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Sexual Precocity in a 16-Month-Old3 p; F, @# o. i8 M7 l2 a; [
Boy Induced by Indirect Topical
1 J" U4 \) V3 c& z5 RExposure to Testosterone
7 H: }0 n7 r& t4 `: j/ uSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ `+ r6 |- D8 S  F
and Kenneth R. Rettig, MD1  o( W$ r4 k' ~3 k9 V6 H4 X3 ~
Clinical Pediatrics: O# D+ L0 W/ {: M. W6 T
Volume 46 Number 6
" Q/ f7 F; }6 {, P: Z# e# pJuly 2007 540-5435 ~9 v4 k6 u  w# D
© 2007 Sage Publications7 h+ {6 ]4 L& v" ]- s: _! {7 g/ v) T
10.1177/0009922806296651
3 h- p( `' u8 t$ z, Dhttp://clp.sagepub.com, }5 O' N1 F8 K- `
hosted at3 |) q- m7 B1 c3 ^3 R" {
http://online.sagepub.com5 T& J$ S' j( J" f7 Z6 p
Precocious puberty in boys, central or peripheral,& N9 E8 O9 r1 a6 X
is a significant concern for physicians. Central! v, I: y* d+ {8 g# m( k
precocious puberty (CPP), which is mediated2 C# l1 E6 F% d
through the hypothalamic pituitary gonadal axis, has
$ i0 V" X$ I9 [+ s% I5 n, |a higher incidence of organic central nervous system) S8 F1 j; R! o# P# p
lesions in boys.1,2 Virilization in boys, as manifested
6 }/ e6 L( ~% ~by enlargement of the penis, development of pubic
% {4 H8 [9 _# {2 j2 X( T! chair, and facial acne without enlargement of testi-% ]- p. x  j8 j& I. L. o0 S
cles, suggests peripheral or pseudopuberty.1-3 We1 _& ~; x9 d) ~6 V& o
report a 16-month-old boy who presented with the
9 D3 M( v$ g* q0 n! B5 Venlargement of the phallus and pubic hair develop-
* e* t0 d$ \; F* a; X1 ]ment without testicular enlargement, which was due* S  m5 b% ~: O8 {' I; q: @
to the unintentional exposure to androgen gel used by( E# t$ i& {& i: f. L
the father. The family initially concealed this infor-  |7 d$ F6 y# C/ m# c3 q& c) ]
mation, resulting in an extensive work-up for this$ {$ [# v8 N6 h+ }  X$ H
child. Given the widespread and easy availability of! z5 U/ a4 ?) C% n" U0 n
testosterone gel and cream, we believe this is proba-# p6 r9 v' ^* G1 n' F
bly more common than the rare case report in the+ Z  m5 W5 W* n, ^; M
literature.4& T1 ?. o+ y8 H8 U
Patient Report
' w/ ~: ?) Y0 _( g7 w+ J$ Q3 QA 16-month-old white child was referred to the+ ?$ h( r; [. G
endocrine clinic by his pediatrician with the concern
. g/ {3 c& o/ L" P8 }" e! Qof early sexual development. His mother noticed: |! h9 Y+ b: z) X
light colored pubic hair development when he was9 B7 Z$ o) @8 y$ ?7 Z, w% N
From the 1Division of Pediatric Endocrinology, 2University of6 L2 g% j! F3 b, J. x$ i
South Alabama Medical Center, Mobile, Alabama.5 t6 B  z) m9 j6 U, K! u" O) K
Address correspondence to: Samar K. Bhowmick, MD, FACE,- y" h$ A" a. U7 [- z6 _* z
Professor of Pediatrics, University of South Alabama, College of
1 t, b1 ~7 q. [Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! _6 M4 c( A" f& ]6 s& I  g; H
e-mail: [email protected].' r7 ~' y* P* V% V+ B7 u2 f
about 6 to 7 months old, which progressively became
$ n/ j5 J- `2 r% f4 G. H! U- g. ?darker. She was also concerned about the enlarge-' `7 H  v1 B% q6 _$ X
ment of his penis and frequent erections. The child" E$ G" ]7 b( `+ J$ K
was the product of a full-term normal delivery, with7 H- @9 b  A2 K/ t- N" H
a birth weight of 7 lb 14 oz, and birth length of
6 V* D; |3 O" ]: L. b; J20 inches. He was breast-fed throughout the first year0 ^: B9 w, E0 X; X4 y2 W
of life and was still receiving breast milk along with+ x' H" p+ ^! O. E# M
solid food. He had no hospitalizations or surgery,! j4 E6 O* p/ O: |8 e+ [
and his psychosocial and psychomotor development+ `! f! U: w$ o' A9 I6 _" Z
was age appropriate.) A5 A; U- x# A6 n: Z; T1 }; J7 E
The family history was remarkable for the father,* I& |$ b* |8 v7 f
who was diagnosed with hypothyroidism at age 16,* u5 c( L& X& I3 t4 F" Z. ]  h; r2 g! W
which was treated with thyroxine. The father’s
. _/ y" X6 R; q: P! Zheight was 6 feet, and he went through a somewhat" z+ u# U' H: n# B8 c5 v( K1 x
early puberty and had stopped growing by age 14.
! y& B) c5 L- XThe father denied taking any other medication. The+ b! c0 M* c  ]# X' \
child’s mother was in good health. Her menarche
# {7 g( ~3 u! I' ~5 P! p" d: {- Cwas at 11 years of age, and her height was at 5 feet
  H9 o2 }, L8 S" W$ l; A1 S5 inches. There was no other family history of pre-: ~( B* Q1 Z  Y7 T3 X. m- ^
cocious sexual development in the first-degree rela-
2 ~$ x* d; S$ [. U- U- Q0 _7 [tives. There were no siblings.6 ^) r- ^+ O+ ?# F( j( t
Physical Examination1 m  W; E( F( l8 K
The physical examination revealed a very active,
+ ?. S9 h( D6 L! p# bplayful, and healthy boy. The vital signs documented
# Q% |  |$ O& E3 \4 L5 g$ z( Ra blood pressure of 85/50 mm Hg, his length was' ~. m9 n6 K  q* w7 {% Z
90 cm (>97th percentile), and his weight was 14.4 kg
1 X% \( P% j" _9 w(also >97th percentile). The observed yearly growth
% f) v$ r/ e1 `# |/ H& S8 i6 }  @velocity was 30 cm (12 inches). The examination of
7 d; B% N# g3 t: Mthe neck revealed no thyroid enlargement.
! A; y; s. a  |; R$ T+ N7 {The genitourinary examination was remarkable for( |  L2 ]- t& s8 s: {, `% O
enlargement of the penis, with a stretched length of
8 [: L$ c0 F$ S& d1 ^; N8 cm and a width of 2 cm. The glans penis was very well# x! q+ h/ e3 \# @: s5 n
developed. The pubic hair was Tanner II, mostly around. }# w8 {4 a) P/ V3 u5 v3 j
540
, S  a  f- ?, U* ?at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; z! f; l5 H; }: W; P
the base of the phallus and was dark and curled. The
- p/ I2 d8 P% K4 K6 |/ Ctesticular volume was prepubertal at 2 mL each.
* T, H8 `, ^1 t2 P5 o" i( DThe skin was moist and smooth and somewhat
4 n0 Y, A4 o, k' d7 o9 o3 V9 Hoily. No axillary hair was noted. There were no3 L) i' g$ k, B/ `" ^* [4 V
abnormal skin pigmentations or café-au-lait spots.+ E; M/ A0 a- v9 {! M
Neurologic evaluation showed deep tendon reflex 2+
9 X8 L" |! v" B( }+ ^) h7 ?8 j- Tbilateral and symmetrical. There was no suggestion: d6 J* G9 w' c0 \- Y4 s$ ]
of papilledema.
+ {% s) [: @$ p/ ]# y, |3 ^Laboratory Evaluation4 N( |- v) Q) o
The bone age was consistent with 28 months by$ ?' ?) w0 A  u5 _8 `
using the standard of Greulich and Pyle at a chrono-8 n7 Z. D7 B: z1 ?6 @
logic age of 16 months (advanced).5 Chromosomal; c6 ?! q7 T2 S: V+ Q) _
karyotype was 46XY. The thyroid function test1 }- A! e, o4 f" P4 R
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
. P  j6 n7 q/ Wlating hormone level was 1.3 µIU/mL (both normal).
' j) ?8 ^: i+ s" ~/ f; Y" O& `The concentrations of serum electrolytes, blood
+ \# N/ H1 H; k% _urea nitrogen, creatinine, and calcium all were
5 h# Y1 v0 ]8 j% c& g; wwithin normal range for his age. The concentration
1 M) m' T1 v5 rof serum 17-hydroxyprogesterone was 16 ng/dL
/ [/ l% m0 m' T2 l(normal, 3 to 90 ng/dL), androstenedione was 20
0 P$ ?9 B$ \7 h4 P- s2 ]( lng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-8 F/ x+ B6 M: }7 h3 Y
terone was 38 ng/dL (normal, 50 to 760 ng/dL),% X* r# F; a9 E3 @* K
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
. d7 K9 u3 R% c. g  D( y49ng/dL), 11-desoxycortisol (specific compound S); S* w% e3 d( D7 s
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-5 q& K2 U5 K7 C4 E0 @, k
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 w, b  l8 z- @testosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ r8 L* p( t1 }* j
and β-human chorionic gonadotropin was less than' @8 B( w9 \5 R$ M$ l8 o# a- Z
5 mIU/mL (normal <5 mIU/mL). Serum follicular
! H- i4 o2 M6 n. G2 R+ Lstimulating hormone and leuteinizing hormone
+ i- Q+ @4 i) t, K& C/ W; D6 kconcentrations were less than 0.05 mIU/mL
7 W' z5 B1 {) s  W9 [0 w$ ?(prepubertal).
1 F+ R& U! I8 i1 |! g3 yThe parents were notified about the laboratory
: P$ D$ J4 }3 j3 p' bresults and were informed that all of the tests were  h+ E0 F* y0 n4 s6 M
normal except the testosterone level was high. The
* C; J- S7 g+ k' Q& b" dfollow-up visit was arranged within a few weeks to: x# S5 q; Y3 R( x) C0 f
obtain testicular and abdominal sonograms; how-
6 ]$ u( C+ I, _+ }4 Bever, the family did not return for 4 months.
/ B- q  B( `$ W6 e/ UPhysical examination at this time revealed that the
. ^4 y! [/ ~' t$ J  [4 Bchild had grown 2.5 cm in 4 months and had gained( a, d7 ~' a  {% |" j: I5 ]
2 kg of weight. Physical examination remained0 E8 x$ ~/ H4 e
unchanged. Surprisingly, the pubic hair almost com-, x, P' M& q* {/ l9 v- g  b
pletely disappeared except for a few vellous hairs at/ e1 m$ v) w# G; O5 H  P
the base of the phallus. Testicular volume was still 2
4 e% h8 Z' y- b! A4 FmL, and the size of the penis remained unchanged.
# `% N% k1 U) Y+ p+ X( \The mother also said that the boy was no longer hav-) L$ N/ T+ z$ s! K% @& p1 Q. u
ing frequent erections.
$ r# ^# Y8 J9 ^3 q2 i+ e* S+ [Both parents were again questioned about use of! q! \) i1 r, J7 r( R- ]
any ointment/creams that they may have applied to
+ ]& L0 c( ?) z4 m5 Ethe child’s skin. This time the father admitted the! W3 S, C9 n7 R- ~, L# R% L
Topical Testosterone Exposure / Bhowmick et al 5417 X( k; `; |3 i7 {, _
use of testosterone gel twice daily that he was apply-6 x4 w$ p: a+ l1 S4 i# o
ing over his own shoulders, chest, and back area for4 W* m: X9 D- T- [7 |' Y: l
a year. The father also revealed he was embarrassed
. e; Y1 S$ g+ W9 A% ^3 K6 |to disclose that he was using a testosterone gel pre-
/ V) X$ V2 W8 e* x' e! cscribed by his family physician for decreased libido8 c, x6 d* N% P  m. U$ N# ~
secondary to depression.$ T8 n% G5 e. ~" X. q' E- b7 x
The child slept in the same bed with parents.
/ H! N6 G9 @% [The father would hug the baby and hold him on his- X8 X9 s  k+ t. @
chest for a considerable period of time, causing sig-4 `, ~  i8 H$ w5 q1 Y
nificant bare skin contact between baby and father.. s9 _* ]2 _# f; t; @  J  \
The father also admitted that after the phone call,' w5 r) S# j. O( O6 j& O
when he learned the testosterone level in the baby
% I4 c8 P/ O$ q1 ?( [was high, he then read the product information
* Y. C: X, T- h9 npacket and concluded that it was most likely the rea-
1 _8 X% h# U2 o) Z5 r) ?& K, kson for the child’s virilization. At that time, they" F3 _. ^4 t8 M
decided to put the baby in a separate bed, and the5 I, m+ f% X/ f: \, i
father was not hugging him with bare skin and had
$ q, r# }7 L, N* vbeen using protective clothing. A repeat testosterone' l& l7 j+ y1 C' H. q, t5 K
test was ordered, but the family did not go to the1 _* h" R* d' w3 N  O/ Z
laboratory to obtain the test.4 X7 w) h1 P9 Q3 I# A  o( q
Discussion. U+ }" k0 Z7 c) B: S
Precocious puberty in boys is defined as secondary( Y0 B' W' a7 n* x. M
sexual development before 9 years of age.1,4. b4 ?3 l. l2 O) J) Z
Precocious puberty is termed as central (true) when) {) L3 W0 [# P7 N
it is caused by the premature activation of hypo-
' y9 I0 J( ^. r/ n5 o! Bthalamic pituitary gonadal axis. CPP is more com-
; ^# O( J& i" h1 H4 `( xmon in girls than in boys.1,3 Most boys with CPP
  O( n( _  @7 T4 r+ c5 @- U  B8 Vmay have a central nervous system lesion that is  P, A* V# E5 i$ ^* }' s% v' @* i
responsible for the early activation of the hypothal-  {3 C& A" V) G' M" W9 M
amic pituitary gonadal axis.1-3 Thus, greater empha-+ r$ \7 a# y: j1 s: b' Q8 D/ }
sis has been given to neuroradiologic imaging in* \" x. F$ Z6 }" a5 b: v
boys with precocious puberty. In addition to viril-
; e  [  |7 m1 T5 \% t9 y2 lization, the clinical hallmark of CPP is the symmet-
. m; P! {3 x/ c' s5 \9 e( R6 m( `rical testicular growth secondary to stimulation by
# l, t/ C( a& P; {4 ?gonadotropins.1,35 x3 S  s4 S* ?) S
Gonadotropin-independent peripheral preco-( Y/ r2 {, _+ u8 E! B
cious puberty in boys also results from inappropriate
7 G9 e) l  R- _) m- xandrogenic stimulation from either endogenous or
9 u9 a/ B0 [! N, Fexogenous sources, nonpituitary gonadotropin stim-: y! ^9 J! q' d$ |' G7 b4 N
ulation, and rare activating mutations.3 Virilizing
* d$ Y' S+ M( u" \. z0 |congenital adrenal hyperplasia producing excessive
' B2 P% `  d* a+ zadrenal androgens is a common cause of precocious
  f2 w6 _9 h+ N/ g2 qpuberty in boys.3,4$ Q0 j: P& f1 k' P4 m
The most common form of congenital adrenal
; G+ o6 a" t$ d6 U* u, Vhyperplasia is the 21-hydroxylase enzyme deficiency.+ w* N+ W8 K, G2 e
The 11-β hydroxylase deficiency may also result in
' `6 P' K# X7 p! g. g% o. o+ ^3 Qexcessive adrenal androgen production, and rarely,
* K- L, C% Q) C' A9 \5 ran adrenal tumor may also cause adrenal androgen9 ?) j. @' ?; K$ L
excess.1,3, m1 v, r9 ]! P8 |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 i% g: c# k2 ~: \1 U542 Clinical Pediatrics / Vol. 46, No. 6, July 2007) ^/ o) a" P  `/ Y% d' C+ Q! J
A unique entity of male-limited gonadotropin-
4 E+ p1 p/ p& ?" p8 gindependent precocious puberty, which is also known0 l; e% H7 {! v
as testotoxicosis, may cause precocious puberty at a
& H8 Z% y9 G# x/ [/ Dvery young age. The physical findings in these boys' j2 Q! c( `' V' x7 \
with this disorder are full pubertal development,
- v" h& N, H& |1 i) Hincluding bilateral testicular growth, similar to boys7 t) _/ t1 ~7 O
with CPP. The gonadotropin levels in this disorder# R* k* D( K( P  [  s
are suppressed to prepubertal levels and do not show. I0 `  a5 Q$ B! b9 |4 D- ~* q" i) |
pubertal response of gonadotropin after gonadotropin-
. ~2 f6 B( t. ?, ^; Yreleasing hormone stimulation. This is a sex-linked
# ^. R1 I6 _; c4 ^: aautosomal dominant disorder that affects only) T" c) U+ x) W
males; therefore, other male members of the family
: h9 T# z* t! z1 Y8 {5 ~) c6 fmay have similar precocious puberty.3
; ^4 Y$ }( }$ M, b4 X" QIn our patient, physical examination was incon-3 C9 }- i4 r" N1 U6 J
sistent with true precocious puberty since his testi-
- O; G1 A# y5 M; ]cles were prepubertal in size. However, testotoxicosis: Q# N6 e3 k! V* p* O
was in the differential diagnosis because his father& F5 B# a) ~' m, f. V/ |4 ~
started puberty somewhat early, and occasionally,
: |1 E. M# C5 g# P+ b( Ztesticular enlargement is not that evident in the, e! u$ @& b9 Q3 r- n9 u
beginning of this process.1 In the absence of a neg-4 }3 D3 m5 a7 A9 i$ y6 e2 C
ative initial history of androgen exposure, our
4 G. b& d$ Q6 \" \0 Ybiggest concern was virilizing adrenal hyperplasia,
- R7 V9 ^' n" g2 Zeither 21-hydroxylase deficiency or 11-β hydroxylase
) e' z* b; R+ Odeficiency. Those diagnoses were excluded by find-
# C8 j, o& |1 F+ o' ning the normal level of adrenal steroids.; ?& Y+ K  L2 K% [$ O
The diagnosis of exogenous androgens was strongly
! c5 U% _1 ?3 [3 P$ msuspected in a follow-up visit after 4 months because
, @: Z% V* Q& a  H/ ^the physical examination revealed the complete disap-8 w& {- S, o  u, n/ }
pearance of pubic hair, normal growth velocity, and; T) _9 s! d" J& b
decreased erections. The father admitted using a testos-
8 s% n* F  s" c3 Oterone gel, which he concealed at first visit. He was6 o7 i( p( G' a
using it rather frequently, twice a day. The Physicians’
- f: M9 w2 T8 P; K4 h& V1 mDesk Reference, or package insert of this product, gel or
- n# y# G7 F$ J+ g7 r, xcream, cautions about dermal testosterone transfer to
. ?: p: F& G' Q* P; w3 e# \* u1 Runprotected females through direct skin exposure.
, Z3 N6 e- t' Y9 t* s# }8 R0 d' DSerum testosterone level was found to be 2 times the
  K- {5 _# Q# ^% k9 z' v* Z- \0 bbaseline value in those females who were exposed to
7 v4 `4 j0 }$ g& K) I. F$ _even 15 minutes of direct skin contact with their male6 k1 b1 C. @$ G2 O$ v
partners.6 However, when a shirt covered the applica-
/ q' L* R) {4 A4 I/ ntion site, this testosterone transfer was prevented.  w/ q2 @, B+ U* ^
Our patient’s testosterone level was 60 ng/mL,- }7 M" |& m/ Q: M8 I
which was clearly high. Some studies suggest that
9 y0 u1 ]/ h' _1 cdermal conversion of testosterone to dihydrotestos-5 p& L/ Z/ _4 u! h  H1 I# {* U
terone, which is a more potent metabolite, is more6 a0 E5 U, w/ l7 V& T2 z% X5 ^
active in young children exposed to testosterone1 S0 z& T& V; u: G& U/ B& s2 n2 H
exogenously7; however, we did not measure a dihy-
1 L4 p$ O9 u2 edrotestosterone level in our patient. In addition to) g( o+ r9 I: @3 ~2 I$ I
virilization, exposure to exogenous testosterone in& n. a) r! [7 K" i7 c6 d! m; ]
children results in an increase in growth velocity and
( w8 {% F5 T6 I: f9 dadvanced bone age, as seen in our patient.
3 T7 g: X8 v2 c4 JThe long-term effect of androgen exposure during$ p# ^* r$ J! n& k& u
early childhood on pubertal development and final
+ }& J7 g+ W' _6 I/ Jadult height are not fully known and always remain
- n  b7 n+ b+ t/ H, B* P/ Na concern. Children treated with short-term testos-* z: C( J  R7 b# C& a
terone injection or topical androgen may exhibit some+ O' o# _- t; d
acceleration of the skeletal maturation; however, after
8 m0 R" \5 }# Q4 N/ a6 Jcessation of treatment, the rate of bone maturation
0 z; t8 J- b  ]- g- A5 H) j* idecelerates and gradually returns to normal.8,9
7 g! Q# G; A/ _6 ]4 pThere are conflicting reports and controversy
" o6 @: i: I9 V" P, m, M; Sover the effect of early androgen exposure on adult
6 K5 y' z; i& H8 T, s  }penile length.10,11 Some reports suggest subnormal
% B5 ?7 n/ X- jadult penile length, apparently because of downreg-- A; Q+ t& J2 b/ n* Y/ L1 q+ I) N# u% h; n
ulation of androgen receptor number.10,12 However,
( H8 H% y  X0 M- ?Sutherland et al13 did not find a correlation between
) N. r+ @% [9 lchildhood testosterone exposure and reduced adult7 |7 s6 X" k* @
penile length in clinical studies.
$ r) {' ^% T% J+ i5 w+ B) f) wNonetheless, we do not believe our patient is* T- q/ F3 F7 Z8 Z  J
going to experience any of the untoward effects from
1 h9 Z6 i: i9 P- Otestosterone exposure as mentioned earlier because
9 K$ P& a( k- Fthe exposure was not for a prolonged period of time.
4 |, b* K; g- M; T' p2 q/ A4 eAlthough the bone age was advanced at the time of
+ E& j! ~" x9 y6 Pdiagnosis, the child had a normal growth velocity at
0 e6 M$ V! f: f* ]0 [the follow-up visit. It is hoped that his final adult
4 w& Q! `# \) j$ b9 g, _# u' Iheight will not be affected.
1 f4 L1 a9 f# V; ?$ `" @/ fAlthough rarely reported, the widespread avail-7 @- ^6 C, D$ a5 d) B& N: Y
ability of androgen products in our society may. v( v4 u1 g! @' T
indeed cause more virilization in male or female3 d8 \$ Z/ ]7 Z: V5 e9 K$ s/ y
children than one would realize. Exposure to andro-
& @0 }$ G# g8 I) |gen products must be considered and specific ques-
$ I' d  q: p) z& m) Y# htioning about the use of a testosterone product or: p+ Y0 h9 G1 B* J& R3 M. Z2 w
gel should be asked of the family members during4 S( J4 S3 G/ p/ T; B' b
the evaluation of any children who present with vir-# y. X! Q7 @( F( C+ q
ilization or peripheral precocious puberty. The diag-
% f: \! J: q/ |9 Znosis can be established by just a few tests and by3 l5 s3 o) o* n; W0 `0 c
appropriate history. The inability to obtain such a$ @0 v) S. A( G6 \
history, or failure to ask the specific questions, may4 ?3 A/ u) O% _5 o* }6 K5 Y
result in extensive, unnecessary, and expensive
1 ^* o3 ^' }7 T. D% _investigation. The primary care physician should be) v" G, Y/ M4 _
aware of this fact, because most of these children
9 U' _7 J' ~0 {! K2 A3 _  Qmay initially present in their practice. The Physicians’
5 w6 g9 E* ^4 y' \8 Z# w5 G/ O4 qDesk Reference and package insert should also put a
+ R- U. Q+ N2 J5 d) Y* M- uwarning about the virilizing effect on a male or
( m" v5 b8 B9 [% R$ V5 L6 \6 X2 Vfemale child who might come in contact with some-
4 H) V% G0 N* b, W7 s  Jone using any of these products.
) e/ e) a8 o" ~, q( r$ RReferences# L  |* H. H# c( l( O1 m4 y
1. Styne DM. The testes: disorder of sexual differentiation6 B! r% X8 d3 F- p! [/ K
and puberty in the male. In: Sperling MA, ed. Pediatric- G( u  c3 [9 Q9 V; B
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
1 }: S1 C5 ?( X7 f1 a3 @& L2002: 565-628.5 o# k8 @8 }, s) g8 n. r' i7 w
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
  N+ ~3 U) J) ], H  m- e. v$ B. ~puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old0 j- a6 k5 C. U3 s
Boy Induced by Indirect Topical( @$ t; i: R) r1 v* F) Y. [6 g' W
Exposure to Testosterone+ {1 n2 W/ V5 z/ R. f+ |
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ b7 x* s! w! Z! r: P! I: _
and Kenneth R. Rettig, MD1
1 i! g/ D  u# B8 o' aClinical Pediatrics
$ @. m" ?8 c# ~/ p' _Volume 46 Number 6
0 C- B- Z7 D' w. Y/ S( G( wJuly 2007 540-543
: ?. r; W. I$ @0 i' A© 2007 Sage Publications
3 l! v6 T0 C3 U10.1177/0009922806296651
" c# {( N# Y7 i+ d% _5 shttp://clp.sagepub.com" V7 |8 F3 v6 q- d9 m
hosted at* \( T9 ~( K6 A1 N
http://online.sagepub.com! ^( Z6 o+ F( T( J
Precocious puberty in boys, central or peripheral,
& X$ M  M# b& _; W- `, h% g/ iis a significant concern for physicians. Central
; {( w0 l6 @9 u+ ?3 v) D+ f- Vprecocious puberty (CPP), which is mediated
+ U2 a0 s1 m' Q2 nthrough the hypothalamic pituitary gonadal axis, has3 I* W  H( a1 g: j7 C
a higher incidence of organic central nervous system$ I* Z  n# e1 h( N/ M
lesions in boys.1,2 Virilization in boys, as manifested
0 r" v+ h+ E7 ?9 s+ w5 |. fby enlargement of the penis, development of pubic9 v. d  h( a: o
hair, and facial acne without enlargement of testi-/ M) b# |$ t# o. o. R, h
cles, suggests peripheral or pseudopuberty.1-3 We
/ ]# b. `" `. ~/ ]8 P  r5 Nreport a 16-month-old boy who presented with the
, A+ W* S  Q9 N1 V2 `enlargement of the phallus and pubic hair develop-
" z, k% n' U* V- g% K; y/ Z0 wment without testicular enlargement, which was due
6 E9 m; T2 k, S6 i+ _/ Sto the unintentional exposure to androgen gel used by
; u( [2 P8 g0 u7 K+ e" ^2 a  Q* ]the father. The family initially concealed this infor-
; Q* M  u: N5 A& R5 g; Pmation, resulting in an extensive work-up for this
1 [; P5 J. X* m9 I5 Ichild. Given the widespread and easy availability of
! ]' a' t% X- d* htestosterone gel and cream, we believe this is proba-
: d8 W* K$ X+ `8 }# L4 Mbly more common than the rare case report in the( _0 X1 V3 B) m
literature.4
2 B6 e8 J, W: S: d$ H/ xPatient Report
& ]5 G0 m# `; p' L& l8 ?; _5 X. G$ G0 wA 16-month-old white child was referred to the
2 H( Y7 g- C+ p0 L7 [4 \1 N, e5 [endocrine clinic by his pediatrician with the concern' M/ _7 k% F% Z, E9 T
of early sexual development. His mother noticed9 q# }# h1 h1 Y0 P  {/ D) g
light colored pubic hair development when he was7 w5 B! Y: t# n: R, E$ ^
From the 1Division of Pediatric Endocrinology, 2University of
% O. F2 D( C# {South Alabama Medical Center, Mobile, Alabama.
. _; p# Y2 N/ M: g( L% T& \5 wAddress correspondence to: Samar K. Bhowmick, MD, FACE,3 |5 V4 y1 h2 D! M
Professor of Pediatrics, University of South Alabama, College of
0 N6 @1 v! Z$ d9 a2 r& K9 c; sMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! L$ C& d5 D/ `- ^6 G/ K+ M" G
e-mail: [email protected].
# [- e% F: v1 V  c" ], k4 ]$ K  E, Vabout 6 to 7 months old, which progressively became
$ W( z2 T6 |* t: r* D( p! e- Z! ldarker. She was also concerned about the enlarge-
# V' B; Q3 K  G: w" |, W& s* c9 Xment of his penis and frequent erections. The child
4 u2 X# G2 D: dwas the product of a full-term normal delivery, with& V( s: {7 ~" K5 e+ k, d
a birth weight of 7 lb 14 oz, and birth length of. }: K# y( ^4 ^; [9 t/ m9 V7 n
20 inches. He was breast-fed throughout the first year7 Y* V' d4 ]4 N) m: q
of life and was still receiving breast milk along with2 a$ O! X* U4 E. |- ]  l( V! D
solid food. He had no hospitalizations or surgery,3 {1 A& p/ q7 O- }+ y3 z
and his psychosocial and psychomotor development
3 G( B3 g5 c4 a+ Xwas age appropriate.
) K) m( v/ t) I7 rThe family history was remarkable for the father,
3 _4 \. U7 U5 p3 S  N# t3 hwho was diagnosed with hypothyroidism at age 16,
8 `# h9 h7 h2 t& K) k6 A/ Qwhich was treated with thyroxine. The father’s7 c5 R% v, X8 d0 D5 x, r: Y
height was 6 feet, and he went through a somewhat  A, U# x# D7 O. ]! z0 \
early puberty and had stopped growing by age 14.! {& ]3 V$ I  h' E( W2 Y( H: S
The father denied taking any other medication. The
0 P8 L3 O7 |2 L: Achild’s mother was in good health. Her menarche
, d' u+ e- R! j5 }4 Swas at 11 years of age, and her height was at 5 feet4 t. Y% o' u- s2 |3 ?: R
5 inches. There was no other family history of pre-
# t" ?  T' v7 l  G& x& \, \* _+ Jcocious sexual development in the first-degree rela-
* G8 d" Z% g$ P% [. xtives. There were no siblings.
2 Z; @0 |2 r, u% V9 BPhysical Examination7 N% v, R6 A3 P, `: ?
The physical examination revealed a very active,
: b3 l* M2 q" |* v# D. zplayful, and healthy boy. The vital signs documented
! T; G% _$ H  q- @a blood pressure of 85/50 mm Hg, his length was/ B# U1 @# K9 |9 }% g
90 cm (>97th percentile), and his weight was 14.4 kg$ l" T# U5 h9 V' e( A6 F7 L8 H3 }
(also >97th percentile). The observed yearly growth& c  h4 |, {3 q7 x8 A4 `1 O
velocity was 30 cm (12 inches). The examination of
  S% Z5 {. k6 p. [0 j) H7 jthe neck revealed no thyroid enlargement.
" Q8 j1 D- M/ Z: C( q: ?The genitourinary examination was remarkable for
) G5 f9 p% t( R% y* P# Nenlargement of the penis, with a stretched length of
. H6 B# O9 E) q& S% Q3 \8 cm and a width of 2 cm. The glans penis was very well, T" L  [: r- ~# ?8 ?- j5 R
developed. The pubic hair was Tanner II, mostly around# U, Q" o: y+ u4 S2 `$ c3 O2 w
540' V& `+ k/ e/ F; _4 |9 g+ j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! E1 H/ S, Z! |$ Y6 K
the base of the phallus and was dark and curled. The. j7 B' B; J; ?5 A. q! y
testicular volume was prepubertal at 2 mL each.3 @9 I8 K3 t- K& S9 q2 Q& M
The skin was moist and smooth and somewhat$ R- s+ ~  _( ]( M" q) b% h
oily. No axillary hair was noted. There were no
  S4 F8 R5 `1 W1 D- dabnormal skin pigmentations or café-au-lait spots.
5 s& |8 [( ]0 N; ?Neurologic evaluation showed deep tendon reflex 2+
  a! a( n; X1 }) D1 r8 _bilateral and symmetrical. There was no suggestion: k. D8 }+ s% k) d
of papilledema.  L4 T4 _9 _" C$ A
Laboratory Evaluation& T( @/ {! }& G0 Z8 c. [8 J
The bone age was consistent with 28 months by
. I5 P8 X$ L$ x6 I6 ^5 ~using the standard of Greulich and Pyle at a chrono-' G- T# W0 a1 `  R) d
logic age of 16 months (advanced).5 Chromosomal
7 {- }9 b% g% ?1 h8 E; L0 ]karyotype was 46XY. The thyroid function test
' ]4 T* G! W3 s4 h4 Pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-9 r6 M7 l- k( [2 m, V5 y! ?
lating hormone level was 1.3 µIU/mL (both normal).& @( k4 l* |) P7 L
The concentrations of serum electrolytes, blood$ R4 K9 `  t/ [6 j* }4 m' Y
urea nitrogen, creatinine, and calcium all were
5 J, Q# _9 h  n8 dwithin normal range for his age. The concentration" F, `  t, U# W, \" N
of serum 17-hydroxyprogesterone was 16 ng/dL, O6 {! u/ _( i; L+ o3 i9 ^
(normal, 3 to 90 ng/dL), androstenedione was 20% q& A* t% \( W
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 }$ V& m- h6 i: o% C6 Z3 `. J6 A
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
+ {1 W: L5 X: t- R6 g1 q' n$ x, \8 Qdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 S1 o$ {; H7 @3 B6 L/ H1 a& n49ng/dL), 11-desoxycortisol (specific compound S)
& l. P; f9 ?! o1 V  i' v1 Jwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: \7 i* ]2 u  g3 I! }  I1 ftisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 Y/ _  o- y+ T$ \2 P1 ^& q+ Y0 xtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),, @3 r4 _0 A  ~( t# @
and β-human chorionic gonadotropin was less than
% Q6 L* @, Y4 i, F# Y5 mIU/mL (normal <5 mIU/mL). Serum follicular9 `3 ]8 v3 A4 T' ]% l- D  C
stimulating hormone and leuteinizing hormone) F3 w) h! Y+ F3 r. f% Y
concentrations were less than 0.05 mIU/mL7 [" C3 Q  W) d1 k
(prepubertal).' k& R: k/ D( T
The parents were notified about the laboratory
8 R5 m+ _5 I3 p- Nresults and were informed that all of the tests were
0 W9 i6 \+ y2 S* x9 X# d# Anormal except the testosterone level was high. The
- U" w" x6 \( j4 _follow-up visit was arranged within a few weeks to
* \4 I" Z$ }3 m, Y9 }! }  Cobtain testicular and abdominal sonograms; how-1 ^$ i; S% j2 L) Y5 a
ever, the family did not return for 4 months.
$ k2 N. {. I6 f: W+ Y5 ZPhysical examination at this time revealed that the8 F$ F" E' _0 a! S/ ?6 @, q
child had grown 2.5 cm in 4 months and had gained
" a% p! \! _# ]- W4 {- K2 kg of weight. Physical examination remained
& x# X; @+ E0 P. i+ O) Kunchanged. Surprisingly, the pubic hair almost com-
. O) W0 C7 I9 M6 W9 _3 Qpletely disappeared except for a few vellous hairs at
  D- u0 {* s1 t& l8 Pthe base of the phallus. Testicular volume was still 29 E6 f0 k7 k1 U7 p+ ~
mL, and the size of the penis remained unchanged.( ^3 K: U: z5 V' O6 S/ N
The mother also said that the boy was no longer hav-6 ]8 l4 f7 E5 Y6 t5 ?& n
ing frequent erections.+ U) m; U$ h9 M
Both parents were again questioned about use of6 t  M! t* S" t
any ointment/creams that they may have applied to
) ]5 x; X) w& Z4 F8 ^the child’s skin. This time the father admitted the
1 E$ R! x6 k3 K+ JTopical Testosterone Exposure / Bhowmick et al 541& j. j5 s. ?7 f4 ^
use of testosterone gel twice daily that he was apply-
3 a6 \8 |- `* j. M4 G6 Uing over his own shoulders, chest, and back area for
  a, A; s3 O) J5 x$ ^a year. The father also revealed he was embarrassed" W" O/ |# g6 v" M6 t7 h+ Y
to disclose that he was using a testosterone gel pre-9 F5 q8 }7 ]- |$ r2 V! g9 k
scribed by his family physician for decreased libido
9 Y  N' k$ m# q8 O5 @secondary to depression.
" b$ Z, n7 E/ G  l0 IThe child slept in the same bed with parents.
4 x' P6 C# _+ ^' ]The father would hug the baby and hold him on his! R/ G( t3 ?' L# n6 J* K& n
chest for a considerable period of time, causing sig-5 V) D% a- m& D$ Q$ Y9 ?
nificant bare skin contact between baby and father.
0 R% `6 l) e0 Y; y, _The father also admitted that after the phone call,+ p1 J! s0 b: i2 |- @9 g
when he learned the testosterone level in the baby* ?6 A3 C- W# `: B0 M+ u
was high, he then read the product information
' R% i/ O: P* J. t. B  m" p" ^packet and concluded that it was most likely the rea-
6 @) c6 K1 G5 ison for the child’s virilization. At that time, they# ?# b$ P" S8 m' T6 A
decided to put the baby in a separate bed, and the
+ E6 r( o2 n) N( y( `+ d) ffather was not hugging him with bare skin and had9 K3 d8 a4 g7 _* i
been using protective clothing. A repeat testosterone
& N% i6 `' x7 ~' c+ ytest was ordered, but the family did not go to the
: ?# f, U% J2 g& [( u8 ]5 K( q2 Ulaboratory to obtain the test.
: W; X1 v5 z' `. eDiscussion
* T. D& J8 q/ }  O; jPrecocious puberty in boys is defined as secondary: v8 N7 d4 E" L' I) |2 [$ y
sexual development before 9 years of age.1,4
# W0 N' W# `+ ^; V* M! KPrecocious puberty is termed as central (true) when
' u" Q' v+ k1 Eit is caused by the premature activation of hypo-
* O0 p7 a0 _9 F4 rthalamic pituitary gonadal axis. CPP is more com-
4 u) j( R0 p- e% w9 Rmon in girls than in boys.1,3 Most boys with CPP1 L/ k! f: V$ I- k% U4 \
may have a central nervous system lesion that is
# V" C' C; `! ]' T8 F6 Lresponsible for the early activation of the hypothal-2 V, ~* u. V) c) ^& x
amic pituitary gonadal axis.1-3 Thus, greater empha-
* i" ~! K* o, v0 E: Asis has been given to neuroradiologic imaging in
: E) ^# O6 w7 a0 Bboys with precocious puberty. In addition to viril-
( A5 ]2 m0 Y  l2 l* d/ ]ization, the clinical hallmark of CPP is the symmet-
. ]! [) ^* s- d6 ^& [rical testicular growth secondary to stimulation by
; F2 T1 q; a4 ^/ r2 kgonadotropins.1,36 X* k" m" @& v, X9 ^4 c. Y
Gonadotropin-independent peripheral preco-
8 h8 F. f8 B1 x9 Ccious puberty in boys also results from inappropriate
' P  Q" Z) ^- t3 mandrogenic stimulation from either endogenous or& ^% l6 R' |* k0 |% j0 W
exogenous sources, nonpituitary gonadotropin stim-
3 d, |. H7 t9 Q5 Y+ B7 l: \2 Q! Culation, and rare activating mutations.3 Virilizing, H, o# ], @2 L+ w; j
congenital adrenal hyperplasia producing excessive7 K, W6 n/ Q5 M4 q1 i
adrenal androgens is a common cause of precocious6 Z3 x2 y1 Z  {; Q1 x) u. o
puberty in boys.3,4
5 e4 |3 }% N# W- UThe most common form of congenital adrenal
  n! D( E; i2 e. @) C( uhyperplasia is the 21-hydroxylase enzyme deficiency.
% I- [6 h5 I6 I& Q1 I" B; D$ J0 JThe 11-β hydroxylase deficiency may also result in' L9 f  _- f5 Z
excessive adrenal androgen production, and rarely,: |- R9 r2 s/ h& L9 z! x
an adrenal tumor may also cause adrenal androgen
* }* G7 t( r& G$ r$ M% nexcess.1,3
) _) V6 e3 G+ L. _7 p3 K/ U) W9 hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from/ e0 C7 {. Y" l5 A* d& r
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
. ~' ^+ l( p0 u3 s5 l5 Q* i7 [A unique entity of male-limited gonadotropin-$ J* v2 X% F) X+ J
independent precocious puberty, which is also known( Q) u) m3 S. [$ i6 W" y
as testotoxicosis, may cause precocious puberty at a
8 ]0 d% _# A* w! C9 c* Yvery young age. The physical findings in these boys
% r0 u6 t' {! |: b; P7 [" k8 Gwith this disorder are full pubertal development,
+ L  S, r) Y, ]including bilateral testicular growth, similar to boys
2 u8 a6 A$ H( t9 r+ awith CPP. The gonadotropin levels in this disorder8 H1 m2 A0 _/ M5 Y
are suppressed to prepubertal levels and do not show+ O% `: [  h1 N/ D5 A
pubertal response of gonadotropin after gonadotropin-# d4 M) ^; M) B# [, x9 y& B) c
releasing hormone stimulation. This is a sex-linked* c6 K/ c* b- P3 N
autosomal dominant disorder that affects only) w) G! c& [$ v9 L9 @  K
males; therefore, other male members of the family* O+ r9 o. \- W( m
may have similar precocious puberty.3$ Q8 Z) R) P9 c* p
In our patient, physical examination was incon-
7 X3 @; i& b- }; V' L( Fsistent with true precocious puberty since his testi-
- Q) P( [; K  P' _) Y" ncles were prepubertal in size. However, testotoxicosis
& F% t2 j0 j6 h0 }was in the differential diagnosis because his father
  Q. {6 U/ v+ L. F% tstarted puberty somewhat early, and occasionally,! M% ?7 @0 j& }9 d/ g
testicular enlargement is not that evident in the9 b) I- W% g4 K4 t9 c$ S  j
beginning of this process.1 In the absence of a neg-
6 L  g* p! C& T* k  {7 `2 oative initial history of androgen exposure, our
9 i1 U' ]0 ]3 Ibiggest concern was virilizing adrenal hyperplasia,
* ^0 B4 S  {7 _, T( C$ @( J( @either 21-hydroxylase deficiency or 11-β hydroxylase
7 V) _0 `' Y- S+ c, `deficiency. Those diagnoses were excluded by find-5 v4 n+ k& T2 A5 z: r+ D6 M  V1 c3 e
ing the normal level of adrenal steroids.& _+ s7 \; u+ `! h
The diagnosis of exogenous androgens was strongly
8 ?4 O, s- g6 ]suspected in a follow-up visit after 4 months because: C9 L3 }- V9 t( v
the physical examination revealed the complete disap-
9 {' ?% J  L, t( P( ~pearance of pubic hair, normal growth velocity, and9 y. t$ K2 z7 ~6 h0 R* e# @# Z7 c3 D
decreased erections. The father admitted using a testos-* \; J! S* ?; }: t1 k
terone gel, which he concealed at first visit. He was
0 g' v# X$ S5 w* s+ ?& E0 tusing it rather frequently, twice a day. The Physicians’  m3 r- S- i2 \/ [/ a& h
Desk Reference, or package insert of this product, gel or
* A4 Q1 p7 ^  [0 {  `6 t+ rcream, cautions about dermal testosterone transfer to
4 N! F0 O$ \& s( f  vunprotected females through direct skin exposure.
* X6 N( G3 S" D. x: |' jSerum testosterone level was found to be 2 times the& S" \6 c# d, n) C. J
baseline value in those females who were exposed to
$ t& M8 S5 z, m7 X0 g4 Ueven 15 minutes of direct skin contact with their male7 z0 b1 j+ J# D* G
partners.6 However, when a shirt covered the applica-' u! _2 j* r3 `" X9 C0 N
tion site, this testosterone transfer was prevented.
3 d# W% e1 l$ [4 \; zOur patient’s testosterone level was 60 ng/mL,4 R7 N+ W4 t/ w0 V$ i, c7 {
which was clearly high. Some studies suggest that
7 x* w0 R! z  p3 ~) m4 i* m& Mdermal conversion of testosterone to dihydrotestos-
) q- l, y6 O$ W: i' Zterone, which is a more potent metabolite, is more
4 o; A% ~) g) B$ c) iactive in young children exposed to testosterone
3 }" R% y# l; f  |$ e# f6 K& Vexogenously7; however, we did not measure a dihy-6 y$ R3 h1 I9 ?9 _( `3 A
drotestosterone level in our patient. In addition to5 B" x, `! M) X9 I  _& f9 I3 x6 a
virilization, exposure to exogenous testosterone in
" K- D& p  G$ D5 ], ~children results in an increase in growth velocity and8 U/ F& l; p% q, G
advanced bone age, as seen in our patient.  _4 h0 x9 ~: W1 D5 T  C
The long-term effect of androgen exposure during  F, \* D, S& f2 P: y4 y; P- j
early childhood on pubertal development and final: u7 H, z" x  N5 }* A5 [
adult height are not fully known and always remain
' |* A! w3 _- {9 v& O7 w/ Na concern. Children treated with short-term testos-/ |8 m  W$ [% Q, e- m! S
terone injection or topical androgen may exhibit some
/ B$ [- j0 F. t' [  a% Cacceleration of the skeletal maturation; however, after0 D! p3 ]8 Z6 @5 n. W7 I: @: }* c! f
cessation of treatment, the rate of bone maturation
" _3 w# ]) ?. q& T% p0 |9 Jdecelerates and gradually returns to normal.8,9. B1 a6 ]0 n/ f% r. G
There are conflicting reports and controversy5 Z- r+ f3 i- D* V- X9 F. x
over the effect of early androgen exposure on adult
% _  _4 y3 F; H/ |0 E1 r9 u$ ]penile length.10,11 Some reports suggest subnormal, `: D. _( S. F  k$ T5 }& u! O
adult penile length, apparently because of downreg-
: A, B9 Z) \2 R; ?# x' Dulation of androgen receptor number.10,12 However,- A6 R- y; N/ Z0 t$ ~: h( v4 v
Sutherland et al13 did not find a correlation between( l! k% l, ~* R8 R" Q- \
childhood testosterone exposure and reduced adult
! b3 E8 V3 `+ x# h, u" Ipenile length in clinical studies.
5 N* e7 g0 w0 i: O; GNonetheless, we do not believe our patient is
# H% b1 z0 P' g# f& n& mgoing to experience any of the untoward effects from; M$ W' ?' U. D1 T+ C
testosterone exposure as mentioned earlier because, `( y8 i7 J) |9 H; c) |. _# X
the exposure was not for a prolonged period of time.0 }' K) h6 Z$ [  L
Although the bone age was advanced at the time of6 M" R* \  [: X
diagnosis, the child had a normal growth velocity at
6 ?4 ~2 R. r* T; h" Ythe follow-up visit. It is hoped that his final adult
& `! r) S* S, Y" [+ T. sheight will not be affected.
# K4 V, }* P3 |Although rarely reported, the widespread avail-
9 S+ S( _- F( `9 Q! j# X6 Q* Xability of androgen products in our society may
: r9 R/ m5 R# Vindeed cause more virilization in male or female
" J9 H4 T+ \3 x: P0 Dchildren than one would realize. Exposure to andro-
9 `8 R' B' A* Q0 d% Mgen products must be considered and specific ques-
; c, l) Q9 F* w# E) Ltioning about the use of a testosterone product or7 O. n" y. L! ~7 q) J
gel should be asked of the family members during
0 F% R, z- ]  r7 [  B( }! Jthe evaluation of any children who present with vir-
8 C  i) y; U5 ]ilization or peripheral precocious puberty. The diag-+ Z! V, ~5 ^" k/ D+ F& {8 W
nosis can be established by just a few tests and by( Q4 y: n2 I: g" Q
appropriate history. The inability to obtain such a7 K) {& h8 P9 e7 C& y
history, or failure to ask the specific questions, may
& x  \0 k! u: x8 H& Q. eresult in extensive, unnecessary, and expensive! W5 N+ p6 U1 V, u5 ~: `
investigation. The primary care physician should be- J2 h+ m  g8 }
aware of this fact, because most of these children/ e% _7 u0 c% a; n
may initially present in their practice. The Physicians’3 y0 }; E9 L" y
Desk Reference and package insert should also put a& R/ {. }+ R- [6 `. L% C0 _4 R
warning about the virilizing effect on a male or
2 m7 O8 n$ O" {% H" v% pfemale child who might come in contact with some-. r& X% u' M, g5 c
one using any of these products.0 K; P, c& B' ?, o  }
References. s/ ^! a5 u5 g, r
1. Styne DM. The testes: disorder of sexual differentiation
/ P5 b. @; }! U( X) I" ^) F: L4 t8 \and puberty in the male. In: Sperling MA, ed. Pediatric
1 s5 T8 e) [9 g2 l1 e& A6 XEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;* e/ c- `( N  K. f1 x! R
2002: 565-628.
9 r$ A0 P, a  `4 t! g/ Z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) W3 t/ e( @3 y
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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
; a8 ^- z( B# u1 r, u
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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