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Sexual Precocity in a 16-Month-Old" O2 R0 B8 Y* P7 v6 O
Boy Induced by Indirect Topical
! I2 y. r8 Y1 \1 p# A! SExposure to Testosterone
- ]1 Q1 [$ X- s! }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
& m4 l- s$ N" }and Kenneth R. Rettig, MD1
" f( q3 U1 |2 f) o6 e. C% xClinical Pediatrics
0 W1 e0 ?. O9 _" }3 f( \% [Volume 46 Number 6
& [. @, X) E! W! ^( }# [July 2007 540-5439 P# I+ [3 L* r: |. t
© 2007 Sage Publications
  q7 k% h/ c: l7 Y9 W10.1177/00099228062966515 Z  E3 D9 C4 e# x% o2 R2 p* i% [
http://clp.sagepub.com
& N% N# H8 h# d% Ahosted at
+ @. f  L  M$ e+ J4 }( Rhttp://online.sagepub.com
  ^" u% ~3 k/ r8 b  |2 C* KPrecocious puberty in boys, central or peripheral,) }! h3 }! R! V' u  |0 S0 H: E
is a significant concern for physicians. Central8 h2 A: _. ]# e# a
precocious puberty (CPP), which is mediated" P) p0 h9 D+ }: X* E3 F$ R
through the hypothalamic pituitary gonadal axis, has" m$ `8 X. b8 G7 y
a higher incidence of organic central nervous system" `3 Z) m4 i) [4 S& e) W; }: }* u
lesions in boys.1,2 Virilization in boys, as manifested
4 U+ J4 x8 g/ Cby enlargement of the penis, development of pubic
3 M+ ^: e% t! o. ^4 E/ Lhair, and facial acne without enlargement of testi-
- c4 r, M9 N" @3 k0 M0 S. ?' Zcles, suggests peripheral or pseudopuberty.1-3 We
  f) D4 y4 Q" s& L* |& }9 \report a 16-month-old boy who presented with the
4 e+ y' ^9 `8 `$ b+ t4 Wenlargement of the phallus and pubic hair develop-
  [7 L$ I! b; o0 k7 L& @- ^ment without testicular enlargement, which was due
9 B6 N% N' y  kto the unintentional exposure to androgen gel used by$ D" a/ n" L; `3 y1 y9 ^9 ~
the father. The family initially concealed this infor-6 U: ~% c1 V' q; u
mation, resulting in an extensive work-up for this* X; I) _$ Y$ t1 j7 n7 m: j. ]
child. Given the widespread and easy availability of
' q) M; |+ r  o" E3 _testosterone gel and cream, we believe this is proba-
) o' a# o4 W  c) m0 U4 u5 ]2 @$ ubly more common than the rare case report in the; b( J' L4 B& k
literature.44 y7 ]# ~4 G, i
Patient Report8 E" E$ m. E7 p* E+ n1 J" S2 O
A 16-month-old white child was referred to the
( b* w: o* U. ^. e. j5 z9 ^' Sendocrine clinic by his pediatrician with the concern
4 H6 B! x/ o+ R1 zof early sexual development. His mother noticed9 ]1 H& y& W' |6 h# l
light colored pubic hair development when he was
4 C- M3 s( V: x/ G+ k8 ^From the 1Division of Pediatric Endocrinology, 2University of3 x0 E! I% N  K' \! l
South Alabama Medical Center, Mobile, Alabama.
4 Z1 C5 [( @6 \, S7 cAddress correspondence to: Samar K. Bhowmick, MD, FACE,% G* f. m: A! ~+ @: o9 B0 p- Q
Professor of Pediatrics, University of South Alabama, College of
1 H) k* P* z3 g5 z0 C7 c) TMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;( K% F) i2 @9 N! e7 w* H/ Y% y
e-mail: [email protected].! h' J, g* \7 p# c4 S  a* E- {
about 6 to 7 months old, which progressively became" ~( k! d/ T( w; `/ z
darker. She was also concerned about the enlarge-
/ c! J6 j) f2 s0 I! ^/ wment of his penis and frequent erections. The child" B; P& C8 P& }5 k
was the product of a full-term normal delivery, with
3 J- l4 V( x2 n6 v3 f' W8 V; ma birth weight of 7 lb 14 oz, and birth length of% z  ]# ~7 ]8 G4 s
20 inches. He was breast-fed throughout the first year
; L8 f( V& t' |: J/ _* j, Hof life and was still receiving breast milk along with
: N- o5 u( |, C7 H7 ksolid food. He had no hospitalizations or surgery,
0 H0 f+ x( ?5 k1 V/ E/ `+ U/ J( o4 }and his psychosocial and psychomotor development
2 W  h# _8 f# j% S/ lwas age appropriate., N0 u, O! _5 n; v; ]$ N. i
The family history was remarkable for the father,
2 R7 q& ?& C; ~& X- j7 o  D' @3 Fwho was diagnosed with hypothyroidism at age 16,# {, a0 P, o$ _$ n0 ^
which was treated with thyroxine. The father’s
# s7 L4 e' L8 e' Sheight was 6 feet, and he went through a somewhat
  p  [& ]0 d: ?  [6 d, kearly puberty and had stopped growing by age 14.# E! h2 F5 B* }7 D2 j
The father denied taking any other medication. The, A7 }0 p+ i$ E$ f# O7 Y0 q& K& Z! k
child’s mother was in good health. Her menarche
1 a6 n; }. s0 Q, ?was at 11 years of age, and her height was at 5 feet
5 M8 @' t) @: a9 i3 S5 inches. There was no other family history of pre-; Z; V& i/ }. v) V5 w
cocious sexual development in the first-degree rela-
! j+ f2 x& Q5 M3 M, d4 c9 Etives. There were no siblings.( N% H4 W$ @( K! u# P
Physical Examination0 u& @9 l" b  Z  X
The physical examination revealed a very active,
+ c. s$ U  m! _/ Y/ oplayful, and healthy boy. The vital signs documented
1 c5 `/ l; X2 i9 Y% T, G. L0 ua blood pressure of 85/50 mm Hg, his length was
9 b. K* M6 {" w90 cm (>97th percentile), and his weight was 14.4 kg
" h- H" |. K% V3 M8 g1 X1 [( [' [(also >97th percentile). The observed yearly growth
- W1 u! o! G1 a0 p4 y  A4 Dvelocity was 30 cm (12 inches). The examination of
  L4 l% h3 a  `  r' n; Ythe neck revealed no thyroid enlargement.
' @) o# R4 s$ r4 R/ w  R$ ZThe genitourinary examination was remarkable for
+ T& {! d& D6 j4 Q# s; |enlargement of the penis, with a stretched length of
2 F  l4 H9 V2 A; j4 ]8 o8 cm and a width of 2 cm. The glans penis was very well8 y4 t9 h/ O6 S+ L, p; U7 Z
developed. The pubic hair was Tanner II, mostly around( Y  R+ ?5 ]' _7 T1 h
5402 e8 ~, h- |! [/ H
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 s! z; K8 `. g7 J3 f8 M& H  `the base of the phallus and was dark and curled. The
% p+ n' U% G6 ^$ `4 S4 n3 ^, b1 Qtesticular volume was prepubertal at 2 mL each.
3 @7 P2 Q6 ~# i+ ^+ b9 T- yThe skin was moist and smooth and somewhat
: {" K% t3 Q/ a- V, {0 ioily. No axillary hair was noted. There were no
0 c9 [3 n& C+ R* [$ qabnormal skin pigmentations or café-au-lait spots.
3 ?7 f+ ?& c% W" W" Y& @9 QNeurologic evaluation showed deep tendon reflex 2+/ W+ k  O) W9 G
bilateral and symmetrical. There was no suggestion
. J+ v" X8 t4 Z, ]1 m" cof papilledema.( O9 }" ~* G3 L7 D) y8 i4 \- I; ]
Laboratory Evaluation
( ^- n1 v7 k% W' y, \; H$ |; xThe bone age was consistent with 28 months by# i6 U6 s/ m, N( ~: E
using the standard of Greulich and Pyle at a chrono-
+ J" t$ w8 A; D* |% b) c6 O! plogic age of 16 months (advanced).5 Chromosomal
; h9 d- Z0 d2 ?# q4 R/ Ckaryotype was 46XY. The thyroid function test9 }/ w! g: x9 d3 {* k
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
; G6 A) q9 D: g% U7 W2 H0 [* rlating hormone level was 1.3 µIU/mL (both normal).' R' A9 I4 C, k! U- r/ f6 s
The concentrations of serum electrolytes, blood
, Y9 `" g3 I4 ^- ^3 surea nitrogen, creatinine, and calcium all were
8 j# X; b$ B! y/ K7 r. ?within normal range for his age. The concentration
* P  a- L5 {9 jof serum 17-hydroxyprogesterone was 16 ng/dL
& G- `1 k+ s. ]; n( t: E(normal, 3 to 90 ng/dL), androstenedione was 20
8 M& y2 ^: T) K6 zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-4 ~5 C/ L  u$ m& z
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
; o# P7 J4 b. V* i6 odesoxycorticosterone was 4.3 ng/dL (normal, 7 to: C  I6 U' f# Y
49ng/dL), 11-desoxycortisol (specific compound S)
( P! Z: j) D5 `2 fwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' W( R9 |! I7 @- p( \7 x$ y, ztisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
( ]' A# d7 p9 Stestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; x: c- O1 k( Band β-human chorionic gonadotropin was less than
# a: H3 I4 o0 N8 n$ G, C8 F5 mIU/mL (normal <5 mIU/mL). Serum follicular! s, E3 B" [" C' P5 S& q! A
stimulating hormone and leuteinizing hormone
! k2 d1 K% M$ D, y5 s5 ]concentrations were less than 0.05 mIU/mL5 o+ `& X  ]3 _8 u! {% o  k3 F
(prepubertal).( M- l' X7 ^$ b/ y! w
The parents were notified about the laboratory
4 m- ~; Y: g. Jresults and were informed that all of the tests were6 |7 p. C. f1 a
normal except the testosterone level was high. The0 ^8 [" n  K) @4 K+ _( i1 ~) S7 `0 M+ \
follow-up visit was arranged within a few weeks to
  _* ?" s' F8 G/ C6 wobtain testicular and abdominal sonograms; how-
0 [7 \7 R/ [$ j- z- z' E3 }ever, the family did not return for 4 months.1 U  i- Q, O3 q' s
Physical examination at this time revealed that the
, s  J+ L5 y3 H* K6 o8 Fchild had grown 2.5 cm in 4 months and had gained
. h' B1 j% R8 O4 [4 I& D4 q- r2 kg of weight. Physical examination remained, n7 J8 r# E! m3 ^
unchanged. Surprisingly, the pubic hair almost com-
, @6 a. Q$ M' c& }( \% wpletely disappeared except for a few vellous hairs at
8 g7 A& J: x0 j7 \, wthe base of the phallus. Testicular volume was still 2+ Z6 @! L1 l5 j6 J6 _
mL, and the size of the penis remained unchanged.! a% |$ W8 Z: W# q1 g
The mother also said that the boy was no longer hav-1 v: V- n" c! L! p8 p( Z
ing frequent erections.( o4 |2 F  q, {: [$ \
Both parents were again questioned about use of6 d; R0 t7 M2 ^% ?+ R0 g1 `$ T
any ointment/creams that they may have applied to
2 |1 d# V& s; G+ _. Zthe child’s skin. This time the father admitted the
7 }, Z# _) b( Y. F+ B) LTopical Testosterone Exposure / Bhowmick et al 5416 x" Q2 |7 [/ m. v  |8 J
use of testosterone gel twice daily that he was apply-' |% _3 K. t# J! r/ C: Q' I
ing over his own shoulders, chest, and back area for- s9 v, I3 L  X5 L9 G5 g) O8 P$ |
a year. The father also revealed he was embarrassed4 q9 k3 _3 V4 s. b! K- B5 E4 \
to disclose that he was using a testosterone gel pre-6 _+ k/ f/ s, I4 c
scribed by his family physician for decreased libido1 t2 q9 t- Q- w' W" _& m; I6 C
secondary to depression.
2 {) B: D4 {$ ~# U% N4 A2 m- \The child slept in the same bed with parents.
, H( p$ T/ w0 Y5 X" d$ f/ d5 OThe father would hug the baby and hold him on his8 \; ~1 p9 D3 @9 k5 J' ?; J
chest for a considerable period of time, causing sig-' G# F2 ?: v* v! m0 D7 w+ v1 u1 _  R- S
nificant bare skin contact between baby and father., G5 [6 P$ I* h
The father also admitted that after the phone call,
8 I0 x# x9 s& ~9 h% swhen he learned the testosterone level in the baby, E3 w( V4 N  M5 v$ e6 P5 o
was high, he then read the product information+ n7 V0 h, G! S# a  H
packet and concluded that it was most likely the rea-0 h! U8 \6 P* h4 n4 K, v0 C/ e" _9 [
son for the child’s virilization. At that time, they2 u9 h' ~( `. w4 H
decided to put the baby in a separate bed, and the
  P+ j+ L$ Z. _, S4 i) a. C8 zfather was not hugging him with bare skin and had# V, Q! g' j% k( t0 `9 {* s# |
been using protective clothing. A repeat testosterone
$ C- V8 T  _9 e. ^/ Qtest was ordered, but the family did not go to the; ?# M+ V" o8 a  M4 ]
laboratory to obtain the test." q" A. n/ U. }! \+ d
Discussion
/ m' D& g6 A4 _Precocious puberty in boys is defined as secondary) B( x6 s4 C$ V- I, p% E% j& I
sexual development before 9 years of age.1,4% K% e4 v( f$ m5 v1 F" ?4 ~
Precocious puberty is termed as central (true) when& e. u2 W# F* R9 y0 d$ a
it is caused by the premature activation of hypo-( M, Y4 V: B9 K5 @1 a4 j
thalamic pituitary gonadal axis. CPP is more com-% t: `% T2 _8 A# ^/ R
mon in girls than in boys.1,3 Most boys with CPP; ]& h8 D2 t* \5 u) E
may have a central nervous system lesion that is; i; G, I: }# H5 u+ ~) C( B
responsible for the early activation of the hypothal-
: f2 s$ t" U9 M, n2 camic pituitary gonadal axis.1-3 Thus, greater empha-
4 V' K9 O1 s4 A9 H* _3 D8 c5 M+ h8 ysis has been given to neuroradiologic imaging in
3 x  ]/ w9 U$ M. A) _! b) bboys with precocious puberty. In addition to viril-$ A$ o- m" S. Z  V7 z, t
ization, the clinical hallmark of CPP is the symmet-9 G* B! Q. B, s1 S' C
rical testicular growth secondary to stimulation by( ]9 J! F0 [0 c
gonadotropins.1,3
+ W6 D& y. o5 @( F) D( iGonadotropin-independent peripheral preco-
$ n* Q! r) |3 `& `cious puberty in boys also results from inappropriate1 m4 i5 O  A: q) ^
androgenic stimulation from either endogenous or
4 ?% t" S; {7 W8 u- p& Fexogenous sources, nonpituitary gonadotropin stim-7 q) q: y! b  @- i  }# l9 D
ulation, and rare activating mutations.3 Virilizing, L( O/ C+ \* p* ~* D3 E
congenital adrenal hyperplasia producing excessive
- z* j! G& y) x7 ?! l' dadrenal androgens is a common cause of precocious- h" I) N6 J  }% X  Y1 g  ]
puberty in boys.3,4
) C7 q; I4 I; iThe most common form of congenital adrenal
! y/ ]4 w& L& g2 i. u1 `: _hyperplasia is the 21-hydroxylase enzyme deficiency.' d. i! D; d2 d7 ?5 B
The 11-β hydroxylase deficiency may also result in. b/ o9 C  \* x. c" o
excessive adrenal androgen production, and rarely,
+ s2 ]6 w6 F# S5 u+ Fan adrenal tumor may also cause adrenal androgen
) T, w" [* o$ ~0 H0 M9 `- ~( j/ L) g5 wexcess.1,3
5 n, a# {# O" e% n; @/ Xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
: I+ t2 q1 f' r542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! h0 R) }7 q% I8 S/ U
A unique entity of male-limited gonadotropin-
, R# k: ~. N& R) t2 r8 pindependent precocious puberty, which is also known
1 Z& s1 o: W: Cas testotoxicosis, may cause precocious puberty at a% R; E9 v* g) U3 \: b
very young age. The physical findings in these boys- V/ k' _. e9 _3 N( B+ ]2 ]
with this disorder are full pubertal development,' {& S" `! k8 b, E& Y, B3 |
including bilateral testicular growth, similar to boys
( K" X. o/ \# c$ [& q) s$ Twith CPP. The gonadotropin levels in this disorder
1 }$ U1 s# H# N# v( Iare suppressed to prepubertal levels and do not show3 f+ f+ r) Z2 W
pubertal response of gonadotropin after gonadotropin-% h; a4 b, t+ @: K" d+ G5 b: f
releasing hormone stimulation. This is a sex-linked
8 P0 A: H) d# C' k+ aautosomal dominant disorder that affects only
  U0 k% _! u$ m( R6 ~males; therefore, other male members of the family6 }0 V6 y% ~- n6 }
may have similar precocious puberty.3
3 `5 A8 O+ z/ \  EIn our patient, physical examination was incon-
; V! ]2 w8 Y# d3 c5 v0 l* [5 A1 Csistent with true precocious puberty since his testi-
/ M% v1 t$ b3 e. b+ @cles were prepubertal in size. However, testotoxicosis. x  A; E5 m% H5 a$ E( B
was in the differential diagnosis because his father  l& d2 t5 E$ d% z. ]- k
started puberty somewhat early, and occasionally,' L- G+ |7 k" ~8 z
testicular enlargement is not that evident in the) A: n( U6 g7 Y6 Z! _/ B9 b; z
beginning of this process.1 In the absence of a neg-# X7 I) R& `, r) {' N, n
ative initial history of androgen exposure, our2 m& X/ M5 w. k5 U; p$ J
biggest concern was virilizing adrenal hyperplasia,1 }0 s( C) J% [2 s  ]3 l
either 21-hydroxylase deficiency or 11-β hydroxylase
. r% f' f0 w$ r+ G- t+ r& A4 S9 bdeficiency. Those diagnoses were excluded by find-
* ~, }4 q4 R8 f" T6 i, |$ z  xing the normal level of adrenal steroids.
4 M( {2 `$ k/ ~The diagnosis of exogenous androgens was strongly+ {" e- s2 q9 \9 i/ O5 t
suspected in a follow-up visit after 4 months because
& X8 m4 Y( Y" M( y; t# G% T  Gthe physical examination revealed the complete disap-
) u* ~) n" k% Y$ K8 ?3 l# A8 y9 n0 zpearance of pubic hair, normal growth velocity, and
% D" {  e' A6 o, \; ~9 U6 Q; L( Sdecreased erections. The father admitted using a testos-
& Z" v" P2 T" h" v0 S6 `terone gel, which he concealed at first visit. He was
& u! D7 q' t: d; Q( R4 y4 pusing it rather frequently, twice a day. The Physicians’
6 |2 \, ~7 z, Q( Q6 H+ ?: u4 O4 W# TDesk Reference, or package insert of this product, gel or9 C' P) E0 Q8 j2 h. N1 y: B
cream, cautions about dermal testosterone transfer to
! {9 S) A+ U" d1 X+ cunprotected females through direct skin exposure.
8 k0 ^7 m) K( E- q$ t5 }1 n9 A$ lSerum testosterone level was found to be 2 times the
; T. o! ]) G" z1 t' b+ |baseline value in those females who were exposed to
- }* V( T- E. Seven 15 minutes of direct skin contact with their male
( t3 L  l% e8 Q5 N8 Tpartners.6 However, when a shirt covered the applica-8 L; c/ I& ~+ T! [
tion site, this testosterone transfer was prevented.6 O" t6 U& s" y! r9 q
Our patient’s testosterone level was 60 ng/mL,
% s( ]) d" z8 \3 P2 K+ R/ jwhich was clearly high. Some studies suggest that
2 M4 Z7 R: e( j7 c! m1 ~5 ^' c9 Fdermal conversion of testosterone to dihydrotestos-
8 E# S. r3 a2 c  N$ F+ U5 \0 v) dterone, which is a more potent metabolite, is more
- F  X2 r" J2 _* P+ C: M1 Tactive in young children exposed to testosterone# c' K- h$ W  P; c; D+ ~+ F6 G9 v4 l
exogenously7; however, we did not measure a dihy-- m5 Z+ q4 I0 Q( y) ]& O
drotestosterone level in our patient. In addition to6 [7 z7 }# M+ o' j
virilization, exposure to exogenous testosterone in
9 J" t0 S( q3 u; l. X7 A5 @8 Schildren results in an increase in growth velocity and
+ E8 V# B3 X) V1 ^advanced bone age, as seen in our patient.2 W& s1 A1 \5 y
The long-term effect of androgen exposure during
: s1 _& M$ c/ X* T  Tearly childhood on pubertal development and final
' w) P' m" }$ Z( G  ^+ ladult height are not fully known and always remain
; X' B* a. D' z8 O" T3 ya concern. Children treated with short-term testos-
( T. e5 ?# T& E' b1 A5 iterone injection or topical androgen may exhibit some% V% C% \7 U" X% t$ o
acceleration of the skeletal maturation; however, after+ m% L) Z( P. h4 \+ M
cessation of treatment, the rate of bone maturation1 b8 c, z2 ]9 I% l' |3 [7 M8 m8 [
decelerates and gradually returns to normal.8,9  _2 U8 e- x2 S& K% V
There are conflicting reports and controversy
" u2 \7 f; P* D' A* xover the effect of early androgen exposure on adult
$ d) L& F5 z- a( ]* Jpenile length.10,11 Some reports suggest subnormal
3 {- I1 R$ q3 h7 q, i1 p7 ^adult penile length, apparently because of downreg-2 z$ V7 m( f( l9 v' k" J
ulation of androgen receptor number.10,12 However,
: x( X# @! h  q8 r3 b3 B/ `0 l8 ySutherland et al13 did not find a correlation between
" p+ D; I& N2 f( @childhood testosterone exposure and reduced adult
2 B# q6 ^+ F* ]" ]4 T5 U4 }* ^penile length in clinical studies.
3 q, N6 g8 c3 l: q2 M' \6 T4 _Nonetheless, we do not believe our patient is
( h6 L; G9 y& A# s4 d2 A* N- Tgoing to experience any of the untoward effects from8 ~; b% v2 B2 s6 U9 t( M
testosterone exposure as mentioned earlier because. d3 [6 A. c; S+ W# \1 P. X! Y: R
the exposure was not for a prolonged period of time.
) p9 Z  q/ {. ]/ h1 i9 ^+ K+ SAlthough the bone age was advanced at the time of
; l; `7 b$ f0 f# Fdiagnosis, the child had a normal growth velocity at- S# A: F1 e2 j+ V) J3 V" O
the follow-up visit. It is hoped that his final adult  m- I  S/ h# f; L
height will not be affected.
( f. G7 J0 F4 oAlthough rarely reported, the widespread avail-/ U, g0 ?! D7 X$ L# t4 T  \2 h
ability of androgen products in our society may
1 `& n# D2 x- E5 ]indeed cause more virilization in male or female5 }# t, {# ]4 I
children than one would realize. Exposure to andro-
7 B% U" g* a2 z+ N% pgen products must be considered and specific ques-
# _0 ?% G5 [0 j( E' c: N; h' ?# Ztioning about the use of a testosterone product or( [, `- Q- V8 \; e  H, S8 r. W. D
gel should be asked of the family members during
* B2 Z% Y% {* a0 ?! i* rthe evaluation of any children who present with vir-
! u& a& x$ `0 ?9 |: cilization or peripheral precocious puberty. The diag-4 Y5 W, Y5 }. P* g& d
nosis can be established by just a few tests and by
0 B+ C  Y3 r4 Z+ t/ fappropriate history. The inability to obtain such a/ T# r. F* s3 l2 w+ e
history, or failure to ask the specific questions, may
; w7 d4 S. w3 [$ H2 m3 sresult in extensive, unnecessary, and expensive' q8 ~4 p8 C+ k. W$ P4 F
investigation. The primary care physician should be' |' M6 Y# ]5 T# e! P% ]
aware of this fact, because most of these children" g9 _/ E3 j- y( d% Y1 d" C# O
may initially present in their practice. The Physicians’
& R: S# n0 g/ Q+ b* pDesk Reference and package insert should also put a
9 I0 e8 w/ w  s. X, Z2 W' jwarning about the virilizing effect on a male or
5 j) _! w; O! [: s) L- M1 [female child who might come in contact with some-
# F8 N$ `! L, [( a" Mone using any of these products.* o0 q8 n3 Y, M! R
References
( Q4 e& v+ s% D& _2 D" _3 D1. Styne DM. The testes: disorder of sexual differentiation
$ g* `& U) [+ u  \& m: d. Dand puberty in the male. In: Sperling MA, ed. Pediatric; F4 i7 s/ f  n# o- O
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
0 V' X- Z) v3 o/ m: G' z5 c* V2002: 565-628.+ [! w; V! d  q) M+ T" s* M
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 P. y* R" A# D
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old# _. y* J! C) K
Boy Induced by Indirect Topical
: X2 C+ n0 Q( L/ E, @$ O( z3 O- BExposure to Testosterone3 B# e3 T9 H& Z$ e
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
  O3 Y, S  i# y+ |and Kenneth R. Rettig, MD1
9 d* ^" s" ^9 S9 G+ n0 Z0 x/ lClinical Pediatrics: X# {2 I9 M3 X% f& S4 M4 Z
Volume 46 Number 6
; C& ]1 h  V8 C7 mJuly 2007 540-5432 Y2 F+ U+ O3 X/ x
© 2007 Sage Publications
( J7 T$ X( n9 |5 A- q3 C( O10.1177/0009922806296651# [- P9 V# T1 E3 L1 U. k0 |. z
http://clp.sagepub.com
( S' d1 \+ Z( |* i% |6 chosted at: `0 _4 Y9 ~0 e/ k  V  i
http://online.sagepub.com
9 u9 K) Q- Z' }Precocious puberty in boys, central or peripheral,/ x, l, g0 g4 z5 {6 y7 l. g8 \
is a significant concern for physicians. Central9 b! s' s$ `: Y" V0 N
precocious puberty (CPP), which is mediated; S! e- S8 [, ?  k( Q+ k# x
through the hypothalamic pituitary gonadal axis, has. U% Q" ^" q) O4 w* h
a higher incidence of organic central nervous system  A% ~3 k# p3 E4 a' x* S  k8 t
lesions in boys.1,2 Virilization in boys, as manifested( C+ R/ r0 v4 |& W; |+ c
by enlargement of the penis, development of pubic
! f. i3 a2 i& E) Y1 c4 Fhair, and facial acne without enlargement of testi-! [) D: R: c: n+ R$ `* D3 q7 e0 u
cles, suggests peripheral or pseudopuberty.1-3 We& H3 v$ q- N% q; {5 F
report a 16-month-old boy who presented with the5 ]6 [$ |" j* X, a' w5 w
enlargement of the phallus and pubic hair develop-
- B) G6 E  L# P# |ment without testicular enlargement, which was due
7 F7 \9 c6 h+ oto the unintentional exposure to androgen gel used by/ O; x% G4 `9 Y9 H
the father. The family initially concealed this infor-! w1 j% ?- R# y3 ^: L( D3 ?  s3 @: m
mation, resulting in an extensive work-up for this4 a0 Z/ I: o3 ?1 e
child. Given the widespread and easy availability of  ~( x/ r; K* [! }# {
testosterone gel and cream, we believe this is proba-
) _( U) I( X$ Bbly more common than the rare case report in the
' h' f$ q- n* a0 W# m6 l7 B5 {; cliterature.4
5 a0 s3 Y' \0 g5 v3 Q, D1 X( ePatient Report% m" K& @$ M' T; T8 O! h6 Z
A 16-month-old white child was referred to the  A3 H6 ?; H" l% t7 Z4 b. y: c
endocrine clinic by his pediatrician with the concern: \2 H( i$ b4 z5 y9 ]8 h) x% f
of early sexual development. His mother noticed
3 z' K: F; |$ C4 olight colored pubic hair development when he was
4 b2 A& n8 x- G6 Z. F3 R, N0 lFrom the 1Division of Pediatric Endocrinology, 2University of
8 d/ j* W9 [0 v, i1 E9 hSouth Alabama Medical Center, Mobile, Alabama.
7 w1 R2 n! Y0 d& \" |$ Z$ K2 k% e! hAddress correspondence to: Samar K. Bhowmick, MD, FACE,% N9 q6 {5 c% }0 f' a
Professor of Pediatrics, University of South Alabama, College of. D1 q- l* R7 a3 V) A1 S/ e
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;3 P5 M- O2 O0 ?& n: L. C/ Q/ c
e-mail: [email protected].
9 j/ S2 u1 f3 E+ E: m7 ]  uabout 6 to 7 months old, which progressively became9 @# [0 [! v0 E: T6 J9 t9 J% F
darker. She was also concerned about the enlarge-
: B- }2 A4 y$ D7 j. Zment of his penis and frequent erections. The child
! i+ N; _7 f! Z/ g# |was the product of a full-term normal delivery, with9 V/ w; j' ~: W! k  i$ y& K0 ?6 J
a birth weight of 7 lb 14 oz, and birth length of4 x0 X2 u% ^5 D5 e! @
20 inches. He was breast-fed throughout the first year* S5 ~4 x& E8 ^% O5 p
of life and was still receiving breast milk along with/ T# h- S/ h6 b- C8 D" G% T7 Y: k
solid food. He had no hospitalizations or surgery,
; S! D4 Y' x, ]and his psychosocial and psychomotor development
, Q+ r; d- `# n) y$ G% d! E$ zwas age appropriate.
/ l: |! S% D2 x: X2 V8 n4 bThe family history was remarkable for the father,0 |4 _  Y% u( k" [' p4 m
who was diagnosed with hypothyroidism at age 16,7 j8 K- z4 F3 H4 J7 s
which was treated with thyroxine. The father’s
' Z+ c+ U% A3 `, Q9 ]1 X+ wheight was 6 feet, and he went through a somewhat9 _* H- a! L$ }: L, ?
early puberty and had stopped growing by age 14.
; y! g) P6 h2 i8 s5 ]8 @0 @& x% zThe father denied taking any other medication. The
/ M- c( E+ D& xchild’s mother was in good health. Her menarche
; g( Q% {0 b' s( [9 ^6 N* Awas at 11 years of age, and her height was at 5 feet; M! l% E  I3 ~2 v
5 inches. There was no other family history of pre-' a! p2 Q+ }9 x9 d0 d% z  V9 h! n4 y
cocious sexual development in the first-degree rela-
" w/ X: m9 l$ i: `# R( k/ C0 rtives. There were no siblings.) c+ [0 R; J& ^# r$ `
Physical Examination
* q% ~/ p) M  A! W5 V0 l/ RThe physical examination revealed a very active,
8 `! X$ G- v# q: i6 iplayful, and healthy boy. The vital signs documented( \# p2 u' N1 x" {" t, d8 A
a blood pressure of 85/50 mm Hg, his length was
" w8 r0 @' _8 o' D6 }; T90 cm (>97th percentile), and his weight was 14.4 kg- p. z6 g/ L2 f' F3 D/ W! a. x
(also >97th percentile). The observed yearly growth
' d. K- u$ i+ x8 a9 Mvelocity was 30 cm (12 inches). The examination of
1 c/ y5 G; f8 O( |! q2 @the neck revealed no thyroid enlargement.
/ l( U9 q  A7 _' W5 b' _+ uThe genitourinary examination was remarkable for  a. @- d9 j' ^# v4 ?0 n7 H
enlargement of the penis, with a stretched length of7 [: \8 I. t7 y
8 cm and a width of 2 cm. The glans penis was very well
( @, @: a9 I3 u2 p7 e  e% Y) P" gdeveloped. The pubic hair was Tanner II, mostly around$ z, P6 k! Y6 ?& p7 |7 H
540& P& G/ [& Y' g; p$ g' u
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
& k0 ?. E/ E' @5 e5 nthe base of the phallus and was dark and curled. The
# C; W& F# i. n: Jtesticular volume was prepubertal at 2 mL each." X% G, k! K. \, |8 {
The skin was moist and smooth and somewhat8 `/ X/ Z  R) p. }% B+ H
oily. No axillary hair was noted. There were no
7 h4 I1 g$ T! f+ vabnormal skin pigmentations or café-au-lait spots.
) H: C( n- Q. F3 \Neurologic evaluation showed deep tendon reflex 2+
) {7 Z0 G7 c% _( Abilateral and symmetrical. There was no suggestion$ g9 O& S6 R3 L, z( E
of papilledema.
  J, d7 r" T" I: U4 R- iLaboratory Evaluation+ |- K7 S5 y* M0 P/ q
The bone age was consistent with 28 months by" W: e% }* O: T; v1 f! o2 \
using the standard of Greulich and Pyle at a chrono-
' `, G) \$ l' T1 C  E0 y1 hlogic age of 16 months (advanced).5 Chromosomal) Z$ [$ j+ w- f' Z% {. t
karyotype was 46XY. The thyroid function test
% p* G1 v. e& M8 H/ \showed a free T4 of 1.69 ng/dL, and thyroid stimu-- m5 C2 @& S: ^: e6 S8 _7 N9 }
lating hormone level was 1.3 µIU/mL (both normal)." v% Y. g# w3 `7 E
The concentrations of serum electrolytes, blood3 T& E; H, U4 d$ c8 k. Z
urea nitrogen, creatinine, and calcium all were; v, Y* A/ Y4 p1 K
within normal range for his age. The concentration' O2 f' \, B+ ]' W5 I9 s% P
of serum 17-hydroxyprogesterone was 16 ng/dL
$ w6 F4 x8 i% I% X8 m; @+ M) c(normal, 3 to 90 ng/dL), androstenedione was 20
, c! ~9 k  ^* ]. n& I1 Lng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- V  s3 J  K0 F4 E$ Oterone was 38 ng/dL (normal, 50 to 760 ng/dL),+ _  E2 r* [. b! N# {% v8 h
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
* E* r' C; H6 j3 L% v! v49ng/dL), 11-desoxycortisol (specific compound S)& `1 W2 n( D& Y& r
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' s* ?+ c* N; E# P8 l; I( Ktisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
0 f, N0 `: X! k$ b  @* Etestosterone was 60 ng/dL (normal <3 to 10 ng/dL),( t, P) }5 p5 `
and β-human chorionic gonadotropin was less than
6 M3 u! t  {0 m, w2 R; X5 mIU/mL (normal <5 mIU/mL). Serum follicular' G4 P9 ~& e+ b; n& w; `  o0 w
stimulating hormone and leuteinizing hormone
8 x7 |1 w( U- H# S# Tconcentrations were less than 0.05 mIU/mL
/ v, @; w& }9 ~/ d(prepubertal).: }: N/ w7 b9 [, @' u: }
The parents were notified about the laboratory
+ e! O7 z1 X2 H% v+ F7 J/ xresults and were informed that all of the tests were( i: I. F- e" n8 c, y+ q
normal except the testosterone level was high. The
# f& Y3 |$ q6 t* ?* b% |1 U5 Bfollow-up visit was arranged within a few weeks to
. @4 D( Y5 P8 T: n# zobtain testicular and abdominal sonograms; how-
* ^! S+ j1 k4 ]# {! A6 yever, the family did not return for 4 months.
( H" \. M' _! f$ L9 {: [Physical examination at this time revealed that the
) ?: ~7 O8 p: @4 w! Zchild had grown 2.5 cm in 4 months and had gained  {1 r7 a2 V6 B( Z8 w# ]: k
2 kg of weight. Physical examination remained
% u/ Y9 H7 d; I" A  K2 Nunchanged. Surprisingly, the pubic hair almost com-
" ?1 u4 ^$ A3 b/ ?3 fpletely disappeared except for a few vellous hairs at# E5 W7 h7 Q8 \# s4 b
the base of the phallus. Testicular volume was still 2
2 r! Q; [1 X0 d) W6 v- r/ g5 w' ]  ymL, and the size of the penis remained unchanged.8 ]2 G. L2 q6 {
The mother also said that the boy was no longer hav-
6 @7 C# I  Y0 m1 U8 \" H4 E/ \ing frequent erections.% M8 W& ^7 r7 V) e
Both parents were again questioned about use of
+ H, b2 A, y+ Z8 s! f& b; a" D- n+ {any ointment/creams that they may have applied to
0 \  T7 |# K; L- zthe child’s skin. This time the father admitted the# a; k4 C9 d+ a7 p
Topical Testosterone Exposure / Bhowmick et al 541- u: B- R' C; V* i( `
use of testosterone gel twice daily that he was apply-) n1 V3 F# r- Z, G- i% b; y) v* d
ing over his own shoulders, chest, and back area for
* h" Y# ~$ S, na year. The father also revealed he was embarrassed
% g  C3 S  |+ U$ f- ]; H& ?to disclose that he was using a testosterone gel pre-
& F+ H1 ^5 L) I/ O9 Q, Oscribed by his family physician for decreased libido
" ?+ K8 H1 J+ V9 o/ a+ e6 csecondary to depression.
: D, d: r$ @8 R- uThe child slept in the same bed with parents.
* N) v0 d4 o, m$ K* ~2 _6 c0 }The father would hug the baby and hold him on his
# ?% j6 \+ }! ]# O: f8 P# |( I. zchest for a considerable period of time, causing sig-  ^8 U* P' t6 C! M
nificant bare skin contact between baby and father., [) M. J) f* _2 j5 R2 a
The father also admitted that after the phone call,  G: W+ s9 @; e. {0 q
when he learned the testosterone level in the baby- v7 m, i9 y. v6 o9 u( v% }( p
was high, he then read the product information
: y/ W* H: G" V3 I, d9 k2 G  \0 Rpacket and concluded that it was most likely the rea-3 u, ]# S( {! X* r
son for the child’s virilization. At that time, they0 g% D& O+ O0 k8 z
decided to put the baby in a separate bed, and the
: H5 g4 k+ T% {% ^- Ofather was not hugging him with bare skin and had- B3 `1 s- A8 J4 A& R
been using protective clothing. A repeat testosterone; V, r1 G/ C. c' w. ]
test was ordered, but the family did not go to the
' j/ x6 E: N. a/ H" A3 Flaboratory to obtain the test.
( n3 P6 S. a; i, g, e3 R/ s7 WDiscussion
& A% {5 r7 T5 `+ MPrecocious puberty in boys is defined as secondary
! o+ A5 e5 w5 e% }$ s% N# ?sexual development before 9 years of age.1,4
) m" r% R8 K& o" C+ e' uPrecocious puberty is termed as central (true) when
% Y2 A1 y  u1 M0 z4 O. f; Git is caused by the premature activation of hypo-6 |- f' ~1 M+ a- q6 p/ V
thalamic pituitary gonadal axis. CPP is more com-% H/ p6 Z( K: L5 x; X$ v4 W- f
mon in girls than in boys.1,3 Most boys with CPP
8 d0 x. x' G, {! Imay have a central nervous system lesion that is
# n6 a2 ^3 t, j' G& A: Qresponsible for the early activation of the hypothal-
3 T5 V) K( @5 E* g4 l1 namic pituitary gonadal axis.1-3 Thus, greater empha-
* D7 l9 P$ r6 J1 o, n8 ^sis has been given to neuroradiologic imaging in
3 u2 l; b* u5 D  N1 ]boys with precocious puberty. In addition to viril-
, H- l0 a( N, G7 P3 Gization, the clinical hallmark of CPP is the symmet-
  U+ u- i; x) ~3 J7 Prical testicular growth secondary to stimulation by1 r+ S  r- T9 ~" [- z
gonadotropins.1,3" r9 e% @$ Y# h6 l: ]
Gonadotropin-independent peripheral preco-9 B. S! A# x$ I1 w
cious puberty in boys also results from inappropriate
5 ~' e! x+ ~  G6 @: fandrogenic stimulation from either endogenous or
, L/ `7 l7 I: E* E# C4 Hexogenous sources, nonpituitary gonadotropin stim-# [7 [! X4 t2 A' L- Q
ulation, and rare activating mutations.3 Virilizing
/ l* m4 t& v5 a. z0 g6 h0 P# bcongenital adrenal hyperplasia producing excessive8 f  Z( L2 k1 ?- {1 \- X) Y
adrenal androgens is a common cause of precocious3 ^! I- G! t8 l. ]- A
puberty in boys.3,4
3 a$ Z) c1 ]& l2 U6 f" K3 MThe most common form of congenital adrenal( C' c6 o9 J$ M  @3 q) n# H& R, V7 z
hyperplasia is the 21-hydroxylase enzyme deficiency.( c$ s; g  a: a% N. e7 z/ s, H
The 11-β hydroxylase deficiency may also result in% E6 g% z# E3 ]! @7 ?8 `" t$ Y+ u: N. A
excessive adrenal androgen production, and rarely,1 S) f: k1 l7 g
an adrenal tumor may also cause adrenal androgen2 Z+ I* a+ Z. r) l5 R
excess.1,3, Q, r9 T/ P3 ^$ ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from9 c2 o3 F& Q  r, ]- \  w
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
9 d2 K5 L6 E1 J# S4 F% WA unique entity of male-limited gonadotropin-
) N4 ]5 K0 d/ n' f( windependent precocious puberty, which is also known% f/ n, p" H9 ^* Q1 z" @- J  d
as testotoxicosis, may cause precocious puberty at a
# n% v9 x2 ^+ H$ Q  hvery young age. The physical findings in these boys/ C- t( F0 d; u4 c. C6 i! e! W3 v
with this disorder are full pubertal development,) n( Z; l1 o4 U8 S
including bilateral testicular growth, similar to boys, N$ r# k2 N4 c1 u
with CPP. The gonadotropin levels in this disorder
6 P1 k7 v: T3 ^- p6 Nare suppressed to prepubertal levels and do not show+ A' d6 y+ W: Y8 d4 n- u6 q
pubertal response of gonadotropin after gonadotropin-' Z  C: A! J0 m
releasing hormone stimulation. This is a sex-linked
' p, v6 P+ y. Fautosomal dominant disorder that affects only0 `( X6 S8 A. K  t
males; therefore, other male members of the family
2 k3 @! i! q3 m- h6 L; k8 W) Ymay have similar precocious puberty.38 ~* d% [( i7 Q0 i$ ?
In our patient, physical examination was incon-
! g, `" j5 K, g$ C# O6 Z  ^sistent with true precocious puberty since his testi-
3 J3 P2 O2 M; r1 ^$ jcles were prepubertal in size. However, testotoxicosis
6 U0 Z+ \+ Z+ C+ kwas in the differential diagnosis because his father  K- h% a8 k0 l2 O) z9 a5 h
started puberty somewhat early, and occasionally,+ A+ c* C0 R- H2 Q3 c- M) I
testicular enlargement is not that evident in the  k& M* S3 q. j- @3 D9 O' _
beginning of this process.1 In the absence of a neg-4 @, u. l* n! `) ]# T: m) h: _
ative initial history of androgen exposure, our
' @: k7 e8 X7 I" n5 V! X2 rbiggest concern was virilizing adrenal hyperplasia,
" d# n( l: l- B' H2 p. g/ Jeither 21-hydroxylase deficiency or 11-β hydroxylase
6 _/ y( i$ B# w7 {deficiency. Those diagnoses were excluded by find-5 W* R% Z: j' K1 Y9 Z5 G0 D3 c) Y
ing the normal level of adrenal steroids.
1 ]" x- n& [* H: HThe diagnosis of exogenous androgens was strongly. \' G' I8 J( _3 G& O& n! q
suspected in a follow-up visit after 4 months because- l  m) d7 L3 Y8 ^& K
the physical examination revealed the complete disap-+ F$ X5 `6 X8 K3 D: i
pearance of pubic hair, normal growth velocity, and5 k4 t- K" R3 p2 f2 H/ X" [; Y& d
decreased erections. The father admitted using a testos-1 H$ Q4 w  U* ?- T1 u% d
terone gel, which he concealed at first visit. He was. v* b+ f. K3 H; y: o; X
using it rather frequently, twice a day. The Physicians’) h9 G, F3 [9 F( n
Desk Reference, or package insert of this product, gel or
8 k8 g0 N& G: J# tcream, cautions about dermal testosterone transfer to6 t5 W0 L$ d# C0 W3 ~
unprotected females through direct skin exposure.; x8 D; `3 \" {$ u. k
Serum testosterone level was found to be 2 times the. X  o7 M' @* h: N* D
baseline value in those females who were exposed to
4 S+ b5 f! D* V9 }even 15 minutes of direct skin contact with their male
8 o8 R% O, r4 }; M, ]0 [6 |. Lpartners.6 However, when a shirt covered the applica-5 U' U, H% _7 H- g
tion site, this testosterone transfer was prevented.
0 y* u1 N; L4 c8 _6 P# ~8 X3 `Our patient’s testosterone level was 60 ng/mL,
2 T  }# v9 W5 L4 Hwhich was clearly high. Some studies suggest that
! t5 H1 e8 d: i8 S( `/ q  ?dermal conversion of testosterone to dihydrotestos-# Z- Z) j; v+ ?$ l4 ^# {7 J! t: J
terone, which is a more potent metabolite, is more
1 f% H+ p: F) k' t$ L& r6 p+ Gactive in young children exposed to testosterone
: t! i3 H$ O( B5 }exogenously7; however, we did not measure a dihy-* R) w, @6 B$ I) `
drotestosterone level in our patient. In addition to/ z; o" T/ D; w' I$ D6 w% m
virilization, exposure to exogenous testosterone in
& r8 r! S# w' t8 ]children results in an increase in growth velocity and
% ]) o* k: n- ]& @6 U7 B, q8 D4 _advanced bone age, as seen in our patient.
1 c& P' ^6 ~- j6 ZThe long-term effect of androgen exposure during* n+ c2 r& [1 O/ {, d/ U
early childhood on pubertal development and final# ?! n1 m6 Q6 f, X' D9 f* V; T
adult height are not fully known and always remain; ]( B" [) m6 x/ B3 w. Y
a concern. Children treated with short-term testos-
- |3 ]7 m- z+ q) Gterone injection or topical androgen may exhibit some+ ^+ q4 P  _/ Z9 ^
acceleration of the skeletal maturation; however, after' ]/ o  v$ d. R9 B
cessation of treatment, the rate of bone maturation
) h1 W- E' k8 s2 X9 fdecelerates and gradually returns to normal.8,9% j9 U) B, K8 \0 d$ ^
There are conflicting reports and controversy
" h4 b# g2 q: G( d1 x4 eover the effect of early androgen exposure on adult
; X: T3 A8 d. J; Apenile length.10,11 Some reports suggest subnormal5 m* v* X$ J6 w: t! ?' E- {
adult penile length, apparently because of downreg-2 j$ ?, d$ y6 I
ulation of androgen receptor number.10,12 However,- S( \7 R: `$ B
Sutherland et al13 did not find a correlation between; o; ?: G9 |4 f- N
childhood testosterone exposure and reduced adult+ P& e% k1 H% U
penile length in clinical studies.
- `4 ^7 _  P5 q! bNonetheless, we do not believe our patient is) @( ~7 T) ]" ?) F- R* a6 l; e; @' z
going to experience any of the untoward effects from
% ~- G  T' g6 ctestosterone exposure as mentioned earlier because% n6 }+ E& g0 K" n. E
the exposure was not for a prolonged period of time.
/ `* E7 g) \6 J# U! m8 B( i6 G1 }Although the bone age was advanced at the time of
( z' X3 S4 [: y* V  b9 V3 Tdiagnosis, the child had a normal growth velocity at4 d9 t% N0 ^9 e- u! C$ P2 T
the follow-up visit. It is hoped that his final adult
! `/ f- h. `' @! ^7 {# qheight will not be affected.
0 K' ^1 S) ^: y2 P3 D5 p& oAlthough rarely reported, the widespread avail-. s+ S  f$ Y' k: i! `% {
ability of androgen products in our society may8 Q9 V) h6 d3 {2 z* Y$ |
indeed cause more virilization in male or female7 [  T- f5 J* J/ ?& t9 s; \% h
children than one would realize. Exposure to andro-+ p5 W5 K. c: E9 r$ O
gen products must be considered and specific ques-# g  V/ z- `; ~
tioning about the use of a testosterone product or- n) o8 ^& n6 z$ N  m4 ?- b9 V6 M- J
gel should be asked of the family members during
, [9 r8 |. K8 s* B7 f+ ~5 h, jthe evaluation of any children who present with vir-( w8 f. C! T. X# L$ L/ n7 i
ilization or peripheral precocious puberty. The diag-
* b  X! U* a7 C; {nosis can be established by just a few tests and by$ |2 ~* s7 q6 c3 |
appropriate history. The inability to obtain such a
8 o+ V# |, s# v8 o( E9 w% bhistory, or failure to ask the specific questions, may6 c. Y! G* j$ M* d
result in extensive, unnecessary, and expensive  f. n. u8 n3 W
investigation. The primary care physician should be
/ A" F; D7 y0 H2 p; Maware of this fact, because most of these children
  E. R' ^& U5 N$ z5 H- Rmay initially present in their practice. The Physicians’/ M, j8 g. K  Y  @' ?6 x; f
Desk Reference and package insert should also put a
3 j+ e) w9 r3 ?/ Z6 u4 e; r! Uwarning about the virilizing effect on a male or) Z* M7 ^) e7 O: \' L
female child who might come in contact with some-8 ^" t( n5 U2 o. d* [4 g$ ^
one using any of these products.
4 B* p# B9 g1 E- N# i, d. E& @: KReferences4 y+ }! u9 K6 K& `/ h5 U$ a
1. Styne DM. The testes: disorder of sexual differentiation
( n% D& j- }4 s7 P$ X8 ^4 Land puberty in the male. In: Sperling MA, ed. Pediatric- y* J' x/ g; ]$ z, o
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 ?3 K" @' {1 A* R. f
2002: 565-628.+ I' o) y8 _7 u; o* i! F* o% J% A
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 d9 k, V/ B: H0 L; R
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
- l2 p8 G* `& u) i9 u" `/ o' y
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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