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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; z) U- q  Q* u+ ?& ~
Boy Induced by Indirect Topical& k  o# [- m1 C& O7 h
Exposure to Testosterone6 g. y, u& \, t: \+ m
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 E/ x$ E; F" V
and Kenneth R. Rettig, MD16 g3 |# y0 x; e6 Z0 p8 J
Clinical Pediatrics$ X0 y8 ]* j5 L, g
Volume 46 Number 6( V+ O0 [' g2 O7 T
July 2007 540-543
& y" r1 ~3 y- z9 R: |) D© 2007 Sage Publications
3 _  G2 W* @+ E/ ^# D+ Y# {" h0 Z10.1177/0009922806296651
9 F6 {% s. W- b# G' Bhttp://clp.sagepub.com- S+ F4 z. f% W# W
hosted at: V) _) x* }' S3 w5 ?* d1 z; i. X
http://online.sagepub.com1 ~9 Y; @1 W0 m+ J. f
Precocious puberty in boys, central or peripheral,
+ f4 {5 k. J: d% d' Wis a significant concern for physicians. Central/ w: C* J4 F/ `/ o. F( _0 x) T" }
precocious puberty (CPP), which is mediated
9 s4 p! c  e) Xthrough the hypothalamic pituitary gonadal axis, has
  a' A: \  j" K( T2 I, Pa higher incidence of organic central nervous system- V/ \5 D) e7 p
lesions in boys.1,2 Virilization in boys, as manifested
& `9 z* B: ]+ ^9 h+ m" x$ K$ Oby enlargement of the penis, development of pubic
2 }- C' }( h; K6 k/ G+ Jhair, and facial acne without enlargement of testi-- |, v6 e& u: k# o6 [* b$ Y
cles, suggests peripheral or pseudopuberty.1-3 We2 ^3 R  F4 q: ~1 k
report a 16-month-old boy who presented with the
& b) i" }% b! M( o: o" Senlargement of the phallus and pubic hair develop-4 q/ c* V# U$ P3 P
ment without testicular enlargement, which was due
- I2 X  {' Y+ J8 V$ Tto the unintentional exposure to androgen gel used by& m) i. K7 B* o2 W4 ^: Y
the father. The family initially concealed this infor-  [- z+ J& d6 y# M% C6 F
mation, resulting in an extensive work-up for this
. x7 }/ B3 J) o6 @! H$ Ichild. Given the widespread and easy availability of1 }4 c/ k" R/ f% B7 @' t) R' K
testosterone gel and cream, we believe this is proba-
; U( L% k8 V4 z6 d. Rbly more common than the rare case report in the' u1 N5 f7 c# ~. f; E
literature.4
' i& P5 {5 A5 x% jPatient Report8 u! X9 V8 I, I
A 16-month-old white child was referred to the
0 U% A) j& t% ]' o4 Yendocrine clinic by his pediatrician with the concern9 t+ E' o( `( k
of early sexual development. His mother noticed
: K  \. n  s: r8 N, hlight colored pubic hair development when he was
- A4 H% ?  {' ~- G2 y, tFrom the 1Division of Pediatric Endocrinology, 2University of5 ?; G4 u3 ^. B1 j. w$ _
South Alabama Medical Center, Mobile, Alabama.# p* N7 ^& R, @) D1 ~) P  V
Address correspondence to: Samar K. Bhowmick, MD, FACE,* C$ ~2 a, Z. \
Professor of Pediatrics, University of South Alabama, College of/ \/ o7 `3 |/ N. E1 `; b
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. V9 H  H7 Q8 b$ Me-mail: [email protected].
; x' M4 u  D" s$ V( Z3 _! Uabout 6 to 7 months old, which progressively became; q: D5 ~. m2 @9 k4 Y- }
darker. She was also concerned about the enlarge-: e% [2 |+ ?" I8 N0 a% V
ment of his penis and frequent erections. The child: C  W9 h2 U0 s, N  O: D  s1 ~6 i
was the product of a full-term normal delivery, with/ D# f- G: y. G) x( _; |9 W$ y
a birth weight of 7 lb 14 oz, and birth length of
6 W2 `. {' t. D  L% \20 inches. He was breast-fed throughout the first year7 O; S5 U6 q4 n, F
of life and was still receiving breast milk along with
6 z# Q" F& G% O$ B" t1 Dsolid food. He had no hospitalizations or surgery,% {' u% M- K" ?! B6 C+ R
and his psychosocial and psychomotor development
1 h9 E$ I: W$ p4 Z2 Vwas age appropriate.  }( y# A) Y7 B+ Z' r  ]5 q
The family history was remarkable for the father,
) c7 o$ X1 N! z" i. gwho was diagnosed with hypothyroidism at age 16,
' S& n9 H1 t. v4 e2 O. l: Ywhich was treated with thyroxine. The father’s- [6 D& ]2 ~5 T
height was 6 feet, and he went through a somewhat
9 }( _& T  X7 t( W* I' nearly puberty and had stopped growing by age 14.
0 O9 P& u" V. h- wThe father denied taking any other medication. The
( N- T/ K5 F$ T9 Pchild’s mother was in good health. Her menarche, }% g" T& }: j" }; Z2 Q) r" Y
was at 11 years of age, and her height was at 5 feet
( z7 P4 C% q" ~9 {4 [. p, e5 inches. There was no other family history of pre-
0 ]- U& @1 @9 _0 B: \1 scocious sexual development in the first-degree rela-
5 O! ~0 Y1 p2 [" etives. There were no siblings.5 {, g0 h( Z4 h/ h, q
Physical Examination
/ u8 w( H0 a: ZThe physical examination revealed a very active,$ q6 o. V( h, @- y# T( ]( G
playful, and healthy boy. The vital signs documented
$ M5 y* _# c4 P- @4 F* c- J/ Ba blood pressure of 85/50 mm Hg, his length was
  k" Q  \' v& q- K+ {1 |4 G5 R90 cm (>97th percentile), and his weight was 14.4 kg
$ J( L) s6 X2 W" T(also >97th percentile). The observed yearly growth! b) X) `/ J2 Z8 p& a* P8 w
velocity was 30 cm (12 inches). The examination of
0 u/ @5 d1 N2 W) s, ~the neck revealed no thyroid enlargement.
3 ?9 w: ?7 C/ q# Y4 y4 U- K2 QThe genitourinary examination was remarkable for
2 A' k4 N% Y: T# G* K/ aenlargement of the penis, with a stretched length of9 w# S9 v2 L% o8 Q* K( S4 J6 E
8 cm and a width of 2 cm. The glans penis was very well
0 i1 p( x( L0 S6 n* g& x$ Ndeveloped. The pubic hair was Tanner II, mostly around  u2 b6 W5 ?! o" U
540$ n# c" Y6 p: {6 _( b: s5 ?! J/ o
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ l' l# f. B  X0 c/ G
the base of the phallus and was dark and curled. The5 z3 K- P" B; f  ?
testicular volume was prepubertal at 2 mL each.2 o5 i% U* c; t& U8 X
The skin was moist and smooth and somewhat
+ _  ^! t! [; @' t& Q& Aoily. No axillary hair was noted. There were no
, z3 l; o4 H  B5 Tabnormal skin pigmentations or café-au-lait spots.
& G) y  a( v$ c4 d0 lNeurologic evaluation showed deep tendon reflex 2+
0 ?1 F3 P3 c* S0 g( ?bilateral and symmetrical. There was no suggestion  k: H" M& h2 i- n6 ~6 \# m
of papilledema.
: k1 P3 h1 V: v9 H/ D. iLaboratory Evaluation
% K* J% F* b, h- K. yThe bone age was consistent with 28 months by, X- N+ i- K$ Z0 O1 t
using the standard of Greulich and Pyle at a chrono-
" D- _  z( C9 u& {, e& Glogic age of 16 months (advanced).5 Chromosomal0 X) p' `6 R1 a9 w/ C( N2 M
karyotype was 46XY. The thyroid function test
: U# D- W8 x3 Y; ^" g3 Wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
, B4 b4 E; D3 R% V! a% N6 D" ?lating hormone level was 1.3 µIU/mL (both normal).
6 s; w; k2 r1 X( h. |The concentrations of serum electrolytes, blood# i  v8 }! j$ w4 d: I& Z
urea nitrogen, creatinine, and calcium all were; m2 Z, F' Q3 C$ j+ y) M1 Q
within normal range for his age. The concentration
/ b; d* P7 ^7 n0 T0 Sof serum 17-hydroxyprogesterone was 16 ng/dL3 `' k) T* U: y1 O
(normal, 3 to 90 ng/dL), androstenedione was 20
$ c( Z' \; I9 f( u& xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: |  ~  |, e1 o6 s3 V
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 C  k- O) @! R! bdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
# _! H% f# y7 Z7 J$ Z1 Z49ng/dL), 11-desoxycortisol (specific compound S)& p3 M! H1 O9 e
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ O: W% D" [6 P, B8 x
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ |3 @4 i& z) d' R1 U
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 \5 \! C: T9 ~: D  k
and β-human chorionic gonadotropin was less than
0 \+ F- ^# j. Q6 H0 V& ~5 mIU/mL (normal <5 mIU/mL). Serum follicular
* Z) h& K: |' y% z6 nstimulating hormone and leuteinizing hormone
7 y. y+ }4 u, y( Y; jconcentrations were less than 0.05 mIU/mL' Q5 r1 P: m( c3 Y; p( ^& P
(prepubertal).
9 y9 T( x, q7 i3 ~* v3 B# aThe parents were notified about the laboratory
3 J4 X5 g% `* @' x2 \1 c* W+ ~- S7 g# mresults and were informed that all of the tests were
. M( K1 u3 w' V3 rnormal except the testosterone level was high. The
+ V  e! {& Z: T2 p1 Xfollow-up visit was arranged within a few weeks to; N, f) }# }6 r0 m% |
obtain testicular and abdominal sonograms; how-! S% U( }" v: E3 V! P, `( V
ever, the family did not return for 4 months.7 j9 h& r: A9 m' v( ~6 w
Physical examination at this time revealed that the
% G$ U5 L  f! ?/ f$ Uchild had grown 2.5 cm in 4 months and had gained
6 R( h; h2 M1 V9 P+ _* v2 kg of weight. Physical examination remained
5 w0 ?/ ^- b$ E: k8 S; c5 Bunchanged. Surprisingly, the pubic hair almost com-
- J7 k: ~# d! Ppletely disappeared except for a few vellous hairs at! x# k: t( ?2 E  ?# b
the base of the phallus. Testicular volume was still 27 x2 p% [' L* N- M3 n, P0 i
mL, and the size of the penis remained unchanged.
* }* X3 a2 u# a. hThe mother also said that the boy was no longer hav-  l1 M: c2 D' X$ Z' S8 Z& ~
ing frequent erections.+ W! f/ W( o, l. P" i6 P
Both parents were again questioned about use of: m& E+ I7 @6 E4 i% k. s1 ]$ W
any ointment/creams that they may have applied to
% J* h- G6 R) G/ T+ Athe child’s skin. This time the father admitted the
! a% J9 w# _) H% n" q  zTopical Testosterone Exposure / Bhowmick et al 5417 n4 K. c$ x! _4 z: ~% d
use of testosterone gel twice daily that he was apply-# w/ H: L1 ~3 `* Z6 w2 Z. k
ing over his own shoulders, chest, and back area for
( t( s+ B2 h5 p! ^3 d; O. o* sa year. The father also revealed he was embarrassed  N; }' ^  ]. P& Y
to disclose that he was using a testosterone gel pre-
5 {6 I* N5 E6 @* M. L# @% Vscribed by his family physician for decreased libido
, R' u  J0 \. ~secondary to depression.
2 f( E, d. G1 d" X1 L6 z( SThe child slept in the same bed with parents.
, `% h. B6 E2 ^* }9 AThe father would hug the baby and hold him on his
7 _2 R, D) f; y& [9 ^chest for a considerable period of time, causing sig-
% f( I. y& O, {3 M: i  snificant bare skin contact between baby and father.! d9 s4 x, v* H1 e, J9 X( v
The father also admitted that after the phone call,
. U3 D( o3 v7 ]* @% y" Ywhen he learned the testosterone level in the baby& N' b9 {( C/ U2 M# O
was high, he then read the product information/ X2 ?1 _+ o! u
packet and concluded that it was most likely the rea-' Q5 X9 X+ ?7 H
son for the child’s virilization. At that time, they. Q* I, [, ]7 v3 d+ q& ?  Q; s0 T. k
decided to put the baby in a separate bed, and the$ B- `6 M* {6 ^. D
father was not hugging him with bare skin and had1 W* ?! p7 q. T' ?' G) \
been using protective clothing. A repeat testosterone
1 B1 l8 `8 w# u; u7 K% Gtest was ordered, but the family did not go to the
6 i) l8 }0 j0 Zlaboratory to obtain the test.
0 q% A8 V% \4 A8 @Discussion
$ ~1 {$ n0 I. x4 {$ M3 N7 K$ l9 xPrecocious puberty in boys is defined as secondary/ _/ ?! A$ ~7 c) }# A: w8 g
sexual development before 9 years of age.1,4
9 F/ C5 ~- [; r+ S( c7 FPrecocious puberty is termed as central (true) when
. L  D: r, \! |$ }6 H* X  Kit is caused by the premature activation of hypo-$ g0 j/ X$ S0 U2 X/ Z" m
thalamic pituitary gonadal axis. CPP is more com-
) O$ w9 R3 l0 h8 @mon in girls than in boys.1,3 Most boys with CPP5 C. W  H5 z" ]4 s* q
may have a central nervous system lesion that is
6 b# k/ r6 }& W: [& G. r) I( ^responsible for the early activation of the hypothal-5 @* L" {) c2 N
amic pituitary gonadal axis.1-3 Thus, greater empha-, Z; p1 T' Y/ `. h4 n
sis has been given to neuroradiologic imaging in6 M& L" ]% I5 W/ w
boys with precocious puberty. In addition to viril-) N- r5 x1 _$ s# P" y
ization, the clinical hallmark of CPP is the symmet-
! E: G/ ]) ~( I) Z* {3 k  rrical testicular growth secondary to stimulation by
7 s1 i# e% z/ n( w& _. Egonadotropins.1,3
2 U$ ^# a6 K, d) M( n4 G, oGonadotropin-independent peripheral preco-( d. I* q; N9 @8 H  N+ l
cious puberty in boys also results from inappropriate
7 D1 g2 h( U9 B; F+ ~; r% _androgenic stimulation from either endogenous or
/ W: q! g# c/ r* Z7 R8 ]exogenous sources, nonpituitary gonadotropin stim-
* j1 I2 q9 a# y$ ~* bulation, and rare activating mutations.3 Virilizing
3 l; \1 Z0 ~2 econgenital adrenal hyperplasia producing excessive
, h+ E, l$ v+ E) s7 F1 }' uadrenal androgens is a common cause of precocious
* \+ N- `% r- G* o0 _1 V5 y3 gpuberty in boys.3,4
5 _1 d* {- k8 i4 iThe most common form of congenital adrenal
1 f+ O  A3 D$ h  thyperplasia is the 21-hydroxylase enzyme deficiency.
( f# P% l: D; k0 FThe 11-β hydroxylase deficiency may also result in; C  ?% j* u" _1 _
excessive adrenal androgen production, and rarely,
9 F5 j  s  e) f, }+ y+ X* n( D( `an adrenal tumor may also cause adrenal androgen6 \" K* ~$ ?* d- ~6 W: j! p
excess.1,3
8 }. Z$ y: ?% n6 X6 e7 D+ ]at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 e1 ~. S2 `- y- K' n2 |( A
542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 u# Y$ ^9 D4 E+ B" X$ x! s* u
A unique entity of male-limited gonadotropin-' m+ |$ V; P9 r. o
independent precocious puberty, which is also known, R7 Z- W5 M9 U& u
as testotoxicosis, may cause precocious puberty at a5 C) l4 d' f+ C$ l
very young age. The physical findings in these boys
$ o* h" H$ q3 \3 b5 S$ Y/ xwith this disorder are full pubertal development,/ ?  o1 E" Y! ~8 C5 R6 v
including bilateral testicular growth, similar to boys# I4 C$ a2 d" m
with CPP. The gonadotropin levels in this disorder
/ G3 e  @" z* @* D3 N. xare suppressed to prepubertal levels and do not show  d; D2 g- \/ ^$ W
pubertal response of gonadotropin after gonadotropin-
  C( y# y4 K# hreleasing hormone stimulation. This is a sex-linked
8 P4 c( k9 r2 T% m% x: V2 Gautosomal dominant disorder that affects only
, H5 K' X! \1 r/ P7 tmales; therefore, other male members of the family* [( p/ n( I" i: K+ \( x
may have similar precocious puberty.3/ u, _: }3 C* U& I  t8 Y! I. A
In our patient, physical examination was incon-
2 H$ ~2 @, G; Y/ ]4 ?$ Tsistent with true precocious puberty since his testi-$ w6 m) }$ a' |7 x+ o
cles were prepubertal in size. However, testotoxicosis
4 w1 H! n0 O4 p8 h: E' v3 hwas in the differential diagnosis because his father" M% X5 h$ j. D  Q2 z6 S8 o
started puberty somewhat early, and occasionally,( z, y; p( x) _2 ]# Y- S
testicular enlargement is not that evident in the$ E4 Z: {9 V/ E) s
beginning of this process.1 In the absence of a neg-2 W, S; x! a7 L+ L7 W' u
ative initial history of androgen exposure, our
; f  M; Z! A( l" S7 x2 bbiggest concern was virilizing adrenal hyperplasia,$ ?! G, P- ~) j
either 21-hydroxylase deficiency or 11-β hydroxylase
( }! S6 r8 l# }& X& sdeficiency. Those diagnoses were excluded by find-
/ B2 e3 k8 v3 U% b# X& a# Q7 @; Ving the normal level of adrenal steroids.
/ Q# F8 h: f6 d; KThe diagnosis of exogenous androgens was strongly: C$ _2 U2 o2 }( J8 k
suspected in a follow-up visit after 4 months because) L7 P. I4 ?# A- [  Z. R- Y
the physical examination revealed the complete disap-
; t: H" k: F4 y5 A$ O4 l9 xpearance of pubic hair, normal growth velocity, and
1 H, n  t8 H8 ^" M* h$ R; Wdecreased erections. The father admitted using a testos-7 g; V: U! R* u2 d$ L, n+ M
terone gel, which he concealed at first visit. He was% d, {4 s! J* ^- h( d
using it rather frequently, twice a day. The Physicians’
" w1 m6 B) ~7 ?Desk Reference, or package insert of this product, gel or
* `8 S8 ?/ d0 b, ccream, cautions about dermal testosterone transfer to
! V& w4 a2 }. A2 {: P! b  z: Nunprotected females through direct skin exposure.2 G5 u6 _" a8 b6 c
Serum testosterone level was found to be 2 times the
3 h. n* Q/ c" lbaseline value in those females who were exposed to4 t1 e% `% J! ^) g
even 15 minutes of direct skin contact with their male, O/ x2 h- P, h, X$ L( J
partners.6 However, when a shirt covered the applica-; Q, B- Z' Y3 Q1 R$ ~: s" T# e
tion site, this testosterone transfer was prevented.) I; |  g- l. n" t* T( D( `* `
Our patient’s testosterone level was 60 ng/mL,* {4 B; e, R- F1 @) Y
which was clearly high. Some studies suggest that
/ ^1 M8 [: w# L) Ldermal conversion of testosterone to dihydrotestos-" K  K8 t2 H6 P( e1 y
terone, which is a more potent metabolite, is more  G1 q- B' v2 H- y
active in young children exposed to testosterone' U/ `% R8 Q/ s9 f
exogenously7; however, we did not measure a dihy-
- w* a  o  ~) J1 J& V' K0 t" I7 hdrotestosterone level in our patient. In addition to! ~1 I! _! U- A+ O& J0 z1 i: i
virilization, exposure to exogenous testosterone in& E0 a# p5 o5 q# P( }; Z! r
children results in an increase in growth velocity and. o- h) D2 G4 P
advanced bone age, as seen in our patient.
7 e) v/ k! ~6 J: M. cThe long-term effect of androgen exposure during  \1 I: F, f9 p6 s
early childhood on pubertal development and final
6 ]5 ^; P9 f+ U" s& ?adult height are not fully known and always remain
+ c4 i$ c+ K, r" @a concern. Children treated with short-term testos-! {: |, e0 d. a9 @7 h
terone injection or topical androgen may exhibit some
2 r! W7 n  U: u8 Uacceleration of the skeletal maturation; however, after
' e% y% E/ p! t) ]* p  Fcessation of treatment, the rate of bone maturation) Y0 y) f5 _* S  H( e
decelerates and gradually returns to normal.8,9
* B+ {7 ]0 `) h+ c, jThere are conflicting reports and controversy$ v& N7 m, \$ A, a- D+ S  B
over the effect of early androgen exposure on adult# ^# @! |' c1 I9 Q9 \
penile length.10,11 Some reports suggest subnormal$ z+ r/ Z5 r9 s
adult penile length, apparently because of downreg-
. Y" N' Z  n  e# i+ V9 M% nulation of androgen receptor number.10,12 However,
" i6 c  i' E# X/ g6 A' aSutherland et al13 did not find a correlation between$ z( ?5 _, Y5 {8 N; x6 w
childhood testosterone exposure and reduced adult
8 W5 d  E# O& }# kpenile length in clinical studies.
7 a4 J$ F- b" \0 nNonetheless, we do not believe our patient is, V* S/ O6 r  j( c
going to experience any of the untoward effects from6 [; Q* v/ m# g7 j2 E4 g9 m/ `
testosterone exposure as mentioned earlier because
9 Z7 @$ s; w' E. `2 i3 C0 \% Sthe exposure was not for a prolonged period of time." ^" j0 S$ T; b7 q
Although the bone age was advanced at the time of; t' X  \2 @& J8 |9 M
diagnosis, the child had a normal growth velocity at
* A6 n" L  Q: Y% Dthe follow-up visit. It is hoped that his final adult6 `2 X( \9 m# D  v- ?) \, i$ T
height will not be affected.
, V' e. R/ n& |* L  Y5 ZAlthough rarely reported, the widespread avail-2 l3 S& d* r/ l1 a4 s5 r
ability of androgen products in our society may
6 h$ Y4 h' K% Q& Y" n9 p" O! s4 Jindeed cause more virilization in male or female; W9 f9 }) A* y2 ~4 z
children than one would realize. Exposure to andro-9 y" }. G$ X6 e5 Z' X
gen products must be considered and specific ques-
' d1 y3 H, @% l# f5 z8 e6 b) r7 F, ctioning about the use of a testosterone product or) ^4 m6 \& V$ C8 Z+ Z' P6 S/ A. X
gel should be asked of the family members during
; B1 |: |2 Q, n7 x* {: f1 J7 Ethe evaluation of any children who present with vir-' Z- v, ~# r+ c" ?. P1 s: {
ilization or peripheral precocious puberty. The diag-; s: x2 E+ B& t4 M/ }
nosis can be established by just a few tests and by7 g& I, q' s0 }/ C
appropriate history. The inability to obtain such a
# Z& @) `: ^! Z4 L1 Nhistory, or failure to ask the specific questions, may3 }( V% F: T, E1 i8 L
result in extensive, unnecessary, and expensive
  u+ C# w+ R9 p' x% Tinvestigation. The primary care physician should be2 `/ P. K9 V! F
aware of this fact, because most of these children
& F0 a& N  d: `1 [may initially present in their practice. The Physicians’+ k0 r1 V2 c; P# @
Desk Reference and package insert should also put a
1 D4 ^' ^" @) k* W+ |warning about the virilizing effect on a male or0 @& z% P4 \+ h5 o" N, I( L
female child who might come in contact with some-, l% G1 Q) ^- g: y7 W" {
one using any of these products.
7 o0 I% v6 f" jReferences* I9 E! s' L7 _' n
1. Styne DM. The testes: disorder of sexual differentiation
$ O4 ^9 m  o% O; ]  Eand puberty in the male. In: Sperling MA, ed. Pediatric, _' k- |1 G% K& ]
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 T" M" ^2 X/ E+ x2002: 565-628.
& Q6 g3 S# L: m; `/ G% ?2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% J9 |9 v: [' d) u3 V% B" c1 m+ vpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
- J& ^) V, ?- a$ {* n4 C3 LBoy Induced by Indirect Topical
, G  f$ j6 J1 \4 q# E1 `3 tExposure to Testosterone& b7 r5 `- d( p2 M  W
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
$ P+ d# }2 v5 L' z3 |and Kenneth R. Rettig, MD14 v& Y' F  G+ Z, m8 H9 P3 w0 H
Clinical Pediatrics
& ~) j$ M! m. T9 N$ lVolume 46 Number 6% m8 l6 B0 d: ~; f5 A$ d5 W2 N5 _
July 2007 540-543
. c" S) o, E/ I+ O& B0 r4 v7 W. R© 2007 Sage Publications
! d% s( e8 Q: z0 {$ m- S10.1177/0009922806296651* D3 G8 I; b: ]% N
http://clp.sagepub.com
4 [3 J; j' B8 v7 m& a5 {+ Dhosted at
  m4 ]3 g  z4 }0 [6 E) H; rhttp://online.sagepub.com
' C9 ?, u3 B7 {1 r' ?! v2 C* l& }Precocious puberty in boys, central or peripheral,* M; l& j  K" O2 s$ X
is a significant concern for physicians. Central
2 x1 C2 i% O- F0 j2 Hprecocious puberty (CPP), which is mediated" W' L+ _4 Y0 v$ ^9 Z
through the hypothalamic pituitary gonadal axis, has  P% V: H7 q( T: z) {$ O" S5 }/ _
a higher incidence of organic central nervous system' h8 p7 w4 Z& s. M* w6 W) }# p$ s
lesions in boys.1,2 Virilization in boys, as manifested1 A9 r2 l* P! U5 `% l/ P  V
by enlargement of the penis, development of pubic
& c5 B; ?3 h( }8 `' a/ ?# m; nhair, and facial acne without enlargement of testi-
, v+ o! ^# g2 T. zcles, suggests peripheral or pseudopuberty.1-3 We9 r  U- a, E( Z1 ?0 ^
report a 16-month-old boy who presented with the
, u; A' ^0 x/ u0 B1 {# P# Genlargement of the phallus and pubic hair develop-
" K( M$ }3 `/ ^+ dment without testicular enlargement, which was due" ]& l" ~. B  x3 o. q+ P
to the unintentional exposure to androgen gel used by
3 S- o: L' E2 Y/ G, E8 i( T3 i' ]/ _the father. The family initially concealed this infor-9 ]. h7 u: a& m& d
mation, resulting in an extensive work-up for this* U! E3 T1 r! @; X) E8 r2 M3 {: {% H" Q
child. Given the widespread and easy availability of) H5 @4 Z9 {2 R& z. b9 x
testosterone gel and cream, we believe this is proba-
/ f4 C; F& ^' `; r  X! z9 d1 \bly more common than the rare case report in the
" l+ k/ ~6 ~" ?/ wliterature.4
; X$ P, b. C  i8 APatient Report
1 E1 x, N! F; k; TA 16-month-old white child was referred to the$ `, d2 l% D: K
endocrine clinic by his pediatrician with the concern
) M9 b# f/ ]' l0 `' C; rof early sexual development. His mother noticed
. {( c. \, A/ Z2 R8 j( z; ~0 G) dlight colored pubic hair development when he was
: h/ X* v/ m1 ~" i# ~- u7 cFrom the 1Division of Pediatric Endocrinology, 2University of
) \! W6 d9 G4 }- U1 g, k6 cSouth Alabama Medical Center, Mobile, Alabama.
1 U/ q, R. E7 _5 n6 X% w; mAddress correspondence to: Samar K. Bhowmick, MD, FACE,
3 y' h! r: X: ?+ f: L0 |* NProfessor of Pediatrics, University of South Alabama, College of& N% }0 W. U  h% O/ f' Y3 p4 C2 R
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
: B7 B1 M1 q: \: @- xe-mail: [email protected].
$ y3 M; {- g# u* M$ [  Xabout 6 to 7 months old, which progressively became
, ~  K& u: E$ ]darker. She was also concerned about the enlarge-
- R& n2 q% z! Y% z0 G& E6 _4 |/ Ament of his penis and frequent erections. The child3 Y, j4 K% U+ h  t, z
was the product of a full-term normal delivery, with
4 s+ d7 T8 s1 i4 Da birth weight of 7 lb 14 oz, and birth length of
1 b, [/ I  A0 E! h& Q20 inches. He was breast-fed throughout the first year& Y( G& l" q' s3 b7 L- W( P
of life and was still receiving breast milk along with$ f! J: E8 H/ |6 r3 m+ c
solid food. He had no hospitalizations or surgery," h) I, {+ R1 p: U5 V
and his psychosocial and psychomotor development
6 N) u5 Y- U0 m. Cwas age appropriate.& E! ^1 q  E# s2 k! ]4 p
The family history was remarkable for the father,: U  }4 ^1 C7 W) `
who was diagnosed with hypothyroidism at age 16,
& T) Y# n5 K* B4 R; N5 G/ ?9 twhich was treated with thyroxine. The father’s
1 m* k& f5 }. ?5 w! n9 |height was 6 feet, and he went through a somewhat, C  C7 _9 p6 v2 B; W" O$ w
early puberty and had stopped growing by age 14.: `6 z+ o# g; D3 ?
The father denied taking any other medication. The
% }& P: D4 d: x% q* O# }child’s mother was in good health. Her menarche& I# M2 P- `$ r
was at 11 years of age, and her height was at 5 feet6 m1 @) ^0 f' m- S
5 inches. There was no other family history of pre-
3 G7 B7 o7 m- E0 u( E* [cocious sexual development in the first-degree rela-/ j5 I4 d  M- R! B3 J6 P2 k4 G  u
tives. There were no siblings.7 H+ a$ b1 `  Z9 ?' k
Physical Examination
. P. g2 C; J- FThe physical examination revealed a very active,
. O3 F6 K4 K! Y/ }playful, and healthy boy. The vital signs documented
/ [# T# e5 M( R# r4 j, Fa blood pressure of 85/50 mm Hg, his length was
  e. |: r* `' N( q2 g90 cm (>97th percentile), and his weight was 14.4 kg
8 G! s' v3 L  T(also >97th percentile). The observed yearly growth
/ a( p$ J4 X8 lvelocity was 30 cm (12 inches). The examination of+ N0 l+ e5 T; c3 M' e. X# {% A
the neck revealed no thyroid enlargement.
4 h, z/ d0 y9 A5 Y- Z& L) \" TThe genitourinary examination was remarkable for, Z/ ~* z; h+ r9 h/ x& Y+ U0 |( v
enlargement of the penis, with a stretched length of
0 ~* }/ V0 N9 O/ A, e8 cm and a width of 2 cm. The glans penis was very well: E% D% y( U8 p+ j) E
developed. The pubic hair was Tanner II, mostly around
& J* T3 k5 x, O' g540) c1 _2 o" L6 y( Y7 n  I: ~- ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 o% z: a' ^1 p, e; \! T1 x
the base of the phallus and was dark and curled. The
# n6 p9 ]+ u# Q. L. g1 Atesticular volume was prepubertal at 2 mL each.
# g: v, r4 @: I+ p/ Y6 I& K1 EThe skin was moist and smooth and somewhat
" m3 D0 {, Z2 I* t6 j8 L) _" Yoily. No axillary hair was noted. There were no+ _6 a  E+ B7 F/ o
abnormal skin pigmentations or café-au-lait spots.
: A9 |7 J! |0 O4 B% u0 Z( I( CNeurologic evaluation showed deep tendon reflex 2+
5 d% d/ [% `. X. ^8 Y! Wbilateral and symmetrical. There was no suggestion
6 O0 [* M6 q& A, e$ {of papilledema.. m& S( O+ l% j! }0 L
Laboratory Evaluation
2 v% E: k% R: r# @) j$ v- yThe bone age was consistent with 28 months by
4 n: ?' V& x9 g/ ~using the standard of Greulich and Pyle at a chrono-
! G2 a( j2 H9 l6 x0 b5 c# _9 U! D9 Hlogic age of 16 months (advanced).5 Chromosomal7 i+ ^" D) y( o
karyotype was 46XY. The thyroid function test
& J2 @$ ~6 l% F. K6 ?5 r. q+ G6 oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
: a- k! F0 P% m9 @9 A4 y3 alating hormone level was 1.3 µIU/mL (both normal).
, V8 c6 o& \; F3 _The concentrations of serum electrolytes, blood, H, S4 U, C) ^' K
urea nitrogen, creatinine, and calcium all were2 T9 O# k) C3 F8 |. I
within normal range for his age. The concentration/ O) `' g+ r% B7 X
of serum 17-hydroxyprogesterone was 16 ng/dL: T( ~( D% t( f- l' ^9 \
(normal, 3 to 90 ng/dL), androstenedione was 20
0 S8 |1 r3 P3 F/ L8 L+ ]  fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( s# R* H7 `4 ^& wterone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 ], m' F0 d; [8 @/ b, Ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 @5 x9 H  g% [: c& f. ^4 S49ng/dL), 11-desoxycortisol (specific compound S)
: q8 V0 U5 f  c1 nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, x# i# R9 f! R1 F& X( Z6 b
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( j3 o! X2 J+ T8 W8 D8 E7 `- ^
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 w; C) }7 K* r
and β-human chorionic gonadotropin was less than
1 G! e( o# r- S& j: r6 t0 z5 mIU/mL (normal <5 mIU/mL). Serum follicular) t8 ?; g: n5 i4 e5 d; b
stimulating hormone and leuteinizing hormone
2 M+ j7 O' a+ o5 V+ Uconcentrations were less than 0.05 mIU/mL
7 ~7 r: g6 [. F8 ~(prepubertal).  Z9 f+ T; u- Y" \7 x
The parents were notified about the laboratory
. @9 w% Z8 X7 D/ P, k% {: l  l1 I6 gresults and were informed that all of the tests were; P$ L9 ^' _' I2 x4 \0 D- J$ J
normal except the testosterone level was high. The
$ v7 |* z3 H# z7 }. h/ Ufollow-up visit was arranged within a few weeks to
1 S6 Q% j' ^3 c: n- M( [# e# kobtain testicular and abdominal sonograms; how-. @: |/ Z) u* o
ever, the family did not return for 4 months.. i8 Y% \* W$ ~/ g
Physical examination at this time revealed that the& a  v: [  r3 A& F8 V
child had grown 2.5 cm in 4 months and had gained* w5 ?# N' [, _( Y
2 kg of weight. Physical examination remained4 ]4 b6 L/ G$ r  ?8 Y0 \
unchanged. Surprisingly, the pubic hair almost com-. b) q& L- _# E$ K5 s8 _* h) @
pletely disappeared except for a few vellous hairs at( N/ ^, u" C# x: `
the base of the phallus. Testicular volume was still 2( E7 [# I, |' C; [3 b& m
mL, and the size of the penis remained unchanged.7 d; L8 K8 \* t
The mother also said that the boy was no longer hav-8 v: Y6 O3 H, H. K$ [) i
ing frequent erections.  U( |% f, Y! J9 T! r2 x+ |! [
Both parents were again questioned about use of
# r/ ?% h. }' l5 @4 u2 `$ b3 Hany ointment/creams that they may have applied to
* j* _8 y& y# k) v7 ]! }. H4 \* dthe child’s skin. This time the father admitted the) C* o# a* f$ @, n2 c$ E% m
Topical Testosterone Exposure / Bhowmick et al 541! o! @2 t6 X& @. h- N0 {
use of testosterone gel twice daily that he was apply-1 E6 ]. @$ R1 M  s# C
ing over his own shoulders, chest, and back area for* N7 W+ h: l" H. h, q4 a! v$ w
a year. The father also revealed he was embarrassed! u) R# z! O) v6 V" M, ^  k6 I
to disclose that he was using a testosterone gel pre-- Q! n  J' j+ C9 ?9 K' |
scribed by his family physician for decreased libido; {/ I' e! `6 Q  R7 [8 ^' B
secondary to depression.
9 s$ A/ J: D7 _8 l+ Q# q$ U& IThe child slept in the same bed with parents.* _# z. [9 Z! H2 i
The father would hug the baby and hold him on his. c+ f; `5 y& v" t, c4 w5 j$ j
chest for a considerable period of time, causing sig-8 g7 y, R5 H# P
nificant bare skin contact between baby and father./ b2 Q# F3 Q5 P# t
The father also admitted that after the phone call,, p6 ?. i. t( V1 `: h$ ?# F
when he learned the testosterone level in the baby
  n# q' M4 w0 S8 |$ l  Xwas high, he then read the product information
" v& |8 ^- P( E  Q( Spacket and concluded that it was most likely the rea-
: ?( m2 g: F0 ^3 t5 C+ zson for the child’s virilization. At that time, they
4 r) I9 u7 Z% ddecided to put the baby in a separate bed, and the
/ S( B4 f% c, F0 x7 I& @father was not hugging him with bare skin and had
; G) L9 Y0 M) h7 Kbeen using protective clothing. A repeat testosterone# D+ i1 C) r% T, V
test was ordered, but the family did not go to the
7 M$ S0 R. }6 V4 |# }. vlaboratory to obtain the test.; j5 r0 J7 F: i) f
Discussion' M) S6 E7 |- Q& |; x
Precocious puberty in boys is defined as secondary# R. }- I5 }3 E; n* M7 j
sexual development before 9 years of age.1,4
) t0 Z& W" C, @0 a, a" C5 ePrecocious puberty is termed as central (true) when
# p  C. h/ |; Mit is caused by the premature activation of hypo-
$ ~! y2 G4 ^+ ?, q6 G4 Uthalamic pituitary gonadal axis. CPP is more com-
+ }& m$ Y8 s# W+ Wmon in girls than in boys.1,3 Most boys with CPP; k% W6 ^3 U% A6 V
may have a central nervous system lesion that is, l/ K# X' t8 m1 u& T4 _5 b
responsible for the early activation of the hypothal-2 @$ ?8 V, ^+ @- z5 K3 S) V# a
amic pituitary gonadal axis.1-3 Thus, greater empha-% y# m  ?, ^" k* `" [
sis has been given to neuroradiologic imaging in1 ?" x' L. A9 N* `) a
boys with precocious puberty. In addition to viril-) v1 \9 M- d, j" W0 r
ization, the clinical hallmark of CPP is the symmet-
. y( S0 D: Z% X; p4 a1 krical testicular growth secondary to stimulation by
  ~- ~# f, u) Wgonadotropins.1,3
! Z% P+ V) t5 M' G5 e0 _Gonadotropin-independent peripheral preco-8 p2 h- B0 b7 q# U
cious puberty in boys also results from inappropriate
$ u. z9 J9 k; P. j2 E! ?androgenic stimulation from either endogenous or4 B  t2 z- M) j, ~4 e
exogenous sources, nonpituitary gonadotropin stim-
# `: ]8 E! A. m' l+ u' aulation, and rare activating mutations.3 Virilizing1 I; u  b4 i* T0 o. [
congenital adrenal hyperplasia producing excessive# h; W+ l0 j# G  [& t1 f( @
adrenal androgens is a common cause of precocious; s$ v( C/ u4 d2 n% v' n
puberty in boys.3,4
+ ^, ]. M/ P  I) S5 WThe most common form of congenital adrenal3 R6 c8 D) ^# p# J& [& K  G* b
hyperplasia is the 21-hydroxylase enzyme deficiency.4 ?- u9 B* ^6 p; F
The 11-β hydroxylase deficiency may also result in
! n& X" n/ @# h, C( y. n) i" |$ j) N- Mexcessive adrenal androgen production, and rarely,
6 K" c$ m8 x% p& I. [an adrenal tumor may also cause adrenal androgen
, L4 p, q* g3 M$ E8 Rexcess.1,31 _. x8 M, r  K$ o
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ M3 M% _; c5 v! w9 N* t
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 S; {& m: [  D# Q6 vA unique entity of male-limited gonadotropin-" q3 s4 I- j9 [3 p  i( X, q8 j
independent precocious puberty, which is also known* n. F4 J" _) l, Y
as testotoxicosis, may cause precocious puberty at a
5 ?- T/ D4 K5 N) o1 p6 z, E, zvery young age. The physical findings in these boys
/ K0 [1 H9 F8 `. [( B: Gwith this disorder are full pubertal development,
  A4 x* @6 ~% s0 e8 Q5 L$ v5 }including bilateral testicular growth, similar to boys
: J: `* ?0 c% ^, q# L8 zwith CPP. The gonadotropin levels in this disorder
8 y/ r! w% ^+ {6 U7 P" C3 Ware suppressed to prepubertal levels and do not show
3 J2 ^! J: n; Q& H9 k, g8 S& ^0 hpubertal response of gonadotropin after gonadotropin-" \1 B$ o/ m1 @5 x; f4 t2 w
releasing hormone stimulation. This is a sex-linked) X; G8 F. k" }
autosomal dominant disorder that affects only$ n- G5 Y' H" P' z( p& F! d1 ^
males; therefore, other male members of the family
" q1 m% W% b1 u9 @; y, Emay have similar precocious puberty.3$ b* C" e( ]6 q9 S4 @* r& C3 ?
In our patient, physical examination was incon-/ J3 e* ?$ ^  C9 a/ Y! x7 _
sistent with true precocious puberty since his testi-( c) F$ d0 [! j: _9 ?1 Q
cles were prepubertal in size. However, testotoxicosis+ g+ l, P* y) W7 I2 O( H( X
was in the differential diagnosis because his father2 T0 I5 Z7 _% x
started puberty somewhat early, and occasionally,
8 e- t8 k0 O/ e; K9 q& \9 |testicular enlargement is not that evident in the
) z/ ^7 M8 z" K( Y0 {% [1 A7 H! ibeginning of this process.1 In the absence of a neg-8 {) c1 g7 }, f& r+ B4 ^0 N( I' ~
ative initial history of androgen exposure, our
$ Q4 Y+ }2 M# A# g1 Qbiggest concern was virilizing adrenal hyperplasia,( Q! K- H4 g; a4 M- j  g! f
either 21-hydroxylase deficiency or 11-β hydroxylase. J+ C. C! K$ D  j9 b" {) C& K
deficiency. Those diagnoses were excluded by find-. c/ m: K) G, |2 r
ing the normal level of adrenal steroids.
6 d; d7 [6 i% A. a. i, lThe diagnosis of exogenous androgens was strongly  P( u0 Z) z+ [* k% T
suspected in a follow-up visit after 4 months because) l( Q* C3 G2 W6 B. q, S
the physical examination revealed the complete disap-
  }" v8 x# E8 npearance of pubic hair, normal growth velocity, and
3 r& e) D6 n# L3 g# ?( Xdecreased erections. The father admitted using a testos-0 F% V/ g- {% m3 u7 a0 k( X
terone gel, which he concealed at first visit. He was- t$ a: E% n3 g# S7 r* q
using it rather frequently, twice a day. The Physicians’- l7 x; A$ g* F* \4 {3 K8 @: P
Desk Reference, or package insert of this product, gel or
" r5 F8 d9 H4 L1 Zcream, cautions about dermal testosterone transfer to  P( Y( d" ]7 c9 O+ I" y% [
unprotected females through direct skin exposure.  L; @5 J6 u0 `) d+ w$ k" k( ]- B# s
Serum testosterone level was found to be 2 times the
8 v" f) E, m0 @baseline value in those females who were exposed to
/ q! P( h" M' s( A- B  aeven 15 minutes of direct skin contact with their male
+ E" ~$ K' P* T% vpartners.6 However, when a shirt covered the applica-; I4 U6 h# J" f
tion site, this testosterone transfer was prevented.; ^8 M; i0 ?2 s7 z& f1 D6 s
Our patient’s testosterone level was 60 ng/mL,
- \) f6 A6 Y& }- F& owhich was clearly high. Some studies suggest that
& ?* j& }" l: `% R* o; H! n% `dermal conversion of testosterone to dihydrotestos-& X8 {; E! m+ r" C
terone, which is a more potent metabolite, is more
* p3 Z6 R4 c/ k* hactive in young children exposed to testosterone% j: {5 N, a1 P$ @* L2 A
exogenously7; however, we did not measure a dihy-
0 T; C6 e# P7 b/ c. P4 Fdrotestosterone level in our patient. In addition to
& `. q6 T( F2 Z% vvirilization, exposure to exogenous testosterone in
0 n8 Q' y$ ]. }  ochildren results in an increase in growth velocity and
# P* w# i: w) c0 ~3 P& i7 Jadvanced bone age, as seen in our patient.
. @1 ]2 H5 r1 n2 Z% PThe long-term effect of androgen exposure during, A7 E. L  o% A( C
early childhood on pubertal development and final# ?  m( b' A# |
adult height are not fully known and always remain
5 h  f3 |) G0 V! m( Y/ [1 Ca concern. Children treated with short-term testos-
/ z2 N) r# |& X  x0 f4 Aterone injection or topical androgen may exhibit some
* s8 I! B& Z! Facceleration of the skeletal maturation; however, after% L9 Y: q8 w- D% z- l! d
cessation of treatment, the rate of bone maturation
: O9 k. M6 @" e. pdecelerates and gradually returns to normal.8,9
+ `: n3 }5 l2 R/ J5 KThere are conflicting reports and controversy
3 E- K. U( b; W5 d5 j* iover the effect of early androgen exposure on adult8 H5 M- U4 G; E
penile length.10,11 Some reports suggest subnormal
- x1 @3 Y) d' g9 e: dadult penile length, apparently because of downreg-
; G, n  u( A0 Zulation of androgen receptor number.10,12 However,
( p/ {. d+ G, a% H8 ^' YSutherland et al13 did not find a correlation between+ J0 K- }, U# B7 H2 i9 S2 E1 O
childhood testosterone exposure and reduced adult5 }, B) X3 G! ?4 J2 w' a- `
penile length in clinical studies.
0 Z7 l# ]5 i+ E3 F+ jNonetheless, we do not believe our patient is
- n9 {+ V! M# d' F' cgoing to experience any of the untoward effects from; o5 L( E, ~# ~) ?6 u1 Y# g2 @
testosterone exposure as mentioned earlier because: m: ?8 G  d) {4 [( I  U$ }
the exposure was not for a prolonged period of time.$ @+ R2 S8 [+ e! x# i1 b$ v
Although the bone age was advanced at the time of) u' C/ G' W% M1 [7 M9 ^& @0 l$ S" E
diagnosis, the child had a normal growth velocity at7 X& J# c- S) ?' S; b# Y$ q) p) u
the follow-up visit. It is hoped that his final adult
' E9 Z! A. v9 S# X1 Uheight will not be affected.# a. E3 Q( F7 }2 b) r/ y
Although rarely reported, the widespread avail-
. I1 ^( i$ X3 \! G3 uability of androgen products in our society may
$ R3 |8 Y* R3 S% V* X! a+ d/ \8 c( \6 Sindeed cause more virilization in male or female
2 f9 g, `3 r2 c" }children than one would realize. Exposure to andro-
) _0 D2 ^" k4 T& Ugen products must be considered and specific ques-: m( d; t1 I" I5 Y7 J- M
tioning about the use of a testosterone product or/ L# s1 x5 P  F' Q4 V
gel should be asked of the family members during) p% p. l; q* R
the evaluation of any children who present with vir-6 {2 V) h( |1 k" Q, ~$ E3 S: W
ilization or peripheral precocious puberty. The diag-
% @2 Z2 m  ~4 y5 ?' S2 `nosis can be established by just a few tests and by
2 L* m3 k! j' C: O0 E' m4 \appropriate history. The inability to obtain such a
/ l1 b. y) }1 Z' S3 g: |history, or failure to ask the specific questions, may
7 @3 R+ d4 V% G3 a3 _' A% }+ qresult in extensive, unnecessary, and expensive
% L4 \3 b/ G; m1 X) h8 V" E/ Finvestigation. The primary care physician should be
1 a, \& @7 h* @3 N. s( ^8 J5 H" vaware of this fact, because most of these children) Y. D% [" K! G0 N, `
may initially present in their practice. The Physicians’
* ?; @) |# {6 d6 Y  LDesk Reference and package insert should also put a
) P- Z0 |, j# m* Z* M5 Rwarning about the virilizing effect on a male or
# c) O( e0 N  [/ Y+ e) n7 e4 s+ a% ofemale child who might come in contact with some-
' |* h! f1 _$ rone using any of these products.8 q! E# E- b. i/ C7 l
References
4 n; S+ |% f0 _8 A9 Q1. Styne DM. The testes: disorder of sexual differentiation2 W. z! O2 H+ d7 }% e4 z$ J1 o* D8 H
and puberty in the male. In: Sperling MA, ed. Pediatric: p' u# Z9 @% J9 [3 q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- E( S6 G, s* Q( a
2002: 565-628.
' a4 f' N0 ^+ m+ f* U7 i2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  H0 F0 I# f* U
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

5 D' D, M6 t6 r5 y9 X/ r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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