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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
  B( \  O5 {8 gBoy Induced by Indirect Topical: H9 H$ E: Q4 X$ R! K5 C
Exposure to Testosterone2 D% ^' J7 @" J/ K
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 h1 ^$ D7 A9 d) ]: X
and Kenneth R. Rettig, MD1! {' b; J- U3 l
Clinical Pediatrics4 ^+ K) |  e" U0 g4 a& V, c
Volume 46 Number 69 V2 V; w3 D" b( c
July 2007 540-543
( d# p8 r! z1 g( F0 B8 ^© 2007 Sage Publications
* m) l2 I, L, R4 K6 h1 G7 ?2 b& p10.1177/0009922806296651  H. P9 D+ p) H
http://clp.sagepub.com
/ V$ U, H( J3 A. a: v. u& Thosted at
: M. o+ B3 {! ]* }  w4 T9 Chttp://online.sagepub.com
* w7 D6 M' e4 C+ CPrecocious puberty in boys, central or peripheral,1 J% j. p7 Z" r4 N8 E+ w
is a significant concern for physicians. Central
* A. M0 k; p) b- k3 oprecocious puberty (CPP), which is mediated
4 u" S2 Q% j% }through the hypothalamic pituitary gonadal axis, has
. m3 N# c8 S6 g# g8 t: K5 @, Oa higher incidence of organic central nervous system
0 j  H. `" H2 S$ a- w* Nlesions in boys.1,2 Virilization in boys, as manifested  y; s1 t3 _7 y8 \0 a6 i/ l# H  t
by enlargement of the penis, development of pubic
2 U6 e3 J9 R) n* L+ v$ p: \" |$ ihair, and facial acne without enlargement of testi-
. \) ^* d: B* Rcles, suggests peripheral or pseudopuberty.1-3 We& a) g# u8 R# b& X6 L4 y* l- A
report a 16-month-old boy who presented with the- y+ `+ Y! n6 `# [& A, e0 z. a
enlargement of the phallus and pubic hair develop-5 ~. J! [5 Y/ d% F; g2 n
ment without testicular enlargement, which was due3 |! a5 N3 M# a% H
to the unintentional exposure to androgen gel used by
( j" v* a0 N/ `" s0 N) Y7 {the father. The family initially concealed this infor-) |  X' F  y" x7 ^1 R
mation, resulting in an extensive work-up for this
. k/ C  h& R9 Xchild. Given the widespread and easy availability of
* y$ k6 ]  I' l# w5 _6 stestosterone gel and cream, we believe this is proba-( F. m" }* s/ P  s5 A0 S' O+ i7 f
bly more common than the rare case report in the
0 L! ^6 o: t7 ?( `5 B9 Jliterature.4
) s& J) ?7 a6 ?Patient Report& v* S6 y' n( N- s  u( {
A 16-month-old white child was referred to the
& [4 p% ^/ H! e& p5 R3 Dendocrine clinic by his pediatrician with the concern
: `5 ^% v. Y& k3 D( X) Q4 [  Iof early sexual development. His mother noticed; D( ~6 I$ o+ o- }- }6 o
light colored pubic hair development when he was% S' o" U! s7 X2 B$ Q- f# k( a' |
From the 1Division of Pediatric Endocrinology, 2University of
0 o1 L# Y& ?; X( A9 X. @8 USouth Alabama Medical Center, Mobile, Alabama.
! `( e' }0 H3 D( H3 V. V  o* rAddress correspondence to: Samar K. Bhowmick, MD, FACE,- C( G' R: @9 h/ W% R
Professor of Pediatrics, University of South Alabama, College of
2 _& b: I6 l# ]7 }0 pMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
3 ]# j: i; x" p7 ]$ ue-mail: [email protected].+ @4 R) h' S- W- N8 M: Z
about 6 to 7 months old, which progressively became1 X0 ?6 K! I  e0 ?( ~! \
darker. She was also concerned about the enlarge-
7 Q' D& a' b& b  _' E5 vment of his penis and frequent erections. The child
% V# c9 C: h% rwas the product of a full-term normal delivery, with
4 z2 r3 y+ d% h; f0 }a birth weight of 7 lb 14 oz, and birth length of
6 |* G0 P+ |) T& H. c9 u  j7 g20 inches. He was breast-fed throughout the first year* _- [  W+ m" f; B! ]: ]
of life and was still receiving breast milk along with
4 ?* F8 [) d, q& psolid food. He had no hospitalizations or surgery,3 g/ p- _9 S# x5 L* J  q& W) _( E
and his psychosocial and psychomotor development
4 I6 c, o( Y& A/ r  q: m% Qwas age appropriate.2 `7 p7 X7 R. \
The family history was remarkable for the father,
4 P- H6 ?& m. C  P) k9 owho was diagnosed with hypothyroidism at age 16,) t; h. m) \( o2 Z
which was treated with thyroxine. The father’s
% `. @0 u  a8 {1 F8 ~; E6 D4 Theight was 6 feet, and he went through a somewhat
8 b/ e2 R2 H% ]early puberty and had stopped growing by age 14.- o- v( ~4 q3 M, e# |
The father denied taking any other medication. The
% \# y5 R3 G; u* ychild’s mother was in good health. Her menarche
- v- l- W9 Y, N5 Mwas at 11 years of age, and her height was at 5 feet
) @0 A* J) N" Z1 \% ~2 D  I+ H4 Z5 U5 inches. There was no other family history of pre-
! v% O$ C& V- l4 tcocious sexual development in the first-degree rela-
0 m8 T8 F9 ~& S7 I- l$ G1 Ltives. There were no siblings.
2 R- {/ f2 O3 o+ p- E8 ]8 uPhysical Examination3 \& S, |: W" e: z3 w0 G7 z! {
The physical examination revealed a very active,9 Y! x1 i' P, M! g7 u
playful, and healthy boy. The vital signs documented
* [# l! y8 B- H+ q2 S5 q# @. oa blood pressure of 85/50 mm Hg, his length was
' G8 c' W% I9 z5 X90 cm (>97th percentile), and his weight was 14.4 kg  f% \3 f2 k4 d3 U! ?" P
(also >97th percentile). The observed yearly growth
! n# |2 F* ~7 G. n7 E4 e% N+ Bvelocity was 30 cm (12 inches). The examination of2 T4 b. h* e8 b1 Z1 ~
the neck revealed no thyroid enlargement.; ~# K7 v# M" X! D. o! q' r6 u" y5 G
The genitourinary examination was remarkable for$ c- g1 K! F. J( g" [
enlargement of the penis, with a stretched length of7 F5 u/ Y7 d; v! R" ~  v0 F. f
8 cm and a width of 2 cm. The glans penis was very well
5 D6 ]" A; b5 L3 pdeveloped. The pubic hair was Tanner II, mostly around
, J. N3 @' `- j- E7 K540
5 b& q, _+ u6 P, u4 pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- o8 B2 J$ K7 c% r$ cthe base of the phallus and was dark and curled. The8 H# G! w$ t+ V: @
testicular volume was prepubertal at 2 mL each.
) V2 M( w: j) i0 d% Z7 k  ^+ ?$ R: \The skin was moist and smooth and somewhat
/ c; O8 @0 h; T0 S- Goily. No axillary hair was noted. There were no% U, }3 k7 [* }7 [
abnormal skin pigmentations or café-au-lait spots.
% f6 r3 ?  S- n5 T  SNeurologic evaluation showed deep tendon reflex 2+5 R2 r  E1 V. O" R( T& j9 {& d
bilateral and symmetrical. There was no suggestion
$ _0 H- Y$ t) `) m9 Nof papilledema.& _7 P7 O% {, k0 ^- [- z4 n
Laboratory Evaluation# @7 Q- x5 s! y) ^8 C7 a# g
The bone age was consistent with 28 months by" |0 w: [+ i$ z
using the standard of Greulich and Pyle at a chrono-
0 l% |. i) y1 j5 K1 J- i$ Alogic age of 16 months (advanced).5 Chromosomal
8 F& q6 {; ?- c$ \5 I6 v- Ekaryotype was 46XY. The thyroid function test
9 |8 w3 o/ z' X3 \3 I% {showed a free T4 of 1.69 ng/dL, and thyroid stimu-) h  u& s# h0 X
lating hormone level was 1.3 µIU/mL (both normal).
1 ~& W5 F  X* l# M+ [/ q! aThe concentrations of serum electrolytes, blood( e: Z7 R( o2 {4 }$ R5 m( p
urea nitrogen, creatinine, and calcium all were3 S: u' Y& ?7 l" L! T
within normal range for his age. The concentration
, k, E5 M8 d. I+ h/ g7 Y, y4 y( cof serum 17-hydroxyprogesterone was 16 ng/dL8 i* M- n# M6 X9 l- A& Y
(normal, 3 to 90 ng/dL), androstenedione was 20" K) {9 M2 F) `: m
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ H2 A# D1 p6 L" l
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
$ V6 {# U8 J7 y, W! wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ K+ Y# \* v" ~9 V& }# ?49ng/dL), 11-desoxycortisol (specific compound S)
5 L- ^) K* e: U- N* \" Hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 t( @! P( @8 @: t9 t/ G
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. T; x2 |& `% d& Utestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 p# h) [0 \/ `' Q1 g$ a( vand β-human chorionic gonadotropin was less than2 n1 O- }6 i' m1 [$ r- D* U8 E
5 mIU/mL (normal <5 mIU/mL). Serum follicular
: W! b/ Q7 K, i5 q1 cstimulating hormone and leuteinizing hormone
9 S3 T" _, r4 Sconcentrations were less than 0.05 mIU/mL
& Q1 A: V- K  d* v1 [(prepubertal).
1 {: w( e/ f2 a% }, C5 {' h6 x# RThe parents were notified about the laboratory! q) v" l5 h# F) J0 H0 a7 T2 F& Z
results and were informed that all of the tests were
% v: n/ A# g# k( L( o+ gnormal except the testosterone level was high. The6 I$ o; R3 K8 G5 `7 l8 w
follow-up visit was arranged within a few weeks to- C. H0 p& \5 L2 @! H6 c
obtain testicular and abdominal sonograms; how-% g9 V( q4 ~: a' p7 Q! f: i
ever, the family did not return for 4 months.$ u+ r3 o; m# q: Y5 g5 O
Physical examination at this time revealed that the
2 R6 I7 s" @: w0 r; ~child had grown 2.5 cm in 4 months and had gained+ P2 d' Y8 G% F2 }
2 kg of weight. Physical examination remained
% C- |, i& u. j$ N" Z, }unchanged. Surprisingly, the pubic hair almost com-
5 p- {/ P+ |' V$ F+ C; |pletely disappeared except for a few vellous hairs at
) z% r, E6 a# Ythe base of the phallus. Testicular volume was still 2
1 ~# {3 c/ r$ g7 ~, M1 ]- DmL, and the size of the penis remained unchanged.
6 d& k8 M$ \* l2 CThe mother also said that the boy was no longer hav-% Q# a# c3 P5 X( n3 T% g
ing frequent erections.( |5 ?3 I$ F5 u  U# x* C
Both parents were again questioned about use of& S  g$ R, s4 m
any ointment/creams that they may have applied to- h! m7 L& _: d% S- U2 r
the child’s skin. This time the father admitted the
6 f$ g% W* [: j" \7 `0 FTopical Testosterone Exposure / Bhowmick et al 541- b% z2 P9 Z# e- M, O
use of testosterone gel twice daily that he was apply-7 {; q2 ]6 I! D
ing over his own shoulders, chest, and back area for
  l& p6 Z6 `" T9 g' k( C9 s  Ta year. The father also revealed he was embarrassed8 N) c. O2 {, b# s6 h
to disclose that he was using a testosterone gel pre-! Z/ {6 p* `: u# u& x
scribed by his family physician for decreased libido4 Z& f1 h: Y3 Z0 r7 g3 h0 ?5 r
secondary to depression., O) t7 s5 L# U+ P
The child slept in the same bed with parents.
' F. {' \& Y' @. WThe father would hug the baby and hold him on his
% \1 @: T% E, u3 z* {chest for a considerable period of time, causing sig-
4 k1 N; b1 ~' y0 Wnificant bare skin contact between baby and father.# m5 s$ T- N, a/ p% X, r
The father also admitted that after the phone call,. G3 G  G/ q& @" @
when he learned the testosterone level in the baby7 F; b' h, `6 G% g
was high, he then read the product information
& Q6 ?& n3 E$ ^' C( X+ \packet and concluded that it was most likely the rea-' Z: R$ P* R# @& J) D
son for the child’s virilization. At that time, they
; x$ W! I+ E" q& f) w3 ]" C& @( edecided to put the baby in a separate bed, and the7 Z7 z( m2 M9 m
father was not hugging him with bare skin and had
2 A  s4 A2 X# Ibeen using protective clothing. A repeat testosterone. {7 \+ f$ A0 u1 ~7 A' k
test was ordered, but the family did not go to the( I' ]  k% B3 {6 O. o, N
laboratory to obtain the test.
8 L/ m6 Z: `" O6 I: W, x( n# EDiscussion8 [* U+ e' p" L6 j7 U% x! d
Precocious puberty in boys is defined as secondary' E$ L. g% L8 D3 j, z) q, C
sexual development before 9 years of age.1,40 F* X$ h# l9 W- t6 W1 A6 @9 X& l
Precocious puberty is termed as central (true) when
, j2 _& U4 i8 n  i" o- N7 ?it is caused by the premature activation of hypo-
- \: G" }' l) i! \thalamic pituitary gonadal axis. CPP is more com-# \3 G" c* t! B6 a, Y
mon in girls than in boys.1,3 Most boys with CPP
9 H( _. b( {2 h' h+ jmay have a central nervous system lesion that is" w1 M3 K3 E' l% v0 b; l0 r
responsible for the early activation of the hypothal-8 s  D* v4 I( ^& c- _, m6 c. y
amic pituitary gonadal axis.1-3 Thus, greater empha-) w3 ^9 O$ P7 i: ^
sis has been given to neuroradiologic imaging in
& j$ i: Z! O% |! xboys with precocious puberty. In addition to viril-
. P# {4 A, Q0 {0 l; \) w$ Y1 Nization, the clinical hallmark of CPP is the symmet-
. @8 w& ^+ C) }4 W8 C. [rical testicular growth secondary to stimulation by
$ `3 T! \6 S0 S# Z# Hgonadotropins.1,3* `2 Y0 N' ^2 K6 G9 M# I# h
Gonadotropin-independent peripheral preco-0 ~$ C0 U1 ?) u* t- |) @: l+ O9 i
cious puberty in boys also results from inappropriate
4 i9 B7 r% p7 M' j9 {$ o* ?9 i7 T9 Vandrogenic stimulation from either endogenous or
4 y; n* |2 N  |2 w0 I' Wexogenous sources, nonpituitary gonadotropin stim-
( g$ X2 O2 ~" i/ Wulation, and rare activating mutations.3 Virilizing
9 F) t" t2 Y0 e8 ~congenital adrenal hyperplasia producing excessive+ B, M9 }% ]: U+ q4 i7 ~
adrenal androgens is a common cause of precocious
. Q4 j. b% n$ g0 z0 Rpuberty in boys.3,4
" |0 @1 z; |& n" N- H' w- W7 |The most common form of congenital adrenal
% f2 B0 O  B3 T. yhyperplasia is the 21-hydroxylase enzyme deficiency.; @) W$ U4 Q; Q
The 11-β hydroxylase deficiency may also result in. D& s9 y2 Y8 H8 ]
excessive adrenal androgen production, and rarely,
0 q+ T7 y1 f' kan adrenal tumor may also cause adrenal androgen
) g9 S6 _, P' ~" \8 }excess.1,3
; C) k+ E6 s2 V9 t, Y% b0 h" Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# C& [% w7 H! d1 ~542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# Q' I/ ?  A0 n* t4 U9 M: d
A unique entity of male-limited gonadotropin-
/ ]# V) X& x3 ^( W2 {; m9 D; sindependent precocious puberty, which is also known
6 s; }( y  K! b1 `, Xas testotoxicosis, may cause precocious puberty at a$ [/ ?( A# w  Y' S3 X  A
very young age. The physical findings in these boys
' J9 f4 B3 d; a. s/ J0 zwith this disorder are full pubertal development,: [' t8 s  l* ]! a
including bilateral testicular growth, similar to boys
" a" c8 J8 K$ q$ F% [with CPP. The gonadotropin levels in this disorder
& j" i( ~# L$ g( c8 n, i1 Care suppressed to prepubertal levels and do not show% E) @: }; B) Z& E  N
pubertal response of gonadotropin after gonadotropin-
: [/ Q" t9 ~& {$ a8 F; [# _1 Ureleasing hormone stimulation. This is a sex-linked
$ }2 `) W  K+ B; i1 o$ ?& Cautosomal dominant disorder that affects only5 |& |- n. J" T$ X
males; therefore, other male members of the family
6 M9 t( y# h  G& Smay have similar precocious puberty.3
, l% n9 |) ~) t7 V3 N% yIn our patient, physical examination was incon-' |, v6 K! \' P$ i
sistent with true precocious puberty since his testi-
& q# e+ m. z% v% V" Ecles were prepubertal in size. However, testotoxicosis) ]3 C' k: c7 z" \  o5 z
was in the differential diagnosis because his father. U* N4 _* {/ H# O7 F& J
started puberty somewhat early, and occasionally,
3 C" x0 ?; w) v0 Ctesticular enlargement is not that evident in the
/ @$ I/ {5 F4 G$ Ibeginning of this process.1 In the absence of a neg-
2 I, D' T( n. kative initial history of androgen exposure, our$ Z4 I# H3 P1 V" z  F
biggest concern was virilizing adrenal hyperplasia,
) h( \% O6 X0 j, _9 S' I- ?either 21-hydroxylase deficiency or 11-β hydroxylase
* m, A5 i0 Q$ ideficiency. Those diagnoses were excluded by find-' z" F; ~5 M, I: q/ z" Z
ing the normal level of adrenal steroids.
, l) g9 _9 z0 b1 P+ bThe diagnosis of exogenous androgens was strongly; N/ y9 A6 ]' {$ e2 M' Y5 M, i# M
suspected in a follow-up visit after 4 months because
# n3 k, d( O( s1 F. ^) Y9 P1 ethe physical examination revealed the complete disap-5 @; C, h  ^6 k  x
pearance of pubic hair, normal growth velocity, and
4 ]+ r1 u/ D/ zdecreased erections. The father admitted using a testos-
/ h% A" H6 t, gterone gel, which he concealed at first visit. He was
5 |$ C0 |2 ]8 k( s1 @' yusing it rather frequently, twice a day. The Physicians’
0 x. o6 G: C6 `7 A% @: n) |$ p$ sDesk Reference, or package insert of this product, gel or
  o( x' O/ M% b' F' E  fcream, cautions about dermal testosterone transfer to
/ \/ M- S- b- C. j  d/ c; funprotected females through direct skin exposure.5 X. B9 Z: Q) }/ V+ Q
Serum testosterone level was found to be 2 times the
5 v7 m9 @6 D$ A1 \3 C8 Ubaseline value in those females who were exposed to8 c. G+ U9 |3 W
even 15 minutes of direct skin contact with their male
/ a( A7 M  ?! ^) Z# e2 y. R+ L: Vpartners.6 However, when a shirt covered the applica-
' Z  v+ z  n  H& T: @8 H& d0 v9 s; \tion site, this testosterone transfer was prevented.& U4 F9 [9 h( k6 q4 [* Q3 _
Our patient’s testosterone level was 60 ng/mL,2 W5 W5 h* H1 t$ _* n. O
which was clearly high. Some studies suggest that
; v: \- X5 @) `dermal conversion of testosterone to dihydrotestos-
2 _0 s! j/ f! R. l& Z4 i7 oterone, which is a more potent metabolite, is more1 n% a+ z  ?& G; i% o
active in young children exposed to testosterone, d* h$ V6 ~2 Y, P& ?* g8 h% q
exogenously7; however, we did not measure a dihy-( F& @$ @( B9 c( ?
drotestosterone level in our patient. In addition to
: P: r, b0 H; C( U6 a  vvirilization, exposure to exogenous testosterone in
! M) q) S8 y8 C4 x3 o( ichildren results in an increase in growth velocity and) q2 A, o6 R5 }+ q
advanced bone age, as seen in our patient.
$ H: e, l) g$ p; f4 p7 [The long-term effect of androgen exposure during7 a0 Y( x+ ?) w* f, p
early childhood on pubertal development and final4 i0 [6 \) e& N! l
adult height are not fully known and always remain
- v5 i$ Z; ?% h( j3 A+ e, aa concern. Children treated with short-term testos-: V+ ~0 P; c% N7 M( {0 j5 K+ s
terone injection or topical androgen may exhibit some, P( Y7 `+ |* E' [: R: o( H# B
acceleration of the skeletal maturation; however, after
8 K; k# i( B, G% }) [cessation of treatment, the rate of bone maturation4 s3 s4 H7 c% y7 Q
decelerates and gradually returns to normal.8,9
7 ?  o8 C, ]& ^0 P6 a& L  h8 AThere are conflicting reports and controversy2 A4 G  V) j7 {% Z
over the effect of early androgen exposure on adult+ N3 B5 Z8 f. b9 B
penile length.10,11 Some reports suggest subnormal8 o. x! a2 |! H/ j& J( p/ `* a( a
adult penile length, apparently because of downreg-
' e+ B6 ~# p8 Dulation of androgen receptor number.10,12 However,
; i' U8 e0 w5 hSutherland et al13 did not find a correlation between
+ x) F  e; H/ C. a6 |& o4 ]childhood testosterone exposure and reduced adult' ?% W2 ^& a  p0 w, L4 ~
penile length in clinical studies.6 k3 f1 D8 ~7 h" |# K7 V
Nonetheless, we do not believe our patient is" c& c! Y1 a7 y
going to experience any of the untoward effects from4 c- {8 ?' M; `+ i" M1 \
testosterone exposure as mentioned earlier because* v9 W0 e$ R6 C
the exposure was not for a prolonged period of time.
( {. A( R5 [* D& x0 u6 X) w& o* xAlthough the bone age was advanced at the time of
) M1 K( b, {& S6 O* L- ydiagnosis, the child had a normal growth velocity at1 C: E, u/ Q" o' v1 T
the follow-up visit. It is hoped that his final adult" R4 H( U7 D1 @; f& h2 ~- f# m  M
height will not be affected.7 v1 ^: I  Z5 G# g8 A/ f* K0 p- J
Although rarely reported, the widespread avail-
8 ^3 _: C7 ]% B: z  S5 Yability of androgen products in our society may
4 t4 |4 R# W" H( @indeed cause more virilization in male or female+ x  t, z1 u: y8 j, v; p
children than one would realize. Exposure to andro-
/ [; w9 E$ x: c0 ?' D7 `gen products must be considered and specific ques-7 _3 r. F) i5 N1 W
tioning about the use of a testosterone product or2 i# r% `' x# [( P6 y  C
gel should be asked of the family members during
/ p( P! u+ \( o) b7 _the evaluation of any children who present with vir-
- ^9 q8 N  ~7 @+ c0 uilization or peripheral precocious puberty. The diag-
1 E1 z* g" a8 U' O8 mnosis can be established by just a few tests and by
. E8 f" w9 [+ a6 kappropriate history. The inability to obtain such a
, ]" S  o+ R# l' zhistory, or failure to ask the specific questions, may
$ q0 a, I5 m+ @5 D( S9 G8 H/ Vresult in extensive, unnecessary, and expensive
' n. O4 w1 e  t7 hinvestigation. The primary care physician should be8 j1 C$ @7 K& G0 T
aware of this fact, because most of these children4 {' U4 x; X! k; ^2 A/ Y0 p
may initially present in their practice. The Physicians’
/ K% v& N6 g0 MDesk Reference and package insert should also put a
/ Z. h( c& x( Q8 \& _, gwarning about the virilizing effect on a male or
- }, H+ x9 Q( s& P  [- Z) E" t& Nfemale child who might come in contact with some-  \7 T; g4 G1 l& A! i
one using any of these products." S" `" D% A" X) }: x
References
: T+ r& Q& l& Z/ t8 l/ y1. Styne DM. The testes: disorder of sexual differentiation
- A3 h9 @4 N% i: dand puberty in the male. In: Sperling MA, ed. Pediatric0 b- F$ X/ ]& E* L# k( i
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 D+ z) |' ^) }  H- U
2002: 565-628.8 U4 L7 x6 m* r: R4 M) @% q
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 [' \  k* S; P8 L4 k1 p7 V  h, Hpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old+ `; F1 B  Z/ F1 @+ C+ J7 o/ K2 `' H
Boy Induced by Indirect Topical
. `$ O# Z8 n: G1 d" l  zExposure to Testosterone  \4 F7 s) R; i8 N1 p+ L
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! K7 `4 ]  v% ]2 `0 a  X9 ]# H
and Kenneth R. Rettig, MD1
; z* N( i; l2 \" a1 x$ xClinical Pediatrics# y) c$ t: H9 H$ N& v
Volume 46 Number 6+ d; Q+ p: q2 [% k- Y
July 2007 540-543
2 U) y( i3 Z! g2 b) t: R© 2007 Sage Publications+ k& q9 t0 C* q8 W3 h
10.1177/0009922806296651
# L0 ~) u  {7 f+ I& |$ ~http://clp.sagepub.com
+ }$ A3 }# l' L6 j9 @hosted at
! r  k" ^: B" P( x, rhttp://online.sagepub.com: _& x( E! Q$ d! W% V! b  |; V2 b
Precocious puberty in boys, central or peripheral,5 r8 C2 ]  o* G' W% q  Z( E; [
is a significant concern for physicians. Central3 X* B5 _: |7 E
precocious puberty (CPP), which is mediated% c: p+ }% V/ b7 R
through the hypothalamic pituitary gonadal axis, has
. m! P  L! s1 ta higher incidence of organic central nervous system, V, W. V2 w2 }: V/ q0 u
lesions in boys.1,2 Virilization in boys, as manifested8 H0 r7 g) S' s2 }+ T* ?/ J$ S
by enlargement of the penis, development of pubic
; v! S% u, U& P" ^9 D0 _# Chair, and facial acne without enlargement of testi-' m4 s1 v( Q5 `4 p$ j' p7 {1 s& Y
cles, suggests peripheral or pseudopuberty.1-3 We1 z+ K2 ?! c! v. ?8 X
report a 16-month-old boy who presented with the
& A& Z: ^3 a) j& v" G3 [# Wenlargement of the phallus and pubic hair develop-5 L" N4 z- w0 U: m5 B! Y
ment without testicular enlargement, which was due' C: O. G) G* [7 I
to the unintentional exposure to androgen gel used by0 j$ R' b7 G1 `. d: n/ w
the father. The family initially concealed this infor-
2 @( |$ K* X8 V! ]mation, resulting in an extensive work-up for this
, H( _6 j- i5 y1 P1 ^; hchild. Given the widespread and easy availability of/ Z$ A# X5 C1 ]- H( z9 z
testosterone gel and cream, we believe this is proba-" a  G& ~8 T% o( ~2 m5 O7 |
bly more common than the rare case report in the
; V1 f' `& L5 s' ~8 z+ d4 Pliterature.4
, {& C3 O$ p. }. J2 k, N2 T) s7 ]Patient Report
  E+ X( g! l# z! g& f/ B/ e* ?. O2 `A 16-month-old white child was referred to the, T3 w3 S9 \6 w1 g8 y% [* E4 m
endocrine clinic by his pediatrician with the concern, X4 I2 ]; q1 ^0 U0 a  ^
of early sexual development. His mother noticed8 o3 e- ?( }  u' I  _  q2 `3 l( P
light colored pubic hair development when he was" w" [+ B( A1 V1 o' M! Y4 c" c
From the 1Division of Pediatric Endocrinology, 2University of0 |" |! f) ?7 g9 v
South Alabama Medical Center, Mobile, Alabama.
3 o& X! Y+ U/ L+ mAddress correspondence to: Samar K. Bhowmick, MD, FACE,
+ u  Y3 X" m+ Y7 z4 [+ n. y0 TProfessor of Pediatrics, University of South Alabama, College of7 @6 \% I; D% O+ q8 {
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: s+ h! O3 t: Ae-mail: [email protected].5 I9 y) O; L! b# j$ A+ L
about 6 to 7 months old, which progressively became
* |" N" u6 _. u7 C% l8 A, U- Wdarker. She was also concerned about the enlarge-$ }" i7 s& A$ J9 c! q
ment of his penis and frequent erections. The child
# P4 C+ Y, {% d2 R" K3 H' Swas the product of a full-term normal delivery, with
3 \( f" @) O3 o) K3 Oa birth weight of 7 lb 14 oz, and birth length of8 Q' d1 ?" p  m2 Z1 |7 @
20 inches. He was breast-fed throughout the first year
" A- N1 P2 @- c- b0 hof life and was still receiving breast milk along with
* F) z4 U9 ^4 }! @1 d$ U( bsolid food. He had no hospitalizations or surgery,* r. q/ X& @9 \' L( k+ |
and his psychosocial and psychomotor development
9 _: J7 t+ Q/ g  |* Hwas age appropriate.* u, Y5 H  |2 @; v; X
The family history was remarkable for the father,  `- G+ Z: p" z6 M2 Y4 K
who was diagnosed with hypothyroidism at age 16,
$ K  \0 x7 h' `& ^which was treated with thyroxine. The father’s
6 S3 N+ P5 W0 A' bheight was 6 feet, and he went through a somewhat
& b4 v; a! {; V' cearly puberty and had stopped growing by age 14.. _3 C' l$ g: [' n, ~) \% h2 q
The father denied taking any other medication. The* T) q. x6 X/ x0 C8 @: g
child’s mother was in good health. Her menarche
4 k5 ?2 l* H6 R  n, n# |. fwas at 11 years of age, and her height was at 5 feet, h- S0 [8 V$ _
5 inches. There was no other family history of pre-
& Q) l& ~. k, \0 D0 ~cocious sexual development in the first-degree rela-
8 Q8 u# D: \8 F$ e( X: Ytives. There were no siblings.
9 N: u& C$ b  ~# mPhysical Examination
# T& w& }* R  ~4 g4 \The physical examination revealed a very active,( T: J7 {) z. E
playful, and healthy boy. The vital signs documented
- O% M4 t6 t. z& t2 u; va blood pressure of 85/50 mm Hg, his length was$ i: V, q0 H) y. n0 l# h5 T" n
90 cm (>97th percentile), and his weight was 14.4 kg' I& r. o- J. L/ `2 z; E' [3 e0 @
(also >97th percentile). The observed yearly growth- p4 X8 b2 `7 N! Q' o
velocity was 30 cm (12 inches). The examination of/ I8 Q: N% d' _
the neck revealed no thyroid enlargement.
1 P1 h; Y2 Z: K/ m+ WThe genitourinary examination was remarkable for
( n5 C9 `0 K2 E! s; _$ Q1 X$ oenlargement of the penis, with a stretched length of8 ]- b2 J! i) i: d9 s6 C! H: s
8 cm and a width of 2 cm. The glans penis was very well5 R" c( m- n& F+ u4 `
developed. The pubic hair was Tanner II, mostly around
8 n, z, f9 M# {" X5407 Z( T* \+ I# J) I/ y. I
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' {$ ~6 ]% g3 q2 j; ^
the base of the phallus and was dark and curled. The. _3 M! W. R0 h; U. K* J& L) U( m& ~
testicular volume was prepubertal at 2 mL each.
: Q2 K" o: B4 g8 f$ c/ r/ c7 d% rThe skin was moist and smooth and somewhat) O6 T/ I3 n# P. H' M; m
oily. No axillary hair was noted. There were no3 ]! Z4 z3 T1 V- Y1 x! V; B
abnormal skin pigmentations or café-au-lait spots.: F" Z# O9 d7 D8 O& t6 p! b- S
Neurologic evaluation showed deep tendon reflex 2+& X1 ~( c- k# a# V7 h
bilateral and symmetrical. There was no suggestion/ N/ S/ W- Q" q/ W& _# j
of papilledema.
/ F  S. R6 g5 F3 Q5 oLaboratory Evaluation
0 D- `4 \/ M% H( N2 ~The bone age was consistent with 28 months by3 T" m6 d' d% k$ X& g* r
using the standard of Greulich and Pyle at a chrono-
) l' }- [: Z3 Vlogic age of 16 months (advanced).5 Chromosomal
( p3 J4 p+ Q) p2 ~karyotype was 46XY. The thyroid function test
: s7 `0 e& l# }6 ?6 r+ n& L3 ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-
) T2 D! I( `3 H, f  E3 H  Ulating hormone level was 1.3 µIU/mL (both normal).' o9 M8 N% s  k9 I# f  a
The concentrations of serum electrolytes, blood
  ~3 r4 U) p* vurea nitrogen, creatinine, and calcium all were
5 i$ O" M2 i: w" rwithin normal range for his age. The concentration4 F2 w/ G4 ?& q
of serum 17-hydroxyprogesterone was 16 ng/dL
$ E* R# B& B. j- Q, d" n! \(normal, 3 to 90 ng/dL), androstenedione was 20
: u$ J; i; E( g& Q4 o9 wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 s- w" ?) H+ S8 bterone was 38 ng/dL (normal, 50 to 760 ng/dL),
; P! P# d* N* G9 sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to5 |+ z% w1 _$ O2 Y! ?$ h
49ng/dL), 11-desoxycortisol (specific compound S)7 V' O# O$ j- v: b1 Q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
$ a5 j3 r: s, N: K# r! z8 ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 c( w* s& M- V  U- `: p1 {
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
( a1 U: L6 T$ {' e: ~* d; P5 d4 O8 t0 Vand β-human chorionic gonadotropin was less than
' p2 A* \; t* J2 z, o4 v* A5 mIU/mL (normal <5 mIU/mL). Serum follicular( X+ F2 F5 O4 Y, ]4 \
stimulating hormone and leuteinizing hormone
& d* [) J7 U7 \  n( g- G! ?6 y! zconcentrations were less than 0.05 mIU/mL
% ^$ J( w" E% o" N4 X) [' p(prepubertal).
( _# l; @2 r$ v' PThe parents were notified about the laboratory' I! n$ R6 P4 {, D" }6 E
results and were informed that all of the tests were
  \5 l+ Y* y3 k1 F( J$ znormal except the testosterone level was high. The
- Y2 l, o) C8 u- A. _, bfollow-up visit was arranged within a few weeks to
* l8 ?1 @( R9 q6 v3 N  a( t7 Aobtain testicular and abdominal sonograms; how-  _9 U9 p2 `3 z$ z8 l  q
ever, the family did not return for 4 months.6 ]% s$ y. e7 W% P
Physical examination at this time revealed that the+ W+ L6 K) s% S" P" j6 t& Z8 J
child had grown 2.5 cm in 4 months and had gained
; l& A& G. S0 w/ |. k" f2 kg of weight. Physical examination remained) f  H, r/ t7 w. F7 U* q/ z! e
unchanged. Surprisingly, the pubic hair almost com-+ H6 f  v6 l7 C8 O
pletely disappeared except for a few vellous hairs at# y/ P5 a+ {" B4 f7 ^" _
the base of the phallus. Testicular volume was still 24 w, I" k- ~0 ~6 x. F. n. ~- _: n
mL, and the size of the penis remained unchanged.7 a3 I" t9 A4 F5 v7 j+ F
The mother also said that the boy was no longer hav-0 D, I; F" }% S0 }& M) P" Q' I5 ~, V
ing frequent erections.
$ |; i) w+ j4 V! _Both parents were again questioned about use of
/ s9 x1 P2 s- ?" a) z' x# @any ointment/creams that they may have applied to  V; J/ a1 n) t- l* T$ I' y# r" r
the child’s skin. This time the father admitted the. C6 k. H- ]; e5 `: D
Topical Testosterone Exposure / Bhowmick et al 541
! H: T" o. Q5 v' u6 F/ U+ m3 f, v0 |use of testosterone gel twice daily that he was apply-
4 r9 F4 ^  {8 c, r: eing over his own shoulders, chest, and back area for
9 G. O. v  a4 i: s, ta year. The father also revealed he was embarrassed
0 S5 r- }' S; u" ?) q. ~to disclose that he was using a testosterone gel pre-
" w8 W& e( q9 p) s4 Y; oscribed by his family physician for decreased libido
* J* y' K$ Z% s7 C: d; |3 _) Usecondary to depression.
8 y; a* O& j& q2 M" m' A+ x/ oThe child slept in the same bed with parents.% E; F- z! O1 V4 h. ~) e( }/ ^
The father would hug the baby and hold him on his3 f* }( f  |$ {1 s0 j
chest for a considerable period of time, causing sig-
  z6 e- E; q' U) N8 B4 @nificant bare skin contact between baby and father.2 X' c) }9 l% W& n
The father also admitted that after the phone call,8 s" t" ~1 K6 J* M) x; m$ f, Q4 R+ ]
when he learned the testosterone level in the baby
% n9 t# q( j6 w7 E, O$ @was high, he then read the product information
* v. C' f- W% w: n" `packet and concluded that it was most likely the rea-2 ?5 a: c) x9 b# C# h+ l! v
son for the child’s virilization. At that time, they
( Y( @- m; I0 R. d7 edecided to put the baby in a separate bed, and the
  W" F* T1 K( H  v% afather was not hugging him with bare skin and had
; R1 T) k' `8 ~9 ~6 G& [8 Pbeen using protective clothing. A repeat testosterone
) i1 f" p: E+ G0 S. @test was ordered, but the family did not go to the
* |$ {2 h9 p' Vlaboratory to obtain the test.
4 l8 D4 }* h6 [9 HDiscussion
4 _  C, k4 c7 \6 b! K, _1 M2 wPrecocious puberty in boys is defined as secondary8 s- \  F: f2 r, ]- V  q' e) E
sexual development before 9 years of age.1,46 G6 Q4 Z! `* k8 `& X* t; \0 T
Precocious puberty is termed as central (true) when1 ~1 L9 k6 X: l
it is caused by the premature activation of hypo-
3 J8 w' a6 j$ v9 p6 W6 N% pthalamic pituitary gonadal axis. CPP is more com-
0 d9 {7 s! l/ e7 n# D5 \+ jmon in girls than in boys.1,3 Most boys with CPP1 b; |# O; l& N; M( d  M. i! p) I
may have a central nervous system lesion that is
7 ^  g3 d$ X  kresponsible for the early activation of the hypothal-
4 w: D/ z( B) p  bamic pituitary gonadal axis.1-3 Thus, greater empha-7 m- C  x7 J0 i
sis has been given to neuroradiologic imaging in2 ]# F/ t' H6 w  k" `" g
boys with precocious puberty. In addition to viril-
: Z! M/ s- \# H! e- f% T4 jization, the clinical hallmark of CPP is the symmet-
' c% w0 A4 ^3 f0 H3 Krical testicular growth secondary to stimulation by4 C+ k4 K) v( p0 }% H$ f
gonadotropins.1,35 t6 D9 m# L3 h
Gonadotropin-independent peripheral preco-0 G7 {1 F7 }# C/ b8 e: g, \# u
cious puberty in boys also results from inappropriate
% F1 f1 x" `7 X0 candrogenic stimulation from either endogenous or
$ f8 F3 p: N& ^4 {# q( ]exogenous sources, nonpituitary gonadotropin stim-
$ j6 N5 \2 T' p0 A% M% Hulation, and rare activating mutations.3 Virilizing
3 a# T$ r; ~  c: n% Z& U: Ucongenital adrenal hyperplasia producing excessive2 P2 {6 U. J4 _' ?
adrenal androgens is a common cause of precocious5 _6 O* z0 `+ |+ k6 G, U% Z
puberty in boys.3,4, f3 _1 H( f1 B3 h
The most common form of congenital adrenal5 R$ V; @/ R' V$ c5 `5 [
hyperplasia is the 21-hydroxylase enzyme deficiency.
# n! I" J- ^* d3 y7 F. u2 ?The 11-β hydroxylase deficiency may also result in
. y" W6 l) ?% texcessive adrenal androgen production, and rarely,4 h4 d+ Z/ A" {+ W+ |4 l
an adrenal tumor may also cause adrenal androgen+ B9 T% X8 v' `- s7 Y  g! L
excess.1,3
, a; U7 G! Z' R% U, A+ c( e, h$ U$ Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 v" p% y( b- s$ l4 `4 r7 W542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: ~% W# h* J6 J5 g& J1 B5 ]/ h/ xA unique entity of male-limited gonadotropin-2 {6 b/ b% i- g% [
independent precocious puberty, which is also known
4 T! u4 w. |6 c2 U! v+ n0 sas testotoxicosis, may cause precocious puberty at a
0 W5 t+ d2 P8 {3 _5 wvery young age. The physical findings in these boys
, }# l/ r. J% a5 k, s$ u  P, f- Dwith this disorder are full pubertal development,; I$ p: t9 e) _1 M
including bilateral testicular growth, similar to boys% Q* ^) S$ ]0 G' a
with CPP. The gonadotropin levels in this disorder; ~. s, Q9 a$ m0 O# Z4 J2 @
are suppressed to prepubertal levels and do not show
$ B" S- g, U& P+ Q! ipubertal response of gonadotropin after gonadotropin-4 {$ ]1 w  v+ {6 J+ U4 m% ~
releasing hormone stimulation. This is a sex-linked
; D# H; `  s+ t+ dautosomal dominant disorder that affects only
; `) u! ^- r9 cmales; therefore, other male members of the family
/ @5 x, o' A- }5 }5 {3 V- Zmay have similar precocious puberty.3) r, a3 P  m  ]3 m/ n
In our patient, physical examination was incon-
9 X2 h, g* r+ C! Qsistent with true precocious puberty since his testi-/ @: ]6 }( t, X# v
cles were prepubertal in size. However, testotoxicosis
; C( N; t9 L* E2 |' B" L) D$ G$ mwas in the differential diagnosis because his father
. |: j8 j; H3 ~started puberty somewhat early, and occasionally,5 H. ]6 o/ C9 `' e, L$ n4 l
testicular enlargement is not that evident in the
# K7 Q6 T6 P' n2 K* R/ d+ B8 zbeginning of this process.1 In the absence of a neg-
/ Y" Z& C; {+ c& g8 Z: E1 C0 P4 }4 zative initial history of androgen exposure, our
4 @# H" S0 o& r# j5 [' bbiggest concern was virilizing adrenal hyperplasia,
: \4 ^/ p3 g# g& ?6 {% s  y2 ^, eeither 21-hydroxylase deficiency or 11-β hydroxylase9 l4 y6 \0 C# V! Z0 T
deficiency. Those diagnoses were excluded by find-
8 \: H% x8 |# R* Y- D' Oing the normal level of adrenal steroids.
/ o3 t* c& L9 o& F! t3 a) P# FThe diagnosis of exogenous androgens was strongly
4 e1 v& V- ~+ m% X% r, isuspected in a follow-up visit after 4 months because7 c( Z2 ]: s- V2 i
the physical examination revealed the complete disap-% z: P% u$ D. G3 K0 }( M" i# ?
pearance of pubic hair, normal growth velocity, and4 a! b# U1 e0 j" ~/ S% n6 \/ y
decreased erections. The father admitted using a testos-
. E6 g: ?; K( R0 x+ c& Q1 f! [) Xterone gel, which he concealed at first visit. He was
) I: V, g% R' ~! w* Kusing it rather frequently, twice a day. The Physicians’
" |$ @" i/ h: p4 e6 PDesk Reference, or package insert of this product, gel or; a+ y- g$ F5 `* g: U- @
cream, cautions about dermal testosterone transfer to4 f. K# P$ D6 M1 N7 V" s, H
unprotected females through direct skin exposure.. D3 S% H% v% T" s( E& i1 h# v0 x
Serum testosterone level was found to be 2 times the
  K- x8 Z4 |: A% [( z) jbaseline value in those females who were exposed to
) {0 C* ?$ t7 |+ W6 h9 ?even 15 minutes of direct skin contact with their male
6 H$ q$ [, g; Npartners.6 However, when a shirt covered the applica-! \! W( z/ u- a* p3 J9 M* E! i/ ~
tion site, this testosterone transfer was prevented.; u* t" ]# S( ], Z% x% K7 O5 B
Our patient’s testosterone level was 60 ng/mL,
% i( r- N  C& }1 W6 x! Lwhich was clearly high. Some studies suggest that
5 s' Q- F+ p0 l* b9 s7 Tdermal conversion of testosterone to dihydrotestos-2 s, W* b9 c, h: y0 Y  h  J# ~# R
terone, which is a more potent metabolite, is more
- {2 N4 Q3 ]6 x9 b: R% u: a6 y- aactive in young children exposed to testosterone
' A0 w6 a/ ~$ Z# v* aexogenously7; however, we did not measure a dihy-9 n. O* S% g: X3 z7 Z$ M% I( l4 X
drotestosterone level in our patient. In addition to
: D$ {: E8 _  G+ A! N9 nvirilization, exposure to exogenous testosterone in
4 l- A0 G% ]0 H# s% D! u5 V( i. Gchildren results in an increase in growth velocity and
  \) \# Z% X3 `& X- t8 O. ], \advanced bone age, as seen in our patient.$ @1 c, h- E6 K! {* j6 p2 J# L1 n
The long-term effect of androgen exposure during2 y& g, d  o% s8 ?$ q
early childhood on pubertal development and final
* Z2 A, g. ?* vadult height are not fully known and always remain6 M; v  p% J9 [0 D6 z4 T. N$ }
a concern. Children treated with short-term testos-! J( e, Y( w6 \( p( \
terone injection or topical androgen may exhibit some2 s; K# l  |0 f4 I+ t4 G
acceleration of the skeletal maturation; however, after
5 a! r# O! P1 C+ p: ]) xcessation of treatment, the rate of bone maturation
( V( F7 N& U; U; ~3 K; i# Xdecelerates and gradually returns to normal.8,9
& I# `+ Y0 j7 b6 w+ y0 wThere are conflicting reports and controversy4 V0 N0 H8 K0 s7 a
over the effect of early androgen exposure on adult
+ F3 G' o1 N' j8 B& Ipenile length.10,11 Some reports suggest subnormal
( V  I! J( n8 [) M: yadult penile length, apparently because of downreg-
5 \% o! J* a( T: t( L6 Tulation of androgen receptor number.10,12 However,6 S& g( }. g1 w: |" H
Sutherland et al13 did not find a correlation between
- z# h( m" E; jchildhood testosterone exposure and reduced adult
2 V0 A# t# H/ L0 ]/ ppenile length in clinical studies.
2 q; B* u+ V+ w1 ENonetheless, we do not believe our patient is
+ l- ~3 j0 c. Y" agoing to experience any of the untoward effects from
- V6 \# {5 t0 o% Btestosterone exposure as mentioned earlier because  j  k% U9 u$ x4 {/ W; p) M
the exposure was not for a prolonged period of time.
9 g& u: ~, h, x' IAlthough the bone age was advanced at the time of- g# q" H3 f; s* c" V" h: T. U( {/ d
diagnosis, the child had a normal growth velocity at8 G$ a# V9 n; @0 y5 ^
the follow-up visit. It is hoped that his final adult1 y( @# y4 L+ ~% u
height will not be affected.
% u5 p' e, `. K. I# T& g3 f6 lAlthough rarely reported, the widespread avail-
/ }" s' m% H) r1 P8 p4 Gability of androgen products in our society may  c# q/ e' J% C1 g* H7 a, r
indeed cause more virilization in male or female
( j/ U& o( Y! q: Gchildren than one would realize. Exposure to andro-
, I' w+ p4 H/ vgen products must be considered and specific ques-
* a" e8 w/ O+ ?- b0 F" k* Ntioning about the use of a testosterone product or% L8 Y3 ^$ f/ f5 [$ I# P
gel should be asked of the family members during
( T! N) E9 m1 ?8 d' I$ q& h4 ~: othe evaluation of any children who present with vir-
3 |: C' F2 T/ f0 Pilization or peripheral precocious puberty. The diag-
- I- G! f, N& z$ Z8 H; bnosis can be established by just a few tests and by
) d& R6 k" o" M9 y2 Zappropriate history. The inability to obtain such a
1 C; M) v& v: w9 C' Chistory, or failure to ask the specific questions, may  P4 n6 M6 x% F0 E
result in extensive, unnecessary, and expensive
  `- ]# P$ f0 h$ @( T" Dinvestigation. The primary care physician should be. O# }6 M) x1 m1 {4 |8 J" H
aware of this fact, because most of these children
- U4 H" z5 d; V6 fmay initially present in their practice. The Physicians’8 b! ?7 M( S1 i& M3 F" U$ p* T# [
Desk Reference and package insert should also put a( k0 c6 v$ m7 B; y7 ~1 ]8 O% P' Y1 i
warning about the virilizing effect on a male or6 a0 k7 L; {; \$ ]/ g; e$ n/ B
female child who might come in contact with some-+ {; N) V: E. D: B) D4 {( S2 G: y
one using any of these products.2 r- H# ^8 ]# S8 Z
References
' Y# n& Q# T  \! u. U( r  k0 ?1. Styne DM. The testes: disorder of sexual differentiation
' l( S% M' l' U0 T1 v" F  h8 \and puberty in the male. In: Sperling MA, ed. Pediatric
( b2 u% D- m3 w; n- ^Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 z7 q0 D( w$ Z4 U- A2002: 565-628., `. n8 Q+ _2 s1 `. o% `. m: g
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious6 z, t+ v2 {/ `6 j* Y9 H) Z1 x
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

3 h! L# }, P% q4 ]1 G, e2 o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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