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Sexual Precocity in a 16-Month-Old
; S9 [. ]5 q/ H( X. Y* e) p7 @, |' fBoy Induced by Indirect Topical% y; E; u6 O# d+ k: @4 Q% i* F4 x0 z
Exposure to Testosterone3 _, G2 t0 m8 T$ a) f; t. \
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 N9 m# _! f+ X3 Jand Kenneth R. Rettig, MD1
5 g8 b5 N: a6 yClinical Pediatrics6 Y% J. M. \1 D+ s. f
Volume 46 Number 6
2 r5 O/ S/ v0 p1 hJuly 2007 540-543- `6 ^/ S* U$ R) C1 b
© 2007 Sage Publications9 k6 \0 j7 e+ ~2 y
10.1177/0009922806296651
% z8 a0 s( ^& C3 s- F4 }/ R  |http://clp.sagepub.com. F) S' b: n* b# \1 x
hosted at
; d  ~) n8 m: C3 S/ k2 W3 xhttp://online.sagepub.com; x; k( J8 F( [: D) o# M
Precocious puberty in boys, central or peripheral,
; e0 D, k$ e9 O  R9 I2 Pis a significant concern for physicians. Central
/ M1 R) Y; E" E2 Sprecocious puberty (CPP), which is mediated) O& u" w( ]8 {6 b& K
through the hypothalamic pituitary gonadal axis, has
, [2 `8 _  ]4 y& k, f7 I1 Ca higher incidence of organic central nervous system
: ^. u9 O* }2 W8 ilesions in boys.1,2 Virilization in boys, as manifested
+ q# U# _1 f, u! s/ J5 fby enlargement of the penis, development of pubic  G! F5 L" e+ b" E7 ?: l& s9 M
hair, and facial acne without enlargement of testi-$ B0 v  U& r6 z) s
cles, suggests peripheral or pseudopuberty.1-3 We
0 O- z3 i; d$ h1 y1 M& P8 a* wreport a 16-month-old boy who presented with the7 F3 r, `) K% U, @4 S
enlargement of the phallus and pubic hair develop-
5 ?9 ^! g7 |+ i3 Pment without testicular enlargement, which was due
/ I  s0 K: ]' W0 nto the unintentional exposure to androgen gel used by7 ?- Q+ Z$ U2 a9 R5 U+ K' j( ~; m
the father. The family initially concealed this infor-7 l/ j* u5 B. P' i3 o7 S
mation, resulting in an extensive work-up for this
9 Y/ {7 C/ y3 B+ C- {7 vchild. Given the widespread and easy availability of
2 j& Y  n- ]9 {, A  L# r1 Ttestosterone gel and cream, we believe this is proba-4 F; Q" Q, D9 c6 T
bly more common than the rare case report in the
4 y: }) K7 J+ c1 b- gliterature.44 }6 n& r: X5 _
Patient Report
) l' M/ n3 b+ ~A 16-month-old white child was referred to the1 o# r4 r# p6 ]5 z. j0 i
endocrine clinic by his pediatrician with the concern! C& W: A% Z' h
of early sexual development. His mother noticed
' }2 C. T! e7 j. w) t3 Rlight colored pubic hair development when he was
& H# b: F+ S4 R8 KFrom the 1Division of Pediatric Endocrinology, 2University of. L7 i7 O! b& R4 m
South Alabama Medical Center, Mobile, Alabama.
- b% [, ~. _& |% UAddress correspondence to: Samar K. Bhowmick, MD, FACE,
0 r' r+ D2 _  X8 kProfessor of Pediatrics, University of South Alabama, College of
4 O3 k, A8 [/ aMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;: x7 T1 N  L8 Z. d. l: q; b+ c! P& B
e-mail: [email protected].
, J; K- @; {8 Q3 T4 xabout 6 to 7 months old, which progressively became1 X4 i* i  F$ Q4 t. p" V! P& [
darker. She was also concerned about the enlarge-/ r: i3 t+ y5 M/ E
ment of his penis and frequent erections. The child
1 s6 x% ~. f0 H! }- T0 Kwas the product of a full-term normal delivery, with! }) c6 V& u8 y9 a6 q
a birth weight of 7 lb 14 oz, and birth length of
9 g" `& ?" \" h( H, Z2 L20 inches. He was breast-fed throughout the first year! C5 L6 v) M% {3 L, M9 F8 [: q5 d
of life and was still receiving breast milk along with
. r/ N3 X2 G  D9 g; k# h4 psolid food. He had no hospitalizations or surgery,
$ b3 U6 N9 j" I( V1 V0 h9 q, Mand his psychosocial and psychomotor development
& r5 Y! M4 I  l# Mwas age appropriate.9 a# D% N; s( f/ a+ C. n" x' S; D# z
The family history was remarkable for the father,
% j0 R8 s% {/ w" {# a. U2 nwho was diagnosed with hypothyroidism at age 16,& a% g9 W% K' @
which was treated with thyroxine. The father’s% S- ^' ]/ P/ T
height was 6 feet, and he went through a somewhat% J; d& f1 x, C* n5 }
early puberty and had stopped growing by age 14.' d- w. i, {2 M' L" D  m- B3 b: V& M
The father denied taking any other medication. The
, m# ^' }. S* K5 A7 Rchild’s mother was in good health. Her menarche
) _1 x- Z4 M/ P, Mwas at 11 years of age, and her height was at 5 feet
0 J% ^7 K! y8 ~' @. T5 inches. There was no other family history of pre-, F/ g& m4 ]" p! t5 I9 J( S
cocious sexual development in the first-degree rela-/ z( G) ]9 y3 A  z+ T
tives. There were no siblings.6 m6 G6 c" [& l' Y" }  \# _
Physical Examination
& W2 z( a1 F* P/ _The physical examination revealed a very active,( q) R3 `* c2 Z
playful, and healthy boy. The vital signs documented% T  p/ L8 b: F5 |1 K6 Z' \
a blood pressure of 85/50 mm Hg, his length was
+ i" E: l1 O& E7 b# d90 cm (>97th percentile), and his weight was 14.4 kg! S4 B( x( [$ [
(also >97th percentile). The observed yearly growth; K7 Q& u- a. W0 q/ t3 `7 d. O6 K- X
velocity was 30 cm (12 inches). The examination of
) X4 N5 Z( |7 d! g+ x; g3 N* q0 Rthe neck revealed no thyroid enlargement.
9 v. I8 R/ h# B: ^The genitourinary examination was remarkable for5 X6 e* |4 m# c6 H
enlargement of the penis, with a stretched length of
) W# l9 i& N- a9 A2 G7 R0 I. ^* j8 cm and a width of 2 cm. The glans penis was very well
# W( a: V5 O" {* D2 Pdeveloped. The pubic hair was Tanner II, mostly around
: ^/ h0 R+ N, }0 T  t540& S4 c1 {& j% P1 G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 h8 c0 H! Y# @$ ?- Nthe base of the phallus and was dark and curled. The2 {' a! _/ [) o/ }! }5 d* F
testicular volume was prepubertal at 2 mL each.
% v4 L$ G  n& N  H6 _The skin was moist and smooth and somewhat2 o. O8 U# A2 o
oily. No axillary hair was noted. There were no0 t- y' S3 X; _3 H
abnormal skin pigmentations or café-au-lait spots.
: w. d9 B1 `' MNeurologic evaluation showed deep tendon reflex 2+
" y( Z5 M1 t6 m: J% }bilateral and symmetrical. There was no suggestion
1 ~; s+ H! f& f" Wof papilledema.
' \) V% a9 q8 X' I- oLaboratory Evaluation( A  S, t6 U3 @3 P" V( h
The bone age was consistent with 28 months by. c3 s3 }5 d2 D$ g! F
using the standard of Greulich and Pyle at a chrono-. o/ R! ~& F5 [+ X: z; S6 J
logic age of 16 months (advanced).5 Chromosomal3 I" `5 z5 g4 s5 ?) _1 j. u  n
karyotype was 46XY. The thyroid function test
$ C7 D6 y! X% |4 j5 q# j9 @! Ushowed a free T4 of 1.69 ng/dL, and thyroid stimu-
/ y4 {9 I9 ~/ d8 `lating hormone level was 1.3 µIU/mL (both normal).1 M' o4 r' P9 A& C
The concentrations of serum electrolytes, blood& S/ e& s. g( W3 |% ]# B: C, E
urea nitrogen, creatinine, and calcium all were
. W" _2 L, |  n3 J4 W1 \* T4 W4 gwithin normal range for his age. The concentration
  z, o9 {1 X, v3 u2 D7 ^* kof serum 17-hydroxyprogesterone was 16 ng/dL
+ ?" [/ R9 I5 i# [0 [2 E(normal, 3 to 90 ng/dL), androstenedione was 20/ k9 O$ t  Y9 [8 C0 r6 S
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: t& H% o  m& z. s) z/ Xterone was 38 ng/dL (normal, 50 to 760 ng/dL),7 R5 N9 O$ |. i- M7 R: O' r
desoxycorticosterone was 4.3 ng/dL (normal, 7 to& Z8 L* z7 W' n$ V$ v2 v2 \8 u2 d
49ng/dL), 11-desoxycortisol (specific compound S)5 B8 ^% N0 O& d$ ^8 T
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* B: p1 J% ]5 U; c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
: w. O  ?1 K' l% Ftestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 k" d/ n; Q" Sand β-human chorionic gonadotropin was less than
" a. I( Y; n1 M5 mIU/mL (normal <5 mIU/mL). Serum follicular6 @5 d* D2 a( J6 S6 j  r1 ?
stimulating hormone and leuteinizing hormone7 T* w: o. ~  n- b, S( Y$ D3 f
concentrations were less than 0.05 mIU/mL
3 m7 }- Q& E2 R0 B( n(prepubertal).
( s: Z9 {# ~# q: ~( EThe parents were notified about the laboratory
+ L% ?; c( X4 n/ x7 M! Xresults and were informed that all of the tests were$ L# i2 v2 n4 O- e. q
normal except the testosterone level was high. The2 O; a& X2 g" B. S2 l8 c8 t
follow-up visit was arranged within a few weeks to
1 w8 D9 K2 s+ |. Oobtain testicular and abdominal sonograms; how-
2 F2 e" ~4 [/ k7 ^$ m# kever, the family did not return for 4 months.- R7 d- Y, W, h  }6 A7 @, w
Physical examination at this time revealed that the
5 _6 R8 O2 p" \7 ?. mchild had grown 2.5 cm in 4 months and had gained8 i& \1 D: Y0 `* l. r- Z: _
2 kg of weight. Physical examination remained
0 u# M$ X) z# Z, p! iunchanged. Surprisingly, the pubic hair almost com-
; _# X! v9 n$ M# W- ~pletely disappeared except for a few vellous hairs at  V6 A6 x0 R. @: l2 V/ S, }! w8 c
the base of the phallus. Testicular volume was still 2
* A; C( B$ q1 s. |: G  j' {mL, and the size of the penis remained unchanged.
9 v2 W- J9 W4 ]; }2 ?% s. FThe mother also said that the boy was no longer hav-
8 Z! I# i8 W2 G4 L, T; Z( c& P% q$ Eing frequent erections.# u: U) S! m$ `1 W7 V- v
Both parents were again questioned about use of
, s( q& E; T0 m7 m7 {9 \. Qany ointment/creams that they may have applied to# Z7 w; c2 q; [  ?7 Q* A
the child’s skin. This time the father admitted the
2 F2 x0 E- O3 t) X3 cTopical Testosterone Exposure / Bhowmick et al 541! ?' R8 P2 M- r9 x) K# Q* L8 m
use of testosterone gel twice daily that he was apply-
* n& `7 U" K2 t$ iing over his own shoulders, chest, and back area for
4 p3 ?0 H1 F9 k; ^0 O  f& r& Ua year. The father also revealed he was embarrassed2 o% p& @) y% j. `7 C
to disclose that he was using a testosterone gel pre-
( T5 E  ^" Z) Xscribed by his family physician for decreased libido
0 H1 e0 @% H, \1 E6 ~) `9 bsecondary to depression.
( ~5 o9 ]7 L  d9 e  l" |The child slept in the same bed with parents.! v! O) H- R1 l- n# c) ?( g  Z0 }
The father would hug the baby and hold him on his1 ~  H( K; d* y
chest for a considerable period of time, causing sig-% o; F  S& w0 g4 }1 l; J7 U
nificant bare skin contact between baby and father.) \. K5 O$ f& x+ J
The father also admitted that after the phone call,
% b  b! @) E: uwhen he learned the testosterone level in the baby" E; b# O6 f; X* O2 t" ?+ S
was high, he then read the product information
  h3 @  X; [, l# W' Kpacket and concluded that it was most likely the rea-
  Z# A! I$ S4 J  e" ]son for the child’s virilization. At that time, they
. G8 c1 _0 P/ V/ A) Xdecided to put the baby in a separate bed, and the
+ l4 c5 z8 ^: _9 h9 z6 {father was not hugging him with bare skin and had4 t6 m& G7 X& Y9 ^6 l
been using protective clothing. A repeat testosterone
. d# }$ g5 g9 T2 e+ Ttest was ordered, but the family did not go to the' U6 E- m. u* J1 K) a) _
laboratory to obtain the test.$ S  N0 S, i- V" D/ K7 E
Discussion) l) L, U& |$ ]/ |- V
Precocious puberty in boys is defined as secondary! n, y6 a8 Q( E# N& }# s$ S) I
sexual development before 9 years of age.1,4) m1 V% E/ R. M- z6 E
Precocious puberty is termed as central (true) when9 l1 {8 z  W$ |9 ^: p
it is caused by the premature activation of hypo-( u+ \7 s) S2 J1 i- R
thalamic pituitary gonadal axis. CPP is more com-8 I* }$ j4 M* n8 r4 P
mon in girls than in boys.1,3 Most boys with CPP3 W) ^. ?  `7 l9 F7 T6 x7 O2 Q& U; s" s2 A
may have a central nervous system lesion that is8 ?' g5 b# d& S7 b# W1 `
responsible for the early activation of the hypothal-
+ j( {4 r- K- b: r3 }3 Q7 namic pituitary gonadal axis.1-3 Thus, greater empha-! ]7 V/ o& ?, d  A, M/ s
sis has been given to neuroradiologic imaging in" o1 x, {# C" n. r* k# L5 F: @' C
boys with precocious puberty. In addition to viril-( B, |8 ?9 A- t3 F- P9 v3 }
ization, the clinical hallmark of CPP is the symmet-' X0 ]/ F7 D4 D7 f
rical testicular growth secondary to stimulation by
0 z+ F" o) A1 H1 K0 \$ ]: h& U" Vgonadotropins.1,3  j0 }8 o5 q' c5 k& C, g5 q
Gonadotropin-independent peripheral preco-& }' t2 {5 B1 S, }
cious puberty in boys also results from inappropriate
, q- u. Z3 I8 v9 f& T# c* Handrogenic stimulation from either endogenous or3 a7 C) G8 F- W$ w* k
exogenous sources, nonpituitary gonadotropin stim-
: L8 z: I# K7 @/ W% `ulation, and rare activating mutations.3 Virilizing
* k# O# y9 q- |. A  m+ x! ccongenital adrenal hyperplasia producing excessive" b3 P& `1 B, N4 ^5 \
adrenal androgens is a common cause of precocious/ I* e0 E: P- c
puberty in boys.3,4
! s$ \+ _) U: cThe most common form of congenital adrenal. j% B. q* I& g8 j% R* N; {
hyperplasia is the 21-hydroxylase enzyme deficiency.
% P6 l! {6 P3 l4 m, G0 w+ _, a8 l% hThe 11-β hydroxylase deficiency may also result in
  c8 F; u8 I( l+ L* _excessive adrenal androgen production, and rarely,  x+ X& L/ X  I" c! \$ ^
an adrenal tumor may also cause adrenal androgen
& Y8 j4 p6 h6 r0 V5 K' B! S# m/ Hexcess.1,3
/ i8 x% R8 z8 [  v$ K2 Sat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: c& l; _! s; j* }0 Z- B542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( i! ]6 X% {$ k% V$ ^6 }: ^
A unique entity of male-limited gonadotropin-
$ r  `+ s! w4 P0 |independent precocious puberty, which is also known% f7 ~; x* X  {, @( I! Q, `
as testotoxicosis, may cause precocious puberty at a' z# i" p& K$ m3 _8 [
very young age. The physical findings in these boys
% I% A. f$ R9 o' t) D! ?) swith this disorder are full pubertal development,
- C5 G1 Q6 U  v7 X; tincluding bilateral testicular growth, similar to boys& ]4 X$ q1 m$ A  x6 s# }! x
with CPP. The gonadotropin levels in this disorder
3 k" P; e: U" b" X$ g/ Z/ D; w% Bare suppressed to prepubertal levels and do not show
' w# t& `8 G1 p0 ?pubertal response of gonadotropin after gonadotropin-" J. u, ?( q/ m1 q& }8 P
releasing hormone stimulation. This is a sex-linked
+ {2 c  @0 n% V, z* S  d0 S0 xautosomal dominant disorder that affects only0 ?; S" v2 x8 J  F. I0 `4 @
males; therefore, other male members of the family( W9 j( \" g/ _! v
may have similar precocious puberty.3
+ X' V8 k, g7 O: T6 aIn our patient, physical examination was incon-+ i* i9 ~4 D+ B3 Z
sistent with true precocious puberty since his testi-5 u; n( U& I+ f( A$ L
cles were prepubertal in size. However, testotoxicosis3 Q: r0 e( Q  K# a7 B
was in the differential diagnosis because his father
, b5 T5 |- J7 Tstarted puberty somewhat early, and occasionally,
9 L2 J( q9 d& s  _testicular enlargement is not that evident in the
5 C, h2 Y$ M' p8 o2 [beginning of this process.1 In the absence of a neg-
6 e0 q8 S( b. }) }  ]ative initial history of androgen exposure, our" P; P$ s* D* D7 ~2 C4 `  X
biggest concern was virilizing adrenal hyperplasia,
+ Z, [& u: K$ F3 Heither 21-hydroxylase deficiency or 11-β hydroxylase7 R+ A: M2 I6 t% y; P! L! w, o
deficiency. Those diagnoses were excluded by find-9 n; E# O; ?. c, D# @* D' R
ing the normal level of adrenal steroids.
8 S5 x' U( I' DThe diagnosis of exogenous androgens was strongly- x: T  ^" \9 |3 H3 L  _! P( y
suspected in a follow-up visit after 4 months because
+ h3 h) b1 M" a! j# I/ ^, Vthe physical examination revealed the complete disap-
7 U5 g! l4 T; ~! S. |$ \' o2 ~pearance of pubic hair, normal growth velocity, and- U  w1 h. i' p2 g% P$ I
decreased erections. The father admitted using a testos-( X, n' C/ I& f; w; o
terone gel, which he concealed at first visit. He was" [' h: R* k! c
using it rather frequently, twice a day. The Physicians’
% G# l; l* ~' ~; t# ]9 b$ pDesk Reference, or package insert of this product, gel or# x- G7 \- M- X# {; j# g
cream, cautions about dermal testosterone transfer to
) y0 r2 A' B8 z0 ?7 tunprotected females through direct skin exposure.. a) L, l2 r1 b6 F4 J) C/ p
Serum testosterone level was found to be 2 times the1 u1 T5 r! ~* o0 w3 F
baseline value in those females who were exposed to
8 M, M' U0 V, E- I% Geven 15 minutes of direct skin contact with their male7 p/ B. I! K9 |8 e: `; S( ^( K
partners.6 However, when a shirt covered the applica-- J& y8 {; e: O% j4 D, s8 _9 p- H) M
tion site, this testosterone transfer was prevented.. G7 f* Y, I1 r2 a1 R! g6 `- w
Our patient’s testosterone level was 60 ng/mL,
4 P# N1 v$ T  a/ e/ i( _% e: E; zwhich was clearly high. Some studies suggest that
9 X) r# ~9 L* g2 Qdermal conversion of testosterone to dihydrotestos-
; M+ o; p7 S3 }0 K/ vterone, which is a more potent metabolite, is more
/ `  G& R, S! F, |active in young children exposed to testosterone! p( ~9 K9 ?: V7 \/ E* _/ |
exogenously7; however, we did not measure a dihy-8 K: w  Y7 ?! \" Y- J* W7 k# r6 w
drotestosterone level in our patient. In addition to: b2 ?% W# k. F0 ?: u8 w
virilization, exposure to exogenous testosterone in& S9 ?) e/ h! a7 S% s- o7 W8 P, s6 X
children results in an increase in growth velocity and) d6 {4 H* J% O4 w, E/ c
advanced bone age, as seen in our patient.
2 t8 v6 |6 {* R" L4 T" L, U7 S% _5 bThe long-term effect of androgen exposure during, O0 z( i; S: Z$ w  J
early childhood on pubertal development and final0 Z) k+ h( h  d
adult height are not fully known and always remain
1 M" y. p8 m# u- u* F+ c3 Pa concern. Children treated with short-term testos-
; x, f  ]% f) r3 K8 a) [# Cterone injection or topical androgen may exhibit some
/ Q% K6 N+ u3 m" [; P6 {acceleration of the skeletal maturation; however, after
3 ^2 M7 y+ N$ ~7 F9 {+ Q# c, Gcessation of treatment, the rate of bone maturation
$ U9 |! z% n5 S' }' ndecelerates and gradually returns to normal.8,9
+ M( _$ |% T3 ]. L; @& |; _  C% MThere are conflicting reports and controversy
6 v* J; s& B4 R0 S4 _over the effect of early androgen exposure on adult  g3 ]  E$ q- H# G4 c% w/ G
penile length.10,11 Some reports suggest subnormal
$ v& i" n3 J& C* t! `, s! ?6 Dadult penile length, apparently because of downreg-1 k8 K/ I$ [$ d( q
ulation of androgen receptor number.10,12 However,
% y: m# S1 d! s1 \% u0 _/ O2 iSutherland et al13 did not find a correlation between& j; Y, z' R, b, P1 e3 B8 W% t) `' o
childhood testosterone exposure and reduced adult  W7 ]: ]3 j$ {- J# X5 q/ c) J/ m
penile length in clinical studies.
" ]  l  M2 h. s5 |& bNonetheless, we do not believe our patient is/ S/ _. F. d/ q* i$ y$ {1 ]
going to experience any of the untoward effects from
9 }# \6 b- g/ k/ }# S* g* ktestosterone exposure as mentioned earlier because
8 G+ s5 q# i- Q& `! Y5 a  f& vthe exposure was not for a prolonged period of time.
7 l8 M% v7 C! N! D$ PAlthough the bone age was advanced at the time of
$ U6 n8 |/ |1 V# D  Zdiagnosis, the child had a normal growth velocity at6 L8 r/ _% E7 k2 m" J, T' j4 l" U
the follow-up visit. It is hoped that his final adult# o, f* c# ^3 Q7 J! ?2 Q% h
height will not be affected.
* M4 E) s, E$ a9 T7 a. TAlthough rarely reported, the widespread avail-1 z* H3 t( A. t0 f8 U
ability of androgen products in our society may  A& ^! ~5 B2 p/ w7 q& U, H& R
indeed cause more virilization in male or female# Z8 \) @8 I9 j* s  }
children than one would realize. Exposure to andro-( V9 S+ _( v- V) [! T0 V9 ]
gen products must be considered and specific ques-/ ?0 l& K9 e! Y& O4 Q8 U
tioning about the use of a testosterone product or% h* b- V9 l: w0 F* {6 H
gel should be asked of the family members during
% {) ?" _: l# b' ~3 e9 P5 vthe evaluation of any children who present with vir-
* Q0 E: F; H# \7 T8 x) K8 Qilization or peripheral precocious puberty. The diag-4 k0 V' t1 w: d1 t
nosis can be established by just a few tests and by
  V- o/ R9 s, _7 f: ]appropriate history. The inability to obtain such a% ?# s& O# g/ d- d) O
history, or failure to ask the specific questions, may
! a% {" o6 j  l/ Fresult in extensive, unnecessary, and expensive
, S1 O# n" t8 ?3 sinvestigation. The primary care physician should be
2 c+ r. q. s1 l* h; V& laware of this fact, because most of these children' e% I4 S$ R4 u5 S0 Y
may initially present in their practice. The Physicians’" M( V) I, U2 ^8 x1 X
Desk Reference and package insert should also put a
- }3 Y2 {6 m, C6 A2 I3 bwarning about the virilizing effect on a male or! h9 T3 J" _4 Q4 b* m
female child who might come in contact with some-
; v9 a$ I% G8 m! M8 ]9 Wone using any of these products.' n! w* @$ N" `% }) q8 Q1 P5 c
References+ T% h' v* `! J
1. Styne DM. The testes: disorder of sexual differentiation" V) I# ]/ n7 \  `6 {! N4 g# ^* x
and puberty in the male. In: Sperling MA, ed. Pediatric
- v$ R1 ~0 o" t2 tEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; v9 N6 n( ?) C2002: 565-628.; `9 q9 A! I2 d4 L0 y1 l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
) e( a3 d" `0 I, Rpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
) w1 M" `6 V1 l5 V9 GBoy Induced by Indirect Topical
+ e. U* V& u( F; L9 \: p1 }/ AExposure to Testosterone
* ^( W5 R' I0 d- B& wSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 p) w6 R, h' h9 K
and Kenneth R. Rettig, MD1
( B- t- p: y6 L7 n9 G# Y3 i/ `' @) yClinical Pediatrics
7 u* H: Y1 w. B1 F' J, K! hVolume 46 Number 6
& j) V; O3 k- m. c& ~" CJuly 2007 540-543, v$ t, p. J8 \  l7 j+ q' H
© 2007 Sage Publications. Y2 x" w- e0 e3 O
10.1177/0009922806296651- ]9 I, U- x; L% B! N
http://clp.sagepub.com: F' A4 f2 I/ q8 d0 |- s
hosted at8 k8 n) V3 m, P* q6 z8 W  V9 O
http://online.sagepub.com# V/ ~4 J8 V+ n9 e
Precocious puberty in boys, central or peripheral,+ k! E3 ?& S2 ?9 g4 P6 r+ Y4 t2 t
is a significant concern for physicians. Central
2 E% ^' P. O7 X  \2 Tprecocious puberty (CPP), which is mediated
; i, g; D' ?! f8 d: Qthrough the hypothalamic pituitary gonadal axis, has
6 ^, K9 ~0 ]& ~/ z# x  g+ la higher incidence of organic central nervous system
9 V, u/ j- ]0 K1 x: I: \lesions in boys.1,2 Virilization in boys, as manifested- r' }' t0 h; K" a! r
by enlargement of the penis, development of pubic
: L5 S8 D- y, R. l4 rhair, and facial acne without enlargement of testi-
4 W0 L8 @3 E6 W! {# ], m1 t# M' Fcles, suggests peripheral or pseudopuberty.1-3 We
; g- E/ Z- }' p# v8 T3 ^6 {report a 16-month-old boy who presented with the% S0 a; T4 a6 B2 B( Q
enlargement of the phallus and pubic hair develop-
9 ~/ m* x' {! \3 L5 kment without testicular enlargement, which was due
0 B6 M0 V! w' j" i9 P$ Mto the unintentional exposure to androgen gel used by. G2 T/ b# O% S# ?
the father. The family initially concealed this infor-
2 f) P5 i/ J5 d* t  I. s. W/ h. Gmation, resulting in an extensive work-up for this
1 \! T0 }3 Q5 a! @. P/ Lchild. Given the widespread and easy availability of4 }/ m  H) }1 o6 Y3 I
testosterone gel and cream, we believe this is proba-7 p" v( T5 R% k
bly more common than the rare case report in the  e- J8 e6 B8 j
literature.4# C7 S: U/ `9 N  _& o+ ?! L$ k8 d; `9 |
Patient Report: b/ n" V& R7 |- g  P
A 16-month-old white child was referred to the
  o% Z' f# c8 N1 Y' V, ^, g) V! qendocrine clinic by his pediatrician with the concern
  H7 t$ I7 a1 v$ k# Wof early sexual development. His mother noticed
, V# M+ J5 C% [% g3 h7 [light colored pubic hair development when he was1 _: P$ Y/ O6 f. t
From the 1Division of Pediatric Endocrinology, 2University of  i  @. ^( X3 w/ g% x' I% J/ y
South Alabama Medical Center, Mobile, Alabama.
3 a8 B' w8 U, S; i* [; \) {! p, ?Address correspondence to: Samar K. Bhowmick, MD, FACE,
/ h$ }8 u' C1 O; m( B# yProfessor of Pediatrics, University of South Alabama, College of- _! l% S# o% L! g
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. E" t8 F/ U0 }1 Y+ r0 A4 `e-mail: [email protected].9 O1 ]* M; |5 ]. ?! ?7 B
about 6 to 7 months old, which progressively became
9 Z& k. k4 @# X# k# kdarker. She was also concerned about the enlarge-+ e: X2 E. @& z
ment of his penis and frequent erections. The child, ~' S3 k6 {/ t( c2 |
was the product of a full-term normal delivery, with# u2 ]1 s8 ]% K  f' h
a birth weight of 7 lb 14 oz, and birth length of
; L- Y" e$ X+ ]4 d' j20 inches. He was breast-fed throughout the first year9 @' e# j3 ]! w
of life and was still receiving breast milk along with
5 j+ p0 y8 _5 ]solid food. He had no hospitalizations or surgery,
9 ?. X. k# Z7 G$ s5 O6 D( Q8 ]# L3 [and his psychosocial and psychomotor development
5 z- J/ r8 Q4 m& |1 e( j7 O5 Y% Mwas age appropriate.
5 F- I- j) k" |4 DThe family history was remarkable for the father,
4 z% B# f3 F5 twho was diagnosed with hypothyroidism at age 16,+ U* W, [6 M' k4 a: s* l8 v
which was treated with thyroxine. The father’s$ \0 O* y2 }1 p& a) u
height was 6 feet, and he went through a somewhat% E$ L& O; Y, w4 [
early puberty and had stopped growing by age 14.
  \( N) M4 h, [- }The father denied taking any other medication. The! j9 W4 F% v0 c. N( `5 l7 U$ F
child’s mother was in good health. Her menarche
6 u4 h& Y! t( j5 X: R/ D( Cwas at 11 years of age, and her height was at 5 feet: X+ i& \+ e) Z1 l8 k0 c
5 inches. There was no other family history of pre-# c9 |' W# D6 P, a; F. E) v
cocious sexual development in the first-degree rela-% V! V6 m& X3 E1 _# F( e
tives. There were no siblings.! _9 y2 v$ A8 n6 H$ c
Physical Examination* d3 L" m9 i$ e0 q7 U; B% t  p
The physical examination revealed a very active,( q& ^3 c' s; j1 ^0 \- G: d7 m& ?
playful, and healthy boy. The vital signs documented& D, W2 Y1 v7 R
a blood pressure of 85/50 mm Hg, his length was
& u6 r; p" X  c4 P; d8 f90 cm (>97th percentile), and his weight was 14.4 kg
7 l; a) Z7 \; Y; @(also >97th percentile). The observed yearly growth
+ i$ G' E$ R5 q. ~velocity was 30 cm (12 inches). The examination of
- \1 f+ T8 K: w& u8 Uthe neck revealed no thyroid enlargement.# Y9 R" B; B7 V- T8 n  q% r' @+ r& {
The genitourinary examination was remarkable for' N8 o0 S! ?1 A% L0 `- S7 K! F
enlargement of the penis, with a stretched length of
# m. x6 _* U8 N, n8 cm and a width of 2 cm. The glans penis was very well
9 d9 `' N9 S" f% J# N% L- gdeveloped. The pubic hair was Tanner II, mostly around- w3 L5 a- f6 t) l) z' b4 m
540
$ H' `1 h0 W7 y% X0 v, bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 d" m# n4 C! g2 bthe base of the phallus and was dark and curled. The
2 w) a% @, g+ c7 r9 Dtesticular volume was prepubertal at 2 mL each.
& d1 D9 l& ~1 \3 Q. yThe skin was moist and smooth and somewhat
& `5 A; T# b0 v' F0 P5 N, x' Doily. No axillary hair was noted. There were no
( Z7 n! |! s3 z1 E) M, Zabnormal skin pigmentations or café-au-lait spots." t- |6 m" p: M2 Y
Neurologic evaluation showed deep tendon reflex 2+1 v/ [- K7 k7 Q9 ?0 l# e
bilateral and symmetrical. There was no suggestion4 L" _0 `; w! g8 y/ [9 ?
of papilledema.$ j+ q0 I8 _5 E. ]$ [  P, ?
Laboratory Evaluation
( R: y1 X! \' U# x1 ^2 z# E  dThe bone age was consistent with 28 months by% D( G* F6 O$ l
using the standard of Greulich and Pyle at a chrono-0 w4 }1 o* D8 P" l* w
logic age of 16 months (advanced).5 Chromosomal
; d8 d$ r2 ^9 U# p0 h' vkaryotype was 46XY. The thyroid function test
1 O1 Q# ]- {- o! H+ Pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-, Y1 S( J  ~' v+ ^; _- w+ J- Q
lating hormone level was 1.3 µIU/mL (both normal).# t$ w) W0 S  G: k" o! E
The concentrations of serum electrolytes, blood0 B5 A# i. ~9 c) l0 k4 `
urea nitrogen, creatinine, and calcium all were
. K  n' ~, k' _within normal range for his age. The concentration
9 h3 D2 ]2 ]+ [. T8 G" G/ n6 c; |; c# vof serum 17-hydroxyprogesterone was 16 ng/dL
% v  G& t/ u: v% a(normal, 3 to 90 ng/dL), androstenedione was 20
+ S4 n* h1 F/ F& h) `/ Mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' m7 k% W2 q3 t+ l- P9 J
terone was 38 ng/dL (normal, 50 to 760 ng/dL),8 T- F. y) [3 x* w, ~) V
desoxycorticosterone was 4.3 ng/dL (normal, 7 to1 `$ i- M: J' @$ |
49ng/dL), 11-desoxycortisol (specific compound S)
1 j4 X3 x/ W, W% u+ iwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) i% _& r, D3 n8 V( j! A! s* ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, R& K- t' z# G& d& rtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 b0 [/ j# t* z# s7 E
and β-human chorionic gonadotropin was less than
; O9 l- t9 o+ |6 v5 mIU/mL (normal <5 mIU/mL). Serum follicular
" {6 P; v- c, W( H7 F: ]% F9 M* nstimulating hormone and leuteinizing hormone
5 J0 f- s, d6 ^6 fconcentrations were less than 0.05 mIU/mL
2 B$ T/ N# U4 J4 O5 h5 @(prepubertal).
* Z' |$ ?6 Z* U* b* A0 J! kThe parents were notified about the laboratory
8 s  R  {& p/ ^3 c% d9 e3 Bresults and were informed that all of the tests were
; v# U6 B9 i, w/ ^9 X; |normal except the testosterone level was high. The; u" p; \5 E; {' N
follow-up visit was arranged within a few weeks to1 \1 ]$ ?7 G2 i& w: f) s
obtain testicular and abdominal sonograms; how-
8 u9 r# l: _5 ?+ S+ @0 Y% Bever, the family did not return for 4 months.
4 L8 x$ t, K8 _/ IPhysical examination at this time revealed that the
! q, |: u# E7 ^: h! c' d) P" Ychild had grown 2.5 cm in 4 months and had gained
9 p$ o" F0 G6 `% }, T0 M* I8 J. E2 kg of weight. Physical examination remained7 t7 s, {2 d& @+ C8 i; E7 V* n
unchanged. Surprisingly, the pubic hair almost com-/ w( @. M+ g% l
pletely disappeared except for a few vellous hairs at
0 D, l# |& ?: `. H4 tthe base of the phallus. Testicular volume was still 2; |! ?' c; K( k0 c
mL, and the size of the penis remained unchanged.# A( q6 i; {! ~9 c9 Y
The mother also said that the boy was no longer hav-7 {1 f* c0 V. t9 L8 j
ing frequent erections.  r% _6 @! ]2 H1 o4 |1 Q& \% M( w
Both parents were again questioned about use of
2 X5 B6 T  R0 G# F% p- k8 jany ointment/creams that they may have applied to
5 j  }, v0 i: ?  R& ~the child’s skin. This time the father admitted the6 s4 \0 _6 t, Z, }5 j! a  |8 A
Topical Testosterone Exposure / Bhowmick et al 541
# u2 L4 t2 E, o2 f) M. Z) Tuse of testosterone gel twice daily that he was apply-0 X) c. I9 G5 u: y# p* _
ing over his own shoulders, chest, and back area for: Y; B! E# M5 p3 Y
a year. The father also revealed he was embarrassed
2 e2 R0 l, ]8 H& |2 Bto disclose that he was using a testosterone gel pre-
: A9 g; p5 |- Kscribed by his family physician for decreased libido) a: H; v( `5 h( u* s; H) Z' ~
secondary to depression.
$ n" r1 A& Q6 o- V1 m! [The child slept in the same bed with parents.1 |8 j# f2 v) s) E7 C
The father would hug the baby and hold him on his! `% t# w* X8 N- Q; @+ c5 u; v( ]  ]1 i
chest for a considerable period of time, causing sig-
1 t7 j: H, u( {4 B+ a5 g% T% knificant bare skin contact between baby and father.' c* x5 c( q9 ]: d" z) q
The father also admitted that after the phone call,
& Z, y, r$ _, |1 m& j' wwhen he learned the testosterone level in the baby/ M6 [& m% D/ z; J+ b, P
was high, he then read the product information4 o/ b& H1 A! O5 K0 j. e
packet and concluded that it was most likely the rea-
/ R! }1 n7 D+ k6 @8 W1 n- ason for the child’s virilization. At that time, they
  T0 ^0 y- O4 Fdecided to put the baby in a separate bed, and the
" N1 t4 x8 e  Nfather was not hugging him with bare skin and had
5 V$ e; p9 [; ybeen using protective clothing. A repeat testosterone
& [4 K/ }' B! \7 X+ `/ vtest was ordered, but the family did not go to the
8 k. @/ e( I* D4 z4 f! I# qlaboratory to obtain the test.3 @. \. ?# L. v
Discussion
+ x; W: b1 a- j: B4 m8 i3 aPrecocious puberty in boys is defined as secondary# N- p0 F+ I# X# D& ]
sexual development before 9 years of age.1,4- W3 @( n3 z4 ?) A" a/ g
Precocious puberty is termed as central (true) when' w) H0 d1 s( }4 x( k; d
it is caused by the premature activation of hypo-9 C$ Z* f  N2 T
thalamic pituitary gonadal axis. CPP is more com-: Q* w( r7 E# b7 P" Q- i0 t8 ]6 }5 h2 z
mon in girls than in boys.1,3 Most boys with CPP
- K  v. K: W1 U1 r$ Cmay have a central nervous system lesion that is0 p  {& x4 G4 z( ^) `$ ~$ Y
responsible for the early activation of the hypothal-
" b! o4 |6 J5 R5 _% @4 g4 Jamic pituitary gonadal axis.1-3 Thus, greater empha-1 ~9 K" E2 H/ `3 y
sis has been given to neuroradiologic imaging in
& ^; ~1 N, S! ?9 ^boys with precocious puberty. In addition to viril-
( X4 ^  O8 j7 w+ }6 n4 u( Q: Dization, the clinical hallmark of CPP is the symmet-3 P) ~9 R7 r0 n! @
rical testicular growth secondary to stimulation by; t; c) L; t$ `: h  q
gonadotropins.1,3
3 u, _" T( R  X' Z+ h# h# ~Gonadotropin-independent peripheral preco-2 O* z/ {" Q5 q! h6 s0 B
cious puberty in boys also results from inappropriate2 b0 Y1 s2 J# W" P& y- P. X7 u
androgenic stimulation from either endogenous or
8 Z) p5 E% i0 mexogenous sources, nonpituitary gonadotropin stim-
% ~4 y( q; _% A1 G, n1 Z- R0 hulation, and rare activating mutations.3 Virilizing9 J1 M! d* C7 T5 x
congenital adrenal hyperplasia producing excessive
$ z' D5 ^: ]3 o8 padrenal androgens is a common cause of precocious
8 g1 i) f8 c' Kpuberty in boys.3,41 g/ F: K& r5 F! `0 y
The most common form of congenital adrenal
2 y( y& r0 F. T$ S* t  ahyperplasia is the 21-hydroxylase enzyme deficiency." @2 V" a1 w3 p* C: A5 F9 _
The 11-β hydroxylase deficiency may also result in
) F0 t$ n1 O4 ~4 zexcessive adrenal androgen production, and rarely,5 i, V6 m" A/ m1 A4 j; e
an adrenal tumor may also cause adrenal androgen$ w/ H) Z4 h! t& k/ O4 G8 W
excess.1,38 V. T; q. T( [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 @9 n/ ~/ }1 {: ]+ v542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; h, ?+ G& o) K
A unique entity of male-limited gonadotropin-
! `" f/ l( i1 }: f  O' ^6 D8 C, b3 Tindependent precocious puberty, which is also known# u" J* F, Z$ G% c/ I
as testotoxicosis, may cause precocious puberty at a
& ^( ^4 Q6 Y* l8 E4 dvery young age. The physical findings in these boys( F0 {. C5 W: e: j* e! ]: o2 |
with this disorder are full pubertal development,
$ n. o3 I6 H6 {$ e( ?1 Q  u* uincluding bilateral testicular growth, similar to boys
7 o  d9 e1 o; K0 j5 M# ]& mwith CPP. The gonadotropin levels in this disorder$ o7 b4 {8 Z- f) a
are suppressed to prepubertal levels and do not show# R/ O3 B$ G4 e" x$ G; j
pubertal response of gonadotropin after gonadotropin-
3 g/ x. b/ Y0 @) P% ureleasing hormone stimulation. This is a sex-linked7 U  S# r9 I. R" |
autosomal dominant disorder that affects only4 n; _; O, Q9 W7 Z: |* w
males; therefore, other male members of the family6 q: U! U/ D  c6 v7 @
may have similar precocious puberty.3
- e) l7 ^$ D0 b+ ~- ]% tIn our patient, physical examination was incon-
6 n1 x# e' T# O) asistent with true precocious puberty since his testi-5 `- n, [" P9 T* u: Q0 O1 Q
cles were prepubertal in size. However, testotoxicosis" @% w: n/ u) f7 y$ }- o; k
was in the differential diagnosis because his father
" k$ x+ H5 V6 z8 E: T7 p' Ystarted puberty somewhat early, and occasionally,
, K! h  j0 C5 Rtesticular enlargement is not that evident in the3 s; V; T, r3 ]! P. A# K* p
beginning of this process.1 In the absence of a neg-3 t4 T8 F# ^6 ~' x" p, a% `7 E6 Q
ative initial history of androgen exposure, our' ?: l: e6 E* r2 n& x& {) z
biggest concern was virilizing adrenal hyperplasia,; N2 t' [) o. p
either 21-hydroxylase deficiency or 11-β hydroxylase
3 n  N4 W: @% \: n1 Hdeficiency. Those diagnoses were excluded by find-- [3 ]* _. o8 B4 _1 R
ing the normal level of adrenal steroids.
! {: u* K1 |8 ?5 JThe diagnosis of exogenous androgens was strongly
) o1 T5 l4 ]+ z( Csuspected in a follow-up visit after 4 months because
6 U- e/ B( A" E2 z- g) w: qthe physical examination revealed the complete disap-
3 d- ~8 P$ Z& l2 y6 j  Apearance of pubic hair, normal growth velocity, and9 o) l8 c. A3 t" S
decreased erections. The father admitted using a testos-2 I# H2 N( c* u. `. _. A
terone gel, which he concealed at first visit. He was
! C& @+ ?' C. {, f5 Busing it rather frequently, twice a day. The Physicians’' n0 H; {1 B( p- [
Desk Reference, or package insert of this product, gel or
0 v! O& e) y+ l; }: ?% g4 ~  M( acream, cautions about dermal testosterone transfer to
) @0 M4 \# u" s0 e: b; funprotected females through direct skin exposure.
5 w* J( M* U' y+ t( _Serum testosterone level was found to be 2 times the
+ J; n! Z+ z) ibaseline value in those females who were exposed to: }$ S8 R: @6 T3 a+ U
even 15 minutes of direct skin contact with their male
) s/ u8 m3 l9 e1 U4 f5 dpartners.6 However, when a shirt covered the applica-4 U: U- x. L# g, d2 x  F) a, A1 ~) u) E
tion site, this testosterone transfer was prevented.6 z4 K" c& W: d0 v) ^6 o: I2 o
Our patient’s testosterone level was 60 ng/mL,
: W) L2 u, S& a! k5 Cwhich was clearly high. Some studies suggest that
' ]0 f  I  O# g- m3 Y+ c8 ydermal conversion of testosterone to dihydrotestos-
# Z; G. V+ z+ h9 x/ Z6 N9 `terone, which is a more potent metabolite, is more$ r/ K. |: W" @/ y2 k
active in young children exposed to testosterone
  B9 [2 q  n' Z7 Texogenously7; however, we did not measure a dihy-: Q# ^7 K0 D- T  m: m
drotestosterone level in our patient. In addition to
0 [- W4 c. O9 v& ]8 h) Ivirilization, exposure to exogenous testosterone in2 q+ \, j/ e0 a, z9 e
children results in an increase in growth velocity and
0 E4 i. N/ [5 t  Madvanced bone age, as seen in our patient.- U2 h' ]$ Y- b! K: O- g  \
The long-term effect of androgen exposure during) M" d8 }+ g# X0 L% M9 l+ l+ I- [
early childhood on pubertal development and final
/ _* @3 v6 o8 o7 Badult height are not fully known and always remain
, s" N% c4 w9 j$ ua concern. Children treated with short-term testos-. k9 u. `6 w& ]* R8 |/ J4 Y5 ?- b* e
terone injection or topical androgen may exhibit some
6 d- a1 ?8 J+ eacceleration of the skeletal maturation; however, after
7 [7 Z! {% F& Y+ L$ s  ?cessation of treatment, the rate of bone maturation& b% u0 K/ H1 s: d# }( O+ S
decelerates and gradually returns to normal.8,9
, h* Q3 [" G  ~' VThere are conflicting reports and controversy( D$ i$ V7 H5 V2 n1 Z; c% b
over the effect of early androgen exposure on adult1 j4 \/ p8 }9 q" m5 D
penile length.10,11 Some reports suggest subnormal8 n: Y& v& R. [" f) m' D8 p$ W( ?
adult penile length, apparently because of downreg-
1 e8 G% f. ^& U) |! D( i  zulation of androgen receptor number.10,12 However,
0 z2 ^( ~  R2 a7 RSutherland et al13 did not find a correlation between
3 C- k2 a6 l  c# J2 z( K% \childhood testosterone exposure and reduced adult! p; q7 n8 H( w' Y
penile length in clinical studies.! c, [5 J$ H) T- `& U: L0 C
Nonetheless, we do not believe our patient is
, p/ L' ?8 j& Q$ k' ]( u- Agoing to experience any of the untoward effects from8 W# C) o  t0 a2 v
testosterone exposure as mentioned earlier because
$ T+ x' \% k8 ^, uthe exposure was not for a prolonged period of time.
- q8 w0 X& x: D/ `' ]+ ^, w$ OAlthough the bone age was advanced at the time of
8 D4 R+ u2 `7 E6 ]diagnosis, the child had a normal growth velocity at
) \3 e# {/ x; c  s4 h5 p9 g2 Ythe follow-up visit. It is hoped that his final adult
6 q3 w) ~6 J, i/ {" |2 \height will not be affected.
% w7 U- a) E5 G/ d& lAlthough rarely reported, the widespread avail-; O) c- o  t+ x4 d
ability of androgen products in our society may5 e4 W; H) \1 r' \. S/ h" P
indeed cause more virilization in male or female% k5 s  o1 e" ~9 G
children than one would realize. Exposure to andro-
2 O3 x9 _( y" l! c8 @  Vgen products must be considered and specific ques-
$ @0 A4 t" A( Ltioning about the use of a testosterone product or
5 t0 U/ H4 \% q! fgel should be asked of the family members during
2 {/ c( G8 _3 w( Vthe evaluation of any children who present with vir-
$ |( o/ D% n2 ~, b5 r& N" g* m0 nilization or peripheral precocious puberty. The diag-
6 d- H- g6 S: h1 wnosis can be established by just a few tests and by8 \4 F# ~" O; Z5 X2 \3 W( v
appropriate history. The inability to obtain such a' C2 p; l" n- I( _* @( C$ x7 ~% F: t6 J
history, or failure to ask the specific questions, may: Y, J& F0 C0 j) ^
result in extensive, unnecessary, and expensive
; ]( ]7 G! F' N, minvestigation. The primary care physician should be
9 [7 J. `- W5 z7 c1 H' \& V% Maware of this fact, because most of these children$ w; L0 ]0 r+ ~
may initially present in their practice. The Physicians’
3 R9 l; a; v4 RDesk Reference and package insert should also put a
5 Q5 w; Z4 Y- F5 W& b8 k" c( Gwarning about the virilizing effect on a male or2 P  E, J8 S" a& J/ Z* L
female child who might come in contact with some-- S, S' M5 r* A% G2 a4 \( F* @7 P
one using any of these products.
1 T  c. R/ m9 U; [: q, t4 zReferences: x1 j9 N- i# {! K5 z3 B4 n
1. Styne DM. The testes: disorder of sexual differentiation
) F9 ?' z9 \6 X6 j7 A5 hand puberty in the male. In: Sperling MA, ed. Pediatric
; ?9 u6 i8 Q3 s) wEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- `3 ^$ g1 n  [+ K! _; N2002: 565-628.) b7 l8 J" c) B+ x% n
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
5 F) ]( h# ]  C5 m* A- Xpuberty in children with tumours of the suprasellar pineal
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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!

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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!
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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

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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?
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發表於 2025-1-19 02:41:05 | 顯示全部樓層

6 ^6 f2 y0 R( B3 H6 W; y4 T- h精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
 分享同時學會感恩,一句感謝的話語,就是最大的支持!  歡迎交流討論
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