and smooth and somewhat# l0 j+ j8 x. i) ~7 t( s* R  E" W
oily. No axillary hair was noted. There were no( O+ ^; M- D9 j( y  Z
abnormal skin pigmentations or café-au-lait spots." A7 l+ b+ L5 R1 b
Neurologic evaluation showed deep tendon reflex 2+
8 {, j3 w+ A; y& Y4 d3 y, S9 wbilateral and symmetrical. There was no suggestion( [6 @4 N4 s. N# o! C  E% m3 `
of papilledema.4 W. L! g7 W! e4 n7 {3 n, D4 l
Laboratory Evaluation
" Q! H/ F# p7 E/ }2 Z4 }. M4 kThe bone age was consistent with 28 months by8 z' g6 G* p' N# H
using the standard of Greulich and Pyle at a chrono-6 T  |) x3 @( E, x
logic age of 16 months (advanced).5 Chromosomal
. S) R. Y" \0 Z. G; fkaryotype was 46XY. The thyroid function test
! k( A* V" n3 ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-% z2 Y5 p# U1 T1 r; k' ]$ m
lating hormone level was 1.3 µIU/mL (both normal).% t5 r$ k5 T  h2 f
The concentrations of serum electrolytes, blood4 E% D7 h6 g  d$ h
urea nitrogen, creatinine, and calcium all were+ L* l( E7 x* M+ d5 l
within normal range for his age. The concentration/ F5 k. E* y' j; e; c1 ?# e9 Z
of serum 17-hydroxyprogesterone was 16 ng/dL
2 X$ l$ x7 T! ^( Q# D: l(normal, 3 to 90 ng/dL), androstenedione was 20
' o/ r! T" Z+ d, S; u" nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 s7 ~% |  g* B# @: `# `% g
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 ?5 r3 q0 v* `9 }" ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to* q! S4 u# E: w! }( Z
49ng/dL), 11-desoxycortisol (specific compound S)
* [3 d  K" J- p4 @$ R& ?was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 O8 n6 q+ r5 Q7 P5 ^( t
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( q4 R$ |) @7 |3 k
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 N) W+ T( P# D& H8 Gand β-human chorionic gonadotropin was less than
5 v& v2 y% G0 L) G7 k( Q5 mIU/mL (normal <5 mIU/mL). Serum follicular
" G$ y' o0 ^! u  s2 N; d8 qstimulating hormone and leuteinizing hormone
5 M1 N/ @2 g- ]4 w- w2 ]concentrations were less than 0.05 mIU/mL$ W8 g8 o! s( \- [% ?
(prepubertal).& m3 Y  o0 _6 Q7 k5 ~) k, L+ \
The parents were notified about the laboratory* m9 \( j4 U  G/ t
results and were informed that all of the tests were, d5 y0 J  S' o' v( X7 g
normal except the testosterone level was high. The
* B( h% L0 e2 V$ d0 ofollow-up visit was arranged within a few weeks to. m/ _6 h  m$ t1 J
obtain testicular and abdominal sonograms; how-" c3 c" r7 J5 [% W  D$ k- W. i
ever, the family did not return for 4 months.
6 L$ {$ h# v' n+ XPhysical examination at this time revealed that the
3 X) k  O( X2 ?* Zchild had grown 2.5 cm in 4 months and had gained7 f; y/ k8 B- ?$ t9 j+ _- T. _1 z
2 kg of weight. Physical examination remained5 u: R2 O+ s0 ?+ i* r' Z
unchanged. Surprisingly, the pubic hair almost com-; Q2 [- ^0 _9 s# U
pletely disappeared except for a few vellous hairs at2 ~' ^) ?8 A' n0 ?3 m
the base of the phallus. Testicular volume was still 24 Z5 b0 X* g- R0 r* N% Y, v
mL, and the size of the penis remained unchanged.6 A: N# ?) m6 y9 u9 A
The mother also said that the boy was no longer hav-
3 U+ ]. e* r: |2 Y1 b6 m0 `ing frequent erections.
' x* B4 I& O' X5 O0 Z$ c, Y0 zBoth parents were again questioned about use of  y2 U- V& f# K  \$ s( X* h$ ?
any ointment/creams that they may have applied to
4 g  N# P: o" bthe child’s skin. This time the father admitted the
' V, ?9 r: z1 }Topical Testosterone Exposure / Bhowmick et al 541
  }+ L- \6 d& n* F& U& [use of testosterone gel twice daily that he was apply-: E: S5 R2 F6 K. Q
ing over his own shoulders, chest, and back area for
0 r+ K- f3 @4 r! {3 O% I1 W* W! k9 Ia year. The father also revealed he was embarrassed: Y& K) `1 e2 @6 o8 j
to disclose that he was using a testosterone gel pre-
$ T6 a3 V, a9 u* ^scribed by his family physician for decreased libido
, a6 y3 O; `) X! N7 jsecondary to depression.
# J" F& k! f6 h  pThe child slept in the same bed with parents.
9 W. W* e& J2 K3 h0 |The father would hug the baby and hold him on his
8 U' Y7 e1 d* V0 uchest for a considerable period of time, causing sig-
" _6 ~0 D% B% ?  ~/ a4 Ynificant bare skin contact between baby and father.
# J0 \6 C! Z& W4 R; ]/ s* ?7 cThe father also admitted that after the phone call,& `) o) K1 p8 G' l# ^( w
when he learned the testosterone level in the baby
6 |1 ?( k: M) a; V9 M) ^was high, he then read the product information0 J$ L; j4 s3 N: I
packet and concluded that it was most likely the rea-+ N) v) i0 j+ J  M  V. m4 G
son for the child’s virilization. At that time, they! R& }/ C8 `% B0 D
decided to put the baby in a separate bed, and the
4 W  ~7 x9 d9 b* y1 \8 Z" Q7 tfather was not hugging him with bare skin and had+ M% {. L4 z9 a  P, b- L& l+ D% J4 \$ L
been using protective clothing. A repeat testosterone- _: t$ L6 `+ k* X9 P
test was ordered, but the family did not go to the
1 \0 A$ w, Z1 l+ y# m7 klaboratory to obtain the test.
8 E. Q& T& j. V3 nDiscussion
5 {* v# K! |" e# {' }Precocious puberty in boys is defined as secondary
, l* i" t2 Q7 R; ~sexual development before 9 years of age.1,4
: @% w% ^- m6 C- GPrecocious puberty is termed as central (true) when3 D, c& Z) p( X. E7 O; ?# ^
it is caused by the premature activation of hypo-
# T, y9 z9 i. d8 U" {. hthalamic pituitary gonadal axis. CPP is more com-
" e! S) Z! Z0 x& hmon in girls than in boys.1,3 Most boys with CPP
4 e0 b$ V, v1 w/ _1 ?( o  zmay have a central nervous system lesion that is
: O" h1 ]- s; ?8 l' kresponsible for the early activation of the hypothal-: K7 I8 U+ B2 i8 N, x% `
amic pituitary gonadal axis.1-3 Thus, greater empha-
1 d' c" P$ N9 m4 T5 }2 zsis has been given to neuroradiologic imaging in8 S6 g* K5 q) c% h( h3 Y. N" y
boys with precocious puberty. In addition to viril-
, b2 B( t& Y+ F" v# d6 tization, the clinical hallmark of CPP is the symmet-
# k7 o4 d; M9 S3 Irical testicular growth secondary to stimulation by
0 v5 U- `1 V# _8 ygonadotropins.1,3
9 |( h- B$ `; e5 b" Y" AGonadotropin-independent peripheral preco-
0 B5 |+ u. s+ b: s# A* Pcious puberty in boys also results from inappropriate
2 e: y1 L  q; Z5 H' Landrogenic stimulation from either endogenous or- X$ h* d/ H1 h% ~( g% @
exogenous sources, nonpituitary gonadotropin stim-
+ m+ [1 h# K& [8 o- yulation, and rare activating mutations.3 Virilizing9 p) }6 l) }1 D  p% t# n  R; L
congenital adrenal hyperplasia producing excessive
3 ~( y! n" q5 K( ]2 Uadrenal androgens is a common cause of precocious
, B. w: |. U0 N2 h. p! H+ Zpuberty in boys.3,4
1 A' Q3 @" Z: z5 o2 Z4 k& g7 FThe most common form of congenital adrenal9 L/ C  v1 s# m: V! Y* ^
hyperplasia is the 21-hydroxylase enzyme deficiency.
: t7 T% q  Y/ U) d) d7 hThe 11-β hydroxylase deficiency may also result in
9 |( L( ~7 j- D7 dexcessive adrenal androgen production, and rarely,
4 W5 ^! L" }* H- Ran adrenal tumor may also cause adrenal androgen0 W( ^. Q4 z+ R5 s
excess.1,3: s( C) F* n5 R" e  Q) W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  a! ?; b$ d4 N4 G! f4 h
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* ?) }1 u" K. O# z' `+ @$ x2 t
A unique entity of male-limited gonadotropin-
3 D3 w+ v2 X; I3 u5 k. N. [' dindependent precocious puberty, which is also known
2 D9 E# o9 s2 u2 T& sas testotoxicosis, may cause precocious puberty at a* ?" p+ l2 u- T! ]8 u6 ]: g8 L
very young age. The physical findings in these boys
& Y0 V1 G9 u$ a! U4 z( Iwith this disorder are full pubertal development,: g; L& G$ a* e3 K+ x/ j
including bilateral testicular growth, similar to boys
/ Q. l8 ?+ O8 U- `0 K$ }with CPP. The gonadotropin levels in this disorder
/ T  v" [$ P" h' i1 g) nare suppressed to prepubertal levels and do not show
$ ^  M- t: _2 q- i% R1 dpubertal response of gonadotropin after gonadotropin-! S8 o0 t6 _4 n
releasing hormone stimulation. This is a sex-linked0 V6 }' }* n, i# w- {
autosomal dominant disorder that affects only9 k3 e4 H0 r9 c# ~' x
males; therefore, other male members of the family: r6 O$ p* k2 k! l1 \  ?1 L
may have similar precocious puberty.3
, _$ m* H/ d& NIn our patient, physical examination was incon-3 `8 M' d0 j0 s/ D5 h
sistent with true precocious puberty since his testi-1 `* v( k3 B- g: o) x- h4 |
cles were prepubertal in size. However, testotoxicosis$ ~2 T5 d+ O2 Q  A8 x" ^
was in the differential diagnosis because his father
" L! O+ V7 ^% ]/ _/ ]started puberty somewhat early, and occasionally,
& i: ]8 l3 b& u' Y6 c  Ctesticular enlargement is not that evident in the
& D  D' b/ S# q$ x1 {( |beginning of this process.1 In the absence of a neg-
# z! g: l( z2 J" m( f9 ]ative initial history of androgen exposure, our* U6 k% R! x3 U2 h$ b$ @
biggest concern was virilizing adrenal hyperplasia,
+ g) I% a9 {$ E5 {; a7 O9 Ieither 21-hydroxylase deficiency or 11-β hydroxylase
/ D6 B7 T+ J. e3 q8 c3 Ldeficiency. Those diagnoses were excluded by find-
( ]' [9 l! g* `" l' u$ g4 Jing the normal level of adrenal steroids.8 \$ o# m& G& K/ z
The diagnosis of exogenous androgens was strongly
7 z! m) n) A! m0 Rsuspected in a follow-up visit after 4 months because) `! s+ U1 D- \4 j4 f
the physical examination revealed the complete disap-; u3 h/ ]) S/ G3 o! T) s
pearance of pubic hair, normal growth velocity, and
) O6 c8 a5 z2 `# G7 ?8 K; z8 Tdecreased erections. The father admitted using a testos-
# E9 q$ Z. Q3 l( i; ^. Kterone gel, which he concealed at first visit. He was9 V6 t9 w' u  q  x# s
using it rather frequently, twice a day. The Physicians’( m6 L. Q1 {/ T
Desk Reference, or package insert of this product, gel or
4 {, a0 X# h! q7 N% p$ O2 Z; Wcream, cautions about dermal testosterone transfer to: K- G- V- z% k- ~" I. U
unprotected females through direct skin exposure.
* `5 X9 t' y1 w7 @Serum testosterone level was found to be 2 times the
# M' r) s3 V; tbaseline value in those females who were exposed to- S5 j$ P# Z1 ^1 _5 }3 Q
even 15 minutes of direct skin contact with their male
- Z9 x& z0 U. a9 l8 ]/ xpartners.6 However, when a shirt covered the applica-, K' i8 Q' H& s) r& Q9 h1 {
tion site, this testosterone transfer was prevented.0 a5 _. s' ?8 V8 _
Our patient’s testosterone level was 60 ng/mL,
. _# m: s+ {# twhich was clearly high. Some studies suggest that6 o/ [% ~$ z$ \) S! A0 L
dermal conversion of testosterone to dihydrotestos-2 d: |2 O, q* x, A+ o0 t
terone, which is a more potent metabolite, is more
+ c4 {7 A, m/ }- y  E$ hactive in young children exposed to testosterone
' k" |0 l2 U) k' E* W. ^exogenously7; however, we did not measure a dihy-
3 F/ c2 [+ k/ P8 n3 r  [4 n1 y' ~drotestosterone level in our patient. In addition to( O, Q, E; j' V5 W& e
virilization, exposure to exogenous testosterone in  e( U# ?5 J, r3 B( ]$ J) F
children results in an increase in growth velocity and+ X& R! |9 `; l; }6 _6 U
advanced bone age, as seen in our patient.
7 U) a5 M9 E* s8 J4 lThe long-term effect of androgen exposure during
- [, x: ^& ]) R7 w- v9 S  a2 Nearly childhood on pubertal development and final
. m0 |4 U) S& N: T5 Z5 Tadult height are not fully known and always remain
5 f8 B+ f: {5 w2 m% X: Ia concern. Children treated with short-term testos-8 T) C- K! Y4 ^  V1 A, W, v
terone injection or topical androgen may exhibit some
6 s7 _; P% o" {1 Racceleration of the skeletal maturation; however, after0 y( j5 F$ Y) C7 `2 Y
cessation of treatment, the rate of bone maturation
& c' N, e; c# o. {8 C. S( h6 k. Pdecelerates and gradually returns to normal.8,9+ ?5 ]3 O* d3 g  A. L
There are conflicting reports and controversy
5 V* E7 [# [5 W; ?, b$ ~" Q& I$ Zover the effect of early androgen exposure on adult
6 ?  c6 j8 A5 @1 I6 |penile length.10,11 Some reports suggest subnormal
- ]; j6 w% C1 Z: W  {1 Gadult penile length, apparently because of downreg-
: }  Z! n4 Q$ w9 z$ b% w; J1 gulation of androgen receptor number.10,12 However,
) G( p: l0 T5 H* kSutherland et al13 did not find a correlation between
# Y4 t$ {/ N: O/ g% T+ |childhood testosterone exposure and reduced adult
6 x: ]$ R" F- {* _5 R3 p. ppenile length in clinical studies.0 }. r$ o4 z# `
Nonetheless, we do not believe our patient is2 _: O  O9 X$ r. @7 p! ]$ d9 r9 |6 s
going to experience any of the untoward effects from& w( c+ r& h4 q
testosterone exposure as mentioned earlier because: H4 G6 r0 E# l" j, Q1 d% g4 U
the exposure was not for a prolonged period of time.: |4 T9 l) X& z3 V% ~
Although the bone age was advanced at the time of
( `; _3 k4 O: M9 vdiagnosis, the child had a normal growth velocity at7 |5 d) r4 R; k8 @; T$ P. L
the follow-up visit. It is hoped that his final adult
+ q- Q& o" A: h1 z4 Rheight will not be affected.
, W- @0 V, }* n* d5 U) ?9 }# tAlthough rarely reported, the widespread avail-
' |5 l! m# w( ^, p; |. K) k. k$ j+ yability of androgen products in our society may" M! m7 G  Z" q& c2 I) M
indeed cause more virilization in male or female2 W9 e- W5 ]" e" X+ E8 }
children than one would realize. Exposure to andro-# b# q* K& I3 a  u/ O  q' O% b! T
gen products must be considered and specific ques-6 Z  x6 R. [1 V4 @
tioning about the use of a testosterone product or1 }1 X1 L" b! l8 z) ^
gel should be asked of the family members during; D/ Z6 G/ r- @$ g
the evaluation of any children who present with vir-
  T: |& X) b% Y6 Yilization or peripheral precocious puberty. The diag-
. @9 {) F" H. D0 N" L9 Fnosis can be established by just a few tests and by
* S8 R0 s' _' s' \appropriate history. The inability to obtain such a; H4 _* S( \- z* p9 J0 A
history, or failure to ask the specific questions, may$ `1 E& `6 F& @- U9 o
result in extensive, unnecessary, and expensive! X  A& G% v9 \5 v* ~9 h
investigation. The primary care physician should be
8 w# @6 C- J  [! \$ e7 X( |0 Uaware of this fact, because most of these children7 @* ~0 N% @8 D: V
may initially present in their practice. The Physicians’# B3 J1 u2 C3 V1 F
Desk Reference and package insert should also put a; b6 S0 O, C8 T
warning about the virilizing effect on a male or
. G8 n; n6 I3 q: a# Z& G6 Yfemale child who might come in contact with some-
0 v* D. k6 l; ~8 }) Q+ z0 lone using any of these products.
. `1 V/ A6 F5 X* A  c5 mReferences
/ a' j2 i$ H: e+ J  j1. Styne DM. The testes: disorder of sexual differentiation! h" Z+ R; F# f+ U0 Q" [7 u
and puberty in the male. In: Sperling MA, ed. Pediatric
/ R/ I* V- B; _+ pEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- o7 E9 K8 Y* m& p) u9 H' h2002: 565-628.5 N  H& g) l4 B& m% t" L4 N
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 U5 E' \, G- j% ]( q( ]
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
5 E5 p- {5 M5 g6 v1 KBoy Induced by Indirect Topical
; q( P' x$ x5 S+ I* n  u5 G# ^Exposure to Testosterone9 p, B( n4 k' K
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) @4 @( p" l9 }8 j  a2 A% N
and Kenneth R. Rettig, MD1) z  U- L1 k  v4 I  V
Clinical Pediatrics$ h$ k; X( k9 y3 X
Volume 46 Number 6$ T% |7 M; n* s. i# d  w/ c
July 2007 540-543
/ \: r+ ?. n0 b$ W- S© 2007 Sage Publications
" z! Q6 D' C0 p. ?2 \5 F" P. [$ `% k10.1177/0009922806296651
5 _4 I* M/ Y" \0 ahttp://clp.sagepub.com
) Y# V4 C1 {, `6 T; d  Uhosted at
: }8 ]) [6 E) n: w% shttp://online.sagepub.com8 c! A1 {' [* J# K2 y/ {
Precocious puberty in boys, central or peripheral,
2 z/ `7 K6 y5 N% h" t$ I3 N( \& q5 [is a significant concern for physicians. Central
( |, z& f6 p0 Zprecocious puberty (CPP), which is mediated
9 B% q2 {+ m3 f- _+ O$ M; ~% Kthrough the hypothalamic pituitary gonadal axis, has8 P. N* q9 Y# V, {8 `
a higher incidence of organic central nervous system
6 y+ d9 K  A  G. R* Vlesions in boys.1,2 Virilization in boys, as manifested
2 U3 v, O3 u7 V; V+ b6 n/ k+ N6 q, K  fby enlargement of the penis, development of pubic
- \$ b6 W2 a3 o, [! w/ J* bhair, and facial acne without enlargement of testi-( q1 _! b) w! ]
cles, suggests peripheral or pseudopuberty.1-3 We
2 X/ ~4 t6 m3 o3 H7 @report a 16-month-old boy who presented with the
- o4 o# p  l4 c+ L* @enlargement of the phallus and pubic hair develop-/ H! e- K* Q4 d) l: C
ment without testicular enlargement, which was due8 I- [! n0 i  n6 @
to the unintentional exposure to androgen gel used by
* \# m7 m0 }3 G8 D$ O/ ~* y7 @, b, |* Sthe father. The family initially concealed this infor-& B/ Y5 Y# B$ j' B
mation, resulting in an extensive work-up for this
; b$ L! e4 C2 t) s) Q  w+ Ichild. Given the widespread and easy availability of
, b4 i- i. z0 [7 `9 ltestosterone gel and cream, we believe this is proba-
' V0 X* X& o4 Cbly more common than the rare case report in the3 c* y; q. T7 Y& P; H# `
literature.48 j/ R- R: S7 f
Patient Report- D) a: \2 e$ F$ ]1 j- o8 e
A 16-month-old white child was referred to the( a" R  b$ u' e4 ~) U' J4 i
endocrine clinic by his pediatrician with the concern
- G' N" m# u: N) [* B7 |of early sexual development. His mother noticed; R! [" B4 c1 h3 b% Q
light colored pubic hair development when he was# Q8 v! o% P) ~$ i2 {$ x6 A
From the 1Division of Pediatric Endocrinology, 2University of2 n% B/ V; J$ X
South Alabama Medical Center, Mobile, Alabama.9 O- I% n( G4 y, O
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* h5 w& z+ r# f$ `Professor of Pediatrics, University of South Alabama, College of. O" M. y; J, Q6 M0 F0 o
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ D) v8 ]6 r, @) ^* {3 `6 ~* m
e-mail: [email protected].
7 I7 b0 K) W8 _about 6 to 7 months old, which progressively became. u1 e3 B. a% s
darker. She was also concerned about the enlarge-
9 ^1 o+ |6 g' _' B+ {$ F% _ment of his penis and frequent erections. The child! q1 T* S' _7 H
was the product of a full-term normal delivery, with
/ P! T# A8 ^) Z: m) m- W$ u! La birth weight of 7 lb 14 oz, and birth length of
- g' ^6 K% i- ]' }# t20 inches. He was breast-fed throughout the first year
9 O2 D' X3 `+ Q8 R5 q* wof life and was still receiving breast milk along with
! j$ h* Q% o" s  g9 Ssolid food. He had no hospitalizations or surgery,  l% z/ z) A5 K2 F4 K- X
and his psychosocial and psychomotor development5 s8 W" X3 y( R5 p  x
was age appropriate.4 U$ R' S( i0 B! r5 F+ y) Q6 f
The family history was remarkable for the father,
9 [% t! U* r) C. J" ^9 Jwho was diagnosed with hypothyroidism at age 16,1 e2 {! w/ R5 M, P7 p
which was treated with thyroxine. The father’s, G, k  K2 |3 |
height was 6 feet, and he went through a somewhat  f" K, E! A  [* g, N8 d2 A
early puberty and had stopped growing by age 14.! ]$ k1 ^" F9 T! P! g
The father denied taking any other medication. The
8 Q; |0 Y' N6 y$ B. T3 cchild’s mother was in good health. Her menarche: C7 ]- Q+ I1 o4 \. J# C
was at 11 years of age, and her height was at 5 feet; ~1 e! J- L7 @; `2 t$ k
5 inches. There was no other family history of pre-: G$ R5 k2 d' h2 A
cocious sexual development in the first-degree rela-! f+ H% _1 ~$ h: q
tives. There were no siblings.
( h6 T$ r# D) \. I) i9 `5 s0 LPhysical Examination
" K% x- k7 ?1 GThe physical examination revealed a very active,) |8 g6 H2 ^% Q, b9 K9 z5 f+ j# y" |
playful, and healthy boy. The vital signs documented/ |- g* n+ j9 ]2 U, j" X
a blood pressure of 85/50 mm Hg, his length was/ E3 E5 ]7 v# y8 z8 c
90 cm (>97th percentile), and his weight was 14.4 kg2 L" z! P! }! h
(also >97th percentile). The observed yearly growth
2 [) D) }" L9 Y5 d: d. H( Qvelocity was 30 cm (12 inches). The examination of
  k& ]9 V. V4 M) ^the neck revealed no thyroid enlargement." X+ A/ s! X' d5 p( `/ F% j/ }, o
The genitourinary examination was remarkable for
: L* B* }, y. g8 @enlargement of the penis, with a stretched length of
2 }* A, J  K( \. Q8 cm and a width of 2 cm. The glans penis was very well6 U. c4 @) S) J7 |
developed. The pubic hair was Tanner II, mostly around
0 C. V) W% E, Q" ]3 t0 c7 s540( e" i& p0 o# [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ B. z- ?& M( y( r5 [& ]
the base of the phallus and was dark and curled. The( M) h% B8 W5 k- W
testicular volume was prepubertal at 2 mL each.
3 [9 O* w* W; ~0 E& j) f0 T0 qThe skin was moist and smooth and somewhat
) d  u! M( L8 coily. No axillary hair was noted. There were no  {2 p, t( y# W" _% b1 \
abnormal skin pigmentations or café-au-lait spots.3 h; D4 n" `3 R( M5 Z2 i$ i3 D, {- t
Neurologic evaluation showed deep tendon reflex 2+
# j- P% Q3 r( D2 d2 y- Obilateral and symmetrical. There was no suggestion0 i$ R6 Q' S8 w& d! |2 C3 K* Y6 q1 M! H
of papilledema.
8 }9 x8 l# k# n4 z7 nLaboratory Evaluation" b, ]4 c/ d* i! b/ O* K* Q
The bone age was consistent with 28 months by
3 F& l9 e+ r5 D! C1 F4 V5 f2 Y( m' Jusing the standard of Greulich and Pyle at a chrono-
+ w+ p, ~/ ~* s( j: i# @logic age of 16 months (advanced).5 Chromosomal
2 L  i' j+ \9 @karyotype was 46XY. The thyroid function test
9 ~% d) c& k6 Q, v% k$ ^showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 L, s8 Q+ Q: U; e9 T
lating hormone level was 1.3 µIU/mL (both normal).
. h7 A: H% c4 k- _1 G( t4 P8 p/ vThe concentrations of serum electrolytes, blood) f& _0 W: j; g" x
urea nitrogen, creatinine, and calcium all were
; C& R+ T! N: \within normal range for his age. The concentration; w* y6 C  U% O5 K' z2 f5 g+ Q* O  e
of serum 17-hydroxyprogesterone was 16 ng/dL
. ?. l7 f$ j( M6 N( @(normal, 3 to 90 ng/dL), androstenedione was 20
. d: _8 ?3 h; K2 G, }: S% U5 w4 Png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% r0 [! N$ H, }( @5 v
terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 ]0 @( i, M! d7 k6 a6 w! b
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
  C* M9 l. [" ?" N* p" C49ng/dL), 11-desoxycortisol (specific compound S)
, M% R/ \1 p& z: T& Y0 L: qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 v. Y5 r( h7 ]5 C7 e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 l2 K! B. b. V" M1 f7 E6 b. A% y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),) J! `+ r1 X( D; x! Y7 x0 Z3 [
and β-human chorionic gonadotropin was less than
- M* t; X6 m% [' v0 z9 U5 mIU/mL (normal <5 mIU/mL). Serum follicular
' L9 {7 L! J: F$ Nstimulating hormone and leuteinizing hormone; h, O) J3 F  m/ }$ c4 y7 V
concentrations were less than 0.05 mIU/mL
/ q$ P3 J/ x: S: f5 r; r(prepubertal).
) r' \+ l  {# @, O: E  u/ |The parents were notified about the laboratory
9 _3 b0 s+ J6 I' D% B7 kresults and were informed that all of the tests were
1 ]1 c$ i; [1 C# Hnormal except the testosterone level was high. The
/ r7 C' A8 S& v4 m" jfollow-up visit was arranged within a few weeks to9 h0 X1 V; s( z
obtain testicular and abdominal sonograms; how-4 M( i7 j8 i% u  b5 U
ever, the family did not return for 4 months.. Y& g5 C/ U" p) k
Physical examination at this time revealed that the# A- a2 E7 |( |' u" S/ t. p# Z. Y0 H
child had grown 2.5 cm in 4 months and had gained' G( D  G$ G) J1 g4 ?3 q
2 kg of weight. Physical examination remained
6 O" ?% P4 X' b/ Q0 F+ N% v) }unchanged. Surprisingly, the pubic hair almost com-4 e" d9 {* C0 V
pletely disappeared except for a few vellous hairs at
5 Q$ F0 C; G/ Z0 O: C+ ~* nthe base of the phallus. Testicular volume was still 2; {/ p! c: S5 d) K- e
mL, and the size of the penis remained unchanged.
5 n: x# M: }- M! U3 F' EThe mother also said that the boy was no longer hav-! y- f! y& a2 z
ing frequent erections.7 q& O" T- L6 I3 s6 p
Both parents were again questioned about use of
" Q7 Z: H2 {+ S7 J* j8 C1 O8 vany ointment/creams that they may have applied to
. }# [. |, ^" ]0 a' s' gthe child’s skin. This time the father admitted the
2 b( Y- \# @' j4 |Topical Testosterone Exposure / Bhowmick et al 541, a# `1 L# e3 S& z$ {
use of testosterone gel twice daily that he was apply-8 N& M( w" r* h6 m; N
ing over his own shoulders, chest, and back area for
5 A* R9 t5 B% Z1 ea year. The father also revealed he was embarrassed
& S: C3 k) k) ]! [' Fto disclose that he was using a testosterone gel pre-2 j$ q5 t, M  n8 c2 g8 C  t
scribed by his family physician for decreased libido- T# h% H0 \. ]& z# _0 D; a, r
secondary to depression.
- C- F/ T( w$ WThe child slept in the same bed with parents.: }$ v0 ^7 E* t: u1 R; d5 Q
The father would hug the baby and hold him on his
# i/ T4 z0 _" R) echest for a considerable period of time, causing sig-, H, s8 s1 l  O, B5 J; n
nificant bare skin contact between baby and father.
, O+ }% X2 \! `* L, l" |0 N# T4 a& rThe father also admitted that after the phone call,1 b: w( c; D: Z  A/ _
when he learned the testosterone level in the baby
. e. N/ x4 D3 E. @) swas high, he then read the product information
6 B5 x6 y& }+ t2 z" W0 I3 ?packet and concluded that it was most likely the rea-
2 \/ V; r* ?& C$ h- i( dson for the child’s virilization. At that time, they
7 E: G6 M. c: s0 @decided to put the baby in a separate bed, and the
* @0 [; }( k% S% U" h) c8 |  u$ j! h8 vfather was not hugging him with bare skin and had
! u' J/ y+ b7 L/ Z. K0 D: fbeen using protective clothing. A repeat testosterone
1 u. E& F9 W% Y. Htest was ordered, but the family did not go to the
% M8 E; `! m& Zlaboratory to obtain the test.
3 b3 I, k5 K9 f0 CDiscussion! \) Q. w7 T, f6 G1 N8 E5 H
Precocious puberty in boys is defined as secondary& f. H) }- X* x, I: v6 `  C
sexual development before 9 years of age.1,4  I: F, n4 P) H1 s) o
Precocious puberty is termed as central (true) when4 |& _+ w9 v# e  K0 E$ a# ]1 r$ @
it is caused by the premature activation of hypo-
& N5 [9 Y7 ~+ }9 d7 [+ b7 Vthalamic pituitary gonadal axis. CPP is more com-
0 p$ j: Z/ ^6 ]' [5 Z, ]3 {8 Gmon in girls than in boys.1,3 Most boys with CPP  ^. P6 P. G* Z0 D$ J3 B' J5 C
may have a central nervous system lesion that is
& P( v* P  r5 `2 C/ Iresponsible for the early activation of the hypothal-* k' `- G# V" b1 U! c, n7 m& G
amic pituitary gonadal axis.1-3 Thus, greater empha-( `+ U2 z; _% O5 _/ l0 ?' a8 l7 W
sis has been given to neuroradiologic imaging in
, ?& Q. r4 H3 C: F) S3 j4 ?4 @! ]/ A* Yboys with precocious puberty. In addition to viril-
7 V0 ]$ `, n. Y7 R4 b) a- l2 n6 ?ization, the clinical hallmark of CPP is the symmet-9 K( K, N% u$ j  F
rical testicular growth secondary to stimulation by
7 t1 r; o0 D* c& Tgonadotropins.1,3# b: f# k/ k, D3 o; g
Gonadotropin-independent peripheral preco-: F7 m. C' D& W1 o! I
cious puberty in boys also results from inappropriate
  \/ h# `% J: c1 T9 S" S  `/ ^# s) Wandrogenic stimulation from either endogenous or
. z( e0 A' u2 E6 h- [2 X1 sexogenous sources, nonpituitary gonadotropin stim-1 {( w4 o9 G3 @$ Z" W
ulation, and rare activating mutations.3 Virilizing2 _1 m- v9 w! V# R( n
congenital adrenal hyperplasia producing excessive8 H3 H9 |: m7 N6 C! U
adrenal androgens is a common cause of precocious5 i, t) l$ o+ h5 _7 t3 O
puberty in boys.3,4# d! w; `, ?: r/ Z7 a' f; T' J+ O
The most common form of congenital adrenal
% {0 I6 k) D4 w8 |, P' d% Ghyperplasia is the 21-hydroxylase enzyme deficiency.- ^; X% ^& f$ h( c  C: i4 a- V9 y& C4 ]( v
The 11-β hydroxylase deficiency may also result in
9 u- B2 U  Q4 a3 eexcessive adrenal androgen production, and rarely,. |! k: c: k: x/ _1 e: h
an adrenal tumor may also cause adrenal androgen
; G+ Q; ?, s- G5 Z) c+ n! Eexcess.1,3" A) d, {; J5 V* K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" ?7 m% Y& Q5 j  U% |542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 ?& P4 \$ O7 a' V4 w! w  @) e, |
A unique entity of male-limited gonadotropin-4 d7 W. @# Z# ^. O5 b/ Z. J2 q
independent precocious puberty, which is also known
; \. D( f/ N  U; P: K7 ~as testotoxicosis, may cause precocious puberty at a
$ s! P3 ?/ f, P4 s& }# V9 d5 E" Rvery young age. The physical findings in these boys$ v: T/ Z. n/ B7 B$ j0 N$ W
with this disorder are full pubertal development,+ h3 Y6 `( x0 W$ \: o( f9 a
including bilateral testicular growth, similar to boys
8 T0 y, l8 N# ?6 H. hwith CPP. The gonadotropin levels in this disorder
: y  ]4 @4 U0 q  Q+ O( a& O" care suppressed to prepubertal levels and do not show
/ Z) r/ `+ f/ g9 F( rpubertal response of gonadotropin after gonadotropin-) b- l1 t4 O2 l
releasing hormone stimulation. This is a sex-linked7 K# [6 I7 Y1 d  `  w9 m
autosomal dominant disorder that affects only
; R" [: G/ U" v; Qmales; therefore, other male members of the family
$ p) c7 [% G* Q1 D. o9 }! k: Cmay have similar precocious puberty.3
/ z3 {. J  h& I& oIn our patient, physical examination was incon-/ p4 Y. n* b/ t3 Y+ @: O
sistent with true precocious puberty since his testi-
: E' L: F3 A/ J, x$ q8 L, z& ?cles were prepubertal in size. However, testotoxicosis) s, N. G- s! b9 [
was in the differential diagnosis because his father/ m4 J& p  S7 B% c
started puberty somewhat early, and occasionally,
3 e. D& k! }$ v+ Ptesticular enlargement is not that evident in the( ^" |& p: L! n7 Z# E* k/ @
beginning of this process.1 In the absence of a neg-
9 E+ s& M# u. R# |& i3 F! lative initial history of androgen exposure, our
: `5 y2 A' |7 E3 O# D/ U2 {biggest concern was virilizing adrenal hyperplasia,
% B. V; H( E! E; n- r! Keither 21-hydroxylase deficiency or 11-β hydroxylase1 M$ l' }0 o& n+ |. A
deficiency. Those diagnoses were excluded by find-4 A0 a$ k8 G+ J4 _
ing the normal level of adrenal steroids.
# m( Z% W3 H/ g% |# L! ^4 xThe diagnosis of exogenous androgens was strongly: L% {/ m' J2 ~3 a' v
suspected in a follow-up visit after 4 months because& B$ v( }/ V" v0 B# t9 H
the physical examination revealed the complete disap-) e; q" A& `, c) z% b, x
pearance of pubic hair, normal growth velocity, and
$ s# i. |, b2 q: cdecreased erections. The father admitted using a testos-: C# C' `3 P6 d4 w( `$ S# k/ E
terone gel, which he concealed at first visit. He was+ T6 O, x2 q; x+ I7 u0 c, D
using it rather frequently, twice a day. The Physicians’0 `% L( u1 c, q: d
Desk Reference, or package insert of this product, gel or
5 i; v, f5 K' N9 S. Kcream, cautions about dermal testosterone transfer to
1 I( G3 ^9 T! t5 munprotected females through direct skin exposure.
  E9 m* M5 M0 {; _) N  N. @. oSerum testosterone level was found to be 2 times the
' Z' @! w, N8 Ubaseline value in those females who were exposed to2 H% n( l5 y) K; X. M
even 15 minutes of direct skin contact with their male
- g3 H  X: G) J0 L; M0 Tpartners.6 However, when a shirt covered the applica-: q: J4 x6 C: Z3 @1 o) J
tion site, this testosterone transfer was prevented.
4 b2 T1 I0 J) {3 V' uOur patient’s testosterone level was 60 ng/mL,4 ]+ i0 h, F( z( @9 t& _
which was clearly high. Some studies suggest that
% F5 n$ `  H5 }0 a2 k4 Gdermal conversion of testosterone to dihydrotestos-
$ m1 m8 o9 d1 Y' n3 t0 j$ h- e# |terone, which is a more potent metabolite, is more% j: o& P8 V' V( C0 \4 F
active in young children exposed to testosterone' g2 H1 w* I4 V% o6 S' M
exogenously7; however, we did not measure a dihy-, t4 [" U5 d) x% ~. k9 B* W
drotestosterone level in our patient. In addition to, C$ Y1 G8 q& c. E
virilization, exposure to exogenous testosterone in
. Y/ V, {: m+ g0 b" |children results in an increase in growth velocity and
/ s7 C! `0 T! T, M1 T+ I# Yadvanced bone age, as seen in our patient.. Q8 _7 [1 N" p# r6 x+ R! n9 B
The long-term effect of androgen exposure during8 A/ I4 \4 v* t. R% ~* L! c: @
early childhood on pubertal development and final0 m' w- n* o5 ~4 r( h& p1 e. ~
adult height are not fully known and always remain! Y2 _% g3 l  K' V) G5 A, d5 s3 A
a concern. Children treated with short-term testos-; o, [0 h( b; w5 E! w( u
terone injection or topical androgen may exhibit some9 [! c; J# ?5 [, e- |; }3 r4 s
acceleration of the skeletal maturation; however, after
2 C0 H% b5 {& L, \5 r, G) ^cessation of treatment, the rate of bone maturation: f( ]1 W) Y4 }8 e& C# A" H3 `
decelerates and gradually returns to normal.8,9
  |5 {6 _% f4 p+ b" ~% NThere are conflicting reports and controversy+ W' ?0 r' \" }, x2 p6 m0 j
over the effect of early androgen exposure on adult
/ q7 B3 H4 I/ m2 a. V- ~penile length.10,11 Some reports suggest subnormal
* U4 Z% v  O7 X- y$ J$ s8 }1 {( Padult penile length, apparently because of downreg-- j/ @5 f* i  Q0 O6 Q9 Z- G
ulation of androgen receptor number.10,12 However,
4 N  b' K; V% ^9 U( C0 v0 dSutherland et al13 did not find a correlation between" e4 [; r5 n8 W5 Z/ ?+ x
childhood testosterone exposure and reduced adult, \+ O! B, \% N
penile length in clinical studies.9 s% ?; Q# y" H1 Q
Nonetheless, we do not believe our patient is! v; G8 @8 E% P6 o9 w1 z: T
going to experience any of the untoward effects from
9 ]0 g. u3 C5 w/ P2 c, s$ C7 `testosterone exposure as mentioned earlier because
4 O) g! C% S; w- I  Gthe exposure was not for a prolonged period of time.( F! y/ J9 F8 p1 L$ c
Although the bone age was advanced at the time of1 ]8 W2 }' p7 K- i& q" U. [# ]
diagnosis, the child had a normal growth velocity at! Y+ \' ^/ t( ^, h  h# J
the follow-up visit. It is hoped that his final adult
6 C; g1 \9 Y4 N  ~  `; M- yheight will not be affected.9 p+ X0 |- Q6 v* S& ^+ |7 S6 r* ?$ N0 f
Although rarely reported, the widespread avail-, v. S9 D5 h9 x
ability of androgen products in our society may
* e4 D7 K4 p- J+ d" e# Y5 h7 Windeed cause more virilization in male or female1 a+ Z8 |/ P. o
children than one would realize. Exposure to andro-7 B/ [1 c  r% H/ ]1 _
gen products must be considered and specific ques-
# g8 ?; x8 B7 |/ i7 W" ~. ytioning about the use of a testosterone product or
2 a" g" p# U) D" s" y/ Egel should be asked of the family members during
& l1 [( D9 ~7 u3 J) e0 L$ t" {the evaluation of any children who present with vir-! j* }9 ]5 Q3 Y9 C% M# Y3 H
ilization or peripheral precocious puberty. The diag-' m- o8 _) G8 ~3 P6 @4 \9 x2 s: x
nosis can be established by just a few tests and by: ]. W7 R" g* P* N; p3 A+ Q
appropriate history. The inability to obtain such a: i/ m% c3 W6 Z$ s
history, or failure to ask the specific questions, may" G% C; |# `- Y2 r9 z. K
result in extensive, unnecessary, and expensive
7 A! x" P" q3 b1 m# pinvestigation. The primary care physician should be2 w" |' q1 P2 y
aware of this fact, because most of these children1 E! `4 s& B6 G3 D- `( m! M
may initially present in their practice. The Physicians’
$ p0 q7 c% Z1 d9 Z7 e! Y; dDesk Reference and package insert should also put a
5 B" I8 @/ h: D1 _& q! ~4 Gwarning about the virilizing effect on a male or" y7 Z9 [1 L, }3 F
female child who might come in contact with some-
# D- s  q, v5 |! mone using any of these products., c3 l% G0 A) A; R3 t1 u! I* K5 n
References
& r* C. |* U; n8 _- ^1. Styne DM. The testes: disorder of sexual differentiation! G) _* R7 Y! y/ B6 w- v
and puberty in the male. In: Sperling MA, ed. Pediatric6 f/ j# k7 k, z. T4 q8 o6 Q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ e5 Z8 w- ]% Q  Q. w/ o, x2002: 565-628.
0 u5 m- y6 e1 b: s; k5 c2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) D7 S/ v5 ^: G4 f8 ?; ]# l
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

5 q3 I9 e; s4 n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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