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Sexual Precocity in a 16-Month-Old
! R2 F3 `' O- y4 P2 s' lBoy Induced by Indirect Topical
8 T# s& ]; O  MExposure to Testosterone
+ A, _  Q- b% J6 f9 CSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% Y  s& _- y& b1 V+ u/ Oand Kenneth R. Rettig, MD1
: B  t+ z' _* k' eClinical Pediatrics
. Y6 q5 L( }$ @$ d2 DVolume 46 Number 6
) `5 x* y% I% j0 cJuly 2007 540-5434 D" r# {- [" N. F# V" W. N# b% e
© 2007 Sage Publications
1 H+ p( o6 H- C0 ~10.1177/0009922806296651$ s& H7 A$ M) R- w# n
http://clp.sagepub.com0 o! B3 E# W3 q
hosted at
) t& t8 @4 s" E0 r% Rhttp://online.sagepub.com
% H* f9 Z5 i% k- t* ]7 OPrecocious puberty in boys, central or peripheral,
6 u3 ~/ t" g5 i+ ~- D; o7 G  Nis a significant concern for physicians. Central3 v1 A  c0 F1 B; w" S' c
precocious puberty (CPP), which is mediated0 |: q/ R) B9 A
through the hypothalamic pituitary gonadal axis, has3 l4 i' n: r7 ?
a higher incidence of organic central nervous system- A: V% B- i9 Y
lesions in boys.1,2 Virilization in boys, as manifested
9 B$ h$ o1 g  _2 s8 r4 jby enlargement of the penis, development of pubic, h3 I8 K+ F& X* R+ c% X
hair, and facial acne without enlargement of testi-
) Y* \: v' M" Ncles, suggests peripheral or pseudopuberty.1-3 We
( p2 p2 K+ n+ \, u; preport a 16-month-old boy who presented with the( r3 N" |( i6 F$ l. U
enlargement of the phallus and pubic hair develop-
8 J4 O- a) M4 P  E, lment without testicular enlargement, which was due
* j6 @6 m& M& x- K+ S+ r7 nto the unintentional exposure to androgen gel used by! _+ s) D1 u0 P' L2 ?
the father. The family initially concealed this infor-
& p, ~! C& s& W; g" v+ C7 Emation, resulting in an extensive work-up for this
0 Y# P& x, ?# h, T+ X' Dchild. Given the widespread and easy availability of) r7 p3 t# j+ j# r
testosterone gel and cream, we believe this is proba-
6 t1 ~+ {# I0 r0 M4 i- r1 Sbly more common than the rare case report in the
/ t, _4 X" p4 P7 l' H9 z; @literature.4
" ?6 B% |* b' b! n0 ~2 V% j; Y+ K! JPatient Report/ J- G$ H9 r% J' c2 Y. o- B, |- S* ]
A 16-month-old white child was referred to the
( g5 \; u( U9 Sendocrine clinic by his pediatrician with the concern0 K& f8 q/ v* z+ N
of early sexual development. His mother noticed4 f7 V- Y5 q8 M. U: n
light colored pubic hair development when he was7 N( E$ t) ~/ x) Z3 e, Q; S
From the 1Division of Pediatric Endocrinology, 2University of0 p  t, h- ^5 J) z8 K. Y
South Alabama Medical Center, Mobile, Alabama.
) {( W- \. c$ p  Z9 q, J1 C* |Address correspondence to: Samar K. Bhowmick, MD, FACE,+ |6 I8 P+ |7 W# s% _0 p8 v6 I
Professor of Pediatrics, University of South Alabama, College of
# E7 A( a2 a$ j4 o) C: KMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, D) N, a% D. _- @- }6 X
e-mail: [email protected].3 Z, [+ I& L! d( w* @; e
about 6 to 7 months old, which progressively became. Z" E' ]4 B; r7 O& Z
darker. She was also concerned about the enlarge-7 R; \7 v4 T0 y2 x' F
ment of his penis and frequent erections. The child' c) Z$ r) y5 l" B% H, a1 J5 \
was the product of a full-term normal delivery, with7 s; `- S* d) E% B+ a* }" S
a birth weight of 7 lb 14 oz, and birth length of& e# E8 W* W. I, S& @0 D7 L1 j
20 inches. He was breast-fed throughout the first year
' _( ^) e0 e) L- e6 _of life and was still receiving breast milk along with
4 A6 @, D. e8 l1 E$ Zsolid food. He had no hospitalizations or surgery,
; x; @7 |# J1 p. ]- g' Wand his psychosocial and psychomotor development$ Q( c4 b4 U( W; w' h! p( s
was age appropriate.
1 v' N4 h! r. e+ h; k; p5 _" CThe family history was remarkable for the father,
" O8 N3 P" ], B3 Z- q1 Gwho was diagnosed with hypothyroidism at age 16,
5 N. T6 q6 C! ?7 S% Q. ~- Iwhich was treated with thyroxine. The father’s8 o0 O3 V6 _, X2 H- r9 V
height was 6 feet, and he went through a somewhat$ q3 p$ |  B# N, T1 X
early puberty and had stopped growing by age 14.+ ~2 F6 n1 d5 V9 u# X
The father denied taking any other medication. The' O! \! N4 v; Y; N  \' _0 \, N9 z
child’s mother was in good health. Her menarche
9 ^; j( v% X3 v( f) o% \was at 11 years of age, and her height was at 5 feet
* c1 o" z/ [; o# o9 U, D5 inches. There was no other family history of pre-5 T" d8 O+ g6 B9 R) g$ w% D) N: w
cocious sexual development in the first-degree rela-% S  ]2 O- _6 W: g
tives. There were no siblings.
. f. Q- L8 S7 E. LPhysical Examination& E9 X# B" ?& B& l: ~6 r+ t) b" C$ \
The physical examination revealed a very active,
5 k" D4 U; ?! P* C" R1 ~playful, and healthy boy. The vital signs documented6 Z" v5 k& N4 ?+ Z. z
a blood pressure of 85/50 mm Hg, his length was8 L; F' n: J8 F2 a
90 cm (>97th percentile), and his weight was 14.4 kg  H6 w% ?9 C5 A9 Z) k
(also >97th percentile). The observed yearly growth# g: B/ T, P, o& i& L) Q8 C' s' w
velocity was 30 cm (12 inches). The examination of! e5 m7 y0 j' {9 j- f& w6 r# `3 r. \
the neck revealed no thyroid enlargement.
5 F4 x/ Y! N5 J; J( |The genitourinary examination was remarkable for3 m2 }- Z- r9 ?' s) N
enlargement of the penis, with a stretched length of
. B* A9 x. I, a6 ~5 q8 cm and a width of 2 cm. The glans penis was very well4 Q, A  f& q" N) T
developed. The pubic hair was Tanner II, mostly around5 G" [) S: ^( ^$ ]2 Q, F4 g
540
) r+ G( r% ^2 S/ d# p- P7 O& ]: yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ N+ L1 d% B! v" h" d/ X
the base of the phallus and was dark and curled. The' g' n0 ?0 }! L* T& I# b4 O
testicular volume was prepubertal at 2 mL each.& l" e; B0 j# B$ Z% v6 n
The skin was moist and smooth and somewhat
1 D* O7 f+ @, @- \. H$ u7 toily. No axillary hair was noted. There were no
# P" y  I0 j/ J" L  u5 |4 [% c7 [abnormal skin pigmentations or café-au-lait spots./ ?. C* x! ~# I
Neurologic evaluation showed deep tendon reflex 2+' i$ {- _: F6 a( G' Q
bilateral and symmetrical. There was no suggestion- h9 l0 ^# _3 h+ J% M2 t+ D# J
of papilledema.
5 g  K  z7 ]/ aLaboratory Evaluation9 T& {" M, K* E" @- D; A
The bone age was consistent with 28 months by
, X& \: r+ n7 P2 c0 u2 Tusing the standard of Greulich and Pyle at a chrono-5 C1 l& I; s  D! w
logic age of 16 months (advanced).5 Chromosomal7 \8 ^* K# C& Z0 B
karyotype was 46XY. The thyroid function test
! S4 U9 E# \# I! X2 T  n2 Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
; W& R1 O" J+ b! f7 I2 ^+ Dlating hormone level was 1.3 µIU/mL (both normal).+ c+ w8 ]* q. ]9 k( C8 i
The concentrations of serum electrolytes, blood0 \( j( O# }( \. A& ?, s
urea nitrogen, creatinine, and calcium all were& R% f$ C8 d! M$ C
within normal range for his age. The concentration2 \. p; @' q( Q8 _) R+ `$ g
of serum 17-hydroxyprogesterone was 16 ng/dL5 l, a' C) D$ V) U
(normal, 3 to 90 ng/dL), androstenedione was 20
7 B* }$ l7 |" ^2 H0 Kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ c: n. _$ C5 N, v& w( Jterone was 38 ng/dL (normal, 50 to 760 ng/dL),
5 A# P( W5 m9 fdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
" ^8 I6 \7 m! m2 G49ng/dL), 11-desoxycortisol (specific compound S)
5 W: Z- p" A/ w& zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
# ~0 O, ]* s5 O0 q0 Utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 h0 J* L3 T$ K* g2 rtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ Y% t: z' R4 U8 k4 A
and β-human chorionic gonadotropin was less than
+ M3 a5 V: }: H0 I5 }6 E( Z5 mIU/mL (normal <5 mIU/mL). Serum follicular& j) j  y& X7 @/ Z" [  J
stimulating hormone and leuteinizing hormone
; q2 s; i/ ]. ]0 K7 `concentrations were less than 0.05 mIU/mL# _) V$ u" q" T: c4 e7 M" j$ Y; K
(prepubertal).
4 o9 e$ e+ H. ^  u9 TThe parents were notified about the laboratory- F' D: m/ |( y8 Z
results and were informed that all of the tests were$ w3 [6 C) E, s$ L" q+ a* W. X
normal except the testosterone level was high. The- B" D" S6 u0 _+ t
follow-up visit was arranged within a few weeks to4 E# m7 E* `; b" b9 ]
obtain testicular and abdominal sonograms; how-
* `) i8 S4 g# Oever, the family did not return for 4 months.: }/ o" ^+ _4 ~- K  s1 h
Physical examination at this time revealed that the3 E, Z; X( N) M5 v
child had grown 2.5 cm in 4 months and had gained7 f$ Z: \, d7 c+ Y! \
2 kg of weight. Physical examination remained+ d  G) X( w/ @
unchanged. Surprisingly, the pubic hair almost com-7 g) Y  b% q* N, u( A3 R4 ~
pletely disappeared except for a few vellous hairs at6 s  K/ I; d8 m; U7 [. t
the base of the phallus. Testicular volume was still 2
4 z% {) b$ z2 o  i' B2 K# xmL, and the size of the penis remained unchanged./ T- i& M; l" W5 l0 m
The mother also said that the boy was no longer hav-
1 {! ?) {7 A  V0 C* H4 e6 uing frequent erections.
" e" e5 l; J8 @9 ]( E7 I* TBoth parents were again questioned about use of4 N( }" W3 |# v1 }, ^: A( k/ k
any ointment/creams that they may have applied to
9 I9 t6 l6 d; M2 n  Gthe child’s skin. This time the father admitted the
8 O+ z( ]! |  _) l7 l. k$ j# ?7 XTopical Testosterone Exposure / Bhowmick et al 541
8 g7 r' q; B, W' N1 b& duse of testosterone gel twice daily that he was apply-
2 V; x/ x9 j9 A4 q; king over his own shoulders, chest, and back area for
. p! C# q' k& g* X& ?0 la year. The father also revealed he was embarrassed
) _9 a: t8 v, }3 {8 e) E1 T: o) vto disclose that he was using a testosterone gel pre-/ D/ [3 ]! |) i
scribed by his family physician for decreased libido# u7 J  c/ \( ?' Z  `- N( n; r1 \
secondary to depression.
: v5 ~7 i' t$ Q& h# \The child slept in the same bed with parents.& }& R9 Z1 k, y8 U
The father would hug the baby and hold him on his
' f0 @: h0 B& Z$ X2 schest for a considerable period of time, causing sig-
  p/ |7 G! U7 t+ [* s. Fnificant bare skin contact between baby and father.
) f5 u$ s6 |' mThe father also admitted that after the phone call,
% O, k$ w" Y' o7 v- Iwhen he learned the testosterone level in the baby( U+ L8 S3 ]: j
was high, he then read the product information+ X/ n7 G0 k+ T1 p: ~3 R; C" h
packet and concluded that it was most likely the rea-
$ r( Y: Q5 X5 d1 uson for the child’s virilization. At that time, they; O! D- m7 \( ^: P" w$ p7 ~6 l
decided to put the baby in a separate bed, and the8 Q2 [" `  w$ u/ U. b/ d
father was not hugging him with bare skin and had
! I/ |7 `1 F/ ~  ^" X2 W0 I% y$ hbeen using protective clothing. A repeat testosterone3 U  \" M' o- K
test was ordered, but the family did not go to the
" S! ^  U( G4 D0 _laboratory to obtain the test.
0 ?7 @" K  ]  N8 w5 M+ uDiscussion
0 G: t, T# c" X, [5 APrecocious puberty in boys is defined as secondary7 B3 [+ `- C2 Y9 p
sexual development before 9 years of age.1,4
+ y" U0 y8 j* TPrecocious puberty is termed as central (true) when
- D7 B3 j, d3 ^# j$ {7 e* D0 x3 _it is caused by the premature activation of hypo-+ K: x4 [& o/ D
thalamic pituitary gonadal axis. CPP is more com-3 V4 W" `% i) H3 |. L) b2 H
mon in girls than in boys.1,3 Most boys with CPP  c! ^6 `# u/ e- d% y
may have a central nervous system lesion that is5 ?# E. L: x7 T3 D, b% W" [
responsible for the early activation of the hypothal-
4 e9 z' f, v* N- Pamic pituitary gonadal axis.1-3 Thus, greater empha-
5 r0 T4 P2 T* k- @; G5 ysis has been given to neuroradiologic imaging in
/ o9 H5 n; b* ]1 L7 bboys with precocious puberty. In addition to viril-' l" {# e7 t9 I4 @* ], J9 O: s
ization, the clinical hallmark of CPP is the symmet-( g1 b! @" d% I5 L7 a' x3 t
rical testicular growth secondary to stimulation by7 c0 m8 A1 n6 @" Y0 r7 ^6 F
gonadotropins.1,3
0 [2 H! s4 T4 A( rGonadotropin-independent peripheral preco-
3 q& l3 _) O1 f" i3 Ocious puberty in boys also results from inappropriate
' d2 t; e' z. y8 B/ r' y' N5 nandrogenic stimulation from either endogenous or7 f# c2 ~8 R( U" R1 T+ B% M
exogenous sources, nonpituitary gonadotropin stim-$ m6 h) D# j% q) E* T
ulation, and rare activating mutations.3 Virilizing5 C( i5 [5 R3 ~2 h/ b/ G' `
congenital adrenal hyperplasia producing excessive
) h7 N. {, T& y: i% E  J1 v0 Tadrenal androgens is a common cause of precocious
! Y+ d( V4 B7 k: }9 f7 rpuberty in boys.3,4+ Z) `/ {- t6 n  v. Q2 ?
The most common form of congenital adrenal
1 f. c4 b' h* T! D' Z! u& thyperplasia is the 21-hydroxylase enzyme deficiency.
: e/ ^( m% T5 X  V% W/ z: IThe 11-β hydroxylase deficiency may also result in, b3 ^9 h3 V; Y0 W
excessive adrenal androgen production, and rarely,: n/ |2 B# Z; B, f, n9 g
an adrenal tumor may also cause adrenal androgen
6 t1 X1 n- y5 j1 @! t8 `2 wexcess.1,3
  z; s& z& O2 ^2 R% s8 v1 Kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. l! n! K! e. g; a1 \4 m8 x- D+ m5 s9 ^/ E
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
, A! @4 D4 n. p: a* ]A unique entity of male-limited gonadotropin-
; a1 A. C$ A- a2 `independent precocious puberty, which is also known5 m! h. w3 J  K1 q6 j  v
as testotoxicosis, may cause precocious puberty at a
) h$ l& m- b8 ~. W: m8 m3 \- hvery young age. The physical findings in these boys
# V+ [" S: d+ D# qwith this disorder are full pubertal development,
/ n0 f  E. Q& i# m8 |, ]: tincluding bilateral testicular growth, similar to boys
7 c. ~" a/ p0 e1 K6 @* W& |! G3 W# twith CPP. The gonadotropin levels in this disorder
. X+ I$ d; |& a  l; t, k% {are suppressed to prepubertal levels and do not show
" V/ b4 x$ I' [0 Vpubertal response of gonadotropin after gonadotropin-
% N$ T/ ]) n0 i  ?1 Lreleasing hormone stimulation. This is a sex-linked* S5 c$ z& D$ h8 V9 t1 M; _  ?
autosomal dominant disorder that affects only* [2 }" U" Y( N$ l
males; therefore, other male members of the family
/ W. J7 A/ L! d  A4 k  }5 S/ ]' ?may have similar precocious puberty.3
! b- b' _' Q( V  G( P5 _In our patient, physical examination was incon-6 g' t, F, R8 R- S' Z* Z9 c# p1 O
sistent with true precocious puberty since his testi-
+ N& d- D% s6 e6 D' Wcles were prepubertal in size. However, testotoxicosis
: _4 s( s$ a  V  j9 l- Swas in the differential diagnosis because his father
& k5 x) w$ F3 o$ K+ w: {+ o6 c. I1 p2 Fstarted puberty somewhat early, and occasionally,
& A. d# C" [# btesticular enlargement is not that evident in the
) ^2 s+ p' U; r; Sbeginning of this process.1 In the absence of a neg-
+ x* _/ [, C! ~, E' _ative initial history of androgen exposure, our
. I1 q" Q( M3 e- s1 I. Fbiggest concern was virilizing adrenal hyperplasia,  P+ @* M3 K$ P. C3 I! F
either 21-hydroxylase deficiency or 11-β hydroxylase- P+ A  b" s5 `1 r7 o4 A
deficiency. Those diagnoses were excluded by find-
; S* j$ C+ t( E' L  ding the normal level of adrenal steroids.
) l6 D! ?0 o( S; VThe diagnosis of exogenous androgens was strongly; C& Q3 A* H3 u. s& G
suspected in a follow-up visit after 4 months because! ?7 F3 v2 G" L/ f
the physical examination revealed the complete disap-) m' T0 p8 V  o9 k
pearance of pubic hair, normal growth velocity, and4 D9 o, v. D% q9 d0 L  |6 g' s
decreased erections. The father admitted using a testos-/ @% f, @. \5 k' c$ {
terone gel, which he concealed at first visit. He was
5 }- Y. L* V# C/ {using it rather frequently, twice a day. The Physicians’
& Y0 _+ O' ?5 R# o, cDesk Reference, or package insert of this product, gel or
: t9 z" R: P9 \$ ~6 lcream, cautions about dermal testosterone transfer to
0 t0 F" Y% p2 ^  s+ q' [( Yunprotected females through direct skin exposure.2 c' n) A8 N( K* Q1 K* q
Serum testosterone level was found to be 2 times the. k! G' B; u) }& K8 Z  ?
baseline value in those females who were exposed to
% {: p+ I1 w  t7 f( s& \9 Aeven 15 minutes of direct skin contact with their male4 e3 I& X' S0 ~+ s
partners.6 However, when a shirt covered the applica-# O4 l9 D: S5 V+ [9 t" Z+ l' C
tion site, this testosterone transfer was prevented.
! u7 B6 ^( Z* o( v% wOur patient’s testosterone level was 60 ng/mL,+ t" u7 B% M4 _* N
which was clearly high. Some studies suggest that
$ F7 N' B; ?, o3 R' J% Ydermal conversion of testosterone to dihydrotestos-
% v0 D- w  f8 Sterone, which is a more potent metabolite, is more
. e( G' f) L$ R& K/ C6 Iactive in young children exposed to testosterone
8 Z" R4 R8 A+ Q2 I0 i) F0 f/ xexogenously7; however, we did not measure a dihy-% i# Q3 u# d9 j( \! c% I3 V
drotestosterone level in our patient. In addition to
! y/ \8 {' D- qvirilization, exposure to exogenous testosterone in' S% ]! j' H: c: ]+ b  E& z( t
children results in an increase in growth velocity and
3 O4 s9 G$ R+ i* Q5 j, b1 J2 wadvanced bone age, as seen in our patient.0 e) [0 g8 {) t  C* I$ ^& ]
The long-term effect of androgen exposure during/ G- _& ]6 C0 w" ~
early childhood on pubertal development and final- }1 f" m) N1 C6 S6 `1 S
adult height are not fully known and always remain
0 |) t/ K/ S3 V7 Ya concern. Children treated with short-term testos-2 S6 u' V3 {- T/ H( Q# t0 a* L# n$ w
terone injection or topical androgen may exhibit some
  D' l" ]9 A9 a! A; b4 Jacceleration of the skeletal maturation; however, after
# n2 G" B1 Q3 C& k6 L! D6 n& Ucessation of treatment, the rate of bone maturation
/ o1 A0 P/ A" r. wdecelerates and gradually returns to normal.8,9
8 D6 w. u# j8 }( I+ pThere are conflicting reports and controversy, t; l% ~# q! @+ o8 S6 {  |2 j
over the effect of early androgen exposure on adult1 S1 f! v  C0 }2 n# T( `
penile length.10,11 Some reports suggest subnormal
2 a; [: b9 ?" C$ A7 n& |adult penile length, apparently because of downreg-
) ^9 `4 d4 J' c* Y( L" vulation of androgen receptor number.10,12 However,
& ]4 J) x+ v0 a6 eSutherland et al13 did not find a correlation between
) C* E7 V( k$ r& b2 _' ]& {childhood testosterone exposure and reduced adult
; u" s3 |7 h, K6 ]  d; hpenile length in clinical studies.
" m! o$ a& j1 x) d4 NNonetheless, we do not believe our patient is
, B: b: V5 G/ Mgoing to experience any of the untoward effects from1 \$ T% d! ]3 J$ D
testosterone exposure as mentioned earlier because' ^1 f. S# l6 [" V
the exposure was not for a prolonged period of time.+ t# K5 |/ b, e9 n
Although the bone age was advanced at the time of- X; o3 X( H( A' ~% p
diagnosis, the child had a normal growth velocity at+ J" I$ r. e- _) o
the follow-up visit. It is hoped that his final adult
- D1 m2 o8 F6 U) Z8 wheight will not be affected., e) l$ v5 x" x% q4 P* L
Although rarely reported, the widespread avail-8 R, R& [% r3 o& B% \* ?4 E( m
ability of androgen products in our society may! ^8 C# p5 B' _; U5 u
indeed cause more virilization in male or female
2 R' x; C' x$ p5 u. d" [children than one would realize. Exposure to andro-
0 j) B1 F7 l+ }: h) `6 ~( Cgen products must be considered and specific ques-
( {8 A- h: u! H2 |$ Dtioning about the use of a testosterone product or7 P8 O# K" D, N
gel should be asked of the family members during: ?7 B: l; g8 U  b" t5 i
the evaluation of any children who present with vir-% |6 l( [9 A# r7 O0 Z
ilization or peripheral precocious puberty. The diag-
+ Q/ x. \0 j! H  Y1 |. Qnosis can be established by just a few tests and by
8 x9 U/ N0 Z, m5 Q% fappropriate history. The inability to obtain such a
  O; Z; [' R9 y# shistory, or failure to ask the specific questions, may
6 R4 O3 Q$ g5 M0 m+ eresult in extensive, unnecessary, and expensive" m4 N! }% h5 g8 V0 S+ R
investigation. The primary care physician should be
. b+ W8 E0 z9 p; ?' `: {aware of this fact, because most of these children
* ^( A- g+ B2 Y9 X# Bmay initially present in their practice. The Physicians’. J. d! f# {8 d, o4 c" I  Q5 P! f
Desk Reference and package insert should also put a9 |3 l6 e$ m! J% O& x3 m4 d
warning about the virilizing effect on a male or
4 O$ S! \8 B6 v) O- |7 Rfemale child who might come in contact with some-6 X% ]/ t) u) f* h$ b# q
one using any of these products.
  x8 g: c1 ]' `; L3 cReferences% B$ ^3 D. c7 Y5 [
1. Styne DM. The testes: disorder of sexual differentiation
9 s& r/ g0 R# ?and puberty in the male. In: Sperling MA, ed. Pediatric  v, ?, t9 a1 S# z) z
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- T2 {" Z) r7 B4 Q
2002: 565-628.
9 S& n* H% d+ M* J4 V0 X- W2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 O: W# }4 v4 N/ S8 Y; h) Opuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old2 K% J" G8 G! K0 G" V( R
Boy Induced by Indirect Topical8 g/ s6 W. P" Z. r% r
Exposure to Testosterone; A) q1 J/ |# o( }) Y
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* o) \2 U# F7 {4 W7 a1 }
and Kenneth R. Rettig, MD10 i, R+ \; u: E2 }
Clinical Pediatrics  s6 d0 `# {8 k8 l& {
Volume 46 Number 61 q4 P7 M! @" ]+ f
July 2007 540-5437 c  C# S: X% L6 m! @9 H  b
© 2007 Sage Publications+ C% [. F3 ?8 l( v
10.1177/0009922806296651$ c) _& G5 n5 V1 N: Q
http://clp.sagepub.com0 o6 p) j3 F( k+ E5 @
hosted at/ M9 `$ ]& g) X- e6 l
http://online.sagepub.com% ]9 k- C( e8 b/ q7 A: ^
Precocious puberty in boys, central or peripheral,
  p! H4 f  Q- U1 T* lis a significant concern for physicians. Central
/ g; P2 q+ S1 j" gprecocious puberty (CPP), which is mediated
  N+ [8 [. b, p; ~+ rthrough the hypothalamic pituitary gonadal axis, has
: s; e0 S* b2 L, N* O$ Fa higher incidence of organic central nervous system6 T' ^  m" a" T7 G; M
lesions in boys.1,2 Virilization in boys, as manifested
0 _8 `6 Z. ?" tby enlargement of the penis, development of pubic# `' C, _) Y' J( _
hair, and facial acne without enlargement of testi-
* g/ ~0 T* W7 q- U  ?8 rcles, suggests peripheral or pseudopuberty.1-3 We
) x( L& }( }$ \/ h) Sreport a 16-month-old boy who presented with the: C  ~+ Z% Y$ h/ L9 p0 c' G
enlargement of the phallus and pubic hair develop-1 E$ t1 f' z4 r4 k$ c, y, {  Q, U! @
ment without testicular enlargement, which was due4 M% i' Z$ a3 E0 S
to the unintentional exposure to androgen gel used by
' D# B  N, k" ?, k! O/ H* u, zthe father. The family initially concealed this infor-
; e4 q9 p% U5 w2 g7 H- m: tmation, resulting in an extensive work-up for this* t* D$ X7 |3 P3 p4 B
child. Given the widespread and easy availability of- P  m, F' \+ P; l! N6 ~
testosterone gel and cream, we believe this is proba-6 ~9 p; U; i. V2 c5 S5 L
bly more common than the rare case report in the
; U( k+ @0 b" Pliterature.4; [8 D8 a. D2 s
Patient Report
( t: ^1 e9 Q" z& s, U2 SA 16-month-old white child was referred to the, c, o4 }" O( Y) c7 A5 _$ v
endocrine clinic by his pediatrician with the concern
1 d8 ^( n8 |9 T( S: d/ S: Cof early sexual development. His mother noticed
$ ?" H5 K+ }- H8 R9 o8 ulight colored pubic hair development when he was/ v5 h. j0 J' P% R7 z
From the 1Division of Pediatric Endocrinology, 2University of  F, x- U; N5 r, I3 f3 S
South Alabama Medical Center, Mobile, Alabama.
( ?6 y$ S! ]/ tAddress correspondence to: Samar K. Bhowmick, MD, FACE,8 u$ _! L" Z% R8 ~' l
Professor of Pediatrics, University of South Alabama, College of
) K. q5 U8 H4 d1 FMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
( {. n3 k( H0 \! X& C6 e6 Ke-mail: [email protected].
% M- ]; Z" V; g* I8 j" U& cabout 6 to 7 months old, which progressively became" Q3 j  x$ `3 }4 s. Z
darker. She was also concerned about the enlarge-
5 T; [: O  {/ e0 h% Kment of his penis and frequent erections. The child
( d( a6 ]( @/ w2 nwas the product of a full-term normal delivery, with  S* D- a  k. [0 V3 A( x) Q
a birth weight of 7 lb 14 oz, and birth length of
, _# |7 s9 u6 ^20 inches. He was breast-fed throughout the first year& t! {  r" N+ i/ a
of life and was still receiving breast milk along with
: ]+ _) z  U- v8 w# Q1 F3 ssolid food. He had no hospitalizations or surgery,
# t5 N0 H, K! a3 f9 {and his psychosocial and psychomotor development
" V+ M0 F1 v3 ?! x' I5 Rwas age appropriate.8 V' X/ S: |4 p
The family history was remarkable for the father,* v; o' R7 N! A* F1 p1 u7 W
who was diagnosed with hypothyroidism at age 16,7 Q  t4 a3 m) p
which was treated with thyroxine. The father’s- N& p6 M& |1 S! k. }9 \
height was 6 feet, and he went through a somewhat3 w7 o; i" D1 T& I) S, v
early puberty and had stopped growing by age 14.
, E* V" E* q# h# _# q# }- E) HThe father denied taking any other medication. The9 q8 F+ S( w# N, V4 K; K
child’s mother was in good health. Her menarche# j& v" g& l0 _" W9 o+ [5 r  Y+ I
was at 11 years of age, and her height was at 5 feet
8 R2 ~) ^! A* [5 inches. There was no other family history of pre-5 a0 C. y. u" v, v
cocious sexual development in the first-degree rela-
9 V: {2 H; j% ltives. There were no siblings.
! u5 n/ b" b! \6 K- ~Physical Examination* H$ v! i5 d" ^. L1 J# M5 ]& k
The physical examination revealed a very active,2 y/ x+ A+ ~3 B: c: i2 s$ r- [  o
playful, and healthy boy. The vital signs documented
) Z, Q# L* |8 o# `+ ~$ f' c& ca blood pressure of 85/50 mm Hg, his length was  W7 q0 [0 G0 b+ I
90 cm (>97th percentile), and his weight was 14.4 kg# J6 U* f* h3 t9 j. G
(also >97th percentile). The observed yearly growth. a' D) w# Z* ^  d+ a4 I9 J+ U5 U
velocity was 30 cm (12 inches). The examination of
! K$ z) F, l) H! nthe neck revealed no thyroid enlargement.+ j4 i" O+ Z0 y6 S0 }; H
The genitourinary examination was remarkable for0 ]: q' ?2 K7 w2 {8 J' q4 T
enlargement of the penis, with a stretched length of0 \1 K. U( f" r8 K' X7 n
8 cm and a width of 2 cm. The glans penis was very well4 s2 q4 T! S& O. z
developed. The pubic hair was Tanner II, mostly around
9 ]3 |9 c2 f' `8 M* f; j540! i4 i1 E' X2 l! G3 L
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 E' s- ~$ K& l* \( F/ _% h: w: t
the base of the phallus and was dark and curled. The
, W, ~8 f$ ^- B  \) O. V/ ?! M& f9 X/ gtesticular volume was prepubertal at 2 mL each.
! y% B7 A' |+ S: q8 @The skin was moist and smooth and somewhat
+ U; \# T) Y4 y' w$ t! aoily. No axillary hair was noted. There were no; X, ]5 f9 I9 }8 |
abnormal skin pigmentations or café-au-lait spots.5 M: p' @: ^# j( b
Neurologic evaluation showed deep tendon reflex 2+2 _$ Z: t8 i0 r% n/ X6 V
bilateral and symmetrical. There was no suggestion
( c4 S3 w. O1 A7 w6 ]0 k, Nof papilledema.
4 F- F# x- d2 }% q; aLaboratory Evaluation4 k! _# `" e, [& p; ^; C3 |
The bone age was consistent with 28 months by
0 Z& _( F4 n# I7 Qusing the standard of Greulich and Pyle at a chrono-' g; s7 i6 C' o
logic age of 16 months (advanced).5 Chromosomal
' s% H/ a% Y* B: s7 Z  {karyotype was 46XY. The thyroid function test6 e( X7 o9 ]# n5 L- ~
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 B( M7 m. U0 n* b" wlating hormone level was 1.3 µIU/mL (both normal).
: _* v1 z6 c8 E1 X3 U; g# {The concentrations of serum electrolytes, blood
7 G% O& M8 j' s  V2 Surea nitrogen, creatinine, and calcium all were
/ G4 J1 q1 p$ c) f/ q, W0 ]! cwithin normal range for his age. The concentration+ P' T! ?( D) T- |* z
of serum 17-hydroxyprogesterone was 16 ng/dL
3 `) s; z( s" {(normal, 3 to 90 ng/dL), androstenedione was 20
+ u, T3 y6 B' P* Dng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-. ^% e( s+ w! c) @% J5 }+ W4 l
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 ]: y* ]+ V; ^! F( [" Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 V- I; y0 ~3 Y' l" o49ng/dL), 11-desoxycortisol (specific compound S)& A- i7 e) S( u* v* G; @' V
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 ?, N/ Z! ?8 d( V, B; y) r2 X& etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. n4 o# c" g  t2 N3 N. G4 q  U
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& f( f* D( r+ W' b( U+ Xand β-human chorionic gonadotropin was less than
# U, ?2 I) {: i: j" g5 mIU/mL (normal <5 mIU/mL). Serum follicular
+ Q9 N1 F- ]( Dstimulating hormone and leuteinizing hormone, `& g* {. V9 T5 g* x2 M0 U
concentrations were less than 0.05 mIU/mL
4 x- v3 |, u  d8 j5 M$ D- ](prepubertal).
0 l" }" m# e0 L4 G# k" d+ pThe parents were notified about the laboratory  ?9 H5 _' x" t
results and were informed that all of the tests were
* r2 r6 Q  w3 V& s( J2 T' cnormal except the testosterone level was high. The. D4 l6 ^( r1 h0 ^( {
follow-up visit was arranged within a few weeks to
6 E$ j& o- E- q6 mobtain testicular and abdominal sonograms; how-! b2 H2 p: O, C) H3 x
ever, the family did not return for 4 months.* H7 n$ }: _4 C* [) ^5 v, @6 f. n6 |
Physical examination at this time revealed that the4 M& l* l/ r4 D6 q8 }% d9 z1 Z7 L
child had grown 2.5 cm in 4 months and had gained1 g$ O6 e+ Q8 S; K8 D# O
2 kg of weight. Physical examination remained
) P. A: i4 ^6 |0 C0 ]% sunchanged. Surprisingly, the pubic hair almost com-" X: T2 M4 L# X' L
pletely disappeared except for a few vellous hairs at/ Q+ S% P* b( Q5 M( l+ k& [! R6 H5 n
the base of the phallus. Testicular volume was still 2
0 X, k7 {, O9 O3 d* lmL, and the size of the penis remained unchanged.
  C2 A  [) n5 FThe mother also said that the boy was no longer hav-
+ k! X! d' R  c& b! |- ning frequent erections.3 g1 l# q+ R* o8 A9 |
Both parents were again questioned about use of  N5 a+ A5 p" ^* V0 ^' C; t
any ointment/creams that they may have applied to' N2 Q/ Z/ L& k4 e4 s
the child’s skin. This time the father admitted the
1 }; Y9 b, X( H& xTopical Testosterone Exposure / Bhowmick et al 541
4 }; {" }% B' S/ I$ Juse of testosterone gel twice daily that he was apply-
: q  P$ a. ^( A( ^' s1 |. iing over his own shoulders, chest, and back area for* d' |5 l6 [, Y
a year. The father also revealed he was embarrassed
! a  y* p0 b9 p; _. Y' Zto disclose that he was using a testosterone gel pre-
; E. ]2 ?* j* O) l% a$ i  n# \( g% ?scribed by his family physician for decreased libido
, J8 Q4 \9 {& h$ ]: x6 Osecondary to depression.: Q) e) i  K2 y+ T
The child slept in the same bed with parents.
% l; N$ [/ n! s0 F% bThe father would hug the baby and hold him on his6 ^  j$ \/ g/ v, f- o
chest for a considerable period of time, causing sig-
7 a+ E3 i  {7 [9 Anificant bare skin contact between baby and father.
6 u: r8 e3 X& q1 O5 P' oThe father also admitted that after the phone call,0 M5 D: v4 _8 I8 g) W0 `" |
when he learned the testosterone level in the baby: E4 _) x2 b. P/ b: k" @
was high, he then read the product information2 c* {& ?( V. W# ^/ g. S1 [7 A- z
packet and concluded that it was most likely the rea-
4 z; y, O$ M6 b7 c+ f7 lson for the child’s virilization. At that time, they
- P& j' b1 f* Q4 Q  Edecided to put the baby in a separate bed, and the
6 J& S+ D& v, `father was not hugging him with bare skin and had
8 e; S' A' {  _$ {, {( f) f( Ibeen using protective clothing. A repeat testosterone1 X, ~' ?( z" d
test was ordered, but the family did not go to the1 @# M6 s8 j' u, U, F# X  ~
laboratory to obtain the test.) E7 ^% @. L4 u( x2 @6 D  r' U
Discussion! F& E8 h, t9 ^8 J
Precocious puberty in boys is defined as secondary# Y5 J& y; s1 F$ w. l5 A6 i
sexual development before 9 years of age.1,4) w9 v% ~3 y3 P7 W
Precocious puberty is termed as central (true) when
( `, C; x7 {2 A7 u! H+ i# {it is caused by the premature activation of hypo-
5 C- [8 g5 s: [- q; Pthalamic pituitary gonadal axis. CPP is more com-
2 p' n7 X9 ^" Z# Umon in girls than in boys.1,3 Most boys with CPP  |8 n4 u# d# z: I& z/ S* M
may have a central nervous system lesion that is
9 T, s: g% k8 S) ^* ^! R9 wresponsible for the early activation of the hypothal-  l' \7 ^7 Q( V3 d
amic pituitary gonadal axis.1-3 Thus, greater empha-% n, ]% g+ k: [4 j
sis has been given to neuroradiologic imaging in
) t5 k! A9 n( k6 _4 f2 C; Jboys with precocious puberty. In addition to viril-
5 s- [$ e+ n# }4 m' Y# v' o5 k! Lization, the clinical hallmark of CPP is the symmet-
+ K; @8 U2 e& c% b. R, P, m+ Y% Prical testicular growth secondary to stimulation by
. W, T2 D+ y# R3 P' l: R6 Rgonadotropins.1,30 C- O- T5 z  T/ ]( t( e
Gonadotropin-independent peripheral preco-7 P) |1 M" \) r8 ]- F" x2 {  G/ A
cious puberty in boys also results from inappropriate0 l0 T' A  ^( ~
androgenic stimulation from either endogenous or! G0 q6 L3 y5 y* y
exogenous sources, nonpituitary gonadotropin stim-
4 p% \4 T9 I$ `) L5 M# Vulation, and rare activating mutations.3 Virilizing: b  T; H6 S% d! g4 e
congenital adrenal hyperplasia producing excessive
; m* n  O: i+ @2 V& dadrenal androgens is a common cause of precocious, J. K1 X1 O% S1 ~/ f+ q8 H) b3 C
puberty in boys.3,4- A7 Y. F+ x6 {% D* h1 V
The most common form of congenital adrenal% [& n0 }3 o$ L" l0 b
hyperplasia is the 21-hydroxylase enzyme deficiency.
5 K, `* m# x2 t4 rThe 11-β hydroxylase deficiency may also result in
/ Q; ?+ h7 L/ b9 jexcessive adrenal androgen production, and rarely,
$ L4 P& F% I& H# ]an adrenal tumor may also cause adrenal androgen6 C3 K/ w0 t! D$ l; z+ ]& x
excess.1,3
5 n6 D5 z3 x" _( p/ ~at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% Z7 l7 y' k6 g& K. i1 M542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& ^6 r# r, B  p$ j: ~" c3 bA unique entity of male-limited gonadotropin-0 H$ c1 @/ [0 m& h
independent precocious puberty, which is also known6 n$ @# c! W* M& V5 v+ E# U
as testotoxicosis, may cause precocious puberty at a/ e# w/ k# R  g1 y3 @* d# ?  _
very young age. The physical findings in these boys
/ R' c) [0 J% ^with this disorder are full pubertal development,
- y+ f" F  _/ |* t& E! Mincluding bilateral testicular growth, similar to boys
' o/ |) C/ t8 a% \, |$ @( Bwith CPP. The gonadotropin levels in this disorder
: J& y: e4 B9 x3 ware suppressed to prepubertal levels and do not show
! g) P& Q$ i2 f- ]- H- Hpubertal response of gonadotropin after gonadotropin-- e4 Y% w) Q% z! F4 `. F  B
releasing hormone stimulation. This is a sex-linked
+ a6 V( L4 x9 t; nautosomal dominant disorder that affects only
9 b' ~* @* F" f2 Tmales; therefore, other male members of the family
0 X& D4 ?' E' n  z" Fmay have similar precocious puberty.3
3 Y  z- J0 i0 F) |7 n: S1 A( i) TIn our patient, physical examination was incon-. g* C& d. x* X/ @1 g/ u5 s# A- o
sistent with true precocious puberty since his testi-0 k+ e1 _# Y, C$ v8 Y
cles were prepubertal in size. However, testotoxicosis
; @5 m3 E- H9 Swas in the differential diagnosis because his father
, |  |* {' b; W5 L" N0 }$ a: Ystarted puberty somewhat early, and occasionally,6 V) K# Q1 Y$ E6 c
testicular enlargement is not that evident in the. {. V9 U: a0 w( @' d
beginning of this process.1 In the absence of a neg-
& @& c$ n( `6 Native initial history of androgen exposure, our- s+ ?% H$ j( X; \2 ]+ H
biggest concern was virilizing adrenal hyperplasia,
; p4 b+ Z: ^* O" \6 S% @# }either 21-hydroxylase deficiency or 11-β hydroxylase
8 _* P4 F( q' j* wdeficiency. Those diagnoses were excluded by find-
  e* H% u" U) v7 @0 Ning the normal level of adrenal steroids.
! T/ c+ L3 q' ?' [. V# I/ R" UThe diagnosis of exogenous androgens was strongly
3 ]! d$ \; W# z, jsuspected in a follow-up visit after 4 months because
# M  `) F- o2 A8 u2 H- z6 z2 zthe physical examination revealed the complete disap-
# r- [5 {6 f( S6 b5 v$ D$ Vpearance of pubic hair, normal growth velocity, and) }) M. F/ \1 W  B
decreased erections. The father admitted using a testos-
$ X( X* K! F; o; Aterone gel, which he concealed at first visit. He was
- n4 O0 s5 ~( f6 Jusing it rather frequently, twice a day. The Physicians’4 e& a' ]) @% ?' N8 a
Desk Reference, or package insert of this product, gel or
9 i* M  n* t* P( ?& ucream, cautions about dermal testosterone transfer to
* @# k$ E( c) k: g9 i# K1 Xunprotected females through direct skin exposure.
/ O" B: ~7 m" R2 X$ Z2 N, B4 e" wSerum testosterone level was found to be 2 times the1 M+ R2 S, x8 `# f
baseline value in those females who were exposed to: _9 E( ~, F# A5 y9 r; g
even 15 minutes of direct skin contact with their male- f. @( w1 m# l9 S3 u
partners.6 However, when a shirt covered the applica-
' ?7 R! L8 J8 }" M+ u, P. F9 ction site, this testosterone transfer was prevented.
! G# v, h' H* u* L* ?$ r: B" h4 HOur patient’s testosterone level was 60 ng/mL,+ I1 p# q0 a% R  d% ]
which was clearly high. Some studies suggest that& H7 ~* f: v6 l! X
dermal conversion of testosterone to dihydrotestos-1 W5 ?  U/ o2 Q/ `! o
terone, which is a more potent metabolite, is more. m* A( _- e/ M2 e8 q6 D) M
active in young children exposed to testosterone
% t: l4 d8 v! I$ j; p/ Aexogenously7; however, we did not measure a dihy-
( M. C' i/ r& N5 {1 _7 a5 I# Kdrotestosterone level in our patient. In addition to* F1 n0 |; _' j
virilization, exposure to exogenous testosterone in
* B: a+ [* i* \  d% Dchildren results in an increase in growth velocity and  O4 b5 f0 F/ I; L+ F1 u
advanced bone age, as seen in our patient.
0 T6 G( V+ j4 ]The long-term effect of androgen exposure during
" W/ h' ^' J- X! `early childhood on pubertal development and final
3 R0 |6 u" W% Z/ W' }; ]! `& radult height are not fully known and always remain' J& n5 ?1 Z0 v( i) m
a concern. Children treated with short-term testos-6 e0 f3 }" v0 B8 ?. i( e# T
terone injection or topical androgen may exhibit some
- K4 s+ I' D% D% m- j, C6 f: Kacceleration of the skeletal maturation; however, after
7 L7 V* ]7 t2 p7 F+ Qcessation of treatment, the rate of bone maturation. |9 ]! N9 h$ W" F
decelerates and gradually returns to normal.8,9
& I* v- d- `) XThere are conflicting reports and controversy
+ a+ d: ~( ^  A! tover the effect of early androgen exposure on adult
5 N! V7 e* \4 t6 J6 ?/ wpenile length.10,11 Some reports suggest subnormal
3 f0 B, p; b4 }* F, g1 Radult penile length, apparently because of downreg-
  b% ]: I& C7 b! M9 F! N: mulation of androgen receptor number.10,12 However,  \/ Z. P( k2 y/ v; v
Sutherland et al13 did not find a correlation between
4 W; P0 J8 K& v) F2 }$ ^+ m3 `childhood testosterone exposure and reduced adult- p( v( C/ J* O; N: D( S
penile length in clinical studies.
- j1 ^, P4 r. H, z- a% y. l1 XNonetheless, we do not believe our patient is
* \0 S9 e1 H, F* A; \- m+ Ugoing to experience any of the untoward effects from! E: |" @8 Y% U4 S, z1 F
testosterone exposure as mentioned earlier because
4 G* d. l6 t# y% a* A/ @the exposure was not for a prolonged period of time.6 p: K% X/ c, ]( \: r! j7 w
Although the bone age was advanced at the time of
2 g4 ^5 z8 V: T: Ddiagnosis, the child had a normal growth velocity at
) x( s4 B" u0 X  X& g& P9 ]' D: Hthe follow-up visit. It is hoped that his final adult0 \; w7 d/ G  d, q0 H
height will not be affected.
! T) ]2 a, V) E0 C4 d/ V; `Although rarely reported, the widespread avail-1 ~  w$ g! a2 @9 Z
ability of androgen products in our society may5 p8 z- m# X1 t
indeed cause more virilization in male or female
" Z  j' A+ Y3 u, qchildren than one would realize. Exposure to andro-
$ r; U1 p. h( D: ~0 i% J5 _gen products must be considered and specific ques-
" T3 }- W5 i3 Z& Htioning about the use of a testosterone product or
. o* m7 M% I- z. `+ j) O3 v" ugel should be asked of the family members during
# j0 n# i9 ]  _! s3 X& o$ [the evaluation of any children who present with vir-
8 G8 q0 ~, O" ], e, Q1 {ilization or peripheral precocious puberty. The diag-
, D$ K% E6 o' unosis can be established by just a few tests and by
/ b, c0 `. [# m- J( w& Iappropriate history. The inability to obtain such a1 I( u" c, G; |7 d& Q/ W! p' U
history, or failure to ask the specific questions, may
8 @" d* \& w3 z6 B2 qresult in extensive, unnecessary, and expensive
- F/ E6 \9 m" |/ H( Winvestigation. The primary care physician should be) t; y; P2 t. d. O9 W+ c
aware of this fact, because most of these children: m# P( S/ d) l4 {4 L
may initially present in their practice. The Physicians’3 N' b" f2 d7 ^. F8 \3 i- u
Desk Reference and package insert should also put a4 e7 y5 A- R! o' }# f7 X
warning about the virilizing effect on a male or! {: n$ A7 ~5 }
female child who might come in contact with some-
! z6 |9 u3 i3 H. o% L! vone using any of these products.+ X8 ^) U! }* q) H
References
* ~5 q5 G7 k# T: \9 l$ {0 m( s1. Styne DM. The testes: disorder of sexual differentiation7 L$ f9 E) p& ^$ C  m
and puberty in the male. In: Sperling MA, ed. Pediatric
6 c2 [0 b/ f1 ?8 PEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;+ h* v1 h# S) D
2002: 565-628.
" F' u" T) z. O2 m2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
0 J! r5 }, y/ }puberty in children with tumours of the suprasellar pineal
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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!
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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
. ~1 F- i/ W4 _
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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