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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
. D( |9 U9 M: s- G' e; ZBoy Induced by Indirect Topical
* p5 P) T) [- ]; q: }2 `Exposure to Testosterone% [; w1 b8 `4 k, R7 h4 S  I- a  L
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, [) g8 q7 i0 `8 [and Kenneth R. Rettig, MD11 u  Y2 N, y. X( s" y: q/ X$ R/ e1 v' G
Clinical Pediatrics6 n+ E3 X% B- f
Volume 46 Number 6
' T- k$ [; ~! R% e( y0 s" }July 2007 540-543* m4 {) S# @7 p+ U
© 2007 Sage Publications
3 [4 x, A9 @4 E  M; ]10.1177/00099228062966519 f4 b4 d! ^3 t0 R" f. E, o" i
http://clp.sagepub.com7 `% ]9 g5 j; V, T- `* J
hosted at7 a- L6 [8 K1 p. A$ b
http://online.sagepub.com
" q+ v% W( J  ?, ^9 `* ZPrecocious puberty in boys, central or peripheral,
1 D) z8 {) W' C, W  f, y+ tis a significant concern for physicians. Central4 S) o( @0 u: e' ^- e. V; a5 _  q2 m
precocious puberty (CPP), which is mediated* J7 T# Q) t' l& h8 ?" z0 e8 m
through the hypothalamic pituitary gonadal axis, has
+ U  ^0 O- J* N; _a higher incidence of organic central nervous system$ \. J# X, \( O. ^
lesions in boys.1,2 Virilization in boys, as manifested# ?; w& A' X6 u" z: ?2 u/ I9 {, r3 @
by enlargement of the penis, development of pubic) F4 c: Q7 R/ m
hair, and facial acne without enlargement of testi-
5 r& ^( s' h' Ocles, suggests peripheral or pseudopuberty.1-3 We
* o% i( Q8 V5 \% }6 k: `7 zreport a 16-month-old boy who presented with the6 B, a+ [* q# _1 T5 x
enlargement of the phallus and pubic hair develop-% \; Y* r2 t+ q
ment without testicular enlargement, which was due
1 p! P0 d1 d5 Q( K% _7 e! f' A! Kto the unintentional exposure to androgen gel used by
- _( }7 J3 p' b! v7 bthe father. The family initially concealed this infor-
" z( a" p. [- ]' {: P- _/ hmation, resulting in an extensive work-up for this) U5 B3 J( e6 @0 k' ~
child. Given the widespread and easy availability of
$ T6 ^! V( E0 {* q+ ?8 ctestosterone gel and cream, we believe this is proba-  {0 U3 o  K, ^7 v( e& }) p2 z
bly more common than the rare case report in the
/ _3 A4 |/ {9 b' A; }literature.4& U5 T1 i, v! r8 W5 `
Patient Report
2 m9 f' J  I4 x0 F5 E% v) K2 fA 16-month-old white child was referred to the
: G% L8 k6 ?( @# c! xendocrine clinic by his pediatrician with the concern
3 \  ^* }) K$ n2 I7 Fof early sexual development. His mother noticed+ f4 F+ t3 q4 T* `8 H9 K
light colored pubic hair development when he was
) b2 [2 l5 b% Z* uFrom the 1Division of Pediatric Endocrinology, 2University of
. ]4 R/ j4 l1 C( K& oSouth Alabama Medical Center, Mobile, Alabama.
+ |& r  ]  d4 vAddress correspondence to: Samar K. Bhowmick, MD, FACE,
& g" {; n; X) G4 I" e  p# oProfessor of Pediatrics, University of South Alabama, College of
  O" M% L* E: Y. n5 o5 m0 G' kMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ n8 \* A* U- Q2 C- p2 a: he-mail: [email protected].& _% u) d  U5 {+ I2 T1 l% \1 r
about 6 to 7 months old, which progressively became
5 _& o$ F* d8 c8 L( C7 _darker. She was also concerned about the enlarge-, `+ }8 a6 x6 ]) }8 h. h, h0 Z1 F
ment of his penis and frequent erections. The child
% ?6 O4 l- M0 A5 |' k; V  Z# Pwas the product of a full-term normal delivery, with- S0 d; U, W# W: N: l* Z
a birth weight of 7 lb 14 oz, and birth length of
: h1 e! r7 G/ _. {0 w8 f  Q20 inches. He was breast-fed throughout the first year0 N4 V# J; W: H8 j
of life and was still receiving breast milk along with/ G' X8 ^: n- E+ u
solid food. He had no hospitalizations or surgery,
4 _3 K( u4 U4 p$ Mand his psychosocial and psychomotor development
! |4 h6 C4 H. }( Q- a, `was age appropriate.0 `1 g& i" y; Z3 r5 a0 O
The family history was remarkable for the father,
5 g3 u9 l6 g! C. @/ Uwho was diagnosed with hypothyroidism at age 16,
7 o8 E1 C  t% t( f5 Awhich was treated with thyroxine. The father’s/ i% A* }0 u0 b  g* z6 R
height was 6 feet, and he went through a somewhat* t7 d+ f0 J3 L  _4 A9 g0 f5 b4 w
early puberty and had stopped growing by age 14.
6 r" r( J! w3 O9 R% C) G  [" q5 FThe father denied taking any other medication. The
& |0 X; f& p3 x9 B6 ^child’s mother was in good health. Her menarche2 o, U( l3 ^: Q9 r% q1 o+ _
was at 11 years of age, and her height was at 5 feet  X6 F& P; `% K# n
5 inches. There was no other family history of pre-8 A; Z1 @" t+ E' X
cocious sexual development in the first-degree rela-
$ h% B* r$ M. j  ?tives. There were no siblings.9 G& f. V, V$ Y0 p1 O: w. ]
Physical Examination
9 ~0 r3 R9 R1 C- R8 H1 cThe physical examination revealed a very active,( N  ~' k3 p& k  M3 T& W& b7 @
playful, and healthy boy. The vital signs documented0 b: O) C. G0 L% N. ~
a blood pressure of 85/50 mm Hg, his length was3 Z/ {6 r2 |* `
90 cm (>97th percentile), and his weight was 14.4 kg
( o6 j5 }' R& W' Q(also >97th percentile). The observed yearly growth
6 j% g" e: `) z5 Gvelocity was 30 cm (12 inches). The examination of
2 w1 B  `& T! f6 ^+ `the neck revealed no thyroid enlargement.
- o9 w! \2 e' k( G7 x' f9 ]+ @The genitourinary examination was remarkable for
& `/ ?5 A7 V0 ~7 benlargement of the penis, with a stretched length of- Y8 |0 z4 i4 R& T8 B7 @
8 cm and a width of 2 cm. The glans penis was very well8 L* P6 [1 U+ x
developed. The pubic hair was Tanner II, mostly around, y" w9 F5 o/ ^: K: f) R) W& J  S
5404 }3 K9 Y/ ]% `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& U7 K9 \8 J) L6 _4 @: t  sthe base of the phallus and was dark and curled. The" u  R! j. H. w2 l% e5 y5 y
testicular volume was prepubertal at 2 mL each.
0 n) v" |: W) O6 R3 qThe skin was moist and smooth and somewhat
  N  X9 p; A  }( D, m6 O6 ooily. No axillary hair was noted. There were no
$ l. s* U- {9 a& Gabnormal skin pigmentations or café-au-lait spots.
* H& X& O9 K5 gNeurologic evaluation showed deep tendon reflex 2+
# L, ^7 J4 b" U* g  Y" Wbilateral and symmetrical. There was no suggestion
( Y# e8 s. K% ?6 |of papilledema.2 r5 F8 ?0 f0 G; B* g6 n" a
Laboratory Evaluation
0 n' v2 k1 _, X) F" OThe bone age was consistent with 28 months by3 r( B3 q* Z' ^; s6 x$ S
using the standard of Greulich and Pyle at a chrono-
! m' X; }7 [4 p( clogic age of 16 months (advanced).5 Chromosomal
# R3 F0 _; j) z& T0 Kkaryotype was 46XY. The thyroid function test) [0 }6 g  V$ O  i# i
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ E# m- T, I& ]/ {& T) [lating hormone level was 1.3 µIU/mL (both normal).8 I- A9 U2 h8 Z# e
The concentrations of serum electrolytes, blood
1 K; _7 m/ `+ X9 yurea nitrogen, creatinine, and calcium all were1 H- M% T7 U6 q
within normal range for his age. The concentration
+ b- N! J  f! b+ g! r7 a% i4 n- Rof serum 17-hydroxyprogesterone was 16 ng/dL3 e& V6 E, ?) g7 f
(normal, 3 to 90 ng/dL), androstenedione was 20
8 `4 o0 p5 _0 N$ Nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
/ H+ T0 [/ S  pterone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 [. M8 o& `, H$ p0 b/ `  Bdesoxycorticosterone was 4.3 ng/dL (normal, 7 to% Y9 v: M! U3 F/ U6 h
49ng/dL), 11-desoxycortisol (specific compound S)
6 c' ~% K& \2 Ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-1 A4 Q$ }8 F: x8 Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
; d- [; s9 n  Wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) `. m4 B$ F, m0 Qand β-human chorionic gonadotropin was less than
0 S; r# |/ N* @( |; ?5 mIU/mL (normal <5 mIU/mL). Serum follicular# I3 z! A$ K# S, s; r! l7 ]5 T& R
stimulating hormone and leuteinizing hormone
8 e9 B3 A. r) k5 vconcentrations were less than 0.05 mIU/mL
$ ?' a7 v* D; A+ q3 Q(prepubertal).
' v! c) Z- X3 e$ s/ p* sThe parents were notified about the laboratory) b9 }/ y1 b% U  \+ ^
results and were informed that all of the tests were! J' l  {! @* Q
normal except the testosterone level was high. The
6 s- d3 z# J4 r% ffollow-up visit was arranged within a few weeks to  H5 @' H/ v. _' \
obtain testicular and abdominal sonograms; how-
; V4 o5 H; p6 Y/ S4 _+ h1 Vever, the family did not return for 4 months.
4 ~. u, M. E$ r& i3 sPhysical examination at this time revealed that the/ `4 e8 I4 @, Z2 V
child had grown 2.5 cm in 4 months and had gained
% `# ?7 t# }& T% O9 |. w% {+ U2 kg of weight. Physical examination remained- `8 |6 Q9 `) I9 d5 S
unchanged. Surprisingly, the pubic hair almost com-/ O, ?6 N  d1 `! Y* c, a/ k# f
pletely disappeared except for a few vellous hairs at
! P+ U! Y2 S6 Z+ Pthe base of the phallus. Testicular volume was still 2( c, i0 W1 b  ]7 M  w! ]
mL, and the size of the penis remained unchanged.
$ c- I; x9 I. k; N# xThe mother also said that the boy was no longer hav-
7 P% g% D# H  \' F( x# cing frequent erections.
) {/ {* c- Z! X1 v# T$ P# T, \Both parents were again questioned about use of
) W9 D2 d. c4 a& e) W9 C! Dany ointment/creams that they may have applied to
7 y- [. _" X; r, ]8 u7 r! O- Mthe child’s skin. This time the father admitted the
% i# U  q9 _! D; `6 }Topical Testosterone Exposure / Bhowmick et al 541
0 ]; F- E: \+ b; Tuse of testosterone gel twice daily that he was apply-
9 H* Y5 n9 Q6 H: Z2 q- Wing over his own shoulders, chest, and back area for$ T+ {2 l5 H' N" ^0 L
a year. The father also revealed he was embarrassed
4 K# c6 H) Y5 D: N1 D1 `to disclose that he was using a testosterone gel pre-; y2 Z  @/ }: _% Z, }
scribed by his family physician for decreased libido; ?- A! y* J- P
secondary to depression.
+ A' s! S. l" {The child slept in the same bed with parents.( I( c$ L* [! q# h0 z; Q8 [, o
The father would hug the baby and hold him on his' Q, H7 p; z+ B8 d9 K. D
chest for a considerable period of time, causing sig-* S: o9 {0 p- d( I! Z! p
nificant bare skin contact between baby and father.( Y8 @0 g! Z# U, l4 V
The father also admitted that after the phone call,
. j  w+ k. q+ Q) X* q7 N6 R9 Z* qwhen he learned the testosterone level in the baby" Z8 Q. `( K2 E6 z
was high, he then read the product information
/ y3 ~! y0 @4 {- c4 e5 M+ kpacket and concluded that it was most likely the rea-
& ~- E3 |0 k8 kson for the child’s virilization. At that time, they. ?. B& _6 R/ \8 j: F2 {+ g
decided to put the baby in a separate bed, and the6 X! V1 X1 @3 S( m0 p4 J
father was not hugging him with bare skin and had1 P% v) ]$ D( s1 G  V. K
been using protective clothing. A repeat testosterone
: J, N# q) w0 W3 Y' itest was ordered, but the family did not go to the4 I% |5 H7 A7 l7 P. N0 V9 t6 N" o
laboratory to obtain the test.* E7 q; C" C8 R& ~9 J+ K& _
Discussion- W9 l6 m1 v- D- Y' y
Precocious puberty in boys is defined as secondary
" E/ [8 X0 l% M- Z9 L+ L- _7 Zsexual development before 9 years of age.1,45 B" k& u0 o0 u3 d3 T$ z" X2 A
Precocious puberty is termed as central (true) when
, W" q* `2 g6 ?6 J; q0 {& \it is caused by the premature activation of hypo-
- R2 e" q( C- j& Z) Q9 ]! Rthalamic pituitary gonadal axis. CPP is more com-  i. t! p" E9 ?4 |$ S
mon in girls than in boys.1,3 Most boys with CPP
* _1 ~/ e0 Z- L9 ?/ ~. b; G/ C. i' rmay have a central nervous system lesion that is# {0 P  U8 |8 |3 E; ]$ m6 S& r1 a
responsible for the early activation of the hypothal-4 O: R1 e! M7 l' M
amic pituitary gonadal axis.1-3 Thus, greater empha-! j6 Y* a+ {+ ~6 o& R# a; n) C
sis has been given to neuroradiologic imaging in* ?% K9 F( O0 p6 H- G2 T/ i
boys with precocious puberty. In addition to viril-
4 j: J. y( x% ^ization, the clinical hallmark of CPP is the symmet-
5 |- E8 B( d0 k1 Jrical testicular growth secondary to stimulation by* t. p% Y+ B3 w. m$ j
gonadotropins.1,3
5 [+ x+ ?1 E- ~Gonadotropin-independent peripheral preco-0 U$ t% S) h3 Y3 F) I) R( h
cious puberty in boys also results from inappropriate
+ v( x+ E  r. d7 A; Sandrogenic stimulation from either endogenous or
( g6 o) \' p8 g$ t& T; yexogenous sources, nonpituitary gonadotropin stim-
0 h. e$ l: u$ R9 w' L* l, yulation, and rare activating mutations.3 Virilizing
+ w5 T- ]" {8 m# h2 i- u$ P0 Bcongenital adrenal hyperplasia producing excessive
$ M. h# u1 E" t7 T6 `+ B  c- Yadrenal androgens is a common cause of precocious1 B, ?1 k* _( H: T
puberty in boys.3,46 b3 j' Z3 |/ x+ R4 c; [
The most common form of congenital adrenal
  V. K% @4 M4 i5 D; |+ thyperplasia is the 21-hydroxylase enzyme deficiency.
! N! J4 y& m5 |The 11-β hydroxylase deficiency may also result in
( @* C* h* ]: G7 }0 _excessive adrenal androgen production, and rarely,8 n) B& {/ F6 M  ^
an adrenal tumor may also cause adrenal androgen9 H! X* w) V- }" z6 \+ F
excess.1,3
. [  _! F" ^$ eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
% M3 P/ a6 a! J5 y$ }542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 Y2 K0 ~& A6 c; O$ ]A unique entity of male-limited gonadotropin-
( x2 P! O. l# z9 Z; h5 E) Z3 qindependent precocious puberty, which is also known
' Q6 e. i2 l/ ras testotoxicosis, may cause precocious puberty at a0 W* ~0 \# W5 c% o2 e
very young age. The physical findings in these boys
3 z+ J6 d. S: k- W% O7 T( Z5 ?with this disorder are full pubertal development,
$ J3 t$ i! k* O- D* a9 B( |including bilateral testicular growth, similar to boys
3 Q/ V2 p7 D9 c4 ]* P, mwith CPP. The gonadotropin levels in this disorder0 y0 O+ q$ o8 N
are suppressed to prepubertal levels and do not show
% V8 {/ @4 E& U7 p1 W8 r1 T, j/ T& Bpubertal response of gonadotropin after gonadotropin-  O. S% \' F' r" Y
releasing hormone stimulation. This is a sex-linked
: P- H$ q+ l  r" h8 r0 S" Dautosomal dominant disorder that affects only
# V6 ^  |  y; Q8 H( Tmales; therefore, other male members of the family
0 w; i" k' v/ `6 ?7 ~may have similar precocious puberty.3
0 Q) ~/ w) J8 v; q; I8 t) RIn our patient, physical examination was incon-
2 e- [, d9 F7 B6 l0 i- t' D. ?sistent with true precocious puberty since his testi-, z; S( H7 c0 d+ M3 k3 U, M/ A
cles were prepubertal in size. However, testotoxicosis
4 U! f8 a) n" iwas in the differential diagnosis because his father
5 x! S  R  A4 F0 j  `" O& Cstarted puberty somewhat early, and occasionally,: F  U1 q. k$ k9 s0 V
testicular enlargement is not that evident in the: p+ P6 C7 i. i" T+ |+ M: j) P9 q$ q  T
beginning of this process.1 In the absence of a neg-
2 |; t  S; |) Y9 Mative initial history of androgen exposure, our: m9 X/ }6 v; v/ U, h
biggest concern was virilizing adrenal hyperplasia,) F! d) d$ k: p! S5 A$ R3 e
either 21-hydroxylase deficiency or 11-β hydroxylase3 o# G4 M! U& R; F7 D, ~: ~0 s
deficiency. Those diagnoses were excluded by find-% n4 I6 G( W8 e3 O, ~0 H* ~
ing the normal level of adrenal steroids." @3 P: v0 t. P/ Z* _1 |
The diagnosis of exogenous androgens was strongly: L, v1 i( H9 l. o
suspected in a follow-up visit after 4 months because
! g) L* b2 L0 z# Pthe physical examination revealed the complete disap-
/ v- d0 Q- p+ hpearance of pubic hair, normal growth velocity, and
$ B( D' v; {: O* cdecreased erections. The father admitted using a testos-
+ n8 n$ G- l1 T7 Xterone gel, which he concealed at first visit. He was
2 u" b. l; {7 o5 n" x# yusing it rather frequently, twice a day. The Physicians’6 ]* y* n4 A) c0 F% c2 b' Q
Desk Reference, or package insert of this product, gel or
# ~) A% z- v  A  a7 K- Q: @# wcream, cautions about dermal testosterone transfer to
( p- v! P! y8 a" N9 Qunprotected females through direct skin exposure.+ g3 a' T' [) G2 _: E( j
Serum testosterone level was found to be 2 times the& f% w1 j1 n- G3 l: ~6 s
baseline value in those females who were exposed to
; N! O" d" ?" q# H9 g$ Neven 15 minutes of direct skin contact with their male
$ A* U5 T! N# ~- s5 M8 x4 `& ~partners.6 However, when a shirt covered the applica-
+ }0 H9 s" P2 `2 Z- Dtion site, this testosterone transfer was prevented.
6 j7 ?" k9 `3 s( ~2 \# UOur patient’s testosterone level was 60 ng/mL,
# D' ?9 F# {5 V  L& H9 Mwhich was clearly high. Some studies suggest that
! b+ C/ J4 G( U7 ^, `. Fdermal conversion of testosterone to dihydrotestos-" G6 z, f% i6 L4 S# \
terone, which is a more potent metabolite, is more
) n+ r( U( ?0 M3 b0 z, mactive in young children exposed to testosterone
+ g" q$ p% z! H+ Z* G4 e+ E5 t8 d6 uexogenously7; however, we did not measure a dihy-
5 y8 x) y0 I7 p/ Jdrotestosterone level in our patient. In addition to
* a# I9 {/ F4 w- D% ?* ~8 Cvirilization, exposure to exogenous testosterone in
: [. N- A8 f0 ~: g. M) ^: Zchildren results in an increase in growth velocity and) t( E+ H- ]( Q5 h0 ~3 u
advanced bone age, as seen in our patient.
7 K. T3 [# \4 P* f3 _The long-term effect of androgen exposure during8 U& n8 T0 y3 Q
early childhood on pubertal development and final
9 n% T$ C5 y0 `* G& Y) j2 v1 Zadult height are not fully known and always remain6 A% r* q& n, e* F" G
a concern. Children treated with short-term testos-. Q$ T1 Q0 ]! [7 n
terone injection or topical androgen may exhibit some
. ^+ {* i  ]! t/ ]acceleration of the skeletal maturation; however, after: |$ s. ]: q1 b( T5 A$ K/ A- q) _
cessation of treatment, the rate of bone maturation
% K/ A& x/ r) m! h+ Ldecelerates and gradually returns to normal.8,9
- y5 @0 i; W7 D' I5 d. |There are conflicting reports and controversy2 ~1 y5 l# _! Q( j. F6 v
over the effect of early androgen exposure on adult/ I5 H  I( R/ _6 ~# g
penile length.10,11 Some reports suggest subnormal& c7 E8 b/ \% F8 j3 J* n  m! V
adult penile length, apparently because of downreg-
4 A! y3 }& E7 X" |) J, X; culation of androgen receptor number.10,12 However,3 A0 g$ _! q$ x% K6 ]& E5 p- u; S
Sutherland et al13 did not find a correlation between9 ]2 b* w' Q4 f: k2 S% i  L' C
childhood testosterone exposure and reduced adult" j& f% o( n# P* i
penile length in clinical studies.; m* ^5 @- m/ K  h- g# ?% U$ q
Nonetheless, we do not believe our patient is1 ?7 [; W1 D8 S. `  b8 ^. ^+ j
going to experience any of the untoward effects from
4 _# g0 U5 `$ R/ e; l% M1 Z. ptestosterone exposure as mentioned earlier because
- b- c- G7 B0 N; u% |+ o8 x- Dthe exposure was not for a prolonged period of time.; O) h" K: {5 {6 ^* A/ ]" W# A' ?
Although the bone age was advanced at the time of8 ~2 U5 b- ?: s. m/ E( P5 N
diagnosis, the child had a normal growth velocity at
/ O& v5 o  V, X; \the follow-up visit. It is hoped that his final adult
5 _- e) {+ z3 Rheight will not be affected.; {% S2 s) d; W% ]5 R
Although rarely reported, the widespread avail-  p: `# ]+ G4 _+ ~- d
ability of androgen products in our society may8 z3 `) u+ w  L8 ?( U, k
indeed cause more virilization in male or female
8 o1 Q1 C9 l: L. i; [9 {6 Pchildren than one would realize. Exposure to andro-
& S1 g5 ?. I; W' ugen products must be considered and specific ques-* u' Z* ^8 y8 O1 ?3 j; c8 H& C+ h" r
tioning about the use of a testosterone product or
5 A/ l8 q* u6 W$ E$ h6 Igel should be asked of the family members during5 N# R+ Z! f" h$ z) o
the evaluation of any children who present with vir-3 @9 }4 Y# Z: d8 n+ [% P" t
ilization or peripheral precocious puberty. The diag-
1 k$ T1 k% U* n, s: Inosis can be established by just a few tests and by
! V, u' N( ^8 j& ^( Q: |5 O. H9 oappropriate history. The inability to obtain such a: b! i$ ?+ E8 @
history, or failure to ask the specific questions, may
1 J4 \1 t5 P/ I# n8 A8 fresult in extensive, unnecessary, and expensive
& T8 w0 I  b3 c* minvestigation. The primary care physician should be. d2 j; F; X. `: k
aware of this fact, because most of these children
1 V) b( ]+ l9 R( g; H- Omay initially present in their practice. The Physicians’
3 e% u. H0 U$ MDesk Reference and package insert should also put a
# C- O: R) _+ d6 B4 bwarning about the virilizing effect on a male or
; w8 t* E! F0 a" O: ~6 Zfemale child who might come in contact with some-& l6 t) j' g8 a
one using any of these products.
/ N( j1 e& n4 `- sReferences
  }0 y; S9 }$ S9 ~3 r1. Styne DM. The testes: disorder of sexual differentiation8 H- A& P( D: F( w
and puberty in the male. In: Sperling MA, ed. Pediatric
" f, K, z2 G: F3 P: K, _Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' G7 z' u4 |' w. }2002: 565-628.; Q, O* w( G% a' B  @/ o- c- {
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, Q0 c% w# K, _puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old3 _; z8 C( ]" S. N+ |
Boy Induced by Indirect Topical
( \  t; y2 L% p. F, c* Q% qExposure to Testosterone
% T+ q$ W% @$ W* A7 M7 nSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! X+ ^/ d% E, Hand Kenneth R. Rettig, MD1
0 O" j& T; q# b. tClinical Pediatrics$ X+ c5 c; W. w# p
Volume 46 Number 6
. H6 q7 ?# [" \1 ]; f9 @: TJuly 2007 540-543
% u( s( u* r( e© 2007 Sage Publications
. X% X; {+ x8 G$ `10.1177/0009922806296651# J- M; a5 g: r! z" ~, Z
http://clp.sagepub.com! M' P! q7 N* M. f: J" D6 e
hosted at
* s5 x& j! u& J2 O6 {: h5 E# _http://online.sagepub.com
3 t! v! V* F8 A* {: |4 cPrecocious puberty in boys, central or peripheral,
$ @- t9 s$ [/ G9 His a significant concern for physicians. Central0 i# E, l2 I6 ~. m0 ^. F% |; g
precocious puberty (CPP), which is mediated% G, v- P, \, [  a- c1 N
through the hypothalamic pituitary gonadal axis, has
9 n! j) }3 o  j: v+ [/ ya higher incidence of organic central nervous system2 O2 |& ^0 e  @/ D: ?, Q  ~' _5 Z
lesions in boys.1,2 Virilization in boys, as manifested
6 F+ C( Z9 \+ K1 h. `  O4 F2 Uby enlargement of the penis, development of pubic
3 f: o/ [$ \; r, j$ v. Phair, and facial acne without enlargement of testi-% o! F; F/ w3 p. I  j1 B$ g
cles, suggests peripheral or pseudopuberty.1-3 We
2 {; p' V" y* B- Breport a 16-month-old boy who presented with the
# J( `! S4 N5 t/ S, @enlargement of the phallus and pubic hair develop-
3 u0 x5 o  I6 G) @ment without testicular enlargement, which was due; u  T' I; z3 r; w$ E
to the unintentional exposure to androgen gel used by( n/ v) R) k- c
the father. The family initially concealed this infor-
% z. `7 q8 p# U9 Z6 J( ^- emation, resulting in an extensive work-up for this5 G. o6 e. ?3 Y/ O, P( Z
child. Given the widespread and easy availability of8 e7 j6 n' m9 W& c4 R( M, y
testosterone gel and cream, we believe this is proba-
1 Y- d) _2 @) W) lbly more common than the rare case report in the
$ D* n9 f. U+ E6 N* k5 q1 l% iliterature.4
! e: O/ `0 G0 I: O) q4 ^Patient Report' I; M5 w/ j6 f$ D$ L, A- ^! J' Z" t
A 16-month-old white child was referred to the/ j% b5 d" o& o7 d0 k) Z: Y, c% j( {
endocrine clinic by his pediatrician with the concern
7 b* L5 d' F/ S4 A; p6 e) dof early sexual development. His mother noticed2 s: m/ a* q. o7 O
light colored pubic hair development when he was+ F, {4 W3 ~7 b- V- m
From the 1Division of Pediatric Endocrinology, 2University of* M5 F/ Z5 E3 G
South Alabama Medical Center, Mobile, Alabama.
' i! ]1 \3 x% @0 S. D7 ~Address correspondence to: Samar K. Bhowmick, MD, FACE,- `2 G5 L" Z; f" d4 ^
Professor of Pediatrics, University of South Alabama, College of* @: C) J: o& C- U1 x4 i
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 @0 a% F! ?" s7 E) n# \# K0 me-mail: [email protected].
2 B/ F3 _6 a# H& ~( f3 z7 S  Eabout 6 to 7 months old, which progressively became0 N& K% m0 \( Y* @: k. c
darker. She was also concerned about the enlarge-4 L8 x) A/ \9 u  T7 ?1 Y1 {0 K; B# g1 F
ment of his penis and frequent erections. The child
0 M# g0 X1 d6 Ewas the product of a full-term normal delivery, with
2 c- t3 b$ C( i3 I- y# @% ea birth weight of 7 lb 14 oz, and birth length of0 [* i% l/ e7 {0 M6 i9 b9 E
20 inches. He was breast-fed throughout the first year
, J9 w$ O* Z# X% m3 l# f1 Sof life and was still receiving breast milk along with" S4 v- U8 I( x; h6 A3 F# E$ `
solid food. He had no hospitalizations or surgery,
% Y( A$ L  ?7 ?5 jand his psychosocial and psychomotor development* g' j# _" O) w1 [2 r& W
was age appropriate.. m4 f. [5 h5 e* F) ^+ M
The family history was remarkable for the father,3 f8 l& A" M! N3 `8 F, I4 o3 K
who was diagnosed with hypothyroidism at age 16,( X0 T: y4 x/ J
which was treated with thyroxine. The father’s  ^5 o4 h  G, l1 D
height was 6 feet, and he went through a somewhat
' J8 ]8 x4 C7 Z+ h' a) S  N5 i0 @early puberty and had stopped growing by age 14.
) O8 p! R  ?- m. C5 V6 BThe father denied taking any other medication. The4 ~/ `" ^' \+ O. V  _# r
child’s mother was in good health. Her menarche5 r+ I: U1 e; |! L
was at 11 years of age, and her height was at 5 feet- H9 j* [0 s9 `7 U: k' R6 E$ f
5 inches. There was no other family history of pre-2 y4 t" W4 J% d$ @% o1 U
cocious sexual development in the first-degree rela-: j* N0 ], y1 L, n
tives. There were no siblings.
  l# [: ~  D& x/ B9 ]. TPhysical Examination
7 v, I" }: Z7 n4 Q- |# O: gThe physical examination revealed a very active,
& K8 \. q1 N4 E% V7 m- Q' p, aplayful, and healthy boy. The vital signs documented9 N% y) e( v) G  `+ l4 c! Y( ]
a blood pressure of 85/50 mm Hg, his length was# i" c8 j$ x3 l4 @/ M- v1 f/ Y
90 cm (>97th percentile), and his weight was 14.4 kg
8 l( V. c; i# X' K6 I(also >97th percentile). The observed yearly growth
) ?3 j6 `! Z0 S/ [% Hvelocity was 30 cm (12 inches). The examination of8 O2 f) G( c2 ?# c  }4 q! `5 O& W
the neck revealed no thyroid enlargement.+ H6 ]# s$ I9 k) ~) P( A$ I* |% y
The genitourinary examination was remarkable for
' u2 o$ ~- X$ u+ a/ p& W* benlargement of the penis, with a stretched length of
' h- V9 W' d. C5 S8 cm and a width of 2 cm. The glans penis was very well
! Q: e- ?/ b7 M$ j7 i1 Wdeveloped. The pubic hair was Tanner II, mostly around
2 ]0 M! ?) y3 k' V4 M' ?: m9 G540* V4 l6 x, O) `  t6 r3 ?: E: F- H( g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. ^+ ]9 I/ I. u
the base of the phallus and was dark and curled. The1 j' H# V* ^' M7 H: L  {
testicular volume was prepubertal at 2 mL each.
5 T6 H5 G% k; ~: e4 k* u. eThe skin was moist and smooth and somewhat) s5 ]6 [8 a. K+ s+ U; S
oily. No axillary hair was noted. There were no2 s" W8 S: f, R5 ]4 N
abnormal skin pigmentations or café-au-lait spots.4 f  r9 z6 i3 n4 L: w7 s# l
Neurologic evaluation showed deep tendon reflex 2+
1 U: S+ F$ X2 D! F( n( K' }/ n1 {' m' Cbilateral and symmetrical. There was no suggestion9 m9 L1 ?1 D2 m( n7 }. g
of papilledema.
. f! [* x. m) V5 ^# T4 X( r' gLaboratory Evaluation
6 u- a- ~5 t. W2 Q/ pThe bone age was consistent with 28 months by5 \+ f! }6 h) n* D5 }: d
using the standard of Greulich and Pyle at a chrono-" \) o% P6 d+ A8 N. i4 _0 C8 t
logic age of 16 months (advanced).5 Chromosomal' u" N% v6 f: s+ w( \) M
karyotype was 46XY. The thyroid function test; M! s8 |  h" k* {6 d! J
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
7 P1 X6 K6 L* y/ |lating hormone level was 1.3 µIU/mL (both normal).
6 Q/ m# ^# ~. Z8 cThe concentrations of serum electrolytes, blood
- j* [+ b. {  `4 r7 {+ _urea nitrogen, creatinine, and calcium all were
+ x6 K8 ~1 w2 \% D, Kwithin normal range for his age. The concentration5 b: B) }- Y4 V9 y( G  e" @
of serum 17-hydroxyprogesterone was 16 ng/dL
5 ]( h( m2 r: I7 p4 d(normal, 3 to 90 ng/dL), androstenedione was 20) h- O- i$ y# F% l
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 t2 y) ?, _, T+ |terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. J9 o! c) {/ `: O& a2 S* Hdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ ]7 W* q; m# D7 j# h! a0 ^49ng/dL), 11-desoxycortisol (specific compound S)
# \) v6 q! P) ?/ kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-+ E% r) L, D" i) ?: w7 ?
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% C  ?( n4 r! h" U5 n
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
1 p- |! s5 Z8 \" e7 T8 Iand β-human chorionic gonadotropin was less than
1 r8 u$ l8 B* {6 j5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ v  n. v# Q) E9 H5 ^stimulating hormone and leuteinizing hormone, d" Y" e  g) l) D: X
concentrations were less than 0.05 mIU/mL
, _" N& j0 e* v: m1 u0 y(prepubertal).
( m" i5 V2 W7 |7 P$ S# N$ LThe parents were notified about the laboratory% W0 C' |, L1 L0 f! B
results and were informed that all of the tests were
& q6 g4 H' e; v; Inormal except the testosterone level was high. The3 U3 v9 A4 X2 S- Q) S/ L- I2 a8 ?
follow-up visit was arranged within a few weeks to
3 F, j; [$ H0 |5 S* _' u5 Aobtain testicular and abdominal sonograms; how-
# b  c$ P5 y0 W: T" T( Z8 Qever, the family did not return for 4 months.! h2 A* [( Z* F2 Z* e; |
Physical examination at this time revealed that the
) {, s6 K: H5 |; F, Nchild had grown 2.5 cm in 4 months and had gained
4 c, n! I: o' l! g$ G. D! L+ \& p2 kg of weight. Physical examination remained: U: W# z- S; \( d9 H0 W% i
unchanged. Surprisingly, the pubic hair almost com-
: W- \; d0 M2 k+ y! m, }! Gpletely disappeared except for a few vellous hairs at
8 E$ K& O* I  _0 g. _& qthe base of the phallus. Testicular volume was still 23 K+ |/ r/ v# s
mL, and the size of the penis remained unchanged.  h: F6 R5 o% W$ f
The mother also said that the boy was no longer hav-1 \; D% g* [" E. ~
ing frequent erections.  E4 I* @( i) I8 c# v, u
Both parents were again questioned about use of0 ], C2 y+ R, }9 _) d8 h8 n
any ointment/creams that they may have applied to
6 ]% T: v/ D( k- p  {% R3 O3 gthe child’s skin. This time the father admitted the
" m5 V: i$ T- @' `6 a3 ATopical Testosterone Exposure / Bhowmick et al 541
1 m" ?5 q2 V! n. K# {% ]use of testosterone gel twice daily that he was apply-6 d( C( D& g) V" s
ing over his own shoulders, chest, and back area for
8 A& V% |" Z* d; U4 Sa year. The father also revealed he was embarrassed- K) h% H# Z1 |& r  ~. r
to disclose that he was using a testosterone gel pre-
  I" b% z, s' ]1 T) Fscribed by his family physician for decreased libido6 V1 ]% \9 @! }6 K9 D1 v+ @
secondary to depression.1 k" R1 \! y0 i- H( H' [7 f& W4 h1 n
The child slept in the same bed with parents.
) r6 z( A4 o9 @( i, d& wThe father would hug the baby and hold him on his0 ]" u, M3 u# l5 B7 X* c
chest for a considerable period of time, causing sig-7 r% x& d6 V6 I( J: A+ y! K
nificant bare skin contact between baby and father.
7 Y5 s' p7 A, h/ b  [The father also admitted that after the phone call,9 j4 g& A" R; m% F3 D: j" k0 h
when he learned the testosterone level in the baby
8 |8 D9 l. z0 q0 C7 f+ n% p0 B* U' E1 vwas high, he then read the product information9 y( V& y6 {$ k# w/ O9 B
packet and concluded that it was most likely the rea-. n) D8 i7 s, ~9 a' t! P$ I
son for the child’s virilization. At that time, they. x8 K/ t8 ~, L. u: u: Z  S
decided to put the baby in a separate bed, and the
3 Y7 S1 @( t" K/ T' lfather was not hugging him with bare skin and had2 x1 a6 w- Y" p$ o, u' Y
been using protective clothing. A repeat testosterone$ P8 i# T. U% T- W
test was ordered, but the family did not go to the
5 L; v* ?$ M. R. n- C; N( Ilaboratory to obtain the test.5 E0 L3 H; ]; r+ j1 C5 n
Discussion
% Z% v( f: O% l  \$ Z1 a/ b  {Precocious puberty in boys is defined as secondary/ ~5 V5 k2 D. F7 C1 M* n- o
sexual development before 9 years of age.1,4* k0 W. U$ x/ _9 D) c
Precocious puberty is termed as central (true) when
; ~7 v6 z( m# r, Nit is caused by the premature activation of hypo-) t4 q1 D6 P7 ]& R6 Q3 A! e
thalamic pituitary gonadal axis. CPP is more com-  J, o* F* l0 i* _6 M; \1 J) I# ^
mon in girls than in boys.1,3 Most boys with CPP) K, v1 i/ z) ?% G
may have a central nervous system lesion that is! Y9 j& B  r5 |/ }5 H0 M. K+ B
responsible for the early activation of the hypothal-
# X' f; A# h) A; C% Tamic pituitary gonadal axis.1-3 Thus, greater empha-
5 \: ^3 R+ }. Rsis has been given to neuroradiologic imaging in
. V; q& C6 B5 Y! rboys with precocious puberty. In addition to viril-
! J8 C: a+ O& F1 w: t. v' Wization, the clinical hallmark of CPP is the symmet-
# x* u* ~7 y1 h) |3 T, crical testicular growth secondary to stimulation by$ i2 J0 |; y* s, i3 x7 s6 f
gonadotropins.1,3( Q# o- j2 r: X+ q- d# c
Gonadotropin-independent peripheral preco-6 d" |; ]6 U! j
cious puberty in boys also results from inappropriate1 l* l3 G9 Y! Z) E& v
androgenic stimulation from either endogenous or1 y, ^' z% g$ n. k7 I
exogenous sources, nonpituitary gonadotropin stim-
( n  h" J, W3 ~1 U6 h) o" ?; f" R1 xulation, and rare activating mutations.3 Virilizing$ V8 h1 q0 r9 l
congenital adrenal hyperplasia producing excessive+ Q$ ?& J' H8 o! _, l5 Y( ?0 c. F$ z
adrenal androgens is a common cause of precocious
1 R: g3 i3 Z5 l8 lpuberty in boys.3,4
2 p' ?1 `/ _7 \: T  _! G' s" S; eThe most common form of congenital adrenal
8 v6 u# d2 S1 B% q: a, hhyperplasia is the 21-hydroxylase enzyme deficiency.
: z6 ^. e, Y' v9 w, u0 O0 w8 wThe 11-β hydroxylase deficiency may also result in
+ m" G& |2 q3 z$ l- B! h/ fexcessive adrenal androgen production, and rarely,2 c% A- m# Z9 T& @- h* u2 u
an adrenal tumor may also cause adrenal androgen
9 o9 A3 w6 I) F; e% fexcess.1,32 N  I! V: C0 ~2 A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* A' `+ ]5 K6 W9 T. k" U
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* r, f  r0 B9 k7 O" y
A unique entity of male-limited gonadotropin-6 y7 k7 u1 ^' Z) c5 R8 n1 g, Y
independent precocious puberty, which is also known
1 Q' S" r" C) j7 }4 Vas testotoxicosis, may cause precocious puberty at a# w6 E; m1 s% Y3 |* ^, q1 G& L
very young age. The physical findings in these boys- @4 \* }* S2 r* r" _2 U# d
with this disorder are full pubertal development,
' I' L- Y- e; z/ W7 nincluding bilateral testicular growth, similar to boys+ c2 y0 L1 u4 j0 k2 ], `) G
with CPP. The gonadotropin levels in this disorder/ g: L! m4 d4 c
are suppressed to prepubertal levels and do not show( b- z" O3 x' `/ `
pubertal response of gonadotropin after gonadotropin-
# E2 U) \7 Q% Oreleasing hormone stimulation. This is a sex-linked
' ~/ c4 K  ~/ O/ V9 f  _autosomal dominant disorder that affects only
" F2 Q! u3 q: \5 Y3 lmales; therefore, other male members of the family
1 M( Q* M! @' [may have similar precocious puberty.3! C4 A! c$ Z5 p$ p  [
In our patient, physical examination was incon-
# D& a1 O4 G( X* K* E$ Esistent with true precocious puberty since his testi-' `4 T3 I# ]8 L  f. v$ ]
cles were prepubertal in size. However, testotoxicosis
8 e, T, P7 h$ y7 ]! [was in the differential diagnosis because his father: S1 ?& E0 Y2 p+ p$ Z9 E
started puberty somewhat early, and occasionally,, W! E4 s5 g$ F. @0 \
testicular enlargement is not that evident in the# n: K) O2 _0 s, h% T$ m  W: ?# b
beginning of this process.1 In the absence of a neg-& Q: m4 K) x& F/ Z
ative initial history of androgen exposure, our' k, L) o8 H2 e" w6 _
biggest concern was virilizing adrenal hyperplasia,0 s$ q6 G! A7 u7 O0 D* I0 i
either 21-hydroxylase deficiency or 11-β hydroxylase( M2 `/ ]6 I, Z' r! a2 q
deficiency. Those diagnoses were excluded by find-8 S8 m! ?! z% u1 K) U$ m7 x
ing the normal level of adrenal steroids.& b' R" |* j' k& [% l
The diagnosis of exogenous androgens was strongly( M6 D$ k) A% v. }& L
suspected in a follow-up visit after 4 months because8 T: e+ C. i* \; I( U9 G$ s
the physical examination revealed the complete disap-( @8 g+ S. P( S' ]
pearance of pubic hair, normal growth velocity, and& t9 D6 _. L9 w# f6 L
decreased erections. The father admitted using a testos-
: }- _) A& [9 C% Aterone gel, which he concealed at first visit. He was
. G5 {, h+ _; g8 Y2 Cusing it rather frequently, twice a day. The Physicians’1 }% ]3 Z" j3 ?' M0 Q' l
Desk Reference, or package insert of this product, gel or
0 B" m( r, Q1 [% ocream, cautions about dermal testosterone transfer to  k% I+ u8 {" I. H0 Z$ h) {4 w! N
unprotected females through direct skin exposure.
: u6 Z! b! K6 g, d$ _Serum testosterone level was found to be 2 times the
% p& D5 V" e2 O6 Y: Y# F9 sbaseline value in those females who were exposed to" j' m6 K9 u" K8 i/ q7 `
even 15 minutes of direct skin contact with their male
/ y9 w; O, f; T6 y! U1 S( Mpartners.6 However, when a shirt covered the applica-
* }- V- `8 A7 G& z. ^0 ?tion site, this testosterone transfer was prevented.
6 X: R9 C5 R$ Z' u. I3 \Our patient’s testosterone level was 60 ng/mL,
3 u0 m+ F+ I: n0 A* hwhich was clearly high. Some studies suggest that
' U) k( f) `& x+ N; ^dermal conversion of testosterone to dihydrotestos-. h# I/ z( h1 D4 |0 N+ v$ q
terone, which is a more potent metabolite, is more& Q, ^( Y' |6 E$ _& U( s
active in young children exposed to testosterone
7 y% ?* |$ T& D4 L3 U( nexogenously7; however, we did not measure a dihy-
3 ^' e, G8 u/ V2 a: A$ _& Mdrotestosterone level in our patient. In addition to0 @" y4 Q+ ^: w
virilization, exposure to exogenous testosterone in0 W% X/ c8 i5 Q
children results in an increase in growth velocity and
% B! x( B9 p. R  d4 [advanced bone age, as seen in our patient.
/ X; u, Q! e6 R7 `) A$ mThe long-term effect of androgen exposure during3 I3 ~5 O" F. \2 [* s
early childhood on pubertal development and final
  G1 l7 }' U8 u, K! ?adult height are not fully known and always remain
  P4 }' W7 [4 B8 K" i; s5 ha concern. Children treated with short-term testos-" n9 h  I6 B- l  Q( `* A
terone injection or topical androgen may exhibit some" @; o; o8 d7 ~. Y
acceleration of the skeletal maturation; however, after
/ J% L8 {% M) F0 n$ p, bcessation of treatment, the rate of bone maturation( P' r! f5 p1 ?- A
decelerates and gradually returns to normal.8,9
6 _1 s7 [1 j* R3 m1 x1 V. y# SThere are conflicting reports and controversy
! p" q  A. |: n5 E8 Sover the effect of early androgen exposure on adult$ y) m/ N5 g4 j: E
penile length.10,11 Some reports suggest subnormal
* r* G5 n+ ?' w) `( N9 e3 hadult penile length, apparently because of downreg-* _+ S! a' p/ n2 k
ulation of androgen receptor number.10,12 However,
. N( U1 n3 Z, z6 l: k& P0 ]Sutherland et al13 did not find a correlation between3 V! `% z. u) ~2 ]3 A
childhood testosterone exposure and reduced adult' T# L/ z; L: L1 w" T  N* s/ C
penile length in clinical studies.- |) r, C0 R- T3 z
Nonetheless, we do not believe our patient is
1 z# P' P4 z! S  Sgoing to experience any of the untoward effects from
* I2 t; i- o0 n* y( ptestosterone exposure as mentioned earlier because( `. Q5 h4 U9 U+ J4 m5 V# ]* d1 H
the exposure was not for a prolonged period of time.
8 v0 y4 b! L9 G5 aAlthough the bone age was advanced at the time of
$ h, V9 d$ E0 c% adiagnosis, the child had a normal growth velocity at
$ x& m' {( H& y% |( @the follow-up visit. It is hoped that his final adult
; r1 S8 _; T- aheight will not be affected.
6 @2 R, z) v/ G. r7 M3 bAlthough rarely reported, the widespread avail-8 @+ s* t1 G9 X4 z
ability of androgen products in our society may- Y0 B% G3 M: z$ q' V4 m2 n9 e8 s- D
indeed cause more virilization in male or female
& U! `5 F5 Q7 w$ ?children than one would realize. Exposure to andro-
8 \9 t5 o+ ^5 e# M+ Z! ?' ^& {" Cgen products must be considered and specific ques-
/ r, e. Y" G: C" M# x0 w3 \tioning about the use of a testosterone product or$ a" U* n/ b  Y9 o  }8 Q- s
gel should be asked of the family members during$ M8 u2 L2 {+ j' [. O
the evaluation of any children who present with vir-5 g' U, D, _- Y/ |" \
ilization or peripheral precocious puberty. The diag-! \- K0 S% f, X7 k( K! ]8 e& d1 r
nosis can be established by just a few tests and by
8 C# k/ d; }- {7 i& D5 ?7 kappropriate history. The inability to obtain such a! t' B2 ]4 Q( G& X
history, or failure to ask the specific questions, may
' ]# m. ]3 q; P1 Z4 nresult in extensive, unnecessary, and expensive
- z: a3 }9 @- `! minvestigation. The primary care physician should be2 k. o2 T0 [1 \# c  c) n6 v. i7 G2 U9 Q! J; G
aware of this fact, because most of these children4 }! Y+ B+ ~  K0 ?+ M) g* x9 B  S4 @
may initially present in their practice. The Physicians’% p) V0 G5 F; _8 O1 k/ ?4 H
Desk Reference and package insert should also put a/ E: v6 b1 ^: a1 ^, I5 y
warning about the virilizing effect on a male or
# N- ]8 s$ s0 W/ yfemale child who might come in contact with some-4 `2 g+ y" E4 a' D
one using any of these products.+ F$ z0 `6 K) C. n. c  j3 w
References
; |. I4 a* x) }1. Styne DM. The testes: disorder of sexual differentiation1 E3 a! J$ v9 l0 G# _6 p  x1 o
and puberty in the male. In: Sperling MA, ed. Pediatric
+ ^+ ^- v3 u; S; f! T; W/ {Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 p. F9 g- b0 x
2002: 565-628.6 m2 V. @$ }) ^$ I( I' @9 h' b( D
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious2 U( i* e8 ~5 s
puberty 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
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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
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

' Y+ v0 c: F; ]6 K( P7 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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