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Sexual Precocity in a 16-Month-Old8 d8 f% M5 z2 T, C/ D. f
Boy Induced by Indirect Topical
: Y9 r9 S. N% D7 R9 ~3 s- vExposure to Testosterone
9 E1 R& e4 n9 U* a2 BSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( w7 w' W2 \/ n" nand Kenneth R. Rettig, MD1- h$ k% x0 G/ m- ~+ S. a5 G2 j9 @
Clinical Pediatrics; h  B( Y& T9 r5 ]1 K7 e
Volume 46 Number 6
( Z5 w7 e5 {9 j2 A/ u. `July 2007 540-543
. G4 E$ ?" a1 F, ~# d© 2007 Sage Publications* v5 m9 N& O  n
10.1177/0009922806296651
& q: f9 _3 T+ s3 X: Uhttp://clp.sagepub.com
. z9 ?! ~6 @1 E- n* Chosted at$ C; c- ^8 P" _
http://online.sagepub.com* V( @7 w1 x( l, W  Y9 P6 Z* d
Precocious puberty in boys, central or peripheral,
! a# F7 U: T' h6 Bis a significant concern for physicians. Central
+ j5 u0 G- J; h# F5 b1 d0 tprecocious puberty (CPP), which is mediated
' Q) r$ O' `( M% ]through the hypothalamic pituitary gonadal axis, has
& V) C/ ]! T2 e% x% h$ D) aa higher incidence of organic central nervous system
' w- d! \8 l4 B& Z) K# R5 V3 i, clesions in boys.1,2 Virilization in boys, as manifested
$ I: c5 Y2 w$ I1 h7 z' S( a. }6 |  {: Mby enlargement of the penis, development of pubic3 d- r2 V: v; z& V! m2 z8 _. E
hair, and facial acne without enlargement of testi-' Y4 B. b" Y' J, f- @
cles, suggests peripheral or pseudopuberty.1-3 We
. X, _: d( Z  [2 U0 ?- ]1 s( areport a 16-month-old boy who presented with the
+ g1 \# o( `: |6 `, ^enlargement of the phallus and pubic hair develop-
8 E0 u" L4 U) g: N: W! cment without testicular enlargement, which was due
4 U1 J& A9 }5 V  O9 y) nto the unintentional exposure to androgen gel used by
# h4 o& |+ Y+ i# y% D6 p* Bthe father. The family initially concealed this infor-6 D; K0 T  D1 O, @' e. U
mation, resulting in an extensive work-up for this
( L; Q7 D0 k# T" J, @. @child. Given the widespread and easy availability of; e! h0 s0 w. }# U: K- R- g, a3 t
testosterone gel and cream, we believe this is proba-7 v" ^8 O+ }; y8 f, O0 `
bly more common than the rare case report in the
8 V% s2 U5 b! M/ g% [( \literature.4
+ Y* ^4 ]( s& [$ cPatient Report$ J8 _, u! Z% L* u9 N9 f
A 16-month-old white child was referred to the& n, k: X) {$ q6 X. j& P
endocrine clinic by his pediatrician with the concern
! p8 V4 y& D3 j3 v3 G" sof early sexual development. His mother noticed7 O/ \' y" W4 `3 c! j
light colored pubic hair development when he was1 |6 {- {; y8 c9 y% r6 H" [
From the 1Division of Pediatric Endocrinology, 2University of) ], X4 K: F6 A3 U# w$ j
South Alabama Medical Center, Mobile, Alabama.
2 K& @, U% X% B# `1 `% m) z* oAddress correspondence to: Samar K. Bhowmick, MD, FACE,
0 p4 K+ g: B0 b# n" R, `" f; WProfessor of Pediatrics, University of South Alabama, College of; l. ]6 e+ ?. l# {3 o3 Z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;  G+ U; Q+ Y/ O2 C2 c6 V: I9 R- x5 M
e-mail: [email protected].
# P: T5 U7 _1 ~5 E# babout 6 to 7 months old, which progressively became( Z5 P* E  p2 d
darker. She was also concerned about the enlarge-' u; z9 w) e* J1 U' u# Q
ment of his penis and frequent erections. The child
+ W9 j2 ~- v. |8 Jwas the product of a full-term normal delivery, with0 M" \" B$ o& O/ {
a birth weight of 7 lb 14 oz, and birth length of: b4 b6 A% i- ~& @# u+ ]+ q
20 inches. He was breast-fed throughout the first year
4 x5 n$ ~* D" J" d) U0 ^% ~of life and was still receiving breast milk along with' @  `4 b3 b, B5 P
solid food. He had no hospitalizations or surgery,
4 q9 I. G4 x0 H( ^/ l% p3 `( kand his psychosocial and psychomotor development) y- a3 h( x) A" i6 J
was age appropriate.
4 l5 f6 J# T9 l! CThe family history was remarkable for the father,
3 ]" i/ u2 o# P" s8 E# X0 s  U4 Nwho was diagnosed with hypothyroidism at age 16,2 V2 z2 e) _$ Z% x9 |" R0 I
which was treated with thyroxine. The father’s
, {$ C$ ~5 T0 d( X# t+ Pheight was 6 feet, and he went through a somewhat5 J' p( b- Q; k/ K. C/ P$ L* {0 N
early puberty and had stopped growing by age 14.
/ E/ |' |/ E5 M! Y) wThe father denied taking any other medication. The
1 |9 ]$ z9 z" ^& O+ Dchild’s mother was in good health. Her menarche1 M1 H' |! G  a3 A9 b
was at 11 years of age, and her height was at 5 feet
! J) L* V: `0 A! F* w5 inches. There was no other family history of pre-
8 ~3 C$ U. b# Hcocious sexual development in the first-degree rela-
! G& _" i6 Z: e) F6 Ztives. There were no siblings.
8 B# [; m$ B1 V4 y5 T0 fPhysical Examination/ q2 J( z$ g6 a. f
The physical examination revealed a very active,
; J1 H: g6 \2 F! _playful, and healthy boy. The vital signs documented2 `1 B& W- A! O# V4 y
a blood pressure of 85/50 mm Hg, his length was
1 h/ s, Y: X* n# L90 cm (>97th percentile), and his weight was 14.4 kg
& g+ d/ {# K7 b: D, m% k# j(also >97th percentile). The observed yearly growth8 a0 |& O% @5 b/ e  ~1 d2 C6 F
velocity was 30 cm (12 inches). The examination of+ L5 E/ E7 b. J2 U& N* w5 }
the neck revealed no thyroid enlargement.
4 Z/ M# k1 Q. P0 aThe genitourinary examination was remarkable for: n2 q5 s1 ~5 u
enlargement of the penis, with a stretched length of
4 F. w( y, h4 g4 I( y8 cm and a width of 2 cm. The glans penis was very well) \- t8 Q9 y' V( E3 T
developed. The pubic hair was Tanner II, mostly around( T$ U# @; x; ]! X* Y5 ^, p
540
- U0 Q5 A7 M! x; \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) K, L7 p' f/ X0 D) ?9 e+ }the base of the phallus and was dark and curled. The2 U) ?& f- P: c
testicular volume was prepubertal at 2 mL each.
/ s! |& e5 I* N; F' k" JThe skin was moist and smooth and somewhat
1 ^" F6 J( b6 ]2 z: q& w2 Xoily. No axillary hair was noted. There were no
6 c7 Y! L6 t( i: [7 Sabnormal skin pigmentations or café-au-lait spots.
) H$ i7 P* x: L/ B6 t4 SNeurologic evaluation showed deep tendon reflex 2+/ [( Y5 F$ `* S
bilateral and symmetrical. There was no suggestion. o, G4 T; ?/ j. [+ }
of papilledema.  r( P( B8 E* o5 ?
Laboratory Evaluation+ m6 U! o8 C4 P3 g) O3 h! A7 O
The bone age was consistent with 28 months by. N. F. U' T0 c
using the standard of Greulich and Pyle at a chrono-
6 C( p9 [  z0 j" I# C  N2 V5 \logic age of 16 months (advanced).5 Chromosomal
8 e5 o: R" D) w5 Y4 j0 ]6 fkaryotype was 46XY. The thyroid function test
/ L+ B  r0 _% E' R/ U7 W" m3 g7 f1 lshowed a free T4 of 1.69 ng/dL, and thyroid stimu-4 Z- S, }* L' w9 s. s0 q
lating hormone level was 1.3 µIU/mL (both normal).- ?- w3 W7 {7 ~9 A( M  q! C
The concentrations of serum electrolytes, blood  v. A* m. B( X$ p) b7 Y4 @- H
urea nitrogen, creatinine, and calcium all were( u1 v, A3 o: Y7 [
within normal range for his age. The concentration
5 t' w. D/ V/ j# Hof serum 17-hydroxyprogesterone was 16 ng/dL
) n. A* f! Z" i2 f& U- o# Z(normal, 3 to 90 ng/dL), androstenedione was 20
! f% _8 _" \* k& z0 M3 `( m: Qng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& Q# N- Q0 v( A' Z- [
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
( d0 i- S3 P- t* \7 v% N" _desoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ g1 ?( `" j: T1 C. J# L! e49ng/dL), 11-desoxycortisol (specific compound S)- X4 r: i1 {9 l2 z
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
$ I) m/ g  B$ o5 `' X- ctisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) k& Z! v& P8 H2 }9 Z! Etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ q0 C. }/ F! l" x; I+ {* D% rand β-human chorionic gonadotropin was less than
  Z" `2 W0 y' _/ x5 mIU/mL (normal <5 mIU/mL). Serum follicular
, Q: W# L" Y" T% |7 vstimulating hormone and leuteinizing hormone
- a: g1 ?/ y5 P0 Lconcentrations were less than 0.05 mIU/mL
2 |# O+ b9 g; j$ D5 f2 r(prepubertal).
$ u: T: r- J' F/ FThe parents were notified about the laboratory
' ~+ y  l2 k5 m/ aresults and were informed that all of the tests were
! i( z7 O, ], M1 bnormal except the testosterone level was high. The4 ~2 O& a6 a) [
follow-up visit was arranged within a few weeks to2 [  N3 N2 ]1 |
obtain testicular and abdominal sonograms; how-9 E# x5 E5 w& Z/ ]4 D. H
ever, the family did not return for 4 months.
( X7 D) I7 N1 Z  S3 t1 |( KPhysical examination at this time revealed that the
- F8 ~1 r; r1 Tchild had grown 2.5 cm in 4 months and had gained
- I& `$ [" _/ H) ]  Y, M/ f2 kg of weight. Physical examination remained7 H! }3 U( M0 s9 D8 X" ^
unchanged. Surprisingly, the pubic hair almost com-
* S+ Z9 J! \& Q# ?pletely disappeared except for a few vellous hairs at
# G, K1 C5 r( }/ O4 J* ?the base of the phallus. Testicular volume was still 2$ U& v8 B# s+ p/ t5 ^  C" V
mL, and the size of the penis remained unchanged.
' D. N- S0 G: V. Z7 ?0 k6 s0 S- YThe mother also said that the boy was no longer hav-0 q/ y5 @0 j. P; M9 U8 V, m
ing frequent erections.
! G+ h8 [/ v2 ]' S5 @" ]Both parents were again questioned about use of
3 I4 J4 R! N, B4 q8 ]: R. l# Nany ointment/creams that they may have applied to3 P2 s4 X9 X. |% Q. p  ]" A) d- R
the child’s skin. This time the father admitted the; u% U2 b9 o' ?4 k
Topical Testosterone Exposure / Bhowmick et al 541
" T6 b$ Q- {; Guse of testosterone gel twice daily that he was apply-! ]) ~* B3 \- l2 z
ing over his own shoulders, chest, and back area for
! }* l% X- t+ i# }) r' ]a year. The father also revealed he was embarrassed
9 p* r! k. C" X, P( wto disclose that he was using a testosterone gel pre-
& s, |( D# w: _7 _scribed by his family physician for decreased libido9 W' O0 O8 g3 c4 P1 ]1 ]; O0 q
secondary to depression.
% M# D& L: A- p0 V9 ?& x9 N& EThe child slept in the same bed with parents./ U9 r0 x9 c! C
The father would hug the baby and hold him on his# j9 {; E# d/ G4 O0 ~1 _3 F
chest for a considerable period of time, causing sig-( J6 _* b7 ~2 t2 O
nificant bare skin contact between baby and father.
4 w$ }( \  @- d: L# ^6 R0 n' gThe father also admitted that after the phone call,
. u4 f( g1 f6 w. d( j( u' jwhen he learned the testosterone level in the baby
9 O  ?$ J5 y3 f2 O* m* [was high, he then read the product information) d' X( d4 J2 g+ D0 [
packet and concluded that it was most likely the rea-
8 e* _! t5 w, s. `$ U6 vson for the child’s virilization. At that time, they! A# [; O6 `" d8 N/ ^4 H3 n
decided to put the baby in a separate bed, and the$ C. C- z$ S7 V; {! a! G
father was not hugging him with bare skin and had
2 e% j$ d( B% u3 Q9 [7 u: C' obeen using protective clothing. A repeat testosterone
# f4 N+ h* D/ R2 Vtest was ordered, but the family did not go to the( n8 }8 k* U4 v8 g) m- N0 \
laboratory to obtain the test.
& L/ r$ ]) @' z# a" F- pDiscussion
* X; T0 s% r' X9 w  TPrecocious puberty in boys is defined as secondary
$ Y  h* Q9 }6 O  ]sexual development before 9 years of age.1,4* g1 w0 g# p7 K+ a
Precocious puberty is termed as central (true) when
+ [% T. B/ l- i% Z. h2 t% b( |it is caused by the premature activation of hypo-& L1 L, @/ Z9 J/ ]6 |7 t4 P
thalamic pituitary gonadal axis. CPP is more com-
: ~) p+ B  u: o: x" fmon in girls than in boys.1,3 Most boys with CPP$ A3 N3 t0 D- g5 `: }. r
may have a central nervous system lesion that is
5 D+ _3 j( r7 D' m: Xresponsible for the early activation of the hypothal-, \8 M# t: Y* L
amic pituitary gonadal axis.1-3 Thus, greater empha-, I) q" X& U9 E, P1 U" E
sis has been given to neuroradiologic imaging in2 n: h2 A7 D* k+ r9 h
boys with precocious puberty. In addition to viril-8 H7 Y, j. t4 Z6 Q5 \; u
ization, the clinical hallmark of CPP is the symmet-  t8 W8 F/ F/ v
rical testicular growth secondary to stimulation by
. I4 H; x; r  d% D& j3 i7 Rgonadotropins.1,3, J0 ]; a8 L7 a  p
Gonadotropin-independent peripheral preco-; n. G: b3 t1 i" U: `: w6 D  B
cious puberty in boys also results from inappropriate7 s5 F" r' [( Z0 D  u" ]
androgenic stimulation from either endogenous or! c8 J: Q  U2 t% @3 z
exogenous sources, nonpituitary gonadotropin stim-
$ _2 ~( x( a& v- B& o" }ulation, and rare activating mutations.3 Virilizing" Y8 q$ w- C% d# J- m5 ?
congenital adrenal hyperplasia producing excessive
) ~+ Y) p- d% M" J3 gadrenal androgens is a common cause of precocious+ Z( E# @7 m- E( A. t
puberty in boys.3,4, M" O3 P1 D, R2 P5 ^: `  W
The most common form of congenital adrenal
4 @+ H$ S: X9 ]& \* q6 L8 G% Ahyperplasia is the 21-hydroxylase enzyme deficiency.
" _, r" ^4 ?$ E: C. \. `The 11-β hydroxylase deficiency may also result in
1 w& o2 G9 t% u% A9 N/ k; A5 Nexcessive adrenal androgen production, and rarely,0 X( A6 ^' \" W% [* x! ~' b) E
an adrenal tumor may also cause adrenal androgen: ?- ]6 {$ M. s9 W2 \! }9 R
excess.1,3, t: W, r+ N6 [/ F
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: o# `2 d$ S4 j3 O+ }8 S4 K
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007$ w: ?% H! B" N5 [% r5 m) W  _
A unique entity of male-limited gonadotropin-4 X! b4 a6 b3 X# ~
independent precocious puberty, which is also known) H3 [0 J' @9 j2 A* G+ `. P2 I
as testotoxicosis, may cause precocious puberty at a( k# n: e: p3 U& l( h0 y
very young age. The physical findings in these boys
/ I( R! m0 |9 wwith this disorder are full pubertal development,
" S' U4 h% F  dincluding bilateral testicular growth, similar to boys7 L9 |, T3 o5 y1 Z6 L- W. K6 H
with CPP. The gonadotropin levels in this disorder3 u" a# b. C" G6 b& Q
are suppressed to prepubertal levels and do not show
8 ~: l% h+ i* Z# xpubertal response of gonadotropin after gonadotropin-
9 {$ X, Q4 N( B5 ireleasing hormone stimulation. This is a sex-linked; R5 Y  E6 k1 H# u  v7 R3 \% W- m
autosomal dominant disorder that affects only  a! Q6 C2 f) B- V
males; therefore, other male members of the family3 x/ A9 f6 ^$ }
may have similar precocious puberty.3
: C* x1 a0 d% O; t* G$ ^2 sIn our patient, physical examination was incon-, i& d1 g4 c9 q( U
sistent with true precocious puberty since his testi-6 ]) e7 K  N5 d6 y9 j5 p3 T2 z
cles were prepubertal in size. However, testotoxicosis, X0 n. w0 g6 e& `" B6 w* W! I5 g; T
was in the differential diagnosis because his father. V% _( ^0 g6 @2 T" {: f( y9 x5 x& D1 r1 g
started puberty somewhat early, and occasionally,1 t# w) D2 \7 ~2 |; @6 `2 [
testicular enlargement is not that evident in the  g8 ?2 s8 W$ O, u
beginning of this process.1 In the absence of a neg-
* J5 F! y" @) b/ mative initial history of androgen exposure, our- A  E, E* `* e: C, x
biggest concern was virilizing adrenal hyperplasia,. O- B5 S2 }7 p* o
either 21-hydroxylase deficiency or 11-β hydroxylase
& x. G; n" G+ Z3 Y$ ]/ k, s; w+ {& U  ydeficiency. Those diagnoses were excluded by find-
5 m( }7 N6 T) T+ R2 q& H* _6 ging the normal level of adrenal steroids.5 U+ v7 X0 u4 U! D/ o: e% t! z3 c
The diagnosis of exogenous androgens was strongly
) Q' L% \  N9 a* n* X+ |suspected in a follow-up visit after 4 months because' q  W$ P+ g* }0 Y
the physical examination revealed the complete disap-
5 w9 q; A4 O/ {$ [# ]+ k2 W: ^pearance of pubic hair, normal growth velocity, and/ e* y- Q9 i$ }8 j  s( Z: i5 P
decreased erections. The father admitted using a testos-
. @5 T9 H+ B- Q8 I  }terone gel, which he concealed at first visit. He was
# {& M4 Y4 w! b4 Kusing it rather frequently, twice a day. The Physicians’- ~3 ~. [) w0 e0 _6 c  X
Desk Reference, or package insert of this product, gel or3 g0 r) H. n" X* l! W
cream, cautions about dermal testosterone transfer to2 V, {3 ]( Y% q' M) J8 {6 f5 Q1 Q: Q) W
unprotected females through direct skin exposure., u# t7 O6 P9 W9 R
Serum testosterone level was found to be 2 times the9 I3 S9 J3 @" V' E
baseline value in those females who were exposed to5 n2 Y( x% l5 |: ^1 n) c/ M+ j. m
even 15 minutes of direct skin contact with their male
" ]5 y6 ?; a; T* p5 K$ Cpartners.6 However, when a shirt covered the applica-7 m! {7 k. ~3 g) ?4 ~6 v# k+ L- W
tion site, this testosterone transfer was prevented.; p) z% k. y- m# ^6 _6 y( K
Our patient’s testosterone level was 60 ng/mL,6 _4 l. `7 ~: K8 @; T5 K, }% S
which was clearly high. Some studies suggest that: m2 j8 A/ P2 O. r, u% v
dermal conversion of testosterone to dihydrotestos-
1 @. s# b2 a8 zterone, which is a more potent metabolite, is more" K1 C8 [: e* s$ S0 O* _+ `( ]/ |
active in young children exposed to testosterone% P9 ?3 }+ y; M' c8 n1 L+ L5 F
exogenously7; however, we did not measure a dihy-
- v9 u7 {; T$ Q" L4 U, e/ Odrotestosterone level in our patient. In addition to
1 Z1 f# ?, J9 }8 k* y/ m5 q: pvirilization, exposure to exogenous testosterone in
+ {2 s  j$ Q, Pchildren results in an increase in growth velocity and
( x# d. d( P3 l$ H1 b' r! v% k$ ladvanced bone age, as seen in our patient.
/ B0 c" H: d) D" T$ D' JThe long-term effect of androgen exposure during6 R+ c- H0 w3 `5 D- ^' c+ E0 l- \
early childhood on pubertal development and final
0 w' X# Z' B6 R$ E) g* @4 Hadult height are not fully known and always remain
; E! s* V" J# F+ `5 F9 G$ Ia concern. Children treated with short-term testos-
) G1 ^( T1 e1 V/ G  V6 Q2 U1 h2 Uterone injection or topical androgen may exhibit some
: s- V! W3 h/ d1 P+ P: p- p7 xacceleration of the skeletal maturation; however, after
1 H+ }+ d1 S, J/ R. lcessation of treatment, the rate of bone maturation% I" U2 N+ p; I5 e8 U9 G8 ]9 z8 R3 s
decelerates and gradually returns to normal.8,9
' l  j  Y0 [8 s% ~1 u  a% [" XThere are conflicting reports and controversy
: s, x1 A1 d1 m2 t5 H  eover the effect of early androgen exposure on adult
5 r6 G) Z5 @# X0 L- fpenile length.10,11 Some reports suggest subnormal
+ w5 f7 C6 z% S& R1 m- ladult penile length, apparently because of downreg-! D! H, {+ \$ V! V5 _% Z3 m
ulation of androgen receptor number.10,12 However,
3 m2 o: s6 |) u2 B: JSutherland et al13 did not find a correlation between6 x$ ]& G; W. i' l6 l& c
childhood testosterone exposure and reduced adult# o7 H' R) H5 ^. `; F
penile length in clinical studies.. w1 i0 _! E2 ^
Nonetheless, we do not believe our patient is% }  ^6 r# w3 f8 |) r" T/ N
going to experience any of the untoward effects from0 ^4 l6 q% f3 a3 D% g
testosterone exposure as mentioned earlier because
: X, [2 D8 |9 `4 t/ t2 Y# v& a7 A3 Gthe exposure was not for a prolonged period of time.
/ v3 s1 p. U) w0 w; N5 Z$ rAlthough the bone age was advanced at the time of" o0 Q2 T2 \2 A, d" _1 G
diagnosis, the child had a normal growth velocity at
! X, L0 _6 _& y( B! d7 hthe follow-up visit. It is hoped that his final adult2 \0 Y1 ?) o2 C1 U3 \" G2 ~
height will not be affected.
; u* u1 v$ X2 j: a% a) D" B. nAlthough rarely reported, the widespread avail-
8 V/ k" L$ R! f1 A  H! M- Zability of androgen products in our society may+ K7 K4 M* D2 `% B
indeed cause more virilization in male or female
( A  z- z/ j: ], v" tchildren than one would realize. Exposure to andro-# A: r" X0 ]8 Y" a' o
gen products must be considered and specific ques-! S7 m6 _8 ?. _* V: [0 O' e
tioning about the use of a testosterone product or, U! N$ D+ e0 V* f
gel should be asked of the family members during, U3 }: j( J& o6 R4 E7 G
the evaluation of any children who present with vir-1 b0 F: R5 U& _
ilization or peripheral precocious puberty. The diag-
# o5 E" G9 g* unosis can be established by just a few tests and by) i0 I# ^1 @1 l. I
appropriate history. The inability to obtain such a8 H! q! R5 l0 T+ m* T
history, or failure to ask the specific questions, may( F3 G* j8 L, F' H9 x
result in extensive, unnecessary, and expensive; b1 A  s2 n# u# l0 t
investigation. The primary care physician should be! k3 K6 v0 P) m$ N+ \3 V
aware of this fact, because most of these children
6 X# g) c9 m; n% x% dmay initially present in their practice. The Physicians’
9 a8 W4 s: t" R1 C+ ?& t4 dDesk Reference and package insert should also put a( S  M; n, K; R% v
warning about the virilizing effect on a male or
7 N* |  v% H5 u! j3 G8 Q5 I2 mfemale child who might come in contact with some-; u( t$ m2 W* e- q" W
one using any of these products.) m1 S4 _& }+ u. ^. g) ?) r1 [3 k0 N
References
4 [% o/ l6 x  w8 m; Z* n1. Styne DM. The testes: disorder of sexual differentiation
7 ^$ D: m2 k( q" land puberty in the male. In: Sperling MA, ed. Pediatric- z8 ^) w: W) r( X& u
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;8 ^/ v! G( R7 d6 r+ g; L% V
2002: 565-628.
1 o* E0 {% K+ h2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
# `  P& [0 `9 t) }. }, cpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old% p, ]; P8 ^( {" g8 B/ O9 Q
Boy Induced by Indirect Topical
& q( f( S, J$ U. v# oExposure to Testosterone+ O5 M, G4 b9 f% Y1 y2 ?$ A  p9 R* j
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. R& N4 @1 e( j7 J' g3 Oand Kenneth R. Rettig, MD11 c* T, x0 Z. J- R. }
Clinical Pediatrics& t/ K. Y6 h4 o+ H, w3 e! B
Volume 46 Number 6
! j4 u# X" w! c7 k# hJuly 2007 540-543
: v! T7 ]( @0 x0 A© 2007 Sage Publications
* ^. X) f$ t8 h1 {8 A10.1177/0009922806296651
* d. Y+ e6 i( i2 A% ?http://clp.sagepub.com
9 Y8 p. ?" c, e9 i3 K0 J8 Qhosted at
4 q7 X) O+ [% i0 R5 u  i5 G! khttp://online.sagepub.com; V. L+ L: V- k& c' L
Precocious puberty in boys, central or peripheral,7 a- e. ]4 |1 r  p8 }  p. p( }
is a significant concern for physicians. Central% d) ?) I1 w4 Y) s& Y1 W5 n
precocious puberty (CPP), which is mediated
6 \' F8 S8 s1 cthrough the hypothalamic pituitary gonadal axis, has3 q. R' n8 U7 j6 u- P
a higher incidence of organic central nervous system8 W: C4 z1 ^0 S: U0 v( `) l4 J5 ^
lesions in boys.1,2 Virilization in boys, as manifested2 n, u/ R8 t, R- h; K4 X
by enlargement of the penis, development of pubic  Y: \4 J3 ]  r+ {" l4 Y
hair, and facial acne without enlargement of testi-0 Q+ f: b8 I) J1 n. l4 U2 w) `. z
cles, suggests peripheral or pseudopuberty.1-3 We! A$ N4 H4 z% @# l7 M  s4 D
report a 16-month-old boy who presented with the
, l+ ?$ [. [% M3 g) [+ Genlargement of the phallus and pubic hair develop-
* x7 n7 F( ?' F( Zment without testicular enlargement, which was due" ~! G; x; b6 m# |! R& Z# D
to the unintentional exposure to androgen gel used by
5 {/ V! O) I% o8 _- b5 t6 i; n4 dthe father. The family initially concealed this infor-
  S% F- z% P* e* U4 U7 r! Emation, resulting in an extensive work-up for this
+ H, V# [9 y! s7 C& q: N* Q% n5 _4 Pchild. Given the widespread and easy availability of
& E; `9 ~* R; R3 B6 w% h6 ttestosterone gel and cream, we believe this is proba-
* w" U/ k- {& ?0 B. Y7 U. B$ Wbly more common than the rare case report in the) T+ x. M3 M' |7 ?- P. l
literature.4
: I* Q8 p; X5 [# i& hPatient Report5 X( H2 s  N( P
A 16-month-old white child was referred to the" {" v' v: X3 h. s, a& m  w  ?3 u
endocrine clinic by his pediatrician with the concern5 r- e& r+ p* I" f( W5 e! [+ o
of early sexual development. His mother noticed( ^6 G$ K" G3 R* f/ a( ^2 c) h8 L
light colored pubic hair development when he was! j" F# `: x2 q6 y- \' T
From the 1Division of Pediatric Endocrinology, 2University of+ y6 a) Q- E5 K  R  t# j3 J+ p
South Alabama Medical Center, Mobile, Alabama.
  c# C1 C( s: H- d! G. XAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 h/ u9 z5 b* j8 k3 y: a$ w5 z
Professor of Pediatrics, University of South Alabama, College of
6 D8 i8 e0 ^: h3 [: `. zMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
- A8 f  W+ @: g! W, e) h. ne-mail: [email protected].
* q" h& Z! t; E( n6 M& \* Vabout 6 to 7 months old, which progressively became
" Z4 M$ ~! f- Q$ L  M' Z( z- pdarker. She was also concerned about the enlarge-3 J- g! |' i$ H
ment of his penis and frequent erections. The child
8 _/ p. o3 X% S  Uwas the product of a full-term normal delivery, with
) ?7 l/ l; Y4 R# m6 X& K% x3 l; ca birth weight of 7 lb 14 oz, and birth length of  D& s8 U& j/ k6 Y3 ^4 J4 z
20 inches. He was breast-fed throughout the first year
* Y# R5 W! v1 r9 H8 I5 r  @of life and was still receiving breast milk along with: X$ y. \9 p3 {* ?1 p) S& G
solid food. He had no hospitalizations or surgery,
6 ^4 s9 K5 T7 d! R9 nand his psychosocial and psychomotor development9 t! G" h9 S. l; Q6 B( M& Y" V8 G
was age appropriate.3 L  E& R, t- U6 t4 L
The family history was remarkable for the father,9 h+ M; u3 e. F, a7 O9 e4 f6 |; F8 Y
who was diagnosed with hypothyroidism at age 16,
* g4 f& F1 J9 ]which was treated with thyroxine. The father’s
% K; ~0 y' w$ v; Wheight was 6 feet, and he went through a somewhat1 ^9 E2 X( O, }9 q* V
early puberty and had stopped growing by age 14.+ E) K" S* m" |( I+ }5 z
The father denied taking any other medication. The9 n  c2 D0 P3 i0 ~; D3 B  |
child’s mother was in good health. Her menarche
9 `7 I# y) a/ f/ R, U. awas at 11 years of age, and her height was at 5 feet7 j; r$ \. N9 e; n( _$ G  I* m
5 inches. There was no other family history of pre-, w; B0 a$ B7 z* L6 m
cocious sexual development in the first-degree rela-
+ w/ g+ H+ C- L- m, N. \2 ~8 A' Gtives. There were no siblings.6 H9 D* c, l3 p+ {& k1 Y3 S
Physical Examination
! W$ x  F- l; h# n( j6 x9 EThe physical examination revealed a very active,  L7 D1 O2 A8 I4 K& u
playful, and healthy boy. The vital signs documented* C2 b7 k4 i0 R- I7 M- i0 A2 W
a blood pressure of 85/50 mm Hg, his length was5 U6 x; u. @- u
90 cm (>97th percentile), and his weight was 14.4 kg+ u0 ?" X8 w$ B" Q
(also >97th percentile). The observed yearly growth' q1 k; j: U  G- Q( V0 B7 z
velocity was 30 cm (12 inches). The examination of% f. b  t, p  U' t/ h% `& f  A
the neck revealed no thyroid enlargement.
2 ^% j+ T' |- VThe genitourinary examination was remarkable for' g$ g  ?0 o# `% j* C8 Z$ b; S% u
enlargement of the penis, with a stretched length of4 o; U4 c1 }5 g7 l4 o8 v1 S1 v& l
8 cm and a width of 2 cm. The glans penis was very well
" c: F$ Q% \, kdeveloped. The pubic hair was Tanner II, mostly around3 T* `% ?3 b; `. g4 F+ Z6 j  C- I/ ]
540, c/ e! w* V6 E3 F6 j# T
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ j) z, L* g3 g1 Nthe base of the phallus and was dark and curled. The
: o1 [& P6 i; [testicular volume was prepubertal at 2 mL each.
& |+ N5 g) d. g: XThe skin was moist and smooth and somewhat: {$ W6 @2 v: z; N9 P, ^' S
oily. No axillary hair was noted. There were no. ~( m) B8 ^  I, |
abnormal skin pigmentations or café-au-lait spots.
" s+ }# n( b- D* O$ }, a/ yNeurologic evaluation showed deep tendon reflex 2+* u1 t# @; ~& A1 v* a/ v% R
bilateral and symmetrical. There was no suggestion4 K9 R( B* E  m& v
of papilledema.
7 Y+ h6 M9 g2 u# A8 X3 _9 M' qLaboratory Evaluation& w' R1 Q% Z+ p/ U1 z
The bone age was consistent with 28 months by
! J4 P$ r. E& ^( ^using the standard of Greulich and Pyle at a chrono-# j2 D! A: T. h* C# k
logic age of 16 months (advanced).5 Chromosomal
6 |& \0 Q% U0 |. ~karyotype was 46XY. The thyroid function test
) r4 ]# D+ v8 c3 U( ]1 A" d* U. r* xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! i- C: z7 C) P8 Wlating hormone level was 1.3 µIU/mL (both normal).* v" j$ Z5 s! t, W
The concentrations of serum electrolytes, blood; S2 e1 [( Y, h+ Z* N1 L0 j
urea nitrogen, creatinine, and calcium all were% I6 u- ?7 e4 U: L
within normal range for his age. The concentration8 a- M0 G1 Z+ f* r
of serum 17-hydroxyprogesterone was 16 ng/dL
& u* N' r; q3 x, a(normal, 3 to 90 ng/dL), androstenedione was 20$ ~2 O2 x, {% f/ V
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; a0 B: F4 d, J- M
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
% K2 w7 p# f* F4 @desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 l, [; i+ }- v7 {. ~5 j49ng/dL), 11-desoxycortisol (specific compound S)' ?( z* Y: S& @# _- C! Q& s. V
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& H- k1 ?3 w3 q  j) j- L" btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" w: @5 s9 `8 S2 Atestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 r+ X9 a7 ?  p% d) ?1 E& J& pand β-human chorionic gonadotropin was less than
4 \6 m7 q% c5 T5 Z# i5 mIU/mL (normal <5 mIU/mL). Serum follicular
; o- t6 c- q! |7 G/ j4 ?stimulating hormone and leuteinizing hormone
, ?/ C. w, ]6 d( j/ ^% a. vconcentrations were less than 0.05 mIU/mL
+ [& w6 V8 z$ T- ~& p% Y(prepubertal).
' W9 ~2 U4 O# b2 ~- n6 G& k6 @8 IThe parents were notified about the laboratory# Z) E0 P5 A: M
results and were informed that all of the tests were$ w, R' n6 e* M: g
normal except the testosterone level was high. The; k% B5 ]: A- C; L+ q# A: C' c$ ~0 B
follow-up visit was arranged within a few weeks to. N# X. w' P) d6 o6 V
obtain testicular and abdominal sonograms; how-7 j- J6 `' f% S' h+ {( K+ v3 o
ever, the family did not return for 4 months.
3 K# i: w- d) jPhysical examination at this time revealed that the
5 q* @& @: I  j7 t/ R) Wchild had grown 2.5 cm in 4 months and had gained: K0 E- S( p9 J! g" o
2 kg of weight. Physical examination remained
1 `- W/ j8 M/ i9 D7 Y; h0 @unchanged. Surprisingly, the pubic hair almost com-
9 z/ C) f8 w# ?pletely disappeared except for a few vellous hairs at
" Y8 c# c" u; ~+ ^* V2 ythe base of the phallus. Testicular volume was still 2
& s* s$ Z# D, Y: K' ]& i5 RmL, and the size of the penis remained unchanged.6 }5 S7 Q" R" P1 \7 H1 F, o' }
The mother also said that the boy was no longer hav-
6 u) S1 B! ?+ d; qing frequent erections.+ _  `+ K, `1 a8 S- D  V
Both parents were again questioned about use of
8 X3 N. G2 ^! l) \% Y; ]1 Kany ointment/creams that they may have applied to# |: f$ k8 M2 c3 V
the child’s skin. This time the father admitted the* D) ?, f, w/ G9 i
Topical Testosterone Exposure / Bhowmick et al 541* m& L0 {6 K& ?% y+ Q
use of testosterone gel twice daily that he was apply-/ d+ s  g- d+ u3 q7 f! e, V
ing over his own shoulders, chest, and back area for
% E+ v  r/ g& N3 aa year. The father also revealed he was embarrassed
' q' |. l0 a1 i# e& [6 Z+ Jto disclose that he was using a testosterone gel pre-
. H2 U9 q  c7 sscribed by his family physician for decreased libido
4 V  [( T9 n0 @: x. p2 Xsecondary to depression.
* Y' h. N4 J/ |0 n: _; {9 HThe child slept in the same bed with parents.
/ Q5 p: M! j2 X3 }5 sThe father would hug the baby and hold him on his% w2 I& o3 d' W& V0 p' ]4 H& e+ a
chest for a considerable period of time, causing sig-
; y# G" d* z6 Snificant bare skin contact between baby and father.
/ ~; D  J4 G9 l& M' `The father also admitted that after the phone call,
3 e) M: l- e8 P) {4 Ywhen he learned the testosterone level in the baby1 {* y+ i2 H/ g  e( y8 \0 [. ~
was high, he then read the product information4 S  k& _% m5 R6 U% H
packet and concluded that it was most likely the rea-4 F* I/ m5 F' s5 n, d5 T1 a8 P3 Z' _
son for the child’s virilization. At that time, they
5 W" W" I1 }3 s( B4 i+ tdecided to put the baby in a separate bed, and the
  T  o- P7 d% X" Sfather was not hugging him with bare skin and had8 k  o  f8 }' g# y
been using protective clothing. A repeat testosterone
/ T, d) |& X; C$ ^test was ordered, but the family did not go to the; I! K( c  D, l% \9 a6 K* z6 {* O
laboratory to obtain the test.9 Z6 T0 \+ l: }" Y4 y
Discussion
5 P1 R% Q' X: V- r! WPrecocious puberty in boys is defined as secondary0 C3 G8 {( u7 u$ I- `* k
sexual development before 9 years of age.1,4$ C$ d+ R" V$ E- f# f/ r- H
Precocious puberty is termed as central (true) when
6 w$ Y. e  S0 C1 y; E3 qit is caused by the premature activation of hypo-
1 c# x2 V* Y1 {: \4 [+ V) O  vthalamic pituitary gonadal axis. CPP is more com-* b: E. q/ A: B# X$ L. m
mon in girls than in boys.1,3 Most boys with CPP
1 M' b+ O; R4 u. ?2 ]: V- Lmay have a central nervous system lesion that is% N- y6 u  K9 ^1 d) N/ R
responsible for the early activation of the hypothal-, _( Z4 D6 K* D2 D/ V+ H) Q$ o
amic pituitary gonadal axis.1-3 Thus, greater empha-
. `; o5 m- J! bsis has been given to neuroradiologic imaging in- w- }0 B  W. M) b  x+ {  A$ b
boys with precocious puberty. In addition to viril-3 P6 V7 u! o9 C# |8 q# Z
ization, the clinical hallmark of CPP is the symmet-  F$ D, O; w5 z
rical testicular growth secondary to stimulation by# j) E# E" W  B3 g# c% }. e) z5 o
gonadotropins.1,3
, }2 @6 f0 ]! T/ fGonadotropin-independent peripheral preco-6 i5 O9 q: S/ }* ]# G
cious puberty in boys also results from inappropriate
8 Z. f6 t9 m1 o/ Pandrogenic stimulation from either endogenous or
' J+ K1 J9 o( Y0 H9 C9 hexogenous sources, nonpituitary gonadotropin stim-
  v# }0 C& W1 \& D( D9 W: `2 B& culation, and rare activating mutations.3 Virilizing
* G4 B7 t! k5 Wcongenital adrenal hyperplasia producing excessive
0 ~  ]/ _8 n5 Tadrenal androgens is a common cause of precocious' L( c& [* m" `1 `
puberty in boys.3,4
3 D* j( L* \& y9 N* {; |1 ]7 X, xThe most common form of congenital adrenal! L+ d4 F6 i7 [$ Q4 {9 N
hyperplasia is the 21-hydroxylase enzyme deficiency.
* C1 q& f* y, x- mThe 11-β hydroxylase deficiency may also result in. L0 g+ Y( p" U- p" @
excessive adrenal androgen production, and rarely,
0 ?1 D3 u; }# n- d1 O* uan adrenal tumor may also cause adrenal androgen; A6 s1 ]; _7 K9 N/ m" ]
excess.1,3
' V; l  W6 Q. ^* }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 [/ J* Y2 }* x" {$ p" d' `4 s542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& B( R+ o  ?& U) Z- A
A unique entity of male-limited gonadotropin-
/ |  c" R- o$ Gindependent precocious puberty, which is also known
7 U6 h6 `" v3 g5 M4 {1 C* O  \as testotoxicosis, may cause precocious puberty at a
9 h% Z; h. [1 C5 a/ Rvery young age. The physical findings in these boys$ w4 N: M8 K" v$ C. K/ i* m+ \
with this disorder are full pubertal development,
& w) D7 T$ R9 S3 l2 _$ {including bilateral testicular growth, similar to boys  N0 R3 a3 w! Y9 y
with CPP. The gonadotropin levels in this disorder
  `' E: n% H' b5 ~% |are suppressed to prepubertal levels and do not show% }8 L' F6 A9 F3 W
pubertal response of gonadotropin after gonadotropin-7 w+ v7 O3 T" Z9 F3 G
releasing hormone stimulation. This is a sex-linked
# l2 H  O1 V/ }: }- W- G, }autosomal dominant disorder that affects only; i/ J0 m! v! B3 R
males; therefore, other male members of the family
8 `: i1 c5 O+ Y8 ~" smay have similar precocious puberty.3
3 f" U* f+ f0 \/ O  S4 tIn our patient, physical examination was incon-
1 x# u4 w, c, p& wsistent with true precocious puberty since his testi-
5 z) E, p) A& r  ], _' O! i" Scles were prepubertal in size. However, testotoxicosis4 J2 T0 J8 y4 H) v
was in the differential diagnosis because his father
' E6 w2 J6 f# L5 T  G/ [started puberty somewhat early, and occasionally,
! A& ^% E3 x5 j( k6 q( T- Vtesticular enlargement is not that evident in the
# |+ m$ g. G6 u* s) W, @( r7 Abeginning of this process.1 In the absence of a neg-
. P* M* d1 {- }  w1 Eative initial history of androgen exposure, our' i. M4 ]$ a) M3 s) X* z$ M; y
biggest concern was virilizing adrenal hyperplasia,
' J( ^+ Y& d6 t: b( H4 I) j! ^either 21-hydroxylase deficiency or 11-β hydroxylase" b: s. g2 h+ O* d6 i, U9 H
deficiency. Those diagnoses were excluded by find-, U1 p: V9 r/ q; K1 E# Z5 }
ing the normal level of adrenal steroids.7 t+ W. ~* @/ s* t4 V6 u) \
The diagnosis of exogenous androgens was strongly7 i. S! j- h! q: h" I
suspected in a follow-up visit after 4 months because
4 h4 t0 L6 R9 T' i8 Vthe physical examination revealed the complete disap-0 W/ ~: O7 v/ \: |
pearance of pubic hair, normal growth velocity, and
, j( e+ ^7 P/ I* }+ L" hdecreased erections. The father admitted using a testos-3 _6 X; m$ p, \% C1 J2 \
terone gel, which he concealed at first visit. He was1 z7 m+ U3 `3 G* ]' |, }) u9 x
using it rather frequently, twice a day. The Physicians’4 j' X# x1 L& h% Z: K( D
Desk Reference, or package insert of this product, gel or- Y* [; v* ?, P% i* n7 v7 G! @3 x
cream, cautions about dermal testosterone transfer to+ f+ ~8 Q$ v' K- m8 t5 G
unprotected females through direct skin exposure.
$ Y: I5 E0 b: g) VSerum testosterone level was found to be 2 times the8 l) D6 J! e0 _
baseline value in those females who were exposed to
1 B0 r0 P0 y# heven 15 minutes of direct skin contact with their male3 g9 j( K9 ]! |. U) h( [
partners.6 However, when a shirt covered the applica-
: ?2 |! y) H# A2 O! w( rtion site, this testosterone transfer was prevented.' q$ O' y: l2 R) `$ N3 n) g; K
Our patient’s testosterone level was 60 ng/mL,
& r, t4 g6 P" W- A/ Qwhich was clearly high. Some studies suggest that
! r8 o0 Q0 c0 }$ Wdermal conversion of testosterone to dihydrotestos-
2 G+ h& h5 a8 g) x$ B3 C8 c5 K9 Tterone, which is a more potent metabolite, is more
- u9 C, T7 ^" D9 lactive in young children exposed to testosterone
: B; k3 F: b! _exogenously7; however, we did not measure a dihy-  R, `/ r$ J: f- m5 t
drotestosterone level in our patient. In addition to) }1 X3 C  a1 z9 h
virilization, exposure to exogenous testosterone in
. T+ U$ k/ B. i" a  v# ^children results in an increase in growth velocity and
7 H, w5 c/ k- Qadvanced bone age, as seen in our patient.9 t* F/ v7 c5 u2 u. G2 Y- @
The long-term effect of androgen exposure during% Y6 O) O; X$ c1 A
early childhood on pubertal development and final2 j+ |+ ^& R. V7 a' I3 e
adult height are not fully known and always remain: R7 b7 D( i& ~8 a
a concern. Children treated with short-term testos-% h& U) s7 Z+ |' _6 J: N
terone injection or topical androgen may exhibit some
/ N, t/ h' m, p1 v( B/ M3 Racceleration of the skeletal maturation; however, after
& l) U. ^2 f6 U9 [cessation of treatment, the rate of bone maturation
6 y/ {! Z, D( H7 Z! s8 j7 ddecelerates and gradually returns to normal.8,9
* T- N: B/ v+ m1 v7 x+ HThere are conflicting reports and controversy/ z* B8 _$ v  B* L" ]) Y2 J
over the effect of early androgen exposure on adult
6 ?1 S, q8 l! y- \! f. l& xpenile length.10,11 Some reports suggest subnormal. H7 u7 K" {" E5 J: @. W  {
adult penile length, apparently because of downreg-
  Q" {3 M9 y9 E3 Z8 C, x8 M" Rulation of androgen receptor number.10,12 However,
5 @% q7 c. A* Q) |, t& {Sutherland et al13 did not find a correlation between  ^, q# ?3 v, w5 Q) Q; a' v, A
childhood testosterone exposure and reduced adult
) I) O  j0 p+ m& I( {. t2 L' P( ^penile length in clinical studies.. X5 j1 d: D" a
Nonetheless, we do not believe our patient is: E: ?3 G( d' \- ]- R3 w
going to experience any of the untoward effects from
# q% r/ T: B/ f. h% T% a  ~5 g) {testosterone exposure as mentioned earlier because
+ r+ Q+ t& }! w' k- }+ {the exposure was not for a prolonged period of time.3 h( R  B: N, F; C
Although the bone age was advanced at the time of
1 x4 U, Z* ^5 C+ M, @% mdiagnosis, the child had a normal growth velocity at
! E: r! Y& G3 i0 S* jthe follow-up visit. It is hoped that his final adult- t* o1 u# J* e) z
height will not be affected.
3 @0 I" M& t# d7 j0 x+ q4 ?* M% r+ MAlthough rarely reported, the widespread avail-7 i1 K) y+ z/ J* E9 q
ability of androgen products in our society may
! c' u# [# ~( R9 X' L; Z+ Sindeed cause more virilization in male or female& {3 Y. l  i1 f# e0 T
children than one would realize. Exposure to andro-
* ^, x( n9 `- |- M: sgen products must be considered and specific ques-
2 e' n4 M" u! |) @tioning about the use of a testosterone product or9 S, p5 k. ~+ E5 \% l- j2 @, B7 \" V
gel should be asked of the family members during
& n, }" q9 S* Z4 \1 q$ y/ Tthe evaluation of any children who present with vir-
1 i0 P/ Q3 n3 f3 Cilization or peripheral precocious puberty. The diag-
# S8 X+ H, O! a& g! S# e( X3 j4 znosis can be established by just a few tests and by
6 e+ r9 W0 ~# {$ h3 U; y0 T# rappropriate history. The inability to obtain such a, F' e$ Q" m0 }! d8 T
history, or failure to ask the specific questions, may8 q) h$ |" Y5 V* t: T3 n
result in extensive, unnecessary, and expensive
$ ]7 _9 G3 o) F' x, H  Xinvestigation. The primary care physician should be
. d4 \5 {4 L0 p" ^aware of this fact, because most of these children! ?6 c& m# b7 a2 a& g/ m0 C
may initially present in their practice. The Physicians’
. m4 |) e; |! U9 QDesk Reference and package insert should also put a
) H; V8 f1 |; j; |warning about the virilizing effect on a male or$ {: L% q+ _2 M% f* R& ^
female child who might come in contact with some-; n1 p: z2 N4 S
one using any of these products.+ w8 Y5 b- i) V& X  q7 q1 W# R
References. ~7 O- I  x! T3 d/ ^- U
1. Styne DM. The testes: disorder of sexual differentiation
: i+ @" d  \; tand puberty in the male. In: Sperling MA, ed. Pediatric) r8 D! \, G2 t( o$ K! q4 Z+ M8 |( r# @
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 _+ L: l# d5 D+ O: u) p
2002: 565-628." \, L$ O; [$ `. f# Y5 ?
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- `* M, \# z: `" s/ epuberty 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

/ g+ H4 A" |. P$ [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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