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Sexual Precocity in a 16-Month-Old* N& Y2 n' F8 v% g! l" D
Boy Induced by Indirect Topical
: A( n. T. ^4 L& i% Q, l2 fExposure to Testosterone
. h8 r0 L4 N* v6 P! m7 g8 KSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. W0 b% V0 i4 b) g3 r( V
and Kenneth R. Rettig, MD1$ _# [( S/ p! m& {' b9 T. z1 \7 x$ \1 R
Clinical Pediatrics- L+ r7 M" D/ o" U# B: R7 {0 i
Volume 46 Number 6
$ r5 L* ?7 v( y* FJuly 2007 540-543) r. G/ M) k1 `$ {8 S5 C+ @
© 2007 Sage Publications
" `: W7 L- s! t, u" D$ W7 x10.1177/0009922806296651, R' F& `! t2 {! Y
http://clp.sagepub.com* g0 J- k% `% a, I- }7 b6 B
hosted at
" V) M. d% u) H; L. c. L; W. t& Chttp://online.sagepub.com
  w9 c4 e5 j. q* i0 [' BPrecocious puberty in boys, central or peripheral,/ J# z) z# Y2 |" Z
is a significant concern for physicians. Central
- I/ ^( y: G7 ^4 \precocious puberty (CPP), which is mediated
5 R! w- a' O' B% q. m* q1 {through the hypothalamic pituitary gonadal axis, has9 `: w/ D6 G, ~, m
a higher incidence of organic central nervous system
% M# c, ^, k6 l  p5 v. l- elesions in boys.1,2 Virilization in boys, as manifested% \+ J: H8 G: m* ~, z8 p; Z
by enlargement of the penis, development of pubic
: r* U) {' W$ D. B1 b. T* Uhair, and facial acne without enlargement of testi-
4 }# l4 l- B% A9 G& F4 Gcles, suggests peripheral or pseudopuberty.1-3 We% `! n' Y( c- W9 q, [3 v2 R% t# V
report a 16-month-old boy who presented with the
5 @$ j6 g+ z6 ^. Fenlargement of the phallus and pubic hair develop-/ A' p" E2 l4 T0 Y" A5 Z
ment without testicular enlargement, which was due) M7 u% @& c  w; U, r$ N- K
to the unintentional exposure to androgen gel used by# A! y( I! c& t% f; `* ^. I( D
the father. The family initially concealed this infor-
4 M3 y# d! {0 `% F+ amation, resulting in an extensive work-up for this) e7 C3 D1 ]/ y5 |  u+ z% l  q
child. Given the widespread and easy availability of/ ^; S5 [  E1 Z# B( B, a. g4 B# d( u+ u5 f
testosterone gel and cream, we believe this is proba-
, d/ s) L0 Z) o. b: i" q" rbly more common than the rare case report in the: O. b' h( c. K$ v2 }
literature.4
9 @& ]' a- z: ^) C$ T8 U7 F. `Patient Report
5 [9 D- j, {) P1 N; f( rA 16-month-old white child was referred to the% S0 F4 u6 F9 c# ~# X0 J1 U# M
endocrine clinic by his pediatrician with the concern* B7 C8 Z$ _- s& U
of early sexual development. His mother noticed, w0 d+ Z2 m3 g, f4 b
light colored pubic hair development when he was
# C8 o1 M0 b+ ]+ NFrom the 1Division of Pediatric Endocrinology, 2University of
; P3 K- c7 G# n# W$ X; k$ o2 JSouth Alabama Medical Center, Mobile, Alabama.6 \0 b+ m2 ~, z# k: J( N
Address correspondence to: Samar K. Bhowmick, MD, FACE,  ^  ~+ s( Z  S& L/ d+ W8 O
Professor of Pediatrics, University of South Alabama, College of
6 D1 ]! I- D1 a! u, Y, b# |5 l9 _Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 j0 l3 d0 v" e9 J$ c
e-mail: [email protected].' L4 T0 e) T! u$ z. ^
about 6 to 7 months old, which progressively became
7 X% p3 a% m, v8 ?0 v  ]; M: mdarker. She was also concerned about the enlarge-  P1 f' V/ \9 \" z
ment of his penis and frequent erections. The child8 j+ L2 u8 e& O7 S/ E
was the product of a full-term normal delivery, with4 A+ j& o8 `2 ~( X! Z! Z
a birth weight of 7 lb 14 oz, and birth length of
, D- N: {! Q" Z4 X) G20 inches. He was breast-fed throughout the first year
# d9 ]7 @1 p& j* \- X7 \( Lof life and was still receiving breast milk along with
( e* z  z& m; Y: E$ y2 Dsolid food. He had no hospitalizations or surgery,
  F" R8 O! s# V7 Fand his psychosocial and psychomotor development
* E. a- M+ T% \; ~  ~- zwas age appropriate., j- G; I& @. u; e
The family history was remarkable for the father,1 _. x1 b9 i- m  ]" B! N
who was diagnosed with hypothyroidism at age 16,; b% P" f; m# R& @( m' r: h
which was treated with thyroxine. The father’s
* q! O# j/ X- H9 j( r& Dheight was 6 feet, and he went through a somewhat
" Q: o% ], Z9 f$ ]early puberty and had stopped growing by age 14.
/ O. ?# Z7 t& \3 PThe father denied taking any other medication. The
( z/ ^  t4 F! b& ^9 vchild’s mother was in good health. Her menarche$ m5 Z# P8 V- u
was at 11 years of age, and her height was at 5 feet
5 s  {# [4 z' ^5 inches. There was no other family history of pre-
- c" P5 }1 {* Icocious sexual development in the first-degree rela-0 r8 o( M: y# u: m% Y' K: |' s
tives. There were no siblings.
2 ^& z) T3 J) U2 d) o0 ~) @Physical Examination" F8 l% H! d( B6 I
The physical examination revealed a very active,
- v8 v' ^; {: W# mplayful, and healthy boy. The vital signs documented" X% x% j3 R; \& {6 q
a blood pressure of 85/50 mm Hg, his length was
3 t7 b9 k( c3 n0 v. ~& ]$ f90 cm (>97th percentile), and his weight was 14.4 kg
' u7 K, B3 ]0 w(also >97th percentile). The observed yearly growth3 L% ~" {, g: f! t
velocity was 30 cm (12 inches). The examination of0 e( y7 Q$ g0 u4 N$ N" C0 p
the neck revealed no thyroid enlargement.
, l$ W6 `9 }! M# U! fThe genitourinary examination was remarkable for* [6 L* Z  g: Z0 c
enlargement of the penis, with a stretched length of6 f1 T6 K, g: N5 M, d$ Y/ U/ Y( c& B: {
8 cm and a width of 2 cm. The glans penis was very well- y8 A( t: h6 i% v: S
developed. The pubic hair was Tanner II, mostly around# R  [5 w+ A5 v8 S  ~" ^
540
( w: Y5 E& h/ i! aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; _7 R9 l( a- m" W
the base of the phallus and was dark and curled. The6 K4 R9 x$ I3 F8 _+ ]
testicular volume was prepubertal at 2 mL each.
& `$ C4 e2 ^9 ?) p4 m# I+ SThe skin was moist and smooth and somewhat) O2 t6 r9 _( p
oily. No axillary hair was noted. There were no
7 V3 O- `- x$ d! O8 @abnormal skin pigmentations or café-au-lait spots.
: N; x, h& |8 g0 sNeurologic evaluation showed deep tendon reflex 2+- n" M3 X" O5 _  X
bilateral and symmetrical. There was no suggestion
. V6 v5 ]  G2 f& s+ cof papilledema.- }+ _$ e4 \2 h6 |5 x( S4 {
Laboratory Evaluation
( u- ?" ~# H7 n) R4 Y5 s0 mThe bone age was consistent with 28 months by  o+ M6 b: k; k" N
using the standard of Greulich and Pyle at a chrono-
  W6 a; O6 L/ Z7 c7 V9 llogic age of 16 months (advanced).5 Chromosomal4 d  r7 h) i2 U3 k+ \6 ^/ c
karyotype was 46XY. The thyroid function test
2 W1 `: a/ w* V/ b# o, ^showed a free T4 of 1.69 ng/dL, and thyroid stimu-" S9 Y% P: v4 B4 s
lating hormone level was 1.3 µIU/mL (both normal).
2 ~6 z6 ]5 W3 m% HThe concentrations of serum electrolytes, blood
: _" }( @& w! m% k( X; \8 Eurea nitrogen, creatinine, and calcium all were
0 h$ u6 B! y% ?8 u5 X, ewithin normal range for his age. The concentration
+ k9 E+ G  _# f2 N. C  Yof serum 17-hydroxyprogesterone was 16 ng/dL1 ?3 y8 @7 c7 k3 L) K( A
(normal, 3 to 90 ng/dL), androstenedione was 20: b+ ?2 y* u, K
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 q: z& _+ k$ B% o4 g$ F0 L+ Wterone was 38 ng/dL (normal, 50 to 760 ng/dL),
, p/ \/ G4 i8 \desoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ g% y" h+ F8 _; |49ng/dL), 11-desoxycortisol (specific compound S)0 e4 ?% q, Y5 N
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-, J( x! U3 _. _3 x9 h1 P( s/ I
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
' V/ Y8 Y6 J' _: Btestosterone was 60 ng/dL (normal <3 to 10 ng/dL),& e; C! y8 E$ J% ?
and β-human chorionic gonadotropin was less than! h+ P1 F$ l# W9 H) c
5 mIU/mL (normal <5 mIU/mL). Serum follicular
/ u7 b9 a4 L9 l! C# A/ qstimulating hormone and leuteinizing hormone$ r& e' T% [' _3 U) ?7 t  y0 B/ O' ~
concentrations were less than 0.05 mIU/mL
$ h& T4 S. L" P0 {2 W(prepubertal).5 X8 ]4 }6 ?) K& x6 Z: w5 A1 R
The parents were notified about the laboratory/ Q7 g# `' u. K' {
results and were informed that all of the tests were
5 N& s; R$ }4 Znormal except the testosterone level was high. The
3 M: e8 ?7 a# b0 `follow-up visit was arranged within a few weeks to6 u+ G* Z2 _& |6 C  V0 ?! h1 ~" {, I
obtain testicular and abdominal sonograms; how-+ f6 V- X' _1 m
ever, the family did not return for 4 months.
6 e' c6 p$ |+ b$ ^( A, i+ TPhysical examination at this time revealed that the
; u" h* M/ J7 echild had grown 2.5 cm in 4 months and had gained
! u4 d; r+ F) @2 ~' I2 U% M0 X  {2 kg of weight. Physical examination remained) n& o5 |# ]0 U& A! ]6 a2 _
unchanged. Surprisingly, the pubic hair almost com-) n1 d4 o4 N3 `# `' h
pletely disappeared except for a few vellous hairs at
6 F/ @  R. Z' V3 d( Ythe base of the phallus. Testicular volume was still 2
- a2 x( j4 Q, m. Z; @mL, and the size of the penis remained unchanged., s3 ^0 r' z7 h2 J; F2 Y
The mother also said that the boy was no longer hav-1 y. l* D8 a6 u, U2 y2 k) e
ing frequent erections.
1 ]* y; `$ D+ W% g6 tBoth parents were again questioned about use of5 a* e, m. P" `, m; \  t
any ointment/creams that they may have applied to
1 k% Z- o) n/ M2 Z" j% Zthe child’s skin. This time the father admitted the
  L) i4 \* t+ i4 K9 v' @6 S& ^& E5 CTopical Testosterone Exposure / Bhowmick et al 541
1 n+ ]) z$ `# _$ O5 `$ @& Muse of testosterone gel twice daily that he was apply-: r5 X: a* k9 T7 a+ z) f
ing over his own shoulders, chest, and back area for* g4 n) q! Z" @. g" n% i
a year. The father also revealed he was embarrassed
" X( ]& a  ^: Z) ~& `- U+ Yto disclose that he was using a testosterone gel pre-
0 f; F( V8 g/ v+ u6 O: @8 P+ @2 `scribed by his family physician for decreased libido
! I$ l9 _8 T" _/ H3 Vsecondary to depression.: S, Z5 T, [# A: v: r1 `$ l7 Q8 L
The child slept in the same bed with parents.
# R8 B4 q* v  E8 d& tThe father would hug the baby and hold him on his1 Z0 L. c5 ]8 k" L4 {
chest for a considerable period of time, causing sig-
* @; E; L8 X' o8 X  B4 lnificant bare skin contact between baby and father.
3 e& m) v" E$ s0 g  b4 }" V) {The father also admitted that after the phone call,8 V5 F4 w% Q& H
when he learned the testosterone level in the baby  C+ u0 y1 K/ d9 I# t
was high, he then read the product information( o* m% D/ f- _3 `; J) h5 h9 G1 j
packet and concluded that it was most likely the rea-1 ~) v" }* u- p3 E  t  S* \
son for the child’s virilization. At that time, they. p5 H0 B& y- |  i
decided to put the baby in a separate bed, and the7 L6 e; S! r# {
father was not hugging him with bare skin and had
4 |# ~" w0 g$ J5 v5 Q( ^been using protective clothing. A repeat testosterone/ U- G& c3 h, M% ]7 }+ f6 j
test was ordered, but the family did not go to the
" i2 ?' o# O% t" {' ^3 @+ s9 x+ Ylaboratory to obtain the test.) Z8 C# |: j' ?6 L* h% g+ Y
Discussion
) }- h; x% z# B7 Q" zPrecocious puberty in boys is defined as secondary
5 @- ~5 C7 W' z7 Hsexual development before 9 years of age.1,41 u: y' P& Q/ {8 _0 s6 @
Precocious puberty is termed as central (true) when
2 A6 d: J% X! q  yit is caused by the premature activation of hypo-
6 H3 y- c  Y" F' R* Dthalamic pituitary gonadal axis. CPP is more com-
7 N- l. t; l8 w. Y6 Smon in girls than in boys.1,3 Most boys with CPP! L# X' x/ M. K; @  R& Z9 K/ U" t& o
may have a central nervous system lesion that is
4 e. ^  J) O) t8 B: e& Bresponsible for the early activation of the hypothal-
) u# v9 U# p  M! P2 ]! Lamic pituitary gonadal axis.1-3 Thus, greater empha-% q4 a; d" L# t/ H5 _! b! C
sis has been given to neuroradiologic imaging in
0 K  A' V# a7 {& ^$ y5 k# oboys with precocious puberty. In addition to viril-
3 }% }' t5 x4 Pization, the clinical hallmark of CPP is the symmet-! E- {1 P- z" s4 U
rical testicular growth secondary to stimulation by6 u* I1 A% X$ r: `  n
gonadotropins.1,3
  h: [$ Y1 G0 K6 F- V& N6 `: dGonadotropin-independent peripheral preco-9 r7 K7 O* w/ j! W: H
cious puberty in boys also results from inappropriate
- |7 q0 z& U) F5 t+ randrogenic stimulation from either endogenous or  T; \# y" y6 ?# [
exogenous sources, nonpituitary gonadotropin stim-) Y2 M7 a  b1 I8 u( k7 n
ulation, and rare activating mutations.3 Virilizing1 }1 L( Q) ~8 g* ~! p
congenital adrenal hyperplasia producing excessive
8 M1 Y/ O2 [( F$ Q4 Z5 `' t" Q, dadrenal androgens is a common cause of precocious9 @0 H: B$ \7 q0 v6 l+ q4 L
puberty in boys.3,4
* G  J% Q% F: ]* I0 `The most common form of congenital adrenal- |+ E" j% p( q. @! g4 s
hyperplasia is the 21-hydroxylase enzyme deficiency.) e( c9 N5 T* e1 U* v8 o5 |' C
The 11-β hydroxylase deficiency may also result in
" H; |( Q9 u7 w7 b9 {; h1 Mexcessive adrenal androgen production, and rarely,
, j/ A% B  }& N( j2 ]) G( Ban adrenal tumor may also cause adrenal androgen
- v4 C  t, X$ h6 Iexcess.1,3
  G7 O+ m8 J5 q- {7 E. Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" `8 {  J& K2 G7 G4 m1 V, |542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 D/ s% p$ N/ ]3 r5 b+ L) H% WA unique entity of male-limited gonadotropin-
6 T) s6 F; v9 L1 e3 C8 b2 Mindependent precocious puberty, which is also known
7 Z3 _' A+ Y2 }; \, T3 X. E$ [/ jas testotoxicosis, may cause precocious puberty at a
' O, H; r( R% J0 zvery young age. The physical findings in these boys3 A# s5 F( n3 K5 y3 T2 i, y
with this disorder are full pubertal development,
1 q$ e2 }. e. L' I- L! ?: dincluding bilateral testicular growth, similar to boys
3 r0 t/ Q- t& J; f/ O" j- Bwith CPP. The gonadotropin levels in this disorder
& v( ?% ~! b+ W3 d& V/ Kare suppressed to prepubertal levels and do not show* b5 _/ `0 j1 m# E- u
pubertal response of gonadotropin after gonadotropin-; a: @- R0 h" Y; o' U3 Q  {  B
releasing hormone stimulation. This is a sex-linked, O) W& r$ y* i; t
autosomal dominant disorder that affects only: q+ u" c5 h6 n8 d
males; therefore, other male members of the family
0 D% n( @$ b+ Y! O+ O/ Y4 @4 Amay have similar precocious puberty.3
7 ~) F, f0 h! _' |2 hIn our patient, physical examination was incon-
$ h3 C* G$ d7 b0 H5 `7 @! U. H) |4 s& osistent with true precocious puberty since his testi-
1 v& n3 ?6 ~0 m3 m* Y' lcles were prepubertal in size. However, testotoxicosis
# K0 u3 A( J5 k4 n" ?was in the differential diagnosis because his father9 O* L8 ?* R  k! |
started puberty somewhat early, and occasionally," g8 m; q( F% E1 d6 L( G6 a
testicular enlargement is not that evident in the4 w7 S/ }: w+ C5 \
beginning of this process.1 In the absence of a neg-/ {5 y" `$ u( e5 M  x4 |
ative initial history of androgen exposure, our3 d" d, r9 b0 u. T' q: |
biggest concern was virilizing adrenal hyperplasia,
. \( Z+ U( f7 r4 {0 l2 \either 21-hydroxylase deficiency or 11-β hydroxylase
6 z" S" g; a% u& \0 J! Vdeficiency. Those diagnoses were excluded by find-
; Z: `+ B* M6 \ing the normal level of adrenal steroids.
8 E. Q& m4 f9 D% M& `9 g" d) YThe diagnosis of exogenous androgens was strongly
/ c/ r  H% o1 Y5 Tsuspected in a follow-up visit after 4 months because
  i' _& x* U0 y' Z7 l2 nthe physical examination revealed the complete disap-2 @1 A8 K9 t  o' B' w/ h9 S. o
pearance of pubic hair, normal growth velocity, and+ M# c2 }6 y4 t# h  |9 `
decreased erections. The father admitted using a testos-8 b1 H0 z- L* f+ f& R! U$ I
terone gel, which he concealed at first visit. He was
- Q& K, l1 p9 a* iusing it rather frequently, twice a day. The Physicians’
' M, y# r, x% x( M- X" R& {% ~Desk Reference, or package insert of this product, gel or
0 x* A: Z$ R2 z# I3 x$ Y6 R* n6 j( gcream, cautions about dermal testosterone transfer to0 t* X1 c) w  W1 K  t
unprotected females through direct skin exposure.
3 v& S" g/ p# ]( H6 B8 ~' e, tSerum testosterone level was found to be 2 times the; b, `2 |1 S* `
baseline value in those females who were exposed to( [. R1 Q; S5 \/ Y& q
even 15 minutes of direct skin contact with their male
& j1 e+ r! X- q4 I% t$ R9 Lpartners.6 However, when a shirt covered the applica-
; U9 O4 U1 L! M' Ition site, this testosterone transfer was prevented.
; g3 V6 [/ F( Q+ @Our patient’s testosterone level was 60 ng/mL,
3 u$ Q# D2 O5 V! k8 c- c, iwhich was clearly high. Some studies suggest that
* h6 }  s, J! P0 T4 F: A1 E+ c  L/ {' cdermal conversion of testosterone to dihydrotestos-
5 z' ?2 ~, K3 Yterone, which is a more potent metabolite, is more% t0 J2 u5 ~- L( L
active in young children exposed to testosterone
! h- `" f" I' O, D( Y+ |exogenously7; however, we did not measure a dihy-
" K7 B4 o  T0 n$ o; |6 h! Hdrotestosterone level in our patient. In addition to
  @! U0 H: X3 x3 a* w: n. r2 B1 fvirilization, exposure to exogenous testosterone in4 h; b" O7 Q: |( H
children results in an increase in growth velocity and$ s( S6 i( u3 I6 F3 z. Y' H
advanced bone age, as seen in our patient.& I9 ]9 C$ R6 F; B5 M4 f8 S
The long-term effect of androgen exposure during6 a& j# `2 D! O0 b6 \
early childhood on pubertal development and final- i5 Q' }' |$ z( S7 {: [& b! f
adult height are not fully known and always remain5 f6 T6 d7 Q: k! Y, f0 w
a concern. Children treated with short-term testos-$ h) h3 e2 M; ~  M6 Y: h: _' a
terone injection or topical androgen may exhibit some! R. I2 P# ^7 P; g( Q, f- q$ \$ u" p
acceleration of the skeletal maturation; however, after2 {) e$ F. M- b% x4 O# C1 K$ k# g: j, L
cessation of treatment, the rate of bone maturation- F. B2 ^5 P  c2 Z: @* }
decelerates and gradually returns to normal.8,9! |, B$ ]- Z; t9 l" S$ |
There are conflicting reports and controversy) Y9 k1 j+ z; I! l
over the effect of early androgen exposure on adult
, j+ R. w% x/ X# R* fpenile length.10,11 Some reports suggest subnormal8 ]" L+ X: z: c* e5 H9 C! h5 q6 t
adult penile length, apparently because of downreg-7 i& p. r: ]' a5 ~
ulation of androgen receptor number.10,12 However,. }$ w$ `. D' K
Sutherland et al13 did not find a correlation between
5 {: d+ ^3 f7 }2 I5 P" Z' {. Kchildhood testosterone exposure and reduced adult
" \. s5 w! `. E# ]$ f9 Q8 @penile length in clinical studies.
- h: `3 O7 p" Y" `7 u' WNonetheless, we do not believe our patient is
- j0 f) i! n7 g' ]/ \, I7 cgoing to experience any of the untoward effects from) X  C& N4 L0 n1 S9 Y9 A& I3 v
testosterone exposure as mentioned earlier because8 J1 I/ z# `8 T4 W0 N0 f- {: j
the exposure was not for a prolonged period of time.
- l2 ^3 @4 L( K  T0 ], a/ LAlthough the bone age was advanced at the time of
  V4 a1 ]1 e" k$ R% ndiagnosis, the child had a normal growth velocity at$ |( {4 v( h% n4 j3 L" U1 U
the follow-up visit. It is hoped that his final adult
1 q3 s! y5 f' i  ~; o9 d( m" Aheight will not be affected.
/ K9 I- D, n0 Q9 fAlthough rarely reported, the widespread avail-
" Q3 W) K& L& }! aability of androgen products in our society may: ^' f4 e3 z- F7 B' K+ E& P/ V! `
indeed cause more virilization in male or female
& `4 k* @  r/ l2 C' [9 wchildren than one would realize. Exposure to andro-
( Q# @4 C5 B: R$ ?0 M0 ^gen products must be considered and specific ques-3 V5 P2 T0 u- P+ e7 U0 a
tioning about the use of a testosterone product or1 N5 z4 }3 `/ _- e: s
gel should be asked of the family members during5 K( {) M# R, V- z' g! |0 R" P
the evaluation of any children who present with vir-
% `0 ~( A1 W( }; l5 v7 _# [ilization or peripheral precocious puberty. The diag-
% b6 h0 @7 E' h' nnosis can be established by just a few tests and by6 e8 y+ l. a3 m4 A) K( t
appropriate history. The inability to obtain such a
; |: s) s" `0 N# }  z( @, d3 T8 ghistory, or failure to ask the specific questions, may
) T; H$ H( o. S& u, _result in extensive, unnecessary, and expensive
) d$ e( C" F4 C$ {2 Qinvestigation. The primary care physician should be
6 ^  c: p: q& L: L& @4 `9 I. \4 ]" vaware of this fact, because most of these children
; y& H2 P) y9 V) X- g5 Lmay initially present in their practice. The Physicians’
6 x7 w" s7 E& J6 f! p- ?* T1 MDesk Reference and package insert should also put a. W$ l2 _) `3 D
warning about the virilizing effect on a male or
$ W. F' f* ~% f* f5 j- Nfemale child who might come in contact with some-1 ~% Y4 j  A& A5 R/ M8 V. F. i9 [4 J% h
one using any of these products.  Z: |# z" L& @% c9 z" @1 x
References. z$ N" V$ J- m; c
1. Styne DM. The testes: disorder of sexual differentiation( Y1 S' t+ u( r3 [" `7 G
and puberty in the male. In: Sperling MA, ed. Pediatric# u. a- U% v+ }) P$ i9 w8 {
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 [: m+ `; C0 ^! e0 _: O9 T0 ]2002: 565-628.
( S" T* y) E3 n) A% V: U) @2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious) H/ m5 r! r( L+ g! _' @" E
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
. z/ H" t  j- i8 Y* g  FBoy Induced by Indirect Topical+ R7 ]* f* M4 X" c
Exposure to Testosterone
% B/ P& R/ \4 `1 n2 g! A3 Q4 ^# z8 fSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2; L& f# T9 x. O8 }/ H" b* }2 p
and Kenneth R. Rettig, MD10 H. Q- e) f0 b; [2 C
Clinical Pediatrics" F/ I/ g% `6 T" x
Volume 46 Number 6
9 j( O. U5 t" _! E- wJuly 2007 540-543% t* q  U/ P$ ]4 ~" t$ n3 A6 z3 {
© 2007 Sage Publications% v6 T! }2 u. p5 g2 X* U1 ]
10.1177/0009922806296651
7 ]" q- t2 S( n" F1 e4 t2 Ehttp://clp.sagepub.com
# @& l# h( u5 a) R7 Khosted at- `7 T3 |) q2 y6 A9 T
http://online.sagepub.com% F/ @2 }& l/ [" }: S; C
Precocious puberty in boys, central or peripheral,
) O5 n1 _6 W2 B$ F8 zis a significant concern for physicians. Central
, G' |. ^6 A4 \' s5 g/ lprecocious puberty (CPP), which is mediated+ P% Y% [) M+ m4 j' g5 {: N" W
through the hypothalamic pituitary gonadal axis, has1 I; f/ {6 d5 W$ [9 F. h: F# n  f' J
a higher incidence of organic central nervous system8 k% \) [; F2 E+ k3 w* F( \/ |
lesions in boys.1,2 Virilization in boys, as manifested
, o  @  U! y7 S. ]4 \7 {by enlargement of the penis, development of pubic7 |' Y5 ^5 V1 C6 b/ O
hair, and facial acne without enlargement of testi-* w, J/ D; E8 r) Y" W" k
cles, suggests peripheral or pseudopuberty.1-3 We' D0 w  E; Y, n' o8 G
report a 16-month-old boy who presented with the
- b' _! P* S' [0 Q$ qenlargement of the phallus and pubic hair develop-. o; L4 A# E' s4 V
ment without testicular enlargement, which was due
9 M. v6 A& K% tto the unintentional exposure to androgen gel used by3 ]0 \+ u! ?9 x, X' y
the father. The family initially concealed this infor-
9 d. W, _0 Y4 Q: Umation, resulting in an extensive work-up for this
! o/ o% R" k! p- J. C1 hchild. Given the widespread and easy availability of
/ P' a# x) c7 R# jtestosterone gel and cream, we believe this is proba-; L$ u/ Z: R- K
bly more common than the rare case report in the6 ^7 s; a# N. r9 d  Y
literature.4
: }* `2 \/ s, N  m2 g& [5 L+ {3 p$ aPatient Report
. ^' w: f# l3 U- P$ h: }% uA 16-month-old white child was referred to the8 U8 L+ j0 x: E! f2 J
endocrine clinic by his pediatrician with the concern
% _" z2 H3 D  jof early sexual development. His mother noticed
; u, }6 p6 P* H# e2 _light colored pubic hair development when he was
9 {( s* s$ S/ |From the 1Division of Pediatric Endocrinology, 2University of/ t. Y' R# m9 u' m
South Alabama Medical Center, Mobile, Alabama.
4 X: T0 a) p$ |- QAddress correspondence to: Samar K. Bhowmick, MD, FACE,
9 ?1 m2 ?4 J0 m( V2 tProfessor of Pediatrics, University of South Alabama, College of
7 c1 i+ N/ |' H0 N: B' EMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 v  B( A* C5 Q8 d$ ?. _7 Y$ i* w
e-mail: [email protected].- H4 V) J2 l# X: b9 X
about 6 to 7 months old, which progressively became$ m4 G/ `. n. i* p" H$ u1 x
darker. She was also concerned about the enlarge-
: j4 \1 n, a: S8 I2 ]8 `- O/ bment of his penis and frequent erections. The child: `, N# N' o& Q. s
was the product of a full-term normal delivery, with
! ?9 l& n2 D: U$ f, n# A8 `a birth weight of 7 lb 14 oz, and birth length of+ A6 S/ u9 m' {2 T8 G9 Y* I2 R5 n
20 inches. He was breast-fed throughout the first year1 w7 j) E) d/ V# k3 W7 F
of life and was still receiving breast milk along with
/ h- N2 {& B, usolid food. He had no hospitalizations or surgery,, t  v) Z7 f2 v. ^. N8 p0 z
and his psychosocial and psychomotor development
3 ~/ _* R6 o0 q! Z/ T, cwas age appropriate.9 o2 l$ E3 ]4 x: a( o9 e  Y
The family history was remarkable for the father,
, q, v9 X. i$ s& Bwho was diagnosed with hypothyroidism at age 16,
7 E, {& X3 s; I* U9 ?9 X: R" Cwhich was treated with thyroxine. The father’s
) [- |9 o, D/ [7 l9 _height was 6 feet, and he went through a somewhat
3 M$ h% l& X6 ^early puberty and had stopped growing by age 14.
& V0 U4 ^& p! T6 l+ u( yThe father denied taking any other medication. The
: {' _8 r; S' p* echild’s mother was in good health. Her menarche
4 K+ `3 C3 D1 M6 o* @% wwas at 11 years of age, and her height was at 5 feet
' F3 ^9 l8 p. D! L5 inches. There was no other family history of pre-  s. Y5 S7 g6 `. `
cocious sexual development in the first-degree rela-* c5 }* Y# C$ N
tives. There were no siblings.
( q) h  Z' ~- @0 b+ u* g- T5 qPhysical Examination
& }# F& t0 E8 q: d! l4 ^The physical examination revealed a very active,& G- k; @8 G% w8 D- K! K3 e% g7 j
playful, and healthy boy. The vital signs documented/ s) _4 [' L4 \! C5 g1 ]+ S
a blood pressure of 85/50 mm Hg, his length was) _- d! ], e& W. Q& a6 ?
90 cm (>97th percentile), and his weight was 14.4 kg; X9 C  Y  H2 K  O( T
(also >97th percentile). The observed yearly growth
$ T6 L6 r) U" ]" H4 q; D7 P. ?velocity was 30 cm (12 inches). The examination of
/ Z0 E: {9 m- w2 z9 Y/ N, _the neck revealed no thyroid enlargement.
% ?% j4 g. }2 e3 _6 t( i5 G2 ^0 IThe genitourinary examination was remarkable for
/ n3 r% Q. j0 F. W# Nenlargement of the penis, with a stretched length of' C6 N. b) i) u$ u0 G* M
8 cm and a width of 2 cm. The glans penis was very well
( C/ A+ W' G* e) Tdeveloped. The pubic hair was Tanner II, mostly around+ n! a; E2 O$ L9 _/ \4 j0 I
540
! v. S- K& X( f; j& Z$ L& V( @at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
) l1 w* b) Z+ P. v3 l; U/ x& |the base of the phallus and was dark and curled. The6 H1 r; K5 B) a. h
testicular volume was prepubertal at 2 mL each.
- c7 ~) s  T  E' r4 R) R; U- ZThe skin was moist and smooth and somewhat/ {7 S1 l+ k7 |# R$ r
oily. No axillary hair was noted. There were no
$ Z# m! W, |4 H8 ]! P: Q1 kabnormal skin pigmentations or café-au-lait spots./ ?  {$ r" R7 [1 b* P
Neurologic evaluation showed deep tendon reflex 2+
: p7 t; i& y) N  C1 ?- L# \. z, A2 ?% C) ?. ?bilateral and symmetrical. There was no suggestion3 C9 v. Y) M% f' t9 Y4 I
of papilledema.
4 r" j5 S: r/ ]& z7 o. X- MLaboratory Evaluation
) U9 G4 g: I& I% W/ eThe bone age was consistent with 28 months by+ B$ i1 O3 \7 u' k; m- I
using the standard of Greulich and Pyle at a chrono-
1 A3 R- }* S( |2 Llogic age of 16 months (advanced).5 Chromosomal
5 E' N3 \$ _% d! P3 g( Pkaryotype was 46XY. The thyroid function test
' i2 x# A$ S! O. [showed a free T4 of 1.69 ng/dL, and thyroid stimu-; @$ _. x6 c0 T2 g. @5 m5 Y
lating hormone level was 1.3 µIU/mL (both normal).
( A$ F3 H/ \9 AThe concentrations of serum electrolytes, blood% P; x! O0 |6 ^
urea nitrogen, creatinine, and calcium all were& ~& I5 b6 z. ?
within normal range for his age. The concentration# w+ m6 L. J3 @9 U6 I
of serum 17-hydroxyprogesterone was 16 ng/dL
0 O$ C2 f6 E- N3 K# x9 k(normal, 3 to 90 ng/dL), androstenedione was 20. ]. S% X, ~$ t6 g" @! `8 S
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
4 M5 j- Y9 s; X( ?/ T# fterone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 ?8 w- k. x8 ~' \. b/ Tdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
* e) \2 ]' a$ X49ng/dL), 11-desoxycortisol (specific compound S)
" v% [  U. a* ]6 C7 s* w: t+ ^5 Mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-# G" w" d$ h* `" D. q
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
* S7 b8 U* D3 B) `4 M0 ktestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
- [/ g. P) r8 B5 q2 L9 V: @and β-human chorionic gonadotropin was less than4 W0 m4 S9 S  L) h0 m2 I
5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 K; G2 g/ C8 F! mstimulating hormone and leuteinizing hormone
& Y3 X$ ]; @; E1 E2 fconcentrations were less than 0.05 mIU/mL  M- V7 m7 [- \) _7 H/ P
(prepubertal).: }/ c4 M- k# P# o/ ^% E
The parents were notified about the laboratory- h) g, p8 n: Z! X
results and were informed that all of the tests were
5 `3 c) q" G" e4 cnormal except the testosterone level was high. The. u! A. d' d1 m1 R: c
follow-up visit was arranged within a few weeks to
: @& C% e: A" w. ~+ d9 Hobtain testicular and abdominal sonograms; how-- y: B: X/ Z# S0 g0 R+ k* ]9 Y
ever, the family did not return for 4 months.
+ T. n" P9 `& S! |' }Physical examination at this time revealed that the3 Z  i+ Y/ n5 B' D0 L$ N+ e
child had grown 2.5 cm in 4 months and had gained
) q5 R, }' S: ]+ ^6 T  U2 kg of weight. Physical examination remained$ `0 D0 _- Z/ D* y. N
unchanged. Surprisingly, the pubic hair almost com-
! s3 M7 D! s  }' Z% I! tpletely disappeared except for a few vellous hairs at6 e- x4 Q1 _, Z5 i5 x5 Y2 S6 d& V
the base of the phallus. Testicular volume was still 2
( i; j% U( E8 V1 d+ J: q; cmL, and the size of the penis remained unchanged./ Q: m! e9 u0 t
The mother also said that the boy was no longer hav-% Z! a2 P, j; Q' P
ing frequent erections.. ^1 O! G: l, [+ @. f
Both parents were again questioned about use of- ~5 f9 k4 R' ]# S- D
any ointment/creams that they may have applied to1 X+ N$ {% |% P/ K# c# I, |
the child’s skin. This time the father admitted the
  E5 k1 e4 V$ Q, P4 G) {: ETopical Testosterone Exposure / Bhowmick et al 541
& q  C0 ^5 }1 Yuse of testosterone gel twice daily that he was apply-
0 l9 u) N- I! Z" _- h/ q! T- x" Ling over his own shoulders, chest, and back area for
$ o# P* ]6 ^/ R5 o) pa year. The father also revealed he was embarrassed" h: _% O/ f3 k' Q' w
to disclose that he was using a testosterone gel pre-
( Y& w6 L! e4 I7 K* B5 ~scribed by his family physician for decreased libido
( D6 m8 J0 @- hsecondary to depression.  \% y% z4 ^# w  Z/ O9 l
The child slept in the same bed with parents.
, k9 I; i. [4 _6 X2 l5 C0 C, Y( zThe father would hug the baby and hold him on his
% N9 N' }+ O2 `9 c: |! }4 p" Nchest for a considerable period of time, causing sig-
; ~) x2 z; q. Anificant bare skin contact between baby and father.
3 H0 a: \/ i8 w- Z7 [; m9 QThe father also admitted that after the phone call,  b! e. v, Y% j# W9 I3 l
when he learned the testosterone level in the baby+ G" |3 `- D+ ^" U* J) ]; W
was high, he then read the product information& u/ g9 K, m4 d% P
packet and concluded that it was most likely the rea-( d- b) u+ s6 q/ D, J- S- U: a, x
son for the child’s virilization. At that time, they
4 y2 {; @1 n6 W; N5 s( i! i8 ndecided to put the baby in a separate bed, and the
; ?( ?0 O% K  p; bfather was not hugging him with bare skin and had1 g/ L8 A- G; l
been using protective clothing. A repeat testosterone
, l# e7 n3 M) ~9 l' @3 W* Ytest was ordered, but the family did not go to the, B' M8 N4 N# U2 O
laboratory to obtain the test.. k! n2 y) H6 T, i) h
Discussion
' E9 Q5 q  X5 Y: _- O1 R" VPrecocious puberty in boys is defined as secondary
( w* L0 ^+ X+ S3 n. Dsexual development before 9 years of age.1,4
: c/ X, |" J+ y$ i! kPrecocious puberty is termed as central (true) when
3 S) G5 {1 K( jit is caused by the premature activation of hypo-
7 Q9 q  O! \/ z* X1 j7 t$ cthalamic pituitary gonadal axis. CPP is more com-$ L6 |5 }4 {7 h7 u0 r; x. K% V. v
mon in girls than in boys.1,3 Most boys with CPP5 M  C3 o4 m& _/ h: {* k
may have a central nervous system lesion that is
( ^: s. I/ F! }; f4 [" d5 X; g# Vresponsible for the early activation of the hypothal-/ [9 u; ?' H# {  E6 L
amic pituitary gonadal axis.1-3 Thus, greater empha-
  A1 a  }/ p0 q% _! X! Nsis has been given to neuroradiologic imaging in
% Z9 h% V+ [; b* A4 F+ mboys with precocious puberty. In addition to viril-
& n3 s2 [* I. ~4 yization, the clinical hallmark of CPP is the symmet-
9 J2 a6 J* d1 D- ]6 D8 S' Wrical testicular growth secondary to stimulation by
5 E! f: f- u0 r" V! J8 z& O! I" ~gonadotropins.1,39 ~) E, Z6 }; G3 j! y$ H) e
Gonadotropin-independent peripheral preco-
7 Y" T5 t% J; J% l# Xcious puberty in boys also results from inappropriate
. {6 O8 j  Y' v/ @; C5 I% ?3 ]androgenic stimulation from either endogenous or
1 L+ j+ K3 k$ |7 l; ?" ?0 _exogenous sources, nonpituitary gonadotropin stim-
3 E4 V& M- @0 c( wulation, and rare activating mutations.3 Virilizing+ Q0 w9 D# Z; g1 s! B7 h
congenital adrenal hyperplasia producing excessive
& L  n9 S5 c  uadrenal androgens is a common cause of precocious/ B; t" i. B/ Y" ]
puberty in boys.3,49 q5 E% ~/ `+ j- ]% @- d, |( ]# Z
The most common form of congenital adrenal
' K' F% @2 w8 R' a2 ?$ Shyperplasia is the 21-hydroxylase enzyme deficiency.3 o6 s$ b5 t% V# o# j0 {9 ~
The 11-β hydroxylase deficiency may also result in: ~- J; |. K8 f' F- l3 k% J
excessive adrenal androgen production, and rarely,
+ }( ~9 ^; i, U: i0 xan adrenal tumor may also cause adrenal androgen
3 L  j  O6 I: \- L& Hexcess.1,3  K8 H: Y2 I& w0 t
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
0 |& l) K" m; `" C; ~542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
/ P- F4 l; n5 S7 z. F8 V* xA unique entity of male-limited gonadotropin-
( v2 k* W+ ?& r2 X4 ^0 ^independent precocious puberty, which is also known
" n! n/ o/ Y0 P6 ]* G: a. C+ qas testotoxicosis, may cause precocious puberty at a
) E' ~. e9 p# F  {# {3 ?0 zvery young age. The physical findings in these boys
) a0 y( k) U' i' _& k/ x# s& ~with this disorder are full pubertal development,& f+ W$ R7 D: h7 x- p- s
including bilateral testicular growth, similar to boys
0 t$ ?  b6 a: X# L  w$ ~/ C) mwith CPP. The gonadotropin levels in this disorder: V! b2 X& Y4 s7 e# L8 W! K( I
are suppressed to prepubertal levels and do not show0 D, B! v, ]+ j; d; w. D
pubertal response of gonadotropin after gonadotropin-
' b( _/ D# V  x! ereleasing hormone stimulation. This is a sex-linked
  }4 L" b; z  e# _( Dautosomal dominant disorder that affects only$ F  Y. Z0 T1 c' B) w. _
males; therefore, other male members of the family; X6 |' v2 I' ?$ w2 Q
may have similar precocious puberty.3
" a$ F( [  |) p  B$ N* k4 {4 v0 ?In our patient, physical examination was incon-
" y' Y8 `2 R% V- ^6 ~* `! T1 Dsistent with true precocious puberty since his testi-
& x4 N0 a3 H$ vcles were prepubertal in size. However, testotoxicosis
1 Q2 @) \6 ~- L1 o+ J* h3 Twas in the differential diagnosis because his father
; G; d" \9 W- v6 ?/ E7 ^5 N. Ustarted puberty somewhat early, and occasionally,
0 n" ?' u, x4 z; M. ?testicular enlargement is not that evident in the4 S. M5 e: b( |8 E1 G5 M
beginning of this process.1 In the absence of a neg-
, w7 M. |4 G8 t) h5 y# n$ kative initial history of androgen exposure, our7 `+ U. M" T% i5 q; V
biggest concern was virilizing adrenal hyperplasia,
, E- t) L% q( h, f0 k4 Ieither 21-hydroxylase deficiency or 11-β hydroxylase% V2 g6 A9 _% l/ n' Y
deficiency. Those diagnoses were excluded by find-  f5 K4 r# L0 g, k& B
ing the normal level of adrenal steroids.
7 \1 N  N- r% K6 ZThe diagnosis of exogenous androgens was strongly
; P6 t6 o8 Z9 c% w" a& D# Ysuspected in a follow-up visit after 4 months because; o) S  f2 {4 b! [5 O
the physical examination revealed the complete disap-* z7 v" B  g5 y! D. r3 S
pearance of pubic hair, normal growth velocity, and( o- u% @& c, q. F! i, t
decreased erections. The father admitted using a testos-+ t& W6 W% _$ `$ ]7 d, Z8 F: t
terone gel, which he concealed at first visit. He was. \4 y- w* a4 y" d1 {( [
using it rather frequently, twice a day. The Physicians’1 P. w3 n. y/ R- h
Desk Reference, or package insert of this product, gel or
  X* a$ i0 Y  }cream, cautions about dermal testosterone transfer to/ c9 X% f8 v- R6 h# v
unprotected females through direct skin exposure., O! X3 ?2 u% S% }# A
Serum testosterone level was found to be 2 times the
4 \" _- I, H. _4 B, Ibaseline value in those females who were exposed to% f0 S) ?( u, C& v
even 15 minutes of direct skin contact with their male
6 D; A* p- i: dpartners.6 However, when a shirt covered the applica-/ c! }; ~+ x8 ?- ~$ e
tion site, this testosterone transfer was prevented.
+ i& H& m4 `0 y' _Our patient’s testosterone level was 60 ng/mL,! W8 a7 y; h! A9 Z+ `- M# A3 M8 ?$ D
which was clearly high. Some studies suggest that
2 @% b5 N/ I" k8 {: G- adermal conversion of testosterone to dihydrotestos-# B' w+ t9 n& z1 B: l9 M8 F
terone, which is a more potent metabolite, is more4 F$ }1 T  `( f. V
active in young children exposed to testosterone
2 c9 d3 o4 c* Aexogenously7; however, we did not measure a dihy-
) O0 [! E  T$ c6 [! E: P" N2 adrotestosterone level in our patient. In addition to
" Y) ]0 A3 V. }: k' B9 _" Ovirilization, exposure to exogenous testosterone in# N- U9 K4 W" `" S
children results in an increase in growth velocity and
7 X" ]4 L$ z7 C3 fadvanced bone age, as seen in our patient.$ `; o4 D! _2 P
The long-term effect of androgen exposure during
  j. M& K/ ]  _6 M5 C% {early childhood on pubertal development and final" D" e2 Y* [2 s6 A% I* u
adult height are not fully known and always remain% z, _0 Y1 g( v! w; ?
a concern. Children treated with short-term testos-
" g3 q3 }/ ?" a3 |9 q# X' G" zterone injection or topical androgen may exhibit some3 k# ], z9 u! ?  W( M
acceleration of the skeletal maturation; however, after8 w; r& |) w0 m/ w4 q; f4 j
cessation of treatment, the rate of bone maturation
+ M; Y( ?* K- X9 x: Jdecelerates and gradually returns to normal.8,9# l$ w# f1 i7 C+ p: @7 b8 ~+ Z
There are conflicting reports and controversy
) F+ T5 E! c- x4 p7 \" P: Cover the effect of early androgen exposure on adult
5 p$ R4 d4 y, R) U. U4 w# epenile length.10,11 Some reports suggest subnormal4 v1 k& `4 I+ a9 Z
adult penile length, apparently because of downreg-
. m" q% g7 f2 u2 ~: Mulation of androgen receptor number.10,12 However,6 M2 E  E! ~6 K) S& W" e
Sutherland et al13 did not find a correlation between
4 d% N6 ^: P: |childhood testosterone exposure and reduced adult
4 z) K4 F: e+ L' q+ ?penile length in clinical studies.
# \# _1 a% M+ ENonetheless, we do not believe our patient is
( {7 Z' c6 j2 V3 `/ }7 I% R3 H0 wgoing to experience any of the untoward effects from
. l% |0 m5 H! t/ o' x  Q! E4 J/ U: Btestosterone exposure as mentioned earlier because
6 Y9 f: J/ s$ h' j0 Ithe exposure was not for a prolonged period of time.
% D4 G+ q% P0 ~5 @8 P: f0 U8 FAlthough the bone age was advanced at the time of
) L; d! l7 v+ t  Wdiagnosis, the child had a normal growth velocity at% L: S0 ^! M. _3 g9 T& c) E  t* B! e
the follow-up visit. It is hoped that his final adult% Q4 ]  X) W; L
height will not be affected.
* K: N- s+ _% I- s" i+ H& ~Although rarely reported, the widespread avail-
" e1 I' n4 u+ n2 n/ w- Mability of androgen products in our society may
7 D2 m, l; q" {. O% @indeed cause more virilization in male or female
: x3 G8 r3 t) k% C# ]5 Y, K) n3 mchildren than one would realize. Exposure to andro-
; O+ E/ r0 ^" Q$ W  k' j! C8 J8 G* Dgen products must be considered and specific ques-, d6 V# R9 ]1 i; R& m/ x9 i
tioning about the use of a testosterone product or
0 b, d4 y  o$ Y+ }: ]3 |1 G2 egel should be asked of the family members during
+ J! w" \  _$ P* \9 l" G- U. w; D$ ^the evaluation of any children who present with vir-
7 u/ ]$ ]' a9 z' bilization or peripheral precocious puberty. The diag-' D9 V9 w1 o' A
nosis can be established by just a few tests and by6 ~% T4 X- _4 p  U  F- T/ F
appropriate history. The inability to obtain such a% F8 ]/ S' ]9 U1 x3 Q8 [, `
history, or failure to ask the specific questions, may
. V* @& w) Z! y# F- Z1 x5 dresult in extensive, unnecessary, and expensive
  e5 R6 v( I1 S! linvestigation. The primary care physician should be
# O8 K0 t" ]9 N$ z3 t+ vaware of this fact, because most of these children
) ]8 ~9 {+ a5 Qmay initially present in their practice. The Physicians’( {; s) j- `& K0 @$ M
Desk Reference and package insert should also put a. H. A* B8 |/ y3 B$ T7 M# K
warning about the virilizing effect on a male or$ A! u7 j3 O' ~& P1 G
female child who might come in contact with some-1 }+ B, G; o+ t. n
one using any of these products.
0 W. n  H2 g" h# u$ K. Y  {, ?1 eReferences! d% f9 D: _4 \8 Y' W( ~- H% w% J
1. Styne DM. The testes: disorder of sexual differentiation
4 c# S5 m6 D9 nand puberty in the male. In: Sperling MA, ed. Pediatric
: }: k/ A4 o  r) [! M5 L  T* |Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;) z% R) ?2 }5 E2 \
2002: 565-628.
$ V8 h# q# n1 H2 _- R2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" R% d- M: a( v- s7 |+ A- I
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
0 G4 A' I+ {9 \% ~
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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