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Sexual Precocity in a 16-Month-Old$ b% ^9 [  P( q0 H6 x
Boy Induced by Indirect Topical
9 e+ V! z* i6 U' BExposure to Testosterone
+ u: w  j7 W3 T- N% q1 E  U9 t6 dSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2' p& u. u  q+ ]- b. F/ u, {
and Kenneth R. Rettig, MD1( _7 H; ~; l) _+ x- ~1 G
Clinical Pediatrics/ P/ d0 r2 Q6 ]9 W, l5 V
Volume 46 Number 6
. I5 u8 }' i* SJuly 2007 540-543( U! B; H/ R/ ]" q1 A
© 2007 Sage Publications
7 E+ Z2 H& F: q6 D9 O/ E10.1177/0009922806296651
2 ]9 A: t5 {$ g3 H9 e. w  }" ]4 ehttp://clp.sagepub.com2 X) x+ C+ Q. f* I: Q* H. Y
hosted at5 A6 d) @6 P; M
http://online.sagepub.com
& w8 K) g) w: b4 i, b( _" \& [Precocious puberty in boys, central or peripheral,
% b: ?! z+ p5 J% M% v! vis a significant concern for physicians. Central
9 m  E9 `' Z6 C6 h( wprecocious puberty (CPP), which is mediated
  N, X& g, o( v8 L  b% \- _7 A' ]3 nthrough the hypothalamic pituitary gonadal axis, has: j7 @9 a7 _1 x+ j0 `
a higher incidence of organic central nervous system
. }5 Y! A( Z6 hlesions in boys.1,2 Virilization in boys, as manifested0 l; r- j8 i7 I, p
by enlargement of the penis, development of pubic
, h! V/ ~' O4 G1 U. ^0 }hair, and facial acne without enlargement of testi-$ P  A: q4 D: }. ]- P; ?7 K
cles, suggests peripheral or pseudopuberty.1-3 We
; {, m0 m+ i" Ureport a 16-month-old boy who presented with the4 s# q" _; }8 Y: R" y2 U
enlargement of the phallus and pubic hair develop-1 ]# q5 m( J# o+ y4 Q9 Z
ment without testicular enlargement, which was due
3 V% C' \( A2 Z0 G8 A3 C( q* Dto the unintentional exposure to androgen gel used by
* y: S. o9 |9 J0 Q/ E3 Ethe father. The family initially concealed this infor-+ C2 `% T, _9 p8 u/ w: @) o
mation, resulting in an extensive work-up for this# S. Z* G9 i) o& [, B- R* t2 Z5 Q
child. Given the widespread and easy availability of( ]: D8 D  M9 p  T
testosterone gel and cream, we believe this is proba-
1 x6 X8 l% f( n8 h- Q- Pbly more common than the rare case report in the4 V; `' t( y* [' T- \3 F; G6 H
literature.4& N( y6 D& f# i, h$ c* p
Patient Report
% C# y$ t" m  r  S3 X/ M- dA 16-month-old white child was referred to the7 N8 V* ?" _* L/ F0 q7 R: G; e, h
endocrine clinic by his pediatrician with the concern9 M7 w$ g1 ]) ], B
of early sexual development. His mother noticed) A2 n3 \8 b: N0 L/ J  U
light colored pubic hair development when he was8 p; ?+ L" B6 v& B/ h: T3 |9 C
From the 1Division of Pediatric Endocrinology, 2University of
; T! C6 m# e) q) [4 c. a3 ASouth Alabama Medical Center, Mobile, Alabama.
& \% X% F( p  c3 F+ yAddress correspondence to: Samar K. Bhowmick, MD, FACE,. J6 J: \  t: [
Professor of Pediatrics, University of South Alabama, College of& y& H1 ]& @. \0 g1 ]$ u
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
* H' J  ~; a9 c* n1 j  s  le-mail: [email protected].
7 i( f' z6 F$ |; y5 qabout 6 to 7 months old, which progressively became" }& T0 l, Y, d5 I4 v2 ?% X
darker. She was also concerned about the enlarge-
) h) ]+ ?; h  [+ \' h5 j6 cment of his penis and frequent erections. The child; Q$ E% a+ f- C! u
was the product of a full-term normal delivery, with3 \' v  Y( d' O0 Z$ o% L3 b( J+ p
a birth weight of 7 lb 14 oz, and birth length of
0 j2 e7 L* z  {8 O2 G20 inches. He was breast-fed throughout the first year: D% S! P, ]2 B/ k7 ^, C+ D' g
of life and was still receiving breast milk along with
4 L; I, o/ C8 n3 jsolid food. He had no hospitalizations or surgery,9 C! l$ M  Y5 P; V$ T
and his psychosocial and psychomotor development7 s" Z9 ^7 u; h6 d1 N# i6 Q- Z7 S, J
was age appropriate.
9 W- P9 l% D3 S6 J/ t' d4 uThe family history was remarkable for the father,
! o/ {  _9 b8 Y. ywho was diagnosed with hypothyroidism at age 16,+ h2 ^4 e& V# }0 ?  ?! T
which was treated with thyroxine. The father’s
' e$ v  Z/ D- X9 `5 Z2 V2 Mheight was 6 feet, and he went through a somewhat
6 W/ ~. R, e4 t# Q& I1 l  Oearly puberty and had stopped growing by age 14.* C, a- L( ]0 m0 f8 ]
The father denied taking any other medication. The
- T; j: v3 w' L' L. F  @% vchild’s mother was in good health. Her menarche0 |: U( N& W8 B! Y
was at 11 years of age, and her height was at 5 feet
8 w8 O0 C$ L5 p1 M- c9 T/ L0 W1 A5 inches. There was no other family history of pre-- g5 ]4 s0 K, K4 j
cocious sexual development in the first-degree rela-
) @& Q  M9 W, e2 X3 F) B1 a: K2 ptives. There were no siblings./ ?% g& k! g9 a+ v5 C
Physical Examination
* r3 ~5 k% g; b' i0 i* wThe physical examination revealed a very active,
! D1 j6 I" ?$ rplayful, and healthy boy. The vital signs documented# j) ?- {0 u7 d, r/ S+ J1 ?
a blood pressure of 85/50 mm Hg, his length was# Y; G6 A% o  ]" {: v
90 cm (>97th percentile), and his weight was 14.4 kg
' Y, P  U, R& e, D(also >97th percentile). The observed yearly growth# P3 I0 P: w. N7 b. a
velocity was 30 cm (12 inches). The examination of
$ P& F, v- B+ A3 r: Gthe neck revealed no thyroid enlargement.: Q6 {. D* }1 v6 @7 n1 n: d( o
The genitourinary examination was remarkable for1 Z" v$ @, Y+ f+ Z: L) z
enlargement of the penis, with a stretched length of
2 F# q, N# d3 w0 x& s8 cm and a width of 2 cm. The glans penis was very well2 y, B  v+ Z) Z: n
developed. The pubic hair was Tanner II, mostly around
. X6 r( v# R; N5 w6 j, _5 l/ a540
" V/ m3 D. ]0 ?# V9 i2 Eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* H  @) `0 K# m1 D3 @9 @0 a
the base of the phallus and was dark and curled. The
$ p0 v: U' w& b* E' stesticular volume was prepubertal at 2 mL each.
/ @! K+ Y2 x% C5 k$ gThe skin was moist and smooth and somewhat
! ?% ~& [$ S' _0 y) u0 boily. No axillary hair was noted. There were no
+ r$ R8 ]' r0 V. [$ |/ r2 P# U+ S' r8 |abnormal skin pigmentations or café-au-lait spots.
& {  n* z) M, v4 V: |) fNeurologic evaluation showed deep tendon reflex 2+: V" ~6 B( D& I( |
bilateral and symmetrical. There was no suggestion
  S+ d4 [1 A6 eof papilledema.8 a* }5 d% b9 ~+ C
Laboratory Evaluation/ ~3 d, s" z. r6 _4 C  k* k# ]
The bone age was consistent with 28 months by  T8 m- E8 S' O) h
using the standard of Greulich and Pyle at a chrono-
: L& X8 g: Y: o- ylogic age of 16 months (advanced).5 Chromosomal
9 S, P" s1 S$ k# `8 b. w, kkaryotype was 46XY. The thyroid function test: H1 @1 ^. ?$ Y3 \1 Z
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
  K6 G7 b  O, Clating hormone level was 1.3 µIU/mL (both normal).
0 e5 g" ^) w2 ?1 fThe concentrations of serum electrolytes, blood* x, g6 h. g' M8 K/ G  ?
urea nitrogen, creatinine, and calcium all were
: J4 J+ p6 k: N0 \within normal range for his age. The concentration! Y/ f% a0 Q9 ]% }4 y; [
of serum 17-hydroxyprogesterone was 16 ng/dL
8 v& @: r# Y+ Q& }1 [(normal, 3 to 90 ng/dL), androstenedione was 20# k1 X7 O3 i$ k8 T: F4 B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-( S+ c0 |" m2 O+ t) `
terone was 38 ng/dL (normal, 50 to 760 ng/dL),7 B) F' Y( z* K
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
, E. Z0 ^) q, Q" h49ng/dL), 11-desoxycortisol (specific compound S)1 w5 G4 k7 H1 w
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
! A8 z6 u! A4 k$ Htisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
$ d4 j$ n" k8 M% g1 i  j% T5 m* Vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),% g+ b5 f, a: z& o# ]1 S
and β-human chorionic gonadotropin was less than6 b7 C$ l5 T$ }: \* u# N
5 mIU/mL (normal <5 mIU/mL). Serum follicular' z+ \2 r% z$ v. s+ o4 b7 X7 E
stimulating hormone and leuteinizing hormone
. D* e) b! N: c$ Q2 zconcentrations were less than 0.05 mIU/mL
3 J1 w6 u5 y% ^2 P& j(prepubertal).
+ d) o+ A! p, j- a. A* aThe parents were notified about the laboratory( c: W" Y! T( K7 a# p! Z$ f1 I: n' [
results and were informed that all of the tests were
8 y9 s1 B2 B) c5 W4 ~normal except the testosterone level was high. The
# H8 D1 [' D8 q4 s4 mfollow-up visit was arranged within a few weeks to
- ^0 ?% N( {2 G2 Hobtain testicular and abdominal sonograms; how-
4 p4 i- u: Z" a0 V, J6 aever, the family did not return for 4 months.
* r1 s1 |7 V, l" N& `. N7 g: g" W- n9 Z& _Physical examination at this time revealed that the
( h9 P4 {5 C; z* g" X  ichild had grown 2.5 cm in 4 months and had gained& D% ~. ~2 ~# P* ~0 ~  s: _1 {
2 kg of weight. Physical examination remained
/ b; C1 d% p9 z$ u- tunchanged. Surprisingly, the pubic hair almost com-
8 ~$ z* y, ?7 G, y: Jpletely disappeared except for a few vellous hairs at- l5 T; z- ^# K0 C7 \$ z
the base of the phallus. Testicular volume was still 2# {9 L. G" o7 ]: h1 o
mL, and the size of the penis remained unchanged.
5 f9 Q, S% m- i4 I4 |  x5 }8 [4 \$ cThe mother also said that the boy was no longer hav-8 z* H# N  S* n/ u$ X9 n
ing frequent erections.
! R1 ]. y9 W6 r$ P6 t! m! ZBoth parents were again questioned about use of  ]+ s% T/ f7 h! e# W1 t- t  i
any ointment/creams that they may have applied to
8 p7 S, y( P3 \the child’s skin. This time the father admitted the8 C$ s% S( g% }4 o8 O
Topical Testosterone Exposure / Bhowmick et al 541: R7 T2 R2 [0 [( M6 u. r
use of testosterone gel twice daily that he was apply-  R3 i3 s5 }- `4 z1 ^
ing over his own shoulders, chest, and back area for& ?9 B1 V. }! E" M" v
a year. The father also revealed he was embarrassed/ Y5 ], ~/ }, a2 t$ |
to disclose that he was using a testosterone gel pre-
5 _; e+ ^7 f! V2 M) cscribed by his family physician for decreased libido. P5 ~: |2 Z8 ?% ^9 U* s& Y% Y
secondary to depression.
2 ]. M' v8 ?7 x! wThe child slept in the same bed with parents.  v/ |+ v: E% x7 \' J
The father would hug the baby and hold him on his+ f7 J8 k& P7 D1 ~" c
chest for a considerable period of time, causing sig-
7 u: M6 O/ x7 ^# q0 f: r" Lnificant bare skin contact between baby and father.
' n, U' x6 w* v8 M# YThe father also admitted that after the phone call,
. b, M% S5 K; E7 O" x0 Cwhen he learned the testosterone level in the baby: c/ N% H, {- n
was high, he then read the product information
- o! a; y1 B5 T& upacket and concluded that it was most likely the rea-2 R3 }. c# a. }8 S1 |$ C. [
son for the child’s virilization. At that time, they% G1 @' a( H7 h5 F) [; X8 e& l" d
decided to put the baby in a separate bed, and the* \7 q2 `- i8 t6 \* I
father was not hugging him with bare skin and had4 t; I( a' V$ ~
been using protective clothing. A repeat testosterone- T4 w( F# G) O$ b' L
test was ordered, but the family did not go to the- f( q( Z# x! S1 x2 c! X% e9 \
laboratory to obtain the test.
; `1 {7 [+ a" vDiscussion
: c1 Y) ^9 ?5 u9 |) T9 B9 D5 hPrecocious puberty in boys is defined as secondary
. e/ F, ?7 K6 E* f; usexual development before 9 years of age.1,4
  n# A: P+ \4 [Precocious puberty is termed as central (true) when# A1 P* N4 P2 S! |9 t# D; S) _' Z
it is caused by the premature activation of hypo-$ _" i6 k5 L% H8 ]/ o3 E
thalamic pituitary gonadal axis. CPP is more com-
0 d/ i+ ^- d* _, Gmon in girls than in boys.1,3 Most boys with CPP4 D) p7 ?; D. \, W
may have a central nervous system lesion that is7 C+ V3 {' j1 l0 z
responsible for the early activation of the hypothal-' O( V5 I' W- S6 F0 v" s# z2 h
amic pituitary gonadal axis.1-3 Thus, greater empha-
' i# J, P9 ], T' [3 d( Asis has been given to neuroradiologic imaging in
; n; b: w8 G7 ^. ]; ?4 x# C7 z) a) Gboys with precocious puberty. In addition to viril-6 u9 H- F; N1 }( b2 ^) _
ization, the clinical hallmark of CPP is the symmet-) D, ]/ y2 {& J4 I- E1 p$ P* b
rical testicular growth secondary to stimulation by6 o- ?4 W1 n$ s( Y
gonadotropins.1,3
3 m4 `- J) S9 {' I  NGonadotropin-independent peripheral preco-
% a1 i$ E* v8 X/ `+ Wcious puberty in boys also results from inappropriate
$ d/ `2 L" p4 S0 Y% f* V# F* landrogenic stimulation from either endogenous or! V  p% z; q* n4 L% G7 v
exogenous sources, nonpituitary gonadotropin stim-
& T  q# n+ ]1 B1 h! [ulation, and rare activating mutations.3 Virilizing+ y: U1 I6 o2 p! e/ M& Z
congenital adrenal hyperplasia producing excessive
# ^3 B3 g8 k# S9 V0 r( e- `adrenal androgens is a common cause of precocious
. h% u( x* B; I+ e7 q/ Lpuberty in boys.3,42 ~: c* d: t0 ]* U/ x
The most common form of congenital adrenal
6 }) f$ P  }' L" nhyperplasia is the 21-hydroxylase enzyme deficiency.
! E4 G  E+ g0 e( Y. t4 EThe 11-β hydroxylase deficiency may also result in" w" R. j7 {- v3 }: Y2 n& `5 q
excessive adrenal androgen production, and rarely,* R6 D- X4 W3 U3 z! \
an adrenal tumor may also cause adrenal androgen9 d4 [3 o% z3 a8 P
excess.1,3
7 n- x( j: j. l$ @at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( Y  ?7 g  q; R  \$ z542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
2 ~1 m9 |0 N" B$ U8 OA unique entity of male-limited gonadotropin-
" E) R0 D0 N4 g( i5 k) O5 Nindependent precocious puberty, which is also known0 |+ L3 E" N1 c/ P
as testotoxicosis, may cause precocious puberty at a
5 l" _5 T+ q# h9 b" n3 nvery young age. The physical findings in these boys
3 Y( }0 O$ o, [3 k* j9 C% ywith this disorder are full pubertal development,6 m6 J5 u! j: B! @- T
including bilateral testicular growth, similar to boys7 d# _8 |) y6 t" f0 ^, `
with CPP. The gonadotropin levels in this disorder4 B5 k. X8 m# h' i/ K
are suppressed to prepubertal levels and do not show9 @" w1 E5 B  S( U: ^/ a
pubertal response of gonadotropin after gonadotropin-
- J& l* u% `& B+ D+ C+ Kreleasing hormone stimulation. This is a sex-linked
" M7 C" A7 u! g0 G8 [autosomal dominant disorder that affects only
$ _! b/ o; _4 A. {* }males; therefore, other male members of the family
! S; F! N) i; L( i4 L# g( W. o. }0 \. tmay have similar precocious puberty.3. i' ?0 {7 _8 l! l) f4 c% m! z. M( p
In our patient, physical examination was incon-
% V7 o% t6 r2 p9 q7 r! N* isistent with true precocious puberty since his testi-5 ?( p. S) Y' f/ n" f! Z
cles were prepubertal in size. However, testotoxicosis) ~$ N" Z  x% T
was in the differential diagnosis because his father6 [0 j; d. y% s* ?" l$ R% A6 z: s* c
started puberty somewhat early, and occasionally,
$ k* U# P1 M! J; _testicular enlargement is not that evident in the5 H+ l' _0 e" c
beginning of this process.1 In the absence of a neg-
" s& l1 Y7 {% u* \- w5 s; U/ zative initial history of androgen exposure, our5 ^+ |3 h" v9 H& L2 t$ B9 w
biggest concern was virilizing adrenal hyperplasia,
+ t8 h  }9 P; z/ I1 u% Seither 21-hydroxylase deficiency or 11-β hydroxylase
; B/ f% r+ k0 {6 Ndeficiency. Those diagnoses were excluded by find-& H) f. e" w; m7 b- ?1 i
ing the normal level of adrenal steroids.* K' u. \  }( `) M3 }$ V! h
The diagnosis of exogenous androgens was strongly9 o1 l9 U6 P& I1 G- J
suspected in a follow-up visit after 4 months because
1 E5 O+ i' N. N, e7 G* ~the physical examination revealed the complete disap-
0 B( f. g2 E# y" cpearance of pubic hair, normal growth velocity, and
4 u# m0 y4 s+ l6 @1 Z) x" K8 Sdecreased erections. The father admitted using a testos-9 l1 H+ Z! `2 ]1 x6 u- O0 a
terone gel, which he concealed at first visit. He was
) d. c$ x# G$ h; W7 p- n) Busing it rather frequently, twice a day. The Physicians’" n+ j. r8 o) b6 i# p  e
Desk Reference, or package insert of this product, gel or& Y" i$ Y! `3 d0 I- T9 f
cream, cautions about dermal testosterone transfer to4 {' {9 b+ p  O8 q# V
unprotected females through direct skin exposure.2 t! i9 j: J' ^" o8 n9 b
Serum testosterone level was found to be 2 times the
/ O' D. s4 V' @2 \7 A2 N& z5 ybaseline value in those females who were exposed to
' `9 i$ E$ r$ |3 o4 A2 U+ R5 ueven 15 minutes of direct skin contact with their male; K. m- W6 c2 i) R
partners.6 However, when a shirt covered the applica-
/ x! N1 C1 d1 {# r' stion site, this testosterone transfer was prevented.
2 b- m8 u* n# l/ U! OOur patient’s testosterone level was 60 ng/mL,
9 o5 k! P# E6 K  z7 y8 M: z& O7 Uwhich was clearly high. Some studies suggest that
3 K: h  V$ d" t) i4 w; T+ Zdermal conversion of testosterone to dihydrotestos-
" F7 z$ h- ~: ^/ G% Mterone, which is a more potent metabolite, is more
9 ?* v1 f  H5 q2 |3 v" bactive in young children exposed to testosterone0 |* Q5 e% Y1 `/ X* E& n9 }# A
exogenously7; however, we did not measure a dihy-5 M2 Y9 @8 J. t4 r
drotestosterone level in our patient. In addition to
2 g4 j* L8 p2 N1 R5 pvirilization, exposure to exogenous testosterone in
' E% V$ l+ z7 j$ n3 p8 \children results in an increase in growth velocity and/ j! ~( s9 p& a- y
advanced bone age, as seen in our patient.! M' `! B. C8 M4 I9 |8 V
The long-term effect of androgen exposure during5 n( e6 V0 w6 ~7 }
early childhood on pubertal development and final
0 m& Z% \$ X( e5 Cadult height are not fully known and always remain
# s5 `6 e& n' D9 p- M) z- }a concern. Children treated with short-term testos-$ l6 ~  }+ A& u; j1 ^0 m* a9 y
terone injection or topical androgen may exhibit some: S' J% X" r# N8 D7 J: s- u5 w
acceleration of the skeletal maturation; however, after
& |) ~$ _" F% `0 zcessation of treatment, the rate of bone maturation" ]. g4 X' H4 I& [, w# m5 ~
decelerates and gradually returns to normal.8,94 Z4 W2 @+ P( m
There are conflicting reports and controversy" F' ?  w: C' Q. `. O6 l
over the effect of early androgen exposure on adult
* D! }7 r( O0 }, o$ fpenile length.10,11 Some reports suggest subnormal
  `$ @5 m* Y. D  W; W5 I9 c5 b) Y& xadult penile length, apparently because of downreg-; s% ^" h& p" b/ I
ulation of androgen receptor number.10,12 However,! d. ~. ?; J( c! \; Z# z
Sutherland et al13 did not find a correlation between* P/ J+ |6 l! c$ X4 x5 e
childhood testosterone exposure and reduced adult
8 y7 w' E0 t+ B  f2 S8 l; b- Q2 lpenile length in clinical studies./ e5 q3 ]+ m' j) H3 f. G+ i# W4 n( i
Nonetheless, we do not believe our patient is0 ?5 w% _; c6 i
going to experience any of the untoward effects from
1 j- {4 s/ P  R# f" n; ytestosterone exposure as mentioned earlier because
* L# I& p) ?+ H8 _5 O& vthe exposure was not for a prolonged period of time.
' i0 j" S4 C9 M* F# P+ S+ PAlthough the bone age was advanced at the time of8 s7 O" I+ @& F4 J6 @# v
diagnosis, the child had a normal growth velocity at% z. @( z2 T; K& d
the follow-up visit. It is hoped that his final adult
+ v5 d; k1 Q6 }' Z8 mheight will not be affected.
0 @- ^2 x, B" c3 N- bAlthough rarely reported, the widespread avail-
3 W' B9 e! ^6 p0 s4 b+ _  Xability of androgen products in our society may6 V- W% ^7 V3 M4 {- V; v
indeed cause more virilization in male or female
* u! R: m4 y$ c3 S: y0 m+ I/ a& Y8 Y4 ?children than one would realize. Exposure to andro-
9 R: z, {$ q: F0 X& e; P3 ]4 ~gen products must be considered and specific ques-" d4 m6 z" g! K8 Q4 B7 H4 V/ F
tioning about the use of a testosterone product or
2 `6 i) Q/ m- }$ S: ]gel should be asked of the family members during- V* X) @4 U( a. ~% b: U; J3 O: U
the evaluation of any children who present with vir-" E/ O: \( V2 c& H; c+ k0 L7 {
ilization or peripheral precocious puberty. The diag-5 N7 [% u7 q7 O9 h" x2 O
nosis can be established by just a few tests and by4 r, O" x+ H; L$ U$ e  ~3 u% o
appropriate history. The inability to obtain such a! x7 e( h( V, K# r7 C  r
history, or failure to ask the specific questions, may
' m3 O0 B4 m3 z0 wresult in extensive, unnecessary, and expensive6 h; I- J' B4 A) d2 I) g' L
investigation. The primary care physician should be
5 J1 G+ O, [4 D$ r7 P3 R0 taware of this fact, because most of these children
+ o# ?# j  @8 z: c3 |may initially present in their practice. The Physicians’* I! _* w% [! e( q# f4 j5 i
Desk Reference and package insert should also put a) h4 J. u4 Z8 f# \% d2 ~  e
warning about the virilizing effect on a male or( G2 A& F3 F. D2 a# ], R
female child who might come in contact with some-7 R5 ?" L! g9 j+ M
one using any of these products.. {9 _7 z4 z; n  N/ d: K
References. Y& \- _! |, h7 m, A# x! ]
1. Styne DM. The testes: disorder of sexual differentiation
$ P$ e$ U" x7 l* F* ?and puberty in the male. In: Sperling MA, ed. Pediatric
, @* m& X4 E. aEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
$ t* y9 n' b1 w% k9 |2002: 565-628.$ W- U( H0 N8 O  A2 Q
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* j4 Z; U1 e# D
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
5 S% E5 [2 d% I+ uBoy Induced by Indirect Topical  G2 N" z( x3 ^. L
Exposure to Testosterone
9 f4 O' r* K  b. W/ j7 ?# MSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
9 M8 ~7 Q  g: fand Kenneth R. Rettig, MD1
: d9 r% t( N& B$ a3 y& X, eClinical Pediatrics
: X, t3 M& @* uVolume 46 Number 63 E) ]0 B6 @. C  M8 x$ @
July 2007 540-543# B* t$ w* |* G) V' W/ j
© 2007 Sage Publications, i( D: c: r" A' d
10.1177/0009922806296651; r( _* I5 X4 N# i
http://clp.sagepub.com6 F/ `, r) i5 i& X, }
hosted at3 q% g) K. i! x& I9 V" E
http://online.sagepub.com. e. t! w6 A) e/ Z5 K; U1 g
Precocious puberty in boys, central or peripheral,; Q8 p7 Z& s4 @$ n% p6 A+ R6 A/ [) g
is a significant concern for physicians. Central
) s) _- \# o1 n) y7 s3 N& J. Zprecocious puberty (CPP), which is mediated, v4 g6 n9 I9 d
through the hypothalamic pituitary gonadal axis, has$ a1 J' M! a( d, d9 F
a higher incidence of organic central nervous system
$ I3 D5 b! t3 ^; Jlesions in boys.1,2 Virilization in boys, as manifested7 R/ @$ ]7 k; W& N6 P
by enlargement of the penis, development of pubic
9 l, D4 V3 x' ?& u5 r: ^( ]3 z# d% Xhair, and facial acne without enlargement of testi-
  p( r) W% L( j2 J8 i/ L& pcles, suggests peripheral or pseudopuberty.1-3 We! k; W* A9 E& Y! I, D7 B
report a 16-month-old boy who presented with the3 l4 a5 I9 d! ^3 p* w  R4 m) O. _
enlargement of the phallus and pubic hair develop-6 a# C8 ?) N  R7 \1 W
ment without testicular enlargement, which was due9 m5 c1 M* m3 k# E) Z+ t' r5 D
to the unintentional exposure to androgen gel used by3 k1 Z7 r+ t0 J# z  f
the father. The family initially concealed this infor-
* ]9 V2 m' W% x9 F- r5 u) `mation, resulting in an extensive work-up for this
: ?. P: ?& f" hchild. Given the widespread and easy availability of: |3 }( Y1 n% s" V4 j3 u/ g
testosterone gel and cream, we believe this is proba-
  _1 o  ]6 K+ O! I, z' ybly more common than the rare case report in the: W! V, D5 W& x
literature.4. l/ I# w$ }( i! `9 u2 W$ e
Patient Report, O" B; J5 W, P0 C' u0 G$ [) l1 q" J* E0 r
A 16-month-old white child was referred to the# v9 Q7 P) u8 _" E( c
endocrine clinic by his pediatrician with the concern4 w, m3 u$ T; \- x
of early sexual development. His mother noticed  `& t& f# p2 N4 ^
light colored pubic hair development when he was
7 P& M! c1 g. T. R3 OFrom the 1Division of Pediatric Endocrinology, 2University of
' D. E# z3 \% ~0 jSouth Alabama Medical Center, Mobile, Alabama.- A; p7 n2 c- u. {" x  c$ w
Address correspondence to: Samar K. Bhowmick, MD, FACE,& ?7 Z6 }) s# a  {
Professor of Pediatrics, University of South Alabama, College of
9 z6 H) y$ X, ~7 u, MMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
9 A4 |& Y' r4 m  @3 o" Q/ q" J, P3 [e-mail: [email protected].
7 b8 c7 g( X6 K! Uabout 6 to 7 months old, which progressively became
, ^' o& y8 p; F9 z7 vdarker. She was also concerned about the enlarge-
0 ?/ L) i; t+ a" ~$ G9 D% X1 Gment of his penis and frequent erections. The child/ F3 u. N& f3 S$ u
was the product of a full-term normal delivery, with4 `) w) |0 C( P$ T! l' o
a birth weight of 7 lb 14 oz, and birth length of0 c2 S3 x8 x1 |! }! b# S/ R0 x" F
20 inches. He was breast-fed throughout the first year# u. F- W% [& L( g  X- t/ {! Y
of life and was still receiving breast milk along with9 {5 v7 j/ }1 ~; ^1 i
solid food. He had no hospitalizations or surgery,
8 S  K  k( U8 }2 G/ wand his psychosocial and psychomotor development! U- W; Q- h* l  E
was age appropriate." Y. l" c9 T, ?# s
The family history was remarkable for the father,
$ N$ @5 r4 p4 W' ^  S8 \who was diagnosed with hypothyroidism at age 16,
- _) W2 P4 g5 [* Owhich was treated with thyroxine. The father’s
- K, P: W$ _1 ?; W( _) qheight was 6 feet, and he went through a somewhat
% m8 m  [2 i) ^0 j) qearly puberty and had stopped growing by age 14.
( ~8 b6 }! I7 dThe father denied taking any other medication. The
, T. r( \( b& x& L* ^child’s mother was in good health. Her menarche
5 q. N3 P* k0 F( I( dwas at 11 years of age, and her height was at 5 feet
. |* T/ |! G4 N  m+ ~+ {5 inches. There was no other family history of pre-
# [" V7 F+ p  ^4 \. x9 D0 E! V# _cocious sexual development in the first-degree rela-( s  d" `7 `# W& s' G* v
tives. There were no siblings.+ F6 K3 F( e% ~9 j* T
Physical Examination+ F4 d5 e' j- N7 }! j
The physical examination revealed a very active,6 u  {" B& I- G6 X* A
playful, and healthy boy. The vital signs documented
& C9 C* Q6 ~/ i( Q4 za blood pressure of 85/50 mm Hg, his length was
1 c7 U  M& D7 J4 ?+ n$ H  X90 cm (>97th percentile), and his weight was 14.4 kg# s: ~8 d' q* ~4 z1 n
(also >97th percentile). The observed yearly growth
8 ^# g2 J4 m# A& S3 {# ovelocity was 30 cm (12 inches). The examination of- N* o8 o( N/ ~* l3 i
the neck revealed no thyroid enlargement.4 V" t7 N' y- I6 t6 m0 k* m4 y& i
The genitourinary examination was remarkable for- X5 a) A( ?% e3 a
enlargement of the penis, with a stretched length of
8 o2 q$ R: ]# Z7 Q8 cm and a width of 2 cm. The glans penis was very well
3 u4 [  z9 c! t/ E$ d/ s) g( tdeveloped. The pubic hair was Tanner II, mostly around
6 X7 c1 v* v' {  z+ i540) p/ l9 c/ t% Z
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the base of the phallus and was dark and curled. The. c2 R9 g. ~7 R. |, z
testicular volume was prepubertal at 2 mL each.
  s# V. C; g  }; E, C/ u0 CThe skin was moist and smooth and somewhat
+ Z7 [6 j' Y* A- L$ Noily. No axillary hair was noted. There were no' @0 j) D! i8 o; D  S
abnormal skin pigmentations or café-au-lait spots.
! X0 H& Y& [1 }4 W7 m! d1 T! kNeurologic evaluation showed deep tendon reflex 2+& w" ]9 V) H# G) K( W% s# T9 O
bilateral and symmetrical. There was no suggestion
, c7 I; e7 H% [$ U; hof papilledema.3 ]! e4 S1 t0 d7 |! h- Z
Laboratory Evaluation* K/ i3 ~0 d  ?! d9 m
The bone age was consistent with 28 months by
) `# F( u! G+ W# v+ W  Vusing the standard of Greulich and Pyle at a chrono-
: ]2 T% n% B* s/ |6 |$ |logic age of 16 months (advanced).5 Chromosomal
, T$ u8 x* L3 k3 x& Y0 v9 @5 w- skaryotype was 46XY. The thyroid function test
" V% N+ `* V& O0 N& }7 Ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-
) r5 @8 E& |6 Ulating hormone level was 1.3 µIU/mL (both normal).
( ~- V0 f( ?) v: d0 Q5 W2 y; }; WThe concentrations of serum electrolytes, blood
; M1 S) |+ J* N6 m" `$ Uurea nitrogen, creatinine, and calcium all were" `) c& r) S- T; b3 U7 d1 [7 T/ ]# }
within normal range for his age. The concentration- M" L/ N3 {4 Q: L9 ~
of serum 17-hydroxyprogesterone was 16 ng/dL
# h9 a! q6 ~8 F2 p(normal, 3 to 90 ng/dL), androstenedione was 20
. M! u: Z  q4 v9 ?ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-, g$ {1 {8 ?. e, U/ |- I
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' p) \0 n# i5 \: U8 c) n8 v7 l6 B
desoxycorticosterone was 4.3 ng/dL (normal, 7 to9 {( ~9 w) q& F; Q/ w9 G1 c$ ?
49ng/dL), 11-desoxycortisol (specific compound S)
* K: V' {& ?9 `was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' X$ V  A9 ^1 L) h* T3 _1 [tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ V0 A# M& k& o0 `+ R5 c3 C; g
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; R2 R; L1 }3 a2 w- ]2 Mand β-human chorionic gonadotropin was less than, k! @+ L1 W% Z2 N$ C. Z
5 mIU/mL (normal <5 mIU/mL). Serum follicular4 [: q- C! C9 v9 ]" X
stimulating hormone and leuteinizing hormone" F9 ]* @" {* N( z6 q! Y/ g: \- V5 B' r
concentrations were less than 0.05 mIU/mL: I3 C; D0 i) B# p& E
(prepubertal).
7 n) M: E# R5 kThe parents were notified about the laboratory
, Z; Y, K# n+ l8 _  I/ @  m5 `2 Bresults and were informed that all of the tests were
1 g, o& O2 F7 I4 u9 ?( J+ unormal except the testosterone level was high. The
1 s5 L% l" J$ q3 ~follow-up visit was arranged within a few weeks to
# P7 g9 H+ \. S5 R1 zobtain testicular and abdominal sonograms; how-
1 y+ G8 o/ c% U( z% n1 S: aever, the family did not return for 4 months.
( K5 K% N) m4 x& ]8 K; h7 d+ ZPhysical examination at this time revealed that the9 y) ?2 o# b5 `; @. U  d: v
child had grown 2.5 cm in 4 months and had gained' @. ]+ J7 `- c$ [% Y7 z
2 kg of weight. Physical examination remained
* O6 d0 N1 r" E% `unchanged. Surprisingly, the pubic hair almost com-
" x- E- x# i/ ]pletely disappeared except for a few vellous hairs at- Y. ?! _' ^3 e7 `% Q, e' V
the base of the phallus. Testicular volume was still 24 o/ O- q$ p8 d* ^$ D8 p, l
mL, and the size of the penis remained unchanged.! W" D, ^* A& Z8 j& Q/ G! X) w
The mother also said that the boy was no longer hav-
3 M/ [6 V/ ]1 Q6 p% ming frequent erections.
! v. w* j- y( O' b7 ^) oBoth parents were again questioned about use of1 z7 H( a. g/ J' z
any ointment/creams that they may have applied to2 B% M) D7 K9 i) l
the child’s skin. This time the father admitted the' l* V+ \& r/ R3 a. A
Topical Testosterone Exposure / Bhowmick et al 541
5 V8 t) h+ u( X6 I2 V# E. _; L. }use of testosterone gel twice daily that he was apply-9 s: e1 j" P( {6 ^5 o8 ^
ing over his own shoulders, chest, and back area for! e9 S* }3 t3 E& c  W  Y2 }
a year. The father also revealed he was embarrassed
3 u  O  B! M8 R% B5 }( O! n2 ]to disclose that he was using a testosterone gel pre-
4 ]" X% F  V  [! M. lscribed by his family physician for decreased libido2 F- N( ?6 o! U3 [- I! A1 ~; v: n
secondary to depression." n) s$ R1 `& A, E9 ~
The child slept in the same bed with parents.
# v2 k! t' ]9 r7 W+ ^The father would hug the baby and hold him on his" J# H% k2 f6 F% x. L, q! h/ G
chest for a considerable period of time, causing sig-
1 ?6 n" C! P# ]# \5 S% s% h+ ~* vnificant bare skin contact between baby and father.2 O0 W% m8 s4 B9 `( E
The father also admitted that after the phone call,8 ?4 J8 J% l+ Z' S8 K* d) o) y9 I
when he learned the testosterone level in the baby- p" A* t7 N# ]! z0 {
was high, he then read the product information
) d; ]$ _3 R. bpacket and concluded that it was most likely the rea-  \. R" s5 q7 U
son for the child’s virilization. At that time, they
- |* g9 m) O8 A& b9 N: J: k; Odecided to put the baby in a separate bed, and the
7 D* o" C, |& P0 z$ ?' ^1 Afather was not hugging him with bare skin and had
! z, a" H' \: B+ `4 ?been using protective clothing. A repeat testosterone$ _8 d: \$ c! v; G- p+ W
test was ordered, but the family did not go to the* u; Q2 g+ Y, ]( [
laboratory to obtain the test.
# z9 }6 x4 j8 H6 N! W5 b% ]Discussion
( B$ J9 t+ \* Z- Y$ }4 OPrecocious puberty in boys is defined as secondary
3 A$ l4 O4 [/ a* D1 {sexual development before 9 years of age.1,4
2 X0 j/ S: y# |! f* \4 {9 cPrecocious puberty is termed as central (true) when" o- d0 C. n' _# ^# m
it is caused by the premature activation of hypo-  o  g0 A! p* p5 h
thalamic pituitary gonadal axis. CPP is more com-
+ H  P( |0 m6 F7 B7 K+ o" jmon in girls than in boys.1,3 Most boys with CPP
# y7 v  s1 e5 ]3 hmay have a central nervous system lesion that is
3 Y. v6 @- H  s! b) K3 oresponsible for the early activation of the hypothal-* T+ R0 ]6 u8 ]6 E; G1 ^: S7 l8 d
amic pituitary gonadal axis.1-3 Thus, greater empha-
1 \( l  r% {7 Y2 }& Psis has been given to neuroradiologic imaging in
7 u: W& {( U0 S; Z# o  j+ }0 A0 U  i9 oboys with precocious puberty. In addition to viril-
  ~% G: c0 ~$ T0 B0 D  mization, the clinical hallmark of CPP is the symmet-
% n5 y5 q5 {# t0 i9 s1 urical testicular growth secondary to stimulation by/ _4 y( ]- X+ ~# m& {4 n
gonadotropins.1,3& V8 S! e( Y3 v5 V; w8 s4 h
Gonadotropin-independent peripheral preco-
  e7 }+ ^/ Z; icious puberty in boys also results from inappropriate
1 m( X4 H- X, J% a7 [6 landrogenic stimulation from either endogenous or$ r( H/ e5 k0 b) U7 z" J& G
exogenous sources, nonpituitary gonadotropin stim-
6 A( M; I# d/ y0 nulation, and rare activating mutations.3 Virilizing2 @8 u4 R, z& c5 b& O6 y! l
congenital adrenal hyperplasia producing excessive8 ^. C5 E  U- b/ B
adrenal androgens is a common cause of precocious0 a# y/ H- v/ o1 k) O
puberty in boys.3,4/ R1 }; J) |3 l" @. Y
The most common form of congenital adrenal
2 X+ F4 u5 g; h0 a" J& y4 X# Shyperplasia is the 21-hydroxylase enzyme deficiency.
- g/ i$ N& k& y* p# qThe 11-β hydroxylase deficiency may also result in
) L- @1 J  s' _% @' oexcessive adrenal androgen production, and rarely,( x+ A/ O/ g- `! D
an adrenal tumor may also cause adrenal androgen& x! T/ Y% z) M. V2 }) j( b7 p3 ]
excess.1,3- F1 B( v& D' C( u. m! n: S& e& |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  L: l( a1 j( k7 x$ M542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- f) j+ Z  _& pA unique entity of male-limited gonadotropin-5 P# ?( U* e" a
independent precocious puberty, which is also known, y" y$ C% V3 k4 I; q6 c5 m! {, E
as testotoxicosis, may cause precocious puberty at a+ Q$ O/ G0 b% T
very young age. The physical findings in these boys0 G" P9 q! T- X0 g
with this disorder are full pubertal development,
9 o/ I) a% x% d+ y# `5 r/ Nincluding bilateral testicular growth, similar to boys8 g5 Y5 U. s; ^8 f% Q
with CPP. The gonadotropin levels in this disorder3 W8 R0 a- I4 w; K0 y5 Q
are suppressed to prepubertal levels and do not show% Z8 f* t1 ]& k3 e% K" Q7 }
pubertal response of gonadotropin after gonadotropin-
" [6 T& l$ q* k1 a4 Yreleasing hormone stimulation. This is a sex-linked, D( {( n  C) n8 y* h
autosomal dominant disorder that affects only% H1 u3 r/ ?( D7 c/ o
males; therefore, other male members of the family
3 y7 K/ ~( w- ^( d* R7 Z1 emay have similar precocious puberty.3: [7 d% D! P% g6 P5 _  p
In our patient, physical examination was incon-/ U3 X8 y0 c2 }
sistent with true precocious puberty since his testi-
( C$ O# d  Q- p/ \* |' _& Dcles were prepubertal in size. However, testotoxicosis; u/ ^5 A8 b  O0 c# N& ~
was in the differential diagnosis because his father% ^& Y1 u+ D4 }; Y! V( T# o
started puberty somewhat early, and occasionally,
; D! D2 T, X0 x$ H+ }, P% Ptesticular enlargement is not that evident in the
: C2 T/ \3 B8 v3 x/ }beginning of this process.1 In the absence of a neg-6 q' P# c) {6 G" y7 t& a
ative initial history of androgen exposure, our
6 A8 ?% R% s/ y# Cbiggest concern was virilizing adrenal hyperplasia,
. U% h! f- u+ F) oeither 21-hydroxylase deficiency or 11-β hydroxylase& J! o& N# C" ?7 T
deficiency. Those diagnoses were excluded by find-, M& A' D% n0 S+ S( `1 m* T3 O
ing the normal level of adrenal steroids.
( k" l7 X" e9 a1 eThe diagnosis of exogenous androgens was strongly. J. I1 t- T2 x8 S* ]  r$ i
suspected in a follow-up visit after 4 months because# J& a; j0 Q: C
the physical examination revealed the complete disap-
* E  i6 E, n$ j5 K, @4 I! @7 I% c+ w: \% dpearance of pubic hair, normal growth velocity, and
/ w  |9 T8 ]( f5 {' m" Wdecreased erections. The father admitted using a testos-
8 M) Q0 L" }# k1 V- b$ f% |terone gel, which he concealed at first visit. He was# i) R7 u6 K4 w8 A9 O, b9 Y
using it rather frequently, twice a day. The Physicians’
" @5 S% M: S7 s$ b, U5 _3 SDesk Reference, or package insert of this product, gel or4 ~3 S! m. n3 ^+ X8 ~* J
cream, cautions about dermal testosterone transfer to5 [" L( t+ B6 Z8 ]
unprotected females through direct skin exposure.) J6 ~7 m0 `. f+ r& m" I! w" W
Serum testosterone level was found to be 2 times the$ h3 W1 a! C+ L- Y
baseline value in those females who were exposed to
% O9 Q5 Q. }7 U, e4 Weven 15 minutes of direct skin contact with their male
. N9 E: T) `: w2 _8 Q0 }partners.6 However, when a shirt covered the applica-4 }+ J* e! }. h2 E3 b3 r/ L
tion site, this testosterone transfer was prevented.0 ?3 ]. Y  |! ]8 @, e$ C9 \7 o7 f
Our patient’s testosterone level was 60 ng/mL,
& ^4 K! K# |- f9 swhich was clearly high. Some studies suggest that+ U2 ^& W' \5 x3 W
dermal conversion of testosterone to dihydrotestos-6 K1 w5 c# v1 L% M$ k
terone, which is a more potent metabolite, is more% n( W) Q+ f% `3 ~: E+ b8 T2 W
active in young children exposed to testosterone! C  C" j  |% c+ k& t* e
exogenously7; however, we did not measure a dihy-7 |- i1 G; e; a# k8 n- `, \& x. N
drotestosterone level in our patient. In addition to9 }) F+ c4 K" F( Q0 ?
virilization, exposure to exogenous testosterone in& {3 v1 \$ f& p4 D$ R7 [( m" d
children results in an increase in growth velocity and
5 K/ \; i. I5 X: c1 [% A2 {advanced bone age, as seen in our patient.
$ T' Q! b% o- d: W% W2 S- gThe long-term effect of androgen exposure during' A, J6 g9 o! T' t% R
early childhood on pubertal development and final. R( U5 p  {# _1 `" n5 i6 ~
adult height are not fully known and always remain+ C  m7 S& U% @6 t
a concern. Children treated with short-term testos-
+ @' ~* G" p. O& `1 e' ]0 }( }terone injection or topical androgen may exhibit some& j4 O  `9 f. C7 C3 z/ S( F
acceleration of the skeletal maturation; however, after
8 R2 h4 ^: _  [" Q% o% E- jcessation of treatment, the rate of bone maturation
! I( c. C1 t7 c1 Y5 wdecelerates and gradually returns to normal.8,99 o, z9 _* B6 C0 s  B
There are conflicting reports and controversy
! ?1 O) q! V+ T  S9 ~0 Dover the effect of early androgen exposure on adult
: Q( V* u( B: A: p6 t& npenile length.10,11 Some reports suggest subnormal( ~" ^2 p) D& {/ C4 }
adult penile length, apparently because of downreg-- g8 H' r! A! c' ~
ulation of androgen receptor number.10,12 However,
" h: S2 V8 f+ ESutherland et al13 did not find a correlation between
3 u, l: E# \- I, ^( I( ]# vchildhood testosterone exposure and reduced adult9 F$ `6 K; r% e9 P5 \  L
penile length in clinical studies.
2 L2 C$ a# p' W/ W! h, |$ T- vNonetheless, we do not believe our patient is
" y) R. S5 r& L& t* cgoing to experience any of the untoward effects from
4 m9 L: o) }1 O0 N# ]& p1 X0 ztestosterone exposure as mentioned earlier because
- d3 C0 k# s, G& q& Fthe exposure was not for a prolonged period of time.2 q3 c8 X* U' F4 x) H% `9 U- |
Although the bone age was advanced at the time of3 R  a, b& Q4 T3 S) m2 q  Y
diagnosis, the child had a normal growth velocity at
0 q; h& ~9 b& Q3 I7 J" Qthe follow-up visit. It is hoped that his final adult
9 `8 }- e  V$ c4 [" ^height will not be affected.: t3 X( C# E' i6 i: X
Although rarely reported, the widespread avail-
& W/ u: F5 `* j1 fability of androgen products in our society may
9 t2 s0 |7 j0 F9 Z9 Uindeed cause more virilization in male or female: i+ l) l) s' }; M2 d* }* K
children than one would realize. Exposure to andro-
% H& i7 A: U# N. P3 {gen products must be considered and specific ques-/ \' D/ r9 p3 a+ M
tioning about the use of a testosterone product or$ d0 I! I$ \3 R7 l* D+ F$ [
gel should be asked of the family members during4 B: k5 y5 Y( _  V" f
the evaluation of any children who present with vir-9 t$ |* d# I% b" S  m3 [7 p, `+ F  z
ilization or peripheral precocious puberty. The diag-- R/ h! y- [* c, A1 Y0 v1 _: T
nosis can be established by just a few tests and by3 b9 i0 ^* S( }! @  ?* A
appropriate history. The inability to obtain such a
6 o! V1 K& G' l2 c. H: ~$ c' Vhistory, or failure to ask the specific questions, may
8 k: F: Y0 j( Y1 T+ i6 E* Kresult in extensive, unnecessary, and expensive' [2 ?, S! @5 T9 R6 e# ~
investigation. The primary care physician should be
! v2 P1 A. q( o+ W) r! faware of this fact, because most of these children
# _- C1 {* i5 Y: |: n7 s2 |may initially present in their practice. The Physicians’( y$ Z6 j6 W9 h; E
Desk Reference and package insert should also put a3 M* X. N' x1 T3 ~/ j. o& x! n
warning about the virilizing effect on a male or/ r! H# v: J2 A2 d( E5 q' m' K7 L/ Q
female child who might come in contact with some-
. ]% E; S; K. ione using any of these products.
: T! Z  v; A6 D! ~7 D5 tReferences
5 Z, ^; R3 P0 R) U8 C  B  ?$ a1. Styne DM. The testes: disorder of sexual differentiation
( ~* g/ `9 f' n4 f/ E; ~and puberty in the male. In: Sperling MA, ed. Pediatric
) d1 K; _+ ]; l' X/ R# L1 ^Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
) y- @% Q9 Z9 B1 z4 {- U; H2002: 565-628.
. Y; Z3 o0 F1 S, ~% K9 }+ c0 \2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. P7 T) ~' b0 {1 k
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
/ X/ J: E8 c( y  V% |0 x" Q
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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