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Sexual Precocity in a 16-Month-Old% N4 V$ x' h# |. s
Boy Induced by Indirect Topical0 }) Z, G4 ]$ h
Exposure to Testosterone+ J0 I6 b- K! l- o- [2 `8 q
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 P! k; `$ Z+ B+ @5 d. M' c6 n( m
and Kenneth R. Rettig, MD1' B# k6 K# b( x
Clinical Pediatrics6 W1 ?, Q  d# Q; ^) ~% y, q! u
Volume 46 Number 6
! u/ r0 X7 i$ y* l9 w$ P8 AJuly 2007 540-543. F2 P/ `4 |, o' y( u$ _
© 2007 Sage Publications, o; {4 j2 |  F+ d6 |8 e+ q
10.1177/00099228062966510 k+ _9 N9 Z7 G; ~
http://clp.sagepub.com/ O6 M, d# ?% u& @" |9 j
hosted at% c# d' [1 P& Y; o0 y
http://online.sagepub.com
* W" B! F% X/ W( O+ O& m9 cPrecocious puberty in boys, central or peripheral,0 i& E' H1 ]5 T0 c
is a significant concern for physicians. Central" {3 U: x6 a/ l; [( @& n
precocious puberty (CPP), which is mediated
. N+ X. f# h$ X% c" L% Othrough the hypothalamic pituitary gonadal axis, has
- s- U8 Y4 Z: ta higher incidence of organic central nervous system
& B& A; N7 z6 O7 H1 J& p7 q: Dlesions in boys.1,2 Virilization in boys, as manifested
: X! m+ u% z; w$ ?, d) aby enlargement of the penis, development of pubic. t* y5 I, I; i' C: @' F: j1 E
hair, and facial acne without enlargement of testi-
! I7 i  `" O+ {3 Z( z; ?( w6 g5 bcles, suggests peripheral or pseudopuberty.1-3 We
* r9 H5 e9 E, |& E' u7 jreport a 16-month-old boy who presented with the
' Y4 A6 }- w) fenlargement of the phallus and pubic hair develop-" f+ ?9 u) J$ v% T8 w/ \, B* a
ment without testicular enlargement, which was due% m+ w& d. m2 x% t
to the unintentional exposure to androgen gel used by& y1 E8 V: }; v" @' t
the father. The family initially concealed this infor-8 H, X" Z, @6 A5 x# F
mation, resulting in an extensive work-up for this
, Z% Q6 e1 c% W. ]child. Given the widespread and easy availability of
9 s) B: L( _$ C, r: L; Jtestosterone gel and cream, we believe this is proba-" v4 b& I; N+ M( h- e
bly more common than the rare case report in the& f, c' m8 n* t
literature.4& ], \8 C" {0 L% g+ m" e
Patient Report/ i$ v0 z$ `: K  z0 X9 K: F% @
A 16-month-old white child was referred to the* A+ ?/ q1 g) \
endocrine clinic by his pediatrician with the concern6 }* |2 N- a. h8 P
of early sexual development. His mother noticed+ \% I5 n6 }" v  a" I' [
light colored pubic hair development when he was- ^: K' U' h5 D
From the 1Division of Pediatric Endocrinology, 2University of
$ \/ ~' ?4 ^7 h& e* B$ l7 v  Q+ pSouth Alabama Medical Center, Mobile, Alabama.. F# i! d+ J4 I+ C" ]
Address correspondence to: Samar K. Bhowmick, MD, FACE,. `; D! f6 s8 ]) [4 d
Professor of Pediatrics, University of South Alabama, College of4 N' Z" P: d( H/ N! L. Y7 W" y# @
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( l* w  [* h" E: Y: R) G* @% \e-mail: [email protected].- @7 i- S. E2 U# E
about 6 to 7 months old, which progressively became1 |* f+ C5 l* v$ E0 s
darker. She was also concerned about the enlarge-
6 x) K- p5 ^' x7 nment of his penis and frequent erections. The child# C! p: J3 k) g/ |7 b& d$ g
was the product of a full-term normal delivery, with
) h- H! g  z. x8 Z5 }  k1 fa birth weight of 7 lb 14 oz, and birth length of( P5 l7 W4 u( ?8 q) ]
20 inches. He was breast-fed throughout the first year! k" Q9 |+ t0 q5 @( V
of life and was still receiving breast milk along with
& P8 F1 G  ^# K% E/ q' dsolid food. He had no hospitalizations or surgery,/ e% }$ ~, S* I& Z+ n, ^
and his psychosocial and psychomotor development0 _' c' |7 Y& s1 [
was age appropriate.6 |( q# ?+ D. I4 R' u2 k( i
The family history was remarkable for the father,
% `" t) H  i; C" @0 Kwho was diagnosed with hypothyroidism at age 16,, J, a$ X  }9 W* K: W. u1 a7 M* K
which was treated with thyroxine. The father’s7 B8 {: t$ ^. {9 V- o" Z6 ^
height was 6 feet, and he went through a somewhat. u! o  `, \( J$ V6 d
early puberty and had stopped growing by age 14.
  Y4 z: r* L0 `  Y& VThe father denied taking any other medication. The
$ O$ Y3 v' G/ c% {* h! vchild’s mother was in good health. Her menarche; q7 ~7 N+ P: G2 R5 G
was at 11 years of age, and her height was at 5 feet
9 u5 p, Y) c6 [5 inches. There was no other family history of pre-
( F7 \* P  `7 Ccocious sexual development in the first-degree rela-, _: n" C. t, D0 m3 A2 L9 Y+ K
tives. There were no siblings.
; {9 q; b. K/ {* k& n8 mPhysical Examination
- F; B. N+ c% P7 g, l& t" CThe physical examination revealed a very active,
1 I$ @' U7 l9 h& {0 splayful, and healthy boy. The vital signs documented
: V- I' y  W5 l, g. ta blood pressure of 85/50 mm Hg, his length was) X: O8 X& F# g) A2 |
90 cm (>97th percentile), and his weight was 14.4 kg9 b4 v; h6 F- `4 d8 P* \2 w" ?! U
(also >97th percentile). The observed yearly growth3 g; |# H8 B3 @6 o3 [* V/ c. X
velocity was 30 cm (12 inches). The examination of
: f9 I6 f& @! N7 othe neck revealed no thyroid enlargement.
! q7 X% o! |& B6 x) C4 i6 CThe genitourinary examination was remarkable for6 g# E2 [  F7 f' \% G* Z- b
enlargement of the penis, with a stretched length of
8 G# S# W" P& Q- Z" r8 cm and a width of 2 cm. The glans penis was very well
3 W/ p& }, v. k9 s; Bdeveloped. The pubic hair was Tanner II, mostly around
7 m; ?9 d; E1 f8 b: ~540$ `( t  q. h! a* E5 K0 ~7 t5 A3 r2 N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* n; n: @( x) ]3 J4 ythe base of the phallus and was dark and curled. The
' a# B+ w4 e; P. a" atesticular volume was prepubertal at 2 mL each.! a$ z) C& @7 Z
The skin was moist and smooth and somewhat
- n4 v+ r0 Z1 W+ b1 a5 V- doily. No axillary hair was noted. There were no& ?  q# r5 _& R+ o* x) B5 p1 @
abnormal skin pigmentations or café-au-lait spots.
4 _% `3 q) P4 d, ?( m) r- c' {; fNeurologic evaluation showed deep tendon reflex 2+! _9 X( @: a+ n, z% \7 f2 n7 }
bilateral and symmetrical. There was no suggestion
: p. c. f+ R5 a4 c# u% f) Z  yof papilledema.  x2 p, W6 _& v) F# u9 V4 Y  O. s
Laboratory Evaluation
# X( Q3 {8 Q% X0 i7 s2 LThe bone age was consistent with 28 months by
/ ^- r3 |/ {5 ]2 X0 Z; fusing the standard of Greulich and Pyle at a chrono-" S: n4 G! s# P$ Z1 r9 u- p
logic age of 16 months (advanced).5 Chromosomal
' u; ?. E+ }/ A# ?. v' a6 xkaryotype was 46XY. The thyroid function test3 ]( Q4 v% M' i3 e' A
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
$ u, j( n* D4 U" `lating hormone level was 1.3 µIU/mL (both normal).
$ }; O; M$ d' MThe concentrations of serum electrolytes, blood
, H( U1 n7 A* @! _3 \1 T3 gurea nitrogen, creatinine, and calcium all were
' S! w! V* h* o3 O. l0 uwithin normal range for his age. The concentration
& H- V8 L: M) o* D9 b5 @! w9 V# ^of serum 17-hydroxyprogesterone was 16 ng/dL' o- O8 z8 r8 h, ^3 q; t
(normal, 3 to 90 ng/dL), androstenedione was 20
, W9 t9 a: [8 _  ]1 Y3 b9 zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 _5 P' h! X9 j& {* dterone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 H! a/ ?5 g: p  Y  D  d& rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to5 d( m/ c( I" W( [8 ~( P# P: I) v/ J
49ng/dL), 11-desoxycortisol (specific compound S)
, h; O% h, t3 g; _( i3 fwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-  f4 ?* |  [9 b5 ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! C/ W* M! _! W. ]; A+ ytestosterone was 60 ng/dL (normal <3 to 10 ng/dL),$ B6 \% Z& ^( e  j/ D/ Y
and β-human chorionic gonadotropin was less than' p; Y" r3 b# L
5 mIU/mL (normal <5 mIU/mL). Serum follicular- @/ ^1 t8 a7 `' ]% q' I. ]
stimulating hormone and leuteinizing hormone9 E8 O, ]8 b$ D* b
concentrations were less than 0.05 mIU/mL
- N$ P1 y1 y3 F+ X$ F9 t- J6 [6 q(prepubertal).' q9 f# \$ t; t8 i+ ?
The parents were notified about the laboratory2 b  f! B! z  w8 k9 S
results and were informed that all of the tests were3 v( n; i' ]. t  }7 J
normal except the testosterone level was high. The
4 U4 Q' E3 B2 [1 p* k  X2 |4 ufollow-up visit was arranged within a few weeks to1 G/ j$ g) {6 p3 l
obtain testicular and abdominal sonograms; how-- v+ }' i6 g. J& J
ever, the family did not return for 4 months.7 x+ C7 \& A+ L' j. k9 _
Physical examination at this time revealed that the5 r& d  ?! \2 ]* o3 {& c  P  [
child had grown 2.5 cm in 4 months and had gained
9 A4 k7 Y1 h3 }. n$ }2 kg of weight. Physical examination remained
" i  g4 Q( \& ?6 e7 D8 W' ]8 h0 zunchanged. Surprisingly, the pubic hair almost com-4 j9 P) g, a5 @4 U, D
pletely disappeared except for a few vellous hairs at
8 K8 W' c1 S5 V) ]2 C4 Z8 S- Mthe base of the phallus. Testicular volume was still 2. Z% l  t: d4 u
mL, and the size of the penis remained unchanged.* U- C" e! l! C7 M) _
The mother also said that the boy was no longer hav-
0 T2 N9 Q, q1 E/ E" zing frequent erections.; D3 C# c7 H9 J" H/ _9 F8 I
Both parents were again questioned about use of& u! K" H% s! x& j8 U
any ointment/creams that they may have applied to% M* G4 y8 I- K  |' }! R' A
the child’s skin. This time the father admitted the
: p. b' P. X) B, iTopical Testosterone Exposure / Bhowmick et al 5414 k- ^$ Q/ d2 S+ ?1 o" m  }$ u
use of testosterone gel twice daily that he was apply-
& U  c7 q2 V+ u/ y0 r7 }$ wing over his own shoulders, chest, and back area for
+ b  Y# r" \9 t: Ja year. The father also revealed he was embarrassed  b% i- L5 N: I
to disclose that he was using a testosterone gel pre-8 `+ u4 w, s( T
scribed by his family physician for decreased libido2 X2 F5 e+ J% D4 l* p  G) \
secondary to depression.( `% L! K/ v6 d0 Z  Q) I
The child slept in the same bed with parents.
6 F6 V0 X& ?3 p4 F2 m( fThe father would hug the baby and hold him on his' Q' |5 N0 S, o# c  y, B+ h
chest for a considerable period of time, causing sig-
. E& K# ?& k; a8 F0 F& ?nificant bare skin contact between baby and father./ v; o0 l2 e9 A. z( t
The father also admitted that after the phone call,
/ ]/ C- }1 e5 B' }6 @8 lwhen he learned the testosterone level in the baby2 I) H0 i! P$ ]
was high, he then read the product information4 t1 S4 k$ F; U  y7 ]! d6 v
packet and concluded that it was most likely the rea-
. O9 Y' }1 i9 A9 S& d% g% x* b1 lson for the child’s virilization. At that time, they; G7 e( _9 H) f4 z1 u9 m
decided to put the baby in a separate bed, and the
; P- ~; f" c& a( m6 O  w0 t0 Cfather was not hugging him with bare skin and had
, i! b" |) B1 H8 V. [* h# xbeen using protective clothing. A repeat testosterone3 K( D4 ?% K2 h
test was ordered, but the family did not go to the  W& J5 g% o5 m2 v
laboratory to obtain the test.. w  F& _% {' J. P( x% w2 I
Discussion
* Q) z' B9 \, \  c/ n: S: t# dPrecocious puberty in boys is defined as secondary" T& `1 U! s6 I7 s/ ?% Y; G
sexual development before 9 years of age.1,4
; p( c5 E2 w4 e2 e2 k3 h1 lPrecocious puberty is termed as central (true) when
- ^% _3 c# L0 l+ P2 K3 m& Eit is caused by the premature activation of hypo-
9 x. r6 r  u4 P( {7 Othalamic pituitary gonadal axis. CPP is more com-
/ S6 M5 F* n, xmon in girls than in boys.1,3 Most boys with CPP
$ O% d- D/ L3 U1 G. Z. hmay have a central nervous system lesion that is
% ]5 P1 r3 [( O1 U+ Kresponsible for the early activation of the hypothal-
! l. m' ~9 g: v8 @$ y9 Eamic pituitary gonadal axis.1-3 Thus, greater empha-& ]& q1 h& f2 \+ N# [
sis has been given to neuroradiologic imaging in  ]5 j9 R, h$ D. _, R$ I+ q
boys with precocious puberty. In addition to viril-+ @9 ?1 j, D6 P0 C0 V: c
ization, the clinical hallmark of CPP is the symmet-
+ t* Y; f. w0 s1 h% rrical testicular growth secondary to stimulation by3 Q! t3 H9 `5 n6 Z& s! Q
gonadotropins.1,3
) ]* p) h4 r, G3 kGonadotropin-independent peripheral preco-
3 [& D" x2 n0 x! @* s& r' }  |' y1 S. [cious puberty in boys also results from inappropriate
; z# }% E: J9 W8 `' ~) ~8 {androgenic stimulation from either endogenous or
' x; D7 L, A* sexogenous sources, nonpituitary gonadotropin stim-: Z4 V) a: |- n) ]% U, b
ulation, and rare activating mutations.3 Virilizing+ T6 Z) k0 Z% M% L  c" g
congenital adrenal hyperplasia producing excessive
8 {1 V& t; l7 P/ U$ l* Sadrenal androgens is a common cause of precocious" Y8 b# w  n+ J( o: |1 O/ v0 b
puberty in boys.3,42 L/ m: L1 R+ z" Z- U: A6 F/ P. i
The most common form of congenital adrenal
' O# P. d7 ~. _/ Z; N9 Rhyperplasia is the 21-hydroxylase enzyme deficiency.
! F% _/ S, h) c; uThe 11-β hydroxylase deficiency may also result in9 U8 e$ i2 F( |( c5 D2 o* t9 E% O
excessive adrenal androgen production, and rarely,$ M1 |: i) D" R; p5 c
an adrenal tumor may also cause adrenal androgen8 a6 N- Q2 p" [
excess.1,30 S% {) w) {0 V3 I; t2 u( H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# D3 v' u0 V! r542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 ^- g3 \6 U/ I5 N) T
A unique entity of male-limited gonadotropin-
3 [6 I- P0 c9 v' K9 Xindependent precocious puberty, which is also known
% o' D1 q$ u! b2 a- jas testotoxicosis, may cause precocious puberty at a
2 U& `% \- z* R' qvery young age. The physical findings in these boys, d2 H) R* g& |; H1 X9 p: P4 @
with this disorder are full pubertal development,
: \; z: j1 j, p' W4 ^2 x# E0 Jincluding bilateral testicular growth, similar to boys  k6 k4 u+ h8 E" C, x; F' C
with CPP. The gonadotropin levels in this disorder
3 m- S1 h' s7 |  G* U$ ^) ]& C( `are suppressed to prepubertal levels and do not show
3 d, e* u( n' R: hpubertal response of gonadotropin after gonadotropin-* A1 r! z+ {* ^  _5 R) P
releasing hormone stimulation. This is a sex-linked
9 ?( q7 L$ ?/ ^- |2 [" [2 X+ A4 cautosomal dominant disorder that affects only
) S# j  ]% W$ gmales; therefore, other male members of the family' E; d; ~7 [1 i4 R5 L% `8 I9 H
may have similar precocious puberty.3. U( g' |' p$ @9 n
In our patient, physical examination was incon-% H2 G' ^3 |& I
sistent with true precocious puberty since his testi-! [1 A9 x$ j; q" Q
cles were prepubertal in size. However, testotoxicosis6 N: `: y6 a/ Y
was in the differential diagnosis because his father9 n+ h) ]. ]7 Z5 ?% A+ f4 N
started puberty somewhat early, and occasionally,
: S1 o+ w6 E3 t2 V) v. otesticular enlargement is not that evident in the
! g* k3 j! d3 m' M. ybeginning of this process.1 In the absence of a neg-% |7 F/ X3 i( Z$ M3 H7 t/ z, U
ative initial history of androgen exposure, our
* D: [2 |* ~/ b1 s4 Q3 ~6 @biggest concern was virilizing adrenal hyperplasia,
& i2 T) w3 a$ {' {* n2 `" s7 Qeither 21-hydroxylase deficiency or 11-β hydroxylase% I9 G" _6 J* }: I. y
deficiency. Those diagnoses were excluded by find-
  r, C! k' T8 N* ming the normal level of adrenal steroids.
" Q, e/ ^& N, {7 A8 R! yThe diagnosis of exogenous androgens was strongly
3 J; Y0 b$ y# |" \9 bsuspected in a follow-up visit after 4 months because7 B! L% s- ^8 f) A6 W
the physical examination revealed the complete disap-& J* x; p0 L! A) U, M+ u) n8 Y
pearance of pubic hair, normal growth velocity, and6 V, X% E& q  f2 N4 V
decreased erections. The father admitted using a testos-+ `% ]1 Q: G! s* K3 g/ }
terone gel, which he concealed at first visit. He was" G1 W& T  ~! ~
using it rather frequently, twice a day. The Physicians’
* W4 H& }) B; L, F0 w) cDesk Reference, or package insert of this product, gel or  _4 A( p8 _8 G4 j) ~
cream, cautions about dermal testosterone transfer to
: `4 z7 T) e* f$ P  t6 E: U7 y# {# tunprotected females through direct skin exposure." ^* @# |3 w; X$ f. K% Q
Serum testosterone level was found to be 2 times the' W5 [+ P8 E# e* A
baseline value in those females who were exposed to9 s/ `3 v% G& U8 p
even 15 minutes of direct skin contact with their male! V) n. T: ~+ q8 x: A1 f
partners.6 However, when a shirt covered the applica-
, U! C) J+ d) O0 N) Wtion site, this testosterone transfer was prevented.) P: {7 d  X. x' X
Our patient’s testosterone level was 60 ng/mL,
' t6 F- s% c0 B" Vwhich was clearly high. Some studies suggest that
4 j; d! y# X6 ~. l  Hdermal conversion of testosterone to dihydrotestos-' D/ ]2 l+ V4 F) N% p$ I1 v
terone, which is a more potent metabolite, is more
8 V' H9 `9 a9 ~- Cactive in young children exposed to testosterone# Z( Y1 L* ~0 r$ |
exogenously7; however, we did not measure a dihy-+ L2 A: y+ Q& @3 f2 d
drotestosterone level in our patient. In addition to4 @: M/ v3 G) C9 z
virilization, exposure to exogenous testosterone in* ^* m- U# N: `1 Z7 b) m
children results in an increase in growth velocity and* L3 t6 R7 W* q2 E# q( d/ {
advanced bone age, as seen in our patient.
6 m$ N! P4 Q4 BThe long-term effect of androgen exposure during* i8 j8 K! G% h8 a9 O) O: r6 [4 y
early childhood on pubertal development and final
/ n  n4 \+ ?8 B; F, Kadult height are not fully known and always remain, g% Z# ~7 X5 K" V/ X0 M
a concern. Children treated with short-term testos-
4 K% b/ J2 r9 }: A# a) ^6 a+ g" |terone injection or topical androgen may exhibit some
$ ^$ l% S* z6 \- cacceleration of the skeletal maturation; however, after
, q- m& n: s$ p8 K7 S" acessation of treatment, the rate of bone maturation5 l9 G9 X( w& ]" R
decelerates and gradually returns to normal.8,9
( r" X% w& V. ^2 A, @There are conflicting reports and controversy- q& K% `( m, U
over the effect of early androgen exposure on adult
& }# C) |; [; K6 a* k5 I  |penile length.10,11 Some reports suggest subnormal7 i& J- A+ s: A- l. I' i# q( g: q: Z
adult penile length, apparently because of downreg-
6 E! a/ Y8 z: d/ o/ Iulation of androgen receptor number.10,12 However,
: Z, B) l' }3 k# r" U, v$ LSutherland et al13 did not find a correlation between
, R5 I8 b8 V* ^4 Xchildhood testosterone exposure and reduced adult
/ R0 ~6 {* R" cpenile length in clinical studies.4 }+ E4 s$ w6 K3 u  l7 }$ _
Nonetheless, we do not believe our patient is5 [% |; Y2 k) W$ Y- {, j- x
going to experience any of the untoward effects from  @# @5 c. z) n
testosterone exposure as mentioned earlier because
( x: V9 T) c) U5 b+ H! Tthe exposure was not for a prolonged period of time.1 K+ S' B2 L% R7 F, V
Although the bone age was advanced at the time of0 ~8 X2 s6 D! i2 r; p( ~
diagnosis, the child had a normal growth velocity at
+ C' d5 [. O% B8 m- u; kthe follow-up visit. It is hoped that his final adult
& k7 X4 i  d/ N! hheight will not be affected.# p, y: _4 ?6 A. f  G$ D
Although rarely reported, the widespread avail-
  K; ^8 a1 N6 o( E$ |# `. A9 gability of androgen products in our society may  s3 T" J9 m6 n: G/ `/ W
indeed cause more virilization in male or female
' W& w$ ^; f% \) E- @( m9 t9 {children than one would realize. Exposure to andro-
) {' }) p- J: d5 G+ R% D$ a+ jgen products must be considered and specific ques-
( @# ^1 Y) e2 J- xtioning about the use of a testosterone product or
; b6 q, c! q6 x9 E" H) b. o' Kgel should be asked of the family members during& ]+ n3 ~0 Q  F* M
the evaluation of any children who present with vir-" N; V& K# e- c" z
ilization or peripheral precocious puberty. The diag-
3 C' |/ w& i' I% V7 O8 K( Enosis can be established by just a few tests and by/ ]) ^5 p" F: O2 W+ ^- ^
appropriate history. The inability to obtain such a
0 p+ J2 Q+ }3 v# Xhistory, or failure to ask the specific questions, may
6 M6 z* I4 J) p% ], |result in extensive, unnecessary, and expensive
7 ?2 l; F. n- {3 i$ h( T' Cinvestigation. The primary care physician should be
  L; J, @: f3 u$ E% }8 zaware of this fact, because most of these children
  _# l' O8 f% M+ Z/ T1 T9 zmay initially present in their practice. The Physicians’
  k' X* t/ b2 W5 t* B( u/ I/ t9 MDesk Reference and package insert should also put a
$ j1 i% S) h7 x9 Y/ t$ z, ywarning about the virilizing effect on a male or1 d4 j! h% M) d( D$ h8 f
female child who might come in contact with some-: D- }$ Z$ [# v6 q) T2 p
one using any of these products.
5 E; \' o: Z5 I. N+ zReferences; W9 E! k! G, S* ^$ s
1. Styne DM. The testes: disorder of sexual differentiation
! N8 Z- V3 f. p. F4 band puberty in the male. In: Sperling MA, ed. Pediatric
# l" n7 r4 E- [" f0 a8 I; r5 ]& hEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 [+ u# [: }) C& a3 s6 N9 N$ U2002: 565-628.
( _0 |! [" z( N) [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! F- I' `5 K1 Y0 s7 V% Gpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old6 `; P4 g6 E! U7 I  R
Boy Induced by Indirect Topical
! n$ D) D% }5 J& zExposure to Testosterone% p( G% ?) K) E, L; @! O
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- u( O/ k+ H; \3 \1 C
and Kenneth R. Rettig, MD1% z# E& H1 ^6 C4 ]  h) n) X
Clinical Pediatrics$ [, x* w: I/ f$ b5 ?
Volume 46 Number 6
5 b& J2 K7 s- m  SJuly 2007 540-543, ~8 X' m! \, t3 C. n3 j
© 2007 Sage Publications9 n/ n) K" f8 C- F
10.1177/0009922806296651
# S5 M" V0 C; q+ I, F0 I' I$ mhttp://clp.sagepub.com. ^: k2 ~% u* Z0 d
hosted at5 c0 J$ t7 d' \8 h8 ]/ I6 j
http://online.sagepub.com, x( Z( A* S' A) c5 `
Precocious puberty in boys, central or peripheral,. a  I  h5 Z) x3 Z+ y+ `
is a significant concern for physicians. Central% X- D! i( [) z6 z: }& a, G
precocious puberty (CPP), which is mediated4 Y  r- Y( ?, \% _$ `" D+ k5 A
through the hypothalamic pituitary gonadal axis, has
- L3 S+ D6 G7 Pa higher incidence of organic central nervous system' [, [! j/ G  J$ R0 j2 [  v
lesions in boys.1,2 Virilization in boys, as manifested3 J$ x( P; P/ o6 d
by enlargement of the penis, development of pubic2 n6 a( e" ^. H, l
hair, and facial acne without enlargement of testi-
/ e0 H' P- L7 ^9 Hcles, suggests peripheral or pseudopuberty.1-3 We) _4 S4 e1 R. e' ^1 F  B
report a 16-month-old boy who presented with the2 G) c+ r( _% c6 K7 o* l% h3 |
enlargement of the phallus and pubic hair develop-# D5 Y0 d: z9 u( i$ V! p
ment without testicular enlargement, which was due
! d2 g6 X) Y4 D2 ~5 Wto the unintentional exposure to androgen gel used by* }! Y  n0 o! _& ?
the father. The family initially concealed this infor-
! k  q2 ?1 X; @" F" Hmation, resulting in an extensive work-up for this6 ~) U1 n- w1 o5 a, O
child. Given the widespread and easy availability of
6 A, I1 N$ d8 o! i* e% Etestosterone gel and cream, we believe this is proba-# r0 L: E. q2 s! H/ c1 j
bly more common than the rare case report in the1 r* @4 g: t7 i6 {, \( s) k. X3 u
literature.4
: _4 W; @' f) R0 RPatient Report, n3 F4 l9 |* f0 C( Y
A 16-month-old white child was referred to the4 g+ W- @/ @% p1 q7 N! P) c6 ]9 P
endocrine clinic by his pediatrician with the concern3 M  s- J8 f1 F. n
of early sexual development. His mother noticed
8 f  V% Z9 @7 d/ o( \* k6 r( z5 Wlight colored pubic hair development when he was
2 C" T8 `- o3 Z/ P' O: ~From the 1Division of Pediatric Endocrinology, 2University of! E1 ^1 n, r* s3 V. n
South Alabama Medical Center, Mobile, Alabama.
- A# n' ]0 z, @& x( {! O4 z9 JAddress correspondence to: Samar K. Bhowmick, MD, FACE,0 }+ z+ c" M' I1 h  i
Professor of Pediatrics, University of South Alabama, College of' R. u$ J) @! g( V6 T
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
3 R) ~% F5 e, s$ h$ ge-mail: [email protected].# y) ^: d5 [) i/ Y  I. z. v% C: a
about 6 to 7 months old, which progressively became5 k- {+ R0 y1 o
darker. She was also concerned about the enlarge-
4 w" U  ?# C4 f& T4 lment of his penis and frequent erections. The child- k- `0 O5 s0 S# j
was the product of a full-term normal delivery, with* a$ T3 B- C- ?8 ^' ?# E
a birth weight of 7 lb 14 oz, and birth length of% `+ P& q; E3 F8 P# ?  g5 [: ~& w
20 inches. He was breast-fed throughout the first year0 Z* j' P8 h6 E
of life and was still receiving breast milk along with3 k7 q* P+ X4 M! z. a8 y5 ?( L
solid food. He had no hospitalizations or surgery,8 V; ]$ B. n$ Q# f- t2 u7 @6 m
and his psychosocial and psychomotor development
1 c- f+ Q+ X% h' D3 H, nwas age appropriate.) B  r0 _6 V3 K5 E- Q  ]
The family history was remarkable for the father,' J" c4 w2 |7 E6 ^* r- }
who was diagnosed with hypothyroidism at age 16,
2 \( X0 x/ V  |+ g4 Iwhich was treated with thyroxine. The father’s
. P6 @% V  m: ~( y6 m8 c- m! mheight was 6 feet, and he went through a somewhat
# U7 K$ x7 }/ N3 O5 K6 E# Aearly puberty and had stopped growing by age 14.& \# ~$ y! V) r$ ^
The father denied taking any other medication. The. z& }; A6 ]: g8 \# M& W2 j5 b
child’s mother was in good health. Her menarche
' `1 s( Z  O& u( o, v1 O/ wwas at 11 years of age, and her height was at 5 feet+ G2 _8 B, m! r5 v' C
5 inches. There was no other family history of pre-
* \9 Y2 w8 T+ B" @+ D4 F! V+ ecocious sexual development in the first-degree rela-
, ]+ x, y  M, k- a0 u! N3 s6 etives. There were no siblings.
, N. I" X" k* uPhysical Examination' T" U* e9 K5 u! e/ q/ P
The physical examination revealed a very active,, H! G0 X. l8 ~
playful, and healthy boy. The vital signs documented
  D3 I- h: |7 ua blood pressure of 85/50 mm Hg, his length was
4 j8 |$ L' Y( K; W2 C2 ~90 cm (>97th percentile), and his weight was 14.4 kg
% c# K) @- v- M: S(also >97th percentile). The observed yearly growth# M. O6 k6 M) j; z8 K% b$ l$ M
velocity was 30 cm (12 inches). The examination of
/ F  W6 A( f$ h( C1 M$ [the neck revealed no thyroid enlargement.
* ?: A+ ~5 b/ ~" K1 n5 q. S" EThe genitourinary examination was remarkable for, u8 i# h6 \  ?; J
enlargement of the penis, with a stretched length of
$ l4 _* }/ M' v( _7 b& @& f8 cm and a width of 2 cm. The glans penis was very well2 g1 r# }. h/ \7 l9 u# t
developed. The pubic hair was Tanner II, mostly around6 {8 Q; V) G! U& D% W- N
540
8 h9 Y# V  b% w) |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# }' p9 v( ~6 F' C( f1 _& u3 m/ u
the base of the phallus and was dark and curled. The
+ C' J8 Z7 |! D6 D/ N& H1 n0 btesticular volume was prepubertal at 2 mL each.# I: K- r6 H+ \9 {+ s" o& e
The skin was moist and smooth and somewhat- j$ G6 ^4 s! N8 D. H
oily. No axillary hair was noted. There were no7 z1 ?& a  A- ?& e& v* ?# ~
abnormal skin pigmentations or café-au-lait spots.7 K% x" y0 s  L1 c0 o5 t6 W9 U+ b
Neurologic evaluation showed deep tendon reflex 2+4 X9 g0 ~1 s2 _& r
bilateral and symmetrical. There was no suggestion  _# a2 J6 W1 y6 L
of papilledema.
4 m8 N* |. [" CLaboratory Evaluation/ P6 N0 V) P, A* y( U
The bone age was consistent with 28 months by
, U: L+ X4 d' N8 f7 g3 gusing the standard of Greulich and Pyle at a chrono-" K/ G$ |7 r2 h3 C4 I& {4 d9 e
logic age of 16 months (advanced).5 Chromosomal
! \8 `$ }1 E' U% f+ l) Z! ~karyotype was 46XY. The thyroid function test( d4 o8 @% y; O6 ?2 A5 e) H) F& Y
showed a free T4 of 1.69 ng/dL, and thyroid stimu-- Q6 m: o' p& C& ]3 Y9 {% e
lating hormone level was 1.3 µIU/mL (both normal).
0 Q& ^6 }1 C) P" NThe concentrations of serum electrolytes, blood  r' e* z; H1 B1 H/ }  R+ }, y! m
urea nitrogen, creatinine, and calcium all were' @8 V* ^' u$ K, V1 B$ g1 K
within normal range for his age. The concentration/ @0 L7 c7 Y7 w3 b  O+ ~/ A
of serum 17-hydroxyprogesterone was 16 ng/dL) {* n: O( G- O$ {; s; K% D
(normal, 3 to 90 ng/dL), androstenedione was 20
) u( D: A3 ?# R8 J0 R7 Fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
, `! \: y# x$ {( wterone was 38 ng/dL (normal, 50 to 760 ng/dL),
, E. N% Y' `! x8 q5 @8 Gdesoxycorticosterone was 4.3 ng/dL (normal, 7 to' @5 |$ k$ E* J7 B$ D3 f# \
49ng/dL), 11-desoxycortisol (specific compound S)! h+ B! v! `$ D+ O* E0 @/ }
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 z! g3 w/ ]- e- i" C
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& p( r: t4 s3 w; Mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),  c: N# P. O/ z
and β-human chorionic gonadotropin was less than8 |3 z* H- \( j' c  o7 }
5 mIU/mL (normal <5 mIU/mL). Serum follicular
/ j5 V, @' |' jstimulating hormone and leuteinizing hormone. Y% T3 X" k7 z: B' Q7 q+ Y
concentrations were less than 0.05 mIU/mL
4 C' g% Q3 g9 B' J$ m7 h' y(prepubertal).5 q) ^+ J* B  T+ ]& a5 s3 a
The parents were notified about the laboratory% D" p3 u% j% L" K
results and were informed that all of the tests were" f  [4 ?" ~3 d7 G- J7 I
normal except the testosterone level was high. The
+ o1 p& ^& ]4 V* d3 @: h3 @follow-up visit was arranged within a few weeks to
, }7 {, b9 G( i" }obtain testicular and abdominal sonograms; how-) H* d) }2 _+ I2 x" u
ever, the family did not return for 4 months." E3 P* v( R; c; a
Physical examination at this time revealed that the
+ H. x4 Z1 c; i4 @9 a- bchild had grown 2.5 cm in 4 months and had gained
" h; C- [% k$ O6 q/ e2 kg of weight. Physical examination remained, C+ q; \* ?8 R* }: b6 l
unchanged. Surprisingly, the pubic hair almost com-) e. [& G3 x' g3 J, Z8 Q
pletely disappeared except for a few vellous hairs at& c* L6 ]- z, z3 s/ E
the base of the phallus. Testicular volume was still 2% W9 ?& g. l* r, u8 b
mL, and the size of the penis remained unchanged.
' w& [. W  }& x" R6 FThe mother also said that the boy was no longer hav-0 V- _8 D. x; {5 F
ing frequent erections.5 f4 R, {. B, }# p# b5 e
Both parents were again questioned about use of
3 L5 T. v- d$ `4 t3 i( Bany ointment/creams that they may have applied to5 l0 d1 O& p6 _4 Y) |- a+ n
the child’s skin. This time the father admitted the- C  d/ G( b+ I# W
Topical Testosterone Exposure / Bhowmick et al 541, d, [8 t$ |( B/ Y& L
use of testosterone gel twice daily that he was apply-
4 X& `  b% c6 k' ]) }! V! Oing over his own shoulders, chest, and back area for3 o- K- i" H$ x/ {' |/ T* j
a year. The father also revealed he was embarrassed
8 B2 D2 g9 G! |5 L- nto disclose that he was using a testosterone gel pre-
) G2 W- d  w6 j0 k1 I: M" Iscribed by his family physician for decreased libido3 d; F# d- |6 i/ N
secondary to depression.2 Q8 ]3 D2 }9 C, \
The child slept in the same bed with parents.0 L, Z5 p# `* m/ R
The father would hug the baby and hold him on his0 `+ T" `* W& }* r0 X
chest for a considerable period of time, causing sig-" l: _2 L8 `/ y$ z, b
nificant bare skin contact between baby and father." l% p5 L9 v  x: h# T  N# C
The father also admitted that after the phone call,( {( f& o& _& e
when he learned the testosterone level in the baby
2 v& i' }; o, \% B- kwas high, he then read the product information
% C: e, H3 b3 D2 U- cpacket and concluded that it was most likely the rea-
# O  k" o; G; m: I2 Rson for the child’s virilization. At that time, they
# z+ h1 J: m, |. s  Gdecided to put the baby in a separate bed, and the
5 a! U/ a$ ?% Lfather was not hugging him with bare skin and had
) O4 w! g& G, A$ b" r5 ubeen using protective clothing. A repeat testosterone
0 t9 G  I( r# M( gtest was ordered, but the family did not go to the6 U: i% |5 w5 p
laboratory to obtain the test.6 V! L. `9 I! y9 m* N' `+ v5 b
Discussion/ N1 d1 h# [0 P3 i! p
Precocious puberty in boys is defined as secondary; e5 R; D+ I0 M4 m3 E
sexual development before 9 years of age.1,4# \2 v' {. I5 H+ L8 j) I
Precocious puberty is termed as central (true) when
" q' ?) S7 \! ]( }: {9 ?- e4 w  ^it is caused by the premature activation of hypo-1 l: N6 y9 c- |7 a* u5 Y# p( R
thalamic pituitary gonadal axis. CPP is more com-1 f3 l5 X0 E$ P' z% Q" k' U
mon in girls than in boys.1,3 Most boys with CPP
* l- X% V& g" Cmay have a central nervous system lesion that is
, W( w, q" |3 ]  r5 U% ~; G9 jresponsible for the early activation of the hypothal-6 A% y) N2 s& c$ n" _& ?8 ?
amic pituitary gonadal axis.1-3 Thus, greater empha-
- u; v8 B8 i/ K" Psis has been given to neuroradiologic imaging in
5 x: a- z8 C1 T8 h% P9 |boys with precocious puberty. In addition to viril-
( f9 l4 L! q9 c; b4 s3 H8 fization, the clinical hallmark of CPP is the symmet-
* R$ R; a$ y6 xrical testicular growth secondary to stimulation by* l" y3 n! n+ ?5 u4 H' K
gonadotropins.1,3
9 v' s: e- Z, V8 Q* G( ?, }Gonadotropin-independent peripheral preco-
" k2 s* f- Z* n; C- r+ i3 j0 Rcious puberty in boys also results from inappropriate+ n$ R2 }0 Z$ I  b% T3 X, T
androgenic stimulation from either endogenous or  e# R* C  J" @5 V
exogenous sources, nonpituitary gonadotropin stim-: H) ^1 r' C( d9 ]/ X7 _! e
ulation, and rare activating mutations.3 Virilizing! A! B8 ?# X1 ~/ Q
congenital adrenal hyperplasia producing excessive
' I% V3 F) b6 @  i6 T2 @adrenal androgens is a common cause of precocious
1 u/ j1 T" C4 I" _* D: @6 _6 [8 ^puberty in boys.3,4
5 O8 {' L! B! G, A, EThe most common form of congenital adrenal
7 p1 N. S$ y. i- J! \hyperplasia is the 21-hydroxylase enzyme deficiency.
7 U) B6 h# D0 g& X' iThe 11-β hydroxylase deficiency may also result in/ z2 P+ c$ t& K2 x
excessive adrenal androgen production, and rarely,
7 r) t4 \1 k" ]: B; m. q3 ^& _an adrenal tumor may also cause adrenal androgen: D; n2 O: ^7 [+ a1 H5 j) d4 o8 h( D* g
excess.1,30 C6 {+ P! g0 n% \3 M. j: f% L
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: _2 |5 U* A$ K' x2 ]7 }8 \542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( f+ i: E; s1 g5 W
A unique entity of male-limited gonadotropin-
$ X" f/ V0 p0 k& q/ sindependent precocious puberty, which is also known
2 U" Z2 Y& l  H; eas testotoxicosis, may cause precocious puberty at a
7 {8 g0 z4 p  @1 s# lvery young age. The physical findings in these boys
! M! F. D& m+ Y' fwith this disorder are full pubertal development,
0 c& }1 D$ q2 ?! Eincluding bilateral testicular growth, similar to boys: u: S- G3 Y: `3 O5 O$ _
with CPP. The gonadotropin levels in this disorder
, S! v2 c  `1 G# R- \. C" sare suppressed to prepubertal levels and do not show
8 }# E8 F& [$ T/ ~pubertal response of gonadotropin after gonadotropin-% D; F' s2 Q5 S0 F' k
releasing hormone stimulation. This is a sex-linked  V* e( t: m' C
autosomal dominant disorder that affects only
' P- Y, h" v& `! }$ smales; therefore, other male members of the family6 G5 P7 Q( r* @% ^
may have similar precocious puberty.3  l- u6 D! I$ W- f. M1 z7 l% `; Z1 A% F
In our patient, physical examination was incon-
, W/ y- l" d* \, M5 D9 ^3 lsistent with true precocious puberty since his testi-
8 a5 }( S- p" S# W' }cles were prepubertal in size. However, testotoxicosis: P: [: q4 I2 ]% o/ U; h
was in the differential diagnosis because his father
) n$ D3 ?4 B+ \3 pstarted puberty somewhat early, and occasionally,& B- A( f* N& p  H; v& F' o6 q- Y+ o
testicular enlargement is not that evident in the
& R: f' W8 C) p* X- Xbeginning of this process.1 In the absence of a neg-4 B) G8 z2 ^/ C: T& \
ative initial history of androgen exposure, our
! b; E9 P' b0 b& V; F. }) gbiggest concern was virilizing adrenal hyperplasia,
& g+ `7 f4 [) d) G6 ceither 21-hydroxylase deficiency or 11-β hydroxylase; Y5 Z4 L4 @8 C' Q' N
deficiency. Those diagnoses were excluded by find-* t/ D/ q& v! s5 x" ^
ing the normal level of adrenal steroids.
$ `; w, A: `% ]" K' U$ sThe diagnosis of exogenous androgens was strongly- G. A# I, Q5 P, ]) ]1 P
suspected in a follow-up visit after 4 months because
7 r0 \7 N' l4 i1 j/ L& Zthe physical examination revealed the complete disap-3 ~3 }+ Y$ B6 b9 T8 [) f
pearance of pubic hair, normal growth velocity, and
4 g; B8 ?- H5 J+ b+ l. fdecreased erections. The father admitted using a testos-
( Y# {& T' ?+ zterone gel, which he concealed at first visit. He was# r5 K4 X) M' y7 o: b  t, }  j
using it rather frequently, twice a day. The Physicians’. R! Z$ n0 i! Y% m& B
Desk Reference, or package insert of this product, gel or; m. q2 B# c/ p: L$ m' ]6 c
cream, cautions about dermal testosterone transfer to! e3 S6 F9 @# }, a9 y/ V' |
unprotected females through direct skin exposure.
0 _* [* |6 f! \8 j; G) |4 ISerum testosterone level was found to be 2 times the
  X+ h( V. ?/ d# v0 V1 l5 Sbaseline value in those females who were exposed to
9 D* u& i( c0 q2 Meven 15 minutes of direct skin contact with their male5 n4 b& R0 u$ n8 O! q
partners.6 However, when a shirt covered the applica-
' }" p. R# \; r! g  Gtion site, this testosterone transfer was prevented.% s; f2 l9 U  m7 l1 n
Our patient’s testosterone level was 60 ng/mL,
6 M% y; A9 B. q! T; x5 I* M* e6 \which was clearly high. Some studies suggest that
) c& j: I! E" I" }4 X5 W  Vdermal conversion of testosterone to dihydrotestos-( m! M, }* m* S% @+ B" D  ^
terone, which is a more potent metabolite, is more
' S: f! z6 P& a8 ]1 g7 T( R* K5 Y6 }active in young children exposed to testosterone% k; ~+ v$ }2 ?' U
exogenously7; however, we did not measure a dihy-
/ H- [" H  I  X6 u$ G7 Kdrotestosterone level in our patient. In addition to
# ^( J2 q& D3 z' \9 k+ B, Avirilization, exposure to exogenous testosterone in
8 F2 Z$ ?3 L; f+ x2 k! fchildren results in an increase in growth velocity and
, i0 k! l; n3 A. Z5 x( A7 Z; Gadvanced bone age, as seen in our patient.9 }2 w, _/ H' b* s( l, y
The long-term effect of androgen exposure during
" b$ v- V7 X" \+ {early childhood on pubertal development and final6 m( J- n) `6 L% i
adult height are not fully known and always remain
& d# {2 P9 C! {2 l' s5 xa concern. Children treated with short-term testos-0 Z. V) O$ \! U: [
terone injection or topical androgen may exhibit some/ Z' S' ]. w" A8 v* u7 ~
acceleration of the skeletal maturation; however, after
3 S4 v* h; I+ R# {$ t( bcessation of treatment, the rate of bone maturation# A" H/ B  F+ ~! r' y
decelerates and gradually returns to normal.8,9
7 c5 B+ ?2 }  b+ _  q* f, }% [There are conflicting reports and controversy
8 F0 w" \# |/ _: B8 Cover the effect of early androgen exposure on adult
+ p# j& D) o6 Kpenile length.10,11 Some reports suggest subnormal
, s" f; ?! J) }; {/ ]adult penile length, apparently because of downreg-" D) O: s5 T! n4 t
ulation of androgen receptor number.10,12 However,7 ~2 e- n% e" ?7 M8 t
Sutherland et al13 did not find a correlation between
7 u7 m3 D/ U" _5 t0 u8 T# Fchildhood testosterone exposure and reduced adult& f2 Y/ b; k2 K4 ?+ j7 P
penile length in clinical studies.' h0 `+ K! m4 T% j# M
Nonetheless, we do not believe our patient is
( ^3 _$ X9 p. x3 f" F: Kgoing to experience any of the untoward effects from9 d, v( F9 O% X5 V! q0 u, \5 N( Z
testosterone exposure as mentioned earlier because
8 A8 G% G; \( ?2 J3 gthe exposure was not for a prolonged period of time.
7 V6 b% F( `9 o" s+ U) c" C; JAlthough the bone age was advanced at the time of
  z5 S4 |8 P# ediagnosis, the child had a normal growth velocity at
5 E8 g! ^6 d7 M& Kthe follow-up visit. It is hoped that his final adult
% Q; c& g& e7 t) W. bheight will not be affected.- k* q. e8 {  v2 E, ]; l) h7 ]9 w
Although rarely reported, the widespread avail-4 N, N- a; F: t
ability of androgen products in our society may
; \* L, U3 `0 l) Eindeed cause more virilization in male or female  v; s- E* S4 h
children than one would realize. Exposure to andro-
$ s0 y% X" M: V3 j3 @* H* Q, @gen products must be considered and specific ques-8 }# l5 D0 t3 O. q9 Z& Z7 _6 F9 V
tioning about the use of a testosterone product or+ N2 S  t5 O" u8 p& ^6 _( u8 E- ]
gel should be asked of the family members during5 F5 O& m# S& z3 H
the evaluation of any children who present with vir-
  G$ q, ~; ^: s0 Iilization or peripheral precocious puberty. The diag-* s7 M% F6 z. |, l4 @* w
nosis can be established by just a few tests and by
2 R7 p& y. K. A4 G5 D6 _appropriate history. The inability to obtain such a& ^, ~3 O( n, Q- M0 b9 K4 M5 g
history, or failure to ask the specific questions, may
+ O  T" p2 k7 C% d+ u" f, M  Wresult in extensive, unnecessary, and expensive
: S; a; r: V$ }$ Winvestigation. The primary care physician should be% K. d3 ?5 `* y/ w, D' N  f
aware of this fact, because most of these children4 @) _; B$ f+ e) O
may initially present in their practice. The Physicians’
# ]" D' H" T4 P1 B9 j+ X! `Desk Reference and package insert should also put a
8 ~$ T/ J8 M5 r% D- f& \warning about the virilizing effect on a male or0 e( g7 P6 N+ G+ |+ M6 f$ P
female child who might come in contact with some-
& @9 @8 s8 d; |: r6 O1 d! eone using any of these products.2 Z6 M8 F6 T( s0 ]- [& l
References( c/ Z: O' D+ r2 i/ |; @
1. Styne DM. The testes: disorder of sexual differentiation& N: z  M" W9 }
and puberty in the male. In: Sperling MA, ed. Pediatric
6 Z; S2 y3 w2 ~$ nEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( A( w& J  t6 Z3 h2002: 565-628.% E8 D) K% D7 l1 l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 E& P7 I, h8 |: Y; n1 l
puberty in children with tumours of the suprasellar pineal
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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
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

3 H& u  s- A: j" @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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