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Sexual Precocity in a 16-Month-Old
: H+ O' |. ~5 j6 |: q# a& z  l- ZBoy Induced by Indirect Topical8 }6 o7 ^! D5 `  k+ [3 Z
Exposure to Testosterone
; o7 y# E8 V2 l9 ?Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# t3 c, V1 i0 band Kenneth R. Rettig, MD1
2 s7 f  M6 V# O6 r0 i% y0 ]Clinical Pediatrics
  H" ?& A# g8 K2 R' eVolume 46 Number 6( x: G( L6 f  S3 x% G+ G1 y5 Y
July 2007 540-543
0 }( ~( n6 D) [© 2007 Sage Publications7 R: O$ V! p. |. @. d
10.1177/0009922806296651
4 A% ~# ~" |8 a" lhttp://clp.sagepub.com
6 |# d, z! [, r( Hhosted at
* V7 j' z5 f- s: Q0 @1 \http://online.sagepub.com
4 s. Z: l6 H. Q2 x8 A1 x; APrecocious puberty in boys, central or peripheral,
1 ?* _: H' \9 ~( ~is a significant concern for physicians. Central( |( G1 E" P8 V4 X! z
precocious puberty (CPP), which is mediated
- h& N  S1 g- t1 y0 m2 vthrough the hypothalamic pituitary gonadal axis, has
* v) Q# C- ~) u( K0 |- aa higher incidence of organic central nervous system6 ~% h! ]8 U/ H, Y1 V
lesions in boys.1,2 Virilization in boys, as manifested9 e' X2 y0 c% c! l! o6 V# y* C
by enlargement of the penis, development of pubic/ j7 n; z. p3 k8 k6 D
hair, and facial acne without enlargement of testi-+ F* |+ s& ^! v, \& k- b: l
cles, suggests peripheral or pseudopuberty.1-3 We
. u$ u8 G1 C5 z! p: V4 E( rreport a 16-month-old boy who presented with the" h7 D3 R) G3 c4 Y1 q1 b( C
enlargement of the phallus and pubic hair develop-
) ]- h5 O9 G8 {3 e: Q7 _7 X. Iment without testicular enlargement, which was due
; P" h4 P! V' B& L, v, x+ gto the unintentional exposure to androgen gel used by4 I4 v2 W, t: k3 O# p3 g7 j/ u
the father. The family initially concealed this infor-
) G6 x' w' V9 _! F# D& P1 {7 Cmation, resulting in an extensive work-up for this% w, {2 Z& b8 Z  e9 T* p
child. Given the widespread and easy availability of
9 `6 ]- b& h) v1 Itestosterone gel and cream, we believe this is proba-
! n6 ], C% ~3 r  i& d3 S) V0 w. Xbly more common than the rare case report in the
; k, J; q4 s8 }& uliterature.4
- l( r: s, v. i4 R" q6 x* i: `Patient Report7 c/ S5 E& M$ d
A 16-month-old white child was referred to the
# z+ Z+ ?+ u+ E8 {1 zendocrine clinic by his pediatrician with the concern9 b6 O( C- j' h- B; Y
of early sexual development. His mother noticed' D* }0 H6 ?' M& Y8 E
light colored pubic hair development when he was& y9 K8 g" g% S. f! O' q
From the 1Division of Pediatric Endocrinology, 2University of- q$ G/ G8 W0 n" C6 ^- M% c* r
South Alabama Medical Center, Mobile, Alabama.
4 ^( s3 I* K% r4 J) UAddress correspondence to: Samar K. Bhowmick, MD, FACE,; G1 L! [* _# i0 _% F5 Y0 p
Professor of Pediatrics, University of South Alabama, College of3 T1 ?% R# n% M$ u; W2 f: D
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 ?5 j  i( n, n) c2 `6 t# u
e-mail: [email protected].. d- _8 _. P5 C) H7 U+ Z
about 6 to 7 months old, which progressively became4 _' O" z9 V1 D3 A  L
darker. She was also concerned about the enlarge-% G; q9 R; ^" m; F0 @; I
ment of his penis and frequent erections. The child
. o. j5 b" n( s5 \1 H! \$ J) Q9 fwas the product of a full-term normal delivery, with
- l& N5 v2 F; c. Xa birth weight of 7 lb 14 oz, and birth length of1 a" g+ F! F" f; B! C$ f0 F% b
20 inches. He was breast-fed throughout the first year
- Y" ^+ ^/ g, {0 t9 \% oof life and was still receiving breast milk along with
+ x$ {: ?8 M/ f* z) u* q, m' Nsolid food. He had no hospitalizations or surgery,0 S6 \9 @3 f. p' d* {5 b$ N
and his psychosocial and psychomotor development
6 H# A" F- A4 h* w; Y* b: ewas age appropriate.+ J' ~  X6 i& r9 |) a1 q" \& O- ?, [+ M
The family history was remarkable for the father,8 c( ^$ L2 v3 E, ?
who was diagnosed with hypothyroidism at age 16,$ V7 t( S; Q0 J! [; m
which was treated with thyroxine. The father’s
- u: U6 K: l9 y" Q- t5 {* oheight was 6 feet, and he went through a somewhat  C8 n9 b; k# O
early puberty and had stopped growing by age 14." F8 k& }; u5 f1 X6 Q, }3 Y8 x
The father denied taking any other medication. The/ c6 ^) U* X) C' ?" V# A
child’s mother was in good health. Her menarche+ a; J( l( q' j9 j1 y4 I# a! n, m/ B
was at 11 years of age, and her height was at 5 feet& L* c; q0 Y, d* P2 L2 }5 K+ U4 q
5 inches. There was no other family history of pre-( l8 G- j& {! p* J3 o
cocious sexual development in the first-degree rela-
; D1 R  ^- [& |) H; B, Wtives. There were no siblings.
, E. [  m( q/ v4 S/ S. r4 ?  rPhysical Examination
8 C4 X: K7 P" D" C9 P: VThe physical examination revealed a very active,
2 L  O" K+ y: bplayful, and healthy boy. The vital signs documented
1 Y2 X& V' B; ]' o; a7 j4 Ka blood pressure of 85/50 mm Hg, his length was
. p! V  i. v2 f/ A- @6 w3 c# ]0 V90 cm (>97th percentile), and his weight was 14.4 kg7 i) S8 @2 F. Z9 B
(also >97th percentile). The observed yearly growth
- y$ `: m. X3 evelocity was 30 cm (12 inches). The examination of
6 _; }) U+ g% B0 uthe neck revealed no thyroid enlargement.
( V2 l2 w3 v1 B$ F/ a+ h; IThe genitourinary examination was remarkable for
6 J; a5 ?- Z0 j6 ^8 E; E) ^enlargement of the penis, with a stretched length of! f% l& U! s( L1 x# X
8 cm and a width of 2 cm. The glans penis was very well
' Y" a6 A6 m4 q0 Z1 i- Ndeveloped. The pubic hair was Tanner II, mostly around6 S& U( C2 w; N8 L$ ?7 p' r* b; q
540
% i) t" N5 K, X2 j  ^8 Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 [$ ~8 u! W$ ~  W& X0 D
the base of the phallus and was dark and curled. The& q5 J7 x' Z3 ~. S2 d; n# f6 H
testicular volume was prepubertal at 2 mL each.# r$ y3 y4 m6 Q  _+ H
The skin was moist and smooth and somewhat$ D, P" n: S0 \% r4 S' Y( ^$ J
oily. No axillary hair was noted. There were no
/ E1 N# n" a+ A# xabnormal skin pigmentations or café-au-lait spots.
9 C+ x6 L0 ?' _) a, Y9 \$ F. q0 `7 G4 ]Neurologic evaluation showed deep tendon reflex 2+
  _! K& U% ~3 t7 T7 lbilateral and symmetrical. There was no suggestion" b+ Q7 `( f* ]" o* z
of papilledema.
( H, U9 [9 n+ c# sLaboratory Evaluation
0 w8 K- ]2 K0 ?The bone age was consistent with 28 months by
4 o3 J# L4 B) Z" D0 Z0 M" xusing the standard of Greulich and Pyle at a chrono-
9 S; ^, }1 X0 {+ i( L. i- ^3 Mlogic age of 16 months (advanced).5 Chromosomal
5 a& d9 G3 U" A7 ]+ ?karyotype was 46XY. The thyroid function test
7 r' ]5 M/ G) n5 j$ wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-2 E; @3 p' `0 Z
lating hormone level was 1.3 µIU/mL (both normal).
9 X1 O2 h. L0 Q" b# E  {& CThe concentrations of serum electrolytes, blood
5 l8 M/ j6 H- Nurea nitrogen, creatinine, and calcium all were
* \# x) ^8 k" l$ Uwithin normal range for his age. The concentration* s' y  m7 K. x* l( Z, K5 W4 X# a2 x4 T
of serum 17-hydroxyprogesterone was 16 ng/dL2 u/ }$ d  y' T9 y( W1 N
(normal, 3 to 90 ng/dL), androstenedione was 20
" X* }% |+ Q& u$ q+ t( f: r! G8 Tng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 @0 g  j; f  [$ K& \
terone was 38 ng/dL (normal, 50 to 760 ng/dL),& Q+ a3 @4 j0 h
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
) v# m' b; a/ ~4 H49ng/dL), 11-desoxycortisol (specific compound S)
' D' P  D/ C1 G3 e. _+ G# x7 j( w) D/ cwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* b  r( \! h6 Z$ J' a2 f) Ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' j; w$ F" L% C, w( W8 ?; Itestosterone was 60 ng/dL (normal <3 to 10 ng/dL),) s* v/ V6 o% U9 E+ a
and β-human chorionic gonadotropin was less than! t" [, I( u8 {4 Z
5 mIU/mL (normal <5 mIU/mL). Serum follicular
" T: s( O( }; i7 r2 ~stimulating hormone and leuteinizing hormone' j; }4 W1 O. C: I8 l* d
concentrations were less than 0.05 mIU/mL
$ p! u2 U+ O6 s& d& F(prepubertal).% O" J4 X' ^) I- C' L( Y8 s0 }0 E. Q7 Z
The parents were notified about the laboratory
( v" L3 q: m7 D3 Q7 Z) K$ \results and were informed that all of the tests were
$ }) ~2 }/ M& K0 d, A5 R0 R. M/ i' j8 \normal except the testosterone level was high. The& Z1 X" R& N$ v6 n
follow-up visit was arranged within a few weeks to# H. {/ d- l  @; B/ o8 `7 k
obtain testicular and abdominal sonograms; how-
2 a' j5 `* Z! Q$ L. wever, the family did not return for 4 months.
# @% F/ _# }6 R- APhysical examination at this time revealed that the
! S. g6 m3 f! m3 vchild had grown 2.5 cm in 4 months and had gained3 \6 Y! [( J/ [9 t
2 kg of weight. Physical examination remained* g; b8 i% o  n1 P- H
unchanged. Surprisingly, the pubic hair almost com-& i. x6 C8 C/ k5 ]7 V( t
pletely disappeared except for a few vellous hairs at2 [% [  M8 D* \8 q2 `
the base of the phallus. Testicular volume was still 2
' c2 f0 p% F9 i8 S7 e$ F6 A! |  gmL, and the size of the penis remained unchanged.
$ J& Q# c0 a& q, _The mother also said that the boy was no longer hav-( H4 c0 j% z7 y+ Q
ing frequent erections.# I+ ~# H/ ]: c; U# ^. ?' f
Both parents were again questioned about use of$ h% S6 c8 Y  L6 W( H4 U$ D( b
any ointment/creams that they may have applied to
2 l- m* H6 \5 Jthe child’s skin. This time the father admitted the
8 v* G  }$ Z9 VTopical Testosterone Exposure / Bhowmick et al 541
8 w2 I. i1 Q9 S& J. U( a$ cuse of testosterone gel twice daily that he was apply-
$ q) L, \' `5 t* V6 Ling over his own shoulders, chest, and back area for
. O) g9 Y+ E- O( d5 t/ wa year. The father also revealed he was embarrassed! f+ S( a0 J$ z! m+ `
to disclose that he was using a testosterone gel pre-# h4 O, S1 V/ F. ]
scribed by his family physician for decreased libido
5 \9 ~0 n- c' K0 I; b# Lsecondary to depression." P- @5 L, L) f3 ?
The child slept in the same bed with parents./ B, d7 J- ^+ s5 M9 F6 @% u- I, d
The father would hug the baby and hold him on his5 ^% C9 r; X/ v6 B# X
chest for a considerable period of time, causing sig-
7 W, Z" M# N) a$ ^4 S9 Gnificant bare skin contact between baby and father.
$ I. b( u2 l6 Y7 F2 }% I) c! cThe father also admitted that after the phone call,
% h/ o% O; B  d0 o- T) Ewhen he learned the testosterone level in the baby
9 @$ k& U7 S$ ^8 J$ t2 d5 twas high, he then read the product information
4 O' T" N) l2 [packet and concluded that it was most likely the rea-
- U  S0 M& K; V. u/ z; tson for the child’s virilization. At that time, they
( |& C, k0 q7 P, r' [: x$ tdecided to put the baby in a separate bed, and the; P" `5 o1 o/ G& f. g1 P" j& I
father was not hugging him with bare skin and had
( |4 K! p! n% s( Q4 \9 obeen using protective clothing. A repeat testosterone: q0 ~  S# }) T9 I  b3 ]0 v3 e
test was ordered, but the family did not go to the
' h+ k" K% W6 }$ [4 `2 P6 e: wlaboratory to obtain the test.! b# ?7 l+ f) j
Discussion& W3 {: L8 B* Y4 S8 B# Z
Precocious puberty in boys is defined as secondary
$ e* i2 u4 w; M$ E* D; [sexual development before 9 years of age.1,43 I4 S5 E* X: O+ P
Precocious puberty is termed as central (true) when
. \: g0 q( r/ Z3 H! g8 j, `it is caused by the premature activation of hypo-: l. H4 b% L9 W; Z! r9 X; v
thalamic pituitary gonadal axis. CPP is more com-
$ Z; i& [! g2 C* C2 [mon in girls than in boys.1,3 Most boys with CPP! C' q, t  O- h; R# p. h
may have a central nervous system lesion that is2 f/ ]$ m) h! E
responsible for the early activation of the hypothal-* n! Q+ x' ?9 E, u7 b) Z! i
amic pituitary gonadal axis.1-3 Thus, greater empha-
+ T& b# ?, ~: M; b8 H5 \, b$ O2 Tsis has been given to neuroradiologic imaging in0 S9 ]2 \; K. V" T& Z% a* D
boys with precocious puberty. In addition to viril-! i9 w$ b- t# ]7 u; z
ization, the clinical hallmark of CPP is the symmet-1 x; Y" ~& _1 ?6 @/ N5 t6 h
rical testicular growth secondary to stimulation by1 Z4 e7 b  `) x, l' @, W2 s& ~7 A: C
gonadotropins.1,3, \7 b4 s5 E/ |: v) a
Gonadotropin-independent peripheral preco-2 n$ b4 e7 A. l, M( X6 o2 t6 x
cious puberty in boys also results from inappropriate0 x8 V3 d& `) u6 ~$ k" B' D9 F
androgenic stimulation from either endogenous or0 A2 o& E7 G4 _: I# F
exogenous sources, nonpituitary gonadotropin stim-+ g3 y9 v$ g$ m( v) I# s$ Z
ulation, and rare activating mutations.3 Virilizing( ?  e/ ~: Y9 f+ B( `
congenital adrenal hyperplasia producing excessive
3 \, Z% l2 z! Xadrenal androgens is a common cause of precocious
9 ?/ z& I4 N; Xpuberty in boys.3,4$ O3 o, H& d# D. ^& E; @
The most common form of congenital adrenal
/ m' ^* J9 X2 }8 Q5 dhyperplasia is the 21-hydroxylase enzyme deficiency.1 r6 K8 V: a4 Z: n, U$ i' }6 {
The 11-β hydroxylase deficiency may also result in3 D( A" k; G$ O5 s1 W- F2 U
excessive adrenal androgen production, and rarely,2 `) ?* X$ F2 Q$ P& j1 W
an adrenal tumor may also cause adrenal androgen
$ ~+ E: B9 T' z; v$ Eexcess.1,3' A. J( C" y  z9 ]. ]/ d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 r3 e; d8 }: O; X# m' R9 w
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 l; L' |! f$ y. AA unique entity of male-limited gonadotropin-% g0 J& n3 t' }/ g
independent precocious puberty, which is also known
5 M5 c# L6 \& Ras testotoxicosis, may cause precocious puberty at a2 ~! p7 ]! L% K; F7 {, a5 D
very young age. The physical findings in these boys% i6 a# G8 R2 D. ]; J7 ]3 k' R
with this disorder are full pubertal development,
) ~$ t* f, p, q0 T- q( ]9 M$ lincluding bilateral testicular growth, similar to boys; V6 e, u! A9 e5 E  f
with CPP. The gonadotropin levels in this disorder* }8 q& ~% N( r9 ^' x& k
are suppressed to prepubertal levels and do not show- h- V5 t7 B/ J+ m: @6 V0 S
pubertal response of gonadotropin after gonadotropin-
5 x) y& k( d8 Jreleasing hormone stimulation. This is a sex-linked
$ ~: }( i  \" v  j7 Dautosomal dominant disorder that affects only
5 y; ]; Y) F1 U: c: d9 y0 q+ k4 Mmales; therefore, other male members of the family
9 M9 D, E! c) o6 R( j& z( Dmay have similar precocious puberty.3$ d- E  a# i' u8 ]$ N
In our patient, physical examination was incon-( K6 Q  g4 M% X: s7 z- m2 \- V/ [5 R
sistent with true precocious puberty since his testi-3 L0 x* w  S+ l
cles were prepubertal in size. However, testotoxicosis5 F" y% d9 k% A7 n
was in the differential diagnosis because his father' [3 Q9 P2 F/ R9 K1 H
started puberty somewhat early, and occasionally,% y. Z! g1 K9 m$ `
testicular enlargement is not that evident in the
+ C( ~4 M: B2 Xbeginning of this process.1 In the absence of a neg-
- ], Z4 ^: n. {3 W" N+ z/ d& M1 B) Qative initial history of androgen exposure, our
  \3 D1 q$ k: tbiggest concern was virilizing adrenal hyperplasia,
6 K* e0 V9 O) W6 Feither 21-hydroxylase deficiency or 11-β hydroxylase6 Q: ?. u: B  X$ W7 U2 \
deficiency. Those diagnoses were excluded by find-5 y- f& C! M9 Q6 F
ing the normal level of adrenal steroids.
1 A. k1 K5 l4 o0 l6 b8 EThe diagnosis of exogenous androgens was strongly7 w4 p( c* y) q. f
suspected in a follow-up visit after 4 months because
- F1 H/ a( X; [the physical examination revealed the complete disap-9 Q; q0 ~- B8 G& B% H" T# [
pearance of pubic hair, normal growth velocity, and
1 H9 U) e; R- H) _* f) i$ W% Mdecreased erections. The father admitted using a testos-
: b/ z: l& x9 d6 rterone gel, which he concealed at first visit. He was# T! _' c& D; A: A" m3 u. i; E! ^
using it rather frequently, twice a day. The Physicians’% z# ~% \  P/ @# _* b. _' x8 }- E
Desk Reference, or package insert of this product, gel or
( `6 V3 l# F; ~. w, \, f" A1 Qcream, cautions about dermal testosterone transfer to" m7 V7 a7 O( i5 H+ a; I( z
unprotected females through direct skin exposure.
& c! s  x8 U, D2 w2 kSerum testosterone level was found to be 2 times the
  Z; N: V& \7 \7 Z# r9 ~! }: qbaseline value in those females who were exposed to
+ e* ?% I: Q; D. z& X% J/ x( oeven 15 minutes of direct skin contact with their male
; y7 |& x/ p7 p& ypartners.6 However, when a shirt covered the applica-) B1 V  X) T: D8 T/ |$ y8 ]8 O2 f; y( ~
tion site, this testosterone transfer was prevented.
% y9 F7 K3 ^$ D2 QOur patient’s testosterone level was 60 ng/mL,
" Z, A2 }1 v- kwhich was clearly high. Some studies suggest that
6 b) G. q  A+ a8 a$ _dermal conversion of testosterone to dihydrotestos-
8 M" E6 ]( I( _% v8 A/ l0 ~terone, which is a more potent metabolite, is more& v3 A; ]& _6 n7 R
active in young children exposed to testosterone/ Q4 y* p+ |& l
exogenously7; however, we did not measure a dihy-
& ~- O9 z: M  O' I; Sdrotestosterone level in our patient. In addition to
, t( q7 o' t, S; c! \virilization, exposure to exogenous testosterone in* N  R* X( T% ^* C! a
children results in an increase in growth velocity and  Q% R: b$ D! j1 v0 @" t0 f: _
advanced bone age, as seen in our patient.
& N# X+ q3 \0 l. N* IThe long-term effect of androgen exposure during
% w5 h! z, {' z# aearly childhood on pubertal development and final
" l6 B& c1 }; A% Qadult height are not fully known and always remain
# ]5 q2 y6 [3 \$ J3 d& ^3 M7 U7 Ta concern. Children treated with short-term testos-
; i9 W3 P; r. E( m% W. X0 W5 h2 Y1 hterone injection or topical androgen may exhibit some3 x: W, T& L: I& f; Z' d
acceleration of the skeletal maturation; however, after2 @/ W$ e! D9 z6 ^: c$ A5 g
cessation of treatment, the rate of bone maturation
7 E2 l+ L) Y8 r0 _9 K5 tdecelerates and gradually returns to normal.8,93 U- P$ e3 l, u( b+ @9 v2 X( ?* v
There are conflicting reports and controversy
+ @6 W8 X1 r1 Sover the effect of early androgen exposure on adult
# {. x& d2 J- Z1 B, openile length.10,11 Some reports suggest subnormal- c3 [( H) E, W1 D8 a7 o
adult penile length, apparently because of downreg-
& z) M( c, u- }/ q6 Yulation of androgen receptor number.10,12 However,
* h2 \" \* h" C$ C  H$ \/ _- [$ USutherland et al13 did not find a correlation between1 T0 I: y* Q% x3 @2 u# c
childhood testosterone exposure and reduced adult. }9 x  T3 r1 N, O9 Z+ v/ o
penile length in clinical studies.3 a9 j  n* c3 `) U3 Z- n
Nonetheless, we do not believe our patient is$ d3 Q  [! ^) K8 k( V9 Q- x
going to experience any of the untoward effects from4 I: ?1 W2 h0 z& G; N
testosterone exposure as mentioned earlier because" ^8 B$ l$ S* G4 t( s8 W0 W
the exposure was not for a prolonged period of time.
$ ^$ C% Y3 N! x) hAlthough the bone age was advanced at the time of
$ X4 _  X: t9 m% ?8 Kdiagnosis, the child had a normal growth velocity at2 q7 t; Z5 ]6 o
the follow-up visit. It is hoped that his final adult7 J5 m5 K# C( X6 G& }8 }
height will not be affected.2 t/ \# f! E! J. J% b2 [+ d
Although rarely reported, the widespread avail-
' p: m) A7 Z: L7 m+ B6 oability of androgen products in our society may. ^8 J, U. o0 U6 O
indeed cause more virilization in male or female
* d- @/ w" F0 S- m6 U' m$ ^children than one would realize. Exposure to andro-
  R% M* A2 H3 Zgen products must be considered and specific ques-6 f) t2 x$ Y2 T) m
tioning about the use of a testosterone product or. G+ g1 K, e4 e3 O
gel should be asked of the family members during$ e- V/ {: M& s2 i
the evaluation of any children who present with vir-, ^5 @3 U9 F' k$ N" K! u* @: Z
ilization or peripheral precocious puberty. The diag-
2 L$ X! c' i7 D- J1 [+ I% Onosis can be established by just a few tests and by
5 f/ P! C# p$ sappropriate history. The inability to obtain such a
0 X3 B+ p+ K/ R2 Q, B3 khistory, or failure to ask the specific questions, may7 q( h7 m& |* ]: O$ S
result in extensive, unnecessary, and expensive
: ^/ ^  A3 Y( Y' g" ainvestigation. The primary care physician should be0 N+ n* i  A2 u- S/ ^) ]
aware of this fact, because most of these children
3 y) A8 h5 _4 z* M$ l5 V: Amay initially present in their practice. The Physicians’. q/ n  T1 n+ s; j
Desk Reference and package insert should also put a
% s( g& y2 A" v- m3 u! D5 A! Rwarning about the virilizing effect on a male or
5 t5 z/ H7 {) h- }6 o& T4 kfemale child who might come in contact with some-
# E3 X6 R' s+ B4 j$ w) T) {' B# Yone using any of these products.+ N! }/ o' x. T( A$ r  |
References
2 G+ [! `2 a6 P6 Z3 {1. Styne DM. The testes: disorder of sexual differentiation
6 r' t4 g# g* ~' Yand puberty in the male. In: Sperling MA, ed. Pediatric
) A# V( t- V! D+ kEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;  s. l2 U0 ~3 q, f3 I
2002: 565-628.
9 S; [8 X2 ]( L8 V1 g, z' ~7 B2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* J! E1 V  X1 T* vpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
* t1 ^. ~* f* X- H( n. u, _) CBoy Induced by Indirect Topical2 A2 K+ R) M( q0 u
Exposure to Testosterone
6 _, A0 N% r( R+ D" W/ aSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  f" e: L: K+ h* ]" Land Kenneth R. Rettig, MD1  T" h9 z5 P  ^
Clinical Pediatrics% V; `. ?+ J- C6 l
Volume 46 Number 6! s  Q! h) s; @
July 2007 540-5433 v+ l' s9 x0 }& z' o
© 2007 Sage Publications* `7 {4 `5 S7 S" G
10.1177/0009922806296651$ C9 T+ T! Q) {3 p9 j
http://clp.sagepub.com7 o. u) y7 |) @$ p$ L" X' W3 T& P
hosted at
9 w; q+ d3 w) `! V. L9 i( u9 Jhttp://online.sagepub.com
4 R, y7 j! `& u% Q$ L& [Precocious puberty in boys, central or peripheral,
/ P2 d/ b5 n9 l4 a2 N9 s0 R; jis a significant concern for physicians. Central* S& d' a% ?2 M4 C; t) j
precocious puberty (CPP), which is mediated, _, l/ }4 D! Y) h- \$ a1 y" G" O
through the hypothalamic pituitary gonadal axis, has
9 S+ _/ A: {( w! |- n7 za higher incidence of organic central nervous system
! E5 M9 Z6 Q8 I3 W: mlesions in boys.1,2 Virilization in boys, as manifested( {% A$ r4 M) l2 E( `1 T, B" \" j
by enlargement of the penis, development of pubic
* J& H/ W% A* W  Q+ B& ^5 ohair, and facial acne without enlargement of testi-# W5 v+ ^" `: Y6 P. M# U
cles, suggests peripheral or pseudopuberty.1-3 We
! j$ b( s3 R7 d3 F  Kreport a 16-month-old boy who presented with the
4 O& L# |- b" O* Benlargement of the phallus and pubic hair develop-# P* N$ ^, d- A- [
ment without testicular enlargement, which was due
5 ^/ ]$ Y% A1 T; ]to the unintentional exposure to androgen gel used by
+ d% P( p4 z' A1 ~) ithe father. The family initially concealed this infor-
$ Z! L% m, x3 t7 c9 s, nmation, resulting in an extensive work-up for this
4 r* `% ~  i6 }) v$ f6 J; Ychild. Given the widespread and easy availability of2 t: S5 A7 g+ }% L( b% P6 E
testosterone gel and cream, we believe this is proba-' l) a$ G6 D% ]
bly more common than the rare case report in the& i  F- U( ]7 r/ ?+ O
literature.4& o& o" k' c3 m0 m- L/ \6 X
Patient Report
$ a8 ?4 ]- \/ F6 m, [7 FA 16-month-old white child was referred to the' t# g& N5 t& {$ s4 g5 M5 Z! S: H) I
endocrine clinic by his pediatrician with the concern6 ^2 N9 L" [/ p- j8 K9 E1 G% t
of early sexual development. His mother noticed
# H- D1 n+ n+ m: v9 Y& s7 zlight colored pubic hair development when he was
: J, b! Q" `6 g" [From the 1Division of Pediatric Endocrinology, 2University of/ N8 a5 H% V4 M+ g, t
South Alabama Medical Center, Mobile, Alabama.
5 r5 W0 h1 J6 Y' ?! eAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 w6 i8 w* p' V' c
Professor of Pediatrics, University of South Alabama, College of
0 d& [) }5 \4 M% R/ ]3 Q/ K3 ]/ Y4 MMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 ?" F3 i: H  O0 r& H6 E8 ye-mail: [email protected].; {3 w$ R7 P5 t- ^6 q+ Q  q
about 6 to 7 months old, which progressively became
* Y# x( [* r- ?( p: d; Z1 Q" h( o, q# ndarker. She was also concerned about the enlarge-
/ ], {+ h" L" J  l  Q8 _4 m5 ament of his penis and frequent erections. The child
& U9 p$ p6 m& E1 L# o) Nwas the product of a full-term normal delivery, with
9 B5 u" ]: T; a6 D7 t. ta birth weight of 7 lb 14 oz, and birth length of, M0 O" T1 V  [6 }3 o: k2 a3 G
20 inches. He was breast-fed throughout the first year/ Z& C$ q5 V- J4 b) G2 O, F
of life and was still receiving breast milk along with+ r* `4 m/ C) r' s
solid food. He had no hospitalizations or surgery,9 Z! c6 [( E! E7 ?/ Y
and his psychosocial and psychomotor development3 V, h% w/ N( [
was age appropriate.$ I# Z/ Y$ L) Q& J7 I
The family history was remarkable for the father," a" k8 g& Y5 |! x% ~% Z3 S  i
who was diagnosed with hypothyroidism at age 16,$ ]* r, j' p5 k
which was treated with thyroxine. The father’s
3 f2 j" y8 s) I. F: p' S. Bheight was 6 feet, and he went through a somewhat
) f# R& r3 G- r% b% @early puberty and had stopped growing by age 14.
  ?1 l6 v- z" SThe father denied taking any other medication. The7 r$ d: _% o! x1 Y& t, X- \: [! @2 |
child’s mother was in good health. Her menarche
' c8 H" i0 }3 ?4 Xwas at 11 years of age, and her height was at 5 feet
6 e; m9 I# ]7 A- t5 l4 \$ j  k: j# |5 inches. There was no other family history of pre-' Z) t* g. ?6 z$ k1 b: {- o
cocious sexual development in the first-degree rela-! J7 m  t7 c+ M0 X
tives. There were no siblings.. F2 N3 n! W$ h1 V+ b# Q& i( Q
Physical Examination
5 r: n" s8 z5 k! @) b# ]3 p- A' C# {The physical examination revealed a very active,
; }4 o7 M" g6 ?1 \/ bplayful, and healthy boy. The vital signs documented$ y2 L" Q8 K2 z( P
a blood pressure of 85/50 mm Hg, his length was
7 _$ D2 ^3 f, d& y90 cm (>97th percentile), and his weight was 14.4 kg% ], @. X  S: U8 ]) i, i* r' [$ W0 c
(also >97th percentile). The observed yearly growth7 o2 Z& h1 {: W1 h% _, q  C
velocity was 30 cm (12 inches). The examination of
6 x+ O* h5 H4 _the neck revealed no thyroid enlargement., L; Y4 X& K# I8 T% ^  G7 w& Q( c1 r
The genitourinary examination was remarkable for
' s; D: b1 D1 y7 _! Eenlargement of the penis, with a stretched length of! Q" R' k0 _$ @. K
8 cm and a width of 2 cm. The glans penis was very well
! Y3 X& P' }  O1 Ideveloped. The pubic hair was Tanner II, mostly around& A$ p: C7 g% _5 Z! n
5404 Q# f  |" J& G$ Z! Q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) b. b2 _' F$ K$ v5 B8 G4 \3 jthe base of the phallus and was dark and curled. The8 b7 T* j* Y& g. g6 F) S+ X5 R+ j
testicular volume was prepubertal at 2 mL each.
# R) _' E% l9 `  uThe skin was moist and smooth and somewhat
$ {3 ^( ~. ]( d+ K) g/ |oily. No axillary hair was noted. There were no' Q5 ?! u$ ~9 Q2 I- n, l
abnormal skin pigmentations or café-au-lait spots.
$ G9 w, J% J$ Z& |' |  d9 ~; WNeurologic evaluation showed deep tendon reflex 2+
" n) V- U8 Y6 ?: v2 f, xbilateral and symmetrical. There was no suggestion# }% [9 ^9 Q  z1 |" ~  m
of papilledema.
9 `  P9 j9 M. K5 N9 P% D, PLaboratory Evaluation
4 X% o* W7 c; w2 u5 r3 yThe bone age was consistent with 28 months by
1 \2 G! b1 Q1 m+ M0 eusing the standard of Greulich and Pyle at a chrono-1 G$ z! _: D" J
logic age of 16 months (advanced).5 Chromosomal
+ c% T4 |5 X0 I; K" bkaryotype was 46XY. The thyroid function test7 I  N$ `+ H1 r# H
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 U1 w& }+ q0 e+ flating hormone level was 1.3 µIU/mL (both normal).
9 n3 j( {3 W8 R) rThe concentrations of serum electrolytes, blood
; m% Y: P3 E) v9 d$ D: furea nitrogen, creatinine, and calcium all were+ n8 q6 H3 B) o% z: c. p- k# \& v4 {
within normal range for his age. The concentration
% i" R- P' `+ e  G$ K& I' o2 K9 c) Bof serum 17-hydroxyprogesterone was 16 ng/dL
, Q& S9 S. w2 K8 [( L7 m  \(normal, 3 to 90 ng/dL), androstenedione was 20
- I. v% v; a8 e* H2 |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 y. k0 ~* g6 K# Z
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 a- Y* T4 ?2 x! Ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to- D5 c+ l  y7 M! P0 x/ M! d/ G
49ng/dL), 11-desoxycortisol (specific compound S)5 d1 ?" I+ t- ^9 V, m6 _
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
/ L$ f! V5 a- `% H2 {. Z9 Q$ wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 b) K: |# F; c  P4 j2 @' ttestosterone was 60 ng/dL (normal <3 to 10 ng/dL),; J' M5 w: F( i; w+ Z" y3 B
and β-human chorionic gonadotropin was less than
3 S5 l" u8 {5 a& g0 f5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 f4 ]8 \5 O* L% Nstimulating hormone and leuteinizing hormone
% E& k7 Z( |( T* {% [& V( b+ \concentrations were less than 0.05 mIU/mL
9 J$ S% S2 u3 Z; M5 ^+ z. q/ N  |6 T3 @(prepubertal).( L" S0 s2 M3 y+ N
The parents were notified about the laboratory
: u) o+ C7 K9 B, c& x) ?results and were informed that all of the tests were' w7 G% a3 q( P: [/ q
normal except the testosterone level was high. The
. W( U& t5 F3 d  ofollow-up visit was arranged within a few weeks to' c" {$ m5 h7 @2 J9 w( H6 V
obtain testicular and abdominal sonograms; how-
7 j+ a2 o* K9 Q9 e$ g( @ever, the family did not return for 4 months.* F( U) s4 e7 L, Q5 x) h* V& X
Physical examination at this time revealed that the
) z) p: D/ C4 w- Ochild had grown 2.5 cm in 4 months and had gained/ R0 a6 `% u$ H/ R$ d8 n. O. `
2 kg of weight. Physical examination remained" l( o2 R% a6 {
unchanged. Surprisingly, the pubic hair almost com-
: k, O7 e- `( Opletely disappeared except for a few vellous hairs at
! z# U# R7 \& u$ lthe base of the phallus. Testicular volume was still 2, h  [; b  }2 n9 y
mL, and the size of the penis remained unchanged.
: _& b( K) d% A1 Q, x3 sThe mother also said that the boy was no longer hav-
' U' @, P+ Y( Z, O3 xing frequent erections.+ o5 J, K7 `4 A6 T* z% h
Both parents were again questioned about use of
% y% j+ M4 a2 V1 {5 [8 Dany ointment/creams that they may have applied to# \8 R) i. s$ G* f# x3 D9 p, j
the child’s skin. This time the father admitted the
. l4 u/ C* ?$ B5 |9 i$ `Topical Testosterone Exposure / Bhowmick et al 541. G( [5 z* |$ n: Z) F7 K2 R
use of testosterone gel twice daily that he was apply-
; Q) d3 J7 ~, y) P; |ing over his own shoulders, chest, and back area for
0 p. ?% }1 E( r8 P9 da year. The father also revealed he was embarrassed3 K0 m4 C' T7 i  L9 l8 A
to disclose that he was using a testosterone gel pre-9 m# o! ^( {$ x* m" J8 j
scribed by his family physician for decreased libido+ ?' t, N) }' G0 o7 v( S7 c/ J
secondary to depression.
3 M& o' h9 ^( z* Z6 M4 f4 {' h5 UThe child slept in the same bed with parents.0 o/ v+ }7 o4 Z# u
The father would hug the baby and hold him on his
8 B& ^' S9 B+ ?& B& gchest for a considerable period of time, causing sig-
0 X& r1 g* {+ Enificant bare skin contact between baby and father.
+ O1 A+ ~+ K2 X- f& S6 D! H! tThe father also admitted that after the phone call,
0 M8 l9 T: H& o- u- f, c  V: m4 v  nwhen he learned the testosterone level in the baby. h  L" w) h9 \- r. x  X8 T
was high, he then read the product information1 g! c% J" F3 V# X# c" E
packet and concluded that it was most likely the rea-
- d9 m! e2 O2 e/ K5 Y0 \son for the child’s virilization. At that time, they
: \. w- U" @3 X. D! S; w" Wdecided to put the baby in a separate bed, and the, M+ C) Z5 y0 F1 `5 y& R
father was not hugging him with bare skin and had
% U; r. l9 U  N& Q- Hbeen using protective clothing. A repeat testosterone: `3 M" ^: H5 G2 i6 Z
test was ordered, but the family did not go to the
1 M* x& j$ C2 R! B2 `5 i+ _7 ?laboratory to obtain the test./ n: \3 m6 I  M1 ?& k
Discussion
) t/ y- W) V6 L7 w' iPrecocious puberty in boys is defined as secondary  y, u0 K( }" _, r9 V& R8 r) C
sexual development before 9 years of age.1,4
, A/ @0 ~. M- uPrecocious puberty is termed as central (true) when
$ C1 V% s' ]9 y; ^( rit is caused by the premature activation of hypo-
: R; A4 N, |9 e8 E5 L! k% U4 f2 xthalamic pituitary gonadal axis. CPP is more com-! U6 o* W9 m( r, M5 O9 F
mon in girls than in boys.1,3 Most boys with CPP
' L9 V' r9 }- b% D) e( R' m9 Amay have a central nervous system lesion that is9 C5 h4 w0 ]% x
responsible for the early activation of the hypothal-- L+ Z& M$ \8 ~$ z" I) \* w
amic pituitary gonadal axis.1-3 Thus, greater empha-  ]& C5 D8 i& R- o
sis has been given to neuroradiologic imaging in
- _9 O" Y# h. Z6 H$ h8 Rboys with precocious puberty. In addition to viril-# F) ~- |( R; j2 A0 L1 v1 P
ization, the clinical hallmark of CPP is the symmet-6 E/ G* Q2 B9 k1 O2 {; P
rical testicular growth secondary to stimulation by5 m( {' E8 p" r6 j! n
gonadotropins.1,30 S* W+ F; t& F$ {2 n% F
Gonadotropin-independent peripheral preco-
  q8 u8 Z2 N5 S( F! L2 ^: fcious puberty in boys also results from inappropriate
$ A$ q( m7 L7 Wandrogenic stimulation from either endogenous or
! b; u, S) A( x4 W5 O, n) V9 sexogenous sources, nonpituitary gonadotropin stim-/ v8 s# _" C0 j" v
ulation, and rare activating mutations.3 Virilizing
: m; T8 P* Z% U8 |) K9 U4 vcongenital adrenal hyperplasia producing excessive2 i; |2 ]1 W+ N# K. N( j5 O7 b
adrenal androgens is a common cause of precocious$ F6 {) ?1 |4 k+ k$ M6 s
puberty in boys.3,4
% Y# x+ Z+ W( E' y4 G# q. HThe most common form of congenital adrenal
& j& e2 g- v' _* y4 F4 \$ Vhyperplasia is the 21-hydroxylase enzyme deficiency.& S! K; y0 g9 j5 @# R7 @4 h
The 11-β hydroxylase deficiency may also result in# _) L" m- R' G$ N: U2 a
excessive adrenal androgen production, and rarely,
' M# M3 o3 S* k# M, c! h' y, uan adrenal tumor may also cause adrenal androgen7 R* ?  N5 H; m% C) Q. I5 Y
excess.1,3; M6 U+ A/ N* m) p* H+ \
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 s5 T- q. N6 t
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007% x9 l; N+ b& e4 @
A unique entity of male-limited gonadotropin-$ ?7 ~$ E. l9 f% o
independent precocious puberty, which is also known
9 M; M2 B- Z* @. @8 ]as testotoxicosis, may cause precocious puberty at a9 r3 \0 v' j5 _0 J& c+ Q3 o
very young age. The physical findings in these boys; B7 J: U7 W+ b% q/ }+ P' E' f& m
with this disorder are full pubertal development,- S; T2 M% ]0 i/ @! f
including bilateral testicular growth, similar to boys
4 Z4 T  q+ Q# w) U, [% T8 r) hwith CPP. The gonadotropin levels in this disorder
* G# Z! O+ q+ o( P! Aare suppressed to prepubertal levels and do not show
5 ]' A+ E, D* p/ c0 Q1 m/ o2 K/ mpubertal response of gonadotropin after gonadotropin-' V' h; Q7 ^( ?. n* v9 |/ i4 I
releasing hormone stimulation. This is a sex-linked
' O& D: U5 l! ?; E3 r3 `autosomal dominant disorder that affects only& f. J; H0 @% A6 v/ q
males; therefore, other male members of the family
( @' m2 u2 H/ Imay have similar precocious puberty.3) [4 ^) P- g% w3 ~
In our patient, physical examination was incon-' J* f- c& t$ t/ f5 F
sistent with true precocious puberty since his testi-
/ Z) l4 M- t2 ~& scles were prepubertal in size. However, testotoxicosis) U6 z& f# o- v) A* u
was in the differential diagnosis because his father: Y* f3 U, B( v  o- u# A$ `( D
started puberty somewhat early, and occasionally,
0 W3 G1 X+ c8 ^+ {  T7 Y1 Htesticular enlargement is not that evident in the
. w$ ^2 l7 T' T1 \4 r# `8 F3 Kbeginning of this process.1 In the absence of a neg-/ B$ w* v  O9 Q8 w- S
ative initial history of androgen exposure, our8 p# P4 O" {. U( R& ^+ N5 L
biggest concern was virilizing adrenal hyperplasia,8 d) |! B5 ]8 l  r: ^- Y- R
either 21-hydroxylase deficiency or 11-β hydroxylase
2 I2 F, @$ J- n/ O4 h# u* `* [deficiency. Those diagnoses were excluded by find-
) T6 s" I" z% s% wing the normal level of adrenal steroids.
& w6 n& D1 n5 G% F) g% rThe diagnosis of exogenous androgens was strongly
% b! A  m2 ^6 b0 {/ k+ @$ qsuspected in a follow-up visit after 4 months because
1 w& m; P2 P, f! c2 Pthe physical examination revealed the complete disap-1 y4 A2 S3 C1 G. k6 q: F
pearance of pubic hair, normal growth velocity, and
/ e1 {' M% q; O" t7 Wdecreased erections. The father admitted using a testos-
' Y  d# K5 Y2 v8 aterone gel, which he concealed at first visit. He was( P4 w1 t5 g( x" N7 K/ I. b
using it rather frequently, twice a day. The Physicians’0 N: @& y8 e" r8 J' x
Desk Reference, or package insert of this product, gel or% ~. S  w! g2 J7 X
cream, cautions about dermal testosterone transfer to4 R) y5 B5 ?3 ^4 k
unprotected females through direct skin exposure./ [* G) \& M4 @' j3 w
Serum testosterone level was found to be 2 times the# r, n/ m* Q% a  y
baseline value in those females who were exposed to2 C) E6 k0 H% F1 ?
even 15 minutes of direct skin contact with their male4 p$ k/ F, \- \: a# j2 M
partners.6 However, when a shirt covered the applica-
& t1 C- o' ~) y! O0 B- rtion site, this testosterone transfer was prevented.* b. G! g  g* ?; U! j/ _9 O) n. O
Our patient’s testosterone level was 60 ng/mL,
' c+ U0 x. H1 E$ @+ `which was clearly high. Some studies suggest that
. V  }* r& D, I& J# j1 Ydermal conversion of testosterone to dihydrotestos-
% s& ^4 l, U/ r9 |! {$ I: tterone, which is a more potent metabolite, is more
" b9 h2 e9 M' v# j+ g1 k; Zactive in young children exposed to testosterone
+ M* W& O0 {1 }5 {2 B( u% rexogenously7; however, we did not measure a dihy-2 L8 T! e+ v" S. n+ J! }. N
drotestosterone level in our patient. In addition to! d4 }* M8 {& Q* Q: m' p
virilization, exposure to exogenous testosterone in
1 Y' g0 N; t% dchildren results in an increase in growth velocity and
% l* o% N) z' D9 _8 {2 |* Z* n% aadvanced bone age, as seen in our patient.
9 a3 s0 f& v6 r/ M, s8 iThe long-term effect of androgen exposure during
/ `. x& G/ X+ M1 P9 searly childhood on pubertal development and final1 t3 t9 C; J3 f, s
adult height are not fully known and always remain
0 W* [- Y( e# ^) v+ z( Qa concern. Children treated with short-term testos-* B0 A* c& `3 i9 j
terone injection or topical androgen may exhibit some
) G4 {1 X  c3 e, F; X6 l7 Xacceleration of the skeletal maturation; however, after
; |! d; G, j% H% k4 Lcessation of treatment, the rate of bone maturation/ U( r+ L8 A7 p5 P1 O  ^
decelerates and gradually returns to normal.8,9
- L- t! ?: E1 R9 G( k1 `There are conflicting reports and controversy
9 n. Y5 s1 `6 a2 X1 Pover the effect of early androgen exposure on adult
, Y/ L9 L  ?! @6 Ypenile length.10,11 Some reports suggest subnormal
1 f8 r, y( `* f" radult penile length, apparently because of downreg-
- R; w9 p8 m) g0 `. {. bulation of androgen receptor number.10,12 However,
0 K  e% N" C8 ~; _( u* X! iSutherland et al13 did not find a correlation between, `7 [; ?; T4 M! C: c
childhood testosterone exposure and reduced adult
$ c- D" ], M  ~% H" v' ]( bpenile length in clinical studies.$ x* U+ y( w1 s6 K/ Q& c/ \
Nonetheless, we do not believe our patient is6 w/ t9 x3 @8 o& x$ d! @' o7 B
going to experience any of the untoward effects from/ l/ U4 R' t, a- r; u5 t! x8 ?. O
testosterone exposure as mentioned earlier because
, W* @# U- D8 Tthe exposure was not for a prolonged period of time.
$ u# ?7 v6 E( t( w2 \4 rAlthough the bone age was advanced at the time of
* M: T6 W. F& h2 wdiagnosis, the child had a normal growth velocity at
$ t% q" w3 o8 X' ethe follow-up visit. It is hoped that his final adult
* K8 U+ g4 }$ h8 dheight will not be affected.. o  j" Q, |4 ^- V8 [  ]
Although rarely reported, the widespread avail-* W" X' b. |, {! f: d- G- C: @- d
ability of androgen products in our society may
% s8 j. k' O6 y3 j8 `! Q1 \& G0 pindeed cause more virilization in male or female
) A2 o% N3 i; X: y3 m2 Q7 Schildren than one would realize. Exposure to andro-. x) i1 c6 b" ~3 I3 S3 A
gen products must be considered and specific ques-
" |) @" D0 }' h2 x+ l: E( Ctioning about the use of a testosterone product or3 z# v/ W" V9 D. O9 l
gel should be asked of the family members during' T, U: w' n+ N# ~; Z
the evaluation of any children who present with vir-4 M$ j; s7 e+ h1 u+ f
ilization or peripheral precocious puberty. The diag-5 \% t5 ?8 g! l) v
nosis can be established by just a few tests and by2 V. [5 P* I1 N( g3 X
appropriate history. The inability to obtain such a
  U9 P( p& Z" n" Y. xhistory, or failure to ask the specific questions, may5 a& O; m6 p! ]6 j  S( \, x
result in extensive, unnecessary, and expensive& h2 i2 ]  V3 g& h/ n3 w7 I7 \; z+ F
investigation. The primary care physician should be
* K" l. B) a! Y: W5 M5 l6 C, Faware of this fact, because most of these children
8 l; D: B6 u7 bmay initially present in their practice. The Physicians’6 }* J7 g( O3 w# ]
Desk Reference and package insert should also put a7 _3 {- s/ x/ x/ T
warning about the virilizing effect on a male or
$ N9 B" R& c  A. w( G% m/ Yfemale child who might come in contact with some-
2 o- q) S$ v& \8 z0 L" vone using any of these products.
- z* }/ [& J  ?5 e$ HReferences
. E  c% t! k, X( O9 h1. Styne DM. The testes: disorder of sexual differentiation
9 R- `6 u. P3 Y# i; l3 Kand puberty in the male. In: Sperling MA, ed. Pediatric2 S- c  L( Z$ Y% b* v
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 h, j4 @+ ^7 Y6 Q, s6 r9 M4 I6 x2002: 565-628./ X( R) P  D' T; e8 ]6 v2 K) l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" l- F8 S- J" c; f4 V+ ppuberty 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
' c; H9 K1 U! Y* D" F5 k8 z, d
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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