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Sexual Precocity in a 16-Month-Old
% a% B6 `/ z1 c0 X. eBoy Induced by Indirect Topical
0 n% y5 Y- p# P* F$ @- iExposure to Testosterone# [0 f5 z9 {3 h, N5 k6 g1 \. Z- @
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2 ]6 n9 H% ]! p9 p9 F
and Kenneth R. Rettig, MD14 t; i% Z' c/ r1 w6 c9 c# d
Clinical Pediatrics2 g7 i* c3 C8 x8 W7 V4 _
Volume 46 Number 6
+ Q: i0 y$ T u1 X c9 y4 ~July 2007 540-543
, b& z3 Y( Y+ s! w8 g0 {© 2007 Sage Publications
8 K& i% b% l: C10.1177/0009922806296651
- Y1 q. j! q; zhttp://clp.sagepub.com
, U" _& \% h0 \" d6 ] F, [hosted at" v$ M0 M, Y( Y! i+ P" f
http://online.sagepub.com5 M {8 |0 j) i0 z" p* @# a( J! m. w
Precocious puberty in boys, central or peripheral,
4 S8 f, {, f$ M* G9 }# _is a significant concern for physicians. Central$ |* `+ s: S! ]" |; K9 Z; |
precocious puberty (CPP), which is mediated6 y8 `0 G( A" Q
through the hypothalamic pituitary gonadal axis, has
_+ u5 k0 W2 Ha higher incidence of organic central nervous system" }* ~& I2 c6 {1 J) L& \- {( F* i
lesions in boys.1,2 Virilization in boys, as manifested R3 r3 `: l, W
by enlargement of the penis, development of pubic2 ~: Y1 v- K' ?
hair, and facial acne without enlargement of testi-
6 s" b4 F5 ~: D. q) F, z$ b( t" S/ Mcles, suggests peripheral or pseudopuberty.1-3 We$ E+ A) C4 U) W0 b& h" I
report a 16-month-old boy who presented with the. X! X8 L& y" a1 g, T/ K
enlargement of the phallus and pubic hair develop-
: b' ?' ?' o; {: M: Qment without testicular enlargement, which was due% v+ d% N l" n. E0 g7 ]- B
to the unintentional exposure to androgen gel used by
% n' a/ }. j8 E6 O, P9 O* tthe father. The family initially concealed this infor-0 D9 ?9 `5 \ j1 e: }( `
mation, resulting in an extensive work-up for this+ f- B: x0 C+ V1 n2 G+ R s$ \
child. Given the widespread and easy availability of
# F/ P- ? U5 n1 [ utestosterone gel and cream, we believe this is proba-
! k6 m3 m& |/ l$ s# m% ^4 Dbly more common than the rare case report in the
5 q8 ^7 @. T( k. r: g/ {4 Yliterature.4 X) r, O8 W1 P
Patient Report4 q. g8 n4 o: y+ I) `# h
A 16-month-old white child was referred to the
0 I ?! b" M" j2 V2 Nendocrine clinic by his pediatrician with the concern
& P$ F, K/ n3 J5 w' O: X) s, b2 Fof early sexual development. His mother noticed
/ d4 Y/ r% g5 N4 R! {light colored pubic hair development when he was' j$ {* l, D+ f+ }' }% ?+ w
From the 1Division of Pediatric Endocrinology, 2University of
( }1 x- V2 W% z7 ~' ?* L, w; SSouth Alabama Medical Center, Mobile, Alabama.
7 N+ A6 ^0 Z$ ]& l5 e o6 u4 P! h$ fAddress correspondence to: Samar K. Bhowmick, MD, FACE,
1 x3 V3 X/ Z% A# EProfessor of Pediatrics, University of South Alabama, College of* G4 m5 t) Z, W7 r6 v
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 n' V4 [0 O' Y/ P9 Q8 d
e-mail: [email protected].* O. S& N' }; Q% N; a- W
about 6 to 7 months old, which progressively became$ H1 ]$ l5 d; } i" r
darker. She was also concerned about the enlarge-
2 ^: F* s$ X, y6 N0 D2 o7 i+ n; D* fment of his penis and frequent erections. The child9 I0 s4 b$ v+ [, T6 J/ {7 ?
was the product of a full-term normal delivery, with& ?5 s. G3 _9 }) M+ S! i
a birth weight of 7 lb 14 oz, and birth length of) t6 A: X0 l' U& F/ V: n
20 inches. He was breast-fed throughout the first year
/ |9 s+ ~1 _( L$ _7 w* Oof life and was still receiving breast milk along with; ~, ~* ^1 n) O3 F# k# d, @. O
solid food. He had no hospitalizations or surgery,& v& ^6 t6 Q/ n' E! Z
and his psychosocial and psychomotor development2 h0 }7 R, q* e& I/ t
was age appropriate.& V" n0 M8 w3 W l
The family history was remarkable for the father,
; C' p; i! J* o: `0 s0 Z% W H4 Pwho was diagnosed with hypothyroidism at age 16,
5 r2 z& a1 s' m& P% p) _5 Cwhich was treated with thyroxine. The father’s
" y+ t# p+ b: ^5 e# g+ X: xheight was 6 feet, and he went through a somewhat
s# a4 C$ g- P; ]& t6 ^9 bearly puberty and had stopped growing by age 14.
8 U' m& _1 B5 ^2 cThe father denied taking any other medication. The
* f' S2 N, Z: \+ T$ n/ |child’s mother was in good health. Her menarche
, T6 ]3 p; q/ O1 k# j fwas at 11 years of age, and her height was at 5 feet
6 ^* w5 s8 E3 o6 V) B) M5 inches. There was no other family history of pre-
1 j; e7 ?6 \* W5 U' E) H% Jcocious sexual development in the first-degree rela-6 ^+ }2 U& u! ]( t9 ]8 ?
tives. There were no siblings.( q/ ?/ s% }5 S8 l, `: d% S
Physical Examination5 T) s8 k+ @ n2 k
The physical examination revealed a very active,
+ I+ S- A( f% w/ c) Y! rplayful, and healthy boy. The vital signs documented0 g) D* H L. K9 p7 n
a blood pressure of 85/50 mm Hg, his length was
, p! f: [; V0 m: m$ R$ J90 cm (>97th percentile), and his weight was 14.4 kg8 I5 l+ g9 i2 T) k% {& q
(also >97th percentile). The observed yearly growth
$ L5 [; S/ t1 bvelocity was 30 cm (12 inches). The examination of
5 L& l! ]& d8 @the neck revealed no thyroid enlargement.
% o' r. `/ D5 N$ \) w% l- |The genitourinary examination was remarkable for- k+ Y# w1 W9 n) Y/ C8 r: B
enlargement of the penis, with a stretched length of
( ]* o/ `; M0 ^+ N8 cm and a width of 2 cm. The glans penis was very well9 h" T; n6 t, K* R8 R5 D: |( O
developed. The pubic hair was Tanner II, mostly around+ j$ Z8 U4 r+ I6 l8 u3 u8 M
540! Z: { E5 c5 u2 O$ B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 r8 y* q F! N( w& ]the base of the phallus and was dark and curled. The; B# j$ g# ?" G |8 e, t1 p* }
testicular volume was prepubertal at 2 mL each.- z5 U/ Q! U5 \0 o
The skin was moist and smooth and somewhat" F8 @7 a3 x/ M8 i9 W5 _5 R
oily. No axillary hair was noted. There were no
' ~3 { y7 v. a3 R" Rabnormal skin pigmentations or café-au-lait spots.5 T5 X3 X. b+ n: j- |
Neurologic evaluation showed deep tendon reflex 2+; \( I: i1 H2 K% S" W, U3 `: H$ [
bilateral and symmetrical. There was no suggestion
. D; b3 F. \2 Y4 C9 _6 g, B# yof papilledema.# o% U3 C- _, d) G+ [- J" k0 j9 y
Laboratory Evaluation
& |3 C7 F2 Q6 hThe bone age was consistent with 28 months by7 [" B4 |" U# \9 Z# j f
using the standard of Greulich and Pyle at a chrono-
+ {$ Y) A% w8 K3 elogic age of 16 months (advanced).5 Chromosomal
( K1 k: [5 X+ ukaryotype was 46XY. The thyroid function test- a3 k. e. A$ T, o# r% r4 W! j( F
showed a free T4 of 1.69 ng/dL, and thyroid stimu-+ W$ M8 J+ n* v1 ]. ~$ F/ j
lating hormone level was 1.3 µIU/mL (both normal).% z2 [5 i4 k4 b' ^+ A
The concentrations of serum electrolytes, blood9 W* T) ~1 W1 s3 s; x; g3 O* a
urea nitrogen, creatinine, and calcium all were0 ` p9 g3 [! R, S+ E5 P" T) o
within normal range for his age. The concentration
3 e" T5 ]4 f+ j9 W! Q+ ^3 }" p7 m5 Dof serum 17-hydroxyprogesterone was 16 ng/dL* \$ b- l" K$ I4 t% _
(normal, 3 to 90 ng/dL), androstenedione was 20
+ U4 z) n5 {6 G% jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
U5 P7 p" N8 N& u' F" G# d9 Q# ]terone was 38 ng/dL (normal, 50 to 760 ng/dL),$ H: Q( O8 \6 c* j% D
desoxycorticosterone was 4.3 ng/dL (normal, 7 to$ K7 E+ N, ?" C4 Z1 @
49ng/dL), 11-desoxycortisol (specific compound S)
+ P/ z% |+ i v5 jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 @9 [% D! }2 h- t- J
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ k" k/ U+ i) H
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 u; u, {; b W; G* |; Cand β-human chorionic gonadotropin was less than
9 e% z, H* @6 d9 X6 S8 C1 [5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 z2 |0 r: U3 f' b, f! r1 W" Astimulating hormone and leuteinizing hormone
2 h, w6 _! F1 B/ ?% l' g+ vconcentrations were less than 0.05 mIU/mL
0 h" s, G& l0 v+ a(prepubertal).# i1 e8 F, D9 _; w
The parents were notified about the laboratory
. P2 A8 `2 [- H& V7 A+ Gresults and were informed that all of the tests were+ h7 z3 ]4 e: Y4 p8 V
normal except the testosterone level was high. The
# W$ M$ M; K4 [+ ?1 W# u0 Jfollow-up visit was arranged within a few weeks to2 T' P% @8 i5 f4 j9 {
obtain testicular and abdominal sonograms; how-/ r! z) i' e; d7 j6 v. g: p
ever, the family did not return for 4 months.# ~4 k$ \7 S3 _* j
Physical examination at this time revealed that the
6 f8 T9 c+ H0 _! T6 A# ychild had grown 2.5 cm in 4 months and had gained: I7 l0 z& _1 z/ U) V; `0 c; |) M/ }
2 kg of weight. Physical examination remained- `5 T2 T9 s' w! G6 E" s
unchanged. Surprisingly, the pubic hair almost com-
+ D8 z- x6 J& A) @4 Mpletely disappeared except for a few vellous hairs at
8 K( z2 W; _' ]' V! [7 C. qthe base of the phallus. Testicular volume was still 2
* c1 D$ r7 o, a8 I" ^9 amL, and the size of the penis remained unchanged.
+ J, p! q, ]. l0 w% M+ F7 CThe mother also said that the boy was no longer hav-
6 \1 n( w! D9 qing frequent erections.
; Q: d' [: F1 |1 W; ?" D, V/ l0 jBoth parents were again questioned about use of
; m% k" ?2 r( E; xany ointment/creams that they may have applied to1 @3 B) r% U) h# d+ y0 i# J/ F& \7 C
the child’s skin. This time the father admitted the
0 Z* h+ g" a0 s h! T$ |5 H6 LTopical Testosterone Exposure / Bhowmick et al 541
# B$ ~0 Z, f ?$ R6 ~! e6 ]use of testosterone gel twice daily that he was apply-3 v4 s# w' Y* W0 B. W9 g$ z7 N
ing over his own shoulders, chest, and back area for
2 r5 w3 ~' F( L( r3 _0 h5 J3 Aa year. The father also revealed he was embarrassed
A* b; D% k: J* D) i2 i( lto disclose that he was using a testosterone gel pre-
# P& A! o% K0 m5 w+ Escribed by his family physician for decreased libido
8 ]2 [! q* f: ~9 ^0 V- v& ^$ R4 vsecondary to depression.
+ g$ b& }$ u3 mThe child slept in the same bed with parents.
4 \/ w u d G& R. n1 {The father would hug the baby and hold him on his
9 r6 Q( |: R4 a! R( t) xchest for a considerable period of time, causing sig-
5 I$ j' C1 {: r2 S3 Bnificant bare skin contact between baby and father.
* i! v- R2 Q" a7 m0 g3 A) v/ l2 A8 x; ^The father also admitted that after the phone call," W `1 Y- i6 e, |3 |7 B
when he learned the testosterone level in the baby
: l, p0 v% q% p9 @2 m" C) b8 Pwas high, he then read the product information
( q7 C' J+ w" s7 [' k1 ipacket and concluded that it was most likely the rea-
3 W! U/ q, F7 t; C% e6 G% Ason for the child’s virilization. At that time, they6 } B& J5 F' ^3 d0 G
decided to put the baby in a separate bed, and the0 r) U7 l3 X/ G: ^ m" d3 m
father was not hugging him with bare skin and had
# F0 r$ c0 s% s/ C1 G: O Abeen using protective clothing. A repeat testosterone
$ E- x0 I) m- B& L1 Mtest was ordered, but the family did not go to the
/ P! e3 m2 S" z4 J' \1 l* v7 Xlaboratory to obtain the test.# O7 H! [) k6 E1 G) A5 P i3 f
Discussion
# N7 b+ R! r# T2 B# x. oPrecocious puberty in boys is defined as secondary: p2 R( K" d3 X( k: n0 J) o* }
sexual development before 9 years of age.1,4
2 r7 ]3 I6 V: G3 ^& l. ?Precocious puberty is termed as central (true) when' i. N4 i4 D* P7 F% ^& l( |
it is caused by the premature activation of hypo-; Z! i) E1 ?( a, R+ Y- s: M
thalamic pituitary gonadal axis. CPP is more com-
, |8 A& \; g0 @' k& u/ @! `! w3 }mon in girls than in boys.1,3 Most boys with CPP. l' B! [( d: ^' i1 K* B; B, A+ m+ x
may have a central nervous system lesion that is
5 Y% Z; a. K7 \4 uresponsible for the early activation of the hypothal-/ ~5 Y) U. z: S1 s* L( Q j* A
amic pituitary gonadal axis.1-3 Thus, greater empha-+ a; k0 Q( ]; z$ ~3 w: U5 _
sis has been given to neuroradiologic imaging in" w' E. }: K/ [; y1 a2 P5 ^+ n' a
boys with precocious puberty. In addition to viril-* i$ X# j1 ~( B) I7 V
ization, the clinical hallmark of CPP is the symmet-
# s" ~. z: u. U) Y( L+ Nrical testicular growth secondary to stimulation by
$ H1 d* H8 s( _! i; ygonadotropins.1,3
& p: e/ y) U! [6 J: m1 CGonadotropin-independent peripheral preco-, f0 @! W0 v# `: X4 P+ g. q0 a
cious puberty in boys also results from inappropriate
- C% C# i g5 Sandrogenic stimulation from either endogenous or1 _! f7 x1 z4 L" k
exogenous sources, nonpituitary gonadotropin stim-
% A2 i5 R! l$ T8 r' x7 o% m% W/ Uulation, and rare activating mutations.3 Virilizing: c/ F) F, \/ O1 J( A5 y1 A
congenital adrenal hyperplasia producing excessive' h Y, q) k0 |. ~6 U' J5 y( X
adrenal androgens is a common cause of precocious" k- ]6 ^+ R k' A B- M
puberty in boys.3,4
/ {( N' x( }4 y: z9 \$ h; ?2 eThe most common form of congenital adrenal$ s$ n0 _8 `& y0 c3 O
hyperplasia is the 21-hydroxylase enzyme deficiency.4 ?: q3 X5 m; b& y( ]
The 11-β hydroxylase deficiency may also result in
% l& V. Z# {0 o6 H8 kexcessive adrenal androgen production, and rarely,
" \1 b% d9 ?1 tan adrenal tumor may also cause adrenal androgen
* \$ X" ^4 V9 S$ Oexcess.1,3' C$ P" n5 C6 K2 d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- V" t1 R. D: p- c4 B; [542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ h4 u7 @9 S; R- ]9 t" K( E& v
A unique entity of male-limited gonadotropin-
* D9 k- Q+ y2 {. r, @7 `0 U0 Windependent precocious puberty, which is also known
6 p; R# F* c2 s" B+ T: U+ H9 e9 g+ das testotoxicosis, may cause precocious puberty at a F$ E: |/ |# K: Y2 Q3 T) h
very young age. The physical findings in these boys
! C7 S! s7 Z x: swith this disorder are full pubertal development,6 v: A% p# C8 P4 g" Q, O
including bilateral testicular growth, similar to boys
: V9 i+ }3 C! `( d$ y! K! iwith CPP. The gonadotropin levels in this disorder
1 W3 ~5 y) T0 n2 J- yare suppressed to prepubertal levels and do not show. X. R) Z5 k9 l* A
pubertal response of gonadotropin after gonadotropin-
4 m3 R6 h X% J! t) ]( j8 d' Sreleasing hormone stimulation. This is a sex-linked! R1 K% Q1 k, l, h- o6 P- T* V
autosomal dominant disorder that affects only
1 |0 g g$ M: J( E4 c' Ymales; therefore, other male members of the family
; G1 u" O+ I3 w: v" P7 |may have similar precocious puberty.3
- J5 [$ ~2 V/ h3 X- N# C& _9 lIn our patient, physical examination was incon-& Q, e! k6 i% W# x
sistent with true precocious puberty since his testi-
3 |, ]! l, e4 ]* _( Ecles were prepubertal in size. However, testotoxicosis
& i7 \- L6 j! `9 k, \2 Mwas in the differential diagnosis because his father* O) p) f: ^. x
started puberty somewhat early, and occasionally,: R" k" c! `# o, @9 E7 q. C/ W3 c
testicular enlargement is not that evident in the; A$ F: g0 i/ W, N- h
beginning of this process.1 In the absence of a neg-
3 G4 h1 _+ X% k6 q2 D7 `ative initial history of androgen exposure, our' `7 u' A, W5 d1 E0 H4 l
biggest concern was virilizing adrenal hyperplasia," s0 t, t- I, J
either 21-hydroxylase deficiency or 11-β hydroxylase
, d4 R) _/ K5 l" D6 Edeficiency. Those diagnoses were excluded by find-
/ g, a# v7 ?. Q% |+ H+ H, |. ~ing the normal level of adrenal steroids.
; O$ _! H! `: k% S* i" `: fThe diagnosis of exogenous androgens was strongly% u4 Q$ X& `5 l$ q: L8 d0 v# N
suspected in a follow-up visit after 4 months because
! |! j* V: d! P* r2 }% ?; k( p8 tthe physical examination revealed the complete disap-
|/ P* _! v. V' Bpearance of pubic hair, normal growth velocity, and
4 Z/ m* s; y* b: x1 u3 G. o! edecreased erections. The father admitted using a testos-
8 G3 G; s! ?2 b5 w" w. e% j$ Pterone gel, which he concealed at first visit. He was
9 A& J) l# E& \# a" eusing it rather frequently, twice a day. The Physicians’
# v9 R3 I, S$ IDesk Reference, or package insert of this product, gel or: l7 i6 D/ T" f, J& i3 j
cream, cautions about dermal testosterone transfer to7 g( x: c7 ]" f
unprotected females through direct skin exposure.
9 j. V, E- e3 ?; [! N, |9 V( LSerum testosterone level was found to be 2 times the
2 ?% S! R R1 bbaseline value in those females who were exposed to
2 {2 j; |; P# u8 a! ceven 15 minutes of direct skin contact with their male1 v! t; f. M9 U- T. n/ O
partners.6 However, when a shirt covered the applica-6 |! ]1 [; s5 I* M% S
tion site, this testosterone transfer was prevented.
1 e @* ? G% W. A5 GOur patient’s testosterone level was 60 ng/mL,1 Q8 i3 R z! u, d2 x
which was clearly high. Some studies suggest that
- k; s# t+ t" l, R; g* Z& _& ]- g: xdermal conversion of testosterone to dihydrotestos-
! i- ~+ _+ F9 w) G8 R hterone, which is a more potent metabolite, is more
; K$ U. u7 O. U& factive in young children exposed to testosterone
( r4 s( s, k& E1 ^ [; _' y. ]exogenously7; however, we did not measure a dihy-
+ m9 [4 f& o' x5 F5 Idrotestosterone level in our patient. In addition to- S% v9 D" n' K' o$ L& N v2 R$ K
virilization, exposure to exogenous testosterone in8 J$ g# m& o/ I6 {4 L
children results in an increase in growth velocity and
* w3 n: Z z1 N$ ?) ]4 b6 h! G) Fadvanced bone age, as seen in our patient.
[$ j- v+ Y; D5 jThe long-term effect of androgen exposure during
# g6 l, B/ ^- B( O3 oearly childhood on pubertal development and final* k: s( x) g5 ]# S$ u6 B6 I
adult height are not fully known and always remain
! F5 l# q+ x7 N) \+ _ U0 Xa concern. Children treated with short-term testos-
0 M& U K: g) Qterone injection or topical androgen may exhibit some
) G3 b8 }+ U# b+ t. h- L/ }acceleration of the skeletal maturation; however, after C7 |$ G; D5 S6 O c8 C @
cessation of treatment, the rate of bone maturation' |& I) Q0 O. c( ~7 o+ c/ i$ t% c* K4 \
decelerates and gradually returns to normal.8,9" `$ G, Z5 l6 Q5 ~( r. r( k
There are conflicting reports and controversy( G( u. E7 @" f5 H. E
over the effect of early androgen exposure on adult
+ G" q! ~: L$ Q* Hpenile length.10,11 Some reports suggest subnormal
- O$ [$ L: @$ }' uadult penile length, apparently because of downreg-
4 P0 V3 D, g3 ~. F9 a! nulation of androgen receptor number.10,12 However,7 W9 c1 ], r8 R) c4 A
Sutherland et al13 did not find a correlation between. R" K% f, z4 ]9 _* `7 c7 |6 ]1 a
childhood testosterone exposure and reduced adult
( U" `6 a3 i) I/ D! Z8 m3 h% i6 ppenile length in clinical studies.
: e4 d( n! F3 x7 PNonetheless, we do not believe our patient is3 s4 ]# \, p# j+ O2 C! ?1 \! P
going to experience any of the untoward effects from
! u6 f `* ~/ g7 r. }: Y' jtestosterone exposure as mentioned earlier because& P& W2 x# N$ }) |
the exposure was not for a prolonged period of time.
! S# N2 I' U3 m+ OAlthough the bone age was advanced at the time of) M% m( f6 c$ `3 V5 g1 [" ?
diagnosis, the child had a normal growth velocity at
7 F9 X; P+ T$ X0 H$ o! @the follow-up visit. It is hoped that his final adult T! ^6 F: W- q; n" i. U. u
height will not be affected.
6 c/ I7 c0 X5 j; s. q: ^: X' zAlthough rarely reported, the widespread avail-
* b5 o8 Q8 N; a sability of androgen products in our society may: {* t" r- T' s( W( a" o- z
indeed cause more virilization in male or female
7 C4 @- C) U0 K% H' Hchildren than one would realize. Exposure to andro-
# J+ c7 d. \! \gen products must be considered and specific ques-
. h' K) f0 X% Btioning about the use of a testosterone product or; F5 R; x+ a1 H* S! U/ f
gel should be asked of the family members during
% e( _$ _6 j1 h. [% `the evaluation of any children who present with vir-
* C8 R/ \6 }; k9 G0 oilization or peripheral precocious puberty. The diag-
: D9 w6 g" |- y1 I4 c) Pnosis can be established by just a few tests and by8 o6 o# O+ D1 |, D! j
appropriate history. The inability to obtain such a
9 {! M. _7 N9 h$ k& h* dhistory, or failure to ask the specific questions, may' G# V: b7 b: N, ^: t
result in extensive, unnecessary, and expensive
+ R8 U- M5 L6 T* Hinvestigation. The primary care physician should be
. C# T" Q9 z* i" ^. U' Raware of this fact, because most of these children
- n3 G7 Q7 o7 @2 V( I# Ymay initially present in their practice. The Physicians’; V8 E* W1 _. w* f& ^: F
Desk Reference and package insert should also put a
; H% }# X/ y( p! k) M/ k/ l# Kwarning about the virilizing effect on a male or1 o: y0 [( Y( c! e( Z' l6 R
female child who might come in contact with some-
" |) R3 Z0 n6 d6 k9 f4 jone using any of these products.7 c/ Z# Y: r" m/ g1 s
References
: A) Z1 l* K& w1. Styne DM. The testes: disorder of sexual differentiation7 { m+ O0 k, G; B( l8 x
and puberty in the male. In: Sperling MA, ed. Pediatric1 p' ~! h- H2 R7 C
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;5 t# C+ o! g* V y
2002: 565-628.5 ~! q4 @! r# F$ @: {% I. D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! }1 j' v3 J- \8 Z9 c
puberty in children with tumours of the suprasellar pineal |
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