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Sexual Precocity in a 16-Month-Old! A5 L7 d1 s) b& s
Boy Induced by Indirect Topical
/ q: r* A. l; Y5 Z  g+ N/ JExposure to Testosterone+ H4 Q$ Z& K* E1 s) |* a
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& ~* ]0 u# j: O9 d
and Kenneth R. Rettig, MD15 j* B* e& S, |3 U+ \2 q
Clinical Pediatrics
7 s+ N# T3 z" Y; |' a2 ^  K+ wVolume 46 Number 6
) O2 a- @3 c2 [' b, Q, }* lJuly 2007 540-5433 V" s9 [& \" w2 A! J! d( {
© 2007 Sage Publications
' h, Z3 w8 ^0 l) e& e2 ]10.1177/0009922806296651: w- U) N+ Z8 D
http://clp.sagepub.com
) F1 w# j, `" ~  y# f! u& C% @hosted at/ t+ l  i6 U2 t" s7 D2 x- A
http://online.sagepub.com( g+ w; q3 ?4 l0 ?  \
Precocious puberty in boys, central or peripheral,1 A  X3 [2 J4 z
is a significant concern for physicians. Central3 `0 U: B4 Y) }5 F
precocious puberty (CPP), which is mediated
# _0 |' v/ w7 ~) e) Dthrough the hypothalamic pituitary gonadal axis, has! K6 q! C1 f' E& X2 H" @: v$ Z% _4 p: Z
a higher incidence of organic central nervous system' A, O1 a5 `0 ^" D
lesions in boys.1,2 Virilization in boys, as manifested
* U6 Y& N* e7 b1 C3 aby enlargement of the penis, development of pubic
! |4 w; R3 C: j" b" Hhair, and facial acne without enlargement of testi-% a. n/ ^& ?0 e$ m, G
cles, suggests peripheral or pseudopuberty.1-3 We
* f  {& b# \9 a, P. E! Qreport a 16-month-old boy who presented with the
- C; ], ~' c/ B+ Fenlargement of the phallus and pubic hair develop-
! L2 A+ q7 v5 [ment without testicular enlargement, which was due' K7 x3 O3 |, E; E3 M& b* S% `  v% ?
to the unintentional exposure to androgen gel used by3 g+ c9 Y9 J* P* a/ F* w+ n8 X
the father. The family initially concealed this infor-) X4 T; r) X. c" Z1 P7 a  P# d
mation, resulting in an extensive work-up for this2 ~; P0 L( j  e! K5 U4 E: c9 U5 e
child. Given the widespread and easy availability of; D( \% X/ u1 Q
testosterone gel and cream, we believe this is proba-1 K; l8 W6 w/ H* G) b
bly more common than the rare case report in the
0 h8 x6 |  H- L. U) hliterature.4$ [6 U: U( R, j+ b% m+ g, [
Patient Report
) Q7 p. D' Q8 vA 16-month-old white child was referred to the9 y+ `2 @5 g& n6 w) l0 @( [
endocrine clinic by his pediatrician with the concern! _: q% F8 g- l$ t+ I
of early sexual development. His mother noticed9 i# t) Y, \" Y2 [1 M$ }( p) i
light colored pubic hair development when he was$ L% ^7 P3 n: p8 m& w
From the 1Division of Pediatric Endocrinology, 2University of! v0 D0 p: [4 t% L
South Alabama Medical Center, Mobile, Alabama.
5 L5 d6 u9 b8 @; O- }0 Z- p5 \Address correspondence to: Samar K. Bhowmick, MD, FACE,
8 m& ^# I+ N' M1 `! a$ KProfessor of Pediatrics, University of South Alabama, College of9 A5 c. _. G  q  f
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 a" s2 m4 V- f2 t$ |9 T6 ]3 {" Te-mail: [email protected].
  G2 [. D- n7 u9 t  babout 6 to 7 months old, which progressively became
5 h4 J0 v8 L' M7 {9 W, Jdarker. She was also concerned about the enlarge-
1 U0 I7 C$ Z$ |7 G4 Rment of his penis and frequent erections. The child' n( O, b6 Q; {7 l" R; I3 \! j
was the product of a full-term normal delivery, with, Z8 f! a0 u$ b4 g) n- z& G
a birth weight of 7 lb 14 oz, and birth length of
% z  g: N3 v( ?6 K4 Y20 inches. He was breast-fed throughout the first year( W& B0 o# x6 ?
of life and was still receiving breast milk along with4 b. A% X: W) u2 V5 t
solid food. He had no hospitalizations or surgery,& M2 m* i) C/ D+ D9 T
and his psychosocial and psychomotor development
# H  l* |' S% _  L: B. awas age appropriate.1 d8 b! t- s8 W; j
The family history was remarkable for the father,7 c8 S) S1 ~1 V. Q0 y8 w# ~
who was diagnosed with hypothyroidism at age 16,
* ]# M7 A+ b: T' \2 T4 h! B! j+ [+ I/ bwhich was treated with thyroxine. The father’s
6 g& {, w& L6 _( e( X2 X4 e  s* _height was 6 feet, and he went through a somewhat
+ q# m3 {! y8 b+ R- `$ R# {early puberty and had stopped growing by age 14.
, h+ H  D+ E% m5 u- d$ LThe father denied taking any other medication. The% I! h) U' ]- _
child’s mother was in good health. Her menarche
& i( Y( g. @8 O: Owas at 11 years of age, and her height was at 5 feet8 \, Z# S+ B) y6 }( k( W8 D
5 inches. There was no other family history of pre-
6 J# S+ H) s+ T1 A9 ycocious sexual development in the first-degree rela-7 V9 N- f  e: R8 L) L
tives. There were no siblings.
3 C3 |3 q! g0 D! I& GPhysical Examination
1 a" p9 i; N( }  |6 T0 B" TThe physical examination revealed a very active,* Q4 p9 O9 z# ~  f4 l/ u
playful, and healthy boy. The vital signs documented, W: w/ G  j4 d3 i1 Y) F- s
a blood pressure of 85/50 mm Hg, his length was
( _; M& t$ r2 I0 F2 u6 K90 cm (>97th percentile), and his weight was 14.4 kg! U% H0 O  @' w' C9 i4 S) u. J
(also >97th percentile). The observed yearly growth
; W. ^$ b% X- c8 `velocity was 30 cm (12 inches). The examination of
9 `0 d9 Z4 ~: {) xthe neck revealed no thyroid enlargement.% q' N5 O- V7 S& O
The genitourinary examination was remarkable for2 z; E, B3 i* e
enlargement of the penis, with a stretched length of/ P1 L0 x, a. {3 Y; A' U+ D
8 cm and a width of 2 cm. The glans penis was very well
+ n8 f$ J" T% G% o. J7 ~developed. The pubic hair was Tanner II, mostly around
" s8 N8 t0 v& p8 F2 M540
0 i3 Z$ l6 N! e5 Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& k! f) Z2 B0 X, F# dthe base of the phallus and was dark and curled. The
/ b$ Q' V. v/ x; ~) m* x) E0 j7 htesticular volume was prepubertal at 2 mL each.
& y* H: A1 |% f) j" C: r! pThe skin was moist and smooth and somewhat( }: ~$ ?& |# M. q
oily. No axillary hair was noted. There were no- `7 i( M% H- F3 P) U9 D: s* d
abnormal skin pigmentations or café-au-lait spots.! Y4 t. Z* c, p& c& M( Q. B
Neurologic evaluation showed deep tendon reflex 2+' {1 P# x' ]9 F) d7 [
bilateral and symmetrical. There was no suggestion) @- Z  I8 S+ [8 P0 {2 t3 I
of papilledema.
1 y3 A- M4 O9 u. e5 I4 C3 PLaboratory Evaluation
3 A1 ], `/ ?0 D1 S. _, x4 ?( T% KThe bone age was consistent with 28 months by5 I6 D0 R' I6 g5 J- _
using the standard of Greulich and Pyle at a chrono-
% A* [$ d: M. Z4 g8 {logic age of 16 months (advanced).5 Chromosomal: k+ p2 `0 s4 [+ _+ I) }% C2 B
karyotype was 46XY. The thyroid function test
" z' k8 h, }' s/ v5 [) xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-! Z# E3 P8 Q+ G( S5 X: \5 |; w
lating hormone level was 1.3 µIU/mL (both normal)./ ~/ n' E2 ?- |7 L6 J
The concentrations of serum electrolytes, blood
( G% V. k! Z# y: v) p% X8 Q2 ?& nurea nitrogen, creatinine, and calcium all were# M7 Y2 P3 m  ~3 Y) q
within normal range for his age. The concentration6 H1 ]; Y" t; P$ G4 _9 l
of serum 17-hydroxyprogesterone was 16 ng/dL
' T' t) {9 k; Z5 O/ p(normal, 3 to 90 ng/dL), androstenedione was 20
, P3 H; D% ?4 w7 ~ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% }# |! C% p$ m7 U5 p4 k7 m* A
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. H- C5 G/ }: ]4 d$ [1 ^/ Tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to: {. [8 r8 Y% P: f6 T
49ng/dL), 11-desoxycortisol (specific compound S)" W8 F3 _4 Z# s9 y% s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-6 O' {7 P0 C( V7 Y/ z5 _+ G
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- I4 L2 E7 o; E4 W! u
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 H6 Z8 |1 ~) J' U' ?
and β-human chorionic gonadotropin was less than
! _3 ~# \* D& ]! K- h0 j) ?5 mIU/mL (normal <5 mIU/mL). Serum follicular5 `+ C& s) Z2 f4 w( R7 ~( O
stimulating hormone and leuteinizing hormone: v! p: V4 s; p0 _, w% a
concentrations were less than 0.05 mIU/mL  e8 p' Q. a, A* h- \
(prepubertal).
* g& F& A# B( N: EThe parents were notified about the laboratory; |5 n5 f  X! u
results and were informed that all of the tests were
9 E$ [, I* O5 l+ B4 dnormal except the testosterone level was high. The! r, \9 ?( P2 s2 @. h# r  n
follow-up visit was arranged within a few weeks to
# F1 N9 R4 v" x. M. Wobtain testicular and abdominal sonograms; how-
4 ~  T% t: n0 t( \ever, the family did not return for 4 months.
8 u# W" r* y7 X& H/ k# A+ cPhysical examination at this time revealed that the% r2 C7 l' q# U( X$ I' D; A0 y
child had grown 2.5 cm in 4 months and had gained
; c% s  a3 ^7 I9 k# d2 kg of weight. Physical examination remained0 P: D1 y* e# ?* C$ ~0 N% G
unchanged. Surprisingly, the pubic hair almost com-0 z8 y& {% ^  x4 O7 c4 d8 N9 u- N- C
pletely disappeared except for a few vellous hairs at
- L3 v4 |6 z; Y0 y! [0 k0 }  ]1 o) ^the base of the phallus. Testicular volume was still 2
7 u& a) b5 n' A' N3 `mL, and the size of the penis remained unchanged.
0 `) |/ J3 |( O  Y. gThe mother also said that the boy was no longer hav-3 T/ e" v* O! I; [9 y1 x
ing frequent erections.
- @6 q) l% E7 A; R1 wBoth parents were again questioned about use of1 u. B  c5 i  Q' f$ k$ R6 N
any ointment/creams that they may have applied to, o$ p' Q5 _7 x# O% |9 W
the child’s skin. This time the father admitted the4 ^% m% a7 d7 r2 w4 C# k
Topical Testosterone Exposure / Bhowmick et al 5410 T) g0 y  M; w" b0 E- ]$ C8 `2 D
use of testosterone gel twice daily that he was apply-
9 w6 w7 M6 o! W7 Bing over his own shoulders, chest, and back area for" X3 ]" m: k5 d
a year. The father also revealed he was embarrassed
  n* Y3 ?: p% zto disclose that he was using a testosterone gel pre-* M  t3 }5 `9 o. [* V; `2 @2 H" n+ t
scribed by his family physician for decreased libido
! h2 k8 ^  T: I& i' e! Tsecondary to depression.
, G" a6 y* w$ j, c+ a" d- ~The child slept in the same bed with parents.- k. I0 \1 ?2 g8 ]1 s
The father would hug the baby and hold him on his
+ I2 I) u% O/ o2 ^% e$ fchest for a considerable period of time, causing sig-' r3 S9 s( W( r/ ?# Z2 t  U2 ]) s. T
nificant bare skin contact between baby and father.2 J7 q7 ^5 p2 E- n2 m
The father also admitted that after the phone call,
" Z! A2 f* p9 H  m* ^7 Twhen he learned the testosterone level in the baby% t- r% D  C1 j1 t
was high, he then read the product information
& Y* Y4 P9 |. ?# ppacket and concluded that it was most likely the rea-# n- @$ A5 m2 p/ o. q
son for the child’s virilization. At that time, they
* Z# o' v$ O1 H( zdecided to put the baby in a separate bed, and the
# u% @  V4 p% Q# ~9 y- C; I# L8 ifather was not hugging him with bare skin and had9 g6 R  I! f! M) e  L; H
been using protective clothing. A repeat testosterone6 z  r! \5 V' Z2 H: C3 _6 S
test was ordered, but the family did not go to the" ~" T% G; U+ K0 }2 O% R, S4 O
laboratory to obtain the test.
. d# z+ y& G7 W1 E" eDiscussion3 Y) q" m$ B- A0 t$ s9 U5 _/ j
Precocious puberty in boys is defined as secondary
8 n" Y. d! A# M* W; b" Tsexual development before 9 years of age.1,4+ g" [0 j+ q: @' M# b% x
Precocious puberty is termed as central (true) when% e2 E! Z9 H. c) {- t
it is caused by the premature activation of hypo-" Q9 y  Y' I/ z% @3 n% L/ j# f9 g
thalamic pituitary gonadal axis. CPP is more com-
* L& V8 h8 C' Gmon in girls than in boys.1,3 Most boys with CPP
" v0 p0 `' w2 z* h0 q0 @may have a central nervous system lesion that is) I! t1 t! w% T) C1 P8 `
responsible for the early activation of the hypothal-( [5 ?$ q# q" v4 j4 D) ]
amic pituitary gonadal axis.1-3 Thus, greater empha-
$ I3 u: m" N$ [1 @sis has been given to neuroradiologic imaging in
* S" }9 C4 e3 L/ _5 v- Iboys with precocious puberty. In addition to viril-' M/ Z, ^; G( B; D
ization, the clinical hallmark of CPP is the symmet-
4 H# C( b+ P, a4 {& P7 wrical testicular growth secondary to stimulation by
2 c, ]8 b7 s/ M3 V$ mgonadotropins.1,3
* a( A3 \& V1 O+ c( pGonadotropin-independent peripheral preco-
! B" o2 {4 }( x/ r2 I3 Zcious puberty in boys also results from inappropriate2 j) M1 m  [& t4 Q8 G( }
androgenic stimulation from either endogenous or( t8 A. N2 A* d, w
exogenous sources, nonpituitary gonadotropin stim-7 o+ }1 I9 s8 i
ulation, and rare activating mutations.3 Virilizing
: F6 D! w% C. S; g$ fcongenital adrenal hyperplasia producing excessive. f6 {6 X  c5 ?- ^+ k
adrenal androgens is a common cause of precocious# a% n3 f5 y# E9 s' z' p3 s6 j$ f# R2 g
puberty in boys.3,4
; t3 O+ G( \/ v7 ]) zThe most common form of congenital adrenal
0 V+ Z- l/ b6 @/ E" ehyperplasia is the 21-hydroxylase enzyme deficiency.( N& y- X8 M' a' P0 M
The 11-β hydroxylase deficiency may also result in2 S* G+ b+ g1 T6 s; U& _9 T8 c3 ^4 b
excessive adrenal androgen production, and rarely,
' D8 K( K4 P! \- M' Man adrenal tumor may also cause adrenal androgen3 a2 i) Q8 q; o# V8 E3 p2 D* R5 y
excess.1,3: @: @( D% s& Q% {$ B3 y8 P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 j( c  f, j' t, n$ V# E+ d542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
% d  C& p- E& u! O. I  }! dA unique entity of male-limited gonadotropin-! a* R& K" p4 z; z4 V
independent precocious puberty, which is also known3 F9 X. Z8 M5 u5 F7 B
as testotoxicosis, may cause precocious puberty at a
8 M% c8 M9 S( s  |+ z' I# fvery young age. The physical findings in these boys
) ^  `2 |/ `3 n6 b( t# D% }with this disorder are full pubertal development,, o1 h' p# l3 U7 O4 @  t
including bilateral testicular growth, similar to boys
. J2 g# ^3 M4 [8 e; k( ^# [with CPP. The gonadotropin levels in this disorder
& [" t5 |5 `2 e$ n) q: qare suppressed to prepubertal levels and do not show
5 v  Q: O" x1 d5 v& u' s. Ypubertal response of gonadotropin after gonadotropin-0 x5 _1 Q, C* R5 D% ~5 p
releasing hormone stimulation. This is a sex-linked3 o9 o: ]4 e" Q9 _1 o; r% A
autosomal dominant disorder that affects only8 H# X5 }' x0 w# l( h" U
males; therefore, other male members of the family
. i& {  W# ~$ k* J2 H8 m" r: d4 f3 h2 Nmay have similar precocious puberty.3
) ^6 ^9 Q5 P  ?9 d0 PIn our patient, physical examination was incon-. F6 F9 v2 ?6 o, ^' O9 I$ Z5 @
sistent with true precocious puberty since his testi-
: T2 |( c6 m9 `8 v& pcles were prepubertal in size. However, testotoxicosis
7 v, w- O. J( }8 }2 Ywas in the differential diagnosis because his father
6 b. p- k7 D/ T- [) \# e2 Z0 hstarted puberty somewhat early, and occasionally,
4 r0 D' x0 ^" _: U2 Z+ j8 b4 u8 mtesticular enlargement is not that evident in the4 `2 r4 v/ f, i* l
beginning of this process.1 In the absence of a neg-
" p& t" G: Y5 |3 Oative initial history of androgen exposure, our1 |3 ]/ }) p" r5 A
biggest concern was virilizing adrenal hyperplasia,) u: F( l) h" L" a( X
either 21-hydroxylase deficiency or 11-β hydroxylase3 v5 ^7 h" q+ }" J" i' A! c7 E' B8 n
deficiency. Those diagnoses were excluded by find-, f" q/ k: ~- G: C
ing the normal level of adrenal steroids.
6 X1 ^# A5 J& S' zThe diagnosis of exogenous androgens was strongly# k. i# z3 ~$ Q- {" z4 c
suspected in a follow-up visit after 4 months because1 c3 M3 t: x8 v* R0 w& t) `
the physical examination revealed the complete disap-# L' f8 \1 I% G! g, }, N; q* s
pearance of pubic hair, normal growth velocity, and% S0 m7 x- X7 G- P
decreased erections. The father admitted using a testos-
  u0 w4 f/ E7 U9 X, }terone gel, which he concealed at first visit. He was
! s6 Z' q, z' g2 I( Qusing it rather frequently, twice a day. The Physicians’
! h$ y, m9 R5 h/ d" i. [1 zDesk Reference, or package insert of this product, gel or6 y+ u9 `# p" `' b0 `' _; m  G- b
cream, cautions about dermal testosterone transfer to
$ A. X; v& a4 ]  ?; ~; T  Gunprotected females through direct skin exposure.4 F+ F2 v; }" u4 A$ I/ E
Serum testosterone level was found to be 2 times the
; ^/ k: r, p. g) J) Tbaseline value in those females who were exposed to
. w* M4 J& |/ Q* {even 15 minutes of direct skin contact with their male  M# Y7 T% X" P. v9 M0 J* T9 z- ~
partners.6 However, when a shirt covered the applica-
& a) Z* L0 r# s* U1 Htion site, this testosterone transfer was prevented.
+ P2 s" Q+ b1 t+ S+ _) ]Our patient’s testosterone level was 60 ng/mL,9 ^9 L0 u8 C. @! R
which was clearly high. Some studies suggest that2 N- ?# X- z8 E- y2 z
dermal conversion of testosterone to dihydrotestos-% R; t: s9 d+ S3 |4 W
terone, which is a more potent metabolite, is more/ C- g: I) ]+ y
active in young children exposed to testosterone1 [. e* S- c# ^: V7 Z8 b
exogenously7; however, we did not measure a dihy-
8 \0 R8 ~4 \/ Y% ]+ t" ^7 R0 hdrotestosterone level in our patient. In addition to
# U1 j$ O: Q" g2 o" R. hvirilization, exposure to exogenous testosterone in
3 u; r5 C8 S# ~0 {children results in an increase in growth velocity and4 M$ O' G- p( C
advanced bone age, as seen in our patient.) [# ^6 y$ N$ z& ~& C
The long-term effect of androgen exposure during
8 J. y: h7 N2 y- P  d( ]early childhood on pubertal development and final
: L3 Z1 \, i8 {adult height are not fully known and always remain7 J9 r  y/ a- Y7 X0 P' ~/ A- t
a concern. Children treated with short-term testos-: E5 E, @/ G0 @9 P& I/ s, q  E  U
terone injection or topical androgen may exhibit some; B7 w2 h' W4 U0 O" z
acceleration of the skeletal maturation; however, after
- v+ {) T" E# pcessation of treatment, the rate of bone maturation
% \7 J! B; E- y: Ydecelerates and gradually returns to normal.8,9# _& O- p! W0 O7 x+ j; i$ |! q( b7 C
There are conflicting reports and controversy
3 U: ~( R. y6 R( x& _# mover the effect of early androgen exposure on adult
3 ?, R* e% S2 P& kpenile length.10,11 Some reports suggest subnormal6 q! {1 J( F7 l' c
adult penile length, apparently because of downreg-
) V' x$ c3 r: D3 Kulation of androgen receptor number.10,12 However,  e9 w9 k' F5 e
Sutherland et al13 did not find a correlation between7 U. R4 W8 V8 f# Y  Y
childhood testosterone exposure and reduced adult
+ [/ G+ P# E+ ~2 l9 R8 I8 ?penile length in clinical studies.
4 A/ ^% h% G6 F; @' k, `Nonetheless, we do not believe our patient is
6 w% B4 P$ g: w0 v5 J6 @going to experience any of the untoward effects from
0 }' K  a2 H3 L) ?' Utestosterone exposure as mentioned earlier because
! L% [$ n. M, \, X/ {0 p( athe exposure was not for a prolonged period of time.! v# ]/ U8 ^7 R
Although the bone age was advanced at the time of( N) G9 M" D  S3 B) o
diagnosis, the child had a normal growth velocity at0 c# w" J- f" ?; K. I  r
the follow-up visit. It is hoped that his final adult
, A6 V* W5 ]5 L/ s( t3 m! Fheight will not be affected.
6 C7 J: h- u) r$ G8 n/ g% A% \Although rarely reported, the widespread avail-8 E% P& I0 ]! W  n: J0 G% B
ability of androgen products in our society may" m" K) |4 K+ \. Q7 }4 d
indeed cause more virilization in male or female4 B0 w$ c. |) J3 k
children than one would realize. Exposure to andro-3 d( n) d5 V3 Z. L5 _7 n4 D" z. b
gen products must be considered and specific ques-* D2 @3 L! z" E8 X- f
tioning about the use of a testosterone product or! W/ t: r, ^: _. f: T  e6 g- P
gel should be asked of the family members during( Z7 G2 l6 L# P1 \8 a% i& u
the evaluation of any children who present with vir-
- n) X. j1 @0 A1 k8 O6 [! w* k( `$ @6 `ilization or peripheral precocious puberty. The diag-
" r( F$ ?1 G/ z: ^7 snosis can be established by just a few tests and by
8 X9 x9 W( E; f& W- U( g+ u$ Wappropriate history. The inability to obtain such a+ u+ G- C  f& \6 `+ X) l4 f2 `
history, or failure to ask the specific questions, may1 h8 O% }9 D! F2 G' S# m' S
result in extensive, unnecessary, and expensive
$ K  r/ d/ L* Y2 r& K0 Vinvestigation. The primary care physician should be
6 ^% r6 B* @4 o6 u( Gaware of this fact, because most of these children
% N: T* D: m" z. Lmay initially present in their practice. The Physicians’8 g7 M! ~1 @9 f6 i  y6 m8 S
Desk Reference and package insert should also put a9 H' T$ s' H, U
warning about the virilizing effect on a male or" N8 s, H8 f  K  m* k0 M
female child who might come in contact with some-
# V8 g6 E2 ^% ]) v, P* mone using any of these products.
  L; P* P( r5 O4 d' iReferences
  o# |1 G8 D. V9 J% K- j% Y1 d7 ?2 P1. Styne DM. The testes: disorder of sexual differentiation
+ h4 k& m1 C( k# [: @( T5 M" _and puberty in the male. In: Sperling MA, ed. Pediatric
! k# v! d; I. @! ~2 w: x# m. yEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 s8 R' K; b, g1 `% e7 T: H9 l% C
2002: 565-628.) z& G0 u$ n7 q
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. v. [; x9 m7 @! U- Rpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old" J% @7 [0 [5 e4 ~
Boy Induced by Indirect Topical
" O- `$ D$ D0 BExposure to Testosterone0 P" J& O/ B4 l, U# e" i- N6 c* p
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; `8 R- E5 \5 _- D5 X+ U2 H
and Kenneth R. Rettig, MD1
7 i+ ?/ F/ E, t$ W! SClinical Pediatrics
: @( U! ~$ y: uVolume 46 Number 6( L2 O  q* M8 h! \. D/ J! U
July 2007 540-5433 f4 G6 {' f/ W# s- H8 ]& Z7 |! C8 H
© 2007 Sage Publications) n8 d& J8 B+ ]8 J! |. j
10.1177/0009922806296651
; {6 _7 Z+ b6 w2 W+ k/ whttp://clp.sagepub.com
7 Z7 R9 e3 \  u. ^6 K& D2 d  ^hosted at  A% {, @  Y; q1 F
http://online.sagepub.com
4 {& A& F8 w+ _+ gPrecocious puberty in boys, central or peripheral,
9 C* ?. K; l' Q* N) Y6 yis a significant concern for physicians. Central9 s' Q1 ?! e4 X$ {) ]
precocious puberty (CPP), which is mediated) a9 e; M9 z/ ^" x
through the hypothalamic pituitary gonadal axis, has! Y% y( |% y9 U- j4 z/ t
a higher incidence of organic central nervous system! b0 }, @# ^: r5 w( ~
lesions in boys.1,2 Virilization in boys, as manifested( D/ C% s$ D7 s6 m- j
by enlargement of the penis, development of pubic
9 z2 ]& E* i. V9 w2 _) C; Uhair, and facial acne without enlargement of testi-
, i% u2 r5 K9 N! pcles, suggests peripheral or pseudopuberty.1-3 We
3 D9 S6 Q- a0 e5 P/ M4 ^report a 16-month-old boy who presented with the
' P) L4 X/ ~  c9 G" x2 `: Qenlargement of the phallus and pubic hair develop-) C: o$ }- x- J' v, ]
ment without testicular enlargement, which was due
" X1 d- l( L6 T/ ito the unintentional exposure to androgen gel used by
( e3 ^4 y- h7 `, Pthe father. The family initially concealed this infor-
5 _' K' Z  n/ n5 Ymation, resulting in an extensive work-up for this; e7 ^6 I8 B5 h9 k' }* f
child. Given the widespread and easy availability of
/ n6 S5 F) [# H7 F# k9 M) @, Qtestosterone gel and cream, we believe this is proba-
# R' u) N& O, k# }$ v$ a5 I7 s# _bly more common than the rare case report in the
! B6 r/ j  s9 w" uliterature.41 G2 u/ l6 @3 K. n; L3 r1 |
Patient Report
% Z" @# ]9 i+ [A 16-month-old white child was referred to the
* \2 Y  O% x$ `+ d! R6 E# Rendocrine clinic by his pediatrician with the concern- \  y% U( F2 d& k1 g
of early sexual development. His mother noticed
& I9 }3 a" T6 [' [light colored pubic hair development when he was
7 w8 u. U* w4 {' n7 \From the 1Division of Pediatric Endocrinology, 2University of
" B! ~3 V; K3 s+ ESouth Alabama Medical Center, Mobile, Alabama.
; h! R4 {8 J# q3 t  OAddress correspondence to: Samar K. Bhowmick, MD, FACE,* w% f& h1 P. u8 A; ^
Professor of Pediatrics, University of South Alabama, College of
! S+ ]3 B8 }7 Q6 t& _/ n" sMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# c3 @2 y: K3 p' {5 f0 Je-mail: [email protected].
' y! J6 R7 I/ N7 f# m# V" kabout 6 to 7 months old, which progressively became) r& c* ~" t0 e. ^
darker. She was also concerned about the enlarge-
' w6 t4 |  N" a  M. h2 ?; Ument of his penis and frequent erections. The child3 E9 t) K2 w) x( {2 T' }
was the product of a full-term normal delivery, with
! m6 P5 k. @- ~0 q5 ra birth weight of 7 lb 14 oz, and birth length of& ?7 O) I- h2 P2 g5 M1 w( L
20 inches. He was breast-fed throughout the first year. R; r8 W) O8 J# P, p; k
of life and was still receiving breast milk along with
+ i; L* I5 p" W* \4 \solid food. He had no hospitalizations or surgery,
$ x: T; M& e+ ?; k2 Tand his psychosocial and psychomotor development
  O; w9 \# P, l( _* |% wwas age appropriate.
5 p- w' R: X/ N, y7 s. \The family history was remarkable for the father,; W0 a8 C% |- Y- d9 f  h
who was diagnosed with hypothyroidism at age 16,
# H5 u% |& h$ M; w3 ?5 lwhich was treated with thyroxine. The father’s
8 L2 n' R8 P' F+ vheight was 6 feet, and he went through a somewhat
' L" ]) _2 I( x+ z4 b; m5 mearly puberty and had stopped growing by age 14.
2 b' P. v9 E* ]7 e1 ~% GThe father denied taking any other medication. The
4 E% h1 b- R7 ~5 v3 e9 Y+ achild’s mother was in good health. Her menarche
6 e$ J2 C) w* d4 g# rwas at 11 years of age, and her height was at 5 feet9 m, \9 ]) [# d" D6 O+ q* w
5 inches. There was no other family history of pre-
2 j7 m4 h) `6 Ncocious sexual development in the first-degree rela-, N) v5 _& M3 C6 _
tives. There were no siblings.
, Z) O, m5 k" ^" TPhysical Examination0 y0 E( }* E# b/ ]
The physical examination revealed a very active,
+ y4 ~1 X& B) M! Jplayful, and healthy boy. The vital signs documented6 u; R3 s% ^5 C$ i- n' d% U
a blood pressure of 85/50 mm Hg, his length was
# p' Q) T. A$ W* u! D5 ^: L90 cm (>97th percentile), and his weight was 14.4 kg
* R/ l2 J8 V! V5 ]* Y' o+ v' [(also >97th percentile). The observed yearly growth
5 F$ G( v3 ]+ j7 fvelocity was 30 cm (12 inches). The examination of
* C5 [% A/ V) }the neck revealed no thyroid enlargement.
4 T3 t5 o. o1 ?5 m+ jThe genitourinary examination was remarkable for2 Z3 f' f7 q0 m6 X5 a
enlargement of the penis, with a stretched length of) Q. T* Q0 N7 |, n1 ]7 r( n
8 cm and a width of 2 cm. The glans penis was very well' E5 f& f5 ^+ N; g
developed. The pubic hair was Tanner II, mostly around
  s. J! b* A8 U6 g5 Z0 V5405 G3 o+ k6 @! r) n2 V# E3 F1 g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# p0 x9 F- x3 |# Wthe base of the phallus and was dark and curled. The/ b9 c8 M; X# S, s5 B! L# G
testicular volume was prepubertal at 2 mL each.. }9 Q  Q# ~! b* X7 O
The skin was moist and smooth and somewhat
2 D/ G2 P8 X. H# u# C8 s& coily. No axillary hair was noted. There were no
; F$ X4 U8 ]$ m  i8 y4 [abnormal skin pigmentations or café-au-lait spots." l% I, b8 [3 `8 E
Neurologic evaluation showed deep tendon reflex 2+; f1 Z9 ]' W, ]
bilateral and symmetrical. There was no suggestion8 V- ?& u7 ]1 E6 v& V
of papilledema.
( {+ v3 T& B) T6 D  B& iLaboratory Evaluation
, @7 }5 \3 l" Y& WThe bone age was consistent with 28 months by
5 H3 ~1 X1 ]6 Ausing the standard of Greulich and Pyle at a chrono-
% w' ^  D4 E# W8 k; Ulogic age of 16 months (advanced).5 Chromosomal7 B# z/ r* `( z- ]
karyotype was 46XY. The thyroid function test
5 @0 T' c2 A" W8 V7 B% x1 fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
: b5 D: Z3 F6 D/ T- O; h4 {( I; Vlating hormone level was 1.3 µIU/mL (both normal).) R0 a, u5 T$ k- O/ F% D
The concentrations of serum electrolytes, blood
1 O. a3 S4 F; N( N  r, X( D) v: surea nitrogen, creatinine, and calcium all were/ D# {2 k* ^! i. A- m6 f
within normal range for his age. The concentration
/ C# F% E# p* C" Dof serum 17-hydroxyprogesterone was 16 ng/dL
5 m$ c8 N* v, G, h* L# i(normal, 3 to 90 ng/dL), androstenedione was 20$ C% [% R' S4 M/ c
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ f! J) \4 V$ o* N8 t8 Rterone was 38 ng/dL (normal, 50 to 760 ng/dL),
% S7 X) L4 [. L& {desoxycorticosterone was 4.3 ng/dL (normal, 7 to
' |! d! c) ~$ H/ g4 {' Q% q49ng/dL), 11-desoxycortisol (specific compound S)+ s# S- ^, B! q4 n8 j3 `; }4 x
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 g6 {* M( l. j4 [* _& f
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: Q9 O) `5 N  L" S' ?testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, ]/ J# W& @3 P" }, ?
and β-human chorionic gonadotropin was less than  O7 W! B  O3 U' A2 s' v$ g
5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 V/ X# W) ^. N5 ?, Q7 bstimulating hormone and leuteinizing hormone
7 o9 ]; f. p# T5 y3 nconcentrations were less than 0.05 mIU/mL& J  A+ Z* n+ U; G
(prepubertal).9 O" D. e* ^- K5 Z7 }$ G( Q: @+ Y
The parents were notified about the laboratory8 R- e0 I6 L! S) a8 Y  W
results and were informed that all of the tests were
8 z2 v9 e& A! S8 ~% A- Onormal except the testosterone level was high. The& y4 y& E8 ^2 j8 w1 o3 Q! \
follow-up visit was arranged within a few weeks to
- t* [* u% m( O6 b& {: vobtain testicular and abdominal sonograms; how-
. W2 W' Q' K$ N0 O7 g' tever, the family did not return for 4 months.
/ [: n$ Z/ r3 G# h2 w* H2 IPhysical examination at this time revealed that the
6 d# r9 Q5 a$ o5 X2 b& Vchild had grown 2.5 cm in 4 months and had gained
" B( S/ v! L9 `4 b! M2 kg of weight. Physical examination remained. ]; Y% z2 t9 O1 a) s8 P& \7 F
unchanged. Surprisingly, the pubic hair almost com-; U: Q! l* e# R! w
pletely disappeared except for a few vellous hairs at
; `5 `- Z( H! ], K5 Zthe base of the phallus. Testicular volume was still 2
' }% K2 Q1 K4 S# C& Z) {mL, and the size of the penis remained unchanged.% e. K. B6 H9 H' ]* @2 [% c% C
The mother also said that the boy was no longer hav-
: k$ ^3 F  w. T, h" }6 X) g, cing frequent erections.; u1 m: z' `% g) t* I
Both parents were again questioned about use of( o, q0 ~9 K* t$ Z0 U
any ointment/creams that they may have applied to: }( J6 u1 _9 ~- i. }0 r6 u" v4 i
the child’s skin. This time the father admitted the0 S' ~5 d! e* m: w& c5 F( X! [
Topical Testosterone Exposure / Bhowmick et al 541. R* }, P- D& |1 l+ b0 u1 s
use of testosterone gel twice daily that he was apply-
0 _0 Q/ \2 E1 r" j! f# S# Ping over his own shoulders, chest, and back area for
4 O( R/ O2 \' D: _# Ba year. The father also revealed he was embarrassed
- A& D, ~5 a* Ito disclose that he was using a testosterone gel pre-2 ?2 k# b# l9 s* _7 g! s
scribed by his family physician for decreased libido
8 C7 s) _4 e  [+ M* q8 {secondary to depression.& w* i5 j3 N# Z* |4 W, W
The child slept in the same bed with parents.
' H" U8 m& Y& R) @2 n1 P9 I3 y4 SThe father would hug the baby and hold him on his
$ w! d: U, [# Z: c" [0 N" uchest for a considerable period of time, causing sig-
) T( O- l" R5 z' u( C! U2 t, tnificant bare skin contact between baby and father.
, m# q) a( e- l& i4 ]+ I: e6 d, PThe father also admitted that after the phone call,
+ f5 ~6 V& _; C. mwhen he learned the testosterone level in the baby
, y  K! O$ k* X: ]$ L3 `: Nwas high, he then read the product information! k! f. P+ g% `' y0 D3 Q) f; `1 ]
packet and concluded that it was most likely the rea-
8 o# L3 H) a/ V1 Q7 gson for the child’s virilization. At that time, they
* y: ?$ g9 g& A6 a* Ndecided to put the baby in a separate bed, and the; L4 S0 B% A" I4 `4 Y
father was not hugging him with bare skin and had; h0 l, O: C4 e- N- Q
been using protective clothing. A repeat testosterone( G, F: b) Y4 V* j5 j+ a" j
test was ordered, but the family did not go to the6 Q- Z, ]: H3 f: z9 z
laboratory to obtain the test.
/ `1 ~0 p0 i2 W" `, LDiscussion
3 J2 H& I" N- j& Z2 e+ bPrecocious puberty in boys is defined as secondary
9 y! n( t5 @7 t& b1 bsexual development before 9 years of age.1,4) D* T# J  N; q8 D. s
Precocious puberty is termed as central (true) when6 c4 e) w5 X3 E1 M) U5 E
it is caused by the premature activation of hypo-
* }& Q0 k- H, q4 {6 cthalamic pituitary gonadal axis. CPP is more com-
4 I. E+ }' E& y! imon in girls than in boys.1,3 Most boys with CPP
, E1 y3 I/ o1 ^% W, @) ?: L# S" s$ h5 Gmay have a central nervous system lesion that is
* f9 W" M) F# H# X9 G8 @9 Nresponsible for the early activation of the hypothal-
- h: m& a7 E* xamic pituitary gonadal axis.1-3 Thus, greater empha-
' q- k  U5 D  e9 R  Fsis has been given to neuroradiologic imaging in: H# {0 t: C/ r2 j3 F% \7 E
boys with precocious puberty. In addition to viril-
2 B5 R" u8 G' Q* [  P3 j  Cization, the clinical hallmark of CPP is the symmet-
, d* V) l3 E' q5 _2 H. B5 \rical testicular growth secondary to stimulation by
& S) Y% Z  C/ e2 d! t3 Lgonadotropins.1,30 k) o/ G; \$ E9 E* s
Gonadotropin-independent peripheral preco-
" |; c! z, ]) ~' _) R1 jcious puberty in boys also results from inappropriate9 r' W# `3 u5 a6 O, Z' N
androgenic stimulation from either endogenous or
* V2 I4 h7 k9 s" |) x1 c) Cexogenous sources, nonpituitary gonadotropin stim-9 D$ [  a: |" f( f- |3 H- _
ulation, and rare activating mutations.3 Virilizing6 N) v' Q& B0 d7 Q, x  v
congenital adrenal hyperplasia producing excessive
- ]# |1 _" f/ V. a- madrenal androgens is a common cause of precocious% P0 o' a% G* P9 T' u: ?
puberty in boys.3,42 e1 x! F8 Y( a  g3 W( X
The most common form of congenital adrenal
  C" ~2 W) r+ ?* `2 thyperplasia is the 21-hydroxylase enzyme deficiency.
. K5 T6 l- X- K5 u8 x+ D) T8 z. tThe 11-β hydroxylase deficiency may also result in0 x+ ^! H6 r  G# T* ^& S/ p
excessive adrenal androgen production, and rarely,0 U: G/ |8 g3 e( J8 [
an adrenal tumor may also cause adrenal androgen
1 I' Z$ y3 @- |# Texcess.1,3  N/ E" s' j' s# y' j+ [7 C
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542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: k( U* p( t6 o  f  ]) Q# d
A unique entity of male-limited gonadotropin-% Q) e6 G, q: z) ?
independent precocious puberty, which is also known
1 G4 l6 n# e9 Nas testotoxicosis, may cause precocious puberty at a7 \5 A- H5 w! `2 L5 G. m; H: `
very young age. The physical findings in these boys
, n1 k- L- T0 y' H0 Vwith this disorder are full pubertal development,! H$ a* h# ^. ~/ L, Y$ f7 L' H/ _
including bilateral testicular growth, similar to boys
8 i9 L  @5 a% X( y* w" w" `2 O. gwith CPP. The gonadotropin levels in this disorder
% A% t, }( @  l8 [# P# H$ R' nare suppressed to prepubertal levels and do not show* x+ M4 T" n! ~/ v7 }, I
pubertal response of gonadotropin after gonadotropin-
! `6 k& [/ P; w  Q, ^1 i3 oreleasing hormone stimulation. This is a sex-linked
6 ^5 z) ?5 N8 B7 f! L, s; D9 xautosomal dominant disorder that affects only
+ w% e  g$ Y! K# R; `males; therefore, other male members of the family
0 `5 K, X- `: Q: Tmay have similar precocious puberty.3
& y3 U. o6 M3 ?4 P7 zIn our patient, physical examination was incon-7 |& ^* `! u" Z4 I1 K
sistent with true precocious puberty since his testi-$ B# y. R0 k; b' F% q3 h; C
cles were prepubertal in size. However, testotoxicosis
. {  C4 P% Q/ U/ uwas in the differential diagnosis because his father, A: ]8 M  R' q& k3 o
started puberty somewhat early, and occasionally,
+ X/ r2 T# e8 ktesticular enlargement is not that evident in the- i7 X, _8 X. x4 E0 u
beginning of this process.1 In the absence of a neg-- u7 F$ l( b8 C/ T* i, F& t( }3 {
ative initial history of androgen exposure, our* ~% h! Z" o6 {1 Y
biggest concern was virilizing adrenal hyperplasia,
0 h8 ?2 e2 ]. L5 J$ _! k0 meither 21-hydroxylase deficiency or 11-β hydroxylase
. \+ O5 X9 h+ Y" \0 }- H! O0 p$ adeficiency. Those diagnoses were excluded by find-8 n) ?! R" \" P( H: X$ R( D
ing the normal level of adrenal steroids.0 Y) N+ D$ U$ ~2 D% l
The diagnosis of exogenous androgens was strongly
9 Z4 A$ J& Y& X# p1 d6 Osuspected in a follow-up visit after 4 months because% k2 h1 i& A& ?0 X  K2 ]
the physical examination revealed the complete disap-: |! H9 s1 }6 z
pearance of pubic hair, normal growth velocity, and
7 V, D7 a8 c$ `9 |- l: ]decreased erections. The father admitted using a testos-
4 |( N. i5 _7 ~: b2 ^terone gel, which he concealed at first visit. He was
7 k+ T( F* Y3 x& S9 u: xusing it rather frequently, twice a day. The Physicians’0 X6 g2 o8 ^2 l9 b) J7 z
Desk Reference, or package insert of this product, gel or
- q, U' X- C( j) ]2 N5 J8 Wcream, cautions about dermal testosterone transfer to2 W0 V' H: t1 X- T- S- f1 h6 H+ I
unprotected females through direct skin exposure.; l5 b* Z% V" e+ c
Serum testosterone level was found to be 2 times the
  r7 m0 c3 y- p2 @4 i" Sbaseline value in those females who were exposed to+ y1 g% H  `- t* k2 L  D
even 15 minutes of direct skin contact with their male
4 G7 m* G3 s9 P1 h3 w' i1 Ppartners.6 However, when a shirt covered the applica-
+ t6 P7 v$ q! f1 f! d& ition site, this testosterone transfer was prevented./ c- G' B3 B2 V' W
Our patient’s testosterone level was 60 ng/mL,
# z$ j& i% S6 r# gwhich was clearly high. Some studies suggest that& K, v+ b6 E/ e& h  K
dermal conversion of testosterone to dihydrotestos-; C. Z' Q2 P) j0 E; v) `$ F
terone, which is a more potent metabolite, is more* r, Z* H0 u. O* M
active in young children exposed to testosterone6 h% i) x. @8 e4 O* H
exogenously7; however, we did not measure a dihy-5 ?* A, ~$ v. M" q
drotestosterone level in our patient. In addition to
+ H8 G7 ]7 u6 Rvirilization, exposure to exogenous testosterone in
/ P- O4 ]  ~9 ^, ]  q( U. Ychildren results in an increase in growth velocity and" Z4 h) i7 x9 D- u) a- k9 c
advanced bone age, as seen in our patient.
; Y! |- C" {2 p* o# i$ [The long-term effect of androgen exposure during# a- r# g" d: X1 j2 u
early childhood on pubertal development and final# A1 t! p6 ?9 R$ F; @* b" i
adult height are not fully known and always remain/ K1 K3 }5 m# ]6 q; j
a concern. Children treated with short-term testos-, a% [  l7 H: A3 B' |
terone injection or topical androgen may exhibit some8 x' N9 q, {1 R7 [- \
acceleration of the skeletal maturation; however, after1 z1 O8 k. F3 \' Y9 V1 d% i  b7 k
cessation of treatment, the rate of bone maturation
+ @7 l5 a( U! g- v3 w5 B+ G# Mdecelerates and gradually returns to normal.8,9
; ?+ D: X$ B9 L( F% \4 t1 f$ OThere are conflicting reports and controversy2 X+ z' B6 k; X, E3 c
over the effect of early androgen exposure on adult
4 L* ~3 R9 N; J# @6 R7 x1 ~' C9 Rpenile length.10,11 Some reports suggest subnormal0 d9 `# j# a7 p" ~
adult penile length, apparently because of downreg-3 v3 F" X9 j  i- ~* c3 ~6 ^* {
ulation of androgen receptor number.10,12 However,
9 K" K. b& j! }) D# USutherland et al13 did not find a correlation between
( v% i3 N" R/ N2 Q0 Dchildhood testosterone exposure and reduced adult' s5 V& ?3 h2 }/ a. q
penile length in clinical studies.
6 T' f0 e5 h% O: Z* PNonetheless, we do not believe our patient is0 E8 o! U4 _7 o) V/ ?3 B" H7 m
going to experience any of the untoward effects from  g" \" ?4 X; J- q
testosterone exposure as mentioned earlier because
# }; |% y6 }: ^+ N. Ethe exposure was not for a prolonged period of time.
0 K6 O' y$ u6 J& M9 T' ~% c3 UAlthough the bone age was advanced at the time of% Y" B  d* A* Y3 `( R& Z7 g! @( L
diagnosis, the child had a normal growth velocity at
  A" R4 [& o& z  Othe follow-up visit. It is hoped that his final adult
# ^* p" }4 A2 Z9 V" {! w% Theight will not be affected.2 y. J. M. i: K8 j- K& v
Although rarely reported, the widespread avail-
% Y% t" L! B# w: r3 @' tability of androgen products in our society may
* k/ M" U8 E  b$ g9 o% p* D$ D6 Vindeed cause more virilization in male or female
( e* `: _$ k+ b$ Gchildren than one would realize. Exposure to andro-
9 `0 Z0 }% t! v2 q7 ugen products must be considered and specific ques-( p% X6 Z" G( r
tioning about the use of a testosterone product or
# H) b% t' }6 n$ v6 t2 g, {gel should be asked of the family members during
* ~; Y/ N3 o3 T  i, c2 Tthe evaluation of any children who present with vir-
" z4 K. K: P. O! A: k4 ?# yilization or peripheral precocious puberty. The diag-7 {! ]9 r7 b0 i% ^! p
nosis can be established by just a few tests and by" {+ ^$ o( B' S! n: g) F
appropriate history. The inability to obtain such a
1 k9 H  {, K  d# Ahistory, or failure to ask the specific questions, may
3 h- f' Z1 i, I3 B$ D; w1 r9 ~result in extensive, unnecessary, and expensive
6 ~! b' P! w! uinvestigation. The primary care physician should be
/ z) i0 T. P- b  W+ L. daware of this fact, because most of these children3 q' n/ ]4 j+ P' U5 K
may initially present in their practice. The Physicians’
# G; A) R; e: B. l  j/ U& YDesk Reference and package insert should also put a
4 y$ p+ Q- O7 t  _' H" i' J0 Qwarning about the virilizing effect on a male or
8 c6 B' b3 F, Afemale child who might come in contact with some-
' C+ S  j4 z. B0 y3 Wone using any of these products.  ^+ @' k% ~+ d7 r6 Y1 d" H" U
References
, X. k7 P7 L% a5 v( v1. Styne DM. The testes: disorder of sexual differentiation0 v' V$ E$ P  D# S! c) H
and puberty in the male. In: Sperling MA, ed. Pediatric
+ O# q) h1 H. u( oEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 F1 c, J  h7 l" B4 ^! {
2002: 565-628.
5 G2 l( u0 b8 |! O+ N2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( T9 Y8 S% B+ H0 ^5 j2 L9 N
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

' e7 T: N  U0 O4 h  Z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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