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Sexual Precocity in a 16-Month-Old5 U1 O) R6 }5 D6 G( o
Boy Induced by Indirect Topical' w6 \$ _- ?1 |3 L, }1 I
Exposure to Testosterone9 K/ p) ^* y- B* A) q1 J4 c# ~- B
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
) a3 [! z* [, e8 s. Y, h) Sand Kenneth R. Rettig, MD1
# W- I9 c( I% H$ D5 k! O5 \Clinical Pediatrics
3 a* s' q% D; kVolume 46 Number 6
# w- o% ]# P1 o$ }July 2007 540-543
, g+ _) W' H7 a6 p: I9 v© 2007 Sage Publications
: Y, |6 C- }4 z5 Q1 A" n10.1177/0009922806296651$ J8 d5 U2 O$ \& h
http://clp.sagepub.com1 E) s) @7 O. ?' W  U7 w- s
hosted at
& g$ ^) ^0 m! N8 F' _+ f' Nhttp://online.sagepub.com, F$ O# g. T/ U8 P0 G$ k8 A
Precocious puberty in boys, central or peripheral,% u, r1 p; J8 a' P
is a significant concern for physicians. Central4 ], q; o0 i+ h/ m
precocious puberty (CPP), which is mediated+ G! O- W7 i8 o5 Y. c# C) X
through the hypothalamic pituitary gonadal axis, has
) Y1 R- T" Z2 L# v; p% R7 o& J1 da higher incidence of organic central nervous system9 R, C& E7 `& d% J2 \2 G
lesions in boys.1,2 Virilization in boys, as manifested
0 B2 K2 o# B: z4 h( P3 Xby enlargement of the penis, development of pubic6 S* `: w- l' L. Q: p
hair, and facial acne without enlargement of testi-
* R2 Q1 i' }7 ?$ ]; fcles, suggests peripheral or pseudopuberty.1-3 We$ e' A  X% t! O# w1 r
report a 16-month-old boy who presented with the
7 d1 ?6 ]+ a$ x3 t7 B- R6 ]1 f& Eenlargement of the phallus and pubic hair develop-
/ a. S9 w. D, E- b$ [ment without testicular enlargement, which was due
3 c% C" B1 n2 |6 ^" Tto the unintentional exposure to androgen gel used by
' R( j8 G9 ^6 [: \the father. The family initially concealed this infor-
# Q" A3 B% `7 y% ?mation, resulting in an extensive work-up for this
& @9 C% y9 x8 @3 r- }- Achild. Given the widespread and easy availability of1 s; k' t; _8 [
testosterone gel and cream, we believe this is proba-, b+ e4 b& n6 T" d! @" z; N
bly more common than the rare case report in the
2 V' C. M. V- U7 x- T; r% S% Pliterature.4! K0 Y6 a# K( l# X$ l" u1 W% H* V
Patient Report$ R' L  {" p! [1 R" [1 V( [5 O
A 16-month-old white child was referred to the( c) m' q' y- O7 _* I- M
endocrine clinic by his pediatrician with the concern
, D- G) G$ C. `) j1 w! }of early sexual development. His mother noticed
) `0 K  u; t; C: X" m3 i: rlight colored pubic hair development when he was2 o; }8 b0 V5 o( u9 G2 O7 N/ y
From the 1Division of Pediatric Endocrinology, 2University of- m0 I# L( g, f5 T, P  T2 N9 i
South Alabama Medical Center, Mobile, Alabama.% v* m: V0 z# U' I4 S: ~" b8 ~6 O
Address correspondence to: Samar K. Bhowmick, MD, FACE,
$ y- [$ C# {7 ~! d8 r6 }Professor of Pediatrics, University of South Alabama, College of
2 l( c) A5 I! g% m2 |Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# \. w3 [; o' k' O& oe-mail: [email protected].7 a) @- z! g3 |8 B8 e0 r
about 6 to 7 months old, which progressively became
: O! g8 S2 v# A9 kdarker. She was also concerned about the enlarge-
+ D  W* B8 E0 m% g0 f! s& `+ |ment of his penis and frequent erections. The child
/ O/ h% {7 t: p8 u6 c$ F. iwas the product of a full-term normal delivery, with) r- \* ~9 I3 r& P8 E6 E4 b
a birth weight of 7 lb 14 oz, and birth length of7 o) z+ }/ h0 Q: n
20 inches. He was breast-fed throughout the first year
- V8 W! }, C( c6 ?of life and was still receiving breast milk along with
8 @5 w3 h# r1 i& e& Gsolid food. He had no hospitalizations or surgery,- u; S# F0 ?0 t$ v
and his psychosocial and psychomotor development
* m9 `; s6 E+ B6 d. @, Xwas age appropriate.% A, ?( m; X1 P  @! \" J
The family history was remarkable for the father,
7 F( H1 D8 D- T6 V2 ]3 o: Vwho was diagnosed with hypothyroidism at age 16,
: ^7 H. K8 L# W9 Vwhich was treated with thyroxine. The father’s
$ K0 J  _" N1 {+ v" Mheight was 6 feet, and he went through a somewhat5 Y: b' o1 I. r3 @+ [3 U( a
early puberty and had stopped growing by age 14.
# [+ c! w2 D2 ^3 H: ?) Y9 jThe father denied taking any other medication. The8 v- ?" v& j; F& F7 u. i) K) h
child’s mother was in good health. Her menarche# q$ K5 d: y  k1 A2 w* C
was at 11 years of age, and her height was at 5 feet
$ d' K5 C7 B# c# N5 inches. There was no other family history of pre-5 ]& \: V4 D9 F4 ^
cocious sexual development in the first-degree rela-
8 r  m4 t# u1 }: g" s! w. ^tives. There were no siblings.
7 j  M: J5 T2 V/ TPhysical Examination: K5 v2 J% b1 i: i
The physical examination revealed a very active,
# {1 _$ M" U1 `% E. Y# E' Gplayful, and healthy boy. The vital signs documented* B8 _8 O0 N$ x; ], S6 a* @
a blood pressure of 85/50 mm Hg, his length was% l6 H' D/ i7 o  e% o
90 cm (>97th percentile), and his weight was 14.4 kg
0 N& @" {" y. h2 O' i1 Q. _3 G% r(also >97th percentile). The observed yearly growth
) E) o9 O" q  f: U$ O, zvelocity was 30 cm (12 inches). The examination of* w. ]% k- [: D+ E0 S9 T/ D' {
the neck revealed no thyroid enlargement.
( _5 @! M6 Z$ e; o; ^# k& K+ NThe genitourinary examination was remarkable for: }4 {, X8 r5 M- z  }0 a
enlargement of the penis, with a stretched length of$ o% l$ @% A" L& @* [0 E
8 cm and a width of 2 cm. The glans penis was very well
( H! E6 X0 |$ j. Sdeveloped. The pubic hair was Tanner II, mostly around
# r, f1 }+ z% ]- }* w, M5409 ^. a" {9 n7 s; @) A4 N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 `7 o0 |/ W6 @) fthe base of the phallus and was dark and curled. The+ c' t3 G, l! b  F& A: C
testicular volume was prepubertal at 2 mL each.
* |& \- q. ]! k' u( M! r3 r7 |( eThe skin was moist and smooth and somewhat
# s3 ?7 q/ d3 h( r# E: s9 ]oily. No axillary hair was noted. There were no
" j1 d0 t5 k( \+ W& |abnormal skin pigmentations or café-au-lait spots.
! l2 a9 j" l  F) @Neurologic evaluation showed deep tendon reflex 2+
" n: D- }- v- I. `bilateral and symmetrical. There was no suggestion
3 a7 B5 ~) V& N$ U6 B7 u0 yof papilledema.
9 x1 Q5 D% H, l9 I" B- yLaboratory Evaluation
) K' Q; i: n: F$ h7 ~2 A9 |3 lThe bone age was consistent with 28 months by
3 ]* m# j: x& H, ]6 ousing the standard of Greulich and Pyle at a chrono-
- P0 W0 K8 }4 @# D! ]8 W$ U6 Clogic age of 16 months (advanced).5 Chromosomal8 P8 u. K; @. y2 Z8 G: X& h
karyotype was 46XY. The thyroid function test# O' g" {+ c5 S7 I2 _+ v; t" \' ?' \
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
2 y6 m" M( y$ b; dlating hormone level was 1.3 µIU/mL (both normal)." j+ \( t% I0 J* C2 S8 F3 d
The concentrations of serum electrolytes, blood
  h. S. [/ r9 M- f( N4 j3 Hurea nitrogen, creatinine, and calcium all were
3 o0 ]4 J8 u& Y4 y; W+ K8 Jwithin normal range for his age. The concentration3 [; V4 ^1 T! @7 R# d6 q2 A7 j, ~
of serum 17-hydroxyprogesterone was 16 ng/dL
" z1 b. v$ O! @! M& c7 l(normal, 3 to 90 ng/dL), androstenedione was 20- K3 Z3 h1 m. z7 w
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& M+ {- v' K" W" P4 mterone was 38 ng/dL (normal, 50 to 760 ng/dL),
. `: m, m% K4 ]% Q2 mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
. r$ T, R8 ~* Z49ng/dL), 11-desoxycortisol (specific compound S)
+ i3 X# B- r( e& r$ \2 t% B% i1 kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
% F: l  v% i) |' R! _  A9 O$ ?tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 L% u# T1 g0 y* h6 X4 R- ]testosterone was 60 ng/dL (normal <3 to 10 ng/dL),. ~: Z& D2 P& ~- U8 _1 i3 i8 X2 ^8 j3 v
and β-human chorionic gonadotropin was less than
7 ~/ T( @2 \, I) P2 z5 mIU/mL (normal <5 mIU/mL). Serum follicular1 x0 M! }( j0 N
stimulating hormone and leuteinizing hormone+ s* S  u6 j& s
concentrations were less than 0.05 mIU/mL; ^6 _. h4 W* y
(prepubertal).
" n; T/ ^( _9 o: ]% GThe parents were notified about the laboratory: \% q* V1 h+ _* ~4 {  K
results and were informed that all of the tests were
- s3 ~, G0 a# s- P4 r3 fnormal except the testosterone level was high. The( [+ h% i  b8 _0 v" I! _& y
follow-up visit was arranged within a few weeks to
( G* t1 S% D  S: M- Sobtain testicular and abdominal sonograms; how-
" H$ H: c& T" m. uever, the family did not return for 4 months.
" R  F. F( X% g, {% R& }Physical examination at this time revealed that the
4 O$ T5 ^6 e% p: ichild had grown 2.5 cm in 4 months and had gained6 q4 e0 z: C, m0 T7 F' t
2 kg of weight. Physical examination remained. u8 a  Z0 y  e
unchanged. Surprisingly, the pubic hair almost com-
# ^* W& I$ o# W1 g- {pletely disappeared except for a few vellous hairs at
7 w* S# B. z5 O4 }# n; F  pthe base of the phallus. Testicular volume was still 2
! G! C5 ?( m  M8 t# u0 t$ vmL, and the size of the penis remained unchanged.
: Y( R" i% }$ k. S1 `! \+ YThe mother also said that the boy was no longer hav-
! g. g1 g* R$ oing frequent erections.' i' r+ K7 @# k. s6 ~
Both parents were again questioned about use of( u$ d% U2 l; H1 z3 p" J
any ointment/creams that they may have applied to
8 X6 ~$ t' ^$ d. G/ W$ ?the child’s skin. This time the father admitted the
6 E6 F& L- n- h# h- z, Q2 x: ?, rTopical Testosterone Exposure / Bhowmick et al 541
& U) w! l0 L- |  {% K0 Cuse of testosterone gel twice daily that he was apply-
' s9 L/ [0 V1 o2 T0 Z- k* ~; Sing over his own shoulders, chest, and back area for
0 e* x  J8 x% q, ]a year. The father also revealed he was embarrassed
5 ]. j& N7 f% L) H/ k. U0 z% zto disclose that he was using a testosterone gel pre-3 o/ l4 }* F. m$ ^; R2 N
scribed by his family physician for decreased libido
* N2 S8 i3 g5 q/ |. }secondary to depression.
6 x% o" R% b3 ]5 Q9 f2 k" z- H1 nThe child slept in the same bed with parents.9 B$ p; X0 B9 }. l/ x
The father would hug the baby and hold him on his
  [6 T! {2 r1 J) mchest for a considerable period of time, causing sig-$ \- s% u; H2 ?4 U
nificant bare skin contact between baby and father.1 ~% o  m' T6 ], C) k- N
The father also admitted that after the phone call,3 l2 H1 q* W( u
when he learned the testosterone level in the baby2 ~/ I- u3 D: G9 p/ O/ G
was high, he then read the product information/ _7 ]$ J4 j9 O4 v
packet and concluded that it was most likely the rea-
  W( @* t- E- d+ }: ]son for the child’s virilization. At that time, they
( L  U% \+ `6 d% C0 pdecided to put the baby in a separate bed, and the
2 y# Z5 P& W" X- b9 v8 s' F+ _father was not hugging him with bare skin and had
# y4 X1 s$ x* J8 q  s, ]) p" Hbeen using protective clothing. A repeat testosterone* r. y, [0 X+ p8 ^, A  d  ~
test was ordered, but the family did not go to the
& j& a8 U: A" vlaboratory to obtain the test.: t  V( I9 G7 W$ \$ J2 T
Discussion
  A3 ^/ M+ Y. JPrecocious puberty in boys is defined as secondary) z6 \8 x- ~( e8 c% a# _
sexual development before 9 years of age.1,41 @* E& v0 ?9 |$ ~
Precocious puberty is termed as central (true) when( q& ~8 B4 w. v$ [8 x5 B; I
it is caused by the premature activation of hypo-/ t- F0 @0 n; i
thalamic pituitary gonadal axis. CPP is more com-
& x  l# A" n/ \6 v9 |5 q( e8 g5 p' X7 m9 gmon in girls than in boys.1,3 Most boys with CPP
2 A8 X) o+ }6 T' |9 x- u9 ]" |may have a central nervous system lesion that is' _1 |5 A/ W/ `$ T0 g8 Z4 k& ?
responsible for the early activation of the hypothal-) |4 _' [( u( U! i7 g) }, k
amic pituitary gonadal axis.1-3 Thus, greater empha-+ R1 N" A" X/ m& j
sis has been given to neuroradiologic imaging in
9 L3 |8 k' ?! q) Hboys with precocious puberty. In addition to viril-" e1 {/ R9 O5 C! n) j
ization, the clinical hallmark of CPP is the symmet-
9 a& O6 }/ ~& Y; G9 ]3 e2 I% v1 G: frical testicular growth secondary to stimulation by
$ r" g; r6 g+ }; S, e1 M8 l% c4 Qgonadotropins.1,3
4 N. u' o7 E8 m/ D4 fGonadotropin-independent peripheral preco-
: [/ ?9 ]) H4 z0 Vcious puberty in boys also results from inappropriate
. Y0 N, v. t* c1 q' Nandrogenic stimulation from either endogenous or& Y8 w& ?: q, H  L, c
exogenous sources, nonpituitary gonadotropin stim-
1 q7 p+ U0 Y/ N9 e8 r) iulation, and rare activating mutations.3 Virilizing5 H" k. z6 i2 }. G7 M! B/ C
congenital adrenal hyperplasia producing excessive$ u; G% z) N& l2 e, t
adrenal androgens is a common cause of precocious( f# O' {# I. ~& w8 @
puberty in boys.3,4( v3 H  f! d8 _  z3 }
The most common form of congenital adrenal
7 r) A$ D2 R$ r( R. c: y7 ?1 }hyperplasia is the 21-hydroxylase enzyme deficiency.
+ V5 P. N( u9 @4 L7 X; h3 cThe 11-β hydroxylase deficiency may also result in, e! G9 o+ X2 E- i( F
excessive adrenal androgen production, and rarely,
1 }7 U5 E4 F3 h+ t/ B- han adrenal tumor may also cause adrenal androgen' C, J9 j3 u% H/ t4 y
excess.1,32 ^9 i8 j, z5 A. l( d" l7 ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 v2 Q3 a) q$ a+ Q- [542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
/ D+ ?* W1 O" }7 P7 {1 nA unique entity of male-limited gonadotropin-
9 Q: u; @0 z$ }' U) d4 z! J0 tindependent precocious puberty, which is also known
, c( F/ m3 s3 l& h$ Was testotoxicosis, may cause precocious puberty at a
) E  D+ ?9 U. W5 ^9 \8 Gvery young age. The physical findings in these boys0 Y$ A" B! T" r: p2 g
with this disorder are full pubertal development,
- {! G% a7 o3 C8 v& j0 v- Nincluding bilateral testicular growth, similar to boys% {8 B( P' x& W' `( K, _
with CPP. The gonadotropin levels in this disorder0 k5 B# E3 s" d  a: W& T4 e
are suppressed to prepubertal levels and do not show$ T+ C3 e' R- N3 u" G5 k) `
pubertal response of gonadotropin after gonadotropin-* j5 a0 Q% E9 [0 v% B! w4 M
releasing hormone stimulation. This is a sex-linked
% J# T6 B, l' d0 \% c$ [autosomal dominant disorder that affects only$ X9 M* V, F' b4 y. Y
males; therefore, other male members of the family
& N! C7 j* B2 [8 N& ]3 Q" s3 ~may have similar precocious puberty.3' z8 e5 r9 J' p& I) }6 B
In our patient, physical examination was incon-; m/ n% s( ?% v3 R
sistent with true precocious puberty since his testi-
; E- w+ E: m3 {cles were prepubertal in size. However, testotoxicosis' y2 T9 k5 M: h) w: u
was in the differential diagnosis because his father; ^& h6 ^" ]0 C7 z4 p# F: R4 u1 W
started puberty somewhat early, and occasionally,; ?6 h+ I! n9 V1 d& d/ o
testicular enlargement is not that evident in the
( w" U$ X* A1 a) K0 F- lbeginning of this process.1 In the absence of a neg-
$ L  p3 v4 g. Y: H% e8 w* O  Kative initial history of androgen exposure, our
9 R; Z/ c, O8 _0 X) k' _+ p1 P- e- jbiggest concern was virilizing adrenal hyperplasia,3 ?! t; |# v; d5 [) p: T
either 21-hydroxylase deficiency or 11-β hydroxylase! Y: s) _( R4 f' E8 m% C4 p7 Y
deficiency. Those diagnoses were excluded by find-
( L+ M" v+ J0 w% U. Cing the normal level of adrenal steroids.% \. L' W4 \0 c# K
The diagnosis of exogenous androgens was strongly
% b. U  U3 ]" ~& Vsuspected in a follow-up visit after 4 months because) x/ S" d$ \0 X6 F7 ?
the physical examination revealed the complete disap-" ~9 A$ D+ J+ y% }1 q9 n# g
pearance of pubic hair, normal growth velocity, and
! D6 v# E/ O8 {' U1 O+ v8 V+ e% `decreased erections. The father admitted using a testos-
' C$ {2 G) `& j9 pterone gel, which he concealed at first visit. He was& Z" m7 w8 P$ Q0 {. M$ w
using it rather frequently, twice a day. The Physicians’
4 q2 G0 L  T: q. j- SDesk Reference, or package insert of this product, gel or5 g! O, N+ p+ l; o# X% n% s5 J% c
cream, cautions about dermal testosterone transfer to) a7 [, A5 v0 a+ c
unprotected females through direct skin exposure.
4 m: U# m8 w5 x# E# B# d  MSerum testosterone level was found to be 2 times the" i2 ~7 I6 H8 C+ ]# k
baseline value in those females who were exposed to
& n4 ^( z; F# j1 Neven 15 minutes of direct skin contact with their male
$ Q$ q6 {+ b; u- zpartners.6 However, when a shirt covered the applica-
; z: y3 _" X3 W0 c. \9 rtion site, this testosterone transfer was prevented.
) D& p9 O. |* h+ `Our patient’s testosterone level was 60 ng/mL,
1 R0 b. p  Z* z8 dwhich was clearly high. Some studies suggest that
, Q& a1 Q* Z0 ?/ K: I6 n& Rdermal conversion of testosterone to dihydrotestos-
; Q5 }. l: n9 E6 q: X4 x) }4 Qterone, which is a more potent metabolite, is more( r; P0 r. A( A( G. a: r$ t' a3 Y
active in young children exposed to testosterone
8 _7 \9 i& S+ l3 P! M! Z5 Sexogenously7; however, we did not measure a dihy-+ ]. M3 T( `  {* H
drotestosterone level in our patient. In addition to
( u& U! [& r# y' @# `/ m( Dvirilization, exposure to exogenous testosterone in* v& a4 E4 [8 r( L% w
children results in an increase in growth velocity and
! @( D1 }8 n7 x. padvanced bone age, as seen in our patient.
& i1 w4 y: R5 V8 F# FThe long-term effect of androgen exposure during
( p0 N8 h! E  A& }' e: N5 j9 qearly childhood on pubertal development and final
4 z( @4 L5 n) r  Dadult height are not fully known and always remain
9 f% _. Q' }" X& B8 Ba concern. Children treated with short-term testos-5 G, i/ y$ B% v6 Y" t- K( P+ R+ }  c
terone injection or topical androgen may exhibit some" D3 j+ W6 |" l  C% s, p
acceleration of the skeletal maturation; however, after
1 a' N. V, n0 Ucessation of treatment, the rate of bone maturation
  \* Q5 _& @$ b. d: E4 zdecelerates and gradually returns to normal.8,9
- `' C$ `7 o/ x+ cThere are conflicting reports and controversy
" ~9 b7 _0 b2 R* lover the effect of early androgen exposure on adult* Q7 L; g. y7 i6 O: ^; e
penile length.10,11 Some reports suggest subnormal  i7 Q$ b/ c( ^
adult penile length, apparently because of downreg-
2 _7 G  h: i2 W5 Hulation of androgen receptor number.10,12 However,. g& g; O" @' |4 ~
Sutherland et al13 did not find a correlation between7 x5 c6 J8 R( b) u& a" r4 a4 i
childhood testosterone exposure and reduced adult2 N3 G0 F- \4 L! G$ O. @0 p
penile length in clinical studies.+ j6 u" q5 C5 r& y3 P: p: ?
Nonetheless, we do not believe our patient is1 d  A- W$ r1 b- r1 ^  n
going to experience any of the untoward effects from7 ]: Z- i! E) r, ?1 w
testosterone exposure as mentioned earlier because3 B: U7 ^' u- t4 V" ^
the exposure was not for a prolonged period of time." T, B! o6 o3 {7 R% S* G* w
Although the bone age was advanced at the time of- Q; O6 k, {' y4 W; Y8 _
diagnosis, the child had a normal growth velocity at- v% t) w. t* i7 l! @; _; u5 c
the follow-up visit. It is hoped that his final adult
* [5 q$ e3 \- W; t2 mheight will not be affected.0 P' L# j; X9 }% k- j, Q
Although rarely reported, the widespread avail-
( r: R7 t+ h" j; tability of androgen products in our society may
0 f8 b3 U6 o$ d" F4 jindeed cause more virilization in male or female9 L* g+ n8 T5 n$ Z
children than one would realize. Exposure to andro-
' j. d; H2 ~' ?4 F4 T; A% Wgen products must be considered and specific ques-
; ]% [3 f3 C. s7 C9 Htioning about the use of a testosterone product or
+ v' k* l# U5 Z7 W# Wgel should be asked of the family members during5 i, {% k8 \0 N' t9 j/ J( Y, s; T3 N- j
the evaluation of any children who present with vir-" G4 N; m$ `' \% d7 _  M
ilization or peripheral precocious puberty. The diag-
# N7 q$ T: C2 n) Jnosis can be established by just a few tests and by3 ?- e5 l9 J" ^: ]6 Y
appropriate history. The inability to obtain such a% J- ?  p1 g; \7 D! \$ G+ Y. h' u4 l8 z
history, or failure to ask the specific questions, may2 s5 d& p1 p5 L( V7 I: s6 U6 `" X
result in extensive, unnecessary, and expensive' Z( K5 q1 B) G0 j$ Q
investigation. The primary care physician should be
8 y% t3 T7 H; z% Zaware of this fact, because most of these children6 \, V. N" e0 T$ }. o& F- k; i% [
may initially present in their practice. The Physicians’
' t0 T+ }4 s; ]$ c6 @4 yDesk Reference and package insert should also put a) `3 H+ S7 k! D  I; C. n4 x8 f
warning about the virilizing effect on a male or
& t) s. @5 T# @7 |/ zfemale child who might come in contact with some-
! D) x5 A3 O1 J( s0 Ione using any of these products.
8 _, [2 _4 x- f/ O- w5 e4 k/ W0 BReferences
8 W$ V& h) h8 K+ I: V+ K2 b9 A1. Styne DM. The testes: disorder of sexual differentiation9 z2 _' _* B/ R  ~( G% v
and puberty in the male. In: Sperling MA, ed. Pediatric
& l3 W& G6 G$ W% U9 nEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
% L( z, n2 ~) j3 q6 o2002: 565-628.' }  A5 Q0 F) v' m+ S! A
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* g+ B, Q7 N6 L
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old% w+ v9 l/ m  b$ z; c6 d
Boy Induced by Indirect Topical
- E" _* ?% N6 P0 }0 C* K( EExposure to Testosterone2 [0 G; `$ h* ?0 i6 R' y
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 ]* g! c) h# d7 j  B% d5 c0 Nand Kenneth R. Rettig, MD1/ z. z$ f$ l6 E' v9 L; T- S8 d
Clinical Pediatrics
8 Y4 U6 Q5 |5 kVolume 46 Number 6
' [  o" I% G( o8 P: m: F2 VJuly 2007 540-543
+ F1 y( k4 `% @© 2007 Sage Publications  l- L9 [5 a' H2 l
10.1177/0009922806296651
1 l2 G- f: N$ }; ?; l- shttp://clp.sagepub.com3 N" r$ ^% }9 D
hosted at' F- x6 A4 t# e7 S* \/ H" p
http://online.sagepub.com1 o/ a% {2 V! j9 J( a' C$ m! C8 ?* p3 ]
Precocious puberty in boys, central or peripheral,
; T: e' ?- H5 y& }  lis a significant concern for physicians. Central
* Z% V% N# @$ t, j) x! Eprecocious puberty (CPP), which is mediated7 n9 e, \5 @' F" `5 e, Q
through the hypothalamic pituitary gonadal axis, has
9 l4 b: _) D' }a higher incidence of organic central nervous system0 i$ l* c2 V  c: u7 B4 m
lesions in boys.1,2 Virilization in boys, as manifested
' d5 L$ o& s3 _9 V. Y3 Hby enlargement of the penis, development of pubic
( y2 c7 p0 R# g4 c+ ?hair, and facial acne without enlargement of testi-4 Y. g- z5 W! s* y9 K
cles, suggests peripheral or pseudopuberty.1-3 We
) r+ Q7 J& m8 I1 Freport a 16-month-old boy who presented with the
1 k' u! L, a2 Lenlargement of the phallus and pubic hair develop-
6 b5 A% x9 \  `! Yment without testicular enlargement, which was due
6 X( [. R4 q% G  V& J4 xto the unintentional exposure to androgen gel used by  z( z9 ]0 |/ C. I$ C& d
the father. The family initially concealed this infor-8 `  j0 M  ]9 X1 f4 l
mation, resulting in an extensive work-up for this
% U4 F) ?+ E! `( W- O* q% achild. Given the widespread and easy availability of" b$ p( y3 X4 |
testosterone gel and cream, we believe this is proba-5 v( R6 @# f1 v
bly more common than the rare case report in the! Q! n3 F5 b) Z. W. B
literature.49 p: a; M% J6 i& ]4 a7 M
Patient Report
" B! w3 o7 Y0 T* o" e  ]A 16-month-old white child was referred to the1 d" }" W- J7 c
endocrine clinic by his pediatrician with the concern
  F" e$ y8 X5 R: L2 Bof early sexual development. His mother noticed
1 d: Y4 ?, ^- Z3 g2 t6 wlight colored pubic hair development when he was
9 M* x. z" X* I2 P" a  u& g/ _3 ?From the 1Division of Pediatric Endocrinology, 2University of
& N/ o) Z6 f6 }- h1 h2 iSouth Alabama Medical Center, Mobile, Alabama.
/ g: @8 Z( e8 ?+ a- J, QAddress correspondence to: Samar K. Bhowmick, MD, FACE,
& Z7 E/ o* ^: V4 t. ~Professor of Pediatrics, University of South Alabama, College of- H& }( H9 v) P) @) g- j
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# B5 k& M1 {4 @* I' be-mail: [email protected].
% k7 O: z6 Q$ ~' {about 6 to 7 months old, which progressively became& w1 p: N+ X/ ]( L
darker. She was also concerned about the enlarge-1 b- t( n% q; \7 i2 T& H
ment of his penis and frequent erections. The child
, o% s1 a: B6 _2 L3 ~  G: U2 iwas the product of a full-term normal delivery, with
8 B2 x- p6 H: s+ F, K6 N7 L. ~9 ?9 fa birth weight of 7 lb 14 oz, and birth length of: `& O" m1 w* Z5 j# s$ ^
20 inches. He was breast-fed throughout the first year
+ s" I3 Q* |2 }- M( [2 Fof life and was still receiving breast milk along with
" l. s- n  q" G$ L  i" Usolid food. He had no hospitalizations or surgery,
+ j/ @9 F7 F4 z* S( U4 Y1 P" Sand his psychosocial and psychomotor development9 q3 |6 [% l0 Q$ L6 E; v
was age appropriate.6 _8 a9 }. C1 A1 v6 f) F! E
The family history was remarkable for the father,
0 D4 L& ]. B( U2 D* `* Xwho was diagnosed with hypothyroidism at age 16,
% n) r. ]5 m6 Q$ cwhich was treated with thyroxine. The father’s
$ f. a5 m' z. jheight was 6 feet, and he went through a somewhat
, o* v, `8 J& I3 C* ]" oearly puberty and had stopped growing by age 14.  ]" A  \* `, v4 A% D/ ?  V: {
The father denied taking any other medication. The, e# ?6 t: i8 N# s7 U8 a5 H
child’s mother was in good health. Her menarche5 A6 v- z5 g' Q, i) ?9 |
was at 11 years of age, and her height was at 5 feet; I0 t3 j1 L6 b& x: j  Q
5 inches. There was no other family history of pre-
" A4 ~' r7 J9 K! c( E, w+ Z% i9 Acocious sexual development in the first-degree rela-
$ X6 W6 k! s/ f! u  H' Xtives. There were no siblings.* d& ]( z7 D! l, q0 }
Physical Examination) G# I- O1 q1 M5 D% `) K9 W1 }! U
The physical examination revealed a very active,, W+ o! t- d! d
playful, and healthy boy. The vital signs documented" _' _2 l% _' ~1 ]% W
a blood pressure of 85/50 mm Hg, his length was/ M" _7 M4 E! M" O
90 cm (>97th percentile), and his weight was 14.4 kg0 j( i3 S/ t) b" w* E4 T9 ^0 F, @
(also >97th percentile). The observed yearly growth( z& D: T% Q0 o
velocity was 30 cm (12 inches). The examination of: }5 k& f+ r0 t9 A9 y
the neck revealed no thyroid enlargement.
1 v/ p* k' `3 k9 mThe genitourinary examination was remarkable for% h  N2 K% W" E8 c( J$ e
enlargement of the penis, with a stretched length of+ G+ d$ O, ~' O; a  }5 d: C# h/ ]
8 cm and a width of 2 cm. The glans penis was very well
- A( m4 i. M% A) K0 b+ kdeveloped. The pubic hair was Tanner II, mostly around! F6 u" q* E, S' q2 c
540
9 I5 v3 k: P! i2 `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from6 L- p, @+ `- C; G& P# p4 N( ]
the base of the phallus and was dark and curled. The/ \1 L) j/ F' g2 [( Z& W5 u6 B/ `
testicular volume was prepubertal at 2 mL each.0 j1 o0 a6 F! }8 C4 W- p
The skin was moist and smooth and somewhat
: \0 r1 q7 ?  E/ m; D( E; Ooily. No axillary hair was noted. There were no
* d  Z6 r7 o6 a0 k* Kabnormal skin pigmentations or café-au-lait spots.
7 W# r0 a0 i7 c9 Q# O' LNeurologic evaluation showed deep tendon reflex 2++ }6 S5 p6 A/ O% }  u# \. i
bilateral and symmetrical. There was no suggestion# D( m( F% V* w) O) s8 {/ k
of papilledema.
9 D: N" s! K* O; b: {% N" Z: _Laboratory Evaluation
: [! X2 e9 |. BThe bone age was consistent with 28 months by7 ~% y; J/ D1 w) Z$ a
using the standard of Greulich and Pyle at a chrono-
0 A1 _* S. N! p- n" Ilogic age of 16 months (advanced).5 Chromosomal
+ o7 t) J+ ~2 ^% skaryotype was 46XY. The thyroid function test
% P) m1 |5 i3 n6 V( U( ^+ V) |showed a free T4 of 1.69 ng/dL, and thyroid stimu-  W8 o3 ~' G( s9 [
lating hormone level was 1.3 µIU/mL (both normal).
2 x! h* ^! H6 N5 A3 {+ mThe concentrations of serum electrolytes, blood
+ f$ B! c" W% T, y% aurea nitrogen, creatinine, and calcium all were
: v  c% {0 s* U  G' l) W( }within normal range for his age. The concentration
. Y6 `/ d( z! Q/ _of serum 17-hydroxyprogesterone was 16 ng/dL" p4 q/ T$ m0 C
(normal, 3 to 90 ng/dL), androstenedione was 201 F( H3 O! O' O/ O
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& h/ B( Q% Y- x& k9 g2 B& oterone was 38 ng/dL (normal, 50 to 760 ng/dL),
" G/ B# {# k2 ]: _  r; E: ~: ]" cdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
  P8 ^% O+ [( h5 ~, A49ng/dL), 11-desoxycortisol (specific compound S)3 M, K' n8 T( P' ?
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: w  m! U7 z# V2 ]: atisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total& r/ o' s4 [* e# _# F. d) h0 e/ [  y
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ B. ?& t0 a, S) qand β-human chorionic gonadotropin was less than
1 l6 B' l5 E, W+ _$ t5 mIU/mL (normal <5 mIU/mL). Serum follicular
, |5 s8 }9 b6 jstimulating hormone and leuteinizing hormone) r# N- T6 o6 S% G
concentrations were less than 0.05 mIU/mL6 S2 c6 s* O5 P* b5 c
(prepubertal).
: L0 U, @9 m7 J6 ?% P7 LThe parents were notified about the laboratory
9 b; L8 w: }# F2 a* Uresults and were informed that all of the tests were+ c& a3 {. e  d" P# _9 Y% ^( x
normal except the testosterone level was high. The0 h- M. E. B/ ^( R; n1 B0 B
follow-up visit was arranged within a few weeks to
# O2 t4 f" u8 Y8 y4 iobtain testicular and abdominal sonograms; how-
6 v. f8 J) K) M7 _1 w7 Mever, the family did not return for 4 months.7 ?5 `0 X. }) k% w7 s6 s  t' D
Physical examination at this time revealed that the
; f$ S/ C1 O  M7 l1 c, I6 Ychild had grown 2.5 cm in 4 months and had gained
  e( [9 e9 m) _4 [2 kg of weight. Physical examination remained
% G: E$ x. M" yunchanged. Surprisingly, the pubic hair almost com-
; z/ J2 F) w, h3 N, Spletely disappeared except for a few vellous hairs at
  g1 v) ~$ L% s$ ithe base of the phallus. Testicular volume was still 2; @7 m) G5 U" k- Q
mL, and the size of the penis remained unchanged.
/ n5 I- j  Y. p. Y" MThe mother also said that the boy was no longer hav-
6 H( ]; f& Q1 @+ I& _: Q! f' C# Ming frequent erections.
( Q* `; }1 {6 H! E! RBoth parents were again questioned about use of
6 Q* q# U9 a4 j' I4 O7 _any ointment/creams that they may have applied to
0 d% ^/ R; Q5 J) rthe child’s skin. This time the father admitted the& Q# R) J* k9 Z$ q: T
Topical Testosterone Exposure / Bhowmick et al 541& Y2 S6 ~- `4 J' c
use of testosterone gel twice daily that he was apply-3 p  n  Z  s) ]+ R3 p+ R' W
ing over his own shoulders, chest, and back area for
. {6 h1 [, j+ F  {% R5 na year. The father also revealed he was embarrassed
) z0 e; t1 ]: O1 l! Hto disclose that he was using a testosterone gel pre-0 {. d' e9 d1 s& `6 x
scribed by his family physician for decreased libido, B- k: F0 F7 e8 J$ W, `' L5 L
secondary to depression.
8 D' @1 Q/ X, w+ ]$ r1 \# {The child slept in the same bed with parents.
. a9 m2 P) h5 F# ?" tThe father would hug the baby and hold him on his, R+ _4 e& ^0 s) f& N7 j
chest for a considerable period of time, causing sig-) r4 D: r% i4 y; W7 \0 T8 H; G
nificant bare skin contact between baby and father.
+ V4 J6 x/ }& o) {* _* g: RThe father also admitted that after the phone call,5 j% L" N0 o4 Z+ X1 ]6 h
when he learned the testosterone level in the baby5 [* p# M: f: O7 S  e( b/ y# K% N6 ?
was high, he then read the product information
5 p7 I% Y6 o8 ]$ L/ s( npacket and concluded that it was most likely the rea-# _0 P. p3 n7 Z+ r
son for the child’s virilization. At that time, they( V1 K' t& ]5 D% S
decided to put the baby in a separate bed, and the) J' y8 j7 U: f) m: P
father was not hugging him with bare skin and had, }; _4 T9 T% C6 n! b: Q
been using protective clothing. A repeat testosterone
- S7 x9 }7 Q1 e- a7 K$ G- Utest was ordered, but the family did not go to the
) i/ Z2 i6 z4 E8 Z8 p! Alaboratory to obtain the test.3 w  d8 w1 [8 k
Discussion
3 R0 ?/ H# J! s; q3 l4 }. ^Precocious puberty in boys is defined as secondary" k% P, q7 d5 |
sexual development before 9 years of age.1,4. K- ~, P# M; X2 E  S+ `0 X
Precocious puberty is termed as central (true) when5 F0 z) a' `! H
it is caused by the premature activation of hypo-
+ Q/ f7 i3 \5 G1 Z& |' mthalamic pituitary gonadal axis. CPP is more com-
4 K( `( U- D2 w- S8 }mon in girls than in boys.1,3 Most boys with CPP  D. U; P+ h* ^( e0 |8 u6 h- V2 S
may have a central nervous system lesion that is
0 @& @, R* f% Y# r4 Wresponsible for the early activation of the hypothal-" `; n- J9 j1 R5 j: R3 j
amic pituitary gonadal axis.1-3 Thus, greater empha-
6 \( b+ m* ?3 X9 i% K- A" P* Lsis has been given to neuroradiologic imaging in6 M1 o2 C0 f$ H8 f
boys with precocious puberty. In addition to viril-! U8 M' v* G0 G% I
ization, the clinical hallmark of CPP is the symmet-
7 H2 Q5 h3 g7 z0 l3 Brical testicular growth secondary to stimulation by9 f3 c" N% w. r+ ^
gonadotropins.1,3( P1 @# [1 D: k& `7 O1 `( L
Gonadotropin-independent peripheral preco-
; ~' Y% Y& o- `- R' n1 O( k5 }; Icious puberty in boys also results from inappropriate( M( D, }. ^# ]- R; [% ]( h0 m
androgenic stimulation from either endogenous or
$ F( D. x. u+ M5 M5 S7 ~, Gexogenous sources, nonpituitary gonadotropin stim-
, P( V& W3 L, e/ G5 e$ zulation, and rare activating mutations.3 Virilizing
# E8 u3 A  c1 Z  ?congenital adrenal hyperplasia producing excessive9 l5 z3 O# e2 r7 Y- F" e& T
adrenal androgens is a common cause of precocious
/ X$ g* A4 s. Y& @puberty in boys.3,4$ C4 o0 o; E$ U9 _% s5 [
The most common form of congenital adrenal- |5 Z5 t/ Z( L& \4 h1 y
hyperplasia is the 21-hydroxylase enzyme deficiency.# Q. H3 \, d$ E& p
The 11-β hydroxylase deficiency may also result in
* P6 h2 a  x, Xexcessive adrenal androgen production, and rarely,
9 j; d; n  W, t8 e3 l, n$ I, ^an adrenal tumor may also cause adrenal androgen
; e; U: w; W( ]" u5 {6 Z- X4 L/ Sexcess.1,3
2 p: P3 V3 b* d- j. `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 {1 _; d3 p) C542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
4 O4 e( _, h+ aA unique entity of male-limited gonadotropin-) w! u6 x4 i* G- F, q9 o; v, H0 Z
independent precocious puberty, which is also known/ A& Q( z, W# ?
as testotoxicosis, may cause precocious puberty at a7 P, F1 o: G8 L" \
very young age. The physical findings in these boys; D+ Y* F: ]* p9 D  d
with this disorder are full pubertal development,
( Y+ \5 P& \$ q# @- i" c2 `  y8 bincluding bilateral testicular growth, similar to boys
# g+ Q$ a7 t& Qwith CPP. The gonadotropin levels in this disorder
$ q3 p6 `5 T+ i+ Nare suppressed to prepubertal levels and do not show& N5 q) B# t" W8 u; G
pubertal response of gonadotropin after gonadotropin-$ a" N9 _% e+ k6 a# R
releasing hormone stimulation. This is a sex-linked7 E" Q2 e! G2 n" L1 p
autosomal dominant disorder that affects only5 `2 q! K2 R& X9 w/ s
males; therefore, other male members of the family
2 z* S; _  J4 F" rmay have similar precocious puberty.3
" x3 O+ W' y% d+ p# bIn our patient, physical examination was incon-# M% |+ |8 N" u) w3 Q: @
sistent with true precocious puberty since his testi-
) \. y8 K: d; a$ Z+ jcles were prepubertal in size. However, testotoxicosis
& k0 S! ~* v  E/ m5 i# ewas in the differential diagnosis because his father
$ m/ |, d9 G4 m5 istarted puberty somewhat early, and occasionally,
% X* d' r: \5 S( T" ?3 Gtesticular enlargement is not that evident in the& N$ D( j' y5 @
beginning of this process.1 In the absence of a neg-6 U7 D6 B" _5 d' d* X
ative initial history of androgen exposure, our) d; V7 S3 L; f7 Y2 ^
biggest concern was virilizing adrenal hyperplasia,
1 ^9 ]; R' r) X4 J; q5 xeither 21-hydroxylase deficiency or 11-β hydroxylase
1 y. c0 R3 F! L0 ~; S) S# gdeficiency. Those diagnoses were excluded by find-4 D" t! a* U' v8 b6 }9 d2 G
ing the normal level of adrenal steroids.
' u/ W1 {8 Z. N' _8 e# t8 OThe diagnosis of exogenous androgens was strongly
  M% W! E. e% `  T( Z, tsuspected in a follow-up visit after 4 months because! A0 O2 m; J, ?$ Z
the physical examination revealed the complete disap-
) `9 c# W' [7 L$ k/ A, Gpearance of pubic hair, normal growth velocity, and7 F) R% M3 g7 a2 k
decreased erections. The father admitted using a testos-7 T$ ~+ O9 S1 ]1 h( g
terone gel, which he concealed at first visit. He was6 K  V' a2 u( m, y6 s
using it rather frequently, twice a day. The Physicians’: a2 T- H1 J# V* q( Q& [* a
Desk Reference, or package insert of this product, gel or/ ^; _9 X) A( N2 _
cream, cautions about dermal testosterone transfer to9 `8 e* Q4 z6 S5 |- _) d& V
unprotected females through direct skin exposure.
% a8 @0 a- ^6 USerum testosterone level was found to be 2 times the/ {4 {* B/ [+ |! [. Y' k4 \
baseline value in those females who were exposed to
) P( \3 ~0 o' d# Q" u3 _3 Xeven 15 minutes of direct skin contact with their male" W' c" K6 I( _
partners.6 However, when a shirt covered the applica-# Y6 G5 p3 A" {9 u  Q
tion site, this testosterone transfer was prevented.0 _; n: ?) A2 y7 r( v
Our patient’s testosterone level was 60 ng/mL,
: d+ @9 h1 Q; j- J' Xwhich was clearly high. Some studies suggest that
( L2 m, F& A  m" c0 qdermal conversion of testosterone to dihydrotestos-
6 o. g% M  a' h& [  N# rterone, which is a more potent metabolite, is more
0 [/ H. d* z" l+ ~active in young children exposed to testosterone
/ ]4 n3 Y& t/ [5 u0 `exogenously7; however, we did not measure a dihy-
7 ?- }" D0 i$ W; Ddrotestosterone level in our patient. In addition to
& a# ~! z3 m# |% F2 n2 i9 bvirilization, exposure to exogenous testosterone in
: h* c8 I' c5 b; \children results in an increase in growth velocity and
% v" v- i5 Q1 p% k- {7 w. i3 h8 }7 sadvanced bone age, as seen in our patient.
% ]& l& h" a- t8 t3 \6 Q2 WThe long-term effect of androgen exposure during
4 w) e; j/ M  j4 B, v) }5 xearly childhood on pubertal development and final
. e1 R, m2 k2 K6 T- n! X6 nadult height are not fully known and always remain3 x/ G% P- w' ^. Q) v) ^
a concern. Children treated with short-term testos-. J8 Z/ B7 j4 \/ i4 _+ M' L  \" ?2 L" x
terone injection or topical androgen may exhibit some" D7 l7 _4 z) |# [* \
acceleration of the skeletal maturation; however, after
+ `, R# S' d5 a4 g; m) f/ \cessation of treatment, the rate of bone maturation' l0 t3 e/ _7 }' `# t
decelerates and gradually returns to normal.8,93 C( ?7 B- x, {" j9 u; f, [
There are conflicting reports and controversy+ _- q+ c+ L3 B* ?
over the effect of early androgen exposure on adult' k: z% C. b5 ]4 x0 s
penile length.10,11 Some reports suggest subnormal
5 s3 `# K7 w' J! z3 radult penile length, apparently because of downreg-
5 T4 d; b( k4 W9 Y- G$ W! pulation of androgen receptor number.10,12 However,
7 L+ n! a4 I3 h7 x$ M. z5 i* r/ ASutherland et al13 did not find a correlation between8 {& a6 M0 x) Y) R3 T' G
childhood testosterone exposure and reduced adult
: R; G, K& h* ^% @9 npenile length in clinical studies.9 |: v6 \; R0 r8 E" k4 b+ Q
Nonetheless, we do not believe our patient is% E  Z2 w( a" u! J8 }6 U
going to experience any of the untoward effects from* A% d. e0 Z$ a7 M, V, g
testosterone exposure as mentioned earlier because! r% u: U3 M2 W. D* ?2 X+ v
the exposure was not for a prolonged period of time.
3 z' Z! ^5 g5 c# }% a( p! NAlthough the bone age was advanced at the time of2 |) _4 r1 m; e  x8 N( b/ w: {( z$ O
diagnosis, the child had a normal growth velocity at" q$ _# `# ?% X
the follow-up visit. It is hoped that his final adult
* h+ n  z7 ^- t4 ]' x4 l# Sheight will not be affected.
& {3 M0 O$ v. w: ^/ XAlthough rarely reported, the widespread avail-
& Y8 w3 r( U8 d1 K% k  V; C5 g1 Aability of androgen products in our society may9 b3 n) }) t+ O3 P" }) R. m/ ^
indeed cause more virilization in male or female
8 ?' A6 U/ R: zchildren than one would realize. Exposure to andro-- V3 I2 q0 ]+ ^3 l0 _! A3 ^
gen products must be considered and specific ques-
' w: `, u. }4 Gtioning about the use of a testosterone product or+ N9 O# L' L5 P/ E5 h9 J
gel should be asked of the family members during$ w5 @. N7 R; }1 [7 ~! V! {
the evaluation of any children who present with vir-: ?* A: }- W' m6 h0 b
ilization or peripheral precocious puberty. The diag-
* [$ C- M: G) c# |& |+ fnosis can be established by just a few tests and by, }6 h, t* D. N& ?7 h4 x6 I
appropriate history. The inability to obtain such a5 n6 T/ }8 k0 J9 q
history, or failure to ask the specific questions, may/ z+ Z# y8 o  {9 ]; P* T6 ?$ g
result in extensive, unnecessary, and expensive8 U6 I( a' }0 F' X9 m$ Q: Z! R
investigation. The primary care physician should be* C0 `( }5 I* M/ n; B
aware of this fact, because most of these children& c6 r6 G" ]) d" k  \+ E" e
may initially present in their practice. The Physicians’: U. y$ i" m9 b0 B* R* i
Desk Reference and package insert should also put a
& ^( p; e" t% l/ p! Q1 f6 Fwarning about the virilizing effect on a male or
9 Z* {% S7 H% n' cfemale child who might come in contact with some-! A" M& `) f8 A- d+ s1 g# f  M6 Z
one using any of these products.3 ]9 W( l7 {8 g6 w( q( M5 U/ W: p
References
2 Y. Q3 H7 _+ Z2 k$ ~6 Z( n1. Styne DM. The testes: disorder of sexual differentiation
3 U1 a/ K, a. f& }  h. uand puberty in the male. In: Sperling MA, ed. Pediatric
9 F: ^6 @5 \6 p. e; |: n6 rEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
9 g( k$ N, ~8 i4 E) X5 U2002: 565-628.6 i! G* R+ N& T8 K3 |* w+ O
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* e, |$ J2 A+ p3 j+ `: m) h, Ypuberty in children with tumours of the suprasellar pineal
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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
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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
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
* s, ^! Z7 U9 _5 \. L! N. R: \& }
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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