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Sexual Precocity in a 16-Month-Old
" N! B! c" F+ Y6 X) o0 Q9 D8 iBoy Induced by Indirect Topical
0 g6 l& D9 y2 D' v1 h0 oExposure to Testosterone
3 c3 L7 h# I# R/ w/ YSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. L4 r* g2 r8 L1 ]! ^
and Kenneth R. Rettig, MD1. b5 d5 x5 M; M' i* H6 a4 K$ b
Clinical Pediatrics  s  }+ y4 R+ F7 K7 \: @9 M
Volume 46 Number 6
) {3 [+ k. H, UJuly 2007 540-5431 ^2 {' D  j5 T6 z0 D
© 2007 Sage Publications
; a3 N1 W& x; T  x6 b8 O10.1177/00099228062966510 G0 l* P2 ]1 b9 Z9 p; _; Y# L
http://clp.sagepub.com
) G1 ^* n. ]+ y# U+ Phosted at
, d  P+ B& x' F/ |) xhttp://online.sagepub.com: X/ @+ w  {3 y' J
Precocious puberty in boys, central or peripheral,
3 V1 N+ j8 _) [! Yis a significant concern for physicians. Central
' V' v% c6 I" Z- t5 v) cprecocious puberty (CPP), which is mediated5 P. I5 n2 E: [) {
through the hypothalamic pituitary gonadal axis, has
6 ^+ S) q2 K' B% `a higher incidence of organic central nervous system# ^, x" ~0 q6 X( w  g8 o& u
lesions in boys.1,2 Virilization in boys, as manifested+ T3 K! y8 q8 y% U& [+ T0 W7 Z
by enlargement of the penis, development of pubic
" X3 M, u7 T! J1 Phair, and facial acne without enlargement of testi-
: _: n9 u' e4 D! Mcles, suggests peripheral or pseudopuberty.1-3 We' k; J+ i0 I/ e' r& B6 U$ `
report a 16-month-old boy who presented with the# \$ s+ O% y/ o% o& r
enlargement of the phallus and pubic hair develop-/ P8 `9 d7 v) [
ment without testicular enlargement, which was due3 x' C! t" i# q2 B7 y" K
to the unintentional exposure to androgen gel used by, {, H' G# u1 b
the father. The family initially concealed this infor-6 u6 ?* K/ x  A+ u
mation, resulting in an extensive work-up for this. `/ W: z0 t% k
child. Given the widespread and easy availability of3 i1 Q. K* w0 O, G
testosterone gel and cream, we believe this is proba-% i9 {  h9 S6 c
bly more common than the rare case report in the8 ]+ O3 z) B3 u2 m9 T6 i8 ^2 o0 j3 {
literature.4
5 B8 ]8 z' r# u  G$ T# Y5 YPatient Report7 ]& ]: E5 }' Y- }% [
A 16-month-old white child was referred to the# y9 j; O' U. o/ ~) c6 L
endocrine clinic by his pediatrician with the concern. k4 |1 }* j4 o% w+ s, Z) e# O
of early sexual development. His mother noticed! v( U3 m8 g  H3 T; X
light colored pubic hair development when he was* j! G5 O8 O3 m8 p* d
From the 1Division of Pediatric Endocrinology, 2University of
4 \+ L2 `4 \) J  G4 FSouth Alabama Medical Center, Mobile, Alabama.
; j: @) R# b1 I4 e7 I8 e0 ?9 UAddress correspondence to: Samar K. Bhowmick, MD, FACE,
2 _& [- O$ @  k3 c( _Professor of Pediatrics, University of South Alabama, College of
' R0 i4 z1 c& z" M( VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;, k0 M" u) e4 l! }% V2 Q( X
e-mail: [email protected].
' |) R- N- m$ T- G# \5 Vabout 6 to 7 months old, which progressively became8 U, C" e- y4 @- `, m
darker. She was also concerned about the enlarge-- G% \3 k8 b( c9 l$ k
ment of his penis and frequent erections. The child. }. q9 R5 S! Q/ @
was the product of a full-term normal delivery, with
; u( w5 p0 E; k2 s- L+ O6 o9 Q+ b1 Ea birth weight of 7 lb 14 oz, and birth length of
2 j3 z& A- T* G! p4 ~  d- i7 s; w$ j20 inches. He was breast-fed throughout the first year
5 i2 Y1 U- v" D3 D4 @of life and was still receiving breast milk along with; l1 ?, f2 N  h( r
solid food. He had no hospitalizations or surgery,0 F3 K: ~4 H: A: a
and his psychosocial and psychomotor development
2 k4 n' z6 o  Iwas age appropriate.
& b6 N( q& H0 N  X. DThe family history was remarkable for the father,
2 a" |/ E8 G) a& C3 X" Fwho was diagnosed with hypothyroidism at age 16,
& \) S+ X6 B, p( Rwhich was treated with thyroxine. The father’s
* X! s3 S( s! ^, S8 s% gheight was 6 feet, and he went through a somewhat
; {; A3 i' J, cearly puberty and had stopped growing by age 14.; w9 y# `3 u- i
The father denied taking any other medication. The
  N/ S) {4 k$ T' p7 ~child’s mother was in good health. Her menarche
2 X* D! D+ J5 S7 m3 b) w6 g( Qwas at 11 years of age, and her height was at 5 feet
4 K* K. J5 d9 f8 y, {; ^5 inches. There was no other family history of pre-
  _! A& r( z% l7 Vcocious sexual development in the first-degree rela-. E1 Q% B. H) z  @" G+ y& ~
tives. There were no siblings.
; Q3 L$ i( p) B& {& T! vPhysical Examination1 y7 _& n8 i& B
The physical examination revealed a very active,& S5 P" @2 f; ?+ @
playful, and healthy boy. The vital signs documented0 j( g. G! R1 z' _6 @/ n2 ^
a blood pressure of 85/50 mm Hg, his length was
# ]% J1 f/ B2 @8 }6 ~- F/ N4 s90 cm (>97th percentile), and his weight was 14.4 kg
) M( H6 b+ y! b5 m: z. @5 W(also >97th percentile). The observed yearly growth$ q6 [1 l' S1 x8 x% `
velocity was 30 cm (12 inches). The examination of+ K8 n7 Y2 w6 l2 v
the neck revealed no thyroid enlargement.2 W. x) W2 B* t/ x7 h( L
The genitourinary examination was remarkable for6 s( l5 j' f1 y; Z' j
enlargement of the penis, with a stretched length of- k1 ?4 C$ I. p& [2 [4 O4 b9 B% W7 R
8 cm and a width of 2 cm. The glans penis was very well# g( b5 q6 G. I' y& A
developed. The pubic hair was Tanner II, mostly around' K) n+ o$ V& f8 h6 a& D
540
7 f: f. V$ i8 ~$ T% Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* v, l1 c' e  A. j! Ythe base of the phallus and was dark and curled. The2 I1 u+ g: B1 B7 t3 J$ P+ j
testicular volume was prepubertal at 2 mL each.
! [. @! y" ?4 y+ `The skin was moist and smooth and somewhat
2 \, A# n2 R+ f/ P/ j1 Loily. No axillary hair was noted. There were no" L0 B9 ]. p8 _* X. A
abnormal skin pigmentations or café-au-lait spots.
( C# u+ o! r. C& e/ ~& MNeurologic evaluation showed deep tendon reflex 2+
6 O- \; H3 M7 `' x- Ubilateral and symmetrical. There was no suggestion: X3 S% V8 w4 F& J) H( @1 P
of papilledema.5 G7 g5 I0 d* i0 j% r8 B* F( A" _# {
Laboratory Evaluation
, k/ p  H5 `( c7 R$ j7 jThe bone age was consistent with 28 months by7 _. N, v$ g- Q! T4 @: R
using the standard of Greulich and Pyle at a chrono-1 E/ D; E2 C1 {4 ]9 d8 [: j7 d& q
logic age of 16 months (advanced).5 Chromosomal
( B1 J9 D# P) C& D  W; L2 A0 ikaryotype was 46XY. The thyroid function test
2 L' Q$ f' h/ f) j) V! yshowed a free T4 of 1.69 ng/dL, and thyroid stimu-0 Z% [' l) B! f' e3 v
lating hormone level was 1.3 µIU/mL (both normal).
5 V# t: ^6 R4 |: p: e! v; v1 CThe concentrations of serum electrolytes, blood
2 e8 d1 p5 Z+ ]8 ourea nitrogen, creatinine, and calcium all were# w3 ?; p- Y2 c9 k# e
within normal range for his age. The concentration
9 x1 X- r* y" _1 J5 ~of serum 17-hydroxyprogesterone was 16 ng/dL
7 q( p7 s1 D( Q: `* y) q(normal, 3 to 90 ng/dL), androstenedione was 20
8 R$ E7 ^' Z/ x" E# rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-: H( [7 o% X: ^. J2 {
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
  |  h" _% [% ^& v+ _! c4 edesoxycorticosterone was 4.3 ng/dL (normal, 7 to( S7 e5 u; F" Y- \8 s. R$ _
49ng/dL), 11-desoxycortisol (specific compound S)
4 T$ a0 F: m6 ]! }# h( K4 ewas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
  `" D% Y' m: Y; k: Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' @/ h: `( U' btestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
3 b, J8 _/ k* x6 {and β-human chorionic gonadotropin was less than
; f$ U' f; J  p# e: y# ?, {5 mIU/mL (normal <5 mIU/mL). Serum follicular  Z$ `. ]3 j! K6 S$ G, e6 N5 s# v
stimulating hormone and leuteinizing hormone
7 }% _' H& G. g4 C1 N! Nconcentrations were less than 0.05 mIU/mL
+ d/ X3 Q& D% H- e7 q(prepubertal).
1 k. a( W/ ?- s+ r, N! y, y# DThe parents were notified about the laboratory
8 ?: q: I! l4 ?* Gresults and were informed that all of the tests were
7 l4 o1 n% a, t3 O) m6 l' Y; o: @normal except the testosterone level was high. The
$ S' R4 t' s1 F- gfollow-up visit was arranged within a few weeks to& u& ]- j8 F5 ]
obtain testicular and abdominal sonograms; how-
* L& P" M1 M4 T# W# jever, the family did not return for 4 months.8 x* t) S1 G4 k$ X& \" P. s
Physical examination at this time revealed that the# S7 W; a7 e& ?
child had grown 2.5 cm in 4 months and had gained8 }3 T" D) k8 q! p* b8 [
2 kg of weight. Physical examination remained
" @& B2 L+ g) m, J" f: runchanged. Surprisingly, the pubic hair almost com-
/ e3 G. ?4 |5 U( u+ m# rpletely disappeared except for a few vellous hairs at/ \# |* D5 _: G5 T; L9 x
the base of the phallus. Testicular volume was still 2. ?0 x. O$ F& u; y
mL, and the size of the penis remained unchanged.
; {* O0 |5 O$ z! P2 }; \& rThe mother also said that the boy was no longer hav-
+ ]3 v3 ^  y5 q( sing frequent erections.
: ^+ V! U8 ~* {; eBoth parents were again questioned about use of" a, P- S, K4 ?) x  \
any ointment/creams that they may have applied to
) o% w) ~0 Y$ K+ A. k: Qthe child’s skin. This time the father admitted the
9 y2 V' {- r- s$ E5 PTopical Testosterone Exposure / Bhowmick et al 541" i) a5 H) z0 j
use of testosterone gel twice daily that he was apply-
2 x0 i0 @. D2 Y+ l6 k5 Cing over his own shoulders, chest, and back area for
5 w' ?  _1 R* O9 q3 Wa year. The father also revealed he was embarrassed& J7 g$ J" S- w: c# o9 [3 t+ Q7 O' N
to disclose that he was using a testosterone gel pre-3 t! I# F2 {8 E; N# |3 A# d+ k
scribed by his family physician for decreased libido4 \$ a. y+ _& p- P
secondary to depression.: P% c  ^% F5 Y6 X* j- S
The child slept in the same bed with parents.
: M% g, |9 {& R; E: K, T1 z$ K6 \The father would hug the baby and hold him on his
! h( U1 I4 \4 E5 _" \! xchest for a considerable period of time, causing sig-1 H( k# u; e, L/ x4 m8 F: A1 x
nificant bare skin contact between baby and father.
; @9 E8 @0 W0 @9 |  W6 p9 EThe father also admitted that after the phone call,
. r# C: L+ C3 G. ^8 V% h4 ~# C6 Nwhen he learned the testosterone level in the baby
2 U) m; J. Z1 P6 K4 p( |3 k7 Z9 swas high, he then read the product information
* J& u0 l) b, |9 {, n$ d3 `+ Dpacket and concluded that it was most likely the rea-" G- N7 B2 Z3 @) r: H) a. e" T7 c
son for the child’s virilization. At that time, they
  q8 W1 z% h4 `3 Ydecided to put the baby in a separate bed, and the5 W% \2 l5 C4 |. Q, K6 d; N, F) ^2 e
father was not hugging him with bare skin and had7 u* }, @2 ?2 I+ L! A8 @
been using protective clothing. A repeat testosterone- D; @, J; W8 j! J9 \$ F
test was ordered, but the family did not go to the9 A' V7 h, H  F( ^, m
laboratory to obtain the test.
1 |0 T  ~; c! C  z5 C0 X" IDiscussion# R: v  f  S. z7 Z7 H: a
Precocious puberty in boys is defined as secondary
- ^9 y2 M: u7 K3 o! A& ~sexual development before 9 years of age.1,4: f9 Y0 ~$ M& B% ^! a
Precocious puberty is termed as central (true) when/ T( y9 V8 B2 s6 S( g1 B! g
it is caused by the premature activation of hypo-
) ]3 {9 f4 m2 {4 t" R$ jthalamic pituitary gonadal axis. CPP is more com-0 P' H. @( ~0 d0 c+ ^
mon in girls than in boys.1,3 Most boys with CPP
+ ^' u$ q) R# e7 x. o/ {, E- Kmay have a central nervous system lesion that is
5 G; ?/ X' b0 W0 M2 U( v' E( L" Bresponsible for the early activation of the hypothal-
  r$ }* J6 z) y3 c' t  @amic pituitary gonadal axis.1-3 Thus, greater empha-
& k6 U" f1 P/ F/ N4 O& asis has been given to neuroradiologic imaging in
( ^  q2 `& Z3 [. ?boys with precocious puberty. In addition to viril-
" ^6 Y/ H/ K, C4 y$ f6 }ization, the clinical hallmark of CPP is the symmet-! Y9 E6 G! B4 ?/ Z
rical testicular growth secondary to stimulation by# V8 z- R; [: V8 V. ?/ i; c5 x
gonadotropins.1,3
$ G1 q! m$ l$ Y) |Gonadotropin-independent peripheral preco-* N. y& R7 i  u# r* t. b$ D' E4 l* [
cious puberty in boys also results from inappropriate
2 L  G5 k7 [/ ]1 X- N7 M/ J$ tandrogenic stimulation from either endogenous or2 {# ^& T8 ~$ m% s
exogenous sources, nonpituitary gonadotropin stim-3 _1 y2 @% c* ^* @1 d; J
ulation, and rare activating mutations.3 Virilizing5 g% z2 Q0 z1 I, c7 ?% O- H
congenital adrenal hyperplasia producing excessive8 q9 Y$ D% J- S
adrenal androgens is a common cause of precocious! q, B$ E. g  T' S, B$ g- G8 Q" M
puberty in boys.3,4
1 G3 B: T& y) r2 f! ]The most common form of congenital adrenal' }+ \  w# f) r! R: \, b
hyperplasia is the 21-hydroxylase enzyme deficiency.
% `, _$ w% D  d  R% U9 |$ UThe 11-β hydroxylase deficiency may also result in+ X3 X; ?) O. L) p" E6 O
excessive adrenal androgen production, and rarely,
' t$ Z6 o- ?& h. X5 u+ ?5 L; Can adrenal tumor may also cause adrenal androgen' R. e4 N$ s: ?& g# N$ Z3 t; T
excess.1,3
# t% Z" O, F% _0 i/ oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from, V0 o6 `. t/ u- r3 o( I
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007% M; G# f' {) U
A unique entity of male-limited gonadotropin-
! E' @+ {, [' i2 Y' S* g7 zindependent precocious puberty, which is also known1 q2 q* {9 i7 q% |1 s
as testotoxicosis, may cause precocious puberty at a# Z1 A3 u4 T' s
very young age. The physical findings in these boys
/ r$ j  l+ B% Owith this disorder are full pubertal development,( r. N; Q4 a1 p6 m5 m6 y6 s
including bilateral testicular growth, similar to boys
) U1 `* e4 j) F4 S* o) p5 B/ N+ K/ Gwith CPP. The gonadotropin levels in this disorder
7 H2 |( D4 J- W) L  S1 fare suppressed to prepubertal levels and do not show
, R. s) F7 B4 ~6 Q4 |9 f0 spubertal response of gonadotropin after gonadotropin-
" K! z6 x6 P5 @/ ~, o# qreleasing hormone stimulation. This is a sex-linked! |, h2 I5 r1 t3 \
autosomal dominant disorder that affects only
4 B0 t  H; M: _% G3 }5 B3 Y. }males; therefore, other male members of the family0 t/ j2 ?( v* W" H; w( c, e
may have similar precocious puberty.32 m) T/ z2 A; v1 U1 g- b
In our patient, physical examination was incon-
9 [1 ?7 i* f4 `# \2 q) z) ~4 ~sistent with true precocious puberty since his testi-) N# v3 Y! S' y5 X4 Z( V
cles were prepubertal in size. However, testotoxicosis- ^0 Z4 w  @( L0 N9 ^8 z7 g
was in the differential diagnosis because his father
* R2 Y" g& x7 a; z1 R. z8 Q! zstarted puberty somewhat early, and occasionally,' r3 D( k* k% S' U# }  w
testicular enlargement is not that evident in the: I) Z' _* v; j6 H) l
beginning of this process.1 In the absence of a neg-" d0 O3 p( D8 c$ b. m1 V, a+ R
ative initial history of androgen exposure, our
2 X7 j& q/ ]- [1 U6 Ubiggest concern was virilizing adrenal hyperplasia,9 ^( s" o+ S' D7 r( D( r0 R; ^
either 21-hydroxylase deficiency or 11-β hydroxylase
7 m# d/ I/ c+ d* t8 d$ T" xdeficiency. Those diagnoses were excluded by find-
0 k+ E* e( t) S4 B8 |ing the normal level of adrenal steroids.# m3 o8 c! E$ z8 c9 D' l
The diagnosis of exogenous androgens was strongly
* z* m, g. G. }  E/ q4 fsuspected in a follow-up visit after 4 months because8 K# P% P: ?/ `2 Q; x* \
the physical examination revealed the complete disap-
3 B0 G; @9 g* @! B# ypearance of pubic hair, normal growth velocity, and
: X# y( J. c; {9 fdecreased erections. The father admitted using a testos-
, u4 d+ q/ H4 z8 G- lterone gel, which he concealed at first visit. He was+ Q7 B" @  Q+ p2 x% D
using it rather frequently, twice a day. The Physicians’) U! k8 I* }: L3 X
Desk Reference, or package insert of this product, gel or
- D9 p; A  E2 W6 Q  u. k+ D: Gcream, cautions about dermal testosterone transfer to
1 H8 t" I5 D4 s+ O' [unprotected females through direct skin exposure.
" l# @$ Q& a" K# y# R9 V0 y$ tSerum testosterone level was found to be 2 times the/ t8 \2 X& b6 t& o) v% U3 `9 C/ q
baseline value in those females who were exposed to
! K3 D0 J% J* Veven 15 minutes of direct skin contact with their male
5 j8 ?/ u% ^  l% I) mpartners.6 However, when a shirt covered the applica-
) \5 g, _& z! M7 j7 _3 b, ~9 }/ i& Ktion site, this testosterone transfer was prevented.8 R7 |5 C3 [; L, X/ t# B9 N1 w
Our patient’s testosterone level was 60 ng/mL,
: F! c$ }# G3 hwhich was clearly high. Some studies suggest that/ s6 O  `& R. `( i  V2 ]
dermal conversion of testosterone to dihydrotestos-
0 t3 b7 h9 o* r) ]; {- zterone, which is a more potent metabolite, is more  o% v% {) f" N6 q- W8 \! M, }; d
active in young children exposed to testosterone
- P( V( \2 E4 g2 eexogenously7; however, we did not measure a dihy-  J' z  h. G- Q) i8 n8 {4 F
drotestosterone level in our patient. In addition to2 c4 I8 b: o$ Z6 o5 O
virilization, exposure to exogenous testosterone in
: F0 R0 L. x. F$ p4 h9 ?/ pchildren results in an increase in growth velocity and
" ?" I# G. [% uadvanced bone age, as seen in our patient.
( p1 q, b1 L% oThe long-term effect of androgen exposure during
3 ]# J6 p& l( A6 B6 j- Cearly childhood on pubertal development and final
& i  ]1 f( k1 [/ nadult height are not fully known and always remain
4 X! b' I, u# h. y+ za concern. Children treated with short-term testos-
, b6 ]$ M7 x6 k4 I& Gterone injection or topical androgen may exhibit some
( c* |$ L( N* v, o/ u# ^% Qacceleration of the skeletal maturation; however, after1 o$ T8 k6 v6 m
cessation of treatment, the rate of bone maturation
, F$ G+ g$ I8 u" A/ ?3 Edecelerates and gradually returns to normal.8,96 h* i, y: t. F. }
There are conflicting reports and controversy/ \2 i1 t* m2 k; R* L
over the effect of early androgen exposure on adult7 w6 O" ^5 _( J" w1 b' ^$ f
penile length.10,11 Some reports suggest subnormal
8 _7 T1 w/ c9 f0 p/ P/ ~5 I$ l6 ]7 jadult penile length, apparently because of downreg-
8 r& n& M; i$ h9 M8 @6 u/ iulation of androgen receptor number.10,12 However," h& t% K; ]9 O# G7 M; Z* B
Sutherland et al13 did not find a correlation between
2 ~4 U' i6 ^( g- `; h2 c; x4 ^childhood testosterone exposure and reduced adult, Q, J! {! E, F( q4 `9 D5 B' i2 n& w
penile length in clinical studies.8 O4 z6 J4 X+ ?; ^4 z
Nonetheless, we do not believe our patient is
1 j* O; E4 W) q' u9 }going to experience any of the untoward effects from) P5 D# @8 g" W( D7 w3 a
testosterone exposure as mentioned earlier because/ W' e* v4 \; D: }. U. T  g# d* p
the exposure was not for a prolonged period of time.
% M. q5 n  n8 U8 g" oAlthough the bone age was advanced at the time of& j! L- n& x! ~8 ~( Z4 G9 [# V" R
diagnosis, the child had a normal growth velocity at; Q  B+ E( w/ O! D! k5 r" M
the follow-up visit. It is hoped that his final adult. F3 G8 G; W) A& r1 o( ?4 `
height will not be affected.5 ~. z* b1 M4 U& O9 t6 i
Although rarely reported, the widespread avail-5 y; {+ H2 l8 r, r, v. v/ L
ability of androgen products in our society may$ g" Y7 r& \, Z- |
indeed cause more virilization in male or female4 P2 I9 P. p) A& f* x- T& T; X
children than one would realize. Exposure to andro-4 a5 {& s) n9 T' d. J' e' Y) Y4 |
gen products must be considered and specific ques-2 N. }' R& r3 I5 M9 Y
tioning about the use of a testosterone product or
6 ^. R: b1 v. I6 U# }+ s1 E7 bgel should be asked of the family members during* X# m% P1 ~* j" C8 A0 g" K' _
the evaluation of any children who present with vir-- g: ]- z) \) n7 G- r4 b, u" i1 ]$ E
ilization or peripheral precocious puberty. The diag-) J5 }1 ?$ @) t, r
nosis can be established by just a few tests and by
6 R2 E: Y0 k* ]2 Q3 U. g- }3 Oappropriate history. The inability to obtain such a. L' J7 f2 X  h- f8 B
history, or failure to ask the specific questions, may
% @3 c8 U$ {  ]9 l( \result in extensive, unnecessary, and expensive
3 L9 B5 U7 R, h- ?& h  S7 Sinvestigation. The primary care physician should be. t' L" j9 N; t% _! P. [4 c
aware of this fact, because most of these children
! L  w3 c9 r9 ?/ [may initially present in their practice. The Physicians’
, H. a* T# c8 ]9 X# hDesk Reference and package insert should also put a2 f5 q; L3 W2 m% _. ?2 x* @
warning about the virilizing effect on a male or! a  q6 j% O1 d1 N) F! }, x- D
female child who might come in contact with some-
" G8 K+ K( x% L  g& cone using any of these products., N; ^& V5 d6 x  V) r0 b. u1 q  P; T0 Z
References
+ M2 t% V+ s2 z' A4 b' b) M% g1. Styne DM. The testes: disorder of sexual differentiation
# `  l! M0 e6 N2 vand puberty in the male. In: Sperling MA, ed. Pediatric+ l) i) ~- b: h& F' c
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ D4 M9 s# ~8 W' p( o; ?2002: 565-628.5 K4 f/ s1 }: U/ @
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious! @& _1 O1 R) i  W# N! [  e
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
9 N0 e  n; ?4 R8 _" j$ WBoy Induced by Indirect Topical$ P3 S( |' e" t' D& ?  E2 \& A% g$ j
Exposure to Testosterone
4 B- u; i& q$ P( A/ `  G& q0 JSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 }0 q5 A9 J: v2 H1 g, K. iand Kenneth R. Rettig, MD1: B  S$ H9 H6 J" f& V
Clinical Pediatrics
0 I! G+ L+ |$ D8 _& k+ l" wVolume 46 Number 6
: ]/ Q6 P3 B; ~! f) hJuly 2007 540-543
6 J! ?8 ^4 s( a+ P4 x2 ^% V© 2007 Sage Publications: J( t- F6 j$ s9 n
10.1177/0009922806296651, x2 _2 _8 G5 `' {7 D: M
http://clp.sagepub.com5 E' B/ J! R  t$ l0 O# H/ @
hosted at
! ^1 z& g" n, v8 `4 O; Phttp://online.sagepub.com3 y) w: W1 ^3 k. r
Precocious puberty in boys, central or peripheral,
% E4 `( z0 j4 U5 L0 {$ f! O$ ~- ris a significant concern for physicians. Central* @* g. E4 R' B7 E9 T
precocious puberty (CPP), which is mediated
6 D/ J) z. R4 V2 ythrough the hypothalamic pituitary gonadal axis, has
" G2 K) h, ~% `2 n% M1 `6 Na higher incidence of organic central nervous system
3 {7 r8 K: M) |+ R3 m% q- zlesions in boys.1,2 Virilization in boys, as manifested
9 i6 J8 G4 n- F8 e5 k1 W: Kby enlargement of the penis, development of pubic
$ K$ I; k6 @  ?hair, and facial acne without enlargement of testi-# m! K1 I8 ^/ H) B
cles, suggests peripheral or pseudopuberty.1-3 We
. r0 I" B: Y: z4 Zreport a 16-month-old boy who presented with the
+ j1 x1 o$ U) I6 }8 D& Q6 ^enlargement of the phallus and pubic hair develop-
; f3 }) [$ p/ H, iment without testicular enlargement, which was due
! j2 ]6 b" Y- i# Cto the unintentional exposure to androgen gel used by
' j9 Z/ d; o5 T9 Lthe father. The family initially concealed this infor-4 |7 c% a$ Z/ w. I" p+ x" r
mation, resulting in an extensive work-up for this
* H+ r3 }) s+ c- }( N% tchild. Given the widespread and easy availability of3 j  @3 s  L; m: Y1 z5 h- @$ r
testosterone gel and cream, we believe this is proba-
& z! v3 S" u9 }bly more common than the rare case report in the
- v  E( {0 k- `6 e) Hliterature.49 r3 ?9 V; n+ A/ [9 h; _
Patient Report
) F% X1 v9 L, y4 q! f$ SA 16-month-old white child was referred to the
1 ~/ @; [' N7 a" ^6 `+ G: kendocrine clinic by his pediatrician with the concern  Z- ^7 \# N- `: L) k
of early sexual development. His mother noticed# U9 L/ c! N- W5 v; J0 l, \
light colored pubic hair development when he was4 Q1 y$ h# B. ?9 H" K( N7 p
From the 1Division of Pediatric Endocrinology, 2University of
4 b% c; F( J8 o/ t7 Y& FSouth Alabama Medical Center, Mobile, Alabama.; F% k' Q5 d5 J. p  O' @
Address correspondence to: Samar K. Bhowmick, MD, FACE,
7 v; q+ S4 ]& M+ X5 o3 \# aProfessor of Pediatrics, University of South Alabama, College of
) i) Q" M( q: A/ c" F; \$ k- |Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# o% _" {: g8 O$ Z
e-mail: [email protected].  A6 z9 Q; `8 w7 Q, |* k  _
about 6 to 7 months old, which progressively became. d1 x6 |1 F% c6 D
darker. She was also concerned about the enlarge-
$ K9 x1 C6 Q3 ]5 p7 ?. K% Lment of his penis and frequent erections. The child
' D7 [3 l1 Y( owas the product of a full-term normal delivery, with0 Z8 v# ?# f' Z. ], K: L
a birth weight of 7 lb 14 oz, and birth length of( Q5 y- P( p5 h  f  @, N4 E# [: H
20 inches. He was breast-fed throughout the first year; [( \" Q% O! h% U, P  h. Y
of life and was still receiving breast milk along with/ ?( D5 ]5 n, R
solid food. He had no hospitalizations or surgery,5 J8 l, P; D# ^5 F" ~- c
and his psychosocial and psychomotor development
% C1 m  e1 L" `was age appropriate.) j9 H1 `: @3 [# G- F- O
The family history was remarkable for the father,
/ a( A  Y8 I: x. |who was diagnosed with hypothyroidism at age 16,
7 y3 n- t8 i4 @$ D* {' bwhich was treated with thyroxine. The father’s
2 v9 ~) F( b& bheight was 6 feet, and he went through a somewhat
: Q/ c: X" I3 z; f- Qearly puberty and had stopped growing by age 14.+ Y2 w- k" J& a. s1 \- {
The father denied taking any other medication. The
: h; Q. V( N' W6 {child’s mother was in good health. Her menarche# a( C1 t6 W$ ?9 A
was at 11 years of age, and her height was at 5 feet
. U8 ]( f: [6 V. _" Q. a5 inches. There was no other family history of pre-/ ?+ l: T& e' D4 P4 v1 t7 ?* l# [
cocious sexual development in the first-degree rela-
5 V: `8 v3 [$ _" L7 B6 `tives. There were no siblings.
6 L' S  o. [( n7 N, QPhysical Examination
; w  ~) \7 B6 `$ R' ~The physical examination revealed a very active,
$ J5 I* d# [4 g6 lplayful, and healthy boy. The vital signs documented
& H  ~. @% x, O; W% ja blood pressure of 85/50 mm Hg, his length was) I7 `7 J# E( k1 D6 R& M& R, l& \
90 cm (>97th percentile), and his weight was 14.4 kg
* U* T1 F# d/ ?; |9 F) o3 ](also >97th percentile). The observed yearly growth( W8 q" q& H. D& k3 s
velocity was 30 cm (12 inches). The examination of) M: L  {% D& y5 ^5 h
the neck revealed no thyroid enlargement.
7 l2 _  B) D" ]8 ]; MThe genitourinary examination was remarkable for! z3 A4 `& ^5 a' x7 ^3 B
enlargement of the penis, with a stretched length of) ~1 H5 X/ y% \. V- l( n
8 cm and a width of 2 cm. The glans penis was very well4 [; o* a; o/ C
developed. The pubic hair was Tanner II, mostly around% c3 X5 D; B5 z+ [+ x1 ^( O
540' H: j7 x1 o" ~4 t: @- g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# _" m" }7 A% s" j7 fthe base of the phallus and was dark and curled. The1 q) j+ S; n1 o) T& P# `
testicular volume was prepubertal at 2 mL each.
) @4 P4 i* ?0 XThe skin was moist and smooth and somewhat
3 [  f6 W5 O( V# [6 ~, g1 _! `7 uoily. No axillary hair was noted. There were no9 X4 j  V1 G  q% I
abnormal skin pigmentations or café-au-lait spots.8 s- P2 I- q0 U* g
Neurologic evaluation showed deep tendon reflex 2+
3 \5 h+ ~* }9 _7 @3 b' dbilateral and symmetrical. There was no suggestion! W8 U0 j! r- U1 l6 D
of papilledema.
' |' C8 h/ I5 `: G3 x7 i3 W% ]3 {* ALaboratory Evaluation
% d: y7 I0 W3 e8 l" C  l& E( qThe bone age was consistent with 28 months by
0 ^$ s8 c# O$ m+ b' H4 Dusing the standard of Greulich and Pyle at a chrono-
$ q2 q) S7 [/ m; g0 Rlogic age of 16 months (advanced).5 Chromosomal
: f0 C) K0 ]( o) _karyotype was 46XY. The thyroid function test
* u( C2 Q4 k0 c9 X2 I& @* dshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
( A, {  r2 M4 R& @( Elating hormone level was 1.3 µIU/mL (both normal).
% L  S; }' G$ G! p+ jThe concentrations of serum electrolytes, blood' a* R! G+ {) `  O
urea nitrogen, creatinine, and calcium all were) @$ h# a7 F+ D, C+ y; \
within normal range for his age. The concentration
' X5 Q. E* d$ n8 h" Nof serum 17-hydroxyprogesterone was 16 ng/dL
0 i6 P2 {# Z  Y; \' t(normal, 3 to 90 ng/dL), androstenedione was 203 s2 Q0 E1 Y% `6 ~! g, a
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! r, ?8 u9 n& s/ Hterone was 38 ng/dL (normal, 50 to 760 ng/dL),; |! g1 Y8 _2 u9 M
desoxycorticosterone was 4.3 ng/dL (normal, 7 to! M/ ?' T, n% E8 y* [& c" P( V
49ng/dL), 11-desoxycortisol (specific compound S)
* e$ v3 V! F/ ^& p; f0 fwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 l( w4 }1 h" o# u
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ K4 z; w" \; a4 E" O1 Vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),  d" i6 U) M' `5 ^* k& Q1 D
and β-human chorionic gonadotropin was less than
/ @( e6 m! }! J1 i5 mIU/mL (normal <5 mIU/mL). Serum follicular
( {0 r, u4 |6 Ustimulating hormone and leuteinizing hormone+ y6 N' u0 x8 \
concentrations were less than 0.05 mIU/mL# B7 ~; Q" r. V/ F4 y$ ^3 Y+ m
(prepubertal).1 l3 @4 t& z) v! e5 k
The parents were notified about the laboratory
3 j5 P* s5 Z0 H2 J* c7 [! @results and were informed that all of the tests were4 `7 n( c- r: N  t0 r( z: b
normal except the testosterone level was high. The
3 J  m- |$ m. @9 }1 K( Y' g/ `follow-up visit was arranged within a few weeks to
  p- X$ r# O& S8 Y  I/ Iobtain testicular and abdominal sonograms; how-
0 R, q$ _1 M6 J4 H0 S/ ^ever, the family did not return for 4 months.
  t% u. h9 X# V- d/ fPhysical examination at this time revealed that the+ u* M( e1 z+ E
child had grown 2.5 cm in 4 months and had gained
. k2 Y! B/ S" Y, c2 kg of weight. Physical examination remained
% N; S4 x3 N9 A& V! H# Munchanged. Surprisingly, the pubic hair almost com-. c( y) w. c2 S) v+ ~. I" U
pletely disappeared except for a few vellous hairs at5 Z0 ^$ W3 n7 Y4 B6 _7 j* Y
the base of the phallus. Testicular volume was still 2
$ z2 j2 J: P! H. X! I) ymL, and the size of the penis remained unchanged.
0 s0 O% H# `  i" AThe mother also said that the boy was no longer hav-. l7 ~( _9 J- A9 _* \4 U; P0 d
ing frequent erections.
% [( _  V3 h4 ~4 m. R) J' fBoth parents were again questioned about use of
3 G# y8 }, h2 g, b0 gany ointment/creams that they may have applied to
! U1 z% j3 E; j- m8 ~8 Cthe child’s skin. This time the father admitted the0 \4 ~1 d0 [7 |6 r5 f4 J3 M/ p( U
Topical Testosterone Exposure / Bhowmick et al 541
( l3 ~6 B: T- p, o* Z3 xuse of testosterone gel twice daily that he was apply-
2 [' K( p) r3 g: c5 u( v. V4 ting over his own shoulders, chest, and back area for
9 N! M  W- M( |" L& C0 Pa year. The father also revealed he was embarrassed
2 T( Z; E3 u  c; ~8 ?; Zto disclose that he was using a testosterone gel pre-
" ~# j7 r5 ~, ~% D4 Q. N9 }scribed by his family physician for decreased libido5 G8 w& I3 \% f3 o
secondary to depression.$ `2 z/ }0 D! \1 X% G* c
The child slept in the same bed with parents.! e% F8 _9 B; {5 L9 Y9 T
The father would hug the baby and hold him on his" R3 `+ s9 R% T# |5 ]. v
chest for a considerable period of time, causing sig-1 J- v' m; H2 c- `0 I! q0 [
nificant bare skin contact between baby and father.( G9 c6 I2 j, p$ F" X+ T
The father also admitted that after the phone call,
) S* i8 I2 U! Z- @4 \when he learned the testosterone level in the baby
6 t' Q! O! u, `- x$ {" C3 f% Nwas high, he then read the product information
" p: f% v& n$ P  t6 \( V$ }) Bpacket and concluded that it was most likely the rea-
3 M- V' O7 E. Uson for the child’s virilization. At that time, they3 @! k+ r( R% m: |* z/ c6 f
decided to put the baby in a separate bed, and the2 q* p/ ^) D# d
father was not hugging him with bare skin and had
! F- W$ {' _2 mbeen using protective clothing. A repeat testosterone
: P0 X; q" v6 t2 y: P9 a5 P3 otest was ordered, but the family did not go to the& h2 X% D: L1 n$ T* z0 ^$ s  |
laboratory to obtain the test.
$ b* s/ b7 r3 B* S. W3 d, lDiscussion$ _0 _' v; [+ |( v
Precocious puberty in boys is defined as secondary
9 [" C6 [) G/ B' H9 ?2 U; W& ^& isexual development before 9 years of age.1,4( d) v% E; j1 O5 {0 ~( n
Precocious puberty is termed as central (true) when. H3 q% o, M* z7 K  o9 m; F
it is caused by the premature activation of hypo-
. U6 S) z; U4 c* Q2 T5 Ythalamic pituitary gonadal axis. CPP is more com-3 S/ r/ b' p4 G7 s+ @; c/ A, y
mon in girls than in boys.1,3 Most boys with CPP( a; V9 c( E/ ]: e
may have a central nervous system lesion that is
, F' z, Q: `# _' J, Vresponsible for the early activation of the hypothal-: C5 S3 \: `3 W6 O- L
amic pituitary gonadal axis.1-3 Thus, greater empha-
- q/ a: \' i- Isis has been given to neuroradiologic imaging in
1 |3 |# j3 p5 M, D1 v4 Hboys with precocious puberty. In addition to viril-
6 i: ~/ D* V' Z- Wization, the clinical hallmark of CPP is the symmet-
( ]( ]$ b4 Z/ `. M$ Brical testicular growth secondary to stimulation by
) o5 M9 i# ^4 H: ~% h" Zgonadotropins.1,3% s$ z# {: o$ t8 ]% S. n; t
Gonadotropin-independent peripheral preco-
  ]0 \2 q2 d* h: u) mcious puberty in boys also results from inappropriate2 i" P- X1 n- @- V6 Q
androgenic stimulation from either endogenous or. O/ z( k# N! ?& u9 }3 y* W
exogenous sources, nonpituitary gonadotropin stim-+ x! q& D8 J. y
ulation, and rare activating mutations.3 Virilizing0 a5 @$ j9 t* {# i
congenital adrenal hyperplasia producing excessive
1 n5 S6 G9 G4 _) H4 J; A5 Q$ aadrenal androgens is a common cause of precocious, j% p! J4 N  ?5 m- m( s: o' G
puberty in boys.3,4) ^  H" w1 X/ @! ]
The most common form of congenital adrenal. y" u& S0 i  r% h; H, a
hyperplasia is the 21-hydroxylase enzyme deficiency.
+ Y! G) P0 K- [8 aThe 11-β hydroxylase deficiency may also result in4 t0 E( Z  a2 D% g
excessive adrenal androgen production, and rarely,) Q. q% K3 s5 E
an adrenal tumor may also cause adrenal androgen4 P3 S1 p0 M+ k3 ^* U
excess.1,3; U4 k3 A6 a; c" L- P3 W6 K
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 U' A3 F- J  s- X542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) d: Z+ r, v: W: c  H) GA unique entity of male-limited gonadotropin-% K" L4 K; e- O/ m3 j3 V
independent precocious puberty, which is also known: Z/ s$ ?3 y/ k4 Z# l9 k
as testotoxicosis, may cause precocious puberty at a
- R; C  b$ g& {2 E8 zvery young age. The physical findings in these boys
# u0 x  Q+ k* `6 kwith this disorder are full pubertal development,
3 [: A8 \! r% `2 Q% Qincluding bilateral testicular growth, similar to boys7 y) }" {" T! ?( {9 Y
with CPP. The gonadotropin levels in this disorder
9 M% A$ M. c- L& N3 N! aare suppressed to prepubertal levels and do not show
, s1 v) d+ s' D5 z4 Epubertal response of gonadotropin after gonadotropin-$ S% w) K; L" e* n! h+ e
releasing hormone stimulation. This is a sex-linked
: }9 Z2 A; E8 |5 I6 p! a0 Q6 uautosomal dominant disorder that affects only
, }6 j( L3 }3 E3 h! \0 |, j" R  qmales; therefore, other male members of the family$ }, }2 b2 W* T8 t& s4 {
may have similar precocious puberty.3$ R# T8 q7 w; r' [
In our patient, physical examination was incon-3 m6 K$ a. N9 D% @4 I) Q/ |5 W$ V/ f
sistent with true precocious puberty since his testi-  Q5 w& r4 b8 G0 p$ p% M5 Y6 V4 M
cles were prepubertal in size. However, testotoxicosis
) B; L1 T) M9 r! P4 kwas in the differential diagnosis because his father0 Y% v9 K7 s7 k) h0 h% ]; i
started puberty somewhat early, and occasionally,2 E1 h' U+ l3 l7 {: w
testicular enlargement is not that evident in the
4 ]) K# E8 ]+ d" Qbeginning of this process.1 In the absence of a neg-
- w& v( a8 N. ]$ w0 t, p, e) Pative initial history of androgen exposure, our. r) L. N8 h' T( c4 c
biggest concern was virilizing adrenal hyperplasia,
+ p- {$ P' N' C9 X8 _8 p( e3 oeither 21-hydroxylase deficiency or 11-β hydroxylase! s8 k$ g3 ^% U9 H' ^
deficiency. Those diagnoses were excluded by find-5 G9 U% c/ h+ V; `* y. W3 |
ing the normal level of adrenal steroids.
; r4 \0 j8 B  e  i4 BThe diagnosis of exogenous androgens was strongly
7 f2 A3 @; i3 \! G. I2 b. vsuspected in a follow-up visit after 4 months because) ?- l& i, Q3 n' p7 [+ q
the physical examination revealed the complete disap-' V8 D$ n. k7 v: l$ o. a* x
pearance of pubic hair, normal growth velocity, and
3 F- H3 q/ a3 g( v( M" M0 ]2 M+ ~; _decreased erections. The father admitted using a testos-
' ^( w! ?: w  J4 B; T- `terone gel, which he concealed at first visit. He was
- M# ], l; b) q5 D% @; P# X+ ousing it rather frequently, twice a day. The Physicians’
" {0 x! w  d& q! m& b/ h3 W4 I0 NDesk Reference, or package insert of this product, gel or
- B! G7 p/ l% x% b: v  u+ Pcream, cautions about dermal testosterone transfer to
) ]0 \$ g8 Z/ \  L$ R7 }unprotected females through direct skin exposure.( i. y  C4 H4 c3 o* }7 D
Serum testosterone level was found to be 2 times the
& O. i8 _6 E2 y; M8 N$ v3 ~( bbaseline value in those females who were exposed to8 [2 w7 n9 T4 l# v
even 15 minutes of direct skin contact with their male3 C" L6 ?$ ~# o4 N
partners.6 However, when a shirt covered the applica-8 V5 A% S; y8 K3 ~
tion site, this testosterone transfer was prevented.; E9 h- l6 U, h) j
Our patient’s testosterone level was 60 ng/mL,; x, W! @3 |& v9 N3 r8 T
which was clearly high. Some studies suggest that
' x* ~7 Q9 I' Y! z3 Z+ U3 adermal conversion of testosterone to dihydrotestos-$ \1 I4 f, v# |  y1 C- w: C1 S
terone, which is a more potent metabolite, is more) {, ~2 E) M2 A7 p/ a
active in young children exposed to testosterone
7 M% G" V) e1 Z, P+ }. O1 ?exogenously7; however, we did not measure a dihy-
3 I. C& e; b. F' L9 v9 X8 Gdrotestosterone level in our patient. In addition to
( T0 i% c# Q" z+ A3 {+ dvirilization, exposure to exogenous testosterone in
) }, v5 C" J! Bchildren results in an increase in growth velocity and6 l4 h# r4 d3 y7 q+ ^; l
advanced bone age, as seen in our patient.; a: c+ r" K1 G+ }) c/ v) c
The long-term effect of androgen exposure during6 M) ^. u- b: D/ [. Z" o# \( C) E
early childhood on pubertal development and final! X6 y" P3 q6 C- V! `3 [: n1 f
adult height are not fully known and always remain6 ]0 h9 S( x/ O3 C4 B9 {7 R
a concern. Children treated with short-term testos-
) [6 v3 P( p( G, u4 [% Iterone injection or topical androgen may exhibit some; |. u. {, O$ |; \$ {; ?! U" K
acceleration of the skeletal maturation; however, after( T6 |, N4 O5 j
cessation of treatment, the rate of bone maturation5 B' l& }" \1 ^9 P
decelerates and gradually returns to normal.8,9
3 l; e% b. \5 r. S/ [1 Q& EThere are conflicting reports and controversy( G% N5 C4 b- v0 s8 E/ M8 J7 T
over the effect of early androgen exposure on adult
; t1 F$ Z& c4 H& l: e& G  |! ppenile length.10,11 Some reports suggest subnormal
/ r) q' v. Q0 b5 dadult penile length, apparently because of downreg-
: s8 F. h! s9 B: L  b! Iulation of androgen receptor number.10,12 However,' s( |0 ]  h0 I# Y+ D7 b% n) \
Sutherland et al13 did not find a correlation between
% l. u" P9 Q: @% C! F: Y9 vchildhood testosterone exposure and reduced adult) O/ }! N9 M8 Q# ~% D' y
penile length in clinical studies.( H4 m4 P' K' I+ n- x
Nonetheless, we do not believe our patient is) {7 ]+ Z: I; ?4 g
going to experience any of the untoward effects from" Y1 {* D# f6 t( K0 N/ T
testosterone exposure as mentioned earlier because$ [2 X  T; m$ W# `0 r2 g( G5 f3 w
the exposure was not for a prolonged period of time.8 T3 r& O$ _& z- l' b$ ~
Although the bone age was advanced at the time of
) u0 L" ^3 m/ }6 R2 ]diagnosis, the child had a normal growth velocity at8 \2 O, b: B5 C
the follow-up visit. It is hoped that his final adult' u' s( W, v1 Y+ `
height will not be affected.
7 t5 H" E& A( B, b# yAlthough rarely reported, the widespread avail-
! [) d7 u! `3 h) C  uability of androgen products in our society may, \, b- M/ @5 ~
indeed cause more virilization in male or female$ E8 R  _8 d( Y8 G# Y# D
children than one would realize. Exposure to andro-. w- h5 B. T& l8 _# W# _- p
gen products must be considered and specific ques-! r* L( h. i" k; t$ t  c4 x6 A. X
tioning about the use of a testosterone product or+ D( e" \0 m9 Z2 L5 h
gel should be asked of the family members during6 X2 J! g( q$ f
the evaluation of any children who present with vir-1 g% @6 i2 `' I$ A, ~
ilization or peripheral precocious puberty. The diag-1 U$ ?1 @8 e6 E, F
nosis can be established by just a few tests and by
* A. @3 O5 v/ y* S( @8 E' ]0 ?appropriate history. The inability to obtain such a" z1 g0 P# x4 ?3 r6 Y& t
history, or failure to ask the specific questions, may
* O" c( t0 `9 H+ @5 B0 s. Eresult in extensive, unnecessary, and expensive
9 V; ]1 l6 ?& T$ A0 Qinvestigation. The primary care physician should be
* X7 }$ O$ A8 R" Gaware of this fact, because most of these children2 H' F6 S* n4 \/ p
may initially present in their practice. The Physicians’+ K) d9 u& A+ q1 Y3 S0 m
Desk Reference and package insert should also put a+ ~3 x4 I7 h6 H! D. X: \! e
warning about the virilizing effect on a male or
  ^7 y7 l% G! @; G: l# r( F; u) Ffemale child who might come in contact with some-( |5 U6 j) [( Z% L& `1 U9 w
one using any of these products.
6 m" U' o3 }  V0 sReferences3 ^" u# X! g3 w+ T
1. Styne DM. The testes: disorder of sexual differentiation8 a% z' `% F/ N2 g% h
and puberty in the male. In: Sperling MA, ed. Pediatric
, i3 ]5 V0 z7 jEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 x3 L6 ?7 f* M- h/ i2002: 565-628.
" |2 [3 S2 R$ w0 N  f" A9 C. ^/ M2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* U  e0 q/ Z, w0 n6 F( Y, mpuberty 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

/ D* Z/ S1 T: h+ Q5 ?; C# R9 @9 M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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