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Sexual Precocity in a 16-Month-Old, f, v% x, Q( z7 v' k2 D5 p' d8 e0 O
Boy Induced by Indirect Topical) n5 c* t0 u6 r
Exposure to Testosterone- K6 ^( L" {0 c$ v" R5 Q$ ^9 q% E6 v
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 R5 q) p" v7 F* x$ i
and Kenneth R. Rettig, MD1) B; v, ~9 G* h! t6 H5 x/ N
Clinical Pediatrics1 Q# Z. G" G5 ~1 N% ]# e5 z8 h, ]
Volume 46 Number 6
/ F6 N# f* z2 L! W+ FJuly 2007 540-543! I; x6 H6 c, L2 e0 H
© 2007 Sage Publications
# P" P& k% r3 r0 ^10.1177/0009922806296651
. @' l( U$ r, [/ v$ ^http://clp.sagepub.com
, A6 }  L2 A4 R( ]8 p, O, r3 a& y1 jhosted at
  R( u) H0 C0 V  q( G/ ahttp://online.sagepub.com6 k! W' k8 x- \& z# i& w8 V
Precocious puberty in boys, central or peripheral,3 i  B- z9 T) I: p
is a significant concern for physicians. Central7 i2 a1 S2 W  x5 l
precocious puberty (CPP), which is mediated
6 W) k5 X2 Z/ w! {3 N/ L% o% Hthrough the hypothalamic pituitary gonadal axis, has
$ A6 u" r9 _1 E" y" v8 t" d4 Ja higher incidence of organic central nervous system' V. l0 K+ w9 j' N1 c
lesions in boys.1,2 Virilization in boys, as manifested, x+ a* y0 {; l% X( V) D
by enlargement of the penis, development of pubic# f/ V2 z# N8 q) d' @, `
hair, and facial acne without enlargement of testi-
$ j7 o5 q) T% g3 i$ \3 E3 n; Y  @cles, suggests peripheral or pseudopuberty.1-3 We$ F& F0 P1 }* o$ j
report a 16-month-old boy who presented with the
7 w3 u  V- t. r8 e- Yenlargement of the phallus and pubic hair develop-
- ]: M+ e1 j, I' Gment without testicular enlargement, which was due! f: Z0 z& ]* Z; F" {/ r
to the unintentional exposure to androgen gel used by
1 E7 u# \$ g1 j) ~' q4 Bthe father. The family initially concealed this infor-( g* b, J1 S$ J. L
mation, resulting in an extensive work-up for this
4 R$ ~- c/ w" [3 @' M: l) Achild. Given the widespread and easy availability of' z5 L  X5 z5 [
testosterone gel and cream, we believe this is proba-% t  ^4 Q  k3 a: o% n
bly more common than the rare case report in the2 ~7 ^2 }+ n  ?; X. b8 L
literature.4- P( H; ~% o6 P! y
Patient Report4 `# N' _: m: b$ ]
A 16-month-old white child was referred to the. V- M) D( W* \
endocrine clinic by his pediatrician with the concern
  o- `" i; J. aof early sexual development. His mother noticed7 u# w! o( ?6 k. `2 f( w
light colored pubic hair development when he was
/ o3 A2 K9 D3 u/ {! j" c! |8 XFrom the 1Division of Pediatric Endocrinology, 2University of
2 s3 l5 L0 B! e+ HSouth Alabama Medical Center, Mobile, Alabama.
$ _6 V$ v, `; G7 E' Y$ c$ |" cAddress correspondence to: Samar K. Bhowmick, MD, FACE,
, \8 K9 y) h  y1 cProfessor of Pediatrics, University of South Alabama, College of- Y9 v2 C: r% _) Y$ F4 E  N' n
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 ?8 N% [0 q( R8 ?8 y* K* P
e-mail: [email protected].
7 O8 ^6 f! d8 G  v: ?9 Uabout 6 to 7 months old, which progressively became1 ?1 L+ n6 s) l$ z" ]
darker. She was also concerned about the enlarge-
& H8 m& u5 i% l) |6 P2 y: {ment of his penis and frequent erections. The child
: h* ^; V; V1 C6 J% C; K4 V, kwas the product of a full-term normal delivery, with* v3 C. G' R% L6 G& U
a birth weight of 7 lb 14 oz, and birth length of
+ S' X! b; T$ x$ O20 inches. He was breast-fed throughout the first year( N8 {* i$ l0 b7 w5 O
of life and was still receiving breast milk along with
& m! z# m: ~* k) F, Qsolid food. He had no hospitalizations or surgery,
# ^4 p( `2 J! |3 p0 \8 I' v. `% n3 wand his psychosocial and psychomotor development4 p. p6 O* _8 N' E! a" @" B
was age appropriate.; a9 ]4 b' Z% ^- {8 U3 t
The family history was remarkable for the father,* I' Y! x1 K8 W! @' F
who was diagnosed with hypothyroidism at age 16,
. y) x: y/ s* M% g# r4 [1 _% C4 Twhich was treated with thyroxine. The father’s# G) }6 e8 [0 ]3 [
height was 6 feet, and he went through a somewhat7 }" U3 [/ g2 w3 T2 U- m" I
early puberty and had stopped growing by age 14.
' r& Y$ j) b7 H7 ^+ D. q2 `* {3 nThe father denied taking any other medication. The
! B* K* i9 u" t# f9 O3 Achild’s mother was in good health. Her menarche: X3 a$ W7 Y" e( v% m
was at 11 years of age, and her height was at 5 feet/ l7 S" L2 n2 ?6 V
5 inches. There was no other family history of pre-. j+ r+ N1 R$ v& h# }! A' U
cocious sexual development in the first-degree rela-
0 F- B3 ?' w) [tives. There were no siblings.  \+ P. c  ~) [) P$ d  l
Physical Examination! a6 [4 Z+ O7 F9 S" d: ?9 b
The physical examination revealed a very active,
/ ]( {" n. ~$ y1 S1 b, l) Zplayful, and healthy boy. The vital signs documented- z( h' G! _9 n$ ~! O
a blood pressure of 85/50 mm Hg, his length was
( m5 D. s& B' R% @90 cm (>97th percentile), and his weight was 14.4 kg
; G+ |$ a7 v; c(also >97th percentile). The observed yearly growth
( H( Z) }8 C3 ?0 {6 avelocity was 30 cm (12 inches). The examination of2 S- o: Z4 S% ]* B; M$ e
the neck revealed no thyroid enlargement.+ }' H$ h# B" a
The genitourinary examination was remarkable for* ]; U4 x! n% o$ @/ H0 E
enlargement of the penis, with a stretched length of  j, E+ r8 Z; w: r9 a  _6 ^0 t. {
8 cm and a width of 2 cm. The glans penis was very well% ?- v/ U# S: u& \
developed. The pubic hair was Tanner II, mostly around9 b1 E# s- u, a5 {
540
8 D# k% L2 m9 l( Dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 B# }: U" v' X
the base of the phallus and was dark and curled. The
6 \" q$ ?# x7 Z4 |3 D' ]testicular volume was prepubertal at 2 mL each.% }+ K. C! f& B' e" C% L* c
The skin was moist and smooth and somewhat4 A3 X; i4 P' S# a
oily. No axillary hair was noted. There were no6 M) G8 J8 _6 c+ C- P
abnormal skin pigmentations or café-au-lait spots.7 s1 l+ C- W3 Z3 X- a  j
Neurologic evaluation showed deep tendon reflex 2+# p5 @6 G% O! q( K3 X- l
bilateral and symmetrical. There was no suggestion- c' E5 t" ~5 a6 t+ P
of papilledema." D. L# b+ P% D) c
Laboratory Evaluation; r  B; |; ?7 p# m" |. D
The bone age was consistent with 28 months by
7 c( A. j5 {6 O4 pusing the standard of Greulich and Pyle at a chrono-% o& x5 p3 j4 r" k6 @
logic age of 16 months (advanced).5 Chromosomal6 F1 o. n/ o/ U' @/ p8 B
karyotype was 46XY. The thyroid function test
& g) o0 V" R  \$ U# zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
: A& z2 L6 _+ k6 L. D, `lating hormone level was 1.3 µIU/mL (both normal).
2 V  Y. e+ G( @5 Q! ZThe concentrations of serum electrolytes, blood; j$ A4 A. b. u# `7 D: D  x
urea nitrogen, creatinine, and calcium all were
1 {' J- \$ Y8 `) A" x8 C. Fwithin normal range for his age. The concentration) k* }2 i$ s( P- t: u1 n+ I4 g9 a
of serum 17-hydroxyprogesterone was 16 ng/dL% g* u( t0 c# H2 [. G
(normal, 3 to 90 ng/dL), androstenedione was 20- s/ F: A6 p( p3 p4 o( Z# Y
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-% e- H* M7 ?7 t4 L
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 n! Y/ ~- r+ F! Z5 B9 u1 Rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ e; P( q5 o0 W& O  b" A# ]49ng/dL), 11-desoxycortisol (specific compound S)
! W& l8 w# k3 A- ]was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& n$ }/ x3 s! ]. {- |2 f) y0 qtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 c, M1 L/ `7 ~* K7 W+ dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  L! S6 u, u( I" W/ {! V$ cand β-human chorionic gonadotropin was less than
" ~: |. Z. [8 k0 W5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 M, b' A4 N& H8 w) Ostimulating hormone and leuteinizing hormone7 n( E) r* Y. o* R1 N
concentrations were less than 0.05 mIU/mL
2 f3 x' ?6 y/ V' u4 Y# ]$ t(prepubertal).% p1 C7 R1 I  _" n8 p1 F
The parents were notified about the laboratory" c1 _  J$ I" v$ i& y
results and were informed that all of the tests were
9 C; j5 V# y& U* A4 n: X! p6 ]* T7 `+ Znormal except the testosterone level was high. The6 g2 y6 r3 w; w! T0 R8 L- t# h
follow-up visit was arranged within a few weeks to) B" Q; A  ]: A" {3 f+ |0 @! _
obtain testicular and abdominal sonograms; how-
7 y+ {+ K8 P, f2 V- ?ever, the family did not return for 4 months.
6 R; }# R' P% d: zPhysical examination at this time revealed that the8 \) t+ t8 N0 X
child had grown 2.5 cm in 4 months and had gained) n) t% Q7 V% X. _
2 kg of weight. Physical examination remained& l6 T1 U) a- X* g. k* x4 O
unchanged. Surprisingly, the pubic hair almost com-
% N9 N  ^, \5 epletely disappeared except for a few vellous hairs at
  r9 ?7 p6 k1 f# w2 z* T7 o% Xthe base of the phallus. Testicular volume was still 25 }3 ^1 [& t! r
mL, and the size of the penis remained unchanged.. f- B8 F' g6 M4 {, e1 J( X
The mother also said that the boy was no longer hav-/ g# g' z6 l" h. h9 l3 F2 k
ing frequent erections.- L! m3 P9 J% i; @8 }+ r1 g& T
Both parents were again questioned about use of
6 w. y9 `; T9 U7 {any ointment/creams that they may have applied to
/ G4 h* a- l; g& Z. L3 T1 g% nthe child’s skin. This time the father admitted the* V  e2 f, p& y3 ]
Topical Testosterone Exposure / Bhowmick et al 541+ `* b5 ?  |+ `0 S
use of testosterone gel twice daily that he was apply-' d( |% S6 o; j1 j
ing over his own shoulders, chest, and back area for
( u% a% L6 A' x0 Y8 ~a year. The father also revealed he was embarrassed
# N3 t" J3 Q' ?. g- P; `to disclose that he was using a testosterone gel pre-
+ ?. I6 L! g# {+ v4 @scribed by his family physician for decreased libido0 F4 `, I% }/ z4 G" N' \1 h
secondary to depression.9 J7 b/ c. M5 T6 O1 n0 H
The child slept in the same bed with parents.
, m( j, B- c0 _- X! M: ^  X" c- O: W. yThe father would hug the baby and hold him on his
/ ^! K* U& y; k# G9 Vchest for a considerable period of time, causing sig-/ q3 E& Q2 O- N  I, i6 U
nificant bare skin contact between baby and father.
: |0 n. h" E, ^: Q& O0 L$ @The father also admitted that after the phone call,
9 U/ b' O6 B/ f6 Lwhen he learned the testosterone level in the baby9 H5 k( U4 J4 j
was high, he then read the product information
% A" W0 r+ d$ s, @packet and concluded that it was most likely the rea-
+ |# u2 D/ C$ O- ?$ Y: k* U! Y# Mson for the child’s virilization. At that time, they  g9 V. z( l0 k$ n# g" X4 ?0 W- M7 ^
decided to put the baby in a separate bed, and the9 `. Z( c& n2 J4 y5 }
father was not hugging him with bare skin and had* i+ d5 d" L9 @9 C+ I8 n8 x% l$ k
been using protective clothing. A repeat testosterone
4 \: A7 ~/ f) N$ {8 V# Y4 ~test was ordered, but the family did not go to the
, {' V3 ?& U% ^% Rlaboratory to obtain the test.. G  G  ]6 e& c# P' Y3 ]- i6 I
Discussion
/ Z, V- E- K3 z% B  APrecocious puberty in boys is defined as secondary$ u9 h; V5 z% ?& M- Y% R
sexual development before 9 years of age.1,43 ]- ~, i) o6 G# K! Z1 P7 h  [
Precocious puberty is termed as central (true) when+ |" ~: q) U/ r6 Z" v! e
it is caused by the premature activation of hypo-, Y, k5 b$ }3 S$ @) H
thalamic pituitary gonadal axis. CPP is more com-
5 N8 O9 a( Q; m, c3 n2 q, f, Rmon in girls than in boys.1,3 Most boys with CPP
/ k, M: @0 t* J) y, d$ Rmay have a central nervous system lesion that is
) ]* E6 ]5 Y9 w" Sresponsible for the early activation of the hypothal-' L) C( p! @1 N
amic pituitary gonadal axis.1-3 Thus, greater empha-; E+ o  m! p" ~* v0 Y1 M" L7 E
sis has been given to neuroradiologic imaging in/ ^7 _7 i# B; e4 f1 ]
boys with precocious puberty. In addition to viril-/ R, ^9 W# d/ |, n9 q1 `7 O+ `
ization, the clinical hallmark of CPP is the symmet-
2 V& ~, U0 y, R, y2 j9 \rical testicular growth secondary to stimulation by* U% l; X- {& `4 B8 y" j# y% C! c
gonadotropins.1,3
% Q6 a! h; K  }; V% R4 XGonadotropin-independent peripheral preco-
* K" V8 v9 q- s4 x* d% J5 s; Jcious puberty in boys also results from inappropriate8 u6 i' m3 B% P5 K
androgenic stimulation from either endogenous or
3 z2 B9 C" L& r/ Y2 u4 r5 L5 rexogenous sources, nonpituitary gonadotropin stim-
: H* [( M- h0 [9 p' culation, and rare activating mutations.3 Virilizing9 N" C: \! s) X+ C0 Z
congenital adrenal hyperplasia producing excessive
$ y! b) {* _, y" T$ Tadrenal androgens is a common cause of precocious
0 h( @  k8 g/ d9 B# Q1 Wpuberty in boys.3,49 C$ i$ R; G# A6 L' G, T: F7 R
The most common form of congenital adrenal% F, h5 _' Z( X: z' k
hyperplasia is the 21-hydroxylase enzyme deficiency.# x- X3 R9 ?6 z
The 11-β hydroxylase deficiency may also result in
2 K7 Q& {& i6 o+ kexcessive adrenal androgen production, and rarely,2 U8 s' y: G$ X- T" ?9 R1 E6 x* e
an adrenal tumor may also cause adrenal androgen$ V, Q8 h' G1 Q0 J
excess.1,3
- [/ c" v8 ~* ]+ b1 ?* ~at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& d* A# X7 Z: z& W1 R542 Clinical Pediatrics / Vol. 46, No. 6, July 20079 y7 m7 q0 N/ X
A unique entity of male-limited gonadotropin-+ G' l) W) o$ }9 G' z' y0 S+ s# D
independent precocious puberty, which is also known, j9 p3 `# B9 M9 i& u9 W$ p
as testotoxicosis, may cause precocious puberty at a
/ T5 i6 E) w7 @. [% j' f- `! Fvery young age. The physical findings in these boys
  q0 J2 q4 ~( ~% Jwith this disorder are full pubertal development,
  @0 K* d% I# D- nincluding bilateral testicular growth, similar to boys6 v7 S% W- B/ O
with CPP. The gonadotropin levels in this disorder: o0 j: H+ s6 Z7 u: }$ L3 O
are suppressed to prepubertal levels and do not show
; d5 W/ j$ f# |& Q- L4 jpubertal response of gonadotropin after gonadotropin-5 q* o' c! @8 Y" i6 R& A5 [
releasing hormone stimulation. This is a sex-linked( U! N- z7 ^$ \) t2 o" O
autosomal dominant disorder that affects only+ w3 [: B2 A9 W9 a9 t" @: v
males; therefore, other male members of the family
! w- h5 E8 f8 C# Y2 emay have similar precocious puberty.30 d6 P  l* R8 n+ L
In our patient, physical examination was incon-
: V5 o8 q3 p9 ^8 [" Vsistent with true precocious puberty since his testi-# J9 ?5 `4 G* ?7 [1 B
cles were prepubertal in size. However, testotoxicosis+ D9 A% B9 S1 Q
was in the differential diagnosis because his father
3 {9 G# T% V" m& G# J. Cstarted puberty somewhat early, and occasionally,% z" m! e& l; W, ?4 |  v
testicular enlargement is not that evident in the4 p1 l3 m' U% n& `/ ~
beginning of this process.1 In the absence of a neg-' e; D9 F  p0 t  ]; D6 Z; `
ative initial history of androgen exposure, our1 ]: S# A) B8 \- ^+ ]1 Q( V5 R* b
biggest concern was virilizing adrenal hyperplasia,: ^+ \: r+ `* \& v# d) x  B& O
either 21-hydroxylase deficiency or 11-β hydroxylase
% c" U4 c2 a$ wdeficiency. Those diagnoses were excluded by find-
- ?/ K. w, O/ y6 {# G! ?ing the normal level of adrenal steroids." C* g& l1 v  H: H9 ~! E
The diagnosis of exogenous androgens was strongly
0 \: Z) L5 w5 h( R7 }( vsuspected in a follow-up visit after 4 months because, }, P* j. q9 P- k
the physical examination revealed the complete disap-' `1 |$ x8 f/ I+ A# J
pearance of pubic hair, normal growth velocity, and( D3 W: r2 |* C; W9 b
decreased erections. The father admitted using a testos-
2 }: D. E5 x  B# V+ ^  @terone gel, which he concealed at first visit. He was
, W6 l! V" F* C2 [7 vusing it rather frequently, twice a day. The Physicians’0 H1 C: ?1 L% U& z& o
Desk Reference, or package insert of this product, gel or
* s6 f& m. u6 k* p, }# l9 f& Jcream, cautions about dermal testosterone transfer to( u/ D6 u" E/ o& i( J
unprotected females through direct skin exposure.
, S0 A" V4 |: e/ [Serum testosterone level was found to be 2 times the
9 E: n- z/ v" t' `4 Nbaseline value in those females who were exposed to1 ]9 C, S5 M, r* ^( d/ x3 z" ]$ @
even 15 minutes of direct skin contact with their male/ M1 _6 f) F% h, ~* n& e4 C5 B/ |
partners.6 However, when a shirt covered the applica-
6 K- M! U+ J6 B5 \  f0 ?tion site, this testosterone transfer was prevented.
$ ^: P; Q$ _* l9 W# X" BOur patient’s testosterone level was 60 ng/mL,+ \+ `3 W! O( _9 Y9 @; y! d
which was clearly high. Some studies suggest that
/ [* S" e3 H; A! xdermal conversion of testosterone to dihydrotestos-' }/ i; x/ \6 [; u; T
terone, which is a more potent metabolite, is more
0 p* y3 e6 m# Jactive in young children exposed to testosterone
8 U# V' \* e- M& wexogenously7; however, we did not measure a dihy-
) Q+ U4 U- k% t4 `& i- Edrotestosterone level in our patient. In addition to. R! {. e' E" d- u
virilization, exposure to exogenous testosterone in1 @: P" t+ B) ?$ b) @' p8 s
children results in an increase in growth velocity and
8 h$ k! l# Q$ a4 Fadvanced bone age, as seen in our patient.
; o0 C# m3 n/ S- V$ z* k$ A0 {The long-term effect of androgen exposure during) n0 E5 _- X- N
early childhood on pubertal development and final% ^9 B" v* E. G! n  F+ L9 ?7 y
adult height are not fully known and always remain
' d- O8 Z8 N. B4 p' q" Z3 S5 |* ma concern. Children treated with short-term testos-* k4 n! F9 l0 F* Z; d# e
terone injection or topical androgen may exhibit some% n+ q: J6 k0 p
acceleration of the skeletal maturation; however, after: [8 ^$ v" }2 j& M7 `/ J* r
cessation of treatment, the rate of bone maturation5 R5 P& h3 L/ Q2 X2 u. U+ b- f
decelerates and gradually returns to normal.8,9
8 \$ D. H) I7 x4 _7 p# V2 aThere are conflicting reports and controversy
9 V4 L+ L4 F+ v( l2 A- G/ H+ F- zover the effect of early androgen exposure on adult
5 N2 R1 p% \* c7 i1 `8 R& Jpenile length.10,11 Some reports suggest subnormal& R! d/ y0 p3 D9 c" _6 e3 O8 P
adult penile length, apparently because of downreg-
: \+ |) q4 Z$ n( F8 nulation of androgen receptor number.10,12 However,
; S$ H+ b& H9 }" R8 }% K+ JSutherland et al13 did not find a correlation between
7 i9 {0 H  [. Q" i7 w; S. M% q# r& vchildhood testosterone exposure and reduced adult! r, `/ {: P$ C5 O
penile length in clinical studies.
8 D$ S7 T  Q2 cNonetheless, we do not believe our patient is
( b9 X3 r6 j' R, c1 E9 y) O1 ]( Wgoing to experience any of the untoward effects from+ s+ b9 Z4 {( M6 x
testosterone exposure as mentioned earlier because
0 s. a4 k# n4 F3 n8 Xthe exposure was not for a prolonged period of time.
* I/ f! p% D" H& D8 q+ QAlthough the bone age was advanced at the time of: I; W' n) B: q: O$ y) R
diagnosis, the child had a normal growth velocity at$ \" l( ?. U  \- C3 Z# b" V5 v) H
the follow-up visit. It is hoped that his final adult! e6 _5 R8 J& W- q/ V3 J7 X0 {+ m
height will not be affected.8 ^( S& A3 R- b$ V4 V5 m; ~+ \
Although rarely reported, the widespread avail-
+ t; B  w& Z4 Kability of androgen products in our society may7 G) T& @" B1 N: u& a
indeed cause more virilization in male or female0 M1 q5 a8 e4 i( O
children than one would realize. Exposure to andro-
5 j+ f8 a9 I9 o# B( r4 fgen products must be considered and specific ques-1 o. r. R+ ^( q( w3 h- W
tioning about the use of a testosterone product or9 O0 M, b7 a) H' H! T9 B6 R$ j
gel should be asked of the family members during2 ~9 t: ~1 ~7 |. _9 O
the evaluation of any children who present with vir-
( C% m, i  f$ k$ ~' f" Lilization or peripheral precocious puberty. The diag-
' I% y! p/ g* r' C- s3 s2 H9 `nosis can be established by just a few tests and by
% C# o/ L6 y2 R/ F' N# Oappropriate history. The inability to obtain such a' I$ j6 C8 s) s. _
history, or failure to ask the specific questions, may
7 P# o, L/ O; L/ M9 k' u8 k! lresult in extensive, unnecessary, and expensive
$ q5 F8 i( C2 B% y& Finvestigation. The primary care physician should be7 B1 p" |+ J+ [+ }* G
aware of this fact, because most of these children
5 U; R/ d- k1 {6 Vmay initially present in their practice. The Physicians’
; z& k- p- X8 i! ~& ]Desk Reference and package insert should also put a
$ k! R7 X  g  c, C7 Wwarning about the virilizing effect on a male or
5 d! M) B' f4 ~  z) V: v3 g& ?female child who might come in contact with some-
- h' g. a' R3 i* o# E0 w( H) |one using any of these products.
3 B# \$ G7 O: D9 VReferences* a0 @$ _& w2 y! h3 ], s
1. Styne DM. The testes: disorder of sexual differentiation3 q- v+ U# Q6 S
and puberty in the male. In: Sperling MA, ed. Pediatric
0 i7 M& f1 L1 c! lEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% u1 A' y9 N  J# A2 c4 w- P8 ~2002: 565-628.5 W! a/ `+ b& E
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- s) c# G( Q2 Q/ ^! x* U9 L6 A  ipuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
3 ]1 K% [  b) j# c7 M: F. D- C, CBoy Induced by Indirect Topical! v* ?" X% S/ p$ j% q
Exposure to Testosterone
2 h2 @, c& o) Y3 K7 n) KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2) @8 s8 Y& v/ S) n& `
and Kenneth R. Rettig, MD1+ K2 s4 q8 ^$ R) p! l, D. `2 Z
Clinical Pediatrics
% k% G5 W5 `) E( E( RVolume 46 Number 69 d3 S4 V, k9 r5 l3 a6 O
July 2007 540-543! t$ j" A9 A1 v, q, s5 v& _3 Q8 ?5 o
© 2007 Sage Publications9 i( q: `" Z6 K  B; |. h
10.1177/0009922806296651
, e+ H/ {+ b. H2 D. {( ?+ nhttp://clp.sagepub.com
. v) T/ R* H0 A2 v- U! ^' dhosted at3 a  N. T! G: q' g  `6 n
http://online.sagepub.com& T1 J6 U! C5 e- x/ y9 c
Precocious puberty in boys, central or peripheral,+ ~# o3 l  o' y. E& c7 `, b$ ]& N
is a significant concern for physicians. Central( K0 C3 n# m" v; C* D
precocious puberty (CPP), which is mediated
0 ~. l, A& V: [  Z7 p! @: {$ Y0 s* qthrough the hypothalamic pituitary gonadal axis, has, Q% d& x5 A8 C' u0 \+ K
a higher incidence of organic central nervous system6 c* \+ |5 _; C7 A5 A) U- E
lesions in boys.1,2 Virilization in boys, as manifested
8 @: k1 J7 K. J- nby enlargement of the penis, development of pubic! U0 u( Y9 s9 ]- I$ @
hair, and facial acne without enlargement of testi-
3 P6 W4 g! U5 i# o6 [* o6 K8 Ycles, suggests peripheral or pseudopuberty.1-3 We
4 I: y2 [6 }' g" L6 Wreport a 16-month-old boy who presented with the
: @" P5 N/ V% [2 M" genlargement of the phallus and pubic hair develop-
, i& i5 A# T( _* `ment without testicular enlargement, which was due$ g( l* a; S- X' q+ d7 u2 Y
to the unintentional exposure to androgen gel used by
' w4 W: Z- O0 A1 y2 }4 _the father. The family initially concealed this infor-
/ ^, |% ^! `! b6 Smation, resulting in an extensive work-up for this2 Y4 j, w+ A- ?6 e5 l6 a
child. Given the widespread and easy availability of7 L" {) m2 W" o5 K8 |
testosterone gel and cream, we believe this is proba-  d% R/ u+ }* V8 h% z$ {0 y
bly more common than the rare case report in the
) e9 a, I1 g  s, Wliterature.4
. t+ I+ }9 ]8 e& J) V" APatient Report$ [7 `7 K, l- B0 _" l+ f  r1 E
A 16-month-old white child was referred to the8 S* f  |( `2 a) ~# A
endocrine clinic by his pediatrician with the concern
3 g) i. L, O# X+ ]/ Iof early sexual development. His mother noticed
7 F8 A% ^+ ?; A' r# Y0 Y5 Hlight colored pubic hair development when he was3 ^) Q2 ?- A7 x. C) C
From the 1Division of Pediatric Endocrinology, 2University of1 k" x" ?% R9 S0 ~. l, Y
South Alabama Medical Center, Mobile, Alabama.
, _$ Z+ U( a1 F/ ]Address correspondence to: Samar K. Bhowmick, MD, FACE,4 r# B; V9 t- I/ r4 f3 }
Professor of Pediatrics, University of South Alabama, College of
) S; ?/ @3 o, t% y) eMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;  K2 ?! k( Q$ @" |( R' t
e-mail: [email protected].
2 p5 y8 d# l' L9 M/ R# G/ l) Kabout 6 to 7 months old, which progressively became/ ]! V% a/ V8 k& t
darker. She was also concerned about the enlarge-2 w. @3 x2 }3 C( Q5 r/ U: y
ment of his penis and frequent erections. The child& @5 [. i5 t( l
was the product of a full-term normal delivery, with
# h2 P+ s$ z2 ?: Da birth weight of 7 lb 14 oz, and birth length of
9 `6 T, W) C- l7 Q  f% P. \20 inches. He was breast-fed throughout the first year( Z) G, c/ s; X( S# y1 _
of life and was still receiving breast milk along with2 U; I  K+ V5 k' u8 P0 {- g
solid food. He had no hospitalizations or surgery,
2 @- p9 k: a( L" o' p9 A8 Y" Xand his psychosocial and psychomotor development- e; i* q1 ~1 M' L/ [: Q
was age appropriate.
$ S3 h) g4 D' {$ E3 f/ @6 A. uThe family history was remarkable for the father,+ Y* U/ y9 J& L9 G( e; k& a
who was diagnosed with hypothyroidism at age 16,) F  @! j2 R( \- Q9 i* a3 i
which was treated with thyroxine. The father’s
: M8 _6 r$ q$ e- A+ r' hheight was 6 feet, and he went through a somewhat
8 v/ B' K; L% q3 k! Jearly puberty and had stopped growing by age 14.
% n% T& s+ Y  X  \% sThe father denied taking any other medication. The
: g) J( b+ I3 t; w/ V$ f0 V, Schild’s mother was in good health. Her menarche, M$ u3 I! R& g9 Z
was at 11 years of age, and her height was at 5 feet! z$ I7 F4 v; R6 D5 K4 i
5 inches. There was no other family history of pre-) T& K* x. |6 z) W7 [$ N5 v" H
cocious sexual development in the first-degree rela-+ k9 |% p3 `1 t7 n" c" a5 B/ h& |
tives. There were no siblings.  }7 P; r; A1 L. ~) H5 i
Physical Examination
) H1 f; Q* \4 }( R. J9 V7 MThe physical examination revealed a very active,7 F- J( z6 {  p: b4 W
playful, and healthy boy. The vital signs documented
3 m4 T% q) L) G# n5 Ma blood pressure of 85/50 mm Hg, his length was
( j- Q$ {0 n) x  c90 cm (>97th percentile), and his weight was 14.4 kg+ A# S4 q( o9 ]; k: _6 Q
(also >97th percentile). The observed yearly growth
6 U: R4 U; X( Kvelocity was 30 cm (12 inches). The examination of8 |. j" e( {& r; l6 v  ~! s
the neck revealed no thyroid enlargement., }4 C3 L/ `+ }& H
The genitourinary examination was remarkable for8 P7 |$ K% n! T, M4 m- N, w- i
enlargement of the penis, with a stretched length of2 R, L# k9 Z" T& t. h; w# ^9 N
8 cm and a width of 2 cm. The glans penis was very well+ J- B5 }/ l4 a7 K/ a( X. @
developed. The pubic hair was Tanner II, mostly around  L2 ]  U7 u5 w0 s  i. J
540* r3 i3 `" c! T8 {  N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 [* P2 u- D/ o4 d: o
the base of the phallus and was dark and curled. The
* [3 C) ?0 m; btesticular volume was prepubertal at 2 mL each.9 ~2 j4 {* L* ]: l( O
The skin was moist and smooth and somewhat
' s8 F0 ~3 j/ noily. No axillary hair was noted. There were no
! d( s  \% \; |: L8 ]* e8 k# @abnormal skin pigmentations or café-au-lait spots.
& J: ?5 {5 l2 @$ ?/ ~Neurologic evaluation showed deep tendon reflex 2+
5 K; g# v6 l, ]- x! D8 O  w, ibilateral and symmetrical. There was no suggestion
& K; r; M% ~/ J. W8 A$ A; e( tof papilledema.
! w% q7 ?& b  d1 O9 FLaboratory Evaluation$ {* M4 X; K+ D8 U5 w( j' s! s# E
The bone age was consistent with 28 months by
  ]$ L/ R! C, R5 J4 G& g# v' z& l1 \3 Qusing the standard of Greulich and Pyle at a chrono-
3 p% h! D9 E- ^6 D5 Y% \logic age of 16 months (advanced).5 Chromosomal& {# Z) {8 t7 B2 z
karyotype was 46XY. The thyroid function test
- T3 c% ^0 K1 Q- \0 D& kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
/ c8 m1 l  K, v/ s! D/ _  x# {lating hormone level was 1.3 µIU/mL (both normal).
5 g4 c/ L+ J0 d0 w! xThe concentrations of serum electrolytes, blood
- D  Q# x; W# a1 }2 Nurea nitrogen, creatinine, and calcium all were; o! {+ R9 I  V' F
within normal range for his age. The concentration/ T" h8 T1 M. q, c$ I. ^3 l4 O
of serum 17-hydroxyprogesterone was 16 ng/dL
8 A0 `; N( D+ u0 Q/ F(normal, 3 to 90 ng/dL), androstenedione was 204 s# \' f' M( ~
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-. _, k8 T1 w: x/ \
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
; Q" Y" I& r5 ~( T/ Gdesoxycorticosterone was 4.3 ng/dL (normal, 7 to4 S' @, f% X3 H% [: W& H. `
49ng/dL), 11-desoxycortisol (specific compound S)' d! K* k  R) M: Z, R2 s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
9 G) e9 Z- q+ ~# w0 T4 @4 h5 H  Ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 c+ O7 }0 O3 o" X( q* Mtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
/ W* \/ V; P% ^: c! U, ]4 wand β-human chorionic gonadotropin was less than" a1 b& ]1 T& e1 U4 o
5 mIU/mL (normal <5 mIU/mL). Serum follicular
( M' {& {% Q$ R% [; l, Fstimulating hormone and leuteinizing hormone
  c; b; K  h. }concentrations were less than 0.05 mIU/mL! k+ T: y+ H( S
(prepubertal).
0 P& D; g) S% h6 H* G. bThe parents were notified about the laboratory
, D7 ^! X: I$ q7 ^/ ]0 }2 [5 eresults and were informed that all of the tests were
5 x& O3 l( ?; [) u6 [' l1 m! c- ]0 Pnormal except the testosterone level was high. The
1 t9 N5 i  l% V7 q/ ?' e1 Xfollow-up visit was arranged within a few weeks to* y- U) w5 U& z1 m" p3 y3 o
obtain testicular and abdominal sonograms; how-8 ?# |9 j1 w  ^& c% E6 ?
ever, the family did not return for 4 months.
, W% a4 j+ X5 k. `- fPhysical examination at this time revealed that the# ^+ p4 u# ^; n# G! `& V
child had grown 2.5 cm in 4 months and had gained' i, y. B4 ?+ l. r1 v: {" ]* M
2 kg of weight. Physical examination remained2 [# O9 H! s( p
unchanged. Surprisingly, the pubic hair almost com-. W3 t0 x' w. F1 @4 J% i
pletely disappeared except for a few vellous hairs at' ~4 K$ I' x5 r9 M. n4 c
the base of the phallus. Testicular volume was still 2
" u) m8 ]9 ]' {& g: k* ymL, and the size of the penis remained unchanged.
6 I$ s# c& O1 n# m/ TThe mother also said that the boy was no longer hav-4 x/ ^" p& h+ B! U$ u
ing frequent erections.
& J% j  W( I- oBoth parents were again questioned about use of
  |' B# F: i8 A% ~2 j6 J/ |" v" ^any ointment/creams that they may have applied to
' Z6 y/ k$ Q2 ^8 O' A5 ~the child’s skin. This time the father admitted the0 }) V" u! D: A
Topical Testosterone Exposure / Bhowmick et al 5410 C3 e2 z0 d; X8 w* F
use of testosterone gel twice daily that he was apply-  v0 ]8 M! ^! g' D0 ~. Y
ing over his own shoulders, chest, and back area for7 H2 ?( n9 e1 P8 s
a year. The father also revealed he was embarrassed
$ ~& ^8 x( S6 q4 E9 q* O1 |" C9 }to disclose that he was using a testosterone gel pre-; l% E% Y, n0 U: M  u
scribed by his family physician for decreased libido- ^: z2 y% P; Y
secondary to depression.
2 k5 |& K: `6 q1 gThe child slept in the same bed with parents.
+ w9 q) }* F3 g2 K" u7 c, iThe father would hug the baby and hold him on his. f( b. B; [7 H; v
chest for a considerable period of time, causing sig-) q. p! S: M/ [( B; L; }& n$ b
nificant bare skin contact between baby and father.
$ ~( e! o) c# a' i0 o! Q0 D2 \4 _6 DThe father also admitted that after the phone call,
2 |9 Q2 C# o+ A3 P' T% R: Kwhen he learned the testosterone level in the baby% c3 C2 W$ `( \; S% v% @5 k
was high, he then read the product information
1 p3 Y! x) W$ O' Y8 npacket and concluded that it was most likely the rea-/ ~" j: }3 V3 E, d3 X# @3 {( U
son for the child’s virilization. At that time, they% w3 d3 K/ D# ?
decided to put the baby in a separate bed, and the
4 s* y  S9 T$ ^& I! |% ?6 F; B% tfather was not hugging him with bare skin and had
& F/ J0 [; n) t1 i  _: _. M3 r$ \been using protective clothing. A repeat testosterone( ~8 Z/ b) K' m! Q. a7 e/ z
test was ordered, but the family did not go to the
4 A( P. }9 J: N# hlaboratory to obtain the test.+ p: T; Z& b, F% U' H5 n* T
Discussion1 D) b6 j  A$ N1 B0 M; O
Precocious puberty in boys is defined as secondary, S$ l' j1 s0 c9 a) {
sexual development before 9 years of age.1,4# h5 g3 N. K3 M0 Y/ F, w. F
Precocious puberty is termed as central (true) when
! D( |) Q5 V$ f; d7 @- Eit is caused by the premature activation of hypo-
# g' g# j/ m- g# K5 pthalamic pituitary gonadal axis. CPP is more com-$ E+ Q8 p1 g/ C1 U& {5 J
mon in girls than in boys.1,3 Most boys with CPP
5 x4 Z/ g+ E- f, q8 J2 j1 U# Fmay have a central nervous system lesion that is
3 t) _9 G' T" J, {* Mresponsible for the early activation of the hypothal-* X! u4 r0 m' i5 O+ e2 A# J; @9 d
amic pituitary gonadal axis.1-3 Thus, greater empha-* l& C9 h9 d. S$ G
sis has been given to neuroradiologic imaging in
# p: u, _5 ~/ V8 d! ?% a) pboys with precocious puberty. In addition to viril-
. Z) H7 W3 a$ V: aization, the clinical hallmark of CPP is the symmet-2 w# S: y# |6 O$ W9 F) q% W. B
rical testicular growth secondary to stimulation by, z4 ]7 g3 Q5 O4 [5 R9 x. z
gonadotropins.1,3. T3 }+ N3 d8 b( J9 U8 Y' F& R
Gonadotropin-independent peripheral preco-( g3 J$ |( _* k) C% m% y
cious puberty in boys also results from inappropriate$ F) @5 {) |* s% j6 r6 q, P' J$ R
androgenic stimulation from either endogenous or! S9 t6 w$ P& t2 ~& L' `& L; L5 q
exogenous sources, nonpituitary gonadotropin stim-
! E2 U  p$ ^' `2 y4 v' N/ xulation, and rare activating mutations.3 Virilizing5 Z/ J8 B! z0 O/ m, _7 {
congenital adrenal hyperplasia producing excessive* }/ l  D. X% X9 Y  v" e2 u
adrenal androgens is a common cause of precocious
" Q' r: F, p$ z! p+ r5 ypuberty in boys.3,4
: Z! N9 b- Q2 e' N% [5 @1 O' ]The most common form of congenital adrenal
$ X! q  K" D0 ]6 n( a3 I# e2 thyperplasia is the 21-hydroxylase enzyme deficiency.
  ?% i+ E+ ]6 R/ {- ^The 11-β hydroxylase deficiency may also result in
7 E! J2 W4 x( T* m% Jexcessive adrenal androgen production, and rarely,9 C  [, Z9 Z7 {; m2 ~  Z" C: n
an adrenal tumor may also cause adrenal androgen
4 l7 ]7 p  [: r- O: [excess.1,36 P/ |5 Q) ~$ b' b' _6 g$ b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' o9 w4 k/ ^6 \
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
$ j( K! O7 g2 N* G, k' _$ x4 q0 b% u. m  UA unique entity of male-limited gonadotropin-
- |! j+ a+ n( y# M: ?7 m3 H- Zindependent precocious puberty, which is also known
: k$ Q4 m7 y5 P" k5 p" o- gas testotoxicosis, may cause precocious puberty at a& a! J" ?# o# _( y  w0 N! g: g) @
very young age. The physical findings in these boys
% ?2 {/ S2 R4 {- C8 {with this disorder are full pubertal development,
" K/ e0 J1 e" bincluding bilateral testicular growth, similar to boys
( a- p9 p1 J! b* e( f1 _with CPP. The gonadotropin levels in this disorder1 n. {5 Q, x& k
are suppressed to prepubertal levels and do not show+ d+ H; n6 A7 X" e( M0 M% c) I
pubertal response of gonadotropin after gonadotropin-4 C' q  i3 E/ G' I+ j) _& _+ \% a
releasing hormone stimulation. This is a sex-linked
/ i  g1 b# y* ]7 Nautosomal dominant disorder that affects only
! n& y: o6 R0 _1 |males; therefore, other male members of the family8 f/ S- @) f/ S  ?1 |2 n0 Y
may have similar precocious puberty.3
/ q/ a  A1 a- W! I9 cIn our patient, physical examination was incon-
/ d/ d( P  v2 C9 b( S: \9 t7 G8 J  vsistent with true precocious puberty since his testi-
4 E+ z8 \' [: b) \/ ^" f9 D+ Mcles were prepubertal in size. However, testotoxicosis& M- x* I5 {1 K5 }4 C$ o. s
was in the differential diagnosis because his father
6 E) F7 p1 J5 F" qstarted puberty somewhat early, and occasionally,3 u% q+ }- b# k: r
testicular enlargement is not that evident in the. f# E# v8 u  b
beginning of this process.1 In the absence of a neg-
) m6 P/ i; Y! s. T/ @" mative initial history of androgen exposure, our
" L2 r7 z8 F7 b6 e) N4 Bbiggest concern was virilizing adrenal hyperplasia,
+ G) h+ _+ C9 B! Xeither 21-hydroxylase deficiency or 11-β hydroxylase
; {3 T5 U2 p% E' c: h9 Vdeficiency. Those diagnoses were excluded by find-& P8 ?9 l( F3 q) b& R5 |
ing the normal level of adrenal steroids.
! K( c) G) ]1 F. ~3 _) MThe diagnosis of exogenous androgens was strongly
7 ]' a. R. m- t7 ~0 @+ e7 B% lsuspected in a follow-up visit after 4 months because
/ Y* g, z5 Z( c; tthe physical examination revealed the complete disap-
* L% n8 z8 `% r6 w3 hpearance of pubic hair, normal growth velocity, and: s9 G4 [  x) A4 c
decreased erections. The father admitted using a testos-8 s$ W3 z  ]5 l0 z: D
terone gel, which he concealed at first visit. He was1 K% \* r5 {. w  z; I
using it rather frequently, twice a day. The Physicians’7 q7 O. b) X1 o
Desk Reference, or package insert of this product, gel or
1 j) N1 Z: X# H7 Ncream, cautions about dermal testosterone transfer to
- X4 C2 N- F& u: @4 xunprotected females through direct skin exposure.. ~7 d1 F- ]1 p' }( m
Serum testosterone level was found to be 2 times the
4 d+ n5 D; a/ Kbaseline value in those females who were exposed to
: S' g) w$ c# K1 L3 e# o1 q2 U/ zeven 15 minutes of direct skin contact with their male
: d' x( F! o" jpartners.6 However, when a shirt covered the applica-
# a0 v! F" \1 d8 t2 @$ Xtion site, this testosterone transfer was prevented.
' S4 Q' Z' {4 b2 @) qOur patient’s testosterone level was 60 ng/mL,# T5 ]  K  |" a3 ]; d
which was clearly high. Some studies suggest that
" f; D# M0 {8 v9 ~$ Fdermal conversion of testosterone to dihydrotestos-% R" @# d1 j' ~% b9 F/ f8 H( R
terone, which is a more potent metabolite, is more- [0 Y9 S' F0 Z2 G0 ^. i# @# g
active in young children exposed to testosterone  P7 s$ s8 t' f  i9 t  _2 _
exogenously7; however, we did not measure a dihy-
6 Q. c2 c) Q; ?$ J' Ndrotestosterone level in our patient. In addition to7 X  r' u4 G' v
virilization, exposure to exogenous testosterone in2 D" h' t3 l2 c" S+ b% t2 a8 P3 Z
children results in an increase in growth velocity and) Q* v8 R) a; X! q* k# k
advanced bone age, as seen in our patient.: I0 B2 g) P8 A  A+ k- H8 \
The long-term effect of androgen exposure during
' A0 V4 ?: Z( d4 Y5 _early childhood on pubertal development and final8 {$ |7 [: k7 ^# Y
adult height are not fully known and always remain% e8 H/ A1 c: m7 L* E5 u% T" P
a concern. Children treated with short-term testos-) B4 F7 u6 D# ?3 ]; }4 Y
terone injection or topical androgen may exhibit some
5 e+ Z5 E5 x* lacceleration of the skeletal maturation; however, after
! H5 t+ \" {: M! i4 [cessation of treatment, the rate of bone maturation
( o# ~, O; Y: Y* W/ ldecelerates and gradually returns to normal.8,9
* @7 m1 o" o8 ~There are conflicting reports and controversy
" V; }2 x# ]* M' U5 q3 M' Bover the effect of early androgen exposure on adult
0 o9 p; Y$ q0 |5 I, ^' Q7 upenile length.10,11 Some reports suggest subnormal
( M7 `3 ^: ?& F0 Gadult penile length, apparently because of downreg-6 [) b9 N" O' s1 g2 _
ulation of androgen receptor number.10,12 However,& \0 q8 L5 T9 E4 j9 q  B
Sutherland et al13 did not find a correlation between4 d( O+ U; n$ g% H/ ~
childhood testosterone exposure and reduced adult* t+ Y! X% ~# |
penile length in clinical studies.
  r& p7 N; ]; T% f+ D1 H1 P+ HNonetheless, we do not believe our patient is7 J$ _+ A2 F7 W8 P5 e1 W: o' C  V
going to experience any of the untoward effects from
. Q, n  i9 S% J, n: ^testosterone exposure as mentioned earlier because
* g9 Z7 u" l7 t& sthe exposure was not for a prolonged period of time.
3 I! ]$ k; ~  h& vAlthough the bone age was advanced at the time of
" l0 F2 x; M% A! ddiagnosis, the child had a normal growth velocity at
% ]" a2 u$ u8 {! `9 W/ f7 Rthe follow-up visit. It is hoped that his final adult6 B8 D- a6 j: O9 |9 s
height will not be affected.
" i$ l  D' a3 S7 }8 K- jAlthough rarely reported, the widespread avail-2 u, K$ X0 X% e& K2 T8 ^0 _. j
ability of androgen products in our society may6 x, I% M+ p1 {* J7 W3 d& K; h
indeed cause more virilization in male or female
$ m; b. B/ {8 J) C3 l0 q9 I4 u% Rchildren than one would realize. Exposure to andro-0 T0 v- B% q6 a  d
gen products must be considered and specific ques-' Y! e5 b# U* t/ Q+ e# A
tioning about the use of a testosterone product or/ B. ], @* U$ E4 U1 g7 Z' ?
gel should be asked of the family members during
, [1 N( ]( O8 H. Z6 Q6 hthe evaluation of any children who present with vir-
( p( y0 a! B' xilization or peripheral precocious puberty. The diag-0 C0 C7 F& {; S0 k; `0 |
nosis can be established by just a few tests and by2 \* Z- n3 T0 K- U+ y0 |
appropriate history. The inability to obtain such a
* e+ [" j# R3 P" I! ^9 ehistory, or failure to ask the specific questions, may
" _1 ^) M1 ^% ^0 dresult in extensive, unnecessary, and expensive
5 q) s- M8 g4 Q, V4 ?investigation. The primary care physician should be" s2 \! f* F, ^
aware of this fact, because most of these children6 j7 r; `8 w! d
may initially present in their practice. The Physicians’' f- J$ a/ D$ h9 R% M
Desk Reference and package insert should also put a
4 s) g6 y+ w7 ?' X8 ^warning about the virilizing effect on a male or
/ \% ]- \0 _# wfemale child who might come in contact with some-
( F. F* T& ~: ione using any of these products.% S9 b6 ], b4 j% j! W+ W1 t7 c
References5 w0 Z. R  d2 Z* `9 t3 ~  c
1. Styne DM. The testes: disorder of sexual differentiation
; B8 U+ Y% |0 U# xand puberty in the male. In: Sperling MA, ed. Pediatric
5 a/ j2 n% \2 M" D2 L- Z; BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
7 f* j: ?. D% W) S" i2002: 565-628.
' e8 |4 E! o0 {+ Q- U2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
2 p' ~0 [/ A- ~  t& Ppuberty 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
$ Z( E7 r: s9 b- i
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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