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Sexual Precocity in a 16-Month-Old
9 a7 {0 V# `) D' M( L$ P: Z% P1 WBoy Induced by Indirect Topical
5 g2 K1 v, ]7 Z. EExposure to Testosterone" h4 E5 h+ C6 _( o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& c0 ]/ y1 O9 Z* ]0 j3 P
and Kenneth R. Rettig, MD1; u# C& |. L9 e7 l- k1 Z0 _# ?
Clinical Pediatrics9 r  b. `' H" V' F9 \% o7 L- N. X2 C
Volume 46 Number 6
& ^, s+ P- J* v$ a6 H3 v5 x2 AJuly 2007 540-543
* l! N4 U2 q  e1 K& _  K; U© 2007 Sage Publications/ s+ N* G* g- r% ~- M
10.1177/0009922806296651& t* J' W  O( P- v
http://clp.sagepub.com& b! ~' S6 D0 i% b9 D* V) |( \  l
hosted at
% w2 C( p/ y, G' Ahttp://online.sagepub.com9 @1 P* O5 }/ @) _6 `: [: ?& ^
Precocious puberty in boys, central or peripheral,
0 s4 `; b0 G8 R" `  @is a significant concern for physicians. Central7 I; Y3 t% K' h8 _
precocious puberty (CPP), which is mediated
( f9 F8 b) J, {2 x' J2 w3 T4 H3 ethrough the hypothalamic pituitary gonadal axis, has
, J- g1 a5 Q: N( Ia higher incidence of organic central nervous system: u* f2 Z  |$ C9 t
lesions in boys.1,2 Virilization in boys, as manifested; \' f& w6 f) m% S' J
by enlargement of the penis, development of pubic" ?* p! [0 y' ^2 B/ t' C# V$ g
hair, and facial acne without enlargement of testi-
  ~, s0 Q* N! \- i& M2 _$ Mcles, suggests peripheral or pseudopuberty.1-3 We) K* ^- n! B1 c, n6 w5 X
report a 16-month-old boy who presented with the
) g: ?. b0 k6 X; `# cenlargement of the phallus and pubic hair develop-
. |4 g  b& J3 L! A, ?# Ument without testicular enlargement, which was due
/ f. Z: [8 ~1 l0 |6 o- }0 `to the unintentional exposure to androgen gel used by+ O1 b( r4 |/ a
the father. The family initially concealed this infor-& }, n) j3 B+ _- \7 W+ U) o) \  o
mation, resulting in an extensive work-up for this- T9 F. }! g3 ?) p
child. Given the widespread and easy availability of4 H0 Q4 _1 h  D6 \, M
testosterone gel and cream, we believe this is proba-
0 R9 q0 w3 L7 `* [! V1 jbly more common than the rare case report in the
( }6 P+ {2 K: z, Lliterature.4
: d1 P# Y* G2 X" oPatient Report2 K4 W" X4 N' I/ A( p
A 16-month-old white child was referred to the
% ^) S+ S4 b4 {6 H' zendocrine clinic by his pediatrician with the concern
+ c; v: y  v$ yof early sexual development. His mother noticed
  g* j( B6 J  r/ L4 [( {light colored pubic hair development when he was
- O( h: \  E7 O9 I5 e3 l9 ZFrom the 1Division of Pediatric Endocrinology, 2University of
# R# _- b" _( v  i2 ^( aSouth Alabama Medical Center, Mobile, Alabama.9 U' q7 T: G: Q4 G$ U3 o/ b- K
Address correspondence to: Samar K. Bhowmick, MD, FACE,
# y% _8 Q' e  j9 O, i5 Y# }# m2 uProfessor of Pediatrics, University of South Alabama, College of! e1 H8 u0 ~) M/ Z- ~
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. q4 e+ i  }, C) se-mail: [email protected].; M! M( R9 z9 e9 f: V' M
about 6 to 7 months old, which progressively became* J- X# b& _, E: n2 M
darker. She was also concerned about the enlarge-
4 z% K- \# t' t! ?* ]ment of his penis and frequent erections. The child. U* K& D& {: [3 v
was the product of a full-term normal delivery, with% S6 N( x5 U0 g3 }5 e# h' G
a birth weight of 7 lb 14 oz, and birth length of) O' H) y# l5 ~+ F5 j9 D% r
20 inches. He was breast-fed throughout the first year4 z5 n* z& G$ l6 V) P
of life and was still receiving breast milk along with; |7 C; ^  n3 G: P8 p
solid food. He had no hospitalizations or surgery,7 d% K8 u& c+ d) L' m7 Y9 s
and his psychosocial and psychomotor development" U2 r$ P" P* v& r  I/ s
was age appropriate.% ]8 r2 o/ g, S- b. v
The family history was remarkable for the father,
  h% h8 Z* L1 V" [- ]9 Zwho was diagnosed with hypothyroidism at age 16,5 Q9 o; ]) F9 p2 ~
which was treated with thyroxine. The father’s  `; Y. }$ X2 f0 A  d
height was 6 feet, and he went through a somewhat
, j% V! P. n% f( R/ |2 ?early puberty and had stopped growing by age 14.& C+ F. z* _0 ~3 N# B2 n
The father denied taking any other medication. The
3 v+ X, H2 @! s- G, ochild’s mother was in good health. Her menarche
( r+ w  q/ p- Kwas at 11 years of age, and her height was at 5 feet' r# Z1 u+ Q- I3 K* X! s
5 inches. There was no other family history of pre-  U! Z% h7 d1 I, p5 Q9 j2 E
cocious sexual development in the first-degree rela-5 ?- \) Q( ^! X4 R
tives. There were no siblings.$ N+ ?4 k- d0 `. o+ r  x+ W
Physical Examination' A$ i) `9 @4 W3 G( j* `
The physical examination revealed a very active,/ ?/ \& b6 Q2 m* r3 J
playful, and healthy boy. The vital signs documented7 w9 ?  Y4 |1 |8 T
a blood pressure of 85/50 mm Hg, his length was
( E9 d% ~* F+ o: b90 cm (>97th percentile), and his weight was 14.4 kg% R5 |: _; @# l/ n4 n5 p! K
(also >97th percentile). The observed yearly growth) V: E# @$ w2 o( @- V" W2 _. Z+ E: T
velocity was 30 cm (12 inches). The examination of
' j7 c% i! T* B3 H/ b' z/ ~the neck revealed no thyroid enlargement.
! B) e9 k$ b- c4 b1 VThe genitourinary examination was remarkable for
5 M7 _" c0 T5 R- }- Uenlargement of the penis, with a stretched length of( j+ m: M4 }0 X) C) |% S" |( T
8 cm and a width of 2 cm. The glans penis was very well4 Y' [4 I, k5 ]) ]2 C* |7 a
developed. The pubic hair was Tanner II, mostly around) [7 }0 `1 j) a' X3 e
5402 _' ^: _$ I$ L5 e. ?/ ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& m6 i; ?  E& T  Kthe base of the phallus and was dark and curled. The7 e. X! [8 w# |7 n
testicular volume was prepubertal at 2 mL each.& ?  E5 C4 ~! U4 r; }6 y' a
The skin was moist and smooth and somewhat
2 J# U% O5 f5 Y6 M9 toily. No axillary hair was noted. There were no
0 U8 `" O7 @0 g8 f: n( X1 z3 E& fabnormal skin pigmentations or café-au-lait spots.! g7 D2 z/ U) X8 d& a  Z
Neurologic evaluation showed deep tendon reflex 2+
2 W* y- C. s. b4 a# b! Lbilateral and symmetrical. There was no suggestion4 e& v9 O+ v3 F1 H8 |7 T& O" J/ B9 I
of papilledema.
9 e5 c1 ~2 U* FLaboratory Evaluation
" o4 x0 p) X. {- Q, ^The bone age was consistent with 28 months by
5 S3 U+ `& U9 a  d8 m* [using the standard of Greulich and Pyle at a chrono-- C) e% p. H. W# s5 f3 _0 f
logic age of 16 months (advanced).5 Chromosomal1 \9 L" m- \: p9 ?7 ]
karyotype was 46XY. The thyroid function test' L" V& F5 B# m
showed a free T4 of 1.69 ng/dL, and thyroid stimu-; D" u4 a& G- R. M
lating hormone level was 1.3 µIU/mL (both normal).
; A: e9 @/ g/ O2 }8 KThe concentrations of serum electrolytes, blood7 Z1 y' \7 C) p1 a3 a
urea nitrogen, creatinine, and calcium all were" O  w* y, j; y% f
within normal range for his age. The concentration
- [% G* U2 y; `+ Y8 q" z- H; Qof serum 17-hydroxyprogesterone was 16 ng/dL0 q  M7 l0 f. w& Q
(normal, 3 to 90 ng/dL), androstenedione was 20
5 i. V' b) G, Z# p3 E3 }0 Vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ D; K5 G' o; X# |; L0 P: B5 b4 }! x; \terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 S" T7 ]$ ^6 a4 m' G5 B
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 L' F4 x& V9 N# d( U. @: [* A49ng/dL), 11-desoxycortisol (specific compound S)
9 z5 u. i  g3 f5 D  v1 Uwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ l! [, I; \/ T  h: j
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: q1 I$ Z( u) R% p0 P
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),1 Q; P# _4 _2 ~7 `- S' ^5 h
and β-human chorionic gonadotropin was less than
4 h- J2 i; o& M6 D- u5 mIU/mL (normal <5 mIU/mL). Serum follicular) I. h6 w! S$ [! l3 t
stimulating hormone and leuteinizing hormone
/ n' t# ?. U  L& _1 e: F3 wconcentrations were less than 0.05 mIU/mL% m0 a# H2 j1 U
(prepubertal).; O; G( B/ q2 W
The parents were notified about the laboratory7 E+ M6 s% ~  k3 c: ^
results and were informed that all of the tests were
# o& X9 ?4 y5 K! V% jnormal except the testosterone level was high. The' E' `- F) e$ U2 t% N
follow-up visit was arranged within a few weeks to
% R1 K/ }2 e% @  M* uobtain testicular and abdominal sonograms; how-
% X# l8 g, G% N  E! A; V, kever, the family did not return for 4 months.
. j% R" d' y. ~$ }9 T; |% bPhysical examination at this time revealed that the7 o: `+ O& j$ P' D& B$ _* p- a
child had grown 2.5 cm in 4 months and had gained
5 H& j' k. T9 d2 kg of weight. Physical examination remained4 q7 K7 A) |6 F- p$ |' c0 f
unchanged. Surprisingly, the pubic hair almost com-
! S. u' n1 e7 v) Ypletely disappeared except for a few vellous hairs at
$ s% K6 e+ t0 ^% J+ `$ Y; V- Nthe base of the phallus. Testicular volume was still 2
' d; k# A; [! ?7 g' w+ }! @mL, and the size of the penis remained unchanged.
; v" c: ]7 n* q9 z! EThe mother also said that the boy was no longer hav-1 y$ H/ ^* ?2 w. X4 Z! u
ing frequent erections.4 I6 j  e3 a4 {% g
Both parents were again questioned about use of, f+ m6 ^' C& _9 _; ?5 B6 w& \
any ointment/creams that they may have applied to) B' [' i' Y, K( P
the child’s skin. This time the father admitted the
3 W" t+ T7 U- t$ [/ yTopical Testosterone Exposure / Bhowmick et al 5412 U- ^$ ?; r( |7 ~" h
use of testosterone gel twice daily that he was apply-
1 |/ k- L4 g* `9 {! D% \! Hing over his own shoulders, chest, and back area for0 f6 \* O% p( \
a year. The father also revealed he was embarrassed
$ Z& M+ y6 k" O! _' q7 u# M1 B) N$ Sto disclose that he was using a testosterone gel pre-
- r+ @6 h0 j& \5 `: l5 vscribed by his family physician for decreased libido+ z. H' m1 \; t8 Q- |# E: Y: [( `
secondary to depression.
- V- [) k) [+ \& y' s% l5 OThe child slept in the same bed with parents.
1 V0 U7 {5 _: S" |& nThe father would hug the baby and hold him on his% z' A* W1 h0 U4 I% ~
chest for a considerable period of time, causing sig-1 r/ @! y; a$ J. t; K
nificant bare skin contact between baby and father.
5 w: r' L5 W# J7 L8 O$ QThe father also admitted that after the phone call,
3 z5 z6 y4 t1 a# [when he learned the testosterone level in the baby
+ }( c- t6 c2 W9 e; a+ swas high, he then read the product information" n5 V) z8 }3 {- {  Z
packet and concluded that it was most likely the rea-
8 O+ N7 [; O& m) n# Lson for the child’s virilization. At that time, they
& w: [4 m; E9 ]1 |1 Zdecided to put the baby in a separate bed, and the
5 w1 A! O2 P5 r8 _father was not hugging him with bare skin and had, E) J4 ^6 m7 t  I4 K
been using protective clothing. A repeat testosterone$ ?3 F" k: h" O9 N$ i
test was ordered, but the family did not go to the
, G; J) m2 ?; |& ^! e* x1 A; Claboratory to obtain the test.( }) c9 A) l& T) |) K7 t
Discussion
% a! N0 h% W, {! \' \. a, ePrecocious puberty in boys is defined as secondary  I: C; ]% Y  i% a7 S; }% q: U
sexual development before 9 years of age.1,4
+ C! Y& n$ Z  e- R/ l1 }& S5 KPrecocious puberty is termed as central (true) when
5 h, M" {3 G% ~0 }it is caused by the premature activation of hypo-/ L# ], Z' q) D; Z' U- ?3 C
thalamic pituitary gonadal axis. CPP is more com-
  G6 l9 U7 j1 @mon in girls than in boys.1,3 Most boys with CPP" j3 w7 D) g' O4 `- F8 k2 k
may have a central nervous system lesion that is/ \- g$ j5 o& Y% _3 n' U" x
responsible for the early activation of the hypothal-
/ c0 R% K- H. I/ Iamic pituitary gonadal axis.1-3 Thus, greater empha-
8 d, |9 O/ t# x' T& C2 ?, ysis has been given to neuroradiologic imaging in
+ t1 y/ E* M# O5 Mboys with precocious puberty. In addition to viril-
; ]: I2 m. E: h3 T+ Tization, the clinical hallmark of CPP is the symmet-7 B' c; P9 j. B6 M) a
rical testicular growth secondary to stimulation by9 Z# G6 H& a) e$ v- W: c9 r# }
gonadotropins.1,3
  L+ [6 v2 w/ P' J2 @' K5 BGonadotropin-independent peripheral preco-0 K/ x6 y% R/ f5 n; L# r- O
cious puberty in boys also results from inappropriate
! g+ g) |$ w5 _# [) L2 Candrogenic stimulation from either endogenous or
+ L0 x5 q$ d- [# A1 sexogenous sources, nonpituitary gonadotropin stim-' ]3 c$ c/ h/ L
ulation, and rare activating mutations.3 Virilizing
6 H' O0 Z/ W! v8 Bcongenital adrenal hyperplasia producing excessive) }/ L( C# n+ x# e( U9 @' h0 L
adrenal androgens is a common cause of precocious
! y: p( u1 ^# F/ Upuberty in boys.3,48 t" A. ~$ U& T8 \9 c; Z
The most common form of congenital adrenal
9 D) G- V% D# M. u5 _1 C" Y" ]3 k) j1 Ehyperplasia is the 21-hydroxylase enzyme deficiency.' y5 Y% E) O" F5 o$ l
The 11-β hydroxylase deficiency may also result in
* v" k7 E) b6 {) Yexcessive adrenal androgen production, and rarely,
, j) a, B# q5 j% H* n2 X: W# z5 han adrenal tumor may also cause adrenal androgen
, A) `  j# {/ [. q# c" Zexcess.1,39 \" R4 ^7 J; y% @# n1 t  r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* G  W( h& ~  J1 }* F6 U8 E0 s542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ _& J4 G( l6 T5 O4 ~A unique entity of male-limited gonadotropin-  N& W! h; j& R/ [0 A! e/ e" l( H
independent precocious puberty, which is also known! q, w, u/ J8 q5 t; a: d
as testotoxicosis, may cause precocious puberty at a9 F- M3 Z% ?" I6 b" o
very young age. The physical findings in these boys
& K7 \1 D5 G7 x  t; Z( ^  Bwith this disorder are full pubertal development,5 E# o. l- V  D" K, I# U- j8 s
including bilateral testicular growth, similar to boys6 ?3 [" i8 ~3 t* }6 o1 _2 D
with CPP. The gonadotropin levels in this disorder
6 g( ^' A: o2 F- Care suppressed to prepubertal levels and do not show; O' h9 _) }8 S6 y" ]7 _1 ^
pubertal response of gonadotropin after gonadotropin-# C0 V) z( v! ~" {: }7 O
releasing hormone stimulation. This is a sex-linked
& V' s( y' z5 D9 x3 E! _$ Xautosomal dominant disorder that affects only' L- k& u" B: a! l
males; therefore, other male members of the family
$ b+ K" h+ V8 j; rmay have similar precocious puberty.3
7 a# V1 m$ \4 _$ KIn our patient, physical examination was incon-
) T/ g& z, X* A- V* b5 D5 y" Nsistent with true precocious puberty since his testi-# `2 @' m7 X2 y7 M/ M
cles were prepubertal in size. However, testotoxicosis
+ S) N. f2 H/ Z8 _was in the differential diagnosis because his father
1 i7 X6 |' [0 r* m; wstarted puberty somewhat early, and occasionally,' z0 J$ }- I" j- Y5 B1 ~. T$ m
testicular enlargement is not that evident in the4 C  z/ c# n" z4 b. f8 n
beginning of this process.1 In the absence of a neg-
) A  W. \4 k5 |. p4 N5 t1 F# ?ative initial history of androgen exposure, our
3 w4 c* w* u# J1 }# vbiggest concern was virilizing adrenal hyperplasia,
. b' c1 l) m/ C; Z" Leither 21-hydroxylase deficiency or 11-β hydroxylase
: }( X: b3 {- Vdeficiency. Those diagnoses were excluded by find-% Z! N. A# `% [7 }5 v
ing the normal level of adrenal steroids.
7 r1 c  A3 X7 Z9 N, d+ W0 MThe diagnosis of exogenous androgens was strongly
& V" T0 Z# l0 N' ^$ }* N9 g% ssuspected in a follow-up visit after 4 months because7 X4 k! I# E' M
the physical examination revealed the complete disap-
' m6 \' q! ^! e, N7 Ipearance of pubic hair, normal growth velocity, and
& J+ t. J. X& ]# N' x: z- Ydecreased erections. The father admitted using a testos-# P. ]3 m/ }8 p+ c" E& E. x
terone gel, which he concealed at first visit. He was
$ k$ B5 A6 H' Z+ pusing it rather frequently, twice a day. The Physicians’9 n8 D  O, q# Z+ \/ t- x2 }
Desk Reference, or package insert of this product, gel or! V7 ]8 X: U5 ^5 I2 w
cream, cautions about dermal testosterone transfer to
; c9 j& _2 k5 F% k- h; D2 w* p0 E/ gunprotected females through direct skin exposure.
5 b% g$ a1 @" r& ASerum testosterone level was found to be 2 times the
) ]5 ?$ K0 |9 Pbaseline value in those females who were exposed to' Z1 {) ~0 C7 z0 T/ ^
even 15 minutes of direct skin contact with their male
9 o  D' O& f& ~* Q, R0 ]% y2 Mpartners.6 However, when a shirt covered the applica-8 T% @& ?2 g7 ]. N8 J1 E* ^3 A' U
tion site, this testosterone transfer was prevented.0 v$ O) w. t  ~  F
Our patient’s testosterone level was 60 ng/mL,
4 c: }! t0 x  m( F2 \, Rwhich was clearly high. Some studies suggest that
9 X$ f3 m. K3 `- T+ l# Mdermal conversion of testosterone to dihydrotestos-
! U% n7 S' Z4 ], X0 y: c- W1 jterone, which is a more potent metabolite, is more
& ~# B/ K4 |' y/ vactive in young children exposed to testosterone
; @& a( ?$ A& F/ cexogenously7; however, we did not measure a dihy-
% t  ^# T7 ?0 X1 i6 hdrotestosterone level in our patient. In addition to6 p6 i5 h# S5 h6 E- U- b
virilization, exposure to exogenous testosterone in
+ M9 i3 b2 g3 m% y0 Rchildren results in an increase in growth velocity and! Z# ?8 B: e8 o/ K
advanced bone age, as seen in our patient.  r: A; N+ c$ t7 E0 B
The long-term effect of androgen exposure during
, r& z& z* j$ Z* x% t4 Dearly childhood on pubertal development and final
; v' \* r+ f( C6 S/ p. `adult height are not fully known and always remain) S# \7 t$ C2 f8 I6 P
a concern. Children treated with short-term testos-
- K# D9 Y* v& @$ e9 gterone injection or topical androgen may exhibit some4 w0 B" W4 W+ a/ ~# G9 p4 K  C
acceleration of the skeletal maturation; however, after* Z. h8 H0 g" Y5 c
cessation of treatment, the rate of bone maturation
# O) }( d. k1 ~4 Zdecelerates and gradually returns to normal.8,9" H8 p2 X& P% ~/ I
There are conflicting reports and controversy5 X% d% R6 D( a, B) Z. x  _$ Z
over the effect of early androgen exposure on adult+ Q  e: f& I' h1 i+ O8 V) _
penile length.10,11 Some reports suggest subnormal& E$ V. `' ?, T0 R$ n
adult penile length, apparently because of downreg-
% d' u# `2 m$ U. X6 O( wulation of androgen receptor number.10,12 However,: i0 I5 F  U% n& z" B1 p
Sutherland et al13 did not find a correlation between! h+ h7 P( w0 U  _2 {4 A
childhood testosterone exposure and reduced adult  @( o; D; s$ ]9 Z8 j5 h# X' I* W3 W
penile length in clinical studies.
# |* G+ z/ n5 E0 ]3 ]; oNonetheless, we do not believe our patient is
" u6 x( P2 i% ]going to experience any of the untoward effects from4 T- M$ Q5 J& o0 C1 T* `/ o+ i
testosterone exposure as mentioned earlier because; {9 z3 v. s( D
the exposure was not for a prolonged period of time.
- m1 S5 H# ]8 I5 @* b7 GAlthough the bone age was advanced at the time of
  W4 c; M& s8 s' w9 Wdiagnosis, the child had a normal growth velocity at2 T2 A% T, C1 i, o! w
the follow-up visit. It is hoped that his final adult
+ d" t) g- {: _! bheight will not be affected.
& s+ R+ _. o9 G  O# H9 a. }1 k' GAlthough rarely reported, the widespread avail-
$ @4 j$ |; r9 ~ability of androgen products in our society may7 N9 [) X9 I9 h; d4 z
indeed cause more virilization in male or female, M: y4 X; ^% m# `8 }9 D. a0 `
children than one would realize. Exposure to andro-1 Y6 |' c! k+ h- |& a4 J! Q9 ~
gen products must be considered and specific ques-. b" I) ?5 Z) ^9 v3 P# P; e
tioning about the use of a testosterone product or
( J9 i7 R5 j6 Q" Xgel should be asked of the family members during
9 i  p/ s( S; nthe evaluation of any children who present with vir-1 W* L4 q" ^! d
ilization or peripheral precocious puberty. The diag-
( |( y5 a  U; b3 b6 ]! a0 @0 a% nnosis can be established by just a few tests and by
) Q( K" u+ o$ i9 f, sappropriate history. The inability to obtain such a8 ?/ ?) z7 H9 K
history, or failure to ask the specific questions, may- z7 t( U1 x) j  Q( \4 }, e  a
result in extensive, unnecessary, and expensive- ~8 z9 D7 Y! [9 Z
investigation. The primary care physician should be8 B4 v6 i: I8 P2 q" R
aware of this fact, because most of these children/ A0 p3 o6 H0 h% W4 m
may initially present in their practice. The Physicians’
4 ^- W6 Z, `5 i1 a# gDesk Reference and package insert should also put a2 v4 |0 x3 C& m( V
warning about the virilizing effect on a male or8 q+ S" M4 B- t9 d
female child who might come in contact with some-
$ _6 |! k  R# eone using any of these products.% Y% S, F7 \% R/ A; M5 d
References
! o8 [, }; k% f5 Q! G$ I8 p1. Styne DM. The testes: disorder of sexual differentiation
5 L3 q' y5 g6 a, y' Mand puberty in the male. In: Sperling MA, ed. Pediatric  o' t! w/ }$ ^3 ]# i- A# Y; N
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  ~* Z1 B7 X- g, Z! D1 R2002: 565-628.
; ]9 _6 C! K, H8 u% Z* m2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. q* d4 u2 e2 |8 E2 ~; V+ opuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
9 {' c1 C* j, e/ p, |& RBoy Induced by Indirect Topical
. m0 l4 @8 Q$ SExposure to Testosterone
; U. _/ U8 M+ }7 hSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! T3 v) g1 A: N5 X  h( H# V- E
and Kenneth R. Rettig, MD1
4 T$ a: F4 Y0 X9 n( G6 P- tClinical Pediatrics  J3 k! v3 B8 R, q: |* ]  W
Volume 46 Number 6
3 h$ P' K0 M4 oJuly 2007 540-5435 n3 l" k% t) u7 R" D
© 2007 Sage Publications
0 l' \$ ^  J0 J" s* E& z3 M10.1177/0009922806296651
$ v" P5 l0 S( fhttp://clp.sagepub.com6 a0 _  a4 ]8 o3 r& H4 Y9 I
hosted at
9 }2 f8 H! a" m. s6 E: i1 t- Nhttp://online.sagepub.com
% L, A* L% m. @5 D# J2 WPrecocious puberty in boys, central or peripheral,2 Q% L: p* V; `# Q% {+ U3 j
is a significant concern for physicians. Central7 F) W/ B$ W" t5 X
precocious puberty (CPP), which is mediated
, u: M! W6 Z. h, N/ o# uthrough the hypothalamic pituitary gonadal axis, has+ ?9 W3 S. f3 q) T' o% m
a higher incidence of organic central nervous system
, t- z  c: ]( f; J* K+ ^% hlesions in boys.1,2 Virilization in boys, as manifested
: ?( W, t3 ]$ mby enlargement of the penis, development of pubic
/ F7 X+ r7 G+ }6 v2 U' Q$ \hair, and facial acne without enlargement of testi-% V9 j: H6 z) N3 O6 X5 ^8 N# M; M4 [1 Z
cles, suggests peripheral or pseudopuberty.1-3 We
! ^$ R; x0 n. C; z1 z# Wreport a 16-month-old boy who presented with the
* {8 Z* v! a5 Oenlargement of the phallus and pubic hair develop-
0 C6 Y1 l4 j4 Z' j% D2 I  e5 Iment without testicular enlargement, which was due
; }8 h( M9 U5 ?! D9 J% {to the unintentional exposure to androgen gel used by
8 D! T/ I- o4 a; G* T, lthe father. The family initially concealed this infor-
. @5 M6 z+ M% J) Ymation, resulting in an extensive work-up for this; \! O2 ?* Q" l4 g" a. E% e6 `5 I
child. Given the widespread and easy availability of5 B$ ]9 [+ L: g8 k1 n( [7 u9 i4 |
testosterone gel and cream, we believe this is proba-5 G# i" s) y0 Q" l6 P! \: N
bly more common than the rare case report in the
8 G* J% `+ b$ _4 zliterature.43 h$ E8 N) k% b8 \+ V; |. d
Patient Report" a$ x& g7 `+ L& O& L
A 16-month-old white child was referred to the
8 v! s& R5 W. B/ w! ^7 p, W0 ?endocrine clinic by his pediatrician with the concern! d  S# q9 `3 w1 X( y
of early sexual development. His mother noticed) Q/ ?. \+ C/ C% t1 C2 \
light colored pubic hair development when he was
  b; N8 p  w4 d# i; PFrom the 1Division of Pediatric Endocrinology, 2University of
# o4 e6 j/ z$ j! m, HSouth Alabama Medical Center, Mobile, Alabama.
% B3 @0 `0 R$ S; `8 I' v: LAddress correspondence to: Samar K. Bhowmick, MD, FACE,
6 T+ U' r& k, l9 OProfessor of Pediatrics, University of South Alabama, College of- T  N3 U1 ^- Q' s
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! I3 N, s) E6 V& _( j* z% Re-mail: [email protected].- \# B' u' r8 ]. ^
about 6 to 7 months old, which progressively became
2 n7 y" T1 V( N* y5 H/ T! I( f( adarker. She was also concerned about the enlarge-
+ w! ~; ?( y% I- }6 v# A* Sment of his penis and frequent erections. The child
! E/ W- M8 z( D, k7 mwas the product of a full-term normal delivery, with, c3 ^6 ^, S' T% x' u( ?2 u
a birth weight of 7 lb 14 oz, and birth length of
8 g4 v2 A/ X+ A& f5 |5 ?' n5 J20 inches. He was breast-fed throughout the first year" I! J4 D! w: \; I
of life and was still receiving breast milk along with
" w  A  p! U% r/ ^, xsolid food. He had no hospitalizations or surgery,
/ ?: G2 ?; w5 I1 x9 J& H9 wand his psychosocial and psychomotor development
2 Q2 k: u" W- L$ ?  c. kwas age appropriate.
1 D& q. z( W9 E& {- vThe family history was remarkable for the father,' X7 F- v% P! O* j
who was diagnosed with hypothyroidism at age 16,$ {# y) j+ `! Y/ ~
which was treated with thyroxine. The father’s* \4 y; s6 B% V$ D% L. e* d; v
height was 6 feet, and he went through a somewhat) H* L. d  g1 B' u9 g& |1 M
early puberty and had stopped growing by age 14.% J0 r. y3 G& b4 e; U
The father denied taking any other medication. The/ r/ e$ O- T4 w4 Q4 Q! H7 Y
child’s mother was in good health. Her menarche, ]0 M7 a+ `( s) {( {/ S
was at 11 years of age, and her height was at 5 feet
3 p3 q( M. @: [( K( j3 r5 inches. There was no other family history of pre-; A5 W2 K* f/ ]/ @( g; t# L7 T
cocious sexual development in the first-degree rela-
: s" k5 d" C9 x" W, ^/ M$ `/ Stives. There were no siblings.; h$ P6 z; A2 K
Physical Examination
, C2 a9 @2 p' G. z$ QThe physical examination revealed a very active,- r( v: x# l' H* @
playful, and healthy boy. The vital signs documented
, L$ q5 V- I( r, Ma blood pressure of 85/50 mm Hg, his length was
" Z1 p% ?# l- b& q/ m3 }2 }90 cm (>97th percentile), and his weight was 14.4 kg6 n5 H3 Q. j8 Z: R' @& T% |- p
(also >97th percentile). The observed yearly growth% l. Y9 O' ?1 N& M1 K
velocity was 30 cm (12 inches). The examination of$ ~+ C) z! [  Y1 k) e. B
the neck revealed no thyroid enlargement.
8 Z/ o) f! Q9 F3 A0 D) KThe genitourinary examination was remarkable for2 O' e0 ]9 ~* O/ g) S8 Y: Y2 _
enlargement of the penis, with a stretched length of
' K- p& q( c" w& J2 T! a8 cm and a width of 2 cm. The glans penis was very well* a6 v" J1 m% P6 N+ I
developed. The pubic hair was Tanner II, mostly around
4 |5 w' P. g) r+ r' z& O4 ?540
% Z; E6 h. m. Q, O) R# u- iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 ~( j) f5 e6 L5 ?the base of the phallus and was dark and curled. The$ F6 U9 k: u" H0 n9 m
testicular volume was prepubertal at 2 mL each.7 I3 I( t: t' `. [' S
The skin was moist and smooth and somewhat
7 f' O) ~0 C1 ^7 [: k0 s1 y. Roily. No axillary hair was noted. There were no4 P. h3 |5 a2 Q9 _0 z
abnormal skin pigmentations or café-au-lait spots.
6 ]0 E8 a. c8 W# I' L" A! J$ rNeurologic evaluation showed deep tendon reflex 2+
% X* N8 F/ Q8 x9 Abilateral and symmetrical. There was no suggestion
: K* R2 X5 ^3 {5 ]of papilledema.5 e: d( {% M# }, k' z  O
Laboratory Evaluation
- @' ]2 U9 V% u7 G% c$ sThe bone age was consistent with 28 months by
; F1 z4 N( P: e4 ]using the standard of Greulich and Pyle at a chrono-7 L3 o! U  w7 z
logic age of 16 months (advanced).5 Chromosomal
. C- \- {( U6 D0 E6 f7 u- q& ?karyotype was 46XY. The thyroid function test
6 Z4 M1 Y9 W, s. |( l( R% hshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
  p# Q1 s+ v, [7 O7 K8 b7 klating hormone level was 1.3 µIU/mL (both normal).
3 o- H: \0 z4 r4 c1 ?The concentrations of serum electrolytes, blood  `+ Q  n" H0 O  `% G
urea nitrogen, creatinine, and calcium all were
+ }3 I0 e4 H2 m' D, D! Xwithin normal range for his age. The concentration
" N, o3 K$ [2 ~$ z/ A; K: K9 yof serum 17-hydroxyprogesterone was 16 ng/dL
+ f- G1 h* n6 f! u9 s(normal, 3 to 90 ng/dL), androstenedione was 20
. c- {, s4 U) G* K9 A, I  Wng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) O# m) ?8 X( y- [% `5 Vterone was 38 ng/dL (normal, 50 to 760 ng/dL),! a) l, W0 }; k9 G! x
desoxycorticosterone was 4.3 ng/dL (normal, 7 to/ \# F, K$ j6 b3 c! G. p
49ng/dL), 11-desoxycortisol (specific compound S)
  \) d; d& c" X' ^0 r5 Uwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 k' z9 l5 [# e5 o: D
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 ?. p5 O& V2 p: M
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
: V2 O( b: p5 Jand β-human chorionic gonadotropin was less than
$ v) ~, J7 }( q/ T; d7 J5 mIU/mL (normal <5 mIU/mL). Serum follicular
( M5 w$ y& W- l# z2 h: O% }. bstimulating hormone and leuteinizing hormone" X2 q( B  [& d0 G
concentrations were less than 0.05 mIU/mL; _" o- O! q0 L, C2 G; r& t+ h* M
(prepubertal).$ A  y+ e0 G6 C$ M
The parents were notified about the laboratory
% T5 ?3 U' \4 w$ t5 lresults and were informed that all of the tests were
  S+ `! y8 v5 W& z% Lnormal except the testosterone level was high. The
4 R, Y" d" {7 Ofollow-up visit was arranged within a few weeks to6 i9 s8 E3 L: n9 h
obtain testicular and abdominal sonograms; how-
# s8 c- }1 o6 `& Y1 y  i# jever, the family did not return for 4 months.. Z5 m$ l2 U5 P( g% c3 a
Physical examination at this time revealed that the
& E. j  G; q# s1 f. R- G* s# ~child had grown 2.5 cm in 4 months and had gained+ {6 z% w& p) w
2 kg of weight. Physical examination remained4 |7 G- d& N6 I
unchanged. Surprisingly, the pubic hair almost com-) C. ]( S4 `  P, `* A" `5 c
pletely disappeared except for a few vellous hairs at
4 l. a0 C8 @' m! t1 M( gthe base of the phallus. Testicular volume was still 2
9 Z1 a& g5 N* {# N6 a: BmL, and the size of the penis remained unchanged.! w* ^" B( f( t- s
The mother also said that the boy was no longer hav-; R8 {. [( v4 u7 X' s! N/ _
ing frequent erections.9 w' X; t( T6 ^: r
Both parents were again questioned about use of5 E# B1 m3 D- k' ^% h
any ointment/creams that they may have applied to
9 x+ F! D  @: a2 o1 zthe child’s skin. This time the father admitted the
  E$ q6 Z3 |4 ]2 }) t# C& U1 ATopical Testosterone Exposure / Bhowmick et al 541
" t/ s/ I* l1 u9 D, ?use of testosterone gel twice daily that he was apply-
2 Y! ^" @4 P4 eing over his own shoulders, chest, and back area for
, S  W) E, V! T$ Aa year. The father also revealed he was embarrassed
8 u$ w  B7 z4 a( Dto disclose that he was using a testosterone gel pre-9 u; H: z  c# j. s& \% U
scribed by his family physician for decreased libido* j- b7 t  W: m. H1 ]
secondary to depression.9 Q: P  @4 x  b$ m* O* V
The child slept in the same bed with parents.  m. I; f& t( C; B
The father would hug the baby and hold him on his& ^$ {1 [7 W: L. ^" V; z
chest for a considerable period of time, causing sig-3 y; n% S# Y( T6 s2 `# [6 K+ \
nificant bare skin contact between baby and father.1 G, @. L' J% r
The father also admitted that after the phone call," o" T, D; s4 u
when he learned the testosterone level in the baby
: P. V+ Q8 t; C' b+ Twas high, he then read the product information* ]: c' i. _4 [/ p9 F' S: Z
packet and concluded that it was most likely the rea-
: |6 `! A+ u+ V( `* ^4 eson for the child’s virilization. At that time, they2 o' j% f1 v9 R! V7 a0 c0 b
decided to put the baby in a separate bed, and the, t4 E7 ?- j, U/ g
father was not hugging him with bare skin and had
& r, F3 R; o4 [( Obeen using protective clothing. A repeat testosterone
0 q  q6 r. P4 }! U9 ztest was ordered, but the family did not go to the: ?* F2 E! o9 d2 {' v; S
laboratory to obtain the test., B( j4 v  Y9 A- x2 b8 o  ^  M
Discussion8 g, w/ s% d- Z: u; Z7 y& M" {
Precocious puberty in boys is defined as secondary
: t' ~. X) A8 xsexual development before 9 years of age.1,40 w  Y& @+ i. }9 {* d! z1 C
Precocious puberty is termed as central (true) when
4 c; I0 }2 B- Q) j' z; {it is caused by the premature activation of hypo-$ n* W2 Q% w1 }+ o
thalamic pituitary gonadal axis. CPP is more com-
  v- v) Y: F& K0 mmon in girls than in boys.1,3 Most boys with CPP" F- p* z3 M, a: `. l
may have a central nervous system lesion that is6 j6 S3 k( g( _6 v" l  b0 L
responsible for the early activation of the hypothal-$ L5 v2 w0 l5 Q# g# s# t
amic pituitary gonadal axis.1-3 Thus, greater empha-
7 {! G( _0 r+ l: wsis has been given to neuroradiologic imaging in3 a* }$ h! g$ S
boys with precocious puberty. In addition to viril-
$ n- m& F5 v$ `* b0 J. u/ Tization, the clinical hallmark of CPP is the symmet-, y3 }! }3 S1 H4 P. c* y
rical testicular growth secondary to stimulation by% C5 M& }, p7 ^& H' N/ B4 k% ^+ H
gonadotropins.1,3/ u! R8 x+ K& J1 z! j$ k! q
Gonadotropin-independent peripheral preco-
& K$ O* \4 s4 {cious puberty in boys also results from inappropriate
1 X& H' ?- G: G5 `3 {9 eandrogenic stimulation from either endogenous or* K* d* _- }) i, G  r  w3 n8 B
exogenous sources, nonpituitary gonadotropin stim-2 n2 K- s1 t! Z5 \. X
ulation, and rare activating mutations.3 Virilizing" t  f1 }& r6 Q5 H
congenital adrenal hyperplasia producing excessive
; W4 j9 E5 g4 A9 Q7 P) Aadrenal androgens is a common cause of precocious
- `) ^7 K+ Y! {7 L& j% W+ t9 Mpuberty in boys.3,4
1 b$ J, e7 e1 _6 HThe most common form of congenital adrenal
+ u3 `* V  X: yhyperplasia is the 21-hydroxylase enzyme deficiency.$ d3 u* i1 s9 ^' {
The 11-β hydroxylase deficiency may also result in
( n1 V# x- h" m7 Hexcessive adrenal androgen production, and rarely,/ j6 D. D  g' N8 W
an adrenal tumor may also cause adrenal androgen/ L7 O: |9 y& F% H% g/ \5 _
excess.1,3# L5 I1 L  M: G' T! C* n' H! s
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% P9 N2 g. q4 K3 }! G
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! a, e) U8 Q" t# m) wA unique entity of male-limited gonadotropin-
: `4 ]7 Y: j# M& r1 Windependent precocious puberty, which is also known
1 S9 B3 p2 q6 q, [; ]9 b$ xas testotoxicosis, may cause precocious puberty at a; _6 i% ^7 o2 M& B; h0 s6 b
very young age. The physical findings in these boys9 t( R, p9 G' K( G& b
with this disorder are full pubertal development,# l) ?; ~' r1 a
including bilateral testicular growth, similar to boys+ m% U4 H5 e( |' _! {8 j! {' d
with CPP. The gonadotropin levels in this disorder
; \/ I. r; i2 b/ }0 Qare suppressed to prepubertal levels and do not show" \$ N8 a5 B& s) O+ E8 Z- u$ w
pubertal response of gonadotropin after gonadotropin-
% S! O: k( X7 W1 [: @: ~releasing hormone stimulation. This is a sex-linked- Q( M) r! g) w% ~
autosomal dominant disorder that affects only4 j+ q" K+ M# O$ T  i
males; therefore, other male members of the family6 g. F% t$ Z7 s5 D
may have similar precocious puberty.3; Z9 S8 W1 k( y; R' _$ n  S3 V
In our patient, physical examination was incon-
& r7 W# L% P" G/ `  B, ?2 Z: B$ O5 ksistent with true precocious puberty since his testi-7 i9 I; G4 ?. [7 q2 x
cles were prepubertal in size. However, testotoxicosis
% m1 V( J" ^7 U. h+ p- C8 Swas in the differential diagnosis because his father
6 x% m% k/ `- P0 P- k, C/ qstarted puberty somewhat early, and occasionally,% \4 i) ^9 O0 j- G* [' \: N7 _" i
testicular enlargement is not that evident in the0 b- d# f% |: r5 k' ]- H
beginning of this process.1 In the absence of a neg-- x) ~, U! l2 @) n8 P1 g
ative initial history of androgen exposure, our
2 Z) O2 z/ I& j& v. {biggest concern was virilizing adrenal hyperplasia,
5 j5 ?$ _# g0 L3 O! l- Feither 21-hydroxylase deficiency or 11-β hydroxylase
# p! n6 X. C) Hdeficiency. Those diagnoses were excluded by find-: K6 k9 w! M6 \
ing the normal level of adrenal steroids.
1 S6 z' s$ Z* `6 V# c+ m, P0 dThe diagnosis of exogenous androgens was strongly+ t( H; r* r0 p& Q; C! L' ?8 s: U
suspected in a follow-up visit after 4 months because7 e  z% F1 [5 @' [9 h7 C
the physical examination revealed the complete disap-
! m4 j+ d% `$ K$ ~' J) xpearance of pubic hair, normal growth velocity, and
# z$ a% A+ C" `  D2 s3 ndecreased erections. The father admitted using a testos-+ b0 f5 `& f! M( G1 I
terone gel, which he concealed at first visit. He was; V0 g* L! o: s0 {2 Y
using it rather frequently, twice a day. The Physicians’
. x1 B8 I4 X- a) O# N" FDesk Reference, or package insert of this product, gel or  |; I( }$ U) _2 u/ j
cream, cautions about dermal testosterone transfer to# E. l, |  T! T8 @4 m8 V, N
unprotected females through direct skin exposure.0 E- j  x: h* M& t
Serum testosterone level was found to be 2 times the1 U% t; A: S5 y. @/ C3 W
baseline value in those females who were exposed to
- Q& h* ~: d/ I  C+ @* [" ]even 15 minutes of direct skin contact with their male* E8 U4 {0 G; o  t! r6 l8 w) M
partners.6 However, when a shirt covered the applica-
( ?+ o+ f4 ^. k& \  v" H% ition site, this testosterone transfer was prevented.
- R3 \& e8 X0 lOur patient’s testosterone level was 60 ng/mL,
' a- |  _# }: e& iwhich was clearly high. Some studies suggest that" V/ Q' i; j6 s8 T( z7 w
dermal conversion of testosterone to dihydrotestos-5 q: U- a0 ~3 d* z% {
terone, which is a more potent metabolite, is more8 m& M& J" b$ V8 z# }- S9 Y6 v
active in young children exposed to testosterone! [6 }$ P: H, U/ ?5 u7 B( V
exogenously7; however, we did not measure a dihy-( G5 G4 n" `  l, w/ S- h3 _  k
drotestosterone level in our patient. In addition to
/ j1 d0 Y! X& B: w7 C  c. cvirilization, exposure to exogenous testosterone in0 X$ J0 V( _! F6 b
children results in an increase in growth velocity and
  D6 C( a  ~: b' Q2 }/ }advanced bone age, as seen in our patient.
8 \7 s' {# N: K  c  g) u7 {The long-term effect of androgen exposure during
" N5 @1 x2 J) M- `early childhood on pubertal development and final2 ^+ ~- ^% k: N' q+ o7 H) l
adult height are not fully known and always remain) r+ ?2 d& ^  I" }& Q+ F
a concern. Children treated with short-term testos-$ M8 [6 O2 H+ Q6 L3 t$ i
terone injection or topical androgen may exhibit some
: D& t! C8 |8 `acceleration of the skeletal maturation; however, after
! X" j& B! o% t$ ^( y& }cessation of treatment, the rate of bone maturation
* \: ~" F3 o5 X) n8 cdecelerates and gradually returns to normal.8,97 Y& m' z7 z! K6 m8 G$ n# l
There are conflicting reports and controversy
5 j3 m& V  u+ H9 S2 R& @; Fover the effect of early androgen exposure on adult" J2 L6 ]$ s' X
penile length.10,11 Some reports suggest subnormal; h  j( C( ?# \' b
adult penile length, apparently because of downreg-
% Y' E; `7 n. p6 Qulation of androgen receptor number.10,12 However,# J0 o& n: e# b0 d' N+ ~( A3 j
Sutherland et al13 did not find a correlation between
2 H1 t; P8 x1 F" {7 Lchildhood testosterone exposure and reduced adult
+ d6 Y  }6 a: y2 g. Npenile length in clinical studies.! |/ O' k$ v; B! K  B/ |8 `
Nonetheless, we do not believe our patient is- O. Q9 t4 k' ?% p" c) f- ~! x, E1 T
going to experience any of the untoward effects from/ k2 o5 ^3 W$ T5 z3 A+ _  o# Y- p
testosterone exposure as mentioned earlier because2 [+ C. V, E/ T! t
the exposure was not for a prolonged period of time.9 d& c  f! f& X
Although the bone age was advanced at the time of
$ I8 }* B, u* E, q7 f8 ~  C4 U" ydiagnosis, the child had a normal growth velocity at7 y# Y7 J8 g" B1 Z& f( A$ |# _
the follow-up visit. It is hoped that his final adult( I+ f& z* W% @, B( {' z# t
height will not be affected.
9 t! C9 K+ X: u+ ^Although rarely reported, the widespread avail-/ N2 |- T, \. I
ability of androgen products in our society may
% I! c0 x" {6 }; ~  mindeed cause more virilization in male or female( c2 u, j# e' e2 p. I
children than one would realize. Exposure to andro-
7 |9 v0 m2 {# U( C1 o, n0 P6 }gen products must be considered and specific ques-4 |6 y! P: M7 G7 a& E
tioning about the use of a testosterone product or
' f7 {. d2 ]( H1 u. Hgel should be asked of the family members during
  t7 b+ _9 Q( a% Y: T$ z7 xthe evaluation of any children who present with vir-
0 L' Y4 n* k% {/ G  p! T( `ilization or peripheral precocious puberty. The diag-5 ?- X( o! u0 ]4 Y/ R) G5 j, I
nosis can be established by just a few tests and by
9 ]4 Z- Y. u- o! u, xappropriate history. The inability to obtain such a
5 x% T; Y  p7 ]! f* D9 Z  phistory, or failure to ask the specific questions, may3 _# G$ t8 _) B
result in extensive, unnecessary, and expensive, m* m& a( l8 v  \! x7 p6 g" d
investigation. The primary care physician should be
/ ?# O' u' ?8 u! }4 xaware of this fact, because most of these children- S, ~5 C* s% x
may initially present in their practice. The Physicians’6 H9 v8 f, p3 L" H- z
Desk Reference and package insert should also put a
- V$ K6 _) ~  Z; b9 nwarning about the virilizing effect on a male or
, @9 c( l5 u9 `) f: Ffemale child who might come in contact with some-
* }2 [( p: k6 Z2 N! _  done using any of these products.$ t, Q5 o- z7 h/ z1 m
References
1 u7 G5 ~' R; |, `1. Styne DM. The testes: disorder of sexual differentiation
3 I; w8 n) p2 X' F6 k, e0 F& xand puberty in the male. In: Sperling MA, ed. Pediatric4 j: `# H# h  `
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;9 L/ E& }. k9 F( S9 M
2002: 565-628., A; C. o1 @1 F9 D. F2 K
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# q) M+ Z( {! {3 z
puberty in children with tumours of the suprasellar pineal
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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
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?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
# u3 y: f+ q3 d4 \5 Y9 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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