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Sexual Precocity in a 16-Month-Old" j. h3 s, b: O" F/ b9 s# ?' m
Boy Induced by Indirect Topical
5 M, _3 ~4 E+ W0 ]2 Q( @+ B5 K+ FExposure to Testosterone
/ Y. r1 j2 A& D. j1 B' XSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 A% E* N6 H0 W
and Kenneth R. Rettig, MD13 a! N6 A# Y) h" j3 F8 `
Clinical Pediatrics1 Y, z& n7 v' i+ t
Volume 46 Number 6
2 F( Y! K. X  h$ F# z# e* _July 2007 540-543& }9 F  o3 X/ f% X. N& X
© 2007 Sage Publications/ ~- U6 Z- O/ c# J- r, H4 I0 ~
10.1177/0009922806296651; H; t& d- K$ q3 z' T! a% T: I: d
http://clp.sagepub.com7 h7 z& v$ H; t% S
hosted at6 N: g* i; \. d6 P. a; E$ M/ m
http://online.sagepub.com+ j/ B5 J# @. Q( [
Precocious puberty in boys, central or peripheral,1 m7 o% O2 v! v& Z7 N) i7 S1 ]4 c6 h
is a significant concern for physicians. Central( }3 J' D" a( I( n2 n) @
precocious puberty (CPP), which is mediated/ I9 J# A7 A& f7 l( X% B) x
through the hypothalamic pituitary gonadal axis, has  g! w  _0 J: k# _* L( |, g
a higher incidence of organic central nervous system
. [- `/ x& {* U0 zlesions in boys.1,2 Virilization in boys, as manifested
! N- A2 ?/ ?: H  Pby enlargement of the penis, development of pubic
1 T2 H9 @8 j: H* M/ ^0 f% v! [5 ahair, and facial acne without enlargement of testi-
* C( V" D7 Z# f8 L0 X9 hcles, suggests peripheral or pseudopuberty.1-3 We
' {8 N  I- Y2 i: z+ breport a 16-month-old boy who presented with the
( a( ~) S- Q9 P4 x3 w! G0 senlargement of the phallus and pubic hair develop-6 Y1 ~; P- Q* x! z& X. }
ment without testicular enlargement, which was due5 r. ~0 x  J8 M; Y! A; W
to the unintentional exposure to androgen gel used by
( y: o, e( h7 D+ ]; cthe father. The family initially concealed this infor-3 s) U5 x* d* D; u# |5 M, a; {
mation, resulting in an extensive work-up for this
7 n' l4 i& ~3 q; c' {' I  N1 `child. Given the widespread and easy availability of- @7 [8 G! ?) H! a! E. V* K  Q
testosterone gel and cream, we believe this is proba-
6 L! `& o1 G% i" K1 M( \3 W! z" gbly more common than the rare case report in the/ j. K  X5 `" A
literature.4! w# ]$ }8 B1 Y
Patient Report& y9 m2 u: v' [2 h
A 16-month-old white child was referred to the0 v9 K  c1 A. ^3 E$ F
endocrine clinic by his pediatrician with the concern
0 x* |$ f% g0 l# l3 x8 Kof early sexual development. His mother noticed
- ]5 k* w& k2 o4 klight colored pubic hair development when he was' n8 @% r$ ]  I- d0 B% `# p* R. w
From the 1Division of Pediatric Endocrinology, 2University of
- U3 V7 c7 g  W# T; GSouth Alabama Medical Center, Mobile, Alabama.
2 x8 b& [0 m, c: G  w7 |Address correspondence to: Samar K. Bhowmick, MD, FACE,& \1 }" v$ P# F7 s7 U+ I
Professor of Pediatrics, University of South Alabama, College of( i! E# z/ X% j' I2 y$ |
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
; H! X- b/ H2 L& J! k. i4 N5 k" we-mail: [email protected].1 o' I4 G  o$ V" m
about 6 to 7 months old, which progressively became
. D) W. N& I/ x4 qdarker. She was also concerned about the enlarge-
. |& M( m8 S: j# L( E1 Bment of his penis and frequent erections. The child8 D9 j; j) l; m& u
was the product of a full-term normal delivery, with
4 }" u" R5 [" ^0 w! r/ {/ k  xa birth weight of 7 lb 14 oz, and birth length of7 Q9 \! ^! b! S4 h& Z
20 inches. He was breast-fed throughout the first year6 ]0 S* C7 y4 E' `* [
of life and was still receiving breast milk along with3 G" ?" M, a( D, \, D. a* l" \
solid food. He had no hospitalizations or surgery,
+ \# H. D, C6 W6 W: Aand his psychosocial and psychomotor development
# s1 V" J6 g$ ~5 K7 d8 J. uwas age appropriate.
; W, N0 D0 `2 I: ]0 JThe family history was remarkable for the father,0 T7 X. t9 @; g9 m1 Q* Y
who was diagnosed with hypothyroidism at age 16,! L$ C3 m( S' o2 l3 ^3 l9 I# Z
which was treated with thyroxine. The father’s
: M$ N* s+ D; X7 T  e+ {: n" wheight was 6 feet, and he went through a somewhat2 T# `7 M- N( F  m* |
early puberty and had stopped growing by age 14.
7 {( V5 h/ F8 f! H6 E' g" tThe father denied taking any other medication. The( Z+ w1 V- i- q6 m4 r7 X
child’s mother was in good health. Her menarche
  z1 ?$ u8 s0 }3 kwas at 11 years of age, and her height was at 5 feet3 Q0 C# a( i% h
5 inches. There was no other family history of pre-
6 \3 d/ u: s4 s  S. bcocious sexual development in the first-degree rela-
5 I  D+ }$ y* [+ W, |8 |2 Mtives. There were no siblings.
( F" j% h; h3 z* J5 N, ?& qPhysical Examination: D: @3 l( G! Z$ ^* |
The physical examination revealed a very active,
$ J* c  Y2 h( H: `$ @. pplayful, and healthy boy. The vital signs documented! z$ r! p9 G9 ~. [5 }; v
a blood pressure of 85/50 mm Hg, his length was
( I9 ^! `2 w2 {' h& ?& [6 t( ^3 `90 cm (>97th percentile), and his weight was 14.4 kg) U* x  M" H: n% r7 D
(also >97th percentile). The observed yearly growth4 _* R! ~6 s0 n! T" u+ O, P- e
velocity was 30 cm (12 inches). The examination of5 l* c5 D) `) A, j9 A8 Z
the neck revealed no thyroid enlargement.) M+ K- E) B6 w  ?& k4 G0 o2 i& z
The genitourinary examination was remarkable for
; \/ p: c2 j! v1 |; d% P8 I! c8 b# ]enlargement of the penis, with a stretched length of- p5 _' F* n. `
8 cm and a width of 2 cm. The glans penis was very well
9 `7 c$ w( \4 ]  b8 O9 x% ydeveloped. The pubic hair was Tanner II, mostly around- Z  ?4 }0 Y0 U0 b% t( U
540
6 y, H, w1 O) G% J" Y" x7 cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* |% C+ X; I$ q5 s5 @% v2 Z( B" \
the base of the phallus and was dark and curled. The' [% U, F  V; c" T4 I/ ?
testicular volume was prepubertal at 2 mL each.; F7 ]* s! N+ {
The skin was moist and smooth and somewhat
1 e9 T  E+ }8 q% l, o- b* V$ Goily. No axillary hair was noted. There were no
. D$ t! }+ O$ ]abnormal skin pigmentations or café-au-lait spots.
- M- n; _. g1 z. ?Neurologic evaluation showed deep tendon reflex 2+' }, N/ D; l6 R& ~' N
bilateral and symmetrical. There was no suggestion
" ^! M3 I2 H) ~5 g, ~of papilledema./ H3 R( M6 j1 I
Laboratory Evaluation
7 X* f8 R3 c; b6 XThe bone age was consistent with 28 months by0 f+ v$ ~; T2 u/ r5 Y
using the standard of Greulich and Pyle at a chrono-; b" j" M. G" k7 p5 V
logic age of 16 months (advanced).5 Chromosomal; ]% A$ k' z1 S& |% M" T: x
karyotype was 46XY. The thyroid function test5 B% Y1 [2 G) }; e' P
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
5 |. ]2 k9 J/ o& Wlating hormone level was 1.3 µIU/mL (both normal).. `3 x! z0 t" k0 `: F3 e
The concentrations of serum electrolytes, blood
" E2 M9 C! @, N; i* `; j9 gurea nitrogen, creatinine, and calcium all were
1 V4 ]  V6 L) }* a: qwithin normal range for his age. The concentration
  B" F5 {9 e& I4 C7 }of serum 17-hydroxyprogesterone was 16 ng/dL3 @6 M' ?5 H( p5 R$ p: h4 Q7 q3 i
(normal, 3 to 90 ng/dL), androstenedione was 20
6 Y6 u/ y0 p) n& W; X0 Ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) {' S2 y% Z8 fterone was 38 ng/dL (normal, 50 to 760 ng/dL),; _$ F1 Y2 g4 a) g) N1 v" ^' F# S$ `
desoxycorticosterone was 4.3 ng/dL (normal, 7 to" O! ], s1 z) s$ _
49ng/dL), 11-desoxycortisol (specific compound S)5 J* j+ S: \- Y1 j9 \9 Z  c9 y
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: O. |4 I' r1 r0 j% v5 Q3 \- Ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
5 u1 r: n$ |) E! W. b* Ytestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
7 L' _' O( d2 i1 m2 fand β-human chorionic gonadotropin was less than
& v( n; [& {: a5 mIU/mL (normal <5 mIU/mL). Serum follicular; h! L9 I# ?# p3 F: J( |0 Q- F& {
stimulating hormone and leuteinizing hormone$ I) y' k* K! _* ?- G) @1 L7 M/ @8 c
concentrations were less than 0.05 mIU/mL; l" R$ m" {1 w2 H
(prepubertal).4 W1 y: X+ ]( N& a/ n3 R4 A
The parents were notified about the laboratory, d$ M( c# g- r; R0 t
results and were informed that all of the tests were
6 c) y4 f- _& o' b3 J8 g6 unormal except the testosterone level was high. The! A- h% N3 \8 F* \8 x
follow-up visit was arranged within a few weeks to
' l1 _" c9 a' ?4 g# ^1 J* N7 gobtain testicular and abdominal sonograms; how-$ w# s# A3 h4 v) W
ever, the family did not return for 4 months.
6 Q: D0 L4 E6 @" W8 X4 DPhysical examination at this time revealed that the0 L& m4 s( j, g. {
child had grown 2.5 cm in 4 months and had gained# ^8 b1 j1 ]: T( v
2 kg of weight. Physical examination remained
  E/ t8 G6 J9 b. Junchanged. Surprisingly, the pubic hair almost com-
* Y2 U; J: X' L1 B; tpletely disappeared except for a few vellous hairs at
# O6 _. q: Q3 T% `the base of the phallus. Testicular volume was still 2
, I5 [# @; e! b( e' |3 G0 t2 ~mL, and the size of the penis remained unchanged.+ l- F7 B& M# c$ S2 ~
The mother also said that the boy was no longer hav-
8 X  U/ _3 x3 \- u* w  D+ \; ?0 w" Ging frequent erections.
* Q" L' ]- h: m9 bBoth parents were again questioned about use of
5 M9 }+ ?* J% g2 U" M9 A' ~3 Dany ointment/creams that they may have applied to
. G4 F+ Z. f; f& j1 Dthe child’s skin. This time the father admitted the: C: M) Q7 k& s1 [* q% V
Topical Testosterone Exposure / Bhowmick et al 541  }0 C; b" r4 P9 a& {2 t+ C
use of testosterone gel twice daily that he was apply-
* t  F" f: F" v6 ying over his own shoulders, chest, and back area for
' J1 `% K0 I4 k+ A1 ~3 z7 qa year. The father also revealed he was embarrassed& v4 L" y( F& c, q3 n: u
to disclose that he was using a testosterone gel pre-
( N/ r4 d1 k9 Xscribed by his family physician for decreased libido
) x; g, A* E. l$ a  I3 S. r4 Nsecondary to depression.
4 L% ~. }, K0 u9 [( w$ y7 fThe child slept in the same bed with parents.
1 @- g- C2 b. M: S8 ^/ O7 G- QThe father would hug the baby and hold him on his
$ C1 Q2 X1 y) L9 m6 P) zchest for a considerable period of time, causing sig-3 g) m! X0 P3 W3 v" B
nificant bare skin contact between baby and father.
" {; B0 R! {; |" {6 N+ SThe father also admitted that after the phone call,
$ t! i( C' q% O( s+ V6 ]3 [when he learned the testosterone level in the baby2 {  A4 ]. \3 R8 `$ w2 e+ i
was high, he then read the product information0 M7 I& d  e3 Q2 t
packet and concluded that it was most likely the rea-
7 u5 @- @; `+ e3 d. }- l0 ison for the child’s virilization. At that time, they" {+ K6 X4 `' k6 D* V
decided to put the baby in a separate bed, and the
, y; B/ y. J- D: jfather was not hugging him with bare skin and had' v; F  r1 a6 p; O) w% ~" {
been using protective clothing. A repeat testosterone
- [+ G; E8 |: v1 ]! K7 v* P3 Etest was ordered, but the family did not go to the
$ l1 `4 U+ x! x4 P- Wlaboratory to obtain the test.
6 c6 C  m1 Z6 ^" v1 u9 U- o* mDiscussion( j9 D2 J' `1 j5 o
Precocious puberty in boys is defined as secondary
7 p+ S  d4 I: x$ k! m' ?! ~sexual development before 9 years of age.1,4& s# f% M5 C! d7 s$ M, x7 z
Precocious puberty is termed as central (true) when! E( B7 m+ I) g' b4 n  }& f
it is caused by the premature activation of hypo-9 D& O( P3 E2 _5 j3 k' t: f
thalamic pituitary gonadal axis. CPP is more com-
* N7 {! a% z6 emon in girls than in boys.1,3 Most boys with CPP
( f: @) f8 i; D1 y; E3 R9 E1 @" v% cmay have a central nervous system lesion that is
- A/ |' O( @8 U; oresponsible for the early activation of the hypothal-
- h' g9 ^6 u. V* |9 Z. R) j- mamic pituitary gonadal axis.1-3 Thus, greater empha-
( \. f/ a' k' |$ osis has been given to neuroradiologic imaging in
: r1 ?3 C: o4 ^' _# _( D  Iboys with precocious puberty. In addition to viril-
( J( V: \  U2 n0 u, iization, the clinical hallmark of CPP is the symmet-
) t( }/ {6 K8 Q! A, Qrical testicular growth secondary to stimulation by1 D$ K3 o: t# U) E. D# @. R, b1 U
gonadotropins.1,3
3 q' h4 C- N7 n/ V4 GGonadotropin-independent peripheral preco-7 \& T: H. a: P% X2 D
cious puberty in boys also results from inappropriate0 K- j, k$ f' q" [- d% C
androgenic stimulation from either endogenous or
! f8 G1 N$ ?2 F& Sexogenous sources, nonpituitary gonadotropin stim-) p7 `0 q9 |5 w+ e' b" R) Q3 O
ulation, and rare activating mutations.3 Virilizing
4 r& n/ C; r; tcongenital adrenal hyperplasia producing excessive( q2 C! N* f) V: d3 B
adrenal androgens is a common cause of precocious) V5 h4 E$ m3 c4 u# q; h7 h1 d
puberty in boys.3,4$ S& g* R/ q* K2 J6 C5 @9 m
The most common form of congenital adrenal
( O: Z5 I/ s# _- ehyperplasia is the 21-hydroxylase enzyme deficiency.1 X( L/ K4 ^; A0 L
The 11-β hydroxylase deficiency may also result in
% a& t, j2 ^0 M9 S$ u! `excessive adrenal androgen production, and rarely,2 k! K& Y9 ~* n8 h0 c! m% y! k
an adrenal tumor may also cause adrenal androgen, ~$ H  K; Z: f7 {5 C* o( W& u; R
excess.1,3
# H7 H8 f, g9 i6 Nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" M  D3 c/ y7 r0 R7 g0 U7 P# ~
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* m9 M6 O; `5 |) V) `" c
A unique entity of male-limited gonadotropin-
$ \% n4 U3 B/ V6 I& i, J3 hindependent precocious puberty, which is also known
1 i, ?2 U$ [9 Q1 B6 B$ a* E" uas testotoxicosis, may cause precocious puberty at a
! |, a" J3 O0 J. Y" Vvery young age. The physical findings in these boys
/ I* H' N! y) ^) R& kwith this disorder are full pubertal development,
3 M/ H# ?! R: E+ Y" v# C7 gincluding bilateral testicular growth, similar to boys
9 Z' m% C- U! y/ n5 ?* P2 K2 p6 K6 u% Pwith CPP. The gonadotropin levels in this disorder& t- x0 P7 N/ X3 a1 E3 {2 `
are suppressed to prepubertal levels and do not show8 @* W# {9 L: P) R) P: ~
pubertal response of gonadotropin after gonadotropin-
, L1 o/ \8 f1 sreleasing hormone stimulation. This is a sex-linked; }! x, Z; m: K5 Z
autosomal dominant disorder that affects only
, L, h( |9 k1 e2 Tmales; therefore, other male members of the family
# a; V8 \5 x5 M6 H7 s+ y' K5 p$ `( Wmay have similar precocious puberty.3, k8 Q3 s5 u$ U/ G8 Z
In our patient, physical examination was incon-: N( f- ?, k8 i
sistent with true precocious puberty since his testi-
( `6 X9 c/ ~9 i9 A& o* {cles were prepubertal in size. However, testotoxicosis
: W' j, X, A' p+ H/ r$ Iwas in the differential diagnosis because his father
4 A/ Z: |3 k. H. {% Qstarted puberty somewhat early, and occasionally,7 t3 j/ l- B* p5 t7 c+ B* Q
testicular enlargement is not that evident in the
, E7 ]  k) Z; r% f4 D( `' ubeginning of this process.1 In the absence of a neg-
6 s, k2 g6 u0 c2 Oative initial history of androgen exposure, our1 d% Y7 K1 [! n% ^
biggest concern was virilizing adrenal hyperplasia,+ ?- D! ^- h. ]- f
either 21-hydroxylase deficiency or 11-β hydroxylase2 l5 o" |: h. r
deficiency. Those diagnoses were excluded by find-8 F- Z+ P  v- c$ ?5 ~
ing the normal level of adrenal steroids.5 k' s% g9 Y2 U* P! s: h. ?
The diagnosis of exogenous androgens was strongly
" K, [; y+ |$ ?: R, S3 p- wsuspected in a follow-up visit after 4 months because/ O" R; b$ y& V* x0 M( T
the physical examination revealed the complete disap-
! ~! s2 d  r6 s. ~/ I6 Qpearance of pubic hair, normal growth velocity, and
; W7 q- J8 N! {0 U3 z6 ]: ]decreased erections. The father admitted using a testos-; c4 j- j3 r0 g) f. q8 w9 V
terone gel, which he concealed at first visit. He was( R: o' n8 Y& ?
using it rather frequently, twice a day. The Physicians’
3 U% x, ], S0 W3 a8 Q4 E/ FDesk Reference, or package insert of this product, gel or3 U0 L, t/ ]7 P4 ]3 ~3 X
cream, cautions about dermal testosterone transfer to3 u- E% p3 P2 ^8 D
unprotected females through direct skin exposure.
3 K4 ?4 K- U% e7 T5 Q% tSerum testosterone level was found to be 2 times the
# |9 E2 P5 H  P, e9 J5 Fbaseline value in those females who were exposed to9 y1 }0 C2 Y  Z* }
even 15 minutes of direct skin contact with their male
7 i! ?) B- d5 }+ U. U% r4 Lpartners.6 However, when a shirt covered the applica-5 {5 \' H6 C3 R
tion site, this testosterone transfer was prevented.
- L  D/ p. s4 C# g3 h/ I( P2 wOur patient’s testosterone level was 60 ng/mL,
1 w: W4 D$ ~- a# Y. ]which was clearly high. Some studies suggest that
$ l. J; J2 r' r1 H2 X$ Jdermal conversion of testosterone to dihydrotestos-
' W5 {8 D+ V: i' y7 Jterone, which is a more potent metabolite, is more
5 i- W5 _6 H" s; F* tactive in young children exposed to testosterone
3 H: }$ Q" G- }7 P4 s: Eexogenously7; however, we did not measure a dihy-
4 p+ i% t/ X; Z3 m, ^$ @drotestosterone level in our patient. In addition to
6 ~9 Q: H! f8 [" V, Q' U1 O9 m. C1 Mvirilization, exposure to exogenous testosterone in
9 }* y, x7 J5 h/ zchildren results in an increase in growth velocity and
9 D* q" i* [+ O/ Uadvanced bone age, as seen in our patient.9 k5 J4 }/ Y  N
The long-term effect of androgen exposure during
' a$ G; k0 n9 P& D2 g! vearly childhood on pubertal development and final
: M: \7 l2 y4 P5 ?* z4 ?adult height are not fully known and always remain
- {) U$ Z, N4 r3 D! ]3 Xa concern. Children treated with short-term testos-) G) t# [% }# i
terone injection or topical androgen may exhibit some/ ~' }  i. m, I/ u( I5 o8 v3 h
acceleration of the skeletal maturation; however, after
6 ]# t% q% A/ }( y' [! J7 j/ [' |cessation of treatment, the rate of bone maturation/ D# G6 |# W6 o
decelerates and gradually returns to normal.8,9( O/ |* C. P' _4 t4 P
There are conflicting reports and controversy1 ^. Z- @, k, I# e" l
over the effect of early androgen exposure on adult
) X  F9 o. y* Ypenile length.10,11 Some reports suggest subnormal1 P+ {8 A6 s/ M3 `' ~2 X
adult penile length, apparently because of downreg-
% o  C9 m8 m- Hulation of androgen receptor number.10,12 However," r7 a# T2 c# Y: s; W$ d- D5 l
Sutherland et al13 did not find a correlation between$ O0 u# h0 k- G5 ]" c
childhood testosterone exposure and reduced adult/ a9 n4 S) |4 ~% U8 [- f1 P' k. K( i
penile length in clinical studies.
0 Q: t* j6 i. r; }4 ^; VNonetheless, we do not believe our patient is" K! u0 f$ r' m
going to experience any of the untoward effects from
2 V" g2 p1 L: ]: [. ?: Q( L& x  \testosterone exposure as mentioned earlier because
, `- S6 g9 ]! f' S. }the exposure was not for a prolonged period of time.
$ N( \5 M1 N6 T: Y- D7 K% U# BAlthough the bone age was advanced at the time of
! Q: Q( w$ s8 Z( P, b, [diagnosis, the child had a normal growth velocity at7 {2 ~% ^1 W& }
the follow-up visit. It is hoped that his final adult! Y& ~' B9 d" b; f3 r+ n. b
height will not be affected.
9 h/ E+ N9 J! `' m  Z. aAlthough rarely reported, the widespread avail-
0 R  M9 B' A( `& [/ {. s. Pability of androgen products in our society may: M& @! ]0 ?4 n( g  ^
indeed cause more virilization in male or female* p' ]" z, n. `! H1 s4 j
children than one would realize. Exposure to andro-) T; t" c) k: H2 j, M0 o
gen products must be considered and specific ques-
$ \' D: J; }4 I; w" J9 vtioning about the use of a testosterone product or
" E4 r1 m% }9 w! t  u" y( Qgel should be asked of the family members during3 N& \& L# `" i' }
the evaluation of any children who present with vir-
. `9 M7 r" Y0 U% w" N! R# ^ilization or peripheral precocious puberty. The diag-0 F+ T0 T" L0 z9 I
nosis can be established by just a few tests and by, Z1 U7 z+ V$ P/ \+ D
appropriate history. The inability to obtain such a. \0 y* V, H! t/ V3 V" h
history, or failure to ask the specific questions, may
# L/ q0 e0 j% ?% Y9 M) Sresult in extensive, unnecessary, and expensive, N- y2 @$ D$ v5 Y/ }7 v$ Y+ f5 q5 Q
investigation. The primary care physician should be" q& `* F0 k. i/ h# _2 e2 m( g7 r; E
aware of this fact, because most of these children
) a" ^3 I, z- S, O/ Fmay initially present in their practice. The Physicians’
8 q. Q* ~) c7 N# DDesk Reference and package insert should also put a
& V# g, @( a$ B/ x4 Swarning about the virilizing effect on a male or
, D/ c; P0 ?$ V" r9 Y0 Q  t/ ^female child who might come in contact with some-' a) n* A3 V/ u( x
one using any of these products.% ~& f' x% P# t( h6 W/ `6 W9 j6 A
References  B$ F# R2 i* Q$ h( i* F
1. Styne DM. The testes: disorder of sexual differentiation2 ?/ f0 k$ W0 M& ~( o% [0 H+ {
and puberty in the male. In: Sperling MA, ed. Pediatric
4 i9 a$ n/ O1 p& V, H* s1 q5 [Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* D& ^/ o8 @; G
2002: 565-628.+ C* Q5 h: _5 D- `. Z& X
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
' c4 C$ r8 Y" T( T1 P* rpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
8 J1 a# ~, [+ X3 U, ~, lBoy Induced by Indirect Topical
# [; G" J4 B4 s& wExposure to Testosterone
4 f, P) O' g% O4 k6 `$ D5 Z$ |; n+ i  kSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' {  g7 a5 H5 Gand Kenneth R. Rettig, MD16 L+ T3 ^3 [: L, S! p9 P
Clinical Pediatrics) p1 P0 L0 X; [$ [! P! I) N7 z( P
Volume 46 Number 6
3 o5 p3 L, a/ n: `July 2007 540-543
) l' Q" `3 [  T7 o© 2007 Sage Publications
2 B/ C- y/ w) x: f10.1177/00099228062966512 m, }9 }9 }/ l  B4 {
http://clp.sagepub.com0 [6 p! A  E) ]. ^( b5 Q: X2 c8 i7 F
hosted at
1 w7 E! D0 n, Hhttp://online.sagepub.com
: B" r- f, G& v. s& z" Y5 {Precocious puberty in boys, central or peripheral,, P7 B. _- X, H# L& A% H. P
is a significant concern for physicians. Central
/ t& o/ v) _  v$ A  Q1 Y" yprecocious puberty (CPP), which is mediated1 k! [1 G7 H" A  N
through the hypothalamic pituitary gonadal axis, has7 l# N4 r# F( ^2 G' b  T3 `
a higher incidence of organic central nervous system
% z4 O7 t+ K# R3 y$ flesions in boys.1,2 Virilization in boys, as manifested
% g$ T9 q0 U, U2 d# l( Y5 hby enlargement of the penis, development of pubic* D5 f# w. V# e- \% Z. y! z
hair, and facial acne without enlargement of testi-% J/ p$ Z+ K! p3 I
cles, suggests peripheral or pseudopuberty.1-3 We( l9 H/ b* E) b. c* r
report a 16-month-old boy who presented with the. P  p9 t4 z5 X: D* O7 S; _9 {
enlargement of the phallus and pubic hair develop-
3 p: ]) I$ V' M" a+ m$ nment without testicular enlargement, which was due: Z/ |8 N: f7 ^4 x% q
to the unintentional exposure to androgen gel used by
5 M9 a4 K9 ^: R; x% f9 K4 {the father. The family initially concealed this infor-
6 G+ n3 }# V2 U; T0 `. D0 j' L1 b) fmation, resulting in an extensive work-up for this( @& r) m( Y5 k( M$ _7 E7 m/ R( O
child. Given the widespread and easy availability of
+ J7 M1 J) A- Z9 \5 otestosterone gel and cream, we believe this is proba-! C5 D5 z7 y5 J/ {. r% A6 P. d
bly more common than the rare case report in the+ h  O/ _9 H8 j+ s" r* g
literature.4
9 s' n2 w0 h9 t( v: \& V, |; SPatient Report
$ O6 Q( H8 c% D$ C) fA 16-month-old white child was referred to the8 @, `$ i8 h# x! B$ _
endocrine clinic by his pediatrician with the concern
' ]9 [' V  C* ^; \+ wof early sexual development. His mother noticed
2 p- f' T" D4 \* R7 ~& d  jlight colored pubic hair development when he was7 R4 N; G( l) w: k9 v
From the 1Division of Pediatric Endocrinology, 2University of7 V0 N/ d) ]; W7 b1 Z
South Alabama Medical Center, Mobile, Alabama.4 V2 F# e$ x5 l; g+ k( b
Address correspondence to: Samar K. Bhowmick, MD, FACE,
3 f: b# h# B- k+ HProfessor of Pediatrics, University of South Alabama, College of/ o( h% A& K* j' r& w; G! d% E
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ e; C: r$ q" a( j1 y& ee-mail: [email protected].' p! @; M5 r/ O4 N9 x
about 6 to 7 months old, which progressively became8 P: B0 |' q) B
darker. She was also concerned about the enlarge-
4 y' }' f7 @& E0 vment of his penis and frequent erections. The child  v) N" M0 _, ?+ S
was the product of a full-term normal delivery, with
" A) U8 P  X, M/ }! Y' L; oa birth weight of 7 lb 14 oz, and birth length of: [* {" P6 U' g9 @
20 inches. He was breast-fed throughout the first year3 U$ e8 L, h, ^# }. {% Q+ _# k
of life and was still receiving breast milk along with
3 N3 O3 T8 W, p- H/ ^solid food. He had no hospitalizations or surgery,' I+ d/ F/ U! \" l; M, a
and his psychosocial and psychomotor development
: ?! R5 `) O3 b# Jwas age appropriate.
# l, |1 Z. W4 B) A, \) W* m( gThe family history was remarkable for the father,
; R9 f' U, [* O# S. u. ~2 \2 `/ D* zwho was diagnosed with hypothyroidism at age 16,
& _: |% E5 g& K. \; r6 \5 dwhich was treated with thyroxine. The father’s
' L7 X$ R2 Y3 yheight was 6 feet, and he went through a somewhat. [* I) Y+ d; g) s; @% ?2 L* F; C
early puberty and had stopped growing by age 14.
0 X( Q" G- B- _& q- M/ c9 ZThe father denied taking any other medication. The+ a3 i% m' ]  x+ `3 x, J
child’s mother was in good health. Her menarche
9 m/ E: O& o4 \6 ]0 uwas at 11 years of age, and her height was at 5 feet
3 Y0 h: v. q9 ?; V3 @7 z5 inches. There was no other family history of pre-
; x" q% c* ?  ^0 ucocious sexual development in the first-degree rela-
' g! ?5 D9 s2 y1 W3 ntives. There were no siblings.
' ?5 _4 e$ ^5 _) W! R1 z& A9 |& pPhysical Examination7 I: F3 b% t- e6 T1 {# |0 n
The physical examination revealed a very active,& K+ f/ X+ J, U( t
playful, and healthy boy. The vital signs documented: l6 n6 u$ T2 |3 k4 q9 a$ h
a blood pressure of 85/50 mm Hg, his length was7 G' g, Z8 g# M
90 cm (>97th percentile), and his weight was 14.4 kg
& R% W9 [9 H+ j% a(also >97th percentile). The observed yearly growth, D. E5 s3 Z, d  T
velocity was 30 cm (12 inches). The examination of
( [% q1 f5 B2 C8 l) Y" W! m% Xthe neck revealed no thyroid enlargement.4 E4 e$ k" W8 J0 r* D# ]
The genitourinary examination was remarkable for
9 r! O. I. h( ~enlargement of the penis, with a stretched length of6 C) \  j! O3 C6 t) s8 H
8 cm and a width of 2 cm. The glans penis was very well
! ~# J0 b3 D/ v& y* L/ Xdeveloped. The pubic hair was Tanner II, mostly around2 ^. e9 C# [" q
540
6 S1 p& Y! b# {. n4 Yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 c: U' L4 h0 y7 m  U
the base of the phallus and was dark and curled. The6 ?! P, H8 f! g! j% M
testicular volume was prepubertal at 2 mL each.
+ b, q+ M6 D2 |1 uThe skin was moist and smooth and somewhat' o1 v% z0 L5 a
oily. No axillary hair was noted. There were no& V. }9 p' f9 T
abnormal skin pigmentations or café-au-lait spots.
5 Z4 G* I! v! y8 VNeurologic evaluation showed deep tendon reflex 2+! H8 A  M! S- f! I* l$ X# x8 [
bilateral and symmetrical. There was no suggestion; b: [' d5 v8 v6 ?0 c' J
of papilledema.
# i7 @) ?/ k. u3 q4 v0 t- DLaboratory Evaluation4 x& o/ Z: u+ R% S
The bone age was consistent with 28 months by, u/ H$ b, ^; i$ X. k8 r, v2 A
using the standard of Greulich and Pyle at a chrono-1 K& Z. M- n7 w. [
logic age of 16 months (advanced).5 Chromosomal: r) D3 R1 l+ m
karyotype was 46XY. The thyroid function test
# B- u7 s0 \/ x7 \7 H% q. }showed a free T4 of 1.69 ng/dL, and thyroid stimu-% {5 c( y9 W3 C5 x
lating hormone level was 1.3 µIU/mL (both normal).0 W, P" x2 u: ^( `4 w
The concentrations of serum electrolytes, blood
! v7 d2 A% r' Ourea nitrogen, creatinine, and calcium all were* C* T4 x% l, Z
within normal range for his age. The concentration8 \* H- Z' Y0 n: I
of serum 17-hydroxyprogesterone was 16 ng/dL
) n( F& J: E2 {% K7 F9 E% [(normal, 3 to 90 ng/dL), androstenedione was 20
) d# Y* L4 Q+ o7 [; I; }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( [/ q7 E& d2 |/ F+ @0 N
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
% ?5 k8 D% k4 H5 }desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 T% x8 R0 c1 ?& l
49ng/dL), 11-desoxycortisol (specific compound S)9 p0 Z$ _( n$ E$ r( ^4 O* [! t( @4 T( e
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' H3 I: U+ x  H7 `1 R" T# Utisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 G: @9 i  P( I6 n
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),7 h) s5 y6 g( O. R. E  ]
and β-human chorionic gonadotropin was less than: C0 c4 ]8 C9 Z" _, J9 v
5 mIU/mL (normal <5 mIU/mL). Serum follicular: }& \% R. \0 [8 @9 n
stimulating hormone and leuteinizing hormone0 I/ Q4 u" o; V1 ?! P/ @
concentrations were less than 0.05 mIU/mL/ G! @" Z+ o/ Q" l2 L2 f. h
(prepubertal).
  K& B7 K5 r& a1 x; \2 {! |6 cThe parents were notified about the laboratory
" o1 e: A' F6 w' M- _0 p4 }results and were informed that all of the tests were9 F8 d6 j( [) t8 m; H- K
normal except the testosterone level was high. The
+ R+ k2 t' r/ X. Q) d* Bfollow-up visit was arranged within a few weeks to4 h: Z& e: \( V3 a7 l
obtain testicular and abdominal sonograms; how-- [; i, o% f$ k! J* H, D
ever, the family did not return for 4 months.
4 Z/ f+ E5 u) |( UPhysical examination at this time revealed that the
0 n  X+ B1 Q# pchild had grown 2.5 cm in 4 months and had gained
4 I' N* |1 J5 p. r) c4 u" F2 kg of weight. Physical examination remained, ^" N3 r- v* l2 E8 t
unchanged. Surprisingly, the pubic hair almost com-0 \5 c$ k3 T0 S' d/ ?
pletely disappeared except for a few vellous hairs at
) M& e" f, q; p7 c" H4 Nthe base of the phallus. Testicular volume was still 2
/ P2 d7 r: k7 b) f8 H" c" ^) e) emL, and the size of the penis remained unchanged.
- W8 M3 n% r( j8 `4 XThe mother also said that the boy was no longer hav-6 D7 o" C% d% c! Q9 f( `( y
ing frequent erections.
+ O7 R, [  }" g( ]" F- GBoth parents were again questioned about use of5 D3 y/ G; M4 t. @) J
any ointment/creams that they may have applied to7 d7 j: P7 i+ Q6 l$ u1 K+ q
the child’s skin. This time the father admitted the# H  @- i4 c, z( E
Topical Testosterone Exposure / Bhowmick et al 541
2 r* B4 ]0 i5 G8 e) w1 i/ puse of testosterone gel twice daily that he was apply-
; x6 X0 S# r& G  f) ^2 L1 A# }ing over his own shoulders, chest, and back area for
* Z& H. j, v3 s: ea year. The father also revealed he was embarrassed
8 I7 U. z7 h( ~1 f: Rto disclose that he was using a testosterone gel pre-
% r3 X1 g0 n* ~% k: ]) H% U; wscribed by his family physician for decreased libido2 {1 H# q% I# y
secondary to depression.
! P- O: S  G$ |! t3 I8 L9 z9 x$ NThe child slept in the same bed with parents.
  p  a+ [) A. }: D3 `The father would hug the baby and hold him on his
  u( ^, g! |7 h; n. k1 B+ }chest for a considerable period of time, causing sig-
; d: s# C. w7 K& D5 N" d  {7 Cnificant bare skin contact between baby and father.
& e, _5 c6 Q; ?8 kThe father also admitted that after the phone call,
7 w4 v7 G: A/ lwhen he learned the testosterone level in the baby" ?7 h- T+ W# [0 G
was high, he then read the product information
( n: A5 N9 e) T# L5 Apacket and concluded that it was most likely the rea-
+ N& C$ h$ c5 F3 ]4 `* Json for the child’s virilization. At that time, they
) N5 s! A+ Z( l9 e0 t$ g0 Tdecided to put the baby in a separate bed, and the
$ |3 a+ B) D1 S5 X" Q( k2 h* yfather was not hugging him with bare skin and had
+ |7 J4 y6 a# a1 ~2 kbeen using protective clothing. A repeat testosterone
2 i( [% F) s  Q0 Stest was ordered, but the family did not go to the9 f5 J4 S6 S5 {! t" u
laboratory to obtain the test.
) B$ j) O" u' `4 cDiscussion- F" }1 e; I" u; V
Precocious puberty in boys is defined as secondary
( d( u# K3 V9 u1 b- p3 _sexual development before 9 years of age.1,4# b! J# k( [7 [8 W/ S3 o" Q
Precocious puberty is termed as central (true) when
3 _" m% s4 g( }; p; h0 Pit is caused by the premature activation of hypo-
4 \% X! B/ k. _: S$ J& ]6 ]thalamic pituitary gonadal axis. CPP is more com-) {, b+ R* w2 N
mon in girls than in boys.1,3 Most boys with CPP
  N: t! z4 \! b! I8 R0 Vmay have a central nervous system lesion that is1 C% j. u' }1 C6 _0 C2 ~4 o
responsible for the early activation of the hypothal-; O1 j2 d" _. C  |) r2 X
amic pituitary gonadal axis.1-3 Thus, greater empha-4 Y! P2 [' m( `( u2 s/ |) M
sis has been given to neuroradiologic imaging in
+ }# X) ?' Y. d* |boys with precocious puberty. In addition to viril-
# f- A% n( z1 n" x1 nization, the clinical hallmark of CPP is the symmet-
3 r$ u. o% P; I( A6 p* q2 Arical testicular growth secondary to stimulation by
+ b. f, r" i0 U, J  z8 Q1 k* W2 bgonadotropins.1,3+ f! u6 i! I% s8 @" M
Gonadotropin-independent peripheral preco-- B. x; d8 N2 G2 c. e% F; M8 h
cious puberty in boys also results from inappropriate% \- J- |. F/ r
androgenic stimulation from either endogenous or
2 ?/ H3 T( J# Q) O" T) Pexogenous sources, nonpituitary gonadotropin stim-
2 O- x! r9 G0 G# r: H* vulation, and rare activating mutations.3 Virilizing
; w' {. G2 x( l3 \+ ]: F+ i7 @( hcongenital adrenal hyperplasia producing excessive
  X! }5 I- [9 |/ Y, Wadrenal androgens is a common cause of precocious0 W8 N! d! [3 f" A9 P
puberty in boys.3,4
6 W/ @. m! u1 |The most common form of congenital adrenal
6 M. E4 ]* d. q# s) Ehyperplasia is the 21-hydroxylase enzyme deficiency.
: M5 e3 {1 d1 zThe 11-β hydroxylase deficiency may also result in1 D8 x6 h$ j& u" R. S% R
excessive adrenal androgen production, and rarely,2 X3 V9 `6 q, b! V
an adrenal tumor may also cause adrenal androgen9 X4 k5 t( u: a1 b3 Q# S
excess.1,3
8 N" i2 c9 D6 W' C( r" Aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. R" u! y0 U5 C
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
; c; o6 o# Q4 q) j- CA unique entity of male-limited gonadotropin-7 P! l' z" N2 o7 j9 N
independent precocious puberty, which is also known
( f, D. H3 V* q* X) E3 z! cas testotoxicosis, may cause precocious puberty at a
' S& I0 Q, {. F* Y! t# ?9 e7 qvery young age. The physical findings in these boys+ {) K1 `* \* Y9 L( G
with this disorder are full pubertal development,
8 a# y/ A. Y. F  t5 T% J$ b. Gincluding bilateral testicular growth, similar to boys
0 X  B! S6 l/ t8 ]% d& |* bwith CPP. The gonadotropin levels in this disorder6 ~& T5 K8 Q5 Y! D
are suppressed to prepubertal levels and do not show( U9 }" \& r6 n4 w2 o: m; M
pubertal response of gonadotropin after gonadotropin-! A9 j$ q7 Z0 @0 Z6 K
releasing hormone stimulation. This is a sex-linked
+ k7 @* O8 ?8 \; z* ]) Y) |+ uautosomal dominant disorder that affects only. r' u$ Z: F9 D. F$ U* u
males; therefore, other male members of the family
, z' `. M! L8 J2 x: ~  _% f) K1 Zmay have similar precocious puberty.3: q( f! m8 _" G. h
In our patient, physical examination was incon-1 _) r* P& G, O# O$ o! r
sistent with true precocious puberty since his testi-. Z2 w. D( I7 w  c" J1 a# H3 V
cles were prepubertal in size. However, testotoxicosis( P7 A6 }# M: H! G
was in the differential diagnosis because his father  F1 s9 U' T0 O) \& e6 n- u
started puberty somewhat early, and occasionally,
7 e0 P# z( ]5 J. ^/ itesticular enlargement is not that evident in the
9 V6 R# [! J) D' s" ibeginning of this process.1 In the absence of a neg-5 w5 G2 G2 I% X+ Y  D5 D4 `* j
ative initial history of androgen exposure, our
" I3 {  w% U/ f  a5 |& g0 t7 z) Xbiggest concern was virilizing adrenal hyperplasia,
4 l/ S- @9 `! x3 x4 W" Ieither 21-hydroxylase deficiency or 11-β hydroxylase
7 D+ g  M) c) D. E; edeficiency. Those diagnoses were excluded by find-
1 t7 l  [$ }( T" oing the normal level of adrenal steroids.* H0 H1 c# R6 l# J9 ~
The diagnosis of exogenous androgens was strongly
7 K& o+ [8 q+ c8 k4 m6 R( T. {suspected in a follow-up visit after 4 months because& `  i- R' I/ S
the physical examination revealed the complete disap-6 R4 I' Q( F: @+ G( ]: `: Q6 C
pearance of pubic hair, normal growth velocity, and0 d/ |/ D5 f+ V
decreased erections. The father admitted using a testos-" H% ~4 O! }6 B7 y
terone gel, which he concealed at first visit. He was
5 ~5 U1 `$ @( T! R' tusing it rather frequently, twice a day. The Physicians’! }' b. e4 Q& T  k5 q. L* p
Desk Reference, or package insert of this product, gel or+ ^% ], T; c/ R
cream, cautions about dermal testosterone transfer to0 k: w# O: A8 }. z: Q1 m9 v
unprotected females through direct skin exposure.1 j& ?# Y5 W8 h* C  h1 u' L5 [
Serum testosterone level was found to be 2 times the
! I: i0 I, d  L' _' |' xbaseline value in those females who were exposed to6 f0 x( p! ?. U$ {' g
even 15 minutes of direct skin contact with their male
5 \! Y* z" N4 Q! s  jpartners.6 However, when a shirt covered the applica-% i, C. o" y5 j! I6 E# h3 W
tion site, this testosterone transfer was prevented.
. g# m% A. e/ s. t8 Y, H! ~4 @Our patient’s testosterone level was 60 ng/mL,
! Y) t4 H- n2 E+ d" b( [2 d& twhich was clearly high. Some studies suggest that
$ E+ s  C: u4 o8 r3 T7 [dermal conversion of testosterone to dihydrotestos-1 i) q2 I5 Y% Y' q
terone, which is a more potent metabolite, is more
! e0 P% }! N9 C! eactive in young children exposed to testosterone5 E! x) c8 O! }
exogenously7; however, we did not measure a dihy-, Q9 }; B; p) f
drotestosterone level in our patient. In addition to
( I" r3 |9 W0 A3 |- W/ @virilization, exposure to exogenous testosterone in
( y) y7 v' N+ J( U7 U7 L* vchildren results in an increase in growth velocity and# X8 k; j1 Z; M# ^" R) U! M
advanced bone age, as seen in our patient.# E9 t2 a, w0 `2 }' R
The long-term effect of androgen exposure during# g# I; I* L- Z/ n. {5 W! H
early childhood on pubertal development and final5 P% ]8 v( {+ g9 S0 q: {
adult height are not fully known and always remain* I5 a% G/ b& E9 J! \1 p) {
a concern. Children treated with short-term testos-
# J7 i* z  A7 K1 D, ^- Y* @terone injection or topical androgen may exhibit some5 I' y" A: c3 t
acceleration of the skeletal maturation; however, after& G+ |7 o4 D: p7 n! y
cessation of treatment, the rate of bone maturation2 d, t: k1 t! A3 D7 l* H# S; z
decelerates and gradually returns to normal.8,9
3 n2 Y- e* e7 kThere are conflicting reports and controversy2 K* u# i% K  y/ }+ u4 _) W
over the effect of early androgen exposure on adult, R% O+ g/ C8 h' A, D
penile length.10,11 Some reports suggest subnormal
( ?% T6 b" m5 G+ N+ R. yadult penile length, apparently because of downreg-
( O. M5 ]9 G5 h  Hulation of androgen receptor number.10,12 However,
& h+ C3 A% g  K1 K& l, uSutherland et al13 did not find a correlation between# Q% D/ w2 @3 G. j
childhood testosterone exposure and reduced adult: u! D# \- j1 ~- Q
penile length in clinical studies.
+ G, u+ _' P# x! D/ A6 e4 vNonetheless, we do not believe our patient is5 G3 v% Y9 E8 g5 e- `
going to experience any of the untoward effects from% U. U# Z: u- k, i, h
testosterone exposure as mentioned earlier because
8 c# v$ E! {/ j, hthe exposure was not for a prolonged period of time.
+ m& E9 u3 |* t8 @Although the bone age was advanced at the time of
- p" B# m9 ^9 ?9 m0 sdiagnosis, the child had a normal growth velocity at+ [: W7 n* z% P- t
the follow-up visit. It is hoped that his final adult4 k+ n% c- q, [( k0 i/ `
height will not be affected.8 g. X' S( u( V7 {% U
Although rarely reported, the widespread avail-) G9 @$ F$ e) z" C
ability of androgen products in our society may( y/ `- Z9 I) j) s) C8 k0 z
indeed cause more virilization in male or female
  E2 u' G0 x8 j6 h& ichildren than one would realize. Exposure to andro-% f+ [6 L7 F+ ~2 z7 C
gen products must be considered and specific ques-
1 v4 S  D/ K( O; _- I5 k2 b0 ^tioning about the use of a testosterone product or# y; h* L" G1 G" \) l
gel should be asked of the family members during3 y3 S; P7 R' Z  ]9 m9 R
the evaluation of any children who present with vir-$ I' z1 x$ l% [& K
ilization or peripheral precocious puberty. The diag-
& H$ R3 u9 [1 Bnosis can be established by just a few tests and by
" R9 V: _5 G7 d* W% p; b8 |7 Happropriate history. The inability to obtain such a
$ D: G/ F9 [8 j% a) m* Y* xhistory, or failure to ask the specific questions, may2 {( ]& k/ N1 |4 R$ N7 o$ v
result in extensive, unnecessary, and expensive
" h1 @& M% L4 F, ^" Vinvestigation. The primary care physician should be
" ?8 q  n4 C- k1 F% Aaware of this fact, because most of these children( L3 y! J6 n6 H# f' x1 @
may initially present in their practice. The Physicians’
8 G. ^1 u& B! S8 P9 ADesk Reference and package insert should also put a. z$ E1 m- N) K* ~0 u6 U
warning about the virilizing effect on a male or- C( V( G9 _! L- P; z% ~4 A
female child who might come in contact with some-
9 Z5 i# \: e* \" N9 [) q% ^2 ^one using any of these products.
, q2 J% o# d: I$ c; s' sReferences
7 V4 n6 z3 x8 u5 D1. Styne DM. The testes: disorder of sexual differentiation
7 Q/ M: @4 S4 Qand puberty in the male. In: Sperling MA, ed. Pediatric
8 a" ^" B1 y2 J* rEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( Z, X$ f. H- T! g$ @4 Q2002: 565-628." z6 n+ S( @& ^& z/ ^/ b) v
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
5 }0 D5 m8 F  ^! m8 d; M. U5 Q# xpuberty in children with tumours of the suprasellar pineal
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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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加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
2 n8 q% q7 a5 [! |
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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