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Sexual Precocity in a 16-Month-Old) g$ r3 j7 A+ F8 ^
Boy Induced by Indirect Topical% k5 o; e* N5 ?% u
Exposure to Testosterone
' ^# [' O' Q0 e7 ~3 u8 dSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% {& @# V2 Q3 l* `" z5 N( {# Dand Kenneth R. Rettig, MD1
/ [! X3 _5 q, S6 t0 RClinical Pediatrics
: c: f: ?" T4 n! A  AVolume 46 Number 60 K- ^4 F; k* s& q
July 2007 540-543
) w+ i; D1 I. O2 ?$ m© 2007 Sage Publications2 ?+ B7 [9 q# u
10.1177/00099228062966516 X. e/ t! ]  n7 N/ G
http://clp.sagepub.com
8 g8 j6 r4 k! V9 ?hosted at
( E0 {5 t/ E& ?) P3 r1 [2 q! Y2 phttp://online.sagepub.com% m3 e9 U) U5 Q' l7 ]
Precocious puberty in boys, central or peripheral,) E4 }6 R" Z: M( {
is a significant concern for physicians. Central
2 c8 H. v' ~9 G9 i" |) zprecocious puberty (CPP), which is mediated% h! t, C8 P6 e, I
through the hypothalamic pituitary gonadal axis, has
1 g) a& v0 w' G5 c" d* L6 g1 A. w' wa higher incidence of organic central nervous system- o" Y. g) s' v: `7 G' @
lesions in boys.1,2 Virilization in boys, as manifested
0 c5 C3 D  J% w7 ^/ k$ t; wby enlargement of the penis, development of pubic
* G# N' p$ y" mhair, and facial acne without enlargement of testi-) z5 N! v3 s' ?; E+ g( v
cles, suggests peripheral or pseudopuberty.1-3 We
' d! ]5 q8 v1 L0 M! Zreport a 16-month-old boy who presented with the
# d. M* L" ^" H, ~; g* `5 z* Jenlargement of the phallus and pubic hair develop-
( C, J, A/ @; j" @# O1 r. y& G! Zment without testicular enlargement, which was due
8 ~+ |# E9 W3 gto the unintentional exposure to androgen gel used by
# X4 u+ C* ?) H/ F" k( [the father. The family initially concealed this infor-
* f! c' i2 X: {9 A1 o- J% \mation, resulting in an extensive work-up for this
. m4 Z$ h8 v' D) u; ^: dchild. Given the widespread and easy availability of% e+ n/ l& j! W- K8 W3 M$ z2 W- I
testosterone gel and cream, we believe this is proba-
# l( d$ h6 u6 y- Ebly more common than the rare case report in the( c' G0 ?# r1 H% m
literature.4
4 T/ _2 k4 [' g  Q9 H5 qPatient Report0 F& R; G  i1 J) E9 C9 A
A 16-month-old white child was referred to the
0 Q% r" b) @9 D0 ^$ eendocrine clinic by his pediatrician with the concern
# ~3 x. y: M( a5 sof early sexual development. His mother noticed
. o, H3 d; s8 S/ L2 S  E5 e1 H6 Ilight colored pubic hair development when he was
1 l# M7 ?9 s% I' }8 D1 m1 vFrom the 1Division of Pediatric Endocrinology, 2University of7 g* ~8 l) E% E9 K) O, Q
South Alabama Medical Center, Mobile, Alabama.
  j/ U: `: x3 g8 j( O- `* gAddress correspondence to: Samar K. Bhowmick, MD, FACE,
) h8 p1 x# c$ t2 ^: d" [2 T* JProfessor of Pediatrics, University of South Alabama, College of0 X/ a+ r: c) E4 F- C0 |: q
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( e* c& s  a5 k* m0 L- K# M
e-mail: [email protected].5 O* N. C9 M4 V
about 6 to 7 months old, which progressively became
/ i6 Z8 Z/ q( f# h. ~# edarker. She was also concerned about the enlarge-4 P3 q3 U" E* |. ]5 \3 J0 S* k0 g
ment of his penis and frequent erections. The child
' U1 ^6 ^5 ]3 B" W" M: T) Xwas the product of a full-term normal delivery, with
% g- J# X4 C8 P4 w- H# {4 ea birth weight of 7 lb 14 oz, and birth length of
6 e' ~1 o! O2 T2 M8 ^, W6 g8 x20 inches. He was breast-fed throughout the first year
, B, U" T6 V& j7 Iof life and was still receiving breast milk along with5 Y; h2 d; D- \) E! c& |/ M- W) A% e
solid food. He had no hospitalizations or surgery,
1 e. t  r( x9 C! |- N3 L+ F. nand his psychosocial and psychomotor development3 O2 b/ u3 C. @* u+ t
was age appropriate.
: J. T! ?4 Z( L0 sThe family history was remarkable for the father,
* L0 q% y2 [& i# |& Uwho was diagnosed with hypothyroidism at age 16,
8 N& D) z' M) Iwhich was treated with thyroxine. The father’s
! Q. a7 V0 c- B* F( P$ g. ^$ }height was 6 feet, and he went through a somewhat
5 Y5 |) U: c' O! X1 \2 i" }early puberty and had stopped growing by age 14.) }  P) q4 U. x* W3 `1 ?9 c
The father denied taking any other medication. The2 M3 w/ z# X# H4 _( B4 n
child’s mother was in good health. Her menarche
4 B. @: M* y4 p9 n, T: C* E% Z! Bwas at 11 years of age, and her height was at 5 feet3 ^, m8 b; S8 @7 ^) s, o
5 inches. There was no other family history of pre-; C5 L. l' `2 a1 t: Y
cocious sexual development in the first-degree rela-
2 I+ t  ^# r3 {tives. There were no siblings." |- p  i1 T0 f3 [) {
Physical Examination- @5 y. V% r. K& F& K+ C' g. S7 z! e
The physical examination revealed a very active,
* c& a! g6 R$ iplayful, and healthy boy. The vital signs documented
3 _5 z' S& `% {+ G) C  ja blood pressure of 85/50 mm Hg, his length was
1 a7 Z# ?  ~4 `/ A- \# y- z90 cm (>97th percentile), and his weight was 14.4 kg5 `1 q' ?, N0 e' k8 m
(also >97th percentile). The observed yearly growth
5 j% D" r( [3 Z3 g! J5 E; s2 Svelocity was 30 cm (12 inches). The examination of8 m6 r8 n4 o, A& E8 E
the neck revealed no thyroid enlargement.
& ?4 k( ?+ @1 s  e8 A, XThe genitourinary examination was remarkable for$ Y( h0 x0 g3 p
enlargement of the penis, with a stretched length of  V: K/ p8 O5 G2 @. f
8 cm and a width of 2 cm. The glans penis was very well8 n/ ^" L5 B* I5 a
developed. The pubic hair was Tanner II, mostly around) u' ^7 c6 y$ \- {7 N' F, G* C$ f
5409 G2 X' ]1 A+ W( o. X8 K1 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: o7 _7 p" s6 {% x3 z* d6 Q9 [
the base of the phallus and was dark and curled. The" |1 x/ f5 b, G; M* V" j
testicular volume was prepubertal at 2 mL each.  H! x9 }% ~. q& u# }- T  J
The skin was moist and smooth and somewhat
) z% E3 T+ p" u0 aoily. No axillary hair was noted. There were no1 G/ C. o+ f8 F! J7 W6 g9 y
abnormal skin pigmentations or café-au-lait spots.+ g2 e8 u. E( H  A9 d% d& f
Neurologic evaluation showed deep tendon reflex 2+2 y* @% o+ Z. c, r
bilateral and symmetrical. There was no suggestion
$ Y3 W/ D, a4 ?8 r5 B7 \# oof papilledema.
" c  [7 D7 b' {' U- L9 \Laboratory Evaluation0 J8 H: c6 n) W7 W% l, c" v
The bone age was consistent with 28 months by
& E$ h- i' J% e8 e2 J, Z* {using the standard of Greulich and Pyle at a chrono-
5 z7 v7 Z* {3 D' @7 C3 Blogic age of 16 months (advanced).5 Chromosomal
4 l0 @1 X  l# y+ o0 skaryotype was 46XY. The thyroid function test5 H- I( s% ~* W4 k. r. _
showed a free T4 of 1.69 ng/dL, and thyroid stimu-( I$ _. A$ ^3 N; e" a
lating hormone level was 1.3 µIU/mL (both normal).) V+ K- W$ P: D$ _, E
The concentrations of serum electrolytes, blood
/ ]! }. v9 c5 S9 \+ S9 `urea nitrogen, creatinine, and calcium all were
2 G: B. K6 f# A! \, I. q+ kwithin normal range for his age. The concentration
5 v# A, N. g8 W# T8 kof serum 17-hydroxyprogesterone was 16 ng/dL* a) B" f$ `8 p  r9 _- c
(normal, 3 to 90 ng/dL), androstenedione was 20& D* e( _( C" Z% C
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- A) h! C4 k' Y$ [! cterone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 k; F0 A0 t) n) @, k3 p: T. Edesoxycorticosterone was 4.3 ng/dL (normal, 7 to
' T( h" g& n0 \49ng/dL), 11-desoxycortisol (specific compound S)
' T8 ?* f% x' g( q8 h* Jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-. D' ]* [" c- t1 z5 R, `/ [, e; n$ K# D
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& Y  D) X+ ]! y! E2 l- `testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! t- L- L9 t5 L6 ]* l; V  pand β-human chorionic gonadotropin was less than
+ V& E/ `, V4 q; x7 C( C5 mIU/mL (normal <5 mIU/mL). Serum follicular# W6 _0 z1 F5 \$ Q! b  T
stimulating hormone and leuteinizing hormone
: p% H" |9 }7 _* ~" P3 G) Gconcentrations were less than 0.05 mIU/mL: b* h5 E9 A; c; B9 }
(prepubertal).3 ^+ ^$ B; o* z# m! Y; ?
The parents were notified about the laboratory
) K" S8 U9 D7 eresults and were informed that all of the tests were( o# P' W* Z0 c8 G! x$ w: {1 Z5 Q& p
normal except the testosterone level was high. The0 s- Z7 D$ @* |+ g0 k8 x
follow-up visit was arranged within a few weeks to
2 C7 F( O& |- B- j- V' o( lobtain testicular and abdominal sonograms; how-' P2 S% Q. g0 Q. Z! m& {
ever, the family did not return for 4 months.; D! m) m0 ]) E' T: b  v
Physical examination at this time revealed that the
% z0 z+ p0 W& T! i( @+ s" Q/ _child had grown 2.5 cm in 4 months and had gained$ I  `8 i& L+ }9 |1 Z
2 kg of weight. Physical examination remained& S0 O, W3 ]5 G5 M) x3 T5 D! x
unchanged. Surprisingly, the pubic hair almost com-
2 g. J* N0 O) V0 C. ]: |: }2 Wpletely disappeared except for a few vellous hairs at
4 }# T$ ^3 ^8 qthe base of the phallus. Testicular volume was still 2: u4 ]! O4 v9 Y% C1 I; s( p2 o2 e; ~
mL, and the size of the penis remained unchanged.
9 q' Q' }  }' L6 o' g' |% s3 y* BThe mother also said that the boy was no longer hav-. w* [/ V. g2 V3 g- u8 W1 |9 t6 ]
ing frequent erections.
+ Z" o3 S  Y. ^& J2 H: m/ X$ m) X; h4 KBoth parents were again questioned about use of7 J6 ]4 r, ^# I
any ointment/creams that they may have applied to7 q0 d8 G8 v& ]0 k" x
the child’s skin. This time the father admitted the
0 L/ {% B! V% K6 B# Y9 `Topical Testosterone Exposure / Bhowmick et al 5411 Z1 G( N9 r/ P" a4 b2 T6 ?
use of testosterone gel twice daily that he was apply-
. c7 o* }5 N% Q+ ^/ _3 P3 \ing over his own shoulders, chest, and back area for& O  @% W: A& u* X4 d% P. C/ w
a year. The father also revealed he was embarrassed$ F2 z6 F; i; p
to disclose that he was using a testosterone gel pre-
$ E: Z+ \/ w% N) Q& tscribed by his family physician for decreased libido
" H; n" p7 z' Ssecondary to depression.! o8 B: T% T2 e) I
The child slept in the same bed with parents.
* m; b+ s# V( m3 m" N* U" a# JThe father would hug the baby and hold him on his
4 F; R1 x9 F' q$ ~! Wchest for a considerable period of time, causing sig-' C. S4 J8 `' d; H
nificant bare skin contact between baby and father.
4 F+ A  {% j! ]3 M& mThe father also admitted that after the phone call,0 T6 `; g! t- L7 o' e! c- S9 x
when he learned the testosterone level in the baby
4 O0 h' E/ B/ J. G- K* Iwas high, he then read the product information- U  H( y$ Q) d% {
packet and concluded that it was most likely the rea-! [, Y4 _9 m% V1 R- q
son for the child’s virilization. At that time, they/ o: Y9 i' k! p6 c- R9 O1 j7 f$ U4 O* ^
decided to put the baby in a separate bed, and the# D9 H3 j" l. C# L
father was not hugging him with bare skin and had
) [5 H. n0 k, @been using protective clothing. A repeat testosterone) X% _. n( s; _4 Z5 {  ]9 h
test was ordered, but the family did not go to the. B& ^2 I& T$ K1 P  j
laboratory to obtain the test.
/ U' r4 r* _! @! y. `4 ?( GDiscussion7 q, ~' z% C/ P& }
Precocious puberty in boys is defined as secondary; `3 y, {2 k  E  b7 d+ Q8 o
sexual development before 9 years of age.1,4! [; q8 E1 F7 |- {4 T% G  a$ o% s0 R% D
Precocious puberty is termed as central (true) when
+ o( W- x+ I* o  [- \6 ]it is caused by the premature activation of hypo-
/ L5 u: |  m! Q8 kthalamic pituitary gonadal axis. CPP is more com-
$ k$ u4 o: I4 e/ Lmon in girls than in boys.1,3 Most boys with CPP
# P; ?7 O% T5 u3 z6 h* Omay have a central nervous system lesion that is1 X/ s- s0 g$ P8 n& G% `
responsible for the early activation of the hypothal-
( [$ I, v6 G( a* l7 m  xamic pituitary gonadal axis.1-3 Thus, greater empha-; Q/ U+ X+ ]& A( j
sis has been given to neuroradiologic imaging in
+ _' x, I* t# m. @; X9 I- Rboys with precocious puberty. In addition to viril-
+ [9 o! F- T  P' E$ e  wization, the clinical hallmark of CPP is the symmet-$ E* h5 g. d- U5 k
rical testicular growth secondary to stimulation by
; z3 a3 P* [6 u, egonadotropins.1,38 E6 K0 E: q6 ?8 I# g
Gonadotropin-independent peripheral preco-
, y4 ^/ H  Q# i& a4 e. d3 Bcious puberty in boys also results from inappropriate
6 a4 C" f5 p# g* g- v' `androgenic stimulation from either endogenous or) V7 Y5 F) f8 E9 t
exogenous sources, nonpituitary gonadotropin stim-
  u% X  V) [4 m+ u' V1 q( {ulation, and rare activating mutations.3 Virilizing. L5 a( @/ m. C* L5 U; r* R1 Y1 A
congenital adrenal hyperplasia producing excessive
) U- k6 s+ Z* s# q3 d  O) G! aadrenal androgens is a common cause of precocious
! U" ~, w- J# [8 W6 w" t& {' K/ _puberty in boys.3,4- o: D1 X, Q6 s# i9 \! l
The most common form of congenital adrenal
' s( C% b) Q% `& q6 zhyperplasia is the 21-hydroxylase enzyme deficiency.
; C, x  W4 S+ z( GThe 11-β hydroxylase deficiency may also result in" q+ E* L" e& L/ k/ E
excessive adrenal androgen production, and rarely,
- Y6 B$ X0 b% x( xan adrenal tumor may also cause adrenal androgen
3 M8 Z" c4 G& V( Q" X9 E7 r3 Cexcess.1,3
( C/ n3 `& z$ Hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* s# P; O: E3 E& E: C1 a542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 y0 l! r5 f9 X; P
A unique entity of male-limited gonadotropin-
! R, g7 N6 a# i+ a4 v% j1 Z4 ?! Bindependent precocious puberty, which is also known6 c. x5 p! ^2 V' V6 g  I1 c
as testotoxicosis, may cause precocious puberty at a' Q, G8 L- x6 V% `, t! M, Y% Q
very young age. The physical findings in these boys* t0 q! W# Q3 O
with this disorder are full pubertal development,
! n8 h+ K' i. B5 W: _including bilateral testicular growth, similar to boys
8 Q# r* J* J0 a+ g6 Rwith CPP. The gonadotropin levels in this disorder$ ^2 _. r2 z$ J
are suppressed to prepubertal levels and do not show
3 M6 F# g5 }+ h2 L, l% X0 kpubertal response of gonadotropin after gonadotropin-
2 m- Y1 a, |8 M. R' m% R- jreleasing hormone stimulation. This is a sex-linked* T* O3 N) u9 m+ h5 k4 X# |0 z. G- h
autosomal dominant disorder that affects only# y- a* e1 U$ W$ A
males; therefore, other male members of the family, ]( d* t" b  h2 s: ]* u
may have similar precocious puberty.3
" k5 X, `2 v* G' R9 B3 L* sIn our patient, physical examination was incon-5 ^' L. n1 |% n: w( {" \
sistent with true precocious puberty since his testi-6 T$ d! X5 s' A. _3 z
cles were prepubertal in size. However, testotoxicosis% |  m  D1 @$ I
was in the differential diagnosis because his father
: @/ ?2 Q6 }8 y9 {. Hstarted puberty somewhat early, and occasionally,- k2 c4 t6 H& Q. F8 r8 r! _
testicular enlargement is not that evident in the
! s$ T( p% p! j1 h6 Obeginning of this process.1 In the absence of a neg-
9 P. g8 P. J# ~; t6 v& J6 h& w+ V# y% Sative initial history of androgen exposure, our* O# \/ V: d, K
biggest concern was virilizing adrenal hyperplasia,
! o# k7 X4 {7 B; ?0 v9 Y& z4 Seither 21-hydroxylase deficiency or 11-β hydroxylase6 T$ b' L3 [  z; L4 ]7 k' d( q
deficiency. Those diagnoses were excluded by find-4 J( Y* @! w5 y) O1 ^# X
ing the normal level of adrenal steroids.
. L. P7 M, h0 C. d9 H: ^The diagnosis of exogenous androgens was strongly8 ?$ }" g2 ~& P1 p7 U9 }/ X$ B& e
suspected in a follow-up visit after 4 months because
1 R* O3 z$ I6 ]# I3 G8 c( R1 Y9 j( Uthe physical examination revealed the complete disap-( I. L5 O; M4 E6 A' t7 k
pearance of pubic hair, normal growth velocity, and, X5 q+ @- C1 j7 p6 Y
decreased erections. The father admitted using a testos-: _* X4 b1 c2 v! K, u' S
terone gel, which he concealed at first visit. He was
5 C/ Y4 o" ?- T) g9 yusing it rather frequently, twice a day. The Physicians’8 [1 M, q# E: R: e. t8 W3 [9 _
Desk Reference, or package insert of this product, gel or
5 h6 X* h5 e# W3 {5 Rcream, cautions about dermal testosterone transfer to
) g; h4 Q. Y1 f+ {unprotected females through direct skin exposure.
3 V1 \! S; h/ K9 f% @* p; D7 SSerum testosterone level was found to be 2 times the# ~3 v4 e$ V2 |6 g& f* q6 t& c  C
baseline value in those females who were exposed to7 c8 N# n7 Q9 ]" H0 X0 J& E2 `
even 15 minutes of direct skin contact with their male
0 O: X; F$ B  ], }partners.6 However, when a shirt covered the applica-/ A; i3 g* I0 y; D8 n8 F# l
tion site, this testosterone transfer was prevented.  y2 d2 M1 `( ?9 g. f
Our patient’s testosterone level was 60 ng/mL,
, b: C% i! B/ E4 S# z1 Xwhich was clearly high. Some studies suggest that- j- E# G9 B" Z4 W
dermal conversion of testosterone to dihydrotestos-! l1 r: l. e% i- c% L$ i0 V  o. m1 X
terone, which is a more potent metabolite, is more
8 D" j9 _  {* e1 Y  Factive in young children exposed to testosterone
# x5 ?& T. m1 B# {exogenously7; however, we did not measure a dihy-, ~' M: d6 y+ Y. z8 ]/ f
drotestosterone level in our patient. In addition to
/ P5 {  U( u4 Jvirilization, exposure to exogenous testosterone in
' H* ^% `% X) S$ O7 tchildren results in an increase in growth velocity and: e# _+ z  v; G& h  [# I
advanced bone age, as seen in our patient.; F& e% A$ ^' f8 q4 S
The long-term effect of androgen exposure during
  q: ?7 B9 j+ `5 P! eearly childhood on pubertal development and final
; ]4 Z8 R  E( C' G( j$ b) C' nadult height are not fully known and always remain6 n* r- x. i3 |5 r! S4 d# x
a concern. Children treated with short-term testos-
3 D6 [. d- {8 c- \; Kterone injection or topical androgen may exhibit some
2 \; Q6 E+ U- m. {, Q4 Qacceleration of the skeletal maturation; however, after2 V/ Q/ P+ p% h' q6 U- O
cessation of treatment, the rate of bone maturation  L  x2 A* S, T9 ?7 n, _0 x4 V: ~
decelerates and gradually returns to normal.8,9. ?( h3 J2 j# s# _
There are conflicting reports and controversy
% ]7 W5 q' H" F' Y0 a6 _. ?over the effect of early androgen exposure on adult
8 G& }; \% j9 m/ [7 kpenile length.10,11 Some reports suggest subnormal+ s2 G" h, p# T
adult penile length, apparently because of downreg-
# ?! K0 A# v; O" O4 t' t# U4 x# dulation of androgen receptor number.10,12 However,
2 \. I) P7 T9 J% R* P4 B2 PSutherland et al13 did not find a correlation between* r2 k" ?! q/ o8 S+ w2 o
childhood testosterone exposure and reduced adult! u' J+ o2 G5 u/ k5 Q1 V
penile length in clinical studies.
  |: q2 c! E0 g1 a& Z+ ~Nonetheless, we do not believe our patient is
; ]# |/ y4 J; n1 {7 D! O5 a! Jgoing to experience any of the untoward effects from% ]% t0 [- x3 j& E4 j
testosterone exposure as mentioned earlier because7 z' ~5 o; f+ {  s3 g2 L7 g" Q
the exposure was not for a prolonged period of time.
! C3 x6 A; s) R: yAlthough the bone age was advanced at the time of, f# I/ d/ \7 i( K9 G1 d* l7 W, t' q
diagnosis, the child had a normal growth velocity at: Z9 U+ p) p% T! D  h- s
the follow-up visit. It is hoped that his final adult2 S8 e! r( W3 I( K3 _$ f' ?7 J+ W2 ^
height will not be affected., Z6 C( W% M# P
Although rarely reported, the widespread avail-2 {1 j$ S3 g% H
ability of androgen products in our society may
' k  m5 t' p: `4 Pindeed cause more virilization in male or female
2 R$ a; A" T/ _. K1 q7 R$ C. W2 zchildren than one would realize. Exposure to andro-
& I" ]2 a+ N3 m/ \$ I6 e$ t. I: |gen products must be considered and specific ques-
1 t. y4 Q2 u) L9 A0 W. W' Jtioning about the use of a testosterone product or- A3 y& j$ X( y5 ]8 I: ~  m% Z6 [
gel should be asked of the family members during
# {7 J$ V1 P  `the evaluation of any children who present with vir-
1 g, q% d( e6 g0 @4 x- v$ Silization or peripheral precocious puberty. The diag-/ t$ Z; s3 [2 S' D- ]7 `: M, j1 v  K8 I- _
nosis can be established by just a few tests and by
5 i; t, y3 C% h4 T* J& R7 pappropriate history. The inability to obtain such a7 f% H& j% y% x1 }2 Z
history, or failure to ask the specific questions, may+ i3 `5 {- h8 ]3 l4 ?- U8 O( ?4 ~! M
result in extensive, unnecessary, and expensive
$ Q; U) v/ A# l" p6 n0 Y3 Dinvestigation. The primary care physician should be
2 E: T' m; d+ }7 k7 C, r+ waware of this fact, because most of these children
% q9 ^7 E- e( O! I; X  d( nmay initially present in their practice. The Physicians’
- F1 ?  J  V$ l, G, j# d7 e$ PDesk Reference and package insert should also put a- K4 H0 K/ J- M* z
warning about the virilizing effect on a male or
4 |  z0 v. a* \  g) [female child who might come in contact with some-
& z$ a  l* b& U% d. ~one using any of these products.6 t) L- C0 L6 \& X* _+ n: l
References
7 e: w% q. V# H! h2 r/ t1. Styne DM. The testes: disorder of sexual differentiation* b" @. u1 P  V. b) T& N4 a% |
and puberty in the male. In: Sperling MA, ed. Pediatric
2 {5 b4 Z$ T! Y$ G3 LEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ n4 ?! C$ R' a& q6 }; N- T7 z( H2002: 565-628.1 C7 y7 q  Q" \& }. s
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 x( X* M/ r( \1 y- }9 f
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
4 W- b  b0 K9 V& bBoy Induced by Indirect Topical
. u7 e. ^0 v5 d$ W8 y6 \! e) kExposure to Testosterone# H5 w8 t4 T4 V3 H2 a. D
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( `) J/ A6 o/ \6 Y0 G* l$ g; z( B* W& `
and Kenneth R. Rettig, MD1
- ]0 w; V! t' `Clinical Pediatrics
0 \/ v9 U5 ^5 DVolume 46 Number 6
% g7 X% K. G  z* i7 @July 2007 540-543* f! g  {# j' m- @( W  f7 n
© 2007 Sage Publications3 E( R8 y& \6 K0 }3 f0 t
10.1177/0009922806296651' L: g+ r) Y8 H
http://clp.sagepub.com
% j" }3 J* v- N3 Y( r+ `hosted at
( u% a) \9 \+ N2 hhttp://online.sagepub.com& ]* N5 S) d* m  i$ K
Precocious puberty in boys, central or peripheral,* ~  R0 `  x* R% p% l# _
is a significant concern for physicians. Central0 P% A2 U) O! R" [
precocious puberty (CPP), which is mediated0 ~8 [& i# t0 u
through the hypothalamic pituitary gonadal axis, has
5 ^4 ]1 ?+ v: f8 w2 ]a higher incidence of organic central nervous system
$ v( l, `3 t" Alesions in boys.1,2 Virilization in boys, as manifested4 ^8 F7 Y1 [! T7 h2 ^
by enlargement of the penis, development of pubic) Z$ l) ~2 N6 U# h" q: X. I
hair, and facial acne without enlargement of testi-$ p4 @5 W" |* I1 {; _
cles, suggests peripheral or pseudopuberty.1-3 We
: ?$ Q! l1 \5 j2 g: Sreport a 16-month-old boy who presented with the4 h& @  J  q! _# K
enlargement of the phallus and pubic hair develop-+ Q( r% |1 S) a4 d5 ^# X
ment without testicular enlargement, which was due
, s" C: ^( t. Rto the unintentional exposure to androgen gel used by
+ @5 Z7 p" [$ e/ u/ [; [# j* Y7 J9 jthe father. The family initially concealed this infor-
8 h& z1 z8 w$ B8 }: F2 Gmation, resulting in an extensive work-up for this- P  i' @$ p0 ?
child. Given the widespread and easy availability of
3 F. u5 E- I9 W9 m- htestosterone gel and cream, we believe this is proba-
; {4 [* U% I' g% Fbly more common than the rare case report in the
% s5 n7 z* i) X0 L- u. S6 J9 pliterature.4% Z% ~; P, I. J8 A) c
Patient Report
  K; ~+ s  t& a. i, P, L! @! B$ ZA 16-month-old white child was referred to the2 |; i9 Z+ v6 V" I0 K6 M
endocrine clinic by his pediatrician with the concern" O% n0 X  _6 b
of early sexual development. His mother noticed  c: m# a9 o  p, V9 }$ P7 x1 Q
light colored pubic hair development when he was  c- X% h  P, a  D& S1 n$ o+ Z" E
From the 1Division of Pediatric Endocrinology, 2University of
8 ]# x% u- H% z, m0 WSouth Alabama Medical Center, Mobile, Alabama.6 }- W, \4 W9 l! q* ]% @( F, `
Address correspondence to: Samar K. Bhowmick, MD, FACE,
0 U; L6 H7 g( G. QProfessor of Pediatrics, University of South Alabama, College of
3 `3 H& H' g/ D0 WMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 y# P8 `% K. W' ^
e-mail: [email protected].
( s# I( l5 g0 \1 _7 aabout 6 to 7 months old, which progressively became
; C' T& E8 ?  H! ]8 [) A# d2 _5 fdarker. She was also concerned about the enlarge-0 x: D" v' V* ^4 M  {  b1 j
ment of his penis and frequent erections. The child
# t5 p# f( U9 @' b- o/ c0 g4 d0 Zwas the product of a full-term normal delivery, with+ x) ^* k6 e: P3 O/ q' S7 X
a birth weight of 7 lb 14 oz, and birth length of
8 b  G, `0 \& T; G20 inches. He was breast-fed throughout the first year
" v" z+ K8 W0 Q( x1 p6 wof life and was still receiving breast milk along with
7 w' K) O( M( X6 S) e; fsolid food. He had no hospitalizations or surgery,/ ^% @* o/ o! P; X# \! v/ h, |# C
and his psychosocial and psychomotor development
3 }+ Q* W& x: }. r. x, owas age appropriate.' B  w+ d! G; g  X5 M
The family history was remarkable for the father,- Q  i9 ?* D2 ?
who was diagnosed with hypothyroidism at age 16,$ \8 @# O5 c3 v) _, g. }& e
which was treated with thyroxine. The father’s
* ]) U+ e4 c) s; B) Z4 d# y6 s' _height was 6 feet, and he went through a somewhat( c# H9 F% r" b& u( i& x6 A
early puberty and had stopped growing by age 14.
6 |3 ^5 |# t) i+ Z! A5 qThe father denied taking any other medication. The, J; d4 c( S- p
child’s mother was in good health. Her menarche
% E7 }* _: M3 A9 K: M/ i' M. B9 ewas at 11 years of age, and her height was at 5 feet: r" [, D  o& r( v' g5 W
5 inches. There was no other family history of pre-
) x- ^2 N" g+ s, S' X; Pcocious sexual development in the first-degree rela-: b4 C7 l5 ~+ _2 k  J( f! u$ |' b
tives. There were no siblings.
9 R5 ?- o* {% P. u3 t, ZPhysical Examination
! s: ?* M" R5 h3 n5 d9 GThe physical examination revealed a very active,
# Z8 K/ Q% T9 {- v1 t. J5 Wplayful, and healthy boy. The vital signs documented
% n9 e* \7 d% P* aa blood pressure of 85/50 mm Hg, his length was- W4 L5 n, H% [! l
90 cm (>97th percentile), and his weight was 14.4 kg8 _+ t& z" M3 }* |* k) l
(also >97th percentile). The observed yearly growth0 E/ S  }1 R: |8 k3 p
velocity was 30 cm (12 inches). The examination of2 m0 J' L, t. T( D6 Q7 H5 E
the neck revealed no thyroid enlargement.
0 k5 }# h9 v8 P4 I5 o3 M. E6 r. G7 ~1 iThe genitourinary examination was remarkable for5 A9 }/ ]; z/ \4 G6 i3 A+ o  |
enlargement of the penis, with a stretched length of% H) c/ @( m# N2 L8 G! r) N
8 cm and a width of 2 cm. The glans penis was very well
5 }  N$ W9 F" w- i4 Bdeveloped. The pubic hair was Tanner II, mostly around; L8 m) o# I5 c5 ^
540
: n+ D7 P8 b! t& ]" K, p/ Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ K' L7 \' z' S' L. ~3 cthe base of the phallus and was dark and curled. The
. t. O5 f* `* ~1 O3 Ctesticular volume was prepubertal at 2 mL each.& {' Y: h( {# a: u0 z
The skin was moist and smooth and somewhat* J8 V5 C8 v8 q
oily. No axillary hair was noted. There were no
5 A6 w* z/ F( [+ [, Oabnormal skin pigmentations or café-au-lait spots.- }5 I4 a4 {  b9 p6 X" z; p' [
Neurologic evaluation showed deep tendon reflex 2+
: n8 \4 B, ?: p" o: s8 Jbilateral and symmetrical. There was no suggestion
) N$ p, Y- ^" n- ?of papilledema.
% S- \( `3 Y3 Q  l& Y2 iLaboratory Evaluation
& t; a/ J' U: ]' e1 `0 AThe bone age was consistent with 28 months by
; C; M# i, C- I, T" v* [using the standard of Greulich and Pyle at a chrono-. x! e" L4 j2 y2 u; A; }7 }" I/ @
logic age of 16 months (advanced).5 Chromosomal
0 z1 o  }& a0 N" x4 Hkaryotype was 46XY. The thyroid function test
8 R+ z+ b$ f7 A2 ^* N0 vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-' v+ `8 P) |2 O6 [% P, i
lating hormone level was 1.3 µIU/mL (both normal).
% w. t+ U. L: yThe concentrations of serum electrolytes, blood
8 Y  Q8 F, Z. j( j  D# \6 s/ Ourea nitrogen, creatinine, and calcium all were2 t( ^0 G: C+ z
within normal range for his age. The concentration
( D6 n1 f: _$ z8 dof serum 17-hydroxyprogesterone was 16 ng/dL/ K& [6 p, F! D; P0 Z* g+ R
(normal, 3 to 90 ng/dL), androstenedione was 20
6 }' B, k  v" f  p, G0 Mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 A: K* y9 ?3 b; V! j/ S5 @
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 ?( O, g8 [6 L( b7 F/ edesoxycorticosterone was 4.3 ng/dL (normal, 7 to$ M+ o: H7 F- I8 w
49ng/dL), 11-desoxycortisol (specific compound S)
, {& t9 n  Q- [$ ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- z% w0 F8 o' L/ T% U2 R& g
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. o( c8 ]) H4 l3 U, t
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),* C$ O: `. w9 ~/ X4 b) F+ F
and β-human chorionic gonadotropin was less than$ x2 T2 x! _# T; ~5 O2 y
5 mIU/mL (normal <5 mIU/mL). Serum follicular
, d' h( r* L4 K$ k( J/ tstimulating hormone and leuteinizing hormone( K: C% {2 d) z4 g1 U* Z& ?" m" s
concentrations were less than 0.05 mIU/mL$ o8 E4 I' n* v
(prepubertal).
: ]7 [* y# p6 O. Y4 C0 x* bThe parents were notified about the laboratory
; i, p4 i0 G1 _+ m- I) |results and were informed that all of the tests were2 J9 j8 N# A( c' U- j
normal except the testosterone level was high. The7 V& H5 H* G5 }' a
follow-up visit was arranged within a few weeks to0 o% e6 j: {8 d7 p9 Q' a: _
obtain testicular and abdominal sonograms; how-
, {6 }  j  p% mever, the family did not return for 4 months.  {& V: W0 V+ F/ Z, S% y% O& P; i9 Q2 @
Physical examination at this time revealed that the7 h: ]3 \# S- W8 E# ^: K/ d; `
child had grown 2.5 cm in 4 months and had gained
) F2 F  K3 U5 I' _2 l/ {" |7 W2 kg of weight. Physical examination remained2 Y1 o5 x$ S, x- h" F
unchanged. Surprisingly, the pubic hair almost com-0 y2 _* x# O9 N3 j! ?. Q
pletely disappeared except for a few vellous hairs at
4 t/ @; q  U" v( z, D/ R2 B. I( wthe base of the phallus. Testicular volume was still 2
; d( [' ?* L/ H( Z0 VmL, and the size of the penis remained unchanged.
; j9 N  A6 H. ]% z' HThe mother also said that the boy was no longer hav-
, t  }5 P" l' M7 F0 j2 J- iing frequent erections.
) }  @1 N: D0 ZBoth parents were again questioned about use of
* @1 a; A' F# x3 p# Z2 W  a0 cany ointment/creams that they may have applied to$ r) ?2 y. D( B
the child’s skin. This time the father admitted the) B# I* ?% o$ p1 L. J; @( m
Topical Testosterone Exposure / Bhowmick et al 5410 _' m, n8 i2 w* s
use of testosterone gel twice daily that he was apply-3 u; z! q+ P9 M3 x
ing over his own shoulders, chest, and back area for
  x; }# y1 @# K8 d) o6 ]a year. The father also revealed he was embarrassed
( I" z  W0 r9 P' A. w8 mto disclose that he was using a testosterone gel pre-+ ?9 m8 A: c$ {% M
scribed by his family physician for decreased libido
5 K& V1 R( \8 E5 @% I! ssecondary to depression.
2 y4 L) C5 `$ g8 |: ]! ]The child slept in the same bed with parents.* a3 ^+ S" `& ?; j4 [
The father would hug the baby and hold him on his, N1 Z8 E3 Y+ }5 j6 N" U1 a4 P0 ?
chest for a considerable period of time, causing sig-
: l1 E4 E/ f9 ]9 A& S7 Znificant bare skin contact between baby and father.2 Y3 Q0 l* \8 X  I$ ]& w
The father also admitted that after the phone call,
& r" p# l) J0 A1 U1 G' X6 K' ~when he learned the testosterone level in the baby  |' M2 O- h# z3 z& a7 I
was high, he then read the product information  M' L- J: S4 ?0 q/ [5 }
packet and concluded that it was most likely the rea-
7 F: \, g- a5 I/ U) B0 nson for the child’s virilization. At that time, they) u& `) t. Q( _0 ?
decided to put the baby in a separate bed, and the
9 F$ ]1 J! j, T, v. ufather was not hugging him with bare skin and had
/ E$ H) l; E- i) _5 ubeen using protective clothing. A repeat testosterone4 K9 h7 ]  u+ V5 k$ e1 V; Y; W
test was ordered, but the family did not go to the
8 [  n) N$ y+ ~, ?laboratory to obtain the test.+ H6 F! V, d0 V
Discussion" w2 |2 r, R9 S* u
Precocious puberty in boys is defined as secondary
" A" ?, B" H5 h. \- {; bsexual development before 9 years of age.1,4
) Q2 S! [" v$ [" T" N7 ~Precocious puberty is termed as central (true) when" W8 `1 h' o8 ~" o
it is caused by the premature activation of hypo-/ P2 G! m; r. |/ q9 J
thalamic pituitary gonadal axis. CPP is more com-
- a' W7 b0 c# r% }mon in girls than in boys.1,3 Most boys with CPP
9 U. M. M( C  Vmay have a central nervous system lesion that is. h! |$ B  M' \# h1 G
responsible for the early activation of the hypothal-
  C+ ~. \( O2 B+ [amic pituitary gonadal axis.1-3 Thus, greater empha-
2 ?, l  S3 G2 L5 B, d- M0 K0 P* c; wsis has been given to neuroradiologic imaging in
$ Q; |) ]5 H" @boys with precocious puberty. In addition to viril-& t0 L" h' P$ V* H
ization, the clinical hallmark of CPP is the symmet-- ?* \/ }& _7 i, C9 [. D6 }
rical testicular growth secondary to stimulation by
4 u! o) _5 \, l4 K/ pgonadotropins.1,3. ^& P9 a5 ^( p5 R
Gonadotropin-independent peripheral preco-
& d8 y0 C: ]: x' |' Ycious puberty in boys also results from inappropriate& I2 Y; Q" K1 |
androgenic stimulation from either endogenous or. J) g# r- I, i/ u
exogenous sources, nonpituitary gonadotropin stim-
" L/ m, V! F1 Y  dulation, and rare activating mutations.3 Virilizing) N- O3 V* u; l& _3 Q! M
congenital adrenal hyperplasia producing excessive
# w7 A1 b" [7 {  Zadrenal androgens is a common cause of precocious) W6 w3 k- {& a) M1 {
puberty in boys.3,4
/ I, A* V0 ]; R$ O5 ?1 G( BThe most common form of congenital adrenal
8 A! k( Y) h% Q; L2 ?8 J7 @7 Q+ Thyperplasia is the 21-hydroxylase enzyme deficiency.- Z3 F  A! z8 d
The 11-β hydroxylase deficiency may also result in
3 Y! n5 L( u( f/ m+ x6 R7 Q0 q, Fexcessive adrenal androgen production, and rarely,
" Z& y: f1 k) ?! Zan adrenal tumor may also cause adrenal androgen
# }1 H6 [! e3 m" Oexcess.1,3
: Q" n$ k- H! g4 Tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& W: k0 l; N- z& [+ [
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 v8 j. X# u, E  MA unique entity of male-limited gonadotropin-1 j9 U  ], X4 _+ C: V8 M7 }
independent precocious puberty, which is also known  g' q% p3 z. }2 j0 }
as testotoxicosis, may cause precocious puberty at a
3 j, _. ]- c7 l5 Q4 Xvery young age. The physical findings in these boys
3 L) a% {, [7 X9 G8 ?2 q" Kwith this disorder are full pubertal development,; x4 S! s$ ~  D4 R! S9 |
including bilateral testicular growth, similar to boys
) D+ \6 d7 q" s9 A0 ~, [with CPP. The gonadotropin levels in this disorder
6 P" \9 w5 j- k. Y1 mare suppressed to prepubertal levels and do not show
7 a* j4 Q+ Y, Z1 P) a8 W- {& Ppubertal response of gonadotropin after gonadotropin-
4 U( }7 G6 w! b: Mreleasing hormone stimulation. This is a sex-linked; \2 K1 S/ N, D) {/ h! Y
autosomal dominant disorder that affects only
) V, |6 p  Z. |! g, umales; therefore, other male members of the family* a0 T2 [, z$ d$ `- S
may have similar precocious puberty.35 S- K) _8 x) _& Q% Z- F: |% O; K
In our patient, physical examination was incon-- y, a3 x6 G0 y/ D4 F4 O
sistent with true precocious puberty since his testi-
- ~, ^3 M* a6 c  m% ccles were prepubertal in size. However, testotoxicosis
3 h/ B% [4 g! I4 b' Z1 Twas in the differential diagnosis because his father- J8 C* `$ g5 D: P* m6 _; q9 @2 R
started puberty somewhat early, and occasionally,! M. V4 R% i* s7 f: Z9 [& d2 j
testicular enlargement is not that evident in the1 B+ ]% O  _3 N4 q; u1 U- p3 B
beginning of this process.1 In the absence of a neg-
" ]' y3 \7 Y1 O- k4 Eative initial history of androgen exposure, our
( N% n' |5 ]! \1 f- }4 I. a/ Q4 n' gbiggest concern was virilizing adrenal hyperplasia,
5 e3 A" L, s; f; w, Leither 21-hydroxylase deficiency or 11-β hydroxylase/ }, T2 y1 N( M3 d
deficiency. Those diagnoses were excluded by find-2 r- k6 _: q; H& W1 ~
ing the normal level of adrenal steroids.. Z0 M% l$ d3 r3 _0 m# Z
The diagnosis of exogenous androgens was strongly
9 |% t% i6 C6 U( Zsuspected in a follow-up visit after 4 months because
' [( Y+ L3 j3 p2 B  g3 bthe physical examination revealed the complete disap-
( t7 I) e% {) c7 y5 Epearance of pubic hair, normal growth velocity, and# i' `" c- q5 \+ G' D8 ~6 q
decreased erections. The father admitted using a testos-( V5 ^9 @# ?4 ?3 c$ G8 h/ x
terone gel, which he concealed at first visit. He was
; S4 }- E  M) ^  d- @6 [using it rather frequently, twice a day. The Physicians’) d9 |/ k! ?' R' a3 g1 \
Desk Reference, or package insert of this product, gel or, M3 n( z9 r2 z% e
cream, cautions about dermal testosterone transfer to* N4 P+ ?5 j% D( F% g
unprotected females through direct skin exposure.5 y. z) {2 x8 Y) h# `$ l+ u
Serum testosterone level was found to be 2 times the" c' c6 n( G" o% [4 F0 |/ z* E
baseline value in those females who were exposed to
# w6 N$ k* z% c& oeven 15 minutes of direct skin contact with their male+ m, U( e& Y3 G! v: {  o8 S
partners.6 However, when a shirt covered the applica-2 ]$ k+ D$ P6 g# G: O
tion site, this testosterone transfer was prevented.
! \) S0 I$ R) s* e/ D4 hOur patient’s testosterone level was 60 ng/mL,& p6 a1 g% \7 u0 w4 m
which was clearly high. Some studies suggest that
- V9 W' i. v  F. [: j9 kdermal conversion of testosterone to dihydrotestos-
2 {. P5 e2 m# E9 j5 `! |& Bterone, which is a more potent metabolite, is more
) n. x6 p8 l" U* c# Z& _  r# o+ Kactive in young children exposed to testosterone
2 E( S- F2 p2 K% P. P" gexogenously7; however, we did not measure a dihy-9 H9 {. L) h. w; K6 f5 e
drotestosterone level in our patient. In addition to( \7 C1 t2 `& ]. f7 D
virilization, exposure to exogenous testosterone in
, }* G& j/ g; @children results in an increase in growth velocity and! j* s7 Q5 O3 o+ c# P! p+ ~
advanced bone age, as seen in our patient.
. X% _$ i$ m" i& uThe long-term effect of androgen exposure during9 |# M7 q& d+ E
early childhood on pubertal development and final" w4 ?, g- U$ D& C) Q' u$ a
adult height are not fully known and always remain
! {1 u" ~% R, H: g4 p" Ra concern. Children treated with short-term testos-7 I/ K- s! ?3 r- z+ _
terone injection or topical androgen may exhibit some2 C7 K( x# `" w
acceleration of the skeletal maturation; however, after* b9 K- @7 M* U: _) V* a, `
cessation of treatment, the rate of bone maturation
; Z& L6 j0 @7 v, v: V4 v8 d3 p+ Edecelerates and gradually returns to normal.8,9: k" B# m/ S# N
There are conflicting reports and controversy* m5 C1 ?' J% n' o; X/ }4 }2 W
over the effect of early androgen exposure on adult
2 b; ~2 @; p- @7 H% B) l5 ?penile length.10,11 Some reports suggest subnormal: V$ e9 m# q0 s  T) E1 D
adult penile length, apparently because of downreg-
" @+ X' B- \# _7 o  n/ M5 `3 J! Nulation of androgen receptor number.10,12 However,
/ \$ P& j* Z' S7 CSutherland et al13 did not find a correlation between
: A) @- y8 W, H1 `& b: G0 X' G( rchildhood testosterone exposure and reduced adult" g. [( {& X0 A
penile length in clinical studies.
" i- P5 D7 i  |# ~+ nNonetheless, we do not believe our patient is
; D( A6 O4 p! `" y! a7 ~; Tgoing to experience any of the untoward effects from# K; L% j5 _6 g; t
testosterone exposure as mentioned earlier because) e) g# F$ c3 b' H% h7 k! m' |* C; V) L
the exposure was not for a prolonged period of time.% K3 R# n9 O1 h/ T- z
Although the bone age was advanced at the time of( l1 |2 @- z, x
diagnosis, the child had a normal growth velocity at
# b/ w1 d& H. H2 y" L1 l, Y0 `the follow-up visit. It is hoped that his final adult+ Q) o. _9 f; G. u* ?$ _" B8 [1 K
height will not be affected.
; _# S( F1 R2 ^- G' _: SAlthough rarely reported, the widespread avail-# j  L9 S% R, R/ G9 l
ability of androgen products in our society may. d1 ]/ {2 S% y, p. a; T* h+ J7 o
indeed cause more virilization in male or female
( J- A5 K7 H/ h7 Xchildren than one would realize. Exposure to andro-5 s/ T% B/ t  ?( Y* L
gen products must be considered and specific ques-
3 s, x+ o: f) ?tioning about the use of a testosterone product or) v4 n% ~1 \, X( g( f1 J8 _
gel should be asked of the family members during' j, @: F: F& z& n) L
the evaluation of any children who present with vir-
! g% P' F3 {/ u1 [ilization or peripheral precocious puberty. The diag-3 q" V1 l; [" O5 v* I
nosis can be established by just a few tests and by# B3 |0 T- T& Z  d) F5 t& a
appropriate history. The inability to obtain such a( [  u5 j) f! D( q1 ^6 Z1 R
history, or failure to ask the specific questions, may
) c8 E* L9 ]5 D! Z7 mresult in extensive, unnecessary, and expensive" p3 [  {2 Q: p
investigation. The primary care physician should be* t- M( j+ n' Z  T# z* v$ P
aware of this fact, because most of these children
- Y& U7 X% M. Q$ mmay initially present in their practice. The Physicians’
9 d! r3 F7 G" a% X) Q& sDesk Reference and package insert should also put a# ?- \" u2 J/ m" l0 v) a" q
warning about the virilizing effect on a male or& ?9 A6 Q1 j  \! L: D0 n6 F
female child who might come in contact with some-0 K, C6 Y& u  F. K; A: ^
one using any of these products.
  K5 C1 g! y2 \* z5 \1 X7 T* OReferences
1 |; ]) v. n( e. |1. Styne DM. The testes: disorder of sexual differentiation& y, D+ Z  N" H# V- G; Z/ W
and puberty in the male. In: Sperling MA, ed. Pediatric
5 `8 ~0 `8 C( q! HEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
$ @- q& B% V2 O2002: 565-628.
6 C+ V9 q2 u2 c$ q) ^" b0 R: h( o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) J/ b; \4 T) i5 t% c4 D
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

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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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