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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
  P6 h& f+ i2 w$ yBoy Induced by Indirect Topical* P* h1 P, b3 l' t
Exposure to Testosterone5 R7 I6 F( x% X' a4 u
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% z" S- J5 T7 V% R, \and Kenneth R. Rettig, MD1
* X' H" X2 i) `* j. CClinical Pediatrics3 Z) k0 I( N9 E* `2 L* H
Volume 46 Number 6
- T  S, ]/ K0 SJuly 2007 540-543
$ q, A  _7 `% n5 i& R; }© 2007 Sage Publications
# ^6 \2 i% {+ \9 i+ p. B; u10.1177/0009922806296651
: A) E+ D% E9 `6 R4 i1 Uhttp://clp.sagepub.com
: Q4 T2 {# u  Q' lhosted at: q, \% n! o' i& h' n
http://online.sagepub.com3 ]% n8 A5 n0 H5 v0 o8 O& |
Precocious puberty in boys, central or peripheral,* J1 O$ F3 e) o+ l
is a significant concern for physicians. Central
- G+ d# y8 X- ^. E- X8 iprecocious puberty (CPP), which is mediated4 N. F6 L( X9 ^; Z6 D' Y! l
through the hypothalamic pituitary gonadal axis, has
' N. c; r0 x2 G- N$ x# t# c* la higher incidence of organic central nervous system
: Z3 I8 M& `+ q- G* Vlesions in boys.1,2 Virilization in boys, as manifested
7 n9 |+ k% L* y6 ^6 V+ Wby enlargement of the penis, development of pubic
% t* v, e: a4 fhair, and facial acne without enlargement of testi-
0 P* E4 ^5 @; p$ `% ~cles, suggests peripheral or pseudopuberty.1-3 We
& ^" a! b3 g2 I0 c+ N! U7 zreport a 16-month-old boy who presented with the
/ d% |. m& U6 V  Venlargement of the phallus and pubic hair develop-
, p( \/ o. Y: [! P3 R* wment without testicular enlargement, which was due
% @1 @! e* @- y& H% Pto the unintentional exposure to androgen gel used by1 d9 n& u& b# j4 ]) V) ?, Z/ ]
the father. The family initially concealed this infor-9 x( Z9 D, i5 ~; D& j( \
mation, resulting in an extensive work-up for this% D/ [5 X6 R" ^' H3 m% d7 b
child. Given the widespread and easy availability of
& S$ U- f; w' b5 G* }/ W" Ltestosterone gel and cream, we believe this is proba-# I* c1 O" a" V9 M
bly more common than the rare case report in the
- C2 p2 O2 A/ ?' Tliterature.4
" d7 e) z! d% a4 cPatient Report
# y+ ]1 {# J( x; p+ u, u+ ]A 16-month-old white child was referred to the
! H8 }$ C# W1 {! p, _/ yendocrine clinic by his pediatrician with the concern
1 P6 ]* S/ i/ Vof early sexual development. His mother noticed5 I" w- t6 }7 d9 e* _
light colored pubic hair development when he was0 ~( R3 }$ |* a4 H
From the 1Division of Pediatric Endocrinology, 2University of' ^' l8 z4 m, O& d1 z
South Alabama Medical Center, Mobile, Alabama.
8 x1 z' L0 q0 N: h. S- @Address correspondence to: Samar K. Bhowmick, MD, FACE,! h8 p. u! R8 S  `
Professor of Pediatrics, University of South Alabama, College of) J  m' ~9 l$ r( {5 a
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 [7 w0 u6 G. Z. Ye-mail: [email protected].
' ~/ B8 X0 O, b5 K1 }5 habout 6 to 7 months old, which progressively became
) R$ V5 e* L# Q% Adarker. She was also concerned about the enlarge-
5 }4 @4 j0 \& w5 Ument of his penis and frequent erections. The child0 e. A# S: P: h$ O) C9 Z
was the product of a full-term normal delivery, with% s/ x1 W! O$ Z  t$ h
a birth weight of 7 lb 14 oz, and birth length of0 I% y  |9 s3 D# x" ], c
20 inches. He was breast-fed throughout the first year
3 Y" x2 \5 \+ K- }; R$ Wof life and was still receiving breast milk along with8 o) D0 j; J6 g9 N
solid food. He had no hospitalizations or surgery,
' |: H! i) i2 B3 S  m$ I! o9 }and his psychosocial and psychomotor development
, G8 j' A3 J% xwas age appropriate.
% G6 ]- r6 J' q# C# m  g7 q( kThe family history was remarkable for the father,
3 M, V# k' I: i" E) Ewho was diagnosed with hypothyroidism at age 16,% _7 y9 z9 \  [& ?3 ]& y: o# z8 h
which was treated with thyroxine. The father’s7 G+ v2 _* s8 f* E
height was 6 feet, and he went through a somewhat" X" g! n- e3 O  n- G1 E$ D; K3 u
early puberty and had stopped growing by age 14.3 P, [8 m3 X, L) H8 Q7 s! `/ O: o
The father denied taking any other medication. The; f1 N3 O. B7 d) s* `1 z! g
child’s mother was in good health. Her menarche
# c9 S# }  O+ v7 D) Iwas at 11 years of age, and her height was at 5 feet
  M% v' N$ g) L4 i- u. w5 inches. There was no other family history of pre-( U: `. R3 X# H! g$ U2 D4 T
cocious sexual development in the first-degree rela-8 h! T' V& W/ _$ o' \5 F
tives. There were no siblings.
. C9 ]& w3 n" ]* U8 m0 T/ I1 B6 mPhysical Examination7 j2 [6 I* E+ |+ n; t1 S/ Z7 t6 y# Y. o
The physical examination revealed a very active,7 j/ u/ v* O8 t
playful, and healthy boy. The vital signs documented; t4 W' L4 h# ]3 L) u
a blood pressure of 85/50 mm Hg, his length was/ E7 V$ v" G% [( w6 F4 C  l/ \
90 cm (>97th percentile), and his weight was 14.4 kg" Q/ [) o8 _: C! k
(also >97th percentile). The observed yearly growth
- K4 C1 U# @  @7 D2 H. gvelocity was 30 cm (12 inches). The examination of+ L: L6 v7 F3 v
the neck revealed no thyroid enlargement.  P2 o' n$ {) u) U  p
The genitourinary examination was remarkable for
+ e$ v8 g+ c( E/ N! j1 ?enlargement of the penis, with a stretched length of
( i% p) n7 _8 r- _8 M8 cm and a width of 2 cm. The glans penis was very well
+ A1 r- [5 m# G2 E/ r! K3 rdeveloped. The pubic hair was Tanner II, mostly around, Z' r) A/ P0 i" }5 J, }$ {
5408 {! _) I: e- k4 t( ]( l1 V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ Z+ w4 }  y* t) n. z: P5 Z. dthe base of the phallus and was dark and curled. The
6 S) Q$ `& \. \# ~testicular volume was prepubertal at 2 mL each.% l1 s, m0 u/ X$ |2 u
The skin was moist and smooth and somewhat
2 T* d. {! x8 J, {9 D, R% Uoily. No axillary hair was noted. There were no! O$ I" A+ m- @. M1 a( ]/ h
abnormal skin pigmentations or café-au-lait spots.: u* a' w1 ~+ e+ ]# V7 h, j
Neurologic evaluation showed deep tendon reflex 2+
  p. W' ?' S2 \; n' c* ]" fbilateral and symmetrical. There was no suggestion5 f: Q6 x8 w$ X9 k% f: Q/ p7 f
of papilledema.: M5 n3 Y; \% A- m
Laboratory Evaluation
- X" d; K# Y) f1 o! E& lThe bone age was consistent with 28 months by
, U% c& b7 R# c/ |8 _, Q2 S( Busing the standard of Greulich and Pyle at a chrono-- z6 J& {% @. H! b+ _8 `5 V. M
logic age of 16 months (advanced).5 Chromosomal6 Q4 y: t+ z- T) h
karyotype was 46XY. The thyroid function test
9 U" f$ l8 i8 G/ ^& P$ N" dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-, @: {/ S6 p# u; h0 C2 l' C
lating hormone level was 1.3 µIU/mL (both normal).
4 a7 I# {# `- c; `/ }The concentrations of serum electrolytes, blood+ N4 e* l( v$ Z
urea nitrogen, creatinine, and calcium all were  N8 V7 P& e# ~6 _
within normal range for his age. The concentration4 b3 d( K6 ^8 Q7 e" O) y+ v
of serum 17-hydroxyprogesterone was 16 ng/dL
4 N& f# F4 m4 [8 S0 o) p4 \- K(normal, 3 to 90 ng/dL), androstenedione was 20! F8 i; J" A; P. R+ K, g# t5 ^
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 o6 W0 @1 o* k" t* z, ^/ q+ {. gterone was 38 ng/dL (normal, 50 to 760 ng/dL),( `; B) g- U1 c
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 I7 i! c1 }# C# `8 j1 o49ng/dL), 11-desoxycortisol (specific compound S)
+ B* p' z2 F4 |9 {was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' ]4 c6 V, T+ Q. Gtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ B8 ?. x2 J. Z9 Q+ U
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( i* U8 m  B2 w) k
and β-human chorionic gonadotropin was less than
' e! A" a& s" E" o* P& ?: G5 mIU/mL (normal <5 mIU/mL). Serum follicular- `7 D7 q7 W" G; V8 M+ X; A
stimulating hormone and leuteinizing hormone
7 c1 w. G4 |; [& e  ]: W* vconcentrations were less than 0.05 mIU/mL& m& u4 ^" W- K% \
(prepubertal).
& k, M) `/ ^( w! v- h* n7 wThe parents were notified about the laboratory7 o  _6 ]- A" i0 L2 _$ j- @
results and were informed that all of the tests were0 k: m, |$ z3 c) {6 y
normal except the testosterone level was high. The  M! G3 }* S% @' C; Q
follow-up visit was arranged within a few weeks to
0 r& s! \! C! q, R6 |0 a, z5 ~obtain testicular and abdominal sonograms; how-
# K4 |/ |2 o1 L2 ]! U8 Vever, the family did not return for 4 months.
. D1 s; ]5 I& u, N- aPhysical examination at this time revealed that the; _" n5 K  _4 Z. n
child had grown 2.5 cm in 4 months and had gained! h# g( t' N- x# M- j3 T, I
2 kg of weight. Physical examination remained) B2 g* e, T  c; c
unchanged. Surprisingly, the pubic hair almost com-. u- W' Z! `* s" a3 S
pletely disappeared except for a few vellous hairs at( X- L9 j* L. o% M; b- S& _3 k$ |$ f
the base of the phallus. Testicular volume was still 2
- ?* {; y% ]7 u: _7 y1 j9 a8 j( rmL, and the size of the penis remained unchanged.
& j$ ?9 n3 n& U1 iThe mother also said that the boy was no longer hav-
1 N. z% _  `$ n% Oing frequent erections.
7 n. W& e; y$ N4 tBoth parents were again questioned about use of. ?) o. n1 q4 ?0 f5 G5 o* o* ~! H
any ointment/creams that they may have applied to
! ?/ q" D/ |( X/ g% ithe child’s skin. This time the father admitted the
# d/ D* |( j5 O& y5 rTopical Testosterone Exposure / Bhowmick et al 541# ]7 Q) f& c6 G, a# O# S
use of testosterone gel twice daily that he was apply-& i8 e/ K9 `  `0 x- i$ m
ing over his own shoulders, chest, and back area for- t  d' z& H7 S1 s' I$ j9 X
a year. The father also revealed he was embarrassed  Q8 O! ?+ B# ^% x' `" c9 \1 N: ~
to disclose that he was using a testosterone gel pre-' Z( |& q! R9 N2 q
scribed by his family physician for decreased libido1 ?( @1 Y7 _/ g
secondary to depression.
% G, m. ?/ G8 R3 O* e9 e/ `7 AThe child slept in the same bed with parents./ ^7 s" R4 U0 a  |& V
The father would hug the baby and hold him on his
! a) y# _4 c% o1 e5 Fchest for a considerable period of time, causing sig-
* D& `5 C6 Q. `1 O/ ^3 B- ~nificant bare skin contact between baby and father.
& b; v' r' M8 I4 Y. J! F1 }6 tThe father also admitted that after the phone call,
$ a4 b, V& q" y- @when he learned the testosterone level in the baby
& f9 O" E1 J" I" k3 C5 h# G, q' owas high, he then read the product information
" V0 b6 }* q, z% [+ N: k! npacket and concluded that it was most likely the rea-1 C  H; B) ^) e1 {1 \0 n+ x) @
son for the child’s virilization. At that time, they
# n0 z. C+ w9 Odecided to put the baby in a separate bed, and the4 {' r* J+ C5 V5 r6 u
father was not hugging him with bare skin and had
6 K6 C9 E' Y1 R' N3 x1 X$ i$ xbeen using protective clothing. A repeat testosterone
) ^3 Y- Z2 E& K5 i; {test was ordered, but the family did not go to the& `7 w1 K& s8 \. R
laboratory to obtain the test.
# C% [+ T& g' `& g+ |) i' sDiscussion
$ l) i3 Q! U/ T4 n0 r  ~Precocious puberty in boys is defined as secondary1 ]  |+ C/ c- y
sexual development before 9 years of age.1,4
  T& }5 t1 G  Q1 HPrecocious puberty is termed as central (true) when
4 @% @9 ^2 ]' s8 bit is caused by the premature activation of hypo-
. k* u# [5 g. S. W( F. lthalamic pituitary gonadal axis. CPP is more com-5 V' \4 P% A/ a8 H/ `
mon in girls than in boys.1,3 Most boys with CPP
$ N  `6 e8 [  Y7 P& bmay have a central nervous system lesion that is0 }9 a9 d; L* E! T
responsible for the early activation of the hypothal-
+ O8 m/ f2 c1 ~8 ~5 ?+ u7 a* I* e+ y/ tamic pituitary gonadal axis.1-3 Thus, greater empha-# m% \7 ?. Q6 q" L
sis has been given to neuroradiologic imaging in
; N  k+ \% P+ q" Cboys with precocious puberty. In addition to viril-
6 B2 B4 a" e: p- J: t  k; oization, the clinical hallmark of CPP is the symmet-2 \! R) N' x& `+ ~: n7 M( ]
rical testicular growth secondary to stimulation by0 G/ Q  `% N$ A
gonadotropins.1,3
3 ~# t, ^* y  |1 RGonadotropin-independent peripheral preco-
- U/ `8 y; Q+ Z5 h! E3 [  Ccious puberty in boys also results from inappropriate
3 k2 H4 g" f$ u0 B1 Wandrogenic stimulation from either endogenous or
7 @0 D0 O+ @- T8 Z2 A5 oexogenous sources, nonpituitary gonadotropin stim-$ e$ p1 Z; o5 z! T  L
ulation, and rare activating mutations.3 Virilizing8 i' w+ h2 d4 Q, }9 l$ ]% |; S0 x/ C
congenital adrenal hyperplasia producing excessive5 X4 o  j" [  A* @5 e! T
adrenal androgens is a common cause of precocious; Q3 K/ @9 k8 _$ \
puberty in boys.3,4  u' U6 s/ r: i3 @$ b7 o
The most common form of congenital adrenal
+ Q3 v* q" E. V$ n: H: fhyperplasia is the 21-hydroxylase enzyme deficiency.! [7 h3 o- i4 [7 s
The 11-β hydroxylase deficiency may also result in. M: w# ~1 t( q- u
excessive adrenal androgen production, and rarely,  R' H( o& T+ @9 g5 a
an adrenal tumor may also cause adrenal androgen
/ I5 k; h' C- B! \/ M6 cexcess.1,3& H+ K. ~8 g# R' U. S
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) b  B8 R& k# h- S542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 [1 g- q. n8 g0 A4 A! pA unique entity of male-limited gonadotropin-3 L* ?' [& [+ P7 W: t3 o5 o
independent precocious puberty, which is also known
7 F  n3 w! }8 W: c6 E' I' Xas testotoxicosis, may cause precocious puberty at a) J- y, S, V* ]
very young age. The physical findings in these boys7 {8 s2 ]" Y1 W( K$ ^" I
with this disorder are full pubertal development,( f5 f1 y4 y2 l" p$ N$ ?/ B; Z' B
including bilateral testicular growth, similar to boys/ d4 S: y" {; K$ u: ?/ Y
with CPP. The gonadotropin levels in this disorder0 Z$ {6 N8 a8 V6 Q. m1 N6 f. D1 h6 W
are suppressed to prepubertal levels and do not show
/ v5 ~1 u2 O0 v& Q# l( N4 Zpubertal response of gonadotropin after gonadotropin-
! j1 F2 I4 e! ?/ S0 h, M' v* v- s3 Qreleasing hormone stimulation. This is a sex-linked
% L5 g  ~) Y# m- F. Iautosomal dominant disorder that affects only" a, A+ m" h' d3 }+ t8 K
males; therefore, other male members of the family
9 F/ c. C5 v( Z! V8 V; @' |6 ]8 Jmay have similar precocious puberty.3* r$ S" d! |' c6 ^8 ~3 s
In our patient, physical examination was incon-
2 Z. U( l# Z6 E  qsistent with true precocious puberty since his testi-. S" L6 Y$ E9 p* M" X8 p
cles were prepubertal in size. However, testotoxicosis
1 g& X( m9 j! [7 D$ Hwas in the differential diagnosis because his father
- @$ n1 P1 y5 S& {started puberty somewhat early, and occasionally,/ R# b+ ~4 D7 A- ~: n" D$ |
testicular enlargement is not that evident in the
3 r5 S* W2 v7 ^/ Hbeginning of this process.1 In the absence of a neg-
. Y) ]/ m; H- kative initial history of androgen exposure, our2 L+ N3 t0 f+ r  N8 T$ z
biggest concern was virilizing adrenal hyperplasia,! O3 j$ f8 u, ^$ h1 [
either 21-hydroxylase deficiency or 11-β hydroxylase
. [. x1 m, b, G- x2 Vdeficiency. Those diagnoses were excluded by find-
. d) P5 w! n) q; E: R0 p3 x1 `ing the normal level of adrenal steroids.
! i! E1 n* D! N4 k1 w1 dThe diagnosis of exogenous androgens was strongly
6 B$ `2 h& _9 W% i, y9 ~suspected in a follow-up visit after 4 months because
9 Z" s8 o" k+ S0 T& Fthe physical examination revealed the complete disap-
6 P" t/ e) u1 a5 Spearance of pubic hair, normal growth velocity, and
9 ]. g; @1 I6 u" X) g8 d. T( kdecreased erections. The father admitted using a testos-8 R" \7 I1 J" m
terone gel, which he concealed at first visit. He was7 G4 W5 O8 C/ O  m( B4 o
using it rather frequently, twice a day. The Physicians’4 R/ f7 j5 K/ ?( y3 }
Desk Reference, or package insert of this product, gel or4 I! K( b7 O2 t& i6 f6 |* P
cream, cautions about dermal testosterone transfer to5 ^, E* w3 p2 i
unprotected females through direct skin exposure.
: t3 l/ \7 i, vSerum testosterone level was found to be 2 times the
: `- }4 Q) z% S" `9 K% Kbaseline value in those females who were exposed to
, y/ ^& \& }, z/ z+ seven 15 minutes of direct skin contact with their male
, G* Y3 T. m; Z! O2 v* Q, y: ?partners.6 However, when a shirt covered the applica-
8 I* e( g( U& v! g, `4 Y; Y0 Ktion site, this testosterone transfer was prevented., k. T' b; i/ b8 C
Our patient’s testosterone level was 60 ng/mL,
; Y" `# I1 u% _8 F% t9 gwhich was clearly high. Some studies suggest that1 a' K' H6 ]( u
dermal conversion of testosterone to dihydrotestos-+ W3 |2 z8 `" a5 A$ a9 A: h7 R6 e
terone, which is a more potent metabolite, is more
$ y0 d& [( O7 E0 `" s9 yactive in young children exposed to testosterone
/ o1 K/ ~; w' q) Z9 H# yexogenously7; however, we did not measure a dihy-4 ?: A. p1 d+ r, Z4 P1 |
drotestosterone level in our patient. In addition to
1 g. P+ p+ @1 u3 o" n' ^+ Y) U6 pvirilization, exposure to exogenous testosterone in
' F) t" N6 M% V' K* Pchildren results in an increase in growth velocity and8 q( i4 T* K( G, y3 R
advanced bone age, as seen in our patient.
3 ?* H4 g5 G1 O' {# _; M% XThe long-term effect of androgen exposure during; ^, [; v9 x. S! s1 O
early childhood on pubertal development and final
* B$ z. e* ]6 p  w9 eadult height are not fully known and always remain
9 ~! ~3 ~, \& V# g8 f" Y/ x+ Za concern. Children treated with short-term testos-
+ r% k8 x. v; F' }1 V) h. Oterone injection or topical androgen may exhibit some
, d  E5 ]. g: n& r& x% Qacceleration of the skeletal maturation; however, after, D$ _7 @: d& R( Q
cessation of treatment, the rate of bone maturation
8 ]6 [1 a# B2 I! k, @: c3 |& Sdecelerates and gradually returns to normal.8,9& |% d. R# N' x% R% [
There are conflicting reports and controversy& W, u. y( `; }, r& j% e
over the effect of early androgen exposure on adult
# p3 G% N+ t+ W% L# Apenile length.10,11 Some reports suggest subnormal  k/ @9 [! L2 F' k
adult penile length, apparently because of downreg-
) B) {  t( w" lulation of androgen receptor number.10,12 However,
* e! c9 a$ S; u4 Z# P$ N: z4 \Sutherland et al13 did not find a correlation between4 ]( ~0 E* ^- }
childhood testosterone exposure and reduced adult
1 W' _2 E3 }, Q( Z9 C  npenile length in clinical studies.  D6 |7 `+ Q9 I" O. ~
Nonetheless, we do not believe our patient is
; G# d0 c! y3 Y" t: agoing to experience any of the untoward effects from
0 w! W, [* V0 [6 Itestosterone exposure as mentioned earlier because9 b% e  ]' N' v# o! j4 {
the exposure was not for a prolonged period of time.
  q* _/ f8 }8 T1 ~Although the bone age was advanced at the time of% |" \/ s" P8 C# m2 G
diagnosis, the child had a normal growth velocity at
. F- k- W0 Z9 W, @8 jthe follow-up visit. It is hoped that his final adult
0 V0 x$ n8 G$ }, pheight will not be affected.
5 m" N: x! t3 y+ I  S2 W: BAlthough rarely reported, the widespread avail-
5 {( ^& r5 ^  g& C" Lability of androgen products in our society may
- `3 Z+ t, w* J& Yindeed cause more virilization in male or female
. m9 T# }7 g  @4 X% ^$ ochildren than one would realize. Exposure to andro-
1 H) I# h, r1 y- o1 mgen products must be considered and specific ques-
% B# H5 h; |5 {7 \& S* i1 stioning about the use of a testosterone product or  K9 m% E& Q  n; s6 N8 Q6 t
gel should be asked of the family members during
9 x  s6 V% R2 U( k) othe evaluation of any children who present with vir-
9 w4 `" E2 I8 a* W+ g6 {ilization or peripheral precocious puberty. The diag-
. \+ X! y  \* [0 X9 c, Knosis can be established by just a few tests and by4 A$ q+ ^7 `6 i. q* V
appropriate history. The inability to obtain such a$ @, D% J: M' l# h) R
history, or failure to ask the specific questions, may) \0 F' ^- E/ a; `3 e: e
result in extensive, unnecessary, and expensive' G' C- k$ ~) b$ t$ y/ \0 h# R
investigation. The primary care physician should be4 d. p9 v1 j* E& K3 k/ W4 _
aware of this fact, because most of these children
- _/ n* L( Y: k3 tmay initially present in their practice. The Physicians’: s( C3 {7 _& X
Desk Reference and package insert should also put a
7 ^. k; A; }: z  S3 m3 W) \warning about the virilizing effect on a male or
8 }. |. y1 |" R& O/ a4 rfemale child who might come in contact with some-# P7 R" a) m  Z2 O2 `5 V
one using any of these products.
. D3 h" e& M9 O) aReferences
8 q; c2 \) f5 J1 j3 J% {) g1. Styne DM. The testes: disorder of sexual differentiation
* _; w  B3 P7 N$ V- i: L, Dand puberty in the male. In: Sperling MA, ed. Pediatric
5 Z# c* x( E& @7 e" DEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: L1 @8 w- ~& Y( N) [
2002: 565-628.
( q& k4 ~! Z& _* k$ Y2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 K  n" e' E8 g$ Y- jpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
! ^( P( ]8 t2 a7 `Boy Induced by Indirect Topical9 n( ]! d7 Q& r  ]. H
Exposure to Testosterone
6 C9 b" {" H- uSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; l' X) X' m$ Q
and Kenneth R. Rettig, MD1' _  M- q. m0 n$ ]  ~9 A
Clinical Pediatrics
! K0 [$ [: \, {# AVolume 46 Number 6: `  ^  i0 M' K2 Q# \* {& R
July 2007 540-543( A% q( j" v9 T9 Y
© 2007 Sage Publications, q, |4 E' Y$ s! k" ]. l% l
10.1177/0009922806296651
6 W# _5 D( l7 Khttp://clp.sagepub.com5 a7 E- I+ y! l' G& U! j6 \$ v( q  g
hosted at
2 Z( \/ U3 L+ z& Thttp://online.sagepub.com2 b: N/ k3 S: q2 W9 i, h+ k; X& A4 @
Precocious puberty in boys, central or peripheral,
6 f) V4 d! [( o, p% {+ }is a significant concern for physicians. Central: k5 P. c2 s) W! Z* j  O
precocious puberty (CPP), which is mediated1 @) p" D* N( F( r
through the hypothalamic pituitary gonadal axis, has
1 @$ l1 p) G" D1 Y. O$ ~1 O* w' }a higher incidence of organic central nervous system9 Z, w; D  \  L6 k
lesions in boys.1,2 Virilization in boys, as manifested) p. B, ]% G# S; j: K1 V* ~; {! f% D
by enlargement of the penis, development of pubic; M8 I, m7 o: R. O5 b' y7 c6 k
hair, and facial acne without enlargement of testi-
  X' s/ X4 Y$ V# H7 c$ acles, suggests peripheral or pseudopuberty.1-3 We$ {8 e$ P, S/ ]) l! n( X
report a 16-month-old boy who presented with the
) L2 f( D  J) E, b( L( Z7 `enlargement of the phallus and pubic hair develop-0 F7 B, w4 I! g4 p& d
ment without testicular enlargement, which was due% ?& [; u( T$ I8 ?" Z' c3 Q! F$ o
to the unintentional exposure to androgen gel used by- u: q- u8 E" P5 s1 k7 D
the father. The family initially concealed this infor-
5 Q% A; P! C/ |5 emation, resulting in an extensive work-up for this, B7 S0 Q% n7 u( _0 D2 s# N
child. Given the widespread and easy availability of
" z, V7 V, {( M" e7 rtestosterone gel and cream, we believe this is proba-+ l' p$ W: R1 O% C
bly more common than the rare case report in the
! z( V& K& H' l2 f7 D3 O* G! H+ \literature.4. {9 c9 @3 ]5 A. I$ d* D/ [
Patient Report, B  ]0 E, K) \- c* Y. O8 g  t& H
A 16-month-old white child was referred to the5 @( P1 ~6 `# k5 J! B6 M
endocrine clinic by his pediatrician with the concern! i5 y7 `. l8 ~
of early sexual development. His mother noticed
4 o& l. f. p! \! `7 B/ {1 ?9 Xlight colored pubic hair development when he was: Y! ]  p' m: p! P  G8 o& ~' b
From the 1Division of Pediatric Endocrinology, 2University of
6 O/ o' B! [! V7 Q* i7 v$ O( lSouth Alabama Medical Center, Mobile, Alabama.% o6 {" P( B! B$ [5 w# ~
Address correspondence to: Samar K. Bhowmick, MD, FACE,
- h2 Q' v* _3 ^" cProfessor of Pediatrics, University of South Alabama, College of
8 z1 z1 K: ~; wMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 e. A1 p; o# \  r3 Z# {  X+ T2 Oe-mail: [email protected].
" Y" B" c. t4 {+ Nabout 6 to 7 months old, which progressively became
4 s% c2 R( Z7 n6 b% p, Ndarker. She was also concerned about the enlarge-! Y% m' V6 B8 ]
ment of his penis and frequent erections. The child) O" D) k* ?/ G
was the product of a full-term normal delivery, with5 V: J3 N/ }- i& a, A
a birth weight of 7 lb 14 oz, and birth length of9 A1 F& R2 k1 j4 R
20 inches. He was breast-fed throughout the first year
! B! e5 {! }7 r& @7 ^+ J9 dof life and was still receiving breast milk along with6 w7 @5 |! X: Z% D9 ]( U3 U1 y7 S9 H
solid food. He had no hospitalizations or surgery," m7 w: F9 h/ K: B+ K" F4 G
and his psychosocial and psychomotor development, k$ @6 e* @$ c) x" \; k
was age appropriate.
8 C1 j. k2 g" a5 g$ H( OThe family history was remarkable for the father,
5 L9 I+ f* m  i0 j" {  b1 N' bwho was diagnosed with hypothyroidism at age 16,  p5 c  j; F( K1 h6 {& P
which was treated with thyroxine. The father’s
1 `8 c0 x; a6 A/ I# hheight was 6 feet, and he went through a somewhat
/ z% J7 ^" i( K: b0 X- D0 x6 M8 ^  A- Dearly puberty and had stopped growing by age 14.
& {: K- w* P3 [( ~" jThe father denied taking any other medication. The
- s3 S$ \" B( X0 D* \* {child’s mother was in good health. Her menarche
* u7 k; C% a+ N* p9 wwas at 11 years of age, and her height was at 5 feet$ }8 i/ m& G1 T$ N$ H* u
5 inches. There was no other family history of pre-
+ G" J; |' Y. \4 y0 fcocious sexual development in the first-degree rela-, G& Q3 y* X6 r0 N/ _% p! I
tives. There were no siblings.% f2 B) I; a; c6 P
Physical Examination
- e) j' H  }9 \' M% `The physical examination revealed a very active,
% X& D% x# K2 V/ v; u( f/ {playful, and healthy boy. The vital signs documented# c  c6 ~: G0 U  j) \
a blood pressure of 85/50 mm Hg, his length was: [1 J; X2 B5 U9 n- P
90 cm (>97th percentile), and his weight was 14.4 kg
! _0 j" A! X2 q( C( a2 k(also >97th percentile). The observed yearly growth
3 ?/ M1 j% o( q1 |+ S% J9 vvelocity was 30 cm (12 inches). The examination of
, x; d( k7 \5 a5 C& ^the neck revealed no thyroid enlargement.
2 Z+ Y* H' N: h9 H% ^$ v9 g! KThe genitourinary examination was remarkable for, o8 Z8 A2 H4 d
enlargement of the penis, with a stretched length of. m- H; }2 M  j( _( k
8 cm and a width of 2 cm. The glans penis was very well
( w* Q6 ^  m3 T9 ?9 Qdeveloped. The pubic hair was Tanner II, mostly around
- A) d9 f9 x: X( G% O$ F/ X540
# K/ T+ A: J3 p2 J/ T/ |+ u4 Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ @! Y$ M# J" s9 W  Gthe base of the phallus and was dark and curled. The
3 _" `* F) G7 C0 ^7 Atesticular volume was prepubertal at 2 mL each.
  |$ }% G% N0 ~The skin was moist and smooth and somewhat
  G* C7 y' z: T* Z& Zoily. No axillary hair was noted. There were no1 H0 ]2 g9 h# B+ v  a8 V
abnormal skin pigmentations or café-au-lait spots.
* O( c# }+ ?# t, t9 zNeurologic evaluation showed deep tendon reflex 2+
  X6 p4 J1 d& q# U- g6 Mbilateral and symmetrical. There was no suggestion( V5 O0 K2 N% T8 r& d  E: X
of papilledema.
+ Y4 n  X# ~6 qLaboratory Evaluation4 h* i) o+ T6 M. V
The bone age was consistent with 28 months by
0 [- t' O1 X/ q8 k8 A/ G& lusing the standard of Greulich and Pyle at a chrono-
( z5 z7 V/ \  q- @- A  blogic age of 16 months (advanced).5 Chromosomal3 E+ r, P  W( d8 p& ]) G. P* @
karyotype was 46XY. The thyroid function test- b" x' P1 c' l; l
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 N/ W- j! i) s6 rlating hormone level was 1.3 µIU/mL (both normal).
; P  J( h2 Y5 _! O) X9 f4 v/ iThe concentrations of serum electrolytes, blood
3 }; B6 E8 E; g6 T2 ~2 r/ y! murea nitrogen, creatinine, and calcium all were
" Z; \- Z2 u# `within normal range for his age. The concentration
$ u) ^) F5 T# h8 P- [of serum 17-hydroxyprogesterone was 16 ng/dL
0 y: u! Z9 T3 v: t) n+ U  M(normal, 3 to 90 ng/dL), androstenedione was 20
/ R: ?/ A' p3 W1 Z. _ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-9 O  ~! C$ T2 A) {( }1 o4 R" b- l
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
( m" x8 N5 O" p& D1 T7 q) w; ndesoxycorticosterone was 4.3 ng/dL (normal, 7 to+ g5 ]% H+ }8 k* }4 N; d
49ng/dL), 11-desoxycortisol (specific compound S)
; k7 ]- t: H& V* p  e$ Rwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-; Q  b2 A% ^( S8 J& `3 x' i
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: Q9 f/ S  w$ j4 G; z$ H) f7 Vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 p) y7 X8 }+ W6 h4 n* F& T- B
and β-human chorionic gonadotropin was less than0 U2 n. t7 ~2 W% z* J& O, U
5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 w) U! D' ~0 X4 b& I1 t# ystimulating hormone and leuteinizing hormone
3 r5 W$ O1 ?+ O% ^% L( Y% Tconcentrations were less than 0.05 mIU/mL+ J8 o# ]" o1 ?: A- R3 L* \
(prepubertal).4 n% \$ h7 F1 u+ ^. x
The parents were notified about the laboratory( X( O' e& U6 @" H8 y
results and were informed that all of the tests were, g, Z* z" \/ g
normal except the testosterone level was high. The4 g3 {0 x0 N* [
follow-up visit was arranged within a few weeks to
4 s1 L! ?) ^5 c4 S% U4 @* _obtain testicular and abdominal sonograms; how-; x3 i% v* Z( v
ever, the family did not return for 4 months.6 u# s! \4 X/ m  W
Physical examination at this time revealed that the
/ t3 [& Y7 K% g: B9 s; vchild had grown 2.5 cm in 4 months and had gained
  R1 r4 g/ p" \  W8 j- Q& P# R  V2 kg of weight. Physical examination remained3 {* G, h3 {# H% [& Q, Y3 J, P
unchanged. Surprisingly, the pubic hair almost com-- o" H0 g  ]. o# Z$ H7 u( u: P/ r  j
pletely disappeared except for a few vellous hairs at% E" B5 P9 i/ o
the base of the phallus. Testicular volume was still 2
) s: @2 a( p( H: D8 B7 y1 ImL, and the size of the penis remained unchanged.
" P4 I& a8 S4 s$ m8 nThe mother also said that the boy was no longer hav-
: @& u5 G0 x) i, R& Z9 X7 iing frequent erections.
  m9 t9 B7 {" o/ O: Y7 bBoth parents were again questioned about use of" _, t3 _: `/ x
any ointment/creams that they may have applied to
6 @# o' V! \- j7 {! ^2 Lthe child’s skin. This time the father admitted the
/ o4 `6 q6 q( J  H5 O& p1 ITopical Testosterone Exposure / Bhowmick et al 541& N7 o. |+ e- H( S3 R2 _
use of testosterone gel twice daily that he was apply-
- z; |# Y4 s! W% v. King over his own shoulders, chest, and back area for- ~- M- a0 E: g, D2 K9 Y
a year. The father also revealed he was embarrassed. L& |+ b+ Z% W$ N" q
to disclose that he was using a testosterone gel pre-
4 H" f& S. w, Escribed by his family physician for decreased libido9 t, T3 J+ k% D% ~  @
secondary to depression.6 B8 \  I4 l0 C% m6 C
The child slept in the same bed with parents.+ _6 D4 h$ ~  H
The father would hug the baby and hold him on his& I- ^# x0 ]! G: w
chest for a considerable period of time, causing sig-
+ K/ }0 n  `" k9 E! Unificant bare skin contact between baby and father.# P1 I  \4 F) o$ ]0 c. M' q4 [
The father also admitted that after the phone call,
3 y( @$ J' ?% hwhen he learned the testosterone level in the baby4 D7 A9 n. n% j0 U
was high, he then read the product information9 G- i' \) g9 {- A; _5 T/ S
packet and concluded that it was most likely the rea-
/ R% y% ^& a/ i  H$ }3 [/ zson for the child’s virilization. At that time, they5 ~* B( X# l: D9 u; y' e0 P
decided to put the baby in a separate bed, and the
2 r/ \. _+ I6 q9 k/ v' }. f: G* ofather was not hugging him with bare skin and had
! o0 o* W) W  z9 P) Mbeen using protective clothing. A repeat testosterone
+ @  ]0 n* ]) O! ctest was ordered, but the family did not go to the; B6 I  R5 D/ a2 n! q
laboratory to obtain the test.* a# T+ A) q+ B0 I4 u* z% s9 F9 ]
Discussion& u0 N* _! ]7 ]' p& P0 p* a
Precocious puberty in boys is defined as secondary0 ~, x" e1 r7 i' S: K
sexual development before 9 years of age.1,47 A3 k" h% V* ^
Precocious puberty is termed as central (true) when
* B. i; c, {' g8 K5 b) K- U8 a) \it is caused by the premature activation of hypo-5 u* y# g( O; r; Z  L
thalamic pituitary gonadal axis. CPP is more com-/ u. ^6 d. e8 C
mon in girls than in boys.1,3 Most boys with CPP' H. W1 x& H4 t- J3 i1 w
may have a central nervous system lesion that is
/ ~; V2 k3 q; n/ B; R, v: Y+ ^responsible for the early activation of the hypothal-
" S) W6 q( \" ramic pituitary gonadal axis.1-3 Thus, greater empha-
( Y4 o, Z; T3 M) esis has been given to neuroradiologic imaging in
0 P1 A: P. p9 Y5 C+ F/ y# mboys with precocious puberty. In addition to viril-
5 j  F- I1 H/ T' m- M7 X0 [ization, the clinical hallmark of CPP is the symmet-" A5 w( t% T* Y7 F
rical testicular growth secondary to stimulation by
3 `; ^1 S- v) a7 b9 n! [# ]* Qgonadotropins.1,3% [* C# m  {8 a4 r3 U, u& U  i" o
Gonadotropin-independent peripheral preco-& E* {7 r+ ?& R6 b$ i7 S8 e
cious puberty in boys also results from inappropriate7 i4 N  w8 p/ M7 Z4 Q
androgenic stimulation from either endogenous or* L' c3 f% r% D  V' L! ^2 P9 |
exogenous sources, nonpituitary gonadotropin stim-, s% O0 E, ?3 Y$ a
ulation, and rare activating mutations.3 Virilizing, L1 e: a' N0 x' T% S; S% J
congenital adrenal hyperplasia producing excessive& i8 s7 g6 @/ c0 G4 ?
adrenal androgens is a common cause of precocious
0 E& S$ g+ P' t& {) R4 ^puberty in boys.3,4
, g+ e& m( s" j" `2 s. U# _The most common form of congenital adrenal% a/ t. r# {) O
hyperplasia is the 21-hydroxylase enzyme deficiency.
( O! @; C. r# k2 T) ]The 11-β hydroxylase deficiency may also result in+ o* w  K' _6 x2 l6 X: t
excessive adrenal androgen production, and rarely," g9 K& T7 `" l. V' S$ O
an adrenal tumor may also cause adrenal androgen
2 S4 n! r! m5 B1 z* @# K! Gexcess.1,3
: {  s, O) @# L. W0 xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" G8 B1 b( k) I  U542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 m; y/ |7 E1 U, A
A unique entity of male-limited gonadotropin-. C7 K4 b6 o  Z% j. b
independent precocious puberty, which is also known
$ G9 l! x% @9 ?0 l! f" a/ _as testotoxicosis, may cause precocious puberty at a; K+ z4 R9 G3 \: t9 H. S
very young age. The physical findings in these boys6 H% ~7 j+ G) b% @
with this disorder are full pubertal development,
6 K" N5 b! M, r; J7 c: cincluding bilateral testicular growth, similar to boys
3 ^$ _9 h1 z5 L/ e! Lwith CPP. The gonadotropin levels in this disorder
& q6 {; c  m2 _are suppressed to prepubertal levels and do not show  f3 O9 l7 E0 f$ r9 m
pubertal response of gonadotropin after gonadotropin-5 i' M" s$ H& {1 a- [' e; i. b
releasing hormone stimulation. This is a sex-linked
4 B# p* n% Q% F3 F6 vautosomal dominant disorder that affects only9 X0 @- S. k0 C/ o0 r0 T
males; therefore, other male members of the family# b% p4 k0 K& w  [" @( |
may have similar precocious puberty.3
% f, S! U$ z6 l+ ]  mIn our patient, physical examination was incon-; F9 ^1 P, {& f3 k+ V
sistent with true precocious puberty since his testi-
- Z+ T3 N, ^( T: Ecles were prepubertal in size. However, testotoxicosis
% K+ {9 V1 T" A( |. Y( Cwas in the differential diagnosis because his father
8 M) u; ]8 p+ Z. j2 |- [. [started puberty somewhat early, and occasionally,( K4 D# H9 a# ], g9 x. a& |7 I
testicular enlargement is not that evident in the( z# h" y2 O# G+ \3 L; B  D0 J/ }7 l
beginning of this process.1 In the absence of a neg-
: [+ `3 V' u+ K! j5 H8 D9 zative initial history of androgen exposure, our& S4 z" y1 p( Z1 c1 L! K- y
biggest concern was virilizing adrenal hyperplasia,  O1 I; h0 X* M9 @" o( D& I
either 21-hydroxylase deficiency or 11-β hydroxylase
' B4 G/ `6 }+ U9 k* gdeficiency. Those diagnoses were excluded by find-
/ o: [) }% l2 [. U; X5 Q5 _6 [ing the normal level of adrenal steroids.5 g3 `* `) r. P
The diagnosis of exogenous androgens was strongly, x) T8 |; U: d' ?
suspected in a follow-up visit after 4 months because
* m1 a9 ?" Y, m5 p# g2 }* o5 Pthe physical examination revealed the complete disap-
  `; K& \7 j" O. k5 W* i' Bpearance of pubic hair, normal growth velocity, and
% {' ?* W4 d0 J3 N: Y, H' l! |" vdecreased erections. The father admitted using a testos-
) T" F8 g) ~, y8 o8 |' n4 nterone gel, which he concealed at first visit. He was
% B7 J2 O9 [2 F5 E/ ?( T% o3 d! j0 S# wusing it rather frequently, twice a day. The Physicians’
# g  M9 M  _& F0 Z7 }Desk Reference, or package insert of this product, gel or% ~/ j( r. `( {
cream, cautions about dermal testosterone transfer to6 z  l: }5 F7 w$ _
unprotected females through direct skin exposure.
3 V6 t& V" X: A7 uSerum testosterone level was found to be 2 times the
7 h+ b) ~- F$ J  K5 Q0 [baseline value in those females who were exposed to
- J" ~5 z$ N, q" l* S( reven 15 minutes of direct skin contact with their male2 a# ^  G( ~1 K4 K* U
partners.6 However, when a shirt covered the applica-
9 T  R6 g2 w( X" z& q6 i+ d" e$ ^tion site, this testosterone transfer was prevented.# [  a8 |  t  `* I  }8 Y0 ^
Our patient’s testosterone level was 60 ng/mL,: P9 X8 [+ e- U0 A$ `
which was clearly high. Some studies suggest that
; @1 n* l2 y% L5 I4 C1 o5 `4 Mdermal conversion of testosterone to dihydrotestos-: M/ e0 L6 }2 q& h) S
terone, which is a more potent metabolite, is more
$ K" B# }/ x( [. }4 v+ c8 lactive in young children exposed to testosterone
& F6 r9 G7 T' K( L* ^. sexogenously7; however, we did not measure a dihy-
% q5 X/ I8 ^0 X% X2 i2 udrotestosterone level in our patient. In addition to- B( }5 f, `. M9 p* g$ m7 C3 y( u
virilization, exposure to exogenous testosterone in
% n! h" r) r6 ^8 S! Q1 x& jchildren results in an increase in growth velocity and
2 N" O7 B2 x9 `# M6 c9 U' D* j- _advanced bone age, as seen in our patient.
# u: q1 H9 g* U/ qThe long-term effect of androgen exposure during
' Y# G6 T5 T8 Fearly childhood on pubertal development and final
0 I# \  J% u; P9 cadult height are not fully known and always remain
" ~4 w! U; }9 r$ ya concern. Children treated with short-term testos-
) Y1 n3 j2 z: _: Vterone injection or topical androgen may exhibit some
& ~$ Z7 j4 p/ R# a) }' S/ @acceleration of the skeletal maturation; however, after. D* W, W, g2 s# N
cessation of treatment, the rate of bone maturation
4 w' E" B/ D  Vdecelerates and gradually returns to normal.8,98 G/ }  `. o" H, H* F
There are conflicting reports and controversy" X$ ~& d8 n* N3 M/ ~
over the effect of early androgen exposure on adult
! u" V/ a# g; w1 [& K, B* c% qpenile length.10,11 Some reports suggest subnormal
* d8 _, _1 V7 k$ C: Sadult penile length, apparently because of downreg-
2 y" m+ u. I3 ~0 K$ o4 Nulation of androgen receptor number.10,12 However,
! U( B; G2 @9 H# f1 xSutherland et al13 did not find a correlation between
- M+ G' K9 E" t+ n; S/ n; G/ lchildhood testosterone exposure and reduced adult+ l7 j+ e, N8 B" h" u
penile length in clinical studies.: x8 w) F- f( o( r; f8 f
Nonetheless, we do not believe our patient is1 X( U5 t6 Q$ X; P6 c
going to experience any of the untoward effects from' _4 j9 X5 V6 R7 Z/ M( j
testosterone exposure as mentioned earlier because
+ ]" b& d/ P+ W9 v* h' D" \+ Zthe exposure was not for a prolonged period of time.
# v- J: |* y. q# h* C2 Y1 @Although the bone age was advanced at the time of- o* L. n, g' E2 D& X! n9 t
diagnosis, the child had a normal growth velocity at4 t& ^8 p; L) g5 J) x
the follow-up visit. It is hoped that his final adult1 F( f: Q. X: [8 R. k* O
height will not be affected.
5 J. b( Q* U9 M# W1 V3 z+ d; AAlthough rarely reported, the widespread avail-+ m" R' U/ w( Y4 p0 o" Y2 T0 I
ability of androgen products in our society may. ?: o0 E; E$ ~: b
indeed cause more virilization in male or female. k! T7 x9 _1 v7 }" s
children than one would realize. Exposure to andro-( b) O; u8 a2 }0 @
gen products must be considered and specific ques-
9 U: v! A2 W. {6 ?3 x1 N- P3 Ationing about the use of a testosterone product or
8 ]5 |+ G8 ?' ]2 t3 T4 Zgel should be asked of the family members during3 a3 @# }, C, r. ?! b% R
the evaluation of any children who present with vir-
! s+ U3 P6 I: q* G, x- e1 }1 jilization or peripheral precocious puberty. The diag-, o) C1 y# g) T& K8 k) h
nosis can be established by just a few tests and by
' v$ w- P$ `* F+ U6 \* s& G8 A" lappropriate history. The inability to obtain such a
5 {) N7 W( W$ ^history, or failure to ask the specific questions, may
, g7 Z8 H3 c- I8 f. O: ?result in extensive, unnecessary, and expensive0 I+ Y) V1 J& k) j5 z
investigation. The primary care physician should be
. j1 `# V' ]! ]. Caware of this fact, because most of these children
& ]: L- N, E% \3 v8 Xmay initially present in their practice. The Physicians’
2 H" O5 i) t/ v- F# P: t0 X" B& h$ LDesk Reference and package insert should also put a
1 f9 n" y/ E) x9 U8 _$ V) Y9 gwarning about the virilizing effect on a male or
) M1 y' s2 E# @: ?$ V, s' nfemale child who might come in contact with some-; L/ O! B  I: p3 ]
one using any of these products.* @3 @6 g+ o% r. m  G8 `
References
! l" F, `1 s3 F+ R1. Styne DM. The testes: disorder of sexual differentiation; R3 ^( x7 j9 S+ Y, a& P
and puberty in the male. In: Sperling MA, ed. Pediatric7 V1 z6 W8 ]) u7 ?( L
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" Z; L1 j3 k/ U- g5 w9 Y$ a
2002: 565-628.
& z8 M9 Y6 F( B$ h9 N' b2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ p9 a3 p, h& a: w" r  Y
puberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

: h6 T' t/ K/ x5 o9 A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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