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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
. d* {: B* [, x' J. k6 |0 L% x( ABoy Induced by Indirect Topical% s9 p- M1 r4 j# Q4 V8 \
Exposure to Testosterone
% N% D" P6 Z  d& nSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 j- n" F7 Z! G+ `  P
and Kenneth R. Rettig, MD1: w+ E  A8 ?! G- k0 R/ R. E
Clinical Pediatrics! s) `, t/ o: x2 M% V+ U- ?
Volume 46 Number 6) {# L. H! w8 s! F( G( W; l
July 2007 540-543
; p4 T4 Y5 v4 z4 g, n© 2007 Sage Publications
8 L9 [1 P3 S4 Z, w/ d* R" s' l% l5 x10.1177/0009922806296651
1 P, d& a! U  chttp://clp.sagepub.com
; @5 N  K4 G6 h1 C  r- s) Ohosted at
+ A  d- c3 Z6 H* X, Z' Qhttp://online.sagepub.com
9 G* s5 w% G; h+ M5 g& z& m$ @Precocious puberty in boys, central or peripheral,
* X+ Q1 \* a2 ]( a5 A8 uis a significant concern for physicians. Central+ B8 B% D/ C0 X* z* R( B
precocious puberty (CPP), which is mediated
7 W9 D& z& S; {0 C# z5 `through the hypothalamic pituitary gonadal axis, has
- C! s  ~' u+ w  E4 f8 ja higher incidence of organic central nervous system
1 Z4 c; Q% e; v; j$ ~/ ylesions in boys.1,2 Virilization in boys, as manifested4 \% o. `! l, i, b$ h5 n- ]
by enlargement of the penis, development of pubic! Q9 x9 W: m# ?4 X5 H
hair, and facial acne without enlargement of testi-
4 I! j* J+ O# ~. }% Bcles, suggests peripheral or pseudopuberty.1-3 We
0 s. d$ d1 K, _; M" H, T* Qreport a 16-month-old boy who presented with the, O4 ]- G& k7 S2 P- N4 ~7 u) q: R% z
enlargement of the phallus and pubic hair develop-
, V; {! i( Y% nment without testicular enlargement, which was due9 a4 d6 ~, q0 l
to the unintentional exposure to androgen gel used by! [: G& q4 P6 t4 ?$ n$ ~* R
the father. The family initially concealed this infor-
! I6 r4 j3 \8 q9 ymation, resulting in an extensive work-up for this+ a( }" Q) r) Q+ j% ~& n( N
child. Given the widespread and easy availability of5 t) K+ g( C; X* p6 P" G
testosterone gel and cream, we believe this is proba-' M: s, M0 o! m, A3 h
bly more common than the rare case report in the
1 p5 @& x) ^$ c. X& v  w, pliterature.4
6 q% T2 @5 L: G# qPatient Report$ Z2 U* ]7 ^! a* a
A 16-month-old white child was referred to the
8 ]. f+ @7 |6 c; X$ |endocrine clinic by his pediatrician with the concern6 G6 f7 D: Z) _* G
of early sexual development. His mother noticed
0 A3 ~* o, o0 [. K0 Slight colored pubic hair development when he was0 x4 z2 ~6 j# J2 ?
From the 1Division of Pediatric Endocrinology, 2University of
% G) h& l* G- K7 ~& s9 lSouth Alabama Medical Center, Mobile, Alabama.0 J1 r$ g& L/ M1 r9 w0 b9 i! }5 [
Address correspondence to: Samar K. Bhowmick, MD, FACE,
" u1 ]* [& T+ [% u4 v5 rProfessor of Pediatrics, University of South Alabama, College of
; c. v8 u& Q9 `% A. u6 aMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ g) ^3 [, ]& P& ke-mail: [email protected].7 w( E& r- Q7 ~
about 6 to 7 months old, which progressively became* s2 R/ k( P6 h( |) K9 ^
darker. She was also concerned about the enlarge-' @/ Y8 u: k0 U
ment of his penis and frequent erections. The child
6 y' F$ y3 y0 l+ Q; A' Cwas the product of a full-term normal delivery, with3 @$ v/ ?/ }9 c1 c: f# |! [+ ^
a birth weight of 7 lb 14 oz, and birth length of
0 B9 A% [( u2 w% e20 inches. He was breast-fed throughout the first year
, B7 G- s# Z8 p1 E2 ]* V" `1 }of life and was still receiving breast milk along with9 x9 l1 a, i2 U7 b! ^
solid food. He had no hospitalizations or surgery,4 J1 W( p* J" b3 n9 ]
and his psychosocial and psychomotor development
) Y, [/ Q& p( {2 Z: [- Lwas age appropriate.  c( @( i1 m  k# E
The family history was remarkable for the father,2 ?. ]; \4 R9 E
who was diagnosed with hypothyroidism at age 16,0 C; d6 _6 D" `1 y* F
which was treated with thyroxine. The father’s4 }8 B6 y( I& w0 i9 [$ j
height was 6 feet, and he went through a somewhat
% ?/ U* u; A" Z% I, C) h  L0 Bearly puberty and had stopped growing by age 14.( e) T" m% ~$ \: G3 z. z: H0 ~, {
The father denied taking any other medication. The
7 G6 l8 ^3 o& s  V; \( y; Nchild’s mother was in good health. Her menarche3 E. J4 P( c6 O
was at 11 years of age, and her height was at 5 feet, }' p: ^: H# n9 [* |: t$ }
5 inches. There was no other family history of pre-
! a% Z. \) [( a3 ]) dcocious sexual development in the first-degree rela-9 |8 V" \) D# Q  }0 G3 x4 u+ N
tives. There were no siblings.; t8 t. N- r9 l0 r/ F
Physical Examination" ?6 W6 O  t0 _
The physical examination revealed a very active,  {3 x' R+ W( W
playful, and healthy boy. The vital signs documented
) U4 f8 u7 D7 o0 v/ T, x% Ha blood pressure of 85/50 mm Hg, his length was
* [+ b$ ?; ~8 K90 cm (>97th percentile), and his weight was 14.4 kg$ x& Q. f0 C1 B
(also >97th percentile). The observed yearly growth( u1 V2 G; N, A4 U
velocity was 30 cm (12 inches). The examination of
' n. g, M+ G% c' n+ j3 B4 xthe neck revealed no thyroid enlargement.# L% n7 G& K. ]* Q. w9 P! n
The genitourinary examination was remarkable for
  ?+ x6 O5 W6 Benlargement of the penis, with a stretched length of
% N+ b% C  ^) @% U0 h8 cm and a width of 2 cm. The glans penis was very well, [) y# p6 E2 X* ]3 v, p8 v
developed. The pubic hair was Tanner II, mostly around  `9 a: c1 M2 ?  E3 O& D. J
540
8 P/ W& v% c1 e* wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: c/ ^+ `2 m4 W+ \4 bthe base of the phallus and was dark and curled. The
$ u  q- i0 ~! stesticular volume was prepubertal at 2 mL each.$ ~0 R2 R/ Y& P1 ^: e
The skin was moist and smooth and somewhat
3 h( j! C$ E: T' E- [7 _9 Foily. No axillary hair was noted. There were no
, C" P# n$ O$ h+ ^* Labnormal skin pigmentations or café-au-lait spots.: Z# j/ u+ k0 r3 X: g: [
Neurologic evaluation showed deep tendon reflex 2+
" j' t- o1 j/ }: wbilateral and symmetrical. There was no suggestion% e5 x! Q% I4 H0 ?! k( N
of papilledema.0 G& ~  s" Y( E# R/ m0 G
Laboratory Evaluation
' v7 [# y- G! d6 ZThe bone age was consistent with 28 months by
# }% l) F" F+ r8 ~" ?$ R/ z/ Xusing the standard of Greulich and Pyle at a chrono-( j* g, r- [- G8 ^4 V: X
logic age of 16 months (advanced).5 Chromosomal& L+ P$ N0 K/ ^; D9 l' D5 H
karyotype was 46XY. The thyroid function test
& K9 w8 S% _: Z5 g4 D9 ^; Kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
* f1 O: d. C: \8 j4 |lating hormone level was 1.3 µIU/mL (both normal).
; H% V/ N4 k/ J" eThe concentrations of serum electrolytes, blood
- i& G' [1 `8 E) s' K* \  [( Eurea nitrogen, creatinine, and calcium all were) t8 U3 G  o7 L0 f
within normal range for his age. The concentration" N3 @! U0 W- w  d
of serum 17-hydroxyprogesterone was 16 ng/dL6 n  p; i  R- L2 h9 B. m
(normal, 3 to 90 ng/dL), androstenedione was 20
/ s+ ~+ t8 t6 ^5 l  Bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) d4 w: y' y; M! c/ z6 T
terone was 38 ng/dL (normal, 50 to 760 ng/dL),4 }* b; h% b! N
desoxycorticosterone was 4.3 ng/dL (normal, 7 to* F5 e# O; X1 X8 ]  r
49ng/dL), 11-desoxycortisol (specific compound S)$ B9 \+ D; m% A$ N, j( [6 }6 `" n
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 ]# t0 K! D' A, b- e
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 }5 |4 L2 W/ ttestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  ?. e0 l6 L) P& `, ^and β-human chorionic gonadotropin was less than9 r1 s! a3 G. `) X
5 mIU/mL (normal <5 mIU/mL). Serum follicular- e9 ]4 Z! G' n6 p) d% I
stimulating hormone and leuteinizing hormone
' J5 D- J9 j' Pconcentrations were less than 0.05 mIU/mL: Q: w  X$ i! [+ r
(prepubertal).$ [2 _+ b  E- x" L6 R/ t
The parents were notified about the laboratory
/ D$ |5 b, J) N$ h$ R2 Tresults and were informed that all of the tests were8 e5 ?6 \' E& x& b; t4 c
normal except the testosterone level was high. The- p5 q8 S% H1 I/ o* f
follow-up visit was arranged within a few weeks to
6 s) @. D9 \: @7 Z$ T# ]obtain testicular and abdominal sonograms; how-
! z0 q4 _; n7 j/ V7 {1 i- B4 Xever, the family did not return for 4 months.
( n2 H; G. [0 v6 g) jPhysical examination at this time revealed that the
$ z7 @2 i  o1 d" u2 V* p$ Uchild had grown 2.5 cm in 4 months and had gained' W& A9 G- B  d# L9 i2 N# d* @
2 kg of weight. Physical examination remained- q# ]$ ?$ [% p4 D. t# W3 t
unchanged. Surprisingly, the pubic hair almost com-
; k, Z( {, k4 V: O, q5 Bpletely disappeared except for a few vellous hairs at" @! S9 ]) M% V9 l/ D) _" K2 u
the base of the phallus. Testicular volume was still 2
  Q0 f3 c% q* [% t$ AmL, and the size of the penis remained unchanged.; A8 x! I, D  }3 ]$ A0 n1 E8 L: g
The mother also said that the boy was no longer hav-3 q$ p& V+ |3 ]0 O) Z" ?# ?
ing frequent erections.
4 z6 `0 H, o; S4 Y3 VBoth parents were again questioned about use of
$ N) R) A; L  w( |( l% h0 lany ointment/creams that they may have applied to. E# \$ [( e5 I* a$ y
the child’s skin. This time the father admitted the
$ k% L' @  W7 `" ]* s6 q( ITopical Testosterone Exposure / Bhowmick et al 541
4 h$ u% b( |' I/ }! c3 x2 K5 Xuse of testosterone gel twice daily that he was apply-( s; E+ ~  z5 j* Z
ing over his own shoulders, chest, and back area for. b6 c9 D6 m1 H" ~+ K( w
a year. The father also revealed he was embarrassed6 ~1 I8 B/ R/ Z" R4 F) C# j0 _
to disclose that he was using a testosterone gel pre-
2 a4 ]) H3 l/ X4 Z( ?% Qscribed by his family physician for decreased libido
( ?! e9 I% T, p: @, f8 J# Bsecondary to depression.
5 {: P1 Y3 D, s' U8 BThe child slept in the same bed with parents.
2 v9 R% |2 w% W* J5 {The father would hug the baby and hold him on his
1 T0 o' ]+ P9 b0 N( B+ O  fchest for a considerable period of time, causing sig-. e! Q7 h$ y/ T8 E2 k: e. f
nificant bare skin contact between baby and father.% L# |$ B7 c' K( i) K# |
The father also admitted that after the phone call,
5 X1 b, H& u# h9 _! Dwhen he learned the testosterone level in the baby2 {+ s# E; k. Z# ~: D, B+ |4 l
was high, he then read the product information
5 d9 M6 }$ U  p4 T3 Npacket and concluded that it was most likely the rea-
$ A7 O: X4 ]% ~/ K0 c6 c, Y! Qson for the child’s virilization. At that time, they9 z* y. c5 }  e+ S/ |) [
decided to put the baby in a separate bed, and the
' [/ I2 A" g: r% y- ^( J  B: Z& Yfather was not hugging him with bare skin and had8 b: T) j# u3 [, ]  r4 t
been using protective clothing. A repeat testosterone
2 ^, \! s0 O, C7 O6 n! `9 Ltest was ordered, but the family did not go to the9 }1 v* i% l) F& H5 a5 x4 }
laboratory to obtain the test.1 M+ l: l# a9 H5 W' X6 P, O
Discussion9 l( n$ F' @# J  y$ u
Precocious puberty in boys is defined as secondary
# E7 W/ X3 h: {; q8 q% Dsexual development before 9 years of age.1,4
' W% Q  U# f" GPrecocious puberty is termed as central (true) when4 F- H+ B8 h% `6 H, c, y8 e
it is caused by the premature activation of hypo-5 U9 B/ p/ ^4 r) k' c" a; H
thalamic pituitary gonadal axis. CPP is more com-
3 f, ]6 q* O! m2 v- c# imon in girls than in boys.1,3 Most boys with CPP4 c5 |2 Y9 D7 s. u1 T. H
may have a central nervous system lesion that is3 i& @2 [+ O$ a& K7 b# Y
responsible for the early activation of the hypothal-
, N1 l0 f0 J2 \8 P$ Namic pituitary gonadal axis.1-3 Thus, greater empha-
" ]% \& ]. C/ _0 a$ Y# n0 k8 Qsis has been given to neuroradiologic imaging in1 p) ]3 w: T% M' f8 @- R$ C2 m
boys with precocious puberty. In addition to viril-
5 P; }, [: h7 T) N! Jization, the clinical hallmark of CPP is the symmet-
! Z9 }4 o* Y& n. o0 erical testicular growth secondary to stimulation by
% `+ @$ P2 U( |gonadotropins.1,33 ?+ |4 J4 Z( z0 b1 D
Gonadotropin-independent peripheral preco-) N" f( W& Y: I4 t% I8 Z
cious puberty in boys also results from inappropriate
) E* I$ ]# Y5 A% U# Nandrogenic stimulation from either endogenous or
  ]& a! ?$ Q9 h+ ], Y& O& hexogenous sources, nonpituitary gonadotropin stim-
# p/ O& C  V# i  T2 m9 D' dulation, and rare activating mutations.3 Virilizing
. W* m7 N+ W+ [+ g& p4 }congenital adrenal hyperplasia producing excessive
% q! _5 X% E: j. h) Q% Fadrenal androgens is a common cause of precocious4 x& _% {, n3 {6 l
puberty in boys.3,40 q- e6 ]: u! i' M
The most common form of congenital adrenal
5 o+ K  O5 s2 g9 [, ]! u/ r9 i. H0 thyperplasia is the 21-hydroxylase enzyme deficiency.
6 N. N. J! M9 k$ wThe 11-β hydroxylase deficiency may also result in
- \2 A0 U$ v) B/ P) f% z  aexcessive adrenal androgen production, and rarely,
7 H* M( H2 L5 R: nan adrenal tumor may also cause adrenal androgen8 G4 I8 E8 Y$ q3 A
excess.1,3
8 M" Q, A$ D4 J! [; rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( Z9 Y! L2 l4 l1 _" R542 Clinical Pediatrics / Vol. 46, No. 6, July 20073 r/ J" `) @+ I: V1 Q" f8 B0 h1 s
A unique entity of male-limited gonadotropin-
  x8 o5 T- i* D& \# v4 `independent precocious puberty, which is also known) @- }$ A+ D" Q1 ^3 ~" Z* ]
as testotoxicosis, may cause precocious puberty at a" v/ o( ]) ]$ B
very young age. The physical findings in these boys
) P& Y- G+ C# M4 K+ pwith this disorder are full pubertal development,! n( \& H+ F6 |
including bilateral testicular growth, similar to boys
7 Q  r, w$ D# p" jwith CPP. The gonadotropin levels in this disorder
  _) T; X, y5 B( A# b7 W% k3 aare suppressed to prepubertal levels and do not show
7 B- W& J; f6 J* j, Y  bpubertal response of gonadotropin after gonadotropin-
5 S6 `$ P1 O0 [5 B- L( sreleasing hormone stimulation. This is a sex-linked) e" l  Q+ M! d- \
autosomal dominant disorder that affects only: ]1 U  k: R0 }6 l
males; therefore, other male members of the family5 d& q! {2 @" w% |
may have similar precocious puberty.3
* c/ W0 F" j4 Q4 }. d( V0 @8 ?In our patient, physical examination was incon-
; g: z9 K' h2 F; r# x# fsistent with true precocious puberty since his testi-9 \0 ~0 f  X7 u
cles were prepubertal in size. However, testotoxicosis
! `+ z  @6 p& Y8 W' {was in the differential diagnosis because his father% A. r1 A% r) G) `3 r6 N
started puberty somewhat early, and occasionally,  s8 I7 c" T# C2 x
testicular enlargement is not that evident in the
6 I' d( ?7 N( ?9 g" S2 [% }beginning of this process.1 In the absence of a neg-/ `. v* w+ I5 I& t
ative initial history of androgen exposure, our
% E5 ~- v7 v& tbiggest concern was virilizing adrenal hyperplasia,3 V- q6 P0 T& `2 I' O
either 21-hydroxylase deficiency or 11-β hydroxylase5 @0 O. Y4 P* M! I
deficiency. Those diagnoses were excluded by find-
$ V6 _5 }5 l0 t' z2 [ing the normal level of adrenal steroids.& P* B3 V4 j  ^2 F
The diagnosis of exogenous androgens was strongly
0 k: O% q: i8 j0 P* Rsuspected in a follow-up visit after 4 months because! k) [. Q8 ^! M. R5 l  f. d/ G! X
the physical examination revealed the complete disap-# C, K* C* d5 I' D
pearance of pubic hair, normal growth velocity, and1 ~+ B6 q3 T' T' q2 a) @5 y! B. N
decreased erections. The father admitted using a testos-4 H. j( Y( K' y
terone gel, which he concealed at first visit. He was& S3 q8 S7 a6 v  }: v) f4 d4 |1 U
using it rather frequently, twice a day. The Physicians’
/ Z3 W7 J, M* H5 i4 r5 _% `Desk Reference, or package insert of this product, gel or9 J3 b. w8 U# R0 A
cream, cautions about dermal testosterone transfer to2 W" l! C8 j% }- ~% @2 l; f2 K
unprotected females through direct skin exposure.
0 e% C+ B: ?/ D, h7 ySerum testosterone level was found to be 2 times the& D# L, [- A+ M( p3 L
baseline value in those females who were exposed to  Y4 r  h' o0 g9 w$ z/ S& z
even 15 minutes of direct skin contact with their male
8 A  g6 T5 Y" x( ~: i" o, vpartners.6 However, when a shirt covered the applica-
6 I  K/ @1 @% htion site, this testosterone transfer was prevented.& V& V3 U) V* F/ F& ?* b0 v3 N% }
Our patient’s testosterone level was 60 ng/mL,4 `; r5 d4 u% A# T
which was clearly high. Some studies suggest that% d- m, z0 A5 N: F+ Q
dermal conversion of testosterone to dihydrotestos-2 J# F2 p4 q& z4 L" _, T
terone, which is a more potent metabolite, is more
# ^' J6 b/ p. Q  u$ D- e! N- E$ `; Lactive in young children exposed to testosterone  k/ y' e' M2 l! G1 w! z: ~9 B
exogenously7; however, we did not measure a dihy-3 Q  v) n& X9 ^0 U7 e* h0 M
drotestosterone level in our patient. In addition to, r- d) z  {0 I- [2 s( e
virilization, exposure to exogenous testosterone in
- o) p9 [4 H  qchildren results in an increase in growth velocity and
. S% F' W( ^" p  Y2 ^advanced bone age, as seen in our patient.8 }# c. P3 \3 O# G) E. |
The long-term effect of androgen exposure during
9 j4 W; a" I9 f2 B1 Eearly childhood on pubertal development and final
9 ]; w1 s. ~/ f0 O4 P" C1 K5 H! Sadult height are not fully known and always remain0 b  Z6 p/ }6 m, _# `3 u
a concern. Children treated with short-term testos-. J, Q8 A; L* |" z
terone injection or topical androgen may exhibit some
, g  o) |: F; hacceleration of the skeletal maturation; however, after1 ~6 Q$ E0 w. `& ^" g: U
cessation of treatment, the rate of bone maturation3 P- E+ P8 K8 w) f  S7 j
decelerates and gradually returns to normal.8,9
( a' p) T2 e% u8 n5 [- i- wThere are conflicting reports and controversy$ [8 Q8 \& x; g# \9 W
over the effect of early androgen exposure on adult, @3 J8 D- E! u1 u8 W* Z  [6 `
penile length.10,11 Some reports suggest subnormal
' t; D: O. }5 q; ]adult penile length, apparently because of downreg-+ c& W- r6 z" n7 q; J
ulation of androgen receptor number.10,12 However,
4 n# r, k7 A9 @/ h& p3 C) [Sutherland et al13 did not find a correlation between+ b; G3 Y6 k) v& T- Y4 H
childhood testosterone exposure and reduced adult, b0 Q- k- L1 {1 K7 W3 K$ m, e
penile length in clinical studies.
- d1 d" `! j, q+ b8 o0 E$ |Nonetheless, we do not believe our patient is) u% ]' b% T* s. F. F
going to experience any of the untoward effects from
' b% V: H( B& C0 O* L& _testosterone exposure as mentioned earlier because4 C; J) N$ x5 S; U9 o2 t/ W
the exposure was not for a prolonged period of time.6 P+ W* o3 C6 y4 e
Although the bone age was advanced at the time of
! }+ |# M. t5 r5 l2 L+ P# U2 A/ Ddiagnosis, the child had a normal growth velocity at
/ K7 V- i) A2 g& {" athe follow-up visit. It is hoped that his final adult$ i0 F9 @2 F/ c
height will not be affected.& x0 `7 f& J* e+ X4 s1 u
Although rarely reported, the widespread avail-/ p. {* g6 I, u+ H5 G4 `
ability of androgen products in our society may: G8 R+ e/ }* ]$ o& h
indeed cause more virilization in male or female
% ?  G1 i- c+ V" Y$ Bchildren than one would realize. Exposure to andro-
# {! E1 C8 Q' I8 T  Kgen products must be considered and specific ques-, j  A* _3 g* t6 ]6 c
tioning about the use of a testosterone product or
4 G  O$ S4 l/ w. \) C5 Egel should be asked of the family members during
6 R2 W2 m2 _+ |5 F4 |! K5 E3 Vthe evaluation of any children who present with vir-
" g! f. p6 t- m9 j$ P2 oilization or peripheral precocious puberty. The diag-
7 e- w( ~. ^! j3 g5 @nosis can be established by just a few tests and by% a0 D; K& N1 ~  c$ e
appropriate history. The inability to obtain such a2 j7 g; t$ a  [
history, or failure to ask the specific questions, may2 Y/ z4 Y, P, w6 Z
result in extensive, unnecessary, and expensive
& u6 T* Q8 ?3 L7 l' N# Yinvestigation. The primary care physician should be
5 m; X& O3 c3 V% eaware of this fact, because most of these children3 v* R% _- n% Q- @
may initially present in their practice. The Physicians’
! e; U  t9 Z$ ?) \& {! iDesk Reference and package insert should also put a( s3 I# n9 [5 @0 ~8 ]
warning about the virilizing effect on a male or6 L1 R' @% O  A* z2 F' j
female child who might come in contact with some-
4 q' `3 Y( k) a$ {3 I" _" \one using any of these products.' C. \" U$ C+ E& i2 |5 h8 j  L
References
/ o/ a' z% i. {) j4 s' T* D. b1 Y1. Styne DM. The testes: disorder of sexual differentiation' M3 h( F) \; A# E
and puberty in the male. In: Sperling MA, ed. Pediatric5 z8 m7 u4 C0 {
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' _& T: X2 Z7 a1 c9 ^) l2002: 565-628.
$ \0 }  L1 ^) ?8 K, e$ s" p9 L4 P2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' I) r1 `6 Z& M* V' ~puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old/ r+ c" S8 G+ x/ u6 x
Boy Induced by Indirect Topical
4 j# K  y8 f! ~2 u, |" u9 ?Exposure to Testosterone) m( R; V* J7 J, k
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. j  b9 y# r9 A2 I0 hand Kenneth R. Rettig, MD1& t5 t( m( n8 b2 ^) C; s- o5 a
Clinical Pediatrics
5 {+ _# P; }9 o, D* f: sVolume 46 Number 6& c9 C( E# A/ R* W. V# a
July 2007 540-5433 H, M/ c% d! r7 h& ^
© 2007 Sage Publications
: v7 a# i! t: B' T1 F& \% d10.1177/00099228062966511 k& {  e/ j: G/ C6 Q
http://clp.sagepub.com
+ w1 I- v7 Z9 V6 f/ E5 ]hosted at
$ Q3 @) |# B" j! h% k# chttp://online.sagepub.com! n% H* s5 d) r; I: |2 |, ~; o8 W
Precocious puberty in boys, central or peripheral,
  c: M. h( G6 j; Y- His a significant concern for physicians. Central: q  u; ^. i8 u3 A: p7 l
precocious puberty (CPP), which is mediated' y) B5 T$ r' _6 ]( _. T& n
through the hypothalamic pituitary gonadal axis, has
1 f+ E& P2 ^' J7 ?6 la higher incidence of organic central nervous system# z# R1 n6 R. w/ ~; X4 F; k: Y, y, i
lesions in boys.1,2 Virilization in boys, as manifested
' h) E) y7 v& x6 x. @by enlargement of the penis, development of pubic
0 y& Y) o* Q5 l+ j1 hhair, and facial acne without enlargement of testi-+ d; X+ ?" G( \" S: G/ b. U
cles, suggests peripheral or pseudopuberty.1-3 We0 |/ g: o4 ]- E( h5 H& M5 \
report a 16-month-old boy who presented with the: K2 k  C; l. H$ b: {' d
enlargement of the phallus and pubic hair develop-& Y4 p2 U6 v* z/ a
ment without testicular enlargement, which was due, z& ?# K8 f/ T0 u9 \- {
to the unintentional exposure to androgen gel used by
1 s! b! C# t3 u' F5 |the father. The family initially concealed this infor-
7 @- v8 D8 ], X9 n( w0 I2 n# Y  jmation, resulting in an extensive work-up for this
; U% I, z% B  i! Z# c* achild. Given the widespread and easy availability of
3 S& X  [7 Q  @, L8 w' s/ T0 t5 Qtestosterone gel and cream, we believe this is proba-8 C) p3 l0 \7 B5 p
bly more common than the rare case report in the  f+ T7 j: i7 j6 ?+ i, m
literature.4, E- h: E: [2 v6 u; J) l
Patient Report! ?+ l- C  N& B; ~8 Z6 N
A 16-month-old white child was referred to the8 o+ I# a  n  k6 ^& H, z3 t
endocrine clinic by his pediatrician with the concern
$ E, q" s! i" s& O! X! T' Wof early sexual development. His mother noticed
. l6 A" S) Q! I4 {light colored pubic hair development when he was7 ]( n# n8 j4 J- g4 @: V$ ~1 G" p1 [
From the 1Division of Pediatric Endocrinology, 2University of2 ^7 Y: X$ [" Y9 U
South Alabama Medical Center, Mobile, Alabama.8 ?% Z; G1 |9 ?3 E$ S# s: y
Address correspondence to: Samar K. Bhowmick, MD, FACE,+ u: U3 F7 _' F+ G
Professor of Pediatrics, University of South Alabama, College of
/ w/ i: q! |5 @: O4 Z! ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 M$ p3 i3 l- f3 qe-mail: [email protected].
: d# Y$ `/ d0 _+ o, k: J1 Z4 gabout 6 to 7 months old, which progressively became+ a4 ~7 Y: [3 m6 Z0 {5 j
darker. She was also concerned about the enlarge-
2 [. T4 v5 u  `; N& ?, _+ f$ ~& xment of his penis and frequent erections. The child6 I& c2 I) r. m  [* x4 G
was the product of a full-term normal delivery, with, j! K7 D5 n5 _4 q5 H0 F+ a0 @
a birth weight of 7 lb 14 oz, and birth length of
7 X8 ?! ]$ T+ P) C20 inches. He was breast-fed throughout the first year
% ]# d, j3 g  [9 W5 w" c% h# gof life and was still receiving breast milk along with+ V; ^! z/ M% s2 b7 t
solid food. He had no hospitalizations or surgery,9 q: c0 @( u  f& p' @) p5 k
and his psychosocial and psychomotor development
# B# M  f, K9 l0 X4 U8 awas age appropriate.
  e, E9 X% h* G/ F: X$ \The family history was remarkable for the father,5 ~, S- d" X# c0 G: w
who was diagnosed with hypothyroidism at age 16,
, M1 k3 X  V3 u; Cwhich was treated with thyroxine. The father’s2 j* O- J1 a# o( _1 H4 P
height was 6 feet, and he went through a somewhat
: ^. Z) Y# `6 Searly puberty and had stopped growing by age 14.
* |& s0 c5 h  ^& M( SThe father denied taking any other medication. The0 T0 F, [! ?0 A  U$ B+ }8 R6 m
child’s mother was in good health. Her menarche
; W; X: A' q* @4 {0 pwas at 11 years of age, and her height was at 5 feet
; W; ~0 u8 D& I1 s+ U, k; ~0 ]0 x5 inches. There was no other family history of pre-
) o$ q7 S8 s$ G+ U: Ecocious sexual development in the first-degree rela-- Y  G1 x' s' D) ^
tives. There were no siblings.
! G4 r1 N: R" V- w7 E7 ZPhysical Examination6 p% V  O/ F9 L0 Y  |3 V6 s$ `
The physical examination revealed a very active,
  O- S2 p$ _7 O! ^/ Vplayful, and healthy boy. The vital signs documented
4 A- ?% z7 P# R1 f% m9 Ga blood pressure of 85/50 mm Hg, his length was
* O) }: z  @9 P) f; G( N7 Y90 cm (>97th percentile), and his weight was 14.4 kg( f9 ^* x; |# y" ?/ C- X! l
(also >97th percentile). The observed yearly growth
% g& I, K$ S! i  [: E3 j! svelocity was 30 cm (12 inches). The examination of
4 t6 Z# Q6 W  Q2 O- \5 _the neck revealed no thyroid enlargement.% L% Z# n7 A: n2 `& r$ f& Q# n
The genitourinary examination was remarkable for$ W6 b. @6 K) u. M% A- S9 M) I
enlargement of the penis, with a stretched length of
  r  `! y' w8 {  ?% u( ~' z8 cm and a width of 2 cm. The glans penis was very well
  F0 g& @  B% I) i# j( F$ R. Odeveloped. The pubic hair was Tanner II, mostly around3 [+ ]# Z+ K. s" T# K  {8 T6 O
540: W6 N* r% V1 ]% F! P2 F
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: T3 C  m7 @0 [* j+ q
the base of the phallus and was dark and curled. The
7 k4 @  S2 B) R) W1 v( s5 h" Htesticular volume was prepubertal at 2 mL each.
; h$ q7 \$ s" Q  h5 i3 F5 JThe skin was moist and smooth and somewhat
: ^$ S# t$ A1 C3 u* Foily. No axillary hair was noted. There were no
; U- J, O+ O4 f# S# m5 Q, l5 pabnormal skin pigmentations or café-au-lait spots.: ^0 x" p2 m% _/ ^
Neurologic evaluation showed deep tendon reflex 2+/ a1 h# y& A6 _. F* {5 O' K. _" K
bilateral and symmetrical. There was no suggestion
+ ?8 W# J& Z/ z$ y6 @' {of papilledema.( D! A* r4 g! }" P
Laboratory Evaluation
0 n/ i( \* _! r7 ~0 t, t& BThe bone age was consistent with 28 months by
# L& v6 O5 ?/ O  ?- |using the standard of Greulich and Pyle at a chrono-
- H& o' w+ Y/ @0 ilogic age of 16 months (advanced).5 Chromosomal
% F5 O5 v1 T5 e% Q! m& j9 Ikaryotype was 46XY. The thyroid function test
2 s8 {# r* \, P/ P2 mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-" _; P8 i) D& o
lating hormone level was 1.3 µIU/mL (both normal).
, K0 q6 [$ K& X# d% SThe concentrations of serum electrolytes, blood
. e  A# I* Q: O1 J7 hurea nitrogen, creatinine, and calcium all were
& U4 l9 s+ k; g4 Awithin normal range for his age. The concentration5 d4 s# P. r% [3 {
of serum 17-hydroxyprogesterone was 16 ng/dL1 Y' D8 t+ H1 E; e
(normal, 3 to 90 ng/dL), androstenedione was 20
# E9 p" Z! }% y2 Vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, q* d0 ]3 Y9 P3 @terone was 38 ng/dL (normal, 50 to 760 ng/dL),
, j, _% z& y7 I; E3 jdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
' V  c) C( O! l. L/ G/ U# U49ng/dL), 11-desoxycortisol (specific compound S): ^) W; J) x6 a6 R
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% Y. G1 u" D0 y$ M( B" i2 V( r7 S
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total3 U* d( z, T8 P1 y# d8 P- G
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 i! g1 x& g5 {& i
and β-human chorionic gonadotropin was less than; E" `6 N7 J% o( K3 L& S: X! f
5 mIU/mL (normal <5 mIU/mL). Serum follicular2 P( K  ^5 s5 n6 C
stimulating hormone and leuteinizing hormone
( |' I' N" O* P- C4 C/ ?concentrations were less than 0.05 mIU/mL0 p  Y/ H  E1 f2 O8 E
(prepubertal).
3 b- x4 w$ p2 l( b; {) i7 q" g  vThe parents were notified about the laboratory- H# M5 S0 X' ^: u; H" l
results and were informed that all of the tests were
5 \/ e  [; N' [# f$ C4 b4 Tnormal except the testosterone level was high. The) r. n* Q" \9 t) Y
follow-up visit was arranged within a few weeks to
0 L4 _. ]! P8 Y" b# L$ Mobtain testicular and abdominal sonograms; how-
3 _. p1 o: u) y4 ]  ~ever, the family did not return for 4 months.5 k) s5 d1 z+ N0 x* q
Physical examination at this time revealed that the1 h( \. l, j; R( T
child had grown 2.5 cm in 4 months and had gained
9 L1 [* s7 R$ \' _8 a2 kg of weight. Physical examination remained
) b4 t6 t1 c7 H- S, ~  ^2 |: B9 F3 nunchanged. Surprisingly, the pubic hair almost com-5 ^0 B$ B6 w! e8 {( }
pletely disappeared except for a few vellous hairs at
1 Z9 v! a4 f9 R# O7 q- B, pthe base of the phallus. Testicular volume was still 2% A7 [% `; [$ }( j% \# v5 O
mL, and the size of the penis remained unchanged./ _- }8 l9 s3 z0 c' b3 G4 Y1 ]) i
The mother also said that the boy was no longer hav-1 l' W/ y/ h# p8 ]- A
ing frequent erections.
: H+ _9 P8 z  E: YBoth parents were again questioned about use of
+ h% g* o& ?5 |# `any ointment/creams that they may have applied to
, X% G  |" q+ I6 i' r! N4 E7 bthe child’s skin. This time the father admitted the
* F/ s' @  l$ NTopical Testosterone Exposure / Bhowmick et al 541
* Z! S$ c1 z3 x) W3 z6 d+ Uuse of testosterone gel twice daily that he was apply-
/ V- X0 Y1 L" N; Bing over his own shoulders, chest, and back area for
, h- A9 Z3 p+ n; l+ Wa year. The father also revealed he was embarrassed' O9 }5 T. }; n2 X+ \% W
to disclose that he was using a testosterone gel pre-/ p# ?" M) A) {
scribed by his family physician for decreased libido
' G3 @, p3 Z  P7 z, Y" C* K* ssecondary to depression.
1 E# D$ c8 t; o- N. C. AThe child slept in the same bed with parents.2 O3 D! N3 o  V$ r( B
The father would hug the baby and hold him on his) `0 @( ?# w- h! Z3 N& G0 Y
chest for a considerable period of time, causing sig-4 Z& y! v8 W  w: r
nificant bare skin contact between baby and father./ d: Y- K$ ?0 [& c
The father also admitted that after the phone call,
+ \0 b8 U" C% lwhen he learned the testosterone level in the baby+ Q6 c- L' f/ I
was high, he then read the product information
, p% b" d0 E3 B! \) I5 upacket and concluded that it was most likely the rea-- o6 M0 \2 w5 `, X8 l
son for the child’s virilization. At that time, they
2 i6 U; _% S1 T6 `* ndecided to put the baby in a separate bed, and the
# R5 t3 o; A5 r* mfather was not hugging him with bare skin and had: w- w8 ]1 N* [) e0 Y( f
been using protective clothing. A repeat testosterone
; F0 r1 P) r$ |$ N+ d# Dtest was ordered, but the family did not go to the
$ o! y/ s, N; n5 slaboratory to obtain the test.
; a* E$ P, i% w( v* E& k! r4 MDiscussion
3 S  i/ k1 b7 g$ \; O5 jPrecocious puberty in boys is defined as secondary
! D% \/ ?* n6 p" T3 H* ^# Esexual development before 9 years of age.1,4
! a0 n! h; {! M4 Q6 F4 q& [( S1 w: d& TPrecocious puberty is termed as central (true) when
! D; k: B0 T& L  o. t, \it is caused by the premature activation of hypo-
8 K9 ]+ x! s! |0 w6 I9 w+ Bthalamic pituitary gonadal axis. CPP is more com-
, [, O2 l6 F- T% Z6 @. Qmon in girls than in boys.1,3 Most boys with CPP. R6 R8 @( d; J: {
may have a central nervous system lesion that is7 {# j( n/ r( [+ x: @$ `: w
responsible for the early activation of the hypothal-
' J9 H8 a0 ]4 }# s- h. o& _& o% m4 B' Jamic pituitary gonadal axis.1-3 Thus, greater empha-$ l% x) Y8 e, V: v9 l
sis has been given to neuroradiologic imaging in
4 {; G5 d4 f4 u0 Fboys with precocious puberty. In addition to viril-
$ p: b& f; P$ P2 V5 R; o/ Pization, the clinical hallmark of CPP is the symmet-
/ l# W; V3 l: ~* @4 {8 Rrical testicular growth secondary to stimulation by) @; K( c  [% [2 A
gonadotropins.1,3
( m9 w$ a: L9 d, b0 l  xGonadotropin-independent peripheral preco-" R: K1 Y/ ?0 [& O/ V
cious puberty in boys also results from inappropriate
% ^7 s. v" H8 w! landrogenic stimulation from either endogenous or
" N6 E: B* t: ?& D, ^exogenous sources, nonpituitary gonadotropin stim-
1 A$ \8 n7 h7 S7 j& \1 Wulation, and rare activating mutations.3 Virilizing0 x8 Q6 ?" p: ?: b) ^$ P
congenital adrenal hyperplasia producing excessive; ?6 `6 p) |7 S* u
adrenal androgens is a common cause of precocious
+ x6 a# \1 ]& k" I3 m  R. ppuberty in boys.3,4
3 u. U2 a1 ?# U. _The most common form of congenital adrenal
( U& e8 H6 V2 X. P3 G* g  xhyperplasia is the 21-hydroxylase enzyme deficiency.
; L$ v* e  `* H# f; vThe 11-β hydroxylase deficiency may also result in
/ e9 ]5 T! i" H: N& qexcessive adrenal androgen production, and rarely,0 I) Z6 L- A$ P! i4 R8 c8 @
an adrenal tumor may also cause adrenal androgen
  h2 F- w+ \' R7 ?( a2 Yexcess.1,3& @  |, j* M8 z9 N0 k& \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: O8 R) v! X, A, b* H0 S  }7 F; g542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. s5 t! i1 _* q9 e3 u1 fA unique entity of male-limited gonadotropin-" H! p+ j- z/ C
independent precocious puberty, which is also known& Z, K/ V3 `9 f0 J- S
as testotoxicosis, may cause precocious puberty at a! l& r! m. p' Y+ a9 h
very young age. The physical findings in these boys
" X/ g" k6 h# X# H$ H9 R9 |, lwith this disorder are full pubertal development,
) k8 ?) ~+ _4 a$ E( B5 c- B' Eincluding bilateral testicular growth, similar to boys3 Q4 ]0 s" ?2 T
with CPP. The gonadotropin levels in this disorder
8 N& G0 w- L2 U$ Yare suppressed to prepubertal levels and do not show) x7 _- S- ~7 b7 U" M( `' u+ i( |
pubertal response of gonadotropin after gonadotropin-# `. ~' R$ y  f; d
releasing hormone stimulation. This is a sex-linked0 {# O; z2 h# c4 v4 p
autosomal dominant disorder that affects only
1 y, o) m+ x1 R  \males; therefore, other male members of the family3 r; O" Y8 d+ R3 a; _
may have similar precocious puberty.3
+ T- h9 U+ ^9 N3 CIn our patient, physical examination was incon-. L3 c) O. p' S. S# D
sistent with true precocious puberty since his testi-  E1 Q: q* v9 @2 P* q& Z1 f
cles were prepubertal in size. However, testotoxicosis
4 b) W6 z; A2 pwas in the differential diagnosis because his father
+ g& S* W# y+ U4 R: s4 [+ Estarted puberty somewhat early, and occasionally,
, \4 ?( e: N1 a) Q4 h, ]testicular enlargement is not that evident in the5 M; X; \! g7 b" g6 u
beginning of this process.1 In the absence of a neg-
1 N# D  @2 [0 O8 B; c* Hative initial history of androgen exposure, our
7 D/ X8 j" A) P0 n" y; f- zbiggest concern was virilizing adrenal hyperplasia,
+ `, w1 O# b: Keither 21-hydroxylase deficiency or 11-β hydroxylase6 r# s2 {+ ]) K& a" b( @
deficiency. Those diagnoses were excluded by find-% z5 ^' s7 k9 ~5 u3 p7 X/ U
ing the normal level of adrenal steroids.
5 d, S( N% I  {2 c% H6 bThe diagnosis of exogenous androgens was strongly2 N1 M9 c0 X- ]/ R7 z
suspected in a follow-up visit after 4 months because8 [. }) W2 ^+ s9 o
the physical examination revealed the complete disap-
- q) C4 `7 F, f4 y7 Wpearance of pubic hair, normal growth velocity, and( N% g8 g- t1 q7 R' P9 x3 |7 k
decreased erections. The father admitted using a testos-8 ~- s& p/ ?; N, `
terone gel, which he concealed at first visit. He was
& M) t1 i/ z" [8 l) I# t2 Vusing it rather frequently, twice a day. The Physicians’( ?, C& e7 }6 n9 x
Desk Reference, or package insert of this product, gel or5 K1 R' w& _9 b/ b! Y: E
cream, cautions about dermal testosterone transfer to
: R" G# [! _2 n/ x5 z1 T. [unprotected females through direct skin exposure.' R3 B) N1 v' s. j, ?0 T- D
Serum testosterone level was found to be 2 times the
* L, e; u) G: \# a1 ]. Mbaseline value in those females who were exposed to7 H8 i- r- U% M8 ~3 c
even 15 minutes of direct skin contact with their male
- v1 L# V& e* Tpartners.6 However, when a shirt covered the applica-3 _" i- i, M7 d0 e
tion site, this testosterone transfer was prevented.
$ U) ^4 Z; X1 o' o% Y% _+ b  e5 NOur patient’s testosterone level was 60 ng/mL,( ?8 J8 M4 ?3 I7 W' J) J
which was clearly high. Some studies suggest that; i# o8 L) P9 o; w5 \! c. w
dermal conversion of testosterone to dihydrotestos-6 J% W$ k( J/ F2 B5 |6 z% P( p+ u
terone, which is a more potent metabolite, is more# E% {9 L7 U( J: g) b8 c: l
active in young children exposed to testosterone9 a8 _# N, H7 [$ v1 G* V2 e7 y$ q
exogenously7; however, we did not measure a dihy-8 {. p7 C' E4 y: w7 y
drotestosterone level in our patient. In addition to& H% C2 C, p/ _1 t8 t, _! m# Z
virilization, exposure to exogenous testosterone in* f* `& L* U  O
children results in an increase in growth velocity and
8 l9 e# M% `! T2 R, H" Eadvanced bone age, as seen in our patient.
# V' F( N  B. FThe long-term effect of androgen exposure during4 d% Z$ b% [9 r; j+ x' O
early childhood on pubertal development and final1 ^/ c7 }4 p( y" w/ U& Y; f6 N) ^8 I
adult height are not fully known and always remain" I* K7 h( Y" `" G: U
a concern. Children treated with short-term testos-/ k% P2 p4 h4 t  R8 s  R
terone injection or topical androgen may exhibit some
7 |) k& w( _" ^- E# W4 ]acceleration of the skeletal maturation; however, after/ h% Y4 M+ ]# c5 c- P" S5 C
cessation of treatment, the rate of bone maturation
- ?5 o# G3 l! k8 ]- ^) Sdecelerates and gradually returns to normal.8,9
7 N  `1 I; ]0 R; F# k' aThere are conflicting reports and controversy
3 u% S8 ^$ j' L  C- u+ Uover the effect of early androgen exposure on adult* G$ s1 M8 Z  N* ]; c2 _: P
penile length.10,11 Some reports suggest subnormal$ q' N  {! q7 t  n4 a7 X- u
adult penile length, apparently because of downreg-
3 e+ l8 e' R$ L: ]. e5 I' culation of androgen receptor number.10,12 However,/ t  M% x% w& J! B
Sutherland et al13 did not find a correlation between
1 U1 m8 c$ |- echildhood testosterone exposure and reduced adult
$ U: U- |: {! w$ Zpenile length in clinical studies.0 Q% U( i% u7 E5 ], S
Nonetheless, we do not believe our patient is
8 z( S: Z$ O& K1 U/ }' [: X) ^( [going to experience any of the untoward effects from4 ?$ u1 [3 R/ W0 k. x: B! m4 K
testosterone exposure as mentioned earlier because+ M$ v; [% G* s) F/ w$ }
the exposure was not for a prolonged period of time.& X* B5 d9 E3 k/ x
Although the bone age was advanced at the time of
! a- x* l% H) w( d: Y3 z2 tdiagnosis, the child had a normal growth velocity at5 ^, a  i: k# g. Q, G
the follow-up visit. It is hoped that his final adult6 f  ^; W) h" ]* I" Z6 l
height will not be affected.
/ }5 _, a5 L  v) a# Q) sAlthough rarely reported, the widespread avail-& m2 W- {! a5 f+ Y3 M8 g" k
ability of androgen products in our society may# X, e: q, u8 x" N3 f' e# a
indeed cause more virilization in male or female
4 E! O: b0 g; |# l0 Vchildren than one would realize. Exposure to andro-
! Z7 f$ R! W& _% ~. Igen products must be considered and specific ques-4 r. [* D" t" c3 u+ Y
tioning about the use of a testosterone product or
. W+ h9 f& @+ K0 C/ tgel should be asked of the family members during2 M) a( l/ Z* \
the evaluation of any children who present with vir-& e" e9 f: F: a9 H$ A
ilization or peripheral precocious puberty. The diag-) z& S" G9 r0 w- y+ R
nosis can be established by just a few tests and by6 U6 k/ L* V6 U) a- t
appropriate history. The inability to obtain such a
8 ~2 _/ ]. e: Uhistory, or failure to ask the specific questions, may
2 Q$ K. }' v9 v+ Hresult in extensive, unnecessary, and expensive
& n$ p- R5 v- ]. Dinvestigation. The primary care physician should be5 p2 P4 T; v4 W- o+ ~7 O& z$ A7 g
aware of this fact, because most of these children1 D8 L7 N, k0 o& y. e& t' p1 _
may initially present in their practice. The Physicians’' b' \0 c: \8 Q6 B8 C/ d8 x
Desk Reference and package insert should also put a
/ g' D" I2 f# t+ R9 k5 C6 q( Uwarning about the virilizing effect on a male or
* n" W, d) ?, `% {female child who might come in contact with some-6 q: T" d( }: E1 S3 v- m* g. C
one using any of these products.
, M. f! @2 b$ A' y5 S  C' ^References
9 x7 a2 p" O+ r- X6 q2 @1. Styne DM. The testes: disorder of sexual differentiation
# F, Z  \7 n7 a) Land puberty in the male. In: Sperling MA, ed. Pediatric. P2 P+ K7 n6 X* V
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- l) K3 V8 ?2 |! z6 q( l
2002: 565-628.
1 e1 W" F* N* T7 J. t6 k1 s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
; w% F+ p' E) E6 ?6 [/ I& [puberty in children with tumours of the suprasellar pineal
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

$ w/ H8 a- e  O  {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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