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Sexual Precocity in a 16-Month-Old# e0 `4 D: G- \7 O* F6 S+ B
Boy Induced by Indirect Topical
# [9 z( d9 j# GExposure to Testosterone
- [4 j( ]5 r" R  m1 NSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
3 `% Y6 S2 C- i- u3 y5 R0 zand Kenneth R. Rettig, MD1
4 k9 s' m1 Y; p/ _6 S2 B) i* dClinical Pediatrics' V7 z$ w: H" P" f' g/ ^: W0 R  e
Volume 46 Number 6, W; M; A! O5 c: @7 p9 Z
July 2007 540-543
; ~5 Z; F# ^9 l; ?; Z© 2007 Sage Publications* [, a) d; |2 T/ Z/ ^0 {+ C3 q
10.1177/0009922806296651
4 \- H6 F4 B% e6 \& V4 nhttp://clp.sagepub.com. g, L2 H, J" T% c6 E. c9 ?" |
hosted at
/ x- `5 x! k9 Q7 ~% Hhttp://online.sagepub.com. X1 V8 n: d9 a: P9 n# n, p
Precocious puberty in boys, central or peripheral,5 i& |7 P5 m0 Z
is a significant concern for physicians. Central
6 x& p5 ?+ @" V* ?precocious puberty (CPP), which is mediated2 t& I) N+ K6 z: k
through the hypothalamic pituitary gonadal axis, has
, w, |. }7 W8 a$ ?9 Sa higher incidence of organic central nervous system
5 u% D8 H6 ^/ [* j, clesions in boys.1,2 Virilization in boys, as manifested8 |2 V1 v. a' C; G
by enlargement of the penis, development of pubic
! c& D  x6 J: Yhair, and facial acne without enlargement of testi-& H$ _" e$ q2 {! U8 ]6 Y5 r- q+ D$ e+ V7 F
cles, suggests peripheral or pseudopuberty.1-3 We$ L7 s5 m1 Z9 _9 q
report a 16-month-old boy who presented with the4 J0 y4 }3 e% k! X0 a& f6 x' g
enlargement of the phallus and pubic hair develop-' `& f8 x1 L3 Q3 W0 d# d$ a
ment without testicular enlargement, which was due
& e  D" e5 F/ N3 E& V  ?. }to the unintentional exposure to androgen gel used by% \* v/ O* _/ A( o
the father. The family initially concealed this infor-
2 w) L- y) \: w, E% B  smation, resulting in an extensive work-up for this
( _  b( r9 S4 A6 H6 J6 K$ achild. Given the widespread and easy availability of4 D# j7 Q9 H% y8 c
testosterone gel and cream, we believe this is proba-
! |" \8 q/ K0 o$ n" ~! P6 \bly more common than the rare case report in the6 g% C: R* N7 B+ ^
literature.4
2 V. a' G8 @& i0 IPatient Report! M" z7 t" P0 R! q" n+ s( o
A 16-month-old white child was referred to the
' o' v3 @  Z8 j' d) uendocrine clinic by his pediatrician with the concern
, B, c' Y' ~8 T. Q# kof early sexual development. His mother noticed% N2 b/ a6 |) D
light colored pubic hair development when he was: h8 S  A) {/ F2 N( I9 f3 B9 o
From the 1Division of Pediatric Endocrinology, 2University of
6 }7 q1 f1 b! G3 ^, l) ~South Alabama Medical Center, Mobile, Alabama.
! Q7 P4 B3 j) zAddress correspondence to: Samar K. Bhowmick, MD, FACE,, T$ K8 j# ?$ F* Z; V! j4 Z
Professor of Pediatrics, University of South Alabama, College of5 F; c9 P: N! z
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 I- I9 P  B3 N7 B1 J# E
e-mail: [email protected].
+ [- G" C: |8 v$ ]/ A" T: Labout 6 to 7 months old, which progressively became
! }5 J/ w* B& r' s# z/ Jdarker. She was also concerned about the enlarge-  m9 o. G5 J+ h9 |! x
ment of his penis and frequent erections. The child
4 c( l+ w# p9 Q9 u$ h/ p  A* ^was the product of a full-term normal delivery, with
3 R' J1 E; H" n% la birth weight of 7 lb 14 oz, and birth length of
! t, Q% z4 V( i, |20 inches. He was breast-fed throughout the first year% Q: f; N- s/ r+ Q; Z
of life and was still receiving breast milk along with
2 F; W- [6 A. H3 r* `; Nsolid food. He had no hospitalizations or surgery,1 M4 \! I" E# q
and his psychosocial and psychomotor development; D5 U2 \" u8 x+ h9 n" `
was age appropriate.
8 j; F$ i1 _$ ~. p3 L) v; _8 V* zThe family history was remarkable for the father,
+ o# O  T: Z& I. R' x' nwho was diagnosed with hypothyroidism at age 16,
, K% G# S& I1 ]: Kwhich was treated with thyroxine. The father’s
  l0 J% d9 k& b; D9 {9 zheight was 6 feet, and he went through a somewhat
4 b+ e( f$ x0 T4 a+ R6 mearly puberty and had stopped growing by age 14.: t9 m' K, o& B8 Z& X
The father denied taking any other medication. The
+ O+ i1 p9 M  D2 R, rchild’s mother was in good health. Her menarche
4 `+ U" ^! q- Q3 Twas at 11 years of age, and her height was at 5 feet
& V  t3 T8 e1 ~9 t2 I/ g7 X5 inches. There was no other family history of pre-& B6 G- a8 r7 c! x  D
cocious sexual development in the first-degree rela-
* D6 M6 n8 S. ?- Z' O( [3 rtives. There were no siblings.
, |5 r, R+ c5 k; iPhysical Examination; H  t5 N' U0 ]& u6 i
The physical examination revealed a very active,
5 O, ^0 p" x' K) I; |& yplayful, and healthy boy. The vital signs documented8 _( H! V, n9 L7 H! d
a blood pressure of 85/50 mm Hg, his length was
5 F( Y3 V( u* p& d9 d& v  h+ J90 cm (>97th percentile), and his weight was 14.4 kg4 b" }$ f  T" K
(also >97th percentile). The observed yearly growth& p5 f9 V; o5 e
velocity was 30 cm (12 inches). The examination of
: ^! X; B. |! d( u1 uthe neck revealed no thyroid enlargement.
3 @9 f1 h& P0 D4 w# rThe genitourinary examination was remarkable for
: \% C+ W* ]$ O( k' o& |enlargement of the penis, with a stretched length of
* V* \! H. O/ Z, |8 cm and a width of 2 cm. The glans penis was very well
. m. O. @  t% d  m/ g* Z" `developed. The pubic hair was Tanner II, mostly around$ r( e& n, G' h; R( N. z' a
540' j( \2 d9 j. ?
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the base of the phallus and was dark and curled. The4 P3 C; n* w( k; V# S) G
testicular volume was prepubertal at 2 mL each.
; ^. K3 c7 L% ?  e/ WThe skin was moist and smooth and somewhat
. N- b* G' z1 ~" n- Z- l$ I( a& Goily. No axillary hair was noted. There were no) v0 y. C6 j$ R% ]1 k7 [' d' ^
abnormal skin pigmentations or café-au-lait spots.! T3 h. c$ n% m
Neurologic evaluation showed deep tendon reflex 2+
. K9 }* `2 r4 s) U# Rbilateral and symmetrical. There was no suggestion
' Q1 \, [" B- rof papilledema.
; e* R: l5 N1 V& _1 e+ ALaboratory Evaluation
+ F  n( d4 V0 n) uThe bone age was consistent with 28 months by2 A4 J" e$ ^+ n8 w
using the standard of Greulich and Pyle at a chrono-+ k8 b5 `% c0 f2 ?
logic age of 16 months (advanced).5 Chromosomal
6 Y0 A6 J+ x) N5 v$ dkaryotype was 46XY. The thyroid function test1 k" u* ^6 g* }
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 w, p6 h" x5 c; P/ Q7 f- [lating hormone level was 1.3 µIU/mL (both normal).0 E& d+ `' v; X. y0 M
The concentrations of serum electrolytes, blood; _* Z+ _9 b% ?, ^) t/ k4 Z/ }$ C0 k
urea nitrogen, creatinine, and calcium all were- c! o9 e  j% ~
within normal range for his age. The concentration
2 g3 U, d+ z/ T3 Q, Z$ n' Dof serum 17-hydroxyprogesterone was 16 ng/dL9 Z; T' G- F3 N. Z! {4 l) V; x
(normal, 3 to 90 ng/dL), androstenedione was 20
1 L8 F, P4 q/ l8 V$ Zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* P1 f2 \& ~- J  J
terone was 38 ng/dL (normal, 50 to 760 ng/dL),6 x; _; ]$ L# V- j: |  T
desoxycorticosterone was 4.3 ng/dL (normal, 7 to( v- E2 x6 a' {( R  p& z/ Z4 {+ o
49ng/dL), 11-desoxycortisol (specific compound S)5 I& z8 w0 `. ]8 l9 V9 l% K# N, Y
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" q! ~& H5 x7 I% H) v% k
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" w, V+ e7 k2 h5 r6 O0 z% \
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 S+ n! Q# H4 u/ x; b: l, {, m$ |% ~and β-human chorionic gonadotropin was less than
" G' }" `7 A1 g+ x5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 Z" i9 C3 l. B7 b) ?( d+ f) ]+ dstimulating hormone and leuteinizing hormone
5 g+ q4 _/ }/ x( a  \concentrations were less than 0.05 mIU/mL
/ X. L9 V2 ?# K9 K7 j: k(prepubertal).8 f8 o, _3 S0 M$ {* ]
The parents were notified about the laboratory; a, [4 A+ O! b! T/ N: b
results and were informed that all of the tests were
  G5 u, h6 N  A! A: O' \normal except the testosterone level was high. The5 p) t- y$ Q& g
follow-up visit was arranged within a few weeks to
" I$ `9 d0 T! O' w& k$ J$ c( \obtain testicular and abdominal sonograms; how-# I8 @3 a% L- s% B: R4 n1 q. b
ever, the family did not return for 4 months.; ^  f5 ~1 i' U) K# a/ j
Physical examination at this time revealed that the1 M) F1 E: h& g) K
child had grown 2.5 cm in 4 months and had gained9 B8 y% O. Z) K( Y; X5 \2 Z. F) @
2 kg of weight. Physical examination remained
9 y0 S: O& i  m1 b. [8 U, A* Sunchanged. Surprisingly, the pubic hair almost com-
# v. i; d% o8 O0 V( D; {% @7 F$ x1 mpletely disappeared except for a few vellous hairs at
7 ?. o8 |( X+ }3 X, r5 I/ G$ Cthe base of the phallus. Testicular volume was still 2
7 f. A! l: j; k$ \' t3 a2 TmL, and the size of the penis remained unchanged.
# l! d( J8 N1 x2 `& G( F" QThe mother also said that the boy was no longer hav-
( e  G- r* z* v5 ?5 w7 cing frequent erections., n  o; E& a) l2 x
Both parents were again questioned about use of/ L5 n1 u: X+ r1 l; A
any ointment/creams that they may have applied to
' c0 g, s; B' C& R4 B0 Kthe child’s skin. This time the father admitted the; \% b( \" d2 A! j1 f
Topical Testosterone Exposure / Bhowmick et al 541+ p* `) U" C1 P' F) }  B
use of testosterone gel twice daily that he was apply-7 K. @; ~/ u) r: i1 S( c( ^# l
ing over his own shoulders, chest, and back area for
- X5 \) ]6 X8 a- M! ^a year. The father also revealed he was embarrassed
( K3 q2 E; `- J+ X8 n( y2 [% Mto disclose that he was using a testosterone gel pre-
2 @6 _& Z" {$ D: I* f* `* `scribed by his family physician for decreased libido5 n* F% O9 F5 Q% q4 `
secondary to depression.
6 P; W$ b: h0 O" k) S* AThe child slept in the same bed with parents.
& O5 o+ n. b+ y* AThe father would hug the baby and hold him on his
3 Z" j! G/ T! ichest for a considerable period of time, causing sig-
4 ^$ I- |6 x9 ?$ \/ enificant bare skin contact between baby and father.4 i; \9 s0 t9 j2 z0 F  a, f' G, q
The father also admitted that after the phone call,
- x0 |% Q5 i2 g' h; i" Swhen he learned the testosterone level in the baby; n6 h! G& R. {$ J
was high, he then read the product information' C/ R" T# }1 F& u4 ^2 g& X/ d
packet and concluded that it was most likely the rea-
0 z! l  |8 ]( i1 bson for the child’s virilization. At that time, they$ u$ e' _! |# |9 Y$ Y3 t/ j
decided to put the baby in a separate bed, and the
. z9 P' L: s) i5 E; F/ x/ I2 Ufather was not hugging him with bare skin and had
1 R$ F$ M6 A( G9 D3 ?) \5 gbeen using protective clothing. A repeat testosterone
9 i3 G2 y* Z. v: ltest was ordered, but the family did not go to the
& D% T7 O8 v  i) ^$ H) rlaboratory to obtain the test.
8 K/ b; j% I" |% [; B2 _7 hDiscussion4 H) g4 ^/ Y) J3 _: N' h
Precocious puberty in boys is defined as secondary+ r* _& C1 O2 N% b6 X$ O7 v# V
sexual development before 9 years of age.1,4
3 _/ ^  Z3 V+ L! I. O3 vPrecocious puberty is termed as central (true) when' M' X* r9 |' w  `& y# q0 u# q4 c* W
it is caused by the premature activation of hypo-
3 i. i: Y, Y  B6 l, i: Zthalamic pituitary gonadal axis. CPP is more com-1 r+ g. Y- |5 o7 B: `
mon in girls than in boys.1,3 Most boys with CPP
- ~' p* t) b' Q$ r' |$ D/ Hmay have a central nervous system lesion that is
0 k$ o/ T) n% `& m9 Fresponsible for the early activation of the hypothal-! v% n, R4 T7 |" O  r' ]6 T( X
amic pituitary gonadal axis.1-3 Thus, greater empha-
; X' M5 K6 R7 t8 C8 u- U' xsis has been given to neuroradiologic imaging in
: s: [$ N3 X, ]$ q# R9 d% Nboys with precocious puberty. In addition to viril-3 ^  r% h# b2 O7 O& `
ization, the clinical hallmark of CPP is the symmet-: Z2 g0 G. C4 L/ ~0 ]8 l
rical testicular growth secondary to stimulation by/ r  x- n' T+ b8 ]/ ^% z
gonadotropins.1,3
. `3 S" d' c  [" Y- W+ sGonadotropin-independent peripheral preco-
) e: @, l0 l+ h+ e4 K6 h; U/ m# zcious puberty in boys also results from inappropriate
6 P0 p" @% l1 }" U6 l7 ?androgenic stimulation from either endogenous or9 y, a+ g. R1 t4 u, o7 B
exogenous sources, nonpituitary gonadotropin stim-+ G* g. T6 C  l( V' Q
ulation, and rare activating mutations.3 Virilizing. n  M, c) p; B8 ?3 G  [
congenital adrenal hyperplasia producing excessive# O& q3 z5 s: \2 D% v" ~8 k+ Y
adrenal androgens is a common cause of precocious
# @( E. _! |7 c4 k  Opuberty in boys.3,4
# e. J. Q$ ~* P5 C$ h, oThe most common form of congenital adrenal
, [3 R6 _/ ^: ?# g. Yhyperplasia is the 21-hydroxylase enzyme deficiency.
( e  f: v, \# y% Z* i  Q( ZThe 11-β hydroxylase deficiency may also result in: R% [8 S: j0 a0 E1 Z1 M
excessive adrenal androgen production, and rarely,5 z: g  Z; n# J1 e& @/ B
an adrenal tumor may also cause adrenal androgen6 W% @: F* A! g- Z8 B" j7 Z+ n
excess.1,36 m! W9 K) S/ L5 k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 t% b5 i9 H2 y: D* A
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 ?) _! e! }0 ^1 z+ |, RA unique entity of male-limited gonadotropin-
8 v' V3 d2 v6 I  p# p3 }: Lindependent precocious puberty, which is also known1 }+ l! v& @9 P5 o+ j7 B5 [3 K
as testotoxicosis, may cause precocious puberty at a
( k# V9 [, b3 E1 l* X9 Ivery young age. The physical findings in these boys0 u  d' n' `: y9 a& Q
with this disorder are full pubertal development,: b( c+ f( ~6 C) f
including bilateral testicular growth, similar to boys7 _9 l9 ?3 I% g8 N$ G
with CPP. The gonadotropin levels in this disorder
+ [& U& j6 D" F# T. A; iare suppressed to prepubertal levels and do not show6 i' P: S; Z' |( P; Q8 A3 `
pubertal response of gonadotropin after gonadotropin-
) t- W4 T/ A3 C% t$ b9 H' Z3 Greleasing hormone stimulation. This is a sex-linked
8 k3 [& f; B' k) \autosomal dominant disorder that affects only+ `: D* C% d" U( n+ W( d
males; therefore, other male members of the family/ i# f8 b( e# r/ [+ u1 Z/ j
may have similar precocious puberty.3
$ f% v) `/ w- E5 A# y/ e; ]: K& c- e& ZIn our patient, physical examination was incon-
( U" O0 Q0 b/ [+ L$ S7 P/ zsistent with true precocious puberty since his testi-
* I, W  V7 s1 z+ v$ |: m8 Wcles were prepubertal in size. However, testotoxicosis1 c6 S" _, ?+ E2 x
was in the differential diagnosis because his father% r% {: }/ G7 Y2 v+ }' ~  @
started puberty somewhat early, and occasionally,* X3 ~1 F$ E! d: a
testicular enlargement is not that evident in the& ?1 s  G6 O& A( C1 @9 Y
beginning of this process.1 In the absence of a neg-
+ h# }8 B7 p. R1 d, ~+ J! d! jative initial history of androgen exposure, our# Z+ t: i* B' M
biggest concern was virilizing adrenal hyperplasia,: x2 R! |/ _/ P* _1 s7 a
either 21-hydroxylase deficiency or 11-β hydroxylase
5 e  A" m1 q) y* Q! l* `deficiency. Those diagnoses were excluded by find-! k! a7 G7 X) U' f: g' s. N( _
ing the normal level of adrenal steroids.
6 A2 w! i0 [6 h* r- k' CThe diagnosis of exogenous androgens was strongly
7 C1 P, H4 C0 i1 ~suspected in a follow-up visit after 4 months because
  `, y4 g: w# R2 S0 ?the physical examination revealed the complete disap-
- L! W" g/ a$ J: A8 Zpearance of pubic hair, normal growth velocity, and
4 p3 k# q; ]) ]$ Adecreased erections. The father admitted using a testos-" O  Q" h) n# E% [
terone gel, which he concealed at first visit. He was
7 N5 `0 a* O- s+ V) @; |using it rather frequently, twice a day. The Physicians’
- K, a2 N9 {% m& e* r7 e! jDesk Reference, or package insert of this product, gel or* i3 X: |  Z  P/ {0 J
cream, cautions about dermal testosterone transfer to' f+ G( \* g/ v1 j
unprotected females through direct skin exposure.
0 H8 R9 V0 G2 M3 n. s5 u! ySerum testosterone level was found to be 2 times the5 ?& C7 ?* B; G5 y! L* g
baseline value in those females who were exposed to1 C1 P; p0 l) d3 n, \/ I
even 15 minutes of direct skin contact with their male
. R9 n7 Y* d& D6 w* mpartners.6 However, when a shirt covered the applica-5 U. e) |6 Q5 M; i
tion site, this testosterone transfer was prevented.+ X: c: w) n. y$ I$ P4 {0 a# j
Our patient’s testosterone level was 60 ng/mL,5 Q* y1 J6 u! a6 S" F  p5 h/ r$ I: b
which was clearly high. Some studies suggest that
  l' S: e. O4 G- R2 m$ Qdermal conversion of testosterone to dihydrotestos-6 k5 w) h- ?! ?  N/ v  _" u( l
terone, which is a more potent metabolite, is more' ^2 ]2 r. S' J0 T* b" W! ]) Z6 b
active in young children exposed to testosterone( q$ m! u8 F- m  y
exogenously7; however, we did not measure a dihy-2 S/ l) i$ G0 t$ b% i( X: B
drotestosterone level in our patient. In addition to2 `5 Q3 X; V6 Z) {8 Z- L- {1 v
virilization, exposure to exogenous testosterone in" s* I6 @' J8 F5 v! p
children results in an increase in growth velocity and
" I0 F2 ~% o& P; R7 w; yadvanced bone age, as seen in our patient.3 C" c7 j: v4 d7 J  J
The long-term effect of androgen exposure during* N: Y4 j8 M7 K: @' |
early childhood on pubertal development and final
% M, Y- `* l9 x3 N, Q/ jadult height are not fully known and always remain
4 _; H' \. i, y& h! }a concern. Children treated with short-term testos-+ b8 {3 R) B1 \- j. Y- z
terone injection or topical androgen may exhibit some
+ Z0 o& _) j# x9 E- `! c) u, jacceleration of the skeletal maturation; however, after: Q8 |5 d" X2 i9 @. z6 T+ D
cessation of treatment, the rate of bone maturation( K0 c3 Y! q" d8 D% ?; K6 I4 n
decelerates and gradually returns to normal.8,9
2 v- r7 U9 I* S$ I1 mThere are conflicting reports and controversy
8 g0 \' y$ a2 M0 N0 y" lover the effect of early androgen exposure on adult9 l8 a$ B) Z- {
penile length.10,11 Some reports suggest subnormal
$ {& g* X  m  G8 N% e5 _3 T% Zadult penile length, apparently because of downreg-
' N, ?0 c% S: f4 A+ }8 ^ulation of androgen receptor number.10,12 However,
" g- |' a* w$ Z4 v1 N5 ]/ ]5 lSutherland et al13 did not find a correlation between# u* [6 _8 z& R7 d6 e8 q' J0 `% t9 F; @% e
childhood testosterone exposure and reduced adult
; |0 u1 i, o; M9 R* E/ j( Ipenile length in clinical studies.9 `: w. ]% y! ^/ A  ^0 x
Nonetheless, we do not believe our patient is  B" I- Q! u+ e' Q* I" a7 T
going to experience any of the untoward effects from
' o0 `9 N  D9 Y5 ^+ ^9 R' ytestosterone exposure as mentioned earlier because" a2 Q5 S( p; a; B/ w) \6 X# D
the exposure was not for a prolonged period of time.
; N  [: X$ I% X: @3 D7 d' _Although the bone age was advanced at the time of
/ |0 m$ ]# X0 j/ |$ Odiagnosis, the child had a normal growth velocity at# w  Q, v3 U/ n6 n+ V
the follow-up visit. It is hoped that his final adult
$ ]# \* E1 W& n7 gheight will not be affected.
; K1 U1 H$ D/ j% x$ MAlthough rarely reported, the widespread avail-; W# x! @+ s  J' J/ O2 W
ability of androgen products in our society may/ t# z! h8 ^+ T! m
indeed cause more virilization in male or female: }1 }( S6 ^& d0 |
children than one would realize. Exposure to andro-1 D  \8 V, |( D0 F
gen products must be considered and specific ques-
' l& n  `, A4 W1 Y6 k1 b  _tioning about the use of a testosterone product or
3 c5 ^. P" w" b; i( Fgel should be asked of the family members during
/ m6 I- }* c/ qthe evaluation of any children who present with vir-, Y7 P4 f1 K  i3 p1 P5 m
ilization or peripheral precocious puberty. The diag-
4 c  a! v# A% d4 cnosis can be established by just a few tests and by7 C& A1 U3 X  M$ N1 v
appropriate history. The inability to obtain such a
& J3 l$ o( Y& u8 Dhistory, or failure to ask the specific questions, may
9 F2 \: _* ^/ O$ H2 d1 Oresult in extensive, unnecessary, and expensive
9 |( U+ r3 _3 ^  X2 W, Hinvestigation. The primary care physician should be
0 u  W; }4 l6 Paware of this fact, because most of these children
& e1 N3 d! ~1 K2 d. k1 Lmay initially present in their practice. The Physicians’" A+ G) X6 X% h  }* f0 ^
Desk Reference and package insert should also put a
: @: e* A, X, {0 Lwarning about the virilizing effect on a male or( a0 j- @; p" u% |0 j" s
female child who might come in contact with some-
7 ?/ n6 a* }- g2 W5 y& wone using any of these products.
) G6 D8 O* r! G3 v7 iReferences
7 y) Z( J1 T, r  `7 M0 P8 j1. Styne DM. The testes: disorder of sexual differentiation
5 Q/ e4 R1 k1 o4 Iand puberty in the male. In: Sperling MA, ed. Pediatric
+ ]! i/ O8 `- ~1 UEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
) O3 u" y8 m+ w2 s2002: 565-628.
$ K7 ~" `5 E* C& r5 d2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  D$ Y5 |; {9 H7 r6 W) G: W
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old, G! J# S$ c* x! q, c" o
Boy Induced by Indirect Topical5 b5 x' K$ o: D# j
Exposure to Testosterone- L8 s5 ?( W  L+ P) u% h
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% z, z. `' F; ]5 k& Pand Kenneth R. Rettig, MD1
% n3 ~, M/ |! f  T/ D3 m; ~, O6 NClinical Pediatrics8 l' N+ V4 j, Z# n3 {
Volume 46 Number 6% u! u5 {- b1 L5 f1 u9 G* ]
July 2007 540-543! K) P- s8 q- d1 p$ b! _; J
© 2007 Sage Publications
# s2 ^0 X7 G. \# \10.1177/0009922806296651, w( T1 S5 Z. S/ t
http://clp.sagepub.com
+ A/ N2 U/ [/ q, b- ^* F8 ?hosted at2 O; |  ^( ]2 J& s, z2 e, v3 Y
http://online.sagepub.com, [  M1 L  P2 A" w/ V- ~2 Z
Precocious puberty in boys, central or peripheral,, V5 b3 ^  e! G) c
is a significant concern for physicians. Central8 U7 ~" f7 t  Y' ?/ Y
precocious puberty (CPP), which is mediated% Z. P3 F% D" z  i. h
through the hypothalamic pituitary gonadal axis, has
# A* B* X# c' b) ja higher incidence of organic central nervous system6 W1 C# `, c3 Y: W6 V
lesions in boys.1,2 Virilization in boys, as manifested
9 i! i. A# E# V& X9 Vby enlargement of the penis, development of pubic
/ Y* ~  P7 i) u4 Y" ahair, and facial acne without enlargement of testi-0 }4 j/ j3 ^7 c& x' X6 K3 ]8 _. K
cles, suggests peripheral or pseudopuberty.1-3 We
( L* g" [' {: M( W! t/ ]( `report a 16-month-old boy who presented with the
) y8 C. s  B. T1 T" Jenlargement of the phallus and pubic hair develop-, [6 s" b# t; v6 e
ment without testicular enlargement, which was due' V9 q: }2 }! n3 R' m
to the unintentional exposure to androgen gel used by: M) J& ^  F! F, A9 {  w
the father. The family initially concealed this infor-  G$ I, }. h( R1 W
mation, resulting in an extensive work-up for this
# t8 y, P& l. T# Wchild. Given the widespread and easy availability of
5 l% x" d. c: |5 o8 Ttestosterone gel and cream, we believe this is proba-' c0 e7 k; C1 t0 ]- ^9 Q
bly more common than the rare case report in the% d( ^% W3 y4 h4 x2 I8 |3 a- {4 q; T
literature.4+ h9 O5 V7 v5 W! i
Patient Report
$ |7 K9 C$ g1 Q9 ?A 16-month-old white child was referred to the
2 S) i5 t) a8 K/ O0 i8 ~- dendocrine clinic by his pediatrician with the concern9 L4 f( N2 U# G# e' v7 V; y# f
of early sexual development. His mother noticed
: ]9 \  F5 P2 K& N) c* [light colored pubic hair development when he was
( {! m% X0 R1 ^* b9 k2 UFrom the 1Division of Pediatric Endocrinology, 2University of2 J1 W$ u( `; `  k7 w
South Alabama Medical Center, Mobile, Alabama.) N; \5 a$ }2 U+ O
Address correspondence to: Samar K. Bhowmick, MD, FACE,
/ w/ p$ I, {9 v5 }Professor of Pediatrics, University of South Alabama, College of
" l" H7 S# P1 X9 B& r: z5 p, fMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
3 K5 y8 q2 j6 M* p( C/ Ie-mail: [email protected].
! j# z7 O# \: _: Sabout 6 to 7 months old, which progressively became
- z1 w4 B! p4 K( u' \4 t$ D# J1 ldarker. She was also concerned about the enlarge-
& s: b4 J' o1 v1 _ment of his penis and frequent erections. The child
  r3 O: e; G$ S- B% Bwas the product of a full-term normal delivery, with
6 z" D, H( Y. ]+ r" ~5 V6 n2 ma birth weight of 7 lb 14 oz, and birth length of  k0 o" E  m7 W. V
20 inches. He was breast-fed throughout the first year
3 @$ O4 _+ F; e% pof life and was still receiving breast milk along with$ V- d3 n4 U! h, p
solid food. He had no hospitalizations or surgery,- u/ ]' e8 X. v0 A7 [  M
and his psychosocial and psychomotor development
. n2 l8 N9 U5 vwas age appropriate.
  Q+ L7 ~% v0 y. I! hThe family history was remarkable for the father,- s( ~+ q% T" b& _
who was diagnosed with hypothyroidism at age 16,0 R5 a# ?* p1 K
which was treated with thyroxine. The father’s+ q& u6 ?% T8 G/ A: I; D$ W/ \! y
height was 6 feet, and he went through a somewhat& l( x" M. q8 n* S1 K* t
early puberty and had stopped growing by age 14.
; D2 L- g2 z8 `  U& ]5 r. x9 V* gThe father denied taking any other medication. The9 @* F* d2 K, u  z# r
child’s mother was in good health. Her menarche
* i9 E% T- G; b: |was at 11 years of age, and her height was at 5 feet# p$ L# s9 }& C- r, q" l3 N2 I
5 inches. There was no other family history of pre-5 C2 ~( B2 }; k& y) q! X7 j/ H
cocious sexual development in the first-degree rela-
8 z; T9 z/ ]( P5 S; etives. There were no siblings.
: e. h- l2 y) a. o; ~Physical Examination$ ]. ^/ _! S5 K. T: b; s
The physical examination revealed a very active,2 g/ c) p0 i; T- s  _
playful, and healthy boy. The vital signs documented
# g  h' @" k9 b  s1 x# Wa blood pressure of 85/50 mm Hg, his length was8 v/ `2 {8 b0 ^2 ?; O+ P% S
90 cm (>97th percentile), and his weight was 14.4 kg. g6 e/ t5 D9 ?/ q3 S% I. @. q8 }
(also >97th percentile). The observed yearly growth( t8 n2 \# o2 l& \" c3 a
velocity was 30 cm (12 inches). The examination of2 |) C0 n, ?$ J0 B
the neck revealed no thyroid enlargement.. z$ E/ `% x% R- F* l! m' C
The genitourinary examination was remarkable for
! x. i; Y6 i4 y$ c8 s% Aenlargement of the penis, with a stretched length of5 K9 ]# ^$ ~5 i. }2 A* m
8 cm and a width of 2 cm. The glans penis was very well
: J; Y: S. ~2 rdeveloped. The pubic hair was Tanner II, mostly around+ M, [/ c( {. ^6 a
540
6 _% c# c/ ]4 y  `: M) qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 K' I, r$ f( b! U" c- [the base of the phallus and was dark and curled. The
, q, z; \" r+ `5 Ctesticular volume was prepubertal at 2 mL each.
2 ?4 S* Z) t9 l  N. NThe skin was moist and smooth and somewhat
6 m; G% G  M* Doily. No axillary hair was noted. There were no
2 Q( a( {1 \4 B' M* s! Y- O$ U" H- D  }abnormal skin pigmentations or café-au-lait spots.5 n3 I1 w; V) h9 b$ n, Z
Neurologic evaluation showed deep tendon reflex 2+
" t: i4 e! [9 I- C1 j/ t) Y+ z  zbilateral and symmetrical. There was no suggestion
6 U) t4 P1 t3 W' L9 |. hof papilledema.
# o# r8 c$ T) ^2 o# W1 NLaboratory Evaluation
8 n- U& W- w0 [/ eThe bone age was consistent with 28 months by1 {) c' c" C: Z1 X
using the standard of Greulich and Pyle at a chrono-' }3 R- C& |- i9 H' Z
logic age of 16 months (advanced).5 Chromosomal
/ X8 j9 `! F9 A6 p" R% Ekaryotype was 46XY. The thyroid function test1 E% i4 y8 y5 B/ y* }$ J! n
showed a free T4 of 1.69 ng/dL, and thyroid stimu-; h; }" c; }" V; G* s4 X  D  f4 d! S
lating hormone level was 1.3 µIU/mL (both normal).
5 E% ?& H: x: x$ K$ nThe concentrations of serum electrolytes, blood* O4 X# U$ f4 c- {. b4 E1 M% L
urea nitrogen, creatinine, and calcium all were
, z1 I# }3 s% Iwithin normal range for his age. The concentration* ^8 ~2 ~& O' z) J
of serum 17-hydroxyprogesterone was 16 ng/dL
3 s! X- r# N) Z! t3 \4 |  O9 d(normal, 3 to 90 ng/dL), androstenedione was 20
% f3 c/ h# ]9 Eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# T# `0 I, {3 D! Y. J8 @
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 o) F' E; v0 n9 v" s& g; X# y2 {desoxycorticosterone was 4.3 ng/dL (normal, 7 to$ D' o" ?' k2 R  |1 N4 z& |
49ng/dL), 11-desoxycortisol (specific compound S)
* Z: W/ m5 {8 n. x' r+ z4 t5 {was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' e7 Z; ^) c( K* Vtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* g$ ?# i8 ?8 o+ E7 p) B5 Q
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 [  o( o. P3 I9 Xand β-human chorionic gonadotropin was less than
3 I+ T  d; i6 l# A/ r9 g5 mIU/mL (normal <5 mIU/mL). Serum follicular9 ~# G7 E, q2 U" ?) q
stimulating hormone and leuteinizing hormone) O* [7 l* W$ R- Q/ j. ~9 D
concentrations were less than 0.05 mIU/mL* @- j# H6 k; y+ n
(prepubertal).8 Y6 W- a5 Z% x# u* n
The parents were notified about the laboratory
# T; T. y# U# b( }# D" Iresults and were informed that all of the tests were, F# c, k' c- @2 h* z
normal except the testosterone level was high. The7 s( D( h4 E) w
follow-up visit was arranged within a few weeks to7 w  M6 |  T- C4 |& j/ K" Z( h
obtain testicular and abdominal sonograms; how-0 x' s* H- i  l" t5 _
ever, the family did not return for 4 months.5 A  d. P( d: S- i( ]+ ]
Physical examination at this time revealed that the
' `. O- a- r( n' I# D6 Z  \+ dchild had grown 2.5 cm in 4 months and had gained$ c6 ^7 b! ]+ m5 t! J
2 kg of weight. Physical examination remained* g8 B4 `& w" [1 J9 [  w2 \
unchanged. Surprisingly, the pubic hair almost com-
, Z' j6 B4 ~1 L3 F% O9 F) C# Vpletely disappeared except for a few vellous hairs at" S3 K0 n  ^7 i: U
the base of the phallus. Testicular volume was still 2- H( y  y8 m+ e4 \' v! S
mL, and the size of the penis remained unchanged.
. l( C) O; O! w( ]The mother also said that the boy was no longer hav-
' i4 @+ {4 c% P6 ~8 Q4 uing frequent erections.
; A0 `3 M2 @  {. m. gBoth parents were again questioned about use of
  H3 d+ x, M8 K+ E* N0 kany ointment/creams that they may have applied to
  w( j$ B! W0 f) Z' R" a% _the child’s skin. This time the father admitted the
9 B: n/ h: ?* f. S. g8 h" uTopical Testosterone Exposure / Bhowmick et al 5415 U( G" f: p) `! C9 o; R
use of testosterone gel twice daily that he was apply-' l& B) G: K$ G9 ]% D
ing over his own shoulders, chest, and back area for
9 q; c+ f. l. Y1 a' Ba year. The father also revealed he was embarrassed
5 K- P; F0 Z; k6 |3 Vto disclose that he was using a testosterone gel pre-+ t3 W0 {5 L, V0 x% n
scribed by his family physician for decreased libido5 x# F6 T! _( a  t8 H0 k% P- F# G+ K
secondary to depression.
8 T' Z- x  F0 n% d# b  Y5 {The child slept in the same bed with parents.
* e; h! f' K  y1 r/ o! E- v8 {$ hThe father would hug the baby and hold him on his* E* w. s- |3 g' H% |
chest for a considerable period of time, causing sig-
$ D( v  H, s" E/ pnificant bare skin contact between baby and father.
3 L: r2 W& |5 s6 A. M3 KThe father also admitted that after the phone call,& l- V! A- A6 H# Q: }6 l$ `
when he learned the testosterone level in the baby
& M6 ?& v3 `- awas high, he then read the product information
9 J1 ^/ I6 F/ d1 M+ Ypacket and concluded that it was most likely the rea-
5 S9 i9 S; o! u2 ?son for the child’s virilization. At that time, they& m7 j. Q* m1 z" G6 A# f" c6 ~* \
decided to put the baby in a separate bed, and the
# N9 D' b; t& d  T9 Ifather was not hugging him with bare skin and had
+ V# K" |, h! E$ F7 d+ o" M8 T1 _been using protective clothing. A repeat testosterone
0 D. W8 A6 l: x5 Z) c" X5 _test was ordered, but the family did not go to the* C7 d1 w& b7 }6 r- k, v  E* P: x
laboratory to obtain the test.% e3 f: i! p4 \; i9 C
Discussion
. c" _! S  k* {, }  V1 t" k1 Q+ ^Precocious puberty in boys is defined as secondary( i5 a  W# e$ H$ e/ @$ p' k
sexual development before 9 years of age.1,4, s, b% g1 \" B+ g$ X9 l
Precocious puberty is termed as central (true) when
6 M) S9 S3 S: Z$ Nit is caused by the premature activation of hypo-
6 |& E& T( a) `3 r! Bthalamic pituitary gonadal axis. CPP is more com-
0 M6 T- a; `, Pmon in girls than in boys.1,3 Most boys with CPP5 q7 ]7 I' g3 L! m
may have a central nervous system lesion that is
3 i- X: ^( {5 m% _; r9 c& n3 nresponsible for the early activation of the hypothal-( w  l. H! \! y5 `
amic pituitary gonadal axis.1-3 Thus, greater empha-9 l$ h+ u6 ]+ Q4 R5 j
sis has been given to neuroradiologic imaging in2 s7 c- w3 Z( _" R$ b3 O
boys with precocious puberty. In addition to viril-: o" L7 b/ s( x, P! i5 Y1 ^; B
ization, the clinical hallmark of CPP is the symmet-
6 x2 w; V$ P. D! I5 Vrical testicular growth secondary to stimulation by% e0 x4 N" s! K! l
gonadotropins.1,3
; D# o8 _8 p4 Z. S( ^Gonadotropin-independent peripheral preco-
' O# b# k* F* \6 {) tcious puberty in boys also results from inappropriate5 n2 y" K) ?$ O6 V) Y3 f' M
androgenic stimulation from either endogenous or
2 _' G! B( d2 V4 x! Fexogenous sources, nonpituitary gonadotropin stim-, A$ s4 q. k. w4 r2 p- ^$ g
ulation, and rare activating mutations.3 Virilizing1 e% ?& [, W# ~' v! t  x3 _
congenital adrenal hyperplasia producing excessive7 t# V) d4 a* {; a4 B! t- h" o
adrenal androgens is a common cause of precocious
4 S( `2 q) X  p7 Spuberty in boys.3,4
2 A0 n6 X/ A2 R7 i1 E+ MThe most common form of congenital adrenal
3 W8 a8 i# |6 M' S" J1 Vhyperplasia is the 21-hydroxylase enzyme deficiency.
3 u" ^6 T! L$ O/ B* `) c$ }The 11-β hydroxylase deficiency may also result in
1 a. U7 o8 J1 R3 mexcessive adrenal androgen production, and rarely,4 ~( P- f( c+ G/ O7 F0 u- @
an adrenal tumor may also cause adrenal androgen4 I6 G. f3 e- T& M) V( V
excess.1,3
' J( W0 u/ j: ~3 a' T" _6 D9 Aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from  G5 s* H' ^# y. A) H$ S4 A
542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 \4 m" V5 W" |# c5 G
A unique entity of male-limited gonadotropin-
& Z5 U7 K" K5 w4 |* W1 Findependent precocious puberty, which is also known! A; g5 ]3 ~! @; A! a
as testotoxicosis, may cause precocious puberty at a3 u  J/ `1 N5 }' }/ O9 l
very young age. The physical findings in these boys7 W8 O3 s3 H& w& z
with this disorder are full pubertal development,
3 f3 [; x' h3 g: J( Hincluding bilateral testicular growth, similar to boys2 V8 B* S- e8 ^6 w
with CPP. The gonadotropin levels in this disorder  [, t' K' V- n; @
are suppressed to prepubertal levels and do not show) ~1 p; E# T  t/ k
pubertal response of gonadotropin after gonadotropin-
: }; y9 Z. m5 {) l/ s- O/ xreleasing hormone stimulation. This is a sex-linked
! k/ o3 N4 w; M  k* p( fautosomal dominant disorder that affects only
( N0 t5 W2 |" e& u  C: ^males; therefore, other male members of the family. \* f/ X7 H+ p
may have similar precocious puberty.3. _2 d; I' t5 I' b
In our patient, physical examination was incon-' O+ W7 ^7 C& y  a
sistent with true precocious puberty since his testi-8 Z; b, H3 o' m2 }9 h( n" {7 Z( {" y
cles were prepubertal in size. However, testotoxicosis# g0 }  ^# L: r1 A- B
was in the differential diagnosis because his father
  ~/ M, |' `' L* j6 _8 c: Tstarted puberty somewhat early, and occasionally,5 L6 t( n2 A0 F( W0 B, s2 }: U$ G
testicular enlargement is not that evident in the7 Z9 ?8 m% v* K9 \
beginning of this process.1 In the absence of a neg-
  F' c: u/ ]0 N% \5 Wative initial history of androgen exposure, our
  y  r* e/ h; tbiggest concern was virilizing adrenal hyperplasia,2 e2 i2 y7 ?$ t) n  m: H# y
either 21-hydroxylase deficiency or 11-β hydroxylase
3 k8 }$ P' m) Jdeficiency. Those diagnoses were excluded by find-
- C) X7 B0 Y2 F+ ?8 Hing the normal level of adrenal steroids.
& z. f8 Q9 B5 BThe diagnosis of exogenous androgens was strongly3 g8 v! Z0 X, f2 U$ ]
suspected in a follow-up visit after 4 months because
4 o, C5 X, X6 w* c) Hthe physical examination revealed the complete disap-# t- e9 ?* R2 a" |% y# O/ Y4 t
pearance of pubic hair, normal growth velocity, and
0 K0 D9 D/ Z2 d5 S4 s" {5 adecreased erections. The father admitted using a testos-
0 N, A& X/ T5 \terone gel, which he concealed at first visit. He was
0 U5 I# H# h  d" T. q; ousing it rather frequently, twice a day. The Physicians’
, ^7 {# k( e$ uDesk Reference, or package insert of this product, gel or. `4 _' @& y6 g+ }
cream, cautions about dermal testosterone transfer to
3 U( _( R2 M5 @/ s0 Z2 yunprotected females through direct skin exposure.
5 F4 D, {3 T8 h- }; }' B' ?# J0 DSerum testosterone level was found to be 2 times the& u# x; F+ p- e1 h/ F" v
baseline value in those females who were exposed to( B: a* r6 }" e1 Q0 z. m& f4 _
even 15 minutes of direct skin contact with their male/ ?! Y8 W8 `0 v( y- k+ h. v0 T
partners.6 However, when a shirt covered the applica-
- k  L  \, W0 m' A6 x  ytion site, this testosterone transfer was prevented.
+ m2 c. f3 v+ wOur patient’s testosterone level was 60 ng/mL,
5 W0 e8 ^. ^$ _- u* dwhich was clearly high. Some studies suggest that
) m  [2 J( E: O7 M6 x- xdermal conversion of testosterone to dihydrotestos-. V' |6 b) V9 J* U( z3 ]
terone, which is a more potent metabolite, is more2 |# ]; r0 }6 @: D* S& t! _
active in young children exposed to testosterone
3 X$ A+ N( \% N5 bexogenously7; however, we did not measure a dihy-  J$ t3 ?0 p( N) ~
drotestosterone level in our patient. In addition to3 M/ D) F6 I3 O8 g
virilization, exposure to exogenous testosterone in" W2 D. o6 Q# l; \$ r# ]5 a: f
children results in an increase in growth velocity and
; w! w2 ?) P9 {advanced bone age, as seen in our patient.
8 p1 k, e/ Z) j, O7 h* T- jThe long-term effect of androgen exposure during
3 }; _& P3 x/ E8 k, n! w& e" Jearly childhood on pubertal development and final
; v# z# g; [8 Qadult height are not fully known and always remain2 B( d9 n2 L! w' G
a concern. Children treated with short-term testos-5 {$ z- y9 H$ m+ N8 G. V
terone injection or topical androgen may exhibit some
; |  J1 ~& j& M5 A; `" Yacceleration of the skeletal maturation; however, after
3 ]3 l6 r3 u2 r3 {$ X" z( t7 ycessation of treatment, the rate of bone maturation. j- }5 l! s6 D) z* e9 Y
decelerates and gradually returns to normal.8,95 X# s+ Z* a. G; D/ l3 i6 i
There are conflicting reports and controversy4 u% A9 q( s& v7 s/ z5 Z) D
over the effect of early androgen exposure on adult
1 v0 j, c" U: _2 I2 apenile length.10,11 Some reports suggest subnormal1 [5 M$ P5 o- l- g
adult penile length, apparently because of downreg-
( A4 j+ c0 }( A7 @$ W: z0 \ulation of androgen receptor number.10,12 However,0 I! H6 h' f' Y* W7 X) C
Sutherland et al13 did not find a correlation between: U" M; @" q% M# b, {
childhood testosterone exposure and reduced adult: r9 R0 g7 A/ i
penile length in clinical studies.' T& a5 ^+ g+ f+ n  t/ W1 U' d
Nonetheless, we do not believe our patient is, I# W  Z" e2 e" O4 r4 r
going to experience any of the untoward effects from
3 V4 w& J3 ~0 L5 K  F. r1 }6 }testosterone exposure as mentioned earlier because0 w, @& }: A7 z$ B/ }9 @
the exposure was not for a prolonged period of time.
( }; Q3 u: l7 {  ^6 A! o6 J, K0 X- GAlthough the bone age was advanced at the time of. [9 ~, s0 D8 B+ \/ \
diagnosis, the child had a normal growth velocity at8 s  ^/ n* Q% c
the follow-up visit. It is hoped that his final adult
' h9 g6 f  r% `" L1 Nheight will not be affected.
! l# o, m& h% [0 _; l4 V- ^& yAlthough rarely reported, the widespread avail-- _4 p1 Z# ?. f# G# u5 e9 d
ability of androgen products in our society may+ N% x2 d1 J; l$ _6 k! U' }0 G+ l' i
indeed cause more virilization in male or female4 Y- u' Z5 }6 o' G
children than one would realize. Exposure to andro-; ^, R5 b/ e4 w: j' l9 G
gen products must be considered and specific ques-
9 |# V9 H1 _, f& F8 Ytioning about the use of a testosterone product or' g. R+ e8 f+ z! t$ ~1 t9 M# u
gel should be asked of the family members during6 a: ^" Q, F# a  ]$ |7 \
the evaluation of any children who present with vir-1 {" C* d1 x) R. z3 D
ilization or peripheral precocious puberty. The diag-
6 b2 Z0 R4 s0 _; l% nnosis can be established by just a few tests and by
# ?) [3 J7 n7 k. X2 Happropriate history. The inability to obtain such a
" ^9 c3 p$ m  Thistory, or failure to ask the specific questions, may$ j/ c: m; d& b: b' j4 ]: {
result in extensive, unnecessary, and expensive
- ]; V4 T3 R1 S* `! Y) Binvestigation. The primary care physician should be0 S: v8 B% w  o4 `, ~
aware of this fact, because most of these children
9 ^# E4 a% R# V+ F& f0 [may initially present in their practice. The Physicians’
/ E& }! p/ h. T- i" x* I' @/ QDesk Reference and package insert should also put a( X# z( r( Q' l( S
warning about the virilizing effect on a male or
6 C# r% Q9 [( O: f8 tfemale child who might come in contact with some-
" v" p* Q, G/ q" B' Oone using any of these products.
+ J) V  R) f  D7 J( DReferences# f% n( }1 @% J1 X. P; @
1. Styne DM. The testes: disorder of sexual differentiation
8 \9 W8 p3 t! m& jand puberty in the male. In: Sperling MA, ed. Pediatric
2 @. L) w% X. w+ c5 S% C4 t4 tEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 y% K: X+ B# f4 G3 r3 H2002: 565-628.
7 }1 v3 z1 @0 r6 x5 S+ }, s2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 V- o& u3 d: A' h0 m9 dpuberty 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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

8 Y+ U, C8 ?! Z) a9 e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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