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Sexual Precocity in a 16-Month-Old7 e" v" ]' d8 L# K. F$ G
Boy Induced by Indirect Topical9 l2 b" ?3 D$ e3 P2 g' m
Exposure to Testosterone
- E, i8 m  j2 w) x" u+ B% X. ?Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
6 W  ]  l. m- H& s* \$ I: gand Kenneth R. Rettig, MD1- W( e8 Y( M5 U' J! u5 n, O# m
Clinical Pediatrics' ]/ [8 \2 o; }" T0 v% _0 u8 J7 t
Volume 46 Number 6: d9 I& u& U% Y9 Q: O- p
July 2007 540-543
3 o1 u' z3 G# c; A7 m) y6 ]9 a© 2007 Sage Publications$ r1 k9 L* ~0 @: T$ f/ `, I: b
10.1177/0009922806296651# S, I7 q4 M- ^3 K' f
http://clp.sagepub.com
4 p4 @+ G9 r9 [, |8 Mhosted at6 ?! H; N/ K4 D+ ]+ t: [9 u$ K
http://online.sagepub.com
, \4 q/ t2 v' \* x7 \8 KPrecocious puberty in boys, central or peripheral,* W* [& }7 F* ~* D- O2 X4 X
is a significant concern for physicians. Central1 _$ b0 O* C, H, W1 u5 w
precocious puberty (CPP), which is mediated7 W, A/ f, q* l0 S! G0 q
through the hypothalamic pituitary gonadal axis, has
! _( g6 \- Y( e' v: ^* ga higher incidence of organic central nervous system9 @' r' L, R) F+ C
lesions in boys.1,2 Virilization in boys, as manifested8 z$ |. A2 C+ ~4 Q; u
by enlargement of the penis, development of pubic$ Z8 t9 \; Q5 t6 w' y4 N2 j
hair, and facial acne without enlargement of testi-& }& R  `) }7 x8 ]' _* g2 k
cles, suggests peripheral or pseudopuberty.1-3 We
0 t" s0 I" x8 dreport a 16-month-old boy who presented with the$ l- Y: e. z" h/ T% K- d& M3 z
enlargement of the phallus and pubic hair develop-; v' O9 B+ t5 p$ t4 g. e
ment without testicular enlargement, which was due
' j) E( t( M8 Y7 Z& B" U1 `; \; T2 i# u( }to the unintentional exposure to androgen gel used by( {+ C% F. m+ B7 k) ], x
the father. The family initially concealed this infor-
3 [* V; ]! M* U# o' w2 ?' Emation, resulting in an extensive work-up for this* M4 w4 c3 B. {% j/ b6 d
child. Given the widespread and easy availability of/ M6 Y0 [8 l, T6 K1 Y8 |
testosterone gel and cream, we believe this is proba-2 m, B" @5 [# }  i. l" R
bly more common than the rare case report in the
' G, m* h; I. z8 a, _+ hliterature.4
( o+ d9 P( ~. d$ q- \1 K0 QPatient Report
' W( a; L  [  [" iA 16-month-old white child was referred to the- f! ~5 U8 W+ g5 k* G6 \
endocrine clinic by his pediatrician with the concern2 h# }4 S+ i" d5 a0 P) H
of early sexual development. His mother noticed
# J' g  e% c* c) d. mlight colored pubic hair development when he was. @' H8 o3 x: C; ~0 f- A/ ~9 j. I, |1 D
From the 1Division of Pediatric Endocrinology, 2University of
  a$ I# _' L5 A. l, C* ^" n9 aSouth Alabama Medical Center, Mobile, Alabama.) n& u4 v1 j- B; [4 S  F
Address correspondence to: Samar K. Bhowmick, MD, FACE,. i! Y7 Z2 r% L1 e8 m. F
Professor of Pediatrics, University of South Alabama, College of1 P8 p& e0 \2 G+ M
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ R9 x4 {( T- C* s9 Ke-mail: [email protected].  f. P) I2 U- B! v! F
about 6 to 7 months old, which progressively became
1 f( N# C9 V+ q/ Mdarker. She was also concerned about the enlarge-
6 u+ k2 ?5 m4 c; h5 Q& y" f! tment of his penis and frequent erections. The child
4 n. H7 }; f% {$ x  x& C: p: j& P' H3 vwas the product of a full-term normal delivery, with
6 O& F1 z4 K6 Q) _; f# A( Va birth weight of 7 lb 14 oz, and birth length of
1 a4 K7 v1 P* r9 \! ?2 `: z20 inches. He was breast-fed throughout the first year
4 H* ^+ P1 l* l7 C/ e( qof life and was still receiving breast milk along with
( R. x0 X1 o0 w8 G) o, q. Bsolid food. He had no hospitalizations or surgery,
" r- ?3 l  H+ X* ^and his psychosocial and psychomotor development1 r7 c! t: [1 n! k
was age appropriate.
# R* b; Q5 p$ U2 X# hThe family history was remarkable for the father,2 {) ?# l* y" A+ W7 i
who was diagnosed with hypothyroidism at age 16,
) q! E: J5 X1 _3 q  [) a% ?which was treated with thyroxine. The father’s9 H( G; _- s% `, ?4 S
height was 6 feet, and he went through a somewhat
% p( J& H3 \3 H* I8 tearly puberty and had stopped growing by age 14.
6 c- M  i3 l: N* I$ WThe father denied taking any other medication. The/ D$ U- x+ \: s
child’s mother was in good health. Her menarche
4 ]9 {7 i6 M9 U6 m: f4 D, q) \# b+ Ewas at 11 years of age, and her height was at 5 feet
$ d0 s" A4 k8 e' C5 inches. There was no other family history of pre-2 v$ u' |1 O( H4 |
cocious sexual development in the first-degree rela-: S& o! C4 Q* ?: n
tives. There were no siblings.
, |  W3 I  F) N  I4 A  ^Physical Examination1 Y# N8 V7 l( w
The physical examination revealed a very active,
/ o! z% b% K: W6 p- Lplayful, and healthy boy. The vital signs documented1 \! W7 |# o; \4 p$ e  B3 {; n
a blood pressure of 85/50 mm Hg, his length was
& \( p- A! q5 O- E4 ^90 cm (>97th percentile), and his weight was 14.4 kg
( F8 A9 K) T- `/ [8 d) i$ A. H- K(also >97th percentile). The observed yearly growth/ c# O. f4 E2 b% b9 o8 H
velocity was 30 cm (12 inches). The examination of! |" a* P% W2 Q% {7 w
the neck revealed no thyroid enlargement./ F2 ]- u5 Q, o) s4 t
The genitourinary examination was remarkable for
) I9 @, b4 r/ zenlargement of the penis, with a stretched length of
+ W- w. _: w' R- E" Q+ G( t8 cm and a width of 2 cm. The glans penis was very well# D% c# [) j' u. E+ ~$ S
developed. The pubic hair was Tanner II, mostly around+ {3 T8 w  U2 Y7 B
5405 {4 c" i; x* o8 x2 y" I$ B
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 `, g+ ?: m) W, _$ o# xthe base of the phallus and was dark and curled. The  {0 ~0 k$ r( s* h  q
testicular volume was prepubertal at 2 mL each.
* K6 T4 C6 ?2 F$ o# zThe skin was moist and smooth and somewhat
6 V. ^  h9 B! C# s0 H4 boily. No axillary hair was noted. There were no1 J# q' G1 ^' y& i4 {. Y+ V* n
abnormal skin pigmentations or café-au-lait spots.! ]) J' k) O1 T" @1 N
Neurologic evaluation showed deep tendon reflex 2+
9 O; v2 s+ I$ I2 g0 F) W1 X: e! cbilateral and symmetrical. There was no suggestion; ^' f' ~- e  {1 e4 `
of papilledema.
7 K  C3 m0 A( K& H8 r0 yLaboratory Evaluation( e8 B/ b9 ?. P
The bone age was consistent with 28 months by
5 a$ O0 ^& x& [4 A0 B8 Tusing the standard of Greulich and Pyle at a chrono-
2 ^) y- e2 m% i: Ulogic age of 16 months (advanced).5 Chromosomal
# K+ ?' q6 N- Zkaryotype was 46XY. The thyroid function test( }  Z, F1 b$ R* Z) _
showed a free T4 of 1.69 ng/dL, and thyroid stimu-1 v0 C- Y) F) L9 h2 L
lating hormone level was 1.3 µIU/mL (both normal).6 B, X' O4 S9 f  E
The concentrations of serum electrolytes, blood
% q1 Z+ J+ |3 F0 g9 L+ A$ ~urea nitrogen, creatinine, and calcium all were
, w9 ]5 r# ~2 j- rwithin normal range for his age. The concentration! U4 X- K9 b( P7 M) C9 G" Y/ ^* O9 O. g
of serum 17-hydroxyprogesterone was 16 ng/dL
" ^! A5 q7 L- v& L5 D7 g$ H' g: J(normal, 3 to 90 ng/dL), androstenedione was 20
" o: k, B6 t1 @: o9 T" s7 Ong/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# O: {3 f. U, m! l% M
terone was 38 ng/dL (normal, 50 to 760 ng/dL),7 R) `/ {6 a+ W" {6 D
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 P- M5 l& v% i5 m- K49ng/dL), 11-desoxycortisol (specific compound S)0 }+ g1 b1 l. L& f. y% i; J
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-' Z$ P/ e1 G/ _" e+ b( A) P3 R- ^
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
! n5 W, \7 h& v. E6 stestosterone was 60 ng/dL (normal <3 to 10 ng/dL),. S0 n0 ^) t- K9 B; c4 f
and β-human chorionic gonadotropin was less than
: G9 }+ u# f$ b8 g5 mIU/mL (normal <5 mIU/mL). Serum follicular
" D1 D2 `- {9 ]7 O; G* ]0 qstimulating hormone and leuteinizing hormone8 ]0 }; p8 h" [0 I2 ], J
concentrations were less than 0.05 mIU/mL  a3 r* \5 k* t$ s1 P
(prepubertal).
0 I8 {- r' I1 T# q9 Y) r2 u2 PThe parents were notified about the laboratory% P- y( W% n9 R1 j' O. m  M) H
results and were informed that all of the tests were
; g+ |, S5 a: Q" ?1 h/ J* r) z/ Unormal except the testosterone level was high. The
$ J" T' Q% c% ]" Wfollow-up visit was arranged within a few weeks to
$ \3 T4 v  E* I& W% |% H* M1 ?obtain testicular and abdominal sonograms; how-" w- u( }7 G" [8 F3 J
ever, the family did not return for 4 months.
6 z3 a* _9 v+ k# {0 ~0 f, A6 J2 kPhysical examination at this time revealed that the
0 ?1 n' q' I! _& Uchild had grown 2.5 cm in 4 months and had gained
$ N/ h! D& d* j; @7 ?0 y* G2 kg of weight. Physical examination remained
2 \7 ^# c& _. [+ u9 Q) m- Junchanged. Surprisingly, the pubic hair almost com-4 l0 [+ l6 K" \: A; a
pletely disappeared except for a few vellous hairs at
7 H6 {4 D- e/ |# J0 \the base of the phallus. Testicular volume was still 2
; E. N" \) b  T! {8 amL, and the size of the penis remained unchanged.$ ]' H& y5 c  z9 ~2 o
The mother also said that the boy was no longer hav-
9 o! ]1 Z9 ~1 g- n8 Qing frequent erections.
+ H9 Z1 w  _/ h3 ]5 x6 UBoth parents were again questioned about use of
& j8 J; Z8 T0 Rany ointment/creams that they may have applied to8 d" i1 x2 O( F: s1 H
the child’s skin. This time the father admitted the, ~/ {; L/ `/ g
Topical Testosterone Exposure / Bhowmick et al 5417 w# s3 v) A% t! T) [5 H
use of testosterone gel twice daily that he was apply-
( x, ~# v$ O! I3 Q! {$ ving over his own shoulders, chest, and back area for
# N) N* G1 _6 E) a5 p' Va year. The father also revealed he was embarrassed
' f' Y5 F1 ]  {2 {/ W7 nto disclose that he was using a testosterone gel pre-+ I3 J  b+ n+ i! @3 F6 ^9 P) Z+ }# @5 N: _
scribed by his family physician for decreased libido, G8 }  ?( r6 E8 u( @4 n% D5 K
secondary to depression.( B% l/ i  R3 C. F2 `$ P7 B
The child slept in the same bed with parents., f# Z* B5 f+ {4 T
The father would hug the baby and hold him on his
. l4 _  N2 U' z# K0 ?chest for a considerable period of time, causing sig-
! W! V5 b1 R" P/ x7 f/ Rnificant bare skin contact between baby and father.
* f  U% S) @' Y: q" x) zThe father also admitted that after the phone call,. x( I8 e3 i8 G8 A( X$ M
when he learned the testosterone level in the baby' J8 b# Z+ V8 t+ m7 H
was high, he then read the product information
& [1 ^8 a! Z$ a' x) ?( wpacket and concluded that it was most likely the rea-
9 l5 D/ n6 Q. ~7 U2 X$ o: Uson for the child’s virilization. At that time, they& \  ^) h( G$ O3 p
decided to put the baby in a separate bed, and the2 S" }. x2 |( c6 l
father was not hugging him with bare skin and had
* c6 u1 g  d5 O" U8 y0 A6 Jbeen using protective clothing. A repeat testosterone9 P# w8 D* Y$ ^0 C% [
test was ordered, but the family did not go to the
3 F4 f/ w: _( o9 r: h6 b+ n" qlaboratory to obtain the test.% |- v* u, ?+ Z# v
Discussion( {+ z4 |6 S$ V
Precocious puberty in boys is defined as secondary! |  O2 I% J0 F3 q# |- z' e
sexual development before 9 years of age.1,4; h3 `' z  j- s
Precocious puberty is termed as central (true) when
) T7 ]3 N( u$ K. [! _7 i& A: Dit is caused by the premature activation of hypo-0 A' a4 E0 Z& O2 Z
thalamic pituitary gonadal axis. CPP is more com-
, n% q  c; d1 p) M3 k( d+ dmon in girls than in boys.1,3 Most boys with CPP3 z) Y" m% g9 h' |
may have a central nervous system lesion that is/ d- {- p& t- j& {. |0 e3 M
responsible for the early activation of the hypothal-7 k/ F4 ]! u3 z! ]" o+ z
amic pituitary gonadal axis.1-3 Thus, greater empha-
: U7 F, ]0 p% Isis has been given to neuroradiologic imaging in
0 x' ~, A% Z7 qboys with precocious puberty. In addition to viril-
3 c. d9 ?0 e! `9 {ization, the clinical hallmark of CPP is the symmet-
' N& K# a) R3 Y; }' Y/ r* Qrical testicular growth secondary to stimulation by; }& B* {4 l( S" J' a
gonadotropins.1,3
4 x, g* A) v, w; bGonadotropin-independent peripheral preco-" e; ]  R: y1 I
cious puberty in boys also results from inappropriate" Q  Y) e5 T. [2 r+ N! [# S# [
androgenic stimulation from either endogenous or* r" a; u& ~; U' h1 r% p8 M3 u2 O
exogenous sources, nonpituitary gonadotropin stim-
' ^: u9 V% B- Rulation, and rare activating mutations.3 Virilizing$ K. ?( q6 m; s. L& S
congenital adrenal hyperplasia producing excessive9 W/ i" \7 W. A0 X3 t
adrenal androgens is a common cause of precocious2 [% ~4 K8 G( M( B
puberty in boys.3,4
. O/ |/ ~$ q# ~+ X/ s7 GThe most common form of congenital adrenal
0 m8 T2 ^3 O* B( i: E  _hyperplasia is the 21-hydroxylase enzyme deficiency.
9 l5 K1 X" E+ s. _1 s4 ]+ UThe 11-β hydroxylase deficiency may also result in# z% @/ s$ K/ k! b4 b# R1 q4 _' a
excessive adrenal androgen production, and rarely,
7 l- A: z0 P+ x0 gan adrenal tumor may also cause adrenal androgen
6 H  ]7 b1 O9 |- Zexcess.1,3
7 u) G) ]8 @0 f* G# }at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. M% R4 t/ @4 d5 P; `, i- R542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* r+ n+ m! P- f; @3 ^
A unique entity of male-limited gonadotropin-4 {- W. Q, D7 [( p3 Y2 H. Y
independent precocious puberty, which is also known: O" T0 z- b% G2 c) K. V
as testotoxicosis, may cause precocious puberty at a
$ ?, l  N2 s1 O) |& P9 }7 k6 Avery young age. The physical findings in these boys  `0 Y% }. ]; J0 }
with this disorder are full pubertal development,$ X* D. ~' U7 \# H0 B
including bilateral testicular growth, similar to boys
6 j+ G' X5 p# g! v' a$ zwith CPP. The gonadotropin levels in this disorder  y8 u- p' g% J; f( L6 ?
are suppressed to prepubertal levels and do not show: M" O; w% g& {! x6 H+ B
pubertal response of gonadotropin after gonadotropin-
0 P' ^2 s5 @" @* Kreleasing hormone stimulation. This is a sex-linked# C( [" O) `: ?4 {' F* A# R
autosomal dominant disorder that affects only3 {* C+ p* w4 m9 |
males; therefore, other male members of the family# B. C- d* H6 |) ^2 H' A
may have similar precocious puberty.36 a& v2 e, Q1 \. T" g& c
In our patient, physical examination was incon-! U, |  i6 T5 i
sistent with true precocious puberty since his testi-
2 r" z6 e5 ?: e4 F6 f& @, J+ acles were prepubertal in size. However, testotoxicosis
7 Z: P* U: M% A" k  s5 m, N+ ?was in the differential diagnosis because his father. z& _3 e0 C; s  y- b! T; U- B2 E- G  ]
started puberty somewhat early, and occasionally,
( {  r8 i& m: S" stesticular enlargement is not that evident in the- R9 A6 x! s% N2 G8 v
beginning of this process.1 In the absence of a neg-
) N: f( U( _$ S" p9 u+ |ative initial history of androgen exposure, our( Y% u# v( f, g  {
biggest concern was virilizing adrenal hyperplasia,
* G2 @6 [* i8 l8 b9 P/ t0 i& T, Yeither 21-hydroxylase deficiency or 11-β hydroxylase- m# `' H6 Q( |6 r/ V
deficiency. Those diagnoses were excluded by find-6 S* c/ m$ l* c6 \( Y2 X
ing the normal level of adrenal steroids.( h, Q6 c  z% {  o. O. ~" n2 ?0 w
The diagnosis of exogenous androgens was strongly. i" o; S7 ^) N5 ^: I& ?
suspected in a follow-up visit after 4 months because6 Z) K4 H' \& Y: k: m5 f1 @
the physical examination revealed the complete disap-
6 J: O, i8 Z4 M, \9 ?' mpearance of pubic hair, normal growth velocity, and
7 C7 k& e% _' B5 a: I' jdecreased erections. The father admitted using a testos-
" F$ W; @8 O) r* g- C3 [$ h* jterone gel, which he concealed at first visit. He was
( A: n, E" T. musing it rather frequently, twice a day. The Physicians’
% R. |2 q% W* q' o) WDesk Reference, or package insert of this product, gel or
& V8 @: S) a7 g; F/ v( Ucream, cautions about dermal testosterone transfer to
; A. r# b2 ?  _$ x# \- p2 x' funprotected females through direct skin exposure.
8 s4 c, @- ?9 m8 Q4 q* PSerum testosterone level was found to be 2 times the
8 y& S  P. L- O8 r; X1 X' bbaseline value in those females who were exposed to9 m% t4 \  b& B
even 15 minutes of direct skin contact with their male6 }) u8 }1 L. ^+ r5 r
partners.6 However, when a shirt covered the applica-3 I* g2 ?0 {; ~
tion site, this testosterone transfer was prevented.
" M. |- Q/ R8 \/ F+ yOur patient’s testosterone level was 60 ng/mL,! d; A) E) l3 J9 f% H+ B
which was clearly high. Some studies suggest that; A3 s- }1 q# G4 P; U* W% P# v
dermal conversion of testosterone to dihydrotestos-
* D% I% B* p2 e# qterone, which is a more potent metabolite, is more
, X3 l8 W" ~' k! i" W: y5 t1 xactive in young children exposed to testosterone: B4 M( B1 h4 H1 S
exogenously7; however, we did not measure a dihy-" s" b# S! h8 M) u! ]9 w  T4 n0 q
drotestosterone level in our patient. In addition to
- L& r; ^/ x9 Mvirilization, exposure to exogenous testosterone in* |! I8 `2 T2 K' r4 P+ d; W
children results in an increase in growth velocity and2 [2 I2 s) \( @9 D2 v1 p$ }+ ^; Q# h
advanced bone age, as seen in our patient.
4 {6 T8 z; M2 S3 j- @  U+ x2 kThe long-term effect of androgen exposure during
; f4 h* n( c! r0 wearly childhood on pubertal development and final
! j$ K! E8 |1 N( W' @" {adult height are not fully known and always remain
3 G$ x9 m# ]2 j& T$ pa concern. Children treated with short-term testos-
) u/ C5 P3 G. f2 Q7 r* wterone injection or topical androgen may exhibit some8 _! ]% z' d9 A- K+ z9 Y) K
acceleration of the skeletal maturation; however, after: _* A% ?. K) ^. k( w
cessation of treatment, the rate of bone maturation
! E4 q- d- P, Pdecelerates and gradually returns to normal.8,95 m" K# n' Z  x) O4 y% z6 X  V
There are conflicting reports and controversy) R' M) I1 V: k8 V6 r, \% g
over the effect of early androgen exposure on adult5 @+ V4 |4 u" o0 K2 A
penile length.10,11 Some reports suggest subnormal4 A8 ~% t2 a& C% u. r
adult penile length, apparently because of downreg-
& W- D4 y: k7 h4 pulation of androgen receptor number.10,12 However,
+ ?' A; f+ D, q. e* {Sutherland et al13 did not find a correlation between  x, c+ J: p. G' O# D/ J7 ]( P8 Z
childhood testosterone exposure and reduced adult" E1 M; W( X: g. u6 c0 B# j
penile length in clinical studies.
4 M7 A7 N+ f/ a: i: X3 b* Y; ?. TNonetheless, we do not believe our patient is
: z. Q6 d: b# {& C# Zgoing to experience any of the untoward effects from4 }% M# D3 Y. A: z( i- c
testosterone exposure as mentioned earlier because( q. V. A1 S8 Q) P+ [8 A6 g1 r
the exposure was not for a prolonged period of time.# n  f$ E0 Z( B, G
Although the bone age was advanced at the time of
  b, i+ i  |! O1 T$ p9 M* L5 r: d! @diagnosis, the child had a normal growth velocity at9 z# e( r1 K4 T! l! z" j9 X
the follow-up visit. It is hoped that his final adult6 N" y+ x2 r7 D7 `2 r* |* l3 T. \
height will not be affected.
/ q# o1 D% L2 Q3 {3 dAlthough rarely reported, the widespread avail-% y( Y! _6 d* {- d' O& r# V
ability of androgen products in our society may8 f. x3 z% f# Z, k
indeed cause more virilization in male or female- [3 l4 S% Z" C
children than one would realize. Exposure to andro-
! @& D/ H4 K& D/ x6 G  Sgen products must be considered and specific ques-
1 G; n( l0 \. H2 Ltioning about the use of a testosterone product or
4 l* h3 t; v. U( \1 I& Y# Pgel should be asked of the family members during
7 S6 T2 z# i( y8 Y$ othe evaluation of any children who present with vir-. O- K% Z4 ?8 ]' t2 J) y
ilization or peripheral precocious puberty. The diag-% e+ p- ^6 n+ d  D" _  @
nosis can be established by just a few tests and by
  K' x& Y! Q; l) o9 _7 ^9 Iappropriate history. The inability to obtain such a
& f# J8 `3 Y" A- n. H' ^6 s6 M4 ahistory, or failure to ask the specific questions, may2 T4 e4 U- C# ~+ N6 F0 h: t
result in extensive, unnecessary, and expensive
& l5 L. Q) A) G* tinvestigation. The primary care physician should be
+ {+ i  t: B7 {: }/ {aware of this fact, because most of these children
% Y8 S9 l: K2 t/ U) J& omay initially present in their practice. The Physicians’
; @$ c) B  ^1 f- ADesk Reference and package insert should also put a
4 v1 u7 d4 k) ]' b# \6 twarning about the virilizing effect on a male or
2 A8 m+ `7 r. k- k: D; z: B. e- xfemale child who might come in contact with some-4 l; }) Y( K+ p% ^
one using any of these products.8 g  y2 f" M5 E" l9 \- ^9 p
References
9 b$ k5 g( Z/ ^+ X& i9 r1. Styne DM. The testes: disorder of sexual differentiation
7 E- Y* \0 }# [$ J  p. Uand puberty in the male. In: Sperling MA, ed. Pediatric
8 g1 |4 e- ]! O; p+ N) |2 X, H/ q& zEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;6 x2 w7 F1 j" x6 l4 I# U0 u: X
2002: 565-628.
7 R0 ]: `" |7 y2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; h1 |7 I! U/ ?! k! \  |' H* ?% C
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old. a# k- u. |& I) Y& M
Boy Induced by Indirect Topical
: L1 w% ~$ [! U- cExposure to Testosterone8 d6 m5 G8 U5 L0 z, K* z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 s' }6 F# {1 T- X7 X5 aand Kenneth R. Rettig, MD1
( M7 V( W3 a5 X) t+ b& ^2 dClinical Pediatrics
. n9 r* v, M1 `Volume 46 Number 6  q9 n( x! C" s
July 2007 540-543
1 Y8 H, B: D* m© 2007 Sage Publications
+ d  q- L, c, ?3 k' ]( ?10.1177/0009922806296651
# c! \/ N+ X- S$ ^& `5 ]http://clp.sagepub.com/ d" j  J( _6 o# D. m- S. \9 M
hosted at( P' X1 K% A0 f9 \
http://online.sagepub.com
2 T* d) \/ K  D* Y5 rPrecocious puberty in boys, central or peripheral,+ Q( m3 ^- H9 b4 L4 d
is a significant concern for physicians. Central
) {- R9 d, i* G/ ]! iprecocious puberty (CPP), which is mediated  Q! v+ `1 f2 Q6 o
through the hypothalamic pituitary gonadal axis, has
$ R$ c/ _$ k! }* b) i5 ~6 ~$ Xa higher incidence of organic central nervous system$ U5 z& q/ F6 w
lesions in boys.1,2 Virilization in boys, as manifested
- X3 v+ ~" }% Q, G. ^/ a: u$ Yby enlargement of the penis, development of pubic$ _: m* C/ ^) ~9 J
hair, and facial acne without enlargement of testi-
: _6 f1 A$ j0 f3 ]cles, suggests peripheral or pseudopuberty.1-3 We6 B1 [% n( S2 s
report a 16-month-old boy who presented with the+ p5 i5 v! D. m0 z0 e4 j+ ~$ a1 O) [
enlargement of the phallus and pubic hair develop-2 R6 c# d/ d5 z* ^, T. N' u
ment without testicular enlargement, which was due
5 U2 {( e6 q3 O6 H& o3 q$ i0 Nto the unintentional exposure to androgen gel used by
0 o% q7 S9 H2 f9 K' s' I5 I: g& _8 ^the father. The family initially concealed this infor-6 |$ Z/ `: P9 X/ e" b5 H  y% |# x
mation, resulting in an extensive work-up for this# u& |3 ]9 F  c% w
child. Given the widespread and easy availability of
5 c* Z5 F' b. Ktestosterone gel and cream, we believe this is proba-8 w  C8 i  o+ C
bly more common than the rare case report in the  {% H5 _  D( D
literature.43 P: ?2 {4 c0 j, b% T1 S
Patient Report
5 X. K) d7 Q, f, j9 D$ xA 16-month-old white child was referred to the0 ?1 p4 O* p5 ]2 v! f! N: G
endocrine clinic by his pediatrician with the concern
6 J6 o# p6 T) Q* {9 G8 n# ]: lof early sexual development. His mother noticed2 X! s. T" q  j3 i
light colored pubic hair development when he was1 \8 r8 v6 j* u  ~; ^1 J" q
From the 1Division of Pediatric Endocrinology, 2University of
3 m4 Y+ b7 k7 Y# Z- USouth Alabama Medical Center, Mobile, Alabama." \2 ~# [% z3 t- @
Address correspondence to: Samar K. Bhowmick, MD, FACE,
) C0 F* [9 i: U9 b/ UProfessor of Pediatrics, University of South Alabama, College of( w' d) O, a+ i1 _0 N; q0 y: ]
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. F) ]" [" R0 f6 F# s) o
e-mail: [email protected].5 L: d. Q: A9 ^& u6 ~$ r% m
about 6 to 7 months old, which progressively became
" H% q7 z; O- U) ]. I! f4 Ndarker. She was also concerned about the enlarge-
9 l% U" S) q7 B* n. zment of his penis and frequent erections. The child6 M& @( ~/ S4 x+ c' r" a  c1 m+ y
was the product of a full-term normal delivery, with
5 C0 D. o* U+ |; ya birth weight of 7 lb 14 oz, and birth length of
# \9 V6 Y3 [" ~2 C! e& g! O& L" d( Q20 inches. He was breast-fed throughout the first year- A8 e3 O* M( J3 T4 a
of life and was still receiving breast milk along with
% P; a" m6 }, Z8 I; msolid food. He had no hospitalizations or surgery,/ p; f2 M7 _1 w. v" R  I
and his psychosocial and psychomotor development0 @: {. D+ R- g" x$ {, ], ~4 Y
was age appropriate.
: Y3 \5 }  @0 U+ Z3 J7 P. F) }The family history was remarkable for the father,
3 M9 a) e5 V2 t% ?$ r# F# dwho was diagnosed with hypothyroidism at age 16,: K. Z) k, D5 O; K' `$ r+ g
which was treated with thyroxine. The father’s
3 C- `6 }* R' G8 `height was 6 feet, and he went through a somewhat: X9 }4 @2 g' c5 K8 x0 D
early puberty and had stopped growing by age 14.
! m2 ]: V7 {( q; S0 l/ XThe father denied taking any other medication. The
; B. d( H  @4 }' kchild’s mother was in good health. Her menarche& N! M& i* Z8 o3 w0 t. W4 u$ \
was at 11 years of age, and her height was at 5 feet4 n4 z+ G% Q$ g1 [
5 inches. There was no other family history of pre-2 ^! R5 Q& B6 o: N+ d# ^
cocious sexual development in the first-degree rela-3 c5 t2 i7 j2 x3 h
tives. There were no siblings.
2 b# \) ?, u" T% o$ q0 vPhysical Examination
* ]. _4 o4 d- Y# h8 OThe physical examination revealed a very active,
8 ]& W6 ?7 i6 o9 q+ T+ w! pplayful, and healthy boy. The vital signs documented  B( G% Q+ d0 D4 }0 H+ i0 a
a blood pressure of 85/50 mm Hg, his length was
8 M7 i4 \$ L& i7 O! C+ Y90 cm (>97th percentile), and his weight was 14.4 kg
. T  P, M, S6 {( x(also >97th percentile). The observed yearly growth
4 d. z! h, r1 k  s' k: \velocity was 30 cm (12 inches). The examination of
# K  z4 w0 ]( m1 Vthe neck revealed no thyroid enlargement.3 d3 B. T. y$ Q! V  f# t
The genitourinary examination was remarkable for( y# h: i; \& {5 Y& a- h  i
enlargement of the penis, with a stretched length of
0 N2 X' G: m- V2 j& E$ c' f8 cm and a width of 2 cm. The glans penis was very well
5 j: s- p$ K" }developed. The pubic hair was Tanner II, mostly around
5 k/ D3 r- T/ @! e2 g# B540
6 z* y7 X& {3 Q6 ?2 W# Q+ [8 Dat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( y- j" B2 s$ t
the base of the phallus and was dark and curled. The
- b* F8 I/ b1 i7 Ctesticular volume was prepubertal at 2 mL each.: Q3 A1 V+ b* v& @# {+ k% \; k
The skin was moist and smooth and somewhat
5 ^  ]- o: [! E9 {  t3 v9 ~" roily. No axillary hair was noted. There were no  _; t9 Z5 _# }; q
abnormal skin pigmentations or café-au-lait spots.3 S/ o/ l4 J: u( m/ ]. U
Neurologic evaluation showed deep tendon reflex 2+1 s( z9 v3 W4 c+ X. E' y
bilateral and symmetrical. There was no suggestion, o' e# c8 u* \3 Q# B
of papilledema.
: L: }- ~" m+ ?- }' i- C$ S) X) [Laboratory Evaluation
# M, V; A3 G3 A( J  Y* rThe bone age was consistent with 28 months by
: V6 k$ I/ v! F3 ]using the standard of Greulich and Pyle at a chrono-( `% z& }$ E! j6 u5 N7 v% w
logic age of 16 months (advanced).5 Chromosomal
1 n8 Q1 h! ~6 b1 u& O7 Ykaryotype was 46XY. The thyroid function test  z: {" l2 b; n* v
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
& [$ A; |* y# m: @0 c! Y  F7 xlating hormone level was 1.3 µIU/mL (both normal).
% ^. Y% G* S8 W. m7 r' aThe concentrations of serum electrolytes, blood
$ s) C- g2 _7 G8 w" D( Vurea nitrogen, creatinine, and calcium all were
6 }, s9 Z0 v; ?1 D- ewithin normal range for his age. The concentration
3 N8 c. F4 \7 L9 i3 v/ k( H' @of serum 17-hydroxyprogesterone was 16 ng/dL
# `( ~  c5 h( Y% t& \1 b(normal, 3 to 90 ng/dL), androstenedione was 20
1 m, m( b7 ?- o! h3 bng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
3 G# m  _( W. B* g! Dterone was 38 ng/dL (normal, 50 to 760 ng/dL),
: n$ q. b) ~) |desoxycorticosterone was 4.3 ng/dL (normal, 7 to; [3 Q/ Z; k. E) s6 n; \: X; o
49ng/dL), 11-desoxycortisol (specific compound S)  L4 y9 t2 l7 d. i9 P! b/ l, }. d
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- M1 e2 i5 ]% G$ o4 H5 M
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& k$ G+ C, r4 T8 Z) {/ L& _" Ytestosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ N+ t6 N7 H' w( {
and β-human chorionic gonadotropin was less than7 n/ F, l2 g" @6 ]
5 mIU/mL (normal <5 mIU/mL). Serum follicular7 F) Z( m/ J" ?" ~. t( [1 G
stimulating hormone and leuteinizing hormone+ q- p' \1 t8 o# J. c/ ^) L' N
concentrations were less than 0.05 mIU/mL4 d. P3 o3 v& Z0 ?- E
(prepubertal).  N1 j, v. x- b9 |
The parents were notified about the laboratory
0 q+ j/ u6 }$ }6 H. t' Nresults and were informed that all of the tests were! H8 z4 N" R, Q% B
normal except the testosterone level was high. The
+ Q9 L8 I+ c: k: `3 V4 P7 p  h% Mfollow-up visit was arranged within a few weeks to8 M& z9 b4 ?5 R: _  j$ J
obtain testicular and abdominal sonograms; how-0 k5 t5 P1 B0 D; `. R) K7 H
ever, the family did not return for 4 months.
( S& H* w- Y) Q0 SPhysical examination at this time revealed that the: N; C  g; U6 X  N% Q+ ~- Z$ u( D
child had grown 2.5 cm in 4 months and had gained' I7 b- Z3 E1 k0 m9 c
2 kg of weight. Physical examination remained. h( n, m! S7 r- {5 {: u! X
unchanged. Surprisingly, the pubic hair almost com-  f) d! n: D% [& \
pletely disappeared except for a few vellous hairs at
6 j5 q: P) C- m. b/ f7 tthe base of the phallus. Testicular volume was still 2
$ V( A( }1 ?. e" B; ^mL, and the size of the penis remained unchanged.
2 A, R& o8 M9 b& ~4 kThe mother also said that the boy was no longer hav-
2 I' e) ?5 N1 _: Q& {9 A3 C* Y5 J3 n, ying frequent erections.
$ S# @# `5 d* g& \Both parents were again questioned about use of* F7 n3 m& D0 ?4 ]& B
any ointment/creams that they may have applied to
) F5 i( c8 @. R) T) h) P% Wthe child’s skin. This time the father admitted the$ F% l# _, Z2 N5 T- b8 _
Topical Testosterone Exposure / Bhowmick et al 541: i  y- F( p2 Z
use of testosterone gel twice daily that he was apply-& W2 K: B4 C# U
ing over his own shoulders, chest, and back area for
& R5 q2 U6 m+ Sa year. The father also revealed he was embarrassed
; B2 I# N. Q- h4 t; H1 i% bto disclose that he was using a testosterone gel pre-
+ n  O/ _$ I  f$ r( Pscribed by his family physician for decreased libido
3 D: O+ U6 l* ^' e9 F* j  @* C! Hsecondary to depression.  z) ?* d' i& Z: _" U
The child slept in the same bed with parents.
; f0 W5 D- R, ^: `: u, k5 fThe father would hug the baby and hold him on his
; }# X4 D8 j: }/ H% T2 D- Nchest for a considerable period of time, causing sig-1 P0 o# Q% m6 h1 ?  U
nificant bare skin contact between baby and father.8 e# S7 u- I# Z+ i5 r" U: P
The father also admitted that after the phone call,* q" f4 r, [; Q& ?; q
when he learned the testosterone level in the baby
% B5 F  i% g3 V, {3 d: D, C, `was high, he then read the product information! u. e, Z8 d9 K' \8 f
packet and concluded that it was most likely the rea-
5 o" F! I8 j* R$ q  K3 Ison for the child’s virilization. At that time, they
1 b; ?2 M" U9 l7 T. o, c( Z$ pdecided to put the baby in a separate bed, and the
/ h6 ^6 {0 b# t& v! C# Lfather was not hugging him with bare skin and had+ o; k; z& W3 r# T+ B
been using protective clothing. A repeat testosterone
% @0 E' e2 z0 f' `test was ordered, but the family did not go to the
" z$ A5 E; q: R' Wlaboratory to obtain the test.
& p6 W7 y) c8 f9 g2 w* oDiscussion
% m" z- a, o6 Y0 W' xPrecocious puberty in boys is defined as secondary9 F/ m* }" L- L8 y: \# X
sexual development before 9 years of age.1,4/ r. u4 N# t  J4 a& P7 ]  {
Precocious puberty is termed as central (true) when  _& T2 o7 f0 h9 U' k/ t- B" k* j
it is caused by the premature activation of hypo-; u' a. B0 f& Z9 `& N
thalamic pituitary gonadal axis. CPP is more com-- y5 n9 y6 H% R0 r1 }: f! [: t$ c
mon in girls than in boys.1,3 Most boys with CPP; s# u6 i0 N& B2 Q
may have a central nervous system lesion that is+ P$ t$ X- J4 r! C3 K3 ]
responsible for the early activation of the hypothal-
4 m% j) b" ?- C, |, Q: j0 jamic pituitary gonadal axis.1-3 Thus, greater empha-' M; w4 t* E: q3 F
sis has been given to neuroradiologic imaging in% V" R# x% i1 y1 s. ]% [
boys with precocious puberty. In addition to viril-1 m! |( C) i9 n% H% g/ H/ f" `
ization, the clinical hallmark of CPP is the symmet-
! i' C' V8 z% {! U( mrical testicular growth secondary to stimulation by, t, ^* O6 A1 E* r+ E
gonadotropins.1,36 |' A( C% g( C  w: B' C; g7 t. T
Gonadotropin-independent peripheral preco-0 _4 `" i0 K& N
cious puberty in boys also results from inappropriate1 m- C+ v9 M, o4 Q
androgenic stimulation from either endogenous or
1 l' c( @- v, c! Dexogenous sources, nonpituitary gonadotropin stim-# y5 W! {/ `9 Z
ulation, and rare activating mutations.3 Virilizing9 Z9 ]3 U, w: ]( m" d
congenital adrenal hyperplasia producing excessive
+ s: n0 R! s) L0 N9 uadrenal androgens is a common cause of precocious
! h8 _) o" N3 u) m. c3 Rpuberty in boys.3,4# X! \3 E3 ?4 p3 D. \
The most common form of congenital adrenal* d3 v7 _! h& \7 n! g
hyperplasia is the 21-hydroxylase enzyme deficiency.4 `% I+ z# @- ^% Z3 Y9 s- Z
The 11-β hydroxylase deficiency may also result in( K4 K% O! G5 P
excessive adrenal androgen production, and rarely,
3 |. \$ L/ c3 _% c% Fan adrenal tumor may also cause adrenal androgen
7 b: K7 ]7 `0 r8 N8 {excess.1,35 s: j6 J9 V7 l
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
. L+ X9 w: x6 e1 O542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 o# U2 _$ e, h  u) M$ u: U
A unique entity of male-limited gonadotropin-
+ q% A. J- y; Q) C& c( sindependent precocious puberty, which is also known
! U$ x0 c0 Y3 O8 yas testotoxicosis, may cause precocious puberty at a
! W" u' r# c$ H3 pvery young age. The physical findings in these boys
5 E( w- M3 v$ k& pwith this disorder are full pubertal development,
5 l: J: Q  K" W% Aincluding bilateral testicular growth, similar to boys
, C" _( x: _$ u7 a7 u9 ^! Hwith CPP. The gonadotropin levels in this disorder
: Z& |4 w6 b5 _  B; U9 }0 q. D7 {. iare suppressed to prepubertal levels and do not show
2 u/ _9 s* x3 I; dpubertal response of gonadotropin after gonadotropin-
  C! G# p1 h( K3 n9 C3 Ireleasing hormone stimulation. This is a sex-linked
5 ?6 }: \2 c, g/ {1 m; W. ^autosomal dominant disorder that affects only1 C4 Q% N( k: k5 Z8 q  W$ X
males; therefore, other male members of the family: J" S/ z6 a5 D- w
may have similar precocious puberty.3
+ z4 S7 }, L! X; `6 ZIn our patient, physical examination was incon-
1 N6 O/ b  K. C" N/ Tsistent with true precocious puberty since his testi-, g. J: x1 s8 M2 z7 I1 M/ I: |
cles were prepubertal in size. However, testotoxicosis1 |$ i% {* B4 C. o% w& @: c, U
was in the differential diagnosis because his father% P+ [' k# l, X. X: s
started puberty somewhat early, and occasionally,2 Q2 c3 F; G; D3 \! Z" F1 p& ?5 s9 r. `
testicular enlargement is not that evident in the
, S6 x4 G8 t+ K$ ]" x% ^' sbeginning of this process.1 In the absence of a neg-! o" y' F6 Y. R$ Z$ n
ative initial history of androgen exposure, our; T( y( i$ P% Z: h( X4 K
biggest concern was virilizing adrenal hyperplasia,/ l) a6 N- a; n6 B
either 21-hydroxylase deficiency or 11-β hydroxylase
) ~9 V! \8 M, @( K4 T5 w6 Edeficiency. Those diagnoses were excluded by find-% w2 n$ |3 I! B7 v5 w7 U+ L
ing the normal level of adrenal steroids.5 L4 e" d$ R' Z' w- _
The diagnosis of exogenous androgens was strongly3 K2 ^! O$ D7 Z5 ~( t
suspected in a follow-up visit after 4 months because
( o1 f' g5 k$ C2 y3 @$ R3 rthe physical examination revealed the complete disap-  k8 a" a7 ?" c& x; j$ f0 u
pearance of pubic hair, normal growth velocity, and
% V# O: T9 I! n  v" mdecreased erections. The father admitted using a testos-
; n) V0 b: l; L5 H* [" Mterone gel, which he concealed at first visit. He was
. x: m$ C9 O+ }% u9 i9 T" z* Musing it rather frequently, twice a day. The Physicians’
6 {" b, a; U, K& T7 h0 YDesk Reference, or package insert of this product, gel or: J2 Y2 h0 X. k4 I7 c
cream, cautions about dermal testosterone transfer to! Z, V( T0 w6 l# o( L5 p
unprotected females through direct skin exposure.
# ^7 q. f  i, p) g5 L3 Q- n( F7 aSerum testosterone level was found to be 2 times the" K) F- F  s% Q; A1 X* J
baseline value in those females who were exposed to
7 R, y' T2 c8 A6 M9 B5 Q) Heven 15 minutes of direct skin contact with their male0 B; ]! D; N4 `* i" ^. R
partners.6 However, when a shirt covered the applica-
: m( _* O# g. z+ J. a2 o! ttion site, this testosterone transfer was prevented.+ G3 E! ^' F+ |. l1 a4 H
Our patient’s testosterone level was 60 ng/mL,
4 d" {* G9 F! J0 T' A/ kwhich was clearly high. Some studies suggest that$ f9 g. z. Z$ O9 L
dermal conversion of testosterone to dihydrotestos-$ J4 I4 J$ S. l% m+ v4 E6 Z: Z
terone, which is a more potent metabolite, is more9 d" t  W( X0 J0 {  F, |
active in young children exposed to testosterone
2 M9 m; A$ k' H1 M. W5 }. z9 d; jexogenously7; however, we did not measure a dihy-# O' k4 g. F$ W8 o4 H. h
drotestosterone level in our patient. In addition to8 c/ F$ V3 Z$ T  M  a
virilization, exposure to exogenous testosterone in
7 J4 i( F1 E+ ]# e  bchildren results in an increase in growth velocity and3 P: \7 c% I% t' L; v# V+ r
advanced bone age, as seen in our patient.; A) C% P/ \- ~
The long-term effect of androgen exposure during
# K. \- {& b" r2 K# O  |early childhood on pubertal development and final
8 y; b1 f7 \& E. wadult height are not fully known and always remain% j- ^# Y! P# I# i, O; Z
a concern. Children treated with short-term testos-
1 t, J5 o, o! @7 t; t- t% j2 ~( Aterone injection or topical androgen may exhibit some
) b* R5 E" X! Y: m+ n  |acceleration of the skeletal maturation; however, after" J- V# X+ o2 L: N' r1 j' I
cessation of treatment, the rate of bone maturation
- H7 O' i( c" b% {& h4 H' idecelerates and gradually returns to normal.8,9+ w4 q. ?6 a- R
There are conflicting reports and controversy
* J: K# N8 [. g8 Q# d, z2 Mover the effect of early androgen exposure on adult
/ ~7 x* u2 b& q& Lpenile length.10,11 Some reports suggest subnormal8 I, g: F* c8 F) j/ O6 `
adult penile length, apparently because of downreg-
# I# K; b! y( M1 M- i" E9 b* vulation of androgen receptor number.10,12 However,) q: p( A7 W; ?0 t. X7 R4 r, _
Sutherland et al13 did not find a correlation between
8 m' x* r+ m/ s4 a2 p$ g5 J( q+ H5 Qchildhood testosterone exposure and reduced adult( ~/ \) o6 a/ F. C* i8 t9 ?: x
penile length in clinical studies.
: [8 a0 E7 r- a( r/ rNonetheless, we do not believe our patient is4 ~, O: s( S( H3 d: M4 q0 D) E( @
going to experience any of the untoward effects from% H* K) V/ v  {% T" n
testosterone exposure as mentioned earlier because
/ D/ {* e9 X; k6 othe exposure was not for a prolonged period of time.# K. M1 d7 j) Q0 `: x$ P7 K
Although the bone age was advanced at the time of
% D$ U5 {; w5 ?% L6 ?* \6 Vdiagnosis, the child had a normal growth velocity at, g5 Q3 S# U; s: G% P
the follow-up visit. It is hoped that his final adult
2 j# Z2 p* r9 o+ m( Cheight will not be affected.! [$ I- a2 r" u+ @' G9 N% s4 i. j) ?
Although rarely reported, the widespread avail-
/ k4 n! t* V3 ^7 b7 iability of androgen products in our society may
* u. W3 D8 v* d/ o' V5 B  mindeed cause more virilization in male or female
7 ~# |. E' |9 Gchildren than one would realize. Exposure to andro-7 s: j! ?+ R1 `) }6 t; @
gen products must be considered and specific ques-# |3 {8 ]5 H2 B- J+ p
tioning about the use of a testosterone product or
3 |/ J' m4 w9 l% U3 i6 f7 d. s4 E* e2 ?gel should be asked of the family members during2 h& s% H  h. v. h2 E3 \" S- I* A! f
the evaluation of any children who present with vir-0 n, m; V! F" J# U! u
ilization or peripheral precocious puberty. The diag-" j* v+ u! `2 |6 G5 l
nosis can be established by just a few tests and by
3 d  Y9 ]/ X+ ?! E2 Y% C: Xappropriate history. The inability to obtain such a( r: o: w" r/ u5 q( a) I
history, or failure to ask the specific questions, may) c1 z, w: W, l
result in extensive, unnecessary, and expensive3 P# c3 `- X6 C- T
investigation. The primary care physician should be4 I! D  H4 ^! f/ q. \
aware of this fact, because most of these children
( R7 V: R! |9 H( Z1 P) l9 X$ Rmay initially present in their practice. The Physicians’. ?9 {% {+ b' Z- ?- ]; J
Desk Reference and package insert should also put a
3 C8 j% n/ w2 A- q5 N2 Nwarning about the virilizing effect on a male or
3 V* ~0 r0 Y& X( i. g2 Lfemale child who might come in contact with some-
" \+ F/ y% y( {3 z+ w7 Wone using any of these products.
. L9 a! Y( Q- C& S: p0 l7 i. oReferences4 t, A/ f0 Y, \. [4 q" B. D, D# w& z
1. Styne DM. The testes: disorder of sexual differentiation
# n# I. c: f# u6 @0 y9 n6 o+ z! _; kand puberty in the male. In: Sperling MA, ed. Pediatric, s& E9 o9 C9 B7 W
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ a# c9 e8 P& _9 z, N2002: 565-628.# T8 [2 _* c7 T8 y1 ]" _
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 w# p3 H& t2 J+ ]4 G
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
/ @. r+ Q& d: W6 ?
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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