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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& J, t3 x6 a- s6 ~
Boy Induced by Indirect Topical
+ M0 Z) x7 f. p( Y3 C1 _Exposure to Testosterone. s' J) U4 B$ T  [* q7 D
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  _- J- Y% C- s5 Uand Kenneth R. Rettig, MD1$ j; p2 G) Z  ]4 K0 ~9 H+ X
Clinical Pediatrics
2 ^1 ]  k2 z: B% [6 p: ]# uVolume 46 Number 6
. y* ]7 |  N; {4 lJuly 2007 540-543; @: x+ f/ e& Q- V8 b4 K
© 2007 Sage Publications
! q3 K" A( F: n0 C10.1177/0009922806296651' [% M, W* M- w+ t
http://clp.sagepub.com
" K) g9 \) X, P* [" ^$ S7 a9 {hosted at
% h3 v$ `) U3 p8 g" ?http://online.sagepub.com- ~! N1 N- z; M! j' ^
Precocious puberty in boys, central or peripheral,
) x: R! b( M3 Y6 ]is a significant concern for physicians. Central
2 L' {/ s4 _% O: G, n7 tprecocious puberty (CPP), which is mediated/ H) o' q* o. ~: J: M) }
through the hypothalamic pituitary gonadal axis, has
) ?+ V' J/ h- _: Ha higher incidence of organic central nervous system
& @: u5 a& y3 d6 D# J; nlesions in boys.1,2 Virilization in boys, as manifested
* D+ n2 C! Z5 A: N" o+ uby enlargement of the penis, development of pubic+ g- P6 r- Y/ u6 M
hair, and facial acne without enlargement of testi-( B$ b: w* _4 D* i& ]: F, `- |
cles, suggests peripheral or pseudopuberty.1-3 We& a- C' E% n. |8 ~. v1 d
report a 16-month-old boy who presented with the
* R: L6 y5 I5 D% l- `) Nenlargement of the phallus and pubic hair develop-
" i% U: a& s! m5 ~2 U' [* Kment without testicular enlargement, which was due
/ }* A4 x* K1 q5 q& t4 y0 o! p3 g' \9 v1 sto the unintentional exposure to androgen gel used by
4 J9 a$ j! t  E6 R$ Lthe father. The family initially concealed this infor-
7 q% x+ o% K/ K1 Q  Rmation, resulting in an extensive work-up for this
  j7 Y' |' U& M$ T0 Schild. Given the widespread and easy availability of0 @7 L1 P* S2 V7 J% F
testosterone gel and cream, we believe this is proba-
( n, W: }+ B; C# Ybly more common than the rare case report in the
4 C7 _$ I3 e9 n' Xliterature.46 {) G+ w; I) R8 x9 P
Patient Report7 b: ^, ]- O4 \* l3 z' x0 A+ @
A 16-month-old white child was referred to the
3 w# {; G& ?, y0 C$ Y* vendocrine clinic by his pediatrician with the concern
% V' |6 \- d4 ?0 M: W. w/ P, g2 W2 bof early sexual development. His mother noticed& K! n3 q7 }! H" T
light colored pubic hair development when he was
! q0 \: J- O' X2 z8 r+ _From the 1Division of Pediatric Endocrinology, 2University of
* |* ~* x: n" gSouth Alabama Medical Center, Mobile, Alabama.* R  W1 K1 q& p: C5 j
Address correspondence to: Samar K. Bhowmick, MD, FACE,5 M: \6 @% N6 R5 c
Professor of Pediatrics, University of South Alabama, College of8 n( f( W$ O: @
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 N( A# O8 o, S& ]7 {9 {: y
e-mail: [email protected].- r# }5 A/ G3 V' M/ V0 G
about 6 to 7 months old, which progressively became
. `0 y3 b8 A( mdarker. She was also concerned about the enlarge-
) D0 c* L% T5 d/ ]( H* _ment of his penis and frequent erections. The child
' C) ^3 F. ]* V! I9 C" [, Ywas the product of a full-term normal delivery, with
* x8 E$ z9 Z& N1 r, `a birth weight of 7 lb 14 oz, and birth length of
" s. F# w! I- z$ D4 I9 o20 inches. He was breast-fed throughout the first year( V- n* X9 K) V# T/ M& }+ X" Y6 v. F
of life and was still receiving breast milk along with8 O2 q+ B2 e$ ]# C' A2 T# M  B7 V
solid food. He had no hospitalizations or surgery,% q6 u  g2 ^5 ]( Q6 j. g9 Z
and his psychosocial and psychomotor development. ^% Q& a5 ]; ]7 l4 n
was age appropriate.3 c$ a$ L5 H( I2 {; T$ L
The family history was remarkable for the father,
( C/ I6 q" S! I* ]who was diagnosed with hypothyroidism at age 16,, p* k3 p2 _$ ~7 b
which was treated with thyroxine. The father’s1 m3 r: s* _# p
height was 6 feet, and he went through a somewhat' M. G, Z6 s; r9 x
early puberty and had stopped growing by age 14.% m% X6 ^8 Z: I0 q& I
The father denied taking any other medication. The
" O0 G+ f" D* B: Y8 [2 D$ rchild’s mother was in good health. Her menarche
& S4 K! R5 M6 Gwas at 11 years of age, and her height was at 5 feet
0 s& B2 M# z* U# _& ?, c4 V: ~0 L5 inches. There was no other family history of pre-
3 @* K, u$ x) R+ s1 Mcocious sexual development in the first-degree rela-
* q7 `- V, J+ y& M7 Xtives. There were no siblings.
3 P$ n# M' m% v2 s5 u6 _Physical Examination0 s; U1 p/ o5 R( ]8 B- I8 E
The physical examination revealed a very active,
+ j: w. O% y  Yplayful, and healthy boy. The vital signs documented' b0 P0 G8 W( V5 F2 \/ \* V( G
a blood pressure of 85/50 mm Hg, his length was3 f# a  |. Z! X
90 cm (>97th percentile), and his weight was 14.4 kg
% l8 W4 z0 T+ n7 v4 e  m(also >97th percentile). The observed yearly growth# m* t6 B; m' n
velocity was 30 cm (12 inches). The examination of
. I- K6 ^+ G, b1 r, athe neck revealed no thyroid enlargement.5 O! D: W! r9 r2 z0 Q+ B
The genitourinary examination was remarkable for
1 p/ n" r) G( O; T- ]  Jenlargement of the penis, with a stretched length of
7 k' D6 T$ w4 W9 i* A8 cm and a width of 2 cm. The glans penis was very well
1 ]% ^; X1 w7 j4 @) _3 X7 r" Fdeveloped. The pubic hair was Tanner II, mostly around4 ^& z/ B! E4 N' b
540
" k7 z7 C3 a9 `. y' c7 O% D3 Wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! _( r% i& P3 B9 w2 v: Jthe base of the phallus and was dark and curled. The+ L' o5 H: F/ e4 }$ K2 E" B6 R
testicular volume was prepubertal at 2 mL each.6 D( }/ a8 K* G
The skin was moist and smooth and somewhat
% k% t1 R/ `; o0 F/ y5 u  w; c1 ?oily. No axillary hair was noted. There were no% ]& U1 _8 A/ c. ]% N' E
abnormal skin pigmentations or café-au-lait spots.( ~! H( I5 Z0 i( ~0 q! Y
Neurologic evaluation showed deep tendon reflex 2+
4 u/ k, `' t$ I  M1 X, |7 q" x8 `/ {bilateral and symmetrical. There was no suggestion
+ e8 W6 p( `1 k/ o+ Oof papilledema.
1 l- e9 S) k+ j0 \: jLaboratory Evaluation7 M* m+ b7 D# U
The bone age was consistent with 28 months by# B; G5 K% g8 O/ Z8 n: Z
using the standard of Greulich and Pyle at a chrono-5 f6 A  [. T% ~( w# m  Z
logic age of 16 months (advanced).5 Chromosomal, g8 Q/ G2 r2 M( d* E* W6 {. P
karyotype was 46XY. The thyroid function test
( x8 d, d8 `- S6 t7 M/ N3 zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
* q; \: U( P( s) \# k# Z( Nlating hormone level was 1.3 µIU/mL (both normal).; P/ @! s9 w- O- U+ `# L7 q1 Y; `, t
The concentrations of serum electrolytes, blood) z7 }3 g7 M  Y$ M; P3 p
urea nitrogen, creatinine, and calcium all were
  U. y1 g4 O* o$ W/ uwithin normal range for his age. The concentration4 L( I6 k0 f% y' K1 q
of serum 17-hydroxyprogesterone was 16 ng/dL
! p; ]4 t5 g5 P* Q) O/ g(normal, 3 to 90 ng/dL), androstenedione was 20
, Q% h) Q8 N, r" png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 b8 {: S* Q9 a- ^; b3 z- }& c/ L
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
5 l# n4 V1 M! F- V2 `( s9 Edesoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 H8 t- s8 X- K- U, c49ng/dL), 11-desoxycortisol (specific compound S)
+ i6 n) L: u& a1 p9 i/ Iwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* r; x+ Q6 F5 k+ U( @: V) H
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 w0 N1 @" ]5 M+ q/ Ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),' G  _$ s9 R9 }$ D
and β-human chorionic gonadotropin was less than4 K% S0 ]3 [5 o' A# J
5 mIU/mL (normal <5 mIU/mL). Serum follicular& z" `4 H& w4 r, a
stimulating hormone and leuteinizing hormone2 v" S) n9 z6 P# R" l7 `- n
concentrations were less than 0.05 mIU/mL. R. H8 M/ i+ D! f
(prepubertal).
; m' ]0 u! A& JThe parents were notified about the laboratory
4 [9 ]" F  f$ o' hresults and were informed that all of the tests were- S) e) {$ Q3 i" Q0 ]5 w
normal except the testosterone level was high. The; y' Y7 P4 {- |5 y7 ?
follow-up visit was arranged within a few weeks to
" c  L8 J! y8 ^, D3 D0 xobtain testicular and abdominal sonograms; how-
! R4 X( k" e+ S3 P9 O8 yever, the family did not return for 4 months.7 Q- b+ T& V5 T
Physical examination at this time revealed that the
3 m6 _/ Z6 m5 w! w# Y  a+ h5 achild had grown 2.5 cm in 4 months and had gained
3 s  t3 K0 U( r/ p. v: X2 kg of weight. Physical examination remained
0 o/ A  A$ X  punchanged. Surprisingly, the pubic hair almost com-; P' F( m! f0 [# X( Q$ e) H/ q0 R
pletely disappeared except for a few vellous hairs at# x# t! w3 C& `1 I
the base of the phallus. Testicular volume was still 2
; g% M5 r( A3 ~1 l3 z0 VmL, and the size of the penis remained unchanged.. h& l: G+ z3 o2 v: B9 @
The mother also said that the boy was no longer hav-
# d: m- J2 w) J8 Ying frequent erections.
& C' s+ c6 H" N5 F6 C: qBoth parents were again questioned about use of3 |$ ~/ `1 |2 [9 g3 F+ f
any ointment/creams that they may have applied to. d/ ~2 z: w" p7 j
the child’s skin. This time the father admitted the! B+ {, P- l9 F0 r+ @1 n4 k6 P+ A
Topical Testosterone Exposure / Bhowmick et al 5413 i" J4 x/ J1 o! \. z
use of testosterone gel twice daily that he was apply-
, \0 n8 i; w& F6 h, Ming over his own shoulders, chest, and back area for
( ?. p% s# ~) T3 b" Xa year. The father also revealed he was embarrassed
- ]& f+ h6 E- e9 D1 Hto disclose that he was using a testosterone gel pre-; F' O# M# r; A; l
scribed by his family physician for decreased libido
7 t' j& U2 U0 h$ d: d* ~2 L$ Fsecondary to depression./ \: ^2 i0 I( h" K9 o
The child slept in the same bed with parents.' y* {/ f: W' ?' ^& d
The father would hug the baby and hold him on his
, T; b3 n" F; y4 ~9 c! B  Wchest for a considerable period of time, causing sig-
) X) L1 ^$ _5 c6 _7 x$ wnificant bare skin contact between baby and father.! c: H7 v' }* \" `0 U# G
The father also admitted that after the phone call,' M9 H" a) C6 g+ X7 o7 n3 m
when he learned the testosterone level in the baby& b, s  M  T$ ^
was high, he then read the product information
. K1 z: I$ B! z7 U% {. X2 Zpacket and concluded that it was most likely the rea-" Q$ v  \( g$ J% v7 G6 m! J0 \
son for the child’s virilization. At that time, they9 _9 ~: t/ j4 p
decided to put the baby in a separate bed, and the
# h! @$ @, J( M5 \4 n" ]father was not hugging him with bare skin and had
3 q; \8 d" v1 r! x9 V5 i' ~been using protective clothing. A repeat testosterone
# z0 F" l# O4 O% X& ^( Vtest was ordered, but the family did not go to the/ z$ {& P6 ]8 J- }# Q1 M
laboratory to obtain the test.: R+ X; v! k9 v9 t' Y* [) m) N
Discussion
; c9 {+ @% w8 E. [2 U1 i) tPrecocious puberty in boys is defined as secondary/ `) n; t# n) ?& J1 ~9 x! a
sexual development before 9 years of age.1,4
  ^- T. L$ z: O9 f" TPrecocious puberty is termed as central (true) when
1 M4 U9 W* }, T7 W; N% b& E. [it is caused by the premature activation of hypo-; L9 M3 {. b6 T# T" X
thalamic pituitary gonadal axis. CPP is more com-
; @9 ^: X5 e- H+ ^mon in girls than in boys.1,3 Most boys with CPP( P: J- U3 }; ~# K8 f7 ~0 E
may have a central nervous system lesion that is% r" c. y! K2 l; ~% u- c, A3 r5 \
responsible for the early activation of the hypothal-9 {& T! }) u' S+ m6 E2 u1 o- r8 A! u
amic pituitary gonadal axis.1-3 Thus, greater empha-
8 y! {5 @2 P! K8 a2 Osis has been given to neuroradiologic imaging in: ^! c( a* v4 a5 e- q+ e
boys with precocious puberty. In addition to viril-+ p: b' _6 l' B1 a* @* i" C
ization, the clinical hallmark of CPP is the symmet-. k8 P! O5 r( n
rical testicular growth secondary to stimulation by
6 |* c7 x9 z2 W' y, \# Agonadotropins.1,3) Y. A# ?  x& z
Gonadotropin-independent peripheral preco-3 Z2 T( t( l% ~$ v$ N# W& L
cious puberty in boys also results from inappropriate4 @7 B) J9 K# \; @- H2 S; Y
androgenic stimulation from either endogenous or' \5 [& v* U$ ~# D' {) u5 X( y  C1 T
exogenous sources, nonpituitary gonadotropin stim-3 ?* ]# I8 x8 |: [) s( s8 @
ulation, and rare activating mutations.3 Virilizing
; V, I( ^4 ]  H) w& fcongenital adrenal hyperplasia producing excessive
0 D* _' C* ^) {& G( |+ S% Gadrenal androgens is a common cause of precocious* M# T% _8 S' \8 Z7 r
puberty in boys.3,4
# O5 z2 y$ s6 I& ^The most common form of congenital adrenal3 r6 I4 m1 G' v) W7 @/ S
hyperplasia is the 21-hydroxylase enzyme deficiency.7 b) X: L7 h' W5 F0 O% ?& P0 a
The 11-β hydroxylase deficiency may also result in8 D7 k( Y4 C/ v0 z3 r1 M
excessive adrenal androgen production, and rarely,. Y- \& R5 g+ r, c
an adrenal tumor may also cause adrenal androgen
  d& S2 u$ Q0 gexcess.1,3* H0 [' e* }4 D* p) T( l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. T  z  Y  D8 C
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* G9 F& j6 s3 ]! G2 \, g1 N
A unique entity of male-limited gonadotropin-/ g  O' E8 x- `" G( t7 B# u9 J
independent precocious puberty, which is also known
8 w) u) C2 _7 Y* ^& R' Mas testotoxicosis, may cause precocious puberty at a
2 v# U. Z5 {2 \8 j. T" a* `very young age. The physical findings in these boys
" {) s# }; W' x$ B$ wwith this disorder are full pubertal development,& B" o; I6 L  `+ |: j7 o4 F/ [
including bilateral testicular growth, similar to boys$ w# P% d( y% \- n
with CPP. The gonadotropin levels in this disorder" |# m# y4 K2 S# p) h
are suppressed to prepubertal levels and do not show
3 z1 z* t$ j! S3 P9 ~+ G* Q0 l. B# {pubertal response of gonadotropin after gonadotropin-. F# Y$ b, U$ y6 m' z* g4 V
releasing hormone stimulation. This is a sex-linked
2 f; o  r6 ~3 N  a6 \2 |autosomal dominant disorder that affects only
7 L: ^2 ~" m4 G( D# R& J. N" omales; therefore, other male members of the family
$ s9 r. `" v4 K* \) D6 c; Z# u$ F, {may have similar precocious puberty.38 s0 V  A4 b3 n; \
In our patient, physical examination was incon-+ q+ P; d; G5 Q3 ^( I7 T3 q1 b* y! A
sistent with true precocious puberty since his testi-
; W* y+ ]4 {4 b% P  r0 i2 l; r% |cles were prepubertal in size. However, testotoxicosis
9 L# @% b/ j/ F2 y# owas in the differential diagnosis because his father
% x2 r6 T9 N6 G( Fstarted puberty somewhat early, and occasionally,( g5 L, k2 J" X- W' h  o: }1 o
testicular enlargement is not that evident in the
8 e; L! D( }. H& Q7 _beginning of this process.1 In the absence of a neg-
9 X; `& H# G2 [# z6 f; iative initial history of androgen exposure, our7 h7 i: R3 w8 b5 R, L& Y
biggest concern was virilizing adrenal hyperplasia,% h. k3 n4 D- P. d9 O
either 21-hydroxylase deficiency or 11-β hydroxylase
4 v3 H( _6 w- jdeficiency. Those diagnoses were excluded by find-
+ H. Z& ^) D# G7 R5 a* _ing the normal level of adrenal steroids.9 {6 e' i5 g* _6 W6 a3 q
The diagnosis of exogenous androgens was strongly
: a, W# s  }6 {/ ?; osuspected in a follow-up visit after 4 months because
: z6 l! z  d( C0 Y% ?8 l$ c& ?. Ythe physical examination revealed the complete disap-0 w7 }# ~& l  @  [* Y& v
pearance of pubic hair, normal growth velocity, and2 n; O$ [% ?5 [
decreased erections. The father admitted using a testos-
8 b4 _: f6 U) \9 Pterone gel, which he concealed at first visit. He was6 R% u, {) i  O
using it rather frequently, twice a day. The Physicians’) w+ c- D' z+ M; N$ s
Desk Reference, or package insert of this product, gel or
5 N$ N& h$ ~# H* k, p3 Ycream, cautions about dermal testosterone transfer to
4 K" i" R$ p. V* b* d, y" u" `/ Z# |unprotected females through direct skin exposure.  s' @( e% n0 @: }+ x
Serum testosterone level was found to be 2 times the/ P" u8 V: ?3 v  Z# M3 G
baseline value in those females who were exposed to3 O+ U$ h9 g* B3 ?1 h  {9 S: J! C8 a* z
even 15 minutes of direct skin contact with their male- _! @' `: d! o
partners.6 However, when a shirt covered the applica-
% l: s5 X% x' W5 ~tion site, this testosterone transfer was prevented.; |9 h! A" Y! B4 o# e
Our patient’s testosterone level was 60 ng/mL,9 Q9 ^- ~, {, j. I3 b" S
which was clearly high. Some studies suggest that) e5 M+ Y" |; P" P' p2 n; O( E
dermal conversion of testosterone to dihydrotestos-
4 z+ N! r; z) |4 U) A6 _# U: t& Oterone, which is a more potent metabolite, is more
+ b1 Q- @: a8 aactive in young children exposed to testosterone0 \! j- n' R# ^! [% i1 q
exogenously7; however, we did not measure a dihy-! _" `$ x8 B7 ?
drotestosterone level in our patient. In addition to4 r, r) T! A) L* ~: D# z1 f
virilization, exposure to exogenous testosterone in/ U  [* q8 X( g* {$ e: ]3 T" U
children results in an increase in growth velocity and
/ j- M  V4 ?7 W* A' g) c& d7 Q) {advanced bone age, as seen in our patient.
) R. K: _3 `1 m  B- tThe long-term effect of androgen exposure during
! W0 V) V; R9 }" W+ Nearly childhood on pubertal development and final; {0 F" m; g# C* X- [: S
adult height are not fully known and always remain6 G' b" W& u* x: z- ]0 w3 S
a concern. Children treated with short-term testos-) o/ n- ^' p0 R. H$ ~
terone injection or topical androgen may exhibit some
, q/ K0 t# d8 H/ a6 uacceleration of the skeletal maturation; however, after, N" a4 J+ D2 I! C- j5 I4 a
cessation of treatment, the rate of bone maturation, ^/ U# N% [( ]0 f% C) x
decelerates and gradually returns to normal.8,92 I- g0 G7 M: f' M5 E
There are conflicting reports and controversy
6 c, `0 A3 h; |, Y7 K4 }over the effect of early androgen exposure on adult( {, A( H1 t# F0 ^8 }
penile length.10,11 Some reports suggest subnormal
" ?! a' g! Y( B1 oadult penile length, apparently because of downreg-
% t; S6 d+ \1 h" m, |& L+ k' mulation of androgen receptor number.10,12 However,4 e# ?# [" C, l% ]5 j
Sutherland et al13 did not find a correlation between
! T! v) }1 `7 Uchildhood testosterone exposure and reduced adult
+ ^: r8 ]" a7 ^0 l* bpenile length in clinical studies.+ z- o/ O9 v# _5 [$ b
Nonetheless, we do not believe our patient is7 M* u7 K/ j7 k: {6 u% _
going to experience any of the untoward effects from4 R0 j& p9 X# z5 x& }
testosterone exposure as mentioned earlier because
& k5 b* S. |8 b) d& J# |7 y- ^the exposure was not for a prolonged period of time.% `% D( x$ P: T4 X$ p+ {" c
Although the bone age was advanced at the time of, q7 t8 i+ ]: T5 X0 H5 y
diagnosis, the child had a normal growth velocity at6 b% |- N  s2 b9 W- k9 u
the follow-up visit. It is hoped that his final adult
# Y3 F9 B" u8 f# ]4 Fheight will not be affected.- G/ W1 Q/ G1 ?1 q! N& ~
Although rarely reported, the widespread avail-
( Z, v8 w) [  U' c3 ~, }ability of androgen products in our society may: ~) D9 a6 g0 ?# Q6 s0 z) y- B
indeed cause more virilization in male or female
6 b4 G1 |6 r$ echildren than one would realize. Exposure to andro-+ \9 f; a9 ~0 o' x# E6 I& M$ Q0 c# M$ d
gen products must be considered and specific ques-
! ~8 c9 t4 I" \+ r2 c  `; Ctioning about the use of a testosterone product or
* F5 H7 Z4 d0 u8 K8 x- i9 O$ M9 cgel should be asked of the family members during
8 ~: K& C0 z' F& _. k; v* l, Y9 Ythe evaluation of any children who present with vir-
- t+ A8 D6 _& R/ uilization or peripheral precocious puberty. The diag-
8 B7 k7 y  B# b7 lnosis can be established by just a few tests and by8 V9 R- @3 y% I0 U; T2 p
appropriate history. The inability to obtain such a8 s9 n$ W% }/ Q4 _( X1 |2 v
history, or failure to ask the specific questions, may$ Z/ A% {- z; Y7 V
result in extensive, unnecessary, and expensive
4 H1 Z3 _4 j$ d& G- X0 \investigation. The primary care physician should be
! e" {+ A" R- _6 I1 Yaware of this fact, because most of these children$ U) W6 A3 h+ A/ F7 v$ z8 _
may initially present in their practice. The Physicians’# k0 u) O* v* f, j$ S$ I
Desk Reference and package insert should also put a* I2 k6 x' q, j* v
warning about the virilizing effect on a male or
4 \; L2 [8 ^9 l% Jfemale child who might come in contact with some-
) n% E% O8 x6 Yone using any of these products.
5 S2 k5 i% _# a; {References
, u( r2 }4 C4 Y1. Styne DM. The testes: disorder of sexual differentiation
1 v, J8 Q$ I' X0 _and puberty in the male. In: Sperling MA, ed. Pediatric; R4 u" [) r; G3 `9 |+ ]9 b, ?" `
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;7 h) P$ ]- u/ ~( D% V" |3 }& c8 K
2002: 565-628.
* p  S3 E6 ]2 {4 s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: L+ c* v+ ]' v) B3 y" v$ J  Vpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
5 {, R1 q3 b5 sBoy Induced by Indirect Topical
8 n) O6 {/ b: L6 IExposure to Testosterone
8 u( G9 H  B% @& Y. YSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 z8 \$ D$ P7 w5 y% L$ n
and Kenneth R. Rettig, MD1
/ p- J+ `" z& t/ O1 @0 A8 G! ^Clinical Pediatrics
5 h, P* t" E& ]Volume 46 Number 6$ _- V4 B' y+ D+ ~$ o/ L/ {7 w' W
July 2007 540-543, N$ g, O6 l. {! _
© 2007 Sage Publications
9 T/ [: s* T& N: K10.1177/0009922806296651- ]6 s7 ?; t# c/ a2 y
http://clp.sagepub.com
! ]2 _8 r# y1 Rhosted at
4 d  H% u$ `# Z! Ihttp://online.sagepub.com1 x# q' f  O+ n4 Q$ G: q
Precocious puberty in boys, central or peripheral,, E' G: |% t' E" r2 L4 H9 {2 S
is a significant concern for physicians. Central  t( Q+ q; L3 o. o; C" u1 D
precocious puberty (CPP), which is mediated
- X3 }* i/ v  Y6 n9 o6 Pthrough the hypothalamic pituitary gonadal axis, has
. t! h8 T' S! Ya higher incidence of organic central nervous system; U; C3 a) P- z# u
lesions in boys.1,2 Virilization in boys, as manifested, J. a2 a+ a! H+ n8 k6 _6 H; `
by enlargement of the penis, development of pubic$ x5 n+ O7 h5 s
hair, and facial acne without enlargement of testi-
* W+ M6 K& ^- P0 p9 Mcles, suggests peripheral or pseudopuberty.1-3 We( m5 e: p$ Z+ R' X
report a 16-month-old boy who presented with the: r: }. ]* G2 p
enlargement of the phallus and pubic hair develop-
5 n) v5 d8 ?% m' Bment without testicular enlargement, which was due
/ z6 L7 y: V) ]. }% p/ E; qto the unintentional exposure to androgen gel used by
7 @+ ~' D* F5 I7 Y  wthe father. The family initially concealed this infor-3 Q7 \1 r! n4 `  A) K! j& j$ Y
mation, resulting in an extensive work-up for this
2 ~4 A7 m2 ~, E3 r( d! _child. Given the widespread and easy availability of/ ~) j. z; N6 M9 b$ G6 E: h
testosterone gel and cream, we believe this is proba-  y# U1 L4 _' k& N$ n; y* W
bly more common than the rare case report in the
3 W1 b4 z$ v1 p& O) Oliterature.42 C2 Y% Z' S: k
Patient Report
6 Z) ]5 J( o+ Q7 ^6 k! hA 16-month-old white child was referred to the: k& |" ^4 j8 U  N
endocrine clinic by his pediatrician with the concern
2 d+ b3 c  K- B8 ]! m# Fof early sexual development. His mother noticed
: w6 @5 R* }, b' i, ?4 O; Plight colored pubic hair development when he was
( S" H/ P* R4 h' xFrom the 1Division of Pediatric Endocrinology, 2University of
! z/ q8 ^# N. H, v& xSouth Alabama Medical Center, Mobile, Alabama.; l) b# ~" R) b$ w4 w/ u' z7 a& g
Address correspondence to: Samar K. Bhowmick, MD, FACE,. k$ k% R, E& @+ H1 V1 p
Professor of Pediatrics, University of South Alabama, College of
) e4 v+ A' ]* C5 j: ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 F! B; L) M3 ye-mail: [email protected].
) u7 U- g7 q3 P3 W& l! y' J$ Rabout 6 to 7 months old, which progressively became
( q( v" F5 m) E4 @, z' Cdarker. She was also concerned about the enlarge-
( D$ |4 ?8 V, `  A$ u# p' P& Hment of his penis and frequent erections. The child0 n, B" h$ B! }& |" _
was the product of a full-term normal delivery, with' X4 Z! Z! W. R3 U+ x* `4 G  @
a birth weight of 7 lb 14 oz, and birth length of
* m! T& j' O' N) P/ N+ X6 {20 inches. He was breast-fed throughout the first year
( Y; {' C4 ?7 cof life and was still receiving breast milk along with
: {! q) I% _  P1 ~$ L0 J0 v; B, Esolid food. He had no hospitalizations or surgery,
- ]" t  @1 q: Xand his psychosocial and psychomotor development6 F) i! y8 a$ F  [6 v2 Y0 e; b
was age appropriate." D/ u: g. ~( Z. Y" p
The family history was remarkable for the father,
6 `8 s8 q6 B. Cwho was diagnosed with hypothyroidism at age 16,
& l9 e# [' B1 [8 L- Y8 [which was treated with thyroxine. The father’s
8 Q/ t8 W1 p! t- C  O! s4 Mheight was 6 feet, and he went through a somewhat! u/ e/ }4 h6 x/ M$ d) M4 E
early puberty and had stopped growing by age 14.
- L9 ^6 l, f+ kThe father denied taking any other medication. The
+ ~( O! T/ v( H) s% ychild’s mother was in good health. Her menarche1 i+ d  z, B7 d
was at 11 years of age, and her height was at 5 feet; p1 \" J: \% K; z, M1 t/ e9 P' J
5 inches. There was no other family history of pre-
; f4 ^. Z: p4 A% q7 scocious sexual development in the first-degree rela-
! U8 x; E) r; w5 V# rtives. There were no siblings.7 R4 K$ @' f/ c' d$ D
Physical Examination
' m6 }# r0 u6 w9 W8 i/ RThe physical examination revealed a very active,3 C6 j' Y9 O9 w2 H0 N6 i/ W
playful, and healthy boy. The vital signs documented" |2 i# P; R% F# D$ V" x% ^
a blood pressure of 85/50 mm Hg, his length was) n) K( U0 {2 Q. d% k  j0 T
90 cm (>97th percentile), and his weight was 14.4 kg
# d+ c! u3 H! K& e- W& _% u$ ^(also >97th percentile). The observed yearly growth
2 e% |2 v# m; ^* V2 \7 P" F0 Qvelocity was 30 cm (12 inches). The examination of
* O6 Z# c" w: p1 p4 E. Cthe neck revealed no thyroid enlargement.6 l9 S3 a: W9 f3 `$ ^" e9 l# C
The genitourinary examination was remarkable for
1 L6 i% H& a8 s5 ~* j' n3 Senlargement of the penis, with a stretched length of0 N( b) {$ [2 P: X1 V( k" i2 j
8 cm and a width of 2 cm. The glans penis was very well( Z0 o. C+ d/ d
developed. The pubic hair was Tanner II, mostly around
8 \* g( u0 `+ D* y# ~540, l) A2 ~7 @, W. g# ~/ k" M
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ _* s* E- d/ P7 n) [
the base of the phallus and was dark and curled. The7 U* p" c; m: _* I5 E) H. U
testicular volume was prepubertal at 2 mL each.
2 Z9 e7 n. ~! G6 a- s" j" MThe skin was moist and smooth and somewhat8 J7 O7 a+ O$ C2 W( j! S9 C
oily. No axillary hair was noted. There were no
4 ^/ r0 V4 k) U: s' c) labnormal skin pigmentations or café-au-lait spots.
/ x8 m: N- q% K0 v# ]Neurologic evaluation showed deep tendon reflex 2+
1 A* R6 R. O* b5 J1 E" Obilateral and symmetrical. There was no suggestion
4 B: Y' o# [% p6 c7 u) Bof papilledema.
1 U; D+ ?; N5 a* K( H+ K( r6 uLaboratory Evaluation
0 Q! F# X3 P1 F$ tThe bone age was consistent with 28 months by
! m0 ~0 ?) X: Q" \1 {using the standard of Greulich and Pyle at a chrono-% t: h, u& {  z' n
logic age of 16 months (advanced).5 Chromosomal
: w- T& A1 o4 J/ ckaryotype was 46XY. The thyroid function test
: E- v. u7 _; L6 K7 Qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 Z- ^  N$ E% B. D: V5 Hlating hormone level was 1.3 µIU/mL (both normal).1 p4 J3 g( G; ]) N! b8 O
The concentrations of serum electrolytes, blood
$ _" s; k: o) ]5 ^+ Hurea nitrogen, creatinine, and calcium all were
8 O+ Q3 z9 v' g1 K8 Y! l# swithin normal range for his age. The concentration& y: t0 V+ b8 |: D
of serum 17-hydroxyprogesterone was 16 ng/dL; p+ a" h% Y% e* J" f3 `
(normal, 3 to 90 ng/dL), androstenedione was 20: {3 O/ W2 T& Q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ _3 z& S, G# I0 D7 |3 U
terone was 38 ng/dL (normal, 50 to 760 ng/dL),7 b; C1 R6 ~' Z% X! o" R
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 w  L* t, z. U5 q' Z
49ng/dL), 11-desoxycortisol (specific compound S)
6 \. _6 K5 Q2 e( S/ N3 _was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( t" P; a; [% X- i
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
# h( N: t  J4 o3 c8 q) etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 K5 c: n, ^! h% u
and β-human chorionic gonadotropin was less than4 B1 P; H- y- l9 I9 g
5 mIU/mL (normal <5 mIU/mL). Serum follicular% x( s* ?! T  e7 S7 ?9 q8 B$ o
stimulating hormone and leuteinizing hormone
; m5 \8 Y! u, U( \2 p3 d0 Vconcentrations were less than 0.05 mIU/mL
& Z7 s% E7 F" T0 P(prepubertal)." l4 a- F5 m6 Y6 ?0 m4 L
The parents were notified about the laboratory- v% e# A5 N: Z$ l
results and were informed that all of the tests were
% o3 w2 |0 S7 H7 Q4 x! k- c5 \normal except the testosterone level was high. The
% ]: x& g/ g; k/ F5 l9 w! P& L6 j+ n/ wfollow-up visit was arranged within a few weeks to
, D5 `2 b: G/ q# j# M( q& i7 h) M" dobtain testicular and abdominal sonograms; how-
3 e5 ^+ L3 H2 |, o" p& Q. Q, B$ Zever, the family did not return for 4 months.$ r! m9 z3 z8 O! ]- j
Physical examination at this time revealed that the, v& k& R6 E9 e) V- c) C9 u
child had grown 2.5 cm in 4 months and had gained# X3 d* ~9 S# `/ L% a- c2 _( R
2 kg of weight. Physical examination remained
4 Z3 ^3 X  _& G# iunchanged. Surprisingly, the pubic hair almost com-
  h2 s$ S+ Q& V" npletely disappeared except for a few vellous hairs at
) a" T! O% O7 W8 ?. g3 k9 Bthe base of the phallus. Testicular volume was still 2* y+ l9 w0 {) {' t* {
mL, and the size of the penis remained unchanged.
2 O: B) _& M  C) D' k1 \* `The mother also said that the boy was no longer hav-
2 r& ]+ e$ `$ k" ming frequent erections.5 ?) v9 `& x: A- f- K& e8 O& l! A5 {6 q
Both parents were again questioned about use of
% u7 g" A0 Z" y- M' Jany ointment/creams that they may have applied to
) `7 i3 p% @+ x" P/ k; [: ithe child’s skin. This time the father admitted the
; q; |, C. M) ]7 k0 c. ETopical Testosterone Exposure / Bhowmick et al 541
9 h( ]2 U( B1 V3 {" q: B6 ?use of testosterone gel twice daily that he was apply-
. F) H1 a! p+ Ling over his own shoulders, chest, and back area for
$ I" v0 a0 P' h% i) k- y. xa year. The father also revealed he was embarrassed
; e5 N; Y; W, J; ]9 ^& {, ato disclose that he was using a testosterone gel pre-5 M% i/ b5 `/ t* D' m1 i
scribed by his family physician for decreased libido  l; {& j' a8 ]4 v' t, B
secondary to depression.
5 ]  Y2 w7 U5 k! ~* C8 hThe child slept in the same bed with parents.& J; `! F( i: j0 |# D
The father would hug the baby and hold him on his
) b) W/ h0 L! D# ]9 o# Tchest for a considerable period of time, causing sig-
) |; L; G- W& f5 a. ^* _nificant bare skin contact between baby and father.
) ?* e. i3 C( f) V6 lThe father also admitted that after the phone call,3 Z$ o. j% a% u" k. k- _  e
when he learned the testosterone level in the baby
. l) s( o: s! ?# w' f5 B( w! kwas high, he then read the product information2 _/ n2 w' `4 `6 E" O% H
packet and concluded that it was most likely the rea-1 F) a& r5 X) E& L0 B9 @$ x
son for the child’s virilization. At that time, they. d, W  ]( q* `% b# [* q
decided to put the baby in a separate bed, and the9 W/ ]- ]# O; ?" Z" z/ f5 n
father was not hugging him with bare skin and had- I% }6 y9 X8 q7 Y" J  g+ v+ S/ K2 J
been using protective clothing. A repeat testosterone
/ M% [/ a4 y" y& l# b3 Q. dtest was ordered, but the family did not go to the
6 H9 h& ]( O5 ~- }. q9 Vlaboratory to obtain the test.
0 L6 Q4 X; F- P4 L* i! _Discussion5 D! r/ [$ x- T& t' W" v
Precocious puberty in boys is defined as secondary
% P* p  c5 r7 L+ W- Jsexual development before 9 years of age.1,4
6 |( i* K/ d4 U5 V3 f7 g4 wPrecocious puberty is termed as central (true) when4 Q( {8 ^9 R' |- `2 H
it is caused by the premature activation of hypo-/ N- [+ n* N! c) b) s( A
thalamic pituitary gonadal axis. CPP is more com-
2 ?. ^% i2 y6 G( C$ v/ t- cmon in girls than in boys.1,3 Most boys with CPP
: l( t* ~: V& A( b: M) Nmay have a central nervous system lesion that is
" Y: l. l+ m7 o! d! ^) j* vresponsible for the early activation of the hypothal-  }2 U9 \0 A! q) x9 n
amic pituitary gonadal axis.1-3 Thus, greater empha-- g" q6 W1 v3 b2 }* j
sis has been given to neuroradiologic imaging in( Q9 g+ D8 u% `+ @
boys with precocious puberty. In addition to viril-1 ^1 ~9 v$ T% t8 L$ {, N" R
ization, the clinical hallmark of CPP is the symmet-5 o- [2 u4 c  ]( o/ _' W/ P
rical testicular growth secondary to stimulation by
( {3 b. a' j, A' L3 Ugonadotropins.1,3& O5 h. p  [4 @; `
Gonadotropin-independent peripheral preco-, [& a" H! e5 h# T& c5 `
cious puberty in boys also results from inappropriate
. I8 |  L' r* g) `/ H7 Handrogenic stimulation from either endogenous or
8 l3 k; o, ?! W" f3 Cexogenous sources, nonpituitary gonadotropin stim-" `9 \- P. Q$ q; v( a! Z9 v- _7 |
ulation, and rare activating mutations.3 Virilizing
* i3 }. f) \8 |3 d4 {# Tcongenital adrenal hyperplasia producing excessive4 K6 x/ B' ~6 Z3 m% ^' m! y
adrenal androgens is a common cause of precocious1 o5 H( s. z, `- M9 y) ?
puberty in boys.3,4  n) ^* g  ?6 o+ h9 g2 B4 s6 H
The most common form of congenital adrenal
/ g5 u) {- A2 g& x" j8 P  _" p6 U$ Rhyperplasia is the 21-hydroxylase enzyme deficiency.  G* r4 U5 V" p) [5 r
The 11-β hydroxylase deficiency may also result in* {" }& m8 o% l. T; s9 v* c" a
excessive adrenal androgen production, and rarely,
5 A/ A: B9 @# {an adrenal tumor may also cause adrenal androgen
- y6 E) N6 V9 ?9 G* D4 g- Qexcess.1,3
) Y& t- `2 q$ @) i: P0 bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 U9 _* K9 w8 B( I+ J
542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 N" K7 f# D& \- m
A unique entity of male-limited gonadotropin-
) E% r9 Z* t( w8 }. F6 \independent precocious puberty, which is also known
0 T. `1 o5 }5 K' S& H& R) gas testotoxicosis, may cause precocious puberty at a
2 D; t8 @  j8 a1 X1 T0 Wvery young age. The physical findings in these boys
) r/ o; r* S( B: D+ }0 P& @& dwith this disorder are full pubertal development,* Y- c2 Y! m/ Y* d) z
including bilateral testicular growth, similar to boys
; L2 I: n1 ^* Z/ `0 r8 ]with CPP. The gonadotropin levels in this disorder
5 y% M& F+ f/ Z6 ?are suppressed to prepubertal levels and do not show% I3 W9 N1 p7 h8 ^
pubertal response of gonadotropin after gonadotropin-
$ L) N; H, Q" Y& W' Wreleasing hormone stimulation. This is a sex-linked
3 o, D3 l) q; ?6 k/ e: tautosomal dominant disorder that affects only
" o* }1 |$ e$ bmales; therefore, other male members of the family
! F9 g  n: V& {3 `may have similar precocious puberty.3( v0 O2 ?, E" R6 U% Y0 A! v. |
In our patient, physical examination was incon-; {7 K/ C9 F2 ^3 [9 b3 T( K
sistent with true precocious puberty since his testi-
5 D  X! Y1 ?2 \: E! G5 w# O. e1 o& wcles were prepubertal in size. However, testotoxicosis
. Z, ^* y3 [: s( \was in the differential diagnosis because his father" s$ X. _+ w  A' H% h7 _7 @) {
started puberty somewhat early, and occasionally,$ \4 B! U3 v# y+ n$ J3 p
testicular enlargement is not that evident in the
  ]) h& N7 Z5 b+ G. s9 G$ Xbeginning of this process.1 In the absence of a neg-
5 @+ D( r, h; T6 H& q/ k# _ative initial history of androgen exposure, our
& N' B$ K# V3 c. u& J5 H4 V5 dbiggest concern was virilizing adrenal hyperplasia,  \* d" v+ s' a# ^2 @6 J
either 21-hydroxylase deficiency or 11-β hydroxylase
5 Q  u7 _6 {. W) |7 d4 xdeficiency. Those diagnoses were excluded by find-
( R: l; x/ F' \/ cing the normal level of adrenal steroids.) M" k$ R9 x+ Y6 x# M
The diagnosis of exogenous androgens was strongly
: t& e7 L; y7 _8 l! Qsuspected in a follow-up visit after 4 months because$ S# V1 R- N( L2 l5 e
the physical examination revealed the complete disap-
3 ^; m8 [+ {$ ?0 D6 L5 mpearance of pubic hair, normal growth velocity, and2 ~9 g% j; m4 F1 y4 E. z
decreased erections. The father admitted using a testos-
* r% a7 t3 a/ ~. c3 b- R. Y6 lterone gel, which he concealed at first visit. He was3 z' ?9 ^' d, j% A! ]
using it rather frequently, twice a day. The Physicians’
% e3 I8 I. V0 i; s% C( a' a: |Desk Reference, or package insert of this product, gel or
$ l! H  r* S: G" bcream, cautions about dermal testosterone transfer to
6 U7 Z: a, W, I  w+ aunprotected females through direct skin exposure.
" c! |" m! l4 LSerum testosterone level was found to be 2 times the0 `1 }) U4 X. ~
baseline value in those females who were exposed to5 @7 i6 m4 }# l4 s' F" M- K
even 15 minutes of direct skin contact with their male$ D1 C* J8 @9 F) ?# Z6 I8 U
partners.6 However, when a shirt covered the applica-
7 o  b% @4 p9 e4 S. q' {2 }& `tion site, this testosterone transfer was prevented.. k. g9 V1 L3 W( T) j
Our patient’s testosterone level was 60 ng/mL,+ d5 H& Q) h/ A4 p( `
which was clearly high. Some studies suggest that
# _5 P" q2 k, l8 ~dermal conversion of testosterone to dihydrotestos-' I, O5 t1 V2 K$ o! G' j
terone, which is a more potent metabolite, is more9 x0 O4 Z, P$ A2 M$ E+ D4 K- o
active in young children exposed to testosterone
0 l$ P$ z  x1 b. T, v  \- Z& A; {exogenously7; however, we did not measure a dihy-
# H8 P) G; W4 g# A, e( pdrotestosterone level in our patient. In addition to' A* I. @  q( ~; j# Y
virilization, exposure to exogenous testosterone in" m' }5 ?! j, O8 h, I7 l( R0 ~
children results in an increase in growth velocity and
# O; T/ F  \9 Madvanced bone age, as seen in our patient.# D5 |  d$ S, p7 W: h. v
The long-term effect of androgen exposure during, n) J# |$ R) k* t% _! u  n. T
early childhood on pubertal development and final" t  J/ O, n$ b
adult height are not fully known and always remain
, [. {: @8 J% ^6 W& x% G2 La concern. Children treated with short-term testos-
1 n1 n( p2 ?5 i/ Nterone injection or topical androgen may exhibit some0 U$ S  A$ \7 J% w$ H- Z  `
acceleration of the skeletal maturation; however, after* T+ f- w% N% G. y3 a1 |
cessation of treatment, the rate of bone maturation
" h2 f: O4 T) q, ~1 K2 r- C6 ]decelerates and gradually returns to normal.8,9) \1 i% M6 F' z6 I2 w5 {  `, b
There are conflicting reports and controversy
+ W4 l1 W& C$ S) m; _over the effect of early androgen exposure on adult9 n% l) P$ d6 n" i; O
penile length.10,11 Some reports suggest subnormal
4 J3 l* I2 f7 s8 uadult penile length, apparently because of downreg-
) B5 @0 B/ ^( I" Tulation of androgen receptor number.10,12 However,' X4 U3 F. Q+ G( W: d1 c
Sutherland et al13 did not find a correlation between6 J& I( ?; L; `6 S" }4 F
childhood testosterone exposure and reduced adult
) I4 F1 z1 N* X2 k; Z5 ^penile length in clinical studies.
- ^( `' X6 R8 h0 F. ~' i! s9 h$ vNonetheless, we do not believe our patient is5 Z+ Z' t3 d! f
going to experience any of the untoward effects from* f+ i: f8 c, j4 y4 O
testosterone exposure as mentioned earlier because
; u. w& }% s3 H. ethe exposure was not for a prolonged period of time.8 \4 a! [8 g4 ?, q
Although the bone age was advanced at the time of
0 Y5 A/ A; G' `4 k' L5 \; ]- e1 Ndiagnosis, the child had a normal growth velocity at
! j, n' V. w1 Y9 o$ ?; cthe follow-up visit. It is hoped that his final adult$ y  J( Z* [" k- S5 S$ j: q
height will not be affected.
1 K3 F5 O$ s4 W* e0 G1 q. J, _. tAlthough rarely reported, the widespread avail-3 }; M& F+ q- s( @, ~
ability of androgen products in our society may: t: n! c* E% W8 {0 x
indeed cause more virilization in male or female
+ X( J$ e' l) t4 E. B0 c3 mchildren than one would realize. Exposure to andro-
' E4 z8 W; L: j$ r) k4 mgen products must be considered and specific ques-' |7 K% A* w  [: T; B
tioning about the use of a testosterone product or
; q( }- Q1 a/ `  ^6 n0 Ggel should be asked of the family members during
7 j  R9 w0 R5 K% h. g9 a: Fthe evaluation of any children who present with vir-
( z/ u. c- Y: v6 `2 U% gilization or peripheral precocious puberty. The diag-& W! ]7 b! I- {) i+ S
nosis can be established by just a few tests and by
: M. b' F$ D0 C, s6 `/ gappropriate history. The inability to obtain such a
3 ?$ Q4 Q1 \- shistory, or failure to ask the specific questions, may! T0 L. X2 H; f; e. q" n; N; o
result in extensive, unnecessary, and expensive4 f, P. o- L5 \. a$ t
investigation. The primary care physician should be
- Y; P7 S3 z3 a! U3 faware of this fact, because most of these children8 ~# |  L* F  O( e$ z: |4 Q! F; P
may initially present in their practice. The Physicians’
0 |- Q3 k3 R: z+ R' t' z- @+ F; W+ XDesk Reference and package insert should also put a
# R& x$ k  b5 [warning about the virilizing effect on a male or
* h$ V- O4 B6 z1 C* ]- l" K( q8 ]" yfemale child who might come in contact with some-4 w+ z, \8 }& s
one using any of these products.& T' F& k4 R# c: \0 Q% ~$ g6 }$ {: g
References
2 |1 ~" U# ~+ g, d1. Styne DM. The testes: disorder of sexual differentiation
* c  S2 q5 r( G4 U7 yand puberty in the male. In: Sperling MA, ed. Pediatric
9 n6 I4 G! R; e" tEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ N0 W1 m. w5 D3 ~2 }4 `: g7 E4 W2002: 565-628.- i( V4 q  E# F. y; h1 E2 n
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ o3 q) F. Y, k8 E& {% [9 q/ G+ ?puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

$ H/ `. o0 z. l4 k( X4 F/ D& _7 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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