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Sexual Precocity in a 16-Month-Old, ~# n) f- h& S. M/ i& D2 B
Boy Induced by Indirect Topical% j5 T+ Q$ [) M
Exposure to Testosterone
, P6 r$ L3 X4 _) x& }3 CSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
4 }0 c' O, ~" p; u6 [; A- a8 E1 zand Kenneth R. Rettig, MD1/ O  P& \0 P$ g3 Y( i9 U
Clinical Pediatrics
* G# v4 V  k8 ?6 Q7 I3 M5 P9 {1 wVolume 46 Number 6/ ^" d! Q$ _, l( I
July 2007 540-543& Z; S8 @1 e; H0 C
© 2007 Sage Publications5 t" E+ F" \0 y" W" Y
10.1177/00099228062966512 s( V; y2 \& c4 l! `
http://clp.sagepub.com
# x/ z4 Z. D7 N% ^hosted at; @5 I; T& g3 w' q- s/ |
http://online.sagepub.com
1 d. l" s: Q% z" SPrecocious puberty in boys, central or peripheral,! d1 {& J' }/ \5 U( V# L
is a significant concern for physicians. Central7 T5 M6 z, s7 g4 n" u: m- D
precocious puberty (CPP), which is mediated4 K2 Y% p. y( p& X7 c. a" v
through the hypothalamic pituitary gonadal axis, has
9 _1 m8 G  [7 q5 E! @a higher incidence of organic central nervous system# h9 n: n+ `* ^+ l0 B  m
lesions in boys.1,2 Virilization in boys, as manifested! p$ c4 m5 g' x0 o
by enlargement of the penis, development of pubic2 H" \$ ?4 W* O9 U. Q8 w1 U/ _5 t0 T
hair, and facial acne without enlargement of testi-5 P7 H2 T* Y8 B+ H9 ?
cles, suggests peripheral or pseudopuberty.1-3 We
& c3 T/ W* z  a, c2 W- V8 U" Vreport a 16-month-old boy who presented with the
) b  N& k; Q8 D% k1 F4 \: T4 m: wenlargement of the phallus and pubic hair develop-
  i8 j! n% _! @+ D- n- i& l1 }; N2 zment without testicular enlargement, which was due
) {; ^# x2 @; j9 X5 |0 B9 lto the unintentional exposure to androgen gel used by! r: }9 w. g+ \
the father. The family initially concealed this infor-
) _7 Q9 F! K% h9 o: q% K( wmation, resulting in an extensive work-up for this8 o9 t1 c9 ~4 M
child. Given the widespread and easy availability of
5 @' s" @* \' w3 o$ a9 rtestosterone gel and cream, we believe this is proba-5 a( F% g; S/ J
bly more common than the rare case report in the
+ w) H  f# d( M: B% Yliterature.4* }4 S5 A6 k9 N* F9 m! w
Patient Report
' f& k8 u- Y. p* E% [A 16-month-old white child was referred to the( B1 D* f5 u5 m% \# V2 g) _
endocrine clinic by his pediatrician with the concern! m2 \; i. Q! X: [- j
of early sexual development. His mother noticed" c" J/ \! ]! W5 s# ^% G
light colored pubic hair development when he was$ K2 f' J4 t) z) Y: C. `
From the 1Division of Pediatric Endocrinology, 2University of" Z$ W# Y/ W9 ?/ {
South Alabama Medical Center, Mobile, Alabama.5 C! e8 A* o: S3 K. R3 C4 l; E
Address correspondence to: Samar K. Bhowmick, MD, FACE,) P- f  I: p3 P% S8 P2 h0 L
Professor of Pediatrics, University of South Alabama, College of" r8 a0 {2 u( l; \$ d0 J
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 w6 A/ [/ \. x9 y4 Q, L% p
e-mail: [email protected].) w! z+ a2 Z7 p" Q# F
about 6 to 7 months old, which progressively became
2 P6 G- U1 ^- _, X7 v# ]5 bdarker. She was also concerned about the enlarge-
* k. S. e* |& }3 ^; @  ]ment of his penis and frequent erections. The child1 A3 t- H. E: h4 m; C
was the product of a full-term normal delivery, with& {8 _6 m( \: Q( {) h
a birth weight of 7 lb 14 oz, and birth length of' W' H1 y; o# J8 C5 D
20 inches. He was breast-fed throughout the first year5 J, h$ {0 `% T/ S: }, S" {; A
of life and was still receiving breast milk along with
7 ^0 \  ~1 f7 [4 ~# m8 Msolid food. He had no hospitalizations or surgery,
8 m" y/ q+ t7 L, o* k- Kand his psychosocial and psychomotor development
; O  H+ t- _, R5 e) A/ u# lwas age appropriate.
& J6 ]3 z( M. _# g7 YThe family history was remarkable for the father,
4 ?, I7 R% P7 o0 F+ m4 ?who was diagnosed with hypothyroidism at age 16,
' c0 l( H" f  z9 y- xwhich was treated with thyroxine. The father’s
& l( |7 F) O4 rheight was 6 feet, and he went through a somewhat
2 n! S( }* c; @& ?0 e9 dearly puberty and had stopped growing by age 14.( z5 h& ?& S# p7 y+ u7 X1 I8 ]
The father denied taking any other medication. The
  C$ K& v$ n: Y8 mchild’s mother was in good health. Her menarche% m) n5 w  [. Y# k$ Z/ K& ^; t3 n
was at 11 years of age, and her height was at 5 feet
. O. {# I8 `- ]  d: }1 Y6 F5 inches. There was no other family history of pre-" t6 _; O7 i; e/ A" R
cocious sexual development in the first-degree rela-# G* A. f( G) K' r  p: ], X
tives. There were no siblings.# P  e* U- m' r, y  I( `; p7 Y1 z
Physical Examination2 ?9 `3 V1 o- Z6 J
The physical examination revealed a very active,$ b# \5 P6 T) R3 B
playful, and healthy boy. The vital signs documented
; W% z1 ~- z, w% q) la blood pressure of 85/50 mm Hg, his length was; {) L& h5 ^! d7 P* ^8 z
90 cm (>97th percentile), and his weight was 14.4 kg! D2 S4 J  y6 D1 O; F* l
(also >97th percentile). The observed yearly growth- B! I- ~# A2 e! E! Q3 Q( ^
velocity was 30 cm (12 inches). The examination of) F9 L; s" W6 c
the neck revealed no thyroid enlargement.
( f/ [7 |6 S  w$ J7 q( ~, S# BThe genitourinary examination was remarkable for/ _. M+ P# F) a8 a, \! T
enlargement of the penis, with a stretched length of' n0 B' U2 a0 B: m
8 cm and a width of 2 cm. The glans penis was very well
$ @7 \3 w; d/ e9 e3 {, I! v- bdeveloped. The pubic hair was Tanner II, mostly around; t3 F7 O$ p2 ^4 |; k, b
540
" G- O% R2 w4 K" {6 t" zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, N0 _; }7 {+ D7 \5 l9 u1 u+ kthe base of the phallus and was dark and curled. The
+ O0 k2 |4 }! f6 Ytesticular volume was prepubertal at 2 mL each.
4 A. X5 U$ o; yThe skin was moist and smooth and somewhat& W0 X$ T& C$ Q- A9 `/ A9 Q% Y
oily. No axillary hair was noted. There were no" L( w$ H1 u  i6 f. f: f
abnormal skin pigmentations or café-au-lait spots.* K( `  }0 J/ A8 g- \- B6 b% a. Y% I4 h( E
Neurologic evaluation showed deep tendon reflex 2+
" D$ A% ?7 ^; k5 N) }( |bilateral and symmetrical. There was no suggestion
. r% K0 N0 k; i6 p7 Fof papilledema.
0 z/ y4 O/ X4 I. _- V8 ELaboratory Evaluation' T, R4 `0 ]# j+ j7 |
The bone age was consistent with 28 months by/ k1 v0 K' |- k2 m+ R' D8 E# o
using the standard of Greulich and Pyle at a chrono-0 L- X3 @2 X" `+ a) A3 I6 @
logic age of 16 months (advanced).5 Chromosomal& r: J+ G; {& P1 w
karyotype was 46XY. The thyroid function test) r9 M( Q3 R4 ]  }6 i# ~$ W; X
showed a free T4 of 1.69 ng/dL, and thyroid stimu-) ?1 m- w; F! D/ y3 M
lating hormone level was 1.3 µIU/mL (both normal).+ X/ b: h# p. X0 P
The concentrations of serum electrolytes, blood1 y& C8 G5 e3 l" e
urea nitrogen, creatinine, and calcium all were+ T* x3 F2 F# u. G! _5 k6 \: T
within normal range for his age. The concentration
. U: S7 P  f; z( M3 g% Sof serum 17-hydroxyprogesterone was 16 ng/dL) r- k" x% {: x) T+ W9 @4 Y' S1 ~
(normal, 3 to 90 ng/dL), androstenedione was 20
+ p# ?- b, e5 a# F6 m, mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ H5 ~( k/ m) o" S) [9 p, i
terone was 38 ng/dL (normal, 50 to 760 ng/dL),9 S' _2 u! j- J$ @
desoxycorticosterone was 4.3 ng/dL (normal, 7 to+ g4 ^! Y: j7 }! v5 R# c! v
49ng/dL), 11-desoxycortisol (specific compound S)/ D: h. F7 C/ s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-+ T6 |) X) z9 x- p
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* t" M! V% k1 v5 G1 H* Wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ Y: |8 o9 q  o! K9 j3 L8 ?and β-human chorionic gonadotropin was less than
1 z* H# ^+ R4 Y% L* |4 Y; E8 ?  |5 mIU/mL (normal <5 mIU/mL). Serum follicular+ B% ~: D* _6 O
stimulating hormone and leuteinizing hormone+ o' G4 _) ~! O. k7 S' s7 u# R. g
concentrations were less than 0.05 mIU/mL2 T! c/ I1 A' k' G; }8 B9 a/ ^' Q  E3 y) |
(prepubertal).
, y  j* R7 h6 k1 {2 y( NThe parents were notified about the laboratory
( H; k. G' t4 F+ vresults and were informed that all of the tests were
9 z+ q& w) f, z5 H! C( c' E7 gnormal except the testosterone level was high. The4 G0 [3 B5 E7 _% A2 m
follow-up visit was arranged within a few weeks to
5 V4 n1 t2 P3 u4 Yobtain testicular and abdominal sonograms; how-
, m) `2 R  g- [* M% Kever, the family did not return for 4 months.
7 Q/ h* c8 w& c% P& i* D/ iPhysical examination at this time revealed that the- R0 S& s9 {7 X7 H! E9 m
child had grown 2.5 cm in 4 months and had gained' ]9 [7 v, n* `+ o6 p1 z
2 kg of weight. Physical examination remained; ~& l% G; f$ u( ~- v. j
unchanged. Surprisingly, the pubic hair almost com-
7 A& _  t6 d9 E% D2 ipletely disappeared except for a few vellous hairs at1 D4 s2 a& H2 P
the base of the phallus. Testicular volume was still 2
; x# U6 U. S2 H0 B- @mL, and the size of the penis remained unchanged.' N+ r* s! `9 [9 U8 Z; l8 _1 p- A
The mother also said that the boy was no longer hav-
$ l3 A4 M# y) ying frequent erections.6 G' M4 I5 ^7 R
Both parents were again questioned about use of. M$ ?0 Q+ t7 `9 Y
any ointment/creams that they may have applied to% }$ t8 w" W8 f) F2 o) ^
the child’s skin. This time the father admitted the
5 W7 x% x9 g1 G  a7 f+ _Topical Testosterone Exposure / Bhowmick et al 541
; p6 G6 X# V" Y8 Euse of testosterone gel twice daily that he was apply-5 v0 _/ R2 k4 w4 n% B
ing over his own shoulders, chest, and back area for
, D+ B, g: O2 ya year. The father also revealed he was embarrassed
; X0 E1 c) C9 b  O/ ato disclose that he was using a testosterone gel pre-) F  _6 X) i' }% {! M# I9 r
scribed by his family physician for decreased libido/ S' G" `1 Q+ \; ?. Q
secondary to depression.
0 U8 u& Q, s. \# X( V) Y: ^The child slept in the same bed with parents.; Y+ w% K" i: {! @) [
The father would hug the baby and hold him on his
7 W% X( m1 t% Xchest for a considerable period of time, causing sig-
- m8 s2 F; [0 F5 t2 ]8 d8 fnificant bare skin contact between baby and father.; J6 v1 t. H1 S' ]' v$ v9 l7 h
The father also admitted that after the phone call,
: I* m' }" U( b5 M* ]when he learned the testosterone level in the baby2 |& o  x5 }8 R" m
was high, he then read the product information
8 O: R, k$ }! l. l8 [' t* T$ n; Y$ ?packet and concluded that it was most likely the rea-
2 u8 ~1 H3 a- E! mson for the child’s virilization. At that time, they
9 H) ?! I5 v' D. `( n0 [7 r+ Tdecided to put the baby in a separate bed, and the7 \5 ^! \; Y0 w
father was not hugging him with bare skin and had: E$ Q5 z7 W4 w& d8 y; O
been using protective clothing. A repeat testosterone$ H( `- X& v+ Z! l; {3 c2 g
test was ordered, but the family did not go to the
# M1 p! y1 `" h* d+ H+ L; Dlaboratory to obtain the test.
1 w1 q0 f! s2 {0 i* }/ k" y& E8 TDiscussion
5 N( d" @8 v& w: y9 _3 S7 d& H6 bPrecocious puberty in boys is defined as secondary
, g  s% z2 D* Z- z+ J; Ksexual development before 9 years of age.1,4( q$ e! p( B% H+ f1 R, l/ C
Precocious puberty is termed as central (true) when7 o" e# d; ]0 ]; t
it is caused by the premature activation of hypo-2 h: y! j) n  Z0 r
thalamic pituitary gonadal axis. CPP is more com-
' S. R8 m6 P! I* Z! }mon in girls than in boys.1,3 Most boys with CPP: Z2 }0 O. m1 E* h, w" ~% G
may have a central nervous system lesion that is% [. t7 D  e2 Z. \
responsible for the early activation of the hypothal-- X- t1 K$ M  k4 g$ f2 b9 ~# v
amic pituitary gonadal axis.1-3 Thus, greater empha-
, D0 {, I% {$ `" P' Nsis has been given to neuroradiologic imaging in
3 F; N5 B: S& pboys with precocious puberty. In addition to viril-3 ^$ U5 W9 U- q; M7 S# L
ization, the clinical hallmark of CPP is the symmet-# K, I, k9 h: `# a% c
rical testicular growth secondary to stimulation by
, Y; F! b( t4 A9 X/ X8 Z7 F: X& zgonadotropins.1,3& ^. o) H! M$ X% d* U, F& K% S
Gonadotropin-independent peripheral preco-
; d# ~4 _. r8 j" ncious puberty in boys also results from inappropriate
9 d' @5 o' g$ t# xandrogenic stimulation from either endogenous or1 b" c  S6 h( z5 }( [1 g
exogenous sources, nonpituitary gonadotropin stim-
9 ^: n* j3 B' pulation, and rare activating mutations.3 Virilizing7 f( t5 J0 a# Q; N8 h5 N
congenital adrenal hyperplasia producing excessive
6 a$ X1 p( i/ l# sadrenal androgens is a common cause of precocious
/ I1 y  C6 [' [; c1 ^  Xpuberty in boys.3,44 T, z' j3 @* b$ R" i; b
The most common form of congenital adrenal6 `8 K. O* u# ?' n! p
hyperplasia is the 21-hydroxylase enzyme deficiency.
1 ]0 M" s$ a! e* K! ZThe 11-β hydroxylase deficiency may also result in
9 s  w& b+ p. [excessive adrenal androgen production, and rarely,
# E& s7 R' E, e, ]% Yan adrenal tumor may also cause adrenal androgen
8 R( U7 U8 R0 R& x) k' cexcess.1,3& D& j  J" V) K& a8 f# Q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& x& S% h& d% w! ^$ R542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- Y$ d! W, k  @& `/ d
A unique entity of male-limited gonadotropin-: D5 ~3 ]0 \: N6 u- ~  X2 }
independent precocious puberty, which is also known0 u# ]8 t+ ~7 f9 r7 r7 I
as testotoxicosis, may cause precocious puberty at a; J# V& X& v( D- \! ~+ W
very young age. The physical findings in these boys7 E2 X  F( n, c, ~: l2 _( `, _* d
with this disorder are full pubertal development,! N/ u) M( @% V# H
including bilateral testicular growth, similar to boys9 @4 _4 x" b1 v6 u
with CPP. The gonadotropin levels in this disorder
# R% R- t& D" h0 care suppressed to prepubertal levels and do not show2 o2 B* ~/ s' e# f3 |$ P( F+ P
pubertal response of gonadotropin after gonadotropin-
) W3 f5 d* W  J) @/ `releasing hormone stimulation. This is a sex-linked' s3 B, b% F& k' O7 J8 n  f
autosomal dominant disorder that affects only6 R0 \7 v- f; l  e6 H' k) r
males; therefore, other male members of the family( a3 \& P2 p' ?. P9 X$ B4 O- w$ N
may have similar precocious puberty.3
% o. `5 ^5 h' z5 M9 kIn our patient, physical examination was incon-
4 y% y4 g% y8 ?4 W3 y& E& P: t1 G. ksistent with true precocious puberty since his testi-
# e* j; A: c% U/ C8 L1 zcles were prepubertal in size. However, testotoxicosis
$ K3 z) f3 L) S$ Twas in the differential diagnosis because his father8 A, k3 A, J2 Q& m- `7 k  @
started puberty somewhat early, and occasionally,, X% I+ B3 q8 k  ^; ^& I! K
testicular enlargement is not that evident in the9 A, W8 @; c: L" x" v8 @
beginning of this process.1 In the absence of a neg-
6 I2 I4 s7 F  d8 [4 mative initial history of androgen exposure, our; P* d0 ^6 [6 }( k1 n# V% @, }0 z6 T
biggest concern was virilizing adrenal hyperplasia,
0 \. o- y4 e# ~/ M1 p1 L( x; ceither 21-hydroxylase deficiency or 11-β hydroxylase' i, O! C5 d+ F- {  ?1 S1 ]
deficiency. Those diagnoses were excluded by find-! p# @0 Q1 b* P: y% }
ing the normal level of adrenal steroids.
8 h; W/ ]: W* z. Y2 H/ xThe diagnosis of exogenous androgens was strongly+ @/ U* e9 I3 s( t5 f5 e0 [' Z
suspected in a follow-up visit after 4 months because
# E" r' r3 W$ m& w8 J: ~- N6 Bthe physical examination revealed the complete disap-
3 t, N/ ~" V" k" ^+ N+ ^$ S+ c- Xpearance of pubic hair, normal growth velocity, and
- t' Z3 i* H, Z2 D8 N6 Ldecreased erections. The father admitted using a testos-
/ n2 H2 j0 v& F2 Kterone gel, which he concealed at first visit. He was
$ \8 \0 M9 m5 s- d; D! Rusing it rather frequently, twice a day. The Physicians’
1 H. }$ C3 l+ O' F& ]6 uDesk Reference, or package insert of this product, gel or9 i' I$ K) ^) T7 G7 o( V% ?; |# _
cream, cautions about dermal testosterone transfer to# A4 q0 U" a" ]% o" n& g3 b8 h
unprotected females through direct skin exposure.4 f9 H2 Z2 O$ t8 {8 Q% k- m1 _
Serum testosterone level was found to be 2 times the$ S$ v# |5 `  T: J: `. I( |: h
baseline value in those females who were exposed to
/ p) H, u& t" Seven 15 minutes of direct skin contact with their male
( c) L$ T& o& _5 D& N* v. I" Y8 G- Upartners.6 However, when a shirt covered the applica-' u: i" D! ?, `
tion site, this testosterone transfer was prevented./ ^4 Z. A) {* B, G
Our patient’s testosterone level was 60 ng/mL,1 Q, p( \1 a  v5 g7 M) x3 s. k
which was clearly high. Some studies suggest that# C5 f2 G# o7 ~9 O5 Q: G5 ]
dermal conversion of testosterone to dihydrotestos-
; Z* v+ y" X- j2 `terone, which is a more potent metabolite, is more4 S6 Q/ Y. m6 q/ R
active in young children exposed to testosterone$ G# J1 f4 x) W0 z( Q' W$ ?" e+ k/ F
exogenously7; however, we did not measure a dihy-& Y( s- t1 R( X3 I
drotestosterone level in our patient. In addition to
+ v* {/ T9 A. n( n+ ^0 Lvirilization, exposure to exogenous testosterone in& G6 K; A' b3 u; ]- S
children results in an increase in growth velocity and
6 A5 I" X7 D% d( D( r4 L: ~% i% Eadvanced bone age, as seen in our patient.
% C0 D+ [) O, T  DThe long-term effect of androgen exposure during
! o+ I/ o1 K3 M* w7 B& bearly childhood on pubertal development and final$ h8 e  f6 |: H$ s
adult height are not fully known and always remain
* v+ `$ D- c# m& D7 A- j+ L& t6 Ma concern. Children treated with short-term testos-0 M5 ]% t. J  ]6 w  x  y
terone injection or topical androgen may exhibit some+ ^/ \! K9 _3 |" w
acceleration of the skeletal maturation; however, after
3 o/ [- [2 ?: V% L4 Lcessation of treatment, the rate of bone maturation
; n. C2 t" L. o8 S! X- Z4 ^decelerates and gradually returns to normal.8,9: T" b+ L- q9 F' j1 \: u* z& \. J
There are conflicting reports and controversy1 x* c/ z  C! C1 F
over the effect of early androgen exposure on adult
7 x$ \- v' Y! q0 [penile length.10,11 Some reports suggest subnormal
: ~% V1 x% W5 B3 {( a! q) ]adult penile length, apparently because of downreg-+ Q) c3 A( _% n; z! r
ulation of androgen receptor number.10,12 However,! W6 I# K0 V3 u4 _9 r# S
Sutherland et al13 did not find a correlation between
0 v/ ]" c) I+ e3 Bchildhood testosterone exposure and reduced adult" t" v0 e$ l, ]. M- }+ n# V4 |
penile length in clinical studies.
4 w/ S  b. K8 H8 P5 r& gNonetheless, we do not believe our patient is, g- c; M3 C6 E. \7 Y* n6 h4 V$ i5 G
going to experience any of the untoward effects from. m5 c. ?! g! N6 |
testosterone exposure as mentioned earlier because
, A1 `/ M  g' @. R! H$ \the exposure was not for a prolonged period of time.  P' [% E/ B3 |7 w9 _
Although the bone age was advanced at the time of- o; Y2 M- f9 s8 x1 y  h
diagnosis, the child had a normal growth velocity at0 P" m. L& j1 M9 V7 c
the follow-up visit. It is hoped that his final adult. k, R# N5 s& f  Q/ I% r2 o
height will not be affected.
- C. ~  P8 v; _, x" d* MAlthough rarely reported, the widespread avail-
; O0 R5 t4 F* v/ n( fability of androgen products in our society may3 @+ K" z8 A9 h7 A
indeed cause more virilization in male or female
3 t. D! p0 W( B* Jchildren than one would realize. Exposure to andro-
  @8 f5 Z# C( I0 j& T; p- T! tgen products must be considered and specific ques-
3 F$ s( F5 q( R3 F, S: I3 J5 wtioning about the use of a testosterone product or  X; W2 y% ^: s
gel should be asked of the family members during
' y( w" W) B9 Wthe evaluation of any children who present with vir-
$ V) g# O& S+ pilization or peripheral precocious puberty. The diag-) c/ U2 t8 P: j! ~- B* X
nosis can be established by just a few tests and by
* z; @3 P: B; Y- Q! W8 rappropriate history. The inability to obtain such a  r, D, G9 P& z: Q& |
history, or failure to ask the specific questions, may
6 B; }  J' q! w  [* n/ @2 Dresult in extensive, unnecessary, and expensive
9 B/ I6 M/ s+ ainvestigation. The primary care physician should be- Z4 W; o+ w, P" u" p
aware of this fact, because most of these children
( i2 n7 ?% x* R* A4 B+ ~may initially present in their practice. The Physicians’/ n, j& J( ]7 X6 r
Desk Reference and package insert should also put a; T1 R) F1 A# |! ~
warning about the virilizing effect on a male or( y; J8 X; `' e9 n
female child who might come in contact with some-* C0 _& S: t  |7 _; ?
one using any of these products.
( O& m6 e: u, p8 x4 ~5 LReferences
$ q4 x1 Y  M; m  s1. Styne DM. The testes: disorder of sexual differentiation
  |  I% p; ^* I0 R$ S0 eand puberty in the male. In: Sperling MA, ed. Pediatric
2 d( j' E' k! ^( Z  l1 vEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* C6 B! |. ?0 @) E' @& ?4 h1 X2002: 565-628.
9 l4 B4 \  Q, M* C2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# s7 k3 n) l8 D( S; r6 W
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
7 A$ x* K8 y- d+ D* MBoy Induced by Indirect Topical
. B0 }* {2 a! U5 FExposure to Testosterone
  A! n0 [0 b  b) ]Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
5 a5 {( ?7 u/ m% O) Aand Kenneth R. Rettig, MD1  `' ^( G2 U2 r5 j9 ~
Clinical Pediatrics1 |, [0 K5 e5 }' ~
Volume 46 Number 6
; w$ r6 [$ W) f  p! jJuly 2007 540-543
; U. ^! Z% B. ]© 2007 Sage Publications- L9 a$ T# S9 c
10.1177/0009922806296651  L  u0 T" a) g' f
http://clp.sagepub.com( G0 d+ d7 i1 v8 C
hosted at; Q" [3 S8 e7 R) ]3 _1 b1 s% S$ b4 ]
http://online.sagepub.com
" `$ I$ g2 e3 f+ a3 P1 bPrecocious puberty in boys, central or peripheral,8 }" {5 W1 N6 S5 W! K7 z+ n
is a significant concern for physicians. Central5 z& Q0 a9 c) d  t5 ]- H
precocious puberty (CPP), which is mediated
. Z1 b5 _4 A) T4 Dthrough the hypothalamic pituitary gonadal axis, has
$ k( ?1 j% D0 a8 t% la higher incidence of organic central nervous system6 p4 Y# l1 V  h7 d" Z! E( Z& [
lesions in boys.1,2 Virilization in boys, as manifested
9 X9 s$ {5 P. C& w0 }. W: Vby enlargement of the penis, development of pubic$ U) q- a" l& t0 q- ?; K6 J6 w
hair, and facial acne without enlargement of testi-7 c  d& R6 u  n
cles, suggests peripheral or pseudopuberty.1-3 We; W+ u" K- v6 Z  s1 j0 G
report a 16-month-old boy who presented with the
9 M/ Z  t, Q5 s# h/ X9 u3 A, Aenlargement of the phallus and pubic hair develop-# m0 ]8 ?. ?0 F- U9 o' ?
ment without testicular enlargement, which was due
0 A1 W1 Y, Y# C* p" s/ o1 F3 |' [to the unintentional exposure to androgen gel used by
& R4 D& t8 f+ \1 J+ a" M3 Q- U/ Athe father. The family initially concealed this infor-
0 z; |1 I0 f+ [% u: S2 K; Wmation, resulting in an extensive work-up for this
) b' |8 @. H9 G( a3 i5 t( ~8 tchild. Given the widespread and easy availability of
+ J% j& [- R4 {" [# {+ ~0 Itestosterone gel and cream, we believe this is proba-0 w% O- L$ G5 c( p# a; H/ I
bly more common than the rare case report in the
" Q% x5 U& z8 Sliterature.4
. x5 p  [1 ]( [( j4 Y: B) a% R1 aPatient Report
/ a8 z; A! ]3 n9 kA 16-month-old white child was referred to the1 o% s$ v6 Z. h1 x2 K, N
endocrine clinic by his pediatrician with the concern
- Y! T1 f; z2 u1 {8 h9 Cof early sexual development. His mother noticed& z, y: ]" G, |$ @' y: ]
light colored pubic hair development when he was
0 `3 R# o. V& DFrom the 1Division of Pediatric Endocrinology, 2University of
# N- L4 X5 p+ C; v( c* D- vSouth Alabama Medical Center, Mobile, Alabama.
8 {- Q  n' E9 _Address correspondence to: Samar K. Bhowmick, MD, FACE,- q1 ?5 h. d" H" z
Professor of Pediatrics, University of South Alabama, College of
0 H& ^, y/ {3 C$ }0 w, \Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ O/ r8 F9 w5 G+ S. ^+ h( |& re-mail: [email protected].0 S$ H/ E; I! ^& C# b
about 6 to 7 months old, which progressively became
8 G6 ~9 Z5 @, y! Q  i: c4 fdarker. She was also concerned about the enlarge-
; j- G8 R0 w, k( mment of his penis and frequent erections. The child
4 O: J$ H" K. |  Z6 A  Lwas the product of a full-term normal delivery, with
$ R) P# Z3 ]% `* T$ g. u( ja birth weight of 7 lb 14 oz, and birth length of& _& ]# M, S7 H  |
20 inches. He was breast-fed throughout the first year
) p5 E$ K6 o4 F3 T4 J3 Iof life and was still receiving breast milk along with% ?  x6 s& `9 u! y* X/ @2 l
solid food. He had no hospitalizations or surgery,  }  K5 \) x* ]: |" y0 q% B! |
and his psychosocial and psychomotor development8 V+ z: D+ t; K& }9 h
was age appropriate.
$ c6 f5 r) q$ c; b" aThe family history was remarkable for the father,
) L* d! X, O! [" bwho was diagnosed with hypothyroidism at age 16,
' l) S1 i$ g9 }3 T* Z3 b1 H$ v2 H( jwhich was treated with thyroxine. The father’s
+ U% v6 \2 D% n, i; w2 pheight was 6 feet, and he went through a somewhat8 U7 @( ^- g+ N3 s1 k: K( w
early puberty and had stopped growing by age 14.
" [4 ]# o- `/ [! y- S, SThe father denied taking any other medication. The* E& D8 p. B+ r5 a
child’s mother was in good health. Her menarche* V. _! S7 d  \
was at 11 years of age, and her height was at 5 feet
" a. V+ E+ G  ?" j5 inches. There was no other family history of pre-& r) c8 L) G) c
cocious sexual development in the first-degree rela-- r* a9 x7 S" }* [
tives. There were no siblings.* N& T6 ]2 B- ]) d8 ]; ?
Physical Examination
5 ?, ~# T$ z; j# }8 |The physical examination revealed a very active,
7 o8 r+ h& \, Y6 Fplayful, and healthy boy. The vital signs documented
- \% ]. l0 R- M* s& da blood pressure of 85/50 mm Hg, his length was' }1 v* r+ u  c! G/ w. L
90 cm (>97th percentile), and his weight was 14.4 kg+ a" [8 R( ]! ?1 _
(also >97th percentile). The observed yearly growth* d1 D/ B0 o% s: ^. q
velocity was 30 cm (12 inches). The examination of
+ A1 S  S" v% Athe neck revealed no thyroid enlargement.; h' Q6 M0 `3 x' H
The genitourinary examination was remarkable for
$ N; r* y. D1 T4 x0 j' k" y4 t* Henlargement of the penis, with a stretched length of
/ r  H" Q+ B: [8 cm and a width of 2 cm. The glans penis was very well
% z9 ~3 ^- a) D3 H6 t# S# T0 R$ p9 qdeveloped. The pubic hair was Tanner II, mostly around( V& [0 K7 L% H/ F' c* `
540
. Z% Y5 v$ T. n" Aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: P. U, z" L, J% Z' O( o  U# C
the base of the phallus and was dark and curled. The9 L* c5 ]% G; ^, E: D
testicular volume was prepubertal at 2 mL each.0 l$ e1 G; L4 C( y6 _9 n- F
The skin was moist and smooth and somewhat; L4 [' q) \3 _2 l6 V  |% `9 d
oily. No axillary hair was noted. There were no
5 n/ a. \8 I0 r* O0 p4 y& Babnormal skin pigmentations or café-au-lait spots.
1 R" p1 N, S3 }: ^Neurologic evaluation showed deep tendon reflex 2+
2 R9 p( E/ @1 {& b" a8 [' Abilateral and symmetrical. There was no suggestion
/ x+ m- ~( m' g  Q* yof papilledema.
. O/ D+ _+ |3 h+ c  Z- a8 Q( ~2 HLaboratory Evaluation3 H6 ^# W( P# s& }& z( u
The bone age was consistent with 28 months by
+ M2 c* M; k3 B3 B7 e0 busing the standard of Greulich and Pyle at a chrono-
. f8 P; G- Q) C8 d* y) Y+ plogic age of 16 months (advanced).5 Chromosomal
3 G+ \! _6 ]' k$ m5 I  Bkaryotype was 46XY. The thyroid function test
0 T# {0 n5 B+ i8 m( p/ kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-' z1 D, ]4 V/ L$ b- v( V
lating hormone level was 1.3 µIU/mL (both normal).
% ^* I; U) Y- v5 H: RThe concentrations of serum electrolytes, blood' z& Y+ N) v6 n; S0 z* S6 e
urea nitrogen, creatinine, and calcium all were) E8 e  X6 y* f% Z
within normal range for his age. The concentration! v6 D# `, D# Q8 O& C# b* t) r% i3 B8 S
of serum 17-hydroxyprogesterone was 16 ng/dL; |. F( I) |9 D! l1 K& ^6 E6 a1 @2 x
(normal, 3 to 90 ng/dL), androstenedione was 200 {1 p7 O. g! }
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-9 L# Y5 `0 u0 l) s( x
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
: B3 G# G7 p* Ydesoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ ^3 \# y6 g1 |! |& T8 b49ng/dL), 11-desoxycortisol (specific compound S)* _, c% j; {5 w+ o: _
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 \8 R. Q0 T7 Htisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# ^3 X9 k# _3 t
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),; f+ _2 s$ F7 E$ O
and β-human chorionic gonadotropin was less than4 s+ ]+ P  \$ w8 P: R3 B8 ]: [
5 mIU/mL (normal <5 mIU/mL). Serum follicular* ?$ M6 Q0 z/ J1 |! d; _& s
stimulating hormone and leuteinizing hormone
% r  h5 ^3 N, h8 `0 [concentrations were less than 0.05 mIU/mL4 M9 ]; p% n, V( d* \
(prepubertal).
% a) h, k. K* o. A% V' o, UThe parents were notified about the laboratory2 g+ ]4 }* f8 Q8 S% k
results and were informed that all of the tests were
3 O& `9 V! L& J8 Y% u3 ?+ ]normal except the testosterone level was high. The
% A* D* h( r+ r' {4 {, qfollow-up visit was arranged within a few weeks to: O2 p" p# b/ }( \
obtain testicular and abdominal sonograms; how-
. o. p& P+ q& n9 [. S0 ^ever, the family did not return for 4 months./ ~+ _* L5 Y: }" i9 T
Physical examination at this time revealed that the; R  o2 u+ h" U3 u
child had grown 2.5 cm in 4 months and had gained4 o+ \( R& q0 k- H8 {% J7 g  I) j
2 kg of weight. Physical examination remained
, u! L9 |5 r* A, @3 P! }unchanged. Surprisingly, the pubic hair almost com-4 F5 R" h# M. X
pletely disappeared except for a few vellous hairs at
% M* P4 ]0 c6 a; A5 ethe base of the phallus. Testicular volume was still 27 \" `% ^6 F2 X7 K( w4 e6 v
mL, and the size of the penis remained unchanged.& w1 e- O$ h8 l7 S, ^" m) o  }
The mother also said that the boy was no longer hav-' c1 P, A0 H* m7 ?) r
ing frequent erections.
$ M1 o4 a5 o) r. |, VBoth parents were again questioned about use of
: m# e9 O6 d1 p4 b% I0 F  dany ointment/creams that they may have applied to/ Y1 T" K) o; ^5 W! ]7 b" L3 Q" S" O
the child’s skin. This time the father admitted the
5 J% \4 z3 f' W5 v" g3 tTopical Testosterone Exposure / Bhowmick et al 541% |5 c1 K0 G4 E' n6 G/ r
use of testosterone gel twice daily that he was apply-
( Z! R  J7 J6 m! e2 oing over his own shoulders, chest, and back area for
6 J" k* g& X" D6 O/ ^a year. The father also revealed he was embarrassed
4 ]$ b+ f7 [% H/ n: T: q; `to disclose that he was using a testosterone gel pre-
. |) y+ i/ ^0 N) F* Sscribed by his family physician for decreased libido
& d* k& o7 U' ^) Usecondary to depression.6 q& p; y) `! h: {4 V$ a
The child slept in the same bed with parents.
  }3 r4 \  Z% |; @! UThe father would hug the baby and hold him on his
: ^1 w, W; n/ I( j! F9 t0 @chest for a considerable period of time, causing sig-
: t) t) v- m3 c. Pnificant bare skin contact between baby and father.
7 B& U+ o& ~1 u9 m$ V6 N+ kThe father also admitted that after the phone call,
* g, h+ n/ r! x" P& T8 L7 }when he learned the testosterone level in the baby
+ J  L+ _9 T- Q$ Y% `was high, he then read the product information
- @! g8 Z& D) D* w; |packet and concluded that it was most likely the rea-1 F6 Z: K6 ?1 A3 N. @/ b/ _# `7 n
son for the child’s virilization. At that time, they9 x7 Z& L7 m/ e( \! ?8 P* u
decided to put the baby in a separate bed, and the
" p  K8 L1 r1 ]: }# I2 {& K, Lfather was not hugging him with bare skin and had
/ n5 A3 F$ w+ O9 O- }9 @  m$ ]8 kbeen using protective clothing. A repeat testosterone
4 n( `- z& M7 f5 Z4 T9 c4 j  |test was ordered, but the family did not go to the% {+ ?* L1 V' d) W) z' E
laboratory to obtain the test.- P/ D6 A5 Z3 M, n2 W
Discussion
9 U# O/ d' p0 o$ f- ^  |Precocious puberty in boys is defined as secondary
0 r9 m. P7 \5 ~  l# Fsexual development before 9 years of age.1,4" ^: [' |3 e0 M; Q
Precocious puberty is termed as central (true) when: T3 i8 K% }8 g' r: ^' b- g
it is caused by the premature activation of hypo-( m3 S& F% }* S/ O  Y3 x
thalamic pituitary gonadal axis. CPP is more com-
7 y0 W; ]" X7 D5 m. N9 cmon in girls than in boys.1,3 Most boys with CPP
$ C$ h3 U* B( \. {4 m3 {may have a central nervous system lesion that is
/ v; \! o0 c* S! S* {4 Aresponsible for the early activation of the hypothal-& y, C2 H* y3 x6 K9 N6 a# D7 w
amic pituitary gonadal axis.1-3 Thus, greater empha-
8 S2 l5 y) {3 a3 y( z5 ~sis has been given to neuroradiologic imaging in& Q: {$ }. L; G* G, y( w
boys with precocious puberty. In addition to viril-
8 ?! z; I2 b& }1 Rization, the clinical hallmark of CPP is the symmet-* L& c! M: ?9 {! O5 ~/ S( |
rical testicular growth secondary to stimulation by* X' [5 _: s( F5 T" V1 }' d' b' f
gonadotropins.1,3. y0 l- h3 C8 m
Gonadotropin-independent peripheral preco-
% c5 K, S' `; {/ u$ m& Wcious puberty in boys also results from inappropriate
: W' q. _+ s2 g& sandrogenic stimulation from either endogenous or
9 b9 z+ w6 B; h4 ~1 i& zexogenous sources, nonpituitary gonadotropin stim-* y: u+ |% t' h
ulation, and rare activating mutations.3 Virilizing
: k" i& s9 ?7 j& Zcongenital adrenal hyperplasia producing excessive
( c) E8 K7 k) ^% M4 W: z8 Ladrenal androgens is a common cause of precocious* f8 e# u0 @' d7 j4 J9 n. U1 ?( g
puberty in boys.3,4
; V+ Z% w& W+ S7 F4 \( e3 S4 ?The most common form of congenital adrenal( s: `+ W7 B7 T+ e! {. u
hyperplasia is the 21-hydroxylase enzyme deficiency.
  s; _+ C- n: v& G; d; X' |The 11-β hydroxylase deficiency may also result in
5 }7 v1 Q: R" {  i  yexcessive adrenal androgen production, and rarely,! a9 H6 d* s0 _) i' I3 J  w
an adrenal tumor may also cause adrenal androgen
, A- p2 d3 V8 p3 aexcess.1,3
+ S8 m% N+ _1 ?! c4 L$ [at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
/ a4 o( m- O/ T& w$ ]1 N. {542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 Y$ S* q2 U. M" l: |: P9 v7 r+ J$ c/ IA unique entity of male-limited gonadotropin-
1 r9 e, a+ t+ S6 n* Jindependent precocious puberty, which is also known
; t" ^: g: B$ G: E) j% f, [as testotoxicosis, may cause precocious puberty at a+ Q  T$ L( ]0 }8 A4 u
very young age. The physical findings in these boys, h3 F" r0 o/ h2 J- _8 G  n/ G
with this disorder are full pubertal development,  g  z% P6 }# k* l" m7 ?2 S" g
including bilateral testicular growth, similar to boys
7 _) W$ F3 z  j: b/ ~6 V3 D0 Mwith CPP. The gonadotropin levels in this disorder4 I6 q' r5 ]) M3 z
are suppressed to prepubertal levels and do not show) P! r! K3 B3 P
pubertal response of gonadotropin after gonadotropin-2 x' M& z0 h! a. F# `  y8 k
releasing hormone stimulation. This is a sex-linked7 L# M/ r2 _; n! b
autosomal dominant disorder that affects only
5 i1 _9 @# q. S$ M& vmales; therefore, other male members of the family
! w0 F8 ]4 Y! G6 A# ]3 m! umay have similar precocious puberty.3
9 s  y* d! Z: V  d3 B, p8 @. _In our patient, physical examination was incon-
+ |4 M* `% [' m& K8 T) Y' esistent with true precocious puberty since his testi-
1 D$ p. S2 R) E0 \( }cles were prepubertal in size. However, testotoxicosis
# k! A4 h8 B* D2 {" vwas in the differential diagnosis because his father. H9 l: _3 m. m$ K) |
started puberty somewhat early, and occasionally,* j  G  J+ b, }6 f7 Q
testicular enlargement is not that evident in the/ [. E3 Z; L4 s* j- j  e9 t
beginning of this process.1 In the absence of a neg-/ G. i7 x+ w3 O! p" q
ative initial history of androgen exposure, our% ?/ V1 W, N( L% R4 _$ F
biggest concern was virilizing adrenal hyperplasia,
4 b( ?& c0 D* y6 h9 U1 heither 21-hydroxylase deficiency or 11-β hydroxylase* |/ }) x( A& B
deficiency. Those diagnoses were excluded by find-
  w' g5 M. [) `. oing the normal level of adrenal steroids.) c) [. {! |% a6 N/ r& K6 Y
The diagnosis of exogenous androgens was strongly8 d1 n: Q% {! Q1 F
suspected in a follow-up visit after 4 months because
# m$ V7 \" o- n% J$ Q) k% ?- ~& ithe physical examination revealed the complete disap-
* h: j4 k. F: k# Rpearance of pubic hair, normal growth velocity, and
- O) K5 [% i9 @3 C& U& J) Udecreased erections. The father admitted using a testos-
' J' i' y; H+ w! m% nterone gel, which he concealed at first visit. He was
9 h) Y/ R# }2 iusing it rather frequently, twice a day. The Physicians’
. X( {. M# [2 l+ y, z9 V: F, d9 uDesk Reference, or package insert of this product, gel or0 _; w; v) Q3 U, _
cream, cautions about dermal testosterone transfer to
6 \9 ^: B1 U2 H+ nunprotected females through direct skin exposure.4 o+ [. [( Y, p4 u, t( C
Serum testosterone level was found to be 2 times the
/ Q1 q7 ^7 B7 v! x# [baseline value in those females who were exposed to2 x: O$ |+ O% s8 b
even 15 minutes of direct skin contact with their male- \! w6 w) N; l7 _) G
partners.6 However, when a shirt covered the applica-
7 c3 m4 J6 B0 Q: Q/ ?tion site, this testosterone transfer was prevented.  t+ o  }4 [- F
Our patient’s testosterone level was 60 ng/mL,
  f9 O4 \) `4 k% ?5 H6 \which was clearly high. Some studies suggest that
8 s0 X( y/ |4 y1 N' ^) h6 Qdermal conversion of testosterone to dihydrotestos-# {% F4 H& G7 D8 z9 L; Q( `
terone, which is a more potent metabolite, is more
- `8 u' G0 `7 t0 G- n6 z8 u: r* Pactive in young children exposed to testosterone0 C# s9 y% a) a. j
exogenously7; however, we did not measure a dihy-8 W, n! P* `, h0 {* \8 P/ j
drotestosterone level in our patient. In addition to  n, n$ s& G9 R5 U) B  U$ C0 c
virilization, exposure to exogenous testosterone in
0 W" n: ~. }+ @0 _: K. Hchildren results in an increase in growth velocity and
/ P/ k2 w4 B- U, `1 C/ Vadvanced bone age, as seen in our patient.& l4 X2 ^# g' h9 C* P
The long-term effect of androgen exposure during
& T" z+ I6 c& I' R6 z1 O$ zearly childhood on pubertal development and final
. }) {! W. X2 x  @- \$ t8 J! m1 yadult height are not fully known and always remain
2 ]7 @: x+ D* ~$ {( u! ~0 ga concern. Children treated with short-term testos-
" C  B9 l1 B. ?& |8 o; N: xterone injection or topical androgen may exhibit some
4 L: r4 k) _* m! B7 Iacceleration of the skeletal maturation; however, after) u2 h* N3 h6 F8 h; i3 b0 [
cessation of treatment, the rate of bone maturation5 }+ P( d; u! }' S/ x& [4 `; W, m
decelerates and gradually returns to normal.8,9
3 V  j7 p  Y& D( l; Z% v+ M+ ZThere are conflicting reports and controversy
8 {7 V" r8 g- I" Bover the effect of early androgen exposure on adult
* s/ [1 I5 H, c' @$ ~7 G, @, S  cpenile length.10,11 Some reports suggest subnormal
! z* _& R) e  Z( i( J+ Jadult penile length, apparently because of downreg-) R! m0 M3 x2 s, Y
ulation of androgen receptor number.10,12 However,
2 F4 t" ]& K( n/ |) g5 V$ JSutherland et al13 did not find a correlation between5 j' D) \( M; x! l
childhood testosterone exposure and reduced adult7 m" \  J2 v9 R5 p, [, q2 L
penile length in clinical studies.$ _7 x" u/ K- j* \7 k5 }9 U
Nonetheless, we do not believe our patient is
9 W5 ]: L8 q3 a' Wgoing to experience any of the untoward effects from
) G  @, z, _$ F0 ]testosterone exposure as mentioned earlier because6 K0 X% l% D. v- {6 H( P
the exposure was not for a prolonged period of time.2 R9 m" F- F1 V" M4 b* A" W
Although the bone age was advanced at the time of
1 h5 Q) z1 U; U7 D( L% Ediagnosis, the child had a normal growth velocity at5 y. a+ a& W" _
the follow-up visit. It is hoped that his final adult
7 o& S5 a0 ?6 ^# o. g9 Bheight will not be affected.% i* e* M( O7 D, K& u4 B( ]
Although rarely reported, the widespread avail-
/ n- X; J7 M) ~+ T& [6 Wability of androgen products in our society may- ^2 S; N! v4 g* u5 A# m
indeed cause more virilization in male or female
4 g  V  _* G8 S7 qchildren than one would realize. Exposure to andro-
9 \) p1 j8 U$ B: n$ K4 L  h3 N, \gen products must be considered and specific ques-
# y6 n5 \2 h* [+ e: |tioning about the use of a testosterone product or2 _0 I6 l7 ^6 P
gel should be asked of the family members during. ^. i/ ^0 s. W
the evaluation of any children who present with vir-. `" p# E: g4 j+ _
ilization or peripheral precocious puberty. The diag-# T! |6 M: g3 S# M
nosis can be established by just a few tests and by# W4 G3 y5 ?' F/ Q
appropriate history. The inability to obtain such a
0 \1 s9 m% }& H8 l/ _1 i+ _" Ehistory, or failure to ask the specific questions, may( o. Z. f% O  G6 c/ V
result in extensive, unnecessary, and expensive
$ n1 B( ]0 o, t4 {0 M6 uinvestigation. The primary care physician should be
* v. N5 @6 i7 ^) a2 h: h" P. M6 ?+ {aware of this fact, because most of these children
# j( t5 o2 K! O: G  |  l/ vmay initially present in their practice. The Physicians’
9 e" y$ w$ Z% ^1 ?! v8 ^Desk Reference and package insert should also put a
3 ^& P) H* Y6 N3 Q' nwarning about the virilizing effect on a male or# Z- l, X6 [# Q
female child who might come in contact with some-2 m- h' H6 c3 e: O  k
one using any of these products.
) b. v. N) H/ yReferences
! _" Y8 x' o: {  M# O1. Styne DM. The testes: disorder of sexual differentiation1 {$ F9 H9 Y8 K) D8 L$ l' B7 e
and puberty in the male. In: Sperling MA, ed. Pediatric8 t# C+ x8 H) T* J  N) H" [: c
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. H; R0 a# N: x  p
2002: 565-628.
; i2 l$ M; F/ R% I# g2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# C# N+ x3 S) i  A* ~! t0 G
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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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

& H9 E& r% ^4 Y, X* y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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