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Sexual Precocity in a 16-Month-Old
8 I3 G1 L" `- r, O( b6 zBoy Induced by Indirect Topical
: E6 x4 v7 B6 v, A0 TExposure to Testosterone! K3 @  t( Q$ c& A9 ~; o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2# S- y( i4 z' e9 j0 {7 {
and Kenneth R. Rettig, MD1
1 I5 a7 r/ i$ dClinical Pediatrics3 L# w. E6 h* d8 d0 R4 W
Volume 46 Number 6
( D5 n7 q( K8 n& _July 2007 540-543
8 r1 x( w1 d* K3 j2 j: E© 2007 Sage Publications3 l" a) D: Q4 H6 S; E
10.1177/0009922806296651
7 e; ~, g. ?" P$ b; C* f( F8 phttp://clp.sagepub.com
* x5 o. n$ m$ j, ~% n7 jhosted at( i  U  r5 X& s: L% I/ v9 u& T
http://online.sagepub.com
1 m, U& ]  b9 i0 d6 ?Precocious puberty in boys, central or peripheral,( z2 Y$ h, m: \; \
is a significant concern for physicians. Central
" O1 Y" I' @4 s. o9 X0 fprecocious puberty (CPP), which is mediated
) q4 y9 T* l  I1 |9 g; R  r4 `, H; Ethrough the hypothalamic pituitary gonadal axis, has2 p, n7 W6 t9 ~- [: [! R
a higher incidence of organic central nervous system
3 G6 n; c8 w% ]+ @6 B% O# G+ }2 Jlesions in boys.1,2 Virilization in boys, as manifested! d: C$ M5 g. j  m& @
by enlargement of the penis, development of pubic
. S' F0 O, |* N$ }hair, and facial acne without enlargement of testi-
; ]1 Y  b% s! D- r, p% x# Lcles, suggests peripheral or pseudopuberty.1-3 We- }' M3 J: c( B" t4 X. `
report a 16-month-old boy who presented with the$ y$ ?; R% l9 i. S9 v5 h% H
enlargement of the phallus and pubic hair develop-
1 D: P; Q$ G4 N- {$ k5 @ment without testicular enlargement, which was due
: q2 T. c: V4 [% |$ ^* y; R, Ito the unintentional exposure to androgen gel used by5 i+ o1 f- A8 v/ x  w9 Z
the father. The family initially concealed this infor-
5 t9 t. Q- Q3 _mation, resulting in an extensive work-up for this+ F- b- r! k2 U. f8 ]
child. Given the widespread and easy availability of
# l+ X% @, U' C- W5 H4 J" o, k  _testosterone gel and cream, we believe this is proba-
/ x. `( [2 {6 }6 ^5 z6 `bly more common than the rare case report in the
; }" G$ G  Q" I0 [: Hliterature.4( k3 g7 }; x9 Z9 }
Patient Report
2 Y; `( A# k3 t7 f% rA 16-month-old white child was referred to the& o; ^6 I! g9 G) @3 ^2 T
endocrine clinic by his pediatrician with the concern
& {' T( w3 y& u, U3 h/ s! `* `of early sexual development. His mother noticed
/ U  r* }# n9 K4 @" H5 n* Y+ wlight colored pubic hair development when he was0 w* D" ~/ P! c( e8 y4 g4 p
From the 1Division of Pediatric Endocrinology, 2University of
# ?: W3 v7 I# W' i; F0 n( kSouth Alabama Medical Center, Mobile, Alabama.
' n0 y1 {; N  |3 H( t, o4 `Address correspondence to: Samar K. Bhowmick, MD, FACE,$ `% v9 Q3 ?, {$ @' \8 Y
Professor of Pediatrics, University of South Alabama, College of
" {2 {. o& r: R) c. L- PMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* {$ J8 D8 [1 U  h# E. v- y+ g0 g
e-mail: [email protected].
/ ]3 k$ s) K5 f: J: E* fabout 6 to 7 months old, which progressively became
8 a4 w: p9 _% A" [' Adarker. She was also concerned about the enlarge-( l# f* s  ?" G. |! P6 S" n& `+ s8 ?
ment of his penis and frequent erections. The child
7 W2 y) {8 P- l6 J, {+ o& Gwas the product of a full-term normal delivery, with
7 ~. C  p) N' O# v- |7 ]a birth weight of 7 lb 14 oz, and birth length of, g2 U, ^- x* G# I, d1 v- r& ]
20 inches. He was breast-fed throughout the first year+ F; {; g$ q1 m1 E# A  X+ t: c
of life and was still receiving breast milk along with7 c, ^7 G! M- g$ m
solid food. He had no hospitalizations or surgery," r* |( m3 @4 i
and his psychosocial and psychomotor development
+ s, i+ @, n# `0 iwas age appropriate.+ f$ K. h* y& d) g4 W- W
The family history was remarkable for the father,
% e" R0 x3 w+ k& N# Pwho was diagnosed with hypothyroidism at age 16,
6 ~2 }9 d- _5 a+ c) Kwhich was treated with thyroxine. The father’s  v' H) w% p5 s4 b. g, F/ X
height was 6 feet, and he went through a somewhat8 _  w5 y$ ]- L# s/ {# b
early puberty and had stopped growing by age 14.
* J/ p$ c7 Q" x( h" r+ VThe father denied taking any other medication. The
. B  l" K! A" Qchild’s mother was in good health. Her menarche
7 [$ n3 j; u+ j; }) M2 uwas at 11 years of age, and her height was at 5 feet  ]: V/ f1 y$ I6 P- V' ~, c
5 inches. There was no other family history of pre-, S- o4 g/ o! ?* K, |" U
cocious sexual development in the first-degree rela-2 j, H1 K) W4 v# d4 C
tives. There were no siblings.2 i1 Q! i' B* C5 y4 y1 o
Physical Examination8 Q7 Y' E* p3 S4 e3 \
The physical examination revealed a very active,% U8 w" Z4 W9 u0 R2 D
playful, and healthy boy. The vital signs documented: A% T* _. I! L
a blood pressure of 85/50 mm Hg, his length was7 O  X4 c8 M, O! X
90 cm (>97th percentile), and his weight was 14.4 kg, |2 r# t; S" I2 k' Y: @5 M
(also >97th percentile). The observed yearly growth1 U; `- }. Q) u( g# H: n
velocity was 30 cm (12 inches). The examination of
- \! o: z) `6 J# u( C9 pthe neck revealed no thyroid enlargement.
/ q! L; a0 o9 }" Z4 j- R" gThe genitourinary examination was remarkable for; Z; T" y. T1 w/ \, l( o3 d
enlargement of the penis, with a stretched length of
/ a2 u  p( c1 D8 cm and a width of 2 cm. The glans penis was very well1 X  C0 h( B( f! |& O
developed. The pubic hair was Tanner II, mostly around) z; |" Q( q1 |2 w& J8 \
540" m2 h+ D$ m: W+ V8 }! I6 [) ^7 h
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 r. ^8 ~6 F8 ~0 G3 u& S: L; f. {& }0 L
the base of the phallus and was dark and curled. The# f- }6 O. N1 V. G% o; _  a7 E
testicular volume was prepubertal at 2 mL each.) r+ s$ Q8 O  p7 l
The skin was moist and smooth and somewhat$ F6 I+ W' Z' t' w5 G  N! m
oily. No axillary hair was noted. There were no% ~- }% {2 W5 g. N8 h
abnormal skin pigmentations or café-au-lait spots.7 \' o5 s# l* y
Neurologic evaluation showed deep tendon reflex 2+! R# C. g( J- @6 P! G  U  \
bilateral and symmetrical. There was no suggestion$ T4 @, c  u8 w8 @% |1 I) L
of papilledema.
* m. ]7 j) N9 S" p% M& eLaboratory Evaluation
9 z0 n' ?/ d# iThe bone age was consistent with 28 months by
+ x% _& z5 G, ^# o6 O5 uusing the standard of Greulich and Pyle at a chrono-
' a9 f8 Q& p4 c# B+ D$ blogic age of 16 months (advanced).5 Chromosomal
- [4 v6 h8 x4 j8 k( R7 F  Zkaryotype was 46XY. The thyroid function test; x2 [* m# n0 {- g% S* O
showed a free T4 of 1.69 ng/dL, and thyroid stimu-  g" c" N- l! s% w/ N* [  d" F6 F- r
lating hormone level was 1.3 µIU/mL (both normal)./ a  |* Y' {( c' f& K
The concentrations of serum electrolytes, blood/ D. ~! z) M! B5 j( t$ d7 O
urea nitrogen, creatinine, and calcium all were
$ g/ E" t$ f8 K0 G/ U& swithin normal range for his age. The concentration
2 S0 k1 d4 Y, y  c$ ^6 ^, Kof serum 17-hydroxyprogesterone was 16 ng/dL2 Y4 ]3 G$ G: H2 \: {
(normal, 3 to 90 ng/dL), androstenedione was 201 r  m: h6 [" Q$ Q( M0 B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 U0 O) ?3 u0 _1 k: c  t6 Cterone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 o+ z) S# ~- c6 T8 qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to9 c6 p8 M5 z3 ~: K0 y
49ng/dL), 11-desoxycortisol (specific compound S)
, k! S3 b! n/ y/ w8 \8 a9 j% B* w$ swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* D: d8 A  l: }tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 Z1 P1 ^  `% X& O6 o8 btestosterone was 60 ng/dL (normal <3 to 10 ng/dL),- P) G/ `9 a; G  I/ E0 N  H
and β-human chorionic gonadotropin was less than
6 T! h7 c, ~5 p1 [) [5 mIU/mL (normal <5 mIU/mL). Serum follicular
- k1 x1 B& j' w* P0 t; {7 dstimulating hormone and leuteinizing hormone2 Y8 y3 m& t4 J) A5 `/ [3 q
concentrations were less than 0.05 mIU/mL. {2 ^% {8 t2 k5 ?/ b! T6 Q: ]  M- B
(prepubertal).
' T: c, R( b% m6 `0 p3 OThe parents were notified about the laboratory
/ S6 k, `0 |3 f: o2 p0 F7 Y5 u( P! oresults and were informed that all of the tests were
, Q, p$ V3 q2 k1 n& @6 P) Tnormal except the testosterone level was high. The0 S1 m+ A1 O; |7 k2 A
follow-up visit was arranged within a few weeks to: g3 x1 k; k$ ?7 Z
obtain testicular and abdominal sonograms; how-
6 T* K: _% `# s2 Uever, the family did not return for 4 months./ Z# g# n; L4 {3 {! ^" w; _1 M
Physical examination at this time revealed that the: A- G' e! D" k$ x9 R8 ^: Q( g
child had grown 2.5 cm in 4 months and had gained
- h* X; Z( M8 ?# _+ x' D2 kg of weight. Physical examination remained, ?3 Q- f! [- N; k+ x3 E
unchanged. Surprisingly, the pubic hair almost com-/ @1 A. f, r0 W5 _
pletely disappeared except for a few vellous hairs at
+ |8 D9 }$ v' L3 e! F; [the base of the phallus. Testicular volume was still 28 @6 r9 B% r0 n* n5 c
mL, and the size of the penis remained unchanged.4 A: m! K# Y! \3 U  h- h& E
The mother also said that the boy was no longer hav-
3 a3 i4 J6 h2 A3 _. r9 v6 m& jing frequent erections.
) H" q& g$ y: MBoth parents were again questioned about use of
' ]  P. N! j) t6 L; y" a7 Tany ointment/creams that they may have applied to& Z7 |* I" c( a  m' r* z
the child’s skin. This time the father admitted the
" U. n0 E$ h0 U6 N! W9 d7 ]Topical Testosterone Exposure / Bhowmick et al 541
: d  A' `9 O5 {4 M3 W# R8 wuse of testosterone gel twice daily that he was apply-
  l" y$ e# ^: i, D8 a6 j+ ]ing over his own shoulders, chest, and back area for
6 s" F! Q) n4 f; k3 N2 ba year. The father also revealed he was embarrassed
& D2 P' R7 C; o5 m( `, e' r- U; z4 @: qto disclose that he was using a testosterone gel pre-
9 j, ?# M2 S, Kscribed by his family physician for decreased libido
; G3 F2 a/ y1 Y) _: J) rsecondary to depression.
! E# c+ o4 @7 a' E+ i. YThe child slept in the same bed with parents.
! v0 Z$ O4 J7 v  kThe father would hug the baby and hold him on his4 G1 g  ^  q2 S6 E$ d! X/ l6 n
chest for a considerable period of time, causing sig-
8 U6 [, F* D( w! ?nificant bare skin contact between baby and father.
# O# R+ N7 N4 ?. U# k- n4 e7 s5 A# HThe father also admitted that after the phone call,6 @+ _$ K( n) U
when he learned the testosterone level in the baby8 p0 o0 U# z! I0 w( _
was high, he then read the product information$ x# @. [+ \# d) e( m
packet and concluded that it was most likely the rea-
8 |) a5 [( r$ l1 N2 J2 t: Qson for the child’s virilization. At that time, they
- A! B! H/ Y4 U9 U( E4 `+ h- Zdecided to put the baby in a separate bed, and the
( G! |7 f6 y+ N7 |+ Sfather was not hugging him with bare skin and had
  g* s7 Y  O4 g* J" tbeen using protective clothing. A repeat testosterone
7 `$ f( e6 K9 p' @! e) U, vtest was ordered, but the family did not go to the; b4 b. _" U. D! G
laboratory to obtain the test.
: t+ L% _4 m( a& }. @( eDiscussion
$ `$ p2 @3 ^  m" b1 aPrecocious puberty in boys is defined as secondary
2 G( P2 C( Y$ @7 U, L: hsexual development before 9 years of age.1,4
2 F* k6 P% f! f0 j5 \* X" ]Precocious puberty is termed as central (true) when; p* C" C; m2 d8 @& ~
it is caused by the premature activation of hypo-# J; ?. {* @6 g
thalamic pituitary gonadal axis. CPP is more com-& Y- ]. t6 x  n* s7 y+ I
mon in girls than in boys.1,3 Most boys with CPP9 V3 x( }& }( @" h' ?# i# @4 \
may have a central nervous system lesion that is( t$ I8 j) V. v' `; I6 L
responsible for the early activation of the hypothal-
; L1 i" h+ _! v8 A) k0 Zamic pituitary gonadal axis.1-3 Thus, greater empha-
6 \% r' r$ o6 ^% D# T* |/ T( f3 Isis has been given to neuroradiologic imaging in
; y6 M' f: d' S$ t7 Wboys with precocious puberty. In addition to viril-
3 }2 ?4 x! ]0 @" lization, the clinical hallmark of CPP is the symmet-7 f! B$ `- N8 L/ f0 T5 p
rical testicular growth secondary to stimulation by+ B8 I: z; G* Z) l2 g
gonadotropins.1,3
: W6 F+ a, d) O$ e) P  k. q0 dGonadotropin-independent peripheral preco-
: v2 |2 N9 R. {/ h7 e( h! q7 [  ocious puberty in boys also results from inappropriate& M  h3 @1 s4 M& h9 }8 S
androgenic stimulation from either endogenous or6 K/ K1 r/ D5 [: y
exogenous sources, nonpituitary gonadotropin stim-  @5 a, }3 R, @# v+ H' n/ I
ulation, and rare activating mutations.3 Virilizing' m. e( w, b, B. j/ _' u4 ~5 Z, s
congenital adrenal hyperplasia producing excessive6 x% P, K$ c( b, |
adrenal androgens is a common cause of precocious7 z* d% i$ L  C' T6 h, Y
puberty in boys.3,4
8 N% E( j+ X; p% i' OThe most common form of congenital adrenal- o* ^- g! m0 C3 J$ X7 e
hyperplasia is the 21-hydroxylase enzyme deficiency.& S. m; ]' e1 {/ n9 K$ B& o
The 11-β hydroxylase deficiency may also result in
5 W* Q% e9 J2 `/ M' r, V* j# t! G' }excessive adrenal androgen production, and rarely,8 L' i% Z: X8 l$ t5 ]
an adrenal tumor may also cause adrenal androgen5 Q% w9 }$ M+ Q$ O) q
excess.1,3! w) E2 |9 f$ r  b9 {$ t
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* T) f% e/ P/ ?542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ S- }( j/ `0 t& ?2 D$ m6 c1 u
A unique entity of male-limited gonadotropin-2 G! a+ Y* }' ]' {5 n1 A8 p
independent precocious puberty, which is also known! X* n: q, E  o+ t) f4 t
as testotoxicosis, may cause precocious puberty at a
- n  B* v/ m" P- L( c9 D9 \very young age. The physical findings in these boys
& g4 |; A+ \/ r0 pwith this disorder are full pubertal development,
. a! \" t! j* r5 u  ]4 l) @; c( Fincluding bilateral testicular growth, similar to boys% U# a; I3 u1 t: }. i1 N/ R
with CPP. The gonadotropin levels in this disorder& c, n! T9 r% e+ j( `4 o/ Z
are suppressed to prepubertal levels and do not show( X3 n. W* l  Y* w
pubertal response of gonadotropin after gonadotropin-
7 A4 X: P- \7 @9 v& {. Preleasing hormone stimulation. This is a sex-linked- [8 Q$ g; N9 A. |# T
autosomal dominant disorder that affects only6 Z/ X1 P: r, R6 ~4 W
males; therefore, other male members of the family/ @7 T& d- Y; X6 U8 B* o6 [& B0 I+ ^
may have similar precocious puberty.3
9 }/ K9 y  n  t2 i4 Y+ uIn our patient, physical examination was incon-
& J$ v- @; j& lsistent with true precocious puberty since his testi-
, |( ?  K, m. B& c( `1 qcles were prepubertal in size. However, testotoxicosis& g% i3 x2 T: k  ?9 j
was in the differential diagnosis because his father( g5 _. K2 E6 N- N. E# ~+ O3 G0 h
started puberty somewhat early, and occasionally,2 i; b% d% g. L, M2 ^7 M$ h7 K
testicular enlargement is not that evident in the
: G6 X* d0 Q  x7 o- x( l& Hbeginning of this process.1 In the absence of a neg-% X8 [$ v# p5 ]2 [& C
ative initial history of androgen exposure, our4 L  a& ~1 o6 k  I
biggest concern was virilizing adrenal hyperplasia,
. V8 g7 [' l3 k: G! n+ meither 21-hydroxylase deficiency or 11-β hydroxylase6 Z# i  M; U9 h% Q9 D% f9 P1 U
deficiency. Those diagnoses were excluded by find-1 }, |6 q7 l% [' e* M4 n/ l! ?
ing the normal level of adrenal steroids.6 }, X9 w# ?; F  _
The diagnosis of exogenous androgens was strongly
9 s2 t* R7 P5 `suspected in a follow-up visit after 4 months because% D5 M6 j# b$ G; P9 Z1 E! x
the physical examination revealed the complete disap-
  J& O6 j' O, W6 K; K) cpearance of pubic hair, normal growth velocity, and. G, ~; p/ @0 C" O
decreased erections. The father admitted using a testos-' T; j) }4 q; w
terone gel, which he concealed at first visit. He was) L* x, W3 {3 F$ ?9 q! Q
using it rather frequently, twice a day. The Physicians’3 N1 T. P, I: @  x. V; I
Desk Reference, or package insert of this product, gel or
2 b/ X: G" q& n9 Vcream, cautions about dermal testosterone transfer to
6 C, z  J1 y, l9 b- y, Hunprotected females through direct skin exposure.; i; y4 C" ~7 y0 B# X2 N4 d
Serum testosterone level was found to be 2 times the2 E3 B$ p8 z. H% ~( c9 ]3 `- O' N$ B
baseline value in those females who were exposed to
* s" u# J6 @* H+ N) weven 15 minutes of direct skin contact with their male: h) _9 ^6 t: B9 n
partners.6 However, when a shirt covered the applica-2 }5 H) s+ l* n) W7 T
tion site, this testosterone transfer was prevented." B$ [: l+ I. p) `* R& I* c
Our patient’s testosterone level was 60 ng/mL,
; R0 Y8 h! o: R( \) s; |/ w0 Gwhich was clearly high. Some studies suggest that
- q' w9 T. H. A) ^/ }$ _* ldermal conversion of testosterone to dihydrotestos-
. ]: k$ f- X9 |  c+ p* bterone, which is a more potent metabolite, is more) A5 X4 R4 f1 H+ g
active in young children exposed to testosterone
6 g  N+ {8 Q3 S5 \! zexogenously7; however, we did not measure a dihy-
* ], I* k& Y! |% h8 Ndrotestosterone level in our patient. In addition to
+ w2 y3 H4 J9 H3 nvirilization, exposure to exogenous testosterone in
8 w- _; C. e% b0 Z. P; O, jchildren results in an increase in growth velocity and! r% [* Z# Q/ a" h( A. z1 ^
advanced bone age, as seen in our patient.* i2 j5 E4 @% G: N5 o" ^& c/ O
The long-term effect of androgen exposure during
+ q9 e$ O- P1 a; k0 }5 _early childhood on pubertal development and final
; w4 r7 n2 D' t  tadult height are not fully known and always remain
: q0 N: ?( f6 h# xa concern. Children treated with short-term testos-
2 U% A: a( r, ]* z( @terone injection or topical androgen may exhibit some& ?% e0 q( A- F5 o5 h8 F' [+ B) a
acceleration of the skeletal maturation; however, after
6 T9 B( g! B4 L+ m; w' Tcessation of treatment, the rate of bone maturation) P( a/ g' O, K3 `; h2 m
decelerates and gradually returns to normal.8,94 ?4 d. L% {: H+ s) q( f& R
There are conflicting reports and controversy
3 m& q! g" N$ b3 v- qover the effect of early androgen exposure on adult
$ k# n/ l4 ~1 J, j% |penile length.10,11 Some reports suggest subnormal
! o, j' W+ g$ j/ i/ s$ ~- r4 P4 x" oadult penile length, apparently because of downreg-
0 Z0 I9 [3 |8 v. w' U5 Z% q  v" J: culation of androgen receptor number.10,12 However,
  a; O6 [  `" d) X2 ~& |! b1 wSutherland et al13 did not find a correlation between
4 t+ W9 S& h$ _8 I# Gchildhood testosterone exposure and reduced adult
9 V; E* b3 h9 ^3 R% Mpenile length in clinical studies.0 z3 C  K, K9 r1 ~2 w# p/ W, `
Nonetheless, we do not believe our patient is% ~; w( r5 \* V3 @  @# `! p
going to experience any of the untoward effects from
+ ^6 o+ b, r# c% |" E% ?testosterone exposure as mentioned earlier because
5 x4 y9 u2 ^- }3 ?' `the exposure was not for a prolonged period of time.2 Y- l  o5 w3 N, v$ C$ \
Although the bone age was advanced at the time of4 u3 o% h, ]2 i8 b5 b
diagnosis, the child had a normal growth velocity at
6 y7 u3 ]4 D& H2 r6 Zthe follow-up visit. It is hoped that his final adult
7 }- [! p7 K. m! f" h% Mheight will not be affected., @2 J9 }6 F* ?6 h9 b& v6 e$ }
Although rarely reported, the widespread avail-9 E4 W. I/ e8 _( \% O. Y: V
ability of androgen products in our society may0 ?2 C+ x  H1 A6 d+ Q
indeed cause more virilization in male or female$ ?  M) v' `0 v; S# r7 ?
children than one would realize. Exposure to andro-
9 l& Q" }+ m5 [% x7 x4 B. rgen products must be considered and specific ques-
& D* ?+ u, r4 O6 ^+ Etioning about the use of a testosterone product or
3 W$ v- g7 ]" U" d( dgel should be asked of the family members during
; h. N: Q$ k7 m2 e) Rthe evaluation of any children who present with vir-# I: d* H" I; v  f/ N
ilization or peripheral precocious puberty. The diag-
2 ]; S2 U4 f. {! anosis can be established by just a few tests and by- _" D( c2 ^0 b5 N0 q
appropriate history. The inability to obtain such a; x: _- J9 D" ^- Z% y
history, or failure to ask the specific questions, may
( n2 c2 F+ P: Q6 o" }  X, @result in extensive, unnecessary, and expensive! y* `+ \- d1 \9 d" g% a8 F# @
investigation. The primary care physician should be
1 |" s0 @) [2 C$ [/ z& J% D3 z# Uaware of this fact, because most of these children
- c. N  `) m/ h* X& B: l  H1 r8 Vmay initially present in their practice. The Physicians’
- L! q0 M  s" o. i4 H3 kDesk Reference and package insert should also put a8 l0 x8 x2 D8 W; o4 _: @4 Y9 s
warning about the virilizing effect on a male or$ M, X) ~; K) t
female child who might come in contact with some-
9 X2 B$ H! Q2 O$ [- S! P1 M1 l$ Xone using any of these products.4 w$ P- z: q. x
References
- S9 n# `$ Q- U4 A3 v1. Styne DM. The testes: disorder of sexual differentiation
' I. |% A. A! X8 Sand puberty in the male. In: Sperling MA, ed. Pediatric; S" v7 W! h8 F8 |
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* W2 w! ]% d+ a3 e9 R" g# J8 r2002: 565-628.
7 r2 G* l& F) m) w3 c2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' j1 c8 t4 [9 P/ F* h1 h1 P0 f9 ^4 x: j
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old- E6 q, W1 M4 Y' ?: s0 y
Boy Induced by Indirect Topical# h4 P8 g; k* [9 K
Exposure to Testosterone
+ v& ^2 \. s# Y* R, h$ x+ B$ _Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2$ ?0 z8 {7 C# p  Y, M8 W
and Kenneth R. Rettig, MD1. N! h! K4 M( O. b
Clinical Pediatrics" z5 V; g* i; H7 d/ L% `8 d
Volume 46 Number 6
: ^+ i, h8 ?( E! F  `3 a& z" Q) ZJuly 2007 540-5434 q( L4 }3 u0 S1 F/ G' h- I
© 2007 Sage Publications
+ L5 M# i* ^2 J3 H: m10.1177/0009922806296651# k+ ]& h$ z" @( N% B- d+ |% q
http://clp.sagepub.com
: P, l$ I. j; I* I1 x' ^% ]hosted at' s" g5 Z9 Y  r1 R7 v9 @
http://online.sagepub.com8 p8 \+ ?2 \; B6 q
Precocious puberty in boys, central or peripheral,' P" r( ]7 C/ f. D1 W3 G
is a significant concern for physicians. Central
& w( G3 E; X) d* c& jprecocious puberty (CPP), which is mediated
4 n: ~/ n+ e( I" l: ?- }8 _. w) sthrough the hypothalamic pituitary gonadal axis, has' W' f8 K0 U/ x. Y
a higher incidence of organic central nervous system8 l* _# X* w7 J+ ]+ t
lesions in boys.1,2 Virilization in boys, as manifested% D3 Z: C% F1 N* l
by enlargement of the penis, development of pubic
9 \' K- E7 S/ Vhair, and facial acne without enlargement of testi-7 D+ @, n+ n6 x$ T6 f
cles, suggests peripheral or pseudopuberty.1-3 We* n7 l6 r3 K# G9 g
report a 16-month-old boy who presented with the
3 X$ Y1 j: T2 }+ T1 menlargement of the phallus and pubic hair develop-2 F+ l. Y2 u8 m3 u2 G% k7 S
ment without testicular enlargement, which was due
0 c6 C! d( \; T  h( ^to the unintentional exposure to androgen gel used by; J% j" Z& \1 q/ G& M
the father. The family initially concealed this infor-
# C' B$ \1 }4 F  k& C2 fmation, resulting in an extensive work-up for this; r  r% u* h8 ]. B: N
child. Given the widespread and easy availability of
# n( Z: X- q0 G4 [( B2 O- h4 ztestosterone gel and cream, we believe this is proba-
2 v7 S7 w* X. t/ e6 T/ _bly more common than the rare case report in the: T0 o9 z3 x* G0 Y" |- g- f
literature.4* q/ S1 l' `: G9 w/ Y
Patient Report7 `# j2 x7 C+ }3 d
A 16-month-old white child was referred to the/ D7 E/ \& u0 \6 K* N3 u
endocrine clinic by his pediatrician with the concern
1 M" k5 d& ~5 tof early sexual development. His mother noticed
; N: k: m4 ^* h4 m; e( b0 X2 Ylight colored pubic hair development when he was8 i; G& n0 {, l# R, @
From the 1Division of Pediatric Endocrinology, 2University of6 B" f+ j9 F* b( `1 Z- `9 m
South Alabama Medical Center, Mobile, Alabama.# f  q% Q0 J$ l( S% Q) P& B2 S4 m
Address correspondence to: Samar K. Bhowmick, MD, FACE,
2 G4 z1 c( b5 n) j8 R: S  |Professor of Pediatrics, University of South Alabama, College of0 k; z0 n7 n( K3 F/ r
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
& e3 B) j4 k7 N. l% r% Me-mail: [email protected].$ S& x$ V& {, h4 Q
about 6 to 7 months old, which progressively became$ C2 G5 s; Q* S2 V( r- z- [( D' y
darker. She was also concerned about the enlarge-
% y2 S- U# q+ C6 I! M* G8 Q. Cment of his penis and frequent erections. The child$ X6 _1 j0 V* y( @2 q
was the product of a full-term normal delivery, with* a1 [8 w  h) C3 g* F% I
a birth weight of 7 lb 14 oz, and birth length of
3 m% F+ \" d5 K- l20 inches. He was breast-fed throughout the first year" [  }6 Q  D2 h
of life and was still receiving breast milk along with
$ i' P4 _+ y7 ^9 C8 {solid food. He had no hospitalizations or surgery,; e; _( P% l3 g0 Y7 M
and his psychosocial and psychomotor development7 I; A  A+ D& `" l: B5 K1 G$ l( z1 p
was age appropriate.5 i2 r, {: F0 ?7 T& Z" v3 G
The family history was remarkable for the father,
$ W& \9 Z" e( K8 Owho was diagnosed with hypothyroidism at age 16,+ l2 V; s! \/ s0 z7 u6 Y( r4 ]- G3 k
which was treated with thyroxine. The father’s+ O0 I* O( A8 `- t) _% H; h; \
height was 6 feet, and he went through a somewhat; n  g1 v! w6 [- H
early puberty and had stopped growing by age 14.
) _4 C; V% `' |* w6 L4 y8 }8 C" t! HThe father denied taking any other medication. The
" ~' g- M" k* ~child’s mother was in good health. Her menarche' a$ J9 {/ {2 O" Y
was at 11 years of age, and her height was at 5 feet
& d3 @% e+ J9 D) M, t0 T5 inches. There was no other family history of pre-" J' F+ Z- _# }2 i, S
cocious sexual development in the first-degree rela-5 Z6 Q0 w1 Q  w3 F( {; J+ T
tives. There were no siblings.- e' \. |  J7 V
Physical Examination% E( O2 I' ?3 S, `/ Z
The physical examination revealed a very active,
) h) }- G3 }- o4 fplayful, and healthy boy. The vital signs documented
5 O1 d# x' t2 @! o( y+ b, @: Pa blood pressure of 85/50 mm Hg, his length was! h  t& O! t" A" s8 A
90 cm (>97th percentile), and his weight was 14.4 kg% V. ~9 c2 \" R$ Q
(also >97th percentile). The observed yearly growth( B; K1 Q0 B. L5 Y1 \
velocity was 30 cm (12 inches). The examination of* E4 A: X/ O( z
the neck revealed no thyroid enlargement." x8 c- X9 Z3 \$ p/ ]& s# `- n
The genitourinary examination was remarkable for2 Q8 v) C/ w" J. @$ L5 u
enlargement of the penis, with a stretched length of( C) Z  k: D1 z; A1 s! z4 j. U. J
8 cm and a width of 2 cm. The glans penis was very well4 M# y, D; D3 N: w3 t1 B
developed. The pubic hair was Tanner II, mostly around
. c7 V- W/ R) @& f6 c, P% x; s. g1 |540
3 F5 T4 l; V# O4 s* F. |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ h( o1 a2 \1 p% p
the base of the phallus and was dark and curled. The$ y( Z- z+ f- ^
testicular volume was prepubertal at 2 mL each.
& P; K2 `$ p9 r# iThe skin was moist and smooth and somewhat
# |$ ]2 N# T3 y. J% K4 n/ ]) Roily. No axillary hair was noted. There were no
. ]$ O: l& K5 K: P/ Labnormal skin pigmentations or café-au-lait spots.- v1 U) V+ {& {0 i# _( H& I2 n
Neurologic evaluation showed deep tendon reflex 2+; s3 N) Y+ s2 D& l3 z; t
bilateral and symmetrical. There was no suggestion6 e9 k5 G' i' E; M( V
of papilledema.+ x1 e5 Z! x" n( i: U+ \
Laboratory Evaluation
8 t0 }% [6 V% k# RThe bone age was consistent with 28 months by) Q" ^$ p- d* [& m" r( v( N1 ~
using the standard of Greulich and Pyle at a chrono-( Z3 l7 A1 K; ^1 B& s
logic age of 16 months (advanced).5 Chromosomal9 U6 ~5 E, [; x& M6 x
karyotype was 46XY. The thyroid function test+ d$ D* P+ X% i, g3 O
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
! T3 F1 {' @1 u# P1 }3 l( Ylating hormone level was 1.3 µIU/mL (both normal).1 P- _, i( Z. ]) M7 Q6 R
The concentrations of serum electrolytes, blood
* F- y% {- D4 ~6 uurea nitrogen, creatinine, and calcium all were
) J( `' B. n. a+ Iwithin normal range for his age. The concentration+ V" z, ?5 ^* \* P. z
of serum 17-hydroxyprogesterone was 16 ng/dL
& u3 ]! Y* v  o2 J: |/ u(normal, 3 to 90 ng/dL), androstenedione was 20
# c2 A$ N- x$ a; w5 Vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( @% H8 d( d; w1 I$ [( \
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
* {$ u& G& C. ]' d6 i# x3 L# cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
4 |1 L8 D. e. ?1 g; k$ {8 L49ng/dL), 11-desoxycortisol (specific compound S)* f* Q8 s5 n6 K& Q! `7 V. E
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
( z# I4 D, o( Q! K7 wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 A6 ?3 d' g' S( e& I2 ?5 Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),* u* J4 Q+ S3 |( |
and β-human chorionic gonadotropin was less than
" `" M4 i# y; s1 m! M3 n5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ Q# _( [1 X4 Q% \! ^* nstimulating hormone and leuteinizing hormone
0 B2 v. k7 Q  Q+ U: ?; Z, J% ?concentrations were less than 0.05 mIU/mL
7 J3 W5 ~% D; N(prepubertal).
1 K2 D4 N2 V# T( nThe parents were notified about the laboratory
# a; ?0 x6 H6 l! B7 _5 k) X3 i4 presults and were informed that all of the tests were  p3 |: c+ f% {- v( Q* J, V$ c5 Y
normal except the testosterone level was high. The2 {/ g5 T9 f9 i
follow-up visit was arranged within a few weeks to
. I+ J' O6 H$ ~& T  a3 jobtain testicular and abdominal sonograms; how-' X$ e8 ^* O) k: a* ^' E7 k& g4 O
ever, the family did not return for 4 months.- u2 S. B# F; f( ~% B
Physical examination at this time revealed that the
4 w3 H4 a' \) v9 i! l+ `6 |! m2 w9 Wchild had grown 2.5 cm in 4 months and had gained
. U; A" |+ o/ C* p9 N" J2 kg of weight. Physical examination remained7 E8 P( v8 n0 h, l  x9 q& r0 n( j
unchanged. Surprisingly, the pubic hair almost com-
# Z9 o3 f+ N5 i- i0 X  e: |pletely disappeared except for a few vellous hairs at
) a) F4 Z2 Q/ R% c5 @1 }4 _the base of the phallus. Testicular volume was still 24 b" D; s+ N4 b% I1 k
mL, and the size of the penis remained unchanged.
! R1 H$ u7 Q9 OThe mother also said that the boy was no longer hav-
, L  C/ @" U6 L+ ?9 k& Aing frequent erections.
5 e1 ?! Y/ `8 P& o9 {1 rBoth parents were again questioned about use of
* u5 C* ]8 k- X  n7 i1 _' Z- a4 Qany ointment/creams that they may have applied to; M& [& P# d& {& i5 i7 ~
the child’s skin. This time the father admitted the: l6 S5 q& _5 F  ^( U$ @1 K
Topical Testosterone Exposure / Bhowmick et al 5419 C7 B8 W# Q2 }1 H/ D: a! P
use of testosterone gel twice daily that he was apply-
  q, }9 B8 q0 E8 G# Y+ Ming over his own shoulders, chest, and back area for" U' w% w" f4 _' k, G; g2 O
a year. The father also revealed he was embarrassed4 I- g* m/ Z. j
to disclose that he was using a testosterone gel pre-
( A, c4 N! _8 o2 Pscribed by his family physician for decreased libido$ u# y6 x+ J% M! L* c
secondary to depression.
9 X( l/ D: `' M3 p& q6 BThe child slept in the same bed with parents.. \) H5 m# P1 S+ [5 o" K
The father would hug the baby and hold him on his
- T' n5 J% V  }8 F( u& X0 k3 Q! s9 Y. bchest for a considerable period of time, causing sig-
6 V4 Z/ j8 S' x6 W/ r/ Ynificant bare skin contact between baby and father.
, I9 F( z" ]3 K/ T. Q/ j* [% `The father also admitted that after the phone call,
$ [  e) X5 E9 k3 X; Wwhen he learned the testosterone level in the baby
+ m5 D- C7 }) F5 z# ^/ Nwas high, he then read the product information
6 u; [2 y4 B0 E( L& W0 Bpacket and concluded that it was most likely the rea-2 i7 h6 S' ]0 r
son for the child’s virilization. At that time, they2 T7 t, n. Z8 N* ]
decided to put the baby in a separate bed, and the
2 j7 D+ p. _  Mfather was not hugging him with bare skin and had
9 a; z% g$ z! L7 S  [) w# a. ybeen using protective clothing. A repeat testosterone
1 _4 ?0 V4 r0 k2 t. g. K/ {. ^test was ordered, but the family did not go to the; E1 ?' N3 o3 g* P& Z
laboratory to obtain the test.  _' V/ x* k& J
Discussion- B4 L! t) m/ r' K" [
Precocious puberty in boys is defined as secondary
: S) F! v( r) w4 Gsexual development before 9 years of age.1,4
; Z- U6 g1 Q( M) k( @4 NPrecocious puberty is termed as central (true) when0 T. C' Z! A. p
it is caused by the premature activation of hypo-0 o" T/ |" H( [' v4 L$ K: u
thalamic pituitary gonadal axis. CPP is more com-
# q% \0 _. ~) c. j. f0 K1 g5 Ymon in girls than in boys.1,3 Most boys with CPP
8 u" h& U, g. Q6 T& Q7 \may have a central nervous system lesion that is
9 T+ t; P2 c* [$ o' ?. aresponsible for the early activation of the hypothal-# e5 {7 [0 L& X
amic pituitary gonadal axis.1-3 Thus, greater empha-
9 G* F2 u: W, T; a8 ~sis has been given to neuroradiologic imaging in
: H3 b8 R2 @# w; \8 B% A, r7 \boys with precocious puberty. In addition to viril-
- A" X! g8 Y. r% X/ q( mization, the clinical hallmark of CPP is the symmet-$ r) U( j1 y+ p8 [  ?1 ]) X6 q! ]
rical testicular growth secondary to stimulation by9 S8 S8 m$ W! M
gonadotropins.1,3
, S5 N9 Y" o- F% y) {Gonadotropin-independent peripheral preco-
( O1 k" T1 L/ Y8 N( j, Dcious puberty in boys also results from inappropriate
: B' s0 x" t1 vandrogenic stimulation from either endogenous or* R$ y% M6 e# R' d" U0 F& p
exogenous sources, nonpituitary gonadotropin stim-; I% v8 [8 T/ i8 \! a2 U
ulation, and rare activating mutations.3 Virilizing: s# k8 _$ K! {2 X- t7 C. Y
congenital adrenal hyperplasia producing excessive( K3 Y2 q2 T2 N7 \( ^! l6 m# [7 a
adrenal androgens is a common cause of precocious
* \# [) n+ C5 }2 Jpuberty in boys.3,4
# P/ C# D# g; Z) x% D1 E' f7 KThe most common form of congenital adrenal" F& r/ S0 e0 r$ R8 F* p/ h3 b9 ^
hyperplasia is the 21-hydroxylase enzyme deficiency.6 e. A4 S  b; f( F& ~0 v- _
The 11-β hydroxylase deficiency may also result in7 u1 K& y' a3 d7 a
excessive adrenal androgen production, and rarely,& j# `2 i8 O  ~* o1 T' V4 c
an adrenal tumor may also cause adrenal androgen
9 P; m4 N8 F$ H) a# Q  C2 H. texcess.1,33 k$ U5 I% [* s! N% d; L& Z8 S
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( G  F( }" y% j5 B; u. k542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 O) i7 K! E: T6 l3 hA unique entity of male-limited gonadotropin-
# p& I  P7 n, K+ T2 Z- m/ V" {independent precocious puberty, which is also known9 A2 y5 }, |, m: s* ^5 D& o2 d
as testotoxicosis, may cause precocious puberty at a* o" \0 F4 H  Y" \* x
very young age. The physical findings in these boys( i$ Z' q/ D5 P' t
with this disorder are full pubertal development,
. b+ i1 J7 B! ]  a6 J1 |including bilateral testicular growth, similar to boys
9 F6 j  d, J' Y! awith CPP. The gonadotropin levels in this disorder
( u; \6 K) ~) ?5 A8 o; ?5 z  c2 q9 n/ tare suppressed to prepubertal levels and do not show; s5 L# R0 k: Y; U% t8 n" U$ E
pubertal response of gonadotropin after gonadotropin-# |) j' M/ W; x% _
releasing hormone stimulation. This is a sex-linked4 \' @3 p9 Z2 e  _5 b; Y3 k
autosomal dominant disorder that affects only
0 l* R' ]/ }* [8 V7 C" nmales; therefore, other male members of the family
9 P  Q4 t8 [$ K- F. [& t7 tmay have similar precocious puberty.36 K, C1 n* D/ B. Q- f
In our patient, physical examination was incon-
9 u3 ]+ P; C$ `4 k% Osistent with true precocious puberty since his testi-
7 M( f; q- I' o' y; W: c) scles were prepubertal in size. However, testotoxicosis6 S. N( m% a* m3 d/ }. Q
was in the differential diagnosis because his father
, _# c: W9 \. ~1 T( m" Nstarted puberty somewhat early, and occasionally,# a( `0 M. i: j& h
testicular enlargement is not that evident in the6 t$ j& P" a$ X( O/ m' ~7 j8 Q; R; ~- l' B
beginning of this process.1 In the absence of a neg-) m; n$ G& R/ d, J/ u/ G* Y0 S: J
ative initial history of androgen exposure, our
. B! q7 w1 p& W2 Obiggest concern was virilizing adrenal hyperplasia,
# Z# z  [5 z7 t0 G3 N: v1 f. ueither 21-hydroxylase deficiency or 11-β hydroxylase
9 k) ]  K9 T& i& I0 j, D7 ]* ?deficiency. Those diagnoses were excluded by find-: W/ n4 {  `! H+ ], h2 R5 L
ing the normal level of adrenal steroids.
, l! N( r) a$ U& r6 Z- mThe diagnosis of exogenous androgens was strongly. U* u) O: I' Z8 }
suspected in a follow-up visit after 4 months because4 U2 E! a, H/ B' a  u
the physical examination revealed the complete disap-/ j( J5 C5 F$ t7 p( ~0 W$ m- e" L
pearance of pubic hair, normal growth velocity, and- r: z: ~. I9 O% w# d
decreased erections. The father admitted using a testos-0 {8 j! Q8 {( q
terone gel, which he concealed at first visit. He was
& t: s- N* H) x2 v$ n  i5 tusing it rather frequently, twice a day. The Physicians’: H, S7 M/ h" q  ]) @8 |3 f( G7 E
Desk Reference, or package insert of this product, gel or0 R' C5 m) x8 z1 e5 i! C' P0 |/ z0 L
cream, cautions about dermal testosterone transfer to
5 W+ O( f+ X; S3 junprotected females through direct skin exposure.5 B0 T9 X9 N+ U( `" [4 m( t3 L
Serum testosterone level was found to be 2 times the
- R% i6 a6 d% ^baseline value in those females who were exposed to5 |: c4 K7 W! U6 R0 @8 D
even 15 minutes of direct skin contact with their male% ^5 J/ }% ?: H$ R9 ]/ a
partners.6 However, when a shirt covered the applica-+ L7 i+ q: B' q0 c& f
tion site, this testosterone transfer was prevented.5 c  `; I# d9 p# G: h1 b; v
Our patient’s testosterone level was 60 ng/mL,* _+ z5 N) U/ y$ o
which was clearly high. Some studies suggest that8 L1 L4 z& a; A1 S, F  F. i
dermal conversion of testosterone to dihydrotestos-/ v3 }% t3 _9 V3 J- V
terone, which is a more potent metabolite, is more; e7 e: S4 [+ z
active in young children exposed to testosterone
, `5 ]4 F: m5 F. ?4 m  Vexogenously7; however, we did not measure a dihy-
& H( l! G+ H3 r/ o, Z$ ?! n' udrotestosterone level in our patient. In addition to
0 V) S, l* V. avirilization, exposure to exogenous testosterone in
# V( B' \; f9 m5 u4 bchildren results in an increase in growth velocity and
  ~3 H" a; F6 g; T+ j, e$ I7 k3 Padvanced bone age, as seen in our patient., F' S, ]( O! m  c
The long-term effect of androgen exposure during- s/ i& h  o+ `2 _$ Q
early childhood on pubertal development and final$ m! W1 ~2 `1 j: Y+ |) O8 N& v4 w
adult height are not fully known and always remain
  J3 p* ?7 j7 [3 R1 L, [( j$ Ya concern. Children treated with short-term testos-% {$ j$ i9 Z* |: p. K; v  \8 I
terone injection or topical androgen may exhibit some3 Y! z& X/ H% R
acceleration of the skeletal maturation; however, after
$ [& f9 Z  Q- _cessation of treatment, the rate of bone maturation
7 [& S: _3 J! J1 adecelerates and gradually returns to normal.8,9
6 R/ G2 v8 i6 V1 H" [  mThere are conflicting reports and controversy
! u/ f6 P4 o- G6 e1 ~( Dover the effect of early androgen exposure on adult
9 _* ?* P! F4 l: y3 cpenile length.10,11 Some reports suggest subnormal
/ n, Q( @& T) G# i" R3 Wadult penile length, apparently because of downreg-
% S& U" L% m: L3 i8 H# r6 ^' Iulation of androgen receptor number.10,12 However,- g& C' ^! k. n( ^0 r
Sutherland et al13 did not find a correlation between
2 C# q% P) `3 |: E2 h& Qchildhood testosterone exposure and reduced adult# T4 s2 r+ K. q  Z: S
penile length in clinical studies.& |' i: K7 G* u2 G, h& _# i
Nonetheless, we do not believe our patient is
" T# \0 X6 U5 Q8 I- |8 c* Egoing to experience any of the untoward effects from
9 I5 t4 V; b2 l3 Atestosterone exposure as mentioned earlier because
5 u  |6 z* o8 w) ^2 `8 Cthe exposure was not for a prolonged period of time.
# p7 b1 [4 T6 I# v" z. V5 XAlthough the bone age was advanced at the time of
. E( \; ^4 t2 ndiagnosis, the child had a normal growth velocity at1 J, t7 c+ D  o4 D* d% O0 w
the follow-up visit. It is hoped that his final adult
3 J+ P2 R6 g+ ^height will not be affected.
) b2 N% f! {* W8 o. H' Y; @4 MAlthough rarely reported, the widespread avail-
1 N- {+ V$ n! r8 C0 [( Oability of androgen products in our society may
& _2 J. k# Y- Q0 _; Iindeed cause more virilization in male or female+ H- Z4 |6 u2 f& [$ R7 z
children than one would realize. Exposure to andro-: _9 Y& W. o% B$ m
gen products must be considered and specific ques-
" Q0 B! W6 s, ]9 gtioning about the use of a testosterone product or
4 v7 H) m3 K3 j5 V, o4 E" o2 @gel should be asked of the family members during9 {$ j" w- t  ~% H
the evaluation of any children who present with vir-
; s' o% Q2 H. g9 x6 H, r1 {* Zilization or peripheral precocious puberty. The diag-* K7 Z9 R. m; O& t4 X
nosis can be established by just a few tests and by0 J6 n7 ]' P$ w2 v* W1 G, Y9 w5 r
appropriate history. The inability to obtain such a. H  D9 O. _# G( S1 x% R0 k
history, or failure to ask the specific questions, may4 Q5 C; p' E) l3 t
result in extensive, unnecessary, and expensive9 t2 T* S* M# k; m+ a9 \* U
investigation. The primary care physician should be  j/ v; k9 Q) a/ v/ e8 R
aware of this fact, because most of these children
% I: S3 i9 L' h# Pmay initially present in their practice. The Physicians’
  n4 k# Y" g% d; H3 w6 _Desk Reference and package insert should also put a
" K9 _2 J& d1 i% k+ A9 zwarning about the virilizing effect on a male or0 d' w/ w+ y" j$ @+ N* T& }, U( ]% g  p
female child who might come in contact with some-8 u& H8 L% Y1 k" W& l; f
one using any of these products.
7 y, b- B( c# U/ C! v7 Q  [4 L6 cReferences
' U  w# A; l& n9 }( u  g" j1. Styne DM. The testes: disorder of sexual differentiation
  z# C* v& y4 r. z; _and puberty in the male. In: Sperling MA, ed. Pediatric/ {, q; g" S% Q+ T1 S
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 l2 }$ G. F- m: j; f. \2002: 565-628.
5 H% b. F$ t1 P0 f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& B4 P9 @! I# b& mpuberty 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

% W4 g. f* X" f- Q# m+ l  L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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