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Sexual Precocity in a 16-Month-Old
8 O  S% K# n$ C: u! f6 _7 xBoy Induced by Indirect Topical
" Y/ b- h. u' w0 D) I; V2 jExposure to Testosterone
( l4 B9 @$ F2 |; H, k) S3 [4 ASamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 b3 b. l) N0 S: ~$ zand Kenneth R. Rettig, MD1
: Y2 _4 ?% U" W/ VClinical Pediatrics
6 |" g; T# _0 x, L6 Z8 W& _Volume 46 Number 6
* ]& y) H* r" J7 U7 S+ ~$ T# jJuly 2007 540-543
  Y& l; ~1 K) `- J2 k© 2007 Sage Publications
7 I4 ^+ I8 J2 R# E10.1177/0009922806296651
5 V$ u# s7 q9 x, x' {http://clp.sagepub.com8 ~6 J1 c9 S! ^9 M
hosted at2 c/ t8 Z& M; D
http://online.sagepub.com
& ?$ z; P- J4 O- p+ j2 Q/ \5 F( VPrecocious puberty in boys, central or peripheral,2 g0 F/ D8 u! A4 ?( \( [& |: W
is a significant concern for physicians. Central
& U* w3 H, }8 ~$ zprecocious puberty (CPP), which is mediated) P' ?7 I2 E; ?2 ^( C, t
through the hypothalamic pituitary gonadal axis, has$ O$ e! \1 V+ y% p1 ?* ]1 T( }
a higher incidence of organic central nervous system' A2 i- {3 ]4 M, t3 h
lesions in boys.1,2 Virilization in boys, as manifested7 Y: c1 ^! O- t& `% J2 e* R' O
by enlargement of the penis, development of pubic7 c! k: ~! Q4 H$ G# U2 F
hair, and facial acne without enlargement of testi-9 ~; u! D3 B: ?8 R0 W4 A$ R
cles, suggests peripheral or pseudopuberty.1-3 We
0 B4 i: S1 \7 [+ Breport a 16-month-old boy who presented with the
: \9 _2 y( [$ U, L( |; O, t6 r. venlargement of the phallus and pubic hair develop-0 K5 [. v3 W% C: T9 J/ \: s
ment without testicular enlargement, which was due
# N" @7 u1 H) i7 Vto the unintentional exposure to androgen gel used by
+ v' |4 I* B2 k0 Tthe father. The family initially concealed this infor-+ M( j% G6 M$ y5 ^  u* a5 M
mation, resulting in an extensive work-up for this
$ l9 `5 e4 H# z( }% Z" D7 Kchild. Given the widespread and easy availability of
2 v  b% \0 t5 L+ n, M, v2 H% atestosterone gel and cream, we believe this is proba-  z! ]) A' G5 L4 ^7 T
bly more common than the rare case report in the
2 l6 \& c6 k" b! V. Dliterature.4
4 c1 }# Y1 r. G" |Patient Report
8 x) o8 N# _& C) r! LA 16-month-old white child was referred to the( ]' I2 J/ D1 I% K; o% a. N+ Q
endocrine clinic by his pediatrician with the concern) r% m) Z% Z  h7 ?) R4 E$ Y& n
of early sexual development. His mother noticed) a4 _& H( ]2 b) f
light colored pubic hair development when he was& p4 `# y+ m$ c9 i+ G* w" _( b9 t
From the 1Division of Pediatric Endocrinology, 2University of7 D/ F& T  w5 A1 w% O2 s( ]
South Alabama Medical Center, Mobile, Alabama.
# V) L( r9 W  g, EAddress correspondence to: Samar K. Bhowmick, MD, FACE,5 S8 D- J, E0 F) Z
Professor of Pediatrics, University of South Alabama, College of- \) j- _+ m( Q( @$ V, i  W: _
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! ^7 N8 Q7 J, h* O2 R- m
e-mail: [email protected].
+ |+ P- u, M+ G& m  I+ A4 Y$ Habout 6 to 7 months old, which progressively became  Q0 d) d" g1 s6 J
darker. She was also concerned about the enlarge-
6 X3 L  V- N6 h1 H- |/ Sment of his penis and frequent erections. The child
; R& v6 i$ r& a- gwas the product of a full-term normal delivery, with- j& F2 S+ j$ V& Y1 J
a birth weight of 7 lb 14 oz, and birth length of
  s, H' R" @; b% [20 inches. He was breast-fed throughout the first year: C1 `% q$ M) r: D) N- }4 I: V- `
of life and was still receiving breast milk along with1 t; k3 r% N3 ^1 j$ L! ~0 ]  M* N
solid food. He had no hospitalizations or surgery,; K9 f* ~- s" \3 P7 H4 z1 V! w
and his psychosocial and psychomotor development; t# L7 s5 F+ S7 \( I; j- r* N
was age appropriate.
+ ~* B  |/ }! Z5 W8 m, ]The family history was remarkable for the father,
* f; I1 G3 C! L" @who was diagnosed with hypothyroidism at age 16,
3 L3 c# j3 m& P* C( y: U5 O8 H+ Qwhich was treated with thyroxine. The father’s- }2 s6 A( z) Q# `& a- {
height was 6 feet, and he went through a somewhat# g" [' U5 M4 @" L0 T' q9 Y
early puberty and had stopped growing by age 14.
# z$ U! K& V8 {  H( S& uThe father denied taking any other medication. The
# W1 B0 [- e- o& ~child’s mother was in good health. Her menarche+ d0 {% J1 E$ g% t/ m8 ]/ f
was at 11 years of age, and her height was at 5 feet
8 l/ J0 F! }* |  u9 D5 Z5 inches. There was no other family history of pre-9 G" d( T7 L5 C1 ]4 m# \" X: C
cocious sexual development in the first-degree rela-! }6 Z0 {) J2 l5 n! L3 J
tives. There were no siblings.. h+ y) P; M0 u  u6 S3 `2 k* C1 y/ t
Physical Examination4 J% I+ E0 c4 g
The physical examination revealed a very active,4 b8 }2 E& ?# J* q6 v/ Q2 J# g- J
playful, and healthy boy. The vital signs documented7 s' ]  A9 C' F- w. \
a blood pressure of 85/50 mm Hg, his length was
, s! ^; t! I$ `1 V90 cm (>97th percentile), and his weight was 14.4 kg
4 t1 |# M0 Y9 i9 K(also >97th percentile). The observed yearly growth
7 h# v* y, {5 N- I- ovelocity was 30 cm (12 inches). The examination of/ s) O; z4 n; f; H2 k
the neck revealed no thyroid enlargement.4 U  e$ `% U/ w: }, V
The genitourinary examination was remarkable for
1 S8 S' C+ ?6 y. a5 W2 z: Zenlargement of the penis, with a stretched length of
) x( d  i, U7 x1 @, g# o8 cm and a width of 2 cm. The glans penis was very well
  K1 P6 u& J2 Jdeveloped. The pubic hair was Tanner II, mostly around
6 E" y& j3 d; `, e5409 q0 ?, T$ v" H6 C" f& V
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 h: y6 Y8 g/ @* E" V
the base of the phallus and was dark and curled. The1 \  |6 h1 m  e: X' o; S
testicular volume was prepubertal at 2 mL each.
& d$ C7 h' g1 e2 b: |7 MThe skin was moist and smooth and somewhat
' Q) f4 q1 b2 z+ H4 c/ F/ L2 `oily. No axillary hair was noted. There were no
2 M7 \1 _4 s! g; g$ W( N( v. _abnormal skin pigmentations or café-au-lait spots.0 j7 S8 n5 g6 n
Neurologic evaluation showed deep tendon reflex 2+# G) B3 |3 }- t2 {* m
bilateral and symmetrical. There was no suggestion$ d/ \( [( A! P  ^$ X: K- u
of papilledema.) G" T1 ~* y; z( d
Laboratory Evaluation1 c6 p+ t9 v) z3 d8 x% S. P/ l
The bone age was consistent with 28 months by; G0 M* y% ]" P1 Z. p  ~& H
using the standard of Greulich and Pyle at a chrono-0 _2 ]3 w2 h! _& c" Y5 {& ~1 v
logic age of 16 months (advanced).5 Chromosomal
- J! @  |3 _5 d, h- rkaryotype was 46XY. The thyroid function test
2 T. \. |$ U/ i* |( f2 Dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-: s# a/ S: N$ x: I
lating hormone level was 1.3 µIU/mL (both normal).
: \* g  }/ ~- Z3 kThe concentrations of serum electrolytes, blood
4 E: `) N* L0 k# \urea nitrogen, creatinine, and calcium all were
% r$ u# s  r. x5 cwithin normal range for his age. The concentration8 E9 n; w0 ?& G3 i' {
of serum 17-hydroxyprogesterone was 16 ng/dL
$ z* l% c; G" n" l! ]" d) n2 L3 T(normal, 3 to 90 ng/dL), androstenedione was 202 }5 z0 }1 L- D7 C5 ^
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-' u! K6 n0 ]& H* @8 b# M
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
( I: f2 p# G+ U; Z8 V( d  Udesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( ]+ R7 Y- r1 u49ng/dL), 11-desoxycortisol (specific compound S)
- m2 Y7 D' u1 jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 |& N" w: X% E& \: h2 n
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
- y# H5 \4 n6 Y+ }& {testosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 O; g0 F! k- _% [+ d" R6 {- B& ~: U, E
and β-human chorionic gonadotropin was less than
$ A% T9 `, y; x: N( s5 mIU/mL (normal <5 mIU/mL). Serum follicular
1 Q( e! o5 w* Q& n- @0 Istimulating hormone and leuteinizing hormone; ?- C, t3 }" H) p; P% Q
concentrations were less than 0.05 mIU/mL. F6 D( Q) l4 K; [% D' n' Z
(prepubertal).2 E7 o$ d) a. D5 S* H% g  E8 t; t% ^
The parents were notified about the laboratory) J0 c' q8 w4 U
results and were informed that all of the tests were) G, n! S' [8 C
normal except the testosterone level was high. The+ x1 Z: z1 c3 z
follow-up visit was arranged within a few weeks to
5 N3 _, F# }: L5 m" D8 Aobtain testicular and abdominal sonograms; how-/ v  T& H  \7 d9 I5 I* [
ever, the family did not return for 4 months.7 l0 g% o* u5 e. O
Physical examination at this time revealed that the+ j/ n) T1 L0 F3 R. ~1 l2 k
child had grown 2.5 cm in 4 months and had gained, ?: Q5 G. _. n& h) ?% ?6 i
2 kg of weight. Physical examination remained& W% m" M* w. b* @% O
unchanged. Surprisingly, the pubic hair almost com-) F. J: O6 S8 R; V4 @
pletely disappeared except for a few vellous hairs at% S9 w* w* o$ F: p& [9 J! B$ R( O
the base of the phallus. Testicular volume was still 2$ }0 i' r/ Z0 v( t1 g6 L
mL, and the size of the penis remained unchanged.' }' q$ ?) n7 j' ~: I. r
The mother also said that the boy was no longer hav-
$ ?& S) S/ _3 g/ T3 Cing frequent erections.1 \+ j0 ~. x4 }5 `
Both parents were again questioned about use of
/ r; c; U. l) Oany ointment/creams that they may have applied to
& }9 E8 u- D2 Ithe child’s skin. This time the father admitted the5 u' P$ {+ K0 V* H0 x
Topical Testosterone Exposure / Bhowmick et al 541
$ K8 V% |( U+ J* M7 }use of testosterone gel twice daily that he was apply-
& {* k' ]; X. u. p$ @ing over his own shoulders, chest, and back area for1 P! o1 |4 l, @% ~: N0 C
a year. The father also revealed he was embarrassed
( y% F; D3 Z4 @4 w; Bto disclose that he was using a testosterone gel pre-" Y4 Y  P6 l- H4 I7 Z3 f; o
scribed by his family physician for decreased libido( Y8 Y! m; t' V# J' z) _  y
secondary to depression./ v3 Z* \6 D5 J& L7 V, ^0 i
The child slept in the same bed with parents.
2 [$ O5 n. M* }7 C- C/ M2 iThe father would hug the baby and hold him on his
$ `8 ?6 S/ }+ G3 X* o6 N: Dchest for a considerable period of time, causing sig-
6 z8 s3 C; e4 w' V* Z1 X7 m6 Mnificant bare skin contact between baby and father.
8 K9 R  l( R6 Y) V( h1 HThe father also admitted that after the phone call,
* @9 @6 t! T! k# ^) N# W2 f3 bwhen he learned the testosterone level in the baby* \/ A& u# V  z
was high, he then read the product information
7 C* y& L) f* P2 X: n& ipacket and concluded that it was most likely the rea-6 d4 O( }2 Z* ~9 Y
son for the child’s virilization. At that time, they
+ O& P5 z$ j) m  V9 q* ~$ }decided to put the baby in a separate bed, and the1 n2 C% R  m! k7 i: X$ ~% B
father was not hugging him with bare skin and had
5 }$ S* A; E) y! V4 \; p3 Bbeen using protective clothing. A repeat testosterone4 r" @6 ~* p( J. ?$ s2 j
test was ordered, but the family did not go to the
" C& |2 ~( z% dlaboratory to obtain the test.
" l" F8 c. T# B: R: HDiscussion" ~+ T6 x- Z, ^' b* Y; @& q
Precocious puberty in boys is defined as secondary! f, Y( s- N0 B
sexual development before 9 years of age.1,4/ t! @5 }! W! k: d4 [1 a' X, k
Precocious puberty is termed as central (true) when
7 l( M. m$ `4 b0 f& A0 B2 m- @4 ^it is caused by the premature activation of hypo-' a1 Q& m, Y6 }! O. t4 H3 d( m
thalamic pituitary gonadal axis. CPP is more com-
+ ?% L* k* Q1 Y+ e9 Pmon in girls than in boys.1,3 Most boys with CPP
8 e. t: ?/ w- t8 C! k5 [may have a central nervous system lesion that is/ t9 U9 B0 a: Q# e4 R  w  o4 X
responsible for the early activation of the hypothal-
* _7 O" z' D4 E) U) famic pituitary gonadal axis.1-3 Thus, greater empha-
. g* L- A  s- t# H0 A4 v8 |% O* Fsis has been given to neuroradiologic imaging in
; `9 v8 H9 Q- \* Mboys with precocious puberty. In addition to viril-
2 E) l3 l% F) U  bization, the clinical hallmark of CPP is the symmet-
9 L# @! V. n' y2 P4 y# Yrical testicular growth secondary to stimulation by. Y! Y- [! m" V1 E9 a. D; `
gonadotropins.1,3
, q7 m8 x- \* ?- h3 H' P1 t. U1 IGonadotropin-independent peripheral preco-* C6 j, ~6 Q' b- K+ t  P, @# _: |& h
cious puberty in boys also results from inappropriate
6 }9 O0 _, N, b2 }0 pandrogenic stimulation from either endogenous or( ?$ G/ W( }9 ~9 v: u
exogenous sources, nonpituitary gonadotropin stim-
% P! T6 ~) D3 X. ]0 }6 hulation, and rare activating mutations.3 Virilizing
. @  N" @" |8 Z1 I1 T7 r2 Acongenital adrenal hyperplasia producing excessive9 u# p1 u- p/ _
adrenal androgens is a common cause of precocious9 \3 ?$ Y: ~; b+ r0 p# e
puberty in boys.3,4
, L% g2 J* k1 S, BThe most common form of congenital adrenal( k% ^' q; c, d' f4 F. W/ k
hyperplasia is the 21-hydroxylase enzyme deficiency.  g5 ]: o) {, U) R" N
The 11-β hydroxylase deficiency may also result in" h3 d- `1 x! d2 L
excessive adrenal androgen production, and rarely,3 ?5 R' \6 a+ K5 J( h) c% b+ o
an adrenal tumor may also cause adrenal androgen! b, _6 G5 b% S! ^7 R# w( h
excess.1,3
* k0 p( t! @/ g( u7 t5 Aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. ]& @9 H3 T* c( v+ O4 M/ F: y4 [
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
  \. N2 X6 k% \7 v2 i# rA unique entity of male-limited gonadotropin-
5 R2 e& |9 B, `9 V2 gindependent precocious puberty, which is also known
( L# l6 r) Q* ^5 Ras testotoxicosis, may cause precocious puberty at a0 A! M5 E# N: m4 W; @) c* ^
very young age. The physical findings in these boys8 M  k7 n, ?! C7 l9 r
with this disorder are full pubertal development,% f! T& D+ x, |  j. j1 F3 q
including bilateral testicular growth, similar to boys  r) f$ u( ?. {
with CPP. The gonadotropin levels in this disorder
: E* H! b7 U' s; e' I% c# b. V6 Dare suppressed to prepubertal levels and do not show3 M) E7 |2 M3 K6 s3 |1 [
pubertal response of gonadotropin after gonadotropin-
# K, `! X2 E( d: r1 q3 W1 V. |releasing hormone stimulation. This is a sex-linked+ j8 h- w' s* j3 L
autosomal dominant disorder that affects only
2 L3 b. r: O* m. ~males; therefore, other male members of the family+ b& r0 T* k; g) n! D0 z8 M
may have similar precocious puberty.3. ?0 w* }6 _$ R: ?
In our patient, physical examination was incon-6 c6 C% n- ]- y4 ?6 ]/ l1 I
sistent with true precocious puberty since his testi-
- M& X" G1 a/ G, w, }8 ^cles were prepubertal in size. However, testotoxicosis
  N. Y8 U3 ]: dwas in the differential diagnosis because his father6 I4 D* u  \0 a7 Y
started puberty somewhat early, and occasionally,$ h2 N5 b7 O* y& t0 C
testicular enlargement is not that evident in the
: j' z3 f& m$ G4 G* A# r  cbeginning of this process.1 In the absence of a neg-
6 _% j! X% i; f! N- q" ?ative initial history of androgen exposure, our
- i1 q# U- K5 {. ?1 j" Gbiggest concern was virilizing adrenal hyperplasia,
2 F/ X3 g  Q% M2 ]: jeither 21-hydroxylase deficiency or 11-β hydroxylase* j; e/ Q+ K; e' \
deficiency. Those diagnoses were excluded by find-0 j$ f/ U, Q7 a& a6 @
ing the normal level of adrenal steroids.& E: t  d# \1 d4 j  g* r4 S8 H
The diagnosis of exogenous androgens was strongly# C6 p: ]1 X( A) }: e+ u
suspected in a follow-up visit after 4 months because: n6 ?0 w$ a; [$ g/ g; E/ Q" o
the physical examination revealed the complete disap-
2 ]( Z( m/ m( F% ~pearance of pubic hair, normal growth velocity, and
6 b! Y3 z, A# h6 G8 E& s5 `decreased erections. The father admitted using a testos-
. R; ~0 G4 d5 o0 ~' wterone gel, which he concealed at first visit. He was+ P; L& Q; {9 E" B. ]) p
using it rather frequently, twice a day. The Physicians’( ]9 f0 t6 U- f
Desk Reference, or package insert of this product, gel or" D, r6 p* z. n' u( @$ e
cream, cautions about dermal testosterone transfer to
/ k$ I* s+ x6 ^8 S# T4 }unprotected females through direct skin exposure.2 s8 J. A" w- h! V! V" C: J: L
Serum testosterone level was found to be 2 times the
; m! p- `2 I, `2 A* Lbaseline value in those females who were exposed to3 a5 ]: S4 [6 D9 v) @7 g8 w
even 15 minutes of direct skin contact with their male
4 P8 {# V+ \! b; @9 ~9 U* L6 fpartners.6 However, when a shirt covered the applica-
3 }, b2 y0 `3 s; t( x1 ltion site, this testosterone transfer was prevented.
  ~( }  x, {7 vOur patient’s testosterone level was 60 ng/mL,7 |; d5 r3 F' i0 ?7 U
which was clearly high. Some studies suggest that2 d( i/ A0 r8 a0 ~, d+ c* `
dermal conversion of testosterone to dihydrotestos-5 Y6 ~0 ?/ c  _" W4 i
terone, which is a more potent metabolite, is more
& @4 l2 Y0 h3 y1 }8 _* zactive in young children exposed to testosterone
5 x5 x  m3 u% t% l$ Iexogenously7; however, we did not measure a dihy-. z) p7 O% b8 U6 h- m( r
drotestosterone level in our patient. In addition to1 \$ Y* s9 H  f) U$ U* _- r
virilization, exposure to exogenous testosterone in8 f/ T; V+ E) n& d6 w$ T! y
children results in an increase in growth velocity and
6 A6 M  y$ ]/ a( Radvanced bone age, as seen in our patient.  b, {5 F  M4 l9 i9 I9 I
The long-term effect of androgen exposure during/ B  r9 E9 E. F# U3 z3 J
early childhood on pubertal development and final
9 w+ {, t9 q0 e: k; ?0 v" ~& {5 q' ]adult height are not fully known and always remain
) N, L5 _# q- d% y; _9 K" ]a concern. Children treated with short-term testos-
9 e7 x% ~! ]( D$ dterone injection or topical androgen may exhibit some9 \; g7 F  O/ g
acceleration of the skeletal maturation; however, after4 i% A; y' W& K9 m* N) X
cessation of treatment, the rate of bone maturation1 K0 O/ M: a# r) [7 \5 [3 |2 c% @  _
decelerates and gradually returns to normal.8,9+ g- u6 Y( ]6 I" W8 I. B% `
There are conflicting reports and controversy
  E) e$ Y9 B5 `. ^0 nover the effect of early androgen exposure on adult% X% s, d& p) |, y; J6 F
penile length.10,11 Some reports suggest subnormal, ?, m; d* g' u9 B" {
adult penile length, apparently because of downreg-8 g: Z( c* k' D2 D; ]
ulation of androgen receptor number.10,12 However,+ Z' j0 O0 @; Z; [& ?6 u0 i0 Q
Sutherland et al13 did not find a correlation between
* f" G1 ]. T4 ?) `5 mchildhood testosterone exposure and reduced adult6 Y# }7 l1 g7 d7 T  i
penile length in clinical studies.* D% v) B7 Q# J) b
Nonetheless, we do not believe our patient is* i# V/ `+ j9 C/ ^8 I3 [& H' T2 w
going to experience any of the untoward effects from
6 _. X2 i. x& P2 o0 o3 Xtestosterone exposure as mentioned earlier because9 |# S3 ^( k2 p* |+ b$ ^4 l& ?
the exposure was not for a prolonged period of time.
4 y2 ~: t( m5 b7 \# x/ aAlthough the bone age was advanced at the time of
$ p0 F. k, D2 f& v  pdiagnosis, the child had a normal growth velocity at
  o3 a# s, b3 e7 b, ^5 u1 U- j) `the follow-up visit. It is hoped that his final adult
1 o- |7 P% I: Q; M9 W0 V3 U# ?height will not be affected.- z8 d9 {& E* S9 z) M6 D8 X) o  e- [6 Y
Although rarely reported, the widespread avail-* M; g1 s9 @8 j" A/ {$ i& \5 S, E; N
ability of androgen products in our society may
: w+ a% \  ^# s+ Q4 W% I  kindeed cause more virilization in male or female
( r* C$ `/ l# V; qchildren than one would realize. Exposure to andro-) m6 p$ z7 o  a
gen products must be considered and specific ques-
( M8 Q& F; _3 ?- P7 ^tioning about the use of a testosterone product or& e, o, @# _3 ~! L* q
gel should be asked of the family members during
$ S& w9 v( c" r( h9 v4 I$ cthe evaluation of any children who present with vir-+ s6 T( q( B/ R& m! T9 w9 [4 n# U
ilization or peripheral precocious puberty. The diag-
1 W. J, ~7 Z" A8 M1 E0 O+ A& enosis can be established by just a few tests and by
9 o% ^6 h2 a) ~9 u( B, V6 _appropriate history. The inability to obtain such a
1 @7 q0 @8 B3 Yhistory, or failure to ask the specific questions, may& d8 A7 V3 Q( B2 d& q
result in extensive, unnecessary, and expensive2 g( D2 S; F$ v9 k& y6 [3 Z. Y3 f
investigation. The primary care physician should be0 Z9 H. c8 r( l+ z- U+ J
aware of this fact, because most of these children
/ {5 i+ L$ a- `3 r1 Xmay initially present in their practice. The Physicians’* {" F9 R" G/ n' E7 n
Desk Reference and package insert should also put a
; T/ O- I; f1 _$ owarning about the virilizing effect on a male or
. v% `6 S' E* y+ w2 s. A3 efemale child who might come in contact with some-
! i! V; O9 b1 ~$ E/ None using any of these products.* e8 L/ p. C/ t) L7 }
References
) h( p. y/ C5 `( a$ J1. Styne DM. The testes: disorder of sexual differentiation& L6 r$ H+ ~. s; f, W& U, n% e
and puberty in the male. In: Sperling MA, ed. Pediatric
3 A. L' }# \" n( DEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 F& X+ P% y' L2 [3 @2 J- t2002: 565-628.
, f1 z2 M' K8 S9 u2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% a# Y6 L' d* S7 f; G7 `
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old  S6 {9 |6 F. e$ T
Boy Induced by Indirect Topical
% _. M1 |& N+ ^# c& xExposure to Testosterone
! p% I1 B  g4 Z2 j. BSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 p) E1 u% B: h: z1 Q( V; gand Kenneth R. Rettig, MD1  p2 x) p; T$ y- n+ f
Clinical Pediatrics
$ z6 ]  e! B" P( ^8 ]Volume 46 Number 6
1 O. G+ y: b0 g2 |; H" h1 ?July 2007 540-543+ p5 P' z$ ]: ~; C$ t6 ?3 Z
© 2007 Sage Publications: m* p- l% l0 s/ a/ P: F- g
10.1177/0009922806296651, C' @, d7 b) x$ Z: Z+ p4 `3 v% d
http://clp.sagepub.com
# M. a& R. d+ Y4 D  ihosted at  `5 @) u3 a: `# F
http://online.sagepub.com
* a: l% W0 x' y- m: EPrecocious puberty in boys, central or peripheral,9 f  r. e1 h. {. c3 j
is a significant concern for physicians. Central# j" q7 |- }8 i  t2 `; T  r" i
precocious puberty (CPP), which is mediated4 \( r2 |7 M2 y, x* u* G$ C5 |' L
through the hypothalamic pituitary gonadal axis, has
8 L9 o5 ]9 z# E! I* D9 R5 P: b  ka higher incidence of organic central nervous system% s! J' `$ ?/ f- D; q) q5 v
lesions in boys.1,2 Virilization in boys, as manifested7 D# v4 S  t5 ]5 l) n/ }$ B
by enlargement of the penis, development of pubic
( U. p$ B+ L* i; L( h! hhair, and facial acne without enlargement of testi-' ~9 q$ e3 V2 G9 J  u; y
cles, suggests peripheral or pseudopuberty.1-3 We" o: P) [* s/ L% A
report a 16-month-old boy who presented with the
! V: F! ?5 r7 J, _  K! b1 Menlargement of the phallus and pubic hair develop-3 b0 {# @; X6 ~" d) o% t* Y
ment without testicular enlargement, which was due
: _2 J( T' }( a* s3 Hto the unintentional exposure to androgen gel used by" q( W* o, I4 e- c
the father. The family initially concealed this infor-3 _% Q. s$ L" q+ X. e8 @
mation, resulting in an extensive work-up for this
: Z  \$ r1 J% Gchild. Given the widespread and easy availability of
5 d! F7 d2 X( @& x$ |8 g: o3 a( gtestosterone gel and cream, we believe this is proba-
. n0 B7 l6 \: ^bly more common than the rare case report in the+ @1 \! z$ G" k$ H
literature.4( i2 y( H) e- v3 n! t
Patient Report0 y) ^+ x% S1 R& o$ b1 c/ ~3 g, v# x/ p
A 16-month-old white child was referred to the! B& U  m, J  L9 J* k; d
endocrine clinic by his pediatrician with the concern
. [5 q5 I) @: L+ g$ }of early sexual development. His mother noticed8 h. K5 u/ M: Q& k3 K1 w& b* n
light colored pubic hair development when he was
: u1 g& X: q; j$ F7 f. n% u+ r! `* NFrom the 1Division of Pediatric Endocrinology, 2University of
( ?. K5 j# e3 ~8 W5 QSouth Alabama Medical Center, Mobile, Alabama.7 U* g5 n1 w8 W* Y$ @1 Q6 d
Address correspondence to: Samar K. Bhowmick, MD, FACE,# L8 d% M# s5 Y2 o0 {
Professor of Pediatrics, University of South Alabama, College of7 {$ G4 Q+ i8 D) I9 d
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ N; _4 W- A4 u) D: q
e-mail: [email protected].
. k# ?* w0 ~! i& m& [& n( \2 habout 6 to 7 months old, which progressively became$ C5 S: ]% d4 T
darker. She was also concerned about the enlarge-8 o- N2 P$ h/ z& [' P
ment of his penis and frequent erections. The child
8 q' y6 c. i. m$ g( Lwas the product of a full-term normal delivery, with
6 Z; m" C. \/ ]1 w, }/ xa birth weight of 7 lb 14 oz, and birth length of
! f( Y0 L7 [9 z2 Y' ?2 ^/ z. h% R20 inches. He was breast-fed throughout the first year8 |  ]& ^% Z% X% P! ]! C4 E
of life and was still receiving breast milk along with
/ L1 h( N" O# u  R- u5 h( y/ x" ksolid food. He had no hospitalizations or surgery,
# l' m2 u; S# }2 `. l! Aand his psychosocial and psychomotor development1 G3 m, r% Z; h' Z0 t# W" D$ r
was age appropriate.! }; |7 ~6 K2 _
The family history was remarkable for the father,
8 K- h' ^0 ?+ T. G- bwho was diagnosed with hypothyroidism at age 16,
5 t0 I$ r$ O+ [which was treated with thyroxine. The father’s- k4 y3 T' w& H' I7 c; f
height was 6 feet, and he went through a somewhat
: ]" {! m' I, J3 D5 ?' ?" R2 Z/ h4 E# yearly puberty and had stopped growing by age 14.& N0 U7 s3 P4 G9 U3 k
The father denied taking any other medication. The
) t4 L+ V' v! p' ?& ~* }# jchild’s mother was in good health. Her menarche
4 I0 w( n. r0 O; {was at 11 years of age, and her height was at 5 feet- x: }) F9 b0 j' [* W; r
5 inches. There was no other family history of pre-4 E0 w8 m3 X  k7 w
cocious sexual development in the first-degree rela-# O3 l. W9 j) J# {
tives. There were no siblings.
. s( a' _2 d+ d$ n6 |; s; PPhysical Examination
, L/ b: N$ \# W5 G* _& oThe physical examination revealed a very active,' R- @# q+ p: P
playful, and healthy boy. The vital signs documented
# Z3 F6 x/ z4 g) N  c& Ya blood pressure of 85/50 mm Hg, his length was2 \. X: |! p7 m" r: l
90 cm (>97th percentile), and his weight was 14.4 kg
9 X1 ?* S4 `; v7 U(also >97th percentile). The observed yearly growth
- b4 H. p0 T# [9 l" W( Y# H- cvelocity was 30 cm (12 inches). The examination of; f! w# Q* w5 V
the neck revealed no thyroid enlargement.
3 y! t" O' l% nThe genitourinary examination was remarkable for
' `# x- g- L. P2 z! k* k4 Xenlargement of the penis, with a stretched length of
3 R  s, r  p6 c8 cm and a width of 2 cm. The glans penis was very well
2 ~: C$ o+ z; y1 }1 ?5 ndeveloped. The pubic hair was Tanner II, mostly around
1 \( A0 q, o: O1 [3 \540
) b& f" J' V; Mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ f8 }+ H& f; \+ m! E6 L0 Jthe base of the phallus and was dark and curled. The
# F: h* E$ g+ S$ p2 z9 g% D8 O4 {testicular volume was prepubertal at 2 mL each.
  [) }# E5 P  \$ C" lThe skin was moist and smooth and somewhat
' \3 M* e/ O7 t5 w; g/ I/ Ooily. No axillary hair was noted. There were no
2 ?7 e9 i0 A. f& j3 T7 q. S/ Jabnormal skin pigmentations or café-au-lait spots.
4 V$ N$ B0 g3 U: C( i& yNeurologic evaluation showed deep tendon reflex 2+/ t* p8 A( o4 E$ M. ~
bilateral and symmetrical. There was no suggestion9 W( @( ^2 _* h
of papilledema.
8 U' W/ S% ]) s+ h) C# W! I. ~2 G) fLaboratory Evaluation
8 u3 G+ u! k* V3 r& z1 D$ a8 Z6 TThe bone age was consistent with 28 months by
" l. o9 R, [+ _* Vusing the standard of Greulich and Pyle at a chrono-$ _+ ?& p  x' M+ X: G
logic age of 16 months (advanced).5 Chromosomal  N% S9 j+ f- @
karyotype was 46XY. The thyroid function test
- j! j8 {, I; A5 Hshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
, \( }% l5 `3 V$ b9 O: Plating hormone level was 1.3 µIU/mL (both normal).
) g* L" d- T% D9 JThe concentrations of serum electrolytes, blood: \$ N# G4 b# l* p7 {1 M1 D* x
urea nitrogen, creatinine, and calcium all were3 W- k/ n: J1 y" y" W
within normal range for his age. The concentration1 F2 P8 _) x( T. A
of serum 17-hydroxyprogesterone was 16 ng/dL
* Q1 H% g' y, S: r1 V: T(normal, 3 to 90 ng/dL), androstenedione was 205 n3 G3 ~0 u0 |
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-+ h- ^2 c/ R  o
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 q1 [4 T( m( B$ W! r; Ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to9 h4 e: F. ^) o
49ng/dL), 11-desoxycortisol (specific compound S)2 d$ ~1 x% h4 J/ @8 I
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-6 Q) T( d  t& J! [5 E8 B9 h: J
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
. n2 h) ~% @" Q/ rtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! ^0 ~+ R6 U) `( d9 p( H6 F, t  Pand β-human chorionic gonadotropin was less than) @. m, \! x. l- N9 i
5 mIU/mL (normal <5 mIU/mL). Serum follicular
% B, \# d* w9 N- }8 ]$ Estimulating hormone and leuteinizing hormone
1 C% m  y* t( g6 ?concentrations were less than 0.05 mIU/mL
: T' u- i6 a% D2 m/ O7 K  |0 p& f(prepubertal).$ X7 e0 s# d3 J( s4 D
The parents were notified about the laboratory
$ z3 @) ?, R* ~4 k( Oresults and were informed that all of the tests were/ Z0 s- v" g+ c% A1 g0 h. j" \. ?
normal except the testosterone level was high. The0 r3 r. C, L" V/ w" _; \
follow-up visit was arranged within a few weeks to
% Y8 ~; [! L; yobtain testicular and abdominal sonograms; how-
6 l5 j* G# o, Qever, the family did not return for 4 months.
9 D. l" c% o. DPhysical examination at this time revealed that the
! k  ?' l8 V3 S8 y+ N; Cchild had grown 2.5 cm in 4 months and had gained
5 k" }/ R/ x5 m2 kg of weight. Physical examination remained9 Q. Y3 @; \) I: X* w8 ?1 q9 x
unchanged. Surprisingly, the pubic hair almost com-" M1 F2 w  |  E% j
pletely disappeared except for a few vellous hairs at( }+ B4 B6 C5 B3 ^
the base of the phallus. Testicular volume was still 2
- U8 r3 [* r0 I+ qmL, and the size of the penis remained unchanged.- j- x6 T  y, \; u9 S) n
The mother also said that the boy was no longer hav-' ?0 f4 @6 I/ }; E1 m0 w& F
ing frequent erections.) d* g3 w9 {8 A+ T$ n; g
Both parents were again questioned about use of
  }' e- E: o* j9 E# i7 F9 e6 W6 m/ Bany ointment/creams that they may have applied to
, K, ^1 ~$ w/ j  U+ h* z, q1 Vthe child’s skin. This time the father admitted the$ g  \4 z2 u* V( m
Topical Testosterone Exposure / Bhowmick et al 541$ j9 S* G$ ^' g0 X8 `  S  p
use of testosterone gel twice daily that he was apply-4 f( h; |% p- U3 p3 }
ing over his own shoulders, chest, and back area for: }* ]" O  s  O/ g/ k
a year. The father also revealed he was embarrassed) ?1 ^( S- j0 t$ |9 J" K+ Q$ {
to disclose that he was using a testosterone gel pre-- p; z! {; ?. l! U
scribed by his family physician for decreased libido3 X- t2 i3 C4 q- G, P4 p* H
secondary to depression.
" J$ `( c. Q2 }8 d. X( j; ?3 CThe child slept in the same bed with parents.: ]7 ~7 R+ G9 T% O
The father would hug the baby and hold him on his
( F8 w$ F5 o, T0 r# U* ^" nchest for a considerable period of time, causing sig-+ s/ b: j2 q* d' v; i) [8 I: B
nificant bare skin contact between baby and father.
/ C) e0 R: |; u8 H: h8 e- `The father also admitted that after the phone call,
; |) [# H+ Y2 W. q2 Kwhen he learned the testosterone level in the baby' J$ E: s4 r! E! r
was high, he then read the product information7 l& N4 i' J9 f3 h
packet and concluded that it was most likely the rea-9 m  [9 q7 z4 Z
son for the child’s virilization. At that time, they* v  ]4 T1 s; J: A
decided to put the baby in a separate bed, and the  {! {( e2 ~% Q! d% B8 E( C* i
father was not hugging him with bare skin and had
$ p. r7 Y2 }/ a! P  qbeen using protective clothing. A repeat testosterone. S3 x$ r0 Z& B. L7 Y9 o' F/ U9 _
test was ordered, but the family did not go to the
/ E4 O. H# W1 s4 f, b' ~/ p" e+ q# S8 |laboratory to obtain the test.7 T5 {+ a7 M" \$ s7 U
Discussion
1 W. }9 D5 b1 c1 z0 ?5 YPrecocious puberty in boys is defined as secondary
. D) D+ \* W! K: R3 n$ ~. ?  Dsexual development before 9 years of age.1,4
) t/ H9 ?2 h  WPrecocious puberty is termed as central (true) when+ R$ Q+ l: J. T1 [6 v6 ]5 W
it is caused by the premature activation of hypo-
* ~8 M1 r$ ^7 ?thalamic pituitary gonadal axis. CPP is more com-
& e* S4 D) i2 p6 U' K: ^mon in girls than in boys.1,3 Most boys with CPP/ V  c; H9 }3 w2 c8 v* s
may have a central nervous system lesion that is( Z) l# A" o+ ?! H6 `( [+ Y
responsible for the early activation of the hypothal-
6 r2 Y; K  _+ {7 q1 H. ramic pituitary gonadal axis.1-3 Thus, greater empha-
0 {8 x! r+ ]1 u9 nsis has been given to neuroradiologic imaging in
) L6 I9 L9 o5 u$ I, E( o! ~boys with precocious puberty. In addition to viril-
/ [) S  Z: M) x( K" @4 |2 Q9 ~ization, the clinical hallmark of CPP is the symmet-4 d/ {& G7 I! G
rical testicular growth secondary to stimulation by3 u6 w3 b  m& y! T) F) ^
gonadotropins.1,3; \# Q9 f, e1 L2 c  K8 |
Gonadotropin-independent peripheral preco-; O$ O/ a" w, m5 k- R) B  D: J
cious puberty in boys also results from inappropriate+ _+ B/ m8 ^( j. w  d* L
androgenic stimulation from either endogenous or
0 I) {1 Z/ O, \. K- mexogenous sources, nonpituitary gonadotropin stim-
. u: s1 E1 k4 S; i1 W9 M+ P! Julation, and rare activating mutations.3 Virilizing! H0 }+ F5 x2 S1 a" e
congenital adrenal hyperplasia producing excessive2 R. t4 W* C! |3 E! T3 F
adrenal androgens is a common cause of precocious
. {; C9 m+ J+ v: Y/ ]0 k; xpuberty in boys.3,4
9 u) V) I! V; _5 EThe most common form of congenital adrenal
6 J5 s% O$ n" J: X2 c# L$ ^hyperplasia is the 21-hydroxylase enzyme deficiency.
8 b5 J$ ~7 l8 q0 x, ^4 mThe 11-β hydroxylase deficiency may also result in0 T* h3 B5 c7 g" ~* f) l- u! J# L
excessive adrenal androgen production, and rarely,
6 n% J" K: T) \  man adrenal tumor may also cause adrenal androgen! x2 |9 K2 `3 `  Z* o3 l
excess.1,3
) i( y4 @% J" ?) i& t+ \at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; C3 g1 _% d; k! c8 d& {
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007- V' X$ s/ n  \
A unique entity of male-limited gonadotropin-, k5 f6 `: E. E* V( b
independent precocious puberty, which is also known
( g6 f. t% p) d' K) C6 Z$ Tas testotoxicosis, may cause precocious puberty at a
* h& U. c) ^! ~$ i7 T9 X! m+ \very young age. The physical findings in these boys2 n+ S* v  i0 g+ Q5 Y8 P
with this disorder are full pubertal development," Q2 s# z" @% ?% x0 y% z+ M% {6 Q
including bilateral testicular growth, similar to boys
! {  c2 H/ p; c7 C/ k- e3 }5 bwith CPP. The gonadotropin levels in this disorder0 Q4 ^3 o  t- H" ~( N5 |* i
are suppressed to prepubertal levels and do not show
/ F" ?9 ~/ h2 G/ J% \pubertal response of gonadotropin after gonadotropin-+ A2 t! c/ M: s8 [. p) h
releasing hormone stimulation. This is a sex-linked
9 N5 n$ `9 A+ j) q+ jautosomal dominant disorder that affects only8 x1 S+ B) l: j; ?
males; therefore, other male members of the family
, A, f; H, c. Q# P! K2 }may have similar precocious puberty.3
, [7 W$ M1 B/ T6 V0 Q. Y, l* U) yIn our patient, physical examination was incon-
% a4 A' ]6 I+ x; h+ d8 z$ z# psistent with true precocious puberty since his testi-3 K4 p# k2 n: K/ @$ ?, w
cles were prepubertal in size. However, testotoxicosis" ^# M7 ~4 p, w  h
was in the differential diagnosis because his father
# c1 h# Z( u- k/ j4 c0 R: Lstarted puberty somewhat early, and occasionally,
& K/ m2 v0 M5 M6 g( {7 M% otesticular enlargement is not that evident in the
# [' v- r8 Y3 Z3 U  A) X, F3 vbeginning of this process.1 In the absence of a neg-
) s4 d* [5 S  y1 Wative initial history of androgen exposure, our
: w. p/ V: V. a4 u- _biggest concern was virilizing adrenal hyperplasia,
) X9 n. _; S* P4 Keither 21-hydroxylase deficiency or 11-β hydroxylase
- _( ~9 a* a2 T: M8 Y8 h( pdeficiency. Those diagnoses were excluded by find-. {' `7 P' ~4 _! ~( x
ing the normal level of adrenal steroids.6 x4 y6 {" R; x+ d' W- e8 B
The diagnosis of exogenous androgens was strongly9 Q* g4 W) ?  ]: k
suspected in a follow-up visit after 4 months because# S; O5 W+ ^/ t4 R
the physical examination revealed the complete disap-  ~- J+ v( ]! E# g
pearance of pubic hair, normal growth velocity, and" s8 k" f+ E: b1 T/ c
decreased erections. The father admitted using a testos-
* S$ `2 A' h  Wterone gel, which he concealed at first visit. He was* K7 G  Y4 K& ~" F  e
using it rather frequently, twice a day. The Physicians’' K' u  y  \' L) l4 C  g" [$ N
Desk Reference, or package insert of this product, gel or) G7 R( Y3 h! g5 ?" J& F
cream, cautions about dermal testosterone transfer to
4 D2 c6 m0 U; g( ~unprotected females through direct skin exposure.# f) Y4 T* r( g) `
Serum testosterone level was found to be 2 times the
& H6 X" I! e! }7 O4 E/ \baseline value in those females who were exposed to
  ?+ _, m, Q+ K0 \1 B& Eeven 15 minutes of direct skin contact with their male
' |& Q& {0 Y2 B  }$ B* Gpartners.6 However, when a shirt covered the applica-4 _5 N) U' W1 @
tion site, this testosterone transfer was prevented.
/ z5 G: ?" b# B: P* K- aOur patient’s testosterone level was 60 ng/mL,8 _" Z4 a" i- @6 V% M: @
which was clearly high. Some studies suggest that7 ~% D' N! s: T8 V$ m4 j- Q
dermal conversion of testosterone to dihydrotestos-: F+ P( e' c! j
terone, which is a more potent metabolite, is more
% }/ A( D' G4 }! ^8 `active in young children exposed to testosterone. E3 m+ V: M$ o6 j+ v! a
exogenously7; however, we did not measure a dihy-
6 I5 J( {* J$ ~2 Ldrotestosterone level in our patient. In addition to
+ Z8 G4 P6 F% s/ `virilization, exposure to exogenous testosterone in% Q: K% b$ H6 w, v
children results in an increase in growth velocity and
" o1 g6 A$ t) t) ~7 {  x; z+ Tadvanced bone age, as seen in our patient.- m# r0 x1 \) a2 t" e8 `
The long-term effect of androgen exposure during
2 z; L: q! h/ m4 v4 K4 k( V2 dearly childhood on pubertal development and final
2 Q; o) K5 E7 F" `0 xadult height are not fully known and always remain* ], F3 ~# F0 w/ B4 v
a concern. Children treated with short-term testos-+ \) N6 C* O0 U: q+ E
terone injection or topical androgen may exhibit some- q  v$ y6 Z! u1 O7 A
acceleration of the skeletal maturation; however, after% x, G1 c5 h! V+ X# J% i
cessation of treatment, the rate of bone maturation$ h0 b4 O6 ^: F& H4 J1 X6 g/ j# Z
decelerates and gradually returns to normal.8,9
& B7 j( P3 d, {5 q) O  uThere are conflicting reports and controversy
: O1 r# m& N7 q8 x* y6 Uover the effect of early androgen exposure on adult8 o* l; I$ w+ Z+ Z
penile length.10,11 Some reports suggest subnormal1 w8 P1 s8 P3 o2 w! m
adult penile length, apparently because of downreg-# w4 O& V) U& r. \
ulation of androgen receptor number.10,12 However,! C, F; u7 Y; x' M8 i2 a: p
Sutherland et al13 did not find a correlation between: s" u- O) E% |+ ?% k$ `
childhood testosterone exposure and reduced adult  W' H9 j! u) w; r7 z4 z0 O5 b% k$ @/ `
penile length in clinical studies.
  G1 W3 r- w6 ?/ D# I+ rNonetheless, we do not believe our patient is% n) i+ ~- k2 G# S( F, J0 ~: P
going to experience any of the untoward effects from* A& Q3 z2 {' m0 K4 y/ M$ t$ |
testosterone exposure as mentioned earlier because
4 R' _5 M1 s7 Z% Pthe exposure was not for a prolonged period of time./ J$ i% w& G8 [9 T" Z. Y
Although the bone age was advanced at the time of4 M4 U6 `8 b$ s
diagnosis, the child had a normal growth velocity at8 |- L! i5 r! s3 u$ r+ d9 C$ x0 r! F+ `
the follow-up visit. It is hoped that his final adult
$ S. `& K* n- @: s9 T0 w0 N% Eheight will not be affected.) y3 _8 E. G$ ^0 [5 n$ p2 C$ j
Although rarely reported, the widespread avail-$ ~* \/ y3 J* l9 I3 e( }! s
ability of androgen products in our society may
& V% X3 j1 @, L/ uindeed cause more virilization in male or female: J' |" {, a5 ^2 ~) c; `$ u
children than one would realize. Exposure to andro-
4 \7 ?6 ^! z" x% [2 d7 _& A3 Cgen products must be considered and specific ques-
! w" Z; m6 j  `& Ntioning about the use of a testosterone product or$ Y: t0 j  @% o' K
gel should be asked of the family members during; o3 q9 C  n! p; X
the evaluation of any children who present with vir-
0 c* ?, R5 D# [: K( `  O& k' {ilization or peripheral precocious puberty. The diag-
+ [; v5 Z6 p% y% D2 Unosis can be established by just a few tests and by5 @- L6 l& ^' _  J7 g
appropriate history. The inability to obtain such a
% s7 K6 h/ }1 T4 }0 c6 mhistory, or failure to ask the specific questions, may
+ E2 [' S" r) c/ Vresult in extensive, unnecessary, and expensive
4 \/ Y' }) d. L* Y. {" ]8 U' w) Z6 Finvestigation. The primary care physician should be
) B' p+ z3 e1 P' O* w$ Z- O: b/ uaware of this fact, because most of these children$ I( `) b7 Z& E' w' v2 i& I
may initially present in their practice. The Physicians’
) t* n' A' [& M& I# sDesk Reference and package insert should also put a; b! u* z6 w9 [. T  K
warning about the virilizing effect on a male or
% N7 E5 a! _. o/ T- Vfemale child who might come in contact with some-/ K' U! v9 h- a0 w' M1 c
one using any of these products.
" \- O( z0 B2 U* T7 t7 q, wReferences
6 S4 ?2 {& J; e% `- E1 e6 f/ F  h1. Styne DM. The testes: disorder of sexual differentiation1 g4 b6 ~; M+ B7 ^1 h, M
and puberty in the male. In: Sperling MA, ed. Pediatric2 y+ i* q: F, j+ A, s6 C
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, y, c) H& v( f0 r3 o0 `8 c2 Y0 x" _3 Y
2002: 565-628.0 C% s: ?6 N; J1 |
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious8 k9 q) a0 ]$ `4 u; l5 D
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

4 d& H5 ?' G9 g% [8 K+ y$ x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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