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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
5 {( `: G9 _4 M. j4 q0 t6 |: G$ NBoy Induced by Indirect Topical
% v+ r( h+ {9 O) j" UExposure to Testosterone2 j4 |/ b' d- z+ J
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2, Q) j1 b* a. H: u# f/ a( S/ k2 x1 v
and Kenneth R. Rettig, MD1" m6 ?$ _: ^( R3 k+ Z# G/ l* U
Clinical Pediatrics. ?8 [1 `/ U9 }
Volume 46 Number 63 S4 O( _  o, O
July 2007 540-543- c+ F) O3 i* Y
© 2007 Sage Publications
" ~, S* i* o1 g10.1177/0009922806296651
- g' f+ X( k4 Y" |" U+ a' D% zhttp://clp.sagepub.com
# b4 p+ U3 Q* ?( A" K/ v% ^" O  Mhosted at
+ S- w6 ~6 y3 ahttp://online.sagepub.com
* n5 ?' y3 J$ k$ Z6 `, M( q- v' |Precocious puberty in boys, central or peripheral,
* o* a; X) f. I! qis a significant concern for physicians. Central
( w. H& {' Z2 Y9 @precocious puberty (CPP), which is mediated
' ?5 s6 G3 v0 {7 _' ]$ Q1 Fthrough the hypothalamic pituitary gonadal axis, has" O6 w* G6 ~0 H
a higher incidence of organic central nervous system
1 o( f, M  p* e' `9 g# R. E: ^lesions in boys.1,2 Virilization in boys, as manifested4 [  A6 q2 m: ]: \. o
by enlargement of the penis, development of pubic2 s) w7 A6 L$ @! q0 m: j. m$ Z
hair, and facial acne without enlargement of testi-
' _7 R6 Y+ E& o8 U( T( vcles, suggests peripheral or pseudopuberty.1-3 We  h8 r: y: K* V8 I9 ]7 a
report a 16-month-old boy who presented with the
: Z) B( k1 {* |$ i) B. m5 ~7 Eenlargement of the phallus and pubic hair develop-- B6 H- J  I3 ~( l, v
ment without testicular enlargement, which was due
$ D0 P5 R6 @/ H, m5 F4 W/ J' Gto the unintentional exposure to androgen gel used by! _" [0 O0 ~. E. C* }3 ]
the father. The family initially concealed this infor-
8 F# ~$ L; V) L3 C. ?mation, resulting in an extensive work-up for this
% v+ R1 A4 W% p7 \- Mchild. Given the widespread and easy availability of
1 I1 y* p' y3 g6 ^' J" s* ptestosterone gel and cream, we believe this is proba-$ |: b: l2 P: h8 S# Y& I7 b' o, j
bly more common than the rare case report in the& Q$ C" X  r# a& G. P1 r% t3 ?
literature.4* V' f8 R5 O. v* |8 e
Patient Report
5 q9 Q/ _* ?) {, ~6 H7 VA 16-month-old white child was referred to the
3 p  e6 T' F1 E/ K+ u. q" }8 g$ O* sendocrine clinic by his pediatrician with the concern5 G2 a* V' n8 p$ W: y) t
of early sexual development. His mother noticed
& @8 z. T: t, o" ?9 |( Jlight colored pubic hair development when he was
4 ]0 o7 l3 N; v# I' H4 {2 a) h4 eFrom the 1Division of Pediatric Endocrinology, 2University of
) k# L, {2 G' L* K! ESouth Alabama Medical Center, Mobile, Alabama.
. R6 R' K/ X5 j/ N2 X6 G! c# eAddress correspondence to: Samar K. Bhowmick, MD, FACE,
( D) R  @, |4 S2 I& L  ^Professor of Pediatrics, University of South Alabama, College of9 y8 r9 R1 T3 s+ K
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ d0 ^2 [/ b6 M0 M$ |% I! ~e-mail: [email protected].
) n2 Z7 r( X# n! [, ?about 6 to 7 months old, which progressively became
& P/ ]- w0 Q; tdarker. She was also concerned about the enlarge-' T+ s9 G: Q# v% f
ment of his penis and frequent erections. The child2 [  k/ U. L$ m( f1 W9 W
was the product of a full-term normal delivery, with1 F0 u/ k- E* y) F* t1 |- v5 a
a birth weight of 7 lb 14 oz, and birth length of1 \5 [# @3 P, r- K4 n1 o
20 inches. He was breast-fed throughout the first year
8 |" d) b0 ~2 U! Nof life and was still receiving breast milk along with
: M6 l4 F0 Z$ ?- x4 K+ Tsolid food. He had no hospitalizations or surgery,4 m7 X# z" b8 h4 d" S2 J
and his psychosocial and psychomotor development
/ j! M  E' G7 M  ewas age appropriate.% p" ^+ |( H- n. v, O9 }
The family history was remarkable for the father,0 E* N* f3 G8 a9 W$ I
who was diagnosed with hypothyroidism at age 16,6 D4 K& g1 Y8 `, g4 P
which was treated with thyroxine. The father’s
5 K. E8 N5 r8 L# eheight was 6 feet, and he went through a somewhat+ t3 n# q+ A3 ]1 j) R7 `# J. k
early puberty and had stopped growing by age 14.5 f0 B+ R: |% C5 W) o, e- y
The father denied taking any other medication. The
! V) w7 X# R) h4 n  w; L- Gchild’s mother was in good health. Her menarche& q( n( R3 j, ~& u% @1 P  T
was at 11 years of age, and her height was at 5 feet
9 E$ A6 L" }; C8 B  c5 inches. There was no other family history of pre-- X: u  J& m7 [+ N  C5 H
cocious sexual development in the first-degree rela-# Y- `( s: D6 A2 R3 Z) e# L6 v/ c1 o
tives. There were no siblings.' E/ ?, C* n5 C' S  M% f
Physical Examination7 R/ x! y+ R" z9 C/ z* I5 w
The physical examination revealed a very active,0 j7 r1 j+ H/ [. R( o' R2 O
playful, and healthy boy. The vital signs documented, D  f: g( z9 A
a blood pressure of 85/50 mm Hg, his length was
" H) `3 a8 Y- G: m+ h: k7 f, I90 cm (>97th percentile), and his weight was 14.4 kg; M6 w1 o- s8 \( G7 K( v
(also >97th percentile). The observed yearly growth
* S% h/ U# A5 b0 l- wvelocity was 30 cm (12 inches). The examination of
- v# S# s+ a+ ?4 K# a2 F, n+ rthe neck revealed no thyroid enlargement.  W+ g7 Y. y8 G
The genitourinary examination was remarkable for* q+ D0 l/ ]* |+ `/ r
enlargement of the penis, with a stretched length of
5 R$ v% w% n1 S$ A+ p8 cm and a width of 2 cm. The glans penis was very well" s$ ~7 }: u7 q6 |
developed. The pubic hair was Tanner II, mostly around. ~9 N8 Y/ z( [: X
540# l4 o2 V- w$ G  ]
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 C2 W5 ]' t* L0 Xthe base of the phallus and was dark and curled. The6 Q3 n( T+ |0 g2 u
testicular volume was prepubertal at 2 mL each.
  [& \& z7 ]& fThe skin was moist and smooth and somewhat5 F3 p3 e- v! t3 ~4 W, O
oily. No axillary hair was noted. There were no
  P! X% q' c, }8 a/ w" q  Yabnormal skin pigmentations or café-au-lait spots.
8 S2 h" n5 z4 W9 rNeurologic evaluation showed deep tendon reflex 2+/ H3 a) @6 i; N) A" ~
bilateral and symmetrical. There was no suggestion; A1 j) j( {% T6 r( O
of papilledema.8 U& X* R1 g2 s* m$ ^" Z7 m
Laboratory Evaluation
" i' I4 Z. X& s8 I9 N- _$ BThe bone age was consistent with 28 months by
0 i- z" f# F( e- i3 Pusing the standard of Greulich and Pyle at a chrono-
, G8 b/ n8 _1 U2 C; K& K- t$ Xlogic age of 16 months (advanced).5 Chromosomal5 z# s6 M# a: L3 h, C+ ^3 ^: P
karyotype was 46XY. The thyroid function test2 e# ?# Q% D* z5 D/ a
showed a free T4 of 1.69 ng/dL, and thyroid stimu-( F+ O6 h# Z& A6 g. g* }9 y
lating hormone level was 1.3 µIU/mL (both normal).
$ a9 R" L# \- y6 Z* A8 V0 C* }" SThe concentrations of serum electrolytes, blood3 l2 [9 R; B$ a2 W" K
urea nitrogen, creatinine, and calcium all were
5 p( t- ?' S. Y4 o3 U3 ^0 @' \; O+ |within normal range for his age. The concentration
! p$ C: Y* L) ^; Q$ d. H' }of serum 17-hydroxyprogesterone was 16 ng/dL
7 r! J* N% L/ J$ G+ s" P$ ~# J(normal, 3 to 90 ng/dL), androstenedione was 20
7 i  w0 n0 q, v* u* p7 J9 @' e# w9 ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) s: l2 m' N# ^3 b
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' [' C/ ~& U' c0 q1 @1 G
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 V9 I/ j2 H, ?9 T7 P49ng/dL), 11-desoxycortisol (specific compound S)+ `# p  d2 l" Y* T( G
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# i8 Y6 g1 i- U; i7 _
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 r( G) {$ f: t/ Gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),  ]. _0 z6 @1 J! Z: n8 _% S
and β-human chorionic gonadotropin was less than
8 u+ }4 m4 j3 D  I5 mIU/mL (normal <5 mIU/mL). Serum follicular! O/ J& A8 C7 b+ X, c  B
stimulating hormone and leuteinizing hormone5 ?. B$ R: o8 z& r7 E
concentrations were less than 0.05 mIU/mL( |3 ]8 h" h% w
(prepubertal).! X) h& S+ v) j$ ~* Y  ]9 K
The parents were notified about the laboratory
+ h$ p) S: _  yresults and were informed that all of the tests were9 \$ @$ b& @1 n0 B2 L
normal except the testosterone level was high. The
* A+ k# y4 U& g$ z2 _! }follow-up visit was arranged within a few weeks to( `/ K, `' t1 F) ^2 J5 i3 Q
obtain testicular and abdominal sonograms; how-0 P. P( d; v# b
ever, the family did not return for 4 months.
- ~+ D  ?: G" `Physical examination at this time revealed that the( J" I% p9 U6 ^) o6 R7 r2 l, {
child had grown 2.5 cm in 4 months and had gained! s9 e. B* _) f% r" D! l
2 kg of weight. Physical examination remained; u6 H4 r" I" B/ t
unchanged. Surprisingly, the pubic hair almost com-
- H" g2 M8 o1 }& Vpletely disappeared except for a few vellous hairs at
: ^$ @; @  M& @, Sthe base of the phallus. Testicular volume was still 2
  z1 a  H9 b7 D# V9 JmL, and the size of the penis remained unchanged.. |& M8 G& f! J  S! V: B
The mother also said that the boy was no longer hav-7 l6 z$ n. {5 f0 B( e$ u1 B' R
ing frequent erections., Y7 ~: H& m9 h+ A
Both parents were again questioned about use of
- I  N. p/ {- H7 n/ H- Z0 Vany ointment/creams that they may have applied to7 d- \: U# I3 H* J
the child’s skin. This time the father admitted the1 S8 o- n9 h7 \/ Q
Topical Testosterone Exposure / Bhowmick et al 5419 d  s, N' x; p+ f; |$ m) N* `
use of testosterone gel twice daily that he was apply-
& i# v) Q0 b2 z6 king over his own shoulders, chest, and back area for
+ k% u  E* z6 m0 f; R/ Ya year. The father also revealed he was embarrassed2 J7 `0 k0 J+ S* e1 z
to disclose that he was using a testosterone gel pre-2 H& z& Z2 g  ]9 |
scribed by his family physician for decreased libido
5 @2 z: `8 O8 _secondary to depression.
# p; u$ g. x& AThe child slept in the same bed with parents.
( o5 E) b( {4 I0 ~4 k7 n, k. e# iThe father would hug the baby and hold him on his  O( t/ f; q: T+ l) ^' Q
chest for a considerable period of time, causing sig-
2 d7 q# |- O1 E5 [5 pnificant bare skin contact between baby and father.' _( ~# \' E# k: n8 G& E
The father also admitted that after the phone call,
6 M" o/ D+ G$ q0 ?3 R; ]when he learned the testosterone level in the baby
+ X! m2 C, h& p/ X& Jwas high, he then read the product information$ R  t% I( K" V+ h9 p# W! S
packet and concluded that it was most likely the rea-
7 ?$ ?' j" s5 r* _' Q* Z' Gson for the child’s virilization. At that time, they2 W* Q4 l8 W! C- f  B
decided to put the baby in a separate bed, and the
& }" }4 Z! K8 P1 Y0 y/ tfather was not hugging him with bare skin and had
2 v3 w' u! j4 Z: d1 b: n% Obeen using protective clothing. A repeat testosterone
0 o0 g  ?& ?& q7 v( x" N9 _  \; ^  |test was ordered, but the family did not go to the
: @, o7 P0 i# q2 g5 Glaboratory to obtain the test.# z6 X! `$ n- K! o. t$ I( t
Discussion3 X" [* A2 K2 R+ d4 [! w7 R( e  J
Precocious puberty in boys is defined as secondary& t$ O1 n; f. h/ Z( z* r  }
sexual development before 9 years of age.1,4! b5 f' V9 g2 J' k; G+ m
Precocious puberty is termed as central (true) when
9 L$ ~3 O8 w3 k' J9 _+ n/ E0 fit is caused by the premature activation of hypo-
* }; h( r) L; A9 N7 Z& \thalamic pituitary gonadal axis. CPP is more com-/ x! r6 q4 p1 ?7 v5 h9 y1 k% N
mon in girls than in boys.1,3 Most boys with CPP
. }& ]: N/ w7 i! Q9 S7 nmay have a central nervous system lesion that is
! \7 p% \$ u7 C; m( Aresponsible for the early activation of the hypothal-0 ]3 B9 \0 A" {  o6 e! ]7 f$ h: x
amic pituitary gonadal axis.1-3 Thus, greater empha-
2 s# U; |+ l2 t; y" wsis has been given to neuroradiologic imaging in9 j. Q# e% w3 u! ]; \0 C
boys with precocious puberty. In addition to viril-
/ q5 E% R6 N7 k- x4 n- Y: iization, the clinical hallmark of CPP is the symmet-
2 y2 D7 i" `3 t1 [. V4 w% S0 arical testicular growth secondary to stimulation by
5 ^+ p* K' g: D. h& `gonadotropins.1,3
( u$ z6 B0 O; |& yGonadotropin-independent peripheral preco-
! r" Z) M8 `9 j1 H- S, Ecious puberty in boys also results from inappropriate
7 S8 o$ A" J( G! handrogenic stimulation from either endogenous or
( H/ u" f  y. \6 }/ Mexogenous sources, nonpituitary gonadotropin stim-
0 c1 c% A, G& Z/ C8 xulation, and rare activating mutations.3 Virilizing
4 u9 W! A; X& {: A3 h* Acongenital adrenal hyperplasia producing excessive$ B& m1 G8 Q% Q9 F
adrenal androgens is a common cause of precocious
2 k* K+ K" \) Epuberty in boys.3,4
) s$ y/ E* ^8 T0 W3 iThe most common form of congenital adrenal
- a- P! d# \* p# l) E5 |# Xhyperplasia is the 21-hydroxylase enzyme deficiency.& p- ^9 J: o* N6 K4 t
The 11-β hydroxylase deficiency may also result in
9 e; y$ Z! @! ]/ [& O0 sexcessive adrenal androgen production, and rarely,
+ \1 d, S, v# G3 N2 R3 nan adrenal tumor may also cause adrenal androgen
7 J2 V+ y6 l' }( x; N" G! w; s* R" K9 Jexcess.1,36 o" V% f. ^$ n  X# n# P7 m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 T& G3 M5 v6 [* s0 p542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- E1 Z4 K1 X+ `: [3 h$ N$ iA unique entity of male-limited gonadotropin-+ E. o% R; t! c* R
independent precocious puberty, which is also known
( f4 ?5 \1 d* \) xas testotoxicosis, may cause precocious puberty at a
2 V% g  Q+ Y; s* t+ v! j; Y' qvery young age. The physical findings in these boys) u. E9 S* }- X. Z7 v
with this disorder are full pubertal development,. k* J' B. f* m1 n
including bilateral testicular growth, similar to boys
# N0 O' k1 W, u* H0 [with CPP. The gonadotropin levels in this disorder' U3 V+ E/ Y& a1 {
are suppressed to prepubertal levels and do not show5 c" L# c; E0 }" L' s4 z  l+ g
pubertal response of gonadotropin after gonadotropin-- y1 V" S3 d7 R# a0 D6 Z! t
releasing hormone stimulation. This is a sex-linked
# s# j# O" x1 n- ]& Eautosomal dominant disorder that affects only
# A2 J& Z; }) H& Emales; therefore, other male members of the family5 l; ^$ y. P+ x7 J3 Z
may have similar precocious puberty.3
* F4 k9 p& G. s) m: {' w" vIn our patient, physical examination was incon-
: v: j/ |0 _* e; j# F) E$ f& Wsistent with true precocious puberty since his testi-
) x' P% E: a& o) K) `) m  ccles were prepubertal in size. However, testotoxicosis+ ?1 _- c" `$ @0 s
was in the differential diagnosis because his father
: b2 }3 Y  M' P3 }  nstarted puberty somewhat early, and occasionally,' h. i8 J0 S% W* l- ]  b: Z- `
testicular enlargement is not that evident in the
* Z3 I4 s6 w) r5 I! t8 s7 j0 F) Zbeginning of this process.1 In the absence of a neg-
' \( ^7 \' L+ K' |, tative initial history of androgen exposure, our/ `3 C4 {! u5 y/ B. ]8 c* B3 |
biggest concern was virilizing adrenal hyperplasia,6 e! D4 X: k# f  ~
either 21-hydroxylase deficiency or 11-β hydroxylase* g7 m, t. v# ^5 j$ v# z4 I
deficiency. Those diagnoses were excluded by find-5 {* }# r5 }/ V
ing the normal level of adrenal steroids.' h7 u2 e2 E# p! G8 g8 `! o
The diagnosis of exogenous androgens was strongly( {# J4 B' n* I
suspected in a follow-up visit after 4 months because
( J# u& G% c) c$ d" y% ~+ othe physical examination revealed the complete disap-
1 V9 R( i* ]5 `! L3 d! vpearance of pubic hair, normal growth velocity, and
* b: l7 `3 }. f, ddecreased erections. The father admitted using a testos-4 w/ ^9 v+ N: P" J' F4 P; e1 Y
terone gel, which he concealed at first visit. He was* u+ n9 x) Z6 d1 Y( U7 t6 j
using it rather frequently, twice a day. The Physicians’2 k# [7 y% u' ~# Q6 C
Desk Reference, or package insert of this product, gel or
3 m9 e$ D9 Q& O/ scream, cautions about dermal testosterone transfer to! C' ~+ D+ _$ C% Z% F2 F0 U* e( g
unprotected females through direct skin exposure.* @5 A) t2 x" a6 |& P6 m
Serum testosterone level was found to be 2 times the
  W( s4 |8 l  r4 Hbaseline value in those females who were exposed to
- k# S! M- i& F& y* S$ m0 Seven 15 minutes of direct skin contact with their male
, n2 |+ b+ I4 M5 q2 xpartners.6 However, when a shirt covered the applica-- i' w2 z7 S* Q1 ^  q* o
tion site, this testosterone transfer was prevented.
* B& E: @) l' o1 POur patient’s testosterone level was 60 ng/mL,- v& _/ C, y8 z7 O9 M5 U- q
which was clearly high. Some studies suggest that
( D) P! _3 P9 O- B  vdermal conversion of testosterone to dihydrotestos-& A3 B9 d! v  q# u* \  |3 T" ^
terone, which is a more potent metabolite, is more
6 Y" k& t, K3 f+ i, W1 wactive in young children exposed to testosterone
8 [0 i4 A* L( K3 R1 I! oexogenously7; however, we did not measure a dihy-
# j' |8 r% e2 i* xdrotestosterone level in our patient. In addition to: p/ w% z# e: H# g
virilization, exposure to exogenous testosterone in2 o4 z# z) C8 x& _
children results in an increase in growth velocity and1 k) q! V& K0 y& c
advanced bone age, as seen in our patient.2 F7 c5 m8 m. n
The long-term effect of androgen exposure during
6 t$ E" k% }. gearly childhood on pubertal development and final
9 ?4 U( A3 d* R. q1 hadult height are not fully known and always remain
8 q8 y/ Z; e6 ~3 B' C+ Ua concern. Children treated with short-term testos-
6 V2 E, e5 `" t6 ?2 ~2 a+ K, x  Rterone injection or topical androgen may exhibit some6 |+ N% Q2 i5 c( ]! ~
acceleration of the skeletal maturation; however, after3 E. s; \' [( l4 U% b
cessation of treatment, the rate of bone maturation. F- |2 C2 s% F- M5 `9 c
decelerates and gradually returns to normal.8,9; N3 M! c0 G) D1 F0 G- t5 u
There are conflicting reports and controversy6 C' ?0 `' L9 b
over the effect of early androgen exposure on adult- b. J2 A; Y' y7 P$ m1 m
penile length.10,11 Some reports suggest subnormal
2 k" Z3 W, R$ P7 B1 P3 Padult penile length, apparently because of downreg-- T# R) [+ b/ K. `
ulation of androgen receptor number.10,12 However,. l8 O: C3 M2 I) V
Sutherland et al13 did not find a correlation between% Y# Q0 \% W7 O* {0 T$ H* K
childhood testosterone exposure and reduced adult% C0 C5 P" e# K( q( t4 l7 B. S* w
penile length in clinical studies.' i0 L- d) M6 D# w2 u5 K( r
Nonetheless, we do not believe our patient is
! `7 i# o* \! r* [7 ~$ @" R2 Pgoing to experience any of the untoward effects from
' e1 y/ n/ a# Z* ytestosterone exposure as mentioned earlier because3 [3 s0 h" Q  X2 I
the exposure was not for a prolonged period of time.. v  R, c; T) G
Although the bone age was advanced at the time of5 g$ y9 D) l! X& i3 H% E
diagnosis, the child had a normal growth velocity at6 Q1 v& m; d5 D( p( p/ w* G$ H6 j* V
the follow-up visit. It is hoped that his final adult! `7 j, x) J5 ^' z2 ?6 \
height will not be affected.1 j" L: N$ F& F6 b
Although rarely reported, the widespread avail-. E4 \$ k! t1 V3 |" p+ `- {
ability of androgen products in our society may/ H* [- j' r% @
indeed cause more virilization in male or female' L5 d6 p/ {: f" \% A" ^$ D
children than one would realize. Exposure to andro-1 }2 D. K0 J1 M* B7 h' ]
gen products must be considered and specific ques-
5 s3 V: G8 N2 P8 z0 A! Ptioning about the use of a testosterone product or
" p+ B4 z9 w( H" z9 Tgel should be asked of the family members during9 d5 W7 d; o+ b1 o; E0 R
the evaluation of any children who present with vir-
2 r& @* j0 y  S1 o7 V& B5 V" iilization or peripheral precocious puberty. The diag-
3 f8 v% h% Y( b- c+ W$ bnosis can be established by just a few tests and by
- h  L; {; }2 u2 x; `appropriate history. The inability to obtain such a
' s8 \2 g$ |: u& ehistory, or failure to ask the specific questions, may
4 N% S5 q2 D/ R8 E  X& cresult in extensive, unnecessary, and expensive6 i# A  L- c9 C( m. H: J6 v. }% ]# t% y
investigation. The primary care physician should be
( V; c* k  }  ?( x# a3 Z4 }$ Iaware of this fact, because most of these children5 |. `" _, u' f; Q0 G
may initially present in their practice. The Physicians’
$ c7 N" o3 q+ A# B3 tDesk Reference and package insert should also put a& ]* W  g, }" m: O/ M: ?
warning about the virilizing effect on a male or: ^6 n6 y0 \1 b, n1 S2 \
female child who might come in contact with some-
$ G5 _8 ?9 K: lone using any of these products.
  a' p, n) V9 E1 Q* ]4 bReferences
: D; s0 r* d# ], c7 ~1. Styne DM. The testes: disorder of sexual differentiation
  Y! o" Q3 t$ p8 Zand puberty in the male. In: Sperling MA, ed. Pediatric* ^7 n9 A& m' X+ B+ K6 p
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" c* _: {: a* _% @! h2002: 565-628.
$ \. Q, ]& I( A7 I& _' }5 o. k2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( y- f. x1 K* o
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old6 b$ V( P# R5 ^/ t) X5 h
Boy Induced by Indirect Topical, o0 z, B: C+ N. H
Exposure to Testosterone
2 I" A6 G* S+ K+ w1 @/ oSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. ]4 H3 b) E! o  dand Kenneth R. Rettig, MD10 `# M3 \3 Z/ c( G
Clinical Pediatrics
" D/ x! M" Y: r0 \% |" O' GVolume 46 Number 6
3 b2 u" k6 d" g' ~: UJuly 2007 540-543
  b- T' H% l; d$ C+ w- B© 2007 Sage Publications% u& q) h- Q& m# R
10.1177/0009922806296651
; @/ p" d" U( `1 `: Chttp://clp.sagepub.com
4 _: B& {, w; Y) H; N4 U- Uhosted at
, J7 W( x/ M& k6 e8 Hhttp://online.sagepub.com
4 q  m1 n+ N( C- F7 qPrecocious puberty in boys, central or peripheral,8 v- O( R/ s' n0 |( u1 b% \( n/ k( G
is a significant concern for physicians. Central
4 J0 X% w) u) ~7 d$ Uprecocious puberty (CPP), which is mediated
" d  X5 X& }7 y! G* w4 |through the hypothalamic pituitary gonadal axis, has. a$ B/ u: t# R5 {" G  O& W
a higher incidence of organic central nervous system
8 `4 L+ C3 t3 @* jlesions in boys.1,2 Virilization in boys, as manifested
. ^1 B2 I( V. p: ]5 Q, y* D# hby enlargement of the penis, development of pubic+ {) f; W" l, O' k
hair, and facial acne without enlargement of testi-
0 z8 a3 y7 l2 ], Icles, suggests peripheral or pseudopuberty.1-3 We
# {" Z; k) C9 L4 A. ^8 U- ^report a 16-month-old boy who presented with the
' n; D/ i) g9 O2 f0 j' h" d5 S# x" s% Lenlargement of the phallus and pubic hair develop-
4 N6 S1 Y! o! m8 d7 K9 `$ k2 ement without testicular enlargement, which was due
! W* d8 ~! G6 T, j% \, Rto the unintentional exposure to androgen gel used by9 R& k! A% p% [. U& n
the father. The family initially concealed this infor-
9 L; y# I, G, l& emation, resulting in an extensive work-up for this2 b7 n  i" ?7 E* J
child. Given the widespread and easy availability of; ]9 u4 s2 O8 H9 q9 R4 r
testosterone gel and cream, we believe this is proba-: I* S' \4 b, b
bly more common than the rare case report in the
, ]3 a3 M0 z6 y+ Eliterature.4
9 C0 {2 l* z( w/ J3 T/ zPatient Report; a% \$ W. v$ F0 `
A 16-month-old white child was referred to the
8 v( [8 r. w  h+ E- q/ xendocrine clinic by his pediatrician with the concern" ^* N5 g9 @/ P8 Y0 v7 j. P
of early sexual development. His mother noticed
0 ~# S9 N# |% F2 A: ]light colored pubic hair development when he was
2 ?- ?$ @* T4 i; M2 S- H2 V# i( dFrom the 1Division of Pediatric Endocrinology, 2University of3 Z! h% o5 F( Z/ z2 Y( ^& w& W/ |/ v
South Alabama Medical Center, Mobile, Alabama.! p" V' k; r+ t& i- Q/ p
Address correspondence to: Samar K. Bhowmick, MD, FACE,- s6 ?; Y) \2 h/ d' T( P5 e
Professor of Pediatrics, University of South Alabama, College of8 X2 ~# o& j( t! P
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
4 u7 P# h7 E& H0 J- x/ N1 \! Ue-mail: [email protected].
7 j) A( K7 u1 r7 ]1 f% C& oabout 6 to 7 months old, which progressively became) e) `6 m2 H( q% Q0 @8 d  I* d5 b
darker. She was also concerned about the enlarge-+ T6 j1 \4 v$ m5 n) g; N
ment of his penis and frequent erections. The child8 `/ U2 s+ E% c& h
was the product of a full-term normal delivery, with$ o7 i# U1 ?; T/ \) Y+ c. R- z  C
a birth weight of 7 lb 14 oz, and birth length of* t( o  Z0 x9 K: u: A; m
20 inches. He was breast-fed throughout the first year* ?( ?6 h9 B/ |4 S9 M* r; c
of life and was still receiving breast milk along with
$ M# M* d& ], s7 I! osolid food. He had no hospitalizations or surgery,2 ?$ ]+ S" s1 r: Z
and his psychosocial and psychomotor development
5 X$ r$ M% ~' O4 ]( Xwas age appropriate.
9 W& ~+ {! ^2 H' WThe family history was remarkable for the father,+ E& P! @0 h/ B3 B3 l) p, g3 ^# j
who was diagnosed with hypothyroidism at age 16,
: `1 ?7 y' l0 f+ y" l: Xwhich was treated with thyroxine. The father’s( B8 l$ Q- g1 v5 Z3 L
height was 6 feet, and he went through a somewhat% h& y% ~1 f  e- i+ [
early puberty and had stopped growing by age 14.
9 F" x6 |7 z+ d- R2 O4 FThe father denied taking any other medication. The" T& q& D9 S% w# d- d% l3 P* J
child’s mother was in good health. Her menarche
5 C  b, Z  A/ o9 ~/ twas at 11 years of age, and her height was at 5 feet
8 o! }7 N: z9 F8 B1 _" ^* ~5 r5 inches. There was no other family history of pre-
9 m; t8 p' z4 E1 n: kcocious sexual development in the first-degree rela-2 g& z& W8 e: O& C! J  v9 W& G
tives. There were no siblings.; F, ?1 X# w, l& i7 p
Physical Examination. B9 w: E  f% [1 K2 N% {' A
The physical examination revealed a very active,9 m5 \# X7 e( _3 \$ X/ l2 r
playful, and healthy boy. The vital signs documented1 @, }3 a8 N1 V; D  [
a blood pressure of 85/50 mm Hg, his length was3 x% M: E! L6 j, ^+ p! J4 ^) R
90 cm (>97th percentile), and his weight was 14.4 kg" f' W6 L# @) H3 Q" R1 @
(also >97th percentile). The observed yearly growth% b) g  o3 J' ], ^8 M& \9 V
velocity was 30 cm (12 inches). The examination of
- d. V7 h0 a3 o9 k+ \the neck revealed no thyroid enlargement.
! L. S8 k  f) n8 R$ k1 O  `The genitourinary examination was remarkable for
$ s8 E4 l1 P3 q# _4 B' q; }. lenlargement of the penis, with a stretched length of
6 H, |  D+ @( S! j! O6 e7 N5 B1 a5 @3 k8 cm and a width of 2 cm. The glans penis was very well1 N# n* N2 H! F9 F  ?8 n
developed. The pubic hair was Tanner II, mostly around+ v/ \- R+ ?; s8 H( ?; a/ G- F
540, B! y$ L# g2 }
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 X3 j: s( {- e5 Q  f2 f5 w% [
the base of the phallus and was dark and curled. The* o7 d4 q5 \8 B/ Y
testicular volume was prepubertal at 2 mL each.
# d/ [7 r0 R4 ~2 _* ]The skin was moist and smooth and somewhat
0 p3 x! u% ~% W( x& d" M" N9 Y5 yoily. No axillary hair was noted. There were no
. W, |& @: T1 R$ cabnormal skin pigmentations or café-au-lait spots.7 x/ ^3 M7 P( K+ P% b, z1 Q! q, M
Neurologic evaluation showed deep tendon reflex 2+5 w* E) ~% \" |. L; k9 {$ ^
bilateral and symmetrical. There was no suggestion0 x/ _" _" V- n' @6 z9 F4 J/ {8 r
of papilledema.
  t! ]/ w  n3 ~" u5 j, T9 Y" JLaboratory Evaluation! ?, `0 U8 |/ g# t& H( J, S
The bone age was consistent with 28 months by
* O' N$ D# ?: V7 _* Z8 ]using the standard of Greulich and Pyle at a chrono-: h' r2 k. f' A- K- D1 W1 b
logic age of 16 months (advanced).5 Chromosomal4 I$ K) ]' v' y! v5 y0 ~0 U
karyotype was 46XY. The thyroid function test% c5 Y7 O  d: o8 G3 @* B
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 Y* Z* a$ d. E6 `$ A' l& `lating hormone level was 1.3 µIU/mL (both normal).
4 m1 Z. p* Z4 V* s' yThe concentrations of serum electrolytes, blood
6 w1 p" a$ Z. W, Y- }! furea nitrogen, creatinine, and calcium all were
0 Q4 [% E" r8 t# \3 }3 K& d% ?within normal range for his age. The concentration7 h4 h' b. l9 J, E
of serum 17-hydroxyprogesterone was 16 ng/dL
# e% F- q: F' h, d6 h; H7 h& L% w8 Y(normal, 3 to 90 ng/dL), androstenedione was 20& F+ ~7 h0 m$ z: b& G7 o
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" r9 S  d; p7 ~/ G# B
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
9 y- v6 u0 a0 Z7 ~2 ]2 m/ Y6 @2 Wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to5 ^. i( u' q, y2 Y: A! Z
49ng/dL), 11-desoxycortisol (specific compound S)) u- ]/ u! A, T4 j. W, M- j/ \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( w4 B% a: l; m
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ o- d' b5 a* n# Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 ?9 W* j3 i9 ]$ nand β-human chorionic gonadotropin was less than
* e6 S; o( ]( w, j2 Q5 F2 ^5 mIU/mL (normal <5 mIU/mL). Serum follicular- e. z. Z$ Y+ \0 P8 M
stimulating hormone and leuteinizing hormone$ u4 x9 c+ F+ C# F. p6 A7 S
concentrations were less than 0.05 mIU/mL
8 Z: J, E% f0 P- m( Q" W(prepubertal).
: B6 [1 k' Q9 f" h# ^/ {The parents were notified about the laboratory
9 C9 y& C4 K6 C; `results and were informed that all of the tests were
  c7 H/ G) Q( L* c7 Tnormal except the testosterone level was high. The
$ R- m1 Z. [& r( F8 Tfollow-up visit was arranged within a few weeks to
0 f+ |" z# ]$ b# P5 Nobtain testicular and abdominal sonograms; how-3 U) U0 }. n% I! d, h" F; w
ever, the family did not return for 4 months.
! S+ v# [( ~) S" a1 O) T7 A1 h: |5 IPhysical examination at this time revealed that the
0 u  b0 f* i' k4 }! r$ b! |child had grown 2.5 cm in 4 months and had gained* S/ U. S; X6 T" n# I* U) E
2 kg of weight. Physical examination remained4 {3 o; ^; o& A% X, G' T
unchanged. Surprisingly, the pubic hair almost com-
/ f: p. h, G5 u. P8 R' q6 vpletely disappeared except for a few vellous hairs at
+ t7 O+ r' _' I; Nthe base of the phallus. Testicular volume was still 2
2 ^6 J  R1 f. G+ @mL, and the size of the penis remained unchanged.# Y. G* Y# I" W7 m  F0 z
The mother also said that the boy was no longer hav-
. B/ p' `( w4 c+ h9 `" \7 jing frequent erections.3 ?  b, A; A- {4 W% e0 b
Both parents were again questioned about use of
! f# E- G3 Y# o1 ^8 R3 a# D" {5 Fany ointment/creams that they may have applied to, b" l1 }. d3 x6 R% m6 o$ v3 a/ Z
the child’s skin. This time the father admitted the% e7 T( O, @  ?9 A5 D4 k) M* z
Topical Testosterone Exposure / Bhowmick et al 541. ]8 F$ n0 l: y5 g' h
use of testosterone gel twice daily that he was apply-: U( r. Y: W- N# y& G6 B
ing over his own shoulders, chest, and back area for$ u2 o& O) f+ A7 ~# P3 u  ~
a year. The father also revealed he was embarrassed4 [0 a! {1 F" G
to disclose that he was using a testosterone gel pre-
( G  M6 {$ n+ z; H# p2 }' a9 j8 kscribed by his family physician for decreased libido2 \; n/ B: \! f* i: s! A. Q
secondary to depression.3 q7 {# O8 z9 }8 X9 c! H% S7 w; J7 a
The child slept in the same bed with parents.
, A4 {) D3 m: ^% j7 `+ I) G% a* S7 jThe father would hug the baby and hold him on his8 P6 A5 s6 i0 K1 x3 T
chest for a considerable period of time, causing sig-9 U- O: p! v1 ~' e
nificant bare skin contact between baby and father.6 o9 r8 s" B9 [2 G; A
The father also admitted that after the phone call,( c4 P( E% Q( S0 T" \. K! }
when he learned the testosterone level in the baby
7 ?' f  M! L+ [8 \; t6 C& a- U+ h& ?was high, he then read the product information
# w9 d4 N$ G( @8 wpacket and concluded that it was most likely the rea-
0 e4 v) v7 z6 B* {% sson for the child’s virilization. At that time, they
' X% ?- T6 j1 Q; n2 r  X+ i2 q; zdecided to put the baby in a separate bed, and the1 C7 u8 ^. E& S- P) i2 S# m. y
father was not hugging him with bare skin and had8 D9 [3 c/ X! j) x& H
been using protective clothing. A repeat testosterone
3 v# z- Y, Z/ h" Y5 Etest was ordered, but the family did not go to the
' _9 [7 w) A. Q! O' Jlaboratory to obtain the test.* i: x5 A$ v* U7 h
Discussion
4 e: r* o% u7 ~/ U( Z1 @% F2 {Precocious puberty in boys is defined as secondary
) ~9 g; B) }" h: T. I. g8 u9 dsexual development before 9 years of age.1,4
! O! M) O: [& C1 H7 K8 `+ C- _3 f: RPrecocious puberty is termed as central (true) when  _4 m# ^' K7 \  h. }1 ~0 Q5 z+ w
it is caused by the premature activation of hypo-
! d( S/ \2 I5 [$ [thalamic pituitary gonadal axis. CPP is more com-$ c, r5 {! v) \% F* C9 Q! E
mon in girls than in boys.1,3 Most boys with CPP: x( `  r! `" h0 l. S' K
may have a central nervous system lesion that is* o, u- O! v* y# k
responsible for the early activation of the hypothal-) ~. p4 ]& V9 |6 p8 i2 h3 \
amic pituitary gonadal axis.1-3 Thus, greater empha-
7 ^3 J$ g" C) @/ V$ j, csis has been given to neuroradiologic imaging in
# X) n: X/ y+ l! I6 Nboys with precocious puberty. In addition to viril-
/ \. p' R; ^; s" vization, the clinical hallmark of CPP is the symmet-
0 @3 J7 C4 a* Wrical testicular growth secondary to stimulation by1 q- P4 ]# ]& L8 \+ t
gonadotropins.1,3
: _' n) G- y2 Y7 V# I: FGonadotropin-independent peripheral preco-/ ~9 _9 |1 t$ @- A
cious puberty in boys also results from inappropriate6 M8 l; Z: B! _# Q
androgenic stimulation from either endogenous or! V" y: b3 p4 ?
exogenous sources, nonpituitary gonadotropin stim-. m0 v" [/ j/ j( W1 R' S
ulation, and rare activating mutations.3 Virilizing
) ]& \0 J7 F% b0 q# _; Qcongenital adrenal hyperplasia producing excessive
$ v2 n/ h  [1 u# Nadrenal androgens is a common cause of precocious
3 @7 X1 {, b$ w" w. O9 P* H6 ]puberty in boys.3,48 U" r/ x- ^$ Y7 [/ ^
The most common form of congenital adrenal
: I, _8 L) N8 Xhyperplasia is the 21-hydroxylase enzyme deficiency.. F$ w- S, N; r) ?6 o
The 11-β hydroxylase deficiency may also result in
4 Y! E+ z( Y" Q% Eexcessive adrenal androgen production, and rarely,
. d9 ~& ^  M( Uan adrenal tumor may also cause adrenal androgen) v) u; S6 \% T% v" e) y: G
excess.1,3
/ |% B7 d5 J5 B' W( t) _$ F$ {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 _" u/ U4 p) `9 c8 E6 W542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 z7 S6 ]9 K& S; g# d, k! x+ M
A unique entity of male-limited gonadotropin-) _" R; @8 c7 q% C7 e
independent precocious puberty, which is also known" s1 j/ \) I7 O0 X6 X4 c4 h
as testotoxicosis, may cause precocious puberty at a
% r( y( Z- q+ |4 L. Mvery young age. The physical findings in these boys
1 D. j; Y  M7 l# v0 N- @; [with this disorder are full pubertal development,5 K" D( |  i, ?( \- d& @" _& W" ^9 }
including bilateral testicular growth, similar to boys
1 |$ [( k$ C5 \  W. Nwith CPP. The gonadotropin levels in this disorder: D0 n5 H! G; H* N
are suppressed to prepubertal levels and do not show
' b0 i7 @/ j4 D& M- Gpubertal response of gonadotropin after gonadotropin-2 [1 M( Y5 S; g% f6 w) i; c
releasing hormone stimulation. This is a sex-linked3 G0 x6 J/ m/ p, j" C
autosomal dominant disorder that affects only  O) |: V' o! ~: M) [) ?
males; therefore, other male members of the family8 g& P: }* Z) {7 M5 ^  O
may have similar precocious puberty.3
; F6 A) i1 Q) L! L4 [7 M3 q; A. uIn our patient, physical examination was incon-; l% s1 W2 {8 O! t
sistent with true precocious puberty since his testi-5 b! `- k+ ^6 o4 s: ^0 N. P
cles were prepubertal in size. However, testotoxicosis
" @$ J+ Q0 e2 \- T: E! k$ R+ dwas in the differential diagnosis because his father
* }% m0 e! A8 R" y' ^# T7 G2 L0 Qstarted puberty somewhat early, and occasionally,
2 b: ?0 B! T6 Ntesticular enlargement is not that evident in the# t/ m& A: r% x$ s  D8 }' L" C; U; Q
beginning of this process.1 In the absence of a neg-0 e9 s, s4 {8 O/ J; u- R9 V
ative initial history of androgen exposure, our9 h) M, R' N  g- n/ s6 v
biggest concern was virilizing adrenal hyperplasia,
) l. [( F! ^* l7 m4 e* s9 |either 21-hydroxylase deficiency or 11-β hydroxylase* j  A% o  k+ r- F2 K* U/ }
deficiency. Those diagnoses were excluded by find-# N4 U+ n3 S" Y2 H/ H( p
ing the normal level of adrenal steroids.% L& r( ~' j3 q& `) w# `% q
The diagnosis of exogenous androgens was strongly5 G8 W; {! @& C8 f/ R
suspected in a follow-up visit after 4 months because
1 Y, b5 `3 b- b6 r7 bthe physical examination revealed the complete disap-& A4 e6 l: X( c* [
pearance of pubic hair, normal growth velocity, and0 f# A2 Q0 f6 a3 `$ B# d$ L
decreased erections. The father admitted using a testos-
5 W3 D. Z" h3 I3 f" H/ a+ hterone gel, which he concealed at first visit. He was" R2 N( \1 S/ d- z  r6 U4 Q# v
using it rather frequently, twice a day. The Physicians’
2 H$ W' I4 P& e. T) S% rDesk Reference, or package insert of this product, gel or9 m1 W: p/ D1 M( e3 s
cream, cautions about dermal testosterone transfer to
8 K0 A& H# |  Y) ?unprotected females through direct skin exposure.
. M8 [( _. p  G( U: D7 tSerum testosterone level was found to be 2 times the+ H: I- b- ?( o2 l, E6 Y( P0 V
baseline value in those females who were exposed to
# x: y8 X- }3 {+ f5 b; d+ l: yeven 15 minutes of direct skin contact with their male3 n$ F, w2 A1 ]( Y8 A
partners.6 However, when a shirt covered the applica-5 M5 k, Y2 k8 ?" T( B- c
tion site, this testosterone transfer was prevented.
. l. O' N5 G9 kOur patient’s testosterone level was 60 ng/mL,' p$ ]0 l5 t8 y; r/ J; d5 E( l
which was clearly high. Some studies suggest that5 x8 n* k% }0 R3 p
dermal conversion of testosterone to dihydrotestos-! ], u: A" @. x* `/ S
terone, which is a more potent metabolite, is more
. x' v6 C! U/ n6 _active in young children exposed to testosterone3 d) ^: j+ |" \* c" R; @
exogenously7; however, we did not measure a dihy-
8 h+ T, Z" R/ v8 a7 X8 i: h6 idrotestosterone level in our patient. In addition to
: T3 [) s9 C" g% _* N1 {, Vvirilization, exposure to exogenous testosterone in4 Q* d8 f6 {2 V! z( [% @; p
children results in an increase in growth velocity and
$ c+ R7 W! K1 M1 b9 Zadvanced bone age, as seen in our patient.
7 l: {& U( \  k+ ?The long-term effect of androgen exposure during
7 Q/ a' z% s9 C  [1 u# Wearly childhood on pubertal development and final( p8 Z7 e& U) [- }
adult height are not fully known and always remain
8 _% v4 q/ M! V# x: Ba concern. Children treated with short-term testos-
  ~2 \& b+ C, R8 q' F$ Tterone injection or topical androgen may exhibit some& G* j7 s5 l; e4 |* d  P
acceleration of the skeletal maturation; however, after
0 L) F5 e* S' P% R; F2 P- acessation of treatment, the rate of bone maturation6 F- u% h8 E4 o/ u8 d" `
decelerates and gradually returns to normal.8,92 V- _2 z8 R( L  c2 m" g
There are conflicting reports and controversy' o6 t' c+ A0 g& `9 M2 T
over the effect of early androgen exposure on adult0 p! j8 F- F- T5 L
penile length.10,11 Some reports suggest subnormal. R1 X( H% I, S2 j) v( k
adult penile length, apparently because of downreg-- ~3 ?/ y- e- Y$ F
ulation of androgen receptor number.10,12 However,( ^: g2 \) \- r% e3 x  R0 @3 ?
Sutherland et al13 did not find a correlation between
  }  e0 O( K# ]childhood testosterone exposure and reduced adult5 Y8 j; B9 k: s& |4 }
penile length in clinical studies.
0 }$ M8 c, O0 a, a( n! L0 [' T/ JNonetheless, we do not believe our patient is
( L6 X# y1 p  ?6 m) D( Wgoing to experience any of the untoward effects from
: Z4 A5 x. i* g% O' j7 ~) |  Btestosterone exposure as mentioned earlier because  _  C# s& I9 k
the exposure was not for a prolonged period of time.
& F2 L; ?" |, Q! d0 p( @: GAlthough the bone age was advanced at the time of
4 U8 z. }1 W4 M1 a4 Mdiagnosis, the child had a normal growth velocity at
% }% D: v: ?% s/ N% D# J) tthe follow-up visit. It is hoped that his final adult9 ?6 G: P( g+ \; G
height will not be affected.0 K! P+ N1 v. m$ n4 e8 Y  l
Although rarely reported, the widespread avail-
+ J% k1 _6 ~0 e! Yability of androgen products in our society may
$ b5 _6 D, H* I9 l( Y7 U5 W+ Uindeed cause more virilization in male or female
. S* ~& ^5 W9 }2 g( Y: i+ Achildren than one would realize. Exposure to andro-
  i0 g3 B. b% K( b/ v  tgen products must be considered and specific ques-5 V& {. E8 v. M! R
tioning about the use of a testosterone product or9 k# ~# x+ Y2 j5 s
gel should be asked of the family members during
3 G" \+ E: ^, j3 J$ n7 vthe evaluation of any children who present with vir-, M0 {- ?/ y" X1 w9 w" l
ilization or peripheral precocious puberty. The diag-
' A% \! d- o$ J; P  L! \; Knosis can be established by just a few tests and by( @' q3 s0 m4 B
appropriate history. The inability to obtain such a
6 D  O/ O' S* d+ P) Q% I, mhistory, or failure to ask the specific questions, may
( L3 |% _! s& Eresult in extensive, unnecessary, and expensive
5 ~9 m. R8 f  ?' {) ^6 Xinvestigation. The primary care physician should be
; V# a8 j3 [# M! J& e0 R- k' M5 Raware of this fact, because most of these children+ a: P$ f4 o. a0 a4 [" v
may initially present in their practice. The Physicians’
1 W8 k/ G4 [! XDesk Reference and package insert should also put a
, R, o! o  V4 c9 lwarning about the virilizing effect on a male or5 h# Z$ w. f  L4 w  A; o+ F
female child who might come in contact with some-
- ?4 l1 y/ W  z( [  [' y# [- Kone using any of these products.
/ i; o* n5 D. F/ p0 j+ f4 z- dReferences
7 J  P  o+ F3 s: ?4 m; F1. Styne DM. The testes: disorder of sexual differentiation9 T- J; R* h/ o( h3 R, P
and puberty in the male. In: Sperling MA, ed. Pediatric0 N4 [( u( d' O7 E% [
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& w% S) Z0 [' d" c% s; B7 l" \
2002: 565-628.
$ W# S5 B' T* S0 _5 C/ V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* G  o* d9 e) \' t9 }( w
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
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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
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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
2 ]( N/ i# P% e3 ~+ c% _( G
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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