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Sexual Precocity in a 16-Month-Old8 R1 q, S; j( A7 R4 x
Boy Induced by Indirect Topical
: |0 ]8 k8 k: JExposure to Testosterone
7 j/ \0 H" |- e u! RSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 W7 G% y0 m+ Z: {& H1 |
and Kenneth R. Rettig, MD19 w. Z% L% h+ ?/ i
Clinical Pediatrics
7 U3 N6 ]" D/ AVolume 46 Number 6
- Y: O* ~! X' |2 w4 Q G3 hJuly 2007 540-5439 K6 V/ G- V" s! j, {) ?
© 2007 Sage Publications; S& L) c& z, d, E0 y% Q
10.1177/00099228062966514 q- r, N {& P# l
http://clp.sagepub.com% d/ k! w6 Y! G- n7 _& y
hosted at. m9 P/ z4 W( ^1 Q
http://online.sagepub.com
, j/ K$ M4 z. v/ Y$ b8 BPrecocious puberty in boys, central or peripheral,+ v% k( f2 w9 _+ |
is a significant concern for physicians. Central |& U( v; i1 b5 ?+ e
precocious puberty (CPP), which is mediated1 b+ u( O, q8 W
through the hypothalamic pituitary gonadal axis, has/ }( h& g! K, S% s+ Z* B; o& K
a higher incidence of organic central nervous system( I% ]1 W2 B, q' H2 K1 A) G3 h
lesions in boys.1,2 Virilization in boys, as manifested( Y0 y5 ?5 ^* `% n9 W. T1 y& X3 G
by enlargement of the penis, development of pubic
. p, A2 q4 w: C1 Q2 w7 dhair, and facial acne without enlargement of testi-
, ]$ \3 s4 ~: ~2 F6 w, h) V7 G) Zcles, suggests peripheral or pseudopuberty.1-3 We
& s+ v9 c- ^. f& x% Ureport a 16-month-old boy who presented with the
" y2 G2 T# f5 [: Denlargement of the phallus and pubic hair develop-5 X; @. L2 S; s! x5 I0 w4 @% s
ment without testicular enlargement, which was due
; \1 A" }$ A/ W( R! }6 ]to the unintentional exposure to androgen gel used by5 E9 \. a; F5 Q& o2 j
the father. The family initially concealed this infor-
8 s W7 q. x$ C/ c8 u$ Kmation, resulting in an extensive work-up for this
: s- |9 g8 `4 }) i; c9 echild. Given the widespread and easy availability of8 ]" @' O. h. A' K: ~" L+ T( W
testosterone gel and cream, we believe this is proba-
+ _( j n( E) Q1 Z9 M' Ably more common than the rare case report in the
5 N* f8 _5 S1 Q0 u7 j" G& J wliterature.4
6 V$ ~# g* }2 x; u/ Q7 i1 `2 {Patient Report
8 a' {3 ]5 W' N1 ]9 mA 16-month-old white child was referred to the1 e0 x7 r) L X g5 e9 |. h
endocrine clinic by his pediatrician with the concern a7 l6 T6 @. K D2 B
of early sexual development. His mother noticed6 O, E. h" l; p7 |$ @8 P
light colored pubic hair development when he was3 t+ ~5 ^. z, w( T! L
From the 1Division of Pediatric Endocrinology, 2University of" P3 z1 w! U1 ~4 \- l0 g
South Alabama Medical Center, Mobile, Alabama.( P' B( b# p6 l. G! q
Address correspondence to: Samar K. Bhowmick, MD, FACE,# M8 Y+ n7 {* D$ |8 J
Professor of Pediatrics, University of South Alabama, College of! o! R0 m1 Y3 o: \; |8 e' R! K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;5 z0 q- R* c% T2 r
e-mail: [email protected].
4 T; `# S4 z3 ~" K( L( V7 Oabout 6 to 7 months old, which progressively became
) w" k# s* [! s& E( s9 {darker. She was also concerned about the enlarge-1 i, d$ W9 w' ?
ment of his penis and frequent erections. The child
) b& {( d3 q, x! }1 pwas the product of a full-term normal delivery, with
$ n8 m' t' W; r2 m* Ka birth weight of 7 lb 14 oz, and birth length of6 T3 i9 q9 z( N
20 inches. He was breast-fed throughout the first year' s. O: v+ d8 G
of life and was still receiving breast milk along with
$ f4 ]* Z, [) w! \: ysolid food. He had no hospitalizations or surgery,( X6 n6 [5 Q1 p& H
and his psychosocial and psychomotor development
" x( I* h: J) }5 j" Qwas age appropriate.
! |& y+ R' |1 y* `& f. kThe family history was remarkable for the father,
1 w |0 V6 Z n, \who was diagnosed with hypothyroidism at age 16,
, e: x6 k9 u5 L0 O4 x1 Gwhich was treated with thyroxine. The father’s, @8 S: M* C* v7 E3 K$ Y
height was 6 feet, and he went through a somewhat
4 _+ f$ U y# n6 E1 }% E: A) | Bearly puberty and had stopped growing by age 14.4 ~+ Y0 a6 W5 D, d
The father denied taking any other medication. The
; j4 I1 {6 V. h7 t, [child’s mother was in good health. Her menarche
9 v! X& H) n" N+ J% bwas at 11 years of age, and her height was at 5 feet2 [- q; T, r! G: W
5 inches. There was no other family history of pre-
M3 i9 X6 C% V! ?cocious sexual development in the first-degree rela-
6 @* D& L+ d- u v. _% X+ g( utives. There were no siblings.- P1 B) O; Z { O, R8 o6 J6 a
Physical Examination
% l: K Q6 D' ~# x7 m& a& J+ g( V! EThe physical examination revealed a very active,. F1 y1 S+ w3 H+ K A6 _+ V% A
playful, and healthy boy. The vital signs documented
( j9 W7 H6 u& O! x* fa blood pressure of 85/50 mm Hg, his length was9 }) E5 U" H" s2 _
90 cm (>97th percentile), and his weight was 14.4 kg. i9 P# N, C2 x N
(also >97th percentile). The observed yearly growth
- B; r& }3 o$ m7 M7 h& O; Qvelocity was 30 cm (12 inches). The examination of
+ b0 m a' o+ M+ hthe neck revealed no thyroid enlargement.2 R; g, r, a F% m
The genitourinary examination was remarkable for6 Q$ h1 f U! P' _7 S
enlargement of the penis, with a stretched length of7 S m% m: H8 e& u& Z2 N8 z4 f
8 cm and a width of 2 cm. The glans penis was very well4 U! t3 d2 r* A/ ], L5 p
developed. The pubic hair was Tanner II, mostly around
& ~4 A- V, t, |9 F540 ~* G0 L% F9 l: }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 i* O1 h# P' pthe base of the phallus and was dark and curled. The
0 v: ^$ `6 x5 J/ {$ v8 z' ]. X2 g! I; Ytesticular volume was prepubertal at 2 mL each.
7 G B& m/ \! uThe skin was moist and smooth and somewhat9 m: a: y4 i8 y' w4 R
oily. No axillary hair was noted. There were no
: A/ z V: u% Dabnormal skin pigmentations or café-au-lait spots.4 I4 F& D7 U& o5 u7 Z
Neurologic evaluation showed deep tendon reflex 2+
" Z/ w9 X* a% @% Ebilateral and symmetrical. There was no suggestion
! @; w$ a( N1 c" cof papilledema.% U. h$ H* l6 K+ h, B$ N( I( ]
Laboratory Evaluation
9 t8 O7 _. R$ b4 gThe bone age was consistent with 28 months by$ @+ l! z( \7 O& T6 o
using the standard of Greulich and Pyle at a chrono-
8 x/ ^$ A/ M: X7 ?4 qlogic age of 16 months (advanced).5 Chromosomal& ]5 C; w- q/ i' W& |4 s
karyotype was 46XY. The thyroid function test
+ ^+ p6 Z- A, X7 ~- d9 Z( Fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 e+ I4 s! l, H8 c7 flating hormone level was 1.3 µIU/mL (both normal).* W J, [( L0 L4 P' r6 R- k" V
The concentrations of serum electrolytes, blood& C# K6 Z, h7 D. D5 Q: T
urea nitrogen, creatinine, and calcium all were6 t8 G1 m ]) Z. y7 m. y
within normal range for his age. The concentration
+ k" i, q/ G4 `4 O! p; [ u4 {of serum 17-hydroxyprogesterone was 16 ng/dL
, V7 l4 H5 h, l5 p7 g1 ]; R(normal, 3 to 90 ng/dL), androstenedione was 20* T% X( g! \% l
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
2 t" q( n" y( B& J* E9 qterone was 38 ng/dL (normal, 50 to 760 ng/dL),
8 ^8 H" J( L+ h/ qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
9 N3 k, R: B1 \5 v! W49ng/dL), 11-desoxycortisol (specific compound S)
8 R4 h* Q. B* t1 t( r/ ~( g Bwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 V- }( L O; `3 W" {0 L8 r) Gtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 t3 l; ~* d; r% f* x+ k/ V
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 d6 {$ a# x( J; x7 `5 b3 ?and β-human chorionic gonadotropin was less than
$ Y$ q2 b! H+ [& K c2 O5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 O1 O% X, t/ Z) t0 C2 sstimulating hormone and leuteinizing hormone
3 l, C6 I8 P8 D3 b* Q/ U% t) D; y8 hconcentrations were less than 0.05 mIU/mL
' E5 O4 i" l0 \(prepubertal).
" u2 _9 j3 X: c- aThe parents were notified about the laboratory
5 Q9 R" ] s; [1 \6 cresults and were informed that all of the tests were; m/ c. ~& `7 ^
normal except the testosterone level was high. The
/ k$ ]( [$ o2 C4 r) o7 y7 ~ bfollow-up visit was arranged within a few weeks to( Z6 {2 G( }" r% R7 ?# h
obtain testicular and abdominal sonograms; how- ~6 \7 r+ B3 B- ~0 ^6 G; E
ever, the family did not return for 4 months.
% X* x! \$ ?) T( @' O) pPhysical examination at this time revealed that the
% j5 _% X. U8 @1 t- g/ w/ c/ R0 U) fchild had grown 2.5 cm in 4 months and had gained
9 ~, ]- h9 ]/ U, U- d2 kg of weight. Physical examination remained3 m- }. M9 `, Z7 Q
unchanged. Surprisingly, the pubic hair almost com-) W, t# m8 q" X- ?+ k8 G! C
pletely disappeared except for a few vellous hairs at+ J8 G5 k, I V! g2 l, ^3 f
the base of the phallus. Testicular volume was still 28 m# t$ O) B% ]$ u/ F* {$ @7 C1 n
mL, and the size of the penis remained unchanged./ o0 q( ^- U! d# j
The mother also said that the boy was no longer hav-6 F2 P+ M# d: t" f: H7 Y
ing frequent erections.
( ?; Z: |# S; b, c6 ^( e9 ]+ _Both parents were again questioned about use of$ _( w* i& w Q" ?4 `. A% t# }9 l+ S5 W
any ointment/creams that they may have applied to
: N; p3 N& j6 r3 _& }( g" Cthe child’s skin. This time the father admitted the
, k7 s, k2 A3 kTopical Testosterone Exposure / Bhowmick et al 541
, k7 G7 R2 a& v! d1 Euse of testosterone gel twice daily that he was apply-
" U7 l' i- d8 _2 H) }! wing over his own shoulders, chest, and back area for$ ]6 R: L( Q. s
a year. The father also revealed he was embarrassed
8 `* @! S7 T/ B! c0 A: `to disclose that he was using a testosterone gel pre-$ W$ Q1 z% m0 t) P; Q, M0 l6 `
scribed by his family physician for decreased libido+ y& B/ a- V6 M% p, b! a
secondary to depression.1 S# K$ J$ q( W1 n$ _5 ]
The child slept in the same bed with parents.
1 h" \* y0 H& Z* Y0 @* H4 @The father would hug the baby and hold him on his8 J. h }7 F- b
chest for a considerable period of time, causing sig-
) O) f+ a! ]' ]/ f" qnificant bare skin contact between baby and father.' r6 C/ h1 U7 x) e9 p6 a; j
The father also admitted that after the phone call,
- l+ t* [; i9 q4 k+ U$ f; bwhen he learned the testosterone level in the baby# W: \6 T# O8 |# g
was high, he then read the product information% Q) ~5 r4 a1 p3 I' \2 j
packet and concluded that it was most likely the rea-
) @+ x& j+ I3 J/ Json for the child’s virilization. At that time, they& y/ G+ m% s" [
decided to put the baby in a separate bed, and the/ o% i2 W5 ^. m; _8 p( X2 Y# T
father was not hugging him with bare skin and had. {. w, |% W" c7 x$ i8 ]
been using protective clothing. A repeat testosterone0 j- w5 ^" j5 ]) }
test was ordered, but the family did not go to the
7 Y0 u2 }4 x0 e" `9 alaboratory to obtain the test.
' Z2 V& J/ T* R# o7 V% I* `6 jDiscussion' Q- ]: f4 f1 A* @0 q
Precocious puberty in boys is defined as secondary
7 O0 ^7 u: P: O Wsexual development before 9 years of age.1,4 ^ X c3 H6 k* ]' f( W
Precocious puberty is termed as central (true) when0 Y/ V9 [& Z; j3 `
it is caused by the premature activation of hypo-
: P7 [$ W+ T- I; j+ @; f" [& Bthalamic pituitary gonadal axis. CPP is more com-* U. j6 ?4 F1 }2 y( J
mon in girls than in boys.1,3 Most boys with CPP
& f0 e. q3 F; B# C8 O+ e# @) q' }may have a central nervous system lesion that is" z* L$ h: l4 A/ ?/ [
responsible for the early activation of the hypothal-/ m9 @* H. k5 A: u- ~) h, H
amic pituitary gonadal axis.1-3 Thus, greater empha-
3 e- U3 g' d4 v ~5 j: hsis has been given to neuroradiologic imaging in
2 S" o& j% ]3 T$ v Fboys with precocious puberty. In addition to viril-! ` B6 m# d; u1 b* ]3 h
ization, the clinical hallmark of CPP is the symmet-$ ^; u% y1 g- ]
rical testicular growth secondary to stimulation by
X' Y- H0 v5 s/ Rgonadotropins.1,30 z+ F3 m, e. x4 h* H/ ]
Gonadotropin-independent peripheral preco-
$ `5 T; w" a' h! Kcious puberty in boys also results from inappropriate
$ ]' X! b8 M- K/ C1 R7 Tandrogenic stimulation from either endogenous or% |1 V- X) r/ _" u% g) X5 Z
exogenous sources, nonpituitary gonadotropin stim-
5 `+ o; K! [6 D4 |ulation, and rare activating mutations.3 Virilizing
7 Q p! i7 F7 {, j/ s* j2 qcongenital adrenal hyperplasia producing excessive
3 J7 d8 }/ Z+ G$ a; R/ Xadrenal androgens is a common cause of precocious
0 K8 ^' }3 O$ ]$ l8 opuberty in boys.3,4
3 N- h0 X; \9 _6 H7 OThe most common form of congenital adrenal% E6 m6 v: F5 b0 F. e* s
hyperplasia is the 21-hydroxylase enzyme deficiency.3 C( ~6 Z& g; Z( U8 S
The 11-β hydroxylase deficiency may also result in
3 k8 b8 c+ q; W) Z% Wexcessive adrenal androgen production, and rarely,
1 e$ u) O! F" v" Qan adrenal tumor may also cause adrenal androgen4 S2 o) S' i) \
excess.1,3
y8 n9 \6 E) y7 O7 y4 c2 uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. b' H0 K3 h' W+ e
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007. `: Z4 `" O7 o0 A* R
A unique entity of male-limited gonadotropin-
+ y. S; R; ]8 y* ]independent precocious puberty, which is also known' U( k. a: I% A$ N" Y
as testotoxicosis, may cause precocious puberty at a1 E+ U7 n. f" v* }* P7 W
very young age. The physical findings in these boys
1 q: o0 h' e0 E e' v8 Bwith this disorder are full pubertal development,
. y2 `8 j2 j- z* nincluding bilateral testicular growth, similar to boys
5 R! c5 `- r! Qwith CPP. The gonadotropin levels in this disorder9 O, ]6 H* s- H4 e! c
are suppressed to prepubertal levels and do not show
' g# `- e1 D1 P, ~7 Gpubertal response of gonadotropin after gonadotropin-
+ j# _' ^+ L* z$ n( F. R6 j" t$ ?releasing hormone stimulation. This is a sex-linked) V$ U; W/ a( S0 S! l
autosomal dominant disorder that affects only2 p2 h+ C [% X0 ~6 Q& |+ W
males; therefore, other male members of the family0 m# ~" G D* S7 l' [, g# i1 q
may have similar precocious puberty.39 H) X# H% S) g3 L1 ~# b! i
In our patient, physical examination was incon-. R/ w$ _) Q, S' b
sistent with true precocious puberty since his testi-
0 c" Y( ?1 _' Q+ C/ S1 [& Ccles were prepubertal in size. However, testotoxicosis( n: _% I3 a$ j4 Y$ _
was in the differential diagnosis because his father- q( |# q7 z1 y% Y3 }7 M2 }
started puberty somewhat early, and occasionally,% H, N: M4 W1 x) n5 Y6 j0 J% A
testicular enlargement is not that evident in the! T9 J0 e p: A, X; c; |* K
beginning of this process.1 In the absence of a neg-8 c5 k. C) _7 t& S! l4 b, t
ative initial history of androgen exposure, our! u( j( i$ e3 J# d% }
biggest concern was virilizing adrenal hyperplasia,8 e7 J T, T4 q& R" q$ C
either 21-hydroxylase deficiency or 11-β hydroxylase" K- U+ W! Y7 L1 g. |- H
deficiency. Those diagnoses were excluded by find- _$ V" z1 i0 t0 S5 \0 u: ^
ing the normal level of adrenal steroids.. C& z( F4 S8 ], _* I9 ~
The diagnosis of exogenous androgens was strongly g X# { P; F1 k1 |8 K9 a$ Q% K
suspected in a follow-up visit after 4 months because
0 z; l1 m9 N: g, athe physical examination revealed the complete disap-, @4 z5 r& y3 g- ?5 S2 i2 x' Y, T
pearance of pubic hair, normal growth velocity, and1 s1 j1 E! {5 d$ t
decreased erections. The father admitted using a testos-
/ u$ r9 |! o; R8 j' Fterone gel, which he concealed at first visit. He was
. N/ A9 ]# q2 j# _using it rather frequently, twice a day. The Physicians’
; e/ u7 ?* f" w' I$ A. DDesk Reference, or package insert of this product, gel or& P1 d) X4 X/ M; o. N8 Z; h
cream, cautions about dermal testosterone transfer to
% H8 y" V0 } t2 b. W6 b" Uunprotected females through direct skin exposure.! O0 f5 A* ~! x
Serum testosterone level was found to be 2 times the; m9 I/ W$ J* Q: ?7 Z! H' D2 d7 C
baseline value in those females who were exposed to
) [) v+ \7 `" c" U; v- M" Geven 15 minutes of direct skin contact with their male
! U) w) K) E# n3 D0 S4 v. _/ vpartners.6 However, when a shirt covered the applica-
' \; r. G: g* ?) P5 a; X, Ttion site, this testosterone transfer was prevented.
. e# q2 R8 ]& S; E6 s8 ?% r; SOur patient’s testosterone level was 60 ng/mL,& u' Y! f. j* L3 V# ]9 \
which was clearly high. Some studies suggest that+ u( U5 H, k6 N! S% h8 d- A+ S
dermal conversion of testosterone to dihydrotestos-
" B: p0 b7 s; K+ B4 ?terone, which is a more potent metabolite, is more
" f0 K/ O1 R" d; Mactive in young children exposed to testosterone) [) o) D7 ^% V: g# G
exogenously7; however, we did not measure a dihy-7 f0 f( M+ ?% I) f
drotestosterone level in our patient. In addition to
4 [3 P* G; v7 bvirilization, exposure to exogenous testosterone in
1 |8 u5 t; j* ?' _3 ~- d" Mchildren results in an increase in growth velocity and, |, P9 N1 a1 b# g0 X
advanced bone age, as seen in our patient.3 F0 F& b' b) @& `$ A( s$ @' n9 f
The long-term effect of androgen exposure during4 z( A, y$ g! M
early childhood on pubertal development and final
, P6 ~2 y( X! u1 _, h, Jadult height are not fully known and always remain& K. Q5 i+ r; r+ `3 F- I
a concern. Children treated with short-term testos-
% X# x a* A. v! A9 ?- sterone injection or topical androgen may exhibit some! x+ \) s1 S: M' y" G
acceleration of the skeletal maturation; however, after
m: V+ Z6 m5 S/ N" t' o Rcessation of treatment, the rate of bone maturation
( d% @7 v# Q9 z+ pdecelerates and gradually returns to normal.8,9
- p6 {1 i# W9 rThere are conflicting reports and controversy$ S0 Q- V8 x9 J% w5 a, }
over the effect of early androgen exposure on adult3 J2 X% D( |7 x" w
penile length.10,11 Some reports suggest subnormal
, P( X' s9 `0 M7 S+ [, W+ Xadult penile length, apparently because of downreg-4 I& w# F+ v& Z
ulation of androgen receptor number.10,12 However,
& D8 L% j" s% ^' @& VSutherland et al13 did not find a correlation between
; B" F5 e2 z) m! w: k- Echildhood testosterone exposure and reduced adult" R9 Y. [) N. F, H# i, S
penile length in clinical studies.
1 X. j( S! n' Q" @4 G9 kNonetheless, we do not believe our patient is( D3 F/ o3 {; k6 N3 R. H
going to experience any of the untoward effects from
. z5 K8 c3 a& @9 m2 y1 Ptestosterone exposure as mentioned earlier because
" R+ ~' j7 \) J$ v# Q0 Cthe exposure was not for a prolonged period of time.# D! L- c) n4 H K" }9 L
Although the bone age was advanced at the time of
R6 C7 e- f0 b! Y5 Idiagnosis, the child had a normal growth velocity at* X- N' c$ i8 Z- l
the follow-up visit. It is hoped that his final adult
3 \1 h+ S% ~- t# S- }height will not be affected.5 ^' e3 g+ n! x1 J8 g) H
Although rarely reported, the widespread avail-
2 q+ r+ f& B f7 {ability of androgen products in our society may& }4 v- ?, p/ Y
indeed cause more virilization in male or female. B1 Y/ s5 _1 y. L5 j$ k! e2 a9 w
children than one would realize. Exposure to andro-
! {: g8 r, H/ g7 W; e3 cgen products must be considered and specific ques-2 O& s1 p8 V7 V" L! P2 Y4 c2 } r9 g
tioning about the use of a testosterone product or5 P8 u5 j, b) S( |+ ~9 V6 m
gel should be asked of the family members during
, S2 t/ d) a* }the evaluation of any children who present with vir-. y0 x8 z# A4 B2 O
ilization or peripheral precocious puberty. The diag-. F! E: b! j. K5 m& H/ n
nosis can be established by just a few tests and by
* D4 A$ o" B) z% U' Jappropriate history. The inability to obtain such a4 P+ Z0 c" J" o1 I( {7 j
history, or failure to ask the specific questions, may. q. |8 \+ Z# |5 K' @. J' n, X
result in extensive, unnecessary, and expensive
$ M+ H [$ i4 O2 M' Z4 g _+ kinvestigation. The primary care physician should be P0 S8 C, N/ D# Y* K4 ]
aware of this fact, because most of these children7 z2 W: p3 r8 L7 I$ @2 r, ^
may initially present in their practice. The Physicians’1 \' \" j6 d+ ~$ b3 }
Desk Reference and package insert should also put a: _$ x; ]0 o1 d* a4 {) j
warning about the virilizing effect on a male or: W! D! O; a7 p" n
female child who might come in contact with some-. r9 V6 w& [% G0 ~( t
one using any of these products.# v6 c- |5 h& [
References
9 p) Q' v9 P: k. u. n! C1. Styne DM. The testes: disorder of sexual differentiation
/ E; }! ?5 u' `3 u: N kand puberty in the male. In: Sperling MA, ed. Pediatric
* _7 r/ V- W6 F" [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders; d# V8 A* M- r2 M
2002: 565-628.
+ u H7 y" K5 m2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious5 U, {' G0 X: N' F5 w% y: ^/ {0 r, H
puberty in children with tumours of the suprasellar pineal |
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