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Sexual Precocity in a 16-Month-Old
+ V2 {$ c% X+ A# ^2 @/ H0 C" W, l4 `Boy Induced by Indirect Topical
. {/ d% S/ Q' O/ b# oExposure to Testosterone
  W8 o$ }' U2 R. YSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, `! I2 @4 [2 X9 B+ ]  cand Kenneth R. Rettig, MD1
/ S. q4 g6 y/ MClinical Pediatrics
8 X' M0 s; _5 I* AVolume 46 Number 6, ^7 w# J: {  B) R3 T8 m* [2 O2 F
July 2007 540-543
4 U# _/ \/ n. r8 {2 L# c$ n© 2007 Sage Publications
5 u5 y2 {) C" @* ]5 u( ~10.1177/0009922806296651/ ^3 _& z4 h; o
http://clp.sagepub.com( Y3 P/ u) g0 J& ^
hosted at+ R% z# E, Z" T/ |; D) V
http://online.sagepub.com
* M& h' S; _& ?Precocious puberty in boys, central or peripheral,+ |' e5 {4 K6 j5 J) w" |  y
is a significant concern for physicians. Central
" Y2 S' D' G/ u' J1 E; @precocious puberty (CPP), which is mediated
( R- ?1 f  [/ q  xthrough the hypothalamic pituitary gonadal axis, has
& ], x; e5 \- y; y/ ^a higher incidence of organic central nervous system
: h6 B) X' l5 _8 B) Q6 l, ulesions in boys.1,2 Virilization in boys, as manifested1 n7 [% n0 Z% h: o& F. @" t
by enlargement of the penis, development of pubic: w& z, Y! j# h" ~% S4 d
hair, and facial acne without enlargement of testi-
+ r. V/ z% B: m0 r: s5 `; wcles, suggests peripheral or pseudopuberty.1-3 We& r$ F5 J% G) F$ s% P" E2 W
report a 16-month-old boy who presented with the: f- U0 E( o7 W9 w) e  V! U0 g& \
enlargement of the phallus and pubic hair develop-! E* g: W8 o/ A8 `( L) d
ment without testicular enlargement, which was due
9 t( ~" _8 k% ]to the unintentional exposure to androgen gel used by( `2 A4 }% E6 m+ c
the father. The family initially concealed this infor-3 T! f2 v0 E0 M# i) I; G5 t' y
mation, resulting in an extensive work-up for this( ]. c( c$ M* Z2 ~: n: E
child. Given the widespread and easy availability of0 d" J. O) k1 D2 B3 k9 C
testosterone gel and cream, we believe this is proba-
( z( M' B( w; ~( H  E1 Sbly more common than the rare case report in the$ x4 Q+ u& b) E  n0 K: f  y# V) z
literature.4  P5 Y4 ?, x+ @) v+ k8 i/ }
Patient Report8 ~" i. e! Q9 q* x9 {
A 16-month-old white child was referred to the( D# c% f' O* M, s' L5 ?
endocrine clinic by his pediatrician with the concern
5 j& L  g) p4 m" b" s) F3 h# Gof early sexual development. His mother noticed
" }- z. S. S- f# k4 Rlight colored pubic hair development when he was
8 f1 o: ]$ X) q8 pFrom the 1Division of Pediatric Endocrinology, 2University of
1 \- w' }  b" W. OSouth Alabama Medical Center, Mobile, Alabama.
0 V0 W5 ]% L' iAddress correspondence to: Samar K. Bhowmick, MD, FACE,8 O7 ?$ Y9 @! ^: U4 F" y4 j0 E, T
Professor of Pediatrics, University of South Alabama, College of1 y+ y  }( Y; b3 L
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
% r3 N6 a: ]: m7 F. te-mail: [email protected].
  D/ r) c- u0 W/ m% c( U" x& Yabout 6 to 7 months old, which progressively became
- q& [" L4 P( x/ mdarker. She was also concerned about the enlarge-
3 x$ G* p. J" ]9 u( }ment of his penis and frequent erections. The child: I+ Q, n$ _0 f0 Z0 v5 K' v/ d! J: a
was the product of a full-term normal delivery, with. \0 q( z" V0 x9 K8 N5 |+ S
a birth weight of 7 lb 14 oz, and birth length of
9 }9 U1 h6 V  G; G& y: X/ X! }1 U1 }" I20 inches. He was breast-fed throughout the first year6 Q$ P* L# A, Z5 ]) Y* j
of life and was still receiving breast milk along with. {) ?9 }/ o( _9 }* \
solid food. He had no hospitalizations or surgery,
. X% X, Q) d8 J3 K8 f; Dand his psychosocial and psychomotor development: O; u+ O/ x. }8 [
was age appropriate.* X  _9 c! }7 q* `1 |5 t
The family history was remarkable for the father,
6 N* y* s' B8 @& R6 Z2 Gwho was diagnosed with hypothyroidism at age 16,/ F- M% |/ A3 G2 j; a5 i$ o
which was treated with thyroxine. The father’s; U! o; [0 t/ |" H, {# }) i
height was 6 feet, and he went through a somewhat: P$ y+ o' f3 P
early puberty and had stopped growing by age 14.
" |) W0 X: G6 H/ ZThe father denied taking any other medication. The6 G: p7 y9 D. v
child’s mother was in good health. Her menarche/ p  a0 Q! X1 O5 X* x0 y0 l1 G
was at 11 years of age, and her height was at 5 feet
+ t" h2 ~5 o3 `* H5 inches. There was no other family history of pre-. Z: `# j2 h. r' }
cocious sexual development in the first-degree rela-8 |. I, c( ~7 \1 d& b
tives. There were no siblings.5 D4 K4 {* m2 H# Y5 }" s
Physical Examination
6 u" e# t' X9 {8 `& NThe physical examination revealed a very active,) E6 m& m8 A$ c. V5 S
playful, and healthy boy. The vital signs documented+ [: Z1 v9 [. R0 I; A
a blood pressure of 85/50 mm Hg, his length was
# M2 X& s; h# E( D9 }! X90 cm (>97th percentile), and his weight was 14.4 kg, @- M  F: Z, w+ a" ^' |& e% n* n
(also >97th percentile). The observed yearly growth
9 s3 N9 {$ K2 m4 g! |' ]9 ^velocity was 30 cm (12 inches). The examination of& {3 @- U; Z5 B2 M; d" i1 |
the neck revealed no thyroid enlargement.' B0 s' ]9 }7 M
The genitourinary examination was remarkable for+ z( J: h  J7 b
enlargement of the penis, with a stretched length of
7 u/ y  p7 p" C9 h3 c8 cm and a width of 2 cm. The glans penis was very well1 {) _" t8 Z, D2 r. P# M
developed. The pubic hair was Tanner II, mostly around, q3 q1 C' _, d3 H  r+ Z1 G
5408 E5 M) a: L# z& O5 T
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the base of the phallus and was dark and curled. The1 t$ G4 S& e, k  }& ^- p
testicular volume was prepubertal at 2 mL each.* p9 Q1 u; P/ H2 h1 k
The skin was moist and smooth and somewhat
8 a% e2 ?4 _+ c$ N: f7 yoily. No axillary hair was noted. There were no
$ W: d  @3 C" ^  b. ]abnormal skin pigmentations or café-au-lait spots.7 Y' x# K# ?8 r- V1 i) g4 ~
Neurologic evaluation showed deep tendon reflex 2+
. N5 z. R6 s* Z# ^( ebilateral and symmetrical. There was no suggestion
) K9 K+ g7 x) ^: Bof papilledema.
. [- ^' {1 F2 y3 x/ P  nLaboratory Evaluation
8 S# w6 {# f9 y# p' ^! z% {The bone age was consistent with 28 months by
% }  B* a# j; k6 R+ _/ a; a% Musing the standard of Greulich and Pyle at a chrono-+ m' E) ^1 l+ R/ z' W+ y( Y3 W. F
logic age of 16 months (advanced).5 Chromosomal
1 z. B# Q: D! O8 I% ]karyotype was 46XY. The thyroid function test* z- ]8 J6 w7 Q" c
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 O, _& J# i; D% p. o- X$ O+ p
lating hormone level was 1.3 µIU/mL (both normal).
: D+ w! }" b0 f0 u# H4 `- hThe concentrations of serum electrolytes, blood8 i" D# t, L6 S1 B) Q+ i7 u' P
urea nitrogen, creatinine, and calcium all were
% g$ g5 Y- q5 K0 O" y( B( j: R2 Ewithin normal range for his age. The concentration
, ~) r# _8 V0 ]7 I( v3 L7 ]( xof serum 17-hydroxyprogesterone was 16 ng/dL
+ d, _7 A/ `0 J* e(normal, 3 to 90 ng/dL), androstenedione was 20
* M, f* s. |# u" Qng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-. v, E) x# |6 H/ ~
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 G% i  B; f# W. p3 z/ b) I/ edesoxycorticosterone was 4.3 ng/dL (normal, 7 to' k# f- L5 N4 F3 W2 s7 I
49ng/dL), 11-desoxycortisol (specific compound S)
$ F+ H- M% L9 D2 Z. wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& J, l+ y7 i0 y' Z$ ~8 y  A* U1 dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( F' m5 T; o  k0 t/ }
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! r  ~1 t$ w2 x: X6 Xand β-human chorionic gonadotropin was less than( d- Z7 V, U' C' Q- ~
5 mIU/mL (normal <5 mIU/mL). Serum follicular6 @7 n$ N8 K9 ]
stimulating hormone and leuteinizing hormone6 M2 S, u7 x" A; F* C
concentrations were less than 0.05 mIU/mL7 w7 f" E: K$ P- @: }6 G! V9 [
(prepubertal).: w3 ]5 ~5 |& U/ @! M
The parents were notified about the laboratory8 d0 F5 T5 q5 |/ e9 E
results and were informed that all of the tests were
/ j0 Y3 R: D& J1 j$ enormal except the testosterone level was high. The/ {/ H" F! T, P! v$ c
follow-up visit was arranged within a few weeks to$ t1 Z0 s% l4 D
obtain testicular and abdominal sonograms; how-
% O$ n$ Y8 M+ A/ U6 x. b9 G1 i2 @8 Iever, the family did not return for 4 months.
' }$ f; r+ k6 @Physical examination at this time revealed that the7 {  H8 U$ u( E! D  `8 y" U  s
child had grown 2.5 cm in 4 months and had gained  J, }( X  Q( j/ ?1 H7 R) e4 K! ?9 M
2 kg of weight. Physical examination remained
, w! M- n+ k/ G  S( K( V' {' x7 U( Tunchanged. Surprisingly, the pubic hair almost com-0 k7 t" _2 [( q: e
pletely disappeared except for a few vellous hairs at
8 \, n: [) C& l: `8 _the base of the phallus. Testicular volume was still 2
1 q* A/ K/ p% H" \mL, and the size of the penis remained unchanged.4 x+ \! T5 h8 \- p! w
The mother also said that the boy was no longer hav-1 J) i5 V6 [+ P
ing frequent erections.
, [- G8 A. [; lBoth parents were again questioned about use of
/ Q: t2 \2 n  r6 j$ d: y7 P, P% ^any ointment/creams that they may have applied to! M6 t6 R9 Z  l  N
the child’s skin. This time the father admitted the5 S; I3 G) j3 ^4 B
Topical Testosterone Exposure / Bhowmick et al 541
& @9 j7 x- {7 s4 Yuse of testosterone gel twice daily that he was apply-; P8 S+ t" A0 y4 c
ing over his own shoulders, chest, and back area for
+ e8 g$ f. I1 N: V( L1 k* L( ca year. The father also revealed he was embarrassed) w6 }7 w8 y+ f9 v# [/ a
to disclose that he was using a testosterone gel pre-2 H, c5 @7 w- o" Z
scribed by his family physician for decreased libido
" r/ Y6 Z5 h6 j# w% t( U% vsecondary to depression.8 C- O& u8 O; J, W
The child slept in the same bed with parents.
7 A% E$ G- p- y2 K  SThe father would hug the baby and hold him on his
2 j1 d/ C: e# U$ X; _4 }chest for a considerable period of time, causing sig-
4 e; _& D) j; c2 w# Z; G9 x/ o1 knificant bare skin contact between baby and father.
0 O' G7 i% a# PThe father also admitted that after the phone call,) ^* W3 d9 @; X# c9 d
when he learned the testosterone level in the baby% Y$ [6 `- x& J" U( A) _" [
was high, he then read the product information1 h7 ^4 ]; P* G+ B* t
packet and concluded that it was most likely the rea-% a4 q9 S0 m8 ~1 n
son for the child’s virilization. At that time, they
/ ?; L  I5 u, f6 E; t2 udecided to put the baby in a separate bed, and the: j: ?1 Y" ?1 @6 H
father was not hugging him with bare skin and had0 ]0 Z# }9 N3 z! K/ A& r3 r
been using protective clothing. A repeat testosterone
/ P2 g1 x2 D6 n/ L% L7 ttest was ordered, but the family did not go to the
5 [/ G& k- \( H  n+ }6 qlaboratory to obtain the test.- v( v  f0 z: h& g$ c
Discussion
' V- a8 C2 l7 k+ A% d9 U9 _- J8 I8 ^Precocious puberty in boys is defined as secondary
, J6 m0 A. n7 N6 J& Y7 ^sexual development before 9 years of age.1,4% A# Z$ q" W6 G/ B* ~6 p/ k" O" R
Precocious puberty is termed as central (true) when
& R: z: Z* m+ W5 x3 z8 Xit is caused by the premature activation of hypo-
8 S% u, _. f0 {6 C$ S" m  X( X! f& zthalamic pituitary gonadal axis. CPP is more com-; d  Y% }0 e3 D5 N( G' J3 E, @- u
mon in girls than in boys.1,3 Most boys with CPP
) V5 C; n- p( b3 L7 ]& vmay have a central nervous system lesion that is
4 U/ c) m! _9 W6 O1 x$ @responsible for the early activation of the hypothal-0 K6 T: h! _( c
amic pituitary gonadal axis.1-3 Thus, greater empha-! d5 V4 k; P6 f0 y$ M0 n& R
sis has been given to neuroradiologic imaging in
- ]* g/ x$ x$ ?( e3 ]0 M" Jboys with precocious puberty. In addition to viril-
8 a- x1 r' D. ^: `2 {7 n) Kization, the clinical hallmark of CPP is the symmet-/ i3 x$ G/ m, W; K
rical testicular growth secondary to stimulation by
0 A' g2 H' E5 O9 p: R# D) b) i! `gonadotropins.1,38 Q' d; F: v: k1 F. J$ |  r
Gonadotropin-independent peripheral preco-# \" ?# k) z, Y, h: J9 I1 ?, K3 ~
cious puberty in boys also results from inappropriate
( Y4 U; w+ A- [  Landrogenic stimulation from either endogenous or- k1 g8 v( @' K' J+ G3 k' C; g: F
exogenous sources, nonpituitary gonadotropin stim-8 m8 o+ h. ?: m
ulation, and rare activating mutations.3 Virilizing* }# n1 H1 U# o: B
congenital adrenal hyperplasia producing excessive; w$ w) Q0 y3 d$ M
adrenal androgens is a common cause of precocious( g/ |' g: n- U! p7 O
puberty in boys.3,48 u9 J0 ^" Y: b$ G( c% V
The most common form of congenital adrenal
+ L( ?' ]9 d, i# U" Bhyperplasia is the 21-hydroxylase enzyme deficiency.+ y7 b2 S) J# A" Z
The 11-β hydroxylase deficiency may also result in- k$ O% g, c' H8 L& f- l
excessive adrenal androgen production, and rarely,
, _! ~6 c5 c% I: c6 k- g. y4 nan adrenal tumor may also cause adrenal androgen) R: K7 j& v0 [  p4 @7 H3 }! l
excess.1,3  @2 m, o0 `; C, z' ?
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ G, \- \3 H+ h4 i
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' c0 `8 ~* }$ c+ }' j# ]A unique entity of male-limited gonadotropin-
4 G1 u1 v! r4 R8 E# |  Rindependent precocious puberty, which is also known
! ^0 e/ q0 a9 Has testotoxicosis, may cause precocious puberty at a
$ E) Y7 c+ f) y$ \! B, {1 Pvery young age. The physical findings in these boys/ S$ w3 w3 k  c* W( x! c8 \( o( F
with this disorder are full pubertal development,+ a% ^7 v$ P7 F" e$ ^8 _
including bilateral testicular growth, similar to boys) Z( g6 Q3 }: @* U
with CPP. The gonadotropin levels in this disorder
$ j. P- E" k, A7 [8 ]; ^8 Tare suppressed to prepubertal levels and do not show
0 N# z/ ^# C9 Fpubertal response of gonadotropin after gonadotropin-6 q4 D2 Z+ {- b
releasing hormone stimulation. This is a sex-linked1 U: ?8 w0 j2 i' d# ]9 B$ Z: L4 |
autosomal dominant disorder that affects only) w# t+ N/ J$ c' p( ^
males; therefore, other male members of the family
. V, R1 O0 B  N5 i2 [4 Xmay have similar precocious puberty.3
6 f  w+ u4 s, z# a0 y1 ]  r$ F3 LIn our patient, physical examination was incon-
) I2 d) E, }, E; S' T1 ^# Fsistent with true precocious puberty since his testi-
; |, _9 i0 M# m$ \7 c2 W* Hcles were prepubertal in size. However, testotoxicosis
5 e% @9 w3 X& Zwas in the differential diagnosis because his father/ h5 K. U1 w4 V7 d
started puberty somewhat early, and occasionally,
, Z  h( p  I) B6 O9 T3 D  B( }' qtesticular enlargement is not that evident in the# s+ N8 o0 D, r$ m* K6 ^6 T3 ~
beginning of this process.1 In the absence of a neg-1 z$ y+ k0 h, ?# T" w0 s) ?! @! {
ative initial history of androgen exposure, our
/ b% K6 l1 I" W( S$ p% z+ R% \9 sbiggest concern was virilizing adrenal hyperplasia,
8 h4 d7 E7 c0 Geither 21-hydroxylase deficiency or 11-β hydroxylase5 i- D, d, H# D- H
deficiency. Those diagnoses were excluded by find-
8 [: v0 i3 s0 ~% H) N; ^8 ]ing the normal level of adrenal steroids.
" T% |; Y: D3 b  _: LThe diagnosis of exogenous androgens was strongly/ \+ b7 y9 [1 Z2 W
suspected in a follow-up visit after 4 months because
; o4 K+ ]1 o: L* o- jthe physical examination revealed the complete disap-5 P' F2 e2 F) F) Q( J$ K
pearance of pubic hair, normal growth velocity, and
" E8 M, Q6 P' P9 Ydecreased erections. The father admitted using a testos-. x6 J0 L; w! q* T& E+ d  C* Y! P
terone gel, which he concealed at first visit. He was
1 s+ D! u8 N- [; [' Cusing it rather frequently, twice a day. The Physicians’
  P/ b) q; d, p* Z6 B1 bDesk Reference, or package insert of this product, gel or9 z! B1 I/ d" n  z" e0 ]
cream, cautions about dermal testosterone transfer to
, U2 W- `4 z2 I* `0 ]7 yunprotected females through direct skin exposure.
- X) a) L6 k5 L0 ]8 [1 }Serum testosterone level was found to be 2 times the
/ p$ {0 L6 ]2 |. ~0 `6 |baseline value in those females who were exposed to
1 K1 `& B3 O: ], k8 g: R  x& X3 Seven 15 minutes of direct skin contact with their male* I% ^2 _1 u9 F/ A% ?( l
partners.6 However, when a shirt covered the applica-1 S# e; {; h. u: B4 b* k/ |9 _
tion site, this testosterone transfer was prevented.
& q4 k6 j$ a2 u1 s4 cOur patient’s testosterone level was 60 ng/mL,
: X) o. N4 O9 V" r# {which was clearly high. Some studies suggest that' H& F8 j+ ]+ {; F4 T6 z
dermal conversion of testosterone to dihydrotestos-5 Y; p: e/ [( f$ i7 V+ ?
terone, which is a more potent metabolite, is more: t9 I6 ~) k. c9 J  A# h& M
active in young children exposed to testosterone0 y3 h# D. j! N: |- e7 M& c
exogenously7; however, we did not measure a dihy-, W2 A$ _3 {- g+ _- F
drotestosterone level in our patient. In addition to
/ c1 n; Z. m) @- u5 u' Tvirilization, exposure to exogenous testosterone in4 x) {, Z2 v. ?2 O, W+ `& ?
children results in an increase in growth velocity and
  d5 J8 ~: m; l8 c9 Q! o5 |- `advanced bone age, as seen in our patient.
  i- \! Q6 h3 F) S3 o8 E' qThe long-term effect of androgen exposure during
% U  q! E% p4 }  j2 |early childhood on pubertal development and final
9 t  s' ?: {! T$ k6 Q" ]0 ^adult height are not fully known and always remain
" r3 @- X* K4 Ya concern. Children treated with short-term testos-: D, @' R4 o' }& D4 i$ J  O
terone injection or topical androgen may exhibit some
* m9 H+ m- ?8 O4 c) @0 Xacceleration of the skeletal maturation; however, after: k0 b2 c9 y4 H
cessation of treatment, the rate of bone maturation' N0 o* c# A$ k, w' ^6 n
decelerates and gradually returns to normal.8,9
" q% [/ i  G! O) P) h4 |There are conflicting reports and controversy0 V5 V+ R2 _' b# \# x9 H0 e
over the effect of early androgen exposure on adult+ i. T$ y! X/ q1 V  \; z, u
penile length.10,11 Some reports suggest subnormal
7 j7 N. w" G3 q: R/ ~adult penile length, apparently because of downreg-
1 U2 @' l* I' s) a' ?  |ulation of androgen receptor number.10,12 However,
7 `- N2 H4 Y- y3 T$ o% [Sutherland et al13 did not find a correlation between: r% g8 p* x9 M+ _; f
childhood testosterone exposure and reduced adult/ h( x% e% G0 V) N9 _- ]
penile length in clinical studies.
/ }  P* P: h5 v  N' H1 R! iNonetheless, we do not believe our patient is
* v( b6 \) c( l4 {! t$ n! qgoing to experience any of the untoward effects from- V! O6 ^. J( a2 X" P1 R* M( O
testosterone exposure as mentioned earlier because8 m1 a. i0 i  I8 w$ {
the exposure was not for a prolonged period of time.
1 n# h9 R$ B2 i( ]. J  ZAlthough the bone age was advanced at the time of- h& @/ J& e6 K. J
diagnosis, the child had a normal growth velocity at
: u8 j3 @) t! h0 S: \1 {the follow-up visit. It is hoped that his final adult
6 F' p8 U2 F. F2 h  g7 e3 iheight will not be affected./ ~5 ^5 e0 a7 k! A; Z; g* _
Although rarely reported, the widespread avail-% h6 D; s  M+ e& u# c
ability of androgen products in our society may  D) \2 _! S0 L! {9 x! D6 ~3 D
indeed cause more virilization in male or female9 A: q" F+ [1 b1 ?; t1 L
children than one would realize. Exposure to andro-
$ S6 ^* |3 S& U9 o' l. ~# A, A: o1 q/ ^gen products must be considered and specific ques-7 }4 g: g' u+ @% K/ p
tioning about the use of a testosterone product or
# i& T8 h4 }7 P5 tgel should be asked of the family members during
0 J6 ~# Z+ P# q! d9 e2 {6 Jthe evaluation of any children who present with vir-( ~( l* ]3 U' f/ |" }
ilization or peripheral precocious puberty. The diag-
- H2 S6 ^9 ]$ m  Y0 t0 V- y: ~nosis can be established by just a few tests and by9 [" ^" a) c( e2 u% J  z0 R
appropriate history. The inability to obtain such a
* I& H, |" C0 m9 n7 u7 z  t" Bhistory, or failure to ask the specific questions, may
& w8 k9 J& Y# u  S0 wresult in extensive, unnecessary, and expensive
/ f) J/ ?8 S) g* z' ~$ hinvestigation. The primary care physician should be
' m7 E8 Q$ v$ O0 uaware of this fact, because most of these children4 W& \: T/ s/ m  o4 o% d% n- L
may initially present in their practice. The Physicians’
# d$ _$ B0 N$ g4 T3 r2 J$ bDesk Reference and package insert should also put a
/ Z9 L  Q* P0 m: A9 Lwarning about the virilizing effect on a male or7 [. C& \, s. B
female child who might come in contact with some-
6 h$ h9 Y6 c" y" Z* G, _one using any of these products.
- }; d1 a4 D0 j, r! h$ LReferences
0 @2 H  A# ^9 t) y* W3 a7 b" G3 r0 {1. Styne DM. The testes: disorder of sexual differentiation- z3 \7 }. n4 u# b9 ]) v/ `
and puberty in the male. In: Sperling MA, ed. Pediatric1 i/ N$ F& ?, p$ c6 m1 N
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( Y; k) s! W, |$ S2002: 565-628.
$ o0 @8 t0 Y" C' c2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 {: t5 B" j) x4 [8 K
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old5 V0 o# @7 C* w2 l* w: K1 w9 D# d
Boy Induced by Indirect Topical4 u0 Q0 ?) j+ H) Z" S8 K
Exposure to Testosterone
) q7 F" A1 o; @/ ?: A2 bSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 _) [, \; l- U* H; d' ~6 P$ R
and Kenneth R. Rettig, MD1$ _% A7 n8 m9 K
Clinical Pediatrics
) |3 |$ B: [8 T; H: x4 cVolume 46 Number 6( \5 ]# O5 x6 _
July 2007 540-543: _& v! ^; ~, c, Z! h
© 2007 Sage Publications
1 d4 E, v7 i: k( W# }10.1177/00099228062966510 b1 k2 R: r( X
http://clp.sagepub.com
: j) B; Q4 k* Zhosted at2 O$ K) \$ ~9 @
http://online.sagepub.com8 Q4 H0 r7 Q( v( @7 Y
Precocious puberty in boys, central or peripheral,) I6 n  l7 A/ H1 J/ z# e3 ]
is a significant concern for physicians. Central4 C4 y9 \+ _4 W. B: v' {
precocious puberty (CPP), which is mediated
3 r- I/ h; }& O2 J# h# n% R7 Tthrough the hypothalamic pituitary gonadal axis, has# A7 u3 a5 \3 E7 r+ A) E
a higher incidence of organic central nervous system$ G  H) ]- q) @) u. n$ M
lesions in boys.1,2 Virilization in boys, as manifested
# g1 e8 \3 J  c9 w- t. Tby enlargement of the penis, development of pubic
4 k' q& Y* y3 m7 d2 j  I" Zhair, and facial acne without enlargement of testi-5 k. w" K  d/ e8 [( y
cles, suggests peripheral or pseudopuberty.1-3 We
, M* `; D) N! B: Sreport a 16-month-old boy who presented with the
9 h( Y- H  l, `) P& eenlargement of the phallus and pubic hair develop-% H. A  [' ^! w! o! l
ment without testicular enlargement, which was due
9 U. n' d* O5 ^/ D% C' m4 H( pto the unintentional exposure to androgen gel used by
4 g0 n+ O3 H2 Dthe father. The family initially concealed this infor-3 M! d& I4 A. E
mation, resulting in an extensive work-up for this
5 @9 G# Q8 q. `$ o; K; Z3 k! lchild. Given the widespread and easy availability of
* o4 S7 J, K, v# H6 xtestosterone gel and cream, we believe this is proba-6 T; g- y; ?7 M; ^
bly more common than the rare case report in the7 W1 y; y: n+ f& t# ~6 [( i
literature.44 s# Q" I4 L9 r) `% m
Patient Report
$ X0 u+ x9 B0 H. f/ vA 16-month-old white child was referred to the
8 H- S" r8 f1 z% C* tendocrine clinic by his pediatrician with the concern* f6 c+ v! A; D8 q0 p; F
of early sexual development. His mother noticed
9 P# ]7 S5 X3 W  h1 zlight colored pubic hair development when he was
: a/ d& I- M9 b8 Y& @) FFrom the 1Division of Pediatric Endocrinology, 2University of" a; Q: E) L- a
South Alabama Medical Center, Mobile, Alabama.
0 E0 X6 @3 ~9 x! p4 k- |( zAddress correspondence to: Samar K. Bhowmick, MD, FACE,
8 c$ x4 F' N. l- p, @" ]Professor of Pediatrics, University of South Alabama, College of' h& O/ ?! w$ c0 a! z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! @! U/ a3 a$ B/ Z# k. oe-mail: [email protected].
  h% K. l+ p- j/ V1 u0 y! aabout 6 to 7 months old, which progressively became
7 S* F6 s! C. \5 ^- Ddarker. She was also concerned about the enlarge-
3 F/ `6 d4 l6 ]$ y6 t6 [" \ment of his penis and frequent erections. The child
, e3 r$ c3 s" wwas the product of a full-term normal delivery, with
1 z0 c  j1 U1 b/ N! K1 Wa birth weight of 7 lb 14 oz, and birth length of- V2 h0 v6 z' ~( k0 e; w1 L
20 inches. He was breast-fed throughout the first year5 t# F8 y& A. I& n6 C
of life and was still receiving breast milk along with
8 I/ Y& c  j4 S  lsolid food. He had no hospitalizations or surgery,
/ ^: Q$ W7 x  A" xand his psychosocial and psychomotor development8 ^9 J; F' B) T- {" ~8 @: O
was age appropriate.
/ ^, j/ a# C/ g1 h) hThe family history was remarkable for the father,
) j. I/ E2 R' {" ~4 [2 ~who was diagnosed with hypothyroidism at age 16,% M& @- P% d! b$ }, Q& m
which was treated with thyroxine. The father’s
9 B, _  u6 x6 ~- R7 @$ v0 @height was 6 feet, and he went through a somewhat
! m+ w7 r' d; Z! m) W# W# q) hearly puberty and had stopped growing by age 14.
) Y2 V! e4 I, m; I+ e" VThe father denied taking any other medication. The& _6 e( j- c$ ?1 c$ b  m6 s/ n$ h
child’s mother was in good health. Her menarche7 ~7 _0 H" B+ r, c* y2 ~5 b
was at 11 years of age, and her height was at 5 feet$ R7 M3 H6 @" N  O! H/ L2 ]
5 inches. There was no other family history of pre-
: `" t* P4 U, g/ D/ \) Rcocious sexual development in the first-degree rela-' [1 P) i9 W6 ^# E
tives. There were no siblings.
6 T2 V4 P4 `! `# Y7 g2 X. S: S& TPhysical Examination2 f$ [  ?$ V% L. j+ a; [
The physical examination revealed a very active,3 y% ^% O) h# W3 G+ L# c# q4 f
playful, and healthy boy. The vital signs documented
; n, m/ a( }* o. Y9 ]& wa blood pressure of 85/50 mm Hg, his length was
! b0 d" [4 a; D" [! F90 cm (>97th percentile), and his weight was 14.4 kg
4 o% K* Y) K4 c3 C" P: E" g(also >97th percentile). The observed yearly growth
) b5 c/ Z$ m. P  B" z: Uvelocity was 30 cm (12 inches). The examination of
+ d# ^& L( r' B' n: d- x6 Qthe neck revealed no thyroid enlargement.$ {( \! A' M8 F& b
The genitourinary examination was remarkable for
$ y3 x3 Q; H: r" Jenlargement of the penis, with a stretched length of
# |5 a' s6 C3 G  a  a" w! r8 cm and a width of 2 cm. The glans penis was very well
* r8 R, g: E6 ~( m  vdeveloped. The pubic hair was Tanner II, mostly around3 ^: c; g0 ?6 ?% N1 m( C: }* ?
540
, j1 o3 r1 ~' j+ s* h7 L5 G4 t% Vat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& `1 ^( S0 O  C: e+ W+ _
the base of the phallus and was dark and curled. The+ A0 U, H  O' o9 C5 b
testicular volume was prepubertal at 2 mL each.
" M4 d2 [& P) ^% {The skin was moist and smooth and somewhat, ?: F6 e/ ]4 a) c
oily. No axillary hair was noted. There were no
. W5 h4 U& U: t# r# wabnormal skin pigmentations or café-au-lait spots.
  _9 i( o5 a( T- k3 ]Neurologic evaluation showed deep tendon reflex 2+0 N: C) ^4 w8 e7 D
bilateral and symmetrical. There was no suggestion: U$ K, G: k( |# F( C  H* W9 `
of papilledema.
. |' l5 W/ }) f" ~/ l* F# `. GLaboratory Evaluation
8 ~' ?9 T0 l  W9 Q, UThe bone age was consistent with 28 months by
# U* x9 ^6 v* e3 |3 W% z8 ]" k/ @using the standard of Greulich and Pyle at a chrono-, q' U! o9 ?) P2 w! S5 m& H
logic age of 16 months (advanced).5 Chromosomal
4 ]5 k6 }" u4 X: B: lkaryotype was 46XY. The thyroid function test; c% l& k; x6 c; o
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 l( v2 v9 w$ x  Y2 O3 ylating hormone level was 1.3 µIU/mL (both normal).
  e9 y- n. X0 \$ M, Y2 j: \2 ^The concentrations of serum electrolytes, blood  O( o! ?0 t4 O" @" `* P2 {. c
urea nitrogen, creatinine, and calcium all were
: Y  i2 f$ h* L9 Z" P! rwithin normal range for his age. The concentration
* _& B: @$ f* r, d5 `of serum 17-hydroxyprogesterone was 16 ng/dL
8 x. M- ^* W  @1 b(normal, 3 to 90 ng/dL), androstenedione was 204 M8 N; H+ d/ h0 x; O) a4 w; V) x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 G2 A8 J$ K9 J/ o1 N. P1 p; b* _; }terone was 38 ng/dL (normal, 50 to 760 ng/dL),+ M* S8 e9 C6 E# E
desoxycorticosterone was 4.3 ng/dL (normal, 7 to( G% w( a2 C% t
49ng/dL), 11-desoxycortisol (specific compound S)# Z0 x# u* a0 M0 z) c
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 c" H4 E. A2 ]: o3 x
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& C5 L5 s) _' @4 m. _& Y$ k. Ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),. g7 S$ h; E5 J& \5 ~. G4 k
and β-human chorionic gonadotropin was less than1 t7 p' z& X6 Q" c3 m/ d8 p+ n
5 mIU/mL (normal <5 mIU/mL). Serum follicular5 e$ j& f! K- \4 [, E
stimulating hormone and leuteinizing hormone
+ F0 v4 H  K2 [) J6 u1 e$ nconcentrations were less than 0.05 mIU/mL
( w2 [; J0 |6 S& ]4 E( z# x(prepubertal).+ I( \+ D0 p. \! [! L
The parents were notified about the laboratory, t' U2 b0 x/ @% p
results and were informed that all of the tests were
+ ~' _) D; k) f1 Lnormal except the testosterone level was high. The
. `/ y( ^. n6 Y5 t$ ofollow-up visit was arranged within a few weeks to
, B6 G3 L5 f9 e1 _obtain testicular and abdominal sonograms; how-, P7 D; k) E+ F% O1 m' Z, }+ p2 R
ever, the family did not return for 4 months.
! u: o3 l' `  tPhysical examination at this time revealed that the
- M- G- X( l5 ?* W. [/ b4 b) J/ s8 dchild had grown 2.5 cm in 4 months and had gained) P7 B# Z1 V) u+ W' K0 F  _
2 kg of weight. Physical examination remained
: I5 @, b8 c( C2 S( wunchanged. Surprisingly, the pubic hair almost com-! a5 Z( ~3 w( d! |* R$ I
pletely disappeared except for a few vellous hairs at
( S' U9 ?2 \9 K0 e3 {. E, T4 rthe base of the phallus. Testicular volume was still 2! O4 C. Q/ ~8 k  m7 b
mL, and the size of the penis remained unchanged.9 d, V5 z" M! T; ^: r" I
The mother also said that the boy was no longer hav-, H2 j9 r2 Q" T9 Y9 W1 B
ing frequent erections.
7 o5 G- G% [2 |% X" x7 }Both parents were again questioned about use of8 S! j, M% P# `. H
any ointment/creams that they may have applied to
2 l; S% J6 b$ g! ]1 U3 d! J6 H! Wthe child’s skin. This time the father admitted the
9 r- X+ g; Q. {& D* a4 ^2 q% I, kTopical Testosterone Exposure / Bhowmick et al 5410 J. g4 \, x# \7 h
use of testosterone gel twice daily that he was apply-
0 j1 \! t* S$ T7 n' Ming over his own shoulders, chest, and back area for% y  ^5 H* d. M
a year. The father also revealed he was embarrassed, b4 b8 @7 Q8 r; J
to disclose that he was using a testosterone gel pre-
' M( P- l* v2 L# ?. ?* oscribed by his family physician for decreased libido+ x0 N- F8 R2 C" F
secondary to depression.
) f0 ?! X1 ^* d- LThe child slept in the same bed with parents.7 P( ?& ~3 C& k3 t: U
The father would hug the baby and hold him on his
6 O. Z2 e6 r7 z5 I0 d3 Nchest for a considerable period of time, causing sig-' c0 C# F- ?$ g0 ?$ e
nificant bare skin contact between baby and father.
& Q* W& l/ z( Y' v. D& T5 l& eThe father also admitted that after the phone call,# H% ^7 |2 D+ u1 f: l# n# H5 [; h$ `
when he learned the testosterone level in the baby  E/ \" b/ m: ~# C
was high, he then read the product information
' I6 V  _+ X3 ^6 I; {packet and concluded that it was most likely the rea-
4 A5 R9 a3 B9 w, S* ?- gson for the child’s virilization. At that time, they& f) q9 S! S, z! s, R8 ~- P* N6 n2 X
decided to put the baby in a separate bed, and the
; e) V3 Y; x. x* O5 W; _9 {( qfather was not hugging him with bare skin and had
3 {4 E: e6 ~9 N6 J8 Gbeen using protective clothing. A repeat testosterone1 `  m4 M) M$ K% F; x; {4 [
test was ordered, but the family did not go to the: ^& o" f( h0 q$ z' O( ]
laboratory to obtain the test.
* F) Q, Z6 y1 g' gDiscussion& I  W* U& s* {
Precocious puberty in boys is defined as secondary
5 n2 W3 I1 d, T8 h& W- Rsexual development before 9 years of age.1,4: r) l5 A2 I0 b6 v
Precocious puberty is termed as central (true) when
& f' I9 t: s& ?, W  u. q1 Kit is caused by the premature activation of hypo-
- m' h& Z, t" v9 G1 Y( Wthalamic pituitary gonadal axis. CPP is more com-
5 Q; N1 S; U; N% q  d3 imon in girls than in boys.1,3 Most boys with CPP
! Q0 S& \+ G7 _6 gmay have a central nervous system lesion that is+ u) k7 [& a, m& N2 b0 z) t4 s
responsible for the early activation of the hypothal-# q1 @  A6 s) i4 ]
amic pituitary gonadal axis.1-3 Thus, greater empha-
; p5 P+ G; S0 `7 A& v( ysis has been given to neuroradiologic imaging in
! b# i" q  _) [2 H" ^9 g/ {, pboys with precocious puberty. In addition to viril-
$ t; R7 }% R! Z7 yization, the clinical hallmark of CPP is the symmet-
: G, o( q0 ~. o: O" rrical testicular growth secondary to stimulation by7 p7 C) p8 K2 D- O6 p# p3 y
gonadotropins.1,3
" [7 k+ c( ]* Q# G& k( |8 cGonadotropin-independent peripheral preco-
8 i8 l; _5 \3 x. x9 vcious puberty in boys also results from inappropriate; C9 P/ b6 n" [3 T
androgenic stimulation from either endogenous or# C  F4 m4 G. r6 y
exogenous sources, nonpituitary gonadotropin stim-
9 @6 _3 v7 Z# ]" |! julation, and rare activating mutations.3 Virilizing9 P' B  X$ }: w1 m
congenital adrenal hyperplasia producing excessive3 e( T3 j' o& ]" b
adrenal androgens is a common cause of precocious
! }7 |7 B0 [; N' ^$ Ipuberty in boys.3,47 k. @" K2 @8 L7 Q  i5 Y
The most common form of congenital adrenal- K$ h2 c$ d% X0 ~# p% L& o5 d
hyperplasia is the 21-hydroxylase enzyme deficiency." E5 J. j$ ^9 x9 l' A
The 11-β hydroxylase deficiency may also result in
5 M( L5 f2 S* A; h8 Gexcessive adrenal androgen production, and rarely,
& F9 ^( _1 i. K1 ^7 W3 N% |an adrenal tumor may also cause adrenal androgen! A8 Q2 x1 N2 i6 }5 ?
excess.1,3
) p8 N5 r$ r) N7 w, o0 Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 k3 c5 f) G( u
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; y( k% n/ ]# {+ f4 I
A unique entity of male-limited gonadotropin-, Z* E: p  Z  y" i5 a& N+ _" u, H
independent precocious puberty, which is also known9 M9 {2 x# N% V
as testotoxicosis, may cause precocious puberty at a! I2 p0 E1 k# q/ p
very young age. The physical findings in these boys2 O% v; Q  t+ e4 _1 I
with this disorder are full pubertal development,, Y' p8 V2 @' r5 f* |; D$ [# B
including bilateral testicular growth, similar to boys  k" Q0 B7 V% N2 z: z- C
with CPP. The gonadotropin levels in this disorder+ w) G* ^/ m( X6 A& Z9 H
are suppressed to prepubertal levels and do not show& }3 I0 m0 N* y+ k) G% M
pubertal response of gonadotropin after gonadotropin-
/ Z1 [, y! T5 oreleasing hormone stimulation. This is a sex-linked# B  W- y5 K4 \& l( r
autosomal dominant disorder that affects only
6 k0 Z$ v  ^7 a* T' A* c- m3 ?  Emales; therefore, other male members of the family
: N3 L  h8 a% Smay have similar precocious puberty.3
3 x  h$ Z- L- b- w. a9 \: ~In our patient, physical examination was incon-
  K9 _( ~) X7 V  f5 }% esistent with true precocious puberty since his testi-
; R$ ~' R/ \9 ^+ i5 F7 `7 Bcles were prepubertal in size. However, testotoxicosis) D8 g. A- D5 Z1 {# V3 u/ b" v
was in the differential diagnosis because his father" A0 g% A3 o" T$ }) {0 z( D5 A
started puberty somewhat early, and occasionally,
0 W- i! p6 n/ F+ d1 M/ otesticular enlargement is not that evident in the
- ?. J; @: ~$ ]9 ?( i& _4 p$ pbeginning of this process.1 In the absence of a neg-
" X: x( G( J- S5 dative initial history of androgen exposure, our
1 [# W( A4 v* f* `' x% I$ dbiggest concern was virilizing adrenal hyperplasia,
% R8 C9 E$ R, O" C9 Jeither 21-hydroxylase deficiency or 11-β hydroxylase
3 f1 v4 |7 k( g8 A# d) ?5 ^deficiency. Those diagnoses were excluded by find-7 e$ ~' _. H) M: [  i; u
ing the normal level of adrenal steroids.
9 U' w4 H$ y, ]4 `The diagnosis of exogenous androgens was strongly
" v0 ~5 G/ B7 i! k* W( o* y' xsuspected in a follow-up visit after 4 months because
8 R9 k2 _8 k9 W7 q& \; V. Bthe physical examination revealed the complete disap-
  S( o$ A9 N( D: P9 @+ a; w1 @pearance of pubic hair, normal growth velocity, and7 z; ?4 `: u# B4 L6 G( j
decreased erections. The father admitted using a testos-
7 M# ]' U6 O" i- jterone gel, which he concealed at first visit. He was, S" h0 g: Q+ x
using it rather frequently, twice a day. The Physicians’- i9 B0 k9 L/ F7 c+ `( q6 s/ W
Desk Reference, or package insert of this product, gel or
( d) O' Y( e, vcream, cautions about dermal testosterone transfer to' H- B4 `9 m$ \  a! @- T8 m6 W# o
unprotected females through direct skin exposure.
& Z5 r* c) @. Q) f8 ESerum testosterone level was found to be 2 times the
% b# `$ `; {, r; y) ~baseline value in those females who were exposed to: W: H1 h5 d3 g3 }* [0 G
even 15 minutes of direct skin contact with their male* T$ c9 p# C& j) U
partners.6 However, when a shirt covered the applica-
" @' A8 }! C: T5 H8 Ttion site, this testosterone transfer was prevented.8 g, d- D9 j: d. {
Our patient’s testosterone level was 60 ng/mL,5 U) m, Z; S( }2 e: o0 b: A8 k
which was clearly high. Some studies suggest that  p/ D1 I& E% Q" T: x
dermal conversion of testosterone to dihydrotestos-2 R% ?/ N& z  O* I( S1 U
terone, which is a more potent metabolite, is more+ y' O) |7 |+ o0 w% k
active in young children exposed to testosterone
& h1 w! k' j4 D6 E7 @: D3 Dexogenously7; however, we did not measure a dihy-( ~3 X8 [$ K& D, x: o5 |: [
drotestosterone level in our patient. In addition to$ K( O+ a- d" R: J
virilization, exposure to exogenous testosterone in  @; M( w7 E* j; r
children results in an increase in growth velocity and
6 J1 X$ l: \9 T9 V1 r2 M* S  V$ {advanced bone age, as seen in our patient.5 W7 B0 ^$ A1 T9 a$ u8 L, @9 b8 \- w: l
The long-term effect of androgen exposure during  s! x7 z/ X) j$ u
early childhood on pubertal development and final, a: ?, x& [! o, X% I
adult height are not fully known and always remain7 c9 L4 h# U# s9 R5 n
a concern. Children treated with short-term testos-
% ]1 D, _6 I- V; k/ \. Fterone injection or topical androgen may exhibit some" Z& b0 m- Q7 F1 @( {" T: ~% x
acceleration of the skeletal maturation; however, after3 G9 L5 U3 |" |% E- g) v) O4 g
cessation of treatment, the rate of bone maturation
* V0 E2 ^! v4 y/ S- ^decelerates and gradually returns to normal.8,9  W) c0 |, _: v7 M
There are conflicting reports and controversy
: o8 m9 ~/ j9 ?- D, |# L% iover the effect of early androgen exposure on adult6 [( d8 S8 [/ J" f) F; G
penile length.10,11 Some reports suggest subnormal
; |. E( a8 X) e) E# w. a- Eadult penile length, apparently because of downreg-' I2 O. J1 A6 _) M' b
ulation of androgen receptor number.10,12 However,# z& d6 }$ M7 r( W, V
Sutherland et al13 did not find a correlation between
6 }1 M3 c% C. Achildhood testosterone exposure and reduced adult
% L: V, X) k9 c9 U/ dpenile length in clinical studies.
) V) c  j6 ~) H5 O# O' FNonetheless, we do not believe our patient is$ M4 F  F9 v8 L
going to experience any of the untoward effects from
' Z2 o* W: M7 ^  U0 w/ jtestosterone exposure as mentioned earlier because. U8 n+ Q8 f) E0 c( [. T2 A5 K' M
the exposure was not for a prolonged period of time.( w8 ~& G) ^3 g( e* l, D+ N0 L* H
Although the bone age was advanced at the time of& J$ |+ |4 x' D
diagnosis, the child had a normal growth velocity at& H3 r3 C8 ]! `' V/ ~0 w
the follow-up visit. It is hoped that his final adult" U# Y& |+ Z! n" E- E/ w# ^+ b4 R
height will not be affected.5 ?/ V9 }$ u3 L) P2 C9 ^% p4 u
Although rarely reported, the widespread avail-
, O4 {% o9 D' R8 [8 @1 Jability of androgen products in our society may) n' `0 o# }" m9 O9 \9 }7 W
indeed cause more virilization in male or female
) S; O( ^; v8 f# s" \children than one would realize. Exposure to andro-
3 r9 L& ]6 T. fgen products must be considered and specific ques-" ~" \8 W7 x( u0 t
tioning about the use of a testosterone product or. A" [# C' R2 j% {
gel should be asked of the family members during. r7 u. L* L: U& `
the evaluation of any children who present with vir-4 F* Z# Z0 H/ C& B
ilization or peripheral precocious puberty. The diag-
/ {  K# i3 ]" r0 c. w1 W! lnosis can be established by just a few tests and by
, ]- i9 s: W+ \% Nappropriate history. The inability to obtain such a
9 d* }. H* i' \* M2 Yhistory, or failure to ask the specific questions, may
. i- h  g0 Y4 xresult in extensive, unnecessary, and expensive
9 S/ V) x$ v% j1 L' S. tinvestigation. The primary care physician should be4 O# Y  O8 c/ v9 D/ H% t' o1 F$ F
aware of this fact, because most of these children8 C0 U/ i) `7 V: H  V) Y8 l
may initially present in their practice. The Physicians’2 X1 ?6 m. C: d  z- u% i
Desk Reference and package insert should also put a( p( e% a- o$ Y6 ^
warning about the virilizing effect on a male or
9 G1 t6 s- K8 y3 Kfemale child who might come in contact with some-
0 J# w' t5 l8 M7 U; j: Oone using any of these products.) L  K2 Y) X7 ]" _' z6 U- I& H
References
3 V# B/ L3 R/ ]2 ^1. Styne DM. The testes: disorder of sexual differentiation
' }/ F% u' {0 d3 iand puberty in the male. In: Sperling MA, ed. Pediatric9 |' c2 A3 D4 S% b# A+ B
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 M4 j6 [6 T& ^2 H. B7 |) y2002: 565-628.5 t! z# w8 [$ |2 p3 k
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( s' b  V  p: B% K& Jpuberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

* m7 k. `% ^* `- |# ^: h2 {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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