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Sexual Precocity in a 16-Month-Old' M- l  B" x/ G/ f! ~+ e) d
Boy Induced by Indirect Topical* a$ J3 q' L  j3 d. m+ L$ m5 G
Exposure to Testosterone; q# {* R/ I2 W" W& a# X4 m
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
* M& @/ m& j  H7 F# sand Kenneth R. Rettig, MD1
9 t$ Q5 e! G" B: JClinical Pediatrics
% T4 t6 y: f  a* I$ \4 m% gVolume 46 Number 6+ R3 x% L: P- {* a6 G& z/ H
July 2007 540-543
4 E! t$ Z+ E: Q  I7 E1 M© 2007 Sage Publications% y! w, }" j/ |. D8 d
10.1177/0009922806296651
. h/ U  K( X6 O* G. d1 r3 Fhttp://clp.sagepub.com
; B9 ~# H6 d0 a8 \9 i  O# `! Dhosted at
, [  m7 n* V) E% Vhttp://online.sagepub.com0 Z: C$ k' I. V& i1 J$ q, f. Y# C
Precocious puberty in boys, central or peripheral,
6 M. ]0 |& J$ Pis a significant concern for physicians. Central
* |6 n/ ~! K8 L( Q) Mprecocious puberty (CPP), which is mediated
$ Y7 [9 `# i) t0 l+ P( q) g4 S( Athrough the hypothalamic pituitary gonadal axis, has# Y- x& j  Y# J
a higher incidence of organic central nervous system" e$ V9 Z0 \" A5 m/ G* n8 P: n( r
lesions in boys.1,2 Virilization in boys, as manifested
& H; ?2 V2 P; B) N1 b+ V2 Cby enlargement of the penis, development of pubic
: i$ B% k1 u2 O/ X: }hair, and facial acne without enlargement of testi-
6 Y5 N) y0 W0 y( b" H: i: ccles, suggests peripheral or pseudopuberty.1-3 We- Z, r+ g# e  b$ n
report a 16-month-old boy who presented with the! j8 P: L+ r6 k, B) F1 _
enlargement of the phallus and pubic hair develop-
, k" H9 `& n  Y/ q7 ]; Rment without testicular enlargement, which was due7 ~# z! B& ]3 t. E8 V9 a
to the unintentional exposure to androgen gel used by
3 R3 o; ~5 f  d% j, u  Qthe father. The family initially concealed this infor-: q& r" ~  H. [+ _; @3 h, J  H; h- n
mation, resulting in an extensive work-up for this
: r! S% _3 q1 x2 u* Schild. Given the widespread and easy availability of
8 ]3 j2 h0 l! E1 [) atestosterone gel and cream, we believe this is proba-0 q4 A% V' }+ k; K
bly more common than the rare case report in the, {) c* J2 X% Y6 M1 j. \
literature.4
5 J% b/ D; B$ qPatient Report! m" F8 t- H4 T+ E* i6 B9 R; |
A 16-month-old white child was referred to the' [: }; b7 w- ^9 n0 s- O0 y
endocrine clinic by his pediatrician with the concern- y5 l9 o  G) \: Z6 d( c# ?  E
of early sexual development. His mother noticed5 k, U" O/ W+ K
light colored pubic hair development when he was
+ T+ \7 e- g7 i! j9 EFrom the 1Division of Pediatric Endocrinology, 2University of' p% x- `, \9 O9 r! l% M; h7 N2 P
South Alabama Medical Center, Mobile, Alabama.( r, `8 q0 y6 Z" C, K. L
Address correspondence to: Samar K. Bhowmick, MD, FACE,( f9 y5 g5 [) F3 I
Professor of Pediatrics, University of South Alabama, College of9 z! c( _9 g1 x1 {* M8 S* N8 s* A
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;! b* z( W& \9 s
e-mail: [email protected].
) Z' `; ]% p. u9 o) Z1 ^2 @; labout 6 to 7 months old, which progressively became
& V/ o/ C2 t- Zdarker. She was also concerned about the enlarge-
3 |' N) `; E1 o* a$ U" B7 ~- N9 Fment of his penis and frequent erections. The child
1 E* @- A; \8 p  Xwas the product of a full-term normal delivery, with
# J( ]6 b; ]1 N+ J. |. ka birth weight of 7 lb 14 oz, and birth length of8 g) G) h: L3 w& N1 C- ]& Y, F5 f8 i6 t
20 inches. He was breast-fed throughout the first year
" R# y0 u$ u( ~; {* |of life and was still receiving breast milk along with
. X/ k9 V- U" G* \1 q5 Gsolid food. He had no hospitalizations or surgery,$ `& z0 |+ w% e
and his psychosocial and psychomotor development  n! k8 y% X( U2 }: x
was age appropriate.
3 `8 e" B! ]  V7 X8 \# s- O8 }The family history was remarkable for the father,
7 ^" u, d4 y* w) I0 d- V' iwho was diagnosed with hypothyroidism at age 16,' k2 K0 U8 u4 n3 j5 L
which was treated with thyroxine. The father’s
6 i8 H) Y3 D+ B: J7 V1 F% n9 vheight was 6 feet, and he went through a somewhat
& _: S: K* j' d$ n. hearly puberty and had stopped growing by age 14.$ s; k& g; H2 C0 n& |) z! L
The father denied taking any other medication. The
( R! U% K' |. m% Qchild’s mother was in good health. Her menarche
6 W8 c( A5 Z' q1 Kwas at 11 years of age, and her height was at 5 feet1 z( ^- X% R+ \
5 inches. There was no other family history of pre-6 _/ _/ |, F; A) r# {7 ]  H
cocious sexual development in the first-degree rela-
1 Y! F' q5 {+ `/ etives. There were no siblings.+ [. x  I  ^+ g
Physical Examination1 k$ `; T+ b) y$ D1 a
The physical examination revealed a very active,
& e- |% |* s( i+ M% J$ dplayful, and healthy boy. The vital signs documented; H4 y1 @: `: E$ O9 {
a blood pressure of 85/50 mm Hg, his length was( D8 V3 g% M3 @+ A$ ?' i( b1 A3 a
90 cm (>97th percentile), and his weight was 14.4 kg
& `- a& m5 M% Y1 K* b' J& T(also >97th percentile). The observed yearly growth
6 G8 i' g) Q7 g  T: d: N# H. ivelocity was 30 cm (12 inches). The examination of' z8 s& m: T# O9 ?9 n
the neck revealed no thyroid enlargement.
) j7 m: m$ _1 ]& @% R* n, N3 d- }% X: v% zThe genitourinary examination was remarkable for( T- b; U6 B! y( D. _
enlargement of the penis, with a stretched length of" g  b- Z8 X0 O4 X
8 cm and a width of 2 cm. The glans penis was very well& n5 r8 `- z; y. A! A
developed. The pubic hair was Tanner II, mostly around8 h# f$ r5 {9 B; t4 U; N
540! ~# ]8 Z( Y' b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 E, t, E) ?  p
the base of the phallus and was dark and curled. The: ]) f; a. m" q3 `: ]6 v
testicular volume was prepubertal at 2 mL each.
* {5 K8 o8 E6 p/ B1 WThe skin was moist and smooth and somewhat
- U: m3 r& G. i6 U; Koily. No axillary hair was noted. There were no
7 u( F4 c' T  i. j- G5 y2 }abnormal skin pigmentations or café-au-lait spots.8 z8 \  n) N8 V3 L* D) Y2 R
Neurologic evaluation showed deep tendon reflex 2+
! T' |9 I# d+ p6 {/ Tbilateral and symmetrical. There was no suggestion
5 ~/ [' e3 F) u) {7 p3 C) bof papilledema.
9 a7 W0 V4 A4 u- Q0 N0 [Laboratory Evaluation
% T8 M& ]8 V* T. J9 nThe bone age was consistent with 28 months by
8 Y# n  m( G- P) h. I" w8 Lusing the standard of Greulich and Pyle at a chrono-
) }% r, [' R" s5 p( s, Z6 Klogic age of 16 months (advanced).5 Chromosomal
5 d' t6 S2 C# O% y* pkaryotype was 46XY. The thyroid function test
' p, t; r7 L! z; a0 U' nshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
# @* H+ M1 [8 |* O9 L5 clating hormone level was 1.3 µIU/mL (both normal).
* v9 @  x  W# C# |3 yThe concentrations of serum electrolytes, blood: E: u% y, x- @: _) K3 c0 W
urea nitrogen, creatinine, and calcium all were
5 C3 b; c; I/ M8 Vwithin normal range for his age. The concentration
* S, h; l# n. R# Xof serum 17-hydroxyprogesterone was 16 ng/dL0 z2 D& B, `& L9 }
(normal, 3 to 90 ng/dL), androstenedione was 20. l+ p. G7 g7 ^' v% R6 ?9 G% m' m
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 `3 D8 x' a" D; F% ]  f
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
' k' o6 s7 c: @3 `, ^desoxycorticosterone was 4.3 ng/dL (normal, 7 to
$ n" M# V1 u" z4 M  h; y& h49ng/dL), 11-desoxycortisol (specific compound S)% A, C( M; _) S6 `1 b! k- \
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
) D# v" j3 h: o0 Y$ }tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
6 f, q9 p& y" U4 s5 i: {( }testosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 H0 Q0 J- D# b, n
and β-human chorionic gonadotropin was less than1 Z# p  r; S" w1 y/ M4 P3 U0 `2 Z
5 mIU/mL (normal <5 mIU/mL). Serum follicular
% C9 i1 q% b9 x3 x6 d* fstimulating hormone and leuteinizing hormone
  {4 o- @$ j+ @1 A5 F4 zconcentrations were less than 0.05 mIU/mL7 g: Q& \% U; U1 u. s! T9 {0 `3 P
(prepubertal).
# y! r+ m$ ?0 V* D# q/ i' H  L& MThe parents were notified about the laboratory; {; |7 X' L+ j! @5 b8 `
results and were informed that all of the tests were
+ R+ ]+ F/ h, |normal except the testosterone level was high. The; o7 U& f% B+ F4 R5 Z: ~
follow-up visit was arranged within a few weeks to
0 Y  s5 O) N  i; f, i, w! jobtain testicular and abdominal sonograms; how-5 m* `  Q: _$ B) h8 P' U1 e% q
ever, the family did not return for 4 months.& |7 p) C- U/ L- }7 u
Physical examination at this time revealed that the; E& Z6 S) N) x* M; \3 b
child had grown 2.5 cm in 4 months and had gained7 ~* W9 Y( e% ?5 t) B8 S
2 kg of weight. Physical examination remained
$ S" Z$ w! w8 Y* Runchanged. Surprisingly, the pubic hair almost com-% E9 V3 {5 C" P
pletely disappeared except for a few vellous hairs at
+ r5 F9 T  Y) l$ B7 g5 Hthe base of the phallus. Testicular volume was still 29 B! M6 M% u- j+ ^3 L. G5 H
mL, and the size of the penis remained unchanged.; T( s8 B  h+ N  D% c' ]) ^
The mother also said that the boy was no longer hav-
' U& w, m1 @9 R  ]1 ?ing frequent erections.
, K4 w6 a9 H2 W- Z# y# JBoth parents were again questioned about use of/ P! N3 {0 n% w  @" [/ s4 k. Q* P
any ointment/creams that they may have applied to# H6 p2 _2 u: R2 s, o5 z
the child’s skin. This time the father admitted the
9 j6 l2 i, q- `' ^$ o0 |1 k  @Topical Testosterone Exposure / Bhowmick et al 541
  i0 O& q4 C0 Y6 h1 S2 {! e* kuse of testosterone gel twice daily that he was apply-
" Q6 l' x6 @* m  x3 y3 g% \ing over his own shoulders, chest, and back area for
% }. M' `5 R! r- ]# y+ Oa year. The father also revealed he was embarrassed
8 i5 k  ~- L0 v; r( j6 ]4 uto disclose that he was using a testosterone gel pre-
4 l& a, g6 F* ~! j+ ?scribed by his family physician for decreased libido
9 {. h4 ?. l+ l! L" q8 n* U7 Rsecondary to depression.
- a0 V0 b' z5 _# g1 g% \; UThe child slept in the same bed with parents.' T( u5 [( ]6 H8 Y' ?* O
The father would hug the baby and hold him on his
0 H1 N2 a1 j. f8 S2 n5 @5 Dchest for a considerable period of time, causing sig-/ e0 s! Q: r" `3 N$ L& ?) R7 v4 l
nificant bare skin contact between baby and father.
# D9 K, ?  w# K& T) P* yThe father also admitted that after the phone call,
+ w3 s( A, g  D6 ?when he learned the testosterone level in the baby
$ A6 ^2 F" q0 L" h" T# owas high, he then read the product information# s+ R8 P, U0 l8 J' ]& s
packet and concluded that it was most likely the rea-" \$ e% {: _3 _/ p" j' T( s
son for the child’s virilization. At that time, they# _* l( D4 c& a0 }' O/ `
decided to put the baby in a separate bed, and the: m; @7 m! R1 x1 Z4 |* A
father was not hugging him with bare skin and had1 c. S. E* p- c7 N0 F
been using protective clothing. A repeat testosterone
1 ~, E3 _! {/ xtest was ordered, but the family did not go to the  T. i0 ^7 b) _. A) u+ h3 ~! S
laboratory to obtain the test.3 |" ~/ a8 b0 O( S
Discussion
1 x$ u  `6 y% |. y% c' w. tPrecocious puberty in boys is defined as secondary3 f0 ^# L* [5 E1 v- z
sexual development before 9 years of age.1,4
3 G+ w0 X" r/ jPrecocious puberty is termed as central (true) when
% A) G2 }& |  b6 i3 qit is caused by the premature activation of hypo-* J6 `5 ~! i6 P9 u
thalamic pituitary gonadal axis. CPP is more com-; `& l1 ?$ H7 n- o( D/ w
mon in girls than in boys.1,3 Most boys with CPP( `3 b' N5 a* u$ @( \% G
may have a central nervous system lesion that is
: z6 b4 D/ d* z+ sresponsible for the early activation of the hypothal-1 F2 p1 y" M# o0 c8 e+ W
amic pituitary gonadal axis.1-3 Thus, greater empha-
, a: h1 l- d4 Bsis has been given to neuroradiologic imaging in
  I2 X& r* v8 t  ~/ _boys with precocious puberty. In addition to viril-
% M- @! i3 [3 o. u' t3 b$ q8 vization, the clinical hallmark of CPP is the symmet-
5 F3 t5 ^# f0 w3 t& Q) |: Jrical testicular growth secondary to stimulation by, K1 O# T1 X8 D# n) Y
gonadotropins.1,3; [( H) ~, Q; O& E2 @6 W
Gonadotropin-independent peripheral preco-
  ^7 ~* |+ _) j% n% t+ F( ?% [" p) ^cious puberty in boys also results from inappropriate0 P! _4 R: G! e/ ]3 g
androgenic stimulation from either endogenous or+ u' l$ c3 G0 b6 {4 q# R2 y
exogenous sources, nonpituitary gonadotropin stim-
* U( d- b/ e6 q% ?8 aulation, and rare activating mutations.3 Virilizing- i0 ^3 S! \! @2 B* T: K
congenital adrenal hyperplasia producing excessive
# @3 x  c/ t' x2 t! ~, R: qadrenal androgens is a common cause of precocious
, ?. g) z0 ?- O0 G2 d, bpuberty in boys.3,4) o2 d6 b+ ?+ h! a2 w- u) a
The most common form of congenital adrenal. X) X. X7 a1 G  @, @& x3 e
hyperplasia is the 21-hydroxylase enzyme deficiency.
6 }; O$ m2 M# O$ t; oThe 11-β hydroxylase deficiency may also result in
+ D) t0 m- x/ C0 s$ h& W) xexcessive adrenal androgen production, and rarely,. s, o- m8 L) l# @
an adrenal tumor may also cause adrenal androgen' G. a# K4 |) a& e$ D9 V# ?
excess.1,3
2 z, H7 c7 |0 M# x; {at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( a5 g+ Z0 U" ^% C9 s! S542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
1 B0 _& ^* n. d% nA unique entity of male-limited gonadotropin-+ e5 F& R# ]% l2 t3 d, w) F: ]
independent precocious puberty, which is also known( y: M8 \7 t, i+ L( {
as testotoxicosis, may cause precocious puberty at a
* A! Q. G8 E+ i0 T# o) Avery young age. The physical findings in these boys4 U3 U& t! }1 r) w
with this disorder are full pubertal development,. K0 ~- i! q- H' _. Z, q7 w# Q8 X% b
including bilateral testicular growth, similar to boys' ]1 q+ h* e+ ]3 w2 R
with CPP. The gonadotropin levels in this disorder
( @8 o0 ?& Y" o5 Pare suppressed to prepubertal levels and do not show
& q  x1 K2 P6 o/ j& Jpubertal response of gonadotropin after gonadotropin-; [1 i7 w; l0 \! |
releasing hormone stimulation. This is a sex-linked
* I* r& f1 M$ mautosomal dominant disorder that affects only
, L, \3 B! u+ o1 W' `2 S5 Pmales; therefore, other male members of the family
- {2 K; S; u) [* y7 E1 Emay have similar precocious puberty.3
1 ?  n$ x' T, N& B, vIn our patient, physical examination was incon-
1 O6 d% O" {0 d5 C' ssistent with true precocious puberty since his testi-
/ p2 V6 _9 T7 t1 z+ tcles were prepubertal in size. However, testotoxicosis
. h/ X+ p7 M" [4 Uwas in the differential diagnosis because his father& H7 h) }+ h& \" N  q' `
started puberty somewhat early, and occasionally,/ U: R! H, s# x; C
testicular enlargement is not that evident in the& \- L: ?$ |" K2 f
beginning of this process.1 In the absence of a neg-. M/ Z4 M5 ]5 D
ative initial history of androgen exposure, our) V+ S% t4 O; _2 s0 t* l
biggest concern was virilizing adrenal hyperplasia,* @1 `) s! {+ C$ b
either 21-hydroxylase deficiency or 11-β hydroxylase% z; |9 q" u: R* n
deficiency. Those diagnoses were excluded by find-; L- y5 z; V& N& S, X# k
ing the normal level of adrenal steroids./ M2 o+ A- @& {; S0 o
The diagnosis of exogenous androgens was strongly& m9 m8 B1 ?4 t2 J7 G
suspected in a follow-up visit after 4 months because3 K' B8 V0 Y+ ?; \; I- G
the physical examination revealed the complete disap-
# D3 `1 N0 ]6 g) Z, f' q: ?3 Wpearance of pubic hair, normal growth velocity, and
/ X5 c% @$ S5 B0 N) rdecreased erections. The father admitted using a testos-
6 ~9 ^' j5 [; ?  ~4 ]terone gel, which he concealed at first visit. He was  |9 W" I6 L( N+ O4 _  ]
using it rather frequently, twice a day. The Physicians’3 w& e# d' s- D) d; a" j) m1 V
Desk Reference, or package insert of this product, gel or
6 [- m, p; S, }) h5 S. L  a& n, Rcream, cautions about dermal testosterone transfer to
. R8 H! l+ j3 }  L* {& K. sunprotected females through direct skin exposure.6 A8 O- r% h& Z" x8 @
Serum testosterone level was found to be 2 times the
* h! v) p. ~; r2 g1 J/ fbaseline value in those females who were exposed to
+ `7 _) f) e3 L+ q1 j" o( |even 15 minutes of direct skin contact with their male/ m( c+ P; ?8 p/ I# P# k" a" r
partners.6 However, when a shirt covered the applica-. E/ K. V0 z$ X( r6 B0 v
tion site, this testosterone transfer was prevented.3 e# ~) k' Z/ G& v1 R/ n! ^- d' W
Our patient’s testosterone level was 60 ng/mL,2 v! O; Y$ N/ U9 {% d* A" p
which was clearly high. Some studies suggest that" O1 a0 i4 V1 f# ~
dermal conversion of testosterone to dihydrotestos-
# W5 F& D  a  Rterone, which is a more potent metabolite, is more" O0 V3 `6 Y3 e" Q8 T% t3 Q
active in young children exposed to testosterone# C' g% K" i. u, d- _# O
exogenously7; however, we did not measure a dihy-
, e$ s( t5 F7 B" S; r& idrotestosterone level in our patient. In addition to
& L, \: c4 x& L. L7 A  \+ jvirilization, exposure to exogenous testosterone in
( ]8 V- X, a. X. X1 ^: W4 Q# w" xchildren results in an increase in growth velocity and
. e5 _' J' M9 ^( e* Padvanced bone age, as seen in our patient.
* c  i" v9 n  s+ }# b0 R6 UThe long-term effect of androgen exposure during
) ~7 H4 x. U% `3 Z. uearly childhood on pubertal development and final6 u) j6 H& J" ?
adult height are not fully known and always remain0 H' z& k+ E1 M6 R/ t
a concern. Children treated with short-term testos-* i  O' f" O+ v# e; u9 Z9 E0 {; k: F
terone injection or topical androgen may exhibit some3 }4 Y5 ~9 P6 U! {  T
acceleration of the skeletal maturation; however, after. Y; @# W2 A- A0 \
cessation of treatment, the rate of bone maturation1 \; h, u# N' B
decelerates and gradually returns to normal.8,9% W6 \; t  y! Y  p8 P$ X7 T  g
There are conflicting reports and controversy/ J( \( r3 `7 D. n/ [
over the effect of early androgen exposure on adult
; _$ I4 I0 C" E6 @) [4 xpenile length.10,11 Some reports suggest subnormal" u# l) O- @* ^, [* H
adult penile length, apparently because of downreg-
/ @, n8 S+ x' Rulation of androgen receptor number.10,12 However,
* Z* M, I  M3 b+ hSutherland et al13 did not find a correlation between
4 _& ]' d* l" V- d# h2 Nchildhood testosterone exposure and reduced adult- h/ L8 Q( |4 B5 d* g1 D
penile length in clinical studies.
" b/ I3 d/ U, I6 P! i% l6 XNonetheless, we do not believe our patient is
/ W* k+ p5 H' F3 z8 W) M, n4 \$ lgoing to experience any of the untoward effects from5 o0 O! \4 P" `$ S/ d
testosterone exposure as mentioned earlier because( y8 R. n, ^( Z
the exposure was not for a prolonged period of time.3 l7 q1 |) J' ^% e4 i! G4 F6 m
Although the bone age was advanced at the time of6 u* R/ \: E; f' P+ I1 o) S
diagnosis, the child had a normal growth velocity at
5 d" J( T- g; ^; q1 dthe follow-up visit. It is hoped that his final adult
; d6 P# W( `, o( d5 u, `5 P% g/ I$ K  sheight will not be affected.* _  o8 X( G3 n* Q
Although rarely reported, the widespread avail-' ]& d+ Y4 Z; Q; P- s( u6 y; W
ability of androgen products in our society may0 p+ F7 p1 [* J; D. X7 q3 m
indeed cause more virilization in male or female
" U5 B0 F# g+ ^2 B0 `children than one would realize. Exposure to andro-/ E- D$ ~4 G6 ^+ ?5 {% C1 ?
gen products must be considered and specific ques-
- n: \, X1 W# Z; gtioning about the use of a testosterone product or
/ C3 k/ L! w  A+ Kgel should be asked of the family members during1 {3 @# k0 K+ Q0 k
the evaluation of any children who present with vir-1 h$ V8 {: ~1 l  l8 e% H% p% S' ^% j
ilization or peripheral precocious puberty. The diag-
8 N0 I6 @) Y! K+ N& {$ Tnosis can be established by just a few tests and by, g# i! Y/ H) Z) ?
appropriate history. The inability to obtain such a0 _) t4 v* |# v, R
history, or failure to ask the specific questions, may5 |: u( J7 P* f' Z$ j- ]) J
result in extensive, unnecessary, and expensive" ^; p  k, Y. w/ X- O* p7 ^
investigation. The primary care physician should be, L. K( z* E  U
aware of this fact, because most of these children; q* Z& J1 \8 K  ~
may initially present in their practice. The Physicians’
& Z( }2 V9 ?3 e2 o- }" v/ m" ~: TDesk Reference and package insert should also put a
0 X& d) e- Q. x/ @: w3 {7 Ywarning about the virilizing effect on a male or
# |2 L. C" U! ^' |* _7 Zfemale child who might come in contact with some-
' \, K2 }% ~& p+ A' q, U7 aone using any of these products.' M6 G4 Z: `1 v5 u5 q
References
0 T! z* X2 H! X3 @9 s4 S; o1 k1. Styne DM. The testes: disorder of sexual differentiation
2 x7 ]( L3 Q- e+ e! x. o+ b& D; \* Land puberty in the male. In: Sperling MA, ed. Pediatric
$ h$ X. b; ]! ?3 D7 g3 `7 FEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
) ?8 g2 \3 l- _# [5 J2002: 565-628.
2 D* x6 Y" ^8 p/ L3 Y- F2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# U, _( ]0 O3 _4 t: R3 M# w
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old8 B% ]' A. J* z( ]+ E8 y
Boy Induced by Indirect Topical
% H; a6 c5 d- ^6 ?3 a6 m3 NExposure to Testosterone0 @0 h6 L' v: _) I' m7 u) c, o% R
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2- l) Z( W; p  R: g
and Kenneth R. Rettig, MD1
* @) z7 n5 f; c7 JClinical Pediatrics
, z9 v& C. Y& `( f0 cVolume 46 Number 6
1 T- {7 [7 z: L; {# TJuly 2007 540-543# o- a+ A1 z% j4 F3 z* O& O
© 2007 Sage Publications
9 o5 m, I0 u* w$ e) I- n: W10.1177/00099228062966513 V: e8 V% k$ O5 t  N' h( l2 r
http://clp.sagepub.com$ V# c  X# w! ?' W& n7 J1 K% {9 I
hosted at
: E6 P2 e. ?. W; \1 n8 xhttp://online.sagepub.com
9 O: z* h. |- d/ H  H  Z2 nPrecocious puberty in boys, central or peripheral,& A9 H) E5 \+ w) N/ F) Y
is a significant concern for physicians. Central
" N3 H6 i9 b- O* _% ]precocious puberty (CPP), which is mediated
9 X! b0 m' K" {! W  [2 o2 I# _through the hypothalamic pituitary gonadal axis, has
+ [4 T, A  Z# w) a: T9 v; V0 ca higher incidence of organic central nervous system
4 A/ g( g8 Y& t: X5 h, X( a/ qlesions in boys.1,2 Virilization in boys, as manifested9 D1 s/ T+ x; N+ Z. ~7 s3 [' q
by enlargement of the penis, development of pubic# y2 S$ F  i- e* `$ x% i! _
hair, and facial acne without enlargement of testi-
9 B# W, [0 P$ X  ?$ D6 Ocles, suggests peripheral or pseudopuberty.1-3 We/ r3 |% W% C6 l; c
report a 16-month-old boy who presented with the
; R# Z. f/ u2 I  yenlargement of the phallus and pubic hair develop-
% F# q: W/ O# [- w$ t) dment without testicular enlargement, which was due2 v4 R: S. T7 g# h* V" J
to the unintentional exposure to androgen gel used by" r$ |( p7 Y' k3 l/ }9 k3 S( G
the father. The family initially concealed this infor-
% y* {( P! d; R& m) }9 Bmation, resulting in an extensive work-up for this  H# r. I% b; Q: A4 b# J2 Z. a
child. Given the widespread and easy availability of
& w0 V0 P/ I. i$ P. ^* ?7 \testosterone gel and cream, we believe this is proba-) d( r( R; E# d: p5 ^# T2 a# [
bly more common than the rare case report in the0 A3 C( t( c: g0 @
literature.4
& u; z' w9 I  p# j! h3 S- i6 UPatient Report1 n% |# k' R" B$ }
A 16-month-old white child was referred to the* e. a9 L% m0 C
endocrine clinic by his pediatrician with the concern
7 W) d8 T) k3 f; Y6 G3 X8 }of early sexual development. His mother noticed
2 M: M& o3 @, mlight colored pubic hair development when he was
1 V4 k* s' t! X$ A: lFrom the 1Division of Pediatric Endocrinology, 2University of7 _  G, K0 L! [$ t, _; c! _
South Alabama Medical Center, Mobile, Alabama.
5 r9 M! F6 g. u5 F( @Address correspondence to: Samar K. Bhowmick, MD, FACE,  p+ F! R+ f2 n( U
Professor of Pediatrics, University of South Alabama, College of
7 ~4 ~4 y9 y( h( J/ _Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 u4 v; L9 S* Me-mail: [email protected].: c% w. e% t4 v6 Z
about 6 to 7 months old, which progressively became
# A# R/ c, {0 I/ b- Z+ l" T+ E8 Odarker. She was also concerned about the enlarge-# a2 E1 P7 _; A  \5 ?6 W5 B6 _# A
ment of his penis and frequent erections. The child
0 M* [9 D4 s. T$ S$ Q5 Nwas the product of a full-term normal delivery, with
- {% K2 v( U6 E1 j& S; \7 t5 P& C2 p  Wa birth weight of 7 lb 14 oz, and birth length of3 r/ E; t( o" S: ~  R% Q
20 inches. He was breast-fed throughout the first year4 p+ @, k9 l% ]$ O8 Y
of life and was still receiving breast milk along with
0 P3 K6 D# W$ m: t) Hsolid food. He had no hospitalizations or surgery,
- J: I) R- z3 X; yand his psychosocial and psychomotor development
2 @/ T. R* ~- H; q  Z! Owas age appropriate.- k5 X' D- u( N' o4 b8 Z/ s2 O6 W5 F
The family history was remarkable for the father,
$ K3 }, J6 c' C  Z* xwho was diagnosed with hypothyroidism at age 16,  o+ v- B9 x. P" c$ h7 ^; y
which was treated with thyroxine. The father’s" |& u7 `" Q% n/ m( Z* s
height was 6 feet, and he went through a somewhat: U- \/ y" w6 M  N$ k2 q' s
early puberty and had stopped growing by age 14.
4 A  g6 E+ ?% j, h( V1 s" ^The father denied taking any other medication. The. f/ x6 N% G% w% z- c+ t2 v3 c
child’s mother was in good health. Her menarche7 y- `( C7 e6 t* O. \- i
was at 11 years of age, and her height was at 5 feet
* D" J; k; G! M) e) F. I" [3 k5 inches. There was no other family history of pre-
+ `& R6 w0 w- x9 n- |. C5 h& Ococious sexual development in the first-degree rela-! e1 M" [# O. ~9 L
tives. There were no siblings.
: O" P; S  k+ y0 IPhysical Examination: F6 E0 q/ x3 g( y
The physical examination revealed a very active,
2 d0 b/ h; z8 H) [2 nplayful, and healthy boy. The vital signs documented
. D! F8 g* L, x  a  Ba blood pressure of 85/50 mm Hg, his length was# x, J1 V' g) `9 u- i
90 cm (>97th percentile), and his weight was 14.4 kg
9 @6 |0 p9 G/ q' S& L6 H0 Y, `$ [8 c' |(also >97th percentile). The observed yearly growth
" u$ ]( C/ ^/ |; T0 N3 A' v. m  hvelocity was 30 cm (12 inches). The examination of
" A9 M1 ]2 {/ j5 k# h+ ithe neck revealed no thyroid enlargement.
  D* i- }1 {$ D* T+ [The genitourinary examination was remarkable for! l3 {% g! N  M3 p0 G3 @
enlargement of the penis, with a stretched length of- |% ~- Y4 o* ?
8 cm and a width of 2 cm. The glans penis was very well" k. ^. r+ O( N' w. T6 Y% n) Z
developed. The pubic hair was Tanner II, mostly around
5 }" Q4 r# p( b& g( b1 X% b540" T* C. T' P. H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( x; e" @/ W; s' m  Kthe base of the phallus and was dark and curled. The5 G( h3 m  K6 ]/ f7 T* P% ^
testicular volume was prepubertal at 2 mL each.
& K4 s9 y2 V  I) Q6 OThe skin was moist and smooth and somewhat- ?9 {0 C8 C. ]" S
oily. No axillary hair was noted. There were no6 V& r( T1 h/ u* ~  j' L
abnormal skin pigmentations or café-au-lait spots.
9 J: K( y& @, n" N/ T) {Neurologic evaluation showed deep tendon reflex 2+3 d$ R; V/ Y6 u) x0 ]
bilateral and symmetrical. There was no suggestion
8 f! v) P5 B8 `1 i- Uof papilledema., ?1 @% A7 u, i& o: s1 P' X) Y
Laboratory Evaluation
$ n' |+ V8 J% _6 e2 U- D  [/ rThe bone age was consistent with 28 months by- s6 m0 J  U) A1 R+ @9 a4 r
using the standard of Greulich and Pyle at a chrono-0 w' |& \" w( [/ I
logic age of 16 months (advanced).5 Chromosomal
( s! r6 X, r: O6 g/ Okaryotype was 46XY. The thyroid function test
8 H$ C" Q' y  \! x; }: y" k1 Q! Xshowed a free T4 of 1.69 ng/dL, and thyroid stimu-* N) j8 C8 Y# o- K1 E$ P
lating hormone level was 1.3 µIU/mL (both normal).4 U, K" t% R/ y1 J8 i' ?8 S
The concentrations of serum electrolytes, blood
) c: }7 c) r7 x$ U- B! j2 }urea nitrogen, creatinine, and calcium all were( u# B6 L1 u0 R9 I8 E
within normal range for his age. The concentration
. ?' Z/ m) A- oof serum 17-hydroxyprogesterone was 16 ng/dL! ?" v: T' {! U7 ^+ a0 S
(normal, 3 to 90 ng/dL), androstenedione was 20
, Q  g7 P$ _! n4 Q% V7 Z; Q& H' g1 }ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-* X& Q3 `1 t. Q6 x% c
terone was 38 ng/dL (normal, 50 to 760 ng/dL),: \8 E2 C! a2 Z  G2 r# [% P
desoxycorticosterone was 4.3 ng/dL (normal, 7 to7 K; j7 ]8 t1 r9 A+ {6 U
49ng/dL), 11-desoxycortisol (specific compound S)
* P2 ^6 _- v5 N+ ?was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
9 f6 Y5 W6 v/ t8 ?% btisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
) G& e, L4 h# ^4 ?3 _3 Wtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),4 U* u( ^8 r( f' V3 d9 a
and β-human chorionic gonadotropin was less than0 g9 v! r5 u% ?4 \
5 mIU/mL (normal <5 mIU/mL). Serum follicular. F& G! Z  t7 y2 S& U
stimulating hormone and leuteinizing hormone
+ H) u+ l* {" d" o: o. Tconcentrations were less than 0.05 mIU/mL* f$ D0 v2 ^5 Q% x% X3 L
(prepubertal).
- l2 l* f4 u& M) K7 i& R/ r; _The parents were notified about the laboratory" Q4 N3 ~% W6 d6 q3 a; j1 j1 x& w
results and were informed that all of the tests were
! A+ }$ V: u+ Ynormal except the testosterone level was high. The/ x/ g8 _1 F$ d$ |. M% z2 J" F
follow-up visit was arranged within a few weeks to5 G& G) B5 @7 Y6 b4 C
obtain testicular and abdominal sonograms; how-* h. E8 V: v, Y# f7 u5 R) ^+ ?
ever, the family did not return for 4 months.
& N( i4 h5 @% d1 O" P$ ?0 _Physical examination at this time revealed that the+ m1 N! D7 l* a& A3 ^+ y, }9 s* S
child had grown 2.5 cm in 4 months and had gained
% P" l$ V4 l+ Y* W2 kg of weight. Physical examination remained4 |% b+ F2 \; R1 x& B) J
unchanged. Surprisingly, the pubic hair almost com-
( s1 |3 u( k! L& Opletely disappeared except for a few vellous hairs at
: w  |; E$ a+ D; zthe base of the phallus. Testicular volume was still 2' c9 u& p% H7 u( I
mL, and the size of the penis remained unchanged.
  @9 G" L5 K' IThe mother also said that the boy was no longer hav-
0 _) ]3 ?) n% A; h( |% |: `3 uing frequent erections.
% w4 @1 E- _: ?Both parents were again questioned about use of
0 N6 l2 v5 h# y1 c) Pany ointment/creams that they may have applied to
" p/ k1 @. n& Y0 n8 U$ ]the child’s skin. This time the father admitted the
4 b# W9 }$ w+ h4 x3 Z$ OTopical Testosterone Exposure / Bhowmick et al 5419 h) {1 p# ~2 f" G0 Z9 j0 p
use of testosterone gel twice daily that he was apply-
, A1 S0 A  t5 ?+ k  v- \* a$ I! m1 g* Ling over his own shoulders, chest, and back area for+ G. x8 g+ j6 }3 n+ E- W7 ]+ |8 ]
a year. The father also revealed he was embarrassed) O1 g' d" Z* C7 J7 I" U, I# l5 v; e
to disclose that he was using a testosterone gel pre-2 R1 k3 h+ o1 F% {; ?
scribed by his family physician for decreased libido
9 }7 l: f, Y1 n( t# O) msecondary to depression.
- C8 W. V4 [# x: R& ^The child slept in the same bed with parents.! Z/ S2 p' X& G5 i5 _4 w
The father would hug the baby and hold him on his$ W' Y5 Q0 ?. X( y# h0 y
chest for a considerable period of time, causing sig-/ o4 ]& a4 C" }) S+ h8 `
nificant bare skin contact between baby and father.: t' _% z, m) I9 j  }' B: H% j
The father also admitted that after the phone call,: m" f- `! A: S% o) d5 M
when he learned the testosterone level in the baby  y) @2 _9 n0 W( h/ x
was high, he then read the product information
8 F: O! y" H, xpacket and concluded that it was most likely the rea-
# |8 O% x2 K" X' M, u5 f: xson for the child’s virilization. At that time, they* Q/ B: p6 g6 c9 a6 Z2 ?% K
decided to put the baby in a separate bed, and the+ b/ }% v# o7 v7 A5 h
father was not hugging him with bare skin and had9 }$ ?5 S8 D$ U
been using protective clothing. A repeat testosterone
; b4 n' u- e& B( k* F5 j6 Ytest was ordered, but the family did not go to the  ~; L4 i9 ?% G
laboratory to obtain the test.
" C& I  T8 f( }0 K7 M0 |Discussion
0 O$ P! b2 x0 q  G% p- S# XPrecocious puberty in boys is defined as secondary0 S; [- q$ v: M8 H8 N0 F3 H9 ]* P0 O
sexual development before 9 years of age.1,4
' K) |9 X" o* {+ b! BPrecocious puberty is termed as central (true) when
# _. e5 m5 z; t" F4 Kit is caused by the premature activation of hypo-
6 {/ F3 S& x4 _thalamic pituitary gonadal axis. CPP is more com-
7 v! w( Y* p1 A: Omon in girls than in boys.1,3 Most boys with CPP
, k0 G1 o) e/ m- D2 l1 R2 lmay have a central nervous system lesion that is2 u) S* L- `* o# W+ I
responsible for the early activation of the hypothal-
9 s# ^7 P5 }' m! V2 Damic pituitary gonadal axis.1-3 Thus, greater empha-  y, k* q3 w: u) Z0 {% W
sis has been given to neuroradiologic imaging in
% Q2 M4 W' u, A8 F! r( gboys with precocious puberty. In addition to viril-. g( Y0 i4 R3 d' }
ization, the clinical hallmark of CPP is the symmet-1 t' E: R' i6 v  }$ L! N
rical testicular growth secondary to stimulation by2 Y! l( D& ]3 N  |4 o6 @* ^
gonadotropins.1,3
/ _, U0 }9 j  M2 aGonadotropin-independent peripheral preco-1 r4 l/ L. T% f- @! @( H' G
cious puberty in boys also results from inappropriate
" j' y' f  i; L: j: F3 ~4 z1 u5 Gandrogenic stimulation from either endogenous or
. F" s/ \- R; _# ~3 _4 e2 gexogenous sources, nonpituitary gonadotropin stim-* e* z0 o) i: G
ulation, and rare activating mutations.3 Virilizing( \; D4 e" u, g& ?2 S3 z: n! g
congenital adrenal hyperplasia producing excessive
  o/ `9 A9 ~2 k( L2 J# M  h6 ~* _adrenal androgens is a common cause of precocious, L( W3 O- X9 t' R5 y: ?
puberty in boys.3,4
( \% p0 ]5 H$ Y3 e+ N& [The most common form of congenital adrenal2 k' J, B- a& ^% t0 ^, U
hyperplasia is the 21-hydroxylase enzyme deficiency.$ P4 i* A( A/ u7 C
The 11-β hydroxylase deficiency may also result in
- c5 r2 y1 S$ g2 q" kexcessive adrenal androgen production, and rarely,
' T/ F* @2 y/ ^* K' ?# }& C9 ran adrenal tumor may also cause adrenal androgen. r# y( e7 j% I2 [1 ^
excess.1,3
5 K! [+ D2 f4 ?1 u; N% h* Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. ]& p$ h; @7 {4 w" B
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
* w' W5 M5 p) H% Q3 |) WA unique entity of male-limited gonadotropin-
( H: i- |( L" oindependent precocious puberty, which is also known$ f# x" ]% V& G/ j; j, B. V' E
as testotoxicosis, may cause precocious puberty at a
; i3 g" F! U* mvery young age. The physical findings in these boys. q& |7 j9 M" L2 h, X
with this disorder are full pubertal development,
  }0 E  U# V" D$ H- f/ tincluding bilateral testicular growth, similar to boys$ ?: k2 N4 p7 A, F) I
with CPP. The gonadotropin levels in this disorder
+ v, N/ c% e/ A+ H. e2 g' Dare suppressed to prepubertal levels and do not show/ v3 Z" f. R6 h# m6 D; `
pubertal response of gonadotropin after gonadotropin-
- \1 u7 E4 N6 l2 G2 f3 [releasing hormone stimulation. This is a sex-linked# [7 d. n, l, n( b" F* i& v4 \
autosomal dominant disorder that affects only+ f, i; E: e3 E( A2 `5 _0 q7 {, Y* @
males; therefore, other male members of the family9 h- o0 P4 l5 ]) }, I
may have similar precocious puberty.3/ _. n( Z  {* m* n
In our patient, physical examination was incon-
' K4 ~3 o# s  ]6 w5 ?2 T  ssistent with true precocious puberty since his testi-0 d1 I. E- n, p  \' k' Q
cles were prepubertal in size. However, testotoxicosis
" ?* G: k! ]; A1 Q9 L* g5 C( p) Lwas in the differential diagnosis because his father
. q1 P  w1 D1 e$ r7 j( l; f0 N# M5 Ystarted puberty somewhat early, and occasionally,. R  H. r- b6 s3 m
testicular enlargement is not that evident in the! N$ `' C* Z9 \- h$ |$ l% Z
beginning of this process.1 In the absence of a neg-
6 \( T- R  Y% g' s" A$ V/ p' yative initial history of androgen exposure, our
. N0 }( e/ K3 o" v1 gbiggest concern was virilizing adrenal hyperplasia,* x8 X2 V+ I" ^# A0 y. y2 _" R: |
either 21-hydroxylase deficiency or 11-β hydroxylase9 o+ I5 v- b. C( a
deficiency. Those diagnoses were excluded by find-
0 H9 N; f7 P3 S* B4 N# sing the normal level of adrenal steroids.
5 \* }9 }; c6 c8 R& x9 U7 TThe diagnosis of exogenous androgens was strongly
6 b$ H$ _' v0 O. C. P4 fsuspected in a follow-up visit after 4 months because1 S. d+ A; X3 ^- F' V* r
the physical examination revealed the complete disap-
) H' ]# n% F0 G$ m" I/ u1 Ipearance of pubic hair, normal growth velocity, and: [$ h0 L5 G# f& l  I: v
decreased erections. The father admitted using a testos-1 d0 G  X/ a& Z9 {7 g) ~
terone gel, which he concealed at first visit. He was
- o3 ?  I2 _+ wusing it rather frequently, twice a day. The Physicians’. W, P4 s9 }2 y$ R5 X
Desk Reference, or package insert of this product, gel or
# b  f0 W( ~0 w7 \* L% icream, cautions about dermal testosterone transfer to
/ x1 \5 x1 g6 X0 N! {5 u( r3 Kunprotected females through direct skin exposure.; G+ n5 O% p+ h. ~& H
Serum testosterone level was found to be 2 times the
$ @; W5 A7 @9 c4 H, C+ gbaseline value in those females who were exposed to
; j( t8 h' q6 V/ S7 @. A; W( z# Yeven 15 minutes of direct skin contact with their male
$ o5 I, Y9 _! Q; Ipartners.6 However, when a shirt covered the applica-$ z7 Q5 f; m* q# U/ t
tion site, this testosterone transfer was prevented.
) I6 g$ u* P, r( S  |; D) |/ l' @Our patient’s testosterone level was 60 ng/mL,6 N7 F+ N3 z1 i. @7 \- U2 `* p
which was clearly high. Some studies suggest that$ g+ `$ b4 F4 l2 Q; `% K1 M+ W
dermal conversion of testosterone to dihydrotestos-
7 V$ S% H0 o/ n: kterone, which is a more potent metabolite, is more
. S9 Y2 Q& @8 Y* y, aactive in young children exposed to testosterone3 Z; O. T: B% c2 j) ?$ }
exogenously7; however, we did not measure a dihy-
! v# T  i# v# ^/ W; m7 l$ cdrotestosterone level in our patient. In addition to
( g! E* g8 e+ V1 X5 u+ g2 r! T  U  ~virilization, exposure to exogenous testosterone in6 f$ I3 D" T5 |
children results in an increase in growth velocity and8 M6 ~3 r0 O  y+ o) o* U
advanced bone age, as seen in our patient.
) m, n' y) q) F( }; N- RThe long-term effect of androgen exposure during  B0 `# B/ f0 u
early childhood on pubertal development and final/ t! B. o& q" W- ], C# G2 L
adult height are not fully known and always remain
3 f+ u, b9 l( O% |3 u( f6 D5 ]a concern. Children treated with short-term testos-9 \& I4 x. T+ ]# m, l0 g
terone injection or topical androgen may exhibit some
: E: E) u. m( n' vacceleration of the skeletal maturation; however, after
0 p3 d/ v) F: M1 u' @3 h  w' F% gcessation of treatment, the rate of bone maturation
0 f: \! ]$ K4 k* E: U, \# p  u' i! Kdecelerates and gradually returns to normal.8,9. b9 D$ X7 |. s& O, T
There are conflicting reports and controversy. _, m. K* A8 k% u" I  Z0 x
over the effect of early androgen exposure on adult7 N% F  S/ ^/ ~5 X5 ?, |; E/ d( |
penile length.10,11 Some reports suggest subnormal
, I# R: C3 {" f, y6 k7 e% d! cadult penile length, apparently because of downreg-
. I" @3 ]& X( L+ W6 Gulation of androgen receptor number.10,12 However,  E4 h- q  e9 I2 P
Sutherland et al13 did not find a correlation between
6 m3 X( ?  K. T* o% kchildhood testosterone exposure and reduced adult; X- f, k8 ]' j! i! B5 I
penile length in clinical studies." \; b0 a. v# W! z" o! \/ T% R
Nonetheless, we do not believe our patient is
0 t9 q: C6 v1 j4 Cgoing to experience any of the untoward effects from6 o  C, p+ {1 L" p
testosterone exposure as mentioned earlier because
6 p) `( S9 e0 e2 r% T, ethe exposure was not for a prolonged period of time.
: g1 N3 u" J* xAlthough the bone age was advanced at the time of
- y' H6 i' C' }- R, ldiagnosis, the child had a normal growth velocity at
, @+ j; z! l  L) @: j, ~* Xthe follow-up visit. It is hoped that his final adult; x/ c1 t6 Q4 d2 b# g
height will not be affected.
2 M2 v7 e) q: {* `- j8 K& c0 jAlthough rarely reported, the widespread avail-
6 B9 K$ L3 v! ^ability of androgen products in our society may
7 o8 t; [1 L9 `+ y0 x" m" H7 Eindeed cause more virilization in male or female
1 [% B  G. d! m" G) N3 R, L& achildren than one would realize. Exposure to andro-$ n" x7 X1 C" @. \! X9 `
gen products must be considered and specific ques-
/ {+ e) }5 M: P( Btioning about the use of a testosterone product or
1 T) x" G* g8 Dgel should be asked of the family members during
  ?" T" p( A% @' Pthe evaluation of any children who present with vir-2 R5 E, c7 g/ T' F! O! j
ilization or peripheral precocious puberty. The diag-% G0 z- y# d- f
nosis can be established by just a few tests and by& Z/ z$ P8 F* i
appropriate history. The inability to obtain such a3 B# Q" z( H) I9 e: N
history, or failure to ask the specific questions, may7 |3 K# y- S; t# Y6 d
result in extensive, unnecessary, and expensive
" K8 Z& F& ~9 h. `$ R' c2 n5 Zinvestigation. The primary care physician should be
) t, c! D" @# ?/ d) n! z; _; _aware of this fact, because most of these children
8 y& [& \1 A% D5 N  Wmay initially present in their practice. The Physicians’
$ T1 I2 b) v* U8 E9 ~- F2 UDesk Reference and package insert should also put a. s5 k% v( g* ]% l6 N
warning about the virilizing effect on a male or
9 E0 k% ~0 \  e+ hfemale child who might come in contact with some-
4 G" a' ]+ W6 d5 s4 L8 Kone using any of these products.
9 O7 g# B, N+ y" a7 lReferences
" Q8 p# D$ p' p. j1 _1. Styne DM. The testes: disorder of sexual differentiation& f' ^3 Z" _, n/ j8 J% j
and puberty in the male. In: Sperling MA, ed. Pediatric7 L% Q; }" u$ `: w
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- S! I$ A; Y; n2 s7 T2002: 565-628.. c/ o& I/ C3 B3 a& J
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- y; \4 L! h7 K# ]: `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
  |) H9 q+ N- E2 e2 m/ I
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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