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is a significant concern for physicians. Central* Q! Z3 j3 l8 a' v
precocious puberty (CPP), which is mediated y1 v$ T. O* S& L
through the hypothalamic pituitary gonadal axis, has' B2 Y- V3 n4 s
a higher incidence of organic central nervous system" V- P7 `3 L6 a1 [) z, }
lesions in boys.1,2 Virilization in boys, as manifested$ @1 { A, A/ S+ k. n! I' z5 A
by enlargement of the penis, development of pubic o$ o6 U" Y) Q/ s- h1 v
hair, and facial acne without enlargement of testi-
% D1 ^, v* ?! ?cles, suggests peripheral or pseudopuberty.1-3 We4 A, h* u: A/ e3 s9 T1 Y# f/ H
report a 16-month-old boy who presented with the
1 I8 B( x! d4 q% n7 wenlargement of the phallus and pubic hair develop-/ Q. h, w' v* X8 @
ment without testicular enlargement, which was due
; e |" x$ l5 f5 D3 `+ e- q6 Jto the unintentional exposure to androgen gel used by5 y7 E9 Q+ g6 i ?& M) n) ?2 R( f
the father. The family initially concealed this infor-
9 L8 p! j& U1 c& t. ?/ e" Xmation, resulting in an extensive work-up for this
+ D+ L) d) G- Ychild. Given the widespread and easy availability of' [0 \2 T* W+ V d
testosterone gel and cream, we believe this is proba-; [ J3 `7 Q9 U' I# G
bly more common than the rare case report in the
I- a" Y% Q% o& ]+ S5 i3 vliterature.4
: h& M& V5 Z! Y& n+ U( c2 S" ^Patient Report6 g" b. X: c) x7 F I3 T
A 16-month-old white child was referred to the, q4 y a! [8 J4 Z r* ?: t0 L
endocrine clinic by his pediatrician with the concern
0 q/ ?- g* Z7 W0 C6 a0 Y X3 Uof early sexual development. His mother noticed: W1 f: X1 N5 N. k$ W
light colored pubic hair development when he was: w6 u5 {. N+ O! e0 M% n9 f
From the 1Division of Pediatric Endocrinology, 2University of8 Z8 |8 O8 G9 N
South Alabama Medical Center, Mobile, Alabama.
" \# w( O) o. dAddress correspondence to: Samar K. Bhowmick, MD, FACE,+ W7 G0 ]0 N4 m1 a7 Y2 B. O
Professor of Pediatrics, University of South Alabama, College of
H3 h1 ~" W/ I( yMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ A* b* P# q0 o7 i! b8 P1 H! ?" w
e-mail: [email protected].
1 f7 ^- v9 Z4 t. j/ W( ^! w$ V$ Cabout 6 to 7 months old, which progressively became/ Z9 J( D$ B. s
darker. She was also concerned about the enlarge-8 }+ q0 W5 O" ?) \ d
ment of his penis and frequent erections. The child; \, b. n3 v. h6 U" s
was the product of a full-term normal delivery, with
5 h, E8 X. N: ?* ia birth weight of 7 lb 14 oz, and birth length of& D; H- [5 D' I ^* U4 q
20 inches. He was breast-fed throughout the first year. v3 U, X; R9 A
of life and was still receiving breast milk along with
- L2 j* v2 q: ^0 T) Osolid food. He had no hospitalizations or surgery,. V; e% L/ r+ f1 C; O0 L f% O
and his psychosocial and psychomotor development
# o8 L4 d) w* U0 |" Wwas age appropriate.. c8 H0 A' s: [% c% U: ?4 m
The family history was remarkable for the father,2 y' B H$ H! B" `& }8 X
who was diagnosed with hypothyroidism at age 16," ?, b( x) i x/ ]. B
which was treated with thyroxine. The father’s
5 K4 M0 R, P: V. Aheight was 6 feet, and he went through a somewhat" F/ C5 e- s$ ^
early puberty and had stopped growing by age 14.
4 S2 q3 q6 F9 i5 G. GThe father denied taking any other medication. The
8 Z1 T* O: G+ k" |$ nchild’s mother was in good health. Her menarche/ K* x6 y- z9 ^' M
was at 11 years of age, and her height was at 5 feet5 P/ m1 I+ n& S: j2 t
5 inches. There was no other family history of pre-
4 u$ [/ n: e; J$ ]/ }( f2 icocious sexual development in the first-degree rela-
" r2 `0 N, ]. k v2 q9 ktives. There were no siblings., d* y0 z$ C8 M5 M5 O$ h( U( F
Physical Examination
" N& e( S7 I( u! bThe physical examination revealed a very active,0 r0 A2 m$ J6 M- F4 P' S E5 a+ O
playful, and healthy boy. The vital signs documented: E! }6 f9 j/ N4 x0 q6 ]! _
a blood pressure of 85/50 mm Hg, his length was% [6 n% _0 V/ |3 y7 j
90 cm (>97th percentile), and his weight was 14.4 kg; {/ \$ |+ o+ }$ N p0 W+ i9 Z2 D
(also >97th percentile). The observed yearly growth
+ D1 G! P4 J( K! \% `/ F2 {velocity was 30 cm (12 inches). The examination of
: ]# B# V# e T& b; v/ G* P% F9 Rthe neck revealed no thyroid enlargement.
1 ~; G! Q0 K1 `5 a$ mThe genitourinary examination was remarkable for
4 D' L$ o5 S$ e2 t# p6 Qenlargement of the penis, with a stretched length of& E U- \" y3 @9 D/ e0 e
8 cm and a width of 2 cm. The glans penis was very well
- ^& ^; ~7 A0 f5 r9 `( u9 O5 |; P7 odeveloped. The pubic hair was Tanner II, mostly around$ D# S6 u3 ~ w
540 N8 y6 f7 x) e) V! v( J- I+ n
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 j/ W0 H" n& j. pthe base of the phallus and was dark and curled. The7 a6 q1 ?& q9 F8 ?
testicular volume was prepubertal at 2 mL each.0 D7 j7 ] P- n
The skin was moist and smooth and somewhat6 _* [9 O* i/ K$ g+ s5 |# Y
oily. No axillary hair was noted. There were no: T0 }4 M& e4 Z
abnormal skin pigmentations or café-au-lait spots.7 x3 c( z+ O4 W: ~4 L E4 h
Neurologic evaluation showed deep tendon reflex 2+
$ L# P4 K, T) v b/ Y0 w3 Sbilateral and symmetrical. There was no suggestion& O1 Y6 g+ f' P: m( G. ^
of papilledema.
' H4 c6 @- ]: I6 zLaboratory Evaluation- |" Y$ L h, L) ?# {
The bone age was consistent with 28 months by
% e- k a8 c0 lusing the standard of Greulich and Pyle at a chrono-
$ ?- o- X5 g$ a- Alogic age of 16 months (advanced).5 Chromosomal
% }, G W2 O9 C7 R o, Fkaryotype was 46XY. The thyroid function test% I7 b! X# x# L9 g, ~
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
. ^8 G: b, d3 ~5 q1 olating hormone level was 1.3 µIU/mL (both normal).2 a# p0 j9 v7 d1 C* ]9 F
The concentrations of serum electrolytes, blood
2 h/ ^1 P: Z- |6 f* g" o/ ]urea nitrogen, creatinine, and calcium all were Y' z9 w6 ?+ g8 q- V7 b% h
within normal range for his age. The concentration# [2 x5 c' p1 T% _# x6 x) y
of serum 17-hydroxyprogesterone was 16 ng/dL
( E: U" u: I4 U- l( U% r(normal, 3 to 90 ng/dL), androstenedione was 20
9 B! v: I" Y* _- L* vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 }6 Y; D" m4 e1 m, e/ }terone was 38 ng/dL (normal, 50 to 760 ng/dL),
$ i% V! s) K* |- l6 `8 e6 Ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to$ h" v2 t C+ k; e& S
49ng/dL), 11-desoxycortisol (specific compound S)+ ?+ }% E# X+ |* j0 L
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-1 _) R( D, _8 _- j4 c& K# t
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' b; W1 e r$ d% e
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% R% c! g5 A: b( U/ xand β-human chorionic gonadotropin was less than6 t0 D9 Q2 g0 V
5 mIU/mL (normal <5 mIU/mL). Serum follicular
' J6 [5 n3 L9 G" h1 y1 ]stimulating hormone and leuteinizing hormone
& u7 @( H9 x% h" k' Rconcentrations were less than 0.05 mIU/mL8 g$ `4 F9 M0 I5 ?; H6 p/ _
(prepubertal)." u; G7 w+ H4 y) i, \7 h$ j
The parents were notified about the laboratory; u* t1 f* u7 C* W* ^: A0 p0 `# r
results and were informed that all of the tests were0 V+ F, U: L2 b0 b- o
normal except the testosterone level was high. The; T/ b+ Q( |/ p1 ]4 C
follow-up visit was arranged within a few weeks to+ m+ I9 d& u6 V F3 `4 y$ z! E: V
obtain testicular and abdominal sonograms; how-* |2 @' z# v8 S7 [ T
ever, the family did not return for 4 months.8 f; |2 p% ~% T" y9 Z
Physical examination at this time revealed that the4 c& _5 |1 X( i3 ~8 K5 A( `
child had grown 2.5 cm in 4 months and had gained
5 X* v4 t( D/ M' r2 `2 kg of weight. Physical examination remained& }" q; o9 ]9 a& c2 V) t
unchanged. Surprisingly, the pubic hair almost com-6 D* J5 w" t4 o( G
pletely disappeared except for a few vellous hairs at& y; t$ T$ d3 p- A( [
the base of the phallus. Testicular volume was still 20 z: G6 }7 ^ X0 o y) o+ x2 \. D# T4 g
mL, and the size of the penis remained unchanged.% T" W3 A S: T/ l/ y1 m0 M. n2 B8 G
The mother also said that the boy was no longer hav-
, i, v' J. O9 \ ?ing frequent erections.) L, \5 m+ s& E+ T7 H
Both parents were again questioned about use of* ~& g6 P* P+ ~: U5 Y
any ointment/creams that they may have applied to
" ^: ?5 m" }: e, q1 Nthe child’s skin. This time the father admitted the; e. c& e3 g& m
Topical Testosterone Exposure / Bhowmick et al 5410 D! g2 s9 P4 G0 K% S! {
use of testosterone gel twice daily that he was apply-
" B" C: m$ ^5 oing over his own shoulders, chest, and back area for6 g+ G$ I' w# f- i
a year. The father also revealed he was embarrassed3 ^- r1 m& \4 A6 L& N7 b' T
to disclose that he was using a testosterone gel pre-
- o7 R7 }" d" K w- [# Rscribed by his family physician for decreased libido
% p) u' i6 b7 ^5 T' T! Gsecondary to depression.
* `7 ^9 p6 ?( f' L G1 FThe child slept in the same bed with parents.
: D8 B" f4 Y2 V3 R1 mThe father would hug the baby and hold him on his
1 q; N- }; a4 y3 hchest for a considerable period of time, causing sig-! v8 C3 u7 b3 B1 V3 c+ c
nificant bare skin contact between baby and father.
0 ], R; j) t0 r# E4 hThe father also admitted that after the phone call,
' O, d: E0 i0 k3 r; l5 A6 iwhen he learned the testosterone level in the baby
W- g( M1 x; q, y! j+ @was high, he then read the product information3 `6 [: z9 _1 }; \6 U* F6 y
packet and concluded that it was most likely the rea-
3 Y8 R: F# M) J$ hson for the child’s virilization. At that time, they3 {! m* s. K8 x& S
decided to put the baby in a separate bed, and the U' U- S. l) I% c+ u
father was not hugging him with bare skin and had
5 B& Q# j# C9 ?2 tbeen using protective clothing. A repeat testosterone
) E- R/ [( U6 A# o2 Itest was ordered, but the family did not go to the) {" }5 o; y, ~3 C
laboratory to obtain the test.
! G7 w6 f4 w4 E3 C- D; h# CDiscussion
! ~( V m$ Z7 APrecocious puberty in boys is defined as secondary1 X0 g" ~* Y# g( ~/ ?. |
sexual development before 9 years of age.1,4
3 n, g9 s' I* Z. j4 m2 [: ]) _Precocious puberty is termed as central (true) when
# T' S3 Z! w, B. R3 N N. |9 jit is caused by the premature activation of hypo-
: L1 t! B" ^4 D- Nthalamic pituitary gonadal axis. CPP is more com-
" e/ Z* B4 F/ ~: F1 P7 J- d+ _mon in girls than in boys.1,3 Most boys with CPP/ P. M" i s9 H1 }: s% _
may have a central nervous system lesion that is
* V: Q8 B* |# G+ p# L4 gresponsible for the early activation of the hypothal-
/ S/ [ ?0 b. B0 Gamic pituitary gonadal axis.1-3 Thus, greater empha-3 N. N A+ T+ k: {. y/ t! I1 [
sis has been given to neuroradiologic imaging in6 y' h2 M, F& y9 A- w
boys with precocious puberty. In addition to viril-# s: u% {4 g, m- A9 j7 x* t. c
ization, the clinical hallmark of CPP is the symmet-
: B7 P2 c2 [ L3 Y7 |3 }& krical testicular growth secondary to stimulation by1 |/ O& Z U6 t; Y+ ^
gonadotropins.1,3
& Z% L+ }! C" }Gonadotropin-independent peripheral preco-
7 g7 D2 T7 D* l' {$ F3 b& r& y; r1 `cious puberty in boys also results from inappropriate& N) D8 _- E% a) ?
androgenic stimulation from either endogenous or7 E* H3 F3 t5 B& Y2 h! h4 u
exogenous sources, nonpituitary gonadotropin stim-
- D+ V6 `9 C: ]) X" K8 ~6 wulation, and rare activating mutations.3 Virilizing
1 c7 s1 Q6 Q. n1 P3 H7 G. }6 @congenital adrenal hyperplasia producing excessive
7 E6 g1 i. T8 v3 Y; \; y9 {adrenal androgens is a common cause of precocious
c) Y6 A5 G) A* `! Vpuberty in boys.3,4. S+ v3 T% }2 w& p ~9 o
The most common form of congenital adrenal
3 j5 g2 S$ D1 N, hhyperplasia is the 21-hydroxylase enzyme deficiency.
; v! N' D9 U+ [9 v3 n- o& YThe 11-β hydroxylase deficiency may also result in
0 ^, b* h' k' Y& e- }1 v2 Z6 |excessive adrenal androgen production, and rarely,# W7 q# W6 q4 K: t& b9 { a
an adrenal tumor may also cause adrenal androgen0 g4 r4 x; T# x
excess.1,3( u! j- j$ Y, X4 r- F) X
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' T" ~+ t; ]0 D! }0 f8 f542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 i2 b+ R, r# u
A unique entity of male-limited gonadotropin-
8 w- r- B( q4 b$ Findependent precocious puberty, which is also known
" Y8 P2 M2 p# u9 o5 F; R3 s4 qas testotoxicosis, may cause precocious puberty at a; P7 s& X8 A! W, P) M2 C- o! Z
very young age. The physical findings in these boys6 d* G/ }, o* o$ w" ]7 ?4 B" ~: }
with this disorder are full pubertal development,
, Z! l0 U9 E# v7 Y$ r; Y# \* eincluding bilateral testicular growth, similar to boys
5 d2 Z4 u3 X7 T+ K: V \* Z+ v& zwith CPP. The gonadotropin levels in this disorder
A2 }& b8 O9 hare suppressed to prepubertal levels and do not show6 t2 t, j; e+ {& e1 {8 z
pubertal response of gonadotropin after gonadotropin-# X) N( O' |# q4 Z% Z( S5 b$ b
releasing hormone stimulation. This is a sex-linked
% G' e( Q3 `& u$ z# c2 K( O, aautosomal dominant disorder that affects only) S5 s* i, Z5 ?% n G, x+ e
males; therefore, other male members of the family: `( f$ X' H; W4 O
may have similar precocious puberty.3
5 \. Q; |2 H6 N! U# Z0 ]% xIn our patient, physical examination was incon-
& l3 x) V7 N3 S+ Isistent with true precocious puberty since his testi-
+ g" W0 o' L3 G* b" B- [( Wcles were prepubertal in size. However, testotoxicosis2 ^) ~) h6 `3 Z; C
was in the differential diagnosis because his father
5 B" T( W; V6 B( c: @0 ^$ qstarted puberty somewhat early, and occasionally,
" n) ^5 @7 P3 @/ n+ I6 U. T! X. G) Rtesticular enlargement is not that evident in the+ h9 A" _/ J( k" F
beginning of this process.1 In the absence of a neg-! o' D2 P; J7 p
ative initial history of androgen exposure, our
+ a/ } y& ^2 z4 f8 _7 G& }. abiggest concern was virilizing adrenal hyperplasia,; D p) ~* s3 n9 D
either 21-hydroxylase deficiency or 11-β hydroxylase' X& ^1 i% E& i7 D' y+ ]$ S& b% N/ p: I
deficiency. Those diagnoses were excluded by find-, W: }5 U1 z/ F- n7 M
ing the normal level of adrenal steroids.
6 w! P4 b3 ?9 R( h+ ^% R+ i6 dThe diagnosis of exogenous androgens was strongly- m1 ]4 @! `0 n! v0 r
suspected in a follow-up visit after 4 months because) o. {. u! F% A
the physical examination revealed the complete disap- ~; e& B& m2 h
pearance of pubic hair, normal growth velocity, and
. u4 b3 G6 j& C* Y$ t- S: I3 S$ adecreased erections. The father admitted using a testos-4 Y* ~* s' E: K" I
terone gel, which he concealed at first visit. He was; ?) L: c1 l3 o* U
using it rather frequently, twice a day. The Physicians’
- r% ]8 [$ J; z; R, C' E, U/ mDesk Reference, or package insert of this product, gel or# }! ~, X: V. a
cream, cautions about dermal testosterone transfer to0 @& o, c8 E1 G* p- ~
unprotected females through direct skin exposure.
5 N; R: g; ?0 `4 A: cSerum testosterone level was found to be 2 times the
: r3 r4 u5 j- ?7 s: T9 Ybaseline value in those females who were exposed to: T; Y3 O# F! U2 k# a% o0 K
even 15 minutes of direct skin contact with their male/ r" H2 b( p$ n: y g! \- _
partners.6 However, when a shirt covered the applica-
1 r6 R6 V- g3 j/ d8 @2 ftion site, this testosterone transfer was prevented., c2 Q/ k7 g5 K" I7 v
Our patient’s testosterone level was 60 ng/mL,6 h {; b+ L$ h+ q: K* v
which was clearly high. Some studies suggest that
; ~" z2 v7 S( ?: Xdermal conversion of testosterone to dihydrotestos-
4 z- [; f F2 {) U5 i7 k6 W0 c) bterone, which is a more potent metabolite, is more
& h3 q* F) S: S8 |# eactive in young children exposed to testosterone
4 v7 S i2 |2 E- O. }- N8 D2 texogenously7; however, we did not measure a dihy-
3 _4 b+ A+ E' Qdrotestosterone level in our patient. In addition to' @. u M% x' Q7 r& U6 G) ]* h; Q! W
virilization, exposure to exogenous testosterone in
# S( L: {) A7 J1 m& E' Y( J# X4 Schildren results in an increase in growth velocity and6 U2 M9 d% k% t7 h
advanced bone age, as seen in our patient.
) z$ C( s. C% ?# U" W6 ZThe long-term effect of androgen exposure during
& ]5 c" j$ H$ B/ m4 q! Q. yearly childhood on pubertal development and final
' c4 E; W5 z8 I+ z2 h" radult height are not fully known and always remain) N' B& N: E1 _. d( K8 t7 Z1 d
a concern. Children treated with short-term testos-# @ ^4 @4 c1 f5 X1 V
terone injection or topical androgen may exhibit some+ h+ M. ?5 ?7 s% m+ B6 V& z
acceleration of the skeletal maturation; however, after
. Y; H- A5 @% v) f% `$ K( Scessation of treatment, the rate of bone maturation1 C p* l: K% D/ d" n
decelerates and gradually returns to normal.8,9
$ C8 g$ _4 |$ ~2 Q: {6 V& C( S! l( ZThere are conflicting reports and controversy
1 ~/ s- Z1 n1 I5 W l2 oover the effect of early androgen exposure on adult) F: t' J& F3 H& E; m+ w7 |
penile length.10,11 Some reports suggest subnormal6 R* s2 p8 l. ^6 c, _6 g
adult penile length, apparently because of downreg-
1 V9 i- t/ {! l/ A8 x' E* gulation of androgen receptor number.10,12 However,
9 R' M: Q2 p0 Q; mSutherland et al13 did not find a correlation between* R0 u x" A1 a# m. h; B, c
childhood testosterone exposure and reduced adult# h% W4 }/ h5 m# p( H
penile length in clinical studies.
4 \+ O9 E" G* r7 a' e+ ANonetheless, we do not believe our patient is; Q. y7 \1 D1 p, `6 A( q
going to experience any of the untoward effects from( p: [' j! t" W; A) i
testosterone exposure as mentioned earlier because- l& p) w! Y0 ~& `& w: ^
the exposure was not for a prolonged period of time.8 j' }7 E) a @
Although the bone age was advanced at the time of8 }! \# K2 k0 n8 z7 ^$ m# a0 E
diagnosis, the child had a normal growth velocity at) {$ ^4 z4 U9 _( r0 A9 Z' R
the follow-up visit. It is hoped that his final adult
- q% ?# b( S, B! Z! j7 a( Eheight will not be affected.
2 X# a5 W* M8 _0 f$ J7 }' LAlthough rarely reported, the widespread avail-! [. N' y2 d5 {+ G
ability of androgen products in our society may s; D7 A! ]$ l) g, h {% K+ h4 {
indeed cause more virilization in male or female
9 i! x+ p% z! Q- s5 X, B8 ychildren than one would realize. Exposure to andro-+ Q8 r; p" V. @
gen products must be considered and specific ques-
5 m! G, r0 R/ Y( Jtioning about the use of a testosterone product or# o0 d+ x+ n. X" k7 K% q; A) j
gel should be asked of the family members during* u: |3 j8 u; l7 j9 ]7 ?
the evaluation of any children who present with vir-' r+ s' G) l" `: k
ilization or peripheral precocious puberty. The diag-" Z/ \/ O2 v" _4 n
nosis can be established by just a few tests and by4 B, P0 m) B7 R+ E
appropriate history. The inability to obtain such a, R* t& H- I0 m6 N8 t4 I
history, or failure to ask the specific questions, may4 y$ L9 J6 z/ j! }, j2 W
result in extensive, unnecessary, and expensive" ]3 x- X8 E* K* D/ F6 L
investigation. The primary care physician should be
# u: X# k6 k9 }7 I0 {aware of this fact, because most of these children
3 r( d0 h# L' z) G5 D0 `& d- Nmay initially present in their practice. The Physicians’6 q$ `8 A. ^, `' Q- R) ^
Desk Reference and package insert should also put a
5 o+ j* l3 o9 v$ ]5 Jwarning about the virilizing effect on a male or
* U- I' p" G( L1 Q* o$ @female child who might come in contact with some-
$ t4 p3 S+ ~- {9 N' _8 Kone using any of these products.( u: Z/ B1 P8 g$ i: p
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9 T; `1 _ A I+ `) f, j1 O2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' P% Z W2 e7 e! e9 X J4 d4 Kpuberty in children with tumours of the suprasellar pineal
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development in a two-year-old boy induced by topical
) o) D( v5 Y0 pexposure to testosterone. Pediatrics. 1999;104:e23.
! R; k9 l* w6 ^7 Q& t4 ?; l- I. b5. Greulich WW, Pyle SI, eds. Radiographic Atlas of
. Y/ G% O; \ p. l. T& _3 ?& }" j- @ eSkeletal Development of the Hand and Wrist. 2nd ed.
* _; E* w. R- ^" {7 oStanford, CA: Stanford University Press; 1959.& |9 Q' S J$ R; R
6. Physicians’ Desk Reference. Androgel 1% testosterone,: H4 `+ H. S# Y) c
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Economics Company, Inc; 2004:3239-3241.
6 {# F- ^1 i5 y8 |) r7. Klugo RC, Cerny JC. Response of micropenis to topical
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