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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, Z3 s0 {/ q( O, t- }1 x! z1 @9 R
Boy Induced by Indirect Topical
# H, O0 |8 A& I8 F9 p0 L& c) ]Exposure to Testosterone
1 Q8 w2 n0 `' [5 c5 T/ JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 ^8 I* f9 ]" m) `
and Kenneth R. Rettig, MD1
: I+ R9 C# J# b, X6 A' ?; }, qClinical Pediatrics- ~, W* q0 T4 X0 ~  g
Volume 46 Number 6
) J0 g# T4 E: k) {0 }, O# s/ s  lJuly 2007 540-543- U' o. ~8 U) n7 O& ]% C* a4 ]
© 2007 Sage Publications
, W% @; X/ r& o7 B& z% {% k9 u10.1177/0009922806296651& s. \" e! F! C% I0 n& G" f+ @* u
http://clp.sagepub.com
0 }# J% r- m: G0 [* t4 ~% ?& thosted at
1 W# ]! c1 K5 z9 `) Thttp://online.sagepub.com
3 U/ m. E* i  k: c& ^+ l) dPrecocious puberty in boys, central or peripheral,
! b4 ?9 t( g* q* ~7 q! Y1 B$ ois a significant concern for physicians. Central0 H5 J% ^+ f* U+ m) w
precocious puberty (CPP), which is mediated7 ^, l7 C6 R. U# v7 r
through the hypothalamic pituitary gonadal axis, has
3 S5 W) _( ]8 K) a  ?8 A: ka higher incidence of organic central nervous system
% O: ?8 D9 J) s$ _: A( Z% s9 hlesions in boys.1,2 Virilization in boys, as manifested
/ [% S1 v; X4 ~9 O3 r& B+ Sby enlargement of the penis, development of pubic9 w1 U1 h3 g. [
hair, and facial acne without enlargement of testi-
8 L% @! D7 \% |9 {6 ~1 Pcles, suggests peripheral or pseudopuberty.1-3 We: ?- A/ E9 w7 g% _0 U( e* D& j$ ]
report a 16-month-old boy who presented with the: F1 p' c8 b/ n
enlargement of the phallus and pubic hair develop-
* l. R6 m) l0 w  Ement without testicular enlargement, which was due
1 D" J) O: C( T) U) e% ]to the unintentional exposure to androgen gel used by
" w4 s% [  b$ M( @; |1 Dthe father. The family initially concealed this infor-
! z# [' C7 n0 c1 Y+ G% \- Amation, resulting in an extensive work-up for this4 y! J9 ~, E% f; u: l
child. Given the widespread and easy availability of6 @4 n( Q/ t2 `
testosterone gel and cream, we believe this is proba-
# ]$ \: ^1 c1 ]0 Lbly more common than the rare case report in the! Q2 i  Q- c1 S! i8 `* L. k5 P
literature.4' T" V) [5 `: \
Patient Report
* b/ ~/ y1 @4 A" UA 16-month-old white child was referred to the9 T4 C( g+ i$ z" y/ W: P8 Q: F
endocrine clinic by his pediatrician with the concern' X' W( n- H( N2 I4 Y  ^
of early sexual development. His mother noticed5 [, q! T; U* h* m
light colored pubic hair development when he was
7 j* j! a  f* p0 f9 z! R# iFrom the 1Division of Pediatric Endocrinology, 2University of
6 `. L; y/ \" Y3 {" u+ ~South Alabama Medical Center, Mobile, Alabama.
* S. [/ h4 F: }" W. v# ~% KAddress correspondence to: Samar K. Bhowmick, MD, FACE,
0 c# o. i8 ^. n4 A/ w4 S2 S" i6 K. A' DProfessor of Pediatrics, University of South Alabama, College of, c' n, t. i; B& e8 a6 p/ e
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; e$ R, ?* a9 a
e-mail: [email protected].6 y( h7 ^; f0 L: U7 ^
about 6 to 7 months old, which progressively became( Z! k4 W  b& S( z* m+ u3 Y
darker. She was also concerned about the enlarge-, W! M# G% A3 u8 x4 n
ment of his penis and frequent erections. The child, g8 S" b- Q3 V) X% g  Y3 l
was the product of a full-term normal delivery, with
% o. E$ m1 o2 M  d* a4 H8 Wa birth weight of 7 lb 14 oz, and birth length of
1 @' s+ a$ U% _: ~$ C6 G20 inches. He was breast-fed throughout the first year
7 z) h3 |4 b* Z4 w4 q# u  |of life and was still receiving breast milk along with) w0 I& d( F- @
solid food. He had no hospitalizations or surgery,0 L" M9 J& q0 V
and his psychosocial and psychomotor development0 f7 X8 z; k! `( f) P  z; d
was age appropriate.
1 t6 F& y7 E0 f# S2 q2 ]The family history was remarkable for the father,
1 `. f; L( ~3 t8 vwho was diagnosed with hypothyroidism at age 16,% i, W$ |4 f8 H; K1 f8 H4 G
which was treated with thyroxine. The father’s
! i& D7 ]6 ^4 O1 Hheight was 6 feet, and he went through a somewhat
. K3 z8 x( ~( @  b4 \early puberty and had stopped growing by age 14.
9 u2 q  g) b2 i9 B1 X# ~$ c+ ^The father denied taking any other medication. The% g3 P3 `: E' g0 n- T
child’s mother was in good health. Her menarche; O( D8 o6 ^# z$ R5 h3 E
was at 11 years of age, and her height was at 5 feet6 g  G% {  T1 u) b
5 inches. There was no other family history of pre-0 p, M( K, P. Z  v2 F
cocious sexual development in the first-degree rela-
2 u$ z; D0 @$ Q+ r5 Htives. There were no siblings.! P# m" u/ f6 G
Physical Examination- j$ F1 j1 z  I1 u+ D, S4 B$ m  T5 }* [
The physical examination revealed a very active,
1 X& O0 m: v" S$ \playful, and healthy boy. The vital signs documented
0 F5 z, T: R2 j% S6 Ca blood pressure of 85/50 mm Hg, his length was
) X3 H) Q4 K/ M* s' q90 cm (>97th percentile), and his weight was 14.4 kg$ {  m2 C' H# B) W& t) J! o* U
(also >97th percentile). The observed yearly growth( z$ K. C, Y: d9 t9 S' e$ R
velocity was 30 cm (12 inches). The examination of
6 Y# s' t5 L' e; hthe neck revealed no thyroid enlargement.- ]; e# j; g% x- F' o# P
The genitourinary examination was remarkable for
# l( f6 s: V& o+ [enlargement of the penis, with a stretched length of+ q7 L" o0 _4 S6 K( D
8 cm and a width of 2 cm. The glans penis was very well4 G9 b- N- \- p8 J
developed. The pubic hair was Tanner II, mostly around" l8 V1 p( A2 s
5406 p* ~0 f" E9 \% r) r8 ?& d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 z; W5 d" F& r# u( [. n
the base of the phallus and was dark and curled. The
  }7 y. ?" _0 Etesticular volume was prepubertal at 2 mL each.
4 c/ c) n& C8 A& w. OThe skin was moist and smooth and somewhat
8 [  s5 u, E/ t3 Yoily. No axillary hair was noted. There were no; a$ V% p- V5 s& e6 H) L; A3 \
abnormal skin pigmentations or café-au-lait spots.# e3 ^& Z' H, ], ~$ K, A
Neurologic evaluation showed deep tendon reflex 2+
2 o2 u9 ?. I: {bilateral and symmetrical. There was no suggestion) j/ H) G* s" P
of papilledema.
3 K+ q2 h' e2 X, ?; A, X, @Laboratory Evaluation* q# E. S5 h2 E  P4 J% Q
The bone age was consistent with 28 months by
2 t' s% F/ A7 p+ r; Y& f, U8 ]using the standard of Greulich and Pyle at a chrono-5 ~5 i0 k/ O& _) p1 l
logic age of 16 months (advanced).5 Chromosomal
0 D: H& h% n; Q( rkaryotype was 46XY. The thyroid function test
: H$ [' ^* ]. Nshowed a free T4 of 1.69 ng/dL, and thyroid stimu-% Z7 h! U/ F; v0 d3 M2 _# Z
lating hormone level was 1.3 µIU/mL (both normal).
3 v+ e7 \5 M, M1 ^, C& v0 \The concentrations of serum electrolytes, blood
0 x6 ]9 V+ c. u# D' Ourea nitrogen, creatinine, and calcium all were
4 u4 P2 h3 }5 ^) e; g- a6 W5 Rwithin normal range for his age. The concentration" M# f5 z! C) h: g6 \
of serum 17-hydroxyprogesterone was 16 ng/dL
& q! C5 ~8 W( y. w+ s4 m& p(normal, 3 to 90 ng/dL), androstenedione was 205 ]7 Z, f$ c* c" q8 E
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 ~$ l% ^9 z# [; ?, `9 K% C  Iterone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 `* A. b% G- [$ _4 Zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to3 [( C4 f. w/ P
49ng/dL), 11-desoxycortisol (specific compound S)2 ?4 }1 M. l0 l1 m! O
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: _  {7 x9 s' |9 Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
+ j$ X$ b9 [) N9 ~) w. Gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL)," g  j& u; |' k% x
and β-human chorionic gonadotropin was less than$ _/ v7 P5 o, y3 h8 {# N2 P
5 mIU/mL (normal <5 mIU/mL). Serum follicular1 }% A7 s1 ~* A% t: S2 E
stimulating hormone and leuteinizing hormone5 q+ H& i' P' U+ j
concentrations were less than 0.05 mIU/mL
' D3 Z7 P, Q6 q( W8 b(prepubertal).
6 k3 S$ P* q+ s7 H* _8 N9 b. pThe parents were notified about the laboratory6 |# P$ h* r1 m% P6 B
results and were informed that all of the tests were
: b+ P8 y9 A: r& d% |normal except the testosterone level was high. The$ u8 x8 J) F1 P1 n# e2 S, i
follow-up visit was arranged within a few weeks to- x! \% u; M& c' Q% N
obtain testicular and abdominal sonograms; how-# F1 Y( h% n6 @. G  T5 L4 l
ever, the family did not return for 4 months.
- \# V3 ^7 L* H2 _Physical examination at this time revealed that the6 k) Q/ A( k5 ?  {
child had grown 2.5 cm in 4 months and had gained
3 r% I  W) v# @6 j! G7 l2 kg of weight. Physical examination remained
9 K5 S- s2 v& Hunchanged. Surprisingly, the pubic hair almost com-+ p: x: b1 p5 ~7 U
pletely disappeared except for a few vellous hairs at
! C* u+ P$ }" a; \/ Sthe base of the phallus. Testicular volume was still 2% w; O$ P" X& R- v$ d
mL, and the size of the penis remained unchanged.* h6 v/ v# Y4 S/ ~2 y6 N+ _
The mother also said that the boy was no longer hav-
  g* E" J% H9 S% z. @. A5 O# ting frequent erections.5 Q* X1 _# `; y* b* n7 h
Both parents were again questioned about use of
. W/ m& a: a8 c* h3 Tany ointment/creams that they may have applied to0 g- W: j9 D, J0 `/ A, B; p
the child’s skin. This time the father admitted the
; C0 b2 B  ~/ k+ P3 U  [  `* nTopical Testosterone Exposure / Bhowmick et al 5416 h* K) t! K* Q+ |/ W
use of testosterone gel twice daily that he was apply-! Y; C* ]2 R6 |! K, Q9 P
ing over his own shoulders, chest, and back area for# E. J# F9 C0 b9 g3 j7 @) s
a year. The father also revealed he was embarrassed
0 F2 E6 C" @8 u' E8 Bto disclose that he was using a testosterone gel pre-
3 C9 d: N  `3 x+ g1 O3 ^scribed by his family physician for decreased libido; o7 x. ]" I; @3 A  k! ~
secondary to depression.
+ Z* T8 r- \. \The child slept in the same bed with parents.
( m* R/ b7 _6 |8 |3 ]The father would hug the baby and hold him on his
" b: ]/ n( z# ]" _1 b/ V* p% Ychest for a considerable period of time, causing sig-( o* y+ b" X$ w8 {5 j
nificant bare skin contact between baby and father.+ R. v0 ]9 X8 k6 w: g) u7 `
The father also admitted that after the phone call,
: Y. C. x" E+ q: g, m& _+ ewhen he learned the testosterone level in the baby5 c( X( {! i( E* O0 R, P+ J
was high, he then read the product information! r  s; F( g+ M# K9 W+ n6 t
packet and concluded that it was most likely the rea-
' J/ E$ }# I$ Z$ G7 Pson for the child’s virilization. At that time, they
7 H9 J. E7 }1 P' E  ^8 Mdecided to put the baby in a separate bed, and the
0 P5 Y# `  H; H7 Ffather was not hugging him with bare skin and had9 X/ Q* m% E" {- Q( [
been using protective clothing. A repeat testosterone" M7 I4 M- k, M0 V! C) S, {
test was ordered, but the family did not go to the  X/ D6 R, l$ E9 L, x3 _; w5 c
laboratory to obtain the test.: ]3 ^9 R7 [5 k7 U
Discussion& q2 s+ T# J" a1 R( g( C, p, |) |
Precocious puberty in boys is defined as secondary4 y" C' _' A+ U* q0 b% P0 H* e
sexual development before 9 years of age.1,4  [) H# C5 L  y- `  z- [
Precocious puberty is termed as central (true) when( N4 M; {7 x  O) d
it is caused by the premature activation of hypo-5 Q# O! `5 C  `+ b, L% R
thalamic pituitary gonadal axis. CPP is more com-3 x# c. U$ K4 G1 J5 `' |9 l! `8 p
mon in girls than in boys.1,3 Most boys with CPP* n) r, Q6 ?% |: r" ]
may have a central nervous system lesion that is/ k. S+ M& p1 M8 Z  G) b
responsible for the early activation of the hypothal-* x0 S5 k6 q2 K8 |% N8 b8 }" t
amic pituitary gonadal axis.1-3 Thus, greater empha-, A+ ]' {3 ^' [/ M9 c( l: }  c( L% a/ d+ y
sis has been given to neuroradiologic imaging in# h$ o+ m6 v2 X$ W, @5 I: j  a# L
boys with precocious puberty. In addition to viril-  L' U: y7 x4 P' |1 F+ x
ization, the clinical hallmark of CPP is the symmet-
0 i* P# q0 C* b9 N$ p# nrical testicular growth secondary to stimulation by& g4 S$ n5 h! q& ?6 L
gonadotropins.1,35 w5 {" R9 J" p. ?5 ^+ _
Gonadotropin-independent peripheral preco-4 [+ B+ h% x* B3 {; w7 ~0 L0 M1 h+ s
cious puberty in boys also results from inappropriate! ~7 p, h( ^9 z2 T: M* _
androgenic stimulation from either endogenous or! m( w5 S  e. I  \$ O
exogenous sources, nonpituitary gonadotropin stim-
0 S: k: C0 u3 Y3 sulation, and rare activating mutations.3 Virilizing
1 h. Y6 t, {# T3 G  {" acongenital adrenal hyperplasia producing excessive
' X$ d9 c0 I8 u) \adrenal androgens is a common cause of precocious
* c8 u7 Y8 j2 ~( d& @puberty in boys.3,4( \4 |, Y4 W& p' V
The most common form of congenital adrenal
, y: g) Y% Z1 [( \hyperplasia is the 21-hydroxylase enzyme deficiency.
7 {  |% A  _+ H! HThe 11-β hydroxylase deficiency may also result in
/ n& |7 C) P3 }7 w& G. Gexcessive adrenal androgen production, and rarely,
0 `/ s. Y/ u& w$ p" d' lan adrenal tumor may also cause adrenal androgen8 Z( ?; {: R2 G8 n* f0 p' ^
excess.1,3
% D. p# L8 T, q/ X) i( sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) i: Y! M$ t6 _& y+ P
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
" N: b3 O# I3 W+ ?, i+ AA unique entity of male-limited gonadotropin-
. U; o+ _8 K. \9 uindependent precocious puberty, which is also known
/ I& J, b/ a# u" ias testotoxicosis, may cause precocious puberty at a
, H4 y/ }! u2 `- @, ~. l$ ivery young age. The physical findings in these boys9 c: d( M: z! K( \+ k6 m) X
with this disorder are full pubertal development,
! l& E, y' ~# t6 V* Z) yincluding bilateral testicular growth, similar to boys7 X. A: P& h  |6 ]/ Y6 q+ ~
with CPP. The gonadotropin levels in this disorder
  @) b+ {! M# p* y+ b6 Lare suppressed to prepubertal levels and do not show
! d8 o- T" e' H& m! Wpubertal response of gonadotropin after gonadotropin-0 k& S$ E5 J! o! h
releasing hormone stimulation. This is a sex-linked% }  p6 U$ q" s' p3 V
autosomal dominant disorder that affects only" {2 q; b9 Z. u7 V
males; therefore, other male members of the family6 e/ @7 s5 y9 J( q; V9 C) C
may have similar precocious puberty.3
+ K7 U2 K1 ^3 t2 W5 k" mIn our patient, physical examination was incon-
+ }2 J  F( M9 I( Bsistent with true precocious puberty since his testi-
9 ^( P. k* o0 Z5 Ycles were prepubertal in size. However, testotoxicosis7 c$ `% J( F' e' l
was in the differential diagnosis because his father
! I. i, u, M# a0 c, a8 {0 P2 R/ Vstarted puberty somewhat early, and occasionally,
  i6 F: S. M! o5 K' btesticular enlargement is not that evident in the
9 ?  L) @' h8 G& Q% V" Zbeginning of this process.1 In the absence of a neg-
0 E- K2 c8 ]4 A" A8 ]/ q& Lative initial history of androgen exposure, our
+ R/ i. F  c0 M' jbiggest concern was virilizing adrenal hyperplasia,' I  o4 N- I) r. P3 @
either 21-hydroxylase deficiency or 11-β hydroxylase
# ]6 k! s" S2 z3 {+ rdeficiency. Those diagnoses were excluded by find-9 X4 |! l# b- x( r; J9 s
ing the normal level of adrenal steroids.: v3 w8 d0 B& Z# f' ]+ @$ h
The diagnosis of exogenous androgens was strongly2 Y' u' ^4 J% _. ^  [( n2 ~6 A( e2 S
suspected in a follow-up visit after 4 months because3 }1 E8 f  `' H! j" n# C* t
the physical examination revealed the complete disap-+ \8 G2 V( B1 N, h2 ]4 h
pearance of pubic hair, normal growth velocity, and4 [8 f: x+ D! H( ~9 [
decreased erections. The father admitted using a testos-
2 `6 u7 n6 q1 D0 p+ ?) q$ wterone gel, which he concealed at first visit. He was
/ ]7 U+ E- K1 J$ \using it rather frequently, twice a day. The Physicians’
) D/ g9 D  i' ZDesk Reference, or package insert of this product, gel or
" M( T# Z3 E# R1 l; Wcream, cautions about dermal testosterone transfer to. J$ o( x$ V/ g
unprotected females through direct skin exposure./ @3 w" h- G1 Y
Serum testosterone level was found to be 2 times the. a- @, L* D6 Q2 w- I2 C* p
baseline value in those females who were exposed to/ _) _4 D+ ^/ |8 P
even 15 minutes of direct skin contact with their male: ^' L4 R* M; O: X
partners.6 However, when a shirt covered the applica-. R; U4 b% }) z" ~
tion site, this testosterone transfer was prevented.0 m" G, k4 E* {: V6 S- n
Our patient’s testosterone level was 60 ng/mL,
3 C+ t4 G! J9 ?: ]which was clearly high. Some studies suggest that  _. a3 b: |4 E: g  k
dermal conversion of testosterone to dihydrotestos-0 ], `. D' U4 E
terone, which is a more potent metabolite, is more
$ c1 R+ T1 J1 B  \9 N% p7 Pactive in young children exposed to testosterone
3 c1 o  k8 Z: b6 U0 Iexogenously7; however, we did not measure a dihy-
& i! T# C( k' K8 d% @; }" M! idrotestosterone level in our patient. In addition to2 f! A! T: Q3 A- u4 J
virilization, exposure to exogenous testosterone in+ O1 f( m! {, W$ e9 s
children results in an increase in growth velocity and
# W& A, z9 ?7 Nadvanced bone age, as seen in our patient.
( d0 k8 l# L8 u5 R# l$ ?The long-term effect of androgen exposure during
7 z: ^4 d0 ]4 r6 S- }6 ]" aearly childhood on pubertal development and final' e! m* F3 m" n/ y' e, R
adult height are not fully known and always remain& L2 d8 g* a- j1 `- _
a concern. Children treated with short-term testos-
% r% S0 y- @4 S0 D& ?0 Kterone injection or topical androgen may exhibit some) N; [  I) e6 P
acceleration of the skeletal maturation; however, after. |0 T% u# c$ z
cessation of treatment, the rate of bone maturation( ?2 v! J7 s( m% Y" t
decelerates and gradually returns to normal.8,9
7 E9 z9 N# O2 y: w/ oThere are conflicting reports and controversy4 C- N5 {! I) E4 X# v
over the effect of early androgen exposure on adult: X* ]' S+ t  W
penile length.10,11 Some reports suggest subnormal
; t- Z: j' B. N+ D2 yadult penile length, apparently because of downreg-5 |1 A9 @. B, s/ b8 y
ulation of androgen receptor number.10,12 However,
2 K) O6 t3 v2 h" O2 @' I" CSutherland et al13 did not find a correlation between
3 y6 e% h" j  J( achildhood testosterone exposure and reduced adult( {  A8 c( W1 U( R  h) ^  a9 V
penile length in clinical studies.
2 J0 I2 v& O/ {: _; Q8 ^Nonetheless, we do not believe our patient is1 u( j  e) v7 O+ C6 c
going to experience any of the untoward effects from
. W3 {& B. ?& A1 z  z  etestosterone exposure as mentioned earlier because! N3 N1 W' y3 v3 I( ]( e
the exposure was not for a prolonged period of time.! j8 m. w5 h/ ~  x6 ?0 j: B" G
Although the bone age was advanced at the time of
) g: |; E9 E8 K5 F1 t' p' f  odiagnosis, the child had a normal growth velocity at) b- d& @6 j! s* R, X( w$ ^0 w
the follow-up visit. It is hoped that his final adult
* Q/ r2 N8 T: aheight will not be affected.( o8 l4 A( C, P% ?
Although rarely reported, the widespread avail-4 l" l. O5 \8 ]# @3 h3 n) x! k8 @
ability of androgen products in our society may
$ h4 R& P) D' L* [( y! Z( uindeed cause more virilization in male or female. A" p% k$ R# a5 U/ m' n* s" w
children than one would realize. Exposure to andro-. ^( d' _1 |* h) W9 d" |+ R
gen products must be considered and specific ques-1 u  B6 s$ `. |, V8 d
tioning about the use of a testosterone product or, I# ^; F4 W9 c
gel should be asked of the family members during6 \* {+ Z2 `+ U& Q* u
the evaluation of any children who present with vir-
" c) z% h- A9 qilization or peripheral precocious puberty. The diag-
9 C1 d) G: H8 L. e' ?3 Rnosis can be established by just a few tests and by
9 f7 o% l5 G( t% a' b2 Mappropriate history. The inability to obtain such a
& s0 H: W* G2 K9 ohistory, or failure to ask the specific questions, may
% N* N4 s2 w0 Z7 P2 Zresult in extensive, unnecessary, and expensive% m! a+ U( s* U% M" r: W' E( [
investigation. The primary care physician should be
4 R+ b! x5 B! W9 R3 u% C' g: C7 gaware of this fact, because most of these children
2 W$ ^. L% Z9 k$ omay initially present in their practice. The Physicians’% l2 f/ L! p3 u$ ~
Desk Reference and package insert should also put a) \- K- @' s% [2 b, b3 y. O
warning about the virilizing effect on a male or0 l' t# l, j" c9 t+ G& K
female child who might come in contact with some-# I0 }# S: a* C* U
one using any of these products.$ E* U9 |4 c# H8 I* D
References  S1 f: A8 J5 _) U+ H5 o
1. Styne DM. The testes: disorder of sexual differentiation
4 B: z1 D4 W2 i" j0 H' Hand puberty in the male. In: Sperling MA, ed. Pediatric
3 R3 q/ Q: E) N0 V( v) @Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
) a1 C" h+ ^" E( M" `2002: 565-628.- f9 n4 E  m; N7 E3 Q  w
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 S0 y1 J1 H. Y3 D! @, L# |2 O
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
$ G0 h  Q$ C- g1 y% QBoy Induced by Indirect Topical) H; m: s0 v, Q
Exposure to Testosterone
' Y% Y% ?* c: W( ~- _Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 N  }. B* @9 P  cand Kenneth R. Rettig, MD1
8 n' k) f1 B- j/ _0 i) cClinical Pediatrics; G/ z1 V3 f' b
Volume 46 Number 6
3 f# e6 f3 e5 }/ a# O/ l: `July 2007 540-543# B5 y4 z) c" ]6 \
© 2007 Sage Publications
! B$ Z' `9 |2 P/ ^& ?% i* J8 A10.1177/0009922806296651
' u8 S3 B" |$ o( \+ _http://clp.sagepub.com. z$ l: B0 V* h8 E5 g5 N
hosted at" A* M/ `  O/ X/ _9 d, c
http://online.sagepub.com
' Z6 g  I/ d2 E) W& yPrecocious puberty in boys, central or peripheral,- A3 w4 k, a- o3 x7 R. I
is a significant concern for physicians. Central
6 c% R* x' }* g/ f9 {7 Y7 Uprecocious puberty (CPP), which is mediated
3 a- N: j9 N& Uthrough the hypothalamic pituitary gonadal axis, has
9 J. y9 S, c; j" U1 `+ ^, V1 Qa higher incidence of organic central nervous system  e! k0 D5 Z  A
lesions in boys.1,2 Virilization in boys, as manifested6 m7 s/ K* c* x7 f" I# y
by enlargement of the penis, development of pubic$ I* P7 B, d3 R. l) V# ^! b# M
hair, and facial acne without enlargement of testi-
* U$ z$ |7 `- ~2 h# U0 _3 |cles, suggests peripheral or pseudopuberty.1-3 We
" Q) M! `$ Z, i& p* {& Treport a 16-month-old boy who presented with the
4 R' V- X4 S) {enlargement of the phallus and pubic hair develop-) J' r2 i" h; L: J7 T. G1 D
ment without testicular enlargement, which was due4 ^7 h3 N7 I$ O; L- V
to the unintentional exposure to androgen gel used by' c# Q' e0 B' s6 b4 k7 O% S! ?) ~* z" x
the father. The family initially concealed this infor-
  S& V  B* D0 U: Wmation, resulting in an extensive work-up for this! [( v* Z- d) F; B( }! z5 F
child. Given the widespread and easy availability of
$ V7 S4 R$ C8 O! w# vtestosterone gel and cream, we believe this is proba-# u( g# ]# {9 e9 `
bly more common than the rare case report in the
- i; z2 r- ?. ]literature.4
$ r, q0 n- e: }: KPatient Report, Y9 h% j! L0 q0 D4 X/ u
A 16-month-old white child was referred to the$ G4 ~' t& o0 Q5 j3 R5 p0 T6 |- S- J
endocrine clinic by his pediatrician with the concern( }7 d+ p0 P$ j& n5 B4 [
of early sexual development. His mother noticed. ^' z8 n( [, N6 p* w2 y- k6 M. U- j
light colored pubic hair development when he was
9 t  P0 a0 @, s5 c. VFrom the 1Division of Pediatric Endocrinology, 2University of
1 m- D# o  t4 H' U' t# g7 s% f3 TSouth Alabama Medical Center, Mobile, Alabama.
) c3 Y' V$ ~" @9 M& r$ w( tAddress correspondence to: Samar K. Bhowmick, MD, FACE,* U0 N& S& \, b0 a/ `/ S
Professor of Pediatrics, University of South Alabama, College of. V9 A! g( E2 W3 P
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) {0 h8 D( V: K) R5 D- \e-mail: [email protected].6 {- A& }! H0 r8 H6 w5 h
about 6 to 7 months old, which progressively became
3 d8 P0 i/ f& ^2 S! Hdarker. She was also concerned about the enlarge-
: j2 K) Q# Q& Lment of his penis and frequent erections. The child. a1 Y) {# Z# J2 O1 t: z- Q9 d, q
was the product of a full-term normal delivery, with; n( J" e7 Z  \" a8 c4 z* X3 L8 q0 F
a birth weight of 7 lb 14 oz, and birth length of* r! p& ?2 f' I$ @
20 inches. He was breast-fed throughout the first year5 T: Y# f) F1 {" C' X2 A! T
of life and was still receiving breast milk along with: Y6 i( ^' @2 [6 @! J) a
solid food. He had no hospitalizations or surgery,
$ x( r9 V2 J; ?) b, cand his psychosocial and psychomotor development
; _& F6 K& H. k( l. m% swas age appropriate.
" `* x! V2 E6 W% lThe family history was remarkable for the father," J: x* {  D; o9 D4 [
who was diagnosed with hypothyroidism at age 16,
4 w1 i1 U, z  t8 t3 L0 Y0 hwhich was treated with thyroxine. The father’s& x1 w1 O: K% l' `0 \& m2 h, ~
height was 6 feet, and he went through a somewhat3 f' ?- h" V4 e7 B8 ]
early puberty and had stopped growing by age 14.) K/ g7 C) i* B. A
The father denied taking any other medication. The
0 V4 {  ]/ v7 Y* D- Xchild’s mother was in good health. Her menarche" z/ `) Z7 Q0 z
was at 11 years of age, and her height was at 5 feet
/ Y0 N* d1 _9 A) _& \* ]+ r5 inches. There was no other family history of pre-& Z2 ]) d; G& N0 x. j5 |
cocious sexual development in the first-degree rela-, x- F6 @: C6 X
tives. There were no siblings.9 X, D% C. I  i1 f; D* V: Z
Physical Examination
5 ^0 Z) L2 u7 N, Q7 q+ D. H* Y7 |/ DThe physical examination revealed a very active,
! c+ l( w1 ^4 g1 t0 ^, E! }8 Lplayful, and healthy boy. The vital signs documented2 |. A$ E& w- j& T  F/ h3 ]
a blood pressure of 85/50 mm Hg, his length was+ }$ ~) q9 g0 ?6 T. T8 K3 N5 o
90 cm (>97th percentile), and his weight was 14.4 kg
, h3 p! a' W8 S9 m' g1 [# C(also >97th percentile). The observed yearly growth% N: ]) k8 u, F+ K3 ]: ]/ i4 n
velocity was 30 cm (12 inches). The examination of
' G; \' G; o4 w& A5 Wthe neck revealed no thyroid enlargement.
& T7 Z7 h+ K9 tThe genitourinary examination was remarkable for
; d0 C" n! z) ~+ ?: denlargement of the penis, with a stretched length of
8 O% g/ c9 a! z+ y4 T0 u8 cm and a width of 2 cm. The glans penis was very well7 N6 N6 S1 H4 q& m) V$ v
developed. The pubic hair was Tanner II, mostly around
+ f9 ]/ Q+ D$ z8 U3 K+ C540: d4 a/ I: S0 \" q# `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 d, q$ E3 k& g! h$ Dthe base of the phallus and was dark and curled. The
7 B' u5 V9 d- T# u# O1 \testicular volume was prepubertal at 2 mL each.
) W  Q3 p# K+ i# j$ o8 XThe skin was moist and smooth and somewhat) e( c. ?- E( I% H. _( P7 K# N
oily. No axillary hair was noted. There were no
/ d" }2 g$ ^: W1 `. M9 Habnormal skin pigmentations or café-au-lait spots.1 H: p/ Q; G0 C- W+ A7 t
Neurologic evaluation showed deep tendon reflex 2+; Z/ {% _8 }% ?) \! C' n5 W
bilateral and symmetrical. There was no suggestion$ r# I% U, k! E8 L" G
of papilledema.
% u+ Y0 G5 Q1 tLaboratory Evaluation
7 w- V/ u  e  D4 t) A* n/ t! fThe bone age was consistent with 28 months by
+ u' h- m7 A8 X. e9 m2 K4 _2 a' husing the standard of Greulich and Pyle at a chrono-0 X. h9 a' b, F! N$ U4 Q. q
logic age of 16 months (advanced).5 Chromosomal( V& q) x3 X& P/ ?% F& t
karyotype was 46XY. The thyroid function test
& u* G: b' C3 V4 Yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-% O2 a  V4 n  n! s! w. b
lating hormone level was 1.3 µIU/mL (both normal).
6 w- i1 \7 ~/ s" ?$ D) R5 M- YThe concentrations of serum electrolytes, blood
7 Y3 o; P/ u5 U; n9 Gurea nitrogen, creatinine, and calcium all were
9 j; X! a" m1 cwithin normal range for his age. The concentration
; R( U( y3 I  J1 N$ d: yof serum 17-hydroxyprogesterone was 16 ng/dL
3 m# N3 G5 T& Z7 U0 ~8 H(normal, 3 to 90 ng/dL), androstenedione was 20
, Q) X5 ]8 P! {2 [2 J9 G$ Y& C3 hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, n- v, w5 a& @. k' h$ `terone was 38 ng/dL (normal, 50 to 760 ng/dL),, r1 x" @9 B! [$ n- A1 w$ N% E0 T: R
desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 t9 B  W# P4 L) P& z$ h3 _; s5 w
49ng/dL), 11-desoxycortisol (specific compound S)7 j# R2 w% Q8 J5 N2 ^2 s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  t9 h& x4 ~* Q9 z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& d( K5 p: n) i$ g$ g3 ~! `testosterone was 60 ng/dL (normal <3 to 10 ng/dL),# x$ W& h+ x7 h& d  L8 G
and β-human chorionic gonadotropin was less than
1 B3 s/ }4 K! c9 M9 k5 mIU/mL (normal <5 mIU/mL). Serum follicular  j. x0 K$ [; O$ y6 `* S  _
stimulating hormone and leuteinizing hormone9 {; w6 }, U- X
concentrations were less than 0.05 mIU/mL
- M0 |9 r, u( ](prepubertal).
4 H' c+ Z3 G2 n# w5 t$ B& j5 u8 S" ]7 LThe parents were notified about the laboratory% W8 j1 S- L% o* S
results and were informed that all of the tests were
; O. A) Q# E2 `5 vnormal except the testosterone level was high. The# Y3 ?5 J& r8 K0 a0 {" @: |- N% A$ ^
follow-up visit was arranged within a few weeks to" W! c6 S/ H) h' y( r4 L
obtain testicular and abdominal sonograms; how-# `3 l+ S+ C5 Q
ever, the family did not return for 4 months.
% g* B* [% b! gPhysical examination at this time revealed that the" \$ }- B+ A5 J4 U  j
child had grown 2.5 cm in 4 months and had gained
1 _! ?. f* J, Z, Q! e, s9 I2 kg of weight. Physical examination remained
; H/ x6 S6 S* C" vunchanged. Surprisingly, the pubic hair almost com-/ h& \4 x1 V2 X9 j% o/ W* t, S
pletely disappeared except for a few vellous hairs at; {) ^' O7 ~* ?/ a" ]: _+ e' x4 [
the base of the phallus. Testicular volume was still 2/ f/ X- B' g' W, {7 B  N; _! _' z# G
mL, and the size of the penis remained unchanged.
, \3 E! [( N/ }! gThe mother also said that the boy was no longer hav-8 }" i) @( P  ]8 x
ing frequent erections.! F3 Y% ^+ Y2 }0 p% ?3 I
Both parents were again questioned about use of
" Q% C1 k' k, O$ B& O/ C% J) Cany ointment/creams that they may have applied to9 X6 w2 N- c8 I2 j
the child’s skin. This time the father admitted the$ y( u( F$ @8 d, f9 f( f
Topical Testosterone Exposure / Bhowmick et al 541# M3 l: C' H3 i; M8 `$ G
use of testosterone gel twice daily that he was apply-1 R5 A. j0 ^3 S* N6 `8 Q
ing over his own shoulders, chest, and back area for7 x; A* f5 P& A' @
a year. The father also revealed he was embarrassed( t$ f- D) s3 i# W. N: F" r
to disclose that he was using a testosterone gel pre-8 m8 }' B% @  M( q
scribed by his family physician for decreased libido
* \! y! u3 n- M- z4 ysecondary to depression.( a2 O, I1 U3 k) I* H' \  p- E: Q* _  I. n8 f
The child slept in the same bed with parents.
9 _) T6 h, b5 ]9 @The father would hug the baby and hold him on his$ @  |- |8 ~. G
chest for a considerable period of time, causing sig-
6 S' R. A/ {! z2 G$ h8 Inificant bare skin contact between baby and father.
. X; W0 w! w/ \$ M- R* j! H/ D+ CThe father also admitted that after the phone call,
8 d: ?3 F2 ?1 U- ^* \3 o5 Gwhen he learned the testosterone level in the baby
/ q) m1 b# F- p8 ~1 hwas high, he then read the product information5 h. R6 |4 Y! ~+ W3 |3 Y5 o
packet and concluded that it was most likely the rea-' V. M6 Z" Q7 W% m2 a. R# S
son for the child’s virilization. At that time, they5 \3 K3 t4 P0 a$ M' p
decided to put the baby in a separate bed, and the
0 l4 Y- r1 I$ Vfather was not hugging him with bare skin and had, z. }( U) A( m
been using protective clothing. A repeat testosterone
3 t) F3 R3 S3 w: ~% \3 ~5 @test was ordered, but the family did not go to the
1 ^& G7 d2 R4 [+ Olaboratory to obtain the test.
- k, z$ a% R1 c6 ^Discussion( Z) b8 g1 Y' P; T
Precocious puberty in boys is defined as secondary5 V$ U( W; O$ t2 l. {
sexual development before 9 years of age.1,4
5 Y  R) `8 H# H% \& p- w! O4 xPrecocious puberty is termed as central (true) when/ c+ }+ y! c( d
it is caused by the premature activation of hypo-
8 s) Q; B# ~9 K0 t' ]# l& fthalamic pituitary gonadal axis. CPP is more com-
* ]3 B# j+ v, y+ m: s! z1 qmon in girls than in boys.1,3 Most boys with CPP6 n+ V  I1 V' f4 b1 J% v
may have a central nervous system lesion that is/ r+ p! V0 }! |3 w. G
responsible for the early activation of the hypothal-
, A, D8 e6 b' I  p6 H  xamic pituitary gonadal axis.1-3 Thus, greater empha-
, N1 z3 I: k6 f; R8 gsis has been given to neuroradiologic imaging in$ q9 D: W: x8 C
boys with precocious puberty. In addition to viril-
* K! |/ X8 @+ j, a1 `3 q# Oization, the clinical hallmark of CPP is the symmet-
: \& k: c; r% E% Grical testicular growth secondary to stimulation by: X, P+ ~5 V& T9 [$ G
gonadotropins.1,3# e" h8 J9 o; m* D) v' C( H/ b
Gonadotropin-independent peripheral preco-
. A$ r/ c) Z4 R7 ucious puberty in boys also results from inappropriate7 L( M+ }1 `4 w4 s
androgenic stimulation from either endogenous or  t; U) ^- e1 r" A% E1 s/ w- s
exogenous sources, nonpituitary gonadotropin stim-. [+ H( v; g. M7 l) C8 n
ulation, and rare activating mutations.3 Virilizing
2 Z2 b  t1 n1 M4 Z, X8 l0 ?4 Scongenital adrenal hyperplasia producing excessive" ~4 R7 n6 D$ K& z' t! n; P
adrenal androgens is a common cause of precocious
( P/ j  r6 I' ^& i$ Npuberty in boys.3,4
+ k( {. B" \# r8 ^" k  oThe most common form of congenital adrenal$ ~; i, x0 }% m# t& s4 {% R- E
hyperplasia is the 21-hydroxylase enzyme deficiency.
. _5 l1 r7 H, i/ f. X; SThe 11-β hydroxylase deficiency may also result in- ~' G; j. @: a" X* r/ B1 e" F
excessive adrenal androgen production, and rarely,7 m' j1 |/ S! Q* _! n
an adrenal tumor may also cause adrenal androgen
# N4 {* g7 J+ J% L) T+ N/ Texcess.1,3/ k* ~% x0 T& x7 b; Z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 `7 W! @! x& Z' I) r* I542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
1 s5 `9 n# N( |  ^& K& J' ^$ s. ~A unique entity of male-limited gonadotropin-: E; R) z  m: w4 H! `
independent precocious puberty, which is also known3 B9 W2 ^' u4 X: S: T) L+ Q4 x8 G# M
as testotoxicosis, may cause precocious puberty at a. M; l7 Y! T0 O- E# e1 [
very young age. The physical findings in these boys
8 W5 v" W& ^- C! rwith this disorder are full pubertal development,
2 z: a$ [) }( A; {, P( Aincluding bilateral testicular growth, similar to boys
" n7 {' P4 i; G3 D) O) ywith CPP. The gonadotropin levels in this disorder. a+ k+ e0 I1 k
are suppressed to prepubertal levels and do not show
" N2 y2 ^- k1 f# Gpubertal response of gonadotropin after gonadotropin-: h; [- ]9 [: ?+ M! R1 q
releasing hormone stimulation. This is a sex-linked
; c" t: c" {2 Y8 l- i# Kautosomal dominant disorder that affects only
+ W+ W% ]" `2 T, h; c. ?. umales; therefore, other male members of the family6 m$ `7 W1 E5 U
may have similar precocious puberty.3) G  C( W9 P' B8 b0 B/ H
In our patient, physical examination was incon-* }* Q$ E6 }4 i. D
sistent with true precocious puberty since his testi-+ F# i& B) I0 [9 {: t
cles were prepubertal in size. However, testotoxicosis- Y! {0 K8 y6 r$ ?! R: Y# Q
was in the differential diagnosis because his father
$ f8 D0 t7 L3 M7 n& zstarted puberty somewhat early, and occasionally,& m- O( V: i9 E1 C! z. B( s# |
testicular enlargement is not that evident in the
' y0 n* U7 l. ~: V/ z* sbeginning of this process.1 In the absence of a neg-( {# z( G. w3 W5 @9 C- i
ative initial history of androgen exposure, our
2 _3 t+ E# o9 l7 Z3 Jbiggest concern was virilizing adrenal hyperplasia,7 t# f8 J) n4 o: H
either 21-hydroxylase deficiency or 11-β hydroxylase& w3 O. }% x' r- ^7 X$ T
deficiency. Those diagnoses were excluded by find-
7 u: |6 S4 t- C  w2 p5 `  \; eing the normal level of adrenal steroids.
5 W) Y# _' x# B- kThe diagnosis of exogenous androgens was strongly
" B# N; K' ]$ c1 K1 b0 msuspected in a follow-up visit after 4 months because
/ T, ]' P& F0 \9 e. v- ?; ]6 kthe physical examination revealed the complete disap-
. G( y% B' N/ W) ~' {pearance of pubic hair, normal growth velocity, and, e. w. K; `, e5 J( ]+ h- ^, j
decreased erections. The father admitted using a testos-
4 Q: p  V: D' R# o1 Oterone gel, which he concealed at first visit. He was
5 {5 N2 x, \! P3 s3 q$ jusing it rather frequently, twice a day. The Physicians’
' X! k* K6 i  `6 Q/ cDesk Reference, or package insert of this product, gel or
% a( U2 y: |0 ]* Ncream, cautions about dermal testosterone transfer to1 t/ x3 l0 t$ I1 b# h
unprotected females through direct skin exposure.
: L9 e' I4 J) ?0 ]Serum testosterone level was found to be 2 times the
( G. }) h# v3 E1 }baseline value in those females who were exposed to1 q2 `( d7 C$ o2 W
even 15 minutes of direct skin contact with their male
6 y: b% q+ r7 Q) U$ bpartners.6 However, when a shirt covered the applica-
2 _9 \+ O: d- K5 P* Q% C- Ftion site, this testosterone transfer was prevented.) l4 ^9 m8 r" ~
Our patient’s testosterone level was 60 ng/mL,
1 Y7 q. W4 F& q, l2 x4 I, Z; Z- Pwhich was clearly high. Some studies suggest that: D: c, n; J9 {- {0 U3 J
dermal conversion of testosterone to dihydrotestos-
% D. T% n% C) B5 Q8 vterone, which is a more potent metabolite, is more
$ k9 x" O0 J3 J8 Lactive in young children exposed to testosterone
, a& M. f" a- Hexogenously7; however, we did not measure a dihy-
+ Y4 U+ i2 \1 \; h4 ?drotestosterone level in our patient. In addition to3 Y0 [) ^% @% S, m$ _& z
virilization, exposure to exogenous testosterone in
: O7 [9 X8 X. _children results in an increase in growth velocity and! h: O+ ^  w0 D. i
advanced bone age, as seen in our patient.
9 d' u/ W& t4 ^( @9 C: YThe long-term effect of androgen exposure during
/ J! h3 t! I/ D6 D  Y: T2 {8 \early childhood on pubertal development and final- h9 T% I" a4 q% m* m- t  g
adult height are not fully known and always remain% C, o1 U" T  m  W: {2 n3 n
a concern. Children treated with short-term testos-( K! \: i$ I" d1 I8 L% u8 }
terone injection or topical androgen may exhibit some7 |' V0 l, y! v6 s: \+ S3 }* j6 B
acceleration of the skeletal maturation; however, after
4 Z2 W( D: G5 E4 T" kcessation of treatment, the rate of bone maturation
- k, u& C; j) Kdecelerates and gradually returns to normal.8,9) G0 e& q' t8 ?
There are conflicting reports and controversy
7 ~. h8 M. w8 w$ ?over the effect of early androgen exposure on adult
  t! v# H6 j/ E" M* Zpenile length.10,11 Some reports suggest subnormal% v* |* x  y; e3 I0 W( G# M
adult penile length, apparently because of downreg-
8 P- C7 x$ k* E* r- \+ Iulation of androgen receptor number.10,12 However,
2 g  F6 R* x" C) oSutherland et al13 did not find a correlation between
; p2 w- {/ r5 Y; Q% Cchildhood testosterone exposure and reduced adult' q3 ?$ P. a5 A# y
penile length in clinical studies.
7 K7 S# w% {1 \  A; n) cNonetheless, we do not believe our patient is
# ?0 N4 Y9 G  E6 ?+ x/ tgoing to experience any of the untoward effects from
  C0 N6 t% B6 V5 L( qtestosterone exposure as mentioned earlier because; Y3 L9 d) C2 }- X0 j* D
the exposure was not for a prolonged period of time.
4 S0 o1 A& T& n! cAlthough the bone age was advanced at the time of
( X7 S6 E( P( D0 ]% ldiagnosis, the child had a normal growth velocity at
) k5 |8 |8 Q2 v" W2 O  M  Nthe follow-up visit. It is hoped that his final adult3 M: C; P  o% P. A
height will not be affected.
. T9 P- X3 a& O: C9 m3 u9 m( `& n8 }0 CAlthough rarely reported, the widespread avail-
5 g6 y1 u- e  v( I  A# K6 Yability of androgen products in our society may* L6 V2 P' S3 R* H5 k$ D' V
indeed cause more virilization in male or female
4 s4 M) T% `& p  Qchildren than one would realize. Exposure to andro-; p" i0 L0 n* [& A
gen products must be considered and specific ques-2 q7 ?7 ?: t$ U$ k
tioning about the use of a testosterone product or
6 W4 O! K, v5 F, f1 `gel should be asked of the family members during( |* {# V, {: m( q, K! c
the evaluation of any children who present with vir-
& B2 T7 K5 h. [1 l6 gilization or peripheral precocious puberty. The diag-! E$ w3 H5 X+ v3 K# N: G2 j. l; W
nosis can be established by just a few tests and by
  l, }7 ~: v: d) r4 Iappropriate history. The inability to obtain such a
9 z. ?1 ^9 W! U$ N& zhistory, or failure to ask the specific questions, may
4 H/ @; T, W: C* s' bresult in extensive, unnecessary, and expensive" O% e6 b% V7 c. f
investigation. The primary care physician should be
" E; x/ D6 e3 J! Qaware of this fact, because most of these children
: B8 R% G2 Z" {5 }; Z/ y; Kmay initially present in their practice. The Physicians’
. p$ u7 R% C0 s% |. i% dDesk Reference and package insert should also put a
: }8 E- ]" n+ p8 ~( a) C# g4 Lwarning about the virilizing effect on a male or* N5 H6 t* O0 }, F, C4 _, g
female child who might come in contact with some-& W$ t% z' i+ J
one using any of these products.
% y/ P$ Y' ]6 c- O( @$ O* p6 zReferences
5 W2 I4 R# O8 o; P. ]! ?, ?% l1. Styne DM. The testes: disorder of sexual differentiation
* o" A; i+ n6 pand puberty in the male. In: Sperling MA, ed. Pediatric
2 X+ w6 v1 d6 Y! EEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" K- A5 q; }* j  `" \2002: 565-628.
# K0 k6 u, |$ d; j+ `# [) [5 |2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 H. C; J! K6 j7 v# L, n
puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
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女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

: Q8 c( c3 z7 z7 f! G. `% ]! K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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