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Sexual Precocity in a 16-Month-Old
3 k; x7 v. C- d5 m) e/ b5 lBoy Induced by Indirect Topical! B4 p" L* h! |
Exposure to Testosterone
4 R9 d0 P9 |) }0 J; K' u& @Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 b5 d2 I( @0 I
and Kenneth R. Rettig, MD1% Z9 i* s6 s# D0 p+ n5 G8 o, h& B+ j
Clinical Pediatrics
  D% @: F' c: g7 o6 ]Volume 46 Number 6
/ x* l3 n+ a8 C# D, JJuly 2007 540-543; @5 A1 J- {6 v2 Z
© 2007 Sage Publications
7 O" B' S$ {3 `" x10.1177/00099228062966516 Q8 |, C  Q. v
http://clp.sagepub.com
7 q  f: `/ i+ _6 K$ s2 W. r% Rhosted at
$ E- s! r: G$ T& o% k, k$ [http://online.sagepub.com4 F$ k$ J" D  `( @) w
Precocious puberty in boys, central or peripheral,4 v; a& n5 T) ]% K- \) g
is a significant concern for physicians. Central* s0 V# j3 @( q" \% \, h8 j
precocious puberty (CPP), which is mediated* S- Z* W+ `( T: p/ m: n6 ]: ^
through the hypothalamic pituitary gonadal axis, has
0 q* _& `% e9 u% w) l" G% La higher incidence of organic central nervous system! m1 t: i. U4 @- [* ]3 C' N; S+ `
lesions in boys.1,2 Virilization in boys, as manifested
. u% h7 L: `9 l8 L% hby enlargement of the penis, development of pubic  J) m5 i% Y% ~2 y  D- U9 T4 U( {1 r
hair, and facial acne without enlargement of testi-
8 I% k" E5 O5 h1 Z8 w# vcles, suggests peripheral or pseudopuberty.1-3 We5 i/ g6 g2 r7 s6 b2 j2 a
report a 16-month-old boy who presented with the# R" J: W& u% s- }8 R" a
enlargement of the phallus and pubic hair develop-) a+ j. N6 R  F$ E1 T
ment without testicular enlargement, which was due& b% I7 q- c1 X/ Z8 r
to the unintentional exposure to androgen gel used by
* d3 }* ?  I7 ?* P0 _7 _  Qthe father. The family initially concealed this infor-
5 _) z; n/ \' |4 Q/ d9 rmation, resulting in an extensive work-up for this
# d" j4 ]/ b) J8 ?child. Given the widespread and easy availability of& d& H: Q0 \! W6 f' J. J" r2 z
testosterone gel and cream, we believe this is proba-; O& {# z" Q) k  }! i# P
bly more common than the rare case report in the4 L5 z* _" {! W8 t; [5 u9 Q
literature.4" X  j3 N" Y3 _' [1 O* _9 [
Patient Report
" F# v1 m3 \0 ~. V5 y0 gA 16-month-old white child was referred to the
' T$ P+ ]' d; C: f9 L3 eendocrine clinic by his pediatrician with the concern
8 B4 {* j- w& X. ~8 b% vof early sexual development. His mother noticed
; q: F0 s  a2 xlight colored pubic hair development when he was
9 n6 X6 i3 D! rFrom the 1Division of Pediatric Endocrinology, 2University of; b- Y5 F$ D% C/ _& a
South Alabama Medical Center, Mobile, Alabama." [1 S# d8 ?, D: X' ?/ ?+ e
Address correspondence to: Samar K. Bhowmick, MD, FACE,9 r8 S" E9 f& u4 L" D3 q  Q" c
Professor of Pediatrics, University of South Alabama, College of
, d" h' R% u) r/ M) X+ f) X/ aMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;# c5 y. B+ Y' d7 A0 B8 D5 ?4 Y& P
e-mail: [email protected].
0 g6 v) ^3 a; ~  Z! T& ~about 6 to 7 months old, which progressively became/ R- b' b& e7 u3 x* n' j8 R4 d
darker. She was also concerned about the enlarge-+ M) R3 ]. D' ]& q$ C  O2 j
ment of his penis and frequent erections. The child
4 f7 q6 I/ z7 G# z! v5 ywas the product of a full-term normal delivery, with
, I- q: b9 v. c2 Y- Ma birth weight of 7 lb 14 oz, and birth length of8 F3 t, @4 N3 C  l1 B$ Z
20 inches. He was breast-fed throughout the first year( z! H1 P) u3 \* D3 y0 j- N
of life and was still receiving breast milk along with! a; E2 J2 K) x; b% h  P* H
solid food. He had no hospitalizations or surgery,0 Q6 S1 ~, S' l4 N0 i; E" r- |
and his psychosocial and psychomotor development
9 \0 a' F9 S1 \. Qwas age appropriate.
: k; |" D; ]. ], r2 f. E3 w3 }The family history was remarkable for the father,
+ V0 U- j* o! x; Uwho was diagnosed with hypothyroidism at age 16,; U& [2 B2 m1 L; a8 A
which was treated with thyroxine. The father’s8 y: j1 z+ B. Y1 m4 i2 o! T& R! V9 j
height was 6 feet, and he went through a somewhat
! X+ W2 k0 |  T" l5 L6 jearly puberty and had stopped growing by age 14.
8 M$ a; q) x+ ?4 kThe father denied taking any other medication. The7 P; r* k. v6 w) N; n
child’s mother was in good health. Her menarche
5 p8 A$ e2 x$ ^was at 11 years of age, and her height was at 5 feet
  p9 |$ W* i! M; S) m2 v. t5 inches. There was no other family history of pre-
5 A. P# |, d% X8 Z; @* }8 h( ?; Ycocious sexual development in the first-degree rela-
* [' k# P! C. M) p! A1 l! Etives. There were no siblings.( k4 G" n4 ?5 @9 B; |
Physical Examination$ E8 R6 G: r/ k6 [9 }* R
The physical examination revealed a very active,+ J0 l+ T# o$ e- |5 O# M
playful, and healthy boy. The vital signs documented6 w2 t' S; }5 m" A
a blood pressure of 85/50 mm Hg, his length was
! v$ F4 v4 f1 f. }90 cm (>97th percentile), and his weight was 14.4 kg
1 }8 P2 [. i1 y, f3 b& F% X(also >97th percentile). The observed yearly growth
6 t8 F: |+ A+ t0 M* d! Avelocity was 30 cm (12 inches). The examination of9 @( A; n8 Y8 n+ c
the neck revealed no thyroid enlargement.
" V# b9 B  z! B1 [% S5 \- oThe genitourinary examination was remarkable for
7 _1 [& E$ `  L* W; u  d; Y5 Renlargement of the penis, with a stretched length of4 D" H# u- N# K0 A/ b
8 cm and a width of 2 cm. The glans penis was very well- R' [9 Z: }' y4 S5 w5 R2 H# x- s
developed. The pubic hair was Tanner II, mostly around
1 ?  c1 g! G( O: n2 i5 p9 U6 z540
/ H: g% Y+ a2 d) ]. Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 l- R1 }1 Q# E; qthe base of the phallus and was dark and curled. The
6 G% C; l' r4 `8 w6 G4 Rtesticular volume was prepubertal at 2 mL each.4 k* g2 Y* T" V/ b
The skin was moist and smooth and somewhat5 r" Y* S1 x; \+ }9 a
oily. No axillary hair was noted. There were no, T4 f$ o/ f, i/ |& v
abnormal skin pigmentations or café-au-lait spots.9 V- |" n' p5 f" G$ g- Z
Neurologic evaluation showed deep tendon reflex 2+
6 \& f+ g* ?+ o: f$ \1 j1 m. Bbilateral and symmetrical. There was no suggestion
# \) w5 ~) P0 ?' ^) t4 F2 tof papilledema.) F% X% m) j. C9 j, ~* Q. K' S7 O; ^. ?
Laboratory Evaluation
: w5 ^0 i- L" d% C! d5 y" f1 D2 @The bone age was consistent with 28 months by; x# p, ~) ~2 v' z$ q
using the standard of Greulich and Pyle at a chrono-' d+ Z$ v+ A; q$ ~  N; m
logic age of 16 months (advanced).5 Chromosomal! H' U1 Q; l  u
karyotype was 46XY. The thyroid function test* \% \7 g0 k8 Z$ f
showed a free T4 of 1.69 ng/dL, and thyroid stimu-! m  m: e/ a6 T! |5 I( U
lating hormone level was 1.3 µIU/mL (both normal).
& l8 Q" _% G9 {* O7 XThe concentrations of serum electrolytes, blood
5 X6 n/ H& w8 S# D- Nurea nitrogen, creatinine, and calcium all were0 I  i5 x  y1 l
within normal range for his age. The concentration
5 @0 \# E0 o' jof serum 17-hydroxyprogesterone was 16 ng/dL. N) _8 S& d1 z5 s. x+ [! B; [
(normal, 3 to 90 ng/dL), androstenedione was 205 N' j) Y! g9 L1 t
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 M' e  e# d, f  M; d" e+ {terone was 38 ng/dL (normal, 50 to 760 ng/dL),) B8 o# P/ o0 Y1 {2 S
desoxycorticosterone was 4.3 ng/dL (normal, 7 to3 c8 e4 f7 _: I4 r3 j7 O7 F2 m5 C2 \
49ng/dL), 11-desoxycortisol (specific compound S)
! d; h! t3 u+ `9 nwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 J7 D9 P) O9 s. Y4 y* E+ a
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
" [- g. D# j# W+ ^6 Dtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' Z: P. ~7 Y0 J4 P% D6 land β-human chorionic gonadotropin was less than' {0 H$ p4 O6 U6 k) c5 \/ ~: x# F( Y
5 mIU/mL (normal <5 mIU/mL). Serum follicular3 R! l, K1 R9 M( K  Y$ Z
stimulating hormone and leuteinizing hormone9 j+ \9 G. h4 ?4 N9 X
concentrations were less than 0.05 mIU/mL7 S6 s4 H3 J/ ~9 G5 l9 K0 v6 f
(prepubertal).$ [# s6 h5 y" V. E9 Q! m
The parents were notified about the laboratory
8 |4 @) G8 ], _; e, P( t: ?7 \results and were informed that all of the tests were
  h, d- T+ P% a1 p" E1 ]# tnormal except the testosterone level was high. The
) Z! e# f8 W- x7 Q4 y" i! n, ffollow-up visit was arranged within a few weeks to
& F0 e% t, l) K4 lobtain testicular and abdominal sonograms; how-
  c: @$ ?# |6 ]5 ^1 ^, ?ever, the family did not return for 4 months.8 G6 X& q! K5 `% |7 n, \
Physical examination at this time revealed that the: C4 O6 J: A" s+ D! y8 }- h
child had grown 2.5 cm in 4 months and had gained! e8 g9 ~/ K/ u. [7 I' o' t
2 kg of weight. Physical examination remained1 E+ f( k2 ]3 E' k: G
unchanged. Surprisingly, the pubic hair almost com-1 X6 R9 M9 p& `6 `1 I
pletely disappeared except for a few vellous hairs at
, N: C  H7 T! R( Athe base of the phallus. Testicular volume was still 2
5 K$ \0 |6 N. |+ k: \7 v. cmL, and the size of the penis remained unchanged., }) e# s% D! E% l" ~( R- X6 r
The mother also said that the boy was no longer hav-
6 u; C5 q8 U. Z) F$ F) A4 P) Ling frequent erections.
4 c: V: a! s" m" u  v3 _Both parents were again questioned about use of) V1 ]/ k3 A/ I1 S
any ointment/creams that they may have applied to
) p( T9 M  Y9 ^. _the child’s skin. This time the father admitted the
0 b" }4 e0 p- ?* v% o9 STopical Testosterone Exposure / Bhowmick et al 5413 }# i' q' ^" A& h& `4 u& L4 ^2 d
use of testosterone gel twice daily that he was apply-
& {. v; {. E! f( [ing over his own shoulders, chest, and back area for+ H, J) L- U* |3 d
a year. The father also revealed he was embarrassed" D- i" W' k% F. v5 s) A6 r
to disclose that he was using a testosterone gel pre-
5 p4 O) z) ?# fscribed by his family physician for decreased libido
& C0 B7 Q- b9 k( |9 }( H' }secondary to depression.
  G0 B; e( g/ j  H0 \- y) dThe child slept in the same bed with parents.
7 I7 o: V2 C6 D; dThe father would hug the baby and hold him on his8 U7 X* J" |! y* p+ R4 E& a
chest for a considerable period of time, causing sig-
7 [. C7 M6 c/ W" b  v& S  F6 |nificant bare skin contact between baby and father.
5 H3 J* b4 x3 C) i& {. n- xThe father also admitted that after the phone call,% T5 N! b! K  S: e9 R) P) z
when he learned the testosterone level in the baby' ~: s- w$ b6 p% T1 d! }
was high, he then read the product information1 @1 U; s3 N, s6 q: x
packet and concluded that it was most likely the rea-
  v: Y( e* B- P0 t0 B+ ?9 s5 ^son for the child’s virilization. At that time, they! V% B$ y0 t7 U' r
decided to put the baby in a separate bed, and the. K8 r1 ~9 I# B% L" l0 L3 ~/ O
father was not hugging him with bare skin and had
) H) J- o/ M) m" n6 vbeen using protective clothing. A repeat testosterone+ {. Q6 l  [$ b. j9 c5 j
test was ordered, but the family did not go to the
: t! C5 v' `5 s* s1 mlaboratory to obtain the test.
' l$ U! s0 ]- b& ?8 ^6 b; |Discussion' S9 l. |! `/ d; {) A+ k% h: y
Precocious puberty in boys is defined as secondary
: E- _6 H+ b. A3 d  Asexual development before 9 years of age.1,4
+ ], F- ^& v. G  IPrecocious puberty is termed as central (true) when
6 J- ]# z( V5 H: Fit is caused by the premature activation of hypo-
; q5 B3 f$ ]% Qthalamic pituitary gonadal axis. CPP is more com-* Y5 J8 s4 R& N& k8 w3 N* x* ~  Q
mon in girls than in boys.1,3 Most boys with CPP, B6 }% |+ O+ M+ x: ]# F
may have a central nervous system lesion that is
  e) k9 M' r7 d- F9 f- l2 kresponsible for the early activation of the hypothal-, E! z  v$ i9 \( R- G
amic pituitary gonadal axis.1-3 Thus, greater empha-) X, L. N% S4 ~/ [) m  P: z& W
sis has been given to neuroradiologic imaging in! ^( C4 H* u0 O! j9 d
boys with precocious puberty. In addition to viril-0 {7 f+ @. M7 t, a
ization, the clinical hallmark of CPP is the symmet-
4 o% G, F* W0 ^0 m- Y  srical testicular growth secondary to stimulation by
" T0 W9 ~  o0 Fgonadotropins.1,3( r% o! f8 ]+ O4 G$ J( }! V
Gonadotropin-independent peripheral preco-8 p" s! ~3 m& c  s3 C; F8 C6 [
cious puberty in boys also results from inappropriate
( P: D& ?% |. f) Y7 Fandrogenic stimulation from either endogenous or
6 ]1 n1 I8 i, W( A2 s) r- {exogenous sources, nonpituitary gonadotropin stim-: y  k" ~$ a" ~: ?; ^
ulation, and rare activating mutations.3 Virilizing0 P8 L+ v8 c; S1 p, v* S: k
congenital adrenal hyperplasia producing excessive
) V) @0 I) C- A' s1 M9 D7 w5 ?6 [8 madrenal androgens is a common cause of precocious( F$ h6 Y+ G" q+ T) ?) l3 v% a
puberty in boys.3,4: v  A; Z( d  }" T
The most common form of congenital adrenal( F9 w+ C3 V3 |) M3 b
hyperplasia is the 21-hydroxylase enzyme deficiency.. F* J5 a- M; I1 `+ j
The 11-β hydroxylase deficiency may also result in
* P! `# y# E* {: U) x7 o/ x) Jexcessive adrenal androgen production, and rarely,9 D* b. U. t8 [% X3 V5 S& J6 H
an adrenal tumor may also cause adrenal androgen
$ ~# U6 a! f$ F7 G# Q  }2 h( \excess.1,33 r$ @  s; k8 y* N7 ?7 Y  e
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from4 o; _: [: ]. n9 G! K) G4 [% g
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: G; J. G. J5 i
A unique entity of male-limited gonadotropin-2 f; k* [' \( B8 l. m
independent precocious puberty, which is also known
. b; x1 S  a/ Y$ @! o: B- C: G& k: Eas testotoxicosis, may cause precocious puberty at a
4 d$ w6 B  s) }6 }# Rvery young age. The physical findings in these boys
% \  u5 G! y5 j5 R% T5 t& S4 N! Rwith this disorder are full pubertal development,/ B7 A% n& e" S
including bilateral testicular growth, similar to boys8 A# b1 h4 S  g; E2 [" T& X6 K
with CPP. The gonadotropin levels in this disorder
7 A/ q, g# a% Y# Kare suppressed to prepubertal levels and do not show
* |6 W5 E7 Y2 ~+ Q6 C( d8 Lpubertal response of gonadotropin after gonadotropin-
; p& _( X- }& f( Q" |releasing hormone stimulation. This is a sex-linked
% z2 [- @! |6 s2 m& Y' `+ _autosomal dominant disorder that affects only
9 j5 a4 ^$ b; J% V1 r& }males; therefore, other male members of the family
) {: D8 t$ D+ ]may have similar precocious puberty.3
9 g6 b- x8 j+ Y- |* wIn our patient, physical examination was incon-& o' F  A8 q  |8 g4 B2 `; M. R8 x
sistent with true precocious puberty since his testi-
; c  b9 F# R! f. acles were prepubertal in size. However, testotoxicosis
* Z* z7 ]; b  Mwas in the differential diagnosis because his father  N3 N* K* f" ~8 [6 R1 Z8 s
started puberty somewhat early, and occasionally,4 {9 F) M1 e% P
testicular enlargement is not that evident in the4 ?& W( a( b) ?9 Z2 V
beginning of this process.1 In the absence of a neg-
- x$ c6 Q8 P- \4 cative initial history of androgen exposure, our, n4 [5 C* Z- F) U0 p, m! _
biggest concern was virilizing adrenal hyperplasia,. ^$ J  x: c, Z( e" P  W4 q
either 21-hydroxylase deficiency or 11-β hydroxylase9 E0 C5 a5 [0 v
deficiency. Those diagnoses were excluded by find-7 j$ D) K$ s5 H3 v- [: i5 I
ing the normal level of adrenal steroids.
- S# ?$ I$ c- [4 ^- _The diagnosis of exogenous androgens was strongly& }" r! ^. D' L. e: ]1 i
suspected in a follow-up visit after 4 months because* l2 D0 C3 y6 Q
the physical examination revealed the complete disap-
/ [+ J: Q+ H& q; p" \8 Cpearance of pubic hair, normal growth velocity, and
  ~( p+ y# n, a5 k8 |decreased erections. The father admitted using a testos-
  M$ d# [# S. W  h* h0 qterone gel, which he concealed at first visit. He was
9 z' T9 `/ C5 G; L( Z9 Dusing it rather frequently, twice a day. The Physicians’
" c) R- z3 O. K7 z# FDesk Reference, or package insert of this product, gel or
1 r* D$ D* Y& w5 v1 Z! Xcream, cautions about dermal testosterone transfer to9 P8 U& g$ n, g5 j4 ^7 A
unprotected females through direct skin exposure.
  O: Q$ |. U7 `Serum testosterone level was found to be 2 times the
0 m* f% B. K( J$ ~2 Fbaseline value in those females who were exposed to. P& J1 \7 i2 ^; r4 k* }9 M, L
even 15 minutes of direct skin contact with their male( v6 P+ i% A) P
partners.6 However, when a shirt covered the applica-* ^$ U$ p) d7 t# D, X. b
tion site, this testosterone transfer was prevented.' _+ f% B8 Z5 i: N
Our patient’s testosterone level was 60 ng/mL,
# Z0 i6 L. u7 u/ x6 j5 D0 Gwhich was clearly high. Some studies suggest that
7 e: q0 s: }+ H% z. @+ pdermal conversion of testosterone to dihydrotestos-2 W$ w  ~& z; ~1 d7 s" Z$ o
terone, which is a more potent metabolite, is more
/ D0 d( F9 |5 T5 l; ~7 v$ |4 ?active in young children exposed to testosterone
( ?7 p6 }: v! \& iexogenously7; however, we did not measure a dihy-" k% O- s4 y' S% c7 X
drotestosterone level in our patient. In addition to* d8 Z% b% _% |7 c: z
virilization, exposure to exogenous testosterone in& {5 I0 w' r" B, R. D3 R
children results in an increase in growth velocity and, E; t; K. H6 W/ B
advanced bone age, as seen in our patient.
$ M7 N0 X+ o5 C5 L7 e  AThe long-term effect of androgen exposure during
6 z' R8 \! V( B$ O! N- N. H  Eearly childhood on pubertal development and final6 @4 H, ?. c2 `! W4 h  ~* s
adult height are not fully known and always remain
: u6 @! K/ x4 p: ^" m" J: ka concern. Children treated with short-term testos-
. k( ]" A1 n: Q) D8 Qterone injection or topical androgen may exhibit some3 |; J) Z- x' Q+ k$ O
acceleration of the skeletal maturation; however, after
+ {7 i0 c: S& q/ F8 X+ Q0 [cessation of treatment, the rate of bone maturation1 T2 k: C: W+ r
decelerates and gradually returns to normal.8,9
( y8 K  G/ j0 z5 |There are conflicting reports and controversy* \# o) e9 e/ A1 s
over the effect of early androgen exposure on adult" {  b3 v8 c/ ]) y6 M: ~& S0 ?/ D
penile length.10,11 Some reports suggest subnormal
8 ~* h' T9 q9 W  v1 R1 v8 y1 L% L0 kadult penile length, apparently because of downreg-' B1 D; ^  o% A. K" Y4 L! |
ulation of androgen receptor number.10,12 However,1 j- i% O% r5 {
Sutherland et al13 did not find a correlation between9 W) c3 L" ?- T# h) ^
childhood testosterone exposure and reduced adult! W- v4 O) O2 v' f1 }- V
penile length in clinical studies.
& G' Y- U! y& h5 |# nNonetheless, we do not believe our patient is) z/ Y( n8 O8 l$ ]- _' k
going to experience any of the untoward effects from7 Y5 B; }# @2 C! x: K+ A0 R
testosterone exposure as mentioned earlier because
5 c) H2 x- _9 U4 A+ e" ~the exposure was not for a prolonged period of time.$ Y. F! Z6 q, n1 L! h
Although the bone age was advanced at the time of
* c/ p2 c# m6 R3 wdiagnosis, the child had a normal growth velocity at
: U% X4 V9 U+ ^2 }$ uthe follow-up visit. It is hoped that his final adult8 d# N; }) E/ |9 A. t  d2 S9 @7 f
height will not be affected.
! o9 |3 U% \  M; bAlthough rarely reported, the widespread avail-
: g, e& k9 T. H7 y% U. [; I# Zability of androgen products in our society may+ `  ^; b+ g) U- Q' m! V0 V
indeed cause more virilization in male or female! \# R# w$ w' A1 N
children than one would realize. Exposure to andro-* L1 Q, L) ^' ?6 s8 t
gen products must be considered and specific ques-. ~, @1 M  ]- Q/ e$ V: v' y
tioning about the use of a testosterone product or2 z  G6 }2 s& \. ]( ?
gel should be asked of the family members during# x4 d% V. Z, F+ n# I; u
the evaluation of any children who present with vir-
, E! Q, w% p1 g9 @: G& d$ s; `ilization or peripheral precocious puberty. The diag-2 U5 y' H3 J- E3 R% V0 [
nosis can be established by just a few tests and by
  ~/ k8 e4 e& h- {8 Wappropriate history. The inability to obtain such a
! t6 G0 K1 \  n$ ahistory, or failure to ask the specific questions, may
% Z0 d* s, ^# ]$ S4 }) `result in extensive, unnecessary, and expensive6 \" _( }# M  Z. d1 \, o# m3 L
investigation. The primary care physician should be
0 E: A& [* Y& x/ e+ k9 C9 gaware of this fact, because most of these children
  t5 w7 v/ {/ N7 G0 {) Xmay initially present in their practice. The Physicians’
8 E, R9 `  S/ e$ |0 [Desk Reference and package insert should also put a. O: y3 Y0 P$ f9 v
warning about the virilizing effect on a male or
+ {1 K1 ~1 S. Y% N  z) z$ Qfemale child who might come in contact with some-: k: o% Z$ h. _5 H2 z5 F. }0 J
one using any of these products.
* T1 d* H. {6 Z  E# W- y1 C0 HReferences
' Z9 p. ?7 I; T: P1. Styne DM. The testes: disorder of sexual differentiation
* o+ o+ A1 D) v) R6 O  j& n2 h2 F# Mand puberty in the male. In: Sperling MA, ed. Pediatric
' _5 i' H! L9 M* Z, BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
4 Q; D9 _: E2 c- K/ A# f% H2002: 565-628.
6 w  M$ `! f. V% i2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; P7 b" e9 u6 n! P/ ]
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
8 V' j7 P- ]4 Y  KBoy Induced by Indirect Topical: z% h9 |- w% j
Exposure to Testosterone* z" w2 M" X; [. j* [) e
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,23 ?8 v! X+ T+ Z( J, N
and Kenneth R. Rettig, MD1: a; {3 o# p3 Y9 r! w; M  d
Clinical Pediatrics1 `+ S- V% R& R+ _  ~) u+ \
Volume 46 Number 6
% @: \8 ^6 \) p$ g% m( rJuly 2007 540-543
" f; x7 Z& @) w+ H6 y7 g© 2007 Sage Publications' S3 x/ _; T2 b1 n; O( W
10.1177/0009922806296651
+ N+ @- x2 C, T! P" i" Shttp://clp.sagepub.com
' ?3 K2 U8 U. ihosted at
; S! Q8 S2 S0 k1 c2 ?3 w2 Ihttp://online.sagepub.com
1 a' P, v3 g! P. o3 \& o4 V; ~Precocious puberty in boys, central or peripheral,2 g$ g+ b: a" w) ^' N  a5 `
is a significant concern for physicians. Central
, _0 P" B  C# P4 c/ |- O! F# ]+ b% bprecocious puberty (CPP), which is mediated
+ z- i8 X* n2 g1 b; K6 j( pthrough the hypothalamic pituitary gonadal axis, has: G) Q/ K, t! W- c
a higher incidence of organic central nervous system- r3 a6 f6 m3 x4 |% y5 n: O) m
lesions in boys.1,2 Virilization in boys, as manifested
8 C# ^! l; }3 {$ iby enlargement of the penis, development of pubic
7 ^% |+ |1 x1 I% G, v# k9 mhair, and facial acne without enlargement of testi-0 L1 c' X* A( i) I! W1 ^
cles, suggests peripheral or pseudopuberty.1-3 We
* y3 |% q8 N, w0 w5 y  Mreport a 16-month-old boy who presented with the
+ [& O# D) }5 Zenlargement of the phallus and pubic hair develop-9 ?2 ]' M% h8 B1 u
ment without testicular enlargement, which was due' A/ P, U. u# B5 y( V
to the unintentional exposure to androgen gel used by9 ]+ w8 \3 c5 i; T7 v* Q5 |
the father. The family initially concealed this infor-
& H2 S9 `( `$ l( Wmation, resulting in an extensive work-up for this# s9 p  `! p0 \* M3 f/ v, ]
child. Given the widespread and easy availability of7 K* u- g4 P1 U: R$ W
testosterone gel and cream, we believe this is proba-$ Z5 _0 z& ]) w1 s4 W4 L  k
bly more common than the rare case report in the
( k* J: k$ D8 q! o* L6 E1 \  I, ^literature.40 q; C( B/ K; N. v7 R
Patient Report
  W  N1 W2 F( T, _! MA 16-month-old white child was referred to the: z3 D) O# W4 D0 g6 s9 j
endocrine clinic by his pediatrician with the concern: H  V. ~% A6 B+ t! s' `* Z
of early sexual development. His mother noticed  o% j; N. G. U  k9 @
light colored pubic hair development when he was' W" r. k3 `9 L  }6 u5 _
From the 1Division of Pediatric Endocrinology, 2University of
; `# o& y* y, ~9 ?4 SSouth Alabama Medical Center, Mobile, Alabama.
& }. W# ^1 b* m2 J8 e6 ^/ Z4 FAddress correspondence to: Samar K. Bhowmick, MD, FACE,4 [$ S6 W* P; u7 _
Professor of Pediatrics, University of South Alabama, College of
0 e% p8 A+ U& C- ~Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
8 \1 I3 D/ u  D$ Q* v7 w0 _! [1 }e-mail: [email protected].7 e% }+ {) o; J0 @( n
about 6 to 7 months old, which progressively became# W" [' m$ d7 R
darker. She was also concerned about the enlarge-
  y! n" o/ K+ f' [2 s! gment of his penis and frequent erections. The child& }" v6 L5 Q8 n4 d4 _
was the product of a full-term normal delivery, with; F+ Y( g- \3 a' }) y
a birth weight of 7 lb 14 oz, and birth length of! g5 Z8 N  s4 K- j# T& Z$ I6 }: b
20 inches. He was breast-fed throughout the first year
+ U6 _# Q) X9 X6 U" lof life and was still receiving breast milk along with/ U# E* A7 t. G; A9 Y9 K3 x0 F  p
solid food. He had no hospitalizations or surgery,
* P; u% T( u3 B: Aand his psychosocial and psychomotor development
( @/ y: t9 u, a& `3 ]$ lwas age appropriate.: U+ w" b& l% c
The family history was remarkable for the father,2 U0 s! i. O# U3 M# i4 e) I  Z/ `
who was diagnosed with hypothyroidism at age 16,
( L$ ~* d$ \/ g1 q) P7 \& [' |" k2 {0 lwhich was treated with thyroxine. The father’s
( g0 W5 D) D9 y: Rheight was 6 feet, and he went through a somewhat# @! ~; Q2 @- u9 M4 A, g3 W* M: [0 g5 z
early puberty and had stopped growing by age 14.
/ |: Y; q) A! A. r  pThe father denied taking any other medication. The
' k% Z8 G% k( ~% ?- e! Vchild’s mother was in good health. Her menarche
  T8 _7 N: B( v5 \2 x7 M  x* P' b: Cwas at 11 years of age, and her height was at 5 feet
3 D( l8 m* H/ ^# N( B9 Q5 f5 inches. There was no other family history of pre-( f' ]# b& C: _6 |; s! `; L0 E2 E. C
cocious sexual development in the first-degree rela-. y, P4 m7 H% f; G
tives. There were no siblings.
7 U. e) }. i) v; ~) i$ G& vPhysical Examination
& _" m7 l1 m4 u' q9 g  vThe physical examination revealed a very active," Z& G: ?, u7 z1 d3 r
playful, and healthy boy. The vital signs documented
% ]- {; }8 N+ ?6 [9 g, |, O2 `a blood pressure of 85/50 mm Hg, his length was* U; ]: o( w% b* H# F  `, {" e
90 cm (>97th percentile), and his weight was 14.4 kg" y0 h) K8 L8 h1 q. l. t. w+ x
(also >97th percentile). The observed yearly growth+ u& g% u: D' X) W" A; |! i
velocity was 30 cm (12 inches). The examination of
' f+ r5 l0 w& k$ l7 V3 wthe neck revealed no thyroid enlargement.
. z5 R; r  B7 @+ |The genitourinary examination was remarkable for% }8 Q0 Y, k" |$ _
enlargement of the penis, with a stretched length of$ r7 s# S! N, q
8 cm and a width of 2 cm. The glans penis was very well
" K7 Z( F0 G% R' l$ n2 F# jdeveloped. The pubic hair was Tanner II, mostly around  S- ~+ ~+ s1 j7 ]( p
540
' x6 A$ |* B: M3 L5 w  oat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! i0 |3 W6 J: g
the base of the phallus and was dark and curled. The5 X$ O( X% U7 X; r- ^2 K2 Z" q
testicular volume was prepubertal at 2 mL each.
0 J, r" ]) h5 i( _# L& Z1 WThe skin was moist and smooth and somewhat
# M. n& L4 h  Z, r# [* Koily. No axillary hair was noted. There were no
: |1 o4 k  q+ e' a1 e# u' pabnormal skin pigmentations or café-au-lait spots.
) x$ n. }( ?+ m3 M4 rNeurologic evaluation showed deep tendon reflex 2+. g/ ^+ t; a3 @& u1 v) }" ?
bilateral and symmetrical. There was no suggestion' K1 N) V3 W9 Q
of papilledema.' }  e/ u" n3 i/ e" {+ M/ e
Laboratory Evaluation* L' l( q) Q3 L1 q5 Y9 P  t/ K6 o3 Q
The bone age was consistent with 28 months by
. {* F; W2 O$ v3 [& Xusing the standard of Greulich and Pyle at a chrono-& V0 h* j! s  _5 j7 C
logic age of 16 months (advanced).5 Chromosomal/ U; ~9 z% t' E0 k; W( Q1 s
karyotype was 46XY. The thyroid function test
* Z/ q; G0 V1 b* r% J; D- @showed a free T4 of 1.69 ng/dL, and thyroid stimu-3 q- `) G) H( ~( \
lating hormone level was 1.3 µIU/mL (both normal).
" Y2 n2 b- f  LThe concentrations of serum electrolytes, blood
8 d$ Y; F/ f+ I9 T) H5 f5 e  ourea nitrogen, creatinine, and calcium all were5 p; P5 i- I+ W: I$ ^5 V& M
within normal range for his age. The concentration( C8 O5 K, q- l* }- G  b9 F
of serum 17-hydroxyprogesterone was 16 ng/dL9 f: Y) x; ^: Q$ E( K# Q  v  a: J% A  B
(normal, 3 to 90 ng/dL), androstenedione was 20
/ J/ P" q$ v4 p) nng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-& I  H1 C1 R7 v* F" U) B" y
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
* t( o8 I0 s" s: {) s, o3 s6 o6 wdesoxycorticosterone was 4.3 ng/dL (normal, 7 to8 z" W8 D# {! H7 Y
49ng/dL), 11-desoxycortisol (specific compound S)
$ C/ _" b- z1 g2 x$ _2 e+ x( Mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
9 ]- l: t$ S) t/ i/ `& wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ j- ^9 r$ X1 `( W* J
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 t9 Z0 u" y% D9 ^& r, I" mand β-human chorionic gonadotropin was less than
* |0 ]3 V3 y3 i: ]6 S5 mIU/mL (normal <5 mIU/mL). Serum follicular
2 l. V' m( L* {/ U" pstimulating hormone and leuteinizing hormone6 G4 p( ~6 N+ h/ O7 q! C/ l8 [6 b
concentrations were less than 0.05 mIU/mL2 x! P5 V7 t/ ?" }$ @1 R. O" d& b
(prepubertal).2 C6 J# C3 q- U: Z0 r; ^
The parents were notified about the laboratory1 p5 d! S6 S1 L! d0 W+ n" U, ?7 H
results and were informed that all of the tests were
/ w  a, _5 B- i  Jnormal except the testosterone level was high. The
& x) l3 H) f3 W5 f6 m) f9 ^6 Bfollow-up visit was arranged within a few weeks to- z8 R3 u; m5 E, c3 I
obtain testicular and abdominal sonograms; how-2 r: R+ _4 x7 w2 V
ever, the family did not return for 4 months.
: y5 l. V- W" c( H5 o5 _2 xPhysical examination at this time revealed that the
2 h8 A$ Y+ U0 N" D- _child had grown 2.5 cm in 4 months and had gained1 X' `; O5 f, ^9 B! y9 j$ r$ W( O
2 kg of weight. Physical examination remained
, p- K; y9 \; u9 H- }5 Uunchanged. Surprisingly, the pubic hair almost com-
  K9 |$ `( H8 [; b, e, `pletely disappeared except for a few vellous hairs at
7 j& `+ G* E- y- Uthe base of the phallus. Testicular volume was still 2
, N3 K4 n1 C1 B- S. T, r8 d& WmL, and the size of the penis remained unchanged.
7 I7 N  a) G9 p. @8 EThe mother also said that the boy was no longer hav-
4 Q$ ?( F8 v4 U7 E( g& Zing frequent erections.
0 p( l' {  I$ g. Z& RBoth parents were again questioned about use of
9 n- Q# {) i: P6 q7 n8 ]' Oany ointment/creams that they may have applied to
2 B+ ]& o% [' ]- Uthe child’s skin. This time the father admitted the
/ C8 M3 }$ _3 \' h2 w& @Topical Testosterone Exposure / Bhowmick et al 541
) A/ k2 o% q, ]use of testosterone gel twice daily that he was apply-
; Q* t  W" W& J6 X% c' I; Z6 E1 `ing over his own shoulders, chest, and back area for' E6 g3 u6 u: u
a year. The father also revealed he was embarrassed2 f; N) ^5 a2 R/ T$ }
to disclose that he was using a testosterone gel pre-) b- G1 H  [6 S$ D9 @; D
scribed by his family physician for decreased libido* i* K8 a# r+ F/ E; I/ U
secondary to depression.
$ H' W# A3 D( I$ @The child slept in the same bed with parents.
& K) Z2 Y! W; H' {  T: G6 _The father would hug the baby and hold him on his5 }7 T: F, i* v$ M6 M. r+ U9 z
chest for a considerable period of time, causing sig-6 a$ Z, `) D8 j# W6 O
nificant bare skin contact between baby and father.
4 u$ A% n- }+ {7 {; A0 \8 O, pThe father also admitted that after the phone call,
+ d3 |& b1 T0 \8 Iwhen he learned the testosterone level in the baby
' m, {) C$ q- Ywas high, he then read the product information
% {) [5 k2 i6 a; M8 Z6 s: opacket and concluded that it was most likely the rea-
0 s, M6 \, H3 H6 t2 {. ~3 m6 oson for the child’s virilization. At that time, they
8 ~0 V7 C0 r& y, ldecided to put the baby in a separate bed, and the3 `) ^- F4 Q" n# E+ H
father was not hugging him with bare skin and had% V" J8 Q7 p& h2 T
been using protective clothing. A repeat testosterone
9 A! r! V7 u7 L, V: A, Ntest was ordered, but the family did not go to the
  {0 f7 w! u, E: r& O7 [laboratory to obtain the test.& {* ?6 ^! q7 J( R
Discussion+ Y; o: [! ^; O( r( Z
Precocious puberty in boys is defined as secondary- `3 J4 Z4 f1 \) r2 |. d  H
sexual development before 9 years of age.1,4
5 z; T" N8 n$ i$ _: V0 _Precocious puberty is termed as central (true) when
% r3 e* v0 h; L( M- z  n) git is caused by the premature activation of hypo-
7 v) k: R2 X7 Wthalamic pituitary gonadal axis. CPP is more com-
: d1 m( }* _' S5 L0 Mmon in girls than in boys.1,3 Most boys with CPP
: p, Z3 b' Y7 J, f, b: ?& Umay have a central nervous system lesion that is) M, W& Z1 K: ]# V* O+ c
responsible for the early activation of the hypothal-
& g; L0 T- U0 x; Lamic pituitary gonadal axis.1-3 Thus, greater empha-
; V/ ~& R( M$ c$ A/ Psis has been given to neuroradiologic imaging in
( [# d6 B8 x) X2 {9 ^boys with precocious puberty. In addition to viril-4 t& @# n" o. E- K- |1 C, f, ?' q
ization, the clinical hallmark of CPP is the symmet-. V+ N$ X) O6 {3 O6 M6 n
rical testicular growth secondary to stimulation by
+ Y; n0 Q- b9 K  R, u4 t+ k- {0 t; ggonadotropins.1,3
/ p3 N2 l* ]4 V7 `" h& J& r. b5 EGonadotropin-independent peripheral preco-7 Q( R& S% s. |& M' U
cious puberty in boys also results from inappropriate7 D) ^$ T2 _. q8 z, z
androgenic stimulation from either endogenous or
" S' ^& z) _! R  d1 rexogenous sources, nonpituitary gonadotropin stim-# Y+ F5 g/ ?7 Z* ~' R
ulation, and rare activating mutations.3 Virilizing0 T/ L$ p# ~4 _3 u5 c
congenital adrenal hyperplasia producing excessive" X6 C- |$ ]0 e# u. ?% g
adrenal androgens is a common cause of precocious
$ i  c- V8 b& t# I2 T4 A) V7 K, Hpuberty in boys.3,4
" u, ^6 j4 j7 C; OThe most common form of congenital adrenal
, K4 B2 {5 |5 p3 M! o4 L! lhyperplasia is the 21-hydroxylase enzyme deficiency.
# o1 \6 \# ~' mThe 11-β hydroxylase deficiency may also result in. i. i$ P  O( D' B; }  g0 {
excessive adrenal androgen production, and rarely,
. w3 V" m1 P; J* C9 Man adrenal tumor may also cause adrenal androgen
0 {/ m1 e9 Y. U; eexcess.1,3  g2 i; C. r+ B1 N# y- F% k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: a/ P/ f: ~6 Z% n" M
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! Z3 w# Z1 ~$ @! RA unique entity of male-limited gonadotropin-
, Z# B) l  B% D3 kindependent precocious puberty, which is also known
. m( m6 S& h8 U% T! \% J  F( `as testotoxicosis, may cause precocious puberty at a
1 N8 r/ M* g( O* T: D* f( ~4 fvery young age. The physical findings in these boys" ~+ ?2 a  A& E, x1 z
with this disorder are full pubertal development,1 l5 z# O3 Y( F! H9 G! J, M
including bilateral testicular growth, similar to boys: a- g4 f7 s" S2 T" ~! q1 x. `3 b
with CPP. The gonadotropin levels in this disorder
* l+ T3 ]$ o* k8 r/ \are suppressed to prepubertal levels and do not show  P. `0 E( o, A8 V& p# a
pubertal response of gonadotropin after gonadotropin-
. S: p1 J; F6 o3 v& Preleasing hormone stimulation. This is a sex-linked) N1 d+ w5 P/ x4 J# g+ m
autosomal dominant disorder that affects only
2 x; Z& P' U+ o- G$ Q$ ^9 m) R+ A6 P( Xmales; therefore, other male members of the family: V# X; f- J8 C% _, |( i  I
may have similar precocious puberty.3
( l' ~3 E! d: r8 \In our patient, physical examination was incon-
' K' v7 G$ R. G0 }, a  z+ c0 E! h0 H' qsistent with true precocious puberty since his testi-
& l& F) {, g% B- h+ }6 j. hcles were prepubertal in size. However, testotoxicosis
; A0 E8 u  Q5 e5 mwas in the differential diagnosis because his father
' u9 P; ?0 V$ d( ]started puberty somewhat early, and occasionally,! i+ z* H* g) ^5 R9 M4 D
testicular enlargement is not that evident in the
( t  r9 ^; [: y' abeginning of this process.1 In the absence of a neg-
- d! F: r, u4 ^: bative initial history of androgen exposure, our3 O5 t5 o3 x9 q  J8 a
biggest concern was virilizing adrenal hyperplasia,
4 t4 j7 ]) b  B, Yeither 21-hydroxylase deficiency or 11-β hydroxylase
. C1 p7 p2 f1 Q: }) K! a7 Ldeficiency. Those diagnoses were excluded by find-
0 R1 F) T  S4 j/ Z" i' ^5 h5 jing the normal level of adrenal steroids.4 y8 _" L. [0 j; p7 I
The diagnosis of exogenous androgens was strongly5 h' h: c, e* |* J& a* Z
suspected in a follow-up visit after 4 months because" y7 O( U% R6 W# @& ~+ @3 o
the physical examination revealed the complete disap-$ h0 P: j* @  E+ ]: t* A* w! M/ V
pearance of pubic hair, normal growth velocity, and
) r( @  }- G+ Tdecreased erections. The father admitted using a testos-
, A) i8 c$ w6 X4 g, \* i% g# o! hterone gel, which he concealed at first visit. He was6 |, N1 S& `: s/ B* J
using it rather frequently, twice a day. The Physicians’
5 t( Y  @( G$ ?Desk Reference, or package insert of this product, gel or' D' P/ f9 ^* F: v
cream, cautions about dermal testosterone transfer to3 }/ X* J( `& y5 R9 ~
unprotected females through direct skin exposure.3 {8 M2 |0 }! M9 N
Serum testosterone level was found to be 2 times the
: e$ X  z7 J- T0 j1 c5 B0 ^! ~baseline value in those females who were exposed to
9 l# I* _3 ~8 e0 Y3 @  Reven 15 minutes of direct skin contact with their male
; a' d+ W" Y! Cpartners.6 However, when a shirt covered the applica-. l2 j: L  g9 N& \1 s
tion site, this testosterone transfer was prevented.
4 v+ t$ d" L5 y1 o6 H8 b' _$ _Our patient’s testosterone level was 60 ng/mL,. [# {, w4 T& D: [+ H$ ]
which was clearly high. Some studies suggest that" J/ k6 ?9 c. O. R4 O4 Q
dermal conversion of testosterone to dihydrotestos-
9 Y: p( H) `3 Aterone, which is a more potent metabolite, is more
1 z# C1 l2 O& l0 G/ x0 R+ Zactive in young children exposed to testosterone
+ z( ]* j$ v& E' ?, V9 Gexogenously7; however, we did not measure a dihy-! e- m2 R- k  H6 h3 q2 `0 J
drotestosterone level in our patient. In addition to
$ n/ I% F8 w! C% ]5 \2 dvirilization, exposure to exogenous testosterone in
2 e/ x( P% \' F4 a$ G+ m/ b3 {- nchildren results in an increase in growth velocity and; M! g8 V0 I4 C/ T: \/ h
advanced bone age, as seen in our patient.
, {3 K: h4 W# x: s* w) hThe long-term effect of androgen exposure during
3 p/ e6 i* u; h7 v& dearly childhood on pubertal development and final' e* r% y$ P' V, O4 L$ C8 y
adult height are not fully known and always remain$ d$ z, \" b. S$ B
a concern. Children treated with short-term testos-; g) L, O3 f, ?
terone injection or topical androgen may exhibit some5 l) x& S4 p% F7 o5 E5 C
acceleration of the skeletal maturation; however, after7 u9 f# l2 ]( K! ~# V, w
cessation of treatment, the rate of bone maturation4 W0 I% k' W: Y, w$ W9 W5 c- X
decelerates and gradually returns to normal.8,9
6 h$ U, f# ]3 VThere are conflicting reports and controversy) H; z/ p' B# T( ]
over the effect of early androgen exposure on adult
9 z" {8 h! _: ?( d' I2 k( u2 upenile length.10,11 Some reports suggest subnormal
/ ]# e8 ?/ z8 K% U- uadult penile length, apparently because of downreg-
4 v" K: l# Z$ E- ?9 q! tulation of androgen receptor number.10,12 However,
+ }$ a$ R3 f" [' u; ]) U4 J# Q3 Y2 ZSutherland et al13 did not find a correlation between5 D3 P- }' I, A& e# l7 R
childhood testosterone exposure and reduced adult
0 S7 `: O( F& R0 cpenile length in clinical studies.
. I" k3 D9 C6 x& e3 M% c* g( UNonetheless, we do not believe our patient is
) }4 f- x4 _, tgoing to experience any of the untoward effects from+ B) b+ m: t6 f& a6 T* I4 G$ S
testosterone exposure as mentioned earlier because6 ^( _# g1 G# F( X" x1 Z  Z7 K
the exposure was not for a prolonged period of time.
5 A  h9 u7 u1 ?# o8 L  S1 eAlthough the bone age was advanced at the time of% l- A3 q9 j% h2 F" g
diagnosis, the child had a normal growth velocity at
& H" M+ l: l, `( ^$ O# Qthe follow-up visit. It is hoped that his final adult
' l# p; o" p7 f" I4 L. q' eheight will not be affected.
4 N# K# G) E) a' _! x7 MAlthough rarely reported, the widespread avail-
- \9 m# Q# y9 [6 j9 Q+ j6 o0 bability of androgen products in our society may
3 S7 T  A& `& g. }3 T7 `indeed cause more virilization in male or female
0 a8 V* P8 o7 i" J- }/ Cchildren than one would realize. Exposure to andro-
1 N8 v6 e3 z- z& b3 z3 lgen products must be considered and specific ques-$ i* N6 O1 P2 b7 H# a/ O! T
tioning about the use of a testosterone product or
  q; q2 }/ U: J1 h+ Bgel should be asked of the family members during
& z7 k5 o( M, t, C: g/ Wthe evaluation of any children who present with vir-4 }/ e2 ~" f4 H& s- H+ Y
ilization or peripheral precocious puberty. The diag-3 q; d6 t0 d1 x9 ?
nosis can be established by just a few tests and by6 w4 E8 w' Q' N3 }
appropriate history. The inability to obtain such a8 W! l8 X: ?. C! K" S
history, or failure to ask the specific questions, may
( \5 W  w0 M- l; N' nresult in extensive, unnecessary, and expensive
; g3 d2 L" u( w" P  O" ^investigation. The primary care physician should be5 h8 t" V' I% f" |* y
aware of this fact, because most of these children) x( m  e' n9 h" [# }  M% y
may initially present in their practice. The Physicians’
' F" r) h0 Y+ F8 U  HDesk Reference and package insert should also put a
, E% A7 `3 n) |; s/ W& p7 Mwarning about the virilizing effect on a male or
1 }2 A) e2 I% K5 Nfemale child who might come in contact with some-* L- w, S# C# G$ E: k- f4 [
one using any of these products.
% L. d- s% B4 B& R4 b, UReferences3 M# m- ^2 O3 I% S; y% [$ h
1. Styne DM. The testes: disorder of sexual differentiation
' M$ N9 @+ B- w) E9 ^) p! H% D) Tand puberty in the male. In: Sperling MA, ed. Pediatric9 D3 z& P# w" A! _& }/ B8 B
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
/ f: a0 W! E7 }2002: 565-628.+ w! y) \/ }* {. R( [
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
! \2 \: C- Q; dpuberty 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

! I$ G* m1 F3 w" M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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