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Sexual Precocity in a 16-Month-Old/ a  L+ m# v$ d0 q. V! [& [+ t
Boy Induced by Indirect Topical- z* Q0 k9 o2 t, h1 w8 b) I; w, p
Exposure to Testosterone
, o5 K7 V" \% A% {% |Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; I0 \) ^- N, O! E9 E. `1 _- T% Qand Kenneth R. Rettig, MD19 A8 v, j5 q0 h% Q7 v* ?$ `5 s
Clinical Pediatrics6 D  P8 Y* F  G
Volume 46 Number 6
3 n: G  H2 \3 R9 y! d; Y3 ZJuly 2007 540-543
: o% h3 ~% w8 z© 2007 Sage Publications( d* Q9 R. j, F0 y+ g
10.1177/0009922806296651
6 Z- j8 p7 F4 O* |; A( {* j0 _! Zhttp://clp.sagepub.com- O, P* b& P$ Y- w; V) [9 D
hosted at4 b$ o3 b0 C1 q; L# Y& D* B- T
http://online.sagepub.com, y" Q% W1 k' O/ Y* m1 Q; z
Precocious puberty in boys, central or peripheral,! v* m  A$ ^& w8 c3 W( i8 G0 X
is a significant concern for physicians. Central
& W9 {7 W3 g+ B0 X# `( y, vprecocious puberty (CPP), which is mediated
: T+ b! o0 Q& D- ]7 Xthrough the hypothalamic pituitary gonadal axis, has
+ O# D) Y$ d& A" I" ia higher incidence of organic central nervous system
4 C+ A6 ?2 o) f& z& E! f- Glesions in boys.1,2 Virilization in boys, as manifested; b0 m. d. W1 \& A  ^7 v
by enlargement of the penis, development of pubic/ e$ D; G9 h& s- _4 H2 g
hair, and facial acne without enlargement of testi-
/ P: K& S+ W; z$ I0 ^  Pcles, suggests peripheral or pseudopuberty.1-3 We  v# r5 d9 w. i, d# ^" R3 o
report a 16-month-old boy who presented with the+ t7 ]9 R- S- ^. [0 X* O2 z
enlargement of the phallus and pubic hair develop-
2 a: Z, Y: D5 d9 c+ Yment without testicular enlargement, which was due, H0 _5 `! l" n- ~- F& s3 Z
to the unintentional exposure to androgen gel used by
+ [4 ~- @9 i' d# othe father. The family initially concealed this infor-
" R3 `$ N" }! }$ l( {mation, resulting in an extensive work-up for this
3 h4 ^2 m' `; Y  k. Cchild. Given the widespread and easy availability of) L8 m8 k1 \8 b8 z; [
testosterone gel and cream, we believe this is proba-- i6 L5 X/ c5 p& ]
bly more common than the rare case report in the5 `) }2 b2 R/ H7 O2 e0 Z# w
literature.4
$ C2 a0 O. y% K3 D8 F* I+ ~) v$ p# ]Patient Report, x+ P9 a  ?5 t3 J. |& S
A 16-month-old white child was referred to the+ G- ?& c+ ^7 n' u
endocrine clinic by his pediatrician with the concern0 l. F0 [: j4 m
of early sexual development. His mother noticed6 y9 e# S' t0 u0 c
light colored pubic hair development when he was
+ i/ c/ L$ y7 d, z& H7 {& H* @From the 1Division of Pediatric Endocrinology, 2University of# q) j( t/ F$ e. q3 ?
South Alabama Medical Center, Mobile, Alabama.. O; q: g1 v% a) _+ v. L
Address correspondence to: Samar K. Bhowmick, MD, FACE,
/ \# @) u  O9 ~4 e9 @Professor of Pediatrics, University of South Alabama, College of
. a, U$ j" x) k2 UMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 T% Z8 ?: \0 n- m0 c5 ke-mail: [email protected].
! B' }3 @6 U$ e% Labout 6 to 7 months old, which progressively became
) u% D' ]. Y* S4 R2 l  g1 k) m5 c* _darker. She was also concerned about the enlarge-' U8 a- ]5 J, ]9 z: o
ment of his penis and frequent erections. The child
$ o6 e7 o: Q# G. Ewas the product of a full-term normal delivery, with4 o; t  G- ]6 U7 L6 }1 l4 F
a birth weight of 7 lb 14 oz, and birth length of/ m0 k/ h# w5 n) t. n# O7 r/ ]& m
20 inches. He was breast-fed throughout the first year
* }7 ]. [  Q* @5 S4 j5 ^0 Pof life and was still receiving breast milk along with: s& N# p8 D' V' s
solid food. He had no hospitalizations or surgery,; M- r  z+ g( o! [5 }5 e) y) t
and his psychosocial and psychomotor development8 Y  }' Y1 R3 n7 ^! n5 F9 r
was age appropriate.2 q8 d/ Q- X6 p3 I
The family history was remarkable for the father,
  X+ G$ M* n# _5 s( E) _who was diagnosed with hypothyroidism at age 16,
# o) x5 r; f3 B- F" S3 ^7 o; _which was treated with thyroxine. The father’s* b; q* _/ M& a& Z. J
height was 6 feet, and he went through a somewhat& j! L7 i2 E5 W9 r5 f6 }
early puberty and had stopped growing by age 14.
4 z1 `* S. Y+ p# h  XThe father denied taking any other medication. The
+ p2 o# v9 v% k# ichild’s mother was in good health. Her menarche" W& {5 H1 ]8 T* q( m/ i% H4 G+ Y3 P
was at 11 years of age, and her height was at 5 feet, e3 Y- k+ S- U
5 inches. There was no other family history of pre-
" ], ~* ^& N  ?6 ^cocious sexual development in the first-degree rela-
- ]0 J- f2 a/ m  t6 _5 @; ~tives. There were no siblings.9 I2 l, [: d* h3 r( o. \
Physical Examination
! i! m" h7 T1 f7 RThe physical examination revealed a very active,( W  {: ]4 x0 r# |9 \* M
playful, and healthy boy. The vital signs documented
4 H7 A: F8 q5 p" v. b3 za blood pressure of 85/50 mm Hg, his length was4 N2 w8 x) |. L/ l
90 cm (>97th percentile), and his weight was 14.4 kg
) {1 D1 P1 b! R  \7 C(also >97th percentile). The observed yearly growth
  y- Y7 |  B5 xvelocity was 30 cm (12 inches). The examination of
! K  t0 u4 ~, O9 Nthe neck revealed no thyroid enlargement.+ r1 h5 m4 b( x0 J5 r! ^0 i1 U9 k
The genitourinary examination was remarkable for
5 R+ M8 Z# c7 M' a, n$ ienlargement of the penis, with a stretched length of
: O5 T+ K# F7 R" F; g- A" B0 d1 p8 cm and a width of 2 cm. The glans penis was very well) Q/ d4 |' X6 M, B, Y( I
developed. The pubic hair was Tanner II, mostly around+ @5 d+ H- s/ ?. H
540
; M1 X: T* p* A3 R# _at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 J) @1 |: \- S# D, {$ u9 ithe base of the phallus and was dark and curled. The
, n8 Q: Z7 _# R. s1 Qtesticular volume was prepubertal at 2 mL each.
5 T; }, [$ j# B' d' ?4 g9 \The skin was moist and smooth and somewhat
- H, N8 r: j) }! }6 d( q* C+ n0 Boily. No axillary hair was noted. There were no$ X1 G1 q8 K, h* F6 {4 s
abnormal skin pigmentations or café-au-lait spots.- M/ L, ~& I/ x$ s7 \3 f
Neurologic evaluation showed deep tendon reflex 2+7 Q" f3 C3 ?2 [0 B# P; d# m
bilateral and symmetrical. There was no suggestion# A% Y) X& |0 Q/ m6 N( r; J. m
of papilledema.
2 N  e7 ^' X7 J- DLaboratory Evaluation
/ v; ^) l5 d0 z( c( Y. n  ?The bone age was consistent with 28 months by0 F. ~7 Z, \- Q" |( k) Y$ i
using the standard of Greulich and Pyle at a chrono-
# @- j0 E4 ?& y% \8 Z" o: h" Zlogic age of 16 months (advanced).5 Chromosomal) p- I  p  a  {7 K
karyotype was 46XY. The thyroid function test" F6 ]; Q" ~  b. A* Y) |+ @8 F
showed a free T4 of 1.69 ng/dL, and thyroid stimu-6 V- w$ s8 c' ]
lating hormone level was 1.3 µIU/mL (both normal).: m! k  f, a8 Y# ^* }/ w/ }
The concentrations of serum electrolytes, blood) t( d: D# a$ s" b$ l4 }
urea nitrogen, creatinine, and calcium all were8 m: w/ Y% l0 C
within normal range for his age. The concentration
/ f5 c3 @0 c# w( p3 f9 Y' ]- eof serum 17-hydroxyprogesterone was 16 ng/dL0 N! n/ {" `- ^8 I1 x# U
(normal, 3 to 90 ng/dL), androstenedione was 20
! y: f$ N" V0 I. m! @: [1 ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ v& T# H8 D, _
terone was 38 ng/dL (normal, 50 to 760 ng/dL),4 ], O# {! x- i2 S1 D
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
: p% m; i% k" Y7 Q49ng/dL), 11-desoxycortisol (specific compound S)
4 C6 q9 g3 Y8 P8 P! k- Wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-1 K/ f; E' l# I  L+ {
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# r; f4 i( x3 A1 C
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 i' l; h! f" [! h4 S. f
and β-human chorionic gonadotropin was less than
9 c6 {6 K( b% u" A9 w/ Q5 mIU/mL (normal <5 mIU/mL). Serum follicular
- z2 C  ?3 w8 ^) l2 J: r7 Nstimulating hormone and leuteinizing hormone
$ h+ |5 G' m; Y0 u( D. M  Y  fconcentrations were less than 0.05 mIU/mL2 n* \/ O  u- a+ ^
(prepubertal).
6 B) i# d) g$ |7 bThe parents were notified about the laboratory
/ c/ D& R* T( `4 O; ~* E1 fresults and were informed that all of the tests were
! E( J: i: s" S; X8 fnormal except the testosterone level was high. The6 i6 k( f8 c* w1 d
follow-up visit was arranged within a few weeks to
3 g- J0 D% r8 L8 F+ G/ i$ r& \/ ]obtain testicular and abdominal sonograms; how-0 F1 ?5 f. {. Z( u8 s5 T8 |
ever, the family did not return for 4 months.' M+ d+ z# r. ]( |
Physical examination at this time revealed that the$ S8 A  b2 c9 m; q
child had grown 2.5 cm in 4 months and had gained" G# u% p' x* K: F/ S. B
2 kg of weight. Physical examination remained# e% x/ S" n$ o3 m- o# I/ C
unchanged. Surprisingly, the pubic hair almost com-$ v$ H- ]5 ^/ Q0 H9 z+ o1 N) [0 V) L
pletely disappeared except for a few vellous hairs at+ {3 P" A/ S  Z9 z9 v( E: k
the base of the phallus. Testicular volume was still 2
  B7 z& \0 Y) }, GmL, and the size of the penis remained unchanged.
$ v5 H, T4 n' w! uThe mother also said that the boy was no longer hav-4 O8 J' y1 B# G
ing frequent erections.
9 F5 C# D4 a8 \" iBoth parents were again questioned about use of, U, Y5 C3 m' Y  @$ e* Q
any ointment/creams that they may have applied to
  v3 p. I) M( ]5 T7 [0 H" ithe child’s skin. This time the father admitted the
# z5 u: S/ ]" C8 x# L6 i2 {Topical Testosterone Exposure / Bhowmick et al 541* ?6 T" V' B" J3 J+ H6 K' I
use of testosterone gel twice daily that he was apply-
0 K9 b& l, q3 [ing over his own shoulders, chest, and back area for% q0 Q+ [& C6 ^6 r  n# ~
a year. The father also revealed he was embarrassed
' D3 m3 E  B( v* V4 `; Kto disclose that he was using a testosterone gel pre-7 ?% M  d) H, {; N. n
scribed by his family physician for decreased libido! \* o, S7 t0 e5 o2 w
secondary to depression.
$ l3 i5 D* N: @8 l1 XThe child slept in the same bed with parents.* g  D2 U+ M( {/ `+ Y- Z
The father would hug the baby and hold him on his
  _& _$ K' V* Pchest for a considerable period of time, causing sig-
; C! ^) R& p: y4 x9 L  Lnificant bare skin contact between baby and father.( w2 q- }. v8 P# i& V, n( o
The father also admitted that after the phone call,
9 h  {5 _: h6 w9 S# d# uwhen he learned the testosterone level in the baby
2 |; _9 _% Y- g1 _) P7 P$ W# xwas high, he then read the product information
  y1 f7 [; e% M' ?* S- d4 ^- lpacket and concluded that it was most likely the rea-
- e# `& n: R9 Cson for the child’s virilization. At that time, they
. |3 e/ `) c! h. K: G. M0 |decided to put the baby in a separate bed, and the
9 h: w: T+ C& efather was not hugging him with bare skin and had7 s( N3 F7 c* t, b: A# ^7 w+ J
been using protective clothing. A repeat testosterone
2 _. C3 C* w4 B; v, q4 |test was ordered, but the family did not go to the4 @3 {2 Y, N4 I
laboratory to obtain the test." j. s% h8 W9 [$ X( ~$ q! L
Discussion
1 u$ H/ z1 ~* k2 tPrecocious puberty in boys is defined as secondary
2 ]( `' e; z5 J. j& G% L( n& q  Hsexual development before 9 years of age.1,4
$ V9 T4 b( Y4 J4 ^+ T0 V2 Q7 ~- K% YPrecocious puberty is termed as central (true) when6 W: I* Q( ^% H+ U" C
it is caused by the premature activation of hypo-
" C2 e! n! w4 |! ~7 y9 j1 w' a7 pthalamic pituitary gonadal axis. CPP is more com-8 p# T* t% E+ y. C& L- T
mon in girls than in boys.1,3 Most boys with CPP
3 c' }4 v# \! B7 Bmay have a central nervous system lesion that is
- }" L$ p6 y3 t: y1 Y% w) ]responsible for the early activation of the hypothal-- ^# Q( f- [& U$ @! D' A6 r
amic pituitary gonadal axis.1-3 Thus, greater empha-$ t9 O( G0 r% n& s' `( J
sis has been given to neuroradiologic imaging in
- X, ~8 b' \( I( s+ ]boys with precocious puberty. In addition to viril-
! T& w1 j4 I- a: nization, the clinical hallmark of CPP is the symmet-
/ d* V6 X* {# [6 Q! hrical testicular growth secondary to stimulation by% |8 q% W3 q: N) T# J, ?* Z7 [0 @
gonadotropins.1,3, B& h. }6 z* V
Gonadotropin-independent peripheral preco-
' J" a, O  j: |$ Rcious puberty in boys also results from inappropriate. m$ Y6 l) s3 f3 F" z* [! X, @
androgenic stimulation from either endogenous or! h: \4 T/ y; p6 ?. ?
exogenous sources, nonpituitary gonadotropin stim-
3 N# L( y  v" Zulation, and rare activating mutations.3 Virilizing. y! W' S' a, k) ~7 b( H! y* w
congenital adrenal hyperplasia producing excessive5 x1 D, A5 _# o% N% l8 t
adrenal androgens is a common cause of precocious) t2 {8 E1 W# A8 S+ l5 ~+ C
puberty in boys.3,4
$ {4 r3 U  ^9 E  qThe most common form of congenital adrenal; o( H1 q- A, f: j
hyperplasia is the 21-hydroxylase enzyme deficiency.+ d. F' ]: B0 v. [; {# m+ |
The 11-β hydroxylase deficiency may also result in
2 z! R' [# v. d$ E+ m& texcessive adrenal androgen production, and rarely,
$ V0 Z  E4 G1 B' ~an adrenal tumor may also cause adrenal androgen, q8 g- O2 ?% r* E1 F
excess.1,3
( X6 d1 L" ?7 pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ |$ j8 `9 H" |& ~% F; k7 o
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& a* l) `7 G1 X
A unique entity of male-limited gonadotropin-
% I% d# w0 v, r. `1 E( E8 ?4 zindependent precocious puberty, which is also known
" H% {6 c+ l6 Z4 [5 m5 }+ Zas testotoxicosis, may cause precocious puberty at a5 `! v8 `# n' K7 l. W
very young age. The physical findings in these boys
1 K! N; s2 L- s0 z: Owith this disorder are full pubertal development,
/ m; ~& L& B( @; Eincluding bilateral testicular growth, similar to boys
4 R+ B9 p! _$ X+ s9 a" l: X: q5 Lwith CPP. The gonadotropin levels in this disorder
8 O$ @& z/ w7 g( S1 n7 s( W, `( ]  L! a+ Zare suppressed to prepubertal levels and do not show: H' _2 A- O0 D8 r* l) m% E! {
pubertal response of gonadotropin after gonadotropin-7 C& M+ Z) B- Y! r0 S5 `
releasing hormone stimulation. This is a sex-linked1 \% p& a$ y4 \% s9 r% t( [  M
autosomal dominant disorder that affects only
4 T4 L0 ?* m! s4 `males; therefore, other male members of the family
, H! @0 X3 e3 S. Umay have similar precocious puberty.3; h5 B; i6 M) q
In our patient, physical examination was incon-: P$ w; ~+ j- N# q+ m* E5 j
sistent with true precocious puberty since his testi-6 d- j( J* v3 X/ Y4 F* F
cles were prepubertal in size. However, testotoxicosis' Q/ k3 W5 o* Y0 o0 F3 W1 ]3 Q3 g
was in the differential diagnosis because his father
2 K( c6 ]+ d& @; n) p; W, Cstarted puberty somewhat early, and occasionally,
) E6 S2 B2 B# otesticular enlargement is not that evident in the
" `5 b8 [' B8 h; Sbeginning of this process.1 In the absence of a neg-
1 B8 I3 H1 {) R/ Aative initial history of androgen exposure, our  F; }& {4 _2 p+ m: D
biggest concern was virilizing adrenal hyperplasia,
1 K% z$ h. y8 H( L- r7 Weither 21-hydroxylase deficiency or 11-β hydroxylase1 Q2 M* C5 \9 A! L, g1 z
deficiency. Those diagnoses were excluded by find-" n" d& R  {; A9 z/ e- e
ing the normal level of adrenal steroids.
  `1 ?) F1 H, W1 |The diagnosis of exogenous androgens was strongly
' I) \9 A# r3 b+ lsuspected in a follow-up visit after 4 months because/ e( n, B6 h# S
the physical examination revealed the complete disap-
$ t6 u$ q, V" M8 d, Q! h7 Lpearance of pubic hair, normal growth velocity, and' ?. e! Z+ B7 C1 t) T
decreased erections. The father admitted using a testos-" A. n. t5 k  B# M
terone gel, which he concealed at first visit. He was7 A; b# E7 R% s$ {
using it rather frequently, twice a day. The Physicians’* }7 w8 q6 {# j0 y* M2 Y
Desk Reference, or package insert of this product, gel or( y, S4 V% h5 [" {  p6 _# i
cream, cautions about dermal testosterone transfer to, ^) `2 Q" t! {; u" m* H6 {
unprotected females through direct skin exposure.& w. }+ e6 w1 L0 l, \5 h$ V  v
Serum testosterone level was found to be 2 times the
& C0 W: a  n1 e' Jbaseline value in those females who were exposed to& R6 Q; Q" e$ g+ n( T% P
even 15 minutes of direct skin contact with their male" k$ e2 i8 q* a) u! @8 p
partners.6 However, when a shirt covered the applica-
$ n$ I7 s+ D9 h) ution site, this testosterone transfer was prevented., A* Q- s8 H1 Q5 J) J8 u- [  |
Our patient’s testosterone level was 60 ng/mL,
' M# {1 C4 }+ N* P! {which was clearly high. Some studies suggest that
; d2 p, m- m. T. N# [. g  x; Fdermal conversion of testosterone to dihydrotestos-
, }; e: {2 ]  t  X3 ]% o1 wterone, which is a more potent metabolite, is more
1 y6 R' V) m7 S1 T. X9 `active in young children exposed to testosterone- W3 }/ t) u& R  I, V& f/ j: b
exogenously7; however, we did not measure a dihy-' S/ g/ z1 H" C- W2 x" ^: r
drotestosterone level in our patient. In addition to
1 A7 {7 |  {) W$ z; M$ nvirilization, exposure to exogenous testosterone in
1 R$ j. I! P$ ]3 S$ h/ kchildren results in an increase in growth velocity and
* g$ J9 e& B: y) \$ _9 dadvanced bone age, as seen in our patient.( @) t* L  T! W- N3 Q! [
The long-term effect of androgen exposure during% a( E5 y; l# }2 Y6 D1 _4 z
early childhood on pubertal development and final
. c. x1 B; v0 B4 k+ A" ^adult height are not fully known and always remain
3 f& w# F% Y8 Da concern. Children treated with short-term testos-& T$ G) ^! I& P, B2 m: b, V
terone injection or topical androgen may exhibit some
4 [; w/ }# F- Racceleration of the skeletal maturation; however, after5 C0 K3 @2 O  L' l
cessation of treatment, the rate of bone maturation
' Z* e$ R- J! D# O! edecelerates and gradually returns to normal.8,9
+ O5 o9 D& S% m' B: u2 `* {8 ZThere are conflicting reports and controversy
  z$ }& F+ A! k" M8 J$ gover the effect of early androgen exposure on adult+ h9 d; |& q/ g1 a: C2 Q0 @
penile length.10,11 Some reports suggest subnormal
  O& \. R3 T8 P7 D' Z7 t8 kadult penile length, apparently because of downreg-5 u: Y8 j1 i1 K+ K
ulation of androgen receptor number.10,12 However,
; f- S7 {2 x# X( g: R' WSutherland et al13 did not find a correlation between4 [* ^3 O( T/ S% P( G
childhood testosterone exposure and reduced adult+ t: i7 L1 P# Y' Z5 x6 T
penile length in clinical studies.6 l" I/ d: E$ c
Nonetheless, we do not believe our patient is. x& A- J% i0 O) x6 p& X, [& V
going to experience any of the untoward effects from# O) g# u8 i5 \! _$ `# ?' n
testosterone exposure as mentioned earlier because
$ T+ i' g- D0 ?" e9 _the exposure was not for a prolonged period of time.
' I5 s) H/ b5 o' j7 qAlthough the bone age was advanced at the time of
) p' K- Q5 {' adiagnosis, the child had a normal growth velocity at2 d8 i" N) B6 a0 s1 d
the follow-up visit. It is hoped that his final adult
; u+ r4 N& S( L: ^; M. f8 `& pheight will not be affected.
" O' j$ G" f" VAlthough rarely reported, the widespread avail-  V9 e+ v" t* w3 D
ability of androgen products in our society may! g: F# f+ T2 i" o
indeed cause more virilization in male or female: a; K8 L/ r7 P4 h: }/ N# b
children than one would realize. Exposure to andro-
% Z2 a0 ?5 T( R. vgen products must be considered and specific ques-
* c1 j- Z9 M0 s9 K9 m, L8 t& O( ]tioning about the use of a testosterone product or
2 J! [8 s3 Z/ S- dgel should be asked of the family members during
* w# Y; L( |1 E# k6 Kthe evaluation of any children who present with vir-
& q2 D  x" _5 b' B/ Yilization or peripheral precocious puberty. The diag-5 G7 R2 |! t/ K6 p; K$ {2 T
nosis can be established by just a few tests and by1 H5 g, H1 n8 j0 e
appropriate history. The inability to obtain such a- [/ L6 E4 R6 q. {0 @
history, or failure to ask the specific questions, may
6 [8 b: O5 C; A: V- K- \result in extensive, unnecessary, and expensive* @! V& p- N; @) }8 t, a! n
investigation. The primary care physician should be
+ ?1 X- x  ~# h1 t8 i9 Taware of this fact, because most of these children6 t+ d1 O3 P6 a& m8 J) _: w+ O
may initially present in their practice. The Physicians’, X- f9 ?* H% b- a- y. U
Desk Reference and package insert should also put a
' e2 d1 W* Z. h- r& M) F8 Rwarning about the virilizing effect on a male or: d8 N) _1 u* c) F2 [: p7 \
female child who might come in contact with some-) {" V& }! B4 [. Y" m
one using any of these products.+ d) s, E& b! R8 @6 }( B9 `
References
* {; U' @5 t, S7 f) `, U1 a# p7 N1. Styne DM. The testes: disorder of sexual differentiation- ?" h2 ^) w, K3 B7 v
and puberty in the male. In: Sperling MA, ed. Pediatric5 r( o% E9 }! B' ~% ?
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 L/ f3 i3 M8 V1 h
2002: 565-628.
2 m0 v* e) Z5 }0 Y* T# K5 b2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ ?9 _9 y  j. ipuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old, r, T: h4 x' P9 F+ `
Boy Induced by Indirect Topical' l# c8 x8 C9 o
Exposure to Testosterone% K2 P2 h0 J: W- W% I; {* }
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) L1 C; |9 J& Q( }, ]! U+ |8 C. L
and Kenneth R. Rettig, MD1
2 w# G* S. [( JClinical Pediatrics
; O1 f: O7 ~1 J2 q8 l4 JVolume 46 Number 6
/ P: u" _+ K* J. \* r& [) c4 FJuly 2007 540-543
) `! ]3 p2 l+ ~( t& s, A© 2007 Sage Publications5 r' M9 v$ u) @/ |: ]6 h
10.1177/00099228062966512 k7 f: c, H* k! i
http://clp.sagepub.com
( S8 c  A2 R. H! f. Z2 }! ghosted at+ ^4 E: K) u, N( O! M5 o4 R
http://online.sagepub.com
3 N) l: j; o$ ?2 m' ~9 q" \( XPrecocious puberty in boys, central or peripheral,
+ c  {/ y% W- {( F7 J5 R3 v0 L8 ?is a significant concern for physicians. Central: P/ V9 R7 J: o9 H
precocious puberty (CPP), which is mediated
8 `+ U. _+ ?/ W! u# w* ethrough the hypothalamic pituitary gonadal axis, has
7 Y% e9 Y  B, A' m/ ka higher incidence of organic central nervous system
9 `' @7 p0 o' k* ?3 V+ x7 }* P% ?( Hlesions in boys.1,2 Virilization in boys, as manifested
- }# h, o$ c& S0 j" g# qby enlargement of the penis, development of pubic
0 Z1 B+ y4 T- x$ `. _hair, and facial acne without enlargement of testi-5 x2 d9 Y% B8 o: r8 V) }8 s
cles, suggests peripheral or pseudopuberty.1-3 We
3 m  H0 @; Q' b& I0 X2 Nreport a 16-month-old boy who presented with the
9 y: G* H9 o% ^$ \* \3 Tenlargement of the phallus and pubic hair develop-7 a5 ?& l0 \' B* t: t
ment without testicular enlargement, which was due& }' x5 G& X0 q
to the unintentional exposure to androgen gel used by
6 D0 [  n, |1 o4 kthe father. The family initially concealed this infor-) e& v9 w. C2 C& G0 q$ V. B+ }) t' E" h
mation, resulting in an extensive work-up for this
, V7 q- X- X/ a3 P0 schild. Given the widespread and easy availability of2 W9 S6 c6 h# t! e. l
testosterone gel and cream, we believe this is proba-
' x& x; }( ]8 ?, L- T* X2 fbly more common than the rare case report in the
, N% K! J: g9 [2 ]: j. Sliterature.4
2 b' V. f# b- f1 P9 [1 ?! hPatient Report& E* i5 Y/ Y  t; E: U; Y
A 16-month-old white child was referred to the# b$ R9 V! J9 S
endocrine clinic by his pediatrician with the concern
: w- k# P: c* K& O2 mof early sexual development. His mother noticed* f3 ]* w9 ~- U# d) r' K: d
light colored pubic hair development when he was5 t$ a8 ^" `# D* n
From the 1Division of Pediatric Endocrinology, 2University of
  y# }) h1 T) h* X0 {, }4 PSouth Alabama Medical Center, Mobile, Alabama.
: f. L+ p* ^) G# N7 L( fAddress correspondence to: Samar K. Bhowmick, MD, FACE,
: p! C6 ?  Q9 L2 K# Z7 Y, }7 W/ ]Professor of Pediatrics, University of South Alabama, College of& s3 b" |$ A) R0 i
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ b- y' s% z: X4 `: P# Ae-mail: [email protected]./ |/ ]3 O7 B9 g, g
about 6 to 7 months old, which progressively became
' u  ]) c/ n, N, Y" W8 qdarker. She was also concerned about the enlarge-: `, \9 t2 F; A& G1 w* Q
ment of his penis and frequent erections. The child
" F5 J) A5 J; ^was the product of a full-term normal delivery, with
8 {2 l3 J4 P; d" ^2 t; V1 |/ Xa birth weight of 7 lb 14 oz, and birth length of
$ G2 i( p  Z7 F/ e8 R) d20 inches. He was breast-fed throughout the first year
$ q* c& ?: P* S4 R8 i, Z# {of life and was still receiving breast milk along with1 r' ]8 g* L+ _: ?; n2 e- e9 l
solid food. He had no hospitalizations or surgery,
* y( e+ l8 c4 ~, V1 u2 \$ Q  _and his psychosocial and psychomotor development
( K+ ^- f% S# @) s3 h6 ~8 fwas age appropriate.: l/ i* @) f% x
The family history was remarkable for the father,
$ \: B2 ~  R! B( g# ^who was diagnosed with hypothyroidism at age 16,
) D, h; ?% R3 X: g2 S' u0 S  d' fwhich was treated with thyroxine. The father’s
/ i, B% ]% o1 o1 Fheight was 6 feet, and he went through a somewhat% u2 A. O8 |9 ~( |
early puberty and had stopped growing by age 14.- g0 v8 K) l9 h  z
The father denied taking any other medication. The
% n1 S+ O1 A6 W2 X2 n7 S" Y& zchild’s mother was in good health. Her menarche
% W7 n* q' K/ r/ x+ @7 q; {5 owas at 11 years of age, and her height was at 5 feet, ~4 g5 _! n5 M! I% J9 d
5 inches. There was no other family history of pre-
& _; T, X! ^# w2 Vcocious sexual development in the first-degree rela-
8 `7 M9 ^' I# V8 Q9 vtives. There were no siblings.% ^, p& Q; z/ X, B0 V3 a
Physical Examination* T& B0 A2 Q: s* W) _
The physical examination revealed a very active,
- d0 c# \; C: Y& f0 ~) O; hplayful, and healthy boy. The vital signs documented
" s6 h/ ]' b! ]* M; E) g4 J7 k  Ea blood pressure of 85/50 mm Hg, his length was
& E1 \/ V5 i8 v6 C/ R; H( J+ z, L/ V90 cm (>97th percentile), and his weight was 14.4 kg
: m' L, N, m, S) y(also >97th percentile). The observed yearly growth
" g0 c7 F# ?; C7 |) Fvelocity was 30 cm (12 inches). The examination of9 l7 Z3 {% @" ]
the neck revealed no thyroid enlargement.
  I3 R& @/ N3 f6 @: @& r  a$ x+ qThe genitourinary examination was remarkable for" v- p' Y  e7 T$ P
enlargement of the penis, with a stretched length of
1 c  K: P6 M0 I. S8 cm and a width of 2 cm. The glans penis was very well
* N! M0 Q  A' ^developed. The pubic hair was Tanner II, mostly around8 U& z0 I$ q; s2 O
5407 S% ?- w6 B8 T; a, j% b8 E- R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
$ ?" |, W% @* J$ P2 L' O1 o2 Tthe base of the phallus and was dark and curled. The7 ~5 |$ V8 j4 ^* V2 w: O2 v6 S
testicular volume was prepubertal at 2 mL each.
5 C( r' w; H5 F  ^( `* i$ _The skin was moist and smooth and somewhat. u4 C1 S% d, F$ j$ c) ^8 ^8 B
oily. No axillary hair was noted. There were no
; h: a9 o7 X8 {# g' R0 Babnormal skin pigmentations or café-au-lait spots." y& v2 ^) ~- Q8 @
Neurologic evaluation showed deep tendon reflex 2+# g6 S# T* k; M8 ?+ _0 u: ^9 w
bilateral and symmetrical. There was no suggestion3 q8 j+ {- b$ W) {
of papilledema., R  T! N" a! m" s# [$ Y2 n4 K$ z
Laboratory Evaluation
! r' O+ J; g$ q$ @The bone age was consistent with 28 months by
6 t: Q4 p8 C, Susing the standard of Greulich and Pyle at a chrono-/ `% I, G: L* X
logic age of 16 months (advanced).5 Chromosomal; `! K( f$ L& E" {9 y& R- j* J- i' B
karyotype was 46XY. The thyroid function test' r. U/ F8 p2 R  x
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
$ E8 O( r& f- i% M5 i! ?lating hormone level was 1.3 µIU/mL (both normal).1 {- u" f- x) o! B( y
The concentrations of serum electrolytes, blood
, o2 [+ z* a: T  Q2 rurea nitrogen, creatinine, and calcium all were& _. D2 }  p4 R
within normal range for his age. The concentration: q( ~- V* k! z  q4 T$ F( s
of serum 17-hydroxyprogesterone was 16 ng/dL( }1 ^0 t3 z. Z* P) l* m
(normal, 3 to 90 ng/dL), androstenedione was 20% u! Z) _' E, s
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
: E, Z" O: k" m% m0 y( t% `terone was 38 ng/dL (normal, 50 to 760 ng/dL),
; B8 N# s& M) Z4 c' C! @3 zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to$ }  E% {% {: d
49ng/dL), 11-desoxycortisol (specific compound S)
; \0 ?6 r5 Q. c% {& c" v- nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, w; t! O2 _/ q( s& `tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* h& P0 Y; o* P& ]( U/ @+ s
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 W1 y3 @" P: r" N, y5 h
and β-human chorionic gonadotropin was less than8 J) u4 R" l( E! f8 ?
5 mIU/mL (normal <5 mIU/mL). Serum follicular
: }6 S- A  q, ^! v: E  vstimulating hormone and leuteinizing hormone
! l8 X" K3 D" ]8 c" a1 I# L) A; nconcentrations were less than 0.05 mIU/mL
3 S9 l# s1 Z/ R(prepubertal).
: T  y9 [2 @% d% a6 aThe parents were notified about the laboratory: ~$ O! E5 `, {  F& M
results and were informed that all of the tests were- s$ i- S( ^5 m' x  L3 d
normal except the testosterone level was high. The
  U4 \1 n( h8 M! h5 I. Yfollow-up visit was arranged within a few weeks to. o, i0 i9 O! g$ T3 v
obtain testicular and abdominal sonograms; how-4 o% N, |( j  K, }, t
ever, the family did not return for 4 months.* T0 ]7 i$ O" M
Physical examination at this time revealed that the
- i# ~& j$ k2 Echild had grown 2.5 cm in 4 months and had gained
% _5 a8 T: X/ I2 kg of weight. Physical examination remained
8 R2 a9 Q8 r$ \% C& o) p0 vunchanged. Surprisingly, the pubic hair almost com-9 {4 D2 s+ H! G) \! O' E
pletely disappeared except for a few vellous hairs at
$ p" X: H: S4 {3 ?6 b" |$ r: [* @the base of the phallus. Testicular volume was still 2
+ X: G: ]7 b- E$ u$ P! imL, and the size of the penis remained unchanged.
9 E2 c& d+ A( a" Y2 a8 X+ I" q1 sThe mother also said that the boy was no longer hav-
0 n7 `- Z- Q- w) x0 ting frequent erections.
( y5 S/ ]8 @6 W3 e) h  LBoth parents were again questioned about use of! h, K0 e9 `2 x8 O+ N9 X0 f$ u* \
any ointment/creams that they may have applied to" v% A6 l8 g5 i+ ^8 e
the child’s skin. This time the father admitted the& u1 Z. y7 \1 f
Topical Testosterone Exposure / Bhowmick et al 541
  E3 U5 R: o$ G# \$ suse of testosterone gel twice daily that he was apply-' p. P: d7 l  q& r; {- J& d
ing over his own shoulders, chest, and back area for" f, F  v0 `2 X. B
a year. The father also revealed he was embarrassed
2 j2 D* c5 t6 xto disclose that he was using a testosterone gel pre-$ T" R( s8 U% M5 T# E6 g
scribed by his family physician for decreased libido4 {" z" t. ^% l
secondary to depression.
# _5 a) f( C% c- m: YThe child slept in the same bed with parents.9 R& j1 B4 Q$ y
The father would hug the baby and hold him on his
( O, O, L( _+ L4 s1 A8 Fchest for a considerable period of time, causing sig-
, ~5 q. z/ e2 g6 w. xnificant bare skin contact between baby and father.1 R8 Q* E2 e$ p
The father also admitted that after the phone call,- `) I" e! p$ Q9 A& j4 t% n! a
when he learned the testosterone level in the baby2 c: M: ^3 M# j) K' [) V. U
was high, he then read the product information& l# T' y  `) Z* X; Y5 b5 G
packet and concluded that it was most likely the rea-
3 W+ J0 h) Q/ G) e, Y; Hson for the child’s virilization. At that time, they7 q0 @; c% O. g6 n
decided to put the baby in a separate bed, and the/ C+ N' L/ o8 s/ U% Y" m( d5 g9 |
father was not hugging him with bare skin and had& S* A7 p$ y, s6 x
been using protective clothing. A repeat testosterone. i7 s# ^/ m( Y6 I3 a; V, H0 Z7 R
test was ordered, but the family did not go to the
- q( |" Q4 Y" S8 E: p/ Blaboratory to obtain the test." N# Y3 {4 N0 K+ b
Discussion5 p( m% Z& E' s7 M
Precocious puberty in boys is defined as secondary5 i- R6 i& r* t7 h& c7 ?
sexual development before 9 years of age.1,4
9 C7 V! t5 z! F/ ]: NPrecocious puberty is termed as central (true) when, W5 F' p1 S6 ?' n
it is caused by the premature activation of hypo-" R$ f9 N3 }5 w3 O1 \. T
thalamic pituitary gonadal axis. CPP is more com-4 O7 l) o, S: j! v. a4 V
mon in girls than in boys.1,3 Most boys with CPP
+ A, A5 A1 ?8 y: ~$ ^may have a central nervous system lesion that is, w( d* H) g) h/ z* ]% p  `3 s
responsible for the early activation of the hypothal-, ~) n3 ~/ Z# N+ _' J
amic pituitary gonadal axis.1-3 Thus, greater empha-& O& X" U% |* W1 {
sis has been given to neuroradiologic imaging in
: g# _! [4 w+ `/ [/ V0 d' g" }+ Yboys with precocious puberty. In addition to viril-  K9 M4 h9 q7 F6 O5 N; ?
ization, the clinical hallmark of CPP is the symmet-& ?) a1 G) p( z% K- N
rical testicular growth secondary to stimulation by
! V! D# c5 J1 X/ Xgonadotropins.1,33 f$ q$ m9 X% c+ C) e0 h
Gonadotropin-independent peripheral preco-7 s' C5 q& d* [8 l' r- @
cious puberty in boys also results from inappropriate5 D2 q, l* \! J7 d1 |
androgenic stimulation from either endogenous or
+ P$ _9 u' H8 Yexogenous sources, nonpituitary gonadotropin stim-, N2 M' l# x9 [* c5 L
ulation, and rare activating mutations.3 Virilizing
- r6 b/ W% e6 ^& K' R1 H8 |congenital adrenal hyperplasia producing excessive
7 C5 F5 k; w, @/ ^- uadrenal androgens is a common cause of precocious/ Z+ P  q9 O7 ~% Q3 B. Y
puberty in boys.3,48 v2 c* R1 x  g! O2 p9 U
The most common form of congenital adrenal8 H; x7 Q* c3 h
hyperplasia is the 21-hydroxylase enzyme deficiency.
. k* R8 B' [3 n- Q6 |The 11-β hydroxylase deficiency may also result in1 \5 D$ M& @6 c# l% J
excessive adrenal androgen production, and rarely,
1 b% i* C% j- ~' t5 I9 uan adrenal tumor may also cause adrenal androgen
  L0 |/ O& R+ x! O; L' e" u: a6 ~1 R" M( rexcess.1,3
  \! v8 n. ]* I- M2 Q+ h9 c2 L# Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ \, S( O' n! x0 _5 {
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
+ t5 u3 [+ h6 y& yA unique entity of male-limited gonadotropin-2 ]) G, J( L4 `! f. y3 N
independent precocious puberty, which is also known) c: b8 f& D3 Z, k9 {7 P# q* _
as testotoxicosis, may cause precocious puberty at a
, |- f: p& C6 U3 T4 Z+ Gvery young age. The physical findings in these boys' @. F. J4 c0 l0 {
with this disorder are full pubertal development,. j  C6 f/ P9 I% E% o- L7 F! C
including bilateral testicular growth, similar to boys* E+ w3 ~, v4 \$ Q! u
with CPP. The gonadotropin levels in this disorder0 F6 x! q/ }7 u. ^, M
are suppressed to prepubertal levels and do not show0 n7 Y. z! L/ L& n
pubertal response of gonadotropin after gonadotropin-
, M! p7 P. k) k7 s5 hreleasing hormone stimulation. This is a sex-linked
" D: R/ h7 U; S" X/ p! Oautosomal dominant disorder that affects only
& x$ x+ k4 C5 M& umales; therefore, other male members of the family
- U% H0 ~+ p/ ?2 nmay have similar precocious puberty.3
  F7 O0 D; O! s# \. H( h1 T! bIn our patient, physical examination was incon-- }7 ^  R& Z. J5 Y' J* x, ~
sistent with true precocious puberty since his testi-
  p' c4 i* F5 L5 E, _+ f; D, Acles were prepubertal in size. However, testotoxicosis
3 E9 g. a8 K- E. V/ g, Z2 |+ `was in the differential diagnosis because his father
7 v5 P# a( ^- `' p. @' Astarted puberty somewhat early, and occasionally,* f) l( L* E; [4 g; V: B
testicular enlargement is not that evident in the
+ i% O( N5 e& [' ~beginning of this process.1 In the absence of a neg-
0 A6 k6 p5 o8 |2 G. Aative initial history of androgen exposure, our
, n. [- R/ N' H* Gbiggest concern was virilizing adrenal hyperplasia,
1 T6 F# m0 B' ]+ R  R( Veither 21-hydroxylase deficiency or 11-β hydroxylase
+ m2 e0 t( i/ m/ }' K- H) _0 |deficiency. Those diagnoses were excluded by find-. {3 e/ i. W$ w; `5 O$ F' ]$ I
ing the normal level of adrenal steroids.
% @; w2 w: z1 K9 F4 pThe diagnosis of exogenous androgens was strongly
8 X1 v8 `) m: B+ A3 O  w$ z8 Tsuspected in a follow-up visit after 4 months because" q7 n+ x0 X2 R" O% U* M2 r
the physical examination revealed the complete disap-; |7 f2 i. F$ D* m/ V
pearance of pubic hair, normal growth velocity, and
' I% d0 c; A4 o0 mdecreased erections. The father admitted using a testos-, ]- x  w; Q8 O* _1 j* u9 @. J! e1 C% w. `
terone gel, which he concealed at first visit. He was, }) S# P6 o5 p0 N. O
using it rather frequently, twice a day. The Physicians’
" u4 {! x) }$ }, y) ?Desk Reference, or package insert of this product, gel or
& ]* T/ ]5 G! f5 Q4 Ycream, cautions about dermal testosterone transfer to6 o7 ?- ^) w8 Z
unprotected females through direct skin exposure.7 z. I$ n- \: }% A
Serum testosterone level was found to be 2 times the
* h! `& t: F( g6 B/ ubaseline value in those females who were exposed to; ~" u' `% K, i$ Z
even 15 minutes of direct skin contact with their male
# K. W5 G/ K7 L9 p6 z5 r/ epartners.6 However, when a shirt covered the applica-* l, w) s% u/ r" d4 K
tion site, this testosterone transfer was prevented.
2 W; U1 i1 |, w; SOur patient’s testosterone level was 60 ng/mL,0 K% c& f9 e7 B2 S1 Q$ P2 o& v; F
which was clearly high. Some studies suggest that
% Q3 S. h$ d# ]" e  Fdermal conversion of testosterone to dihydrotestos-7 G+ ?% w& D1 T% t( d
terone, which is a more potent metabolite, is more
  A* o) W2 g6 ^( xactive in young children exposed to testosterone
" a+ G% e8 [/ ^" m6 D$ p! ~- k6 |0 z- qexogenously7; however, we did not measure a dihy-
8 E% C  Q5 ?* u3 G! Q: l* c; ^drotestosterone level in our patient. In addition to6 z: z, x. v; F% B
virilization, exposure to exogenous testosterone in2 r7 e  k! ^) W3 U! q$ K
children results in an increase in growth velocity and
0 z& ~) x  f' ?- o# O6 Eadvanced bone age, as seen in our patient.) G  y$ z& P/ G; p. _, _9 q4 |
The long-term effect of androgen exposure during% V2 c# i7 U4 ?. l
early childhood on pubertal development and final
/ {* u- M9 ^/ F5 Q1 \# C3 }1 g. Y3 n4 madult height are not fully known and always remain
# \. _2 c0 e# P$ l  ma concern. Children treated with short-term testos-
/ ^, f8 L! J) V# z' Mterone injection or topical androgen may exhibit some$ b1 Z* o! v- V  U. m
acceleration of the skeletal maturation; however, after' H. E; J0 D6 V# m! S
cessation of treatment, the rate of bone maturation6 H* J$ Y4 w7 M% J0 X2 u3 G
decelerates and gradually returns to normal.8,9
+ U0 O9 W' i$ t5 \; T' m1 O: NThere are conflicting reports and controversy
1 ~# {( n& g7 l  f4 A* f' ]over the effect of early androgen exposure on adult. M- F( J& @0 ~4 p
penile length.10,11 Some reports suggest subnormal7 P4 N; A8 S# C! a& t7 N- \
adult penile length, apparently because of downreg-* m0 J$ w, `) L
ulation of androgen receptor number.10,12 However,
% I( p4 u# v+ |% _* XSutherland et al13 did not find a correlation between
+ G. X* H2 I/ F8 \+ Fchildhood testosterone exposure and reduced adult
  O8 b7 L3 J2 E1 \' Y1 Fpenile length in clinical studies.* R% C0 i& K) u* _
Nonetheless, we do not believe our patient is
7 l6 ?: K5 p% E" t& [going to experience any of the untoward effects from
7 ~5 Y/ K) Q" V( Q7 Qtestosterone exposure as mentioned earlier because; N1 j; Z9 W3 k5 b* G
the exposure was not for a prolonged period of time., L3 M& ?" I1 ]: W* I/ K0 D
Although the bone age was advanced at the time of
7 A2 R9 F0 [& E1 h* Ediagnosis, the child had a normal growth velocity at8 Y+ v% x8 B% D
the follow-up visit. It is hoped that his final adult. I6 T& C' P0 `9 m! M
height will not be affected.7 O9 b* o' V, f8 ?( t7 h
Although rarely reported, the widespread avail-! z" G8 s: p# E$ E1 g9 B
ability of androgen products in our society may+ [9 o. L9 @; B) X
indeed cause more virilization in male or female- ?/ b, O/ ~0 Y- V2 K
children than one would realize. Exposure to andro-
( Y6 C# Q, O' n1 vgen products must be considered and specific ques-
/ j0 Q2 V4 s- N/ M* m1 I& ]tioning about the use of a testosterone product or7 O7 T1 y  Z& r
gel should be asked of the family members during  T' s" j( ]" N6 l. m/ ^! _3 `
the evaluation of any children who present with vir-
6 c/ q- W& E! Z5 zilization or peripheral precocious puberty. The diag-; m. T- d% [. D0 I  y
nosis can be established by just a few tests and by
# c5 G7 X, D! z5 b5 Jappropriate history. The inability to obtain such a( S) f9 G4 U; E/ ?. E
history, or failure to ask the specific questions, may' D+ Z& p8 F  e6 i) g* V2 r* R. M
result in extensive, unnecessary, and expensive
) j7 m- w8 F' `investigation. The primary care physician should be, g: k7 X+ R6 x3 m- T$ v; t
aware of this fact, because most of these children
4 W$ `8 A; k6 n2 smay initially present in their practice. The Physicians’: |. e! H0 M* ~$ l! f  K
Desk Reference and package insert should also put a
# x7 X. S& R+ r0 `& z! |warning about the virilizing effect on a male or
2 P! C$ [2 D  I; c4 @female child who might come in contact with some-
" B. P1 ~/ m8 h0 [6 {one using any of these products." P+ M9 G- P! I3 }: O
References( i( D4 r0 J8 U$ X  s- @* U2 G6 Q
1. Styne DM. The testes: disorder of sexual differentiation3 @4 U) n3 O2 d8 n3 o* y
and puberty in the male. In: Sperling MA, ed. Pediatric) o# `8 z  \( e/ _& @6 n  c
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% T7 ^# ]8 c9 o3 s/ Z" B0 a$ o3 v2002: 565-628.
2 U% s8 v# P- j' I6 m, @2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 W$ q& y' K. k4 R3 Z
puberty in children with tumours of the suprasellar pineal
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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

- w4 Z5 ^% a" V" 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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