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Sexual Precocity in a 16-Month-Old- P5 W5 P( S5 i* `- p- e; H
Boy Induced by Indirect Topical
: T" D1 [* x( U( |4 V8 ?, @) QExposure to Testosterone
) C1 V+ `% M, x5 R  }6 D. ESamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! l$ Z/ p# J8 E! V( d. I; [" q
and Kenneth R. Rettig, MD1
; N/ m, ]' h5 V, y1 U, O1 sClinical Pediatrics
2 r& j" X; B# {' d& |Volume 46 Number 6
8 i$ L3 f; t) i, l3 ~  W! [/ p* R/ F( aJuly 2007 540-543
9 g4 P& w4 [+ r6 y) l, @© 2007 Sage Publications
/ H9 i$ v" l2 `10.1177/0009922806296651
. w  g1 {1 z+ p! E& t: ]: e# {% Qhttp://clp.sagepub.com( F! q2 Z8 o  ?
hosted at$ |7 D" Y: t# ~& h- z+ x* q' e
http://online.sagepub.com0 |0 z9 i$ Z  [: M7 f: v& k
Precocious puberty in boys, central or peripheral,
  k1 x' N6 L# L, P5 Z4 O5 `is a significant concern for physicians. Central
* O2 s* t8 r0 Aprecocious puberty (CPP), which is mediated
3 Q: U) ^' L/ O9 ~through the hypothalamic pituitary gonadal axis, has
9 I% q5 p. k0 ba higher incidence of organic central nervous system
0 i' r! Z# T7 z. e& Plesions in boys.1,2 Virilization in boys, as manifested- k0 o7 @! n: a& T% J  i7 O4 @7 }
by enlargement of the penis, development of pubic  T" D0 E! J4 k, D/ @$ Z3 ?" }
hair, and facial acne without enlargement of testi-  x2 @0 m0 Q, u# {0 ?' f" N2 J
cles, suggests peripheral or pseudopuberty.1-3 We
& U) k( {- v& H, P% Qreport a 16-month-old boy who presented with the
2 D" m' W2 k9 d6 kenlargement of the phallus and pubic hair develop-
4 b0 W$ W# z4 {ment without testicular enlargement, which was due2 \4 T4 T0 }; w& E3 K# I) P
to the unintentional exposure to androgen gel used by
, q1 F0 P' F) _: q" ~the father. The family initially concealed this infor-
# Y* Y% l* f) P- dmation, resulting in an extensive work-up for this
; i8 `4 L5 |& c$ x. Bchild. Given the widespread and easy availability of
! T, X  C  i% |: G& J7 otestosterone gel and cream, we believe this is proba-
0 e  |2 J" e; ^0 lbly more common than the rare case report in the
! G3 q. H! T7 zliterature.4; l2 T3 i5 W* C. o9 `
Patient Report  x) e- S; ]; ^- G4 P/ R
A 16-month-old white child was referred to the- \6 J. Y# c0 v
endocrine clinic by his pediatrician with the concern
2 Y0 P7 _: l( ^6 m; dof early sexual development. His mother noticed
' v5 T( G8 d/ z* Z1 i# x* [( {light colored pubic hair development when he was
4 c/ f+ \. ?  s8 X0 ~* v, w( fFrom the 1Division of Pediatric Endocrinology, 2University of
9 I# ^* b; F2 b6 P; \" S3 q& H. K& O& QSouth Alabama Medical Center, Mobile, Alabama.  m9 t3 h/ q* \
Address correspondence to: Samar K. Bhowmick, MD, FACE,
$ r- R) X; ^4 V6 H7 p1 \Professor of Pediatrics, University of South Alabama, College of
- C  q/ }4 P' f( O) aMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) i- K  G9 r. B: l6 t
e-mail: [email protected].: N2 D3 j4 }* v' o# q8 u
about 6 to 7 months old, which progressively became
. ]) a' C8 e" Q6 edarker. She was also concerned about the enlarge-
$ J7 W3 G1 N( Z; e0 K  {% ament of his penis and frequent erections. The child
% n3 Q5 m% T+ Z  i$ j/ {was the product of a full-term normal delivery, with9 Q% w( b7 G. p& ]" J
a birth weight of 7 lb 14 oz, and birth length of6 C' \8 A- Y* w% |; W9 ~- r5 D
20 inches. He was breast-fed throughout the first year
1 |9 W( J) T8 r8 e2 A5 W4 [of life and was still receiving breast milk along with
) e) ]% i0 q5 @4 usolid food. He had no hospitalizations or surgery,
! j5 k% t) `7 C5 b& j! Nand his psychosocial and psychomotor development
2 O* c* m1 d% bwas age appropriate.3 r! i( F6 g0 \2 [+ B
The family history was remarkable for the father,$ c& m& a" G8 _0 R' u
who was diagnosed with hypothyroidism at age 16,
  v9 k( W6 L9 o& g+ O! E1 Owhich was treated with thyroxine. The father’s% P9 ]  D% {3 i1 N
height was 6 feet, and he went through a somewhat% J( y# T$ q4 R1 ?  B2 h4 l3 |. H, A$ F; C
early puberty and had stopped growing by age 14.& A- p7 R( R" Z# v. S" @
The father denied taking any other medication. The* [% E$ q& x- v- s9 P6 Z5 o
child’s mother was in good health. Her menarche
, Q( ^0 s8 h, I& c) Zwas at 11 years of age, and her height was at 5 feet
1 R% k" V2 _! f4 K9 X& J8 J6 L* C' ^5 inches. There was no other family history of pre-2 Z* J7 i7 O* [) _) M# w. V
cocious sexual development in the first-degree rela-) [+ g' R3 k! l
tives. There were no siblings.& {! ?5 g# R* h, \% x; w
Physical Examination( S3 E& @( x% m$ t2 d* n
The physical examination revealed a very active,+ T) c% m3 D8 Z" `7 h3 v- B
playful, and healthy boy. The vital signs documented0 s+ V% I7 S% p0 G: I0 X
a blood pressure of 85/50 mm Hg, his length was3 C+ m, }' t' [7 \
90 cm (>97th percentile), and his weight was 14.4 kg
9 W9 @' u( T. Y1 A2 z' X0 H/ v(also >97th percentile). The observed yearly growth8 V& q! ~* S: e$ Z8 G* V* Y9 ^( Q
velocity was 30 cm (12 inches). The examination of% C" Q9 E# d' M% B
the neck revealed no thyroid enlargement.
1 ]8 s8 [' y$ I( V) G0 qThe genitourinary examination was remarkable for
8 q- a' j, e/ m( y& W0 ^& E+ `enlargement of the penis, with a stretched length of$ g) z; \% O/ x4 m/ O% y* R. i
8 cm and a width of 2 cm. The glans penis was very well5 ]& G$ H6 C% N0 L/ d2 a
developed. The pubic hair was Tanner II, mostly around, m7 t) v, `" L6 b) t' E& {7 ~
540
+ l) z, C8 v/ b2 [( ~9 ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; t0 A  [1 k* z' K& X  N4 m2 R8 j
the base of the phallus and was dark and curled. The
# B0 G. @3 E; U( R- S5 ztesticular volume was prepubertal at 2 mL each.
5 a& d$ Y" t" ~% p6 ~The skin was moist and smooth and somewhat
6 y6 f) ?. I* w2 u; l. S- t8 l: foily. No axillary hair was noted. There were no! n# S) `9 c( f% S2 Y7 H
abnormal skin pigmentations or café-au-lait spots." w5 I' Y: _6 M# {4 a# A- U
Neurologic evaluation showed deep tendon reflex 2+
0 s) A0 {4 t6 A& {/ sbilateral and symmetrical. There was no suggestion
1 U) c! m% ^8 m" F0 H( y* M& M: _* ~of papilledema.
5 `1 _$ r% x( D- Z' Q8 iLaboratory Evaluation7 U! Z2 A: M% m/ q; c+ O
The bone age was consistent with 28 months by
/ F. S0 J: j* Vusing the standard of Greulich and Pyle at a chrono-
$ k' P5 V  [$ F  xlogic age of 16 months (advanced).5 Chromosomal
! Z% T9 _! I9 N" xkaryotype was 46XY. The thyroid function test+ F5 W" T* }1 U# t' d
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
  ?" W* @% u8 o6 A$ D2 [lating hormone level was 1.3 µIU/mL (both normal).9 I9 W0 J+ j6 `" B
The concentrations of serum electrolytes, blood
6 i& C  y" L9 I( Eurea nitrogen, creatinine, and calcium all were( n: Q2 w, u3 F/ ]; i  G5 y
within normal range for his age. The concentration
8 S0 ]9 T5 e+ Y9 `% _! r3 Y2 aof serum 17-hydroxyprogesterone was 16 ng/dL! g! @2 m. n) ]! ~% N. A" ]- \. I
(normal, 3 to 90 ng/dL), androstenedione was 20
; f2 d: f/ T; [% U1 Fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 B8 d" w0 i0 u" @terone was 38 ng/dL (normal, 50 to 760 ng/dL),# K6 y' ]% C& P6 ?
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
4 A* Q3 \" X1 p5 P& X49ng/dL), 11-desoxycortisol (specific compound S)) z( m! `5 A$ B' @/ U3 L" o
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
( y& r+ g4 |" @# a6 q3 }! N. |+ Ftisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& R- A) J2 G; u; K: r( l+ Q4 y0 @
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),! O0 y8 Q, \# T( n
and β-human chorionic gonadotropin was less than" `* G% N- H, M+ h/ }
5 mIU/mL (normal <5 mIU/mL). Serum follicular; x, e7 w% u" |0 E4 x
stimulating hormone and leuteinizing hormone
' ^; s3 ]2 y1 nconcentrations were less than 0.05 mIU/mL5 [4 {5 G7 z- R1 C. V
(prepubertal).
* I, q6 ]- q6 d0 o5 m6 R! S! OThe parents were notified about the laboratory
2 O1 e# N5 @2 M" ?7 }results and were informed that all of the tests were' t! S; d! X% H% ~3 y
normal except the testosterone level was high. The  D. u( T, Q4 q; i; P( X
follow-up visit was arranged within a few weeks to
+ w5 v' t3 z/ o; x: _obtain testicular and abdominal sonograms; how-' l' ^9 ]. s, G5 S* k" u0 N/ q1 ^
ever, the family did not return for 4 months./ N* r; U# A0 `
Physical examination at this time revealed that the2 a. W5 B4 f; q: A9 h1 u% ^
child had grown 2.5 cm in 4 months and had gained
) N9 o' K/ U; T% B5 [1 Q$ B2 kg of weight. Physical examination remained3 k$ S+ I2 p1 `4 l/ e
unchanged. Surprisingly, the pubic hair almost com-# R' z; w. O3 ^
pletely disappeared except for a few vellous hairs at+ P% p# Q6 A6 T! @4 e4 V8 u
the base of the phallus. Testicular volume was still 2- s5 E3 L4 }0 \" I: }  U, ?4 I1 G  F
mL, and the size of the penis remained unchanged.
  Z' N4 d0 ~0 n% `* O+ IThe mother also said that the boy was no longer hav-
3 [! S" O0 ?( A/ u1 }5 ping frequent erections.; f% X$ D! d5 |5 x+ N9 N8 t
Both parents were again questioned about use of
* O# P* O' H- ^* g8 W2 N/ c! wany ointment/creams that they may have applied to  z6 L9 @2 P( }; U. H
the child’s skin. This time the father admitted the
7 n9 k. N. F* ?" F% JTopical Testosterone Exposure / Bhowmick et al 541" h' X8 }/ f# ?8 m2 L1 M  t
use of testosterone gel twice daily that he was apply-
6 l& ?1 u; g$ @( zing over his own shoulders, chest, and back area for9 H: I/ W3 k$ p! A2 Z& G, B: H
a year. The father also revealed he was embarrassed' N0 w5 N* o) O' c1 w
to disclose that he was using a testosterone gel pre-
( W% o$ {! N5 o5 _3 i- xscribed by his family physician for decreased libido
/ \. A6 r( o+ n7 a' O1 y6 F: O  msecondary to depression.7 h+ ^) t* X8 z9 s/ g1 V* U7 c
The child slept in the same bed with parents.! d$ F2 |% n, D/ N. f# Z
The father would hug the baby and hold him on his' X: |  L  {9 T; s" E
chest for a considerable period of time, causing sig-$ |0 ~8 e; {' i0 r! q7 r8 z
nificant bare skin contact between baby and father.. W8 P) O* `: ]* y% E: S
The father also admitted that after the phone call,; c0 A" a; F6 R3 r
when he learned the testosterone level in the baby, B- L, n+ a8 J4 w1 c8 g
was high, he then read the product information0 m" N/ L3 h& N" j! z% X/ e+ f
packet and concluded that it was most likely the rea-: n5 L" J, ^4 }  J
son for the child’s virilization. At that time, they
1 p- _. @) x; S# g/ Cdecided to put the baby in a separate bed, and the
) c5 {  {# v+ R8 yfather was not hugging him with bare skin and had
# h2 s8 O& _; C) d/ lbeen using protective clothing. A repeat testosterone
/ g; W3 ?% t# R4 B5 x1 Otest was ordered, but the family did not go to the( m0 y6 d, L: q& D$ K/ N) N
laboratory to obtain the test.6 u" V5 U) m- d2 `, H0 o# g, L
Discussion1 I4 e2 J& H7 E" |4 \& o
Precocious puberty in boys is defined as secondary- R% }: T7 \/ t8 J# i
sexual development before 9 years of age.1,4
  `5 \) y' k* xPrecocious puberty is termed as central (true) when0 }5 h4 r6 C: k- W: G
it is caused by the premature activation of hypo-4 k6 |* Z" H! \5 [5 @/ E7 Q( y4 s: q
thalamic pituitary gonadal axis. CPP is more com-$ Y& i3 z( Z% O: ~* p3 i
mon in girls than in boys.1,3 Most boys with CPP
% ?4 z2 L$ s+ c; ?3 }  ~may have a central nervous system lesion that is
+ z3 o, {/ ]% u( R9 ?$ mresponsible for the early activation of the hypothal-
- g' ^6 ]7 R& \; L2 E- G& F1 [amic pituitary gonadal axis.1-3 Thus, greater empha-
! P2 O% [9 l9 o* o/ Asis has been given to neuroradiologic imaging in
. D3 t  T2 O  B* o7 [/ y8 l+ Gboys with precocious puberty. In addition to viril-4 t# F" u4 t" N
ization, the clinical hallmark of CPP is the symmet-
; T- f% M, ^: [1 f- w) ^- Xrical testicular growth secondary to stimulation by) b4 B. l( x/ i# ^
gonadotropins.1,3( m' B/ Q4 k* k3 g- e/ N% Y
Gonadotropin-independent peripheral preco-
9 P; q5 ^- ^# a# v. `cious puberty in boys also results from inappropriate
9 `6 I1 Q' Y% T5 Pandrogenic stimulation from either endogenous or  D* Y5 M/ u1 b$ n7 `
exogenous sources, nonpituitary gonadotropin stim-! A! X$ [: ~. ?5 D) ]
ulation, and rare activating mutations.3 Virilizing# v4 ^1 A$ r3 P5 J% r
congenital adrenal hyperplasia producing excessive
* O' m! L! [0 g: O) D7 ?/ v2 Jadrenal androgens is a common cause of precocious
! h; W8 Q* E- o# T* I0 Upuberty in boys.3,4+ J- ~% w7 W# a. `' U, y) h- l
The most common form of congenital adrenal/ M6 C; r% r# M( G4 v8 B/ A
hyperplasia is the 21-hydroxylase enzyme deficiency.
1 h. q) T, r  ZThe 11-β hydroxylase deficiency may also result in6 ?) a! P2 [8 }9 C* X
excessive adrenal androgen production, and rarely,
  Q2 F* K) M$ r  `) e4 P7 n  yan adrenal tumor may also cause adrenal androgen
$ U* o1 q( A+ S9 \5 Q0 y! r- o& O3 ]excess.1,3
- `9 G0 }) z9 ~5 u2 E( }/ Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& J1 L6 z8 [8 X% e' |542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 r1 i/ S  ~5 H2 f! x, _A unique entity of male-limited gonadotropin-
+ v2 [4 {# Z, L, jindependent precocious puberty, which is also known# z& e1 i# @  o  J: f
as testotoxicosis, may cause precocious puberty at a) d6 ~! n+ }* ~* y) k0 e  a, z
very young age. The physical findings in these boys. W# p! o' G) n& O' X1 ^
with this disorder are full pubertal development,
3 q; G" H( k5 xincluding bilateral testicular growth, similar to boys
8 D, [6 e! H9 J: Qwith CPP. The gonadotropin levels in this disorder8 U' J& m7 `: t$ b* j- e
are suppressed to prepubertal levels and do not show0 i6 H# B+ j" V' S. T- H
pubertal response of gonadotropin after gonadotropin-& |2 P$ r2 b! h. a$ k! \
releasing hormone stimulation. This is a sex-linked" i/ J" D& ]2 ?7 Y
autosomal dominant disorder that affects only5 j* B: o" w. T: r: m3 z
males; therefore, other male members of the family! F0 P3 i0 g7 M, ]; o, i
may have similar precocious puberty.3/ ?% Z4 c( Y# A! ]) q' N. @
In our patient, physical examination was incon-
! n) C6 `$ c4 o9 Dsistent with true precocious puberty since his testi-
1 Y' ]( J( s; b' L5 V7 H, Icles were prepubertal in size. However, testotoxicosis1 k. H( r2 X+ a1 J& `* c7 U! N  h
was in the differential diagnosis because his father
" `+ H9 H" ], t  x0 X8 m9 ^started puberty somewhat early, and occasionally," {2 w9 C: Y- I
testicular enlargement is not that evident in the/ U$ [8 Z* f1 m0 C# L$ C3 I
beginning of this process.1 In the absence of a neg-: N3 w" ], m1 L- Q& @/ g7 Z
ative initial history of androgen exposure, our
% r* g% R& _$ D% \biggest concern was virilizing adrenal hyperplasia,
% I: Z8 X, u; u- `1 t0 B- ?* {* K9 veither 21-hydroxylase deficiency or 11-β hydroxylase! g9 U/ r( e1 J3 ?1 f+ n% q
deficiency. Those diagnoses were excluded by find-5 X9 I9 q6 Y% \. e; L
ing the normal level of adrenal steroids.4 y; |% S. n0 |; X0 u. f0 z
The diagnosis of exogenous androgens was strongly
$ z( N6 Y& E# L0 M8 @suspected in a follow-up visit after 4 months because" c4 D5 N' h  j) v0 C
the physical examination revealed the complete disap-- |9 T! `1 x+ ~7 l
pearance of pubic hair, normal growth velocity, and, h2 A% t5 ?0 G- A4 y8 h
decreased erections. The father admitted using a testos-
/ p( N1 P3 x& b: X) vterone gel, which he concealed at first visit. He was
" i4 {  y7 U8 u5 J+ ]using it rather frequently, twice a day. The Physicians’
; v. d0 _" N: B8 ^Desk Reference, or package insert of this product, gel or" R, [/ l4 Q% A0 a7 ~
cream, cautions about dermal testosterone transfer to7 e+ c" W  M+ n. x
unprotected females through direct skin exposure.
# _- ~: v+ s+ J+ p4 k  bSerum testosterone level was found to be 2 times the6 A% Y  L' D5 n/ B, {
baseline value in those females who were exposed to  W6 F/ [4 J, L3 p+ {2 Z7 s
even 15 minutes of direct skin contact with their male
4 l* Y- f' K- |partners.6 However, when a shirt covered the applica-; V0 _5 @4 g9 D1 a5 |; {5 ]! r7 W
tion site, this testosterone transfer was prevented.5 s' X) i' Q0 N6 G
Our patient’s testosterone level was 60 ng/mL," ^. q( W5 @0 ~& x
which was clearly high. Some studies suggest that
# \& N, Z, t5 l; Ydermal conversion of testosterone to dihydrotestos-6 ^" E8 [! i6 z' U0 U
terone, which is a more potent metabolite, is more6 h' T3 h7 ]* }
active in young children exposed to testosterone* w/ A9 R# W7 R9 E/ S6 ], J
exogenously7; however, we did not measure a dihy-3 P! L, w+ U: v. ~2 w4 H
drotestosterone level in our patient. In addition to) a* ^  T) H9 T. a, @
virilization, exposure to exogenous testosterone in
  E% b: C' p& @6 A7 M4 Wchildren results in an increase in growth velocity and6 O+ `$ ~1 |! R* A9 Q
advanced bone age, as seen in our patient.
! \3 d' K3 @$ A3 B# x% YThe long-term effect of androgen exposure during8 R2 ]1 A, y5 a/ ?% _2 k1 C
early childhood on pubertal development and final
" i! u' @* ~- Z5 y+ }8 M* G& @% wadult height are not fully known and always remain/ P% z% |. h# Z) L" L6 X4 d
a concern. Children treated with short-term testos-
' C2 Q- v" o! Lterone injection or topical androgen may exhibit some% |8 w+ R# p. ]+ [2 _5 I
acceleration of the skeletal maturation; however, after
( x5 k) R8 ]9 u0 R6 ~cessation of treatment, the rate of bone maturation
- |( ], p5 e% R; K5 [* z# X/ s4 [decelerates and gradually returns to normal.8,9" v; V( w# z( V0 M! y
There are conflicting reports and controversy3 Q$ T. m2 P1 H
over the effect of early androgen exposure on adult
* b7 L& t) J3 C- l& A, bpenile length.10,11 Some reports suggest subnormal
5 W5 Z7 T. A. \) J. yadult penile length, apparently because of downreg-0 e2 P$ e1 H& T: ]2 e' {- W
ulation of androgen receptor number.10,12 However,1 F; F0 ~" T, c/ L5 I% K. p) v
Sutherland et al13 did not find a correlation between7 v: o7 B5 G2 }, ]& e, e
childhood testosterone exposure and reduced adult
) S* ?& R( {/ W# t' J: rpenile length in clinical studies.0 [" ?& W2 F# h
Nonetheless, we do not believe our patient is
8 A) G( Q8 `# Q+ M! a- S$ ]; mgoing to experience any of the untoward effects from* b7 G: K4 O% g
testosterone exposure as mentioned earlier because
/ D2 Z/ a- T5 J& H/ Othe exposure was not for a prolonged period of time.- V3 F5 y- {3 }' {  u
Although the bone age was advanced at the time of1 K4 P# }) o. w% X  N, k& m2 {: ?
diagnosis, the child had a normal growth velocity at, g! D; k6 f& B7 X" X% I
the follow-up visit. It is hoped that his final adult" C* e) l% B' @$ \
height will not be affected.- `( p% n2 R, D* O; t( t
Although rarely reported, the widespread avail-! K3 d1 s) z9 R) e4 ]1 o
ability of androgen products in our society may- y2 Y: P3 e6 e! _% e
indeed cause more virilization in male or female
' l2 ~1 l- R9 i5 g0 U8 ichildren than one would realize. Exposure to andro-4 F3 n0 O2 S2 t) w4 H
gen products must be considered and specific ques-
, B4 Q) ^% O! I( T! Z. ytioning about the use of a testosterone product or8 I1 E: p2 g& P/ J7 X
gel should be asked of the family members during) U+ E) a, e' k8 Q# u' {
the evaluation of any children who present with vir-3 P% a$ e) c7 H- y
ilization or peripheral precocious puberty. The diag-
" H" g" T& S, e2 U4 wnosis can be established by just a few tests and by3 I5 S& ]0 e' Y+ L4 X1 z4 p* q
appropriate history. The inability to obtain such a
+ G& `7 Q6 j, S8 o8 c! E7 H3 v6 vhistory, or failure to ask the specific questions, may
7 {1 b4 A8 E# v  Yresult in extensive, unnecessary, and expensive' h: t( K: H% H7 M3 Z
investigation. The primary care physician should be9 N% U( ^- l  k7 w( v1 Q. L9 I$ t2 ^* W6 H
aware of this fact, because most of these children
. C+ `+ d( @# kmay initially present in their practice. The Physicians’# Q* e8 G- q; b4 e/ A9 g; p
Desk Reference and package insert should also put a4 ?# I# W& Z! V: u  l
warning about the virilizing effect on a male or/ ?, r8 e# f4 j& g0 i
female child who might come in contact with some-- I9 [' b* R' ~- T) }% `
one using any of these products.. g2 j$ R. @3 N+ Q' W
References7 g/ D$ q* {, A- p' K( Z: Q4 G7 z
1. Styne DM. The testes: disorder of sexual differentiation
# F  q9 e4 |8 r1 b' k0 Iand puberty in the male. In: Sperling MA, ed. Pediatric
* A6 r/ w3 M) g  Y9 B6 F2 sEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' h5 G4 M+ o" R2 J2002: 565-628.
7 i1 b+ |/ Z0 X1 R, s6 `5 w/ G' Y2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 Q. D7 v5 h0 J; ]* ipuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
- m% J% H2 z. c7 u( I$ c; [# oBoy Induced by Indirect Topical
2 K7 o2 [2 Z9 u) g( f0 `% l0 L9 nExposure to Testosterone* L# F) H, C- R2 X* x5 _
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, l; `9 t2 a! ~) a
and Kenneth R. Rettig, MD1" P: O  k2 x3 F" n2 J9 d- ^
Clinical Pediatrics
" W" b( W. u7 j5 _5 KVolume 46 Number 6
/ K8 T4 j( I* ^- k: e. J2 K1 U0 vJuly 2007 540-543
$ z8 i9 I! n/ X. S* p( U© 2007 Sage Publications
6 ?/ @: t: b. M10.1177/0009922806296651
+ E  _- x$ b. M2 ]& fhttp://clp.sagepub.com9 _0 c$ Z& X5 V) F) t" J+ ?
hosted at; p+ J+ r+ T8 j1 m
http://online.sagepub.com
) c; D3 I0 K" mPrecocious puberty in boys, central or peripheral,
0 ?: M9 M( u! s% g+ r. V' qis a significant concern for physicians. Central
- t3 S8 y9 {' }5 R5 b, aprecocious puberty (CPP), which is mediated
: n/ n: m0 P' `through the hypothalamic pituitary gonadal axis, has
" g! Z( u) Y  }& @; Ca higher incidence of organic central nervous system
+ X* s& X% ]- V) Z  Z6 `0 Zlesions in boys.1,2 Virilization in boys, as manifested$ P+ @- J/ I2 W0 _5 i9 I
by enlargement of the penis, development of pubic
$ N8 d) x: _$ f7 t" A& |1 z2 i0 Lhair, and facial acne without enlargement of testi-
+ e. V) P) s' [cles, suggests peripheral or pseudopuberty.1-3 We
( z( k6 B# ]8 [2 M$ z7 ^report a 16-month-old boy who presented with the8 ^' J* ^  I  q; y
enlargement of the phallus and pubic hair develop-
, `- H% @$ u$ i" ~6 xment without testicular enlargement, which was due
- d& z" T3 B3 Q+ }; j, x9 ~to the unintentional exposure to androgen gel used by
( [& e) `& W% ]( C/ _  ]the father. The family initially concealed this infor-4 v+ d6 m0 q: t' B+ {
mation, resulting in an extensive work-up for this: f! \4 E2 ^, b  q- m
child. Given the widespread and easy availability of
) r/ g" r7 b; Utestosterone gel and cream, we believe this is proba-
3 p; @& A& X! b/ R$ |. mbly more common than the rare case report in the
3 g* Y& `8 o& b0 E2 Aliterature.4
8 @- A" a3 ^9 m) j! O: i9 ]) NPatient Report
) f2 W1 U4 V0 Z/ F% _& N2 oA 16-month-old white child was referred to the6 ^" f# \$ o7 W* D
endocrine clinic by his pediatrician with the concern
- l5 g0 a3 i+ |3 C/ qof early sexual development. His mother noticed
2 Q% Y8 I5 Z" _# d; Slight colored pubic hair development when he was+ z" Z6 b) g! r4 V
From the 1Division of Pediatric Endocrinology, 2University of- j( x, r' @8 f. t2 B7 `* @/ ^
South Alabama Medical Center, Mobile, Alabama.
; U7 W: o  v* G6 f4 }; xAddress correspondence to: Samar K. Bhowmick, MD, FACE,
3 O" f1 o2 M8 J8 D- K" g; r# I+ fProfessor of Pediatrics, University of South Alabama, College of
. F( F# ]" a: k2 [' R$ BMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
9 r' z+ s$ [; y' V+ \2 R- ve-mail: [email protected].
* k% S- {3 Q0 X" ^about 6 to 7 months old, which progressively became
8 q% \. v2 n$ }darker. She was also concerned about the enlarge-
; f$ F" _5 A2 R6 hment of his penis and frequent erections. The child
( Q2 Z7 M# C: n6 v! Rwas the product of a full-term normal delivery, with* S+ s- h. f! I) W
a birth weight of 7 lb 14 oz, and birth length of
- Y( @) k" M: U( ^' [9 U- S20 inches. He was breast-fed throughout the first year0 k" H7 }7 @8 |
of life and was still receiving breast milk along with: ^2 [3 a7 |4 T& _2 [) X  w9 Q1 q
solid food. He had no hospitalizations or surgery,4 H/ k( g0 |0 E8 C4 `7 y8 V
and his psychosocial and psychomotor development
. u" s% w; I; N; o5 |was age appropriate.
4 [' p  A7 Q8 ^( mThe family history was remarkable for the father,0 F4 `: ~% e3 W7 l  L
who was diagnosed with hypothyroidism at age 16,1 ]' g0 b& i% q" g9 z& {! R0 g
which was treated with thyroxine. The father’s
% R: X! T/ `4 |7 d% Nheight was 6 feet, and he went through a somewhat# C% J. a8 B! U5 t
early puberty and had stopped growing by age 14./ k1 o! j( x7 i2 M7 J) I8 J
The father denied taking any other medication. The) ?5 i: r9 `- w( @/ N
child’s mother was in good health. Her menarche
: e$ x2 }9 [4 u' Q; m, j2 }was at 11 years of age, and her height was at 5 feet$ W* h! E$ X6 m. i4 @7 M
5 inches. There was no other family history of pre-9 B4 o  J: ^6 U3 ^
cocious sexual development in the first-degree rela-
* m, c8 f( u& g1 y9 l  }; i- X3 xtives. There were no siblings.
. {, {8 P- H( f3 D6 `* G  nPhysical Examination
- b3 z) C; L( j& lThe physical examination revealed a very active,) J+ X# P: j, b. e$ i; O
playful, and healthy boy. The vital signs documented7 N. f3 P- Z% V1 p$ X6 B# P5 _
a blood pressure of 85/50 mm Hg, his length was" K7 W0 @' E8 s* B
90 cm (>97th percentile), and his weight was 14.4 kg7 u) L9 x/ K7 l
(also >97th percentile). The observed yearly growth$ k2 E/ i8 H' ?, u6 {, m
velocity was 30 cm (12 inches). The examination of" t  Z7 B; M1 F0 y! p
the neck revealed no thyroid enlargement.
% L7 n/ y' e- D* U5 V, YThe genitourinary examination was remarkable for
3 D% Y4 }: |5 J6 O0 W& u3 Ienlargement of the penis, with a stretched length of
' g1 b) q# i. h0 B; h. P( v* w3 o8 cm and a width of 2 cm. The glans penis was very well; E; ?, y" Z% V8 Y1 v5 W# Q
developed. The pubic hair was Tanner II, mostly around
( r; M+ d- e+ I" a540
6 w2 U6 ], @  U* W0 N2 ]4 J3 aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 I/ n) _/ y; R: `! l' zthe base of the phallus and was dark and curled. The
& o3 x0 r! Q! |testicular volume was prepubertal at 2 mL each.
0 B5 z$ d; F$ k% @0 |The skin was moist and smooth and somewhat; L6 w* G5 L4 e9 w$ ~) E- e: @. M
oily. No axillary hair was noted. There were no
9 Y5 _$ X" q: ]; }8 Aabnormal skin pigmentations or café-au-lait spots., Z; n5 l7 m1 s' \) C
Neurologic evaluation showed deep tendon reflex 2+  B1 u& ], ?" A8 h, @8 `
bilateral and symmetrical. There was no suggestion
" \1 L2 Z( f" B( j% pof papilledema.3 ~8 X5 I4 M: L( L/ b
Laboratory Evaluation: }/ r0 d/ m% \8 M! Q4 h+ T
The bone age was consistent with 28 months by
* g7 u* a, c* Y# a, Q9 xusing the standard of Greulich and Pyle at a chrono-
+ r- p* ]8 O* m9 Ulogic age of 16 months (advanced).5 Chromosomal$ E0 V; w/ ?) H- W( L  s
karyotype was 46XY. The thyroid function test
% a0 m# G& f) w$ \. v7 pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
: B- V- _7 P& N" X/ x6 ^lating hormone level was 1.3 µIU/mL (both normal).
6 D  O% I" a% gThe concentrations of serum electrolytes, blood$ N3 b9 I6 j0 E5 Y8 E- Z( Z
urea nitrogen, creatinine, and calcium all were4 t& n+ O. I) W, S1 r( w% _
within normal range for his age. The concentration) T0 i2 u- S; `$ ?
of serum 17-hydroxyprogesterone was 16 ng/dL0 f) Z5 z# h0 M
(normal, 3 to 90 ng/dL), androstenedione was 20
( s8 W- u9 C5 W' [! S/ `* w: }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& o$ X$ F" e% f' F& P: v# qterone was 38 ng/dL (normal, 50 to 760 ng/dL),  B0 M) {3 x$ T2 A9 T5 K
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 @3 b! t/ p+ }49ng/dL), 11-desoxycortisol (specific compound S)- u8 L+ h* m/ W2 i8 Z4 f- R
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" W2 E$ x+ Z) ^+ o
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
2 G) O4 p- y2 N) mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" l: S2 @* s/ B/ Nand β-human chorionic gonadotropin was less than
& z5 v2 ]# H4 W6 T+ M& @. r5 mIU/mL (normal <5 mIU/mL). Serum follicular
) t- ]' w7 h4 X. d- Estimulating hormone and leuteinizing hormone
, K4 f' y# Q, J0 C6 z* Yconcentrations were less than 0.05 mIU/mL; ]9 N0 W0 P# a. V5 F
(prepubertal).& B$ S3 @+ G9 \+ X8 W) s
The parents were notified about the laboratory
0 T; R$ M  @* [* z; Q' m' `2 [results and were informed that all of the tests were% M/ |0 w- g5 _* p7 w) I8 h
normal except the testosterone level was high. The
9 H9 q# {* q* Z: Hfollow-up visit was arranged within a few weeks to5 h' ^' _. W/ ~7 Y# T& e
obtain testicular and abdominal sonograms; how-
/ K# _$ K" d: Z. B- Mever, the family did not return for 4 months.
4 ~5 `. [0 T) @; X  {% ~) oPhysical examination at this time revealed that the8 S8 g6 p; E, f: x8 D
child had grown 2.5 cm in 4 months and had gained
' }- X+ T7 W" p+ M  Z2 d/ P2 kg of weight. Physical examination remained
. Z% e& \. D2 s0 Z, q1 L9 P) vunchanged. Surprisingly, the pubic hair almost com-9 ?5 p+ o7 b% y: a) L% @
pletely disappeared except for a few vellous hairs at
# X6 A7 C; d& u1 n9 o/ T/ ithe base of the phallus. Testicular volume was still 2* {: Y# I7 A  Y" \7 e4 v$ `
mL, and the size of the penis remained unchanged.: q4 M- Z% j) v) T3 t# g- Z1 b
The mother also said that the boy was no longer hav-/ o. i" ^1 r$ z$ U0 c
ing frequent erections.0 u# {# G5 R6 N5 H
Both parents were again questioned about use of+ N0 D1 e$ ~. R9 b8 y! h
any ointment/creams that they may have applied to
6 r" x- y# K; o+ W& f& @$ Vthe child’s skin. This time the father admitted the# j6 X  A8 O1 d  `8 A0 b
Topical Testosterone Exposure / Bhowmick et al 541
/ B% c5 m. H3 N5 F, J1 Muse of testosterone gel twice daily that he was apply-! |4 v( n# `  F) i8 Q$ F- ~7 }
ing over his own shoulders, chest, and back area for2 d/ H" V1 g( b
a year. The father also revealed he was embarrassed# l, B" p  ~! j; w& Z0 J; i
to disclose that he was using a testosterone gel pre-0 y* o$ k2 @, W3 @
scribed by his family physician for decreased libido
. \0 D1 F( V9 Z" ^( M+ j# Wsecondary to depression.
" ^5 o1 j$ k3 Y7 ~3 T/ y& x* P. S4 z& jThe child slept in the same bed with parents.
. H& U: L) p) N" @3 D( ^4 \" {; ZThe father would hug the baby and hold him on his
( A4 ^& `% }8 x  ~# j  _chest for a considerable period of time, causing sig-
' `4 G4 v0 m5 u* ~! `1 Anificant bare skin contact between baby and father.
; _0 U4 g" e2 B  S4 rThe father also admitted that after the phone call,
+ J) B) k* a$ J6 X4 a9 Swhen he learned the testosterone level in the baby; v4 @* D' x7 t8 d  `
was high, he then read the product information
+ l8 c3 `* K* I3 Ppacket and concluded that it was most likely the rea-) a! n7 h1 \: J9 N
son for the child’s virilization. At that time, they
. Q8 J6 v8 L5 g9 F% u) ^decided to put the baby in a separate bed, and the
! x) M8 H1 }; O7 v7 d* {0 gfather was not hugging him with bare skin and had
1 C; t/ F1 o6 |been using protective clothing. A repeat testosterone9 C+ W/ e% Y4 X* ?
test was ordered, but the family did not go to the
8 j% A9 o9 f& l; ]' u, Alaboratory to obtain the test.! b+ K) f6 e- y& V1 ?1 E9 }
Discussion
. {$ k# @! B8 g. dPrecocious puberty in boys is defined as secondary1 A7 c; M* e: }) w+ s, L
sexual development before 9 years of age.1,4
' D" f4 I* [( N: e8 ^- H, H: i4 oPrecocious puberty is termed as central (true) when4 }: u* ~) q7 l9 m. y( Y
it is caused by the premature activation of hypo-
( l' m% x5 d$ d* w6 {thalamic pituitary gonadal axis. CPP is more com-
# D5 f& U% a- G1 E" Cmon in girls than in boys.1,3 Most boys with CPP- e* F5 E3 {( b0 o, ^
may have a central nervous system lesion that is2 a, h9 x1 e' w+ B
responsible for the early activation of the hypothal-
* [2 X# Q) ]: \! k( B" c' Ramic pituitary gonadal axis.1-3 Thus, greater empha-
5 k' U0 \+ X- F$ D' ]1 _. `' U: Qsis has been given to neuroradiologic imaging in
! M# W+ x' v) q- r9 J2 N2 Eboys with precocious puberty. In addition to viril-$ E3 J- v$ D' I1 y, H3 p
ization, the clinical hallmark of CPP is the symmet-
6 u. V; M  |1 Y2 I5 B; Mrical testicular growth secondary to stimulation by
+ |3 |" S. [5 |8 n+ @' F0 a/ Ggonadotropins.1,3
! e7 S: K; h* A, n7 S- ^2 q1 E! X* ZGonadotropin-independent peripheral preco-) q, T) y) |6 f
cious puberty in boys also results from inappropriate
/ }2 [$ f4 Z6 ?9 y, L9 I6 ?  P7 Yandrogenic stimulation from either endogenous or
# |; j6 T6 u4 U- gexogenous sources, nonpituitary gonadotropin stim-
" V0 F# s7 G$ U" L9 Zulation, and rare activating mutations.3 Virilizing3 m5 [5 a! t1 d( @- l
congenital adrenal hyperplasia producing excessive' \, w  |8 Z" [  j6 o. M% g3 p
adrenal androgens is a common cause of precocious5 R/ F' ^6 }, J1 p1 X2 i8 F
puberty in boys.3,4+ T2 Z( v$ u2 t; \5 U" r
The most common form of congenital adrenal% O* d: s0 w$ C: x6 i
hyperplasia is the 21-hydroxylase enzyme deficiency." x; K6 n; c; X* _6 j* L  L$ {
The 11-β hydroxylase deficiency may also result in
" r( [3 v" K& oexcessive adrenal androgen production, and rarely,
& ^. K$ @1 [. F1 b5 xan adrenal tumor may also cause adrenal androgen
/ Y$ r, p9 ^, e, @excess.1,3
' q. ~( [2 E' M. g3 N4 b' I- y! tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* b5 U2 J9 D2 n( U, {
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ P7 c  L7 A9 S8 m
A unique entity of male-limited gonadotropin-# e8 ]% q$ n+ Y
independent precocious puberty, which is also known
: p4 y; ~. i! qas testotoxicosis, may cause precocious puberty at a
" ~; C, V" @3 s& l# |  Z3 Avery young age. The physical findings in these boys
8 i' b8 `  m9 C$ \' r5 r- V/ ~5 Pwith this disorder are full pubertal development,2 M  M3 b3 h2 \8 g1 l0 k( c
including bilateral testicular growth, similar to boys8 Y) `6 x0 b1 j9 u/ l
with CPP. The gonadotropin levels in this disorder* m7 x$ I: A8 u# ~0 ?# d9 d6 k
are suppressed to prepubertal levels and do not show5 f# \9 |, n' _# p1 Y
pubertal response of gonadotropin after gonadotropin-
: N: l9 u3 E+ ~4 X9 jreleasing hormone stimulation. This is a sex-linked
% {1 \0 L- C* @9 @" J* P. |& Fautosomal dominant disorder that affects only! D) |" r0 I3 X
males; therefore, other male members of the family) V5 C  b  T$ Q- ^( Z0 o5 L
may have similar precocious puberty.3
# ]' _* V: a, n6 p; n& |In our patient, physical examination was incon-! A) L! j' V- Z; M6 P" O
sistent with true precocious puberty since his testi-; V' b$ N) Q" u3 s8 p7 |% h
cles were prepubertal in size. However, testotoxicosis
. }& A0 s& z9 `3 ]( U6 Xwas in the differential diagnosis because his father; e4 p: d0 a: L% l4 l
started puberty somewhat early, and occasionally,
1 ?( l9 ]* W& C" _/ R9 Ktesticular enlargement is not that evident in the
# W4 r9 q; I& mbeginning of this process.1 In the absence of a neg-" W% _9 R1 N( P5 B, T. T: v) T
ative initial history of androgen exposure, our. l- ^% }- }; G
biggest concern was virilizing adrenal hyperplasia,
9 k& g- p9 X; `3 qeither 21-hydroxylase deficiency or 11-β hydroxylase
$ @. Y( m6 b& n8 W9 a) Ddeficiency. Those diagnoses were excluded by find-
+ B4 Z: m! o9 t5 e% J8 ]4 N. ping the normal level of adrenal steroids.
. Q! N8 w& D& {- }; ?5 L  NThe diagnosis of exogenous androgens was strongly
6 ~1 H3 a& `( S% o) C0 esuspected in a follow-up visit after 4 months because  E6 a3 T* K: \; M, X2 j
the physical examination revealed the complete disap-9 b: M( h+ v9 m: F
pearance of pubic hair, normal growth velocity, and
; M* W3 V- f2 y* cdecreased erections. The father admitted using a testos-, h! C3 q: b. Z& q2 [
terone gel, which he concealed at first visit. He was
6 H* p4 Y) P) j- T. n) F: D- U8 Iusing it rather frequently, twice a day. The Physicians’
: a- t  N) a  IDesk Reference, or package insert of this product, gel or# y$ N2 l& u( w' C7 b
cream, cautions about dermal testosterone transfer to
4 @  r$ ^4 r% U0 Z5 w% w- O, t+ Punprotected females through direct skin exposure.8 E* n! v2 w1 m" n/ ?: H  [1 Q9 _
Serum testosterone level was found to be 2 times the
  I+ ^2 ^: ?" T% i5 Q4 Sbaseline value in those females who were exposed to2 q' ^, A! d; M7 z0 o
even 15 minutes of direct skin contact with their male
5 x) f  R  Z; v9 s. F9 c& ]7 p8 Qpartners.6 However, when a shirt covered the applica-
) p- y! Q3 m- ?) e  y1 X, ption site, this testosterone transfer was prevented.' q! T) l; }$ F% ~1 H- s* P
Our patient’s testosterone level was 60 ng/mL,1 R4 r+ l, Z3 [: C
which was clearly high. Some studies suggest that* O$ @/ Y  W2 Y- y' \, N. |
dermal conversion of testosterone to dihydrotestos-  ?7 Z' J( J; D- W
terone, which is a more potent metabolite, is more
+ t$ H# M; o$ j, h' g  sactive in young children exposed to testosterone! X) o' e7 p9 M- {* u
exogenously7; however, we did not measure a dihy-9 D4 q1 o' \- t7 |4 C3 Q4 f" d5 K
drotestosterone level in our patient. In addition to* k; F: U4 D# d* R3 k
virilization, exposure to exogenous testosterone in* _7 B; s0 b* N
children results in an increase in growth velocity and* y; ]7 m  q0 S
advanced bone age, as seen in our patient.- ?. ~  I9 z; S: n1 j
The long-term effect of androgen exposure during% M) d1 `; q" |9 f# K) _# v5 X
early childhood on pubertal development and final
9 i: H+ p; j) Y/ S2 madult height are not fully known and always remain
0 p! K9 L3 o8 F! |, D+ o% Ya concern. Children treated with short-term testos-7 s& m9 E6 R* o
terone injection or topical androgen may exhibit some
/ y# ]( E, \. U4 d$ ~* U8 kacceleration of the skeletal maturation; however, after! p$ H! }7 T' r' `% W  Z4 ?
cessation of treatment, the rate of bone maturation
+ B. \0 k# L$ W: V8 V2 I2 X3 ^3 j1 Zdecelerates and gradually returns to normal.8,9, {/ \% m& z7 X6 ^4 {- ^3 _; ^
There are conflicting reports and controversy, Q+ u5 u9 g! V1 P( Y3 M8 D  v
over the effect of early androgen exposure on adult
) z( f+ C1 Q$ q! V1 S- lpenile length.10,11 Some reports suggest subnormal0 d+ T( R) j6 `+ ?- B
adult penile length, apparently because of downreg-
6 @4 S2 V' I' _2 u4 c6 {8 sulation of androgen receptor number.10,12 However,
0 v+ T/ |- p4 f: s1 x1 SSutherland et al13 did not find a correlation between, m# o/ m! ?- @1 H. t. z+ L+ Z
childhood testosterone exposure and reduced adult3 S& P" ~1 B- q# v' n+ m
penile length in clinical studies.
4 B& ~# M( G9 c% X2 C$ MNonetheless, we do not believe our patient is( _& x4 w" k6 A. a& z
going to experience any of the untoward effects from+ \5 g0 `9 K5 x7 I) A" N+ D
testosterone exposure as mentioned earlier because! H8 u+ ?" Q) I- M6 L0 A* d! K' V7 q' w
the exposure was not for a prolonged period of time.
; s! d' @6 E, r$ VAlthough the bone age was advanced at the time of0 _+ \6 j" q* \( b, n! {
diagnosis, the child had a normal growth velocity at% H) V8 J8 M* F
the follow-up visit. It is hoped that his final adult$ f' Y4 b. V( n7 u5 `2 M" m% d6 E
height will not be affected.% P/ p: R5 q; e# z
Although rarely reported, the widespread avail-6 i1 W2 @5 b" H3 B
ability of androgen products in our society may5 T- D) ?. I. S3 ~+ v0 n
indeed cause more virilization in male or female: e, k( h8 J# S) m# ~
children than one would realize. Exposure to andro-
& k, G$ E! Z0 k% |2 [gen products must be considered and specific ques-/ Y  X& _/ u, [$ I& U% f
tioning about the use of a testosterone product or  W& `" Q' J- ]' ~  ]
gel should be asked of the family members during
! n9 W- m% y. U& q0 o( {the evaluation of any children who present with vir-
7 N: f; V  B6 d8 G- ~0 |6 m9 G1 @: cilization or peripheral precocious puberty. The diag-" }/ q% M# n1 K9 A$ a
nosis can be established by just a few tests and by
0 `- k/ e3 ~6 `" B/ {- xappropriate history. The inability to obtain such a; R! c: R3 E4 Z2 t* j9 j/ @
history, or failure to ask the specific questions, may: N/ U7 r* i+ \1 R" E- j
result in extensive, unnecessary, and expensive* j6 {% p' [' w0 t* B
investigation. The primary care physician should be  J/ u/ D1 Q: s2 H( d
aware of this fact, because most of these children
( v: u! d: |: c0 ^. Z0 f2 Cmay initially present in their practice. The Physicians’
1 ?. ]  G9 s. I% R1 V3 FDesk Reference and package insert should also put a* N: S- r2 w2 g. B6 y  \7 r9 J4 E
warning about the virilizing effect on a male or* A9 K' f  B) P# _
female child who might come in contact with some-
4 H0 A9 \5 g* L: U6 S; z2 ~2 U7 Pone using any of these products.2 X" g7 n% t2 G, X6 Z9 C
References
# }: S, Q' z3 ]" u3 Y1. Styne DM. The testes: disorder of sexual differentiation
/ ]2 V; M+ Q; B5 x) eand puberty in the male. In: Sperling MA, ed. Pediatric! x( `. V1 a1 K# p) ?
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( n% x" z! Y/ ^5 a) J" n8 y  @2002: 565-628.6 I+ A$ r3 E) t2 l2 V
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- e$ o2 F* k: V8 W7 U) xpuberty 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

2 @) _* }% [5 L  X* A/ Q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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