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is a significant concern for physicians. Central0 ?4 X7 x) t |$ j" n
precocious puberty (CPP), which is mediated
1 r9 _% D$ h) W+ t6 U6 N$ Ithrough the hypothalamic pituitary gonadal axis, has% e! l8 Q! W. L' w! {
a higher incidence of organic central nervous system
3 i. d z2 V( O! s9 Alesions in boys.1,2 Virilization in boys, as manifested# q6 m: I2 s: A3 [5 o: g
by enlargement of the penis, development of pubic
! N& d- H) I g5 thair, and facial acne without enlargement of testi-
+ ?- g. R. k5 `5 _$ ?# d0 G" ?cles, suggests peripheral or pseudopuberty.1-3 We0 }' o6 u! g7 u4 K. B3 G
report a 16-month-old boy who presented with the
) a. T# t0 u" d* \1 ]7 ]% ?4 N4 cenlargement of the phallus and pubic hair develop-! r) ]: ^3 v4 a5 J
ment without testicular enlargement, which was due
* R4 g) T, S$ s2 O Qto the unintentional exposure to androgen gel used by' ~2 j8 o2 x% f+ S- L4 @( v0 c( p
the father. The family initially concealed this infor-% M+ n7 S+ K% q) b1 R7 X
mation, resulting in an extensive work-up for this
2 {9 x+ X9 [9 }" u) O" L5 m3 Qchild. Given the widespread and easy availability of
# `' K" n) H5 \( i9 p& }; J0 stestosterone gel and cream, we believe this is proba-4 C/ [8 g! r; I: W
bly more common than the rare case report in the1 F7 z' ?( Q& `& k# J0 v# l
literature.4& \5 u6 F5 \& F9 K: v3 Z
Patient Report) f0 a6 K0 v# T0 ?& m* m
A 16-month-old white child was referred to the( t: }4 D6 N* e
endocrine clinic by his pediatrician with the concern
$ \* q9 ]( y$ Y0 P, b0 pof early sexual development. His mother noticed: m4 w, l a" o5 V
light colored pubic hair development when he was/ N' O. G$ F: w( S. y9 Z" M
From the 1Division of Pediatric Endocrinology, 2University of' _# e3 d7 P; ^9 q3 I
South Alabama Medical Center, Mobile, Alabama.! q: N& B! h: H* {" J+ @) P3 u
Address correspondence to: Samar K. Bhowmick, MD, FACE,
% [4 X1 i% P+ _3 T4 V* c2 p1 k, U- K2 ]Professor of Pediatrics, University of South Alabama, College of; j2 t" x7 W+ Z' Q# {/ A3 d
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 ~; k! O+ l1 z8 r( T+ Q g
e-mail: [email protected].4 ~! p2 Q/ b1 ]0 t) U
about 6 to 7 months old, which progressively became
9 M3 H) @' C; G0 w8 G$ l6 xdarker. She was also concerned about the enlarge-% ^7 X8 ^' Q- n6 } N
ment of his penis and frequent erections. The child$ W# e# ^& C M# E, N' l# y
was the product of a full-term normal delivery, with
. c: N$ w- Q& R, ha birth weight of 7 lb 14 oz, and birth length of4 r- I* o6 a! W$ t+ @$ O2 Z3 I3 U, h
20 inches. He was breast-fed throughout the first year
8 h* Y& Q |) s. e* s& M( Y% `of life and was still receiving breast milk along with9 q/ F9 e3 V- o @) A: s
solid food. He had no hospitalizations or surgery,2 P/ d I1 i; [) `' O
and his psychosocial and psychomotor development
: J$ J x# X/ e" }# D" awas age appropriate.) L" [, `6 [; b" f3 i ]* t
The family history was remarkable for the father,) E0 g; l0 g3 x( i/ G$ h
who was diagnosed with hypothyroidism at age 16,
4 s$ A6 l+ G& O: M3 `which was treated with thyroxine. The father’s
% h$ S2 x* h, Wheight was 6 feet, and he went through a somewhat
. _- N0 A3 \' x' Y3 ^early puberty and had stopped growing by age 14.
/ [: J4 U7 e; c# S5 fThe father denied taking any other medication. The V; j1 ]5 F0 d" A# u
child’s mother was in good health. Her menarche" z) U7 M1 ~% b T# }
was at 11 years of age, and her height was at 5 feet' F6 H" q2 @ |& w( R" N
5 inches. There was no other family history of pre-
) [: N( ?) j1 `1 }- ycocious sexual development in the first-degree rela-: l1 L. U- V5 a; W
tives. There were no siblings.# o, U7 T" T: {9 l
Physical Examination
/ Y# J- z8 |4 a' \The physical examination revealed a very active,1 h/ |* G8 O5 t
playful, and healthy boy. The vital signs documented
9 g1 M" g% p+ j# a( m6 Za blood pressure of 85/50 mm Hg, his length was
7 K4 `% ?8 R: A P. ?( b% G90 cm (>97th percentile), and his weight was 14.4 kg% ?3 W0 z. Q6 A1 X2 w
(also >97th percentile). The observed yearly growth" ?$ _* v# o6 |) _5 ]
velocity was 30 cm (12 inches). The examination of# p* O$ u5 j6 G* J1 `6 Y
the neck revealed no thyroid enlargement.
^9 {9 v G( n$ M! {The genitourinary examination was remarkable for, n: Q: G P/ }7 `2 L0 Y1 i. b
enlargement of the penis, with a stretched length of; L- d8 f9 ]* y# |
8 cm and a width of 2 cm. The glans penis was very well* p/ V+ g5 Z+ J0 X
developed. The pubic hair was Tanner II, mostly around
. I- X& M' Q/ h- l4 `- ]+ f540
* X! {4 ?* ]" Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from X0 a: j6 g: N Z9 d/ s; v; `
the base of the phallus and was dark and curled. The
) y8 b! A3 I! k( n* w1 `testicular volume was prepubertal at 2 mL each.* c9 Q* a. o9 _% R
The skin was moist and smooth and somewhat: B ]) R; _: u" D2 U
oily. No axillary hair was noted. There were no" H/ W( o4 k2 d
abnormal skin pigmentations or café-au-lait spots.
* v8 x6 O0 V' ], @$ c- {1 ENeurologic evaluation showed deep tendon reflex 2+0 O2 U1 G4 k( W
bilateral and symmetrical. There was no suggestion2 P5 S1 T7 g; {8 G" j' D/ S
of papilledema.* F* _' U! h0 N7 q+ X* K; t
Laboratory Evaluation4 |; e/ ^/ z6 F7 `$ Z! g
The bone age was consistent with 28 months by
2 K5 V# n: e- x/ @& z' \. ^. b( susing the standard of Greulich and Pyle at a chrono-
$ M/ [3 c+ ]( a# F: nlogic age of 16 months (advanced).5 Chromosomal
4 R) W& S8 T& T9 k2 pkaryotype was 46XY. The thyroid function test
1 r: @7 {8 k+ P$ E$ f7 ~showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 x! \, ^+ j2 D& B
lating hormone level was 1.3 µIU/mL (both normal).
/ s- N% L8 o: V2 X4 lThe concentrations of serum electrolytes, blood& v) D3 Q1 W5 v! t
urea nitrogen, creatinine, and calcium all were6 K+ o3 Q- t3 S4 {% h3 H' n
within normal range for his age. The concentration
9 y, M/ L4 Q5 j. f/ W; x) aof serum 17-hydroxyprogesterone was 16 ng/dL
# W$ f9 d' Q+ L5 {- Q# Y(normal, 3 to 90 ng/dL), androstenedione was 20( o/ I3 j) q" m0 l }1 V
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* D8 l9 a- J1 Y0 i; K
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- c1 T1 x# U$ O6 fdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
" D$ K4 q# C9 H; k% `! a49ng/dL), 11-desoxycortisol (specific compound S)$ d% ] R+ p" x0 C5 i
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# }( f \# }: C: F: [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 E% u _+ ]8 X0 d3 ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) O: c" E. W- ]* u/ n8 gand β-human chorionic gonadotropin was less than, @0 e8 Q; [& U3 l% V5 x
5 mIU/mL (normal <5 mIU/mL). Serum follicular
) j0 ]4 ~1 A+ ^! bstimulating hormone and leuteinizing hormone
& s2 \1 s* y9 y7 ?9 wconcentrations were less than 0.05 mIU/mL
( X6 S( e* e5 ^3 s5 e4 z(prepubertal).6 E5 r' n, u+ Q& _
The parents were notified about the laboratory
6 @* V! R. W l$ z& d, [results and were informed that all of the tests were! Q+ @7 X- @% @1 x
normal except the testosterone level was high. The/ ?* ~+ J/ Y/ h
follow-up visit was arranged within a few weeks to
! J# Y) g: V- {- D Jobtain testicular and abdominal sonograms; how-
; e5 L6 C: S- h, I3 never, the family did not return for 4 months.
4 d" h' R v/ \# ]$ V) SPhysical examination at this time revealed that the
- C/ }8 [+ e! V; p6 `0 mchild had grown 2.5 cm in 4 months and had gained8 U7 s6 @% Y1 ^* r7 y0 I
2 kg of weight. Physical examination remained: }1 r9 {' j3 O3 T5 {! |
unchanged. Surprisingly, the pubic hair almost com-
6 A% D* I8 g. \pletely disappeared except for a few vellous hairs at' N7 Y0 Z( B7 Q J/ p
the base of the phallus. Testicular volume was still 2
, i( x( u. J0 Q: c5 O+ q4 bmL, and the size of the penis remained unchanged.
" s) y- D$ Y5 bThe mother also said that the boy was no longer hav-
" c# y! G: ?. m" aing frequent erections.
4 @9 f6 ~' S- }. @: HBoth parents were again questioned about use of8 Q& A0 k& M+ {" {, Z( L( I( ]$ m
any ointment/creams that they may have applied to
0 _: \( w* e+ H" \3 ~the child’s skin. This time the father admitted the: f3 g/ V/ o7 E5 q0 D2 \6 Y* \
Topical Testosterone Exposure / Bhowmick et al 541
; b7 v1 C t; uuse of testosterone gel twice daily that he was apply-6 a2 u X$ p9 q1 y) |" m x$ |
ing over his own shoulders, chest, and back area for
m+ o, {. a% ?6 r. Ya year. The father also revealed he was embarrassed
/ b6 z' S) A% N6 M+ nto disclose that he was using a testosterone gel pre-6 T+ N/ W$ x+ _, o0 ]
scribed by his family physician for decreased libido' g a7 c* |+ q+ g
secondary to depression.
u! ]) l9 L/ t- T6 TThe child slept in the same bed with parents.
" p* r% p2 C) j* M% E% a TThe father would hug the baby and hold him on his9 S5 e+ [) Y5 x! s0 Y* J8 o3 P
chest for a considerable period of time, causing sig-% e7 d. c1 K2 n' T" b9 o4 V) N
nificant bare skin contact between baby and father.
/ f% m7 x j4 IThe father also admitted that after the phone call,; y. E' t' ^6 o7 l9 W
when he learned the testosterone level in the baby
! r3 u; Q. J2 a( q( C! twas high, he then read the product information
) L/ D/ w+ [3 Ppacket and concluded that it was most likely the rea-/ K+ g( K4 i, k+ `3 K: ^2 A% Y5 p3 h7 v
son for the child’s virilization. At that time, they
4 Z2 ]* ?& e# ?; x( u$ j/ I- N9 }decided to put the baby in a separate bed, and the1 Y# L: k# o7 z U; ^) P
father was not hugging him with bare skin and had& W' W# j" v9 [8 B X7 Q2 W9 Q
been using protective clothing. A repeat testosterone
; \2 S' ]% P' x! Y& ctest was ordered, but the family did not go to the
' k- K0 K5 _) Q* j& h) Claboratory to obtain the test.8 u$ D7 k6 N3 c- @
Discussion. N4 s8 S% I, I0 c
Precocious puberty in boys is defined as secondary
" h' U' y5 g- K3 |4 rsexual development before 9 years of age.1,4
; w* S; Z; ~+ H/ Q1 NPrecocious puberty is termed as central (true) when/ Y5 u/ T% z7 a9 {) C; S' S
it is caused by the premature activation of hypo-
+ x& A: B5 z0 {* e" z6 Kthalamic pituitary gonadal axis. CPP is more com-2 V3 \4 f& j* ]. T
mon in girls than in boys.1,3 Most boys with CPP2 Y0 s! G! \2 a6 ^- [$ v9 h3 m' k
may have a central nervous system lesion that is% v v! |( P# q* ^5 i G
responsible for the early activation of the hypothal-/ U( D1 P% c# o8 W5 d; G+ t
amic pituitary gonadal axis.1-3 Thus, greater empha-& \9 n- [$ |5 S! v1 s2 J0 d
sis has been given to neuroradiologic imaging in+ J$ b2 h: t: ~9 b, C3 d8 Z
boys with precocious puberty. In addition to viril-
7 ^# M$ x0 |1 eization, the clinical hallmark of CPP is the symmet-# D2 t$ }: P9 {. u" c" ^
rical testicular growth secondary to stimulation by8 { I6 E, d8 n7 O: l
gonadotropins.1,3* } B7 w( ~- [
Gonadotropin-independent peripheral preco-
% F( e3 j7 ]0 }$ v1 E' T. lcious puberty in boys also results from inappropriate# E! g1 _1 ] o: w1 e: Q" ^
androgenic stimulation from either endogenous or, l' ]% G% O5 m i0 M2 K: _
exogenous sources, nonpituitary gonadotropin stim-7 ^7 Y) s" e- _3 ]4 D
ulation, and rare activating mutations.3 Virilizing
7 \+ n4 g; E! J! f2 X5 Y5 ocongenital adrenal hyperplasia producing excessive
+ }- {" `2 K3 A% d+ F5 C: Eadrenal androgens is a common cause of precocious+ S* D/ [' o m6 m
puberty in boys.3,40 S- X5 m, G8 y! ^
The most common form of congenital adrenal
% L. i# z; B' f& |: m4 s! phyperplasia is the 21-hydroxylase enzyme deficiency.7 Z9 D" m0 c& m! V
The 11-β hydroxylase deficiency may also result in
( U0 r# N( z; G o+ R" T8 xexcessive adrenal androgen production, and rarely,
4 X9 x K; @! q5 ~0 ^* X: Can adrenal tumor may also cause adrenal androgen6 ?; n0 I5 ]4 ^* Z: T4 ?( C
excess.1,36 @9 O' \; z( t2 [7 ^" L$ u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 N R% ]' M0 C( T" U. n5 @542 Clinical Pediatrics / Vol. 46, No. 6, July 2007# n* F1 L }& N
A unique entity of male-limited gonadotropin-3 ~) Q, q, y; f
independent precocious puberty, which is also known
# a4 M) F: g( v* e) i$ las testotoxicosis, may cause precocious puberty at a4 s$ O$ q8 A2 |/ V+ Y8 [
very young age. The physical findings in these boys
5 ?; y$ M! L7 E8 J" @. zwith this disorder are full pubertal development,7 J H! b3 Z0 X* k
including bilateral testicular growth, similar to boys
U5 u7 X9 p h$ }# e( E: awith CPP. The gonadotropin levels in this disorder. n0 O- _# r% O$ w
are suppressed to prepubertal levels and do not show
. [! a; p2 p3 ^% q6 A- X2 A0 Wpubertal response of gonadotropin after gonadotropin-
; N, G1 e( E3 u% s$ i+ areleasing hormone stimulation. This is a sex-linked
/ _0 b2 l7 P) n( s8 r6 e7 W! Nautosomal dominant disorder that affects only
5 u" f6 t: r4 d4 }males; therefore, other male members of the family
. U3 E3 ~2 D6 P0 B. c! [$ r4 Amay have similar precocious puberty.3* X2 h* d0 a% X# L' _. S
In our patient, physical examination was incon-- a! G& Z1 z9 _9 |" o" H) _
sistent with true precocious puberty since his testi-
5 J( h/ o0 k- x5 j- \) H; Vcles were prepubertal in size. However, testotoxicosis
' L e4 ^8 [' f. s- Pwas in the differential diagnosis because his father1 g9 z2 t6 w+ b* F( S# D
started puberty somewhat early, and occasionally,
6 B- D3 ~* p, a9 L0 a7 ?testicular enlargement is not that evident in the% M7 P# }: N! e7 M
beginning of this process.1 In the absence of a neg-0 n) m! I# O; w+ Z9 ^
ative initial history of androgen exposure, our
9 w, A4 T6 o! J; {( T, F" hbiggest concern was virilizing adrenal hyperplasia,7 H6 v% n1 z2 C1 x: \( d9 ]/ I1 S
either 21-hydroxylase deficiency or 11-β hydroxylase8 ^+ F/ R7 C8 P) R4 p8 v. }
deficiency. Those diagnoses were excluded by find-
) U( W8 K: }* @3 N Xing the normal level of adrenal steroids.
1 Z8 o% W& o, T D& eThe diagnosis of exogenous androgens was strongly* j6 J- {+ m0 \) Y# }/ z% e- c6 H
suspected in a follow-up visit after 4 months because4 k" V7 l( N+ j. _2 c( y
the physical examination revealed the complete disap-% E/ o; S& \% C- ]2 b
pearance of pubic hair, normal growth velocity, and2 u: a; z0 @* B0 }# ]. I
decreased erections. The father admitted using a testos-; I/ G9 M. m& H3 U+ D' `2 n
terone gel, which he concealed at first visit. He was, ~: h3 R- g1 \5 s+ Z4 F5 a$ ~8 Q9 G
using it rather frequently, twice a day. The Physicians’
, B. f D6 C& r9 oDesk Reference, or package insert of this product, gel or
# a: d4 l8 A' J1 t6 s7 p% vcream, cautions about dermal testosterone transfer to
/ V, X' Q. y( l! |* `) ^; v1 Ounprotected females through direct skin exposure.4 w) s7 {$ H% s* E& n/ Z
Serum testosterone level was found to be 2 times the8 r0 \% I6 F ~2 S% a
baseline value in those females who were exposed to) s! q- F3 i2 v7 s( `6 ~
even 15 minutes of direct skin contact with their male
" z3 u8 w, x9 p4 [' J9 z6 N. n1 }partners.6 However, when a shirt covered the applica-3 a& l, ]# Q8 |+ C( c5 M+ b2 ^
tion site, this testosterone transfer was prevented.6 I2 [5 _( m: n+ w& Q E
Our patient’s testosterone level was 60 ng/mL,8 E' U2 q9 s% g+ [% l& T
which was clearly high. Some studies suggest that8 i! E8 j) G: W6 s6 N: `: |
dermal conversion of testosterone to dihydrotestos-
, ^1 N5 a6 v$ u# x8 H Q7 u# P* V+ cterone, which is a more potent metabolite, is more
2 V4 G* \2 s8 c3 v Eactive in young children exposed to testosterone+ l, A- q. k8 R& t/ t8 [
exogenously7; however, we did not measure a dihy-. u7 l' r6 E' k e4 e) v* b2 U
drotestosterone level in our patient. In addition to' b. U+ c9 U$ {. a! t0 H: D
virilization, exposure to exogenous testosterone in
. d$ Z) |# x5 {( M9 kchildren results in an increase in growth velocity and5 A- a( X$ j/ [# X2 U" I& ^
advanced bone age, as seen in our patient.
+ N) L2 y! _6 jThe long-term effect of androgen exposure during
" \2 N8 W$ W5 m1 F) ?early childhood on pubertal development and final$ J) I: C e; c4 `
adult height are not fully known and always remain
, Q0 C! h+ p( F" Za concern. Children treated with short-term testos-) {7 P# H% b$ q9 I' i. L! p9 p9 @
terone injection or topical androgen may exhibit some
9 c" r7 _, M; @; {5 O. Gacceleration of the skeletal maturation; however, after
, ]4 b' @% Y7 n5 j* F$ Ccessation of treatment, the rate of bone maturation& T3 o- ?3 s8 ^# F
decelerates and gradually returns to normal.8,9+ b& i; n# }: l: I
There are conflicting reports and controversy* r% f `0 Y6 Q7 X& }9 I7 Q
over the effect of early androgen exposure on adult
( t% G( Y4 T* e3 w5 x* C dpenile length.10,11 Some reports suggest subnormal
1 j9 H) g# T) x4 ^) {+ c9 Nadult penile length, apparently because of downreg-- E! d/ @& L, f7 s4 {
ulation of androgen receptor number.10,12 However,: I% L! y- Q6 x5 x" k* d
Sutherland et al13 did not find a correlation between
. v' P+ {5 V: B' R5 _. x; ^& F2 K/ t, {childhood testosterone exposure and reduced adult* N) X* p$ Q8 }$ c+ N
penile length in clinical studies.
. G V/ ^1 ]! g7 Z |5 F- l# ^Nonetheless, we do not believe our patient is* d9 V, @& q6 s
going to experience any of the untoward effects from
: @- r- V, D8 T2 Gtestosterone exposure as mentioned earlier because
{( o( v8 S( g% Ithe exposure was not for a prolonged period of time.
' F9 ^$ ^; ?( W' }Although the bone age was advanced at the time of( |9 C: v$ t: T: U# s% P
diagnosis, the child had a normal growth velocity at& {* Q+ O5 L2 Z' X- F& B X
the follow-up visit. It is hoped that his final adult" R# ?% W+ `3 J q& K
height will not be affected.
, @8 x( ]2 e1 W; ~3 m! YAlthough rarely reported, the widespread avail-7 n8 F" H% `; ]4 d# k$ S! _
ability of androgen products in our society may
2 A: D* U" ]0 c* q" w2 l7 z/ _indeed cause more virilization in male or female, B6 V' ^) T( K/ B! D
children than one would realize. Exposure to andro-
* ?& Z3 n2 q7 s! K# rgen products must be considered and specific ques-9 ~- `* I, a( U+ [3 F
tioning about the use of a testosterone product or1 v! I. y) u" c' M# S
gel should be asked of the family members during
6 H! `% _0 }: \. u& Uthe evaluation of any children who present with vir-
f1 b# H Q+ q7 _2 Milization or peripheral precocious puberty. The diag-* ^$ x5 `+ Q' V; J m- G
nosis can be established by just a few tests and by6 E0 s/ z2 J% ?; X7 \0 [
appropriate history. The inability to obtain such a
+ ?! ~3 n" z- m/ U3 thistory, or failure to ask the specific questions, may! e7 l; R4 Y! a" w% Y0 o
result in extensive, unnecessary, and expensive
7 v3 a# K" q1 J5 \8 L7 Finvestigation. The primary care physician should be
* C& q8 W$ i. \- I' a$ naware of this fact, because most of these children8 {9 f& q% X* K2 m: P
may initially present in their practice. The Physicians’% V" @- S! F" L
Desk Reference and package insert should also put a4 w$ j* ?# k+ Y/ b% {
warning about the virilizing effect on a male or
* ^" v5 L( M' f* afemale child who might come in contact with some-" q* k/ {( q" m" R/ L6 ]
one using any of these products.
( A! L. ]) Y P' J+ RReferences
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Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- b. I& s. [8 }, n& ?2002: 565-628.1 n" }. i0 W9 x& Q( i i% ^2 R
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
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Dekker Inc; 2003:211-238.
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development in a two-year-old boy induced by topical0 ^) H$ G# W, U" G4 z
exposure to testosterone. Pediatrics. 1999;104:e23.
$ L! F1 `' H, P x. ?5. Greulich WW, Pyle SI, eds. Radiographic Atlas of8 c4 j1 ~6 y3 E' ~
Skeletal Development of the Hand and Wrist. 2nd ed.- ^' b: {, ^3 C. Q
Stanford, CA: Stanford University Press; 1959.
0 V% G' z4 R5 c; G( ?& i/ U5 B6. Physicians’ Desk Reference. Androgel 1% testosterone,
* M% v0 f N$ |, zUnimed Pharmaceutical Inc. Montvale, NJ: Medical8 f! y9 J5 B [6 {
Economics Company, Inc; 2004:3239-3241.; g' T1 z7 C* a
7. Klugo RC, Cerny JC. Response of micropenis to topical
/ B9 P) s+ l. y! f3 [! Ltestosterone and gonadotropin. J Urol. 1978;119:
; m- g9 M1 [ {" X, q" G& w667-668.
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