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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
) n0 o; J2 y# A& ?9 UBoy Induced by Indirect Topical
# z+ i# o) b, F8 s0 p( uExposure to Testosterone) I/ c9 U1 m5 b/ j, p) k4 C
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
- F2 S, c1 B; g0 r. jand Kenneth R. Rettig, MD1
0 P. A. U, M- P1 n  lClinical Pediatrics
; }8 b  `( L* a. {+ {$ h' RVolume 46 Number 6
. l0 U) k$ o6 u: DJuly 2007 540-5432 M! \4 w  @! g  r
© 2007 Sage Publications
1 S! E4 r" Z- Y7 x% o10.1177/0009922806296651
0 _1 B2 }+ `1 N6 }- L, z0 U! ^8 P# t8 lhttp://clp.sagepub.com
- H3 v2 v8 V, Z$ {. H( Mhosted at
& H5 r" S  ?$ j* r9 x9 G2 Q9 V" Z$ Dhttp://online.sagepub.com7 u  [; c: U2 Q/ i6 w
Precocious puberty in boys, central or peripheral,
: [- S5 N' Z2 b, h5 His a significant concern for physicians. Central% O5 X) D% A5 L4 ^3 w# |/ p
precocious puberty (CPP), which is mediated8 Z/ u1 c% Z0 w
through the hypothalamic pituitary gonadal axis, has
" D; Z3 H, j9 o7 ^- j' ~3 ]( T  {9 [a higher incidence of organic central nervous system. F) [* d1 x5 u. {2 `6 K' H
lesions in boys.1,2 Virilization in boys, as manifested
; F  W7 d% g# F* dby enlargement of the penis, development of pubic
8 C: G0 C( @6 Ghair, and facial acne without enlargement of testi-( m* L/ u% u6 Q* ^% e7 Z
cles, suggests peripheral or pseudopuberty.1-3 We" U: m: M4 b* w4 R
report a 16-month-old boy who presented with the- _( N  o) m& |. E1 P0 X' r+ E
enlargement of the phallus and pubic hair develop-1 E" ~, e4 S3 r2 j$ c) ]; |. r- F
ment without testicular enlargement, which was due8 d/ O: s6 d6 @
to the unintentional exposure to androgen gel used by0 L$ P! y- T; f! @6 j/ {
the father. The family initially concealed this infor-/ Z2 x# }9 j" U: w& k
mation, resulting in an extensive work-up for this0 b6 h( q& C% i2 R3 K/ o$ W
child. Given the widespread and easy availability of
: ]' g+ d! K  i! \5 etestosterone gel and cream, we believe this is proba-
1 R* r" e1 H) X& j. rbly more common than the rare case report in the' ~& S1 s' H& _
literature.4
$ \9 q+ w  T6 o/ y) {Patient Report
" z4 I# P; ~6 r# L/ q6 G8 I" vA 16-month-old white child was referred to the, s( T% h/ w: n' \/ b! \
endocrine clinic by his pediatrician with the concern& N8 x# r. X* h# u0 c; g2 o
of early sexual development. His mother noticed
" T, i. p$ e+ a9 s: l# Tlight colored pubic hair development when he was7 V2 @+ W  K' C! E) r1 j( V, X7 m6 T
From the 1Division of Pediatric Endocrinology, 2University of
4 b. t) B7 `- |9 {# b8 U6 WSouth Alabama Medical Center, Mobile, Alabama.: y) |: J" y, Q7 T- K7 f0 v
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 _) ?' k$ I8 Z& ZProfessor of Pediatrics, University of South Alabama, College of) L4 Y" e8 V' o, {0 S
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 W4 n6 g* H/ J0 @e-mail: [email protected].$ s8 K9 i' t  X# O  p" ?- b- d
about 6 to 7 months old, which progressively became: u% Z3 Q3 e; Q9 Q  }- j- W
darker. She was also concerned about the enlarge-5 F0 E) U4 ]% v
ment of his penis and frequent erections. The child) P: F, p7 h$ T+ O! [2 r+ w
was the product of a full-term normal delivery, with
# Y4 X( w. o1 F2 }1 M+ Ha birth weight of 7 lb 14 oz, and birth length of
' m7 |9 m6 w2 V. Q4 y20 inches. He was breast-fed throughout the first year! e9 O% X1 i# o, N7 c1 |
of life and was still receiving breast milk along with1 b, {, e. M8 y+ t
solid food. He had no hospitalizations or surgery,
% Z' \% ~+ }" Q1 n. r/ eand his psychosocial and psychomotor development% y& z0 Q8 ^/ l+ r$ y! d' S) x
was age appropriate.
) @6 A/ g8 m2 cThe family history was remarkable for the father,
6 m$ r% l; s3 |( y  F' lwho was diagnosed with hypothyroidism at age 16,
  d. ^5 f' E4 _: c' t' Q2 [) Hwhich was treated with thyroxine. The father’s
2 g( p7 u. V. R* l9 Uheight was 6 feet, and he went through a somewhat
. v$ f( V* N' P6 x+ o" uearly puberty and had stopped growing by age 14.
/ u( b8 W! w0 G% d9 wThe father denied taking any other medication. The
7 c2 H6 \* e; s- h6 m- t# Kchild’s mother was in good health. Her menarche
& c$ k' d: ?7 J. {was at 11 years of age, and her height was at 5 feet
/ t$ |+ D2 P3 y& m) G" |$ Z/ ~5 inches. There was no other family history of pre-
$ A9 \: J  N( |7 J9 Y2 ?$ tcocious sexual development in the first-degree rela-
/ M- u  j) J( m% s* c' p+ ^tives. There were no siblings.* k) f3 K' Y  o/ k! x
Physical Examination* T) V  l1 M5 ^! ~" d& V
The physical examination revealed a very active,* M8 P" t4 h# x$ R* q
playful, and healthy boy. The vital signs documented
- T$ t" F, W; E6 g5 l  p  Y) H8 }a blood pressure of 85/50 mm Hg, his length was
0 J3 S/ L" w/ |. c( O90 cm (>97th percentile), and his weight was 14.4 kg. U6 h; p: q1 y; V- Q$ N0 u
(also >97th percentile). The observed yearly growth0 @* b$ G+ l* ]3 a. P  g, w% N
velocity was 30 cm (12 inches). The examination of
% c' h% ?0 ^5 W& Z% n2 Gthe neck revealed no thyroid enlargement.
% v4 S8 g/ R6 rThe genitourinary examination was remarkable for
6 J0 ^9 ^- e: I+ n+ Nenlargement of the penis, with a stretched length of/ N0 }" a4 W. n
8 cm and a width of 2 cm. The glans penis was very well
$ \. p, P4 }8 C0 Ideveloped. The pubic hair was Tanner II, mostly around
' I; h0 Q4 h3 e7 X/ U! F# G540
+ ~- ~# ^: K  N4 o- iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# B* @6 v4 d' l- ^# E! p9 L$ U" B
the base of the phallus and was dark and curled. The! H2 a6 Z3 d" z! d" ?
testicular volume was prepubertal at 2 mL each.
, w  I! O  g# `9 k! WThe skin was moist and smooth and somewhat
8 c! t- |, H2 Z) O  O& Ioily. No axillary hair was noted. There were no
( }) r9 c, }# {0 |9 U# w( G3 |, ~abnormal skin pigmentations or café-au-lait spots.
0 I4 F8 M8 d" J* fNeurologic evaluation showed deep tendon reflex 2+
5 F' e5 P# y9 T' W/ S& zbilateral and symmetrical. There was no suggestion
, P) L5 W+ q- D; o5 S: A- m& xof papilledema.
7 O- V& H& B' c& eLaboratory Evaluation' \  e- b+ i( n) j0 q+ v
The bone age was consistent with 28 months by7 j  ^$ |& C! I) X. I. v: b# S  R
using the standard of Greulich and Pyle at a chrono-2 U0 M8 @" W+ l, R
logic age of 16 months (advanced).5 Chromosomal1 W" [/ d  D$ g+ t) F
karyotype was 46XY. The thyroid function test1 f0 O( X$ E( d$ }, l/ C7 G7 l2 S
showed a free T4 of 1.69 ng/dL, and thyroid stimu-$ {6 T) s" l$ U" G/ J$ [
lating hormone level was 1.3 µIU/mL (both normal).
2 H: ?  f% k4 J$ w7 k( `, D7 BThe concentrations of serum electrolytes, blood
+ r- H" W2 k* t( f8 k& p+ ]urea nitrogen, creatinine, and calcium all were- Y! _3 b6 l3 R
within normal range for his age. The concentration
# v* A- e- O$ o) b9 G' Aof serum 17-hydroxyprogesterone was 16 ng/dL
$ f" s* z. V% j) s; \(normal, 3 to 90 ng/dL), androstenedione was 20
  Y, n  \$ A% t4 ?* ~ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 b3 y6 ?4 ]* j4 D" C: |
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' ]# \3 P5 V) g0 @: v2 b! l
desoxycorticosterone was 4.3 ng/dL (normal, 7 to2 z$ h; k* G- |
49ng/dL), 11-desoxycortisol (specific compound S)7 V5 Q) m0 v6 C% ^% |6 |, l& m1 g
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
  s2 f, }& ^% |8 A+ v0 n7 [4 t2 ]6 @tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 B8 d- w8 q  O  _
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, I* W# I7 G7 K% }7 i
and β-human chorionic gonadotropin was less than/ b& |4 f  |' [0 t9 o4 l  A3 i
5 mIU/mL (normal <5 mIU/mL). Serum follicular( J6 t3 S4 n; E7 f2 o5 F& D% ^, ]: P# B
stimulating hormone and leuteinizing hormone
- @3 [0 V4 H+ V9 i' Lconcentrations were less than 0.05 mIU/mL
0 u4 Y" u$ R1 C$ q, h) P(prepubertal).9 k% Z( D* N5 Q! v8 y/ Z2 M5 a. M; \: K
The parents were notified about the laboratory( f- c# e9 F* s# W/ d
results and were informed that all of the tests were
1 ~+ \- l0 u& ~7 xnormal except the testosterone level was high. The
7 y. v8 ]% F6 g$ R* g& ]% Hfollow-up visit was arranged within a few weeks to
# r3 n" A5 N- e3 v! J, nobtain testicular and abdominal sonograms; how-
% i0 D- o6 V2 c+ K4 s& zever, the family did not return for 4 months.8 L) G8 `) q# N4 |) m* [9 J, x
Physical examination at this time revealed that the4 l" `8 r9 P7 E( }+ ^9 o
child had grown 2.5 cm in 4 months and had gained
% b% L. O8 K8 q5 e5 [2 kg of weight. Physical examination remained" F$ z' Z6 g% ^* t: `4 ?0 f9 E
unchanged. Surprisingly, the pubic hair almost com-. ?$ h$ H( G* n
pletely disappeared except for a few vellous hairs at
* D" n- Q( J- F8 mthe base of the phallus. Testicular volume was still 2
+ ^+ v! ~9 _" N1 x" o" {0 dmL, and the size of the penis remained unchanged.. t" p$ e' v6 {3 b' {' r1 ~  |
The mother also said that the boy was no longer hav-" G# A; q" z3 o4 U4 k) ?
ing frequent erections.) Q# k; o0 I9 ~: c* ~, X& [* U
Both parents were again questioned about use of5 a' m/ |$ e5 A+ V' |
any ointment/creams that they may have applied to5 |, C$ J$ ~1 R
the child’s skin. This time the father admitted the# q( f/ n2 L* U& q/ n
Topical Testosterone Exposure / Bhowmick et al 541, r0 a2 F) L; ]9 T# d
use of testosterone gel twice daily that he was apply-
. z0 Q/ A$ }4 n2 A# A( Cing over his own shoulders, chest, and back area for
# U: _: S) N9 t: b& i9 Y- |a year. The father also revealed he was embarrassed
3 d: q4 f8 s# A& rto disclose that he was using a testosterone gel pre-
! F! {! Z* ]% rscribed by his family physician for decreased libido8 Q2 \! I5 b, n0 _; q
secondary to depression.
* J8 s9 R8 I, O# A: tThe child slept in the same bed with parents.% [! a8 \) T& j
The father would hug the baby and hold him on his
0 M, {9 ^% }, e# P% @( F* N- p6 Hchest for a considerable period of time, causing sig-
# @% O! g: M. S3 q# nnificant bare skin contact between baby and father.
8 h; a+ T& s5 H" F3 D  I3 PThe father also admitted that after the phone call,/ F/ ~% J1 H7 m
when he learned the testosterone level in the baby
- A: K0 m: {/ s/ ]3 y! W" rwas high, he then read the product information
& w, w# x& x; S; ?: fpacket and concluded that it was most likely the rea-
4 l. x  P% c9 h3 o  g/ Sson for the child’s virilization. At that time, they
0 A2 u" V* A& p2 vdecided to put the baby in a separate bed, and the
' M: d( u/ l& g* A& G0 Z( Ifather was not hugging him with bare skin and had- T/ M0 a. `1 E: u8 _% C
been using protective clothing. A repeat testosterone2 }/ K) p0 G2 U9 j* E( Y
test was ordered, but the family did not go to the1 K9 @# D( o$ X; B/ j
laboratory to obtain the test.( _% {) P+ N0 @
Discussion
9 O  U" h/ o5 M$ @+ B. q5 z9 \; dPrecocious puberty in boys is defined as secondary  q% j8 R. M4 t
sexual development before 9 years of age.1,4
, g: C: x1 q( f, s. ZPrecocious puberty is termed as central (true) when  y: S- r& p" u9 q4 |
it is caused by the premature activation of hypo-; r4 Q* l% z8 i, S; \
thalamic pituitary gonadal axis. CPP is more com-
4 f8 e4 B, i# h8 _3 O2 emon in girls than in boys.1,3 Most boys with CPP
+ e, I9 K6 q. q" D  Q- L1 Bmay have a central nervous system lesion that is/ b5 A+ e0 a- H) B$ w0 `: B8 Y" ~
responsible for the early activation of the hypothal-9 D9 j7 m& z% v6 y
amic pituitary gonadal axis.1-3 Thus, greater empha-7 m! u3 Z3 X5 u) C  L& x0 q6 c% i
sis has been given to neuroradiologic imaging in
4 |! ?$ B( n/ V3 f: C, q" c( v- i# }boys with precocious puberty. In addition to viril-
$ k) z; M1 t2 @% h0 |% Aization, the clinical hallmark of CPP is the symmet-5 p  j3 U* F  M$ C1 E) T; R8 l
rical testicular growth secondary to stimulation by
1 S& E& x, g) q: Ugonadotropins.1,3
3 B! @& O7 Y- {' _Gonadotropin-independent peripheral preco-
+ w7 |3 }1 [7 h* Zcious puberty in boys also results from inappropriate
4 T, z3 o0 s. G# handrogenic stimulation from either endogenous or) a" _/ s8 @, d7 ]4 A# e( k3 M
exogenous sources, nonpituitary gonadotropin stim-
; x! S2 x! Y0 b$ Bulation, and rare activating mutations.3 Virilizing
& C/ K9 a$ ?2 Q( _: N2 e9 ~3 R! xcongenital adrenal hyperplasia producing excessive! j) X# Y+ c, k0 W
adrenal androgens is a common cause of precocious
$ ^6 e/ c: C! |puberty in boys.3,4
, _1 F! V, W$ n, KThe most common form of congenital adrenal2 |1 S; z: A0 b. Q8 W3 C% W
hyperplasia is the 21-hydroxylase enzyme deficiency.
$ a1 Y- H- F; ]; ]The 11-β hydroxylase deficiency may also result in+ m% C2 N. o4 Y$ [
excessive adrenal androgen production, and rarely,
. X& Y- T! l+ x! E/ ban adrenal tumor may also cause adrenal androgen
0 [& F$ y& `! f- h! Jexcess.1,33 r3 l; X" C: _7 ~4 M9 `5 W  `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# J! @( J: ^3 T$ N
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. ^& R- `5 \8 K6 |A unique entity of male-limited gonadotropin-
8 m2 U9 e. y6 f+ g. q2 r( D# o* d9 Kindependent precocious puberty, which is also known
2 |1 ?. z, g7 X$ X. [8 [% Vas testotoxicosis, may cause precocious puberty at a
- E, r, e9 ?! m- G4 H, q, K; @very young age. The physical findings in these boys
3 p2 r3 P5 g" dwith this disorder are full pubertal development,
  X1 x& f. X8 P7 ~! O# L' gincluding bilateral testicular growth, similar to boys
; T2 l& q, w. ]with CPP. The gonadotropin levels in this disorder
; [: Y3 t6 I$ w; f; Uare suppressed to prepubertal levels and do not show
9 \3 `7 S6 m2 `1 a$ ^7 Z* v, I5 U' V( Vpubertal response of gonadotropin after gonadotropin-9 u. Z8 L! O& n7 M5 l
releasing hormone stimulation. This is a sex-linked
; s- ?# `! i2 P) x/ K% Jautosomal dominant disorder that affects only& d$ B. z0 R) K8 y7 V2 D% ?
males; therefore, other male members of the family
2 [- ]& t! n4 I# ?- w1 {may have similar precocious puberty.3
3 B  M0 t& I3 T. E3 eIn our patient, physical examination was incon-2 g: N0 w' `- B
sistent with true precocious puberty since his testi-8 w; S4 f8 A0 q2 X3 T
cles were prepubertal in size. However, testotoxicosis3 [9 E) z/ q+ ?+ h# v
was in the differential diagnosis because his father1 n$ `9 _* b1 [+ [% V( T1 ^
started puberty somewhat early, and occasionally,8 `3 j3 q+ K  j1 r6 P
testicular enlargement is not that evident in the
: Y: P# \' k* ^8 L$ a0 d* {beginning of this process.1 In the absence of a neg-
; F4 U6 K0 g0 {8 [- ^* X, p$ }! Wative initial history of androgen exposure, our+ Q/ w$ n" I/ }# x+ n0 G& \
biggest concern was virilizing adrenal hyperplasia,
, |* o; k- \8 n: g6 ?1 E& {! Deither 21-hydroxylase deficiency or 11-β hydroxylase: Q# \* j! J) j' H  q, @* z3 g
deficiency. Those diagnoses were excluded by find-& F" B6 B$ O( M1 i" g& \' @
ing the normal level of adrenal steroids.
: d* C' V4 f+ U1 o& V8 \The diagnosis of exogenous androgens was strongly
7 J- q& @* u7 l, @4 s& l- ^3 nsuspected in a follow-up visit after 4 months because) l( t" I% h. g: P: Y
the physical examination revealed the complete disap-
. a! r+ T% e* |) Qpearance of pubic hair, normal growth velocity, and1 j/ |- M* {3 }, g
decreased erections. The father admitted using a testos-
6 k) }  a, q' @# j2 qterone gel, which he concealed at first visit. He was
+ z+ E2 _0 A9 H; y. jusing it rather frequently, twice a day. The Physicians’" X8 @$ C! W1 H, F( w
Desk Reference, or package insert of this product, gel or
4 M$ `0 D3 h' Dcream, cautions about dermal testosterone transfer to. d& l! A1 ?' t
unprotected females through direct skin exposure." _3 R0 |; ~9 V# l+ w- k5 y, w" v. _" H
Serum testosterone level was found to be 2 times the/ m6 y2 s+ C5 C, T4 W8 X6 [- c- [
baseline value in those females who were exposed to
" [2 K9 N) }' k2 Q; [3 C- h% feven 15 minutes of direct skin contact with their male
, `9 @" `0 }( u6 mpartners.6 However, when a shirt covered the applica-
- L, W, c; ?( z3 z" u3 Gtion site, this testosterone transfer was prevented.- `. n" g; O/ X/ @- d0 J/ L
Our patient’s testosterone level was 60 ng/mL," m/ x5 V, ]" P, s- }
which was clearly high. Some studies suggest that: X8 P' H) K3 [+ G7 r
dermal conversion of testosterone to dihydrotestos-
( [; `. r9 \: z) j' J' hterone, which is a more potent metabolite, is more; f& `/ M5 v) [8 A
active in young children exposed to testosterone
% a' m6 {1 u8 S) d8 m) \) m7 gexogenously7; however, we did not measure a dihy-: e) d0 L( B6 I, q* D1 O7 \
drotestosterone level in our patient. In addition to
8 |6 e, ~2 a: x# T5 Yvirilization, exposure to exogenous testosterone in
$ ]: \4 J  Y: {: bchildren results in an increase in growth velocity and
5 o1 `# K  f' r; }9 z' r5 `advanced bone age, as seen in our patient.
- {4 a/ l" o( s' lThe long-term effect of androgen exposure during# x; s0 A/ \5 q; ]9 M/ M) G5 ^
early childhood on pubertal development and final
6 E. s. `- R# j6 V, b% Fadult height are not fully known and always remain
' o: F4 Z# |  ~a concern. Children treated with short-term testos-
! p5 Z  e9 D) g& v$ rterone injection or topical androgen may exhibit some2 S$ f" X4 ~. m. i1 C
acceleration of the skeletal maturation; however, after
0 x( Q7 ]8 ^/ \+ \9 e4 |4 ncessation of treatment, the rate of bone maturation0 X2 F# `$ W# q. w  Y
decelerates and gradually returns to normal.8,91 x' w) _" k- l$ b  J
There are conflicting reports and controversy
( e5 U: \3 k) q1 S9 Nover the effect of early androgen exposure on adult
! Y' K0 B0 U& ]: N* Z7 Xpenile length.10,11 Some reports suggest subnormal
3 y* q6 q: C$ w) d' Z7 l, qadult penile length, apparently because of downreg-
7 x/ K( P8 u& N- culation of androgen receptor number.10,12 However,
% f: P3 G* ?, o3 N; H  b6 oSutherland et al13 did not find a correlation between
9 _  U% t/ Q3 ]# X+ Z) |childhood testosterone exposure and reduced adult  [; X" M: b4 x! T; I( Z) N: B
penile length in clinical studies.$ ]. c" m6 G: q
Nonetheless, we do not believe our patient is
7 c/ O' b- X- \going to experience any of the untoward effects from- p6 x$ w* E) p  _+ t2 h
testosterone exposure as mentioned earlier because- Z+ B9 B* e% i6 R! v
the exposure was not for a prolonged period of time.
0 b8 f7 P2 W" c" kAlthough the bone age was advanced at the time of
/ u6 p" X4 r/ j+ @8 t- y5 e% Fdiagnosis, the child had a normal growth velocity at
  d: Z  J( N* P' d1 ^1 {the follow-up visit. It is hoped that his final adult
2 K/ E) I- p; g& F& }height will not be affected.
; n# d9 _1 l  q! v* [Although rarely reported, the widespread avail-7 K9 f9 [' E. [! L, J' S9 Q
ability of androgen products in our society may
) @4 Y5 v( b/ @" h/ N/ ]+ K- Cindeed cause more virilization in male or female
- m0 h5 b( p$ X, G. e# a1 rchildren than one would realize. Exposure to andro-
) G8 }7 }: y  @1 ggen products must be considered and specific ques-
+ @3 l( y% h2 ktioning about the use of a testosterone product or
" m3 V; D3 ]8 pgel should be asked of the family members during
0 ^4 G2 g" Q; L& `5 B0 H# sthe evaluation of any children who present with vir-' {7 a& @+ D3 u# H
ilization or peripheral precocious puberty. The diag-& @& w1 V* B) s' e
nosis can be established by just a few tests and by+ V) l8 o0 r7 K! k9 e
appropriate history. The inability to obtain such a
& e! I$ U, p4 d# xhistory, or failure to ask the specific questions, may
% S# J+ j' G: i* ^& L4 C1 Xresult in extensive, unnecessary, and expensive  D. D% G2 a5 J
investigation. The primary care physician should be, n% e9 ?( c  g  Z5 V* s1 M9 V
aware of this fact, because most of these children, d' e' @0 v2 |$ G5 U
may initially present in their practice. The Physicians’* D) O8 D; c! f
Desk Reference and package insert should also put a
0 d1 C" ?+ o2 }warning about the virilizing effect on a male or
& i* G& y9 c1 }. E( z( l. K1 vfemale child who might come in contact with some-
% B+ q9 J* \, B; `8 Xone using any of these products.
) R- [( x0 O$ m, _( b# IReferences1 `/ g: G+ l3 H7 _# s' V
1. Styne DM. The testes: disorder of sexual differentiation
2 Y+ L2 x+ d* m% ]5 Qand puberty in the male. In: Sperling MA, ed. Pediatric
- Y) i4 L* c& ^% B6 @& o4 kEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, y& ?4 A2 A6 R1 h9 x9 n2002: 565-628.
/ b# W2 q( S- L( o* {+ {2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious' m2 E  B' v4 k' n  u
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
; P0 s; \! i8 a% g( c. C. R3 `; `Boy Induced by Indirect Topical
% B* ?+ O; ^5 E1 RExposure to Testosterone" o0 O5 g7 m+ c# s2 d! x. e
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' L. F  F; F! u' B( Q" ~' U
and Kenneth R. Rettig, MD1! v/ h* h4 |8 U' A+ r( x
Clinical Pediatrics, e# ^; g0 R+ ~# S( Z( H
Volume 46 Number 6, [# |! k$ N  Z. t
July 2007 540-543
: f2 b3 ]5 I$ o8 }7 h0 a; z© 2007 Sage Publications; r4 {3 M9 H, X/ p, a7 Z" K$ G, ~
10.1177/00099228062966518 d- B* O' N3 Y) V
http://clp.sagepub.com- m8 A) C  b& [8 b; B% H& g
hosted at
$ g& b6 p$ R+ v; ghttp://online.sagepub.com! E. W# g6 E7 _4 x$ e+ k
Precocious puberty in boys, central or peripheral,7 r) |2 g3 X% _1 O, |
is a significant concern for physicians. Central
0 x, C4 z; L+ b# p+ Wprecocious puberty (CPP), which is mediated0 [6 \9 u" S6 b! F$ Z3 N+ X
through the hypothalamic pituitary gonadal axis, has
+ L6 q! u1 p8 ua higher incidence of organic central nervous system
3 a% f# U  Y% `0 j8 n8 `6 w8 Hlesions in boys.1,2 Virilization in boys, as manifested2 Q6 e( Z8 o3 y% b9 k: n& B
by enlargement of the penis, development of pubic
% U- a; ]4 N( S- Q- ~$ ]+ Yhair, and facial acne without enlargement of testi-
. T7 K1 ?# `1 ?* W# @# R# bcles, suggests peripheral or pseudopuberty.1-3 We
: K8 |* m3 g. Freport a 16-month-old boy who presented with the
* `. i: t# o$ e) K' ^enlargement of the phallus and pubic hair develop-
# v8 M: B9 g" s2 Pment without testicular enlargement, which was due4 k5 C& ?; G/ t$ y- @' G
to the unintentional exposure to androgen gel used by
# ~0 C0 k4 w7 @8 a7 p" I# k+ Jthe father. The family initially concealed this infor-
- L% x  S9 p5 a: V5 Amation, resulting in an extensive work-up for this! ]/ C8 H" Z% W7 m8 y
child. Given the widespread and easy availability of
& U' b4 {( J# A( ttestosterone gel and cream, we believe this is proba-6 E- x$ a6 H& E* W  m! @& o+ M
bly more common than the rare case report in the
8 e3 o2 Y1 Y$ D/ b# F( Rliterature.4
1 c. o6 m9 o; O& O3 m! N: _; NPatient Report6 s" R- d* c7 U% R/ u; M4 E8 q
A 16-month-old white child was referred to the
. w  R( Y& p: e+ x2 w7 I; Sendocrine clinic by his pediatrician with the concern) r. E' u3 X7 Q) h( J
of early sexual development. His mother noticed  Z4 r& B/ ~% `6 C% C: E
light colored pubic hair development when he was
8 k+ @, L( R8 |) w  m1 g/ {From the 1Division of Pediatric Endocrinology, 2University of
+ ^' `% j" s) e- ]$ eSouth Alabama Medical Center, Mobile, Alabama.
( z+ c7 J" C0 k! _& SAddress correspondence to: Samar K. Bhowmick, MD, FACE,
  x+ v' m8 C9 c$ o6 kProfessor of Pediatrics, University of South Alabama, College of9 M% `6 g/ f# A$ Z3 R8 m6 U
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
9 W5 n" }+ E, m  ^& [& J- @e-mail: [email protected].- v) X+ K4 _7 v+ v8 }* `
about 6 to 7 months old, which progressively became! ]6 C2 r5 O5 t
darker. She was also concerned about the enlarge-6 g( I3 D! D! a" ~
ment of his penis and frequent erections. The child
7 V0 x. f1 z+ `, [3 e# T4 xwas the product of a full-term normal delivery, with
6 w& ]* b! H6 y0 T- C/ za birth weight of 7 lb 14 oz, and birth length of8 k- p, ?1 w' e* L7 |: M2 P
20 inches. He was breast-fed throughout the first year) R  _7 m8 l) `; o* ?
of life and was still receiving breast milk along with; g  A, j8 F2 j& x* j% N! V
solid food. He had no hospitalizations or surgery,
, e+ h2 `0 i  C2 V; {* {and his psychosocial and psychomotor development
& z# J2 i. H! {; [# Nwas age appropriate.
. Z3 w, f! r- B) l1 uThe family history was remarkable for the father,) S+ A4 f) Q& U* j7 V' I7 J/ n4 G& c
who was diagnosed with hypothyroidism at age 16," ]# x3 C0 k) N: A
which was treated with thyroxine. The father’s) d# p+ a6 x! |6 H1 a% z8 ^6 z$ A  I
height was 6 feet, and he went through a somewhat
/ k$ N2 P3 @' @% c8 W" K- fearly puberty and had stopped growing by age 14.
' l6 d$ ~3 D8 D8 w" TThe father denied taking any other medication. The
$ e9 f0 W3 n! B! Hchild’s mother was in good health. Her menarche) w+ g. K! `- B  X
was at 11 years of age, and her height was at 5 feet" {9 v; B6 f% F2 ]
5 inches. There was no other family history of pre-
& r* P  A0 g" @7 C( f' ?/ Mcocious sexual development in the first-degree rela-
/ O: I* _4 n. E, p- etives. There were no siblings.
8 I( D! ]) v% |" C! X0 P) WPhysical Examination
* D! E6 o$ U0 Z6 l9 _3 rThe physical examination revealed a very active,
- ~, @8 {* E' \# }0 Rplayful, and healthy boy. The vital signs documented
& ^5 w5 y: |& W6 aa blood pressure of 85/50 mm Hg, his length was/ U  o  J$ ]2 Q7 V
90 cm (>97th percentile), and his weight was 14.4 kg4 ?8 j: G5 T9 a, [
(also >97th percentile). The observed yearly growth5 l  A0 _# T& a0 v, U7 U0 s
velocity was 30 cm (12 inches). The examination of7 @* J2 [- E, d
the neck revealed no thyroid enlargement.6 w) v2 K+ K% I6 b
The genitourinary examination was remarkable for
7 Q7 \; f/ L/ ?% [7 h9 J0 A* d% Oenlargement of the penis, with a stretched length of6 q$ e  k5 P7 j2 ]# _
8 cm and a width of 2 cm. The glans penis was very well4 p+ M% J* I: B: N
developed. The pubic hair was Tanner II, mostly around4 X) c) a# m! C
540
1 x1 @( X# }4 J) u+ _7 M8 Dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ u9 B& o# K& m* L
the base of the phallus and was dark and curled. The
+ G; H3 q2 v) w* d; Etesticular volume was prepubertal at 2 mL each.6 ^& v1 l' S5 ?
The skin was moist and smooth and somewhat
+ t' U# Q. {3 d& q4 f+ A" |' Hoily. No axillary hair was noted. There were no4 ~5 G! r: l1 y* p/ r* G' a
abnormal skin pigmentations or café-au-lait spots.
, t6 z9 W6 x' E2 y% b+ x, _, n& @Neurologic evaluation showed deep tendon reflex 2+5 b4 X6 ~2 h4 f( l. A
bilateral and symmetrical. There was no suggestion
) `8 l$ a; b7 X3 l7 Iof papilledema.& v/ S) ]* |; N0 _( n
Laboratory Evaluation* }/ y9 Q! ~1 {, [
The bone age was consistent with 28 months by
! J! b6 N( M0 e. E" m- {/ Cusing the standard of Greulich and Pyle at a chrono-* W8 `4 j; o/ C) f1 F
logic age of 16 months (advanced).5 Chromosomal
8 H/ |& T# D3 ~6 ^. u5 I. wkaryotype was 46XY. The thyroid function test
, j. x# d" K* G2 q# Rshowed a free T4 of 1.69 ng/dL, and thyroid stimu-/ g$ m% d  V* A' U: X
lating hormone level was 1.3 µIU/mL (both normal).
- A4 i9 h0 _% ]4 M- fThe concentrations of serum electrolytes, blood
4 H# T5 X5 B: f! _2 S: T1 W. Rurea nitrogen, creatinine, and calcium all were; n" W! u# R( B
within normal range for his age. The concentration  m; J! S+ m6 U5 ?$ s
of serum 17-hydroxyprogesterone was 16 ng/dL5 k0 S+ N/ v& f7 @* u
(normal, 3 to 90 ng/dL), androstenedione was 20
$ D# g# V3 |0 k& g5 K4 ong/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ v! S: a% F( G; X$ Yterone was 38 ng/dL (normal, 50 to 760 ng/dL),
' z, f. `7 h. G5 ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to4 P6 Q4 t/ ?) v
49ng/dL), 11-desoxycortisol (specific compound S)9 @; P( e) l( p
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 b, B0 o% }7 X" G( {
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, I1 `  ]1 r7 i# Q3 J& C3 Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  ^; \) w# m( h! @& Cand β-human chorionic gonadotropin was less than
: _9 I& f+ r5 d4 s7 u$ y5 mIU/mL (normal <5 mIU/mL). Serum follicular
( Q) z$ I' ?1 y6 Z2 x( u+ Istimulating hormone and leuteinizing hormone* |1 P7 Q3 C: ^. d
concentrations were less than 0.05 mIU/mL, K5 ?+ i2 u' g+ J
(prepubertal).
% R7 w; O& \+ H" _2 i6 q" x  CThe parents were notified about the laboratory$ R  r+ Q9 \4 ?7 C0 `. L# M
results and were informed that all of the tests were
6 @# A8 P; d- L2 onormal except the testosterone level was high. The
: H% V# H- E! j( R9 x% v! Bfollow-up visit was arranged within a few weeks to
9 a( _' w5 |0 nobtain testicular and abdominal sonograms; how-3 R5 ~1 e8 T) ~1 [) @
ever, the family did not return for 4 months.- g* O  K3 ~! C! {
Physical examination at this time revealed that the
3 u$ Y: @# G3 Tchild had grown 2.5 cm in 4 months and had gained0 I! O. P. S2 Y; d
2 kg of weight. Physical examination remained
/ J9 a% P0 n5 A+ zunchanged. Surprisingly, the pubic hair almost com-+ B9 q: A# [' L
pletely disappeared except for a few vellous hairs at
6 g* A) b  P) w- ]* r1 F  Y; n) I' zthe base of the phallus. Testicular volume was still 2
& L' W3 Z. @" Q  i; O$ LmL, and the size of the penis remained unchanged.0 q6 d8 W& t9 ^6 {) o* s( W
The mother also said that the boy was no longer hav-
8 ~7 ^0 q# Z8 [9 [% `ing frequent erections.5 k# v: M; w. u
Both parents were again questioned about use of& P0 g; P# D" H! C2 E# x& v9 V
any ointment/creams that they may have applied to1 _& ?+ D7 P! e6 o$ g1 z) n
the child’s skin. This time the father admitted the
7 C( v  q2 d* OTopical Testosterone Exposure / Bhowmick et al 541* E) h! N& p5 ?
use of testosterone gel twice daily that he was apply-
+ G$ z2 g# |& f0 O) q( W  y0 u  e. ^ing over his own shoulders, chest, and back area for
  ?; C6 y; W. H  @a year. The father also revealed he was embarrassed3 Z4 t/ s4 L. h
to disclose that he was using a testosterone gel pre-
- |3 K! I$ d7 c: o' Vscribed by his family physician for decreased libido- ?. u7 _3 i, ^
secondary to depression.
4 ^( \. m+ ~" t, c0 W$ A7 CThe child slept in the same bed with parents.) w- U- Q  U" P# a# N
The father would hug the baby and hold him on his0 d; Y/ \6 t) Q
chest for a considerable period of time, causing sig-
7 s* a7 `# N1 `, {+ Enificant bare skin contact between baby and father.
2 N6 r  @# ^/ E  h; r7 P4 F) KThe father also admitted that after the phone call,# P. R- ]: ~4 a9 k1 v7 B5 f
when he learned the testosterone level in the baby" w0 R. _+ U- q( ~
was high, he then read the product information3 c  R8 H( N( u9 r
packet and concluded that it was most likely the rea-  O- n& p  C+ E) e# k8 F
son for the child’s virilization. At that time, they
( i7 b" B" f8 fdecided to put the baby in a separate bed, and the+ r/ P" W- t# u
father was not hugging him with bare skin and had  }) C5 \. p' R  _9 l
been using protective clothing. A repeat testosterone
. q+ p' c' b1 G- L$ }test was ordered, but the family did not go to the3 u- W# i  T* I, y' V# P% E
laboratory to obtain the test.
* [) X0 H: r+ D3 h* ]& q$ h& q8 IDiscussion
- w( @5 w( y* _% D3 l' NPrecocious puberty in boys is defined as secondary4 ]# C* i3 i- B1 s
sexual development before 9 years of age.1,4. d7 N1 t5 K: ]* @7 H; e
Precocious puberty is termed as central (true) when) X$ X, h5 I+ K7 [) [! G
it is caused by the premature activation of hypo-
+ I9 E* L2 l8 l* A6 k6 }thalamic pituitary gonadal axis. CPP is more com-+ A; ?+ x7 s. ^) x0 R- c
mon in girls than in boys.1,3 Most boys with CPP9 G/ K- i7 R* m, V
may have a central nervous system lesion that is4 _5 D6 ?- y- r6 N
responsible for the early activation of the hypothal-
2 P' g2 c/ h- h) P) {7 }0 v1 {amic pituitary gonadal axis.1-3 Thus, greater empha-
" s2 i% T; h( n) C* hsis has been given to neuroradiologic imaging in& U/ w$ O/ w# s
boys with precocious puberty. In addition to viril-
* P+ w; o& b: \; O: p# u  b1 Pization, the clinical hallmark of CPP is the symmet-1 k8 h/ L& ~. j$ ]' f& T
rical testicular growth secondary to stimulation by
, b# |% `4 |( F' u' D2 tgonadotropins.1,36 B3 Y4 O& ~' l
Gonadotropin-independent peripheral preco-
: l- e) ?& `. g& m* a  e9 r0 qcious puberty in boys also results from inappropriate/ A, |' I. e4 l! A/ @
androgenic stimulation from either endogenous or- C2 k& g( S7 \' {. F
exogenous sources, nonpituitary gonadotropin stim-! |5 x; ?5 A# x
ulation, and rare activating mutations.3 Virilizing
+ A$ R' P4 @7 i3 rcongenital adrenal hyperplasia producing excessive
" V9 u6 b& q7 P" c% ], [adrenal androgens is a common cause of precocious
$ P* |  I; g- cpuberty in boys.3,4
7 K! }. N5 J6 z4 l9 i- ]: iThe most common form of congenital adrenal1 s6 I5 h% ^  b7 r
hyperplasia is the 21-hydroxylase enzyme deficiency.
" t' ~' \6 ?  ]$ GThe 11-β hydroxylase deficiency may also result in
/ h7 {& x0 {3 z* Iexcessive adrenal androgen production, and rarely,5 ?: m4 P$ e3 w7 {6 i4 W
an adrenal tumor may also cause adrenal androgen
7 m9 m' j: S% @5 w* w) I( zexcess.1,3
! y" I1 |4 X6 v) o8 F% D/ Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" b9 b( Q7 P- q" ^6 L' M. Q542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& g4 L0 _: W: X0 @8 g& ^
A unique entity of male-limited gonadotropin-
) T1 Y: Z& S8 j7 ~8 gindependent precocious puberty, which is also known
+ o$ |. p( R6 U8 W* U/ _/ o8 Oas testotoxicosis, may cause precocious puberty at a$ t( l6 Y$ O! D9 I4 L$ {; x  b
very young age. The physical findings in these boys
& d# W- m7 N5 X% Vwith this disorder are full pubertal development,
. `( B( ]4 J3 r- Y1 H7 jincluding bilateral testicular growth, similar to boys
  o8 ~4 q$ S# R! B+ bwith CPP. The gonadotropin levels in this disorder$ q2 n( g  ^( C6 j+ |/ r' r
are suppressed to prepubertal levels and do not show$ f2 ~5 H# u2 n5 I" {0 c6 K" ^
pubertal response of gonadotropin after gonadotropin-
" @+ J7 O7 S6 b/ z9 l- C( N8 j  kreleasing hormone stimulation. This is a sex-linked% Y( Z; L0 k* `% v7 a5 z8 m* _
autosomal dominant disorder that affects only
1 n6 j: h' [7 F6 S% [, K4 J8 Xmales; therefore, other male members of the family
+ Y9 ~0 S$ a# Wmay have similar precocious puberty.39 P. g4 t' G& |$ l( W( _5 u1 @* K
In our patient, physical examination was incon-0 z' a: M  `! @% U4 z; ?
sistent with true precocious puberty since his testi-
0 A5 `! {; J5 ]; i0 }3 O( ncles were prepubertal in size. However, testotoxicosis
' n% T/ k5 S% ^: U) l, Y# Swas in the differential diagnosis because his father
6 l& L9 U6 G; a9 v7 W: p) P8 {started puberty somewhat early, and occasionally,' A) D8 f$ b: T1 I) ^
testicular enlargement is not that evident in the
  ?% O' _5 |4 g1 i1 O5 mbeginning of this process.1 In the absence of a neg-4 g5 V4 [6 I3 g" ^" u( U6 d9 S
ative initial history of androgen exposure, our6 a4 f( `! c& K
biggest concern was virilizing adrenal hyperplasia,
  y0 d( E: L6 |either 21-hydroxylase deficiency or 11-β hydroxylase, w8 i4 Y$ z9 \4 P  W. J% _- l, `5 X3 R
deficiency. Those diagnoses were excluded by find-3 a% n( l8 m4 c" k  W% h
ing the normal level of adrenal steroids.
- I+ }% s" b2 E  v! E( sThe diagnosis of exogenous androgens was strongly" w$ o# J/ a+ o4 }0 Q8 A+ i+ F
suspected in a follow-up visit after 4 months because
& G1 n! g# {% Sthe physical examination revealed the complete disap-( P( g3 K. ?0 u' X& d% G- F: b
pearance of pubic hair, normal growth velocity, and
- n: r# x5 [1 ~" s# j& Zdecreased erections. The father admitted using a testos-( i9 |& C) {; K+ q
terone gel, which he concealed at first visit. He was
' ~4 D& b9 t9 L6 N' e# Jusing it rather frequently, twice a day. The Physicians’
, V# D1 Q9 m+ D0 iDesk Reference, or package insert of this product, gel or
/ E. w; k+ R% K/ ?  _8 r1 s( X& M6 `cream, cautions about dermal testosterone transfer to, r* ?6 C/ S4 ~/ q$ I& Y
unprotected females through direct skin exposure.
3 A9 m1 U- {/ Y  d: J6 ASerum testosterone level was found to be 2 times the, B6 Z/ n1 V* W' ?) z
baseline value in those females who were exposed to
1 k5 I7 L& q! `even 15 minutes of direct skin contact with their male$ h+ U8 p) `3 \; b
partners.6 However, when a shirt covered the applica-* J1 Z9 Y7 E6 i6 ^, F
tion site, this testosterone transfer was prevented.
4 W+ k5 T. j. B! [Our patient’s testosterone level was 60 ng/mL,
: l- ]( A  R/ N2 T1 V. H; cwhich was clearly high. Some studies suggest that
2 j: m" [7 L& q6 k7 q7 X- t% Y0 |dermal conversion of testosterone to dihydrotestos-: b! [2 G2 Y' n! n0 @% r
terone, which is a more potent metabolite, is more
5 \% T5 a% Y! ]$ Z( z3 wactive in young children exposed to testosterone
  x/ Q/ b" v; n7 E8 n% qexogenously7; however, we did not measure a dihy-
/ H6 v5 B4 {2 |/ b: Rdrotestosterone level in our patient. In addition to
0 ?# G) G! J' x( Zvirilization, exposure to exogenous testosterone in
1 X; I  e7 ~& v; @5 `0 Rchildren results in an increase in growth velocity and7 W5 K) F- H8 H* l: s6 I4 S
advanced bone age, as seen in our patient.
; ~- ~& \5 {2 x( f/ gThe long-term effect of androgen exposure during
' G$ t% {, G9 \9 J( n' H8 Yearly childhood on pubertal development and final
$ |- i7 f4 e: [& c" oadult height are not fully known and always remain( ?) l1 Z, g6 z% B" d2 W  A6 ~" x
a concern. Children treated with short-term testos-
( {9 x+ Q0 U0 s# Y/ uterone injection or topical androgen may exhibit some0 A  ^: g. M7 }: ]
acceleration of the skeletal maturation; however, after3 L  ^+ t6 C$ y' k0 p
cessation of treatment, the rate of bone maturation& u( [+ I: z0 A2 i3 N, O$ R$ `% J& A" b) I
decelerates and gradually returns to normal.8,9
# T* ?# M6 g- PThere are conflicting reports and controversy4 d( g- ^% j+ k1 m. d' e% ?; c( K
over the effect of early androgen exposure on adult
$ ^* F6 c8 H4 k* `6 S  n4 [# k" upenile length.10,11 Some reports suggest subnormal
- Q2 o, ?9 |: ~/ radult penile length, apparently because of downreg-
" B: s$ X) o0 z7 ^* Tulation of androgen receptor number.10,12 However,
& T, H0 ?( J1 ~: _( v( uSutherland et al13 did not find a correlation between. T0 p  k9 y7 p2 c$ {
childhood testosterone exposure and reduced adult
9 S; t/ v& T# C3 b; upenile length in clinical studies.$ m* X9 |3 w' }5 W
Nonetheless, we do not believe our patient is, w8 k7 v! A* g4 t, D, T4 M
going to experience any of the untoward effects from' E. [- t. V; p
testosterone exposure as mentioned earlier because& G! I0 c7 W) S/ a! }
the exposure was not for a prolonged period of time.
. I* q! {+ A- F# LAlthough the bone age was advanced at the time of( e% S, l& E0 y
diagnosis, the child had a normal growth velocity at$ J4 D" e6 D0 q# d, W' d1 U, e7 ^
the follow-up visit. It is hoped that his final adult
& l2 e- z0 S, ~6 m+ N* Fheight will not be affected.# H: L8 I) B) r; |& i
Although rarely reported, the widespread avail-
( l1 h; s( i9 _( p6 Y+ f7 zability of androgen products in our society may9 E# P/ h' }- n
indeed cause more virilization in male or female0 o. z* S. \; W- O
children than one would realize. Exposure to andro-( F0 h/ H: y4 A8 W: t$ r. B* z
gen products must be considered and specific ques-
" y5 e2 ~% b% k% Ytioning about the use of a testosterone product or
1 F, t% l1 n: [/ ~% d) F5 fgel should be asked of the family members during
+ J) x# ?1 Q3 lthe evaluation of any children who present with vir-
6 O6 O9 b  W. v& w' A# e4 Vilization or peripheral precocious puberty. The diag-
; G4 v% {$ ?3 h' ^" jnosis can be established by just a few tests and by
( j1 A# Q2 x! z/ `. m  q1 p0 }) Yappropriate history. The inability to obtain such a
$ c* x; s! Z* R. {: |9 M! v  Zhistory, or failure to ask the specific questions, may
. J% r2 B( j/ g* q1 d$ Jresult in extensive, unnecessary, and expensive+ j- s4 [7 V" D% i
investigation. The primary care physician should be5 s4 Y3 l8 [( s6 |+ V
aware of this fact, because most of these children& s0 ]- q6 L# j/ s1 n
may initially present in their practice. The Physicians’' @" |: O- \* I. _
Desk Reference and package insert should also put a8 M4 v  i9 e  |; e% Z: _
warning about the virilizing effect on a male or1 I& ^& |# I9 F7 v2 ^* K5 W
female child who might come in contact with some-
* S% Y( |3 L5 {# |/ Oone using any of these products.
1 s7 J$ `8 m& M: d& J; J; X/ g' MReferences  X8 T: g( O* a2 k# M
1. Styne DM. The testes: disorder of sexual differentiation
" n5 |" W& L1 M' C( r- `and puberty in the male. In: Sperling MA, ed. Pediatric7 o/ c# ]9 h- ?2 r& z$ z) n/ }/ t  \
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;0 m: b* g3 F+ z+ @7 S7 p
2002: 565-628.
" h# ?% G0 ~  T: c, p$ v% n) j2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious, I  z2 x2 ?) o- H
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!
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

* n) {/ f  y4 B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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