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Sexual Precocity in a 16-Month-Old1 j; K/ F8 v* o( e7 S/ @
Boy Induced by Indirect Topical. n3 n2 z2 O1 j! I1 M  k
Exposure to Testosterone5 p/ s+ ^: |8 k# C0 W
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ |: s. B4 B# t3 ~, zand Kenneth R. Rettig, MD11 n: U$ u/ M" }, b' ~/ s/ V
Clinical Pediatrics3 `* q3 W; ~- I: @4 B, P: ]0 ^
Volume 46 Number 6: [& H) t& R2 U8 S# b! ?
July 2007 540-543
9 N3 x0 @# a6 j3 S1 R6 J© 2007 Sage Publications! c2 W, v( G: j! B: b4 i6 n2 O0 \
10.1177/0009922806296651
0 O7 \/ A# B; h8 w" W! Qhttp://clp.sagepub.com' R) g) ]& m8 a  M
hosted at
* d3 X  n; x; b+ }# q9 a) B3 Shttp://online.sagepub.com
, u, h" B9 C3 o" L/ h# {! a4 R0 s# iPrecocious puberty in boys, central or peripheral,! {3 l, A0 b! p3 i' E; z
is a significant concern for physicians. Central& w+ A/ o5 `: w  C& v& x/ ]; G
precocious puberty (CPP), which is mediated+ Q+ y) e: L4 L: X0 T3 p
through the hypothalamic pituitary gonadal axis, has: T6 g6 Z+ }. b2 _5 z, E
a higher incidence of organic central nervous system5 K; D# ~; v4 q
lesions in boys.1,2 Virilization in boys, as manifested
  \: n3 J+ k) S& f3 `5 t, A! Y' Q. [# tby enlargement of the penis, development of pubic
- o! }2 `' m. q5 Y9 w5 l( yhair, and facial acne without enlargement of testi-
: O+ f8 k( k6 R8 a0 icles, suggests peripheral or pseudopuberty.1-3 We7 }" u+ F- B8 b# K  R' F5 e
report a 16-month-old boy who presented with the
9 z3 j9 n/ R. @5 ~8 ]( J  }2 X6 X$ ^enlargement of the phallus and pubic hair develop-5 ~" t/ p1 o8 m2 G% j! {
ment without testicular enlargement, which was due
! N% z1 ~  w& f; `6 d  u; ?7 ]+ dto the unintentional exposure to androgen gel used by9 r( f. Q) O6 G, e2 d3 E
the father. The family initially concealed this infor-9 C' E1 |% W2 r& C
mation, resulting in an extensive work-up for this8 Z! Y8 @7 {0 O( H* i
child. Given the widespread and easy availability of
: Y5 g# c2 ]( mtestosterone gel and cream, we believe this is proba-, `1 ]; q6 [1 n1 I: Q; C0 a2 w0 w+ ~  B
bly more common than the rare case report in the/ u: m3 ]* }8 @/ g% a' y  ^
literature.4
7 t5 d8 X" y4 T) i: z1 Y8 y# yPatient Report
7 r5 f) I" }( R. x; G" @A 16-month-old white child was referred to the
" l0 W$ g  }# Fendocrine clinic by his pediatrician with the concern
" F. i) U! ?, p8 pof early sexual development. His mother noticed9 e  b$ I8 o, m; [& _) M7 D
light colored pubic hair development when he was# C% m7 X7 i, Y3 n0 Y6 m1 ]
From the 1Division of Pediatric Endocrinology, 2University of! B1 e$ {: R0 H* `% p2 o
South Alabama Medical Center, Mobile, Alabama.
3 o3 B# @* E2 i/ |4 L) J, tAddress correspondence to: Samar K. Bhowmick, MD, FACE,; h/ v# \1 c4 y% ~3 O
Professor of Pediatrics, University of South Alabama, College of- }( e7 V9 k  u5 G. n5 ^, O& W
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* H5 f( q: u/ U
e-mail: [email protected].
+ A! K. Q- d2 z3 L. habout 6 to 7 months old, which progressively became
& b* y4 v) J7 j% |/ b3 j5 `) udarker. She was also concerned about the enlarge-
% q) }" u7 Q/ xment of his penis and frequent erections. The child. q) z' W0 {4 @# z  a. y. s
was the product of a full-term normal delivery, with+ O" L1 g# S" |. y! X# ~! \# E2 f5 d
a birth weight of 7 lb 14 oz, and birth length of# b, d4 d1 u' ?" K0 @
20 inches. He was breast-fed throughout the first year
- S3 x3 m$ r8 Z% cof life and was still receiving breast milk along with  c$ H8 _+ M" G
solid food. He had no hospitalizations or surgery,
4 W" s/ ^" V; S; C7 Iand his psychosocial and psychomotor development
0 i0 O, g% G5 @. N0 J5 D* t* Gwas age appropriate.
$ d, {9 j$ `, u7 Y! _# VThe family history was remarkable for the father,
. u( @$ D, X$ Vwho was diagnosed with hypothyroidism at age 16,
$ j7 e+ ]* E- ~0 }, I+ ]3 @3 \which was treated with thyroxine. The father’s
0 ]1 x  u2 z7 I* J4 \& o* Zheight was 6 feet, and he went through a somewhat
  L$ |0 |! ]" Z) e4 S( rearly puberty and had stopped growing by age 14.* ?4 N1 I# I0 h( [
The father denied taking any other medication. The$ Y% P2 g, c) G- y9 E9 y+ L
child’s mother was in good health. Her menarche
3 H6 T( M6 e3 wwas at 11 years of age, and her height was at 5 feet0 Q6 ^; T& f* E% M3 G4 E3 L
5 inches. There was no other family history of pre-3 v' z# g  \3 W/ t( u! ?% ]
cocious sexual development in the first-degree rela-# x) {2 j( I5 y: c
tives. There were no siblings.! ?: j- c# ?& q/ S
Physical Examination9 u1 G1 M: Z, o0 p6 n: n
The physical examination revealed a very active,( w* g  i6 j7 T4 B/ b
playful, and healthy boy. The vital signs documented/ ^% K0 ]  D) F! V2 a: E7 x# F, H
a blood pressure of 85/50 mm Hg, his length was
3 {8 Z4 h8 j0 B9 J4 e! v9 s90 cm (>97th percentile), and his weight was 14.4 kg
' }6 n# |- L  W  [(also >97th percentile). The observed yearly growth+ t* n: i' d, X  A+ e8 F; V9 w8 [" V
velocity was 30 cm (12 inches). The examination of2 o) l. e' Y! f0 `  e
the neck revealed no thyroid enlargement.3 E1 ~* d+ q0 Y5 a- z5 o
The genitourinary examination was remarkable for5 F# C( G3 P6 R! L0 a2 k
enlargement of the penis, with a stretched length of1 G* @7 H0 M' n! L: |) j- V1 V
8 cm and a width of 2 cm. The glans penis was very well6 V( q8 S) n9 G- a, G5 g7 l- y5 @
developed. The pubic hair was Tanner II, mostly around
. q% U1 a; J) R0 e540& x  ?& y0 K" }/ ^0 H" u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& @: E3 ~5 L# H, ~4 L' W
the base of the phallus and was dark and curled. The
4 K! A5 `6 @3 otesticular volume was prepubertal at 2 mL each.
& {- z, C; A8 Q3 G) f9 |8 RThe skin was moist and smooth and somewhat
7 w4 B: a2 E  k) m3 Eoily. No axillary hair was noted. There were no
" W+ B9 ^+ H6 o7 Q8 `, ~abnormal skin pigmentations or café-au-lait spots.$ E. I+ g, J1 d1 C5 l: k3 J0 c
Neurologic evaluation showed deep tendon reflex 2+8 X' I' R, @/ Z! l2 s" G6 X9 B. k
bilateral and symmetrical. There was no suggestion1 _8 [5 ^! i& T2 l  K6 E$ U4 n0 C
of papilledema." U/ e4 L8 G$ ~' T) k- q& m( O
Laboratory Evaluation
7 X( I0 ~+ U  W3 A4 D% VThe bone age was consistent with 28 months by
7 i$ ?1 V' b% w1 R* M: Uusing the standard of Greulich and Pyle at a chrono-
; p& ]$ K3 ?. v( D! S! n; i2 plogic age of 16 months (advanced).5 Chromosomal
2 |' T" b8 H  O) N' C" N/ kkaryotype was 46XY. The thyroid function test
6 `/ O: V+ k9 E% kshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
) e3 n8 x4 ^! _7 z8 J8 P5 c3 `lating hormone level was 1.3 µIU/mL (both normal).
7 c; D4 E! e) }0 f4 `/ kThe concentrations of serum electrolytes, blood
9 e0 t# n0 I" u; }, u' n7 Xurea nitrogen, creatinine, and calcium all were
& s4 [" @6 m! X+ u# N4 pwithin normal range for his age. The concentration# _) W& b6 H% |1 ~9 q
of serum 17-hydroxyprogesterone was 16 ng/dL
# Q. P" K) a' R9 @* T- b(normal, 3 to 90 ng/dL), androstenedione was 20- x9 A+ F& P. R3 F* S# G2 p1 F$ ~
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
) X* d$ J; z- u. t/ `8 S. Oterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 l  T8 M+ G2 X0 M( r% v
desoxycorticosterone was 4.3 ng/dL (normal, 7 to- N6 O) e/ a9 j/ Y; e
49ng/dL), 11-desoxycortisol (specific compound S): l3 L, G$ M4 y1 g+ {7 S. C
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 w, B" p) G5 g. D/ d" y- m$ [
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 D) m, t, K9 K5 T- z4 ztestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
* _9 q$ C6 a) Iand β-human chorionic gonadotropin was less than9 }2 E  V8 {9 e9 y& w1 p- ?
5 mIU/mL (normal <5 mIU/mL). Serum follicular
( V  j# T5 N7 F( [4 o* d6 dstimulating hormone and leuteinizing hormone
. e9 ^8 i8 T2 I3 d+ s" c& Nconcentrations were less than 0.05 mIU/mL
' j% I' P4 V9 m* i3 m, m" u, D(prepubertal).. D3 S6 O& C. k! Y* W$ s" P5 |1 U
The parents were notified about the laboratory! N8 r& R! f2 E5 ?
results and were informed that all of the tests were
1 C8 G. r% Q; Jnormal except the testosterone level was high. The5 W. p; H/ N5 b, p
follow-up visit was arranged within a few weeks to8 K4 v8 p9 C9 y( ~1 W3 u0 J$ ]/ V
obtain testicular and abdominal sonograms; how-7 B' f8 @: T! e* H, M' i
ever, the family did not return for 4 months.
' u0 e0 D/ Q) k7 n$ nPhysical examination at this time revealed that the' i6 ]2 r# I: c( ]* j& I1 m' i. @
child had grown 2.5 cm in 4 months and had gained9 Q; i4 o# h3 i
2 kg of weight. Physical examination remained8 ^  Y6 `! P. `
unchanged. Surprisingly, the pubic hair almost com-
$ R& p3 g* q7 P% U) X7 Y% Spletely disappeared except for a few vellous hairs at
0 t; C8 d- R8 ]5 p) k7 J, zthe base of the phallus. Testicular volume was still 2
* j1 [; K. n7 V9 y. G! y( k& |5 |mL, and the size of the penis remained unchanged.
$ |( v! W( f+ HThe mother also said that the boy was no longer hav-
' H  T0 @) x- v" y3 U% Ring frequent erections.
" b8 z4 K$ i  l8 m3 f1 aBoth parents were again questioned about use of
) m3 l+ ?0 Q6 e; r# l/ d* sany ointment/creams that they may have applied to
5 W4 Z& p7 X1 Ethe child’s skin. This time the father admitted the. m6 O+ k# j0 x) Y4 J
Topical Testosterone Exposure / Bhowmick et al 5418 y& i! z4 G/ J
use of testosterone gel twice daily that he was apply-3 H4 f. e, z4 D' a2 @. y
ing over his own shoulders, chest, and back area for+ N5 ^3 J3 X' B5 ?
a year. The father also revealed he was embarrassed
: ~4 s8 s- M1 K& sto disclose that he was using a testosterone gel pre-6 I" b% j+ k2 B( M+ P1 d1 q$ ?
scribed by his family physician for decreased libido. ^3 u' k" D1 |; F
secondary to depression.
9 ]" ^  Z+ E9 t8 m8 C1 }2 MThe child slept in the same bed with parents.! t# ^2 o" u* _, P$ Z- e7 Y  t& s
The father would hug the baby and hold him on his
% g6 R- Y& I3 P. o! Ychest for a considerable period of time, causing sig-
2 u- q9 J# C) F* ~) i8 Tnificant bare skin contact between baby and father.2 N; ?& h! L+ x3 M' v+ U, J
The father also admitted that after the phone call,
* |3 M, |& y$ i( B5 |( Twhen he learned the testosterone level in the baby
! i- a- g; H- w( h6 d7 E7 Xwas high, he then read the product information! W9 ]) w& |& P- Q6 `
packet and concluded that it was most likely the rea-
9 x# C9 @# p) J/ a" fson for the child’s virilization. At that time, they
4 g4 K- L4 g. ~: `) n1 Kdecided to put the baby in a separate bed, and the
% b% S8 W, U$ J2 q0 Ffather was not hugging him with bare skin and had
6 j7 ?' w) e7 b) ~been using protective clothing. A repeat testosterone
5 D6 z7 h# ^; etest was ordered, but the family did not go to the; f) K! C1 z6 b  i
laboratory to obtain the test.
& Y) Y5 J6 J% g. S( Z7 KDiscussion
; v4 S! x% Z8 i% H6 m( kPrecocious puberty in boys is defined as secondary/ J( J1 S, O" j; p9 m. ]# E9 x
sexual development before 9 years of age.1,4
: t" \) M' Y) [! |6 Y- C8 nPrecocious puberty is termed as central (true) when+ N" s& N$ `: e4 `( h. r, O) p
it is caused by the premature activation of hypo-
1 b* r, [" [( J4 tthalamic pituitary gonadal axis. CPP is more com-
/ O0 m+ W# ~9 c4 Ymon in girls than in boys.1,3 Most boys with CPP
, @9 d) v5 }% w7 Nmay have a central nervous system lesion that is
( }* K; x: M) w" [9 W/ y- Bresponsible for the early activation of the hypothal-1 w1 @% G0 w" C+ p) W! S
amic pituitary gonadal axis.1-3 Thus, greater empha-
8 G" `: m1 X; d. {3 h; N& p. Rsis has been given to neuroradiologic imaging in2 D( v; M% K" }! P% @1 j* Z6 h+ g
boys with precocious puberty. In addition to viril-( S1 J- E; q3 \! B2 T! j' ?
ization, the clinical hallmark of CPP is the symmet-
+ W4 X% T7 r$ b  Hrical testicular growth secondary to stimulation by, m7 X4 C$ X1 v1 M
gonadotropins.1,3" }9 }8 w8 n9 O0 n1 D; f2 L+ b
Gonadotropin-independent peripheral preco-" S  L1 T* V# a! |5 s
cious puberty in boys also results from inappropriate  z! U# V1 N1 k5 i2 s  _
androgenic stimulation from either endogenous or  t- v, l6 z. _" k& s. p
exogenous sources, nonpituitary gonadotropin stim-
/ Z+ r5 Q! ?1 d2 |ulation, and rare activating mutations.3 Virilizing
" j+ s3 h! W2 x7 q8 W/ ^2 i5 |congenital adrenal hyperplasia producing excessive
: u: e* {$ Y3 v" Hadrenal androgens is a common cause of precocious& u" o' ?1 @$ c: S) A  X- w
puberty in boys.3,4
/ S9 P. E5 G  ]The most common form of congenital adrenal5 F, ~0 o4 w. o% g/ o% R/ _  W
hyperplasia is the 21-hydroxylase enzyme deficiency.& J+ d# H5 d" a
The 11-β hydroxylase deficiency may also result in
0 h" O- }: D2 l/ n2 L. W1 s" Cexcessive adrenal androgen production, and rarely,. J' c9 g+ R* K# s* ^/ [
an adrenal tumor may also cause adrenal androgen$ p, o& U% S; ^3 e. o- X
excess.1,3
2 k8 l/ C4 U$ f9 b. N, H) A0 Kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
7 N1 C, i4 d+ Z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- g9 F( S0 {! ]" [+ r- ]. \A unique entity of male-limited gonadotropin-
/ K' A$ m% c( g% L7 V# J( \& Q+ |8 hindependent precocious puberty, which is also known
" Y- ~9 I0 L: k/ p7 h' bas testotoxicosis, may cause precocious puberty at a
- A3 G5 R% Z1 h* j1 H3 F& e1 Every young age. The physical findings in these boys
7 u" z1 |1 v! ~' Z2 {6 uwith this disorder are full pubertal development,7 y7 I- d- F! \+ ^
including bilateral testicular growth, similar to boys; i/ U/ j/ M; k, H3 o
with CPP. The gonadotropin levels in this disorder; u, o% j' j- ]0 k$ f7 P' ?& Z3 k
are suppressed to prepubertal levels and do not show; S9 Y! b1 I- Q2 W, `) H3 w. k! N
pubertal response of gonadotropin after gonadotropin-
% y8 T( N" ~+ v- vreleasing hormone stimulation. This is a sex-linked
5 b% ]: ]/ H' L9 j+ C" I3 W( o, ?autosomal dominant disorder that affects only
1 D( G2 a! a) Q0 J' ^3 @males; therefore, other male members of the family9 a% F5 ^4 |5 k8 ?# g. [( p0 K
may have similar precocious puberty.3# n5 I) H' l4 N
In our patient, physical examination was incon-
! G* ?/ f2 ~0 k% c. m" fsistent with true precocious puberty since his testi-
0 \9 z* |3 n9 }7 p) v' @' a0 g: xcles were prepubertal in size. However, testotoxicosis' j+ W9 w& |, m( G# c8 g6 a
was in the differential diagnosis because his father
  {* Y) L- c) [- o3 \8 jstarted puberty somewhat early, and occasionally,4 }- g1 k  ^/ K4 X: X
testicular enlargement is not that evident in the- \% a9 X# v3 j5 o
beginning of this process.1 In the absence of a neg-
" N8 l. {7 c% r# X) wative initial history of androgen exposure, our/ b# X, t; e' ]; a5 c9 L
biggest concern was virilizing adrenal hyperplasia,
8 b4 Z1 Y7 q8 D! t1 Eeither 21-hydroxylase deficiency or 11-β hydroxylase5 ?% o0 l2 l+ R' `9 g" ~
deficiency. Those diagnoses were excluded by find-* N8 h- ^- D3 T# I
ing the normal level of adrenal steroids., |5 i4 ]8 D$ U" M- V5 ~
The diagnosis of exogenous androgens was strongly/ Z& j. a  m" u" l
suspected in a follow-up visit after 4 months because8 m" _5 Z3 _0 S' t
the physical examination revealed the complete disap-
6 p! a5 |/ t8 ?% p1 dpearance of pubic hair, normal growth velocity, and
+ g4 n/ J7 \, C" v0 K& jdecreased erections. The father admitted using a testos-7 g$ Z- x- [* s( i% }
terone gel, which he concealed at first visit. He was
+ }- `* d. p; ~using it rather frequently, twice a day. The Physicians’
# [6 x9 G. r$ q8 |Desk Reference, or package insert of this product, gel or5 K8 N+ S- B/ {4 z
cream, cautions about dermal testosterone transfer to8 y, @2 T! ^8 W: u* d/ G
unprotected females through direct skin exposure.5 o0 v1 M* a( j) {
Serum testosterone level was found to be 2 times the
  G9 p) T8 `; Dbaseline value in those females who were exposed to" b& q# B& \+ z4 j, W- \
even 15 minutes of direct skin contact with their male4 z* I0 x$ a) A8 D0 ]9 D, e. R3 c
partners.6 However, when a shirt covered the applica-
0 H5 l+ ^9 ?, w& v4 y& ftion site, this testosterone transfer was prevented.8 F  I9 ], u  V$ }$ @
Our patient’s testosterone level was 60 ng/mL,. u" |3 Q, E, I' A" f
which was clearly high. Some studies suggest that6 D3 Y( K  p% z) Y* ^' Z
dermal conversion of testosterone to dihydrotestos-
$ b( W( k( \% p: |( l" _0 q6 cterone, which is a more potent metabolite, is more8 Q% f  ?; G* S4 R" ~
active in young children exposed to testosterone
7 f* f5 I, Y$ `6 \- c! Texogenously7; however, we did not measure a dihy-: I0 g, n* u: N7 U& o7 o
drotestosterone level in our patient. In addition to* l( d5 J, ^0 j4 F
virilization, exposure to exogenous testosterone in) `- ]+ a1 ^( H2 t5 Q& B2 r
children results in an increase in growth velocity and) z2 U4 P6 w' I- d
advanced bone age, as seen in our patient.) l( |: f" B8 h
The long-term effect of androgen exposure during* I+ X9 B* Z5 `7 }
early childhood on pubertal development and final2 J# Y& x  L+ ~0 G9 X2 u# t, ]
adult height are not fully known and always remain# c7 l  J! ~4 `" {
a concern. Children treated with short-term testos-) |( O2 F1 u# d4 y
terone injection or topical androgen may exhibit some* l( g% o4 z9 v& a8 n. I. l1 H& z
acceleration of the skeletal maturation; however, after9 Z* f' X- d8 p6 n
cessation of treatment, the rate of bone maturation. F% h6 f4 f9 p' s4 k5 N
decelerates and gradually returns to normal.8,9
+ @- U" B+ b, ^  [% _There are conflicting reports and controversy( R+ W7 T' S0 [+ @) O% v: F4 O
over the effect of early androgen exposure on adult
' s7 C& r, q5 r' ~9 W0 x  ^penile length.10,11 Some reports suggest subnormal
& O7 S. J& t/ q$ Yadult penile length, apparently because of downreg-- q+ g* E7 ^% V# E8 s8 u
ulation of androgen receptor number.10,12 However,' ^5 A- g4 I% g$ X; w( g! Q# R
Sutherland et al13 did not find a correlation between
- Z: e$ N5 \" x5 _, x. Achildhood testosterone exposure and reduced adult( I7 G6 z6 z: q9 B/ h1 A
penile length in clinical studies.( x% P( i- s! m$ @
Nonetheless, we do not believe our patient is
* D6 F/ w+ d, I% \going to experience any of the untoward effects from
# ^1 X8 d: p: h# B7 `3 v% g& a3 L+ ?testosterone exposure as mentioned earlier because
, g* [# f% S( P/ J" rthe exposure was not for a prolonged period of time.
( ^1 x- |0 O* Y5 _! bAlthough the bone age was advanced at the time of
% n- q' I6 s. u+ O* Vdiagnosis, the child had a normal growth velocity at
8 q2 \+ B/ @' T' _the follow-up visit. It is hoped that his final adult
  S/ i8 t* e( z- I3 L1 L) \6 mheight will not be affected.. T" G5 ]+ L+ F7 ]- i2 q/ p
Although rarely reported, the widespread avail-+ p2 J) I' Q0 T7 ]3 Y( l; U
ability of androgen products in our society may8 q% Z; H- a# y9 f3 ]: Y0 O1 u
indeed cause more virilization in male or female
; U1 L3 S- a8 r' G! z$ Qchildren than one would realize. Exposure to andro-
% e5 D* t$ y1 v0 bgen products must be considered and specific ques-: {$ _1 @: n. K% V$ ?
tioning about the use of a testosterone product or
- K1 |$ ^9 y  s& l& j- [1 Y! d; bgel should be asked of the family members during1 i: J4 X1 j9 D8 y0 i
the evaluation of any children who present with vir-* }: i: Y) l9 _! Z6 w! m! f
ilization or peripheral precocious puberty. The diag-# e! e2 R/ a  a! M' Y; q% t
nosis can be established by just a few tests and by
, [! d- J; J6 c2 M' }appropriate history. The inability to obtain such a9 ]1 S$ e; T! K* I9 Y4 e/ |
history, or failure to ask the specific questions, may
8 m/ u1 O/ x* P9 N# K) m% D/ }2 eresult in extensive, unnecessary, and expensive
. k/ ?# ?, N3 |: E; \* Sinvestigation. The primary care physician should be
8 N5 R5 [( M: |1 caware of this fact, because most of these children& Y2 W! U/ B. P, N1 O# i! J( M
may initially present in their practice. The Physicians’9 d) t& {6 `/ t+ c  Q
Desk Reference and package insert should also put a
- G2 y3 I0 W  K7 D, K6 M$ jwarning about the virilizing effect on a male or
/ g1 H5 h- W# j$ o& ifemale child who might come in contact with some-
7 G# k5 V0 F; ~: I' Z2 E2 Yone using any of these products.
) W2 X/ O& M2 l4 R9 D# v, e8 JReferences
" }) V9 `3 v( T8 \6 l1. Styne DM. The testes: disorder of sexual differentiation! |1 J! l9 T9 Y
and puberty in the male. In: Sperling MA, ed. Pediatric
- ~( e! J$ B5 q6 h. p" o9 ?0 IEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 q1 r/ j! {3 J& m% N2002: 565-628.* ~" [. z/ t& p# y- v2 W# O8 L* C
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" q3 M) B2 j! J% xpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old. x5 V2 v2 A* F* K1 W* ^. |! }
Boy Induced by Indirect Topical
: t4 `: k# r+ gExposure to Testosterone
( P: c: N$ Y1 `. [0 n, X: aSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
. X- Y5 y5 ]/ w/ c/ S% Gand Kenneth R. Rettig, MD1
) L. h# T! ^! H$ Q" ?+ [Clinical Pediatrics! t) Y2 Q% w* a& U
Volume 46 Number 6
3 Z) t6 I9 x5 f! ~0 eJuly 2007 540-543
! `6 n: m9 g, c© 2007 Sage Publications2 q- p' p! J2 N
10.1177/0009922806296651
/ f9 O4 ?( o) [( c) l' T  o, s" z5 rhttp://clp.sagepub.com" B/ Z$ {: v! \* _: t
hosted at
1 \* Y# ?8 W$ ?/ S3 J' k3 A$ xhttp://online.sagepub.com
5 P4 R8 _1 a2 L7 `2 s5 W, tPrecocious puberty in boys, central or peripheral,$ |* r* D2 }5 \) R) O$ k% \7 R
is a significant concern for physicians. Central
- p6 l4 Q1 {7 m, l: J7 Qprecocious puberty (CPP), which is mediated
8 W3 Z& V+ _2 n0 S% |/ ~/ ^through the hypothalamic pituitary gonadal axis, has
" v; t- v+ f' L6 k+ |a higher incidence of organic central nervous system3 Z7 U# D3 E' Y- Q/ l# O
lesions in boys.1,2 Virilization in boys, as manifested
9 S" `2 |- d. z! w, z" g( Dby enlargement of the penis, development of pubic* n! U) P- a  r  e3 k' S  ^) M. r
hair, and facial acne without enlargement of testi-
9 i8 J# A6 V. q/ p( j6 zcles, suggests peripheral or pseudopuberty.1-3 We
/ \" H& I2 t0 ~4 r% @report a 16-month-old boy who presented with the! c$ r4 \. g6 ~3 Z
enlargement of the phallus and pubic hair develop-
, G$ M6 w9 G2 e/ Q6 [5 V) kment without testicular enlargement, which was due
. m  b" n2 Q$ [' S4 `* a3 H+ X  Jto the unintentional exposure to androgen gel used by
3 {1 `) e) \" w" i- f3 Q$ D! jthe father. The family initially concealed this infor-
6 |' L  k3 Q, ~4 p2 gmation, resulting in an extensive work-up for this$ t+ ~6 X7 C. O) r+ Q
child. Given the widespread and easy availability of
* N( ?6 Y; c$ s8 v/ Ktestosterone gel and cream, we believe this is proba-4 |2 O, K/ S  x& X
bly more common than the rare case report in the
! l8 u( Y3 n) |: [$ I( jliterature.47 {7 b( O' E3 O1 }9 D- S
Patient Report% n. k% e8 p9 e+ L8 l5 `8 B5 ~
A 16-month-old white child was referred to the
; ?2 T/ O7 r, g5 p7 n6 m* w: s) j1 E3 \endocrine clinic by his pediatrician with the concern2 o: C" V% B9 o% a# T
of early sexual development. His mother noticed- w& K% e/ \2 X+ _
light colored pubic hair development when he was
  n: ]# A) x. R! K- @9 bFrom the 1Division of Pediatric Endocrinology, 2University of# s5 _+ p& `& g% S( @
South Alabama Medical Center, Mobile, Alabama.
& i% u6 p6 X5 J* NAddress correspondence to: Samar K. Bhowmick, MD, FACE,/ q3 c, i* `% X, h' x" P
Professor of Pediatrics, University of South Alabama, College of* _6 h. P5 b" p2 J+ H. r# s
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ ?& V- [+ O3 F+ J% Z# E& @e-mail: [email protected].
$ U, D3 O5 L' ^. H% v8 D* Vabout 6 to 7 months old, which progressively became
, |! u. @/ L* Y/ rdarker. She was also concerned about the enlarge-9 g2 [' o( R# m( X: f
ment of his penis and frequent erections. The child
# N' B4 B  k) R* hwas the product of a full-term normal delivery, with
" f: B& ~) ?' Z4 F9 Ra birth weight of 7 lb 14 oz, and birth length of
$ L) u3 d- D/ ^4 F% M% Y* U$ a6 c20 inches. He was breast-fed throughout the first year
* @0 T; H/ L4 L2 ^* Y2 L' Q4 aof life and was still receiving breast milk along with$ V. t, Z2 H. {2 \9 x% _5 k  c5 l
solid food. He had no hospitalizations or surgery,8 ]8 p: k: ^2 e$ J, F7 p' a
and his psychosocial and psychomotor development
* N* `) a2 ?" p, bwas age appropriate.# X# F$ B  }9 Y% E0 Y2 J) r
The family history was remarkable for the father,9 F5 D% }; _) `' K
who was diagnosed with hypothyroidism at age 16,; ?/ J; i- V7 R7 [
which was treated with thyroxine. The father’s
  P5 m& K! _7 @+ U8 L% Jheight was 6 feet, and he went through a somewhat& N$ V- }: t% N4 V
early puberty and had stopped growing by age 14.
( X. t$ {3 s3 l* Z$ ^% v, K$ q, f. SThe father denied taking any other medication. The
& ~) l6 W4 j2 [8 L4 q4 O9 Kchild’s mother was in good health. Her menarche* c; |; A2 M0 q) ~, I8 d1 L7 P
was at 11 years of age, and her height was at 5 feet
4 L) O7 a9 d  w7 o/ l% o6 B& g5 inches. There was no other family history of pre-
6 \% @- S0 H  E2 ~cocious sexual development in the first-degree rela-
' x: e6 [0 b6 b7 \. O+ `2 jtives. There were no siblings.6 @2 D/ T1 F$ K' X" G6 x
Physical Examination
5 J$ u( C, F& s/ ^The physical examination revealed a very active,. n, }- z- ~6 ?9 v
playful, and healthy boy. The vital signs documented
3 ]9 f! B, D/ U, F- G2 M+ \a blood pressure of 85/50 mm Hg, his length was9 u' p! d% a5 K
90 cm (>97th percentile), and his weight was 14.4 kg) p  J* ^7 k3 F0 C5 o
(also >97th percentile). The observed yearly growth
2 {* |6 d3 r. }velocity was 30 cm (12 inches). The examination of* `5 `- e1 D3 ~$ I% @7 F% u
the neck revealed no thyroid enlargement.
7 p/ t% W  G& x% t' h1 m' R8 {) b  ?# OThe genitourinary examination was remarkable for
' g7 o8 i" i. penlargement of the penis, with a stretched length of. M7 n7 Z  r/ J/ w8 O, i2 _5 n
8 cm and a width of 2 cm. The glans penis was very well
$ K# l4 [# _/ ~' L& [developed. The pubic hair was Tanner II, mostly around
$ [: |/ \( W9 B. S1 Z2 L+ B" [: U; [6 @0 e540) }6 f9 S- x7 I. d
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 C- x" H1 L. f2 |+ G2 K, R+ ^
the base of the phallus and was dark and curled. The
* R% a$ N; v7 S" \% |6 Itesticular volume was prepubertal at 2 mL each.5 N+ a9 V8 L. }$ d- p
The skin was moist and smooth and somewhat
  V/ ]) P: E; V8 W1 s. xoily. No axillary hair was noted. There were no/ X/ r" n! Y3 C$ m" o6 c% @
abnormal skin pigmentations or café-au-lait spots.& L, n; ?# L! e* I
Neurologic evaluation showed deep tendon reflex 2++ t+ m+ ~2 y8 e1 L: s, S  Z, o
bilateral and symmetrical. There was no suggestion7 |; o/ i" @) I3 B5 C- O
of papilledema.
. @1 ~5 o! v5 l4 a2 K$ uLaboratory Evaluation) V! Z( s# W9 q6 g! p4 G) G* a
The bone age was consistent with 28 months by: v# \/ a! m  h" Q
using the standard of Greulich and Pyle at a chrono-
$ {& \# s4 u& `  c9 R0 ?) Llogic age of 16 months (advanced).5 Chromosomal
- j. z9 N2 [" s1 P. [karyotype was 46XY. The thyroid function test* |. {$ A6 r0 `: O% Y- p4 _4 Z0 y
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
* O* m& [! y  Ulating hormone level was 1.3 µIU/mL (both normal).8 @- K) y( {/ U% v
The concentrations of serum electrolytes, blood$ t' N! T  O' v0 m# d* y2 k$ o( L
urea nitrogen, creatinine, and calcium all were
" z0 ?1 x" ]  x# @' o. @" f! @% dwithin normal range for his age. The concentration
7 {* R" ^  E& f' D: ^of serum 17-hydroxyprogesterone was 16 ng/dL* r" z4 T& z: u4 N) C( S: L; U$ m
(normal, 3 to 90 ng/dL), androstenedione was 20
* Y) ~- T8 W& ?+ J  Ong/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 s2 f) K1 k4 ]' P1 ^6 r- q) U" Zterone was 38 ng/dL (normal, 50 to 760 ng/dL),: \) P9 F4 w6 [( Y$ o( q" j3 {; d( D
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
7 V$ C0 _5 U. g* I6 m" E, `49ng/dL), 11-desoxycortisol (specific compound S)
! G- y3 o) \) }- G4 H2 t- n4 Zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-4 p, z7 H, u; z" S$ p  n/ ]
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 h: G2 ?' Y$ f
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
& _% q; ?* i! r; M4 K" Band β-human chorionic gonadotropin was less than
# q9 t% u" o+ o1 ]0 {/ H) ~5 mIU/mL (normal <5 mIU/mL). Serum follicular" O, K2 P' w8 {- v
stimulating hormone and leuteinizing hormone. ]8 U+ k8 A. M; h
concentrations were less than 0.05 mIU/mL! o# z6 H0 \1 ^* A
(prepubertal).6 O( A3 V1 y1 c. A
The parents were notified about the laboratory! Q1 j* ~9 m0 N4 ]8 b
results and were informed that all of the tests were
, g8 u1 m% x$ g; U' U8 Fnormal except the testosterone level was high. The: o8 C2 S& l( G4 ^6 p/ z
follow-up visit was arranged within a few weeks to
2 L7 L7 ]$ q" p9 S! ~9 kobtain testicular and abdominal sonograms; how-
" ?0 H' `/ _+ ?8 Jever, the family did not return for 4 months.6 _6 A% x1 R7 c! r2 e& O# Y4 R  F
Physical examination at this time revealed that the
4 U  u. m2 @% m- R  @child had grown 2.5 cm in 4 months and had gained: O; ]# J2 F  o* K- _" G- [
2 kg of weight. Physical examination remained
% s3 Q. {& R/ J# }( C0 Eunchanged. Surprisingly, the pubic hair almost com-% Y6 j8 c$ k9 B
pletely disappeared except for a few vellous hairs at
% p3 M/ {& ~3 A) V: U  d, athe base of the phallus. Testicular volume was still 2/ Q) H, s& J4 c. S% F6 u# r4 ]/ k* g
mL, and the size of the penis remained unchanged.
' p1 J$ d' q; xThe mother also said that the boy was no longer hav-1 x9 |8 q& r# ~6 ~
ing frequent erections., J. H. F( [" J
Both parents were again questioned about use of) I# X) D7 W1 u# M2 ]
any ointment/creams that they may have applied to  n& U" H6 w6 {5 `
the child’s skin. This time the father admitted the  y2 }9 H# A8 B9 I1 h
Topical Testosterone Exposure / Bhowmick et al 541
$ G$ M3 i1 Y% I& Z  I  duse of testosterone gel twice daily that he was apply-; R+ N% W/ ?5 G4 x# z
ing over his own shoulders, chest, and back area for  W# V1 X6 d/ U( e0 M: `2 v
a year. The father also revealed he was embarrassed
6 L& q& d2 F$ ?5 Bto disclose that he was using a testosterone gel pre-
: m( [- `; j" @1 ]; U% ]( |- [scribed by his family physician for decreased libido
7 ?7 _" y0 x5 _4 H$ H' usecondary to depression.+ Y' G$ ~# x6 ~
The child slept in the same bed with parents.
  J5 p, t$ f7 Z3 }! B# s3 F% O0 ~( bThe father would hug the baby and hold him on his
: a; a/ ?6 ]' V& gchest for a considerable period of time, causing sig-
5 k3 ]% s7 ]2 J. E2 Y, Gnificant bare skin contact between baby and father.
) A. B5 p! O- C3 w  @The father also admitted that after the phone call,
4 K" H. ]" d0 b& I* X3 f( B, Hwhen he learned the testosterone level in the baby
3 j; k6 N& I. u( m6 n' qwas high, he then read the product information
/ f% @/ G4 B& @: c' h" G  |packet and concluded that it was most likely the rea-3 r' |% s% b) Y+ h# {1 i' Y# P
son for the child’s virilization. At that time, they
2 J  y/ ~! U- Jdecided to put the baby in a separate bed, and the" Y) e1 O! @. f, @6 Q
father was not hugging him with bare skin and had9 ~( I, H9 R7 i8 i2 V5 g
been using protective clothing. A repeat testosterone
7 \( D& W3 t( k. y' g( Htest was ordered, but the family did not go to the
( m# O+ d, x* l% b/ j/ l; Alaboratory to obtain the test.0 l. v4 r6 w+ D  R( Q  O' P0 I
Discussion! H2 N! Z5 T6 X7 }5 `" Q8 u
Precocious puberty in boys is defined as secondary
3 W0 |/ J( M; Z/ `  j1 |sexual development before 9 years of age.1,4+ _6 |. V4 k7 Y3 S, n0 N( ^
Precocious puberty is termed as central (true) when
& p0 p8 E; H9 {% b# d! j, hit is caused by the premature activation of hypo-1 _: j8 K2 r# \$ a7 T) r
thalamic pituitary gonadal axis. CPP is more com-
" i( F1 L- @" Cmon in girls than in boys.1,3 Most boys with CPP# Y( u  ]( F  b$ X: |9 s7 e7 n
may have a central nervous system lesion that is" b% j* V* Q2 }) D
responsible for the early activation of the hypothal-; ~+ W3 A% j  ]6 T5 I: G/ B, P: W
amic pituitary gonadal axis.1-3 Thus, greater empha-
5 A2 P' O& S2 ^  csis has been given to neuroradiologic imaging in2 Q' I4 W2 m2 p; M3 r
boys with precocious puberty. In addition to viril-
; o& C" u, I; f" [; n* s! C" Zization, the clinical hallmark of CPP is the symmet-* g: D5 S+ _8 m0 Y0 m# _
rical testicular growth secondary to stimulation by
1 s7 X1 |+ p, Q8 R: _gonadotropins.1,3
9 K) H' {, T! c$ x7 c. o/ `Gonadotropin-independent peripheral preco-, d4 H) x7 C. `5 l: H
cious puberty in boys also results from inappropriate4 R: z( m7 v7 Q  M; Z4 \& {4 V
androgenic stimulation from either endogenous or+ N1 k8 p/ |) q! T( h
exogenous sources, nonpituitary gonadotropin stim-
2 y2 Q: a5 a; P2 o. g0 Oulation, and rare activating mutations.3 Virilizing* r) ~/ X. X: V" Q) q* W- z3 J
congenital adrenal hyperplasia producing excessive2 T/ ]; B% q/ x5 p- b4 j
adrenal androgens is a common cause of precocious
, R1 [; l& _  ]3 P& Kpuberty in boys.3,4" \1 g/ r. K0 h( Q, c, j+ E" m- l
The most common form of congenital adrenal- L9 h" N9 n2 ]# N) H# D
hyperplasia is the 21-hydroxylase enzyme deficiency.
  u5 _6 H' B; ]# oThe 11-β hydroxylase deficiency may also result in7 a6 m! u1 w6 [. q) N
excessive adrenal androgen production, and rarely,0 q, k. c) h8 ?& p& [/ d: W
an adrenal tumor may also cause adrenal androgen% i& ?6 J+ d- n- z3 T
excess.1,3
+ a+ G1 H, Q: Z( S' }! n' r! nat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% Y5 t9 e$ F5 k1 s: b9 m+ K. E
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 R  o% ~# V6 Z4 FA unique entity of male-limited gonadotropin-! l$ ^4 d; @/ m  d
independent precocious puberty, which is also known
1 \6 H8 ]' n- k/ _: G  B3 Yas testotoxicosis, may cause precocious puberty at a8 [# m5 I  b) f' N7 A: Q% d
very young age. The physical findings in these boys0 b* D% c, m0 p( H) a/ v
with this disorder are full pubertal development,
0 u/ J- G8 T( g; a- Y2 Mincluding bilateral testicular growth, similar to boys
) B" x4 _) z9 n- Kwith CPP. The gonadotropin levels in this disorder
0 c. Y; v/ S* U+ \are suppressed to prepubertal levels and do not show
6 P5 ^+ l3 g: }: \- ^; t% ~: U- Xpubertal response of gonadotropin after gonadotropin-
# z. ~1 r% A7 ^% ]releasing hormone stimulation. This is a sex-linked# O5 D% B! ^9 {/ h" R8 k  Z  o2 v
autosomal dominant disorder that affects only" o  m0 L6 b. c8 q2 o
males; therefore, other male members of the family6 d" L! Y) T: H" n
may have similar precocious puberty.3
2 P) \: C9 Z5 ]4 O% xIn our patient, physical examination was incon-" x2 `$ C) c: j' S' d1 Y
sistent with true precocious puberty since his testi-
3 p  z/ w1 y; o7 O. }" dcles were prepubertal in size. However, testotoxicosis( [) p  H( b  ^  f) e% |3 |* c
was in the differential diagnosis because his father8 k5 w- f3 `& m, Y  w# P
started puberty somewhat early, and occasionally,
& Y  A- z: x+ D3 G+ Q" dtesticular enlargement is not that evident in the$ C0 {2 f" N4 b4 {& z
beginning of this process.1 In the absence of a neg-) z$ A7 f9 L" _
ative initial history of androgen exposure, our+ J( @0 D6 J2 k7 P" n
biggest concern was virilizing adrenal hyperplasia,
9 O  j5 }" @9 X# T! x0 Ueither 21-hydroxylase deficiency or 11-β hydroxylase
$ K1 h' L; G% @& adeficiency. Those diagnoses were excluded by find-
' e$ s, z6 x# _* t* ^" y/ G, q% _8 |ing the normal level of adrenal steroids.
, O4 w4 Q3 {: }2 xThe diagnosis of exogenous androgens was strongly
. F/ e. K3 V+ r+ u0 Wsuspected in a follow-up visit after 4 months because+ b7 b0 @% E2 k- `2 k3 J
the physical examination revealed the complete disap-# r: w& J& w. h  Q: m3 f
pearance of pubic hair, normal growth velocity, and% o% M# V% {3 }6 Y; Z4 @+ }, P; T
decreased erections. The father admitted using a testos-
! b$ I7 u7 D& g& p! tterone gel, which he concealed at first visit. He was
7 }  {  y6 L* Zusing it rather frequently, twice a day. The Physicians’
9 N" k7 q) W6 g7 e: X- pDesk Reference, or package insert of this product, gel or$ n; U) n# L8 Y  |0 r
cream, cautions about dermal testosterone transfer to& f$ M. Z3 j) h# a) b7 `0 _
unprotected females through direct skin exposure.
4 n" W! q7 z# l3 oSerum testosterone level was found to be 2 times the* i* S' ~5 l5 ^- u0 \% l* \
baseline value in those females who were exposed to3 p. B1 M0 r, x
even 15 minutes of direct skin contact with their male
" E0 B% V9 q6 D& p: P3 ppartners.6 However, when a shirt covered the applica-/ A4 q& B4 [% W) \/ j
tion site, this testosterone transfer was prevented.
4 q! ]- v! W' {) w1 `1 rOur patient’s testosterone level was 60 ng/mL,
1 w0 o  I) p% W/ y! M/ f1 |" n- E7 ]# Zwhich was clearly high. Some studies suggest that4 Z4 s  I) M5 B
dermal conversion of testosterone to dihydrotestos-8 l* S- n* d. q4 I
terone, which is a more potent metabolite, is more6 X5 J7 v6 o# q1 K) v/ m' r* G* p
active in young children exposed to testosterone: L- A1 B! Z: `5 i  p7 c  _
exogenously7; however, we did not measure a dihy-: q9 d) o- }1 j2 g2 A
drotestosterone level in our patient. In addition to; R/ _: ?. ?6 r2 U% b
virilization, exposure to exogenous testosterone in
2 G+ P' _/ t! m- \0 F; Pchildren results in an increase in growth velocity and, i" F( w+ s$ v: V  E* v
advanced bone age, as seen in our patient.; u+ d1 _* e- v* t& U2 V
The long-term effect of androgen exposure during" R  o' O" z) I0 m3 I" R* u: m8 s
early childhood on pubertal development and final
9 \) @$ e+ _$ G* B1 T/ H3 f. ~adult height are not fully known and always remain/ O  Q$ \" f4 Q# H, @
a concern. Children treated with short-term testos-
9 G2 C! k' {- B6 Y, S9 y, K  Wterone injection or topical androgen may exhibit some  t  u. @0 B# [6 @1 `/ }. K
acceleration of the skeletal maturation; however, after
6 r' r9 \6 b- S' q8 p: w$ jcessation of treatment, the rate of bone maturation
6 h3 [  K  a1 d; B* `' t2 B+ N4 sdecelerates and gradually returns to normal.8,9
& t7 ^/ p: \5 @$ IThere are conflicting reports and controversy& a% j3 g7 ]1 c, s* D- t' F9 z
over the effect of early androgen exposure on adult
  R# s" ^6 E- G# Wpenile length.10,11 Some reports suggest subnormal' n" h* A$ d! D$ k6 C: Q: W# b8 `
adult penile length, apparently because of downreg-
6 s% M/ `- g( p/ c: K( C" {4 hulation of androgen receptor number.10,12 However,
7 @* s; l" J  w8 E. OSutherland et al13 did not find a correlation between
5 Q+ }- h9 L- {5 P! O. X* Rchildhood testosterone exposure and reduced adult
# x  d- G+ J, _! H: epenile length in clinical studies.
  [$ B, M2 |/ j5 O5 \  JNonetheless, we do not believe our patient is% P+ Y, H) f- W/ p+ v! o
going to experience any of the untoward effects from
9 b6 [9 G. N0 v$ ntestosterone exposure as mentioned earlier because1 ^$ n) `2 A9 h; O& C
the exposure was not for a prolonged period of time.: Y& E& r5 V/ w
Although the bone age was advanced at the time of
& R- \) g, t* p) Ydiagnosis, the child had a normal growth velocity at$ t$ e  F2 L, E7 X/ N8 @7 W
the follow-up visit. It is hoped that his final adult/ S0 N& T: ^1 W4 h% J
height will not be affected.
. {( @( @! _$ f! Y( x! q3 HAlthough rarely reported, the widespread avail-
4 n* y0 K- t7 x" \- Sability of androgen products in our society may9 c5 z% j+ v; i2 Y
indeed cause more virilization in male or female
5 _! _5 Y4 b7 h* }' k, Gchildren than one would realize. Exposure to andro-
1 X% u4 ^5 M/ I  P1 y) K$ Kgen products must be considered and specific ques-( b% u8 C7 W3 B! v4 m3 E0 R
tioning about the use of a testosterone product or4 s" y* S/ j2 B1 ^- Q, d2 \
gel should be asked of the family members during6 E0 B$ L( a+ H1 d) E3 D4 T# c
the evaluation of any children who present with vir-$ S8 m% O0 b' b/ G, c& e! k
ilization or peripheral precocious puberty. The diag-
( J; H5 @6 N) l: K" g5 E# qnosis can be established by just a few tests and by6 ^# {# W! L; ~: Q% ~% e, u$ w  i& W
appropriate history. The inability to obtain such a
" D( Z- \1 x' Mhistory, or failure to ask the specific questions, may
* M! a" a- H  jresult in extensive, unnecessary, and expensive( i4 |$ `# |; {0 l5 A
investigation. The primary care physician should be
$ z$ ]2 D2 ~# caware of this fact, because most of these children: r$ e- L  l7 F
may initially present in their practice. The Physicians’
, d1 G# U+ J! M- t4 EDesk Reference and package insert should also put a) O. M0 N3 ^/ R/ g( L3 _2 M7 R
warning about the virilizing effect on a male or
; U& b1 [; r+ Hfemale child who might come in contact with some-9 S- z6 W" @1 R! a* E/ L
one using any of these products.2 ?) ^% n3 p: g0 j7 z9 J+ b6 c
References
' x3 P8 p, {7 r* a% F+ `1. Styne DM. The testes: disorder of sexual differentiation
+ q* n8 m( V4 U7 _and puberty in the male. In: Sperling MA, ed. Pediatric, o) H8 e$ L) ]) D, ?
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! q0 S. {' t8 Y& L$ K# M
2002: 565-628.
$ w  }+ q: y) \' z+ v$ ]9 [2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( P4 K, g' `. \$ t8 V9 c" c) N
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

% z" E* p' ^  Z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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