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Sexual Precocity in a 16-Month-Old( P3 U, V: D( U$ {
Boy Induced by Indirect Topical
; @  s! ^, ~: KExposure to Testosterone
3 n% A* J2 D  v) o% y6 O& ySamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' R: n# t* y- l+ ~: A7 X
and Kenneth R. Rettig, MD1. d6 ]' ~0 A0 _5 ?1 {; I& Q& f
Clinical Pediatrics
2 R' B" Z- u1 _2 @+ y8 eVolume 46 Number 6
5 V* j) `5 g+ O3 c* s" ^# ]3 |July 2007 540-543
4 b# b, ~9 O: [4 r© 2007 Sage Publications6 z& w) e- ^3 X! Z, D! w# \
10.1177/0009922806296651
$ z0 D  Y, L# Q) i% A# Chttp://clp.sagepub.com
3 m$ h7 c# |8 b, W% C, B; ~hosted at
/ U  T. W% l7 O+ khttp://online.sagepub.com
; B# H: O; P: {Precocious puberty in boys, central or peripheral,; j  i" j' s7 ?8 m: v+ s4 S5 g
is a significant concern for physicians. Central5 R4 m( ~/ J5 a
precocious puberty (CPP), which is mediated
7 [' s( n+ H" `! U* tthrough the hypothalamic pituitary gonadal axis, has
' G# l/ Y; |6 ra higher incidence of organic central nervous system1 j( q" ~7 d" x) M* K5 x/ [
lesions in boys.1,2 Virilization in boys, as manifested, o! O$ Z. ^' Z8 @7 F+ G, O
by enlargement of the penis, development of pubic
7 _8 x: ~  _# k/ N, u1 Ihair, and facial acne without enlargement of testi-3 l: n+ C  `- V# U) n" J" H" U8 r
cles, suggests peripheral or pseudopuberty.1-3 We
4 {) c8 K- O% p! D" greport a 16-month-old boy who presented with the
; G- ]+ U; j. Y7 u0 `" {enlargement of the phallus and pubic hair develop-
) F/ `# w0 C5 ~, Mment without testicular enlargement, which was due
1 k! z1 s; b6 L: g0 S: F" dto the unintentional exposure to androgen gel used by
: R6 C7 M! n, i3 mthe father. The family initially concealed this infor-' s) d3 t/ R; g5 T9 D6 @% z3 e8 ]: ~
mation, resulting in an extensive work-up for this
0 q) B* W. u7 u" Xchild. Given the widespread and easy availability of
" k2 m1 ?! x/ q1 y& G# c$ b. Ftestosterone gel and cream, we believe this is proba-+ j8 I& z! x* h: U/ _. |; e
bly more common than the rare case report in the+ l1 t% c% z+ E2 K5 ]# j
literature.4
! C9 ]4 g" B1 x3 kPatient Report
7 V4 e1 m& Q; X7 n* }; p) t& V9 d7 sA 16-month-old white child was referred to the
; K& S0 o' I7 n" J2 zendocrine clinic by his pediatrician with the concern' {* R) L0 h) q8 F" n+ T
of early sexual development. His mother noticed
& e3 |% Z2 ?; r7 P; o  f1 ]; Llight colored pubic hair development when he was0 m: F5 C0 g; H0 v# c6 a
From the 1Division of Pediatric Endocrinology, 2University of
3 T/ }+ |9 S8 b9 s3 ^South Alabama Medical Center, Mobile, Alabama.
0 z" e* V1 ^# `% O. R" YAddress correspondence to: Samar K. Bhowmick, MD, FACE,
2 m; A9 j" x% {1 Q; i: p; h5 W$ UProfessor of Pediatrics, University of South Alabama, College of
# V2 i( I: D0 M  Z7 U& VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; |7 [0 ?3 j+ t+ A2 ]
e-mail: [email protected].# U( f; V- P/ @% X, g9 J
about 6 to 7 months old, which progressively became/ A/ B& J9 c9 K- g
darker. She was also concerned about the enlarge-) E4 Y3 E# A9 G+ O
ment of his penis and frequent erections. The child" U: @/ j  Z6 u1 d3 r9 n+ p
was the product of a full-term normal delivery, with( {1 p" P9 i) j# [" f) A
a birth weight of 7 lb 14 oz, and birth length of
& B: [! e1 P& f: V8 c  {4 w20 inches. He was breast-fed throughout the first year
/ o4 Z- @1 u/ s' Dof life and was still receiving breast milk along with
- H- |+ M4 \% t( Z+ _( w' C2 Isolid food. He had no hospitalizations or surgery,
( X( P2 U5 h' i* g6 k1 Dand his psychosocial and psychomotor development
7 v4 r; {' G- wwas age appropriate.2 B' r0 d# T9 A) ~/ G+ [* n
The family history was remarkable for the father,
- A+ p  V1 r+ Y- p9 K( U+ ], u6 ?who was diagnosed with hypothyroidism at age 16,$ h4 W" J6 w4 q1 p2 N
which was treated with thyroxine. The father’s$ V0 h* Z- g' I7 \) j
height was 6 feet, and he went through a somewhat
, {/ g  b* J+ s) S# Z0 I$ Eearly puberty and had stopped growing by age 14.
* u  j7 Z5 G+ p. cThe father denied taking any other medication. The+ W, D) O, w; O' e
child’s mother was in good health. Her menarche* p- r/ ~' `- d# z* ~
was at 11 years of age, and her height was at 5 feet+ N: Y$ Z, s6 z+ G
5 inches. There was no other family history of pre-% X! E' ~2 C2 T2 g8 k
cocious sexual development in the first-degree rela-  j( s' C, k2 E. q1 H; s7 C4 @
tives. There were no siblings.
# S5 T8 F4 X$ i, H- cPhysical Examination8 O& U( u3 {" M" A/ z$ o1 e  L4 b& f/ i
The physical examination revealed a very active,
2 y5 n' u) `+ N7 F7 Oplayful, and healthy boy. The vital signs documented
+ F2 C+ ]" S2 `5 z+ qa blood pressure of 85/50 mm Hg, his length was7 @, ?/ m3 _8 v+ g
90 cm (>97th percentile), and his weight was 14.4 kg
& n/ H0 w* |1 k0 J! F(also >97th percentile). The observed yearly growth
' ~- t: U3 B+ b7 x/ bvelocity was 30 cm (12 inches). The examination of& _9 m$ F& Q; A0 q' f
the neck revealed no thyroid enlargement.
& l4 T; \% N, }' g9 q- FThe genitourinary examination was remarkable for
9 z1 x) t4 x& L1 b6 lenlargement of the penis, with a stretched length of$ [: |. F" r# g
8 cm and a width of 2 cm. The glans penis was very well
8 m& l( B* c7 fdeveloped. The pubic hair was Tanner II, mostly around' f5 O8 n+ X6 C$ m7 T: x1 _
540
7 x- F$ N; f" _2 \& L. \: cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  _2 I1 g4 V5 ]
the base of the phallus and was dark and curled. The
' K0 R- d& J8 J( J! P. j9 etesticular volume was prepubertal at 2 mL each.
* ?5 U. q0 P* U2 o- B% aThe skin was moist and smooth and somewhat: X  B/ I. e0 A( e) \) a
oily. No axillary hair was noted. There were no; F9 Z1 K3 ~7 \( B" l1 x! J, v
abnormal skin pigmentations or café-au-lait spots.
+ O6 E! [( g2 ZNeurologic evaluation showed deep tendon reflex 2+" P0 O, _. y9 i; s
bilateral and symmetrical. There was no suggestion
5 J3 [; w# j3 yof papilledema.
8 D4 k1 B/ \1 F( U( E' RLaboratory Evaluation
3 }0 z  h$ p" Z& Y$ Y9 I6 Y( SThe bone age was consistent with 28 months by
6 o6 ^% h4 R4 I/ e) \/ \using the standard of Greulich and Pyle at a chrono-
# f4 ^' e1 I' O/ V+ n) Alogic age of 16 months (advanced).5 Chromosomal4 V" V- v4 D, @" \% W# h% S
karyotype was 46XY. The thyroid function test
+ f, {6 x1 P/ r7 q, k2 fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-& L" ^" w1 I8 ~8 b$ L' A8 w
lating hormone level was 1.3 µIU/mL (both normal).
8 x  r9 C! V5 R5 @0 \7 xThe concentrations of serum electrolytes, blood% Q  |8 z& q7 U5 p5 f' V1 m
urea nitrogen, creatinine, and calcium all were* d4 i! g( l% \/ [
within normal range for his age. The concentration3 F! u- O2 y3 ~* _" d
of serum 17-hydroxyprogesterone was 16 ng/dL
# u. F1 |4 T4 M' Z( H+ b(normal, 3 to 90 ng/dL), androstenedione was 20
) f! F9 A  M6 C, D. k1 ?9 }5 B- Nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; l8 B) @9 q. X2 \8 n( [
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 s; ]. h9 i. }5 M  odesoxycorticosterone was 4.3 ng/dL (normal, 7 to) r& }! b1 A9 O$ D0 O0 ?
49ng/dL), 11-desoxycortisol (specific compound S)/ q* u: h8 E  U( Y0 `  {5 R
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# I( _6 [. U7 |9 `
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* N: s; X3 w% u) n  D
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),2 w8 M- L" {' {+ i5 I
and β-human chorionic gonadotropin was less than1 g/ I: t' |. C+ g/ x
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  J6 P0 o) O" V8 ?& T1 g$ ]% K8 Dstimulating hormone and leuteinizing hormone0 p8 z2 P! U5 \" b: Q: m8 G! C
concentrations were less than 0.05 mIU/mL
, b# ~  o6 q' p  r8 L9 B8 z(prepubertal).
7 L# ?, `2 p, H9 D* o% U6 g, f( mThe parents were notified about the laboratory
( {4 \$ e. h1 j3 H5 b. oresults and were informed that all of the tests were
1 k" ]6 y' o' X# Tnormal except the testosterone level was high. The( }. `4 ~- ]+ _! P% B: O( _2 J( ?
follow-up visit was arranged within a few weeks to7 l8 U7 y+ c$ {
obtain testicular and abdominal sonograms; how-
1 K4 r2 ]* Q" gever, the family did not return for 4 months.
/ f  m6 }) k6 A- a' BPhysical examination at this time revealed that the! y7 X0 j# [: ?# m
child had grown 2.5 cm in 4 months and had gained
7 s$ X5 A. Z1 ?' w% Y& N: l2 kg of weight. Physical examination remained
3 S& b7 u9 ~. j* L! ~0 h0 z" ]% Tunchanged. Surprisingly, the pubic hair almost com-- M* ~, S% R$ \6 [* c
pletely disappeared except for a few vellous hairs at
, L, y8 ]" ]2 U+ [2 Z6 w3 fthe base of the phallus. Testicular volume was still 21 F( R- @! O3 o( ]' p8 t
mL, and the size of the penis remained unchanged.
3 {6 c1 h8 G2 l  WThe mother also said that the boy was no longer hav-
. w1 L6 e+ g. H% h% g2 w5 ying frequent erections.
; f+ N3 E+ t0 T7 s4 H$ n  yBoth parents were again questioned about use of) x+ w% d+ r0 r# H: S' G4 f
any ointment/creams that they may have applied to
/ U$ a7 y8 @3 W2 h2 Uthe child’s skin. This time the father admitted the2 j( y1 i) q, M3 I# q
Topical Testosterone Exposure / Bhowmick et al 541( b9 I; M- Z+ U7 h
use of testosterone gel twice daily that he was apply-8 b  h; `) w6 J9 k( u) R8 f
ing over his own shoulders, chest, and back area for
5 g# ?/ s! t2 v8 Ga year. The father also revealed he was embarrassed* K' @+ N& @3 g
to disclose that he was using a testosterone gel pre-0 I& a" R9 L6 b* y0 L, Q- k
scribed by his family physician for decreased libido
0 ?+ Z. Z5 M+ w6 R" }secondary to depression.
. Z6 t- o* y1 }9 z6 p1 EThe child slept in the same bed with parents.$ `8 {* i5 n2 `3 U
The father would hug the baby and hold him on his
4 l, y/ L2 c! _  _chest for a considerable period of time, causing sig-# O$ B8 A5 I2 V  h
nificant bare skin contact between baby and father.
1 R0 P# y6 A0 b, F- mThe father also admitted that after the phone call,
$ t' R# L/ D- v0 N* f/ ^7 |. xwhen he learned the testosterone level in the baby
3 j% z3 A1 V2 ?; [was high, he then read the product information9 o1 f' P$ [1 l
packet and concluded that it was most likely the rea-2 w1 |! V7 O0 i, E
son for the child’s virilization. At that time, they- n$ M5 Y; \- o
decided to put the baby in a separate bed, and the' O# P9 q1 h- X! H+ h9 V/ O& R
father was not hugging him with bare skin and had
  {2 I1 P& u! {+ z$ zbeen using protective clothing. A repeat testosterone
5 z- W9 O3 A0 itest was ordered, but the family did not go to the+ \( {6 d! N- J- h# x) Q& z; f
laboratory to obtain the test.
# ^( H2 M9 q; D: P& s/ ~Discussion8 I7 c4 e1 e$ G
Precocious puberty in boys is defined as secondary- ^& ^) B3 D1 O% M
sexual development before 9 years of age.1,4
6 q' d0 E+ @' [' N* ?! fPrecocious puberty is termed as central (true) when3 t$ r5 D4 }! K0 E+ o  ]& g
it is caused by the premature activation of hypo-
! i  m! ~& P, X+ P* Q7 Tthalamic pituitary gonadal axis. CPP is more com-" }: j3 r2 L4 H: o. L
mon in girls than in boys.1,3 Most boys with CPP
& V1 I3 i. D) z4 }% I! b, |% n/ O. Rmay have a central nervous system lesion that is
( _2 P, ?, B  Y- S4 V/ xresponsible for the early activation of the hypothal-7 k1 f; I( k4 t) b2 f  _
amic pituitary gonadal axis.1-3 Thus, greater empha-6 z( \0 ]; L' H. I
sis has been given to neuroradiologic imaging in4 Y5 Y5 W; i7 `
boys with precocious puberty. In addition to viril-
+ y: P+ b5 b: ]- S! N: zization, the clinical hallmark of CPP is the symmet-: L* D6 w8 |" {; d" J% k+ g
rical testicular growth secondary to stimulation by  ]4 E& t, l9 i6 W
gonadotropins.1,3( g7 m8 E% J* G% v7 X2 A
Gonadotropin-independent peripheral preco-
# {. P3 g6 d$ X2 A+ J1 R) zcious puberty in boys also results from inappropriate2 [. G: x0 Z8 J6 q
androgenic stimulation from either endogenous or+ U1 d# C( C6 p1 r, F4 ~6 M
exogenous sources, nonpituitary gonadotropin stim-( b1 H. K& w3 _! I% u+ o5 [! o
ulation, and rare activating mutations.3 Virilizing6 \7 m7 R3 E7 L" S  D9 W
congenital adrenal hyperplasia producing excessive( J  W* [; q/ l# c! K0 c+ E3 T
adrenal androgens is a common cause of precocious0 U5 G% p. T7 x) s  b( }; S
puberty in boys.3,4. q3 i9 S0 c. f# g, [4 s0 j; W
The most common form of congenital adrenal" w& \) s* u( y: b+ @# w. j
hyperplasia is the 21-hydroxylase enzyme deficiency.# U# j4 O& M6 m7 L. f
The 11-β hydroxylase deficiency may also result in4 E  j1 F  D* E0 a
excessive adrenal androgen production, and rarely,7 O3 a# M, k1 \8 P
an adrenal tumor may also cause adrenal androgen
. A  A: f/ U5 @excess.1,3
& ~. E' D/ z" u& }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 W" Q9 }7 y: _* s2 _3 k+ b
542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 U9 r  y$ J/ t( ^+ J
A unique entity of male-limited gonadotropin-8 P8 W7 Q% [- s) k5 y0 m4 M
independent precocious puberty, which is also known# S; ?% z  m" g) Z1 |; h8 `
as testotoxicosis, may cause precocious puberty at a4 F# g; k; F6 e% e# ^
very young age. The physical findings in these boys
* T) ]( X8 p) g. Y! \with this disorder are full pubertal development,
- H! @# c9 a1 L9 B+ f, {including bilateral testicular growth, similar to boys& z) v+ ]0 @8 R
with CPP. The gonadotropin levels in this disorder( i0 n  l5 H9 I) y
are suppressed to prepubertal levels and do not show
0 `! b7 _% Q7 u9 I2 n( g6 Upubertal response of gonadotropin after gonadotropin-' t% }& A2 B% h  N9 H$ P' u
releasing hormone stimulation. This is a sex-linked- r* A% k/ }$ Z3 D0 K3 ~2 u/ V. U
autosomal dominant disorder that affects only; f2 l9 }8 \/ I7 _0 m
males; therefore, other male members of the family2 Z+ L" ]4 K8 z5 b
may have similar precocious puberty.3" u: I0 {7 K7 b! Q$ n' V" `( w
In our patient, physical examination was incon-7 G2 N, r! n( l6 o$ a
sistent with true precocious puberty since his testi-9 N, J' Q* n4 M& F0 j0 a6 @/ [
cles were prepubertal in size. However, testotoxicosis
& e' N7 v' s$ }& W* ~! ewas in the differential diagnosis because his father
' ^7 t6 J& C4 n* E2 B" mstarted puberty somewhat early, and occasionally,. e0 N% I" s4 {! I8 |" n/ N$ V
testicular enlargement is not that evident in the7 o( S; }, D# G6 N
beginning of this process.1 In the absence of a neg-# r, C7 _; k" _
ative initial history of androgen exposure, our
! s/ A3 K4 H, t- @6 Pbiggest concern was virilizing adrenal hyperplasia,+ @& c& A) Q: ~3 f" Q
either 21-hydroxylase deficiency or 11-β hydroxylase
$ B- ?4 h% @3 N; p, w  edeficiency. Those diagnoses were excluded by find-
8 Y- T; S' M4 f, d" ding the normal level of adrenal steroids.; a; R1 \/ j- N. b
The diagnosis of exogenous androgens was strongly( U: V' e1 M" v9 V# Y& ^+ t
suspected in a follow-up visit after 4 months because0 K$ H4 O+ ~9 k! x, K8 H' O: b
the physical examination revealed the complete disap-
8 b9 I# H8 \5 u1 `1 V- hpearance of pubic hair, normal growth velocity, and  R& w9 x. P. y; s3 u6 }6 W- s8 ]7 E
decreased erections. The father admitted using a testos-# ~# q* Z  t, i7 F2 k. t
terone gel, which he concealed at first visit. He was
( h6 Y* y+ m) E1 `( ]2 \using it rather frequently, twice a day. The Physicians’
& S) z& d: `5 w# f8 h4 F. |/ N, m' \Desk Reference, or package insert of this product, gel or2 T7 F1 q' M! ]7 ~/ `/ M6 ]( d
cream, cautions about dermal testosterone transfer to5 b- r# d" m7 |9 z* {
unprotected females through direct skin exposure.1 Z4 E! t7 V& t0 W) u
Serum testosterone level was found to be 2 times the- h  m4 H  o; J7 f1 c; e2 o
baseline value in those females who were exposed to; |! }2 A: m. \* ^" D
even 15 minutes of direct skin contact with their male
: H: l! ~4 j, X: fpartners.6 However, when a shirt covered the applica-
/ d1 l. c' a* V$ `9 Otion site, this testosterone transfer was prevented.
% k' k  [6 n( S1 t' @& q4 NOur patient’s testosterone level was 60 ng/mL,
4 Z) M2 ^1 [- O- {0 Hwhich was clearly high. Some studies suggest that
) p( z* D: p: I8 f" j* `dermal conversion of testosterone to dihydrotestos-
, d2 _& a9 t  Aterone, which is a more potent metabolite, is more! Q4 A, i! Y1 U
active in young children exposed to testosterone
( [! K% t6 [- X8 T. ]5 W  sexogenously7; however, we did not measure a dihy-) [2 D: Z9 F# v! M' T% u
drotestosterone level in our patient. In addition to0 G) {1 ~  L# |! e, @! m
virilization, exposure to exogenous testosterone in' s  x) q0 D1 h8 W5 {
children results in an increase in growth velocity and0 |+ E* ^/ E* U5 E
advanced bone age, as seen in our patient.1 l( R) W; n! Z. e5 a' |+ H
The long-term effect of androgen exposure during
+ `. C+ R0 H% s% w( O) Cearly childhood on pubertal development and final
5 g. @2 P# q; N: R. _adult height are not fully known and always remain5 u8 K  k" l* y
a concern. Children treated with short-term testos-
' s* `7 F) [1 w) A. Y/ f7 Iterone injection or topical androgen may exhibit some9 E) t2 _7 ]) ]9 P
acceleration of the skeletal maturation; however, after  E; a" |) z+ V  M6 s2 z
cessation of treatment, the rate of bone maturation
8 q: s0 u/ Y* Z0 b( u" qdecelerates and gradually returns to normal.8,9
* i' T/ o, ^3 e/ j; vThere are conflicting reports and controversy: a( q2 M7 L) ~7 J5 z& j  S( h
over the effect of early androgen exposure on adult
0 H3 w$ N/ }0 n6 {1 dpenile length.10,11 Some reports suggest subnormal
. j& r/ _( r# H0 Q$ ^adult penile length, apparently because of downreg-
, g0 S2 j9 Z, J0 O$ S7 Y3 j* o, hulation of androgen receptor number.10,12 However,
3 z9 y3 m# l3 J$ pSutherland et al13 did not find a correlation between
$ e' v: v8 A, t, f* N% qchildhood testosterone exposure and reduced adult
, n( f  |, I" w  {; Gpenile length in clinical studies.
) [9 @3 y5 g" F) H7 `, ]! @6 g  l! YNonetheless, we do not believe our patient is
$ u3 h: d& r0 y" l7 _5 {- }5 Fgoing to experience any of the untoward effects from
+ h6 v% z' x# }; z' M8 P( l1 n! Vtestosterone exposure as mentioned earlier because" B! x! r1 l7 K2 \( K  z: b2 k8 ~
the exposure was not for a prolonged period of time.
; W" m( u3 {  t6 `; W2 }  L2 LAlthough the bone age was advanced at the time of
7 ]* y5 X0 q+ q( A. ^4 v( Ndiagnosis, the child had a normal growth velocity at
( e5 p/ i$ u7 [. hthe follow-up visit. It is hoped that his final adult: h' U+ e- L% T+ X$ r9 r0 _* g
height will not be affected.4 n1 }7 g6 i. W+ c: ^) ^
Although rarely reported, the widespread avail-
: H: e! u) L5 W' T8 X2 }1 Aability of androgen products in our society may* O# Y2 c% D! T' t/ c* f
indeed cause more virilization in male or female: G1 f* R8 L( K+ ?* ~  ?4 b$ |
children than one would realize. Exposure to andro-( g! T$ ?+ m; o$ D
gen products must be considered and specific ques-' v: W3 H6 y! C, ^- S6 n
tioning about the use of a testosterone product or/ b. }* u- P  C: L
gel should be asked of the family members during) D; c5 l5 y: A; Q, D, j8 v8 O
the evaluation of any children who present with vir-
5 M: ^! o, j7 eilization or peripheral precocious puberty. The diag-
/ C2 k8 t1 j5 O4 h: q; j. W3 \nosis can be established by just a few tests and by
  N* z  @$ d# L4 w* V7 Happropriate history. The inability to obtain such a
, ~. k* s* N# Zhistory, or failure to ask the specific questions, may
6 @' z0 f# [& Lresult in extensive, unnecessary, and expensive: g1 n. @' \6 W* R
investigation. The primary care physician should be+ u2 ]; l7 `8 u7 M% i
aware of this fact, because most of these children' m7 b5 w6 b! O5 V; N) V+ b
may initially present in their practice. The Physicians’
/ d6 R& w- c9 Q% o2 ]4 m% kDesk Reference and package insert should also put a
) P& M! I8 c2 c, w; l% h' w8 i: U9 Cwarning about the virilizing effect on a male or0 B9 _. C$ q# a8 w7 U2 l
female child who might come in contact with some-/ r* ?* m7 L& e' R4 i1 r
one using any of these products.1 V- i, p+ }$ b% C4 V
References9 o- O  L' m. _. m) e& U& b
1. Styne DM. The testes: disorder of sexual differentiation
7 Z! M4 s' `8 D" l( ^; P7 tand puberty in the male. In: Sperling MA, ed. Pediatric. t$ \* ^1 u. w1 A3 Y. w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;6 |' _2 j- Q1 l0 l6 M5 J  V  K; i
2002: 565-628.( J# s6 d( e+ \% `3 ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% g3 C  U0 S) K3 B7 u9 g: |
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old) b' U( @6 B( c1 P
Boy Induced by Indirect Topical
3 k- d. p. X9 J" j+ [% U; vExposure to Testosterone
+ n0 k* ~4 N' E( k4 ZSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2: Q- c& n) P" K. N
and Kenneth R. Rettig, MD1/ f, v$ s0 s( P3 Y
Clinical Pediatrics
) M; w3 b$ |0 a/ _& wVolume 46 Number 6
# s: M. {$ e; I7 f+ V# Z' U5 D0 XJuly 2007 540-543" Z; `1 c/ ^3 P) [
© 2007 Sage Publications
% _2 l  g" w1 e9 o10.1177/0009922806296651
: V, x* B% M: P7 j' w' f) ~http://clp.sagepub.com
. z9 s+ B( u! i8 d$ whosted at2 P: T$ h+ a5 ^( m% f: I
http://online.sagepub.com
: f4 t) h  z* F: ?Precocious puberty in boys, central or peripheral,
7 `3 ]- O5 c& d* O3 E8 F5 ~is a significant concern for physicians. Central) G% n1 m6 u6 E$ K, F
precocious puberty (CPP), which is mediated: B; j' l, Y, q8 K: ?
through the hypothalamic pituitary gonadal axis, has
. c6 h; R) P7 T- Q* }a higher incidence of organic central nervous system$ G% _8 T5 J) A1 v1 n6 d
lesions in boys.1,2 Virilization in boys, as manifested
, U3 \: Q% ]" f. ^' w7 [by enlargement of the penis, development of pubic; E9 A/ d2 O; ?5 _# E5 s5 Q6 F4 r
hair, and facial acne without enlargement of testi-
! y* N# N6 q! a) icles, suggests peripheral or pseudopuberty.1-3 We
5 z8 K8 }1 \' e" G; ]6 M2 Z0 `/ Zreport a 16-month-old boy who presented with the
2 Y" D, d) ]6 _1 k' Henlargement of the phallus and pubic hair develop-" ?$ W9 W8 s2 e
ment without testicular enlargement, which was due8 t; W. p- ?# k- M4 r! n# h
to the unintentional exposure to androgen gel used by
0 u, c: V2 ~! `* B$ H# Lthe father. The family initially concealed this infor-5 J9 V. N1 X3 l) m. e! J2 H
mation, resulting in an extensive work-up for this& L% V( ~% u% b4 A  s& g& D
child. Given the widespread and easy availability of+ }% l, L  k6 s& f  P% ~
testosterone gel and cream, we believe this is proba-
% N- |# u& M$ Z9 G, {. j5 hbly more common than the rare case report in the
7 N" i+ Y, U, K7 ^+ v0 Tliterature.4
3 h+ f6 u! h; }$ M- Q1 m1 k( ZPatient Report
- Z1 F* o- J0 y# ^8 sA 16-month-old white child was referred to the
" {4 @; \2 A" x( g3 m# \endocrine clinic by his pediatrician with the concern
2 c+ a& R6 l8 u4 k3 qof early sexual development. His mother noticed2 D" ^! V: K* y. [8 p
light colored pubic hair development when he was
) y: Z! c% V# L! ?From the 1Division of Pediatric Endocrinology, 2University of
! ^7 j# @" E$ D4 ESouth Alabama Medical Center, Mobile, Alabama.
$ S4 x8 x, M0 m! k* Q: h. uAddress correspondence to: Samar K. Bhowmick, MD, FACE,0 D: a% @! [0 v: F9 w$ J2 q6 Z
Professor of Pediatrics, University of South Alabama, College of. q  t8 _6 K) V
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) y7 |- _9 h# e( ~* P" He-mail: [email protected].7 h8 z; N/ |" I. P6 _1 m* E
about 6 to 7 months old, which progressively became
& a7 q$ X. x; H4 _darker. She was also concerned about the enlarge-
" F! [8 N4 J3 t+ B9 Bment of his penis and frequent erections. The child
" g$ V" N/ J# @, S: z5 W5 {- m& I& xwas the product of a full-term normal delivery, with
8 |! f; T" @1 ]+ Ha birth weight of 7 lb 14 oz, and birth length of3 z" B$ B0 n& M7 J. H
20 inches. He was breast-fed throughout the first year0 ~! n% V. t% z
of life and was still receiving breast milk along with7 Z6 [' Q7 e' D$ \+ R$ s) R/ {
solid food. He had no hospitalizations or surgery,
& s. T* l/ E: `( h6 ~and his psychosocial and psychomotor development7 Z  d; M5 A3 [4 w
was age appropriate.+ m! |+ B; U& G& e; [& l
The family history was remarkable for the father,5 j  U( p) [" p+ `
who was diagnosed with hypothyroidism at age 16,1 n8 k: i0 _# S& m+ o4 b; ~
which was treated with thyroxine. The father’s: G9 J% ?0 c) u# i& d. r( ?
height was 6 feet, and he went through a somewhat
. }6 K8 ]. L- n( R5 Y  cearly puberty and had stopped growing by age 14.
2 }$ L& p) }0 J; N+ ]7 f8 ~/ iThe father denied taking any other medication. The8 q# v. P7 S6 O/ Z. o8 Y5 _
child’s mother was in good health. Her menarche
1 b, q& _% ]& B0 C/ G# Twas at 11 years of age, and her height was at 5 feet
, i5 o8 y4 x" j  K3 r" W5 W7 I5 inches. There was no other family history of pre-. z) n0 u* u9 x
cocious sexual development in the first-degree rela-/ E  `& j$ r5 T' `0 P9 V
tives. There were no siblings.3 l" T4 v: @' T6 L1 _- a/ x: m
Physical Examination
) G4 o. t* _7 q9 `+ k1 h1 ^The physical examination revealed a very active,
+ O/ S' H/ L3 J5 mplayful, and healthy boy. The vital signs documented9 P+ l! U; J$ S! t
a blood pressure of 85/50 mm Hg, his length was/ J4 c, |% ~7 x( o
90 cm (>97th percentile), and his weight was 14.4 kg
3 f' ?. i# C& H+ \" J) @6 B% |(also >97th percentile). The observed yearly growth
' t  @' g( |1 x* R1 U3 O% Xvelocity was 30 cm (12 inches). The examination of
3 z# m. T* Q! S. u3 Rthe neck revealed no thyroid enlargement.
& u8 g+ K# |4 m8 gThe genitourinary examination was remarkable for$ ]9 a. r6 {) [
enlargement of the penis, with a stretched length of; k# |1 L7 w9 t3 w2 `
8 cm and a width of 2 cm. The glans penis was very well
+ H6 H1 M3 L: b- w0 S, I  }developed. The pubic hair was Tanner II, mostly around* x2 Z# I, m% d5 u) K7 B/ f& u: O
5409 J8 o7 _0 P3 t$ f9 `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* B* C" \5 B9 Hthe base of the phallus and was dark and curled. The% u: z, ?. h4 d" H
testicular volume was prepubertal at 2 mL each.# L8 V; i& ]+ I& c# C1 h$ w$ B
The skin was moist and smooth and somewhat
% u" Y5 m4 ?/ d; @/ f* J8 F, Roily. No axillary hair was noted. There were no
2 G* M* P8 L( v4 labnormal skin pigmentations or café-au-lait spots.4 z5 l: k! R: s: v, ]) T$ C( v
Neurologic evaluation showed deep tendon reflex 2+
3 i- G! s8 t6 S7 l( }1 G4 Fbilateral and symmetrical. There was no suggestion
% f, L1 N. I4 k  h2 Y6 rof papilledema.
4 o5 G  |# c& x# v( p1 aLaboratory Evaluation
2 i8 ?4 a* _* O8 o7 [: PThe bone age was consistent with 28 months by4 l2 N6 ^3 |# }
using the standard of Greulich and Pyle at a chrono-, c5 ^% g8 c1 y! a% O4 N  ?
logic age of 16 months (advanced).5 Chromosomal
3 B9 y; U4 Z* U- @karyotype was 46XY. The thyroid function test
: U6 G9 i* I& T) ~3 Oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 q" |% o5 P& X) ]/ T' i0 k/ D/ S9 f0 xlating hormone level was 1.3 µIU/mL (both normal).+ o9 l6 x. s& u5 k+ F
The concentrations of serum electrolytes, blood7 b- m& w6 r; R: N0 q8 @
urea nitrogen, creatinine, and calcium all were/ K: a: F$ o- u9 U. L3 b) C4 ~
within normal range for his age. The concentration/ t! B4 P7 S$ T2 [& ~
of serum 17-hydroxyprogesterone was 16 ng/dL
# Q) g, T& d. N! M(normal, 3 to 90 ng/dL), androstenedione was 208 K8 J. D4 |" A3 Z+ \( Q, b
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ ~  i! n2 d* L. {4 W7 x8 f$ l, Yterone was 38 ng/dL (normal, 50 to 760 ng/dL),  o, x; g" W- G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to* c( @0 ]. \# u9 x8 Q
49ng/dL), 11-desoxycortisol (specific compound S)
4 A9 e% f; E7 Owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
  l" w# u5 G# D3 @8 j7 xtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 v7 t) h7 u' T2 Rtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 x% W4 l+ n. B& M0 N
and β-human chorionic gonadotropin was less than
( ^8 N2 A3 x% Q& ~- x, ]5 mIU/mL (normal <5 mIU/mL). Serum follicular8 k+ R$ B9 m$ M8 o, N* U
stimulating hormone and leuteinizing hormone3 l# R3 E  E) x* f- k; c) [: _
concentrations were less than 0.05 mIU/mL0 A9 I, ]1 x" H* l& L; u1 R
(prepubertal).' v- {) C# _: ~4 g5 \0 W* X' x
The parents were notified about the laboratory: o0 r1 Q5 J* t( n0 W) W
results and were informed that all of the tests were  _4 r$ p0 v- K( d: N" u3 ]
normal except the testosterone level was high. The
2 R$ |" D1 f( S) Bfollow-up visit was arranged within a few weeks to+ ~: O4 B6 v  s: q* R5 }5 h; `3 Q1 F
obtain testicular and abdominal sonograms; how-
- K7 F6 P% A% v: }ever, the family did not return for 4 months.
+ L7 m, p4 h3 d3 i& s8 X$ \Physical examination at this time revealed that the
1 i4 R+ {4 ^+ Z" H$ l7 N2 E4 \child had grown 2.5 cm in 4 months and had gained* u7 l1 {3 u6 F- |# g  `
2 kg of weight. Physical examination remained
1 m: x2 h/ p3 |; H) M# qunchanged. Surprisingly, the pubic hair almost com-
5 T" J3 w' a0 u6 h7 D8 q: I) S! i, Q; vpletely disappeared except for a few vellous hairs at
0 M  P/ X2 z  ?( v: d5 uthe base of the phallus. Testicular volume was still 2
  i1 |2 V8 }2 e, \! y. rmL, and the size of the penis remained unchanged.
9 s. `4 [: n  i" S1 K: _The mother also said that the boy was no longer hav-' A. r9 c' R# @4 J0 \% X
ing frequent erections.' O7 q- }+ ~3 Z' Q8 \: s; G
Both parents were again questioned about use of  A: ~$ ~  A5 P3 i1 u% Y8 k; T
any ointment/creams that they may have applied to
* G" i) z$ Q) i8 tthe child’s skin. This time the father admitted the  `; P6 r; X" z- }6 T; @
Topical Testosterone Exposure / Bhowmick et al 541! |9 z! l% D0 Q- ?" X5 e) g
use of testosterone gel twice daily that he was apply-
1 o- o9 F( W) P1 L4 Y" ping over his own shoulders, chest, and back area for
; A7 I7 p) k( {7 f1 g7 M8 O& }/ H2 Ka year. The father also revealed he was embarrassed
2 t4 I& F$ f0 R3 Zto disclose that he was using a testosterone gel pre-- [/ z- ^. ]  e. F' b8 k4 D+ K
scribed by his family physician for decreased libido
+ N: N$ P$ M* _! O" Isecondary to depression.
% ?& M1 v1 [5 ?  p7 hThe child slept in the same bed with parents.! t0 Y# u" C) J# h9 w
The father would hug the baby and hold him on his
7 N8 {3 Y* g; s! s  r* Z  echest for a considerable period of time, causing sig-
# o2 w# f. X$ H  t2 r  s" Q" l: xnificant bare skin contact between baby and father.8 q. r) R/ l1 O4 ^
The father also admitted that after the phone call,
7 @9 i( Y9 Q( d" I+ w1 K& Y1 fwhen he learned the testosterone level in the baby* r+ `- l4 `0 C: @( |
was high, he then read the product information- Y' Y8 L- {, O/ h' c( d
packet and concluded that it was most likely the rea-# @) v, A3 `( Z* N& n) U+ b2 I
son for the child’s virilization. At that time, they
/ x8 v* x3 `) P7 I% T1 I5 G! ndecided to put the baby in a separate bed, and the0 ], M3 f! p- z
father was not hugging him with bare skin and had/ r! R! u1 K! d( ~; L0 b
been using protective clothing. A repeat testosterone2 r' t4 h) T/ Q* ~; ?0 n
test was ordered, but the family did not go to the
- z/ U8 _( ]4 }$ M1 flaboratory to obtain the test.& b7 G# Q- b8 n6 u' y( Y2 |5 M
Discussion; g5 @7 _4 Q! Z( i$ J" f. A
Precocious puberty in boys is defined as secondary
* U  \3 q: p- f& I" j* }! R' z/ Lsexual development before 9 years of age.1,41 [# s! n/ M5 H$ _! X1 g
Precocious puberty is termed as central (true) when: c3 \9 g& C& P8 d: }) }
it is caused by the premature activation of hypo-
. H* Y  w1 U. E) k& g" fthalamic pituitary gonadal axis. CPP is more com-+ C; [/ q. u' q& n" s' i
mon in girls than in boys.1,3 Most boys with CPP7 R4 M+ g; ~6 F4 k6 f" I9 ~9 ^
may have a central nervous system lesion that is% i1 m3 ?( v  C+ [, p% }) E# ~& Y
responsible for the early activation of the hypothal-1 S) l& U% {/ E* I0 m+ W
amic pituitary gonadal axis.1-3 Thus, greater empha-
6 q( c) m! ~. r# R& [( r% ^+ tsis has been given to neuroradiologic imaging in1 l2 y, R+ ^, X- m& e- b
boys with precocious puberty. In addition to viril-
: |" h; M' ~5 q5 Nization, the clinical hallmark of CPP is the symmet-
( g" }  \& m: Q9 u) v: Z+ frical testicular growth secondary to stimulation by
  d- s2 e$ c3 r9 C9 |1 ]. T% \2 p: Jgonadotropins.1,3
/ m3 l( O' H0 g( g, wGonadotropin-independent peripheral preco-. ?& J4 `1 a" h' u
cious puberty in boys also results from inappropriate
+ T$ ^3 G8 m) G* Xandrogenic stimulation from either endogenous or9 d7 T. \7 c+ X6 u' [& m
exogenous sources, nonpituitary gonadotropin stim-4 J1 w) p# |& A# K* `9 V
ulation, and rare activating mutations.3 Virilizing
& ]) R# w7 n0 a# J! k* mcongenital adrenal hyperplasia producing excessive
8 I3 b' ?( J2 o0 ]0 Zadrenal androgens is a common cause of precocious
  a1 ~: n6 C3 E3 j- mpuberty in boys.3,4) s4 f7 J: ^2 ?4 L2 G8 L$ y1 G1 ^
The most common form of congenital adrenal' j# v, @& P' Y
hyperplasia is the 21-hydroxylase enzyme deficiency.% g! j9 C. W$ `: z+ k' v+ P
The 11-β hydroxylase deficiency may also result in
% s7 G3 O# N" _" M: Dexcessive adrenal androgen production, and rarely,
  L9 g9 \8 f( b8 a" z+ yan adrenal tumor may also cause adrenal androgen
. N; m; E( g; uexcess.1,3- m  v" B- z: ~$ H% a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ ^3 |/ k2 F' d+ K
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; t- a. l1 r& [A unique entity of male-limited gonadotropin-
# Y/ m5 R  {, z! B- t/ Y" yindependent precocious puberty, which is also known9 q: B- B3 V. q6 I# }
as testotoxicosis, may cause precocious puberty at a
- ~/ F4 i5 c5 svery young age. The physical findings in these boys' p/ R2 ?6 }. ~
with this disorder are full pubertal development,
* l& g% t  h6 hincluding bilateral testicular growth, similar to boys
4 s, _  G, }7 c5 b, Bwith CPP. The gonadotropin levels in this disorder
5 \' ]$ G  Y4 C. n, p+ a5 Hare suppressed to prepubertal levels and do not show" n$ O' P4 q: k2 _; j% X& k, T
pubertal response of gonadotropin after gonadotropin-
: G. X$ p! }7 m3 h' Z0 l+ _releasing hormone stimulation. This is a sex-linked& G' L% |  @& t0 @7 ~6 r9 `* w
autosomal dominant disorder that affects only
7 X  F' W9 T3 ymales; therefore, other male members of the family
3 m3 T( ]1 b: M4 Z$ ?! U% Amay have similar precocious puberty.3
. j0 y" V6 E- A8 ?: F8 z& EIn our patient, physical examination was incon-6 S1 |7 h, O# ^6 m- _1 v
sistent with true precocious puberty since his testi-! j7 `+ P- v, W: u5 L  o
cles were prepubertal in size. However, testotoxicosis8 G" h0 \; E% m8 S8 ~2 g/ L7 E
was in the differential diagnosis because his father2 m# T9 k* x. k( e1 k
started puberty somewhat early, and occasionally,2 \; A0 y7 r' X* k/ ^/ b+ c( o
testicular enlargement is not that evident in the+ p; @8 k- B* [  q  Y
beginning of this process.1 In the absence of a neg-
5 m7 [0 D4 H: V1 Kative initial history of androgen exposure, our, Q7 x; O) [0 r- {+ [6 O" l' A
biggest concern was virilizing adrenal hyperplasia,% T# e# F# l4 t. Z* i0 D
either 21-hydroxylase deficiency or 11-β hydroxylase' C8 j/ ]& X: O* S$ n# g) {
deficiency. Those diagnoses were excluded by find-
4 }4 }  W: c1 N5 t! Sing the normal level of adrenal steroids.
: W# G! ]- C) r( q/ q- u3 fThe diagnosis of exogenous androgens was strongly' |) z2 `% g- B$ x4 G8 n2 D/ o
suspected in a follow-up visit after 4 months because- s9 _# t: X, z/ l! X# H! p7 e
the physical examination revealed the complete disap-9 A$ k  I7 H7 H. _9 k, r
pearance of pubic hair, normal growth velocity, and  I7 D& |- |+ I4 g/ `
decreased erections. The father admitted using a testos-
' i  f3 l0 m' w; P6 h; o$ Aterone gel, which he concealed at first visit. He was
) r- T+ O; j; D9 Husing it rather frequently, twice a day. The Physicians’
  @, Q( ^( {# R' dDesk Reference, or package insert of this product, gel or
4 W8 z% D6 V8 X( b  p% Ocream, cautions about dermal testosterone transfer to7 |2 [6 A# g7 r/ V* ]7 u
unprotected females through direct skin exposure.
/ b# h  d$ H) BSerum testosterone level was found to be 2 times the
. u$ w7 e/ Q: I$ u" x) D6 dbaseline value in those females who were exposed to: r- R3 I" S2 s) n& d! w6 I
even 15 minutes of direct skin contact with their male
5 b+ Y5 v. K2 Z; N" Xpartners.6 However, when a shirt covered the applica-
! y3 d6 {$ z4 Q3 D2 s8 M# [6 h; Wtion site, this testosterone transfer was prevented.
. c7 d( J" ]: y0 wOur patient’s testosterone level was 60 ng/mL,1 S" J% t5 F& w: O) c% Q# g
which was clearly high. Some studies suggest that
" u, n$ _# [# E" Xdermal conversion of testosterone to dihydrotestos-: _6 Z% y: g2 H- t
terone, which is a more potent metabolite, is more
7 _; S' G( y  x# D  E+ S  nactive in young children exposed to testosterone
% ]) H$ J9 k* q' H2 fexogenously7; however, we did not measure a dihy-
2 Z  n  l$ [+ A4 H& Rdrotestosterone level in our patient. In addition to! Z2 T8 S+ O6 O! @  Q3 P
virilization, exposure to exogenous testosterone in
9 [6 S, Z. s& x$ Wchildren results in an increase in growth velocity and  ~1 v+ \4 G; R  M
advanced bone age, as seen in our patient.
0 m, g4 c. l1 M# L# xThe long-term effect of androgen exposure during" X! O6 a# {) S- a$ C9 k9 o
early childhood on pubertal development and final
7 U( T% T# f7 _/ F' c+ padult height are not fully known and always remain
0 O0 m1 @' b/ m$ na concern. Children treated with short-term testos-( Q1 S. ?5 V* v5 ^1 x9 q4 Y
terone injection or topical androgen may exhibit some
! Q. {: z. [" b! Y. ]acceleration of the skeletal maturation; however, after
6 A$ E! }; a  a( p; O9 B6 Dcessation of treatment, the rate of bone maturation: Y/ Q; d& t) R3 k6 r
decelerates and gradually returns to normal.8,9* N; Y& b0 }& ?8 V1 \! m. M! U
There are conflicting reports and controversy
. W: b( _( z& t+ o7 _8 l$ uover the effect of early androgen exposure on adult0 }3 O! e4 `7 D. H2 w3 U
penile length.10,11 Some reports suggest subnormal, C! [0 U' _& I6 {" A2 ~: v) R
adult penile length, apparently because of downreg-
" N( x8 u- N: S0 b; d/ w% U+ Kulation of androgen receptor number.10,12 However,9 C$ C+ P! h$ r8 |$ X
Sutherland et al13 did not find a correlation between
: p9 G) @3 v3 x4 Z2 y5 s  uchildhood testosterone exposure and reduced adult; r* _& Y% b8 ^4 V' i" {! Y2 r7 ], m5 Y8 o
penile length in clinical studies.- G& Z# `4 s: j2 `0 o8 H% T
Nonetheless, we do not believe our patient is7 `$ m  q4 P8 i  e: b
going to experience any of the untoward effects from
# Q" N# ~  b1 Ttestosterone exposure as mentioned earlier because
# [9 m% G" X; m1 ^the exposure was not for a prolonged period of time., s$ J, L! L% e$ u5 \$ X
Although the bone age was advanced at the time of
* V: S, D# T" c: c3 o2 f- C  ?diagnosis, the child had a normal growth velocity at
- I- m4 Y# v. z: Q3 W2 e0 }the follow-up visit. It is hoped that his final adult. P8 d; S2 o# J  H; H8 E8 z0 t% i
height will not be affected.  p6 K# D  n. j! m8 a# u2 t) p
Although rarely reported, the widespread avail-
) U. q- }0 g/ G0 x& R/ E' I- {ability of androgen products in our society may
5 W, q$ N1 x9 Mindeed cause more virilization in male or female
9 t, ^2 Y1 t& O4 Q' z2 d6 Cchildren than one would realize. Exposure to andro-
7 D! L: L2 p+ N  H( g) R' N, ugen products must be considered and specific ques-
3 b$ P, {0 {5 I% g6 I9 Ytioning about the use of a testosterone product or% ~6 K; M- A6 h
gel should be asked of the family members during# o# ~( M. N% }( g. e" y
the evaluation of any children who present with vir-
$ u" j) z$ {6 K4 U0 hilization or peripheral precocious puberty. The diag-
" G5 P5 s; p. |( V7 ]nosis can be established by just a few tests and by
3 M* v! A! n3 q' X- M% E# h2 Fappropriate history. The inability to obtain such a
- V( G: M7 x, B& ?% A: jhistory, or failure to ask the specific questions, may! d. W& R) b8 c3 D! T( {6 X; u
result in extensive, unnecessary, and expensive
- F( l; A) I. O' v: D3 I! Vinvestigation. The primary care physician should be+ a6 Y$ E5 n0 z( U4 v) R$ R
aware of this fact, because most of these children
  ^. v: h; o- x6 Z1 ^may initially present in their practice. The Physicians’1 D& P  d+ B/ U, M# x8 i
Desk Reference and package insert should also put a; ^2 q+ ]) z3 ~- d4 D0 L9 [, k+ m
warning about the virilizing effect on a male or8 K# _% O9 H2 Y, y$ v; S* ]2 Q
female child who might come in contact with some-
  [0 V* m0 b& e& a3 H& |  T: tone using any of these products.
* {9 X+ P2 Z( r' u- h3 OReferences/ A/ c( {5 w& o8 V6 h. x. x
1. Styne DM. The testes: disorder of sexual differentiation
  Y8 W- N1 L" hand puberty in the male. In: Sperling MA, ed. Pediatric
- s/ {) O) X6 [2 G( R8 T' K5 cEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 p2 ]  K* D5 _0 U2002: 565-628.
& g: R9 l9 `  f  T; W" ~8 z0 x9 k2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
+ i9 w- z- X7 `" j5 T" e0 D7 Upuberty 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
; q9 D9 b: R0 b( a2 X6 k8 ?# 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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