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Sexual Precocity in a 16-Month-Old& h' T- k% G  {- v0 S7 W/ G5 u
Boy Induced by Indirect Topical
! `3 x2 `: x! s9 J% TExposure to Testosterone9 L7 r0 O1 q, p9 E( ?3 o9 E9 }7 c
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- |# Z: i: O- P
and Kenneth R. Rettig, MD1
7 m+ ^7 E+ o9 f& _2 hClinical Pediatrics7 l. r. K4 M. S; I4 j3 p5 a* x; B
Volume 46 Number 6
) |  u- v- P% v- }3 l' x* s$ fJuly 2007 540-543) g) y7 E9 _0 F  @% L. [6 Q( I# X$ |: Q
© 2007 Sage Publications1 t0 R. x- W" Q4 S
10.1177/0009922806296651
  _  @* w. w6 U  ]0 {1 @1 t; W/ ]http://clp.sagepub.com  k: \( {- d1 ~' B% u( Y# w- a
hosted at
! ~  o! }8 ]! ]* r) w7 Qhttp://online.sagepub.com
  z$ K3 p# w: }3 G( ^Precocious puberty in boys, central or peripheral,3 N- b; k/ {/ H. D5 l
is a significant concern for physicians. Central  x' b( q3 M/ p9 @3 P
precocious puberty (CPP), which is mediated
6 \' n' b' m5 r+ u& t1 vthrough the hypothalamic pituitary gonadal axis, has9 {3 N% V0 E7 H
a higher incidence of organic central nervous system  ?$ ^$ c! r- S" Z
lesions in boys.1,2 Virilization in boys, as manifested8 i5 y8 e6 d1 C3 J
by enlargement of the penis, development of pubic
+ D9 \% C- i8 ^3 k9 }. xhair, and facial acne without enlargement of testi-& S) ]" D/ {- a. n  U
cles, suggests peripheral or pseudopuberty.1-3 We
$ z5 q7 ~6 T( ^) d6 e" B2 Nreport a 16-month-old boy who presented with the
3 I; y" G) l1 [6 Z& cenlargement of the phallus and pubic hair develop-$ S$ i" G8 E4 b& L
ment without testicular enlargement, which was due: q5 A4 e+ X/ a: p% C  P
to the unintentional exposure to androgen gel used by
3 |% L* \9 r& W# t: l/ [6 M/ Athe father. The family initially concealed this infor-' Y5 Q' i* k' N9 y* A7 i
mation, resulting in an extensive work-up for this
' l( ?3 E$ e3 b% k0 }0 ~# Echild. Given the widespread and easy availability of
8 K$ T8 T* B$ U% G- r4 s9 Ttestosterone gel and cream, we believe this is proba-0 |% z: L1 G' B  J- V+ ?
bly more common than the rare case report in the; r; y2 p6 p* K2 Y9 V
literature.42 h+ x/ A8 Z, W1 a1 a
Patient Report8 P9 g5 ?" ?) n$ ?
A 16-month-old white child was referred to the2 D. I+ f. L7 E' Y* |4 A( L
endocrine clinic by his pediatrician with the concern. k, w9 J$ v( Y; c" }
of early sexual development. His mother noticed& r5 y; b) C* V* B0 Y% _/ l
light colored pubic hair development when he was( q/ v* F: r/ V
From the 1Division of Pediatric Endocrinology, 2University of
2 k; h* `6 U/ h5 X( sSouth Alabama Medical Center, Mobile, Alabama.
; d7 y  q5 F$ I) DAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 D4 k# o, t' Z, I4 r! K. D
Professor of Pediatrics, University of South Alabama, College of, R3 i" V6 Z8 n+ H
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# P# b' k7 C+ s$ C6 l5 W: [e-mail: [email protected].
) q8 e) w4 o; Y  O2 \0 Dabout 6 to 7 months old, which progressively became
$ H0 c( s. c& S" O/ r& v% `darker. She was also concerned about the enlarge-; s* m% y1 @) ]
ment of his penis and frequent erections. The child6 w, t+ I+ a1 t& [& }
was the product of a full-term normal delivery, with
+ W) ~9 H+ a6 k# B( \: q- na birth weight of 7 lb 14 oz, and birth length of
# M- Y5 [! q( E5 n2 v20 inches. He was breast-fed throughout the first year$ F% @, R$ |* J* q
of life and was still receiving breast milk along with0 T/ Z, v) J9 @0 U  K+ p
solid food. He had no hospitalizations or surgery,4 A8 r- L7 c  n5 K; o
and his psychosocial and psychomotor development- g! V6 {; Y9 y+ \+ d/ R
was age appropriate.) O- N* N. y* U2 K4 u
The family history was remarkable for the father,' c8 l1 A( t8 R
who was diagnosed with hypothyroidism at age 16,3 \" a8 ]6 ~) `
which was treated with thyroxine. The father’s8 `9 e3 X7 x$ v; J5 o- ]
height was 6 feet, and he went through a somewhat
, l5 I" O- Q. p# F% C0 U. y# w7 Kearly puberty and had stopped growing by age 14.
* H; }" k+ }' x" I$ ]+ ]  ~The father denied taking any other medication. The; b/ J3 W, |( c# W  ~
child’s mother was in good health. Her menarche8 f' G; n6 {$ q/ j
was at 11 years of age, and her height was at 5 feet
+ ^2 W( d' T) f5 inches. There was no other family history of pre-
: L1 w5 {4 T. a# |8 Ycocious sexual development in the first-degree rela-
) f$ r* I0 N) A/ ^0 Q3 ptives. There were no siblings.
1 A/ N, S, z- S8 B7 `# D% P. }/ YPhysical Examination' k" ^- S/ v% ^% L. P  x
The physical examination revealed a very active,4 i) N0 S7 a& f' r0 J9 b4 J; E, ~
playful, and healthy boy. The vital signs documented4 z% m9 y1 m' F/ D( H- b5 W
a blood pressure of 85/50 mm Hg, his length was
; G3 E9 H5 }/ f& V90 cm (>97th percentile), and his weight was 14.4 kg) Z4 G7 X  y( W/ K' e
(also >97th percentile). The observed yearly growth9 H6 {+ O- M* q4 ~' z3 }
velocity was 30 cm (12 inches). The examination of2 [2 F/ t$ L5 m9 N& b' U# l  d; Z$ B& |
the neck revealed no thyroid enlargement.
; N6 S2 A, p  M1 vThe genitourinary examination was remarkable for
1 R; ~: S  U$ O+ henlargement of the penis, with a stretched length of
6 D, r& w. A! W! |) H8 cm and a width of 2 cm. The glans penis was very well# \* ^  G, P1 y, e; K, ]8 U
developed. The pubic hair was Tanner II, mostly around
' i3 N" }7 T, k4 R540
# o4 {/ P6 D# }6 }, I2 @: bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# d" |  u/ ?2 |) ]
the base of the phallus and was dark and curled. The
. f/ k, v4 e; mtesticular volume was prepubertal at 2 mL each.2 K8 z1 ?9 K9 B& N, M7 E
The skin was moist and smooth and somewhat
/ z" \2 S$ f4 k2 }5 ]5 y. M; v/ o7 ~oily. No axillary hair was noted. There were no* Z" U, d( s1 q* K) `1 c4 M
abnormal skin pigmentations or café-au-lait spots.
4 J5 Y2 }2 V9 g# g4 C7 TNeurologic evaluation showed deep tendon reflex 2+
, F2 \) ?; H5 E& B2 y& ubilateral and symmetrical. There was no suggestion
9 q! X3 H$ i( wof papilledema.
8 k: `6 D$ }, A. S. E$ z. j+ _Laboratory Evaluation
8 N) g. f7 ~% o# F8 N+ |5 WThe bone age was consistent with 28 months by
- s  G) B& X8 Zusing the standard of Greulich and Pyle at a chrono-; G$ Q  T9 f( i6 |
logic age of 16 months (advanced).5 Chromosomal
8 D( x$ [0 c4 c7 h4 W' ]karyotype was 46XY. The thyroid function test
7 M  d: @, K) P) B! Tshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
7 {: R9 R$ `' T; w  H, f! Elating hormone level was 1.3 µIU/mL (both normal).2 @) U+ W" g& r) [! O3 ~
The concentrations of serum electrolytes, blood
8 x' P+ w0 X9 z! \% ~3 |urea nitrogen, creatinine, and calcium all were3 l2 X! B1 }1 V- Z$ G/ p) h
within normal range for his age. The concentration- a# @' o1 N+ U- c% u
of serum 17-hydroxyprogesterone was 16 ng/dL) X6 q1 S3 O+ H7 ^- v7 e& C6 G5 b
(normal, 3 to 90 ng/dL), androstenedione was 201 U6 S0 m3 f3 Z6 l  U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* }% O3 _. F9 L- O2 g0 h
terone was 38 ng/dL (normal, 50 to 760 ng/dL),* z3 i+ ^7 W  D- a
desoxycorticosterone was 4.3 ng/dL (normal, 7 to4 d5 Q; z6 `) X* w2 s
49ng/dL), 11-desoxycortisol (specific compound S)
1 e% L- X. H1 |3 l0 u3 ], i3 R* kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ a( s! u6 n& Z# i5 b
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
+ S! W* S. W' W) _0 o8 ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* v* y' z" |# D# F: V& |and β-human chorionic gonadotropin was less than
! i1 U3 A0 c) ^! X3 y5 mIU/mL (normal <5 mIU/mL). Serum follicular
& \7 I0 U3 o" Gstimulating hormone and leuteinizing hormone
9 A  C9 R. n+ \) b+ w0 ?- l* Cconcentrations were less than 0.05 mIU/mL* _9 P& Y' C: K+ m& b; U" U: l: H
(prepubertal).
8 \3 _- p( R; dThe parents were notified about the laboratory
$ f3 A+ f1 k! [( a7 Z" Bresults and were informed that all of the tests were  G& ]% }: |0 ]/ C+ ~
normal except the testosterone level was high. The) d" x( N5 W6 x
follow-up visit was arranged within a few weeks to
# d* g1 g& F7 ]' [# N- cobtain testicular and abdominal sonograms; how-
2 F, a( @$ j6 R3 Iever, the family did not return for 4 months.6 V. J  W: N* I" @/ d" A$ M
Physical examination at this time revealed that the
# R! @3 \. \; ~" C- }child had grown 2.5 cm in 4 months and had gained
5 J0 \$ Q- i" W4 A1 W; N, F  F2 kg of weight. Physical examination remained
8 J# [, Y; x4 J/ q* |! gunchanged. Surprisingly, the pubic hair almost com-
8 q: S" l/ v, w: [8 Dpletely disappeared except for a few vellous hairs at$ y. P# |; ~/ R/ Z' s5 \% \
the base of the phallus. Testicular volume was still 2/ V6 R0 E$ m0 ^3 I& n, t" K
mL, and the size of the penis remained unchanged.
9 d0 k4 Q2 m4 B6 @; c& mThe mother also said that the boy was no longer hav-' _4 Z/ @) T0 |9 x4 j) y
ing frequent erections.. P1 P' @9 y" `) o2 E  x) U
Both parents were again questioned about use of) w8 [0 x: K9 N9 U' H
any ointment/creams that they may have applied to
8 P* t" Y5 T% l8 V. C8 B& i7 ythe child’s skin. This time the father admitted the
* X, w* n4 t' ATopical Testosterone Exposure / Bhowmick et al 541
* R4 G- u0 S  C  F1 t% ~4 X& `! Ruse of testosterone gel twice daily that he was apply-) T* y% C% w3 i* K# G, D" |1 n, }3 S3 X
ing over his own shoulders, chest, and back area for
! S5 l! s, Z* [4 ]a year. The father also revealed he was embarrassed
7 X) N, `; _' K0 P$ i3 V+ rto disclose that he was using a testosterone gel pre-; N2 s( @$ J. }
scribed by his family physician for decreased libido6 \/ W" x5 e- [2 k. ^( b/ @
secondary to depression.* w- N* ?9 A- Y/ q8 e/ G4 B  ^
The child slept in the same bed with parents.; s0 E2 r% l) `2 j. s* K4 ]
The father would hug the baby and hold him on his
' @0 c! q2 X: w; K% Y0 ^chest for a considerable period of time, causing sig-# H7 n* d# O$ d/ v
nificant bare skin contact between baby and father.& }( _0 H) n0 x: a0 q/ q8 P! L$ A
The father also admitted that after the phone call,
. `, ~: w  a7 \when he learned the testosterone level in the baby
3 }* a4 J- H0 mwas high, he then read the product information( H9 ^' E8 X- a8 `2 \* j8 S
packet and concluded that it was most likely the rea-/ M" U5 Q* {& U& j9 ^* }
son for the child’s virilization. At that time, they$ j3 q" p1 c3 o7 C2 ~; E7 U
decided to put the baby in a separate bed, and the
: r; x8 c3 M& `+ P( lfather was not hugging him with bare skin and had
) T. z: j# d0 ^0 ?5 T6 m- zbeen using protective clothing. A repeat testosterone
0 v( |8 Q4 e0 Otest was ordered, but the family did not go to the$ e+ F  F, U6 w
laboratory to obtain the test.. g% X% l" @! s0 K0 W) s- u
Discussion! ~" F- S- N) q% v6 j6 I; b$ [+ p* W
Precocious puberty in boys is defined as secondary$ \) W1 h  L' C7 P% p  m$ P* Y
sexual development before 9 years of age.1,4
. {5 l2 D2 H8 g! ^Precocious puberty is termed as central (true) when
  Z' ]% k% V' k/ u3 Qit is caused by the premature activation of hypo-& w0 ?+ r. z) K" H5 I: Q0 B
thalamic pituitary gonadal axis. CPP is more com-2 T0 I& K# K7 s  C5 |0 B* Q7 {( X
mon in girls than in boys.1,3 Most boys with CPP
  H! v$ [7 M4 R# A+ Hmay have a central nervous system lesion that is+ m' b$ V6 j' x: P; D
responsible for the early activation of the hypothal-
* e2 g8 Y3 [" Z1 a) e. \! tamic pituitary gonadal axis.1-3 Thus, greater empha-1 p# Z! C0 a5 T/ T1 z
sis has been given to neuroradiologic imaging in
: K, T8 H+ |) h! m0 \boys with precocious puberty. In addition to viril-# x( Q6 {4 e* Z, F) A5 ~
ization, the clinical hallmark of CPP is the symmet-
$ ~- {5 O( Z# d* u( Crical testicular growth secondary to stimulation by$ }% G% u! @9 v+ A. E. A" P
gonadotropins.1,3
) m  K) {. z, v. ]5 lGonadotropin-independent peripheral preco-& b# m9 w9 ~2 Z; S5 k# X
cious puberty in boys also results from inappropriate
* L' W5 g) `3 i. a( T* m5 zandrogenic stimulation from either endogenous or5 d4 y- I% X' u& a3 b+ A& Q
exogenous sources, nonpituitary gonadotropin stim-5 l3 i' Q* v/ V% ]# J) u/ }
ulation, and rare activating mutations.3 Virilizing
* E# K5 [8 A% N8 g; Q5 ?' ~# i9 Dcongenital adrenal hyperplasia producing excessive
+ [  ^9 b6 g4 Uadrenal androgens is a common cause of precocious. p6 N; m  p; ~) \' [3 r
puberty in boys.3,4
" g7 G% g" E  ^9 ^% OThe most common form of congenital adrenal
* u( L2 r' s4 A7 D( H* L( Jhyperplasia is the 21-hydroxylase enzyme deficiency.
1 z6 ^0 i. ^% \  ]3 dThe 11-β hydroxylase deficiency may also result in
1 l" a& `' y2 o* f$ T8 d# qexcessive adrenal androgen production, and rarely,
& _1 u" v. m1 l; E' F$ J5 gan adrenal tumor may also cause adrenal androgen9 e. C6 a2 W6 S: Z
excess.1,3" b- u$ U8 R, ]; w! n7 @7 W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% W4 j- ^( C4 j( l. K" g542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ V* Q* {& o7 _7 ]$ b4 Y9 KA unique entity of male-limited gonadotropin-
( v; l9 s9 W$ [% yindependent precocious puberty, which is also known
  B9 f$ M7 |9 w" [' @' l' Gas testotoxicosis, may cause precocious puberty at a$ B# c& }' G, o9 o1 J" ]
very young age. The physical findings in these boys$ a/ v. i4 ~0 G8 \. r) u4 a) J
with this disorder are full pubertal development,
7 b9 [4 e( p5 L; K2 `including bilateral testicular growth, similar to boys
, U7 W& G4 Z, |/ y( A3 v5 Twith CPP. The gonadotropin levels in this disorder! ^4 T# f; V! ]) Y- R. V; M+ B
are suppressed to prepubertal levels and do not show
0 ~  C6 l( C' o) t, d  r+ P+ Dpubertal response of gonadotropin after gonadotropin-
6 O4 j8 y# d4 g0 `releasing hormone stimulation. This is a sex-linked$ X* Z( S9 C9 C9 w" _5 r5 [- H, M
autosomal dominant disorder that affects only- x, V+ N- _% B) a. j1 ^, v! `# X
males; therefore, other male members of the family6 ]' d; y) c. v' o7 N8 f
may have similar precocious puberty.32 q4 m7 C/ s2 |5 i' s
In our patient, physical examination was incon-
1 H! K7 y0 l7 z# j& d+ a  b7 osistent with true precocious puberty since his testi-
, S" L/ k$ J) @0 W" ~* |cles were prepubertal in size. However, testotoxicosis
, |0 h) I. D6 ^* D% @was in the differential diagnosis because his father  @* s) ~, ~" C& h' u! q% w4 l
started puberty somewhat early, and occasionally,
' a* P  M" j% X$ T6 Stesticular enlargement is not that evident in the
$ H) o+ G6 {( g6 Y! Z0 _beginning of this process.1 In the absence of a neg-
1 W3 i4 q) X2 u. v/ hative initial history of androgen exposure, our
8 _* G$ A  v7 \1 i, {, Q! xbiggest concern was virilizing adrenal hyperplasia,5 X3 f3 e8 d, W5 N' s7 T
either 21-hydroxylase deficiency or 11-β hydroxylase( c) {! M* }  x5 |
deficiency. Those diagnoses were excluded by find-2 B  Q$ E$ U& n4 h9 k+ h; E- Z
ing the normal level of adrenal steroids.
& ]* c! W7 }4 H0 F* s( TThe diagnosis of exogenous androgens was strongly
% _7 |7 {, p/ |/ p6 q3 r& Hsuspected in a follow-up visit after 4 months because
) _# F7 v" L& b  y! g: Nthe physical examination revealed the complete disap-
" v& r+ B0 F) T9 j# O# j) h0 Mpearance of pubic hair, normal growth velocity, and
6 P. o2 G9 p; n! e  }4 Ldecreased erections. The father admitted using a testos-
! j, ~5 s7 A, A/ u) H' x/ }terone gel, which he concealed at first visit. He was: w! [  w" q- J8 C; z% y6 g0 l: q( o
using it rather frequently, twice a day. The Physicians’& g5 `4 r+ E& u( y- v
Desk Reference, or package insert of this product, gel or- p- w. J% {- _
cream, cautions about dermal testosterone transfer to6 P* F' \; p% r
unprotected females through direct skin exposure.
3 D+ w. C4 B1 ?Serum testosterone level was found to be 2 times the
4 I, J: G( L' m1 D$ ~( rbaseline value in those females who were exposed to
: E" R1 @) Q$ Q* ^, S5 }; Heven 15 minutes of direct skin contact with their male5 v; I7 U5 a$ L
partners.6 However, when a shirt covered the applica-: ~* K9 V% `; T+ S5 {* S
tion site, this testosterone transfer was prevented.
9 e- i5 J/ a1 E& E9 eOur patient’s testosterone level was 60 ng/mL,+ P1 l1 L! \* l. i6 Q  i3 s3 n
which was clearly high. Some studies suggest that5 S9 s8 Q0 V% ]8 l
dermal conversion of testosterone to dihydrotestos-; r& O6 L1 p+ h3 w1 \
terone, which is a more potent metabolite, is more; [  g3 g$ w' n0 m% Y! ?
active in young children exposed to testosterone
9 z5 L- ^, X! g; r2 ?0 A, xexogenously7; however, we did not measure a dihy-
7 \6 {9 I4 K5 f0 K% ^2 M0 cdrotestosterone level in our patient. In addition to
8 A% V) m5 B9 K( ]) nvirilization, exposure to exogenous testosterone in  ]& N, X1 U5 P& I; @! j, ]
children results in an increase in growth velocity and
1 n! d% a0 b2 jadvanced bone age, as seen in our patient./ o5 x" p% ], q( k" f' p* O% V
The long-term effect of androgen exposure during9 D1 s: N) A# p7 w) m, o# m2 j
early childhood on pubertal development and final
6 [9 R3 Z* K3 A# s* @7 \+ Sadult height are not fully known and always remain
" A2 y$ m* ^5 U, \5 ^' ia concern. Children treated with short-term testos-. r# A1 Z4 `( u  `- J) `5 _
terone injection or topical androgen may exhibit some
; h7 ^* e0 p5 U9 P3 Aacceleration of the skeletal maturation; however, after
- t1 s9 k: F3 s: }5 K9 r! y. Qcessation of treatment, the rate of bone maturation) q' f9 [$ T6 w( ~
decelerates and gradually returns to normal.8,9, G: k8 N) z: q5 A5 _8 {" c
There are conflicting reports and controversy
$ D7 W7 Q0 {$ q. r1 aover the effect of early androgen exposure on adult
. p3 n' S0 Q: }: c" t1 Vpenile length.10,11 Some reports suggest subnormal
: u( R% [/ m' ~  J1 tadult penile length, apparently because of downreg-
& |! T' w2 V( Gulation of androgen receptor number.10,12 However,
, P3 n& d' D2 k+ gSutherland et al13 did not find a correlation between! l* x! D3 Z9 o- Q
childhood testosterone exposure and reduced adult& T' x2 Y# V/ l4 ~/ N  S* @
penile length in clinical studies.. ~% k1 ]7 ^7 `* [5 E/ N
Nonetheless, we do not believe our patient is& Z2 b+ P9 [; `
going to experience any of the untoward effects from
- P+ y/ n# q# o3 Xtestosterone exposure as mentioned earlier because4 B/ p5 V0 T, N4 r( i
the exposure was not for a prolonged period of time., T: K" x8 C$ {& H5 q
Although the bone age was advanced at the time of+ C, v1 D* t8 b& f. z& i3 d3 t, V
diagnosis, the child had a normal growth velocity at6 y2 o. @9 L* }* k+ v: S
the follow-up visit. It is hoped that his final adult: q; J: r2 t, v  R- t- {
height will not be affected.
) \; e/ r" ^; JAlthough rarely reported, the widespread avail-/ i- H3 F% g7 v+ J
ability of androgen products in our society may1 r, A9 L: b; B; d4 ]
indeed cause more virilization in male or female
9 _! P8 L* r+ ~; _/ }# {. dchildren than one would realize. Exposure to andro-& W1 p3 I3 k0 s: f, |* c
gen products must be considered and specific ques-
- @8 B: X  `2 u7 Q& Ntioning about the use of a testosterone product or
! l+ t' c1 }8 V, m4 @( g' Mgel should be asked of the family members during) t) E3 K9 _! @' t
the evaluation of any children who present with vir-
" y6 O& l4 k4 @8 i1 e$ nilization or peripheral precocious puberty. The diag-
+ V) P# Z9 W9 R; D( T6 |nosis can be established by just a few tests and by
8 V, Z+ ?' V+ ~* Y/ |: Cappropriate history. The inability to obtain such a5 N; P- Y0 w' i& n% m. H- Y
history, or failure to ask the specific questions, may
0 Y1 r- v8 C, i: c9 L8 ~1 Oresult in extensive, unnecessary, and expensive
$ I( [: k5 |9 a! G/ B3 ~" dinvestigation. The primary care physician should be
5 p/ q% V$ r3 z7 c% v' S# B' Kaware of this fact, because most of these children, G9 g1 z# p" k5 p* v
may initially present in their practice. The Physicians’9 W7 @# Q; S) j( w, x
Desk Reference and package insert should also put a
6 M0 x- |# F) V( u! owarning about the virilizing effect on a male or
+ v# J: H+ W5 ]8 Q- o. }female child who might come in contact with some-
2 `5 G& t4 y' B* xone using any of these products.
$ B) A/ u# Y8 N- X7 uReferences- r( y  z  b3 O# ]
1. Styne DM. The testes: disorder of sexual differentiation* X6 Q5 Z) z0 \0 k) R
and puberty in the male. In: Sperling MA, ed. Pediatric
' A0 [# ]& r5 d: G7 \( A! AEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 e' k) v4 A; z) s3 ^2002: 565-628.
1 f0 E' f- P" H2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, X" G  N, B+ p# j8 A8 l/ T
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old5 T% E$ \$ A4 a
Boy Induced by Indirect Topical
3 z5 U: o( g, }9 Y! e: HExposure to Testosterone8 `$ j; @( [) ], `; x0 F
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 M) G# n; E. W  ?) ?, M7 k# iand Kenneth R. Rettig, MD1
/ k4 S8 p4 ]+ q6 e/ q6 jClinical Pediatrics7 x+ N. C+ u! e. U6 p7 C
Volume 46 Number 62 j5 |# E& L# O+ J
July 2007 540-543: ~6 y: R6 j# t; h
© 2007 Sage Publications
# W$ Q  g, ]5 T9 n4 K10.1177/00099228062966510 Z; m  {. H' Q: U6 t8 B) ~( t
http://clp.sagepub.com, v5 }& b- Y- _' w" t2 v8 {
hosted at( i9 X/ n- X: s" ^* u( R: u
http://online.sagepub.com! q8 `# t% {, T+ I2 r
Precocious puberty in boys, central or peripheral,9 D% k( Q& G* ?5 e! E
is a significant concern for physicians. Central- A% ]9 t' z* S
precocious puberty (CPP), which is mediated( o0 V+ z8 g, Q& Z7 R: h
through the hypothalamic pituitary gonadal axis, has* l2 |8 d' u+ H0 N$ I
a higher incidence of organic central nervous system: B# X# _  _; y/ X) o
lesions in boys.1,2 Virilization in boys, as manifested
, F: L% Z) z" l, x; I( yby enlargement of the penis, development of pubic, Y: g! p& K; C6 ~# q% z# \
hair, and facial acne without enlargement of testi-
& m3 S9 B( _& {; R, j% R: @5 Ycles, suggests peripheral or pseudopuberty.1-3 We$ U. [  X5 g5 V6 _' W% k" X
report a 16-month-old boy who presented with the
+ f( u4 ~% }. b6 `1 D' {enlargement of the phallus and pubic hair develop-, o1 D0 i0 V. r* b& }
ment without testicular enlargement, which was due
6 I5 M" I8 S: mto the unintentional exposure to androgen gel used by/ z& s6 R  w- |' D
the father. The family initially concealed this infor-5 S" z- V/ _) O3 d3 i
mation, resulting in an extensive work-up for this9 y( y5 x$ t! s6 N+ Z) `  R5 x6 p- j# d
child. Given the widespread and easy availability of: ^% I. d$ I3 L' C) L& _
testosterone gel and cream, we believe this is proba-
6 H/ d. t9 G- L/ S4 [4 c5 P! _8 ~2 ^bly more common than the rare case report in the0 ~: f& E5 Z5 `. G5 |( f8 |
literature.4
$ D$ u4 X' `( t% J' `( C% @  m" |  VPatient Report
0 ]0 ^) S: {. MA 16-month-old white child was referred to the& }4 j) r* w0 e7 \2 \5 D( Y2 d
endocrine clinic by his pediatrician with the concern
) s0 S/ }# ?3 v" N# D& {/ S% Mof early sexual development. His mother noticed2 L* w4 o/ O3 x' C# ]% F, v+ P4 W
light colored pubic hair development when he was' a. l" j) n4 S  u
From the 1Division of Pediatric Endocrinology, 2University of
! F: D/ R) ]+ FSouth Alabama Medical Center, Mobile, Alabama.& z# T/ W" X% C* v( q# [, L
Address correspondence to: Samar K. Bhowmick, MD, FACE,
# u' _/ S( U+ z! R  w% dProfessor of Pediatrics, University of South Alabama, College of* f/ a- F( r9 a, b3 s0 r
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 T  ~$ i+ Q  \, R0 U
e-mail: [email protected].5 m+ L$ L6 ]9 v
about 6 to 7 months old, which progressively became5 R3 T/ w6 s, N2 W! d7 L/ k
darker. She was also concerned about the enlarge-
. ?' W! P7 x. \& t$ a& Cment of his penis and frequent erections. The child
+ w. [9 X6 b" P( A  e, B* ^was the product of a full-term normal delivery, with
3 w0 T+ J5 Q; P+ y+ g0 g/ Ga birth weight of 7 lb 14 oz, and birth length of8 l6 K/ v4 R$ {1 ~( q+ [
20 inches. He was breast-fed throughout the first year& w! c, q9 t2 {- ~3 Q" [
of life and was still receiving breast milk along with
* T2 g  V0 Z' f  ]7 E2 {solid food. He had no hospitalizations or surgery,1 [' Q0 X0 L, y( q# i  ^  H% W
and his psychosocial and psychomotor development
" d# V7 P) F+ U0 k3 i% m1 jwas age appropriate.9 z4 C- E1 y; J9 ~
The family history was remarkable for the father,( C2 G. m- E1 ]8 ?
who was diagnosed with hypothyroidism at age 16,5 r1 r# W& K! u# W' H  c# ]
which was treated with thyroxine. The father’s
, m7 N: i$ k) y7 I6 xheight was 6 feet, and he went through a somewhat
" Q2 N8 R  V( W& V  k# D  U9 b7 Pearly puberty and had stopped growing by age 14.* O* z4 d2 _  j  O
The father denied taking any other medication. The$ w) L. J, p% r1 i) n
child’s mother was in good health. Her menarche& y1 t: s; s0 X
was at 11 years of age, and her height was at 5 feet  P/ i9 ~# a9 x6 u6 e- K
5 inches. There was no other family history of pre-! ^8 ]. D  V8 F  Y2 |& k: f7 `
cocious sexual development in the first-degree rela-( ?$ {' X2 Z9 l1 s9 ^5 X
tives. There were no siblings.
  M+ w; i0 L, C" _+ z! MPhysical Examination
, ?1 N  t9 T/ xThe physical examination revealed a very active,/ M4 S9 a0 P; t) s7 X! k6 ~, H
playful, and healthy boy. The vital signs documented
5 ?7 ]6 E4 n7 @3 e# t& m0 f% E" [a blood pressure of 85/50 mm Hg, his length was- {9 D( o! J& H8 I$ o' F
90 cm (>97th percentile), and his weight was 14.4 kg
7 `7 o5 R" |6 Z; O/ @* W(also >97th percentile). The observed yearly growth) S9 I7 i8 G+ B% |" r/ P* Z
velocity was 30 cm (12 inches). The examination of7 `# G$ f$ i: @* y: Y/ O. N
the neck revealed no thyroid enlargement.' y3 \+ n% [/ l# d# f& {
The genitourinary examination was remarkable for
; ~. E0 a5 y' o* d& X9 Uenlargement of the penis, with a stretched length of0 E; t) a& v6 O8 e# E
8 cm and a width of 2 cm. The glans penis was very well: [1 t7 ~, u% n  A+ o
developed. The pubic hair was Tanner II, mostly around2 G5 `, {2 w+ e8 \3 l
540
' {, }% {8 j' }% q- Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. M  Y! @0 L6 ]; [* F3 G  P: N
the base of the phallus and was dark and curled. The. `, f" R  B. G7 C( t0 N6 j
testicular volume was prepubertal at 2 mL each.
: o8 ?% o8 Z# K! H8 C4 }  lThe skin was moist and smooth and somewhat
3 z& Z( t6 q; c" O( b& w4 xoily. No axillary hair was noted. There were no
1 Z  @3 W7 a& B* b. b  Kabnormal skin pigmentations or café-au-lait spots.6 V0 J6 a) e5 X2 L( }$ K
Neurologic evaluation showed deep tendon reflex 2+1 y3 G* D2 J9 V3 l
bilateral and symmetrical. There was no suggestion0 a  d( m* c2 h; m# i6 {- z$ F+ Z4 I
of papilledema.* M- W0 M9 E( `# {5 F' l" x& J
Laboratory Evaluation9 F  N# ^- D0 \/ m
The bone age was consistent with 28 months by
( b- f9 @) U2 r& f- L, Gusing the standard of Greulich and Pyle at a chrono-, g! j  [7 I. ^3 W7 t
logic age of 16 months (advanced).5 Chromosomal8 G/ h4 l# t1 x& q
karyotype was 46XY. The thyroid function test
+ y8 G7 W, N9 Z+ K& M- t4 |showed a free T4 of 1.69 ng/dL, and thyroid stimu-3 W7 I2 {7 g" d4 F
lating hormone level was 1.3 µIU/mL (both normal).% g7 S9 g3 K/ A: F: w: z/ T' y0 D( m
The concentrations of serum electrolytes, blood: j7 p) J$ W- Q
urea nitrogen, creatinine, and calcium all were
$ m% U3 _( b* E: D0 Q- P( Cwithin normal range for his age. The concentration
5 V1 E% H. G/ P3 k1 E" `6 ]8 hof serum 17-hydroxyprogesterone was 16 ng/dL
( Q( o8 C4 h  O9 j* N0 @4 Z9 g8 \# g(normal, 3 to 90 ng/dL), androstenedione was 206 b' f/ ]7 b: }9 p% S
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; v! k; i( I9 X% a- W
terone was 38 ng/dL (normal, 50 to 760 ng/dL),$ N1 r; w8 a, Z+ S
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
! i5 o3 U' r& d49ng/dL), 11-desoxycortisol (specific compound S)0 Z) _( w6 e( D: ~. K
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
  o$ O3 u5 l+ m# A- a5 ^tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* ?" x( }( L  F% t, F9 I5 stestosterone was 60 ng/dL (normal <3 to 10 ng/dL),# O6 p' |( k6 K
and β-human chorionic gonadotropin was less than
0 y/ w# K8 u$ h1 E# ]/ j6 B5 mIU/mL (normal <5 mIU/mL). Serum follicular  G/ s. \4 c8 m; `' J
stimulating hormone and leuteinizing hormone; @' S: D, L+ V0 ?$ K
concentrations were less than 0.05 mIU/mL
5 M- u6 e# |7 ?0 e2 A0 c(prepubertal).. K& V4 h" w. Q0 H; o9 h
The parents were notified about the laboratory. o3 k% E) U+ c) U* u4 @
results and were informed that all of the tests were) _' [# R) D# K7 G
normal except the testosterone level was high. The
. P9 y- m5 I% x5 ~9 i* qfollow-up visit was arranged within a few weeks to
7 ?8 q( N# m. A" S5 g; E. Aobtain testicular and abdominal sonograms; how-) t: H# Y0 \6 _* l
ever, the family did not return for 4 months.2 C8 k2 l% C) ]7 V; f* a) n
Physical examination at this time revealed that the
- C+ f7 G* ^  v* I" k% J* @child had grown 2.5 cm in 4 months and had gained
, N- ?1 T7 c8 Y& U2 kg of weight. Physical examination remained
0 d% r% L$ R4 T/ G- l$ {unchanged. Surprisingly, the pubic hair almost com-
. r9 Q! }6 H& F; @) m2 E, k  Hpletely disappeared except for a few vellous hairs at& o9 S3 v: z5 _2 o; e* z8 f
the base of the phallus. Testicular volume was still 2
9 [9 T$ p5 C. E, E% @' M% x& HmL, and the size of the penis remained unchanged.
( n& j8 T+ Z) B) S0 V, AThe mother also said that the boy was no longer hav-+ ^& i# [1 U5 ]0 E9 D/ O. {, q
ing frequent erections., U4 @2 i5 e2 H$ x3 m, {
Both parents were again questioned about use of
* y' v$ |& b4 F' n2 @any ointment/creams that they may have applied to/ |& ^9 p% c6 b) T& N
the child’s skin. This time the father admitted the
: P% ?8 d( \5 _, E5 B8 T7 K0 }6 JTopical Testosterone Exposure / Bhowmick et al 541- T% @" B, K' g
use of testosterone gel twice daily that he was apply-
+ e* z8 e5 T4 j$ Ging over his own shoulders, chest, and back area for
0 F% q. k" d" N9 pa year. The father also revealed he was embarrassed
6 |; S  R0 A5 E3 F: Uto disclose that he was using a testosterone gel pre-* l" h9 z: V* h8 q: d! `5 {
scribed by his family physician for decreased libido4 f; }* |2 g. k& }' v
secondary to depression.
$ g# q: q6 u, _The child slept in the same bed with parents.
) y/ D! q% s+ @$ M' i7 d9 SThe father would hug the baby and hold him on his1 @! a" [9 Q, x+ Q
chest for a considerable period of time, causing sig-
: i: \/ @4 q. F% i) Rnificant bare skin contact between baby and father.0 A! f- V* l8 H  M! ~2 [) \
The father also admitted that after the phone call,
  ^' P0 y: s" e! T  A& t) Dwhen he learned the testosterone level in the baby
7 F. F4 h) T8 S" ^& w# Swas high, he then read the product information( m( L+ M% L; ?6 X2 ]+ H* m
packet and concluded that it was most likely the rea-
- K4 b6 C* a+ e5 Ison for the child’s virilization. At that time, they9 {1 l! ~6 J8 P) U  K
decided to put the baby in a separate bed, and the
6 n) V" e# r$ X' u8 Hfather was not hugging him with bare skin and had/ a- s: l4 ~0 B4 G
been using protective clothing. A repeat testosterone
% N  |. F- _# u/ C) a- S7 b8 j" itest was ordered, but the family did not go to the
1 ^! A0 ]# ]7 C$ n. [7 N' P1 l) Xlaboratory to obtain the test.# y- D7 L: }5 l, ]0 P* S2 r# M- S
Discussion9 i6 Z7 H7 M- p
Precocious puberty in boys is defined as secondary) G: [, J9 t# _/ G/ \' e- S
sexual development before 9 years of age.1,4
6 `# O9 k, c& i- _1 F  }% Y/ |Precocious puberty is termed as central (true) when
. v$ ?% J3 M3 Bit is caused by the premature activation of hypo-: B% R7 A, S' C+ c
thalamic pituitary gonadal axis. CPP is more com-9 Y1 V8 D; X. R2 y  E- ~: }
mon in girls than in boys.1,3 Most boys with CPP
3 Y) c6 L. P, t& F7 t0 Bmay have a central nervous system lesion that is
5 ^% i2 n4 O! U4 C6 A# Yresponsible for the early activation of the hypothal-0 I, ?+ `( v  v( k" Q5 J7 a9 A9 g
amic pituitary gonadal axis.1-3 Thus, greater empha-
9 D' {: H5 f6 y/ c5 @9 _sis has been given to neuroradiologic imaging in
# G; S7 s6 q8 y  x' O; g" jboys with precocious puberty. In addition to viril-
: F  o# |& a1 m+ _: |; mization, the clinical hallmark of CPP is the symmet-
0 Y( s2 C% ~5 Grical testicular growth secondary to stimulation by% m- B8 L5 K, [
gonadotropins.1,3
2 ~, `* ~  V. v. ^: pGonadotropin-independent peripheral preco-
, P# j* I9 J7 }' p5 Mcious puberty in boys also results from inappropriate
/ e$ W0 e: e; o7 w# I- O5 `androgenic stimulation from either endogenous or# H3 g1 k$ p4 B' }/ g) W/ g
exogenous sources, nonpituitary gonadotropin stim-
: {: O" b& ~* I1 {: `4 v. l6 Rulation, and rare activating mutations.3 Virilizing
* @6 Q! X5 J4 c0 ?9 n; Acongenital adrenal hyperplasia producing excessive
/ u0 M  H& f; X# y) B. o0 u8 K0 Gadrenal androgens is a common cause of precocious
2 _% y" m5 \. a$ Q- K3 A  Ppuberty in boys.3,4' m" s3 _- i2 a
The most common form of congenital adrenal
2 `1 f# u1 I" m% Y+ f9 dhyperplasia is the 21-hydroxylase enzyme deficiency.8 N3 m) X4 x: H$ w3 g
The 11-β hydroxylase deficiency may also result in
% ~+ A) S; {+ x2 zexcessive adrenal androgen production, and rarely,
7 T6 R$ i( x' K6 ], @2 t1 Tan adrenal tumor may also cause adrenal androgen2 [7 ~* u5 C+ |: I2 J% J
excess.1,3
8 L0 Q  m" ?; A% Q, i' \! H8 E8 oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 A% ]  P- O" [( i, @8 g& O' a542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 D- D3 h0 B* n- o' u
A unique entity of male-limited gonadotropin-2 F- }6 j* r) P9 q
independent precocious puberty, which is also known
! j% v$ h+ Q( x# J% ]" W0 fas testotoxicosis, may cause precocious puberty at a. g$ p" M7 `/ h1 w$ Z
very young age. The physical findings in these boys
8 b5 \1 }; @; R3 Awith this disorder are full pubertal development,
- l. w- r: t, l" c1 R: u3 ~including bilateral testicular growth, similar to boys8 `( _+ J5 o. H. d. F. d
with CPP. The gonadotropin levels in this disorder! X5 U/ j, W7 S2 u) o8 L# F
are suppressed to prepubertal levels and do not show; R/ H+ y4 |& _2 y* Q1 A
pubertal response of gonadotropin after gonadotropin-
! [3 N# S" ]/ d. P1 J+ Ireleasing hormone stimulation. This is a sex-linked
+ @! G8 ]' _; ^; a2 O, sautosomal dominant disorder that affects only
2 i! g$ V; T7 M4 f* \& P9 emales; therefore, other male members of the family5 D! [* k/ n1 D$ W* d$ x4 `5 B
may have similar precocious puberty.34 b6 |% C- e$ m# F- ~
In our patient, physical examination was incon-
% y; R. i7 ?3 ?* r' H) ?& F4 Esistent with true precocious puberty since his testi-
  s: Y/ B5 j5 i7 fcles were prepubertal in size. However, testotoxicosis+ ?4 M3 U, T* V, D  ?9 V
was in the differential diagnosis because his father) i) L& C0 y, @1 A
started puberty somewhat early, and occasionally,
$ j0 `: G0 M% Ntesticular enlargement is not that evident in the
  k- ~. n' H) y3 _4 G% O0 dbeginning of this process.1 In the absence of a neg-+ w" m/ b4 k) N* \2 E
ative initial history of androgen exposure, our6 R( r* K, L  |; u1 F% n, P
biggest concern was virilizing adrenal hyperplasia,
, P# A0 Y/ A9 O$ Meither 21-hydroxylase deficiency or 11-β hydroxylase
$ |. B4 B" [- V# ydeficiency. Those diagnoses were excluded by find-
5 X# l; Z. ~  @7 v5 z  j; {$ c9 Ling the normal level of adrenal steroids.
$ |! N# c  ?  t- ?The diagnosis of exogenous androgens was strongly
. X0 J; n6 |, G! s4 fsuspected in a follow-up visit after 4 months because
) `6 u; _3 S- @) ~8 x0 dthe physical examination revealed the complete disap-
* r% X) \! Q8 c9 ^5 e/ Tpearance of pubic hair, normal growth velocity, and
$ ]& R; s, m7 H7 @# R$ ndecreased erections. The father admitted using a testos-5 H6 \2 _. L- Z% A
terone gel, which he concealed at first visit. He was
! g/ H/ B6 t& O! Jusing it rather frequently, twice a day. The Physicians’, z% y$ S# g' o0 d9 n) b9 ?
Desk Reference, or package insert of this product, gel or
, m# H$ L5 Y! v7 u, \, g8 p0 pcream, cautions about dermal testosterone transfer to
* L: e$ `& ~; m0 T+ ^unprotected females through direct skin exposure.. y: W% e5 C. ]5 {' `# p0 ]
Serum testosterone level was found to be 2 times the
9 [& K3 L& }% W. R* w1 kbaseline value in those females who were exposed to) r' J. ^  ]. t
even 15 minutes of direct skin contact with their male
! o) \9 f$ O& A* k5 B; Wpartners.6 However, when a shirt covered the applica-7 E' O" G6 [/ e; T$ ]
tion site, this testosterone transfer was prevented.
; O& P( G. N5 U) Y8 C: Z; a9 v2 }Our patient’s testosterone level was 60 ng/mL,
/ Q7 ~/ |5 f& [+ `/ fwhich was clearly high. Some studies suggest that
+ W( B6 U9 p9 @$ D. ~, jdermal conversion of testosterone to dihydrotestos-  O" g% x, h, }3 L+ V% A
terone, which is a more potent metabolite, is more
3 }6 U% W  I; d: G- tactive in young children exposed to testosterone
6 F" R$ r& t5 h' K* kexogenously7; however, we did not measure a dihy-$ U! g( s& I. ?% F( V
drotestosterone level in our patient. In addition to0 ^# n- B& F$ |% Z/ x
virilization, exposure to exogenous testosterone in
0 l0 x2 R- `2 E9 rchildren results in an increase in growth velocity and% s/ c( d$ |$ E7 s. A" U! z4 o  Z
advanced bone age, as seen in our patient.5 j1 a* F# l+ b- x7 \6 y
The long-term effect of androgen exposure during
$ d/ P% q* Z2 Y2 C9 I% m" Kearly childhood on pubertal development and final
6 t# L. }- O9 I0 ]; N: Uadult height are not fully known and always remain7 p/ `+ C8 z7 U$ @. y4 A4 V+ u" p
a concern. Children treated with short-term testos-
5 u3 h+ y1 y5 Y; C; Iterone injection or topical androgen may exhibit some
. }7 E, ^8 ~$ e4 u9 L3 Gacceleration of the skeletal maturation; however, after1 ]% F3 V& B" E- p- y' E4 t9 v5 x
cessation of treatment, the rate of bone maturation
6 v2 _! A, q( m' h0 Cdecelerates and gradually returns to normal.8,9
- ~# @4 R7 }  ]# m* bThere are conflicting reports and controversy
5 V& J3 J4 _/ R2 ?" A! ^over the effect of early androgen exposure on adult
: o' y+ u' k1 V  B  Kpenile length.10,11 Some reports suggest subnormal
# A- E) o* Q4 R( l# Tadult penile length, apparently because of downreg-. E+ f$ u6 J  N7 ?) [
ulation of androgen receptor number.10,12 However,
; H% t% _: K0 f; r! H( zSutherland et al13 did not find a correlation between
7 N9 P8 E0 M2 H, J! S/ cchildhood testosterone exposure and reduced adult
: w) d/ T1 T6 Z% ^  _penile length in clinical studies.  p6 N/ ?' p. y5 v
Nonetheless, we do not believe our patient is0 V5 y  n: M# r& j: ?* @
going to experience any of the untoward effects from
) L- q1 `5 A: A1 }6 v# I! Otestosterone exposure as mentioned earlier because
0 |8 F+ q" ~7 V, t' U" ]! {the exposure was not for a prolonged period of time.
/ d7 K: @" T5 `$ b1 cAlthough the bone age was advanced at the time of& |6 M' ~' B: m3 z3 \  d8 d
diagnosis, the child had a normal growth velocity at: W( `& R. T& @) |
the follow-up visit. It is hoped that his final adult
: S0 V, D! E' M5 u: ]* {height will not be affected.: ]9 K+ p; ^" T6 w' }7 q$ S8 w' `, v: Y: y
Although rarely reported, the widespread avail-
, y7 \$ J7 t/ Y4 j! `ability of androgen products in our society may+ S/ o" B" x+ e% e
indeed cause more virilization in male or female& V8 |7 t; @2 `# r& a' ]
children than one would realize. Exposure to andro-: H/ A, z( J4 N: A* k8 c& e# b
gen products must be considered and specific ques-
) p6 @4 {  Z# i# rtioning about the use of a testosterone product or/ Z: X( w& c4 j0 {% {
gel should be asked of the family members during
  ^0 ?" [: h' Kthe evaluation of any children who present with vir-% z7 {$ H* V5 e, H
ilization or peripheral precocious puberty. The diag-, y. n8 X5 e  ?$ s/ v4 p- _' r+ |  J
nosis can be established by just a few tests and by
9 P- {9 ~5 i$ Y+ x3 F. o) O  Oappropriate history. The inability to obtain such a- Z4 d9 K# j5 C
history, or failure to ask the specific questions, may' t5 z* d( u& M7 [9 l
result in extensive, unnecessary, and expensive3 a* }5 V% i: g8 [' u* f) P
investigation. The primary care physician should be
0 w: C# i1 {' V( X* b6 Eaware of this fact, because most of these children% r9 k# |9 l7 M# g5 E. B, m; ]/ y' k
may initially present in their practice. The Physicians’. [/ ?) [, ]$ t
Desk Reference and package insert should also put a
6 @: Z0 t. R. O' {warning about the virilizing effect on a male or
7 K8 h! A- F' G! Q, ~female child who might come in contact with some-
8 ]) G6 \. i" J  Y& V7 L1 B& Qone using any of these products.
$ ^9 f* O  [. c7 i4 c0 a# jReferences+ [8 c  U8 `% h9 m: S
1. Styne DM. The testes: disorder of sexual differentiation" |+ {) j% ^, x, V5 o: `
and puberty in the male. In: Sperling MA, ed. Pediatric
( _; i0 V. x$ `8 d1 x& f3 QEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, g4 Y  W7 E/ |  U! o/ p
2002: 565-628.8 N0 s) e, t# N8 B5 _6 e4 _4 K
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" j  i0 d  G9 V- k8 q9 J+ mpuberty in children with tumours of the suprasellar pineal
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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!

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發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
累計簽到:11 天
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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

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發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
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發表於 2025-1-19 02:41:05 | 顯示全部樓層

$ }. K: u3 Y7 S" e! H, J/ H. N精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!

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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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