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Sexual Precocity in a 16-Month-Old
* f7 l* g0 `7 t/ }- g$ Z- EBoy Induced by Indirect Topical* @- f3 o( T7 ?1 p7 `& i' b
Exposure to Testosterone
# P* E0 b( i; b$ WSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 m" b- G8 L1 N* b& u$ x
and Kenneth R. Rettig, MD15 Z$ ^- d# ?% }# u8 h: G. w8 y$ ?$ L
Clinical Pediatrics
# ?( Y3 D) }  y) t" f) r; cVolume 46 Number 67 C: j, E  |. b& Q6 O
July 2007 540-543
, S" Q9 O9 d; A$ q( J- _© 2007 Sage Publications! Y7 e9 D2 q8 ?3 m6 S
10.1177/0009922806296651  H" u8 E- }$ M/ m+ ], y/ }% y
http://clp.sagepub.com
' a/ h" T, p7 fhosted at2 q8 E9 f: E+ J3 L" P' ]
http://online.sagepub.com
1 K: U% h9 i! OPrecocious puberty in boys, central or peripheral,
7 ]3 W' a2 c. Q- t; {is a significant concern for physicians. Central; q5 u" l0 v& u" m; L6 [" |
precocious puberty (CPP), which is mediated! S2 Y! i) b$ Q. Y2 U( {0 a2 a
through the hypothalamic pituitary gonadal axis, has
5 n- W% w) v$ K( w: b; Ta higher incidence of organic central nervous system
. l. b$ F+ X7 ^; R( ~, N' elesions in boys.1,2 Virilization in boys, as manifested
4 @' J. n  _* {by enlargement of the penis, development of pubic- G) g. U6 U4 H4 q1 W
hair, and facial acne without enlargement of testi-
- |6 b* C0 i3 ^cles, suggests peripheral or pseudopuberty.1-3 We
; A) M, W: n3 {5 @/ ireport a 16-month-old boy who presented with the9 H. ?, ]5 A  T+ |' V4 I* x0 y9 u
enlargement of the phallus and pubic hair develop-% x8 Z6 B! p" P7 s: I3 B; a
ment without testicular enlargement, which was due
4 T1 R. Y% ]( U, f0 k( [to the unintentional exposure to androgen gel used by5 W2 V" g6 b  v# ]" Q7 h( l- m
the father. The family initially concealed this infor-
. ]  d) u3 C# |% @1 i- f5 c: Vmation, resulting in an extensive work-up for this: p* e1 l. I; i# d/ I& y6 e: Z
child. Given the widespread and easy availability of3 C3 e2 I/ f5 [5 z+ D3 G3 U. c/ F
testosterone gel and cream, we believe this is proba-* ]2 H: F/ B9 M# Q# ?6 V  R. z( M: X
bly more common than the rare case report in the) P8 i, J! \9 [7 Y) u$ D4 ?
literature.4
" \3 I1 c; G: y1 j6 O1 ^6 W: `Patient Report
$ z1 E! a3 Z- |8 {$ sA 16-month-old white child was referred to the
+ O8 B& M1 M6 Q- tendocrine clinic by his pediatrician with the concern" o5 c, k: F" F
of early sexual development. His mother noticed
6 s, N' D8 A5 J: g# Clight colored pubic hair development when he was1 m( H8 v$ j4 o6 G4 K( [% b  c8 f" t
From the 1Division of Pediatric Endocrinology, 2University of
* ?& m( q$ P( P% j) j- O& q- GSouth Alabama Medical Center, Mobile, Alabama.
5 ?( t. G: G" s5 {7 iAddress correspondence to: Samar K. Bhowmick, MD, FACE,
2 C8 L! ^9 O- j" C% B6 sProfessor of Pediatrics, University of South Alabama, College of
6 \" ]2 {8 _0 |Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 A. ]/ Z  e- X) Y# D% J
e-mail: [email protected].
$ q# ?- @( K3 G9 @4 mabout 6 to 7 months old, which progressively became
6 ?: S) V) I/ L  l3 c2 Cdarker. She was also concerned about the enlarge-
* M; C) I( q) _9 s9 pment of his penis and frequent erections. The child% d: o% W: [" N- b2 [; }) J: B
was the product of a full-term normal delivery, with9 p: i) J1 h6 [( C+ s7 p) ?
a birth weight of 7 lb 14 oz, and birth length of; D) o* x  E: C4 W$ V+ S9 ^
20 inches. He was breast-fed throughout the first year
8 S, [) \% M/ G( n; w& l+ Dof life and was still receiving breast milk along with
5 X9 j1 c) }. R2 H2 |  \solid food. He had no hospitalizations or surgery,1 I+ Y2 P* B4 U) Z+ z* Y+ `
and his psychosocial and psychomotor development
# O0 [" A' M7 w4 i, T) Qwas age appropriate.9 R) k* S4 L& ?2 z/ b6 A+ k$ x
The family history was remarkable for the father,
. q# _; K/ l% S* p& n/ b4 _- ]who was diagnosed with hypothyroidism at age 16,4 u* ]0 T' a. n! ?! `. G
which was treated with thyroxine. The father’s
' z7 i. U# B$ P1 a, Theight was 6 feet, and he went through a somewhat
7 ?; ~1 I7 F  c9 [9 w5 e+ mearly puberty and had stopped growing by age 14.
2 Y" A% V" Q) _6 B( S" I- eThe father denied taking any other medication. The
/ N* t: ~# D+ E9 v' schild’s mother was in good health. Her menarche2 Z3 k& g; y3 f* t; i
was at 11 years of age, and her height was at 5 feet% L& U2 B' ]) A8 s, b
5 inches. There was no other family history of pre-8 V1 U0 Y( t4 n; q% k- f. N
cocious sexual development in the first-degree rela-6 z  V' E: Y4 E; Y2 e7 k, c% B
tives. There were no siblings.
. W! G/ ^) u4 V2 ?- [- _  FPhysical Examination$ e0 c2 ]$ M/ {5 a( s3 |
The physical examination revealed a very active,
7 x) y1 ~# a9 Y6 zplayful, and healthy boy. The vital signs documented
1 C- |, O$ p; d* va blood pressure of 85/50 mm Hg, his length was
9 I1 K( E7 W0 Z' f' y90 cm (>97th percentile), and his weight was 14.4 kg
7 @, S1 K: ~* n' t: |(also >97th percentile). The observed yearly growth
7 ~* r4 d; ]3 vvelocity was 30 cm (12 inches). The examination of4 V4 h! W" `9 b2 }( ~. u5 U* d
the neck revealed no thyroid enlargement.
# D) R4 i7 h+ }1 o# A+ C. {The genitourinary examination was remarkable for
- O- |: U/ d$ \1 T6 senlargement of the penis, with a stretched length of
% y) ^3 E$ Y3 S% }, S) B8 cm and a width of 2 cm. The glans penis was very well4 V' u* D6 ~6 f% y+ r* u$ z. o
developed. The pubic hair was Tanner II, mostly around
. H6 H8 z7 j8 b6 x5409 L% W4 L4 Y/ W& g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; j: R& K5 W( y8 F# @7 e; `3 t2 Qthe base of the phallus and was dark and curled. The6 L, _: J* W$ W8 J+ k8 y
testicular volume was prepubertal at 2 mL each.
! z3 [& w: i; V+ KThe skin was moist and smooth and somewhat
) i0 u; w" `6 f1 t8 u( toily. No axillary hair was noted. There were no7 {9 d6 a4 |# ]- D3 b
abnormal skin pigmentations or café-au-lait spots.
  f1 ]5 P* e) {& {) c0 ?Neurologic evaluation showed deep tendon reflex 2+- ^) C2 n4 }7 E% k7 }0 A& J
bilateral and symmetrical. There was no suggestion3 Y5 _  y  l# P4 J7 ]9 I$ l; q9 B
of papilledema.
7 Q! Q7 b1 o! a( ZLaboratory Evaluation
' N% e  b- f0 l/ I; GThe bone age was consistent with 28 months by
0 n4 q4 Q* t  V0 ~1 A6 u& gusing the standard of Greulich and Pyle at a chrono-9 ~3 ~. k# ?. G
logic age of 16 months (advanced).5 Chromosomal
5 o) r1 |5 ?7 m* u# ]) a  Lkaryotype was 46XY. The thyroid function test, V( [3 B( ~: u
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 ~1 A6 y6 I+ P0 elating hormone level was 1.3 µIU/mL (both normal).
7 w' V& X, l) p7 H7 \2 {The concentrations of serum electrolytes, blood; V& E1 k5 D4 Y' e# Z
urea nitrogen, creatinine, and calcium all were
# ]* Z- p2 `2 o) {$ e( Mwithin normal range for his age. The concentration
0 b6 _- P4 e/ ~' ~: Y, n6 jof serum 17-hydroxyprogesterone was 16 ng/dL
$ m0 ~0 ]$ V! @0 W+ y' x/ o$ _(normal, 3 to 90 ng/dL), androstenedione was 20
5 B# _; _' ]  g8 [( xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ K& r* `* L. s& R! Z# A; p6 D. J
terone was 38 ng/dL (normal, 50 to 760 ng/dL),$ p+ U' P0 O2 E5 f, |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to6 C. u1 E6 D7 O  K: S' o
49ng/dL), 11-desoxycortisol (specific compound S)) F" u& w* r' A, [, `$ ?7 V
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- z& W! g7 B# Z& R) [7 Z8 V. ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total3 v% S/ |3 u0 {/ g0 P$ N
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 w+ @7 N5 B/ x$ ^1 J1 c% ]
and β-human chorionic gonadotropin was less than& d* D: m; i+ H" f% w+ l% }& ~
5 mIU/mL (normal <5 mIU/mL). Serum follicular6 f* G' c& C  t$ H0 N# k4 p
stimulating hormone and leuteinizing hormone
6 U# ]; q# M8 H) _; U: l; E" }concentrations were less than 0.05 mIU/mL- |- V7 j# |& B% f4 Z
(prepubertal).. r# D/ h! E+ k% Y* f' Z9 X
The parents were notified about the laboratory
+ e4 F0 @9 o1 u* dresults and were informed that all of the tests were
5 G4 o" m! S- M6 t) ^normal except the testosterone level was high. The
) ]  g  C- l6 Kfollow-up visit was arranged within a few weeks to' L) R* @# M8 D' g
obtain testicular and abdominal sonograms; how-
, S- }/ r# ^5 f8 n* Z/ p% F' K1 g) ^ever, the family did not return for 4 months.
; z9 B6 ^; L) _6 t7 TPhysical examination at this time revealed that the5 N4 j* l' \+ c% C3 b4 U2 }  r
child had grown 2.5 cm in 4 months and had gained* H3 Q: O3 J; o4 ?+ c
2 kg of weight. Physical examination remained
4 R/ G& F# [1 y& |unchanged. Surprisingly, the pubic hair almost com-
0 N/ J5 |: c" p; H& \pletely disappeared except for a few vellous hairs at. L' t; B( q5 V7 Q1 N( g# z  J  k
the base of the phallus. Testicular volume was still 2  f) D% M  g% A  ]( f: D
mL, and the size of the penis remained unchanged.
2 k' }$ u3 N; V+ ^% R! J; pThe mother also said that the boy was no longer hav-* u5 L, {" \  I' {
ing frequent erections.
* C# y6 f; {# f1 I+ k+ ~Both parents were again questioned about use of
& |" r5 O$ _3 C% }any ointment/creams that they may have applied to: I7 x/ X! W& J$ w' |
the child’s skin. This time the father admitted the
, ~+ z/ u" o8 q' bTopical Testosterone Exposure / Bhowmick et al 541
9 D9 q% r) q1 {: b8 vuse of testosterone gel twice daily that he was apply-
1 j* F. X5 {* u. Sing over his own shoulders, chest, and back area for
$ U) S6 z1 Q" X: y0 a' ea year. The father also revealed he was embarrassed
2 Y% k7 j3 u$ c6 M- tto disclose that he was using a testosterone gel pre-
9 t/ I5 C7 y# A4 dscribed by his family physician for decreased libido+ f+ w" L. Y1 B% H* I2 P
secondary to depression.
) h" X7 K3 G0 g7 g$ _# A$ U. E! a$ sThe child slept in the same bed with parents.  x5 I; J0 c3 z8 G7 i
The father would hug the baby and hold him on his. q! A  [/ U) D/ l
chest for a considerable period of time, causing sig-
. p& P  W- E; D% knificant bare skin contact between baby and father.
+ |3 ^8 T5 ]: m$ TThe father also admitted that after the phone call,& K6 f4 H+ O' I' l
when he learned the testosterone level in the baby
9 l' |* @0 z9 q) o8 V) K: Xwas high, he then read the product information
2 z$ t( B* Y# ?8 w$ i- [/ epacket and concluded that it was most likely the rea-4 n7 C3 O% b: X, N3 b$ G
son for the child’s virilization. At that time, they
# _; [5 x/ D+ d& {decided to put the baby in a separate bed, and the
# c5 ~- V2 _* ?: ~; C, n" }. B8 y$ Ofather was not hugging him with bare skin and had1 w8 o8 U$ R6 q5 j, O
been using protective clothing. A repeat testosterone; T3 b9 I# I, ?  {; A
test was ordered, but the family did not go to the( Q2 a2 O* U5 d& c$ T6 |' v% t
laboratory to obtain the test.
- Q: _, v7 O9 i: |# fDiscussion
4 ?8 n% ~4 P6 j' U- VPrecocious puberty in boys is defined as secondary/ B( H, J6 ~5 F. ?
sexual development before 9 years of age.1,4
. v( w7 \+ @! W7 @! @1 pPrecocious puberty is termed as central (true) when- d! ?# b! u. {
it is caused by the premature activation of hypo-
! X$ ~- S4 Q# A. U' a# m: Hthalamic pituitary gonadal axis. CPP is more com-4 O0 h+ h5 M/ X; v3 N
mon in girls than in boys.1,3 Most boys with CPP" \; A' V- U+ i& k/ r
may have a central nervous system lesion that is
* Q: {8 F# r8 I% t# tresponsible for the early activation of the hypothal-
( W/ b& v8 o9 T. M- _- Z% iamic pituitary gonadal axis.1-3 Thus, greater empha-9 Z' V. p9 ~2 R0 Y3 Q5 C: _
sis has been given to neuroradiologic imaging in$ V& G3 k+ y1 U, k
boys with precocious puberty. In addition to viril-3 p* w3 x, e! b# b# o7 F
ization, the clinical hallmark of CPP is the symmet-
: \9 X! ^8 [- H. k  Lrical testicular growth secondary to stimulation by
  Q. v8 ]. x" o" o: q  u% ~% }; v% Hgonadotropins.1,3& [4 y! ^+ h0 e" F5 g  A! h
Gonadotropin-independent peripheral preco-1 a1 {1 f. }! Z, J3 T+ F8 g; I# i
cious puberty in boys also results from inappropriate" v# f. @- W; ^2 a7 n8 L* r2 X
androgenic stimulation from either endogenous or
: N% |% ?  ]" k- Z# Zexogenous sources, nonpituitary gonadotropin stim-
$ x2 u1 V/ H- x9 Z  u, xulation, and rare activating mutations.3 Virilizing
+ Y/ d: ?2 M, L) G0 k  n9 ~4 Xcongenital adrenal hyperplasia producing excessive
0 l% F% c5 y% M) V, _adrenal androgens is a common cause of precocious
( v6 K- V. A% K8 _* [. fpuberty in boys.3,40 g: x4 p: Q. `- z
The most common form of congenital adrenal/ H+ m7 |1 Z$ M/ P8 p& U
hyperplasia is the 21-hydroxylase enzyme deficiency.
3 R, B. a' T2 d, V7 |7 g9 y- o- a# ZThe 11-β hydroxylase deficiency may also result in
- o( t# H* P" O% _+ h% [  `  Xexcessive adrenal androgen production, and rarely,# q" l; n. w0 G7 C9 V
an adrenal tumor may also cause adrenal androgen
# p) ?$ C8 c, n, x8 |0 r9 Pexcess.1,3- g# x) G/ P; w0 |2 X8 U# ^2 k, g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from8 \) }; n6 B/ a1 _( ?
542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 v) Q+ A% X( A  m1 W  h4 }
A unique entity of male-limited gonadotropin-! y. w& c4 I, A
independent precocious puberty, which is also known( D, O. j. N1 @
as testotoxicosis, may cause precocious puberty at a1 Y: ?3 ~$ q' ^& a
very young age. The physical findings in these boys8 j- Z) P5 {7 t, C9 J! W
with this disorder are full pubertal development,
+ D5 [& l& U8 I5 y7 o3 k! i1 C% gincluding bilateral testicular growth, similar to boys. Q; d! E# A8 `2 n  ^9 n" U
with CPP. The gonadotropin levels in this disorder5 o! E6 z# a( w# A" q* @( |% k
are suppressed to prepubertal levels and do not show
8 \2 \# a0 S  o, f5 [2 gpubertal response of gonadotropin after gonadotropin-7 F; v; }/ S- U: q6 |) u/ L7 _
releasing hormone stimulation. This is a sex-linked' P; C8 a2 v: T0 \
autosomal dominant disorder that affects only
# c+ U! Q' ^6 Qmales; therefore, other male members of the family
. D" E* C! K; D( @2 A5 |  Smay have similar precocious puberty.3
; D0 i0 ^) A8 q0 Q" J: cIn our patient, physical examination was incon-) T+ x. }+ z# a! b
sistent with true precocious puberty since his testi-
6 D, B3 r/ @* |1 G  scles were prepubertal in size. However, testotoxicosis
- @. x. {& ^$ p0 L5 Nwas in the differential diagnosis because his father1 e# Z" M) @, y1 |1 A4 v) _
started puberty somewhat early, and occasionally,
! m: f  g  N. n( |+ d/ m. _, }( Vtesticular enlargement is not that evident in the
$ f  w$ W) a- m4 T6 B; A3 Ebeginning of this process.1 In the absence of a neg-
7 l( e9 p# g; D$ a# X- K7 Jative initial history of androgen exposure, our% ?: D5 Z9 w$ ]6 x. ~- Y" b
biggest concern was virilizing adrenal hyperplasia,
; }" x9 X. [. S' p1 Keither 21-hydroxylase deficiency or 11-β hydroxylase0 s5 @8 |. |% h: c% }8 X
deficiency. Those diagnoses were excluded by find-
& U$ `: |$ p+ Q; g; l4 Z% V7 ~2 N4 Ling the normal level of adrenal steroids.# ^+ k* T7 J) O3 ~: Y
The diagnosis of exogenous androgens was strongly
$ O. ]  Q8 m8 U& t8 B! ususpected in a follow-up visit after 4 months because
6 T+ D+ P7 N4 Bthe physical examination revealed the complete disap-
5 L3 }" N+ N3 K/ f+ k8 a( gpearance of pubic hair, normal growth velocity, and( M+ J( }  r: Y& K: J( ^6 u; A
decreased erections. The father admitted using a testos-" Z- [) W  Q" j0 s
terone gel, which he concealed at first visit. He was
" D7 o: Y: e* Z1 v. ?( husing it rather frequently, twice a day. The Physicians’
5 i  W3 Z, B6 {7 p* k' ODesk Reference, or package insert of this product, gel or$ T* M0 n3 s2 W  L, N- @
cream, cautions about dermal testosterone transfer to1 Y' U' |/ t/ g2 v1 s' O# Z' S
unprotected females through direct skin exposure.0 ~0 J0 P# Y+ f5 Q3 s8 Q. M
Serum testosterone level was found to be 2 times the: @+ {) w: L5 r) `/ M" N
baseline value in those females who were exposed to$ M# q: `/ T9 U* k
even 15 minutes of direct skin contact with their male
5 U$ [+ ^) |' l: zpartners.6 However, when a shirt covered the applica-
% E- m- Z6 k& s" ~" v5 ?tion site, this testosterone transfer was prevented.8 q* ]. N/ O' X5 ~- R
Our patient’s testosterone level was 60 ng/mL,9 m4 E# G% V5 a+ x2 M# O
which was clearly high. Some studies suggest that
$ U4 v/ x( P. B6 y8 B" n* k& p7 @dermal conversion of testosterone to dihydrotestos-
4 Q6 I  Q: G" U7 Xterone, which is a more potent metabolite, is more
& T* H+ Z7 t/ D; [. I" f4 tactive in young children exposed to testosterone. b7 K* u9 B5 p$ \+ {  W
exogenously7; however, we did not measure a dihy-
( D2 v' Q: e1 j: e) ndrotestosterone level in our patient. In addition to+ Q3 G$ O7 z5 H5 O
virilization, exposure to exogenous testosterone in- u7 `  |0 A8 c8 ]# Y
children results in an increase in growth velocity and
5 }8 Z' |0 O1 s( n5 ^: M1 C% K+ |advanced bone age, as seen in our patient.% e1 w$ s* M) f. J$ X/ F" @. r& g" r0 o
The long-term effect of androgen exposure during
; I: w# I, U: ^& C- f3 Cearly childhood on pubertal development and final
. ^4 T* h% [& G$ ?! V( tadult height are not fully known and always remain4 s5 _; j2 X; p3 F% P' |+ t
a concern. Children treated with short-term testos-  Y. j6 Y% L. m. [- D" G
terone injection or topical androgen may exhibit some
' H; L) f4 ^+ u' C7 K1 _" M( _acceleration of the skeletal maturation; however, after
7 j* U. `! k5 i! j$ g/ Bcessation of treatment, the rate of bone maturation" _, O% e, Y7 w  W# d& q1 Z6 q. O
decelerates and gradually returns to normal.8,9
/ V/ }# J, p. i' gThere are conflicting reports and controversy
9 `8 D! Z( P' Kover the effect of early androgen exposure on adult" B3 b& V! o1 F4 ~6 d( {- j
penile length.10,11 Some reports suggest subnormal4 s2 Z1 d# T# D4 K2 z4 ?5 h
adult penile length, apparently because of downreg-
. o0 Q6 S5 R2 o' aulation of androgen receptor number.10,12 However,
6 D" i. e' ?& dSutherland et al13 did not find a correlation between3 E% o6 ^; c8 _
childhood testosterone exposure and reduced adult( y2 ~' k. \. [0 G0 w' z- ]
penile length in clinical studies.3 Y$ L  v. s, q/ }3 F
Nonetheless, we do not believe our patient is
# p  g, T" V, L; h* Hgoing to experience any of the untoward effects from
$ w4 |5 ^( o# G9 |7 ?" @+ Ftestosterone exposure as mentioned earlier because) a, t1 X8 `& Z
the exposure was not for a prolonged period of time.
" K. x& U# |2 C8 ?$ G$ @- WAlthough the bone age was advanced at the time of
2 |+ Z) `; l/ p; e! ~4 h' t' E' Wdiagnosis, the child had a normal growth velocity at9 t  q2 A4 ?+ G1 c6 G
the follow-up visit. It is hoped that his final adult8 I, v- l% `  x/ E2 X' P$ M
height will not be affected.- Q6 k$ A, L$ J$ r$ m
Although rarely reported, the widespread avail-2 n, y" A; w9 \/ b& [% W! Y: b
ability of androgen products in our society may3 G2 b1 C- a" e* l& @9 p. ~
indeed cause more virilization in male or female; {" S4 i7 f" u7 {2 D3 K# {) ~  n
children than one would realize. Exposure to andro-
; ~. w  G0 F! H0 igen products must be considered and specific ques-$ f! H- u" m$ u& {( R! c; s
tioning about the use of a testosterone product or
5 B7 ~* t. ~5 t9 G( pgel should be asked of the family members during
4 {+ o6 s! g- x6 R8 Jthe evaluation of any children who present with vir-
) Z$ m. _2 l+ \+ Bilization or peripheral precocious puberty. The diag-5 z/ D( v) {2 E  w6 M4 H( X; d
nosis can be established by just a few tests and by
% y, e# p+ n1 X* L( iappropriate history. The inability to obtain such a
, o. D* _  j7 |: W. }history, or failure to ask the specific questions, may
' D% c& |  P' B* n+ E" R$ ]result in extensive, unnecessary, and expensive" l- [5 M! L( I+ ~9 n9 q" R
investigation. The primary care physician should be
: q7 V4 N' Y- o. w! kaware of this fact, because most of these children
1 O( H' }5 `/ x1 |0 Ymay initially present in their practice. The Physicians’; V9 P" t8 u; N* F6 D0 N
Desk Reference and package insert should also put a
8 Y0 L: ^$ ?1 N2 N6 p4 lwarning about the virilizing effect on a male or# e0 M$ X9 t; J: F' e# {* d0 N
female child who might come in contact with some-/ M9 t( X- Q6 `% \$ {
one using any of these products." i9 g% y) ~0 g) ^
References
: \7 X3 l, M- H, I/ E0 V! \1. Styne DM. The testes: disorder of sexual differentiation
" {; k+ n) E5 v0 R+ U  fand puberty in the male. In: Sperling MA, ed. Pediatric9 l6 b+ \! }- s1 R
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
' E9 e8 }7 H- [2002: 565-628.  {4 E& F7 o% n; N. b: h% c. E
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 g$ e  a* c2 o2 y* @
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old+ ^: n! d. n  ?. n2 x8 I5 {5 V
Boy Induced by Indirect Topical/ z* t# j5 ?8 M7 ^  d
Exposure to Testosterone
( X# w5 l5 b2 r6 c' Y/ b& lSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" Y) s+ C4 r9 d  jand Kenneth R. Rettig, MD1- e6 q" e/ \" j& c/ z9 W4 z
Clinical Pediatrics5 U6 G, q$ D: X( h% `
Volume 46 Number 6; x7 B( A) U3 n& o0 s
July 2007 540-543
  h" N) ~- U$ b( j© 2007 Sage Publications
. u2 @0 ^7 U% ?3 _3 M. e10.1177/0009922806296651
# j: j8 @' a% ?http://clp.sagepub.com
4 y7 T  ?! o0 O9 L3 \3 L5 k) ghosted at- V5 k: P3 q# a8 ~" l
http://online.sagepub.com
9 f+ y3 U3 m7 [, B  sPrecocious puberty in boys, central or peripheral,* ]& u4 p/ i: r+ i
is a significant concern for physicians. Central$ r  q9 N6 D7 }# F+ r" {
precocious puberty (CPP), which is mediated' ]5 I6 m) z8 E2 u
through the hypothalamic pituitary gonadal axis, has
8 j. Q. i; `9 x- N# r/ [a higher incidence of organic central nervous system
& \* i+ p9 [2 m' c$ Dlesions in boys.1,2 Virilization in boys, as manifested# x* s+ y+ N- O( ^# g
by enlargement of the penis, development of pubic! T3 R0 H5 O, i5 T' g
hair, and facial acne without enlargement of testi-
, I4 Q, N7 u8 i) N+ X# q! A% {' {cles, suggests peripheral or pseudopuberty.1-3 We
  W4 }! c( W) J$ \$ J: Q. mreport a 16-month-old boy who presented with the
* Z, j7 l. V, y- m" Q7 `) a6 N5 Jenlargement of the phallus and pubic hair develop-
% A; Z' s- |2 |& I4 m  J# s: {4 tment without testicular enlargement, which was due0 z+ G  B# ?4 ^
to the unintentional exposure to androgen gel used by
* H5 |+ g) p6 bthe father. The family initially concealed this infor-
* u" U# c* I0 m+ o+ Q& k# E( Wmation, resulting in an extensive work-up for this
6 ]3 _; W' x, g4 o. Dchild. Given the widespread and easy availability of
+ h, U" {7 p, I1 i7 D: v7 ^* {testosterone gel and cream, we believe this is proba-( Q: W1 T) M7 I4 r  N) V+ H
bly more common than the rare case report in the- z$ L7 R8 N5 \7 B! q6 ]2 ~
literature.43 G/ H. }8 M; Q
Patient Report! ~" c+ y/ y- y4 P9 f: @) J# Y
A 16-month-old white child was referred to the) x3 g. ?7 o) I; a) f
endocrine clinic by his pediatrician with the concern6 n! ^0 `) C% J% r& P/ T9 I5 d
of early sexual development. His mother noticed9 b$ S5 y9 r6 ^
light colored pubic hair development when he was
. P# ^% }5 H! L% K- F  vFrom the 1Division of Pediatric Endocrinology, 2University of
7 x1 \" h! y9 |& s1 d( JSouth Alabama Medical Center, Mobile, Alabama.
! ~. S; ~0 l. _5 d# @Address correspondence to: Samar K. Bhowmick, MD, FACE,3 O2 b4 H) c5 V
Professor of Pediatrics, University of South Alabama, College of, d! E# f+ O4 Q0 y/ h
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- }% Q; ~; m  u; d. U8 ~0 [3 `
e-mail: [email protected].
3 L" x: p% ?8 a, wabout 6 to 7 months old, which progressively became
7 ~3 [$ U2 p( A% ]$ p) zdarker. She was also concerned about the enlarge-/ S# ~/ }, b+ @; K! _: s$ }3 R3 R/ L
ment of his penis and frequent erections. The child- ^$ G: q7 H; D9 |+ C8 l' Z& T
was the product of a full-term normal delivery, with- B) L# {' o8 F7 i- D% T$ t. A
a birth weight of 7 lb 14 oz, and birth length of
# ~: I8 s% v6 v- e/ X- K( F1 i20 inches. He was breast-fed throughout the first year
% B! v: u0 Y  y5 K+ M5 zof life and was still receiving breast milk along with
8 B& p4 E* f' ^& asolid food. He had no hospitalizations or surgery,5 j+ Q2 }$ U' H& W
and his psychosocial and psychomotor development9 p8 |9 Z6 k# ^$ P6 }' D2 s% x9 A' i
was age appropriate.
2 W2 ^1 z4 w+ MThe family history was remarkable for the father,' \* Q3 F; ]7 q
who was diagnosed with hypothyroidism at age 16,
0 e0 Y1 o: Y% b; C4 S# r, ]! \which was treated with thyroxine. The father’s  y9 Y# A3 K! p7 L# D2 j5 _
height was 6 feet, and he went through a somewhat* P! |6 r" }) R4 a8 x9 O
early puberty and had stopped growing by age 14.9 I- ]4 o5 _! J
The father denied taking any other medication. The
" l5 h" w9 G- B- ychild’s mother was in good health. Her menarche  U, q6 |1 }: G6 J* ?
was at 11 years of age, and her height was at 5 feet( T7 F6 i. q6 L3 U9 ~& v- [! t
5 inches. There was no other family history of pre-
, S0 {% B4 H7 @0 }cocious sexual development in the first-degree rela-
. o1 U% s0 _2 {: itives. There were no siblings.
9 {% y: e% G# t" A) o! ?Physical Examination' n. w% {) P3 W+ Y/ U7 Z4 g; V/ W
The physical examination revealed a very active,9 F4 _% ^: h6 |5 t
playful, and healthy boy. The vital signs documented; k4 Z; W' Z3 n! I2 Y7 Y) k$ S! B
a blood pressure of 85/50 mm Hg, his length was; Y0 y7 m9 O: f; y+ N
90 cm (>97th percentile), and his weight was 14.4 kg6 u$ `4 I3 _: [8 R1 b- g
(also >97th percentile). The observed yearly growth
7 a+ w5 j0 D$ B% b+ a- w/ `: V7 {velocity was 30 cm (12 inches). The examination of
; n( w9 Q* `# ]the neck revealed no thyroid enlargement.* E3 n) p$ @, q2 Y8 [
The genitourinary examination was remarkable for
+ B, U$ u/ }' ^- f3 T* i% Yenlargement of the penis, with a stretched length of7 _7 n+ U; S! R& T
8 cm and a width of 2 cm. The glans penis was very well1 `& v& L- k- F5 a, P+ ~4 R9 s
developed. The pubic hair was Tanner II, mostly around
; ^! o: }5 K2 Y, h' R/ @+ o5403 g' ?) ]; b1 S. P' B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& y' i* R9 @  L- G: L! ^
the base of the phallus and was dark and curled. The$ l8 A6 o1 v& |1 _6 F) y
testicular volume was prepubertal at 2 mL each.* w! `7 ^; F, Y
The skin was moist and smooth and somewhat
8 Q; r8 a. {: r" D( Z: Roily. No axillary hair was noted. There were no7 U/ f8 y% |' K; r: e
abnormal skin pigmentations or café-au-lait spots.7 Z4 Z0 j% G& o
Neurologic evaluation showed deep tendon reflex 2+
7 j; a; A( j& g5 s; K$ d" b  \bilateral and symmetrical. There was no suggestion  y! N6 q7 z% K8 ?5 D* u& ^
of papilledema.
. F8 A0 E# f8 V# _; U" S  Q0 T( wLaboratory Evaluation
3 Q/ B: I, w' x- O. V2 R$ ]The bone age was consistent with 28 months by
* S: R+ F, C: n( p9 kusing the standard of Greulich and Pyle at a chrono-4 ]9 U2 w4 P( j; _+ N1 s+ V, ?
logic age of 16 months (advanced).5 Chromosomal' i4 `! @; |4 i% H* B
karyotype was 46XY. The thyroid function test
3 q6 r. e+ O( G/ k; C7 tshowed a free T4 of 1.69 ng/dL, and thyroid stimu-4 J( W* L3 h, N+ u) ]# i, e
lating hormone level was 1.3 µIU/mL (both normal).
7 @9 q; L2 l' v* c( BThe concentrations of serum electrolytes, blood0 I- \# n* L- W/ M1 }8 P
urea nitrogen, creatinine, and calcium all were8 c6 @4 h( D! I# {% L5 ]8 ^+ q+ g6 s
within normal range for his age. The concentration
( ^; Z7 @  z1 R+ _* sof serum 17-hydroxyprogesterone was 16 ng/dL
) J9 ?+ z0 }2 @: Q- K9 Z+ L(normal, 3 to 90 ng/dL), androstenedione was 20
: o  V& j' W0 Tng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 x* J. U0 Q; g/ L- ^6 }( Lterone was 38 ng/dL (normal, 50 to 760 ng/dL),: Z1 F" L$ v" K8 D9 E+ `
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
' B3 o6 A' k, {! ?8 j9 P+ A49ng/dL), 11-desoxycortisol (specific compound S)
  Q" f' I9 }3 U5 Mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: U! E; M' ~; H0 d6 q
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total. z: W9 z3 T" R, u2 y6 I) Z8 h7 n5 }
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 q- A. Y% ~+ ~7 i
and β-human chorionic gonadotropin was less than" N  S, `7 H% R, b0 i2 S
5 mIU/mL (normal <5 mIU/mL). Serum follicular4 g3 a7 Y' ]: N9 }0 R
stimulating hormone and leuteinizing hormone* P0 X/ Z: R( `2 `4 @
concentrations were less than 0.05 mIU/mL
' v1 s0 y, D$ p: ?! y+ `(prepubertal).
9 N) R% I' a; o) J. m. MThe parents were notified about the laboratory7 X% y7 v8 G4 G% G% X: C( T
results and were informed that all of the tests were: z* F! a# t1 p; r* b. q
normal except the testosterone level was high. The0 Z( ~1 T5 B7 A; A' ]
follow-up visit was arranged within a few weeks to/ j/ n  l9 u7 ~1 R; b9 m/ K
obtain testicular and abdominal sonograms; how-
  k8 }! R7 k" F# E4 aever, the family did not return for 4 months./ Y) o1 ?2 X' B6 U) A: o
Physical examination at this time revealed that the) L3 \1 U0 F# ]# d5 e0 A2 U
child had grown 2.5 cm in 4 months and had gained. E# P3 t/ l. x: o8 L6 j
2 kg of weight. Physical examination remained
9 p! w1 }. q8 n# Sunchanged. Surprisingly, the pubic hair almost com-6 I7 [  A- |* n  x  C/ U8 s: k6 {
pletely disappeared except for a few vellous hairs at
3 [" s- Y9 P+ Tthe base of the phallus. Testicular volume was still 20 C* p4 g; D' t; @  E. b5 b
mL, and the size of the penis remained unchanged.
5 \. d# l+ S$ t0 u/ t$ X. XThe mother also said that the boy was no longer hav-
5 Z1 V& J3 E+ G. {' c  D/ e* k7 ving frequent erections.
! y" L/ j  @; E5 j, |! TBoth parents were again questioned about use of8 Y, [5 G* ~# X1 N# I2 h. g& k
any ointment/creams that they may have applied to% Z5 S1 W$ Q- `1 D7 `4 E8 J
the child’s skin. This time the father admitted the
8 ^  v, U" i/ E% |5 kTopical Testosterone Exposure / Bhowmick et al 541
1 s" d. `5 [2 q3 E$ Zuse of testosterone gel twice daily that he was apply-8 |+ n/ X5 h  Q5 }/ U3 `7 ]
ing over his own shoulders, chest, and back area for
: \$ I% z* q9 Y: Sa year. The father also revealed he was embarrassed3 d9 \" t  h( L# N5 c" C2 o7 N
to disclose that he was using a testosterone gel pre-
- |$ d. q0 f- C1 z4 y: n. hscribed by his family physician for decreased libido
$ i: M+ F( C+ ^+ c" e1 b% X4 S% x7 |7 hsecondary to depression.; [9 l$ g% F2 Z; v
The child slept in the same bed with parents.
% D7 T  G. s. e4 lThe father would hug the baby and hold him on his
7 M5 c$ R2 b( e7 D1 \chest for a considerable period of time, causing sig-
1 D$ R( }1 }- ~nificant bare skin contact between baby and father.. E* p/ ~: \$ u9 I" p
The father also admitted that after the phone call,
" Y% ~5 s4 U& [6 _* A/ M- gwhen he learned the testosterone level in the baby" ]& c9 t4 e2 M  w: M  i
was high, he then read the product information
4 y! p7 L7 U1 B) |( L3 b9 Jpacket and concluded that it was most likely the rea-  e2 ~5 y& J; A
son for the child’s virilization. At that time, they
9 ?" c" D  L% wdecided to put the baby in a separate bed, and the
1 r0 ?7 [4 j2 d7 a# D2 a( c( u- j$ r/ ffather was not hugging him with bare skin and had; k* u0 h0 o& j" t& E1 k
been using protective clothing. A repeat testosterone
6 x# K2 ?( X5 M( X! w7 h9 @' Mtest was ordered, but the family did not go to the  |/ }% r5 C! a4 Q$ J  s1 n
laboratory to obtain the test.
* r' r. ?8 ]4 L- r0 x  Q3 ]Discussion
" L7 w2 S9 B$ W* m7 h$ k( ]Precocious puberty in boys is defined as secondary
% f6 t7 y' o" P' o7 _sexual development before 9 years of age.1,4
/ s4 D" {% Q+ o5 E9 a7 h4 A; TPrecocious puberty is termed as central (true) when
/ d! u. a# t: j8 m( }it is caused by the premature activation of hypo-  W; C3 @. @& m$ s- f+ c, l
thalamic pituitary gonadal axis. CPP is more com-
, z2 j) ]& E) A  e3 xmon in girls than in boys.1,3 Most boys with CPP. ^6 H/ X* R0 x* Z4 R: c* j" M$ B! a
may have a central nervous system lesion that is
3 f) {2 `1 ~0 R8 t! iresponsible for the early activation of the hypothal-
% _+ W' \8 ?" C8 v$ w8 U9 jamic pituitary gonadal axis.1-3 Thus, greater empha-
; n# p, C1 s8 ?sis has been given to neuroradiologic imaging in" k5 ]" N1 c3 B" s2 x8 F: |% T
boys with precocious puberty. In addition to viril-7 g% M1 ?3 J- ?4 j5 X6 |
ization, the clinical hallmark of CPP is the symmet-
$ T6 Q- _" O, o. prical testicular growth secondary to stimulation by3 F& m2 o- n- J7 \
gonadotropins.1,3& _' [) |! x* H% E2 A5 L
Gonadotropin-independent peripheral preco-
% V' x& {- v7 I2 u# P4 Y, _& @cious puberty in boys also results from inappropriate
( K: S5 \# @0 e+ F6 z( Qandrogenic stimulation from either endogenous or9 D' r2 }4 J9 A7 o
exogenous sources, nonpituitary gonadotropin stim-
! q1 _; P5 v+ y( X/ ]ulation, and rare activating mutations.3 Virilizing$ m7 L9 Y% ?5 L* \
congenital adrenal hyperplasia producing excessive4 H( I" e8 k* W: c3 \6 Y
adrenal androgens is a common cause of precocious
0 n5 \( u2 e- [1 J, E, c/ ppuberty in boys.3,4# s. H. }: N& }* D' x- |
The most common form of congenital adrenal
5 |& r) [6 _) s: qhyperplasia is the 21-hydroxylase enzyme deficiency.% u1 N( s8 r& h8 q: D  Y
The 11-β hydroxylase deficiency may also result in
1 K& `5 {! j7 s! f1 w, @excessive adrenal androgen production, and rarely," G/ e, h3 U! E' A% s# Y0 H
an adrenal tumor may also cause adrenal androgen
. d, o4 l- g9 Z0 t3 aexcess.1,3; W* ?9 H- ?9 M. X0 a, X
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 D9 s$ z4 G: m* h0 Z542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 U+ I6 N; W& q/ n4 Y3 O4 u2 D
A unique entity of male-limited gonadotropin-. A! b$ r& z% O: H$ R  z) j5 B
independent precocious puberty, which is also known- J$ X( j" a7 t: P" g9 Y& C; p: P# l4 p
as testotoxicosis, may cause precocious puberty at a
# V1 z" j9 F, V( Y, Y# ~- d! \+ Mvery young age. The physical findings in these boys
8 n) u8 X: h  f/ awith this disorder are full pubertal development,% _) N( E. y1 n# }- f
including bilateral testicular growth, similar to boys
+ U6 D2 P- o. @* |with CPP. The gonadotropin levels in this disorder
  M; y. B) ]3 l9 k7 @  fare suppressed to prepubertal levels and do not show
1 O, n; m0 l1 r, tpubertal response of gonadotropin after gonadotropin-- Z* A& H. S+ W/ _  B* ~1 ]
releasing hormone stimulation. This is a sex-linked
. I3 S2 }. C, A; |: }& w0 h0 A5 Fautosomal dominant disorder that affects only0 S& Y, `/ S" S+ q% |  Z( B) M9 X
males; therefore, other male members of the family# ^1 B9 P( T( c6 u7 Q
may have similar precocious puberty.3( M7 }8 J; Z4 k) h& ^6 |' h8 Z
In our patient, physical examination was incon-! g5 W$ c7 a; `: R4 }7 n! S" S
sistent with true precocious puberty since his testi-
3 j2 O* z  x0 d& s0 i8 W) ucles were prepubertal in size. However, testotoxicosis' Z3 B- u6 Q7 I" d1 g! |' h3 Q
was in the differential diagnosis because his father
. k! c- C( ]: ^3 y! i& W* ]) C- v# l6 cstarted puberty somewhat early, and occasionally,$ U3 b. U' _2 v5 L
testicular enlargement is not that evident in the
: u7 P+ G4 B% h4 q2 d5 jbeginning of this process.1 In the absence of a neg-
& J8 p  C9 E! ?6 Q7 R' p4 \ative initial history of androgen exposure, our
5 D( Q- Y7 L- O2 {+ q' i/ {2 Pbiggest concern was virilizing adrenal hyperplasia,$ \" i& b% W* s, F, H
either 21-hydroxylase deficiency or 11-β hydroxylase( H: x8 D7 ^2 V9 z& w
deficiency. Those diagnoses were excluded by find-& ]# D) I, j# Z8 Y
ing the normal level of adrenal steroids.8 t8 P1 q4 U, G; h& f
The diagnosis of exogenous androgens was strongly9 l/ _$ Y/ F0 _! z
suspected in a follow-up visit after 4 months because* u6 s+ d* L2 \  [) b1 z
the physical examination revealed the complete disap-7 I; H% S6 k4 g7 x" A5 }" B
pearance of pubic hair, normal growth velocity, and$ \  y7 q8 J  }; ~& f$ p
decreased erections. The father admitted using a testos-6 n6 q8 U9 |. e9 O: d* }
terone gel, which he concealed at first visit. He was" `) Z6 M# M2 n' \) D
using it rather frequently, twice a day. The Physicians’
. x% c7 }% Q. ]Desk Reference, or package insert of this product, gel or% n9 u6 s4 \' H  Z& _4 ]
cream, cautions about dermal testosterone transfer to
! `% c1 K' m1 P3 S% `( @unprotected females through direct skin exposure.
/ {1 z& \% C: d' P" g3 iSerum testosterone level was found to be 2 times the0 h3 x6 t$ L( q/ }
baseline value in those females who were exposed to- ^" B; g  a2 |' B: q
even 15 minutes of direct skin contact with their male) B: \( H$ R6 x/ t
partners.6 However, when a shirt covered the applica-
( r  t5 q, A: E8 y1 I4 Vtion site, this testosterone transfer was prevented.
4 O# X" s0 }: T+ X/ R0 E8 M! zOur patient’s testosterone level was 60 ng/mL,
; v( Q  t5 i4 J/ Q+ vwhich was clearly high. Some studies suggest that
4 I' ~; P  x! wdermal conversion of testosterone to dihydrotestos-' k+ j1 X$ D2 @' Y0 x# t# ~
terone, which is a more potent metabolite, is more1 @, O4 e7 [, o3 D
active in young children exposed to testosterone
2 T0 h$ o# ^5 f1 zexogenously7; however, we did not measure a dihy-* O( ]9 E- _6 K5 I
drotestosterone level in our patient. In addition to3 S1 Y$ D1 V6 q( X4 C
virilization, exposure to exogenous testosterone in2 w& ?4 ^, k; N9 `- D4 X
children results in an increase in growth velocity and
$ B6 d, T3 [3 hadvanced bone age, as seen in our patient.
* b4 t  {1 N( z) E) f- O9 dThe long-term effect of androgen exposure during/ E4 ]" f+ H! y' q" w+ p
early childhood on pubertal development and final  O; U1 _& x5 P
adult height are not fully known and always remain- B. c$ I1 E+ h, X9 |$ M
a concern. Children treated with short-term testos-
2 f& B. j: `( E, q2 a+ P2 Iterone injection or topical androgen may exhibit some
+ E# N5 i, v. i, ?; d6 Z3 gacceleration of the skeletal maturation; however, after4 |1 P/ g. Y  a5 s7 j% V- M! V# |" ?
cessation of treatment, the rate of bone maturation
2 j  h% [, O4 ?. v' T. edecelerates and gradually returns to normal.8,9
8 N8 {  R& U) sThere are conflicting reports and controversy
: d6 A3 A0 w& n' z6 |over the effect of early androgen exposure on adult
. ~4 d. d% k- e0 W# w3 upenile length.10,11 Some reports suggest subnormal
' p4 E/ l4 B' xadult penile length, apparently because of downreg-
5 u! I4 ]9 ?" nulation of androgen receptor number.10,12 However,
  }; Q' Z7 A. A! T" KSutherland et al13 did not find a correlation between3 \) X9 r  w. a+ _  p6 j$ j( y
childhood testosterone exposure and reduced adult" d0 O) G( n5 Y
penile length in clinical studies.5 n7 D' c" Q9 L/ S# a
Nonetheless, we do not believe our patient is0 P# b0 c8 W  T/ S4 N
going to experience any of the untoward effects from
: g  z6 r) S8 Itestosterone exposure as mentioned earlier because2 o1 b* b; @+ _( B4 n; C9 ?3 q) t
the exposure was not for a prolonged period of time.- c$ I! _; o* Z# t- N3 y
Although the bone age was advanced at the time of6 j, E( W- Z2 ]2 e: Q" G
diagnosis, the child had a normal growth velocity at# _& H, T! M& I& G3 n% A
the follow-up visit. It is hoped that his final adult
, R8 _# y0 o; h4 l0 d& i4 Pheight will not be affected.
8 C+ t/ j- y9 [6 a+ u: UAlthough rarely reported, the widespread avail-8 y% |/ u  c# n# V" X+ X" H
ability of androgen products in our society may
1 A1 ?, ]* d( S: r3 `& Aindeed cause more virilization in male or female
1 Y  a  k  Q+ X; rchildren than one would realize. Exposure to andro-1 ^0 m4 N+ o$ j+ y) t7 A/ N- J
gen products must be considered and specific ques-1 H4 a% u+ n* V3 `# D  [3 i
tioning about the use of a testosterone product or
% U0 o0 z+ k' Pgel should be asked of the family members during
0 s: K: c' k% jthe evaluation of any children who present with vir-
: R2 H/ t7 J+ y) Uilization or peripheral precocious puberty. The diag-9 j8 i* \5 b* d- `, \' U. t( e" O
nosis can be established by just a few tests and by
; m( [8 _1 W; }- Y8 O# qappropriate history. The inability to obtain such a8 r& f0 s8 S9 {9 p& X
history, or failure to ask the specific questions, may  J& x9 \; k* N6 q
result in extensive, unnecessary, and expensive
' i, w, p) U; G2 Qinvestigation. The primary care physician should be
  j! j; W) A( W2 Daware of this fact, because most of these children; `+ w6 N: S* h9 p2 k( m  a
may initially present in their practice. The Physicians’5 x; s6 O( q8 b# `* ]
Desk Reference and package insert should also put a
- h7 L( E9 U. z# M, Mwarning about the virilizing effect on a male or
' j2 a9 _! c7 Afemale child who might come in contact with some-+ t+ p, Y% N4 O( y
one using any of these products.8 _2 N9 G# p" H8 D( ^+ N
References
  j4 q0 {8 h4 ?9 o$ ?6 I1. Styne DM. The testes: disorder of sexual differentiation. E7 V: s) u# b0 w
and puberty in the male. In: Sperling MA, ed. Pediatric
8 Y+ o* Y% A% Z3 M8 x1 m9 F, aEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( u# O! O8 z4 C: v3 q
2002: 565-628.
; K; S6 U' }6 F' Z3 h# N2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
6 e  i. \# O0 y# S8 V# B/ ^: {- ^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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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 p+ u( f7 U) `5 y6 z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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