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Sexual Precocity in a 16-Month-Old
, b" b9 M; m; iBoy Induced by Indirect Topical
" {% Z6 I+ d5 S8 p! n7 pExposure to Testosterone
8 L# a2 G! H5 l9 ^# B0 S- Q6 iSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 i( J. F& E5 d4 Yand Kenneth R. Rettig, MD13 q) C& u: s% O; R1 [$ |/ X7 x0 X8 ^
Clinical Pediatrics+ j8 |" @/ t5 ?
Volume 46 Number 6' w! y- R: @! T/ R
July 2007 540-543+ F& U$ I  b7 p  A/ C, x# _" X
© 2007 Sage Publications1 B+ K- Y3 Q9 k+ B, q* n0 t$ G
10.1177/0009922806296651
2 c7 @4 p, w9 M3 ^1 uhttp://clp.sagepub.com  z4 s- q8 V% `. ]" F; r( L
hosted at
$ z+ c8 T/ M* u* o+ jhttp://online.sagepub.com4 Z/ i* t! d6 x" G: V! j
Precocious puberty in boys, central or peripheral,
; e( |* w' h* E/ p0 wis a significant concern for physicians. Central6 j+ j1 u* H0 r) G% I) t4 I# g& s
precocious puberty (CPP), which is mediated
+ t1 k2 s+ F3 dthrough the hypothalamic pituitary gonadal axis, has+ a% Q+ L2 C, j0 g8 ^- E" m& c
a higher incidence of organic central nervous system6 Q% y" J9 R* k7 @8 G0 `0 y9 Y# q
lesions in boys.1,2 Virilization in boys, as manifested
: O$ b' H5 I9 p2 Yby enlargement of the penis, development of pubic1 G/ P- m# ~4 T; b0 ^1 ~" }
hair, and facial acne without enlargement of testi-2 H, C3 q: L$ B2 [, ~; K( q4 p; t
cles, suggests peripheral or pseudopuberty.1-3 We
! G& ~+ Q- M9 |9 H( yreport a 16-month-old boy who presented with the" H- F) j' l9 K0 ~# ~
enlargement of the phallus and pubic hair develop-
1 L* q( `9 |$ @- L- gment without testicular enlargement, which was due3 i8 O4 R5 \4 }* Z5 [
to the unintentional exposure to androgen gel used by/ ]' m; p( j" U" d2 Q& R
the father. The family initially concealed this infor-
, K! O* H% V* P0 r  Wmation, resulting in an extensive work-up for this
1 J" P8 V1 A# J; S- N5 `) d$ J% e. q( uchild. Given the widespread and easy availability of
- V& ^' j* o6 V* q2 atestosterone gel and cream, we believe this is proba-: W/ K7 Q1 [5 S* Q" E/ O% ~
bly more common than the rare case report in the
8 ]5 p6 Y3 _8 Q; ^: oliterature.4. A( C: P" }$ i+ ~( w; p
Patient Report' F0 i: p/ I/ C, j
A 16-month-old white child was referred to the
5 A  c* A- \. q. m" }endocrine clinic by his pediatrician with the concern
5 W) ?! z$ K, B7 D8 n8 [5 i, ]1 Bof early sexual development. His mother noticed
6 O4 g) n: u7 M) Y8 [# Alight colored pubic hair development when he was
4 u9 d& g9 q; u& {, t6 W! R( LFrom the 1Division of Pediatric Endocrinology, 2University of1 C- y3 x# p& d+ I' N) H1 k4 L& j
South Alabama Medical Center, Mobile, Alabama.+ j8 L( ?0 K; r" G( d) q
Address correspondence to: Samar K. Bhowmick, MD, FACE,. `# P7 D; O' ]( P/ r8 G: G
Professor of Pediatrics, University of South Alabama, College of: ]5 K0 O; y% G
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ s; B) P2 P% ~
e-mail: [email protected].
; B- n* C" W6 Eabout 6 to 7 months old, which progressively became
: Z* W5 `" P. q' a5 u8 B7 gdarker. She was also concerned about the enlarge-
8 S0 x& q: ~* Wment of his penis and frequent erections. The child+ k; N1 L$ a1 A: {' H4 c
was the product of a full-term normal delivery, with0 Q9 i2 j9 y  X  E
a birth weight of 7 lb 14 oz, and birth length of+ S# _% p% ^3 r1 p
20 inches. He was breast-fed throughout the first year3 I" @4 ^* s; l, c9 P7 l: \  Z' P
of life and was still receiving breast milk along with. I% e+ i# e# T. r+ L
solid food. He had no hospitalizations or surgery,6 k& S# D$ }! @/ [" G6 y
and his psychosocial and psychomotor development. s7 O* C8 D% t3 o) r  s/ s
was age appropriate.
9 K: `; a5 m" F5 {1 ~The family history was remarkable for the father,
. x: w  L3 u' awho was diagnosed with hypothyroidism at age 16,) p) o/ P( m0 |0 A' Q. u* r
which was treated with thyroxine. The father’s' o5 W# v& y- t6 b- I6 O) u
height was 6 feet, and he went through a somewhat
5 V/ G% F) w9 P8 ]early puberty and had stopped growing by age 14.
; |# ?' x% b' l' b: ]The father denied taking any other medication. The) _, }9 n6 T" ?4 v& d% P& c
child’s mother was in good health. Her menarche
- j1 y" S: D7 W* iwas at 11 years of age, and her height was at 5 feet4 ]3 t4 \% @# F; w* X% C3 [' Q
5 inches. There was no other family history of pre-% O, w: m) V. H1 C' M
cocious sexual development in the first-degree rela-
# s, I0 T, C! R0 p- r0 p8 }4 c! xtives. There were no siblings." y* q$ J4 A7 \3 n6 O
Physical Examination# |' a' T1 t: A2 F0 o8 A+ n
The physical examination revealed a very active,
3 w; X$ ?' u$ f! t  xplayful, and healthy boy. The vital signs documented
- P7 G* O4 O  z# v9 f9 _' Z/ @6 {a blood pressure of 85/50 mm Hg, his length was1 |. a# `+ I; j% Z: s
90 cm (>97th percentile), and his weight was 14.4 kg8 n( E* r. a, y! M& C) o
(also >97th percentile). The observed yearly growth
" r2 G. y; m5 v' p0 z& ]! b. evelocity was 30 cm (12 inches). The examination of
' }! V& t2 v% Mthe neck revealed no thyroid enlargement.: S: ~& t" X% b/ e0 N  u
The genitourinary examination was remarkable for
1 _" |7 {) F) B( A: c8 ]enlargement of the penis, with a stretched length of
" y2 T9 u* M( m3 i+ S8 cm and a width of 2 cm. The glans penis was very well2 x% I$ b& _$ t
developed. The pubic hair was Tanner II, mostly around2 P# b8 h7 L7 r# K4 ]
540
2 r9 r2 J- {  b6 c! u4 C6 E# Y8 a1 oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 Z( b& v* e0 D9 n2 K" p& h1 P3 ithe base of the phallus and was dark and curled. The
3 j: }/ ^0 ^# j( T/ ]& W: z4 Ntesticular volume was prepubertal at 2 mL each.9 S! q- n0 ~# f5 A% R
The skin was moist and smooth and somewhat' Z' Q# ^& @' e2 H
oily. No axillary hair was noted. There were no
+ d7 D0 n; G. O3 [0 M- ~9 vabnormal skin pigmentations or café-au-lait spots.9 c& [" z* ^- {' x# g
Neurologic evaluation showed deep tendon reflex 2+
: y! P) P: B: R/ O9 _0 }bilateral and symmetrical. There was no suggestion
  L1 W5 ]4 J+ I1 M" o1 g6 M" _of papilledema.% h# O6 q( _' F  F# ~" C
Laboratory Evaluation+ X) r6 F4 a6 h* j8 F1 E$ ]: E* r
The bone age was consistent with 28 months by
" j( k# H6 M# F# K6 iusing the standard of Greulich and Pyle at a chrono-
5 ]7 ^" D1 J( u5 N& z: b& H% @4 L1 Clogic age of 16 months (advanced).5 Chromosomal) z: @( {$ R2 Q+ g4 k  t, T) Z
karyotype was 46XY. The thyroid function test
8 r; G: B; d$ {) {% z) p) e( p, ~showed a free T4 of 1.69 ng/dL, and thyroid stimu-9 c* G5 x$ q2 T, I
lating hormone level was 1.3 µIU/mL (both normal).% v* A. U& q1 j9 X
The concentrations of serum electrolytes, blood9 j1 V9 f8 Z& W! b$ Z$ J  p
urea nitrogen, creatinine, and calcium all were
8 D7 `% ?, ]( jwithin normal range for his age. The concentration
, Z3 f/ k$ ~2 Y' T; q7 {. kof serum 17-hydroxyprogesterone was 16 ng/dL) j& z1 t$ _! F/ ^7 v1 I
(normal, 3 to 90 ng/dL), androstenedione was 205 P6 F- @) y6 J) c7 d" _& R( M5 I1 P
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# b9 ?$ g/ C& V' z" P
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
# x6 C/ `. B( R; j3 |desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 B9 j! @: J7 x( C2 G5 b49ng/dL), 11-desoxycortisol (specific compound S)
6 r+ l  W; `7 m# Z" uwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) f2 h8 G( ]8 T% f8 e" |, B: |" otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
9 ~- q, T0 }! n6 Atestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
- _! V: L9 a7 ]& z+ c: q4 u; k# t/ Land β-human chorionic gonadotropin was less than
; o/ B0 U  v3 |' o& f5 mIU/mL (normal <5 mIU/mL). Serum follicular. e" p$ t: x$ A
stimulating hormone and leuteinizing hormone
7 X  m/ F  \  [; Qconcentrations were less than 0.05 mIU/mL
* h3 J* {7 |0 r) y/ Z0 Q, E(prepubertal).
) u0 B, G. w# x8 S6 |6 Q! g0 t4 _The parents were notified about the laboratory" W; ~/ Y1 r& F6 R0 W' D  c) `
results and were informed that all of the tests were
& [! u; e/ |: e/ J9 n4 Wnormal except the testosterone level was high. The! q* c$ G7 o$ `+ P' U( X
follow-up visit was arranged within a few weeks to
" L5 p  @) H( B$ Z7 J' W8 Eobtain testicular and abdominal sonograms; how-- R5 ]' ~: q; I; W2 B
ever, the family did not return for 4 months.4 e0 v" L: i" y! z$ Q9 V0 N, o$ v
Physical examination at this time revealed that the
% y# L+ ?0 d1 `6 @' wchild had grown 2.5 cm in 4 months and had gained
- g# ]' c1 _: ?2 kg of weight. Physical examination remained& ?) S/ Z6 ?5 m& O& s$ \. o/ P
unchanged. Surprisingly, the pubic hair almost com-
) {1 l/ o  m6 H7 T; q* Rpletely disappeared except for a few vellous hairs at
# x5 I4 {2 o$ c9 Hthe base of the phallus. Testicular volume was still 2" Y( B) s; }* t( K
mL, and the size of the penis remained unchanged.( x$ ]! P3 z5 c+ V" ]
The mother also said that the boy was no longer hav-8 ?) v1 c1 @' j. Z
ing frequent erections.
4 r* c3 T/ F: T/ `* ]* fBoth parents were again questioned about use of
3 V9 @4 X6 x, _& J. {. F5 Vany ointment/creams that they may have applied to" t, A7 u2 |  V$ D, U
the child’s skin. This time the father admitted the
. ]2 S) n4 K) {5 d2 B% ~Topical Testosterone Exposure / Bhowmick et al 541% b0 N2 ~9 G6 c. ~3 [
use of testosterone gel twice daily that he was apply-  j. y* Y! h( m) G+ d  F
ing over his own shoulders, chest, and back area for: y8 Z( |+ }; z2 O2 u: D& ^
a year. The father also revealed he was embarrassed; x: g8 h9 o5 w1 H* T. E; S$ v
to disclose that he was using a testosterone gel pre-
: ~4 l3 X  h0 ~* z8 qscribed by his family physician for decreased libido2 [! u' o/ n& O2 e% a  `
secondary to depression.* U/ A6 x# R: {; N* l6 S9 }! f
The child slept in the same bed with parents.! R% ?) \8 U+ u! `
The father would hug the baby and hold him on his8 j9 y' j9 c1 n3 D$ j7 W
chest for a considerable period of time, causing sig-
: k. \% I; x: \7 snificant bare skin contact between baby and father.& y/ Y, B, l( Y' V+ Z  {2 n6 b
The father also admitted that after the phone call,
$ s4 l& H% ^8 q7 t) A( uwhen he learned the testosterone level in the baby# e- Y- F2 j, q$ }: Z
was high, he then read the product information
+ U! A, S& k2 f1 t) |. npacket and concluded that it was most likely the rea-( @3 a1 d8 O2 K4 I7 i! e
son for the child’s virilization. At that time, they- M9 a! K8 T$ v, E% Z: T  B
decided to put the baby in a separate bed, and the3 u& X3 \* F/ e+ I
father was not hugging him with bare skin and had; Z! }* g! Q. X7 b4 e& O
been using protective clothing. A repeat testosterone2 j6 q4 x- l; Z: X. s8 }; I
test was ordered, but the family did not go to the, ^: x0 z1 R% a" a2 P; z. _+ X. o! f- i
laboratory to obtain the test.
+ b) g+ Q9 Q% R7 oDiscussion0 G, U3 W% }$ B- z" h
Precocious puberty in boys is defined as secondary2 |2 X& u& c3 z3 f& t) v
sexual development before 9 years of age.1,4
( C! Y2 S- z% C, cPrecocious puberty is termed as central (true) when* s8 l3 Y) x" Z! i
it is caused by the premature activation of hypo-
& q& d. C, Q' J( I( A$ gthalamic pituitary gonadal axis. CPP is more com-
7 v1 X; n$ }2 v  q# O) v( q/ bmon in girls than in boys.1,3 Most boys with CPP% f" x0 }. R% T
may have a central nervous system lesion that is
: `4 w1 L* [  s" }+ j% w. Lresponsible for the early activation of the hypothal-
: O% K* j# k4 t5 p; T. H5 T% qamic pituitary gonadal axis.1-3 Thus, greater empha-
* [0 p- D: g0 r8 ~) v6 E5 ~sis has been given to neuroradiologic imaging in
! ]( q. D# }' M* mboys with precocious puberty. In addition to viril-
! \4 [  a! P' \" Y3 e3 n- Q# pization, the clinical hallmark of CPP is the symmet-
8 |. z+ s8 C& |& E' m3 ?# B+ \  o- Erical testicular growth secondary to stimulation by
/ r$ ^; q' L4 ?2 Wgonadotropins.1,3) W. m. q  h* G0 x9 U) b2 M; E
Gonadotropin-independent peripheral preco-' l3 H8 t8 Q3 g2 R5 P! y$ ^
cious puberty in boys also results from inappropriate% J% b* `, U3 i# s8 Y
androgenic stimulation from either endogenous or' V: W. g  s% x! g9 u) w
exogenous sources, nonpituitary gonadotropin stim-
1 s) n9 U! q. z% Julation, and rare activating mutations.3 Virilizing/ B+ i0 y' q6 x; e  F
congenital adrenal hyperplasia producing excessive
: C% k0 R, R% zadrenal androgens is a common cause of precocious9 ?5 b9 Q4 A( \7 ?
puberty in boys.3,4
* `( H" ^! s' m! @3 l1 KThe most common form of congenital adrenal
* d8 E- k1 b( L( _: `0 K0 Q7 P- T2 nhyperplasia is the 21-hydroxylase enzyme deficiency.1 [& F4 p( g) @2 l
The 11-β hydroxylase deficiency may also result in
% {/ |  q" L7 G0 I! W. r/ texcessive adrenal androgen production, and rarely,
! l$ b. A  c1 Lan adrenal tumor may also cause adrenal androgen/ d; q  g& \, _, I9 S9 d
excess.1,3
* p( I/ n: y: G. h5 a4 Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( a/ k8 B8 r( n8 P
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ I% W3 x& p- Z" M1 G" ^
A unique entity of male-limited gonadotropin-& N% M7 @3 a  N" c; e6 e7 |% S
independent precocious puberty, which is also known
- t* H2 T8 S& r* U8 I( }1 R* `1 r2 Mas testotoxicosis, may cause precocious puberty at a
2 v& C0 T' K2 ^9 J) yvery young age. The physical findings in these boys
' ?, ^% I. I! V  u$ P9 w2 r2 Swith this disorder are full pubertal development,
5 L( u% D$ Y9 Iincluding bilateral testicular growth, similar to boys) t! ?. y0 S3 P) S' q
with CPP. The gonadotropin levels in this disorder0 \8 l* B( C0 |! W* D
are suppressed to prepubertal levels and do not show* w) a2 v7 J- _3 H
pubertal response of gonadotropin after gonadotropin-
* E' H6 f" C$ N; l( `: Oreleasing hormone stimulation. This is a sex-linked
' y8 e5 r+ B, M7 W+ g: N' l$ Uautosomal dominant disorder that affects only
! ]/ z0 h8 `' O8 ~$ Z2 b& f" Pmales; therefore, other male members of the family, N3 _, K5 b1 i
may have similar precocious puberty.3
0 `7 t) ]/ J9 f1 U; MIn our patient, physical examination was incon-( M, P* V7 e, o  ^) C7 |
sistent with true precocious puberty since his testi-5 m0 |' V1 B4 J6 h4 |
cles were prepubertal in size. However, testotoxicosis
! O' R) N8 b+ h6 l: i5 d6 V1 fwas in the differential diagnosis because his father. c$ ?" m  M2 V/ F! C2 \# Q
started puberty somewhat early, and occasionally,
3 X' |* w) L* K8 w# _& X, Vtesticular enlargement is not that evident in the! L# j" O4 D7 L7 E7 s7 M
beginning of this process.1 In the absence of a neg-3 r: C; \( l5 ]0 p
ative initial history of androgen exposure, our( k8 e! `0 v3 A  H% N8 h# x
biggest concern was virilizing adrenal hyperplasia,2 Z9 R* U$ e) |: K( v/ N
either 21-hydroxylase deficiency or 11-β hydroxylase
" o$ e- C! a1 A, i8 I6 T: Edeficiency. Those diagnoses were excluded by find-
/ c# X" L/ [) E* n3 ~% A' D9 n: K% K4 aing the normal level of adrenal steroids.& E: _# p% B1 X; w  `/ X
The diagnosis of exogenous androgens was strongly2 c( I( L% {5 K- g# c
suspected in a follow-up visit after 4 months because0 J! g2 U9 D7 u1 T' ?
the physical examination revealed the complete disap-" @6 W8 }5 o* \4 X9 @
pearance of pubic hair, normal growth velocity, and5 f$ E# h% B8 D: b& }* R3 f
decreased erections. The father admitted using a testos-
4 u3 j! g4 {- ?% r3 e1 A' ^6 Qterone gel, which he concealed at first visit. He was1 N2 @( |; ]0 h3 I
using it rather frequently, twice a day. The Physicians’" j* ~$ G$ x8 C/ l6 g
Desk Reference, or package insert of this product, gel or! F9 x4 {8 s+ F5 ]; g
cream, cautions about dermal testosterone transfer to
$ Q4 `+ j6 i1 L4 u8 d( \unprotected females through direct skin exposure.- U6 f$ t& u: @& B9 a4 W
Serum testosterone level was found to be 2 times the
0 F0 i5 p* N, N6 w  f, ubaseline value in those females who were exposed to
  u6 l& f$ G9 R" veven 15 minutes of direct skin contact with their male
) }) p. m" y) L! u, n4 [partners.6 However, when a shirt covered the applica-
" H8 l, V) l- c$ B8 g* T9 \3 ]tion site, this testosterone transfer was prevented.
2 O2 v# L# M* o( q5 OOur patient’s testosterone level was 60 ng/mL,5 {: _$ \5 e  H2 E
which was clearly high. Some studies suggest that" h8 a9 |& Y; u% b1 u7 O% r
dermal conversion of testosterone to dihydrotestos-6 y. z. P9 p% O& i( i9 \7 M! u5 n
terone, which is a more potent metabolite, is more9 K1 Z# @- [" S0 Z" T) Q' P. \
active in young children exposed to testosterone1 K# n2 T0 ~$ X& t2 X
exogenously7; however, we did not measure a dihy-
3 D/ F0 \2 X8 jdrotestosterone level in our patient. In addition to8 a7 U$ _6 i' F( \9 |
virilization, exposure to exogenous testosterone in# H% D9 n8 Q8 f4 j
children results in an increase in growth velocity and- A8 k% N; `, t! w9 `
advanced bone age, as seen in our patient.
0 X  R" `8 K4 g7 vThe long-term effect of androgen exposure during
4 j, v. z* h5 }3 M  zearly childhood on pubertal development and final% a  m1 d3 q- Y
adult height are not fully known and always remain- b+ [+ P7 C- L% w6 O( L& w
a concern. Children treated with short-term testos-
: u% e$ i. s$ V5 G/ G, N) l" Wterone injection or topical androgen may exhibit some, X, k; U: w" n% |
acceleration of the skeletal maturation; however, after& k" i9 c! z7 \0 e$ l% Q. z
cessation of treatment, the rate of bone maturation- z/ }( `* ]2 u6 D
decelerates and gradually returns to normal.8,96 Y" c0 W  F1 l" U! f
There are conflicting reports and controversy
3 u  P9 B6 r0 W4 I! K" h' w" K) ]over the effect of early androgen exposure on adult
+ ~: C/ D& K. i& o' gpenile length.10,11 Some reports suggest subnormal3 a" t, l5 f& _9 r+ K2 T
adult penile length, apparently because of downreg-# i/ i. ^& ~' i8 S& g- @
ulation of androgen receptor number.10,12 However,5 k$ @+ h5 j, M& ?8 z5 @
Sutherland et al13 did not find a correlation between
7 }; `( ]8 s) }7 V% hchildhood testosterone exposure and reduced adult0 H( {# ~7 x( o
penile length in clinical studies.
" b2 {" p6 M! }# g# F+ CNonetheless, we do not believe our patient is. ?2 c% D; v$ {+ @* q* z9 s
going to experience any of the untoward effects from! |4 ~- M. Q$ M8 U
testosterone exposure as mentioned earlier because
+ r1 o8 w% [1 @* Ethe exposure was not for a prolonged period of time.7 l* ?3 B9 P6 H2 E$ X
Although the bone age was advanced at the time of
# V4 c+ i# v7 ]3 E3 }9 Fdiagnosis, the child had a normal growth velocity at" n/ W8 n8 V( z
the follow-up visit. It is hoped that his final adult) r+ n0 `$ i3 |2 E+ d, a
height will not be affected./ S' U1 o% \) J! F
Although rarely reported, the widespread avail-
; f$ y  v" h* S# s: w0 F+ aability of androgen products in our society may* X3 H. Y1 G0 \( \# `, g
indeed cause more virilization in male or female$ M4 ~5 K* z/ N2 z" h  n
children than one would realize. Exposure to andro-0 n" D' B. r8 v8 K! s
gen products must be considered and specific ques-
# c$ E0 h" t  Q* n) O: W8 utioning about the use of a testosterone product or$ ]2 B8 O3 K/ q
gel should be asked of the family members during
. c2 z( F6 ]8 v# ^$ Wthe evaluation of any children who present with vir-
' Q; Z  F( I! T' dilization or peripheral precocious puberty. The diag-
/ @3 J4 K/ o4 ynosis can be established by just a few tests and by
3 Y5 v5 M, G' j( qappropriate history. The inability to obtain such a
4 E: T- W, t5 x* D! R9 Chistory, or failure to ask the specific questions, may
9 K0 ~& I1 l5 B  xresult in extensive, unnecessary, and expensive) V" k; C* O" E. X/ i# A
investigation. The primary care physician should be
, D( e+ H" T* i1 `% H0 Qaware of this fact, because most of these children8 [+ U# P6 {# r+ z# U% r) y
may initially present in their practice. The Physicians’
3 ^6 v+ W1 E, X+ s: s5 E# r4 tDesk Reference and package insert should also put a1 Z; H* \+ \7 ^/ [" P$ N1 k
warning about the virilizing effect on a male or
5 Y' D& Z2 y. d( Q- vfemale child who might come in contact with some-6 y+ q* Y4 ?3 U
one using any of these products.
4 V' g; e+ h9 Z8 ~- yReferences! T% u; ]1 I9 t
1. Styne DM. The testes: disorder of sexual differentiation. Z- i  P6 g* D* W
and puberty in the male. In: Sperling MA, ed. Pediatric
5 t% ~  ?# g0 ~' i+ L' q  T1 eEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 {7 k# ?! P( V
2002: 565-628./ z+ E' @. E1 E3 B% m/ d
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& @4 E7 w6 s5 p# f7 e' J
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old8 R! P$ _6 p$ U" G* r
Boy Induced by Indirect Topical4 s/ `. P- P' p2 P! z7 B5 \
Exposure to Testosterone$ f3 @1 v# Z8 b; w! ?+ E
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" w9 b( [. Z( Y7 u6 Zand Kenneth R. Rettig, MD11 h% G- _- F$ D$ s
Clinical Pediatrics* b% I! H2 O7 ?, y
Volume 46 Number 6# T) a2 q- k' E, F- P" z% l' a) @  S
July 2007 540-5437 [5 k* }1 @* U
© 2007 Sage Publications: X3 N/ [  b3 a" W2 A% {
10.1177/0009922806296651
1 m% x5 ^1 T5 m2 Ohttp://clp.sagepub.com
1 h; f! L# X) Q# C* n/ thosted at/ d$ ~' E$ k2 C+ I+ R1 l0 }
http://online.sagepub.com
3 A6 F1 ]" p" E2 [; {4 `# D% UPrecocious puberty in boys, central or peripheral,
# H  Z* X1 p5 ?+ t3 Xis a significant concern for physicians. Central
" k7 D5 ~2 m1 {# D7 |. qprecocious puberty (CPP), which is mediated
# f- l& @: I+ X. F6 K6 [through the hypothalamic pituitary gonadal axis, has
8 j; U0 d0 I; Ha higher incidence of organic central nervous system
/ k, F3 i' N: q4 n; `lesions in boys.1,2 Virilization in boys, as manifested# d6 N8 W! X- U9 c8 I
by enlargement of the penis, development of pubic" F- i6 o) d0 r9 b
hair, and facial acne without enlargement of testi-5 l, T/ q  i, |3 \+ N
cles, suggests peripheral or pseudopuberty.1-3 We
7 ^( k. B8 Z: F. X, J% r- |" Ureport a 16-month-old boy who presented with the# ~1 @- _: A" u) Z
enlargement of the phallus and pubic hair develop-, j4 W) P5 ^& u9 a+ M
ment without testicular enlargement, which was due" Z/ I# ~0 ]! a' G) _, O
to the unintentional exposure to androgen gel used by
& S& H" X6 ~$ z9 P+ O& O8 kthe father. The family initially concealed this infor-
- n9 p7 a5 J: [( Jmation, resulting in an extensive work-up for this
' q$ v$ R5 S/ X2 f# I, ochild. Given the widespread and easy availability of
7 \4 m/ j3 d# Z+ Ktestosterone gel and cream, we believe this is proba-
) L. F9 [3 T+ Y; Dbly more common than the rare case report in the
1 Y  H* N3 O( `& i  `; [5 V" ~% R: Qliterature.4# H! ?2 \& C1 z5 d7 d9 R% \
Patient Report# b5 i- X1 ^' b7 @7 k% i! @) D
A 16-month-old white child was referred to the) \/ S3 a9 `* W7 d7 |+ ~
endocrine clinic by his pediatrician with the concern6 U! C$ f" H: g2 T8 F5 G
of early sexual development. His mother noticed
3 V% I( z9 O* h: y/ q" xlight colored pubic hair development when he was* l3 I, k7 f# K) G
From the 1Division of Pediatric Endocrinology, 2University of
$ W, N% r7 m5 |* MSouth Alabama Medical Center, Mobile, Alabama.
: D3 v; ], F* C1 `Address correspondence to: Samar K. Bhowmick, MD, FACE,( K7 p4 A( i6 U2 m
Professor of Pediatrics, University of South Alabama, College of  r  v4 S1 @/ R( b& i* n8 `
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( |3 N+ A* l4 B3 p( U0 Q1 Ue-mail: [email protected].
) a% ~; y8 @! b- [! Iabout 6 to 7 months old, which progressively became& ~# r- N* u" ~* \) l- C6 [
darker. She was also concerned about the enlarge-
# X( E, F8 k. C9 `: cment of his penis and frequent erections. The child
* r2 [# j+ R+ i9 f+ {5 N" Qwas the product of a full-term normal delivery, with
# H* t7 u% z# K2 W& Na birth weight of 7 lb 14 oz, and birth length of6 B! R1 C* [6 g, T/ C( E5 j
20 inches. He was breast-fed throughout the first year+ l0 H0 u6 r6 e4 {7 s6 e' ]
of life and was still receiving breast milk along with6 ~! C9 p% V* u, W2 W$ G
solid food. He had no hospitalizations or surgery,
& q* j9 V9 k5 C+ |* ^$ K; i. Fand his psychosocial and psychomotor development
: w; E* f( S4 j% @& Twas age appropriate." d6 w5 s3 D4 `, o+ V% d, G; g
The family history was remarkable for the father,
$ Q! `: v+ h7 w' t& a2 Kwho was diagnosed with hypothyroidism at age 16,
) O. c( w: T, t- o; o# h, \: bwhich was treated with thyroxine. The father’s
4 F/ \* |: q) Y) gheight was 6 feet, and he went through a somewhat
) g+ l$ o; X: h# G# Iearly puberty and had stopped growing by age 14.$ I/ Z3 Z/ J7 O
The father denied taking any other medication. The
: g- U. ?. H7 P& i9 l, S, achild’s mother was in good health. Her menarche% a3 c' a, z9 l) a/ T& k$ l& ?* H
was at 11 years of age, and her height was at 5 feet
; v2 c7 ~% Z) B$ V  I. g5 inches. There was no other family history of pre-, z6 m! b$ t+ i, m/ z
cocious sexual development in the first-degree rela-& K. K  @  w* [! b8 E% P' N
tives. There were no siblings.
( X$ ?8 r4 }- H7 y* K5 @Physical Examination" G( `+ G; `5 \' V
The physical examination revealed a very active,- _8 R# ~" D& `
playful, and healthy boy. The vital signs documented, y0 ]- ~. F3 d+ a6 V
a blood pressure of 85/50 mm Hg, his length was- a$ g% a* S( {% Z0 `8 C
90 cm (>97th percentile), and his weight was 14.4 kg3 ~4 B6 I* P' T+ j7 E! X
(also >97th percentile). The observed yearly growth
, _6 Y/ y8 m9 x8 t' U2 j8 rvelocity was 30 cm (12 inches). The examination of
" w* ^: w5 [( T& wthe neck revealed no thyroid enlargement.
/ T6 ]9 e; C6 R5 ]) n" Y- rThe genitourinary examination was remarkable for
: }7 R, K0 [* e! E/ r; }enlargement of the penis, with a stretched length of
8 ^% V9 N. {& r6 X. Y* Y7 F6 C, l8 cm and a width of 2 cm. The glans penis was very well
( k( [& U! \$ Udeveloped. The pubic hair was Tanner II, mostly around
$ {& @6 u3 G/ ]540
- w5 t. f- h+ J, X/ m( aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 C0 J- D5 n. Ethe base of the phallus and was dark and curled. The
8 M, e* H7 z9 c  j! _% |/ ~testicular volume was prepubertal at 2 mL each.. N: P/ H3 l  O2 X) y& A) X
The skin was moist and smooth and somewhat
( q4 I7 ~0 X9 ^" J. j* K1 l' Noily. No axillary hair was noted. There were no* m6 s6 t/ {( C* R( A9 e) n
abnormal skin pigmentations or café-au-lait spots.
8 U1 N+ k) {/ ]* e6 s' eNeurologic evaluation showed deep tendon reflex 2+8 r, e  b) \7 O7 g& m$ T+ b
bilateral and symmetrical. There was no suggestion4 k# k/ P7 t; m) ~, y$ h
of papilledema.
% m) \$ E+ q/ U0 `/ ~& o% l2 CLaboratory Evaluation- R' Z" U+ x1 F2 C$ B
The bone age was consistent with 28 months by
' p; ?3 f' [0 W# V$ Wusing the standard of Greulich and Pyle at a chrono-
) ]3 Z; U1 w8 v9 Nlogic age of 16 months (advanced).5 Chromosomal
# q  a* r( A& x" R; x- J; v- U: Skaryotype was 46XY. The thyroid function test
0 U: u$ w! Y2 }* e9 P, W. y- pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
  B5 k3 t- {' i6 plating hormone level was 1.3 µIU/mL (both normal).
$ o. A5 U- d, s8 s; b  ?, I+ rThe concentrations of serum electrolytes, blood# p) p( u* Z7 S
urea nitrogen, creatinine, and calcium all were
- J; Q& n: D( L+ A' V- T; D: W5 ~within normal range for his age. The concentration
3 N+ j2 ?! o* A3 ^1 _of serum 17-hydroxyprogesterone was 16 ng/dL
, }/ V$ K, ?7 v8 x(normal, 3 to 90 ng/dL), androstenedione was 20
$ g9 c( \2 Q7 |. d0 ~ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: M- S6 U! I0 K% w( g" I7 C* }) N
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
5 Q1 h- d8 i! @6 u# j  S" ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to" _7 s# f) r9 k' r% o6 e
49ng/dL), 11-desoxycortisol (specific compound S)2 p- A& a; y2 c, h4 ?( |
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 {! K/ h1 W  e; G
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
  @+ m. Y: t" {testosterone was 60 ng/dL (normal <3 to 10 ng/dL),* S! A6 M3 ?% [2 y# V7 b- s7 P
and β-human chorionic gonadotropin was less than4 u3 ^" X6 j& Y* N; V
5 mIU/mL (normal <5 mIU/mL). Serum follicular3 c0 ~1 e; X" n
stimulating hormone and leuteinizing hormone/ L3 B) p9 o3 _# f- P
concentrations were less than 0.05 mIU/mL# X9 N! W! j# S
(prepubertal).
6 u' Q( B( r6 i4 @( z* iThe parents were notified about the laboratory
$ B* ?4 m4 O8 e& v. Fresults and were informed that all of the tests were' t* I$ g; C2 ]" J. F2 {8 h
normal except the testosterone level was high. The! e& P/ P+ d5 h
follow-up visit was arranged within a few weeks to' w# n$ K% _0 O- F4 F% N" b2 j( n
obtain testicular and abdominal sonograms; how-
$ N; H5 Y$ q9 Hever, the family did not return for 4 months.% X% b4 y, a, i2 |2 ~: _  \5 j
Physical examination at this time revealed that the
+ T) x3 a! p) {! x3 M' ]child had grown 2.5 cm in 4 months and had gained
: ^+ U" }/ l. [) x$ C2 kg of weight. Physical examination remained2 u# ?1 _# K: ]- v& _5 D# @3 F
unchanged. Surprisingly, the pubic hair almost com-3 ~  @# l$ b0 }3 Z) a5 j
pletely disappeared except for a few vellous hairs at* H3 X5 }2 h$ \; ?. C- \
the base of the phallus. Testicular volume was still 2: M- D$ E. X/ K  J
mL, and the size of the penis remained unchanged.( r- }* M: F& Y% ~, g- M% \
The mother also said that the boy was no longer hav-
  i/ |3 A) c$ n3 Y5 Y3 q8 h" |3 B* L9 Aing frequent erections.) ~2 m& Z9 y) p$ G; C/ e. H- A
Both parents were again questioned about use of( ]5 W7 o$ h' k; L
any ointment/creams that they may have applied to
: }5 w  G% f, N& Gthe child’s skin. This time the father admitted the
2 a+ q, E, X- _Topical Testosterone Exposure / Bhowmick et al 541( N3 p4 F+ N7 e0 Y, w1 H0 T! t0 t
use of testosterone gel twice daily that he was apply-# J  j8 I+ [0 s% @- s
ing over his own shoulders, chest, and back area for
1 z! ~  |0 p! w4 s+ R' Ea year. The father also revealed he was embarrassed
5 a' s1 `: @& b% `5 \7 jto disclose that he was using a testosterone gel pre-. ]+ y! u. L  S3 A- M4 d& d/ u
scribed by his family physician for decreased libido
7 ]( o2 O6 k6 n0 l; _6 N. Esecondary to depression.
* Z; H4 Y! |) T% LThe child slept in the same bed with parents.6 D- r: r7 }8 w6 p0 {
The father would hug the baby and hold him on his
4 \1 O. K6 U' Q2 `3 ychest for a considerable period of time, causing sig-
+ U# w& O+ r- f6 f5 `nificant bare skin contact between baby and father.
. v0 o, t: T4 `" Y0 d  A$ [The father also admitted that after the phone call,
' v9 g; U/ }2 [! w5 s) Swhen he learned the testosterone level in the baby' h  v" a( A5 P+ }( [& f! Y- l
was high, he then read the product information; k$ b& V, u' {4 t
packet and concluded that it was most likely the rea-
& V. A0 a- s$ O; ?$ _  Dson for the child’s virilization. At that time, they
8 k7 ]) `' ^' _+ R) A, vdecided to put the baby in a separate bed, and the
9 C/ R( e0 X4 d- d- a4 o% `3 \+ Cfather was not hugging him with bare skin and had7 I, W4 i3 }% @+ m
been using protective clothing. A repeat testosterone' K- [- X" @5 L% v8 j5 u; m6 ]
test was ordered, but the family did not go to the
3 Y- y" S4 W9 s6 T1 ?3 olaboratory to obtain the test.
2 c$ Q# R0 y. G4 eDiscussion
: H; P! _# ?, y  t% \Precocious puberty in boys is defined as secondary( r' u9 n/ ~% z9 N8 g+ v
sexual development before 9 years of age.1,4
. ~  w. v  a  R+ YPrecocious puberty is termed as central (true) when+ n5 {9 |! g+ P( K! q' A6 |
it is caused by the premature activation of hypo-
0 V3 W# S# I+ b# \! C; y7 ?thalamic pituitary gonadal axis. CPP is more com-
! H. w; ~0 K/ t. Omon in girls than in boys.1,3 Most boys with CPP
2 Q; G$ B; X! U$ V( E2 q/ Nmay have a central nervous system lesion that is
7 u) o, s3 T1 [responsible for the early activation of the hypothal-
1 Q7 F2 e; u9 O' m7 j4 n* c. Uamic pituitary gonadal axis.1-3 Thus, greater empha-
" P/ d2 ~: D% q/ _sis has been given to neuroradiologic imaging in
1 i' A! b" y2 @% M$ S( }/ oboys with precocious puberty. In addition to viril-' J! [8 K$ v5 L0 V
ization, the clinical hallmark of CPP is the symmet-- q8 y/ y" }  q8 O9 T& v6 v
rical testicular growth secondary to stimulation by! y: I% V* V# G3 N0 a" ]
gonadotropins.1,3; A6 y& z, q& o" P0 L
Gonadotropin-independent peripheral preco-
7 Z+ D! m# X- ^" G6 \( H  ecious puberty in boys also results from inappropriate# L: T' q. W9 t$ B6 B# ~4 r4 ?
androgenic stimulation from either endogenous or9 J6 A. }6 e$ x) y- w' N. k/ i
exogenous sources, nonpituitary gonadotropin stim-/ _2 R2 T0 i& ]) B
ulation, and rare activating mutations.3 Virilizing
/ m5 b1 F7 ^/ L* N, s/ X; A+ C/ Acongenital adrenal hyperplasia producing excessive3 V3 p9 ]- Z. d' i1 Q7 |
adrenal androgens is a common cause of precocious( G2 T3 p( e& A- @+ [
puberty in boys.3,4- ]! U2 s3 B1 {: G) ~2 ~9 t7 I9 T9 d
The most common form of congenital adrenal' g! y  d/ K& N6 ?7 O# c7 e- `
hyperplasia is the 21-hydroxylase enzyme deficiency.1 t7 R+ S6 |; t6 M  u# t. G+ P
The 11-β hydroxylase deficiency may also result in
# b  W6 e+ B# z4 q5 pexcessive adrenal androgen production, and rarely,  t6 u8 g" l0 B- n6 B
an adrenal tumor may also cause adrenal androgen
5 Y0 k; [; w. c% ?- @excess.1,3
1 |5 |2 G: _0 Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 q# b0 D. C% t: Q& P' o* e+ ?# A542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 K/ y1 w$ D- }1 g5 P3 OA unique entity of male-limited gonadotropin-9 K- c5 l5 L# _" J# {* l
independent precocious puberty, which is also known0 v" d1 p" z0 O7 j# k
as testotoxicosis, may cause precocious puberty at a1 y: l8 w' A2 c) t* n; y( j7 |
very young age. The physical findings in these boys3 u0 H, F: X+ [0 I2 w
with this disorder are full pubertal development,
( X- F! F. v4 d! {8 vincluding bilateral testicular growth, similar to boys
  _$ n1 V/ Y# C' o/ e. ^* b. Bwith CPP. The gonadotropin levels in this disorder, A, Y2 [4 J& t! M2 ~5 X7 E+ E! {& D$ o
are suppressed to prepubertal levels and do not show
% B2 h( u) U! Tpubertal response of gonadotropin after gonadotropin-
# v; R3 d1 l# t& ?9 ureleasing hormone stimulation. This is a sex-linked2 @! {8 x  t) N7 |1 ?. _
autosomal dominant disorder that affects only! c$ `) J0 U# o: f, }
males; therefore, other male members of the family
7 _. {% B0 {6 w3 I+ Z" {0 vmay have similar precocious puberty.3# h3 w5 ]/ d: {* O" I
In our patient, physical examination was incon-
7 G( q0 n) F9 ]1 ?8 Jsistent with true precocious puberty since his testi-2 H- P- D. L- l; }- R
cles were prepubertal in size. However, testotoxicosis' W; ~! j: H& m8 Q1 l
was in the differential diagnosis because his father$ b/ W* j& B/ c/ m) e, U  C
started puberty somewhat early, and occasionally,9 ~" m3 t! B2 a, k" a) X! U
testicular enlargement is not that evident in the
/ ?& ]- q) N/ W( Nbeginning of this process.1 In the absence of a neg-' G% I- Z: K# i
ative initial history of androgen exposure, our
/ V- ], C, b# ?/ Ibiggest concern was virilizing adrenal hyperplasia,
- m2 `- Y0 \$ l/ j: p2 z# L% seither 21-hydroxylase deficiency or 11-β hydroxylase" [+ u: a% j& }4 L1 |3 V
deficiency. Those diagnoses were excluded by find-$ d9 u& E( x7 x: c# s. U
ing the normal level of adrenal steroids.
, D/ i! c" n% ]The diagnosis of exogenous androgens was strongly
- U6 `% R1 V8 }5 A4 A+ B/ o) F( z+ R+ rsuspected in a follow-up visit after 4 months because/ r2 w7 C3 k- z% f5 s
the physical examination revealed the complete disap-
' M. |8 R) L  p$ _pearance of pubic hair, normal growth velocity, and
. C3 W2 c1 j3 a& u/ Fdecreased erections. The father admitted using a testos-" c* L4 X8 b/ J' F( L5 v
terone gel, which he concealed at first visit. He was
' t9 B! Z) k$ V' G3 I% P, D( vusing it rather frequently, twice a day. The Physicians’
; S& e1 ]" U  b8 W# }, MDesk Reference, or package insert of this product, gel or
) y: }6 V# B6 |% }cream, cautions about dermal testosterone transfer to& {8 N' ?& M0 }
unprotected females through direct skin exposure.
) k% P* y7 H3 I9 z% c5 B5 H( P$ ~Serum testosterone level was found to be 2 times the6 X- ]. Z6 @9 c) c, L
baseline value in those females who were exposed to
' N* w$ `: u& }# Y- d% beven 15 minutes of direct skin contact with their male
/ i" Z" D$ `, f: |partners.6 However, when a shirt covered the applica-3 M, X" }" V& m& v
tion site, this testosterone transfer was prevented.9 D) Q: D6 y( G3 {0 m
Our patient’s testosterone level was 60 ng/mL,5 V% K0 S9 i& v
which was clearly high. Some studies suggest that
* J( |9 l4 }% ^& Hdermal conversion of testosterone to dihydrotestos-  x0 w2 ~3 c2 ]# Z- p. H. m
terone, which is a more potent metabolite, is more
) w( P3 g5 v0 |6 `, @' lactive in young children exposed to testosterone+ o+ U1 ]  \/ d: _; H* ]) I  V
exogenously7; however, we did not measure a dihy-' }3 z4 d! H( x- r& G2 {$ R
drotestosterone level in our patient. In addition to
9 l) K4 M, Z! i1 c- F/ Hvirilization, exposure to exogenous testosterone in
% g! `: ^. u( Z2 V) o6 S. Wchildren results in an increase in growth velocity and
9 Q) J& j- l6 B# |1 u  p6 I5 Hadvanced bone age, as seen in our patient.. W; n; k6 R  p0 ?% ^' h
The long-term effect of androgen exposure during
3 a/ k( o, i  K3 k, bearly childhood on pubertal development and final
+ }3 o, ~# [  b9 K+ a; ?6 R2 xadult height are not fully known and always remain
. r2 u2 E# e: X. S  L& ta concern. Children treated with short-term testos-
& w6 [& l( ]9 y* b* Bterone injection or topical androgen may exhibit some
3 n9 \/ @5 a8 n# c) H" C1 {0 yacceleration of the skeletal maturation; however, after; ^! y3 o/ y: \" A. \' q9 L% X
cessation of treatment, the rate of bone maturation: `, }2 [3 E0 H5 i3 v! S4 Q
decelerates and gradually returns to normal.8,9
& ?8 J$ U' i) U7 dThere are conflicting reports and controversy
5 x3 A4 v& h" q6 O3 }2 ?2 eover the effect of early androgen exposure on adult
) Q8 l/ Q9 p' Q" l/ |penile length.10,11 Some reports suggest subnormal
- r% T! v' D9 m6 K8 h+ Dadult penile length, apparently because of downreg-: I+ V  e' m' `% o5 R% D
ulation of androgen receptor number.10,12 However,
% |  f# w8 |+ o6 {. e! ]  s2 q: F/ K8 FSutherland et al13 did not find a correlation between4 w$ S& c  T6 h' w1 g2 ^
childhood testosterone exposure and reduced adult
2 s  [6 d9 c* p9 n. kpenile length in clinical studies.
4 d$ B' A0 m, a2 @Nonetheless, we do not believe our patient is1 V" D* A7 l; P0 ]) u, [. N+ m$ g: e
going to experience any of the untoward effects from
6 z% z0 K+ ^; Y* f; ctestosterone exposure as mentioned earlier because
8 |  }- Y$ t  x# a/ e9 }5 mthe exposure was not for a prolonged period of time.0 f: k6 K- m- }; L* K
Although the bone age was advanced at the time of
! s5 s8 H2 x$ ~/ A: d4 bdiagnosis, the child had a normal growth velocity at9 U; Z) E, x7 E  ^* u, C0 ?
the follow-up visit. It is hoped that his final adult
6 A2 l+ `7 H2 [) H, mheight will not be affected.
6 o% g/ ^1 ^7 v9 o9 I4 m4 I$ `$ iAlthough rarely reported, the widespread avail-
. C7 W- l. g2 i4 q* N- T! sability of androgen products in our society may2 R% L, M9 G5 W, W& q2 k6 N
indeed cause more virilization in male or female
% R) e3 j9 ^, H( Mchildren than one would realize. Exposure to andro-& s; T2 _2 G2 m! `. T! }
gen products must be considered and specific ques-
. d1 S8 S( @  ]/ w2 E  W2 S. Ntioning about the use of a testosterone product or) o: g. [! q1 O; D2 q! g' }
gel should be asked of the family members during
7 R- C4 r0 d8 dthe evaluation of any children who present with vir-' Q/ X7 d( R  w# Y( w0 Y% ?
ilization or peripheral precocious puberty. The diag-0 ^) }9 K$ |' z
nosis can be established by just a few tests and by
) w+ A" F/ A, H: J1 U! Rappropriate history. The inability to obtain such a* z7 ^2 @1 ~% E" b: k3 v2 C
history, or failure to ask the specific questions, may
. J% e4 S& W, r; A) rresult in extensive, unnecessary, and expensive0 F5 c! }, F: c1 i2 _8 x
investigation. The primary care physician should be8 `& g( s2 A) |: E$ L) H" K1 L% p
aware of this fact, because most of these children/ z# S; C( m' [& }  k) X
may initially present in their practice. The Physicians’
9 i+ ~0 z. K( nDesk Reference and package insert should also put a/ \1 z* W6 a( d4 e- y( _+ d
warning about the virilizing effect on a male or
7 s' n9 B& \; l/ U* b) O. [female child who might come in contact with some-
) L7 K9 j" b! Y3 A# h% Wone using any of these products., x. E$ @. o5 p, M; F6 O
References5 W; ~4 T: K: B# P, J8 A8 p
1. Styne DM. The testes: disorder of sexual differentiation& F# k+ |$ g; l2 b  ]+ m! w
and puberty in the male. In: Sperling MA, ed. Pediatric0 G( \9 O9 L) m$ N9 {5 p" v/ b
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ ]3 f: n3 w) u$ w- Z, }
2002: 565-628.9 Z. t# h, f1 N  ^$ `* d
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious: [* k1 p. v! J: |* o  E
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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

6 [' {; y1 H  S/ b1 h1 S/ N/ T) e/ ~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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