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Sexual Precocity in a 16-Month-Old/ z6 r8 O- T2 m) W% [" t
Boy Induced by Indirect Topical
, x8 D7 w, h+ Z! u5 uExposure to Testosterone( c) B! o5 z, u" m
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 R4 p' k- F! b7 @3 R
and Kenneth R. Rettig, MD1' k1 \. ?" N( N/ }# j% P# v2 ]
Clinical Pediatrics2 @0 P8 I- {, C3 B5 j) n! E
Volume 46 Number 6) f. ?- X# |3 K* _$ |6 m
July 2007 540-543) m0 L; Y4 A3 ?& {) r9 {& Q
© 2007 Sage Publications: }$ {4 K! a6 n
10.1177/0009922806296651$ e0 A' @' ~6 Q% L# r$ s
http://clp.sagepub.com% S: K, E/ _( I- K
hosted at, ^& d; J3 G& W8 y; X
http://online.sagepub.com; A. }) _" d2 j' O& l, ?  O8 w6 h
Precocious puberty in boys, central or peripheral,, L" E- I" j8 i) H
is a significant concern for physicians. Central# r6 n/ R% A# G8 f
precocious puberty (CPP), which is mediated
6 S( S7 \( X& L- m2 P+ @6 {: y& B7 \through the hypothalamic pituitary gonadal axis, has& ]* ~3 j1 f0 p% F& x* g) t
a higher incidence of organic central nervous system
: J4 U& d3 v- Slesions in boys.1,2 Virilization in boys, as manifested
" T) ]1 S8 R- }by enlargement of the penis, development of pubic( d- {3 E7 m  O3 ]
hair, and facial acne without enlargement of testi-: B8 L7 T* U. H9 Z" l0 d# y! p
cles, suggests peripheral or pseudopuberty.1-3 We
; z* y1 q2 n& {1 g- b; oreport a 16-month-old boy who presented with the) i  J1 Z/ z. [# C  ^4 B$ m
enlargement of the phallus and pubic hair develop-, y  j0 p6 w: q7 O
ment without testicular enlargement, which was due+ z  j% |( C6 ~, B4 m% {6 L. ~4 U4 u
to the unintentional exposure to androgen gel used by3 K5 T3 A; x: ?6 K  p/ m; C
the father. The family initially concealed this infor-, w% v5 Y, F5 x. ]5 [
mation, resulting in an extensive work-up for this
7 z5 c5 {% v8 w+ u/ g" f. Kchild. Given the widespread and easy availability of
  N) S8 e0 e2 b) x5 z' Y& U3 x/ Ztestosterone gel and cream, we believe this is proba-: y. G: Z  |+ `4 \) O
bly more common than the rare case report in the' h, R0 F  n9 Q
literature.4
4 h1 O3 f# g, M  k, tPatient Report- R1 \* u4 @: Q: k
A 16-month-old white child was referred to the
2 b) g; K, T' N4 N& c& nendocrine clinic by his pediatrician with the concern
% e1 n% c( k2 a! O, a- G- _of early sexual development. His mother noticed2 m! {9 `2 p) @$ |; d/ t: o
light colored pubic hair development when he was6 }+ w8 a( [8 g1 Q! v5 N& w
From the 1Division of Pediatric Endocrinology, 2University of
5 |2 i" i5 @- g0 W2 |& v; nSouth Alabama Medical Center, Mobile, Alabama.$ e1 L, t( n; `& d& U* X0 B+ |( P
Address correspondence to: Samar K. Bhowmick, MD, FACE,
2 R% i" g3 n# Q5 G  R+ HProfessor of Pediatrics, University of South Alabama, College of1 c# N, E/ n) v( }  K7 P, k
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  F0 {- t7 H5 v: N$ w$ ?e-mail: [email protected].
4 v% E4 ?, H# ^' j" _: x2 Nabout 6 to 7 months old, which progressively became
! s/ T- \: U2 Jdarker. She was also concerned about the enlarge-
' M1 r* k( ?/ a% ?# q8 D: `ment of his penis and frequent erections. The child: Y# D; i! D: d8 H7 B- M5 y4 y( |
was the product of a full-term normal delivery, with
$ a* M& U, t' P) [% `a birth weight of 7 lb 14 oz, and birth length of
- R+ x* f, C. P" @: w2 V20 inches. He was breast-fed throughout the first year
0 p) Z3 ~9 F6 ?of life and was still receiving breast milk along with& F& o  Y+ {: A( ^$ z
solid food. He had no hospitalizations or surgery,
% K& r8 B9 M* l# C9 i7 [( p, _and his psychosocial and psychomotor development; A; @- c6 [" [" q+ J" h3 @+ W( {
was age appropriate.
1 e7 u; N" H' B' w7 }% W6 BThe family history was remarkable for the father,
/ i) |/ }* S) D8 ]" Z4 z' Qwho was diagnosed with hypothyroidism at age 16,
, ^& W3 Y9 ]# owhich was treated with thyroxine. The father’s/ a7 M, L0 e1 ?
height was 6 feet, and he went through a somewhat
+ S+ ]" c4 W$ G' Mearly puberty and had stopped growing by age 14.
4 c; g9 @2 r6 y/ v+ {# o  EThe father denied taking any other medication. The
5 S7 N* a5 }% Q  o7 Qchild’s mother was in good health. Her menarche5 M2 m) q+ T8 m# d! _3 H
was at 11 years of age, and her height was at 5 feet  R- o+ v- ^* q0 Q" m! M
5 inches. There was no other family history of pre-1 L% q6 N) E) C$ D. G6 I
cocious sexual development in the first-degree rela-
" F1 S) r4 L* O) n+ g( Etives. There were no siblings.
/ z0 K5 {/ }( d6 [Physical Examination% b0 J0 C+ H* f8 h/ Z9 g
The physical examination revealed a very active,4 v, L: j' \, ]" K. V! u  w
playful, and healthy boy. The vital signs documented/ S& L2 Z9 n( H6 Z% b' v# ]
a blood pressure of 85/50 mm Hg, his length was! o  y! C: d* \% a& L4 B$ p  H3 y
90 cm (>97th percentile), and his weight was 14.4 kg
: B: L8 g7 r4 ^(also >97th percentile). The observed yearly growth/ N% [( V. r0 ~' P- x1 {
velocity was 30 cm (12 inches). The examination of
  q2 D+ ~: s+ p1 R) Kthe neck revealed no thyroid enlargement.
: G2 T1 H/ _2 uThe genitourinary examination was remarkable for7 o! k7 n: C$ e0 I7 L& m* a( Y
enlargement of the penis, with a stretched length of
, i# n* U! h& B5 \8 cm and a width of 2 cm. The glans penis was very well
0 [/ J: [/ H. S  ]/ E$ q4 I8 udeveloped. The pubic hair was Tanner II, mostly around
! L/ o- U5 U* t5 `8 `540, a& P- c- m! ?+ t, ]8 B7 [
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" n$ [4 S( h. u+ R
the base of the phallus and was dark and curled. The
5 O6 D; b9 f. i7 U9 V  y1 Ltesticular volume was prepubertal at 2 mL each.) V  ?# O) F& D4 d1 |! P1 x
The skin was moist and smooth and somewhat
; r& {& w5 s5 [3 M! L; e2 Poily. No axillary hair was noted. There were no
9 e1 ~- L% N. A9 i/ |! {9 Vabnormal skin pigmentations or café-au-lait spots.0 w% W1 b1 i% Q. U: z3 a
Neurologic evaluation showed deep tendon reflex 2+9 Z( ^* }# q% H/ z2 `
bilateral and symmetrical. There was no suggestion
. b0 |( r. K8 \: ^1 e( V& tof papilledema.
6 F. Q! b6 ?# y( d- ?, t* n8 `, \Laboratory Evaluation! u/ E5 v5 f3 T8 X0 ?$ ^  k
The bone age was consistent with 28 months by
$ X4 f2 r  F0 y/ S/ y1 rusing the standard of Greulich and Pyle at a chrono-7 Y( g  [4 @% x# ]# [' i8 D# l
logic age of 16 months (advanced).5 Chromosomal/ O7 ~* N$ @$ C, F5 M$ Z$ W
karyotype was 46XY. The thyroid function test* V. `: Z  @2 Z, Z# j/ l
showed a free T4 of 1.69 ng/dL, and thyroid stimu-. Q) f- E2 A0 y3 d
lating hormone level was 1.3 µIU/mL (both normal).
  Y# W$ k7 `1 `; iThe concentrations of serum electrolytes, blood
! d1 x4 V$ ~2 j* ?: n* g- R7 c( @urea nitrogen, creatinine, and calcium all were
8 g: ?4 Z/ ^, w: @0 @9 G2 x+ `within normal range for his age. The concentration/ o3 B' `  c. t1 ]4 n' p. H
of serum 17-hydroxyprogesterone was 16 ng/dL% |( y" c% B* Z, u( i* |5 L
(normal, 3 to 90 ng/dL), androstenedione was 20
' e) W8 J5 l' G) S5 X: R* bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ {, d8 o" b6 @
terone was 38 ng/dL (normal, 50 to 760 ng/dL),8 o0 J' x; u! E' a' s
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 |! U) s# j( h. c2 k5 B" M) y49ng/dL), 11-desoxycortisol (specific compound S)/ ?  l1 E9 x3 [- }' S* U
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* p8 l3 i% x4 Y8 z7 J$ vtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total6 p6 |5 p; V" \7 T7 q
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 @+ ?: [" L8 W+ C/ l' Eand β-human chorionic gonadotropin was less than
6 Z& F- a3 e6 R1 y7 u5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ P& e9 \, w) I$ L7 Y" _stimulating hormone and leuteinizing hormone
- A5 ]0 a1 ]" l$ q8 V) |- F  ?concentrations were less than 0.05 mIU/mL8 h& [& d7 f" O) |
(prepubertal).
7 S4 i" s  w3 ^5 I* X+ x' NThe parents were notified about the laboratory
* v; S2 U; a: J6 P# D  w  yresults and were informed that all of the tests were
) O$ I9 ^) o* N3 O3 G  \" Inormal except the testosterone level was high. The# [3 U( L) [* O) H$ ?1 B; b) b
follow-up visit was arranged within a few weeks to' g9 }# u/ C! Q7 t6 a. d
obtain testicular and abdominal sonograms; how-/ _, ]9 W4 ?9 Y$ h8 u; y) T: q
ever, the family did not return for 4 months.
7 p8 d8 q- b. V9 {9 F7 i1 LPhysical examination at this time revealed that the
6 h, H4 }: T( ^8 Z" K0 [child had grown 2.5 cm in 4 months and had gained4 n4 E" i3 s: k4 v9 T& Q" y
2 kg of weight. Physical examination remained
8 c' L/ ]2 K; F) l1 r8 U* \unchanged. Surprisingly, the pubic hair almost com-
1 Y; U  h, Z1 e, _2 Ypletely disappeared except for a few vellous hairs at
4 s2 M( z/ Y* Z0 b/ bthe base of the phallus. Testicular volume was still 2
  F8 n" p4 F7 x( q8 qmL, and the size of the penis remained unchanged.
" K& W" N* c% h2 \The mother also said that the boy was no longer hav-0 u0 {5 d* p, p8 }6 i' V
ing frequent erections.$ w+ s2 s4 Z( x) P6 x( z
Both parents were again questioned about use of
' {9 p. @7 q; o6 f( [$ b) X- |any ointment/creams that they may have applied to
' o4 b% b( v$ v8 k. }8 ^/ ythe child’s skin. This time the father admitted the# o! o! c+ V0 ?4 ?/ U, I# B
Topical Testosterone Exposure / Bhowmick et al 541
. e/ s  f* _. t" s" Euse of testosterone gel twice daily that he was apply-
" p' J7 |4 F9 f9 ^: @  D9 d' i5 y6 Ling over his own shoulders, chest, and back area for
$ l5 Z; e' h1 F- S" K" B! E3 pa year. The father also revealed he was embarrassed4 C8 P3 ~& C5 t2 X8 J7 h4 e# U
to disclose that he was using a testosterone gel pre-$ }2 A2 M0 S  ]
scribed by his family physician for decreased libido
" D  @3 S/ ?) i2 B, j/ {$ gsecondary to depression.5 T9 j$ W- t$ \
The child slept in the same bed with parents.- u) Z2 m: @$ f2 W/ r4 ?
The father would hug the baby and hold him on his- p7 n, p% A" q# {9 @8 R' k
chest for a considerable period of time, causing sig-" _3 \6 }+ r( a' }  b
nificant bare skin contact between baby and father.
, U1 k" M" W7 h- ]( W4 l* O5 y' IThe father also admitted that after the phone call," `7 }/ M5 @; b) d- p0 U: S
when he learned the testosterone level in the baby4 |% r/ ^& W8 U
was high, he then read the product information
, q1 W: a2 }1 E/ Vpacket and concluded that it was most likely the rea-
( w! h" k  \7 V- a0 q4 y1 oson for the child’s virilization. At that time, they
3 f8 l/ Z9 A, d9 N7 ndecided to put the baby in a separate bed, and the- O4 s( Q$ p) e5 \6 b% q/ x) ]5 M
father was not hugging him with bare skin and had
9 l, b; U9 |/ r* n# ]: |6 Rbeen using protective clothing. A repeat testosterone
) I, ^1 U' J' ?9 Ttest was ordered, but the family did not go to the
0 f: d' [% ~5 C& claboratory to obtain the test.8 y+ c% a7 @. u3 D6 N: s. c9 t
Discussion- L/ c6 u/ e$ E! M& l) E
Precocious puberty in boys is defined as secondary
8 y' O5 R: o& P4 G5 b2 zsexual development before 9 years of age.1,4; f& L" Q1 A4 D
Precocious puberty is termed as central (true) when
. W9 U5 ]% K2 sit is caused by the premature activation of hypo-: L0 Z% {+ o: R; C
thalamic pituitary gonadal axis. CPP is more com-0 [4 S& F! n; e
mon in girls than in boys.1,3 Most boys with CPP
) ~: \8 ]; H' f- [: Nmay have a central nervous system lesion that is
, }7 x; q  ?8 }7 a" y+ m$ S7 C6 C1 x8 iresponsible for the early activation of the hypothal-& S  P0 a; Q% l1 G3 U4 l& L
amic pituitary gonadal axis.1-3 Thus, greater empha-4 g( s  m% H6 K7 I8 g
sis has been given to neuroradiologic imaging in
( N" l5 ~) q! {3 s$ P& m) v8 Zboys with precocious puberty. In addition to viril-# g/ `; h" h, I
ization, the clinical hallmark of CPP is the symmet-( g' m6 U( X9 s! \$ S- m1 H
rical testicular growth secondary to stimulation by" k0 _) v- S/ ^# J* f' x4 M0 Y9 h
gonadotropins.1,3* L' Z5 R4 J9 \4 K; V: Y& c3 n4 @9 y/ P
Gonadotropin-independent peripheral preco-
. X9 R# y* z1 e; `  d, {/ dcious puberty in boys also results from inappropriate
& G% R( B% w) ^6 P3 ~/ w# k& x5 nandrogenic stimulation from either endogenous or; }/ Q+ w0 m8 c! O  M
exogenous sources, nonpituitary gonadotropin stim-
4 y8 l& Y2 `$ W8 A9 _/ dulation, and rare activating mutations.3 Virilizing6 b2 a' U! w' B+ v
congenital adrenal hyperplasia producing excessive5 g, }& d4 A# V  J$ @6 J/ d' e
adrenal androgens is a common cause of precocious
8 k. b- j) r: [& r; R" Q6 Cpuberty in boys.3,4/ {# u( R% r; C- W% O2 ]
The most common form of congenital adrenal* `; H4 C! s) J  g
hyperplasia is the 21-hydroxylase enzyme deficiency.
6 T6 @* K/ n8 w/ ZThe 11-β hydroxylase deficiency may also result in
  ?; R; H( X& e! b% Fexcessive adrenal androgen production, and rarely,+ w3 M' H3 u9 v( H9 G
an adrenal tumor may also cause adrenal androgen/ s4 `. {$ E; E9 j, M/ l5 @% z- c% p
excess.1,3
3 A- p: R5 H. }- Z* `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 p3 G* M% G7 D/ `+ z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 ~; v7 I7 \) K3 @% h2 c6 t; G7 yA unique entity of male-limited gonadotropin-
4 n5 _+ b) \9 e) eindependent precocious puberty, which is also known2 U8 n, v: k4 ^: @
as testotoxicosis, may cause precocious puberty at a0 A$ D  V% F! i' }. X6 W
very young age. The physical findings in these boys
2 }0 r7 f$ V+ \# L7 {8 @with this disorder are full pubertal development,& x8 O- C3 n1 i* w3 V* ]
including bilateral testicular growth, similar to boys
: X* m- o. B; R' S! z' F# kwith CPP. The gonadotropin levels in this disorder
6 ^8 T. W2 m6 hare suppressed to prepubertal levels and do not show
6 A# B" f' ?) X: bpubertal response of gonadotropin after gonadotropin-  R3 {! ^) r9 G: F% i0 M; \$ h
releasing hormone stimulation. This is a sex-linked
9 i7 V; V& L0 `7 ~$ \  s, ^& U( Xautosomal dominant disorder that affects only5 F  g8 n6 O" f; o& F4 {* H
males; therefore, other male members of the family
/ ]; j# U$ d4 K+ \5 _) Emay have similar precocious puberty.37 c# B7 X% Y7 g1 R& V
In our patient, physical examination was incon-
: R5 @3 I. i$ [- R7 U1 k: ^sistent with true precocious puberty since his testi-
9 `3 v4 ^0 I. I& m5 Xcles were prepubertal in size. However, testotoxicosis/ j- f+ E  z) e6 {) T+ A7 z, m
was in the differential diagnosis because his father% _0 K7 a' h1 v
started puberty somewhat early, and occasionally,
$ ^) @- a) o7 l* R" u0 q) U: B6 dtesticular enlargement is not that evident in the' ~- |' R4 a, I0 B
beginning of this process.1 In the absence of a neg-* z" i: V1 N$ s5 X( N" q3 c* e
ative initial history of androgen exposure, our0 |# P8 v/ i/ X( V2 e9 Y7 Q9 @
biggest concern was virilizing adrenal hyperplasia,5 b3 i/ g" E& i7 f$ Q
either 21-hydroxylase deficiency or 11-β hydroxylase
0 @# |$ J5 G2 M+ f0 xdeficiency. Those diagnoses were excluded by find-
  ]; F! W  `5 q. S. X( l! Z% aing the normal level of adrenal steroids.
0 o8 u7 f, I6 x& }3 ^The diagnosis of exogenous androgens was strongly
8 j" t8 ^. u6 \( Z+ \suspected in a follow-up visit after 4 months because  R, w: R4 I6 C7 w" Y# P
the physical examination revealed the complete disap-
# i; f1 ^+ w0 S8 [! y, v- _$ spearance of pubic hair, normal growth velocity, and$ j  u- V: N- v5 Z
decreased erections. The father admitted using a testos-( N: U0 A# q' Z
terone gel, which he concealed at first visit. He was
: l7 z1 W  v0 E8 R! J% ~% |. R( Y, Rusing it rather frequently, twice a day. The Physicians’! S3 @6 N" D9 i% I& a
Desk Reference, or package insert of this product, gel or
# F$ k9 J9 U# {7 Icream, cautions about dermal testosterone transfer to: [+ T) d$ Z5 h' I
unprotected females through direct skin exposure.- R# D0 I% y* v: z) Y9 w: o" M
Serum testosterone level was found to be 2 times the% ~# [( [' h8 U1 f' n/ l
baseline value in those females who were exposed to
3 M3 g* o5 y/ k) H: h* I. _even 15 minutes of direct skin contact with their male1 t0 ^! L5 l) L' q3 O6 y9 \
partners.6 However, when a shirt covered the applica-
4 n3 v6 H+ H! Q/ htion site, this testosterone transfer was prevented.
# w" U/ V! A5 F( ]7 ]7 UOur patient’s testosterone level was 60 ng/mL,
3 _5 m8 p' `& g: {1 X. f( t! pwhich was clearly high. Some studies suggest that
7 o8 i+ B7 ~6 t* ?$ b" m! @dermal conversion of testosterone to dihydrotestos-. u' q# i) b$ r3 t9 z8 g
terone, which is a more potent metabolite, is more
3 Y, w( R) E( @' ?7 uactive in young children exposed to testosterone
* }  D: \' `1 ]2 @exogenously7; however, we did not measure a dihy-+ \. j# Y( T! z: g
drotestosterone level in our patient. In addition to* k3 ^; B  J- t! q* `) U% u
virilization, exposure to exogenous testosterone in
. ]9 t! [6 e5 ~. M2 j% b: b1 Zchildren results in an increase in growth velocity and0 F* a- I/ r3 o8 f; r( u$ r
advanced bone age, as seen in our patient.
5 Z1 g" I' P/ X1 o: FThe long-term effect of androgen exposure during
# h5 {. Q7 m) O% y5 h& q& ]0 W+ F4 searly childhood on pubertal development and final. m1 i: F" c+ }, c8 ]
adult height are not fully known and always remain. V/ |! R1 @5 F- l( H
a concern. Children treated with short-term testos-7 c# E& B  v3 Y. q8 o
terone injection or topical androgen may exhibit some
! O, [+ [2 p; x, B+ P4 Vacceleration of the skeletal maturation; however, after
7 O5 N1 z9 \. V+ `, bcessation of treatment, the rate of bone maturation: K; \" s( C8 i6 R: S
decelerates and gradually returns to normal.8,9& L6 J' |4 v" x# T8 Z. @
There are conflicting reports and controversy8 I' j& \8 {! x: I; x
over the effect of early androgen exposure on adult
" k# k$ Z. d6 ]6 L! W. a. K" Mpenile length.10,11 Some reports suggest subnormal0 a- h! V) R* W
adult penile length, apparently because of downreg-
; G: _  e. m* ~: j3 kulation of androgen receptor number.10,12 However,: J' b  d/ H% q
Sutherland et al13 did not find a correlation between
4 R3 q6 i) |5 P, Pchildhood testosterone exposure and reduced adult
6 Q3 P9 h7 s4 B: d8 ypenile length in clinical studies.6 u! I2 `. B0 q" P7 Y& N
Nonetheless, we do not believe our patient is
& q# o. V- c* A2 |7 ygoing to experience any of the untoward effects from9 p% L+ Q/ }4 J+ B
testosterone exposure as mentioned earlier because
$ W" Y5 ?( i5 ]; c% i% Q0 y2 lthe exposure was not for a prolonged period of time.0 k# t  D) S! o) ?# z7 x
Although the bone age was advanced at the time of1 C9 S  V3 @# ]3 V7 D
diagnosis, the child had a normal growth velocity at! i5 p5 [$ O8 S) B
the follow-up visit. It is hoped that his final adult) N- \3 L# G" r
height will not be affected.
& x8 g# t( ]& p% y$ RAlthough rarely reported, the widespread avail-( L/ q+ r# h+ Q( K% ]
ability of androgen products in our society may) U( O' f+ N7 ]; s  l5 A2 k
indeed cause more virilization in male or female4 Z( X8 _4 D7 _+ M* v5 s2 Z) ^
children than one would realize. Exposure to andro-3 F9 e( k# s. w* w/ X
gen products must be considered and specific ques-( q5 V" z6 [( q6 }% v. s! K" y
tioning about the use of a testosterone product or! V+ c4 A( N4 x/ o5 k' s7 {
gel should be asked of the family members during; n- o  i" m! ^+ `4 F
the evaluation of any children who present with vir-0 M+ Q" ?/ P* w) M: ]4 M. L
ilization or peripheral precocious puberty. The diag-
" v! L/ z& X3 c# \nosis can be established by just a few tests and by
# i& K% D; ]( Z/ |/ e' }appropriate history. The inability to obtain such a* V2 n1 h8 k; q* ^$ t% s5 [
history, or failure to ask the specific questions, may% ?; J) q( h& \- n' x( i
result in extensive, unnecessary, and expensive  j8 Y5 p/ ~: \0 y! R
investigation. The primary care physician should be( _2 A* F3 |  R. ~  l
aware of this fact, because most of these children
9 Q; R( J* v' V6 i) Tmay initially present in their practice. The Physicians’
! L& M  R: b: M% H+ yDesk Reference and package insert should also put a
. |& X0 o: [" A/ g/ z! m4 P; d  `0 d1 N8 Rwarning about the virilizing effect on a male or2 E' Z; _- }5 \( h* l
female child who might come in contact with some-- f: n  M  m6 ?8 ]9 X
one using any of these products.; ^8 M; t, |! T
References! h) ^: S6 S* A' P* J: v
1. Styne DM. The testes: disorder of sexual differentiation$ E2 P: \# T8 k+ ]' ^/ O  t) _
and puberty in the male. In: Sperling MA, ed. Pediatric
+ l. _; P( O0 @7 E3 NEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;/ i9 k: p% V  N. |$ R" @- b
2002: 565-628.2 _1 q# V8 }# z+ L& ~5 P
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ j( b' b+ u+ H( _! ]puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old. k! |4 j: A2 v) Z& g& [
Boy Induced by Indirect Topical7 @/ {& c% }: O0 R, @" `& @5 Q
Exposure to Testosterone
% W) @8 M6 p( D0 PSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; E! F$ d+ Y1 s7 |6 w1 h
and Kenneth R. Rettig, MD1
0 z! i' ^! N3 y1 C& s: `: \Clinical Pediatrics# K% A, r" f' @6 s3 K7 v" i6 i
Volume 46 Number 6' K" z# R; M3 e6 v
July 2007 540-543
9 o% s0 h: ^. G© 2007 Sage Publications
% ~. h, q+ W! `; i1 ^" @10.1177/0009922806296651" U7 Z1 R4 [7 O. m9 v9 R
http://clp.sagepub.com
  k+ }1 v. X6 _1 mhosted at. f1 _3 S9 j5 c
http://online.sagepub.com1 M; W& T) y- X/ L+ P' [
Precocious puberty in boys, central or peripheral,
) W8 `: b4 f, U6 Tis a significant concern for physicians. Central
' X. N5 A0 h4 R4 A+ pprecocious puberty (CPP), which is mediated! K( @8 E3 g7 c# L
through the hypothalamic pituitary gonadal axis, has
7 B9 }) u3 u, z6 Ya higher incidence of organic central nervous system" [# I) V7 m1 S' O8 T% g
lesions in boys.1,2 Virilization in boys, as manifested
! ^7 H3 b  Q) {% d, fby enlargement of the penis, development of pubic9 z% A; Y7 A. d$ @4 q! F% z6 t
hair, and facial acne without enlargement of testi-9 I: q5 L6 w' P% t/ e) ^* l3 F5 F
cles, suggests peripheral or pseudopuberty.1-3 We
& d" G4 i) k" t. }. xreport a 16-month-old boy who presented with the2 ]& L# q5 _5 m! u! y
enlargement of the phallus and pubic hair develop-2 E, `0 ]0 a" F2 Q( S
ment without testicular enlargement, which was due
. v" a+ ~) h+ M3 \to the unintentional exposure to androgen gel used by5 F9 v& W& l8 r$ {# N
the father. The family initially concealed this infor-+ n  A: i6 E3 g/ ?# G1 N. K, A
mation, resulting in an extensive work-up for this
! X. G4 \0 ^, G- M. N# P9 Uchild. Given the widespread and easy availability of
# Y  L8 n% j) _0 z4 _testosterone gel and cream, we believe this is proba-
" n/ h2 _. `4 l% U# Ably more common than the rare case report in the- E+ V* D* @' m: I" ^  U' M
literature.4
8 r& Y( E  C% U* R0 aPatient Report
/ g3 r! q3 k& N6 pA 16-month-old white child was referred to the, d# `' A9 l% k4 G$ n, S
endocrine clinic by his pediatrician with the concern# V% l" g" x1 g* H% D) z
of early sexual development. His mother noticed
# Z, e* N# W% c6 Y6 }light colored pubic hair development when he was* y7 ~5 C( L) V3 |8 o- t/ E
From the 1Division of Pediatric Endocrinology, 2University of
' j* h( v- q5 Z6 Q3 }) d' ySouth Alabama Medical Center, Mobile, Alabama.6 ]" i" G0 A8 Q( v+ x( S% B$ U' J
Address correspondence to: Samar K. Bhowmick, MD, FACE,, k, ^/ X! U) f: @+ s5 {! _6 q
Professor of Pediatrics, University of South Alabama, College of- @. L) m: U) C3 |0 ]7 F$ a' Y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( M& L9 v: S2 c6 \) z# @
e-mail: [email protected]., Q- w0 |+ L( K1 T5 W
about 6 to 7 months old, which progressively became
! j" C+ x1 m8 y- ~: Qdarker. She was also concerned about the enlarge-" L0 ~# A7 H5 P! z  H/ ?  o' ?* P
ment of his penis and frequent erections. The child  e; D: ^7 n+ F2 n7 H
was the product of a full-term normal delivery, with+ [3 e% V& S# a; o
a birth weight of 7 lb 14 oz, and birth length of
" \% h5 _0 x# p. U8 ]# }20 inches. He was breast-fed throughout the first year
& b9 H, X) T- u/ b7 R! v2 i% _0 sof life and was still receiving breast milk along with" C2 t( ^3 Z9 |
solid food. He had no hospitalizations or surgery,
. u. I  c( g. ?6 dand his psychosocial and psychomotor development
. a! J% F. _* V+ A) qwas age appropriate.5 c7 F9 C9 [0 y( p7 j! w! s
The family history was remarkable for the father,
) @+ g/ F5 i) s( n/ Q' |; P* Bwho was diagnosed with hypothyroidism at age 16,- T) L0 ?; D) r4 R8 }
which was treated with thyroxine. The father’s
9 q9 w: `+ I! C7 Jheight was 6 feet, and he went through a somewhat1 v. C$ B% z0 u2 G) Q# U
early puberty and had stopped growing by age 14.5 n, m! L+ z8 k4 s# ]# }7 v5 {
The father denied taking any other medication. The
: N# u7 {# i8 d7 ochild’s mother was in good health. Her menarche
! i' D/ P) `. D7 o/ [, Z& X7 jwas at 11 years of age, and her height was at 5 feet
9 c1 y& W2 L% {5 inches. There was no other family history of pre-
" ~/ p. w4 W1 t6 p4 M; Ococious sexual development in the first-degree rela-  [1 f5 J, a/ i, K1 A; f2 T0 K$ F* ^
tives. There were no siblings.0 U; [: X, p6 C2 K; W+ W
Physical Examination
% t9 k) @# p) B, {3 D  wThe physical examination revealed a very active,7 Z" r% j' z7 O. |4 n# ^$ E. h" Y; y
playful, and healthy boy. The vital signs documented$ @3 }! K6 z0 Z
a blood pressure of 85/50 mm Hg, his length was
3 B+ q1 N) e! t) X  i  ^) Q90 cm (>97th percentile), and his weight was 14.4 kg# j- s. t9 O" f, V6 m6 H% i/ o
(also >97th percentile). The observed yearly growth: H: E! H) j' P& z1 t* F
velocity was 30 cm (12 inches). The examination of4 C2 P: ~- p# z: A* l
the neck revealed no thyroid enlargement.
& F% ?, ]/ _# h% S- mThe genitourinary examination was remarkable for
5 a: f% O8 y1 K" D( O, e: Eenlargement of the penis, with a stretched length of
* f& q$ R& q% Q( c! q8 cm and a width of 2 cm. The glans penis was very well& D+ S# q7 x) s8 e0 p( g0 @
developed. The pubic hair was Tanner II, mostly around
! i- w; e& w3 L$ T9 E$ v, Y& d540/ G; e% n3 {! I9 g4 z6 H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 q$ e2 c) A" T) ?the base of the phallus and was dark and curled. The4 Y) e( J! `9 |8 \% H! T6 C( C
testicular volume was prepubertal at 2 mL each.% J* z" N  X+ Z( a  A. A" P) p
The skin was moist and smooth and somewhat
$ v/ Q+ u5 b) B0 M- doily. No axillary hair was noted. There were no. a. q" m. |9 j. u- c/ K
abnormal skin pigmentations or café-au-lait spots.$ F% K0 ]7 t. c* ?3 E8 ?
Neurologic evaluation showed deep tendon reflex 2+
2 j, B% Q3 z8 i0 mbilateral and symmetrical. There was no suggestion0 \, U# Z+ @  d% u% q5 m% O
of papilledema.
$ x$ }. ?6 U" U# [Laboratory Evaluation
) K* d9 n1 L$ U4 V8 rThe bone age was consistent with 28 months by" m$ B7 c' d  Z1 b- p, n
using the standard of Greulich and Pyle at a chrono-: Y4 Y# A" j  D7 h$ O1 x
logic age of 16 months (advanced).5 Chromosomal% K9 i4 c+ K  Y8 k' M: }
karyotype was 46XY. The thyroid function test
  r" c8 C2 Q7 {( i1 F% Kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ N& a- I0 t$ [9 [& \lating hormone level was 1.3 µIU/mL (both normal).
' O. j/ [) s. d+ s2 a' ^+ cThe concentrations of serum electrolytes, blood
& u% Z7 S6 M0 B4 Surea nitrogen, creatinine, and calcium all were. M! o+ K0 V9 m1 N8 m& e' a4 G
within normal range for his age. The concentration; b/ p! |: {: r! s, @
of serum 17-hydroxyprogesterone was 16 ng/dL/ x8 r* ~& O2 C
(normal, 3 to 90 ng/dL), androstenedione was 20
( Y7 A: Q$ D: bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ Y4 s5 x7 s2 z! wterone was 38 ng/dL (normal, 50 to 760 ng/dL),$ S1 W- ^, @3 K8 m8 V8 g& P7 g' U
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ c+ f' [/ G  t- M  M49ng/dL), 11-desoxycortisol (specific compound S)
$ ~' d# J- }. f6 dwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% h, b/ L! U; u4 Q& ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. W6 ~" T$ k! v! Wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),! P! x4 k5 p8 P5 G* |6 [. q/ A
and β-human chorionic gonadotropin was less than( o) l6 K7 p# \3 B+ F+ G' \
5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 }  W: W% u1 [; E7 e' O" ystimulating hormone and leuteinizing hormone% m3 Q) V. m( |, q  d1 f
concentrations were less than 0.05 mIU/mL; x" F/ b1 o" H  \. n. S
(prepubertal).+ c5 {2 J6 v- o$ E# q
The parents were notified about the laboratory- m; j' k8 g: a/ O+ D
results and were informed that all of the tests were
1 F/ u  _7 l6 u7 znormal except the testosterone level was high. The
, \$ d8 L5 \- w9 Ufollow-up visit was arranged within a few weeks to5 |% S4 _* k  k2 x2 [; Q: {
obtain testicular and abdominal sonograms; how-+ A2 a; w+ N) `9 o# i" q' P# L9 J
ever, the family did not return for 4 months.& D  Z8 g/ v  \- O- Z
Physical examination at this time revealed that the% w' l" e6 q8 w2 d, I8 n
child had grown 2.5 cm in 4 months and had gained
0 m9 T$ j5 y0 x8 U, x2 kg of weight. Physical examination remained
; R! u* g/ r7 V. {6 {unchanged. Surprisingly, the pubic hair almost com-, `7 C  Y' r( ]! L& I+ F- N
pletely disappeared except for a few vellous hairs at
7 F" F* B& d) D  ^9 }1 bthe base of the phallus. Testicular volume was still 2! S& u7 ?/ G* A1 E. z
mL, and the size of the penis remained unchanged.
7 [6 t. g% a1 v- Z4 IThe mother also said that the boy was no longer hav-6 X( J& F6 E9 Q! W, X! V' Y
ing frequent erections.
) X) [  R9 k- x, EBoth parents were again questioned about use of  {+ `" {8 y8 g* y4 p
any ointment/creams that they may have applied to" x) z2 F# j# G5 ]& j( Y. c5 L8 I$ b% s) D
the child’s skin. This time the father admitted the
- v% m4 t( v2 c" C0 DTopical Testosterone Exposure / Bhowmick et al 541
6 t% o7 q+ J! j* Juse of testosterone gel twice daily that he was apply-
) b% G4 k+ X) y9 c: t( z1 E7 `( ning over his own shoulders, chest, and back area for
. M$ V% c' K6 I' A7 S: k% Xa year. The father also revealed he was embarrassed
5 N6 X  W- R, z# }4 Rto disclose that he was using a testosterone gel pre-" d3 ^* g0 K! C. g
scribed by his family physician for decreased libido4 [1 d9 Y! \7 x# n  f
secondary to depression.
& T" A: V6 H6 b  @" E) ZThe child slept in the same bed with parents.
8 s/ l# d# c$ W! {3 JThe father would hug the baby and hold him on his
" Q) c5 y/ D, c- u- W# Vchest for a considerable period of time, causing sig-
6 `4 [/ D$ O' c0 A. F. {: p1 wnificant bare skin contact between baby and father.
+ }0 |$ f, T+ r3 L" O" e. rThe father also admitted that after the phone call,/ H6 U& V2 l. x! V
when he learned the testosterone level in the baby
, r. V+ U( V1 H9 wwas high, he then read the product information' @; V$ X$ x# ?9 y# f
packet and concluded that it was most likely the rea-- J5 o5 c3 D, w$ I
son for the child’s virilization. At that time, they( R1 k8 C, g7 i: ]  A
decided to put the baby in a separate bed, and the
- ^7 A7 [, n" c5 H. Hfather was not hugging him with bare skin and had7 C3 B/ H) z; l! k- q) r* Y0 L5 v
been using protective clothing. A repeat testosterone
% @9 F8 |! n8 y) y# ]0 ttest was ordered, but the family did not go to the& M9 w5 m; C* |# r4 b
laboratory to obtain the test.
- _: ?( i9 H" A) Z: O6 Z( |( }$ xDiscussion
$ H0 g! G! S1 k) y' GPrecocious puberty in boys is defined as secondary
( s2 S& _3 }' A4 a; W4 e7 g, v) psexual development before 9 years of age.1,4/ [+ t% Q/ e( L1 R& s; b. P
Precocious puberty is termed as central (true) when4 k% |2 F- B: p6 g! h
it is caused by the premature activation of hypo-' \/ R3 M5 f8 ]5 E
thalamic pituitary gonadal axis. CPP is more com-$ y. p' r5 @# a! `( @) H: E
mon in girls than in boys.1,3 Most boys with CPP4 r: Z% a$ b1 b
may have a central nervous system lesion that is" J" z6 w  o- m: w2 t
responsible for the early activation of the hypothal-  q/ `: Y% K0 E; \' d' s
amic pituitary gonadal axis.1-3 Thus, greater empha-
  s9 M' M7 Y5 k7 K: u( csis has been given to neuroradiologic imaging in2 L! ]* X: [5 I& C  F9 B$ \
boys with precocious puberty. In addition to viril-
9 j3 e) b* J5 W* Y3 L& Lization, the clinical hallmark of CPP is the symmet-
6 Y& d- u7 Z1 n. {( N2 srical testicular growth secondary to stimulation by3 Y0 w: l- h" j1 l/ S5 d; b
gonadotropins.1,3
9 n9 D/ N" q" Z& d. F& y" x+ [Gonadotropin-independent peripheral preco-; T0 g# q' |2 U/ O. j: y5 x+ W
cious puberty in boys also results from inappropriate* \4 I( Q! W8 M/ V
androgenic stimulation from either endogenous or& ~* _0 E5 m& I$ u% h& f- b
exogenous sources, nonpituitary gonadotropin stim-
; N" l7 o8 Q  dulation, and rare activating mutations.3 Virilizing3 U7 ?6 R4 K. v2 p1 w* S3 t9 {
congenital adrenal hyperplasia producing excessive
/ D; M, d! z7 G4 D: Yadrenal androgens is a common cause of precocious
9 |0 w# |$ C# R: M% {puberty in boys.3,4
  n+ |$ R8 Q$ T6 q: z( A1 tThe most common form of congenital adrenal
9 C; @  Y; P/ ^7 O0 Yhyperplasia is the 21-hydroxylase enzyme deficiency.0 Z" i+ d2 ]4 y7 ^' h" S, `; o
The 11-β hydroxylase deficiency may also result in
+ E7 _$ W& Q) L$ U# wexcessive adrenal androgen production, and rarely,# ?9 s. n1 o) e- C8 s
an adrenal tumor may also cause adrenal androgen/ t) }9 g" ]2 s% s8 `
excess.1,36 [( g$ h* E& V+ I: h
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 L8 X% P- O, a542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 W: N  ^6 b6 k8 h, g! u# T
A unique entity of male-limited gonadotropin-
2 c2 s" U; W/ w' bindependent precocious puberty, which is also known5 E/ q. e& m$ E; b" [  b
as testotoxicosis, may cause precocious puberty at a
0 d+ Q3 V0 W+ C) i8 D! C) fvery young age. The physical findings in these boys0 u/ I( U0 ^0 H: G+ r7 \- U
with this disorder are full pubertal development,
7 m0 o% l# y( m3 r, ?including bilateral testicular growth, similar to boys  Y& N7 W+ d, ^5 |
with CPP. The gonadotropin levels in this disorder+ @0 L) e& z7 C6 V. c. I
are suppressed to prepubertal levels and do not show6 o( ]# r+ I) ]' M! T
pubertal response of gonadotropin after gonadotropin-4 l! Z( j! Y/ y' l6 I) |
releasing hormone stimulation. This is a sex-linked
& H* N% O% Y/ n& z8 Z6 b4 Eautosomal dominant disorder that affects only
& B: E) |4 o8 gmales; therefore, other male members of the family
3 @3 V0 t7 m5 T) Zmay have similar precocious puberty.3) i% W6 q: U. r' M: E$ j
In our patient, physical examination was incon-7 e/ }. I( L0 Q; i/ Y: s; c
sistent with true precocious puberty since his testi-
2 w6 z1 W( S, _! ?* `cles were prepubertal in size. However, testotoxicosis& \7 x: d* T7 _$ X. ~0 y
was in the differential diagnosis because his father
. V" _9 k$ W4 k% t9 ?: dstarted puberty somewhat early, and occasionally,  p% ]- v4 D" H
testicular enlargement is not that evident in the) k- o) h. v4 u6 m! N0 c* ~
beginning of this process.1 In the absence of a neg-
1 F  S$ O- v1 Y  v1 f9 Fative initial history of androgen exposure, our
% h% F5 K1 O$ d6 R# q* Z1 ?6 fbiggest concern was virilizing adrenal hyperplasia,
/ X$ v7 ]! S  v# C- Neither 21-hydroxylase deficiency or 11-β hydroxylase
' P( I; K- Z9 }2 o! P. B5 \. I& sdeficiency. Those diagnoses were excluded by find-
- Y  X5 h$ n, }, U2 }ing the normal level of adrenal steroids.4 f: f2 O# q% d1 r2 v) L% c
The diagnosis of exogenous androgens was strongly
/ Q, N! d8 g- c* _( h7 a; G5 Jsuspected in a follow-up visit after 4 months because2 p+ N/ ^  ^5 `
the physical examination revealed the complete disap-
# S7 s* Y8 q+ l' S  Apearance of pubic hair, normal growth velocity, and; {1 h' q1 f# w2 j# U" l
decreased erections. The father admitted using a testos-
2 ?: {7 C, V# u9 F5 eterone gel, which he concealed at first visit. He was
! p& ^$ L2 Y+ V7 m. }4 s: lusing it rather frequently, twice a day. The Physicians’
4 R: ]/ B6 |5 }Desk Reference, or package insert of this product, gel or  B3 `, o1 ]- V! N  }+ d' q
cream, cautions about dermal testosterone transfer to
# c! d# a; w% z) j+ Z) Kunprotected females through direct skin exposure.; Z9 w0 N7 c7 Z6 ?+ f! A2 x
Serum testosterone level was found to be 2 times the/ q9 e# r4 z8 k$ j0 U$ A; n5 e* b+ s
baseline value in those females who were exposed to4 @0 d4 b: y7 p! v" C3 \* C
even 15 minutes of direct skin contact with their male
& B! {4 ^) q  Z' I1 Rpartners.6 However, when a shirt covered the applica-
# G3 A- `/ m; |4 ^* w$ ^tion site, this testosterone transfer was prevented.% m, Q; S! o( t- q* _
Our patient’s testosterone level was 60 ng/mL,
4 n2 n0 B5 c+ V9 A5 iwhich was clearly high. Some studies suggest that
+ Y. K0 V6 u8 qdermal conversion of testosterone to dihydrotestos-
) P+ A& s( R) u; _/ O, S' Iterone, which is a more potent metabolite, is more( e4 P# J1 a8 ^- ^5 U
active in young children exposed to testosterone3 U! _/ ~  d  [( F/ M4 w8 I1 m; C
exogenously7; however, we did not measure a dihy-$ W6 {: W4 @4 R: n: ?/ S
drotestosterone level in our patient. In addition to
0 S6 H- d+ g; T+ |7 uvirilization, exposure to exogenous testosterone in1 Z, e; H! h1 Y7 B* r
children results in an increase in growth velocity and6 c' t  o: M  z% T6 m3 v2 b" j" P% [
advanced bone age, as seen in our patient.
- |" n5 S6 V2 @1 Y! s# F1 JThe long-term effect of androgen exposure during$ t0 n/ k9 m# [! U, p
early childhood on pubertal development and final
0 c# ?# a) ~4 Q' N" [% q# s1 `adult height are not fully known and always remain8 b; f( B; x& ], Y; M$ f5 c" o
a concern. Children treated with short-term testos-0 O6 ]9 `8 I9 t. |
terone injection or topical androgen may exhibit some
# R' J% b% D/ {# e5 `5 o8 j& kacceleration of the skeletal maturation; however, after. j# k1 A5 z6 k# K
cessation of treatment, the rate of bone maturation, Q7 n, C' B7 f" A2 r% B; ~
decelerates and gradually returns to normal.8,9& H4 H) L4 G0 i: |
There are conflicting reports and controversy
3 k# V) a4 j" K+ y9 P3 x) |; qover the effect of early androgen exposure on adult; Z7 h) Q' j) N; X' D
penile length.10,11 Some reports suggest subnormal. v, v5 @# M- c! a' Q
adult penile length, apparently because of downreg-" P# t& x2 N; N1 y( r8 ~9 N
ulation of androgen receptor number.10,12 However,3 s1 E) F$ e; v9 l9 b. A4 }
Sutherland et al13 did not find a correlation between/ D! W3 m: q# Y. ?
childhood testosterone exposure and reduced adult
0 @; e; b5 F+ I) c! Gpenile length in clinical studies.& {* s4 c  n6 i) L8 E1 b; i
Nonetheless, we do not believe our patient is
/ g+ m0 @6 Y) F+ ~going to experience any of the untoward effects from
: _6 {" k$ c8 A# |testosterone exposure as mentioned earlier because! j4 K6 V- Y; `. |8 ?& [( T
the exposure was not for a prolonged period of time.4 I8 X$ U% D( ^  q# s0 W& W4 o% Z9 Q/ C
Although the bone age was advanced at the time of- \. ^7 B0 t. k1 z* t
diagnosis, the child had a normal growth velocity at5 x- ]% g. e% d% j
the follow-up visit. It is hoped that his final adult
; D2 G. H, Q( y1 ^: `5 Qheight will not be affected.; k2 z# u8 H% p5 v
Although rarely reported, the widespread avail-
: u! ?$ T6 O9 v0 {  mability of androgen products in our society may
  B$ f. g# Q; j0 C, ]indeed cause more virilization in male or female1 O( o) ^) i  ^; `; |: Z
children than one would realize. Exposure to andro-) ?& c/ C2 G) L" p$ \2 U
gen products must be considered and specific ques-
% C8 i+ b/ @3 V6 g1 M; Wtioning about the use of a testosterone product or
# O* p% L  S' Q- H. w, M" C" j4 A6 Xgel should be asked of the family members during/ m. |2 F5 r/ S( n
the evaluation of any children who present with vir-! N! S. D# T, |9 y0 n% G3 N
ilization or peripheral precocious puberty. The diag-+ V! D' G4 t2 p+ R6 k6 U
nosis can be established by just a few tests and by
5 Q/ n. C3 |7 nappropriate history. The inability to obtain such a  k9 D5 \& B7 B( D0 n
history, or failure to ask the specific questions, may7 G7 B- T+ Z3 `, j: {: k& M
result in extensive, unnecessary, and expensive
* n  S# c2 V8 Y( zinvestigation. The primary care physician should be2 h% }, B. |# v+ X7 I) I% _
aware of this fact, because most of these children! L8 Y2 i9 w0 u3 _
may initially present in their practice. The Physicians’+ V& z- ]' e, O5 L8 U" [3 _
Desk Reference and package insert should also put a9 h" C4 D' s  J! h/ ~/ Q
warning about the virilizing effect on a male or1 F8 N* }6 ^" e$ \& q
female child who might come in contact with some-9 W) r) x; S+ m; W7 u% i% a2 E0 k
one using any of these products.
7 w9 g2 _" i% S( h) M3 n! d0 gReferences- d- U5 V4 Y* \1 E1 p( P, b
1. Styne DM. The testes: disorder of sexual differentiation* g0 O0 ?0 G- P! c! U
and puberty in the male. In: Sperling MA, ed. Pediatric
  s/ ~. g! @" f+ V  K( l" z8 [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 [2 [' t# z; z4 ~2002: 565-628.
3 c6 k& R, q8 q; E2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ d: H7 O+ g# D$ g1 \' Lpuberty 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
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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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