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Sexual Precocity in a 16-Month-Old
5 |- b1 n! Y0 N4 ]' b) j* WBoy Induced by Indirect Topical' Z3 Y% O- B1 ]+ P
Exposure to Testosterone
4 p6 T1 m' O1 X0 Z! Q" L8 W+ HSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' ]. ]9 o& ]: @and Kenneth R. Rettig, MD1( r# G4 w4 a- e$ a  t
Clinical Pediatrics0 A( p- z2 J% Y/ [% y/ L7 w
Volume 46 Number 6$ x) p7 C4 B, x
July 2007 540-543
+ k) i5 @$ V7 p8 n7 s$ F© 2007 Sage Publications
% R6 b4 L% Q0 M  ^2 T10.1177/0009922806296651
# r  U5 c/ e- v+ K$ Nhttp://clp.sagepub.com
8 u& W; w$ L4 z, w; H3 Xhosted at5 [4 |! B+ S- D
http://online.sagepub.com: l$ G, s7 n, Y% [0 c
Precocious puberty in boys, central or peripheral,
5 r4 {) B) {: Kis a significant concern for physicians. Central( |  ~7 V6 k  r4 P( `8 T. A: n
precocious puberty (CPP), which is mediated
) W. E7 y' W5 o8 ^; othrough the hypothalamic pituitary gonadal axis, has
2 i) X1 \8 O2 ]; ^1 `3 X; I7 Xa higher incidence of organic central nervous system
' t; ]7 ]6 ?. f! p# t# _* Alesions in boys.1,2 Virilization in boys, as manifested) `6 Q+ n4 s# e0 E* N
by enlargement of the penis, development of pubic
1 B4 \5 w' y5 ]7 s5 }  ?hair, and facial acne without enlargement of testi-, w' ]! P3 }! Y- o' E* ~
cles, suggests peripheral or pseudopuberty.1-3 We
. Z8 n3 Y2 L' A# v9 ^, f$ @report a 16-month-old boy who presented with the1 E6 I% [: R! u( R
enlargement of the phallus and pubic hair develop-+ J* c( ]# k8 R8 s9 T1 j
ment without testicular enlargement, which was due1 p' v) C7 ~/ M- V& u  l
to the unintentional exposure to androgen gel used by
! `# K* q/ ^. C. g* Othe father. The family initially concealed this infor-4 i, z# N1 J- N1 k1 e; _+ }' X0 t
mation, resulting in an extensive work-up for this
9 G6 e: _' R2 A, u- B+ ]: e7 Uchild. Given the widespread and easy availability of' ?; c$ _8 L4 e% B! O
testosterone gel and cream, we believe this is proba-
6 N7 F' F' T: c* Wbly more common than the rare case report in the
. O9 B' T, q. h9 |1 |literature.4  V& A' _5 h4 ~
Patient Report  c- Y5 l( V# I# V# Q
A 16-month-old white child was referred to the1 g) Q2 O% B- \* k2 x+ j, U
endocrine clinic by his pediatrician with the concern( F5 `1 G. l) M( A+ s3 r. L
of early sexual development. His mother noticed
* U9 U) y! y, x6 v# E4 e* Llight colored pubic hair development when he was1 M6 N! o  F$ c3 }% e
From the 1Division of Pediatric Endocrinology, 2University of
8 `9 u  l5 J0 R4 w  N7 }2 \! J  QSouth Alabama Medical Center, Mobile, Alabama.% f( {: N4 i) [, t5 B. k; p6 K
Address correspondence to: Samar K. Bhowmick, MD, FACE,
' L  T6 H$ H; ~5 o# V: f4 lProfessor of Pediatrics, University of South Alabama, College of  I+ z+ o+ P! i( D# v+ Q9 u
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;+ k/ s2 s4 Z- q# R' U
e-mail: [email protected].
& Y1 D2 R  N0 Q, m0 S+ {7 s1 dabout 6 to 7 months old, which progressively became
. p/ K* }5 j- r/ X; H0 j1 A- jdarker. She was also concerned about the enlarge-0 B/ L1 i: r7 {4 c  y' |
ment of his penis and frequent erections. The child
+ L) P0 g# S, w0 T6 X; Bwas the product of a full-term normal delivery, with
" j3 h+ m9 _9 {8 U  m7 f" ]$ Ha birth weight of 7 lb 14 oz, and birth length of5 U  C& I- m7 `1 E# }9 g
20 inches. He was breast-fed throughout the first year; e; d2 M. {4 n6 V) d; l
of life and was still receiving breast milk along with
2 q% x: J$ M. T: {1 W) esolid food. He had no hospitalizations or surgery,
% B, G9 f2 [  W1 ^2 v1 \4 J' `and his psychosocial and psychomotor development
* ^1 P- J. j( G: k2 gwas age appropriate.7 p$ e  D; k2 l" F3 T, L
The family history was remarkable for the father,
( o. F& L" P0 x% B+ w2 P2 A7 swho was diagnosed with hypothyroidism at age 16,
5 g) K; N9 @% R' Fwhich was treated with thyroxine. The father’s: o/ t( U9 t: o# c! c1 o& A
height was 6 feet, and he went through a somewhat& x9 J: C, `( t  x% j+ j
early puberty and had stopped growing by age 14.% I. I/ c5 l& a% [! N5 c
The father denied taking any other medication. The
, ?( L: \7 @& achild’s mother was in good health. Her menarche
' G+ A9 n4 @1 _# Iwas at 11 years of age, and her height was at 5 feet4 o# N2 s" _4 M- Q3 U* w, k3 l0 ]
5 inches. There was no other family history of pre-  _( G/ n3 `- m  c4 c
cocious sexual development in the first-degree rela-0 K  x5 c1 J8 S) [: O3 y# k
tives. There were no siblings.
3 ~/ Y9 [, u$ u6 i9 H( U2 MPhysical Examination1 r: O, ?% x# P# f1 K1 h
The physical examination revealed a very active,* R# ^# {3 n5 a/ c6 e% q# ?
playful, and healthy boy. The vital signs documented9 r+ B1 [0 W- Q( R
a blood pressure of 85/50 mm Hg, his length was
, b/ V+ E0 B& p3 n1 l90 cm (>97th percentile), and his weight was 14.4 kg
5 U/ ^7 o! g. j( j) a  X' S5 p(also >97th percentile). The observed yearly growth5 H( ]) x. B! r% o
velocity was 30 cm (12 inches). The examination of" @# N6 s, Z& L4 S, k; i
the neck revealed no thyroid enlargement." \5 ^! Z- }+ |+ \/ u' s5 R: N
The genitourinary examination was remarkable for
# C  F* ^5 K3 I. kenlargement of the penis, with a stretched length of
% O5 x. F( J: `- D2 b8 cm and a width of 2 cm. The glans penis was very well
- p2 u: b! a8 n9 E) a& h" w- L/ adeveloped. The pubic hair was Tanner II, mostly around, W1 P: \# [- ]0 {: F
540$ X* W8 S: H+ G* {
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 S1 ^8 u* G, S
the base of the phallus and was dark and curled. The
; Q  U. [! f# V$ `, n# Btesticular volume was prepubertal at 2 mL each.
0 {* A4 G  @4 r, IThe skin was moist and smooth and somewhat. p) @8 f6 F/ X% D
oily. No axillary hair was noted. There were no0 L1 D  m% I8 r9 X/ N
abnormal skin pigmentations or café-au-lait spots.
0 [8 j4 {- k' A- H" P5 fNeurologic evaluation showed deep tendon reflex 2+
- N5 z! N+ d& \bilateral and symmetrical. There was no suggestion+ V7 H3 f9 [* Z$ I  H% q9 [7 h
of papilledema.6 O2 L7 l0 d; p- B4 J* L2 @
Laboratory Evaluation
' m& l) w+ r3 [1 ]. F& o& ]' MThe bone age was consistent with 28 months by
2 x* |7 _7 z, T) g! k6 yusing the standard of Greulich and Pyle at a chrono-2 v6 Z( A1 f3 r* @
logic age of 16 months (advanced).5 Chromosomal3 _. {/ m$ e- w8 ^! b. r
karyotype was 46XY. The thyroid function test; k4 l" _7 R/ b0 j
showed a free T4 of 1.69 ng/dL, and thyroid stimu-: \% }* |: |' c' c3 m
lating hormone level was 1.3 µIU/mL (both normal).+ L) A! V7 C4 B2 y
The concentrations of serum electrolytes, blood# {3 t8 k  l' l( V9 t8 |$ B
urea nitrogen, creatinine, and calcium all were
% |. i/ V) J7 |$ @1 Xwithin normal range for his age. The concentration3 `! |3 i$ P/ [$ ^
of serum 17-hydroxyprogesterone was 16 ng/dL' x. {1 }; w. G1 p
(normal, 3 to 90 ng/dL), androstenedione was 20
! p4 z- h& l; V$ t( |5 }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) n# j3 f( q. @$ e8 \0 {5 w
terone was 38 ng/dL (normal, 50 to 760 ng/dL),$ q) o; I& l, ?: U8 k" ^3 H7 M; \9 ?
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ |* i) \( r- s! l+ y/ U49ng/dL), 11-desoxycortisol (specific compound S)
, ?2 }! x9 x- ~5 |- p# Q! B5 |- Qwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% M2 z) b, I8 Otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
8 S. h0 \7 \5 H1 }$ A: htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
8 [5 r0 w, A5 U5 w) X5 z& `3 Yand β-human chorionic gonadotropin was less than
( p7 \7 o0 q: S5 mIU/mL (normal <5 mIU/mL). Serum follicular: O" N1 e/ R, M: X+ a/ n! t
stimulating hormone and leuteinizing hormone
2 a5 c* S7 e1 z" W) B8 p' ~( r+ f4 aconcentrations were less than 0.05 mIU/mL% p! _. z2 h: |5 h8 w" y# A: e! {
(prepubertal).
! C% x/ z: W9 ?: T- p! mThe parents were notified about the laboratory- F$ T+ K2 C6 F) [
results and were informed that all of the tests were
2 e3 x0 l$ @& P8 j/ v0 ]( I8 Dnormal except the testosterone level was high. The
6 E7 z% n( V6 Z! \# k8 f) jfollow-up visit was arranged within a few weeks to/ D3 I. d' b/ X3 f
obtain testicular and abdominal sonograms; how-5 M( }* I) y# \
ever, the family did not return for 4 months.
0 `0 W. b: C, K" d1 p9 S6 ePhysical examination at this time revealed that the7 t* e: k# k4 e) |, d3 I
child had grown 2.5 cm in 4 months and had gained
; t1 V. U3 z) Z4 U4 Y' M' V2 kg of weight. Physical examination remained4 E1 g# F/ M* D/ L
unchanged. Surprisingly, the pubic hair almost com-
) T0 S3 a6 F, t- [, ^! ]pletely disappeared except for a few vellous hairs at
9 s& b& K. j! M. Uthe base of the phallus. Testicular volume was still 2
# t; _: }3 \% T/ VmL, and the size of the penis remained unchanged.
9 O; b5 e( p8 n  _- n/ B+ yThe mother also said that the boy was no longer hav-
; S" G  X" x* bing frequent erections.
) e# M3 t' `; j' O7 O& ]2 Y& ?Both parents were again questioned about use of5 F$ ~/ H, n- O3 ~: R# K2 w6 _
any ointment/creams that they may have applied to
" a9 }4 \% v; z, ]the child’s skin. This time the father admitted the7 `/ W8 i+ }3 n) {$ v5 {3 ?) k
Topical Testosterone Exposure / Bhowmick et al 541
* g2 q( F4 \' X( h3 Ouse of testosterone gel twice daily that he was apply-9 e1 {9 q$ J( c$ N8 c/ }2 J0 J7 G! G
ing over his own shoulders, chest, and back area for
2 W, ~' K) A0 k6 o  Ga year. The father also revealed he was embarrassed
" U6 F! x" g3 G- R, K" ^0 z( }to disclose that he was using a testosterone gel pre-: N: N, `* b) H2 U) N
scribed by his family physician for decreased libido
8 J0 B( C: ~2 r$ W; M/ Z5 p5 Xsecondary to depression.( k* [9 j# L3 M
The child slept in the same bed with parents.
9 D" t% a+ p: }' [The father would hug the baby and hold him on his, @8 G" k* P; i4 h# V/ |% C
chest for a considerable period of time, causing sig-! d" U( l8 T) b( V
nificant bare skin contact between baby and father.
& K* p% X0 K5 t7 [$ M. d( SThe father also admitted that after the phone call,+ ^4 q1 H0 R+ X& }2 v
when he learned the testosterone level in the baby( k0 f/ ]! e* _7 Y% I$ |
was high, he then read the product information
' I7 D! M! O6 Cpacket and concluded that it was most likely the rea-
' c- E# Q% y4 a9 S3 |# zson for the child’s virilization. At that time, they
( _/ n, l, D. K# |: e) y" t+ y$ Fdecided to put the baby in a separate bed, and the
* j" ^) q+ \$ _! {; Kfather was not hugging him with bare skin and had
, U8 k: M4 Y) f/ cbeen using protective clothing. A repeat testosterone2 P$ [9 W$ F3 y" y# N5 }* p
test was ordered, but the family did not go to the
4 a% h9 w& q8 A; olaboratory to obtain the test.1 `& x& x; b0 u7 E  U
Discussion
' |% \9 _" z' DPrecocious puberty in boys is defined as secondary; j0 u' S" u, j
sexual development before 9 years of age.1,4
4 {& [& s2 Y; V' pPrecocious puberty is termed as central (true) when
0 n1 X! R# W2 q  L, Kit is caused by the premature activation of hypo-
* j2 n$ o9 N2 G. kthalamic pituitary gonadal axis. CPP is more com-3 }- U) Y; ]3 e& s' \3 z
mon in girls than in boys.1,3 Most boys with CPP
- l2 O% R2 O( `1 h/ Kmay have a central nervous system lesion that is
, z5 h% C4 Z: F1 ?responsible for the early activation of the hypothal-
+ m3 f. H- u. h0 m1 R5 Samic pituitary gonadal axis.1-3 Thus, greater empha-. n# \& S2 s: J/ a, i% U* q8 z
sis has been given to neuroradiologic imaging in4 d* ?( L7 R2 ^6 c# H1 ^8 O
boys with precocious puberty. In addition to viril-3 N0 Y2 v5 C5 q. C- l0 o6 [
ization, the clinical hallmark of CPP is the symmet-! T1 H& t! M: [/ f
rical testicular growth secondary to stimulation by; N. m+ u! |  Y! I; `8 A4 n) h; W
gonadotropins.1,3  ]! }" z3 `( ~- w% m& \0 m
Gonadotropin-independent peripheral preco-, E0 h; u# [4 q0 d+ [
cious puberty in boys also results from inappropriate
; u2 g& `( t7 @. o" ~8 Mandrogenic stimulation from either endogenous or3 b+ B' t/ H2 x- x  y+ W' }
exogenous sources, nonpituitary gonadotropin stim-
3 I4 U& w7 l& J5 Q, ]" v: e& j% Gulation, and rare activating mutations.3 Virilizing" b5 r* a% D6 k5 h/ D( x
congenital adrenal hyperplasia producing excessive  c" Q$ m) O; j
adrenal androgens is a common cause of precocious1 U+ L) V6 q$ X, L9 g9 H
puberty in boys.3,4
% W0 [2 x- O, h7 e# n1 R: D8 BThe most common form of congenital adrenal+ q' D2 u2 M" _* N  h; B% w3 v3 B
hyperplasia is the 21-hydroxylase enzyme deficiency.5 v* M4 F- f. \+ ]7 b3 E1 L6 ^
The 11-β hydroxylase deficiency may also result in! t) W8 D& h+ X% {  A# c0 c3 p
excessive adrenal androgen production, and rarely,9 d( w" I# ~' K% L
an adrenal tumor may also cause adrenal androgen
" s1 ?( E8 m2 Y9 o7 xexcess.1,3: `; {7 B( A% w8 B% Y$ r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# q! {: X6 j8 Q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; ~( I9 P0 v) I& w
A unique entity of male-limited gonadotropin-
/ g6 u, P% }% j2 Mindependent precocious puberty, which is also known
# I3 u: m0 z0 Q8 y! u; gas testotoxicosis, may cause precocious puberty at a
, {" J, h' x: w+ f/ J) ~8 T* }; Tvery young age. The physical findings in these boys+ N3 e) {. h( u' A- e1 l2 \
with this disorder are full pubertal development,2 K8 f) |5 u0 y
including bilateral testicular growth, similar to boys5 @1 p  J# X0 _+ G% k& i- W. |
with CPP. The gonadotropin levels in this disorder1 _. \4 V1 T  y7 v9 }
are suppressed to prepubertal levels and do not show
( w. K. s( _; N! A. ^pubertal response of gonadotropin after gonadotropin-6 j3 V, ^* E! L: R9 G3 X) O
releasing hormone stimulation. This is a sex-linked
- g# k$ z! ~3 d' Z! Rautosomal dominant disorder that affects only0 R; t4 x; o: w$ k+ V! q% c1 t! S
males; therefore, other male members of the family' b. s! B/ N. B0 [
may have similar precocious puberty.3  P& N+ U2 S/ J' x- n5 c
In our patient, physical examination was incon-
$ M, V2 D% O6 i+ y- E  e$ usistent with true precocious puberty since his testi-4 k7 A# s  t9 O
cles were prepubertal in size. However, testotoxicosis5 a6 r3 w8 a7 n& K
was in the differential diagnosis because his father: h( C) l& l7 c, ]' X( q' H
started puberty somewhat early, and occasionally,
9 _' Z% z) J5 b& C. |testicular enlargement is not that evident in the
" n/ u6 ?# c  Pbeginning of this process.1 In the absence of a neg-2 f4 Z4 r8 C9 ?
ative initial history of androgen exposure, our
; O; W$ A& {" p. E4 e1 abiggest concern was virilizing adrenal hyperplasia,
$ }: K" ]# A  |5 F  beither 21-hydroxylase deficiency or 11-β hydroxylase2 X: [# x) r; W3 g- b7 r& F
deficiency. Those diagnoses were excluded by find-
2 B* X; Y/ i) p3 [* G! Ying the normal level of adrenal steroids.- |6 {6 B  C. B+ h5 S; f
The diagnosis of exogenous androgens was strongly+ Y: f, }2 h' Q  V5 Z* z' ^
suspected in a follow-up visit after 4 months because
9 G  h: b6 c! W& j0 R- G+ ~the physical examination revealed the complete disap-
, |( h9 ]! B  a: U+ ]) `9 x4 Zpearance of pubic hair, normal growth velocity, and$ K, a* ^5 u* X
decreased erections. The father admitted using a testos-
4 j) ]& K' n. G8 _0 H, Tterone gel, which he concealed at first visit. He was
% a5 K2 b+ P+ g2 B2 tusing it rather frequently, twice a day. The Physicians’
( ]4 K3 S$ T' s) ^) S, e. O6 ZDesk Reference, or package insert of this product, gel or3 {; u, b3 I3 L9 r
cream, cautions about dermal testosterone transfer to* Q) u: H, ^0 }8 Z1 S9 c
unprotected females through direct skin exposure.
3 w- Q8 G9 m1 Q0 c. ESerum testosterone level was found to be 2 times the( D/ ?; G! J% d& i7 A
baseline value in those females who were exposed to
( `& H) A( H- u# D7 }7 jeven 15 minutes of direct skin contact with their male) q. a, ~( S% y2 a( `: N
partners.6 However, when a shirt covered the applica-
: Q4 w& o1 |- G; C( wtion site, this testosterone transfer was prevented., J4 \% z0 V8 ~& }  T
Our patient’s testosterone level was 60 ng/mL,
, H4 _0 c5 Y" Z6 ?% ^% `which was clearly high. Some studies suggest that! @& M0 i& y, b0 E  M& m
dermal conversion of testosterone to dihydrotestos-  K& k, q1 P) I7 V
terone, which is a more potent metabolite, is more
) U- {# ^% w% o* |active in young children exposed to testosterone. v: S' v5 k# r  [2 K; M0 x
exogenously7; however, we did not measure a dihy-& M) F" s' i, f+ a8 U2 ~/ D4 {" F
drotestosterone level in our patient. In addition to
+ z: _/ }  n! [' J) Y& e+ u9 hvirilization, exposure to exogenous testosterone in/ b. _6 Y; g) R1 y0 C
children results in an increase in growth velocity and- r( a0 l# {5 ?9 g( M' v
advanced bone age, as seen in our patient.
, a! F- `) P: x9 T; B! cThe long-term effect of androgen exposure during
4 r" O6 Z4 b9 D" ^3 D) fearly childhood on pubertal development and final
: y; m) V: J0 x; c0 kadult height are not fully known and always remain
8 U3 j8 p: B% B5 _" n+ W  ^# n& ma concern. Children treated with short-term testos-
# w, X5 D& w& l4 ~9 {terone injection or topical androgen may exhibit some
, d7 y8 p8 }4 L& `( ~& e/ t3 Iacceleration of the skeletal maturation; however, after# S7 W' L) c/ O) z7 H  m( n
cessation of treatment, the rate of bone maturation: O+ r) ~( x2 `" e. k! f
decelerates and gradually returns to normal.8,9
3 S* B3 Y$ G% v/ i6 p5 E  uThere are conflicting reports and controversy
( n3 W* J7 }+ x0 _8 n1 N& M% f3 ]/ {over the effect of early androgen exposure on adult
; f4 m' c6 [$ I4 a* K5 H. B& C8 Cpenile length.10,11 Some reports suggest subnormal6 Q" F( w0 v7 c! V) o
adult penile length, apparently because of downreg-
# K8 ?5 c/ [; I: z6 Qulation of androgen receptor number.10,12 However,9 e; [4 b2 \' E& U
Sutherland et al13 did not find a correlation between
" B5 M/ M4 R! d0 b* ?childhood testosterone exposure and reduced adult7 }- Q8 m! L9 L- q" A9 c3 r: Y
penile length in clinical studies.
) \0 \+ H) y" BNonetheless, we do not believe our patient is1 T) L5 s  O$ S6 M
going to experience any of the untoward effects from. Z6 e& K: d+ `' f* }
testosterone exposure as mentioned earlier because
4 r* e0 t9 \) Q& D# d  kthe exposure was not for a prolonged period of time.
9 I9 {& Q7 L) C6 I3 z3 q2 pAlthough the bone age was advanced at the time of0 w6 `; |9 @# g
diagnosis, the child had a normal growth velocity at
1 ^. V6 Z- B5 l# \1 T2 Kthe follow-up visit. It is hoped that his final adult# d/ i. p5 Z$ B( n! n
height will not be affected.8 A: W. A. C& _6 Z) ?; y
Although rarely reported, the widespread avail-
+ w4 y! g- s8 {ability of androgen products in our society may0 ]  V' ^" Z5 x4 }# z# G
indeed cause more virilization in male or female
( ^# Z5 h) R# ^# N/ Nchildren than one would realize. Exposure to andro-2 J; t" |: R! r4 P9 j2 x# u. S( V
gen products must be considered and specific ques-
) W; X9 o& n. f  itioning about the use of a testosterone product or; Z! e( d; U$ x! }5 h
gel should be asked of the family members during- d4 G1 w3 O2 Z- N/ h, V2 B
the evaluation of any children who present with vir-5 r" ^: ~5 N% N& a4 d; m
ilization or peripheral precocious puberty. The diag-: |2 o/ H4 S% ^5 o, I) }
nosis can be established by just a few tests and by
: [9 I- e/ L) F, F  U- D7 X. Vappropriate history. The inability to obtain such a
1 ^" u1 m2 f& a: d; ~' [history, or failure to ask the specific questions, may; V) L1 f* B6 i; _# g8 C
result in extensive, unnecessary, and expensive
0 H) ?' K  a  y9 D/ }! C/ e: finvestigation. The primary care physician should be
' N: d/ d, n6 k- K- Aaware of this fact, because most of these children
0 n2 w8 E: i9 ]; J0 [$ {$ ?1 gmay initially present in their practice. The Physicians’8 N  O0 o& ^# t+ ~* h* y, J* j8 ?
Desk Reference and package insert should also put a5 w# a* \. E+ O  a3 g6 y
warning about the virilizing effect on a male or# i* o2 U$ }7 X+ h
female child who might come in contact with some-! _" O# E- G1 @7 u9 h
one using any of these products.
, \% E7 N0 h" [0 vReferences  Y4 h. U1 j, `- C/ R- ~& s  M
1. Styne DM. The testes: disorder of sexual differentiation: B3 r! M" r" C* W* Y  a
and puberty in the male. In: Sperling MA, ed. Pediatric. |' Q5 V; {2 M5 M* v6 U2 i7 ~
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" k# I$ B8 B" N. r0 e+ {4 K2002: 565-628.
! K7 b% y3 H/ M* i2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ d; U0 z1 t2 R$ {% I
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
& E( n# a) y, ]2 [1 xBoy Induced by Indirect Topical
* i2 Z/ K8 e% T# u# |: DExposure to Testosterone; N& y9 e4 _6 p- R8 T: W
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 E- g! C' {0 I' O9 b
and Kenneth R. Rettig, MD12 R! l( y" ?$ j3 x/ h& s& @7 X
Clinical Pediatrics1 b9 |4 i" p4 t. j2 U2 j
Volume 46 Number 6& [$ W" l' j" g6 R! P/ J
July 2007 540-543
5 n% g- S  M7 Z  L2 n3 `- u1 Y8 r) v© 2007 Sage Publications6 ^2 n+ C: k/ @, c3 z( E' g! C2 f
10.1177/00099228062966511 }* \) r0 ]8 Q# u
http://clp.sagepub.com
" G8 ^0 @$ Q8 Z9 W8 Y- \$ yhosted at8 r0 ~2 y9 D$ ~* J5 f
http://online.sagepub.com
3 Q" C3 h0 a& P3 R' k. Y) \Precocious puberty in boys, central or peripheral,$ J; ^8 r8 R3 ~9 m/ [' B% B
is a significant concern for physicians. Central' e1 n+ h  J/ T8 t+ _7 f
precocious puberty (CPP), which is mediated5 Q8 |1 @7 t+ v& e$ _9 A
through the hypothalamic pituitary gonadal axis, has
! l0 E  L: ^! s9 n2 [- U. ma higher incidence of organic central nervous system
6 n. r5 X2 P" U7 c" Flesions in boys.1,2 Virilization in boys, as manifested
9 Z+ f  J  s6 p- I9 Yby enlargement of the penis, development of pubic# @4 \2 q1 j0 Z8 `  @& F
hair, and facial acne without enlargement of testi-7 o0 K4 C" B* r& Y1 S4 l" i
cles, suggests peripheral or pseudopuberty.1-3 We
$ F/ _+ T. I1 ]0 Zreport a 16-month-old boy who presented with the
# o8 l1 `; n* d( z+ Jenlargement of the phallus and pubic hair develop-; @1 p# d5 z$ `- Z( A: X
ment without testicular enlargement, which was due" \  _# n% T7 C7 o8 ~- Y
to the unintentional exposure to androgen gel used by
  G! {! o" W* ]: ^0 k" sthe father. The family initially concealed this infor-
3 D( o% N0 D) I9 d7 I$ Tmation, resulting in an extensive work-up for this
' F5 j+ ?$ z* S4 U% n" ^child. Given the widespread and easy availability of5 p6 m7 F0 @" d0 W+ z, K
testosterone gel and cream, we believe this is proba-7 M- W. J8 s" J
bly more common than the rare case report in the
5 y+ n; S) c9 j' z7 G% U/ Iliterature.4
" f  u- \/ @2 E& P& ]9 q0 C; m# IPatient Report/ [. `/ K" m' P+ c6 K* O" V6 f
A 16-month-old white child was referred to the
* `+ S+ S8 H& L9 {endocrine clinic by his pediatrician with the concern2 [+ y! c/ m! Q
of early sexual development. His mother noticed5 T  o! {5 S- Z  H( B
light colored pubic hair development when he was
. n( a1 U& t9 hFrom the 1Division of Pediatric Endocrinology, 2University of
5 B0 w$ K5 L& q9 e" {! TSouth Alabama Medical Center, Mobile, Alabama.3 }6 g+ a! D* T8 j3 s! t! P7 i$ j3 p/ _
Address correspondence to: Samar K. Bhowmick, MD, FACE,5 B, Y! ^3 O  p3 g6 P
Professor of Pediatrics, University of South Alabama, College of% N4 J+ M$ f* q- U% {& O
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ b6 }0 z0 R5 @+ Q6 e
e-mail: [email protected].0 D0 l1 t) e5 ?3 {% U$ y
about 6 to 7 months old, which progressively became* G1 K; a  f/ @7 G2 f
darker. She was also concerned about the enlarge-0 P8 i, x0 V8 K+ |# ~8 B3 t4 ]
ment of his penis and frequent erections. The child
( S+ u0 C( B' O+ a* g0 Bwas the product of a full-term normal delivery, with
4 k- _, T2 N. z5 {1 }a birth weight of 7 lb 14 oz, and birth length of, @4 p6 s* R1 p7 r; |6 w( \3 D
20 inches. He was breast-fed throughout the first year; o3 y2 a5 ~4 B  C8 f. j/ g
of life and was still receiving breast milk along with
/ u! n0 ?; H! B2 _' f+ b# gsolid food. He had no hospitalizations or surgery,3 D# j% E/ ^  D# V- b5 \. |
and his psychosocial and psychomotor development
1 W$ o1 P4 l$ B0 [5 _4 ^& A( @( C; O) fwas age appropriate.. \; r; q" ~1 S- ]5 \) [: J# }5 }% B
The family history was remarkable for the father,
0 _; I' P5 L+ ~. ]* U4 B$ swho was diagnosed with hypothyroidism at age 16,
9 m1 S+ D4 ]& X4 G: _: v4 s$ bwhich was treated with thyroxine. The father’s6 y! j# |' @! q! m2 ^
height was 6 feet, and he went through a somewhat( n9 a$ U4 a: D3 S& U
early puberty and had stopped growing by age 14." S% R  k& x8 o  ?
The father denied taking any other medication. The
/ h& a$ x1 f# ?& f0 \  Achild’s mother was in good health. Her menarche/ g1 p2 D5 i4 m$ L9 q
was at 11 years of age, and her height was at 5 feet
/ V3 {& z5 u' h* {8 c, k: j! d5 inches. There was no other family history of pre-7 f3 |, V9 T% w; S; c
cocious sexual development in the first-degree rela-
$ K7 P, c4 N7 \. o9 {- P& }tives. There were no siblings.
' i. S) U6 {1 D! vPhysical Examination/ B* h' N7 \6 l% ?2 h
The physical examination revealed a very active,- g: l2 N- W+ s4 J% D+ ]( v2 a
playful, and healthy boy. The vital signs documented: x+ p2 X% R) X+ Z* j
a blood pressure of 85/50 mm Hg, his length was8 V1 ?7 l, m9 Y; i. h) w6 [7 ?
90 cm (>97th percentile), and his weight was 14.4 kg
( |7 Y  h$ ?5 }$ s(also >97th percentile). The observed yearly growth
7 l: s6 f" G" ?0 N5 Gvelocity was 30 cm (12 inches). The examination of' ~' J$ a$ Z+ K9 U6 s$ A5 \# u' x
the neck revealed no thyroid enlargement.) k( Q) T+ L* n! X3 x9 Q+ A
The genitourinary examination was remarkable for$ m$ j) X4 M4 q8 w) I$ Q
enlargement of the penis, with a stretched length of
# ?1 P" |5 T/ `0 Y6 j4 y/ U6 S3 s8 cm and a width of 2 cm. The glans penis was very well; i+ S9 j$ p$ ~- \
developed. The pubic hair was Tanner II, mostly around1 L2 |/ Z- O. p) ]
5406 C6 T/ I& a" i0 Y* A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 r, g  P; i# r) Tthe base of the phallus and was dark and curled. The
9 r  e) X  Q/ ctesticular volume was prepubertal at 2 mL each.
" y0 L6 N$ w$ i' U1 N/ `9 P' F; AThe skin was moist and smooth and somewhat; H: i* F0 B% F7 A1 M
oily. No axillary hair was noted. There were no
/ |. ?: Y/ x' h! xabnormal skin pigmentations or café-au-lait spots.
$ w% k6 c, R4 F# KNeurologic evaluation showed deep tendon reflex 2+
6 @8 R  o# N& jbilateral and symmetrical. There was no suggestion7 q0 P$ P6 W. b6 v+ \5 P1 r
of papilledema.% f- S. v& F0 Y, u9 p! k
Laboratory Evaluation
# V8 O3 F" [, IThe bone age was consistent with 28 months by& z+ b1 u3 o  e( W; T. F8 ?& w
using the standard of Greulich and Pyle at a chrono-
" F: j) O. }$ ~) f5 z: \% B! [; N* n$ blogic age of 16 months (advanced).5 Chromosomal
) n3 i$ L  m: F5 m7 [7 D! wkaryotype was 46XY. The thyroid function test: ?" q, m) X' P' b6 T. ?
showed a free T4 of 1.69 ng/dL, and thyroid stimu-6 S& j. J3 n2 F( z; q
lating hormone level was 1.3 µIU/mL (both normal).
; v/ @& I9 r3 RThe concentrations of serum electrolytes, blood
" Z! M! f! ]4 zurea nitrogen, creatinine, and calcium all were
6 S" z0 l# j! f0 wwithin normal range for his age. The concentration2 X: C" `: E( E+ ~5 L- ?
of serum 17-hydroxyprogesterone was 16 ng/dL
- U. ]: {& ?7 o8 o( t/ z(normal, 3 to 90 ng/dL), androstenedione was 20
* Q) X) ?, C6 N7 @6 A3 fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 I3 V2 t- u" L' r6 d
terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 g. u' m+ X- g0 ?% `, u
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ ~( S  A" I+ j: A, n/ [$ J49ng/dL), 11-desoxycortisol (specific compound S)
6 L6 |; w8 K% t, Bwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
5 M8 K8 \& D! B2 b% u2 x$ [tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# X* v( g0 e+ i
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 n8 r3 ~: U+ ~. l! A9 d
and β-human chorionic gonadotropin was less than
( Q' h: c. |+ H$ b8 i8 ^5 mIU/mL (normal <5 mIU/mL). Serum follicular# z6 i. c9 i+ [% f
stimulating hormone and leuteinizing hormone1 M0 [! [" X% _. Y9 p& ^
concentrations were less than 0.05 mIU/mL
" h4 ?2 x' M) P' d# E(prepubertal).
+ e; c6 O. h7 r4 z: [The parents were notified about the laboratory9 A2 n$ G6 h6 X, e6 r% }4 u  A" \- D* Q
results and were informed that all of the tests were
2 M) Z" f6 P8 o/ U1 |normal except the testosterone level was high. The
* D2 I  X2 w3 M% ^, l+ R) }follow-up visit was arranged within a few weeks to
' Z$ x6 t6 n: a/ Xobtain testicular and abdominal sonograms; how-  v  Q4 x( Q( F
ever, the family did not return for 4 months.; c3 }$ A8 ]1 s; G6 q, A! v
Physical examination at this time revealed that the
% [8 {7 z: l8 j! x; |5 O5 ochild had grown 2.5 cm in 4 months and had gained1 h3 l  M$ x' x% y0 _! ^# ]
2 kg of weight. Physical examination remained
0 e, a: ^: w' n! h5 D" h, junchanged. Surprisingly, the pubic hair almost com-
, C1 `+ Z1 n) ~, X( d( k- i: {pletely disappeared except for a few vellous hairs at& E: I4 {8 D) |) \
the base of the phallus. Testicular volume was still 2
- i& v% N; [& H( l/ x6 a0 L. s. pmL, and the size of the penis remained unchanged.
$ P/ C9 e/ s7 H* J2 kThe mother also said that the boy was no longer hav-# ^$ F  W, l: Q/ o, _
ing frequent erections.6 ^7 @3 U" Q6 @1 w! j+ n$ p- i
Both parents were again questioned about use of4 q- @. F, g; w1 ^* s3 o
any ointment/creams that they may have applied to) X' {% d% P/ m3 ^, D7 g
the child’s skin. This time the father admitted the
1 `1 e5 w6 i5 h: y' HTopical Testosterone Exposure / Bhowmick et al 541
$ D5 @/ n- P/ X# M) X( Huse of testosterone gel twice daily that he was apply-% C9 d( g$ A* Q2 N
ing over his own shoulders, chest, and back area for
+ f- Y2 R2 d# w  \0 E9 t, o  p% Ra year. The father also revealed he was embarrassed
( @: E; u+ h: X7 x4 s! k4 v8 t+ Qto disclose that he was using a testosterone gel pre-8 b/ U2 D0 \# C; ^9 D' L2 k1 V. {
scribed by his family physician for decreased libido- ]4 _+ E' a- b" r# v- J" D( |% m
secondary to depression.
8 X; T4 J' ~: u/ l2 u. i5 S8 _; o" e& mThe child slept in the same bed with parents.
; c" _& a; U( X* `3 B) f/ e) SThe father would hug the baby and hold him on his
. c: G- ~- d- l8 _1 hchest for a considerable period of time, causing sig-
- y! [, V% V/ }0 L& m  N% Inificant bare skin contact between baby and father.- c% F3 {8 G- ~: H
The father also admitted that after the phone call,
# N: N" q  z1 v; x8 Rwhen he learned the testosterone level in the baby/ r9 d9 f) I* l" G5 o
was high, he then read the product information
; Z" t& f1 O7 R5 }+ Z# j  t: [( {packet and concluded that it was most likely the rea-
7 _5 H8 v, b6 o0 Mson for the child’s virilization. At that time, they
- C6 B" o/ ~9 }" Y8 w7 W# Gdecided to put the baby in a separate bed, and the# K4 C! e1 `, Z4 X
father was not hugging him with bare skin and had0 L2 n6 s8 |! }8 C
been using protective clothing. A repeat testosterone
- @7 d* ~! a5 j& U: rtest was ordered, but the family did not go to the
; k% i" I' F/ v3 R1 T( P  l. llaboratory to obtain the test.
2 `5 Z" o$ g# b0 v' X& y6 |Discussion! b. C9 x) p' X8 R
Precocious puberty in boys is defined as secondary( Q. Y$ B5 u, n& Y, m
sexual development before 9 years of age.1,4
; U. H, T( L. t* {+ _+ G  KPrecocious puberty is termed as central (true) when
. B! ]" J) \6 N; xit is caused by the premature activation of hypo-
3 B" d" f6 b3 i* F% X1 T" O) r1 H( vthalamic pituitary gonadal axis. CPP is more com-
. j$ w4 S2 t7 b6 }3 Y. r- h; Qmon in girls than in boys.1,3 Most boys with CPP7 ^  X; Y8 P* N, V8 C
may have a central nervous system lesion that is" i1 L1 A2 C7 V
responsible for the early activation of the hypothal-
1 r7 B5 ]3 [2 i1 N. F' o/ Samic pituitary gonadal axis.1-3 Thus, greater empha-
- o8 N! v. U# `' xsis has been given to neuroradiologic imaging in
/ D5 K0 v9 m1 Y" h) u. s1 X' J3 eboys with precocious puberty. In addition to viril-9 e* g. K+ R% r: |% k  p* @- s3 i
ization, the clinical hallmark of CPP is the symmet-4 @/ p$ d/ i  Z/ Q% m: Z
rical testicular growth secondary to stimulation by
" e; E4 [* j: z) P4 `gonadotropins.1,3; {5 Q' m# }' r, s0 L8 D" X' G
Gonadotropin-independent peripheral preco-% B+ x; i) v( ^6 l
cious puberty in boys also results from inappropriate2 B0 y! z% s& H7 p! F
androgenic stimulation from either endogenous or( w! u4 V4 }( y  x
exogenous sources, nonpituitary gonadotropin stim-
& j2 ~6 Z/ E: Bulation, and rare activating mutations.3 Virilizing% Z. ^" J8 `- q
congenital adrenal hyperplasia producing excessive
8 q" {# i! c1 x! X5 N8 ^: i. J$ m4 }adrenal androgens is a common cause of precocious
5 B/ N4 z' U$ D) X! {puberty in boys.3,49 v2 c3 b8 O1 Z% w# r
The most common form of congenital adrenal
9 @, [7 x% c3 P/ y6 khyperplasia is the 21-hydroxylase enzyme deficiency.
2 D. J$ o5 j! V- Z0 ~The 11-β hydroxylase deficiency may also result in
5 A1 B# @' ^  P4 W; ~7 `8 ^4 P: Nexcessive adrenal androgen production, and rarely,
" x5 h8 O! U* H# ]+ X* S9 g* kan adrenal tumor may also cause adrenal androgen
8 j- o4 }$ |/ p5 mexcess.1,3
4 K! e- [2 a' R, X, T* Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 m1 D* n& i' _! [3 S1 B
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# j* ?. ~( `: U7 G* A( YA unique entity of male-limited gonadotropin-3 m; B/ F' l0 a. L7 E9 t$ n' s3 L
independent precocious puberty, which is also known4 L' g; x. F( U' k% ?1 V4 r
as testotoxicosis, may cause precocious puberty at a
4 Q# f  o& Y3 d) o& ^8 G# Every young age. The physical findings in these boys/ z# ~% D( V; o+ o8 g/ S# E' ~
with this disorder are full pubertal development,
% A6 r3 E% G6 G. z! [* Tincluding bilateral testicular growth, similar to boys
8 R  M+ E, e4 l) a( h1 Z" G  S8 swith CPP. The gonadotropin levels in this disorder9 I* |  E  p- k* t: i( R) D, h2 x
are suppressed to prepubertal levels and do not show$ m2 y% d; o/ |  F* a  P7 F  R
pubertal response of gonadotropin after gonadotropin-
" j% o7 {" w6 ^% C5 T( Treleasing hormone stimulation. This is a sex-linked1 B2 ]4 Q0 r, K5 |& I9 O
autosomal dominant disorder that affects only- [: ~( p8 G4 S+ I
males; therefore, other male members of the family, Z7 q8 `+ R7 V$ X. A* p* U
may have similar precocious puberty.3" M0 y- c( m6 {1 E" I7 \$ \
In our patient, physical examination was incon-
% Q$ @# H9 J5 hsistent with true precocious puberty since his testi-$ d% d0 T* A/ `# E7 S
cles were prepubertal in size. However, testotoxicosis  S. e- C5 c3 C. j
was in the differential diagnosis because his father& E+ ~, g& y: T- D5 j' ~
started puberty somewhat early, and occasionally,
; H2 u$ G1 h. Ftesticular enlargement is not that evident in the. o$ F: J! Q) \4 E* n2 Y
beginning of this process.1 In the absence of a neg-- |, k/ w. u1 A& i0 w! w: x6 I
ative initial history of androgen exposure, our
% j% R5 I$ I  G' gbiggest concern was virilizing adrenal hyperplasia,) R! `$ g/ s0 H2 ~1 {* u9 Y
either 21-hydroxylase deficiency or 11-β hydroxylase
  Q* \; \" W. w$ y, Zdeficiency. Those diagnoses were excluded by find-
9 u' c0 ?. ~4 d# R0 U; `ing the normal level of adrenal steroids.
- @+ R* e# g9 Q# x4 ~The diagnosis of exogenous androgens was strongly, Y3 p8 @" e/ _! H
suspected in a follow-up visit after 4 months because. A; @. z3 f, _$ ]
the physical examination revealed the complete disap-6 N6 c( B9 L1 T' B, \- |- u
pearance of pubic hair, normal growth velocity, and4 @* \; x, P8 `
decreased erections. The father admitted using a testos-
2 V5 F) t/ E. @% zterone gel, which he concealed at first visit. He was
* b5 P1 J/ D8 Y; o( Musing it rather frequently, twice a day. The Physicians’
/ E$ G- C# M: [2 ]: P1 _7 ~Desk Reference, or package insert of this product, gel or1 x. d% L3 K" S+ S. ~7 O
cream, cautions about dermal testosterone transfer to7 V2 s* g3 o$ u( r5 t- n+ r8 U+ \
unprotected females through direct skin exposure.
- A& ~0 c: I$ N" p; r  N) cSerum testosterone level was found to be 2 times the  j! m" d( D, ]1 g
baseline value in those females who were exposed to
$ n$ A5 a( A2 b; ^& |even 15 minutes of direct skin contact with their male5 p( f9 X6 Q6 ?
partners.6 However, when a shirt covered the applica-
5 w5 _; c2 b! }, Xtion site, this testosterone transfer was prevented.
! H0 p5 E: \, }4 J. K6 L" @& b( IOur patient’s testosterone level was 60 ng/mL,1 k) y3 t" L8 i
which was clearly high. Some studies suggest that6 H1 E: O3 @- b( P5 V2 o3 c; l' M% ^
dermal conversion of testosterone to dihydrotestos-# ?' Q( J: s3 R6 s' Z" t
terone, which is a more potent metabolite, is more
, q+ K, a3 O0 Eactive in young children exposed to testosterone
+ W/ v3 T. p( W  s5 I+ \9 }% dexogenously7; however, we did not measure a dihy-$ |2 j9 u1 w' X0 K4 {' P
drotestosterone level in our patient. In addition to
0 F3 O2 b' C0 {% d& [0 _virilization, exposure to exogenous testosterone in
- {* `: t/ R% ]9 wchildren results in an increase in growth velocity and1 v$ l, J$ G, o3 ], g
advanced bone age, as seen in our patient.
! n7 R# L: X* J0 L( n: ?+ GThe long-term effect of androgen exposure during+ R5 ?9 Y' v% ^
early childhood on pubertal development and final) v" G$ K" t# k
adult height are not fully known and always remain6 c: ?3 A* `) Z( y( o: |* U
a concern. Children treated with short-term testos-5 D5 ?& _" {3 S# g: h
terone injection or topical androgen may exhibit some0 J, p; z: G& X, b2 C9 c  L
acceleration of the skeletal maturation; however, after5 w/ v" _& @7 @. Y/ _
cessation of treatment, the rate of bone maturation
# \( j5 g* [  vdecelerates and gradually returns to normal.8,9; V9 O. g) d9 j  a& F" B
There are conflicting reports and controversy
( ?& q6 O0 a/ B$ A* |# Nover the effect of early androgen exposure on adult
/ Q( e/ G( `6 |% ipenile length.10,11 Some reports suggest subnormal
" t  T1 W) ^% j+ _/ @5 H8 p' zadult penile length, apparently because of downreg-/ a6 [  K+ c0 L1 t, q8 k
ulation of androgen receptor number.10,12 However,4 [* h. `6 o5 r
Sutherland et al13 did not find a correlation between
2 b( w" P' J! C7 achildhood testosterone exposure and reduced adult, E# X! o$ Y) U
penile length in clinical studies.& U6 O5 M  o$ e& X; r3 q9 d5 ~
Nonetheless, we do not believe our patient is
$ Z2 H! g. A, F0 w. @9 \7 Egoing to experience any of the untoward effects from9 l& i6 m$ u4 k
testosterone exposure as mentioned earlier because
  }& L, ~: T# Y3 ^3 o' r/ v# Xthe exposure was not for a prolonged period of time." f( V7 S7 q; X' ^
Although the bone age was advanced at the time of6 {; D3 R9 S% B+ ?
diagnosis, the child had a normal growth velocity at- _% x  ]& g  ]6 W9 ~7 r9 b( o# A
the follow-up visit. It is hoped that his final adult
6 l6 a5 f! o9 ?/ {height will not be affected.! M1 G8 o: q9 ]
Although rarely reported, the widespread avail-( u$ r% u# R1 }. \: c
ability of androgen products in our society may
. s, |5 v! u$ \2 Windeed cause more virilization in male or female
' f/ b: Q( D; l  Rchildren than one would realize. Exposure to andro-
3 s: L$ n# A" O& [7 x* P0 ~gen products must be considered and specific ques-
9 z$ @* K; M! `! d3 o, Utioning about the use of a testosterone product or. K9 J' A4 h2 a6 J7 V8 u
gel should be asked of the family members during
; }, R' g* q- uthe evaluation of any children who present with vir-" b; G' C- P# S
ilization or peripheral precocious puberty. The diag-
& L  U: V! e, ]% e/ s' Y0 onosis can be established by just a few tests and by/ U7 v+ p0 L1 p6 l8 t! T' D2 N
appropriate history. The inability to obtain such a8 w, o9 z: n7 _  z/ u% V) q* N6 |
history, or failure to ask the specific questions, may
) d2 v0 O4 c9 u4 ~0 Qresult in extensive, unnecessary, and expensive: C0 I- y% F. y8 V' ^0 W  A% N
investigation. The primary care physician should be
. }# N0 E  @5 t& d9 x  F: ?aware of this fact, because most of these children
6 p: C. s! g6 x, o- j) H9 Smay initially present in their practice. The Physicians’
' Y, c) M2 N( `. U. B- r5 R: fDesk Reference and package insert should also put a: i) u8 z8 E5 Z
warning about the virilizing effect on a male or
) ]7 f  d. q. N' F/ L7 R5 d: tfemale child who might come in contact with some-
# W& j" v, p8 y9 ?9 fone using any of these products.' ?& i% x% O$ P2 {
References9 e1 Y/ f1 P3 M& j0 ~; A: e, ]4 N
1. Styne DM. The testes: disorder of sexual differentiation- G% _) e3 c9 f8 ]" ^* z; j0 g  h' r4 t
and puberty in the male. In: Sperling MA, ed. Pediatric6 }  _1 F. x  w$ O
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;% N  }+ `* G# `  M; ~
2002: 565-628.
! x" b  G& ~- L& k2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious+ }% Y; P% W# G: _2 S
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

* g% ?3 T& I) ?" V) q( T精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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