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Sexual Precocity in a 16-Month-Old
  O2 D* C6 E3 x; k6 V: k, nBoy Induced by Indirect Topical* j/ c+ C1 X4 }, K  J
Exposure to Testosterone0 I+ U# @  M  [* V  u+ A
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 G% q1 m3 H. x+ tand Kenneth R. Rettig, MD1
6 S8 E8 Z$ p: n% M( T' UClinical Pediatrics
) x2 M% M8 y- t. J* B/ Y( jVolume 46 Number 61 m6 ^( W% }' ?  l5 I
July 2007 540-543
. }2 N/ @" c0 x) s4 O3 M- Z© 2007 Sage Publications* P! B0 A1 s9 D
10.1177/0009922806296651# y6 I& b; w5 r! Z% |1 c9 A
http://clp.sagepub.com0 _6 I  Q* f2 j  g
hosted at
, Y5 P( ~9 a4 [$ h$ W2 \7 |http://online.sagepub.com
+ ^9 a3 W) y" ^5 R9 A9 ]# jPrecocious puberty in boys, central or peripheral,: L5 l! u; R+ E
is a significant concern for physicians. Central  C$ L! B6 o/ f
precocious puberty (CPP), which is mediated. [% [+ X8 e- _
through the hypothalamic pituitary gonadal axis, has
: i& x* w5 a  ]3 S  Z: b9 t, na higher incidence of organic central nervous system, d. A' v: a7 K2 Y' ]$ y1 H2 i1 n- T( Y
lesions in boys.1,2 Virilization in boys, as manifested7 V0 ^/ k* z% P; i% ?
by enlargement of the penis, development of pubic  `3 N0 c+ x5 }
hair, and facial acne without enlargement of testi-2 E. g8 [& D* F$ s7 k' S6 ^
cles, suggests peripheral or pseudopuberty.1-3 We
- j% L- v) }. H; d: lreport a 16-month-old boy who presented with the
, d( W% ]1 L+ N  y7 genlargement of the phallus and pubic hair develop-
+ O! _5 X. v; Ument without testicular enlargement, which was due
# Q7 T/ k$ x) \* J& A. X9 ?to the unintentional exposure to androgen gel used by) @* R+ Q) b$ g
the father. The family initially concealed this infor-. n; h& k7 {' q! h( u" J1 j. n
mation, resulting in an extensive work-up for this& L7 H6 D' x- ^2 y# g/ z4 |2 {
child. Given the widespread and easy availability of% K! P2 W2 A8 P% y
testosterone gel and cream, we believe this is proba-
" d2 B* X# C2 ]/ b6 W" Gbly more common than the rare case report in the* @: ~# k1 T$ r1 m* H% y
literature.4
5 f. t4 l1 J6 g9 X' RPatient Report
' i% Z+ G7 f( M+ WA 16-month-old white child was referred to the. W* j! b+ x; m8 z1 {0 {: L9 q
endocrine clinic by his pediatrician with the concern4 P4 v9 R2 F2 z) J' C
of early sexual development. His mother noticed$ H+ M$ R: U7 L" e. e0 ?
light colored pubic hair development when he was
6 h. X( \/ v8 Z# |1 ~6 B3 d8 HFrom the 1Division of Pediatric Endocrinology, 2University of9 q- o" R( f+ h! N- W; g# _
South Alabama Medical Center, Mobile, Alabama.
% R+ c0 B/ ~7 Z* o7 q" y" h2 lAddress correspondence to: Samar K. Bhowmick, MD, FACE,# @- |3 d5 p# y' @, d( y1 ~  g
Professor of Pediatrics, University of South Alabama, College of
" x5 Q& M5 N. i$ v$ M9 Z, e7 @Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;0 ~2 k6 r4 O4 h  A
e-mail: [email protected].
& G( v/ l! M# W$ p8 xabout 6 to 7 months old, which progressively became9 _( W! S6 b+ l  L4 l3 c( i
darker. She was also concerned about the enlarge-
/ \, O7 A  H1 tment of his penis and frequent erections. The child
8 ~1 f7 e/ @7 c) K2 [; K1 B; \7 f& b/ Qwas the product of a full-term normal delivery, with
/ P2 c% a+ b! e) Q) n" }/ da birth weight of 7 lb 14 oz, and birth length of
3 D, `, i, @4 ~. Q20 inches. He was breast-fed throughout the first year
% t! F+ d" v) T. p" dof life and was still receiving breast milk along with
) X' W$ |, v" ]2 Wsolid food. He had no hospitalizations or surgery,
2 Z5 Y. x8 U/ Zand his psychosocial and psychomotor development
7 `& I5 S; J$ G4 Y$ Q, K" i8 b" Xwas age appropriate.# o4 O; }1 j% S% b( f( B
The family history was remarkable for the father,8 f! O6 _7 P' F3 f! l: d
who was diagnosed with hypothyroidism at age 16,
. d- v& ^! r! ^3 t. h; Y* hwhich was treated with thyroxine. The father’s
& E8 c0 x1 h; H3 Kheight was 6 feet, and he went through a somewhat+ w) A" ]* B( ^2 F( P7 |
early puberty and had stopped growing by age 14.( C- [4 ]  O4 H  G1 g) T
The father denied taking any other medication. The
- \1 J$ b* g) h1 {% r7 uchild’s mother was in good health. Her menarche1 M7 [4 z0 k+ f; ^& q0 o  s: l
was at 11 years of age, and her height was at 5 feet
% k( g+ F6 \# N! \5 inches. There was no other family history of pre-/ n. N, a4 Y6 j+ l
cocious sexual development in the first-degree rela-
4 t5 l5 `/ Z( A# ntives. There were no siblings.4 q; u" O. w6 e' s
Physical Examination
% M2 ^# \, _2 X2 m! V9 @. c( G9 K2 VThe physical examination revealed a very active,
3 K2 N8 o" M% ?0 L! Lplayful, and healthy boy. The vital signs documented$ H! C# W$ K5 l/ ]1 l4 p
a blood pressure of 85/50 mm Hg, his length was" ~( I6 }* j5 `$ a1 P9 X
90 cm (>97th percentile), and his weight was 14.4 kg
; k$ L8 L: O4 C/ C( v& ^(also >97th percentile). The observed yearly growth
9 ~9 |9 X" x% m- ]$ yvelocity was 30 cm (12 inches). The examination of
! N0 \$ v+ C! W& E7 ~2 \7 O  Gthe neck revealed no thyroid enlargement.
1 [4 Z2 h0 j! G9 ^7 `! jThe genitourinary examination was remarkable for
. |8 _3 j+ m4 y$ W# Q1 E* S! @" uenlargement of the penis, with a stretched length of
& H$ Q" a( I" k8 cm and a width of 2 cm. The glans penis was very well+ F9 r3 _" z; M7 Z+ {  Q
developed. The pubic hair was Tanner II, mostly around) [$ s; |, j7 \, Y( s
540
- d' G' l) V; m- O8 {, w$ K$ nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; @/ x& K& g( S$ ~; uthe base of the phallus and was dark and curled. The
( V5 B! {5 F) Z7 V# h, T6 E% gtesticular volume was prepubertal at 2 mL each.2 P# P1 P! d5 F1 B7 D: u0 H1 ^
The skin was moist and smooth and somewhat0 b/ L) i" q$ X9 L8 H/ q! {5 a6 J
oily. No axillary hair was noted. There were no; E3 P9 ]3 G9 ?( w$ z% G' d
abnormal skin pigmentations or café-au-lait spots.* s/ s! J6 g3 P$ T+ Q) p
Neurologic evaluation showed deep tendon reflex 2+
7 G# t% z) h. {bilateral and symmetrical. There was no suggestion1 K+ `. u7 k1 _6 W; b* p  O& y
of papilledema.
* J8 A5 ~3 |: s+ r4 S- `7 MLaboratory Evaluation
, ]8 x$ A, c0 E  {1 Z2 VThe bone age was consistent with 28 months by
7 H: e8 K$ R7 tusing the standard of Greulich and Pyle at a chrono-
" u; y* o, k& }( g, Glogic age of 16 months (advanced).5 Chromosomal; h6 e8 u9 y/ p/ L: D3 H( n2 _
karyotype was 46XY. The thyroid function test
. j+ Y* l: }4 J* m: v) k3 Mshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
/ q$ a* A; X1 {7 t& ], a: blating hormone level was 1.3 µIU/mL (both normal).
: i( Z: C$ Z$ H# z  w7 m9 sThe concentrations of serum electrolytes, blood& Y& ]- c$ s9 E# U1 E) X& e$ x
urea nitrogen, creatinine, and calcium all were# `0 j& o& t' W- Y. x
within normal range for his age. The concentration
8 g2 N) q3 _( ?- t5 d$ w/ Hof serum 17-hydroxyprogesterone was 16 ng/dL
6 E' F* U0 d, M* i! X(normal, 3 to 90 ng/dL), androstenedione was 20% m6 f; j4 b) A) D  R! B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- Q- c6 N% h: Y8 _5 Uterone was 38 ng/dL (normal, 50 to 760 ng/dL),1 ^) Q& V( E# j0 g" D  C0 x- C8 [
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 Q& F7 h8 C& x& E
49ng/dL), 11-desoxycortisol (specific compound S)! `1 M3 s# z7 }' I2 h
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
" V6 ]! p, T% s' D, s& Itisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 x. [6 @; K( W1 c6 F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),& p/ c' D0 B4 a1 t- b- J6 ^
and β-human chorionic gonadotropin was less than" q* k) F/ H3 P* E; W
5 mIU/mL (normal <5 mIU/mL). Serum follicular- N0 N" d$ z8 W7 ~0 I9 N2 |
stimulating hormone and leuteinizing hormone# c* M( \$ j6 O) L+ F+ Z6 I
concentrations were less than 0.05 mIU/mL$ J0 h/ O1 v% @. E8 l5 }
(prepubertal).7 t# w" `- u9 E" D+ j
The parents were notified about the laboratory5 f) e+ f2 A9 g/ z, V
results and were informed that all of the tests were
  _7 G/ U" g. z( I/ T. \normal except the testosterone level was high. The& P9 l; [) @( ?& p. h& _" W' |0 N* f
follow-up visit was arranged within a few weeks to
6 a  a) F8 O. z- W: b$ qobtain testicular and abdominal sonograms; how-) t& h: Z. N9 l: Y% ?
ever, the family did not return for 4 months., o- d; [# k5 o3 }' Y, O- V5 Z
Physical examination at this time revealed that the' }+ J9 M1 G( v9 L8 k
child had grown 2.5 cm in 4 months and had gained
6 G3 n) s2 }9 j6 v- t# F3 M) b2 kg of weight. Physical examination remained
$ t! C/ n+ ^; g! F9 r- wunchanged. Surprisingly, the pubic hair almost com-
! a% C5 R, P; mpletely disappeared except for a few vellous hairs at+ C; U- G; v, Q  @) E: j; W
the base of the phallus. Testicular volume was still 2
  R7 |# r/ D2 N5 P5 B/ pmL, and the size of the penis remained unchanged.
# m& F, ^* ?! l3 `1 {' RThe mother also said that the boy was no longer hav-
$ l2 Y) w3 y+ S, ping frequent erections.* M, O" s! A' c/ Z! v
Both parents were again questioned about use of# @8 Q1 u% @& X# `% S; L. o
any ointment/creams that they may have applied to
& x4 C9 V8 c. _" Z7 K9 P: rthe child’s skin. This time the father admitted the; n* R: x, ]! s5 A) r* g0 D2 [
Topical Testosterone Exposure / Bhowmick et al 541
  p9 l- ~6 ~" y9 J  juse of testosterone gel twice daily that he was apply-
" x5 R6 g( a6 G) Z. Iing over his own shoulders, chest, and back area for7 S8 o/ B4 c9 Y- C/ t+ @& |) F  m
a year. The father also revealed he was embarrassed
+ j) i5 H0 ?* lto disclose that he was using a testosterone gel pre-
# E8 [0 w* q6 J6 p7 Mscribed by his family physician for decreased libido  P( n8 f1 V7 c# V6 N
secondary to depression.
" O7 D6 b1 L5 n3 |4 H2 f$ c2 \The child slept in the same bed with parents.
' _$ \: m% K. v7 {- T) FThe father would hug the baby and hold him on his
9 V  V3 r# d0 w% M, C: T: Z2 bchest for a considerable period of time, causing sig-
9 l9 L6 F, m$ J2 j" }nificant bare skin contact between baby and father.
2 R3 e( o/ R% g9 O+ i6 kThe father also admitted that after the phone call,0 q2 Z& E& \$ H% k4 \' _: u
when he learned the testosterone level in the baby3 k' B( `% y' U  X. b
was high, he then read the product information+ v" A+ o) z) X+ n
packet and concluded that it was most likely the rea-- z. p0 u1 r* N0 s1 A0 C) |
son for the child’s virilization. At that time, they. ]  E# I. p9 A! n& Z9 ^1 ?" G. R
decided to put the baby in a separate bed, and the. T& e7 I) y9 r5 [: m( M
father was not hugging him with bare skin and had
* i$ @$ M, Q5 U5 y+ cbeen using protective clothing. A repeat testosterone8 F$ v8 \* S. S# l
test was ordered, but the family did not go to the2 }7 i! @8 ^) h! L
laboratory to obtain the test.9 H& a+ |/ H! A, g5 s# ?& A! h
Discussion+ [* M, N. u6 B: h
Precocious puberty in boys is defined as secondary
+ z9 e/ h; ~' J" u$ R) Q4 A1 Y$ Fsexual development before 9 years of age.1,4! S' ~- b1 q$ _  ]8 M' K
Precocious puberty is termed as central (true) when: y  _. K5 p7 ?4 o3 z
it is caused by the premature activation of hypo-
- c" N) d/ L$ a' z0 L+ Xthalamic pituitary gonadal axis. CPP is more com-
8 \7 S7 Y2 Y; G8 a, b2 bmon in girls than in boys.1,3 Most boys with CPP; ]$ D; ^$ p  ]& P
may have a central nervous system lesion that is2 K2 y" g/ F/ j; K
responsible for the early activation of the hypothal-) L) n( G: }1 `
amic pituitary gonadal axis.1-3 Thus, greater empha-
) j6 ~( ^' [  ~( x6 Z1 I3 s2 {sis has been given to neuroradiologic imaging in
: a0 _% u" W' U1 E) eboys with precocious puberty. In addition to viril-
$ w4 [5 l1 F" Y% O! _ization, the clinical hallmark of CPP is the symmet-
, B6 B  _% i: u7 Yrical testicular growth secondary to stimulation by. V; R* u* j. z; m9 B
gonadotropins.1,3
) W  q; L- X" z- C$ pGonadotropin-independent peripheral preco-
9 O# J6 m% b" q3 Z1 M$ |" Ucious puberty in boys also results from inappropriate
! x; i- u* O$ xandrogenic stimulation from either endogenous or
9 v1 f  M7 f& _$ c' ?exogenous sources, nonpituitary gonadotropin stim-
/ L7 b6 i' k" z( h; ]+ M0 @$ Vulation, and rare activating mutations.3 Virilizing
) v" r! p0 b  ?: scongenital adrenal hyperplasia producing excessive
; s4 N3 Z, Q! Zadrenal androgens is a common cause of precocious
9 a) R/ X! e0 _  N2 Qpuberty in boys.3,4& H7 a: E! s! K" b
The most common form of congenital adrenal
/ M/ O2 Q6 H( z7 a: f) r. H. `hyperplasia is the 21-hydroxylase enzyme deficiency.
/ x2 P" o# i- h! {2 UThe 11-β hydroxylase deficiency may also result in
6 I* n( C0 ]* p* [5 H( e7 R* X! jexcessive adrenal androgen production, and rarely,
4 E$ E' V" T9 m$ Aan adrenal tumor may also cause adrenal androgen
3 z! D. p; e2 X, R( Gexcess.1,3
* r; b7 L- E" W2 k# b* {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 K* z+ s! ?, `  h$ F
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! `7 I7 |$ P+ w: w+ k& A$ U
A unique entity of male-limited gonadotropin-$ {$ {! Z" e' P% B+ y% H* X
independent precocious puberty, which is also known5 z' L, S1 K0 Q; ?. ?: j: z
as testotoxicosis, may cause precocious puberty at a2 b9 N! ^% i0 m
very young age. The physical findings in these boys
) a4 A3 z4 h* N+ `with this disorder are full pubertal development,* R0 P& d0 ]3 C
including bilateral testicular growth, similar to boys
/ P1 s4 C5 A! Ewith CPP. The gonadotropin levels in this disorder
% ?: H. C( T6 g& ~; tare suppressed to prepubertal levels and do not show
$ B+ a: O+ u- n7 b1 Spubertal response of gonadotropin after gonadotropin-
! ~: M! A9 c" x# r9 Ireleasing hormone stimulation. This is a sex-linked
1 K+ I7 |* f/ T& u& mautosomal dominant disorder that affects only8 l1 r5 d6 [  p7 T" ]& n! J
males; therefore, other male members of the family& x. Y  B+ o6 E2 m" a+ J
may have similar precocious puberty.3
  o8 Y  u% h* @; G) fIn our patient, physical examination was incon-
2 G# @: m8 k5 M  tsistent with true precocious puberty since his testi-, u$ v4 F+ x7 z& Q) X$ i7 T; @  _( G0 F
cles were prepubertal in size. However, testotoxicosis
3 D. X  I! ^. k9 ~! _( @was in the differential diagnosis because his father; \0 @3 z3 ?, C- X
started puberty somewhat early, and occasionally,
! n5 m6 i4 \* l9 G4 f8 E6 z+ ctesticular enlargement is not that evident in the- _; O7 l- B0 v" J
beginning of this process.1 In the absence of a neg-, N* c  W% D" a4 t6 g' r
ative initial history of androgen exposure, our+ C8 K4 P# y- e0 Y, ]3 F: d% j, v
biggest concern was virilizing adrenal hyperplasia,
$ w: i. r5 x( qeither 21-hydroxylase deficiency or 11-β hydroxylase' ^4 U! e2 p9 I) ~9 u& l  w
deficiency. Those diagnoses were excluded by find-
! V5 \1 I. F( m$ @ing the normal level of adrenal steroids.3 P" `+ i7 q( K$ M7 G5 i
The diagnosis of exogenous androgens was strongly8 {5 B, \5 G, a; ]/ f9 o0 b
suspected in a follow-up visit after 4 months because6 _7 |7 A7 w% z% @
the physical examination revealed the complete disap-
$ K/ D/ V% d+ A, f7 [! xpearance of pubic hair, normal growth velocity, and1 v6 ^: \  s! t
decreased erections. The father admitted using a testos-
+ p, I! d& f5 y# H: C+ Qterone gel, which he concealed at first visit. He was2 @% Q; F+ i* I. n0 g
using it rather frequently, twice a day. The Physicians’
$ M/ \& n; Y0 J' i$ f, w7 zDesk Reference, or package insert of this product, gel or* C  n3 H# K! \5 r
cream, cautions about dermal testosterone transfer to8 ^! G; u$ {+ w5 K. ~
unprotected females through direct skin exposure.
2 Z% b( E, T. K+ V; Z% s, sSerum testosterone level was found to be 2 times the
+ {9 m+ K% m$ T: @: L( e7 M/ Abaseline value in those females who were exposed to
- l/ w. a& s1 K# ^. S& N- u2 teven 15 minutes of direct skin contact with their male
! k4 Y0 y! w* ?1 [: k, Opartners.6 However, when a shirt covered the applica-
7 ~& l0 d. ]) mtion site, this testosterone transfer was prevented.: U3 u6 C% d- K7 |' G1 O
Our patient’s testosterone level was 60 ng/mL,
9 J9 ^: n/ S3 {& |6 t6 vwhich was clearly high. Some studies suggest that
0 k3 U6 `. H4 ^6 Mdermal conversion of testosterone to dihydrotestos-
% n2 y& e1 ]0 m7 b) [terone, which is a more potent metabolite, is more
8 [$ q+ t1 Z- P$ X& E) vactive in young children exposed to testosterone, E6 V: ?9 h' j- X5 v' p
exogenously7; however, we did not measure a dihy-2 N  |+ e" x. T3 Y
drotestosterone level in our patient. In addition to
7 _  p$ E3 }9 m: e" u% \( ~virilization, exposure to exogenous testosterone in! h( U3 T0 X3 G0 z0 l
children results in an increase in growth velocity and
! Y8 \6 m* R3 ~# |/ D  padvanced bone age, as seen in our patient.; s0 o: R& X- p9 {) a0 F
The long-term effect of androgen exposure during
# o2 O( T, s: x4 D& |+ I4 Dearly childhood on pubertal development and final
* _; u5 f) W3 \9 K# F, Wadult height are not fully known and always remain
- l: ^! n* h: c) }& v! n/ fa concern. Children treated with short-term testos-
8 H# T$ K6 y/ @# |3 o* @terone injection or topical androgen may exhibit some5 g8 M$ p) J5 @* s
acceleration of the skeletal maturation; however, after" ^- E2 s' m) N( l+ F3 T
cessation of treatment, the rate of bone maturation
* ]! c7 D" F. n' f+ A  ?decelerates and gradually returns to normal.8,9
; d, X+ h4 O; y9 f$ C7 x; ]There are conflicting reports and controversy$ S* h+ Y0 O; L! X  r
over the effect of early androgen exposure on adult
( t! C/ ~! s- ~, apenile length.10,11 Some reports suggest subnormal" n# T: s8 Z+ T' K; a5 W# J5 q; z
adult penile length, apparently because of downreg-
9 y5 k6 @! o& G  V+ K0 _ulation of androgen receptor number.10,12 However,. Z; ]2 U0 L- I& j
Sutherland et al13 did not find a correlation between, b/ ?8 z1 z/ J5 E7 `, |3 {4 x
childhood testosterone exposure and reduced adult0 E. ^4 W6 A1 U7 T6 G9 O
penile length in clinical studies.
  [) P4 G) [  JNonetheless, we do not believe our patient is" x: _4 x8 z% P0 s) ]
going to experience any of the untoward effects from/ R/ I' ^# ^0 Z1 _( i. q! A" P
testosterone exposure as mentioned earlier because( g: a3 i- b  Z6 m" Z, j% Z7 W/ @
the exposure was not for a prolonged period of time.2 a9 l2 d* `% ~
Although the bone age was advanced at the time of
& `+ @6 E& x! h, G' ]/ jdiagnosis, the child had a normal growth velocity at/ G0 E! ]  Z, p
the follow-up visit. It is hoped that his final adult
% e+ ^% b5 N9 H. F0 `6 b( |* ~height will not be affected.
" K/ m% I% W5 m5 ?+ qAlthough rarely reported, the widespread avail-
5 u5 A: `6 N7 A: E% Y% G8 ?! E9 sability of androgen products in our society may
% F! E( O5 }8 x5 c4 x" Oindeed cause more virilization in male or female: Z5 R( K$ r# R- x' ^
children than one would realize. Exposure to andro-
+ u) ?+ i/ |- t" F3 B% q1 E( Igen products must be considered and specific ques-2 `5 Y1 x8 Z8 E+ P
tioning about the use of a testosterone product or
; `1 h$ u  y# y4 i& ]gel should be asked of the family members during4 X' \- l* |, l$ {* ]
the evaluation of any children who present with vir-. }# H, `' ?8 z
ilization or peripheral precocious puberty. The diag-0 x$ y2 ?5 R, l; e- t6 U
nosis can be established by just a few tests and by$ d6 s1 E9 n6 ]$ o3 C! _( S# u
appropriate history. The inability to obtain such a
) J% f- h4 a0 h1 C% [5 Phistory, or failure to ask the specific questions, may( Z. g2 K; W  O) c
result in extensive, unnecessary, and expensive
1 d8 U( ]. j' y( W8 K! D# B$ n; Z. ?investigation. The primary care physician should be0 G. L. c9 R6 D3 U( b$ ?6 {' z$ S
aware of this fact, because most of these children' P( Q' l' ?5 R+ x3 \
may initially present in their practice. The Physicians’
' Z$ J" x9 \8 O! k& Q; m/ TDesk Reference and package insert should also put a
  c+ g& L& }7 `" r2 @% uwarning about the virilizing effect on a male or+ X: m3 S0 R# h
female child who might come in contact with some-- d! o, p4 A3 g: w# O! ]+ F  o
one using any of these products.
1 x/ A7 a. g( e1 J) xReferences
+ R7 L' Q1 t- P. T2 f' o1. Styne DM. The testes: disorder of sexual differentiation
$ g7 E2 @7 R7 d% r8 tand puberty in the male. In: Sperling MA, ed. Pediatric0 p5 F& A7 U0 T  W6 P& R
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 o6 G$ v  K  |3 w% j' q2002: 565-628.9 t0 q! p9 e4 O/ _+ _
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. a9 q) Q6 I: p; T4 s0 g$ T
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old$ k  K! S4 Q2 i  f
Boy Induced by Indirect Topical" @  j' {5 c3 d0 n7 F
Exposure to Testosterone
1 O/ G+ s, i, `- R$ XSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,20 a3 x, Y% Y+ L  O, m  j4 |* [$ ~
and Kenneth R. Rettig, MD1
+ c8 U: c' _5 N8 b& y+ n; PClinical Pediatrics# W' w3 h- M, A6 W3 c, ^  Z
Volume 46 Number 6
3 J; l  f: z( h, b) {; m5 `. O+ \4 MJuly 2007 540-5432 w! x% v3 u, n! m/ M$ l$ q7 _( W( l
© 2007 Sage Publications
+ ?' x7 S' x+ _' r3 E7 ]10.1177/0009922806296651: M, ?/ u- Z& ?7 n7 C+ }% l
http://clp.sagepub.com
' M: w, z. t& F7 x$ ^! k/ a" phosted at
7 M6 Q1 }6 Q/ \. h4 ^http://online.sagepub.com, l" \! J. h2 U
Precocious puberty in boys, central or peripheral,
& d" J' y$ F% b+ i2 iis a significant concern for physicians. Central
5 O4 z3 @" K" l; A$ r# @precocious puberty (CPP), which is mediated- T* |1 `# v  Z' A) |, S
through the hypothalamic pituitary gonadal axis, has1 t: R5 h* x* x) ~+ m7 R! C
a higher incidence of organic central nervous system$ z% N, F4 d6 K- R
lesions in boys.1,2 Virilization in boys, as manifested( }8 ?# k' Z- Y" W8 W
by enlargement of the penis, development of pubic8 {. @5 X, ]4 x/ o
hair, and facial acne without enlargement of testi-
& r( l3 u7 Y- u/ T0 a. B/ A4 vcles, suggests peripheral or pseudopuberty.1-3 We
+ d$ o' Y- K5 Dreport a 16-month-old boy who presented with the- L# s2 I/ A! O3 I2 F' |5 e5 p8 C
enlargement of the phallus and pubic hair develop-1 }0 ~" [) B" }7 e7 L0 q8 |. _
ment without testicular enlargement, which was due7 L6 Z( V+ c/ b2 }* h/ ?$ B3 R
to the unintentional exposure to androgen gel used by
7 u6 @" q+ i! D5 `. Vthe father. The family initially concealed this infor-
3 }% G) V$ [5 l6 G; kmation, resulting in an extensive work-up for this
! D) p' N( E& `! Mchild. Given the widespread and easy availability of
* c+ j. q8 s2 dtestosterone gel and cream, we believe this is proba-
  }$ j! q4 _& Y0 L! s9 Hbly more common than the rare case report in the
  g9 F( _/ ^5 P! w* P0 j. C" ^6 Y+ vliterature.40 G) E* Q9 V1 S3 B
Patient Report, n& l: l9 M8 Z7 g' E! q' H# C
A 16-month-old white child was referred to the
2 X3 J  O) G! e: `) U9 jendocrine clinic by his pediatrician with the concern, f' E: o0 T& u7 J' p) c5 o% F
of early sexual development. His mother noticed
/ X) K" t" C/ W& Slight colored pubic hair development when he was
( _+ H) j# _$ ?4 B9 M0 iFrom the 1Division of Pediatric Endocrinology, 2University of
/ K5 y+ Z" C1 V& ?4 g- v: ySouth Alabama Medical Center, Mobile, Alabama.
7 z* t$ N' N4 }# N' x! b5 kAddress correspondence to: Samar K. Bhowmick, MD, FACE,* A" b# [- l  B8 r. c
Professor of Pediatrics, University of South Alabama, College of/ R1 Y: }( Y: R2 P' w
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;- a; H: }9 l, `* I9 [1 z
e-mail: [email protected].9 n4 f. T# o/ w
about 6 to 7 months old, which progressively became
' [' E2 f9 U! \: _! }1 Qdarker. She was also concerned about the enlarge-
) G5 E8 J" Y& _% ]ment of his penis and frequent erections. The child+ @2 o/ j$ X: b9 O8 l
was the product of a full-term normal delivery, with' }. y! F6 ~: I; b7 b  C
a birth weight of 7 lb 14 oz, and birth length of8 O6 A2 L, f0 s! A) X8 Z0 k+ ?- m
20 inches. He was breast-fed throughout the first year
  V3 S; [/ X. O6 W& Z9 f1 g1 N0 Rof life and was still receiving breast milk along with, k: \- d3 |5 `) P1 f# K
solid food. He had no hospitalizations or surgery,( A' p2 i5 H) d! A* e/ y
and his psychosocial and psychomotor development
$ E% |! D+ g; b/ X1 gwas age appropriate.
8 H' X- W: K# _+ K% s. Q9 IThe family history was remarkable for the father,( ]) y6 x  g+ W* H- H5 Q8 _
who was diagnosed with hypothyroidism at age 16,5 M& g) B6 }# X& L) J, b
which was treated with thyroxine. The father’s+ g3 z5 Q" a' [  h, |
height was 6 feet, and he went through a somewhat
, ~# P; @9 M! {* b8 i( Q7 h' iearly puberty and had stopped growing by age 14.& K, J3 g9 J5 s. q
The father denied taking any other medication. The$ n& A; i+ B+ p
child’s mother was in good health. Her menarche
" `  t% x. _& ]( {was at 11 years of age, and her height was at 5 feet* G0 d& \1 V- M6 J' P' ?) }1 T6 m
5 inches. There was no other family history of pre-  N4 r7 [5 O8 S* @5 J
cocious sexual development in the first-degree rela-
' o  v! }, T* S* k& d% H5 ztives. There were no siblings.
7 _, h; S1 o5 m& @Physical Examination) W! h2 e2 w, o! ^6 E/ ~. N
The physical examination revealed a very active,# q6 u+ C, f  W% F3 i
playful, and healthy boy. The vital signs documented
$ {+ h5 O/ t. L) Za blood pressure of 85/50 mm Hg, his length was
' g0 |! N7 j2 b6 ?8 c9 F90 cm (>97th percentile), and his weight was 14.4 kg& J( T# i- g" c1 J
(also >97th percentile). The observed yearly growth/ ^/ B8 k& n8 `! b$ z" Y
velocity was 30 cm (12 inches). The examination of
6 q/ h9 I; x6 Q8 bthe neck revealed no thyroid enlargement.
5 [" Z* Y$ @1 k& c8 i& V" O! ?The genitourinary examination was remarkable for( j( ~( Y0 S4 X/ U5 J
enlargement of the penis, with a stretched length of
) }+ L/ u' _4 s* Y) x0 c$ ^* u8 cm and a width of 2 cm. The glans penis was very well
% f9 _& I! ~# c0 wdeveloped. The pubic hair was Tanner II, mostly around$ {: D7 v: Z4 _5 b! I7 }2 O7 |3 `
540
  b0 |( j) {0 k, t* L% O. c% n$ fat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# l* Q" k$ T* ]: A  O
the base of the phallus and was dark and curled. The/ R( o# F. o8 R$ A8 }9 Y
testicular volume was prepubertal at 2 mL each.5 k% h) K" X4 ]8 S2 R2 K" D
The skin was moist and smooth and somewhat, N7 N0 o4 s: k
oily. No axillary hair was noted. There were no
6 F7 P, H% ]  S& p' Eabnormal skin pigmentations or café-au-lait spots." U* `+ F7 X) V0 K/ D
Neurologic evaluation showed deep tendon reflex 2+) x6 r3 X5 V0 C3 z1 u7 m5 t# X
bilateral and symmetrical. There was no suggestion
( ~  x3 k1 b5 E, l; E1 Qof papilledema.6 \7 x  F4 S# _) k) ?7 `! s
Laboratory Evaluation- x; @( \4 P5 `3 Q0 b
The bone age was consistent with 28 months by; u' Y- r# Z" i3 v2 G5 k( B
using the standard of Greulich and Pyle at a chrono-5 \# r+ l; s8 `5 }6 W; E
logic age of 16 months (advanced).5 Chromosomal1 a  M8 N1 E. Y! \
karyotype was 46XY. The thyroid function test( ~5 d5 L* Q" O0 f. h1 `
showed a free T4 of 1.69 ng/dL, and thyroid stimu-# v( I% I3 E8 Q4 `" g! W
lating hormone level was 1.3 µIU/mL (both normal)." v! |. `" K& t  ~* W4 u& d
The concentrations of serum electrolytes, blood
. z9 b% E( x& S( Nurea nitrogen, creatinine, and calcium all were
& p+ R, p( ^. D6 A; gwithin normal range for his age. The concentration1 W7 f- A1 c3 l# Z+ X% n* v6 ^0 F  ^
of serum 17-hydroxyprogesterone was 16 ng/dL
; o# M, [; I2 c- D/ b4 c- @  p7 f& }(normal, 3 to 90 ng/dL), androstenedione was 20" s. M% \: u; G9 ^& f0 Q
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-- q- y, V3 B$ n
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
# @1 W# x' }( d" Sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to. @% n, r  o0 h8 ~& q' [9 o
49ng/dL), 11-desoxycortisol (specific compound S)0 n* g1 p$ ]9 ?/ G4 k. y% h
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) E8 M; u& q* Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* M! T7 C0 o7 \/ N; @9 `
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, C- G0 Q1 m4 ^) x! Z$ x
and β-human chorionic gonadotropin was less than, [: H% ^9 r) y- J
5 mIU/mL (normal <5 mIU/mL). Serum follicular
# R$ C& A4 U3 Mstimulating hormone and leuteinizing hormone
% ]& ?: Q/ `3 C& d3 k1 aconcentrations were less than 0.05 mIU/mL6 L6 D6 y& @$ {4 ?8 T+ X1 `  S
(prepubertal).
, f- i) J1 B" u9 p' rThe parents were notified about the laboratory
+ C2 }# U, w- i$ |  k7 Y2 e: f" ]results and were informed that all of the tests were
2 ?  c8 I. {2 D$ M( T; S& X! ?normal except the testosterone level was high. The
8 Q$ }5 ?: ~2 U9 rfollow-up visit was arranged within a few weeks to, A: J, O8 e4 K0 o+ X5 w! U+ S7 {- R
obtain testicular and abdominal sonograms; how-! X1 o0 _$ v' w: a- W
ever, the family did not return for 4 months.1 }; J8 [8 \- e* u& d" L% d& n9 e
Physical examination at this time revealed that the
/ G9 J1 k2 c& Rchild had grown 2.5 cm in 4 months and had gained: L% z' t4 e$ Y: R2 s: D
2 kg of weight. Physical examination remained
, Y! k, D7 m( ?unchanged. Surprisingly, the pubic hair almost com-
: N3 D* j0 P* Q' _7 D& m! p; q. `4 k% Mpletely disappeared except for a few vellous hairs at
6 [- k# I, ~! N9 ^1 a6 M8 A/ Nthe base of the phallus. Testicular volume was still 2, g6 R  |/ X' z7 R, [0 j5 u
mL, and the size of the penis remained unchanged.
4 x5 m1 D1 g% g8 ~' _+ r4 HThe mother also said that the boy was no longer hav-
% H0 ]% O9 C. a% {ing frequent erections.$ G$ K* E" K4 t; |& F
Both parents were again questioned about use of
* b1 }7 }; }8 |( ]0 |" Xany ointment/creams that they may have applied to
1 O( Q- e8 J' z" Q5 K, \$ {9 uthe child’s skin. This time the father admitted the0 Q7 X5 C' a- P' ~- Y7 ]- j; p
Topical Testosterone Exposure / Bhowmick et al 541; i4 Q7 A( i7 G0 m
use of testosterone gel twice daily that he was apply-
( l$ }- |, ~6 w3 o; o1 u1 B* D- C+ ving over his own shoulders, chest, and back area for* e: K" f; s/ t$ _4 \
a year. The father also revealed he was embarrassed
: E: F% w2 A! G1 y" zto disclose that he was using a testosterone gel pre-& f2 x  O5 i  I9 }4 H
scribed by his family physician for decreased libido5 {# \; D: [: l) C
secondary to depression.
+ M5 I; h: E. V+ Q! S6 \' K4 ^The child slept in the same bed with parents.
$ ~, e5 ^6 f- sThe father would hug the baby and hold him on his
% d# c3 F& [; \1 ]7 a. E6 T: ^8 P8 mchest for a considerable period of time, causing sig-
( [3 E5 D* W2 |$ @5 S) [( \nificant bare skin contact between baby and father.2 D. B, i; r) `- c' u7 |% j
The father also admitted that after the phone call,( M6 C( h; \! l1 S
when he learned the testosterone level in the baby: x7 a- b4 y, s
was high, he then read the product information
8 N( l9 @+ S4 c& N+ Epacket and concluded that it was most likely the rea-
( [1 U2 V. @+ T) h$ \/ M0 ~' Uson for the child’s virilization. At that time, they
" w! X3 T5 E  t, i0 tdecided to put the baby in a separate bed, and the
* _0 x8 @! @- \father was not hugging him with bare skin and had
6 v: l0 b. b& M: x: ^1 F9 fbeen using protective clothing. A repeat testosterone$ @- K3 R) k( t% l% @
test was ordered, but the family did not go to the
2 E2 L$ y+ `4 S2 mlaboratory to obtain the test.
6 D$ V, b" x- @9 z. \Discussion
4 A/ L5 C! T/ M1 gPrecocious puberty in boys is defined as secondary
( a! m8 p! H' r6 o8 j1 ?, A0 [sexual development before 9 years of age.1,4
9 Q* M) ~6 c' v) IPrecocious puberty is termed as central (true) when
, L6 I' c- m. |3 c1 Lit is caused by the premature activation of hypo-
$ N" G2 o6 S) g6 O" r0 F2 tthalamic pituitary gonadal axis. CPP is more com-% a8 I) `# k7 q: n* [, s8 d
mon in girls than in boys.1,3 Most boys with CPP5 w, Q- F( Q7 q$ n4 o
may have a central nervous system lesion that is  P9 y* ]% J$ l& D9 t
responsible for the early activation of the hypothal-
/ m( r2 r/ L# p- J# Xamic pituitary gonadal axis.1-3 Thus, greater empha-
# q0 ^7 K8 V1 ?; ysis has been given to neuroradiologic imaging in+ e- G4 k4 R4 A7 }! h, S
boys with precocious puberty. In addition to viril-
3 l+ `  E+ H* Zization, the clinical hallmark of CPP is the symmet-1 S3 _" l( D8 _- o( v& c" a" d# U
rical testicular growth secondary to stimulation by
: L: B$ J7 n: ?  l0 Xgonadotropins.1,3
( h2 s& d7 Z$ `9 |1 G* mGonadotropin-independent peripheral preco-
0 R! }4 V7 {* B. L& h/ }, ucious puberty in boys also results from inappropriate
7 T) l7 _0 a- I/ F* N  j; p. Jandrogenic stimulation from either endogenous or
3 S. o, |0 `" p' _4 iexogenous sources, nonpituitary gonadotropin stim-
1 O# E* c( b. M3 W, Aulation, and rare activating mutations.3 Virilizing
5 I/ H. P* F8 N: a& E- ]congenital adrenal hyperplasia producing excessive* F5 T( E3 W, D& G8 I9 |
adrenal androgens is a common cause of precocious# P3 D  d$ i2 @5 A
puberty in boys.3,46 }4 h- s0 t  ~
The most common form of congenital adrenal$ ]+ ]4 V8 [# S: Y" O
hyperplasia is the 21-hydroxylase enzyme deficiency.! c/ n  |2 F( S! v" Z: f8 ^7 Y
The 11-β hydroxylase deficiency may also result in' P1 L; j' `7 {* I
excessive adrenal androgen production, and rarely,. k' {: ?. H5 p+ P, F2 \
an adrenal tumor may also cause adrenal androgen
8 ^) D* ]9 O0 gexcess.1,3
3 N) r7 s1 J& V  j' \4 tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( q! A5 H5 I) a% ]4 U" S7 ~
542 Clinical Pediatrics / Vol. 46, No. 6, July 20077 h" C- u. U4 y2 Y
A unique entity of male-limited gonadotropin-
/ S. V  V0 v: t8 N' Uindependent precocious puberty, which is also known
' b2 t  a+ O' k: ~( q0 @8 o8 Fas testotoxicosis, may cause precocious puberty at a
  C6 ^% _  R* Nvery young age. The physical findings in these boys
: `8 A& x$ l/ {with this disorder are full pubertal development,
* I0 H1 |6 @' a: E0 |+ Tincluding bilateral testicular growth, similar to boys
* P" n- n& k! r* r2 Iwith CPP. The gonadotropin levels in this disorder
  F$ J. Y, ^# x8 W  x4 @/ {% E; R  B% ^are suppressed to prepubertal levels and do not show
  z; i: O  G1 N- fpubertal response of gonadotropin after gonadotropin-: _- l/ d+ I, n+ `( s( f5 D# j7 s
releasing hormone stimulation. This is a sex-linked
1 x- D6 t4 o$ j& l: y  xautosomal dominant disorder that affects only
; @$ G0 ]/ u9 v2 G& M9 f$ Fmales; therefore, other male members of the family
7 x. W4 L& J" M( s' ^may have similar precocious puberty.39 X8 _  n# k) q) L; @3 s. r9 |7 i
In our patient, physical examination was incon-' i. q: u- s. P$ Z2 S6 y
sistent with true precocious puberty since his testi-; {( k8 _1 a/ ^( n* p3 Z. h
cles were prepubertal in size. However, testotoxicosis. H: P. _0 a0 x2 Q1 Q
was in the differential diagnosis because his father3 R: x+ g# g9 p+ h7 Y' t+ K
started puberty somewhat early, and occasionally,
& w  o! A- }6 ^2 H3 v# ?9 ktesticular enlargement is not that evident in the
/ t# l0 f+ u% U6 }/ r) ^beginning of this process.1 In the absence of a neg-. x% F6 b! A) q- j
ative initial history of androgen exposure, our1 k3 J/ g4 O! ]( N
biggest concern was virilizing adrenal hyperplasia,  H9 m. S: B  ~% f/ M8 D5 E% a# \
either 21-hydroxylase deficiency or 11-β hydroxylase. P; M" K! k. R5 s* p
deficiency. Those diagnoses were excluded by find-
' v3 p/ W* M: p. M" \( b$ O. ring the normal level of adrenal steroids.
! g2 Y/ u! Q# z6 P. m) pThe diagnosis of exogenous androgens was strongly8 ^6 P; M; R  Y) @$ {3 Y8 `. W
suspected in a follow-up visit after 4 months because
& ]+ |3 g8 T. }: ?& Lthe physical examination revealed the complete disap-$ U, J* h! x6 {1 S9 x: R
pearance of pubic hair, normal growth velocity, and
$ R; K- B. L5 _. F: Y8 |decreased erections. The father admitted using a testos-
9 j2 x+ I6 W1 N) v9 v$ ?terone gel, which he concealed at first visit. He was9 l( F& o' R7 z. z
using it rather frequently, twice a day. The Physicians’( U4 [) X( P# X5 k3 F4 E, x
Desk Reference, or package insert of this product, gel or
* G* a! d- `4 f5 tcream, cautions about dermal testosterone transfer to2 E0 s+ [2 D# M2 t1 {2 F
unprotected females through direct skin exposure.7 S# D3 V/ v' O- b
Serum testosterone level was found to be 2 times the
+ {; S6 m" p; K! |' r. ]% C) k1 cbaseline value in those females who were exposed to# I& M9 f& O1 e% M7 P  {( X
even 15 minutes of direct skin contact with their male4 F: g0 h0 `" X; B1 e
partners.6 However, when a shirt covered the applica-( H# I2 o8 o0 r( b; q+ V. i
tion site, this testosterone transfer was prevented.
$ O# G% c9 s3 p. c+ y# h& l- gOur patient’s testosterone level was 60 ng/mL,
$ P" `) I: f6 qwhich was clearly high. Some studies suggest that
0 U4 g$ K$ v+ l. i# A, w2 u9 Z/ L: U: c7 |dermal conversion of testosterone to dihydrotestos-
6 e. E5 u1 |1 `  i& ]terone, which is a more potent metabolite, is more
9 x+ i. H  m: s& g/ lactive in young children exposed to testosterone
! e. W1 k' ^7 Q* k6 ]! I; T; uexogenously7; however, we did not measure a dihy-# h0 t3 e4 Y3 q- }6 ]: x% E1 B# o2 K
drotestosterone level in our patient. In addition to
4 W* O9 I, o' @virilization, exposure to exogenous testosterone in( q/ p* ^* L. a  y
children results in an increase in growth velocity and( Z0 E* m3 y: ]1 S
advanced bone age, as seen in our patient.1 o; M, Y7 l% A
The long-term effect of androgen exposure during, P) }! q3 W  ?, @2 ~+ Z# T0 N
early childhood on pubertal development and final! ^, K: h- D, }- N5 U: {4 p
adult height are not fully known and always remain; N3 w8 |4 ?  K
a concern. Children treated with short-term testos-, Z$ m* v# A6 N9 H4 L
terone injection or topical androgen may exhibit some
; l& |" D- \( H) C$ r- G  m$ X0 X0 Lacceleration of the skeletal maturation; however, after, G* M" y% z$ ]
cessation of treatment, the rate of bone maturation: B; w: e% G  O/ G  b
decelerates and gradually returns to normal.8,9
, R3 y9 [/ a+ b: ~5 h. P, rThere are conflicting reports and controversy8 l2 n% I: L9 @; c2 \
over the effect of early androgen exposure on adult
) j0 @! {) o9 ^+ B2 y' x$ K7 ]penile length.10,11 Some reports suggest subnormal' w2 B! D' B) I* b2 Z
adult penile length, apparently because of downreg-
9 i" e- E0 `0 l9 aulation of androgen receptor number.10,12 However,; ?! x5 h$ I9 Q
Sutherland et al13 did not find a correlation between3 g. D, L. k5 x% c% k
childhood testosterone exposure and reduced adult7 |1 N( y3 Q8 V: o9 p
penile length in clinical studies.) H4 z1 Z. J* U. W
Nonetheless, we do not believe our patient is! @+ E7 [6 \# J1 N' r$ \" L7 f
going to experience any of the untoward effects from
$ I5 Z  w$ J$ b" r7 Qtestosterone exposure as mentioned earlier because
3 \4 G  W9 f* ^7 W; E$ athe exposure was not for a prolonged period of time.# F# U+ Z4 U) _" i' R6 E
Although the bone age was advanced at the time of7 u, b; e9 l* S
diagnosis, the child had a normal growth velocity at* U/ h3 B' y* z
the follow-up visit. It is hoped that his final adult- q1 ?- D' P# M7 p( ]
height will not be affected.
$ O: B0 Z# ], V6 a8 rAlthough rarely reported, the widespread avail-: W* z# |1 [6 {
ability of androgen products in our society may
/ f# T- ^9 U% N" G  ^( _/ sindeed cause more virilization in male or female; p" n9 B& j( S; T6 y& [$ a" B
children than one would realize. Exposure to andro-
8 @3 E3 N2 o! r! A) g1 ggen products must be considered and specific ques-
9 j' A1 o' J1 r9 j8 H. Stioning about the use of a testosterone product or
/ \. _' w  p* l8 [5 T# l) O  Ygel should be asked of the family members during
* V$ o9 M) F2 sthe evaluation of any children who present with vir-
4 `( P+ u5 J& U. }2 ^. V' `ilization or peripheral precocious puberty. The diag-% i# A+ \* w* i; e( l1 B
nosis can be established by just a few tests and by
) q) b: D/ V% p, N( `# l% |appropriate history. The inability to obtain such a8 k  l7 c; F' d7 [" d1 |
history, or failure to ask the specific questions, may1 I( \2 o* D3 l& j; K1 M2 _* c
result in extensive, unnecessary, and expensive
  q* J' W1 g7 n  [, Zinvestigation. The primary care physician should be
+ |& G4 \# [4 h1 Iaware of this fact, because most of these children/ }8 J: F" e; s! V
may initially present in their practice. The Physicians’
4 f% ?) I4 F5 H2 I) E/ e# zDesk Reference and package insert should also put a
8 u7 E) A) `( Q; z( w9 S2 q+ c2 Awarning about the virilizing effect on a male or3 R+ D) N6 A; n* d' C2 P( L
female child who might come in contact with some-
$ Q/ q& U5 h- S2 H) uone using any of these products.  i" h* Z. |* q- C& a" b
References
1 h/ o, b' T5 G& {1. Styne DM. The testes: disorder of sexual differentiation
9 Q1 n. {8 E- s0 H4 ^4 i) E6 s; land puberty in the male. In: Sperling MA, ed. Pediatric
. y+ q1 @2 R; \2 W) T" Q8 b; GEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;0 b1 k6 F" J3 _+ E* r! J
2002: 565-628.1 Y9 D/ r" R. s/ u# l' q
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
0 ^7 C8 P: L' Q# R- O# D- ipuberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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 {. Z) n) I/ z7 `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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