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Sexual Precocity in a 16-Month-Old
1 e$ s) N6 R6 R# pBoy Induced by Indirect Topical
6 E. z4 V: e& q' L  l% _6 gExposure to Testosterone
$ D+ t9 M, u1 q) ]  y6 d. r! T0 wSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ f& F7 Z1 Y) X
and Kenneth R. Rettig, MD1
- q( L5 x* c( J4 {( |: iClinical Pediatrics
; g& r) X' n% s: q2 Q: cVolume 46 Number 6/ Z4 w: B- Q7 C+ G/ x3 K3 d
July 2007 540-543
! \6 t5 A( f  k: P0 P$ o© 2007 Sage Publications
$ `8 }/ ~7 D8 H/ m9 i  ?9 k( z10.1177/0009922806296651
8 m$ t/ V) A8 O1 e3 ahttp://clp.sagepub.com
; N, V6 X6 O( h2 `5 Z7 n! [hosted at
. [! Y7 ?5 d! `5 n* xhttp://online.sagepub.com8 c( e8 U8 X) x8 g( `4 v' A) G
Precocious puberty in boys, central or peripheral,
( W( h2 r, _+ pis a significant concern for physicians. Central
) r( R; I1 ]$ b* V* _' cprecocious puberty (CPP), which is mediated7 \+ x- x/ K  \* p& u5 b" L
through the hypothalamic pituitary gonadal axis, has
% K: e! p' \7 G  t9 da higher incidence of organic central nervous system
5 _3 M8 P% y; f7 f. Q7 {$ |- xlesions in boys.1,2 Virilization in boys, as manifested/ z% B( R& u/ S# q3 n
by enlargement of the penis, development of pubic, g; I& y$ \% i1 ?! P% i. R; C3 Q, R
hair, and facial acne without enlargement of testi-2 Y, g) X" z5 |6 I/ V  i0 I  o" ]
cles, suggests peripheral or pseudopuberty.1-3 We
% v5 i+ R* \6 w& k( T( yreport a 16-month-old boy who presented with the" M5 W: s! l6 g! ], P7 S+ I* }/ O2 _
enlargement of the phallus and pubic hair develop-6 ]3 K2 z/ k! z7 h
ment without testicular enlargement, which was due
0 a. N+ j1 a) i2 n) n* Pto the unintentional exposure to androgen gel used by0 S$ {, U( `  N
the father. The family initially concealed this infor-
- g3 o2 r* a& r, |. r% O  Wmation, resulting in an extensive work-up for this; r6 _, N# R: g2 b4 [
child. Given the widespread and easy availability of
6 X0 A: l- o+ D4 p' ztestosterone gel and cream, we believe this is proba-0 ?1 h7 y& S/ J# v  A! L
bly more common than the rare case report in the
; R) T: V& d3 O! S* z! Kliterature.41 ], e  U  ^& u' D
Patient Report
6 e8 C# k& ^8 t; O/ @  @; vA 16-month-old white child was referred to the
# D! d7 L9 E. Mendocrine clinic by his pediatrician with the concern2 I9 G0 T3 T+ p/ M$ K, k# d4 a; _
of early sexual development. His mother noticed
' e3 ^  d4 p. f: Olight colored pubic hair development when he was. }/ W: x9 s" m  k3 U7 [, W  P
From the 1Division of Pediatric Endocrinology, 2University of
, J* J! R. B4 `. N6 m! W! sSouth Alabama Medical Center, Mobile, Alabama.' I$ w2 o5 D  D+ c5 C; |
Address correspondence to: Samar K. Bhowmick, MD, FACE,6 E0 I5 s7 ~* _# ]. r  S3 ?3 X! o/ F
Professor of Pediatrics, University of South Alabama, College of& {+ h9 x7 _1 [: Q
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;1 G& L7 h1 Q: g& ?% I/ G
e-mail: [email protected].
( r7 d0 Q0 A! U1 oabout 6 to 7 months old, which progressively became. F( s8 D' v! T
darker. She was also concerned about the enlarge-
; d9 z$ [* O/ F, Z% e- y  b( B7 \/ Kment of his penis and frequent erections. The child
8 ~) l" h' R/ t" I- _was the product of a full-term normal delivery, with& J% n) n- v3 ^
a birth weight of 7 lb 14 oz, and birth length of
! t: q0 p/ Z" _9 n/ |& x" E( ^20 inches. He was breast-fed throughout the first year6 N! z$ v/ n; ]# n' [
of life and was still receiving breast milk along with
! ]. N, Q& i3 V  _solid food. He had no hospitalizations or surgery,: B9 [% _- f+ o3 B1 X+ i# Y
and his psychosocial and psychomotor development, j, c. B  n# D& ?5 W9 K, c" m
was age appropriate.* @/ N: e! Q: A, a5 K
The family history was remarkable for the father,, l% b* M+ d! e: w4 S/ z
who was diagnosed with hypothyroidism at age 16,
6 I2 h, g0 w! k& c! s. ~which was treated with thyroxine. The father’s
( a6 ?& ]- a) F% t5 `! A% fheight was 6 feet, and he went through a somewhat
& R8 `/ O7 u8 T1 f5 o/ j( Jearly puberty and had stopped growing by age 14.
* ?% n+ m  ?$ X5 O% O% A- a: ~0 BThe father denied taking any other medication. The9 B/ \9 e  R/ L1 G  W  e" y3 V4 F
child’s mother was in good health. Her menarche
3 o$ H* Q$ Y4 M$ f/ @4 _9 [was at 11 years of age, and her height was at 5 feet
$ k6 [7 S0 H2 Q* V( F5 inches. There was no other family history of pre-
/ M8 y, Q+ X0 t* Fcocious sexual development in the first-degree rela-
: A4 e. U; n8 b% etives. There were no siblings.; C& E. p; A3 y$ D
Physical Examination2 z' O1 w. M  a7 |, m& A0 I
The physical examination revealed a very active,
0 T: B+ T) f$ G0 `: [# Bplayful, and healthy boy. The vital signs documented9 U- i  U0 l% f4 r9 g
a blood pressure of 85/50 mm Hg, his length was
. Y+ G# p9 \% @2 u+ V90 cm (>97th percentile), and his weight was 14.4 kg
2 Z3 _5 |& `9 A- P* N" g& e(also >97th percentile). The observed yearly growth
% j8 f& i& F' k9 Mvelocity was 30 cm (12 inches). The examination of! G+ q9 b  |- R2 T$ |
the neck revealed no thyroid enlargement.
/ J( v$ j7 x- P4 \0 |& x% LThe genitourinary examination was remarkable for
% f5 @+ Y. I$ C& ~" V$ ^( \enlargement of the penis, with a stretched length of3 H- `5 B* B# H9 W: [
8 cm and a width of 2 cm. The glans penis was very well; d/ M( j0 b3 @4 B
developed. The pubic hair was Tanner II, mostly around: w5 }; [: Q) j9 k9 B; H8 P
540
/ N: f6 O5 i& U4 Q; X" Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. H5 ^6 Y3 w8 I- X: @7 n/ Y, e/ Y
the base of the phallus and was dark and curled. The0 T4 @% e4 A/ \# ?5 O" V+ a. q
testicular volume was prepubertal at 2 mL each.4 K0 Y/ J9 _  u' C) ^( B5 N
The skin was moist and smooth and somewhat
7 [+ H& w8 s4 i5 Voily. No axillary hair was noted. There were no
6 _( p6 V/ F- B( E" U! P) @- P: ?abnormal skin pigmentations or café-au-lait spots.
4 A1 o9 D0 F! w& }4 L' oNeurologic evaluation showed deep tendon reflex 2+  T/ I! ?' Q% Q& N" j
bilateral and symmetrical. There was no suggestion
5 P1 e3 D0 D% l$ N3 B- jof papilledema.; J' ^7 U+ ~9 p  {4 p
Laboratory Evaluation$ p  P3 \% h8 r7 i
The bone age was consistent with 28 months by, Q: w, s0 F3 C. ~
using the standard of Greulich and Pyle at a chrono-& l3 N0 V" Y; Y. j3 F/ Q
logic age of 16 months (advanced).5 Chromosomal( b" t% j& T$ X5 z5 m( E+ x' s% V
karyotype was 46XY. The thyroid function test
. o3 F4 |6 n+ v; G1 F8 Z' Xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! Y' B6 R( n# Z0 Blating hormone level was 1.3 µIU/mL (both normal).
) A1 {+ Y0 z. z& d! \# s6 \The concentrations of serum electrolytes, blood: \" W9 E' O' {% {
urea nitrogen, creatinine, and calcium all were: M/ x; {; F3 c/ A9 g8 ]) H
within normal range for his age. The concentration
$ ^( w( ~" D; A) D- Oof serum 17-hydroxyprogesterone was 16 ng/dL1 n' o6 f/ ~5 C2 \9 ?
(normal, 3 to 90 ng/dL), androstenedione was 20
4 P# @2 D6 b& x; Bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 i1 }$ k2 @8 Y7 ?! T( w. _terone was 38 ng/dL (normal, 50 to 760 ng/dL),- F: ~6 @  f& C( l$ i
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
; U) w, `% k5 i" H* b- B  R, x49ng/dL), 11-desoxycortisol (specific compound S)# R, |# ?9 r) }9 k. F
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 c5 A$ ?- o1 B: \
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' u3 [& Y  `; e/ r9 C6 l. F- Ctestosterone was 60 ng/dL (normal <3 to 10 ng/dL),1 X' Z$ ~  u' u* P5 |+ \
and β-human chorionic gonadotropin was less than
' `0 x( c2 S9 H5 mIU/mL (normal <5 mIU/mL). Serum follicular
! a/ `' U0 \: e& t, gstimulating hormone and leuteinizing hormone
$ B2 r' H  a) ~+ o. y8 b: uconcentrations were less than 0.05 mIU/mL3 r1 \8 f1 i0 o+ q1 r7 p0 {
(prepubertal).
3 ~: d6 A$ @" b+ A8 iThe parents were notified about the laboratory
& z6 a5 B7 x7 d  L2 X6 Kresults and were informed that all of the tests were
/ p5 f( v8 j9 ^  T$ C, j% ynormal except the testosterone level was high. The
; t9 X( g* h) S1 Zfollow-up visit was arranged within a few weeks to, p5 |8 C* I% B! i: w
obtain testicular and abdominal sonograms; how-
0 e6 k" ^$ O* oever, the family did not return for 4 months.: p$ K* \/ |7 }, g% X6 K
Physical examination at this time revealed that the
6 G: Q  v3 N% Q8 C8 A2 zchild had grown 2.5 cm in 4 months and had gained6 t& q% S1 d! @- X! r9 B  Y
2 kg of weight. Physical examination remained
3 u- `. X+ c2 q' o9 Nunchanged. Surprisingly, the pubic hair almost com-7 Q# f; W7 [% _0 x( f4 A. p( ]- I
pletely disappeared except for a few vellous hairs at
, |2 ~! t0 J$ K. i# gthe base of the phallus. Testicular volume was still 2
4 C8 G8 i# S; smL, and the size of the penis remained unchanged.
: i* a" i$ N" c3 F3 Q4 XThe mother also said that the boy was no longer hav-: d" u8 k5 i: o+ R0 v
ing frequent erections.. U3 d' f. a9 `# H! d7 y2 Y+ o
Both parents were again questioned about use of
7 C$ p( g; {: z( r+ iany ointment/creams that they may have applied to
2 N. B* t9 C2 q3 }- C* b: Ithe child’s skin. This time the father admitted the% u0 s( K0 S1 j# A' a
Topical Testosterone Exposure / Bhowmick et al 541
, `% n+ E1 t* d% r- luse of testosterone gel twice daily that he was apply-0 J, V* Y9 y# d, [& L0 u
ing over his own shoulders, chest, and back area for) [% ~' [8 D/ [6 U  a3 e9 _, G
a year. The father also revealed he was embarrassed. \; `  z4 L" A7 {
to disclose that he was using a testosterone gel pre-8 \# a/ i. @5 \* g6 z/ i6 d4 o- l
scribed by his family physician for decreased libido, ~  [0 ^& I- v- I1 U& f
secondary to depression.' Y7 l' x6 R. n$ ?1 ^9 `2 L
The child slept in the same bed with parents.2 g" E; O4 B  ~7 F# v9 T. ?
The father would hug the baby and hold him on his
" f# G* x" i7 D3 K+ schest for a considerable period of time, causing sig-
) x3 o/ K. @6 G8 x/ i8 onificant bare skin contact between baby and father.7 b4 Q, o! V0 Q+ H; \# ^
The father also admitted that after the phone call,2 @/ _# {* Z5 I7 \/ ?, V! q
when he learned the testosterone level in the baby% D* i) [2 ^+ {% K) k
was high, he then read the product information' X" l9 r% C, m' F' _2 \4 r) j2 q
packet and concluded that it was most likely the rea-
1 C. D8 V/ x& K* c2 S! g6 wson for the child’s virilization. At that time, they
. q' Q* \( b- H: K& _; y6 tdecided to put the baby in a separate bed, and the" r, `1 `1 S$ w( [6 Y4 ?
father was not hugging him with bare skin and had4 h8 B; y7 R/ T! R4 w' w
been using protective clothing. A repeat testosterone* O0 J' V- a" m7 }
test was ordered, but the family did not go to the
* W+ q) a# @% ~: |# b; ~laboratory to obtain the test.6 Y  g- b) D+ V) [: I2 ?
Discussion
# i  q$ W4 }9 @Precocious puberty in boys is defined as secondary) C  c+ `6 q8 r1 l$ b
sexual development before 9 years of age.1,4
2 }2 ?/ f' _  a: r  V1 X7 bPrecocious puberty is termed as central (true) when
- s; s+ W& ?* I' \: g" y4 qit is caused by the premature activation of hypo-, M" _( H) m- m3 D
thalamic pituitary gonadal axis. CPP is more com-: V4 q' Z. `5 \) F1 H0 T5 h
mon in girls than in boys.1,3 Most boys with CPP
. {: w7 ?0 g( h7 F* }: C& P: l  cmay have a central nervous system lesion that is- Z& P! a+ l! N. |. Q8 F0 v
responsible for the early activation of the hypothal-
$ ?+ }! \- l8 C5 S# W' y; vamic pituitary gonadal axis.1-3 Thus, greater empha-9 J+ V& \& u4 \8 D3 m+ R
sis has been given to neuroradiologic imaging in9 ~7 J5 n. b) P1 l1 ?$ M2 F) H
boys with precocious puberty. In addition to viril-. i; E' F8 g1 O) Q  N. M) ~* w
ization, the clinical hallmark of CPP is the symmet-
' K  A* f# p9 c! E7 @" ~/ Z9 ~rical testicular growth secondary to stimulation by3 [2 [7 ?2 v5 a' y( N3 |8 n
gonadotropins.1,3
5 j7 T. U% c/ I6 \Gonadotropin-independent peripheral preco-
5 z7 x' V- r- h$ R& rcious puberty in boys also results from inappropriate$ t$ G+ V; R) u$ h
androgenic stimulation from either endogenous or
# j  @& a7 a2 z6 P8 l# d. Y7 ^1 q1 Bexogenous sources, nonpituitary gonadotropin stim-  N9 _8 e) o4 b" }. r! W, Y
ulation, and rare activating mutations.3 Virilizing
/ E- q$ t3 F3 Y: bcongenital adrenal hyperplasia producing excessive0 Z" a" g/ R' [( q
adrenal androgens is a common cause of precocious* @% ^+ n# y  ~8 [# ^0 {
puberty in boys.3,46 r3 P0 x1 I4 h" g9 q3 t
The most common form of congenital adrenal" F, [6 g3 {& X3 z: ^
hyperplasia is the 21-hydroxylase enzyme deficiency., j8 g2 c* l* G2 H" j) w9 S
The 11-β hydroxylase deficiency may also result in
* ?# r/ A5 v4 r! y3 hexcessive adrenal androgen production, and rarely,( k5 U4 `9 G/ {6 n' L& g8 ]% g' ?
an adrenal tumor may also cause adrenal androgen
1 ?" U5 L3 q$ F/ W) iexcess.1,34 J4 N) z( j( t
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 _$ T' H! Z5 V0 S$ H
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( W, i( d, {& e; P& d( ~
A unique entity of male-limited gonadotropin-
! `$ k0 `$ F  w; Z' v( T( W& ?independent precocious puberty, which is also known1 f* V( s- R0 E& R( L
as testotoxicosis, may cause precocious puberty at a
: S8 ^( i( o) M8 m$ K$ S  \, Z1 @very young age. The physical findings in these boys. W% H' W- A+ A0 S. L
with this disorder are full pubertal development,
1 W+ w( |$ M" y: S4 t, X* r" dincluding bilateral testicular growth, similar to boys
9 _) |# e0 T8 A/ b! F2 H! {3 Mwith CPP. The gonadotropin levels in this disorder
9 {3 n5 I6 v6 t( o- v3 q6 @are suppressed to prepubertal levels and do not show( w. a" Z( S. t0 |+ g% m- t# V
pubertal response of gonadotropin after gonadotropin-! K1 t. ?, y1 }0 b; i
releasing hormone stimulation. This is a sex-linked
8 v, w8 U, D$ E, Y* Dautosomal dominant disorder that affects only
' w* f( P9 U6 w! {males; therefore, other male members of the family; b* L$ f: @6 g3 r6 a- u9 b( {
may have similar precocious puberty.3
9 w- a% `* Q) [' GIn our patient, physical examination was incon-" O& l6 n' D; i$ V/ C( H
sistent with true precocious puberty since his testi-
% O* C6 @8 h! n$ Q; p5 @* bcles were prepubertal in size. However, testotoxicosis
( |) Y0 \5 v) S: x5 b7 Cwas in the differential diagnosis because his father- y" V" Q" i  E: m# t; v
started puberty somewhat early, and occasionally,0 l! j2 q8 n1 w
testicular enlargement is not that evident in the6 k2 F9 E) A% }( {4 X0 `, q. R
beginning of this process.1 In the absence of a neg-9 k: Y0 p: v, C$ d% e
ative initial history of androgen exposure, our* C# V* ]" m3 Y7 |9 d
biggest concern was virilizing adrenal hyperplasia,
, A1 o! I7 @% Peither 21-hydroxylase deficiency or 11-β hydroxylase5 G2 ^$ d7 f% _. `. a1 Z
deficiency. Those diagnoses were excluded by find-
, s+ x6 K' D7 j' @( _ing the normal level of adrenal steroids.7 F/ A3 `  |% q1 H: ~; E  {4 A; c
The diagnosis of exogenous androgens was strongly5 F3 R8 g6 P, _* Y! N
suspected in a follow-up visit after 4 months because$ W! @3 c) e3 B- t3 X
the physical examination revealed the complete disap-1 ]9 t; G- v. h% T5 K
pearance of pubic hair, normal growth velocity, and
) H$ \8 M/ J- mdecreased erections. The father admitted using a testos-$ q/ C4 ^+ D  }4 o0 g/ e
terone gel, which he concealed at first visit. He was8 b3 U2 }* g7 W4 [5 _+ F
using it rather frequently, twice a day. The Physicians’4 J: q" f/ V+ ~
Desk Reference, or package insert of this product, gel or: q3 d$ R0 {0 J7 r4 `
cream, cautions about dermal testosterone transfer to
  N0 V* ?- B! O, r1 q0 cunprotected females through direct skin exposure.
2 i8 d9 h# C8 b* CSerum testosterone level was found to be 2 times the
+ P( g9 P% r9 v4 wbaseline value in those females who were exposed to$ U/ A3 C  s% |9 k' Y0 a
even 15 minutes of direct skin contact with their male
5 i: @% k& D4 ?- t1 dpartners.6 However, when a shirt covered the applica-& X: E6 q7 C, E2 y7 Z2 w- W0 F
tion site, this testosterone transfer was prevented.
+ _! U: z! I7 d* X( {" R- j7 R% eOur patient’s testosterone level was 60 ng/mL,7 S  u8 Y- u7 }; |+ R+ B% m8 K( Y
which was clearly high. Some studies suggest that; f! y" Z- V( G5 R6 v1 g+ |$ H
dermal conversion of testosterone to dihydrotestos-
8 c( @- s* R3 O# j4 p5 B' Q# `terone, which is a more potent metabolite, is more
& @$ B  ~% x( T2 q! X# o5 Vactive in young children exposed to testosterone; A4 e% t4 d$ J4 [8 m; J
exogenously7; however, we did not measure a dihy-; B( i% t2 V1 i# {- i
drotestosterone level in our patient. In addition to1 f" x. e& \4 q" k$ F) C2 e/ Y
virilization, exposure to exogenous testosterone in( \3 q; s& g' J: Z
children results in an increase in growth velocity and
3 X  N8 Z+ Z9 Aadvanced bone age, as seen in our patient.* Z8 W, I" W- o5 w6 t
The long-term effect of androgen exposure during
- J. U# G+ @7 z' N9 w  Zearly childhood on pubertal development and final3 L  Z* s; M, N' p6 Z
adult height are not fully known and always remain5 W& c% N9 R; T# n$ E
a concern. Children treated with short-term testos-5 k* O" K: Q  e2 J9 O3 G% a) K
terone injection or topical androgen may exhibit some
6 ?! m" N( K7 A9 Q0 xacceleration of the skeletal maturation; however, after' U3 p; Q: q3 Q3 B7 B2 h
cessation of treatment, the rate of bone maturation- D! j1 o: _; S- x" _7 K
decelerates and gradually returns to normal.8,9
" c! }- C2 f. c6 f0 b- eThere are conflicting reports and controversy
0 w/ K5 }0 n0 @9 ~over the effect of early androgen exposure on adult  p+ M' p- n8 P# a; Q# G/ n; @, r
penile length.10,11 Some reports suggest subnormal
) h" l1 Z1 ^0 A9 yadult penile length, apparently because of downreg-; ~6 p, A& _/ Y$ O
ulation of androgen receptor number.10,12 However,
: p& U/ N, g" Q2 n6 @Sutherland et al13 did not find a correlation between; p5 _+ B% u6 s
childhood testosterone exposure and reduced adult
1 Y2 E3 T& g1 l4 h* |penile length in clinical studies.
/ _" Q3 g* r8 T' F# a  d& fNonetheless, we do not believe our patient is
! Z" X4 }; \0 P6 T, _0 H; r+ Kgoing to experience any of the untoward effects from+ {  ^! L9 \' I( u
testosterone exposure as mentioned earlier because
% Z, W" ?7 G: G! k: C3 G, {the exposure was not for a prolonged period of time./ M# W6 u0 P1 C' N% c
Although the bone age was advanced at the time of7 |0 c$ {) O1 N2 Y/ [6 }
diagnosis, the child had a normal growth velocity at
3 o% l8 ~1 t* Ethe follow-up visit. It is hoped that his final adult/ V7 R0 B9 R, B  a
height will not be affected.
4 n$ @& _) {9 r& bAlthough rarely reported, the widespread avail-
; N/ Z4 N4 U: C+ aability of androgen products in our society may# g- E: ?) X7 K, @0 Z# y4 [
indeed cause more virilization in male or female
- C* ]* B0 [2 _! M: Y* I) _children than one would realize. Exposure to andro-
! c+ U! `6 [3 a( d0 b: h- @gen products must be considered and specific ques-0 Q* D- a+ k  v5 P, H; z
tioning about the use of a testosterone product or
% V8 ~4 _) b2 m5 Z, J: Mgel should be asked of the family members during' g; @0 \+ r) B4 w  H6 c
the evaluation of any children who present with vir-5 ~8 p* V5 g: {! K- ~3 t. G
ilization or peripheral precocious puberty. The diag-2 ]+ w0 Z- K0 {/ y  l/ A* N
nosis can be established by just a few tests and by
/ l: @- R- _2 O/ Y( F& happropriate history. The inability to obtain such a8 [" N: y: f" q
history, or failure to ask the specific questions, may
( R  M4 x3 U3 xresult in extensive, unnecessary, and expensive, |2 V* I2 O, e. {! m% K* Z
investigation. The primary care physician should be
2 L" O2 P9 S0 R6 A8 E, Kaware of this fact, because most of these children
+ R9 U9 H; S2 r$ Q! g! q' omay initially present in their practice. The Physicians’
" K& t) n5 O2 xDesk Reference and package insert should also put a
8 e9 N; @2 i5 }: P  ewarning about the virilizing effect on a male or
6 b: ~/ L) P2 A; k8 c% |female child who might come in contact with some-0 I  W  J/ K. H6 Z  y! p4 \
one using any of these products.
5 L. Z1 |/ C/ ^2 g0 ZReferences
0 C* E+ {' R4 I) y, \1. Styne DM. The testes: disorder of sexual differentiation# ~# G3 N6 e+ f* c0 g- O9 S9 i2 W
and puberty in the male. In: Sperling MA, ed. Pediatric5 [/ J5 T2 B/ m2 x# y- M# }1 j
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;& Q) G, D+ j  {- a- T; ?/ ~8 h! z) B7 W
2002: 565-628.3 p9 d0 l$ h  F. d& ]7 D7 L4 G
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% c' \# ^2 f2 S$ p8 R5 K
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old, O  s! L. i4 I" K1 M8 z7 x
Boy Induced by Indirect Topical
7 q; U8 `, R6 t0 `$ aExposure to Testosterone
5 O3 o' d3 w( D/ Z& VSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- y) i2 Z2 t3 S6 m% }$ N; L7 l
and Kenneth R. Rettig, MD1
' U) e; z5 x! ?% l) ^  dClinical Pediatrics9 B; |' _' K! s& j& ~' A
Volume 46 Number 6& B5 v4 V/ z# H& ^0 Y
July 2007 540-543
. f6 {: v: V; F5 v/ p$ Z$ _2 B* H© 2007 Sage Publications
/ c" e' R! e3 ?8 }+ K- a10.1177/00099228062966518 m1 L( T6 s2 x$ P
http://clp.sagepub.com( t8 O. V( d/ f9 ]
hosted at
5 {9 r) i9 ]6 G/ M" ^! U6 ^$ Ghttp://online.sagepub.com! {. u2 H1 f: @$ Y3 e
Precocious puberty in boys, central or peripheral,* s: a% b* Z& t' y/ K: k, u! l
is a significant concern for physicians. Central
; w: F" R, z7 K% s9 _precocious puberty (CPP), which is mediated! i& K* k; P% |' g# `! N3 s/ T
through the hypothalamic pituitary gonadal axis, has1 ~" q$ A0 M. E; k4 b! l0 C
a higher incidence of organic central nervous system
' m7 |6 S  f2 L- j4 a1 t& Q9 B) b# klesions in boys.1,2 Virilization in boys, as manifested. M7 U% q3 }8 }
by enlargement of the penis, development of pubic
) ], Y$ W  k  K1 {( `hair, and facial acne without enlargement of testi-% b3 W' R5 g7 E3 p/ L5 ]/ F
cles, suggests peripheral or pseudopuberty.1-3 We
: m: \4 O5 t# J, G, V# |7 X7 ]; ]1 M( nreport a 16-month-old boy who presented with the
( q2 y, f# j) l  y$ E0 [' z1 M0 cenlargement of the phallus and pubic hair develop-5 h5 f7 N- e- ]2 N
ment without testicular enlargement, which was due* k9 A: |! H5 \+ r( v" A
to the unintentional exposure to androgen gel used by
/ L: \4 p" w! j+ D: G- h/ S/ sthe father. The family initially concealed this infor-
( q7 k( h/ t  i. ^" qmation, resulting in an extensive work-up for this, l. ?1 K/ \1 @) K& A
child. Given the widespread and easy availability of5 z# F: B/ O5 S" {( P7 w
testosterone gel and cream, we believe this is proba-
# b0 w: O! w9 Zbly more common than the rare case report in the
' h' q" L' b6 W9 U; R1 Xliterature.4& R+ t$ U8 |( i$ G, h# {
Patient Report
; l0 e6 e# u1 V; {' n" W, DA 16-month-old white child was referred to the7 u/ Z9 r4 m& T  |" T& b& G, _
endocrine clinic by his pediatrician with the concern
7 g% `5 i8 V: w" O- oof early sexual development. His mother noticed* Z$ o/ H3 A0 D/ ?  K$ m# L" D
light colored pubic hair development when he was  l0 g. R; [4 R9 g6 G
From the 1Division of Pediatric Endocrinology, 2University of
, |- r+ j4 h/ S& C% d9 m0 n# SSouth Alabama Medical Center, Mobile, Alabama.7 s2 c. e, e( I6 G) X
Address correspondence to: Samar K. Bhowmick, MD, FACE,5 |+ f% m9 D+ ^* k* X7 Q( K
Professor of Pediatrics, University of South Alabama, College of3 P7 @5 ]( x" k% y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
7 G5 k& T$ u( q. l* K, Y  He-mail: [email protected].
% `3 N& S6 F- h2 _about 6 to 7 months old, which progressively became
2 T9 W2 u5 X8 |) [& Y$ e! fdarker. She was also concerned about the enlarge-4 k7 z2 x+ l7 t# j9 S- O
ment of his penis and frequent erections. The child, ^- a7 K, n, x* r4 _; ?" h
was the product of a full-term normal delivery, with$ I% [6 F- p+ I, E' z
a birth weight of 7 lb 14 oz, and birth length of
! P6 l" V  b, v3 D1 I20 inches. He was breast-fed throughout the first year
9 X/ f% E$ w3 {/ m' aof life and was still receiving breast milk along with
1 s) h1 \  s: ]1 wsolid food. He had no hospitalizations or surgery,3 F6 r: i4 X' w7 k, m3 e
and his psychosocial and psychomotor development4 E) f; J5 z, @5 U- P
was age appropriate.
! u8 i, k3 u& L* |/ B7 S9 UThe family history was remarkable for the father,7 }, ~" _" w, p5 c$ f6 m. [0 {* `
who was diagnosed with hypothyroidism at age 16,
) o  s. C) W! y9 D6 ~1 X. O, d+ v$ [$ qwhich was treated with thyroxine. The father’s# [" G, @7 }! q
height was 6 feet, and he went through a somewhat: h/ c5 L8 J' a$ D1 `, L
early puberty and had stopped growing by age 14.
/ S, ~- Y, r9 W9 P8 N* \The father denied taking any other medication. The) A% b0 v3 g/ [: r4 C
child’s mother was in good health. Her menarche' j# E% G4 u% Q) l
was at 11 years of age, and her height was at 5 feet2 z5 s7 E7 \% X4 C
5 inches. There was no other family history of pre-8 O( e6 Y3 W6 |
cocious sexual development in the first-degree rela-$ u2 d( o4 V& v, S& h
tives. There were no siblings.: o7 S# s  e6 `( H7 K  ^
Physical Examination
1 p& N4 G  |6 P& \0 jThe physical examination revealed a very active,; {' S0 e) F( h3 ~& J
playful, and healthy boy. The vital signs documented
5 l+ _5 I7 O( V& Ta blood pressure of 85/50 mm Hg, his length was
5 [0 L% W$ M6 s  w( {( G90 cm (>97th percentile), and his weight was 14.4 kg
" d7 S3 d& [1 n& ^9 x(also >97th percentile). The observed yearly growth) b' |& O7 o2 Q3 c9 ~
velocity was 30 cm (12 inches). The examination of
7 H. e4 k2 b5 g5 e9 H* H) q; {the neck revealed no thyroid enlargement.6 z2 `: `+ F; T* Y+ [' s+ `( ]8 t- [6 I
The genitourinary examination was remarkable for
6 ^$ V0 s4 [0 x8 k' K/ R) f* aenlargement of the penis, with a stretched length of' q8 q* ]+ o* \& q
8 cm and a width of 2 cm. The glans penis was very well
# |) q( l% a8 \  Ddeveloped. The pubic hair was Tanner II, mostly around) q& |+ y1 G( H4 y# J
540
2 r7 O1 j7 n) ?' a1 o; O0 mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! D9 s) w0 m$ c9 k5 H4 y6 h" [the base of the phallus and was dark and curled. The6 r& ?% h$ W6 \( Y
testicular volume was prepubertal at 2 mL each.8 A1 G+ T* O( M4 v. [8 [
The skin was moist and smooth and somewhat( b/ C. y: V" I$ E* Z! |
oily. No axillary hair was noted. There were no
$ O/ Q9 b" Y+ Kabnormal skin pigmentations or café-au-lait spots.+ h' e" J9 q; ]4 C* v3 Y9 h& N6 F
Neurologic evaluation showed deep tendon reflex 2+
1 {4 _% k5 i! K( s4 s+ C9 w9 A6 fbilateral and symmetrical. There was no suggestion
) r/ g' P8 z' M2 x4 m; z# R! Sof papilledema.  \0 S9 e& J3 T' r& Z
Laboratory Evaluation) P$ a) [" R% O, o6 A. U/ [
The bone age was consistent with 28 months by
- E  U. f. U- Dusing the standard of Greulich and Pyle at a chrono-, X$ A' @$ d: R0 y" r0 P
logic age of 16 months (advanced).5 Chromosomal
- a& p2 I- z% b7 a4 hkaryotype was 46XY. The thyroid function test
$ s: p% d2 Y' H8 Z0 X; o) }showed a free T4 of 1.69 ng/dL, and thyroid stimu-
$ g- f) \$ i8 A; ~# Rlating hormone level was 1.3 µIU/mL (both normal).& g5 n8 F5 q1 u- y, ^6 S
The concentrations of serum electrolytes, blood
! ^0 {) v9 w; a5 \& m4 Qurea nitrogen, creatinine, and calcium all were. p, R) ^4 K7 m
within normal range for his age. The concentration
, c& C7 x! Q0 K4 u# ]of serum 17-hydroxyprogesterone was 16 ng/dL
% D+ G$ h2 Y( s9 U(normal, 3 to 90 ng/dL), androstenedione was 20# v1 S* g' K+ g- T
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
% T9 m% T% O5 M9 i, K0 [terone was 38 ng/dL (normal, 50 to 760 ng/dL),; {5 o/ ^% U0 |# |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to" z, N, S- N, `1 W! f; @6 p
49ng/dL), 11-desoxycortisol (specific compound S)
) z1 Z4 B$ n- R# K6 ^was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, c9 D6 J: o2 v, F2 E3 J
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: T+ ~% h9 X& Y8 X  n  R" K( v! l
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 k3 {' U9 o  l6 u, O' I: ?
and β-human chorionic gonadotropin was less than
3 W* Q9 d7 z7 a- j  [& C4 T5 mIU/mL (normal <5 mIU/mL). Serum follicular
+ d; y5 s$ C( q+ R/ ~4 Istimulating hormone and leuteinizing hormone# O$ `; H: H, w& n9 s) d+ c4 F0 S
concentrations were less than 0.05 mIU/mL* Y0 L. e9 ^8 ~: V, Y
(prepubertal).& f; V) H% z9 B7 `) H7 V( v
The parents were notified about the laboratory) ]- S& K1 u5 Q) o7 \( f
results and were informed that all of the tests were6 Y, C# n6 S) j) @. C
normal except the testosterone level was high. The
8 {; f1 v: q5 ?" z* q7 n1 Kfollow-up visit was arranged within a few weeks to6 f& P8 C  {) s" R: H
obtain testicular and abdominal sonograms; how-! S1 _# s! F- _" B" o1 ]) D
ever, the family did not return for 4 months.
2 H0 [& `- R9 xPhysical examination at this time revealed that the, _3 U4 x2 w+ I1 a. u. a% d' w
child had grown 2.5 cm in 4 months and had gained
+ Z  C* s2 F. L* A2 kg of weight. Physical examination remained: F) M# f1 L, p+ f; n! O3 L
unchanged. Surprisingly, the pubic hair almost com-+ K  A9 }; b, H) l0 c% p- e
pletely disappeared except for a few vellous hairs at
, N! b! H" E' y% Fthe base of the phallus. Testicular volume was still 2
3 M( p  E9 z/ gmL, and the size of the penis remained unchanged.
2 `& Q# D) m" U, d5 J) `3 B" KThe mother also said that the boy was no longer hav-
- E3 L" {% z0 W4 V& Y, wing frequent erections.
4 q) t2 M' `% D) `- K2 G) ]Both parents were again questioned about use of
7 l# ]5 l7 e" ]/ r# Eany ointment/creams that they may have applied to. _7 Q, Z9 G7 Q" r- |1 f
the child’s skin. This time the father admitted the
# \$ t9 `8 D) B) W! tTopical Testosterone Exposure / Bhowmick et al 541
' h4 t- @$ j" t" N- suse of testosterone gel twice daily that he was apply-
4 l, o- ?* y- ?1 V+ Ping over his own shoulders, chest, and back area for3 @1 v0 w) D1 J% J# P% H3 ]" d
a year. The father also revealed he was embarrassed2 Y1 Q& k$ x$ _/ R
to disclose that he was using a testosterone gel pre-
5 g* E9 e# g" J) w1 i' m# b/ ]scribed by his family physician for decreased libido
' H0 M; u( A& W+ Isecondary to depression.
! E# s$ \6 S$ t; V1 ?( `5 y/ XThe child slept in the same bed with parents.& v' D' k( o; ^, P7 l% k
The father would hug the baby and hold him on his0 P: j( V; u' `1 M% r5 M
chest for a considerable period of time, causing sig-6 x! u7 i0 l8 ^* f2 C8 _3 `4 g& k
nificant bare skin contact between baby and father.) Q( F0 T! A  g  N9 L
The father also admitted that after the phone call,5 _1 o  t# O/ C+ ?) h' P1 h$ X- z9 N
when he learned the testosterone level in the baby
& W9 a' H/ x$ ?* {( B5 [, u1 hwas high, he then read the product information
6 C  c2 P: Q+ lpacket and concluded that it was most likely the rea-* p$ N3 @- \# e/ u
son for the child’s virilization. At that time, they/ X' |9 L. S) D* r/ j
decided to put the baby in a separate bed, and the# k0 h0 i( c6 M0 ]' u
father was not hugging him with bare skin and had
4 U7 M. ]4 p" c& ^# V1 X# R$ L  P8 ^been using protective clothing. A repeat testosterone4 C, j7 {5 B( ~" q
test was ordered, but the family did not go to the+ f. Z  j- y$ m& P( g/ N& C
laboratory to obtain the test.
/ N9 ]! K" `) Z3 J. u) y5 L" sDiscussion) @3 r. N! b. {- d, W
Precocious puberty in boys is defined as secondary
1 f  z8 j! e8 H9 hsexual development before 9 years of age.1,4! r" i0 V: p6 Z4 B
Precocious puberty is termed as central (true) when
% k8 J' w- @: S* I4 \7 Lit is caused by the premature activation of hypo-
2 v3 w. U3 {% e. I. Tthalamic pituitary gonadal axis. CPP is more com-
3 P1 ]9 Y5 X! L" Z& x8 \, Kmon in girls than in boys.1,3 Most boys with CPP; r, S8 M! X$ }+ U
may have a central nervous system lesion that is) x) T8 T9 b8 I1 B
responsible for the early activation of the hypothal-. [* H' u- f% F5 a+ }8 A
amic pituitary gonadal axis.1-3 Thus, greater empha-  {) O8 {& I5 I9 ]( u* t
sis has been given to neuroradiologic imaging in- o& q9 v! {6 h* B
boys with precocious puberty. In addition to viril-
9 C4 V" K# B2 d, [. f7 K0 pization, the clinical hallmark of CPP is the symmet-* y) ~# @& C: k% Q; [% I
rical testicular growth secondary to stimulation by
* y8 W0 w) F/ S; S/ I3 Hgonadotropins.1,3+ ]$ Q+ s# Q: {. T" A, ?6 H, a) c
Gonadotropin-independent peripheral preco-) }9 b; N: x  B
cious puberty in boys also results from inappropriate; \2 F  P) G9 z6 L# R' b8 R6 i
androgenic stimulation from either endogenous or
2 B* G, p0 a8 ~- n1 l/ a  J2 Hexogenous sources, nonpituitary gonadotropin stim-; @! I# W# ^. m
ulation, and rare activating mutations.3 Virilizing! o" K, R0 |3 d
congenital adrenal hyperplasia producing excessive
8 h# W0 i( {/ t2 Aadrenal androgens is a common cause of precocious) q0 H8 j. F8 I1 w  {4 q* P. w4 d
puberty in boys.3,4# V  F3 S% d0 \  V( t0 [" y
The most common form of congenital adrenal# F' U( C1 t& H# j6 A6 M2 x
hyperplasia is the 21-hydroxylase enzyme deficiency.1 M6 C& B8 U8 z2 ^- l
The 11-β hydroxylase deficiency may also result in% R! G) h! s( a3 U3 `& t
excessive adrenal androgen production, and rarely,
$ r; J% Z/ s: ~an adrenal tumor may also cause adrenal androgen
. A; z3 X! Q/ b% d4 f2 S9 r  lexcess.1,37 Q/ b+ y8 c: s) s5 |9 y* M& u, R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) ?% E; U7 g; a- x) I7 r) |542 Clinical Pediatrics / Vol. 46, No. 6, July 2007; V1 Q; T+ R5 G/ l  c, B$ K2 Z
A unique entity of male-limited gonadotropin-
/ _! w  N) O" A! @) t# j  dindependent precocious puberty, which is also known
* x% m- E, A7 H2 D2 ]1 xas testotoxicosis, may cause precocious puberty at a( G+ g  L& E$ g+ P# T/ o6 F
very young age. The physical findings in these boys2 L3 b1 i; k) P# G
with this disorder are full pubertal development,
8 u( r/ ?4 M2 B& y5 |4 q) A8 Gincluding bilateral testicular growth, similar to boys
8 H, J0 v: n3 n1 S( v1 @+ {$ gwith CPP. The gonadotropin levels in this disorder4 X# O0 E+ b/ E% e9 g1 P  }
are suppressed to prepubertal levels and do not show
9 o4 [& c+ L& M' e7 `7 `pubertal response of gonadotropin after gonadotropin-
- _, K# \4 g. D( }: u7 N6 J  ?/ }releasing hormone stimulation. This is a sex-linked1 X- \  Q" c9 L9 S+ A& x
autosomal dominant disorder that affects only  s7 q* I' j! S0 P0 j3 ?2 ^/ I% I0 y' Y
males; therefore, other male members of the family
( n1 |" P/ j% ~1 lmay have similar precocious puberty.36 |) r  M# b0 U
In our patient, physical examination was incon-
. H) U7 p2 D9 H% u! O* t' ssistent with true precocious puberty since his testi-  w5 h3 j# f7 d' m+ q! c6 I
cles were prepubertal in size. However, testotoxicosis; t( \( V) a! N& o4 h
was in the differential diagnosis because his father' c6 f0 t( j2 O
started puberty somewhat early, and occasionally,
. E$ \% N7 b+ G8 a! A3 q, E5 ]- n0 {testicular enlargement is not that evident in the  A" O8 A/ Y9 T
beginning of this process.1 In the absence of a neg-
2 E7 F2 F* a( g/ ~ative initial history of androgen exposure, our
4 x: b# K4 x. i1 k. hbiggest concern was virilizing adrenal hyperplasia,
: K0 b8 R# W2 R2 [. L; p8 s2 X; ]either 21-hydroxylase deficiency or 11-β hydroxylase, `) p+ E& A: @5 I: K
deficiency. Those diagnoses were excluded by find-, n0 Q9 |% Z% x1 F" X+ O+ D
ing the normal level of adrenal steroids.
2 {. s1 {! J- O  Y8 J2 H# DThe diagnosis of exogenous androgens was strongly+ Y& z2 Y* z. y% L
suspected in a follow-up visit after 4 months because
9 _2 B  v8 L( E! C2 @7 Ithe physical examination revealed the complete disap-6 X1 @* x+ A2 P+ G9 B9 c5 B
pearance of pubic hair, normal growth velocity, and6 d$ t! E2 d: l
decreased erections. The father admitted using a testos-4 \) J: [  C$ |' B
terone gel, which he concealed at first visit. He was
2 |0 b0 e& e7 S: Cusing it rather frequently, twice a day. The Physicians’
& s$ T' n2 @" V2 g* M0 L5 ]Desk Reference, or package insert of this product, gel or7 X! U) O: r% y5 m- W
cream, cautions about dermal testosterone transfer to
$ {( `- f! x# `5 @' v' tunprotected females through direct skin exposure.
6 ~$ z8 y" I$ x( L" nSerum testosterone level was found to be 2 times the2 t  b! d; ?- S6 _
baseline value in those females who were exposed to# u9 ]: F% o, w$ [
even 15 minutes of direct skin contact with their male! o8 o! |+ g" B! i4 f
partners.6 However, when a shirt covered the applica-
, D: I7 K, s- j% B# @) o2 ~4 ption site, this testosterone transfer was prevented.5 u! v+ M& I  u1 y1 L
Our patient’s testosterone level was 60 ng/mL,2 T/ ^7 T: \: O+ _% Q& I% j
which was clearly high. Some studies suggest that  V1 y# k+ g9 ?9 F
dermal conversion of testosterone to dihydrotestos-/ d5 o! @& t3 I; h" V! \; w/ w7 V( e
terone, which is a more potent metabolite, is more8 x& F6 G7 q8 M# `3 \* o, D
active in young children exposed to testosterone& d) D5 y8 _5 f1 f  A0 v& m
exogenously7; however, we did not measure a dihy-  S) g4 _, P* l+ }1 T! g. u6 |
drotestosterone level in our patient. In addition to2 \4 ?0 ]) c9 ~" d( Z- @
virilization, exposure to exogenous testosterone in
' G$ K/ `8 d3 A3 _$ `0 Pchildren results in an increase in growth velocity and' p$ x4 H2 T. f! B, J/ ^1 z( G
advanced bone age, as seen in our patient.* H- p* ?$ g: S3 D4 k
The long-term effect of androgen exposure during
& D2 y3 Y! r9 g4 Q) d! Pearly childhood on pubertal development and final' o  l0 K0 k& u" h9 _* |. _- Q
adult height are not fully known and always remain5 [( A5 e+ S7 s+ L, t
a concern. Children treated with short-term testos-
9 J; q- H$ R4 Gterone injection or topical androgen may exhibit some
( F# ]/ z8 a% n5 B- y! n$ kacceleration of the skeletal maturation; however, after
" b1 X4 v* X, X) }' Jcessation of treatment, the rate of bone maturation
2 R  {5 e( v# f. ddecelerates and gradually returns to normal.8,9$ W1 a* P5 Z" w/ O1 f! M
There are conflicting reports and controversy
. b0 ~. @# B' g: E' }/ Bover the effect of early androgen exposure on adult
) @2 C) F9 O5 t& q: apenile length.10,11 Some reports suggest subnormal! B- Z  w; ~! M* L) D
adult penile length, apparently because of downreg-
' k' F+ T; s4 m, w( a5 ]% q! sulation of androgen receptor number.10,12 However,
) F6 @  u+ @* a0 I. I" N1 |Sutherland et al13 did not find a correlation between5 V. f: `1 W/ }! _' J
childhood testosterone exposure and reduced adult
+ N3 _+ L; e5 s* w1 D  K2 _; |0 l; Xpenile length in clinical studies.0 Z1 [* H0 C  Y  l3 D
Nonetheless, we do not believe our patient is9 }3 _2 t/ b, X  @3 f
going to experience any of the untoward effects from
+ L$ ~7 {0 U9 ?4 P1 etestosterone exposure as mentioned earlier because
: {0 B6 A% P9 G+ G1 Vthe exposure was not for a prolonged period of time.$ M( t- y+ @) j2 o' V2 |& Y# @
Although the bone age was advanced at the time of
. Z2 i: X4 Y- a. P) Pdiagnosis, the child had a normal growth velocity at
- ^; T3 w. B7 e2 n0 R  ethe follow-up visit. It is hoped that his final adult; Z7 m# w" k/ U4 u5 `
height will not be affected.' b4 p6 z" b% e3 C2 z
Although rarely reported, the widespread avail-
3 O- F5 O" K- i+ [9 i9 ~ability of androgen products in our society may
" r2 A9 {% z# F% {indeed cause more virilization in male or female
& o; W1 S5 Y; y  cchildren than one would realize. Exposure to andro-
% x. `5 u. o/ d- C3 s" Lgen products must be considered and specific ques-
+ L# u2 z% V- d' `$ k+ \0 ktioning about the use of a testosterone product or. Y5 o' T6 ?. T5 K* S" ^0 @
gel should be asked of the family members during
2 r! |8 u! J9 E3 J5 U+ k5 cthe evaluation of any children who present with vir-
6 T  C  w8 w; B1 hilization or peripheral precocious puberty. The diag-
0 v7 \6 D& s( b3 cnosis can be established by just a few tests and by7 n( f' [* G8 q6 ~2 Y2 @/ f  W
appropriate history. The inability to obtain such a
1 H8 T4 m4 d9 `# r/ x# P, Xhistory, or failure to ask the specific questions, may
6 ^6 }& u: R: gresult in extensive, unnecessary, and expensive2 ~5 }: l+ b+ v3 n- E( k
investigation. The primary care physician should be; y/ m% J+ \4 `6 a
aware of this fact, because most of these children
6 t3 ~' k+ l* t  ^1 M2 J7 N: }6 p3 S3 hmay initially present in their practice. The Physicians’
# l, H" p# f- K: K# ODesk Reference and package insert should also put a: D5 y- X+ m4 p2 M. S9 C' p$ E
warning about the virilizing effect on a male or+ g! H2 q* V: d
female child who might come in contact with some-
' S, X* M8 c. S9 `one using any of these products.3 D. b4 J# L/ Q; P9 E- t% V
References* W4 {: M# v, ]) M, V7 W
1. Styne DM. The testes: disorder of sexual differentiation
1 W: W3 Y" ^5 ?* }and puberty in the male. In: Sperling MA, ed. Pediatric
- W0 s  q+ `2 m3 R- kEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( }+ Y: f7 d, q6 Z" x: ^, g
2002: 565-628./ G9 m4 g- w; _' [: ?5 K
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
, c; B5 C* S8 A, E  S* n  d$ hpuberty 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
) Y: X/ G' |) L1 v
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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