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鄉下的妹子太便宜,一次四個都要了[12P]

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Sexual Precocity in a 16-Month-Old% {+ a; p8 V" j- D/ z: U
Boy Induced by Indirect Topical
) K* T3 e6 X, Q4 FExposure to Testosterone
5 }0 P; }0 V" Q9 f8 j& H8 `3 i' `2 lSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
# N8 M8 R6 ?+ u/ _  c4 rand Kenneth R. Rettig, MD1
. _# B4 O/ ^! ]+ {+ {. A2 B% [: kClinical Pediatrics
$ m8 F0 q9 j, \% C! s5 a9 J+ u) uVolume 46 Number 65 L, `. B$ [$ v8 m
July 2007 540-543
2 O3 Z, w5 Q6 K0 ~& W  X' O! i1 }© 2007 Sage Publications7 A. R0 @; D) ?! `" L  Z6 {
10.1177/0009922806296651
# L; w* ]+ a' W- h4 Bhttp://clp.sagepub.com
, _9 Q% v3 K% ?* ?- t% ihosted at0 G8 ]- G9 m# v; s% b
http://online.sagepub.com
/ M3 e' X5 K! Y- f; x1 ~& t9 [Precocious puberty in boys, central or peripheral,; t2 B" |* i) S
is a significant concern for physicians. Central
7 A; N& s7 f; ~$ gprecocious puberty (CPP), which is mediated
) o7 ~$ t% a7 [- k3 U3 W$ d7 ~through the hypothalamic pituitary gonadal axis, has$ L2 X; g1 {, S
a higher incidence of organic central nervous system
& L0 D9 ]' I3 plesions in boys.1,2 Virilization in boys, as manifested/ a3 u. O9 X# N" t2 ~5 L; b$ ?) ~
by enlargement of the penis, development of pubic
! T1 S0 U* W# rhair, and facial acne without enlargement of testi-4 I2 n) B- }, c; V
cles, suggests peripheral or pseudopuberty.1-3 We
  a: p; L3 ?9 @0 ]+ d% |, treport a 16-month-old boy who presented with the
2 v/ I0 W. o; J1 ]' m% e3 menlargement of the phallus and pubic hair develop-! b; I. C; _6 S* `2 r
ment without testicular enlargement, which was due$ }' }; G( Q/ o' i/ g/ S" z7 L! B
to the unintentional exposure to androgen gel used by2 j5 h5 b; ?, D8 f3 `2 y. S3 L5 h
the father. The family initially concealed this infor-
1 x, ]( a6 o' a9 t/ t& }( b9 ?mation, resulting in an extensive work-up for this1 X. N6 m9 |  H' V. f4 X4 l
child. Given the widespread and easy availability of, P7 E5 q5 d: `* u
testosterone gel and cream, we believe this is proba-, C5 y1 Y& e1 z) a  V- t# @
bly more common than the rare case report in the; V' p$ [; J% {8 I$ V; p6 o1 `
literature.4
, W9 b, j* g5 ~$ j7 |Patient Report; _7 T% l  g) ^/ j! b) N7 |
A 16-month-old white child was referred to the
1 G& d/ k& q( tendocrine clinic by his pediatrician with the concern
# `. S. V& U! U5 Gof early sexual development. His mother noticed) i" Q- X- {5 @( [: X0 _
light colored pubic hair development when he was; N3 @' c# i" n: t. f  c
From the 1Division of Pediatric Endocrinology, 2University of/ q" g4 {, J6 d7 Y
South Alabama Medical Center, Mobile, Alabama.& t! H4 {9 N" A. T! I7 j. z% U
Address correspondence to: Samar K. Bhowmick, MD, FACE,. U; n" t0 U8 t# i/ w
Professor of Pediatrics, University of South Alabama, College of
: w$ m2 X5 ~' c  q: |! m- t" y" LMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;) _! o( q7 W5 |* M- z5 S0 p
e-mail: [email protected].
) s8 i+ D- m5 j1 ~+ aabout 6 to 7 months old, which progressively became
* W7 e+ F4 a& f: [  d# z5 E8 Ndarker. She was also concerned about the enlarge-3 t6 l) e4 ]# Q! a* O% `
ment of his penis and frequent erections. The child
$ e8 F& k5 P5 p3 w. I  d" r+ _was the product of a full-term normal delivery, with
1 E, \: H* ]1 \% [$ J: S9 B, W. @a birth weight of 7 lb 14 oz, and birth length of4 G5 [$ z5 J6 f, T; c! A
20 inches. He was breast-fed throughout the first year
% N$ i/ u. V0 i) D4 }3 D- Lof life and was still receiving breast milk along with1 |& }5 ?% A5 }
solid food. He had no hospitalizations or surgery,: U( Q$ O( \2 o/ `; ^
and his psychosocial and psychomotor development
7 V$ z" f. t' p0 Twas age appropriate.0 y, s" T" e, p% H5 `- l/ d
The family history was remarkable for the father,2 a; W% q: h4 f6 z
who was diagnosed with hypothyroidism at age 16,9 k8 M9 R4 P. [: E7 M
which was treated with thyroxine. The father’s/ w# C) \( ]7 t
height was 6 feet, and he went through a somewhat
0 ]- B1 u6 e- F$ m* Tearly puberty and had stopped growing by age 14.
0 C4 n% Z$ ~+ R( W1 D3 QThe father denied taking any other medication. The
5 g& ^' L$ J5 Bchild’s mother was in good health. Her menarche8 z6 Y* ?! G/ l/ O- ?' h
was at 11 years of age, and her height was at 5 feet; @0 w) Y' f/ c/ c0 g& v9 h
5 inches. There was no other family history of pre-
1 `! m8 u5 W$ X( s, V5 j+ N* }; rcocious sexual development in the first-degree rela-
7 C6 t! R8 |! ]$ L5 [tives. There were no siblings.
% X7 ?: v9 Y2 I. N3 [3 z8 UPhysical Examination5 `) B  \2 B8 e3 A
The physical examination revealed a very active,
/ X: ^6 n3 d/ r$ w1 ]( Bplayful, and healthy boy. The vital signs documented
6 T& d' U3 ^% q6 f! S& Y1 Y& ^. o! [a blood pressure of 85/50 mm Hg, his length was8 K- ?) O8 T- V# u$ s, G
90 cm (>97th percentile), and his weight was 14.4 kg/ @# r) z0 R5 B, t* f% m& P8 H8 t: e
(also >97th percentile). The observed yearly growth
! [; r: w; D4 Y0 @2 kvelocity was 30 cm (12 inches). The examination of
2 E! n8 k+ o* `  G) t* tthe neck revealed no thyroid enlargement.
0 E$ q. j* g4 d0 ^, nThe genitourinary examination was remarkable for
' I5 A; V* n. |  ~; Cenlargement of the penis, with a stretched length of& @+ N( N" f' M* g" r$ Z2 O( Z" O9 x
8 cm and a width of 2 cm. The glans penis was very well& C* I4 }  i1 F, x! m" v
developed. The pubic hair was Tanner II, mostly around
  T5 S! j0 x& i5 {) G540. ?* L2 u2 G) f# Q$ f( ]5 e
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, s# y: h" S! g  Q; U& _' ?& hthe base of the phallus and was dark and curled. The# M  w  l8 ^4 E6 w
testicular volume was prepubertal at 2 mL each.6 l/ l9 F! }9 Q7 J* n
The skin was moist and smooth and somewhat
# e! b; J' R7 Koily. No axillary hair was noted. There were no
* }4 t6 Z, n  r, [6 F/ A3 xabnormal skin pigmentations or café-au-lait spots.) ]# j" D6 n0 H9 M
Neurologic evaluation showed deep tendon reflex 2+
+ {, v4 ~7 q7 n" \( O5 Wbilateral and symmetrical. There was no suggestion
0 y3 g6 L; j$ U# L/ uof papilledema.
! W, H1 _) s- W. |  [( g5 nLaboratory Evaluation# u0 t. M  P; f
The bone age was consistent with 28 months by
; q, {1 ]4 r$ n/ Z, g) O! o* l2 busing the standard of Greulich and Pyle at a chrono-
* _+ k4 v. c+ l1 t8 O* Flogic age of 16 months (advanced).5 Chromosomal( u# D& n2 I/ ]% _$ ?5 M
karyotype was 46XY. The thyroid function test5 E0 v" N6 k. E
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 @7 R& M1 r4 z$ w, l4 ^2 \+ D$ ?7 Hlating hormone level was 1.3 µIU/mL (both normal)./ M* T+ b/ W5 W* m6 b
The concentrations of serum electrolytes, blood
# H! K9 z8 Y( t0 Z# h6 uurea nitrogen, creatinine, and calcium all were
" K) k7 z- ~3 P1 c/ N  dwithin normal range for his age. The concentration5 K2 r" r* m% q' k: B5 F
of serum 17-hydroxyprogesterone was 16 ng/dL. ^) ?5 d7 S6 B/ M9 d
(normal, 3 to 90 ng/dL), androstenedione was 20. k' \* @3 t+ v( x
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 {  B' x. P" X/ B
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- H8 M6 Q  |" |/ I2 _. u" d8 mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 v1 K- V* ]; T* E5 T49ng/dL), 11-desoxycortisol (specific compound S)$ Q! h+ Q  q9 P4 W0 o& F
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-$ W0 A. S/ T& @/ D8 K) J8 t3 T, ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
/ v+ T$ V) o, F1 w6 @3 x, P, Q* Wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
. Q( X5 G) b  d) S0 Y2 ~and β-human chorionic gonadotropin was less than0 }5 A2 s# k. p; ~" ]
5 mIU/mL (normal <5 mIU/mL). Serum follicular. s1 o* F! {. S: ~) n% U& j& T
stimulating hormone and leuteinizing hormone& q* [* J, ?8 @
concentrations were less than 0.05 mIU/mL& U5 D8 B* f9 ^
(prepubertal).1 H* W( q& J- J# Y% _" J
The parents were notified about the laboratory! T5 |% d' ]5 @6 x0 [/ i/ Y8 X
results and were informed that all of the tests were5 F' ]4 F8 C0 n( o
normal except the testosterone level was high. The- \5 q8 G% w; x/ G. ?
follow-up visit was arranged within a few weeks to# k, Z* C, X9 q% ~2 m
obtain testicular and abdominal sonograms; how-
* W/ q5 u  u& ]7 ^ever, the family did not return for 4 months.
9 C" U( J  _; G0 c- j- ePhysical examination at this time revealed that the8 T3 L7 P- G, f" A1 n( _
child had grown 2.5 cm in 4 months and had gained
) v9 g/ }' E8 g% N6 d# u4 B2 kg of weight. Physical examination remained
/ {& H0 n/ p! z6 p8 K& t4 yunchanged. Surprisingly, the pubic hair almost com-
1 e0 w( |4 E# Q- p% M8 l8 O, u% hpletely disappeared except for a few vellous hairs at9 y" @" S, G2 L& ]: m0 H
the base of the phallus. Testicular volume was still 2
8 A& n+ @& g$ l' c% q7 I$ d7 ^$ SmL, and the size of the penis remained unchanged.
* h2 p2 U' b; fThe mother also said that the boy was no longer hav-, Q7 ^' s0 |; r
ing frequent erections.
- q! S# m# k/ p. l8 j* N6 ]Both parents were again questioned about use of+ x  B" J4 d3 u: u4 O' w
any ointment/creams that they may have applied to( p1 m3 O% u  m- v9 {' V( m( f, X
the child’s skin. This time the father admitted the  I% A* j3 M8 J1 t
Topical Testosterone Exposure / Bhowmick et al 5411 d# _( ^4 U. O/ a! s& B4 O9 r7 {: [
use of testosterone gel twice daily that he was apply-6 S$ f. G! P) H3 J+ J" V$ T
ing over his own shoulders, chest, and back area for! q) ?9 @# R3 b7 X
a year. The father also revealed he was embarrassed
8 }0 R7 W1 J+ p5 ?& \to disclose that he was using a testosterone gel pre-+ K5 b9 a8 I  V# e( @$ y$ a
scribed by his family physician for decreased libido* f' b1 ^' Y/ w/ l! G) o, K, f& {8 ^5 g
secondary to depression.
( r* E1 W6 f8 O9 U: i4 A, y2 TThe child slept in the same bed with parents.3 Y  m* J- S0 g. l. o
The father would hug the baby and hold him on his9 ]( ^+ `+ ^8 Z% g6 M
chest for a considerable period of time, causing sig-
5 _! H4 t# D; Hnificant bare skin contact between baby and father.8 Y/ V# N1 k* E: Z1 f
The father also admitted that after the phone call,
- Y- o5 u# `$ N, o/ H- T2 Z; _9 j6 Swhen he learned the testosterone level in the baby8 S6 c% [/ i( @$ P1 H4 N1 F
was high, he then read the product information- W" k0 W. k0 H. @+ a7 I# z
packet and concluded that it was most likely the rea-& J& S& I& k2 ~. r5 X. |( A
son for the child’s virilization. At that time, they
. {/ p  k. t+ m2 j, Sdecided to put the baby in a separate bed, and the7 @) K  w/ h1 P1 i5 ?5 a* ~
father was not hugging him with bare skin and had) U* D2 M: h; g4 M! u4 ~; y2 M+ ]- c! Z
been using protective clothing. A repeat testosterone
4 Y, O/ b, T  ^: J3 stest was ordered, but the family did not go to the
- l1 t# J0 N" dlaboratory to obtain the test.. ?7 F% \% S! N  ~
Discussion# A- M1 _& `2 C8 E
Precocious puberty in boys is defined as secondary
0 e% s7 r4 u5 V" z7 Rsexual development before 9 years of age.1,4
% y/ x1 w% b+ v' k1 @Precocious puberty is termed as central (true) when: ]6 t2 B* _3 {0 t
it is caused by the premature activation of hypo-
& L9 b) R: ~  r$ C. Othalamic pituitary gonadal axis. CPP is more com-9 s8 z2 l+ O: i
mon in girls than in boys.1,3 Most boys with CPP& n' K3 T5 n+ j
may have a central nervous system lesion that is5 }  |% a4 r0 s9 x5 d
responsible for the early activation of the hypothal-# O; J: e, F% w0 a  v" ?+ _
amic pituitary gonadal axis.1-3 Thus, greater empha-+ y2 b, u4 e: ?; D, U6 q6 N
sis has been given to neuroradiologic imaging in' ~) g  J9 m/ N' h/ B, P
boys with precocious puberty. In addition to viril-5 O7 S' H0 U+ w
ization, the clinical hallmark of CPP is the symmet-% V/ i: @7 s6 k5 _8 f
rical testicular growth secondary to stimulation by
6 i; w+ r9 q# Egonadotropins.1,3  y' y; D  j1 g, L
Gonadotropin-independent peripheral preco-; c' A: i: ^" H. q. B9 z% O
cious puberty in boys also results from inappropriate
& `/ B! `: r) v, |  E( |0 iandrogenic stimulation from either endogenous or. O' y& D( Z, {
exogenous sources, nonpituitary gonadotropin stim-
! V4 f. [; r3 g& xulation, and rare activating mutations.3 Virilizing% J: O, \# U. R4 g. }( }; V' Z
congenital adrenal hyperplasia producing excessive  e9 d1 u3 y% K- W+ @
adrenal androgens is a common cause of precocious
2 H9 ?' n7 D/ Wpuberty in boys.3,42 Y, M' H) w& o% t
The most common form of congenital adrenal# [$ b. j) o7 L/ F/ C+ |  q( m
hyperplasia is the 21-hydroxylase enzyme deficiency.- O8 c& l+ b# K* ^2 k- S2 b
The 11-β hydroxylase deficiency may also result in" e/ n2 m3 ~6 G; i8 }  D. P
excessive adrenal androgen production, and rarely,
8 @( O4 a# c5 W6 @( ?3 c0 B9 R/ tan adrenal tumor may also cause adrenal androgen
' t- s5 u. i! a( M! F: jexcess.1,35 D5 b* ]! l% v( V  L
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 w# C! x, q! o9 s542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# W/ v+ o* H6 n, k2 k6 X9 pA unique entity of male-limited gonadotropin-1 Z4 x# Z# U! z( L9 d; q
independent precocious puberty, which is also known
/ K! w( W% Z" Y( m' cas testotoxicosis, may cause precocious puberty at a
/ T" E8 p- L- Mvery young age. The physical findings in these boys
5 B9 }- k1 l& O- J& \; m# Rwith this disorder are full pubertal development,
3 X& e. \8 H8 V: Y$ Z  }" m( Dincluding bilateral testicular growth, similar to boys% H9 y) H4 ~# ]8 Q- e7 j
with CPP. The gonadotropin levels in this disorder
. C8 {  b- B$ x1 H' u# p7 D* hare suppressed to prepubertal levels and do not show
" c7 T$ v8 _; K1 apubertal response of gonadotropin after gonadotropin-4 Z( [; a8 y0 J
releasing hormone stimulation. This is a sex-linked4 s. T. o  r2 B* ]
autosomal dominant disorder that affects only5 ?; j3 r$ d+ j! \
males; therefore, other male members of the family
3 y" I; h, M7 Z- R* g6 ^$ bmay have similar precocious puberty.3
. Y! |  h) O" R+ \; W5 m- fIn our patient, physical examination was incon-2 ^+ B4 ?1 k6 j
sistent with true precocious puberty since his testi-. m/ Z. n. f- H
cles were prepubertal in size. However, testotoxicosis4 x$ C0 r8 j6 N
was in the differential diagnosis because his father
0 Z  F- g: A2 I& r; Kstarted puberty somewhat early, and occasionally,
5 v6 P. U' ^( otesticular enlargement is not that evident in the1 `% Z( {9 J+ r
beginning of this process.1 In the absence of a neg-
( f; Y# k1 [( C& ^- tative initial history of androgen exposure, our
( V" o3 l8 k6 ~5 G3 ]. d6 c5 e" Lbiggest concern was virilizing adrenal hyperplasia,
- g6 l+ w7 q' |+ M9 Reither 21-hydroxylase deficiency or 11-β hydroxylase
0 _: B7 G( C: g+ P5 kdeficiency. Those diagnoses were excluded by find-" ]" \0 o  {' V5 V8 z5 p( b; J
ing the normal level of adrenal steroids.
2 g& p/ A: a. ]- n5 GThe diagnosis of exogenous androgens was strongly
8 f/ g" X+ t8 x8 P* T; w. x+ zsuspected in a follow-up visit after 4 months because# N; y' C9 Z- v/ s5 T/ @& k4 A
the physical examination revealed the complete disap-2 V+ T6 r. c" \6 ]+ ]. D/ w' i: p
pearance of pubic hair, normal growth velocity, and7 p: C* u7 E5 t" b
decreased erections. The father admitted using a testos-
- s3 L2 W, I# T  ^6 }  [$ n$ bterone gel, which he concealed at first visit. He was
/ A: Q9 ]5 d" I& e( ^$ ^6 J- Busing it rather frequently, twice a day. The Physicians’
0 Z0 W% Z) B/ p9 yDesk Reference, or package insert of this product, gel or
' S4 w7 E' V" `* K. M4 jcream, cautions about dermal testosterone transfer to+ f1 H6 L: `) E  ]0 s# j# H8 \5 B% l
unprotected females through direct skin exposure.
8 R7 H) N! B8 `6 V' \' MSerum testosterone level was found to be 2 times the
6 t1 [+ j. u" W1 Ubaseline value in those females who were exposed to
1 n+ f) [% e$ Qeven 15 minutes of direct skin contact with their male
4 i, A/ w: ~# Q8 |' Z5 ^1 \3 Bpartners.6 However, when a shirt covered the applica-
' M* U7 v( e' z8 H+ O* Ution site, this testosterone transfer was prevented.% w5 q5 R* e* }5 q
Our patient’s testosterone level was 60 ng/mL,0 ?+ a" n1 I8 a/ x4 z# P6 \7 M1 z
which was clearly high. Some studies suggest that
1 M/ F; @- ~" A" |' O" K) adermal conversion of testosterone to dihydrotestos-4 j7 C5 @3 E; x
terone, which is a more potent metabolite, is more
: J8 Y. o) j/ D' I/ Vactive in young children exposed to testosterone
5 X6 m% ^6 U" u. i1 iexogenously7; however, we did not measure a dihy-
7 B$ X7 l" v9 rdrotestosterone level in our patient. In addition to
8 `- U; n% L: ^virilization, exposure to exogenous testosterone in1 e9 ^: _( [/ o& m# c" j
children results in an increase in growth velocity and9 I2 ~( n6 Z' T4 ?1 L
advanced bone age, as seen in our patient.# v) _9 U7 t0 j$ b7 h' L4 U1 ^
The long-term effect of androgen exposure during9 L0 ]4 X# t( r$ f) N9 J+ x
early childhood on pubertal development and final; {+ R& i4 s% N  H2 Y$ B3 C/ a
adult height are not fully known and always remain  E1 w, x" @7 ]" ~2 T$ q. B2 o, g
a concern. Children treated with short-term testos-
: k# m7 I# z) K) Gterone injection or topical androgen may exhibit some) L& p, W! I8 [- G' R8 h# F+ Y
acceleration of the skeletal maturation; however, after
+ p! i) [8 x8 Ucessation of treatment, the rate of bone maturation  x1 }( m- o2 q( u1 ]) X0 B6 W
decelerates and gradually returns to normal.8,9
; k; `: z- j4 j% `3 I# a) h  dThere are conflicting reports and controversy! R/ I% D# @4 D: H  N- X0 n% m8 i
over the effect of early androgen exposure on adult+ i+ R8 {4 x, d! ~( K* B
penile length.10,11 Some reports suggest subnormal1 ~1 t+ o9 X( R  X* _. T
adult penile length, apparently because of downreg-- X, g  ?$ _2 {
ulation of androgen receptor number.10,12 However,
  C. Z6 U- D2 f: Q( nSutherland et al13 did not find a correlation between
3 S% ?( J) C) O5 \childhood testosterone exposure and reduced adult
/ N$ p* I: Q- |" m- K/ E' T# U3 Ppenile length in clinical studies.. p/ O( f0 J! _: R7 o7 Y
Nonetheless, we do not believe our patient is! N, x' T- B5 U& z; R
going to experience any of the untoward effects from
! o/ R: n0 O1 R% u0 _testosterone exposure as mentioned earlier because7 j/ U% v* j0 Y
the exposure was not for a prolonged period of time.  `2 u2 |: I8 c% r) E& I; N
Although the bone age was advanced at the time of
- \3 S+ q2 a5 hdiagnosis, the child had a normal growth velocity at2 Q3 U  `$ d# p- e* G3 b
the follow-up visit. It is hoped that his final adult
4 {; Z5 |3 g2 p; e) r) f0 P! Dheight will not be affected.
% S; j0 }5 a1 s  BAlthough rarely reported, the widespread avail-8 X  \% G" p, |( r: t- O
ability of androgen products in our society may1 B& V. P0 S. r2 O* C7 q  P; q
indeed cause more virilization in male or female/ ~9 k3 E) x  @/ S1 o
children than one would realize. Exposure to andro-
& i7 w% g7 H8 v1 B6 Zgen products must be considered and specific ques-
. E1 \$ l( c# w  Ttioning about the use of a testosterone product or
, t9 K4 I( b9 L6 Ggel should be asked of the family members during: u" }" N* l: C& C1 B1 C% v
the evaluation of any children who present with vir-' [! V: l6 R. h) p4 [
ilization or peripheral precocious puberty. The diag-7 l! i4 Z/ K1 _! I  r
nosis can be established by just a few tests and by) ?* a! I9 N9 [/ \
appropriate history. The inability to obtain such a
3 b& v: I4 K7 c! [* y% L6 o, Vhistory, or failure to ask the specific questions, may
4 C2 T4 q4 B" V0 D. h% \7 Y9 kresult in extensive, unnecessary, and expensive
0 c/ @: M* q2 ]0 H5 cinvestigation. The primary care physician should be5 M& j6 `  v2 s% S5 Q6 u
aware of this fact, because most of these children
4 s5 J7 S3 ?2 l1 Dmay initially present in their practice. The Physicians’
7 H* X9 c$ z4 `( q( U# RDesk Reference and package insert should also put a9 b; S: L; r8 k2 A, Z
warning about the virilizing effect on a male or
1 S$ |- R; n) }* g) {female child who might come in contact with some-$ D4 O5 |3 r( E/ U! k
one using any of these products.: u1 d$ f' p* }( M, E7 g
References
7 c: @! g8 r3 y) j. ^1. Styne DM. The testes: disorder of sexual differentiation
# x' J, E' K- k5 P+ pand puberty in the male. In: Sperling MA, ed. Pediatric; U$ ~; n2 `$ j: X. \/ p
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- T1 ^9 g+ R% P
2002: 565-628.1 h. a1 z# n/ [  B/ _
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
) S# [. t2 l6 U6 J+ ?puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
" I# l* T! @' k9 m; y3 nBoy Induced by Indirect Topical" R6 u- c# K1 @$ U- A  b
Exposure to Testosterone! B3 l9 p& i( E7 c& P4 y3 f2 v
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 ~/ J" S9 |# g' V! r( Gand Kenneth R. Rettig, MD1. f: a2 K" j! M7 z+ J! l
Clinical Pediatrics+ t7 ~# G1 v) K1 [
Volume 46 Number 6- ~6 c0 o8 l) ]0 W6 c5 D( F
July 2007 540-5436 x; O  l7 Y; K/ a) h3 b4 c+ V
© 2007 Sage Publications- E. e9 Y, H( u# f- @$ x. }
10.1177/0009922806296651/ [) @9 ~% E# k; O; ^* U
http://clp.sagepub.com; t; ?9 A& X3 Y6 H7 J- o' [
hosted at+ f) G; k; S" k: A
http://online.sagepub.com
/ X3 _2 M9 k, uPrecocious puberty in boys, central or peripheral,; \/ Y  g) c# R; `2 y- L
is a significant concern for physicians. Central- e% Y; c7 v* ~) v  g
precocious puberty (CPP), which is mediated
: m& J) w; ?- g% J8 I" E+ u+ r9 l" Ythrough the hypothalamic pituitary gonadal axis, has; ^7 \7 a9 y6 d  F
a higher incidence of organic central nervous system$ B$ G+ Z5 d/ \, f3 A
lesions in boys.1,2 Virilization in boys, as manifested2 m8 P5 n- J* J( [3 g
by enlargement of the penis, development of pubic) b; K$ O6 W( g5 J0 P
hair, and facial acne without enlargement of testi-
; g% k& v+ E+ ]cles, suggests peripheral or pseudopuberty.1-3 We
* U! p# i: e" ?9 U4 Wreport a 16-month-old boy who presented with the
0 {6 q( y9 z$ k7 henlargement of the phallus and pubic hair develop-
4 I" e9 _2 ^  I! ?ment without testicular enlargement, which was due
0 _3 ~  J6 U' D! k+ j, rto the unintentional exposure to androgen gel used by7 _/ f8 W: L+ x( ]; k( K
the father. The family initially concealed this infor-
% H! k4 m  q1 _3 h: k* Xmation, resulting in an extensive work-up for this! q/ m+ b3 x2 x' J
child. Given the widespread and easy availability of# d+ z! {  t5 }  ?& `
testosterone gel and cream, we believe this is proba-$ f( n* P: p. V4 b( K1 K+ z
bly more common than the rare case report in the
) Y2 C7 @, ~5 g0 l! y9 vliterature.4
- J4 l& {  K# E4 {* o9 q% ~Patient Report
2 A& ~5 \, {" T6 b5 o; VA 16-month-old white child was referred to the
/ R$ Q8 X8 H" W$ Gendocrine clinic by his pediatrician with the concern
6 T) U2 g1 U" ~% l) Rof early sexual development. His mother noticed
# X- t9 [' N/ Elight colored pubic hair development when he was
: G4 a+ K1 U9 K! n: bFrom the 1Division of Pediatric Endocrinology, 2University of8 R! s0 t* M- J
South Alabama Medical Center, Mobile, Alabama.
5 `: x- c" P* U& p- c$ g5 yAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 e$ D/ J2 f- V/ i( s9 g0 N" m
Professor of Pediatrics, University of South Alabama, College of
6 X  r" t0 D& R/ S3 A7 UMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; A- P1 X: f" q" ]e-mail: [email protected].9 M, w: `' B; k& i
about 6 to 7 months old, which progressively became
, G+ c3 [  q. D( |/ J9 Ldarker. She was also concerned about the enlarge-
9 J; u+ b+ y# z# I/ F9 a) r! P: Lment of his penis and frequent erections. The child
& U; a  o8 q* P; a5 X' Kwas the product of a full-term normal delivery, with
1 l9 }6 L, ~9 P6 d9 b8 Ra birth weight of 7 lb 14 oz, and birth length of
4 i$ e! _; H' t6 ~, d: u+ f4 z& ~9 d20 inches. He was breast-fed throughout the first year
( e9 k4 q. N3 U9 F9 Z9 s  cof life and was still receiving breast milk along with8 o: C' L8 K; {; d9 M  P  Y
solid food. He had no hospitalizations or surgery,
3 X3 z" F; H5 `% C: w' \5 x  {' M! zand his psychosocial and psychomotor development
5 v0 B, g1 [- W; ^/ c; lwas age appropriate.' b2 w- \$ u  X7 q9 f. p6 B( P
The family history was remarkable for the father,9 R* A7 Z0 s6 ~7 A3 l8 E
who was diagnosed with hypothyroidism at age 16,7 [# e3 u3 B2 C, [! S& U$ Q
which was treated with thyroxine. The father’s
2 _: A' b9 k) Xheight was 6 feet, and he went through a somewhat# {5 b: V* @& ?) A
early puberty and had stopped growing by age 14.7 {5 P+ x) l% h! r
The father denied taking any other medication. The
$ C( U: f2 w! r& V  Ochild’s mother was in good health. Her menarche
$ z- l& s1 b* Ewas at 11 years of age, and her height was at 5 feet) b; j2 {8 J" Z+ {; s' |
5 inches. There was no other family history of pre-
% G  Z3 e. |( @( ecocious sexual development in the first-degree rela-3 ]# l- n6 b6 k! Q% I6 B/ z
tives. There were no siblings.( L* b3 I! E( `( B
Physical Examination
# x7 b' w0 e, b5 S5 lThe physical examination revealed a very active,2 H% r* y% R9 U6 n
playful, and healthy boy. The vital signs documented
: U/ e* j0 Z* M8 g8 I' ta blood pressure of 85/50 mm Hg, his length was
  A7 S9 P3 f/ |- L2 A% x) Y( L! K90 cm (>97th percentile), and his weight was 14.4 kg. u. C2 b$ T  P3 A! B1 M
(also >97th percentile). The observed yearly growth
: j0 _% V2 z$ ]. [velocity was 30 cm (12 inches). The examination of
8 w( k( H3 m' Ethe neck revealed no thyroid enlargement., T6 ?7 f+ r4 a- w+ t. \  f
The genitourinary examination was remarkable for
, Z% q+ ]# s! \- [* [enlargement of the penis, with a stretched length of
7 i' U0 ?" e' |) K% L7 X8 cm and a width of 2 cm. The glans penis was very well
6 C3 {1 \0 u1 D" [7 _developed. The pubic hair was Tanner II, mostly around2 H8 ~' C2 g" w% n7 f
540, t+ g) x$ V) y% J  ~) E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# u4 A7 J! h1 hthe base of the phallus and was dark and curled. The4 t8 _" [0 i% `( X: b& b
testicular volume was prepubertal at 2 mL each.: D& i7 G7 l" V& g2 O
The skin was moist and smooth and somewhat* z5 n+ }) z, a% T
oily. No axillary hair was noted. There were no
# o0 f1 o6 P" a/ a- J4 H# N8 f6 {abnormal skin pigmentations or café-au-lait spots.
& |  U7 t# i) T% F  T' [) e9 Y0 XNeurologic evaluation showed deep tendon reflex 2+
* D- b9 B; d3 o8 X5 x- mbilateral and symmetrical. There was no suggestion6 }; d; w$ ?1 R/ Q: w+ g3 v
of papilledema.% ?6 P4 z" Q/ k; b9 c
Laboratory Evaluation
* j2 q1 {, U% p4 m, qThe bone age was consistent with 28 months by. B  P$ o# j3 u. F. ~/ `* W
using the standard of Greulich and Pyle at a chrono-% B5 y* v0 V6 a" J
logic age of 16 months (advanced).5 Chromosomal
" f+ j2 W4 {% {; fkaryotype was 46XY. The thyroid function test
% a1 U4 d& \( p. J1 A) Z. [2 Lshowed a free T4 of 1.69 ng/dL, and thyroid stimu-+ U* D4 m) m" M: z
lating hormone level was 1.3 µIU/mL (both normal).
! l+ \+ ^1 M2 b1 ^The concentrations of serum electrolytes, blood" j0 d" _8 }# v" d; R
urea nitrogen, creatinine, and calcium all were
* ^. ^$ e& s( c4 t5 Awithin normal range for his age. The concentration' N9 _8 {+ ?0 l) K
of serum 17-hydroxyprogesterone was 16 ng/dL% ~% x2 m7 D! V' J  @- Z8 z
(normal, 3 to 90 ng/dL), androstenedione was 20
: Q1 ^' I% o% P: C1 y  v) Kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' c8 z& B* I) f( H8 I4 ?& g  Iterone was 38 ng/dL (normal, 50 to 760 ng/dL),0 s: _; x% J+ a6 u3 B! T
desoxycorticosterone was 4.3 ng/dL (normal, 7 to# w1 f- r9 v$ j+ s& X
49ng/dL), 11-desoxycortisol (specific compound S)8 I+ X6 Z( C2 q1 ?
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-" x% e( {" D7 {2 I: n5 u) o
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 h2 Z. M) q2 z( e7 p0 V8 a9 U
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 k2 T& M& g- b  V7 }0 z) D
and β-human chorionic gonadotropin was less than
! l; r% @% K8 I: ~5 e/ n4 L7 H, T5 mIU/mL (normal <5 mIU/mL). Serum follicular" b& M0 h' [7 C+ M
stimulating hormone and leuteinizing hormone6 R' p* e1 A0 K1 f4 g3 ~, H
concentrations were less than 0.05 mIU/mL
1 h8 W9 I( Y" q, R0 Y5 H0 M: Q(prepubertal).
- {% i  ]( ~, S, }6 l& x& |) C# ]The parents were notified about the laboratory
) {+ P- j: M1 G- B. A5 Yresults and were informed that all of the tests were
: O  _* Z8 M7 g: g2 d9 }normal except the testosterone level was high. The, R: G4 x8 z5 t, n% n% e! \" u
follow-up visit was arranged within a few weeks to1 ~% x' ]- H' D/ P+ ]% N
obtain testicular and abdominal sonograms; how-% [: }$ @, h8 K# y6 I
ever, the family did not return for 4 months.
2 `& l" ]2 V& z* V) y+ Y* GPhysical examination at this time revealed that the2 P  C' u5 y; t& Z
child had grown 2.5 cm in 4 months and had gained
7 ~3 {2 q" m, }7 h2 kg of weight. Physical examination remained' ]. ?  O( h& ^# k, m! v2 V% ?" @& Y
unchanged. Surprisingly, the pubic hair almost com-' L' e) K3 [* b( v; ?
pletely disappeared except for a few vellous hairs at
  G! W$ w3 S4 c7 Z% o9 lthe base of the phallus. Testicular volume was still 2
. r  x6 q8 F$ S/ I' zmL, and the size of the penis remained unchanged.! G! h) }+ V* ?/ x* `
The mother also said that the boy was no longer hav-
! v2 _; P8 e( n, n: r+ O! Ving frequent erections.
7 Z2 `$ `- o5 ~6 b1 @" O2 [Both parents were again questioned about use of: ]7 l0 D7 e7 M1 \+ Y6 {* e
any ointment/creams that they may have applied to2 `9 B# W; Z7 [" o* d
the child’s skin. This time the father admitted the( M& Q9 v: _  s# D* s
Topical Testosterone Exposure / Bhowmick et al 541% M% s. |4 `& r* i  ^6 K1 J
use of testosterone gel twice daily that he was apply-0 H. K5 s( L( J- j. M: |- b
ing over his own shoulders, chest, and back area for
0 `% V, M# A  Z  R8 k2 F5 ^; fa year. The father also revealed he was embarrassed4 `0 S$ T0 ?& E3 h3 w- X# ^. [
to disclose that he was using a testosterone gel pre-
$ f* x5 w+ [$ T8 p% {! o: pscribed by his family physician for decreased libido
# Y2 A; y+ Z, d7 tsecondary to depression.  m4 [: P) i* G* _  u, V) z; B" G
The child slept in the same bed with parents.
0 p3 _. S- w' t  G5 q4 _The father would hug the baby and hold him on his2 B! v1 s. C8 q( ]7 L, {  U
chest for a considerable period of time, causing sig-
; K7 K3 N1 Y, I7 N2 Knificant bare skin contact between baby and father.
6 r; \. M* ~5 k5 p0 t2 C) kThe father also admitted that after the phone call,
: f+ E7 J2 P+ x; hwhen he learned the testosterone level in the baby# d# T9 C/ r! z2 a9 V, e% j
was high, he then read the product information
* ^3 g3 S8 y* U4 Cpacket and concluded that it was most likely the rea-/ _0 X+ t, x" \$ _( {$ L
son for the child’s virilization. At that time, they$ S' f# }" |+ }+ D; w
decided to put the baby in a separate bed, and the1 @- x3 G0 ?) i1 s  M  |
father was not hugging him with bare skin and had. e( G* C4 Z$ i0 T. P$ G# P
been using protective clothing. A repeat testosterone
0 ^" Q+ K. h0 Y0 T3 a9 Xtest was ordered, but the family did not go to the
( ]- j/ D/ o( rlaboratory to obtain the test.4 {% t/ T, D) B4 J* A
Discussion  d9 d, H% Y: ?' O8 _
Precocious puberty in boys is defined as secondary
6 n" J( S' [5 M& hsexual development before 9 years of age.1,47 u4 ~' e; e$ G( Q0 t
Precocious puberty is termed as central (true) when2 Y! A4 A9 {: F: D
it is caused by the premature activation of hypo-2 h! ~  w" B- V  F5 X/ m
thalamic pituitary gonadal axis. CPP is more com-
. J( d+ ]* U) [0 ^# Qmon in girls than in boys.1,3 Most boys with CPP! r6 ]4 w/ Y3 g* v5 N# h
may have a central nervous system lesion that is9 _: g/ G$ W# K
responsible for the early activation of the hypothal-: N, q- X# ]: K6 ^
amic pituitary gonadal axis.1-3 Thus, greater empha-
# R! S! y5 d3 ]$ L" @/ Isis has been given to neuroradiologic imaging in
, I6 h3 d& s: l7 q4 Qboys with precocious puberty. In addition to viril-& L3 C+ n5 }5 I# e! P
ization, the clinical hallmark of CPP is the symmet-1 g: S) K1 j! ^& B, L; v3 f% L
rical testicular growth secondary to stimulation by
# H9 ]. \8 u$ f  @1 |# mgonadotropins.1,3) u1 C) o* @3 N  q) b7 S  q
Gonadotropin-independent peripheral preco-
# o7 u+ v. j5 M5 \cious puberty in boys also results from inappropriate
8 `( R7 E  q* k" x% uandrogenic stimulation from either endogenous or: s- i* f* a6 d. H7 x+ J) c& d- ^5 H
exogenous sources, nonpituitary gonadotropin stim-
9 m  Z# S2 ~; x7 ?4 [+ ?8 eulation, and rare activating mutations.3 Virilizing% O5 I; M& k2 {" g8 H4 G+ w0 F
congenital adrenal hyperplasia producing excessive+ S& C4 }8 r' r6 B. X( ]
adrenal androgens is a common cause of precocious
6 Y: @/ z0 r" p8 g) Jpuberty in boys.3,4
, r3 M1 z2 S5 P, M/ oThe most common form of congenital adrenal
8 n7 i( T6 m( B) \hyperplasia is the 21-hydroxylase enzyme deficiency.+ ?6 [( v( x1 c' x" h% D
The 11-β hydroxylase deficiency may also result in1 H& V& G1 V* r
excessive adrenal androgen production, and rarely,4 G, d, a4 t, }+ ~0 f% S3 m
an adrenal tumor may also cause adrenal androgen: p- N6 i5 F7 H
excess.1,3
  u9 Q# p5 i2 i, B" E7 Oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 j% m0 m; @- H) q- U/ h542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& y+ {( M1 c; y" ~4 s$ @: j. c
A unique entity of male-limited gonadotropin-: n! H2 o6 F4 N# R/ b- b
independent precocious puberty, which is also known
& e+ w+ k! ~' \8 E1 sas testotoxicosis, may cause precocious puberty at a4 y9 N" G# T) d4 b/ D% ^3 m' O" l
very young age. The physical findings in these boys
- z! W2 U; s, _9 a# Zwith this disorder are full pubertal development,5 q! Y7 P- F& j- P4 H' B8 P
including bilateral testicular growth, similar to boys
) o( ^7 X4 \) W4 ~( dwith CPP. The gonadotropin levels in this disorder
+ H2 U5 k. S# gare suppressed to prepubertal levels and do not show! m" {- M% ]3 ]% a2 S
pubertal response of gonadotropin after gonadotropin-
! m; h1 L0 c- ^9 }; }: R1 breleasing hormone stimulation. This is a sex-linked; {- U  g" e1 V& B( I) w0 T1 l1 A
autosomal dominant disorder that affects only# q( {5 G$ v% `- j+ G! X' e! H
males; therefore, other male members of the family
% m2 e+ L4 e0 {$ qmay have similar precocious puberty.3+ ]5 u. G0 _* c# V
In our patient, physical examination was incon-+ |. N: C: y2 v; w0 Z  }$ _- |9 q, n$ W
sistent with true precocious puberty since his testi-
/ t( g. T; s% F3 ycles were prepubertal in size. However, testotoxicosis6 {. o; {* u! Y
was in the differential diagnosis because his father' p# z3 x3 E0 E8 j: s. u
started puberty somewhat early, and occasionally,3 T3 w  w$ a+ b4 ^, d$ Z7 X
testicular enlargement is not that evident in the
8 `/ [) L6 B5 U4 tbeginning of this process.1 In the absence of a neg-7 y( I! K( ~# A. Q0 M9 j
ative initial history of androgen exposure, our
# m! Q7 |! v- v5 Zbiggest concern was virilizing adrenal hyperplasia,
# w2 i- E' r, p5 l- b% m* y' Ieither 21-hydroxylase deficiency or 11-β hydroxylase
/ n6 f$ \+ M! Tdeficiency. Those diagnoses were excluded by find-7 n) u  J5 O- h$ s) `' E$ {
ing the normal level of adrenal steroids.
& j% k2 {* i% C- EThe diagnosis of exogenous androgens was strongly0 M7 W% l; G5 H2 b
suspected in a follow-up visit after 4 months because7 |9 d/ V+ A5 D8 p- g
the physical examination revealed the complete disap-
8 ^/ Z& l$ }4 Rpearance of pubic hair, normal growth velocity, and
% _0 a1 l4 H5 B  U( ~decreased erections. The father admitted using a testos-
$ G6 u7 M- m  v- ]* t, n, Xterone gel, which he concealed at first visit. He was( k6 ]& \% |6 J, [
using it rather frequently, twice a day. The Physicians’0 X& Q6 x- J! O% P
Desk Reference, or package insert of this product, gel or
7 G- T# `4 s, H& S  k% T1 f: |0 l2 Ucream, cautions about dermal testosterone transfer to
3 |+ [8 o/ h9 U% ?+ {unprotected females through direct skin exposure.
8 T' K( ^% C! T/ @. {Serum testosterone level was found to be 2 times the! `$ g" |$ N2 W9 W
baseline value in those females who were exposed to
: v6 @1 J0 j' ^: o7 teven 15 minutes of direct skin contact with their male
5 p0 ]% `+ H8 @1 x, n$ Gpartners.6 However, when a shirt covered the applica-
+ h9 d; ^! g* M9 ~tion site, this testosterone transfer was prevented.5 ]' U' D8 ~1 Q; J: x) S
Our patient’s testosterone level was 60 ng/mL,
) f* V6 U4 _3 ]4 n: {5 c2 N5 f7 V4 ewhich was clearly high. Some studies suggest that
% T' I1 c2 B5 qdermal conversion of testosterone to dihydrotestos-9 r" q% B/ F" d, n* j$ A
terone, which is a more potent metabolite, is more
' ]0 D+ F: y! C( L2 b8 Tactive in young children exposed to testosterone
0 n+ e5 m- e3 J# v. ]' gexogenously7; however, we did not measure a dihy-
$ W7 {7 \1 Y+ S' e' L6 zdrotestosterone level in our patient. In addition to5 D  O0 D0 w; d, |) e6 B3 a
virilization, exposure to exogenous testosterone in, _: l1 M$ u: q
children results in an increase in growth velocity and
7 b6 R! m+ k$ d) V  O) U' r6 iadvanced bone age, as seen in our patient.
0 y# G) I# b" |6 y, G: ]1 \  R4 uThe long-term effect of androgen exposure during
( o# N- X3 A. eearly childhood on pubertal development and final3 e' z! z2 G# Q) V$ b, `
adult height are not fully known and always remain
5 Q4 y& S* m: {a concern. Children treated with short-term testos-& g  F6 L! S4 b! w. n4 H2 |$ ]
terone injection or topical androgen may exhibit some" T9 q/ W8 L& [' _
acceleration of the skeletal maturation; however, after4 d7 {$ v. Z* F  V* B$ p
cessation of treatment, the rate of bone maturation; P1 C. t& P+ z1 A
decelerates and gradually returns to normal.8,9' l- E# e' q  T2 e% Z) D' w
There are conflicting reports and controversy
6 |6 U8 d/ e# B6 nover the effect of early androgen exposure on adult7 z; O) k/ m% F& m
penile length.10,11 Some reports suggest subnormal7 N2 x/ u6 C1 I
adult penile length, apparently because of downreg-5 h; z9 q2 u: G( [+ T7 }! c- P
ulation of androgen receptor number.10,12 However,# E! O& j" h' A& r2 ?' s
Sutherland et al13 did not find a correlation between
- q& r* W3 ^/ s  |childhood testosterone exposure and reduced adult
6 I4 J1 R9 S" openile length in clinical studies.
, `8 K; q3 I- g/ X/ eNonetheless, we do not believe our patient is
+ }4 i# w8 e1 l( ogoing to experience any of the untoward effects from
2 U: I) O$ h/ ]" }" ~testosterone exposure as mentioned earlier because
) x' `& z, d  c( R6 b: N2 A; j& |the exposure was not for a prolonged period of time.
' R' G$ ~2 W; |; ]: `Although the bone age was advanced at the time of2 g, h' n! {/ c( `
diagnosis, the child had a normal growth velocity at( u8 {* _$ L/ F* ~
the follow-up visit. It is hoped that his final adult7 X1 E4 V* v# H1 ]$ l
height will not be affected.
$ Z, I5 U$ g7 xAlthough rarely reported, the widespread avail-0 S! C# L5 S, y1 E  K; A8 H* {
ability of androgen products in our society may
- d8 ~3 E; E; T( \% Y& k+ tindeed cause more virilization in male or female
) Y: N: J: z# P3 B) ]children than one would realize. Exposure to andro-
+ T" A+ U& g: ]& }- t/ I# i" Pgen products must be considered and specific ques-
% \# k/ L7 n) M* N& s# K. z7 @tioning about the use of a testosterone product or: U# H. b8 w+ l1 I
gel should be asked of the family members during
- C* D* |' ?' m7 ~8 M3 Sthe evaluation of any children who present with vir-8 I+ X  R  `, Z
ilization or peripheral precocious puberty. The diag-
& R; q. f6 t# U: j( U  u+ q$ Xnosis can be established by just a few tests and by
4 p# s) o, E7 A4 `! _3 R: Zappropriate history. The inability to obtain such a- F( U5 H7 }$ K+ `
history, or failure to ask the specific questions, may! F/ x# u# G6 ^3 g6 Y/ |# X$ l
result in extensive, unnecessary, and expensive. x$ l# H. @* a: ~% k
investigation. The primary care physician should be* C$ [- L( r/ j
aware of this fact, because most of these children' p/ o  g5 ^. ~3 @
may initially present in their practice. The Physicians’7 {1 J# b5 ]- ]9 l& @% }' @3 l
Desk Reference and package insert should also put a
& J7 P9 [: A, V, C5 t3 s0 Kwarning about the virilizing effect on a male or
" U2 r* k3 B5 {0 Sfemale child who might come in contact with some-5 P1 }5 L1 `0 }$ F
one using any of these products.& C* o: Y' o( K6 }  T
References
/ k, e( a6 I) K% O, i1. Styne DM. The testes: disorder of sexual differentiation1 w2 @  n) n: Q  i7 x; ?
and puberty in the male. In: Sperling MA, ed. Pediatric
4 `  J: h4 m: ^) V& v. VEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
2 |3 [  L: r0 A9 Y2002: 565-628.
/ f  I& Z- O/ G$ c2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
4 i: b" f0 m* y# K/ X6 Wpuberty 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!
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
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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
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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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