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Sexual Precocity in a 16-Month-Old, X+ h: [4 n8 q7 P1 k4 E/ ^
Boy Induced by Indirect Topical
5 W8 A& q' ^" Z+ E5 [3 TExposure to Testosterone
8 Q$ X# d6 x6 Z+ USamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( E) c; l9 `9 g) P7 q$ d
and Kenneth R. Rettig, MD1; \! e5 r6 v- G' U' ]4 Z; X
Clinical Pediatrics% I' o% N( C3 l- j: c
Volume 46 Number 6
/ w/ a7 d5 {/ FJuly 2007 540-543$ {5 f4 |6 O& i% g2 q4 a
© 2007 Sage Publications
* r8 `. K- S+ m10.1177/0009922806296651
) c7 M, M1 E! Nhttp://clp.sagepub.com# T1 E9 q0 c  I2 e' r. x0 O
hosted at
# e6 W3 _9 S+ J1 I: ^2 Lhttp://online.sagepub.com
) h; ~. b7 T# \7 d5 o, n( x/ e6 j! GPrecocious puberty in boys, central or peripheral,, H1 d2 v$ l5 M+ M$ h* C" s! k
is a significant concern for physicians. Central5 G" \( i8 A6 e' }* G7 H$ c
precocious puberty (CPP), which is mediated
9 u) }& f: _% A5 ?# x0 p+ bthrough the hypothalamic pituitary gonadal axis, has$ u4 A8 g/ Q" ?+ b6 c
a higher incidence of organic central nervous system8 E! v- X$ {2 N) ~4 l
lesions in boys.1,2 Virilization in boys, as manifested) W; X# f) |0 \1 N, G
by enlargement of the penis, development of pubic
& W8 j- _( j4 L# `) S3 thair, and facial acne without enlargement of testi-
/ `2 c0 Y9 |; b/ |0 {9 D+ l* N$ R7 icles, suggests peripheral or pseudopuberty.1-3 We
9 p7 O8 t4 k6 w" p( `0 r& Yreport a 16-month-old boy who presented with the
0 C' V- t" D. Y+ renlargement of the phallus and pubic hair develop-
) V6 n' e/ y* s# tment without testicular enlargement, which was due
( p- c4 k% e2 L. I  |9 Y# K% ~to the unintentional exposure to androgen gel used by) [% |8 g2 E& q8 {# k# f, D
the father. The family initially concealed this infor-. T* I+ `! G* q' R0 x! E6 s; t4 x
mation, resulting in an extensive work-up for this
4 G; m9 P8 X5 ~- D, J, F5 J: achild. Given the widespread and easy availability of
9 m/ q( u8 i/ k2 C5 \% rtestosterone gel and cream, we believe this is proba-4 t4 L; L. R$ m( W, M1 w
bly more common than the rare case report in the
. m0 }  ?0 l4 fliterature.48 l; a& n1 S! {- Z; _! X
Patient Report
& c/ c# H. \; J* s! l) [* b! F$ V0 CA 16-month-old white child was referred to the* F& D$ c- l7 S* i9 t3 [2 x
endocrine clinic by his pediatrician with the concern* ?# Q$ \+ m$ w/ Q$ C% w
of early sexual development. His mother noticed
6 r" g* ]9 @7 E& p. L& G, U1 klight colored pubic hair development when he was
1 l$ j4 b  q( _2 f2 [0 WFrom the 1Division of Pediatric Endocrinology, 2University of  A3 b$ A/ J, r4 U
South Alabama Medical Center, Mobile, Alabama.7 ^8 {) z1 B# Z% w; j9 q$ F
Address correspondence to: Samar K. Bhowmick, MD, FACE,# ]9 P; D& h! j2 c& i; j/ x
Professor of Pediatrics, University of South Alabama, College of6 Q/ E% C- Q4 ^
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;; I; I" ?* O/ f' v9 f! u! b6 u
e-mail: [email protected].5 K* I0 C. i& O4 `3 v5 X
about 6 to 7 months old, which progressively became
) q" h0 @( W; `8 F8 P% y& Sdarker. She was also concerned about the enlarge-' M- c/ E5 ~9 I7 X5 |) {; N4 Z
ment of his penis and frequent erections. The child
5 r* X5 @; e. @% ~$ u/ vwas the product of a full-term normal delivery, with
: B( n- N1 ?9 d7 [4 b2 T* p# Ma birth weight of 7 lb 14 oz, and birth length of
# a% K5 h9 h: d0 m  c% V1 _20 inches. He was breast-fed throughout the first year9 p. k# G' ^" n
of life and was still receiving breast milk along with
- g' G) k) a# v, m6 ~) j9 q2 G: osolid food. He had no hospitalizations or surgery,
+ e: i* ^/ P0 ]8 _. g' {6 U6 @8 Kand his psychosocial and psychomotor development
( U* r9 x4 V2 F& A, @( T. bwas age appropriate., L5 c  ?% L( I7 \+ o. m' e
The family history was remarkable for the father,
$ y, ^0 E; C* D( H+ b- l* Zwho was diagnosed with hypothyroidism at age 16,
, @/ Y+ S3 |" Q+ Qwhich was treated with thyroxine. The father’s3 l5 W& m9 L( T. R. \& d
height was 6 feet, and he went through a somewhat
4 Q# K- K: j: g/ f- u: Cearly puberty and had stopped growing by age 14.+ x" |0 w& \0 H7 \( f; Z" l1 P
The father denied taking any other medication. The3 [. Z4 F+ r/ ^5 m
child’s mother was in good health. Her menarche  c! _8 I2 f7 s* S
was at 11 years of age, and her height was at 5 feet! j, P6 r6 `7 i7 t# X. @
5 inches. There was no other family history of pre-
. d; n0 B6 g! y2 B  U4 Zcocious sexual development in the first-degree rela-
4 d2 y- E7 v# V2 o! `tives. There were no siblings.
2 |: \) O+ J7 yPhysical Examination
4 C5 N  P# C. V7 r# U6 r3 PThe physical examination revealed a very active,# T1 R- k1 b. G
playful, and healthy boy. The vital signs documented
$ a4 H! t) H" B3 w& ]9 ga blood pressure of 85/50 mm Hg, his length was0 Q! D0 ~7 |: _! |: g+ K
90 cm (>97th percentile), and his weight was 14.4 kg
" a( x, v9 M2 I8 e' Q2 k(also >97th percentile). The observed yearly growth( f" ]! y# K6 \+ j0 I
velocity was 30 cm (12 inches). The examination of* m4 K* g4 |& K  `* O: u+ T
the neck revealed no thyroid enlargement." e( g! t/ x/ {' k- x, j* G
The genitourinary examination was remarkable for
  k$ {2 V: ?; }9 e; Oenlargement of the penis, with a stretched length of
: ^7 j7 l0 j+ [, \. h+ k8 cm and a width of 2 cm. The glans penis was very well
" C0 C* [: ]& r) Z# ]' q( @developed. The pubic hair was Tanner II, mostly around  g" L: t* y1 F) C8 [" I" F# O
5402 W6 `/ y6 I% }: R0 B. P. F+ S
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from. B3 g6 y% j0 Z9 d# b6 v  g
the base of the phallus and was dark and curled. The
9 l2 L7 d6 n' `! B; L+ Y! @testicular volume was prepubertal at 2 mL each.) ^1 h4 W/ s9 N8 s0 r" F3 X* ]7 B
The skin was moist and smooth and somewhat
' p+ Z# x* g. F7 v7 h9 _4 L. ~oily. No axillary hair was noted. There were no  w7 [' m9 o2 Y$ u; r! _1 ]
abnormal skin pigmentations or café-au-lait spots.
  {( J. e' |# V3 _  LNeurologic evaluation showed deep tendon reflex 2+
5 {0 I7 `3 L- ~- O2 abilateral and symmetrical. There was no suggestion7 @- H! ~- L/ F2 n. x+ a
of papilledema.  k# }8 E  F6 Z! @# R! a5 D8 ?( p
Laboratory Evaluation
% j9 S- x9 I9 x% S% U+ K) \The bone age was consistent with 28 months by7 u# {9 n1 U6 U8 L- W; J1 T
using the standard of Greulich and Pyle at a chrono-
: @  |. i2 o6 I4 [logic age of 16 months (advanced).5 Chromosomal
4 U9 A7 S/ W( ?8 @& Pkaryotype was 46XY. The thyroid function test4 V/ b' ?9 K7 T4 E$ s4 T* }
showed a free T4 of 1.69 ng/dL, and thyroid stimu-2 T3 I% g' I& y# t7 V' @
lating hormone level was 1.3 µIU/mL (both normal).8 a; L0 x& g% O; `
The concentrations of serum electrolytes, blood7 H0 C% t# i% U0 Z% [* _3 `
urea nitrogen, creatinine, and calcium all were
+ z5 w  {- j2 K, n. }0 Q8 Dwithin normal range for his age. The concentration
1 U9 `' x* I9 ~6 q- K/ _of serum 17-hydroxyprogesterone was 16 ng/dL
3 h" M+ M! Y& `# N! e6 d(normal, 3 to 90 ng/dL), androstenedione was 20
/ V3 g+ H% V, n# I3 g- K  e& fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-# B- z; C. j& E. X
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 g, P  E( P* I" b; B% Ndesoxycorticosterone was 4.3 ng/dL (normal, 7 to+ q' W2 e- p/ m/ h
49ng/dL), 11-desoxycortisol (specific compound S)8 `: H5 |/ y# W; p& R" e
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
7 _. k1 d; j: z' ~tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' Y4 Y$ ~) |# W# {( s
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),+ O" Q+ ]2 v, I- ~
and β-human chorionic gonadotropin was less than& r, b. I) N  i) S0 y
5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 @* O) W2 D$ {2 `# l6 f+ B7 t  Estimulating hormone and leuteinizing hormone
  k0 w* |: {9 R) ]  Oconcentrations were less than 0.05 mIU/mL
* y4 O# y6 }6 C( D, o(prepubertal).
/ n/ d4 f$ ^! E: |  b% PThe parents were notified about the laboratory8 R; ]$ K. ~& l% s$ T( `8 g* G
results and were informed that all of the tests were
% k( V% a) P- c2 r; e  M/ N# znormal except the testosterone level was high. The
# K0 P# r. D' i8 [follow-up visit was arranged within a few weeks to0 p4 g# r9 y% @/ G+ g
obtain testicular and abdominal sonograms; how-/ @5 C9 g, \$ |5 H- A
ever, the family did not return for 4 months.
0 }" ?+ _, P. O9 Z7 _# r/ HPhysical examination at this time revealed that the
: d. n( ~6 k* [& tchild had grown 2.5 cm in 4 months and had gained% f' s' q0 {4 b
2 kg of weight. Physical examination remained
6 a* K% ~/ p' y( z$ dunchanged. Surprisingly, the pubic hair almost com-
: v- J* s, X/ I0 Z7 Tpletely disappeared except for a few vellous hairs at: ]! m/ g+ J( a8 a  z8 Y1 J: ^
the base of the phallus. Testicular volume was still 2- I' W# T  d3 y/ S- ^2 I3 `
mL, and the size of the penis remained unchanged.
4 y( c6 B4 T$ Z  q& HThe mother also said that the boy was no longer hav-
' ]6 d9 \/ p, u: p% ]2 }ing frequent erections.
: C* q, r, [# SBoth parents were again questioned about use of: M+ Q1 _, x  s+ O
any ointment/creams that they may have applied to( R( z  f) g% s$ V
the child’s skin. This time the father admitted the
! e- W+ q% s5 @8 v) B6 n7 ~" y# gTopical Testosterone Exposure / Bhowmick et al 541+ `$ G+ e, Y- e
use of testosterone gel twice daily that he was apply-
9 z) ]( G* e( E% w/ O. king over his own shoulders, chest, and back area for9 {' r/ s  c: k% ]( |" l
a year. The father also revealed he was embarrassed% Z2 }& ~/ Q2 ]( j9 E
to disclose that he was using a testosterone gel pre-& b* s. R- P% S+ L0 L0 E; J
scribed by his family physician for decreased libido
! N/ `, p* l3 ]secondary to depression.
* h2 _5 b0 |  F* vThe child slept in the same bed with parents.0 v& @4 t! X5 S/ u3 P  S2 n: ]
The father would hug the baby and hold him on his
: x6 @. G$ K% M: ^; ?chest for a considerable period of time, causing sig-
8 S# d( a' ^$ N5 Inificant bare skin contact between baby and father., g( Z: w$ g3 {) I/ I
The father also admitted that after the phone call,. Z* n+ I5 d( f' h( Y7 |& o9 J7 ]7 h6 d
when he learned the testosterone level in the baby  c6 @: B; j1 G% k
was high, he then read the product information1 r! s5 D& w, U0 ~% L. [9 Z  B8 C
packet and concluded that it was most likely the rea-
7 Y1 N9 O! I1 U9 R5 _son for the child’s virilization. At that time, they% ]1 H1 R5 L& k5 d2 f+ u- z: r/ m8 k% ?
decided to put the baby in a separate bed, and the
. c. S, q/ _' [/ s( I( h( Ofather was not hugging him with bare skin and had( s3 d4 F9 q; i- B
been using protective clothing. A repeat testosterone
* [- C3 K7 {. m9 n' ~test was ordered, but the family did not go to the
2 s" E" l* @0 R# `+ c/ C" N0 elaboratory to obtain the test.
" \1 K# a+ i- E  |' R4 r& V+ DDiscussion
/ z; b5 C/ `8 x3 t2 K1 W- |4 IPrecocious puberty in boys is defined as secondary1 D' B' a* ?9 Z
sexual development before 9 years of age.1,4( `6 J" w! u6 _( S
Precocious puberty is termed as central (true) when1 ~, ]! M1 C8 T$ x8 W
it is caused by the premature activation of hypo-/ G1 k9 i1 d. Q7 {, v& o
thalamic pituitary gonadal axis. CPP is more com-/ f9 L0 O3 e# i3 V% m
mon in girls than in boys.1,3 Most boys with CPP
/ a9 `( F3 a* T+ B% {; Z' |may have a central nervous system lesion that is
$ p0 p# b! z1 Y4 ^' gresponsible for the early activation of the hypothal-
$ N7 n: d7 \0 m% W6 m  t: Hamic pituitary gonadal axis.1-3 Thus, greater empha-
* ^7 Z3 K1 H" L3 g% qsis has been given to neuroradiologic imaging in5 D& S) I  z4 u  U
boys with precocious puberty. In addition to viril-
+ Z4 Q( J3 g; u. Q+ D% _  ~# oization, the clinical hallmark of CPP is the symmet-3 J1 d# ]2 u* J1 n& q% @$ b* T/ W
rical testicular growth secondary to stimulation by8 B; `5 V4 P( B- ^( d, C' e2 \
gonadotropins.1,30 l% w' T0 y  V* H6 _
Gonadotropin-independent peripheral preco-$ }7 [' b5 ?8 Z  i1 ?. Z% r
cious puberty in boys also results from inappropriate+ M( ^" r9 q( P5 J! [( n
androgenic stimulation from either endogenous or5 d) }2 @1 c1 ]8 J! O. e
exogenous sources, nonpituitary gonadotropin stim-
$ X, J' `+ V8 @3 lulation, and rare activating mutations.3 Virilizing* X( O# B7 O' ]
congenital adrenal hyperplasia producing excessive
, `- h2 r: @3 ]adrenal androgens is a common cause of precocious
" O, z9 ]0 T) ipuberty in boys.3,4* L( `; U: Z9 S, u! s# r
The most common form of congenital adrenal
$ O$ d3 g$ |& _  s# T. d5 ghyperplasia is the 21-hydroxylase enzyme deficiency., O$ z/ x8 _, r5 u- X  b5 e& r
The 11-β hydroxylase deficiency may also result in- j5 E8 e6 w; E  ?
excessive adrenal androgen production, and rarely,
' o# \7 G$ h6 V- r5 \an adrenal tumor may also cause adrenal androgen
3 J! d: l: ~6 J. A+ ]. f( m* Z+ _excess.1,3
8 s9 J. ^) y0 L( \2 w: l' _0 ]5 kat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 t$ D, Z4 N* P+ e( m542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
0 B2 \$ K) x! Q: e: B* GA unique entity of male-limited gonadotropin-
+ _+ W+ Q4 q9 X6 ]. windependent precocious puberty, which is also known0 M' i( ~& H+ z' y, R' C$ P$ J
as testotoxicosis, may cause precocious puberty at a
' @) Z2 X& ^1 T, S% k" Yvery young age. The physical findings in these boys( m' X1 Q6 q1 ?5 O9 b" X; w, b& i
with this disorder are full pubertal development,
! m# e- |5 @% d) mincluding bilateral testicular growth, similar to boys# f8 O+ h- [% U, c
with CPP. The gonadotropin levels in this disorder; p8 }7 u4 e8 `6 f, J7 K
are suppressed to prepubertal levels and do not show7 J- u; ^/ B, [( D1 G! S. j
pubertal response of gonadotropin after gonadotropin-, r7 t. @% F% Z9 {; v  Y' q% @* k
releasing hormone stimulation. This is a sex-linked
% u- F# e2 w. E; H3 ?$ o: K6 cautosomal dominant disorder that affects only
  W; N1 e8 G" w% D) @5 _6 Pmales; therefore, other male members of the family
3 m; ~& \+ G3 `) z2 qmay have similar precocious puberty.3
/ g8 M% e. @$ q- W3 {# X/ |8 A7 dIn our patient, physical examination was incon-
/ z! y( Q5 y* v. Y5 Vsistent with true precocious puberty since his testi-1 G- S/ Z) Q- r# I0 z
cles were prepubertal in size. However, testotoxicosis. [+ T$ l! V( P( J) B$ ^0 }
was in the differential diagnosis because his father
  H: T  X' z; X1 w& {: F! _started puberty somewhat early, and occasionally,, T1 {2 i7 f( C( w/ V( }
testicular enlargement is not that evident in the
) R3 u' K/ @: Mbeginning of this process.1 In the absence of a neg-* t7 O/ y0 k( l  g1 p& k! E5 p
ative initial history of androgen exposure, our
$ ]6 H9 }! C# h0 |: u3 b5 Tbiggest concern was virilizing adrenal hyperplasia,% I# j5 v4 a3 K: H) h& }
either 21-hydroxylase deficiency or 11-β hydroxylase
, u2 X& D* `' q: G) udeficiency. Those diagnoses were excluded by find-
; K2 M: @* F7 T( u7 S; Cing the normal level of adrenal steroids.% u! Q. m) z/ r' r& U
The diagnosis of exogenous androgens was strongly; m" a/ d/ P- |* I
suspected in a follow-up visit after 4 months because
7 R* x- b- y0 E* qthe physical examination revealed the complete disap-
" u5 ~" l5 M. a7 a9 _; V( gpearance of pubic hair, normal growth velocity, and- N$ H; G. k/ q& ]# v! D* t5 H  I
decreased erections. The father admitted using a testos-/ P# _$ [1 b& }0 J$ ~3 g' y
terone gel, which he concealed at first visit. He was
" j9 N6 l/ K* L' @using it rather frequently, twice a day. The Physicians’- F7 I3 A  t& T9 B# _, C  u) n& i0 Y/ l
Desk Reference, or package insert of this product, gel or) I. \' r; k5 G7 H8 U
cream, cautions about dermal testosterone transfer to
, h7 W. v& k6 h( gunprotected females through direct skin exposure.
5 s9 F  c  H; B7 |Serum testosterone level was found to be 2 times the
* G: ?5 f* \0 I# H% d- m* Ybaseline value in those females who were exposed to6 B0 J  I4 @$ Z3 K7 R' F9 v
even 15 minutes of direct skin contact with their male
/ s1 Z  q# r, x/ r5 T' upartners.6 However, when a shirt covered the applica-2 {1 b) t+ C  S$ G1 l
tion site, this testosterone transfer was prevented.
/ d/ p. G# A0 \, YOur patient’s testosterone level was 60 ng/mL,/ {$ n# \) O, n) [% R& H
which was clearly high. Some studies suggest that
* z$ j( r% e9 b/ ^+ gdermal conversion of testosterone to dihydrotestos-5 Y6 p! X& x5 D0 m
terone, which is a more potent metabolite, is more
' G+ y- s% O7 o; C$ W3 \active in young children exposed to testosterone
3 T9 A8 r& v2 j! s" R) ~/ j2 B) X" @9 `exogenously7; however, we did not measure a dihy-8 T% ]8 J6 k! J  B5 i
drotestosterone level in our patient. In addition to
! Y! W$ U0 B/ x3 {& r( {% nvirilization, exposure to exogenous testosterone in
  f) e, Z! `8 g" e& f% ichildren results in an increase in growth velocity and
, ?. e2 ?+ M  Cadvanced bone age, as seen in our patient.) ?& ]: R# ]" O- A2 [: K
The long-term effect of androgen exposure during
3 z+ _% H( d$ b+ S3 T% W8 vearly childhood on pubertal development and final, K3 f3 g/ J' ^5 S5 L3 z" d, T
adult height are not fully known and always remain# E* M& X. W* [- ?3 ?4 {, ^
a concern. Children treated with short-term testos-
7 b8 a7 W2 r6 b& k; Y* y- k( N2 Aterone injection or topical androgen may exhibit some
, t, U% n  w0 v5 V* Aacceleration of the skeletal maturation; however, after; z. \4 \/ U1 b
cessation of treatment, the rate of bone maturation- J# |; h4 {& n5 o- W" E
decelerates and gradually returns to normal.8,9
2 M* i7 [9 `5 Q) w3 [3 lThere are conflicting reports and controversy% A# S0 ]5 C2 s2 k' V
over the effect of early androgen exposure on adult8 ?/ c& M: `# ^2 Q0 R4 Q
penile length.10,11 Some reports suggest subnormal. y/ T$ f7 n& ]: D
adult penile length, apparently because of downreg-
! P! {% L% X' o6 p9 _ulation of androgen receptor number.10,12 However,$ b$ u  G* p2 a7 G( r& z' M
Sutherland et al13 did not find a correlation between9 I$ j7 M1 N& F4 N
childhood testosterone exposure and reduced adult
! K3 s6 o8 C- {" l' ]- V2 ]0 hpenile length in clinical studies.
; p3 j  C& b2 e+ z! ^7 ?" J) D6 |Nonetheless, we do not believe our patient is
8 m) Z4 @5 ?; S, t* lgoing to experience any of the untoward effects from! p/ @) J2 x& I* Q3 V+ I- ?6 l
testosterone exposure as mentioned earlier because/ I" [$ h! O! l) ?  I
the exposure was not for a prolonged period of time.# K! n: b( ~$ b& {3 Z" _
Although the bone age was advanced at the time of+ _  C! ]+ Q8 ]( K! `) P
diagnosis, the child had a normal growth velocity at. T% {6 c4 z$ ^' w! H, [+ T; D
the follow-up visit. It is hoped that his final adult
& Y. i9 H9 B2 P% V# X" g' U5 Fheight will not be affected.
* i" ~% h2 [7 T2 a5 VAlthough rarely reported, the widespread avail-
$ s: ^. B3 f, b/ q7 qability of androgen products in our society may
& h0 i* n# I* h! bindeed cause more virilization in male or female
8 H# ], B. f, Y9 G$ ]% }' Mchildren than one would realize. Exposure to andro-# d6 M  G! o) W- V+ H, B8 V% Q
gen products must be considered and specific ques-# i9 j- L6 Q8 T# F5 x0 S' n
tioning about the use of a testosterone product or, P, n/ ^" R9 Y$ D% K' |9 ?+ E$ D
gel should be asked of the family members during
% I; d* B) L4 Y8 F& _/ cthe evaluation of any children who present with vir-  E  {3 Y+ J1 X
ilization or peripheral precocious puberty. The diag-
5 X  }5 g1 N. L) W0 i$ Cnosis can be established by just a few tests and by
. _% z& b- X# Q- l* Q$ r9 rappropriate history. The inability to obtain such a
) w  O9 R" P, `% C8 [! ~: xhistory, or failure to ask the specific questions, may
0 k& N9 Y; q% Z. C9 `7 R* x0 Dresult in extensive, unnecessary, and expensive2 \2 x8 H3 }4 y' Z/ J& m. B$ s% d% e
investigation. The primary care physician should be
2 n- J- @+ i! s( z4 R; naware of this fact, because most of these children
0 {+ F* U+ O& W% }may initially present in their practice. The Physicians’
' J6 `/ w; s. B8 X7 q% _8 XDesk Reference and package insert should also put a
' n, U  T( R" Cwarning about the virilizing effect on a male or
. A& V" l- w* v3 V8 |female child who might come in contact with some-
" d9 N' ~4 |$ A# C2 U/ S) F* Cone using any of these products./ U/ ?* Z( @& u  t' j# k% l
References7 @7 I" Y% V( q4 t. P' @3 B, q: n
1. Styne DM. The testes: disorder of sexual differentiation- F$ u0 |- x$ ?/ D8 m$ s
and puberty in the male. In: Sperling MA, ed. Pediatric( F9 l7 N# e. s# {. \; a7 g
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 R3 K- E1 Q/ C! C/ K
2002: 565-628.1 ]2 j' ?& M; m8 N
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% T0 m5 Z( I# i5 g6 d( Y. g$ Tpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
! i9 T5 c$ B3 c2 I5 ]Boy Induced by Indirect Topical
2 g/ ~/ z( E! {. p  D" zExposure to Testosterone. F( [# x" U9 ~6 i& ?
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 Z8 C/ K6 L( d2 F, Nand Kenneth R. Rettig, MD1
3 l; _, z0 s) A9 x& d  J( k* SClinical Pediatrics
5 q  i$ E% P. _3 xVolume 46 Number 6
9 N3 p6 T$ z7 @/ `% N4 r% Z! wJuly 2007 540-543
8 W) J4 J0 [) E2 a8 b4 p% i© 2007 Sage Publications9 S  l* L" c5 P
10.1177/00099228062966517 D0 j% M, r1 b0 r& O/ V+ n3 b
http://clp.sagepub.com
; |  T) ^  n" L5 o+ O4 o' V# a% ~' dhosted at
. ^% q- f! m- Y6 ehttp://online.sagepub.com' j. x; e0 ~- M5 A1 f
Precocious puberty in boys, central or peripheral,
/ y, |+ Y9 C, e9 w* ]3 o+ X0 U; Yis a significant concern for physicians. Central4 P' O( P3 \4 A+ V; E5 \
precocious puberty (CPP), which is mediated, c1 o* b; V3 F2 }- Q* i
through the hypothalamic pituitary gonadal axis, has- K2 ~: Q( F4 J) i( W3 B
a higher incidence of organic central nervous system
6 [2 D$ b0 c9 S5 |lesions in boys.1,2 Virilization in boys, as manifested
  P+ T$ k( m( ~$ R% Y; d8 ~by enlargement of the penis, development of pubic5 H7 K, _3 G' M) c
hair, and facial acne without enlargement of testi-6 Y# p5 a, j1 K8 I8 q/ V& [% E
cles, suggests peripheral or pseudopuberty.1-3 We
2 B( b" e  r( a, |9 \" Lreport a 16-month-old boy who presented with the
7 ]7 J* t' A5 a3 _! F4 henlargement of the phallus and pubic hair develop-
( T3 c& J$ a7 S( K4 Iment without testicular enlargement, which was due9 }4 q" {) W1 @! U- b* d! `
to the unintentional exposure to androgen gel used by
1 y- v! f' ~8 Qthe father. The family initially concealed this infor-" h1 `- x/ _3 X
mation, resulting in an extensive work-up for this
7 A4 N" P3 p% x, ~) T. o& [; ]child. Given the widespread and easy availability of3 [8 i( M2 f4 t* p" \0 O/ |' x
testosterone gel and cream, we believe this is proba-- B( D- N& v; H/ _# h: V0 G
bly more common than the rare case report in the
6 ~/ ~4 m0 ~7 Z% V5 f2 Wliterature.4/ c1 ], E4 l0 d' L1 Y' `
Patient Report  `8 g6 Q/ T$ H, w0 ]) w& S
A 16-month-old white child was referred to the' t6 j( k& Q# h  W) f
endocrine clinic by his pediatrician with the concern
% p% o5 E- o1 I1 cof early sexual development. His mother noticed
( x( z. @6 p8 C1 M6 Glight colored pubic hair development when he was! v& X1 E3 D$ A# ^: X2 F
From the 1Division of Pediatric Endocrinology, 2University of
% j* T9 ~: X  F# k7 p, dSouth Alabama Medical Center, Mobile, Alabama.- [: O- ~0 T( J2 T/ u$ V  x$ P! {$ v
Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 b( d! z* z) q7 t4 t) p, lProfessor of Pediatrics, University of South Alabama, College of& l& ^/ z) K, n$ l7 `$ b
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 g3 o8 f' z, E8 z" X7 |) c# \, d
e-mail: [email protected].% o8 z9 z+ W' ]$ ~6 w+ ?
about 6 to 7 months old, which progressively became
% |' Y5 d- o: ]5 X% ^darker. She was also concerned about the enlarge-
, ^+ i, a) R  A0 a# @5 ument of his penis and frequent erections. The child' A. a) v" _8 m$ N# [' v6 l
was the product of a full-term normal delivery, with9 G2 k  v( s) C! r" p* r
a birth weight of 7 lb 14 oz, and birth length of
8 |) U! x# u2 J20 inches. He was breast-fed throughout the first year5 r; S6 [; |' D$ m4 v' A; l
of life and was still receiving breast milk along with) X0 v2 e* a* A2 S& d% |  K
solid food. He had no hospitalizations or surgery,- W- s+ Z- D* v( Z5 F
and his psychosocial and psychomotor development
; D# H0 S; }+ O; @4 f' m' S% D% Hwas age appropriate.
$ l5 }* h' P( v, jThe family history was remarkable for the father,' ^: S7 `) P. W- H, Z- D
who was diagnosed with hypothyroidism at age 16,% U( ^3 c( \. q8 ^
which was treated with thyroxine. The father’s
8 w- f2 }  Z& x2 k/ K/ b8 {height was 6 feet, and he went through a somewhat5 k5 F5 j4 F  X) l
early puberty and had stopped growing by age 14.' Z0 p" `  O1 A6 t1 L
The father denied taking any other medication. The' l( e! v# l7 d* l( l
child’s mother was in good health. Her menarche. {! Y* j- l, m- c: D. K" V- f1 T( n
was at 11 years of age, and her height was at 5 feet
' a4 W3 g! M+ [. b0 W0 n5 inches. There was no other family history of pre-
6 y9 @: E. J# g; d+ |cocious sexual development in the first-degree rela-
. T" g8 O5 U. ~9 M9 U( _* f; }  S& Ntives. There were no siblings.2 g+ o1 R$ a, h- ^& a
Physical Examination
3 F4 o+ Z/ s6 r) E# R, Y- s- UThe physical examination revealed a very active,
# O. X3 n# |( _9 t# ~playful, and healthy boy. The vital signs documented4 [9 p) O- A3 g5 t  J% \% S4 _
a blood pressure of 85/50 mm Hg, his length was; Q) n$ p- G7 j7 Z2 ~
90 cm (>97th percentile), and his weight was 14.4 kg
6 [# ~2 f6 @# [- {(also >97th percentile). The observed yearly growth8 e; n1 ^, r% w. y' i8 P+ _2 F
velocity was 30 cm (12 inches). The examination of
% \# l- H( ~# ~* X' Uthe neck revealed no thyroid enlargement.4 O/ w# g3 m: i1 ~1 {* E
The genitourinary examination was remarkable for# Z' a& U7 x1 ]0 I$ i; R
enlargement of the penis, with a stretched length of* {% q- {( u9 O8 ~( k4 }8 B2 g
8 cm and a width of 2 cm. The glans penis was very well
* Y0 l8 B. M+ _; m' u  ?6 X$ Udeveloped. The pubic hair was Tanner II, mostly around, S+ }% U6 O" K: Y& Q  x3 v1 I/ L
540
5 J7 Q3 `% r/ ]5 m5 p7 y" |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 c* c2 a2 ~4 {' b* rthe base of the phallus and was dark and curled. The
3 [# V; C/ y- s4 i% d6 ftesticular volume was prepubertal at 2 mL each.* y6 B3 t9 y4 p+ ~/ Q& q* X
The skin was moist and smooth and somewhat0 l2 n) f" d  L2 w8 ?
oily. No axillary hair was noted. There were no
- M5 R" r& R5 V9 n7 a, M( c* Habnormal skin pigmentations or café-au-lait spots.
$ j: e, C& C7 Q5 yNeurologic evaluation showed deep tendon reflex 2+
4 U  {9 @2 [: ]8 Z% U" M: [bilateral and symmetrical. There was no suggestion
0 S# h# T2 ?! H  p4 c: Gof papilledema.
% P  T. C' Y' K7 H9 s" u% C6 e6 oLaboratory Evaluation
7 w( p/ G1 x# A4 I7 ^The bone age was consistent with 28 months by
" w) j! k7 J% W7 F- v4 Iusing the standard of Greulich and Pyle at a chrono-9 z' J" }& e5 |3 f4 @+ Q8 z
logic age of 16 months (advanced).5 Chromosomal7 b4 }6 y9 i6 W5 g* l# f
karyotype was 46XY. The thyroid function test0 Z6 G+ p; O, B0 ]2 g; `$ }
showed a free T4 of 1.69 ng/dL, and thyroid stimu-4 c7 q% S+ _& M% X# R. ^! t% T8 G
lating hormone level was 1.3 µIU/mL (both normal).$ a+ H- ]! l6 e1 p* E: ]+ H  S6 H
The concentrations of serum electrolytes, blood
$ L; x" @. B1 T4 G; W  a: c; aurea nitrogen, creatinine, and calcium all were
7 v! Q$ w% ~) xwithin normal range for his age. The concentration* c! q0 ~- I* W( v7 W; t" F& j
of serum 17-hydroxyprogesterone was 16 ng/dL9 n; I& \. c* l4 q0 u  W" n/ i- `
(normal, 3 to 90 ng/dL), androstenedione was 202 `' w( ^) \3 X# S: b
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  x# c- [* C# A4 m& g
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 t- }) M' q7 [  Ndesoxycorticosterone was 4.3 ng/dL (normal, 7 to
/ f$ \: g/ p% c1 p) E49ng/dL), 11-desoxycortisol (specific compound S)# K6 o2 T9 W' T, R  q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
3 ^; s6 \# M* i, r; v3 F% o& V3 Itisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 y; z  j2 t# R! a
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),( K+ v: q; v+ M% w
and β-human chorionic gonadotropin was less than
) \0 B" g$ Z# U2 U% l5 mIU/mL (normal <5 mIU/mL). Serum follicular
. n5 w( h: Q( y' `# Vstimulating hormone and leuteinizing hormone* B; y6 g. s9 C# k( Z; v! b
concentrations were less than 0.05 mIU/mL) _2 I5 y9 ?: v& v
(prepubertal).
+ `& w) Z5 K0 b1 f. {3 o! m' NThe parents were notified about the laboratory
7 Z3 F& P5 c. _! K- zresults and were informed that all of the tests were" f( p9 {  \/ j" V- d6 I
normal except the testosterone level was high. The3 V4 I& B& C, Q( B8 z
follow-up visit was arranged within a few weeks to
6 [& E! v: p7 y3 n6 z2 uobtain testicular and abdominal sonograms; how-0 m3 @6 \) h3 g/ u# K* m; g# @
ever, the family did not return for 4 months.
$ ]' I; @7 B- q8 c9 q% PPhysical examination at this time revealed that the2 l, M5 f" e3 W+ H  k$ T8 s
child had grown 2.5 cm in 4 months and had gained/ P$ R; ^$ ]$ ?: g- G9 S  ]6 M1 x
2 kg of weight. Physical examination remained
8 q! C' X% T9 \3 Y( e' ]/ uunchanged. Surprisingly, the pubic hair almost com-. g9 O: N% j9 H5 C2 q- g5 r
pletely disappeared except for a few vellous hairs at
) M& o# [8 J1 _/ A" K8 Rthe base of the phallus. Testicular volume was still 2
4 b  j2 [, D) |+ R# d3 b6 @mL, and the size of the penis remained unchanged.
) j1 }* Z/ ^, W5 MThe mother also said that the boy was no longer hav-* Y) w7 X8 b& ?) v3 b
ing frequent erections.
% j& a9 I: \: k) _& f$ j# H/ _Both parents were again questioned about use of
; A3 y1 M. d: ?4 j0 j; P# ~; Gany ointment/creams that they may have applied to2 \, @6 S# E' U) P- x
the child’s skin. This time the father admitted the
. p+ ]6 T1 z; FTopical Testosterone Exposure / Bhowmick et al 5415 f& [1 s2 H; t1 B
use of testosterone gel twice daily that he was apply-
* z7 _* f  k8 @, E7 I% I2 C; ling over his own shoulders, chest, and back area for. t3 V. ?/ u% A. X) ?
a year. The father also revealed he was embarrassed; ?0 D3 k; W$ g$ y
to disclose that he was using a testosterone gel pre-! ]! Y4 I  r" g: T# O. V$ w' x
scribed by his family physician for decreased libido
; ^9 O: _6 @) Z- n6 I. wsecondary to depression.) r2 }1 m3 n* {5 h7 a  L) X
The child slept in the same bed with parents.
8 f+ Z8 {% q+ f. eThe father would hug the baby and hold him on his
; v* \/ y% b  r( F% N- [) schest for a considerable period of time, causing sig-" a/ F& P( j1 B: d
nificant bare skin contact between baby and father.+ L+ i# Y9 v$ _8 K
The father also admitted that after the phone call,
. v6 F! }. _9 u/ x* Gwhen he learned the testosterone level in the baby
0 o7 O7 D$ R5 x  D- _was high, he then read the product information6 Q' H8 ~' ~" L" J( b( C& b& d  e5 `
packet and concluded that it was most likely the rea-
, S. f5 U2 t- B0 j! f3 bson for the child’s virilization. At that time, they6 u% P: o( s, J; H5 G
decided to put the baby in a separate bed, and the
8 Y, O* o, X8 j% B+ Pfather was not hugging him with bare skin and had; T* c/ u* p! Y( R! H, z0 }, L
been using protective clothing. A repeat testosterone
9 R* l1 M6 w- T: C+ ]test was ordered, but the family did not go to the
$ L, n$ M+ X0 Plaboratory to obtain the test., A6 e2 V# R9 L; k* s& V) l) h2 a
Discussion$ E7 `0 P4 q: Q3 k% U. l
Precocious puberty in boys is defined as secondary
: j' {4 G: l8 e: `7 k$ k- ^sexual development before 9 years of age.1,4
* Y6 G- J  E; ^4 O6 JPrecocious puberty is termed as central (true) when) ]; U6 P1 l* V% D- d
it is caused by the premature activation of hypo-, f" @: P# N% c) B
thalamic pituitary gonadal axis. CPP is more com-( o6 w8 y* G! T8 \+ \
mon in girls than in boys.1,3 Most boys with CPP
) i# Y: \- D$ g" \may have a central nervous system lesion that is
" S2 _1 s. _! N+ Gresponsible for the early activation of the hypothal-
9 g( Z3 P# E$ e( `5 ^" k+ z" Uamic pituitary gonadal axis.1-3 Thus, greater empha-
2 J4 D' O# ?' {+ |/ M! Asis has been given to neuroradiologic imaging in$ c) D) e: P4 w! }5 [+ l0 p
boys with precocious puberty. In addition to viril-
9 p) F" u! |  X. f+ c& X/ |7 Q4 Fization, the clinical hallmark of CPP is the symmet-
) e$ v6 a$ o/ x. Crical testicular growth secondary to stimulation by
6 t- f* S5 B) \' B! xgonadotropins.1,3
! q; C. U2 X: e+ s4 G% o" nGonadotropin-independent peripheral preco-7 ?8 b' V9 m7 a  e
cious puberty in boys also results from inappropriate  J( A& R" A: h
androgenic stimulation from either endogenous or/ W$ N8 T+ T: r9 _$ Z/ K, y1 v
exogenous sources, nonpituitary gonadotropin stim-. Z- p: v7 u: u" i
ulation, and rare activating mutations.3 Virilizing
0 b! B3 F1 q( i" ?. Fcongenital adrenal hyperplasia producing excessive
' g: T$ R0 ?# _3 ]- m" ?4 Ladrenal androgens is a common cause of precocious
9 P4 J/ [) w- a$ G  \, q* d7 Tpuberty in boys.3,4; {$ d0 ~; H* t; [3 o6 t2 q& z7 g
The most common form of congenital adrenal
& b# T3 F# g5 A8 ?hyperplasia is the 21-hydroxylase enzyme deficiency.
5 L! `. T) D% P9 j: q" KThe 11-β hydroxylase deficiency may also result in# ^( T9 Q' u, \0 ^$ D, S
excessive adrenal androgen production, and rarely,- [$ f( I4 R  ~2 K" o# C
an adrenal tumor may also cause adrenal androgen
! X  f7 y' B% o, bexcess.1,3
3 Z0 _& X  x) l# ~& }/ Gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 T- C/ V& M+ Y3 c% G542 Clinical Pediatrics / Vol. 46, No. 6, July 20075 C) {- g# N+ i& |
A unique entity of male-limited gonadotropin-
7 H* p' t5 j& oindependent precocious puberty, which is also known+ r2 i( _: ^% N, }1 b* N
as testotoxicosis, may cause precocious puberty at a
; B4 j' T' j7 Tvery young age. The physical findings in these boys
1 X2 u$ t2 n" Z2 S* v' Lwith this disorder are full pubertal development,
, Q: P8 {  K' q" ?including bilateral testicular growth, similar to boys
( ]  F, B# M9 Y& ^- k% n& mwith CPP. The gonadotropin levels in this disorder
! b3 u$ w+ D7 }are suppressed to prepubertal levels and do not show
1 N; O9 |) V* H; W; Kpubertal response of gonadotropin after gonadotropin-
2 q% q' y. v2 Oreleasing hormone stimulation. This is a sex-linked9 B5 X4 H: ~4 |5 ?% e* v0 g3 _
autosomal dominant disorder that affects only
/ S0 B$ x$ q* `males; therefore, other male members of the family
  ^2 b  p0 d4 p) ]$ L8 @may have similar precocious puberty.39 n. M$ v' R- n* L' [- I
In our patient, physical examination was incon-
; |, u" N& |* V; F9 O' l: q0 I) J$ |0 Osistent with true precocious puberty since his testi-5 M, K9 ~' _: V1 [) W
cles were prepubertal in size. However, testotoxicosis
6 \: j3 {, R! J7 |4 d) d  V0 lwas in the differential diagnosis because his father
+ z+ w: G8 I4 ?started puberty somewhat early, and occasionally,
! @9 m2 A- W! D% xtesticular enlargement is not that evident in the
- Z4 K, S& r4 B3 O. z+ Vbeginning of this process.1 In the absence of a neg-1 c: W5 R3 l/ ]. C
ative initial history of androgen exposure, our
5 |* V( ^4 W# a5 d# zbiggest concern was virilizing adrenal hyperplasia,
, k* U  ~1 L) Weither 21-hydroxylase deficiency or 11-β hydroxylase
5 ~- k0 W# r1 h2 Sdeficiency. Those diagnoses were excluded by find-
; P( Y% {' Q+ j) @6 B6 k: _- N) c; Ying the normal level of adrenal steroids.
6 |) b4 s. ]4 N; g; e! U3 ?The diagnosis of exogenous androgens was strongly- B5 I  N' c! u9 V0 H7 M/ e
suspected in a follow-up visit after 4 months because
1 U& h" f- l" uthe physical examination revealed the complete disap-
- q( U# S, q0 g; Z7 ]4 C: ppearance of pubic hair, normal growth velocity, and- n' ^1 r% s- l$ k2 P
decreased erections. The father admitted using a testos-
) p8 t7 q2 k5 x/ _terone gel, which he concealed at first visit. He was
8 {' x8 y, A4 @+ L+ e& Xusing it rather frequently, twice a day. The Physicians’
! L9 y: [4 g7 zDesk Reference, or package insert of this product, gel or
: w+ G& v; J2 h- f. v) t7 J5 s8 acream, cautions about dermal testosterone transfer to. a# K* y# v  x9 l3 U4 w9 J0 B
unprotected females through direct skin exposure.$ v: k2 L6 v' H
Serum testosterone level was found to be 2 times the# w3 ?8 q. A: U( D' c1 K  {
baseline value in those females who were exposed to$ H" E9 w9 u2 s6 t
even 15 minutes of direct skin contact with their male1 Q' ^! r) Z0 D; a
partners.6 However, when a shirt covered the applica-7 }5 ]- ?  a: V" K5 d9 n; W
tion site, this testosterone transfer was prevented.
5 \# h: D! g% o: ]. L9 m& I, cOur patient’s testosterone level was 60 ng/mL,; I. {7 A4 j: [5 `0 I% G9 u
which was clearly high. Some studies suggest that
; z( g( z0 `1 [6 S: W+ idermal conversion of testosterone to dihydrotestos-% A6 o; b) j5 r* T5 C7 B( a' A
terone, which is a more potent metabolite, is more  H0 R' g! o+ ?
active in young children exposed to testosterone" e3 Q2 L4 d4 y2 E, z2 z
exogenously7; however, we did not measure a dihy-
' t0 q5 ^! e, _1 B7 c& w5 ?0 Qdrotestosterone level in our patient. In addition to$ F$ t: U" f$ t3 B9 c
virilization, exposure to exogenous testosterone in: @4 W: J5 s1 a8 F$ v% M
children results in an increase in growth velocity and
8 I% O: R2 k# y% u* V" x5 gadvanced bone age, as seen in our patient.
- w: U$ j# r. v7 u; k/ j' ZThe long-term effect of androgen exposure during
: Z  I& H: n7 ^$ Dearly childhood on pubertal development and final
, b: v; q9 E3 B/ uadult height are not fully known and always remain* c7 A( d, \1 @; P0 J
a concern. Children treated with short-term testos-
; `$ ]1 j: ?- v6 R. U8 Bterone injection or topical androgen may exhibit some
+ x# v4 S9 o; I9 R% e" Zacceleration of the skeletal maturation; however, after
& T: `) @6 ~' a* B* P. Dcessation of treatment, the rate of bone maturation' u* y. @  f/ P& E: i8 h: H
decelerates and gradually returns to normal.8,9
! x0 ~3 z/ K4 j* L$ G, u/ n( JThere are conflicting reports and controversy+ q) k6 @' Y& r7 a: r
over the effect of early androgen exposure on adult1 d" i: v& R! g) E6 U+ X7 R
penile length.10,11 Some reports suggest subnormal* T! j$ ~. n& R5 z4 d$ H* i
adult penile length, apparently because of downreg-3 P  t/ N" V* W! q1 ]
ulation of androgen receptor number.10,12 However,
' s/ {& {" l6 ?1 mSutherland et al13 did not find a correlation between. M/ x, g% W& C. F
childhood testosterone exposure and reduced adult  A% o: g. x4 A9 f+ p% H* q1 p' q
penile length in clinical studies.. K  x( A6 y1 z3 S. A. {1 }* u
Nonetheless, we do not believe our patient is
) Z8 ~, i6 f5 D# M4 Agoing to experience any of the untoward effects from
4 m1 D6 x. b2 P4 p# L+ \testosterone exposure as mentioned earlier because
; ^! X+ b8 G! `) ]! v: i: Pthe exposure was not for a prolonged period of time.
( P' ]( O& F; P% v8 WAlthough the bone age was advanced at the time of
/ L* r) C2 u, Q. mdiagnosis, the child had a normal growth velocity at
1 M+ v, M$ o- {. \5 e6 ]the follow-up visit. It is hoped that his final adult
/ g' D( b( V& [2 j8 q1 rheight will not be affected.
; R9 M! h+ N% H& H8 V$ j. [Although rarely reported, the widespread avail-. I3 e5 X; p9 x7 Y7 t0 o
ability of androgen products in our society may
6 B6 {1 Y+ [8 ]0 x9 l; \indeed cause more virilization in male or female
6 @5 p1 G# o. X. l  Zchildren than one would realize. Exposure to andro-
& U3 S& ~: U- W, w# \gen products must be considered and specific ques-
* K7 d6 ^" v  E! ?7 Btioning about the use of a testosterone product or
! i) V% g0 v. v" |3 `gel should be asked of the family members during0 }# r! [9 o7 ?5 Z- n0 G
the evaluation of any children who present with vir-
) \/ n6 F8 N7 T/ V* z. e2 g. hilization or peripheral precocious puberty. The diag-
7 u8 e: U7 B) Y! V& wnosis can be established by just a few tests and by
2 {6 C9 l, E2 \3 a  Z- j8 ]appropriate history. The inability to obtain such a
+ u0 W7 W; u6 Uhistory, or failure to ask the specific questions, may
& l' s4 B. u- wresult in extensive, unnecessary, and expensive
6 u/ L! n2 W& [2 v0 yinvestigation. The primary care physician should be7 X: E4 r+ K1 K! P# h: m( W7 l
aware of this fact, because most of these children
/ |1 H% ?% b. u+ dmay initially present in their practice. The Physicians’
7 d# k% G- w) S* B% W5 dDesk Reference and package insert should also put a- Q1 V! T: ]3 ^: v" }" H
warning about the virilizing effect on a male or
  J" u+ ~+ `9 ], i; n  A- Gfemale child who might come in contact with some-
9 k1 q8 y' l5 k* A9 zone using any of these products.
4 N  h6 e6 A9 wReferences
1 U/ u2 Q6 x! o% e1. Styne DM. The testes: disorder of sexual differentiation2 t! O" C6 h6 J" c
and puberty in the male. In: Sperling MA, ed. Pediatric, C& f* O/ {. @: m0 @: a9 b! X% l
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;! E7 h$ H$ R8 }
2002: 565-628.
; P+ C5 D" H+ u9 m2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
( O  |3 e; J: t( n7 ypuberty 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

: l* ?. \9 i: j  z# I4 T, g. \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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