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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-Old2 h9 B4 w  b1 {. y9 g( J0 P
Boy Induced by Indirect Topical- c: J+ e) T. |
Exposure to Testosterone
- L+ P5 s( J& b) c: M, gSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2" c8 v* _+ w8 \2 ?( I
and Kenneth R. Rettig, MD1
  X6 P) x1 o. G- l1 ]Clinical Pediatrics
: X/ C) \; W! V4 `Volume 46 Number 6
- ?! i* ^2 e1 n' s- DJuly 2007 540-543! M- g( O% ]* g: Q
© 2007 Sage Publications
0 [5 w& M! ~8 e7 t! U$ Y! Q10.1177/0009922806296651! p/ Z5 t$ k. p5 v. f
http://clp.sagepub.com
, J7 s' w6 e3 W# vhosted at
& }# l' k; i( ?5 ]http://online.sagepub.com
+ f; c6 u7 D5 y* G* a' VPrecocious puberty in boys, central or peripheral,9 L- |. [# _$ k
is a significant concern for physicians. Central) j  C# [' r, d4 |- ^7 x/ ?; \
precocious puberty (CPP), which is mediated
# V& k9 ~) c/ r2 P8 Z' `& ?through the hypothalamic pituitary gonadal axis, has: I% P2 \) M, P9 m: b% A  a9 e
a higher incidence of organic central nervous system$ @$ k: f" R4 K
lesions in boys.1,2 Virilization in boys, as manifested$ G' o: H2 [1 ?7 M8 D  W
by enlargement of the penis, development of pubic% s- T, l" f% e# k" l5 K: \
hair, and facial acne without enlargement of testi-7 b# o' c2 j! p- [/ Z% _
cles, suggests peripheral or pseudopuberty.1-3 We
% U( e" D$ D1 ]  L+ v8 j9 Jreport a 16-month-old boy who presented with the  q; G% X  i/ Y5 s. g( D+ _7 J
enlargement of the phallus and pubic hair develop-
5 ~( X7 ^: A! B/ [5 q8 X4 xment without testicular enlargement, which was due) V  ]2 g5 B$ F" d, z1 W
to the unintentional exposure to androgen gel used by
0 |6 \4 D# C/ S. n) Qthe father. The family initially concealed this infor-- j: ^/ M) {5 l1 y
mation, resulting in an extensive work-up for this
4 F5 \0 y$ G* Qchild. Given the widespread and easy availability of
! C% ^; ?: E5 T+ vtestosterone gel and cream, we believe this is proba-5 v3 \& f: X0 Z% h- r
bly more common than the rare case report in the' ?$ q7 z* H  {3 x
literature.4
( I# X3 U* r# V8 UPatient Report% @. Q" v) z( a) ^. B. U
A 16-month-old white child was referred to the. X6 _8 g+ q2 M( V
endocrine clinic by his pediatrician with the concern
" g. L& i! x- k4 d0 }9 Mof early sexual development. His mother noticed
5 R0 ~: o1 R: [" }/ N% z4 W, T* rlight colored pubic hair development when he was
0 J: s* o* c0 y$ PFrom the 1Division of Pediatric Endocrinology, 2University of
$ Z$ d, I# z  Z' w3 k' M$ s' bSouth Alabama Medical Center, Mobile, Alabama.
& g$ y9 g& s4 E/ ZAddress correspondence to: Samar K. Bhowmick, MD, FACE,. c- `, Y  G3 _: y: I
Professor of Pediatrics, University of South Alabama, College of' Y$ m! ^5 @# q8 y( g5 Z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 K1 \2 X" [9 |$ Q
e-mail: [email protected].$ W: F& K6 c) Z2 t
about 6 to 7 months old, which progressively became
8 T$ n% W! E  T1 mdarker. She was also concerned about the enlarge-
# K+ l! @5 |. l) k) u' cment of his penis and frequent erections. The child6 i) t* E( F- J& E
was the product of a full-term normal delivery, with% |* Y" F$ [2 k) V; G
a birth weight of 7 lb 14 oz, and birth length of
& g2 k7 _0 e2 k! B4 ~& j3 m( B20 inches. He was breast-fed throughout the first year
. N6 i6 b3 i0 T/ Bof life and was still receiving breast milk along with( E( l8 z+ z' B1 k
solid food. He had no hospitalizations or surgery,
& |6 {0 x- k& m" mand his psychosocial and psychomotor development: Q6 f8 u; X: H4 x' {# s5 Q
was age appropriate.
1 Q; `6 w$ O' y- W0 J# @+ UThe family history was remarkable for the father,; s* m. S9 E; L; b* G9 i5 `! T8 r* s$ B
who was diagnosed with hypothyroidism at age 16,
2 w, ]6 t8 {4 J# hwhich was treated with thyroxine. The father’s5 s% X" W$ R4 Z  S; I1 r
height was 6 feet, and he went through a somewhat
5 T! m6 U: n  I0 Dearly puberty and had stopped growing by age 14.
; b4 P/ |9 o9 c6 S- [The father denied taking any other medication. The
( |% f! p% N) ^2 p8 b2 J& S% hchild’s mother was in good health. Her menarche' @. j' q! v* h6 M, X5 P, k/ x9 Y8 h
was at 11 years of age, and her height was at 5 feet
6 U  }, v: y  `* T& k$ o5 inches. There was no other family history of pre-
" X6 s' f1 Y- h+ L" @' fcocious sexual development in the first-degree rela-6 W+ k# N: @; k% c: B
tives. There were no siblings.5 o0 w' r% J9 p: }0 p: T: V
Physical Examination  g3 r6 M# b: l# w, F
The physical examination revealed a very active,
3 O* B8 f2 a$ V; G' Q5 P, xplayful, and healthy boy. The vital signs documented" k5 z( @7 i2 X! j7 h6 ^7 L
a blood pressure of 85/50 mm Hg, his length was& t: C3 l9 T+ E6 D. k; _
90 cm (>97th percentile), and his weight was 14.4 kg
5 C% E% T* {" {* Z* ~1 m(also >97th percentile). The observed yearly growth
* j' ^# h/ K  p2 K) h. K( bvelocity was 30 cm (12 inches). The examination of
/ I4 T. u6 Q+ y9 I% fthe neck revealed no thyroid enlargement.8 J" }  {6 S5 ~* {' w3 l- x
The genitourinary examination was remarkable for* I- z$ t3 E6 J/ C
enlargement of the penis, with a stretched length of: m" {0 X+ t9 g. a) c
8 cm and a width of 2 cm. The glans penis was very well0 J2 q' k; G" M" c' [, o' p& t+ U
developed. The pubic hair was Tanner II, mostly around0 Z# H( U, c7 R% H
540
7 t/ S# T* ^7 }0 bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# P8 A6 ]2 ~* T0 x  m8 Q1 s
the base of the phallus and was dark and curled. The
! V7 R% M4 O4 b0 J0 C  y7 ctesticular volume was prepubertal at 2 mL each.% _. l" i/ `2 @. t+ P
The skin was moist and smooth and somewhat
; t, Z3 b6 ?0 aoily. No axillary hair was noted. There were no
. V$ X* ?: |" c. M7 K9 Eabnormal skin pigmentations or café-au-lait spots.6 ?% _; O- Z: c% e
Neurologic evaluation showed deep tendon reflex 2+) F! g  |1 z3 X" Z' W/ i
bilateral and symmetrical. There was no suggestion
& p3 F! x- r. v) y$ N$ T: p. aof papilledema.
" a! W( X* X" z, D  r: M, HLaboratory Evaluation
" R, L+ Z; Y, u4 F7 b1 i" wThe bone age was consistent with 28 months by/ @9 C. J4 @3 y
using the standard of Greulich and Pyle at a chrono-9 [1 F! ]' q5 W% s; T# e4 Q- b  L
logic age of 16 months (advanced).5 Chromosomal$ f& H) L; X" Y9 p4 W
karyotype was 46XY. The thyroid function test! H* F& d* b$ M8 O
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
. \6 p4 m3 z% t5 Ilating hormone level was 1.3 µIU/mL (both normal).
+ h7 a4 Z, \) f2 X0 vThe concentrations of serum electrolytes, blood' @( N/ {: T8 H& r# ^
urea nitrogen, creatinine, and calcium all were
. s' }+ b; a# h: `1 M! jwithin normal range for his age. The concentration% i- }: \6 h8 J, c" l
of serum 17-hydroxyprogesterone was 16 ng/dL
( h7 p/ X2 O# H! _3 [  Y" ](normal, 3 to 90 ng/dL), androstenedione was 20! Y% ~4 R5 x; S! i% L* K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- V" `) u& J9 |6 x. G
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* P3 Q2 j( V' Q+ p4 J, R* A, q  \
desoxycorticosterone was 4.3 ng/dL (normal, 7 to. ]9 c8 h; f7 z8 r. C. n1 y
49ng/dL), 11-desoxycortisol (specific compound S)
4 p5 C' O( Z- ]& }+ Z" [7 swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' c1 Y- c8 U. j/ wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- ~; H3 w- S  ^: N( B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ g* X0 y+ ^+ a
and β-human chorionic gonadotropin was less than
' i: j# @/ i1 q' Q8 V2 v5 mIU/mL (normal <5 mIU/mL). Serum follicular
! I0 l0 o, N2 k* Hstimulating hormone and leuteinizing hormone
. n: ^8 a9 N  E- a' O. J  N8 Dconcentrations were less than 0.05 mIU/mL. Y) Y+ b$ W8 \" S' Q) P" G
(prepubertal).! O/ K! r( b5 y0 C( h
The parents were notified about the laboratory% G$ V" ?& q9 P
results and were informed that all of the tests were) d! B( T. j1 X6 B# e: o
normal except the testosterone level was high. The0 I+ K" h& _  Y9 J3 E
follow-up visit was arranged within a few weeks to
& e8 @0 M& F" V% @. q4 ^- robtain testicular and abdominal sonograms; how-
! [; l% y) d" ]* Mever, the family did not return for 4 months.
7 w( V% R2 S5 r9 T' Q/ |Physical examination at this time revealed that the+ B! ^. B" ]6 O! m
child had grown 2.5 cm in 4 months and had gained- ]" M5 b5 ~6 u" k& Q$ H0 h
2 kg of weight. Physical examination remained/ a. g  @% e) M1 e
unchanged. Surprisingly, the pubic hair almost com-
  m, U% R- R& ?3 Bpletely disappeared except for a few vellous hairs at1 V3 l/ \! o# x$ s! a, D0 L7 z
the base of the phallus. Testicular volume was still 2& F0 u( N8 m8 J
mL, and the size of the penis remained unchanged.
0 C  K5 ?, l# FThe mother also said that the boy was no longer hav-
5 Q* E% z2 ^* L5 b5 m/ j1 f% x. Ying frequent erections.
% m; Z+ x) B9 T& @5 GBoth parents were again questioned about use of
# t& i+ q4 g- Z, f) E- Sany ointment/creams that they may have applied to
3 F! F$ {1 e7 H7 @the child’s skin. This time the father admitted the. U3 ^( g5 W+ h; J' n
Topical Testosterone Exposure / Bhowmick et al 541: h. J9 U/ v- Q3 q' N
use of testosterone gel twice daily that he was apply-& R3 E# H) X: M: K' U6 C
ing over his own shoulders, chest, and back area for
7 Q3 |* [1 e. F1 X* ^/ K/ ?! H& k  Ca year. The father also revealed he was embarrassed+ I3 x* L+ g* B: R! O
to disclose that he was using a testosterone gel pre-2 W3 f- @* s( m$ a, \- Z
scribed by his family physician for decreased libido
- j9 X/ |7 H) Q7 U$ qsecondary to depression.& U  d# v6 P8 s+ t5 s4 n
The child slept in the same bed with parents.
+ f. Z2 r# z* X- N6 lThe father would hug the baby and hold him on his# m. l# \: z6 T& r* a% }2 m3 {
chest for a considerable period of time, causing sig-4 M% @2 o7 u2 J, B& P+ c! k) ~
nificant bare skin contact between baby and father.1 `& O4 D( j: C6 Y, P
The father also admitted that after the phone call,
. K7 I1 C) w; n( ~when he learned the testosterone level in the baby
5 r5 C. @) X) i; y) T/ iwas high, he then read the product information- O/ V, G& J) g. H; Z! R' E
packet and concluded that it was most likely the rea-
' E! u8 S6 b8 H. S6 L* Q0 F+ Sson for the child’s virilization. At that time, they3 Z( u8 ]: N- m- W  q5 M1 M2 z
decided to put the baby in a separate bed, and the# V  W6 u) w) H' F
father was not hugging him with bare skin and had
+ Q/ V7 @1 J: Jbeen using protective clothing. A repeat testosterone2 R" [) e: v9 v! y& l; s9 B
test was ordered, but the family did not go to the
8 o. k$ }; U7 ylaboratory to obtain the test.
9 j- q. _) T/ x- {/ uDiscussion
! j. }) {: h7 L5 F, `Precocious puberty in boys is defined as secondary
" Y% m, F5 H3 l2 U+ [% U4 Ssexual development before 9 years of age.1,49 \" {8 S# {' F, I0 T* ^
Precocious puberty is termed as central (true) when4 ?! e7 g, v! n0 O: S' f0 D
it is caused by the premature activation of hypo-
  t3 b. S3 n6 W7 \, qthalamic pituitary gonadal axis. CPP is more com-
7 i& ^  [  z$ x! b+ S2 ?mon in girls than in boys.1,3 Most boys with CPP& `- x$ a& _+ C2 q# a" O
may have a central nervous system lesion that is
/ ?8 a/ F- P! P4 A- xresponsible for the early activation of the hypothal-2 f6 g: s' \" n5 k3 _
amic pituitary gonadal axis.1-3 Thus, greater empha-& K$ Z) u7 F5 x& f3 V7 Q
sis has been given to neuroradiologic imaging in
1 L7 S7 V) ^# @5 u; Vboys with precocious puberty. In addition to viril-
" l# G3 l" X8 z: T" c4 J9 G9 v) s1 Gization, the clinical hallmark of CPP is the symmet-
2 L8 k1 O& S. y& n0 v' Vrical testicular growth secondary to stimulation by. ?! q) B; B8 s0 S
gonadotropins.1,3) H6 l2 U$ h$ ^& Y
Gonadotropin-independent peripheral preco-
& l9 ^; K2 U- N8 u8 E0 i: o9 Ecious puberty in boys also results from inappropriate
  `5 d- z$ W! r* R" \) Q$ Sandrogenic stimulation from either endogenous or) }7 }0 j- _6 ^9 {+ }9 j# n+ Y
exogenous sources, nonpituitary gonadotropin stim-
8 _+ E7 ~7 \$ C& fulation, and rare activating mutations.3 Virilizing- u5 J, k9 l' T% k' j' f( f+ X( c
congenital adrenal hyperplasia producing excessive4 P* Q/ J, h0 N! b/ u9 Q
adrenal androgens is a common cause of precocious/ m+ @5 m" V3 v$ x) V7 s! ?0 Q' P
puberty in boys.3,4
" w7 I! ?# F( c% P- [The most common form of congenital adrenal
1 p/ e/ E" J0 d1 Ahyperplasia is the 21-hydroxylase enzyme deficiency.& j5 B+ f/ H! r; R% X: k  F
The 11-β hydroxylase deficiency may also result in
. E' ?& h% x* e* S$ X% kexcessive adrenal androgen production, and rarely,+ Q0 }9 A6 K% j1 x! ]# g! V* Y( K& K
an adrenal tumor may also cause adrenal androgen' P/ O$ H0 a" G& I9 m$ l) a5 d
excess.1,3" I+ w! b& K2 {" H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 P: G# @9 N2 F; @* q7 \
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( i1 n+ M. H5 k  Q+ R8 B
A unique entity of male-limited gonadotropin-
* S5 a- o6 J4 N4 findependent precocious puberty, which is also known' G6 e0 `* m1 g
as testotoxicosis, may cause precocious puberty at a5 n& c, E, k) C  C
very young age. The physical findings in these boys8 r( Z# `8 t+ R$ Q' T
with this disorder are full pubertal development,
% S$ b5 _; q0 H# z  e% lincluding bilateral testicular growth, similar to boys
1 ~5 @/ v2 |0 d6 r3 G3 p) owith CPP. The gonadotropin levels in this disorder
* f: r$ L: c$ W" _' Iare suppressed to prepubertal levels and do not show
8 R7 A4 ~, F/ N" D, H2 }pubertal response of gonadotropin after gonadotropin-+ m1 @* V( x9 d0 T
releasing hormone stimulation. This is a sex-linked
2 L- G; E6 c1 m) N! P5 Qautosomal dominant disorder that affects only: r5 n3 u+ I: G/ `
males; therefore, other male members of the family9 u& I' P* h1 v3 E6 n
may have similar precocious puberty.3" J* ~4 d) Z# o8 R2 I
In our patient, physical examination was incon-
' v2 E7 a2 A% n/ ^# Z; hsistent with true precocious puberty since his testi-# y! _) ]: X0 `2 Y+ I. G
cles were prepubertal in size. However, testotoxicosis2 w; ~" L' e$ t9 g/ c; Q" M( u6 f
was in the differential diagnosis because his father6 N& m- G3 d" z. j; P5 s2 g
started puberty somewhat early, and occasionally,
4 K$ v9 C: m1 R) vtesticular enlargement is not that evident in the4 N, Z+ L. P  h; J5 f5 c
beginning of this process.1 In the absence of a neg-
7 ]' J4 M$ K9 Jative initial history of androgen exposure, our# L* C. \* ]. n4 l
biggest concern was virilizing adrenal hyperplasia,. Q1 z; `% Q5 h# b/ b
either 21-hydroxylase deficiency or 11-β hydroxylase
* T6 i4 @# g3 Q$ cdeficiency. Those diagnoses were excluded by find-3 C6 {4 j/ H& V* V/ L+ ?
ing the normal level of adrenal steroids.6 N6 Y9 p' T; f) U
The diagnosis of exogenous androgens was strongly2 s, M6 v$ s' R
suspected in a follow-up visit after 4 months because
3 h7 P- o: |6 i" P: I9 M/ B" nthe physical examination revealed the complete disap-# _1 ^0 f# F$ n3 v" L% d: T  Q4 _) ?
pearance of pubic hair, normal growth velocity, and
- I& s7 M1 _! ?decreased erections. The father admitted using a testos-
8 h8 q  f9 {' k, O! k0 }( Dterone gel, which he concealed at first visit. He was) s7 W' z  C* |: E: s3 K0 U
using it rather frequently, twice a day. The Physicians’
1 o2 Y& M+ [6 h% ^# R6 YDesk Reference, or package insert of this product, gel or. q' I+ q& |0 J8 k
cream, cautions about dermal testosterone transfer to
2 s, ?1 g! p" I3 ]0 ]; L- x$ K( Bunprotected females through direct skin exposure.4 F6 ]+ R8 _7 f5 M
Serum testosterone level was found to be 2 times the
2 e- {1 J4 z+ t; {baseline value in those females who were exposed to3 F$ ~6 E: @+ E4 g2 E
even 15 minutes of direct skin contact with their male
3 i, v3 h8 p: Upartners.6 However, when a shirt covered the applica-
  z* B1 r9 u/ Z  b/ ]1 J+ Otion site, this testosterone transfer was prevented.
9 C5 U1 b+ s) X8 u% KOur patient’s testosterone level was 60 ng/mL,
, F- B/ n' M  p" \which was clearly high. Some studies suggest that
* m; s' _$ m1 p% vdermal conversion of testosterone to dihydrotestos-
3 z, Z, e4 L, b6 Rterone, which is a more potent metabolite, is more
# Y0 l# Q6 c5 A0 v; d9 factive in young children exposed to testosterone* a8 _. t$ G# I5 k3 N4 W8 c* x2 S
exogenously7; however, we did not measure a dihy-
9 }* j4 i1 _& a! c, T0 bdrotestosterone level in our patient. In addition to5 \  u$ K# b+ _8 e1 ]1 B9 D  t
virilization, exposure to exogenous testosterone in( m& Q# S8 O2 Y/ j! k' f
children results in an increase in growth velocity and
! H3 Y( o3 l' q% aadvanced bone age, as seen in our patient." `$ U+ R4 a8 @9 f$ t. C6 h/ V$ K, N
The long-term effect of androgen exposure during' ^5 |0 Q8 X% B6 z2 ]* r4 Z
early childhood on pubertal development and final8 k8 ~  l% N" m
adult height are not fully known and always remain
9 p9 _! e6 R% Fa concern. Children treated with short-term testos-( H6 X! R/ W+ s8 L2 _$ `4 h
terone injection or topical androgen may exhibit some
2 f( r& k, L0 l  h& ?acceleration of the skeletal maturation; however, after8 ^/ H( Z3 S- e3 ]9 b6 J9 C
cessation of treatment, the rate of bone maturation! a8 p, Y4 q- y4 W- v1 w4 K6 K+ G
decelerates and gradually returns to normal.8,9
% V* j7 x& z( o! H) i  E4 JThere are conflicting reports and controversy
0 S- ?% p7 O& S2 q. ]. Zover the effect of early androgen exposure on adult( ^  a, E! A0 K" V$ A, A7 o0 X' G
penile length.10,11 Some reports suggest subnormal
7 K: u  E# Q& B; vadult penile length, apparently because of downreg-
& M( B9 U" e: S0 Fulation of androgen receptor number.10,12 However,- q+ |+ A! E+ x1 i" [
Sutherland et al13 did not find a correlation between1 i  Z4 x( F0 ^
childhood testosterone exposure and reduced adult, u! F2 d- [# K: Z
penile length in clinical studies.! ]2 T' U) @; W2 f
Nonetheless, we do not believe our patient is
5 T5 g7 v; Z9 z6 _; dgoing to experience any of the untoward effects from
$ l8 U7 ^8 U( l( H& H* u2 H* atestosterone exposure as mentioned earlier because5 _, v9 y; k9 k7 f2 i2 `0 s
the exposure was not for a prolonged period of time.* A. H4 z3 `3 @; k/ O
Although the bone age was advanced at the time of
+ a- P; a6 r. l  fdiagnosis, the child had a normal growth velocity at5 l3 w# D& [' n" A) \0 z6 U
the follow-up visit. It is hoped that his final adult( t1 K6 Q7 W. m" w/ y
height will not be affected.# A# {# U+ }: Y( O9 H! ^% y; Y
Although rarely reported, the widespread avail-
1 d6 X; p' [+ F4 iability of androgen products in our society may. l: `- m9 S" M
indeed cause more virilization in male or female
! T& ?% Z' \: R2 e7 Mchildren than one would realize. Exposure to andro-
1 X( Z2 i% g  y1 S) Agen products must be considered and specific ques-
1 C# @+ b9 k$ E* _0 W7 h) ationing about the use of a testosterone product or9 v! L* f4 U/ H7 Z
gel should be asked of the family members during) u' n) r2 x% C4 E6 ?+ Q4 j2 T4 M
the evaluation of any children who present with vir-- ?. q3 U1 G- u3 f
ilization or peripheral precocious puberty. The diag-
! b2 L3 p9 V' [+ G+ ?2 ]nosis can be established by just a few tests and by
. l, g* C4 S, E8 A- sappropriate history. The inability to obtain such a
8 U; d9 O9 Y" S- lhistory, or failure to ask the specific questions, may( u- S( c& L8 S3 H5 n# ]3 q
result in extensive, unnecessary, and expensive4 u+ v) b( X1 O  A5 z/ `
investigation. The primary care physician should be$ a! u. U7 J; }6 i
aware of this fact, because most of these children
8 K1 x5 I+ U' V  n& _may initially present in their practice. The Physicians’( Q5 v. P5 P$ @. H" g0 e
Desk Reference and package insert should also put a: K3 s1 i! H' M0 |2 U. e1 \
warning about the virilizing effect on a male or
0 j  I4 O3 E- S% Ffemale child who might come in contact with some-& w2 {' Z% I7 @  W6 t
one using any of these products.# s- y1 z; R0 R$ U9 M
References
! a0 H* O7 @, d7 L/ f3 @1 R  I1. Styne DM. The testes: disorder of sexual differentiation) V; |! w* Y2 ?+ l1 A  D  q
and puberty in the male. In: Sperling MA, ed. Pediatric% A" `  h0 _$ m
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" c% F( y4 M" }) u( y2002: 565-628.+ t( z9 V( l( I! ?( c
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; ]* `8 D! k) E  P$ Vpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
& A0 W4 J- l8 G' O, l! A- k8 z6 J1 ~Boy Induced by Indirect Topical* E5 H) [: `% y' f4 Y( H
Exposure to Testosterone
" j8 @, ~5 O+ x! ySamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& e" j" F: `/ J* g/ Y9 F
and Kenneth R. Rettig, MD16 P# d9 \0 t6 Q8 ?: j2 t
Clinical Pediatrics
" @& X% D) y8 l/ DVolume 46 Number 64 q9 `& D. |+ p9 ?- ]' m
July 2007 540-5435 W- L* q$ w- I: U; h0 L
© 2007 Sage Publications' i; ?( B2 O% I% ]) @
10.1177/0009922806296651
% v2 E0 s( r4 X; k( Chttp://clp.sagepub.com
- b3 r1 v9 n) ?/ d& g7 Jhosted at2 s  e7 Z! F0 O$ M! i
http://online.sagepub.com
+ Q1 ~* P5 N, A& K; ~2 HPrecocious puberty in boys, central or peripheral,. i7 S( p# u7 S1 r6 O; h# C: V
is a significant concern for physicians. Central4 g! y, ^+ M, B5 I% R. k! V
precocious puberty (CPP), which is mediated( E. u: d9 E& K
through the hypothalamic pituitary gonadal axis, has3 I3 A4 T6 F# B: I" l$ f+ t
a higher incidence of organic central nervous system# ?/ [8 g8 n( O" P' s' ^; ]
lesions in boys.1,2 Virilization in boys, as manifested9 _5 w" Y1 y. g$ J
by enlargement of the penis, development of pubic
+ `* G& B2 j6 U' p/ mhair, and facial acne without enlargement of testi-7 Q* a6 E" V( C  N: }7 q
cles, suggests peripheral or pseudopuberty.1-3 We
3 T/ H% k3 L- i  o/ w* U) z7 {report a 16-month-old boy who presented with the  {( O7 s; }; c
enlargement of the phallus and pubic hair develop-" Q3 L& X+ y8 q4 B- [5 R
ment without testicular enlargement, which was due
( h3 i' U" U) y" c6 H8 l* Y; `to the unintentional exposure to androgen gel used by$ E0 @3 {# C9 R2 v
the father. The family initially concealed this infor-) ?9 C  a% v, _% N5 i
mation, resulting in an extensive work-up for this5 v/ P. n" \: `- J
child. Given the widespread and easy availability of
( P/ q/ O( B3 U2 M7 S6 g. _testosterone gel and cream, we believe this is proba-9 V* q+ S4 s' X# O! ]
bly more common than the rare case report in the: W, x4 L8 W1 {" Z0 i( d2 g
literature.44 i! v" D9 P* C
Patient Report  p) l" w" y; P
A 16-month-old white child was referred to the
1 C& O9 B$ B8 ]* }  L6 f! g- M1 P% Zendocrine clinic by his pediatrician with the concern& P* X  h- h7 @" X  M
of early sexual development. His mother noticed3 @+ H! E  T8 j
light colored pubic hair development when he was" t3 y8 \; r  Z0 M8 d$ N2 m
From the 1Division of Pediatric Endocrinology, 2University of
4 v/ e$ o8 W( C1 `South Alabama Medical Center, Mobile, Alabama.2 _- A4 b" \* i* q/ ~. S5 l
Address correspondence to: Samar K. Bhowmick, MD, FACE,4 ?+ H3 p6 n7 X
Professor of Pediatrics, University of South Alabama, College of
2 O4 X! W& d' oMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& \8 J* t3 F. B  q% V7 i6 k
e-mail: [email protected].9 Q% d! l2 l! {5 E' B% M% a
about 6 to 7 months old, which progressively became
- d$ l( V" R7 i, z4 Adarker. She was also concerned about the enlarge-, Y$ j8 c2 c5 a. b" Z
ment of his penis and frequent erections. The child9 a! O) E; W5 w' t4 M2 d
was the product of a full-term normal delivery, with
" c. c4 [2 G- e# Oa birth weight of 7 lb 14 oz, and birth length of
6 i6 x! C7 T6 b20 inches. He was breast-fed throughout the first year, o' L4 F" d: h% {' i0 E
of life and was still receiving breast milk along with# O2 `7 O# G# k6 w
solid food. He had no hospitalizations or surgery,
' L; e, q& H/ q. dand his psychosocial and psychomotor development0 {+ W& x! i# V
was age appropriate.3 w) [$ D4 o8 t# [# Z: D
The family history was remarkable for the father,
  E; F# ~2 g$ ?" Kwho was diagnosed with hypothyroidism at age 16,5 I6 B* }9 p% R) F+ e
which was treated with thyroxine. The father’s
$ b# u8 m. Y% d, }5 N* v" G% _0 I: U" Nheight was 6 feet, and he went through a somewhat, R% k7 {2 }( H1 K/ l' f1 E8 j: r
early puberty and had stopped growing by age 14.0 V: F1 d4 m+ Q# V& C7 G
The father denied taking any other medication. The
5 j/ c& S: M* A& b0 h- H1 Jchild’s mother was in good health. Her menarche
+ n% L2 F* B& ^7 M* u! N" m5 zwas at 11 years of age, and her height was at 5 feet
" F4 I) r! p+ j# |1 j& s$ e' L; p5 inches. There was no other family history of pre-
& O/ x- E  q' c7 @cocious sexual development in the first-degree rela-
9 A$ l/ d0 Y+ q# E$ \tives. There were no siblings.
3 _5 e! L% ]8 B3 ~+ r! NPhysical Examination" |+ m) z# V. i
The physical examination revealed a very active,2 ~4 @5 s+ U; n  D* o( O- M
playful, and healthy boy. The vital signs documented
# Z, x( H# x$ V0 [7 Ya blood pressure of 85/50 mm Hg, his length was' m) d0 O9 t; V7 \: P7 f/ Q
90 cm (>97th percentile), and his weight was 14.4 kg
6 ^/ ]: @9 `- {  S6 P0 d, B(also >97th percentile). The observed yearly growth
! m# K1 L% F# ]( Q9 Avelocity was 30 cm (12 inches). The examination of
  p- Z1 @: ~+ x: Xthe neck revealed no thyroid enlargement.. f- G( a2 [+ W2 G
The genitourinary examination was remarkable for
+ v2 z, E+ F; V) k+ X. ?/ Q3 Henlargement of the penis, with a stretched length of, h6 t# F4 b: x
8 cm and a width of 2 cm. The glans penis was very well
, w# @- L; L8 E$ ldeveloped. The pubic hair was Tanner II, mostly around- P+ T( ?1 `0 T8 j
540" {7 G) x- J5 ~8 W7 O% M( g6 ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, {9 N( x* l" m. E) J/ V( t0 f5 Ithe base of the phallus and was dark and curled. The. H7 h1 N: o4 I5 }4 X. t+ Z
testicular volume was prepubertal at 2 mL each.
, K- e$ N& P4 T& q3 @- TThe skin was moist and smooth and somewhat8 N' C' `. l3 I* L: O- S0 o8 J% s
oily. No axillary hair was noted. There were no
, A! i8 m8 N' g6 p- `3 Eabnormal skin pigmentations or café-au-lait spots.* i$ w" b# M3 _
Neurologic evaluation showed deep tendon reflex 2+
" {2 ~, j+ ~+ G. A. d! M+ w; wbilateral and symmetrical. There was no suggestion/ l8 J: I6 X! b: p
of papilledema.
- Y3 J2 o% t5 S' c1 mLaboratory Evaluation
7 i! u& ?' \+ p* E& r5 k) \% P9 oThe bone age was consistent with 28 months by- X% b& E7 q6 [8 f, r- e* X
using the standard of Greulich and Pyle at a chrono-
9 _. K; p* U& }; dlogic age of 16 months (advanced).5 Chromosomal5 A( ~& s; S1 g( [2 v5 P" f# e& H1 x
karyotype was 46XY. The thyroid function test
/ e8 u9 B6 \- M4 W- V; sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 ?: d0 l9 @4 Qlating hormone level was 1.3 µIU/mL (both normal).$ p6 `! U( ~" W. z, X3 z  z
The concentrations of serum electrolytes, blood
1 n: d: A- D) _! vurea nitrogen, creatinine, and calcium all were
* ~0 i9 n! B/ `# Z! ~) }within normal range for his age. The concentration
* n* ~& u7 y! t4 ~) @of serum 17-hydroxyprogesterone was 16 ng/dL
6 l; Z( p' M6 |$ `$ H0 a(normal, 3 to 90 ng/dL), androstenedione was 20! E; r7 R4 k& Y+ ]/ B4 j3 W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* }0 x! a+ A- G! l
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ W5 ~: J) u( b! @/ {7 C5 F- Edesoxycorticosterone was 4.3 ng/dL (normal, 7 to) _7 ]+ I2 b' d
49ng/dL), 11-desoxycortisol (specific compound S)
' d' R# }9 R$ i' J3 Twas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' W. A+ R; }- Btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ A: ~% Q7 }# Y) x( M
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! E4 k  C" {0 [! `$ f# w* nand β-human chorionic gonadotropin was less than
3 w3 D4 K, j: Z, l; m# h5 mIU/mL (normal <5 mIU/mL). Serum follicular
5 |8 R% D/ R2 vstimulating hormone and leuteinizing hormone
+ M/ g: a& n7 p$ \) Q' G/ |+ hconcentrations were less than 0.05 mIU/mL
8 t5 Z- w% y8 n' ~6 b% d2 ?(prepubertal).
+ q0 _9 J! B$ x* _0 lThe parents were notified about the laboratory
  |1 ~% C; t, F+ a* ]1 L, _results and were informed that all of the tests were% [: X$ l4 A* O% }
normal except the testosterone level was high. The5 E( J/ b0 b& {: w- h; [6 `
follow-up visit was arranged within a few weeks to
2 z1 c; K% X" `# Sobtain testicular and abdominal sonograms; how-
* C0 J: ^: h! x+ Z9 }5 qever, the family did not return for 4 months.: P& V9 b: y  X$ u% g9 e2 X( a
Physical examination at this time revealed that the. d# n. ^2 r, W9 I; y. D4 f2 n0 l: |
child had grown 2.5 cm in 4 months and had gained: i; {2 b% @5 P/ c4 M6 k- P. {
2 kg of weight. Physical examination remained) U( V5 D  T, I0 Q4 ^$ i+ B1 O
unchanged. Surprisingly, the pubic hair almost com-3 X, W. O# V* G/ t) Y
pletely disappeared except for a few vellous hairs at
0 T5 R% A7 S. w5 p, o) Qthe base of the phallus. Testicular volume was still 2' ^# ]) p0 K, y
mL, and the size of the penis remained unchanged.
# l' E0 \' v: E, |! UThe mother also said that the boy was no longer hav-
$ ~# `5 |  r4 A/ H2 C0 `; x) Bing frequent erections.
- ~2 `- K) E8 ~1 j: ^# M8 \  T7 K$ FBoth parents were again questioned about use of6 i( H7 p" U5 |! b: m, I% o
any ointment/creams that they may have applied to. ]" F; [, N; V- ?& m  k9 r, `
the child’s skin. This time the father admitted the
& Q9 {: L5 Q' o$ R, v$ a* \! bTopical Testosterone Exposure / Bhowmick et al 541
+ h5 o6 S' }  D6 ]& t; }use of testosterone gel twice daily that he was apply-- o7 e' o$ W/ }  J
ing over his own shoulders, chest, and back area for4 d. L6 j& f  d5 G2 N& j3 X
a year. The father also revealed he was embarrassed; _5 x6 j$ B) l' @/ u) c
to disclose that he was using a testosterone gel pre-
3 ?& F( M0 e5 H# ~; r/ z4 V7 Lscribed by his family physician for decreased libido
2 D; I" g: |7 t+ N3 Y9 jsecondary to depression.
8 J" k# j% b9 F  gThe child slept in the same bed with parents.
: v8 d  y$ l3 ~The father would hug the baby and hold him on his
4 Z% U6 X1 o5 `8 j6 X) S1 V; Hchest for a considerable period of time, causing sig-
% U/ [; t$ S8 Znificant bare skin contact between baby and father.1 l7 z- w  }7 S2 R
The father also admitted that after the phone call,
! K  h+ f+ T0 @" ~5 |# F) }" }when he learned the testosterone level in the baby
. G6 Z+ z1 J  ?7 ~# n& }! O, J/ dwas high, he then read the product information' n' n' w! R  U/ `7 |% g! x
packet and concluded that it was most likely the rea-
( {3 {* H9 V& E2 c: a3 sson for the child’s virilization. At that time, they4 D0 ]# _8 s$ D$ @
decided to put the baby in a separate bed, and the
8 i6 h( b3 q6 ]. G$ Qfather was not hugging him with bare skin and had6 g- K3 j8 \  o3 H& `
been using protective clothing. A repeat testosterone
& o% G: Z' [& k+ p) Ktest was ordered, but the family did not go to the
) y8 `! a& o6 k) _9 d; M8 Rlaboratory to obtain the test.8 E& ]' s" t# I/ e/ U/ W) z1 \- u6 B5 u' V
Discussion6 w7 m- b- T! H7 n  Y( @4 S
Precocious puberty in boys is defined as secondary
. \, s9 P) d' Xsexual development before 9 years of age.1,49 @0 ]9 E) _, L1 }
Precocious puberty is termed as central (true) when
. G6 Q4 K/ j4 Q4 n# d: u2 pit is caused by the premature activation of hypo-, c' M) A& b, \( {! [3 I( b: {
thalamic pituitary gonadal axis. CPP is more com-2 d+ F4 X1 G$ h( G8 }" y; i( P/ y
mon in girls than in boys.1,3 Most boys with CPP: H7 k+ o1 G( X# k) ^6 j5 @
may have a central nervous system lesion that is
/ c6 O+ k9 s: Kresponsible for the early activation of the hypothal-
* U4 b! H0 ~+ X& Damic pituitary gonadal axis.1-3 Thus, greater empha-6 A$ c& Q) P% p' \- z3 x0 a
sis has been given to neuroradiologic imaging in
& Z: |4 m) o3 @. P! G) Q6 _boys with precocious puberty. In addition to viril-
* E1 S' X8 O8 e) C+ p3 E& ]5 D3 @ization, the clinical hallmark of CPP is the symmet-
5 Y: o  D# e( z' K- r% U' zrical testicular growth secondary to stimulation by8 h3 b# s9 q+ D3 ~9 N
gonadotropins.1,3
5 \6 G' R1 R+ W! p1 y9 EGonadotropin-independent peripheral preco-5 Q: t. c$ M5 P
cious puberty in boys also results from inappropriate
( r7 m" N) o% W5 z/ Z( A5 |) G% ^androgenic stimulation from either endogenous or; S. w& W4 ]! X: v4 n! ]2 x
exogenous sources, nonpituitary gonadotropin stim-
# p; ]# K/ D0 i3 O3 eulation, and rare activating mutations.3 Virilizing) i' Q( }! b! e' K
congenital adrenal hyperplasia producing excessive
7 [$ b* h% C* Badrenal androgens is a common cause of precocious: `6 f$ h( V! A3 N5 U/ b4 c
puberty in boys.3,4' s; H5 @; G* a4 |$ q- F
The most common form of congenital adrenal- B* ]7 s5 ^6 ^4 a
hyperplasia is the 21-hydroxylase enzyme deficiency.
5 N7 L5 x9 f- i/ j* H$ \The 11-β hydroxylase deficiency may also result in
4 X- R& p, H2 [* `# kexcessive adrenal androgen production, and rarely,4 Q* _$ H( `1 D. p) f* }! S9 Y9 B4 p
an adrenal tumor may also cause adrenal androgen
( y: y( ^4 P7 h7 Q$ n+ Q: sexcess.1,3( U& `. v3 ?3 v' ^1 p; x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 _$ P7 T5 I" r* W& k/ T% ?9 L542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ Y- n2 T, y' @
A unique entity of male-limited gonadotropin-" A% L5 w- K  ~; c7 o" T
independent precocious puberty, which is also known. w7 A/ b, y0 g; @
as testotoxicosis, may cause precocious puberty at a
( j! w- l5 D/ z( v! `5 Rvery young age. The physical findings in these boys( s3 `& E. U# l8 {: C
with this disorder are full pubertal development,
; }0 ]. D0 f7 o; S# I( l/ Wincluding bilateral testicular growth, similar to boys& q  o8 v/ a8 `) |
with CPP. The gonadotropin levels in this disorder* i- [: _1 L" j; ~$ l
are suppressed to prepubertal levels and do not show
1 `2 J, Q  a5 `/ f% P+ U3 ypubertal response of gonadotropin after gonadotropin-3 z5 G3 Z7 Q  B4 S7 S0 ]
releasing hormone stimulation. This is a sex-linked, w5 y' b; K; s8 C* K- ~
autosomal dominant disorder that affects only8 I: D4 Y4 G$ o
males; therefore, other male members of the family
* @4 F1 N$ J4 t* C- ^8 k8 imay have similar precocious puberty.36 ]. p% M" V3 c  w
In our patient, physical examination was incon-
0 a4 [1 Y4 R9 z5 wsistent with true precocious puberty since his testi-
* G) N4 Z2 N% |  m$ A' ?+ r8 G. xcles were prepubertal in size. However, testotoxicosis
" V9 x  [* u# W0 ^was in the differential diagnosis because his father
: Q  K: R3 F* {started puberty somewhat early, and occasionally,2 V6 N; E5 T! v3 m- d' K
testicular enlargement is not that evident in the: _8 n7 x2 Y  @3 O# d
beginning of this process.1 In the absence of a neg-  K" W: d  n/ [: |' p" k
ative initial history of androgen exposure, our. X, M% e: X. p8 _: ^4 i6 {/ j) ?
biggest concern was virilizing adrenal hyperplasia,
8 }; c  K- N0 }" n6 i3 feither 21-hydroxylase deficiency or 11-β hydroxylase
- v7 p2 \5 r9 x. ?& ~0 ]7 I& ?/ jdeficiency. Those diagnoses were excluded by find-
! k7 n' A* U; g" {) u! oing the normal level of adrenal steroids.
$ m: q* y; X  w3 PThe diagnosis of exogenous androgens was strongly% L5 R: C3 }3 H: |' g* @
suspected in a follow-up visit after 4 months because
. B9 |. z- |3 z, g$ t7 t7 M3 `' c) Qthe physical examination revealed the complete disap-
, B- Y+ g9 I# r+ f0 _5 F2 q4 opearance of pubic hair, normal growth velocity, and
; [8 H5 K3 l+ _- ^' }( d6 hdecreased erections. The father admitted using a testos-
- J0 `( y* e5 s& f; M* ^terone gel, which he concealed at first visit. He was
/ u7 X6 C/ c3 Z; u3 G+ m: a, `' rusing it rather frequently, twice a day. The Physicians’$ U  a( g9 ?0 y+ c4 ]
Desk Reference, or package insert of this product, gel or3 n: B7 d2 p! H: ?  \
cream, cautions about dermal testosterone transfer to
& y6 k/ {$ o4 Q/ ]% P* `$ z( runprotected females through direct skin exposure.
: j& i, o3 n3 Z3 B# eSerum testosterone level was found to be 2 times the* x7 H) `' D2 a) v: T9 v
baseline value in those females who were exposed to7 V% Y6 z, W2 M2 d: F9 ^5 x3 e
even 15 minutes of direct skin contact with their male6 f, _# x; u0 [. N
partners.6 However, when a shirt covered the applica-$ r/ X/ i1 z( T1 I4 G
tion site, this testosterone transfer was prevented.
+ b9 @6 l: V4 `* d7 m% C& uOur patient’s testosterone level was 60 ng/mL,( g* O; E' Z+ _* {/ @4 T! S
which was clearly high. Some studies suggest that) K9 M9 }2 w* S+ j
dermal conversion of testosterone to dihydrotestos-4 y; f3 ^8 C4 c
terone, which is a more potent metabolite, is more5 d1 g- x0 ]; Y! _, D# V
active in young children exposed to testosterone
+ I8 }8 q$ A' L. Y1 S8 I/ Jexogenously7; however, we did not measure a dihy-
# O7 s. h  u5 Xdrotestosterone level in our patient. In addition to
! M. o. k/ b" Nvirilization, exposure to exogenous testosterone in
' `4 J" \, D# a" ochildren results in an increase in growth velocity and9 i- }7 l6 C4 p4 t( Q+ n& r4 K
advanced bone age, as seen in our patient.
% l% H" c) j3 h2 L6 ?The long-term effect of androgen exposure during
/ H, F, O! @. S4 Z( u- iearly childhood on pubertal development and final) z1 _/ I2 K! h8 ~& T+ H5 k7 s1 e
adult height are not fully known and always remain
; k7 J- f& c4 P* x6 b7 Oa concern. Children treated with short-term testos-! C4 j) R5 s$ E
terone injection or topical androgen may exhibit some
: n0 x0 t4 _+ D2 N1 o0 p6 Aacceleration of the skeletal maturation; however, after
( l& P& t6 N$ O1 k: R8 xcessation of treatment, the rate of bone maturation
/ @; z: M: w, kdecelerates and gradually returns to normal.8,9% a- D- R9 w1 Z0 _
There are conflicting reports and controversy
9 {" g. g" _* v, tover the effect of early androgen exposure on adult
) M& }& u0 \# C" N& f  }penile length.10,11 Some reports suggest subnormal
- N& b  F; ?, q5 \# tadult penile length, apparently because of downreg-; Y- r6 U, ^1 C8 e6 C( n8 A2 W& g
ulation of androgen receptor number.10,12 However,  h/ q1 S2 r& h2 F5 e
Sutherland et al13 did not find a correlation between
5 u2 h% k; b4 s$ M: j, l. Jchildhood testosterone exposure and reduced adult
  k4 x! \* f, {0 }4 o3 _$ [penile length in clinical studies.
5 f4 P3 W, F% H3 {0 ?' u; ]Nonetheless, we do not believe our patient is; Q$ S- Z" L" l: q3 K4 ?. p& y6 B
going to experience any of the untoward effects from
9 p* Q# @# \. W7 @' N! P* A! ]testosterone exposure as mentioned earlier because) [5 m4 a3 M- }
the exposure was not for a prolonged period of time.! f: q4 M8 s( D% }  `
Although the bone age was advanced at the time of
3 I/ ?$ h0 i! w, `& k5 h4 Rdiagnosis, the child had a normal growth velocity at
# e( T+ J4 `8 o* O' I' [the follow-up visit. It is hoped that his final adult6 h: I$ R3 o: `4 H) v
height will not be affected.+ f% l/ S9 M% m2 v8 E0 ]! g
Although rarely reported, the widespread avail-- r& |- d3 {# e
ability of androgen products in our society may" g* c$ e4 \) k; S& m
indeed cause more virilization in male or female
7 e( B  ]3 I; n& c4 f; |3 mchildren than one would realize. Exposure to andro-
- W2 f7 o& C/ v: dgen products must be considered and specific ques-* U* |. h  C0 S; y5 E8 q
tioning about the use of a testosterone product or* ]2 T" N% a  ^% I0 U
gel should be asked of the family members during
7 S; k/ }1 K; [1 _& q! M2 o3 Nthe evaluation of any children who present with vir-
2 l3 v& s0 w% C: r1 `/ qilization or peripheral precocious puberty. The diag-
# K: I. K( S- R" Xnosis can be established by just a few tests and by  X2 J- v% O1 B3 y$ Z* r, |
appropriate history. The inability to obtain such a$ s2 ~* g+ Q  l1 e2 V5 n: o$ C) N
history, or failure to ask the specific questions, may+ @1 s5 e- }% [  N" T# O1 |5 i
result in extensive, unnecessary, and expensive
- Z8 q% g" X: f/ z2 I. uinvestigation. The primary care physician should be
  w4 M. m- v1 \. Eaware of this fact, because most of these children
' i* H) T( Z0 b) [5 ~may initially present in their practice. The Physicians’: ~# e* H6 ?+ B2 w/ S' l* i7 ~3 F$ C
Desk Reference and package insert should also put a
3 L3 f+ ?4 w  q2 uwarning about the virilizing effect on a male or! c+ E6 @7 F  f4 f  Q. `
female child who might come in contact with some-
" m/ T' j! {/ K$ P, Eone using any of these products.8 j) d+ B4 Q& B9 a
References
+ N# [+ C6 h# u: h4 a1. Styne DM. The testes: disorder of sexual differentiation6 i9 i- ?' f$ P  ^6 [) `
and puberty in the male. In: Sperling MA, ed. Pediatric+ T/ t. K: ?6 w, v
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 {8 S, m* t! \+ t& j0 c4 L7 o4 w
2002: 565-628.
, M' m( i1 K2 V2 g2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  @" ~7 h& a. {1 _% t( x
puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
; U( J  w: |. {8 F, C) r7 k5 ?
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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