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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- l4 u) B) a) [- G- W
Boy Induced by Indirect Topical
( j- G- E) D) z3 V; zExposure to Testosterone
  O9 k  q4 ~/ ~4 [# tSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 e% I1 `* Z2 f$ Kand Kenneth R. Rettig, MD1
; T- A7 ~$ H7 j, cClinical Pediatrics" A7 m3 L* \. h2 M; y
Volume 46 Number 63 I/ x* n/ O, D  e4 B
July 2007 540-543
$ {/ X- V1 z% |5 {8 r4 W© 2007 Sage Publications
& X9 Z( q- R3 e3 Q/ E10.1177/0009922806296651& N' O* M3 R6 O$ Z
http://clp.sagepub.com
) n0 u/ E& H- y' whosted at) G* r) l+ P+ b6 {- r+ x
http://online.sagepub.com. u. U" Z# ^' X& G; B. h" Y
Precocious puberty in boys, central or peripheral,
8 N3 X; G' I+ S2 i6 [- nis a significant concern for physicians. Central8 e, `+ }1 Y0 Y4 B
precocious puberty (CPP), which is mediated+ H+ c% Z3 a: Y% u9 y1 h
through the hypothalamic pituitary gonadal axis, has
/ j, Z  w  ?" a! U- {/ A& ea higher incidence of organic central nervous system, Z" G+ ?# Z5 {1 S8 ~! }6 U
lesions in boys.1,2 Virilization in boys, as manifested/ r4 q4 O# {7 }$ [8 W, ?
by enlargement of the penis, development of pubic
4 R3 `- D  r* z* P: c$ m9 qhair, and facial acne without enlargement of testi-! b% U; g2 Q/ n( ?* l
cles, suggests peripheral or pseudopuberty.1-3 We
3 c5 J  H% q0 y7 }report a 16-month-old boy who presented with the! e* x3 S; b  S0 i6 F' w3 ]4 f! ?
enlargement of the phallus and pubic hair develop-; b( i8 S$ ?8 W2 F5 r0 x
ment without testicular enlargement, which was due, B! f. S" I) Q1 p! ?  @
to the unintentional exposure to androgen gel used by8 E: F" C% I% H1 A
the father. The family initially concealed this infor-
5 z" V1 n1 i: q6 p: H$ N  Ymation, resulting in an extensive work-up for this- r5 z7 }1 e% H# V
child. Given the widespread and easy availability of
. g6 ^2 k  ~' ?  ?+ W4 ktestosterone gel and cream, we believe this is proba-
  r4 h8 S; g6 k4 P" X9 obly more common than the rare case report in the
6 g5 z6 h/ L# s) o0 T& Vliterature.4! \7 ]+ X3 c! N  }7 m/ a
Patient Report
$ R1 w( N7 ?: ], eA 16-month-old white child was referred to the
8 `& u3 ]9 z9 o1 I6 M# Tendocrine clinic by his pediatrician with the concern
2 s# o% }) d# @7 Y" Cof early sexual development. His mother noticed5 ^) P7 }* A+ x3 [9 q8 Y" `7 N  Z
light colored pubic hair development when he was/ \" B' s( x% V' ^3 L# m& N6 ?0 a
From the 1Division of Pediatric Endocrinology, 2University of, o; o$ g& }5 m# L4 {
South Alabama Medical Center, Mobile, Alabama.* l8 k' |/ {. A& [
Address correspondence to: Samar K. Bhowmick, MD, FACE,
& I* X$ H+ L8 P1 e4 aProfessor of Pediatrics, University of South Alabama, College of
' B! e% H* ]; r8 c5 \: @6 H+ T" TMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, @: y0 @. [) W* G- d4 T( }( E7 H
e-mail: [email protected].+ w% u5 M% N* P
about 6 to 7 months old, which progressively became
# K' w$ ~% a( U" {darker. She was also concerned about the enlarge-' ?5 n3 C" K5 O3 l7 K( S" @
ment of his penis and frequent erections. The child
! b( y0 ~3 v& _2 E: ^was the product of a full-term normal delivery, with& a; c6 L2 C  y4 v/ ?% w
a birth weight of 7 lb 14 oz, and birth length of5 f  n. s' }, ~. j
20 inches. He was breast-fed throughout the first year
6 S. ]5 z& T/ q$ I7 [9 kof life and was still receiving breast milk along with
) k) Z+ {/ r- k6 V6 M) |solid food. He had no hospitalizations or surgery,
6 V8 f8 M3 H, G# l3 L- K8 band his psychosocial and psychomotor development
; h1 {$ q  H4 l$ Nwas age appropriate.
6 n/ Y. ]1 ~' ]9 \$ AThe family history was remarkable for the father,
7 A/ G* a  v5 g6 T; Hwho was diagnosed with hypothyroidism at age 16,
2 L, m% N; {" L6 X8 [$ ]% |$ {which was treated with thyroxine. The father’s# n2 h% a: ]' M4 g4 _
height was 6 feet, and he went through a somewhat, q; K0 K6 }2 U) @! o, x) ?2 A
early puberty and had stopped growing by age 14.
+ j. ~) F$ o- I# O; yThe father denied taking any other medication. The2 N3 }! e) R6 f7 r
child’s mother was in good health. Her menarche( m0 [  b5 L* Y# K2 H8 i% w
was at 11 years of age, and her height was at 5 feet
* j1 W- I6 L, Z$ N5 \4 W$ S$ F5 inches. There was no other family history of pre-
/ L! K. Y% _4 o$ g$ `cocious sexual development in the first-degree rela-
$ t# v% Q% h9 ktives. There were no siblings.
' R: K" C% R0 m+ RPhysical Examination
5 s5 l: ]/ C  ^  R% tThe physical examination revealed a very active,
6 F$ m: z' x& {: vplayful, and healthy boy. The vital signs documented
3 @5 x) `) B: A$ a* w& T* ]9 za blood pressure of 85/50 mm Hg, his length was
- C1 L; y1 u0 @$ g& T90 cm (>97th percentile), and his weight was 14.4 kg
6 F5 R3 \2 ~1 v7 S(also >97th percentile). The observed yearly growth
) y9 Q" l2 H: z: i; yvelocity was 30 cm (12 inches). The examination of
  U- w) l* c7 ]1 j) R. O2 f$ _! gthe neck revealed no thyroid enlargement.
/ y7 G/ N9 `9 |The genitourinary examination was remarkable for& M5 Q+ ]" n% I: }! L, ^
enlargement of the penis, with a stretched length of
/ C2 D* x* w; G" m8 cm and a width of 2 cm. The glans penis was very well
, o# i5 q" I1 s) T/ K% W9 Wdeveloped. The pubic hair was Tanner II, mostly around
& Y" v; g1 l! Q( w8 P8 Q5402 P4 B# Z( W! s/ L1 m. A% d- p- K) w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ @! ]! k% {( z4 H- F5 P
the base of the phallus and was dark and curled. The
/ {$ }1 F5 a6 c6 P/ ~; E* J; jtesticular volume was prepubertal at 2 mL each./ f' ?  S3 p2 V  k8 c
The skin was moist and smooth and somewhat
& J( H% n8 u: T0 r% H$ k; J# M- Soily. No axillary hair was noted. There were no
% z' [3 h, [8 U$ g5 qabnormal skin pigmentations or café-au-lait spots.: d4 B/ a6 C9 S0 A1 c+ g& p& }
Neurologic evaluation showed deep tendon reflex 2+' J4 k+ Z+ V  p- H. ]7 `
bilateral and symmetrical. There was no suggestion- U- O( H: X3 F% P6 u% v7 y
of papilledema.
  I3 D# @* o" ~& \4 LLaboratory Evaluation
% k: V" o  F) Q* oThe bone age was consistent with 28 months by5 k" a  G5 v2 n, E8 g% {
using the standard of Greulich and Pyle at a chrono-! K+ b- _8 N; S6 q, Z
logic age of 16 months (advanced).5 Chromosomal
0 v* J' x* B7 G  k  m# ~/ Tkaryotype was 46XY. The thyroid function test6 p3 D1 o$ ]5 W# e5 s
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
" l) t5 V, a7 J. P1 D% Blating hormone level was 1.3 µIU/mL (both normal).
4 S9 Y) S/ Y7 a: Z( @The concentrations of serum electrolytes, blood8 u* @9 G$ d! V5 G
urea nitrogen, creatinine, and calcium all were
1 Y  W- r! B/ Swithin normal range for his age. The concentration- B- [5 w6 R( r0 W
of serum 17-hydroxyprogesterone was 16 ng/dL" b3 n. u) s% Y
(normal, 3 to 90 ng/dL), androstenedione was 20+ S, I  m/ e" ]3 T2 \! N- b
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 U0 j5 Y5 D+ o0 Z, w$ [  Sterone was 38 ng/dL (normal, 50 to 760 ng/dL),  S/ w# }0 U/ o; a: T
desoxycorticosterone was 4.3 ng/dL (normal, 7 to: e- _7 R$ J& [: K  o% F
49ng/dL), 11-desoxycortisol (specific compound S)
7 E+ A4 C/ v/ J- rwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 j+ i( p" c1 u) C+ n
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total  I+ h$ o# Q- u* T( d
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 c4 S" h# X/ k0 @( J. |9 y
and β-human chorionic gonadotropin was less than1 k4 W; x) ~2 r5 @, |5 Y
5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 Z7 ^6 I' t0 I* G7 ostimulating hormone and leuteinizing hormone
4 s: i! f9 z* J2 m/ J- R% T9 Xconcentrations were less than 0.05 mIU/mL; H0 v0 }! q1 C! p$ \
(prepubertal).
+ K1 ^: Z( ], Y1 P. TThe parents were notified about the laboratory2 P/ u8 @3 n. q: f- H4 ~7 n
results and were informed that all of the tests were; B* `9 k) {. Y# \- G0 D) K
normal except the testosterone level was high. The, k  {. U8 b- c# q  x
follow-up visit was arranged within a few weeks to
& b7 I* x/ v5 _% \+ i  xobtain testicular and abdominal sonograms; how-& Y( F/ R. t) b! |* {! U- |
ever, the family did not return for 4 months.
$ b" R4 K( S! R% _' e2 nPhysical examination at this time revealed that the
& L7 d# m. d6 Q4 }3 `6 X8 v7 ]2 vchild had grown 2.5 cm in 4 months and had gained
" L( v4 D/ X: N7 U0 {2 kg of weight. Physical examination remained
) i$ ]% o4 Z+ D8 munchanged. Surprisingly, the pubic hair almost com-9 i$ J6 p7 H8 r  h
pletely disappeared except for a few vellous hairs at2 m  f% h& E6 ~6 c; }
the base of the phallus. Testicular volume was still 29 x  z, J: [$ M& _; @9 r
mL, and the size of the penis remained unchanged.& `) S6 K/ w: P& I  I4 v
The mother also said that the boy was no longer hav-
: S6 j  {3 R/ y1 m4 I- b4 xing frequent erections.5 y0 M- ?/ u  e6 q. l) ~2 Z
Both parents were again questioned about use of
  `% ~6 i8 q/ iany ointment/creams that they may have applied to
4 L  A- x4 V& v& ^the child’s skin. This time the father admitted the
0 n, H9 |8 X& Y( x" }% |Topical Testosterone Exposure / Bhowmick et al 541# }# E4 ?' \$ A
use of testosterone gel twice daily that he was apply-2 {. ?1 a  K4 c5 f
ing over his own shoulders, chest, and back area for
' ]7 Y, s( e/ E4 aa year. The father also revealed he was embarrassed
9 j2 P+ X! S4 S% vto disclose that he was using a testosterone gel pre-
8 I5 Q  @0 ?" i' Lscribed by his family physician for decreased libido7 g7 a- ^1 [: Y- K
secondary to depression./ O) t6 O  v4 r' g8 B) {
The child slept in the same bed with parents.& P  |% t! x7 S" i% B
The father would hug the baby and hold him on his7 m: w' l+ o* E! T( C0 d
chest for a considerable period of time, causing sig-3 ]5 _, p' [3 D+ f- [
nificant bare skin contact between baby and father.7 y# ?; Y, X/ \3 `
The father also admitted that after the phone call,# }& t- z9 }( d, |6 M
when he learned the testosterone level in the baby
- ~$ E$ F, d( {% m4 twas high, he then read the product information5 g. _* s6 l" M2 E- x' t! t5 V8 s1 T; t
packet and concluded that it was most likely the rea-. ]  p4 l2 A0 z  _" Y  R1 `
son for the child’s virilization. At that time, they: p( ^4 N( s+ h, ]: B
decided to put the baby in a separate bed, and the$ b; N2 \( b# j" l( O, H
father was not hugging him with bare skin and had
2 @9 Z1 f. H, Bbeen using protective clothing. A repeat testosterone
7 z5 x9 H/ g# E4 g% q/ ttest was ordered, but the family did not go to the% i" x6 H8 f* `5 h" B4 ?8 N
laboratory to obtain the test.! Q! y( V3 c# B
Discussion- O% G2 U8 U8 Z% Z# C+ }4 Z
Precocious puberty in boys is defined as secondary* r, W  Q5 C! s
sexual development before 9 years of age.1,4
6 t* _5 ~: H1 S0 aPrecocious puberty is termed as central (true) when
& t1 ^/ r; c: ^; Yit is caused by the premature activation of hypo-
8 w2 V! m7 X! |+ o" `+ cthalamic pituitary gonadal axis. CPP is more com-: j7 S3 D& v1 R) c
mon in girls than in boys.1,3 Most boys with CPP2 s$ A7 O% w, X$ z2 r5 Y6 Q
may have a central nervous system lesion that is) D0 b4 I4 i3 R+ d
responsible for the early activation of the hypothal-
' b/ ]1 j( ^, u* D" s0 I4 ^/ k+ Yamic pituitary gonadal axis.1-3 Thus, greater empha-% h3 b' c) E$ Q, N( a
sis has been given to neuroradiologic imaging in6 L! |" b- O* O. o' Y: x
boys with precocious puberty. In addition to viril-
) f6 i0 e0 C- G+ Z8 ]" y% z/ Xization, the clinical hallmark of CPP is the symmet-
+ a4 v1 K  y3 Q& B1 L# l* e% F  jrical testicular growth secondary to stimulation by5 L/ @+ A3 i8 H
gonadotropins.1,3+ Z" E& p  k# o% D/ |
Gonadotropin-independent peripheral preco-6 m/ h, t- d4 a2 |. U
cious puberty in boys also results from inappropriate
  a+ E, x/ l4 U3 c  h& zandrogenic stimulation from either endogenous or0 }1 L5 V3 p* w# R. A% L% v
exogenous sources, nonpituitary gonadotropin stim-
8 Q1 c1 X0 B; S4 z% g; |8 culation, and rare activating mutations.3 Virilizing
! i/ u' ~1 T, R4 O$ f0 pcongenital adrenal hyperplasia producing excessive
+ a" H# m. x# v6 L, hadrenal androgens is a common cause of precocious: |- v1 D$ Q' D( W+ B- z
puberty in boys.3,4
8 c" P3 Q* J% CThe most common form of congenital adrenal* ?- s: D4 N. z' ^
hyperplasia is the 21-hydroxylase enzyme deficiency.
* {9 P" {7 f* R* B+ x- e- eThe 11-β hydroxylase deficiency may also result in6 a. n: ]. |' B# d4 ~6 G
excessive adrenal androgen production, and rarely,
' j9 ^. N3 E* e  b  e+ K. ian adrenal tumor may also cause adrenal androgen
3 }* G; E2 }9 }' Iexcess.1,3: |! L/ i5 y- ]& I; t2 C' B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ j$ M/ K# v; K# n" B# [; }8 s
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# l* u2 @6 T. KA unique entity of male-limited gonadotropin-
2 R# }( X: H0 Y3 a/ z' Eindependent precocious puberty, which is also known
1 F% H4 \0 Z8 ]' }8 w, f6 nas testotoxicosis, may cause precocious puberty at a, }, t% Z1 E! Y9 f5 J# U
very young age. The physical findings in these boys
$ r- d+ `# K2 Y3 h: Hwith this disorder are full pubertal development,7 J2 i+ Z1 c8 O! M
including bilateral testicular growth, similar to boys3 h2 ]- b5 f" @7 I6 U5 }
with CPP. The gonadotropin levels in this disorder( F% x+ w2 h8 i; S( C2 s
are suppressed to prepubertal levels and do not show% ~5 @7 f) }' K! l4 U0 M4 e
pubertal response of gonadotropin after gonadotropin-) a4 S! l9 [( I) P0 t- i4 K5 A
releasing hormone stimulation. This is a sex-linked
, L& z! c' @, M8 xautosomal dominant disorder that affects only& @" L- S6 S1 Z2 f5 g2 l. Q# K" c
males; therefore, other male members of the family1 L' N, }1 s6 M' J) j  G* Z
may have similar precocious puberty.3  ?, f, U& n5 ?- o: L# T# O
In our patient, physical examination was incon-
9 T0 c3 I. F' k( A/ Y8 Tsistent with true precocious puberty since his testi-
. G, [5 o& z9 ]cles were prepubertal in size. However, testotoxicosis! k$ n# Y6 u6 _- V6 C) u7 S
was in the differential diagnosis because his father6 K' S! W! C  f
started puberty somewhat early, and occasionally,
' @( m$ [# N# ], z$ Stesticular enlargement is not that evident in the
, e2 ^5 T7 [3 s& vbeginning of this process.1 In the absence of a neg-7 ]# V0 u) r7 X5 W& Z' ?3 _2 P% M
ative initial history of androgen exposure, our! v/ ?; O( \+ i6 k
biggest concern was virilizing adrenal hyperplasia,
/ r" m5 e" W# b4 ?" Peither 21-hydroxylase deficiency or 11-β hydroxylase% i% t% j# G2 f: f$ n
deficiency. Those diagnoses were excluded by find-
) l# X) F8 N( ?# O+ `, l- e  Ting the normal level of adrenal steroids.
: d! u/ H/ Q8 e6 H: g) w) b6 i& dThe diagnosis of exogenous androgens was strongly
5 p. |% u5 y$ O  J6 ~suspected in a follow-up visit after 4 months because# v7 H4 W2 d+ o. V' \. q6 k; {
the physical examination revealed the complete disap-' d+ o) n4 E1 U
pearance of pubic hair, normal growth velocity, and7 X2 J  j' g- b, P6 Q7 O
decreased erections. The father admitted using a testos-' h+ d& }* d; n
terone gel, which he concealed at first visit. He was
. Q* f. v$ o/ m' pusing it rather frequently, twice a day. The Physicians’0 a: y& D0 h" K( J2 a% A8 r, V# E( @
Desk Reference, or package insert of this product, gel or* ~2 L# w1 T3 t. B  s( O) b
cream, cautions about dermal testosterone transfer to
" T! g; _' n0 o( t: l0 M1 _unprotected females through direct skin exposure.
5 H  w. q4 L) Q& V# x8 oSerum testosterone level was found to be 2 times the
! S; S' A& n! v( }7 t, }baseline value in those females who were exposed to
% ~, k9 t- G. seven 15 minutes of direct skin contact with their male
" {6 k0 w/ b5 y8 Q4 Qpartners.6 However, when a shirt covered the applica-
1 z; L( S' F9 a" {" Q* Q3 ltion site, this testosterone transfer was prevented.
' t! n7 }* M; o! oOur patient’s testosterone level was 60 ng/mL,
( |  m4 [* g# H* o/ {which was clearly high. Some studies suggest that6 o) m! ]4 N$ A, ?: M; O" s5 }
dermal conversion of testosterone to dihydrotestos-9 I$ b- W4 T8 w9 k
terone, which is a more potent metabolite, is more/ `0 R) z; Z' T' w/ u- f
active in young children exposed to testosterone
& o% E3 q9 A) Q+ M8 N3 @, Kexogenously7; however, we did not measure a dihy-7 k5 O3 ~9 S+ X
drotestosterone level in our patient. In addition to5 L' }# {0 f+ ]1 y* ?2 P
virilization, exposure to exogenous testosterone in
4 O* T9 ^; v) i, A% H' S2 wchildren results in an increase in growth velocity and- Y$ `+ O2 T' t; t* J9 J  w
advanced bone age, as seen in our patient.
7 g# c, c* H3 m' k" S# q8 H0 wThe long-term effect of androgen exposure during
9 k& O+ ~1 M6 s& Wearly childhood on pubertal development and final
2 `. A  D  Q: Jadult height are not fully known and always remain
/ O* S2 K; f. T' X% I) qa concern. Children treated with short-term testos-
' S# M. @6 q1 wterone injection or topical androgen may exhibit some$ M$ a+ L- ]' k5 m* R# G
acceleration of the skeletal maturation; however, after2 G* m0 n5 S( Y% `( }
cessation of treatment, the rate of bone maturation2 a# K" P+ d  W
decelerates and gradually returns to normal.8,9
2 C) c; g5 C# J: k; Z9 u& _There are conflicting reports and controversy9 p7 a' e8 I8 N4 d5 h* m, M+ S
over the effect of early androgen exposure on adult
. s2 W; P" F) E" ]9 lpenile length.10,11 Some reports suggest subnormal
9 ^" i6 p. R3 i2 {/ ladult penile length, apparently because of downreg-% G+ ^9 M- s! l, o
ulation of androgen receptor number.10,12 However,
! B) D! \/ I4 ~" K+ F5 iSutherland et al13 did not find a correlation between+ R5 ?& J& @. ]( k
childhood testosterone exposure and reduced adult$ l1 \1 g1 f; ^. e0 g0 a% ^' ~) |" d% c
penile length in clinical studies./ {: y' F/ U& b9 U
Nonetheless, we do not believe our patient is
9 @0 e: v7 N+ Qgoing to experience any of the untoward effects from
5 r  n: X& O/ y& V5 @+ e4 ?testosterone exposure as mentioned earlier because
  d) P7 o- `* \% K4 I  I8 m! v$ Tthe exposure was not for a prolonged period of time.' q% M" K; M( {5 L- w, M
Although the bone age was advanced at the time of
; T2 ?2 J4 s. h" Jdiagnosis, the child had a normal growth velocity at
, X# E: a0 N6 k' r1 I& S7 v' {the follow-up visit. It is hoped that his final adult4 O* `, D# a4 F  X
height will not be affected.( g6 Z8 d1 `/ x- I# _) t5 Y
Although rarely reported, the widespread avail-
; ]3 v0 E9 \5 mability of androgen products in our society may3 `1 }! [! @  T, i- v
indeed cause more virilization in male or female
' b% ^' d, F) b, j/ ^children than one would realize. Exposure to andro-; w: P% {8 v& x% d1 U
gen products must be considered and specific ques-
: p0 L" e. o$ W3 P: Y$ K3 Ytioning about the use of a testosterone product or
+ J  ?/ V5 R$ egel should be asked of the family members during9 `& @0 ~, U# ?' A5 i# `! R
the evaluation of any children who present with vir-8 u6 |: O4 Q- C3 _) e
ilization or peripheral precocious puberty. The diag-
/ a" `6 w! s5 E: g: }nosis can be established by just a few tests and by
/ ?* W8 O; ?( t- A4 g) kappropriate history. The inability to obtain such a, c+ M, w5 K8 _* `! O$ C' J
history, or failure to ask the specific questions, may
6 Z' v& b) A0 S9 ?) S: xresult in extensive, unnecessary, and expensive
3 U) `: X; K8 w- A/ s! U# linvestigation. The primary care physician should be
8 p  U) U. e& B& p. b2 Q5 k9 T* }aware of this fact, because most of these children3 T. L- X9 B" j0 [+ ^; ]
may initially present in their practice. The Physicians’
4 T2 l; s0 l& r/ JDesk Reference and package insert should also put a
$ n, a1 o% |! S0 d" Gwarning about the virilizing effect on a male or4 D' U) i+ g- F$ G
female child who might come in contact with some-
5 n- O, u/ h1 B4 \- Pone using any of these products.
3 s8 U' c. K& U  r  W1 [References3 q, y. k4 _8 s' {- {
1. Styne DM. The testes: disorder of sexual differentiation
. t9 p% N% m9 R9 p$ C6 ]5 vand puberty in the male. In: Sperling MA, ed. Pediatric
- G( S( Y2 [, o3 H  i; |Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 y1 e- v# k% h1 W) ?3 D
2002: 565-628.# ?1 s4 [( m) |; c0 w- V5 I
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 S9 Y; L/ {' u- Y8 Fpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
% }* A1 ~- q! L7 TBoy Induced by Indirect Topical6 o/ t" I& u' d
Exposure to Testosterone
/ P  X  }( X. u6 q! B: cSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 j# f- z- R/ u
and Kenneth R. Rettig, MD1' R# |9 {2 Y% p4 B4 [( E) ~6 S
Clinical Pediatrics0 w2 Z! A# T6 m* v
Volume 46 Number 6, ]0 y' Z  x' m4 E+ U
July 2007 540-543: r5 Q0 x5 K) L/ K5 @7 S) Y1 |( `( p
© 2007 Sage Publications
4 @/ `1 D: q# c( g2 W10.1177/0009922806296651' e! d4 y% l) D! n2 `! g
http://clp.sagepub.com
8 P8 j: _8 V8 s. Y0 `hosted at
# r  t& A" ]# N$ Z* N5 X4 E3 K: ehttp://online.sagepub.com2 A  C- Y2 I% a2 r
Precocious puberty in boys, central or peripheral,2 S5 y; T2 V* M8 z) W3 i
is a significant concern for physicians. Central
) k+ J' I7 h  u  }* e! H8 }precocious puberty (CPP), which is mediated
2 }+ a6 G: K9 g' Q3 ^- r& J2 vthrough the hypothalamic pituitary gonadal axis, has8 y' e7 N7 a: U8 P  L5 ^
a higher incidence of organic central nervous system
/ b6 b0 g, T+ J& h8 z* H% O$ ilesions in boys.1,2 Virilization in boys, as manifested3 T2 j. ^& `5 b3 w( F8 L' o
by enlargement of the penis, development of pubic
# r, [* Y+ E4 \% @  ?+ p2 o  n, Dhair, and facial acne without enlargement of testi-
/ t/ p7 z1 z' t! e6 Dcles, suggests peripheral or pseudopuberty.1-3 We9 h; ]  @/ Y8 E4 n1 h. j* T
report a 16-month-old boy who presented with the6 c1 H) [9 }' [+ {1 q# D
enlargement of the phallus and pubic hair develop-5 \1 Q# }! c' C' @/ I  t  D
ment without testicular enlargement, which was due  R6 ~& Z# b5 d
to the unintentional exposure to androgen gel used by% d0 D$ X0 F, _3 v
the father. The family initially concealed this infor-
9 J9 T7 C- D2 y% `! H" A7 p4 N# Omation, resulting in an extensive work-up for this# O2 ?* w6 I& R
child. Given the widespread and easy availability of
" T* z/ M! S4 _" k- b. Utestosterone gel and cream, we believe this is proba-  \9 _8 ~$ c$ ?8 t, Z2 X
bly more common than the rare case report in the
. v5 F/ i1 H. E4 y% ?- Z  nliterature.42 n# ?$ y- U; o( `( g% W& L3 m! {) i
Patient Report
  d7 S$ P! \% i* ?$ q; l2 Q. M9 LA 16-month-old white child was referred to the
* w* z( ^4 m5 h& C1 hendocrine clinic by his pediatrician with the concern
7 M5 _' C- N# y' n8 `) ^" M) Oof early sexual development. His mother noticed& a6 g) r( Z9 A- |+ D: A
light colored pubic hair development when he was
& f* }/ N0 V# I( L  mFrom the 1Division of Pediatric Endocrinology, 2University of% m, W: _, @. `5 |  ~$ C/ s3 @
South Alabama Medical Center, Mobile, Alabama.  r( C& ?2 ^& Z- R* n' `. y
Address correspondence to: Samar K. Bhowmick, MD, FACE,* u5 ~0 S5 T; J( c; n1 _$ c8 j
Professor of Pediatrics, University of South Alabama, College of- B& v9 j2 x0 r- ]1 ]6 ^
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) X( W. ?; \0 F4 }e-mail: [email protected].# N2 O) Y9 q  ^7 {! r
about 6 to 7 months old, which progressively became9 H& i3 A& @2 ?7 s) p# K  D& X0 v8 Z
darker. She was also concerned about the enlarge-1 z0 j- x4 Q$ ?/ T, [
ment of his penis and frequent erections. The child/ |3 ~( z/ W/ i7 C! l. ~
was the product of a full-term normal delivery, with
7 z- |% U4 |0 |& Aa birth weight of 7 lb 14 oz, and birth length of
1 T( m7 _& f( P+ q& _1 n! D" W20 inches. He was breast-fed throughout the first year, P. y- j$ R7 B* t" N  F2 h4 D
of life and was still receiving breast milk along with
6 d4 E5 w( z% Zsolid food. He had no hospitalizations or surgery,
1 B& y; e; a$ X. x$ }and his psychosocial and psychomotor development2 ]3 Q# D6 c! O. D/ [2 a
was age appropriate.5 |! T! V# @/ w
The family history was remarkable for the father,8 O" C/ n! R3 ?8 s5 c9 ]
who was diagnosed with hypothyroidism at age 16,
1 y3 C% j3 j7 U& |, Dwhich was treated with thyroxine. The father’s: v/ \$ i/ F+ v" @: d" p6 t
height was 6 feet, and he went through a somewhat
$ I+ y- a4 q/ ?3 nearly puberty and had stopped growing by age 14.
( R  r* z7 g& D  B& IThe father denied taking any other medication. The6 D) J% A$ y2 s0 t8 P
child’s mother was in good health. Her menarche1 G& o5 @3 b* D  r& k  t& n
was at 11 years of age, and her height was at 5 feet" ?! J! g2 g, M! K0 W$ B
5 inches. There was no other family history of pre-
( L- i# ]7 ^# `4 ^" j+ h1 ]cocious sexual development in the first-degree rela-; D4 i  t& H; T; ^! Q' u
tives. There were no siblings.1 T1 x1 r, I" \$ I4 P, y% O: q
Physical Examination
' R; l  h. f( w' aThe physical examination revealed a very active,
3 a3 D0 o$ h) H' p5 }5 kplayful, and healthy boy. The vital signs documented# U- P' \0 c4 ]( z* d5 Y) U
a blood pressure of 85/50 mm Hg, his length was+ m3 W9 B) ~, y, C( G
90 cm (>97th percentile), and his weight was 14.4 kg% i4 |- a* O: a7 c9 K) x' P
(also >97th percentile). The observed yearly growth
3 }- {+ a$ _. C2 J- ~" bvelocity was 30 cm (12 inches). The examination of
0 S7 j9 q" _2 u; U0 \, O  ~" x3 e8 Rthe neck revealed no thyroid enlargement.
* K. g1 L9 Q% e3 `The genitourinary examination was remarkable for8 |$ Z. i5 k% N* l# w8 R" g. S4 E
enlargement of the penis, with a stretched length of
( t6 q+ m1 f; l7 [( n7 f8 cm and a width of 2 cm. The glans penis was very well
; J' f6 p% D& n+ Qdeveloped. The pubic hair was Tanner II, mostly around
5 P: X: |/ i( i( g! Z* v8 l540) q# k$ y' i6 Q6 c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  N9 T- X. f5 M2 N+ w# `
the base of the phallus and was dark and curled. The0 z' I  d2 J0 a+ T" y
testicular volume was prepubertal at 2 mL each.
: h( ^" w8 u7 I6 c+ t) q: k. ?$ |5 X) _The skin was moist and smooth and somewhat' w; k% X% u) I: V8 A- n( K
oily. No axillary hair was noted. There were no& l) ~  f3 \! t; J
abnormal skin pigmentations or café-au-lait spots.( n2 A; t/ S1 O7 V5 \+ {# \
Neurologic evaluation showed deep tendon reflex 2+8 U* E7 C2 X$ L" T- R+ @4 N- _
bilateral and symmetrical. There was no suggestion
. M6 Y1 J1 i# R; @' j% v3 }of papilledema.
5 @) g3 l7 T0 X& ]. H& q) `Laboratory Evaluation, y' K' a8 H% d6 I/ q+ V
The bone age was consistent with 28 months by0 e) C% Y: R2 Q% ~# h1 P
using the standard of Greulich and Pyle at a chrono-
5 W8 E1 M3 }) ^  J) N6 T; Q! z- P3 s$ Tlogic age of 16 months (advanced).5 Chromosomal
4 _- e3 r. i$ J: N! C! f6 |karyotype was 46XY. The thyroid function test
6 z" s9 m. J6 V4 W8 S: l$ y! O+ u/ }showed a free T4 of 1.69 ng/dL, and thyroid stimu-6 U/ Y. |9 j7 B6 N! m' L
lating hormone level was 1.3 µIU/mL (both normal).' ~  s; ~! l  S+ I
The concentrations of serum electrolytes, blood( U2 B5 J' W4 p8 ?. F
urea nitrogen, creatinine, and calcium all were" c* F( i$ T0 p  `/ g2 y5 S5 E
within normal range for his age. The concentration6 B, P4 W% S+ n& ]" g# ~& Z) Z
of serum 17-hydroxyprogesterone was 16 ng/dL& L( A& c, K$ v9 e
(normal, 3 to 90 ng/dL), androstenedione was 20' L- a- p! R+ }4 e) D4 M1 A
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 b- ^2 V) v" |
terone was 38 ng/dL (normal, 50 to 760 ng/dL),. }! ^% l7 ^& @" l5 z& F- K" m
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
" [# I- i; m! k* i8 m* T. a49ng/dL), 11-desoxycortisol (specific compound S)
; J6 Q, p4 J1 P/ [6 jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% T/ b- E0 X  L3 F. ttisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) o* f1 U( Z- {+ l  H0 H" E
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),& Z% S" L7 X. m
and β-human chorionic gonadotropin was less than
' f: e$ Z9 t& M8 O- L5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ n+ ~( b: j; t3 N1 @% @! Mstimulating hormone and leuteinizing hormone
& u8 Y& \# ~! Oconcentrations were less than 0.05 mIU/mL$ w/ q( y* O  M
(prepubertal).
% B4 ?: c# y) g- H3 T3 ^: HThe parents were notified about the laboratory+ ]+ K+ A7 f+ H$ t1 O
results and were informed that all of the tests were
% ~0 F2 c1 u' G; _3 inormal except the testosterone level was high. The
5 |$ r! J6 ?5 @" i" o  ufollow-up visit was arranged within a few weeks to, A5 C% c1 {7 L( f
obtain testicular and abdominal sonograms; how-5 y% T" z- O  E3 _% P9 o' \: u
ever, the family did not return for 4 months.! W0 b; m4 q& c$ M' Z1 U+ q1 C
Physical examination at this time revealed that the
# M- o* K9 W, ]) M6 ^/ v) {" K. gchild had grown 2.5 cm in 4 months and had gained
, @# a( X2 N$ F2 kg of weight. Physical examination remained
+ f$ K) T% b/ N6 A  P% Uunchanged. Surprisingly, the pubic hair almost com-* J: g1 B; H; n( G* j) v
pletely disappeared except for a few vellous hairs at
% [  d* G( p5 ^& V' Z/ ?9 lthe base of the phallus. Testicular volume was still 2* j9 z; K7 B1 Q
mL, and the size of the penis remained unchanged.) W/ w" b' {7 J3 A* Y* c
The mother also said that the boy was no longer hav-
2 U6 r! c7 `3 P9 ning frequent erections.
, W. n( L3 }4 m0 }Both parents were again questioned about use of& {5 x  S! p% ?' T. N$ J
any ointment/creams that they may have applied to
  ~4 k* A$ x$ `5 D; y4 O& Pthe child’s skin. This time the father admitted the
& \3 w6 ?/ G  b4 `$ ]+ W4 n5 ATopical Testosterone Exposure / Bhowmick et al 541
4 c  a1 |% i* X* y7 X% E; w3 Z  Kuse of testosterone gel twice daily that he was apply-
$ a* _+ ]- n7 t* A! oing over his own shoulders, chest, and back area for' q! q' V% ~) W( ]0 F
a year. The father also revealed he was embarrassed5 O3 w- g, t  e& }) ?. [. x
to disclose that he was using a testosterone gel pre-
) [' D5 F8 l( {1 Rscribed by his family physician for decreased libido
4 o: ]% @" S* X8 }secondary to depression.
) E' l; F7 E6 d. c* IThe child slept in the same bed with parents.) n# A! o# B! a5 ?' }
The father would hug the baby and hold him on his  ?  u6 H8 H9 ~2 G% C
chest for a considerable period of time, causing sig-
, Z/ d/ I3 b; N- [6 \1 s6 ^nificant bare skin contact between baby and father.% E. V6 P! `  p0 p$ |
The father also admitted that after the phone call,
6 L3 j4 w2 d1 L* c3 _; Jwhen he learned the testosterone level in the baby+ @9 M7 i) B" @- T/ {
was high, he then read the product information3 U- a2 G/ F1 v  m* g
packet and concluded that it was most likely the rea-
1 n1 F( D! V7 W+ R% V9 sson for the child’s virilization. At that time, they% d# f5 o6 d9 n0 u) m5 n
decided to put the baby in a separate bed, and the
. Q  p# D! m6 t8 z- r  U  T1 V9 zfather was not hugging him with bare skin and had( F/ H) A: i$ S! X' E
been using protective clothing. A repeat testosterone9 ~0 U) f0 M0 R0 n% R* Q
test was ordered, but the family did not go to the! s! N$ x. b, }) T" p
laboratory to obtain the test.- e0 a) t9 q. a6 K
Discussion
/ q9 c  H. S$ IPrecocious puberty in boys is defined as secondary
4 y, c- U, ~# xsexual development before 9 years of age.1,4
8 {3 b% m/ F8 S8 X4 APrecocious puberty is termed as central (true) when
* a& ~* N$ w( e. m1 V: `it is caused by the premature activation of hypo-
& T% I0 n/ g' Q. i" U+ e( U) w5 athalamic pituitary gonadal axis. CPP is more com-+ H5 H! W& p' c) Z0 c7 j
mon in girls than in boys.1,3 Most boys with CPP3 |6 K. Q4 U( E- i  y
may have a central nervous system lesion that is
; @0 j+ _. \/ [' K8 M' {responsible for the early activation of the hypothal-
+ w$ b6 o* q0 J; t" m; o" H0 ]$ A5 wamic pituitary gonadal axis.1-3 Thus, greater empha-
. q- Z; E- g% l  i1 psis has been given to neuroradiologic imaging in
1 @5 g( w7 w5 k7 u3 Nboys with precocious puberty. In addition to viril-
3 U: @; d( `  z8 P  _1 Kization, the clinical hallmark of CPP is the symmet-% \6 Q" @0 b; Q: e, R
rical testicular growth secondary to stimulation by! f* o( B$ h  B. D1 @4 Q
gonadotropins.1,3, _7 o, {3 v) G: {
Gonadotropin-independent peripheral preco-) m0 c" T4 q& T/ E
cious puberty in boys also results from inappropriate
' a! v6 e2 i1 H. j+ jandrogenic stimulation from either endogenous or, T, F6 Y/ l: ^
exogenous sources, nonpituitary gonadotropin stim-
; ^6 D" x/ Q: r& X0 u2 Q; w) julation, and rare activating mutations.3 Virilizing
4 R2 T' [8 v2 }" s( ucongenital adrenal hyperplasia producing excessive: q0 [# x1 Q6 `. E/ \
adrenal androgens is a common cause of precocious. M! C- @& W0 ^& i
puberty in boys.3,4- y* i2 B( ]8 A6 ?; T6 _
The most common form of congenital adrenal2 j, j/ ~) X, U( |
hyperplasia is the 21-hydroxylase enzyme deficiency.
1 b' I1 y2 q- f) l. HThe 11-β hydroxylase deficiency may also result in+ Z, D1 H& r" F: Y$ {
excessive adrenal androgen production, and rarely,0 c% X2 e+ N% l$ ?% ~# K- w2 Y7 |3 _
an adrenal tumor may also cause adrenal androgen/ |, `5 |5 [% h$ H, ~( ~' H# e/ o
excess.1,3
) X$ z6 P& t2 c1 L$ L: c. v% E8 |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, G9 H. n. ~' z$ c  w2 p+ j542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ j, F' r2 Z3 k1 }3 hA unique entity of male-limited gonadotropin-
1 u  W; d& w' T8 X* S6 Zindependent precocious puberty, which is also known$ m, K& M' |2 h/ s7 ~) f
as testotoxicosis, may cause precocious puberty at a
% i( K0 A, U. u7 svery young age. The physical findings in these boys) z! b. `1 k5 M; G
with this disorder are full pubertal development,
# S1 j! S4 r  D5 Y# `, H3 uincluding bilateral testicular growth, similar to boys
+ U# h8 v5 T, q, X% Nwith CPP. The gonadotropin levels in this disorder: f9 d3 m3 ^$ v. }7 F6 ^) {
are suppressed to prepubertal levels and do not show
) ?  F, I' h. F% j! g7 K* i1 Bpubertal response of gonadotropin after gonadotropin-
" i# k, p. T- {( w* Z$ U2 o5 Mreleasing hormone stimulation. This is a sex-linked, S& p& K( ]6 |) E9 Z* V* X6 [
autosomal dominant disorder that affects only
: D) m9 }' V; K+ _0 xmales; therefore, other male members of the family; d! q( p; U6 }+ i* t2 j
may have similar precocious puberty.3
4 A# O) e: J2 s5 D2 k/ OIn our patient, physical examination was incon-* h: L# `" K' a
sistent with true precocious puberty since his testi-) C; h$ R5 [% H$ b7 p" X8 k
cles were prepubertal in size. However, testotoxicosis
0 I- Z  z5 m( [  mwas in the differential diagnosis because his father
, S7 e' o' z: S7 E6 istarted puberty somewhat early, and occasionally,
  ~7 Z# Y6 G6 g) P0 s! c! E, g3 Y2 ?testicular enlargement is not that evident in the
& @8 t' U$ P) S/ i& Bbeginning of this process.1 In the absence of a neg-
, D, M+ k4 ~# ]  G2 p- P+ wative initial history of androgen exposure, our- g6 P1 Y. H: R/ q
biggest concern was virilizing adrenal hyperplasia,
2 |1 M; v3 K, J* \$ ?, C' Aeither 21-hydroxylase deficiency or 11-β hydroxylase
# e8 v) s2 b: Q5 k" ~8 gdeficiency. Those diagnoses were excluded by find-9 F( ^$ ?% e" D2 r  y' U: W5 m/ X
ing the normal level of adrenal steroids.
; T, K+ u( \& S9 m. BThe diagnosis of exogenous androgens was strongly8 P$ S8 r- p- {1 \! L
suspected in a follow-up visit after 4 months because, ?4 }6 V$ y+ ^/ t7 v
the physical examination revealed the complete disap-' A  |( d# p2 f: m
pearance of pubic hair, normal growth velocity, and7 u% w- l6 O1 a
decreased erections. The father admitted using a testos-5 @0 d  F3 k% f, A* Q
terone gel, which he concealed at first visit. He was* @. I7 `8 [  _; a9 X8 C3 N
using it rather frequently, twice a day. The Physicians’
. r/ o' n( c' \- u: a/ eDesk Reference, or package insert of this product, gel or: u" T2 j  v6 o1 K
cream, cautions about dermal testosterone transfer to
0 K0 z: Q( G( y7 f: bunprotected females through direct skin exposure.
6 S. c8 b/ J5 W% E% J6 f* V; }9 vSerum testosterone level was found to be 2 times the
5 `7 y6 P  [* `3 g4 qbaseline value in those females who were exposed to
$ W2 Z; _/ q( A+ w8 Reven 15 minutes of direct skin contact with their male& Z1 @# }1 z$ L* l' ?7 l# C
partners.6 However, when a shirt covered the applica-. p: U- t2 `0 t6 h, `( x  p' Y' I2 I
tion site, this testosterone transfer was prevented.6 S' u6 v* i$ R. I* L1 u, t) _
Our patient’s testosterone level was 60 ng/mL,; X- W; B' j& E0 k; z- e
which was clearly high. Some studies suggest that% W/ i$ O7 ]4 J8 l
dermal conversion of testosterone to dihydrotestos-- S/ q  k6 u  `
terone, which is a more potent metabolite, is more1 C4 Z- e9 b6 G0 }$ U; q1 O9 ^8 n7 n
active in young children exposed to testosterone' F( d1 C  g: A7 z8 y
exogenously7; however, we did not measure a dihy-
1 D% m) p! D+ X% W* zdrotestosterone level in our patient. In addition to9 P7 h: g( a2 s) t; Q5 o
virilization, exposure to exogenous testosterone in
) S; p$ ?$ j3 E. l2 rchildren results in an increase in growth velocity and2 ]. G9 T) x( ?  y  ?* N
advanced bone age, as seen in our patient.! _8 M/ d) L/ @# O5 ?1 \, w
The long-term effect of androgen exposure during
0 }5 _  D. S, {! H+ M& a, Yearly childhood on pubertal development and final; b$ R" j0 W( R- b7 D8 |% i2 l
adult height are not fully known and always remain
. f+ C+ j& {# ~, `! }3 @) V4 W; S& Qa concern. Children treated with short-term testos-- l4 ]+ z% D  y0 E2 ?# J( h; \
terone injection or topical androgen may exhibit some) o, D/ Z/ B' H4 \  o+ v3 ]' J  k# @
acceleration of the skeletal maturation; however, after
: }0 T4 E& b/ W1 K; q* fcessation of treatment, the rate of bone maturation9 b! f! [" |0 o9 ]+ U! F$ ^( }
decelerates and gradually returns to normal.8,93 y4 g0 G4 D6 @3 Z, M
There are conflicting reports and controversy
  l) a# p7 L1 s* tover the effect of early androgen exposure on adult
' B; ^- x8 Z. l. P& h0 Wpenile length.10,11 Some reports suggest subnormal, x, u; h  r! c$ b8 }$ t! }
adult penile length, apparently because of downreg-) x* A! T  s, s6 Q/ ]: [: I% y) r, I
ulation of androgen receptor number.10,12 However,2 S  C2 K1 X, e- S& |% B; o
Sutherland et al13 did not find a correlation between- W# Q1 j* C6 C% D
childhood testosterone exposure and reduced adult
# P; Y; `2 H4 L9 t0 rpenile length in clinical studies.! N- H" j1 x2 a( [
Nonetheless, we do not believe our patient is6 h( A6 i6 ^2 q' `4 l1 K3 V4 X1 J
going to experience any of the untoward effects from
9 p: e4 z+ T) U5 a4 v% stestosterone exposure as mentioned earlier because
; \" y$ n" x) Wthe exposure was not for a prolonged period of time.* H- q+ X0 a+ i2 v' e$ w4 e$ x3 a) O
Although the bone age was advanced at the time of
3 Q0 a! g9 N0 c: Gdiagnosis, the child had a normal growth velocity at5 R, R  ~- V! ]' x; K2 w0 L2 _/ L
the follow-up visit. It is hoped that his final adult
' C; w& P" c4 ~$ Y6 W9 D' Iheight will not be affected.7 j* v0 {$ z. Z. \" _6 @# h
Although rarely reported, the widespread avail-" l+ b; J0 E( R; Q; I$ B
ability of androgen products in our society may
7 y& }$ ]1 p3 L/ mindeed cause more virilization in male or female
$ h6 q7 }! I9 Q* wchildren than one would realize. Exposure to andro-
- M% X. B/ p; f" B- j5 J; Qgen products must be considered and specific ques-
2 [  X+ [* @+ ]; ~% z! o$ T' Ftioning about the use of a testosterone product or5 U+ w3 }( g" v3 a. X
gel should be asked of the family members during) Q: H6 Y- _  Q, E& A
the evaluation of any children who present with vir-+ @, ^8 `# }9 C" E
ilization or peripheral precocious puberty. The diag-
' I8 p  }6 i5 @; W) Z) Vnosis can be established by just a few tests and by: H4 x: U: c+ S4 U3 q7 w# |' Y3 X
appropriate history. The inability to obtain such a5 }7 v  ]7 l6 c0 {' O9 ^* D- M6 z
history, or failure to ask the specific questions, may
4 {" P* ?* F  @) ^* M9 J! K* cresult in extensive, unnecessary, and expensive
  O1 n& V7 |- x( U* o+ `( N& s  ^investigation. The primary care physician should be7 i, \1 b4 J4 ?; j$ q( O
aware of this fact, because most of these children! Z, a) Y/ M% ~8 J" y6 I$ m
may initially present in their practice. The Physicians’
+ |  C" t6 Q. y0 v: kDesk Reference and package insert should also put a1 S7 F) G( N% V; m$ R2 J
warning about the virilizing effect on a male or
$ P! X; i( x+ O- L3 ]. ffemale child who might come in contact with some-
" P* E0 H' _% S6 T# R4 _one using any of these products.
* f  u2 ?+ W5 ^2 p7 X6 qReferences
& T, m. Z6 R8 t4 C1. Styne DM. The testes: disorder of sexual differentiation6 l6 p) r5 w& D
and puberty in the male. In: Sperling MA, ed. Pediatric0 ^2 q4 |1 c. ^* s! L3 ?" e; N- P
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, y/ t5 r* f; H5 p- f2002: 565-628.4 i- }4 q, Z/ \6 g7 S
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' w; t0 B' s, Gpuberty in children with tumours of the suprasellar pineal
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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
. {, n% d7 C% P. ]9 m+ H
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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