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Sexual Precocity in a 16-Month-Old
0 S# o" m3 B5 q1 B; k4 FBoy Induced by Indirect Topical
$ S! x: |* {3 M1 T  z5 Z3 HExposure to Testosterone' t( x! r' x8 {: R: v5 k6 L
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. \4 p% @8 d/ N" z# N
and Kenneth R. Rettig, MD1! Q2 q7 `& C3 G$ O5 f  I+ X
Clinical Pediatrics
+ q& c: ?, K2 E9 l+ F+ G6 J1 ^1 HVolume 46 Number 6
, H/ S7 E8 k8 V' fJuly 2007 540-543$ F0 N3 n9 \, S. z" ]8 S
© 2007 Sage Publications
# y3 s! k; u& _/ q2 g( q- b10.1177/0009922806296651
+ }8 [& E3 R' J2 h1 H9 \http://clp.sagepub.com1 V9 A- r% _$ z9 K% L' N& ^8 M( X
hosted at5 z9 Z; W* d( v
http://online.sagepub.com3 c* T2 V8 h2 X
Precocious puberty in boys, central or peripheral,
& d1 N2 E) |5 i2 Gis a significant concern for physicians. Central
, C/ _! J8 \! ?2 kprecocious puberty (CPP), which is mediated1 t- p  G. w! A7 `  f
through the hypothalamic pituitary gonadal axis, has4 X5 p' C# \6 w! E% }5 Z. j2 W
a higher incidence of organic central nervous system# u3 t3 `* n7 i! ~: b2 D1 T
lesions in boys.1,2 Virilization in boys, as manifested1 f* W, N0 W8 }1 [
by enlargement of the penis, development of pubic
5 }; g" v8 A; p( }hair, and facial acne without enlargement of testi-1 X4 r( u0 O: Y' L% C! h" ~; f
cles, suggests peripheral or pseudopuberty.1-3 We" ^6 z6 V! K' _; Q! j
report a 16-month-old boy who presented with the" B0 C  c# R  _2 p$ Z* A& ~
enlargement of the phallus and pubic hair develop-  T6 |: s5 ]- Q/ J4 K. c
ment without testicular enlargement, which was due+ ~( D0 f$ m: o* y- r; ?
to the unintentional exposure to androgen gel used by
, N; ?, p0 P) S1 d+ e6 tthe father. The family initially concealed this infor-2 O" Z1 G% z. r. F  s/ x$ \( x
mation, resulting in an extensive work-up for this9 R4 a4 m, k5 a/ K6 M. G6 C+ f
child. Given the widespread and easy availability of
: w- I- a* H* N5 }. |" G6 R/ \testosterone gel and cream, we believe this is proba-; m' @8 C5 T  f5 G$ Y" J: U8 M, E
bly more common than the rare case report in the
8 |. L% o3 A" Z% Uliterature.4; N" _7 j- x7 [) n9 a3 g2 g
Patient Report
: h$ e% w( v: \/ C" R$ x3 Y" PA 16-month-old white child was referred to the- L: e; ~+ V3 b  x$ V; n" c
endocrine clinic by his pediatrician with the concern
: [+ Y: W% `/ @- S& w; _of early sexual development. His mother noticed( z& s% s& ]( n/ W7 j& S
light colored pubic hair development when he was
) p# M! b, Q+ o! V" ^From the 1Division of Pediatric Endocrinology, 2University of
! ~+ y7 {  O1 Q' RSouth Alabama Medical Center, Mobile, Alabama.7 U# [5 y% b* c6 Q& Y( S/ d
Address correspondence to: Samar K. Bhowmick, MD, FACE,
4 J6 w# D; W, ~. _' SProfessor of Pediatrics, University of South Alabama, College of. m4 R% x. u4 J5 ]/ Z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) M4 {+ [' {; z, T
e-mail: [email protected].2 ~2 M+ x) A  j6 A
about 6 to 7 months old, which progressively became" U3 X' N8 x5 ^5 @  M7 e/ M
darker. She was also concerned about the enlarge-' J' c; u- P# v4 X5 E' k, [" k
ment of his penis and frequent erections. The child
2 b( c. z. M0 b8 [was the product of a full-term normal delivery, with
' P4 V4 d# H7 S: N  i; Va birth weight of 7 lb 14 oz, and birth length of) L- Y3 J& w' F* M1 A
20 inches. He was breast-fed throughout the first year3 r* i; a# Q* V) p+ }' G
of life and was still receiving breast milk along with
# T0 K; _! G: Jsolid food. He had no hospitalizations or surgery,1 f$ P% g1 a: \( R- w: I4 S: r: o
and his psychosocial and psychomotor development
) G! j7 l" K6 L9 _was age appropriate.
  M9 h5 R5 z7 O& ^% i. K3 ]The family history was remarkable for the father,
2 n9 e4 T! G4 d, H" P  o7 m  y0 Wwho was diagnosed with hypothyroidism at age 16,
- Y+ {' R* [4 \! G; [which was treated with thyroxine. The father’s6 c3 v( p- v; n# N0 |, g
height was 6 feet, and he went through a somewhat
# G- V" _) D0 h' ]8 i, Fearly puberty and had stopped growing by age 14.# _3 _3 m7 o* O. t5 G$ k( D
The father denied taking any other medication. The$ t+ B& J, [9 ~$ v' N" `5 P
child’s mother was in good health. Her menarche
. @0 x" Q* l6 ?1 A( |: _; ], R$ uwas at 11 years of age, and her height was at 5 feet
$ B  b9 X- N) U* O+ T3 I6 O5 inches. There was no other family history of pre-" h# v8 [! c3 Z9 q) o
cocious sexual development in the first-degree rela-
, h- v8 [/ C8 J, h* b  Jtives. There were no siblings.1 ]% j. j9 R! y0 f' M/ r
Physical Examination# Z$ [2 v* s) {- @) c
The physical examination revealed a very active,
+ m% o( g! \* @1 Y9 l0 j% iplayful, and healthy boy. The vital signs documented
: D% D- _( a7 j' P: F4 va blood pressure of 85/50 mm Hg, his length was
! k0 u% u: T6 L! R/ v( t3 d90 cm (>97th percentile), and his weight was 14.4 kg, ~/ I, M" O+ o% @
(also >97th percentile). The observed yearly growth% J3 D1 L" b: i9 w; c1 Z
velocity was 30 cm (12 inches). The examination of
2 V1 N) W0 _3 V! I8 E: U( Uthe neck revealed no thyroid enlargement.
6 ^, ?3 j8 u* i# J0 A. M& B$ U, wThe genitourinary examination was remarkable for
; v  z. Q, `" h; I& Aenlargement of the penis, with a stretched length of! F' u# E# y( P
8 cm and a width of 2 cm. The glans penis was very well1 |) t8 L5 }- N1 Z" w# Z5 o  J" m
developed. The pubic hair was Tanner II, mostly around2 E1 n' B& Y$ S3 ?* c0 E
540
8 D* Z. e5 s/ K. ?0 N6 u! uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) s% u' g) n! T5 L  e0 `the base of the phallus and was dark and curled. The$ h3 Z7 D" d7 H. C+ _8 ~* @
testicular volume was prepubertal at 2 mL each.
9 I4 n  R0 T$ W2 hThe skin was moist and smooth and somewhat
2 q' x6 `) `! P( M) o- h3 ooily. No axillary hair was noted. There were no, q8 t7 ?8 k6 ?, @2 U# D) J
abnormal skin pigmentations or café-au-lait spots.
( k+ \( P; ?; ]4 H% aNeurologic evaluation showed deep tendon reflex 2+% F, y  i. T, _( w5 ^) b
bilateral and symmetrical. There was no suggestion  ^; ]/ U# {5 `% x/ K9 S
of papilledema.
; t* t! W( A6 G  Y$ n) ]Laboratory Evaluation2 K! D% G1 j* j( A5 J3 w* U, M& n' @
The bone age was consistent with 28 months by
: a% i! ~* A9 ?7 zusing the standard of Greulich and Pyle at a chrono-# h$ L& a6 H' W: Y$ n5 R
logic age of 16 months (advanced).5 Chromosomal
% e0 k, ?$ S" F2 t. Rkaryotype was 46XY. The thyroid function test
' Q, q: b0 q5 ?4 ushowed a free T4 of 1.69 ng/dL, and thyroid stimu-
# O( w' I3 c( `/ ylating hormone level was 1.3 µIU/mL (both normal).5 G- V9 v6 ]9 ^/ y' O( C: U# H7 H
The concentrations of serum electrolytes, blood8 w, X- E! T. W9 s6 P$ Q2 x# k' I
urea nitrogen, creatinine, and calcium all were
3 I0 u! a# B; p  Rwithin normal range for his age. The concentration
5 \2 I; T2 M6 X9 i' W7 [of serum 17-hydroxyprogesterone was 16 ng/dL) [+ p0 n) d5 S; N- {6 z
(normal, 3 to 90 ng/dL), androstenedione was 20
: c! j* G0 D0 M4 ~ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 ]* L( G$ _- Y% |, jterone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 l( B( N% d. Edesoxycorticosterone was 4.3 ng/dL (normal, 7 to- G5 {1 F( h0 k* c% t, F0 p" q2 f& U
49ng/dL), 11-desoxycortisol (specific compound S); B' J6 r8 A% [6 }+ W* @" u$ }
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* G( M/ G3 X! L9 B& \& qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total  n- x! K! @6 D3 v8 Y7 K
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( M- z. l8 V$ y7 ?: u1 v
and β-human chorionic gonadotropin was less than
4 y( @8 Q0 u2 g) B$ O5 mIU/mL (normal <5 mIU/mL). Serum follicular
) N! C( V1 }- U: s( |: N4 \: Gstimulating hormone and leuteinizing hormone
- O& i. W/ |  M5 Pconcentrations were less than 0.05 mIU/mL/ l* h+ z) c6 s/ l# Y% `( n
(prepubertal).
/ e8 h' f8 P( D$ h% JThe parents were notified about the laboratory
, H) h' ^, ]1 lresults and were informed that all of the tests were
$ T0 ~6 C. I5 [- D" i1 b5 \normal except the testosterone level was high. The4 ^  t, {4 R$ I2 C" D; X* [
follow-up visit was arranged within a few weeks to$ i8 k, F7 @8 Z( D$ H
obtain testicular and abdominal sonograms; how-
( _7 e8 Y6 X% ]9 C6 A7 `9 \6 Tever, the family did not return for 4 months.
% {% \5 q( U( l/ [' R, v# PPhysical examination at this time revealed that the
% R" s/ j$ c9 k4 ?! Z" R* S+ qchild had grown 2.5 cm in 4 months and had gained# R" V: Y$ |# s& B7 h9 }
2 kg of weight. Physical examination remained: a# K) e4 k: p
unchanged. Surprisingly, the pubic hair almost com-* J9 J: W! z6 P& o
pletely disappeared except for a few vellous hairs at
1 V, Q/ i: Q$ mthe base of the phallus. Testicular volume was still 2
7 i, B& I( Z4 F/ a  [" VmL, and the size of the penis remained unchanged.
: [* V4 \3 p: C  H& s. A; SThe mother also said that the boy was no longer hav-" R: U' [- Z, G3 M& m6 ?4 R
ing frequent erections.
" X- M* ^0 u. HBoth parents were again questioned about use of
" k2 M6 \6 S6 b- Q9 n- y  S, O5 Eany ointment/creams that they may have applied to
" h* z) Y3 O8 ~( t( C- x9 xthe child’s skin. This time the father admitted the
9 B# \. \- z+ _6 ^4 D( T4 dTopical Testosterone Exposure / Bhowmick et al 541
' R3 c) A8 g9 x5 B9 {1 B5 U2 buse of testosterone gel twice daily that he was apply-% j- A4 N4 t' v1 K' {2 @
ing over his own shoulders, chest, and back area for
( y3 b5 o0 Y$ c/ U" ~) V; ~% G. J  Na year. The father also revealed he was embarrassed
* m8 i) e& y. P% W- h6 nto disclose that he was using a testosterone gel pre-. X. {/ e" W9 Q% i
scribed by his family physician for decreased libido
# ]# \8 S1 l. Csecondary to depression.) Y" b, T. j! i1 l: @' Y5 k
The child slept in the same bed with parents.* k3 y& l7 C! V& M$ h( K3 a
The father would hug the baby and hold him on his7 Z9 S  C$ w9 ?- M% ]1 T* J8 a
chest for a considerable period of time, causing sig-/ u% v4 N' J+ a" I3 I: D
nificant bare skin contact between baby and father./ m+ r7 @6 E! c
The father also admitted that after the phone call,' [) `3 P) ?' i9 o  m
when he learned the testosterone level in the baby$ a5 Q& U  J% F
was high, he then read the product information8 s# s( C5 r1 O. J  e& s6 y5 Z, @
packet and concluded that it was most likely the rea-( t  y- J! ?) z/ r
son for the child’s virilization. At that time, they
9 {7 O) J" O* Z2 C5 V' I" T/ ], Udecided to put the baby in a separate bed, and the6 R$ t0 u( f& F0 y4 t
father was not hugging him with bare skin and had; X; x* e  a3 d5 c
been using protective clothing. A repeat testosterone
! S& k" W0 u- \$ F7 v* etest was ordered, but the family did not go to the4 f- ?- g" b1 Y: I& Q2 u/ }6 w
laboratory to obtain the test.
' H: i* B( A/ U4 _  p! bDiscussion
! t" u9 C9 F* t  z3 h$ Y! gPrecocious puberty in boys is defined as secondary; \/ X; H+ }; V6 \
sexual development before 9 years of age.1,4
8 f1 M3 P6 N* |9 W% lPrecocious puberty is termed as central (true) when% z8 Y& b* h% d
it is caused by the premature activation of hypo-, r# u# z/ e7 J, r  F, M1 R/ p
thalamic pituitary gonadal axis. CPP is more com-, {2 K0 I1 H- C) Q/ m1 `7 L
mon in girls than in boys.1,3 Most boys with CPP
/ ?& C% O3 E! V( q# u: k. rmay have a central nervous system lesion that is# B) c8 i9 o; z; e9 e. j* D
responsible for the early activation of the hypothal-
( P* E! G* J5 e' uamic pituitary gonadal axis.1-3 Thus, greater empha-, B0 |+ B+ l& v0 X
sis has been given to neuroradiologic imaging in) p5 b) W' N* Q" g" ^  I
boys with precocious puberty. In addition to viril-$ G  ~# w" ]1 V5 L' x
ization, the clinical hallmark of CPP is the symmet-
& W3 P( E4 ^4 ^- G' zrical testicular growth secondary to stimulation by" `6 j7 K/ X8 H# d( |6 ]
gonadotropins.1,33 k" A* d9 [5 v, [% m
Gonadotropin-independent peripheral preco-
4 u! {( c& i4 ]! a* q4 y/ Ccious puberty in boys also results from inappropriate
2 |6 J1 A; U9 k8 Dandrogenic stimulation from either endogenous or# L% y, R3 c) W+ F, j. P7 B
exogenous sources, nonpituitary gonadotropin stim-/ f! N+ g* F+ _2 @  Q$ B
ulation, and rare activating mutations.3 Virilizing
& p: E! b3 [2 l$ M& j' ~congenital adrenal hyperplasia producing excessive7 l" c  A% ~8 A" d! E) |4 e% K
adrenal androgens is a common cause of precocious) J% O. u6 X8 ?) x
puberty in boys.3,4
! Z) E% _  t& h9 TThe most common form of congenital adrenal
! G+ I' Y9 T, B9 d9 P" {: Dhyperplasia is the 21-hydroxylase enzyme deficiency." S  _5 v6 r% J! Q" F+ R
The 11-β hydroxylase deficiency may also result in
( r2 O# N9 }" y7 H: ?excessive adrenal androgen production, and rarely,  e+ I# g) X5 n1 v6 g
an adrenal tumor may also cause adrenal androgen* j9 s, x+ A8 ^
excess.1,3$ q% o( y8 f% _# l$ A2 D
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' R0 T. ]% I* K: O
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 p3 O, h+ [1 w) i# P2 `: P) [A unique entity of male-limited gonadotropin-* l) V5 {4 _4 m* A: ]
independent precocious puberty, which is also known8 r2 l2 K; ~8 S
as testotoxicosis, may cause precocious puberty at a
8 r( J2 U7 N3 u' Z! B  ivery young age. The physical findings in these boys& i. ~; o2 a; a( I
with this disorder are full pubertal development,
9 h5 Q. P5 U6 ]0 a2 {3 y; yincluding bilateral testicular growth, similar to boys$ G9 d# G! `' @9 y3 s( ^
with CPP. The gonadotropin levels in this disorder+ H) n2 o6 P1 e' B2 ^9 Z4 k2 k/ h
are suppressed to prepubertal levels and do not show
7 ]# F+ c/ P5 v6 l9 d' ?# Zpubertal response of gonadotropin after gonadotropin-
% t$ t9 ?5 Q& H3 breleasing hormone stimulation. This is a sex-linked
4 S7 D1 x4 V! O, a2 \) \* _autosomal dominant disorder that affects only
: C, c5 m5 ?7 Y) q: O. Ymales; therefore, other male members of the family  A$ C4 _: z2 k& f0 p
may have similar precocious puberty.3: a3 L& g3 I9 m" |7 e* ~$ V
In our patient, physical examination was incon-
! |* O+ S; J. I# [4 @4 C& d' Ksistent with true precocious puberty since his testi-
( V6 b8 z2 r0 Gcles were prepubertal in size. However, testotoxicosis# ~* f4 \  r7 O8 q9 T9 x
was in the differential diagnosis because his father
# P0 g# Q& E5 _$ [6 _started puberty somewhat early, and occasionally,2 ]2 w/ g9 O0 r
testicular enlargement is not that evident in the! f6 G' o3 f# Y7 [& Q! b
beginning of this process.1 In the absence of a neg-
- r1 ~8 F6 Q- A) J/ Z6 u, \3 G. Jative initial history of androgen exposure, our+ b6 A9 T9 R4 Q4 s  a3 H) k" S. E1 k
biggest concern was virilizing adrenal hyperplasia,
6 S, ]0 }8 B$ M% h  ]7 Heither 21-hydroxylase deficiency or 11-β hydroxylase$ s2 F% c  e4 ~+ e- r6 m! _
deficiency. Those diagnoses were excluded by find-
9 Y6 j: _$ x: R8 m) King the normal level of adrenal steroids.
2 x% Q9 U& h( F9 D1 l3 Y9 ^The diagnosis of exogenous androgens was strongly
: y) u5 ]8 M4 @& i4 @suspected in a follow-up visit after 4 months because
6 O' n  o7 ]5 othe physical examination revealed the complete disap-
* W/ f5 E: x# t# x( O' qpearance of pubic hair, normal growth velocity, and
1 i4 v0 y" A9 i1 r( q4 U4 O' B: [decreased erections. The father admitted using a testos-$ W9 n0 v  L% ^6 q  s' y8 k9 A7 s
terone gel, which he concealed at first visit. He was1 Z- E; Q# K+ R' K$ @; Y
using it rather frequently, twice a day. The Physicians’
( e& v+ m8 E5 h* w* QDesk Reference, or package insert of this product, gel or
  ~. G+ z5 b  u$ }2 h. u, Hcream, cautions about dermal testosterone transfer to) s/ b/ Q0 x( v" D* X2 y
unprotected females through direct skin exposure.
" K1 ]* G4 n4 @$ B* q- Y/ K7 iSerum testosterone level was found to be 2 times the
) u' j" K1 V# D% c: e4 Cbaseline value in those females who were exposed to
2 U+ [2 B" F- p2 f" Weven 15 minutes of direct skin contact with their male
& \* f' I' w8 A* ?; ~' mpartners.6 However, when a shirt covered the applica-9 e8 `3 t7 S* k+ p  I
tion site, this testosterone transfer was prevented.
6 ~* U3 V9 ?2 ~) \) xOur patient’s testosterone level was 60 ng/mL,1 y& b5 _* V' J! T/ ~
which was clearly high. Some studies suggest that
0 W3 G2 {4 B0 Adermal conversion of testosterone to dihydrotestos-
/ `$ j+ y  d/ G: r: p6 pterone, which is a more potent metabolite, is more
- m' V1 w* O5 m$ h& z$ J8 Dactive in young children exposed to testosterone5 b; U- W  W! p# o! w+ g
exogenously7; however, we did not measure a dihy-
2 G; D/ l# Q& k, f& U" |2 }1 ndrotestosterone level in our patient. In addition to3 j7 S3 R( T6 ^
virilization, exposure to exogenous testosterone in
% I9 A7 q% c2 Z! y% tchildren results in an increase in growth velocity and
+ w% I& `/ A7 I. Uadvanced bone age, as seen in our patient.
& k4 D3 d( }8 ]9 b# m9 z4 cThe long-term effect of androgen exposure during& c/ o/ V. Q6 O6 n- E, u
early childhood on pubertal development and final
% R) o) Z5 i1 q. s1 _adult height are not fully known and always remain
+ y2 [( v+ g6 wa concern. Children treated with short-term testos-
% c! M# `- i# h* l+ X3 u4 ^terone injection or topical androgen may exhibit some
7 A% d0 ^7 v1 o) U* ?acceleration of the skeletal maturation; however, after
/ g/ @9 X1 g  J+ ?0 Qcessation of treatment, the rate of bone maturation
. M# g1 x: `0 J8 X7 P, F; Y2 M- {decelerates and gradually returns to normal.8,9
, K( Z  e5 `& ^6 w  fThere are conflicting reports and controversy, H" M) h/ ]$ W4 e, m
over the effect of early androgen exposure on adult3 o5 P% B( R+ {6 T
penile length.10,11 Some reports suggest subnormal
! E; x9 Y/ n6 @. U! Sadult penile length, apparently because of downreg-
* K) P  f7 I' B' V/ Iulation of androgen receptor number.10,12 However,9 D; I9 N. }* W9 z  r, n
Sutherland et al13 did not find a correlation between+ V& P  I5 t' S# t4 ]- q
childhood testosterone exposure and reduced adult, m3 H( X% b' Y
penile length in clinical studies.
- r3 ]; E. Y# F0 V, sNonetheless, we do not believe our patient is
- f$ t9 x2 w: B* Pgoing to experience any of the untoward effects from
6 @% t0 t% O  W' K) e2 Z" W( E4 J2 `testosterone exposure as mentioned earlier because
/ l7 n/ |. W$ h+ cthe exposure was not for a prolonged period of time." m+ v; ?5 r0 e  ~1 }; q
Although the bone age was advanced at the time of5 K& l, D% M' r# z" u& L) C
diagnosis, the child had a normal growth velocity at
3 V0 i# v1 N. X# C0 pthe follow-up visit. It is hoped that his final adult
, @2 _8 \, [7 Cheight will not be affected.
8 E& X3 J$ v# ]/ cAlthough rarely reported, the widespread avail-
. ?) ~) d" ~  b) Bability of androgen products in our society may
7 v* y$ v& C# U5 Yindeed cause more virilization in male or female8 J) e7 x+ P; a
children than one would realize. Exposure to andro-
+ j" v1 I0 ~/ |( B7 g& wgen products must be considered and specific ques-% K; Y" o# P- L" h1 n
tioning about the use of a testosterone product or  S. [" h5 |) R! a7 j8 H0 z" j0 a
gel should be asked of the family members during1 j0 T; [" X0 F
the evaluation of any children who present with vir-
2 J" ]; Y0 {: W* F6 y3 d8 pilization or peripheral precocious puberty. The diag-& |. |( c, Y) ~& q1 P/ R
nosis can be established by just a few tests and by2 I# k6 A/ x2 R5 X3 h  k2 W$ p
appropriate history. The inability to obtain such a( n3 N* F! e& Y+ I2 R7 |0 P3 p% ?
history, or failure to ask the specific questions, may
- _" Z9 {( ?1 S9 J1 W) r# @result in extensive, unnecessary, and expensive5 ?2 l5 W- \# {% ~6 P
investigation. The primary care physician should be
- |( t7 O6 x$ J6 ?% _6 J& w! g4 Qaware of this fact, because most of these children! j8 N- L6 s# z* k8 k6 i  I
may initially present in their practice. The Physicians’
/ N/ [3 G1 u" ^Desk Reference and package insert should also put a
& d  D6 P/ C* `warning about the virilizing effect on a male or1 e8 t" s) g3 L2 p/ K; g
female child who might come in contact with some-6 ~# S; J3 ~7 k
one using any of these products.
  q- h  g* d9 ]/ H" o' v3 Q- g& {References
- E/ z4 f. _+ S4 L; o% q1. Styne DM. The testes: disorder of sexual differentiation
2 v- N( E# R0 K9 g/ \! hand puberty in the male. In: Sperling MA, ed. Pediatric  g0 ]- y8 Y) R7 I) o1 {8 I+ n
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;% h3 H4 N+ n! g' G- V0 Q
2002: 565-628.
2 H; U+ s% q* v& b" V+ D' Y' d% N& Z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( q7 U/ f, x) J% a7 ]# gpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
3 m% O. I3 P9 d3 \0 F4 j9 [Boy Induced by Indirect Topical
% D+ r1 a% W2 y! C/ W5 c6 AExposure to Testosterone' N3 U* x9 t; k9 D3 _3 O) ]4 k3 R
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
) T, B% n  }0 `/ N; Y6 A3 S/ uand Kenneth R. Rettig, MD1
: g- M! Y; m, I5 G. ]% p+ QClinical Pediatrics
  L) r4 @9 L9 z% Z8 k; ?, OVolume 46 Number 6
/ A  M; g5 ], F; T* I  xJuly 2007 540-543
, p8 }$ [. u, C# T5 r7 x© 2007 Sage Publications
4 J/ N9 G1 z9 l3 X. u# Z10.1177/00099228062966518 k* V$ p2 N7 c5 j+ u8 C, p& e7 D
http://clp.sagepub.com( P) [7 S* M3 h
hosted at1 R5 w/ Z( U* ^
http://online.sagepub.com! \, F+ D! k! q! H8 `
Precocious puberty in boys, central or peripheral,& U: Y, y. L0 q! g( N
is a significant concern for physicians. Central
2 c$ x* k, o: M9 ~4 W9 c; ^precocious puberty (CPP), which is mediated. H# z! j2 O1 N, e4 u. Z' Y, {* H
through the hypothalamic pituitary gonadal axis, has
! Q8 S3 J7 Y3 Na higher incidence of organic central nervous system
9 ]' [1 J2 y) ~$ J" Plesions in boys.1,2 Virilization in boys, as manifested+ f0 N! D- {' Y
by enlargement of the penis, development of pubic1 E4 w& M& `; c2 y
hair, and facial acne without enlargement of testi-
0 j( I4 i; x* T4 X. F6 F+ ]& R/ acles, suggests peripheral or pseudopuberty.1-3 We% n6 J2 F; k- f
report a 16-month-old boy who presented with the
% S4 C9 O; G- H  H6 senlargement of the phallus and pubic hair develop-
. W/ Z$ B6 n  T9 E. g3 ^. Lment without testicular enlargement, which was due
6 V/ V/ ^$ V/ M! a  \to the unintentional exposure to androgen gel used by+ o2 R: I: k/ H3 r" y7 t% T( b
the father. The family initially concealed this infor-& y! Z* V- M/ R
mation, resulting in an extensive work-up for this& d! c8 t/ D# L2 f
child. Given the widespread and easy availability of
: ^) s# F+ Y8 M4 ktestosterone gel and cream, we believe this is proba-
/ S5 ]$ ~: h  J  o( |9 K6 Hbly more common than the rare case report in the
" Z" J0 L$ l: _3 Wliterature.4, z3 M' g9 C* z. m' E( c' X
Patient Report
  W9 F7 ]/ v4 `" K+ M- h$ VA 16-month-old white child was referred to the. `6 T6 @* V6 h) h* Z% ]; W  ~
endocrine clinic by his pediatrician with the concern
  l& @% \- A; I5 ^2 Z; I" Sof early sexual development. His mother noticed* d/ I& D5 x1 u" t! v
light colored pubic hair development when he was
3 z* m1 W0 I$ |8 f; |' UFrom the 1Division of Pediatric Endocrinology, 2University of" q: R1 [+ c  A6 c: c& f
South Alabama Medical Center, Mobile, Alabama.
6 o+ j; Z8 Q" ZAddress correspondence to: Samar K. Bhowmick, MD, FACE,( D' C; R' g, {5 M% X1 i
Professor of Pediatrics, University of South Alabama, College of
8 \8 c  Q, N! Y0 c8 i5 S- E$ Y  `Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 W' L. u% B2 P* s+ C8 Le-mail: [email protected].0 Q3 A3 Y. S3 I+ ^# y. V! |# o! o
about 6 to 7 months old, which progressively became
  Z8 a1 o0 d% T+ l& L3 q% [darker. She was also concerned about the enlarge-
0 s: D4 ?3 I) G: i! N( v0 Rment of his penis and frequent erections. The child
' c& }# d$ \. M7 n& O7 Wwas the product of a full-term normal delivery, with
# d) f; ?* I* E% Z8 Q# Ra birth weight of 7 lb 14 oz, and birth length of
2 j6 X& Q7 O1 M  e20 inches. He was breast-fed throughout the first year- ]/ j/ y4 W0 ^) [; a
of life and was still receiving breast milk along with/ s, t6 U+ }' t" w" `
solid food. He had no hospitalizations or surgery,) o) x# ?9 W5 e; L1 G! R
and his psychosocial and psychomotor development
8 h+ Z# Y" i: a& p. D8 S% c5 Qwas age appropriate.4 M0 n: `/ T& a- r
The family history was remarkable for the father,7 ^% C7 }- G7 G8 J% D
who was diagnosed with hypothyroidism at age 16,
$ I; D! h0 ]/ K2 Y8 h3 pwhich was treated with thyroxine. The father’s+ j- S4 c+ K3 ]7 _" X% e
height was 6 feet, and he went through a somewhat: A0 G/ @/ C$ x/ n' z
early puberty and had stopped growing by age 14.
4 l. S$ O6 d. ]2 tThe father denied taking any other medication. The2 W1 S. C1 w4 x* O) T
child’s mother was in good health. Her menarche
. r0 ?" q, n3 F$ h1 ~was at 11 years of age, and her height was at 5 feet# q9 a; q; ~/ |+ P/ u& E
5 inches. There was no other family history of pre-
( i* }* D# Z! W: h! N' xcocious sexual development in the first-degree rela-
8 h5 V% \, k( T# t9 b+ Qtives. There were no siblings./ E, z$ R  K7 d3 E! r/ a) j( h/ ~
Physical Examination' ~" [$ y3 @1 q/ _3 i
The physical examination revealed a very active,
- A% M' S, s$ oplayful, and healthy boy. The vital signs documented
. A1 e& `) e' A6 e; ]a blood pressure of 85/50 mm Hg, his length was1 B! a9 [* N9 j! M1 o; r9 `
90 cm (>97th percentile), and his weight was 14.4 kg5 g/ a& u' M+ L
(also >97th percentile). The observed yearly growth; o/ X0 Q7 Y% m+ x1 V/ A: G
velocity was 30 cm (12 inches). The examination of
! H! H  e7 q1 _the neck revealed no thyroid enlargement.7 o3 W: H2 o' v! L
The genitourinary examination was remarkable for* K* K# y" u$ [. a, t8 c/ ~( ~# v
enlargement of the penis, with a stretched length of
" y3 a5 s: S. |$ Y" Y( S3 p5 E8 cm and a width of 2 cm. The glans penis was very well
% \/ i7 c0 J4 ~1 ]! g9 T: r: ^developed. The pubic hair was Tanner II, mostly around
0 m7 N* @  I5 |5 e; C% v540
& f% d$ P9 }7 u6 F- H  Q3 _6 Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 j! m* v; I5 v* P$ l0 nthe base of the phallus and was dark and curled. The1 I2 Z; X& ]+ u/ K7 ^# u  b+ a" w
testicular volume was prepubertal at 2 mL each.9 _1 x) ]. m( {  i) h2 _
The skin was moist and smooth and somewhat4 Z! ~9 o  ?$ L  E; i
oily. No axillary hair was noted. There were no
# A9 `$ Y+ p0 X; Aabnormal skin pigmentations or café-au-lait spots.
& R$ P2 q: N% a" bNeurologic evaluation showed deep tendon reflex 2+
* P# y6 Z; F$ `. f& F4 m$ t+ o8 Zbilateral and symmetrical. There was no suggestion& x# O  k, U0 T' O
of papilledema.
' k! s. g4 b, f5 {Laboratory Evaluation8 o7 F3 Q1 l8 s
The bone age was consistent with 28 months by, _% P3 d9 O9 l  t3 z3 x0 T
using the standard of Greulich and Pyle at a chrono-
, [& g4 f7 S- g) o  {2 {2 dlogic age of 16 months (advanced).5 Chromosomal
( ?6 l+ y( G, {$ G% U0 M, j. vkaryotype was 46XY. The thyroid function test; P/ m1 Z( H  |" C+ Q7 K8 z3 U
showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 ^5 ^# p3 o3 ^) S
lating hormone level was 1.3 µIU/mL (both normal).* g/ Z  m0 O5 x" E& U6 o
The concentrations of serum electrolytes, blood0 Z# B- b- Z0 D
urea nitrogen, creatinine, and calcium all were1 c/ v) [& h8 M9 p6 _% D& |
within normal range for his age. The concentration
% s  ^8 [. e) T4 O3 tof serum 17-hydroxyprogesterone was 16 ng/dL' o3 a- J/ l/ w, @+ }7 X, F
(normal, 3 to 90 ng/dL), androstenedione was 20
: G# m! l( g. F* [, qng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- B3 o* @3 r. F: ~4 C/ y& Xterone was 38 ng/dL (normal, 50 to 760 ng/dL),
' K) Q& D! Y  j5 xdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 ^! R4 O" s: y* K49ng/dL), 11-desoxycortisol (specific compound S)+ n3 W) T. O& `& c+ D
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. t( p8 P+ Y. n+ Ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
9 N$ S0 n* y8 Q$ W- V( ?testosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 `2 M* G1 Z( f) J( ~% u0 K6 E# b
and β-human chorionic gonadotropin was less than
  H2 ]% ~; l4 K6 i7 z2 U3 E5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 ?8 f$ X  T4 a# R% Gstimulating hormone and leuteinizing hormone
' o7 j. [' W$ B! Mconcentrations were less than 0.05 mIU/mL/ V7 S5 b. |- k3 p
(prepubertal).
) M$ \- Y$ ?/ s0 x: Z5 ^- p5 h: _  f$ H0 PThe parents were notified about the laboratory! L* T3 g+ G& ~% V
results and were informed that all of the tests were- X( i& a+ L" E0 l) J/ r, t
normal except the testosterone level was high. The& U0 t( g% ]6 E$ ^1 q' M9 v
follow-up visit was arranged within a few weeks to& T0 J9 U. [7 v' q2 G3 H6 y
obtain testicular and abdominal sonograms; how-8 L3 k. A7 |' v$ G
ever, the family did not return for 4 months., U5 g4 o- Y3 f4 K' j
Physical examination at this time revealed that the! C3 y* _+ z, y
child had grown 2.5 cm in 4 months and had gained$ [$ }  j1 A% n# d: O) ?0 f( Y' O9 P2 [
2 kg of weight. Physical examination remained. A8 u. Y* U" ?/ D/ y9 b
unchanged. Surprisingly, the pubic hair almost com-
$ q( {4 ?* r, ipletely disappeared except for a few vellous hairs at7 Y. e. ]2 c1 q/ x7 p0 l$ ~, D
the base of the phallus. Testicular volume was still 2
3 i" r, Z, A: \8 \9 w: ]; v# zmL, and the size of the penis remained unchanged.
' Y1 u1 @: _3 dThe mother also said that the boy was no longer hav-
" T% H7 i# L7 oing frequent erections.
* a9 I* O( {$ f4 q! [2 nBoth parents were again questioned about use of$ Z# l4 _! Q& J5 o( y* V
any ointment/creams that they may have applied to/ Y& u5 p7 K% S/ W* U
the child’s skin. This time the father admitted the- f# X5 x/ [$ P+ Y5 V
Topical Testosterone Exposure / Bhowmick et al 541
% x# b: Y* x3 z/ ause of testosterone gel twice daily that he was apply-
+ N$ f; r+ c8 P/ Y7 {) d0 Ring over his own shoulders, chest, and back area for
( ?. U" h: c8 d: oa year. The father also revealed he was embarrassed
2 l$ ^' g% x( N4 s7 bto disclose that he was using a testosterone gel pre-$ u7 `/ H4 r" x8 R$ T7 `" Z! F
scribed by his family physician for decreased libido
' q* T2 M7 P7 ?1 {! E/ @4 vsecondary to depression.
4 \* I8 ]+ Y* l3 |- pThe child slept in the same bed with parents.
; _, }5 |, b6 D& ^The father would hug the baby and hold him on his
6 A$ ]0 {5 T8 k4 D& J: w( G' |chest for a considerable period of time, causing sig-0 S$ f* Z- ]8 @& O+ d; m. e0 n
nificant bare skin contact between baby and father.; I+ ?1 b- d/ E4 f* Z. R
The father also admitted that after the phone call,
. P& `4 S- R  N6 I- hwhen he learned the testosterone level in the baby/ u4 b7 p5 J6 v9 K
was high, he then read the product information
0 @! X( [. Y* v: c7 X% C" h) k( R: _packet and concluded that it was most likely the rea-- s. `9 m7 l6 p# F
son for the child’s virilization. At that time, they
7 P7 Y0 K) n2 Q3 fdecided to put the baby in a separate bed, and the8 ]" \6 }- c( Y1 A' C
father was not hugging him with bare skin and had
' p4 y  z* c- Y) ~7 Nbeen using protective clothing. A repeat testosterone2 J9 f! I, |, D8 I
test was ordered, but the family did not go to the
& \! {  d% x  N- I2 ^! N1 R. h2 Claboratory to obtain the test.2 c2 x8 _& v2 {' l6 S& y- ^) r
Discussion# m+ k4 [# \* n6 c- {) z4 {
Precocious puberty in boys is defined as secondary: n* d. K9 C( E6 j! O8 X
sexual development before 9 years of age.1,47 w! y2 N6 N2 @8 {
Precocious puberty is termed as central (true) when1 ?9 w) h0 _" S7 N( P
it is caused by the premature activation of hypo-
2 ~0 S" q4 [6 s; x/ L. u! e' d# |thalamic pituitary gonadal axis. CPP is more com-6 z( {2 N9 c; T! q8 V
mon in girls than in boys.1,3 Most boys with CPP
; I3 I! `! ]3 o8 `) a+ Lmay have a central nervous system lesion that is
9 |9 f* B' o% \/ ^* W. Wresponsible for the early activation of the hypothal-
9 n8 F& n3 k$ R* g# Mamic pituitary gonadal axis.1-3 Thus, greater empha-
) s" l5 u, ?/ nsis has been given to neuroradiologic imaging in  B8 n# T' _' X$ d9 G) c( Q
boys with precocious puberty. In addition to viril-
$ ]$ L7 @4 I; sization, the clinical hallmark of CPP is the symmet-
& T1 Y4 x, {$ m  Vrical testicular growth secondary to stimulation by0 K9 q" E( x" K. k- ^) R
gonadotropins.1,3+ A3 S1 T4 z0 l8 W7 j
Gonadotropin-independent peripheral preco-+ O' O1 @3 S5 b5 ~2 [# s# r
cious puberty in boys also results from inappropriate
' C( i2 z' ]. ?0 C7 l1 Candrogenic stimulation from either endogenous or
& f4 B( b; |+ O+ J( n' {- ~# ]exogenous sources, nonpituitary gonadotropin stim-
; s7 t  W/ o4 s9 s9 i  G8 @ulation, and rare activating mutations.3 Virilizing2 h7 w$ C: ?" p- t* M. L
congenital adrenal hyperplasia producing excessive
0 o, R) B4 I( M2 Radrenal androgens is a common cause of precocious
% ^' \4 p# p2 k' w' Q- Spuberty in boys.3,4" w1 _1 p, a$ s2 H% y
The most common form of congenital adrenal
* I2 ~" B, ^. E( ohyperplasia is the 21-hydroxylase enzyme deficiency.
: B  g- F( E- [& V! zThe 11-β hydroxylase deficiency may also result in+ S0 L# U. Y' N% y' I& s
excessive adrenal androgen production, and rarely,7 W) \7 l4 W* b+ w: E4 h
an adrenal tumor may also cause adrenal androgen
$ U0 V/ P- t3 L, iexcess.1,3
" n5 ^- l0 j) T4 v5 Z# l& sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( t* c5 @2 {0 H% P542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
  q! n( s# O* [7 cA unique entity of male-limited gonadotropin-
& w% s( u+ @& d: p. i! r4 f0 @independent precocious puberty, which is also known
+ X; l$ r( a/ q, E% ~. ^as testotoxicosis, may cause precocious puberty at a
6 H8 N3 z2 E7 G/ g; Z$ a& T" N- zvery young age. The physical findings in these boys) C- i# V' _, v5 J2 u! [
with this disorder are full pubertal development,
3 T. r$ w! D# d9 fincluding bilateral testicular growth, similar to boys: G* B7 A& G& Y
with CPP. The gonadotropin levels in this disorder4 j8 u, ?5 Y3 Z
are suppressed to prepubertal levels and do not show' k: \. t' g& |8 W' B; _9 ~
pubertal response of gonadotropin after gonadotropin-
) \! j5 V- P! V9 l- [- @. _releasing hormone stimulation. This is a sex-linked3 c; T7 F+ C# y! G3 R
autosomal dominant disorder that affects only- t' U- W1 z& V5 |, m$ F
males; therefore, other male members of the family* ~: C8 ?' G9 q5 h5 {. Z6 P
may have similar precocious puberty.3
3 j5 Y7 }0 h+ J4 A# s7 S( H- x, WIn our patient, physical examination was incon-
' x2 i3 e: G& n* R5 Osistent with true precocious puberty since his testi-( E1 J: a3 Y  V' s
cles were prepubertal in size. However, testotoxicosis
  v7 @+ }9 k! F1 O1 l9 |" Kwas in the differential diagnosis because his father! s% r, \% n; Y/ K
started puberty somewhat early, and occasionally,$ O6 [+ N( V8 k0 l
testicular enlargement is not that evident in the1 o# ^% q9 Y7 a( X- z$ h4 j- k
beginning of this process.1 In the absence of a neg-# ~) o* C- |/ \5 w0 A# z7 {0 W! a
ative initial history of androgen exposure, our9 D/ W& J( ?, p/ [' M- ?3 L4 h
biggest concern was virilizing adrenal hyperplasia,1 H7 r  x1 b9 h) x# `
either 21-hydroxylase deficiency or 11-β hydroxylase% g( T; W2 S2 u* o( J
deficiency. Those diagnoses were excluded by find-! Q8 l+ r# Y4 b  P! e
ing the normal level of adrenal steroids.
* g' V2 j- |% YThe diagnosis of exogenous androgens was strongly
* M# I/ J/ V, ^suspected in a follow-up visit after 4 months because
2 }2 W8 o1 }2 @$ mthe physical examination revealed the complete disap-
8 \! ]  Y- D! v6 G/ gpearance of pubic hair, normal growth velocity, and1 n2 d' K" G1 f: O8 E
decreased erections. The father admitted using a testos-
- ~; o+ [- |; W6 a! n) L0 k! `0 f; Iterone gel, which he concealed at first visit. He was- C' @2 E. O, {7 e! u, ?
using it rather frequently, twice a day. The Physicians’
/ k* E" d$ [+ M& ^' MDesk Reference, or package insert of this product, gel or1 r- u% X6 D+ g2 ?4 B8 f
cream, cautions about dermal testosterone transfer to
* q9 R4 `5 J# X# S& @3 Uunprotected females through direct skin exposure.
, S8 ]$ m: u. L% V$ \" ~Serum testosterone level was found to be 2 times the& h: f$ I! i; `6 N  y; O
baseline value in those females who were exposed to
7 V$ n1 G! H& deven 15 minutes of direct skin contact with their male8 X" f0 d0 i- Y. S8 Z( Q' J( Q
partners.6 However, when a shirt covered the applica-
2 N& _; w' l3 L, z: u1 Jtion site, this testosterone transfer was prevented.3 ?, i9 C, W7 F2 R5 D
Our patient’s testosterone level was 60 ng/mL,
2 s9 `, i4 ]) Wwhich was clearly high. Some studies suggest that4 V0 E5 Q1 z; v* q: Y% g3 @) W9 u$ j
dermal conversion of testosterone to dihydrotestos-
6 x3 s/ l# J! i0 [: N, Tterone, which is a more potent metabolite, is more, ]" F$ H; A( Q$ E
active in young children exposed to testosterone" x1 r+ e& ^3 ~0 g7 L2 G( V
exogenously7; however, we did not measure a dihy-5 G* p% ?9 Z. X, L% T
drotestosterone level in our patient. In addition to
* i1 m5 P0 W1 {2 U5 n1 c* a0 Qvirilization, exposure to exogenous testosterone in' Y: g% q* K3 z! m$ K, X. g* m
children results in an increase in growth velocity and4 {( Y% Q0 B  L" V9 q
advanced bone age, as seen in our patient.8 _1 v. F$ {& \+ `8 M! _' Y
The long-term effect of androgen exposure during
- I. z: n6 y8 l9 Uearly childhood on pubertal development and final; B8 V0 p: ^! e$ g9 |
adult height are not fully known and always remain
" I" N* U5 J$ ra concern. Children treated with short-term testos-
- u4 I% D1 w8 Y" _  m/ fterone injection or topical androgen may exhibit some
3 }) `3 g5 g" D2 }/ v( y1 _acceleration of the skeletal maturation; however, after
1 i2 z- d0 S% p+ w2 G5 \cessation of treatment, the rate of bone maturation4 w9 d* C' Y, q4 X8 ?) W
decelerates and gradually returns to normal.8,9  P3 S9 B4 P3 t# p6 n7 X# Z- t+ L
There are conflicting reports and controversy+ W" l8 o& e% D
over the effect of early androgen exposure on adult- a& f; K' `3 z- ~2 G
penile length.10,11 Some reports suggest subnormal
( M' m" K+ q- k  fadult penile length, apparently because of downreg-
6 [2 D3 J6 W3 M! o/ U* l0 d6 K/ lulation of androgen receptor number.10,12 However,3 z. A0 N) o) l+ A7 w4 q; U
Sutherland et al13 did not find a correlation between$ x: e3 A& E5 U2 ]* Y7 i! @
childhood testosterone exposure and reduced adult& @! e% ], J1 u4 M3 F) Q
penile length in clinical studies.4 @$ o- J8 r6 r8 p' ^) h
Nonetheless, we do not believe our patient is
6 ~8 S! ?0 _& M) A1 B2 e0 ]  }going to experience any of the untoward effects from
) Q6 m. X- [/ T8 R. ktestosterone exposure as mentioned earlier because# [( ]3 L1 M$ O% F7 `
the exposure was not for a prolonged period of time., K& ?1 W; h* H: m$ [. T+ i3 R
Although the bone age was advanced at the time of
2 Z8 A2 H+ p, H$ q5 fdiagnosis, the child had a normal growth velocity at1 c7 {- [9 w4 K/ D$ Y
the follow-up visit. It is hoped that his final adult8 J# N# E: ]- W& I8 m
height will not be affected.0 g2 {& W6 d5 `/ `
Although rarely reported, the widespread avail-
' }5 p0 A5 F6 |ability of androgen products in our society may
9 h& F! {# I) ~! f2 o9 }indeed cause more virilization in male or female
4 q7 R9 d2 ]& @7 d/ pchildren than one would realize. Exposure to andro-
8 @$ K# Q: [0 U; @$ v+ O5 pgen products must be considered and specific ques-' H' S* D  J4 n2 j0 }) _: Z* C
tioning about the use of a testosterone product or. M; G* O7 B$ w! Z6 P4 x1 z
gel should be asked of the family members during
& d1 r3 P- J+ R4 Sthe evaluation of any children who present with vir-- i" P. d& S! O" j. O% ^
ilization or peripheral precocious puberty. The diag-
& z  ^" ]7 j5 g+ c, n  x0 anosis can be established by just a few tests and by
" \* ?+ P2 v, Dappropriate history. The inability to obtain such a7 y3 @4 y- @# ]; G
history, or failure to ask the specific questions, may
3 F- Q% J  P( E( l* Xresult in extensive, unnecessary, and expensive
" H: V+ c, H* E5 n: Ninvestigation. The primary care physician should be& k5 F) L3 ^- W5 V& H" P
aware of this fact, because most of these children0 J" n  O# `; r. R/ F5 _! a# q" s
may initially present in their practice. The Physicians’
# b3 q$ z, i0 A# P4 t6 FDesk Reference and package insert should also put a* v' I" A6 W# J9 E4 d8 Z
warning about the virilizing effect on a male or* ], n2 Q& Q2 y& `
female child who might come in contact with some-7 Z5 `! }2 u( R9 R0 W1 s/ j' A. j
one using any of these products.
- S: P6 Z9 l8 f2 C, G* VReferences
. e5 h5 g: B% U8 z1. Styne DM. The testes: disorder of sexual differentiation
' K6 g, O8 V" _! X+ dand puberty in the male. In: Sperling MA, ed. Pediatric/ k: p$ k& q4 x/ ?& N: h) B9 f
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 A& E  B1 w! F! `& u9 Q
2002: 565-628.
! F2 t9 d  T  V8 e2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious8 V% ~0 N8 B3 |+ h8 L
puberty in children with tumours of the suprasellar pineal
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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!

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發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
累計簽到:11 天
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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

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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?
累計簽到:3 天
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發表於 2025-1-19 02:41:05 | 顯示全部樓層

$ @9 s# {0 l9 X精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!

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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!
 分享同時學會感恩,一句感謝的話語,就是最大的支持!  歡迎交流討論
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