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Sexual Precocity in a 16-Month-Old) e5 H" N* K- q. R) N6 g
Boy Induced by Indirect Topical% D: V5 g: @/ k+ \
Exposure to Testosterone
9 O/ S1 I' Q7 v" ]; P$ W2 tSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- f, B1 u m9 i6 r
and Kenneth R. Rettig, MD1
% [6 d: Z' a4 d& R1 pClinical Pediatrics
# b2 r) V1 @* Y. U. M* ^% O* KVolume 46 Number 6, z& H9 O- e4 @3 O# y
July 2007 540-5432 B0 ^6 B2 y/ d0 S5 \& [
© 2007 Sage Publications
* H! s7 m% m/ |8 b. P2 _7 B10.1177/0009922806296651
1 ]. ^: J! _ U; ?2 E5 }http://clp.sagepub.com
+ V# `! v/ Q2 t. [hosted at
& [$ N5 D% b2 ]6 |$ d T' Uhttp://online.sagepub.com# u1 x6 y: R- S* I8 R+ j1 C* U
Precocious puberty in boys, central or peripheral,
$ o6 v. \; u9 L& Q Qis a significant concern for physicians. Central E) F |4 S5 ?" D% ?' f: f2 D
precocious puberty (CPP), which is mediated+ [( X: ^) t- b9 r$ G% \! n0 r
through the hypothalamic pituitary gonadal axis, has
! {8 B5 ?; f0 ?- o, w1 h2 Ra higher incidence of organic central nervous system6 S% W9 K' Y. B2 R4 v
lesions in boys.1,2 Virilization in boys, as manifested, u& O ^ Z* K: ^; g. d E4 q
by enlargement of the penis, development of pubic( |2 |! V2 a' @
hair, and facial acne without enlargement of testi-
) }. ]/ r- ]2 e4 Dcles, suggests peripheral or pseudopuberty.1-3 We
6 M0 N0 _2 [/ k* V& y1 b; kreport a 16-month-old boy who presented with the
$ [+ s+ e1 M- n! _0 wenlargement of the phallus and pubic hair develop-0 r6 u, a7 Y7 D2 U
ment without testicular enlargement, which was due
( O( E# N4 u7 Z6 ato the unintentional exposure to androgen gel used by5 l# i( k6 T4 e0 v* v1 X3 M
the father. The family initially concealed this infor-
, X: d/ e- K; K, v, V* emation, resulting in an extensive work-up for this; e1 E5 P( W1 @# |
child. Given the widespread and easy availability of
; Y! R/ H1 E3 O; J, rtestosterone gel and cream, we believe this is proba- L1 X% u& ]* h+ k- {
bly more common than the rare case report in the4 d3 u) F( b+ ]: \& }' w M- l& Q+ F7 T
literature.4
, r9 S5 s: B$ H# ^' t8 VPatient Report
1 s/ o% A7 @1 I% u& h! lA 16-month-old white child was referred to the5 \3 d& }+ h3 [; {5 k
endocrine clinic by his pediatrician with the concern- b) U9 U5 R8 {0 l; m/ L
of early sexual development. His mother noticed" b4 V! H0 k, A' S4 |5 P- g
light colored pubic hair development when he was
& H2 H u8 z% qFrom the 1Division of Pediatric Endocrinology, 2University of3 q/ W7 _$ B4 e' i( D8 A/ W
South Alabama Medical Center, Mobile, Alabama.
' n9 j4 ]- ]: A/ {: M7 {4 eAddress correspondence to: Samar K. Bhowmick, MD, FACE,
0 X4 Q) Z+ V0 z- m( FProfessor of Pediatrics, University of South Alabama, College of6 f9 a, O0 x. Y a+ D7 f
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# B% ]; c; h/ R7 d
e-mail: [email protected].
1 k1 u4 _8 Q6 e& u' ?about 6 to 7 months old, which progressively became
1 m' G1 P, {# {8 h9 ], Kdarker. She was also concerned about the enlarge-
& x) s" X! N" ?% m4 L7 Dment of his penis and frequent erections. The child( p$ G7 F, |+ @ ~- G" I E5 h+ L
was the product of a full-term normal delivery, with
3 V1 \% G/ Q. a# t; wa birth weight of 7 lb 14 oz, and birth length of
% ~ y/ y6 j* `/ ?9 f20 inches. He was breast-fed throughout the first year1 n& \7 \/ I) ~, A2 q) N+ w
of life and was still receiving breast milk along with- I) o0 h' E' R- [
solid food. He had no hospitalizations or surgery,
! C x0 z% w: U3 X! \8 B/ {8 dand his psychosocial and psychomotor development) B( I, q; F8 I) k: P$ h) y! X6 D
was age appropriate.1 \% R, u1 @3 j0 W! b
The family history was remarkable for the father,
, _; d x9 V7 s3 Hwho was diagnosed with hypothyroidism at age 16,
$ Q! x! x0 t. t4 k2 N$ Uwhich was treated with thyroxine. The father’s
. X$ q9 Z( l2 {height was 6 feet, and he went through a somewhat* u5 o. `1 u. e; ~0 q) ^
early puberty and had stopped growing by age 14.
8 u {+ ~" F7 U n0 `The father denied taking any other medication. The
0 r# P c" g5 f0 jchild’s mother was in good health. Her menarche. M% Y, V4 |' \8 z6 D& k
was at 11 years of age, and her height was at 5 feet; b' B( p, W y
5 inches. There was no other family history of pre-
$ q8 N$ Z4 u& B3 b% g1 F, g. Q1 f- dcocious sexual development in the first-degree rela-
" X3 A+ l, x( D4 \+ Ytives. There were no siblings.
. Q+ j2 w( w; V* ^* wPhysical Examination
2 {$ C" [. E4 C, B8 @The physical examination revealed a very active,
# a# O$ I- u% c5 F6 V. Rplayful, and healthy boy. The vital signs documented2 X& n5 F3 p, P0 t8 O. N
a blood pressure of 85/50 mm Hg, his length was9 P% A3 E" W) T2 |/ @, x: s
90 cm (>97th percentile), and his weight was 14.4 kg" S+ t" y' H/ a, N4 Q
(also >97th percentile). The observed yearly growth
+ L: O+ w+ E! h# O4 r7 o* r7 f$ J* j/ {velocity was 30 cm (12 inches). The examination of& C4 F7 G/ P8 O( _; p
the neck revealed no thyroid enlargement.1 E* H" ^ z1 X* a
The genitourinary examination was remarkable for# L& C* }1 G2 |) [( x# R8 }9 q" q5 F; q
enlargement of the penis, with a stretched length of
. _" w: t( A, M/ D6 ~0 c8 cm and a width of 2 cm. The glans penis was very well7 x9 [5 J6 `" G7 J9 ~: P7 x
developed. The pubic hair was Tanner II, mostly around
% \3 J' ~: _# V540) U6 N+ ~8 m& n, O- f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ `1 l- J& f5 Z. T5 p; e6 N' j
the base of the phallus and was dark and curled. The8 @0 c2 I) {4 d$ F {3 ?
testicular volume was prepubertal at 2 mL each.& T6 X- `2 J. i- B+ H
The skin was moist and smooth and somewhat
: J3 \/ @, {! Z* yoily. No axillary hair was noted. There were no
- Y/ y; y9 F+ x6 |, e% |; mabnormal skin pigmentations or café-au-lait spots.
2 C3 A3 _2 O" ?Neurologic evaluation showed deep tendon reflex 2+' B5 s/ f# _6 v" K- a
bilateral and symmetrical. There was no suggestion
: Q" r& p- o* w( C* q2 `, }* e' Nof papilledema.1 Z9 K) G7 v* R2 K, O
Laboratory Evaluation
, k) x( N P+ L) o# RThe bone age was consistent with 28 months by' \2 G+ u' y, m* T5 Y1 j% V
using the standard of Greulich and Pyle at a chrono-
4 s4 W) b" m. c! e! Flogic age of 16 months (advanced).5 Chromosomal+ e8 r7 {2 g F( K
karyotype was 46XY. The thyroid function test
2 I, J1 j: ~% g# k7 Kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! X3 ?6 a2 P% |% R2 \6 p* Qlating hormone level was 1.3 µIU/mL (both normal).
3 \: _5 l9 p3 t/ CThe concentrations of serum electrolytes, blood
0 ]* `0 w7 q* w$ d5 jurea nitrogen, creatinine, and calcium all were
! ]; A6 l# |$ G- i3 |within normal range for his age. The concentration9 `1 N( j: \" O# ~4 T0 p: I; x) K! s
of serum 17-hydroxyprogesterone was 16 ng/dL
. e& T" |9 F' e(normal, 3 to 90 ng/dL), androstenedione was 20( i- l- U& X: e" X- R2 W; j+ i$ g) B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: }; |. Q O) r! V& A4 D! h7 r
terone was 38 ng/dL (normal, 50 to 760 ng/dL),% r/ i2 i' w# Y& E0 B7 {9 j
desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 q$ g7 U# |0 K5 t* {, Q) d- k7 d+ A
49ng/dL), 11-desoxycortisol (specific compound S)
( d6 N0 g; |# @4 n5 g- G+ Fwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-& Z; y0 s+ r4 T( w7 A' M
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total e& Z7 `# J1 k6 G$ d9 ~' }
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),9 Y; K2 s, t4 d7 n0 g0 ~
and β-human chorionic gonadotropin was less than3 }/ p! A$ d, ^( l# V4 ?2 k1 Y
5 mIU/mL (normal <5 mIU/mL). Serum follicular4 Q% t& n+ T* P. S$ x7 B
stimulating hormone and leuteinizing hormone
! L0 _* S* I Kconcentrations were less than 0.05 mIU/mL3 N+ X* f, _6 X
(prepubertal).
/ }' c( u" }; [) lThe parents were notified about the laboratory
- H- j; ? {9 N3 [results and were informed that all of the tests were+ F, B/ Q. `$ r$ k ], a4 G0 Y
normal except the testosterone level was high. The
, [* } _. q6 j2 _follow-up visit was arranged within a few weeks to
b/ [# G% k$ v s( |, \2 Iobtain testicular and abdominal sonograms; how-6 n8 i+ k$ c, {8 _
ever, the family did not return for 4 months.
! t" G6 K0 z; n9 c ~8 L3 ^+ s* ZPhysical examination at this time revealed that the$ S4 S& n$ d9 @+ @1 c, z7 Y
child had grown 2.5 cm in 4 months and had gained& M6 j/ X L- L/ f3 E2 o) l
2 kg of weight. Physical examination remained1 `$ }' i9 y- T
unchanged. Surprisingly, the pubic hair almost com-
% x0 d* w' y% C6 e6 z5 O7 wpletely disappeared except for a few vellous hairs at
- D. \# B. ]% i6 Hthe base of the phallus. Testicular volume was still 2% y$ y3 @* B- h# Q
mL, and the size of the penis remained unchanged.* r# _, K% [+ O# c/ }
The mother also said that the boy was no longer hav-. u! Z2 ~# r W/ X# r& ~, Z
ing frequent erections.! N8 g' B2 G/ p5 h4 H9 B; {
Both parents were again questioned about use of V5 S$ L) M4 r! z
any ointment/creams that they may have applied to
1 u* ^, Y* B. o& \5 _the child’s skin. This time the father admitted the% `$ Y( {- h1 H; B o1 ^
Topical Testosterone Exposure / Bhowmick et al 541
Q" o) p% O+ |' wuse of testosterone gel twice daily that he was apply-+ t+ E- d) _( j, v* g
ing over his own shoulders, chest, and back area for
8 K' C: ~9 m9 Ia year. The father also revealed he was embarrassed; ?' [+ P2 e3 S4 G
to disclose that he was using a testosterone gel pre-* }7 @8 f; } Y& A9 `6 s
scribed by his family physician for decreased libido- n7 i8 A+ ?; w& g7 Q4 @) a3 G
secondary to depression.
( Q, S9 ~- }& I9 C/ ?, h' |7 W; g9 OThe child slept in the same bed with parents./ l$ ]: [/ p# m7 S5 q' n) U
The father would hug the baby and hold him on his" w% o/ R6 R: k9 G1 `) F0 E9 z
chest for a considerable period of time, causing sig-+ t' F* A4 E5 g# s% K) ^1 Z# O
nificant bare skin contact between baby and father.
) T: {: @% a$ f& r/ aThe father also admitted that after the phone call,
8 U% q3 i( M* p3 zwhen he learned the testosterone level in the baby
, [' S- `8 F6 U9 q4 @1 Xwas high, he then read the product information
5 x1 O# s" k* @packet and concluded that it was most likely the rea-4 h, k1 z5 X/ M$ q# j( Z% @
son for the child’s virilization. At that time, they# ~: Q/ K- N7 A$ r8 o& {
decided to put the baby in a separate bed, and the
$ w3 }8 N9 P* p2 L' }+ u7 I) Y- `father was not hugging him with bare skin and had/ w+ T: d7 S( V; e+ ^" M% Y. u
been using protective clothing. A repeat testosterone; X+ j0 j( a* s$ ?' E* j" {
test was ordered, but the family did not go to the
+ W. H/ p* |, y) Z" O6 }laboratory to obtain the test.
+ f' T8 K) [4 R3 i1 {: `Discussion
+ Y. c8 C) u, O. V8 UPrecocious puberty in boys is defined as secondary- |7 r! _4 s" @( C
sexual development before 9 years of age.1,4
; A* P! {# n0 @- lPrecocious puberty is termed as central (true) when4 Z" c9 ?# F- R& I+ J
it is caused by the premature activation of hypo-
7 ^0 p( p0 l% s" y; H Ithalamic pituitary gonadal axis. CPP is more com-& W- y0 A* z. r
mon in girls than in boys.1,3 Most boys with CPP. w: g, e/ s i. h* C' e
may have a central nervous system lesion that is
9 M( X* n' G4 E% qresponsible for the early activation of the hypothal-, W0 Z7 Y5 N1 d' v- g
amic pituitary gonadal axis.1-3 Thus, greater empha-
' i5 H* {: y6 F u* m* ?# gsis has been given to neuroradiologic imaging in
+ A+ A# F/ |" I8 G B/ P) f4 I$ N% Mboys with precocious puberty. In addition to viril- v F4 J% A' ^" j4 m* W2 n) ^8 C
ization, the clinical hallmark of CPP is the symmet-
- V& `( x ?- m# g, ]1 [' Krical testicular growth secondary to stimulation by/ |8 M* i- N; r/ Y. h
gonadotropins.1,3: H* R: b& ]0 H: X E
Gonadotropin-independent peripheral preco-! y2 ?" r$ S( F
cious puberty in boys also results from inappropriate; }# \8 w4 D: X& P
androgenic stimulation from either endogenous or' p6 c: T" }* g+ o# m ]7 n0 f
exogenous sources, nonpituitary gonadotropin stim-6 c i) J# y3 N. ^- P
ulation, and rare activating mutations.3 Virilizing( ?& v- `& S* q, ~# q4 R
congenital adrenal hyperplasia producing excessive
. R! o) {5 U% madrenal androgens is a common cause of precocious
Z9 s7 s0 I$ Ipuberty in boys.3,4
9 S! j3 [' O2 x, a/ b5 u% LThe most common form of congenital adrenal& @$ a" @8 p4 h' L B0 X$ q' M+ v( f
hyperplasia is the 21-hydroxylase enzyme deficiency.; U. j; F: B2 w/ E/ j
The 11-β hydroxylase deficiency may also result in
! S0 V9 t1 n R9 }: [8 l( Z; u+ Fexcessive adrenal androgen production, and rarely,
, y! i: C! w$ y) }an adrenal tumor may also cause adrenal androgen* v0 w' z- B1 g
excess.1,3( n# a3 S1 [, U' w# ]( j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, T0 T" L" \! r. `9 @542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
* b: G# ^! K& u; R% N, ~" dA unique entity of male-limited gonadotropin-6 s6 t$ G m. p+ f, h
independent precocious puberty, which is also known+ @$ Z% ~8 R; p y
as testotoxicosis, may cause precocious puberty at a
& p2 P: D- I" G6 v7 N6 gvery young age. The physical findings in these boys% X4 E4 T' Y. ^0 E8 {" x/ f3 }1 d( b
with this disorder are full pubertal development,; Z' C1 M" W8 j) ]# |$ [3 a6 L3 J
including bilateral testicular growth, similar to boys
5 N/ \9 ]7 V. r# `& x" L3 p8 Rwith CPP. The gonadotropin levels in this disorder, P* J$ t- Q) R$ q
are suppressed to prepubertal levels and do not show6 f0 _4 u) ^9 c; g) V( b* E( G$ {
pubertal response of gonadotropin after gonadotropin-
5 g5 N, {3 _# Q# g, b2 ireleasing hormone stimulation. This is a sex-linked
. U1 m5 J/ f, _+ J' L& C4 ]* t* k+ \8 Wautosomal dominant disorder that affects only
9 `& F3 n, g" r" c! x& R$ omales; therefore, other male members of the family
* {( l" ?, y5 w% }% ?4 S. Omay have similar precocious puberty.3, }, }3 D& z8 ^/ @
In our patient, physical examination was incon-
2 {: a. T- ` w8 E3 c! ^+ P) A4 vsistent with true precocious puberty since his testi-1 }) F r3 p# M: ]- O1 j# n1 A3 B
cles were prepubertal in size. However, testotoxicosis
$ k* R6 B4 b; D$ @8 V& Y, r- B5 Fwas in the differential diagnosis because his father' Y+ `% v* M0 }' a
started puberty somewhat early, and occasionally,
0 W/ y6 w$ l. U& gtesticular enlargement is not that evident in the
# b+ ~, H) n/ |beginning of this process.1 In the absence of a neg-( ]0 t- B( w2 C/ _
ative initial history of androgen exposure, our1 C! l* c/ C" n5 }/ `% p' Y2 G
biggest concern was virilizing adrenal hyperplasia,
; M6 F5 s! w5 q% c2 \either 21-hydroxylase deficiency or 11-β hydroxylase8 }, h! v4 \/ `6 ~0 g9 L
deficiency. Those diagnoses were excluded by find-
- l C4 I, _) P% r. ying the normal level of adrenal steroids.
" }' p/ t- d. ]2 ?/ u6 M( kThe diagnosis of exogenous androgens was strongly
9 d, n2 o% \5 \suspected in a follow-up visit after 4 months because
5 c( |, S* ~( zthe physical examination revealed the complete disap-
. _1 |4 p3 g5 O9 s( G4 {1 z6 G t- m% jpearance of pubic hair, normal growth velocity, and- Q8 s+ }, c0 w* Z! [, `! N( V1 B
decreased erections. The father admitted using a testos-% d0 ~* t' O8 L) V- A% \0 W
terone gel, which he concealed at first visit. He was
~! @7 }8 o5 T# J, B! _1 Tusing it rather frequently, twice a day. The Physicians’
e0 Q8 w6 q; d( e, x* UDesk Reference, or package insert of this product, gel or, ~" H6 ?, a1 A( f; m
cream, cautions about dermal testosterone transfer to+ y# W! i6 j) B: l" T! L
unprotected females through direct skin exposure./ G& _, x4 h% \& p r
Serum testosterone level was found to be 2 times the
: B$ s; B' b! z7 B- h/ z3 C: zbaseline value in those females who were exposed to6 V$ V8 y) b# ?$ B# O* B
even 15 minutes of direct skin contact with their male5 {% y) v7 W$ ~) y& P
partners.6 However, when a shirt covered the applica-
5 e0 ?. n j! Mtion site, this testosterone transfer was prevented.
7 t8 O& O& _8 Z& D: T$ Z/ k* {" OOur patient’s testosterone level was 60 ng/mL,8 f5 z% W' g' F# s
which was clearly high. Some studies suggest that
- C0 @0 O' y" `7 {* o9 Cdermal conversion of testosterone to dihydrotestos-2 R- v5 K7 ?- D; q2 n# K4 \
terone, which is a more potent metabolite, is more. f& H. _8 r( Z
active in young children exposed to testosterone/ G R+ H# _+ i3 ?/ f9 f
exogenously7; however, we did not measure a dihy-1 P5 E7 d0 Z+ |! f* l8 i8 e2 R
drotestosterone level in our patient. In addition to& H, ]6 C$ v. c, g
virilization, exposure to exogenous testosterone in# d+ c: a9 ]1 Q! q" }1 d
children results in an increase in growth velocity and0 R% Q3 O4 Z k: d1 A
advanced bone age, as seen in our patient.4 G2 p6 f6 L: V2 i5 Z: ]" h. E
The long-term effect of androgen exposure during
% @* W' b4 D. k0 nearly childhood on pubertal development and final$ m2 o7 [6 k3 I' U6 [% s4 H: a# a& m$ E
adult height are not fully known and always remain2 W a( B4 a, y3 |
a concern. Children treated with short-term testos-
0 l9 v E- L3 ?( r$ i5 @3 F8 V3 p6 Qterone injection or topical androgen may exhibit some
. C, L, k% @" b6 ]& H& K: dacceleration of the skeletal maturation; however, after+ a" y2 z% \! O
cessation of treatment, the rate of bone maturation
- ]6 K2 e$ X( ^& G+ y1 vdecelerates and gradually returns to normal.8,9
6 L; \6 N7 n6 G$ c4 iThere are conflicting reports and controversy
$ P* t0 ?3 d7 [% u- n$ }3 Gover the effect of early androgen exposure on adult9 H3 h6 h6 p! |5 w- f
penile length.10,11 Some reports suggest subnormal
8 T! R8 J6 |: E( V4 W/ Yadult penile length, apparently because of downreg- [3 Y. o/ k7 i. e
ulation of androgen receptor number.10,12 However,1 K9 U! Y. l1 S8 G
Sutherland et al13 did not find a correlation between$ I8 X6 S% w3 s$ `8 G
childhood testosterone exposure and reduced adult8 j' l" ^% `1 O
penile length in clinical studies.1 c2 b9 H. }* X# Z' W# u: a2 ^0 N
Nonetheless, we do not believe our patient is
' |# W9 ^6 d9 h9 R0 Lgoing to experience any of the untoward effects from0 k, t2 H# \ M
testosterone exposure as mentioned earlier because/ H0 Y9 x. z; n9 r; k1 }
the exposure was not for a prolonged period of time.
+ w' `: t4 d- n: }Although the bone age was advanced at the time of. |# `' L+ K5 i+ p/ P5 I) D
diagnosis, the child had a normal growth velocity at: ^$ w! I9 t) N E# O+ w: Y
the follow-up visit. It is hoped that his final adult' l( f, v/ c$ G- h1 V
height will not be affected.
: p& ?: J+ \+ g+ O( Z- i" wAlthough rarely reported, the widespread avail-
8 Q9 g2 Y0 u& a. f2 |4 X" d0 bability of androgen products in our society may$ w1 g9 ?- T4 a, I% u) d) v
indeed cause more virilization in male or female& M8 Y; F; H/ Z/ Q: g2 @& n' C0 Q* j7 X
children than one would realize. Exposure to andro-0 k2 ]4 _$ X. i3 U% S
gen products must be considered and specific ques-
# k/ _% A; ~6 F6 ~tioning about the use of a testosterone product or
0 `$ w9 c) }: z; Bgel should be asked of the family members during
. w: Z2 H/ Q* r( {' I& Lthe evaluation of any children who present with vir-
: ~% T* w& H3 C$ ~. I {8 lilization or peripheral precocious puberty. The diag-* Z$ {( w3 Q, ?& z- ~5 K t% r
nosis can be established by just a few tests and by
; }7 j+ a; K, wappropriate history. The inability to obtain such a
, P1 B& D$ Z- E3 H' Z Shistory, or failure to ask the specific questions, may
# e a. b2 }2 d4 ~8 I# ?0 V! Yresult in extensive, unnecessary, and expensive
/ K& J/ X2 g9 |7 b9 [" l! ^9 minvestigation. The primary care physician should be4 \2 N8 z$ r- D5 l6 d2 E) x
aware of this fact, because most of these children# W& o+ J& L7 F% ^" J, w( w4 W( ]
may initially present in their practice. The Physicians’
- e. d6 k1 |; ^2 c% R1 ]& lDesk Reference and package insert should also put a9 ` u1 E6 W" T9 p
warning about the virilizing effect on a male or8 @6 ^, j K$ {% \
female child who might come in contact with some-1 f- f2 F5 f0 ?9 {% l
one using any of these products.' k5 ~) y. n0 p5 [0 j) W$ a6 N
References
7 @- F1 _$ H; A9 c8 ?4 k9 _7 ]1. Styne DM. The testes: disorder of sexual differentiation
8 e- E5 L/ l, w) X* v8 ^2 qand puberty in the male. In: Sperling MA, ed. Pediatric& v4 q! y3 S# [4 ^5 Q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! D2 B0 X7 F b" l
2002: 565-628.9 Q+ l+ Z# R* E0 o
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
) y$ o0 R6 |# M/ n/ _& W. h1 rpuberty in children with tumours of the suprasellar pineal |
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