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Sexual Precocity in a 16-Month-Old% j# v% H4 c( O2 F$ Y
Boy Induced by Indirect Topical5 w4 `) ^/ Y) F! @  E  y0 M3 Z
Exposure to Testosterone* ^( b+ y1 |% F# \# @4 s+ _8 O
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 V: l: l# g9 W+ {; Jand Kenneth R. Rettig, MD1
. e5 J7 Z3 w& b' l# Y4 p' u9 b1 hClinical Pediatrics( {9 \4 X& y7 U# m/ W
Volume 46 Number 6
: m& d9 c" J) Y, Z4 ?; y% q) [July 2007 540-543
7 B5 F& l+ Z# Q+ ?, e& l% y© 2007 Sage Publications, E% r/ K" D& B( @! N
10.1177/0009922806296651
' a5 X6 v( a/ X8 Hhttp://clp.sagepub.com
) G$ i$ P% }9 J8 V5 I- y( a, b% ?* Whosted at
5 w& e! G5 S& _- d9 m& F/ mhttp://online.sagepub.com
* v0 O2 H3 U; @1 q* K* N, m2 fPrecocious puberty in boys, central or peripheral,6 ^5 O0 z$ V% k7 O
is a significant concern for physicians. Central
; v; k/ r2 w& M+ xprecocious puberty (CPP), which is mediated
3 j0 P( }2 r/ k# @through the hypothalamic pituitary gonadal axis, has% d! z( s# Y4 V; D' K/ w' ?' E4 q1 b$ c
a higher incidence of organic central nervous system
% F0 e+ g5 E3 n, s) q$ Wlesions in boys.1,2 Virilization in boys, as manifested1 M1 `8 y5 v3 F: X) d3 j
by enlargement of the penis, development of pubic% t& D& w: v8 t2 K6 E5 W7 U' L
hair, and facial acne without enlargement of testi-; D* D% _; x9 P. {
cles, suggests peripheral or pseudopuberty.1-3 We. n% h! O8 A* {7 X
report a 16-month-old boy who presented with the
+ {9 c7 }: v, g, ~5 k( {enlargement of the phallus and pubic hair develop-; k2 i5 C+ J3 }" Q) e7 S3 D
ment without testicular enlargement, which was due3 O9 |2 S' d# }& s% c$ b; D/ s' s3 ^5 I
to the unintentional exposure to androgen gel used by; }) P# s4 y4 w+ X3 i4 y
the father. The family initially concealed this infor-
8 t' `0 J# w+ b+ ~( d2 J7 Q( Y) S" omation, resulting in an extensive work-up for this
9 M/ B! P/ O1 H4 ]child. Given the widespread and easy availability of' i9 e8 y/ G6 d" v- v1 n- m
testosterone gel and cream, we believe this is proba-
/ P+ T. C: ^; N5 ~% F5 N. U0 `bly more common than the rare case report in the
8 e0 e5 @3 N" u. pliterature.4
" a1 N: Q  q/ C. j0 nPatient Report) {) W/ k; z- _' M; V0 q. l
A 16-month-old white child was referred to the$ o  {% w- L, W
endocrine clinic by his pediatrician with the concern
& _! v% Y) w0 ~of early sexual development. His mother noticed( H/ [' |& J9 B5 v& _# G# [) J- c
light colored pubic hair development when he was
) R$ p2 v. o) QFrom the 1Division of Pediatric Endocrinology, 2University of' G9 v3 p8 x; U# {. Z( z' U" ^# G
South Alabama Medical Center, Mobile, Alabama.
6 I$ Z; L+ x, g/ pAddress correspondence to: Samar K. Bhowmick, MD, FACE,
) E' J7 d+ S: D( SProfessor of Pediatrics, University of South Alabama, College of, n6 i- H! s( j# n8 a
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 n" t  S6 |: n2 ^( C0 M8 C
e-mail: [email protected].
  k8 k. `1 O, k$ [3 Uabout 6 to 7 months old, which progressively became
! X- L' }' ^9 ]6 |6 Cdarker. She was also concerned about the enlarge-/ \6 \; v% e, f' T; b  {
ment of his penis and frequent erections. The child
9 y. [4 F& H% v7 j+ _was the product of a full-term normal delivery, with
& W) W% T  R$ Za birth weight of 7 lb 14 oz, and birth length of) q, X# [; O2 I" T3 V4 t
20 inches. He was breast-fed throughout the first year
( ?2 [$ q. V; ^9 D# s1 Pof life and was still receiving breast milk along with( P+ V+ o7 Z/ y" ]2 w) ]; t
solid food. He had no hospitalizations or surgery,3 J6 U" F3 [* }1 Y
and his psychosocial and psychomotor development. m# ^7 d+ D1 ], V& D
was age appropriate.
" h6 F# J/ ^; S; I: f- |, n" Y# yThe family history was remarkable for the father,+ P* f2 j& x' g4 F* z+ n8 H
who was diagnosed with hypothyroidism at age 16,
5 f3 O3 p- V8 ]which was treated with thyroxine. The father’s
% L) l- S+ E" W9 Iheight was 6 feet, and he went through a somewhat
  r( m9 Z% x% Y4 F6 z. Dearly puberty and had stopped growing by age 14.
5 X! Y( C9 \7 y% _The father denied taking any other medication. The
$ Y5 h+ ]1 [. Y% Y9 hchild’s mother was in good health. Her menarche
0 V# f7 [  g6 u1 o4 xwas at 11 years of age, and her height was at 5 feet
$ D5 ]* F; n$ M: H; T8 D5 inches. There was no other family history of pre-( c3 ]9 F9 l( }% I2 _( p2 _
cocious sexual development in the first-degree rela-: W# n1 R' [$ t4 E2 x, c
tives. There were no siblings.
8 u/ z* z8 @" S" k8 P- hPhysical Examination5 _& D8 X* Y- w
The physical examination revealed a very active,
7 W; n1 g" N) ^* B6 Wplayful, and healthy boy. The vital signs documented3 o1 G9 G/ [9 l$ V
a blood pressure of 85/50 mm Hg, his length was
: ?& K9 a4 D1 ?/ S' q1 C, C9 e90 cm (>97th percentile), and his weight was 14.4 kg4 G" R% Q- |) @( W, `2 v9 R
(also >97th percentile). The observed yearly growth/ R, |( r9 G  e3 }* f
velocity was 30 cm (12 inches). The examination of0 G7 t9 E8 l8 G- Z& K! z) m
the neck revealed no thyroid enlargement.
5 A& c3 M; m$ ]% V. H  \The genitourinary examination was remarkable for
# g2 M# n6 z" t+ b3 X7 Kenlargement of the penis, with a stretched length of% `7 z! ?4 P9 M# |
8 cm and a width of 2 cm. The glans penis was very well
- o4 c- v* x3 udeveloped. The pubic hair was Tanner II, mostly around8 n& R0 H/ S" o! m) X; F% D+ k5 m. M
540
! r. B! d9 m+ v0 N2 o0 m; wat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
- r" L  o; O. S  mthe base of the phallus and was dark and curled. The
1 U: x6 P8 G1 G5 U$ Ctesticular volume was prepubertal at 2 mL each.8 |7 h: m8 E. c& {. D0 u) q
The skin was moist and smooth and somewhat
' i. P; a9 p" k+ y# }/ Ioily. No axillary hair was noted. There were no$ E& U6 B' m, R1 P+ b, |& k
abnormal skin pigmentations or café-au-lait spots.( t. e/ f3 C0 o8 ~
Neurologic evaluation showed deep tendon reflex 2+; F7 |/ N$ y9 ~1 ^/ R, U* K
bilateral and symmetrical. There was no suggestion
5 C- c+ G1 E: \/ {  A* uof papilledema.' B# j/ [* b: L+ K
Laboratory Evaluation6 M- }" B- b* |  @. c
The bone age was consistent with 28 months by
4 E& J: n( y3 r9 U# q( _! kusing the standard of Greulich and Pyle at a chrono-
1 C9 u! H/ S) i8 n/ W$ F7 h4 vlogic age of 16 months (advanced).5 Chromosomal( d: W' v+ J) q( Q+ m
karyotype was 46XY. The thyroid function test1 t$ K. m9 V- U+ i; u
showed a free T4 of 1.69 ng/dL, and thyroid stimu-9 n- l" v# D4 O2 ]1 L
lating hormone level was 1.3 µIU/mL (both normal).
' B4 M, `7 B( e2 w- zThe concentrations of serum electrolytes, blood, F, S  l3 u0 ~% \9 j/ g" t# C
urea nitrogen, creatinine, and calcium all were( z7 F% `' o: ?5 v3 H# R
within normal range for his age. The concentration
# m4 H0 T( H$ j2 J6 Iof serum 17-hydroxyprogesterone was 16 ng/dL
! y  z9 W- I7 s# s+ Y8 l(normal, 3 to 90 ng/dL), androstenedione was 20
" W3 s0 G4 m# Jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 H" X/ |4 H+ f/ v5 p
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' C6 }- q5 v6 R
desoxycorticosterone was 4.3 ng/dL (normal, 7 to! C9 E4 }' n2 M6 g
49ng/dL), 11-desoxycortisol (specific compound S)
: f1 j7 e6 X0 F6 Fwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
8 e3 D3 a* ~& L! B% ^tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
% }( J% k, _3 Ltestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
: Q4 V, D4 R0 e6 \6 c" sand β-human chorionic gonadotropin was less than
: z+ P. j3 s) }- q4 U" ^5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ x9 [$ ~+ r/ ^  o1 c2 Mstimulating hormone and leuteinizing hormone; h7 b# v& {5 z" X# O  T8 }% b
concentrations were less than 0.05 mIU/mL
  |1 ]% {+ E4 ]! Y  y( u* Y- F(prepubertal).( A+ c5 h& I% Q, R+ j; }
The parents were notified about the laboratory: S9 O. Y. z7 F& z1 O/ m# {
results and were informed that all of the tests were
$ ~. Q9 h5 e( S4 Y* cnormal except the testosterone level was high. The
* o/ Y1 h  H& i( c1 Vfollow-up visit was arranged within a few weeks to
0 Y. q7 J0 @+ ~5 w& Zobtain testicular and abdominal sonograms; how-8 @' \* m0 _7 q+ n
ever, the family did not return for 4 months.7 t% O& F1 [1 d
Physical examination at this time revealed that the
( \5 j0 |1 u# W( @7 [1 l- C$ dchild had grown 2.5 cm in 4 months and had gained( P7 d/ u: o  V8 t7 {& Y  x
2 kg of weight. Physical examination remained( @2 {1 m. }1 g$ D: v' e( ^- I* D+ F
unchanged. Surprisingly, the pubic hair almost com-
" Z# t( v" i& Qpletely disappeared except for a few vellous hairs at
; f+ K" j* U: E  D# dthe base of the phallus. Testicular volume was still 2
- L) x: e' y8 v* s+ R% LmL, and the size of the penis remained unchanged.3 \8 [1 q( S; S4 r, R3 }
The mother also said that the boy was no longer hav-8 ?4 @7 d) l4 O& e- ]7 Z
ing frequent erections.+ \( [1 b( V7 V6 [! w( }
Both parents were again questioned about use of
) ~1 E8 {. b& N5 Oany ointment/creams that they may have applied to/ @( ^# L2 E/ Z8 v7 f2 T
the child’s skin. This time the father admitted the: |3 L! X# O: M- H
Topical Testosterone Exposure / Bhowmick et al 541" d- U2 g) x& x" X+ \" I& d& s
use of testosterone gel twice daily that he was apply-% q- t5 U/ _. e* L, L
ing over his own shoulders, chest, and back area for
# `; O% r3 l" o# sa year. The father also revealed he was embarrassed
( a+ L5 l7 P% c- C% c( L0 ?to disclose that he was using a testosterone gel pre-
- `7 Q- M) Z6 f7 Fscribed by his family physician for decreased libido
+ l8 r& {& C& Z3 _2 ]secondary to depression.: O5 ~* ^& |1 K# @) g6 ?, F
The child slept in the same bed with parents.
! S% I! R& L/ }The father would hug the baby and hold him on his
6 f5 E- e+ ~0 K. H" [9 ~. y" l( c8 echest for a considerable period of time, causing sig-3 T; O' E2 j/ p6 j7 e  d, w+ y
nificant bare skin contact between baby and father.
# P+ [1 Q5 C7 P( M) W# wThe father also admitted that after the phone call,- p+ ^+ x9 Q( E
when he learned the testosterone level in the baby+ T% L2 f8 n& T; u: P* g" g3 }
was high, he then read the product information
# Q+ d# `) s  D8 W( e& }$ gpacket and concluded that it was most likely the rea-# F4 i5 w8 n" @+ L! e
son for the child’s virilization. At that time, they! g  D' [, _# f# N
decided to put the baby in a separate bed, and the
! L% R; {" y7 p) R4 Wfather was not hugging him with bare skin and had% P' ^+ I3 Z# m2 F" D  _; ]& a' G* T
been using protective clothing. A repeat testosterone% F0 P9 ^5 D5 ]' U8 i: [. s# z) |
test was ordered, but the family did not go to the
" |. m( t9 u2 Q  w  Klaboratory to obtain the test.( q$ @+ Z/ a, t" E* y! H" Q: s' E
Discussion
8 c5 }9 [0 Z4 S9 H* n1 \* NPrecocious puberty in boys is defined as secondary
  N8 p3 i: x0 T; g/ ^( ksexual development before 9 years of age.1,4
, @  J7 a9 a" W6 {. s0 K0 rPrecocious puberty is termed as central (true) when
) R6 X( c, g: E% v' n; Y' ]it is caused by the premature activation of hypo-6 U7 T4 P4 u+ h
thalamic pituitary gonadal axis. CPP is more com-8 P0 V( n3 W. Y( i6 D- c
mon in girls than in boys.1,3 Most boys with CPP
" a  p+ P8 l, b! Imay have a central nervous system lesion that is% s) K# m( h; g2 `# i8 J
responsible for the early activation of the hypothal-
/ N/ r( Q/ Q, ramic pituitary gonadal axis.1-3 Thus, greater empha-, R, d" L4 F; ?* A* F4 }# r- ~0 u9 ^
sis has been given to neuroradiologic imaging in
! v7 Z7 x* k) Hboys with precocious puberty. In addition to viril-
& z; h, a! S) _. G/ sization, the clinical hallmark of CPP is the symmet-' G. ]+ C% P) i$ v
rical testicular growth secondary to stimulation by" d# P4 H( e" \3 l
gonadotropins.1,32 e% }/ y' @7 t5 `% ~
Gonadotropin-independent peripheral preco-1 [% _( F6 z1 [; b. ^" \) O& W) u
cious puberty in boys also results from inappropriate9 Z6 U7 p/ Y' r6 r, E/ S
androgenic stimulation from either endogenous or
/ O( X1 p) U4 l) G! ^# sexogenous sources, nonpituitary gonadotropin stim-/ K. s8 R7 I" t  h# _" f# r
ulation, and rare activating mutations.3 Virilizing
, i9 I6 k. B" d- x7 B7 s: q: O! acongenital adrenal hyperplasia producing excessive
" c2 f3 x/ d8 W/ h: J/ a1 A  S  Vadrenal androgens is a common cause of precocious
1 {# p5 a! @6 U: S! t: ?puberty in boys.3,4& I3 o, C; k' d; ~
The most common form of congenital adrenal
  [0 {# Q, O2 S: _4 Vhyperplasia is the 21-hydroxylase enzyme deficiency.* N  w. }/ f  f$ B
The 11-β hydroxylase deficiency may also result in
! i: r' C" i. ?( b' s0 ]excessive adrenal androgen production, and rarely,
1 Y3 J7 o% p5 C) K# {an adrenal tumor may also cause adrenal androgen
1 P; ]5 a$ e% @excess.1,3+ z% r$ V9 V# F3 Q$ p0 i, z; @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 e8 x8 t, |" }- I. n+ @. t
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( @3 V  a3 o/ q4 j' i3 [
A unique entity of male-limited gonadotropin-
4 M+ U# Z# M- ]independent precocious puberty, which is also known
3 E7 p+ `( M, _as testotoxicosis, may cause precocious puberty at a5 ~. W1 ]1 B7 p
very young age. The physical findings in these boys
% r2 \6 H" A2 ewith this disorder are full pubertal development,3 U3 S2 G$ E9 W
including bilateral testicular growth, similar to boys
8 v+ b0 e, ?+ Z" i2 J" zwith CPP. The gonadotropin levels in this disorder
# j* f3 Z6 Z3 F9 h1 Lare suppressed to prepubertal levels and do not show
0 q: x- ~0 M8 N$ q: l- npubertal response of gonadotropin after gonadotropin-
0 C! `0 N! G* m4 ?- M) E# Ireleasing hormone stimulation. This is a sex-linked
8 t$ R) ]0 I- Dautosomal dominant disorder that affects only' M1 ^* T% n; n0 v' m* {
males; therefore, other male members of the family; s# s# ~+ `$ D  Z. X7 X9 D( ]- t
may have similar precocious puberty.3/ u5 P1 M6 ^2 U) i# N$ c
In our patient, physical examination was incon-
) r# {* s& b! Jsistent with true precocious puberty since his testi-
# X4 s' G/ [$ N) N; _cles were prepubertal in size. However, testotoxicosis
" N& \7 t/ ]2 ^: k4 D, i% Pwas in the differential diagnosis because his father
2 B, G+ U9 W) [+ E0 cstarted puberty somewhat early, and occasionally,
# c! L% Q8 m: t& o2 i1 otesticular enlargement is not that evident in the6 l& n  N7 x+ x2 z/ g
beginning of this process.1 In the absence of a neg-
3 ]5 _" ^- J& z' b7 @  j9 xative initial history of androgen exposure, our
$ [% u. h' @& V( Z) Zbiggest concern was virilizing adrenal hyperplasia," {" }* \" |4 f/ i
either 21-hydroxylase deficiency or 11-β hydroxylase9 |# Y5 O% q' t4 l2 W3 W
deficiency. Those diagnoses were excluded by find-6 g. ^* o1 a& z- B' L' C( Y
ing the normal level of adrenal steroids.
" O+ }9 Q9 U, Z# s9 @8 ]' ?3 h8 \The diagnosis of exogenous androgens was strongly
* I' ]. A" L8 I7 B) Z- H9 u" Zsuspected in a follow-up visit after 4 months because7 y5 P: M9 m+ H* Y  f1 v0 C; y
the physical examination revealed the complete disap-
3 {, h- p2 b! x% _1 ^, p+ opearance of pubic hair, normal growth velocity, and
' I4 R- J# l- _! G& @3 Q" qdecreased erections. The father admitted using a testos-) I+ G! F* f* x$ }/ E5 k" H
terone gel, which he concealed at first visit. He was
/ F, r) m) X4 V2 H* F+ _. a5 q7 xusing it rather frequently, twice a day. The Physicians’
/ a: @* K& D9 F2 O  ^; HDesk Reference, or package insert of this product, gel or: j: A4 M  n& b; D
cream, cautions about dermal testosterone transfer to$ g/ l) T# J, I
unprotected females through direct skin exposure.
3 A, X: O+ R7 a$ A* _- PSerum testosterone level was found to be 2 times the
+ E# \# ~, A% S- X: r' j- tbaseline value in those females who were exposed to
( p4 @* O7 p4 @$ F. J2 Heven 15 minutes of direct skin contact with their male
* U( ]! X7 M+ G9 ~/ Mpartners.6 However, when a shirt covered the applica-/ n, Z6 B, T, F) \
tion site, this testosterone transfer was prevented.
" `5 }% \; \  {+ l. i6 }Our patient’s testosterone level was 60 ng/mL,, z) v* g& g' T( Y4 I
which was clearly high. Some studies suggest that# U9 _3 T) T! L! l: t) S
dermal conversion of testosterone to dihydrotestos-
5 W5 S6 V0 k! s+ D8 ~terone, which is a more potent metabolite, is more
( M0 |# B; _, _3 a1 k# r! t# T2 _# W" factive in young children exposed to testosterone
) X$ G5 E1 t  U3 Iexogenously7; however, we did not measure a dihy-
( {7 ]# X) w8 r" o3 b7 Ydrotestosterone level in our patient. In addition to
  l9 L) F/ p4 o* @+ s; Yvirilization, exposure to exogenous testosterone in& o1 J, n/ x( Y5 G, U( l
children results in an increase in growth velocity and7 I, {- r$ |6 {" Z4 m4 `0 ~
advanced bone age, as seen in our patient.3 Y/ y2 d4 R  _5 S$ c0 ?
The long-term effect of androgen exposure during
7 N9 y* {/ K( v' w* nearly childhood on pubertal development and final
( ]: H# |1 m* S2 B6 j, a; X5 B7 Badult height are not fully known and always remain8 N! d2 x; P: G/ O1 [! f
a concern. Children treated with short-term testos-1 m8 _1 p; D3 y" J
terone injection or topical androgen may exhibit some
- I. z+ N% V  C" ?& c( M% [* m: U: @acceleration of the skeletal maturation; however, after9 z2 U+ ?6 R8 n
cessation of treatment, the rate of bone maturation4 @! Z' V& \$ s1 e+ \' Q" N
decelerates and gradually returns to normal.8,9
6 [# Q' l* B4 j0 {8 t' L, p( MThere are conflicting reports and controversy9 b6 h' e, T& b7 n* C3 k. J. }
over the effect of early androgen exposure on adult. Z" f. s% {0 O0 I+ o4 M
penile length.10,11 Some reports suggest subnormal
3 k4 s$ s0 A, z% H) R) M% Gadult penile length, apparently because of downreg-1 \! w8 V5 ^$ r8 b0 }  G8 ?
ulation of androgen receptor number.10,12 However,8 o* G) B/ @8 V5 Y: H$ v
Sutherland et al13 did not find a correlation between# I* `6 z% e# u9 Z! a3 d% I
childhood testosterone exposure and reduced adult
; B& ]1 o! @$ t5 H  w* }; B: apenile length in clinical studies.
% V  P, n' }1 ~; k8 D4 DNonetheless, we do not believe our patient is) V4 m: F, O- f* l* j6 i
going to experience any of the untoward effects from
9 k- ?9 p8 c/ U+ H! atestosterone exposure as mentioned earlier because' c8 m$ l% }# ~0 t& @0 m
the exposure was not for a prolonged period of time.  \2 l' O# q$ J+ J5 F( D
Although the bone age was advanced at the time of
) X4 A. J7 }2 P7 i$ cdiagnosis, the child had a normal growth velocity at1 w+ o: s) Z3 G8 F; x- ^7 j
the follow-up visit. It is hoped that his final adult
- i% |0 H9 A5 m) n1 B7 kheight will not be affected.7 a2 R" O: ^" Z
Although rarely reported, the widespread avail-3 ?3 }2 \. v$ i" b
ability of androgen products in our society may
4 L& {$ }: U0 g& O, [indeed cause more virilization in male or female
# K+ Q+ t9 @& @) kchildren than one would realize. Exposure to andro-
( h  T3 x- w% ~+ d/ qgen products must be considered and specific ques-/ a* ?! P2 @/ _7 H4 s
tioning about the use of a testosterone product or' B. L; j. c) x( ~! H
gel should be asked of the family members during8 v) N% E2 t& o  w' f
the evaluation of any children who present with vir-
/ m% E3 f. L6 `+ Y% b! _ilization or peripheral precocious puberty. The diag-2 v1 P9 l* u" c# x1 C: `. o) u
nosis can be established by just a few tests and by
  T# t- J/ b! j5 {; p" A: `7 Wappropriate history. The inability to obtain such a. C" F/ D7 L; y
history, or failure to ask the specific questions, may
5 n. D/ O, d- I! presult in extensive, unnecessary, and expensive
2 S; J3 @! v% }/ Z1 ^investigation. The primary care physician should be/ x+ Z  r: d$ O$ z* V
aware of this fact, because most of these children
5 W: m. N2 ?% _2 m; }may initially present in their practice. The Physicians’& _# r/ L4 n7 V. w
Desk Reference and package insert should also put a* U2 k$ S, T& k5 t( [. D! j" w( @
warning about the virilizing effect on a male or
) d3 Z! t$ j; W4 U0 E) h- dfemale child who might come in contact with some-6 D9 n- ~0 r$ x, c" t/ C6 J
one using any of these products.6 I5 N2 g- m3 i- ]. e/ T
References
) H+ a6 Z6 H/ l7 o7 B* X1. Styne DM. The testes: disorder of sexual differentiation$ V1 ?. @  A; _* @: n9 O
and puberty in the male. In: Sperling MA, ed. Pediatric, A/ A  P+ c9 C0 M7 N
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;9 ]% {$ U, C. {
2002: 565-628.
1 h' b* @1 H- E0 v1 d2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( S2 J0 s. C- S$ l) @
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old1 o* H& [. F1 y4 X4 z) Q
Boy Induced by Indirect Topical
. m3 D/ H3 v; s! r9 N" P, {Exposure to Testosterone
2 E+ j  p* G& @' {Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, e( v% V7 |4 d1 gand Kenneth R. Rettig, MD1. X6 {: H5 V4 ~3 [
Clinical Pediatrics4 N! k5 k& G6 c6 ^, K% l
Volume 46 Number 6# D5 L! Y3 ]3 u0 n/ J2 |
July 2007 540-543
9 p8 Y( _8 x. `1 ^7 k2 S* L- z© 2007 Sage Publications
9 h. s' v2 H5 Q; W1 @8 M3 O10.1177/0009922806296651
1 H  M; o6 n  Zhttp://clp.sagepub.com
$ h* n- J" E9 @; M% n( B3 N# nhosted at
3 }: b2 [/ U. M9 Y! t& Zhttp://online.sagepub.com. c9 N5 C$ ], R
Precocious puberty in boys, central or peripheral,0 Q2 N! @0 x5 n" o; [& g( R& W
is a significant concern for physicians. Central+ a3 N9 c. a& v. e
precocious puberty (CPP), which is mediated8 l" |3 \$ B& x4 x6 I
through the hypothalamic pituitary gonadal axis, has
" A/ s5 f8 V7 `a higher incidence of organic central nervous system
" W4 T, d# y. ?! q* v  G0 e7 zlesions in boys.1,2 Virilization in boys, as manifested* U- |: E7 G, g4 e
by enlargement of the penis, development of pubic
2 i! a% U+ H. I. ?: Yhair, and facial acne without enlargement of testi-
8 A5 k9 h8 U3 v7 bcles, suggests peripheral or pseudopuberty.1-3 We
4 s0 ~8 @4 n0 X$ G: @; Hreport a 16-month-old boy who presented with the
' P4 I5 Q( b+ L' _: uenlargement of the phallus and pubic hair develop-# t- N$ X/ f; y7 p
ment without testicular enlargement, which was due3 Q3 c2 s* ~! P3 J& M, _# K
to the unintentional exposure to androgen gel used by# y# N. S9 g: a5 e* }) |8 z9 ], P
the father. The family initially concealed this infor-
1 k+ v( ]3 E  F0 u: h$ |mation, resulting in an extensive work-up for this) \' S9 d% d/ T& x3 |( o* t
child. Given the widespread and easy availability of0 l9 \1 F3 i9 Q, |2 l0 f
testosterone gel and cream, we believe this is proba-" |7 D7 \# M0 Z" y. @/ M
bly more common than the rare case report in the! I# J3 @  `7 W, d  m0 P0 T2 h
literature.4
# J6 {1 M# h4 G, t4 f7 U9 ePatient Report9 N' ]) r- v3 n
A 16-month-old white child was referred to the
; y: X! ~1 m( s0 N' f# Jendocrine clinic by his pediatrician with the concern0 l/ R: S8 S, r8 y. n
of early sexual development. His mother noticed( G2 {4 ~% l) j% }
light colored pubic hair development when he was
; x! h( }- m! c; W3 @From the 1Division of Pediatric Endocrinology, 2University of- q* l/ h  P0 [$ o8 R
South Alabama Medical Center, Mobile, Alabama.
" `& u/ a! G/ |2 R' ~Address correspondence to: Samar K. Bhowmick, MD, FACE,
8 t$ s4 U' g' K; ~7 j" y. GProfessor of Pediatrics, University of South Alabama, College of
- {' O! w8 J7 D$ n, S# ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;4 Q8 u4 {: I$ E$ ~
e-mail: [email protected].
$ m( f% H/ ]" i6 N# k, H  Rabout 6 to 7 months old, which progressively became
, b, j1 y/ G7 z/ kdarker. She was also concerned about the enlarge-
4 m+ `  p' ^  sment of his penis and frequent erections. The child
& P+ d$ z8 `# a% O. |& _6 Rwas the product of a full-term normal delivery, with1 K2 C3 J; {/ p0 r
a birth weight of 7 lb 14 oz, and birth length of) E4 _0 Y. `5 O3 Z; j
20 inches. He was breast-fed throughout the first year3 B4 |6 _6 ]( y. o! n. ^8 M
of life and was still receiving breast milk along with/ s  @2 Y( u+ f3 }5 ?
solid food. He had no hospitalizations or surgery,& O" s8 G1 q0 l  Y
and his psychosocial and psychomotor development
: f0 Y) T+ b' cwas age appropriate.
# B# C3 o" _+ l8 \The family history was remarkable for the father,$ Y- C: Y8 E# g* a5 A, _
who was diagnosed with hypothyroidism at age 16,8 ]! G1 E# m7 D$ D' I- K  l& D* O! l
which was treated with thyroxine. The father’s
4 a: x+ P5 F! A# g' W" eheight was 6 feet, and he went through a somewhat: R" o8 e  L2 i+ R0 e
early puberty and had stopped growing by age 14.
. b* C4 b: l# g- h) h1 O, C# D. [The father denied taking any other medication. The$ a  |$ D/ Q: D4 J; l! t4 r
child’s mother was in good health. Her menarche
$ G" E* M0 \1 a* q/ x* }was at 11 years of age, and her height was at 5 feet4 G, L- Q- W0 @( H: C6 c6 W; }3 `! {
5 inches. There was no other family history of pre-- \$ N2 e7 W  p6 S
cocious sexual development in the first-degree rela-$ u; }* A9 s  T8 R& ~
tives. There were no siblings.
8 S; @9 X9 X/ RPhysical Examination
3 i+ Z" |5 q, \/ kThe physical examination revealed a very active,
2 r; L8 d' y7 i# x7 I! {8 z# @1 o$ Yplayful, and healthy boy. The vital signs documented
, \; p  x8 A$ [; qa blood pressure of 85/50 mm Hg, his length was7 A0 ^) B' a. v  o+ u
90 cm (>97th percentile), and his weight was 14.4 kg5 ]' V1 b7 e. T  A
(also >97th percentile). The observed yearly growth) |+ ^$ \9 ^& D" g. @) r' L
velocity was 30 cm (12 inches). The examination of
8 z6 c  d7 h4 H9 y# Nthe neck revealed no thyroid enlargement.
$ \; E+ ^6 M) B+ `' [" o  I  NThe genitourinary examination was remarkable for  }* e3 x* [) c: A+ L% E! t3 s4 ^" f
enlargement of the penis, with a stretched length of3 m$ L" H+ k; u$ e" O# `
8 cm and a width of 2 cm. The glans penis was very well9 _# s8 B& n+ ~+ j* _; c/ y; X
developed. The pubic hair was Tanner II, mostly around, p8 @; e  K$ Z# \& N
540( F( n. S! a* S' M) v
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ g6 B8 c2 F/ u% t" P% ]1 b
the base of the phallus and was dark and curled. The# J1 Z2 M9 Z3 u& v
testicular volume was prepubertal at 2 mL each.7 y3 f; b. E( X
The skin was moist and smooth and somewhat
5 S9 F! `$ P- ^% @% |oily. No axillary hair was noted. There were no/ Y9 i+ o4 H  M- H/ P
abnormal skin pigmentations or café-au-lait spots." B8 A: |& |: ]9 y: @) z2 |
Neurologic evaluation showed deep tendon reflex 2+( H9 M& Z+ o7 q5 p  M0 B
bilateral and symmetrical. There was no suggestion! M7 ]! Z6 X0 I8 G" `
of papilledema./ J6 [2 W9 ]6 ^
Laboratory Evaluation
( y( @& U9 M3 a8 @The bone age was consistent with 28 months by: g7 k  q! E& ^1 v8 f/ [
using the standard of Greulich and Pyle at a chrono-
' Z/ E) L. P' b* W! B& M9 U' s" [1 @logic age of 16 months (advanced).5 Chromosomal
7 Z' O" a6 z2 ]+ f+ Y1 _8 z6 Q: Ckaryotype was 46XY. The thyroid function test
- F1 ~5 d+ R/ e/ i' wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
( d% A5 {7 t* V6 Olating hormone level was 1.3 µIU/mL (both normal).( w( s1 D; @1 f. t4 b& \1 c
The concentrations of serum electrolytes, blood
0 u, V0 x$ l2 Nurea nitrogen, creatinine, and calcium all were+ z0 _3 f5 H, n- T" W5 d! e" U
within normal range for his age. The concentration
$ k+ ^* t; h% Q5 }3 b; Dof serum 17-hydroxyprogesterone was 16 ng/dL# E5 Q3 s/ _* l0 t  E9 k( B
(normal, 3 to 90 ng/dL), androstenedione was 20
# z) a# B" m1 V& {ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 X  |3 E9 y% \4 dterone was 38 ng/dL (normal, 50 to 760 ng/dL),$ n. Q( k2 x1 p4 z- [
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 r, b$ {3 w8 d  H3 x49ng/dL), 11-desoxycortisol (specific compound S)/ I; y. Z0 c( L/ g. D2 N$ N
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, O6 K, Y1 n' e) o. f* Jtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
, Q0 C# _- b# W5 q. htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ ?$ C& O& L8 [1 `. q
and β-human chorionic gonadotropin was less than
, w: j/ w! `6 L$ u! |! ]5 mIU/mL (normal <5 mIU/mL). Serum follicular
% ?2 n+ e2 u# O& j- w# C5 jstimulating hormone and leuteinizing hormone
- s' P) n+ T% n8 a) N' hconcentrations were less than 0.05 mIU/mL
" @$ f" e/ U. e* s  z, l: k! T(prepubertal).5 v1 M( y. N) F6 {( r6 f, T
The parents were notified about the laboratory
2 V  Z2 x9 ~+ p2 i# |5 \% k! u) ^results and were informed that all of the tests were( ^; P6 W4 A- G9 M' u5 M! x+ ]8 {
normal except the testosterone level was high. The! r6 u' v8 ~+ ]; z( v2 x% B
follow-up visit was arranged within a few weeks to( p. B( U' |! T8 {/ A' X
obtain testicular and abdominal sonograms; how-
% y4 E) i& a& Lever, the family did not return for 4 months.
. X" ?& j: [3 ?3 g+ JPhysical examination at this time revealed that the
# n: k  v9 u4 ~: J) ?child had grown 2.5 cm in 4 months and had gained
# d' K! @+ q, K* X; P7 |/ y2 kg of weight. Physical examination remained8 T4 `: U- @4 j( f# S7 Z
unchanged. Surprisingly, the pubic hair almost com-3 L4 h' B6 `/ x7 N, _' E; `
pletely disappeared except for a few vellous hairs at) h2 L, V7 p7 b& N2 \! ^- y1 P: ~
the base of the phallus. Testicular volume was still 22 k* U" G9 z( \, J2 p6 c
mL, and the size of the penis remained unchanged.
  J8 c8 @; s! F# M7 P5 L( x$ IThe mother also said that the boy was no longer hav-7 Z" G( W# J" J% g  E; Z* [( m
ing frequent erections.
, v3 I2 _' `" J5 M* W5 ?Both parents were again questioned about use of
9 \, `0 x; H8 n' Y! U+ T$ Tany ointment/creams that they may have applied to4 V$ o) c7 C  u1 a& a( X
the child’s skin. This time the father admitted the
2 C) m/ Z( b1 g1 X# N+ a* _4 ITopical Testosterone Exposure / Bhowmick et al 541
0 N; x4 y# v/ B& |4 quse of testosterone gel twice daily that he was apply-
, X9 ]% k. T. g: Hing over his own shoulders, chest, and back area for' r. _# k2 A( w4 l$ e: V+ P
a year. The father also revealed he was embarrassed. q9 c  u& S- ^) v
to disclose that he was using a testosterone gel pre-  G# p/ Q* k+ X% j$ k: w# |
scribed by his family physician for decreased libido: \! s& \( b9 E! G( {* z1 k! S
secondary to depression.% F; c5 L- q. L1 Z
The child slept in the same bed with parents.
% M$ @. a9 z* R7 k- x+ _! _The father would hug the baby and hold him on his( N+ ~, i. c* x0 L& ]
chest for a considerable period of time, causing sig-
; J) \# l: w" [" inificant bare skin contact between baby and father., X/ X* C+ g# P( `/ D3 G, J/ b' \
The father also admitted that after the phone call,
1 c) H8 e5 P* i/ ^: Uwhen he learned the testosterone level in the baby7 M; Y# e7 Q; n* r4 l' z1 \7 z  T
was high, he then read the product information( y$ w- z, p  M6 D+ E; m
packet and concluded that it was most likely the rea-8 y3 Q- O9 P+ y& ^$ \
son for the child’s virilization. At that time, they
3 U1 W1 V8 z, E( I$ L' Odecided to put the baby in a separate bed, and the
& p0 k2 L. O2 Afather was not hugging him with bare skin and had9 m+ P. c! _6 B# u% T
been using protective clothing. A repeat testosterone& R6 q' n- l! ~; A
test was ordered, but the family did not go to the
2 v- w. R2 g% U6 N1 klaboratory to obtain the test.
/ K, g/ p$ e% ~$ b' a4 fDiscussion
  `$ |) J; S- E. L0 T' q( F/ |Precocious puberty in boys is defined as secondary
$ t9 X( U1 c7 I. @4 o+ Tsexual development before 9 years of age.1,4
% J- f8 V3 o/ f  \* U3 SPrecocious puberty is termed as central (true) when
/ z1 x. l2 u- `/ _& C; b: Xit is caused by the premature activation of hypo-
) x: U6 Q% O& g1 tthalamic pituitary gonadal axis. CPP is more com-
; c6 h5 D4 b  f$ a, l$ B: omon in girls than in boys.1,3 Most boys with CPP
  g' q4 R6 Q* k: i/ O1 U3 ymay have a central nervous system lesion that is: q7 @* x" I8 E
responsible for the early activation of the hypothal-
# C! i9 V: u6 W* B* J# t+ i( Y* Vamic pituitary gonadal axis.1-3 Thus, greater empha-6 V9 m( S8 H8 v: W% R$ V
sis has been given to neuroradiologic imaging in
4 p( ^/ E6 q9 Z& Bboys with precocious puberty. In addition to viril-
6 x, f4 t8 C9 Y: B- mization, the clinical hallmark of CPP is the symmet-8 R( J% b6 p% E- {& f
rical testicular growth secondary to stimulation by
/ f8 {  j. Q7 vgonadotropins.1,3
" d; p6 o; w. W$ S$ y; ^Gonadotropin-independent peripheral preco-
( ]# o# V4 Z& l3 `cious puberty in boys also results from inappropriate; h& r6 g' I, e7 p
androgenic stimulation from either endogenous or
) k8 M, S7 @: }2 B3 N% t" bexogenous sources, nonpituitary gonadotropin stim-" O+ v- L0 U" n- |0 B/ `" f. u& u
ulation, and rare activating mutations.3 Virilizing
7 g3 w% b& p" L* C: T# Wcongenital adrenal hyperplasia producing excessive
& M1 q3 q  ?. m; [1 G( N- Uadrenal androgens is a common cause of precocious
; s+ O# ^: @: v& M  q: S1 kpuberty in boys.3,4
9 B. `$ P( N. V5 d1 U6 `8 Z2 }6 ^The most common form of congenital adrenal  K/ U8 j3 L( _3 ~
hyperplasia is the 21-hydroxylase enzyme deficiency.
8 _' H8 U+ r4 L3 N- y( YThe 11-β hydroxylase deficiency may also result in
  I6 x% c8 J8 t8 L5 }2 Hexcessive adrenal androgen production, and rarely,
- z$ ~) E0 B# P, W3 `5 San adrenal tumor may also cause adrenal androgen0 k4 U+ u: S$ e
excess.1,3* w$ x- R4 \- ^& X% P
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' T$ Q' I( L# b+ G! j7 m
542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 b; o9 o2 O, k2 ]$ L5 K6 b& Y
A unique entity of male-limited gonadotropin-& U# R. [* |9 E! E+ }
independent precocious puberty, which is also known
9 ^! b5 S/ ?) F3 r3 ^0 b9 v' Bas testotoxicosis, may cause precocious puberty at a/ l7 A( h5 l4 y9 u- p. L3 g
very young age. The physical findings in these boys
, B8 o$ [  T+ a' t+ d  kwith this disorder are full pubertal development,/ c% X$ M4 S: T) @2 L+ A
including bilateral testicular growth, similar to boys0 F$ ~9 v1 i/ J& R
with CPP. The gonadotropin levels in this disorder% ^; T0 U% D% ?
are suppressed to prepubertal levels and do not show
  K8 g" C" a$ t- Z- ?pubertal response of gonadotropin after gonadotropin-
; l4 i9 S" c5 Y) l0 \5 T# d9 ereleasing hormone stimulation. This is a sex-linked
7 f0 H4 }/ q% D' Y! h7 c/ iautosomal dominant disorder that affects only
& I' X* X' Q+ s! E* }4 M# s3 Pmales; therefore, other male members of the family' r) Z; t) s2 N! p0 ?" m
may have similar precocious puberty.34 a: A. e+ w# F6 _, \- v+ @
In our patient, physical examination was incon-
3 O: l, x. V# R- ]2 U2 Xsistent with true precocious puberty since his testi-( \( x& J; V. G, y+ k7 N
cles were prepubertal in size. However, testotoxicosis( W. B* x9 \7 g2 T, I* `; i! u
was in the differential diagnosis because his father/ B. b) c8 o6 f' W3 W0 G
started puberty somewhat early, and occasionally,
  q% R: k, t  @testicular enlargement is not that evident in the
, G7 g. r8 J3 L1 s6 zbeginning of this process.1 In the absence of a neg-
! E) Z- X; ?, yative initial history of androgen exposure, our9 ~# ~8 i- ~/ ?5 Q' Y9 b: {& H4 s
biggest concern was virilizing adrenal hyperplasia,/ |  p0 z6 x7 Z" I, F% b
either 21-hydroxylase deficiency or 11-β hydroxylase
4 p- E9 d2 H- \7 l. G  Z$ Xdeficiency. Those diagnoses were excluded by find-) d9 T" v0 ~( B0 X, H, ]
ing the normal level of adrenal steroids./ a: T4 E1 V' Y+ H
The diagnosis of exogenous androgens was strongly: F% @6 \0 `5 e* T2 w. J' l% w' ]
suspected in a follow-up visit after 4 months because7 n" b! q- c0 I% }
the physical examination revealed the complete disap-+ ?, |9 {  ]/ w! {9 z, v
pearance of pubic hair, normal growth velocity, and
+ u$ O  A$ L. r* j! tdecreased erections. The father admitted using a testos-8 R/ H9 h$ L  _" T
terone gel, which he concealed at first visit. He was
: M# v3 N4 M' r- cusing it rather frequently, twice a day. The Physicians’& g! p7 o8 |/ A9 j: ?
Desk Reference, or package insert of this product, gel or- A1 G4 t9 e) d' k- T4 x
cream, cautions about dermal testosterone transfer to! J; L% s2 A  ^) Z% D  @$ }  \5 _& n
unprotected females through direct skin exposure.) b7 X6 j$ F% l, r) Y( W
Serum testosterone level was found to be 2 times the9 I" _- ^. j0 S8 z7 q. X
baseline value in those females who were exposed to
( g2 r1 x# {% b: l7 P5 Jeven 15 minutes of direct skin contact with their male& E# {- k3 {, \1 ]  Z
partners.6 However, when a shirt covered the applica-3 s& k. a% Z9 n
tion site, this testosterone transfer was prevented.
: [$ |/ e$ v$ h4 _( M2 P0 jOur patient’s testosterone level was 60 ng/mL,- f; k" r' c. r, \- h
which was clearly high. Some studies suggest that
6 ]  r1 t* G- ?9 Ddermal conversion of testosterone to dihydrotestos-
9 D1 {8 ~9 g5 T# Z! o* K  G! Aterone, which is a more potent metabolite, is more
: L# b! U  P  mactive in young children exposed to testosterone
, ]" M! N9 o  s" A* i. q+ y  I' E( rexogenously7; however, we did not measure a dihy-/ H- l+ K, m/ x% `$ P/ G" i
drotestosterone level in our patient. In addition to. F$ r9 |' k, G9 ^4 L
virilization, exposure to exogenous testosterone in' F2 M1 c2 q( H& I* I. N  e! r
children results in an increase in growth velocity and" n* N: u- s0 O4 n
advanced bone age, as seen in our patient.6 q- F4 U( ~- N0 B/ w' |4 e1 r
The long-term effect of androgen exposure during
2 Y  h, w" q1 R4 Eearly childhood on pubertal development and final# g+ O) Z% w4 g$ \. t# n/ K: f- q
adult height are not fully known and always remain3 c+ P; p, x% N
a concern. Children treated with short-term testos-
, a3 n% h2 v! X* F5 E4 n7 e& iterone injection or topical androgen may exhibit some
# V( b$ v/ B) S% B2 yacceleration of the skeletal maturation; however, after
! K: T8 X0 N* u+ [( M' \" z- hcessation of treatment, the rate of bone maturation( ]7 h/ N1 ], E  O" ^, @
decelerates and gradually returns to normal.8,92 b1 d. @! A* A+ r4 T, C( B
There are conflicting reports and controversy
0 S  t/ y7 P5 s* b/ \3 h$ gover the effect of early androgen exposure on adult9 C1 g  o. ]" s+ f/ n( G7 e
penile length.10,11 Some reports suggest subnormal
- i  @( H! e& k$ S3 i3 u0 Uadult penile length, apparently because of downreg-
1 t, `  u6 ^+ a1 \ulation of androgen receptor number.10,12 However,4 g+ F; J  L9 m- w
Sutherland et al13 did not find a correlation between2 C- m, T& T$ ]
childhood testosterone exposure and reduced adult+ e8 q0 ]* G3 O
penile length in clinical studies.
( [% K3 e' T. h0 y. J' P* `9 nNonetheless, we do not believe our patient is0 `$ v( o+ ]3 N3 V! W  k
going to experience any of the untoward effects from* j) t; F: i. _$ S% d* Q* f
testosterone exposure as mentioned earlier because
+ L5 F3 L3 r+ K4 W3 Ithe exposure was not for a prolonged period of time.
4 T# ~6 G0 h8 Z1 f9 zAlthough the bone age was advanced at the time of# X, @7 ]) u' D/ W* F' L
diagnosis, the child had a normal growth velocity at& s2 Q6 {/ E2 {5 v  S: \: p  n
the follow-up visit. It is hoped that his final adult1 v& [: w5 T6 M1 T2 v
height will not be affected.3 ~2 @$ v+ F1 B6 O( C! i- ]0 [  M
Although rarely reported, the widespread avail-
5 X$ a/ M8 \' Y8 ]: m: z0 Oability of androgen products in our society may
$ Q% f* J; @3 q  Yindeed cause more virilization in male or female& y5 h3 v6 X. [+ z6 V+ W
children than one would realize. Exposure to andro-/ y2 C# N% h6 H, k3 E6 ~
gen products must be considered and specific ques-. t" J! s. i$ c3 d% s% k% Q
tioning about the use of a testosterone product or
& R$ @- _& d! F' u- d7 Ugel should be asked of the family members during. j" Q6 z& x* F3 w" O( _
the evaluation of any children who present with vir-& H  u1 ~* F& j  \& y+ P/ _7 M3 t
ilization or peripheral precocious puberty. The diag-
8 X7 X+ M( t* c, r: xnosis can be established by just a few tests and by
/ P, e  x/ Y$ c# i0 r! Sappropriate history. The inability to obtain such a: Q4 s0 V* r$ e' a9 }1 c
history, or failure to ask the specific questions, may
# q- p' Q4 N+ ^, O: k: l* aresult in extensive, unnecessary, and expensive* R4 @# Q! R: ^# W+ m
investigation. The primary care physician should be
$ m. ]( M4 p) Jaware of this fact, because most of these children
4 s! K" w1 S/ X4 Gmay initially present in their practice. The Physicians’; c6 }5 U4 |  R$ I
Desk Reference and package insert should also put a4 Q/ I) T  R+ D3 {" i! B$ K  ~! [
warning about the virilizing effect on a male or. z! r- r! X5 Q( g
female child who might come in contact with some-
& ]; b# j4 O5 k% v0 gone using any of these products.% w% \3 c. Q2 B9 h  U2 i/ L. Z
References( H0 C/ Y+ t/ `1 G/ L; |$ ?) w
1. Styne DM. The testes: disorder of sexual differentiation( D) [) {* a2 k6 Q! Y
and puberty in the male. In: Sperling MA, ed. Pediatric0 R# i6 C; L% [/ t8 ~# [$ J. f% x
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- @; ?3 ]& X& `5 K; ]2002: 565-628.
5 w" z* u" b7 _. s* r9 x2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 I! J5 F1 ?2 O9 v1 u1 V6 Lpuberty in children with tumours of the suprasellar pineal
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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
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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

3 ?  `" A+ F. a9 W, F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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