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Sexual Precocity in a 16-Month-Old/ R# r+ j, F* p3 k0 G2 w! V
Boy Induced by Indirect Topical7 J  s# i' z, P% s* u
Exposure to Testosterone
' d! [; u) j4 N' F( A, _7 ~3 USamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,21 R) z, r- E- Q* _7 i
and Kenneth R. Rettig, MD1
" n$ Y  Y1 q( aClinical Pediatrics) K4 ?2 E6 K" P5 e- d2 o8 C
Volume 46 Number 6
9 T! b3 W5 Y1 l8 C+ \6 kJuly 2007 540-543) T, {: {' I3 c8 [" Q, A8 d
© 2007 Sage Publications. x# C% q$ q* a$ G( a# L- M1 D
10.1177/0009922806296651
% J. I* X0 f$ b, ohttp://clp.sagepub.com
% R& v9 \4 }/ i0 Yhosted at
5 E5 Q2 ^# S4 f0 r. g* chttp://online.sagepub.com
, ~9 W+ ~( q, u  P0 g! S: I, P* N8 vPrecocious puberty in boys, central or peripheral,
1 A9 I+ B, n: b9 K! i/ Gis a significant concern for physicians. Central
1 ?( s$ h, K6 S% Q( k1 ^) q5 K# cprecocious puberty (CPP), which is mediated
2 Q& Y; _2 l+ [9 z. _! R8 S& gthrough the hypothalamic pituitary gonadal axis, has
6 `) n7 ]3 L) g' V4 m( Ea higher incidence of organic central nervous system
: f2 p8 U' \; Q  z5 `& N) @  slesions in boys.1,2 Virilization in boys, as manifested) `9 G- a+ `4 p1 r6 s
by enlargement of the penis, development of pubic- A3 I% S! _5 U) x
hair, and facial acne without enlargement of testi-
% @% R6 [; x1 qcles, suggests peripheral or pseudopuberty.1-3 We
+ ?3 U; A! p% f- @. g% `report a 16-month-old boy who presented with the4 s5 l) D* L0 P! e& w
enlargement of the phallus and pubic hair develop-/ F) w8 D' h4 U
ment without testicular enlargement, which was due
7 s* e) Y# e; S0 [to the unintentional exposure to androgen gel used by
  u/ G5 T- V( T* x( c$ Tthe father. The family initially concealed this infor-- [' K* _- d# p: \2 z
mation, resulting in an extensive work-up for this
: X/ f# m* B: |child. Given the widespread and easy availability of/ Y% `1 c  _, n+ B# J
testosterone gel and cream, we believe this is proba-
; }# b* w# E4 q% L% i& L9 xbly more common than the rare case report in the( ~% S: I# W" T" ^" r% `3 f4 E# J" x
literature.4
/ E% s6 J; Q; [; j$ z  G; y5 rPatient Report
7 V; E) y- D! I: `5 ]9 y9 h$ k1 m8 sA 16-month-old white child was referred to the
5 s' r/ W$ |+ Z& e4 D: Q# Bendocrine clinic by his pediatrician with the concern
% g/ o2 y; n2 b. lof early sexual development. His mother noticed
$ ~9 J& ?; ~  V, g' glight colored pubic hair development when he was
3 b9 Z" v5 [9 O/ Q# d. FFrom the 1Division of Pediatric Endocrinology, 2University of
2 t! x% V4 y5 x4 uSouth Alabama Medical Center, Mobile, Alabama.
7 E- ?. G# F0 B$ _  x  k% K5 eAddress correspondence to: Samar K. Bhowmick, MD, FACE,* y2 D& i- E8 P- @! x, b- t
Professor of Pediatrics, University of South Alabama, College of6 k$ w' @' X! g5 j9 j! E
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. x8 |/ {; U6 j: M$ s5 C
e-mail: [email protected].% ^! V4 _' t0 w8 @0 E- g4 I3 [
about 6 to 7 months old, which progressively became
7 W- Q& _) J# y7 ?2 u7 S! tdarker. She was also concerned about the enlarge-
) l0 w$ {6 |2 I# g0 C; yment of his penis and frequent erections. The child/ E6 k- e" R& ]2 v* P8 l
was the product of a full-term normal delivery, with
- F% s; f7 T2 |- ]. P  Z1 Aa birth weight of 7 lb 14 oz, and birth length of+ S5 F* ?0 k. v7 {7 q" {& D: s
20 inches. He was breast-fed throughout the first year
# l; p6 P- w" k4 \7 R2 dof life and was still receiving breast milk along with7 Q8 B7 D5 P- a, j! l# S6 J" f
solid food. He had no hospitalizations or surgery,
! a5 q; S- X! l2 s* v9 xand his psychosocial and psychomotor development5 H1 c  W& r) ]; Y
was age appropriate., L$ I/ I; x$ m9 A- Z1 T0 H
The family history was remarkable for the father,4 y6 E8 Q5 i7 U* `
who was diagnosed with hypothyroidism at age 16,
5 E6 S3 r7 b- F  [0 R) fwhich was treated with thyroxine. The father’s
$ C  O% S/ B/ V, |( p+ dheight was 6 feet, and he went through a somewhat
/ L4 T5 Q' P7 Bearly puberty and had stopped growing by age 14.
' O0 F! n, ?9 P4 C4 FThe father denied taking any other medication. The
$ [& _& f( ~0 d( A) lchild’s mother was in good health. Her menarche
& x; v! s. @( iwas at 11 years of age, and her height was at 5 feet
# |: n0 ?$ b3 v" C) @5 inches. There was no other family history of pre-+ }7 W; Z( ]- e% ~5 `, ^, Z
cocious sexual development in the first-degree rela-' y. Q5 [( t+ z" d7 C+ _
tives. There were no siblings.8 {' G6 a; ^! l/ G
Physical Examination( t% K  `0 i! R) w/ S" l7 n
The physical examination revealed a very active,' O# `# Y' w! D$ Q0 j- _
playful, and healthy boy. The vital signs documented: q3 l: z% ?/ g( g/ K/ c+ C
a blood pressure of 85/50 mm Hg, his length was
& g) N$ a# Z- d; q90 cm (>97th percentile), and his weight was 14.4 kg
; f. L' Z, z6 T, w/ C( v(also >97th percentile). The observed yearly growth
$ K& d# v" V5 S! z% ]# Wvelocity was 30 cm (12 inches). The examination of
) U1 G1 a$ r/ q$ Ithe neck revealed no thyroid enlargement.
; ]" \, Q/ _6 u% t1 W  ^7 S2 vThe genitourinary examination was remarkable for
$ r/ S4 l2 j- U) E$ ?! Lenlargement of the penis, with a stretched length of
# p* Y) f( f3 Q; D8 cm and a width of 2 cm. The glans penis was very well" h$ c7 E( D! M: {
developed. The pubic hair was Tanner II, mostly around
8 f( G7 g+ i9 M& }' B. Q2 Q( B8 J& x540
% F3 P5 a8 K8 f# F" n; [8 L/ Jat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 w1 }6 h9 C$ X- Q. D
the base of the phallus and was dark and curled. The8 g+ c6 s2 G8 Y: m: @- i
testicular volume was prepubertal at 2 mL each.
7 @7 D8 D$ v6 e4 v1 k; bThe skin was moist and smooth and somewhat
# M  g- `- a  X' ~" k6 soily. No axillary hair was noted. There were no
- e. f% ~' p, x; |  ?abnormal skin pigmentations or café-au-lait spots.
, A! z* Z7 n2 _7 h7 xNeurologic evaluation showed deep tendon reflex 2+% R6 C3 z) x' m  Z1 n$ C+ @% _
bilateral and symmetrical. There was no suggestion
9 C0 p! d! |8 A! T. K0 k7 W" ^of papilledema.
8 V2 Z8 q7 y7 K' O. MLaboratory Evaluation
, E1 M* J' K" ^& R. BThe bone age was consistent with 28 months by
8 M' O) n% @6 u% [* I/ z' \0 @using the standard of Greulich and Pyle at a chrono-3 M% \" l) y4 Q+ p; q$ \
logic age of 16 months (advanced).5 Chromosomal8 \: c5 N- p, p' B! _
karyotype was 46XY. The thyroid function test3 `; {' J' A* x% v0 g1 x
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
, X  h( x( W" |- k; U8 L- o  r/ _lating hormone level was 1.3 µIU/mL (both normal)./ l2 |4 D% [& c8 k, L2 J( m
The concentrations of serum electrolytes, blood9 c( {7 B3 c& {
urea nitrogen, creatinine, and calcium all were. A9 x& ?! j) e% k4 b
within normal range for his age. The concentration
2 W- O; ]8 Y3 M2 y  Pof serum 17-hydroxyprogesterone was 16 ng/dL
3 J, g( K8 s2 e$ Z& j; U(normal, 3 to 90 ng/dL), androstenedione was 20
  b8 I7 a- w! N5 b+ ^  a! Y% Eng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 ]! r" v: G) V1 t
terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 I  L- O' ]- o- q; [6 B
desoxycorticosterone was 4.3 ng/dL (normal, 7 to" }. q  S, Q. Q, _
49ng/dL), 11-desoxycortisol (specific compound S)
) r, X; X. K# L/ Wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-' N8 e5 d0 I. x# H
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 L, v( k  J- |6 g9 q( X4 wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
, w/ h9 T. ?8 o1 d( \2 n* u) jand β-human chorionic gonadotropin was less than; ?) o! ~1 H. s4 r- t
5 mIU/mL (normal <5 mIU/mL). Serum follicular( l3 O1 u' \; v, }' W
stimulating hormone and leuteinizing hormone+ M/ L0 L, t% Y+ E5 L
concentrations were less than 0.05 mIU/mL  B4 }& t; _) |" U& w( q9 P+ H
(prepubertal).
8 v4 Y  M! n$ X7 e, n: k5 q9 mThe parents were notified about the laboratory
% e# L* t7 S2 e6 E5 Aresults and were informed that all of the tests were
; V9 e  `" f7 g! Qnormal except the testosterone level was high. The4 Y% Q( D; a' ?7 B
follow-up visit was arranged within a few weeks to
. k, f# p+ W( _4 eobtain testicular and abdominal sonograms; how-/ b' b$ x6 `8 H# P/ H
ever, the family did not return for 4 months.
+ ^, N6 m. b2 X9 Q' M' f1 E6 qPhysical examination at this time revealed that the
. Q) K" r* v: ~# n8 ^) F4 M3 k& Uchild had grown 2.5 cm in 4 months and had gained9 s0 s- {# \! T) M0 s+ [3 l6 ~
2 kg of weight. Physical examination remained9 p4 S) ~- F. p4 {% F2 O9 r
unchanged. Surprisingly, the pubic hair almost com-5 v0 T3 O9 O( p
pletely disappeared except for a few vellous hairs at
6 n& \2 @) ^/ @the base of the phallus. Testicular volume was still 28 ]0 K* T7 z0 Z1 W- k6 b/ y
mL, and the size of the penis remained unchanged.
# A$ N4 n& D9 [The mother also said that the boy was no longer hav-. a2 ?1 W/ d/ e1 e6 h
ing frequent erections.2 i9 E8 _* E- i( Z2 |
Both parents were again questioned about use of
! J% @1 g8 N" Tany ointment/creams that they may have applied to2 ^3 i5 N4 [* f% C* F, ]; h+ n# e
the child’s skin. This time the father admitted the" [/ F7 p# {8 i9 m$ |: j
Topical Testosterone Exposure / Bhowmick et al 541
$ `, o% R+ T4 y; M4 g! f+ Uuse of testosterone gel twice daily that he was apply-
: K2 x( E5 Z( X# f, I: King over his own shoulders, chest, and back area for
+ b$ _! ]! X9 {a year. The father also revealed he was embarrassed
. }( e4 |0 U, |$ Rto disclose that he was using a testosterone gel pre-, h7 z3 G8 J  K
scribed by his family physician for decreased libido
/ l" G( T; N+ Osecondary to depression.
6 H' p- b4 k' c7 N+ p% CThe child slept in the same bed with parents.
: U' B: @; d8 P; `0 X$ gThe father would hug the baby and hold him on his, P; h$ C" h" G9 a
chest for a considerable period of time, causing sig-9 \/ v* G% [9 E) J- V2 I
nificant bare skin contact between baby and father.
, E% a: k; O# ]# h* B2 P6 ^6 `( IThe father also admitted that after the phone call,) {4 M- @' y" o1 q. a  K' X9 o  z
when he learned the testosterone level in the baby8 A9 F, w* C0 `) k" r; F- g8 V
was high, he then read the product information
" E- W" x) k* r2 q+ k" K  }packet and concluded that it was most likely the rea-
+ p$ O' x9 N& X5 Yson for the child’s virilization. At that time, they
/ |) d: J4 D  j# Z" c8 a- Bdecided to put the baby in a separate bed, and the9 Y' c9 o4 S! ^
father was not hugging him with bare skin and had
. K8 W9 F; |0 b! ?- xbeen using protective clothing. A repeat testosterone5 H9 P8 H8 L' L/ a4 Q$ j. l. b
test was ordered, but the family did not go to the. l3 e/ @! q% h7 R; |! @9 `/ n- ~
laboratory to obtain the test.
! q3 d9 e. z& R/ M* @Discussion, O0 d  [3 |( I6 b
Precocious puberty in boys is defined as secondary
( D% A) M1 m- A: M8 h$ ssexual development before 9 years of age.1,40 E0 P$ ?  I0 ]4 G$ }: j
Precocious puberty is termed as central (true) when
7 a. X$ I. o& K( o9 rit is caused by the premature activation of hypo-
% l- \9 p! E1 O( S; ~thalamic pituitary gonadal axis. CPP is more com-. \3 j1 N. K  @0 ], \% H
mon in girls than in boys.1,3 Most boys with CPP
$ ]; d# a5 A# F6 P& C$ Bmay have a central nervous system lesion that is
; @5 l+ z% x0 {( t6 H: y7 m# ]responsible for the early activation of the hypothal-
' H6 R+ D5 ]/ t5 U& x7 Bamic pituitary gonadal axis.1-3 Thus, greater empha-0 t& h/ `  v  Q; _3 h
sis has been given to neuroradiologic imaging in$ A1 Q( X* r! Q0 ^
boys with precocious puberty. In addition to viril-! s+ r6 r1 S% U9 ?; C$ b
ization, the clinical hallmark of CPP is the symmet-
( a/ k% h3 l1 Frical testicular growth secondary to stimulation by
7 @( [9 L9 i- `3 _0 igonadotropins.1,3
9 T& v& i4 s8 @' X3 YGonadotropin-independent peripheral preco-8 \* U- w  ^1 i; w1 H" k
cious puberty in boys also results from inappropriate3 C. r3 m/ h2 M* S- K7 i* g
androgenic stimulation from either endogenous or9 ]2 g+ Q! s1 ]
exogenous sources, nonpituitary gonadotropin stim-  F8 B) Q. f! }3 I5 c/ S
ulation, and rare activating mutations.3 Virilizing8 D7 q$ ^' z( J- s. x
congenital adrenal hyperplasia producing excessive
" K$ `" n/ n; G1 o3 Z$ U2 Xadrenal androgens is a common cause of precocious+ ~, H, ?4 N8 \7 D
puberty in boys.3,4, L; ~  j; v" b' M; x3 {) p
The most common form of congenital adrenal1 v/ d. Y( J8 V) O6 p) j$ }! Z
hyperplasia is the 21-hydroxylase enzyme deficiency.
* w1 O& M: a1 U# W3 jThe 11-β hydroxylase deficiency may also result in% t* ^. Y( D) c5 ~
excessive adrenal androgen production, and rarely,6 p+ j1 N4 _3 m* E. e, E- v
an adrenal tumor may also cause adrenal androgen. ]4 X$ N& e5 j6 }( d! j* P
excess.1,3. G$ J0 u( s8 |: s1 o
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
1 v) b% a( k. q& o$ g* i542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! K  y  O6 `# ]5 ^# c( V
A unique entity of male-limited gonadotropin-
; ^6 p8 T1 T/ ~# A1 v, C# _1 N% Bindependent precocious puberty, which is also known7 I) J, A  }7 {- _6 C" x$ L% C
as testotoxicosis, may cause precocious puberty at a
3 ~) g( P" b& [4 t4 d/ l8 K5 }very young age. The physical findings in these boys/ t+ T0 A. O! E
with this disorder are full pubertal development,7 S9 z- F9 h, n$ J) J% N) X, k/ c& I
including bilateral testicular growth, similar to boys( V! N! D  ^! ~) g
with CPP. The gonadotropin levels in this disorder
4 k2 Q2 ~# u& k! o$ R/ ?( oare suppressed to prepubertal levels and do not show
8 \+ m$ A8 n. w; {$ ~* xpubertal response of gonadotropin after gonadotropin-
+ z: z( X" A/ m: P( l  V) nreleasing hormone stimulation. This is a sex-linked
; k" h! c. u/ x+ Nautosomal dominant disorder that affects only0 n% A. P/ D4 e1 X+ d' Q" _! t
males; therefore, other male members of the family
: @2 f( s& ~7 D' }9 i6 fmay have similar precocious puberty.3
+ @: e) W9 W9 L8 m  ~7 oIn our patient, physical examination was incon-
  c" t' k$ q( _1 Y' J6 A' nsistent with true precocious puberty since his testi-: W- Z) C5 z3 U5 ]' d. W( s
cles were prepubertal in size. However, testotoxicosis
6 |4 B/ ?" Q5 xwas in the differential diagnosis because his father  c$ ]4 W) C4 c. E# F
started puberty somewhat early, and occasionally,: L* H- f# G- F* T$ u: p' h& w
testicular enlargement is not that evident in the  [8 s- Y, B# R) J' H0 q- d
beginning of this process.1 In the absence of a neg-
/ n( |% t1 D" ~% s4 b' g7 C  mative initial history of androgen exposure, our! j4 U6 O' N+ l$ x$ V# r3 l& j) J
biggest concern was virilizing adrenal hyperplasia,+ p. W! O) `0 y+ ^9 s! N- I
either 21-hydroxylase deficiency or 11-β hydroxylase
' i& B/ I" h6 Z, [deficiency. Those diagnoses were excluded by find-* M4 z+ L1 U4 D. }9 S' |( g) ?
ing the normal level of adrenal steroids.
* i5 `- N# e% p% [The diagnosis of exogenous androgens was strongly
& c" X, x# c$ Y4 p; ksuspected in a follow-up visit after 4 months because7 q* k. }. V/ R. M! A
the physical examination revealed the complete disap-! D* q6 }- x* P; h; H4 i4 M$ n
pearance of pubic hair, normal growth velocity, and6 R4 |- X( q7 Z& d5 V& }+ Z+ q% c
decreased erections. The father admitted using a testos-
+ k8 q" |) h  |# x0 Uterone gel, which he concealed at first visit. He was! W% Y4 R* y4 F$ y$ j
using it rather frequently, twice a day. The Physicians’
9 V# a& c; ~; K1 |6 s6 nDesk Reference, or package insert of this product, gel or
8 k0 h0 {1 o; }( Fcream, cautions about dermal testosterone transfer to* d& \6 p& z/ e* E3 {
unprotected females through direct skin exposure.3 ]; N$ a: P3 U% ^/ |) t
Serum testosterone level was found to be 2 times the. Q) C' G+ x$ O4 |- `3 ?4 _
baseline value in those females who were exposed to
, n. k0 R1 b3 d" M! ueven 15 minutes of direct skin contact with their male+ L7 _7 }2 d) `
partners.6 However, when a shirt covered the applica-
; K/ w7 v1 ]: N  u# v% X' o" v$ ition site, this testosterone transfer was prevented.) a$ K0 W, G. J( C' g0 g3 o, k
Our patient’s testosterone level was 60 ng/mL,
# P! \+ h8 i; R& s  U* Iwhich was clearly high. Some studies suggest that' d! t3 ]' y7 U. M+ w
dermal conversion of testosterone to dihydrotestos-
- j5 M# i5 E$ Y" u. [' ?( jterone, which is a more potent metabolite, is more
  b/ t' r3 Y6 z- R( V( ]active in young children exposed to testosterone
# ~3 D+ S+ z& Q* Z: T6 G1 D' Hexogenously7; however, we did not measure a dihy-
6 S2 ~8 M5 @* T2 Idrotestosterone level in our patient. In addition to3 R& Q. Q$ U0 P. j( E: a1 U
virilization, exposure to exogenous testosterone in
1 m/ r( L8 o! p4 _7 K: uchildren results in an increase in growth velocity and
/ _0 ^* z, V( Fadvanced bone age, as seen in our patient.5 ^1 H9 q. O" v7 b; B
The long-term effect of androgen exposure during
! m& b% ~' K5 |+ c' h+ |early childhood on pubertal development and final
  O" T( _8 @" h7 m9 T$ P7 F" c+ Cadult height are not fully known and always remain( d- r. Q! _+ S
a concern. Children treated with short-term testos-
2 S) E1 ^2 y: I  @: ~2 `terone injection or topical androgen may exhibit some9 H2 Z( I, w1 Y& j& |) q$ h
acceleration of the skeletal maturation; however, after; G2 {' N2 o3 X1 j1 o' Q) i* T
cessation of treatment, the rate of bone maturation
3 v" H; @' s( _, [' X8 X+ O0 Ydecelerates and gradually returns to normal.8,99 _# m9 R" P5 I, z
There are conflicting reports and controversy! M; n9 h  v5 x% ^( j; f) J
over the effect of early androgen exposure on adult3 M5 j3 d( H8 |8 C8 q
penile length.10,11 Some reports suggest subnormal# G# k. p4 G5 ]" B& ?: V
adult penile length, apparently because of downreg-
+ }( Y/ t( C2 k0 `2 `) J1 p5 W2 v. gulation of androgen receptor number.10,12 However,
4 ]  ~0 v8 l1 s- RSutherland et al13 did not find a correlation between
; V9 d2 s; F. l  ~& hchildhood testosterone exposure and reduced adult
: O: w% Q' l( U+ wpenile length in clinical studies.
; m. H4 j+ u) [; H+ VNonetheless, we do not believe our patient is
( @: v, z3 x" w# L" Z2 s6 hgoing to experience any of the untoward effects from/ ?( N. p6 s- C9 V1 C
testosterone exposure as mentioned earlier because
3 h" B8 y, A* xthe exposure was not for a prolonged period of time.
- x: u/ E( ?8 d" aAlthough the bone age was advanced at the time of  b- e3 \' ~! c' T1 B! G+ S$ B
diagnosis, the child had a normal growth velocity at' B4 i- E/ v! \/ [
the follow-up visit. It is hoped that his final adult
  w' i1 M; U! `: o# i2 rheight will not be affected.
# N  V  f+ u) U7 O( ^9 iAlthough rarely reported, the widespread avail-. M. E2 z+ ~' G( i$ ]/ X/ i+ j
ability of androgen products in our society may' B* ~4 j* a0 z% n
indeed cause more virilization in male or female9 T' _" m, h& k3 K8 x
children than one would realize. Exposure to andro-0 h' R* @7 c% O8 h1 g5 z1 ^
gen products must be considered and specific ques-  J4 I# l4 B! c" n5 O% H
tioning about the use of a testosterone product or
$ `1 |  K) l0 z9 i; _& Y0 i) w" ogel should be asked of the family members during  T! m3 z, R& T
the evaluation of any children who present with vir-) h8 F( u6 J- f; a6 s1 v2 u6 C/ k
ilization or peripheral precocious puberty. The diag-
6 X' G5 t  t( f& G9 W1 }1 ynosis can be established by just a few tests and by( V& j* P/ q8 ?5 {+ o! T- N
appropriate history. The inability to obtain such a
, W1 U( t0 y% z9 i4 v( W% o* _history, or failure to ask the specific questions, may( @/ D; P1 d6 ?) Z$ o
result in extensive, unnecessary, and expensive0 R3 f7 D, C: J/ R) _
investigation. The primary care physician should be
& C6 m6 z9 a9 K1 T* z. @aware of this fact, because most of these children+ V: M  Z& R  }% v* J* p$ U; X
may initially present in their practice. The Physicians’
* L3 P( m/ }( S5 q6 @8 IDesk Reference and package insert should also put a
, [: p6 H* ?0 w7 Nwarning about the virilizing effect on a male or
2 m3 d3 h' U9 f" Hfemale child who might come in contact with some-
7 N' `6 p. k( m& j. g* v% `one using any of these products.
6 ~; F* k' j/ _, e* S! g& k, uReferences- Q- p. I$ E( m2 O. i) u% S: |
1. Styne DM. The testes: disorder of sexual differentiation
7 N2 L6 J. Z% q, {; O! @and puberty in the male. In: Sperling MA, ed. Pediatric
1 g8 P4 u& y# w9 b! wEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 p' _' m% a# S4 a9 {2 |% p  }
2002: 565-628.1 W  ~& L  A2 i: i6 M
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
& E$ [: i5 b+ Npuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
$ c! S) r' Y( m3 o* v  qBoy Induced by Indirect Topical( k) L0 Y7 E6 e" o7 a  e0 O
Exposure to Testosterone
+ c( q6 Q; e8 h7 ]' N& zSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% J3 z/ b) R( Q
and Kenneth R. Rettig, MD14 \% b% K% V: {! J' X; [% K
Clinical Pediatrics! Y/ l0 v, i) E9 Z! u( y" E; n5 P
Volume 46 Number 6
% J6 J" Z9 k4 V% t& dJuly 2007 540-543; t6 E3 I& w+ m% b) n# `! _
© 2007 Sage Publications$ }7 h6 N) v+ h4 X# N4 }$ |) n: o
10.1177/00099228062966510 E9 V5 O( Z' ~  K; k
http://clp.sagepub.com$ G; K, ^8 d1 C4 Z$ h3 G
hosted at9 J, a7 W( V* ^& z8 z( @4 B  P
http://online.sagepub.com3 N% d! d% i+ Q) b6 G% L
Precocious puberty in boys, central or peripheral,
# @5 ~' Z+ m7 j9 b3 X$ m- Iis a significant concern for physicians. Central2 X) R, c0 b' B0 q' A8 S
precocious puberty (CPP), which is mediated! t/ q4 x2 @, k0 k" b4 U
through the hypothalamic pituitary gonadal axis, has0 l  \  m6 W# {7 `
a higher incidence of organic central nervous system
0 y* u+ p% H  V9 s( m9 i" clesions in boys.1,2 Virilization in boys, as manifested
8 l# h- M9 e6 I- K& g2 M+ ^by enlargement of the penis, development of pubic
; D6 n2 ~! l  Thair, and facial acne without enlargement of testi-) Z& P8 N+ ]4 h# ?
cles, suggests peripheral or pseudopuberty.1-3 We. n+ x- _9 F. I2 e
report a 16-month-old boy who presented with the, Q7 J6 ^8 P9 Q7 O8 c! A
enlargement of the phallus and pubic hair develop-
8 H  C$ h, S$ ]% h* Q/ W/ Wment without testicular enlargement, which was due9 F' P: K; ]* Z
to the unintentional exposure to androgen gel used by
% ~0 H% C& r3 y# |# K7 rthe father. The family initially concealed this infor-7 G  Q4 i! M5 s' \, U( R  q
mation, resulting in an extensive work-up for this
/ y0 d) k5 d: H# K3 p; g2 Y" Dchild. Given the widespread and easy availability of$ P! J7 q0 ?6 N2 [( c7 E" H
testosterone gel and cream, we believe this is proba-
* `. I# }5 |" u, C/ z+ i( m# bbly more common than the rare case report in the" W7 C7 ]' U) g& ?* }1 q% R
literature.4  f. I  O! H7 v) q0 A( o$ Y
Patient Report/ D' B% d2 Y/ N" Z+ m+ T: J
A 16-month-old white child was referred to the
$ O' ~8 s# t) c% Aendocrine clinic by his pediatrician with the concern4 A4 t7 H7 s! a4 J4 r
of early sexual development. His mother noticed4 K/ m1 G! g  c* c% |
light colored pubic hair development when he was+ J/ k* e: m2 y0 _7 ]
From the 1Division of Pediatric Endocrinology, 2University of
% f- }: d+ _6 n+ Z9 c4 [9 DSouth Alabama Medical Center, Mobile, Alabama.: I- A, m6 y! C* G+ U. D9 ?
Address correspondence to: Samar K. Bhowmick, MD, FACE,6 `8 d2 C% ?" c3 G
Professor of Pediatrics, University of South Alabama, College of4 n3 R0 A' t, T- P% v% C% X
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 \2 S+ Z$ M0 _* p6 S& Ee-mail: [email protected].
$ N: C9 ]) H8 |6 ?$ C4 Babout 6 to 7 months old, which progressively became# ]5 u2 H* n7 Y: ~0 C3 e* r  q
darker. She was also concerned about the enlarge-
  y9 g" b8 w7 x: Rment of his penis and frequent erections. The child
( Q4 |! j+ Z: P8 lwas the product of a full-term normal delivery, with; X5 m1 N, ~' f( z$ u
a birth weight of 7 lb 14 oz, and birth length of
! v) ]2 k& ^! g7 c2 T+ g' X3 h20 inches. He was breast-fed throughout the first year# u3 `4 `& ]( x+ r3 n, L  a
of life and was still receiving breast milk along with
! i$ }, R3 Q5 f4 x1 S8 v) Ysolid food. He had no hospitalizations or surgery,
6 _1 q( C) N1 X6 f0 T9 uand his psychosocial and psychomotor development
) v; @; @4 c& Pwas age appropriate.
+ `* T' f8 i# ~' ^( d, c* vThe family history was remarkable for the father,8 D; ~3 G" W- @# A2 U" j8 e4 |
who was diagnosed with hypothyroidism at age 16,
8 M9 G% O- \  p5 ?4 }2 C' i" Jwhich was treated with thyroxine. The father’s+ s/ \% A% |% V5 C$ N
height was 6 feet, and he went through a somewhat" j, U3 |* P0 R8 [" I3 W
early puberty and had stopped growing by age 14.4 U, u" x# W8 [; f# g& X& y
The father denied taking any other medication. The8 t* L5 u6 U; c- W. w
child’s mother was in good health. Her menarche
2 l  h8 T2 X& W! O% O- [( Ywas at 11 years of age, and her height was at 5 feet
$ H  F  w* i% @8 W) Q5 inches. There was no other family history of pre-8 s1 j! J( S2 m4 ~) G
cocious sexual development in the first-degree rela-) z& C! C  n' D
tives. There were no siblings.
+ N) R; `( O1 R( Z- p4 f# q: Q" mPhysical Examination
- O, H2 R# H" {# G' q) q- n6 v% aThe physical examination revealed a very active,* ~: P- T, B; Y5 T! b/ I' b
playful, and healthy boy. The vital signs documented
4 b6 S/ X$ r- b$ n" R& Pa blood pressure of 85/50 mm Hg, his length was5 V/ U% G$ B" j
90 cm (>97th percentile), and his weight was 14.4 kg" ~" i8 Q- \* U: u; s% Q
(also >97th percentile). The observed yearly growth& L  F+ p7 M6 _* w4 r' N3 V
velocity was 30 cm (12 inches). The examination of- v0 p8 N$ Y% e  p. K
the neck revealed no thyroid enlargement.
; i& r* h6 t$ {4 L( c5 }0 h; XThe genitourinary examination was remarkable for
+ ^: n/ O' }) O* ~2 `3 g( Lenlargement of the penis, with a stretched length of
# B4 }' `; J/ i# H. C8 cm and a width of 2 cm. The glans penis was very well+ w  L% |4 b" o
developed. The pubic hair was Tanner II, mostly around
: U' M' r2 Y( r/ s540- K( r3 F# W& R. S! f
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 x: G$ c+ a/ ?' b6 q+ Q5 \, Lthe base of the phallus and was dark and curled. The
/ K" R1 v! m/ l  jtesticular volume was prepubertal at 2 mL each.
2 H! R7 U$ \* c/ l8 xThe skin was moist and smooth and somewhat4 d0 ?9 ]* }# ?& m& f! x, Z
oily. No axillary hair was noted. There were no4 E. V; `& G' C; T& N
abnormal skin pigmentations or café-au-lait spots.0 R! X# L9 ^) Y+ J
Neurologic evaluation showed deep tendon reflex 2+
3 `2 G! q% l/ [* Y1 u- @bilateral and symmetrical. There was no suggestion
/ n. `1 k: Z3 n* D; G; }/ Iof papilledema.+ B5 H1 U$ O& Q* Y" V- a( h
Laboratory Evaluation3 N( W2 b; [7 I
The bone age was consistent with 28 months by
0 D1 g  r- o) G1 ]using the standard of Greulich and Pyle at a chrono-# q( n+ C6 I+ A: c
logic age of 16 months (advanced).5 Chromosomal
4 W' i2 a1 m3 Hkaryotype was 46XY. The thyroid function test3 U' u0 O1 i1 Z& V6 S! ~
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 O. Q' Q& H5 X& E* _% {2 t2 H0 C% G. jlating hormone level was 1.3 µIU/mL (both normal)., R0 r, g* A* V$ @5 S
The concentrations of serum electrolytes, blood
6 s5 C1 o  t% i* l3 x7 P: y4 A- uurea nitrogen, creatinine, and calcium all were, Q4 L& p! N3 U* f3 Y! h0 p5 C1 a! f
within normal range for his age. The concentration
3 ]5 l- w+ D: B" A0 xof serum 17-hydroxyprogesterone was 16 ng/dL
  ^) d, P) {$ M(normal, 3 to 90 ng/dL), androstenedione was 208 J9 u: j% v5 e% @
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! G+ M! c% M  ?( Q- _8 M0 eterone was 38 ng/dL (normal, 50 to 760 ng/dL),
: T( K  o- W/ D* L1 Gdesoxycorticosterone was 4.3 ng/dL (normal, 7 to4 ~! ~3 l8 F+ P9 Q9 l
49ng/dL), 11-desoxycortisol (specific compound S)  K' ~" D$ a/ M. X
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 O  Q& X$ d5 Z2 y( n( H+ O4 o
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 v- D% k: }+ O& |testosterone was 60 ng/dL (normal <3 to 10 ng/dL),% ], j0 Z4 b9 W. x* l
and β-human chorionic gonadotropin was less than
) s8 g- P' p0 {5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 I7 Z7 S) ^$ F' n: W6 @* b. [stimulating hormone and leuteinizing hormone
- N& U/ L% ^. F! P( Sconcentrations were less than 0.05 mIU/mL+ ?  b: f! D/ j: E$ c5 R8 L
(prepubertal).5 _2 d4 {5 f1 x! v9 \9 l1 {
The parents were notified about the laboratory: I: |  Q+ S2 W$ p" M' ^: x
results and were informed that all of the tests were
8 Y( g  m* ?) x2 i0 u" W" ~normal except the testosterone level was high. The
$ u6 z3 j4 g5 Xfollow-up visit was arranged within a few weeks to
* ]1 p; Z! z4 s* O6 V3 X! Q: oobtain testicular and abdominal sonograms; how-$ {! B, x! s5 _4 O. b
ever, the family did not return for 4 months.
# q) \: p3 v5 M1 x( }Physical examination at this time revealed that the
, _) K8 X+ c  I, J3 B* X1 wchild had grown 2.5 cm in 4 months and had gained- {" R9 c5 \9 G' `+ R; I
2 kg of weight. Physical examination remained7 U: X7 ~+ M9 o4 o5 a
unchanged. Surprisingly, the pubic hair almost com-. D$ {1 A7 {$ O$ `5 Z5 E
pletely disappeared except for a few vellous hairs at; _& w' S1 k3 L5 ~7 f
the base of the phallus. Testicular volume was still 2: H+ `: O" X" c/ }; M- g- q: c
mL, and the size of the penis remained unchanged.
/ V- w3 x4 r/ ]: F6 {The mother also said that the boy was no longer hav-8 |! Y8 d; ~: k9 y; k+ x& g% N
ing frequent erections.7 w& ~$ I6 u6 r, y  l
Both parents were again questioned about use of/ q7 B5 o% V3 I. g
any ointment/creams that they may have applied to
. v7 K4 D' R$ r3 v+ Cthe child’s skin. This time the father admitted the
$ L; _9 i3 L& y" c* k0 O" ~Topical Testosterone Exposure / Bhowmick et al 541
# V+ |" j! a% B, ^1 Uuse of testosterone gel twice daily that he was apply-
( P2 o; z# z" x. u0 \0 p3 d6 xing over his own shoulders, chest, and back area for
' X& t- Q0 f* `: B- [# t3 E: r: ^a year. The father also revealed he was embarrassed" \4 C, M9 }4 O
to disclose that he was using a testosterone gel pre-) H4 H, N  k3 r8 ]8 ]" Z  {
scribed by his family physician for decreased libido1 E4 o+ }4 t- E7 Y- ]
secondary to depression.
3 S9 V. s8 c7 b7 ]: @* D7 Q0 @The child slept in the same bed with parents.
9 w7 _  s, m1 }" t6 w! K$ q1 RThe father would hug the baby and hold him on his
1 j! Z2 w, j+ Z5 }1 fchest for a considerable period of time, causing sig-
/ [  Y7 @  ?4 F" y3 ]2 {nificant bare skin contact between baby and father." R( Q0 h0 R( j3 X) ]% N' j
The father also admitted that after the phone call,7 {0 {* F2 V# L! l8 V) A3 i# H
when he learned the testosterone level in the baby/ p( l5 H* Q; K2 a4 k0 }& `
was high, he then read the product information
8 D. _, g- H! n- a0 lpacket and concluded that it was most likely the rea-
5 z5 P; ?8 j" L' Bson for the child’s virilization. At that time, they2 ]) n& I, V) B5 g' T$ v
decided to put the baby in a separate bed, and the
1 f) U" L# q( M) y1 s% rfather was not hugging him with bare skin and had) I, b5 r+ w. Y
been using protective clothing. A repeat testosterone1 T; h5 X$ ^0 C- a( f7 L, \  l
test was ordered, but the family did not go to the
- ^; r4 [1 h% E2 X3 j5 S3 Mlaboratory to obtain the test.1 T! `0 o$ U: ]) F$ x  B
Discussion
, m# n) I8 \- J! p8 X! ]* d3 aPrecocious puberty in boys is defined as secondary
7 D8 S* k. c' Vsexual development before 9 years of age.1,4( ~$ W- ]% U5 q$ Z& }* n, L
Precocious puberty is termed as central (true) when  h# M$ ?' y& M+ T
it is caused by the premature activation of hypo-
8 \& U# n; q# K/ c+ L0 ~thalamic pituitary gonadal axis. CPP is more com-: P% X$ z' G3 w: c9 A
mon in girls than in boys.1,3 Most boys with CPP- h* i  V) L+ N# S
may have a central nervous system lesion that is5 I7 B6 }* w/ e9 n0 r4 y
responsible for the early activation of the hypothal-. o  j' ]4 d0 S0 K/ ]4 p9 z
amic pituitary gonadal axis.1-3 Thus, greater empha-
7 J4 L7 x  b( d( y& ?sis has been given to neuroradiologic imaging in
3 ]9 W1 k5 n4 |5 [) R' Qboys with precocious puberty. In addition to viril-
% c; ?/ _$ G# L2 ?! k; m# Xization, the clinical hallmark of CPP is the symmet-( k& A: x. I6 n! B4 P3 ^; L
rical testicular growth secondary to stimulation by
) K8 N  _/ h+ Y6 [/ j* Pgonadotropins.1,37 h' x$ n( m. d  L0 n1 q3 w0 u
Gonadotropin-independent peripheral preco-
, s* f/ [; S3 {cious puberty in boys also results from inappropriate# T+ b! I* Z  s' y; e% \
androgenic stimulation from either endogenous or. x/ {# v- U% d: T
exogenous sources, nonpituitary gonadotropin stim-
' Q8 _( X- P# hulation, and rare activating mutations.3 Virilizing
: @% r& f6 g: d& h1 E6 wcongenital adrenal hyperplasia producing excessive9 d1 o) `: m* c7 X0 d
adrenal androgens is a common cause of precocious  t) R/ y5 ?: W3 F& D  A
puberty in boys.3,4: a8 \4 l5 [) n, `: M4 O
The most common form of congenital adrenal7 n5 \, |' ?9 y2 x+ u
hyperplasia is the 21-hydroxylase enzyme deficiency.
6 I  O, H/ H& ]# ~7 t) i$ qThe 11-β hydroxylase deficiency may also result in  y8 Z. e9 e9 T' f7 m
excessive adrenal androgen production, and rarely," t* j. D3 {8 _& ^; z' g
an adrenal tumor may also cause adrenal androgen
) N1 \) k' f: X; V# f  n) lexcess.1,3/ V! q5 J0 K! Z4 ]6 z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 _* [5 V3 `/ b( ~5 L542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! R: w) o$ r. u: g' s
A unique entity of male-limited gonadotropin-9 U) U$ \5 [' @  C0 u) z
independent precocious puberty, which is also known& b+ J' B  z; [
as testotoxicosis, may cause precocious puberty at a1 ?) m6 b/ y8 x' x7 j
very young age. The physical findings in these boys
, g9 h% M: v( C; H3 C  W' |2 Zwith this disorder are full pubertal development,
+ U' @1 U6 k0 c( i( \9 U+ F+ F9 T* Zincluding bilateral testicular growth, similar to boys3 C3 R& f. P2 j3 i  c! X
with CPP. The gonadotropin levels in this disorder( P% l  }) p2 m
are suppressed to prepubertal levels and do not show
# i' N, q- P* ]! l! Z# zpubertal response of gonadotropin after gonadotropin-) u& w% T6 r. [  L5 _
releasing hormone stimulation. This is a sex-linked
- V7 a7 R2 m, xautosomal dominant disorder that affects only6 _% S! Z1 `* E; l. E; v# u
males; therefore, other male members of the family# f' m# B5 q. p1 k# {
may have similar precocious puberty.3
$ _2 Y1 o, N% z% q2 Z6 jIn our patient, physical examination was incon-$ @( Z" Z! s6 D
sistent with true precocious puberty since his testi-
7 y0 d0 j* O1 G9 V( f6 l( N3 q6 _8 rcles were prepubertal in size. However, testotoxicosis
9 f$ g, ^) z4 L; w+ E5 ^8 t" Zwas in the differential diagnosis because his father+ S7 V/ T& r5 F6 {
started puberty somewhat early, and occasionally,  H: ~7 I* Q% K6 v* `% m1 i9 \
testicular enlargement is not that evident in the) N% A$ o1 P  c) _9 e
beginning of this process.1 In the absence of a neg-
# q+ o8 r) v( v' z, {4 zative initial history of androgen exposure, our
7 s7 m9 D( z) `% w. zbiggest concern was virilizing adrenal hyperplasia,
$ Y+ A1 L; P/ T$ {either 21-hydroxylase deficiency or 11-β hydroxylase
  \1 e  W) _6 w3 cdeficiency. Those diagnoses were excluded by find-
3 A, K% o& m: Q% B' L9 jing the normal level of adrenal steroids.
+ J# q5 G8 N1 b+ ?5 e, vThe diagnosis of exogenous androgens was strongly
  l; k1 @; ?5 ?4 G4 a; _suspected in a follow-up visit after 4 months because
' S1 E; ~/ ~2 h5 A" Sthe physical examination revealed the complete disap-
4 H$ @! @- G, b+ l1 Apearance of pubic hair, normal growth velocity, and. k5 J' B8 O+ u6 Z6 P4 T
decreased erections. The father admitted using a testos-
! v0 h, e0 h! q: E; @terone gel, which he concealed at first visit. He was
4 o, D; x5 A' Q# ]# `5 a: ^using it rather frequently, twice a day. The Physicians’
( @) {% t/ e$ [+ |Desk Reference, or package insert of this product, gel or# |# }6 h6 t& L  R. N2 C0 I
cream, cautions about dermal testosterone transfer to6 X; E) |/ g) j; t* a& a: M
unprotected females through direct skin exposure.
: L2 w8 `0 H8 {6 G' M8 MSerum testosterone level was found to be 2 times the
0 T: d( G/ L. u7 G9 [3 w) V& wbaseline value in those females who were exposed to
) x/ }$ o: z. L$ Q0 P& Xeven 15 minutes of direct skin contact with their male
* [+ F7 G. ?8 K8 q1 Lpartners.6 However, when a shirt covered the applica-4 o+ ^, {5 J! ^- Y  A4 o1 Y
tion site, this testosterone transfer was prevented.2 f. {- M( w, x. t- P) B
Our patient’s testosterone level was 60 ng/mL,
  q( G; O6 K  m: j% P$ ywhich was clearly high. Some studies suggest that6 I. S& h, A/ @% T/ {1 _
dermal conversion of testosterone to dihydrotestos-5 q6 g" U' q) H' p- p& B
terone, which is a more potent metabolite, is more
/ i" X9 S" \; V/ {) H8 c* pactive in young children exposed to testosterone. ^# |! c% n' W) J' o( Z
exogenously7; however, we did not measure a dihy-0 s: V- i6 f7 ^" Z/ s3 g
drotestosterone level in our patient. In addition to  O2 w' {' ]8 X; }2 E
virilization, exposure to exogenous testosterone in! ^( p. k  `$ n8 t
children results in an increase in growth velocity and# N" x8 K, j4 c+ x4 x
advanced bone age, as seen in our patient.
: E+ P" G+ A$ p* y' J+ MThe long-term effect of androgen exposure during, E" Z7 [& u( s! q6 `- S
early childhood on pubertal development and final* z1 g- v, Y" k( m( l! @, g
adult height are not fully known and always remain
3 X$ G7 p; n9 M6 s" O! f+ Va concern. Children treated with short-term testos-
4 ]+ ~$ r( ~) U. Y) Gterone injection or topical androgen may exhibit some
+ N; J- x2 I( A2 g; H" }acceleration of the skeletal maturation; however, after
3 i7 l" ]+ \2 J, E" a8 Qcessation of treatment, the rate of bone maturation3 ?5 `9 E9 w: p# o' @6 h2 i4 e
decelerates and gradually returns to normal.8,94 L, Q8 d( H2 S
There are conflicting reports and controversy7 @7 i; ]* q1 e' {1 \4 I+ h
over the effect of early androgen exposure on adult* ]6 I( w- n: z8 G+ l
penile length.10,11 Some reports suggest subnormal
. @2 J$ Z+ r8 radult penile length, apparently because of downreg-) s2 d! `' B  |; j7 d8 z+ V5 N% Y' S
ulation of androgen receptor number.10,12 However,
  C0 O: K2 O: ?Sutherland et al13 did not find a correlation between/ _* P' T9 ^$ x/ U% S& }  O/ k7 \# q
childhood testosterone exposure and reduced adult
* s( d9 ~4 s0 s% J8 G) gpenile length in clinical studies.( ]# y5 I* K! o
Nonetheless, we do not believe our patient is
& ?: j% l" ?: M/ H' x  [# o4 Hgoing to experience any of the untoward effects from
7 [8 x! J0 k! @, ftestosterone exposure as mentioned earlier because- ]2 E# i/ f8 j& `0 n
the exposure was not for a prolonged period of time.
  Q7 A$ W! Q/ @, N0 Y' t& i) S- e4 MAlthough the bone age was advanced at the time of
- w; x2 s/ G$ R2 ydiagnosis, the child had a normal growth velocity at
' d- z9 W6 @2 y+ i+ l9 athe follow-up visit. It is hoped that his final adult% h( Q4 W: k' t/ }; N' i- n. T: C
height will not be affected.- Z2 k5 V4 z5 s
Although rarely reported, the widespread avail-
& ?7 O5 d- O4 q# F( Xability of androgen products in our society may( M3 @' @- k1 s, j7 d
indeed cause more virilization in male or female
$ s, N# E% X( c+ D+ h+ g( zchildren than one would realize. Exposure to andro-
. `: Q4 A6 S; ]' _$ m3 i# }5 O# r! egen products must be considered and specific ques-
- ?8 Q) ^% f) h8 u( w/ Ktioning about the use of a testosterone product or' |, |; j5 w! F2 _: r
gel should be asked of the family members during
! l; g: r7 J5 t7 {. E" K3 Rthe evaluation of any children who present with vir-
1 S8 j& p3 H9 @; F( x$ Lilization or peripheral precocious puberty. The diag-9 ?" q2 {4 l; M+ g
nosis can be established by just a few tests and by; v  m6 c  \! ~/ H9 p6 r' I
appropriate history. The inability to obtain such a
% @' l+ F- L; H- |. v% mhistory, or failure to ask the specific questions, may
& k2 {" N7 t( N  _result in extensive, unnecessary, and expensive+ p8 C0 F9 Z: x
investigation. The primary care physician should be6 ?: |( X" g- E  O5 U6 |8 C3 |. z+ O
aware of this fact, because most of these children9 z: a% N' E$ t% u' C" w/ v$ s' p
may initially present in their practice. The Physicians’+ Q5 B$ f$ N3 y) i, c7 ~, w5 j& r
Desk Reference and package insert should also put a
7 X( i8 W" m. q+ K! C" k# Fwarning about the virilizing effect on a male or
) T2 c  e3 v- |; o0 w+ `female child who might come in contact with some-
) i# i' L6 E: K( a" Z# pone using any of these products.
( X7 b# c* r) CReferences) Q6 w4 C, a/ @( C
1. Styne DM. The testes: disorder of sexual differentiation% |* f9 W2 H1 C3 j' m
and puberty in the male. In: Sperling MA, ed. Pediatric/ j5 D" s2 E) w8 [: f
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ _& j/ F1 _0 M4 y6 Y% v
2002: 565-628.: K* B  A' k& G$ S7 _. R- S0 C
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- j; o' a: \5 S4 t" X
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

( C. K) l3 F  \+ v+ z  m' i2 n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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