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Sexual Precocity in a 16-Month-Old* j  n) n) k2 Q2 P" T
Boy Induced by Indirect Topical
) z, I3 A$ o$ O$ `Exposure to Testosterone
# K3 j) C1 J" VSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! f. L# |/ k! b) }% A0 pand Kenneth R. Rettig, MD1
7 x6 t  s' G2 XClinical Pediatrics% J5 t. [/ f$ W* H% l/ y
Volume 46 Number 6
2 @2 }) W2 M- Z- J# [July 2007 540-543
1 W( `, l1 Y( ]1 A4 }5 g© 2007 Sage Publications
. F$ t6 m+ X5 U0 c10.1177/0009922806296651
: b# L1 n% ]6 n9 J) N' K( bhttp://clp.sagepub.com7 H, B0 m  [; M( n" U+ [6 s' R
hosted at& i1 ~2 A' Q+ L. k. v# u0 ^
http://online.sagepub.com1 A, \" V, a+ B; P8 \( q, H
Precocious puberty in boys, central or peripheral,
% c' e' j1 X* x5 bis a significant concern for physicians. Central+ s* l% g1 ~$ C3 H& N
precocious puberty (CPP), which is mediated
4 m8 i: a  u3 B3 Q. o& Kthrough the hypothalamic pituitary gonadal axis, has
1 s2 u; T/ ~/ h/ T/ B' na higher incidence of organic central nervous system- W" ^5 t  x* {* x0 H; j
lesions in boys.1,2 Virilization in boys, as manifested: T2 E+ ?. J! _' K# e  Y4 I$ K
by enlargement of the penis, development of pubic" g2 T( |* s* H1 b% f
hair, and facial acne without enlargement of testi-
7 F/ h4 p# Z/ \* ^cles, suggests peripheral or pseudopuberty.1-3 We
2 t9 G" K7 O2 b6 oreport a 16-month-old boy who presented with the1 h5 `% `! p0 Z4 h" V8 x
enlargement of the phallus and pubic hair develop-/ W  K& \3 i& w* N! C! Q
ment without testicular enlargement, which was due
% Y7 s  g0 J9 g* P, |  ]! Zto the unintentional exposure to androgen gel used by
! K9 H2 E4 n" k3 n) xthe father. The family initially concealed this infor-
, _* y' n, y& C9 V: e7 ?. [mation, resulting in an extensive work-up for this2 U5 G5 p" }" O/ q& \
child. Given the widespread and easy availability of6 q2 s' ~" v8 a: a$ i% B6 C
testosterone gel and cream, we believe this is proba-  F& c* M& ]7 j1 V, ^6 W
bly more common than the rare case report in the
$ b7 m+ @1 R0 e1 H- F+ ^: Aliterature.4
% z# P# W0 }: M& @- p/ M  rPatient Report2 L! |  K5 t4 }2 H. t) z
A 16-month-old white child was referred to the- \' E$ z4 _8 S5 x+ S) o
endocrine clinic by his pediatrician with the concern
) f; f8 a, p; W5 A" F3 ?1 Zof early sexual development. His mother noticed
6 N; u4 m7 a, d4 u8 U. |8 ]# j& olight colored pubic hair development when he was
; ^  q9 j0 b6 |: `1 nFrom the 1Division of Pediatric Endocrinology, 2University of+ R- S, Q# ^' Y7 ]1 B7 U; q1 K/ Y* h0 K! @
South Alabama Medical Center, Mobile, Alabama.  E5 i  Q7 U0 }/ s
Address correspondence to: Samar K. Bhowmick, MD, FACE,+ ~  J6 g. e( N# a) F1 V+ K; D
Professor of Pediatrics, University of South Alabama, College of
. y' t, a$ o3 w- E. QMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 W% R, @" J; i# r4 F4 Ke-mail: [email protected].6 T! F2 U& ^4 Z' R! p0 y& s& G
about 6 to 7 months old, which progressively became' ], |# Y; T9 T5 A4 V7 Q  c
darker. She was also concerned about the enlarge-' E( E" V* V* D7 @
ment of his penis and frequent erections. The child4 P, o% A- Y5 w+ T5 u4 _. s5 U2 ]
was the product of a full-term normal delivery, with  U6 R0 P! R( J* P3 J7 G  l3 m
a birth weight of 7 lb 14 oz, and birth length of
+ B6 H9 q* B: _20 inches. He was breast-fed throughout the first year* ?6 M, y& ^4 n! k) d0 M9 K: x
of life and was still receiving breast milk along with7 I5 Z1 F- }# H" z2 t9 V6 ~) B
solid food. He had no hospitalizations or surgery,
: B; n) k# v* u+ b; l$ d0 C+ `! land his psychosocial and psychomotor development2 x( k; ?) U$ T% }0 ~
was age appropriate.8 C; ^# P& j0 t& A; P5 E& P3 h2 j
The family history was remarkable for the father,
, n. Y9 v, T$ j( e+ s& M! E1 {' l2 awho was diagnosed with hypothyroidism at age 16,
6 y( L& ^4 }  }) r* ~1 E' C$ Ewhich was treated with thyroxine. The father’s
/ ^. m* X  v$ D. Cheight was 6 feet, and he went through a somewhat; M1 H# r6 X% P" e
early puberty and had stopped growing by age 14.
$ E0 m$ N# }% v3 x2 P; L; i  dThe father denied taking any other medication. The
9 C" ]$ J: x0 r  X& p+ `' c1 Ochild’s mother was in good health. Her menarche4 S& `$ v! R* f$ D; `( w4 |
was at 11 years of age, and her height was at 5 feet
) B( ]$ x4 B- w2 G& D# z5 inches. There was no other family history of pre-
% g3 S) X0 B8 n7 \; {cocious sexual development in the first-degree rela-
2 q( i% v9 p# X- _- Q% y5 a9 Htives. There were no siblings.
0 y2 S3 K8 r$ q* e1 J$ ZPhysical Examination
, e' T9 g! X: Y/ W( b: {+ x! zThe physical examination revealed a very active,
1 [' O8 `. j$ g3 C6 y4 G. K" cplayful, and healthy boy. The vital signs documented* M( }& h2 O. g
a blood pressure of 85/50 mm Hg, his length was
/ ^( D! \8 ?. M90 cm (>97th percentile), and his weight was 14.4 kg
- z; R  _) x- n(also >97th percentile). The observed yearly growth- ~' [7 |7 ]% {
velocity was 30 cm (12 inches). The examination of
" N" M$ ?5 o0 Y7 ]8 \2 u- f3 `0 mthe neck revealed no thyroid enlargement.2 e2 z7 G! z1 W6 Q3 S5 Y& i
The genitourinary examination was remarkable for* b: Z) A7 b+ C
enlargement of the penis, with a stretched length of
+ P5 `) J* g6 Y) a( q4 K3 s1 X8 cm and a width of 2 cm. The glans penis was very well9 P9 p% G9 |. K/ Y; l! |
developed. The pubic hair was Tanner II, mostly around
2 n5 T  a& `, J540
! S& r# j/ s: x* mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ x; s4 Y& f+ N7 k* Y9 Xthe base of the phallus and was dark and curled. The$ l( h: c! u/ X; s$ t/ F
testicular volume was prepubertal at 2 mL each.9 o& K. F2 q! P: a; r
The skin was moist and smooth and somewhat* W: d; Q, G! e- f) g
oily. No axillary hair was noted. There were no8 r6 F2 T" x% z# Z6 i
abnormal skin pigmentations or café-au-lait spots.
1 Y) W& _, {$ `2 N; [* f3 ZNeurologic evaluation showed deep tendon reflex 2+, G' P: U# s9 G9 F% _% x6 l
bilateral and symmetrical. There was no suggestion# n+ n! w) s6 a% F" f$ d6 |
of papilledema.5 C0 [: H% O- M
Laboratory Evaluation4 e' |" }5 }9 r
The bone age was consistent with 28 months by4 K7 Y& l  F% Y
using the standard of Greulich and Pyle at a chrono-6 k1 W0 f# _3 w4 t5 l) k( Z
logic age of 16 months (advanced).5 Chromosomal" e( }# a8 n! i
karyotype was 46XY. The thyroid function test# h/ v* D# B! Z7 I' ?" ?
showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 c$ v0 S+ h0 I' I9 o- t! f* y
lating hormone level was 1.3 µIU/mL (both normal).
! D" D! i9 H9 t" C* p9 D* Q0 T$ g* ?+ ~# DThe concentrations of serum electrolytes, blood
: k( X- {' }8 curea nitrogen, creatinine, and calcium all were
* F0 h+ e$ J( D7 G9 iwithin normal range for his age. The concentration) g( }+ p' u2 Y" L, Z
of serum 17-hydroxyprogesterone was 16 ng/dL
1 B% e; A* x/ W" x/ ?+ N9 G(normal, 3 to 90 ng/dL), androstenedione was 200 \8 ]. d( K7 i+ u' P1 ~
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
# ^4 ]0 V* w" u- I: K0 Eterone was 38 ng/dL (normal, 50 to 760 ng/dL),2 a4 R# }8 o! b1 ~* h. K& P; K7 {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to1 Z% \1 J. Q# s0 @9 x5 d  P
49ng/dL), 11-desoxycortisol (specific compound S)' V. T9 |" w9 W- {0 a
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 o4 t( d8 N+ f3 |$ H: Otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 Q' H" H4 T" o/ n2 {6 `; b0 dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
: I- Y  R; R4 w9 f0 [- Band β-human chorionic gonadotropin was less than
3 H8 j$ C( }+ j* p3 G5 mIU/mL (normal <5 mIU/mL). Serum follicular% L( o3 x* o2 ^
stimulating hormone and leuteinizing hormone9 E2 }6 v0 }" W  E
concentrations were less than 0.05 mIU/mL& a: p% n. w% M2 T( M3 r' H
(prepubertal).7 H  L- @8 A6 T/ G
The parents were notified about the laboratory
' i' D$ Q, R. H+ F7 Eresults and were informed that all of the tests were
& Z2 y  u' k3 A; a  Hnormal except the testosterone level was high. The2 i& |) M6 K3 \) N& h6 p" x% B, {
follow-up visit was arranged within a few weeks to
; j/ ~- q" b2 O& X  cobtain testicular and abdominal sonograms; how-7 [0 J* @8 j) T2 a" q
ever, the family did not return for 4 months.; c( @; ?( P" T/ O6 \: B- k, i
Physical examination at this time revealed that the; u! R7 l: Y1 T3 k% m
child had grown 2.5 cm in 4 months and had gained$ ^. J" g" o% \5 Z, y7 W! K
2 kg of weight. Physical examination remained
, X9 b3 @! p8 N; Eunchanged. Surprisingly, the pubic hair almost com-3 I2 J0 Z+ e& R( J- j5 |
pletely disappeared except for a few vellous hairs at
; ^; _  ^2 H( w+ v/ _& ?. zthe base of the phallus. Testicular volume was still 2
) h: x) k: f! t" s6 k; WmL, and the size of the penis remained unchanged.
; l. J: u5 }6 R& L9 S9 a0 sThe mother also said that the boy was no longer hav-* j$ E5 s* `1 I/ r
ing frequent erections.$ p& x( ~9 W5 l. M. V9 p' A
Both parents were again questioned about use of
% K0 n/ M9 k4 Z# e7 o  G) n+ vany ointment/creams that they may have applied to; O3 j2 c! T6 s9 L
the child’s skin. This time the father admitted the4 c( B9 ]0 X7 @- S0 o8 ?
Topical Testosterone Exposure / Bhowmick et al 541- m1 T: X% O. Q' G
use of testosterone gel twice daily that he was apply-: x) P8 h* p1 r, \0 S6 ?8 n4 b
ing over his own shoulders, chest, and back area for
# E$ S( r. \) ?  c( La year. The father also revealed he was embarrassed; V. ~* n" E& \8 m
to disclose that he was using a testosterone gel pre-
+ m* c( e3 F6 I! {% i6 n& d+ dscribed by his family physician for decreased libido+ x' w" Y% ^; p1 m+ m2 s7 Q9 Y
secondary to depression.
1 z8 k! g" e+ m  \$ t' G$ Z, oThe child slept in the same bed with parents.6 F. v! Q/ K+ h" @) D: j- f- B# L# r
The father would hug the baby and hold him on his! a# g% ?! w! n; I% Y
chest for a considerable period of time, causing sig-
# K, h- w# a7 J) X; jnificant bare skin contact between baby and father.0 f1 b8 h# ?" J* |. c8 S, J
The father also admitted that after the phone call,
0 D% S2 z6 K2 X/ b; p, \. d% fwhen he learned the testosterone level in the baby! ]2 {. S' `' j: X
was high, he then read the product information$ E8 ^$ r4 y5 w  Q, e9 ]5 n: G
packet and concluded that it was most likely the rea-  g( [7 M, n" l' u' J$ K
son for the child’s virilization. At that time, they. i7 m: S$ H" z  Y  k3 Y- @2 z3 [
decided to put the baby in a separate bed, and the7 s7 j/ ~; h3 D3 N) j) H' W$ E% B0 _
father was not hugging him with bare skin and had& L- b2 @* b& c. t
been using protective clothing. A repeat testosterone) C; `# E" E/ _! q+ B. w0 o8 G1 d
test was ordered, but the family did not go to the
) J. N: X! [) wlaboratory to obtain the test.+ E: A$ m% U% s2 K9 |1 p: w
Discussion
' J" N' `3 `- ~/ hPrecocious puberty in boys is defined as secondary. M& r4 k; s: m4 h
sexual development before 9 years of age.1,4+ e) N: E0 ~9 D
Precocious puberty is termed as central (true) when$ A; @1 r) ^9 L( I
it is caused by the premature activation of hypo-1 K& g/ P; a& |8 n9 G! P0 K# i
thalamic pituitary gonadal axis. CPP is more com-6 Z/ P1 ]0 E- {4 x
mon in girls than in boys.1,3 Most boys with CPP- F* `$ f" c* J: R
may have a central nervous system lesion that is
1 A* x8 \$ L9 v0 Mresponsible for the early activation of the hypothal-! R/ x/ v. i* ^' N8 z
amic pituitary gonadal axis.1-3 Thus, greater empha-
, W; q: J( |* S: E: n# o' gsis has been given to neuroradiologic imaging in" |5 `5 \! q) H. B; z- _! c: c
boys with precocious puberty. In addition to viril-
6 h7 e3 S2 I2 x- @* i6 y( w. Sization, the clinical hallmark of CPP is the symmet-
4 _5 l4 R& X2 H7 T) k9 prical testicular growth secondary to stimulation by4 {" c4 H! F) J" Y9 U" C
gonadotropins.1,3# o6 Q! c' x1 y/ ]# n
Gonadotropin-independent peripheral preco-% J0 \5 A; X3 K
cious puberty in boys also results from inappropriate7 z0 {. U- S9 i- F  J" g
androgenic stimulation from either endogenous or. t+ M& Y4 u: Q  f* \( O' b
exogenous sources, nonpituitary gonadotropin stim-4 x+ Q4 v" a* @1 ]9 {
ulation, and rare activating mutations.3 Virilizing
2 b1 G5 B/ Z7 k7 s5 Q0 v( g6 \3 Bcongenital adrenal hyperplasia producing excessive  U0 C+ w( p& t
adrenal androgens is a common cause of precocious% ?5 e% c( J2 l2 ^8 k1 X
puberty in boys.3,4
3 v$ ?% T4 U  s" jThe most common form of congenital adrenal
& \1 ~* {/ V. F: [9 f$ c- I0 qhyperplasia is the 21-hydroxylase enzyme deficiency.! O' p* h) C& L2 |4 A, S1 Q
The 11-β hydroxylase deficiency may also result in+ h8 h1 w/ T/ S$ t2 d4 Q9 ~) t. x
excessive adrenal androgen production, and rarely,
& N2 Q+ U+ U6 T; I; xan adrenal tumor may also cause adrenal androgen
, \# {; S! M* Y5 j: [9 |* g+ x0 Mexcess.1,3, [( u* P6 W" N/ b3 D8 J
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! F1 N4 f1 f$ v542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ C: c1 s4 Y% u6 W' O) Q
A unique entity of male-limited gonadotropin-' [6 F1 t  Q" B- Z
independent precocious puberty, which is also known
% D3 K# q; e9 ?$ P1 Aas testotoxicosis, may cause precocious puberty at a
( u8 E( s& R. p( pvery young age. The physical findings in these boys
( B2 M/ T% i/ Y+ |) B, T7 k) S  P! ~2 Uwith this disorder are full pubertal development,8 C: y/ c) w* L  x  v# n/ o
including bilateral testicular growth, similar to boys; g2 L7 r: Z5 K& ?/ v
with CPP. The gonadotropin levels in this disorder, M; u6 R, c) w! O! L
are suppressed to prepubertal levels and do not show) P8 [$ ~6 ?! G7 K2 [  Q
pubertal response of gonadotropin after gonadotropin-$ J' ^6 j" C& U- w2 ~
releasing hormone stimulation. This is a sex-linked
# S( M7 D1 O( }  n6 J2 I' Dautosomal dominant disorder that affects only
- o( U# a, |& P6 R6 ~. h, zmales; therefore, other male members of the family# n/ Q. R) d8 J
may have similar precocious puberty.3% c- E4 o3 i/ G( e% X
In our patient, physical examination was incon-" m1 B( L4 k1 c
sistent with true precocious puberty since his testi-
6 t1 ?/ [! C# @- ^0 F! pcles were prepubertal in size. However, testotoxicosis
! R5 k' K; x$ `$ a: r' xwas in the differential diagnosis because his father' H. Q/ u9 H# K$ g# P9 X/ Z
started puberty somewhat early, and occasionally,3 C1 v/ X, j6 O! r
testicular enlargement is not that evident in the) v$ _6 W& x# O
beginning of this process.1 In the absence of a neg-
/ g( \( @/ L: C3 Tative initial history of androgen exposure, our
4 {/ ?: x" L2 w" Y4 A4 y9 zbiggest concern was virilizing adrenal hyperplasia,; j, E( \5 t/ ^& O/ J0 s/ H1 S
either 21-hydroxylase deficiency or 11-β hydroxylase! u1 Z1 q* b' f9 [; \$ ^4 |
deficiency. Those diagnoses were excluded by find-( h' ~* O2 x/ a1 x7 I
ing the normal level of adrenal steroids.) n/ Y! K  O' w+ _  S
The diagnosis of exogenous androgens was strongly8 o% f5 f2 S5 J$ k9 |' L
suspected in a follow-up visit after 4 months because
$ g: F* u3 d& l; L- B/ Ethe physical examination revealed the complete disap-
0 E8 v' s% b6 x- xpearance of pubic hair, normal growth velocity, and
$ h: t8 u% H( n# Rdecreased erections. The father admitted using a testos-2 X+ M& k& t8 k. e
terone gel, which he concealed at first visit. He was
2 a: W6 |% y' I' v8 {& F& jusing it rather frequently, twice a day. The Physicians’" E1 f' _0 `0 G$ G
Desk Reference, or package insert of this product, gel or
- K' c2 n. g; L- D" D8 hcream, cautions about dermal testosterone transfer to
( u9 S( A; l" i# Z* l8 y2 funprotected females through direct skin exposure.+ ]+ ?" L: a$ s! p7 Z
Serum testosterone level was found to be 2 times the
" G# e) k" f9 z* k- E! K: Fbaseline value in those females who were exposed to' O) |1 Z% y- d5 k. w0 s
even 15 minutes of direct skin contact with their male
* F7 R/ z: X* H8 @% R; i5 l, Dpartners.6 However, when a shirt covered the applica-3 d1 r0 I9 ?; t# Q2 ^) }
tion site, this testosterone transfer was prevented.9 z; W$ j: I+ m/ N0 c
Our patient’s testosterone level was 60 ng/mL,
! a- h  T2 `9 E+ jwhich was clearly high. Some studies suggest that
( Q/ A( l/ Y! g- o) Cdermal conversion of testosterone to dihydrotestos-
, ]3 j1 M$ |1 `* _8 q) p) q& Tterone, which is a more potent metabolite, is more
3 c5 ~" \" P6 o: a8 ?- V; u$ Lactive in young children exposed to testosterone- G0 d+ N3 O4 B+ O# b
exogenously7; however, we did not measure a dihy-0 w+ ^" q) b& J* q9 b* i) W
drotestosterone level in our patient. In addition to4 [; f0 g% @! Y+ [% J4 ~6 A1 ]# D, D
virilization, exposure to exogenous testosterone in3 L3 r, |. j6 z% a
children results in an increase in growth velocity and3 a4 |+ P2 ]' c3 Y8 h
advanced bone age, as seen in our patient.+ r0 l1 b+ c1 K: X! t+ c4 X: V& K+ B
The long-term effect of androgen exposure during6 E6 C9 o5 p& L3 g7 S- l
early childhood on pubertal development and final- t& j, j0 h. s9 H
adult height are not fully known and always remain
3 q  E) P2 {# c7 [, v  ]- }6 |a concern. Children treated with short-term testos-
5 h3 V0 w1 A6 ?5 A1 l1 ]) E- |terone injection or topical androgen may exhibit some9 k4 e) f# Y& j; M0 ?- _7 ?" Q
acceleration of the skeletal maturation; however, after
. A& |" t, J) a3 l6 ~% ucessation of treatment, the rate of bone maturation9 E% F5 r1 b6 s, G
decelerates and gradually returns to normal.8,9! w  a3 W+ |+ R
There are conflicting reports and controversy1 b" R. n- Z/ F$ R, k8 l
over the effect of early androgen exposure on adult. Z+ b" s/ J) X3 e& u$ \0 p
penile length.10,11 Some reports suggest subnormal
6 W: M) o  P( c; {* ?adult penile length, apparently because of downreg-0 U' P+ K6 g# a7 O, c( X
ulation of androgen receptor number.10,12 However,
1 Z4 Z5 O, ^+ |2 T' S( eSutherland et al13 did not find a correlation between
2 ~5 W6 @9 ~$ ~7 `7 y0 ^* Q) Echildhood testosterone exposure and reduced adult2 J, O# x+ e0 n' ~4 O% k
penile length in clinical studies.( Q2 o, i8 X2 z- F7 `& h
Nonetheless, we do not believe our patient is) l% T4 I% j6 W
going to experience any of the untoward effects from# m2 L& }  `+ |) }" H
testosterone exposure as mentioned earlier because3 I8 {5 m& }8 F4 k3 C
the exposure was not for a prolonged period of time.  j2 K+ D9 B; D* E. y: U& q8 B
Although the bone age was advanced at the time of, |. W9 g. J% n# M: s
diagnosis, the child had a normal growth velocity at) D# S5 i9 }& o- R1 Y
the follow-up visit. It is hoped that his final adult
6 H: Y' v2 b9 z9 Q0 K6 `2 b6 cheight will not be affected.
1 M; f2 }7 K+ b) g' ]5 u- nAlthough rarely reported, the widespread avail-! {& Q1 I# A  }8 Z. T+ s
ability of androgen products in our society may
8 @3 j# `5 K2 C- k- V/ |/ Gindeed cause more virilization in male or female
! k0 `: n6 N6 ?2 b& {children than one would realize. Exposure to andro-
$ ?8 Z: S. N# ~0 T4 H1 qgen products must be considered and specific ques-
+ c# {4 |: d2 O- R; g8 f: Dtioning about the use of a testosterone product or
' Y8 m! i" I, u9 rgel should be asked of the family members during
& m4 A/ ~  V, y9 Hthe evaluation of any children who present with vir-2 T2 s( x8 d- P$ |3 n* x5 q  |1 e' F& |$ [
ilization or peripheral precocious puberty. The diag-
' D/ n5 i6 |+ ^5 {nosis can be established by just a few tests and by# }$ q+ |  D5 D' s$ l4 _* e
appropriate history. The inability to obtain such a
5 P1 q1 s% l- `4 S& T1 G. ghistory, or failure to ask the specific questions, may
# [! d2 o; a, k$ Q9 f# s# e8 presult in extensive, unnecessary, and expensive
$ e- j6 J" a5 z0 Q7 ?investigation. The primary care physician should be
9 q) _- \0 q8 |, X" t. Y' N  }aware of this fact, because most of these children; Z3 a* B) M7 b% m7 h) c$ f
may initially present in their practice. The Physicians’6 l7 U1 b# U8 a
Desk Reference and package insert should also put a
4 j+ `4 }* H. G- M0 ?9 z/ z) u$ rwarning about the virilizing effect on a male or: ^( s, s0 @! F; ?$ ]6 J: b
female child who might come in contact with some-/ W2 q% P. M3 t3 j
one using any of these products.
% g/ w! d* b  b6 D. z- t$ J! MReferences
/ S( i2 p' V) E, ~1. Styne DM. The testes: disorder of sexual differentiation
' W/ M5 j' J) w, N3 wand puberty in the male. In: Sperling MA, ed. Pediatric
) u. Y3 U+ |: x4 |- `& q: a( J: PEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 X* T, n8 S! ~3 J8 C* ]! |4 f6 t2002: 565-628.8 ?% B4 d. c0 N& j, j7 }
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  @+ I0 J  t, _+ ?1 bpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
1 E- ?# V, y( g$ h, A8 K7 aBoy Induced by Indirect Topical
1 P9 V+ E: p7 g2 KExposure to Testosterone8 `  `7 Q9 B. S: |+ A% W4 _4 j
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 B4 l6 \* x" r; ~8 l
and Kenneth R. Rettig, MD10 ~5 K! @6 _2 A4 n
Clinical Pediatrics
* P# v; i" u6 b5 E6 f3 ^Volume 46 Number 6
5 E! O  ~3 E- {3 v) i/ ^5 iJuly 2007 540-543
, D0 j7 ~1 B% _8 M" `© 2007 Sage Publications
; R9 Y3 K; n+ Z10.1177/0009922806296651
/ N% v% d- B7 x. _5 O) ^/ fhttp://clp.sagepub.com$ y+ Z/ E/ ]9 o* E4 F
hosted at) h8 o1 M0 ^4 D& j" Z# H
http://online.sagepub.com
7 |' i3 n* X& o( YPrecocious puberty in boys, central or peripheral,
. {2 u9 W. Q7 P+ \8 g& z, o4 u6 uis a significant concern for physicians. Central" P" T% x1 Z5 M4 l
precocious puberty (CPP), which is mediated
9 T  i+ P* C) uthrough the hypothalamic pituitary gonadal axis, has* t7 z( Y' ^! i. [3 C& |
a higher incidence of organic central nervous system' a% d0 j/ }  i8 X, B! p
lesions in boys.1,2 Virilization in boys, as manifested. P" B9 f/ S" a* I2 I' f+ e
by enlargement of the penis, development of pubic
; I# j6 J& {3 j) E4 b1 Ghair, and facial acne without enlargement of testi-
5 V8 w: i4 a2 v! t& }0 e: x4 scles, suggests peripheral or pseudopuberty.1-3 We0 }' C$ {& l* f4 K
report a 16-month-old boy who presented with the. z+ {# g- `8 p. m3 L' r
enlargement of the phallus and pubic hair develop-) {" I2 E$ x5 F3 v; s! X1 A- r
ment without testicular enlargement, which was due
  G5 s( m+ L' Q. @7 m7 |. K# ^to the unintentional exposure to androgen gel used by
: d$ O5 B7 ^6 u. u& [, Tthe father. The family initially concealed this infor-1 A7 `3 t0 j# q/ ^/ j: ^
mation, resulting in an extensive work-up for this" {& D& L$ Q9 d% U0 x+ k. I3 L
child. Given the widespread and easy availability of
4 c  i3 F) m8 F! J7 l9 L" xtestosterone gel and cream, we believe this is proba-
% U4 S  m$ f$ a1 z8 ubly more common than the rare case report in the3 |4 ~3 f# g. v
literature.4' N: A7 h! K+ k7 g: K1 M
Patient Report
  _- ~; U9 P6 W! l3 y' ?7 g) tA 16-month-old white child was referred to the6 @/ m  y' l9 Q+ o
endocrine clinic by his pediatrician with the concern
' ^+ ~( i! S: J2 o: o6 \# |' iof early sexual development. His mother noticed- B' {+ L* }( a  F
light colored pubic hair development when he was
, l8 e/ m$ o. e' Q& V, LFrom the 1Division of Pediatric Endocrinology, 2University of
1 z7 {! g( Q0 ]0 VSouth Alabama Medical Center, Mobile, Alabama.
" z* S% }- B; V/ G+ [# h" lAddress correspondence to: Samar K. Bhowmick, MD, FACE,5 F  u& ]8 Q# [3 v  b
Professor of Pediatrics, University of South Alabama, College of, }6 p  ^4 N8 w) f6 M9 g5 n# |9 e2 o) _
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
, ^$ l) ^/ l! r, x7 T2 N/ le-mail: [email protected].
9 s5 U8 y1 \) M: D" X$ m7 g4 |. nabout 6 to 7 months old, which progressively became$ }2 |/ x1 b; l. ^0 p% {8 }! V
darker. She was also concerned about the enlarge-' }) |" L8 r* b& }% A3 Y, b
ment of his penis and frequent erections. The child5 \! Q2 k/ x+ H
was the product of a full-term normal delivery, with0 G; ^5 n5 j( }/ x
a birth weight of 7 lb 14 oz, and birth length of0 W! F" \' _- c4 Y+ s2 \3 h
20 inches. He was breast-fed throughout the first year5 ?; L  ^4 I$ U8 S
of life and was still receiving breast milk along with, m8 y0 E8 n8 B; M
solid food. He had no hospitalizations or surgery,
: }# t/ E1 E% N3 Jand his psychosocial and psychomotor development$ o4 d( ?4 l# }5 s& p4 B0 f
was age appropriate." G6 K1 l8 f+ e7 o! i) E8 q( n# g
The family history was remarkable for the father,+ r5 s; |  k: L3 P4 V
who was diagnosed with hypothyroidism at age 16,
0 x0 J8 h) v4 s7 ^. u* d8 Dwhich was treated with thyroxine. The father’s5 g2 t% s0 p3 B) t9 f7 [
height was 6 feet, and he went through a somewhat' C0 j" @8 W  i# P8 J' w
early puberty and had stopped growing by age 14.0 Q+ F* o6 ~2 L4 W/ W  o
The father denied taking any other medication. The
; i* f- U6 y' C0 H! echild’s mother was in good health. Her menarche: i0 l8 U. h: W8 h- \
was at 11 years of age, and her height was at 5 feet
& t1 t. a2 @% A5 inches. There was no other family history of pre-
6 I- a/ k' B* Y/ k' ^" K9 i# ecocious sexual development in the first-degree rela-/ i' j5 N8 M6 N
tives. There were no siblings." Q; y; j! N* X
Physical Examination& f2 L3 m, E, b4 H! F+ s" E( Y; {! T
The physical examination revealed a very active,2 A& L: T+ M: c0 U+ {5 P, {
playful, and healthy boy. The vital signs documented
- F+ q% ^2 }' Ha blood pressure of 85/50 mm Hg, his length was4 g: m$ W( o. u0 [/ b+ |! j7 r/ |8 K
90 cm (>97th percentile), and his weight was 14.4 kg
$ g+ d/ p, K# {/ j  N! j(also >97th percentile). The observed yearly growth  q: G0 r+ {/ D2 a* }' K
velocity was 30 cm (12 inches). The examination of) n) r3 `+ L9 _
the neck revealed no thyroid enlargement.+ y- h# h8 c4 M% H( B! {
The genitourinary examination was remarkable for/ W( q/ `+ j3 G
enlargement of the penis, with a stretched length of7 T1 r( k4 t" O" z5 z/ d
8 cm and a width of 2 cm. The glans penis was very well0 q& [, N0 ^9 ]) p6 n. {
developed. The pubic hair was Tanner II, mostly around  a- F+ N! X" d8 L0 O
540, v4 j1 f* R; H$ k0 N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 W2 [+ H3 T5 }6 X- [the base of the phallus and was dark and curled. The/ E# Y7 G. v2 D" `) Q
testicular volume was prepubertal at 2 mL each.
" o: b) ~1 R8 J2 B% I, SThe skin was moist and smooth and somewhat
7 h7 I+ j8 g! v% w, H0 zoily. No axillary hair was noted. There were no
/ P* P2 P7 _0 X1 R+ C) T4 iabnormal skin pigmentations or café-au-lait spots.$ ~+ w2 N6 e8 r
Neurologic evaluation showed deep tendon reflex 2+6 N0 F; A/ \& A8 E) s
bilateral and symmetrical. There was no suggestion
4 w1 T3 T/ M  `: _! Cof papilledema.
; ?9 N1 L$ U& a" X! ]# r2 R% r; ILaboratory Evaluation) E) E2 \  Z+ w% L0 E9 `) ?3 x$ h
The bone age was consistent with 28 months by
% P% u9 R! Z/ `, |8 k0 ausing the standard of Greulich and Pyle at a chrono-! |2 k+ n; |: m$ {# {5 {7 `! N5 k
logic age of 16 months (advanced).5 Chromosomal/ n% u  Y/ q5 Q. q' s9 X- U. Q
karyotype was 46XY. The thyroid function test
9 ~# s/ ^7 ^1 I) w5 @( r4 |showed a free T4 of 1.69 ng/dL, and thyroid stimu-* m  f  |+ X. p% T
lating hormone level was 1.3 µIU/mL (both normal).0 @3 e3 {* N% `
The concentrations of serum electrolytes, blood
6 G! }3 J8 O% D) G1 D& R; L$ W1 Qurea nitrogen, creatinine, and calcium all were
+ N1 d$ r8 C( U! M" Lwithin normal range for his age. The concentration
, u* ~9 P8 c1 d% i( ^of serum 17-hydroxyprogesterone was 16 ng/dL
2 a% G$ C2 J. G# P( q: C3 X(normal, 3 to 90 ng/dL), androstenedione was 20
0 n+ x7 c% B7 T+ x0 }- e6 xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- ~% t/ ^! n  F9 ?
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
; [( o. c* w( @, G4 P8 bdesoxycorticosterone was 4.3 ng/dL (normal, 7 to/ W1 N7 Z- o2 I* t( C- T3 c  ]
49ng/dL), 11-desoxycortisol (specific compound S)
. Q4 Z: I: P1 k$ n' C; |: S; [( Vwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 x4 g0 j1 I; R
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; k5 O0 b1 x% ?& _! ~1 Ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),( o' t  j. P9 P% F1 _  g& Y
and β-human chorionic gonadotropin was less than
+ a" g+ t5 X% K' `( D, [5 mIU/mL (normal <5 mIU/mL). Serum follicular+ Q" h& d& g7 ^9 D  J) E
stimulating hormone and leuteinizing hormone% T' n5 s& O# v/ Y, L
concentrations were less than 0.05 mIU/mL
% |2 k9 y5 ]" P+ s* t* `(prepubertal).% W3 i  n; Q) n# e) B! i
The parents were notified about the laboratory1 U% A& Y# l% A! R  q
results and were informed that all of the tests were
8 m1 E. a, A4 ?" Qnormal except the testosterone level was high. The
7 z4 i7 c; X8 ~3 F5 {. E/ j! Xfollow-up visit was arranged within a few weeks to# l4 M+ K4 s0 H/ W1 h; }
obtain testicular and abdominal sonograms; how-
, k6 v& P5 S# Hever, the family did not return for 4 months.
. r, k. Z( K! s" l# v# I3 f2 E3 ~( mPhysical examination at this time revealed that the% P& o$ n0 W) M+ G6 ^
child had grown 2.5 cm in 4 months and had gained9 u; h/ q6 x( d" ~0 `2 @8 r
2 kg of weight. Physical examination remained5 N. _% Q6 E$ E
unchanged. Surprisingly, the pubic hair almost com-
, q- M1 Q) |3 [  Epletely disappeared except for a few vellous hairs at  s6 [  X% Q5 C% [* o4 [2 Y
the base of the phallus. Testicular volume was still 2
( |$ _# f/ ?# p% S! ?mL, and the size of the penis remained unchanged.
, b7 ]  o" i1 I. MThe mother also said that the boy was no longer hav-
  [4 r3 |1 f- e: F% x2 ning frequent erections.
4 I8 ^/ [1 D- k, ^Both parents were again questioned about use of7 w. M' Z2 Z$ C. T6 s6 Q0 \; @
any ointment/creams that they may have applied to
) N2 G6 m+ C  k: U: l# Athe child’s skin. This time the father admitted the6 h. X# s) F; z6 R  E. v
Topical Testosterone Exposure / Bhowmick et al 541. W* {- W, Q$ d  S& h* L
use of testosterone gel twice daily that he was apply-/ i  p2 x% ^. J8 E7 E* s
ing over his own shoulders, chest, and back area for1 q' l; F# P2 J
a year. The father also revealed he was embarrassed, f* I4 q7 k5 i; k  |6 k8 S
to disclose that he was using a testosterone gel pre-
! D% v8 |: v) _+ \9 g; |scribed by his family physician for decreased libido$ m: j1 @" ^) o1 h" l2 e" m' F( M, d6 O
secondary to depression.* ?/ p; Q; R1 b" f4 m! _
The child slept in the same bed with parents.
/ Q4 T* ]& K9 E$ R, NThe father would hug the baby and hold him on his
9 U( o8 v% r7 v, a& rchest for a considerable period of time, causing sig-9 P  }7 `3 b2 N) u
nificant bare skin contact between baby and father.+ ?5 V- i0 H! G; P& {
The father also admitted that after the phone call,' ~- ]% A8 k1 v! W
when he learned the testosterone level in the baby, F% E+ ^# E7 ]* M9 Z& c
was high, he then read the product information
( q4 W: @6 G" i& n5 v" jpacket and concluded that it was most likely the rea-
$ r2 Q; g% t8 o! C+ q* oson for the child’s virilization. At that time, they
. V6 B  @) K, T. S- ]( H4 ydecided to put the baby in a separate bed, and the
3 f$ g/ ^7 [! d( ?father was not hugging him with bare skin and had
3 H! F/ T' h: _; Q8 Pbeen using protective clothing. A repeat testosterone
- O- O+ Z/ z- v7 i: P' \test was ordered, but the family did not go to the$ H/ f% q' r- X) h* |8 j# m: m2 d
laboratory to obtain the test.
. U# i: \  q. @) f% DDiscussion
3 \( D4 H2 j- b+ e* f" P  {Precocious puberty in boys is defined as secondary
* H% d5 S2 E+ J! O5 c- n, S. gsexual development before 9 years of age.1,4
* C8 B/ x1 e' w: lPrecocious puberty is termed as central (true) when/ X' P% O- D' |0 R! H- _$ I+ v+ u9 E
it is caused by the premature activation of hypo-
' Y! B" [2 w) l0 Y# f" q+ Uthalamic pituitary gonadal axis. CPP is more com-
2 C/ C1 g- i0 r9 ?1 @" ^mon in girls than in boys.1,3 Most boys with CPP! h# S! n- M) _& a$ }5 J; Y
may have a central nervous system lesion that is
. v4 R" t' y; xresponsible for the early activation of the hypothal-
0 C  _' G$ Z; f: `0 `amic pituitary gonadal axis.1-3 Thus, greater empha-/ G/ o1 s8 p( y* E) e
sis has been given to neuroradiologic imaging in
3 N% a0 Z9 D3 Z( A% `% N( s/ sboys with precocious puberty. In addition to viril-- ]: B- K& _# _- T, o- V
ization, the clinical hallmark of CPP is the symmet-8 w# O: v0 p, ^% s* P- \7 ^
rical testicular growth secondary to stimulation by/ _8 A3 _& `$ b# \
gonadotropins.1,3/ \) Y, A- K# W5 }$ {
Gonadotropin-independent peripheral preco-
' t9 U) N: h) gcious puberty in boys also results from inappropriate
( a; k* f' w" candrogenic stimulation from either endogenous or8 Z, D7 l5 {+ v- u! U
exogenous sources, nonpituitary gonadotropin stim-1 w' ?; ?$ t+ y7 r+ l# f, X: {
ulation, and rare activating mutations.3 Virilizing
& C$ y1 S; d7 c# H2 u7 Fcongenital adrenal hyperplasia producing excessive
( Q) b' n) x" T: \( ^$ p3 m  badrenal androgens is a common cause of precocious' N7 A5 ?# \+ w# P
puberty in boys.3,49 B) G. ^& O+ G, t( ]# @3 }+ g
The most common form of congenital adrenal3 i: H0 A1 B; }3 G
hyperplasia is the 21-hydroxylase enzyme deficiency.9 J( T% E* n: i) Z! W$ j& S- ]
The 11-β hydroxylase deficiency may also result in
6 ]/ k/ a" x5 _. Wexcessive adrenal androgen production, and rarely,
7 j" V' Y. ?- _3 l9 g1 Jan adrenal tumor may also cause adrenal androgen
5 l) p1 z- T# @3 V3 t4 ?: vexcess.1,3
/ q# M+ @% o8 [# S# g+ Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 f/ B/ d0 J2 y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! V! e- i6 K0 ]3 WA unique entity of male-limited gonadotropin-
% Z& s6 O) a: n3 b9 m; S; a6 cindependent precocious puberty, which is also known. S( p7 T- X6 b- K
as testotoxicosis, may cause precocious puberty at a
. U6 V8 `/ X9 k" ~% }% F, nvery young age. The physical findings in these boys3 g. t( }8 @" w$ t% R
with this disorder are full pubertal development,
5 W$ e6 q# z: i# x: A7 I- E$ qincluding bilateral testicular growth, similar to boys
2 p% Q: m3 C0 z& i6 _' M' K$ O8 `, jwith CPP. The gonadotropin levels in this disorder+ c8 S3 C2 I3 b3 f% F# \  u6 t) D
are suppressed to prepubertal levels and do not show
, j4 h0 L; I! V; X% m! L3 ~1 X% apubertal response of gonadotropin after gonadotropin-
) K4 p& u$ p3 x) Qreleasing hormone stimulation. This is a sex-linked
2 g- `$ m/ i. d& N* |5 x  _autosomal dominant disorder that affects only
& k7 m6 v& D" h! |males; therefore, other male members of the family
9 b( y7 F3 ^' i% b( Umay have similar precocious puberty.3
0 j9 o5 Z8 r% L) a6 FIn our patient, physical examination was incon-
/ T  v" }1 D  N1 t1 d1 O' [sistent with true precocious puberty since his testi-
& o, B$ ]1 R5 O3 zcles were prepubertal in size. However, testotoxicosis2 C8 o, ~/ R& H9 e, |! }/ E
was in the differential diagnosis because his father
: g2 j! G/ h$ A& Q6 u! `7 ~( qstarted puberty somewhat early, and occasionally,
9 i- V5 X8 E5 x  A+ rtesticular enlargement is not that evident in the8 X% R2 O4 {% l5 Z  G/ [- r. K
beginning of this process.1 In the absence of a neg-/ i0 H2 f0 ]9 x) ^; w5 N
ative initial history of androgen exposure, our& H& f1 O6 [+ r
biggest concern was virilizing adrenal hyperplasia,
$ j0 {2 A* d! e' }either 21-hydroxylase deficiency or 11-β hydroxylase
3 }3 Y' }& I# k( _+ U: p4 V! Cdeficiency. Those diagnoses were excluded by find-# H) H/ d; @! [1 I' [  E
ing the normal level of adrenal steroids.
  i9 `" ?( D, ~9 HThe diagnosis of exogenous androgens was strongly! |8 _# T! j' a  Q
suspected in a follow-up visit after 4 months because
5 @$ E1 e- q4 l5 {/ A% }6 c9 W4 }  dthe physical examination revealed the complete disap-
) p2 T% n; e/ U# ~) [; Qpearance of pubic hair, normal growth velocity, and8 \. R* Y& ~" ~) J) w7 R% X: n' U& h7 ]
decreased erections. The father admitted using a testos-: }% P& |* T4 \( M* @
terone gel, which he concealed at first visit. He was: Z! @5 q5 E( B; }
using it rather frequently, twice a day. The Physicians’( b9 z6 G6 p; s+ e; Z& p! S
Desk Reference, or package insert of this product, gel or
; G% P2 e3 B6 V, s, scream, cautions about dermal testosterone transfer to
# \. V/ O! H5 _% f/ X; A' ^9 ^unprotected females through direct skin exposure.
+ ~8 L5 E* N5 _Serum testosterone level was found to be 2 times the0 O+ F  _# e4 Z+ @7 W
baseline value in those females who were exposed to4 x, t" `* c5 T7 X0 l
even 15 minutes of direct skin contact with their male
7 Y; H0 ?8 P. W. C3 J' vpartners.6 However, when a shirt covered the applica-6 [* k, ]# T6 A5 _: C
tion site, this testosterone transfer was prevented.
' ?2 j4 w3 y/ a* m! a1 ROur patient’s testosterone level was 60 ng/mL,
* e0 ]7 A; U  I3 C- Rwhich was clearly high. Some studies suggest that
* O' |8 b: C1 b8 L6 j* fdermal conversion of testosterone to dihydrotestos-
0 N& v% G$ K" [( ]2 Sterone, which is a more potent metabolite, is more
/ S" ^0 {  j: |/ V% Aactive in young children exposed to testosterone5 n7 o( a. }. y6 e( i
exogenously7; however, we did not measure a dihy-! C1 t6 A" c: S+ y! B5 ^$ a
drotestosterone level in our patient. In addition to0 B& f* v9 v+ h7 Q) e4 L2 u% |
virilization, exposure to exogenous testosterone in
6 x% M8 p# x. W% qchildren results in an increase in growth velocity and
! C% ^" h. ]1 uadvanced bone age, as seen in our patient./ l6 y: @6 P0 T% Z; E% h$ c# ^
The long-term effect of androgen exposure during
: ]5 v3 @* ~9 Wearly childhood on pubertal development and final1 t6 y9 a, o1 n# r2 T% Y2 m- `: x
adult height are not fully known and always remain
9 E  d1 x: g3 h9 v" t* |a concern. Children treated with short-term testos-3 y) y! i. ^! N: }
terone injection or topical androgen may exhibit some
  _3 \! ^; h" j. \" e+ ~acceleration of the skeletal maturation; however, after+ `/ f0 {9 X) Y8 h7 `; t  q7 y
cessation of treatment, the rate of bone maturation
3 l6 O5 Q7 e6 T" H$ G4 ddecelerates and gradually returns to normal.8,9& x" Y4 x$ R3 _, b
There are conflicting reports and controversy, I, s) y) S' }5 Q9 ^; o: ?, R7 n
over the effect of early androgen exposure on adult
8 f. y% r; Q) a6 t  d' D; Wpenile length.10,11 Some reports suggest subnormal9 u7 u; h' H  D( S# b$ ?& P2 A
adult penile length, apparently because of downreg-( H: z1 A( p- Y
ulation of androgen receptor number.10,12 However,
. Z! `  C/ V% ESutherland et al13 did not find a correlation between( q2 i8 z8 W8 |; m/ W$ U
childhood testosterone exposure and reduced adult
- m2 N4 Y; p( C8 z3 n1 I! ^penile length in clinical studies.
& v9 p; e& e7 j5 m+ D( @Nonetheless, we do not believe our patient is" T6 I  L; c0 f% e
going to experience any of the untoward effects from
. H, x( L$ \0 a. ^testosterone exposure as mentioned earlier because
& r; ^7 y& h6 p7 Mthe exposure was not for a prolonged period of time.
" F. f" J* ^/ H( ?0 LAlthough the bone age was advanced at the time of5 e! k) `7 x/ q
diagnosis, the child had a normal growth velocity at* M3 V5 ^/ H+ [1 `& F3 p" H& k
the follow-up visit. It is hoped that his final adult
5 i2 S% U- n! O! Qheight will not be affected.3 `5 {6 M: |$ q& |' y5 C
Although rarely reported, the widespread avail-
7 k& s+ h7 S. v" I4 r9 {/ yability of androgen products in our society may
! c2 y' c5 u. W+ l1 u$ v! S9 Mindeed cause more virilization in male or female
8 T+ c" v6 ~9 Q% U; Achildren than one would realize. Exposure to andro-  }- R6 l  ~7 b3 i8 i
gen products must be considered and specific ques-. i! ^7 Z" F8 y. W: R
tioning about the use of a testosterone product or' B+ R, p$ e0 Z4 M5 E
gel should be asked of the family members during3 L. W$ [2 s, y8 {! u2 ^+ k
the evaluation of any children who present with vir-
& w* k* g3 c3 C5 Lilization or peripheral precocious puberty. The diag-
; j4 W( N; T/ qnosis can be established by just a few tests and by- E& k' Z6 J) \, I: [  g
appropriate history. The inability to obtain such a& s0 W, s2 h- c1 t6 }7 N7 t" z
history, or failure to ask the specific questions, may
' x2 f8 b  |2 ~: t8 jresult in extensive, unnecessary, and expensive
6 P8 v/ d; h! _investigation. The primary care physician should be  x5 t1 Q7 U7 ]7 q4 Q* r, C
aware of this fact, because most of these children4 u& Q0 M1 n4 _# ]* J' h
may initially present in their practice. The Physicians’
! u& r: Y! o& R0 u, a) x0 dDesk Reference and package insert should also put a3 X) H8 P/ ?( \  C- T
warning about the virilizing effect on a male or; Q  Z' M8 g. {, C& \
female child who might come in contact with some-
3 E/ b3 y& O, S2 ]# Q4 ^one using any of these products.
5 e( y$ s  h8 p1 G! B, gReferences0 M" n+ v; X4 F6 p
1. Styne DM. The testes: disorder of sexual differentiation
7 @  f" ]/ ]5 z; Kand puberty in the male. In: Sperling MA, ed. Pediatric0 z! l! w) D4 V; N) d* |
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  d; G# l( z; N3 J0 \1 L) w
2002: 565-628.
6 M+ |' \' y& ~' j  P2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
8 \, V6 d9 w; i7 Y, _( r+ Npuberty 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
/ p1 k0 h( G) u
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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