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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-Old0 S$ D! J' f/ u, P/ {- @
Boy Induced by Indirect Topical
. K2 b3 v& o; U$ l5 rExposure to Testosterone4 X% _' |. [& u% `/ G0 K
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( q! w: k" V0 i3 ^9 Qand Kenneth R. Rettig, MD12 I! m. W% j7 [$ ]1 F
Clinical Pediatrics$ Q# K/ n/ n' I: C
Volume 46 Number 6
7 E: R# ?) y" \3 ~July 2007 540-543' c- v4 J- }2 r8 B* I- C
© 2007 Sage Publications7 o! }. Y9 c' V0 _: Y
10.1177/0009922806296651
3 B) f5 g8 I' w( e% j5 I. h6 {http://clp.sagepub.com
0 u2 {1 D0 P' h* m, Ahosted at
  S+ [( I: t8 ?/ i: g5 b+ k, A6 ?http://online.sagepub.com# P# ?0 g+ n0 \$ S
Precocious puberty in boys, central or peripheral,
$ v$ w) x' ]: \% G& K0 |1 ois a significant concern for physicians. Central% K8 m. p7 l  w" ^5 z, p8 l5 d+ T
precocious puberty (CPP), which is mediated2 I* C& h' l* M# _8 g
through the hypothalamic pituitary gonadal axis, has
& T* E6 \+ _; S4 h7 v! @a higher incidence of organic central nervous system
( w; g. j- u8 M+ e! q) plesions in boys.1,2 Virilization in boys, as manifested
9 }' q- d" `$ U5 x' Yby enlargement of the penis, development of pubic2 B2 w$ A! U* `$ @$ x
hair, and facial acne without enlargement of testi-7 r3 k0 m1 c* n3 s& G3 \9 ]
cles, suggests peripheral or pseudopuberty.1-3 We
- Z6 J9 W. F+ {report a 16-month-old boy who presented with the
- c- m1 Z  \5 f+ o9 O# q8 r) senlargement of the phallus and pubic hair develop-# u+ D8 }- `) L$ c% H
ment without testicular enlargement, which was due
! X7 D/ W. d$ Xto the unintentional exposure to androgen gel used by
. S9 _$ n8 C) k5 S: \the father. The family initially concealed this infor-
4 l) s; K" M: V, Z: _, B7 Emation, resulting in an extensive work-up for this/ ^* Q. @- [( ]) l; Q
child. Given the widespread and easy availability of( A% A: t/ _6 L+ U# ~( j8 s
testosterone gel and cream, we believe this is proba-
- L1 T$ l, U* }% E7 K4 c! n6 Xbly more common than the rare case report in the
# D' v  q7 M" d, vliterature.4: V; X( H# `2 ]3 D* q
Patient Report6 i% N  m7 K6 ^% ?2 `
A 16-month-old white child was referred to the  e9 r* j9 ~9 a& b. O
endocrine clinic by his pediatrician with the concern- p$ d- {) x+ P' v* n" u$ Q$ G
of early sexual development. His mother noticed
3 k2 q: l& q5 r$ olight colored pubic hair development when he was1 s! @, i5 Z0 V# X
From the 1Division of Pediatric Endocrinology, 2University of3 g, s0 a; o# c( r, {
South Alabama Medical Center, Mobile, Alabama.
1 X  w9 V4 t5 b+ ]2 h2 \% oAddress correspondence to: Samar K. Bhowmick, MD, FACE,! }" [- v9 q" ^9 ]. \3 v  `
Professor of Pediatrics, University of South Alabama, College of
4 k% i6 E1 t  ^; v8 g6 V1 _Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# _. F" H$ l+ S8 je-mail: [email protected].
7 }. o9 w* u9 \about 6 to 7 months old, which progressively became
, A3 y# x! \: Sdarker. She was also concerned about the enlarge-
) i& G* p! U: t7 e& W; Y* ]  ~ment of his penis and frequent erections. The child
6 f( h) C- [* }was the product of a full-term normal delivery, with- i/ i( j% ^: n, \6 j  k
a birth weight of 7 lb 14 oz, and birth length of+ }# o, g2 h& G' u+ M( t5 E
20 inches. He was breast-fed throughout the first year0 ^% k7 }# x* F0 ^4 R( C
of life and was still receiving breast milk along with
2 e2 Z' O  \/ V, F' z9 C# Rsolid food. He had no hospitalizations or surgery,  j2 ?" f, M! G6 o
and his psychosocial and psychomotor development# d. V3 @4 T+ B7 t! @
was age appropriate.
8 s9 K3 N( z& [8 vThe family history was remarkable for the father,! j5 k. F' I) r0 A+ l) m
who was diagnosed with hypothyroidism at age 16,+ t7 V* G/ m0 A) E" n3 ]3 s
which was treated with thyroxine. The father’s/ G3 Q, L6 G6 b/ z$ W2 E/ `! H
height was 6 feet, and he went through a somewhat! l: R# F/ L  \- ?2 d
early puberty and had stopped growing by age 14./ J/ B% H+ p7 P8 p; W
The father denied taking any other medication. The
$ G; I4 f4 }3 ]" k) g- {child’s mother was in good health. Her menarche
9 N( A7 ?7 \) g  Z( y5 O& qwas at 11 years of age, and her height was at 5 feet
) J$ Q' A2 [- O5 inches. There was no other family history of pre-
0 P5 `- h( n: Z( O) G/ rcocious sexual development in the first-degree rela-6 t9 Q, d' u, J2 T+ _, [' M
tives. There were no siblings.
& g# J. ?* ~8 O8 P. G6 ?- ?/ c8 L' FPhysical Examination! @% H% D- R! T% l9 E9 |$ w
The physical examination revealed a very active,
& a! B" G, r! O/ w/ O7 \playful, and healthy boy. The vital signs documented
/ E; R7 m) y  ea blood pressure of 85/50 mm Hg, his length was
8 c. E6 _3 m% L% N. v90 cm (>97th percentile), and his weight was 14.4 kg
  g) d, F+ X, r8 k8 k; c* ?& i(also >97th percentile). The observed yearly growth; H0 S' a6 W9 f3 d# z* M
velocity was 30 cm (12 inches). The examination of  s, z5 L! C' x3 ^# X/ t2 f
the neck revealed no thyroid enlargement.
' s9 b: g, y# XThe genitourinary examination was remarkable for' U4 d- I: N3 x, e2 x6 F1 H
enlargement of the penis, with a stretched length of
& x" ]- ]0 }3 x+ h' ?8 cm and a width of 2 cm. The glans penis was very well0 W. z) y( S2 u1 c) X3 Q
developed. The pubic hair was Tanner II, mostly around# |, X. t# ?% m5 `0 c( G
540
( t% ]0 W. |. X% y+ tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 L5 ]$ u+ O! t  g7 z
the base of the phallus and was dark and curled. The
! B; A" ^. a2 t/ X8 _7 E1 _2 Ntesticular volume was prepubertal at 2 mL each.
2 D- P, W$ w, KThe skin was moist and smooth and somewhat0 Z+ J2 ^6 t7 Z1 L9 {: V
oily. No axillary hair was noted. There were no3 j: q, M9 a4 k. @
abnormal skin pigmentations or café-au-lait spots.4 r) m. Y1 o- W$ ^
Neurologic evaluation showed deep tendon reflex 2+  t8 o3 h5 Z/ |  R
bilateral and symmetrical. There was no suggestion0 Z! j" r5 U1 i" o
of papilledema.
& s8 l3 c6 P4 K4 U$ h1 `Laboratory Evaluation7 I7 s, N7 W( ~: P; k& W' ^
The bone age was consistent with 28 months by$ s) y1 i6 v6 s
using the standard of Greulich and Pyle at a chrono-
: U& O1 y. G3 f( z: s" @! m, Hlogic age of 16 months (advanced).5 Chromosomal
1 U0 W4 d4 K( j. S0 W: skaryotype was 46XY. The thyroid function test
5 A3 t8 [# o/ C; g( Qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 N& K* u  F5 p! J4 d# A; D  plating hormone level was 1.3 µIU/mL (both normal).3 i! W" W+ F' P  G/ G; X" a7 Y, ^$ I7 a/ s
The concentrations of serum electrolytes, blood/ k2 h6 P: Q% V7 y- [( u8 O# ], [
urea nitrogen, creatinine, and calcium all were& X6 L& R  _% H; S
within normal range for his age. The concentration" G2 U  t. Z! x$ K( Z  p6 v( N
of serum 17-hydroxyprogesterone was 16 ng/dL
" c1 y" `  C6 L4 S2 p(normal, 3 to 90 ng/dL), androstenedione was 20
# S* v+ H3 @: Ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( f0 Q3 H; F1 r3 D8 a% I7 x/ d- p0 Nterone was 38 ng/dL (normal, 50 to 760 ng/dL),! z2 L4 q1 z- X& S
desoxycorticosterone was 4.3 ng/dL (normal, 7 to5 Q% T2 C+ u4 p; M1 s
49ng/dL), 11-desoxycortisol (specific compound S)% [$ t. ^9 P8 e1 D: ?
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) p! j! X! S- t4 q# z# c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: G: o9 F% R1 |! y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 }5 f9 d% p% R- i2 p0 [1 Z# Land β-human chorionic gonadotropin was less than# E; N6 s& n+ h/ u0 I/ l
5 mIU/mL (normal <5 mIU/mL). Serum follicular* V8 L8 t: Y% K7 ]
stimulating hormone and leuteinizing hormone; {, Y  P% Y! o1 N7 ?& m4 x3 a# ^  j
concentrations were less than 0.05 mIU/mL
: Z! a, Q/ X, N5 a( D(prepubertal).
% C0 b; d  Y9 {8 n/ hThe parents were notified about the laboratory
8 }7 D; ?- L$ bresults and were informed that all of the tests were: @' J6 P. w9 [7 U4 J
normal except the testosterone level was high. The0 j6 |: K- f# h+ P* z7 S
follow-up visit was arranged within a few weeks to$ t5 `2 v, s2 X0 w0 Y+ J. e1 K
obtain testicular and abdominal sonograms; how-6 y- ^, P7 D, s$ p3 r/ |7 X
ever, the family did not return for 4 months.: a" p% d% P& d4 b0 b0 t2 I3 U# v! a
Physical examination at this time revealed that the2 X+ j% \% W$ S
child had grown 2.5 cm in 4 months and had gained
! Q& |- m- T6 z. z2 kg of weight. Physical examination remained
, t& @5 K; g( D! ]unchanged. Surprisingly, the pubic hair almost com-& z# H& @' f( d& B" V( A
pletely disappeared except for a few vellous hairs at: d! g% c# u  V
the base of the phallus. Testicular volume was still 2* Q1 j) f2 B2 S
mL, and the size of the penis remained unchanged.& e# s* \- P6 g2 a
The mother also said that the boy was no longer hav-1 j  g7 K: f5 \9 R3 B
ing frequent erections.8 O3 D3 C2 m/ Q4 Z, g
Both parents were again questioned about use of7 A5 y3 P$ M8 K
any ointment/creams that they may have applied to
4 @, C% ^8 z9 p- ithe child’s skin. This time the father admitted the: l( k8 z3 X  r" m' t% R5 H5 P5 d
Topical Testosterone Exposure / Bhowmick et al 541  S0 z( a0 n' P/ m3 X" e9 v
use of testosterone gel twice daily that he was apply-% a8 \' Z2 H9 G0 W" K- Z5 s
ing over his own shoulders, chest, and back area for
: t9 A+ h  _; B  K3 |5 M9 u9 E% Da year. The father also revealed he was embarrassed
. }1 e% H# R! Y1 N9 [* a0 H3 ?to disclose that he was using a testosterone gel pre-& i' P. Z& F9 Q, U' n$ p
scribed by his family physician for decreased libido& M: Z: B8 ^! h3 a
secondary to depression.! l6 C* p( o5 ~, `; {0 N
The child slept in the same bed with parents.
% ~- m9 p( N; W3 K9 K8 V: sThe father would hug the baby and hold him on his
  ]; S: D5 ~% echest for a considerable period of time, causing sig-0 D! P% l) T/ J: J( j% r; _
nificant bare skin contact between baby and father.7 z5 }& B0 F0 {
The father also admitted that after the phone call,
% `% X7 L6 c  ?8 b' p+ C5 Q9 c6 Awhen he learned the testosterone level in the baby$ J1 Y& j8 K$ P. `- F" N
was high, he then read the product information
- w  l& ~. x9 f4 opacket and concluded that it was most likely the rea-3 n6 W0 D- \$ L7 o% S- S
son for the child’s virilization. At that time, they. g4 i5 I; p) V: h2 R
decided to put the baby in a separate bed, and the
6 L, I9 o+ c3 e$ Zfather was not hugging him with bare skin and had
9 B- P; n4 U8 X7 Q: X+ A2 Bbeen using protective clothing. A repeat testosterone$ @- {" d" _, P" }$ U8 [* S
test was ordered, but the family did not go to the
; X4 F" O9 L1 v) ]( Slaboratory to obtain the test.: ?3 N8 w: a% g, j" T& ^8 R% P
Discussion
5 [- X& b" g7 CPrecocious puberty in boys is defined as secondary! x, \5 l8 q# O$ k, i/ \! {
sexual development before 9 years of age.1,4
9 G# O# z$ E- a! p$ x  _- XPrecocious puberty is termed as central (true) when
4 [( v  B8 d5 o/ Y* z3 [& P  y5 Qit is caused by the premature activation of hypo-
0 L1 W) i% }5 {# W, F- r# F( V. athalamic pituitary gonadal axis. CPP is more com-- O* I( Z( [* D2 N8 N( J  e
mon in girls than in boys.1,3 Most boys with CPP
% i. i$ i" E/ k+ tmay have a central nervous system lesion that is5 |8 n- G5 S6 H& Y
responsible for the early activation of the hypothal-( E: ~3 a' F3 @) |
amic pituitary gonadal axis.1-3 Thus, greater empha-1 z5 n+ w4 G9 l. v8 G3 ?
sis has been given to neuroradiologic imaging in5 B) Q& F+ m7 `1 b( ]2 k7 E
boys with precocious puberty. In addition to viril-. Y0 E5 s7 A! p" g# o9 [7 j  g- N4 @
ization, the clinical hallmark of CPP is the symmet-
& f: e+ \& }# l/ t/ M' Irical testicular growth secondary to stimulation by+ g5 N0 }* [7 n3 s
gonadotropins.1,3, ^$ e7 S( H4 j1 @+ p9 R3 G
Gonadotropin-independent peripheral preco-
' o6 r# p2 Z/ z+ e- ncious puberty in boys also results from inappropriate
, G% u( I* F) `  K2 ~androgenic stimulation from either endogenous or
! n1 d5 x, r& R( B+ _exogenous sources, nonpituitary gonadotropin stim-
6 K3 T3 p! f( g( C' fulation, and rare activating mutations.3 Virilizing
! y% L6 d# V3 wcongenital adrenal hyperplasia producing excessive" A  Q8 V; Q3 O
adrenal androgens is a common cause of precocious1 C( a2 ]+ w0 P* f& W
puberty in boys.3,4
( e# W# V2 {3 z0 J5 RThe most common form of congenital adrenal" z2 d( G# x+ d
hyperplasia is the 21-hydroxylase enzyme deficiency.  \- _8 D* c5 j4 N% \; s
The 11-β hydroxylase deficiency may also result in0 [. R, L, Q6 n4 @/ z/ S/ X9 H
excessive adrenal androgen production, and rarely,
: N6 M( l  i! B: Lan adrenal tumor may also cause adrenal androgen; V# e4 U7 R5 E9 u" F
excess.1,3! b5 u. {4 O; ~& R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* n/ F, a3 b7 ~% ^
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ f1 @& g, _6 v  y& q
A unique entity of male-limited gonadotropin-/ Q' |, l; N  y. L# P
independent precocious puberty, which is also known$ `# G3 @2 ]# Q7 `5 I# S1 n  X
as testotoxicosis, may cause precocious puberty at a
+ e  L1 L* H, [- B4 Zvery young age. The physical findings in these boys' n/ k3 U4 |4 [" g- n1 y; B
with this disorder are full pubertal development,
) U0 w: s$ T( \" d! G3 J- Jincluding bilateral testicular growth, similar to boys
: ~" \$ E& p  r+ swith CPP. The gonadotropin levels in this disorder
' `2 o. _0 n  e3 ?8 D1 t7 fare suppressed to prepubertal levels and do not show
% ~$ k3 o) b2 G8 \4 t1 l/ _9 Cpubertal response of gonadotropin after gonadotropin-
4 {; A! S6 j, w& h$ X" D* oreleasing hormone stimulation. This is a sex-linked
) e6 R7 p7 W! s# K- L  k  ~5 Kautosomal dominant disorder that affects only, x5 @( h6 Q2 I$ o; ]/ R& ^
males; therefore, other male members of the family
% ~0 `8 j; M- N; Nmay have similar precocious puberty.37 j8 ~2 l& B+ g* Q. O. h$ U
In our patient, physical examination was incon-
- w' F. J) f* xsistent with true precocious puberty since his testi-" ~' _6 a: Q1 I- c" F* F# X/ j
cles were prepubertal in size. However, testotoxicosis( z5 z6 @, w. H3 o/ W
was in the differential diagnosis because his father
/ E" I% y# k7 q+ \  q- j( ]started puberty somewhat early, and occasionally,: c7 o% n  j, o. C
testicular enlargement is not that evident in the( R. d3 e5 f) w2 }: C# s: Y
beginning of this process.1 In the absence of a neg-  c+ @0 U6 C- w% X
ative initial history of androgen exposure, our/ Q! c" r. W( A' {; m6 c& v7 z
biggest concern was virilizing adrenal hyperplasia,2 S* l6 f# `8 \+ q( h# Y# n  G+ J, ~
either 21-hydroxylase deficiency or 11-β hydroxylase
: ?0 }& M4 ?$ U! k" U' `/ hdeficiency. Those diagnoses were excluded by find-
7 O* D) N' \# }0 W* a2 W$ k2 j2 L2 jing the normal level of adrenal steroids.# O- p. r6 ~5 L6 l4 C" g. r
The diagnosis of exogenous androgens was strongly. Q+ {. O5 @* U* `# s# [$ W) w
suspected in a follow-up visit after 4 months because1 k+ N* W$ T* v9 c
the physical examination revealed the complete disap-# s: V' s$ E0 `/ B
pearance of pubic hair, normal growth velocity, and
3 J9 Z3 O  J) z5 m" R: m6 Adecreased erections. The father admitted using a testos-
, p' d4 |" t& ^# V: z1 iterone gel, which he concealed at first visit. He was
/ }4 C4 o6 C1 }7 ?3 y, l% Jusing it rather frequently, twice a day. The Physicians’8 u; X/ N3 V! b/ M2 \" y2 [- O
Desk Reference, or package insert of this product, gel or4 j6 D0 n; ]8 P; a
cream, cautions about dermal testosterone transfer to
' K1 p, t2 k+ Y& U4 O3 Punprotected females through direct skin exposure.4 {0 v2 z! b# e  k1 i4 w( g
Serum testosterone level was found to be 2 times the( Y" U. b9 k! M5 N8 Z3 H4 C
baseline value in those females who were exposed to" h9 h! o! J* `
even 15 minutes of direct skin contact with their male5 d- l5 Z3 X/ I* W+ Q# z& W: ]$ z
partners.6 However, when a shirt covered the applica-
8 e1 X6 F8 b# y( o& ^. g( ^7 _# N. xtion site, this testosterone transfer was prevented.
& w/ D: K3 D/ @0 bOur patient’s testosterone level was 60 ng/mL,0 L; m- z7 r* T0 D9 S& T
which was clearly high. Some studies suggest that
) a2 v; J* `/ N, a1 l* rdermal conversion of testosterone to dihydrotestos-# @' D: n+ Y1 N' A
terone, which is a more potent metabolite, is more
- J" m9 V7 \  R9 Z) Hactive in young children exposed to testosterone
9 g; v8 ]3 O. r& Texogenously7; however, we did not measure a dihy-- p$ ?# t( ^/ b4 k$ o- J; o
drotestosterone level in our patient. In addition to& w* e6 W2 F) M7 f( w
virilization, exposure to exogenous testosterone in6 N2 z% }3 K! s1 e0 \+ h
children results in an increase in growth velocity and
( z0 b! P0 s" l! Jadvanced bone age, as seen in our patient.  N+ \; w+ _- m1 j( w- w
The long-term effect of androgen exposure during( w+ y  E: l6 m" K; b
early childhood on pubertal development and final7 v9 O7 A- S0 M+ C& c7 x& M
adult height are not fully known and always remain
; [. y0 Z. x0 G; T  za concern. Children treated with short-term testos-6 c7 a: H3 O, D9 r5 [2 ?5 F
terone injection or topical androgen may exhibit some
* x1 x- ^4 k1 r, J, E' `! @0 K, Yacceleration of the skeletal maturation; however, after. `& s) Q5 L  H0 h. l
cessation of treatment, the rate of bone maturation
% j) q5 D2 i; ^% j- }) z& Odecelerates and gradually returns to normal.8,9% V/ ?; U8 K& o
There are conflicting reports and controversy+ l3 N1 f6 k$ x% R/ Z
over the effect of early androgen exposure on adult
7 |. L3 x6 d- |; `9 W, O" bpenile length.10,11 Some reports suggest subnormal. Z1 G, E) x7 V; ?) m
adult penile length, apparently because of downreg-4 h1 ^. b# ?. m# A6 @6 N
ulation of androgen receptor number.10,12 However,
3 T& T( A# ?, _Sutherland et al13 did not find a correlation between
  d" m( _% v- V$ Q# }( R- A4 Ichildhood testosterone exposure and reduced adult
  C# q# F$ G, C. B. I( ypenile length in clinical studies.0 H  Z! a& {: T3 ?) @& S
Nonetheless, we do not believe our patient is. W2 b5 ~2 O5 c" c' ^8 T. K
going to experience any of the untoward effects from3 K# i/ P. \# @8 C+ l# \! j
testosterone exposure as mentioned earlier because. w9 Q! u/ O/ t6 X: B
the exposure was not for a prolonged period of time.
* V4 h3 l9 P. \+ L( tAlthough the bone age was advanced at the time of
' g1 P0 X4 \( pdiagnosis, the child had a normal growth velocity at/ ], W( I1 B" g* U4 y& D
the follow-up visit. It is hoped that his final adult
6 k0 d  \6 H! b# X1 }9 t  Theight will not be affected.
3 N7 `/ p, ^4 u9 \$ \Although rarely reported, the widespread avail-6 k" G' s( h. M1 L
ability of androgen products in our society may6 ^- y  }1 G* I  `$ Q2 s
indeed cause more virilization in male or female% M9 M1 P$ i4 d  n+ B5 R
children than one would realize. Exposure to andro-' h/ ]* N. _& l7 Z1 n+ S8 {6 h6 ?( R
gen products must be considered and specific ques-5 k' J: z. N: H8 [; C1 p
tioning about the use of a testosterone product or
3 }7 W( J' ?$ h. ^3 H$ bgel should be asked of the family members during, `' t! T, t/ S) G6 P; J' y
the evaluation of any children who present with vir-$ I% M; m1 }8 r3 _$ B
ilization or peripheral precocious puberty. The diag-
  F, c2 ?6 F" x2 _  r& m+ S/ ~( I3 Hnosis can be established by just a few tests and by
- E( b6 |, |% q- d1 }appropriate history. The inability to obtain such a
0 @& Z! B( }3 Bhistory, or failure to ask the specific questions, may
  Y0 y/ ^) p* I! S' u& R  J8 bresult in extensive, unnecessary, and expensive
* \9 P9 P- m/ {% h& O$ E0 r0 hinvestigation. The primary care physician should be; [9 j! k8 I& D  ]/ s0 l( T
aware of this fact, because most of these children
( b" N) q  b/ e' ~+ L& o0 J- Kmay initially present in their practice. The Physicians’) x6 \  x. i, E# f* F+ b7 r
Desk Reference and package insert should also put a
$ v/ X2 {' |+ g- v7 q6 a3 W! C3 twarning about the virilizing effect on a male or
/ o; f3 d0 o" ]) r% Vfemale child who might come in contact with some-
3 Q7 i) i& g4 g/ u8 |# Tone using any of these products.. _5 P* G: c. u% S; A: j$ Y9 ]
References: A2 `% W* m8 y8 ~9 d. V1 w. z: c
1. Styne DM. The testes: disorder of sexual differentiation
4 V( l3 y7 p5 C+ h1 |and puberty in the male. In: Sperling MA, ed. Pediatric
  u* }1 n7 j) F6 pEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;' J# @$ C; S# c: P1 [- J
2002: 565-628.2 h+ @7 A% q" z( G" U
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious1 _: S; |0 l9 G
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old; e1 J6 n  g# _% u
Boy Induced by Indirect Topical
: q3 W! `! k7 f: yExposure to Testosterone
; V/ b5 O' |2 g3 {% _Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  j! U9 k1 @  @: i
and Kenneth R. Rettig, MD1! i& G5 {- ^$ W) k, d# f5 R
Clinical Pediatrics
6 `3 j5 n9 P# o/ uVolume 46 Number 6/ c& k$ Z" n! l. y- J* n
July 2007 540-543' u9 H0 I0 G2 G4 A& g( p
© 2007 Sage Publications) q* ^9 @' t- C
10.1177/00099228062966519 A# J7 x& x3 Q+ {
http://clp.sagepub.com' M% T; R0 A& k7 W5 S, D
hosted at) _% L& v/ E+ n$ B4 S% I5 i7 }, U
http://online.sagepub.com
/ S, Y" P7 p, HPrecocious puberty in boys, central or peripheral,
7 y6 q3 q6 ~) \7 tis a significant concern for physicians. Central" ~1 s% }: w1 O! c" c7 \  {1 d
precocious puberty (CPP), which is mediated
; R; [# R% ?9 A3 R# E  R' y$ {, nthrough the hypothalamic pituitary gonadal axis, has. E/ O$ \; x6 c( d
a higher incidence of organic central nervous system, H. z+ R+ Z- s3 K
lesions in boys.1,2 Virilization in boys, as manifested
7 a4 X8 P: F' U7 e0 U' r1 `by enlargement of the penis, development of pubic% [: d% Q; q4 b
hair, and facial acne without enlargement of testi-
, N$ i# K2 e  ?/ S( fcles, suggests peripheral or pseudopuberty.1-3 We& l% Q  b% Z# X7 ^3 ?" q; \- @+ d
report a 16-month-old boy who presented with the9 }$ Z+ Y1 t/ ]) S- c" C# s
enlargement of the phallus and pubic hair develop-; {- H* a) o5 [" q/ w7 l
ment without testicular enlargement, which was due
3 P* }$ `# T( j7 T9 |to the unintentional exposure to androgen gel used by  D6 F, m/ C& {, E' f% m
the father. The family initially concealed this infor-& l" l& t+ {4 H% L2 n0 |
mation, resulting in an extensive work-up for this- F. x4 t$ I( \/ k( N1 F( Y
child. Given the widespread and easy availability of' w: j1 i0 W, s* C
testosterone gel and cream, we believe this is proba-+ G2 p, U/ m+ M7 J' Y
bly more common than the rare case report in the4 r2 I$ D6 b2 k" _
literature.4
& l( [9 V6 B5 M$ c- ~, d; oPatient Report7 p( S* a2 K( Z) X$ x: H
A 16-month-old white child was referred to the: a/ E0 _8 {$ l( j  r" v
endocrine clinic by his pediatrician with the concern' ^; B8 `7 [; a/ C8 o) v
of early sexual development. His mother noticed+ X) X2 F, W7 P9 Z* }7 J
light colored pubic hair development when he was
4 F. w% W* O4 `+ @. v  e. O# b. RFrom the 1Division of Pediatric Endocrinology, 2University of, j! \$ b! S9 |
South Alabama Medical Center, Mobile, Alabama.( K$ q! {& }; t
Address correspondence to: Samar K. Bhowmick, MD, FACE,
* u- W* ~7 K7 V! FProfessor of Pediatrics, University of South Alabama, College of
# }3 i+ }8 B, PMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 ~) z/ O) I, m7 @
e-mail: [email protected].8 C& e# R% ]# n1 z% _' W2 Z. G( T- \
about 6 to 7 months old, which progressively became% V; E' J. w* L8 a- x2 Z
darker. She was also concerned about the enlarge-, b1 k2 W- ~; I5 ~3 K
ment of his penis and frequent erections. The child# Q- }6 \7 X( Q- v4 K
was the product of a full-term normal delivery, with+ ]: X0 `% Q5 [1 J8 w  G0 ^7 n
a birth weight of 7 lb 14 oz, and birth length of0 |" i" j& k: b5 B
20 inches. He was breast-fed throughout the first year; ~0 n& e6 h) B
of life and was still receiving breast milk along with
! e5 H* g1 W7 b5 c: m: @( `4 i# }solid food. He had no hospitalizations or surgery,
7 S; c$ R0 `- B# y0 U5 H4 b1 Rand his psychosocial and psychomotor development
" o4 q5 k! B' p' a$ _was age appropriate.
1 N* {1 ~' a* i6 P  lThe family history was remarkable for the father,
; W: A, ?9 I0 M8 c. N  Owho was diagnosed with hypothyroidism at age 16,4 a/ {1 p+ [& \3 p% g8 Q
which was treated with thyroxine. The father’s
& v3 q* ^  |0 |height was 6 feet, and he went through a somewhat
: n# M; \9 ~* Z& pearly puberty and had stopped growing by age 14.
! z( n0 e' m/ jThe father denied taking any other medication. The$ F7 ^% k( ^+ T
child’s mother was in good health. Her menarche
) e2 x; }$ Z; r1 g, ^9 _6 r) O/ Lwas at 11 years of age, and her height was at 5 feet. v) `6 s' G$ B$ A4 h
5 inches. There was no other family history of pre-
2 [4 J# [( F! D/ [6 J5 lcocious sexual development in the first-degree rela-
- D# w5 x: w0 M5 p/ a8 u" vtives. There were no siblings.
) u0 z+ p" v* J0 |8 U% aPhysical Examination
2 l# z# h4 ~$ Q+ gThe physical examination revealed a very active,+ z0 L+ f) E& C: F. _2 a4 E2 P
playful, and healthy boy. The vital signs documented( P$ c7 S6 O0 M% H3 b$ _
a blood pressure of 85/50 mm Hg, his length was
" ?! R3 o. t0 w1 M/ q$ Q$ P5 e90 cm (>97th percentile), and his weight was 14.4 kg
; Y( p# y/ r* s( R' H(also >97th percentile). The observed yearly growth& n) n: l& z$ L/ }% U
velocity was 30 cm (12 inches). The examination of
; q% }# ]3 b9 X5 v2 j4 r) s/ Qthe neck revealed no thyroid enlargement.  M/ U- {5 {  f4 U
The genitourinary examination was remarkable for3 P/ j( l3 V( G: q
enlargement of the penis, with a stretched length of
# O. }$ V" [3 O# a( C8 cm and a width of 2 cm. The glans penis was very well) Z! E! v, n; {  Z: O4 ]% ?
developed. The pubic hair was Tanner II, mostly around
) a6 ^3 ?! B7 N& u4 J540
# i5 x( ?* b1 \: Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) L' Y+ _- R% Q1 a
the base of the phallus and was dark and curled. The7 T- I% t5 [. O1 k4 y2 X8 A
testicular volume was prepubertal at 2 mL each.* f' Y% x7 D  c, f/ P
The skin was moist and smooth and somewhat5 [# r; B4 E0 W% v+ r( u# m
oily. No axillary hair was noted. There were no
3 \7 g3 i/ r0 v3 a: v2 f; j: s8 ?5 C/ zabnormal skin pigmentations or café-au-lait spots.
1 ^" P) M2 R: n# l/ [. E8 ZNeurologic evaluation showed deep tendon reflex 2+
' q/ m* D$ o" y1 C' E; \# @) p* k: ~bilateral and symmetrical. There was no suggestion
% I5 v2 z- J' \: {of papilledema.
# ?" h, y# k" q, s% ?Laboratory Evaluation' f& m3 N2 p; ~( y$ @  g
The bone age was consistent with 28 months by( y4 X, l9 r9 ?0 R$ z
using the standard of Greulich and Pyle at a chrono-
$ X9 w3 y  R* x) j2 q% M4 J/ tlogic age of 16 months (advanced).5 Chromosomal
2 Q: F# [! B$ _6 n1 s3 F2 xkaryotype was 46XY. The thyroid function test  _0 t; T4 e) N, `
showed a free T4 of 1.69 ng/dL, and thyroid stimu-' \. T, B. L! L$ O7 h
lating hormone level was 1.3 µIU/mL (both normal).
5 Z; t  J0 x6 X. E. v+ `& QThe concentrations of serum electrolytes, blood5 }+ B* _8 ~  u9 q
urea nitrogen, creatinine, and calcium all were4 ?" E: i( n0 o4 T! c
within normal range for his age. The concentration  Z3 _* q$ U( h: Y/ ]
of serum 17-hydroxyprogesterone was 16 ng/dL6 z9 s. U; _, Z4 b: ~
(normal, 3 to 90 ng/dL), androstenedione was 209 o8 [& A0 {& V' Y+ y" |2 ]
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; u8 X: }0 L' c  V
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. ~7 ^* P* {% Pdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ C3 z. @8 m/ `; e! z49ng/dL), 11-desoxycortisol (specific compound S); o; _# k; [4 U: F7 K
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* V. Q9 F' G7 D* m% s
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
  n5 S* V& Y5 H$ Otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 c" {1 k+ D9 \' e7 A. Y2 N+ ?and β-human chorionic gonadotropin was less than
  U0 t. t: x: ~! t. l& c- L5 mIU/mL (normal <5 mIU/mL). Serum follicular9 h# c* `& r! f& f9 x
stimulating hormone and leuteinizing hormone
; [) l% U7 q8 ]. Mconcentrations were less than 0.05 mIU/mL7 o5 s1 R# u/ V
(prepubertal).
. D4 Q4 U" c! r5 C! XThe parents were notified about the laboratory* v/ B  x8 ^4 I( R9 e7 |2 ~
results and were informed that all of the tests were
- o( w# G0 y1 D$ E2 F( r) Rnormal except the testosterone level was high. The
5 n- A& D9 y- J" ?: Q8 cfollow-up visit was arranged within a few weeks to5 a" s! R' h2 }. D1 V
obtain testicular and abdominal sonograms; how-6 y/ e2 W$ w+ N7 g! L+ S- U: W
ever, the family did not return for 4 months.
2 m% f5 m7 D6 [' cPhysical examination at this time revealed that the* H7 [& @) e( F" x
child had grown 2.5 cm in 4 months and had gained
0 p  l3 Q; C. ?" q1 B$ x2 kg of weight. Physical examination remained" j- v! C3 Z8 k
unchanged. Surprisingly, the pubic hair almost com-
9 r) ~6 F$ x& B# Jpletely disappeared except for a few vellous hairs at
) Z" a0 h, ?" d( F0 Sthe base of the phallus. Testicular volume was still 2- |! W  j/ H4 j! {
mL, and the size of the penis remained unchanged.( `' T- O1 v, _. x
The mother also said that the boy was no longer hav-% X, ^4 a! p( u8 ]* B
ing frequent erections.
# Y! P! d( H9 KBoth parents were again questioned about use of9 P6 X; z3 R( W) `* T
any ointment/creams that they may have applied to
' T; V* K3 F" W3 l5 sthe child’s skin. This time the father admitted the
/ n, ~6 x6 y: T- F! \5 r6 GTopical Testosterone Exposure / Bhowmick et al 5413 x0 n# Z. ~- ]
use of testosterone gel twice daily that he was apply-" b3 i: B  V# d' Z1 P( E8 q  u
ing over his own shoulders, chest, and back area for
' ]0 z# X" Y, pa year. The father also revealed he was embarrassed; G7 o' k4 S4 `! x1 c0 v8 ]: W  C0 m0 k
to disclose that he was using a testosterone gel pre-
  X; G6 [7 O+ Hscribed by his family physician for decreased libido. Z- ?" o9 g  m
secondary to depression.
3 Z3 j; G7 r) o5 b& eThe child slept in the same bed with parents.# F. f& \0 n3 @7 w4 w8 P8 `1 t7 T* V8 E
The father would hug the baby and hold him on his8 @+ P: \/ K. h+ o3 M- o
chest for a considerable period of time, causing sig-; _- W2 F9 _) }! i/ K: g
nificant bare skin contact between baby and father.
/ ^/ |0 C3 F3 K9 T# R) n+ vThe father also admitted that after the phone call,
, @' X( i% E' w3 Pwhen he learned the testosterone level in the baby1 C9 E9 C6 q! ]/ u7 F
was high, he then read the product information
. c, E- s9 ^: Xpacket and concluded that it was most likely the rea-! y# }+ r/ \  M, f8 w2 P, \) L' Y
son for the child’s virilization. At that time, they' m' z9 X0 r! X( C/ X
decided to put the baby in a separate bed, and the+ J, a6 Q+ H  b0 L1 q# w9 z
father was not hugging him with bare skin and had
4 o; u& d  T/ A; N! Vbeen using protective clothing. A repeat testosterone
5 J$ K- t; N8 k/ [test was ordered, but the family did not go to the) U9 Z5 ~8 a( a% K5 p2 }
laboratory to obtain the test.
$ u+ G1 v0 _/ UDiscussion
0 i; a# I" x3 G+ m& jPrecocious puberty in boys is defined as secondary0 q4 O+ _% v. H# Z" h3 L. ]
sexual development before 9 years of age.1,4
5 M* j% y" q) E7 N8 P" l2 }Precocious puberty is termed as central (true) when
: h, {: Q! h! X6 l- {0 y" Qit is caused by the premature activation of hypo-
8 H6 v. x- }+ A; _thalamic pituitary gonadal axis. CPP is more com-
, j& c. r) |' z* I2 u; K& ]mon in girls than in boys.1,3 Most boys with CPP3 T5 d  ^0 d5 `- [
may have a central nervous system lesion that is% f, }/ d  }! s
responsible for the early activation of the hypothal-. B( W2 q6 d' x3 x) A
amic pituitary gonadal axis.1-3 Thus, greater empha-8 q. _6 O9 |/ a
sis has been given to neuroradiologic imaging in
6 B& T$ r5 F: F1 y) ^boys with precocious puberty. In addition to viril-
4 e) C& \: C: ]$ [" i( Oization, the clinical hallmark of CPP is the symmet-
( i5 |- n. c1 R5 z7 x3 H# Vrical testicular growth secondary to stimulation by
' v: U' G7 R, }* n3 t; Ogonadotropins.1,32 D! L' a$ c, h. b. F5 z9 G6 _: D$ }
Gonadotropin-independent peripheral preco-
9 A* }" g  `7 S8 S7 _* o8 B3 h2 a, mcious puberty in boys also results from inappropriate
/ _+ J* d4 e6 G, F0 Wandrogenic stimulation from either endogenous or
' O6 C6 y, A  B+ R, s# _2 Eexogenous sources, nonpituitary gonadotropin stim-
1 A+ [& j# I4 k% O- E0 Zulation, and rare activating mutations.3 Virilizing
7 W% b- _( S+ S% \congenital adrenal hyperplasia producing excessive
/ X* F3 _. B& f5 S4 g3 Hadrenal androgens is a common cause of precocious' V4 m9 c1 m- p) B, k$ {
puberty in boys.3,4
! V4 h) g& a3 v* C4 a* [0 S) XThe most common form of congenital adrenal
2 Q- H: T( y- I8 y7 s  ^6 H; chyperplasia is the 21-hydroxylase enzyme deficiency.
& Q; z: {7 Z* |9 yThe 11-β hydroxylase deficiency may also result in& G* C+ M% s* r
excessive adrenal androgen production, and rarely,7 m5 Z3 Z" E5 D+ Y  w
an adrenal tumor may also cause adrenal androgen0 s  N/ P* h# O* j! n+ H" v
excess.1,3
- [8 @  U, {% X. z5 Sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 I% l- c& l3 ]' l. I0 {542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. b* a! \# [1 }# k/ N
A unique entity of male-limited gonadotropin-( c! X7 K+ {4 F  c8 Q5 S4 y
independent precocious puberty, which is also known) i& {, `) B2 y, r: f0 O' k+ f* D. D
as testotoxicosis, may cause precocious puberty at a0 `' h; w( W3 {- A, ~. ?6 ~" Z
very young age. The physical findings in these boys
" y0 E3 _8 X7 U  \, R( Nwith this disorder are full pubertal development,* p( @8 |& O$ g) }6 I
including bilateral testicular growth, similar to boys
. I( y; B7 }2 i! @' D/ Hwith CPP. The gonadotropin levels in this disorder
# z( Q- d  q* A5 k" d# b" qare suppressed to prepubertal levels and do not show
2 h* F1 m) H+ M* W- J9 D0 w* }pubertal response of gonadotropin after gonadotropin-1 c$ B" s- s& Z2 Y& J; b3 j
releasing hormone stimulation. This is a sex-linked
( J1 Q( H. U" c5 w2 H5 G5 iautosomal dominant disorder that affects only
2 m: X' C, _4 ]3 V- D5 i' umales; therefore, other male members of the family7 r6 k# J* ]/ B6 k2 B+ Q/ V8 m5 d
may have similar precocious puberty.3
) a7 A  c+ j$ i2 ?+ h; K& U( ~  XIn our patient, physical examination was incon-
- f+ O, `9 b1 @4 R. l8 D+ Osistent with true precocious puberty since his testi-
6 g4 a+ J4 X& D, @$ Pcles were prepubertal in size. However, testotoxicosis
8 }3 o' ~' T7 E- mwas in the differential diagnosis because his father2 p# R3 a5 P# T4 N
started puberty somewhat early, and occasionally,
  E% A5 V8 y) V& Y+ }* ?testicular enlargement is not that evident in the1 q8 F7 }1 \5 T8 C& _8 C
beginning of this process.1 In the absence of a neg-
" X& e0 E1 e2 F* q( [) J3 y' hative initial history of androgen exposure, our
# @2 ^. {! R( B. i: S/ Q5 D3 w' [biggest concern was virilizing adrenal hyperplasia,5 K; j5 e) T2 r6 N; u* p
either 21-hydroxylase deficiency or 11-β hydroxylase
) h  T3 `4 w& m5 o& zdeficiency. Those diagnoses were excluded by find-
# T' R3 ?4 {9 c. M" f9 F7 ting the normal level of adrenal steroids.3 I& k, p. q9 `4 h3 s" @7 w
The diagnosis of exogenous androgens was strongly
: a. [, K/ g; [/ W5 l! Csuspected in a follow-up visit after 4 months because/ F4 R: k0 d# r. a+ a* x
the physical examination revealed the complete disap-
( Y% B4 ~3 l) ^) C7 x- A" Xpearance of pubic hair, normal growth velocity, and% V4 u! d6 `# g  s( K3 s" [
decreased erections. The father admitted using a testos-
& S- X$ b" P1 [* J5 N) ^- Sterone gel, which he concealed at first visit. He was
1 M5 ~: }! x* v  G+ }3 p0 |using it rather frequently, twice a day. The Physicians’5 g; s- E# I1 M1 |, ?$ E* t
Desk Reference, or package insert of this product, gel or
+ }+ F% n7 @( X+ fcream, cautions about dermal testosterone transfer to
& D9 _3 N( W$ ?7 m9 p* Vunprotected females through direct skin exposure.* N1 _: m# ?: R/ Q6 x
Serum testosterone level was found to be 2 times the
$ _, `' H0 L  N& I. ebaseline value in those females who were exposed to
& D/ s% }, `: K% f: r' Weven 15 minutes of direct skin contact with their male" W7 M* B; Q0 q1 [, ?! O+ L
partners.6 However, when a shirt covered the applica-3 X, P9 ]3 s; f; o
tion site, this testosterone transfer was prevented.' k+ m4 d. [2 U6 I6 \1 K
Our patient’s testosterone level was 60 ng/mL,& `" O$ U; e" [1 g  a% I+ o% h
which was clearly high. Some studies suggest that
+ N+ ]3 C% |4 Q: J2 F, I" Gdermal conversion of testosterone to dihydrotestos-
4 ]" h$ K2 B1 @terone, which is a more potent metabolite, is more9 V- T* I0 A: ]
active in young children exposed to testosterone
7 c: L" E, r0 S" Y9 C7 q- B$ kexogenously7; however, we did not measure a dihy-! Y" y( |+ p2 W2 b
drotestosterone level in our patient. In addition to7 a8 Q( a5 @4 W0 X9 U: V
virilization, exposure to exogenous testosterone in4 g, y/ E% q& y6 T5 A
children results in an increase in growth velocity and
; O) ~! n, C& q0 u- ]$ ]0 Dadvanced bone age, as seen in our patient.
/ _+ O- e0 L: E. Y' hThe long-term effect of androgen exposure during# m% e+ \0 @1 N3 }, y4 ^# A4 a
early childhood on pubertal development and final
  S) ?4 j' |$ ?1 P8 K* \9 _adult height are not fully known and always remain1 A( E, I* ?; d: l+ v5 d: F
a concern. Children treated with short-term testos-/ @3 q- w* A: a; H' g  U
terone injection or topical androgen may exhibit some
- n. T! H: ^) Z6 Zacceleration of the skeletal maturation; however, after
- r9 w7 p$ E1 ?" R3 P$ wcessation of treatment, the rate of bone maturation
5 I- J/ |; J& w, f) Ndecelerates and gradually returns to normal.8,9/ v7 p7 _+ u6 d, E$ b8 O
There are conflicting reports and controversy
7 c1 K" t+ q) m' M  r/ ]over the effect of early androgen exposure on adult
# T) O- J; i6 ]8 tpenile length.10,11 Some reports suggest subnormal( X. w5 J& e& H+ J2 w& m
adult penile length, apparently because of downreg-
2 _3 u. Z3 X# ?, Oulation of androgen receptor number.10,12 However,& {6 Q# }9 o8 F; y: Z  Z6 Q+ [
Sutherland et al13 did not find a correlation between
4 _" b3 U% l/ l3 n. ichildhood testosterone exposure and reduced adult% O* Q* S/ H5 ]( v) s
penile length in clinical studies.  I# h5 |8 k* ^- i2 h
Nonetheless, we do not believe our patient is7 @# f2 P8 @: G! f
going to experience any of the untoward effects from. w" T8 q( q2 i; g8 D* R
testosterone exposure as mentioned earlier because, v! t. p) {  X! A" p5 P( ]; Y
the exposure was not for a prolonged period of time.
  W8 i! l- [: p4 Q: S, N) B  HAlthough the bone age was advanced at the time of
) E1 C. {% [! Z7 C; ]+ gdiagnosis, the child had a normal growth velocity at8 b9 b! }5 o$ L; J
the follow-up visit. It is hoped that his final adult
3 S/ M7 g' c1 _' o" Theight will not be affected.2 G& A. l, @3 J5 b$ f% w
Although rarely reported, the widespread avail-+ @, u) U! ~- q4 i+ V- \
ability of androgen products in our society may
$ z' u, |+ R4 D7 v: E' cindeed cause more virilization in male or female, i# c9 F, ]; V9 d0 f
children than one would realize. Exposure to andro-
0 D9 M+ Q7 e- D: Z' d+ [6 ngen products must be considered and specific ques-
  R0 z( s3 y! U3 c3 p. @tioning about the use of a testosterone product or
) l# j6 U& ?8 X! o5 Tgel should be asked of the family members during% T2 h0 w% Q. a2 |2 S, L( k" R6 \
the evaluation of any children who present with vir-; x: a, f5 t: e+ z( _' b
ilization or peripheral precocious puberty. The diag-5 p, J) v2 B: |
nosis can be established by just a few tests and by  R& z- H+ B0 H
appropriate history. The inability to obtain such a$ @1 J4 s) K( F% A( ~( ~' H* j
history, or failure to ask the specific questions, may; B0 j; ~- d, a% p( Y% k, r! a3 z
result in extensive, unnecessary, and expensive
6 |' [; Q( u0 |  t" S; K7 n7 T$ ]7 O/ ~investigation. The primary care physician should be
) c: _$ j" C/ d% U1 ^1 K3 D6 Z" c# oaware of this fact, because most of these children# E0 V+ F8 r! t* O- g& ?
may initially present in their practice. The Physicians’
  `+ m# X. N; k% N7 h2 ^' @Desk Reference and package insert should also put a5 E. |8 x3 O# `7 |# r
warning about the virilizing effect on a male or
9 r! U! E6 e7 }# afemale child who might come in contact with some-! r; p$ W* |" A& }- K% `
one using any of these products.& l" }& H+ _$ Y( D, J
References
- S5 e2 U# e; s% b/ r& G8 G1. Styne DM. The testes: disorder of sexual differentiation* k& W2 r9 r( p+ C  x( R8 L
and puberty in the male. In: Sperling MA, ed. Pediatric: _" V2 L2 E! D7 l
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 v3 I, |0 q, S9 p( d2002: 565-628.2 B+ I+ u" _7 i; A1 a8 J  W
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& e' m2 b, o& A+ P3 b$ `1 Spuberty 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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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

- [/ l& Y% O0 a$ ]* J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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