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Sexual Precocity in a 16-Month-Old: y$ K/ t; D! M5 P
Boy Induced by Indirect Topical/ w# S1 {4 K3 w. u3 W: Z
Exposure to Testosterone  `. a& m3 V& a' O9 I0 q
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ Z1 E6 ~8 X1 D5 d* ?$ l2 cand Kenneth R. Rettig, MD1/ B5 o7 v3 \  n) Y, Y5 Y9 l0 L
Clinical Pediatrics) `# u/ q1 {8 g
Volume 46 Number 6
/ ~5 X: Z" {" Y0 aJuly 2007 540-543
& f" |# D! D, R! D© 2007 Sage Publications; X. l* ^2 H! ?: b- Z$ T3 `0 \
10.1177/0009922806296651. O/ V1 N; p! [# M
http://clp.sagepub.com
0 J3 J. L, _( r& M# m' whosted at
' G' Y+ E: Q; a5 N! uhttp://online.sagepub.com) M$ m: i, K- n0 r8 @; E6 J
Precocious puberty in boys, central or peripheral,
  N* h3 |7 G8 x, H+ Qis a significant concern for physicians. Central
: r6 X) z1 R" i; kprecocious puberty (CPP), which is mediated
6 n/ y4 T/ ?6 I1 G3 i& xthrough the hypothalamic pituitary gonadal axis, has
+ K* G# r" p, ^" u0 fa higher incidence of organic central nervous system
% H7 u% s& J; p) W4 ulesions in boys.1,2 Virilization in boys, as manifested: h; ?: }5 g* @
by enlargement of the penis, development of pubic
$ M+ Z5 m& C2 m9 N; Hhair, and facial acne without enlargement of testi-4 A9 I) ]) }( K. J! v# X7 A
cles, suggests peripheral or pseudopuberty.1-3 We
( P/ i! B8 G5 n, D0 nreport a 16-month-old boy who presented with the) w( S- }7 _* r4 l: a
enlargement of the phallus and pubic hair develop-
( c* B( J0 l9 J( j" U; Yment without testicular enlargement, which was due
* n, I5 U9 ?) q* W% ~to the unintentional exposure to androgen gel used by
0 Z; Z6 z6 K" d, G+ u, Wthe father. The family initially concealed this infor-9 T: q& v5 d6 r% {6 [9 ^! r4 S
mation, resulting in an extensive work-up for this: n7 M: B3 d! L, c* {
child. Given the widespread and easy availability of( \3 q; i) X' z# r: B& F/ Z; p- j& f
testosterone gel and cream, we believe this is proba-" s5 R9 ?3 P! b) n; |2 @& }
bly more common than the rare case report in the
3 ]) V9 _; y. i: S& h0 q/ dliterature.4" p1 w: Q/ g* q6 |4 `; s0 B
Patient Report
6 Q' [7 H9 D" U# DA 16-month-old white child was referred to the# n% \( s8 D5 l5 m1 `
endocrine clinic by his pediatrician with the concern  k" W6 k! W- h$ r
of early sexual development. His mother noticed
3 T7 Q! S$ O0 V3 g, n# Flight colored pubic hair development when he was
0 l$ J9 n7 Y- v" X0 N! X$ W0 G- ?From the 1Division of Pediatric Endocrinology, 2University of
4 Q" _, C6 K" x8 k  T, PSouth Alabama Medical Center, Mobile, Alabama./ a) q! }7 j2 S8 a+ X
Address correspondence to: Samar K. Bhowmick, MD, FACE,
0 y/ p$ H/ {2 D& s3 A, F6 oProfessor of Pediatrics, University of South Alabama, College of
7 i+ X; X& @) [2 _2 ?5 BMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" Z# ?0 G4 U) B$ g
e-mail: [email protected].
- s- ^7 c5 @1 oabout 6 to 7 months old, which progressively became
( |" d. t4 Y! A0 g) l8 Xdarker. She was also concerned about the enlarge-4 I8 F' I8 d; t9 |& r' r
ment of his penis and frequent erections. The child
3 j) |+ @' ^5 a6 K0 m% kwas the product of a full-term normal delivery, with
3 L& j* A+ e. T- j9 a) D1 Ha birth weight of 7 lb 14 oz, and birth length of4 ]3 S0 t6 y6 s1 ?& G9 w* P
20 inches. He was breast-fed throughout the first year2 ?" ?8 e- e* G- g7 Y
of life and was still receiving breast milk along with) d3 ^1 S% b; z8 U3 ?8 x
solid food. He had no hospitalizations or surgery,
6 ]' v7 U. S* e# i/ L: x8 qand his psychosocial and psychomotor development
1 Z2 z% y; b2 i3 d; D3 ?4 I8 owas age appropriate.
1 `+ Z) T2 J. I( o1 w  gThe family history was remarkable for the father,
. X  s- T- g+ {0 V; o! i" M7 }0 jwho was diagnosed with hypothyroidism at age 16,6 t" `+ d' n0 z) C& C" A
which was treated with thyroxine. The father’s' Y3 v! a2 ]( K; N, b8 a
height was 6 feet, and he went through a somewhat
- q7 o/ i8 q6 C5 p+ n: Tearly puberty and had stopped growing by age 14.
" k  T2 Q7 O) W6 aThe father denied taking any other medication. The. l( d7 K9 L6 @$ k
child’s mother was in good health. Her menarche. y& j5 S1 y2 n8 j1 h# U& H
was at 11 years of age, and her height was at 5 feet$ Z) G. |4 z2 I4 F. M
5 inches. There was no other family history of pre-
( g. R/ A. m- ]; o0 m2 v( O. dcocious sexual development in the first-degree rela-) d" V. x$ c" ?( G" ?; O% r( Y+ z
tives. There were no siblings.
$ p* ?0 |+ j6 C! g9 c) IPhysical Examination' w' [5 C* y" A
The physical examination revealed a very active,
2 ?! i" g1 J  {% v9 ^1 kplayful, and healthy boy. The vital signs documented
6 f1 y+ b, u1 s6 ?5 @a blood pressure of 85/50 mm Hg, his length was! N5 C3 A$ {1 Y
90 cm (>97th percentile), and his weight was 14.4 kg/ j0 \8 Z$ b: A2 `0 L
(also >97th percentile). The observed yearly growth4 o5 G- s# E9 X% E0 ^  G$ |7 O! ^
velocity was 30 cm (12 inches). The examination of
2 B9 e- Z8 R( q6 e* T5 Rthe neck revealed no thyroid enlargement.
& n. c+ u. u4 ZThe genitourinary examination was remarkable for( P9 e" l* ^& J$ ]/ `1 H- p
enlargement of the penis, with a stretched length of) e$ T8 P0 L3 j5 f( l
8 cm and a width of 2 cm. The glans penis was very well$ O% L5 c5 i  U) @9 D! X  i! g3 E
developed. The pubic hair was Tanner II, mostly around
' H6 f2 \  ~9 o5409 R' T7 s0 G2 j) \- I# ~) q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: c. _2 `' [! E$ x) W3 E- v" y7 _the base of the phallus and was dark and curled. The9 H9 Q3 E! d/ |. y' A% z  W" S
testicular volume was prepubertal at 2 mL each.8 T# g) [  l7 ^' Z- o
The skin was moist and smooth and somewhat
0 f% z/ C9 @; Qoily. No axillary hair was noted. There were no
2 j0 B$ F5 B% C( V5 v& i) J4 Gabnormal skin pigmentations or café-au-lait spots.
7 z% K# b0 C' }! f# X- \" y1 lNeurologic evaluation showed deep tendon reflex 2+3 {$ t: R$ L9 Q; b; j
bilateral and symmetrical. There was no suggestion
- N; ^5 f/ r* E, n/ F$ l2 D6 Dof papilledema.+ U& c* |  w1 ]- R8 Z6 n' O' }7 D/ W
Laboratory Evaluation
4 Z& E8 O- g2 {6 Y7 C! n/ |8 IThe bone age was consistent with 28 months by
$ U* j$ E, P) ]+ z" n, v" Fusing the standard of Greulich and Pyle at a chrono-) O# p4 Y; y$ X( m
logic age of 16 months (advanced).5 Chromosomal# d! Y, W8 H+ A% f5 N) D. E
karyotype was 46XY. The thyroid function test
9 t* }  H; a* q- O; S) @showed a free T4 of 1.69 ng/dL, and thyroid stimu-% n& \/ N3 M) I8 X' `4 a' l0 O( c
lating hormone level was 1.3 µIU/mL (both normal).
0 m- d' f( |* w) }, a' {9 M' O# kThe concentrations of serum electrolytes, blood
# e, k# G7 B0 V! h5 g8 C' {) Aurea nitrogen, creatinine, and calcium all were
2 f9 _6 N) O$ ]8 p6 ^6 S  U2 Twithin normal range for his age. The concentration1 E5 _% p4 G5 O. u1 y
of serum 17-hydroxyprogesterone was 16 ng/dL2 Q! r8 b: i( g
(normal, 3 to 90 ng/dL), androstenedione was 20
; [1 G& Z0 D  X# }0 ^+ Kng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ h3 f. |9 P0 B3 |5 H' K
terone was 38 ng/dL (normal, 50 to 760 ng/dL),2 z9 k# M( _6 ]' X' q& J; @
desoxycorticosterone was 4.3 ng/dL (normal, 7 to; y; l. h" e  F& d
49ng/dL), 11-desoxycortisol (specific compound S)
' y+ D  Z' K1 ^5 Awas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-: C5 l' R, q: K
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total2 c( e. G/ s7 ?) R+ }
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; x; \. r  k! {7 h( aand β-human chorionic gonadotropin was less than
8 R/ K0 y* S3 j/ f& u* e5 mIU/mL (normal <5 mIU/mL). Serum follicular/ E2 A7 `$ ~% [
stimulating hormone and leuteinizing hormone7 ]  D% N+ Q- ]- h$ f
concentrations were less than 0.05 mIU/mL- S3 a, }! p/ J, T
(prepubertal).
9 p: Y: K; {8 q$ VThe parents were notified about the laboratory2 x1 E) E9 G& Y& B; l
results and were informed that all of the tests were
! V) `* g6 y9 h9 b% c. D4 d9 Ynormal except the testosterone level was high. The
7 |2 ^9 r4 `3 _( \7 R. Gfollow-up visit was arranged within a few weeks to7 s+ c, g9 x- \+ E3 J4 S  X
obtain testicular and abdominal sonograms; how-/ x$ j1 Y; u# [9 M& l
ever, the family did not return for 4 months.$ w. ~( E8 V; m1 _/ N
Physical examination at this time revealed that the
3 m( J2 m3 ]3 M6 n. \1 Zchild had grown 2.5 cm in 4 months and had gained
# }8 r* P$ J" K1 c9 a0 g2 kg of weight. Physical examination remained4 P9 \  y, T, U: Q- b: R/ x
unchanged. Surprisingly, the pubic hair almost com-
- Q' R, ?! E* q, Kpletely disappeared except for a few vellous hairs at
+ t! e$ M% I- B0 Kthe base of the phallus. Testicular volume was still 2
# F0 W9 F9 C1 o' R% B" a  HmL, and the size of the penis remained unchanged.
4 ^& _/ _$ v! s/ S% I2 P  sThe mother also said that the boy was no longer hav-: E  L' o/ n6 i, j" P. [4 \/ S% _: e7 H
ing frequent erections.
2 _; i; s/ C- w; k5 @0 ]$ W( nBoth parents were again questioned about use of
( r! [& \! ]& m; p; P6 @any ointment/creams that they may have applied to- q3 T- F: t  v* R
the child’s skin. This time the father admitted the7 u7 w: h" M' Y0 A" M8 t% X& x
Topical Testosterone Exposure / Bhowmick et al 541
* D9 P/ w* S3 X% Y! Zuse of testosterone gel twice daily that he was apply-
2 y2 C2 A. _: n5 e  k' n) \/ ?ing over his own shoulders, chest, and back area for) {- i$ \9 n+ o$ [- P
a year. The father also revealed he was embarrassed3 f; Q# `& d# ~' Y1 n; c6 S- L
to disclose that he was using a testosterone gel pre-
6 D2 _; f3 P0 ]0 K& Dscribed by his family physician for decreased libido$ N: q) S- y1 {% q" a
secondary to depression.* A% r' r8 I0 I
The child slept in the same bed with parents.
) t' [0 e# x4 C, V! ^. [, i5 KThe father would hug the baby and hold him on his8 N* [1 u1 K/ ]! A! G( \0 p
chest for a considerable period of time, causing sig-
) d9 W. D. s* [: e% E+ Qnificant bare skin contact between baby and father.8 k  W# p6 u3 T
The father also admitted that after the phone call,4 ]6 f! Q# p0 x" w& X7 X  L
when he learned the testosterone level in the baby% n; F  \6 s+ ?; J: e
was high, he then read the product information- K  e: u% Q) B% U) T) o3 [/ H
packet and concluded that it was most likely the rea-
! C# p8 {6 S, z& B6 u3 s- O5 Z# eson for the child’s virilization. At that time, they1 C  r% {+ V$ Y7 E4 c( V
decided to put the baby in a separate bed, and the: R. n( y6 N8 s0 v- X
father was not hugging him with bare skin and had
# U. R, K- x, U' H: b" mbeen using protective clothing. A repeat testosterone' T; t: @9 E: }* k  x: m6 ^4 c
test was ordered, but the family did not go to the1 D! d! l4 g$ l0 i- R
laboratory to obtain the test.
, J. _( |( z6 y# @: a; V0 bDiscussion
& u/ s9 O' p( U, G3 hPrecocious puberty in boys is defined as secondary
, q/ z# J# U4 l) hsexual development before 9 years of age.1,4# s# J1 v4 Y% q1 P
Precocious puberty is termed as central (true) when
) o& A( P0 S5 S9 a/ x# sit is caused by the premature activation of hypo-2 @; a1 V. g# o/ C) [6 z, ~
thalamic pituitary gonadal axis. CPP is more com-; ]% Z+ Z8 d9 I- j* z8 }
mon in girls than in boys.1,3 Most boys with CPP$ I4 [- B! P# z4 J# l4 V5 M; e
may have a central nervous system lesion that is
1 b4 Z0 c+ [7 X2 y" H/ N: kresponsible for the early activation of the hypothal-* [8 }! E* I1 O8 {# m; ^
amic pituitary gonadal axis.1-3 Thus, greater empha-6 A' v0 o8 P7 E* M
sis has been given to neuroradiologic imaging in
1 g0 D( [* I" O  y2 w1 Eboys with precocious puberty. In addition to viril-0 P) K. o3 o6 X9 o/ D
ization, the clinical hallmark of CPP is the symmet-
% D( W# ~* ]2 U) p6 W( S- ?rical testicular growth secondary to stimulation by% G: V" }3 @. a( x( W2 p3 P9 i
gonadotropins.1,33 j7 ?: `1 A+ n5 b8 C2 q: p
Gonadotropin-independent peripheral preco-
8 a5 Z8 h, @2 k( ^/ m7 Q" xcious puberty in boys also results from inappropriate
( {+ v9 d% o4 Qandrogenic stimulation from either endogenous or
, \, P; e8 U6 H' h1 x% `' t6 ?8 ^9 ?% ~exogenous sources, nonpituitary gonadotropin stim-
4 O& J' g! ]3 u- fulation, and rare activating mutations.3 Virilizing
6 y9 A7 ~3 I; G# d/ ?1 Lcongenital adrenal hyperplasia producing excessive2 V/ w6 x1 ?$ j+ m
adrenal androgens is a common cause of precocious, x  x8 H( F- v: S) V
puberty in boys.3,4
/ Y7 P5 O$ l5 g, G% d3 P, h; G4 GThe most common form of congenital adrenal) n# G. I/ z( _# t; v# _
hyperplasia is the 21-hydroxylase enzyme deficiency.
, v$ ~" l, p1 _# ~The 11-β hydroxylase deficiency may also result in
5 x& y2 d' o/ A  Z! rexcessive adrenal androgen production, and rarely,2 Z( S& M- x  D* ?- A
an adrenal tumor may also cause adrenal androgen
' X* j2 Z; q* K  A  b8 w+ nexcess.1,36 ^# B4 U  X7 c3 H. j: m
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 ?, F7 k2 `, s- P542 Clinical Pediatrics / Vol. 46, No. 6, July 2007/ W# [0 e9 N" p2 u3 {: q
A unique entity of male-limited gonadotropin-
* x$ h. F. ~& [& M3 Windependent precocious puberty, which is also known
* Q: U6 t2 _$ F% Z$ O( @" ^. h. [: }as testotoxicosis, may cause precocious puberty at a
6 ?8 k4 G2 S' ?) h) j* \very young age. The physical findings in these boys
4 S: ?4 A6 g/ b$ o) ^! ]; p9 Ewith this disorder are full pubertal development,
  g5 `& `& A- L* b3 e% Dincluding bilateral testicular growth, similar to boys
1 p! U. `+ W) E( Qwith CPP. The gonadotropin levels in this disorder
: e- j( e/ B) d' n. m9 T/ t3 \are suppressed to prepubertal levels and do not show/ j2 N" ?4 z9 y) j$ L0 B4 ^6 z( d0 I
pubertal response of gonadotropin after gonadotropin-" O! X* Y, t. p  W
releasing hormone stimulation. This is a sex-linked
$ S" f+ a3 a6 d! Y# K: nautosomal dominant disorder that affects only
$ X. \$ J$ n0 O4 \$ ]males; therefore, other male members of the family8 G5 L2 v' y; n' A# ]- q1 x2 f
may have similar precocious puberty.33 F+ F% e1 @) ?2 ]
In our patient, physical examination was incon-
9 b: j( _% {8 g( t. y1 r+ Z& Jsistent with true precocious puberty since his testi-$ X, M' g( y0 {# M
cles were prepubertal in size. However, testotoxicosis
  _' {0 ]& P6 P/ a8 Qwas in the differential diagnosis because his father3 ?4 b5 s7 Z& w5 o
started puberty somewhat early, and occasionally,
8 F! X1 b4 _, e9 qtesticular enlargement is not that evident in the2 t1 N0 b1 D, J4 v- s: F
beginning of this process.1 In the absence of a neg-
/ i- w( z2 R9 C" ~4 oative initial history of androgen exposure, our* a0 |1 J% t5 X5 k$ D4 J, C
biggest concern was virilizing adrenal hyperplasia,: G9 Y2 A0 q$ x2 D# F2 I
either 21-hydroxylase deficiency or 11-β hydroxylase6 U& C. @3 U; C4 u( [3 C
deficiency. Those diagnoses were excluded by find-) o6 t1 U8 {, S4 S( M
ing the normal level of adrenal steroids.
4 i0 S* ?, j! F' i: d# W/ _The diagnosis of exogenous androgens was strongly
1 r# a; `( B' ssuspected in a follow-up visit after 4 months because! Y& S9 o; e0 t+ A
the physical examination revealed the complete disap-
/ Y6 L4 @2 L: ], z  t. ^/ ]7 spearance of pubic hair, normal growth velocity, and
8 w$ ]: N1 n3 m1 P, Ndecreased erections. The father admitted using a testos-! _8 \; S) u2 g9 P& p9 g
terone gel, which he concealed at first visit. He was
5 c) \0 m" E2 F1 z* y; z/ P& jusing it rather frequently, twice a day. The Physicians’
+ O' U+ i# b$ B0 sDesk Reference, or package insert of this product, gel or8 n; W5 Z7 v# ^: Q. O6 V* N0 Z
cream, cautions about dermal testosterone transfer to
" i( g$ Y' o0 punprotected females through direct skin exposure.
9 r3 X% G: \- h) L6 A2 ]Serum testosterone level was found to be 2 times the  Z3 O' @& c+ v
baseline value in those females who were exposed to
" W1 C8 c( C  Feven 15 minutes of direct skin contact with their male
/ C2 G; m' G; a+ f) Q3 apartners.6 However, when a shirt covered the applica-$ ?( P: f- \* A6 w, ^- Y/ T
tion site, this testosterone transfer was prevented.
/ N' I# B8 B* a2 a. o' IOur patient’s testosterone level was 60 ng/mL,. h; f: i0 [: k( y
which was clearly high. Some studies suggest that9 q2 B; x. ^5 I- ]' `  d  a2 l+ x
dermal conversion of testosterone to dihydrotestos-
$ R% B, j5 t, l( @1 g) rterone, which is a more potent metabolite, is more
* l2 h3 R( X( S$ x; q: pactive in young children exposed to testosterone
  F6 h" H' q3 I3 l% Zexogenously7; however, we did not measure a dihy-
7 g( ?# q/ p3 w6 p- E' s( ?drotestosterone level in our patient. In addition to
& c6 [' ^- X$ q1 H3 x6 J! B1 xvirilization, exposure to exogenous testosterone in# w* L; g3 c1 ?2 x% x
children results in an increase in growth velocity and# r- U4 [. q0 U; j2 S. v
advanced bone age, as seen in our patient.
+ H  c$ p% }$ X( y4 x. JThe long-term effect of androgen exposure during
% h# j' u4 y( q( Learly childhood on pubertal development and final: C0 h+ o5 Q% Q0 _/ d
adult height are not fully known and always remain
8 X: n1 a  F8 ^. R- N( Ya concern. Children treated with short-term testos-
6 p2 J) V. S4 {: S, @+ p$ y1 @) b$ oterone injection or topical androgen may exhibit some# _( Q7 h# W) O1 ?5 }6 Y
acceleration of the skeletal maturation; however, after* H1 M6 p# H" L( b
cessation of treatment, the rate of bone maturation% K2 E% d0 g. E4 H
decelerates and gradually returns to normal.8,9' C/ C$ W$ `" T5 K5 B: F
There are conflicting reports and controversy
7 h' i5 M  Z; ?6 \over the effect of early androgen exposure on adult
0 W6 P+ f% F! f) Rpenile length.10,11 Some reports suggest subnormal
! H# b$ |7 H& m8 padult penile length, apparently because of downreg-. p9 ?$ |6 r  ^( N: z8 K: K
ulation of androgen receptor number.10,12 However,8 V- g, [! T& _2 l% J
Sutherland et al13 did not find a correlation between( ]+ t1 ^1 m! ^* o! ?2 C) V
childhood testosterone exposure and reduced adult5 ]7 X  x- x% _% \; t
penile length in clinical studies.
) l$ g% |* Q9 b. X/ L6 ZNonetheless, we do not believe our patient is8 {( q& d' K+ M
going to experience any of the untoward effects from
8 h0 j" @) ~0 K1 T8 Y; @4 Xtestosterone exposure as mentioned earlier because
4 ]; \# F& S+ _6 y8 a! Nthe exposure was not for a prolonged period of time.
% @/ s: P9 s2 y( Q, c7 oAlthough the bone age was advanced at the time of( V7 k" T+ k- R8 C4 A
diagnosis, the child had a normal growth velocity at
( y  \/ i! M8 p0 D4 mthe follow-up visit. It is hoped that his final adult6 {7 W9 A5 [& N6 x6 T
height will not be affected.$ g5 n: E8 f* R% n& K
Although rarely reported, the widespread avail-
! M8 L( _0 m; j4 _# gability of androgen products in our society may
, J- T: d8 @% c4 o! W4 x  U3 n* T+ Tindeed cause more virilization in male or female
- U3 m3 H: c3 H( ichildren than one would realize. Exposure to andro-8 D9 ~# W, V' t
gen products must be considered and specific ques-# X" V. v, }6 [/ N  _
tioning about the use of a testosterone product or, ~$ h& O/ q! s  F4 J4 d% w
gel should be asked of the family members during, B& F9 \! c1 ~
the evaluation of any children who present with vir-' ]$ d2 U$ z, l2 z5 o
ilization or peripheral precocious puberty. The diag-% ]/ I% s6 x$ f
nosis can be established by just a few tests and by
' C' X" ?7 u# B2 ?# bappropriate history. The inability to obtain such a# t$ I7 _$ ~; P* K% o+ q; G  N
history, or failure to ask the specific questions, may4 h* W& ]& a4 I  b
result in extensive, unnecessary, and expensive1 _4 c9 m. F- Q# u4 h* V+ r- u  t
investigation. The primary care physician should be
5 B- H# t0 c5 u5 P% d) Raware of this fact, because most of these children9 ?+ S  f7 S, M& h/ S
may initially present in their practice. The Physicians’7 s5 m' g4 u4 I" E1 C, i
Desk Reference and package insert should also put a( T+ L% t) N- f
warning about the virilizing effect on a male or  o7 I" E- w$ a: O
female child who might come in contact with some-
+ e* g" O! U; G; p  i8 @( T. bone using any of these products.
- t& [/ }# n" E8 Y" [+ e, j, `! M( bReferences
& W, P) j0 h9 F2 E  ^/ h# Y" k9 g1. Styne DM. The testes: disorder of sexual differentiation
/ Y, p- C& E( K8 sand puberty in the male. In: Sperling MA, ed. Pediatric
! ^; Y: ~# I, o# T- ~% gEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;: `( S( ^+ j7 x9 i- C5 G
2002: 565-628.
- H! v8 K% Z6 J' G3 ^% y$ l2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious& k/ C. F! q  C7 Y) m
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old0 Y5 y% H$ F( r. q  ]3 h3 e, B
Boy Induced by Indirect Topical
+ }9 k* N8 O, ^+ p. X3 K% S, L' i& zExposure to Testosterone) L/ O- H3 f' Q9 \. i. v! p: t, o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
" G; U1 e( x, A' V/ K+ _/ _+ sand Kenneth R. Rettig, MD12 \0 [. S$ l; @' [  S2 X0 Q
Clinical Pediatrics
8 P3 \* ]5 f$ w8 h$ s$ fVolume 46 Number 6* Z. K% V/ |; ]* [7 K# i; P3 K3 l
July 2007 540-543' S1 s6 @+ K: S
© 2007 Sage Publications
  f7 Q. n( O8 J% t0 F10.1177/0009922806296651
5 Z; H4 E7 h0 d9 W: o' ~" ghttp://clp.sagepub.com) l3 M$ p+ k8 ]0 ]" t7 [8 f6 y
hosted at
- C" p+ G0 K, U; Shttp://online.sagepub.com
% E7 Y9 U! v% r8 l; P  D; APrecocious puberty in boys, central or peripheral,& x8 U6 ~7 `( l- }4 Q: J
is a significant concern for physicians. Central
  r( k5 N5 b. t4 [# Lprecocious puberty (CPP), which is mediated: l* g2 R) l* e. D
through the hypothalamic pituitary gonadal axis, has
3 \5 f' C# @0 j: P' r1 }a higher incidence of organic central nervous system
- i/ B8 e! e: x4 ^' Clesions in boys.1,2 Virilization in boys, as manifested
" {/ y( z. U! |" y7 p1 _/ e# Bby enlargement of the penis, development of pubic
# K8 S) T/ L  o4 Thair, and facial acne without enlargement of testi-; m+ ]3 u; Q. M/ r
cles, suggests peripheral or pseudopuberty.1-3 We
: X/ p; U7 M$ f/ @report a 16-month-old boy who presented with the
4 N' Q" {* W! M: j  A# y/ Jenlargement of the phallus and pubic hair develop-
0 e# X2 O) w; k+ t8 p2 d3 ument without testicular enlargement, which was due! Y6 |2 x4 T% _" h4 E
to the unintentional exposure to androgen gel used by
% p4 V* Y8 H( H8 l. e. @the father. The family initially concealed this infor-
+ C0 V5 E7 {* y- \  Z3 D+ }mation, resulting in an extensive work-up for this; Z. W5 a* C/ k) Q
child. Given the widespread and easy availability of# H$ r# r- X' ~6 X) \8 W) z+ ?
testosterone gel and cream, we believe this is proba-1 c( F( h. M2 S8 ]+ c
bly more common than the rare case report in the. k- q' W' a! p& H7 F1 }
literature.4+ T$ \. r& Y, n. c$ u, [
Patient Report
! |& \" M; O! HA 16-month-old white child was referred to the8 i. V- y* ]- X7 i: J5 j' U3 ?
endocrine clinic by his pediatrician with the concern
% Z, R6 l+ O2 R/ `7 o) x  mof early sexual development. His mother noticed
& X/ y5 t* }6 n4 e7 xlight colored pubic hair development when he was
# a; @  N4 Q9 aFrom the 1Division of Pediatric Endocrinology, 2University of+ A' J* n  I2 r( _: q
South Alabama Medical Center, Mobile, Alabama.. o1 y2 n8 ?/ i# z+ h) M7 a
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 d: ~  q7 p4 A' Z9 H2 v; M. |Professor of Pediatrics, University of South Alabama, College of
' F  Q# _# [! EMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. w$ y7 F) E# m8 e5 o5 N% x) B% Xe-mail: [email protected].4 S/ J: Q" D) H7 ]
about 6 to 7 months old, which progressively became
  X5 A" B( P5 E- K; R/ r' rdarker. She was also concerned about the enlarge-. z/ V! H0 N* q# B! O2 d
ment of his penis and frequent erections. The child* M3 I7 S; G8 c$ B
was the product of a full-term normal delivery, with
" k( n' Z0 L2 Z  ~5 D: la birth weight of 7 lb 14 oz, and birth length of- d+ o/ e4 ^" }* }0 e3 e5 i( a
20 inches. He was breast-fed throughout the first year
! r, ~; `" o5 a3 V- Z( {2 Y% e% Hof life and was still receiving breast milk along with
! T3 e3 w' z0 \! D5 Bsolid food. He had no hospitalizations or surgery,
0 b/ `+ t* Y3 n8 P& c9 Fand his psychosocial and psychomotor development
( A2 C: M* |4 C) n9 d8 M6 {was age appropriate.& o1 M% m. m+ Q' B
The family history was remarkable for the father,
3 ]) x2 {- _, f5 x) owho was diagnosed with hypothyroidism at age 16,- U" Z& p8 y, q1 w5 j
which was treated with thyroxine. The father’s2 Y& g. f5 Z; B, s; N4 H' Q
height was 6 feet, and he went through a somewhat
+ t  Z& p; F6 B" b) Pearly puberty and had stopped growing by age 14.: ~& o3 o' j, a& s$ ~: t9 M' d" o% s
The father denied taking any other medication. The
/ d2 P( n8 c" a" y* Tchild’s mother was in good health. Her menarche6 w- k$ z& z. S2 C  C# S
was at 11 years of age, and her height was at 5 feet8 y- j: O4 h0 w4 a9 j% S2 y
5 inches. There was no other family history of pre-( N3 H, S7 @; T9 c. k
cocious sexual development in the first-degree rela-" Y8 ^3 u2 A' V, Y2 ?; Y
tives. There were no siblings.
+ v  c8 G+ `# h2 |; YPhysical Examination
5 O1 p! w, D& |+ t! UThe physical examination revealed a very active,' V" F' i! I5 r% ?; h
playful, and healthy boy. The vital signs documented& s* W! l$ ^" a- d4 K
a blood pressure of 85/50 mm Hg, his length was
/ e3 d/ u7 H' P& J* p90 cm (>97th percentile), and his weight was 14.4 kg
% ?4 |9 O% w' z& r1 `1 S0 l) i(also >97th percentile). The observed yearly growth
" Z2 ~4 e( }, X) ?; Y2 [velocity was 30 cm (12 inches). The examination of0 a2 W4 \; r8 ~" j8 e' ?. Q  @
the neck revealed no thyroid enlargement.
) n  W0 T% k( X, z; XThe genitourinary examination was remarkable for6 S6 I- N9 B/ S9 @& q
enlargement of the penis, with a stretched length of
' P) m( l* L) o" ~) c6 H8 cm and a width of 2 cm. The glans penis was very well
, s4 @( U& S2 t# Ddeveloped. The pubic hair was Tanner II, mostly around
6 K9 c6 l* F8 X. S3 q+ R540
; S" e- q0 s2 xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" S- j) p0 o; E* k; s1 _
the base of the phallus and was dark and curled. The6 a% d# z4 c+ H$ D/ j6 K& ^. W% i
testicular volume was prepubertal at 2 mL each.
9 w  E, Y* [5 n" _* U1 v6 J" t0 l/ oThe skin was moist and smooth and somewhat
& v7 v; ?, z1 W: g6 Loily. No axillary hair was noted. There were no5 M6 q+ q  ~. t: |1 d: A
abnormal skin pigmentations or café-au-lait spots.
4 I/ [  ^+ E# \; yNeurologic evaluation showed deep tendon reflex 2+
+ M* D8 q2 D# I' j7 a' C) n" }bilateral and symmetrical. There was no suggestion: C9 f2 B% Z6 K; E% ?* C3 a
of papilledema.4 F& W5 x5 ?. j: h2 O- F( g$ ?6 z! e" Z
Laboratory Evaluation) B$ t: C  Y* F" O. s# R
The bone age was consistent with 28 months by3 q& N7 ^0 K# D6 H2 @( A
using the standard of Greulich and Pyle at a chrono-; {7 H7 x! F$ b2 B
logic age of 16 months (advanced).5 Chromosomal
+ {0 m" X3 T0 \7 I! j) |. ckaryotype was 46XY. The thyroid function test4 b% j; f$ P' ^/ M0 B4 M" d
showed a free T4 of 1.69 ng/dL, and thyroid stimu-, m7 }# Y2 r; ^4 \; `, U& g3 Y8 ~) g
lating hormone level was 1.3 µIU/mL (both normal).
8 V3 ?4 {# j( h" `3 k: JThe concentrations of serum electrolytes, blood& c% Z6 h' e# F9 m) ~. i: G
urea nitrogen, creatinine, and calcium all were
1 ~  z7 {/ o8 @- a) H" _' u  `8 l4 Iwithin normal range for his age. The concentration* }% l* V3 L4 x$ f- r9 H
of serum 17-hydroxyprogesterone was 16 ng/dL/ o8 F1 x1 v; j5 J
(normal, 3 to 90 ng/dL), androstenedione was 20
& {% v# t( H" Mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
1 L1 R2 C6 t/ R) k- h7 ~+ `terone was 38 ng/dL (normal, 50 to 760 ng/dL),' h7 O4 s' v- e! W
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 }0 w. K5 ^, U- [! j2 N49ng/dL), 11-desoxycortisol (specific compound S)4 s9 o, |! z! O8 P; I" `+ {& a
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-3 _0 X+ W* I, d2 Y
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" H- `7 Z" o/ d
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& y, H2 z5 {+ J# v1 U* o: V$ g# w( Oand β-human chorionic gonadotropin was less than1 D, s: ?7 d/ |# [0 l7 @
5 mIU/mL (normal <5 mIU/mL). Serum follicular
% J/ R9 c0 S9 L) \, ]( ystimulating hormone and leuteinizing hormone8 L0 q) r, T# @9 d  h
concentrations were less than 0.05 mIU/mL. l) i% f! m9 W
(prepubertal).* S* B9 ~6 f  x( c2 P% d
The parents were notified about the laboratory
. k5 u: t# t) s1 k) e  \results and were informed that all of the tests were) U" U0 [7 `  s, N1 K
normal except the testosterone level was high. The6 K- p! d& N2 M  V
follow-up visit was arranged within a few weeks to5 n& i; u, P9 Q% X, S
obtain testicular and abdominal sonograms; how-
$ o3 {: u3 k3 g3 D9 q" |ever, the family did not return for 4 months.
  r' s+ j2 a  I  q1 Q# E2 \. iPhysical examination at this time revealed that the
8 @$ [. X3 o9 T  ]child had grown 2.5 cm in 4 months and had gained0 O. ~# m' ~/ m6 F
2 kg of weight. Physical examination remained. P! [! p% @' u7 `) n0 `* O
unchanged. Surprisingly, the pubic hair almost com-2 a/ O' p* L  u* |- T
pletely disappeared except for a few vellous hairs at
& I+ H9 h& P* o! S9 z  Othe base of the phallus. Testicular volume was still 2/ E1 ^; R, P9 r
mL, and the size of the penis remained unchanged.
0 p. c% b, v1 d# S7 |9 a' g; XThe mother also said that the boy was no longer hav-$ H" s1 }- i7 p3 G& _* C
ing frequent erections.) _9 N( L- W2 A$ v6 l$ }
Both parents were again questioned about use of
# A8 a0 u. ?1 Z) M! Z3 |& \: fany ointment/creams that they may have applied to2 M* Y# Q' v1 r& |" p
the child’s skin. This time the father admitted the
" _" c- _, P7 ]8 y/ V9 g6 k& vTopical Testosterone Exposure / Bhowmick et al 541+ V. B' |# x  P) d* l/ v1 t6 o
use of testosterone gel twice daily that he was apply-3 j6 d9 f' N& w8 p8 M+ Z" H6 T
ing over his own shoulders, chest, and back area for% {6 _- o- G/ Y5 r- y
a year. The father also revealed he was embarrassed
% a) s5 t$ l" Kto disclose that he was using a testosterone gel pre-  J5 v4 s2 x# J5 {: B, V
scribed by his family physician for decreased libido
  ?% K% p' V6 g7 J6 ssecondary to depression.- J3 \) g3 z1 i8 I& h: c4 S
The child slept in the same bed with parents.# P" M' Y+ f7 r, _. j' Z. L
The father would hug the baby and hold him on his/ [" ]8 J3 @+ e4 o5 r
chest for a considerable period of time, causing sig-
% l/ k, b: x2 Mnificant bare skin contact between baby and father.8 I+ U( S) X" \. ?, q" u
The father also admitted that after the phone call,
8 r4 z8 Q% r2 h4 ~8 `% M+ xwhen he learned the testosterone level in the baby
) }( {* z5 E9 Q3 vwas high, he then read the product information
8 [7 \. E  N. R9 H: tpacket and concluded that it was most likely the rea-8 W" e- b/ ]$ A  F" F: d
son for the child’s virilization. At that time, they0 F/ L/ M/ I( N2 h. U/ j) a
decided to put the baby in a separate bed, and the
2 W. P% U/ o% o; \3 S  Mfather was not hugging him with bare skin and had8 X6 s$ {! V- I4 i) \) L8 e
been using protective clothing. A repeat testosterone
$ C% M  M; k1 L* O' N5 Otest was ordered, but the family did not go to the
6 C5 g. k2 [9 b3 Mlaboratory to obtain the test.
2 L7 `/ Q7 o0 fDiscussion
+ J0 o6 F; z% E9 \: [+ h/ ZPrecocious puberty in boys is defined as secondary- O! R- L6 L7 l" w- g. l/ E9 P5 T9 q
sexual development before 9 years of age.1,4" V# l, _# G7 {) F8 P1 U# C
Precocious puberty is termed as central (true) when9 U+ ?% a! K& B* x6 Q4 O- V: S
it is caused by the premature activation of hypo-5 q% ~; p5 t: U2 O; @& x+ y% s& N: b
thalamic pituitary gonadal axis. CPP is more com-
$ ~: }3 \+ q1 U2 |' R/ |. Q; A* o6 \mon in girls than in boys.1,3 Most boys with CPP, x6 |; _! M# f3 W6 Y
may have a central nervous system lesion that is
  I; n0 z# u5 s: I4 Nresponsible for the early activation of the hypothal-
8 V! F$ W8 q; d* o# Ramic pituitary gonadal axis.1-3 Thus, greater empha-- e9 u% J1 [7 ?) ?( E
sis has been given to neuroradiologic imaging in& D9 z% K% v- H& s4 W" f; O4 I5 @
boys with precocious puberty. In addition to viril-7 i5 x3 g- o4 Y/ Z
ization, the clinical hallmark of CPP is the symmet-
; ]  M$ y$ ^+ Jrical testicular growth secondary to stimulation by/ s" S0 L! H. P7 b) ^  C' S5 G
gonadotropins.1,3
+ t2 i. ^6 c- K, r2 m- tGonadotropin-independent peripheral preco-
: L, F/ P: I3 K7 O4 N* Lcious puberty in boys also results from inappropriate: [- p6 f* K8 [. _+ R* l+ K
androgenic stimulation from either endogenous or+ ]2 d" |8 \& L, h
exogenous sources, nonpituitary gonadotropin stim-
2 m$ Y$ F  k  U# N9 b4 l4 hulation, and rare activating mutations.3 Virilizing
& p# m& w- [+ n& y  B4 ?congenital adrenal hyperplasia producing excessive" O5 S1 {# Q% U6 p
adrenal androgens is a common cause of precocious
. i$ r" K# I' y2 Q! D* N+ E. R4 x% [puberty in boys.3,4' S( [2 T( `7 _' m1 J0 F
The most common form of congenital adrenal; E9 X) p) I! \# D* O
hyperplasia is the 21-hydroxylase enzyme deficiency.
3 ?# X/ T  e. @The 11-β hydroxylase deficiency may also result in
, I$ ~, V& N* ]8 Nexcessive adrenal androgen production, and rarely,
9 Q0 G2 I; t: |6 K7 Uan adrenal tumor may also cause adrenal androgen
7 w+ }$ V) u! @( Lexcess.1,3  x$ X0 B" i2 W  t) g/ w
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from- Q- k+ _, l" t- I  M7 b8 f
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007' f8 O! _0 ~4 \
A unique entity of male-limited gonadotropin-% @- \3 \) r8 ]: Q- ~. {7 |
independent precocious puberty, which is also known- R0 z7 K' e5 W/ \
as testotoxicosis, may cause precocious puberty at a2 M) W) h8 Q2 w$ r: Y* l
very young age. The physical findings in these boys
: N/ g6 T: j1 w8 o: {with this disorder are full pubertal development,
# M; \& T: v) E- Z- v% ^# ?including bilateral testicular growth, similar to boys2 q3 X. S. F" Z
with CPP. The gonadotropin levels in this disorder$ g# q* f6 c$ W
are suppressed to prepubertal levels and do not show5 N5 P4 Z( {2 ~
pubertal response of gonadotropin after gonadotropin-
4 |0 g7 P- k0 Kreleasing hormone stimulation. This is a sex-linked& n  C9 P2 P- x* ~
autosomal dominant disorder that affects only
/ ]- x* o4 X& R. B. Umales; therefore, other male members of the family
, d6 E9 u1 w2 h* W4 nmay have similar precocious puberty.3
% u% Y* K& C7 ^" i% `3 Z3 Y- L0 ZIn our patient, physical examination was incon-" \* M- I, c5 C, P5 A; o. T
sistent with true precocious puberty since his testi-4 @7 b! s7 F: s4 c$ U$ o4 v
cles were prepubertal in size. However, testotoxicosis
6 F. R3 n- c: O( s) Z% ]$ x/ Rwas in the differential diagnosis because his father
! [# ~2 K6 q! lstarted puberty somewhat early, and occasionally,
) p$ h; M- c: a# `$ [- }testicular enlargement is not that evident in the
$ q. K+ C5 w6 X/ _9 N. @7 T' Bbeginning of this process.1 In the absence of a neg-' w4 W9 }) m% a" g: E7 u9 @
ative initial history of androgen exposure, our
2 h: L* [* Q! b  K6 a3 l0 Wbiggest concern was virilizing adrenal hyperplasia,4 C: Y( d4 e6 O$ F) R# R
either 21-hydroxylase deficiency or 11-β hydroxylase
! V) l1 t) b3 m6 Gdeficiency. Those diagnoses were excluded by find-
+ o9 I9 d' k+ d" }, Eing the normal level of adrenal steroids.: C& ?: t) d+ Q% Y4 B& Q
The diagnosis of exogenous androgens was strongly( n% b1 L# T& R- _
suspected in a follow-up visit after 4 months because
  n2 f! D6 h3 p9 `. N1 V" g) _, M1 K% Sthe physical examination revealed the complete disap-& C( x! X" B# B9 h* Q
pearance of pubic hair, normal growth velocity, and3 ?! X' S% B+ _3 q: a# o
decreased erections. The father admitted using a testos-
0 [; b+ L, ?; x: q7 b, m* Gterone gel, which he concealed at first visit. He was% d  q1 p9 y" g6 T
using it rather frequently, twice a day. The Physicians’
8 @  w* O: {, u* `' z) aDesk Reference, or package insert of this product, gel or
  x: q1 [6 [8 M8 E9 Tcream, cautions about dermal testosterone transfer to
2 L% j2 e0 q( z+ \$ iunprotected females through direct skin exposure.! q/ i. y+ |  ~3 \' G
Serum testosterone level was found to be 2 times the, a8 C# T% M4 B4 u+ c5 r/ a, l; J
baseline value in those females who were exposed to
/ Y6 n8 [; D  N0 f4 m$ Neven 15 minutes of direct skin contact with their male
+ V6 c6 J7 ], ?/ Y3 }partners.6 However, when a shirt covered the applica-8 V/ O0 r$ i9 I" o4 A
tion site, this testosterone transfer was prevented./ b% d. L+ n" `- ?0 D% q1 R, d! {2 s
Our patient’s testosterone level was 60 ng/mL,
! k  Q" r+ C5 V0 h. W9 @, u* M8 kwhich was clearly high. Some studies suggest that
& [2 j( c8 m: c  Y/ g: u" z$ bdermal conversion of testosterone to dihydrotestos-
$ B# g, ]: S' I. q$ Z+ ^2 O- Qterone, which is a more potent metabolite, is more
2 f4 m' z" @0 w% p# y: |active in young children exposed to testosterone
& A: O. U& c/ v# W* L/ n% r- c5 ?" u& wexogenously7; however, we did not measure a dihy-5 C* w. d& Q( ^( ]% J3 t$ `
drotestosterone level in our patient. In addition to" ^$ E$ K" @/ `+ {9 T0 A) d% O
virilization, exposure to exogenous testosterone in
2 s" S" R* \+ ?children results in an increase in growth velocity and
+ ^" e. Y! ~/ B, U7 o: b8 _advanced bone age, as seen in our patient.3 |. L' u+ j+ n4 ^) p/ z, ]
The long-term effect of androgen exposure during8 S# k# d( g2 ?* L3 n* i0 v+ r2 T
early childhood on pubertal development and final
. @0 m3 g5 m- Z" j/ }! aadult height are not fully known and always remain% w" I4 a4 i5 w* L# J
a concern. Children treated with short-term testos-6 m: r* d& c% X3 l" }$ X
terone injection or topical androgen may exhibit some4 K; u  C/ Q* Y& f# Y) |
acceleration of the skeletal maturation; however, after
6 l" }' E$ C* o8 Xcessation of treatment, the rate of bone maturation
' j* A# ^6 P/ G# I8 idecelerates and gradually returns to normal.8,9
9 @/ {( j& a8 x/ {; j. e; JThere are conflicting reports and controversy
3 x& O5 F! @2 R& i; W9 j0 d8 _over the effect of early androgen exposure on adult
4 @) r, S9 F4 b2 \4 X" Dpenile length.10,11 Some reports suggest subnormal3 m2 [) R1 E3 a, r& d0 T: `! }
adult penile length, apparently because of downreg-7 H- r7 l. p4 \% [
ulation of androgen receptor number.10,12 However,7 v' g# }- V# W; U+ W3 _
Sutherland et al13 did not find a correlation between$ N+ r  P8 Y% y( p! @
childhood testosterone exposure and reduced adult
4 J! h2 Y' A# i, kpenile length in clinical studies.
2 A9 n2 y" @1 K/ ^Nonetheless, we do not believe our patient is
; ?9 e" m1 n7 _2 I( Bgoing to experience any of the untoward effects from/ S. U/ V: Z" y
testosterone exposure as mentioned earlier because: R; P  G) N9 V2 X
the exposure was not for a prolonged period of time.( u7 n" w* e3 _2 c* ^# ^
Although the bone age was advanced at the time of
, @" x% h4 ?. j. f7 ~2 Y, P  adiagnosis, the child had a normal growth velocity at
: s; D+ m! [/ D8 u3 j' mthe follow-up visit. It is hoped that his final adult' C) f6 Y5 e0 Q, S8 Z
height will not be affected., w$ y" J" H& h4 A
Although rarely reported, the widespread avail-5 ], h# s* |8 r& s+ m; b
ability of androgen products in our society may4 i) K1 ~: R7 B, i# o
indeed cause more virilization in male or female
7 _# q" c# I( M! e) k6 |children than one would realize. Exposure to andro-+ R7 _+ p; }- k8 k& }$ L/ Z. H
gen products must be considered and specific ques-
% p1 ^' s4 Z9 i& T! D/ n! q0 ytioning about the use of a testosterone product or; R: e/ u/ \* P  X- g
gel should be asked of the family members during1 `' H- e1 v9 p3 n  m4 _/ k
the evaluation of any children who present with vir-
+ u) r$ _. _# E' p: Wilization or peripheral precocious puberty. The diag-
3 P  S. B7 Y: u; s, N8 y7 _" snosis can be established by just a few tests and by
9 P/ N5 D! Y, j' pappropriate history. The inability to obtain such a
0 u1 J& L) K4 e1 d% \# O# \- d7 chistory, or failure to ask the specific questions, may. W4 t7 T- `+ ?( e+ |& X2 v! P' J
result in extensive, unnecessary, and expensive" _! Y$ X- p. A2 @$ E
investigation. The primary care physician should be
+ _. ?; r% K' F0 d3 e3 s" T3 paware of this fact, because most of these children7 S0 I" p+ H# ]( v$ f; H
may initially present in their practice. The Physicians’
( s! \% L9 [0 N% L9 t: NDesk Reference and package insert should also put a$ H0 T1 E7 Z) Y& f& B8 ]6 a
warning about the virilizing effect on a male or
  v6 Y7 e: P* [% M' Q6 cfemale child who might come in contact with some-
- B0 N2 A' H1 D2 Lone using any of these products.8 Y  c2 y$ G! D% A, r
References
4 Q+ O: S) k: {5 k7 k$ e1. Styne DM. The testes: disorder of sexual differentiation
; S8 s% h& [) band puberty in the male. In: Sperling MA, ed. Pediatric3 ~  A! H4 T+ [- q% C" z
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;, c# \* A5 }1 U
2002: 565-628., j# C+ c% q( Y1 \0 E* ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious8 c2 b& C- I3 E% M) ]( z
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
" C6 |- ]" C- L
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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