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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old! Z6 m9 x" ?3 w' J% V* M$ F
Boy Induced by Indirect Topical! g: j  F* \% ]
Exposure to Testosterone
9 }+ P7 R& ]& F/ KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
) c: }6 u- |$ k' o5 }; aand Kenneth R. Rettig, MD18 f) D1 s% Z' l; F
Clinical Pediatrics! T# Z& `  W% k& _
Volume 46 Number 6" W+ N- N, s8 V- k" g$ Q, g
July 2007 540-543
4 V) O+ k/ S3 H4 `2 {© 2007 Sage Publications# ]. u( t6 o9 h7 a3 L
10.1177/00099228062966514 p) \/ s$ L; t# Z5 g
http://clp.sagepub.com1 [1 [+ p3 F& Y+ Z; G! a6 a( |
hosted at
) [; @$ m+ F2 d4 A+ p9 `6 jhttp://online.sagepub.com
6 P4 ~% [  `5 DPrecocious puberty in boys, central or peripheral,
! f9 X5 X$ n* ^& H+ W' \6 iis a significant concern for physicians. Central
* Z  n0 l, _% Y. q. dprecocious puberty (CPP), which is mediated3 E% l  Q; m1 F
through the hypothalamic pituitary gonadal axis, has
# n% E3 ~, L6 i1 q+ h2 H; Da higher incidence of organic central nervous system
' Y. S4 ~5 J$ O7 {8 nlesions in boys.1,2 Virilization in boys, as manifested
; _- ?# m- e7 }by enlargement of the penis, development of pubic
/ C- B$ S4 J; Rhair, and facial acne without enlargement of testi-: x+ e7 y( _1 G/ t' q8 U
cles, suggests peripheral or pseudopuberty.1-3 We) b% y1 H0 b& d) z) ]3 D4 v$ P9 M8 r: U7 R
report a 16-month-old boy who presented with the
# D3 S( V" {1 ?. oenlargement of the phallus and pubic hair develop-# {9 y8 S0 P" I) n0 X
ment without testicular enlargement, which was due
- L' O1 S$ y: M* cto the unintentional exposure to androgen gel used by) e" s2 z& O, I: V
the father. The family initially concealed this infor-
3 H" I# Z, t: J% @' E8 P8 H% H# m0 r/ kmation, resulting in an extensive work-up for this
. ^% q9 Z' m! r3 e# Hchild. Given the widespread and easy availability of
- Y9 ^8 D# Q" q, D4 \testosterone gel and cream, we believe this is proba-
8 S2 g0 A) u; h2 zbly more common than the rare case report in the
& W5 K1 f" r- \5 vliterature.4
" q6 X6 X+ L. x+ h6 H* O- _Patient Report
/ A" D, w; G2 ~# A) XA 16-month-old white child was referred to the1 {8 E0 q. Q; i# y
endocrine clinic by his pediatrician with the concern: G/ ~3 C4 m: a" J& N: X$ `
of early sexual development. His mother noticed/ p' z. u$ g9 u9 g
light colored pubic hair development when he was- `0 G4 i5 Y9 O( b0 [1 T0 s6 O  m
From the 1Division of Pediatric Endocrinology, 2University of
2 Q- w1 J  L3 F2 n; J8 hSouth Alabama Medical Center, Mobile, Alabama.; I7 I- N9 h' L
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 F$ \3 `6 o8 P: A$ y# I( xProfessor of Pediatrics, University of South Alabama, College of
9 Y0 t% k5 M) Q* N+ X* CMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;  z3 n+ W" n. d1 [2 {
e-mail: [email protected].; `( F5 n2 T9 u0 n+ r
about 6 to 7 months old, which progressively became
1 u& S  R1 {; |1 m- Kdarker. She was also concerned about the enlarge-( y; p# u9 x4 I# R! I* T
ment of his penis and frequent erections. The child
7 U) B4 P" R" I! R7 ?; Q& m2 ]was the product of a full-term normal delivery, with
. @; f+ c: ^9 Q$ J* _a birth weight of 7 lb 14 oz, and birth length of
* M; K( A$ {: I+ ~20 inches. He was breast-fed throughout the first year/ K( [( |6 q% E( t% v
of life and was still receiving breast milk along with& I# R, ]" b% k
solid food. He had no hospitalizations or surgery,
0 w* j( P/ E) c1 nand his psychosocial and psychomotor development
4 Q: M; f5 v: ?2 Awas age appropriate.! \! J7 g4 K" B4 R3 Y
The family history was remarkable for the father,
, A3 R! K8 s* V/ N& cwho was diagnosed with hypothyroidism at age 16,' v  G. q# j- d8 ]' @; Q3 y
which was treated with thyroxine. The father’s
; c( R% |8 f( J2 |, E3 iheight was 6 feet, and he went through a somewhat
' l  [  o# U1 M% h/ F; g8 |4 K( Dearly puberty and had stopped growing by age 14.1 a  J& L/ p$ ?- ~8 r0 x  k4 j2 w' r
The father denied taking any other medication. The
- \- K9 m) \$ ^9 I0 [: Z0 Wchild’s mother was in good health. Her menarche5 `% R8 w6 e0 V+ g, ~$ ^/ ~! t' D
was at 11 years of age, and her height was at 5 feet
; }7 M, W+ j6 ^9 k3 M$ l) H; }5 inches. There was no other family history of pre-
/ k2 H' ^. ?% J, ~6 D2 E7 Zcocious sexual development in the first-degree rela-  j0 r. m* Y4 q$ X4 Q
tives. There were no siblings.
3 O: A5 Q- T0 F- P$ y& O- kPhysical Examination" w' i! \! i+ y" O0 N
The physical examination revealed a very active,
% Z1 U" m# |3 i% R2 [+ S! J( rplayful, and healthy boy. The vital signs documented! A6 Z; C0 d5 ~, g
a blood pressure of 85/50 mm Hg, his length was, g5 c" q; R4 [1 V
90 cm (>97th percentile), and his weight was 14.4 kg3 A" g( z9 x% l+ t, x  y1 A
(also >97th percentile). The observed yearly growth
3 J% R' l/ G% svelocity was 30 cm (12 inches). The examination of: k( X" x, L: ^, Y; w
the neck revealed no thyroid enlargement.3 y8 F: k, ~& K7 I
The genitourinary examination was remarkable for
5 q- r1 g4 z" A, w- x, N- Xenlargement of the penis, with a stretched length of8 p4 L: J& n9 G
8 cm and a width of 2 cm. The glans penis was very well: F# [( {6 z2 [1 Y; d5 H  l
developed. The pubic hair was Tanner II, mostly around
. L1 l3 b8 a4 B540- R3 Z5 ~5 m& c6 z- b# y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 `: [, }% S' {0 H+ Y) E
the base of the phallus and was dark and curled. The% t; a" Y2 \. H' u
testicular volume was prepubertal at 2 mL each.# ?& l5 H' e# H! e  P" r
The skin was moist and smooth and somewhat' M' b( I) r6 x4 ~
oily. No axillary hair was noted. There were no
# q+ K" q+ ~$ S" Pabnormal skin pigmentations or café-au-lait spots.2 t" X2 O4 }1 k+ o
Neurologic evaluation showed deep tendon reflex 2+
% Y+ _: I& p* e! Ubilateral and symmetrical. There was no suggestion& I  f2 k! a4 J* O; g
of papilledema.
$ v: p0 v% e, I6 _0 qLaboratory Evaluation) G) R- A0 W0 S; |# U8 ]: |# [
The bone age was consistent with 28 months by5 Q5 @: A, S& O' K
using the standard of Greulich and Pyle at a chrono-
( e( q% i6 i7 P- _logic age of 16 months (advanced).5 Chromosomal' q. v+ I5 D) Y! Q* [) j$ u
karyotype was 46XY. The thyroid function test! ?5 B2 X0 X9 D  }
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" Q3 [9 f! N0 ^8 _lating hormone level was 1.3 µIU/mL (both normal).3 [* o+ U  a- X8 X1 P
The concentrations of serum electrolytes, blood- |: A  X  l0 r7 ]% H* x
urea nitrogen, creatinine, and calcium all were, o7 n9 n4 h" Z4 W& g/ w' o
within normal range for his age. The concentration) p4 o* Y! E* i2 D. q3 J
of serum 17-hydroxyprogesterone was 16 ng/dL
% H6 u" q$ _" j& p0 X: j$ t, W(normal, 3 to 90 ng/dL), androstenedione was 20
# |: g; |9 E9 l7 w1 A$ T* Ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% L4 x  H& Z2 V( x6 J  U
terone was 38 ng/dL (normal, 50 to 760 ng/dL),0 y3 z, b  ?% d& d
desoxycorticosterone was 4.3 ng/dL (normal, 7 to1 u3 E8 P$ l3 [3 M0 L
49ng/dL), 11-desoxycortisol (specific compound S)
4 K4 ]1 p/ o( }9 z" Owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 n1 o5 v1 c4 S0 e* c0 _$ s4 wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total6 Y; t2 E# ?2 C7 T. F  v
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ E7 G& {+ ]. y1 i2 ~
and β-human chorionic gonadotropin was less than
9 {# t) B( w- p! @# K5 mIU/mL (normal <5 mIU/mL). Serum follicular! l: q7 I$ }3 e+ p! P
stimulating hormone and leuteinizing hormone( w, V& j" Z) ~- R) z0 c- ]
concentrations were less than 0.05 mIU/mL
) o0 H6 u- z4 k& ]5 u(prepubertal).
+ r$ ~2 k" W. u% Y- X3 F7 I$ c2 U+ H+ vThe parents were notified about the laboratory3 z3 b! {1 ^  @! n9 i
results and were informed that all of the tests were
* ]- S, [) a  r8 A+ ?normal except the testosterone level was high. The
/ n# k$ t9 j2 l: qfollow-up visit was arranged within a few weeks to
$ W0 i9 {- [" o4 ]' k6 Zobtain testicular and abdominal sonograms; how-
) ~! y. g+ M1 n8 w* [3 g- ~( Aever, the family did not return for 4 months.# T+ V. y& o6 N' B! s
Physical examination at this time revealed that the  `7 I7 ?  B! j3 r& b
child had grown 2.5 cm in 4 months and had gained
; G1 g/ p  l. s* R3 R4 O! s+ y2 kg of weight. Physical examination remained
6 v7 i+ ^& U, Q8 e+ P2 w) ~2 d0 kunchanged. Surprisingly, the pubic hair almost com-3 r" V4 a. s; r* r0 [8 x: S
pletely disappeared except for a few vellous hairs at% K( y6 I7 M1 O6 y- b9 `- V4 s' D
the base of the phallus. Testicular volume was still 2
8 _9 Z* t( `+ B4 hmL, and the size of the penis remained unchanged.
$ y9 [6 m! F! ]( RThe mother also said that the boy was no longer hav-
" Z) t# t4 N; W/ n% N+ h% A( ying frequent erections.) P; [9 [% m( H+ O' m
Both parents were again questioned about use of% A! Q% O& F1 k9 q/ ~' P
any ointment/creams that they may have applied to1 Q% U5 t2 u% K
the child’s skin. This time the father admitted the
" q# {( y/ ^, v4 x/ m: g2 oTopical Testosterone Exposure / Bhowmick et al 541
& r( n- c2 u; e, u, m, F# Euse of testosterone gel twice daily that he was apply-! z# T( Q" p8 q5 P2 U! A% v  |
ing over his own shoulders, chest, and back area for$ H' V6 T) v6 Q, e
a year. The father also revealed he was embarrassed
& v1 ^5 G9 v" |8 N# }9 ?0 }2 tto disclose that he was using a testosterone gel pre-
' x: t- y- q' Vscribed by his family physician for decreased libido
1 q1 r8 n: n4 F# s% L/ wsecondary to depression.  ~) O) g* m0 x+ r( T8 M- T# C( o
The child slept in the same bed with parents.
  u# p$ B3 ?2 @  w- KThe father would hug the baby and hold him on his9 S6 K5 s: `" ~4 p
chest for a considerable period of time, causing sig-5 w* Z  o$ l. l" R! \& @
nificant bare skin contact between baby and father.# l" z* }' t8 q
The father also admitted that after the phone call,
% E: p7 e# s6 i% j8 i1 Ewhen he learned the testosterone level in the baby3 T7 d4 _# V6 A5 ]3 e
was high, he then read the product information) L2 l! y: W- [. l* V
packet and concluded that it was most likely the rea-; G$ m" _3 s/ Q: X8 c
son for the child’s virilization. At that time, they
0 e* h/ S2 x! S4 x  ~decided to put the baby in a separate bed, and the" q# [) _% {9 R, _; F
father was not hugging him with bare skin and had; h# X; |5 V) a: v
been using protective clothing. A repeat testosterone
1 G/ i4 O1 u) ~# D* y, \test was ordered, but the family did not go to the5 [# H5 b: E9 I2 _/ O6 v
laboratory to obtain the test.
  d% L  @; v2 W" x. aDiscussion8 |; q9 k- u$ q& S
Precocious puberty in boys is defined as secondary  r+ i! Z2 s9 B' c3 V$ I$ P& l- A
sexual development before 9 years of age.1,4
8 v  U, @0 T# j3 Q3 O) x& nPrecocious puberty is termed as central (true) when: ]4 @: |. d: d# O, R2 c
it is caused by the premature activation of hypo-: E1 y- V; o  ]6 r& j3 [6 L
thalamic pituitary gonadal axis. CPP is more com-
) ^' C; R$ V) ]* v& Fmon in girls than in boys.1,3 Most boys with CPP4 P+ Y" J1 e2 z$ X$ o8 H& I9 I, q
may have a central nervous system lesion that is4 Z% ^6 ~+ ^. R) n, P$ e
responsible for the early activation of the hypothal-7 j  c& y% l/ L  O( x; X
amic pituitary gonadal axis.1-3 Thus, greater empha-
, q% T# N  H5 ?$ e- Isis has been given to neuroradiologic imaging in, J  r1 I9 |7 L( m3 _' p# Q3 Z
boys with precocious puberty. In addition to viril-9 q. X3 a, c$ Q$ ^6 M
ization, the clinical hallmark of CPP is the symmet-$ f- m' `8 z) I8 L3 a5 Q5 t# S
rical testicular growth secondary to stimulation by
+ C' ^1 c3 ^3 T- a8 n. K' Egonadotropins.1,3
8 S5 U- J' ~8 r6 Z8 C+ F9 LGonadotropin-independent peripheral preco-0 K1 N/ F. I$ z- @
cious puberty in boys also results from inappropriate
% T. P: M2 d: m- B3 c, z. pandrogenic stimulation from either endogenous or. G9 G# M7 h/ Z# m6 R. i; m0 j8 J2 Z
exogenous sources, nonpituitary gonadotropin stim-
3 X# E  n# q0 w* ?- K5 W% @ulation, and rare activating mutations.3 Virilizing
5 p; _' [; n) _/ H( h0 z9 `congenital adrenal hyperplasia producing excessive/ Y) y' k( H( {4 U; G! w
adrenal androgens is a common cause of precocious% g/ Q' ?2 i2 g
puberty in boys.3,4
! x) H" G4 H/ S; L! ]The most common form of congenital adrenal+ R5 P9 S7 y( q
hyperplasia is the 21-hydroxylase enzyme deficiency.) _( @3 _; z% o9 g1 q
The 11-β hydroxylase deficiency may also result in6 P0 `% \% x, V
excessive adrenal androgen production, and rarely,& E1 ]4 y1 f0 e2 ^
an adrenal tumor may also cause adrenal androgen
0 ?, y" U9 Z) {) ~" Zexcess.1,3
6 |; |; n; \: h2 v% b" g1 p5 Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; L7 C, m# F% X& J; r% W542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, S; i' l8 @2 z) Y" H! \8 IA unique entity of male-limited gonadotropin-5 z9 F# e2 F; r" o1 i
independent precocious puberty, which is also known! F6 W' a3 ^. R, c0 Y1 g( H' Y
as testotoxicosis, may cause precocious puberty at a
( m' I1 I' q$ tvery young age. The physical findings in these boys
8 A# E! g& f3 B7 v- n7 Xwith this disorder are full pubertal development,# \5 T1 O! B' B# Z7 U
including bilateral testicular growth, similar to boys
4 g" e* Q' {5 a9 L7 W  ywith CPP. The gonadotropin levels in this disorder
1 C  ]; d; w* e: h) ?. k& ^are suppressed to prepubertal levels and do not show6 y' K% a8 H8 Q
pubertal response of gonadotropin after gonadotropin-9 L0 v8 e2 |1 M
releasing hormone stimulation. This is a sex-linked
/ \. t# `- w6 r/ J% ~3 jautosomal dominant disorder that affects only
" q' f1 C5 \/ ?. y* Vmales; therefore, other male members of the family
& S( F  d1 @' h. I; Nmay have similar precocious puberty.3* b. n0 ?4 x  O; a
In our patient, physical examination was incon-
* R1 Z- Y, H; b  Rsistent with true precocious puberty since his testi-
. n+ G# r, _' X. T2 V, z& Hcles were prepubertal in size. However, testotoxicosis
9 f) A# k1 i( g, @- I% F9 Mwas in the differential diagnosis because his father
' T! }0 a. Y$ |, h9 O. xstarted puberty somewhat early, and occasionally,
6 A) F; S* }6 G9 q2 Xtesticular enlargement is not that evident in the( O5 h; d( G4 c4 [5 X; g) _
beginning of this process.1 In the absence of a neg-$ |! @/ @: X& X  ]' J3 T
ative initial history of androgen exposure, our1 I3 v0 v+ m& u4 o1 D  I& `; q# o
biggest concern was virilizing adrenal hyperplasia,) x1 E  {  g* b6 |) n7 L/ j8 c
either 21-hydroxylase deficiency or 11-β hydroxylase
9 `* R4 T. g* k! h# n; Edeficiency. Those diagnoses were excluded by find-
$ C1 G/ \; H- `) d. K8 qing the normal level of adrenal steroids.
- V2 G( b  Y/ q& I+ n- |The diagnosis of exogenous androgens was strongly" e: B6 ?9 ?4 c2 h
suspected in a follow-up visit after 4 months because8 N7 R1 g) u  V/ K0 ~
the physical examination revealed the complete disap-
4 f3 @8 d6 I0 B7 J+ H8 Npearance of pubic hair, normal growth velocity, and
# `/ q+ b  V0 `5 j. O! c* bdecreased erections. The father admitted using a testos-8 ]) l( Z- Z& l
terone gel, which he concealed at first visit. He was
" K7 ^# t; a7 ?" c* g# M# a* Dusing it rather frequently, twice a day. The Physicians’
- ~3 g2 e! I9 hDesk Reference, or package insert of this product, gel or9 O1 ~0 ?0 ^) @
cream, cautions about dermal testosterone transfer to
* M/ C" Y9 X, S: @8 \unprotected females through direct skin exposure.8 G0 |: H6 e8 G" {
Serum testosterone level was found to be 2 times the: G* m0 N$ q  W! T9 x8 m
baseline value in those females who were exposed to
! O$ U# ?' y" ~0 O3 Weven 15 minutes of direct skin contact with their male" S) H! g) S# l5 r: w9 ]
partners.6 However, when a shirt covered the applica-8 a3 B3 `3 P  g- h. ~8 h
tion site, this testosterone transfer was prevented.
( |, v  |- b9 o6 P: e$ nOur patient’s testosterone level was 60 ng/mL,
7 M' r1 d, X" y# h* g& o* Cwhich was clearly high. Some studies suggest that
7 J# c/ n8 W9 I' h' }/ `- K( ~8 @dermal conversion of testosterone to dihydrotestos-
! _. t$ W2 S+ J3 ]0 Kterone, which is a more potent metabolite, is more4 q8 S3 H+ t/ Y+ ^
active in young children exposed to testosterone& Y# N8 Y& W3 j. B- @# |0 }/ m" i
exogenously7; however, we did not measure a dihy-% n2 \/ k- W' r
drotestosterone level in our patient. In addition to
+ O! f. ?, L+ y% v* Vvirilization, exposure to exogenous testosterone in# S0 s6 O* N2 H2 `2 F# J3 c9 J
children results in an increase in growth velocity and9 G8 \' t% C2 O' w+ ^1 E
advanced bone age, as seen in our patient.' ?+ q9 t2 m: k- h$ _  i2 `
The long-term effect of androgen exposure during
+ @8 g  n# U0 T  Q& ]3 w- Qearly childhood on pubertal development and final
. e: l) i; ]5 ]$ I7 n/ ^adult height are not fully known and always remain
5 U1 h- L4 L. b+ D- ?a concern. Children treated with short-term testos-
0 t0 |% u& f" Sterone injection or topical androgen may exhibit some
- h: p# _- x! R3 W# _acceleration of the skeletal maturation; however, after
/ B, g  @1 v% J9 j' ?" pcessation of treatment, the rate of bone maturation( o1 t6 d+ A/ d  P5 s
decelerates and gradually returns to normal.8,9
1 n1 M' a& d0 s+ z& Y! A. V2 V- _There are conflicting reports and controversy% k2 X* h( Z% q
over the effect of early androgen exposure on adult6 F3 K; m0 k' r$ i% i
penile length.10,11 Some reports suggest subnormal4 G9 w& ]: _1 F6 d) L# }3 q
adult penile length, apparently because of downreg-
0 v  A! Z* e& ]) ]( P8 s! julation of androgen receptor number.10,12 However,+ Q, v5 s' @: i6 I9 }& R, i+ c
Sutherland et al13 did not find a correlation between
) `' ^+ u& I9 K7 ?: xchildhood testosterone exposure and reduced adult
+ J+ T0 s9 P" n7 V7 A/ wpenile length in clinical studies.
) m" |. `" P9 aNonetheless, we do not believe our patient is
8 m6 h4 z4 d) D) @- k) i0 h) Xgoing to experience any of the untoward effects from
; I* }9 [0 T/ i' A! V! T' L5 e: ~testosterone exposure as mentioned earlier because
3 ?$ {7 g, G5 Bthe exposure was not for a prolonged period of time.
7 A  J2 o# |( ]' Y' q2 WAlthough the bone age was advanced at the time of+ _/ l9 c5 p6 i+ T% g- V
diagnosis, the child had a normal growth velocity at& O/ a2 i( I. G
the follow-up visit. It is hoped that his final adult% T! X6 Z# q5 ^8 e3 a7 C
height will not be affected.
! W' T# h' L6 y. TAlthough rarely reported, the widespread avail-
( f+ z/ Y) V8 ]7 X- V% Bability of androgen products in our society may
0 j, w! L8 P& findeed cause more virilization in male or female/ O8 d3 V- {* ?# E5 d& H
children than one would realize. Exposure to andro-3 E. ^4 Z: E7 Y; u* U
gen products must be considered and specific ques-; l! K0 ^3 s; r3 M
tioning about the use of a testosterone product or0 @# A& @* ?! m* F" J( l
gel should be asked of the family members during6 Q3 y/ _% |* L' h# E* R* `: ]
the evaluation of any children who present with vir-1 M) t; \* }1 K3 h5 I
ilization or peripheral precocious puberty. The diag-; M6 c; k. }, D* ]  C6 }5 H# F
nosis can be established by just a few tests and by
8 K3 [- i! A; ]( O) Fappropriate history. The inability to obtain such a
3 h; N, G# Q& Ehistory, or failure to ask the specific questions, may) h4 q! P% y% u; f. m
result in extensive, unnecessary, and expensive
: |! A0 @1 F; W0 \) u3 s8 C- qinvestigation. The primary care physician should be/ c+ g* \8 e; J5 D
aware of this fact, because most of these children, i# y) ~2 o0 L
may initially present in their practice. The Physicians’) p) M4 W4 }& j
Desk Reference and package insert should also put a4 S6 \7 P' S. x# G/ o$ A1 \+ T
warning about the virilizing effect on a male or% L7 L' t( [  ]5 F  v; u
female child who might come in contact with some-* g5 l: [3 R- c) `3 I, \) R! `
one using any of these products.
. o5 {$ C8 }4 m. OReferences5 |& T- A4 \+ s" }: P; v9 c
1. Styne DM. The testes: disorder of sexual differentiation
* F  C' O0 |1 r! e3 o9 u1 Jand puberty in the male. In: Sperling MA, ed. Pediatric
6 u. p5 O. _8 p6 c+ AEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: [# U7 g6 z+ P) B( ]) ?2002: 565-628.( }% }. Y6 q% X% W; J, {6 i
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. L' r$ I/ E5 e  z  R( \. x
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old9 E9 k9 ?% @  A4 q# j" `9 d$ Q
Boy Induced by Indirect Topical
6 I2 ]0 k8 _8 t. ^. JExposure to Testosterone% o2 t) Z% h6 j( O
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
3 ^3 o) O, H7 H3 T9 Uand Kenneth R. Rettig, MD1
% ?8 h. N, t- B7 ~2 Z7 f  m* `Clinical Pediatrics0 Q! K* S5 e" l, T" w, y
Volume 46 Number 6
/ r# T" t' Q8 uJuly 2007 540-543% Z/ H6 X6 s# t% ^; n2 [
© 2007 Sage Publications9 o- u4 Z1 v4 v$ Q7 E# {: c7 i" l
10.1177/0009922806296651
, P- ]) t* h' V: r) }# Xhttp://clp.sagepub.com' Q9 P" Y4 b: m  M: s
hosted at
' F# T4 _5 N* V7 chttp://online.sagepub.com
% U+ }; h5 M5 {, S" {Precocious puberty in boys, central or peripheral,2 ?: g$ P+ g( r+ g
is a significant concern for physicians. Central; X' `' r8 j( P0 h, t
precocious puberty (CPP), which is mediated
& X0 e( y3 f) @4 t5 Jthrough the hypothalamic pituitary gonadal axis, has" W6 ]; o* \# o6 k" |
a higher incidence of organic central nervous system
0 E( D7 P+ C5 L% nlesions in boys.1,2 Virilization in boys, as manifested& ^' o0 h  A# Y
by enlargement of the penis, development of pubic
# n' g0 i: b- q+ Shair, and facial acne without enlargement of testi-
: G8 y$ l" Q6 e! F0 A- bcles, suggests peripheral or pseudopuberty.1-3 We
, H7 F8 C0 F5 ~6 P. [report a 16-month-old boy who presented with the: Q; k8 r' w0 ]8 k9 ~- l6 C
enlargement of the phallus and pubic hair develop-1 O! l+ q) @, L! e! @) A4 ~
ment without testicular enlargement, which was due* t  G: `# U; c8 d+ t8 Q
to the unintentional exposure to androgen gel used by
, I6 [4 h- s, f1 l# Sthe father. The family initially concealed this infor-. w( z* U9 ?$ \* }+ Y  J
mation, resulting in an extensive work-up for this& {+ |& P6 n/ D' D) C$ n
child. Given the widespread and easy availability of' K7 ]; g) h, A5 E$ ?8 q
testosterone gel and cream, we believe this is proba-. a2 e* h: D- p2 q- @; c, O
bly more common than the rare case report in the8 {7 w. G" M8 e2 H* ~
literature.49 ^* n! Y- ?) q0 l$ k- I; L* x
Patient Report
3 a" ~( o# p* ~( q+ G: ^7 iA 16-month-old white child was referred to the
  |! }% k& I- }- [8 J: Uendocrine clinic by his pediatrician with the concern
* H- D( I# m* G0 F* `8 uof early sexual development. His mother noticed
9 h! |5 r! X3 C$ Y3 j: xlight colored pubic hair development when he was
- h3 X9 K9 ?6 \From the 1Division of Pediatric Endocrinology, 2University of
4 N  f7 e$ Y7 J& Z' z3 a. a$ m: w0 ESouth Alabama Medical Center, Mobile, Alabama.
- i% U# h& m( t% P4 x! M- @$ c1 R, ?+ \! wAddress correspondence to: Samar K. Bhowmick, MD, FACE,
# Q' [% ?* f0 a* a( WProfessor of Pediatrics, University of South Alabama, College of9 D# o' [- c( m2 L; x9 E# Z0 ^& A
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ I: }; s! V5 h+ X
e-mail: [email protected].: v/ O- x" x( `8 ]7 f4 l9 H
about 6 to 7 months old, which progressively became5 E! F8 a( q7 p( r. q( X9 |" A
darker. She was also concerned about the enlarge-
! A6 L; ~) k6 ?9 o6 U2 Z* @ment of his penis and frequent erections. The child2 F# }$ f/ t/ I! `9 R2 E1 I; K( U
was the product of a full-term normal delivery, with( a" K6 R" K2 Z! t( s3 Y
a birth weight of 7 lb 14 oz, and birth length of1 ^7 \8 ~" i; c8 K( O& i
20 inches. He was breast-fed throughout the first year
7 V* x7 ~: _+ s" t2 Aof life and was still receiving breast milk along with. e& ^; k. `' |3 Q" M; ?, q
solid food. He had no hospitalizations or surgery,
+ s1 z% _  \* I: m3 kand his psychosocial and psychomotor development
: t4 k9 g' @1 F: N- ^( D3 K6 Qwas age appropriate." ~- X7 O8 V! c; ^  j/ n
The family history was remarkable for the father,
$ s6 Y# d/ N; R6 Owho was diagnosed with hypothyroidism at age 16," h, `& o; \, ]& e* m& n3 D
which was treated with thyroxine. The father’s
/ D# n4 U# R6 |8 x9 Pheight was 6 feet, and he went through a somewhat
$ U9 q6 j6 E( h9 m. `  oearly puberty and had stopped growing by age 14./ |7 T8 f% r' K" S! H/ l4 y
The father denied taking any other medication. The% L8 K& c8 E! j) s9 {
child’s mother was in good health. Her menarche% z0 j) X6 b- c/ o8 N/ U' K9 X, O) P- o  M
was at 11 years of age, and her height was at 5 feet
. Y, u3 l. f! O% V5 inches. There was no other family history of pre-4 e! l8 Q. d/ n" j2 r
cocious sexual development in the first-degree rela-7 ^0 L8 @; E4 G/ }! N/ E* z
tives. There were no siblings.3 e( x$ ?9 l; v3 H8 J% j! u  m' ]
Physical Examination2 [$ y" C: M  Y! t! M
The physical examination revealed a very active,; v; z9 p0 ^5 j, E( Q" {
playful, and healthy boy. The vital signs documented2 o" i* [) M. c9 B5 g$ o0 e4 m5 ]
a blood pressure of 85/50 mm Hg, his length was. g" c6 o" @8 P0 q( ]
90 cm (>97th percentile), and his weight was 14.4 kg
3 Z- O0 E2 G+ W+ ^! j% C+ Z6 A(also >97th percentile). The observed yearly growth" I2 }8 P& T0 l  ?# _/ [/ P
velocity was 30 cm (12 inches). The examination of
6 Q7 n: u2 c  @  `* athe neck revealed no thyroid enlargement.
8 @2 k7 ?- D  j( q4 v! q' }/ YThe genitourinary examination was remarkable for
$ Q' |2 y, R  a  s, ?- }enlargement of the penis, with a stretched length of
2 B( J  [, e* r3 t" X$ c/ m8 cm and a width of 2 cm. The glans penis was very well
) a: L2 p* y8 \developed. The pubic hair was Tanner II, mostly around
6 J* x6 F- K- Q3 `& b1 g) |540
. g& Y! Y. [% Q3 R: \9 [  V! B5 Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from3 r. w+ G8 [) v8 @- ~8 G
the base of the phallus and was dark and curled. The
1 I! \4 g# |+ m2 `$ H' i7 Etesticular volume was prepubertal at 2 mL each.
/ U& B  W* N1 @2 e, i4 `The skin was moist and smooth and somewhat
9 V" Z( V! w( B0 H3 noily. No axillary hair was noted. There were no5 g; v9 t" D2 X4 f$ i
abnormal skin pigmentations or café-au-lait spots.- t$ N: A  A7 e, K' h4 B6 o
Neurologic evaluation showed deep tendon reflex 2+  t) i# K( I- d
bilateral and symmetrical. There was no suggestion6 F, S% \6 x' S
of papilledema.
6 Z1 W' Z+ j: u" CLaboratory Evaluation5 c' D: H2 Z* H6 A, Y! z" o. O
The bone age was consistent with 28 months by, R7 u6 O5 w; L
using the standard of Greulich and Pyle at a chrono-0 \( ~+ t; T1 l. b
logic age of 16 months (advanced).5 Chromosomal
$ _6 B9 {! D' {. ?) Q1 c+ nkaryotype was 46XY. The thyroid function test
% Q" _  ?* I0 V- W6 K. Kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-% U4 V# g) T6 W& j2 G, ?2 E
lating hormone level was 1.3 µIU/mL (both normal).7 [( L! ?7 q, z* Q* P$ Z' u
The concentrations of serum electrolytes, blood9 w$ X! X; O' ?; X# N! n
urea nitrogen, creatinine, and calcium all were, R& Y" p+ _1 O5 B' R. O1 d
within normal range for his age. The concentration
! _  [  G& c! }- ^of serum 17-hydroxyprogesterone was 16 ng/dL
: B$ s1 [  _$ l( Q  N2 V9 ?(normal, 3 to 90 ng/dL), androstenedione was 20
& l4 T7 g1 f; v8 V+ a: w0 |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 J! m3 @1 V  Y8 I- [9 e& Y( Kterone was 38 ng/dL (normal, 50 to 760 ng/dL),5 i$ ^- t0 L: U9 q, [5 M
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
: M+ P( a4 S5 E' T8 \" N) h49ng/dL), 11-desoxycortisol (specific compound S)
" b! s% l& q0 twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# Y) x6 h" L* }6 Q  Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; a" L1 x3 I6 Y, v5 D  e) l' O7 [testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" s* f' f( I. {' ?% X. gand β-human chorionic gonadotropin was less than  l0 A6 k& J8 r& b
5 mIU/mL (normal <5 mIU/mL). Serum follicular% _& o7 H- y" H: Y4 M$ [
stimulating hormone and leuteinizing hormone
! r: q& C' M5 q/ T1 T/ U1 c+ Mconcentrations were less than 0.05 mIU/mL0 [2 J6 e, Y7 k1 Z4 Z' Y" m9 Q, X
(prepubertal).
9 n$ K/ c4 X. c$ |' ]The parents were notified about the laboratory
& T" N; P8 ~" h8 e; oresults and were informed that all of the tests were
1 B6 S0 n% x! ~. [! \" {1 enormal except the testosterone level was high. The4 \8 d+ e! p. o& V7 L# a
follow-up visit was arranged within a few weeks to5 ?& d0 I& q* q6 Y1 P* p" `
obtain testicular and abdominal sonograms; how-( f, l8 m' h+ }+ F: V9 c, j
ever, the family did not return for 4 months.
; \. ?( ]0 r5 u8 gPhysical examination at this time revealed that the0 w" J8 V' @; n( P/ E, X
child had grown 2.5 cm in 4 months and had gained7 t8 O8 J. K. p: N! ]/ W7 Z- J
2 kg of weight. Physical examination remained
$ Q/ u4 Z7 |5 }* D% aunchanged. Surprisingly, the pubic hair almost com-: R* C$ C, t# x# I' e
pletely disappeared except for a few vellous hairs at
1 o1 u; l& }9 P' F: t* b. `* Rthe base of the phallus. Testicular volume was still 2
) {2 m3 r8 G- d9 ~# `6 OmL, and the size of the penis remained unchanged.
. \  z6 R* E* W3 t. [) \The mother also said that the boy was no longer hav-* ?( \7 _) H6 d7 b1 D9 ?
ing frequent erections.
# i$ _& J' z* q9 k+ S. cBoth parents were again questioned about use of
: q1 _2 L/ |  K) H1 w) E5 `any ointment/creams that they may have applied to4 c( B! W: D7 v- S3 @
the child’s skin. This time the father admitted the6 u6 M* I9 K2 I7 r. j
Topical Testosterone Exposure / Bhowmick et al 5414 u" o! m+ {" {3 \" B
use of testosterone gel twice daily that he was apply-2 k" \4 D7 c0 f1 T+ ~6 K7 P
ing over his own shoulders, chest, and back area for  z0 J# |1 Q/ B% q2 x9 v0 w
a year. The father also revealed he was embarrassed, d' r  Q$ X8 h1 x# N: `6 G8 s
to disclose that he was using a testosterone gel pre-
  |( s3 f. D$ \% u. `( Mscribed by his family physician for decreased libido
) a  ^1 g$ U- B. e) d) S3 _) Z3 ?secondary to depression.
6 e# q9 {) E0 I) D; m* BThe child slept in the same bed with parents., M( ^$ F2 C* o5 P  v$ s* a0 `/ J2 G9 p
The father would hug the baby and hold him on his
# y2 V( T+ Y) S1 {: p3 schest for a considerable period of time, causing sig-4 X( W8 {! h! {, y1 Q2 {3 k
nificant bare skin contact between baby and father.* M4 N2 g  z+ E% a, u
The father also admitted that after the phone call,5 g8 H9 h2 B" W' s/ u
when he learned the testosterone level in the baby
$ {' y! w- K: V$ x6 cwas high, he then read the product information
$ k5 H, e6 Q! o/ z5 Cpacket and concluded that it was most likely the rea-6 k4 O' ]+ S! P" q
son for the child’s virilization. At that time, they
: ~8 \# E7 P5 b! w- T& S, wdecided to put the baby in a separate bed, and the* z2 |+ h7 U& I: i
father was not hugging him with bare skin and had( z4 g3 b7 Q' s- U8 M9 t3 M( e7 ?. C
been using protective clothing. A repeat testosterone
: E) G- c! c1 L0 Itest was ordered, but the family did not go to the( H6 _) E$ n7 Y0 Z/ I& |+ z
laboratory to obtain the test.
# I  p3 c( @1 p% d$ [; F' EDiscussion
. S4 q& b; J) k2 l) A/ r2 t) ]9 {Precocious puberty in boys is defined as secondary, V1 \) _' v  e. `
sexual development before 9 years of age.1,4( N$ B8 e. \2 o0 O  L
Precocious puberty is termed as central (true) when
' }: b# Q9 _/ I; `% E1 T* Rit is caused by the premature activation of hypo-& s5 i2 n" ?! \" v
thalamic pituitary gonadal axis. CPP is more com-- q# D) M  Q3 |8 ~+ F
mon in girls than in boys.1,3 Most boys with CPP
: j3 Q% q6 t' j6 p( T% ymay have a central nervous system lesion that is( Y- G7 q: [, Q/ Z: T/ G# ]
responsible for the early activation of the hypothal-( T* f) c. e" L' q- S9 D1 l
amic pituitary gonadal axis.1-3 Thus, greater empha-9 l/ }3 r  v' y7 J8 B2 f
sis has been given to neuroradiologic imaging in
; ^/ \" F1 y& g8 d3 h% U% z$ {/ Rboys with precocious puberty. In addition to viril-
3 O5 k8 ~1 N. ~  n* xization, the clinical hallmark of CPP is the symmet-) M! ?; {+ s" {& A3 i# l% p7 E) j; C
rical testicular growth secondary to stimulation by
1 F; {/ J- S; Q, }, g+ R4 x. u+ zgonadotropins.1,31 f4 g/ n' z% o# E0 c$ m. U( O
Gonadotropin-independent peripheral preco-  A% |- T" q! x
cious puberty in boys also results from inappropriate* X; K1 f# N( L+ c$ p
androgenic stimulation from either endogenous or
) g' W4 ?8 \7 k! xexogenous sources, nonpituitary gonadotropin stim-( q8 H% M* w: m3 k& B3 X' w" |
ulation, and rare activating mutations.3 Virilizing- W1 w9 Z: w  I* h, b
congenital adrenal hyperplasia producing excessive
: {3 e0 Y( E/ ?4 I# U1 E1 Hadrenal androgens is a common cause of precocious5 s. J* J# r$ G
puberty in boys.3,40 |- }! O; r% |* J* I; Q3 k
The most common form of congenital adrenal
; j: V. o6 C8 A$ X  [: y7 l  j# o% ~* dhyperplasia is the 21-hydroxylase enzyme deficiency.
2 q7 d) f2 Q$ |" Z" uThe 11-β hydroxylase deficiency may also result in
1 n  g% V. _( {; bexcessive adrenal androgen production, and rarely,
; x! P+ A3 Z- d0 yan adrenal tumor may also cause adrenal androgen) E# [( F' T6 i$ A5 e
excess.1,3
9 q* m; N- ?, d+ Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: N2 }/ x& n9 D$ h& V9 R, N3 T542 Clinical Pediatrics / Vol. 46, No. 6, July 2007  L) M: f2 h; c. z( x  H: d
A unique entity of male-limited gonadotropin-  d, x, L. ]- ~& r
independent precocious puberty, which is also known
1 E# P9 S- i$ Aas testotoxicosis, may cause precocious puberty at a
6 q- N0 g* \+ M2 Z3 ?: n2 Mvery young age. The physical findings in these boys
1 U. e; r6 o4 S6 z5 K6 s4 nwith this disorder are full pubertal development,  ^9 P) y( q& p3 ^+ I
including bilateral testicular growth, similar to boys
- c* e' g9 s4 z0 q/ [with CPP. The gonadotropin levels in this disorder
+ f% Q7 n, Q# @$ o7 c' @% nare suppressed to prepubertal levels and do not show! X( r4 }0 m' e/ M6 u
pubertal response of gonadotropin after gonadotropin-
4 i1 r0 C% W! h% ~4 A2 |9 xreleasing hormone stimulation. This is a sex-linked
- j) x0 Y' m: O% D2 Oautosomal dominant disorder that affects only0 N3 C. E6 z; p: ~# |, X$ h" z
males; therefore, other male members of the family" x  r( V% J! O% y
may have similar precocious puberty.3
2 }8 i! S! q* U  l9 d# a; r; ]9 wIn our patient, physical examination was incon-- k& Z5 S8 J5 @
sistent with true precocious puberty since his testi-
, S  O: U' R3 L+ S7 Lcles were prepubertal in size. However, testotoxicosis
# l, b5 t( s+ W% Y+ iwas in the differential diagnosis because his father
/ D* }2 d" Y3 ~  V6 Astarted puberty somewhat early, and occasionally,
* P, [/ M- ?: L* }4 \( `! z! V" u) Ttesticular enlargement is not that evident in the
4 l) O2 K/ c( b: pbeginning of this process.1 In the absence of a neg-6 k9 @5 X$ U/ I0 M5 y- d
ative initial history of androgen exposure, our
) a  E7 b) W% l8 Dbiggest concern was virilizing adrenal hyperplasia,
# w; ~$ v1 H3 F- `- v/ teither 21-hydroxylase deficiency or 11-β hydroxylase& W/ ^5 z4 T1 E& j
deficiency. Those diagnoses were excluded by find-8 U( ?# T: Q/ E5 Z( W, Z( A
ing the normal level of adrenal steroids.
0 y2 Q4 W5 K- F1 qThe diagnosis of exogenous androgens was strongly
& Y! G5 K7 D# K2 g- \; c% msuspected in a follow-up visit after 4 months because: Z) X8 t5 y; z; u" e$ L% j1 L& u* O
the physical examination revealed the complete disap-
5 i6 x1 ^6 i  ~9 f! dpearance of pubic hair, normal growth velocity, and, N. {& `7 j$ j# m
decreased erections. The father admitted using a testos-* x6 C6 I" k" [7 t5 v' _! i
terone gel, which he concealed at first visit. He was) b+ c% b* u$ t: R& k+ p
using it rather frequently, twice a day. The Physicians’
9 r/ p, n/ k* L0 HDesk Reference, or package insert of this product, gel or% \1 @1 P" p0 N2 [0 u
cream, cautions about dermal testosterone transfer to, @9 m. p4 {) p0 j
unprotected females through direct skin exposure.1 h5 M. V8 O- I( K: p  S8 j
Serum testosterone level was found to be 2 times the
0 v8 X: W4 O% o+ W7 b; c+ l/ Y* b2 pbaseline value in those females who were exposed to
/ z- g2 N6 l; keven 15 minutes of direct skin contact with their male0 P$ i. T  A- W9 |- Z  ?) J9 k
partners.6 However, when a shirt covered the applica-6 h; c) Z) h; B% i* m( Y2 [- u
tion site, this testosterone transfer was prevented.
* i+ E  F, K3 M8 POur patient’s testosterone level was 60 ng/mL,5 _3 L/ b9 p1 G; k/ ~
which was clearly high. Some studies suggest that
9 O4 U( u. g6 F+ e0 pdermal conversion of testosterone to dihydrotestos-
4 X3 ]. m+ K- c7 mterone, which is a more potent metabolite, is more
4 F% R7 R5 [- f5 G; t* j8 _" kactive in young children exposed to testosterone4 o6 k7 R; F# C, E
exogenously7; however, we did not measure a dihy-- P4 C) i& }  e; {5 S, @
drotestosterone level in our patient. In addition to
! n% n  u& R" B3 o! `+ uvirilization, exposure to exogenous testosterone in
- c- w* w3 E4 [children results in an increase in growth velocity and9 v5 m9 m" D  F% x( u
advanced bone age, as seen in our patient.
8 U/ R  `3 B2 V, C: `The long-term effect of androgen exposure during
' v3 A& _: `, _9 J0 e9 s9 ]early childhood on pubertal development and final" [3 v8 ?4 c( V# K. V% F% T
adult height are not fully known and always remain5 Y1 C3 ^& }: t' R" m1 W$ J
a concern. Children treated with short-term testos-& t% P' X2 C% X8 X/ Y: o
terone injection or topical androgen may exhibit some8 W0 M$ l3 B2 m1 C0 Q4 H7 }5 y
acceleration of the skeletal maturation; however, after
$ X# M# A7 T5 l0 x: Zcessation of treatment, the rate of bone maturation
1 M8 ?. _2 r9 E, Mdecelerates and gradually returns to normal.8,9
" S) C6 v. m" E7 v0 h* k5 V8 MThere are conflicting reports and controversy3 i/ H& \/ `8 f. f& |2 |+ ?; H
over the effect of early androgen exposure on adult
1 l7 }. A, k7 P& Y+ W- L, wpenile length.10,11 Some reports suggest subnormal
" W4 U- B( G: Y' P8 g% \0 }adult penile length, apparently because of downreg-( ?" W1 Y& j! w2 [3 j
ulation of androgen receptor number.10,12 However,1 j: G" }2 w! S& ~! Q  x1 k8 M
Sutherland et al13 did not find a correlation between
- t+ n# R0 m. k  K* Jchildhood testosterone exposure and reduced adult3 n: {( }3 ^1 T2 Z' _6 v6 z
penile length in clinical studies.
- F4 p- v; S' Y2 N2 PNonetheless, we do not believe our patient is
& o* _; n  _' y  dgoing to experience any of the untoward effects from/ M$ @1 H1 A2 v8 d2 H
testosterone exposure as mentioned earlier because
8 \* N6 x0 @, p  Z1 w/ athe exposure was not for a prolonged period of time.. B+ W4 E. R5 X7 l
Although the bone age was advanced at the time of
2 U  U: A4 V3 {. udiagnosis, the child had a normal growth velocity at1 x: B1 e1 D- p, n
the follow-up visit. It is hoped that his final adult, s+ D; t/ ], Q
height will not be affected.
9 H0 A' P2 {2 {9 d5 }Although rarely reported, the widespread avail-
! i/ O) v( X) L7 S' Lability of androgen products in our society may1 t1 g/ f1 _7 p9 D3 M/ L) _
indeed cause more virilization in male or female9 a) C. c2 A/ n
children than one would realize. Exposure to andro-
0 u8 I- f6 }2 g% Lgen products must be considered and specific ques-; U! r: Y  i! L6 ~
tioning about the use of a testosterone product or
! l6 I" `2 Q4 g. `( w2 egel should be asked of the family members during7 [0 X. a3 `  v9 Y: K4 X: {
the evaluation of any children who present with vir-
* G( E% W  O: I  G6 E# p, R+ _ilization or peripheral precocious puberty. The diag-
3 b' q4 _2 ^; y# |  Ynosis can be established by just a few tests and by3 y; R- P7 f0 w+ s5 W
appropriate history. The inability to obtain such a( |% z. f  z& i( W* D
history, or failure to ask the specific questions, may, R. Z" U& R0 s  ~- j9 G
result in extensive, unnecessary, and expensive  _8 o, a: e5 x9 z: K5 g& h; n
investigation. The primary care physician should be
, ]5 k( [. r7 j- Laware of this fact, because most of these children: G: H0 @" K5 L. i' g8 l) P
may initially present in their practice. The Physicians’
- z# g- f$ C7 g1 N3 v  L% }2 T( fDesk Reference and package insert should also put a: S; S% H' E6 l8 e0 A( X, C+ S
warning about the virilizing effect on a male or2 v2 e' z. x" y( h: c0 E4 y( p
female child who might come in contact with some-
8 C7 y, K0 d' z0 H4 l- done using any of these products.
6 w- k8 d  \* S1 Z2 D9 n' gReferences
- y" Y7 d3 D% b6 ?1. Styne DM. The testes: disorder of sexual differentiation
) `# j) M1 M2 N, iand puberty in the male. In: Sperling MA, ed. Pediatric- U9 {! m) ~0 ]6 X: M
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 D! t: J: E" l6 U2 u
2002: 565-628.
3 i0 w) L# {) s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
3 K( Y5 e( T( B$ A' m% H+ m8 ipuberty 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!
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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?
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發表於 2025-1-19 02:41:05 | 顯示全部樓層

: `" J- X1 P* B4 g6 a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!
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