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Sexual Precocity in a 16-Month-Old6 m# f: Z+ f- N0 X5 Z+ [9 {4 N& [+ ]
Boy Induced by Indirect Topical- P; g) C, H, `  b* ~2 r9 X
Exposure to Testosterone6 H, G1 ]4 R7 f4 h' E
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) E3 \9 S) [8 N
and Kenneth R. Rettig, MD1
. A0 \' X" H, `/ EClinical Pediatrics
2 C- Q( n+ A; ^3 ~Volume 46 Number 6
% j# Q! N( P( r/ K/ X$ U3 [5 WJuly 2007 540-543
$ ]9 n- ^/ @% {2 w* x, J0 `9 {© 2007 Sage Publications
4 j; O" H3 u2 b- v: _: N* W& ?* F; N10.1177/0009922806296651
! v5 _6 ]/ v, ]1 l5 z" c5 p( \http://clp.sagepub.com
3 [* B, m8 x. c, |hosted at6 J% V9 F! a1 v: ^
http://online.sagepub.com
4 Z# b' |$ C# ~2 _9 K7 NPrecocious puberty in boys, central or peripheral,6 O+ [- B) I- Y# ]
is a significant concern for physicians. Central' R/ X+ c5 L9 O: y: _
precocious puberty (CPP), which is mediated2 U; s% G! i2 F$ E
through the hypothalamic pituitary gonadal axis, has+ R1 v# p! _1 `" @; c4 z% Y
a higher incidence of organic central nervous system" p6 I$ y( S  N. m, B5 _
lesions in boys.1,2 Virilization in boys, as manifested
# D5 }7 D# u* I. ^4 v, q  \2 Bby enlargement of the penis, development of pubic
+ `- y8 ]0 b. |7 O9 shair, and facial acne without enlargement of testi-
5 e) `$ W2 l$ K! |% @( ^cles, suggests peripheral or pseudopuberty.1-3 We
4 r5 z, n; I* z9 ?1 c- Vreport a 16-month-old boy who presented with the+ q* [1 R1 M1 n" C8 Y
enlargement of the phallus and pubic hair develop-. i7 c# L! L4 _4 o6 V
ment without testicular enlargement, which was due
5 |3 V6 |5 e! y8 @1 r) cto the unintentional exposure to androgen gel used by
" t# p( m  N- S! z8 Xthe father. The family initially concealed this infor-) L' x. N) ]1 P8 `) p# S& P
mation, resulting in an extensive work-up for this
! Q  C2 X9 f9 Ochild. Given the widespread and easy availability of
5 Y, d: g+ R6 _6 {% l$ e' ]testosterone gel and cream, we believe this is proba-' O3 r. d& }; @5 X$ m( O  Y6 N4 h
bly more common than the rare case report in the% v2 T! i6 i% K; w
literature.4& I9 K2 q3 w! a9 K$ g" u/ b
Patient Report
" e  h; {4 v0 y! ?3 B# P) r6 s, BA 16-month-old white child was referred to the+ C6 [& \4 y2 e
endocrine clinic by his pediatrician with the concern
9 c2 t' H& N6 d/ N! ?9 v; x- [: yof early sexual development. His mother noticed
9 N! Q4 b, a# |9 S+ ^+ Hlight colored pubic hair development when he was
' e1 s! A* R5 ?3 ^From the 1Division of Pediatric Endocrinology, 2University of
% |9 u4 v) F+ n7 k9 kSouth Alabama Medical Center, Mobile, Alabama.: m; x9 Y& |; t0 }: T7 c2 O
Address correspondence to: Samar K. Bhowmick, MD, FACE,
5 [) b  ?; v5 c/ b. I. T8 k% ~Professor of Pediatrics, University of South Alabama, College of1 K$ e) x5 @& G3 I1 @% H1 d7 _
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ w: `+ w' ?# X% u! te-mail: [email protected]." R6 m# b$ ~( V" @3 |; H
about 6 to 7 months old, which progressively became
. _; \* r: {- q' zdarker. She was also concerned about the enlarge-& b2 }4 T  L8 `
ment of his penis and frequent erections. The child
; c/ P4 P: a0 s4 H, ]" Pwas the product of a full-term normal delivery, with3 T+ S5 c! t5 y8 a( a/ Z. p. t
a birth weight of 7 lb 14 oz, and birth length of3 ?6 k4 w  O5 O4 C  u
20 inches. He was breast-fed throughout the first year2 m. ?$ u8 o5 z6 q8 F! F1 o& m
of life and was still receiving breast milk along with
8 e1 U) G: s7 y, n2 B* lsolid food. He had no hospitalizations or surgery,1 X4 s5 y" E- e, ]) C7 J
and his psychosocial and psychomotor development
$ N* D# ]6 v# C' Y8 A1 D0 nwas age appropriate.
9 f7 S6 Q. W# w  x6 R+ WThe family history was remarkable for the father,
- u' K+ b, k$ R1 Z% Q9 {& xwho was diagnosed with hypothyroidism at age 16,
9 \! E: P0 Q3 p, ]7 Qwhich was treated with thyroxine. The father’s
* s7 S: _; M4 o1 o& U  m4 wheight was 6 feet, and he went through a somewhat
- u$ T% p: W4 t! K1 ]; w0 z  Wearly puberty and had stopped growing by age 14.
1 a$ W( k% L0 q6 I4 g1 IThe father denied taking any other medication. The
- d. L8 y6 G5 V! |; F) O, Tchild’s mother was in good health. Her menarche
) s3 A1 R& W" U2 Y8 g9 U) c! v2 Qwas at 11 years of age, and her height was at 5 feet
# I# y" c" Z) U, Q% [2 M, c. ]5 inches. There was no other family history of pre-- X# k7 \6 F5 d4 v5 S$ q
cocious sexual development in the first-degree rela-
- g% M" j9 n3 H, }tives. There were no siblings.. V& g8 t8 J+ g# j5 l. S" l* h+ ?
Physical Examination
' Z3 G9 ?5 m$ QThe physical examination revealed a very active,; B6 T- [1 q& j( j4 P9 p. N$ F
playful, and healthy boy. The vital signs documented
/ Z1 i: c, M7 D1 [3 y! Ga blood pressure of 85/50 mm Hg, his length was
1 k: w" V, H  b2 y$ M9 B4 s5 [: t0 d$ B90 cm (>97th percentile), and his weight was 14.4 kg- f6 s- O% m# F0 p& p
(also >97th percentile). The observed yearly growth
2 Z6 d" ]( B3 B6 lvelocity was 30 cm (12 inches). The examination of
* @# l+ g- D# D' Xthe neck revealed no thyroid enlargement." u* V" y6 F1 @; @) y& k
The genitourinary examination was remarkable for
$ P  m# x$ M0 \3 C7 xenlargement of the penis, with a stretched length of
' B5 Y0 @+ }, p) s* L8 cm and a width of 2 cm. The glans penis was very well7 c1 M) b7 E& ?7 H5 Q" F& h( u, F
developed. The pubic hair was Tanner II, mostly around! B5 G1 ^! r6 v4 {5 j
540
# o$ X% k1 \: S' Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  ~. S( }' U0 ]$ U( D2 U( Gthe base of the phallus and was dark and curled. The
! f7 O& Q3 A, K+ etesticular volume was prepubertal at 2 mL each.5 D* U, s4 V) I3 a# A' c9 }9 X7 z
The skin was moist and smooth and somewhat, N: k: N& o; w6 c! s$ C9 A. c7 x8 t) M
oily. No axillary hair was noted. There were no5 i2 E2 r' \+ Y. j
abnormal skin pigmentations or café-au-lait spots.
: a. N2 K& o2 Y% WNeurologic evaluation showed deep tendon reflex 2+$ ?% D7 l# Z) X( v8 T& K
bilateral and symmetrical. There was no suggestion
; |2 J: f8 \& Eof papilledema.
$ M: a) I' m0 k: [7 F, h" aLaboratory Evaluation
. n" b0 Q  J/ k8 [  X1 JThe bone age was consistent with 28 months by
& d: g; X. o  B  \, L* x8 dusing the standard of Greulich and Pyle at a chrono-
/ p8 m! _8 [3 z/ d- ~" _logic age of 16 months (advanced).5 Chromosomal- b) X& z5 p6 b
karyotype was 46XY. The thyroid function test
0 f1 A: n5 I0 B$ _% B1 Jshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
) j4 S: L+ D4 @lating hormone level was 1.3 µIU/mL (both normal).
, j3 X: [( \$ }* NThe concentrations of serum electrolytes, blood' g4 y5 Q3 i3 ~1 V
urea nitrogen, creatinine, and calcium all were# f' d  y, S0 V$ ~/ l: H6 d$ w
within normal range for his age. The concentration9 {0 s5 `' P9 ?3 ^1 F% U7 T
of serum 17-hydroxyprogesterone was 16 ng/dL8 ?0 ?8 ~7 E, e4 j& T( Y$ j" w
(normal, 3 to 90 ng/dL), androstenedione was 20
' j9 d9 E- i# Eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) q3 F) ~2 o3 ]* o0 Jterone was 38 ng/dL (normal, 50 to 760 ng/dL),
( z# I- O0 D4 ^/ T- M0 pdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 D3 g1 @& f1 Z1 f/ d4 I# I49ng/dL), 11-desoxycortisol (specific compound S)0 E9 i' t+ x/ b8 t& ]
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# V' F) d, o$ Y( h, Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 U. r5 M! A* a4 ^
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
" L; N9 [" H9 kand β-human chorionic gonadotropin was less than
) w; ]9 k, T+ d5 P: p( ?+ y0 j) \! f5 mIU/mL (normal <5 mIU/mL). Serum follicular
& U  @. F/ f7 R* m9 {- ~3 e) u: G' s* tstimulating hormone and leuteinizing hormone, R3 _' t: J' @
concentrations were less than 0.05 mIU/mL; {+ Y' d  Z$ W: ?
(prepubertal).( N# j- d, E+ R* i: f$ F# Y; q& f
The parents were notified about the laboratory* @6 Z0 r6 q) ^9 {
results and were informed that all of the tests were* v' |0 B9 o' v+ c3 q
normal except the testosterone level was high. The8 T* f' [+ E& z; L1 U* d, t/ }
follow-up visit was arranged within a few weeks to
1 U/ Z* h/ t. A2 @obtain testicular and abdominal sonograms; how-* N) h% p" t1 j& U" Q* d' [* Z, \( S$ M
ever, the family did not return for 4 months.& Y5 a8 J; a4 Y% G$ d4 v3 Z
Physical examination at this time revealed that the6 W5 z$ N0 j3 `- W' k, o
child had grown 2.5 cm in 4 months and had gained
7 a; m. Z$ B) N5 [4 r. S7 ]) g/ g2 kg of weight. Physical examination remained
) D# q$ I' p* {- E9 z/ O8 {8 Bunchanged. Surprisingly, the pubic hair almost com-$ G# }& U( J1 J
pletely disappeared except for a few vellous hairs at( u. i9 H! z, s3 T, v8 O" B
the base of the phallus. Testicular volume was still 2
6 f' o7 q2 j1 u  o4 t/ M2 [, N' WmL, and the size of the penis remained unchanged.
0 ~( Z2 q7 A7 W  |. D. dThe mother also said that the boy was no longer hav-
# p4 ]  |9 u* F: {2 N) ?8 ming frequent erections.  g# c" Q' D1 I, n( H- h
Both parents were again questioned about use of6 t7 m; s; r- p  G( |# `9 x0 E
any ointment/creams that they may have applied to* K4 Q3 U0 U8 u! ?0 W2 M% L& a, d
the child’s skin. This time the father admitted the
8 ^( ^, x4 M2 J8 |, i; uTopical Testosterone Exposure / Bhowmick et al 541
4 ^6 h  [2 W3 l* u+ X8 g; _7 euse of testosterone gel twice daily that he was apply-
8 W- A- h) J  l- cing over his own shoulders, chest, and back area for) g' W2 k. ~( F3 A, b7 E
a year. The father also revealed he was embarrassed2 T1 S# v$ L- `4 b5 U* y1 L
to disclose that he was using a testosterone gel pre-! l4 e( Q* I7 ~$ R% h: v
scribed by his family physician for decreased libido
5 g9 b/ ?2 @7 Lsecondary to depression.. o7 z; O& ?( R
The child slept in the same bed with parents.' {: R* I, O) {8 X
The father would hug the baby and hold him on his
2 m1 i: J, @7 S% W9 Bchest for a considerable period of time, causing sig-
! s4 R( @: n1 j+ o0 P; knificant bare skin contact between baby and father.6 S' u; M! V7 R; Q, f
The father also admitted that after the phone call,+ O  {2 i5 g3 e( ^% r
when he learned the testosterone level in the baby; f* g3 a$ p& |
was high, he then read the product information7 z7 i+ ~. R* w: ^' U
packet and concluded that it was most likely the rea-6 Y& e+ Q& S# U5 J/ z2 z& s
son for the child’s virilization. At that time, they
6 u' _9 X4 b% c; pdecided to put the baby in a separate bed, and the, L8 g' a$ H/ i# ]
father was not hugging him with bare skin and had) D% i" N1 F& h' ?/ B. j
been using protective clothing. A repeat testosterone
. z* e6 z0 q+ g' w+ M( G! E3 }, stest was ordered, but the family did not go to the
3 }3 y) @: |2 H- W3 alaboratory to obtain the test.
+ A# j! E% R: V2 S* X* C  |& mDiscussion6 U# ~- Y: \  D+ v# T/ I5 O
Precocious puberty in boys is defined as secondary. m: v" r( X/ I' D
sexual development before 9 years of age.1,4
1 }% Y+ y, |0 p; ]: K  h- n* z$ s0 l: u& oPrecocious puberty is termed as central (true) when! T0 ?7 q+ t* E
it is caused by the premature activation of hypo-& ~* z  d8 l2 D1 B) x
thalamic pituitary gonadal axis. CPP is more com-) h; a4 d, V' w  J
mon in girls than in boys.1,3 Most boys with CPP
3 i2 p0 p6 o! }$ Hmay have a central nervous system lesion that is
! m4 D3 b# F: j" H5 E# m) P; ^responsible for the early activation of the hypothal-8 |: e2 Q" M: u4 w& \% @9 m3 [9 f
amic pituitary gonadal axis.1-3 Thus, greater empha-3 F7 C2 \# s7 {  y' x
sis has been given to neuroradiologic imaging in5 a, j% A7 \- l6 E5 X5 z- O( z1 _
boys with precocious puberty. In addition to viril-0 N) f% _2 k6 f/ @) i
ization, the clinical hallmark of CPP is the symmet-
" K4 o0 g& D6 L/ Yrical testicular growth secondary to stimulation by4 s  H( l: c# |& [4 O- H
gonadotropins.1,3) s6 A+ Y/ g5 U7 y$ f! o! v5 y, J
Gonadotropin-independent peripheral preco-
' S* A% A+ U, Z# D, ~cious puberty in boys also results from inappropriate
& m8 ]9 b6 U% H6 z* Kandrogenic stimulation from either endogenous or# V: M! A0 J5 \& W6 h. v1 b9 p, F9 D
exogenous sources, nonpituitary gonadotropin stim-* {3 H% h1 }8 l5 L
ulation, and rare activating mutations.3 Virilizing
# D3 F' f1 Y. u' h5 u" s7 Y1 Mcongenital adrenal hyperplasia producing excessive; z3 f+ g( K2 i1 `9 ?$ S6 x
adrenal androgens is a common cause of precocious
$ ^2 @- Q  a  D8 I% d& lpuberty in boys.3,4
7 {1 M2 Z! {5 @" T2 X' Y' lThe most common form of congenital adrenal7 a9 }9 E8 j3 P2 V
hyperplasia is the 21-hydroxylase enzyme deficiency.
$ u/ D1 s8 g! {0 N9 o1 x, J7 T6 W, f' bThe 11-β hydroxylase deficiency may also result in* Q' R0 B% M# P
excessive adrenal androgen production, and rarely,5 E6 ?3 \6 Z! ^# B7 n5 C- h+ u
an adrenal tumor may also cause adrenal androgen
  Z2 }$ n1 E1 W6 e# dexcess.1,3
4 a9 p0 i7 K7 p% L. [% `  d6 M/ {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( B/ e' n2 z+ p542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& f: M. ^  i3 V9 h! k5 q1 i' v
A unique entity of male-limited gonadotropin-
* o! I+ `; v2 A4 [& U* cindependent precocious puberty, which is also known0 ^1 ]* N5 O4 I& F( @7 N
as testotoxicosis, may cause precocious puberty at a
5 d2 N- N! f, c% t# B% ?very young age. The physical findings in these boys
! P$ j' i  O+ Q; Hwith this disorder are full pubertal development,
& Z+ [( h, v+ t# j9 @3 Fincluding bilateral testicular growth, similar to boys
3 T1 D6 J4 P0 |3 dwith CPP. The gonadotropin levels in this disorder
3 }8 M( J2 u8 yare suppressed to prepubertal levels and do not show
9 E6 L" W0 }: |% {4 Z* j; ?pubertal response of gonadotropin after gonadotropin-
- z  @' }0 v! Q0 ?' u* K9 k! xreleasing hormone stimulation. This is a sex-linked- ~5 F$ n7 t! M) t0 P0 \8 \- a% G
autosomal dominant disorder that affects only8 |' E3 l' F& R% M, \& |
males; therefore, other male members of the family
4 z3 q* h6 J* b" I1 dmay have similar precocious puberty.32 A* P5 B( |5 c6 l, \7 r
In our patient, physical examination was incon-4 B# _- e  x+ ?# s8 J: ?) R
sistent with true precocious puberty since his testi-. L1 g5 D, I8 l0 x( _, {
cles were prepubertal in size. However, testotoxicosis( Z) p4 @8 u. c, m$ B
was in the differential diagnosis because his father" a  @# f( L( l7 l
started puberty somewhat early, and occasionally,+ R! J7 ]6 n) {
testicular enlargement is not that evident in the
; m. f  ^( V) e5 ~3 J! w4 w" tbeginning of this process.1 In the absence of a neg-) o& o+ t0 F1 h
ative initial history of androgen exposure, our8 U0 D: B' P5 W7 t7 f6 X, |+ {
biggest concern was virilizing adrenal hyperplasia,
9 |% e: \" b" s7 @either 21-hydroxylase deficiency or 11-β hydroxylase
7 S( c2 K2 d" a! j# udeficiency. Those diagnoses were excluded by find-- [8 E4 g  Q- J6 K. |6 W! Q" h" u
ing the normal level of adrenal steroids.
& J  g* u% y* ], u5 v, H4 }. j1 wThe diagnosis of exogenous androgens was strongly7 k2 y1 C: H3 H& x9 j
suspected in a follow-up visit after 4 months because
& Y$ \$ ~5 C2 X6 \  a: R$ Vthe physical examination revealed the complete disap-1 m) U7 s. ]% r" E( y
pearance of pubic hair, normal growth velocity, and. _. A& k3 C+ R- O& d% `4 Z9 x
decreased erections. The father admitted using a testos-, n6 h; x/ _7 ?! {" ^% O
terone gel, which he concealed at first visit. He was
; ~& |  ~3 z  Z; z" A' g# Xusing it rather frequently, twice a day. The Physicians’
8 L  y2 O( @, O4 f' A2 _* DDesk Reference, or package insert of this product, gel or0 ^: M. u1 t+ `5 Z- o
cream, cautions about dermal testosterone transfer to1 |( z  x# `8 z6 q
unprotected females through direct skin exposure.% k" n  C( x% M" P
Serum testosterone level was found to be 2 times the# d3 P4 D: j* w1 a$ k
baseline value in those females who were exposed to
/ [6 r4 Q# O. `2 zeven 15 minutes of direct skin contact with their male& ^  c' |/ T: x
partners.6 However, when a shirt covered the applica-
1 E2 o1 N4 _: d1 T9 ution site, this testosterone transfer was prevented.. L+ \9 u/ }  x7 x  h# J
Our patient’s testosterone level was 60 ng/mL,: a& V& A, p5 }: J2 X7 K, A! H
which was clearly high. Some studies suggest that- S; w) ]& K# b- w. l7 P3 Z9 V
dermal conversion of testosterone to dihydrotestos-
& P; U$ y2 b) _terone, which is a more potent metabolite, is more
% E6 d$ p( Z( h7 f4 Dactive in young children exposed to testosterone
' \) n% ~7 Q$ G5 S( Aexogenously7; however, we did not measure a dihy-' a' C9 Y9 J) v+ e; F5 \
drotestosterone level in our patient. In addition to6 z  b0 L+ o0 F
virilization, exposure to exogenous testosterone in" A! E/ e) S: t
children results in an increase in growth velocity and
  h! v) F' L  A. U5 ]. yadvanced bone age, as seen in our patient.; p. H# K( o/ v! i7 V
The long-term effect of androgen exposure during: Y, d0 I' u, s& s- R  ^" g& ^6 @
early childhood on pubertal development and final
# ^4 f3 T( q0 B5 `adult height are not fully known and always remain4 e6 |/ t+ Z- o" }& s; q6 ^5 L  K! U
a concern. Children treated with short-term testos-
, {( v% P& N) q% hterone injection or topical androgen may exhibit some
$ S9 t3 s0 c1 M" F4 P: }. dacceleration of the skeletal maturation; however, after6 [# j, ^) D- Q+ s0 d! s# [
cessation of treatment, the rate of bone maturation
# D7 N  t4 q1 q, ~decelerates and gradually returns to normal.8,9# x7 G6 J( J/ O+ c9 u
There are conflicting reports and controversy
9 s1 V$ ]6 n, W1 k- dover the effect of early androgen exposure on adult
% u' n& U9 l% f# apenile length.10,11 Some reports suggest subnormal; J$ l8 @/ U3 J+ i
adult penile length, apparently because of downreg-8 Y8 f  Z, V8 H4 @, `( X
ulation of androgen receptor number.10,12 However,
0 H) b7 m' l( a# J: L0 OSutherland et al13 did not find a correlation between$ ^5 A% P4 k1 f5 o7 F, Y8 }: _
childhood testosterone exposure and reduced adult
! o7 S# \; Y- ^  h  N7 o1 w1 [penile length in clinical studies.
2 p0 O4 d" [5 z" r+ s3 s( w# KNonetheless, we do not believe our patient is2 L3 S0 C" N# `% R
going to experience any of the untoward effects from
. n8 v: K7 @  k0 I% L0 [0 |' Etestosterone exposure as mentioned earlier because
; y9 a/ x8 d, ^* `) U) ]the exposure was not for a prolonged period of time.0 A0 u0 ]* f2 k* ]' J# A
Although the bone age was advanced at the time of
& R0 r: _3 z/ F2 A5 S# v/ hdiagnosis, the child had a normal growth velocity at# G8 Y/ I5 Z! O6 W$ N% a. g  j
the follow-up visit. It is hoped that his final adult
$ H6 x9 z) u- Oheight will not be affected.
, u8 Z! [& i8 h$ A3 P+ cAlthough rarely reported, the widespread avail-
7 n- z+ C8 n2 X4 r- k5 ^4 bability of androgen products in our society may
6 E9 ?9 a( u; E' N5 |. Eindeed cause more virilization in male or female
+ x. c0 z5 L) V7 x* b3 G' ychildren than one would realize. Exposure to andro-  v$ x( @2 R# n- c" }
gen products must be considered and specific ques-0 u& c$ L/ G$ p
tioning about the use of a testosterone product or* ^- q7 V5 ]- G
gel should be asked of the family members during
: j# o5 T' Z8 w. _: K2 Pthe evaluation of any children who present with vir-9 Q# c/ B  H4 X% M: I+ r: {% J, }
ilization or peripheral precocious puberty. The diag-1 z* A' l+ M2 E$ ^' p8 p
nosis can be established by just a few tests and by
- M1 i% l% v3 R* _* b; M% b3 i% tappropriate history. The inability to obtain such a
9 c$ c4 A6 ^: g. U- Y: R# khistory, or failure to ask the specific questions, may
6 o' E4 I0 y( b) i; \8 E$ uresult in extensive, unnecessary, and expensive
8 H# Q7 w- k( t' h7 z3 f7 x" r3 Ninvestigation. The primary care physician should be  a1 J8 [4 h8 W! m8 g+ E4 b9 e5 b
aware of this fact, because most of these children
* j3 u2 {( x8 v1 D4 @; Smay initially present in their practice. The Physicians’4 m; U& \  I8 Q- X1 f/ q- g
Desk Reference and package insert should also put a
" g+ e, |, X  V9 Twarning about the virilizing effect on a male or. H1 m% \+ H6 V
female child who might come in contact with some-- G8 p% p& r" a9 a% u/ ~  z
one using any of these products.  X2 k5 t4 J) |
References
1 }. g# J6 k( D' y1. Styne DM. The testes: disorder of sexual differentiation* [2 f9 }. x# |  N; z
and puberty in the male. In: Sperling MA, ed. Pediatric
2 ^. I( T( e7 V) ~6 N) b9 OEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;/ E6 r( t( t7 J8 k; G
2002: 565-628.
; X. b- `( n7 ~& \4 _" H* G2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious$ b; V3 E) ?  {4 c! ]: O' Q
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old: z0 n  D2 C3 l. J# ^4 K! O1 y
Boy Induced by Indirect Topical. |3 T$ u% f6 l  M) ^
Exposure to Testosterone
+ m% @- b$ C0 k# w8 |, o! FSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ [, F! z$ R, b7 t0 Zand Kenneth R. Rettig, MD1% R" j4 Q6 Z' D5 J: P. ?8 y4 e, t
Clinical Pediatrics
/ _; f0 ]* c6 ]- A) \Volume 46 Number 66 `' ~, n3 F2 i+ L" r1 M4 I
July 2007 540-543
; C: g& T' f& r" F; J0 G* v© 2007 Sage Publications
; m4 q- @; Y) U* K- ~6 v10.1177/00099228062966519 b4 }  Y* V! q2 ~" Z3 R
http://clp.sagepub.com
: p6 n3 @; x2 ~, @# k) U% h& U6 Fhosted at
- ^( o( m- k8 @, C% o. m( P7 t/ Khttp://online.sagepub.com
/ H9 t) p3 F& i+ P9 J; F% GPrecocious puberty in boys, central or peripheral,2 p: s8 I2 I1 ]3 t- N0 U. W  A
is a significant concern for physicians. Central
' E( I& v( ~7 g3 E: E. s3 Tprecocious puberty (CPP), which is mediated
% A! N/ \  [+ n8 e) _( U* N  Vthrough the hypothalamic pituitary gonadal axis, has' l. P& p! S" |: @7 ~/ W+ X" X
a higher incidence of organic central nervous system% K$ J+ R+ o% R( c
lesions in boys.1,2 Virilization in boys, as manifested) c: Q' m& B7 [8 V* P( z
by enlargement of the penis, development of pubic
3 q) Z% Y0 B+ S' {7 shair, and facial acne without enlargement of testi-8 k3 G, R6 C- r
cles, suggests peripheral or pseudopuberty.1-3 We7 N, `+ `; `6 y( Y& B8 F
report a 16-month-old boy who presented with the7 P/ J9 h/ N& b' U
enlargement of the phallus and pubic hair develop-: x! R* R# r# A3 _
ment without testicular enlargement, which was due' O5 K6 [7 |3 j; C( V% M
to the unintentional exposure to androgen gel used by" N  z# v9 e+ s
the father. The family initially concealed this infor-. c3 W( f! C& Q: O! |1 e1 a2 a
mation, resulting in an extensive work-up for this, h3 b5 Q. y5 |$ t
child. Given the widespread and easy availability of
7 K8 l: n2 F" R, ^4 _testosterone gel and cream, we believe this is proba-
: G) q  f8 t# Lbly more common than the rare case report in the
, f4 k/ v% G8 j% j: ]' U& zliterature.4
( X* \$ v1 a" t$ _& P5 _  YPatient Report
/ c: T# |. L0 ?A 16-month-old white child was referred to the( B3 r# v* C1 e! K/ A: l
endocrine clinic by his pediatrician with the concern
# m& }2 `- O1 G1 L/ `of early sexual development. His mother noticed
! u% G% x! ]+ q+ Vlight colored pubic hair development when he was
4 L; o0 J8 }' l$ N' w( L2 f, m' x; c/ L& BFrom the 1Division of Pediatric Endocrinology, 2University of
+ J, B/ _0 t! m- S! V2 Y) @. VSouth Alabama Medical Center, Mobile, Alabama.) a0 D4 w' G5 V# @3 F
Address correspondence to: Samar K. Bhowmick, MD, FACE,) q: ?; w; h' ?% i
Professor of Pediatrics, University of South Alabama, College of
5 |/ V9 i7 ^! R* c: z' ]9 a0 j4 bMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
! R0 q3 A0 D' T. K% L3 Pe-mail: [email protected].
1 L3 K. m, q6 i/ B. ?  k1 labout 6 to 7 months old, which progressively became) s- q3 l) ]5 a7 B+ p. D7 n
darker. She was also concerned about the enlarge-: V6 a% Q# a# X
ment of his penis and frequent erections. The child
8 |* {1 g/ _$ M3 X6 y8 O" Q; M/ Lwas the product of a full-term normal delivery, with
0 P0 k* r' C3 f! _a birth weight of 7 lb 14 oz, and birth length of
3 E' T8 i; f/ g$ j: Y) i20 inches. He was breast-fed throughout the first year# S# `* [) M. H& z+ ^+ c
of life and was still receiving breast milk along with9 Z9 ?! j; I6 b# a
solid food. He had no hospitalizations or surgery,9 O: Z" O; V  E( q( L
and his psychosocial and psychomotor development
( h* B5 W. ~" cwas age appropriate.& @) v+ {4 g' r# z  ?/ P6 b
The family history was remarkable for the father,
- ~1 \, r) Y+ V8 a. v0 owho was diagnosed with hypothyroidism at age 16,
( \; [5 H. h) H* V* g  |which was treated with thyroxine. The father’s8 |* z" }0 a* N4 O
height was 6 feet, and he went through a somewhat8 _/ ^0 K$ h) j( D! h3 ?
early puberty and had stopped growing by age 14.- J( u# ^/ c) G% v2 f4 z
The father denied taking any other medication. The6 W6 Q! o& t; e. }; E2 _
child’s mother was in good health. Her menarche% V% c' J, d. _4 O. `8 u
was at 11 years of age, and her height was at 5 feet
9 t6 E% M! ]& `* S5 inches. There was no other family history of pre-$ h: U% C. o& A& l2 K
cocious sexual development in the first-degree rela-, n" M+ A$ M: S! s; Y% o. D# Q
tives. There were no siblings.
  ]! ]) |9 ~) tPhysical Examination
6 h) O& V" s0 x8 F+ MThe physical examination revealed a very active,
8 y  I! N2 Q9 Y( O5 y6 oplayful, and healthy boy. The vital signs documented
+ ?2 h7 g1 x; k' X9 A7 e2 ^, \# W7 ia blood pressure of 85/50 mm Hg, his length was
( u1 S8 _  `5 `) S90 cm (>97th percentile), and his weight was 14.4 kg9 [* A5 p+ e& Z8 m' c
(also >97th percentile). The observed yearly growth
  Z8 l2 `' E( c& O" m. E! M0 vvelocity was 30 cm (12 inches). The examination of
, m+ J& ~- y* ithe neck revealed no thyroid enlargement.
4 l# D. u2 E, u# F. `The genitourinary examination was remarkable for9 V! p0 a6 @( v; `
enlargement of the penis, with a stretched length of6 S* K: O, p6 j
8 cm and a width of 2 cm. The glans penis was very well
. N. \. q4 D$ y5 [4 g: fdeveloped. The pubic hair was Tanner II, mostly around
0 ^+ A3 @5 T. d0 V  R/ I5404 |9 x: i3 W8 C% I/ H# W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  U' L  {) f+ q7 q% W2 cthe base of the phallus and was dark and curled. The  u0 p5 e% _2 p" @
testicular volume was prepubertal at 2 mL each.1 y8 ~, i' v6 R) b+ e+ M6 t
The skin was moist and smooth and somewhat% x! q; w7 ?  u& u( ?- E) L
oily. No axillary hair was noted. There were no
+ y+ U" D" H* s: babnormal skin pigmentations or café-au-lait spots.
# ^/ ~7 Y0 D+ aNeurologic evaluation showed deep tendon reflex 2+
+ A' U, F3 w. P' v; L2 c+ o/ cbilateral and symmetrical. There was no suggestion5 _/ }* F3 [! F$ ~+ P% o
of papilledema.
) A, O2 `7 s5 Q) n" |Laboratory Evaluation( I2 j$ n* L  N. ^1 b
The bone age was consistent with 28 months by1 L2 M0 V' ?. _8 Z/ o) t
using the standard of Greulich and Pyle at a chrono-
6 C! c: f( U9 J1 Alogic age of 16 months (advanced).5 Chromosomal" |/ H  u1 _2 O% }4 \
karyotype was 46XY. The thyroid function test) W( d! D* B% o
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
6 V3 Q+ u0 M) xlating hormone level was 1.3 µIU/mL (both normal).) H$ k* ~* G1 v: f
The concentrations of serum electrolytes, blood$ |# r" q; @0 ]$ o& }
urea nitrogen, creatinine, and calcium all were6 l7 P/ j, |# J9 B/ d' Q8 L
within normal range for his age. The concentration
$ j0 P: [) s( j. H: Q1 Jof serum 17-hydroxyprogesterone was 16 ng/dL
: n; e; F8 i& {1 w* w$ R6 C(normal, 3 to 90 ng/dL), androstenedione was 20
; x( T& n4 Q) v! ^ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 o% s; f' G2 Q3 G1 I) V( a( ~terone was 38 ng/dL (normal, 50 to 760 ng/dL),/ S0 |0 T$ R5 ?6 o4 \0 C$ ]
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
) X2 ~& e8 K% T( M9 N  g: N0 _49ng/dL), 11-desoxycortisol (specific compound S)3 L" M3 h( Q, T
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 e+ [, I! L( l0 \
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 ~1 n. s5 y& d
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; `5 a: E7 W* A7 h' J: k/ Z* `and β-human chorionic gonadotropin was less than! [, e3 \( S2 u- X
5 mIU/mL (normal <5 mIU/mL). Serum follicular. t. o+ i, Z$ n, E6 `
stimulating hormone and leuteinizing hormone0 c1 ^( s& {; E: \. n
concentrations were less than 0.05 mIU/mL
% `8 \. i6 i8 c; R(prepubertal).
  N- [9 v/ e! v7 hThe parents were notified about the laboratory6 z  d  Q3 @; ?8 A
results and were informed that all of the tests were9 t2 y' E, N4 p+ v3 R/ ~
normal except the testosterone level was high. The7 {" F6 s  d) _5 W  R' L  Z
follow-up visit was arranged within a few weeks to
5 S0 }' G$ D4 X6 ?2 C- ?obtain testicular and abdominal sonograms; how-
) I5 q/ p: D: x2 Mever, the family did not return for 4 months.% y( `3 s) u) v/ l) O" V6 A
Physical examination at this time revealed that the8 f, B3 V# M1 d; ~7 f$ I
child had grown 2.5 cm in 4 months and had gained
. Q! E- @* v* V0 O2 kg of weight. Physical examination remained& u8 Z" }# q$ K* s
unchanged. Surprisingly, the pubic hair almost com-$ k9 a: i: f0 r# R  }
pletely disappeared except for a few vellous hairs at& i. b+ k" a) z+ u' s
the base of the phallus. Testicular volume was still 2! \; f* ?% q6 h3 z
mL, and the size of the penis remained unchanged.
3 W$ H- e! w) ]The mother also said that the boy was no longer hav-
9 D7 g9 |5 \+ ^ing frequent erections.
" H% H6 v8 V9 v$ W" s! u3 Y8 uBoth parents were again questioned about use of6 J; [/ V) D" n+ N! V+ G
any ointment/creams that they may have applied to
  B# @# b, d- R9 V; Uthe child’s skin. This time the father admitted the* ~" @& c; T0 w9 c! D3 v
Topical Testosterone Exposure / Bhowmick et al 541
7 ]) l: G9 l9 tuse of testosterone gel twice daily that he was apply-
0 T% a5 C; v7 wing over his own shoulders, chest, and back area for6 V8 q) n2 R* i  L
a year. The father also revealed he was embarrassed
! _5 c8 C5 @9 n, z3 N# Bto disclose that he was using a testosterone gel pre-
: s; L; R- w2 u# ~  Ascribed by his family physician for decreased libido
! Y# X1 O  g; _/ ^7 osecondary to depression.1 N( u0 ]& t0 ~2 ~  W
The child slept in the same bed with parents.
; g. \7 Y2 u% ]# I' Q. GThe father would hug the baby and hold him on his* h+ ~$ ^8 ^6 x* _8 D& c  Q& P
chest for a considerable period of time, causing sig-& E( d2 x  p* C
nificant bare skin contact between baby and father.
4 U& N) D0 {' C& A! _6 ~  |The father also admitted that after the phone call,2 ]: p# ~1 P. n: \1 F) \3 I" D
when he learned the testosterone level in the baby9 }7 g$ |1 X; M- m* k* |& s
was high, he then read the product information  u# ~; ^4 K6 T5 n( q9 t, G
packet and concluded that it was most likely the rea-% [8 f" g, t8 i+ E7 l
son for the child’s virilization. At that time, they6 J3 h; w( o0 n+ Q  F1 s+ Z
decided to put the baby in a separate bed, and the5 m6 S, Y9 R; M0 q& d2 g
father was not hugging him with bare skin and had  }7 {$ F; U3 B
been using protective clothing. A repeat testosterone4 v" s6 A5 l* @, G% \3 S3 B  e
test was ordered, but the family did not go to the
) V: q3 g6 ^" D2 t6 [8 klaboratory to obtain the test.
( [' U7 h. S0 V4 Y. ZDiscussion
3 q$ Q6 O4 Z  d* D: @! l$ MPrecocious puberty in boys is defined as secondary
/ t9 J/ a: O* i" u4 Ysexual development before 9 years of age.1,4
: ^5 r+ L' u7 _  y$ p1 |Precocious puberty is termed as central (true) when: ]. S- C5 u" l! k/ P* w( n* ~
it is caused by the premature activation of hypo-
  x) R7 g, r' p. Tthalamic pituitary gonadal axis. CPP is more com-# T: A  W& ]4 z
mon in girls than in boys.1,3 Most boys with CPP. a. D! |, e; S& v
may have a central nervous system lesion that is3 N9 o6 Q0 J3 O0 T: p
responsible for the early activation of the hypothal-
& s# {; {0 R. m# z) p- j1 N1 Samic pituitary gonadal axis.1-3 Thus, greater empha-1 o2 a  v) l+ {8 I' x
sis has been given to neuroradiologic imaging in
# [; B  P4 J: F: [' F9 X/ n6 rboys with precocious puberty. In addition to viril-0 o8 l2 O0 b2 [
ization, the clinical hallmark of CPP is the symmet-
" P' I6 j+ f4 G: Drical testicular growth secondary to stimulation by; a( w" r3 G, i  l8 p0 H
gonadotropins.1,3$ ]6 ]8 H: ?6 ^  E; f
Gonadotropin-independent peripheral preco-; ~# ^0 L/ C6 ~5 F( Q! x( S8 n
cious puberty in boys also results from inappropriate$ M! A4 o# o( a( z+ J8 X
androgenic stimulation from either endogenous or: C) ~3 d' h6 e6 E8 X
exogenous sources, nonpituitary gonadotropin stim-
! C/ q9 W' x5 f& s5 yulation, and rare activating mutations.3 Virilizing
' p# o! M0 ]% F/ Icongenital adrenal hyperplasia producing excessive
) A0 s3 ?" h8 c6 ^4 W0 D% Tadrenal androgens is a common cause of precocious
0 V0 p) P. O/ d7 Fpuberty in boys.3,4. ?. o+ }' V9 w  k; w7 R4 m
The most common form of congenital adrenal
6 T2 c1 O6 V5 I. s9 ]3 hhyperplasia is the 21-hydroxylase enzyme deficiency.
; q! z) L7 B, \5 D3 s* ]6 WThe 11-β hydroxylase deficiency may also result in
! P3 l! A! p/ p7 l3 Mexcessive adrenal androgen production, and rarely,! I# C" r1 X# B" C& K. }1 f
an adrenal tumor may also cause adrenal androgen
1 G$ G! s: {" qexcess.1,3
* D5 A7 X2 W4 _$ {0 x) l* e/ `, g  q* xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 Z. T0 r8 r) e* V/ e0 w/ v542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
# C% u0 ~3 b2 \' I+ N# PA unique entity of male-limited gonadotropin-
, c( U- [4 E) S* Uindependent precocious puberty, which is also known& S5 J, ~' C1 p0 U) r2 H
as testotoxicosis, may cause precocious puberty at a
. {$ {8 L3 y0 e& U+ K. e2 lvery young age. The physical findings in these boys4 C) u& j4 d- g3 a% P
with this disorder are full pubertal development,, `( c4 U1 B* n5 i
including bilateral testicular growth, similar to boys
2 o% \8 T3 y+ ?* V9 l& e, Iwith CPP. The gonadotropin levels in this disorder
2 H- g5 W8 P0 ]" G* \7 uare suppressed to prepubertal levels and do not show
9 ^$ p* o+ p% @5 o- Spubertal response of gonadotropin after gonadotropin-0 A2 L" s: I, Z4 m$ q5 r# i; x
releasing hormone stimulation. This is a sex-linked5 w0 ]. q# |& O: g
autosomal dominant disorder that affects only, c3 a$ Y: J! ?
males; therefore, other male members of the family
2 }! \9 N, M! B$ amay have similar precocious puberty.3. h6 L6 X/ `9 D: \
In our patient, physical examination was incon-: `& _; o1 M4 r. k+ l* K6 ?2 m6 c3 G
sistent with true precocious puberty since his testi-3 d. F  o- e' ~, r! a# x
cles were prepubertal in size. However, testotoxicosis
  r9 t/ Y, i' ]4 H# G) [; h; S0 J" Mwas in the differential diagnosis because his father
) y+ L- K# \+ C( w0 x# dstarted puberty somewhat early, and occasionally,
/ `1 ]: d& w0 A% z/ Etesticular enlargement is not that evident in the
: K) }8 w' l6 K: {# X: o; C" nbeginning of this process.1 In the absence of a neg-
5 N, V. _% ^2 z7 i* n" j% Jative initial history of androgen exposure, our
3 m# @2 o! [2 i! }; [# a: ^$ x1 }biggest concern was virilizing adrenal hyperplasia,/ O( g6 S" T/ A% p
either 21-hydroxylase deficiency or 11-β hydroxylase/ K% g7 F, W  i4 j0 [4 H- q
deficiency. Those diagnoses were excluded by find-
) h4 O7 R8 l9 _6 \4 ting the normal level of adrenal steroids.% t0 B  B, c8 l- _7 u/ M
The diagnosis of exogenous androgens was strongly6 T' _8 j  h4 p% G. Z4 R
suspected in a follow-up visit after 4 months because
4 J/ R4 Y# C0 cthe physical examination revealed the complete disap-
  ?$ ?% W# ?" f" \) Ipearance of pubic hair, normal growth velocity, and- |- |5 r- ?& O* f7 J2 j
decreased erections. The father admitted using a testos-8 i$ O- Z! t2 @
terone gel, which he concealed at first visit. He was
2 k$ g& E. O9 A* pusing it rather frequently, twice a day. The Physicians’
3 x4 ~, K1 Y# i% t; X( DDesk Reference, or package insert of this product, gel or3 r+ K; j8 w/ C7 g) A* ^
cream, cautions about dermal testosterone transfer to! d% E2 \4 \7 m/ r
unprotected females through direct skin exposure.
3 A2 T( ^5 E. F. V2 D. U6 VSerum testosterone level was found to be 2 times the
" V# r2 m. a5 P; Ybaseline value in those females who were exposed to
' r3 x/ N9 X: Qeven 15 minutes of direct skin contact with their male- V) a. a2 g# V
partners.6 However, when a shirt covered the applica-
6 e6 ?4 _& l- C) J' Mtion site, this testosterone transfer was prevented.6 b1 I' y: y. r, c3 P
Our patient’s testosterone level was 60 ng/mL,
9 S6 V7 E$ d. V* l5 @& xwhich was clearly high. Some studies suggest that
0 ?9 _; @: ^! I! f8 |$ h7 vdermal conversion of testosterone to dihydrotestos-
9 Q7 @. `# e, m3 pterone, which is a more potent metabolite, is more/ t! |1 @) C5 j" j
active in young children exposed to testosterone" p- W8 D. U" i* n5 L5 ]+ I2 J( Z
exogenously7; however, we did not measure a dihy-/ N) X- ?1 [/ m8 f+ O/ f
drotestosterone level in our patient. In addition to, G& O" v! A# u; E) W. N1 m; \( @
virilization, exposure to exogenous testosterone in) L  T9 d, @, `* t) r# Q8 A- F
children results in an increase in growth velocity and8 ?1 x+ r9 \' p  A9 p1 U# K9 Q
advanced bone age, as seen in our patient.
+ J# _# N% q* s0 N& z. a7 UThe long-term effect of androgen exposure during; s4 t- B$ j( o- d' a3 f9 z
early childhood on pubertal development and final
! H' U  ]: `8 z' s5 c3 b& D2 badult height are not fully known and always remain  c4 P/ m( L* i  z6 m
a concern. Children treated with short-term testos-
' i! j( S9 S9 g+ Q: m7 Z0 A8 cterone injection or topical androgen may exhibit some8 s4 h: a: k& C9 p& ?& A: ?
acceleration of the skeletal maturation; however, after: t6 I" l# t: |
cessation of treatment, the rate of bone maturation6 D* P& S7 ]$ ]5 b$ x" B( r2 [; @
decelerates and gradually returns to normal.8,98 z3 w8 v% s* N* V6 [6 g
There are conflicting reports and controversy& v2 O; r+ |2 M! E0 s  n4 Y
over the effect of early androgen exposure on adult% c- }/ z: l0 d& M
penile length.10,11 Some reports suggest subnormal
/ g1 ?* M2 r1 h0 ^9 {% Q& Eadult penile length, apparently because of downreg-
+ R* I# d. T& }- nulation of androgen receptor number.10,12 However,
( }- X* f2 _' [% NSutherland et al13 did not find a correlation between* c6 V6 Z* f5 W
childhood testosterone exposure and reduced adult
) U: Y" y( U% ?. Z1 Zpenile length in clinical studies.
; Y. c5 R( B3 q" L) J5 iNonetheless, we do not believe our patient is5 r7 P, k# ?% U) q- b5 j% n
going to experience any of the untoward effects from
' U/ R) a; h0 [* c! B' dtestosterone exposure as mentioned earlier because! r6 I, q/ f( J6 U6 e" ?: {( y4 L. i
the exposure was not for a prolonged period of time., F' S' l! P( ~8 q8 M/ q. y5 @
Although the bone age was advanced at the time of
* I* j( b8 k" Vdiagnosis, the child had a normal growth velocity at
2 N4 Y! J: |2 E+ k' k. F, Athe follow-up visit. It is hoped that his final adult
0 N, T- K/ h6 ?" {1 ?height will not be affected./ \( i& p; q0 b- D% D
Although rarely reported, the widespread avail-7 a, X, A# @: R" Q7 g! t
ability of androgen products in our society may2 Z) ]6 U7 V$ q
indeed cause more virilization in male or female! y. z. N# }0 @' ]
children than one would realize. Exposure to andro-
$ i8 m1 w# G( R$ o( G2 z* q8 s1 G. Qgen products must be considered and specific ques-
6 e8 A# Y. n  `1 N4 e: z" stioning about the use of a testosterone product or
; f  D6 V. b2 mgel should be asked of the family members during
7 e4 C: g2 I9 }7 T% E" M' Cthe evaluation of any children who present with vir-
; N) h, C% Z6 l- Bilization or peripheral precocious puberty. The diag-* g4 V6 X# _. I" C# C6 V/ i; [9 j
nosis can be established by just a few tests and by7 h0 J6 a5 s- q3 n* X
appropriate history. The inability to obtain such a
6 Q) S/ N, N: i2 U" c9 H- Z" Q% K% \history, or failure to ask the specific questions, may
  l3 G/ {. h0 c/ B1 t5 Gresult in extensive, unnecessary, and expensive/ S0 B) O' Z. R0 [( }9 @
investigation. The primary care physician should be( R: U$ f# G1 b' _* E
aware of this fact, because most of these children' O1 |4 I; i, `/ V7 z1 N+ I. g
may initially present in their practice. The Physicians’
2 ?& u; `9 W3 m0 _Desk Reference and package insert should also put a
; W$ e, K, N9 W. iwarning about the virilizing effect on a male or
; ]5 {  @, y1 t2 R" x1 xfemale child who might come in contact with some-
- O/ x2 Y/ _& \9 ~, o- ]; Zone using any of these products.
7 a( [  m* k8 y) H' O! n4 o* AReferences1 N0 E$ U7 O% n5 R9 D8 v
1. Styne DM. The testes: disorder of sexual differentiation
- q+ C* h8 A8 K  I5 x; A9 land puberty in the male. In: Sperling MA, ed. Pediatric
2 [; S. Y0 A& d4 d. T+ V& JEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 P  S, r2 D, h1 g2 `1 ~4 f
2002: 565-628.0 S) F- g2 ?  ~; ?+ c9 l
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
# A" {0 K+ L7 Z4 W% s: s$ m5 ypuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
. Q8 N" K2 [; N" S
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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