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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
4 j( Y( A; J( v4 k* j! r2 ZBoy Induced by Indirect Topical$ @  y! j6 r; ^
Exposure to Testosterone, {4 Y. B* H9 R, b  b2 L
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( S+ A8 _0 ^. X5 T" ]8 v
and Kenneth R. Rettig, MD1
3 y" F: Q6 g' o" ^4 NClinical Pediatrics
% U$ g9 f  @* e3 c( I+ Y* j2 `Volume 46 Number 6
& b7 C4 A4 |3 I$ ?' R5 O$ KJuly 2007 540-543& q4 P2 Y& M4 _9 J: a
© 2007 Sage Publications3 n% u. I# v+ v) |& ^! k* P5 K$ x  F
10.1177/00099228062966513 J. b5 r( a3 \* B) u9 T+ w
http://clp.sagepub.com4 g, ~- z) Q3 D- s7 B; ?
hosted at; `7 |" W0 ]! Z6 F7 j# i  Z3 W
http://online.sagepub.com
- l" ~; [! R" \. t% o+ b% `Precocious puberty in boys, central or peripheral,
( V, F& |- B: R0 Bis a significant concern for physicians. Central
/ K9 G8 K8 G; Jprecocious puberty (CPP), which is mediated$ t" g" }! E  ]: O
through the hypothalamic pituitary gonadal axis, has  F" [9 d# m5 [6 Q
a higher incidence of organic central nervous system
/ L: c6 O: `% [+ I2 Y4 u$ H- y8 ?lesions in boys.1,2 Virilization in boys, as manifested
( Q; t3 V1 J% h5 vby enlargement of the penis, development of pubic
; r2 f# p1 G7 Zhair, and facial acne without enlargement of testi-9 T, O9 U# s! `2 I' _5 R' y
cles, suggests peripheral or pseudopuberty.1-3 We8 K' e) |6 j+ S2 s
report a 16-month-old boy who presented with the
' i0 W& s/ X* F2 `* |enlargement of the phallus and pubic hair develop-: n% c8 q# N* \7 d
ment without testicular enlargement, which was due+ R$ o# V) t9 C3 k6 \
to the unintentional exposure to androgen gel used by8 v! T& t( j0 ~0 B/ Y
the father. The family initially concealed this infor-
' v& _1 n3 w  w! R# U) ]mation, resulting in an extensive work-up for this
7 I3 m. f, n: V' Echild. Given the widespread and easy availability of
# H! l; y, l  G* Q$ V4 @  Z# Dtestosterone gel and cream, we believe this is proba-
! U6 K, T2 [' ubly more common than the rare case report in the
: z8 |3 ]1 o& X- D8 c7 f$ n& nliterature.4
# a" b3 M; M/ [2 U3 U9 C; w  V2 ]Patient Report
# O( g6 j( |) E8 J( JA 16-month-old white child was referred to the3 l/ S/ z- e  x* C
endocrine clinic by his pediatrician with the concern
7 z2 K# i6 G, q8 `of early sexual development. His mother noticed6 S" {% ^7 M' j# U" i
light colored pubic hair development when he was
$ @! E/ U! L2 _6 s, ^5 \- E, [From the 1Division of Pediatric Endocrinology, 2University of  s) {, S* [3 ~" m, U8 l. h
South Alabama Medical Center, Mobile, Alabama.  E7 t2 O0 X. t) c8 p
Address correspondence to: Samar K. Bhowmick, MD, FACE,  L3 |7 f. B$ D8 x, R; Q' G4 e
Professor of Pediatrics, University of South Alabama, College of
$ X0 Z1 ]3 O- yMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
3 e/ {$ X- ^! M: P* |- l$ i  ^! Ge-mail: [email protected].0 X, g! K! S( Y% W; a6 [
about 6 to 7 months old, which progressively became/ L7 s  ^# `& N
darker. She was also concerned about the enlarge-, ]3 F. j! x5 E. @8 Q
ment of his penis and frequent erections. The child% y7 U0 o) J$ J  G' C1 n! G
was the product of a full-term normal delivery, with
0 ]! x& M3 z1 F/ s+ K$ K, u3 va birth weight of 7 lb 14 oz, and birth length of# X* ~9 J4 q" |( b& o
20 inches. He was breast-fed throughout the first year
6 d% x8 K: ]/ t3 zof life and was still receiving breast milk along with2 \7 N2 J/ D1 P) F5 n: R, v
solid food. He had no hospitalizations or surgery,
5 ^1 e  C! u" c7 ^" band his psychosocial and psychomotor development
( K3 A* R# `, Y; Q3 ]was age appropriate.6 n' _- e) U# T; C' [
The family history was remarkable for the father,9 X) }& T- V' [+ ~* J! k) Q
who was diagnosed with hypothyroidism at age 16,8 N4 B; ?4 ^3 {1 C# B# a% b0 ^
which was treated with thyroxine. The father’s* g, }+ `4 ]$ p& c) @
height was 6 feet, and he went through a somewhat
& a& G- _0 V  @7 ~8 j, U% S5 G! ^early puberty and had stopped growing by age 14.! k. d% [. j6 ]8 U$ n
The father denied taking any other medication. The
0 L2 a8 y5 ?2 u' \1 k) p" Pchild’s mother was in good health. Her menarche
2 X. }9 \' l5 u! }7 o/ pwas at 11 years of age, and her height was at 5 feet
# T5 b- e8 @- k4 |5 ?. K5 k+ j5 inches. There was no other family history of pre-
. w) {  j9 _! d2 l4 ~" Dcocious sexual development in the first-degree rela-0 l# M: e" {) I( A
tives. There were no siblings.- B8 h" Z' X, p' Z1 w
Physical Examination
4 k/ G/ y! u  x3 O6 Y" ZThe physical examination revealed a very active," `8 F3 r% e  q+ m- A) G# I
playful, and healthy boy. The vital signs documented
2 x: k. N- m6 Xa blood pressure of 85/50 mm Hg, his length was6 U+ a5 a8 r$ ?. A7 |$ M5 L! o
90 cm (>97th percentile), and his weight was 14.4 kg
1 D, K  o  L; ~$ l+ Z+ C6 _$ ?(also >97th percentile). The observed yearly growth
8 }4 [9 s% w7 j$ m' evelocity was 30 cm (12 inches). The examination of" H/ K* O, w+ L+ V+ ^* O; o
the neck revealed no thyroid enlargement.9 ]! ^* C0 @4 n/ U9 y  w
The genitourinary examination was remarkable for
; p& v# z( I/ H* jenlargement of the penis, with a stretched length of% P; i, V  ]+ ^+ _# l3 i
8 cm and a width of 2 cm. The glans penis was very well" A6 f! G% d# U% s" B5 f: G
developed. The pubic hair was Tanner II, mostly around
1 I) @* X% u# h. Y540
) }  C  g9 {- M" J3 W9 N$ Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, x8 t+ e  g. `8 X$ h5 ^9 Z
the base of the phallus and was dark and curled. The
7 x7 c- J( g/ }testicular volume was prepubertal at 2 mL each.
- e- P) `- o! Z8 _6 MThe skin was moist and smooth and somewhat# c! \6 {2 c' Y* t  B. V* Y2 A
oily. No axillary hair was noted. There were no( r1 y0 Z9 ^/ n" J
abnormal skin pigmentations or café-au-lait spots.
0 c+ B0 \& M( N; D9 g+ aNeurologic evaluation showed deep tendon reflex 2+& y% U: s8 H* v; ]5 V$ u- Q: t, B
bilateral and symmetrical. There was no suggestion
& H( Q% J& |6 p! pof papilledema.
2 g" f$ m2 w9 h$ p! B9 j2 U* r8 sLaboratory Evaluation) E+ K/ r: o% Q2 q0 d4 r5 g
The bone age was consistent with 28 months by
) v- l5 g$ S8 @0 ?, |, k1 E* Ausing the standard of Greulich and Pyle at a chrono-
7 w4 j; i% `0 {7 ologic age of 16 months (advanced).5 Chromosomal4 h$ V. T! T* X
karyotype was 46XY. The thyroid function test
; S! w) R7 q3 \2 x* _showed a free T4 of 1.69 ng/dL, and thyroid stimu-
% I( D) A9 J+ N% \8 L/ ], alating hormone level was 1.3 µIU/mL (both normal).
7 x8 h* m/ I5 sThe concentrations of serum electrolytes, blood
0 x  t& W) Q+ h0 J* o  qurea nitrogen, creatinine, and calcium all were
& n' G; ^  _  F# o- u# L2 R& Owithin normal range for his age. The concentration
0 d8 R/ `5 T% L, {3 s# @" M/ c; Pof serum 17-hydroxyprogesterone was 16 ng/dL- ?: V0 Z& ?/ E% E; H% v
(normal, 3 to 90 ng/dL), androstenedione was 20
- `; S# {) `# ]2 ~5 k6 [  v3 Png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 N. O9 ^* I- X" k! I) S1 g( Xterone was 38 ng/dL (normal, 50 to 760 ng/dL),/ l5 E, C, G6 @# V
desoxycorticosterone was 4.3 ng/dL (normal, 7 to& {% t5 X0 S  T  O1 J; k! |
49ng/dL), 11-desoxycortisol (specific compound S)
2 h, l( |. z3 S# gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
- b. _4 ]  |8 }& X3 Vtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 f/ x2 o5 ~+ U
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 U; g1 w% [/ T! @) o) tand β-human chorionic gonadotropin was less than
' c" z4 z8 r; ]& \; Y5 mIU/mL (normal <5 mIU/mL). Serum follicular/ |' e/ ~; F4 Q& \4 ^
stimulating hormone and leuteinizing hormone% T* ~9 ]1 P, C# U) f2 z! D3 _4 S
concentrations were less than 0.05 mIU/mL; j( e* V2 [- _8 S: D
(prepubertal).
; O6 b' ^+ {' E1 g" A! x- XThe parents were notified about the laboratory
8 n- g2 U. O: W0 c& jresults and were informed that all of the tests were
; C6 K! M6 S" M% k1 inormal except the testosterone level was high. The
* h1 {  w3 a( ]# @follow-up visit was arranged within a few weeks to
5 W0 l* }3 q9 j$ x/ Iobtain testicular and abdominal sonograms; how-6 Q3 ]( _/ t9 o* L1 T7 c
ever, the family did not return for 4 months.
* b+ i3 e. ^# ?' \$ ~9 cPhysical examination at this time revealed that the: v6 x1 s4 g: {
child had grown 2.5 cm in 4 months and had gained
& o! _. L! `8 [0 B- g2 kg of weight. Physical examination remained2 P  C$ D) P* ]! d' R" G/ I' @
unchanged. Surprisingly, the pubic hair almost com-
2 {9 t. c" }' u/ J7 gpletely disappeared except for a few vellous hairs at" q9 l! D# @, J# o! N6 X
the base of the phallus. Testicular volume was still 2
0 l1 i. `& w# B5 J" e, S) g; q5 j8 CmL, and the size of the penis remained unchanged.' E  X% G1 P. ^* E) B- q
The mother also said that the boy was no longer hav-8 H  y- n, d" z* T& `
ing frequent erections.% Q% D6 K2 x* B' m, z& ]
Both parents were again questioned about use of
4 n/ l% Q: b; {& ]' E0 p# @% ^any ointment/creams that they may have applied to& ]) \& A) p, `
the child’s skin. This time the father admitted the
* c. D8 W/ K% Y& X# FTopical Testosterone Exposure / Bhowmick et al 541% h0 l0 I  K7 @- l3 Y; a7 l
use of testosterone gel twice daily that he was apply-+ n$ p7 E5 q+ r) {8 E
ing over his own shoulders, chest, and back area for+ L2 ^" U: H8 f& w5 J$ y8 ]- G2 v
a year. The father also revealed he was embarrassed6 I- {# ~0 U- }3 f6 e# ~
to disclose that he was using a testosterone gel pre-; s( q0 x9 i7 @5 L% p( J
scribed by his family physician for decreased libido9 o$ e2 \. t* O
secondary to depression.
/ e  m" d) `4 N" C& p* `The child slept in the same bed with parents.
9 N- _6 t- V+ B0 J9 ]The father would hug the baby and hold him on his
  z7 Z% W% E( H- L3 M, U. L! ^chest for a considerable period of time, causing sig-
1 V5 D' p3 m5 X8 onificant bare skin contact between baby and father.
- q9 f  \$ {$ V/ KThe father also admitted that after the phone call,1 I, v' q! v2 q7 f
when he learned the testosterone level in the baby
6 I* `: _2 ~' c5 awas high, he then read the product information
5 D" P/ V1 d" p: N' y& m+ @packet and concluded that it was most likely the rea-. M& k0 @7 l3 s! E& g( b- A- ^
son for the child’s virilization. At that time, they1 u; p* |7 Q( P- d# Y
decided to put the baby in a separate bed, and the
1 P1 @# M! T, {$ k- U) ~5 Rfather was not hugging him with bare skin and had" M, b3 @" i; b$ x. j% Y
been using protective clothing. A repeat testosterone; n7 m0 j4 h* u8 X
test was ordered, but the family did not go to the
1 @; f4 i  m1 M  u; ^, dlaboratory to obtain the test.
# \  W3 X6 r* V: w. xDiscussion! V5 X$ u' e9 s, u3 Y3 Q0 u. [" x
Precocious puberty in boys is defined as secondary
. T+ [' U; N" p7 t1 |& J' ]. A1 asexual development before 9 years of age.1,4' @( v1 B" G9 R  n. a/ p
Precocious puberty is termed as central (true) when
1 D& y! i) y, ait is caused by the premature activation of hypo-
2 i1 }" c: [4 s+ N: |thalamic pituitary gonadal axis. CPP is more com-
- l. u7 X' F" h$ H& B' _7 H; xmon in girls than in boys.1,3 Most boys with CPP' S  u* T$ B7 i
may have a central nervous system lesion that is
- F$ e: T: P6 Iresponsible for the early activation of the hypothal-# s: m* P) ?" V+ }5 I& A
amic pituitary gonadal axis.1-3 Thus, greater empha-+ A1 e* ?6 S/ p' F4 B
sis has been given to neuroradiologic imaging in0 J& y' H. X; b; J2 X1 h
boys with precocious puberty. In addition to viril-
( _; ?+ h0 b7 Z. q' I' Kization, the clinical hallmark of CPP is the symmet-
4 _; k0 {' H# ?# S: t2 Nrical testicular growth secondary to stimulation by0 J0 d; T% r' O" D
gonadotropins.1,3; O2 M. W" J* \8 z
Gonadotropin-independent peripheral preco-4 F& I2 P0 R: P: q: q
cious puberty in boys also results from inappropriate5 H. m- W' b; i" |) e$ D5 p, _
androgenic stimulation from either endogenous or
4 {: M  C. }' C; g7 Pexogenous sources, nonpituitary gonadotropin stim-5 ~; }7 F# x% q$ `' w
ulation, and rare activating mutations.3 Virilizing: ^6 a+ W0 A/ H. m& e8 K1 E
congenital adrenal hyperplasia producing excessive
, K( R0 h% _9 Y. t9 \5 C/ \adrenal androgens is a common cause of precocious# e7 ]/ H9 s- N( @  B
puberty in boys.3,4
& M3 i/ M5 G1 Z3 A) yThe most common form of congenital adrenal
; h& u) f0 q. |! H6 t( [hyperplasia is the 21-hydroxylase enzyme deficiency.( b# p5 w2 e5 M' U
The 11-β hydroxylase deficiency may also result in
7 T  X- {  D* O* ]excessive adrenal androgen production, and rarely,* q" l' f, r% I
an adrenal tumor may also cause adrenal androgen  v6 }3 s' C6 a, f4 X
excess.1,3
5 V7 @+ H& u: B+ H! Z0 K  Kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' N# j- K- t! Q: Z4 L! a5 v$ q9 x% P542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, h# y: D2 g% l( \% A; s9 YA unique entity of male-limited gonadotropin-) \! r4 H  ^& `2 o  E- h$ U
independent precocious puberty, which is also known! M/ b7 ]8 j& r* ~2 ~' y) ]
as testotoxicosis, may cause precocious puberty at a+ M% Q4 c( H$ M  q
very young age. The physical findings in these boys* I+ u# B& M; P1 C
with this disorder are full pubertal development,
, J1 r+ H) I2 W8 h0 \including bilateral testicular growth, similar to boys
8 x# c# B7 X, {8 n4 Wwith CPP. The gonadotropin levels in this disorder
2 }6 ^9 Y1 @9 l4 g$ }  |2 u; }2 H0 I% Kare suppressed to prepubertal levels and do not show
. \5 N5 k4 n  K& q2 r6 Qpubertal response of gonadotropin after gonadotropin-
, Q' ^" u3 S, dreleasing hormone stimulation. This is a sex-linked* V, _$ X" E6 P: h* p3 U
autosomal dominant disorder that affects only: ^6 T* f, ?, h; K5 t1 l
males; therefore, other male members of the family/ o# A2 p! x3 q- X4 y- v1 x
may have similar precocious puberty.36 E" J" e4 A8 a, `
In our patient, physical examination was incon-, k0 h: p' g$ c* q$ K# J
sistent with true precocious puberty since his testi-7 w4 P( V! r6 \: b5 Q. B  e0 Z
cles were prepubertal in size. However, testotoxicosis+ Z! \* ~7 M" J% ]
was in the differential diagnosis because his father; @2 g1 F- }: L& s& k4 j7 }* ?+ H
started puberty somewhat early, and occasionally,
) \' d$ ~. ]% W' Ptesticular enlargement is not that evident in the/ {- {4 I* Y2 `/ Q4 ?0 G
beginning of this process.1 In the absence of a neg-5 I/ `! M- r; |9 W
ative initial history of androgen exposure, our/ @7 `5 t  U0 W- i3 u- _: u8 B# u& t
biggest concern was virilizing adrenal hyperplasia,  D% S, M& Y# ?) j7 ]
either 21-hydroxylase deficiency or 11-β hydroxylase; r% a" p3 ]0 d0 @# n
deficiency. Those diagnoses were excluded by find-
. n& Z- X" F. y5 A% ^ing the normal level of adrenal steroids.
7 p3 ^1 ^+ D* K2 ^: I2 }The diagnosis of exogenous androgens was strongly0 X8 I. o+ y4 w/ ^9 h
suspected in a follow-up visit after 4 months because1 d1 O+ w3 f: t+ ]5 a
the physical examination revealed the complete disap-+ g! g  l9 e0 V% R
pearance of pubic hair, normal growth velocity, and) k+ ?0 e! c& b  c. m
decreased erections. The father admitted using a testos-
- `) D& b" ]- @terone gel, which he concealed at first visit. He was/ B' ]& U% E+ d9 [1 V& W
using it rather frequently, twice a day. The Physicians’& F$ N5 Z% t# W, w
Desk Reference, or package insert of this product, gel or
% r9 n- X. z# mcream, cautions about dermal testosterone transfer to
' K! \* h7 M1 @$ Cunprotected females through direct skin exposure.
5 f1 [* T- K& Q) }( o. eSerum testosterone level was found to be 2 times the
+ E2 k1 t( m  G3 wbaseline value in those females who were exposed to! Z. m* G2 T0 B% }; C
even 15 minutes of direct skin contact with their male
8 L- l4 ^& C1 k' k  M% spartners.6 However, when a shirt covered the applica-
5 ~3 G: ~5 t5 F7 ]tion site, this testosterone transfer was prevented.
7 f  L) D9 D4 c2 H4 eOur patient’s testosterone level was 60 ng/mL,
2 m  `+ s3 q0 V8 D9 `+ T- bwhich was clearly high. Some studies suggest that4 i. i% F) w$ c, |
dermal conversion of testosterone to dihydrotestos-
/ l9 g: n  |; Qterone, which is a more potent metabolite, is more# @4 T3 g  L2 t3 g
active in young children exposed to testosterone
9 N" b* W) d; ], S. Y3 A+ ^; Oexogenously7; however, we did not measure a dihy-
( t8 q% S  k. k6 c6 V4 }4 x& `5 idrotestosterone level in our patient. In addition to
  `1 k" j* b5 l( `virilization, exposure to exogenous testosterone in
& c+ S( V8 e9 P* Lchildren results in an increase in growth velocity and
1 s' t4 N5 K% aadvanced bone age, as seen in our patient.
6 x; \8 L3 ~3 ^5 P5 WThe long-term effect of androgen exposure during' z3 v% U; c) K+ _% [, x
early childhood on pubertal development and final; v+ I! r4 O% c# [+ f9 U
adult height are not fully known and always remain
, B" R4 t# ^6 @' }! G+ Q& pa concern. Children treated with short-term testos-8 C! I4 {( M1 i% r0 J6 k! h
terone injection or topical androgen may exhibit some( A2 X) E/ M8 c. A
acceleration of the skeletal maturation; however, after6 l5 o! D7 l" }' D$ h6 L- H  f# _
cessation of treatment, the rate of bone maturation
! g) K& O0 r* X& L* J- z2 gdecelerates and gradually returns to normal.8,9
* w9 W' u0 }1 P: H: ?There are conflicting reports and controversy
5 `! `8 H/ r# I: {" O& N' B  @; Z) wover the effect of early androgen exposure on adult
8 z) a" ?9 ?/ }% p' [7 |0 Epenile length.10,11 Some reports suggest subnormal
7 A4 r5 N+ {+ Sadult penile length, apparently because of downreg-
$ @" W# @: I+ w) j9 g. r6 nulation of androgen receptor number.10,12 However,- s/ v3 }2 T! r; s1 @* C/ I& O
Sutherland et al13 did not find a correlation between3 W* o/ V% c$ X. D/ `9 L
childhood testosterone exposure and reduced adult: a9 y  [1 o9 m
penile length in clinical studies.: Y. W) \8 o0 N7 n4 o& T
Nonetheless, we do not believe our patient is
% |* u8 f2 v: J/ }8 A7 cgoing to experience any of the untoward effects from' P" x5 t/ x: \2 N$ p
testosterone exposure as mentioned earlier because9 L( T5 N' G* C- }  p- I- k* e
the exposure was not for a prolonged period of time.! o' e. R; e9 s7 D" n: Y
Although the bone age was advanced at the time of! |3 J! _, l0 z! z) S) D& X
diagnosis, the child had a normal growth velocity at
- l/ w& z# H: Gthe follow-up visit. It is hoped that his final adult
3 O4 U% Y& T# x0 Vheight will not be affected.
% A. }# L3 ?4 I0 Y5 M( u2 VAlthough rarely reported, the widespread avail-9 Q  X" a9 W5 R$ L7 y& N
ability of androgen products in our society may
! u8 d0 a5 y6 F9 }8 M4 Z- Eindeed cause more virilization in male or female9 G) ]9 }$ h3 \" c  q8 i7 J/ j* X
children than one would realize. Exposure to andro-
3 ^2 L6 X( W  O+ u& \gen products must be considered and specific ques-
( P7 R' b* e0 L9 ntioning about the use of a testosterone product or
2 p9 U$ |* ?( p! Z+ ~2 }gel should be asked of the family members during/ c$ ^6 n( r3 M# u
the evaluation of any children who present with vir-6 `, \9 Q: `% G8 K
ilization or peripheral precocious puberty. The diag-
- A! \+ i9 O8 ]1 Gnosis can be established by just a few tests and by
3 l" j2 ]& S) x8 yappropriate history. The inability to obtain such a! v7 K7 R) O  l2 D8 N
history, or failure to ask the specific questions, may% t0 K3 m8 s8 M& L1 y
result in extensive, unnecessary, and expensive
1 f& ]0 P0 I! E1 X& {8 F# P9 Minvestigation. The primary care physician should be7 z5 X0 c, Y/ t2 l/ m; g9 \
aware of this fact, because most of these children
* J, h# y- E9 R( jmay initially present in their practice. The Physicians’9 j$ F* S0 `+ j0 E# {  x
Desk Reference and package insert should also put a
* @9 r" R/ n" P# E3 O3 A! n% Z# Dwarning about the virilizing effect on a male or
* N" j/ Z# E) M+ B3 I; s4 h. Wfemale child who might come in contact with some-
9 A! D, E/ N& \" N. V. C% R  Fone using any of these products.- M, A! ?' V' K, M$ P
References. L9 ?8 g  I" C# L. n. a+ _- U
1. Styne DM. The testes: disorder of sexual differentiation! B  r* q5 P+ `" H
and puberty in the male. In: Sperling MA, ed. Pediatric$ {5 }1 m" D7 H3 Y% @' ]4 n+ M
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 G5 d! Q- P9 [( N  W, R0 j$ q" q2002: 565-628.
7 f+ J1 w' @5 r4 `2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious/ C5 ^+ ?6 U# S: E4 ^
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old" g" l. c7 W# Z7 Z- d$ `( }
Boy Induced by Indirect Topical  A' y( ~) o* i! @$ Z+ O6 d2 Z
Exposure to Testosterone
0 F5 G" N. V2 a2 v+ O5 V, KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 p+ u2 i, b0 p( sand Kenneth R. Rettig, MD1- z9 J& E3 u' ?$ J6 N5 X0 k0 j
Clinical Pediatrics
; G+ ~  Z6 |% RVolume 46 Number 6
+ T9 D; o( F* s' W1 AJuly 2007 540-543
; f9 n3 n* q% X  K© 2007 Sage Publications
6 O$ Q( k7 {( T: e  S% \10.1177/0009922806296651
" L5 I/ I7 b0 N2 F. hhttp://clp.sagepub.com
- I' G$ _0 f% chosted at
$ Y7 b, {( B9 d; g6 R2 `: |3 Q3 Nhttp://online.sagepub.com# i5 w' o( ]% C, k0 p6 v4 K* v/ a
Precocious puberty in boys, central or peripheral,
! G) ~; T  H( {- i% Y+ P9 eis a significant concern for physicians. Central( m- r0 F4 ~# p' e/ l  Y
precocious puberty (CPP), which is mediated  W2 h0 R4 R9 W( ]/ W; t
through the hypothalamic pituitary gonadal axis, has
/ k/ P+ r' E9 a! I* j  Ha higher incidence of organic central nervous system
: S; Q9 A, z7 blesions in boys.1,2 Virilization in boys, as manifested
, O2 g: Z1 K. N  _5 `by enlargement of the penis, development of pubic
- e, }# o% j8 S* y% `6 @. d2 Phair, and facial acne without enlargement of testi-  ?; e' U0 J# U9 v8 d
cles, suggests peripheral or pseudopuberty.1-3 We, Y6 K$ U# g0 g+ I4 X
report a 16-month-old boy who presented with the
2 y0 T+ p0 i' N; Z5 eenlargement of the phallus and pubic hair develop-
4 Z; o  X  q$ G7 k3 S, g/ wment without testicular enlargement, which was due
( g$ o* R% x& ~' j% zto the unintentional exposure to androgen gel used by
0 x4 W; x, p; z# J1 U, ]  {9 Z2 Vthe father. The family initially concealed this infor-
0 [0 j/ [1 _' ?( z0 Y) lmation, resulting in an extensive work-up for this
: t2 g4 n; w! Z& [$ e! u( n* Lchild. Given the widespread and easy availability of
/ p7 a/ K( K& ?testosterone gel and cream, we believe this is proba-- e$ h+ g6 }8 F# f( U
bly more common than the rare case report in the: C' e$ r( ]' l' m' y, X$ i
literature.4* K4 g0 {$ H: {) s" _
Patient Report0 S. T& r: ?1 O9 o7 z) b( @' ?
A 16-month-old white child was referred to the
" e, g1 L" @2 S/ {  Q: gendocrine clinic by his pediatrician with the concern
8 S8 ?; {' {5 _0 q2 wof early sexual development. His mother noticed
* `4 B) ]( }7 L+ K. dlight colored pubic hair development when he was
' g# v# Z- I5 O  X( X: SFrom the 1Division of Pediatric Endocrinology, 2University of8 y: x, V# |. o6 t
South Alabama Medical Center, Mobile, Alabama.
& @3 k1 j; q" }& |Address correspondence to: Samar K. Bhowmick, MD, FACE,
) }7 _) \' s+ t: F, BProfessor of Pediatrics, University of South Alabama, College of1 l' S9 ?5 v& a* v+ u. ^! z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# M- Z) s0 |* ]+ xe-mail: [email protected].
: g: W8 M( B3 O- o) X! ], eabout 6 to 7 months old, which progressively became, ]/ z/ g4 ^" e
darker. She was also concerned about the enlarge-
& n* [1 A% n, q4 r: J6 x! Gment of his penis and frequent erections. The child
1 y0 \, w4 B4 s& lwas the product of a full-term normal delivery, with  g1 z. F2 P- F' W4 |) X6 D9 _
a birth weight of 7 lb 14 oz, and birth length of2 d& c$ c% t- ]* l
20 inches. He was breast-fed throughout the first year
" U- S1 ~* C1 [. C8 v& `of life and was still receiving breast milk along with
* W7 l0 O- y" ^3 s$ s  F3 _7 Usolid food. He had no hospitalizations or surgery,5 q3 a( j4 U" y
and his psychosocial and psychomotor development
0 k: N9 l6 X! @$ Wwas age appropriate.
6 N, L- o# Q* B; M2 EThe family history was remarkable for the father,
/ O+ k( Q7 Z/ P5 F! O) d4 \6 ~/ Ywho was diagnosed with hypothyroidism at age 16,  l1 }" j7 k1 A6 r# i, R: V
which was treated with thyroxine. The father’s; Q- F+ Y, B" ?9 o% @2 ~
height was 6 feet, and he went through a somewhat, }+ Y0 K* y2 W7 E/ `3 U7 a  u
early puberty and had stopped growing by age 14.' [, i2 ~% z3 k, B* U# F& X
The father denied taking any other medication. The
+ G, s! i4 I5 V) G& achild’s mother was in good health. Her menarche+ T+ z( \, |/ `$ Y* ~0 G
was at 11 years of age, and her height was at 5 feet
7 A5 B" z: M% ~5 inches. There was no other family history of pre-6 m% i# z8 {5 j$ h. p! i; m
cocious sexual development in the first-degree rela-
' e+ e, t; c; t( `, i- x7 I0 E. {tives. There were no siblings.
2 y( B1 P9 B0 sPhysical Examination: ^; u7 {( q: f) @* ]* L
The physical examination revealed a very active,
" S7 j2 z; S% s' rplayful, and healthy boy. The vital signs documented
2 ?1 D4 c7 O' a8 Y) {/ \  b! ta blood pressure of 85/50 mm Hg, his length was/ J; G$ |0 @1 w
90 cm (>97th percentile), and his weight was 14.4 kg
+ r: `5 C+ N' S; |( M$ D# W/ u(also >97th percentile). The observed yearly growth! }! Q  G4 H- L
velocity was 30 cm (12 inches). The examination of
+ h3 Y& ~+ ~, m' c0 v) v$ n, Gthe neck revealed no thyroid enlargement.1 R$ R0 I9 e# `4 p% m
The genitourinary examination was remarkable for
8 d5 K" P4 k0 [; K6 E6 Y6 Q. Fenlargement of the penis, with a stretched length of
( V2 ]! ^& x1 A& ?8 U, l8 cm and a width of 2 cm. The glans penis was very well
6 F4 Q# S# y, E$ E4 Z: qdeveloped. The pubic hair was Tanner II, mostly around
( L- e# X9 B6 L. T. ^5405 I0 p/ D) u% p, k- Q/ h/ {- O* H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; Z' A0 V  l1 O3 b8 ~
the base of the phallus and was dark and curled. The  d/ R: a7 `* `5 J2 k3 S
testicular volume was prepubertal at 2 mL each.- J* ^" P3 y9 |, |: x! A" G
The skin was moist and smooth and somewhat
  x) `( q4 S% O0 w& Coily. No axillary hair was noted. There were no, s. B6 g1 g# y/ T$ W" Q0 g
abnormal skin pigmentations or café-au-lait spots.
( V; ?( ^/ V: O- p& Y) P# iNeurologic evaluation showed deep tendon reflex 2+$ M/ m) I9 M* |; g  V
bilateral and symmetrical. There was no suggestion
' x2 g9 A9 O  Rof papilledema.
+ N9 z6 S. {7 l; Z; iLaboratory Evaluation8 s1 @' _! y) a
The bone age was consistent with 28 months by
$ b. U) `1 F& ~" L/ vusing the standard of Greulich and Pyle at a chrono-
5 n" A+ D7 \& o% X! ~1 t' t' k" k# wlogic age of 16 months (advanced).5 Chromosomal6 c& `% p9 K" R6 R6 U$ a
karyotype was 46XY. The thyroid function test
" |1 \" r1 `$ F6 r% F6 p$ Rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 V4 Q( Z  ?% j% J# }( v0 B0 clating hormone level was 1.3 µIU/mL (both normal).
" f* e4 P  i  `; B" R* _7 k3 R5 LThe concentrations of serum electrolytes, blood
! q1 p% l& u0 Z7 ~- k5 \& ?- jurea nitrogen, creatinine, and calcium all were
0 q7 N' Y& V9 \- D" L) W) iwithin normal range for his age. The concentration. ^. o" T7 t! e3 N6 p1 {4 u0 H( Z
of serum 17-hydroxyprogesterone was 16 ng/dL# {1 w  h) }/ L; I& K! Q
(normal, 3 to 90 ng/dL), androstenedione was 20
% A) f0 l9 \, C$ p1 V3 l& Hng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 e4 a. q! |4 U4 X4 T; a
terone was 38 ng/dL (normal, 50 to 760 ng/dL)," J+ ]7 k4 [( W4 j9 K( I" t
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
: Z  N4 F, k* L8 h) y/ b6 L49ng/dL), 11-desoxycortisol (specific compound S)
- Y2 e  b  f. D" lwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 t( Q: U8 F: p0 R& \tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
  n) c( W: Q" J$ k. X6 b' j; jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& N5 d: |8 y4 @# n! Y5 G  c# kand β-human chorionic gonadotropin was less than
+ G7 O: ?' r: b0 ^, T9 n2 ^+ k5 mIU/mL (normal <5 mIU/mL). Serum follicular" K* l3 y" X4 ?
stimulating hormone and leuteinizing hormone
& L+ h" u1 m7 {* ]& q1 nconcentrations were less than 0.05 mIU/mL7 Q# }) S. ^. @7 k4 s- N+ c
(prepubertal).  p7 {: Z! Q$ d) v5 P$ P
The parents were notified about the laboratory1 S0 `1 S4 ?9 D
results and were informed that all of the tests were
  m' Q; ?' l' k( |& l' N+ U; _+ gnormal except the testosterone level was high. The
" c" d- {( u6 ifollow-up visit was arranged within a few weeks to
; \+ f% T4 z5 D8 uobtain testicular and abdominal sonograms; how-( H6 ^8 |4 M3 S- z0 P
ever, the family did not return for 4 months.
4 B% Z6 K  j7 Q4 \: _) r1 nPhysical examination at this time revealed that the- m; K. X9 D& W% M! D
child had grown 2.5 cm in 4 months and had gained. I( t+ G- O" h8 J0 y& C: B
2 kg of weight. Physical examination remained
6 p0 z! w& m3 e; w  Munchanged. Surprisingly, the pubic hair almost com-
) ^; D! H4 M0 Bpletely disappeared except for a few vellous hairs at9 O  X1 @2 f7 K  Z+ v2 v
the base of the phallus. Testicular volume was still 2
3 O7 k4 o+ [- y2 D# N' n5 w/ BmL, and the size of the penis remained unchanged.
$ v1 a; T0 L; _6 _0 Q8 Y' JThe mother also said that the boy was no longer hav-3 c& ^6 H7 Q' q0 e. ~
ing frequent erections.5 G5 |( C/ p# O& \
Both parents were again questioned about use of
* o  J; d, e. Oany ointment/creams that they may have applied to
2 j5 x# @9 i* Y$ N; xthe child’s skin. This time the father admitted the- r% a  X2 f" \. K
Topical Testosterone Exposure / Bhowmick et al 541
3 W! v" J5 ]3 `4 H8 u4 P- ^use of testosterone gel twice daily that he was apply-
- D0 _1 @: V/ F6 I" H# G& @. Oing over his own shoulders, chest, and back area for8 Q' q6 g. |) R6 g6 ?# n
a year. The father also revealed he was embarrassed
) z9 g- E6 W0 s8 c) xto disclose that he was using a testosterone gel pre-
* i; R2 w: F  B3 C9 a! I: h, Y! g. kscribed by his family physician for decreased libido
* n2 d  x& `  {% x) f4 Isecondary to depression.
) p. z- H6 i1 YThe child slept in the same bed with parents.
; i& R! {- Z. \8 X. n9 mThe father would hug the baby and hold him on his
# G% [4 \8 j5 h; \+ `chest for a considerable period of time, causing sig-6 p& I! ]. B5 E2 I' k& x8 c0 p6 f- k/ v
nificant bare skin contact between baby and father.
/ ~9 ^! b* G" y. x" T6 Y. H5 iThe father also admitted that after the phone call,# A/ o- z) j' Z3 D
when he learned the testosterone level in the baby
2 _5 j, n* A" n- c4 k4 R0 g, Zwas high, he then read the product information
% `* m2 Z) N/ b5 g) {packet and concluded that it was most likely the rea-( |5 j% ~9 s9 g! o2 h
son for the child’s virilization. At that time, they
( Y! q* ?7 V+ Z* V2 kdecided to put the baby in a separate bed, and the
0 R9 N  C' n3 I; h) Y! n+ O% Cfather was not hugging him with bare skin and had4 t2 ~  f, ^/ S- t0 d
been using protective clothing. A repeat testosterone
- w; Q1 R, h( `test was ordered, but the family did not go to the
1 k5 Z5 ?; |% z3 C: K& Ulaboratory to obtain the test.
1 |2 r8 Z5 B+ O4 p' W: FDiscussion% f! |; X& D! |! q0 k8 N' W9 F
Precocious puberty in boys is defined as secondary8 S/ T3 {  r9 z" r3 l' M& l9 J4 K
sexual development before 9 years of age.1,4. p. B8 F# H) O0 X, `. x. K4 \
Precocious puberty is termed as central (true) when
* g" b7 U& h' ], y' P( ?it is caused by the premature activation of hypo-
6 O# _  P( l* c3 }thalamic pituitary gonadal axis. CPP is more com-& h/ ?: e2 l- x1 K9 b' n4 Z
mon in girls than in boys.1,3 Most boys with CPP
, G* i, g- m+ u/ k6 I% pmay have a central nervous system lesion that is1 B7 |( _2 D% D( X: \5 W6 G/ |
responsible for the early activation of the hypothal-$ {  H& @7 B* Z! E- J
amic pituitary gonadal axis.1-3 Thus, greater empha-. S8 z/ h0 g; g8 q$ D0 k- v
sis has been given to neuroradiologic imaging in
2 \& ?( K* p! D$ M8 A  s) O) F/ oboys with precocious puberty. In addition to viril-8 n0 t9 b! r% E* @
ization, the clinical hallmark of CPP is the symmet-! p1 r' [; _" G+ s
rical testicular growth secondary to stimulation by( x# `+ c  |+ a) M
gonadotropins.1,3/ N3 _( y1 \' [/ ?& J, v& D7 n
Gonadotropin-independent peripheral preco-" L* ?: T+ J2 f7 N  S4 R  Q
cious puberty in boys also results from inappropriate2 h. u1 z- q, S3 r6 F
androgenic stimulation from either endogenous or
8 g- L7 W5 E( v1 K! h2 iexogenous sources, nonpituitary gonadotropin stim-
- u9 |, @8 O1 F; T  n9 vulation, and rare activating mutations.3 Virilizing
" a8 ~, D9 a, Dcongenital adrenal hyperplasia producing excessive
- Q! @& T6 K  d  ], e2 Oadrenal androgens is a common cause of precocious
. M$ K) `) @. u9 v( B8 A& c5 j9 {# Dpuberty in boys.3,4
' Z: I0 {2 r7 U4 ]9 B+ j# BThe most common form of congenital adrenal! A, u- C! h0 D6 y& P' t  k
hyperplasia is the 21-hydroxylase enzyme deficiency.3 c' R0 }, ~6 W' f4 |) o" [
The 11-β hydroxylase deficiency may also result in
; m- b4 e2 F5 d: y* E* P7 Hexcessive adrenal androgen production, and rarely,1 ^: c* H# g& _* R" w
an adrenal tumor may also cause adrenal androgen5 N' o( F7 I$ n" k
excess.1,3
/ v: }" |# p3 A4 z% f% tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 d# F* ~% W, A/ b: ]; f8 y542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 \7 y& C9 P& \( S0 v
A unique entity of male-limited gonadotropin-
, e! [& T; J1 _9 N$ I6 n  H9 Jindependent precocious puberty, which is also known
# w" v9 R, |! Z7 h' W- tas testotoxicosis, may cause precocious puberty at a7 O! ^# z0 {1 L  x, c" q
very young age. The physical findings in these boys1 w0 \" O1 G% p1 \& T9 i
with this disorder are full pubertal development,
" j- Z# X0 w4 m9 P$ i7 Gincluding bilateral testicular growth, similar to boys# @& U; T  K/ k  O: p  u
with CPP. The gonadotropin levels in this disorder
$ K" M+ O4 c; u! M7 X. q$ vare suppressed to prepubertal levels and do not show/ U+ h+ |0 `& b& ?2 d! w/ g3 v3 B
pubertal response of gonadotropin after gonadotropin-7 [5 L6 I! z  G' t1 W
releasing hormone stimulation. This is a sex-linked$ G' K2 d! [0 ~( `
autosomal dominant disorder that affects only" d# ?/ F1 u' m3 U8 U
males; therefore, other male members of the family0 X: Z- J9 D# h: w. X
may have similar precocious puberty.3, z3 G! d$ A0 Q5 Z  ^/ U, K$ W; w
In our patient, physical examination was incon-( P  E8 u# U# r. t( C  {, D
sistent with true precocious puberty since his testi-. a8 G) M5 \7 x4 s, y* a3 a
cles were prepubertal in size. However, testotoxicosis# d  Y7 W) ~( n1 Q0 j
was in the differential diagnosis because his father. k' _. U2 v# A* J
started puberty somewhat early, and occasionally,/ \) |% L7 P  i  K% ?3 s
testicular enlargement is not that evident in the
# T0 z" |7 O: ^6 y! i) t' J* N' h/ Xbeginning of this process.1 In the absence of a neg-/ C: q4 G. y/ C. w
ative initial history of androgen exposure, our
$ S- |6 M; K9 u2 k5 d) h0 ^, gbiggest concern was virilizing adrenal hyperplasia,
% g6 F& K6 U& f0 neither 21-hydroxylase deficiency or 11-β hydroxylase( ^+ x% R4 G; f) {0 x! _: B
deficiency. Those diagnoses were excluded by find-% |7 j; y; M$ e3 l
ing the normal level of adrenal steroids.
4 `1 s* X' s: ]& l. v. S; c5 ]The diagnosis of exogenous androgens was strongly( s- l7 B. S4 H9 S) z1 o
suspected in a follow-up visit after 4 months because4 i- J. ^4 ]* h: }, z
the physical examination revealed the complete disap-0 Y' N. i. Z4 ^( z; p; \' X. k
pearance of pubic hair, normal growth velocity, and. G$ j% [2 o. G+ k& k0 [$ G( U
decreased erections. The father admitted using a testos-- |" w0 i2 _  T8 H
terone gel, which he concealed at first visit. He was# a) V( i+ v. p" V  z$ E$ @8 n
using it rather frequently, twice a day. The Physicians’8 Q3 Q  C" l7 }
Desk Reference, or package insert of this product, gel or
1 z3 P# P0 e, M! \( Ccream, cautions about dermal testosterone transfer to
6 [  F3 O0 }1 n! n* `unprotected females through direct skin exposure.) o3 U! Z+ a. a
Serum testosterone level was found to be 2 times the6 j6 u: t! P: h: C9 I. Z
baseline value in those females who were exposed to
7 t: ]" y4 q7 P, [2 P6 Reven 15 minutes of direct skin contact with their male
& g0 x: U5 N  m; I9 z. zpartners.6 However, when a shirt covered the applica-
2 k" S/ \5 F6 ~, O% Ntion site, this testosterone transfer was prevented.: H+ H' {: \+ Q8 y; `* \
Our patient’s testosterone level was 60 ng/mL,
( {, I1 V# Q2 C6 U7 ?$ Nwhich was clearly high. Some studies suggest that- I$ }2 J' f: V2 Z; x, Z# c
dermal conversion of testosterone to dihydrotestos-9 m+ E) p! o" `- m; E1 b; T
terone, which is a more potent metabolite, is more
- C% Z& r4 g. Sactive in young children exposed to testosterone
2 c5 }, X# P2 ]; Y/ @exogenously7; however, we did not measure a dihy-. t# A- T8 @9 P' A' b
drotestosterone level in our patient. In addition to
2 B! ~5 p4 ?4 ]" @virilization, exposure to exogenous testosterone in1 J8 Q# w/ h- C' \5 ?
children results in an increase in growth velocity and5 W7 l1 e3 G6 p% W4 k
advanced bone age, as seen in our patient.+ n/ d( _2 K/ i; m
The long-term effect of androgen exposure during
! y6 ?/ m8 E; V% M/ {% mearly childhood on pubertal development and final
' P+ k/ ~7 O% V5 {/ y* Dadult height are not fully known and always remain7 o$ @  J# {+ \- o3 \
a concern. Children treated with short-term testos-
6 N% n3 N& I+ ~1 R, G! Y, K+ N. Oterone injection or topical androgen may exhibit some- g1 h: m) x7 g3 i$ H# l
acceleration of the skeletal maturation; however, after$ q: V1 W9 `% V! A7 a+ A
cessation of treatment, the rate of bone maturation
4 v; N- L: b8 H; H, @0 Wdecelerates and gradually returns to normal.8,93 V! _5 s9 O& N4 n& g1 d
There are conflicting reports and controversy/ j* H0 t- F; }
over the effect of early androgen exposure on adult# M7 W* \: P( y9 c& d: z3 R* x
penile length.10,11 Some reports suggest subnormal/ e2 J8 F, k: t& Q. d2 s4 ?1 r
adult penile length, apparently because of downreg-
+ T7 o8 V/ o  o! dulation of androgen receptor number.10,12 However,
2 m9 S. ]  ]$ ]6 d8 V- ESutherland et al13 did not find a correlation between
, w6 D7 M! Z3 Y% s+ ^childhood testosterone exposure and reduced adult0 u  W- L, I) D7 A$ B2 Q/ w* h
penile length in clinical studies.
# T( l+ h3 E& s8 h$ D2 _3 @Nonetheless, we do not believe our patient is% O; H2 @9 Z5 D/ y' o$ @. \" b5 ?, I
going to experience any of the untoward effects from
8 L, `& d6 s" W  ^# p9 Ltestosterone exposure as mentioned earlier because
2 W9 f+ \% {& U( U0 V. J' A) _7 ythe exposure was not for a prolonged period of time.9 V. s- C0 I" u, e5 E! e
Although the bone age was advanced at the time of
6 |% h' I8 o/ b8 m/ Ldiagnosis, the child had a normal growth velocity at5 `' k0 Y6 S/ |- U8 d
the follow-up visit. It is hoped that his final adult- R. u+ T. Z0 k1 T1 m, v& Q
height will not be affected.  k* c" {& }5 _. A
Although rarely reported, the widespread avail-
2 Q3 s" V) b7 B/ X3 b$ ~0 M5 x( cability of androgen products in our society may
7 K: ]& S# V: s; F4 K( windeed cause more virilization in male or female
- |! b+ I6 t' R8 {5 n4 Lchildren than one would realize. Exposure to andro-' ~; ^" I$ t& W% }( C
gen products must be considered and specific ques-% O; \" \7 W1 e3 L9 M. a( J
tioning about the use of a testosterone product or
, N1 u' t& ~( Dgel should be asked of the family members during
9 s( K/ d) s9 Pthe evaluation of any children who present with vir-
  e, P: l0 {) `8 b" j1 E0 k* Wilization or peripheral precocious puberty. The diag-
9 d. X& }9 f5 k  E$ snosis can be established by just a few tests and by2 h) P- c0 i% v* A0 y  d
appropriate history. The inability to obtain such a+ t$ q! V1 k0 u
history, or failure to ask the specific questions, may
& p' A9 ^" b# t  {8 ]result in extensive, unnecessary, and expensive
' d( _7 f% M; E: d2 j( Vinvestigation. The primary care physician should be1 J$ ?9 F9 Y. r+ f* B% ?" m0 b8 C
aware of this fact, because most of these children
1 N; I6 K9 r( U& X3 s/ N5 Q8 Dmay initially present in their practice. The Physicians’0 R* e( T. q) Z( I
Desk Reference and package insert should also put a
( j, f% H! ?0 ~% c( y7 nwarning about the virilizing effect on a male or) l& p8 x% P. d$ b! B
female child who might come in contact with some-
# L0 ]$ d1 I. b9 G% C5 ?one using any of these products.
) U% D& \$ ]0 p, l# M' pReferences5 z9 ]! ]7 [6 P' t( O  |1 ~! G
1. Styne DM. The testes: disorder of sexual differentiation3 b- Z  i0 g/ f
and puberty in the male. In: Sperling MA, ed. Pediatric, \/ D5 L  b* h: q/ Q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
5 \4 ~  ~! u. Q: B7 \2002: 565-628.
% `: O& X' h" E! Z% o8 y+ B7 n2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. V, a/ f+ C" w
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

: s0 _6 Q, }; Q3 w( G7 R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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