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Sexual Precocity in a 16-Month-Old, i" r. @9 d& R& r( R3 |+ A
Boy Induced by Indirect Topical
4 R! l/ e* G0 l. A0 CExposure to Testosterone
. D  L( k' G9 X7 R7 n% W1 uSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% X/ M2 Y" c0 ~8 r# qand Kenneth R. Rettig, MD1" @8 `/ ^- t$ g# z
Clinical Pediatrics
- q( x$ d1 e7 o5 O& _0 eVolume 46 Number 6
2 ?# E, `: l& r/ p. k: @July 2007 540-543& V# t; Z8 i$ h* Z& F
© 2007 Sage Publications3 ?' b# c& S) @. j# W1 k- |9 m9 U
10.1177/0009922806296651! s+ f: b: h  q: m
http://clp.sagepub.com
, e3 Q9 j/ D- Z. o! nhosted at, R- b4 N7 Y3 ~: ^
http://online.sagepub.com
3 b8 J# v3 i: i$ F& U) x: BPrecocious puberty in boys, central or peripheral,
8 Z/ N0 _, Y" W1 Pis a significant concern for physicians. Central
/ U6 q3 M* m2 u: h9 K0 o, gprecocious puberty (CPP), which is mediated7 E! }8 |3 `! E0 b. C- c
through the hypothalamic pituitary gonadal axis, has- k9 J1 K+ S& \" f4 u
a higher incidence of organic central nervous system
" n) h# E- L* e& o. Y/ Clesions in boys.1,2 Virilization in boys, as manifested& ^+ Z# v7 l5 M
by enlargement of the penis, development of pubic6 H- g$ V6 }) y! b1 ]" E" m
hair, and facial acne without enlargement of testi-
$ w& {' E3 R$ J- D3 d5 [4 w+ tcles, suggests peripheral or pseudopuberty.1-3 We  y0 w8 C' d/ e! u
report a 16-month-old boy who presented with the) q: G  z% ]; V) G5 X
enlargement of the phallus and pubic hair develop-4 t0 j' q0 O/ r$ e2 k
ment without testicular enlargement, which was due! `) k/ ^" X- F, b
to the unintentional exposure to androgen gel used by: h2 c' s9 i( I4 M- i
the father. The family initially concealed this infor-
$ z2 Y$ {3 D- \+ J! z+ wmation, resulting in an extensive work-up for this+ ~0 x( b. ]; v$ d' z( D. L* c
child. Given the widespread and easy availability of
! ~/ s6 Y6 l4 y0 ptestosterone gel and cream, we believe this is proba-5 S/ w1 V! r- |
bly more common than the rare case report in the
; u5 J8 H9 O& S  _5 u' l7 eliterature.4! l4 `( U. H$ F' R2 `' V
Patient Report
5 X1 G) W2 ?5 UA 16-month-old white child was referred to the
" @) D# Z# u: y4 {endocrine clinic by his pediatrician with the concern
2 I% z9 ~7 A5 t: O* Q# rof early sexual development. His mother noticed( \$ |" d, x+ i0 R5 I6 V9 [5 H
light colored pubic hair development when he was
1 M2 y  ]2 S2 \' {% q/ kFrom the 1Division of Pediatric Endocrinology, 2University of4 P; g! y) c7 c  i
South Alabama Medical Center, Mobile, Alabama.; _& h" e2 i- G1 }9 R
Address correspondence to: Samar K. Bhowmick, MD, FACE,( @5 Y! O) X) @
Professor of Pediatrics, University of South Alabama, College of
6 d2 f' N4 `5 D8 K" f8 z1 BMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ L: _0 T8 d6 ^6 Re-mail: [email protected].! _2 ~% O5 d9 K' a! c
about 6 to 7 months old, which progressively became
" b7 m& W; b$ ~' C* W8 xdarker. She was also concerned about the enlarge-
; b& Y! r0 R( C4 l1 `. B# ]' U% sment of his penis and frequent erections. The child& L/ y7 ?( w7 m* j0 A
was the product of a full-term normal delivery, with
: }9 H( t, b8 E- A) ]9 ka birth weight of 7 lb 14 oz, and birth length of2 @$ L6 J& b/ Y0 e( d: g
20 inches. He was breast-fed throughout the first year3 ^1 s; s2 Z% H0 F
of life and was still receiving breast milk along with1 m$ v' y& A/ w
solid food. He had no hospitalizations or surgery,
) I; V6 y% T' r3 C( s0 Land his psychosocial and psychomotor development
7 h+ f: I5 @. p# r: ?2 y9 f8 W7 jwas age appropriate.$ l/ E1 M  M2 w9 p
The family history was remarkable for the father,1 Q, b6 m% a  A0 s
who was diagnosed with hypothyroidism at age 16,
) h* p; B# Q( v0 q' Z  j/ gwhich was treated with thyroxine. The father’s
! m/ K3 O' R# vheight was 6 feet, and he went through a somewhat6 |! L; t) p% _. U  i( Q( w
early puberty and had stopped growing by age 14.0 d' D+ C4 X- Y+ i# U: o4 F
The father denied taking any other medication. The
* E7 u1 Y3 p- a0 I5 K& ochild’s mother was in good health. Her menarche
! T; P$ [0 A8 ~was at 11 years of age, and her height was at 5 feet
# z( H  A9 w: v' U- _) ]: J5 inches. There was no other family history of pre-
+ K& s& i. \1 D) q5 M& g; Pcocious sexual development in the first-degree rela-
6 N2 H/ c, R) N. X3 }$ T- jtives. There were no siblings.* {& s9 O( B  Y* n3 z
Physical Examination
3 M! g' o  Z: N6 R3 y  }. c; MThe physical examination revealed a very active,. ?+ g$ J" A$ Y) D5 g- C4 M
playful, and healthy boy. The vital signs documented
% y1 K6 J& X7 U1 v$ aa blood pressure of 85/50 mm Hg, his length was. ]5 u) o( ?+ Q
90 cm (>97th percentile), and his weight was 14.4 kg# V" E+ J# U9 B" e5 E
(also >97th percentile). The observed yearly growth9 _; s( V8 P8 V& t" \' P* {
velocity was 30 cm (12 inches). The examination of
% r. C. S- p6 J! ithe neck revealed no thyroid enlargement.
0 n( x& h2 |* m- E: I* eThe genitourinary examination was remarkable for* I2 E# {) a( ?% ?9 h( m
enlargement of the penis, with a stretched length of. W; d1 }4 w! O
8 cm and a width of 2 cm. The glans penis was very well5 k# X$ a7 _0 w9 Z6 R7 M
developed. The pubic hair was Tanner II, mostly around
9 H2 N$ V) T5 V5403 u6 p) O& u$ d6 \" O/ }. R# q( l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' Y5 X) A4 r+ A" J+ h7 h
the base of the phallus and was dark and curled. The* E& P9 X- w/ Y2 F' A3 \) g% H
testicular volume was prepubertal at 2 mL each.
9 L0 Z1 F; u* f$ mThe skin was moist and smooth and somewhat. e" I9 h1 H! Y! ]9 Q. M# P! O
oily. No axillary hair was noted. There were no
8 `- C/ [5 x% n' Babnormal skin pigmentations or café-au-lait spots.
3 Q  P9 @( p. V# j* T3 V2 SNeurologic evaluation showed deep tendon reflex 2+: Q+ j" ^; H5 p# q, ]2 G
bilateral and symmetrical. There was no suggestion
) h# |! ^% c. f8 \of papilledema.5 @: R! p7 c) K# h
Laboratory Evaluation3 \0 z3 V1 y1 `1 U
The bone age was consistent with 28 months by  h' H3 {/ X4 B6 Z( r
using the standard of Greulich and Pyle at a chrono-
9 u# z% V/ O  `9 s2 Y! g/ Rlogic age of 16 months (advanced).5 Chromosomal
# D4 A3 @, e% P" `3 R9 Ekaryotype was 46XY. The thyroid function test
1 Y2 p( Z8 V6 J- [. L% A/ vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-  m& j/ J- w+ Q+ d4 J
lating hormone level was 1.3 µIU/mL (both normal).
) H6 U9 y0 h* N- k9 g9 xThe concentrations of serum electrolytes, blood( J( E9 L' Z8 q
urea nitrogen, creatinine, and calcium all were
( v1 m8 z4 Z& m& Y# s- ~" P4 r" l, ewithin normal range for his age. The concentration- _5 B$ P( p2 O4 R7 `
of serum 17-hydroxyprogesterone was 16 ng/dL( c* _" R  g' [- k/ \+ ~
(normal, 3 to 90 ng/dL), androstenedione was 20  l7 [$ o8 r: N' W& o
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 f: X/ s- c/ O  z! R- s: X
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 }! C; P( K( [desoxycorticosterone was 4.3 ng/dL (normal, 7 to
4 m9 D9 T  ^/ i- d1 w! R+ n0 W6 z49ng/dL), 11-desoxycortisol (specific compound S)2 {  V4 ]0 Y4 r9 D" J) W
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) O/ _" i& t2 h2 q% ~6 Utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, E4 c3 t, k/ ^testosterone was 60 ng/dL (normal <3 to 10 ng/dL),- q5 |0 @' k. b2 Z- X9 J) Y8 y
and β-human chorionic gonadotropin was less than* h4 ~( R: e. R
5 mIU/mL (normal <5 mIU/mL). Serum follicular6 v# ]1 a0 h* L. w2 \, N. T7 D2 t& M
stimulating hormone and leuteinizing hormone
  ^9 c: _- o/ p/ ?concentrations were less than 0.05 mIU/mL7 n# J2 Y1 D' s. _/ o) r
(prepubertal).
+ W. S3 D: V# _& u1 s$ _0 @The parents were notified about the laboratory
9 v( L3 S" n( J2 tresults and were informed that all of the tests were+ Q4 T  [+ i; r: K2 U3 x8 ]
normal except the testosterone level was high. The
% m5 }/ V) X& |3 [) [follow-up visit was arranged within a few weeks to! C. u! V6 X" w4 _3 t# ~9 C& ]
obtain testicular and abdominal sonograms; how-4 z8 C: m5 A- W) h% R- a( x
ever, the family did not return for 4 months.
& }9 M$ }( Z2 ^# @# \9 ~Physical examination at this time revealed that the* t4 z1 x% Z* W5 s
child had grown 2.5 cm in 4 months and had gained
/ n" p& o) M+ g. W/ z2 kg of weight. Physical examination remained- ^5 o& Z$ z1 M2 P: E  F- |+ S
unchanged. Surprisingly, the pubic hair almost com-/ ^9 V( i6 y7 h3 A5 c+ E% m) a: x' w
pletely disappeared except for a few vellous hairs at" v  l. ^, |! C+ b5 e& d" W; ^9 G
the base of the phallus. Testicular volume was still 2
  O) d! ?- i. V7 ^+ y+ H4 KmL, and the size of the penis remained unchanged.
7 Y0 Q* O: _5 G+ V: W  F  lThe mother also said that the boy was no longer hav-
' J5 X7 c: m8 y7 j. y5 B& k: \$ `ing frequent erections.
5 K  T# R( A, p9 w  c  w  R+ p. BBoth parents were again questioned about use of
4 p2 y) T7 j' [) }/ q# t  N. p3 Lany ointment/creams that they may have applied to( T/ @# n7 p. _/ O9 k9 g0 K7 k$ h
the child’s skin. This time the father admitted the
9 r. o/ \& v4 f' N/ z. U& s' `Topical Testosterone Exposure / Bhowmick et al 541
5 @+ U0 F0 H% ?  O6 E9 u5 luse of testosterone gel twice daily that he was apply-& W2 K* {$ N& ^8 k3 c
ing over his own shoulders, chest, and back area for; b, k5 {6 @  P( t  m) j4 S
a year. The father also revealed he was embarrassed: ~" O, J$ a- S( M4 ^- g) p( F
to disclose that he was using a testosterone gel pre-
- |+ p" |0 @8 S' cscribed by his family physician for decreased libido
% v5 C5 t  O" s8 `5 l0 W8 \$ e/ U  x( Tsecondary to depression.9 M! p6 C" f$ ?( h- p0 ~* b2 ~! W
The child slept in the same bed with parents.
- E0 p% w% c+ y2 tThe father would hug the baby and hold him on his
# `) `- q1 {: `7 e$ ychest for a considerable period of time, causing sig-
3 ^4 U- b! h( A+ t* `" Jnificant bare skin contact between baby and father., E5 s/ ?- k6 y4 t' j: t
The father also admitted that after the phone call,5 d: y$ B1 E" s2 w
when he learned the testosterone level in the baby
6 _0 l5 [  O& cwas high, he then read the product information
- q6 D6 l4 k$ ]9 U7 |6 H0 P. wpacket and concluded that it was most likely the rea-
/ V+ s: N, ?3 d; T+ x- Uson for the child’s virilization. At that time, they
3 y0 X0 y/ {; @( w9 gdecided to put the baby in a separate bed, and the7 v. k  o) Z% t- z" T- Z! R
father was not hugging him with bare skin and had
2 [4 _' y- I7 C, tbeen using protective clothing. A repeat testosterone$ F2 Q- q6 H( t1 L
test was ordered, but the family did not go to the) Z; k! x( C. i
laboratory to obtain the test.$ Y- W0 \; N  d) k& U4 j% ~! J
Discussion/ w: f& n6 K7 u
Precocious puberty in boys is defined as secondary
# i# i. R" d0 t, i* Z3 G! Rsexual development before 9 years of age.1,45 d- o# {, Y1 k4 s0 N$ L
Precocious puberty is termed as central (true) when
6 z: [1 i1 n1 Rit is caused by the premature activation of hypo-+ m( m; k5 e4 G2 S! @
thalamic pituitary gonadal axis. CPP is more com-, b4 l* U2 q9 G" X$ F" \; F
mon in girls than in boys.1,3 Most boys with CPP
% o, ?- h- N$ B" E5 U# [4 r$ x5 Mmay have a central nervous system lesion that is8 B7 W1 s' H7 ]; \& U: B
responsible for the early activation of the hypothal-
3 b& W  X7 H. G: b9 t" Oamic pituitary gonadal axis.1-3 Thus, greater empha-, H' M. `& c" P2 F
sis has been given to neuroradiologic imaging in
( `0 I1 i+ b! V1 R+ x5 Cboys with precocious puberty. In addition to viril-
" ?9 h. n1 C9 P# A- {$ |ization, the clinical hallmark of CPP is the symmet-1 i& H4 G1 X8 x. \3 r9 c
rical testicular growth secondary to stimulation by( L$ A& D' b" p! ~
gonadotropins.1,3
5 ^) L1 m+ L: K) gGonadotropin-independent peripheral preco-
% j6 E' v, @2 c- J1 g, [3 Tcious puberty in boys also results from inappropriate
2 ~- }# T4 J( d, p1 a; Yandrogenic stimulation from either endogenous or
$ B4 m4 I( l& z. V# yexogenous sources, nonpituitary gonadotropin stim-% H. ]+ h' q& M
ulation, and rare activating mutations.3 Virilizing3 ~$ l$ [8 c7 a. s- c; |7 V/ E
congenital adrenal hyperplasia producing excessive$ Z3 |( q: y4 T
adrenal androgens is a common cause of precocious2 E8 R- k4 W( B. R
puberty in boys.3,4
% \8 F  t/ }% Q9 jThe most common form of congenital adrenal
! B& D) v! c4 R/ U* c0 r" khyperplasia is the 21-hydroxylase enzyme deficiency." |! u4 S/ ?* p  u8 Y
The 11-β hydroxylase deficiency may also result in" Z2 ?  t+ G- v( L$ [. t+ E+ b
excessive adrenal androgen production, and rarely,
6 o4 Y! m2 D$ u8 H/ q9 T7 A" Van adrenal tumor may also cause adrenal androgen
' L% C4 j$ S' h' V4 Fexcess.1,3) [# @% ?( w7 E& u8 T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 J1 F# e1 g" B7 T1 n
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; `4 {  C5 w5 X! s3 `# \
A unique entity of male-limited gonadotropin-5 ]( ~5 Q! y, t* K
independent precocious puberty, which is also known# t3 M  U7 g7 f/ Q8 [  P% J3 D1 D
as testotoxicosis, may cause precocious puberty at a
, O2 z9 s8 _; v0 u! \very young age. The physical findings in these boys
; J" P. M8 b6 m" k+ lwith this disorder are full pubertal development,$ h+ ~$ a7 N2 E- ~" F8 ?! j. L
including bilateral testicular growth, similar to boys
/ D$ n2 F3 s2 w, A+ a4 M% nwith CPP. The gonadotropin levels in this disorder
; G0 G+ ?! W. A: c( Q5 dare suppressed to prepubertal levels and do not show
9 x1 k* y! {" N: Vpubertal response of gonadotropin after gonadotropin-& G; ^$ {. i+ k2 Q: B8 j
releasing hormone stimulation. This is a sex-linked3 v8 \% U5 W" f4 @0 t6 j+ e
autosomal dominant disorder that affects only+ J/ H2 `' |* `/ t
males; therefore, other male members of the family' c! V7 R* {% G4 D, |/ L
may have similar precocious puberty.3
( Q0 Y. l" j/ B1 ^* s$ b3 [  X! E9 ^In our patient, physical examination was incon-4 b* U) |& ?6 _! ~" G
sistent with true precocious puberty since his testi-, }  j7 h1 P6 `0 |# r! i
cles were prepubertal in size. However, testotoxicosis
% c( i4 @% O, x6 ^( ~- \4 L, Xwas in the differential diagnosis because his father$ o; n3 x, L1 l' ?' K( R) g1 i, t, H
started puberty somewhat early, and occasionally,2 i' l. O6 n) \3 W7 ]& A  B0 R6 o& Z
testicular enlargement is not that evident in the9 E0 V( Z' w# N8 ^6 t1 J7 H
beginning of this process.1 In the absence of a neg-
: I% z7 P( f  v; G# t8 mative initial history of androgen exposure, our
2 ~  o$ w- u, r9 P2 nbiggest concern was virilizing adrenal hyperplasia,6 j! Q- K1 S! z
either 21-hydroxylase deficiency or 11-β hydroxylase$ A. V2 d1 R3 l) V! y
deficiency. Those diagnoses were excluded by find-% ^$ U5 Q4 j5 I. R
ing the normal level of adrenal steroids.
/ B: J; [5 ^1 h) n2 }The diagnosis of exogenous androgens was strongly
# K2 Q6 `8 ]. o8 s' J# Jsuspected in a follow-up visit after 4 months because) k/ \) r; v. F5 ^) {
the physical examination revealed the complete disap-" M& J: D+ g+ o2 Z/ E! r: J; e8 L0 t
pearance of pubic hair, normal growth velocity, and. h5 r9 ^0 c$ g; }( Z
decreased erections. The father admitted using a testos-
8 I5 K0 [1 B5 T- i, L) Jterone gel, which he concealed at first visit. He was
2 J* I5 j" M# C7 Iusing it rather frequently, twice a day. The Physicians’
$ Q* B3 x$ I" m7 aDesk Reference, or package insert of this product, gel or
4 B% _  [' K8 e' ]3 q) V1 vcream, cautions about dermal testosterone transfer to- @$ H, P$ S# d$ J
unprotected females through direct skin exposure." q9 A+ m& |* ~! S" @+ p9 x9 s
Serum testosterone level was found to be 2 times the* r/ b& D  l9 T0 `6 i
baseline value in those females who were exposed to
% m: s& K; F. U- H/ a3 Z, {, e3 {! Jeven 15 minutes of direct skin contact with their male
! C7 k) P1 u5 K# Apartners.6 However, when a shirt covered the applica-
  T" m% c2 B. u" \: N* c: Ttion site, this testosterone transfer was prevented.. X( S1 h% E2 O( f; H8 j
Our patient’s testosterone level was 60 ng/mL,1 n0 B/ `$ y/ ?* y/ w
which was clearly high. Some studies suggest that
+ e) {* T& Z/ ]4 d: kdermal conversion of testosterone to dihydrotestos-4 M3 A3 O) j1 r8 X' j1 u
terone, which is a more potent metabolite, is more8 ~1 Z" {9 D% w  b2 w
active in young children exposed to testosterone7 \$ b% @5 h1 T" X9 G9 Z* ]  ~8 b
exogenously7; however, we did not measure a dihy-& ]5 g# ^) D, C$ p% F
drotestosterone level in our patient. In addition to
9 H- l- _$ s( C' Rvirilization, exposure to exogenous testosterone in
( r9 o7 h+ c4 i) K" jchildren results in an increase in growth velocity and
% R2 G/ F! i; l1 }; |  Gadvanced bone age, as seen in our patient.
+ Y/ |5 Q  X  {- EThe long-term effect of androgen exposure during2 B' d  @0 h( J
early childhood on pubertal development and final& B6 ?8 b* s* D- C
adult height are not fully known and always remain- Y, k5 n% J; J8 v( q- x1 m
a concern. Children treated with short-term testos-
- ]5 _$ u  u1 Iterone injection or topical androgen may exhibit some2 c& z* F' |+ @( g
acceleration of the skeletal maturation; however, after6 f7 ]- m1 O, {! o& w
cessation of treatment, the rate of bone maturation
3 f1 a6 v' H5 q* q1 o' udecelerates and gradually returns to normal.8,9  G- R! R0 U" i1 B& n/ ?. ]
There are conflicting reports and controversy
" g# g  c; q% w3 Z% t3 Y/ ^over the effect of early androgen exposure on adult
- N& ?5 Z% {$ j) v! e) a6 spenile length.10,11 Some reports suggest subnormal% }* u  a8 A; B, b
adult penile length, apparently because of downreg-' D* p# D! g/ `) I8 n
ulation of androgen receptor number.10,12 However,) Q" j- H( X+ b% Y
Sutherland et al13 did not find a correlation between3 k3 o  g4 D4 [' T! B9 c) S" z9 w
childhood testosterone exposure and reduced adult6 f; A- V' b1 ~
penile length in clinical studies.
$ a/ ]* L$ @+ \Nonetheless, we do not believe our patient is& Y1 ]  \$ }5 p3 S/ P6 z
going to experience any of the untoward effects from5 p% @% O5 m) |% J
testosterone exposure as mentioned earlier because
, [& A1 }* y2 t$ ?" t& mthe exposure was not for a prolonged period of time.9 Y! i  B2 W3 a
Although the bone age was advanced at the time of
9 u0 ^& }# R4 P8 a! G& jdiagnosis, the child had a normal growth velocity at
0 j2 D/ D# |3 P$ W+ f/ t) K" [the follow-up visit. It is hoped that his final adult& }: s8 V$ m$ }& y: c, [2 ?
height will not be affected.
. G* p- c/ U: N5 e& PAlthough rarely reported, the widespread avail-, a: b7 P) f- t+ C) J
ability of androgen products in our society may5 X) z5 i+ S  \$ n, D/ m
indeed cause more virilization in male or female
+ w& i& u0 Z% E7 Q' `; b7 Lchildren than one would realize. Exposure to andro-& T: W1 k% {6 q! g  Y& n4 @" E
gen products must be considered and specific ques-
7 Y- S7 M* q& l. D: U6 P  ^5 F: [tioning about the use of a testosterone product or
. d0 `0 ^3 ^) \5 `6 M8 r3 [gel should be asked of the family members during
! N; |" t' j( z6 y3 A/ k& |. jthe evaluation of any children who present with vir-
( E) Q# v+ e) P# W% Filization or peripheral precocious puberty. The diag-
& K( K$ n( f/ I" T3 E+ f( ]nosis can be established by just a few tests and by
6 s) O) i5 E, \7 n. p( L: k" `+ D" pappropriate history. The inability to obtain such a
; n7 v1 ~0 C& O4 x+ \2 n' H8 x# Fhistory, or failure to ask the specific questions, may
8 w: z$ k' ^# J4 X) uresult in extensive, unnecessary, and expensive
" r, ~. i* ~) B1 c7 `investigation. The primary care physician should be
# y' z! F$ [" O& s* kaware of this fact, because most of these children
" e4 y5 `/ F. q4 ^0 p4 D" ~may initially present in their practice. The Physicians’
4 U; b: E, H. A( GDesk Reference and package insert should also put a- \* _! e4 ?1 p0 y: _6 j. A
warning about the virilizing effect on a male or
3 J" e! b* ?# d& c/ ~; i' {female child who might come in contact with some-3 H/ X# B! [6 ^- w) D/ I5 x1 q
one using any of these products.
$ p- K7 c/ _0 \) h' T' ^% nReferences5 K( j4 d% O) H
1. Styne DM. The testes: disorder of sexual differentiation
4 Z& h7 Q& t2 t# l3 O, y4 cand puberty in the male. In: Sperling MA, ed. Pediatric7 E) Z; s) o& T' a) @; t7 Y, U
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* Z- s2 q7 N" g6 {2 P
2002: 565-628.
0 p7 D! e6 V* x; W- c( M' e6 t2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- F. E9 @5 q0 _% }1 A! Lpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
1 h) x- p8 t4 U6 K, i+ n' M$ WBoy Induced by Indirect Topical& H. a7 M" X) y% [
Exposure to Testosterone
7 d; ^; Q4 h3 I, @' iSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ `1 R! F7 J& m3 r- F3 P; v; xand Kenneth R. Rettig, MD1
( Y! W% ]* G- i( S# I& QClinical Pediatrics
3 Z! U" G; l$ l7 u- F3 OVolume 46 Number 68 a' I- }! S4 a* o) G  Q( G
July 2007 540-543
0 v& k0 Q' _$ o: G© 2007 Sage Publications
" a( |) c8 L- X* l10.1177/0009922806296651
- E3 w$ o. q& Whttp://clp.sagepub.com! |- \! R" ?% ]. i" w; z2 \2 Q- F
hosted at( K- C# U8 i( Q  I0 Z0 {0 Z
http://online.sagepub.com& F# e* z) q* x- j
Precocious puberty in boys, central or peripheral,
/ c5 F0 ^* R, i- b) J8 Kis a significant concern for physicians. Central) K, w3 w; W: ]% R( \) N# _/ H
precocious puberty (CPP), which is mediated
/ w* s! g# w( m% C' ?$ k( ithrough the hypothalamic pituitary gonadal axis, has; `( i: a( l  Q" I! ]9 }
a higher incidence of organic central nervous system# r* G# l& m- d7 r
lesions in boys.1,2 Virilization in boys, as manifested, d, l4 h4 x( _/ {
by enlargement of the penis, development of pubic
7 Q, U7 J6 l0 o* [  f* m+ Dhair, and facial acne without enlargement of testi-
' l* E% Z% H0 `# r8 |) p- l( D& f1 T, Ncles, suggests peripheral or pseudopuberty.1-3 We
' ^# O) v6 [8 n1 yreport a 16-month-old boy who presented with the6 w* y# D& T  C" v; U3 b) G
enlargement of the phallus and pubic hair develop-
( g6 r: Q# ^1 \ment without testicular enlargement, which was due
6 i; d4 g# q+ }( U/ rto the unintentional exposure to androgen gel used by
$ k0 {$ F) i& l- \! f; jthe father. The family initially concealed this infor-% i% l* P/ C7 V- F+ y1 r
mation, resulting in an extensive work-up for this
7 d% _+ u' e3 D+ \+ J  D/ ?, xchild. Given the widespread and easy availability of8 Y! p4 T# _  W4 r( J; ?
testosterone gel and cream, we believe this is proba-
$ T" f  ^. f+ Lbly more common than the rare case report in the
! g8 [9 O' ?! `4 |1 D8 j; \- t( Mliterature.4$ C) g" s& ?* C/ E; ?; g4 V$ m
Patient Report8 J' @2 R# p8 |: p. D1 y
A 16-month-old white child was referred to the4 n& F' w1 C% a+ {% v. {6 u6 h: [* ^
endocrine clinic by his pediatrician with the concern4 [. n4 A6 T2 ]
of early sexual development. His mother noticed
; H# l3 p5 u4 z; A, klight colored pubic hair development when he was& Y/ G- S, W5 h/ }
From the 1Division of Pediatric Endocrinology, 2University of# M7 u5 d* ?( H$ s, x
South Alabama Medical Center, Mobile, Alabama.
4 J2 [! f8 f* g9 M2 G) F: \8 x7 IAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 @! T1 M% X9 R. y: U: d
Professor of Pediatrics, University of South Alabama, College of
% Q0 j0 s$ L" P* B1 i8 W" \4 y5 MMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 P( b9 o* t( G% D1 Y$ c+ fe-mail: [email protected].; X8 o+ Z6 e" x0 U1 E
about 6 to 7 months old, which progressively became5 r/ X, j2 `1 |# c1 @! N/ a8 z( ]+ L
darker. She was also concerned about the enlarge-( Y: x8 u$ _8 T4 `- f; t
ment of his penis and frequent erections. The child
) l( C* U3 A" O: j7 J( H) |' ?was the product of a full-term normal delivery, with% d% x3 l: s) F, P
a birth weight of 7 lb 14 oz, and birth length of
& p) G! t% k* l- ~7 A# W20 inches. He was breast-fed throughout the first year, D, j2 q( ?7 C) r* i# e
of life and was still receiving breast milk along with
3 g3 n$ Q- M" }- K+ R0 ^solid food. He had no hospitalizations or surgery,
! |3 D) J: a3 M1 y$ {and his psychosocial and psychomotor development2 C3 Q; G7 W$ j6 m" H
was age appropriate.
- h6 Y, N, j, A" G8 @- a- A9 b' LThe family history was remarkable for the father,
5 y  f' e) {" d0 v8 S% B/ Rwho was diagnosed with hypothyroidism at age 16,
) N1 b8 [% K$ q( xwhich was treated with thyroxine. The father’s
4 e  M$ y  j/ n2 S% ~9 P; \5 G7 Pheight was 6 feet, and he went through a somewhat$ s' L# x7 ?: q/ A- a' F" d) @
early puberty and had stopped growing by age 14.
1 u. e1 r: b0 R6 f- jThe father denied taking any other medication. The1 p; _$ }5 q0 i
child’s mother was in good health. Her menarche
7 y( i) @  P1 }7 t8 V2 k; H* d( swas at 11 years of age, and her height was at 5 feet
5 A3 c6 {# n2 I. b5 inches. There was no other family history of pre-
  N# K: e- J1 p  I, Dcocious sexual development in the first-degree rela-
1 h% b! d6 u, [. d' k5 V2 Q7 H. itives. There were no siblings.
/ G2 o7 X  [& o9 V9 |Physical Examination( y! M+ E( S( Y) m3 p' S
The physical examination revealed a very active,' K" k% F" s( ?# J
playful, and healthy boy. The vital signs documented
* v' X1 Y' T5 F1 S) V8 o' ta blood pressure of 85/50 mm Hg, his length was( S. K/ s4 W' v$ M9 \( b+ S; g+ w& U
90 cm (>97th percentile), and his weight was 14.4 kg7 G$ ]' H9 s4 G2 O# _
(also >97th percentile). The observed yearly growth$ Y. D" n* R2 V
velocity was 30 cm (12 inches). The examination of
* H. @2 ?2 u- Q4 f2 g0 q( C8 \" }the neck revealed no thyroid enlargement.
) M; D) s, r- C# Z7 RThe genitourinary examination was remarkable for
; g6 H( \/ s4 L8 Eenlargement of the penis, with a stretched length of0 z! ^4 c$ ^$ j
8 cm and a width of 2 cm. The glans penis was very well
$ [$ [/ ^; h2 T' m& I! kdeveloped. The pubic hair was Tanner II, mostly around
( m# U. {5 k. q5 a: h540
- w! _8 v0 T  @8 H: L; Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. A# g% B+ Z% d& [  r5 g
the base of the phallus and was dark and curled. The2 g9 n1 a, T3 c  w9 _% P* S. X
testicular volume was prepubertal at 2 mL each.
# v9 @0 f1 I: \5 {  D: g' bThe skin was moist and smooth and somewhat
& ?  p. x8 l: A6 B) c! N% y8 woily. No axillary hair was noted. There were no, Y% _$ |$ h: L, ]
abnormal skin pigmentations or café-au-lait spots.
: R5 {) t6 ?- t  VNeurologic evaluation showed deep tendon reflex 2+# J) D0 K, c: y' N7 P1 a$ z
bilateral and symmetrical. There was no suggestion
7 g% B( Y  M2 ?" D" |5 pof papilledema.: s- F) z: l2 v$ E( s# D
Laboratory Evaluation
- ]+ q& X( u& x; Y) DThe bone age was consistent with 28 months by
. q( J% v8 ?. xusing the standard of Greulich and Pyle at a chrono-+ t9 V/ h1 @+ }% X- {8 b
logic age of 16 months (advanced).5 Chromosomal1 R/ {, X) G; \, A: \. l) M
karyotype was 46XY. The thyroid function test% R( e  Q* n! q' l8 ^
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
, F) S/ E! R% U! \- p+ H  m, e: Plating hormone level was 1.3 µIU/mL (both normal).- Z$ J1 p! w1 ?  ^
The concentrations of serum electrolytes, blood
. v3 A5 u  v. X( }urea nitrogen, creatinine, and calcium all were
# V& b& t) P- V0 hwithin normal range for his age. The concentration5 B6 r" c' [/ |6 q" q) R; U
of serum 17-hydroxyprogesterone was 16 ng/dL
# r3 j8 E4 x7 u1 X* Y  ?  j(normal, 3 to 90 ng/dL), androstenedione was 20! o+ n, Z5 P5 m; X
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-. u4 ]' ~: X7 W) {! u! B
terone was 38 ng/dL (normal, 50 to 760 ng/dL),6 M+ H; B7 {; E2 V$ s5 j
desoxycorticosterone was 4.3 ng/dL (normal, 7 to; e$ `; }; d1 z' q
49ng/dL), 11-desoxycortisol (specific compound S)
" L' d: O! V, d3 Kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 N; e5 n1 W& n, p3 z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 ~6 J  O. D5 W$ f8 `1 wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),# K) P; L9 a6 O2 A: X1 E6 a
and β-human chorionic gonadotropin was less than
5 h! V. [3 Y; n' E' z1 N' h5 mIU/mL (normal <5 mIU/mL). Serum follicular
: o& |, b& E4 }7 I% ^& vstimulating hormone and leuteinizing hormone
" T6 s' ^  h* vconcentrations were less than 0.05 mIU/mL) \2 p; F8 L) s+ h8 K; r
(prepubertal).( t+ a; K7 J/ ^- s+ D& V  y* V
The parents were notified about the laboratory
* J7 h2 Z2 p; k! e% U7 N+ Lresults and were informed that all of the tests were5 J* x1 L6 D; x" ], e/ U
normal except the testosterone level was high. The4 n: M9 j! C7 n- M* i+ f/ y9 G
follow-up visit was arranged within a few weeks to
$ b# T( h  u' i% D6 k- p  e2 |obtain testicular and abdominal sonograms; how-
, T% K- C; t* Z! b, `8 s* C: e% Kever, the family did not return for 4 months.
' ~! Y$ Z( ]# kPhysical examination at this time revealed that the8 M. [" X# i, z
child had grown 2.5 cm in 4 months and had gained
/ w. C7 i( H: V  N  g! F) ~2 kg of weight. Physical examination remained. `0 i  ]( F/ |2 m
unchanged. Surprisingly, the pubic hair almost com-
9 I& ]) v! A* m& l' D) P' cpletely disappeared except for a few vellous hairs at+ t; B  }& q: F  R) A% \' m
the base of the phallus. Testicular volume was still 2) G9 u& `1 @; C( [* O& D' R
mL, and the size of the penis remained unchanged.
8 G/ K' A; L: M+ J, o( O% ^The mother also said that the boy was no longer hav-8 ?. L$ u: Z/ q- n. m9 D
ing frequent erections.
; C; d+ O0 ~# \- Z- Y- ~Both parents were again questioned about use of
: H: U9 ~" e, z: w. X# tany ointment/creams that they may have applied to
# ?9 ]) X7 K5 |% m! N5 D* {the child’s skin. This time the father admitted the
6 j% {7 b" n( g  o* cTopical Testosterone Exposure / Bhowmick et al 541  D" e- R6 P1 l% L' x5 b
use of testosterone gel twice daily that he was apply-
5 f5 _+ H# C! ]! Aing over his own shoulders, chest, and back area for
$ X, M- l. z& \0 T' ~1 ]' B2 Na year. The father also revealed he was embarrassed
$ w4 b$ @3 D1 d; mto disclose that he was using a testosterone gel pre-; @  J. K. a! T/ N
scribed by his family physician for decreased libido0 l. o1 b6 U2 s3 \5 l: ?7 b  M
secondary to depression.0 I3 N: k2 T- F$ Y5 a) W9 m
The child slept in the same bed with parents.
* Q+ C! z/ r0 G% UThe father would hug the baby and hold him on his
# F) I4 m7 q! `) `% [chest for a considerable period of time, causing sig-( S3 P0 T1 L. M1 U( r
nificant bare skin contact between baby and father.
* d+ Y$ \* r" }+ i3 a: M4 D$ H3 s3 vThe father also admitted that after the phone call,5 D) F: I6 `# |: e) y+ U
when he learned the testosterone level in the baby3 |' ]1 H" P% q4 o6 k0 \
was high, he then read the product information
) j+ L8 y, _1 B/ s# E; [packet and concluded that it was most likely the rea-) Q' f* y% C3 ~. J* Q7 W/ l
son for the child’s virilization. At that time, they
) v7 a  e/ @4 V% h) R  K! J# udecided to put the baby in a separate bed, and the
2 J2 ?  Z# e( `) ]0 E) l$ Jfather was not hugging him with bare skin and had2 w' p  @. A; h: c  ?6 O. z, k& z
been using protective clothing. A repeat testosterone
' |& y8 |! P9 Ltest was ordered, but the family did not go to the) H, K; P6 l" D+ T! n7 x
laboratory to obtain the test.
$ f) ]- c9 H% u) FDiscussion
: c8 C5 z0 J5 O) U, }( ~' zPrecocious puberty in boys is defined as secondary* L7 G+ P+ \8 b8 U
sexual development before 9 years of age.1,4. `8 d* T/ L5 P) K
Precocious puberty is termed as central (true) when
# I) g1 G. R1 Z6 p# I$ o* B& u/ Oit is caused by the premature activation of hypo-
; c% v% P# }. c$ w) ?9 x7 hthalamic pituitary gonadal axis. CPP is more com-
2 n4 ]/ R; k- [0 F+ _% i  Smon in girls than in boys.1,3 Most boys with CPP2 p  Z2 R* }& C8 a$ b2 n8 K6 F
may have a central nervous system lesion that is: a. f( M' ^# v# W6 {
responsible for the early activation of the hypothal-
$ a: O1 W- P  h. c, I# lamic pituitary gonadal axis.1-3 Thus, greater empha-+ i( E) q0 Y5 n( c7 ?1 Z1 P- g
sis has been given to neuroradiologic imaging in
# H' R" F+ g5 bboys with precocious puberty. In addition to viril-
2 S1 D" U8 |4 x8 k3 zization, the clinical hallmark of CPP is the symmet-
5 u# h7 s2 r: jrical testicular growth secondary to stimulation by
- y" b* B1 r: d: J% o! ^+ Hgonadotropins.1,3
2 c$ L( c9 f7 J2 |: K, MGonadotropin-independent peripheral preco-
+ j( c$ a$ y4 x, F+ ~3 Jcious puberty in boys also results from inappropriate
, d! _( o, F" H# K7 S+ F4 Mandrogenic stimulation from either endogenous or
0 I" K2 w) \& h# o+ yexogenous sources, nonpituitary gonadotropin stim-
+ k: z+ r6 p' i2 Uulation, and rare activating mutations.3 Virilizing0 m8 H, a. `5 P( ^# ^
congenital adrenal hyperplasia producing excessive0 z1 n. p! ^' {. t
adrenal androgens is a common cause of precocious
. V+ p1 J8 Z$ G9 Bpuberty in boys.3,4
( S: v/ @* O  [( jThe most common form of congenital adrenal
% `9 o) N4 x7 O0 t5 W5 A- l! {; Q- Shyperplasia is the 21-hydroxylase enzyme deficiency.
0 Y% R) v3 C3 l, LThe 11-β hydroxylase deficiency may also result in
7 L) _( q7 C! ?4 S8 x% Gexcessive adrenal androgen production, and rarely,
0 k: A& E5 L1 |/ z3 r# w* zan adrenal tumor may also cause adrenal androgen+ _- ]" _8 E' g, P) n8 C
excess.1,39 Q9 ^* [: c( |* z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 S8 G# i1 T# g& Z' _( v0 `. Q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: C7 N1 G& _; }0 ]% |0 Y. |0 R
A unique entity of male-limited gonadotropin-
, V% a( r7 a; h5 }+ c8 Iindependent precocious puberty, which is also known9 J* v& X  _4 ~) j
as testotoxicosis, may cause precocious puberty at a
% R+ Q: o) k* I( lvery young age. The physical findings in these boys
% u7 V& m8 m. K- U/ ^2 q; y; swith this disorder are full pubertal development,
. ~7 N$ ~8 J, o7 nincluding bilateral testicular growth, similar to boys0 V3 w6 b; A8 `
with CPP. The gonadotropin levels in this disorder8 k  O: v$ Z# N5 p; a& P
are suppressed to prepubertal levels and do not show; M1 Y3 N4 k( B' Q2 n+ t# }
pubertal response of gonadotropin after gonadotropin-
% P, C+ K$ Z* v. w; Creleasing hormone stimulation. This is a sex-linked
7 A1 u/ w  u5 a2 x5 m+ u- z& iautosomal dominant disorder that affects only
$ `* m) D5 i/ x* Cmales; therefore, other male members of the family
5 ~: h0 b, z# tmay have similar precocious puberty.3
- q1 B* n4 T5 q3 EIn our patient, physical examination was incon-
/ @# [* |% D7 ?; f* D" ^9 j8 lsistent with true precocious puberty since his testi-
6 S' p, [; p1 K8 y3 C6 G: q! G8 ?cles were prepubertal in size. However, testotoxicosis
! |, u5 ?3 [  G0 @, E8 w. _was in the differential diagnosis because his father
' v, N. L- ^1 l+ P& mstarted puberty somewhat early, and occasionally,
8 H0 W5 d( |6 R, G0 v- u% ]testicular enlargement is not that evident in the% i- d' E# r* p7 b
beginning of this process.1 In the absence of a neg-
: ^" q, Z! |+ \! Fative initial history of androgen exposure, our/ U6 S/ M( v% }
biggest concern was virilizing adrenal hyperplasia,- y6 S# [6 o! H+ V7 _
either 21-hydroxylase deficiency or 11-β hydroxylase5 Y% x: G: x! M; Z+ e
deficiency. Those diagnoses were excluded by find-
  G+ S- Z1 ^9 K+ A3 u$ _# Wing the normal level of adrenal steroids.
7 M% U3 @. X- u! J, I$ fThe diagnosis of exogenous androgens was strongly" o) U0 u' R4 U  t. y8 q
suspected in a follow-up visit after 4 months because
* j6 M( n/ T4 a  u' Pthe physical examination revealed the complete disap-  b8 m$ W6 h6 {. I* j4 q
pearance of pubic hair, normal growth velocity, and
8 B% k; m& Z& i6 Z, u. `. M! y( ^decreased erections. The father admitted using a testos-- U- I% _# c6 ]' F0 ]  C
terone gel, which he concealed at first visit. He was! W$ e7 t( J1 w4 e
using it rather frequently, twice a day. The Physicians’
# B% d& D6 i$ z3 M$ i6 m. U1 y+ d( tDesk Reference, or package insert of this product, gel or
2 L- L; C. `  X/ ~5 x) l/ p6 D- j! Bcream, cautions about dermal testosterone transfer to, I* ?( J$ j8 a2 C7 M
unprotected females through direct skin exposure.! y; g7 q2 m: P. b7 z/ W/ _0 D' A
Serum testosterone level was found to be 2 times the
( L/ i* j1 H" [' H& k  ebaseline value in those females who were exposed to$ r7 t" d* C4 \/ p# D/ I( V
even 15 minutes of direct skin contact with their male8 S1 L1 J) |3 x7 a" ~$ _* [
partners.6 However, when a shirt covered the applica-
+ K" m8 ?5 n4 x. T& Z! A- Ltion site, this testosterone transfer was prevented.7 F, E7 A" \7 O, ]. ~" A
Our patient’s testosterone level was 60 ng/mL," @+ G, W: n7 j! p7 D6 ^
which was clearly high. Some studies suggest that& Q& W, x5 a/ ?
dermal conversion of testosterone to dihydrotestos-
) `' n) Y# |" O8 `# u0 uterone, which is a more potent metabolite, is more
5 w- Q0 Z/ t% T; Aactive in young children exposed to testosterone2 K) P" i! f3 T$ |  a
exogenously7; however, we did not measure a dihy-9 ?, U, \  \8 B: X) M8 @6 K
drotestosterone level in our patient. In addition to) w4 }0 m1 h$ z& b
virilization, exposure to exogenous testosterone in
$ m; c8 \& i, R3 ?, _! j+ ^0 O' nchildren results in an increase in growth velocity and  ?* K% Z5 ]* F
advanced bone age, as seen in our patient.
( Q8 g) X0 }2 m3 kThe long-term effect of androgen exposure during( U( ~8 u; y1 D" M* u' R" T1 X
early childhood on pubertal development and final2 {  v5 P6 O0 z! p
adult height are not fully known and always remain) b% m' b+ p) G) F* c
a concern. Children treated with short-term testos-
! _8 H) U$ M- S4 k) lterone injection or topical androgen may exhibit some& z$ v" t6 B1 l* d3 W) ^  t
acceleration of the skeletal maturation; however, after# O3 s& P& Y3 r: s( j
cessation of treatment, the rate of bone maturation, y: p! ]; g& j! O' o# G
decelerates and gradually returns to normal.8,93 E1 Y* H& \3 G
There are conflicting reports and controversy
- g+ P8 g$ a- }7 Z5 dover the effect of early androgen exposure on adult
. Q+ `& y3 ^( w2 s6 w# L0 hpenile length.10,11 Some reports suggest subnormal
# u* Z- M0 P1 C) `) ]adult penile length, apparently because of downreg-
- W' `% Z4 `( b6 e6 Q6 }% T+ Z- aulation of androgen receptor number.10,12 However,
, V7 A+ V6 b8 ?/ c6 u0 x' b4 NSutherland et al13 did not find a correlation between
+ }# I' S4 A: z! Vchildhood testosterone exposure and reduced adult
% b, \9 `( J1 H( ^! x  u" gpenile length in clinical studies.
0 ]' B; `, v: c6 U+ f5 }( ^Nonetheless, we do not believe our patient is
$ j) I0 I' g1 @7 X& `& Lgoing to experience any of the untoward effects from9 h; o& S3 b7 w* x+ {
testosterone exposure as mentioned earlier because
$ g( l' v+ w  f3 T" V  pthe exposure was not for a prolonged period of time.
7 u7 J; X1 u: ]Although the bone age was advanced at the time of
7 A8 J  G, }# l$ A5 ^4 ^" ndiagnosis, the child had a normal growth velocity at5 p5 f4 J" A8 y) f6 D  Z+ z
the follow-up visit. It is hoped that his final adult
6 v8 y/ d6 `* K6 ^( Y9 w  Kheight will not be affected.& o" H7 \& T- `+ N8 P% ~2 k
Although rarely reported, the widespread avail-
6 y. F* G+ G" Jability of androgen products in our society may
2 X4 U, F# r! h7 X0 a+ m2 u  findeed cause more virilization in male or female
  O9 ]( I& C8 m5 ^) H$ S$ ]! E8 N" gchildren than one would realize. Exposure to andro-
! [/ e( y: l' z" F# x3 F& u# _gen products must be considered and specific ques-
- B# f3 q4 ]8 L; t) ^$ qtioning about the use of a testosterone product or) G3 q6 E: t. I$ i* m
gel should be asked of the family members during' t! r, G& l7 Z" T7 k
the evaluation of any children who present with vir-/ Z( X3 `3 t& q) a3 t4 Y" K' ?
ilization or peripheral precocious puberty. The diag-
1 W; {% [' G. }9 g& i, znosis can be established by just a few tests and by
- ~  w5 O1 D; U) u9 jappropriate history. The inability to obtain such a! P3 _, ~( N6 k$ p5 k2 b3 H
history, or failure to ask the specific questions, may( K" I5 A! S" o+ o+ s
result in extensive, unnecessary, and expensive
- y4 b: w" b) L/ b+ sinvestigation. The primary care physician should be5 p* }% c2 g5 R+ L+ S! m# ^: h
aware of this fact, because most of these children+ N8 v7 s6 _0 V* y6 o# _) A
may initially present in their practice. The Physicians’
$ V+ t/ S3 h1 V8 k* n; n- ?- ~Desk Reference and package insert should also put a% f5 M6 G% Q# V, k. ?! Z+ ~$ g! ?
warning about the virilizing effect on a male or
$ z  C) u( `4 a7 nfemale child who might come in contact with some-
' f; J/ I1 D! None using any of these products.! x) K- X2 ]! _% ]/ H6 A
References
) R( E6 N* X: Y! z4 X+ G+ r1. Styne DM. The testes: disorder of sexual differentiation
4 |) z# V, B6 r* xand puberty in the male. In: Sperling MA, ed. Pediatric1 q' K5 w0 `# k  T0 t1 \
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; ]  _7 z/ K" o1 k. h  T7 Y) G1 B+ v% B2002: 565-628.
2 @, [0 u. n& L  o5 @2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 @3 L6 j2 _" s8 W* u7 O) Y
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
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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

/ x) }+ z$ J- @& }, A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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