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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
4 k$ p( \8 V0 \: M, s3 EBoy Induced by Indirect Topical
" o6 \, o+ v+ {8 v- p& pExposure to Testosterone  Q7 X) k: H* D% `$ K, x
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 s, s6 c0 p  |& z
and Kenneth R. Rettig, MD1+ c0 V$ O# o( r* Q% G# {8 x
Clinical Pediatrics
7 R  |0 M% q  C8 P9 u& {/ y9 o& A* BVolume 46 Number 6+ S! N1 L4 x. w- D# f
July 2007 540-543; y& S  g9 \4 Z* s/ ^- \
© 2007 Sage Publications6 U: c, p4 E5 X0 @4 C
10.1177/0009922806296651/ v2 h# Q0 n3 f3 l1 M6 ~; v  L8 q
http://clp.sagepub.com
  E/ T% S) c* W  B+ `0 Z. hhosted at
" g9 v3 u8 o* Khttp://online.sagepub.com
9 k" C- e; h. d; E/ r2 p8 KPrecocious puberty in boys, central or peripheral,+ y, d! R6 Z0 i! |
is a significant concern for physicians. Central
0 p/ u  D% T7 P! x1 S" w1 w0 Gprecocious puberty (CPP), which is mediated" R( U) t% O. f( `- \
through the hypothalamic pituitary gonadal axis, has
$ E6 Z$ A8 K' Y/ wa higher incidence of organic central nervous system
9 b- Q  m+ [6 Clesions in boys.1,2 Virilization in boys, as manifested3 @1 b' z; O( `: M! D% R" H, ]
by enlargement of the penis, development of pubic1 x% M6 f# a& B2 m6 I3 U4 J
hair, and facial acne without enlargement of testi-: h# Z. o; m5 d  q+ b" B
cles, suggests peripheral or pseudopuberty.1-3 We* F4 L, }! ?$ _' j* r
report a 16-month-old boy who presented with the
, a8 \/ O6 |+ henlargement of the phallus and pubic hair develop-
) \' l- D+ M- g& D/ Nment without testicular enlargement, which was due
: w$ y# _0 ]/ w( ]. ~" |to the unintentional exposure to androgen gel used by& m# F6 c( O: T; E8 @( p+ l. N5 R
the father. The family initially concealed this infor-9 F* S4 k' p9 Q0 n" m; L
mation, resulting in an extensive work-up for this8 P( H- M1 f8 Q6 W( h; {
child. Given the widespread and easy availability of7 [. B& G7 r  Z( O
testosterone gel and cream, we believe this is proba-
& X4 L* G' ]' l6 G$ |: Kbly more common than the rare case report in the
3 V$ {. w8 a# J3 ?; nliterature.4
$ G) E8 G% y" c, X  O  Z; r" W+ NPatient Report6 j6 Z, s1 B% I
A 16-month-old white child was referred to the
6 t; o+ |6 K- J7 r- r) wendocrine clinic by his pediatrician with the concern
& ?+ @+ I4 B$ Pof early sexual development. His mother noticed
% {0 G( l  V$ c" mlight colored pubic hair development when he was  C6 h2 f: K9 R' ~6 b3 X
From the 1Division of Pediatric Endocrinology, 2University of: f4 o9 b& {2 U/ T+ _
South Alabama Medical Center, Mobile, Alabama.% k. O2 j. A9 Y: @
Address correspondence to: Samar K. Bhowmick, MD, FACE,! ~4 W2 o4 ~8 f5 V  c  D
Professor of Pediatrics, University of South Alabama, College of8 M. v3 S" [5 P; E( N( N9 N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ l5 L* J/ m+ i/ W) R* {e-mail: [email protected].
( d. v# |0 {: c0 m/ Vabout 6 to 7 months old, which progressively became
) r! y# \7 D- {2 W$ Y6 O3 o: bdarker. She was also concerned about the enlarge-( ]: u5 Q+ p# H
ment of his penis and frequent erections. The child
; {* _9 A$ t* W% W/ [was the product of a full-term normal delivery, with
1 g" g+ N! A  `- va birth weight of 7 lb 14 oz, and birth length of$ R+ z) k3 `& i; O" L1 d
20 inches. He was breast-fed throughout the first year0 Q( U4 d" e) T
of life and was still receiving breast milk along with/ d3 m1 H9 L. R$ Z
solid food. He had no hospitalizations or surgery,
; T8 I; b9 D7 q: C7 z( [& gand his psychosocial and psychomotor development6 j3 `! h( k) }) M
was age appropriate.$ b! `6 r% R) `* c% Z+ l4 x5 N
The family history was remarkable for the father,
. x9 T, J8 C- k# T- f" Ewho was diagnosed with hypothyroidism at age 16,3 L6 }1 o/ A# m$ @+ ]' f# H8 e
which was treated with thyroxine. The father’s
* I+ Z4 ?; R( L7 Y) j7 E) Sheight was 6 feet, and he went through a somewhat
; P0 P1 w: u# x7 h. q* a+ Fearly puberty and had stopped growing by age 14.& V9 L0 N- ~2 z
The father denied taking any other medication. The" ]7 k4 E2 _2 I( n$ Y: B8 m
child’s mother was in good health. Her menarche
3 r; L- {1 f  g; f/ pwas at 11 years of age, and her height was at 5 feet7 T2 m& w, ?0 J1 Y0 |9 \9 {1 G- V+ |
5 inches. There was no other family history of pre-
2 X) F; `8 ?+ v% ~; u) Mcocious sexual development in the first-degree rela-8 j( w2 z' j2 f  @
tives. There were no siblings.
7 B9 c3 f6 R' ?0 G( \Physical Examination
* L* b1 b  y' W2 n' \! C( OThe physical examination revealed a very active,
# w1 ], h* g+ o1 gplayful, and healthy boy. The vital signs documented) W( X+ Y  m7 A- }- L, v0 p
a blood pressure of 85/50 mm Hg, his length was& e5 _' `  t- b4 h
90 cm (>97th percentile), and his weight was 14.4 kg
$ q! D% D- u" J8 v6 B(also >97th percentile). The observed yearly growth
  R/ D  c5 C% O, [. g2 Yvelocity was 30 cm (12 inches). The examination of
* P9 X, {' D1 b3 j% [the neck revealed no thyroid enlargement.# v: t3 o+ N* V/ `8 c/ M- P2 m
The genitourinary examination was remarkable for, A& q0 p7 m+ D* {* I6 z
enlargement of the penis, with a stretched length of
! s0 X+ a. u% N; e8 cm and a width of 2 cm. The glans penis was very well
  W8 ]2 h6 {4 h, g# w, }( Ideveloped. The pubic hair was Tanner II, mostly around
  H% L/ J7 y! L# E$ T540, G4 X# q6 V2 x4 m6 r6 @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* W& i3 p; S, H7 m
the base of the phallus and was dark and curled. The
% E, {, l4 K1 A3 Ntesticular volume was prepubertal at 2 mL each.
+ }0 a, N  T" o6 s* `. K/ a/ QThe skin was moist and smooth and somewhat
" f# X, o( E7 r  f! Q2 _4 goily. No axillary hair was noted. There were no( L# x- H* K6 [6 C( t7 y
abnormal skin pigmentations or café-au-lait spots.
7 O, F* U1 L( ~- {Neurologic evaluation showed deep tendon reflex 2+
! I! b; r9 c. L2 Gbilateral and symmetrical. There was no suggestion
5 W) |/ T! W! s8 E% x& T. Wof papilledema.. y8 e2 C' r/ A4 ~! n
Laboratory Evaluation
. S1 o; }/ F3 O' l9 j& F+ uThe bone age was consistent with 28 months by
/ g; l5 T- B6 W0 xusing the standard of Greulich and Pyle at a chrono-
8 X) J; I: M) M9 rlogic age of 16 months (advanced).5 Chromosomal$ B7 J! V$ L+ q8 ]
karyotype was 46XY. The thyroid function test
0 k! O' N/ z* G7 F. c1 ]showed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 `5 L8 l* q: o; P7 klating hormone level was 1.3 µIU/mL (both normal).$ Y& S0 j# V& a+ k1 L
The concentrations of serum electrolytes, blood
% h4 a, D9 ?- Q/ @+ G# b* kurea nitrogen, creatinine, and calcium all were
- a: ~' U" Y6 S( Awithin normal range for his age. The concentration
& }$ }/ N* P( _* f$ w, m2 \of serum 17-hydroxyprogesterone was 16 ng/dL
+ j. i1 @. z' ^4 R(normal, 3 to 90 ng/dL), androstenedione was 20
% E6 L& s( f! i0 p/ G* j" X$ Yng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 u8 E; R- G, p$ G: |- nterone was 38 ng/dL (normal, 50 to 760 ng/dL),
: a4 b2 x5 Y8 w; cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ ]+ |9 |9 D' m/ Z0 G6 O9 [49ng/dL), 11-desoxycortisol (specific compound S)
% @* r- @% h4 q* b; d0 uwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-$ O# E3 c1 @4 q$ ]- u% F
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& `5 \; H- R+ b3 n9 K
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ a( V$ }) ~& E+ s" u9 l
and β-human chorionic gonadotropin was less than+ m- d2 F! }2 z0 F- ?& k* f" a( ]; m
5 mIU/mL (normal <5 mIU/mL). Serum follicular
) z0 n6 c. O8 X. G! V2 x5 o8 ~stimulating hormone and leuteinizing hormone4 {, z$ B0 M( _% {  U1 `
concentrations were less than 0.05 mIU/mL) R6 I0 t( Y) |  ~4 S) m
(prepubertal).
, E4 ]& T- I+ T5 g5 [( q; nThe parents were notified about the laboratory
' T4 z. x& N, ]results and were informed that all of the tests were- W4 S- J; N) f6 y9 x2 I5 x2 f
normal except the testosterone level was high. The
. V4 l" N3 S: mfollow-up visit was arranged within a few weeks to
8 T! c' ?: R2 J0 i9 \4 c$ Iobtain testicular and abdominal sonograms; how-
8 j7 G5 O/ a; K2 T$ h6 }0 O- yever, the family did not return for 4 months.
3 I% j. O7 E6 l1 x, j1 K& fPhysical examination at this time revealed that the
4 R3 u) o. B) v0 f: G; Y( c* }child had grown 2.5 cm in 4 months and had gained- o$ B6 x% ^. J- h: X* n" U- T
2 kg of weight. Physical examination remained
: A( @* Q$ t% e+ G+ N6 |: Nunchanged. Surprisingly, the pubic hair almost com-
9 h$ \) j0 W& ?9 b" B0 Cpletely disappeared except for a few vellous hairs at# I: V% {7 D0 q" e
the base of the phallus. Testicular volume was still 2! J( b; v" `" `6 s
mL, and the size of the penis remained unchanged.
8 l* J- T9 c% ^  [2 gThe mother also said that the boy was no longer hav-, h& Y! `+ B! }
ing frequent erections.
* o# h  ~' ?8 U- o" `! OBoth parents were again questioned about use of
- j& j# t( r! wany ointment/creams that they may have applied to  F0 X4 t0 J* Y' B% F0 l: y
the child’s skin. This time the father admitted the9 |$ s) R$ a* u( H4 S
Topical Testosterone Exposure / Bhowmick et al 541! y8 J; N0 Y9 A
use of testosterone gel twice daily that he was apply-& ^1 J% ]/ M( g* v4 i
ing over his own shoulders, chest, and back area for, J( v- s+ m9 i7 {
a year. The father also revealed he was embarrassed
9 W, i" H6 k+ j. c! Zto disclose that he was using a testosterone gel pre-
3 F3 W" b7 R, D7 ~# d2 o6 c: Lscribed by his family physician for decreased libido
1 D" y  t1 @3 v( I0 K( q+ _secondary to depression.# y0 s& u5 D" Z
The child slept in the same bed with parents.
- f2 B$ P6 j& r9 E8 pThe father would hug the baby and hold him on his
& _, r) `' c. |. ^! N+ nchest for a considerable period of time, causing sig-4 j8 K; t" v* t) ]  s
nificant bare skin contact between baby and father.
$ f. d8 \% {8 [. J% H2 |' K" i+ }The father also admitted that after the phone call,, |- A3 ]4 r! H6 q
when he learned the testosterone level in the baby
' p9 f1 o/ w5 N8 H/ u6 l. l8 Fwas high, he then read the product information1 v* M% j; l9 r5 U$ z
packet and concluded that it was most likely the rea-3 l, g7 e! T& X9 w" _' }, o- [: z& F
son for the child’s virilization. At that time, they3 [1 X& C. Q/ N$ x- n, i5 v
decided to put the baby in a separate bed, and the- [9 E0 W; E. W5 P5 H: ?) A& [
father was not hugging him with bare skin and had
; N( D' ^' @# m' Dbeen using protective clothing. A repeat testosterone
$ T2 }  L$ {4 R& `/ J+ v& _8 gtest was ordered, but the family did not go to the! C3 p! |7 T0 E/ f4 O! @
laboratory to obtain the test.% r( S, p- R, }2 ?6 _$ y9 j
Discussion0 ^9 {  `3 t4 Q1 W; H) R& T" g
Precocious puberty in boys is defined as secondary
: r" y# W3 u2 N7 {4 Qsexual development before 9 years of age.1,4- S. R* C* S8 I! s- j4 T3 q
Precocious puberty is termed as central (true) when; R. {! ~( V. d  m+ w; \! D
it is caused by the premature activation of hypo-
2 F! Y/ Q; Q4 E! ~; [# m' uthalamic pituitary gonadal axis. CPP is more com-
! e; _: x% U* `" S2 u* @# ^mon in girls than in boys.1,3 Most boys with CPP& I7 p  e6 k- x
may have a central nervous system lesion that is
: S& n/ k9 v1 N3 E) |8 m1 Rresponsible for the early activation of the hypothal-
1 a1 h4 f9 s! Bamic pituitary gonadal axis.1-3 Thus, greater empha-
# Y2 D1 t! d& r0 @$ J; L# Esis has been given to neuroradiologic imaging in
2 s7 Z$ i+ {7 z* s$ o/ Y0 _boys with precocious puberty. In addition to viril-
& M+ x$ W6 ~1 B2 {ization, the clinical hallmark of CPP is the symmet-9 \* Q6 Q# ~( g% K: [; {7 W
rical testicular growth secondary to stimulation by1 C5 ~4 a$ q9 x7 J5 U. ^) P+ r3 ?
gonadotropins.1,31 ~. P4 K- Q; f7 M
Gonadotropin-independent peripheral preco-' U, U: m+ ?: [: B( Y, \* u
cious puberty in boys also results from inappropriate2 Y: m3 t, g2 `! E
androgenic stimulation from either endogenous or' D7 g* J5 p+ t; p
exogenous sources, nonpituitary gonadotropin stim-9 R) z' @4 w- L
ulation, and rare activating mutations.3 Virilizing
( U  U; p, n5 b/ @congenital adrenal hyperplasia producing excessive
9 F5 `( M, |# uadrenal androgens is a common cause of precocious
0 K5 x# N5 B; C- j! d' p. opuberty in boys.3,4
# m* m  n3 U3 m8 `3 H3 s5 SThe most common form of congenital adrenal9 S: W# \1 {2 ]8 H
hyperplasia is the 21-hydroxylase enzyme deficiency.
' M& P# {  `( L* N4 hThe 11-β hydroxylase deficiency may also result in
& |5 w! _) H5 F  j) w  Hexcessive adrenal androgen production, and rarely,1 z1 ]( D+ `; R
an adrenal tumor may also cause adrenal androgen
9 e, Y( M1 X' i) F# R% zexcess.1,3, j, U- y2 x  t, l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. {% Y) s+ K6 U! C$ P542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
" D! \7 c; I* A: D* ~4 o0 Z% JA unique entity of male-limited gonadotropin-
0 v% Y( u& G* t2 P2 K- ]5 l% ~independent precocious puberty, which is also known) L5 ]# h: C1 z" K1 j
as testotoxicosis, may cause precocious puberty at a  B* H1 W8 _, t* O5 _& C. h
very young age. The physical findings in these boys
( @  P2 A  G( y; `4 P( Nwith this disorder are full pubertal development,$ A4 z2 `5 z7 o4 Q* U1 L9 C# _
including bilateral testicular growth, similar to boys
: ^# R. M3 [1 Kwith CPP. The gonadotropin levels in this disorder( Z7 M% b* L' q8 c
are suppressed to prepubertal levels and do not show
& j1 p  u9 W# X, s( p1 Opubertal response of gonadotropin after gonadotropin-
5 J/ d+ h" E, O/ W" m6 lreleasing hormone stimulation. This is a sex-linked
0 f: d, O' [9 p0 o& g- C# H5 C: Wautosomal dominant disorder that affects only
3 h7 E# N  V: x9 I* t& t( r; omales; therefore, other male members of the family: c$ ]* f, q2 v
may have similar precocious puberty.3
7 O" B# R. |- W  aIn our patient, physical examination was incon-; ~- _# p/ w9 b* _9 z( y4 Y
sistent with true precocious puberty since his testi-. N6 ~2 w% `8 [. d* b" z/ z
cles were prepubertal in size. However, testotoxicosis; v' A; }$ U( t0 f
was in the differential diagnosis because his father. f1 k" q' x1 r  S* c- Q
started puberty somewhat early, and occasionally,+ p5 ~( A: a4 ^( P1 o  S+ P
testicular enlargement is not that evident in the
; h) O+ u# U" d# sbeginning of this process.1 In the absence of a neg-( S3 z) @  W+ h
ative initial history of androgen exposure, our
. J( b8 d# J" }8 {! H% Abiggest concern was virilizing adrenal hyperplasia,
$ d6 J9 m" e9 [; u! |' ceither 21-hydroxylase deficiency or 11-β hydroxylase# d7 v- z) ]5 d0 _3 j  k7 S
deficiency. Those diagnoses were excluded by find-3 |: P/ d2 z' R1 C" L+ {+ b$ M/ d
ing the normal level of adrenal steroids.
2 J; `0 l; N% L$ A" D; gThe diagnosis of exogenous androgens was strongly
: _  D0 @/ ^* B# l) m. W. jsuspected in a follow-up visit after 4 months because' P/ _8 ?& q: W4 T3 N
the physical examination revealed the complete disap-
6 \& I# Y' D# K6 tpearance of pubic hair, normal growth velocity, and
3 a) i6 w! G  x4 M! Bdecreased erections. The father admitted using a testos-/ I, K# s5 u) P
terone gel, which he concealed at first visit. He was% h# \; N, y6 x' t7 `* Z
using it rather frequently, twice a day. The Physicians’
, V7 N4 s3 x8 k8 RDesk Reference, or package insert of this product, gel or# `$ \* ]5 `' y6 B& b% j) ]" y3 [
cream, cautions about dermal testosterone transfer to
; N, i- w: {( [unprotected females through direct skin exposure.
' l% {& y# O3 x: J) h( r$ Z  g( T; S9 qSerum testosterone level was found to be 2 times the0 I$ M" z7 t. P  ~; G
baseline value in those females who were exposed to0 L6 t/ {. v+ \) `% I9 K& z
even 15 minutes of direct skin contact with their male
9 P  {5 i' @0 `! x2 K* p, T/ mpartners.6 However, when a shirt covered the applica-
  {1 ?9 [7 t2 P1 T9 Ition site, this testosterone transfer was prevented.
& z2 r# a+ W4 DOur patient’s testosterone level was 60 ng/mL,: `7 d, P% F% p5 C3 W
which was clearly high. Some studies suggest that
0 k' q2 u9 T0 l( @8 ]dermal conversion of testosterone to dihydrotestos-
1 @( {* w% \  a1 ]/ gterone, which is a more potent metabolite, is more
4 h7 r3 N) x! k4 l: factive in young children exposed to testosterone
2 E; v4 r! C4 ?: D8 \3 Q3 b3 i7 {$ K+ Qexogenously7; however, we did not measure a dihy-& C* ~2 D" T8 K' X
drotestosterone level in our patient. In addition to
6 [# v$ F9 h& Q6 u1 v* a6 Q; vvirilization, exposure to exogenous testosterone in
: e9 C8 O# h& s2 @" O0 o6 Rchildren results in an increase in growth velocity and/ J; n" F% x6 Z8 d& x
advanced bone age, as seen in our patient.$ N% r8 V" `" o8 ^" ~  E1 G
The long-term effect of androgen exposure during
3 V" p! b/ }+ E! ?% D; cearly childhood on pubertal development and final- S9 o+ P! t1 o! l  ^. @
adult height are not fully known and always remain
/ X9 O! [0 H, T2 n+ `; Xa concern. Children treated with short-term testos-* Z- W+ j/ p- ]/ {: D( T2 \. a
terone injection or topical androgen may exhibit some' _, b9 j# K: ?5 ?0 @
acceleration of the skeletal maturation; however, after
; i# A! ?) B! D9 gcessation of treatment, the rate of bone maturation
$ h( k) R. _% p. ^, p! F+ @4 g0 Ndecelerates and gradually returns to normal.8,93 q" g- G( X$ S. n. N
There are conflicting reports and controversy
/ k. b( e$ n2 o- i- O# D& W+ pover the effect of early androgen exposure on adult
9 q# p% n! e, Apenile length.10,11 Some reports suggest subnormal. q5 u( z( Z5 g# ^9 X; }) ]
adult penile length, apparently because of downreg-! q4 W6 m9 }0 ~- P
ulation of androgen receptor number.10,12 However,
% J) _4 x- _0 A) RSutherland et al13 did not find a correlation between
) Q  c' a( V' X2 Z& g4 E5 Achildhood testosterone exposure and reduced adult# a! i/ A9 |7 `9 z9 X2 ~
penile length in clinical studies.4 d8 }8 ~3 m4 f! j+ a  y1 z' w# A: z
Nonetheless, we do not believe our patient is
3 }1 L# y+ B- N5 e7 @going to experience any of the untoward effects from$ ?& u6 K4 W, o' e; \; v" o5 }
testosterone exposure as mentioned earlier because- Y, N& |( m2 B. I
the exposure was not for a prolonged period of time.
% p! Z' d: Y/ A' m, k$ JAlthough the bone age was advanced at the time of
/ ?+ j5 I, w" W: P0 m7 cdiagnosis, the child had a normal growth velocity at9 @4 j+ n, M- G- z' h
the follow-up visit. It is hoped that his final adult' ]. v: b( J9 N7 F0 @8 n, v' a' r
height will not be affected.
6 H# W) F) f/ j* e  O0 AAlthough rarely reported, the widespread avail-$ S: p" \* P2 d( p: u0 ~/ y$ A
ability of androgen products in our society may
4 U/ _8 H) w2 @2 {' V+ Hindeed cause more virilization in male or female6 H5 y: V8 C5 e- L
children than one would realize. Exposure to andro-
: o8 E' a; P0 @; A' A0 S  i3 E" _gen products must be considered and specific ques-# U  z2 K4 O4 I: d
tioning about the use of a testosterone product or5 P% K( [! Q( v
gel should be asked of the family members during' k0 V& O/ r& U
the evaluation of any children who present with vir-6 B- l. Z( O+ L2 G! C0 C- [4 |
ilization or peripheral precocious puberty. The diag-
, n) F" x. c& x8 a  h/ [nosis can be established by just a few tests and by
' y6 r3 l: @. Eappropriate history. The inability to obtain such a
0 m, J$ q1 q/ Phistory, or failure to ask the specific questions, may  P, W: M  O5 k) i
result in extensive, unnecessary, and expensive
" K/ U8 h* b% t- rinvestigation. The primary care physician should be
2 ?+ C% L3 F3 }- X' Q6 p5 h( Maware of this fact, because most of these children: w$ F6 b3 G$ p6 {7 q# x3 j" ^
may initially present in their practice. The Physicians’
8 q9 j5 z* i% P1 I# U8 z2 KDesk Reference and package insert should also put a$ P  M* q! d3 q- n9 ^, o) e1 N
warning about the virilizing effect on a male or
% v. r% [" H$ j4 rfemale child who might come in contact with some-
6 B; \% l+ V! S4 mone using any of these products./ K$ v6 ]6 g4 n
References
; s' L9 Z: V1 K  W. P$ {$ k, l4 c$ S1. Styne DM. The testes: disorder of sexual differentiation0 C4 k8 D8 S! u' w
and puberty in the male. In: Sperling MA, ed. Pediatric
$ S' R8 S  j" a+ {  t) x. E% f( UEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 F' o; d. w0 w  L: s2002: 565-628.
* A* B$ }$ U3 N  M& B8 `2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
/ V5 i- {; P' T4 O/ ~0 u) vpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old; Z$ G' o0 j- L3 \. a- a# l
Boy Induced by Indirect Topical
2 q( l8 W3 u9 P* |Exposure to Testosterone$ \4 r$ A! t: b8 b, F7 |
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. i) f5 t6 h8 |and Kenneth R. Rettig, MD1
' \2 w& p, g! ]2 p8 f8 U6 c. NClinical Pediatrics+ k, F8 G) V/ K, U8 q; J
Volume 46 Number 6) t- c) X4 ?( I2 S2 L- L* ?
July 2007 540-543' e* P4 L0 `# s; I+ a: U
© 2007 Sage Publications- X+ ?5 ]- ]$ H2 T# ?; F( w& e
10.1177/0009922806296651
0 V4 w$ y! ~0 t# ^1 V0 W! R5 Jhttp://clp.sagepub.com
" P) W9 P) R9 o0 V8 o* y) R- `hosted at
' I# _) x( k5 z( thttp://online.sagepub.com
, J6 u" u$ F4 p- j8 N, M; LPrecocious puberty in boys, central or peripheral,
3 i' e/ W; A  o- Fis a significant concern for physicians. Central
" f& S  S  l! d/ a* D4 pprecocious puberty (CPP), which is mediated, ~+ `1 t, ?7 ~( p! S8 _* z4 c( P
through the hypothalamic pituitary gonadal axis, has* |$ {; J! i' q; ?
a higher incidence of organic central nervous system# H) j2 t& N, D+ u% [* l% t5 k
lesions in boys.1,2 Virilization in boys, as manifested
. S  a) b; n( N- H1 E  U' nby enlargement of the penis, development of pubic
( _: X, M! c) C9 a3 s. |hair, and facial acne without enlargement of testi-
$ {9 x2 f4 t' U& ]cles, suggests peripheral or pseudopuberty.1-3 We5 k" b6 f1 x8 C6 R9 e+ I
report a 16-month-old boy who presented with the, h+ T5 t! w4 {# I' R8 c
enlargement of the phallus and pubic hair develop-2 F! {6 `6 z' k: m/ X9 E' c2 @2 i6 C
ment without testicular enlargement, which was due
: m! j2 J( w7 J7 n* \7 Mto the unintentional exposure to androgen gel used by
; j! S' j9 C' Gthe father. The family initially concealed this infor-
8 b5 F; d) A1 @) h# d- A3 ^mation, resulting in an extensive work-up for this$ s8 q/ \1 g3 f8 g+ `
child. Given the widespread and easy availability of4 B4 `' F  d. p0 c
testosterone gel and cream, we believe this is proba-
  J6 g6 A* n& w% L7 I: Tbly more common than the rare case report in the
( e5 D# p! f- L( g* zliterature.4) \! t' i+ m  O' Q) i/ G
Patient Report5 w9 z$ g( ~8 N
A 16-month-old white child was referred to the  |5 M; o# |  k
endocrine clinic by his pediatrician with the concern
9 {$ M6 w% X  j9 U/ \" l: \6 sof early sexual development. His mother noticed
2 H1 m5 T- E* a- flight colored pubic hair development when he was
$ L$ C6 p6 |! }6 Z/ l( `9 dFrom the 1Division of Pediatric Endocrinology, 2University of
4 _9 g, r4 n) M2 XSouth Alabama Medical Center, Mobile, Alabama.$ e2 M2 w& q8 o/ O7 Y1 N3 s) G4 d$ b
Address correspondence to: Samar K. Bhowmick, MD, FACE,0 [- C9 J6 R# n8 x8 |( ~1 f
Professor of Pediatrics, University of South Alabama, College of4 B" T/ B# B- S! n/ h, }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 a" G$ q) ^1 Q
e-mail: [email protected].0 e6 |" c: C( O! \7 x8 Y$ e
about 6 to 7 months old, which progressively became
# p2 h5 B7 Q0 ^( }  b) p# v% Fdarker. She was also concerned about the enlarge-# z4 Q) O& y$ R% x
ment of his penis and frequent erections. The child
  K& U% ]9 C9 j4 }- Ywas the product of a full-term normal delivery, with
  `+ I; F% n8 X- H2 m* Na birth weight of 7 lb 14 oz, and birth length of# P2 R, F5 ^( l
20 inches. He was breast-fed throughout the first year1 a& H" `2 N0 o4 Y6 [3 ^
of life and was still receiving breast milk along with+ c" C  [* W" ^, L) i
solid food. He had no hospitalizations or surgery,+ X  m9 K# u& g
and his psychosocial and psychomotor development
* `5 j5 z, M. Y+ \was age appropriate.
. o+ c; c% z; h6 \+ N8 n9 IThe family history was remarkable for the father,
0 ]6 B9 K9 N4 O4 k( z$ y+ I' pwho was diagnosed with hypothyroidism at age 16,7 b) B/ V: H7 h6 P1 Y2 K5 \3 I
which was treated with thyroxine. The father’s
7 |( U3 s, x) \3 e1 L  Xheight was 6 feet, and he went through a somewhat6 j" ^$ a3 z( B7 w0 @
early puberty and had stopped growing by age 14.) u; A% r- S+ F) m
The father denied taking any other medication. The/ p7 e' e# t& x1 x$ s
child’s mother was in good health. Her menarche7 v( D6 C& G+ U: m6 o, j
was at 11 years of age, and her height was at 5 feet
4 q3 I: Y$ y/ Q" o8 f0 a: n( ^$ D5 inches. There was no other family history of pre-0 m5 o$ v( e0 x
cocious sexual development in the first-degree rela-
# v8 t* R0 i1 j  \tives. There were no siblings.
) `4 |0 q' ?, ]- Q8 xPhysical Examination
( W2 I! `( N5 [9 z8 Z0 P+ ^( }3 aThe physical examination revealed a very active," d# ]7 U1 c8 O$ M' i7 b/ o' p2 n& S
playful, and healthy boy. The vital signs documented
9 @- w6 x9 x- J6 F3 u; wa blood pressure of 85/50 mm Hg, his length was
9 R% @, O  ]& l9 Q90 cm (>97th percentile), and his weight was 14.4 kg
6 N/ n9 [* x2 y. ~' F* Z% j3 w(also >97th percentile). The observed yearly growth
$ Q- }' T# r  L+ z/ avelocity was 30 cm (12 inches). The examination of, k" j4 {+ v. K0 H
the neck revealed no thyroid enlargement.& v! L0 \$ v8 m& h' \, _5 W
The genitourinary examination was remarkable for
8 ~9 n0 D- ?$ Oenlargement of the penis, with a stretched length of0 C- U. ^. [) s# z- e
8 cm and a width of 2 cm. The glans penis was very well$ v; K5 Z0 d. B5 `. Q1 L
developed. The pubic hair was Tanner II, mostly around
! L" C) f4 _+ ^7 i  P5408 z  r- \% B$ F4 u  W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, a9 E' Z- u% G* A9 Y: B9 _
the base of the phallus and was dark and curled. The) R( R8 U; k# E2 K, d; u2 s
testicular volume was prepubertal at 2 mL each.- ~5 X# y3 K. v8 l! C  @& c1 v+ |) K
The skin was moist and smooth and somewhat7 j1 |5 Y5 Y$ G8 ]" Q
oily. No axillary hair was noted. There were no& B1 a4 ?! e5 j
abnormal skin pigmentations or café-au-lait spots.% Z4 e2 m4 X( P5 b' y( `. D
Neurologic evaluation showed deep tendon reflex 2+
3 I  o5 g9 @8 ?bilateral and symmetrical. There was no suggestion
* n1 g( K4 O: t, j2 w. k: Kof papilledema.
1 a% q) M0 |5 dLaboratory Evaluation
5 u- r1 M4 |8 f: ?3 [5 _. uThe bone age was consistent with 28 months by/ W* d% s& r% Y: K! H- t
using the standard of Greulich and Pyle at a chrono-) K# t% R1 U7 B' C3 T
logic age of 16 months (advanced).5 Chromosomal# n& S, k8 {" M: {' h
karyotype was 46XY. The thyroid function test9 f) i9 S3 ]; w6 Z! {* v: {
showed a free T4 of 1.69 ng/dL, and thyroid stimu-6 j* w: y% y( w0 q* p, U3 o; I
lating hormone level was 1.3 µIU/mL (both normal)./ n& C1 T1 X3 a5 r- @4 V  t
The concentrations of serum electrolytes, blood: Z3 E& L& f2 b5 T
urea nitrogen, creatinine, and calcium all were* V$ P: q4 d, r" }- n% U
within normal range for his age. The concentration
" i, C9 a; U8 R! m& @  ^# s7 Oof serum 17-hydroxyprogesterone was 16 ng/dL
& m  `$ d6 U# c- T( B(normal, 3 to 90 ng/dL), androstenedione was 20
8 w, ~. M2 [5 V" Z0 zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 e( O/ q  M, h! b
terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 f) D" N& ^+ s' v0 I
desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 f: f+ {% f  ]# s2 ~
49ng/dL), 11-desoxycortisol (specific compound S)  ~: ~* b  Q  p6 m$ O3 r' U+ u
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
  \+ N! ^2 L9 T# A) ]3 Z& h; }4 Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total9 E, ?" R- i) F- t8 U! N: }/ B
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) i4 ^3 A; z  ?; E1 l# Oand β-human chorionic gonadotropin was less than% `/ W+ E# W& \. `
5 mIU/mL (normal <5 mIU/mL). Serum follicular0 g) v$ r  i' j3 Q! H
stimulating hormone and leuteinizing hormone
( e$ F, ^! n9 _: {' @concentrations were less than 0.05 mIU/mL
2 r/ n# w* i5 X8 X- {* E% j(prepubertal).. L5 G; N; k0 a; a' }9 j) q# e
The parents were notified about the laboratory
7 O. r8 v5 m' K1 B: y% Jresults and were informed that all of the tests were  G  ~' o8 S8 r  v& V( b1 i
normal except the testosterone level was high. The
/ O5 s6 f' P; M4 x( q5 i8 Qfollow-up visit was arranged within a few weeks to
( K( o& a' I7 X( o9 f# {2 Fobtain testicular and abdominal sonograms; how-
/ S  A8 w/ D. _( b7 Q! E8 Vever, the family did not return for 4 months., _6 h3 T$ y5 p: |* }
Physical examination at this time revealed that the/ S. i' Z" F7 P$ E" t* |2 p
child had grown 2.5 cm in 4 months and had gained
6 `7 X  @' i& n4 k, Q, R2 kg of weight. Physical examination remained
, r, E8 R9 X! aunchanged. Surprisingly, the pubic hair almost com-. k: c) B  V+ m- P
pletely disappeared except for a few vellous hairs at
4 ~6 E: A7 |& n& k, Tthe base of the phallus. Testicular volume was still 2
( I( C" u) H6 @2 EmL, and the size of the penis remained unchanged.5 }5 J& R& S& j; D( d) [3 a
The mother also said that the boy was no longer hav-
7 [. L1 ^( x9 G" k# F4 l! bing frequent erections.
' ^0 K1 {5 B' K, {4 o: }! z! JBoth parents were again questioned about use of
' n' ?' |3 l& many ointment/creams that they may have applied to4 {2 g: v3 q  q# N1 |8 B
the child’s skin. This time the father admitted the2 i$ K0 {- ?6 M! r( Z6 P
Topical Testosterone Exposure / Bhowmick et al 541$ L- |+ A! R9 S9 }* A) k% |
use of testosterone gel twice daily that he was apply-' B+ A* J, k7 a& v) {" N: s- j
ing over his own shoulders, chest, and back area for( E8 }: o# x/ j& B/ p" _6 C3 h
a year. The father also revealed he was embarrassed
  j( w6 v, H' Y7 \6 hto disclose that he was using a testosterone gel pre-
7 `, s" u( y$ zscribed by his family physician for decreased libido7 |/ D5 W/ c4 V6 z% k8 }3 y
secondary to depression.; I1 D+ }: Z* {2 c. d, ?
The child slept in the same bed with parents.
4 O) \0 Q. _% s% ]1 nThe father would hug the baby and hold him on his
/ {7 X0 @  n7 i/ P5 k' u1 U  n# y, [chest for a considerable period of time, causing sig-; u0 I& ?) T9 L4 b
nificant bare skin contact between baby and father.8 _  B; f, }7 Y6 a+ j# Q
The father also admitted that after the phone call,9 a, Q4 b- F% M4 Q5 x" c( C
when he learned the testosterone level in the baby, l3 f2 ]8 l6 w/ e  m; r4 d
was high, he then read the product information
% q" w% r$ Q, u$ P+ Ppacket and concluded that it was most likely the rea-  P4 \# C3 `  r7 Z. X  N8 L  u
son for the child’s virilization. At that time, they
, V' w; L7 Z$ j: c( Mdecided to put the baby in a separate bed, and the) H' d3 N( e8 s
father was not hugging him with bare skin and had4 e+ Y5 a* n! k7 [3 e6 N
been using protective clothing. A repeat testosterone
, O/ ~# W/ d, D0 I" xtest was ordered, but the family did not go to the9 A. I5 M/ e) Y# R
laboratory to obtain the test.& l' b% i  j1 Q" n) r: a- t
Discussion5 x7 N0 E" v$ l1 _/ B' e6 G
Precocious puberty in boys is defined as secondary- q; e# M8 Q; ~& D" [& R
sexual development before 9 years of age.1,4
& O1 A+ N, @7 SPrecocious puberty is termed as central (true) when  q! `( w5 i* z
it is caused by the premature activation of hypo-
% C* U" N( v5 ~$ o5 b6 L1 Cthalamic pituitary gonadal axis. CPP is more com-
. ?+ h5 m) i5 C& x- ?% vmon in girls than in boys.1,3 Most boys with CPP) I0 a3 g. s; `  J6 W/ s$ W
may have a central nervous system lesion that is
& ^: p' v: x; }: Zresponsible for the early activation of the hypothal-
+ c* ^$ o+ h: }7 damic pituitary gonadal axis.1-3 Thus, greater empha-  S. ?) ]0 V) A" }- R6 ~
sis has been given to neuroradiologic imaging in( p6 x. J% A! q8 e
boys with precocious puberty. In addition to viril-& ~0 l1 S) }, T9 }& j. E6 S
ization, the clinical hallmark of CPP is the symmet-, T& L0 v; d. C/ S' |3 x& S
rical testicular growth secondary to stimulation by
+ U5 x& C* S) O" l% O, S, Egonadotropins.1,3
4 u+ C+ |9 D4 t) O3 Y* a1 k" tGonadotropin-independent peripheral preco-
  x% j& v2 k1 qcious puberty in boys also results from inappropriate( w1 @; _: s8 h8 w5 [/ \
androgenic stimulation from either endogenous or
- U& R9 T+ o  p7 H- b! k( x+ E- c  m1 Xexogenous sources, nonpituitary gonadotropin stim-$ G' e: G' [7 n; ?
ulation, and rare activating mutations.3 Virilizing) E8 w& c# Z0 w& q, Q
congenital adrenal hyperplasia producing excessive
! J+ }7 E1 {# [9 I! cadrenal androgens is a common cause of precocious" _" l4 H1 B; o9 I4 G6 f
puberty in boys.3,4$ x2 Z" @$ ~7 V$ R
The most common form of congenital adrenal
( ]& Z/ ]  W0 K* U1 X& }hyperplasia is the 21-hydroxylase enzyme deficiency." d$ u5 ~- x9 \* @! y3 n' H
The 11-β hydroxylase deficiency may also result in1 ^& B% u6 k5 c2 E
excessive adrenal androgen production, and rarely,7 t/ N5 \2 [* y
an adrenal tumor may also cause adrenal androgen
: |" t# O* j- ?' Z- [: Oexcess.1,3
$ S. V$ J( I6 w6 v, V; ]+ lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& g0 G- L/ s! b* T& H3 l542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
* n( |: q0 M# iA unique entity of male-limited gonadotropin-$ A2 h5 S$ Q8 s
independent precocious puberty, which is also known
; D# b* ^! L2 L; z5 vas testotoxicosis, may cause precocious puberty at a: d  {4 P7 _! i- I( l  i
very young age. The physical findings in these boys
6 r7 \" S% V. Q: Nwith this disorder are full pubertal development,+ E3 r& w& u, u
including bilateral testicular growth, similar to boys
. I8 S9 k/ i/ u1 G; kwith CPP. The gonadotropin levels in this disorder( P7 U: C9 f5 C5 i4 U) F
are suppressed to prepubertal levels and do not show) m( v/ P6 G; J& \
pubertal response of gonadotropin after gonadotropin-
6 [7 x$ _/ b$ h0 V/ l( t0 qreleasing hormone stimulation. This is a sex-linked
5 T2 @5 C4 d' u" Z3 K* Y8 zautosomal dominant disorder that affects only* E% Z- r0 \) |7 H7 G$ c7 x
males; therefore, other male members of the family3 c8 n: u8 l1 G: v+ C0 o
may have similar precocious puberty.39 p6 c2 _3 [5 p$ m( y& W9 M
In our patient, physical examination was incon-
8 W0 C  U( k0 Q( ]% D% csistent with true precocious puberty since his testi-
' q3 \6 h! I" C- Mcles were prepubertal in size. However, testotoxicosis
2 U2 K2 d; k# b3 l7 n3 l' dwas in the differential diagnosis because his father/ `8 j2 T) E4 J% z$ x9 w# T
started puberty somewhat early, and occasionally,6 u. p8 L9 U1 b+ e/ B7 H
testicular enlargement is not that evident in the
5 s5 ~' o8 O; {beginning of this process.1 In the absence of a neg-
: d: Q% F+ r+ G" c, I2 i1 n& ~ative initial history of androgen exposure, our: _- h$ m" D. K9 ~- M( _) p
biggest concern was virilizing adrenal hyperplasia,6 e: ^0 {. ~4 i
either 21-hydroxylase deficiency or 11-β hydroxylase
4 ]6 D3 b7 p* ^& m% |deficiency. Those diagnoses were excluded by find-7 l0 z& J' _& r
ing the normal level of adrenal steroids.1 D# T0 O* |& \* \$ T2 h
The diagnosis of exogenous androgens was strongly/ E, v( s" s$ ?
suspected in a follow-up visit after 4 months because7 e4 c" t$ J* x- P4 W
the physical examination revealed the complete disap-
5 J2 W" s, r2 R+ qpearance of pubic hair, normal growth velocity, and
$ t3 o9 ?' A4 B3 Ndecreased erections. The father admitted using a testos-" C3 w( C* ~' j0 e: x6 H# o- C% x
terone gel, which he concealed at first visit. He was
$ o+ V2 B. z5 m* t$ Cusing it rather frequently, twice a day. The Physicians’
% \7 i1 o4 E# Y: {Desk Reference, or package insert of this product, gel or
4 ^/ e+ Z! x% |5 r$ d6 d1 {cream, cautions about dermal testosterone transfer to
& L/ ~" A9 T, Q  w5 Nunprotected females through direct skin exposure.) L% V& a$ t) A7 P
Serum testosterone level was found to be 2 times the
% i6 M" r: ?: `* T. k' i9 jbaseline value in those females who were exposed to
) p1 A3 x. h. B/ M3 Meven 15 minutes of direct skin contact with their male$ h6 n1 `5 w/ Q/ O
partners.6 However, when a shirt covered the applica-" a+ s6 N8 y) G5 Q/ X
tion site, this testosterone transfer was prevented.5 H- a5 C/ x5 k+ d4 f( _- E
Our patient’s testosterone level was 60 ng/mL,$ J7 g1 J5 w% J* d8 g
which was clearly high. Some studies suggest that
* f: b4 V+ M. y+ Ndermal conversion of testosterone to dihydrotestos-
' ?- W* _& m: i6 P6 Uterone, which is a more potent metabolite, is more
; ]4 a5 `$ J" e& L4 g" Eactive in young children exposed to testosterone9 Y3 ~' H. E" \1 ?  k
exogenously7; however, we did not measure a dihy-
2 m/ H$ u( f  ^) X9 hdrotestosterone level in our patient. In addition to& s. z1 A% N& R/ G4 k1 J4 D* V
virilization, exposure to exogenous testosterone in
& p' J# @1 I4 m$ zchildren results in an increase in growth velocity and2 i! v0 z  n8 `7 B
advanced bone age, as seen in our patient.
1 d5 }' i0 i! jThe long-term effect of androgen exposure during/ s- Q) U) o' l: c9 Q9 L  h
early childhood on pubertal development and final
2 d7 ?$ U! z( C" x$ g' J( I. H6 padult height are not fully known and always remain; j# B6 s: R5 o" T
a concern. Children treated with short-term testos-) ?3 Y7 p( ~8 I$ j
terone injection or topical androgen may exhibit some/ l7 r4 x! x# w% m% p$ z
acceleration of the skeletal maturation; however, after7 ^; ^' u0 Y$ D
cessation of treatment, the rate of bone maturation
! [, J0 O  k7 Z1 ddecelerates and gradually returns to normal.8,9
  K% y/ u7 V  C( QThere are conflicting reports and controversy
6 e$ a8 O" H6 T9 }- @over the effect of early androgen exposure on adult
, m, |0 t; G2 }/ Hpenile length.10,11 Some reports suggest subnormal# I  s2 B. c# |, ^1 E
adult penile length, apparently because of downreg-
7 C% X3 c  o! culation of androgen receptor number.10,12 However,+ U1 N8 V4 J1 N3 r6 H& }
Sutherland et al13 did not find a correlation between/ C& n1 F# u, m  h4 O' ^( j% N7 I
childhood testosterone exposure and reduced adult
! M% p+ H6 f8 s3 y8 l+ cpenile length in clinical studies.
( y1 C2 d7 Z5 h  a0 ?Nonetheless, we do not believe our patient is
0 v- }! M* K- ]- Z1 t; L" @( Ygoing to experience any of the untoward effects from9 w& B( {/ Q& d
testosterone exposure as mentioned earlier because$ L3 k4 E) Z; z. X) [3 b0 Z
the exposure was not for a prolonged period of time.: y) ?& U! A. ?% @
Although the bone age was advanced at the time of
, k2 a5 {& b1 y7 o8 Vdiagnosis, the child had a normal growth velocity at7 [# R1 N: |9 c+ w3 N
the follow-up visit. It is hoped that his final adult
% b- F# h0 a% f7 eheight will not be affected.2 k" B8 ]2 B/ p, t
Although rarely reported, the widespread avail-4 f, Y* A) Z* \- ]  L0 ^, ~8 s' A
ability of androgen products in our society may, w) ^) n, ^' P* O) `3 R- Z- m
indeed cause more virilization in male or female' k/ T  d6 M. w$ Z
children than one would realize. Exposure to andro-$ w+ }) R  Z- Y; L" z6 g8 }. D
gen products must be considered and specific ques-
" s! j% g! c/ Jtioning about the use of a testosterone product or
* q  b2 N& B! pgel should be asked of the family members during
+ v$ u  w$ e7 \( @the evaluation of any children who present with vir-
4 P; u! c. R) G- Vilization or peripheral precocious puberty. The diag-
0 B) N3 H# e) D' ~3 ~. M$ G0 enosis can be established by just a few tests and by, j) h* H+ j% s
appropriate history. The inability to obtain such a! S, d& n5 D+ z! R$ H
history, or failure to ask the specific questions, may% G4 k) S4 W2 q7 q# S
result in extensive, unnecessary, and expensive
; W/ z4 o. k; I. ~$ ~5 winvestigation. The primary care physician should be
' h9 V" s$ R5 o, Jaware of this fact, because most of these children- E, c5 _6 p5 f) r# s
may initially present in their practice. The Physicians’
" k" q: a9 {3 p, J( x. tDesk Reference and package insert should also put a
4 m( x1 a+ I& |+ Iwarning about the virilizing effect on a male or4 A7 w5 u/ L5 l* [. H/ ]+ C
female child who might come in contact with some-2 |6 E7 A- F( }1 P. A2 z
one using any of these products.1 X/ P$ r* ]" X  T: m* \) Q
References$ M. S8 T2 d6 b& U
1. Styne DM. The testes: disorder of sexual differentiation
( q) C! n6 o2 ]6 s5 F3 nand puberty in the male. In: Sperling MA, ed. Pediatric
- b# f$ V$ y$ eEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: G: H" y; m8 [6 ]% I$ c
2002: 565-628.
( n' e7 {3 {$ d! ^; e3 T3 \2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* e+ J/ w" h9 z6 {5 h
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!
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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
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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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