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Sexual Precocity in a 16-Month-Old- n+ e# C- q# U1 E3 M5 F, i+ o9 H. r
Boy Induced by Indirect Topical" p5 d# U) A  b% Y# l
Exposure to Testosterone
8 j' x/ P6 G+ u: c$ hSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 g8 H) y+ _) g7 Dand Kenneth R. Rettig, MD1
$ I; Y* J) w# G7 cClinical Pediatrics8 V" w% m2 i$ U$ y) K1 L5 B, O2 O
Volume 46 Number 6  t& E! {2 r# P+ l
July 2007 540-5431 S0 b9 r& d7 i" J8 m9 x
© 2007 Sage Publications
* F. z  m  G: W& W: U0 W10.1177/0009922806296651
, o. \  F( W5 Q/ }* c9 U; ehttp://clp.sagepub.com% C' F5 M. C) h- F% m
hosted at+ a8 s8 h' F8 \) @3 f4 ?' y6 N
http://online.sagepub.com( @( N. ^; ]( Y: h" ?! U% C
Precocious puberty in boys, central or peripheral,4 C) L0 x5 U; b7 P  z- |2 I5 g
is a significant concern for physicians. Central* a7 s6 b3 O. @6 B) s
precocious puberty (CPP), which is mediated0 Z1 w( ?  m5 e3 C$ ]$ M
through the hypothalamic pituitary gonadal axis, has
& b# o1 J- G8 X1 E3 L9 G5 Va higher incidence of organic central nervous system
- u5 C9 Z: \+ `) Z) c+ Mlesions in boys.1,2 Virilization in boys, as manifested1 L2 f( C; u3 r% q2 K
by enlargement of the penis, development of pubic
' y9 I$ g0 `6 j6 ^9 y9 Fhair, and facial acne without enlargement of testi-
8 {1 v4 R3 _( C* Qcles, suggests peripheral or pseudopuberty.1-3 We7 T8 Z. u. g) K
report a 16-month-old boy who presented with the
5 j, G" f( \( c8 X, m6 _+ Renlargement of the phallus and pubic hair develop-
9 `9 C2 D/ `' z7 Ament without testicular enlargement, which was due
6 h2 t$ n7 j: }' {to the unintentional exposure to androgen gel used by* S" Z1 r3 D* l2 T; k. B
the father. The family initially concealed this infor-/ w$ [4 k; o7 [' K3 _4 f
mation, resulting in an extensive work-up for this
  x& @8 z# h8 N4 Cchild. Given the widespread and easy availability of
! M$ }( Z0 M# w9 ytestosterone gel and cream, we believe this is proba-
. L3 v3 w, y& h4 ~bly more common than the rare case report in the
3 b5 P7 {8 R9 [, S+ _* P" eliterature.4
& w$ Q! J4 I! ~+ j8 TPatient Report& w+ y) \+ G2 w) K8 N: Q' Z/ h, A
A 16-month-old white child was referred to the
1 [- s( u1 g$ T8 yendocrine clinic by his pediatrician with the concern# `# m0 @. `: a6 c7 X" @: b
of early sexual development. His mother noticed+ N* g! z, j% g2 `4 \1 ?7 k: u3 t
light colored pubic hair development when he was! E3 w+ ^) ^, g$ i) w
From the 1Division of Pediatric Endocrinology, 2University of
- n1 J  T/ Q& r7 }South Alabama Medical Center, Mobile, Alabama.
4 |2 w3 I( I7 Z* QAddress correspondence to: Samar K. Bhowmick, MD, FACE,9 W$ j7 J# i5 F7 F) C* D
Professor of Pediatrics, University of South Alabama, College of4 V0 J2 K( u6 q4 N! P7 D( k
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;& e, W+ A5 f1 ~; q3 m* w4 S
e-mail: [email protected].
& ?1 r2 Z% E& o, u9 z6 u7 zabout 6 to 7 months old, which progressively became
. s! g5 z' y0 Z* ^5 edarker. She was also concerned about the enlarge-% N" V! W$ m/ w8 n
ment of his penis and frequent erections. The child
, N7 ~0 G/ N& V1 q. D% Vwas the product of a full-term normal delivery, with# [$ z3 e! l) a3 A
a birth weight of 7 lb 14 oz, and birth length of
/ x" @; L9 {8 d+ A7 ]20 inches. He was breast-fed throughout the first year
# `/ r; t/ S/ s. K* sof life and was still receiving breast milk along with
( B- S9 f  T* w2 l6 v' ^1 ]4 Isolid food. He had no hospitalizations or surgery,
" S* _& ?% i- n, r1 R* l9 \and his psychosocial and psychomotor development
4 y  D) u$ m1 M' h9 g" b: v  @was age appropriate.: j) K" j# X5 L& z. L
The family history was remarkable for the father,6 R! f$ ^6 ~/ n# Q
who was diagnosed with hypothyroidism at age 16,  Q6 S6 _3 t. n4 {
which was treated with thyroxine. The father’s
0 m$ I/ J. h( P) V) A0 kheight was 6 feet, and he went through a somewhat
3 ^+ m. r% y* V: V8 _3 i& [early puberty and had stopped growing by age 14., E# V, t; e' a  ^. k( A% ]
The father denied taking any other medication. The
( ^! L9 B. o" W; J1 schild’s mother was in good health. Her menarche5 @7 u7 D+ e# C# b! ^' a% F
was at 11 years of age, and her height was at 5 feet
# Y& I4 |, z, M5 inches. There was no other family history of pre-7 Z: b  _6 V3 Q, f* D
cocious sexual development in the first-degree rela-
- d$ q' j& h: u" _9 \' q9 L* ptives. There were no siblings.( c" A% I& O- C' j* _- M
Physical Examination: f0 N8 x+ u" s4 x
The physical examination revealed a very active,
9 F2 J4 {$ k9 }) m9 p8 bplayful, and healthy boy. The vital signs documented
; u" z6 S9 h/ T5 X3 t9 O0 @! Ia blood pressure of 85/50 mm Hg, his length was! C: y+ k$ u0 S& |4 w
90 cm (>97th percentile), and his weight was 14.4 kg% b% d9 R, _5 g6 E0 P: Q
(also >97th percentile). The observed yearly growth
$ O/ X" Z# x8 [6 g% xvelocity was 30 cm (12 inches). The examination of. n* [# h+ l& D5 X3 Q" k3 _
the neck revealed no thyroid enlargement.
  w1 S8 Y# Z2 T/ O, I/ V8 [! V1 ?The genitourinary examination was remarkable for; R$ ]( k+ J9 _* W
enlargement of the penis, with a stretched length of( o$ k7 S) Q2 Y7 t- v/ b& t
8 cm and a width of 2 cm. The glans penis was very well
% a, j+ K8 |/ p" ]developed. The pubic hair was Tanner II, mostly around5 x7 g2 |: h9 d1 N* w7 e7 T! U
5407 o; L9 t1 x( l: q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' i% B2 O; R. K# w  t
the base of the phallus and was dark and curled. The6 ], E, m+ j! S* f$ D1 z, D
testicular volume was prepubertal at 2 mL each.0 B/ _# W* a# f" u: E1 G- n
The skin was moist and smooth and somewhat! @& I; x* y, f5 D' X& x8 q
oily. No axillary hair was noted. There were no1 E) n& a" H- x/ L5 ^
abnormal skin pigmentations or café-au-lait spots.
5 N  d8 c( a9 D) e9 @Neurologic evaluation showed deep tendon reflex 2+! m( T" L/ l9 B# O7 }9 i1 q4 i6 S% L8 h
bilateral and symmetrical. There was no suggestion
- }) q% r* L2 V) d5 Eof papilledema.. W* O3 x: A1 \" q
Laboratory Evaluation$ x# O% T. u; |/ O! w% J: ~4 r/ h
The bone age was consistent with 28 months by! u! n3 X% y+ k# I% Z) ~
using the standard of Greulich and Pyle at a chrono-
0 u8 w8 o# ^: [( h  Q4 llogic age of 16 months (advanced).5 Chromosomal; @* G4 N: v1 ?, E' Y6 Q
karyotype was 46XY. The thyroid function test$ Z; |- b8 k  }' r( |
showed a free T4 of 1.69 ng/dL, and thyroid stimu-) W/ J% K4 c; ~1 m* R
lating hormone level was 1.3 µIU/mL (both normal).
! @! V- |9 m# I5 O" _$ f" P4 G0 _The concentrations of serum electrolytes, blood
* N: L, f9 L2 J: c  N" Surea nitrogen, creatinine, and calcium all were" r( r7 Q$ a, ~$ S
within normal range for his age. The concentration
  H/ z5 R% C4 m4 d2 Cof serum 17-hydroxyprogesterone was 16 ng/dL
" |6 `- `; P/ f6 D+ C3 ^; a; F(normal, 3 to 90 ng/dL), androstenedione was 20( r+ O, I+ s( m9 J" ^( y2 B; `+ k
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 Z% h1 G7 i# W  B$ k$ p; f
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
+ O/ _5 j2 p9 J8 O2 `( T1 `/ g6 q6 ~desoxycorticosterone was 4.3 ng/dL (normal, 7 to  T7 V1 l7 g' v# K' K6 d
49ng/dL), 11-desoxycortisol (specific compound S)
. w  D0 w. f) B" y9 c$ [/ [was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, N9 V% `& X9 F* i6 Gtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 [; J5 \. }- j9 Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
) d; }# [- R% X/ band β-human chorionic gonadotropin was less than, C- k9 \9 i; n5 c# j' ~
5 mIU/mL (normal <5 mIU/mL). Serum follicular' G* u$ y$ A% d! D1 t+ P0 _
stimulating hormone and leuteinizing hormone9 l% s' @- p% F0 y
concentrations were less than 0.05 mIU/mL1 x7 o3 b. W& j6 F4 j/ |( x
(prepubertal).9 N6 M: V& ]3 o4 H
The parents were notified about the laboratory' O- M3 `% F7 p
results and were informed that all of the tests were! k  b3 F) ^+ R# \8 Y
normal except the testosterone level was high. The
; R0 Y* B; d: x+ }follow-up visit was arranged within a few weeks to- u# P0 q* _6 I3 B
obtain testicular and abdominal sonograms; how-+ l7 O3 g3 Y) W$ Q0 f
ever, the family did not return for 4 months.
5 q- N  I7 k4 S. ?Physical examination at this time revealed that the
* g( h$ i& `+ s* [: n# D# O1 [% Mchild had grown 2.5 cm in 4 months and had gained/ {  S$ G# b& g0 M# d- f4 l& M
2 kg of weight. Physical examination remained8 e' s. C1 L+ v3 q' X
unchanged. Surprisingly, the pubic hair almost com-/ e# }2 E" C3 b3 r
pletely disappeared except for a few vellous hairs at
# `; h; b% A% ethe base of the phallus. Testicular volume was still 2
3 q/ Y0 E( c7 |5 {; WmL, and the size of the penis remained unchanged.
" Z/ ^+ g( D' {! M) m+ M  ?The mother also said that the boy was no longer hav-/ y! T) T$ i% x" [: [/ K& b
ing frequent erections.
7 A% r/ h6 W  O- J6 p0 l6 S, ?Both parents were again questioned about use of/ ~+ G/ [! m, s9 d# Z& W
any ointment/creams that they may have applied to
; u8 d9 v% R/ {1 \) Mthe child’s skin. This time the father admitted the
' c* _/ h# g' lTopical Testosterone Exposure / Bhowmick et al 541
1 A0 {6 r4 P, Q/ Buse of testosterone gel twice daily that he was apply-
  h+ f3 ~3 |0 Jing over his own shoulders, chest, and back area for; _/ i& [  ]- g3 `" O6 V
a year. The father also revealed he was embarrassed
: c1 i5 @0 x  `3 h  W* L( {3 Cto disclose that he was using a testosterone gel pre-* k) B  s1 C# b- {$ \9 O
scribed by his family physician for decreased libido
. j7 d+ N( R# e4 S, Nsecondary to depression.
. C$ U$ D  S9 B7 ~' v  l$ V1 lThe child slept in the same bed with parents.
0 W: a8 g$ k; q! q' B7 Z0 gThe father would hug the baby and hold him on his
. a) L* Y) p6 \1 ?% t- Wchest for a considerable period of time, causing sig-
6 S. O% e2 A! V# E8 Q% Y" R' Jnificant bare skin contact between baby and father.) j" r' j# ~7 F# \
The father also admitted that after the phone call,
! b4 ]9 K; `9 [" iwhen he learned the testosterone level in the baby% Z0 g6 j6 ~) w$ K' n
was high, he then read the product information
& b0 P# S: R, ^' Z- spacket and concluded that it was most likely the rea-
' {4 s: U% O) c" A1 o+ rson for the child’s virilization. At that time, they3 g  A+ m0 @. z2 W
decided to put the baby in a separate bed, and the+ z0 p- e/ ~7 v9 j
father was not hugging him with bare skin and had
' T; \$ L: e4 e5 v9 m% ebeen using protective clothing. A repeat testosterone
( E- i+ ^; Z5 {6 c2 h+ _( ?( h. K% Ptest was ordered, but the family did not go to the9 i6 e( s& r2 v2 C: @/ v0 f6 b
laboratory to obtain the test.: Y% x8 t0 N7 w; H# y, m# Y  P
Discussion
; W% q, s, q! ]( ?; j$ Q* D* v/ iPrecocious puberty in boys is defined as secondary! U. y% i2 q4 \
sexual development before 9 years of age.1,4
! Q) |9 W9 S' t7 r% J& h# aPrecocious puberty is termed as central (true) when/ F2 q+ e6 }) V7 B) D3 @5 J  q! M
it is caused by the premature activation of hypo-
8 q4 u" v+ m( r9 ]thalamic pituitary gonadal axis. CPP is more com-
' f  |9 V+ D( L& q5 |mon in girls than in boys.1,3 Most boys with CPP! K3 O7 \  o' G* t% X/ h
may have a central nervous system lesion that is
+ o/ p5 A( m1 X6 x" Sresponsible for the early activation of the hypothal-( x$ u, A  Y/ l3 \/ E% f2 N
amic pituitary gonadal axis.1-3 Thus, greater empha-
: t% `3 z. U$ hsis has been given to neuroradiologic imaging in* k  X- o" K* D# r2 f% |
boys with precocious puberty. In addition to viril-
) d. I# k% S' H1 `, Fization, the clinical hallmark of CPP is the symmet-
7 s) s+ Q  W5 @rical testicular growth secondary to stimulation by9 ?- s! X" z2 n4 s1 _
gonadotropins.1,3
0 ~+ J0 y: Q" g, O- V, oGonadotropin-independent peripheral preco-
7 B+ o  p7 \; Z1 e3 M; Qcious puberty in boys also results from inappropriate7 a( ]! e+ c6 u! H% ~0 D
androgenic stimulation from either endogenous or( R3 v- T* X0 {- w. z5 v, X! w9 W
exogenous sources, nonpituitary gonadotropin stim-
6 _/ }# `: O7 X; o; Xulation, and rare activating mutations.3 Virilizing7 L. }# ]6 H% w3 T# C% ~/ d
congenital adrenal hyperplasia producing excessive$ k# h8 ~* J: B- B9 W) v: h
adrenal androgens is a common cause of precocious
" ]9 u( X1 k$ f) V1 w- _) fpuberty in boys.3,4, A: ~, ~' n3 p# U
The most common form of congenital adrenal
. h9 G3 n. V+ ~5 C. Z9 O8 Fhyperplasia is the 21-hydroxylase enzyme deficiency.
0 Z0 M' L" P3 {& PThe 11-β hydroxylase deficiency may also result in
" c7 _9 F! x+ ]  Z6 L* ], Kexcessive adrenal androgen production, and rarely,
6 I( J/ q* C$ i% L5 E0 ~an adrenal tumor may also cause adrenal androgen# q8 `- c6 T$ T
excess.1,3
! \% Q4 U! d3 g( kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 }. G2 t; b% ^/ z9 G- Y/ r
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 i3 ~8 k8 z1 u, eA unique entity of male-limited gonadotropin-7 j; u' m6 a9 m7 Z/ V$ [
independent precocious puberty, which is also known6 Y3 q$ O. [) J& V# h  k7 H& U
as testotoxicosis, may cause precocious puberty at a
+ L  j# ^0 `- j) S: K" B& hvery young age. The physical findings in these boys# M1 t8 d' e- ~7 f! t; A1 }
with this disorder are full pubertal development,
+ d4 K0 V7 L3 u' ]. U' _/ Gincluding bilateral testicular growth, similar to boys+ e0 E# f# ]3 H
with CPP. The gonadotropin levels in this disorder
+ y2 c4 R& X  b$ x5 K3 [are suppressed to prepubertal levels and do not show
% \5 u& z$ J/ M4 C" ]2 K5 K8 Epubertal response of gonadotropin after gonadotropin-5 v; b) x: B( b; @$ N
releasing hormone stimulation. This is a sex-linked
& W% M! ?1 b" T) ?6 Y$ Qautosomal dominant disorder that affects only0 I8 m3 l0 s) ~( \' U
males; therefore, other male members of the family0 i8 i$ [0 q+ n# y  O' {1 H  D! m4 v
may have similar precocious puberty.3( n2 _; z6 ]/ \/ M" |+ w: [6 I
In our patient, physical examination was incon-
. y5 E% k4 D6 u3 ssistent with true precocious puberty since his testi-1 Z- f6 ?) a' e
cles were prepubertal in size. However, testotoxicosis3 l3 h' h- b5 Y
was in the differential diagnosis because his father
! j. `- C6 C# e: Z/ P" J  wstarted puberty somewhat early, and occasionally,
. t8 _! ^* p0 E! h4 ttesticular enlargement is not that evident in the8 }1 Y" A5 N, T/ n
beginning of this process.1 In the absence of a neg-- N; E5 I8 a/ r( M* l1 ?. E3 C
ative initial history of androgen exposure, our5 g+ @: q0 |# U# w$ y
biggest concern was virilizing adrenal hyperplasia,* o8 E- Y/ ?7 q3 O( y5 i
either 21-hydroxylase deficiency or 11-β hydroxylase
! j- F; h6 l1 h  b1 j4 H2 ddeficiency. Those diagnoses were excluded by find-
) ~4 Z9 V: `- K; @; [* s0 v1 Fing the normal level of adrenal steroids.
8 w2 t0 X3 T0 N7 b7 R$ iThe diagnosis of exogenous androgens was strongly
% m* v8 W& J$ a& @suspected in a follow-up visit after 4 months because# h/ H, C+ W+ E( d+ }; g
the physical examination revealed the complete disap-2 d1 u; M  X' |9 H0 J: K  {
pearance of pubic hair, normal growth velocity, and/ @: W/ u0 z) u, \
decreased erections. The father admitted using a testos-
8 Z+ G; m# [2 y( ^3 [( _% Dterone gel, which he concealed at first visit. He was' B* T  q7 |# X% i# y8 s
using it rather frequently, twice a day. The Physicians’0 S) ?; n7 \& _0 O8 P3 B
Desk Reference, or package insert of this product, gel or8 T' y1 Z+ y$ I  c1 S; F& K
cream, cautions about dermal testosterone transfer to/ n. v6 W+ d% _7 c' b
unprotected females through direct skin exposure.
/ y. L. a: S: G/ y) f/ rSerum testosterone level was found to be 2 times the; H  J; b( Q3 `; Z0 U  x$ c9 P
baseline value in those females who were exposed to
" o8 e/ r  `0 qeven 15 minutes of direct skin contact with their male
/ J& _3 ^" _( K6 E/ ypartners.6 However, when a shirt covered the applica-
2 g" N! {; Q' }tion site, this testosterone transfer was prevented.% Q+ w0 v! L+ ?: h- T
Our patient’s testosterone level was 60 ng/mL,# p# X/ D' W) n- n, w
which was clearly high. Some studies suggest that, X( ]/ {1 I9 }3 C6 i
dermal conversion of testosterone to dihydrotestos-" Q, d# ?" ^2 Q2 W
terone, which is a more potent metabolite, is more& X( f# I& k9 {  ]
active in young children exposed to testosterone; q! M9 h  Q9 f0 W$ C# j
exogenously7; however, we did not measure a dihy-1 r- q* {6 P2 X+ ^" B5 c+ c
drotestosterone level in our patient. In addition to- `$ E/ _* H9 Q7 Y
virilization, exposure to exogenous testosterone in4 C$ t+ G4 @# k# w2 A. E8 X
children results in an increase in growth velocity and) W& t/ k4 _7 p- [
advanced bone age, as seen in our patient.
+ w" u- B- L- j1 ?; O. n6 U+ t8 f& {The long-term effect of androgen exposure during- ^8 Y  w0 v/ [2 w2 @( E
early childhood on pubertal development and final
8 ~1 t* Q. a, J' P! Xadult height are not fully known and always remain0 H) K- V9 X& N' ~( v* e4 r/ ~
a concern. Children treated with short-term testos-
2 {4 z! e  j9 L3 ?( ?" s. I7 O& Sterone injection or topical androgen may exhibit some, c+ V4 t4 h" q- v
acceleration of the skeletal maturation; however, after
9 h# z! R, T, g) [% V$ [5 Jcessation of treatment, the rate of bone maturation
: L3 ~3 t; }8 e$ R/ b4 jdecelerates and gradually returns to normal.8,9
* ]3 L7 U. U, J& Z3 r1 x# [There are conflicting reports and controversy) {/ \4 g& H2 q' B% v1 y5 Q) |1 [
over the effect of early androgen exposure on adult
$ I( K- r& I& q2 y  h* Z- Gpenile length.10,11 Some reports suggest subnormal" C- p7 e, i1 i9 m$ w3 K
adult penile length, apparently because of downreg-& P3 R0 g7 L# B" X, a: g8 g
ulation of androgen receptor number.10,12 However,
/ e# V/ L  M* h2 @. ]7 `Sutherland et al13 did not find a correlation between' x* @5 q4 J- z
childhood testosterone exposure and reduced adult* j# o/ P8 d6 b9 ?, A0 S
penile length in clinical studies.. `. V% n0 p4 L! E
Nonetheless, we do not believe our patient is
6 \& ?8 o+ G: [: _8 S/ zgoing to experience any of the untoward effects from7 ?* Y1 Z( x4 }) V& w" Z
testosterone exposure as mentioned earlier because8 \! {; K  E" o$ o+ P% d
the exposure was not for a prolonged period of time.
4 R" m$ i0 e! y/ J9 _Although the bone age was advanced at the time of
4 Z+ l+ D% g: u( S0 Udiagnosis, the child had a normal growth velocity at
, c! J: {- s  X# w' gthe follow-up visit. It is hoped that his final adult
/ d: m! I+ f7 H3 G* Z; Oheight will not be affected.( h0 A$ E: |2 e% }
Although rarely reported, the widespread avail-3 X  _5 `' }) k. O- b4 ]9 ?
ability of androgen products in our society may
; g8 j! g9 `5 f( N7 yindeed cause more virilization in male or female, ^$ p1 R0 c/ ]9 ~7 ?6 v
children than one would realize. Exposure to andro-( ?7 T/ C. l# A8 I+ u) g  F
gen products must be considered and specific ques-# O5 w8 k" L/ V9 z- @  {# l8 b! R
tioning about the use of a testosterone product or
. T: `# ^; p3 b- _3 I0 Vgel should be asked of the family members during4 |0 x8 x# d. \' `3 F" L) X
the evaluation of any children who present with vir-% T( J8 o  p+ u* ?) L1 e' T
ilization or peripheral precocious puberty. The diag-
: o) e$ B6 N; V& @+ d% O' onosis can be established by just a few tests and by
9 c5 @6 g* q$ p( S  Pappropriate history. The inability to obtain such a
  ^0 E9 d, V) D! V; K5 vhistory, or failure to ask the specific questions, may
" Z7 S' f: t3 A$ Dresult in extensive, unnecessary, and expensive$ K( _% i5 M- R% ]) o( M; d2 Y
investigation. The primary care physician should be
; o: C' D4 i) m  z5 a' F6 h* Taware of this fact, because most of these children
# n3 K; B3 b) o, L2 o/ W) {may initially present in their practice. The Physicians’9 h+ W; k' @& y$ b4 a5 P
Desk Reference and package insert should also put a
4 r" \$ g+ J- Q9 B/ ?. \  ^. Pwarning about the virilizing effect on a male or$ w6 A6 g  U0 }$ ~! R- R0 Y% u
female child who might come in contact with some-; f- u7 g: d& F& K7 @( _% o2 W, y
one using any of these products.
' g4 K! d& _2 y  Z- g) JReferences
% A( r  ^* L9 v9 d1. Styne DM. The testes: disorder of sexual differentiation
. D$ m3 N( ?3 K1 band puberty in the male. In: Sperling MA, ed. Pediatric
$ `& D+ F$ Z3 B7 f0 ^& BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;( E; W- j) B( {' y- H
2002: 565-628.5 l6 l2 O& ]* W
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; }* }! U* B  |" C; D5 T. ]. E
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
8 U2 D. q! G- z0 ?! gBoy Induced by Indirect Topical7 i/ [4 b2 F) j
Exposure to Testosterone5 g/ F* S; s* d  P6 I
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% Y' Q0 V/ \9 t- W) d) s; rand Kenneth R. Rettig, MD1( Y4 ?0 y0 u) x( e: N9 b9 _
Clinical Pediatrics
/ A# w( b0 g7 y5 H0 H: p$ e, u9 E( YVolume 46 Number 6
: Y' V# O: R7 e6 C- yJuly 2007 540-5431 ^( L2 x' g7 f& u
© 2007 Sage Publications- R% H# O9 |) [! B9 w
10.1177/0009922806296651& Y: g' B% W( r* V
http://clp.sagepub.com
# Z  F3 `9 a6 |3 @, @& phosted at- m, P5 C, ~# {# ?2 a5 t
http://online.sagepub.com# w& O& d" ^' O- I0 p
Precocious puberty in boys, central or peripheral,
. P4 }: V2 @$ U: z$ \+ P3 `is a significant concern for physicians. Central
( D7 ]0 n. u3 t1 eprecocious puberty (CPP), which is mediated
0 w  s# w; r5 Y, ~( S  o& j' u) [through the hypothalamic pituitary gonadal axis, has
5 j3 T5 w, o' n1 ba higher incidence of organic central nervous system  y8 {' [* i; f) J, ]
lesions in boys.1,2 Virilization in boys, as manifested
4 G( v- {8 Q0 p3 F$ Mby enlargement of the penis, development of pubic
4 e9 L) ~/ L9 d4 A7 ]hair, and facial acne without enlargement of testi-5 n3 r8 M% M( h: y: R6 _, w% ^
cles, suggests peripheral or pseudopuberty.1-3 We
' y! [) m) b: T6 yreport a 16-month-old boy who presented with the$ r1 j& g1 d8 D9 j
enlargement of the phallus and pubic hair develop-  e( }$ l8 V7 q, q8 M
ment without testicular enlargement, which was due
! q/ Q  g- S7 |; B  d$ J* h) yto the unintentional exposure to androgen gel used by
/ G) o: `6 A0 o' tthe father. The family initially concealed this infor-# U- o. g* Q6 U" R8 [( l- y- S
mation, resulting in an extensive work-up for this9 ?1 F3 k0 X6 W9 o; `
child. Given the widespread and easy availability of% s. y# p2 e( ?+ I, t
testosterone gel and cream, we believe this is proba-# ]& \9 l) X% V% z9 L4 ~  Z- i
bly more common than the rare case report in the  N8 |4 P/ v3 v' l' u% Y
literature.43 N1 E$ B3 b" |$ \% |
Patient Report
( ?# U4 `1 F2 O1 Z; AA 16-month-old white child was referred to the8 g0 h' n- j9 b0 o  v% R
endocrine clinic by his pediatrician with the concern
" s4 L/ J) N, a5 @of early sexual development. His mother noticed
  }- S% _) I8 E; |) G- Alight colored pubic hair development when he was
+ w5 m% H/ W" g2 V1 B( L! PFrom the 1Division of Pediatric Endocrinology, 2University of
. @2 R7 s$ j, B+ KSouth Alabama Medical Center, Mobile, Alabama.
, q5 z2 n! Q/ s2 i/ nAddress correspondence to: Samar K. Bhowmick, MD, FACE,
1 o4 f# P0 i1 B; mProfessor of Pediatrics, University of South Alabama, College of
" |- e9 U6 T7 y, b* ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;: Z: Y% q+ x) n7 V( H. B( m5 r
e-mail: [email protected].
& V/ a- p4 t' Qabout 6 to 7 months old, which progressively became
0 C1 j! q4 b- N5 O! A. T+ Edarker. She was also concerned about the enlarge-
4 L% i2 z8 ~+ y) v# Zment of his penis and frequent erections. The child
% m. `2 o" A/ V+ A8 Kwas the product of a full-term normal delivery, with; m" t5 d6 z$ x- E. @$ l! z
a birth weight of 7 lb 14 oz, and birth length of7 p9 S, k# o6 B/ ~, S! D/ r
20 inches. He was breast-fed throughout the first year
) b" w1 h8 Z) q0 d7 Q4 z9 Bof life and was still receiving breast milk along with" F7 L, x* b+ v0 U3 P! N
solid food. He had no hospitalizations or surgery,
; C: ]2 V. ~4 yand his psychosocial and psychomotor development
9 s7 V4 u5 i9 A6 }' Ewas age appropriate.* \7 P) i2 d" I( S
The family history was remarkable for the father,
) ^. h7 u# k( o3 k; v# H8 Hwho was diagnosed with hypothyroidism at age 16,9 H  `' Z' U4 {( \% j0 d
which was treated with thyroxine. The father’s- a3 H9 p. G! P  h- N
height was 6 feet, and he went through a somewhat% Y! Y; ~& M$ a0 U2 y
early puberty and had stopped growing by age 14." y: j7 i6 U  m$ ]% ~" M
The father denied taking any other medication. The  a0 u. t/ z$ T7 {4 z7 |. G
child’s mother was in good health. Her menarche
! w, L) ^4 h2 E) }, Mwas at 11 years of age, and her height was at 5 feet3 W/ H0 d; m' _$ M2 B: j
5 inches. There was no other family history of pre-
1 A! i* ]- t  ]# B) Z$ X! m& [cocious sexual development in the first-degree rela-
* X* P4 f  {+ H  H6 itives. There were no siblings.
" w0 W: o* H6 v) EPhysical Examination
  X1 m: v0 v0 E! ?& \9 u: WThe physical examination revealed a very active,
! i7 n3 e* M: o! D4 V7 ?! H" W) D( Mplayful, and healthy boy. The vital signs documented
, N( ?) a& _( [1 Na blood pressure of 85/50 mm Hg, his length was0 @$ }4 k: z, d8 G7 M7 S: s" K$ r
90 cm (>97th percentile), and his weight was 14.4 kg( j$ b4 V$ @: O* s
(also >97th percentile). The observed yearly growth0 Y; ^) t3 G4 e
velocity was 30 cm (12 inches). The examination of
* G& O: l: U! ^the neck revealed no thyroid enlargement.
, [% `( Z9 O5 p- h" m2 kThe genitourinary examination was remarkable for
9 c( ~) [( a, j' D! O1 O1 zenlargement of the penis, with a stretched length of
+ f8 Q) k# Y( O5 @: B7 W% J( ^& @8 cm and a width of 2 cm. The glans penis was very well( A4 p! h6 u+ C0 R3 R& M2 z
developed. The pubic hair was Tanner II, mostly around6 p! R# s; n5 n3 G
540# e! }. l7 [0 ~# _. E3 M9 W1 D3 U
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the base of the phallus and was dark and curled. The
/ U3 [8 p$ j  f' k( W4 Rtesticular volume was prepubertal at 2 mL each.
% ^7 X* g0 J; x$ X; K4 Z* t' pThe skin was moist and smooth and somewhat- V% R$ F) e% H1 c6 N
oily. No axillary hair was noted. There were no
+ I) t) f( }2 Q, \% labnormal skin pigmentations or café-au-lait spots.7 f6 u$ V4 W. L% J0 b( Y- Z* A
Neurologic evaluation showed deep tendon reflex 2+
8 n) S0 w: Q6 [3 _! t! Hbilateral and symmetrical. There was no suggestion; c* m" K7 A+ |  S9 A4 Q
of papilledema.
! e9 G' _0 Q' V0 XLaboratory Evaluation6 Y$ R$ W. c0 g
The bone age was consistent with 28 months by; ]( ?  i+ w' v
using the standard of Greulich and Pyle at a chrono-% B! n5 `$ ]% n4 G$ @
logic age of 16 months (advanced).5 Chromosomal# ^: z& M1 |. @8 \7 T* X; O
karyotype was 46XY. The thyroid function test
+ K6 x( I) ]6 B( w3 [4 ishowed a free T4 of 1.69 ng/dL, and thyroid stimu-" H( Y( G  G0 z4 H% \$ _2 Z
lating hormone level was 1.3 µIU/mL (both normal).& ]/ ?0 f5 k& l% v
The concentrations of serum electrolytes, blood
, r1 m3 u$ |% [" X% t. _urea nitrogen, creatinine, and calcium all were
0 u: \5 v' J: Q$ q( k# |/ zwithin normal range for his age. The concentration
- T4 Y" B+ r! v9 ?of serum 17-hydroxyprogesterone was 16 ng/dL, k  Z% ~; C) \$ H& S6 ^) e! T
(normal, 3 to 90 ng/dL), androstenedione was 20
0 m8 r( l4 C$ `6 c& Q" xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* g2 ]: N+ G& L$ i) T$ O: f
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. w0 V* E+ r% k' H1 b  T, `4 V0 `desoxycorticosterone was 4.3 ng/dL (normal, 7 to# P& W7 o% ^" w: ]
49ng/dL), 11-desoxycortisol (specific compound S)7 ?# [2 p# k0 s8 k5 `* u1 J8 E: r
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 {9 [( K7 @, \- f% Dtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total1 f, q9 P6 t% `8 J& X1 |8 I; |6 O; H- W( n
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
% F7 d0 Z" ~, S9 {* {and β-human chorionic gonadotropin was less than
7 ~' G( i4 t" a; f( \8 B5 mIU/mL (normal <5 mIU/mL). Serum follicular  R) H4 t" P2 n6 S! c; a& J
stimulating hormone and leuteinizing hormone: q3 ~& |! l) G8 Y2 z. `5 j
concentrations were less than 0.05 mIU/mL! l4 b: B/ y+ i7 ^
(prepubertal).
) q5 R% B8 J! h1 Q! n/ G( a& HThe parents were notified about the laboratory$ m: ]0 I0 D  `( x/ ]$ B" ~& J, m
results and were informed that all of the tests were) Q. C$ X' {0 \8 B
normal except the testosterone level was high. The4 w) s* V, B' U2 ]
follow-up visit was arranged within a few weeks to) ~& ^0 F) I7 Y" _3 S/ M- z" y
obtain testicular and abdominal sonograms; how-! g+ n+ p) |! L1 ~& V  a+ M
ever, the family did not return for 4 months.5 F; ?8 l/ Y/ `
Physical examination at this time revealed that the  ~1 v* R/ J. J. D% v% ]
child had grown 2.5 cm in 4 months and had gained
+ ]' H8 ~& l0 p. ~' \2 kg of weight. Physical examination remained1 y: Q  A  X& a1 J4 @
unchanged. Surprisingly, the pubic hair almost com-
# V# d; `( _" K4 X, Epletely disappeared except for a few vellous hairs at% t1 K& K: d* q) q  W9 j& o# d0 N3 y
the base of the phallus. Testicular volume was still 2
9 S  n) a# S) S+ tmL, and the size of the penis remained unchanged.
1 T* s  t3 S" Y* nThe mother also said that the boy was no longer hav-$ w6 J1 |1 b5 B* k0 P
ing frequent erections.
! h( ?8 J( P' k/ H2 L8 D6 c$ e: SBoth parents were again questioned about use of
( T- P: s* e; lany ointment/creams that they may have applied to
) N' D8 ~* E4 }" D# ~/ j5 L+ z+ bthe child’s skin. This time the father admitted the9 o( F, \3 v& b& N' }9 x
Topical Testosterone Exposure / Bhowmick et al 541
) N7 R4 K, ~: J7 yuse of testosterone gel twice daily that he was apply-
+ k; d9 H7 ?: g$ B/ Z+ \3 aing over his own shoulders, chest, and back area for" ~% S: T1 P" u- @  @  K9 M) ~$ q( k% k/ U
a year. The father also revealed he was embarrassed
3 n- s6 j$ H$ S1 a( u% d' j3 N' Gto disclose that he was using a testosterone gel pre-
8 D/ u: n% Z/ ?# Z* v9 b: s' Nscribed by his family physician for decreased libido: ~( C5 Y8 n  d. o5 Q
secondary to depression., e" W5 c/ e$ u+ d! g1 t( z7 G0 N
The child slept in the same bed with parents.2 F" Y# Q, k  C+ w, J* j' R, w( F: E* U
The father would hug the baby and hold him on his' j; @, S" F5 H9 O' y. B4 p
chest for a considerable period of time, causing sig-
9 J6 w/ z2 Y6 S1 ~$ ]9 _nificant bare skin contact between baby and father.) C% C, F: _+ d2 S7 O2 K  Y/ u; z
The father also admitted that after the phone call," k" q. W8 v! b3 o0 W/ M  H
when he learned the testosterone level in the baby
+ c+ R* l9 R8 ^7 W" `" j# m) ~4 g# Awas high, he then read the product information
3 `+ d5 Z/ I& Y4 t9 zpacket and concluded that it was most likely the rea-, ]% P! N, Q0 G7 J% l9 ^3 W( C
son for the child’s virilization. At that time, they
3 F; s( ?0 k9 ?decided to put the baby in a separate bed, and the: v  K8 Z0 X+ E: g8 C8 g1 s, q3 C5 c
father was not hugging him with bare skin and had
' T/ Z+ o9 |1 T; N  {' _+ Abeen using protective clothing. A repeat testosterone( `" a9 j0 g* @$ O! n
test was ordered, but the family did not go to the
0 s# x2 T. @$ v# k: W- mlaboratory to obtain the test.) ]% x, v7 X# ?' g) ~
Discussion
+ Y# J0 v/ l  M  H# n, dPrecocious puberty in boys is defined as secondary2 }, s1 J7 K, L: i# }
sexual development before 9 years of age.1,4
( R! N2 \$ S" ^! v( d" X8 GPrecocious puberty is termed as central (true) when
# f  x2 O9 c$ G# N$ L1 mit is caused by the premature activation of hypo-! N- e  ]' b; b
thalamic pituitary gonadal axis. CPP is more com-- O! j0 ]+ `3 `5 E
mon in girls than in boys.1,3 Most boys with CPP, O# u1 p) e8 z, W4 y+ O$ E8 l
may have a central nervous system lesion that is
1 X) ?  p# ^3 S4 Lresponsible for the early activation of the hypothal-
* A5 N9 B. v) A7 N. U7 O2 z% J# Samic pituitary gonadal axis.1-3 Thus, greater empha-
- j  u5 n3 a1 N3 r. t' c# z5 vsis has been given to neuroradiologic imaging in
. I# L$ `+ V9 c* P6 p" mboys with precocious puberty. In addition to viril-
$ y/ [; p" n. Cization, the clinical hallmark of CPP is the symmet-
1 N' r. E  j3 p: urical testicular growth secondary to stimulation by
! x. u' V  p8 A) P& Dgonadotropins.1,3
3 D$ L& \" D2 ?Gonadotropin-independent peripheral preco-
- ~3 e! U' ?8 p. R$ v9 Tcious puberty in boys also results from inappropriate
7 ?" q9 N. \3 d# u5 z: ]7 z% Uandrogenic stimulation from either endogenous or
2 a6 G* D8 h/ U& Y. b5 zexogenous sources, nonpituitary gonadotropin stim-5 G; Q  @3 ^7 i$ r" i8 W
ulation, and rare activating mutations.3 Virilizing
; {' g' x. u3 n! Econgenital adrenal hyperplasia producing excessive# b6 t' u) |' @8 \5 A% B, ?* c
adrenal androgens is a common cause of precocious* V1 l* ^' c6 `& ?1 }
puberty in boys.3,4
% R& i) n' j6 p7 r) }3 E% Y0 F5 F! tThe most common form of congenital adrenal
% ]$ ?3 e; c3 n0 @! ~0 Whyperplasia is the 21-hydroxylase enzyme deficiency.
! E4 x- Z% J) XThe 11-β hydroxylase deficiency may also result in: w4 {5 k& K" X, L) v0 x6 ^
excessive adrenal androgen production, and rarely,
4 N) E- g7 s8 n2 o+ E  Jan adrenal tumor may also cause adrenal androgen
: z+ x0 J5 h' i9 l1 t: ]0 Oexcess.1,3
) R5 [  Q( R5 [, K4 `7 Qat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! P; Y! X& g+ `6 K! V. x5 [
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
/ i+ B% J* \, }  KA unique entity of male-limited gonadotropin-, s& b8 P( F0 b: A* ?: Q
independent precocious puberty, which is also known5 \+ S4 ]/ Y0 ?5 J9 c2 X$ _, b
as testotoxicosis, may cause precocious puberty at a
  I: G0 E, |7 `, Fvery young age. The physical findings in these boys! h4 S: y, u% Y2 u2 q- V; A( I' G
with this disorder are full pubertal development,
$ {9 ^3 F* F; bincluding bilateral testicular growth, similar to boys
/ z* O" ^3 v6 b4 H% Owith CPP. The gonadotropin levels in this disorder
' ^2 A& Q: l2 R4 X+ D+ v* b8 X7 h& {9 U! Qare suppressed to prepubertal levels and do not show3 S) o( P7 L- [
pubertal response of gonadotropin after gonadotropin-
/ k! S3 e. [; Freleasing hormone stimulation. This is a sex-linked
' w& h! F7 p. m, H1 u& Vautosomal dominant disorder that affects only
: j0 }- G6 s# ~0 i- a$ M6 v' kmales; therefore, other male members of the family
9 T" V% o: S/ h; b6 n' k/ Nmay have similar precocious puberty.3. g' P6 o, n; X' k
In our patient, physical examination was incon-/ [3 i8 ?9 r1 @1 E) j- |( C/ ^
sistent with true precocious puberty since his testi-
, g7 P4 W) e. I& Hcles were prepubertal in size. However, testotoxicosis
9 |+ O# C* m7 Q3 d' h: S. K# Nwas in the differential diagnosis because his father
' y" f; D( x+ Z, Z# F1 Q4 i( Lstarted puberty somewhat early, and occasionally,
* y% M% V: V, W$ S1 Ytesticular enlargement is not that evident in the
6 ~! B" o; u5 n# H# F0 [' Ebeginning of this process.1 In the absence of a neg-" C4 n: ^6 z- y% d7 v7 d+ e: ?
ative initial history of androgen exposure, our) k! @% v+ e4 @0 k, Z3 Z/ J: q1 c
biggest concern was virilizing adrenal hyperplasia," C/ u% g0 K) E# P$ v
either 21-hydroxylase deficiency or 11-β hydroxylase" r7 b% }- H  a: t
deficiency. Those diagnoses were excluded by find-/ |. Q$ M9 i5 T# |: e8 Y
ing the normal level of adrenal steroids.
' z- }. B/ N- x, O9 f% {The diagnosis of exogenous androgens was strongly+ j4 q+ J8 [% D* r4 I7 T
suspected in a follow-up visit after 4 months because
# h  b( ^& T0 Q  O5 O$ Zthe physical examination revealed the complete disap-
% {. A- T: V! o, s6 U! Ppearance of pubic hair, normal growth velocity, and
8 o$ A/ @/ g7 l2 x( S8 n4 L' g8 odecreased erections. The father admitted using a testos-
' `5 G9 ^$ G7 P+ Sterone gel, which he concealed at first visit. He was" i& l, K# X+ D$ N
using it rather frequently, twice a day. The Physicians’
; v$ M# v9 n* ADesk Reference, or package insert of this product, gel or8 `$ c6 D* @8 n7 U& I, z. X
cream, cautions about dermal testosterone transfer to4 W8 n( G$ y) i! {3 c( g' k, J
unprotected females through direct skin exposure.: @# n5 |( ~3 f6 e4 A) ?+ D
Serum testosterone level was found to be 2 times the, H& T; L6 g$ c+ i4 m1 A$ k
baseline value in those females who were exposed to  [) m" Y9 i* p/ P+ L
even 15 minutes of direct skin contact with their male
5 ~$ ^* d& z9 e2 Qpartners.6 However, when a shirt covered the applica-) d9 g( l7 o" v
tion site, this testosterone transfer was prevented.
& B0 ^* `  D+ rOur patient’s testosterone level was 60 ng/mL,
" s+ l% I/ k3 K7 U0 @& ywhich was clearly high. Some studies suggest that2 U# j" \% @6 p2 }! t
dermal conversion of testosterone to dihydrotestos-
$ f: P2 B1 j1 E* @" b" Q3 G* ?terone, which is a more potent metabolite, is more
3 h) l8 u! }* a& O; x. \2 R1 S' Gactive in young children exposed to testosterone
" O& `- O, o8 Z6 b% r, g& eexogenously7; however, we did not measure a dihy-
& e5 M! n7 M) e+ Z2 Vdrotestosterone level in our patient. In addition to
( J  q! h; f9 K1 N) g8 w* Fvirilization, exposure to exogenous testosterone in- m6 N/ K- I7 [# T
children results in an increase in growth velocity and
2 g/ o# X( x- d! }' A: Gadvanced bone age, as seen in our patient.
3 p; K% N# i5 d1 KThe long-term effect of androgen exposure during
' \& y5 E2 _  l4 p: Learly childhood on pubertal development and final
; K0 W) R, x+ y  M: A& J# H+ badult height are not fully known and always remain
. r( i. E; J; N+ _* ~a concern. Children treated with short-term testos-
5 V0 F7 b7 {. }7 fterone injection or topical androgen may exhibit some: l! g8 W+ X; ~) p
acceleration of the skeletal maturation; however, after5 R5 L3 v9 D5 j* v4 p
cessation of treatment, the rate of bone maturation* o, `) J/ s6 h7 T
decelerates and gradually returns to normal.8,9" s/ W3 X# z% }7 q/ k7 X9 Y
There are conflicting reports and controversy
% O& G8 N* h: `( T) P: P0 Xover the effect of early androgen exposure on adult
0 T$ [5 S/ B3 Tpenile length.10,11 Some reports suggest subnormal
) k7 G) Q! \. P* ^, g2 [; j$ T7 }adult penile length, apparently because of downreg-  T* [1 c1 e+ e* C. y
ulation of androgen receptor number.10,12 However,, P9 l+ D+ }& v! v& U/ z
Sutherland et al13 did not find a correlation between
9 }. G' G  N: S6 T, b; cchildhood testosterone exposure and reduced adult0 _1 ]% G% y( ~$ U
penile length in clinical studies.* \2 L# G) f  g. \4 m6 F) Z4 E
Nonetheless, we do not believe our patient is0 Q& q9 i& j1 \& o7 h
going to experience any of the untoward effects from
- w  O" y* U! o1 qtestosterone exposure as mentioned earlier because9 n) _7 S" X* G
the exposure was not for a prolonged period of time.5 k. G6 w7 |+ j/ a4 B8 E
Although the bone age was advanced at the time of
. h9 N7 y0 h3 x. L' V! w9 A5 y7 Jdiagnosis, the child had a normal growth velocity at
# j% e% L7 i: Lthe follow-up visit. It is hoped that his final adult: a" ^+ e( V1 p! `1 Z
height will not be affected.
# `: Y% w7 U  O! w' M! aAlthough rarely reported, the widespread avail-' F2 H5 [1 X3 w& k: [8 G9 T
ability of androgen products in our society may6 H' r  p7 {! `
indeed cause more virilization in male or female! D# F$ d4 C- d
children than one would realize. Exposure to andro-
) \4 i) Q  v7 ?. _* ]9 f2 h2 Egen products must be considered and specific ques-
* V+ w( [8 g; Z+ F) R% j2 c6 ^' Ttioning about the use of a testosterone product or& ?  Q/ v  s$ \4 |/ g+ W7 z! G. l
gel should be asked of the family members during" O) g, F6 O6 M4 B
the evaluation of any children who present with vir-! j) C! b( j3 M+ J2 t$ o# S, }% C
ilization or peripheral precocious puberty. The diag-2 \8 \4 {. \" P& x3 G
nosis can be established by just a few tests and by
, p$ _  B* a# ^' ~- Mappropriate history. The inability to obtain such a
8 H' D2 i! v- \3 n$ [history, or failure to ask the specific questions, may
) o0 D: b+ }+ G+ Cresult in extensive, unnecessary, and expensive* n  c6 a2 S$ D( j6 d
investigation. The primary care physician should be
( C4 ~5 d3 }+ X9 naware of this fact, because most of these children
0 v; T$ x/ n) T9 Z9 Pmay initially present in their practice. The Physicians’! S- J5 o* f  f+ }
Desk Reference and package insert should also put a
) V% ~3 B' a. d3 y* X0 }" `3 dwarning about the virilizing effect on a male or
2 c) V4 B# o! V; ^' _9 w1 m6 |female child who might come in contact with some-
& u& W# _8 D/ Done using any of these products.6 M/ n& M/ z/ F8 N
References0 S/ v3 l: ^4 J) {+ I% F+ _
1. Styne DM. The testes: disorder of sexual differentiation# T# j! d' e: b2 I
and puberty in the male. In: Sperling MA, ed. Pediatric
  H; B' p1 Q: }5 R/ {4 k$ S6 i; NEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;" u- D( q9 O6 V- P8 ]
2002: 565-628.
; g1 s% z, I0 d2 A2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
. }5 C; w: `, w$ J. p! mpuberty 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
" H5 R4 v0 y1 }
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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