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Sexual Precocity in a 16-Month-Old% a$ I8 V) W+ R: f; x/ e
Boy Induced by Indirect Topical
  }0 d# T/ P& O& ?: DExposure to Testosterone
# ?" ?" F: R8 \7 vSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 Y$ l( Z( j4 ^+ t6 Band Kenneth R. Rettig, MD1
8 \% T& @3 E$ ?7 WClinical Pediatrics4 V' A2 ?: t6 k: n6 T
Volume 46 Number 6
2 R" \& Y& d# RJuly 2007 540-543! d0 w  U  d+ Z$ m- S2 x
© 2007 Sage Publications
$ B, }) l9 f! S" Y; Q" ^10.1177/0009922806296651- o. v+ u& |, T# s" h
http://clp.sagepub.com
: M! J- `+ C2 ?+ u. ^% yhosted at
( F0 {. t" ]: shttp://online.sagepub.com
+ Y/ ^6 r& r4 t9 oPrecocious puberty in boys, central or peripheral,
* x; ?  o# f$ K' |7 _" G  i: U3 Nis a significant concern for physicians. Central
4 b  A/ a, u: e  `, F/ Tprecocious puberty (CPP), which is mediated
; t+ R. l1 n, B5 x6 ~through the hypothalamic pituitary gonadal axis, has
! k2 t2 ]& M- P$ ]7 Q/ Y* ga higher incidence of organic central nervous system1 A. Y! n3 ]- s+ i  l7 ]  y6 [
lesions in boys.1,2 Virilization in boys, as manifested
  \$ B% N6 R0 f% j  Nby enlargement of the penis, development of pubic
$ r% G/ P, i  X, I, D4 w* u6 H/ n6 ghair, and facial acne without enlargement of testi-+ p+ s. E* n' |1 d+ N  ]; I
cles, suggests peripheral or pseudopuberty.1-3 We* w1 E: a6 |5 R7 }6 a, B9 ~- J7 v
report a 16-month-old boy who presented with the6 v5 d- E# ?5 v
enlargement of the phallus and pubic hair develop-
& D  ~8 f* \$ J* F- R% |ment without testicular enlargement, which was due& s; S2 j: y- T  K, B9 Z" e" e
to the unintentional exposure to androgen gel used by
2 ~1 W' |5 _: Q/ n( b$ Jthe father. The family initially concealed this infor-& n  W5 o$ h7 U
mation, resulting in an extensive work-up for this
8 z' p! O' C& b* dchild. Given the widespread and easy availability of
  r; {' o) w9 |# i& k- \. @$ etestosterone gel and cream, we believe this is proba-
" q2 W! E# Z+ F8 l+ D6 Y3 cbly more common than the rare case report in the, @/ v- `, F6 E" r: ~' X
literature.4
8 @" x' w( {( _5 a+ a5 C; @Patient Report; H" ^. Q, L7 @
A 16-month-old white child was referred to the2 K: w: X+ F0 z* ^" b1 w
endocrine clinic by his pediatrician with the concern3 L0 @4 \; ?' L  J0 F4 x
of early sexual development. His mother noticed
# d1 Y3 Q) S; Z3 ^) klight colored pubic hair development when he was
* |8 i3 e/ ~" a, X$ AFrom the 1Division of Pediatric Endocrinology, 2University of% R1 F1 M% c! E$ }4 K4 S
South Alabama Medical Center, Mobile, Alabama.5 e# n2 g% ?) K3 J
Address correspondence to: Samar K. Bhowmick, MD, FACE,% ?/ U, M7 _. P! N" \
Professor of Pediatrics, University of South Alabama, College of( ^3 C# Z$ Y& M: L
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 O* d7 }7 y$ R, n$ y2 {# N
e-mail: [email protected].% K, N$ I! }( ^8 ]$ X6 l- Y+ ?& j/ s
about 6 to 7 months old, which progressively became  x2 v4 E# [7 ~2 F
darker. She was also concerned about the enlarge-
( Q7 C1 V0 l' Q, O6 q" Bment of his penis and frequent erections. The child
% o0 r7 d. _) gwas the product of a full-term normal delivery, with/ A& I) ~' s8 H5 N1 N
a birth weight of 7 lb 14 oz, and birth length of
& I; f0 e6 V! C. d3 P) s20 inches. He was breast-fed throughout the first year
; j7 E" r. `& v" x5 qof life and was still receiving breast milk along with
7 ~0 q; N1 h: G5 Q* Fsolid food. He had no hospitalizations or surgery,, U1 L7 `% U* E$ c
and his psychosocial and psychomotor development
8 u9 w! D4 f! l9 {) xwas age appropriate.3 m. |  j2 |( v( g) p
The family history was remarkable for the father,6 _7 F" z- y8 m
who was diagnosed with hypothyroidism at age 16,, h% }( A# _6 B3 S2 K
which was treated with thyroxine. The father’s3 ?. w/ W% [6 j) T$ e. ?
height was 6 feet, and he went through a somewhat
* d( W  N+ r; e/ s% ^* H9 t9 E7 |early puberty and had stopped growing by age 14.& _# P7 }: Z, g7 M3 _$ {0 p
The father denied taking any other medication. The
9 N' e! Q( \( M& Y: C$ X& L3 Fchild’s mother was in good health. Her menarche; N( U$ z8 B* A7 C% L& d* X
was at 11 years of age, and her height was at 5 feet% |; d5 `- w# c1 E! l
5 inches. There was no other family history of pre-- H" J# V& P  q- O
cocious sexual development in the first-degree rela-
" X( Z5 T8 D4 F1 htives. There were no siblings.
+ H, q& `, O+ ]6 u" z5 ZPhysical Examination9 R/ L5 P' H: H; U
The physical examination revealed a very active,
: t* m0 t: I4 m0 Zplayful, and healthy boy. The vital signs documented% J  }: x3 d+ [" O# y3 s. v
a blood pressure of 85/50 mm Hg, his length was
" H! ]0 _  M  t% c/ E" c90 cm (>97th percentile), and his weight was 14.4 kg
. }# a. f' Z6 P' ?(also >97th percentile). The observed yearly growth
9 P, E3 _7 e# pvelocity was 30 cm (12 inches). The examination of
! o+ ~* w5 l- H+ X" g# {6 T8 Zthe neck revealed no thyroid enlargement." ~" o6 z$ z4 @% |; C* [1 `. a
The genitourinary examination was remarkable for. }5 b6 @$ z: `$ o7 O! p" k7 @
enlargement of the penis, with a stretched length of
5 a; O2 `4 ^& R5 g/ ~8 cm and a width of 2 cm. The glans penis was very well# m9 o0 T9 A0 R7 l3 |9 M2 L* q/ K
developed. The pubic hair was Tanner II, mostly around2 {9 Z/ [5 d$ T6 l
540: Y' R6 v& u6 z: x' t1 G
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from( i( u. F0 C; l' k" J8 ]. O  V
the base of the phallus and was dark and curled. The
/ F8 G  K* Q" W/ ytesticular volume was prepubertal at 2 mL each." n; e2 t1 [8 S3 ^  w! G! l" {5 b, I
The skin was moist and smooth and somewhat
! v6 H, O& w- j" @5 O' N$ |3 e6 }* Joily. No axillary hair was noted. There were no
; T  {/ q# O( e$ P! I; n$ ]0 Sabnormal skin pigmentations or café-au-lait spots.6 h6 W5 f8 F. @8 \2 n
Neurologic evaluation showed deep tendon reflex 2+
* y) Y( \: A, p% e. f- R' mbilateral and symmetrical. There was no suggestion
! O& X9 I+ x! Z" I+ {' oof papilledema.( b: q& `2 |$ D0 W: f
Laboratory Evaluation
: e: e" h& a9 |) o$ [1 s, q" NThe bone age was consistent with 28 months by
- p5 D1 W; ^$ W1 q$ B! Tusing the standard of Greulich and Pyle at a chrono-* d( {1 B2 c  W9 p" t1 c% T2 r  _
logic age of 16 months (advanced).5 Chromosomal
: E1 w. K) {+ L& B# ]  O0 b" j, j7 Qkaryotype was 46XY. The thyroid function test1 ^1 F: I: i  |# ?* b  m
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
' L" M- ^6 w+ S8 O! S, [& Glating hormone level was 1.3 µIU/mL (both normal).
2 R1 T9 r2 T" M8 k( I; w: gThe concentrations of serum electrolytes, blood. _! H- }8 N5 O) z" d
urea nitrogen, creatinine, and calcium all were/ O. k5 ^- T) @* `
within normal range for his age. The concentration0 M) Z/ X) n. ^' U# ]
of serum 17-hydroxyprogesterone was 16 ng/dL
; ]1 L5 C; p, E: ](normal, 3 to 90 ng/dL), androstenedione was 20
8 B4 s8 N) I7 K# }1 ung/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. K/ C& f5 c- ^- B# ~  Zterone was 38 ng/dL (normal, 50 to 760 ng/dL),% O3 \1 x; W, N, j1 p8 S
desoxycorticosterone was 4.3 ng/dL (normal, 7 to, @; M2 V0 N0 |* F8 ?1 P
49ng/dL), 11-desoxycortisol (specific compound S)
( G6 d  e  O% ~2 pwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-' h6 ^. ~6 l% W, l  b# ]9 g
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ O. @- O8 k: ^! q, i* _  otestosterone was 60 ng/dL (normal <3 to 10 ng/dL),# E. y! R7 f3 q. Y; T+ s
and β-human chorionic gonadotropin was less than, c7 U* J# u& l! U; ~' u- ]
5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 Z! n  ]5 Z/ `/ W$ p, rstimulating hormone and leuteinizing hormone
; W7 E) f5 L6 j+ ]  Hconcentrations were less than 0.05 mIU/mL
; k6 g' ^5 V( J5 \2 H(prepubertal).
/ a7 e4 j: D: s# ?The parents were notified about the laboratory, V( a0 R* D% g7 g7 A* N
results and were informed that all of the tests were
: n0 |/ G7 T+ T. t6 dnormal except the testosterone level was high. The
+ z: d; Y1 k+ F1 v: z* w; Jfollow-up visit was arranged within a few weeks to
1 Q  V) m6 k8 ]; y) K" z" e( @obtain testicular and abdominal sonograms; how-
3 C; w6 m( Q6 \/ u9 `) _! A1 Pever, the family did not return for 4 months.1 P7 v. i' S  v) ?; q9 J; ]7 g! I
Physical examination at this time revealed that the
# ?6 o5 t; O6 E* Lchild had grown 2.5 cm in 4 months and had gained
# t3 W. f! Z. i  k  k: O0 s$ q/ C2 kg of weight. Physical examination remained5 d! A! _9 ?/ b8 }. b
unchanged. Surprisingly, the pubic hair almost com-
' S4 I0 S' Q% S% q/ U0 M, `pletely disappeared except for a few vellous hairs at! Q. J/ K+ _$ c9 `
the base of the phallus. Testicular volume was still 25 m) J  ^. e! U4 I$ W
mL, and the size of the penis remained unchanged.
3 H' i/ t" J' K) G; }/ O' m( YThe mother also said that the boy was no longer hav-, m+ }' v1 x$ l9 p) B9 M
ing frequent erections.
/ A4 y6 ]$ m3 @) \6 i  U! BBoth parents were again questioned about use of& G1 |3 a: f, ]% {
any ointment/creams that they may have applied to
  D7 J# U0 j  A- t3 l+ L1 t" O  Qthe child’s skin. This time the father admitted the
. C0 r/ n% Q) D3 Z# ATopical Testosterone Exposure / Bhowmick et al 541
6 A& z$ |) G4 K0 @use of testosterone gel twice daily that he was apply-
  Q/ Z4 a. G( s; eing over his own shoulders, chest, and back area for, |4 e! m. b. H1 ]9 v
a year. The father also revealed he was embarrassed  {/ u+ p$ p4 c1 e/ X4 |
to disclose that he was using a testosterone gel pre-
* u9 x8 m7 L. `! p3 p5 w- Jscribed by his family physician for decreased libido
; N* }# K7 g4 G4 _! Usecondary to depression.
# }0 p4 b; P0 Z- I  p9 ZThe child slept in the same bed with parents./ ~. E; r6 l: _9 r" g0 s8 v
The father would hug the baby and hold him on his5 w' F# n1 P  V3 Y
chest for a considerable period of time, causing sig-
: q3 A7 F' b$ h; \nificant bare skin contact between baby and father.
6 Y8 S+ j# c2 B' E$ @7 G: {6 v  Q1 ~% nThe father also admitted that after the phone call,; I3 B, j7 ]: A9 e% q( E3 V
when he learned the testosterone level in the baby& u* w' x& O3 s9 m6 P! h) ?5 q
was high, he then read the product information9 p& T: W) F) G6 ]; l0 N
packet and concluded that it was most likely the rea-, h1 x( Q' y# W% ]0 Y
son for the child’s virilization. At that time, they
. {6 z( u. o0 Q* g7 ?: j9 qdecided to put the baby in a separate bed, and the
. `5 S4 [, v. |4 N. Yfather was not hugging him with bare skin and had
' C* P' v# e( ebeen using protective clothing. A repeat testosterone
! t! r: T2 X. o5 j# R5 Etest was ordered, but the family did not go to the
, s+ ?% d( w; L$ Y/ o( {# B( slaboratory to obtain the test.2 o1 f; N; k3 q% {2 N6 Z4 X; j
Discussion/ n$ M# o. R4 T% h
Precocious puberty in boys is defined as secondary4 y9 J: o8 f6 \/ y/ o2 Z
sexual development before 9 years of age.1,4& X! ^7 T- ?+ N4 m3 {- W: H
Precocious puberty is termed as central (true) when
% H2 [( g* C3 z, ^! c, ?it is caused by the premature activation of hypo-( ^# \8 \! y; T7 u& Z/ V
thalamic pituitary gonadal axis. CPP is more com-
4 p" T7 z! B: a3 @7 W* n% }: emon in girls than in boys.1,3 Most boys with CPP
2 z6 G- ^$ M6 E! cmay have a central nervous system lesion that is
$ V0 {+ ]' v" J! j' t! _: g( bresponsible for the early activation of the hypothal-. o5 @. Y0 ]1 H
amic pituitary gonadal axis.1-3 Thus, greater empha-4 g( r& |" ?+ `/ n( n% |# H. d
sis has been given to neuroradiologic imaging in
' V1 l9 h; r  Jboys with precocious puberty. In addition to viril-$ S: v2 ?% n0 m- u9 `' Q
ization, the clinical hallmark of CPP is the symmet-( d4 q3 G7 t! b2 v+ g
rical testicular growth secondary to stimulation by2 L4 E" R# D2 I( ^9 z$ M2 h
gonadotropins.1,32 [& s  j7 E: Q) U7 R! o
Gonadotropin-independent peripheral preco-+ h( J' I- s% Y
cious puberty in boys also results from inappropriate2 Z0 e! \" @* ~* Q0 L
androgenic stimulation from either endogenous or- @$ h/ ]) X+ E: T
exogenous sources, nonpituitary gonadotropin stim-+ H$ |# X* l* N, v7 h# q$ s8 t
ulation, and rare activating mutations.3 Virilizing
1 I2 J; |4 V0 A5 _9 `6 Tcongenital adrenal hyperplasia producing excessive
% `3 t" L/ t6 _" |1 P0 `0 g& ~) Cadrenal androgens is a common cause of precocious
4 a$ G+ b7 E( X8 S" xpuberty in boys.3,4
. c* [/ h( h; j( A, kThe most common form of congenital adrenal
: g$ ?7 S9 I( m9 h' v; ?hyperplasia is the 21-hydroxylase enzyme deficiency.) `* U6 k" E6 m  c
The 11-β hydroxylase deficiency may also result in# b9 l, \9 S0 b7 W# b& Y
excessive adrenal androgen production, and rarely,% r1 ]7 b) S9 y* }" e
an adrenal tumor may also cause adrenal androgen% m+ `8 S6 u+ h* ^
excess.1,3" ?7 s9 J, G6 x: N
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* e4 b5 S6 E$ H542 Clinical Pediatrics / Vol. 46, No. 6, July 2007) I+ d3 c5 B; D2 _. t9 w& K7 M8 C
A unique entity of male-limited gonadotropin-; C2 h' O5 C/ j& |8 o: t3 h( w
independent precocious puberty, which is also known
9 @( @4 V/ J3 las testotoxicosis, may cause precocious puberty at a) F4 N8 j" s8 P2 V8 t" W
very young age. The physical findings in these boys
$ f4 _" c9 I% _! e, f( Qwith this disorder are full pubertal development,7 Y+ N" o9 u3 E6 y& X
including bilateral testicular growth, similar to boys$ h2 M) R5 n, Z, e* B( \
with CPP. The gonadotropin levels in this disorder" \, J% I8 Q% l, R" u
are suppressed to prepubertal levels and do not show# M/ Y0 i* _( L& ^7 C. b* z
pubertal response of gonadotropin after gonadotropin-8 T4 l; {! ^  z" M3 J, q) q4 Z) s
releasing hormone stimulation. This is a sex-linked! z& Z2 n; g; ^. X5 u* E
autosomal dominant disorder that affects only
; R+ J$ D( W# x( i+ n' z7 I( {males; therefore, other male members of the family0 o$ m! @+ ~4 c" g. [- l8 N
may have similar precocious puberty.3
/ a# ]6 [& ^4 E; UIn our patient, physical examination was incon-5 d4 N5 T' _: `& R( y
sistent with true precocious puberty since his testi-6 F% S. O2 A: E
cles were prepubertal in size. However, testotoxicosis
; B+ j2 K) F, Q7 b0 x- ?( [/ U4 nwas in the differential diagnosis because his father
1 T+ X0 f% j3 ~/ cstarted puberty somewhat early, and occasionally,
) a. m' b$ j& Q0 Q' x; jtesticular enlargement is not that evident in the
4 P' l, l6 B" c3 \beginning of this process.1 In the absence of a neg-
+ D6 I8 f) _: k/ ~, }' d# Cative initial history of androgen exposure, our, x5 U, w' @$ S9 y0 S6 y! K
biggest concern was virilizing adrenal hyperplasia,$ m5 Q# a: v# {* k- h
either 21-hydroxylase deficiency or 11-β hydroxylase/ H/ d  O' Z4 i# Y! u4 ]
deficiency. Those diagnoses were excluded by find-
. S5 I5 x0 }, P0 V+ fing the normal level of adrenal steroids./ p) m  h9 V6 w* O) b
The diagnosis of exogenous androgens was strongly( E3 S& Z2 J& m/ V0 P" {
suspected in a follow-up visit after 4 months because  P9 s0 R7 r1 H7 o, E! }
the physical examination revealed the complete disap-# q! Z2 A# i% B" d: Y; k
pearance of pubic hair, normal growth velocity, and
  J* ?: [; `- Q+ Z* f9 M- odecreased erections. The father admitted using a testos-6 e9 N; z% |4 D( W0 V
terone gel, which he concealed at first visit. He was, g' `: }% H* Z$ B) n; u: T
using it rather frequently, twice a day. The Physicians’6 y0 f8 i6 u2 A7 R& n/ _# S
Desk Reference, or package insert of this product, gel or
" Y, F/ S# S$ l. A2 zcream, cautions about dermal testosterone transfer to
& |; ?0 F! W* c- I% k( ]& uunprotected females through direct skin exposure.1 k4 B  q: m) Y' R9 `
Serum testosterone level was found to be 2 times the
1 R" d6 S9 U/ Y. {  x& H% _baseline value in those females who were exposed to
3 r/ k2 B6 @& ^1 K- E+ L" `even 15 minutes of direct skin contact with their male" G8 d, D* F* p# X- I8 D: B, z
partners.6 However, when a shirt covered the applica-
4 U- m" _$ ~& J% E( etion site, this testosterone transfer was prevented.8 j8 \  Z4 U& A+ S% P4 [# g
Our patient’s testosterone level was 60 ng/mL,
6 F# i, ^! I" G2 o- I0 n5 nwhich was clearly high. Some studies suggest that) I; X2 Z2 V5 |% t
dermal conversion of testosterone to dihydrotestos-% {5 e+ B1 y6 L& M
terone, which is a more potent metabolite, is more
7 j4 p; M1 b0 \, K6 X5 Nactive in young children exposed to testosterone
( M2 {$ h. j, @. y7 k4 p+ qexogenously7; however, we did not measure a dihy-, n- ^$ E" m7 N1 |* I( Y7 a6 M- o
drotestosterone level in our patient. In addition to8 {: A% _: _" Y+ ]! w- C3 `0 l
virilization, exposure to exogenous testosterone in) b% I5 V# p: C0 O
children results in an increase in growth velocity and% T1 D, m/ h) u7 {$ k. D
advanced bone age, as seen in our patient.  o+ k) z+ v- k& o
The long-term effect of androgen exposure during
: {5 A! Z8 v3 ]% J: O! ^early childhood on pubertal development and final2 {7 t; N0 f: Q/ Z: ]2 f
adult height are not fully known and always remain
3 o, s) ^0 o' f1 ^a concern. Children treated with short-term testos-( C9 ^/ c! S3 c, O0 o
terone injection or topical androgen may exhibit some
  {6 u* s. R; z+ p5 g0 L: z4 ^acceleration of the skeletal maturation; however, after
0 X5 j  q, Q& `. x) ycessation of treatment, the rate of bone maturation0 S3 y* F- B4 Q  \8 j6 y+ E2 k
decelerates and gradually returns to normal.8,9
7 f% n5 M, g6 W* b+ m9 kThere are conflicting reports and controversy, C6 ^5 \+ j, t: b* z
over the effect of early androgen exposure on adult- G1 {+ w) r8 @  M( d
penile length.10,11 Some reports suggest subnormal  b; Y! A3 ]6 Z0 P+ s0 U8 k, t7 D
adult penile length, apparently because of downreg-9 F! U- ?: `' B2 o
ulation of androgen receptor number.10,12 However,( p- e6 z$ {$ x5 f. M
Sutherland et al13 did not find a correlation between
4 D2 R9 }- c) e4 t6 g) _4 \childhood testosterone exposure and reduced adult
7 ~" Q. v3 G5 }6 ?penile length in clinical studies.
0 U9 b# }( [& l, r% H# CNonetheless, we do not believe our patient is# g$ W7 a$ n; `$ S7 a
going to experience any of the untoward effects from0 I: I7 x1 {& q: D. x
testosterone exposure as mentioned earlier because5 E8 N. x1 k2 L! q; U: p7 Q) [
the exposure was not for a prolonged period of time.0 x5 `  \: Q" m* `. l
Although the bone age was advanced at the time of
& ^- G+ b: X6 Y$ W' j  Gdiagnosis, the child had a normal growth velocity at
5 k+ b2 }4 ^  j/ [  {( L1 |8 A( ]/ C4 Wthe follow-up visit. It is hoped that his final adult
6 B- ^: j& t1 t' g% L) b( k+ n8 Gheight will not be affected.
; \$ {: r, P4 ]1 H, pAlthough rarely reported, the widespread avail-+ x9 e9 I! W# f: ~3 L6 C6 W8 |
ability of androgen products in our society may/ g+ s- N$ z# m$ E
indeed cause more virilization in male or female# s: G5 F! [2 K" i5 v/ j& n
children than one would realize. Exposure to andro-
8 K. @  v/ x& x, n" ~1 ogen products must be considered and specific ques-
7 S$ G1 g6 w$ f# ^# \9 x" X; ^1 ftioning about the use of a testosterone product or
( P9 \/ l$ o8 p+ c/ Igel should be asked of the family members during- |1 F3 H) J: Q# s9 q- ^! }
the evaluation of any children who present with vir-7 F0 q# e) W. c% B4 n9 t0 Q
ilization or peripheral precocious puberty. The diag-8 n7 S0 T+ B% @0 ]' q) X5 c
nosis can be established by just a few tests and by
" [' K, o! j. h; v' g" p& {appropriate history. The inability to obtain such a
! t4 V3 T6 d4 G7 \history, or failure to ask the specific questions, may2 w4 q! g" @/ L# j& Y3 b% M/ o
result in extensive, unnecessary, and expensive( B; t3 x" H( T
investigation. The primary care physician should be
- l5 }' R, R8 d6 D3 U# oaware of this fact, because most of these children
9 p8 ^* q# i$ w: H, u7 umay initially present in their practice. The Physicians’3 J% q' O5 p  q7 V
Desk Reference and package insert should also put a, s% @( n$ l6 F: ?) ?
warning about the virilizing effect on a male or
2 M8 H/ ^  s9 K1 w7 c! J* Kfemale child who might come in contact with some-$ O$ K) ~$ r+ o& A" ?( O
one using any of these products.
0 O9 w- B0 o  d+ Z2 H( F! iReferences
8 p, p! p- _+ x5 w: Q1. Styne DM. The testes: disorder of sexual differentiation& m; Y7 R" D2 _  o% G! k1 i
and puberty in the male. In: Sperling MA, ed. Pediatric% H- j' I, O9 l
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;$ i. D: Y! d* J) z
2002: 565-628.
" A; `! Z) K$ t9 B- w% x) C6 _. i2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. o# q6 z5 Z$ }) g" J
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
% D7 y! M2 K, `* B% y9 fBoy Induced by Indirect Topical) ~) ?5 I- T: F1 W  Y
Exposure to Testosterone( `, M' N' Z0 M
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2+ U- [2 T; q' G. C5 ?. G
and Kenneth R. Rettig, MD11 D. A, X6 W9 Z9 |- Z& V
Clinical Pediatrics
+ e! Q( s& s4 I, H. hVolume 46 Number 6
6 a8 W3 _, X* u! Z) X- zJuly 2007 540-543
. a( I- u5 b" n! p6 y© 2007 Sage Publications
% Z2 U! V! ?9 s5 l* {! Y+ V* m10.1177/0009922806296651
  R, x5 x5 _/ B- l" |6 dhttp://clp.sagepub.com  r) c% \( a0 U5 @+ J
hosted at8 e, D% _' h; l1 `- H/ ?& _: r
http://online.sagepub.com; L4 r$ z; ~* H9 [
Precocious puberty in boys, central or peripheral,/ U6 E% o2 @/ t/ b6 {- C; B- e
is a significant concern for physicians. Central
; K$ F, b8 k4 B" [4 W, Sprecocious puberty (CPP), which is mediated2 i) Q- c+ U1 [1 s  l& b
through the hypothalamic pituitary gonadal axis, has! O+ S* x% o( C& N
a higher incidence of organic central nervous system6 Q) j$ F; [  I/ Q" C7 I
lesions in boys.1,2 Virilization in boys, as manifested
5 P  s) F/ q* S4 G1 tby enlargement of the penis, development of pubic+ ~% b6 q9 A% D% K9 w% k2 s5 ^
hair, and facial acne without enlargement of testi-5 D6 M( W3 t1 `6 e" T
cles, suggests peripheral or pseudopuberty.1-3 We
/ E+ Z0 [! @3 I2 n! j/ hreport a 16-month-old boy who presented with the0 W8 r$ l7 I1 h! o
enlargement of the phallus and pubic hair develop-1 X3 D& E2 Z  ~! }
ment without testicular enlargement, which was due
) a3 H$ l, x6 ~/ n! h% K+ ^, J6 bto the unintentional exposure to androgen gel used by
' d, H' [- e, ^) |8 o! Sthe father. The family initially concealed this infor-, t- G# r! s( q
mation, resulting in an extensive work-up for this& _# i( D' H9 ]9 j$ r  M" o2 h
child. Given the widespread and easy availability of
! ?. n0 F) V6 E4 B( ~testosterone gel and cream, we believe this is proba-6 n7 F  i9 b$ O
bly more common than the rare case report in the+ Y& V& Y+ F7 k1 o1 E& W1 X" r
literature.4
) w" t: N) W2 k4 u& z6 m' ~2 XPatient Report9 V( \4 ?$ t/ X; T8 V4 w5 V( v
A 16-month-old white child was referred to the6 t/ q( p/ X  f
endocrine clinic by his pediatrician with the concern& Z% r, ^4 D' p' N
of early sexual development. His mother noticed8 C) {  v) w* N+ m
light colored pubic hair development when he was
# y7 K. D2 ?  v, Q0 m! V: H# R! x2 aFrom the 1Division of Pediatric Endocrinology, 2University of
% Q' p( h. [9 @5 z( c. iSouth Alabama Medical Center, Mobile, Alabama.# h9 Z# e+ ~3 n4 ?# K: X
Address correspondence to: Samar K. Bhowmick, MD, FACE,: \5 h3 G+ a( c; F/ ?
Professor of Pediatrics, University of South Alabama, College of
3 c( ~) i+ I* B  s) nMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;$ w6 w: T7 e3 L  M
e-mail: [email protected].
, G. w- B4 O7 p% F; _2 Z* Tabout 6 to 7 months old, which progressively became
7 E7 T/ `, Z5 i- U0 C$ y' udarker. She was also concerned about the enlarge-6 Q5 L1 E4 L: ~- p$ v
ment of his penis and frequent erections. The child
) t8 h* l1 F& Xwas the product of a full-term normal delivery, with
1 Z" G+ k9 R, v# @; {& ha birth weight of 7 lb 14 oz, and birth length of6 g& X6 K1 e( E& a5 q$ u" |
20 inches. He was breast-fed throughout the first year2 `1 C1 _2 ^4 {6 o7 I
of life and was still receiving breast milk along with& R% |, ?- ?2 g; f% C8 E0 P
solid food. He had no hospitalizations or surgery,+ h' A5 _5 k& O
and his psychosocial and psychomotor development# A5 h( y7 u  p  Q) ?4 C# A
was age appropriate.9 B) a8 ]5 \  F
The family history was remarkable for the father,' l8 y6 Z! B# K3 K" a3 v6 q  N
who was diagnosed with hypothyroidism at age 16,$ X3 P8 I: N, P, k# X; ?# N
which was treated with thyroxine. The father’s
- Z+ P( g% f) Q+ D# x7 n, |; ?: ~) k) Iheight was 6 feet, and he went through a somewhat
& }7 u# T( S: N+ }# dearly puberty and had stopped growing by age 14.. M- B1 E8 G; S- j7 o/ |
The father denied taking any other medication. The
$ r( q9 r/ H. I( q4 @1 @7 d1 W% \$ kchild’s mother was in good health. Her menarche- d. F8 p! Q! t# s" _9 a  a; N  A* Z) E$ {
was at 11 years of age, and her height was at 5 feet
7 f" N  ]! s  _* w. ^  s5 inches. There was no other family history of pre-# }, }  ^- q/ D1 s6 |
cocious sexual development in the first-degree rela-& X# P$ \2 x; E  J- N. n
tives. There were no siblings.' J+ z2 r3 Z& L6 _
Physical Examination
1 [6 f5 g7 k0 A. V( GThe physical examination revealed a very active,8 D0 R; a9 [3 X$ ]9 i3 l
playful, and healthy boy. The vital signs documented1 V2 d( L/ y% r- q
a blood pressure of 85/50 mm Hg, his length was
7 R: `# D5 b( O+ ]: G90 cm (>97th percentile), and his weight was 14.4 kg
! d: W5 _( l# r0 ~) J2 M5 j(also >97th percentile). The observed yearly growth
$ X) [' U( A9 z, r$ Avelocity was 30 cm (12 inches). The examination of
) Q" G$ h: _8 V" Athe neck revealed no thyroid enlargement.
+ O! W7 q2 s& N: J& l2 dThe genitourinary examination was remarkable for
: A2 k/ A, V# k$ E$ c3 Oenlargement of the penis, with a stretched length of& @1 H, d! f4 B2 n% s: j- c
8 cm and a width of 2 cm. The glans penis was very well
; V+ J- D- J  z1 ddeveloped. The pubic hair was Tanner II, mostly around
) X' o! x4 D9 `540
% K' ?! X' @1 J+ gat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! D- g" h1 n* e1 Y7 z* m0 x
the base of the phallus and was dark and curled. The3 k7 a! q4 C5 A& ?1 Q
testicular volume was prepubertal at 2 mL each.
) j2 a% h; i6 x: XThe skin was moist and smooth and somewhat& U- Z  [. t, a# w! V
oily. No axillary hair was noted. There were no
& G, F; V$ R; e% S; kabnormal skin pigmentations or café-au-lait spots.
2 O; x0 X9 f0 O: [+ D. ^) XNeurologic evaluation showed deep tendon reflex 2+0 u1 B( g; @* W/ h, I+ r0 `
bilateral and symmetrical. There was no suggestion) f- k0 G3 h: ~( z' i, |9 ?2 D
of papilledema.* x/ I( Y) Q! p0 L
Laboratory Evaluation
0 \& |: \4 ^% P: o* f& LThe bone age was consistent with 28 months by1 e1 e7 h* E. H& h; A, j8 }
using the standard of Greulich and Pyle at a chrono-* Y! V1 z# T7 U8 m0 r) ]
logic age of 16 months (advanced).5 Chromosomal6 ^4 b1 ~) N6 u9 x! i6 `1 d0 E7 W4 v
karyotype was 46XY. The thyroid function test
8 u+ R/ J: }/ V$ i/ r) l1 A- b1 qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-: k! A) y- e/ p$ e4 T1 S
lating hormone level was 1.3 µIU/mL (both normal).
6 m( |- u; K- X7 b! W; A! tThe concentrations of serum electrolytes, blood
8 c) C9 ^& I: s0 R) |urea nitrogen, creatinine, and calcium all were
5 C; z/ b6 Q2 ?2 p+ W9 K3 n" Awithin normal range for his age. The concentration
2 c& Q5 o- ~7 O2 dof serum 17-hydroxyprogesterone was 16 ng/dL% ~3 V( b4 E& r0 L' ?: }3 L# X" g
(normal, 3 to 90 ng/dL), androstenedione was 20
$ u7 k. t3 |; Png/dL (normal, 18 to 80 ng/dL), dehydroepiandros-" W8 Z. d8 Q6 w& L$ p! S
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
) D$ B2 O1 m9 J3 j3 Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ E1 }5 @  k- T; D; x49ng/dL), 11-desoxycortisol (specific compound S)
1 V0 l) ^7 |  `was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- s+ w  S- f# ]* S
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
4 v1 S9 \& e: ]0 e) s& `) ^testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 Q6 o- L  d2 H7 eand β-human chorionic gonadotropin was less than: Y/ e$ Z9 R6 m+ D. I$ W
5 mIU/mL (normal <5 mIU/mL). Serum follicular
8 R4 o# U2 ]; R- `! bstimulating hormone and leuteinizing hormone
6 f- z. z# B+ `) D, V) j6 qconcentrations were less than 0.05 mIU/mL
2 j. a8 k) {7 n  _( t; m8 q* h0 x(prepubertal).' S: {6 _9 u% b! |. A
The parents were notified about the laboratory: q3 p0 c( p% `& q1 q  v# a
results and were informed that all of the tests were2 u) X4 g5 |$ s+ N
normal except the testosterone level was high. The' Q+ \+ ]; `* J, p$ \! i
follow-up visit was arranged within a few weeks to
$ Q' ?0 L% Z& `' }2 s( d' R9 Y2 hobtain testicular and abdominal sonograms; how-
  C' ?9 E* }  N5 n7 R% ?5 y* wever, the family did not return for 4 months.
6 R! `* W; y/ i2 y/ Z0 LPhysical examination at this time revealed that the
+ s% D$ [' {5 G& _$ q7 |' z% K  mchild had grown 2.5 cm in 4 months and had gained
7 j; X9 r' m6 }3 o4 L) s2 kg of weight. Physical examination remained
* ]& J2 x: a9 b. {unchanged. Surprisingly, the pubic hair almost com-7 J6 O1 z7 a8 b; H" [$ D4 l
pletely disappeared except for a few vellous hairs at
2 {  p0 @& u% U) c6 \% N% Ethe base of the phallus. Testicular volume was still 2
) @- X$ I$ k- _+ U" jmL, and the size of the penis remained unchanged.
8 k7 C+ S1 v# x0 t0 {" u2 ^# iThe mother also said that the boy was no longer hav-
& `1 F# K/ \& j: [" o& `1 }2 Ring frequent erections.
, l5 O" p  f- {% f. rBoth parents were again questioned about use of; N$ _$ b' W& o3 a  u
any ointment/creams that they may have applied to4 ]2 |5 {& q3 M/ ?) e1 k: I: h
the child’s skin. This time the father admitted the
1 H3 h% A" p1 R$ d+ J% iTopical Testosterone Exposure / Bhowmick et al 5417 H1 T- g( ]" p- K! S" }
use of testosterone gel twice daily that he was apply-
& r# \, c3 s. f7 o, v" D7 hing over his own shoulders, chest, and back area for" s% H4 h: H- a6 O* l( v" O
a year. The father also revealed he was embarrassed; K. l" a& m* A0 C# r6 u+ w
to disclose that he was using a testosterone gel pre-7 F( h! [3 W* m/ T" H8 j
scribed by his family physician for decreased libido5 m5 N! M+ S. c0 E8 z- K* P# C! {
secondary to depression.7 w+ Z! @; V; U! M* D5 f- g
The child slept in the same bed with parents.
! K1 P1 t' S0 LThe father would hug the baby and hold him on his; {/ r9 V/ N% h+ L' [
chest for a considerable period of time, causing sig-
  n) m3 g( `* f4 w8 x0 R( `nificant bare skin contact between baby and father.- ]7 I' k; C0 v4 K$ [
The father also admitted that after the phone call,
- X' s  o: g4 `% C4 Dwhen he learned the testosterone level in the baby; _& N3 ]( k+ ?$ f: c( U/ ~
was high, he then read the product information: f: H  ~" R, e+ p# s2 n0 D4 q
packet and concluded that it was most likely the rea-
2 J/ Y0 Y. C+ C  Eson for the child’s virilization. At that time, they+ ?3 d( j% F$ J3 H4 o9 P$ ~& w
decided to put the baby in a separate bed, and the- x  d' x0 U# p% \+ M! n/ M% f; w
father was not hugging him with bare skin and had
0 C1 ?# Z8 R+ N2 o( d. Qbeen using protective clothing. A repeat testosterone
+ j! I$ X1 ^6 s0 jtest was ordered, but the family did not go to the
4 u7 F9 c2 ^+ y' K$ Z. P/ ylaboratory to obtain the test.; [; z+ l: R7 Z2 t* R, [
Discussion
9 ]9 ~! {/ M6 ePrecocious puberty in boys is defined as secondary0 y8 Q* |: {$ _4 Y8 S: N& @+ D
sexual development before 9 years of age.1,4
, g' ]% d" t  w! @. D/ lPrecocious puberty is termed as central (true) when5 M) T2 V% C/ \1 h9 R: k
it is caused by the premature activation of hypo-
- V6 A7 Z1 z$ Y+ g6 `5 {: J: q! athalamic pituitary gonadal axis. CPP is more com-8 ?! }. T- p5 {; I, _
mon in girls than in boys.1,3 Most boys with CPP
# u3 H( c9 r& N; H8 p! lmay have a central nervous system lesion that is  r6 U6 b: S/ o- W- [
responsible for the early activation of the hypothal-) {! e7 w, q4 I! |4 I2 S3 m5 [
amic pituitary gonadal axis.1-3 Thus, greater empha-, d% N' \( ^4 J3 b
sis has been given to neuroradiologic imaging in
& }( S# e/ M  v% `3 T: r' Qboys with precocious puberty. In addition to viril-2 v9 {; B# w' e5 R. z4 R3 k# m
ization, the clinical hallmark of CPP is the symmet-
. b5 s  H/ O$ |- }4 [rical testicular growth secondary to stimulation by: \2 F9 }8 j$ n+ v* n3 v5 p1 r
gonadotropins.1,3& }; C' L$ W3 k
Gonadotropin-independent peripheral preco-
  |$ S0 j9 t3 W# bcious puberty in boys also results from inappropriate2 d$ k5 j6 G0 [, x9 x4 h! b% P
androgenic stimulation from either endogenous or/ u7 o  T+ ]) g- h0 L
exogenous sources, nonpituitary gonadotropin stim-4 d* Q. I8 @6 r/ i- K- g; Z5 c# D
ulation, and rare activating mutations.3 Virilizing& }% ^0 M3 y, U3 Q
congenital adrenal hyperplasia producing excessive7 P. g- q( b# p2 I8 [9 R3 l, _
adrenal androgens is a common cause of precocious* T$ E2 \8 J+ r! Q0 v- O
puberty in boys.3,47 A- z7 S* L7 k" |4 G+ _5 {: O
The most common form of congenital adrenal
6 N; K. h( \* K' bhyperplasia is the 21-hydroxylase enzyme deficiency.' y, |6 ]) a) ^' K
The 11-β hydroxylase deficiency may also result in! Q5 ]5 _) ~8 I8 v6 [: a
excessive adrenal androgen production, and rarely," F! E* E2 |5 l0 |$ T) P
an adrenal tumor may also cause adrenal androgen% ^: U' S. R. O. s' ~) j8 P
excess.1,35 t/ W1 g2 a. T: r
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% s3 Z8 G3 |  I! Q0 @
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& L0 @& M3 u+ }& I. {: E5 Q2 KA unique entity of male-limited gonadotropin-! ]  _6 s" v( h# b' S6 W8 ?
independent precocious puberty, which is also known
% x! {& G/ p" v8 }% J8 f5 K+ H9 tas testotoxicosis, may cause precocious puberty at a2 h. Z- q$ i  }( P
very young age. The physical findings in these boys
2 V" b1 T4 _8 m* ~# \+ W" cwith this disorder are full pubertal development,
: L& {1 D0 o% j" T( cincluding bilateral testicular growth, similar to boys7 t0 C1 T: w: o
with CPP. The gonadotropin levels in this disorder  i1 t6 A; q  n0 b. G0 m$ t
are suppressed to prepubertal levels and do not show
( a( H! I! `% ]# Z7 }7 ?9 w& dpubertal response of gonadotropin after gonadotropin-5 ~8 S4 B9 W+ n
releasing hormone stimulation. This is a sex-linked
. u* L$ {2 S- [autosomal dominant disorder that affects only
- U3 {) ]. a( H" xmales; therefore, other male members of the family3 e( v- X. a. W" D
may have similar precocious puberty.3
: F. B  l. l$ d; @In our patient, physical examination was incon-
% l9 E9 E1 A8 M! y* I( |4 g) hsistent with true precocious puberty since his testi-
" M1 d, t7 {8 e) q9 N3 bcles were prepubertal in size. However, testotoxicosis
9 p3 z. A' _8 i  Mwas in the differential diagnosis because his father
' @4 ?1 s% d  G# e7 Vstarted puberty somewhat early, and occasionally,3 h% o) R2 n# ~5 O
testicular enlargement is not that evident in the# S9 k5 y$ [2 k- M
beginning of this process.1 In the absence of a neg-
" `4 p7 g; w/ ]! e& K+ kative initial history of androgen exposure, our
) z0 V0 F0 w0 @8 N% ebiggest concern was virilizing adrenal hyperplasia,& g8 j: t4 U7 ?9 c' L
either 21-hydroxylase deficiency or 11-β hydroxylase
% c% Q$ X: C, Z/ @8 V2 Vdeficiency. Those diagnoses were excluded by find-% r. [/ Q" L9 g: q8 ^* s& ?5 w# Q* R
ing the normal level of adrenal steroids.7 {. s; c1 f- C9 C8 k! {3 `
The diagnosis of exogenous androgens was strongly
' m* e  ]% U8 E, _( Tsuspected in a follow-up visit after 4 months because# Y7 z* N$ U" r- d
the physical examination revealed the complete disap-
9 c0 q" a6 y* ppearance of pubic hair, normal growth velocity, and
* \9 ~9 B* s% ndecreased erections. The father admitted using a testos-
* d( _2 ?  L* \6 G8 N( u& W3 Kterone gel, which he concealed at first visit. He was
2 M# @8 J4 b" N8 _0 O  \& Cusing it rather frequently, twice a day. The Physicians’4 _8 v: Z# v6 s, O0 D
Desk Reference, or package insert of this product, gel or" _  ^# b0 G5 s3 A4 J% B3 \7 ~9 s
cream, cautions about dermal testosterone transfer to
% ]2 t7 F1 d7 S2 {) b7 ], `unprotected females through direct skin exposure.9 v4 _9 o# y) V5 H8 H
Serum testosterone level was found to be 2 times the
" N& e8 e) ]5 A, u( r0 a  fbaseline value in those females who were exposed to( c5 v) Y0 C( i/ \* H8 f
even 15 minutes of direct skin contact with their male: k1 ?: M# X0 c1 l
partners.6 However, when a shirt covered the applica-
; A6 p# g; j8 L. |% y4 [4 T  mtion site, this testosterone transfer was prevented.
0 r: d2 n) {* n& f3 T2 w9 O8 wOur patient’s testosterone level was 60 ng/mL,! f+ X5 ]% w0 R  r- P# \6 _
which was clearly high. Some studies suggest that8 L1 A- w" k5 ^4 u( J# v
dermal conversion of testosterone to dihydrotestos-/ g8 \4 @+ D3 N# P+ r
terone, which is a more potent metabolite, is more+ a, `3 G8 _( |$ j0 J
active in young children exposed to testosterone2 t/ c9 z# V0 E0 `
exogenously7; however, we did not measure a dihy-3 a$ U! f% a" T6 _# X2 k! ?4 N0 o
drotestosterone level in our patient. In addition to
# c5 u3 Q( F! S8 ~$ ~5 Uvirilization, exposure to exogenous testosterone in/ t  y$ c) d  U1 f  O
children results in an increase in growth velocity and" [/ S: R, m* ~) p: b
advanced bone age, as seen in our patient., l$ h  f+ b( ?5 U
The long-term effect of androgen exposure during4 z# F" a, [/ {6 ]7 c
early childhood on pubertal development and final
+ G1 z. s! [9 Z9 Aadult height are not fully known and always remain
" [% c3 h4 S9 ^a concern. Children treated with short-term testos-
- ~) n& |; t) S3 t1 D) |terone injection or topical androgen may exhibit some
' K* e& y  p5 F; \, N7 Sacceleration of the skeletal maturation; however, after
8 n8 U' Q' l' j- jcessation of treatment, the rate of bone maturation4 j" ^+ b! }+ z
decelerates and gradually returns to normal.8,9
5 C; b# Z: V5 t! NThere are conflicting reports and controversy
3 j7 k* `: y* Q9 M2 Xover the effect of early androgen exposure on adult
: K3 C# {4 N7 I& ^penile length.10,11 Some reports suggest subnormal
' a& i5 a6 Y  q5 `: V% n% ~5 j! zadult penile length, apparently because of downreg-
! N8 Z8 M" ~- s# [. \7 zulation of androgen receptor number.10,12 However,
  j; O7 i2 I5 C6 ESutherland et al13 did not find a correlation between
( N& i, G0 H5 W) H4 _4 fchildhood testosterone exposure and reduced adult; {4 l" i7 c7 E  N* c
penile length in clinical studies.! b5 }8 R' @: j9 m7 [
Nonetheless, we do not believe our patient is
2 S, ^( g. |3 O7 Z' t6 Zgoing to experience any of the untoward effects from
) T4 x5 E$ s6 C" l6 \testosterone exposure as mentioned earlier because
. K: A0 z7 {" R% S: J* B2 Rthe exposure was not for a prolonged period of time.
7 i3 R2 F5 g" {: \Although the bone age was advanced at the time of
" f' e$ _# s" K: Ydiagnosis, the child had a normal growth velocity at, {( e1 |/ H! u7 }* `; f4 }8 m4 n; d
the follow-up visit. It is hoped that his final adult- X# [1 [* z3 D4 V$ A' |- S
height will not be affected.
, y1 I9 D) O" p; A0 \Although rarely reported, the widespread avail-
& ?% F; L, p* N2 Gability of androgen products in our society may
, I/ F) ^, {0 B' X; @: N5 [indeed cause more virilization in male or female+ T; Z' P5 Y$ `. O+ A
children than one would realize. Exposure to andro-
3 g0 I, ~1 U% Z8 O/ R7 y; ggen products must be considered and specific ques-
. z% F1 G$ w* }+ g9 M" z% ?7 D# Etioning about the use of a testosterone product or
- H- l/ T: w+ ugel should be asked of the family members during+ q7 K; v& E8 j. |6 x0 I
the evaluation of any children who present with vir-
# ~8 v0 j: t  v8 \- H9 _ilization or peripheral precocious puberty. The diag-
; D9 M, S. X( [& x6 c1 vnosis can be established by just a few tests and by
( Y6 p3 z; u; S5 ^" O& Pappropriate history. The inability to obtain such a
/ S0 \! H8 }8 m: p5 N* Chistory, or failure to ask the specific questions, may& i1 Z& N+ s& f& T% n& T
result in extensive, unnecessary, and expensive
% {% y+ q8 U  ^- ^investigation. The primary care physician should be5 J' ^' z6 r+ \% E
aware of this fact, because most of these children
" s; W- n- K2 Dmay initially present in their practice. The Physicians’, G, Y" g; s" r
Desk Reference and package insert should also put a
' Y, h) ?- ]5 Q5 \3 mwarning about the virilizing effect on a male or
, y/ y/ |! U+ F0 f; k$ x0 b& @female child who might come in contact with some-
1 ?5 o  A. p$ g+ y5 Mone using any of these products.
2 m  v  L! Q6 X& KReferences: ^6 f8 ?% C1 Q
1. Styne DM. The testes: disorder of sexual differentiation5 r4 ]) e' V1 r9 y! J$ z# `
and puberty in the male. In: Sperling MA, ed. Pediatric. x' U, R+ [7 r
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 ?+ a0 P% Q3 e% x
2002: 565-628.
1 [* h: F  k: i6 I' l- {5 ?2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
4 x* W& ^# J* Rpuberty 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
0 T' e& i- S* D& X: [# }
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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