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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
" ?0 J6 p/ M; e/ Y. F4 oBoy Induced by Indirect Topical# R8 y$ _4 T" ?- g5 K# E
Exposure to Testosterone
  V  b# ~- E% }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* `) Z+ a0 b0 m9 F9 D, w0 g. _
and Kenneth R. Rettig, MD12 j4 \6 ?1 @( P  Q# K
Clinical Pediatrics, k+ _" ?7 G; u# |9 t
Volume 46 Number 66 K- [; [3 \/ X  r
July 2007 540-5432 J" g5 x# ^6 e
© 2007 Sage Publications, G) @  U: Q" G, \
10.1177/0009922806296651
5 C8 q* X1 Q# M6 k. S3 Nhttp://clp.sagepub.com/ x8 N  O! u5 P1 ?
hosted at
3 c4 t% d  y7 G0 [/ U  L1 Whttp://online.sagepub.com5 N. @" J0 j( R7 B
Precocious puberty in boys, central or peripheral,
& j  L$ Z* E! h- x0 fis a significant concern for physicians. Central+ I5 G6 V* ~5 X0 t6 N
precocious puberty (CPP), which is mediated" A2 e5 O# Q$ ?- A: r$ v
through the hypothalamic pituitary gonadal axis, has
3 p3 y9 q; N$ w8 J1 m) y+ pa higher incidence of organic central nervous system
" x: {9 ?5 G6 f( H! q2 u( h9 slesions in boys.1,2 Virilization in boys, as manifested- @( h+ C9 [2 B
by enlargement of the penis, development of pubic
* X% U! ]* c) Z5 d: Xhair, and facial acne without enlargement of testi-
6 g6 T! ]7 W! ^! n" t# Kcles, suggests peripheral or pseudopuberty.1-3 We! B6 v6 d: `6 L. @+ |  h* z
report a 16-month-old boy who presented with the
6 l$ G3 Q  _7 q: ]6 fenlargement of the phallus and pubic hair develop-
9 V, P5 p1 T4 j# {- P( x# lment without testicular enlargement, which was due
- N0 s- c( r1 P) |  o7 S  Xto the unintentional exposure to androgen gel used by9 Z+ {, c; Y" v- i/ R( E
the father. The family initially concealed this infor-3 W) \8 N* ?# L$ J  ]) K$ e0 C
mation, resulting in an extensive work-up for this
9 L4 k+ y; Q) i+ M/ N6 T0 zchild. Given the widespread and easy availability of$ l. y: z8 l9 k  T
testosterone gel and cream, we believe this is proba-
; i0 T9 }# }4 A: Kbly more common than the rare case report in the
/ ~3 D$ i8 N1 Q3 Gliterature.4
$ d5 [: \1 j7 V- [5 p0 y( E$ ]Patient Report
. ^& X) ?6 M. _% ~4 iA 16-month-old white child was referred to the
1 d$ S& H+ c& D) g2 Zendocrine clinic by his pediatrician with the concern2 x" f/ O4 {3 h9 d4 W5 o  d
of early sexual development. His mother noticed
' Y. }: p: g: [6 |light colored pubic hair development when he was
+ O, l0 l+ ]7 y1 \) FFrom the 1Division of Pediatric Endocrinology, 2University of
$ \+ `! d8 o  E, k& q( lSouth Alabama Medical Center, Mobile, Alabama.
" J+ a; ]9 t% `+ x/ V+ u. ]! @6 uAddress correspondence to: Samar K. Bhowmick, MD, FACE,2 A  m# n1 S; w. q
Professor of Pediatrics, University of South Alabama, College of
* h* G  _6 s6 c$ x  S1 {! _$ CMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ b: q# t7 V8 A% v
e-mail: [email protected].4 T6 R# ~  }* `6 o, t/ g& U$ ~
about 6 to 7 months old, which progressively became
% j1 q  L4 p, t; `  s) \1 H. r& Wdarker. She was also concerned about the enlarge-
7 s# @( j9 q: q: [ment of his penis and frequent erections. The child; c! X! c. k( \/ u. h( U$ C4 b
was the product of a full-term normal delivery, with
2 k* H; w1 ]$ D: R9 k/ |& na birth weight of 7 lb 14 oz, and birth length of
, H; X; u# F/ z+ _+ \) L20 inches. He was breast-fed throughout the first year
/ N# H" c- N$ Pof life and was still receiving breast milk along with
' R4 s4 h5 {5 Hsolid food. He had no hospitalizations or surgery,+ B+ a: y/ t# K
and his psychosocial and psychomotor development
: y6 P7 [! f6 D# x0 v9 dwas age appropriate.+ ?% j( ^0 m& u8 C
The family history was remarkable for the father,
+ ^7 m- i! I& W( q) m9 k, Mwho was diagnosed with hypothyroidism at age 16,
- m  z( d) \; bwhich was treated with thyroxine. The father’s
& c5 ^' S) o: O- H  pheight was 6 feet, and he went through a somewhat
9 R7 a2 W6 ~/ _& Nearly puberty and had stopped growing by age 14.
- P- M# J" Y3 V, B. ?The father denied taking any other medication. The
  y5 i" W. v; |2 U+ Dchild’s mother was in good health. Her menarche: l% Z; G6 m1 @7 ~6 O
was at 11 years of age, and her height was at 5 feet
; S2 @  G0 }9 U- V* T5 inches. There was no other family history of pre-' g7 ^7 {3 n4 @/ u- _2 l
cocious sexual development in the first-degree rela-
1 c5 q: |# H5 N+ D) y/ dtives. There were no siblings.9 s" K/ f+ j6 e/ Q
Physical Examination
6 a' L9 `3 r3 e  ]+ LThe physical examination revealed a very active,
/ p2 n; r' w# m- {- M' jplayful, and healthy boy. The vital signs documented
! ?$ g8 [" @) o+ r- _! A7 da blood pressure of 85/50 mm Hg, his length was
( ^& K4 K( k9 D8 }- I" S6 K' X, p90 cm (>97th percentile), and his weight was 14.4 kg5 i# ]! G1 Z, {) s7 {
(also >97th percentile). The observed yearly growth
; N2 m# `- k. B: Yvelocity was 30 cm (12 inches). The examination of
: C/ H: d; I! i1 cthe neck revealed no thyroid enlargement.$ S# J  g9 w. v  f: g  @# u* q+ W5 A
The genitourinary examination was remarkable for! N* d' o  z+ a/ Z
enlargement of the penis, with a stretched length of* |1 A% \; m5 V
8 cm and a width of 2 cm. The glans penis was very well" |3 q7 O2 J# T
developed. The pubic hair was Tanner II, mostly around' g- R1 t# M. \, W0 h* h
5408 P& b5 L4 G& g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 t. U  y/ H% @* _; P$ B5 `: Kthe base of the phallus and was dark and curled. The
% _: U2 Z0 k; n( q) Wtesticular volume was prepubertal at 2 mL each.) _1 D( Q1 Z  O, j! N& f: Z# T
The skin was moist and smooth and somewhat
# h! \4 A. t% Foily. No axillary hair was noted. There were no& W& W4 M. F* I
abnormal skin pigmentations or café-au-lait spots.. I! N  M7 _( ]! O
Neurologic evaluation showed deep tendon reflex 2+
* Q4 T- ?5 Z8 Ibilateral and symmetrical. There was no suggestion0 \5 [2 l* t$ x/ F$ p
of papilledema.
, d0 b4 z* q  a! V7 sLaboratory Evaluation' Q. y" I: n0 U& M
The bone age was consistent with 28 months by
1 P7 J) P3 x9 g/ ?4 Z' Qusing the standard of Greulich and Pyle at a chrono-
- o& }  s7 E. J1 Ylogic age of 16 months (advanced).5 Chromosomal
  ]; V. ?6 `( Hkaryotype was 46XY. The thyroid function test
0 \) L7 P) E9 m7 ^* l7 Fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
' F1 {* h5 o* j8 L' A7 q. o7 blating hormone level was 1.3 µIU/mL (both normal).
3 ^. V1 N0 V6 k5 o4 Q6 }$ f# P' uThe concentrations of serum electrolytes, blood( c2 {* C  H% v: c/ @: }9 M
urea nitrogen, creatinine, and calcium all were
: {: _6 W" `" n# rwithin normal range for his age. The concentration; x# k0 ], L& f; v8 V
of serum 17-hydroxyprogesterone was 16 ng/dL/ ~8 ^' i. Q9 m  v5 h$ c( i& o9 c
(normal, 3 to 90 ng/dL), androstenedione was 20# i' M3 S6 w& P0 A& a* [0 j8 n- Y9 u
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, \  n; O0 W6 C$ |; {/ ?
terone was 38 ng/dL (normal, 50 to 760 ng/dL),+ Y; g; ~1 ^/ j) V- ]% G+ r
desoxycorticosterone was 4.3 ng/dL (normal, 7 to. G6 ^2 A/ u& l- r0 Y
49ng/dL), 11-desoxycortisol (specific compound S)+ P/ c5 `5 @( Z4 j9 q- b( d$ p! x. Y
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* p  f$ @2 ]- \3 s! G
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total5 i" y* b9 T, ^- ?( _
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),; e* ~1 _: P- d' b0 H1 V7 c+ _
and β-human chorionic gonadotropin was less than: `% E6 h, X9 l0 z3 h
5 mIU/mL (normal <5 mIU/mL). Serum follicular
; B( j# M$ e. H$ Y* j0 fstimulating hormone and leuteinizing hormone
1 G; V. z) ~" I6 h/ q7 Zconcentrations were less than 0.05 mIU/mL
$ M. S7 o! ~# R' z) S5 R# N/ H% D(prepubertal).
: I' F. o8 n8 g% WThe parents were notified about the laboratory
. o8 x1 ~" J  A/ x" presults and were informed that all of the tests were$ Z& \0 h* W1 k, n
normal except the testosterone level was high. The( J" f6 W) F  s* w: T
follow-up visit was arranged within a few weeks to
/ K, g1 R" h4 z. ~  `3 fobtain testicular and abdominal sonograms; how-
/ r( H* Z! z; u* N. _7 ]1 u& F4 Eever, the family did not return for 4 months., Z' v/ i0 d  m5 @9 @
Physical examination at this time revealed that the
0 m' e0 s& ^, {  m% A2 _7 `: Lchild had grown 2.5 cm in 4 months and had gained
# V# m7 \) G# D7 M% u8 m2 kg of weight. Physical examination remained
- a! {6 J8 C$ S0 ounchanged. Surprisingly, the pubic hair almost com-
; s. k7 B3 D4 i/ s( ~( A$ spletely disappeared except for a few vellous hairs at
7 L! W) ]% J/ t- bthe base of the phallus. Testicular volume was still 2
7 \. {6 F# i' c8 F  f" |; G! w' TmL, and the size of the penis remained unchanged.
! k' i. }' G' A0 a- PThe mother also said that the boy was no longer hav-) S1 |) S" r' C: ~" W0 g/ h
ing frequent erections.
; i9 w$ S6 Y7 \+ b8 gBoth parents were again questioned about use of) C* f# f% c, ]$ q. b% v
any ointment/creams that they may have applied to. f9 x5 F4 }& P/ K
the child’s skin. This time the father admitted the: Q* H# _* v& g" ~2 t( ^/ @
Topical Testosterone Exposure / Bhowmick et al 541
7 s# s/ l1 t4 I, R% z- E0 ~9 w/ Buse of testosterone gel twice daily that he was apply-
' ]. ~& w+ K; g. |2 |" ]: Jing over his own shoulders, chest, and back area for
% k3 |' F6 ?) f6 s. N/ Ba year. The father also revealed he was embarrassed
; t  t7 u$ y3 Q. L, w) Eto disclose that he was using a testosterone gel pre-( d, X0 L. ]1 u( ]  |
scribed by his family physician for decreased libido7 L2 P6 Q" U2 ^% o" b
secondary to depression.
6 D% @5 q% C& Z$ t7 }0 XThe child slept in the same bed with parents./ N  H. W1 e) y
The father would hug the baby and hold him on his3 t/ {( X$ k  q7 O- t: s7 R
chest for a considerable period of time, causing sig-
$ r$ c, @7 n- ?- [, u( @nificant bare skin contact between baby and father." }# P5 N9 n4 V$ u0 k
The father also admitted that after the phone call,/ G1 |. r7 _$ @' b9 G* }
when he learned the testosterone level in the baby
- G3 g& U% S% ], p4 f# ]was high, he then read the product information' s5 r& E1 E& c7 f+ A0 q
packet and concluded that it was most likely the rea-0 T% ?: O2 {& X& k6 J  b1 H  y. \; b
son for the child’s virilization. At that time, they
9 v# M" j6 M+ u! Z# }0 T* Bdecided to put the baby in a separate bed, and the
6 @9 t; |% _+ t$ M3 {* _  h  Efather was not hugging him with bare skin and had0 N+ _) L; d! ?2 `7 ?4 L7 d4 S& H
been using protective clothing. A repeat testosterone6 }" k' X6 X9 ]5 c* m8 ?: z! p
test was ordered, but the family did not go to the/ N; k8 Q2 j" N) Y# Z: b- }  u0 W
laboratory to obtain the test.
/ _" r6 d/ ?% J8 _! VDiscussion
6 E. y% V% {- y/ fPrecocious puberty in boys is defined as secondary
* O9 @" L+ B5 {, V$ k$ ]sexual development before 9 years of age.1,48 u' z1 e0 t% s. k- }: K# }
Precocious puberty is termed as central (true) when5 q) _& p0 x2 c% m" J6 P/ B
it is caused by the premature activation of hypo-
! k1 f! N- C4 Tthalamic pituitary gonadal axis. CPP is more com-, p9 j* \. m* l8 a+ B
mon in girls than in boys.1,3 Most boys with CPP
& S- L. [6 \  A1 Hmay have a central nervous system lesion that is8 `8 N9 |" U& H8 u* ^( |  l
responsible for the early activation of the hypothal-
8 }' i2 y$ ]* Q6 S2 Wamic pituitary gonadal axis.1-3 Thus, greater empha-% e1 @' x+ X/ y$ b8 ~
sis has been given to neuroradiologic imaging in; e8 Q) H5 Q6 z$ f
boys with precocious puberty. In addition to viril-6 ~, k, Z/ f. o
ization, the clinical hallmark of CPP is the symmet-
, D; ]! L6 m9 _0 j4 A- prical testicular growth secondary to stimulation by
! M6 A; [  ?  k2 f% m/ I8 \gonadotropins.1,3/ p+ k& }! y6 Y4 M# }" v' T7 r7 _
Gonadotropin-independent peripheral preco-
; B' @% |6 x/ j# `7 K0 Pcious puberty in boys also results from inappropriate. r1 F1 ~2 A! V$ o' D* \! ]
androgenic stimulation from either endogenous or  [6 Z; T7 v8 a( D- v9 B. C% P
exogenous sources, nonpituitary gonadotropin stim-7 Y. k" q* W4 V- f
ulation, and rare activating mutations.3 Virilizing" u3 l  P8 o) R
congenital adrenal hyperplasia producing excessive
) o9 Q0 q1 ?( S7 ?2 iadrenal androgens is a common cause of precocious
0 N' z: l" M. O! p: S- bpuberty in boys.3,45 g$ c$ i) U" K$ Y0 x7 [+ J, `
The most common form of congenital adrenal
, V! z6 k  R7 X$ a1 G. c% nhyperplasia is the 21-hydroxylase enzyme deficiency.' X  b% B8 e7 n. l4 s& o- A
The 11-β hydroxylase deficiency may also result in) o+ g0 x! T/ Z0 u4 h6 q3 ^7 W
excessive adrenal androgen production, and rarely,, C# u: t0 ?3 a, C( C, s6 [
an adrenal tumor may also cause adrenal androgen& R: c& ~& i: q/ l" i
excess.1,3
! I! J: m# b7 w! b" [5 R4 h4 Kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# Q, Z1 J* t9 a  d8 ^3 l+ M
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, x! ~9 }, z) z- I' qA unique entity of male-limited gonadotropin-
9 W) A, C+ F6 x! u: F. Windependent precocious puberty, which is also known
  o- O; Q2 c( U! Z3 `3 o# v, pas testotoxicosis, may cause precocious puberty at a  n/ P& V6 w) M# @/ O5 K0 G
very young age. The physical findings in these boys
) z  x" _, v8 b, lwith this disorder are full pubertal development,& Z8 t) O$ f8 Y: u! i. D" D" R0 r8 v
including bilateral testicular growth, similar to boys2 o. k0 E: `! ^" o) t" c& A0 S- L
with CPP. The gonadotropin levels in this disorder) W9 Y* K) t- \5 H! d( m& O
are suppressed to prepubertal levels and do not show
+ I0 k$ U7 ~& V3 ]% R. q- lpubertal response of gonadotropin after gonadotropin-
8 C+ h: S7 m* r; s9 D- Jreleasing hormone stimulation. This is a sex-linked
5 G, K, C8 V, q& i% w! qautosomal dominant disorder that affects only
+ f7 r$ O: A1 Vmales; therefore, other male members of the family7 F! f! m3 a' ~0 ?2 G
may have similar precocious puberty.3
' ?( d4 t) f/ n) S9 X5 C' C) xIn our patient, physical examination was incon-
/ w' c- u$ c# F2 `5 hsistent with true precocious puberty since his testi-
" m, m2 J. ^8 jcles were prepubertal in size. However, testotoxicosis
( T6 x$ W) z0 O$ _was in the differential diagnosis because his father
( {8 ^' E1 W$ A8 \started puberty somewhat early, and occasionally,
6 v, r5 g2 e' O( _0 otesticular enlargement is not that evident in the8 C$ \2 h4 a0 E  m2 W
beginning of this process.1 In the absence of a neg-
" s) n/ ^3 _6 |ative initial history of androgen exposure, our+ J8 D9 u) d, M  ?
biggest concern was virilizing adrenal hyperplasia,0 O' [# M$ F, V) Q
either 21-hydroxylase deficiency or 11-β hydroxylase
; ]* I$ O4 j6 C0 a0 {deficiency. Those diagnoses were excluded by find-! u5 |  d, W; d. E. ]
ing the normal level of adrenal steroids.% M% F0 d. j9 w/ R
The diagnosis of exogenous androgens was strongly" w* u$ V6 i- m5 T
suspected in a follow-up visit after 4 months because
7 \0 _" p; |( }3 A' Kthe physical examination revealed the complete disap-0 S7 T. N+ ?" v0 X
pearance of pubic hair, normal growth velocity, and7 r; z7 H) i4 O; F9 D* r  Q
decreased erections. The father admitted using a testos-
8 O$ L4 L2 u) [! jterone gel, which he concealed at first visit. He was
% P) T8 j% x) ^, c2 h8 f6 ~8 \using it rather frequently, twice a day. The Physicians’- \+ C# a% A1 |5 o1 ?
Desk Reference, or package insert of this product, gel or. C) c, N$ c9 R1 O5 Z
cream, cautions about dermal testosterone transfer to, G, x. D/ q" x4 c
unprotected females through direct skin exposure.: ?- o5 E" o: R- K. |* `$ _" D
Serum testosterone level was found to be 2 times the8 T5 u3 y( v, {% O
baseline value in those females who were exposed to
" p7 W5 \, b+ Yeven 15 minutes of direct skin contact with their male
# M: ~/ p/ k& }! w2 h8 w/ [' {2 Jpartners.6 However, when a shirt covered the applica-
$ T5 {' Z5 ]% N; ltion site, this testosterone transfer was prevented.
; W" z" j) V1 u  P' j( N2 Z# HOur patient’s testosterone level was 60 ng/mL,
6 ?# |: l. Y; R; B" ^7 q- u6 ?4 @which was clearly high. Some studies suggest that; _% q& V$ x1 j8 C
dermal conversion of testosterone to dihydrotestos-; i& F4 U* s! k! H0 K+ ~
terone, which is a more potent metabolite, is more
3 n- }2 d/ D+ h( }, y( ]active in young children exposed to testosterone( U: r8 o' ^5 \$ W
exogenously7; however, we did not measure a dihy-
4 a% M9 F4 ~$ D! V( |% V, S$ A4 ~drotestosterone level in our patient. In addition to) Y7 u8 }1 {1 s3 Y
virilization, exposure to exogenous testosterone in
0 j+ q3 J0 g# h0 i1 S- _* O0 \children results in an increase in growth velocity and. x, W1 l% X- a. d: \. ^# v" y
advanced bone age, as seen in our patient." Y/ [  F* Q1 X- k& \+ p4 f7 t7 O
The long-term effect of androgen exposure during
0 ?* ~' N" {; ?1 @7 \early childhood on pubertal development and final% C7 I( ?  _# [0 f9 O! `" t: _0 k
adult height are not fully known and always remain/ |3 X! y6 O0 z* ?
a concern. Children treated with short-term testos-; z' A4 `4 V" @7 c7 n
terone injection or topical androgen may exhibit some/ K3 t2 o8 M" x
acceleration of the skeletal maturation; however, after# l7 y- R% E$ ~
cessation of treatment, the rate of bone maturation
, @) w/ m) }1 J6 }, Udecelerates and gradually returns to normal.8,9
3 |, `* G1 I& `2 S- o/ PThere are conflicting reports and controversy0 \1 X% |, L9 u$ E; `
over the effect of early androgen exposure on adult
: v+ y5 X- r$ B. Npenile length.10,11 Some reports suggest subnormal
5 H+ ?. H8 y: Z: c) {adult penile length, apparently because of downreg-
# ]. x5 H: V9 A. mulation of androgen receptor number.10,12 However," g3 Q  D1 I* H, @* d: H. X
Sutherland et al13 did not find a correlation between
4 g! B9 x8 Y7 Uchildhood testosterone exposure and reduced adult
5 C  o$ l( y, d- f# |: Npenile length in clinical studies.$ ]6 T" i6 G7 f3 s, x2 u
Nonetheless, we do not believe our patient is
& S' @4 g; S; [+ Jgoing to experience any of the untoward effects from
! T; n9 h; c) z6 ^$ t+ {" E7 ytestosterone exposure as mentioned earlier because9 v4 E/ G7 l$ s; s. ~1 c
the exposure was not for a prolonged period of time.# H; k* r* ~) p) `  ^& M
Although the bone age was advanced at the time of
2 Q  }/ u4 P# F3 p; E  y" Adiagnosis, the child had a normal growth velocity at2 H3 L; K% |$ j0 r. f1 n8 z
the follow-up visit. It is hoped that his final adult
$ s+ E2 c5 d2 v! o& y, q- ~3 H# lheight will not be affected.
  H7 P* n  }. R& ?! _9 W; w& }! EAlthough rarely reported, the widespread avail-+ [# ~0 E* B. ^6 C" o9 h' E: A
ability of androgen products in our society may
1 V: y! u3 \4 z% m' Nindeed cause more virilization in male or female
3 z  k6 x" v8 uchildren than one would realize. Exposure to andro-
2 l" T& _# R* S- L# r4 |gen products must be considered and specific ques-
# E, f% z. v) ?' ]' D0 \/ Vtioning about the use of a testosterone product or
6 U% [8 C# _) j0 T% c1 c: s; T6 ?gel should be asked of the family members during
6 k# c6 W. t3 [3 ]7 r- R4 K* _the evaluation of any children who present with vir-, z  T& r# r% k/ r7 Z% S
ilization or peripheral precocious puberty. The diag-6 S- Y, I7 r2 c) A" B
nosis can be established by just a few tests and by% n' L5 i( ]/ G" z) M- x
appropriate history. The inability to obtain such a
) c5 N6 e& O0 I/ u( H& [" Ohistory, or failure to ask the specific questions, may$ y6 X2 U7 D2 a# z
result in extensive, unnecessary, and expensive
) i+ r- R2 }) Minvestigation. The primary care physician should be
) t0 D6 C# S0 n" Z: N* g2 Aaware of this fact, because most of these children: @$ Z9 n! l  g. d
may initially present in their practice. The Physicians’
5 _2 m& }& s: N( eDesk Reference and package insert should also put a
- x/ q, D8 O9 Q" _) ]; r* _warning about the virilizing effect on a male or
' C. P: _+ ]% o3 `) K2 Xfemale child who might come in contact with some-
8 }5 V& |5 T' H- q3 Xone using any of these products.
* B  j7 m' ^7 TReferences+ b2 D' e2 T9 W9 ]4 y
1. Styne DM. The testes: disorder of sexual differentiation
) d( ~! f* k' J% u7 jand puberty in the male. In: Sperling MA, ed. Pediatric+ @9 ~% |  `" a% g+ L% p
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: I  G) j! K& Y; [2002: 565-628.4 E7 Q  y8 @0 f
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 A5 z+ s1 X$ C3 Q0 ]9 xpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
, g# o8 Q) W! W6 YBoy Induced by Indirect Topical# l- ?' x) c* G( a7 w8 g% \) F  i
Exposure to Testosterone
' x5 d2 Q" u! \Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& T0 f+ q3 ]& C; u- f
and Kenneth R. Rettig, MD1# s+ H" s' I: Y: F/ f# L
Clinical Pediatrics( Z. }& f, }$ Q6 @  t8 _
Volume 46 Number 6
% T- m' J6 n7 QJuly 2007 540-543: K: c! A6 M5 B) L% L
© 2007 Sage Publications
0 M9 A8 i- O5 n: m6 \6 [  a10.1177/00099228062966517 v" S, x& P: R4 u( H& J6 L' z
http://clp.sagepub.com( M# _4 [/ j; d- m, y1 V
hosted at
" T9 l/ L& G. q: U6 `http://online.sagepub.com$ E* `' F# L" d# \: H9 }
Precocious puberty in boys, central or peripheral,8 U' D: u3 M8 H9 x' N
is a significant concern for physicians. Central6 w: h6 h* F8 f8 B
precocious puberty (CPP), which is mediated/ E1 @. S$ i# n/ E) h3 V# ]& A
through the hypothalamic pituitary gonadal axis, has: F! s, x: t5 i0 o# S% Q
a higher incidence of organic central nervous system
) c! B# T8 S6 b3 @, ]1 z- Vlesions in boys.1,2 Virilization in boys, as manifested
  H) ]  m) W# n% {8 nby enlargement of the penis, development of pubic- d& P) s9 g4 S  o
hair, and facial acne without enlargement of testi-! u+ b. L/ L2 D) w
cles, suggests peripheral or pseudopuberty.1-3 We4 j2 u# k( U6 d  [5 \& M, f" H
report a 16-month-old boy who presented with the
( k% i. G( L* X. N# V1 z6 Xenlargement of the phallus and pubic hair develop-9 @& S; o: U- J) a. _- O4 H
ment without testicular enlargement, which was due
% A9 d0 n8 ?( \1 q' ato the unintentional exposure to androgen gel used by
5 P) m/ W" ~! p: Z: _/ }  Vthe father. The family initially concealed this infor-/ _& J; I: x# o2 q7 O) o0 d. }5 X
mation, resulting in an extensive work-up for this
; S; c# _1 n" N. h- o% K" nchild. Given the widespread and easy availability of
# P9 E; u9 p/ ntestosterone gel and cream, we believe this is proba-2 R( K  C9 {, L! R, _' a! E1 ?
bly more common than the rare case report in the
  E. r6 g% F* t, |+ nliterature.4( l/ J7 V% b, R
Patient Report
7 j/ e5 N/ E1 y* ~% R3 u; eA 16-month-old white child was referred to the
& Y$ _. b8 W9 {+ [endocrine clinic by his pediatrician with the concern/ E5 R$ L3 v' n' J, r9 d
of early sexual development. His mother noticed
& {: C. D: u) U" {9 ilight colored pubic hair development when he was. P7 R4 f3 g! q5 J; u
From the 1Division of Pediatric Endocrinology, 2University of2 d5 W. C) s' u/ C
South Alabama Medical Center, Mobile, Alabama.
. v3 F+ N/ P6 I8 ~) SAddress correspondence to: Samar K. Bhowmick, MD, FACE,/ y% l& r+ {% U6 Z
Professor of Pediatrics, University of South Alabama, College of
. |" O0 }1 J# [( BMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
2 W' e( [$ y6 e$ J, w3 E0 Ie-mail: [email protected].5 M1 b. }# j$ \
about 6 to 7 months old, which progressively became
8 R5 s( L7 o+ Y% A' F% Tdarker. She was also concerned about the enlarge-
  n! \6 k0 ^' \. O. `! w, Q4 Xment of his penis and frequent erections. The child- ]# p- J+ j  T
was the product of a full-term normal delivery, with
- X' k) h& E' o) s( }7 \* Ra birth weight of 7 lb 14 oz, and birth length of
- n- G% O* }8 d# p/ {1 s) w20 inches. He was breast-fed throughout the first year5 N% ]. p- d+ S( ~- V! [
of life and was still receiving breast milk along with$ q' ^8 B' }7 R- b
solid food. He had no hospitalizations or surgery,) J, f6 x1 y. k3 P; X+ H
and his psychosocial and psychomotor development% l" y2 A' Y% C! t( U
was age appropriate.
& o9 A% U$ E, k0 v6 K; iThe family history was remarkable for the father,
+ C0 ~- K" C% k% l' \who was diagnosed with hypothyroidism at age 16,
# V- t2 t  {3 a5 u$ V) Kwhich was treated with thyroxine. The father’s" M( K' ]' p& f1 y# x+ m/ u8 v
height was 6 feet, and he went through a somewhat
  o$ t( ]/ U2 H1 a" dearly puberty and had stopped growing by age 14.
: A+ I4 k3 D" g9 tThe father denied taking any other medication. The2 k! J: D. ~) {0 l. w1 c" [
child’s mother was in good health. Her menarche" q5 K, w; j. V( H& N% k
was at 11 years of age, and her height was at 5 feet" U8 ~4 b' K' V- V7 E
5 inches. There was no other family history of pre-
. B# j( f& l0 `1 Scocious sexual development in the first-degree rela-
: \' e7 |' Q* u" V9 gtives. There were no siblings.
: t; J5 l/ q  S; N! EPhysical Examination) |# s5 H- h( S; D' X
The physical examination revealed a very active,' c- ~6 W6 W0 L
playful, and healthy boy. The vital signs documented* n$ ~/ a* u. z# M
a blood pressure of 85/50 mm Hg, his length was9 R# A7 U+ v4 G/ @& N
90 cm (>97th percentile), and his weight was 14.4 kg
: N; R/ w% Q; C& M7 ^(also >97th percentile). The observed yearly growth! V9 q$ u5 C, ~- e+ ~* ?3 \
velocity was 30 cm (12 inches). The examination of
, ~5 O( ^+ v% V% lthe neck revealed no thyroid enlargement.
. A3 Q5 ~) j% Y6 yThe genitourinary examination was remarkable for& m" K; R1 R1 \7 u6 ^! F  P
enlargement of the penis, with a stretched length of: L, H" Y; _$ w. d) X
8 cm and a width of 2 cm. The glans penis was very well$ Z/ O/ c" e3 f$ ~$ J
developed. The pubic hair was Tanner II, mostly around+ a; k- [- j' q
540
) I7 ?4 A" E+ f; J3 D$ Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 }+ M- x  f& k( O; @the base of the phallus and was dark and curled. The
7 O9 t/ _& T% q8 z3 ktesticular volume was prepubertal at 2 mL each.
# R5 Z1 i- K( W; h' SThe skin was moist and smooth and somewhat- E) h" x" n* K
oily. No axillary hair was noted. There were no
( H9 W: `6 ]4 W6 H: u3 }& [/ \& zabnormal skin pigmentations or café-au-lait spots.
( v  a6 ^4 ?% n+ xNeurologic evaluation showed deep tendon reflex 2+5 `' v% t1 N  o- _1 B
bilateral and symmetrical. There was no suggestion
5 Y: F; q2 M. V$ @of papilledema., y4 E% g7 |- l, b5 o# O8 u  X8 h
Laboratory Evaluation
7 {. Q3 s0 {' Q7 e$ v, N8 n" N% X3 NThe bone age was consistent with 28 months by
0 c" m' r) h1 Busing the standard of Greulich and Pyle at a chrono-
* F8 u+ X8 F+ I; Mlogic age of 16 months (advanced).5 Chromosomal5 Q! ]1 x  B, Y
karyotype was 46XY. The thyroid function test
; l' W: l7 D2 mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 E6 t# c4 W! F* U7 k8 Dlating hormone level was 1.3 µIU/mL (both normal).
0 m& h  I8 q3 ?" @' \* H4 SThe concentrations of serum electrolytes, blood6 r4 R6 @; F) ?. B* \; l
urea nitrogen, creatinine, and calcium all were! u" M2 P9 p; h; \
within normal range for his age. The concentration5 F" e6 V% w. h. u( T4 c
of serum 17-hydroxyprogesterone was 16 ng/dL
. D. Z# i0 ?3 Z: F0 t( U(normal, 3 to 90 ng/dL), androstenedione was 20  [1 N' O! ~) m. R! D
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: n$ W" t! L7 \- R
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
5 ~7 Y! f. d+ D7 v% Tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to9 O1 h# ]5 u* H4 i1 L
49ng/dL), 11-desoxycortisol (specific compound S)2 K  R. i' _  F/ F; K" c% J
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 S6 M6 N. O* h: a; h& v" Z: {tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
  \* z$ F; e  S: Xtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' e! T! I, v) ^$ b; @' j$ oand β-human chorionic gonadotropin was less than! o2 F4 b- b* u2 E1 t2 c5 R
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  S/ f% O1 \; k3 G3 }2 o; hstimulating hormone and leuteinizing hormone6 L8 t8 O8 A; ?
concentrations were less than 0.05 mIU/mL
$ ?2 S6 B5 M3 U  M(prepubertal).
& F) s5 m. S6 C, cThe parents were notified about the laboratory& O8 d/ C9 I' e; m: m. y. ]
results and were informed that all of the tests were2 q  j/ m/ [) a* @# P# `) {, s
normal except the testosterone level was high. The  M9 @7 ^+ n+ p2 G: x
follow-up visit was arranged within a few weeks to
/ G, s( C" m# e, Cobtain testicular and abdominal sonograms; how-6 {0 L9 @- _; [, R- P1 k& X6 C
ever, the family did not return for 4 months.2 E* `+ C' R- k' a
Physical examination at this time revealed that the
% M* G( G2 r/ Ychild had grown 2.5 cm in 4 months and had gained6 x  ~2 i# D7 u8 {3 f. [# a
2 kg of weight. Physical examination remained8 @0 a3 g  |# j7 F, z& d, y( u
unchanged. Surprisingly, the pubic hair almost com-1 a* v9 }2 \* H+ O. L( |- W
pletely disappeared except for a few vellous hairs at) [+ F4 u" [2 G/ p& m3 H( U
the base of the phallus. Testicular volume was still 2# s0 m, e. j* ~$ F/ V
mL, and the size of the penis remained unchanged.
- t0 }) X/ o# k3 |: YThe mother also said that the boy was no longer hav-
% `. z5 L, }  ^$ jing frequent erections.
, O) ]: q& y" R* a5 [$ L9 K' _, _Both parents were again questioned about use of  K/ k, W1 U: ~+ i4 j( }
any ointment/creams that they may have applied to
! m# d  Q9 Y8 h2 a" sthe child’s skin. This time the father admitted the& ?" {  g7 w  F! A5 k
Topical Testosterone Exposure / Bhowmick et al 541
% v: W0 U' V) P- `; \' C) Ause of testosterone gel twice daily that he was apply-
- B/ I' T6 U: i3 k6 [8 L, _ing over his own shoulders, chest, and back area for
0 R3 I( b, O+ P2 o/ Ga year. The father also revealed he was embarrassed
) W* A& ~! ]! y. f6 R+ k9 N% Uto disclose that he was using a testosterone gel pre-
8 r4 o7 R5 F5 U) [9 Xscribed by his family physician for decreased libido
9 s4 n- ~* Q0 B" o3 H1 n. N' k# gsecondary to depression.7 c2 h- r: f( u0 [' g% ?# }
The child slept in the same bed with parents.
, Z: X& A1 j7 L- ?& D5 A: J3 UThe father would hug the baby and hold him on his
0 o/ O9 Q$ j. m0 g" schest for a considerable period of time, causing sig-
8 n6 }; G& r1 m% h' h5 k: X+ ~* \% nnificant bare skin contact between baby and father.
( E: [/ f6 f8 `0 vThe father also admitted that after the phone call,
  c' W. w; F+ n1 M8 J- uwhen he learned the testosterone level in the baby2 _$ {/ t/ Y$ |( x2 y! V( v+ Q' W
was high, he then read the product information, n1 }, A7 b0 M6 ?+ o8 V
packet and concluded that it was most likely the rea-0 {( b8 b' d4 V( h9 ~
son for the child’s virilization. At that time, they
. y6 M0 c4 m% N4 J7 a2 J* [: Kdecided to put the baby in a separate bed, and the
! F  x' S% P" nfather was not hugging him with bare skin and had/ i: [' k" W  g8 V9 w+ \% \
been using protective clothing. A repeat testosterone
8 w! }; e* e4 f# wtest was ordered, but the family did not go to the
4 L( o3 G4 O( C9 x! F* Wlaboratory to obtain the test./ o7 m) o) h  s
Discussion/ k* ~+ \) ~: u; q/ {
Precocious puberty in boys is defined as secondary/ l6 ^! O& G. c6 q
sexual development before 9 years of age.1,4( ]% Y8 H; ^; w7 |2 @
Precocious puberty is termed as central (true) when
: z/ f& P2 {' }it is caused by the premature activation of hypo-$ U. @+ G) y/ r% q( {+ z2 s: U/ `' ]
thalamic pituitary gonadal axis. CPP is more com-
+ p& X# f) H2 q& E. Z' [4 Amon in girls than in boys.1,3 Most boys with CPP
+ ?, T2 M) }4 J6 x8 f2 u5 D" amay have a central nervous system lesion that is6 i1 `6 P. U1 S! q$ z3 ]
responsible for the early activation of the hypothal-; K- G$ p* i" z* b: b1 A/ ?3 ~9 r
amic pituitary gonadal axis.1-3 Thus, greater empha-2 H/ R5 {* Q% g0 L& V
sis has been given to neuroradiologic imaging in
! j  a& U5 J& {, [boys with precocious puberty. In addition to viril-
, ^& O- z* E1 T$ s$ Nization, the clinical hallmark of CPP is the symmet-
7 i+ H* l/ k& e$ A- C) Trical testicular growth secondary to stimulation by- G. k9 o' ]( w
gonadotropins.1,3$ G8 V9 Z  \& ^3 l
Gonadotropin-independent peripheral preco-
. Y- S+ ^9 u( ?0 E4 q. U1 q" M  Ncious puberty in boys also results from inappropriate
1 `% a0 {! h$ y/ n0 n0 Gandrogenic stimulation from either endogenous or
( t5 M5 D+ r. x7 w! {: `exogenous sources, nonpituitary gonadotropin stim-
2 N6 s' J9 p  Z/ _" pulation, and rare activating mutations.3 Virilizing
% O" U' X$ O# p' O4 q! y) W# Xcongenital adrenal hyperplasia producing excessive
2 `, P0 y( o' y  j! X. o% cadrenal androgens is a common cause of precocious
. i5 D  M! i3 l( d9 ipuberty in boys.3,44 I' ~+ F1 z2 ~
The most common form of congenital adrenal* i) C  W1 Z. l+ W3 G# B' ~; h
hyperplasia is the 21-hydroxylase enzyme deficiency.' s; L! ?8 }$ B7 A7 h
The 11-β hydroxylase deficiency may also result in/ v. Z2 t  t! V3 C% [
excessive adrenal androgen production, and rarely,
8 s. h3 d( Y6 u8 n) ?an adrenal tumor may also cause adrenal androgen
5 `7 p4 X- u3 q( Bexcess.1,34 ?2 U  w2 p' D8 f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  U5 f/ K. j6 p# c( ?* k5 \9 S1 j& O. V542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 l# k2 r' E* i4 L
A unique entity of male-limited gonadotropin-
( W8 v0 {- ?3 b+ `6 Oindependent precocious puberty, which is also known: [* K) ?, n# i* t3 Z
as testotoxicosis, may cause precocious puberty at a/ o4 f# R6 h+ }8 J4 M7 e0 ?
very young age. The physical findings in these boys
- F( H$ o' }  w& U* G8 w# _with this disorder are full pubertal development,
! H6 a; |2 z% e$ n* B3 ?including bilateral testicular growth, similar to boys8 P+ x& U" X& i5 w2 Y/ k
with CPP. The gonadotropin levels in this disorder
, t: }  ~4 ?9 f* w9 nare suppressed to prepubertal levels and do not show
& y' s' Q2 H( r8 ?3 ?/ ^pubertal response of gonadotropin after gonadotropin-
2 |& l4 G, |, l+ }  M6 H! ~+ Y  Z) Ereleasing hormone stimulation. This is a sex-linked
  R0 K/ X3 D6 h, X/ m2 kautosomal dominant disorder that affects only# Q6 K/ @, G, [* v" A5 \
males; therefore, other male members of the family
8 w. P# V1 J% Zmay have similar precocious puberty.3/ e7 {& Q/ I4 ^
In our patient, physical examination was incon-1 ]/ i/ j# o0 R2 D3 H
sistent with true precocious puberty since his testi-3 h1 ]- ^8 o3 u% C/ G( v
cles were prepubertal in size. However, testotoxicosis
, \0 r% ~. N+ T, `: L3 bwas in the differential diagnosis because his father
0 k) h. ]- i  l4 N. j+ ^started puberty somewhat early, and occasionally,
5 L0 h/ a0 x- i3 Etesticular enlargement is not that evident in the
2 z$ y' |( s" l' x' C/ M' i) j! s9 Ibeginning of this process.1 In the absence of a neg-
: Z# R, z3 b( ]) Y; c" B. K7 Kative initial history of androgen exposure, our; r6 C* x! x( N4 S
biggest concern was virilizing adrenal hyperplasia,
& }9 L: H) h! teither 21-hydroxylase deficiency or 11-β hydroxylase/ t- `+ k# c# B( o
deficiency. Those diagnoses were excluded by find-
/ d2 l) \$ `5 F3 d# ding the normal level of adrenal steroids.
$ B% c% J& B3 [3 nThe diagnosis of exogenous androgens was strongly
9 ]5 z' E' N: \: s0 R& d- F$ Vsuspected in a follow-up visit after 4 months because0 w- }9 C. N( x  b
the physical examination revealed the complete disap-+ B  Y( a9 Z  ^( }7 h( R% @
pearance of pubic hair, normal growth velocity, and
7 U4 o5 w8 M6 L) F& hdecreased erections. The father admitted using a testos-$ U: z, d, ~; f3 s* u9 U
terone gel, which he concealed at first visit. He was9 [2 r/ Z, e) Y5 V
using it rather frequently, twice a day. The Physicians’0 w; e' o% y# A% h4 U8 F, }* X
Desk Reference, or package insert of this product, gel or
" H1 ]5 P1 B) s$ j' ^  L" Y* ncream, cautions about dermal testosterone transfer to. \3 @% c3 F; f* q* }5 z
unprotected females through direct skin exposure.
6 c5 x+ ]1 ?% [4 M* \: oSerum testosterone level was found to be 2 times the6 j' y5 l- L  R1 t- }' J5 i
baseline value in those females who were exposed to
0 D- l& t2 _9 Z; L' ^2 Ceven 15 minutes of direct skin contact with their male/ M4 }* A2 |9 G# z( C0 X- Z
partners.6 However, when a shirt covered the applica-
( s7 I( |( [9 L+ H' A. f; ]  ?3 Ition site, this testosterone transfer was prevented./ n! y7 O  {" ^, z: |
Our patient’s testosterone level was 60 ng/mL,8 |5 Q$ x. X6 c  k* J0 q
which was clearly high. Some studies suggest that
' b9 J1 a" s3 D' U$ Cdermal conversion of testosterone to dihydrotestos-4 m. k2 u2 u$ c) ~6 T9 y
terone, which is a more potent metabolite, is more
5 m$ V5 p% V/ |0 [& ^  n9 F8 Yactive in young children exposed to testosterone" B! k8 n* n( I9 k$ S
exogenously7; however, we did not measure a dihy-1 E* q4 [0 B& {/ l3 T
drotestosterone level in our patient. In addition to; J& H' k$ T; O. ?" M6 G8 t
virilization, exposure to exogenous testosterone in! i+ b$ l1 N0 F/ m6 D7 {
children results in an increase in growth velocity and5 Z  ~3 c" C% s! H& j
advanced bone age, as seen in our patient., ^9 U: d" p! Q
The long-term effect of androgen exposure during, R2 P, v6 S- I. \& f0 u7 A3 D
early childhood on pubertal development and final
6 D9 }- I: {, j5 [- [0 Kadult height are not fully known and always remain
% C" @: x" f) @& F+ ?# da concern. Children treated with short-term testos-3 m5 q0 `) f/ F. m  T2 W' [! H5 a
terone injection or topical androgen may exhibit some
/ t+ a$ O* D( X4 ^: s1 macceleration of the skeletal maturation; however, after+ A: o8 L' S3 Y5 A3 l3 b/ i, L
cessation of treatment, the rate of bone maturation
7 Q( }" S0 q3 e3 W6 q  `/ Ddecelerates and gradually returns to normal.8,9  ?9 r& O. l, v
There are conflicting reports and controversy4 i$ A" P5 c5 D" r" ^9 E0 @
over the effect of early androgen exposure on adult$ l3 m. V3 I4 L
penile length.10,11 Some reports suggest subnormal
) i+ Q7 [$ A' j, Iadult penile length, apparently because of downreg-
  y* R' ^6 g, w6 rulation of androgen receptor number.10,12 However,3 ~# d8 {0 `1 ]& z8 h6 h, ^
Sutherland et al13 did not find a correlation between
9 v; u# o3 X- q% _* Bchildhood testosterone exposure and reduced adult
# S; z" d% ^7 g7 y0 j- Upenile length in clinical studies.
! v5 o9 @6 K+ r2 \Nonetheless, we do not believe our patient is1 U% P* R5 f& q- g7 y
going to experience any of the untoward effects from
6 x* ?) e0 o" D4 r" E6 j, {. mtestosterone exposure as mentioned earlier because+ f8 A% y- d; [8 l
the exposure was not for a prolonged period of time.
) u# m  K! M7 h) a+ NAlthough the bone age was advanced at the time of" |2 H' L/ P  G, M
diagnosis, the child had a normal growth velocity at
1 i* D' m- }. j7 Bthe follow-up visit. It is hoped that his final adult
; o$ {9 Y' C4 a) {height will not be affected.. ]5 B2 g0 i1 |7 j  F) b2 g: z( `9 D
Although rarely reported, the widespread avail-
2 l+ U& `3 s; N# yability of androgen products in our society may
1 o; [+ F5 Y$ \2 Gindeed cause more virilization in male or female8 L+ V! ^6 C! y& B) b9 I& i1 f
children than one would realize. Exposure to andro-
/ P" `% A6 l7 Ogen products must be considered and specific ques-
- p/ a( R$ p+ F: S* [tioning about the use of a testosterone product or
1 N, u5 N8 T; ~5 A4 hgel should be asked of the family members during( r+ ]4 ?4 [0 [1 v: I0 j" Y
the evaluation of any children who present with vir-% [, J/ C, r7 ~, y4 D; G
ilization or peripheral precocious puberty. The diag-# O8 ^% W1 ]' e( b" P: Y
nosis can be established by just a few tests and by- w. U: M/ N' J: z& f
appropriate history. The inability to obtain such a
# ~+ u2 V! x& |history, or failure to ask the specific questions, may
" m. }( p; b  z+ E: Uresult in extensive, unnecessary, and expensive3 J+ L7 `/ J9 {: E. x
investigation. The primary care physician should be- o( I; z" N- ^4 W* g' R- c
aware of this fact, because most of these children8 h3 P" [' o9 f
may initially present in their practice. The Physicians’
6 Y( S6 Y# X- C3 `4 tDesk Reference and package insert should also put a
& n4 Q! _( O; X5 m, X/ lwarning about the virilizing effect on a male or
$ S, ?& w8 T, H! X$ ufemale child who might come in contact with some-
5 e& c, }3 v3 q2 p. y+ J+ J. }one using any of these products.
- j& W6 c1 L( }4 pReferences+ ~2 h  o6 j( S* q- A
1. Styne DM. The testes: disorder of sexual differentiation) C4 O% I# _5 x. ^# ^/ P' f: w# n
and puberty in the male. In: Sperling MA, ed. Pediatric
$ J6 J0 [0 p; WEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;; L2 G) r9 M6 d" `" L
2002: 565-628.& P6 W5 [1 X* ]* N2 v% \
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 y/ u7 F8 ]  V$ a% Mpuberty in children with tumours of the suprasellar pineal
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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
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發表於 2025-1-19 02:41:05 | 顯示全部樓層

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發表於 2025-3-8 22:04:50 | 顯示全部樓層
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