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Sexual Precocity in a 16-Month-Old
6 Y, @4 D$ B9 |" x4 a% i8 sBoy Induced by Indirect Topical+ o$ v* ?5 @2 @$ k4 _
Exposure to Testosterone
  I, T* g* v' L, @6 c0 A7 RSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& }1 z" l! M0 C( x
and Kenneth R. Rettig, MD15 E. c3 A( z3 ~. l; [! [8 R
Clinical Pediatrics
5 Y/ e& ^# F5 c. V  C- v0 OVolume 46 Number 6
) J+ [& E; a1 G! ^2 F; }July 2007 540-543# s) D0 N9 {* W9 c5 c
© 2007 Sage Publications) G) z  r! X$ p. `. z( e; l3 L
10.1177/0009922806296651
! y' T4 d4 R, K3 zhttp://clp.sagepub.com$ ?/ K$ u. L+ S* x1 V2 U
hosted at% F8 S! o' E; w) g' ^
http://online.sagepub.com& t1 E9 t( y$ }: m- B0 T  n: K" D
Precocious puberty in boys, central or peripheral,) k* R- L3 |9 L5 R$ K
is a significant concern for physicians. Central
3 q) O- j8 P& f2 N6 n; S) m5 b9 @precocious puberty (CPP), which is mediated
: m1 }6 r# {- M; t& z2 r% Uthrough the hypothalamic pituitary gonadal axis, has" M8 H' ~- _; A0 t% f; W
a higher incidence of organic central nervous system
" F; D$ {' |: C; {$ p# z9 B+ G. E* Llesions in boys.1,2 Virilization in boys, as manifested
8 c" |4 v1 e7 V! l( E0 wby enlargement of the penis, development of pubic
- F1 A: M% o" V9 ?9 w. @% \hair, and facial acne without enlargement of testi-: }) J, `8 h1 K& z$ Y
cles, suggests peripheral or pseudopuberty.1-3 We- C; h/ C( f: ?$ t9 a& U& C
report a 16-month-old boy who presented with the
0 K. I+ |- [4 ~enlargement of the phallus and pubic hair develop-
# r; p0 |/ X5 u9 Z$ J+ K& oment without testicular enlargement, which was due3 @8 q+ Q7 O' g8 z" n6 y6 U
to the unintentional exposure to androgen gel used by
: L3 l# \0 A* J2 Wthe father. The family initially concealed this infor-
- f7 s! N0 y7 w2 @mation, resulting in an extensive work-up for this! z6 h( R& X: |
child. Given the widespread and easy availability of
% P# M: {* H" o0 u& g5 dtestosterone gel and cream, we believe this is proba-
! e, q+ F1 |; |2 ?! A: nbly more common than the rare case report in the5 _& x9 r5 ~4 ^! b" g; z
literature.4! j% b; ]1 m0 l' ~1 k! b& r1 c- V" z
Patient Report5 F2 j' w3 B% b* b3 @
A 16-month-old white child was referred to the7 n. M/ [6 ?# `! Z+ |
endocrine clinic by his pediatrician with the concern+ j% Z+ U) H& H: m
of early sexual development. His mother noticed3 X/ ?" Q: h9 D- A0 }
light colored pubic hair development when he was
  f$ `3 j- Z% A1 O* fFrom the 1Division of Pediatric Endocrinology, 2University of
  T7 K% w( H/ s0 ]* E1 m' uSouth Alabama Medical Center, Mobile, Alabama." p7 o, ?: k! _3 R  [) A9 I( u
Address correspondence to: Samar K. Bhowmick, MD, FACE,; D. M4 ~% a3 r
Professor of Pediatrics, University of South Alabama, College of
2 `& d/ H1 G6 rMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
  A) O0 j+ `' I/ i, |2 B3 qe-mail: [email protected].
, J+ B0 `# O! pabout 6 to 7 months old, which progressively became4 R5 u/ z; `; K# h' A) A7 E# L
darker. She was also concerned about the enlarge-! `# N# f+ `% F; ]2 [7 o. @8 M
ment of his penis and frequent erections. The child
1 Y% g: I9 `9 @1 C3 a/ Rwas the product of a full-term normal delivery, with
# _8 n- l: N' V- Y. h( |% D* ja birth weight of 7 lb 14 oz, and birth length of6 x* d" `+ M3 [& b/ E6 U* `
20 inches. He was breast-fed throughout the first year* b) k3 S* |0 T% S) r; n! j
of life and was still receiving breast milk along with
4 R1 I( `# L/ q. {4 ssolid food. He had no hospitalizations or surgery,
: J  [0 F$ m! O) z- e2 B4 band his psychosocial and psychomotor development
9 I& Z) F2 S; j8 h6 ?1 c5 |& Xwas age appropriate.
( n; P& U9 \, M" D9 Q3 U6 @The family history was remarkable for the father,% B+ y  Z$ \2 f2 c( w# B0 ~5 L
who was diagnosed with hypothyroidism at age 16," C0 U5 t# d+ e8 B
which was treated with thyroxine. The father’s
  R3 K( M; A0 o% f/ Sheight was 6 feet, and he went through a somewhat  M/ [7 d4 d) I$ P6 s; j
early puberty and had stopped growing by age 14.0 R+ Q1 d: n- A/ L9 [5 {3 g
The father denied taking any other medication. The
$ m2 l  [4 j2 \5 ichild’s mother was in good health. Her menarche3 W. I# ?4 d0 _+ V
was at 11 years of age, and her height was at 5 feet% i0 G1 C0 j/ i) a
5 inches. There was no other family history of pre-, Q8 Y; n' h+ H9 R+ t9 W
cocious sexual development in the first-degree rela-4 }( h# |) f& r2 m* ?. f6 m
tives. There were no siblings.) m$ H, C" q  x; ]6 @3 t' p2 K
Physical Examination
; {9 e" y9 L2 s3 T5 xThe physical examination revealed a very active,9 l6 P% h; F1 {5 o3 U- x, o
playful, and healthy boy. The vital signs documented
: g3 l. x  a6 Y5 N9 Z% |: h% ja blood pressure of 85/50 mm Hg, his length was. e1 I) V. I( R  v4 S2 p
90 cm (>97th percentile), and his weight was 14.4 kg& p0 j* i  \' f/ u5 K6 O
(also >97th percentile). The observed yearly growth
+ L- _) r6 j' ^- Z( yvelocity was 30 cm (12 inches). The examination of/ G+ g+ C2 w1 K( C
the neck revealed no thyroid enlargement.
' g4 R7 R5 O6 dThe genitourinary examination was remarkable for
% S7 K7 D8 L; O& Henlargement of the penis, with a stretched length of
9 c1 ?  ?+ E# Z+ ], Q5 j  Y, E; x, T8 cm and a width of 2 cm. The glans penis was very well: F3 \- }% Q: ?, B/ \( I$ }
developed. The pubic hair was Tanner II, mostly around
) W# y: Q9 M5 V. A  Y7 i8 ~540
) x2 D. _, B. Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" S" _7 v5 w  E' [, ]the base of the phallus and was dark and curled. The
) U* a# Z) C. A9 Z+ O2 R9 U; Jtesticular volume was prepubertal at 2 mL each.
9 C0 ~8 P7 A- ]- g2 ~! Y4 mThe skin was moist and smooth and somewhat
* S" z, R; ^; Roily. No axillary hair was noted. There were no! G6 Z% @5 T! c4 t
abnormal skin pigmentations or café-au-lait spots.% T+ L7 z1 b5 \. D" c8 b
Neurologic evaluation showed deep tendon reflex 2+2 u* a/ `9 P/ Z/ }& A1 a
bilateral and symmetrical. There was no suggestion
( p6 [9 ^! N4 X% Z* b2 R$ Hof papilledema." T7 f7 q/ z/ f4 f  t
Laboratory Evaluation
) M9 @3 |! f% U1 fThe bone age was consistent with 28 months by% X8 m: r( i2 f$ H& V1 y4 J
using the standard of Greulich and Pyle at a chrono-
. l6 j4 g: a; Y9 `logic age of 16 months (advanced).5 Chromosomal- e6 @  \. @- l6 E% _2 }0 O
karyotype was 46XY. The thyroid function test
4 {6 L3 t6 O' h8 E5 M% Ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-
/ Q+ j% e8 m! Y6 [! elating hormone level was 1.3 µIU/mL (both normal).; q/ k1 w4 _% t# @: ?
The concentrations of serum electrolytes, blood1 Q7 y/ B6 ]% h- C& x$ K. Z' c1 M
urea nitrogen, creatinine, and calcium all were! `$ S4 M$ `9 A/ Q' |
within normal range for his age. The concentration
2 j/ z5 e7 u+ z( x( y1 x3 Dof serum 17-hydroxyprogesterone was 16 ng/dL
+ m. J# c! p" W1 G* F% j/ ?(normal, 3 to 90 ng/dL), androstenedione was 209 v$ X, i7 E2 _, p+ j( z3 N9 H
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 R8 ?$ _% p4 Z0 Cterone was 38 ng/dL (normal, 50 to 760 ng/dL)," t! J8 Z* Q* u  R
desoxycorticosterone was 4.3 ng/dL (normal, 7 to  H( m8 }/ I0 a& b( K- F
49ng/dL), 11-desoxycortisol (specific compound S)
" X; a7 v5 s0 Zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 ^8 P; v) @7 c# btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 o1 @8 j4 J' T9 |
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
7 @" T; v3 s  D2 Dand β-human chorionic gonadotropin was less than
% ~; F/ \: m1 n7 h3 ]3 z1 n% @5 mIU/mL (normal <5 mIU/mL). Serum follicular9 E  J' m4 m; ^: }# R4 B
stimulating hormone and leuteinizing hormone' w7 r( c, E4 I# Q5 t  |3 k6 M
concentrations were less than 0.05 mIU/mL
2 ~2 N6 b# @& p! `' F(prepubertal).( s8 _6 [1 U3 t
The parents were notified about the laboratory2 j3 Q* B7 V/ A& M! s% E
results and were informed that all of the tests were  ~6 z! w% ~1 ]
normal except the testosterone level was high. The( g* z- o1 T, W" w$ O
follow-up visit was arranged within a few weeks to
/ j- E9 S( C+ zobtain testicular and abdominal sonograms; how-
1 `3 M# Z- L& }4 P9 Y+ E+ h3 Mever, the family did not return for 4 months.
0 W$ N( h) c) K2 KPhysical examination at this time revealed that the
- w$ L( s& ]5 M# q! ychild had grown 2.5 cm in 4 months and had gained
/ z' o; N/ S3 ~: |, q. y, s2 kg of weight. Physical examination remained
7 e+ ~; T, g2 ~; z, _unchanged. Surprisingly, the pubic hair almost com-; u% |4 x0 [$ G/ ]7 ~& B
pletely disappeared except for a few vellous hairs at
2 Y/ B- l/ c% athe base of the phallus. Testicular volume was still 2$ F  w3 P) _# D0 a% k
mL, and the size of the penis remained unchanged.
- q3 B8 X0 X3 `8 K+ AThe mother also said that the boy was no longer hav-& U. i' E0 k' A& f' Y
ing frequent erections./ z  V2 Z$ T- F1 Y8 a# x1 ?# g4 L: X! K
Both parents were again questioned about use of5 z8 I/ i' B' ?
any ointment/creams that they may have applied to
* h+ n. f1 H0 s0 sthe child’s skin. This time the father admitted the
/ h' ^$ M( b7 j7 p1 X0 D* W( KTopical Testosterone Exposure / Bhowmick et al 541
2 u, ]& {- z7 U" H" Cuse of testosterone gel twice daily that he was apply-
: V4 t9 C% F0 r6 ?2 Zing over his own shoulders, chest, and back area for  q- ]* H# H( T3 H
a year. The father also revealed he was embarrassed) M6 _9 u0 \% Z$ U5 D: K$ u! a
to disclose that he was using a testosterone gel pre-- P) B& O5 x. L
scribed by his family physician for decreased libido3 u% ^/ [# P2 s/ t
secondary to depression.7 d. K" t* Q" Q" {
The child slept in the same bed with parents.
( v% D; D- a- O) ?5 j9 K, \The father would hug the baby and hold him on his" c* L4 m1 ?% f6 a/ |" U
chest for a considerable period of time, causing sig-5 j# p6 i9 s* @# v8 W. X
nificant bare skin contact between baby and father.
3 R2 m# v: Q9 [# r8 h7 M: ?# _The father also admitted that after the phone call,
; Y+ J8 d% D% T4 ^% Lwhen he learned the testosterone level in the baby
) a' a, x2 A+ z: f7 q# ^" J& e6 G% `was high, he then read the product information
& B! a  J8 \  T4 H$ Z( n- F7 opacket and concluded that it was most likely the rea-
+ {( F9 x& ^) n) S9 @" Q1 Rson for the child’s virilization. At that time, they4 `! x( o! q! I4 ?/ ]
decided to put the baby in a separate bed, and the
4 @$ N  T! Q9 K) z2 _father was not hugging him with bare skin and had0 g) @6 h1 Y" k2 G
been using protective clothing. A repeat testosterone
* h  s4 `+ `+ p$ Q. C: mtest was ordered, but the family did not go to the
; @7 ~! y) j, H9 B2 B, Flaboratory to obtain the test.
0 Y; b# m2 R! [% F% u6 sDiscussion3 h, C' A: k4 B/ \4 D& n4 W/ |1 h4 T+ o
Precocious puberty in boys is defined as secondary
8 l; q+ X' P+ m$ A+ d% H% Isexual development before 9 years of age.1,4
" S; ?( M) O& R6 T% IPrecocious puberty is termed as central (true) when
( A' h" O- V0 K; K: t# c% Sit is caused by the premature activation of hypo-" k) @0 a/ X  c' q3 i1 n! A
thalamic pituitary gonadal axis. CPP is more com-
. H4 }- K* D4 D. C- w* h6 Z% pmon in girls than in boys.1,3 Most boys with CPP
8 l4 w) `; {5 ~8 k. }may have a central nervous system lesion that is3 G5 o/ @1 V& T3 D! V( z( |
responsible for the early activation of the hypothal-
; \2 G) d" X9 M3 i0 Mamic pituitary gonadal axis.1-3 Thus, greater empha-4 E( y, C9 t  e0 h1 }) P
sis has been given to neuroradiologic imaging in* x+ \! I* \, K* U) l2 Q
boys with precocious puberty. In addition to viril-% L: L, x& k* |: J$ l, O" a- [
ization, the clinical hallmark of CPP is the symmet-2 m* |9 F( f$ ]! z+ ?4 [, N; i- z
rical testicular growth secondary to stimulation by- z' p8 ~. h3 d
gonadotropins.1,3, m0 ]! r3 l5 [) d  h, [6 b
Gonadotropin-independent peripheral preco-7 D- j$ B! T/ x+ p
cious puberty in boys also results from inappropriate/ l7 u( _( ?) L9 q  n
androgenic stimulation from either endogenous or) D) X9 \8 i8 o! H5 S/ N
exogenous sources, nonpituitary gonadotropin stim-
$ Q! T1 x! ]4 l3 o* Xulation, and rare activating mutations.3 Virilizing! Y2 W* d% Y6 c  ~' W5 g
congenital adrenal hyperplasia producing excessive
8 X# N4 ]- j# o' R0 _& {/ |+ Fadrenal androgens is a common cause of precocious
" c" w* o( v$ {7 M' M; k; Ypuberty in boys.3,47 q5 \. u: T1 X! ~- \
The most common form of congenital adrenal" A7 ?; Q" L* V1 R
hyperplasia is the 21-hydroxylase enzyme deficiency.
- f- I4 t, b% \& L. C* G1 EThe 11-β hydroxylase deficiency may also result in
" o9 H9 w4 x! G; p* jexcessive adrenal androgen production, and rarely,3 H+ f% X" ?; h6 U' c4 k6 ^7 X7 P: J
an adrenal tumor may also cause adrenal androgen9 Z0 y0 v' L% S9 F
excess.1,3
% e. b% [% d1 `6 g2 W) W( Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- L% ?. X+ _# Z3 S5 E: I9 K  Y
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
  M7 t5 k" e! e: AA unique entity of male-limited gonadotropin-7 D2 n& c6 z/ o7 M2 w
independent precocious puberty, which is also known
# S, B  w- N- Ias testotoxicosis, may cause precocious puberty at a
1 a' o- J% l& m. p4 b; R+ I. zvery young age. The physical findings in these boys: W% T- \9 O3 h$ H
with this disorder are full pubertal development,0 R9 T6 r9 l0 x" _7 L% g2 |
including bilateral testicular growth, similar to boys7 S  ?2 `/ ^; |7 G1 K" j
with CPP. The gonadotropin levels in this disorder
% w" J6 ^7 w: Hare suppressed to prepubertal levels and do not show, H, a  X& d8 C+ K
pubertal response of gonadotropin after gonadotropin-2 r1 e) C- {: }; a. s8 H
releasing hormone stimulation. This is a sex-linked
- A# m( j# k, p+ O! Vautosomal dominant disorder that affects only
( ~' {& ]; m5 Z7 I/ Y2 m& N. omales; therefore, other male members of the family
6 b' ~! @8 o+ [: _* \may have similar precocious puberty.38 |0 s  O9 `0 d" ]( x
In our patient, physical examination was incon-& n" u) G( _( _2 w. s
sistent with true precocious puberty since his testi-! U1 N  u, Q0 I) e' h
cles were prepubertal in size. However, testotoxicosis! F3 p& P& H8 }; h, ]! W) t8 V) c7 t  O
was in the differential diagnosis because his father
, O( m. i) s' k# l8 Z2 g( Tstarted puberty somewhat early, and occasionally,
0 E5 a7 D1 F; Itesticular enlargement is not that evident in the; @5 J$ |' Y% ]4 i5 V" J1 Y. k
beginning of this process.1 In the absence of a neg-" I$ k/ r5 @) N9 t
ative initial history of androgen exposure, our
! {4 D9 d6 e, Obiggest concern was virilizing adrenal hyperplasia,
& O4 v8 n+ t% M- Veither 21-hydroxylase deficiency or 11-β hydroxylase# {4 _! h. Q+ a6 F8 R+ M' q
deficiency. Those diagnoses were excluded by find-% p* Y# k9 }' {: X2 j8 k- j
ing the normal level of adrenal steroids.
! Y" i' o4 L  t8 u8 R6 H$ ^$ H2 qThe diagnosis of exogenous androgens was strongly
* t& A6 O9 D5 isuspected in a follow-up visit after 4 months because
7 x; c1 x3 N+ Q/ V" [- n! v0 qthe physical examination revealed the complete disap-% H# l2 r/ K( {
pearance of pubic hair, normal growth velocity, and
: o$ A+ e2 p: M/ gdecreased erections. The father admitted using a testos-, K' T2 p- n* L( [6 }
terone gel, which he concealed at first visit. He was7 Y- |% D2 q) z% ]/ f
using it rather frequently, twice a day. The Physicians’
* v/ A. [, s8 \% QDesk Reference, or package insert of this product, gel or
6 G- @, ]% h- u% S3 hcream, cautions about dermal testosterone transfer to
& B9 N  r( k8 V1 i# lunprotected females through direct skin exposure.
' C8 u1 j) S  u" s: U& lSerum testosterone level was found to be 2 times the5 n  z" [4 B0 Z7 h9 f
baseline value in those females who were exposed to8 q, A9 N4 Z! X+ E/ @
even 15 minutes of direct skin contact with their male3 o* }& y$ S, `6 c! h6 @: Y
partners.6 However, when a shirt covered the applica-
, z3 R3 k4 e6 h$ ztion site, this testosterone transfer was prevented.8 r; V  }3 h4 ?. Q( @& ~3 m$ J3 \
Our patient’s testosterone level was 60 ng/mL,
3 i& F, z) r+ @0 F5 W2 v! ywhich was clearly high. Some studies suggest that- x* P" M. E7 T9 A. }6 y
dermal conversion of testosterone to dihydrotestos-
' a# \) h+ ~  W0 o. i; d5 cterone, which is a more potent metabolite, is more$ Z, S9 O7 d0 F  A) \
active in young children exposed to testosterone7 y, X; n0 l& j7 `3 W- X
exogenously7; however, we did not measure a dihy-
  W- E  t5 @3 O( ^9 ?drotestosterone level in our patient. In addition to) V# q2 R8 ^3 N0 r& G% @" t" p
virilization, exposure to exogenous testosterone in
/ \, `1 V6 j1 Xchildren results in an increase in growth velocity and! P" z* q$ d& T$ X: v% W. u
advanced bone age, as seen in our patient.2 ^8 |  q, @4 g* i$ j4 ]8 f
The long-term effect of androgen exposure during- I0 M& |" j# D2 C
early childhood on pubertal development and final4 p( D9 A$ H% J# s/ V
adult height are not fully known and always remain
& Y& E. s3 {  e: ea concern. Children treated with short-term testos-1 [# Z' m: I6 ?, j7 ]( q- e  s
terone injection or topical androgen may exhibit some) T6 F" A$ L  c# h9 o- H3 g6 I4 j
acceleration of the skeletal maturation; however, after
. X* U% r5 e! M/ f* E/ Kcessation of treatment, the rate of bone maturation
8 P, o1 M- H- T) f% ], _decelerates and gradually returns to normal.8,96 C/ W$ O+ E% E, L! M
There are conflicting reports and controversy
  ^4 E7 W+ A, J; r0 S* `% @over the effect of early androgen exposure on adult  X1 A9 H; r0 u" T8 c; ]  A7 f
penile length.10,11 Some reports suggest subnormal5 o/ i4 F0 s& s
adult penile length, apparently because of downreg-
; n$ k5 F6 T3 ?. s- @: xulation of androgen receptor number.10,12 However,7 v' ~  G+ C8 }$ I- R7 w
Sutherland et al13 did not find a correlation between$ ], {- Y! |7 U2 F. C# z, f
childhood testosterone exposure and reduced adult
3 v* G! a, N- s2 ?  r8 Z0 y: apenile length in clinical studies.
) s. H% Q5 j, o# \, _Nonetheless, we do not believe our patient is& `8 Q" r3 z4 ~: p: Q8 v
going to experience any of the untoward effects from
( v" ]) ~( u+ ^) @testosterone exposure as mentioned earlier because
/ o( u' b; c( b" W$ W2 B' I3 ithe exposure was not for a prolonged period of time.
* x. a$ W) F6 P7 {+ t5 f. y, @/ jAlthough the bone age was advanced at the time of6 g: z) v& U8 E7 ~6 F5 f4 d' |
diagnosis, the child had a normal growth velocity at
1 }5 R5 m# Y- _4 \1 hthe follow-up visit. It is hoped that his final adult
- D( v4 _' b6 c8 b1 Gheight will not be affected.
% |% a3 W% R% j, ?+ V8 HAlthough rarely reported, the widespread avail-7 K/ A6 |, l( T3 N1 F
ability of androgen products in our society may- b1 ^3 F2 v, S  s4 ]
indeed cause more virilization in male or female6 _* s6 B( Y2 [. o6 M0 N' z+ h
children than one would realize. Exposure to andro-
" J' G1 P  D' C, Cgen products must be considered and specific ques-
0 b1 D* z. [- t& b! f3 }6 |+ S$ f6 |tioning about the use of a testosterone product or, A( H" O! |7 d) y: `8 h3 S8 F
gel should be asked of the family members during
5 h2 K& G5 D2 H2 i7 ?3 dthe evaluation of any children who present with vir-  j4 }1 j, T7 I9 r0 {1 Y# r! l
ilization or peripheral precocious puberty. The diag-
# o& t0 ?9 b6 a, ]9 znosis can be established by just a few tests and by. G  j% y( _# c1 i9 ?
appropriate history. The inability to obtain such a, U0 X/ U  g8 R3 a7 m, x0 b0 k3 ]5 e
history, or failure to ask the specific questions, may
% I7 m! l! Y% Y! _  rresult in extensive, unnecessary, and expensive
- m2 i. T7 g8 T% Y, R0 jinvestigation. The primary care physician should be: G, x2 [& p( c. N" A3 ^
aware of this fact, because most of these children
: s$ K5 T; q5 ?" Rmay initially present in their practice. The Physicians’
2 h' H9 w, g3 V' h, ?4 sDesk Reference and package insert should also put a
% z& ^4 e" e% q8 `( ?$ Swarning about the virilizing effect on a male or# j8 O& g  I+ e; A3 {- z, D8 r
female child who might come in contact with some-
' L2 j. }) S& n  k8 Cone using any of these products.& f2 o9 b. h; _. l, R
References
" M! a+ j# G+ M* V$ _$ F$ F1. Styne DM. The testes: disorder of sexual differentiation
! g, \* m- K1 l& W5 _and puberty in the male. In: Sperling MA, ed. Pediatric: }0 M5 H: g5 T# Y& N4 t' F
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;/ a" B: ?2 h+ z, j- n0 C% S
2002: 565-628." p+ t  U4 y2 w  M7 b  S! c/ K. B' M
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& S( h- I/ `! c6 apuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
. j- N$ ?7 ?% ?Boy Induced by Indirect Topical
9 r' c6 ]/ C0 o0 M6 L5 y4 DExposure to Testosterone# e$ w: O0 X5 n: _6 @
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* H" `  q7 H( L7 t4 L% J
and Kenneth R. Rettig, MD11 n8 N$ w  @9 d
Clinical Pediatrics0 J1 L$ |  t# N& r: M
Volume 46 Number 6, K  `+ k9 y& t& Z
July 2007 540-543& l  {7 c9 ]# T6 r" `
© 2007 Sage Publications1 w5 y% S  g& q5 q! E3 h
10.1177/0009922806296651
$ S6 k  K' |# h' U7 b0 Mhttp://clp.sagepub.com8 @# r0 a1 g1 M6 G* X
hosted at" x  C! K$ g2 a4 Q$ L) I0 m3 S
http://online.sagepub.com
8 N5 ^% F8 @3 f  z2 f' U/ I2 i$ G# IPrecocious puberty in boys, central or peripheral,4 O/ z/ g% I5 T$ i1 D  g: Q6 T& T
is a significant concern for physicians. Central
9 e& U! T3 }. kprecocious puberty (CPP), which is mediated
& \% {0 q6 U1 T3 Ethrough the hypothalamic pituitary gonadal axis, has
/ M: A2 }0 Q3 p* s( u: sa higher incidence of organic central nervous system5 \0 O1 ^( r9 |. j8 D& X6 P
lesions in boys.1,2 Virilization in boys, as manifested
! o: i8 z, B: i) Z% Z0 D) {by enlargement of the penis, development of pubic( y1 w; l) u) J0 E7 `5 o% Y
hair, and facial acne without enlargement of testi-3 h/ A) f: ]! b( _& w
cles, suggests peripheral or pseudopuberty.1-3 We
0 s; y% l# s3 Mreport a 16-month-old boy who presented with the
0 v3 L. F1 x$ ~' l; I3 Eenlargement of the phallus and pubic hair develop-) e  |! H" [% _2 H. x4 o# Q$ ]
ment without testicular enlargement, which was due, o8 Y  ?# T) t; U. h8 m# J
to the unintentional exposure to androgen gel used by& }3 N4 i+ A8 D
the father. The family initially concealed this infor-* m) \( s7 z) o6 Q5 L6 }2 Z1 p
mation, resulting in an extensive work-up for this
& ]6 Y6 {: A( i5 D' v6 Echild. Given the widespread and easy availability of+ O3 X- B8 B. q
testosterone gel and cream, we believe this is proba-9 p6 \" j( O9 F
bly more common than the rare case report in the" v* \* \1 ~* v- v' |" Z
literature.4
* u0 Q2 f& z  Q4 A& |5 XPatient Report  q; G7 p) |- Y- P
A 16-month-old white child was referred to the
3 h# x: C4 y& ]% P6 L1 tendocrine clinic by his pediatrician with the concern
- N8 h4 X4 Y; m* eof early sexual development. His mother noticed
& C( I; C) [! i6 X% Jlight colored pubic hair development when he was) x% S9 Q3 ]) L+ f/ e! [5 Y. W
From the 1Division of Pediatric Endocrinology, 2University of0 |' E1 H* A6 F+ s, ]4 O0 s9 Z. `
South Alabama Medical Center, Mobile, Alabama.7 V: P0 H" |/ C2 \( s' i" ?
Address correspondence to: Samar K. Bhowmick, MD, FACE,
; m, T, m& ?7 T, _% }Professor of Pediatrics, University of South Alabama, College of
) W% d9 X/ X% j$ [! K$ ^Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 m7 s7 o. a2 D$ G# M/ T) u4 E! V- i
e-mail: [email protected].8 i3 [& n1 R4 G! K, W
about 6 to 7 months old, which progressively became7 X! o8 ?" b5 ~9 @5 B
darker. She was also concerned about the enlarge-+ G$ g! a& a% V6 G1 b) {$ g: C
ment of his penis and frequent erections. The child
5 g" H- d: B  j  y- ywas the product of a full-term normal delivery, with7 B8 d* N, y2 Q: e8 F
a birth weight of 7 lb 14 oz, and birth length of
  m5 }8 N' Y  R" {4 O20 inches. He was breast-fed throughout the first year
. z9 G+ E* G/ G8 Q; ]/ nof life and was still receiving breast milk along with
3 t( Z" S6 Q" J6 }6 ~! B4 psolid food. He had no hospitalizations or surgery,
' P1 b+ i! q$ r# ^6 qand his psychosocial and psychomotor development. D, A4 T8 ?7 S5 T( v
was age appropriate.
; P0 R* n$ s2 m$ T* T  E6 d8 h' yThe family history was remarkable for the father,* L9 j0 p1 {5 `
who was diagnosed with hypothyroidism at age 16,( D/ `; J( y; x3 c; u& A
which was treated with thyroxine. The father’s
6 g# k. s' J- k) |* U9 c& P3 c5 B. jheight was 6 feet, and he went through a somewhat. T: J* x/ L  n( H/ J
early puberty and had stopped growing by age 14.1 Z# Y$ B; `- q
The father denied taking any other medication. The
$ C# U8 Q% {! I0 k# ?" Q7 t- Xchild’s mother was in good health. Her menarche
: v  [7 f6 J6 ?$ jwas at 11 years of age, and her height was at 5 feet
! }7 M9 M8 s6 Z  Y! c: Q4 [5 inches. There was no other family history of pre-/ {& `0 D. z0 l* V" n, ]
cocious sexual development in the first-degree rela-
5 x7 V/ r+ B3 Z9 O: S9 Qtives. There were no siblings." \" D9 W) S& V7 a! i( }- x; w
Physical Examination9 T4 e: h( ^  A
The physical examination revealed a very active,
. a6 r& G$ I* ~, h) nplayful, and healthy boy. The vital signs documented7 j# m; M) V8 C& V, T0 p
a blood pressure of 85/50 mm Hg, his length was9 i# z, Q3 S7 J! B3 q; z  U" r
90 cm (>97th percentile), and his weight was 14.4 kg% H/ _  y( V# I
(also >97th percentile). The observed yearly growth5 Q* m* M  B) Z/ \1 G
velocity was 30 cm (12 inches). The examination of
7 Q; a$ T) h! j+ [the neck revealed no thyroid enlargement.) A8 S% y( v+ ]/ D0 b* O
The genitourinary examination was remarkable for
9 T0 |) p, \$ c0 W. cenlargement of the penis, with a stretched length of
! r. Y1 e, m- b8 F3 p0 l8 cm and a width of 2 cm. The glans penis was very well
2 Z( J! W( ^8 `developed. The pubic hair was Tanner II, mostly around
6 W& Z2 T/ s" R7 j) S540
4 u; _' V( e4 E% m3 [2 j$ e5 o' [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) _- q+ r$ V" E: Kthe base of the phallus and was dark and curled. The
6 W5 g  h. V; }0 Rtesticular volume was prepubertal at 2 mL each.& S/ m1 \' b8 x! u
The skin was moist and smooth and somewhat" v+ D1 q$ K1 I7 |( }! d
oily. No axillary hair was noted. There were no! ^/ H  a8 l9 y3 X
abnormal skin pigmentations or café-au-lait spots.5 v; y& {. O4 [, Y7 R& O  ?
Neurologic evaluation showed deep tendon reflex 2+4 E* h5 P/ ~8 v. l
bilateral and symmetrical. There was no suggestion6 H+ |7 z  ?$ ?+ Z, C; d
of papilledema.
' A! R& T+ ?" s3 RLaboratory Evaluation8 t7 a5 I; H% y, ]2 z9 d
The bone age was consistent with 28 months by) X! ^& X1 D; U* x
using the standard of Greulich and Pyle at a chrono-
4 [8 P- c5 `. tlogic age of 16 months (advanced).5 Chromosomal& p5 m, c/ P1 x% [/ g
karyotype was 46XY. The thyroid function test
# u0 f7 d2 Q8 p) C7 _9 D( eshowed a free T4 of 1.69 ng/dL, and thyroid stimu-$ ?6 t" @& ?1 \$ y. j: y1 {
lating hormone level was 1.3 µIU/mL (both normal).
- n/ G6 J& K/ u" l! yThe concentrations of serum electrolytes, blood
" q  W* v/ [5 T3 _% nurea nitrogen, creatinine, and calcium all were
+ u$ ~" \; D2 p4 n  @within normal range for his age. The concentration
- c8 U+ @5 \: B9 e; {- a, ]1 _of serum 17-hydroxyprogesterone was 16 ng/dL
% [: {9 _: z* [+ }0 z; j(normal, 3 to 90 ng/dL), androstenedione was 20
2 z- g7 S# [/ q& E) f. Z! }# |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- z7 a; n2 q/ O% x# w; r; ^2 |terone was 38 ng/dL (normal, 50 to 760 ng/dL),
' H+ B, V/ f) D( F& j$ j3 I9 rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( ~5 _* D1 k3 d; t" @2 h8 ^8 Z& h; ~49ng/dL), 11-desoxycortisol (specific compound S)
7 H  Q% f& r1 T4 g4 qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: Z# v4 Z) F  g) {
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: s" y: x8 m' N1 V7 ^' A  a, _( f/ n
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),6 R. i9 i0 T1 H4 m6 X
and β-human chorionic gonadotropin was less than9 @9 ^7 M" G$ Y! {4 @) V
5 mIU/mL (normal <5 mIU/mL). Serum follicular
5 u  E" |" |5 D  i0 Z) bstimulating hormone and leuteinizing hormone
; f( X  ?* d1 d# Kconcentrations were less than 0.05 mIU/mL
6 ^8 ?4 Y' a3 O, u" o3 K7 r(prepubertal).( `1 n5 \0 l. a( W# V) l
The parents were notified about the laboratory8 i3 l4 C# u1 n9 z  x; g! D
results and were informed that all of the tests were
7 U5 \/ c/ ?* R3 cnormal except the testosterone level was high. The& B: q3 @3 Y7 M+ g) g6 u2 }/ H
follow-up visit was arranged within a few weeks to
7 D8 l6 j$ H3 w- zobtain testicular and abdominal sonograms; how-/ v5 y/ A& g  k: C: Z; C
ever, the family did not return for 4 months.! q5 y- P- {1 r, Z
Physical examination at this time revealed that the6 Z  a: `4 o9 w9 J  w/ y$ \' x& ?7 J
child had grown 2.5 cm in 4 months and had gained
, e* d3 c* O% [4 R2 kg of weight. Physical examination remained/ G3 @; e1 U6 d0 z! H3 K2 [
unchanged. Surprisingly, the pubic hair almost com-7 b5 Q+ c# }$ S5 R. Q/ @
pletely disappeared except for a few vellous hairs at; P: c8 K1 O. \% z1 a
the base of the phallus. Testicular volume was still 2
6 j4 A" g. |: T; emL, and the size of the penis remained unchanged.
# C, h, @! O0 j( L/ xThe mother also said that the boy was no longer hav-4 v6 L( x* [; f; R; v1 E
ing frequent erections.! V! p4 o, r0 u& B$ c# ~
Both parents were again questioned about use of; V. g: x' Z9 q( f' t
any ointment/creams that they may have applied to) d1 ]$ T3 {. H
the child’s skin. This time the father admitted the$ y, `' a# \' N
Topical Testosterone Exposure / Bhowmick et al 541
7 N, G- m8 N' Z7 e3 q, fuse of testosterone gel twice daily that he was apply-
, W; K% _5 |& t% h  d$ sing over his own shoulders, chest, and back area for
( ?! f0 ]$ h9 P* a1 O% w1 La year. The father also revealed he was embarrassed' ~' ]! j, z2 R" G, c
to disclose that he was using a testosterone gel pre-+ o- r0 Z' P6 V. I8 c$ @+ x
scribed by his family physician for decreased libido
4 g+ R) v) X% A, D  ]! Z6 P9 qsecondary to depression." Z2 q" l1 }' O, a8 D9 I9 Y
The child slept in the same bed with parents.
- H3 P" ?& J7 AThe father would hug the baby and hold him on his: B: o% k0 A2 \+ J3 m
chest for a considerable period of time, causing sig-3 N- V8 z5 q( @! O! ~# ?
nificant bare skin contact between baby and father.
' p$ Q( o: _* I, K% Q6 ZThe father also admitted that after the phone call,
$ q- S" k( p8 U$ E- T$ I8 j0 r" G6 swhen he learned the testosterone level in the baby1 o5 C) z2 a: o7 y( i2 O0 `) D% ?
was high, he then read the product information
; H& h& j1 g+ X9 k8 D2 apacket and concluded that it was most likely the rea-
$ S1 W" G, {, ~- s7 a$ B4 _* o) |son for the child’s virilization. At that time, they% I' }# j1 v6 F8 Z- L, P5 k
decided to put the baby in a separate bed, and the5 f7 R" C* t7 `( ?1 E
father was not hugging him with bare skin and had
' b( P' a9 o4 G5 Xbeen using protective clothing. A repeat testosterone
+ r8 f8 N& L2 P+ q3 d- Ptest was ordered, but the family did not go to the
7 Z9 Q# E0 D5 M1 Y$ Slaboratory to obtain the test.$ L" b2 H0 E2 S* {4 C) u; \0 e1 J
Discussion
* J' t( v$ e- E" FPrecocious puberty in boys is defined as secondary
1 J/ Y. B8 h( U+ C# E2 rsexual development before 9 years of age.1,4
. y1 _8 ]7 n0 j1 G5 s4 z  zPrecocious puberty is termed as central (true) when2 g2 Z/ x1 r+ l9 _4 e
it is caused by the premature activation of hypo-
+ }6 A' n5 p0 y) l# U: H3 F9 b  Lthalamic pituitary gonadal axis. CPP is more com-+ G9 |+ x1 m% N/ J- T  i1 p
mon in girls than in boys.1,3 Most boys with CPP
# v( `/ Q* R2 n% ]may have a central nervous system lesion that is
( s; \3 o# {3 M2 N( oresponsible for the early activation of the hypothal-# l3 e) I. b" H: }& |
amic pituitary gonadal axis.1-3 Thus, greater empha-
: e+ Y3 }& B$ Z7 Fsis has been given to neuroradiologic imaging in
! C0 J' ?% w  }0 f; J! Q7 yboys with precocious puberty. In addition to viril-
! e$ Z! O1 _4 j/ s& i, r# ^! Kization, the clinical hallmark of CPP is the symmet-
; M9 s! C$ `3 o4 W* lrical testicular growth secondary to stimulation by
, V3 W# X4 l' ogonadotropins.1,3. S# Q& I( S" h7 z3 X% Q
Gonadotropin-independent peripheral preco-
. D7 y; }+ s6 F- Ycious puberty in boys also results from inappropriate9 E; ^2 i+ x: |! K  S7 j& g7 D* M, ]
androgenic stimulation from either endogenous or
$ r9 w- {2 H6 n: ]exogenous sources, nonpituitary gonadotropin stim-: ]) S: T& z# }2 b' C* w
ulation, and rare activating mutations.3 Virilizing% L2 W* L9 G, K- u. B- h
congenital adrenal hyperplasia producing excessive
# Y) f( A% {) b3 x7 g0 s" M+ {adrenal androgens is a common cause of precocious6 q& I4 P0 j6 A: l5 P  z! O
puberty in boys.3,4
" A5 ^6 U) T9 s* u" [; @  nThe most common form of congenital adrenal: Y% q( W) T  J: P. u$ ]
hyperplasia is the 21-hydroxylase enzyme deficiency.
+ o) _& B8 V& k* ^The 11-β hydroxylase deficiency may also result in6 s; b0 _8 h6 f, l  x
excessive adrenal androgen production, and rarely,
7 x0 p3 P4 q& r9 h& D+ \' _an adrenal tumor may also cause adrenal androgen( m1 P8 e! h: Y5 B  }
excess.1,3
$ c; Q# H5 u- y( ^. Fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% J2 D5 b' M2 Q/ o
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 v1 v7 C5 C  W5 L+ A6 Z) JA unique entity of male-limited gonadotropin-
5 F% K+ s8 L- Z/ kindependent precocious puberty, which is also known
- q4 \1 L9 T: [. C) ]as testotoxicosis, may cause precocious puberty at a
* j: V9 @- U4 i1 }; H% Zvery young age. The physical findings in these boys' u( C8 z5 q+ k: G: a% U3 ^: Q7 y8 g* \
with this disorder are full pubertal development,
4 d) L8 _3 G* @3 R) |, Gincluding bilateral testicular growth, similar to boys
: ^9 v* `5 S2 n8 c) D: x5 Awith CPP. The gonadotropin levels in this disorder: d* {/ C, |; Y3 U. W6 ]
are suppressed to prepubertal levels and do not show
2 C$ `1 g/ M# P+ `( R+ A/ xpubertal response of gonadotropin after gonadotropin-# a6 ^: g7 h4 f: I& D1 f/ X
releasing hormone stimulation. This is a sex-linked1 ~" [3 A. e! O( W# r
autosomal dominant disorder that affects only; `; B0 L6 e; y
males; therefore, other male members of the family5 {- s7 F7 P" E& v1 W
may have similar precocious puberty.31 {7 v1 a1 f" u! w0 Q( X( c9 E
In our patient, physical examination was incon-  y* I" _: [8 u: g
sistent with true precocious puberty since his testi-
4 s, e5 A3 |3 }cles were prepubertal in size. However, testotoxicosis
( y& j, n' J" s. o7 U. }' zwas in the differential diagnosis because his father6 j& K+ k! L" e% f/ T
started puberty somewhat early, and occasionally,/ E1 m1 R# E  y& t( ~' ?% S
testicular enlargement is not that evident in the0 }1 z/ y  T* C2 a, \" u
beginning of this process.1 In the absence of a neg-
+ b# ]  Y' Q. O. R8 f. native initial history of androgen exposure, our. K2 I. ?3 t7 V9 R5 D
biggest concern was virilizing adrenal hyperplasia,
% `1 E* v- D" ?% x7 z8 O+ Q0 Beither 21-hydroxylase deficiency or 11-β hydroxylase5 Y0 Z5 \) R8 S
deficiency. Those diagnoses were excluded by find-
* k" l8 x$ E! f+ Q( Zing the normal level of adrenal steroids.- X8 c) a. Y1 t+ a
The diagnosis of exogenous androgens was strongly
4 {( @; k3 k( F# e- lsuspected in a follow-up visit after 4 months because- d4 Y2 x0 l; d: L, b, L) d
the physical examination revealed the complete disap-+ b1 e0 B4 l& q
pearance of pubic hair, normal growth velocity, and
$ X% a$ \5 a& p. F8 j" bdecreased erections. The father admitted using a testos-. Z" o# ^3 u/ F" h$ y: ?& @
terone gel, which he concealed at first visit. He was9 E) L0 W" o: F0 v) V+ ~  F
using it rather frequently, twice a day. The Physicians’
+ ]+ y7 L0 W# ^Desk Reference, or package insert of this product, gel or
9 h" D8 t& U, k2 l7 c# G4 Xcream, cautions about dermal testosterone transfer to$ K" V3 Y0 x4 d6 `8 ?. d
unprotected females through direct skin exposure.! G7 \/ q% ~8 N  a
Serum testosterone level was found to be 2 times the
0 o9 r6 x3 T; r3 Jbaseline value in those females who were exposed to
- [. `, T3 o! W3 ieven 15 minutes of direct skin contact with their male
" ^( B- C4 _+ k+ \9 l9 p9 zpartners.6 However, when a shirt covered the applica-/ f" X0 N7 N1 ~/ ~
tion site, this testosterone transfer was prevented.
8 ]) L& p! n' t6 \7 j+ b+ ~2 SOur patient’s testosterone level was 60 ng/mL,
4 x$ O8 E- k- y& v* S% owhich was clearly high. Some studies suggest that
! |2 A' ?1 f! M! [& t8 ^) h6 Ldermal conversion of testosterone to dihydrotestos-3 `# R" S) A5 C
terone, which is a more potent metabolite, is more
# U, B: C3 G( Dactive in young children exposed to testosterone+ p1 I% X) M# d: b% {
exogenously7; however, we did not measure a dihy-
+ |- R- Y; |# Ldrotestosterone level in our patient. In addition to/ }- _9 ^6 k7 o3 m7 d
virilization, exposure to exogenous testosterone in
+ q" i5 U0 C8 e% [* achildren results in an increase in growth velocity and
4 K( |4 J2 h+ H& ?2 U* Wadvanced bone age, as seen in our patient.+ }* e9 a) @! o2 T& c
The long-term effect of androgen exposure during: D8 x) ?3 c' A4 @. T( q% t
early childhood on pubertal development and final
, e: Y" O  i; I8 X8 Iadult height are not fully known and always remain
* f/ ~  k9 v, W5 `1 ]1 ga concern. Children treated with short-term testos-
% F) l* Y5 V  b& l7 qterone injection or topical androgen may exhibit some9 x8 b( O6 y7 k
acceleration of the skeletal maturation; however, after  I" b% _% f& h- Z, W$ e5 X" m; ?
cessation of treatment, the rate of bone maturation* Z% A- }* M# R8 {! N" F
decelerates and gradually returns to normal.8,9
1 ?1 Z- k8 R7 E" U- y$ zThere are conflicting reports and controversy
6 d# Y3 |0 g* r* z' u: b" Jover the effect of early androgen exposure on adult! i; H8 a9 V2 _: L: B
penile length.10,11 Some reports suggest subnormal* b, M4 |/ K) z$ Q8 F0 W. c- C
adult penile length, apparently because of downreg-
$ Z# |' M3 M/ g! z' \, j( Eulation of androgen receptor number.10,12 However,5 i# p0 F* r1 S, d
Sutherland et al13 did not find a correlation between! D2 |7 q3 ~4 [0 p( r) c! X9 F
childhood testosterone exposure and reduced adult4 C& \1 b, ^) D: k  y
penile length in clinical studies.
0 I* |# F% P( nNonetheless, we do not believe our patient is
7 I9 @  X% x; G5 M+ T* O6 s$ cgoing to experience any of the untoward effects from! ~7 N6 q: B/ X' }9 a) n+ |
testosterone exposure as mentioned earlier because
0 A$ G, O3 I5 |3 b. j5 t  hthe exposure was not for a prolonged period of time.
3 X# k, y; H' c' J, W0 S, U' o& yAlthough the bone age was advanced at the time of
3 f. ]* [7 G. Ediagnosis, the child had a normal growth velocity at' Y; U0 {. Q. a, P! K; W, ^" R# h
the follow-up visit. It is hoped that his final adult1 {, d1 p( y6 z$ A0 \2 g$ p
height will not be affected.
, t- {0 r7 A- R1 ]' r; ^Although rarely reported, the widespread avail-4 X9 O$ q4 S2 ?+ \
ability of androgen products in our society may
8 c, I& @  Z) X2 m3 q1 R# n8 cindeed cause more virilization in male or female, X6 R2 @: e5 Y3 T, R
children than one would realize. Exposure to andro-
- q. C+ O- c5 F# G) N7 f& v  R; g9 `& }7 Ygen products must be considered and specific ques-0 A6 B# q% U- ]7 s) c' g( A7 [; o! D
tioning about the use of a testosterone product or1 |$ D7 ]% ^: D: `- S$ C( y5 `, t
gel should be asked of the family members during0 o* o7 T4 ^$ }9 x' J" i! Y' z
the evaluation of any children who present with vir-+ `) D$ I, t  t+ i* q$ o/ Y. ]' Q
ilization or peripheral precocious puberty. The diag-! Q7 s2 y! }) b6 I: d% C% ^
nosis can be established by just a few tests and by
4 g' \" e) U+ t# G0 x/ o/ H% `, nappropriate history. The inability to obtain such a  h. d( Z" W9 L7 P6 l% F
history, or failure to ask the specific questions, may3 t# u; b, T. m9 m( y! U5 K* X- H
result in extensive, unnecessary, and expensive
. Z4 D$ _) a1 G. R8 J- P) vinvestigation. The primary care physician should be
! [, T! M5 A- d- G( ~: O: }aware of this fact, because most of these children$ a  [5 A5 k2 h* E/ j: @
may initially present in their practice. The Physicians’
$ O' q% F3 f; r6 m: E3 r" _Desk Reference and package insert should also put a  J$ t* `( [* Q) J, s" l
warning about the virilizing effect on a male or
4 m0 r) q1 R# W/ f1 `2 _female child who might come in contact with some-6 Q: I/ M  c4 E$ J" J: a$ u9 l
one using any of these products.$ c( h! P, K6 }5 _/ E! g; J5 w
References$ v% s- S  ?. u8 f+ F( F
1. Styne DM. The testes: disorder of sexual differentiation) h8 k) A5 s* {* F( B
and puberty in the male. In: Sperling MA, ed. Pediatric
5 ^1 R6 [. G" {! ~Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 c. K+ M9 l5 V" f
2002: 565-628.
3 D& x* }+ M( D$ M1 k2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* Q9 S# ^- Z) n( `3 Z+ w1 ypuberty 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
" y9 Q" c# k- \8 C. R% r
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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