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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% C# R, S  Z, Y
Boy Induced by Indirect Topical
0 t; e( D! u7 i2 zExposure to Testosterone
( V# W) Q0 ~. K( p$ C: [! [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ Q. t9 t8 X. v0 y' N
and Kenneth R. Rettig, MD1- S7 K2 {9 t( _
Clinical Pediatrics8 K% A) U3 r" W0 [, z
Volume 46 Number 62 u; H+ v/ Q/ ?) n7 Q2 a( e+ D
July 2007 540-5437 m  X6 d5 C  X+ D% u- e2 m
© 2007 Sage Publications
2 l' e9 {' T, b9 s" J10.1177/0009922806296651
0 H; V4 @( b8 C# l: V% W& F; phttp://clp.sagepub.com
) n# B7 I" ~3 j4 [; Q) uhosted at) `" Y8 k. g4 U9 l
http://online.sagepub.com- X+ J6 j0 M# x4 t: _3 N8 P% S9 p4 ]! S
Precocious puberty in boys, central or peripheral,( X% k9 `$ L/ ~  c+ ~4 b
is a significant concern for physicians. Central
: b" f9 p% @. aprecocious puberty (CPP), which is mediated
- ~7 E7 y: \- F0 w6 N. Sthrough the hypothalamic pituitary gonadal axis, has
. k7 g# H) a  q0 ua higher incidence of organic central nervous system! L9 Z7 ?8 m4 K* r1 w$ u
lesions in boys.1,2 Virilization in boys, as manifested
  b( E) z# C2 H4 z4 `$ Z. k. J  d! Zby enlargement of the penis, development of pubic- h; b. S: d* j: w
hair, and facial acne without enlargement of testi-
0 Y" p/ ^" Z# t  T& n& Bcles, suggests peripheral or pseudopuberty.1-3 We
. R: p* f) a% E1 b% |( Freport a 16-month-old boy who presented with the
& V9 T) a  L: d$ X( Menlargement of the phallus and pubic hair develop-
# o- R! y) M6 s* gment without testicular enlargement, which was due: n0 ?, J5 s! Y1 I5 o6 G2 A
to the unintentional exposure to androgen gel used by! u% g; g+ l, Q3 k0 ~+ A8 O: s  u% c
the father. The family initially concealed this infor-
# @: ?( J5 o% i( e, pmation, resulting in an extensive work-up for this
9 P1 v3 K, l) M2 S! Q4 J) V. ychild. Given the widespread and easy availability of
& S2 C; o. ]8 M! W8 vtestosterone gel and cream, we believe this is proba-
/ Z: g( ]0 I& X/ }bly more common than the rare case report in the4 ^5 r& g9 h$ ?9 w9 f! t# r; Z
literature.4
% ^* \$ u- o, J+ d/ yPatient Report
4 i: V; Z" y) g. D$ D8 mA 16-month-old white child was referred to the# _- W! q( t5 p
endocrine clinic by his pediatrician with the concern
4 F& R3 N1 n) R% G7 @of early sexual development. His mother noticed
6 A4 ^2 X! N& w2 ?% d9 w& alight colored pubic hair development when he was. w& k# u' L1 ~" E$ F* L
From the 1Division of Pediatric Endocrinology, 2University of
6 S* a! Y5 G% [# u7 ySouth Alabama Medical Center, Mobile, Alabama.: z9 G7 |0 U# W( v( D
Address correspondence to: Samar K. Bhowmick, MD, FACE,; w9 j! f, N; J" A5 s* W
Professor of Pediatrics, University of South Alabama, College of
6 B3 S0 E) h' w+ V4 ]1 f4 ]! R& aMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( a* i9 f. N& k( U# e* G) xe-mail: [email protected].0 S# t0 O( ^* u8 u; \
about 6 to 7 months old, which progressively became
* m' X0 L! X0 ndarker. She was also concerned about the enlarge-
& S; `3 Y) ?* q: \* l: oment of his penis and frequent erections. The child
5 F$ K. `3 H" y0 s8 q2 Lwas the product of a full-term normal delivery, with' h/ d8 i: ]5 H) h7 c# u6 `5 k
a birth weight of 7 lb 14 oz, and birth length of$ i0 U: s) E3 L6 [
20 inches. He was breast-fed throughout the first year
+ v/ h/ N' I+ x8 T( |of life and was still receiving breast milk along with6 i1 }3 \( e. ~- r) r: h& f
solid food. He had no hospitalizations or surgery,) `& ^6 ], |& t- S9 _% ?) f( @
and his psychosocial and psychomotor development
7 |4 y) ?1 h3 k9 Iwas age appropriate.' G9 T- m! k- q3 `  _
The family history was remarkable for the father,
0 q! f7 e3 i: ~4 Q9 }4 uwho was diagnosed with hypothyroidism at age 16,
5 y6 `# F+ U3 f+ u" j' {which was treated with thyroxine. The father’s
0 e) v( ?' ~4 v+ ]9 X9 E0 Rheight was 6 feet, and he went through a somewhat9 t% c3 {! |- i( X5 {
early puberty and had stopped growing by age 14.: B0 Y+ w$ s# c" ]1 P- w" d
The father denied taking any other medication. The7 d9 n7 y* b% W& _, M6 k
child’s mother was in good health. Her menarche
" `5 t: m4 b! l% A1 ^+ e) a7 [was at 11 years of age, and her height was at 5 feet
7 k& I# R: n- _) @5 inches. There was no other family history of pre-6 j' r* q4 z4 E& v
cocious sexual development in the first-degree rela-* h$ D7 c: T' _5 i* D
tives. There were no siblings.
7 C# O5 B6 |2 v% NPhysical Examination5 H  e" P8 B, {3 @/ y$ Y7 I  M, `; B8 Q
The physical examination revealed a very active,
7 E& N/ v) i0 w5 u  l( F" C/ Jplayful, and healthy boy. The vital signs documented
6 H8 n* R. t6 A* m; j0 M0 ra blood pressure of 85/50 mm Hg, his length was
6 P" A' W1 U# s2 Q( F& Y90 cm (>97th percentile), and his weight was 14.4 kg
! b2 [; J* E; |) v! \( I, {: g/ e(also >97th percentile). The observed yearly growth
0 D# n3 n( x% g9 M5 evelocity was 30 cm (12 inches). The examination of$ Q# _0 q) S. r* a* v( C
the neck revealed no thyroid enlargement.3 m; J% i( s# L4 |, m
The genitourinary examination was remarkable for: |# @- d$ F! G
enlargement of the penis, with a stretched length of, H. }$ J" z' ]5 c# V1 B+ n
8 cm and a width of 2 cm. The glans penis was very well* O5 x6 j5 f# u
developed. The pubic hair was Tanner II, mostly around* Q: H% E3 W: u& A, P* z) r& n
540
/ l2 x. E- `& x4 Hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ f! X& n9 Q1 s4 k5 T% E
the base of the phallus and was dark and curled. The
5 p# d" ^8 T3 ^; I/ dtesticular volume was prepubertal at 2 mL each.2 y; V# K! s6 Z& v. _1 @
The skin was moist and smooth and somewhat
5 j2 U8 }- w) ^) V! g2 @; noily. No axillary hair was noted. There were no
) R# ~$ P0 _/ ]3 g4 L( pabnormal skin pigmentations or café-au-lait spots.5 Q9 @/ I% ~, a# o/ K
Neurologic evaluation showed deep tendon reflex 2+
4 ?: w8 Z  W  Cbilateral and symmetrical. There was no suggestion% x2 v+ [3 V' r1 X. D& ?) s& e- X
of papilledema.5 s& s! L9 D9 J* W
Laboratory Evaluation  T+ I/ ?! i' `1 B2 t7 Q
The bone age was consistent with 28 months by+ N' U& u0 @5 p( _
using the standard of Greulich and Pyle at a chrono-
4 H5 X5 Y. G1 o7 }" ]logic age of 16 months (advanced).5 Chromosomal6 x+ P) N: T$ h8 {5 F/ E
karyotype was 46XY. The thyroid function test7 J2 m: s* O- G% ^9 _
showed a free T4 of 1.69 ng/dL, and thyroid stimu-3 B" W3 q( v$ ~3 a
lating hormone level was 1.3 µIU/mL (both normal).
; D9 K, g. B3 ^% H+ E" qThe concentrations of serum electrolytes, blood
" h5 @/ U8 L! X( z7 e8 Kurea nitrogen, creatinine, and calcium all were' j( j/ A* O, b3 m+ W& g
within normal range for his age. The concentration' g; S; s) |; g. N+ e; F
of serum 17-hydroxyprogesterone was 16 ng/dL
0 |% z5 ?" _% c(normal, 3 to 90 ng/dL), androstenedione was 20
5 h3 x1 q  Q9 c1 zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) y; }4 U. I' i
terone was 38 ng/dL (normal, 50 to 760 ng/dL),, d9 T4 \& U$ u& V/ a6 z: T1 z
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 h4 Z5 x2 A$ p8 C" D49ng/dL), 11-desoxycortisol (specific compound S)
  i  z2 o. _/ l6 \+ }$ uwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
9 v, e# R" e0 L# etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* l, ~( g" _+ Q( K, X7 F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),; c- q" d1 u0 K# m# F- h
and β-human chorionic gonadotropin was less than# N/ y# x7 H1 R3 ?/ u
5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 f# G' F2 E% U9 e! T- Zstimulating hormone and leuteinizing hormone
7 X2 i; ^9 q8 x6 L4 S1 l) _concentrations were less than 0.05 mIU/mL
+ [5 c# c# U8 e& }3 ?  [(prepubertal).
7 A' @1 l3 k6 P+ m+ l1 D9 XThe parents were notified about the laboratory
; Z" K1 j  A4 nresults and were informed that all of the tests were
+ i: p! c8 o; Tnormal except the testosterone level was high. The
) ^5 k0 D7 f9 K& Tfollow-up visit was arranged within a few weeks to
& |9 b1 ]8 G! F  b  k: y  q0 v; Kobtain testicular and abdominal sonograms; how-
0 h8 }( r% Y* v5 L/ x8 Dever, the family did not return for 4 months.
0 @6 ^1 ~* H* [: X9 P2 pPhysical examination at this time revealed that the
7 J( J! F1 V- s( G& Wchild had grown 2.5 cm in 4 months and had gained
* k/ T% q" K- E: ?( Z4 y2 kg of weight. Physical examination remained9 _# c  N3 R' {) N+ R
unchanged. Surprisingly, the pubic hair almost com-
( x" o% G, O$ ~( C2 x$ q, W9 Xpletely disappeared except for a few vellous hairs at
2 Z( f7 ?7 [. X+ Hthe base of the phallus. Testicular volume was still 2
3 t& V. U9 o" |% F* y6 ]. HmL, and the size of the penis remained unchanged.
( r% B. r% ?9 _' A. v6 U& TThe mother also said that the boy was no longer hav-- y7 N7 w+ L! a1 y# A
ing frequent erections.
, t0 m  ?( i$ \$ C9 Y, I0 VBoth parents were again questioned about use of
/ X, q' a4 f& w5 tany ointment/creams that they may have applied to/ X* }& z6 R* [' H# W; W/ Z
the child’s skin. This time the father admitted the4 v4 P: t( ^3 [2 S' `
Topical Testosterone Exposure / Bhowmick et al 5412 C% D* C) F" n
use of testosterone gel twice daily that he was apply-
, W4 B3 Y# _( q( M  ~* z# jing over his own shoulders, chest, and back area for
. I4 ~' B$ Y( _% xa year. The father also revealed he was embarrassed
" T0 p7 A+ i. Y1 ?5 s$ S2 ~to disclose that he was using a testosterone gel pre-
2 W* d) r  N3 b( c4 ^: A6 Tscribed by his family physician for decreased libido
. e0 e" f+ s/ \2 S. isecondary to depression.8 x# |0 ]4 {$ R. D) `; H$ z( k
The child slept in the same bed with parents.- u, R) V- B0 c% G+ E# _4 p3 Y# V
The father would hug the baby and hold him on his, @9 j/ A% m% e2 D* z
chest for a considerable period of time, causing sig-
7 w, c/ b# J- U4 m* H3 o  ?7 Mnificant bare skin contact between baby and father., J1 U. i3 p2 ^% h
The father also admitted that after the phone call,
4 c* K' [6 K1 }' U8 P' O5 f2 a  Pwhen he learned the testosterone level in the baby
' N" L( C, r- Y' @# C& z1 k+ vwas high, he then read the product information5 a; ^: d9 b( E2 Q6 C. |1 D8 K9 A, x
packet and concluded that it was most likely the rea-
. q$ s9 T4 ?* ]. i8 X& {son for the child’s virilization. At that time, they
, t; q+ Z4 N, s) |decided to put the baby in a separate bed, and the
( T, G) D3 {% {$ v) Tfather was not hugging him with bare skin and had
/ M3 n  Z5 S9 M: {+ L3 E& Hbeen using protective clothing. A repeat testosterone
  P9 [( F6 D$ n! d) i( Mtest was ordered, but the family did not go to the, a# t* m1 g" E. Z( p8 ?) ]7 ^1 _
laboratory to obtain the test.
+ ~: i2 N  f' [0 U- g, V0 vDiscussion
# Z+ v  w& r& }1 f; d- S' r' KPrecocious puberty in boys is defined as secondary; S# o" T. p9 N3 S
sexual development before 9 years of age.1,4# R5 X8 G0 q& N* @
Precocious puberty is termed as central (true) when* c) d) f* n) M
it is caused by the premature activation of hypo-
! a. w1 c7 `1 \$ d1 hthalamic pituitary gonadal axis. CPP is more com-
# e5 o; d( M' ~, G, A& a0 o) \mon in girls than in boys.1,3 Most boys with CPP) J; u' e' D& F) W. T5 k9 o( [8 u+ Z
may have a central nervous system lesion that is
2 x  R' ?+ d/ P# ]8 \responsible for the early activation of the hypothal-. M* j7 Q8 w! p+ U! q
amic pituitary gonadal axis.1-3 Thus, greater empha-
7 z" s' }4 x  \, Asis has been given to neuroradiologic imaging in
" x3 p$ b# w7 z$ C+ I9 Sboys with precocious puberty. In addition to viril-
. {8 s" v* q9 {5 H* Fization, the clinical hallmark of CPP is the symmet-
6 b7 P- Z7 k6 C7 qrical testicular growth secondary to stimulation by- C4 |7 x: {8 h" Y
gonadotropins.1,3$ M7 T" c$ Q9 I- o# ~9 ^0 k' O# T
Gonadotropin-independent peripheral preco-
: e8 ~, g$ ~2 n, kcious puberty in boys also results from inappropriate( B* [& a4 [+ [  ]2 k: q4 f
androgenic stimulation from either endogenous or
/ w" U' z( C- M* ^# @9 q* e+ y+ sexogenous sources, nonpituitary gonadotropin stim-
/ Z8 c% \$ Y( B+ g* t1 {9 k% U5 Sulation, and rare activating mutations.3 Virilizing
0 s# _5 U7 j# _congenital adrenal hyperplasia producing excessive
* `, Y/ E+ N6 T- m; T! fadrenal androgens is a common cause of precocious* O) J0 F/ f3 i( ~& I6 g0 m
puberty in boys.3,4& D# e) s, P8 c* y0 H
The most common form of congenital adrenal4 U" f+ m. }$ u4 W6 c1 ]" n
hyperplasia is the 21-hydroxylase enzyme deficiency.
/ k! C: x! a/ K3 n; c; y- b6 C2 b6 `The 11-β hydroxylase deficiency may also result in
- L' ]! M4 w' ]excessive adrenal androgen production, and rarely,8 V7 b3 o4 U: V. b
an adrenal tumor may also cause adrenal androgen( L$ o* x. I) g0 k0 @" U
excess.1,32 J: J( B+ K7 Z2 D5 P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! Z! v  N, Y4 G4 R  U0 r
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" C' F& M' O" ~+ G
A unique entity of male-limited gonadotropin-
. _: d3 C9 m0 T' {4 g# }independent precocious puberty, which is also known/ n: X$ q1 R" \% C- l- e7 n3 X# |/ {
as testotoxicosis, may cause precocious puberty at a' O! Q9 m, w3 C0 f7 s# r
very young age. The physical findings in these boys
9 x2 V% [9 i8 Y9 owith this disorder are full pubertal development,6 I! E, D2 J, l$ j' T- d. u
including bilateral testicular growth, similar to boys* A% f  @! h% S7 b& A
with CPP. The gonadotropin levels in this disorder6 z6 d3 \3 t' P' @. e; t: `7 {
are suppressed to prepubertal levels and do not show) `0 }3 e; A6 W% v1 k) t& h
pubertal response of gonadotropin after gonadotropin-: X$ B* Y7 `' Y/ D' Z9 m
releasing hormone stimulation. This is a sex-linked
0 z: O- l# }6 Q% P  H- C. Lautosomal dominant disorder that affects only  e( J4 r/ v) ^2 h% C$ {2 M) o
males; therefore, other male members of the family
0 a4 e1 r, p2 @( ?may have similar precocious puberty.3
4 ~$ |) @+ b, _8 D' s6 [; d( xIn our patient, physical examination was incon-
6 i3 z$ M+ T# S2 m/ [sistent with true precocious puberty since his testi-
/ n/ R: G# Y9 a4 f+ Ycles were prepubertal in size. However, testotoxicosis! ^+ _3 \. o, k; O
was in the differential diagnosis because his father2 l5 m6 o! b; ]6 U2 i
started puberty somewhat early, and occasionally,4 P4 |7 K" l6 w( y, ?2 d
testicular enlargement is not that evident in the
$ e( _+ @" ]) C* dbeginning of this process.1 In the absence of a neg-
9 x- L: I( ]2 l. m* e) P* Native initial history of androgen exposure, our
% p. I8 N) _1 P0 |biggest concern was virilizing adrenal hyperplasia,4 _6 i7 p8 _1 Y4 @* u
either 21-hydroxylase deficiency or 11-β hydroxylase% \" D+ X1 @& v8 `
deficiency. Those diagnoses were excluded by find-
( E: B) _$ P3 T0 R2 W- a$ [ing the normal level of adrenal steroids.
9 T2 E* \1 l) ~& }8 }The diagnosis of exogenous androgens was strongly
. P+ z$ F6 X4 [1 dsuspected in a follow-up visit after 4 months because
3 ~- Y- q) e" _( B- athe physical examination revealed the complete disap-) a" C+ V4 o) M% D1 }4 b
pearance of pubic hair, normal growth velocity, and1 }3 f: K1 j. q6 N; ^% j" v1 D: J" }
decreased erections. The father admitted using a testos-
2 ?0 \* H, A8 _. G, B$ Z# Sterone gel, which he concealed at first visit. He was$ _3 f. A/ |9 }& t  J$ k
using it rather frequently, twice a day. The Physicians’
* m6 q, U* @6 l) y: H" IDesk Reference, or package insert of this product, gel or
( \, G0 Y6 ?% e* pcream, cautions about dermal testosterone transfer to
) y" k" X7 n8 hunprotected females through direct skin exposure.
! i4 [( g" u! p* x* Q& mSerum testosterone level was found to be 2 times the
- {, }1 x$ [5 e  n: F: |0 i: |baseline value in those females who were exposed to
3 T1 A8 F/ v( J  a: H4 ^. g+ |! S$ ieven 15 minutes of direct skin contact with their male
) ?: P0 m1 E1 M6 g# Y' \4 Q- Vpartners.6 However, when a shirt covered the applica-
2 M6 b, B6 {; Ktion site, this testosterone transfer was prevented.
4 r% j* s& F' S3 hOur patient’s testosterone level was 60 ng/mL,2 Z( \* j1 |% j3 ?
which was clearly high. Some studies suggest that/ [' K& G9 y9 Z; W0 P5 s5 h
dermal conversion of testosterone to dihydrotestos-
+ ?3 R) {" T. x: f2 E0 Kterone, which is a more potent metabolite, is more
/ l) j( A% {& t- V$ @active in young children exposed to testosterone
* `) u, W  F6 c! T' ?exogenously7; however, we did not measure a dihy-3 X% T0 Z  G- p8 E0 k
drotestosterone level in our patient. In addition to
: U& Y8 ]0 c4 T9 x% }virilization, exposure to exogenous testosterone in
1 ]  y3 b/ j+ l9 [children results in an increase in growth velocity and
% d- s; |. u/ L, v. _advanced bone age, as seen in our patient., H/ e9 ]4 W$ v) `' b6 k/ z
The long-term effect of androgen exposure during
9 v; T! ?1 a8 Nearly childhood on pubertal development and final1 V( X2 L6 ]3 R5 O
adult height are not fully known and always remain
4 ~2 N0 R* F! {2 |. ~: {a concern. Children treated with short-term testos-' k8 u- h/ ~7 U6 U, t& G
terone injection or topical androgen may exhibit some+ U  M1 ~. e3 Y
acceleration of the skeletal maturation; however, after
1 K5 F0 X& c9 h6 S  d" xcessation of treatment, the rate of bone maturation- N, D- M" r( s! Q* V" U; p
decelerates and gradually returns to normal.8,9
$ |# f" C$ u3 M" E% N( h3 X( n2 p. j( |8 zThere are conflicting reports and controversy
! g; \5 w  H! d: G( tover the effect of early androgen exposure on adult
( S- I% {$ |: lpenile length.10,11 Some reports suggest subnormal
3 d4 [. M- V; h; Qadult penile length, apparently because of downreg-
( G# D9 _' u' @5 F- b$ ]# f1 ^7 e$ yulation of androgen receptor number.10,12 However,9 q; ^# S: e# C% m& R
Sutherland et al13 did not find a correlation between
% Q) M0 u- e# D& s/ N: O# ]1 Y0 q3 Achildhood testosterone exposure and reduced adult6 `# m! I  v+ t, [4 L8 d
penile length in clinical studies.
" d& F8 j% n% ]9 vNonetheless, we do not believe our patient is3 E1 c9 T: ~0 `  |
going to experience any of the untoward effects from
4 N. p6 F0 j- r5 Ztestosterone exposure as mentioned earlier because
* j) b# P* b# I9 g- j: lthe exposure was not for a prolonged period of time.% U1 R: {6 l& b$ u5 z
Although the bone age was advanced at the time of
: n- P# H8 {# r8 ldiagnosis, the child had a normal growth velocity at
1 |( T5 {, W9 N$ [the follow-up visit. It is hoped that his final adult
# A2 R  a# \+ Y8 N8 [height will not be affected.
) a7 h# N' \7 Q! aAlthough rarely reported, the widespread avail-
7 k# ]* c. v6 Y1 J' uability of androgen products in our society may) A- m* Y9 T, F# ^  y
indeed cause more virilization in male or female
: g# y2 m6 K" z( x+ W' Mchildren than one would realize. Exposure to andro-
; n' s" `! X! P6 ?% y. k, Ygen products must be considered and specific ques-
1 f2 ^) F$ }: h2 E3 g3 d: vtioning about the use of a testosterone product or+ i6 V0 z$ n/ |( \. u/ w) ^
gel should be asked of the family members during
! G8 P% O6 }- \2 B) F0 Kthe evaluation of any children who present with vir-: B/ E3 F, @& B0 {6 o$ J- x2 j( _
ilization or peripheral precocious puberty. The diag-
$ a. T9 i3 G$ Onosis can be established by just a few tests and by; M, `" I8 Y3 U. b% C0 V
appropriate history. The inability to obtain such a
9 Z9 {$ s  i- Z- chistory, or failure to ask the specific questions, may
6 X7 Y, I( u( r2 R) n3 Gresult in extensive, unnecessary, and expensive& _' O7 k# v/ W+ T7 b% E
investigation. The primary care physician should be
# o9 e  i0 ~' h2 S0 a2 haware of this fact, because most of these children
% g0 ]+ @0 Z' r( ?# J& Y1 c7 Ymay initially present in their practice. The Physicians’. L+ }9 \# O" a1 Y( |7 H+ [
Desk Reference and package insert should also put a
1 C. S  Z) r( Z4 r9 `warning about the virilizing effect on a male or: P& `% ~5 F! a- f
female child who might come in contact with some-) i9 p7 `- G  R! ]
one using any of these products.
4 U; _3 ~8 ]6 R+ eReferences
! r6 d4 k, f) G4 Q8 O1. Styne DM. The testes: disorder of sexual differentiation
5 z% B' i! i; z/ S" ]) uand puberty in the male. In: Sperling MA, ed. Pediatric4 Q  `9 _' U; ~0 i  w$ g
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: M/ N( f# \. }% D2002: 565-628.
; Z9 e' C& }' L; Q2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ p3 M6 p& C% ^( I! n$ R% Spuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old2 d7 b+ m* Q5 K% X+ c0 H
Boy Induced by Indirect Topical
+ C  O. Y  X) i8 d3 q& CExposure to Testosterone! ~$ ]' b  O1 O7 ^' Z& O. q
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
3 \4 H8 P1 i0 L- R8 p5 o4 d& Iand Kenneth R. Rettig, MD1
, R( l+ j' Z7 I  bClinical Pediatrics
- w/ y: L6 l( X: R* i& UVolume 46 Number 6
' C! }, Z6 R  Y' RJuly 2007 540-543
- b  I. T# O+ ~) N" Y© 2007 Sage Publications
- b, I+ B( y  ]- j10.1177/00099228062966510 r4 Z6 k( R0 e) F/ w
http://clp.sagepub.com
4 P& z% f- {7 ^& Whosted at3 h! K0 ?6 Q* Q9 V2 J2 M
http://online.sagepub.com
  i+ j. m% |5 Q. x, G5 u9 DPrecocious puberty in boys, central or peripheral,$ ^" U9 K+ |; }* f, j, Z
is a significant concern for physicians. Central
8 b6 h( H1 r9 e; @4 y  A9 eprecocious puberty (CPP), which is mediated
* B# x5 g+ t  fthrough the hypothalamic pituitary gonadal axis, has
( H7 z2 J" r) W- r7 K; I# Q4 K% sa higher incidence of organic central nervous system" o8 j: ~# h4 n* [2 h  M
lesions in boys.1,2 Virilization in boys, as manifested8 R8 [2 l; U* k! y) n
by enlargement of the penis, development of pubic$ O0 e" a6 b0 V. b" E
hair, and facial acne without enlargement of testi-5 k, Y0 M( K# I0 r5 Y4 v8 n+ {2 V
cles, suggests peripheral or pseudopuberty.1-3 We9 H( M* g8 n) g
report a 16-month-old boy who presented with the
. o+ ]( k* D. u( l  |. penlargement of the phallus and pubic hair develop-) S) ^# p) V: F$ D' K: v  Z5 D$ f( D7 ]
ment without testicular enlargement, which was due, y% j% [: H: Z' Q, z
to the unintentional exposure to androgen gel used by' B5 r7 F5 K; V5 v4 |
the father. The family initially concealed this infor-
# T' @8 V0 o& C! Vmation, resulting in an extensive work-up for this
  y4 N- x, L7 F; Y6 X$ H2 s2 _7 O, g! \  Achild. Given the widespread and easy availability of; @6 p1 L: y3 k8 y  b
testosterone gel and cream, we believe this is proba-
4 B+ ]( H  V" @0 a8 q9 ~) I% Pbly more common than the rare case report in the- H2 Q& o4 q4 {7 R5 }
literature.4
0 N5 Q& T; ^( C6 O$ oPatient Report
$ P* t6 `0 ~. b6 h& qA 16-month-old white child was referred to the9 B0 U! k2 G1 M8 J! @" `
endocrine clinic by his pediatrician with the concern3 L9 m  Y; Z7 A# s- \/ ?
of early sexual development. His mother noticed- r( B4 v' {% H' \& Y0 R$ X. Y
light colored pubic hair development when he was
! ]6 l) t3 C/ T6 I( KFrom the 1Division of Pediatric Endocrinology, 2University of
  }8 x7 I8 `& A) m/ LSouth Alabama Medical Center, Mobile, Alabama.
# m+ c/ W% c' E0 F. ~4 uAddress correspondence to: Samar K. Bhowmick, MD, FACE,+ u% g; v: Y7 I; c( t4 j/ O
Professor of Pediatrics, University of South Alabama, College of2 W6 @7 |3 Z; l8 R1 @5 _) @* K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# k2 ?- S$ {# Fe-mail: [email protected].: V- s6 q. a8 u, \, a: g
about 6 to 7 months old, which progressively became
1 @# u) s" z" ^6 R9 S% T. X: Xdarker. She was also concerned about the enlarge-
) ?, i' K7 B! e# ^. kment of his penis and frequent erections. The child& p7 p* E# }6 |" U+ m
was the product of a full-term normal delivery, with
. `- G. K- n/ b  ]3 V$ |, Ga birth weight of 7 lb 14 oz, and birth length of
" ~* l/ u# r0 \0 v20 inches. He was breast-fed throughout the first year5 R7 e7 [( {& D# ]7 w4 b
of life and was still receiving breast milk along with2 B0 Q( v: T; {. G3 N
solid food. He had no hospitalizations or surgery,
, A" u+ N4 u& E! m" xand his psychosocial and psychomotor development
% R' X$ e# `3 ]# K# n) P) Qwas age appropriate.
4 w: l  U  a. s! }. \, ]The family history was remarkable for the father,3 ^* t. C! @8 l# K- g. G
who was diagnosed with hypothyroidism at age 16,
' X6 M9 I, c8 J, \which was treated with thyroxine. The father’s
. Z2 Y9 ?4 b4 j2 @, [height was 6 feet, and he went through a somewhat
. q7 ]! N; R/ K& d/ Pearly puberty and had stopped growing by age 14.
& I' v2 M6 M: hThe father denied taking any other medication. The9 F# k* C! m4 _# n: ?
child’s mother was in good health. Her menarche
5 Z& M; K, a/ Jwas at 11 years of age, and her height was at 5 feet
" `% B) _& d- }5 inches. There was no other family history of pre-  \' A. }: m6 n( d( [
cocious sexual development in the first-degree rela-
5 s" z; |, c  _; ~- R' T# ^tives. There were no siblings.5 p% s7 H8 d- p$ S- `4 y
Physical Examination) l( b% ~" i! i. N
The physical examination revealed a very active,
7 J1 P- X1 s" I/ `  uplayful, and healthy boy. The vital signs documented+ y& C. ]$ w* \9 b9 U# e
a blood pressure of 85/50 mm Hg, his length was( `+ e# m5 H) c! Q
90 cm (>97th percentile), and his weight was 14.4 kg
: Y/ f, r* A( u' k$ E' \5 B: `(also >97th percentile). The observed yearly growth- v4 T- h9 u3 i& d
velocity was 30 cm (12 inches). The examination of9 f0 @" [, h( u& y- f5 i; `3 p( _7 s
the neck revealed no thyroid enlargement.
$ z1 y. `+ V$ D' Q) ^The genitourinary examination was remarkable for
- c) |" k" D/ T' m; d2 aenlargement of the penis, with a stretched length of4 F7 ?1 X" H6 x* d
8 cm and a width of 2 cm. The glans penis was very well2 @# p' v1 T0 i6 I1 S$ g2 X+ R
developed. The pubic hair was Tanner II, mostly around+ M7 C" B( M4 {* G) _1 n
540, K3 B$ t) M. S3 G/ ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& h" ?4 j: E: o: L. t9 S4 ~: w$ K9 z9 w
the base of the phallus and was dark and curled. The+ U3 T4 u# a, i0 J
testicular volume was prepubertal at 2 mL each.6 T' R: w3 a. R
The skin was moist and smooth and somewhat
% Q. l! o2 c+ L1 D+ B! loily. No axillary hair was noted. There were no
' Y6 w5 D4 ^# R+ J6 pabnormal skin pigmentations or café-au-lait spots.4 O/ X7 a( `+ z6 r
Neurologic evaluation showed deep tendon reflex 2+
$ i, S$ M- [) j# \bilateral and symmetrical. There was no suggestion6 n/ f7 @+ n& ]! l- K% O% i
of papilledema.0 }: F; k2 n  q" M7 r
Laboratory Evaluation
/ }* u- ]$ G' N. ?9 ~' {  g# P( SThe bone age was consistent with 28 months by2 o% u2 U" a- r8 T8 ]
using the standard of Greulich and Pyle at a chrono-* G. ^: ?6 I$ u
logic age of 16 months (advanced).5 Chromosomal
* _6 W2 r2 s" Z' [karyotype was 46XY. The thyroid function test
: m" p  w. a+ l- Wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 n/ v0 \! z  C) r5 h; X  H+ Ilating hormone level was 1.3 µIU/mL (both normal).
7 O2 Q6 u6 Y5 ?) v3 m4 p+ [. h9 uThe concentrations of serum electrolytes, blood0 ]: b: _5 x, p+ a" Z0 n
urea nitrogen, creatinine, and calcium all were
9 g4 H2 D# ^' {5 f$ M" s, Dwithin normal range for his age. The concentration
0 m, ]9 `7 Z5 i- \3 Iof serum 17-hydroxyprogesterone was 16 ng/dL0 J( z: J( Q) i5 o
(normal, 3 to 90 ng/dL), androstenedione was 20
( `! W2 E4 @! C  H! Cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
+ {- J" i. F7 }3 B% b8 y/ }terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 W! K* m0 n* M% @+ B0 D. |desoxycorticosterone was 4.3 ng/dL (normal, 7 to: X' U5 N$ s$ |* W6 E2 \* V: |
49ng/dL), 11-desoxycortisol (specific compound S)
* y# U1 a7 J) v6 L+ x1 Nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* l+ h( j5 ?( g' f) M  A; e- r; a. ltisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total2 [% U. X% T6 q* t, v; X" n( @
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),1 ~6 n! F+ `5 ^$ j1 n8 t& N2 Y. \
and β-human chorionic gonadotropin was less than* ?1 z2 B; B8 S& ^/ j( T" J
5 mIU/mL (normal <5 mIU/mL). Serum follicular: g) y7 y- i# J6 H. b
stimulating hormone and leuteinizing hormone
; V! }' r$ T" I. Z5 iconcentrations were less than 0.05 mIU/mL9 _8 J; r8 w& ^5 g+ b
(prepubertal).
% j( S  |9 o  e7 K: F& G3 @! e' |The parents were notified about the laboratory
) N! m% j/ \" y  ?results and were informed that all of the tests were
) N" i# l" Q# _, Y, Y  M0 {normal except the testosterone level was high. The
% o, l9 D. u8 j2 _$ @follow-up visit was arranged within a few weeks to6 t$ T0 d" A' M: w5 D1 v! o0 Q$ k
obtain testicular and abdominal sonograms; how-$ P; a. t/ n5 `5 {% D( H
ever, the family did not return for 4 months.! x( e/ ~1 o9 d# f
Physical examination at this time revealed that the
4 n9 K! A3 z6 g( F! z8 \child had grown 2.5 cm in 4 months and had gained
$ \8 G" Q! ?$ x4 o! e2 kg of weight. Physical examination remained5 t) u& Z! `- p! c/ k
unchanged. Surprisingly, the pubic hair almost com-
. O! Y7 d  e8 Bpletely disappeared except for a few vellous hairs at
' q; }! y2 i5 B7 a: O/ b/ R: zthe base of the phallus. Testicular volume was still 2: k3 `7 c/ r) P2 X& M1 _* Z" [
mL, and the size of the penis remained unchanged.
. v0 R" o( ~2 N+ ?$ z6 \" NThe mother also said that the boy was no longer hav-* }: E% E, l4 c8 K& d
ing frequent erections.
+ S# Z. }" R& A2 D6 V) n2 N7 `( `9 OBoth parents were again questioned about use of
% T6 |% T. y5 z: vany ointment/creams that they may have applied to6 E% Y- l$ ]0 ^2 c
the child’s skin. This time the father admitted the
* w) u( g, u. F# a  N! R2 bTopical Testosterone Exposure / Bhowmick et al 541
0 @- g; ~, @$ c& j1 Fuse of testosterone gel twice daily that he was apply-
- n- E7 U5 F8 Wing over his own shoulders, chest, and back area for8 {& G+ W3 v3 z) y
a year. The father also revealed he was embarrassed
) t/ X2 C' q% `( O4 N9 u" w' \, Tto disclose that he was using a testosterone gel pre-# g& |- M. H7 {/ ]
scribed by his family physician for decreased libido- v* X0 e! e2 q: o8 u; k3 V4 M$ i
secondary to depression.: @" O; H0 S3 ?/ d7 K; B* d
The child slept in the same bed with parents.8 [4 P8 o/ ^% F0 U% s
The father would hug the baby and hold him on his( a( ^& ~# i9 A3 ?, H) {
chest for a considerable period of time, causing sig-! _  |  _( ?- F" y# s5 c9 {
nificant bare skin contact between baby and father.
6 U* X& @) Z' J0 c( q8 nThe father also admitted that after the phone call,
) Z, K0 R6 X( gwhen he learned the testosterone level in the baby
. b. {2 w- h6 C$ v) E) M7 b" ]$ Kwas high, he then read the product information( y- @! P: [4 c, o3 ^2 u# Q: p
packet and concluded that it was most likely the rea-
7 c6 U! N, w% V3 W" Lson for the child’s virilization. At that time, they* y6 x! a8 i2 h/ h% J$ \
decided to put the baby in a separate bed, and the
. k/ b+ w* I! ofather was not hugging him with bare skin and had
9 o7 t, r0 a2 F) [; Cbeen using protective clothing. A repeat testosterone
7 M' \8 E& W& p4 n* mtest was ordered, but the family did not go to the/ F$ ~5 P4 A3 v- u
laboratory to obtain the test.
# N3 h' L& ~* ^% ?Discussion5 e2 X. H) J7 j3 j
Precocious puberty in boys is defined as secondary( X: ^8 \5 m9 W9 e
sexual development before 9 years of age.1,4
7 T; r% q; L8 d$ L0 IPrecocious puberty is termed as central (true) when
( m9 ^* L4 P  x; o- k; G4 yit is caused by the premature activation of hypo-
$ N. }+ F% n5 j  wthalamic pituitary gonadal axis. CPP is more com-; y  m+ M: D' v, e, i( t
mon in girls than in boys.1,3 Most boys with CPP6 i6 p5 d) A+ n0 K6 {, {" ?$ H0 w! \1 _
may have a central nervous system lesion that is
. M* w# x* X* X7 Q% s2 Wresponsible for the early activation of the hypothal-
6 O, |* l, ~# b" C4 G, y/ h  zamic pituitary gonadal axis.1-3 Thus, greater empha-# O; W7 z( N5 T
sis has been given to neuroradiologic imaging in$ |- t) l, j) }9 _
boys with precocious puberty. In addition to viril-" y* |- u/ n( S3 \
ization, the clinical hallmark of CPP is the symmet-! T; n% m: F0 I8 \( G& k- V. z: M" k
rical testicular growth secondary to stimulation by
+ N) P/ M) Q5 S' u. r. V, xgonadotropins.1,3$ W4 H9 r% ]9 V5 |4 f, V  X2 S
Gonadotropin-independent peripheral preco-2 V6 A% W* {8 T
cious puberty in boys also results from inappropriate
% R6 ?7 N2 ?7 L1 {androgenic stimulation from either endogenous or
) h2 O) e$ J. Z% P# \  Texogenous sources, nonpituitary gonadotropin stim-
1 p2 p' h  Y" N5 u. f/ o. aulation, and rare activating mutations.3 Virilizing
) \4 u* Y; r: |# A6 T1 z  econgenital adrenal hyperplasia producing excessive% V- F, W/ m- c" @" j
adrenal androgens is a common cause of precocious
' e, E4 u3 {# mpuberty in boys.3,41 x. J  N! _, u
The most common form of congenital adrenal
/ @4 G( c6 q7 p( B: g* w9 ?) |hyperplasia is the 21-hydroxylase enzyme deficiency.
$ x5 u) w' o$ oThe 11-β hydroxylase deficiency may also result in
0 s- v  D/ B/ f, H) G- j5 k8 a4 o5 `excessive adrenal androgen production, and rarely,, |, K4 {3 S' X8 W4 w" P2 ?
an adrenal tumor may also cause adrenal androgen
: S3 p# t$ x2 ^% v- ~# Q2 Eexcess.1,35 ?1 t! x- O* e4 |5 ?- r, r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 Q9 w9 G0 T4 A% ]& D4 u# h; ~% @542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
5 s  d6 y, q9 KA unique entity of male-limited gonadotropin-, _- _( L( x- F$ O, [
independent precocious puberty, which is also known4 p9 S+ W' a* c' E' R0 ~9 C
as testotoxicosis, may cause precocious puberty at a$ N* d$ G& _& U& A9 n; ^; T
very young age. The physical findings in these boys
3 B  B$ n* N2 Z2 Ywith this disorder are full pubertal development,
- [7 f+ `. `+ ~including bilateral testicular growth, similar to boys) i! z7 C' ^/ z; S4 K: ]7 d# ~
with CPP. The gonadotropin levels in this disorder- b/ K% ~3 E5 J
are suppressed to prepubertal levels and do not show  b. X- Z1 ~+ _3 M4 R% G; U
pubertal response of gonadotropin after gonadotropin-
' {7 R  G3 L3 j/ T) [releasing hormone stimulation. This is a sex-linked3 h9 S+ }8 b" r7 W: z
autosomal dominant disorder that affects only; B9 ?- @+ `: C+ A
males; therefore, other male members of the family( E6 n; X" C$ a  {
may have similar precocious puberty.3
# f: s, K' b$ T2 F0 c$ A2 H0 K; B* BIn our patient, physical examination was incon-
; B) Q! P' d% f  ]+ [6 Isistent with true precocious puberty since his testi-
" J; y  f( E8 e+ [- i: n# X) Gcles were prepubertal in size. However, testotoxicosis4 C9 o  G' s1 }: ^% G
was in the differential diagnosis because his father
0 q0 b- ?& T8 L9 ]started puberty somewhat early, and occasionally,3 y2 T& o6 j2 W
testicular enlargement is not that evident in the8 v1 b7 R$ f9 C* N- p
beginning of this process.1 In the absence of a neg-
. N. w/ M1 |8 A" Z; Oative initial history of androgen exposure, our
! M, ?6 H: Z! X, s) D' z( Gbiggest concern was virilizing adrenal hyperplasia,
0 r1 V' Q$ ^3 X% Jeither 21-hydroxylase deficiency or 11-β hydroxylase8 j# X' N/ c; Q5 m! E  d# k
deficiency. Those diagnoses were excluded by find-: Q9 E  T- N0 ^* v; r4 x5 v# B
ing the normal level of adrenal steroids.' d5 M2 D6 R' @. y- t# g
The diagnosis of exogenous androgens was strongly
7 q" y' U4 S' i( [4 Xsuspected in a follow-up visit after 4 months because
/ H, D* F8 c; J: G  S- Mthe physical examination revealed the complete disap-
! [  h& j$ Z1 n- y  @pearance of pubic hair, normal growth velocity, and2 v' r! K0 `1 x9 G2 J( B% l
decreased erections. The father admitted using a testos-% a  S1 F4 w3 D1 k0 a& C# A# k" H1 n
terone gel, which he concealed at first visit. He was! r8 |1 W2 A# ]. h& S+ ?
using it rather frequently, twice a day. The Physicians’" d) O8 L+ ?6 P. J
Desk Reference, or package insert of this product, gel or
: G, [, A: i. ?% K6 Qcream, cautions about dermal testosterone transfer to
* v/ b7 T$ H# v; X0 f5 B2 Nunprotected females through direct skin exposure.3 G" I. I. w. u( j" v3 g8 ~, ^
Serum testosterone level was found to be 2 times the+ m' n' n# g- I7 y' X% c6 P
baseline value in those females who were exposed to
, e7 F& y3 }: r6 L1 z1 K) Keven 15 minutes of direct skin contact with their male7 A9 Y& \6 ^9 o7 K' o3 M8 q8 M
partners.6 However, when a shirt covered the applica-
6 l. @" D: G+ n& _9 h. W* I3 Z7 Dtion site, this testosterone transfer was prevented.9 f: `; }3 j) l
Our patient’s testosterone level was 60 ng/mL,
. z0 f. p4 f6 n, m* i6 f; K3 Xwhich was clearly high. Some studies suggest that
/ r" f8 X# L# Y# J2 J4 Z9 I( V, P/ idermal conversion of testosterone to dihydrotestos-
+ A) D# z$ n" gterone, which is a more potent metabolite, is more% v- V, ^( Z/ B4 _% {* I- A: c
active in young children exposed to testosterone, l1 W/ {% Z8 j& A" |
exogenously7; however, we did not measure a dihy-: }% P% Z/ f2 M
drotestosterone level in our patient. In addition to0 L  h* N# v6 {1 |2 C, t% H2 P' }
virilization, exposure to exogenous testosterone in
0 y$ \! c5 E; ^8 E' ~children results in an increase in growth velocity and* V0 x3 R9 P! M8 P2 T
advanced bone age, as seen in our patient.
- B0 t3 F% S, p4 x" CThe long-term effect of androgen exposure during
& \9 y. f" Y( ^early childhood on pubertal development and final' o  C$ d& Q# H1 d
adult height are not fully known and always remain  x" l1 d6 U- l. C
a concern. Children treated with short-term testos-0 A( n# \- s( H
terone injection or topical androgen may exhibit some
+ q' k7 W5 N8 {$ T/ f1 Eacceleration of the skeletal maturation; however, after
# Y6 w) ]" d) F* I8 T" dcessation of treatment, the rate of bone maturation
$ _: z0 f7 j# }- Mdecelerates and gradually returns to normal.8,9. t3 g9 S5 a4 m+ @0 P8 _  J
There are conflicting reports and controversy3 \; t; u1 p( ~. \  m- A0 K0 c
over the effect of early androgen exposure on adult
8 W7 x4 u6 k3 ]( a! D  Hpenile length.10,11 Some reports suggest subnormal
- \; t& ?3 G( W! H( `adult penile length, apparently because of downreg-
1 X6 l! N- L- `8 I6 O- p9 Y6 @# _ulation of androgen receptor number.10,12 However,
; g1 P  H6 w8 Y8 Z; lSutherland et al13 did not find a correlation between
' C  p' w. D1 h1 J: u/ Pchildhood testosterone exposure and reduced adult: i/ G" B4 A$ Q
penile length in clinical studies.  j: q8 W4 Y' v. D- x( P5 B
Nonetheless, we do not believe our patient is
# h5 I: {- J5 a; l3 \going to experience any of the untoward effects from
5 g+ v. P) @( |& J( l+ M( ttestosterone exposure as mentioned earlier because
0 ]2 U) g* A; ]0 u) z) M4 athe exposure was not for a prolonged period of time./ ?( E) h+ ]6 ^' ]3 Z' C# Z
Although the bone age was advanced at the time of
4 o5 e) x$ W; q  r  @1 k0 M; Kdiagnosis, the child had a normal growth velocity at
/ n/ G" p" S. g' E9 Rthe follow-up visit. It is hoped that his final adult* t8 i( }) `7 F, o! d" O  u# H- w' v; i
height will not be affected.1 U2 n0 Z  _4 b0 X
Although rarely reported, the widespread avail-
' @7 |" }6 G# \- ]ability of androgen products in our society may3 {4 k- J/ m! w0 `/ v
indeed cause more virilization in male or female7 l( t" Y& A' b* F  d; d
children than one would realize. Exposure to andro-
( G* I3 e! J3 |$ O2 Tgen products must be considered and specific ques-' r# Z7 `* w( P9 v+ E! r! B1 B& |
tioning about the use of a testosterone product or: P" S  X) E* Z  c3 n1 D& V
gel should be asked of the family members during
9 C( r  F7 ]9 t% \+ _the evaluation of any children who present with vir-
* w: E+ s7 {/ }# G- l! T" \ilization or peripheral precocious puberty. The diag-
3 |7 J4 N+ X9 n, Anosis can be established by just a few tests and by  W/ ]* h' ^1 d  U2 L6 e8 m
appropriate history. The inability to obtain such a. ~9 `$ [9 ]' {* L! A( B6 W6 ~
history, or failure to ask the specific questions, may
+ z! Y$ h& M  V6 U! v! Jresult in extensive, unnecessary, and expensive- |  I7 ?9 ^" s
investigation. The primary care physician should be
2 u- b3 R7 f% q0 Raware of this fact, because most of these children
+ p6 T1 E0 b7 F) e, Z& {may initially present in their practice. The Physicians’
8 g5 V3 t1 M9 b% x  k( MDesk Reference and package insert should also put a
* t2 V: k  r7 |$ B/ R1 @; M4 X; fwarning about the virilizing effect on a male or; N" E1 G3 L" B+ h
female child who might come in contact with some-8 `0 |& \3 O4 H/ u' i( i" ]
one using any of these products.
; R; m- j$ e8 ~References) s' F# n& i' |3 j6 b
1. Styne DM. The testes: disorder of sexual differentiation
. m8 d- Z+ e7 R* q, Cand puberty in the male. In: Sperling MA, ed. Pediatric7 s) q- [8 a5 h; ?
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, p( D4 K) [9 W8 [9 F, _- T
2002: 565-628.
9 O0 g1 x& m' t) o( U  [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) F/ t% l& b6 U; K
puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
% Y0 W: H1 \5 X7 T4 w" l
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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