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Sexual Precocity in a 16-Month-Old
  q: b& o. I: N; q! B" H4 E3 P8 eBoy Induced by Indirect Topical: f0 z" U$ M3 Q1 w2 O3 c
Exposure to Testosterone
" U( f9 G7 @% G& J4 c3 [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 i" ]" Q4 o/ T4 Hand Kenneth R. Rettig, MD1( @! i4 T( O" r8 y: D- ?- e3 H% |
Clinical Pediatrics
4 M/ f5 P# V( c0 Q" {  nVolume 46 Number 6' Q0 D# w7 ~5 K" Z' R
July 2007 540-543( |( V( v/ `6 ?6 @2 \, x! n9 B; `
© 2007 Sage Publications
' N) `$ g' K: W1 i; F& c10.1177/0009922806296651
& Q% Q0 b/ N" F) c- _http://clp.sagepub.com+ D1 e( e0 g& |3 T" ~
hosted at4 v) S- C8 {3 p1 l; r7 m
http://online.sagepub.com
) ^* Y+ U" V. {* L/ mPrecocious puberty in boys, central or peripheral,  U! B: I; t  k; O% M: [8 c
is a significant concern for physicians. Central% ~) _3 G9 b$ G) K' ?1 a: I5 k8 |
precocious puberty (CPP), which is mediated; Y3 e+ h# U" B
through the hypothalamic pituitary gonadal axis, has
% W( m; B: y: @1 \" V9 z0 La higher incidence of organic central nervous system9 K# I2 [  D( o4 l9 h
lesions in boys.1,2 Virilization in boys, as manifested
; b) O3 G1 Q2 Aby enlargement of the penis, development of pubic
5 g# _* N2 g  z8 qhair, and facial acne without enlargement of testi-7 v; g6 \  d0 i8 p7 X" C& F% {
cles, suggests peripheral or pseudopuberty.1-3 We/ W5 ~9 \- C  X( `$ \; E) P( v
report a 16-month-old boy who presented with the0 e9 c6 B! z7 O
enlargement of the phallus and pubic hair develop-
( `* @1 P# p( n" rment without testicular enlargement, which was due* Q" R/ M0 {7 O4 w6 t0 H
to the unintentional exposure to androgen gel used by
* y' a) ^1 I0 hthe father. The family initially concealed this infor-
9 U! X6 _& l+ E4 ^0 e6 dmation, resulting in an extensive work-up for this
3 m* s" R3 h2 h' ^child. Given the widespread and easy availability of
; y2 U% }3 N" ]5 ^+ atestosterone gel and cream, we believe this is proba-& Z" R* \% b( t, I$ Z9 B
bly more common than the rare case report in the+ p# w1 l6 i! [
literature.4
. U* }/ }  Z) R, o6 q& m) XPatient Report! u6 P+ Y4 g  }) @# Z2 c
A 16-month-old white child was referred to the7 O% I  f3 ~+ B/ I/ ]- k- e, v
endocrine clinic by his pediatrician with the concern. H. M& l6 `& n2 k6 k5 k) u
of early sexual development. His mother noticed0 I0 v% Q  p3 p1 a* m8 n
light colored pubic hair development when he was
5 N: t0 k5 g2 ?" ^% o7 |  H3 WFrom the 1Division of Pediatric Endocrinology, 2University of; L1 E0 Q0 f' d  a: W
South Alabama Medical Center, Mobile, Alabama.
& o/ ?1 U: Q" k/ Y, ZAddress correspondence to: Samar K. Bhowmick, MD, FACE,
2 |9 A9 N6 E& ~- H5 `! tProfessor of Pediatrics, University of South Alabama, College of! u' S5 \& i8 ^2 j! b
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 v2 P7 _9 O0 B
e-mail: [email protected].1 B9 A  m/ `7 n
about 6 to 7 months old, which progressively became
  C9 M7 g+ n, h9 j  ]1 D1 R/ ~darker. She was also concerned about the enlarge-
& F, I' H( ]& S+ Tment of his penis and frequent erections. The child
& S+ d. I( V% e; A( mwas the product of a full-term normal delivery, with, {! l. _6 ]5 v$ d9 U" |  @7 @
a birth weight of 7 lb 14 oz, and birth length of
3 H& a/ |3 d6 y. a( ?20 inches. He was breast-fed throughout the first year
( X" Y. j2 }$ I" \8 A" x- aof life and was still receiving breast milk along with2 }. `% D7 J6 d4 Y- b- z
solid food. He had no hospitalizations or surgery,/ a. M% b! [# v+ S8 e3 Y- H
and his psychosocial and psychomotor development' J% U; X7 p9 o2 ?) i- K
was age appropriate.: K6 {  t/ h0 d) J
The family history was remarkable for the father,
- ?2 B) b# ^. f  O" q" A# d+ H0 ^; X# Cwho was diagnosed with hypothyroidism at age 16,
0 I. ?% G  ]/ K, I, o+ j7 Mwhich was treated with thyroxine. The father’s4 w$ L+ N; j. t6 M2 G) P
height was 6 feet, and he went through a somewhat- N) c8 x* f; @) c% V
early puberty and had stopped growing by age 14.9 q: O( i' G0 m( L
The father denied taking any other medication. The
7 R4 z- z5 N7 e4 }; n0 bchild’s mother was in good health. Her menarche. q* N6 u4 u9 _) S3 Y; K8 z
was at 11 years of age, and her height was at 5 feet  F. h, a1 t9 Q$ ?4 L
5 inches. There was no other family history of pre-5 S* X5 n8 D* G$ n. A  j
cocious sexual development in the first-degree rela-
/ c$ M$ o3 V0 p2 ]3 [tives. There were no siblings.
* V. R$ l" g* ~7 Y# aPhysical Examination
9 ~8 K* h5 r9 h$ m! \2 FThe physical examination revealed a very active,
; F3 B- }* m7 p% D$ F: P7 |0 c- p8 _playful, and healthy boy. The vital signs documented
% ]) C+ E: r) pa blood pressure of 85/50 mm Hg, his length was& x2 q- W7 z9 ]# I" w7 Q
90 cm (>97th percentile), and his weight was 14.4 kg
0 G. P- S9 E) l(also >97th percentile). The observed yearly growth0 Q6 R- ^- W, d2 R  l9 R9 X8 P
velocity was 30 cm (12 inches). The examination of8 Q0 X  G: y8 {* e2 Z7 ~
the neck revealed no thyroid enlargement.
+ ^$ R6 O/ I, b+ ]) x$ Y1 }The genitourinary examination was remarkable for# [& Y# T. }4 k" \, U
enlargement of the penis, with a stretched length of8 w  m2 c6 F+ l9 j+ k9 o
8 cm and a width of 2 cm. The glans penis was very well
2 Q. V, d) Y. n: x+ u, |0 R* gdeveloped. The pubic hair was Tanner II, mostly around/ @" g/ d. ~0 H0 ?& F( r% E
540, q6 q( ]8 v! {3 y8 p8 H5 g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) K  Y) }" a& F4 o3 L
the base of the phallus and was dark and curled. The0 \5 X% d5 O1 d, j! p
testicular volume was prepubertal at 2 mL each.3 `. }( F" V( i8 w* ]# }! E
The skin was moist and smooth and somewhat' N# o0 I7 r- g% J5 Z7 ?3 M! `
oily. No axillary hair was noted. There were no
9 _! N( @+ M+ g  vabnormal skin pigmentations or café-au-lait spots.! ]9 _) S9 T8 b9 [
Neurologic evaluation showed deep tendon reflex 2+0 m3 }5 p0 s4 V$ t+ Q4 j- M
bilateral and symmetrical. There was no suggestion
  D& c9 ]# |$ l% Pof papilledema.
% I+ x( G% G5 @% `7 v- i( fLaboratory Evaluation! P; F5 ?/ {; F2 m8 z; e" o2 e
The bone age was consistent with 28 months by0 B' _% g8 y7 B  `' I4 {- h
using the standard of Greulich and Pyle at a chrono-. y! U& @4 t, B0 t
logic age of 16 months (advanced).5 Chromosomal" j. K: e9 ~9 p) n
karyotype was 46XY. The thyroid function test
) o: H7 k- N. O, M2 N* L1 Yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
" P% D0 D$ |2 L. R1 S8 c$ [lating hormone level was 1.3 µIU/mL (both normal).
, T: d" X8 O$ A( X& mThe concentrations of serum electrolytes, blood9 ]0 A8 O+ z( `# f8 O3 `
urea nitrogen, creatinine, and calcium all were
! T7 R% _$ X7 a! ]7 W7 i# `within normal range for his age. The concentration( @% c1 r7 s3 j" T, ^+ c
of serum 17-hydroxyprogesterone was 16 ng/dL5 e. N" ?% ^3 b1 ^/ f% \3 v/ S
(normal, 3 to 90 ng/dL), androstenedione was 208 m3 K% V- T* {' G+ w, V0 V: b0 T
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, g5 L7 x" S4 R9 |1 J7 v  {terone was 38 ng/dL (normal, 50 to 760 ng/dL),
  J7 b. Y6 w  X  {( a3 wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to" f; E5 [: G! B: m
49ng/dL), 11-desoxycortisol (specific compound S)
- [5 a' S- ~8 q4 S0 L6 Xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 l7 F1 I$ K" m" p6 ^* A. W
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& n# @8 w' k0 g6 W4 R' Q0 F; Jtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
6 i3 h, V: w& {! [# A" oand β-human chorionic gonadotropin was less than
6 s" c/ P3 M8 a. f: K, p8 @5 mIU/mL (normal <5 mIU/mL). Serum follicular
& j# f/ v3 J2 P9 {8 y3 Astimulating hormone and leuteinizing hormone
" `, B9 W. c( s# X$ z# a! i5 lconcentrations were less than 0.05 mIU/mL
+ P' q. c( \$ q! Z4 w2 n2 K(prepubertal).; t" ]9 j# B5 H+ y8 q' ]5 T% [+ l: E+ P
The parents were notified about the laboratory  k+ Q) T% o7 v$ Y- Y# Q( `
results and were informed that all of the tests were+ J$ b3 d4 u% |; K. E0 \
normal except the testosterone level was high. The
* H! z3 L8 m* q0 {follow-up visit was arranged within a few weeks to  }9 B; Q4 e. d+ ]# q0 j& h4 `( D4 I
obtain testicular and abdominal sonograms; how-
: z3 a2 F) I: n* k" f) mever, the family did not return for 4 months.1 n  h+ O" Z0 Z
Physical examination at this time revealed that the
8 }# `& Y3 X- ^' R0 y& o& bchild had grown 2.5 cm in 4 months and had gained7 U  o& _" @7 e4 l
2 kg of weight. Physical examination remained
# ]% l7 H" u- \- b7 b9 {unchanged. Surprisingly, the pubic hair almost com-
  A' j, R) c5 ?- @, ?9 o, F4 C* xpletely disappeared except for a few vellous hairs at
6 H: _1 F, n" e( c/ z+ ~the base of the phallus. Testicular volume was still 2
& ]5 i4 }% p% \- X0 d6 A# NmL, and the size of the penis remained unchanged.
: Y2 a( u& d  p( ]The mother also said that the boy was no longer hav-4 f  @, L  w$ q& M0 F6 D
ing frequent erections.. o$ Z/ A6 r  |4 ]4 I
Both parents were again questioned about use of! g9 z7 M; D3 F, o8 f8 G/ m
any ointment/creams that they may have applied to
' X3 A7 o) M9 N% cthe child’s skin. This time the father admitted the, p( M3 R3 z# w) V
Topical Testosterone Exposure / Bhowmick et al 541
& y# E0 L1 g- s( kuse of testosterone gel twice daily that he was apply-
1 [. E/ S' _6 Q- {& ming over his own shoulders, chest, and back area for5 o3 Z, m+ s7 m' c0 k# j4 V" G! @% ?
a year. The father also revealed he was embarrassed9 g" U1 c* ?$ o' N2 b( S
to disclose that he was using a testosterone gel pre-
# d8 W3 B1 G, x" gscribed by his family physician for decreased libido
6 e& D* m$ i1 R+ o+ Fsecondary to depression.3 Q1 J, x; ^6 B9 p, ]' U8 p
The child slept in the same bed with parents.
9 n! u& ^- C( `8 B4 y6 pThe father would hug the baby and hold him on his7 L* Z: i( p! B
chest for a considerable period of time, causing sig-$ {( ?* R5 ^6 _+ x; m/ W
nificant bare skin contact between baby and father.& A" I% `+ Y1 [3 t" S6 U( I
The father also admitted that after the phone call,
$ \% g  p% `% fwhen he learned the testosterone level in the baby! ]( P( l7 k: z4 m6 S6 q# Q
was high, he then read the product information
3 L8 W* i+ r" b: H, fpacket and concluded that it was most likely the rea-
' Q; z8 v  j. c8 o9 uson for the child’s virilization. At that time, they* R6 R8 X* L$ Y# U3 f- v
decided to put the baby in a separate bed, and the
8 q- f" V" }, ^+ }$ l! qfather was not hugging him with bare skin and had0 s& t$ X4 L& F2 n2 ]
been using protective clothing. A repeat testosterone! r% v$ M& R8 K9 f) m; L0 b' d
test was ordered, but the family did not go to the
( o9 q' o1 z6 Slaboratory to obtain the test.
/ S" g" A  u. ^+ HDiscussion+ k: I. c" D) g- `5 H6 E
Precocious puberty in boys is defined as secondary
% n3 v, U4 D% \) i: usexual development before 9 years of age.1,40 V7 ?1 \$ [4 O; y
Precocious puberty is termed as central (true) when
. c" r% x( m7 Y5 S, dit is caused by the premature activation of hypo-
2 M2 @7 X/ {# i8 I' u( \thalamic pituitary gonadal axis. CPP is more com-  x6 n6 n: i. H: }; w
mon in girls than in boys.1,3 Most boys with CPP, A! B2 C. K; A5 g3 `
may have a central nervous system lesion that is
4 M; g! A  e3 S: B3 j4 Q6 J% `& lresponsible for the early activation of the hypothal-
: x6 k+ D. t, ramic pituitary gonadal axis.1-3 Thus, greater empha-+ l/ |. e, v) E, V3 i
sis has been given to neuroradiologic imaging in6 y+ Y/ O% d9 |: c8 w
boys with precocious puberty. In addition to viril-
" H) E8 d5 i7 v( Aization, the clinical hallmark of CPP is the symmet-
0 ?* a( a5 x$ D9 B  x: c# Y2 Jrical testicular growth secondary to stimulation by
2 h% C! l- q$ I& E. ~% _gonadotropins.1,35 ?% M) Y1 W! p/ f
Gonadotropin-independent peripheral preco-
" B; g$ p* V& I+ v: w7 q4 Xcious puberty in boys also results from inappropriate) m3 ]1 t3 b! P# R# A
androgenic stimulation from either endogenous or
$ w- }2 L0 A; P9 s0 ]. u) yexogenous sources, nonpituitary gonadotropin stim-
/ H6 r" n: C9 q( R  H7 q6 Zulation, and rare activating mutations.3 Virilizing8 i' R; a# [- L% B2 f$ v+ D; g
congenital adrenal hyperplasia producing excessive
1 v- a" F2 r2 |; Q9 {. ~3 kadrenal androgens is a common cause of precocious$ s: j, `4 K! D% a
puberty in boys.3,43 x6 Q, Q. |9 {: C! K: e
The most common form of congenital adrenal
  D0 r5 o$ d& B0 Rhyperplasia is the 21-hydroxylase enzyme deficiency.& w% ~' n; C9 h1 T
The 11-β hydroxylase deficiency may also result in6 F. L# A0 k7 s3 R1 l* s/ T, N
excessive adrenal androgen production, and rarely,# k( f  X- @/ N  n  ^3 T; n! L
an adrenal tumor may also cause adrenal androgen
7 p1 ~) u+ R' W# lexcess.1,3- `7 m% m) l- ]3 D  H& N0 k- U
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 f6 Q  K5 k: T% t  B) i4 S542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, @5 T. M% e# O0 H$ ^8 @A unique entity of male-limited gonadotropin-8 N" l) y- J/ o; U& ~
independent precocious puberty, which is also known6 U8 J( w* j5 L# M0 [0 m' V
as testotoxicosis, may cause precocious puberty at a
: K# d: N; _. i: L8 g, Svery young age. The physical findings in these boys
& M6 H2 s$ W9 X$ ~: N4 m" q4 hwith this disorder are full pubertal development,
$ P/ a8 D3 t/ e# F% [0 cincluding bilateral testicular growth, similar to boys! o, u6 Z9 [0 y! F
with CPP. The gonadotropin levels in this disorder' n' o9 W, t4 l
are suppressed to prepubertal levels and do not show* s" Z3 i! G0 M: p8 K! H
pubertal response of gonadotropin after gonadotropin-  n! K1 g) x# n0 K6 t
releasing hormone stimulation. This is a sex-linked
- x1 x! p  s$ v& Q3 L& aautosomal dominant disorder that affects only1 K, \7 A; C! L! d3 I
males; therefore, other male members of the family: P  J5 q, u: e5 Q
may have similar precocious puberty.3& E- i0 C3 X1 [3 v
In our patient, physical examination was incon-
0 M- {6 C  G8 P) l2 }7 tsistent with true precocious puberty since his testi-
, F9 Z; E' t" x' Gcles were prepubertal in size. However, testotoxicosis# a% u: R9 S) F# z8 c
was in the differential diagnosis because his father# c' |: ^+ b. I# Z" L
started puberty somewhat early, and occasionally,( Y) d$ ]5 _: ], v1 e4 \
testicular enlargement is not that evident in the
) m! ]- N) L: _3 a- L1 f: Ebeginning of this process.1 In the absence of a neg-
) i% ~9 q9 i( p) hative initial history of androgen exposure, our
' B* s* _, _: p, R  ?biggest concern was virilizing adrenal hyperplasia,
0 U* p0 q* {& ^0 F5 M6 q+ f  g5 |3 Teither 21-hydroxylase deficiency or 11-β hydroxylase: i+ N1 U! F, [/ i
deficiency. Those diagnoses were excluded by find-5 A( B1 k4 `) d6 @0 }8 H% }
ing the normal level of adrenal steroids.+ ^  K* T6 w4 N" D- z
The diagnosis of exogenous androgens was strongly- P, F, G; a. k3 `3 U/ [
suspected in a follow-up visit after 4 months because8 U  L" s4 h+ G) _  P" o. I2 u
the physical examination revealed the complete disap-
  _. [2 t  r  h. N" bpearance of pubic hair, normal growth velocity, and: V, {# ]# w* o; c! g  q
decreased erections. The father admitted using a testos-
) y$ t7 I7 E+ T5 fterone gel, which he concealed at first visit. He was. _9 y- o6 V9 ]+ C) x
using it rather frequently, twice a day. The Physicians’2 g- a+ Q* t' u' c; d3 j' d
Desk Reference, or package insert of this product, gel or5 U0 \8 f$ N* q
cream, cautions about dermal testosterone transfer to
# g, m" o- Z- T: f7 I6 kunprotected females through direct skin exposure.
. s+ v+ i! ?( p6 t& l) U7 QSerum testosterone level was found to be 2 times the
0 }4 Z. E# J/ c3 H# w  E3 G  tbaseline value in those females who were exposed to
  Y1 R& b, {+ Y$ Z8 ^5 R; aeven 15 minutes of direct skin contact with their male
$ o- ?6 c/ C* [* G8 U6 w/ npartners.6 However, when a shirt covered the applica-
2 l- {0 A' Y) \3 O- ktion site, this testosterone transfer was prevented.# a, G; b$ s" t7 [9 U: v) ]0 x
Our patient’s testosterone level was 60 ng/mL,  q1 s' _- q* Y) `+ h% T5 c
which was clearly high. Some studies suggest that# f5 R2 F+ Y) T. F
dermal conversion of testosterone to dihydrotestos-
" Q( S8 ~0 T! v. C% e% n2 Oterone, which is a more potent metabolite, is more
5 H, ?) y; {+ F8 |1 j( V' e7 X9 sactive in young children exposed to testosterone
1 y" h- |- w- N" @0 s3 Hexogenously7; however, we did not measure a dihy-
+ c3 }; [- V7 z+ S; k3 s0 f/ ]6 x- d# U, jdrotestosterone level in our patient. In addition to
# J( M& E/ A& D" Xvirilization, exposure to exogenous testosterone in5 P' U: b* Q8 {0 t# H) V" N8 G# D
children results in an increase in growth velocity and
& g5 w+ E2 E7 m+ b% q* ~* @0 gadvanced bone age, as seen in our patient.$ n; |( J0 Z0 F* O3 [8 r' I
The long-term effect of androgen exposure during" D- o. m- M8 C( s" x- w1 X
early childhood on pubertal development and final
* {0 h& ^  q1 `1 l! z, k% Gadult height are not fully known and always remain: A0 o, y0 c% W+ n" j2 Y& r- x1 F
a concern. Children treated with short-term testos-
* j! H4 Z; n; N& H- ~terone injection or topical androgen may exhibit some; h% [5 _! \2 [2 S1 ?
acceleration of the skeletal maturation; however, after$ a  d0 G' ]2 w/ w0 A
cessation of treatment, the rate of bone maturation
# M4 a8 l* m9 e0 rdecelerates and gradually returns to normal.8,9
! S  l; M4 e$ D3 y9 iThere are conflicting reports and controversy
- g9 i/ v; ]5 C2 `, Mover the effect of early androgen exposure on adult
- Q+ F" D) F; x5 Npenile length.10,11 Some reports suggest subnormal
  ], h# ]' q) b: q* R  madult penile length, apparently because of downreg-) v4 ], y% A7 l( N  ?
ulation of androgen receptor number.10,12 However,* ~! K7 r1 B) U+ J$ _
Sutherland et al13 did not find a correlation between& O# `4 y" L3 G) N; k  U; H6 G
childhood testosterone exposure and reduced adult1 N' ~3 g8 m: k
penile length in clinical studies.
. Z) I' X8 u* v2 ~8 pNonetheless, we do not believe our patient is
- ?5 \% l4 I  ?+ P* `% t2 Zgoing to experience any of the untoward effects from! ?( N- S; L7 \; U' B4 \
testosterone exposure as mentioned earlier because; j) e" P5 x. f
the exposure was not for a prolonged period of time.$ U; L' T& W9 s  [3 v# T, K
Although the bone age was advanced at the time of
8 T5 u) X5 i' ~: K& pdiagnosis, the child had a normal growth velocity at; [4 a5 Z3 c0 u+ G
the follow-up visit. It is hoped that his final adult
2 I& m& X5 S; c& }6 M9 z# Yheight will not be affected.
$ k( K9 j& F, W7 K0 s* a: A3 ~Although rarely reported, the widespread avail-9 u! X4 C& s" }
ability of androgen products in our society may
$ f# _% v( X3 R* e2 {indeed cause more virilization in male or female
! S1 a9 ?, v" v6 @0 x, ~children than one would realize. Exposure to andro-* W( h; W5 d! k1 M& x  m
gen products must be considered and specific ques-
1 u6 ?+ |6 E/ p, [  Etioning about the use of a testosterone product or
& |/ [/ @- H% egel should be asked of the family members during
& E  P* A3 T% S  ~the evaluation of any children who present with vir-4 W( Y. [; }* `: }; J6 E3 H% Q. d: Q
ilization or peripheral precocious puberty. The diag-) U( y- f& c; x  z9 c, O) ^# B
nosis can be established by just a few tests and by
+ p& q+ ~' M. F6 iappropriate history. The inability to obtain such a
  X8 V- [$ u1 V# y# ghistory, or failure to ask the specific questions, may2 b1 r; F1 T! \$ U1 b! l) A# {
result in extensive, unnecessary, and expensive
& Q1 q  M4 e7 V$ H! m9 i, J" ainvestigation. The primary care physician should be
# X) Y# |/ z% t$ u* ]$ \$ yaware of this fact, because most of these children! t+ b. {; H) V% \# H4 ^7 J  ]
may initially present in their practice. The Physicians’
( P( A7 X- N0 J, F& qDesk Reference and package insert should also put a
* M8 A2 ~1 Y/ ~warning about the virilizing effect on a male or
0 N2 ?0 f: D  L6 t6 B, _female child who might come in contact with some-
0 _0 s' u7 z6 k: v) b2 U6 pone using any of these products.8 E3 d, Z1 k$ C2 }  J6 G
References
2 p$ S" O/ o- U5 `* @7 J0 P1. Styne DM. The testes: disorder of sexual differentiation' ^4 F' I$ C1 Z8 x' M6 H
and puberty in the male. In: Sperling MA, ed. Pediatric
: @9 Y; ?- t. P3 l: F- IEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 ?& M' |* p6 X& H' h7 {
2002: 565-628.! h4 S% H, S6 f0 L- U
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ ]& W4 }7 j6 f5 B7 S" y8 gpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old( ]9 G+ j5 t9 [
Boy Induced by Indirect Topical
- T6 M* R$ ~4 B# [Exposure to Testosterone
" Q* r/ k% k" R- m2 q( T. }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; h9 t) P8 m3 S) h; J, J
and Kenneth R. Rettig, MD1
4 e+ J$ T4 N# d0 i* c$ T, o9 TClinical Pediatrics
! R& l* r$ L7 T$ _% UVolume 46 Number 6
+ F0 ]7 }% v* T  V# N- a! R  CJuly 2007 540-543) P/ M3 S) U  m, l2 t
© 2007 Sage Publications
; K& y7 D8 ]: {" H9 o: k' N10.1177/0009922806296651
) v) p3 v0 L/ ^' F- @http://clp.sagepub.com
) M% t% f& J# Y1 c7 q. b# thosted at# w' C3 p/ I5 R/ \( o
http://online.sagepub.com
* Y! k% d2 |7 z9 [: {7 t$ XPrecocious puberty in boys, central or peripheral,
0 j$ c- x/ [/ Pis a significant concern for physicians. Central
$ }. l) T3 Y) eprecocious puberty (CPP), which is mediated
) T' B$ d, E4 j* Dthrough the hypothalamic pituitary gonadal axis, has
: u. D7 g2 }: }$ oa higher incidence of organic central nervous system2 X9 |4 J& [# d! U) L& h8 k6 K2 X
lesions in boys.1,2 Virilization in boys, as manifested! N3 h+ x! Z. |, M# p
by enlargement of the penis, development of pubic
  Q6 Z4 V" o$ k! ]/ t0 Z" o" jhair, and facial acne without enlargement of testi-; E4 I3 i: X6 n& A9 H
cles, suggests peripheral or pseudopuberty.1-3 We
0 F4 K' Y" R" G% L) R: ?) vreport a 16-month-old boy who presented with the
+ X  }( s  J1 `' Henlargement of the phallus and pubic hair develop-" ?: {) f' F  m4 F: f
ment without testicular enlargement, which was due
; ^  M, t3 P- ~& f6 q& j7 k; ^8 T9 ito the unintentional exposure to androgen gel used by
4 m/ R  J$ Q' Qthe father. The family initially concealed this infor-
+ o3 g' p0 b/ o1 B5 t/ Vmation, resulting in an extensive work-up for this
4 r% y% h! U) t* T' T8 }' G! Echild. Given the widespread and easy availability of
" t8 g! X0 J/ R6 s# h) K$ R( Vtestosterone gel and cream, we believe this is proba-
: i& R+ ?) Z8 u( y4 K$ x3 p) Qbly more common than the rare case report in the. ?2 E% f5 x) a6 G
literature.45 d* \8 l+ j1 ]% {' i0 q& p4 P
Patient Report  d- H: T. B' c& U. L2 v
A 16-month-old white child was referred to the
. s3 T; l. B" J( ]* s/ D7 Yendocrine clinic by his pediatrician with the concern) v" m- D, T. D" x- Z
of early sexual development. His mother noticed& d- H% N3 O. |! k' k0 A# j# l
light colored pubic hair development when he was8 T. V6 k+ Q, ]$ R; H
From the 1Division of Pediatric Endocrinology, 2University of
, o' ?; Z" g- ~5 y  aSouth Alabama Medical Center, Mobile, Alabama.
5 L- I' P4 |9 @8 PAddress correspondence to: Samar K. Bhowmick, MD, FACE,
/ G2 i5 |/ c3 [Professor of Pediatrics, University of South Alabama, College of6 H4 @' y# |+ g, \& s" ?4 \9 m, |
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* G! e) y0 h( s7 _# z
e-mail: [email protected].( D* a$ c  s- l" {, q
about 6 to 7 months old, which progressively became
/ p" W6 q- C! S" [/ ^1 ^darker. She was also concerned about the enlarge-( S/ N" Q9 F4 Y! e/ u
ment of his penis and frequent erections. The child
6 U; {9 R) y2 H& l# ?- S& e; Hwas the product of a full-term normal delivery, with
, }" I$ R" {5 p7 {1 h# d6 a7 na birth weight of 7 lb 14 oz, and birth length of7 l- Q8 ?/ `3 X  I: a
20 inches. He was breast-fed throughout the first year1 b! ^2 X, N7 b6 {% _: m$ t) j
of life and was still receiving breast milk along with
2 U$ p5 f8 y3 r7 ^# K! b8 Q; Rsolid food. He had no hospitalizations or surgery,7 E. V* X6 T4 k1 |4 L# |) D. p' o
and his psychosocial and psychomotor development
4 j& H" g2 L/ o; rwas age appropriate.
7 u2 r4 E6 o$ U$ sThe family history was remarkable for the father,
, Q8 d8 X, R/ ^$ Ewho was diagnosed with hypothyroidism at age 16,$ l$ A+ S7 t# G# N
which was treated with thyroxine. The father’s
2 U6 q& E6 y( E. J$ hheight was 6 feet, and he went through a somewhat: V7 S; S5 u* C, c2 Y) a
early puberty and had stopped growing by age 14., g  d% g7 i' o- P# C2 f
The father denied taking any other medication. The
; E& Q  n6 O" p& d7 j7 wchild’s mother was in good health. Her menarche& J, d7 q* g- z, i' L# }
was at 11 years of age, and her height was at 5 feet9 @* a& s, [( J- f/ k9 X& x
5 inches. There was no other family history of pre-- k. q: l# p2 W1 T7 ]. ~0 _  C
cocious sexual development in the first-degree rela-
' I9 T' ?4 \8 P# Ctives. There were no siblings.
* v: N3 P( ^% a( T% R0 y  YPhysical Examination
& C6 D% d  `3 u1 S4 dThe physical examination revealed a very active,; n7 }# _# u* R+ h
playful, and healthy boy. The vital signs documented
6 u3 U$ E3 n8 |# Qa blood pressure of 85/50 mm Hg, his length was
+ U( D7 V' w! a. H8 y* W$ H90 cm (>97th percentile), and his weight was 14.4 kg
* E, U9 i3 ~& X( t; Q(also >97th percentile). The observed yearly growth& _& `) k* c9 `% |* H2 {2 d
velocity was 30 cm (12 inches). The examination of. b9 j- v$ V! K) i7 b0 v
the neck revealed no thyroid enlargement.
$ ]) V# Y4 N; L/ l$ rThe genitourinary examination was remarkable for, H6 Y! i: X5 H" b
enlargement of the penis, with a stretched length of
3 O, Y, H+ R7 K" X: S8 cm and a width of 2 cm. The glans penis was very well0 |3 b$ k# C, B5 z7 C' l/ T
developed. The pubic hair was Tanner II, mostly around
  p% ]9 n  d8 e% l" X5 N5402 ?% d- W8 A! v6 R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  O, ^  A. [0 f; C; Y# e
the base of the phallus and was dark and curled. The
, J) O% h/ p5 K' ]/ Ktesticular volume was prepubertal at 2 mL each.9 n% M* I( Y/ C. i1 H- B
The skin was moist and smooth and somewhat4 L# I2 I/ H7 ]! j, `. k
oily. No axillary hair was noted. There were no
: |4 `% _7 A+ P& N$ Xabnormal skin pigmentations or café-au-lait spots.
4 k% n2 S+ ?9 s& b) J1 {* pNeurologic evaluation showed deep tendon reflex 2+
. a$ \0 ?: K$ k2 x8 Y& |" ]6 \bilateral and symmetrical. There was no suggestion7 g' ]1 Q7 @" S% v( ]; g8 K4 ^: A
of papilledema.
$ D8 P& x1 A: E- |' Z- gLaboratory Evaluation
2 R& d, o+ e) E) y4 I& w$ I1 {1 E5 sThe bone age was consistent with 28 months by9 D3 p9 r1 Y$ @* W
using the standard of Greulich and Pyle at a chrono-6 n* o* Y5 z1 D0 c: s! P$ z
logic age of 16 months (advanced).5 Chromosomal
0 O, f6 N$ @& O5 Y: f% k2 B9 Ekaryotype was 46XY. The thyroid function test
; m/ N# Q# s5 q1 Z8 Kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
. F& h7 R: B* `2 W# t. ylating hormone level was 1.3 µIU/mL (both normal).( s5 |! u3 K  c: P* O! T. [
The concentrations of serum electrolytes, blood
( q$ @  U4 y! h/ u( v" b( A' P5 purea nitrogen, creatinine, and calcium all were0 J! u& ]" A; x* H# V
within normal range for his age. The concentration8 p( W( I2 S4 p
of serum 17-hydroxyprogesterone was 16 ng/dL
& v0 R! p0 i( R2 V4 l6 I(normal, 3 to 90 ng/dL), androstenedione was 20
4 Q, V! P' X) @  e# P& T8 V1 xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- U+ `7 t8 U$ G
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* P3 J: h) U/ g
desoxycorticosterone was 4.3 ng/dL (normal, 7 to) j; o0 \- j9 d8 N4 m$ N
49ng/dL), 11-desoxycortisol (specific compound S)9 J* {' r5 q) @4 v- B5 E' e" s. G
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# G$ X0 B9 y2 J& r5 v- C
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ u( Y7 m- _  m8 E+ O7 e. n
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ X4 o9 H$ Y  x: F9 B# G
and β-human chorionic gonadotropin was less than6 D# P& }: ^; r& K0 [* D9 m
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 y9 `* p/ _3 C. _stimulating hormone and leuteinizing hormone
$ H5 G# P8 U* ^4 {concentrations were less than 0.05 mIU/mL  x$ G$ i4 \( w# D' @7 t( d
(prepubertal).6 l6 \$ U, W9 x+ p, P1 z
The parents were notified about the laboratory! X. S/ l6 p- s" w$ q/ \9 O
results and were informed that all of the tests were
1 `- V1 a- m3 a  W8 Jnormal except the testosterone level was high. The  V  J6 k7 ?4 w
follow-up visit was arranged within a few weeks to
% C4 V9 p; T% }  y2 eobtain testicular and abdominal sonograms; how-
( a! u7 J6 J: r: V3 Gever, the family did not return for 4 months.- g& H! S3 G7 s- o* r+ c
Physical examination at this time revealed that the: x! V7 f  p' W) a
child had grown 2.5 cm in 4 months and had gained8 b- x% \+ X1 U, X6 z
2 kg of weight. Physical examination remained
; P% C* n& F0 U" }7 bunchanged. Surprisingly, the pubic hair almost com-
7 n& B& s! |( h. Ppletely disappeared except for a few vellous hairs at: Y1 E& `- E- U
the base of the phallus. Testicular volume was still 2
7 d' e! v+ ]  G3 t6 e" omL, and the size of the penis remained unchanged.
! r/ `# f/ A2 z5 z3 JThe mother also said that the boy was no longer hav-
/ f( [" y. u8 H6 E/ Z5 q, v5 z' ]ing frequent erections.% z1 L: M3 b' ]4 M
Both parents were again questioned about use of( J( K1 j4 [. ?% k: j
any ointment/creams that they may have applied to9 h9 s: g# O) l+ \& X7 ?
the child’s skin. This time the father admitted the9 f/ ^: g0 r$ I+ Y7 T: D
Topical Testosterone Exposure / Bhowmick et al 541
  ^9 Z- Q& z% s+ }" Duse of testosterone gel twice daily that he was apply-
4 x* ~8 L$ M& @  }ing over his own shoulders, chest, and back area for4 M4 P0 H9 f$ p( Z
a year. The father also revealed he was embarrassed2 h) r5 [' u8 B! a5 V7 Q
to disclose that he was using a testosterone gel pre-
3 ~  P9 I9 ^; |* d: J1 ^, l9 k5 Tscribed by his family physician for decreased libido
" t, E3 p+ a5 D8 n7 {0 h$ c& v: jsecondary to depression.
3 o, l  O! J) ~7 m' E* }The child slept in the same bed with parents./ R) p# l& Q! v, j' s  c) _
The father would hug the baby and hold him on his; _& ^) v- o  G$ o5 y7 P4 f1 Q
chest for a considerable period of time, causing sig-* X: t5 E  k# n0 P0 N
nificant bare skin contact between baby and father.; K5 K1 \" u1 k
The father also admitted that after the phone call,
$ D8 H3 q" U8 H4 ]" Owhen he learned the testosterone level in the baby: K( O9 c1 K: j( q% w9 W
was high, he then read the product information
3 b6 W( a% J9 U: n: Opacket and concluded that it was most likely the rea-
; B0 r' a4 k9 p& ^& \" i* w$ fson for the child’s virilization. At that time, they2 Y& M8 l: D0 ?
decided to put the baby in a separate bed, and the
2 S- R7 U1 j7 H. j2 lfather was not hugging him with bare skin and had
  O: U) o, u2 |4 z1 q9 O# e% [been using protective clothing. A repeat testosterone$ `$ {' q& m# z& B9 D
test was ordered, but the family did not go to the
. C. }  k4 q7 n+ Ilaboratory to obtain the test.
  D8 J8 ]* d7 EDiscussion
: V; d/ p; o- x! \) S. N" |9 vPrecocious puberty in boys is defined as secondary4 h* w! Q3 u  ^$ ?, c+ c
sexual development before 9 years of age.1,41 ~( y% l4 S$ s4 v8 L/ X- U
Precocious puberty is termed as central (true) when6 g" T% J' p! X! g( M4 n
it is caused by the premature activation of hypo-6 F- f2 D% s$ Q( y& G
thalamic pituitary gonadal axis. CPP is more com-
/ ?. Z! d. i+ a( a" O7 G/ ~mon in girls than in boys.1,3 Most boys with CPP& @6 p. J; f( @" u
may have a central nervous system lesion that is  C5 ]7 [1 f- h6 V5 [
responsible for the early activation of the hypothal-
8 `3 _- r5 M6 k3 Aamic pituitary gonadal axis.1-3 Thus, greater empha-7 E1 R8 X3 d; a
sis has been given to neuroradiologic imaging in
+ ?6 H' U5 m, |, T( |boys with precocious puberty. In addition to viril-/ e6 K4 e* S  i* ]; U9 W4 u
ization, the clinical hallmark of CPP is the symmet-& _* h1 C4 {$ N9 n7 l) g
rical testicular growth secondary to stimulation by
* q# O1 M8 j: agonadotropins.1,3
2 p+ }1 [# M% r7 q. dGonadotropin-independent peripheral preco-; {4 {; A  A/ Y! n3 S& P- \
cious puberty in boys also results from inappropriate3 O+ N' k) ?. Q& A% |( o
androgenic stimulation from either endogenous or
% c( E$ ?& K% C# Rexogenous sources, nonpituitary gonadotropin stim-
' i0 J9 U( s" J& Nulation, and rare activating mutations.3 Virilizing
& X1 o6 @) i. m( A( m( @" ?. Acongenital adrenal hyperplasia producing excessive
# N! ?1 P* j; H9 ?9 wadrenal androgens is a common cause of precocious
9 Y8 t, b, b) X2 O2 |puberty in boys.3,49 H% o# N7 {: Z+ F: {
The most common form of congenital adrenal+ N0 j/ n* Z0 z( J
hyperplasia is the 21-hydroxylase enzyme deficiency.! \0 w1 M5 d8 N4 c2 z
The 11-β hydroxylase deficiency may also result in
  S; a7 l4 p! V0 p) M# Pexcessive adrenal androgen production, and rarely," ^! v+ s, h0 U# a+ J" q; B
an adrenal tumor may also cause adrenal androgen
! t$ `' T0 ^, J$ B$ r; _# ~) N1 D8 a6 Xexcess.1,3
3 k; G3 p: _$ F* _$ r, E& \& T* Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) p6 x& W4 g" B, ~/ e  W
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, |2 u3 ~9 m6 T; lA unique entity of male-limited gonadotropin-
: ?4 T$ W& c4 B" F) ~: \: ~7 Y& \4 Tindependent precocious puberty, which is also known
+ V4 `) L! Q! ^3 y  f# nas testotoxicosis, may cause precocious puberty at a- J. k. w$ G" s; C4 Y) [0 v
very young age. The physical findings in these boys
" C: \& V$ i2 u8 C  ~' g! nwith this disorder are full pubertal development,- E8 }! u6 h/ }7 [( C
including bilateral testicular growth, similar to boys
4 k$ i& a' L* R. [$ ]& }+ K$ ~8 mwith CPP. The gonadotropin levels in this disorder
$ i' Q0 I7 k4 care suppressed to prepubertal levels and do not show
6 E6 v- b+ q  Y% Qpubertal response of gonadotropin after gonadotropin-
) b) a: U: P+ J, l0 F9 q7 ereleasing hormone stimulation. This is a sex-linked
8 X* f" O/ J0 F* p9 K; H: I) Zautosomal dominant disorder that affects only
+ q% _" X  n& |) J: [; jmales; therefore, other male members of the family
+ H' }$ ?! L+ U; J& J+ |" Cmay have similar precocious puberty.3  P5 t, n3 K: K/ ^
In our patient, physical examination was incon-
% |: o* O& a9 ^0 rsistent with true precocious puberty since his testi-
1 b8 v( R7 y  A5 Vcles were prepubertal in size. However, testotoxicosis
3 F/ V8 h: a( N# Swas in the differential diagnosis because his father
: S5 A6 V; y! s7 Fstarted puberty somewhat early, and occasionally,
! M% x5 n1 ]& h) Gtesticular enlargement is not that evident in the
/ u0 z6 |. p. ^1 V$ E; t4 a. O! vbeginning of this process.1 In the absence of a neg-/ h. P; d/ c$ s, y( q
ative initial history of androgen exposure, our" C) _6 A0 Z6 j
biggest concern was virilizing adrenal hyperplasia,0 _- X. Y3 V* t0 h& v
either 21-hydroxylase deficiency or 11-β hydroxylase. c$ W6 ?% k! u. o/ E& }5 x
deficiency. Those diagnoses were excluded by find-" E& c' _& h9 l* L7 ^; _% A: A+ ^
ing the normal level of adrenal steroids.
. O6 M* w0 A+ qThe diagnosis of exogenous androgens was strongly  f( s- V) ^" o; m6 X: {: E9 b1 E
suspected in a follow-up visit after 4 months because
: o, s+ g+ k$ j4 fthe physical examination revealed the complete disap-
* l0 i6 u9 q' L6 c" Npearance of pubic hair, normal growth velocity, and
- `4 L5 q  V/ W( ?) V" gdecreased erections. The father admitted using a testos-
% Y' E# ?8 I! M, f7 ~; aterone gel, which he concealed at first visit. He was! @3 C4 q" C2 o. z( Z' K( W! a) R
using it rather frequently, twice a day. The Physicians’  }6 h; v& a. o' t
Desk Reference, or package insert of this product, gel or
) o1 X+ H- n, o; M) O& P# ]cream, cautions about dermal testosterone transfer to) A7 t' y7 M' f, Q' |6 }( P
unprotected females through direct skin exposure.( {5 H. d0 Y7 t9 V$ F; a1 d
Serum testosterone level was found to be 2 times the
5 F# J. L& ^& s& i1 ]2 l2 Dbaseline value in those females who were exposed to" X* K- u. w* E. _& g/ x4 o
even 15 minutes of direct skin contact with their male
# G' _0 b  P5 Mpartners.6 However, when a shirt covered the applica-# a0 D6 I) t  T
tion site, this testosterone transfer was prevented.9 s& Q. K$ ^2 I8 I
Our patient’s testosterone level was 60 ng/mL,
% W0 X* _2 _& ^which was clearly high. Some studies suggest that3 U+ J+ x8 B2 Z' z& d1 @0 N  w  A+ f
dermal conversion of testosterone to dihydrotestos-
- x" Q  n1 E, g* jterone, which is a more potent metabolite, is more
& A1 c! W4 @: h  ractive in young children exposed to testosterone. d- n* b1 j% n- K% ]* J
exogenously7; however, we did not measure a dihy-+ O0 ]3 S* _: I0 t4 W
drotestosterone level in our patient. In addition to9 ?' _0 F8 r+ U  O; d
virilization, exposure to exogenous testosterone in
. \7 m( ?; e1 M& l3 r4 c1 zchildren results in an increase in growth velocity and
- y4 q8 @6 x0 i8 r1 j# Z6 u( L8 ]advanced bone age, as seen in our patient./ _( @2 K/ A7 ?6 I) K- Y" N
The long-term effect of androgen exposure during
8 O2 R; e2 o  R% Z% p% r7 U! T9 Iearly childhood on pubertal development and final
3 x% D; k6 ?; Y7 ]  C4 w' Z7 kadult height are not fully known and always remain
! i4 m' \. F' u3 n0 }a concern. Children treated with short-term testos-# q  v$ ]3 ?+ _9 x
terone injection or topical androgen may exhibit some
- E- @# H" X7 j7 t0 @, j4 {acceleration of the skeletal maturation; however, after
$ ^% @7 x+ m1 h( F2 qcessation of treatment, the rate of bone maturation4 `  K) e6 ?7 _( y) j
decelerates and gradually returns to normal.8,9) y: G& w1 |$ l6 Q* U. F# w& A
There are conflicting reports and controversy% L2 m! `* M# g! J8 Y
over the effect of early androgen exposure on adult2 D- _( `2 M1 P% p# M
penile length.10,11 Some reports suggest subnormal
3 M8 \$ s' x3 f, yadult penile length, apparently because of downreg-; z5 P% t- l  U& C6 M  x! Y
ulation of androgen receptor number.10,12 However,3 s+ N2 r. a! R
Sutherland et al13 did not find a correlation between' G8 }# O$ f9 S% k) v5 P- b( D
childhood testosterone exposure and reduced adult9 r9 U5 u2 N5 v! a! j& Z% a4 `0 i9 j
penile length in clinical studies." `& ~8 A: C# d+ I1 i1 [
Nonetheless, we do not believe our patient is; v' B0 V! M9 x) a
going to experience any of the untoward effects from
* W* G% S; N$ P1 `testosterone exposure as mentioned earlier because
8 {$ E) @/ I' Y- d3 D$ }- ?* wthe exposure was not for a prolonged period of time.
+ O: D0 v7 Y+ ~. ^" t- J) ^! DAlthough the bone age was advanced at the time of
# X+ F5 P* }4 ~3 r' [7 D. N& S  D4 Adiagnosis, the child had a normal growth velocity at
) v( ^& s' z: u  T& Uthe follow-up visit. It is hoped that his final adult
, D+ E5 P5 e7 s: n" _0 w% Dheight will not be affected.
% F  Y$ o: }* j8 Y" J/ h' {Although rarely reported, the widespread avail-
' `1 f% B( o' v# h. t+ }ability of androgen products in our society may  I; ^- X1 a% w1 j
indeed cause more virilization in male or female# L+ ^- R$ B/ ~4 v& f
children than one would realize. Exposure to andro-2 P' e% a$ L4 ]
gen products must be considered and specific ques-) v7 w3 s! w& l
tioning about the use of a testosterone product or. X: Y" h' N/ P2 C
gel should be asked of the family members during
- ]. i& q! ]5 c  {the evaluation of any children who present with vir-0 B0 A* s- e% f) x9 c
ilization or peripheral precocious puberty. The diag-" {6 b  Q* K* A- h
nosis can be established by just a few tests and by, m8 [6 j4 u: y  e9 s# X1 j3 E
appropriate history. The inability to obtain such a1 d" e5 F+ P2 s) p
history, or failure to ask the specific questions, may
7 R  e4 e+ N3 A' L4 V  P+ i1 \result in extensive, unnecessary, and expensive
0 M8 p+ t4 E" K+ L. z* T7 m+ N9 k0 Finvestigation. The primary care physician should be
2 S& r2 r. j6 l, Haware of this fact, because most of these children* z5 ]/ K  `: n% i/ G3 M% @
may initially present in their practice. The Physicians’
' U5 W( b/ d4 sDesk Reference and package insert should also put a
* \  N! t; |* w: _* Xwarning about the virilizing effect on a male or
# d/ B# A3 I/ |$ _8 wfemale child who might come in contact with some-) F$ g4 B" `& f0 L; I
one using any of these products.) {+ [5 P0 {  h* W% H+ ^* F4 n
References8 U+ s$ |/ Y; |* Z3 I2 R* L
1. Styne DM. The testes: disorder of sexual differentiation" a* a5 s/ Z" R
and puberty in the male. In: Sperling MA, ed. Pediatric, ]; ^4 A1 D' O9 h2 M
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
3 E+ `7 T; v0 w- f$ ]) S8 i2002: 565-628.
! \, j- F$ m$ }3 m2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 R/ `: ]5 Y* l$ G+ e# b; @4 t+ p+ K. `
puberty 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

3 {6 s" W, |; W8 `: v; h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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