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Sexual Precocity in a 16-Month-Old) d8 p8 e" j5 M" K. ?& a
Boy Induced by Indirect Topical
) V# Z2 {2 {5 s; s3 Y8 _Exposure to Testosterone" y' d) g+ R: a+ M/ w& T
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2" r: S. P6 T) {& W4 Z; H
and Kenneth R. Rettig, MD1
7 u9 V8 d; e3 @Clinical Pediatrics+ [: N& y# z) S; c+ g! h
Volume 46 Number 6) v9 Q7 T! k, {- ]7 |
July 2007 540-543$ D& K4 O" N, t  v4 {3 b1 \" D
© 2007 Sage Publications1 q$ r$ I; V0 |
10.1177/0009922806296651* Z; g+ y$ F$ M6 t& P
http://clp.sagepub.com6 }7 L) r/ c. v0 p
hosted at; D) X; B0 u1 y  m  O# u
http://online.sagepub.com% I/ ^$ y# |2 |8 k5 C
Precocious puberty in boys, central or peripheral,
5 d3 \$ g3 ?& k( ]6 ?is a significant concern for physicians. Central: L" m! m0 H5 I2 V9 |2 i5 q
precocious puberty (CPP), which is mediated
6 j  H3 U8 C6 E* fthrough the hypothalamic pituitary gonadal axis, has
  X3 z$ V& q+ ~4 H8 ta higher incidence of organic central nervous system
% Q. `: H- g' {8 O2 a, R1 |( `lesions in boys.1,2 Virilization in boys, as manifested! I7 U- e+ K) T
by enlargement of the penis, development of pubic2 [5 O; H' [! s
hair, and facial acne without enlargement of testi-
0 L) J+ Z4 ?) e% _cles, suggests peripheral or pseudopuberty.1-3 We" R  |7 i# i3 `2 f; o/ g
report a 16-month-old boy who presented with the
0 }' f! e8 b( {4 Qenlargement of the phallus and pubic hair develop-6 ~2 B" j  E6 E; m
ment without testicular enlargement, which was due; |) Z& y4 W! Q9 ]. v& T; v) O
to the unintentional exposure to androgen gel used by
$ |# d$ F( y6 ?$ W3 n6 w& `6 mthe father. The family initially concealed this infor-) p0 a4 M2 i, D; {/ L9 j7 H
mation, resulting in an extensive work-up for this
; L# @6 {0 i2 X: c& @/ s) G& hchild. Given the widespread and easy availability of
  u$ p3 w, _% q7 f. B% Ltestosterone gel and cream, we believe this is proba-
" e9 S# m. d' u' w: \/ zbly more common than the rare case report in the; w! T4 G& G4 t. C$ o6 z
literature.4
" C# s6 g/ N; |+ D, C3 c5 F0 e- J2 TPatient Report
( {* F0 c: Y9 T: o/ A7 oA 16-month-old white child was referred to the  c2 Y) w! O  l/ L
endocrine clinic by his pediatrician with the concern) O; D. l) m$ g1 H
of early sexual development. His mother noticed4 h; P% d8 b) S! O# }$ @* k
light colored pubic hair development when he was
; |" W' n9 L9 ^4 s7 iFrom the 1Division of Pediatric Endocrinology, 2University of
4 e3 y7 M& U% z5 [* jSouth Alabama Medical Center, Mobile, Alabama.; Y3 O! h" y: y' y; M2 x
Address correspondence to: Samar K. Bhowmick, MD, FACE,
3 W1 Q3 v  ?5 W; @7 t, C/ ?Professor of Pediatrics, University of South Alabama, College of! }5 n' l$ s* J5 B4 t' B
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, ]' b6 g: z+ J  W
e-mail: [email protected].2 g' L/ @7 ]( d9 x: e1 K) y
about 6 to 7 months old, which progressively became; A. i% ?# v( i: C2 V/ {# H
darker. She was also concerned about the enlarge-* f: ]5 G; y% {  x
ment of his penis and frequent erections. The child( w+ k% {: {0 _0 D1 `: u" m
was the product of a full-term normal delivery, with4 P# m! L9 C* S9 E! ]
a birth weight of 7 lb 14 oz, and birth length of$ |+ ?" [- }6 h$ Q- f  Q! Q% N+ v# r
20 inches. He was breast-fed throughout the first year
8 z" w4 Q  n3 b( F1 i0 qof life and was still receiving breast milk along with1 Y7 x$ t0 g& P: `) z
solid food. He had no hospitalizations or surgery,1 `% E6 F( i( Z9 `" T8 g$ r
and his psychosocial and psychomotor development
7 o8 b6 p1 @$ i8 `was age appropriate.
) K2 h* h# o  Y7 s" n8 j8 LThe family history was remarkable for the father,
2 [; Q) h' X' ?+ jwho was diagnosed with hypothyroidism at age 16,
' f5 E' y9 E+ g1 Y' i( rwhich was treated with thyroxine. The father’s
4 J; E- A9 S3 }) Nheight was 6 feet, and he went through a somewhat; y# B- P1 Q* n5 E) O: P
early puberty and had stopped growing by age 14.
2 r5 {" V$ n9 ^8 [# qThe father denied taking any other medication. The
% P9 q# K4 H8 V* Z6 U5 E1 }1 D" jchild’s mother was in good health. Her menarche+ D' f8 O) K7 r* D# K8 B
was at 11 years of age, and her height was at 5 feet
/ C# _* X' [4 S4 J1 k0 `4 O( @5 R- u5 inches. There was no other family history of pre-
9 M* J! S  F7 ]; hcocious sexual development in the first-degree rela-
( z. M- v# `0 m' u! Ltives. There were no siblings.
; l5 j& H1 W2 B& X+ {& X# O0 F1 DPhysical Examination
) I9 x3 a& s, J2 `The physical examination revealed a very active,5 B3 s1 g/ n# Z- |0 u
playful, and healthy boy. The vital signs documented! H; s. d) o: f& y( H3 v4 Z
a blood pressure of 85/50 mm Hg, his length was/ D9 S7 o8 r2 p/ Y! y$ I
90 cm (>97th percentile), and his weight was 14.4 kg/ j" J& F6 r* w4 ]+ w" j( f- J
(also >97th percentile). The observed yearly growth- q8 Q3 }) ]+ e  l/ W$ [9 G
velocity was 30 cm (12 inches). The examination of* J, X2 V4 j! j" D
the neck revealed no thyroid enlargement.
# F! q- b) i$ }- J1 uThe genitourinary examination was remarkable for9 G7 s/ `3 |# d2 ?, N
enlargement of the penis, with a stretched length of; I+ ]8 V- W2 z! Z8 V2 _
8 cm and a width of 2 cm. The glans penis was very well
% h! ~1 I& H6 |4 ^# Z' H& l/ j' m  v% {developed. The pubic hair was Tanner II, mostly around
5 o) t2 R: R. ?- f8 p540
  |; S4 v; P. N0 ?+ d# Jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ K! p7 |5 R5 n' W; a; Y' A5 ]% }, S
the base of the phallus and was dark and curled. The
4 k8 d2 S$ [& h1 v, J# Xtesticular volume was prepubertal at 2 mL each.5 w& ]2 I# v- v+ P
The skin was moist and smooth and somewhat
5 F! i: Q) m6 s8 w; D4 Zoily. No axillary hair was noted. There were no* Q" ~3 u' W# |6 t  E1 o% Z' B
abnormal skin pigmentations or café-au-lait spots.8 @0 j+ }" b* w+ Y. K
Neurologic evaluation showed deep tendon reflex 2+4 g6 K' E3 i6 T7 Q% N" {5 ]- R' B
bilateral and symmetrical. There was no suggestion1 [4 w' G+ ]( M* o# k8 O& ?) e6 b
of papilledema.
5 s& G1 W/ K& W; e: q7 K8 m; c/ ALaboratory Evaluation
/ }2 K3 s. |& L+ t8 s+ V" @The bone age was consistent with 28 months by* B' h6 r' n" A8 g5 E$ ?9 t
using the standard of Greulich and Pyle at a chrono-
4 N" v  Z7 F, v& m/ a' t! N0 Dlogic age of 16 months (advanced).5 Chromosomal3 R) L' P/ H5 P2 ^9 y/ y" B3 H5 B2 s
karyotype was 46XY. The thyroid function test
1 }) o" i2 k% J5 Q. jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-) X! N  |5 ~2 q, @
lating hormone level was 1.3 µIU/mL (both normal).1 ~/ j& R3 A- a, Y8 g
The concentrations of serum electrolytes, blood
+ J/ n, p/ y& `# J, n7 b2 i4 Rurea nitrogen, creatinine, and calcium all were) W6 k" w0 j7 }2 F# m/ H: O( ]
within normal range for his age. The concentration
8 W- M) E0 q6 Qof serum 17-hydroxyprogesterone was 16 ng/dL
+ ?; D; d& G  O) E9 @, q. ?6 X(normal, 3 to 90 ng/dL), androstenedione was 20; |* B% U0 z9 h2 t' N7 |; l
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 V  _/ ]# p$ D" T( X6 x* i' U
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- z2 q2 {- n( tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to1 @& L0 t0 c9 e
49ng/dL), 11-desoxycortisol (specific compound S)
, X7 i; `1 W# h# Y, x" H/ e/ Hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
9 |" ?) G6 k/ q: dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
- u6 k4 i' i3 ^9 R: T$ a- stestosterone was 60 ng/dL (normal <3 to 10 ng/dL),; s2 i* c, w( k, d
and β-human chorionic gonadotropin was less than
/ n7 n6 \6 \: N5 mIU/mL (normal <5 mIU/mL). Serum follicular5 [4 {; l, z3 `/ S
stimulating hormone and leuteinizing hormone
  G2 {. U3 _% z, ]6 L, d# Kconcentrations were less than 0.05 mIU/mL
7 {5 a$ l% A1 A% A9 Z+ g, A0 I(prepubertal).
% Z0 _7 c8 a5 _# R# d1 L9 ZThe parents were notified about the laboratory6 E! X. a2 f/ z  j0 c, Z
results and were informed that all of the tests were
  F" b& ~0 c* inormal except the testosterone level was high. The
2 b' ]3 S! b# rfollow-up visit was arranged within a few weeks to
1 B2 |  T3 k( `& S4 `obtain testicular and abdominal sonograms; how-
9 e/ o8 r. Y, p; x1 p. _* p, F' I' Oever, the family did not return for 4 months.
' f& [' B" e0 p7 m: \' \Physical examination at this time revealed that the
4 y( m) K9 {5 y4 w8 ?- J1 Bchild had grown 2.5 cm in 4 months and had gained
8 Y7 `4 q+ v% z% ~4 f) A' e' K2 kg of weight. Physical examination remained
. Z: p6 m% Z+ punchanged. Surprisingly, the pubic hair almost com-
) q: \! c9 L( A0 P* v; Kpletely disappeared except for a few vellous hairs at
7 Q' C& P1 i% m4 U0 Z7 Lthe base of the phallus. Testicular volume was still 2% ^2 J$ U$ Y, a8 C8 M0 `. N
mL, and the size of the penis remained unchanged.
. S( f, g7 P" x9 _; MThe mother also said that the boy was no longer hav-" B2 P/ Z% P9 U9 t$ w# c
ing frequent erections.5 U6 N; ^8 [# N, L- S, ]* J) F* q/ K
Both parents were again questioned about use of
  @% d, b3 T8 f& B9 O3 h" nany ointment/creams that they may have applied to
+ c$ A: U' c. b1 q( nthe child’s skin. This time the father admitted the
& x. X# W$ {. Y2 U  NTopical Testosterone Exposure / Bhowmick et al 541
0 f# W; r5 N" N% j% t" F8 O0 V8 ruse of testosterone gel twice daily that he was apply-3 Y4 ]# b4 U2 b
ing over his own shoulders, chest, and back area for
! W2 V7 E+ D3 {# J  _a year. The father also revealed he was embarrassed
& q% v6 z2 L' ?& l% |to disclose that he was using a testosterone gel pre-
1 O/ B5 X# y, e: m# t2 \% }( _* Tscribed by his family physician for decreased libido* R) G5 d/ u# J* L8 W/ A
secondary to depression.
8 K1 I& ?+ r- @The child slept in the same bed with parents.8 J* A- ^/ h8 G+ L! x
The father would hug the baby and hold him on his( t5 e% Y1 i% E  d# c6 @2 J0 C8 F
chest for a considerable period of time, causing sig-) h* N/ `6 ~2 j" O  q
nificant bare skin contact between baby and father.: h% l( w; o& X1 \$ \+ P0 E) d
The father also admitted that after the phone call,% l; S* y- \: {
when he learned the testosterone level in the baby
; Q- v. s1 v' X# H3 {8 Kwas high, he then read the product information7 z9 `3 z" a: c5 [
packet and concluded that it was most likely the rea-
/ o, H# R/ \- ?: Z7 p2 Z1 Fson for the child’s virilization. At that time, they; @3 m8 z* N# W& A% }+ M' z; |8 F( J
decided to put the baby in a separate bed, and the2 ~# g# y+ c; F7 F  J+ M
father was not hugging him with bare skin and had
6 B7 d  X# t4 s5 l( c1 Z: c- nbeen using protective clothing. A repeat testosterone7 h7 {$ M+ z. i# _' w' T. z8 B1 S
test was ordered, but the family did not go to the" t0 z% p# W+ m1 h. h* X" {
laboratory to obtain the test.
7 C9 h1 C- t4 S: wDiscussion
+ X) L( J9 L! K# L2 ^, u. nPrecocious puberty in boys is defined as secondary# y* X  l  S' q5 I5 ^9 e+ V9 h
sexual development before 9 years of age.1,4
9 }! @% M  Z5 |8 l2 t" A& E9 j$ ]* jPrecocious puberty is termed as central (true) when
+ c: g7 X9 b' wit is caused by the premature activation of hypo-
" e3 ~4 P. a* |5 Z3 pthalamic pituitary gonadal axis. CPP is more com-
6 K, [7 r8 s5 @  ^mon in girls than in boys.1,3 Most boys with CPP# Z' y4 o/ i1 f7 u; }  p1 U
may have a central nervous system lesion that is+ r" o! k+ u8 C/ P. H) H$ c
responsible for the early activation of the hypothal-' s) `4 T0 I/ \9 @9 G
amic pituitary gonadal axis.1-3 Thus, greater empha-) f* k5 K+ S, c
sis has been given to neuroradiologic imaging in( @' r/ h5 e1 ^$ ^) k4 w5 c
boys with precocious puberty. In addition to viril-
% t. @: ?, o: vization, the clinical hallmark of CPP is the symmet-7 B; Y/ r) Z- w0 |9 Q
rical testicular growth secondary to stimulation by
2 P$ s. l7 @9 X. [# p8 tgonadotropins.1,34 v+ R, z5 J6 m) i' J
Gonadotropin-independent peripheral preco-4 E1 Q" E- O  i. `% x8 ^! s
cious puberty in boys also results from inappropriate
8 f" A9 F1 ]2 @- D* x2 j! ^androgenic stimulation from either endogenous or/ X% O' w0 M" |0 D1 o
exogenous sources, nonpituitary gonadotropin stim-$ Y$ w0 z! @. t
ulation, and rare activating mutations.3 Virilizing
( D0 V3 J3 k4 jcongenital adrenal hyperplasia producing excessive
* k; N% a: [* }+ A$ o# Tadrenal androgens is a common cause of precocious
6 b" Q; W0 G& B. O. wpuberty in boys.3,48 U0 @9 v0 _) P) F
The most common form of congenital adrenal
& H& n7 E1 @. o! chyperplasia is the 21-hydroxylase enzyme deficiency.) R* K' Q7 E1 Q3 {, _
The 11-β hydroxylase deficiency may also result in
2 ?  Z: z8 E* i0 J5 |/ N% C" V/ lexcessive adrenal androgen production, and rarely,
1 e( Y" O- T0 Y- han adrenal tumor may also cause adrenal androgen
% P5 y# M5 Z6 \2 Y2 y& K8 @0 Vexcess.1,3  U! F+ I4 X* z# v8 f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, j1 m- f  \  g. z0 J) y542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 F: G. i4 f9 c9 L$ ]$ I3 ]0 mA unique entity of male-limited gonadotropin-
& p* J) Q) t1 s# T8 mindependent precocious puberty, which is also known
( C* I; E" e8 R" f( W( ], }as testotoxicosis, may cause precocious puberty at a
# [! o! \+ }5 o4 O# Y8 Xvery young age. The physical findings in these boys
8 o, `4 @- \/ i1 J: |; _with this disorder are full pubertal development,
  ], [/ n. a9 Rincluding bilateral testicular growth, similar to boys
8 W5 Z; w# O! v" ]$ V' d& d8 wwith CPP. The gonadotropin levels in this disorder: {2 Y3 J- a# |4 L5 z0 @% M
are suppressed to prepubertal levels and do not show
! j/ @% ^2 R: H0 cpubertal response of gonadotropin after gonadotropin-+ C8 N& r9 Q* @4 o
releasing hormone stimulation. This is a sex-linked! x- |" O: J8 p( [: `
autosomal dominant disorder that affects only
) O+ @; o4 h8 s# o+ \2 H9 }% o2 g& y' cmales; therefore, other male members of the family3 X* z! ~& Z# C1 W! j6 I: @( N- y
may have similar precocious puberty.3
& Y0 Q) N: a2 u! [" a7 GIn our patient, physical examination was incon-
  m( L8 Z. A: K' `8 L3 Usistent with true precocious puberty since his testi-% e! S& O5 r4 g( \  `* R8 v! H& k# R
cles were prepubertal in size. However, testotoxicosis
* t5 z. J2 Q3 x) q2 `* f# U: @was in the differential diagnosis because his father9 S3 s; E! @; t5 u
started puberty somewhat early, and occasionally,* f5 M  s, U5 z) I4 R7 U$ Z& U+ Z
testicular enlargement is not that evident in the
5 W3 o$ Z5 k7 L$ Z/ C! obeginning of this process.1 In the absence of a neg-
2 {+ O3 O" t! b  U3 wative initial history of androgen exposure, our
' {$ {; d) S. [& g, z" P1 Tbiggest concern was virilizing adrenal hyperplasia,- v% r2 r. `- L# O: j
either 21-hydroxylase deficiency or 11-β hydroxylase$ }7 v  s* F% ~7 y, d+ q
deficiency. Those diagnoses were excluded by find-7 D) o$ R- O- {! v
ing the normal level of adrenal steroids.
! j3 t/ v6 z. j$ Q/ T5 X+ H( C4 J$ aThe diagnosis of exogenous androgens was strongly: o0 u- s, K2 \9 ?% Y, j. ?
suspected in a follow-up visit after 4 months because* i* ~  D5 p( u# n: L7 U7 C
the physical examination revealed the complete disap-7 v- t  v" ]2 R" P1 x# P
pearance of pubic hair, normal growth velocity, and0 A! C; S0 n! T8 P3 q
decreased erections. The father admitted using a testos-7 q) T# @/ K+ ~$ ~
terone gel, which he concealed at first visit. He was
$ W7 }# ]% ]7 [# x3 O# husing it rather frequently, twice a day. The Physicians’7 l- l# K$ P# U- w( Q
Desk Reference, or package insert of this product, gel or! P, j% d- E' m! ^6 F2 y
cream, cautions about dermal testosterone transfer to
0 P' u4 {1 [# }4 junprotected females through direct skin exposure.
& P! @1 B+ }5 c' cSerum testosterone level was found to be 2 times the
& z( O* P- y% Y1 }9 G! G6 |3 Dbaseline value in those females who were exposed to, b) r! G; [" M
even 15 minutes of direct skin contact with their male' J3 L/ H  _. W% p
partners.6 However, when a shirt covered the applica-
' i5 t( e9 e# C3 _9 v2 p2 `5 Jtion site, this testosterone transfer was prevented.) P6 N% ^9 E( A! M$ F( R2 v! p7 G
Our patient’s testosterone level was 60 ng/mL,/ R5 ~; x& c2 x3 [
which was clearly high. Some studies suggest that
% ^3 |9 o) m) R" Ydermal conversion of testosterone to dihydrotestos-& X5 d$ W* n- q2 V0 f. S& F- f
terone, which is a more potent metabolite, is more8 c# _, o0 {* M, ~9 w% V4 H
active in young children exposed to testosterone
* u7 _2 m% y1 _; k- Uexogenously7; however, we did not measure a dihy-8 ^* _' z) p+ i' x  q
drotestosterone level in our patient. In addition to
( U  c8 o2 ], w; T5 R2 N9 Yvirilization, exposure to exogenous testosterone in1 p; w% f/ k: d0 Y7 S
children results in an increase in growth velocity and$ T8 ~# S- Y: u4 \) V
advanced bone age, as seen in our patient.
  y# W' h$ Y1 _+ KThe long-term effect of androgen exposure during+ D, T: v/ X0 L8 i' Y; K+ U# s6 p
early childhood on pubertal development and final
/ Y' L  _% W8 Z! p5 V. Fadult height are not fully known and always remain& `; t4 d% W% o- M7 D( z- d9 J
a concern. Children treated with short-term testos-
( S: N" T6 G" n) P5 ^# h" d0 @terone injection or topical androgen may exhibit some
3 f& V: R8 ^" c, z1 d, ?acceleration of the skeletal maturation; however, after
; w* }* @& ]/ b6 Y5 L) z( Ycessation of treatment, the rate of bone maturation* l$ B7 U9 f  c$ n
decelerates and gradually returns to normal.8,9
3 q9 q5 u6 Y( ]: zThere are conflicting reports and controversy3 v/ A. S- M5 ]% w! m( l% v
over the effect of early androgen exposure on adult. m5 O# x& c  H& i+ ~% E
penile length.10,11 Some reports suggest subnormal& m1 Y8 k" ~5 n5 Q6 X! f4 r
adult penile length, apparently because of downreg-
" e$ j) t2 e" g) I3 I2 Zulation of androgen receptor number.10,12 However,* x  C% Z$ S3 J3 W
Sutherland et al13 did not find a correlation between  [) }2 ~- u( }9 G  j7 Z
childhood testosterone exposure and reduced adult1 J4 j9 k# W( P9 Z5 Z
penile length in clinical studies.
. i4 l' }% B9 RNonetheless, we do not believe our patient is& c/ L$ n; o3 L. s0 M% n& ?8 y) e
going to experience any of the untoward effects from
( l$ G3 K' ?4 E! {% Q/ O/ Stestosterone exposure as mentioned earlier because% z+ M, W. M2 Q- h( a( z
the exposure was not for a prolonged period of time.- |7 A3 }& ~( ^- S5 w: `
Although the bone age was advanced at the time of
! g; s6 P. |5 S! f, tdiagnosis, the child had a normal growth velocity at+ [- _5 p; N# r# P6 T5 }
the follow-up visit. It is hoped that his final adult
$ G/ x# q& R6 x2 J: E  }, }5 wheight will not be affected.
; B/ A# E2 d1 X  _; LAlthough rarely reported, the widespread avail-
% P& {  k8 _. O% `ability of androgen products in our society may
3 G  W" f' V9 l; v9 e5 H7 windeed cause more virilization in male or female* o. `- y: O1 B6 b7 e7 \
children than one would realize. Exposure to andro-1 L2 f7 T  @% q
gen products must be considered and specific ques-
/ a4 u& _2 Q& p3 `( Q8 P/ r/ Jtioning about the use of a testosterone product or
& I3 J! I' }$ n3 |% Qgel should be asked of the family members during  b/ x( w, O1 ?% S+ O2 [- N5 [
the evaluation of any children who present with vir-8 x( |# v$ k. c9 O7 F
ilization or peripheral precocious puberty. The diag-
* d( p* T: z' ?+ [nosis can be established by just a few tests and by
$ ]8 ^6 Y& J2 |3 c: C( y8 C4 oappropriate history. The inability to obtain such a5 W# _% s$ x. }# u
history, or failure to ask the specific questions, may
% I( t( a/ s0 Y/ V9 y+ }3 Yresult in extensive, unnecessary, and expensive
) b. k- w$ }' A! i- A6 d" ?investigation. The primary care physician should be
" E. x" x( q2 o4 G; [" Q. ^aware of this fact, because most of these children
( r4 y0 t, r* J( g; O% F! g6 nmay initially present in their practice. The Physicians’4 i& \% U; i3 m; e
Desk Reference and package insert should also put a
) i9 P4 S( G4 t" x% B# cwarning about the virilizing effect on a male or! i, T" \7 q6 ^! N/ w# G
female child who might come in contact with some-8 t7 r. F) w6 |1 l9 X! @: C
one using any of these products.
, _9 i0 _4 M8 I" N. yReferences
: y. z2 x) c; e1. Styne DM. The testes: disorder of sexual differentiation& t0 L+ H, _3 B9 Z/ P9 r) Q% h
and puberty in the male. In: Sperling MA, ed. Pediatric
1 {0 |6 m; S- G! V  k9 S4 t' M* oEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: |  T# `" M( S" @9 A
2002: 565-628.
- h! j' c9 r8 z3 ^$ ^2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious/ m* R. Q/ J' T, Y; C
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
3 m3 G; A% c+ ?8 W- S4 E9 kBoy Induced by Indirect Topical# ^+ v+ b, W( [* e0 k
Exposure to Testosterone1 T9 q1 n6 s3 V5 ^& f
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- Z9 i6 \  n5 u
and Kenneth R. Rettig, MD1
2 V  y, E# B  {Clinical Pediatrics
: S4 q, Z; L5 ^( a7 H3 jVolume 46 Number 6
, {4 @& p" {3 H2 l4 fJuly 2007 540-543
: \& E! o/ C9 k1 x* J: n© 2007 Sage Publications
; n3 y) b" g0 W7 Q10.1177/0009922806296651* A& `/ S8 N- {& h: Q
http://clp.sagepub.com
5 L. K  l7 H: d) [hosted at
8 J! a8 w) ~- I& m) p  z3 Y4 Uhttp://online.sagepub.com" N7 H/ k4 W; F$ b
Precocious puberty in boys, central or peripheral,# V6 P* v/ h5 ?7 |9 l0 @
is a significant concern for physicians. Central) i# o$ p8 S0 S
precocious puberty (CPP), which is mediated! f) \; U- e4 u: E. O
through the hypothalamic pituitary gonadal axis, has
% p0 F+ V/ `4 M5 ^* `# Wa higher incidence of organic central nervous system5 M# _: P8 P& u; h# ~7 O2 i
lesions in boys.1,2 Virilization in boys, as manifested, M7 K: S# A: D- i, t# C
by enlargement of the penis, development of pubic' f/ `& l9 A7 F/ u5 j
hair, and facial acne without enlargement of testi-/ X0 b/ v6 B6 H, F& @
cles, suggests peripheral or pseudopuberty.1-3 We
# y" e* k: z' H1 \# T* j' g  N7 f9 E$ Ureport a 16-month-old boy who presented with the
# d8 K! P: K) g! u5 j1 xenlargement of the phallus and pubic hair develop-) X& t) g- j' y" s0 B
ment without testicular enlargement, which was due& Y& u! W% g, z7 D6 h9 A
to the unintentional exposure to androgen gel used by
8 r% v8 A) F; {8 r" Z4 mthe father. The family initially concealed this infor-
% m$ p3 P% q  b5 Kmation, resulting in an extensive work-up for this
4 d4 Z4 P+ n, n9 D: A" O& kchild. Given the widespread and easy availability of
/ r) E3 n! p( X% ], Qtestosterone gel and cream, we believe this is proba-
$ \, r4 P( A, ]+ pbly more common than the rare case report in the8 a7 Z; H2 H1 q' O
literature.4! S, Q* b6 z2 p
Patient Report0 B1 q; i) L! p: k+ s
A 16-month-old white child was referred to the( h4 {1 N* T% l, |  A, |
endocrine clinic by his pediatrician with the concern
* R% R! X5 \8 a/ Q+ z8 ^$ Iof early sexual development. His mother noticed) |; B3 Y1 q# w- i0 ~3 W& t/ K
light colored pubic hair development when he was
# ?- G( @% _# uFrom the 1Division of Pediatric Endocrinology, 2University of; N0 H) }1 K2 J! N) g
South Alabama Medical Center, Mobile, Alabama.
  T! z7 {* {7 |Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 w& K3 _" Z* C, {3 SProfessor of Pediatrics, University of South Alabama, College of
( U8 U; S# P7 n4 S4 _Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! p, w* a! W% T
e-mail: [email protected]." ^+ ]/ |+ U5 S, G; S9 R8 H: F5 g
about 6 to 7 months old, which progressively became) q, T9 p( c, V, i0 N) }, D7 B
darker. She was also concerned about the enlarge-% `# O, |- ?2 c/ G/ }5 u: l$ k: K
ment of his penis and frequent erections. The child4 E) w/ X+ Y: {& Z- v/ Z9 W
was the product of a full-term normal delivery, with% b/ h' O$ V0 C9 V5 @& o' A
a birth weight of 7 lb 14 oz, and birth length of
: @7 x/ m7 p  c# \3 k20 inches. He was breast-fed throughout the first year2 v0 Q$ W+ D9 \) l
of life and was still receiving breast milk along with- S$ x' c* ?2 d% {
solid food. He had no hospitalizations or surgery,9 C# Y; \$ F* U5 h4 R, |3 m
and his psychosocial and psychomotor development
/ V. L# c, u  Q* w0 W/ P3 R+ iwas age appropriate.: l' _7 e: a( \4 N# |" T6 a
The family history was remarkable for the father,+ u" S- c  K  q! ^9 Y/ ]
who was diagnosed with hypothyroidism at age 16,0 c3 Y% _# t2 X# @+ X1 _( t
which was treated with thyroxine. The father’s9 b4 L2 N8 s) A; E
height was 6 feet, and he went through a somewhat
: `  {$ w6 S; o5 ^early puberty and had stopped growing by age 14.; ]% g$ C1 G! W# g1 r+ n% _" r
The father denied taking any other medication. The
4 k! u+ @5 U  v3 a9 K7 i. _5 ?child’s mother was in good health. Her menarche
  m1 W4 m; ]  _- Zwas at 11 years of age, and her height was at 5 feet+ u! C# z) }7 O; h0 m7 Z
5 inches. There was no other family history of pre-
1 i8 U- C8 D$ u- @& Z# b9 O* U% Zcocious sexual development in the first-degree rela-
. P+ J: x% X5 _/ u, ktives. There were no siblings.( {3 v9 w: U: ~. [; `7 t; _
Physical Examination$ h' Y. F$ R# g" O
The physical examination revealed a very active,6 s  S# A* K2 r3 ^
playful, and healthy boy. The vital signs documented
" o) P" t4 g3 _/ J& Fa blood pressure of 85/50 mm Hg, his length was
" D! |- W) ?+ O/ I4 Z' p* g5 @90 cm (>97th percentile), and his weight was 14.4 kg
7 T) w4 q: Z/ e' e6 G5 R" @(also >97th percentile). The observed yearly growth
# Z6 O' I( @- v4 m; Z( [velocity was 30 cm (12 inches). The examination of
/ X0 Z# T5 r5 f" A1 d- s! Q% j2 `the neck revealed no thyroid enlargement.
) K# X, A9 f2 s8 U/ a" P# g0 \, T/ M2 mThe genitourinary examination was remarkable for3 e! R8 i2 P- p* @5 x
enlargement of the penis, with a stretched length of1 R6 S5 f3 C& @7 i! ^
8 cm and a width of 2 cm. The glans penis was very well- t/ i+ a+ ~! d3 u& y1 _4 W
developed. The pubic hair was Tanner II, mostly around* n2 z; U, V0 q0 t& U
540
+ p( l4 I: o5 U3 Z9 T' K- `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ ]& N; E; @: A7 ?+ C, @
the base of the phallus and was dark and curled. The: d' Y% s6 @/ q3 U* Q. e
testicular volume was prepubertal at 2 mL each.
0 L% P& m- L3 i" F# c3 m( ZThe skin was moist and smooth and somewhat
0 F4 n1 I: C" \0 H7 S, D2 Poily. No axillary hair was noted. There were no+ o, Y1 J1 t. R7 d$ `, W
abnormal skin pigmentations or café-au-lait spots.
5 r% F; }5 C+ Z+ x4 H8 CNeurologic evaluation showed deep tendon reflex 2+# i* O3 Z! {9 y$ Y" b. A4 Q
bilateral and symmetrical. There was no suggestion
( r# I8 D! U: V" ]/ `/ n5 Fof papilledema.
2 ?5 [. a' t4 w; U% @' [8 y7 d! zLaboratory Evaluation" R+ v* O( q; }5 G1 M
The bone age was consistent with 28 months by. x, r3 S  Z/ o) r( L  U- a
using the standard of Greulich and Pyle at a chrono-0 _) \% \2 I# {. Z( E
logic age of 16 months (advanced).5 Chromosomal
+ q  b# U  M+ ]8 _0 o0 u9 h$ w5 G' Ykaryotype was 46XY. The thyroid function test7 Y% ?/ m0 v- J( e4 o$ A
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ \/ r& Y: Z/ y( plating hormone level was 1.3 µIU/mL (both normal).0 [3 R' U  v1 H/ g7 [# q" j+ }
The concentrations of serum electrolytes, blood' ^6 I6 d4 _5 C/ G0 ~* W0 Z1 Y# W
urea nitrogen, creatinine, and calcium all were
8 H5 _4 b; `$ \  k. _+ x6 K8 K. Dwithin normal range for his age. The concentration7 E2 v; `5 d- y4 m/ X! C
of serum 17-hydroxyprogesterone was 16 ng/dL
6 c. ]  B: a2 s  O(normal, 3 to 90 ng/dL), androstenedione was 205 _# R7 Y, Q( p4 Y" ~
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 ]. V% J/ p8 H
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
& ]3 c' d% `6 v+ p. ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
3 j0 c+ B1 k4 ^: K. B49ng/dL), 11-desoxycortisol (specific compound S)) F+ w; p0 b" B
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 w+ h; e; A$ L1 n9 s; Ntisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 f  `, y" r. E8 R! t, dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! k8 W6 I. V2 f0 @3 _and β-human chorionic gonadotropin was less than5 l) T; h  i3 N# d( `. F" y) B
5 mIU/mL (normal <5 mIU/mL). Serum follicular
# V% i+ A3 a" h0 o$ d% `6 mstimulating hormone and leuteinizing hormone% ?& n1 w5 \  p6 q
concentrations were less than 0.05 mIU/mL' ]5 U0 B( }. v2 @& X" A
(prepubertal)." W" Z0 ^$ ]! D% U: s" z# J; ~
The parents were notified about the laboratory
  V+ _4 J1 m8 X1 uresults and were informed that all of the tests were, T1 g. Q8 g# q1 i4 _" ?1 S
normal except the testosterone level was high. The, q' j& W6 |) P, _% u% T$ g* c
follow-up visit was arranged within a few weeks to4 {. \1 p0 m/ x" w
obtain testicular and abdominal sonograms; how-
$ e1 n( F( o: I( z9 }3 iever, the family did not return for 4 months.% I0 R8 i% z$ T
Physical examination at this time revealed that the% i) H4 P8 `+ T; U$ J
child had grown 2.5 cm in 4 months and had gained  g  X. u, E$ O! z# f
2 kg of weight. Physical examination remained
6 W. G" ?2 D3 r" N" F" T% F5 u5 dunchanged. Surprisingly, the pubic hair almost com-% ~" V- F1 ~9 t$ |
pletely disappeared except for a few vellous hairs at
; @( @# `9 C; d+ M$ R" ethe base of the phallus. Testicular volume was still 2
; \) @$ ]% q* Q. w* E  [: j" hmL, and the size of the penis remained unchanged.0 F1 H$ \* T" \, d* a
The mother also said that the boy was no longer hav-& u# S) a" i) q: q. T
ing frequent erections.1 i; a) E) e! a8 \- k7 l3 H5 |8 {: \
Both parents were again questioned about use of7 n) i9 o' Y6 E) x; H4 z' h# d
any ointment/creams that they may have applied to6 r8 |' w: v( W+ b& D
the child’s skin. This time the father admitted the
2 D: o& R4 P% F! D4 R1 ?2 y% |Topical Testosterone Exposure / Bhowmick et al 541
2 y' m' U+ T# ause of testosterone gel twice daily that he was apply-
' m; b0 m! A5 Zing over his own shoulders, chest, and back area for
5 i: E0 g+ ?8 h5 wa year. The father also revealed he was embarrassed( I8 W- u* e; F; D. g5 l, q8 l! S
to disclose that he was using a testosterone gel pre-
* K7 r# R! F. ?2 r' O% n4 Y# [scribed by his family physician for decreased libido' L+ X  h4 n+ B& U; @/ l0 [* M0 X
secondary to depression.
9 [, y  q6 n. ?) d% V/ t+ Z% JThe child slept in the same bed with parents.$ X& ]; \8 o5 C$ y$ N# [
The father would hug the baby and hold him on his
0 {' b) t: h2 d7 G3 ichest for a considerable period of time, causing sig-$ i, i6 x0 ^4 w# H
nificant bare skin contact between baby and father./ ~% o) A8 p: U; x  k6 ^
The father also admitted that after the phone call,
( [. G0 S2 w+ |5 |5 h. Y9 O4 jwhen he learned the testosterone level in the baby
1 w7 p. B# M$ l* lwas high, he then read the product information9 p1 l# @' w# Q: U/ i, w
packet and concluded that it was most likely the rea-! x3 B' I$ ~, Q7 |2 Z
son for the child’s virilization. At that time, they! ~: ^. h1 ^, K- G& U
decided to put the baby in a separate bed, and the
8 q/ m3 b+ k9 a, L, F& Kfather was not hugging him with bare skin and had
2 A, ^' q0 G; ^been using protective clothing. A repeat testosterone
) w0 x! `% }, u0 @test was ordered, but the family did not go to the$ i, ~/ G% o: g4 B* p" M
laboratory to obtain the test.
4 y( m, |: w; a3 G: T1 aDiscussion0 D6 E, A4 ^. j. o5 L2 V
Precocious puberty in boys is defined as secondary
  [2 O! r" g5 z+ O( k# xsexual development before 9 years of age.1,4
2 Q  h3 p8 w8 g' s) M; @$ BPrecocious puberty is termed as central (true) when9 {1 H' z$ }% K& n. _
it is caused by the premature activation of hypo-
. V* v3 }: S1 ?+ d4 |/ ?2 e7 C9 Sthalamic pituitary gonadal axis. CPP is more com-2 R' u& W6 N( R! a* F. H
mon in girls than in boys.1,3 Most boys with CPP2 H  o0 d8 Z  G- T& A! h9 O2 H
may have a central nervous system lesion that is# S+ w8 }1 `+ e- I
responsible for the early activation of the hypothal-" l% h0 h" S, G( ~1 u" v
amic pituitary gonadal axis.1-3 Thus, greater empha-
- n2 l/ y4 ]# m3 e  esis has been given to neuroradiologic imaging in
. P) J9 N8 Q5 L/ kboys with precocious puberty. In addition to viril-
7 ^9 M* b; B0 `# cization, the clinical hallmark of CPP is the symmet-3 `: f6 K0 Q) X0 e$ y
rical testicular growth secondary to stimulation by
5 m! l- }. z" |) ~; N. V; I9 ogonadotropins.1,3. P1 y5 ]' J1 s
Gonadotropin-independent peripheral preco-
- o/ V0 N+ h" w. N' Vcious puberty in boys also results from inappropriate
0 _" A, ^5 ]5 f) X) v5 Landrogenic stimulation from either endogenous or* h# a7 q" o' m2 B6 I$ N
exogenous sources, nonpituitary gonadotropin stim-, ?4 L% o! K/ M* F0 b# D5 I
ulation, and rare activating mutations.3 Virilizing
# Z/ R+ i/ i% |5 [( s. ]congenital adrenal hyperplasia producing excessive
% K& s& N; Q0 H7 z# Kadrenal androgens is a common cause of precocious7 C% l" C  k6 C7 h. I9 Z
puberty in boys.3,4
9 ]( V5 t1 T" b+ UThe most common form of congenital adrenal, Q' k/ X( t1 x' |# ^" s1 l
hyperplasia is the 21-hydroxylase enzyme deficiency.
* Y; W, O4 y% [, |# ]& O# m3 q9 FThe 11-β hydroxylase deficiency may also result in
0 I* e  ^/ H5 q& T; nexcessive adrenal androgen production, and rarely,
9 O( Q: X! P% @  l3 san adrenal tumor may also cause adrenal androgen
4 x4 z% [) x0 [- D2 G# z# hexcess.1,37 o% z& `- S3 c' e6 D7 r8 |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( m4 M+ F" Q* \$ v: E
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) }% l0 ^' s& \% @  q( h$ UA unique entity of male-limited gonadotropin-
/ J# u/ M: Y, o( l0 b+ Sindependent precocious puberty, which is also known/ k* d2 f0 J+ e& V' p9 v% `: {
as testotoxicosis, may cause precocious puberty at a
7 w: n9 u1 B  @6 Avery young age. The physical findings in these boys$ h7 A. L# w* f3 X( ?- r7 Z
with this disorder are full pubertal development,; d& S( V( q2 v' |: w
including bilateral testicular growth, similar to boys
7 Y! o. ~8 c' F) w2 B/ [! mwith CPP. The gonadotropin levels in this disorder" H. k" O0 z' C5 x4 l) U) Y' _+ ^) ?4 U: `
are suppressed to prepubertal levels and do not show" _: m) f: n' h% `' E9 t( C/ u
pubertal response of gonadotropin after gonadotropin-
5 N( D7 c. i8 F2 Zreleasing hormone stimulation. This is a sex-linked
2 B1 k, y1 F4 P% u/ |autosomal dominant disorder that affects only
/ m2 [! K/ Y/ u8 S* E0 |8 X/ Emales; therefore, other male members of the family) ~  c, f8 |! B: p2 R! g
may have similar precocious puberty.3! G3 ^; w2 b0 H
In our patient, physical examination was incon-
- C0 s" B/ }& s( E& Ssistent with true precocious puberty since his testi-
( ^, {4 Z8 d; H: vcles were prepubertal in size. However, testotoxicosis
7 m5 t+ _% N  c; R8 i9 I# @was in the differential diagnosis because his father
6 Y9 S! j* }+ n* n  j# P: O, Ustarted puberty somewhat early, and occasionally,% O  w5 e8 @* l
testicular enlargement is not that evident in the
. [! U0 v, W7 E& {3 f" fbeginning of this process.1 In the absence of a neg-
: C+ K+ B/ W% @0 f. rative initial history of androgen exposure, our5 N2 c+ s8 ?+ d4 }  Z0 d0 v% W
biggest concern was virilizing adrenal hyperplasia,! \' e, O" k, p& }1 x/ j
either 21-hydroxylase deficiency or 11-β hydroxylase
8 q' U- {! f+ M$ zdeficiency. Those diagnoses were excluded by find-( q$ t4 e. ~7 Y# o3 c
ing the normal level of adrenal steroids.4 Q. @0 V7 D% \% b
The diagnosis of exogenous androgens was strongly
9 o, t: F2 t% u. K' S6 ~% Ysuspected in a follow-up visit after 4 months because
' n2 p2 \; p% e; h7 }the physical examination revealed the complete disap-4 u1 D/ q/ W) [6 _9 \0 W& c
pearance of pubic hair, normal growth velocity, and- Y0 R* y) s& w  d% s" a- g0 G2 l
decreased erections. The father admitted using a testos-% t0 O. X1 }4 s( _3 D5 z
terone gel, which he concealed at first visit. He was4 J# c9 u0 B. C- n* p6 A% P/ E# A( j
using it rather frequently, twice a day. The Physicians’
. f% s( U  _+ s" T" }! f4 }: dDesk Reference, or package insert of this product, gel or! b7 S5 c& D) x% @
cream, cautions about dermal testosterone transfer to: m! ]- q. X, t# X
unprotected females through direct skin exposure.
) `( b0 w: L. f6 ZSerum testosterone level was found to be 2 times the3 d* q. {' g) M0 [2 S
baseline value in those females who were exposed to8 L) P5 H0 k( e: y
even 15 minutes of direct skin contact with their male
+ B" ]0 m4 q+ `4 ~9 {partners.6 However, when a shirt covered the applica-
) ^5 K9 w5 P- z1 z4 q( K; ttion site, this testosterone transfer was prevented.7 l* u3 @) y8 j: n1 a2 T
Our patient’s testosterone level was 60 ng/mL,) @' q3 D1 j1 \- N$ T7 E
which was clearly high. Some studies suggest that1 V7 [, k9 n2 [. i( y2 d
dermal conversion of testosterone to dihydrotestos-, d; V3 z0 B: ^5 Q
terone, which is a more potent metabolite, is more2 _8 k, V0 `# u9 t, }8 n
active in young children exposed to testosterone
8 D: J, G. D8 t  {exogenously7; however, we did not measure a dihy-( B* _* _" N  f4 h( F1 d1 z! l4 \
drotestosterone level in our patient. In addition to- `+ U2 [/ k; n! r2 E* W
virilization, exposure to exogenous testosterone in
4 `& z) j9 E& w" \+ xchildren results in an increase in growth velocity and
  S/ X/ b/ B  t0 _* e0 d% Madvanced bone age, as seen in our patient.
( Z. U1 C% M. {& X  bThe long-term effect of androgen exposure during0 n2 x2 G8 N( O7 c) i& |0 H
early childhood on pubertal development and final% \$ M* D1 B- L: Y( A2 C
adult height are not fully known and always remain
$ w3 K& x/ b5 l0 E+ Ca concern. Children treated with short-term testos-
! b9 ~! J6 w( P: J0 p1 nterone injection or topical androgen may exhibit some
1 \+ d" C' k. g+ oacceleration of the skeletal maturation; however, after
& Y" C9 t. ?: S8 Y0 O( J9 Bcessation of treatment, the rate of bone maturation
* M2 L: |8 L% E. u& v2 d9 _decelerates and gradually returns to normal.8,95 c+ I) W# g/ H) n0 l
There are conflicting reports and controversy2 W, U+ s) P4 ^
over the effect of early androgen exposure on adult, x5 D# a  J7 R+ @0 @; ^& X
penile length.10,11 Some reports suggest subnormal' y/ \0 z4 b. q( p
adult penile length, apparently because of downreg-# B2 h! W1 C5 ^# P4 W7 i1 q
ulation of androgen receptor number.10,12 However,
: S. ?5 `- c5 b5 ~* [8 tSutherland et al13 did not find a correlation between
% i- s# n( i$ K+ z9 s: @childhood testosterone exposure and reduced adult% ^3 p  b; z1 E: m2 |
penile length in clinical studies.8 a5 f9 P4 Q( b+ @
Nonetheless, we do not believe our patient is4 q5 ~# K, u/ \
going to experience any of the untoward effects from2 U. n3 @# K, {/ {" v; ~& {$ b
testosterone exposure as mentioned earlier because% b) \. t3 l2 g) m& h  G$ s* B
the exposure was not for a prolonged period of time.
( T5 p! f9 y" ^Although the bone age was advanced at the time of
) d# b8 C3 a/ O1 U' Y1 H+ U& I  v) Cdiagnosis, the child had a normal growth velocity at
. E+ Z/ i8 Q, l& j+ ]5 x& |the follow-up visit. It is hoped that his final adult
" Z6 A& C* _  q1 Dheight will not be affected.
% _5 m" U; Q4 h; d) J. sAlthough rarely reported, the widespread avail-
  N4 @% l( X! s* B; K4 wability of androgen products in our society may0 a; l. |# l5 F, }- B
indeed cause more virilization in male or female$ K+ _. v4 O- O/ H. J
children than one would realize. Exposure to andro-
7 U2 ^0 W$ g8 V) R9 ~3 G6 Vgen products must be considered and specific ques-# T4 U1 v$ A6 y) W; p8 [. ~6 G0 T
tioning about the use of a testosterone product or
, a$ C" I& _' X* e/ W; F3 Egel should be asked of the family members during4 }# e* k, J+ Y" m& V1 ]# `1 g2 J
the evaluation of any children who present with vir-. M. N0 p& S( M" ?# ~
ilization or peripheral precocious puberty. The diag-: M7 B- }8 u6 O0 K
nosis can be established by just a few tests and by
7 B/ m. s% }+ i1 `" o) f# Z: s* Iappropriate history. The inability to obtain such a3 |  j( E4 z1 o) c8 ?" K
history, or failure to ask the specific questions, may% a3 R4 i/ V1 a2 W
result in extensive, unnecessary, and expensive
5 y0 c( D/ y7 ginvestigation. The primary care physician should be
  V+ U, N+ c" Naware of this fact, because most of these children- E2 H" W& }2 z4 w) \. x: F! W
may initially present in their practice. The Physicians’
6 L" N) {8 L0 y1 f5 s4 O' vDesk Reference and package insert should also put a  C+ I/ ]5 K  t$ Z  X: l$ G! m
warning about the virilizing effect on a male or
" Y$ s/ P- z4 b' J7 Mfemale child who might come in contact with some-- K3 z( ?% h  E  q5 E+ V
one using any of these products.
2 [7 A0 Q  ~9 j) N0 I/ iReferences' V- [6 K# l4 V4 A
1. Styne DM. The testes: disorder of sexual differentiation
" y( ?6 L; Q2 b6 E! K6 eand puberty in the male. In: Sperling MA, ed. Pediatric" x9 B) F3 |2 J! {( x: p* e
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 N7 L5 X! z! G  E) Z9 B* b  O  `2002: 565-628.
7 j  p! Z3 d* d  E/ K& X2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
0 Q4 [, h6 h  ^puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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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

4 c% Y3 Z& c7 ~) e5 I* w1 }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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