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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( x1 G! l* T4 q7 A( H; ?$ |
Boy Induced by Indirect Topical
' i5 c2 i2 G- a" l1 M! i( ~1 tExposure to Testosterone, ?4 s& m" N7 T" n( w
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
: \4 `! Y9 I: oand Kenneth R. Rettig, MD1
# o7 \! ^/ |2 M- J5 uClinical Pediatrics
2 l" ?  J: d1 m% N$ B' }( d4 d& TVolume 46 Number 6+ ^0 A" x- K* _9 |" l0 ~
July 2007 540-543* @% l4 c1 z- j6 s! r! T
© 2007 Sage Publications1 y" e- u6 A: c3 t% M
10.1177/00099228062966514 C) [. e7 M0 C9 x
http://clp.sagepub.com6 \% b# g' z# J$ e1 j0 H* u4 K: D9 r
hosted at
- J& l, r; o! I0 {  lhttp://online.sagepub.com. O2 f; d3 {2 {5 u! o
Precocious puberty in boys, central or peripheral,- k" b" W5 R2 u" C3 M/ T
is a significant concern for physicians. Central
6 ]' \$ v( p, F% C, q% p' iprecocious puberty (CPP), which is mediated$ z  Z  E: {# y; X
through the hypothalamic pituitary gonadal axis, has, ~$ _3 r: m+ ~7 D) ~: ~
a higher incidence of organic central nervous system; v8 E) p% r. _3 k! x8 {4 q( A( |
lesions in boys.1,2 Virilization in boys, as manifested; e: ?/ @+ `; D4 }3 k) K
by enlargement of the penis, development of pubic
  H+ L; H; k; ]' Whair, and facial acne without enlargement of testi-$ q0 X2 ^, K/ r0 e$ E
cles, suggests peripheral or pseudopuberty.1-3 We; O$ o9 a; p7 u! r" ^
report a 16-month-old boy who presented with the
+ E5 {& @) S# |2 x  c+ qenlargement of the phallus and pubic hair develop-
% T/ r$ e4 S7 j0 xment without testicular enlargement, which was due0 X3 ?6 g0 l; j; p
to the unintentional exposure to androgen gel used by
" k3 l. V5 J6 Othe father. The family initially concealed this infor-( y! i: U' Z' d& x0 [6 c
mation, resulting in an extensive work-up for this' D* X1 W6 O8 v
child. Given the widespread and easy availability of+ o: L1 w+ A4 ?- T+ `! v
testosterone gel and cream, we believe this is proba-
1 g2 S3 E1 Z. X8 Ubly more common than the rare case report in the
( A% E2 S4 `8 t: o/ xliterature.4* \; _: D; E1 a9 s9 z. M
Patient Report* Z* g$ g! O" m
A 16-month-old white child was referred to the
6 ?; J2 o9 _8 {/ q9 }$ n6 ^- Iendocrine clinic by his pediatrician with the concern
  S! B! [" s! j  r. P6 Y' Vof early sexual development. His mother noticed4 t0 F' K; p% `: Q3 Z% G- T
light colored pubic hair development when he was) @3 T/ \9 ~  Q! w9 k: s' l
From the 1Division of Pediatric Endocrinology, 2University of
& |$ `7 w& l$ t' a9 |South Alabama Medical Center, Mobile, Alabama." T  Q5 X" |! M6 n- M
Address correspondence to: Samar K. Bhowmick, MD, FACE,0 u# _; O( s- M
Professor of Pediatrics, University of South Alabama, College of' u9 j; y5 _; x9 T
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ }6 T6 ?* V# X
e-mail: [email protected].
  Z* y0 l9 X% {! y5 ]/ u3 x! Babout 6 to 7 months old, which progressively became
7 o* K! @' H5 V3 ]. m1 }: ]: }. I% udarker. She was also concerned about the enlarge-; V) ~, T# \0 b
ment of his penis and frequent erections. The child- k  Z( @2 w" m" ~$ K/ p
was the product of a full-term normal delivery, with/ E% \1 N& w* J$ L6 S$ @
a birth weight of 7 lb 14 oz, and birth length of
! ]+ f, _# ?! g' ?8 K4 V3 @! K20 inches. He was breast-fed throughout the first year% T# i& Y, O. g( q' L0 _
of life and was still receiving breast milk along with
6 e5 G2 \* d2 fsolid food. He had no hospitalizations or surgery,
; s+ F! t) @- r  }5 sand his psychosocial and psychomotor development- n1 C/ }8 w- ^1 b
was age appropriate.) ^% b! M( Q0 v2 `9 J' A% O: X  M
The family history was remarkable for the father,
8 D2 v. M7 ?8 H0 p3 f* Twho was diagnosed with hypothyroidism at age 16,  l' W( T' x. G1 X1 I7 o
which was treated with thyroxine. The father’s7 M. _6 A$ e4 p8 q- v+ ]' N
height was 6 feet, and he went through a somewhat9 ~, A( Y; M- }! R  q
early puberty and had stopped growing by age 14.3 Y( e+ u, u) D, G
The father denied taking any other medication. The5 t! @6 a1 t5 P* l: D7 |* v
child’s mother was in good health. Her menarche! s6 K( {% q5 f% I" X6 M
was at 11 years of age, and her height was at 5 feet
. k- m' v* N. a# o5 inches. There was no other family history of pre-
+ t8 g- T1 P' z! xcocious sexual development in the first-degree rela-  w1 x8 Y  G6 x! w" p4 Q% y
tives. There were no siblings.  q/ W4 h9 S6 @. Z  N8 C( X
Physical Examination
% w/ Y9 ~/ \6 b2 f) ^2 lThe physical examination revealed a very active,2 R! h/ Y' {6 M4 p( C
playful, and healthy boy. The vital signs documented* |& T5 \; W2 g% a7 `0 x; i' g
a blood pressure of 85/50 mm Hg, his length was/ t/ M  ]9 E/ s- a0 q4 u% D
90 cm (>97th percentile), and his weight was 14.4 kg
- l! r8 N. q, k% b(also >97th percentile). The observed yearly growth
0 I1 U9 J" `, k8 Vvelocity was 30 cm (12 inches). The examination of! H8 ~* c0 F: ^' {0 Z# b4 o( {0 k/ z: D
the neck revealed no thyroid enlargement.
  b/ s9 N* H' p) v' I8 \- _The genitourinary examination was remarkable for
" ]9 [# r, ^, v1 I) h9 venlargement of the penis, with a stretched length of7 Y: J: X- E2 y% j
8 cm and a width of 2 cm. The glans penis was very well8 ~) U7 I/ {. i9 b7 n6 ~
developed. The pubic hair was Tanner II, mostly around: A2 f& l$ G' l" {) U1 Y5 H* u
5408 [/ g6 ~1 g5 s. r8 K6 I0 ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* J) _2 O2 z3 e7 w" t/ k# ~the base of the phallus and was dark and curled. The
( x5 w& `- A+ J( Z7 j0 r; stesticular volume was prepubertal at 2 mL each./ _  K+ I5 h8 R# X, u- F
The skin was moist and smooth and somewhat# O9 W$ `3 J3 K& E9 s" \; y
oily. No axillary hair was noted. There were no/ p9 l6 s3 ^& r: b7 M
abnormal skin pigmentations or café-au-lait spots.* q) q. C5 Z* m* X/ r6 g
Neurologic evaluation showed deep tendon reflex 2+5 L4 }  `- w- j% `. ]
bilateral and symmetrical. There was no suggestion
- [0 K% N+ c- nof papilledema.
5 @  z& B/ {+ H+ X/ ~6 a0 }Laboratory Evaluation
4 h& l0 ]. @! a9 u+ X  F7 YThe bone age was consistent with 28 months by
: U) p+ k0 ]: N5 [using the standard of Greulich and Pyle at a chrono-' \! F& E/ j3 Z/ g9 l) r/ z' {
logic age of 16 months (advanced).5 Chromosomal
4 ~$ i8 W4 K# _* skaryotype was 46XY. The thyroid function test, k, a! `* O6 T
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
; Q) D' x3 f$ klating hormone level was 1.3 µIU/mL (both normal).
% k! {# p1 ~5 S9 ^! r& fThe concentrations of serum electrolytes, blood3 K8 @" v4 M& E/ j% F
urea nitrogen, creatinine, and calcium all were
9 Z$ t9 a5 R0 V, Y) ?5 d* ewithin normal range for his age. The concentration# s! k7 j: h- s+ W
of serum 17-hydroxyprogesterone was 16 ng/dL
- b8 D0 `! p+ q" [(normal, 3 to 90 ng/dL), androstenedione was 20' P- o" L2 B; M
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: w( D) c4 c# m+ Tterone was 38 ng/dL (normal, 50 to 760 ng/dL),
" T  D. s2 p& \8 |9 x* b* ndesoxycorticosterone was 4.3 ng/dL (normal, 7 to
; a0 Y7 C+ ?; Y* y49ng/dL), 11-desoxycortisol (specific compound S)8 \7 X2 X1 y" W" Z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 z9 F* m0 W, F& d; s2 U. ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
/ t9 ?" ?" i/ V# F$ ktestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) C5 m* f8 x( o0 D& ?- fand β-human chorionic gonadotropin was less than
) ~7 f+ N8 N0 b" O0 a+ Z5 mIU/mL (normal <5 mIU/mL). Serum follicular' b! m$ ?2 ~1 x8 A) ?8 i# K
stimulating hormone and leuteinizing hormone3 L( s" i& K2 W- I5 X
concentrations were less than 0.05 mIU/mL
& s" H. B, m8 D6 Q0 l4 k- o(prepubertal).
' ?: A7 `) z2 l. J! QThe parents were notified about the laboratory$ ~% V; y& g" J
results and were informed that all of the tests were: D/ q# [  V: Y0 }. Z6 c2 }5 w
normal except the testosterone level was high. The
2 `4 h* E2 p2 zfollow-up visit was arranged within a few weeks to: p5 H6 ]2 X5 s" x; G0 T( f
obtain testicular and abdominal sonograms; how-
# \4 z5 E, {2 R  C# ^& Xever, the family did not return for 4 months.. e2 X- u! k* Q" ?! ~
Physical examination at this time revealed that the3 i# y3 u; I: j* c+ E/ e- F
child had grown 2.5 cm in 4 months and had gained, l; O+ l5 s+ b" @$ [
2 kg of weight. Physical examination remained- ~/ v9 D1 `% P2 B
unchanged. Surprisingly, the pubic hair almost com-$ O; C! v# ~9 H5 Y( q, U, Y4 i
pletely disappeared except for a few vellous hairs at
: t; k0 l9 }( g4 Q! X. j% Rthe base of the phallus. Testicular volume was still 2- ]5 ]- e2 H+ a& h5 _- V! U
mL, and the size of the penis remained unchanged.) A2 B5 t8 J2 I* ^" g7 ]
The mother also said that the boy was no longer hav-
7 ?0 f. g3 K; \) U8 `! r9 R7 bing frequent erections.
$ w) f; d8 |1 v. CBoth parents were again questioned about use of8 \% T2 F' [3 L; s: `" A
any ointment/creams that they may have applied to
, u. }2 D1 _5 J/ dthe child’s skin. This time the father admitted the
$ Y7 M. ?) Z+ H. CTopical Testosterone Exposure / Bhowmick et al 541
- }: ]; t" o. ?" zuse of testosterone gel twice daily that he was apply-
7 l; W& d" I2 x. V/ f6 C, ^" A/ {) xing over his own shoulders, chest, and back area for5 ~+ i! ?$ u: p# o1 M$ Q0 J) x
a year. The father also revealed he was embarrassed
* v9 A( s4 T9 q; N  d: gto disclose that he was using a testosterone gel pre-5 J% f7 ]7 ?3 t+ ]4 V  [& k, Q
scribed by his family physician for decreased libido
* D: u: M# l6 S" m; h& i& Zsecondary to depression.
9 z# j- E# |* \1 ^" c6 \! |The child slept in the same bed with parents.
5 m3 k) }: K4 ]8 g2 RThe father would hug the baby and hold him on his0 I& Z5 L" @) y
chest for a considerable period of time, causing sig-' R; s! ^( J% }2 g+ K
nificant bare skin contact between baby and father.
2 _, b/ V6 a2 c3 H" n$ tThe father also admitted that after the phone call,
6 i( q6 q* Y8 m! {' C+ qwhen he learned the testosterone level in the baby! @8 }1 n( ^2 F+ ^( }7 D
was high, he then read the product information, x) ?$ M; E+ T/ ^) M) u. J3 s
packet and concluded that it was most likely the rea-
! p, Y. [. m9 J' F1 k3 R/ G& ^son for the child’s virilization. At that time, they
! N6 H; [( {6 K" G, y( }) Pdecided to put the baby in a separate bed, and the' x" Z6 H+ ?7 M3 ]- w- `$ C
father was not hugging him with bare skin and had& e: F8 V" ?: G* _
been using protective clothing. A repeat testosterone
' ~7 W- `9 `: z3 ?test was ordered, but the family did not go to the6 q! m9 ]" O8 E, G: _
laboratory to obtain the test.
1 N: {2 M' u, E& qDiscussion
7 `- @# G$ A% F9 m, YPrecocious puberty in boys is defined as secondary
& d* q/ Y$ a0 e/ x2 @5 vsexual development before 9 years of age.1,4% ]! W$ {8 U$ W
Precocious puberty is termed as central (true) when0 [7 t0 a- M  B- |0 d
it is caused by the premature activation of hypo-
1 W+ n' Z# _1 G) o6 Y( rthalamic pituitary gonadal axis. CPP is more com-6 `& w. v; I' |9 {
mon in girls than in boys.1,3 Most boys with CPP  V$ n3 A! F' m/ |
may have a central nervous system lesion that is
! ~' t% }4 M4 T5 r2 D& m$ @6 Jresponsible for the early activation of the hypothal-# x# H; ^: J% C" b# E% v
amic pituitary gonadal axis.1-3 Thus, greater empha-
9 J* _" v9 x# z6 L. asis has been given to neuroradiologic imaging in" C9 K9 f2 m/ i3 e
boys with precocious puberty. In addition to viril-
7 a3 }- a4 x7 {0 G6 ?1 Xization, the clinical hallmark of CPP is the symmet-
9 r- F0 h# w* b* V- ?' g8 urical testicular growth secondary to stimulation by" V  Q" @3 j6 X: q5 S$ ?# X
gonadotropins.1,3
! G0 U* P" U% C' }3 a+ w0 r' U' @Gonadotropin-independent peripheral preco-
( F  {; [* h/ {0 A, Z5 {cious puberty in boys also results from inappropriate3 g. O; x  o, p. n+ ~# c
androgenic stimulation from either endogenous or# W( }' l. S3 }9 b
exogenous sources, nonpituitary gonadotropin stim-
+ n, T$ j: l  H$ Yulation, and rare activating mutations.3 Virilizing, G5 l' k7 P$ g
congenital adrenal hyperplasia producing excessive% I( E6 ^6 e2 }1 e
adrenal androgens is a common cause of precocious
% m! I) _) F3 ]7 ~$ q$ Cpuberty in boys.3,48 a2 z8 T, b5 h/ t$ E  k* M
The most common form of congenital adrenal  }7 ?0 B2 D2 z* u- @
hyperplasia is the 21-hydroxylase enzyme deficiency.5 h4 ?9 }* G4 d4 V
The 11-β hydroxylase deficiency may also result in0 \' ~- d8 [  k' `: W1 l
excessive adrenal androgen production, and rarely,# V7 l/ h  F$ i  y
an adrenal tumor may also cause adrenal androgen
( o( H* W* O: ?4 b) Texcess.1,35 e) `9 ]+ [4 [# I9 P2 S
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  D  s9 N( f+ |; U* X2 ?7 a542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ u5 c8 N' P1 E2 l  e
A unique entity of male-limited gonadotropin-
$ w# {: n0 Z" findependent precocious puberty, which is also known9 K1 r8 E! z' m* q' q: E- c, w' C- {
as testotoxicosis, may cause precocious puberty at a
; Y( [' n1 b' S+ g/ t1 k5 Gvery young age. The physical findings in these boys5 i4 z8 k1 L5 S7 ?8 m7 x" s
with this disorder are full pubertal development,$ o6 N4 O3 h6 D# N
including bilateral testicular growth, similar to boys
# P# A) q4 W8 `$ i. hwith CPP. The gonadotropin levels in this disorder
5 F) |4 i* f$ @6 Vare suppressed to prepubertal levels and do not show) J; k$ q6 H) @: ~6 K; I
pubertal response of gonadotropin after gonadotropin-3 j" s% P  c# v; \
releasing hormone stimulation. This is a sex-linked% K* j0 z6 [! g  L1 R7 O4 _" X
autosomal dominant disorder that affects only" ~! I, R9 m& ]* g" S- v
males; therefore, other male members of the family4 W2 ]6 {" F: `" D' ]* U+ a
may have similar precocious puberty.3
/ O. Q+ K4 f7 _! K& P  rIn our patient, physical examination was incon-$ x: p9 K4 }- H; q4 {' V% c
sistent with true precocious puberty since his testi-
( ^! X  y) `$ q( jcles were prepubertal in size. However, testotoxicosis
) @  s- Y2 P( V3 }was in the differential diagnosis because his father$ B8 a8 z3 n" j8 }; Q3 a
started puberty somewhat early, and occasionally,
( g7 F' p: {) t% g9 X8 T1 Otesticular enlargement is not that evident in the, C) G2 H& K1 C0 n
beginning of this process.1 In the absence of a neg-
( E" G( V# X; ~8 @* m4 ]ative initial history of androgen exposure, our
7 v' H" f. R% t( }4 g5 J! lbiggest concern was virilizing adrenal hyperplasia,5 o' j3 A) l' e: l' T) r3 ^) \1 X
either 21-hydroxylase deficiency or 11-β hydroxylase6 g% _% E- c, s% L0 I( K" z* B( C
deficiency. Those diagnoses were excluded by find-
- d; t& m7 `! E- c. Bing the normal level of adrenal steroids.
3 E9 D7 m. ?1 \3 r+ j) aThe diagnosis of exogenous androgens was strongly
/ ^1 v. I$ T& O' X" U: Dsuspected in a follow-up visit after 4 months because/ {: v4 z9 e; b3 H
the physical examination revealed the complete disap-3 C3 g, R. k& u6 g; i: B0 z! g1 B
pearance of pubic hair, normal growth velocity, and( D$ E$ s: N& K6 e  t1 v! k7 ^
decreased erections. The father admitted using a testos-
! R. J5 t6 q! c7 E2 u( g, f8 nterone gel, which he concealed at first visit. He was7 J0 r; m% ~! R# X. W
using it rather frequently, twice a day. The Physicians’
/ T& t1 I$ v4 }+ _$ R) B8 X  V" O5 nDesk Reference, or package insert of this product, gel or7 W2 O- f( X; {
cream, cautions about dermal testosterone transfer to
+ u2 ^% N' }' gunprotected females through direct skin exposure.
; ^/ H9 i+ U/ q. a$ s) _/ ASerum testosterone level was found to be 2 times the
5 W- k& O2 ]8 `: K3 T% M" _' Zbaseline value in those females who were exposed to: g# B  s. k5 D- N3 `
even 15 minutes of direct skin contact with their male) R5 ~) o" ^! W9 o% z4 d
partners.6 However, when a shirt covered the applica-; X2 o8 T' Z3 R. L- H
tion site, this testosterone transfer was prevented.
0 P- o' T$ _2 t- bOur patient’s testosterone level was 60 ng/mL,
: `+ Y( w$ L" Jwhich was clearly high. Some studies suggest that/ X% H9 d9 Y4 t1 o; D
dermal conversion of testosterone to dihydrotestos-* d: f6 {2 P# E6 F) ^
terone, which is a more potent metabolite, is more" l( J  `8 n! ]( f3 E: u
active in young children exposed to testosterone; }" \1 P% l5 v) N: w
exogenously7; however, we did not measure a dihy-
( C4 o  Y, h7 \- d5 Z+ |1 B6 edrotestosterone level in our patient. In addition to
0 e' |2 }( G$ _4 h: @) L# H4 Q  Vvirilization, exposure to exogenous testosterone in
- [" d- i0 G1 V: h$ `children results in an increase in growth velocity and
* q* D  D" q+ l9 i& V3 aadvanced bone age, as seen in our patient.
$ z  z, ]7 d# n) a# F# {- g& GThe long-term effect of androgen exposure during5 f& z7 |! u1 P! b1 `0 j) {
early childhood on pubertal development and final9 E+ y; X, E3 h) c) l$ e
adult height are not fully known and always remain
1 D; Y- ?  A! b2 E) {a concern. Children treated with short-term testos-
2 ~' a! M" K- W/ e* d2 Bterone injection or topical androgen may exhibit some& S! y7 ~) S0 L* F; ~8 U9 Q7 W
acceleration of the skeletal maturation; however, after
2 N; V; g7 J1 `cessation of treatment, the rate of bone maturation
+ U5 f/ d3 }* ^  u, ~3 \: q1 H8 Fdecelerates and gradually returns to normal.8,9& R( {! |  |8 L, h3 X) z
There are conflicting reports and controversy
% c- R  N* @1 u* U- y5 oover the effect of early androgen exposure on adult  N0 G  m. s4 I- A4 D/ t1 E
penile length.10,11 Some reports suggest subnormal+ U8 d" B7 E. H& F
adult penile length, apparently because of downreg-, C& M. @& ]/ V1 X  V3 U
ulation of androgen receptor number.10,12 However,/ v7 G7 H& f& v  V1 c% q; q  S! p
Sutherland et al13 did not find a correlation between
0 j' H# C% _" D1 s9 N+ Pchildhood testosterone exposure and reduced adult$ m4 y4 N4 W: h" K: v  E
penile length in clinical studies.' x9 c' T+ @' d$ k4 ?+ h
Nonetheless, we do not believe our patient is& D) z" S9 T# B0 k2 a  |  [# \  g4 o
going to experience any of the untoward effects from
/ X4 y& o* F7 h4 ]& t3 Utestosterone exposure as mentioned earlier because
8 C) @: O1 G- C/ Jthe exposure was not for a prolonged period of time.
' y1 a% r, j  u6 KAlthough the bone age was advanced at the time of
1 O; n! e4 ^8 ^- p3 ?diagnosis, the child had a normal growth velocity at  }8 I/ E/ \9 a; X3 \) i! M
the follow-up visit. It is hoped that his final adult
& a9 {7 M& c  X6 L/ C- ?9 Jheight will not be affected.6 t( C# H9 j% N" m1 B1 e
Although rarely reported, the widespread avail-
2 b- S7 G' `$ Q( ]  lability of androgen products in our society may+ P1 v, `) q; }" O$ M6 ~* G! O
indeed cause more virilization in male or female
) K& O5 c+ l8 Tchildren than one would realize. Exposure to andro-$ F- z. }0 h0 C
gen products must be considered and specific ques-
% Z# g9 ?; I: Z6 h$ ntioning about the use of a testosterone product or
3 ]% E/ J! p/ g+ h/ m7 Cgel should be asked of the family members during- `$ ]5 a* W/ H- y  E' }" O- |/ u/ h
the evaluation of any children who present with vir-
& ]3 s$ T& p  u9 o! g2 w8 o" c3 gilization or peripheral precocious puberty. The diag-
# v5 i* e' D: M8 Unosis can be established by just a few tests and by
5 t: t% i8 {9 T) Tappropriate history. The inability to obtain such a
) B* P0 j1 b1 @; o6 ~& g1 [8 C$ Jhistory, or failure to ask the specific questions, may
4 K: k: Y* N6 m: _7 B" C7 Rresult in extensive, unnecessary, and expensive, ^9 E8 Y* q' v
investigation. The primary care physician should be9 u* C8 v2 ?# q5 B6 X
aware of this fact, because most of these children
' `0 g$ ~: R  ^) M8 j9 g( L+ }+ imay initially present in their practice. The Physicians’' E* S1 r$ v9 n5 W
Desk Reference and package insert should also put a
) l( t8 r  m1 [* C8 P4 Rwarning about the virilizing effect on a male or
+ X/ d3 G4 L7 L4 _7 M$ efemale child who might come in contact with some-8 K1 [  @* T( g6 }
one using any of these products.
! S. w$ ?( x( Y* y/ F' a+ XReferences
4 z$ a- ?6 _+ x* T5 ?  g1. Styne DM. The testes: disorder of sexual differentiation
  u4 `) b6 F  i4 \( H% [and puberty in the male. In: Sperling MA, ed. Pediatric
0 {- L( n8 u- ?* jEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" e/ I, q- k+ N* d+ ]' d
2002: 565-628.
! M1 D$ r$ C% D9 Y5 _- {2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 J- L# ~9 T9 r, w6 G! `% W1 ]1 bpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
: @- Y  m7 O/ |% O/ cBoy Induced by Indirect Topical
4 X1 p; A* ]4 S/ |7 O- }Exposure to Testosterone
, ]  c. b: [0 s( v4 RSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
) o( x$ _$ M/ c" Fand Kenneth R. Rettig, MD13 n4 N: \/ E5 k, R
Clinical Pediatrics, k2 o# [; I6 }
Volume 46 Number 6
, F7 G8 v" B& r, IJuly 2007 540-543
( `$ W/ ^) v- v4 R" K% o% h© 2007 Sage Publications
. F* ~+ v; h  U6 ?' [10.1177/0009922806296651
$ v. r* s  f9 m+ X+ I# Vhttp://clp.sagepub.com$ R$ O% B2 R" Y; V+ Z7 D
hosted at9 a7 g3 H# V7 |' o4 m; b
http://online.sagepub.com
% b! t" W$ E5 R+ Q+ X: R8 sPrecocious puberty in boys, central or peripheral,
+ T" e6 j8 z2 d/ J* X3 X$ Kis a significant concern for physicians. Central; A- p1 G1 \2 m* v. y* x
precocious puberty (CPP), which is mediated
  Y( _8 o% H: ethrough the hypothalamic pituitary gonadal axis, has6 q; _" E* x5 k& x5 q6 F) f0 F
a higher incidence of organic central nervous system2 U: [/ G8 n2 R8 |8 n$ k
lesions in boys.1,2 Virilization in boys, as manifested
; A# f( h+ {5 j* C0 r3 Mby enlargement of the penis, development of pubic
6 t9 K# s8 k' i5 Q' ~; `+ P% Ihair, and facial acne without enlargement of testi-: l* ?: |& j( y! L
cles, suggests peripheral or pseudopuberty.1-3 We8 ~/ _& M& y  `4 v6 }
report a 16-month-old boy who presented with the
0 _+ P" ^/ y5 Qenlargement of the phallus and pubic hair develop-( d$ c7 _: }3 k+ t
ment without testicular enlargement, which was due: k6 d9 g" G9 G: }, U  [
to the unintentional exposure to androgen gel used by
5 _1 ]' z2 ~' }7 [+ u! m9 Lthe father. The family initially concealed this infor-8 f) t& L# m" H0 d1 [
mation, resulting in an extensive work-up for this$ G: d  I3 q# `( `8 H9 n, ^
child. Given the widespread and easy availability of
4 u8 ?1 G- P. y  ^2 J9 {testosterone gel and cream, we believe this is proba-4 }2 D+ p  e* j9 `* {# }( r! {
bly more common than the rare case report in the6 t: o3 ]$ f6 r8 H) C/ u& }
literature.4
# I. g3 C/ Z, L! t( bPatient Report+ V! Z/ E1 ~# f9 w4 u
A 16-month-old white child was referred to the4 v6 O  U9 P3 J( C4 O
endocrine clinic by his pediatrician with the concern
, g, {+ l2 q4 jof early sexual development. His mother noticed
" J( }  X- n# u6 k7 c- M! E  \light colored pubic hair development when he was
" Q0 x0 a$ h6 E9 WFrom the 1Division of Pediatric Endocrinology, 2University of. @6 o9 S) e" V) i3 W
South Alabama Medical Center, Mobile, Alabama.; x) V* N8 }: L, x
Address correspondence to: Samar K. Bhowmick, MD, FACE,1 w" }8 [* l. J! j1 j
Professor of Pediatrics, University of South Alabama, College of
" y4 b' h4 ^/ v2 a) o6 sMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 x+ \5 g4 {- `3 Y0 n1 \
e-mail: [email protected].
6 N& X- b8 l; H0 l' pabout 6 to 7 months old, which progressively became
1 l; G9 J6 I9 Xdarker. She was also concerned about the enlarge-2 \+ i* E; H, u* n+ W
ment of his penis and frequent erections. The child; e& M& m  e' z2 U/ p. K+ v
was the product of a full-term normal delivery, with5 K3 m7 l0 {3 w
a birth weight of 7 lb 14 oz, and birth length of
4 `; C4 J3 g+ d2 q! J20 inches. He was breast-fed throughout the first year
# j. _5 G: d+ U6 H# ?of life and was still receiving breast milk along with
2 z% R" k2 T; D- P6 s6 L/ O0 [solid food. He had no hospitalizations or surgery,, `# n7 i* N8 Q, B' I4 i
and his psychosocial and psychomotor development; L& ^' L( A& V# G  Q
was age appropriate.
  x* P0 T. o/ X. f! k! ]The family history was remarkable for the father,
9 k  l0 F" }, R/ _7 Vwho was diagnosed with hypothyroidism at age 16,
& s: M3 E, v, vwhich was treated with thyroxine. The father’s; G# {' {6 y) q' ?) {
height was 6 feet, and he went through a somewhat
' I; u) s( K# c2 ~  |4 searly puberty and had stopped growing by age 14.! V) d# Y# B# r  D( c' S
The father denied taking any other medication. The$ x0 N' ?9 O% K+ ^: v1 N5 S
child’s mother was in good health. Her menarche. a. G" b5 Y$ m7 _/ a3 M8 L
was at 11 years of age, and her height was at 5 feet$ K- u* V. i$ Q. m# G! w
5 inches. There was no other family history of pre-9 k+ I2 A6 m& s! W
cocious sexual development in the first-degree rela-+ B! W: @: G( W, v& O5 A
tives. There were no siblings.
( R6 ?; {9 M9 T% @Physical Examination
  i! s% V- r8 k1 A5 V- `7 TThe physical examination revealed a very active,. B) P0 ^. u& C2 \9 A1 ^, z; R
playful, and healthy boy. The vital signs documented$ G  S; f6 I* D) d1 S, |
a blood pressure of 85/50 mm Hg, his length was( D+ S2 Z5 M8 j
90 cm (>97th percentile), and his weight was 14.4 kg
4 L$ @- v8 @5 N( T& E(also >97th percentile). The observed yearly growth' t5 s% r3 `+ c1 o3 R6 {; r5 b( ]
velocity was 30 cm (12 inches). The examination of
1 P' H8 z% W( O1 l' L8 wthe neck revealed no thyroid enlargement.' `7 F2 M& w) H2 n0 g" }% W0 P
The genitourinary examination was remarkable for
- X; w; n6 V6 l8 E/ senlargement of the penis, with a stretched length of% \6 ^  i: S0 E8 Z
8 cm and a width of 2 cm. The glans penis was very well
' @& s6 m. d. p" g8 Z  ]- kdeveloped. The pubic hair was Tanner II, mostly around
. z6 |0 ]  [0 A8 |1 C  s540
) R! C& E. ?  f' @3 j8 k. h& `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 ~" C$ r" q  P$ E
the base of the phallus and was dark and curled. The" L5 g/ ]0 J. Q! t8 Q
testicular volume was prepubertal at 2 mL each.
: b, ?- H% z# `  y3 c3 pThe skin was moist and smooth and somewhat# w: s* W# y: K9 ^
oily. No axillary hair was noted. There were no
; ~8 i3 M0 p2 h; q9 A( K3 I, babnormal skin pigmentations or café-au-lait spots.2 j3 P# R. J" Q6 S
Neurologic evaluation showed deep tendon reflex 2+3 G$ y( t+ p3 D" u( \9 k
bilateral and symmetrical. There was no suggestion
: |, p5 [9 T3 P/ k3 {' Bof papilledema.% H( I" i3 A1 n4 t$ E) F
Laboratory Evaluation9 e, z0 Q- G# L
The bone age was consistent with 28 months by
* ~) `0 D5 R& @: q4 ~& ^- [+ ausing the standard of Greulich and Pyle at a chrono-$ k8 [0 v7 H* p1 m& E
logic age of 16 months (advanced).5 Chromosomal
) M7 V7 \- b$ |, J' x1 Y6 T! Fkaryotype was 46XY. The thyroid function test
- A/ J& T1 @& `5 mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-2 r6 W/ j& j' D, k; M; j
lating hormone level was 1.3 µIU/mL (both normal)., {/ o/ X+ d' a; R. U* g4 G
The concentrations of serum electrolytes, blood
5 Q+ s5 s" X) F* |urea nitrogen, creatinine, and calcium all were* G$ K1 I- `3 j& C" c, L$ U
within normal range for his age. The concentration
6 w4 ~! v/ O6 Q$ n1 Hof serum 17-hydroxyprogesterone was 16 ng/dL7 V0 ?  x5 t6 Q9 ^/ {
(normal, 3 to 90 ng/dL), androstenedione was 20
) V- ^) D( z; q3 E8 ]ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' y5 H2 V' G) M3 i0 `+ G- fterone was 38 ng/dL (normal, 50 to 760 ng/dL),
& {# x2 Z- D( U( Rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to1 V: J. w6 e/ B5 ~$ q& Z
49ng/dL), 11-desoxycortisol (specific compound S)
# m; D! ?7 T8 W" J* u- P$ Nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
+ |8 D* ]; B6 Z" J2 T/ X) Ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% c3 D* i9 o$ w4 f* Vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),) i2 x( V0 M8 D5 O/ U! X0 W- k
and β-human chorionic gonadotropin was less than
% f" q) B, T. I% F3 G8 \5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ V" d; T/ W3 U6 W; @( |. l5 ?( s! \stimulating hormone and leuteinizing hormone
! v1 u7 P- b1 F* }3 ?! uconcentrations were less than 0.05 mIU/mL
3 R4 {$ s0 j' C(prepubertal).
2 v6 Q" j6 {$ k6 r% \: b' K% y. SThe parents were notified about the laboratory8 D3 u- H8 y# K0 J2 D5 ^+ \
results and were informed that all of the tests were
1 M4 E! @( J( C& |. |( |* Pnormal except the testosterone level was high. The% l1 R! b+ l0 ~# J* b4 A1 G
follow-up visit was arranged within a few weeks to1 g! {) a% m  Z9 Y; x0 A  K
obtain testicular and abdominal sonograms; how-
/ w0 i+ Z( N! y% \0 h) z" Kever, the family did not return for 4 months., M0 R( f  i; t
Physical examination at this time revealed that the, t2 _" i7 |7 G( Q
child had grown 2.5 cm in 4 months and had gained+ E5 s6 G8 w/ ^6 d. F. t6 a
2 kg of weight. Physical examination remained
) e( a- I% _# ~* _5 ]6 Punchanged. Surprisingly, the pubic hair almost com-
0 W' J1 O2 G* T2 d' kpletely disappeared except for a few vellous hairs at
+ a) h; K3 Q/ K1 Q9 V; W1 Wthe base of the phallus. Testicular volume was still 2
/ b5 h1 m) n' u' A8 ?mL, and the size of the penis remained unchanged.5 V7 ], C' `2 @5 [
The mother also said that the boy was no longer hav-
, u7 c0 I6 V/ c# Z2 T6 ring frequent erections.
, S1 W$ M" J% \: [' OBoth parents were again questioned about use of
6 a" h$ v/ A( f; g' [any ointment/creams that they may have applied to0 q' b) P& w6 Y% r( M# w
the child’s skin. This time the father admitted the$ f* b: K9 X' S
Topical Testosterone Exposure / Bhowmick et al 541; r4 B, a$ Z/ \7 J) J
use of testosterone gel twice daily that he was apply-
" O5 i  r' x& e8 J. ling over his own shoulders, chest, and back area for
0 E1 B8 e, a7 s4 `a year. The father also revealed he was embarrassed% V6 x& K1 {% N
to disclose that he was using a testosterone gel pre-
$ u+ ]  k- c" s6 |scribed by his family physician for decreased libido
, j$ A  v: g/ ?  a0 d4 k; ?secondary to depression.
9 ?$ y4 ?, g, L- j7 u, m! Q9 h& X, RThe child slept in the same bed with parents.
% Z* o) G% [5 _7 AThe father would hug the baby and hold him on his! z8 L1 l. s7 T# H1 j" u
chest for a considerable period of time, causing sig-
, o: {1 f0 @# N: c$ {nificant bare skin contact between baby and father.* v# E) @8 b% S% r9 P, ]* P' G
The father also admitted that after the phone call,: a0 S. N7 Q3 u& g- }) y: u0 d
when he learned the testosterone level in the baby
; F7 Q' f; [) M5 [, t* P6 k/ @was high, he then read the product information
6 Q% y1 R5 N; R+ q* v8 F" Ypacket and concluded that it was most likely the rea-
% Z+ F; F$ E, _son for the child’s virilization. At that time, they1 _- C; W; ^4 p0 A5 L+ V  K$ k3 s
decided to put the baby in a separate bed, and the/ `* B& L! f  p0 l) u
father was not hugging him with bare skin and had8 J/ t8 B  m. I" O
been using protective clothing. A repeat testosterone
- q/ {: @7 F0 @7 ?. R& y; Y% Z# Dtest was ordered, but the family did not go to the3 H, C- |* W9 k
laboratory to obtain the test.( {* ?" F; R0 s8 Z1 i
Discussion% R: h& }. H' R7 B5 h& Z  t
Precocious puberty in boys is defined as secondary4 s/ c! a  Y5 O- u$ I
sexual development before 9 years of age.1,4, ?; u8 V. |5 J  u- h& i
Precocious puberty is termed as central (true) when
. R2 S; f2 u! W. a" h3 eit is caused by the premature activation of hypo-) G4 q- P- h3 B+ i
thalamic pituitary gonadal axis. CPP is more com-
8 p! O4 C+ J( W' O( o6 bmon in girls than in boys.1,3 Most boys with CPP
+ Z2 B8 u6 o9 B! X7 ?% \0 _, Smay have a central nervous system lesion that is. z: w2 Z' L) ~. d- K: |
responsible for the early activation of the hypothal-
1 f& |2 [  J9 e8 L7 P: famic pituitary gonadal axis.1-3 Thus, greater empha-. ]* E0 u; P+ U, U5 t
sis has been given to neuroradiologic imaging in; }& l- p1 I3 [% ]* |8 Q) c1 m$ _( [
boys with precocious puberty. In addition to viril-
1 R: c4 A/ I/ y1 ?6 \, v# X) W5 D# Tization, the clinical hallmark of CPP is the symmet-. a7 A8 F- b! {, n0 R# |, x
rical testicular growth secondary to stimulation by# F& W0 b/ k2 Z* I
gonadotropins.1,3
/ y3 k/ ]9 _) P/ h, o4 _! tGonadotropin-independent peripheral preco-
! e9 _4 t, t% r- v- o& N3 @+ wcious puberty in boys also results from inappropriate
- S" i0 b% d1 [( B3 K% Aandrogenic stimulation from either endogenous or! Q# }) C/ Y  \3 w' _# \( V
exogenous sources, nonpituitary gonadotropin stim-- [0 x3 H: P, I/ C4 K
ulation, and rare activating mutations.3 Virilizing& S) q1 k& h( W) E, t# F
congenital adrenal hyperplasia producing excessive
/ s2 A3 i8 p2 r; O( Vadrenal androgens is a common cause of precocious- A" G9 U1 H- \: Z5 f
puberty in boys.3,4. V; f  m/ B1 G! o- ?' V- W  g
The most common form of congenital adrenal
" M. m+ G! h' W& fhyperplasia is the 21-hydroxylase enzyme deficiency.
' x2 V1 g  m6 x/ VThe 11-β hydroxylase deficiency may also result in
2 W/ A& N6 U. Jexcessive adrenal androgen production, and rarely,
7 B* n4 a) O9 N3 N2 m- Uan adrenal tumor may also cause adrenal androgen
$ k( W$ y$ G3 a9 H% x2 L; G# Cexcess.1,3' q  [+ P( w7 w% @9 B1 U# `- E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, T5 d. Z  a- |* t" q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
( T" |) H7 j- e# a+ e2 D  ]A unique entity of male-limited gonadotropin-
5 b7 h0 I5 d/ U1 hindependent precocious puberty, which is also known2 M3 m+ r! r) K. W1 h
as testotoxicosis, may cause precocious puberty at a
. \) H  q6 W/ r6 U6 ?! P: Overy young age. The physical findings in these boys
' H- J& ]* U# D7 D1 J! h. b! Gwith this disorder are full pubertal development,
8 V  f6 V. p& |+ t% M% Hincluding bilateral testicular growth, similar to boys
' g, v: P3 u& C3 U( d, ]* h! Ewith CPP. The gonadotropin levels in this disorder9 O8 ^: b, M6 ^4 ?/ Z
are suppressed to prepubertal levels and do not show
! y& {0 o- n- @. S9 hpubertal response of gonadotropin after gonadotropin-0 {( D1 T7 F: j: x  F
releasing hormone stimulation. This is a sex-linked
6 B7 C( M: U( _" L+ x1 Vautosomal dominant disorder that affects only2 X* {  C5 \6 X, y- n1 J
males; therefore, other male members of the family! `" _, K- t5 w- \9 A( v5 R9 J
may have similar precocious puberty.3
( ^8 T1 ]% w6 b5 L1 v6 Y1 gIn our patient, physical examination was incon-
( d/ T5 z0 y9 I7 Q& Fsistent with true precocious puberty since his testi-
# d# ^1 j# n+ r5 N8 P6 i) Scles were prepubertal in size. However, testotoxicosis" I# {+ P+ h/ J0 O: g- k# F5 B
was in the differential diagnosis because his father
8 I# s7 q; ^) {  t" Wstarted puberty somewhat early, and occasionally,2 W# C8 D9 _1 V5 ]1 v  [2 j
testicular enlargement is not that evident in the
( D" X! r2 `/ T9 `- B% Ebeginning of this process.1 In the absence of a neg-3 P( f$ ]9 k9 Q* _8 g/ h
ative initial history of androgen exposure, our" b2 N+ G3 W# }; i" R1 e' {
biggest concern was virilizing adrenal hyperplasia,+ J4 R( ?. c" N8 J) N  l
either 21-hydroxylase deficiency or 11-β hydroxylase
  D. f& J5 r- W2 Hdeficiency. Those diagnoses were excluded by find-0 A0 r% x" ?5 p6 P
ing the normal level of adrenal steroids.1 G! U3 _1 W4 _4 q6 @$ Y2 e
The diagnosis of exogenous androgens was strongly
4 M+ {% p2 }/ v; `suspected in a follow-up visit after 4 months because2 F. l4 r& q' l* l
the physical examination revealed the complete disap-
+ [2 x: V9 e# u6 t* ~4 spearance of pubic hair, normal growth velocity, and, r9 r# ]$ i' o: W8 ]6 \  |- e
decreased erections. The father admitted using a testos-9 `/ f9 D7 ]8 o+ E, U  v5 ~/ T
terone gel, which he concealed at first visit. He was
. l% j6 ~5 i0 X2 q& {9 e* Cusing it rather frequently, twice a day. The Physicians’
1 e5 v) z  ^  Y2 y2 z3 R% lDesk Reference, or package insert of this product, gel or2 \1 X/ U; B- \6 T" E1 L
cream, cautions about dermal testosterone transfer to! R) ?+ G5 |; H# v4 O$ ]1 b
unprotected females through direct skin exposure." o: L2 i4 P* D/ i  _4 Y3 N
Serum testosterone level was found to be 2 times the
. z- l; n$ g- j) j% V* Ibaseline value in those females who were exposed to5 {) P3 ]0 d* J9 K
even 15 minutes of direct skin contact with their male
5 Y  f7 {* _0 C" O' r: K- T5 p4 _* F' gpartners.6 However, when a shirt covered the applica-" f) v: f- [1 @
tion site, this testosterone transfer was prevented.
  E" E% i% _& y0 s; }Our patient’s testosterone level was 60 ng/mL,8 @  v2 O+ v1 Y" n
which was clearly high. Some studies suggest that" W5 g' I4 D3 s* F  }0 S
dermal conversion of testosterone to dihydrotestos-% P7 x9 B# R) e* K: P) [, }
terone, which is a more potent metabolite, is more* u6 |: h( r1 e9 [, y
active in young children exposed to testosterone, G- y- S5 a# E1 |
exogenously7; however, we did not measure a dihy-( K7 N, L' ?3 V! a4 K
drotestosterone level in our patient. In addition to
* }. b% Z8 u+ m( c& T% n+ }virilization, exposure to exogenous testosterone in) u  Y- b% a  X: C$ P. h* {
children results in an increase in growth velocity and
/ [4 K, r& S2 m6 N' s+ p# v; Iadvanced bone age, as seen in our patient.. \$ [9 Z' y+ l" Y7 [
The long-term effect of androgen exposure during$ Q# ?9 g" c" |8 u4 C! q' i) B
early childhood on pubertal development and final
0 A# C' J7 ?1 a) T: ]1 j; ]adult height are not fully known and always remain
; O( T+ l# y. B) z0 S0 Na concern. Children treated with short-term testos-, G9 v& b& M1 D3 q/ T/ f
terone injection or topical androgen may exhibit some
# T2 W4 F4 r. ~/ {; |, r- M" b9 s% ~acceleration of the skeletal maturation; however, after
7 u/ b. O3 _. ~+ ncessation of treatment, the rate of bone maturation" w0 @  q4 G+ p8 n# D
decelerates and gradually returns to normal.8,90 {- V: C. Y+ J2 n) n4 _
There are conflicting reports and controversy
" x1 h; A6 O" U! D& Q' Pover the effect of early androgen exposure on adult# Y; o7 ]" _: _; b  }% Z/ H6 S
penile length.10,11 Some reports suggest subnormal
2 k; |4 @6 M' @adult penile length, apparently because of downreg-
$ V8 c1 [* @+ A$ R1 h% k8 e8 y2 }ulation of androgen receptor number.10,12 However,' g" C5 P" V5 s4 U
Sutherland et al13 did not find a correlation between3 S' z& Z7 g& \6 g. A
childhood testosterone exposure and reduced adult$ s, T* i& H! P% q
penile length in clinical studies.& S, ~$ e6 [, S# s- s$ U/ M
Nonetheless, we do not believe our patient is
: }$ K4 W1 v% Ygoing to experience any of the untoward effects from/ C  }! b' X+ k
testosterone exposure as mentioned earlier because
7 {. _6 A* F9 B# X- h* p8 `, ~$ \the exposure was not for a prolonged period of time.
2 o0 ~3 S0 E( C6 t6 MAlthough the bone age was advanced at the time of
2 h. W" I1 z0 vdiagnosis, the child had a normal growth velocity at# D' |% A& n" O0 I9 @8 d8 }& W
the follow-up visit. It is hoped that his final adult. y5 p* J: A6 n4 e, u* b" Y
height will not be affected.
" I6 |5 K7 Z  f4 IAlthough rarely reported, the widespread avail-
/ {/ x' P5 T% a) u* m) dability of androgen products in our society may# [& }! t# N% C9 U: f: K! q
indeed cause more virilization in male or female
/ P  N! T$ K2 `$ d' R+ dchildren than one would realize. Exposure to andro-
' Y# w( ~& {+ W* bgen products must be considered and specific ques-
- i6 ^# ]6 V5 O! b: U5 Y0 e8 q6 P! vtioning about the use of a testosterone product or
% }# }& Z& c% s. a& H+ Jgel should be asked of the family members during3 ~; K, Y  s  K. s# Z5 C
the evaluation of any children who present with vir-
9 }0 k+ Z$ P6 X( }; V. @0 d% @' |ilization or peripheral precocious puberty. The diag-! \! H; F. V- t6 v& Z% O1 t
nosis can be established by just a few tests and by
9 i: e$ |; o2 ?& pappropriate history. The inability to obtain such a
6 _% u/ ~. `! Q+ L" Rhistory, or failure to ask the specific questions, may# Y) E. z8 I$ \+ F( l
result in extensive, unnecessary, and expensive" f6 n$ f- Z; V
investigation. The primary care physician should be; H; c! k, [! F' Y4 T, m# y
aware of this fact, because most of these children
& |; N0 M8 P! emay initially present in their practice. The Physicians’
3 i, m2 l4 `  R6 K! i/ sDesk Reference and package insert should also put a
# f8 J( R0 Z% c% R, Z: |1 ^warning about the virilizing effect on a male or
+ w; f, f& a9 w: l/ B$ c3 Wfemale child who might come in contact with some-3 P+ Z4 j7 r# Y: x  L3 {( j
one using any of these products.
. x: V# q* w# Z5 X! AReferences
' ]* A1 h. D; I/ P1. Styne DM. The testes: disorder of sexual differentiation
4 |! s% m0 J# ^& H2 }% @and puberty in the male. In: Sperling MA, ed. Pediatric( M  i1 _, L+ E- Q* `
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: s9 D' \5 o$ s2002: 565-628.
1 A2 a4 X) l+ S" Y0 K0 F  c8 P& c4 Q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 _8 a, G! Y5 l8 |5 L" u6 o
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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

9 m" h' w3 H* F" T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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