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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
4 ?3 B: J4 C7 i" X' q! K/ sBoy Induced by Indirect Topical
5 n" h, u5 g$ @, n# y# {Exposure to Testosterone# v5 e! I- J! y
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2& i6 @8 U0 v7 k" H( p( b" Q" f
and Kenneth R. Rettig, MD1$ b4 G! V7 t( A! E9 n
Clinical Pediatrics! f" ^) A, |- y8 ^9 F# p5 m' x  f; x
Volume 46 Number 6
" l- l4 k  q  c3 g, _July 2007 540-543
& N4 s  P% x$ w3 g/ q5 g; w+ _- k. r- r© 2007 Sage Publications* {- t  a. N- w+ u
10.1177/0009922806296651
, g4 o! C3 z# o& W/ ^http://clp.sagepub.com7 D/ J: b# Q# \% J  C
hosted at7 w- X! O9 E& {4 k( d. q( ?2 [1 c
http://online.sagepub.com
  r* u8 X% m0 aPrecocious puberty in boys, central or peripheral,( u; i5 n$ r$ g) u* B
is a significant concern for physicians. Central
% W* @9 k8 S( H6 P; r7 cprecocious puberty (CPP), which is mediated
. U. N8 b$ f% Q6 s- d7 lthrough the hypothalamic pituitary gonadal axis, has7 x/ R, y2 I7 S) u0 g
a higher incidence of organic central nervous system
4 B3 }, M% E  \4 Flesions in boys.1,2 Virilization in boys, as manifested
- [0 G* _2 l; I3 K1 Bby enlargement of the penis, development of pubic
% c0 D3 q' U+ n0 {hair, and facial acne without enlargement of testi-
5 z9 [1 C  G2 l  fcles, suggests peripheral or pseudopuberty.1-3 We' X+ ?9 S; o' c/ i4 V
report a 16-month-old boy who presented with the
& D: x9 A: T" [3 D5 S2 E7 A9 Qenlargement of the phallus and pubic hair develop-
, a* \% s5 C, v( r1 Xment without testicular enlargement, which was due  x3 N0 u+ {4 t; }% z. a
to the unintentional exposure to androgen gel used by" A7 W$ M2 U- t. k
the father. The family initially concealed this infor-) {% ~' x& o" I1 m: d
mation, resulting in an extensive work-up for this
% G5 f' D% w/ f9 ~' j( V  u" f0 hchild. Given the widespread and easy availability of
  n* P! o" I( m% t% ~5 R  [. |) Htestosterone gel and cream, we believe this is proba-* i" L' u' D/ s& ]  y& \
bly more common than the rare case report in the3 |1 v: _& L8 N% K7 E
literature.4# J$ Y6 \) N$ \: G+ k' J! _0 a
Patient Report) b1 C9 r. B8 B8 V- s
A 16-month-old white child was referred to the
; V7 O; y  U4 T3 N9 Hendocrine clinic by his pediatrician with the concern
2 C& v, l8 d! z( G, Y, rof early sexual development. His mother noticed
2 B: F' R  [/ ?light colored pubic hair development when he was( u3 r2 Q( Z& D5 b: I$ \/ ]" v! e
From the 1Division of Pediatric Endocrinology, 2University of( [% M* G# p7 ^
South Alabama Medical Center, Mobile, Alabama.
% X& i% n- t3 W1 n7 ~; t# w4 PAddress correspondence to: Samar K. Bhowmick, MD, FACE," S7 @3 L! W# w2 \% d! h
Professor of Pediatrics, University of South Alabama, College of
( s5 D) e6 J2 t' q+ q9 GMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. x" k$ Y" \. g. D" Ge-mail: [email protected].( s1 q4 n! s5 U& D# l5 c
about 6 to 7 months old, which progressively became! t9 K1 a) m% n' b
darker. She was also concerned about the enlarge-, E5 L- A) j7 k& L% O
ment of his penis and frequent erections. The child2 n& z! o2 u% u7 L
was the product of a full-term normal delivery, with9 r5 s8 O0 M% l" h
a birth weight of 7 lb 14 oz, and birth length of; B, v$ q3 F2 s9 b: M# b
20 inches. He was breast-fed throughout the first year
+ V" D# b8 p' ~2 [of life and was still receiving breast milk along with
- s8 @5 ~+ d5 v& J& t9 }% _solid food. He had no hospitalizations or surgery,& [2 T+ Y% G  I4 y' U% U% P, Z
and his psychosocial and psychomotor development+ ^- ~/ _4 |( l2 P" `/ J7 J
was age appropriate./ h+ h" B$ x1 X( ^
The family history was remarkable for the father,6 y3 }# s( h* r8 f' ]( @, w
who was diagnosed with hypothyroidism at age 16,
9 w3 b: V3 T) |5 b5 }& Owhich was treated with thyroxine. The father’s
& R7 l+ K5 H& K3 z; A4 l0 vheight was 6 feet, and he went through a somewhat$ W: O5 G9 L2 d) J; s. s
early puberty and had stopped growing by age 14.
' C% _0 h; P6 h3 EThe father denied taking any other medication. The+ a/ ^. k1 E! `% g
child’s mother was in good health. Her menarche
& ?3 O0 f2 E$ W  q1 t4 \2 [1 Ewas at 11 years of age, and her height was at 5 feet. ^$ q; L% B# f- }2 _
5 inches. There was no other family history of pre-
( Y5 O" x8 L/ ]- S% r- [3 z- [cocious sexual development in the first-degree rela-- d6 D/ W. Q6 C' Z
tives. There were no siblings., d3 R  `9 i# U7 n4 G" B
Physical Examination
8 t- d$ a+ P9 F+ t: C. D- eThe physical examination revealed a very active,  k. _/ R/ B. @" j
playful, and healthy boy. The vital signs documented
6 E: m" [, _- ^4 }* b% v* `/ Ha blood pressure of 85/50 mm Hg, his length was
; p: R% j8 }5 \  S90 cm (>97th percentile), and his weight was 14.4 kg: D; X. K) b  I# l8 s
(also >97th percentile). The observed yearly growth. m# e7 X. c6 W% e
velocity was 30 cm (12 inches). The examination of
( v4 Y* S! N+ U! }  q2 Jthe neck revealed no thyroid enlargement.6 ]8 Z1 P0 `" t5 F3 ~1 y
The genitourinary examination was remarkable for
: `% b4 j0 w" C) F4 menlargement of the penis, with a stretched length of. |, ?( [  G' b
8 cm and a width of 2 cm. The glans penis was very well7 }2 g' X) ^8 A1 v! x
developed. The pubic hair was Tanner II, mostly around$ M. [0 K0 j; [) M+ x  y
5403 S) W- ^! l' S- C5 B* |. E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ M" I' g: L3 Q  `$ W, K- ^; J
the base of the phallus and was dark and curled. The& x7 e! w6 {& G. ^! W
testicular volume was prepubertal at 2 mL each.  Y9 x( Y$ U- k+ O2 U: B) x: y+ T0 |
The skin was moist and smooth and somewhat: S1 a3 l; p3 q: y4 J* {
oily. No axillary hair was noted. There were no
3 y; \: ~2 `2 Y: b+ Yabnormal skin pigmentations or café-au-lait spots.
4 Y  i5 r  l* V2 G7 }Neurologic evaluation showed deep tendon reflex 2+, X7 Z; I! x' Q9 o6 ^" W9 l, I
bilateral and symmetrical. There was no suggestion
  i) g0 [, r3 |2 Hof papilledema.
9 T3 G# S1 U, q. B7 \$ L* OLaboratory Evaluation
/ ~9 u" P( R7 D2 E) |The bone age was consistent with 28 months by/ b# \) ~5 g( {# s. h6 a, U  Q: Y
using the standard of Greulich and Pyle at a chrono-& t/ t; ?; A/ e) O
logic age of 16 months (advanced).5 Chromosomal$ y- e6 u  a+ k! `
karyotype was 46XY. The thyroid function test
$ M( U$ u3 d+ K" q/ Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-+ V. l' O7 Y# Y
lating hormone level was 1.3 µIU/mL (both normal)." z$ |2 S8 K& Z' U/ A% t2 x5 T8 F
The concentrations of serum electrolytes, blood, o! S/ \) c  `1 \$ g
urea nitrogen, creatinine, and calcium all were8 ]  p% @6 M5 y; a5 d# u* \
within normal range for his age. The concentration
% a# h3 h* f1 r$ Y) I  M. s; m( c; Oof serum 17-hydroxyprogesterone was 16 ng/dL
: G6 @; V# p# G: O, N$ n  b+ t  m(normal, 3 to 90 ng/dL), androstenedione was 20- v, a& V. b! f; W+ O7 f* H) N
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 W/ q; W& p3 \( z0 Oterone was 38 ng/dL (normal, 50 to 760 ng/dL),5 b) g& P* y5 m) [/ U9 X
desoxycorticosterone was 4.3 ng/dL (normal, 7 to' h4 P1 Z# c$ n) _
49ng/dL), 11-desoxycortisol (specific compound S)
1 k- r7 }) M$ M7 s% owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-* R$ n5 p$ m2 j
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; G# J, b& x- _
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! ]/ R3 O3 j  S' `and β-human chorionic gonadotropin was less than
& Y9 G$ \% x- y% Z5 mIU/mL (normal <5 mIU/mL). Serum follicular- X% v9 s- a$ ~2 g
stimulating hormone and leuteinizing hormone# J  V% y7 _. j& W* o9 a/ R: S
concentrations were less than 0.05 mIU/mL8 t6 I4 O/ k, c, S. l
(prepubertal).0 C3 y3 g& [  P8 U; W5 D9 p1 \$ i
The parents were notified about the laboratory
! W; a. G7 K# O: g  r7 xresults and were informed that all of the tests were: y; b& [6 o, a  z1 @9 a6 U
normal except the testosterone level was high. The
) Y5 U) J9 v) G$ r1 E2 sfollow-up visit was arranged within a few weeks to
/ F: |3 @2 o$ @; ?( v: J/ pobtain testicular and abdominal sonograms; how-+ j- _- A2 M% f! x% y* D
ever, the family did not return for 4 months.2 F; B. A' W' \5 ]! n
Physical examination at this time revealed that the+ N' x- t2 G6 U& v3 b- w
child had grown 2.5 cm in 4 months and had gained9 {4 ?8 ^  s  b5 r
2 kg of weight. Physical examination remained' Q3 O. t" G4 D. @$ L+ I% w  r
unchanged. Surprisingly, the pubic hair almost com-0 v9 Y- E! e9 i1 j4 Y
pletely disappeared except for a few vellous hairs at
7 o) R3 u' A1 O. u" }: o# O- A# rthe base of the phallus. Testicular volume was still 2; b& V8 J" {$ d- e' p1 a
mL, and the size of the penis remained unchanged., k2 _3 A, ?+ }3 ?  O* S
The mother also said that the boy was no longer hav-
5 j+ C" ]) s2 |4 sing frequent erections.
( Y, {4 T/ ?# i' q$ I2 G) BBoth parents were again questioned about use of
8 Z0 {3 |# X7 M2 ^* l9 ?any ointment/creams that they may have applied to* M/ h7 }% `* [3 Q) Y
the child’s skin. This time the father admitted the
; v# K& m7 l6 VTopical Testosterone Exposure / Bhowmick et al 541
0 {# x; X/ k' v$ k; Fuse of testosterone gel twice daily that he was apply-2 y, b/ ]' \+ m
ing over his own shoulders, chest, and back area for2 T/ ?: Y5 ^, T& Q5 y+ V
a year. The father also revealed he was embarrassed
5 @- `/ Y: ^) b. R0 d' Eto disclose that he was using a testosterone gel pre-
( F4 r$ }" X! K4 N$ T+ sscribed by his family physician for decreased libido. A* P: @& L% z2 m! W# E
secondary to depression.
! r8 [3 S, ]/ R, e) }The child slept in the same bed with parents.0 q. Q4 N" w( M& ?% @
The father would hug the baby and hold him on his+ c$ k  W  r$ d/ ^9 y
chest for a considerable period of time, causing sig-0 L3 M$ }& g3 t
nificant bare skin contact between baby and father.% ]7 t5 Z2 I# l/ \
The father also admitted that after the phone call,
# R. `- u3 P. {! Gwhen he learned the testosterone level in the baby5 V. t4 [7 I1 k" l
was high, he then read the product information
! s# z: Y0 f; Ypacket and concluded that it was most likely the rea-
9 t3 I$ L8 \/ ]2 ?* }. bson for the child’s virilization. At that time, they( Y: m$ m( L$ N/ l1 l  e5 Z
decided to put the baby in a separate bed, and the
' a3 W* }- D. ]( s% i/ Xfather was not hugging him with bare skin and had
5 k- M' Y  ?" S* D( n& abeen using protective clothing. A repeat testosterone
+ }2 B1 n+ y$ Otest was ordered, but the family did not go to the; Q4 w+ t# U2 W% g
laboratory to obtain the test.
% T& x& ?9 ~1 \Discussion
* k9 @# C6 E8 t! P3 c' XPrecocious puberty in boys is defined as secondary
( M5 ?- {2 q7 Q$ A& ]9 Rsexual development before 9 years of age.1,45 K, K! k1 ]; l
Precocious puberty is termed as central (true) when
1 E& U8 y. p, p' l8 @1 B. L% ?it is caused by the premature activation of hypo-
' W, q6 `6 o' l% v; ]thalamic pituitary gonadal axis. CPP is more com-( Y! j5 F6 N' C" _- ^1 t
mon in girls than in boys.1,3 Most boys with CPP
& E4 ~. p0 }! f6 D5 U$ R% kmay have a central nervous system lesion that is) r$ i# y0 |& g7 L: @$ d
responsible for the early activation of the hypothal-% n% w3 X' m7 R0 h/ A
amic pituitary gonadal axis.1-3 Thus, greater empha-' w+ r' S" D' n7 D! w  y9 [
sis has been given to neuroradiologic imaging in
3 p( |. M/ p6 z& vboys with precocious puberty. In addition to viril-
$ r8 Y) ~+ G2 P1 w3 C3 S5 ?! Qization, the clinical hallmark of CPP is the symmet-
, A, e2 c5 h* l7 v6 K! `: `rical testicular growth secondary to stimulation by) ]0 |6 H5 h% F3 p8 u
gonadotropins.1,3
. s% {8 [% R: l. D( _. qGonadotropin-independent peripheral preco-/ f+ |% h$ {* w+ J  r  S
cious puberty in boys also results from inappropriate
4 O; ~7 l5 g9 ]+ dandrogenic stimulation from either endogenous or
1 U8 W; O! X/ K' {0 {2 ?3 V" Nexogenous sources, nonpituitary gonadotropin stim-1 S4 W! I# C. ]$ P1 A/ _
ulation, and rare activating mutations.3 Virilizing
% I% ~) v; J! u( J0 d' r' econgenital adrenal hyperplasia producing excessive
5 l+ O7 S/ G: P$ Wadrenal androgens is a common cause of precocious
; M$ M, R) l6 ~, Q: Q4 X/ W- ppuberty in boys.3,4
6 w: N1 v0 W+ c8 x: N0 wThe most common form of congenital adrenal
4 s3 I1 e6 \$ d$ P' a! Uhyperplasia is the 21-hydroxylase enzyme deficiency./ [& D4 J7 C7 O9 `% _. k- i" q
The 11-β hydroxylase deficiency may also result in& u0 ^) Q$ e' e7 M4 C- J* v4 @5 b
excessive adrenal androgen production, and rarely,1 `* o* G9 k) H
an adrenal tumor may also cause adrenal androgen* x2 }2 R, [! u. C7 K9 }
excess.1,3* s4 |" ?4 E" j; o" a
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 H+ p- v  ?- V' V0 R542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 m7 L* T4 K  U
A unique entity of male-limited gonadotropin-6 `" Z& N2 G' M
independent precocious puberty, which is also known$ j# Z: L6 E8 i  d! r
as testotoxicosis, may cause precocious puberty at a
- _3 i, }- H9 y: @) S& Jvery young age. The physical findings in these boys
$ N) a3 Q" W# j5 m! `# cwith this disorder are full pubertal development,1 H- e% x& m: K- `1 H
including bilateral testicular growth, similar to boys9 z0 }0 M* F- M) a# y, Y2 u7 M4 x
with CPP. The gonadotropin levels in this disorder
* r9 [6 t8 n# V: L8 Q9 L' c- Bare suppressed to prepubertal levels and do not show
2 O' Z9 M# _9 M- i# l2 O2 Xpubertal response of gonadotropin after gonadotropin-
0 \* J/ O# t( S( E5 y) a' j- k8 oreleasing hormone stimulation. This is a sex-linked
7 @- O& A! T" nautosomal dominant disorder that affects only. p7 t0 `! ~7 s( c) h6 _
males; therefore, other male members of the family
6 l) }1 m  ?/ q8 G7 N. }& F3 j2 Y4 Vmay have similar precocious puberty.3( o% ^/ |% U% v' m
In our patient, physical examination was incon-+ K, k  g+ U" @( P0 Y
sistent with true precocious puberty since his testi-
' z* q9 h  e2 N4 E* f. t7 O- Qcles were prepubertal in size. However, testotoxicosis5 R* k& y4 B6 T- o5 i
was in the differential diagnosis because his father! D) X/ g$ y9 B* a) Q
started puberty somewhat early, and occasionally,  J1 y, H0 U, O( k; h  ~
testicular enlargement is not that evident in the
0 V- P# a  Z0 u" jbeginning of this process.1 In the absence of a neg-0 B" m5 Q$ H$ K
ative initial history of androgen exposure, our
, U) K+ s1 t* t' X1 ^biggest concern was virilizing adrenal hyperplasia,
4 T( e! H. h1 t, z7 Y  P: feither 21-hydroxylase deficiency or 11-β hydroxylase
5 O8 H1 w: R7 Y) vdeficiency. Those diagnoses were excluded by find-! E# [! P. `6 Y0 B: ?% s
ing the normal level of adrenal steroids.2 c4 ]; l' b* N* L; B: [9 J8 b
The diagnosis of exogenous androgens was strongly; g: s3 s$ K+ g- z0 W5 U
suspected in a follow-up visit after 4 months because
- }% C1 E3 l- ?the physical examination revealed the complete disap-
: p9 a0 p# R' ^* n8 V' Hpearance of pubic hair, normal growth velocity, and* T. d& p! p4 B; w
decreased erections. The father admitted using a testos-# m( V1 g6 {5 U9 S& x7 b
terone gel, which he concealed at first visit. He was% O* p8 @* l! a% O( W3 S
using it rather frequently, twice a day. The Physicians’
; ~# d3 A) ^1 |  Z, k  z. ZDesk Reference, or package insert of this product, gel or' L+ i/ g; _* [, T# D* f5 B
cream, cautions about dermal testosterone transfer to
; Z4 J- M! k" U* X2 t4 Runprotected females through direct skin exposure.* \5 r! o! A  j- d5 M" b2 x6 r
Serum testosterone level was found to be 2 times the* A' b, B6 }7 m$ x  p  ]1 y
baseline value in those females who were exposed to4 X& F7 G# \/ A: F- Q+ `
even 15 minutes of direct skin contact with their male4 o* {+ |. i: |) l* M8 t9 L& o
partners.6 However, when a shirt covered the applica-
+ L! ]' N8 a! Y% V; O6 L7 E4 V& Gtion site, this testosterone transfer was prevented.
/ C4 ^& M! h! C; Z% p- j5 v$ ^Our patient’s testosterone level was 60 ng/mL,
: y8 W+ t1 [) y* Cwhich was clearly high. Some studies suggest that4 E! A) ?/ ]) ]2 _4 ~: ]  a
dermal conversion of testosterone to dihydrotestos-
2 i8 [9 A6 l/ r" T" Uterone, which is a more potent metabolite, is more" ^! B3 K1 I# x- {, N3 z' f9 D
active in young children exposed to testosterone
; E- ~3 w3 d3 a' d+ C1 Bexogenously7; however, we did not measure a dihy-/ }/ s8 \4 m2 U0 e& r
drotestosterone level in our patient. In addition to  s. P( `) i; c+ P6 c! ^9 i& B7 {
virilization, exposure to exogenous testosterone in
% b! L% t2 u5 T  ~& Fchildren results in an increase in growth velocity and
1 q+ o$ C/ `+ A& y- M+ o! padvanced bone age, as seen in our patient.
2 W' C" c1 M2 X) L  K) l4 JThe long-term effect of androgen exposure during
! w; l; L5 C! W# aearly childhood on pubertal development and final: L  e% u# c8 d' i3 Z+ V
adult height are not fully known and always remain) z# Y/ {& Y7 h& E0 `5 v
a concern. Children treated with short-term testos-
2 V7 a  e5 M" o6 O2 dterone injection or topical androgen may exhibit some
/ f$ E, i. h6 z0 p4 q- {acceleration of the skeletal maturation; however, after( M% y" y. ~( P  f" R! Y+ @' }
cessation of treatment, the rate of bone maturation; ^4 c% ^9 ?8 \- n8 ]
decelerates and gradually returns to normal.8,9: Y) }& `9 h/ M4 `
There are conflicting reports and controversy
* z1 I4 D: {  Y8 H$ Sover the effect of early androgen exposure on adult
, \# ]; z4 j# {penile length.10,11 Some reports suggest subnormal
3 Z* |5 M$ L5 v3 \4 f1 J# c- t' Padult penile length, apparently because of downreg-
( x  o) Z' p1 G2 W* e- ]ulation of androgen receptor number.10,12 However,& p4 g& S( B+ I/ D* ^! e
Sutherland et al13 did not find a correlation between
4 k  w- I- P' qchildhood testosterone exposure and reduced adult/ a% x7 z" U& G% `7 K* l0 ^
penile length in clinical studies.0 j+ F7 R( A5 y
Nonetheless, we do not believe our patient is
# t5 _; m" D8 f! u8 Jgoing to experience any of the untoward effects from! @  h* f1 f+ V! a( H# e: ~$ }7 A" i% t1 N
testosterone exposure as mentioned earlier because
0 w" D) A: b% F  y! p$ {the exposure was not for a prolonged period of time.% b5 G/ }" R8 k7 B2 Q
Although the bone age was advanced at the time of/ _0 f. G) E; ?& B$ a
diagnosis, the child had a normal growth velocity at4 S  L% y9 Q/ r
the follow-up visit. It is hoped that his final adult
5 x9 P" d  K& }3 |# e8 e8 uheight will not be affected.% C* C. u: u' a& M+ h
Although rarely reported, the widespread avail-
$ @% \& @  B+ j8 k/ qability of androgen products in our society may8 c' G" ^  \! @% b9 v* q
indeed cause more virilization in male or female
* C8 e& q: o# y* u- ychildren than one would realize. Exposure to andro-- F9 V: Y1 z, J; n* `. C
gen products must be considered and specific ques-" Z% o6 X5 ]( e, Y) o% J
tioning about the use of a testosterone product or
; g" B3 n  k3 v8 `: Igel should be asked of the family members during( i% b4 j- U3 X
the evaluation of any children who present with vir-) p/ ~( U( M. l* H0 V0 r/ R0 A! o
ilization or peripheral precocious puberty. The diag-# E3 R4 b3 z/ h! j& h
nosis can be established by just a few tests and by7 L  H: Q' w* y0 n: k8 d6 P
appropriate history. The inability to obtain such a! B. A8 Y& I* ~" Z
history, or failure to ask the specific questions, may
( _+ V6 X+ T5 a0 {) T% q- uresult in extensive, unnecessary, and expensive6 t- n7 G" l1 S( D$ A% G* A
investigation. The primary care physician should be1 Z* t) W! S) q$ B, i  C
aware of this fact, because most of these children6 L# N' a; p/ P# a" E7 d+ L% `6 ^
may initially present in their practice. The Physicians’. `& Q3 P' l5 D
Desk Reference and package insert should also put a* ?! {8 [/ ~: m5 ]. _7 F* L
warning about the virilizing effect on a male or
0 F) t6 `. c2 l. Z4 o6 b5 G1 wfemale child who might come in contact with some-
8 _3 w' T. N7 ^9 I) \3 kone using any of these products.3 ?) J( t" v4 r5 S$ b8 Z
References4 d7 F" y) {. i6 G( H
1. Styne DM. The testes: disorder of sexual differentiation" @3 \5 G: @0 [, V
and puberty in the male. In: Sperling MA, ed. Pediatric
+ O; [  i6 S+ P. O3 \0 ?Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- t3 x4 l: s$ e3 L# f2002: 565-628.: d$ k3 I6 D6 j, x) h: P' A
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, x# p8 z( q+ V6 ]  f4 Lpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
9 f' u2 Q& K3 w8 l! l# T7 \Boy Induced by Indirect Topical1 V& h: U; `. ]1 U7 ^
Exposure to Testosterone* K$ l* s  {" R, q& d) E
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,28 ?0 r! }+ l. b# ]: h# H
and Kenneth R. Rettig, MD1% I7 q7 C# |9 [
Clinical Pediatrics  }9 U+ C% q) ^: ?* F
Volume 46 Number 6  O7 r- [2 v/ u9 R+ v2 A$ Q" L
July 2007 540-543) @  v+ J6 U8 a, H
© 2007 Sage Publications
9 Z+ g3 }3 e) J8 H10.1177/0009922806296651
" F( |. J& M; y, L# c4 uhttp://clp.sagepub.com
0 p/ E3 L" \2 H, i3 ]# Ahosted at- V( l) N9 J5 L5 a4 r; j
http://online.sagepub.com
5 n; y: @" @9 k' R" {: R# h' R2 lPrecocious puberty in boys, central or peripheral,
6 C& l) w3 J  a1 p! ]2 d0 W' V0 uis a significant concern for physicians. Central
8 V9 l/ a+ V; W  k2 X. S6 L$ `precocious puberty (CPP), which is mediated' z/ n$ W4 ^+ s2 W2 \
through the hypothalamic pituitary gonadal axis, has
9 c% f- Y4 z! d1 S  \6 ]a higher incidence of organic central nervous system* ^0 k. \5 Z! B* \4 n
lesions in boys.1,2 Virilization in boys, as manifested
. m- q5 f, k: B' @! oby enlargement of the penis, development of pubic
* W. [* r# E% d: Zhair, and facial acne without enlargement of testi-% y; C0 R0 ?% e7 B* D
cles, suggests peripheral or pseudopuberty.1-3 We: b* t$ f& D1 `; h* F* Y" I
report a 16-month-old boy who presented with the
( X  o, [' k+ ?% @! N; s9 U" fenlargement of the phallus and pubic hair develop-
, J7 L# v% _( q! Jment without testicular enlargement, which was due& ~" g) F+ E; B2 E6 G
to the unintentional exposure to androgen gel used by3 g5 O' W( o- ^. J4 _/ Q
the father. The family initially concealed this infor-% v- p( }$ R: M: s
mation, resulting in an extensive work-up for this
5 B% N( C: r8 P/ @( X9 `child. Given the widespread and easy availability of
0 X" j" x+ [  D/ Q! g0 a8 Ptestosterone gel and cream, we believe this is proba-
- R, s8 _% f6 X1 z, Hbly more common than the rare case report in the6 f) m1 p' a& X: N
literature.4
2 s  w) m/ |7 s# `$ \) v) J/ O! uPatient Report
( w  {" H- [4 }! T5 l* rA 16-month-old white child was referred to the
6 ]4 Q( V+ e1 x9 P/ H, oendocrine clinic by his pediatrician with the concern" X3 W' P+ W# L& d  t
of early sexual development. His mother noticed' w  l8 h) g# Q% @$ r& A0 T! ], `
light colored pubic hair development when he was
( c) y! ~1 k7 P2 Q; W& ^, bFrom the 1Division of Pediatric Endocrinology, 2University of0 Z8 V' `6 M; A/ {% e% e: ~
South Alabama Medical Center, Mobile, Alabama.0 k& e3 J" S0 Y1 t# a* \0 l8 p
Address correspondence to: Samar K. Bhowmick, MD, FACE,( `1 n6 a) A5 _" B" y
Professor of Pediatrics, University of South Alabama, College of
, w. @8 S' b0 i' Z# pMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 j  M$ `( b; Q3 t- I1 s6 U/ Y+ |6 D) k
e-mail: [email protected].
3 r# |9 R8 K7 V6 }about 6 to 7 months old, which progressively became
0 x4 p1 h$ n$ w, B' ^darker. She was also concerned about the enlarge-. D% t/ A( X. c* W$ R6 t, E
ment of his penis and frequent erections. The child
# F% G" ~  P$ ]5 {; Qwas the product of a full-term normal delivery, with+ _8 v& J6 H1 E9 \+ v# b8 {9 m
a birth weight of 7 lb 14 oz, and birth length of
. b# _! v4 D5 y3 @& ]  L0 v+ J+ ?* h! K20 inches. He was breast-fed throughout the first year" Y1 D4 _" ~% z& E
of life and was still receiving breast milk along with. I6 _. q4 h8 E8 ^" z
solid food. He had no hospitalizations or surgery,
  c2 x8 E! f' zand his psychosocial and psychomotor development
/ \: p" ]: a, H6 cwas age appropriate./ \5 O, S( W, R7 z' I
The family history was remarkable for the father,
- |) `3 E( W* q$ ?5 u$ {who was diagnosed with hypothyroidism at age 16,' ?+ Q* V5 D/ @; a' C$ I
which was treated with thyroxine. The father’s4 h1 Z9 ~3 T% r$ }* a; F2 [9 }
height was 6 feet, and he went through a somewhat
/ @$ H0 G0 M9 q+ }8 a' oearly puberty and had stopped growing by age 14.
. E$ }. Y* T) l% B! qThe father denied taking any other medication. The
' u2 j- I  s' v$ H) n& l- wchild’s mother was in good health. Her menarche
- I- R3 S, t' Y2 }9 fwas at 11 years of age, and her height was at 5 feet
- h6 D9 N- o- }% d" |6 I5 inches. There was no other family history of pre-/ l0 q4 I" Q) V! i: E- j
cocious sexual development in the first-degree rela-
! u% p' {" A  c1 j+ R2 ytives. There were no siblings.* e* h: [/ a9 s4 b/ v8 j0 f
Physical Examination
! T( M( m# Q* m; |( VThe physical examination revealed a very active,0 C4 f3 p) |0 c0 p8 ~0 J
playful, and healthy boy. The vital signs documented
  [  `6 }9 {2 e2 K" b! i) |a blood pressure of 85/50 mm Hg, his length was
! h! C4 J3 O# ?! Q% p( ?90 cm (>97th percentile), and his weight was 14.4 kg
* j1 y4 G+ ^; T(also >97th percentile). The observed yearly growth
& Z) X! Y. l; Z/ {5 pvelocity was 30 cm (12 inches). The examination of
( Q/ y8 u8 }+ a+ c+ T) M4 fthe neck revealed no thyroid enlargement.
6 h1 X# T/ w+ H. g' T7 f& AThe genitourinary examination was remarkable for; E! Y' Q2 U. V& z+ M4 W
enlargement of the penis, with a stretched length of
3 n3 H1 c: a8 h( V8 L$ Q8 cm and a width of 2 cm. The glans penis was very well' @/ W. E9 `0 U5 U
developed. The pubic hair was Tanner II, mostly around" v4 g9 W0 b2 h/ l  F2 p  k! j
540( a6 C9 F, D! t) V7 J& m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 J) s$ R/ Z( a8 N& V
the base of the phallus and was dark and curled. The& K0 m, O( }' f! n# K% F
testicular volume was prepubertal at 2 mL each.
6 Q& n9 b1 p1 G$ h( M2 PThe skin was moist and smooth and somewhat
4 `8 Q" \! L9 R( X7 O- @/ ooily. No axillary hair was noted. There were no
0 u! A9 b) J4 G4 vabnormal skin pigmentations or café-au-lait spots.
4 Z8 d' D' \6 n, B+ y8 ^Neurologic evaluation showed deep tendon reflex 2+
% h, x8 n' o3 J! T; V. N" ybilateral and symmetrical. There was no suggestion
' d) P$ D( y/ j/ }of papilledema.
+ q, {: V% }  N& `, e- T: uLaboratory Evaluation
& I; e" S5 r: j9 YThe bone age was consistent with 28 months by& y% M* q7 t$ Q* ]
using the standard of Greulich and Pyle at a chrono-  h# |5 m) L& k  M
logic age of 16 months (advanced).5 Chromosomal
7 }2 f5 c, c! Y+ V- U+ skaryotype was 46XY. The thyroid function test5 b1 A6 _9 V6 E  H, x
showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 Y. `: b1 \1 d7 _" i
lating hormone level was 1.3 µIU/mL (both normal).( \2 y/ R3 g9 [1 K' x6 }9 `
The concentrations of serum electrolytes, blood7 s% p5 Z  b- H5 q
urea nitrogen, creatinine, and calcium all were8 p3 m" A& R! z3 L3 `3 @
within normal range for his age. The concentration* G6 Y% B5 V5 B" n: i- G
of serum 17-hydroxyprogesterone was 16 ng/dL
$ S- Y# M+ X3 G5 \7 s( T(normal, 3 to 90 ng/dL), androstenedione was 20
4 U7 N' b7 y* t  H% Xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# A- O# v. m8 \+ O, W
terone was 38 ng/dL (normal, 50 to 760 ng/dL),; L( g9 ?& `4 q6 J0 F8 v* C
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
% t. c5 D% ^+ Z, u. k* E9 i49ng/dL), 11-desoxycortisol (specific compound S)8 m, a% m( P, W7 O8 O0 H
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-' \8 o9 r" g- B( Z) @/ M! [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, x2 Q4 T+ h# I; ]; g) w' A8 Y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
5 _. Q1 S+ K9 c0 J8 I0 gand β-human chorionic gonadotropin was less than
# Z/ u. Z& C# L* A5 mIU/mL (normal <5 mIU/mL). Serum follicular+ h, M- F9 y& ~8 }2 P9 {( x7 X
stimulating hormone and leuteinizing hormone
: F; _8 H  x- e* ]concentrations were less than 0.05 mIU/mL
( `3 X; F% Q2 y  `' t(prepubertal).4 y3 X/ Q7 H- u/ W* b
The parents were notified about the laboratory
; W6 ?: M: Y! xresults and were informed that all of the tests were0 l6 b$ k- a! c2 O. I
normal except the testosterone level was high. The/ ~$ F* ^  [; q% \: i5 w3 I- S
follow-up visit was arranged within a few weeks to( e4 F0 n1 t. v% H% w1 m
obtain testicular and abdominal sonograms; how-) Y+ O1 g& `/ A, N$ U4 B0 d
ever, the family did not return for 4 months.
7 K3 ?9 [5 Y, t+ P9 }! P; zPhysical examination at this time revealed that the2 [, t% K' L2 m' E- @
child had grown 2.5 cm in 4 months and had gained
/ e, i2 H4 ^- v& n) K( z9 ^) l& Y2 kg of weight. Physical examination remained
5 P% J/ `  p0 I4 ^  lunchanged. Surprisingly, the pubic hair almost com-
0 B/ l6 Y. O: D* m/ O; A. h5 H2 Mpletely disappeared except for a few vellous hairs at4 H% h7 T/ R1 u2 t7 @
the base of the phallus. Testicular volume was still 2: y, _  M, ?& k7 m, c. d2 p
mL, and the size of the penis remained unchanged.+ [5 K, F, M" f) Z5 D+ ^+ t! d
The mother also said that the boy was no longer hav-
; m! r3 A/ _2 e+ \4 cing frequent erections.
' S- X2 L2 u3 B% ]* |: m/ vBoth parents were again questioned about use of& {8 t3 r' x) x* `
any ointment/creams that they may have applied to
0 g1 t1 f8 F* M+ ethe child’s skin. This time the father admitted the, h+ C( q+ g6 K7 i- ]4 c- u
Topical Testosterone Exposure / Bhowmick et al 541
2 o7 p; C- i$ j& j4 Juse of testosterone gel twice daily that he was apply-, K3 g- f# q6 j+ s
ing over his own shoulders, chest, and back area for0 {3 K- N  |! z8 n
a year. The father also revealed he was embarrassed. K! d3 n) r9 P& v! U( Q# F; j( w
to disclose that he was using a testosterone gel pre-2 X/ }0 Y/ T( j( _/ @: B) F- R
scribed by his family physician for decreased libido
2 O  O, \8 p9 Msecondary to depression.8 t2 h  H8 E- y+ V. ]/ A- {3 F
The child slept in the same bed with parents.+ K0 Q0 D( I1 F$ |: {# c
The father would hug the baby and hold him on his
( _! O3 e# z* q( U7 Vchest for a considerable period of time, causing sig-
; L5 c1 V0 C3 x1 [" S9 S2 qnificant bare skin contact between baby and father.% H& J' `$ g' U3 ]- T  w
The father also admitted that after the phone call,
# X) W- P3 }' _when he learned the testosterone level in the baby
4 R1 S# c' z5 n, n+ I  M8 C  t) c$ xwas high, he then read the product information
7 c& G$ A  P2 F% E& G  ypacket and concluded that it was most likely the rea-$ r8 c. A  F/ O
son for the child’s virilization. At that time, they
, D; ?1 [, d( i+ i9 B' ?decided to put the baby in a separate bed, and the; \3 C6 ]% S! j0 A8 E4 p0 V+ y
father was not hugging him with bare skin and had
: ^' E. n1 r" i. e* mbeen using protective clothing. A repeat testosterone
4 y+ I$ f; J( z  Ktest was ordered, but the family did not go to the
) i/ A' o4 [* z, slaboratory to obtain the test.
9 x. R3 m  P8 `% G" PDiscussion: f" C/ E2 h1 l% M$ O0 a* i; H9 ^
Precocious puberty in boys is defined as secondary" A' T+ a# |6 X. S4 Z9 C
sexual development before 9 years of age.1,4/ Y7 z/ J, w) Q/ D/ S5 K
Precocious puberty is termed as central (true) when3 Q9 v  n# t4 r7 D8 [' N
it is caused by the premature activation of hypo-5 |9 q6 B+ Z/ m' U- D4 \
thalamic pituitary gonadal axis. CPP is more com-1 i* h9 r* S7 j/ X* K7 u$ e' `! Q
mon in girls than in boys.1,3 Most boys with CPP
- ]6 V* U1 \- G" Zmay have a central nervous system lesion that is
* [4 e" C: h6 m! jresponsible for the early activation of the hypothal-+ _8 K5 i3 U' v0 ]1 f% D& @
amic pituitary gonadal axis.1-3 Thus, greater empha-
2 G$ I2 U8 ]# _5 M0 X1 hsis has been given to neuroradiologic imaging in
- @  P: S! l* V- h6 S! Uboys with precocious puberty. In addition to viril-
3 }7 O) w% P/ xization, the clinical hallmark of CPP is the symmet-9 {  v- S! u+ o6 f9 u6 F- S
rical testicular growth secondary to stimulation by) F8 }" i. U) b  A$ _; L/ \* J
gonadotropins.1,3
" c5 ]  ?3 \  _0 Y7 Q  K$ zGonadotropin-independent peripheral preco-
5 a& `8 k. H0 W% S: Z  a3 p$ H* ^cious puberty in boys also results from inappropriate
) U1 Y& g# T; L8 o, ?8 oandrogenic stimulation from either endogenous or
' `/ k$ c9 l8 iexogenous sources, nonpituitary gonadotropin stim-
( D  K7 ^7 ~1 e+ j8 ]  zulation, and rare activating mutations.3 Virilizing
/ ]2 c; b" \# c- Y' j% D3 Jcongenital adrenal hyperplasia producing excessive
4 m! r* B" L: K0 j5 m3 O$ Z# gadrenal androgens is a common cause of precocious9 p6 h& h8 y6 A( B1 f
puberty in boys.3,40 W, N  b( Y7 k  M/ O
The most common form of congenital adrenal2 W; S- G6 v* Z$ e; g
hyperplasia is the 21-hydroxylase enzyme deficiency.4 W+ z' y$ e- J5 h$ g! i
The 11-β hydroxylase deficiency may also result in4 P. N, d( l; q$ N( _; p
excessive adrenal androgen production, and rarely,+ [3 ?8 o+ o$ k
an adrenal tumor may also cause adrenal androgen
1 J- Y! j! I& r7 l2 ~# d/ B- W% eexcess.1,3: \( N2 d1 K1 S1 C2 w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! ^9 a- e0 R% i7 R542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
7 o7 m7 z/ \; Q$ zA unique entity of male-limited gonadotropin-: ]: r# F1 F, v
independent precocious puberty, which is also known  z- W1 Y, w$ \( e3 [% y! {# l
as testotoxicosis, may cause precocious puberty at a
/ k" L2 ^+ O* r% `& }- pvery young age. The physical findings in these boys
+ f4 `$ M/ r7 [9 \% O& awith this disorder are full pubertal development,1 P1 n  A# I$ a( w1 V
including bilateral testicular growth, similar to boys/ ?8 S( p9 t1 D% H& ^
with CPP. The gonadotropin levels in this disorder! n# y3 d; k3 L* m$ R( d$ |
are suppressed to prepubertal levels and do not show; k8 \0 {8 l8 i: U, q  P
pubertal response of gonadotropin after gonadotropin-' L( x& w' f! Z$ X4 w
releasing hormone stimulation. This is a sex-linked8 y4 ^! ]* P& s: ^. C
autosomal dominant disorder that affects only
: e: y9 d3 d) @; {males; therefore, other male members of the family, O+ D" h" E8 X8 T6 q
may have similar precocious puberty.3- g# T4 g( q! g% m( `$ ~7 C
In our patient, physical examination was incon-
  r9 a8 ]; \  ]7 `" h9 L5 {( Z2 r" c' T9 lsistent with true precocious puberty since his testi-* l7 {1 \4 U4 ]# B, i  ~
cles were prepubertal in size. However, testotoxicosis
5 b9 \5 E' A; B0 K: _9 V( Cwas in the differential diagnosis because his father) Z: C' M1 W' S0 B0 y# p
started puberty somewhat early, and occasionally,
- q$ p) \9 w# L( Z7 j9 j7 |testicular enlargement is not that evident in the0 H% }( v* ?) q+ t  @- x' L. V
beginning of this process.1 In the absence of a neg-
8 P5 h% `: Q6 U0 w7 A! J. V8 O/ kative initial history of androgen exposure, our
6 q8 {. ?. Q/ U+ n$ mbiggest concern was virilizing adrenal hyperplasia,6 j, q, k6 G6 D$ f& b
either 21-hydroxylase deficiency or 11-β hydroxylase
& h* |, [  Q+ m& edeficiency. Those diagnoses were excluded by find-
" F0 ]* Q! ^( Sing the normal level of adrenal steroids.
- l9 ~# b/ V; CThe diagnosis of exogenous androgens was strongly6 ?6 E  N; H& _. [6 O- ~9 S% {# ]
suspected in a follow-up visit after 4 months because: i8 @# x6 O. B; v+ Z
the physical examination revealed the complete disap-5 R5 N9 x6 s1 N+ O
pearance of pubic hair, normal growth velocity, and
4 s# F: [& @( X! p6 R, L( edecreased erections. The father admitted using a testos-; o+ j$ z5 L7 s" X
terone gel, which he concealed at first visit. He was- ^; m) F+ ?. T8 ^2 a# L# Y
using it rather frequently, twice a day. The Physicians’$ ^5 A3 q) F  A6 |5 H) [4 l
Desk Reference, or package insert of this product, gel or
* x' [; z) x& n! C8 z5 R8 R3 ucream, cautions about dermal testosterone transfer to; B) Z- d) [! b# P
unprotected females through direct skin exposure.
( \$ F5 \" Q# ~1 |4 w: ESerum testosterone level was found to be 2 times the0 q- ?2 m+ }' M( y! _& o
baseline value in those females who were exposed to
) j" |/ F& J6 L/ L2 |. V/ W/ geven 15 minutes of direct skin contact with their male
" q1 ^( B  T5 H. w: t5 B; k0 epartners.6 However, when a shirt covered the applica-
4 C! k' I9 i$ g, k  i9 ltion site, this testosterone transfer was prevented.
' y% ^- Q- b8 ^0 K% sOur patient’s testosterone level was 60 ng/mL,
% [+ ^. b1 R5 `6 }. [which was clearly high. Some studies suggest that# _3 m  h1 T& Z, C$ U
dermal conversion of testosterone to dihydrotestos-1 `% x! z, }0 Q) {8 w
terone, which is a more potent metabolite, is more
5 N. B; W1 d; N& P) ]2 ractive in young children exposed to testosterone& D0 |% M/ ]0 J; M
exogenously7; however, we did not measure a dihy-+ A& q- ^; z; s" d5 i* n
drotestosterone level in our patient. In addition to5 F  P' t5 \1 b+ v2 W0 |7 v
virilization, exposure to exogenous testosterone in
6 L+ K) E9 a$ G/ e8 E5 s  lchildren results in an increase in growth velocity and
( Z5 Q; m4 X5 m" |2 }) M0 E: uadvanced bone age, as seen in our patient.
) a# ^" [# I2 C' k4 |The long-term effect of androgen exposure during
9 Z' K4 K: H1 e+ C( wearly childhood on pubertal development and final& b& [  d# ?2 D
adult height are not fully known and always remain
9 W4 O, {/ Z, @6 Va concern. Children treated with short-term testos-) y( S# B( v, _7 j
terone injection or topical androgen may exhibit some
) ~$ a9 X: ?5 f# {  l: H" c, `9 b# Xacceleration of the skeletal maturation; however, after, z1 t7 l$ ]' t9 V9 f
cessation of treatment, the rate of bone maturation
7 c: `) |  C) a( P! |/ [decelerates and gradually returns to normal.8,9, E% b: k. i5 r/ T% U( B
There are conflicting reports and controversy4 B5 k5 W$ j% I- X3 {" a* e- K
over the effect of early androgen exposure on adult  w/ N' j. m) H: P0 x4 u' b
penile length.10,11 Some reports suggest subnormal3 S) x7 ?0 E. j& a+ _: k: ^
adult penile length, apparently because of downreg-
. A, _. U, R* ^* n5 Lulation of androgen receptor number.10,12 However,) l: W6 q6 c/ m9 A: H
Sutherland et al13 did not find a correlation between
9 S3 h9 m6 y- V; J( W/ k0 u' rchildhood testosterone exposure and reduced adult
* K9 X7 C. g$ B. u) D7 q" Vpenile length in clinical studies.
0 z3 i( u  g- d& [, {; v8 LNonetheless, we do not believe our patient is
3 a, V% v. |: ygoing to experience any of the untoward effects from8 z$ q# y; ?2 z; \' C( w% \
testosterone exposure as mentioned earlier because# _6 N& v9 l) m; f6 B, z: ?
the exposure was not for a prolonged period of time.
2 E1 M1 C; m7 B% _4 |* l! ]4 _Although the bone age was advanced at the time of. e+ ~! f1 @" {
diagnosis, the child had a normal growth velocity at, i+ _( x  k% H
the follow-up visit. It is hoped that his final adult* v% ~* J+ M& G$ g, }
height will not be affected.2 a6 }( s' r) D! ^
Although rarely reported, the widespread avail-: [' x' `: R; {. n9 k
ability of androgen products in our society may
) E& V4 Q5 S3 R) {) l' t; l; Iindeed cause more virilization in male or female, p& R2 H- o9 L# |, x- r8 q+ ?
children than one would realize. Exposure to andro-8 i# _  V! z3 ^1 H- H# X  r5 F$ l
gen products must be considered and specific ques-
  }' f2 p" v! z* Z5 {tioning about the use of a testosterone product or
" o# K6 a, R# a/ u1 sgel should be asked of the family members during
4 z/ i0 Z6 w* o& A3 I3 I# [+ Ithe evaluation of any children who present with vir-: n- U4 l3 W; q3 A+ P2 p1 N
ilization or peripheral precocious puberty. The diag-
- _3 v) w/ o& s1 N' enosis can be established by just a few tests and by: R' r6 ?4 n+ l6 u# ~% e! f4 W
appropriate history. The inability to obtain such a: H, n2 F# v6 G! K# h5 _
history, or failure to ask the specific questions, may# K' @+ j9 {6 u
result in extensive, unnecessary, and expensive
% t: N+ D( `* g3 S$ T  h; c/ `investigation. The primary care physician should be
# X, s2 s0 Z5 O  n, k; O" g0 R8 haware of this fact, because most of these children; }, O# e2 h5 G/ i: R7 y( x# `
may initially present in their practice. The Physicians’
6 T0 u. T) Y( P# p* @Desk Reference and package insert should also put a5 N( R" `! j' N, p' D2 t9 y7 T
warning about the virilizing effect on a male or
. V5 h! l. v; rfemale child who might come in contact with some-+ U% J) {2 g+ {3 n+ E( a
one using any of these products.8 S  d# c6 u$ M2 L, z& p% f
References
7 a3 E# h) ]# ?2 L5 z/ H6 W2 x1. Styne DM. The testes: disorder of sexual differentiation, r, Y: b! @# k% p
and puberty in the male. In: Sperling MA, ed. Pediatric. r0 ~9 w9 j8 `0 j
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- H- y: Z) @. N5 `. J/ ]' ~8 m2002: 565-628.4 ~2 x7 C' u6 L) ]! G
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
5 N6 S3 {; P2 Qpuberty 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
% l  K- C1 {8 f* ^1 d
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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