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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  C  V! P1 [, F
Boy Induced by Indirect Topical/ H' f, {7 H. o
Exposure to Testosterone
( p! z7 b, h$ t- k2 u: sSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, b) X! R) s4 Kand Kenneth R. Rettig, MD1
1 g+ E7 W" S7 Q6 A6 L) lClinical Pediatrics3 {6 S0 [$ h* V  l! z! s0 T
Volume 46 Number 65 A% W& R3 v+ M) r7 G% P
July 2007 540-543
2 u  h7 q- A8 g! O1 U) j* [© 2007 Sage Publications2 `& q/ Y& f/ B% A
10.1177/0009922806296651
) o" V2 f6 f$ F$ T2 t( ]1 }1 m7 Chttp://clp.sagepub.com' L3 h8 p7 U3 m% G& E
hosted at0 [: n& S2 L- T- P
http://online.sagepub.com: }# c, O7 N( u6 b1 |4 h5 @
Precocious puberty in boys, central or peripheral,
# _& I1 u4 x& m" A( Fis a significant concern for physicians. Central
( S2 _: v8 Y. @9 L. @/ @5 cprecocious puberty (CPP), which is mediated
" j# {+ X2 M, Xthrough the hypothalamic pituitary gonadal axis, has
! h: X: m( }# Y) E0 na higher incidence of organic central nervous system3 T0 Y9 s! I; }9 ^7 R; A
lesions in boys.1,2 Virilization in boys, as manifested
- D( s2 o% e5 ~5 A4 s/ Wby enlargement of the penis, development of pubic1 U+ N4 q/ o# U+ O+ I7 L: o9 C
hair, and facial acne without enlargement of testi-' S! B; J# r4 v. v$ L1 f8 |0 i  ~7 T
cles, suggests peripheral or pseudopuberty.1-3 We) I+ ~) J6 ^. K$ y7 K' ]7 h
report a 16-month-old boy who presented with the% g% M$ j2 w& c3 P
enlargement of the phallus and pubic hair develop-
% r8 v, N) f* G+ oment without testicular enlargement, which was due3 C. v8 K) M3 i  ], H* ^
to the unintentional exposure to androgen gel used by
9 ]7 T# u! B! ^) qthe father. The family initially concealed this infor-+ V& r- e+ n& E
mation, resulting in an extensive work-up for this2 r5 Q/ X( U/ K2 l; H
child. Given the widespread and easy availability of
0 `- D# h, z/ o. [5 K; {testosterone gel and cream, we believe this is proba-
$ ~, m4 I; l# h" sbly more common than the rare case report in the4 F8 ]' \- d5 a2 S7 m
literature.4
' [. C: q/ L/ K, o# sPatient Report
) F# ]+ Q8 ]# k% U$ S3 J5 wA 16-month-old white child was referred to the
" K+ ^7 O' x) o/ }7 z  c! sendocrine clinic by his pediatrician with the concern
. h) o0 ~2 T$ ?* s$ m2 k- Uof early sexual development. His mother noticed
7 f* Z) }% y7 alight colored pubic hair development when he was* v3 I0 {: Y8 ]  h0 H* Y9 s
From the 1Division of Pediatric Endocrinology, 2University of
- X, q1 }; i" R0 ]/ z' j0 |; uSouth Alabama Medical Center, Mobile, Alabama.
$ h: v2 R& P% \+ P! JAddress correspondence to: Samar K. Bhowmick, MD, FACE,
9 k, d* v; @: T$ V% \8 R6 dProfessor of Pediatrics, University of South Alabama, College of
+ G3 G6 k9 ^+ VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ y3 U' Z! h, `3 q; I3 Je-mail: [email protected].
4 ~, O' [, a5 F( U7 Z: N3 nabout 6 to 7 months old, which progressively became
! D4 s# Z6 a# O7 \( Rdarker. She was also concerned about the enlarge-
0 n3 y1 O6 N# ?. \ment of his penis and frequent erections. The child
" j. D& w' d! V/ ?  `- Awas the product of a full-term normal delivery, with
7 z# k5 ^( i# u9 ^a birth weight of 7 lb 14 oz, and birth length of# _8 Y/ A3 u( {% q4 {7 ^2 F
20 inches. He was breast-fed throughout the first year
5 O/ z1 _  U( o6 r8 c" [of life and was still receiving breast milk along with# j6 H" r) T. G4 T
solid food. He had no hospitalizations or surgery,
" O2 j* q6 q( e7 ^and his psychosocial and psychomotor development* Z- [& C9 {8 z8 s0 }
was age appropriate.$ I/ k  c0 _1 ]
The family history was remarkable for the father,+ I  @' q6 t0 J0 F
who was diagnosed with hypothyroidism at age 16,. e/ R( I; Y' L5 h
which was treated with thyroxine. The father’s2 r" B9 d! o7 G9 ]8 d4 z3 u
height was 6 feet, and he went through a somewhat
3 c0 R. M: h( t3 S% ^" j& o$ Oearly puberty and had stopped growing by age 14.
/ `, T% U1 q. N5 IThe father denied taking any other medication. The# ?$ Q* B5 h& G( }1 p# I9 G
child’s mother was in good health. Her menarche2 t" ?" w  R+ ]  B
was at 11 years of age, and her height was at 5 feet% _& E! q0 ]6 L/ W# c1 X2 M5 }: v
5 inches. There was no other family history of pre-
% B- h6 _$ T, {2 x! d* Ococious sexual development in the first-degree rela-
& E7 o/ S, a& V- l. |2 Ktives. There were no siblings./ F% O) V( W1 z8 N4 X5 m# j
Physical Examination
) r3 t7 ]0 G- N: a" @- tThe physical examination revealed a very active,
& n8 ?+ c7 V; P; B$ e. r: v; Eplayful, and healthy boy. The vital signs documented
( z7 Z2 ~- B  R: g6 r/ P$ P: @! za blood pressure of 85/50 mm Hg, his length was1 N* O6 s5 V) z
90 cm (>97th percentile), and his weight was 14.4 kg$ ]% A. N4 g- j+ [1 C" ~
(also >97th percentile). The observed yearly growth
/ J; [3 x% `5 Y4 g% Uvelocity was 30 cm (12 inches). The examination of
! R7 c2 x1 l" T7 ethe neck revealed no thyroid enlargement.
0 z' P9 h1 d: o; n5 zThe genitourinary examination was remarkable for
2 e8 b0 K1 d% E. q. @2 F0 u; T9 {enlargement of the penis, with a stretched length of
/ G$ B2 p# Z5 z. ?! c8 cm and a width of 2 cm. The glans penis was very well
; ?3 N  T+ p, Q* n9 u( X! M) ^0 k/ Tdeveloped. The pubic hair was Tanner II, mostly around, y! b8 c2 {9 ]# B9 Y
540" c( X: o5 {/ @+ z* Y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
2 l9 Z) V4 x: s, D: Dthe base of the phallus and was dark and curled. The
* F* _; t( a# |/ {testicular volume was prepubertal at 2 mL each.& h2 H. {( i$ \6 T
The skin was moist and smooth and somewhat& H& v& a7 L$ d; o! D- o& M1 B
oily. No axillary hair was noted. There were no4 |1 \) E" |9 ^, K/ H9 F
abnormal skin pigmentations or café-au-lait spots.
$ r- c! F' Q7 w1 H9 gNeurologic evaluation showed deep tendon reflex 2+4 @: k6 z- Q) k" F; L3 E
bilateral and symmetrical. There was no suggestion5 x3 z# @' O. N: Q9 P: t) i* W
of papilledema.
6 [% L2 ]- n2 _. G3 d1 F7 h$ L$ N) CLaboratory Evaluation
) e: B0 p1 y- r+ U: `7 XThe bone age was consistent with 28 months by; b8 t$ C/ j) H5 a0 i
using the standard of Greulich and Pyle at a chrono-# U) O# n- G; j% f' K: J
logic age of 16 months (advanced).5 Chromosomal
3 N, D" `9 Y1 Y9 y( B5 }- x2 Kkaryotype was 46XY. The thyroid function test/ _2 e* d1 s- O3 h& X  q; [
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 C8 T/ w! s  z+ n" Tlating hormone level was 1.3 µIU/mL (both normal).
0 X, @7 d; w3 x' x& A7 ^The concentrations of serum electrolytes, blood" {; A! X0 a1 E6 ?
urea nitrogen, creatinine, and calcium all were& t  w( Y6 _6 z. _& k% J3 n7 g" h
within normal range for his age. The concentration
( l: \* A5 K1 R0 \1 Aof serum 17-hydroxyprogesterone was 16 ng/dL/ M+ C1 F- c' q) j6 z
(normal, 3 to 90 ng/dL), androstenedione was 20
: P# s3 @/ y3 |& E2 S( i: kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, ]$ ?2 H" T. ~. X
terone was 38 ng/dL (normal, 50 to 760 ng/dL)," {* s& Z( ~8 ?& D; G! j
desoxycorticosterone was 4.3 ng/dL (normal, 7 to: h8 y# r: P: S% }- q
49ng/dL), 11-desoxycortisol (specific compound S)
9 a4 l" |, E+ f# G* x* @was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
$ d+ b; R& R& _. a; i4 G5 Atisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total/ p9 P' W, p0 `) R) \& N
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, t$ A& m; q3 Y6 z, ^and β-human chorionic gonadotropin was less than: v* u1 Y0 f$ o
5 mIU/mL (normal <5 mIU/mL). Serum follicular
# k2 G! q; S" x6 istimulating hormone and leuteinizing hormone% Y, B" @& w  [1 }4 S
concentrations were less than 0.05 mIU/mL7 t  W# N+ H; u
(prepubertal).
1 _8 z* X) u. g) {, WThe parents were notified about the laboratory
5 |0 L2 K: A' ~" Jresults and were informed that all of the tests were3 f, ~9 a5 }  U. K
normal except the testosterone level was high. The
) U+ D; P6 N( ?9 b7 m! b. c5 h3 qfollow-up visit was arranged within a few weeks to
& o# h4 g: s( I. }) b+ oobtain testicular and abdominal sonograms; how-: C0 W& v- x# ?$ t/ ?$ D1 Z/ J: \
ever, the family did not return for 4 months.
( a% k0 `( U/ n3 ]2 [( DPhysical examination at this time revealed that the, s! T' e' y( m8 C
child had grown 2.5 cm in 4 months and had gained
# t8 A7 [* y- a) x2 J3 N+ r2 kg of weight. Physical examination remained
. d3 M$ u  V& o% `+ gunchanged. Surprisingly, the pubic hair almost com-: K& S4 A3 m, {. _+ c0 y8 r
pletely disappeared except for a few vellous hairs at1 O) N& j. b8 `0 F8 g% B; _& m
the base of the phallus. Testicular volume was still 2" O1 O$ z" Q( S; Y; i. r& h- [( M0 u' {
mL, and the size of the penis remained unchanged.) {$ H8 N9 C# O' c/ `" `' W
The mother also said that the boy was no longer hav-+ B; [0 d) j' V4 a5 d
ing frequent erections.
' r* l( S3 Q+ @/ nBoth parents were again questioned about use of0 a, }0 y, v; D9 B' o
any ointment/creams that they may have applied to7 C+ d* [0 X& `$ W, c; p% P
the child’s skin. This time the father admitted the2 v& S0 A5 J/ u% k
Topical Testosterone Exposure / Bhowmick et al 541) m- ?9 t" w2 @$ G  T
use of testosterone gel twice daily that he was apply-9 s3 h* e% \) T4 ^8 j
ing over his own shoulders, chest, and back area for
- m7 N( B1 Y3 g. K0 O  z9 `a year. The father also revealed he was embarrassed9 L1 D+ \) w3 V5 j; r
to disclose that he was using a testosterone gel pre-( \+ _3 W6 e7 Z4 y0 C3 P
scribed by his family physician for decreased libido
( C+ j4 U1 \3 C( k; X! t. H8 Hsecondary to depression.9 C* ~/ P! p0 |6 ~( L6 Y$ ?7 h8 f
The child slept in the same bed with parents.0 [$ N8 x1 k; z+ d" v1 [# J, c
The father would hug the baby and hold him on his; A3 n/ h/ W6 Z5 V3 c3 ?( c) j
chest for a considerable period of time, causing sig-
) s4 m- n1 p3 a2 `nificant bare skin contact between baby and father.- x4 [# ]- H& X2 S7 x* L' ]7 S/ t
The father also admitted that after the phone call,
/ ~* ]5 S8 h/ Ewhen he learned the testosterone level in the baby( x! a, t: f) V5 F' Q
was high, he then read the product information
  B) {7 J3 b" e* ?( fpacket and concluded that it was most likely the rea-0 |2 p. h4 F. Y2 Y( f
son for the child’s virilization. At that time, they4 w" y' E% j* h  S' d& n
decided to put the baby in a separate bed, and the( f  u  v, q4 }
father was not hugging him with bare skin and had
' o$ d7 ~* I9 r1 [$ P5 j, f. Xbeen using protective clothing. A repeat testosterone
. c# k/ X% B/ Rtest was ordered, but the family did not go to the! H1 i0 L: U; B8 Z! ~2 k
laboratory to obtain the test.! a2 s7 `+ Z3 n/ G
Discussion
! b5 v9 @( l; G% CPrecocious puberty in boys is defined as secondary
0 E% _3 Y* F/ V" n: wsexual development before 9 years of age.1,4. k# e2 p& _! {
Precocious puberty is termed as central (true) when( a, M8 {. w6 H
it is caused by the premature activation of hypo-
; \5 e- E  N: nthalamic pituitary gonadal axis. CPP is more com-" @( q& [9 |# R
mon in girls than in boys.1,3 Most boys with CPP
3 O8 q4 g* s3 \& d( g/ Wmay have a central nervous system lesion that is
5 N5 A( ^, u$ Z, ~5 Z6 Uresponsible for the early activation of the hypothal-6 W0 r$ J# |. D: Y( S; _
amic pituitary gonadal axis.1-3 Thus, greater empha-+ U2 S% q: L3 p; P% @' ~" b% a
sis has been given to neuroradiologic imaging in
+ @3 i7 M- u& J* M4 B; b' Bboys with precocious puberty. In addition to viril-
: k2 w: G6 M: _4 Q  Gization, the clinical hallmark of CPP is the symmet-  L9 F$ i$ ?8 N2 a0 \
rical testicular growth secondary to stimulation by' u3 x9 d+ K$ @* j1 p5 f
gonadotropins.1,3+ {8 c- q( Q, f+ j# K2 v+ K
Gonadotropin-independent peripheral preco-
- G% t' L  Z5 l& o( F0 G1 scious puberty in boys also results from inappropriate
8 o/ N2 J1 }* X9 oandrogenic stimulation from either endogenous or8 [: e9 h7 H2 ^7 ?
exogenous sources, nonpituitary gonadotropin stim-( d$ Z7 X: ~0 s" u
ulation, and rare activating mutations.3 Virilizing
3 z9 @3 L3 h1 l- Z4 Z- Xcongenital adrenal hyperplasia producing excessive# M2 P5 e3 p( [! n+ o' W5 N& u) y
adrenal androgens is a common cause of precocious
+ L9 ]9 C5 L/ F' ~puberty in boys.3,4
9 L6 G8 S6 Y& p) u- rThe most common form of congenital adrenal
# Q# P4 ~$ E5 z& o+ thyperplasia is the 21-hydroxylase enzyme deficiency.
7 t. t1 |8 |' r: ~% t' h/ GThe 11-β hydroxylase deficiency may also result in
* P4 t1 u9 \1 s& k8 y$ X+ v# qexcessive adrenal androgen production, and rarely,
3 G0 N8 H. ~8 Y5 u+ D- u* L7 z5 van adrenal tumor may also cause adrenal androgen( X5 b: Z! C1 f; X
excess.1,3
) x- s# v$ {1 `* B$ J- l9 l  n/ iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 ?2 ]: V, }9 S3 T542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 x  j! S8 {7 g7 y) f
A unique entity of male-limited gonadotropin-4 E7 [3 o9 k4 y
independent precocious puberty, which is also known
1 F9 v  k' s  {2 O. j/ kas testotoxicosis, may cause precocious puberty at a% v  G. w# u: A' w/ r! N0 ~
very young age. The physical findings in these boys$ g4 H2 d, p: u& x' P% X
with this disorder are full pubertal development," r% r; z. y% r3 P- X$ V) n2 E
including bilateral testicular growth, similar to boys, f- B2 H& S) J. D' Q
with CPP. The gonadotropin levels in this disorder1 b6 o8 T* f' }& O( Y& o
are suppressed to prepubertal levels and do not show
$ O: c( o% L+ G2 Jpubertal response of gonadotropin after gonadotropin-4 h0 b5 E* `, J% [, o; `
releasing hormone stimulation. This is a sex-linked1 e; a* j  [! Z8 R3 J
autosomal dominant disorder that affects only/ B" ]$ g3 k3 l* s" x/ s
males; therefore, other male members of the family! ?6 H0 W2 T) N+ Q! B3 g: g* k
may have similar precocious puberty.37 X7 V% g  Q  ~( c
In our patient, physical examination was incon-0 f1 H8 e5 C9 Y( Q/ E
sistent with true precocious puberty since his testi-4 h' B' ~# S. o
cles were prepubertal in size. However, testotoxicosis& I& ~- t/ w% e6 f4 H' d
was in the differential diagnosis because his father6 x! W, p* I8 n  y6 g4 W1 g! Y
started puberty somewhat early, and occasionally,* Y* a0 c* ?2 ^$ W, {1 \
testicular enlargement is not that evident in the3 ]; O( h6 ]9 k9 b3 H6 f/ D0 ]
beginning of this process.1 In the absence of a neg-) h7 k: I0 J& E
ative initial history of androgen exposure, our
% l% ~) s! T3 Zbiggest concern was virilizing adrenal hyperplasia,
( L# m+ ^. }+ o& ]9 ]- keither 21-hydroxylase deficiency or 11-β hydroxylase
9 ^' s* Y: e9 p) r; Odeficiency. Those diagnoses were excluded by find-- Y- X0 w3 o/ M
ing the normal level of adrenal steroids., [2 o- N7 G$ l2 J- b9 q* \/ h
The diagnosis of exogenous androgens was strongly
% ^# |3 o' Z3 osuspected in a follow-up visit after 4 months because
* b& O, Q. x. Y' H: }, L; xthe physical examination revealed the complete disap-1 t2 f* m9 o7 l, R5 }* q0 `
pearance of pubic hair, normal growth velocity, and6 D4 O" e, \0 m4 d! \; R9 K7 A& G
decreased erections. The father admitted using a testos-; K" c- h+ n. p" R* l
terone gel, which he concealed at first visit. He was
) K# ?& V0 e# jusing it rather frequently, twice a day. The Physicians’! h' o* c6 |( H' U! i) d
Desk Reference, or package insert of this product, gel or- V' I; D: ]: ]' O
cream, cautions about dermal testosterone transfer to
. i6 s  G! Q+ ?; _# ^% Vunprotected females through direct skin exposure.' d" Q1 J6 T5 L6 m" ~
Serum testosterone level was found to be 2 times the0 j; R. s' m; {5 l$ r7 G4 O3 R
baseline value in those females who were exposed to3 q/ g1 U3 ]7 Y- O
even 15 minutes of direct skin contact with their male9 ?* A* I" q9 |! f9 ^. v& e/ t
partners.6 However, when a shirt covered the applica-& a' r* u4 k$ I; z# z* A5 P7 J
tion site, this testosterone transfer was prevented.) w2 n/ M6 ^! ]0 }
Our patient’s testosterone level was 60 ng/mL,. t$ H9 P+ {/ b" P' Q" _5 T' @
which was clearly high. Some studies suggest that2 ~) z* _) d3 Q8 x# A- K2 ^
dermal conversion of testosterone to dihydrotestos-% ]1 x+ q1 h, u  S" Z8 k, h2 _7 m
terone, which is a more potent metabolite, is more
- j$ h. F3 c" Yactive in young children exposed to testosterone& k* K2 i9 l$ _$ R/ W) l
exogenously7; however, we did not measure a dihy-+ x2 g, O: |3 h2 v% a' {8 t7 r
drotestosterone level in our patient. In addition to
1 ^# n6 P. @. S& @) q8 c& X4 k. i* `virilization, exposure to exogenous testosterone in
( H+ Y, A# H1 y4 f  M1 @; dchildren results in an increase in growth velocity and
/ q8 H. K8 \4 V) Wadvanced bone age, as seen in our patient.# P, v9 z0 K2 W8 G7 p& ^
The long-term effect of androgen exposure during
; c0 X0 Y8 u/ w( @" Fearly childhood on pubertal development and final# y8 c7 W/ c- ^& P3 ]
adult height are not fully known and always remain
# V$ A/ I+ @' F1 Ma concern. Children treated with short-term testos-# j( q2 ~" g2 ~" }& s; N( E& h
terone injection or topical androgen may exhibit some
0 k1 s& g3 Y1 @4 Aacceleration of the skeletal maturation; however, after& Y& |' P; @1 ?, r& o- J  @
cessation of treatment, the rate of bone maturation0 @' e/ D& J0 W& a! J7 J2 J* U
decelerates and gradually returns to normal.8,9* q, I# m0 ^( \. M. l, {( y
There are conflicting reports and controversy; p/ A# i/ L* [: F( a" n; s% i, U8 ]
over the effect of early androgen exposure on adult! f% J$ w5 D8 w2 u9 |
penile length.10,11 Some reports suggest subnormal
" y2 @& C( n7 e, }/ Y" m1 Ladult penile length, apparently because of downreg-
1 F  k. W5 N. |ulation of androgen receptor number.10,12 However,! X0 i3 w; D  }  ~, q
Sutherland et al13 did not find a correlation between1 q1 I$ A5 G' U, w. S. ]& W! k
childhood testosterone exposure and reduced adult
) N+ |& N+ @' g+ k: E/ b( Hpenile length in clinical studies.& z: N9 d5 P5 v  i% I8 W7 K5 d
Nonetheless, we do not believe our patient is
5 e/ T4 W$ W6 T, P4 H% }going to experience any of the untoward effects from2 }# }) q! k6 |, k& k
testosterone exposure as mentioned earlier because" n. W2 g. o% |( |7 a2 V% w
the exposure was not for a prolonged period of time.  d9 x# z2 R. k# ]) X/ X
Although the bone age was advanced at the time of
1 ^6 p/ ]+ h* g7 Sdiagnosis, the child had a normal growth velocity at
# |* X  Q8 m; D, Nthe follow-up visit. It is hoped that his final adult
( }' V! [3 w/ f. }height will not be affected.
, G" t0 A* s8 Y# YAlthough rarely reported, the widespread avail-
' N( o. r/ ~% t; x5 }, wability of androgen products in our society may
1 B3 q8 ?7 ]* {indeed cause more virilization in male or female
5 M7 z! C$ f. e% \3 @children than one would realize. Exposure to andro-) P! C, o! M5 b- W5 r4 h9 f' g
gen products must be considered and specific ques-
" B* J3 V7 z) r1 z$ `# Mtioning about the use of a testosterone product or
& y' [) X( C! s; ^, S: w# Agel should be asked of the family members during
9 U0 |! b- _, G( E4 j' _the evaluation of any children who present with vir-
& |' B2 {$ v& o, S4 u( ]" m( q& kilization or peripheral precocious puberty. The diag-
5 h+ Y* ~, j; B5 s  D( xnosis can be established by just a few tests and by2 |- {* X5 d/ Y( h  F$ I4 a8 g
appropriate history. The inability to obtain such a
# R3 b' ?) ?/ M! z+ B' k6 R' O) Dhistory, or failure to ask the specific questions, may
" k8 ?% @' \$ }* E" q7 Aresult in extensive, unnecessary, and expensive
- E  ]2 w3 |; l* f9 v- Qinvestigation. The primary care physician should be  B5 D+ H# I* y9 \
aware of this fact, because most of these children# _9 g- @) j) J" Z% p1 y
may initially present in their practice. The Physicians’4 U6 A+ M# Z0 D# j& U7 T5 {
Desk Reference and package insert should also put a
9 S7 k0 n1 v; C1 }, Z4 C  Jwarning about the virilizing effect on a male or. Q$ M6 D/ u, A, E3 ?! S
female child who might come in contact with some-
( b9 h3 }% f2 M6 H5 P- y9 jone using any of these products.3 d) K1 \+ k! E( q
References! B# g0 P. \# F) e4 p; j
1. Styne DM. The testes: disorder of sexual differentiation, V6 Z! d- T; p% t" |$ x
and puberty in the male. In: Sperling MA, ed. Pediatric% ?4 C+ x- ^& g; K9 Q& ]7 ?
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 L' E' V$ [, b$ V5 q
2002: 565-628.
5 {  |, M+ A( o8 y2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  ?$ ?" ^6 r3 upuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old7 d( M5 @* V; z( E; k5 f
Boy Induced by Indirect Topical# y% D# E3 j1 p. f
Exposure to Testosterone) K- t; i' x0 ~) R3 A. g% g
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 _, Q. N% f- q1 }and Kenneth R. Rettig, MD15 V- `& M) C. H) W7 J; a& P
Clinical Pediatrics
2 p5 B8 a, u3 v5 t4 fVolume 46 Number 6% z, b" q& A. P2 H! r4 W  P8 |6 y4 @5 ~
July 2007 540-543
" u3 f. c- B/ g5 Z7 A© 2007 Sage Publications
% {: V% e1 O- E+ y10.1177/00099228062966514 e3 _9 H* K% T4 w
http://clp.sagepub.com
& ~' N* c' U7 A1 @3 [7 U1 l# Bhosted at
, o8 i  J# j$ \- q  _http://online.sagepub.com
+ Y+ O) e$ M" \2 m/ N7 aPrecocious puberty in boys, central or peripheral,
( G; X. C8 C  l. B5 W( R5 Q( iis a significant concern for physicians. Central
" B# s+ `7 {# A2 J2 y& oprecocious puberty (CPP), which is mediated2 \' D0 a5 {$ S; J. a  }( [
through the hypothalamic pituitary gonadal axis, has
4 l; h) h+ R  A: m4 ]) t+ e2 ?a higher incidence of organic central nervous system$ u: c9 o. C  N1 ]% `6 P1 G8 {
lesions in boys.1,2 Virilization in boys, as manifested8 |9 Q# M! _; N, V7 j
by enlargement of the penis, development of pubic/ B6 _8 e8 L. O8 {( T4 Z4 M
hair, and facial acne without enlargement of testi-$ D( Y, p9 e8 \9 c! J1 A& E
cles, suggests peripheral or pseudopuberty.1-3 We6 b1 w8 k& t0 p+ |
report a 16-month-old boy who presented with the2 `& q# P8 Z, e& g) ]7 p( U2 Y2 c9 Q
enlargement of the phallus and pubic hair develop-
8 @: s5 o7 d! ]+ t3 \ment without testicular enlargement, which was due
! q/ P/ V  s, R' P4 X1 r. nto the unintentional exposure to androgen gel used by2 t( E- M& n& ]) _' E
the father. The family initially concealed this infor-
2 B7 @) U. Z( f  s% h% @. Y9 Kmation, resulting in an extensive work-up for this$ H4 B; N* j# L4 D; B) O' k
child. Given the widespread and easy availability of6 B: |6 u7 `5 Z1 ]  g& t
testosterone gel and cream, we believe this is proba-% r: K  {8 R/ _* [
bly more common than the rare case report in the
& V, p$ a3 f# O6 nliterature.4
. C9 F0 @/ j1 a3 WPatient Report0 x7 q; z+ D7 u3 k0 Q. @/ b# F1 q
A 16-month-old white child was referred to the; j, ?( h; B+ K
endocrine clinic by his pediatrician with the concern" G' m& B+ t# U0 h1 |. U
of early sexual development. His mother noticed
( B6 W) ]4 P8 }. {$ d8 Wlight colored pubic hair development when he was- I  J7 w5 x' t7 w8 s3 Q
From the 1Division of Pediatric Endocrinology, 2University of
1 e' B5 v9 O8 c' Z9 A, m: MSouth Alabama Medical Center, Mobile, Alabama.: R) P, O% o& }7 |$ a) X. U  I
Address correspondence to: Samar K. Bhowmick, MD, FACE,0 I1 C3 E9 Z0 k& }/ p, ~; K4 ?
Professor of Pediatrics, University of South Alabama, College of+ @3 Q9 \, ]6 l" L0 @# p: \& I* G. ?9 F
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 q% O! G( }, q* o' _; oe-mail: [email protected].
8 y9 R3 U; P" U: Xabout 6 to 7 months old, which progressively became
. M8 e- U' z$ a" Gdarker. She was also concerned about the enlarge-
6 X' n' P. N( E+ B9 U; v- n! qment of his penis and frequent erections. The child
0 H% U) o; a% R; qwas the product of a full-term normal delivery, with
/ \+ K+ u5 G3 S9 Pa birth weight of 7 lb 14 oz, and birth length of  F+ ]* \* |2 K& D
20 inches. He was breast-fed throughout the first year
  ~$ X0 m6 w) L! E% F* Cof life and was still receiving breast milk along with
+ p& y2 W/ L$ E( ksolid food. He had no hospitalizations or surgery,
4 \5 B, V2 O9 F7 K) Qand his psychosocial and psychomotor development. l" h$ u- w; ]8 E
was age appropriate.
) {& L- j3 h$ Q# G! o& ^3 qThe family history was remarkable for the father,- a* K3 Z! a" y! h
who was diagnosed with hypothyroidism at age 16,
8 K9 x* j$ Z. n+ kwhich was treated with thyroxine. The father’s; ^' }9 h5 B; M& Q" y* F7 s
height was 6 feet, and he went through a somewhat
9 ]% o- \: W2 n- P  }early puberty and had stopped growing by age 14.2 E. L, \: x" ]: z" G# |0 C1 v. N
The father denied taking any other medication. The, y7 G4 n2 G# I4 G2 x7 W
child’s mother was in good health. Her menarche
' d" C3 s7 s" [+ O3 p( `3 _was at 11 years of age, and her height was at 5 feet
4 d* A) c2 d: _* D5 inches. There was no other family history of pre-
0 m& O! r$ [7 A# s& q( \cocious sexual development in the first-degree rela-+ r7 O% T1 m: T% p
tives. There were no siblings.
( e2 y3 R& t9 A6 m8 d* mPhysical Examination& Q7 w# \4 |( \$ C4 @! G
The physical examination revealed a very active,: f: m0 X0 U' G0 X
playful, and healthy boy. The vital signs documented
; B8 |/ k& p: G$ p9 O: d/ u  W/ @# E$ ra blood pressure of 85/50 mm Hg, his length was/ l1 W2 E1 c" m  N  J: ~7 F
90 cm (>97th percentile), and his weight was 14.4 kg8 ~) M- u% h5 j& A/ a% |
(also >97th percentile). The observed yearly growth
7 M& o5 C0 u# j! hvelocity was 30 cm (12 inches). The examination of1 w% R9 H, f7 m
the neck revealed no thyroid enlargement.# }$ U  O0 }4 A4 @1 [' T' v
The genitourinary examination was remarkable for3 X1 e! V+ l7 c) ]
enlargement of the penis, with a stretched length of
3 J, l7 u5 }% f2 b6 P3 A' d$ w6 K' p8 cm and a width of 2 cm. The glans penis was very well* {" ?6 \) X- ]. \; X- C! O' }
developed. The pubic hair was Tanner II, mostly around4 x( {( h1 U% J
540# k+ B; J/ G4 R2 x
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! h7 _" |" y2 g9 Lthe base of the phallus and was dark and curled. The
( [3 X/ t8 u7 h0 o: p/ V0 p8 f% Z5 Wtesticular volume was prepubertal at 2 mL each.
+ L! }3 m) w) X2 LThe skin was moist and smooth and somewhat
9 s' L1 j! l/ b6 ]  b- soily. No axillary hair was noted. There were no& Z5 \& G  ^6 a
abnormal skin pigmentations or café-au-lait spots.
* c6 u. X% y; \* uNeurologic evaluation showed deep tendon reflex 2+1 @$ z# A1 q5 Z/ s+ g4 m0 M
bilateral and symmetrical. There was no suggestion
$ z6 _: L$ }% I9 ?( j6 Yof papilledema.
2 {6 S" r. T& U5 [" {Laboratory Evaluation% b, u! T, x$ V& B2 Y/ Z% ]
The bone age was consistent with 28 months by2 F3 d4 c1 N, m& o5 V
using the standard of Greulich and Pyle at a chrono-$ ], f, h5 P) R* [6 C- B3 R
logic age of 16 months (advanced).5 Chromosomal
2 @2 M4 o5 V. ~7 D$ Q. fkaryotype was 46XY. The thyroid function test/ e! e8 L) q& o# K; r) G
showed a free T4 of 1.69 ng/dL, and thyroid stimu-2 x+ Q5 Q- h. a- y2 \
lating hormone level was 1.3 µIU/mL (both normal).
! ^- H5 P8 x; Q4 {) lThe concentrations of serum electrolytes, blood
3 @# n' C/ ^( }* wurea nitrogen, creatinine, and calcium all were8 o$ O- C$ K. w' Z* K1 ?
within normal range for his age. The concentration* ~. a; j# f" ^* M! w! N; j" K
of serum 17-hydroxyprogesterone was 16 ng/dL
, m' G9 p4 Z* n' X0 g(normal, 3 to 90 ng/dL), androstenedione was 20
6 y; ^5 P$ D, [; G* B: y% P& png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-6 E* F8 Z$ ]6 Y# ?) x
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
2 y3 K* s4 \& U! K6 ]. Kdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
! [0 P+ {3 v6 o49ng/dL), 11-desoxycortisol (specific compound S)) m3 ~2 M; T% F, L& f* W" n& ?
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-/ S( z5 O+ @& a7 n5 G1 F
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; c2 A, v6 g, O2 O$ v9 }/ h! O  s3 X
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ v# o! u  B& ^, tand β-human chorionic gonadotropin was less than
% a  V2 \8 f. \5 j& J1 t5 mIU/mL (normal <5 mIU/mL). Serum follicular; e% p) Y2 _  q9 s
stimulating hormone and leuteinizing hormone
. k( e6 ^; z1 ]2 }+ F) P% N5 }0 L. Lconcentrations were less than 0.05 mIU/mL
; z3 Y2 ~) n# V7 @  ~5 q$ u3 C(prepubertal).8 g! z7 B8 o) {$ m9 B
The parents were notified about the laboratory8 G% N8 R8 ~' W: `
results and were informed that all of the tests were" A/ H  L) b& O. G7 R; y. A  M
normal except the testosterone level was high. The5 x1 A; b! l9 G9 W
follow-up visit was arranged within a few weeks to
- ~% M+ t+ w: g8 {; l6 i2 yobtain testicular and abdominal sonograms; how-1 L% y$ T; @+ l/ |7 D2 T
ever, the family did not return for 4 months.
3 B# K2 W9 n6 [- g3 D+ ~Physical examination at this time revealed that the/ v+ ^4 D  I, M& ~- U: F
child had grown 2.5 cm in 4 months and had gained
7 c+ B! a. b1 O7 f/ G3 E% v" ?2 kg of weight. Physical examination remained* P& k$ s8 G  p* h
unchanged. Surprisingly, the pubic hair almost com-
$ g& N. H) u8 V* |6 P5 kpletely disappeared except for a few vellous hairs at
( a& H8 O3 x+ t. n7 G! cthe base of the phallus. Testicular volume was still 2
+ @" z" L0 `* T/ XmL, and the size of the penis remained unchanged.6 B( @, C; ]6 V0 i8 ^4 e# ~' F) w
The mother also said that the boy was no longer hav-# X8 {' F" _' Y- K6 }) s1 c- ]
ing frequent erections.$ q& I8 z4 h4 S7 D8 S2 z& l
Both parents were again questioned about use of/ R' j+ M3 V* j- b
any ointment/creams that they may have applied to
! T4 V8 P. c- j/ Xthe child’s skin. This time the father admitted the* m+ S3 ~- ~5 q8 x# T
Topical Testosterone Exposure / Bhowmick et al 541
2 a8 B1 k& {/ [- n: u% m  Z$ i+ ?use of testosterone gel twice daily that he was apply-; t" Q+ u  Z: n2 l3 B
ing over his own shoulders, chest, and back area for6 a' \4 u- h9 O5 c# z
a year. The father also revealed he was embarrassed$ a' k# |. d* E0 L" t5 P( O1 }7 P
to disclose that he was using a testosterone gel pre-
4 N6 q2 B4 i+ [3 L6 uscribed by his family physician for decreased libido6 r. M- }0 X7 ]5 P! p; x" x$ k) ^
secondary to depression.. }- |& o  c* d
The child slept in the same bed with parents." k4 s5 h* S5 o. t0 R; c- o% |
The father would hug the baby and hold him on his
( U1 d# T/ h- G& Y* D* u$ m% j" f5 Cchest for a considerable period of time, causing sig-" T" P. M. F7 u" \0 k. p/ K! E( Y, \! E
nificant bare skin contact between baby and father.# x. C  u; k. N, f- u$ J( o
The father also admitted that after the phone call,
; O! W0 W4 v4 z& q  L# nwhen he learned the testosterone level in the baby2 G( a. i9 W  k" J0 k6 Q
was high, he then read the product information+ ?" R3 ~9 {0 _9 N
packet and concluded that it was most likely the rea-9 @9 w5 z: |5 G
son for the child’s virilization. At that time, they
9 z7 \6 R0 S+ F" }decided to put the baby in a separate bed, and the; f: s2 s' h* t. C/ k0 U- k% W
father was not hugging him with bare skin and had0 r  j( ^' o. h# n
been using protective clothing. A repeat testosterone& k3 v! @4 O" a& o! r! a. H# {6 L
test was ordered, but the family did not go to the
8 f* I; d+ A6 E! Y$ |: r3 I9 c3 ~laboratory to obtain the test.
& O, F; y6 g! xDiscussion
0 j- h# J! c. `Precocious puberty in boys is defined as secondary" `4 M9 P& c4 z" C1 h4 N
sexual development before 9 years of age.1,4
) R! H/ I# r0 ?Precocious puberty is termed as central (true) when
- H- b' g. U$ B+ _: wit is caused by the premature activation of hypo-
. I% w; `, _( p, J3 v7 Pthalamic pituitary gonadal axis. CPP is more com-
- f8 I. @" ^9 _, b/ e( omon in girls than in boys.1,3 Most boys with CPP0 A, @4 O" ~& k1 l2 I2 m
may have a central nervous system lesion that is: l. f' ~/ _1 H8 F5 W
responsible for the early activation of the hypothal-
7 ]! j' ]' Q6 x* j& Mamic pituitary gonadal axis.1-3 Thus, greater empha-
4 C- q4 g+ B9 S; e6 i# `- b' ?sis has been given to neuroradiologic imaging in
4 E' N5 z$ L1 xboys with precocious puberty. In addition to viril-, e- L" a. P" ~* d$ L  `
ization, the clinical hallmark of CPP is the symmet-
8 ~( p( u3 ]2 ], [4 f- Y  Qrical testicular growth secondary to stimulation by
$ N: N' U  e8 x* Xgonadotropins.1,3, x7 Z' C, g  E* ^- P& g) n
Gonadotropin-independent peripheral preco-
8 O8 U7 o* @+ icious puberty in boys also results from inappropriate
) V3 y  k+ k  `2 c" O; ?- l- ]androgenic stimulation from either endogenous or
$ A6 Q+ B8 c* A/ g% z# k. rexogenous sources, nonpituitary gonadotropin stim-
$ F/ |+ O; [- T4 Culation, and rare activating mutations.3 Virilizing! P3 l, I0 \  D  L" G  L
congenital adrenal hyperplasia producing excessive
0 d- O$ h! N- F/ g- f( yadrenal androgens is a common cause of precocious6 t9 N" n  F" Q
puberty in boys.3,4
2 L9 }) [" J6 l+ A' Q5 gThe most common form of congenital adrenal
* @) z9 M4 j& k- dhyperplasia is the 21-hydroxylase enzyme deficiency.; T/ Z# {. n' _. [: g6 h4 Y# a
The 11-β hydroxylase deficiency may also result in
+ m+ L8 P* Q! d4 ?2 [  g! oexcessive adrenal androgen production, and rarely,
4 {& W3 f( P0 L7 K, f8 g# ?an adrenal tumor may also cause adrenal androgen" g* X; n- U' L+ Z% {5 \
excess.1,3, @# L# j0 i: b# u2 w# g6 ^$ ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. j0 M, h. O: g3 f2 w8 d542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 e& y7 s) W4 W9 A
A unique entity of male-limited gonadotropin-
+ _: C+ M; v- o; [. U! yindependent precocious puberty, which is also known( e& M+ }8 w. Q
as testotoxicosis, may cause precocious puberty at a; S! i4 [# C' b2 r& a# _- m0 {
very young age. The physical findings in these boys4 }) z* n5 E3 ~/ U4 y8 |' A
with this disorder are full pubertal development,. @7 y% W( k# A3 T2 d2 P/ J
including bilateral testicular growth, similar to boys
/ M# |2 c% [  C& _9 Twith CPP. The gonadotropin levels in this disorder
& N2 F* h. U  q. j6 f: [9 f7 @are suppressed to prepubertal levels and do not show
) _4 m+ b3 I+ L3 N; \pubertal response of gonadotropin after gonadotropin-
" V- k) {- ?& ]* creleasing hormone stimulation. This is a sex-linked7 n2 k, B- |4 M7 u& D) {+ P
autosomal dominant disorder that affects only
6 t+ ~8 P$ g0 v* @! o2 bmales; therefore, other male members of the family
" w! N) {: \! x/ ]8 g2 Q. R% m+ Y: lmay have similar precocious puberty.3; G' M9 N2 V9 B5 Y
In our patient, physical examination was incon-3 D' ~# e2 B/ O, m
sistent with true precocious puberty since his testi-
9 X) {% R4 P6 P# a# L, Z# xcles were prepubertal in size. However, testotoxicosis2 ^$ E! `* r' s; I, H6 l! X, [
was in the differential diagnosis because his father, _5 e6 v* p  x9 e( X: U
started puberty somewhat early, and occasionally,8 D7 w- w6 \  m3 v: }8 Q/ m8 w
testicular enlargement is not that evident in the
" P' D. w0 b& k: vbeginning of this process.1 In the absence of a neg-
3 m# r! ^! Z/ H, e! Aative initial history of androgen exposure, our, z( f) q4 d' H. v
biggest concern was virilizing adrenal hyperplasia,1 E. V+ D- |& p" D4 S  G8 t. w
either 21-hydroxylase deficiency or 11-β hydroxylase0 j' p. H7 L8 _
deficiency. Those diagnoses were excluded by find-7 A' g0 N& X7 {% j* E- t
ing the normal level of adrenal steroids.0 w6 T, K  G3 R# Y. u2 v1 I4 p
The diagnosis of exogenous androgens was strongly
4 Y) l# b& E/ U2 K7 csuspected in a follow-up visit after 4 months because
6 A- x2 j) U3 m0 u  `( m$ |, fthe physical examination revealed the complete disap-* Y+ [4 R8 @8 H/ |2 K0 I
pearance of pubic hair, normal growth velocity, and  f( F& l% h+ v- r7 V& u, k% c
decreased erections. The father admitted using a testos-
% ^! [4 o. D/ D: s( G( E; X9 Cterone gel, which he concealed at first visit. He was6 O+ F$ i/ j) x+ z5 J/ z
using it rather frequently, twice a day. The Physicians’. ~) M" W5 f# c* D
Desk Reference, or package insert of this product, gel or9 R! Y7 n: p- ~8 o
cream, cautions about dermal testosterone transfer to
9 {) V& P+ ?8 ~0 c3 sunprotected females through direct skin exposure.
- l5 u- d; y) P" q" ~Serum testosterone level was found to be 2 times the+ T8 V+ m8 q! V0 P% q6 B
baseline value in those females who were exposed to
7 M  f4 c% \. D7 n% Qeven 15 minutes of direct skin contact with their male7 ?) v  u0 T9 G$ u( d/ \
partners.6 However, when a shirt covered the applica-$ Y. p* z4 [# h. j7 T
tion site, this testosterone transfer was prevented." N) U% w9 V1 v: Q
Our patient’s testosterone level was 60 ng/mL," q8 w& Q: \/ |: c, t9 W# J
which was clearly high. Some studies suggest that( X: G/ T  _3 \8 k
dermal conversion of testosterone to dihydrotestos-! |2 q' e: G' X5 G1 D6 V, ?
terone, which is a more potent metabolite, is more9 w/ T; F! h% I4 s$ I( x
active in young children exposed to testosterone
' L! _3 h3 J6 r! m' ?7 bexogenously7; however, we did not measure a dihy-
& H, p7 w/ R: u$ W- Sdrotestosterone level in our patient. In addition to
; Y2 r; {7 E# r8 w  x# M/ w6 Cvirilization, exposure to exogenous testosterone in  W8 j0 c* E2 u+ s
children results in an increase in growth velocity and4 l4 K1 ?+ p7 A' z+ @; b
advanced bone age, as seen in our patient.9 G+ p1 |0 e, M7 ]
The long-term effect of androgen exposure during$ _* v" p& u  g' K
early childhood on pubertal development and final
: [* C* C, m3 N/ c) ?8 ^$ \) Xadult height are not fully known and always remain/ w" d! h9 p5 P4 j  q
a concern. Children treated with short-term testos-
  ~7 g+ J/ ]; F5 B( }$ [  [6 r2 Fterone injection or topical androgen may exhibit some
! }/ g( {+ S1 v! c% Oacceleration of the skeletal maturation; however, after% X. l$ s" Q3 X8 i
cessation of treatment, the rate of bone maturation" O) K5 ]; v1 V7 T+ K
decelerates and gradually returns to normal.8,9
0 D- I. E5 u' d3 T9 |9 V) `There are conflicting reports and controversy
6 T( C4 j( X. z6 T) U; |/ Lover the effect of early androgen exposure on adult
% p7 ]5 f3 Y( [7 b' k: Bpenile length.10,11 Some reports suggest subnormal
' D  V- `# X7 @( Padult penile length, apparently because of downreg-
9 R1 v) |  w+ h+ k' Pulation of androgen receptor number.10,12 However," b, ]* h2 }2 v
Sutherland et al13 did not find a correlation between9 Z! `6 \) W% I9 P" a
childhood testosterone exposure and reduced adult6 k' M( u9 Y4 u/ z5 n; v
penile length in clinical studies.
7 k$ e3 C5 g8 ^* O# u5 f. PNonetheless, we do not believe our patient is
( t# U  j% X" Mgoing to experience any of the untoward effects from4 K% a4 x1 i) w( L2 _) U3 m
testosterone exposure as mentioned earlier because
$ \3 I9 C, y4 P2 H% ^8 Ithe exposure was not for a prolonged period of time.- O$ B# r- w6 q8 x
Although the bone age was advanced at the time of
8 L" k! P) R) ]3 ^3 Gdiagnosis, the child had a normal growth velocity at* w1 G# Y. q( y9 f( o7 ~- j3 u0 Y) S
the follow-up visit. It is hoped that his final adult, v' W( V" u& i4 W7 G8 u
height will not be affected.* Z: u# t1 p* `/ f% U2 S$ N3 y- x
Although rarely reported, the widespread avail-
- C+ ~+ C1 f% i) ^% ~ability of androgen products in our society may
! u: B/ L* b# j) }# A9 Yindeed cause more virilization in male or female9 J& x( ?9 _5 J; @
children than one would realize. Exposure to andro-
9 W5 b4 c. n, {. f! ggen products must be considered and specific ques-
9 X  P& ~+ F1 e+ i( E1 U# h# Ptioning about the use of a testosterone product or
/ O( p' Z* d9 R, P% [" Lgel should be asked of the family members during
3 B5 }6 k, H& d  P) M! x- bthe evaluation of any children who present with vir-
' K# J  I, Z$ `2 Q; q; w* j  u% g. Dilization or peripheral precocious puberty. The diag-
' R  M* p1 ~. C+ dnosis can be established by just a few tests and by( W4 Q& L+ _7 i) q  X6 m* k, z) d
appropriate history. The inability to obtain such a- u" N4 z. U: X1 M1 ~( P
history, or failure to ask the specific questions, may
2 f1 }- M" \. c0 J- ], qresult in extensive, unnecessary, and expensive
0 Z9 w6 W+ ^1 W! Z; q9 E+ ]! B7 ainvestigation. The primary care physician should be9 ]/ l* f* i9 u6 E  D" d! X" c
aware of this fact, because most of these children' y: ]. H7 ]& j1 r
may initially present in their practice. The Physicians’
% E5 X9 @, f, Q* H. \! N" O7 Z/ XDesk Reference and package insert should also put a
7 G; A5 n; P' ^1 F1 r$ U2 @/ `warning about the virilizing effect on a male or- J4 V  [) ~& ^! [! l
female child who might come in contact with some-
3 D( D2 |5 p) e3 i( U- Q- ~7 }% t& None using any of these products.* c9 Z7 T% Z2 S4 J  F5 w: q
References9 |8 k1 l  k  [# K; a
1. Styne DM. The testes: disorder of sexual differentiation
) c6 B$ L6 q6 ~4 s+ }% \) j8 y# R, m) Sand puberty in the male. In: Sperling MA, ed. Pediatric
; m$ a! K" p2 C0 eEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. s" O8 \6 S- F" h* M9 p: p2002: 565-628.$ y5 g2 f  D- I# [5 H* C) N
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) D/ G* \4 e9 J& N" J# a
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
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
/ }2 J9 J" }; y; |/ o4 X
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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