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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
' O$ O4 L6 n) @* t1 oBoy Induced by Indirect Topical* f& N; R" ~# [% Z
Exposure to Testosterone
* Y* x3 ~: Z; FSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 \" z# O$ U2 d6 T2 Fand Kenneth R. Rettig, MD1) n- ?4 z. Y9 ~* z; e2 C' K, [
Clinical Pediatrics7 K* Q( c: i$ e) e/ p+ Y  e
Volume 46 Number 6
, }% |( R4 D2 F& B! S3 ]July 2007 540-543
3 c1 g* w) i" N: }# X9 }2 H© 2007 Sage Publications1 a+ r- ~' w& Z, Q$ T4 b% K
10.1177/0009922806296651$ b' Z6 t( R% y
http://clp.sagepub.com
( `5 \2 |; P( J& mhosted at
5 F' [. Y5 B/ t; l& }http://online.sagepub.com
1 L. A. \' s+ h' LPrecocious puberty in boys, central or peripheral,  N0 K% r$ d. Q0 }5 B; F
is a significant concern for physicians. Central
% J- C9 N4 t/ e; t8 @* xprecocious puberty (CPP), which is mediated6 M+ K: T" V0 ]" q+ |5 k
through the hypothalamic pituitary gonadal axis, has
' J1 h' C3 C% Ia higher incidence of organic central nervous system
1 {) o" R6 P+ c* a  ]lesions in boys.1,2 Virilization in boys, as manifested8 @, I+ c7 ^; K
by enlargement of the penis, development of pubic
( u$ I, @  _' s* u2 x, rhair, and facial acne without enlargement of testi-
0 A0 b9 h- |8 Xcles, suggests peripheral or pseudopuberty.1-3 We
. Y0 l1 t6 ^6 areport a 16-month-old boy who presented with the
* ?* j/ e7 L6 C2 M7 Uenlargement of the phallus and pubic hair develop-
/ `% F: b  ^" _" Vment without testicular enlargement, which was due4 }! Q5 q! T! u4 q9 n, ^. W
to the unintentional exposure to androgen gel used by6 J- ~; n  v& K) W
the father. The family initially concealed this infor-
6 I' t* r7 D# S1 y; E) Z8 Gmation, resulting in an extensive work-up for this$ V4 b3 P2 M5 C. `) N
child. Given the widespread and easy availability of
2 Y" o1 R  g8 e# F+ U% Stestosterone gel and cream, we believe this is proba-% o9 e' L' M+ _6 x; T
bly more common than the rare case report in the
# G0 b3 a1 s& Q7 M4 @3 \- p, I1 Yliterature.4& y5 S$ W4 J( q3 s( a# D0 l) l
Patient Report8 A# s$ G& b' m! b& d6 C: B
A 16-month-old white child was referred to the
1 E8 C7 u/ }! `+ Yendocrine clinic by his pediatrician with the concern
2 e% b, k9 M. _& T1 tof early sexual development. His mother noticed2 K9 O: ~  B. V+ A+ Z: ]! w
light colored pubic hair development when he was
! _, ?, `6 B  i% W4 k; ?From the 1Division of Pediatric Endocrinology, 2University of
" W6 @1 S9 K4 @+ X0 w* B' B% x: KSouth Alabama Medical Center, Mobile, Alabama.
9 a/ Z! R; P4 N7 iAddress correspondence to: Samar K. Bhowmick, MD, FACE,5 X$ D" H" L- Y3 d1 R! }. A: k; F
Professor of Pediatrics, University of South Alabama, College of; I# h# {4 V8 C& T+ Y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" f# W# |* z+ w! M9 w! v% O+ ]" X2 T
e-mail: [email protected].
7 D0 o7 m, q. W) J5 Y5 rabout 6 to 7 months old, which progressively became5 ^, Q& d; }$ N: y# D
darker. She was also concerned about the enlarge-
+ i% v, B  [! w6 @ment of his penis and frequent erections. The child; {, W8 ^% j' T8 L
was the product of a full-term normal delivery, with
# g. F3 a3 i! M1 u1 }' Ha birth weight of 7 lb 14 oz, and birth length of2 N( W0 G3 K, g8 }& H# M. C
20 inches. He was breast-fed throughout the first year1 D- Z1 M! {% X& [+ I5 h$ `
of life and was still receiving breast milk along with
8 T% P7 K4 |% esolid food. He had no hospitalizations or surgery,, T/ D  Y+ U7 i, u2 z
and his psychosocial and psychomotor development
1 p* S! O: x3 I( ~4 r# Vwas age appropriate.: Y0 o0 I" g) Y0 X  y) W, P2 O
The family history was remarkable for the father,- J* [: ^8 N+ [# X. o
who was diagnosed with hypothyroidism at age 16," x; N5 C5 ]: {! R( ^- I
which was treated with thyroxine. The father’s8 [7 V& ]: ], y" [) q/ q* `* h+ Q
height was 6 feet, and he went through a somewhat6 w1 W/ B0 b; ^' P6 M- J
early puberty and had stopped growing by age 14.; T0 A7 {3 V3 R4 l4 Z8 `6 P
The father denied taking any other medication. The
; j6 K  n, O: @9 R6 ichild’s mother was in good health. Her menarche. a, M8 e. T' Y5 ]
was at 11 years of age, and her height was at 5 feet
( f/ ]! {3 E1 }! C' N) i5 inches. There was no other family history of pre-
* J, z. l3 T3 x$ s; h: j- m/ \cocious sexual development in the first-degree rela-
  i$ c# U) R8 {2 k5 ^5 f% }" Dtives. There were no siblings.
% p% H/ s: A* f5 O1 n5 H4 R6 H( nPhysical Examination
* Q* T2 J) n( G, S" s& Y4 bThe physical examination revealed a very active,& V) J; k; f2 ^
playful, and healthy boy. The vital signs documented
% D. M. `' r0 _% |' ~a blood pressure of 85/50 mm Hg, his length was( H' m* x8 Z  \' ~, ]
90 cm (>97th percentile), and his weight was 14.4 kg
2 S+ [( i4 h5 H6 X- r3 ~/ I2 H(also >97th percentile). The observed yearly growth
( z( ^; v( B2 j% l0 d3 @% qvelocity was 30 cm (12 inches). The examination of5 v+ m8 N' }: S. p; s. I
the neck revealed no thyroid enlargement.
, x$ e7 m. Z5 s: |$ m5 Z% `; XThe genitourinary examination was remarkable for4 P# R' K  m4 F( E2 G
enlargement of the penis, with a stretched length of
, f& P, K7 e8 a( N8 z7 d8 cm and a width of 2 cm. The glans penis was very well/ _5 @+ W' V3 h" y
developed. The pubic hair was Tanner II, mostly around7 b9 \3 X# P1 `/ _
540
' F) K* U5 k# ~. W1 G( p9 N& t/ cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: y/ f" Z- }1 g- q* W) |1 @, Ythe base of the phallus and was dark and curled. The
, Q; z5 \. m) B. U6 m7 y9 ytesticular volume was prepubertal at 2 mL each.- S. b. ?$ b  d# _  c1 s& n  O" h
The skin was moist and smooth and somewhat  R. z8 ^0 H' S( l0 e
oily. No axillary hair was noted. There were no0 B3 D# w# R: k  R4 [
abnormal skin pigmentations or café-au-lait spots.& p# A6 u. V' P, F( {9 M
Neurologic evaluation showed deep tendon reflex 2+" w. E$ h7 j' g. ]2 w  r
bilateral and symmetrical. There was no suggestion: r- }2 b7 T3 Z8 p$ I
of papilledema.
- Y' c. G" W0 d* w- `9 @% [2 iLaboratory Evaluation2 f) S2 X; P8 d$ [  ]! B5 N: Z: [
The bone age was consistent with 28 months by
, v4 |1 A7 ~" B3 F: W6 h9 cusing the standard of Greulich and Pyle at a chrono-0 \& ]: Q7 H4 V% G3 Z3 W5 F9 `
logic age of 16 months (advanced).5 Chromosomal
4 E  K/ M& ]$ A# P/ b8 |karyotype was 46XY. The thyroid function test" Y2 a) i7 ]0 i, f7 P! j" [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
! V5 o" }2 c/ r$ C3 S9 P7 dlating hormone level was 1.3 µIU/mL (both normal).
1 I" ~; ~2 T4 W3 ~" O5 v; ?The concentrations of serum electrolytes, blood. T% Z! U* x$ P% E) L, ?; O* G
urea nitrogen, creatinine, and calcium all were2 Q, x! a) W2 E0 o9 e
within normal range for his age. The concentration
+ `  \) W% M5 [5 o* i( X5 D. Oof serum 17-hydroxyprogesterone was 16 ng/dL" Y2 S% s0 ]* {% ~8 Z
(normal, 3 to 90 ng/dL), androstenedione was 20
0 [$ }  a$ H' t3 v. i  Cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-; Z: w$ u& M3 v; @6 n" V" u/ K5 l
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
: w7 Y4 Z" Z( i  ]( x) ^desoxycorticosterone was 4.3 ng/dL (normal, 7 to
& r& Z5 K  z- ?$ m49ng/dL), 11-desoxycortisol (specific compound S)" `; _( Y( d7 O7 V* l
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 E0 t9 v4 i1 q% L+ s. Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 M0 E- k2 t1 D6 M0 Y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, ^4 G' w1 }( e4 m) C1 |' Wand β-human chorionic gonadotropin was less than
+ K( h2 Q- `+ l0 s4 W5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ m* q2 F1 u; M/ n; lstimulating hormone and leuteinizing hormone( r( X1 u# l7 v! O8 _# K/ g
concentrations were less than 0.05 mIU/mL( V, t' C0 G2 Z+ {" F
(prepubertal).
9 C0 _  ~+ F* t8 U5 O- e( m+ ^The parents were notified about the laboratory9 L( \: p$ ^3 p4 q4 _, t
results and were informed that all of the tests were- @! ?$ Q* G$ n# ]9 z1 v
normal except the testosterone level was high. The
  V+ W% ?! J( Q* ~" Hfollow-up visit was arranged within a few weeks to, e' J& G: j2 w5 a. E
obtain testicular and abdominal sonograms; how-: _! k) z6 M9 f" w
ever, the family did not return for 4 months.
2 k# e% I1 F1 e0 u: X4 c- |6 \Physical examination at this time revealed that the
0 J/ Z6 y( D  h8 d) h1 i( lchild had grown 2.5 cm in 4 months and had gained0 Y4 ^: Q; H2 s) \# Q3 X, X8 X
2 kg of weight. Physical examination remained
, h0 l, g) Q1 G6 l- U1 j, Uunchanged. Surprisingly, the pubic hair almost com-; w  I; g9 f6 U2 d2 p" U
pletely disappeared except for a few vellous hairs at, d5 J- E0 q5 O4 n* `
the base of the phallus. Testicular volume was still 29 ~. T6 W# C3 Z7 I' q
mL, and the size of the penis remained unchanged.; ~& Z$ z; ?- o) n) c8 B0 t
The mother also said that the boy was no longer hav-
4 m! n  A5 H6 L2 {  }0 w. @0 m4 Z7 King frequent erections.$ h, |8 M) q8 v9 v5 y2 a
Both parents were again questioned about use of) \4 ?6 l& i: |) x, p
any ointment/creams that they may have applied to
, @1 z, W9 `, d' xthe child’s skin. This time the father admitted the  l3 X  V3 |6 r) M& ~
Topical Testosterone Exposure / Bhowmick et al 5410 C; d. S+ Z, ?. o* B! n
use of testosterone gel twice daily that he was apply-
* K' B* Y1 k( ^0 c# G! N, ting over his own shoulders, chest, and back area for" b) U$ y) I7 V! S
a year. The father also revealed he was embarrassed
! Z, q: @6 S0 E" E! S/ ~3 }to disclose that he was using a testosterone gel pre-
) j4 }0 B3 }) }4 }" H) ]scribed by his family physician for decreased libido& X/ _& o: x/ M0 O( g; T, N2 f/ W# Y
secondary to depression.  U- m5 [+ G. S: L' i! M( ~# g
The child slept in the same bed with parents.# H7 r3 @- b+ h; m/ I8 n  @7 z
The father would hug the baby and hold him on his
7 s! o8 C, c1 U" S( R* lchest for a considerable period of time, causing sig-3 q) d" Q! K$ n, A
nificant bare skin contact between baby and father.
1 A) w! f. J1 ~The father also admitted that after the phone call,
1 y/ _. b/ g* n- ywhen he learned the testosterone level in the baby" f- A% F/ H" A
was high, he then read the product information, s2 ?$ }% w4 {# X
packet and concluded that it was most likely the rea-
1 r( a6 }8 y2 i' nson for the child’s virilization. At that time, they  l0 @" d, B: f+ e/ \% S9 k4 O5 q
decided to put the baby in a separate bed, and the
) y0 r  o0 X) a+ \8 Jfather was not hugging him with bare skin and had
( T, W6 J/ n2 I* b5 _. `) Kbeen using protective clothing. A repeat testosterone$ p1 E3 _( R0 b0 W9 {. Z: x
test was ordered, but the family did not go to the
! B: g- f0 \/ M; C' qlaboratory to obtain the test.: Q% u8 b; N0 ?7 ^
Discussion
3 b" I+ r% }, F0 R: P# gPrecocious puberty in boys is defined as secondary
1 @0 r( _4 P( D+ V2 }sexual development before 9 years of age.1,4/ y) c+ i5 n# j
Precocious puberty is termed as central (true) when
7 b5 K( M# O  m8 G. |/ B* mit is caused by the premature activation of hypo-! U- A  \' G' r1 R2 S: ]# s) x/ |
thalamic pituitary gonadal axis. CPP is more com-
% X' }6 v9 J/ w6 p# g, [& zmon in girls than in boys.1,3 Most boys with CPP2 D6 c2 w; H: P7 m
may have a central nervous system lesion that is" T/ w2 P( F. v% }; U
responsible for the early activation of the hypothal-) [( E; e4 J# ~' N( B
amic pituitary gonadal axis.1-3 Thus, greater empha-
8 \+ D5 ~5 ^* wsis has been given to neuroradiologic imaging in# z! ?: y4 |& O4 W4 b* X
boys with precocious puberty. In addition to viril-
( R5 d+ ~  |/ i2 f1 S; `' u8 Zization, the clinical hallmark of CPP is the symmet-7 f7 n, U+ Z3 E% S
rical testicular growth secondary to stimulation by
! }& s9 O: U0 W' a5 k5 {gonadotropins.1,3; |( g/ z- t; F! Y" _
Gonadotropin-independent peripheral preco-
2 l, q! J& ]$ G, _+ [' Kcious puberty in boys also results from inappropriate
. F( \  F% |& |2 m. v% _! j7 @androgenic stimulation from either endogenous or2 \3 }! C% |4 \5 c& p4 E
exogenous sources, nonpituitary gonadotropin stim-! i5 Q: K1 o% A& {
ulation, and rare activating mutations.3 Virilizing3 R4 K& [- W" _" a
congenital adrenal hyperplasia producing excessive
3 u; C/ ]# V: gadrenal androgens is a common cause of precocious
2 W% ]8 i& W) `$ n6 Upuberty in boys.3,4' h* l1 B& k& h6 d8 F/ h
The most common form of congenital adrenal
. ?; |, U6 K* R' m$ d7 rhyperplasia is the 21-hydroxylase enzyme deficiency., e3 v' U1 c* |! S
The 11-β hydroxylase deficiency may also result in
/ c0 O$ o! g7 P6 ^. `3 f( b: d) z) l5 Y. Oexcessive adrenal androgen production, and rarely,( w3 u4 }9 y; V# [
an adrenal tumor may also cause adrenal androgen
  v% A: e1 X8 @' c7 R0 Pexcess.1,3
; c# ]" x2 X$ d7 j8 Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: F& M' T/ s5 \2 H3 ]542 Clinical Pediatrics / Vol. 46, No. 6, July 2007) m6 g0 s: V% Z; Q5 J
A unique entity of male-limited gonadotropin-
% T  a5 e% z! N" \independent precocious puberty, which is also known! L4 x) e0 u! n. w! |* L0 X  K
as testotoxicosis, may cause precocious puberty at a
/ a6 r( x5 i5 T! K' T0 L) i8 o, z4 ivery young age. The physical findings in these boys0 t( Y8 Z' o3 N7 f, }
with this disorder are full pubertal development,- d3 r- H3 d5 }5 j
including bilateral testicular growth, similar to boys
: Y9 }! F4 B- G+ M8 F( e1 bwith CPP. The gonadotropin levels in this disorder! U! @, ]) i, e: V8 o
are suppressed to prepubertal levels and do not show9 \! K; ?* f) D# s
pubertal response of gonadotropin after gonadotropin-- n; j- d% C3 F& g" H8 B1 U0 W
releasing hormone stimulation. This is a sex-linked$ [$ m- S/ T' V
autosomal dominant disorder that affects only# g! g) P! l4 n
males; therefore, other male members of the family
& I, S. {( }, W7 \1 M8 ^# a- Tmay have similar precocious puberty.3. [" p0 h, x$ ?2 i1 ?; f
In our patient, physical examination was incon-
2 y5 ]8 y' X0 D" ^- J$ n- isistent with true precocious puberty since his testi-
+ _$ p3 [/ R8 M$ x$ A9 zcles were prepubertal in size. However, testotoxicosis' _% W& p# w4 d* ^- m
was in the differential diagnosis because his father0 I6 F* U( ~0 ?8 t- r, w9 a4 C
started puberty somewhat early, and occasionally,
  e; E; }5 j- d0 }( @testicular enlargement is not that evident in the
; C. P7 j  j9 A* m. Y0 t( ~( }beginning of this process.1 In the absence of a neg-
/ g2 B2 k! z- F) Oative initial history of androgen exposure, our
6 w( F1 g$ w6 G: K/ t. nbiggest concern was virilizing adrenal hyperplasia,
! B8 Z0 c7 T# O$ peither 21-hydroxylase deficiency or 11-β hydroxylase
' T2 S5 w/ e2 _; P) Z# qdeficiency. Those diagnoses were excluded by find-
* c% P7 W6 Y3 P: r4 d6 ?ing the normal level of adrenal steroids.) E& w8 x8 C# t  {: A
The diagnosis of exogenous androgens was strongly
4 m- v$ f$ f% [- Q& D9 D$ L. Jsuspected in a follow-up visit after 4 months because1 e% x4 q9 e" U/ v# ?; n- L6 j  u
the physical examination revealed the complete disap-
* Y% g8 a( l+ E0 n5 q' D+ |pearance of pubic hair, normal growth velocity, and
  x& ~( T. }" L; h2 ^/ D$ vdecreased erections. The father admitted using a testos-
: H) g" N1 T! Q5 dterone gel, which he concealed at first visit. He was
# Y& R2 M* E5 w7 x+ f9 vusing it rather frequently, twice a day. The Physicians’
* U" p( i! v" e: |+ H. o+ wDesk Reference, or package insert of this product, gel or; {6 h( c5 t" {+ m
cream, cautions about dermal testosterone transfer to8 b9 r# A/ l# M
unprotected females through direct skin exposure.7 o1 P% G: e% B, A( Z9 O
Serum testosterone level was found to be 2 times the
+ ?$ B0 k* X5 r% ^* `+ q: xbaseline value in those females who were exposed to/ [% e( [0 u7 W1 u
even 15 minutes of direct skin contact with their male
1 w1 B1 m0 ?* O  x! b* T8 Q' E. npartners.6 However, when a shirt covered the applica-
( m; F+ X: b4 T# C3 l$ ution site, this testosterone transfer was prevented.* D8 N2 o7 }/ ]& H+ _
Our patient’s testosterone level was 60 ng/mL,
) Y7 D8 J  V/ T# H- Twhich was clearly high. Some studies suggest that' o6 I# D( a/ b% q
dermal conversion of testosterone to dihydrotestos-
/ K) z; m6 k  [7 p! Y( q7 H$ Rterone, which is a more potent metabolite, is more
# d2 `1 F0 K* `) R4 c. Kactive in young children exposed to testosterone/ ?& O$ O, H# x+ }& C
exogenously7; however, we did not measure a dihy-
- g1 u1 N& U7 g( \5 y+ n8 [drotestosterone level in our patient. In addition to
9 q# u: ~* ?7 p4 E/ ivirilization, exposure to exogenous testosterone in
) f- |4 I2 C1 S* E, cchildren results in an increase in growth velocity and
; z6 h+ N! A+ X$ }2 a1 T$ uadvanced bone age, as seen in our patient.
$ y# q1 U8 G! t$ QThe long-term effect of androgen exposure during
" @5 k0 u7 w# O0 z9 Xearly childhood on pubertal development and final$ k3 ^3 S( R. L  e- V2 |" Q
adult height are not fully known and always remain+ A) h" E, R5 }
a concern. Children treated with short-term testos-" T; L  I9 X* n( h
terone injection or topical androgen may exhibit some
: R. c. t4 [0 ]2 T6 i. racceleration of the skeletal maturation; however, after+ ]* q! p* T- B, _8 R, T: C
cessation of treatment, the rate of bone maturation; P3 i1 c2 @$ J4 x# x1 }8 E; k
decelerates and gradually returns to normal.8,98 C, }, z% B9 N( P; r+ D: l. N8 H
There are conflicting reports and controversy! v8 T) C% y- e6 S; R# P
over the effect of early androgen exposure on adult) m! n/ T0 c" k  R6 c* R7 m* @
penile length.10,11 Some reports suggest subnormal6 v8 M" ]# U7 h1 D7 T* p
adult penile length, apparently because of downreg-
1 ~( R- q* k% {' q; b, Yulation of androgen receptor number.10,12 However,
5 `- `0 `! |" L1 r$ @Sutherland et al13 did not find a correlation between$ D( u5 f: J9 U
childhood testosterone exposure and reduced adult( p% @7 ?  q8 L# b1 G
penile length in clinical studies.
5 |) P" Q( f: }Nonetheless, we do not believe our patient is* m5 [7 w2 k/ u2 l" R4 y) ^( [
going to experience any of the untoward effects from( e# o+ L- _; \3 y% e4 ~
testosterone exposure as mentioned earlier because
- `6 G: E: e0 z9 xthe exposure was not for a prolonged period of time.- b) e+ t$ d4 R
Although the bone age was advanced at the time of
( X* u, f4 ^2 y4 d! adiagnosis, the child had a normal growth velocity at
& p3 I3 `# C. n9 }the follow-up visit. It is hoped that his final adult
+ U( {. D8 J; E; L- Rheight will not be affected.: V' f& I: {7 b/ H% i1 D5 o
Although rarely reported, the widespread avail-. s- {% f3 v/ p' u  G
ability of androgen products in our society may
8 H4 k7 h+ k5 q, K. Zindeed cause more virilization in male or female
: D7 ~/ j8 x* j! O& O- achildren than one would realize. Exposure to andro-) X7 {! G2 e" B4 N( x& C9 w
gen products must be considered and specific ques-& `( ~; C  A* G5 Q% ]1 R; R; V, k; S
tioning about the use of a testosterone product or6 m. Z& n$ Y- `3 J1 S7 o- t! X/ }- @
gel should be asked of the family members during
! n  l& R8 y& Sthe evaluation of any children who present with vir-& @- p/ P7 t5 p/ W. S0 [) f* l
ilization or peripheral precocious puberty. The diag-3 \# N' P, w3 ?8 a- Y- c
nosis can be established by just a few tests and by
) M# q& g" ^1 _  z  W: t( Uappropriate history. The inability to obtain such a
0 P1 N0 Y1 i" Jhistory, or failure to ask the specific questions, may
( v* f! |+ B, M5 n, R& Z! W  eresult in extensive, unnecessary, and expensive4 c( C( L4 q$ d3 b
investigation. The primary care physician should be4 m4 }( W  W, J+ D5 k
aware of this fact, because most of these children9 F1 z, k9 J: O7 p. O9 p
may initially present in their practice. The Physicians’
) {2 h" x7 Z8 _) }Desk Reference and package insert should also put a% k/ u& `2 {3 I7 m
warning about the virilizing effect on a male or+ f' p5 a" ~' ^/ N6 x
female child who might come in contact with some-
) S( X: L/ a6 E5 Vone using any of these products.- g! S+ v" c* Y/ s
References( [3 L% ?% j7 f; \$ p; s
1. Styne DM. The testes: disorder of sexual differentiation- f" [5 p1 Z& H$ {5 W. a( o
and puberty in the male. In: Sperling MA, ed. Pediatric
+ H7 j  Q8 m8 ]7 _$ R+ P9 pEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
2 p! b8 f7 |6 e2002: 565-628.
! n3 h" c; [$ t/ f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
5 t+ [" m0 m$ M: N, f) F) npuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
8 m5 S' r4 c$ y) ~- }1 Z7 iBoy Induced by Indirect Topical/ g% _2 v3 l* {# u' I
Exposure to Testosterone5 e1 b# M4 v4 G- P
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 J) U! u# h  Y5 t% h  gand Kenneth R. Rettig, MD1
/ q+ h9 ]5 _0 }6 u/ W+ h, R5 BClinical Pediatrics
* j. l5 S/ y0 m/ }, @6 `# D# G  P; LVolume 46 Number 6
1 j* s$ o- ]  m+ ]8 W4 hJuly 2007 540-543
: r; A6 {" J  `3 |0 q© 2007 Sage Publications
% N8 z/ v( R; n$ {10.1177/0009922806296651
7 L0 w; D* Q* \" @  L% ^http://clp.sagepub.com. R; Q8 {: J9 L- c
hosted at
$ D8 E* p6 x7 }3 u$ A4 ]( W% ghttp://online.sagepub.com: f* k- ^) U/ x  ?/ J) `8 A
Precocious puberty in boys, central or peripheral,; ^. K9 i' G  A3 A9 t1 {  B
is a significant concern for physicians. Central( F& q; V6 F; [5 H. t5 T8 P
precocious puberty (CPP), which is mediated
/ N5 O% U; j: h# }# |through the hypothalamic pituitary gonadal axis, has6 H$ o' H$ d4 U7 H; g
a higher incidence of organic central nervous system0 ]1 c/ a( W1 Q/ c  i/ C
lesions in boys.1,2 Virilization in boys, as manifested3 L3 v$ z, i- |* H, b; S
by enlargement of the penis, development of pubic& X7 a6 R) p; F
hair, and facial acne without enlargement of testi-! ^9 O; P# R$ `+ n( V. J- l3 t
cles, suggests peripheral or pseudopuberty.1-3 We
6 o! U. O! H! f! g7 ]6 @: f% E9 E" z" ereport a 16-month-old boy who presented with the3 y4 g6 t1 `2 E% M' m% W$ C
enlargement of the phallus and pubic hair develop-% ~% z* I  m) c( k  V$ ~
ment without testicular enlargement, which was due
: ^  V4 P+ S1 c" c/ Jto the unintentional exposure to androgen gel used by1 _4 n3 q5 P* {' W8 x9 a
the father. The family initially concealed this infor-
$ |+ m* N6 l% _0 d" ?5 o* n; ]: \mation, resulting in an extensive work-up for this  S  j7 H; M) T: ]- i
child. Given the widespread and easy availability of
% L7 G+ \5 u, e4 q1 E0 ltestosterone gel and cream, we believe this is proba-( A2 r% {6 Y4 d- Y9 l8 M
bly more common than the rare case report in the6 d. n1 ^' Y4 A  n" D" y8 Q
literature.4
1 v0 @: t; T* F) PPatient Report1 N- h! t/ ]  O- J& d/ {9 G% F
A 16-month-old white child was referred to the% K4 V: z) b5 a) e, r$ K: c* V
endocrine clinic by his pediatrician with the concern
/ S# y. T: M% R2 wof early sexual development. His mother noticed
4 h6 r+ L; Y, k9 s- Q0 Qlight colored pubic hair development when he was
7 W7 T' @) o2 X; aFrom the 1Division of Pediatric Endocrinology, 2University of
$ \) M. z; D0 i6 d* S1 KSouth Alabama Medical Center, Mobile, Alabama.2 E) n4 F! ?) N- `1 u  o
Address correspondence to: Samar K. Bhowmick, MD, FACE,
, _, w# @  L; Y( M. p; }! zProfessor of Pediatrics, University of South Alabama, College of0 `& L& ]" t8 m2 p% r( M
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; o" l8 c: i1 q# J3 _9 G6 g! Q8 ?
e-mail: [email protected].
. l! I+ V$ Y3 Yabout 6 to 7 months old, which progressively became5 D% n" l/ O* t6 H  @
darker. She was also concerned about the enlarge-
8 I: ~! t& j$ d9 e( Zment of his penis and frequent erections. The child
( N" x0 ~# C) f3 R! Swas the product of a full-term normal delivery, with/ u- Y+ [; I5 x4 q
a birth weight of 7 lb 14 oz, and birth length of( p7 |, F- Q% `7 M6 Z% [- H
20 inches. He was breast-fed throughout the first year
7 H, z! d2 L% _of life and was still receiving breast milk along with
1 ]2 `6 d) _$ t  `/ e3 v7 [solid food. He had no hospitalizations or surgery,5 U6 ~/ p6 P6 d
and his psychosocial and psychomotor development% e  y* d% L. g" V7 M* f5 p
was age appropriate.$ W$ J  t  m% I* _
The family history was remarkable for the father,: a3 m/ h" b- d, ^- s* X
who was diagnosed with hypothyroidism at age 16,
$ ]* X5 g$ B$ n' y$ G6 ~* r+ n$ z- H5 wwhich was treated with thyroxine. The father’s& J! U, g- ]3 G
height was 6 feet, and he went through a somewhat$ ^  t! t" p3 q% v
early puberty and had stopped growing by age 14.6 e0 S' g' }' t' c$ @: }
The father denied taking any other medication. The
. {6 w2 C8 w% C, s% ^$ rchild’s mother was in good health. Her menarche
% q3 @) R( ]* L* s$ W8 }was at 11 years of age, and her height was at 5 feet
! {8 n- C3 M4 c: a/ e+ S( f. O8 K5 inches. There was no other family history of pre-
. Q; L3 {- E3 ?$ L* ]9 u, D# dcocious sexual development in the first-degree rela-
. T: y1 n; |. Q/ K5 g- P& J  M* otives. There were no siblings.0 W! a+ }: q8 G) Y  z6 q
Physical Examination
7 w2 h- u# F4 a: fThe physical examination revealed a very active,
1 ]1 l, |2 L4 A. Q1 z$ g- J. zplayful, and healthy boy. The vital signs documented( `  n0 y3 |9 q$ U+ F
a blood pressure of 85/50 mm Hg, his length was
4 ?, w6 |5 C; M- ~: O90 cm (>97th percentile), and his weight was 14.4 kg
9 S: a6 j) q* @2 O1 j8 }(also >97th percentile). The observed yearly growth8 ~- [3 X3 Q5 W1 F7 c
velocity was 30 cm (12 inches). The examination of7 R: J  I% d: o
the neck revealed no thyroid enlargement.7 X  R  @0 i; Y8 h" |; l3 C2 ?
The genitourinary examination was remarkable for
# R6 f/ H0 e% |- H/ b. P8 g3 z4 ]enlargement of the penis, with a stretched length of
5 w3 V3 e1 `- D8 O8 cm and a width of 2 cm. The glans penis was very well
3 v2 M0 B' p( Mdeveloped. The pubic hair was Tanner II, mostly around3 Q* _7 V) }/ O: h% v: J, ^: u
540( l& O. T: ~( C4 r; f4 j  E4 f! d
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the base of the phallus and was dark and curled. The, a; f8 e+ l( d& z; R
testicular volume was prepubertal at 2 mL each.& ]7 D  R, `8 R( `, n" {3 z* d
The skin was moist and smooth and somewhat
( f% q+ a& p/ V, e$ hoily. No axillary hair was noted. There were no0 d; T" p- [3 M8 g2 C, p; P
abnormal skin pigmentations or café-au-lait spots.% ]" a% T+ J. O& L- \. z
Neurologic evaluation showed deep tendon reflex 2+
0 N$ h7 o7 t* ?  ?bilateral and symmetrical. There was no suggestion* J3 _2 `  c# N( v0 V% f
of papilledema.
! q/ }) f% q( f1 }9 b8 L; I" zLaboratory Evaluation
4 c6 T3 n. Q. l' [6 i2 \5 ZThe bone age was consistent with 28 months by
$ ?# _* h1 c; a; D: s1 }using the standard of Greulich and Pyle at a chrono-, l3 ^8 d, t( ?; t; s
logic age of 16 months (advanced).5 Chromosomal
* S! i; ?1 |7 V/ Ykaryotype was 46XY. The thyroid function test( ^# b9 u% ^+ p) T  p
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, b: h( V& ?+ B: V3 B' ~- ]) O
lating hormone level was 1.3 µIU/mL (both normal).
/ ?- \* x: V  r1 j* s" g0 _8 b1 I  [The concentrations of serum electrolytes, blood
' |2 X* g8 z* @4 nurea nitrogen, creatinine, and calcium all were+ k: p& H& v% I' N% I
within normal range for his age. The concentration) u/ l# [9 m$ m1 t. K9 f+ x
of serum 17-hydroxyprogesterone was 16 ng/dL& q$ s; Q9 z' |( W( w: x
(normal, 3 to 90 ng/dL), androstenedione was 20
# i  c: |1 _- c& i9 P8 Z" cng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
( e2 l' T5 o; m3 cterone was 38 ng/dL (normal, 50 to 760 ng/dL),8 b6 s5 C. v/ y' Y* f/ A1 _
desoxycorticosterone was 4.3 ng/dL (normal, 7 to7 Y. B0 f" b0 J% v. a0 Y7 S
49ng/dL), 11-desoxycortisol (specific compound S); ]- ~' `/ `3 S! c0 M
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
. P- q% L. \. B" _/ h6 h* T% ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 K& W1 |% v# Y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
: [) G( L3 y, }0 w6 kand β-human chorionic gonadotropin was less than
" c* \/ ]' N" |5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 x5 W; O' @# G: V$ S) e. cstimulating hormone and leuteinizing hormone
& \: |* R7 B2 m9 Z- gconcentrations were less than 0.05 mIU/mL2 N: C% |! k0 j3 g1 @0 j. L4 j
(prepubertal).( D1 B% N( H/ ]- S4 n, |% K
The parents were notified about the laboratory/ N" [# _% _: o3 O+ t# z
results and were informed that all of the tests were
$ T! M  X5 J0 \normal except the testosterone level was high. The! V0 m& ~3 M: A9 R
follow-up visit was arranged within a few weeks to: e' t+ t) F$ a$ f1 a  ]# Y/ _* i
obtain testicular and abdominal sonograms; how-
5 l; i! ?3 s/ q  aever, the family did not return for 4 months.
) i% [) S  p3 `' kPhysical examination at this time revealed that the7 L$ @, r( \  s8 }3 I) u7 U2 T
child had grown 2.5 cm in 4 months and had gained+ v* d0 ^  B" ?7 R6 o, {4 ~9 A2 B
2 kg of weight. Physical examination remained3 k* G0 e- n& r+ \- i6 I; o7 h; _0 F; K
unchanged. Surprisingly, the pubic hair almost com-. L3 j% H: R3 z: i
pletely disappeared except for a few vellous hairs at) A. W% C- W5 e9 S5 J9 Q/ D
the base of the phallus. Testicular volume was still 2
, d+ ]! d$ g1 d; ?' R8 C: zmL, and the size of the penis remained unchanged.; j: N! c/ E& O; w7 e
The mother also said that the boy was no longer hav-
, G; c: l! p. H# C4 x6 m3 jing frequent erections.
, Q0 a3 ^, b- u& `Both parents were again questioned about use of
2 L! s+ y- c3 a7 ?& xany ointment/creams that they may have applied to
$ b( o  n9 w$ Y3 e8 I4 @" T* M+ U8 v2 Lthe child’s skin. This time the father admitted the+ ?/ x7 @0 L6 P# V3 i
Topical Testosterone Exposure / Bhowmick et al 541& L1 ^0 n/ A; ?/ l1 a! F- C1 P) r) b
use of testosterone gel twice daily that he was apply-
2 K; g  a7 g% Uing over his own shoulders, chest, and back area for& l! }* r! n6 ?, e: _
a year. The father also revealed he was embarrassed
' x% O9 O* J+ f' }0 f1 ato disclose that he was using a testosterone gel pre-
1 f6 H! g( E; T8 ascribed by his family physician for decreased libido3 H6 h- U, Q4 f2 ~) `2 g1 P0 j: v
secondary to depression.
  A* O! p* B; E  UThe child slept in the same bed with parents.: F% ?/ N& {9 w' _' ]* W! E0 U! M
The father would hug the baby and hold him on his
# }+ q3 l( N/ m- Dchest for a considerable period of time, causing sig-9 I' Y# P# O3 }1 w7 F' }' O
nificant bare skin contact between baby and father.
7 m" q4 F6 o! g0 T1 DThe father also admitted that after the phone call,
# x' }& r+ B; d1 \when he learned the testosterone level in the baby$ O7 m1 g( r4 e- S9 O
was high, he then read the product information
: U+ B; D7 w" C% R, Rpacket and concluded that it was most likely the rea-: H" s0 c6 U, `' Q
son for the child’s virilization. At that time, they/ u% @2 `7 e* R: @& j: x
decided to put the baby in a separate bed, and the
2 w" ~! s8 ?& O& Bfather was not hugging him with bare skin and had# X0 N( q! n7 v0 `) F) o
been using protective clothing. A repeat testosterone
+ i* @" M% F# Y1 Z; ~test was ordered, but the family did not go to the, f: d' K7 `* f
laboratory to obtain the test.
3 Q% d# G! y: |/ _  J7 ~Discussion
: ]' y. W) m; P# ]- T* |Precocious puberty in boys is defined as secondary6 Y0 C& V4 ?2 q# }: n- p+ o% A
sexual development before 9 years of age.1,4' h/ G2 r3 `& ^! \7 I  e) T
Precocious puberty is termed as central (true) when
0 P4 R9 M4 t( U0 C. kit is caused by the premature activation of hypo-" U" ^. t( y* R: F$ S
thalamic pituitary gonadal axis. CPP is more com-
! F5 A3 D2 ^6 ?' ]2 Cmon in girls than in boys.1,3 Most boys with CPP8 b3 Z( i1 t& D; q
may have a central nervous system lesion that is
& i# }" D) ]4 ^responsible for the early activation of the hypothal-  S) Y" Q; @6 `2 E7 t
amic pituitary gonadal axis.1-3 Thus, greater empha-
5 @$ Z: b3 p8 o; ?sis has been given to neuroradiologic imaging in" D& W* M1 m: b/ ~  y% G$ _5 V, W
boys with precocious puberty. In addition to viril-
) B1 h0 Z/ B" {5 U  d6 ^ization, the clinical hallmark of CPP is the symmet-
8 M. W, A% a" j+ {  C9 ~3 I: Q; prical testicular growth secondary to stimulation by9 Z9 _1 {) G2 M- t# d
gonadotropins.1,3
- N' t0 K# M! p/ N" OGonadotropin-independent peripheral preco-
* {' e" X7 ^. hcious puberty in boys also results from inappropriate
" d+ U9 }3 X5 Wandrogenic stimulation from either endogenous or0 R- @8 d- O& w7 A& v2 j
exogenous sources, nonpituitary gonadotropin stim-
: f# w$ @3 n/ c7 H3 Gulation, and rare activating mutations.3 Virilizing. W. j2 W& C6 y
congenital adrenal hyperplasia producing excessive5 \# j1 }8 N2 F6 C" ^
adrenal androgens is a common cause of precocious' x1 q  ?3 u' b( }' R& m( w
puberty in boys.3,43 {. l, d$ p1 \6 u! Z& Y6 Z
The most common form of congenital adrenal# K; S! l% o$ |7 t" p9 o
hyperplasia is the 21-hydroxylase enzyme deficiency.8 Z0 \8 z( D; V( W
The 11-β hydroxylase deficiency may also result in
+ c' U! M4 i- W  H% K, ~excessive adrenal androgen production, and rarely,
/ F' w# f5 k/ G: w% van adrenal tumor may also cause adrenal androgen  ~5 H8 U2 w* F* R5 g" _, ]
excess.1,3" Q0 s5 C2 G1 }3 e6 @0 }' R4 F
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 F1 B/ F6 v4 b0 N- _542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: ^7 r! m9 g9 E, Q) W( L- Y
A unique entity of male-limited gonadotropin-' z; F" M( j1 p
independent precocious puberty, which is also known
! u, F; w( Y. ~" kas testotoxicosis, may cause precocious puberty at a
1 \/ a& y3 S) C4 k" every young age. The physical findings in these boys
$ d. n" w$ b  ?: j" q) B) E: t; d+ {with this disorder are full pubertal development,% a, k5 R, j- ~2 @" z9 x$ b+ u
including bilateral testicular growth, similar to boys
, m3 k/ Q6 M7 @$ r# iwith CPP. The gonadotropin levels in this disorder* r$ U$ Y, n  ^, n! \# k
are suppressed to prepubertal levels and do not show
% q8 L, `: h+ N6 [% @, opubertal response of gonadotropin after gonadotropin-4 @  j! `+ @( h, X- f: t8 w
releasing hormone stimulation. This is a sex-linked2 w, ~' f' ?4 `  v. X
autosomal dominant disorder that affects only# p. V: _5 a. i
males; therefore, other male members of the family
+ {( F6 }$ c* p9 Gmay have similar precocious puberty.3: o# D  K. S2 G) }( {: {; B
In our patient, physical examination was incon-7 E* Q$ e; o0 V5 b, v
sistent with true precocious puberty since his testi-
% {. B5 ^' b2 i, d, ^; Kcles were prepubertal in size. However, testotoxicosis
+ t  ^/ d( X* v- C4 ewas in the differential diagnosis because his father; e/ [! V* e( x0 t! F
started puberty somewhat early, and occasionally,
& y& N+ m8 W: S- d+ |  U" ]6 Wtesticular enlargement is not that evident in the/ [; G3 z( `, K' q! W. t3 j2 Y- d5 @
beginning of this process.1 In the absence of a neg-% Y5 Y+ `: m7 P0 |6 }0 I- J
ative initial history of androgen exposure, our
" j5 G! A/ \7 C  gbiggest concern was virilizing adrenal hyperplasia,
2 j) E) o8 @5 O, j) i8 S) I1 Heither 21-hydroxylase deficiency or 11-β hydroxylase2 l' X, O! a0 P5 M  n
deficiency. Those diagnoses were excluded by find-: v: X: S8 q) a1 |
ing the normal level of adrenal steroids.7 \- n( H* z* \$ `8 A+ Q
The diagnosis of exogenous androgens was strongly
5 g5 Y4 _. ~/ {- w: Ksuspected in a follow-up visit after 4 months because
3 Z8 t3 H7 a, [& Z$ athe physical examination revealed the complete disap-
  [( [) P# m( m! x9 T6 `pearance of pubic hair, normal growth velocity, and: a* _. c& Z! `. x' B; C9 I3 m
decreased erections. The father admitted using a testos-
; b3 @; C( H& E. I0 F! zterone gel, which he concealed at first visit. He was" Z; `& Y1 N% D4 A/ R3 i  A
using it rather frequently, twice a day. The Physicians’
4 E9 A% Y7 H5 Z! R; y! p) pDesk Reference, or package insert of this product, gel or
6 Z2 [. {* u" W& J4 m- r0 }cream, cautions about dermal testosterone transfer to0 A# Y3 m" x" J! X; Q  N
unprotected females through direct skin exposure.. l0 _& E5 u2 ~$ S' u! _1 t- a0 V
Serum testosterone level was found to be 2 times the
  P" p$ t- e% z) ^! \baseline value in those females who were exposed to
+ e) Q( E3 @/ p0 S& m# ^1 Eeven 15 minutes of direct skin contact with their male
" U* q* g, i) r! v+ ]" g' dpartners.6 However, when a shirt covered the applica-
# p; j  N% Z6 U6 U1 Ftion site, this testosterone transfer was prevented.
% ^3 y7 @3 f2 B: G9 q( O- @1 mOur patient’s testosterone level was 60 ng/mL,7 W  j2 ]; G1 v/ c; Z( x( t: C. q) V
which was clearly high. Some studies suggest that9 ^5 I1 X. o  A; w; t3 \& L
dermal conversion of testosterone to dihydrotestos-
$ B+ n  m7 H+ Uterone, which is a more potent metabolite, is more7 s0 c5 p0 u9 G+ @; H/ K
active in young children exposed to testosterone: M$ F& p7 s3 P/ d# {" _0 a
exogenously7; however, we did not measure a dihy-" e: _+ i+ o" |
drotestosterone level in our patient. In addition to# c9 L, ?2 d( }$ g- E2 S5 W1 }
virilization, exposure to exogenous testosterone in# Y9 e1 y5 x* x6 i1 k- |  d
children results in an increase in growth velocity and! b9 O+ _" g* e; c1 @
advanced bone age, as seen in our patient.. b% N5 Y9 c9 `
The long-term effect of androgen exposure during( \& W; |- m; a5 C
early childhood on pubertal development and final8 z& C3 Y2 p" Y' ?1 l( ~/ C! s
adult height are not fully known and always remain
9 E6 U3 o- K+ ^. y& p9 Q* `a concern. Children treated with short-term testos-
1 \1 l* q. h. s5 f2 X, eterone injection or topical androgen may exhibit some1 U6 P' `6 h1 n* I
acceleration of the skeletal maturation; however, after, G" ?- C  T, O! G5 ]3 [
cessation of treatment, the rate of bone maturation* J% B  P: n; K- G0 @
decelerates and gradually returns to normal.8,9
0 D' @: l' c6 C( T$ @" l9 PThere are conflicting reports and controversy' H& ~  ]& [; V+ a$ v
over the effect of early androgen exposure on adult
  e7 }3 _7 ?/ r  i( fpenile length.10,11 Some reports suggest subnormal
) }2 s& Y, u: w+ a' R) e7 ^adult penile length, apparently because of downreg-$ Z& k9 P) V- S6 G) J9 G  H
ulation of androgen receptor number.10,12 However,% z7 |/ r& U! w# `/ i: U
Sutherland et al13 did not find a correlation between! `. }8 e7 {+ W- b/ ~% R7 o
childhood testosterone exposure and reduced adult# K. F7 b. k& C2 E9 a/ m
penile length in clinical studies.  K1 C" T* O4 ]7 D4 _+ C6 ^5 Y" b
Nonetheless, we do not believe our patient is
2 l* a- u& {- d7 b! L9 H0 Pgoing to experience any of the untoward effects from% x) o  ]8 n% i$ Y) R- W2 \- e1 |
testosterone exposure as mentioned earlier because
0 b+ u! [' ]! v& v+ qthe exposure was not for a prolonged period of time.$ M2 i6 l% N9 i  B. t! j
Although the bone age was advanced at the time of
% y1 U, b3 R. O2 O" [9 `% N% |! f5 Ldiagnosis, the child had a normal growth velocity at
4 D; u! G, E, T7 Q* Y$ Ethe follow-up visit. It is hoped that his final adult
, q! @7 x, ~, J% Qheight will not be affected.4 \) U9 h4 J# J. ^
Although rarely reported, the widespread avail-8 P5 I, I& Z# t; `5 l
ability of androgen products in our society may2 M! ?# a3 X* J
indeed cause more virilization in male or female
* @9 F9 h3 A9 {! _) h; |- Uchildren than one would realize. Exposure to andro-
6 T5 r. P- y1 v6 p6 Z5 p( H7 wgen products must be considered and specific ques-( B- `: F6 T% s3 O
tioning about the use of a testosterone product or
* W0 Q# n8 {& R" T; Kgel should be asked of the family members during  A' V, |* R5 f
the evaluation of any children who present with vir-' a, J, M0 p6 S9 |
ilization or peripheral precocious puberty. The diag-
3 ]  p+ I! |# f% \- ^5 S0 bnosis can be established by just a few tests and by
: l2 L( P, k$ r7 [7 S, gappropriate history. The inability to obtain such a
! a2 U8 Z  V: P6 i2 S! P& J; Yhistory, or failure to ask the specific questions, may
7 K, U2 O+ S' u+ f) h" c; yresult in extensive, unnecessary, and expensive2 y/ R0 [: S' W+ w1 ^7 T
investigation. The primary care physician should be4 P, ~3 f3 V; f# R- m
aware of this fact, because most of these children
  E  x5 z: w2 {1 f: V" mmay initially present in their practice. The Physicians’
; l5 C( M7 U- s  ~: {3 tDesk Reference and package insert should also put a& D7 @; l0 }. h. O* K
warning about the virilizing effect on a male or5 a. Y! [% B: v% ~
female child who might come in contact with some-4 v( E' A9 M* C1 E, b
one using any of these products.
1 V+ b. A6 A5 P( M7 I& @0 \References' w+ s" \3 V+ M
1. Styne DM. The testes: disorder of sexual differentiation
+ ^" M4 U' Q0 m4 l% O( r2 Q2 Aand puberty in the male. In: Sperling MA, ed. Pediatric
8 A" m4 E1 o+ n& N5 e2 ~Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) M$ c) J  m: _0 O/ c
2002: 565-628.
) m# X, c8 v/ E+ _2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% U3 }) h& U5 i" spuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
+ X3 x- z: v9 s+ y0 V
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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