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Sexual Precocity in a 16-Month-Old* T9 h& C8 m3 V6 R3 i* P' y
Boy Induced by Indirect Topical; Y% T" w$ g; h" t$ J5 k1 }
Exposure to Testosterone4 e' I8 s  o7 G" W3 V2 v. P: q
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ n3 D) r9 J4 q+ Y1 B; Tand Kenneth R. Rettig, MD1! F4 i& @& p. v" M( t' G* F0 p" p
Clinical Pediatrics5 o5 A7 E) h- X4 D5 k
Volume 46 Number 6! V) y( T2 _8 l$ J2 ~! Z0 W: H: K
July 2007 540-543( Q/ b0 C$ _+ G2 i, p
© 2007 Sage Publications  {$ |4 a: t2 p$ y4 h
10.1177/0009922806296651, b# f5 z- R; z- {0 P- A7 z2 f
http://clp.sagepub.com  g/ j8 @6 `  R# U1 M
hosted at
: a, Q* x# C% ]2 ^http://online.sagepub.com- Z3 k, q8 _" \+ F1 h" X
Precocious puberty in boys, central or peripheral,
5 j: B. `1 g7 B2 X$ b5 fis a significant concern for physicians. Central
( M  b# `" S& ], S1 tprecocious puberty (CPP), which is mediated
; ]0 X9 L! u, B2 rthrough the hypothalamic pituitary gonadal axis, has
6 x7 U: ]9 H+ K9 f% Ya higher incidence of organic central nervous system; n. K& ]; X% f" i$ U4 r& `
lesions in boys.1,2 Virilization in boys, as manifested
) o& n) j, j- x4 `+ k* j! kby enlargement of the penis, development of pubic
$ S5 ~* y; p* M! \0 w; \8 W. ~hair, and facial acne without enlargement of testi-
% {" _$ x% r& x2 h0 fcles, suggests peripheral or pseudopuberty.1-3 We
1 ~& I) a/ t) greport a 16-month-old boy who presented with the
6 e9 ^) D) G& _0 {6 c5 Aenlargement of the phallus and pubic hair develop-
/ E; G) Y. t5 r: G8 Dment without testicular enlargement, which was due
+ t! ?+ R8 u( s3 pto the unintentional exposure to androgen gel used by9 P3 ~6 b, f: V4 U' i' \: X5 J
the father. The family initially concealed this infor-$ R# B* c! y& o; S2 v8 u. q, ]
mation, resulting in an extensive work-up for this
9 V8 u) e/ i: F6 C. A+ qchild. Given the widespread and easy availability of
' f4 U6 w9 U- V+ B1 M. E: R+ T- Otestosterone gel and cream, we believe this is proba-
0 o! G' O. h' F. y8 ]bly more common than the rare case report in the% n, S' `: a* d, p1 O
literature.45 g1 Q1 z. I8 Z1 `5 f- M- B+ G# x* K$ ~
Patient Report
, ]" t. c3 i3 J  ]7 l" vA 16-month-old white child was referred to the. Z9 M$ k% O" m- t% B/ X, ^( {# X
endocrine clinic by his pediatrician with the concern
. z0 ?" K3 n; i: Q" @* wof early sexual development. His mother noticed
# H5 ^4 `, @) a) ]light colored pubic hair development when he was3 B: t9 C4 k. T) W. d
From the 1Division of Pediatric Endocrinology, 2University of
5 z# e1 F, N2 ?4 ?5 O" `8 k1 ?+ ~3 NSouth Alabama Medical Center, Mobile, Alabama.* r7 g1 r0 z7 o) g
Address correspondence to: Samar K. Bhowmick, MD, FACE,- L$ l2 ]. t# f8 {2 R' u
Professor of Pediatrics, University of South Alabama, College of  i& \( b: P1 J% ^8 N
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 L: N( ~/ S; Q) g! M" O. Ye-mail: [email protected].- V. s' |; Y# w* C: C
about 6 to 7 months old, which progressively became' s7 j8 G& P; B1 X
darker. She was also concerned about the enlarge-/ p0 u4 w+ @) m& R' l  @2 f
ment of his penis and frequent erections. The child
' E* J. y$ a. W3 ^- m5 x% ^was the product of a full-term normal delivery, with6 L( n# E3 _6 G/ Z! P
a birth weight of 7 lb 14 oz, and birth length of0 k6 v" @+ M+ y, V
20 inches. He was breast-fed throughout the first year/ e, w6 G; F+ d% i" O1 ]$ t
of life and was still receiving breast milk along with& h# Y4 S( z4 k  ^. s. @
solid food. He had no hospitalizations or surgery,
9 S  L. f' V$ x( u: K- E# sand his psychosocial and psychomotor development
3 x, I, \/ |# M8 h6 [was age appropriate.
( t" d7 X% O+ Y1 gThe family history was remarkable for the father,5 ]( e9 K  Q' Q5 L* k3 a
who was diagnosed with hypothyroidism at age 16,2 X( f4 L7 o0 U) c( y
which was treated with thyroxine. The father’s
- w3 E3 v- S+ K2 J, }' t  X& qheight was 6 feet, and he went through a somewhat
' D# V8 D" [/ {, ^* q: h7 `early puberty and had stopped growing by age 14.9 W/ O9 x! e* [! {3 g$ N: K! b
The father denied taking any other medication. The
9 _" y( x8 J: R% f& r3 @child’s mother was in good health. Her menarche
+ @1 C. A. `' g' Awas at 11 years of age, and her height was at 5 feet
" |8 j3 K% J. M- C5 inches. There was no other family history of pre-
- g! I# _. l& Z0 M1 pcocious sexual development in the first-degree rela-
0 ]+ a4 f+ s; O9 ttives. There were no siblings." ?% X) N$ s& r$ H; r6 p- U, |
Physical Examination. f) K0 G5 j' u. k) P( ?$ P
The physical examination revealed a very active,
* t# X0 y+ Z  `8 W2 L, V( lplayful, and healthy boy. The vital signs documented! u0 O9 y6 `' C
a blood pressure of 85/50 mm Hg, his length was
! y3 I: Y6 ]' r1 a/ ]; q5 ?3 Z90 cm (>97th percentile), and his weight was 14.4 kg
9 e0 t, l3 c7 [& [6 \. V4 e) p. a(also >97th percentile). The observed yearly growth+ j+ Z0 @! n" }5 w0 Y6 V3 Z' s) h$ x
velocity was 30 cm (12 inches). The examination of
% n" [2 A( P6 qthe neck revealed no thyroid enlargement.2 x3 a; J2 }( s( T- q/ E* n
The genitourinary examination was remarkable for$ k; k" o/ G* O/ i; k" }; X
enlargement of the penis, with a stretched length of
7 i0 j$ K6 G9 N0 k8 cm and a width of 2 cm. The glans penis was very well
, i* {2 G3 }$ g# I8 g" [/ m- d' Adeveloped. The pubic hair was Tanner II, mostly around- f7 F0 y2 ]2 ?$ u+ f+ b
5401 z0 b; [4 ^( o' \* b& e/ ~9 G; i; Z
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the base of the phallus and was dark and curled. The+ V1 K) `1 w) `* k
testicular volume was prepubertal at 2 mL each.. E( }- k# A$ K2 T$ p
The skin was moist and smooth and somewhat1 {: o8 [, x- {: s4 a9 R" W
oily. No axillary hair was noted. There were no" k; h# t) m2 D2 _- M
abnormal skin pigmentations or café-au-lait spots.
: U/ I! L* a  \/ _Neurologic evaluation showed deep tendon reflex 2+) U) J* a& d* W8 q  p! b
bilateral and symmetrical. There was no suggestion, a6 q7 y3 `5 h5 Z9 W$ l4 x! Z
of papilledema.3 J& q1 j9 s, N$ b
Laboratory Evaluation% U! l; W% J1 k$ ?( T2 n: y0 C3 [
The bone age was consistent with 28 months by. Y6 B$ H0 U4 l; T: i' z- @9 k
using the standard of Greulich and Pyle at a chrono-
2 S! b, a6 f5 v4 S: i7 W5 alogic age of 16 months (advanced).5 Chromosomal2 W5 ^8 r1 C2 V
karyotype was 46XY. The thyroid function test
; Q7 K: c/ a3 r) y7 F. b% H' M1 W% R$ xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-4 ~8 B9 f3 ]2 I: j. c5 e; i
lating hormone level was 1.3 µIU/mL (both normal).2 }# Y* Z  k, M9 \' e  ~
The concentrations of serum electrolytes, blood* H: I7 M  V$ o. R) A
urea nitrogen, creatinine, and calcium all were
# b9 N7 @3 ^" b1 I+ Wwithin normal range for his age. The concentration
, v7 A8 i: \: M2 h" |4 h3 q# cof serum 17-hydroxyprogesterone was 16 ng/dL
! u% n2 R( \. g3 r" k2 Z& y0 i3 O(normal, 3 to 90 ng/dL), androstenedione was 20
  V+ C" d2 g  a8 {0 u( Jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, Q' Q1 \  L" n% b# p" r
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
: c8 z* q" W* Ldesoxycorticosterone was 4.3 ng/dL (normal, 7 to" ]8 `: ?: z; j( u$ e
49ng/dL), 11-desoxycortisol (specific compound S)
% S" m, J/ M& X% l1 gwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 X4 s6 u0 c& d* J$ r$ u# V
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total; s0 @! Z/ Q& o6 x$ `
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),- e% n8 Q$ t. F: n  g- u
and β-human chorionic gonadotropin was less than
; w7 u) w& r, E* o: |5 mIU/mL (normal <5 mIU/mL). Serum follicular
& q% `) z$ `$ F& z9 G- Y: nstimulating hormone and leuteinizing hormone
' R6 G+ D/ @( b6 gconcentrations were less than 0.05 mIU/mL
2 k  p! l9 u  s* K(prepubertal).$ W2 Q6 y0 M' u5 Z. S2 o
The parents were notified about the laboratory
% M% q$ g2 U; B& iresults and were informed that all of the tests were% }2 ?* T) F8 m- }  Z$ K
normal except the testosterone level was high. The
1 \# @# U5 Q3 z3 J- m$ J% B  V( |4 c6 ?follow-up visit was arranged within a few weeks to5 i) ?) }1 q# Y4 [) I
obtain testicular and abdominal sonograms; how-: n/ z, q) @+ X; W; k
ever, the family did not return for 4 months.( I" @% R$ b& n% b( U
Physical examination at this time revealed that the- A3 F3 _0 w! ?
child had grown 2.5 cm in 4 months and had gained
% R$ K5 Y& @2 ?) z2 kg of weight. Physical examination remained; S- f% P+ _7 m4 R, g. l9 t
unchanged. Surprisingly, the pubic hair almost com-7 `8 \% B  S# ~% p
pletely disappeared except for a few vellous hairs at
" M- I/ v9 W: bthe base of the phallus. Testicular volume was still 2. Z, |4 r# d+ z
mL, and the size of the penis remained unchanged.  Q% t. t6 Y" Z4 `3 X' C
The mother also said that the boy was no longer hav-
$ s) a, m# O7 X9 C! r/ Qing frequent erections.
4 H$ F+ T. z0 l/ [9 K% A: |Both parents were again questioned about use of0 r+ m8 p: D/ n8 `
any ointment/creams that they may have applied to& o% d6 @* ^/ _& y( {; N
the child’s skin. This time the father admitted the
4 c# E- [# x" qTopical Testosterone Exposure / Bhowmick et al 541$ ^1 v  {8 _' e# E% M  H
use of testosterone gel twice daily that he was apply-) Q! l0 m4 h- p7 T6 ]
ing over his own shoulders, chest, and back area for7 J/ r  B3 i* e/ u8 K2 \8 Z
a year. The father also revealed he was embarrassed8 b# N' |& U4 e- q4 x
to disclose that he was using a testosterone gel pre-
2 j: ^% r1 p3 y* X: o2 xscribed by his family physician for decreased libido
8 i9 y& O% ?- N4 Gsecondary to depression.5 ]* n$ Z- q. i1 l$ D3 a
The child slept in the same bed with parents.
8 v0 j4 \! t5 D0 V2 t; MThe father would hug the baby and hold him on his/ p) R. h( o1 {1 h# p4 w" R. W
chest for a considerable period of time, causing sig-
- f  ~& j( L+ @" Ynificant bare skin contact between baby and father., a8 T+ X5 V3 U  v: E- h2 ^
The father also admitted that after the phone call,# B/ x1 E3 c9 p' f: j: v
when he learned the testosterone level in the baby
6 e/ V& K' ^3 X* i, Bwas high, he then read the product information" V% `# |% Q1 P. w9 A
packet and concluded that it was most likely the rea-
4 G8 c' J0 o" j3 `) a7 kson for the child’s virilization. At that time, they- D8 R! v( G& U; F0 H
decided to put the baby in a separate bed, and the
- S4 X  I$ j: M' g; J2 q' qfather was not hugging him with bare skin and had
4 N5 {4 q& L7 }$ [been using protective clothing. A repeat testosterone
$ c+ X2 V+ H. O2 v% p. V$ }9 s) Y/ etest was ordered, but the family did not go to the) H9 [1 l; O8 Z& z' ~. `7 P
laboratory to obtain the test.; D0 D2 u3 Q& G# H8 C5 D
Discussion
; x: Y  z6 w8 dPrecocious puberty in boys is defined as secondary( J& T# J1 ^( @& Y; c# a2 v
sexual development before 9 years of age.1,4
, W2 F: _  `, m: H" y% ?Precocious puberty is termed as central (true) when
! k( K0 v5 r  R4 e* xit is caused by the premature activation of hypo-
; y/ S' b3 s, Q  J8 S& @thalamic pituitary gonadal axis. CPP is more com-
* g9 C& G* ~5 j% u5 Pmon in girls than in boys.1,3 Most boys with CPP
; ]2 m' F) L* H+ ?: |- |- W" y+ l( mmay have a central nervous system lesion that is, W: N0 t  `  Q  g" u, d# M
responsible for the early activation of the hypothal-( d4 y3 \7 E& p& p! W5 Z4 ]2 b
amic pituitary gonadal axis.1-3 Thus, greater empha-8 G& D7 Z7 G6 R$ R2 C
sis has been given to neuroradiologic imaging in; N5 z+ E( q5 ]) {% P0 H& g5 T+ W! }
boys with precocious puberty. In addition to viril-
' a  l: x3 L3 Q/ _ization, the clinical hallmark of CPP is the symmet-( w' P  t* w5 W
rical testicular growth secondary to stimulation by8 `' [5 [3 V$ j) B: `- N
gonadotropins.1,37 b. G2 c  @+ r$ r9 ]. ~3 _( P
Gonadotropin-independent peripheral preco-: N& s2 }( T. A- C0 `5 u' R
cious puberty in boys also results from inappropriate2 G8 C& t# A, P$ R* o1 r
androgenic stimulation from either endogenous or
' a! N. E$ o/ w$ B; O. h' v; Wexogenous sources, nonpituitary gonadotropin stim-) |( `/ d. g1 {% `
ulation, and rare activating mutations.3 Virilizing
. S' G8 v- |0 H2 R2 Q3 g! R* Z& hcongenital adrenal hyperplasia producing excessive; ~# g7 \8 H* o& ^* x
adrenal androgens is a common cause of precocious8 |- Z/ E, k0 n0 L
puberty in boys.3,4. o# M) @% _2 i9 \; y
The most common form of congenital adrenal" p0 K$ Y: \4 V1 z: A6 }+ X
hyperplasia is the 21-hydroxylase enzyme deficiency.4 c3 q# A( E6 ]
The 11-β hydroxylase deficiency may also result in
7 \. S) _8 A) ~0 @' L  hexcessive adrenal androgen production, and rarely," i' @: R5 j- _1 E1 T( v% G# M
an adrenal tumor may also cause adrenal androgen) H& [& n0 j- v  ^9 }! D7 M
excess.1,3
, o" M" M( ]+ Z: U( |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from) j" K! W2 _: A: M) s7 k
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007+ {( S% N3 n3 m4 @, q% B
A unique entity of male-limited gonadotropin-( [5 _9 `+ [2 p" @2 [
independent precocious puberty, which is also known
* o& t/ M0 v" A8 i( Cas testotoxicosis, may cause precocious puberty at a5 e. X( ?. s' T) K, O  X& J/ `
very young age. The physical findings in these boys
$ Z! [+ i0 i8 x, ]5 L7 jwith this disorder are full pubertal development,& b8 |5 J( P! m3 W% T3 Q9 S
including bilateral testicular growth, similar to boys% D$ V+ _7 x, h
with CPP. The gonadotropin levels in this disorder) u2 J" }1 J" n/ R$ ~' B
are suppressed to prepubertal levels and do not show4 t# F0 p' h2 a, {4 b7 S5 o
pubertal response of gonadotropin after gonadotropin-
  U) e# B( w4 ~* c' Nreleasing hormone stimulation. This is a sex-linked
) p% \" K+ H  V8 Jautosomal dominant disorder that affects only
2 ?8 W" G/ G, Umales; therefore, other male members of the family
6 Q: R8 F2 n* [  Omay have similar precocious puberty.3
6 w( H* e& M/ bIn our patient, physical examination was incon-
6 \# y) e0 W; k6 [9 e1 N' Q* ysistent with true precocious puberty since his testi-0 b# L. @8 c; P" D$ K0 |  n
cles were prepubertal in size. However, testotoxicosis1 g3 N, J! v- z0 e- R# v. A
was in the differential diagnosis because his father" p+ X% `$ r' o- P& v* x
started puberty somewhat early, and occasionally,; B$ h7 [6 ]1 J* g$ H
testicular enlargement is not that evident in the
9 T3 _; F$ j: Y& gbeginning of this process.1 In the absence of a neg-
: `7 e; i. l  [$ n5 e9 zative initial history of androgen exposure, our
0 i9 F0 x4 k8 Mbiggest concern was virilizing adrenal hyperplasia,
, E0 ^6 f- j1 Y% X1 a6 @/ Eeither 21-hydroxylase deficiency or 11-β hydroxylase% ]. a# T  F+ w  ^$ ^" E
deficiency. Those diagnoses were excluded by find-
; L' d8 i  d4 |3 t: V: p' x/ oing the normal level of adrenal steroids.7 k* [  v" v( v9 m9 @( J/ A' j
The diagnosis of exogenous androgens was strongly. o' S9 @2 u* Z
suspected in a follow-up visit after 4 months because
. t9 n6 U4 U$ c: Tthe physical examination revealed the complete disap-; y) Z& x! \# n$ j  J. d
pearance of pubic hair, normal growth velocity, and3 U* v  e! w7 G/ t" Z  T
decreased erections. The father admitted using a testos-
$ N: X: U. Q3 t' O: mterone gel, which he concealed at first visit. He was
6 z  F: a$ k- `) Vusing it rather frequently, twice a day. The Physicians’
6 l) q9 c5 F2 K9 `Desk Reference, or package insert of this product, gel or
! u: \+ |3 }; d1 Ucream, cautions about dermal testosterone transfer to
+ z; G/ e, G! J9 i* Eunprotected females through direct skin exposure.
" X0 |5 U: ]* r; I1 w% _' a3 N  I  lSerum testosterone level was found to be 2 times the
6 @! l% q& \& q6 c3 w# {0 X7 Obaseline value in those females who were exposed to
. T  F; G4 ^8 yeven 15 minutes of direct skin contact with their male
* @( A+ g% T* q$ U1 xpartners.6 However, when a shirt covered the applica-
" E; M, T9 O# N3 k5 c; E# N% ition site, this testosterone transfer was prevented./ `8 a9 n. P5 U- p7 _& {- g; ]
Our patient’s testosterone level was 60 ng/mL,- L& F" i6 j5 ~% \9 l0 ]
which was clearly high. Some studies suggest that* V/ q: C8 D/ Q3 }  r
dermal conversion of testosterone to dihydrotestos-
- h" A# |2 w8 |8 eterone, which is a more potent metabolite, is more
$ E$ ]6 o4 _" @& F& z5 xactive in young children exposed to testosterone
, d3 T$ a; R$ n6 n" ?exogenously7; however, we did not measure a dihy-" `9 O8 s% Y% n, Y6 O' }* [, h3 s; f7 r
drotestosterone level in our patient. In addition to
& z) Z* M8 s0 O! U  R( S0 b) J7 {7 @" Xvirilization, exposure to exogenous testosterone in" R0 ^1 W9 o6 c" [
children results in an increase in growth velocity and  B' V! m. N& N5 i
advanced bone age, as seen in our patient.$ h1 J1 V8 c( C) }7 O% R
The long-term effect of androgen exposure during
9 S7 {( n6 p2 T" R( I6 Uearly childhood on pubertal development and final
) g, t. A; D; t" W& gadult height are not fully known and always remain
4 o1 A3 b7 {2 Z) ~; [9 J7 a! v" f# O% T7 S- ca concern. Children treated with short-term testos-
. N  i, k! Y/ o  Q( i# G6 _terone injection or topical androgen may exhibit some1 W  r, a4 }9 N/ a) }- I2 K
acceleration of the skeletal maturation; however, after
0 k) E, L2 J$ {4 lcessation of treatment, the rate of bone maturation
  G9 y; K2 f- o* f" \; b) F$ Odecelerates and gradually returns to normal.8,93 Z' x- Y) D8 P  B
There are conflicting reports and controversy* l- }3 B0 ^5 V
over the effect of early androgen exposure on adult
! \) `& w( j* B! z2 X4 c2 dpenile length.10,11 Some reports suggest subnormal
5 k6 }8 W: Y6 k0 x1 R4 X! Tadult penile length, apparently because of downreg-
- ~; x( m* P( lulation of androgen receptor number.10,12 However,
/ ]. m2 \5 a; WSutherland et al13 did not find a correlation between
! V. Y7 K0 o8 a1 Kchildhood testosterone exposure and reduced adult
- t+ N2 C/ `2 [( ^+ dpenile length in clinical studies.. C& Z2 d; o" j% e; A) c
Nonetheless, we do not believe our patient is2 e8 Y9 x0 ~( k! w% @2 _4 ~
going to experience any of the untoward effects from
. V: a; Q6 w, ]3 N( Ytestosterone exposure as mentioned earlier because( F  Y2 ?$ F; N
the exposure was not for a prolonged period of time.
4 ^" Z: K* i9 D/ h" D6 k6 s1 |Although the bone age was advanced at the time of
0 t8 E7 C" a) X" A4 sdiagnosis, the child had a normal growth velocity at
( {1 P7 e0 A: @$ z  ~! bthe follow-up visit. It is hoped that his final adult
+ |/ H9 E0 y" N9 ?6 L2 A% _- Dheight will not be affected.  Y, l; P, i% a; ~
Although rarely reported, the widespread avail-  k* p9 {6 L( m1 v! ]4 e
ability of androgen products in our society may
- J, a' M/ u: Y# N' o$ g$ ?indeed cause more virilization in male or female' J" D9 Q: X" F* T2 `& z
children than one would realize. Exposure to andro-( A3 [; e1 K" [. N. R
gen products must be considered and specific ques-
% l' k9 G0 d6 D3 |& itioning about the use of a testosterone product or
, M" A. b2 L% W3 N* W$ K# Ogel should be asked of the family members during6 x* |2 ~7 y4 z! {! w0 F7 m& U
the evaluation of any children who present with vir-0 K7 c4 v$ k$ m# L! k. i0 a
ilization or peripheral precocious puberty. The diag-
+ G) ^* K# A2 P: @  {% O, Cnosis can be established by just a few tests and by
. o4 l: X, x) w4 Z  q7 i9 ?appropriate history. The inability to obtain such a0 J' D6 Z: G! v: S( k% L- D4 `
history, or failure to ask the specific questions, may/ Y4 D/ m  _8 \/ {
result in extensive, unnecessary, and expensive6 ?4 p! c; l8 ?: P
investigation. The primary care physician should be8 t7 a9 @2 T3 O, F- }2 A4 y  x
aware of this fact, because most of these children' o" |$ r0 c9 ~" {- S) R% p
may initially present in their practice. The Physicians’/ V% w7 F. l2 k  ^+ T% c) c9 e
Desk Reference and package insert should also put a
& w# M; d7 ?4 \( owarning about the virilizing effect on a male or
: G9 k; j3 Q3 L, @* ^female child who might come in contact with some-
4 C" C7 }2 {/ A/ \- l6 D* M8 Cone using any of these products.8 e& h6 j# s0 X# H
References
  [& [) P0 R5 i# b% A, Y8 X( _: [1. Styne DM. The testes: disorder of sexual differentiation
, g- W9 w: f/ \and puberty in the male. In: Sperling MA, ed. Pediatric
7 w0 S. L: _4 Z; z) NEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
& Q' C* v7 q5 M& F2002: 565-628.
; D2 R8 L3 z- w; P  ]! z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 D4 Q" e6 o/ v& H6 U9 k0 Q# R
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
! y0 M/ w8 B7 \( C8 v, fBoy Induced by Indirect Topical
0 t( C5 `1 F8 oExposure to Testosterone
0 J' m0 h% E$ m7 B; _9 q1 VSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2/ K, E- f; g5 E) B  r
and Kenneth R. Rettig, MD1
; }4 P/ X- c1 ?" U3 [Clinical Pediatrics% Z- {& y1 h) S$ w1 G: R, v
Volume 46 Number 6
, j( ~/ r3 D. F8 S) x5 v6 c- jJuly 2007 540-543
0 Z3 O- P* X, ]0 t$ T© 2007 Sage Publications6 s( J5 @0 E' X8 @6 x6 o# |
10.1177/0009922806296651
, n7 a, W: ?7 D+ b: _' \( yhttp://clp.sagepub.com
) G' O# i+ {$ U9 {; nhosted at
* P; a8 c5 p  }http://online.sagepub.com! V) Y/ ?/ I! @) D/ |7 A
Precocious puberty in boys, central or peripheral,
' D+ E) i, B, n  |0 Pis a significant concern for physicians. Central9 \1 M5 g1 u1 G/ T9 I
precocious puberty (CPP), which is mediated
( l( H4 r- _' I  r/ s7 a4 Z4 Q6 Hthrough the hypothalamic pituitary gonadal axis, has& J3 j2 e% y. I/ l+ [; }. w( }
a higher incidence of organic central nervous system
! e0 I, e/ n& j& y5 v/ rlesions in boys.1,2 Virilization in boys, as manifested
) Z2 u2 y; G* r- J$ p  K' f+ ?by enlargement of the penis, development of pubic
. t9 M5 c; |5 r% shair, and facial acne without enlargement of testi-  H) r+ J! [/ ?- l3 \* |* b
cles, suggests peripheral or pseudopuberty.1-3 We
/ {+ ?5 b. `# W4 t" |# O7 mreport a 16-month-old boy who presented with the
+ H+ ^: Z  S# menlargement of the phallus and pubic hair develop-
0 S" z/ D3 V' o# e3 O+ x: yment without testicular enlargement, which was due, ^3 O% y1 ~) U6 l
to the unintentional exposure to androgen gel used by
6 Y9 ?4 p! g) S' L; |& `$ C- }the father. The family initially concealed this infor-4 w7 V+ u7 C# m
mation, resulting in an extensive work-up for this
+ ^  z2 [5 v, L$ r* l1 ychild. Given the widespread and easy availability of
' |9 I" C2 M  V+ T9 F, Ttestosterone gel and cream, we believe this is proba-5 B3 m4 \4 {  g8 X
bly more common than the rare case report in the
4 E' y" B) e- j* Cliterature.40 U6 a( D* V- Z' H$ m8 o
Patient Report
' E/ F2 f: d" s: pA 16-month-old white child was referred to the
/ x" _$ [" A( {9 {& vendocrine clinic by his pediatrician with the concern& K5 [7 M1 e+ |9 z8 _
of early sexual development. His mother noticed
" |0 @" Q8 A; B# Z& P+ I  dlight colored pubic hair development when he was
. S0 p- P( i2 I" WFrom the 1Division of Pediatric Endocrinology, 2University of; u' z& d& y8 H: H
South Alabama Medical Center, Mobile, Alabama.8 n* U' x& t$ t) @) p6 K% S- G0 X9 z
Address correspondence to: Samar K. Bhowmick, MD, FACE,
( `  Y' h  W% r( X& F- HProfessor of Pediatrics, University of South Alabama, College of
4 g( t2 \% H9 w8 s7 i  m, W  BMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 j1 P7 Q9 u9 z: I
e-mail: [email protected].: B9 Q& @5 a# ]- Q, H
about 6 to 7 months old, which progressively became
8 }8 _2 b" F; u1 I. P& Y% }6 G$ T& P, [" tdarker. She was also concerned about the enlarge-
3 k+ D1 l6 m  \0 ament of his penis and frequent erections. The child
; f5 n/ v; @" ]+ ?# _was the product of a full-term normal delivery, with
3 U/ S/ Q2 ^% |! z# ~+ ha birth weight of 7 lb 14 oz, and birth length of
5 n6 E0 b" e6 H% ^) h5 q. j20 inches. He was breast-fed throughout the first year- `* K$ |+ W) V: W1 [- }" I3 L
of life and was still receiving breast milk along with: }- Q8 j; g. _
solid food. He had no hospitalizations or surgery,$ T4 _* R$ @4 o9 W
and his psychosocial and psychomotor development
+ G8 C6 ?- z8 y' hwas age appropriate.% c7 `9 b3 M$ M
The family history was remarkable for the father,
. ?4 i0 V5 ?- G3 Uwho was diagnosed with hypothyroidism at age 16," \& U& g$ z' w5 c) J3 W2 y
which was treated with thyroxine. The father’s+ j- w3 m; Y8 y- m: a9 f9 ?. j
height was 6 feet, and he went through a somewhat" o9 Z  e+ e1 z; J5 z- i3 h
early puberty and had stopped growing by age 14.+ O9 }6 K/ w' j; G# K# V
The father denied taking any other medication. The
4 _3 Y& J5 n. W! B( [child’s mother was in good health. Her menarche2 r, |. e# {3 O) u$ ?
was at 11 years of age, and her height was at 5 feet: l* t  t7 J  A1 b1 J2 p; v
5 inches. There was no other family history of pre-7 w+ v3 m+ f7 T9 }6 {0 m
cocious sexual development in the first-degree rela-
; T5 R: X! W3 w. u( E5 r9 z/ Ttives. There were no siblings.
+ C  y% B1 U! a; v/ F4 @Physical Examination
! r6 D: z! b4 UThe physical examination revealed a very active,
- h0 l" Z7 w5 [  U, Jplayful, and healthy boy. The vital signs documented& V7 ?" c0 c8 t- d
a blood pressure of 85/50 mm Hg, his length was
1 [; F; ~* {9 ]* f; t90 cm (>97th percentile), and his weight was 14.4 kg- j3 E; C9 T$ `% V2 U
(also >97th percentile). The observed yearly growth
, L0 H, Z) K& y- k, ]5 G+ o% zvelocity was 30 cm (12 inches). The examination of. k: b6 @, {* Q, w. T* Q$ F
the neck revealed no thyroid enlargement.: O! n1 M. h8 f- h' ?' i0 `
The genitourinary examination was remarkable for7 b) z6 K( S0 d4 d2 i; E6 x8 J
enlargement of the penis, with a stretched length of. R6 Y) H& {) X% K0 F  d6 `4 f
8 cm and a width of 2 cm. The glans penis was very well
9 j$ S+ |8 v+ B  W( \3 xdeveloped. The pubic hair was Tanner II, mostly around
$ F5 a7 D4 l9 |( v, h4 H$ G5407 g* @9 J6 P0 B) t0 E' I
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the base of the phallus and was dark and curled. The
( |4 f1 O* ]: \1 P' f* L! {testicular volume was prepubertal at 2 mL each.8 h( j* u: w5 @0 k) q& J/ y
The skin was moist and smooth and somewhat
- F4 H3 R( w* @( V/ p4 }6 z' y0 Aoily. No axillary hair was noted. There were no: H4 |% w( f5 @  P7 q
abnormal skin pigmentations or café-au-lait spots.4 j: A& \' i! K/ F4 R% B
Neurologic evaluation showed deep tendon reflex 2+! i) J+ t8 M/ S2 m( D/ y( E& s: T
bilateral and symmetrical. There was no suggestion
0 y1 K! {, |- H( l* {8 I$ ~; q7 }of papilledema.1 v; k# b- C0 k( J8 q8 Z
Laboratory Evaluation5 `" D! w8 [' t$ |# \0 m
The bone age was consistent with 28 months by: d) b: ?' n+ ]1 W; D, ~7 e! l# O% |
using the standard of Greulich and Pyle at a chrono-- Y. B- q" [, U" J# m5 R
logic age of 16 months (advanced).5 Chromosomal6 V9 G) A& l& C+ L
karyotype was 46XY. The thyroid function test
! s' w" c6 T2 z8 [) C0 w  Fshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
1 V" `( }# m8 N& O) B: xlating hormone level was 1.3 µIU/mL (both normal).; c4 `7 x: p5 x. J0 {2 J; Y
The concentrations of serum electrolytes, blood
0 A8 e6 h1 u# i7 R  w# [0 surea nitrogen, creatinine, and calcium all were3 n1 E! ]1 A8 i# F+ N9 C
within normal range for his age. The concentration
3 E* l+ |. ?( a' f/ R7 gof serum 17-hydroxyprogesterone was 16 ng/dL- r( {5 U( ]( T$ h  N7 d9 n! y
(normal, 3 to 90 ng/dL), androstenedione was 20: D) s6 B* t* ^2 D5 J# d6 a+ n, H
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-0 {4 Z2 a' U" j7 i) X7 M7 p
terone was 38 ng/dL (normal, 50 to 760 ng/dL),; W! c4 ~  B0 d2 `3 e+ I
desoxycorticosterone was 4.3 ng/dL (normal, 7 to1 Q- ?0 V7 [3 [3 D% c
49ng/dL), 11-desoxycortisol (specific compound S)
# m. M+ P' J! d* G5 R2 J  U% Swas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 r% t& d/ F- ^5 S4 D& Ftisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 J( }2 @! Z5 p0 y4 h4 Stestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! j4 A! c) f" _' R& Pand β-human chorionic gonadotropin was less than
6 Q7 Q0 i9 g% ^5 mIU/mL (normal <5 mIU/mL). Serum follicular
& O8 d: E- Z2 Z( C; b  ]stimulating hormone and leuteinizing hormone
8 V) u# i- U2 m" F7 J) ^5 |concentrations were less than 0.05 mIU/mL
$ I" h9 `( H/ V: u  n(prepubertal).
3 x( m4 B4 u$ K) d) W) C1 SThe parents were notified about the laboratory
+ H( W! f4 D- W+ A7 fresults and were informed that all of the tests were
8 ^- e; x# k& W' x1 rnormal except the testosterone level was high. The  U+ U0 P1 {1 b. c# R" w
follow-up visit was arranged within a few weeks to+ R4 ]0 v# B) P7 c" u
obtain testicular and abdominal sonograms; how-) z- ]4 x% `* z9 z6 w
ever, the family did not return for 4 months.
+ z& s  L3 p4 _3 N1 p) CPhysical examination at this time revealed that the: J3 t, n2 z: U9 R6 N
child had grown 2.5 cm in 4 months and had gained; }9 g& \" N0 i: p
2 kg of weight. Physical examination remained
/ S% G9 d; d2 r/ Z6 t; Vunchanged. Surprisingly, the pubic hair almost com-
- U( K4 ]; O* ]' Qpletely disappeared except for a few vellous hairs at
5 R2 L. ]$ f+ fthe base of the phallus. Testicular volume was still 27 A2 B5 ^. _& f
mL, and the size of the penis remained unchanged.
, e; w& P" R! }2 U$ A. Y3 D3 @) ?2 {The mother also said that the boy was no longer hav-
5 f( A3 h+ ~- P# ]- N0 V# Fing frequent erections.3 w  L3 }( W+ L0 Q
Both parents were again questioned about use of" h1 j% b: _3 j) f8 m- e" c4 H% w
any ointment/creams that they may have applied to& h6 D, Z  D) B# ^! L/ n5 A# o
the child’s skin. This time the father admitted the6 @( ?$ z1 L# U0 y3 ~! U5 v' |
Topical Testosterone Exposure / Bhowmick et al 541  B1 W) ]! N- }7 A0 R
use of testosterone gel twice daily that he was apply-" b  h  Q$ k5 N) Q9 v$ q! Z
ing over his own shoulders, chest, and back area for
' ]: V6 {% @! R: H+ n+ Ma year. The father also revealed he was embarrassed
' h; b, W" Z' Rto disclose that he was using a testosterone gel pre-
1 r$ v4 A( m! w( W0 ?scribed by his family physician for decreased libido
0 A& W! ?: U- C& N, Ysecondary to depression.5 ]4 y0 W4 c' _; J0 O
The child slept in the same bed with parents.. }8 _- S* r: K9 t' |$ Q, a
The father would hug the baby and hold him on his9 C% x' X0 ^. l# j4 u# N
chest for a considerable period of time, causing sig-
# |- n" ]- y$ s; X; C& I: z" ynificant bare skin contact between baby and father.
" v$ W/ j  k( k# c4 p1 M$ PThe father also admitted that after the phone call,3 [% m0 |* l  W/ V
when he learned the testosterone level in the baby. [4 ~4 {: F# U8 i% F: W
was high, he then read the product information
* ~1 t3 B: q0 Y4 ypacket and concluded that it was most likely the rea-: U- B0 k. D) y5 R7 C
son for the child’s virilization. At that time, they, m, P2 O( O6 Y7 l
decided to put the baby in a separate bed, and the0 G9 M$ P0 v+ }
father was not hugging him with bare skin and had. `8 o4 e( h& {. F6 I5 n1 i" |. o+ y) d
been using protective clothing. A repeat testosterone0 l1 p  C" `0 h2 u5 x# i
test was ordered, but the family did not go to the, x  ]' @! [# E2 A: Y& V9 m2 x6 b
laboratory to obtain the test.
! W! E  E; g# u1 k% E1 \& ?Discussion
) b/ f, m" Z$ F. uPrecocious puberty in boys is defined as secondary
1 V4 N% [9 l: n" N4 s3 ^sexual development before 9 years of age.1,4+ p' L% r7 s' D1 k$ [: N# ?2 ]8 j
Precocious puberty is termed as central (true) when
% u3 W" v9 O9 a1 B6 ?4 q4 fit is caused by the premature activation of hypo-. D0 s5 {; o" h8 C
thalamic pituitary gonadal axis. CPP is more com-
5 Y8 O  d# t% Y8 w2 Bmon in girls than in boys.1,3 Most boys with CPP) i7 u' H# I( w4 Y4 t( Q. ?3 F
may have a central nervous system lesion that is" F7 s. M9 z0 {0 ]( @9 c! C
responsible for the early activation of the hypothal-; _8 ^+ S% K. t7 \' m3 U& \, L
amic pituitary gonadal axis.1-3 Thus, greater empha-
' _7 k, F, K& D2 [1 Fsis has been given to neuroradiologic imaging in
4 H$ J8 j* _6 o; Y+ \boys with precocious puberty. In addition to viril-
) H5 h' e  C' g- w& V8 Qization, the clinical hallmark of CPP is the symmet-5 t6 w) k( p# A
rical testicular growth secondary to stimulation by( B" C5 N" M  n* G, N
gonadotropins.1,37 _4 w$ s$ B& D! ~- E5 Q
Gonadotropin-independent peripheral preco-8 x# B7 b$ o- {( b% X
cious puberty in boys also results from inappropriate' S2 z/ ^* n6 Z
androgenic stimulation from either endogenous or
4 Y- s  A$ X, i' mexogenous sources, nonpituitary gonadotropin stim-) {4 S/ m* H$ y/ k5 e0 k: S
ulation, and rare activating mutations.3 Virilizing1 o  @/ N" U' T' p* p
congenital adrenal hyperplasia producing excessive
0 b, o/ y, X3 {adrenal androgens is a common cause of precocious
% O: p! Q$ w( g8 ypuberty in boys.3,4. h  I( A6 p1 |+ c+ X* S
The most common form of congenital adrenal# X6 x% o+ r/ S/ ]& R1 H
hyperplasia is the 21-hydroxylase enzyme deficiency., Y1 E; m7 l: y! d, Q1 B1 v
The 11-β hydroxylase deficiency may also result in0 Z& @5 l2 J9 L5 z
excessive adrenal androgen production, and rarely,
2 c& l, g% \1 L' h" y# \an adrenal tumor may also cause adrenal androgen
% D- l- h8 e( n& n$ A/ Cexcess.1,3+ z2 P; N2 V3 ?0 H: y+ v7 ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: d( q9 Q, u9 h- E; F$ W: f
542 Clinical Pediatrics / Vol. 46, No. 6, July 20070 Y: Y1 Z9 k, I
A unique entity of male-limited gonadotropin-$ D0 v/ m$ W" }1 a, Q0 R
independent precocious puberty, which is also known
, [% @% O. h$ E: m$ zas testotoxicosis, may cause precocious puberty at a
- z3 e7 z# W) T$ Z5 {very young age. The physical findings in these boys' T8 A1 i$ F% z: x
with this disorder are full pubertal development,  F) j' V5 A' K* ]& ?
including bilateral testicular growth, similar to boys% ]' f6 B8 a  s( X4 m1 n( m- l
with CPP. The gonadotropin levels in this disorder9 j' {# @$ U- Z& O
are suppressed to prepubertal levels and do not show
( [% j- O* [2 H2 O4 ?5 U  x* Dpubertal response of gonadotropin after gonadotropin-  B, u! k/ ?4 [
releasing hormone stimulation. This is a sex-linked; W; m7 r6 `0 E  D
autosomal dominant disorder that affects only
9 {( P. R$ x' i% C* pmales; therefore, other male members of the family
* X" [2 t1 y+ ]- tmay have similar precocious puberty.3  a' O( `" a1 |- {" _) K2 Q
In our patient, physical examination was incon-6 b: z, G! X4 `& u. r4 Y
sistent with true precocious puberty since his testi-  J7 P8 b8 c% f1 c+ }0 [0 r% @- x4 J
cles were prepubertal in size. However, testotoxicosis9 {/ l  o$ R7 z$ I2 r+ {: L% S7 s
was in the differential diagnosis because his father
+ Z1 c& ?# A9 M0 jstarted puberty somewhat early, and occasionally,2 F( {  ~- D7 ?8 {$ ?& B
testicular enlargement is not that evident in the
3 o: c5 b+ T. S' A: [8 H' Z* Ybeginning of this process.1 In the absence of a neg-; D3 R. T- R! f7 _1 q5 i! s
ative initial history of androgen exposure, our* |! S0 u+ l& c8 D& b7 o: T
biggest concern was virilizing adrenal hyperplasia,
% |( B, E( |. d* E( N7 _2 ~either 21-hydroxylase deficiency or 11-β hydroxylase5 C$ r! v' }" ?1 R2 ^6 x( U
deficiency. Those diagnoses were excluded by find-' N8 K" O( n; T9 k4 F- W6 M
ing the normal level of adrenal steroids.! W& K+ M( d1 A7 c  ]3 I
The diagnosis of exogenous androgens was strongly0 Q9 v& a- N: R( Y( e7 j) F% m
suspected in a follow-up visit after 4 months because
/ |* d! B& q2 M) P! B. |0 a! lthe physical examination revealed the complete disap-
" ?0 y1 l, n7 npearance of pubic hair, normal growth velocity, and
: B9 O1 f# f" _* w0 ]# hdecreased erections. The father admitted using a testos-
) z7 m! [% k) A5 z0 X' Hterone gel, which he concealed at first visit. He was
/ n+ N; Q6 i+ U! e: v5 \( Busing it rather frequently, twice a day. The Physicians’! p- X1 |+ u% C3 L8 t
Desk Reference, or package insert of this product, gel or9 c+ O4 T6 E" R; H  k
cream, cautions about dermal testosterone transfer to
4 u- m- W5 g1 c/ E- C: Q2 [unprotected females through direct skin exposure.+ b& _2 Y- R- X7 I# V4 i) x9 L, r
Serum testosterone level was found to be 2 times the7 x* @8 ]; a" u- v! H* X% M6 z
baseline value in those females who were exposed to, Z; d, ]7 `7 F
even 15 minutes of direct skin contact with their male
! l8 i7 o6 d$ E2 I" C' L/ Tpartners.6 However, when a shirt covered the applica-; i  o* X' b9 N/ j2 M: H: _2 S) E
tion site, this testosterone transfer was prevented.7 O7 r! ?- m) E+ w
Our patient’s testosterone level was 60 ng/mL,
6 l7 J! T$ A1 |which was clearly high. Some studies suggest that
2 J+ A- P- y8 C6 Zdermal conversion of testosterone to dihydrotestos-' f$ T* {; z) f$ x
terone, which is a more potent metabolite, is more0 H, G' T# t' q2 E' m2 a
active in young children exposed to testosterone
/ [( F, K, x: z% p+ lexogenously7; however, we did not measure a dihy-
  I, L& u: y7 T- Ndrotestosterone level in our patient. In addition to
5 t1 t8 ?) S" i* ivirilization, exposure to exogenous testosterone in; K$ `# t% b1 c
children results in an increase in growth velocity and8 U: i, n- _4 s2 E) L
advanced bone age, as seen in our patient.
( {. p5 J% q7 b& J. C/ O4 ]The long-term effect of androgen exposure during% v' O7 p, K  n' y2 q
early childhood on pubertal development and final* R1 d1 O# b5 a; |9 Q% H) n2 ?
adult height are not fully known and always remain# B7 L* L3 i! W4 r5 w/ g& D& P
a concern. Children treated with short-term testos-& K) t, F$ K1 }% R
terone injection or topical androgen may exhibit some
/ p- u1 _* r' j" B# z7 qacceleration of the skeletal maturation; however, after1 C0 r3 l7 z+ e9 i. l
cessation of treatment, the rate of bone maturation
/ s* x% ]7 l$ U4 L, S# qdecelerates and gradually returns to normal.8,91 D( L' a+ Q3 w% n9 L, }2 k. ^% O
There are conflicting reports and controversy1 c9 U# v; r/ b# r) w9 K3 O' L
over the effect of early androgen exposure on adult
5 U+ R/ X" r' Qpenile length.10,11 Some reports suggest subnormal* r: p$ V4 N; r. b/ I
adult penile length, apparently because of downreg-
1 K5 L& G$ v/ x7 C5 W1 t# Yulation of androgen receptor number.10,12 However,
* n* }9 e6 E: `* X- g, WSutherland et al13 did not find a correlation between
, Y9 \& R3 w" p" _# \) ]4 D+ r- ochildhood testosterone exposure and reduced adult1 B" h! E+ }, N. S8 A. m
penile length in clinical studies.
' O0 T+ ~' r8 B$ G# w' DNonetheless, we do not believe our patient is" T' b; s; V2 \0 p1 q8 o' n) g
going to experience any of the untoward effects from6 o% H$ Q( ^( [& Y4 {8 [
testosterone exposure as mentioned earlier because) ]0 I! t+ N# d0 |6 |2 t3 _# e
the exposure was not for a prolonged period of time.& {5 ?8 V8 M6 o; u+ `! v
Although the bone age was advanced at the time of* t; R8 f0 ], s" U, w$ y
diagnosis, the child had a normal growth velocity at% c$ @+ F9 i5 E9 U* }/ N
the follow-up visit. It is hoped that his final adult
2 U& d$ o1 j, r2 ?9 pheight will not be affected.  n1 y* U% Y$ v" Y
Although rarely reported, the widespread avail-
% A+ L, P/ Z" |0 Q' Xability of androgen products in our society may2 c3 d" x% K9 R
indeed cause more virilization in male or female
$ s7 q3 ?. C; Q2 _" Q$ J. ychildren than one would realize. Exposure to andro-
. L! r7 h! l  E9 \7 mgen products must be considered and specific ques-
3 ~' Z  ~& v5 [7 xtioning about the use of a testosterone product or0 M$ ^/ {, R& ]' H+ `
gel should be asked of the family members during! \7 Q3 N9 S0 v9 X
the evaluation of any children who present with vir-, H/ w. {9 Q' u+ y. j' I
ilization or peripheral precocious puberty. The diag-" c1 G/ H- Y  q( e+ f0 l4 [4 l/ |, X
nosis can be established by just a few tests and by
4 j' c) r8 k+ l9 Gappropriate history. The inability to obtain such a
7 p4 x' Y0 ~$ e- @. ~6 X8 nhistory, or failure to ask the specific questions, may! A) n% m5 \( s- s
result in extensive, unnecessary, and expensive9 A8 D7 e. e+ S6 g. ]
investigation. The primary care physician should be/ v0 N: }# N6 h0 S6 e& T
aware of this fact, because most of these children2 e' a# P; c$ y$ Z; X. P% `5 f& K
may initially present in their practice. The Physicians’# z+ z+ E- b4 c; O9 [2 \
Desk Reference and package insert should also put a, i/ c! {* A0 F9 M7 E
warning about the virilizing effect on a male or0 p8 h$ i6 e% m( B( y, p4 ^: X- v
female child who might come in contact with some-
0 ~. a6 Y' B& ?* zone using any of these products.5 n+ Y9 r& m/ ^9 e
References% s! s% U9 z  a
1. Styne DM. The testes: disorder of sexual differentiation
, Y/ g" m$ q# n# T) _and puberty in the male. In: Sperling MA, ed. Pediatric% ^' |7 J9 @0 z: ^& c8 o6 z
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;0 S" u% p+ }( E/ j6 H/ u
2002: 565-628.  I5 z* d/ A. z$ }1 s' I( O0 h
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 c2 e! ?7 m" p; Z( @; |$ v5 R% a5 E
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
! p8 x0 g  ?$ R$ i' g
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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