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Sexual Precocity in a 16-Month-Old) z) t/ O8 h* l. u
Boy Induced by Indirect Topical
) T3 J5 i9 j/ ^1 \) ^Exposure to Testosterone3 r* A! R: B, Q: d
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; ]8 h0 a6 ?4 J! L0 Rand Kenneth R. Rettig, MD1
& W4 C( ^0 v" |+ j; E4 }Clinical Pediatrics
( K( v+ {6 E" zVolume 46 Number 66 L: Y" L( C  H8 a' Y: }; b
July 2007 540-543
+ @* f# o! v/ Q# b) T( K- a/ h% R© 2007 Sage Publications) T. l6 W7 d, A1 o  k  f: X
10.1177/00099228062966513 X9 L$ u, h( B5 X  }1 b( C; D
http://clp.sagepub.com7 L* H6 T3 }0 n
hosted at1 o) R. {2 }- y, R  F  {( _
http://online.sagepub.com
4 n$ I- L6 A) w# f+ YPrecocious puberty in boys, central or peripheral,
5 d+ h8 `6 E, a2 @is a significant concern for physicians. Central
; k* P) O- ]7 B( P+ K& x  m3 Xprecocious puberty (CPP), which is mediated
+ ]# F1 ^# X; `through the hypothalamic pituitary gonadal axis, has- t* e" B" R5 P3 ?1 o  m* h
a higher incidence of organic central nervous system1 T1 Y! [3 @: j% x# T+ G9 e
lesions in boys.1,2 Virilization in boys, as manifested2 ]9 a5 {: Y2 S2 R
by enlargement of the penis, development of pubic, A+ J3 e; ?6 r8 L( t
hair, and facial acne without enlargement of testi-
2 J& F* ^9 u: R+ v$ F, Acles, suggests peripheral or pseudopuberty.1-3 We
. \8 U  Q+ _3 I  A% ?report a 16-month-old boy who presented with the
* G, G: _% C( L2 u2 H. R! `0 Zenlargement of the phallus and pubic hair develop-
6 {" [: S/ C* Y4 ]& b/ \ment without testicular enlargement, which was due
2 E4 `1 |) I5 cto the unintentional exposure to androgen gel used by
  {) u. K7 ?8 }# z( X6 d! Xthe father. The family initially concealed this infor-
" N* {, f$ j0 ~2 i% Qmation, resulting in an extensive work-up for this; d# d: ]( t8 k/ y! l6 {
child. Given the widespread and easy availability of
3 w5 ]9 @( A2 ?* e! J' Itestosterone gel and cream, we believe this is proba-
( F% r7 D0 Q6 q) T) J7 ]1 T1 pbly more common than the rare case report in the) e. O& \- Y/ L  [+ n6 u
literature.4
& d( D0 x/ H/ A5 t* ~5 `Patient Report
* f( g1 v! w! i* ^A 16-month-old white child was referred to the
2 Y. w8 N* m+ h( R6 v: pendocrine clinic by his pediatrician with the concern
- T, D& C5 l0 z" ?. L5 H) \0 A: jof early sexual development. His mother noticed
& {5 f2 e2 S) F* i: N  D2 ^; H% Mlight colored pubic hair development when he was4 x' s% B, }: f
From the 1Division of Pediatric Endocrinology, 2University of
6 U" e/ o) x! ?7 \2 T5 jSouth Alabama Medical Center, Mobile, Alabama.! M7 [$ o) `: F- m' @5 u0 Z
Address correspondence to: Samar K. Bhowmick, MD, FACE,
/ F4 D; x5 T# f) F& ?" g0 XProfessor of Pediatrics, University of South Alabama, College of2 i0 n6 ]% s# _: ^% y
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
# m; c  i7 e0 I' N8 Te-mail: [email protected].; ~4 m' m9 I- l, n/ h
about 6 to 7 months old, which progressively became$ A6 n  ]6 {+ b" b+ T
darker. She was also concerned about the enlarge-
+ X; B3 T9 q# v! A& P+ ement of his penis and frequent erections. The child7 b' |8 x+ _$ ~- X. M1 K9 W, q- k
was the product of a full-term normal delivery, with( w, ]- Y/ T/ Z
a birth weight of 7 lb 14 oz, and birth length of
9 y& k7 f0 x- R* w20 inches. He was breast-fed throughout the first year# V) y4 k( k# }! @
of life and was still receiving breast milk along with
4 \( D' t2 }: g) j: e8 _) ^solid food. He had no hospitalizations or surgery,
3 G- z# @  _/ Y* }and his psychosocial and psychomotor development
' f, y9 a9 V; ^( k8 a4 d4 ?  |was age appropriate.
* e, r: i  U5 t! y8 [' PThe family history was remarkable for the father,) B; |# c. ~( G  _7 j9 F- s
who was diagnosed with hypothyroidism at age 16,, e( T: U  x& f' o
which was treated with thyroxine. The father’s
( x) _$ b! L& M* R; h3 t: X1 q) D$ ^height was 6 feet, and he went through a somewhat
0 f: a( v6 `$ G' Gearly puberty and had stopped growing by age 14.
4 T1 U) K7 U# N: NThe father denied taking any other medication. The9 y: m( M1 [7 m+ `4 s. \6 J
child’s mother was in good health. Her menarche
# z# B0 L8 r* X: Wwas at 11 years of age, and her height was at 5 feet+ Z1 C3 \3 Z( ~5 ^5 M( w: N" e$ o
5 inches. There was no other family history of pre-
- |- y- _7 }4 c( Q7 Bcocious sexual development in the first-degree rela-
2 N+ Q1 q2 W% M: Y, Htives. There were no siblings.
) _- S' G0 ?3 v0 E% Z) HPhysical Examination
4 B/ h( r* b3 \1 w( t9 MThe physical examination revealed a very active,
) Y) g7 a( p' J$ i) x# nplayful, and healthy boy. The vital signs documented/ k2 f* h, M9 p* A
a blood pressure of 85/50 mm Hg, his length was, d4 m6 p) u$ D7 p7 M4 W
90 cm (>97th percentile), and his weight was 14.4 kg- q) `9 k! n% u! A$ ^, i1 k, U
(also >97th percentile). The observed yearly growth
: r& `( C/ k. E, ~, R: U. Wvelocity was 30 cm (12 inches). The examination of* y. w: q/ @$ a/ Q9 M
the neck revealed no thyroid enlargement.! N# F) W' j. W. B
The genitourinary examination was remarkable for
0 p6 B1 n5 U, m- \4 Y( Zenlargement of the penis, with a stretched length of
- w" B6 u2 A" o9 s1 a( H; U. Y8 cm and a width of 2 cm. The glans penis was very well
" a8 I& J, [3 b) Q* e! \developed. The pubic hair was Tanner II, mostly around4 i" ~5 B5 c, T7 }& m7 Q
5401 n$ Z6 o# G) X1 C1 B+ q( A# C
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( M) D5 s. r1 @" T5 s5 T5 Zthe base of the phallus and was dark and curled. The
5 ?( R( s' E5 |; Atesticular volume was prepubertal at 2 mL each.$ _0 N. f  A2 h. U: R* F
The skin was moist and smooth and somewhat
0 f) o7 w- f* y5 g" U* Doily. No axillary hair was noted. There were no) @& P  F) l: D8 e: i# |  @9 s
abnormal skin pigmentations or café-au-lait spots., ^; E+ t% N- J0 K
Neurologic evaluation showed deep tendon reflex 2+
1 c/ Q7 A+ \+ Zbilateral and symmetrical. There was no suggestion
0 i! B2 V0 Y3 o6 oof papilledema.6 u4 P: H& n7 p. z+ F. \7 K
Laboratory Evaluation
  \3 F5 B- H1 ]8 XThe bone age was consistent with 28 months by. a) h% [1 ]2 M: t- b% Y. ?0 {! O8 [* k
using the standard of Greulich and Pyle at a chrono-
; ^% t9 g1 s5 z4 Glogic age of 16 months (advanced).5 Chromosomal1 C, X3 }0 \3 D# u# L
karyotype was 46XY. The thyroid function test
& N, k' S4 C) }' \4 Oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
( Z' H2 w2 c: _6 r! S' clating hormone level was 1.3 µIU/mL (both normal)./ g  f/ V/ ]6 O2 B# Z0 w
The concentrations of serum electrolytes, blood
' R3 N; w! _% j' F. Z, Ourea nitrogen, creatinine, and calcium all were
* u2 j: K* ?5 u7 O' L2 T* uwithin normal range for his age. The concentration
9 x7 H5 V# I' F8 }% k6 V$ L) s- W2 M+ r% Gof serum 17-hydroxyprogesterone was 16 ng/dL  G: L. k2 e3 F! q
(normal, 3 to 90 ng/dL), androstenedione was 20
3 ~# j0 ]* L' m8 h# Z) r( ^  k( Sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-5 \4 }8 A5 K5 f
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 H$ l3 L( y6 U, e  E6 q1 Rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to$ f- N- f) I  W( u& H" l
49ng/dL), 11-desoxycortisol (specific compound S)
3 C' R* @3 P. c, Q6 M5 e4 Zwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- F- ~2 {% j# b2 l+ G* [& L
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 q! m+ e/ R- D& N% Q- _  b9 Ntestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
2 n& |: A0 {$ Q$ ~and β-human chorionic gonadotropin was less than6 k+ p" n+ v3 ~7 o
5 mIU/mL (normal <5 mIU/mL). Serum follicular
9 J. P, m$ S0 k. f# y  d. Tstimulating hormone and leuteinizing hormone5 F% p! Z1 I& [1 V8 a, K
concentrations were less than 0.05 mIU/mL
% q& O6 {( q! E  p(prepubertal).0 H! \8 a0 r2 i' H) N! v
The parents were notified about the laboratory
2 ^' `, O, {- e1 j, S6 F9 W/ Zresults and were informed that all of the tests were
$ ~$ ~1 v8 r* Y" xnormal except the testosterone level was high. The
9 n  n4 t7 W7 m+ h) Hfollow-up visit was arranged within a few weeks to
3 z# r' H9 t! k$ e; Zobtain testicular and abdominal sonograms; how-* l8 f6 _$ i  v) l7 k& @
ever, the family did not return for 4 months.6 @6 G3 Z  X' a8 i+ r! S
Physical examination at this time revealed that the6 `; {+ l$ p; m7 W, N: n$ h& ]/ I1 I
child had grown 2.5 cm in 4 months and had gained8 ^; f% H  S- k% t# |" V, Y
2 kg of weight. Physical examination remained. c# [2 l, a3 o
unchanged. Surprisingly, the pubic hair almost com-
' H3 S+ ?- q& I; j# n1 p7 Dpletely disappeared except for a few vellous hairs at
1 Q% C. u4 t0 [the base of the phallus. Testicular volume was still 2
6 a1 H7 ]7 j+ y# t5 wmL, and the size of the penis remained unchanged.
) T$ T) z/ k( \9 j0 l" C, @The mother also said that the boy was no longer hav-2 o- E. i0 j1 Z, i9 e7 U/ v
ing frequent erections.
0 F$ P4 \$ H- uBoth parents were again questioned about use of
% k* B; L2 ?3 h# A* h+ h# ?. I* T7 _' cany ointment/creams that they may have applied to
7 B: l" E2 L2 V* @3 dthe child’s skin. This time the father admitted the
3 p4 v, n. O6 L; F. ETopical Testosterone Exposure / Bhowmick et al 541, F4 E& l5 W  M0 L" m, D
use of testosterone gel twice daily that he was apply-
9 M: M) q0 A3 H% @8 @! S& Ding over his own shoulders, chest, and back area for, `; w+ s. F! D' Q) ]9 H
a year. The father also revealed he was embarrassed
/ \# ~$ n8 n- _8 n' N! xto disclose that he was using a testosterone gel pre-. M6 i3 L+ P, R' s. O# k" m
scribed by his family physician for decreased libido
: X3 r8 Y: [6 \) [9 A& L4 @% ]secondary to depression.
+ F% n6 V! j: w$ W; @& o! o  ~4 fThe child slept in the same bed with parents.
& a+ Q, S# a: E( m) k. U; z+ ~The father would hug the baby and hold him on his9 Q2 C; o; V' a0 U6 m- c) L
chest for a considerable period of time, causing sig-# z! [/ C. ^( K/ t* {7 j
nificant bare skin contact between baby and father.
, W; w: B0 N" R' ~% z) o2 gThe father also admitted that after the phone call,. V) T& @3 J8 v" z/ [5 D  t
when he learned the testosterone level in the baby+ B$ R. ~" ?, o7 {, x8 Y5 i
was high, he then read the product information
8 E- O* s9 l# g  y& kpacket and concluded that it was most likely the rea-2 X2 s, }) v. h* b
son for the child’s virilization. At that time, they
) r  j7 e4 h% K! A( u2 t: w% e1 C) adecided to put the baby in a separate bed, and the" t$ D3 a/ Y, d4 S. X3 f
father was not hugging him with bare skin and had
) f8 g8 B+ B  |; ^' sbeen using protective clothing. A repeat testosterone9 G9 t& C, K" Y  r4 ~- e8 T: K
test was ordered, but the family did not go to the; \( j7 c" f6 S7 B- X  e; z
laboratory to obtain the test./ B- j6 b! p- F& O0 [" Q3 h
Discussion
$ Z+ e, M5 w# V8 f6 G0 S0 @4 L& PPrecocious puberty in boys is defined as secondary
3 P$ ^$ H/ q7 m3 r% H7 Wsexual development before 9 years of age.1,4
1 I; i. M. k3 p0 bPrecocious puberty is termed as central (true) when
8 a6 ]! F% ?0 r; M5 j3 B+ @8 ait is caused by the premature activation of hypo-
5 Z2 B: U9 l( h6 hthalamic pituitary gonadal axis. CPP is more com-. x7 P3 A4 d& K% Z" R( v4 Z) e# C3 J  p
mon in girls than in boys.1,3 Most boys with CPP! e0 O1 \  S, _
may have a central nervous system lesion that is9 J7 \1 e+ Q! m. h! i4 Q. [2 O
responsible for the early activation of the hypothal-
, G0 z3 v2 W5 F* Vamic pituitary gonadal axis.1-3 Thus, greater empha-
2 O0 g0 l. x7 L0 ^) M' {% E& K; a( |sis has been given to neuroradiologic imaging in. g( u$ |$ d7 l3 T, c8 _
boys with precocious puberty. In addition to viril-  b. D' k; h0 G6 \$ L" `9 M& [
ization, the clinical hallmark of CPP is the symmet-2 A- z( S: c3 o; Z# `7 k
rical testicular growth secondary to stimulation by. ~  x7 k( z4 }# e
gonadotropins.1,38 k; h9 b) F/ e
Gonadotropin-independent peripheral preco-; r9 G9 l/ `! ^' Z2 c3 U  b
cious puberty in boys also results from inappropriate
! F4 j9 O/ k" \- ?& s; H  B* sandrogenic stimulation from either endogenous or
& i- I4 s- Y& c& U" f5 Aexogenous sources, nonpituitary gonadotropin stim-
( M7 @% H$ p- b' ?* J! e5 @* d' ~ulation, and rare activating mutations.3 Virilizing, N0 w6 H3 w0 }& _
congenital adrenal hyperplasia producing excessive
/ u; i: f( w) zadrenal androgens is a common cause of precocious3 V/ J5 o7 C% B; s& ]2 U8 P
puberty in boys.3,4
2 _! D. q3 Q7 T- G  `7 QThe most common form of congenital adrenal: A: B7 I) T, c/ o
hyperplasia is the 21-hydroxylase enzyme deficiency.* A- f4 _2 e* E" [7 A
The 11-β hydroxylase deficiency may also result in% w0 J- `, {' \* N7 p- c
excessive adrenal androgen production, and rarely,* N; F  s$ B/ i& t5 H8 X
an adrenal tumor may also cause adrenal androgen8 W, q8 F1 T2 ]6 `5 N) S
excess.1,3  g9 F" u2 H' [' y. T3 E
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 g- U/ _  T4 M, H4 A5 s5 E; W
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: k- p) U) w# x  i/ DA unique entity of male-limited gonadotropin-
% y, i5 `8 a0 D5 }4 Jindependent precocious puberty, which is also known
" N; ~3 F0 ^) e' o, Yas testotoxicosis, may cause precocious puberty at a
2 O! Y! f2 L! m) u6 qvery young age. The physical findings in these boys
! X- T1 h/ y. k) T8 i7 Ywith this disorder are full pubertal development,
: E9 Q. ?8 X9 t$ J6 F3 Cincluding bilateral testicular growth, similar to boys
9 Z" g5 l: r% L' r$ U3 ?: ?with CPP. The gonadotropin levels in this disorder4 K, J" D( m' v$ M# @
are suppressed to prepubertal levels and do not show- x$ P; Y& g4 W* A  ]" N% l
pubertal response of gonadotropin after gonadotropin-
  \2 k- Q( K% Greleasing hormone stimulation. This is a sex-linked
: Q+ h! X/ h4 T1 q# K9 b% Oautosomal dominant disorder that affects only+ ^; O, R' Y- ]( K& K
males; therefore, other male members of the family: s, G) x; T3 N5 }  z% ~
may have similar precocious puberty.3
9 k% Y8 V6 H2 B0 e1 O% N$ B& w) G5 hIn our patient, physical examination was incon-
  F! t# A3 I2 q, |' M9 ^sistent with true precocious puberty since his testi-3 {5 z: N) I) a  r2 f: n
cles were prepubertal in size. However, testotoxicosis. F9 q! Q: F% f/ }% d* ^) J1 K
was in the differential diagnosis because his father7 }7 S6 j$ G2 M+ @
started puberty somewhat early, and occasionally,4 V- Q4 j5 N. ~1 p6 Q0 p
testicular enlargement is not that evident in the( h5 B6 U5 @7 \* W4 e
beginning of this process.1 In the absence of a neg-( |" n1 G! F) Y: a- h! k0 d
ative initial history of androgen exposure, our  F! |) T( D/ k; q6 \
biggest concern was virilizing adrenal hyperplasia,
7 `+ K) r6 ^8 w: T' S# G! _% Feither 21-hydroxylase deficiency or 11-β hydroxylase$ R' _# u! [" u% D: s5 [' N- g5 z
deficiency. Those diagnoses were excluded by find-. E; H/ T. }  w0 l
ing the normal level of adrenal steroids.
, a0 s- n8 ^1 N, n( KThe diagnosis of exogenous androgens was strongly' N* h6 c& U/ S* c) ~
suspected in a follow-up visit after 4 months because
6 _9 r# m( }& a+ G4 Nthe physical examination revealed the complete disap-/ Q% c: ]: I; m1 S
pearance of pubic hair, normal growth velocity, and9 X; ]  u* a* G
decreased erections. The father admitted using a testos-
3 O- T: ~" P1 l" N: r4 K* x; |  bterone gel, which he concealed at first visit. He was# a! K7 ]+ K; I, `
using it rather frequently, twice a day. The Physicians’) L0 Y% o; P2 D& T0 V
Desk Reference, or package insert of this product, gel or! Q" q( ?# n& [8 T3 c( i5 P3 ^
cream, cautions about dermal testosterone transfer to' o# v% j+ u3 r1 J' s
unprotected females through direct skin exposure.
- [" p) p, W# s1 K6 M9 \3 TSerum testosterone level was found to be 2 times the
; U* ~5 C; ?; pbaseline value in those females who were exposed to5 ~2 f( l7 S! x; n# S/ {; l* Z% f
even 15 minutes of direct skin contact with their male
' ~9 S/ d9 S4 L" Wpartners.6 However, when a shirt covered the applica-" l1 x3 P1 O5 b( a$ j$ I2 r
tion site, this testosterone transfer was prevented.$ t+ ?! U  O% R+ D4 ^3 V" i
Our patient’s testosterone level was 60 ng/mL,
+ [/ F0 N; w/ a- V  {, hwhich was clearly high. Some studies suggest that
, i# x# T0 W3 s/ B% ?( ]dermal conversion of testosterone to dihydrotestos-& }. U4 B) p+ S! i' H* D) m
terone, which is a more potent metabolite, is more
. A, d) m1 {. Jactive in young children exposed to testosterone
3 t  F5 l; z8 T8 k8 P* \exogenously7; however, we did not measure a dihy-
. {( V! d8 |$ I% k  fdrotestosterone level in our patient. In addition to
9 d) ^% l+ R" g! J+ lvirilization, exposure to exogenous testosterone in: @( W4 B% B& H$ h
children results in an increase in growth velocity and! m- P/ {8 E( H$ v$ l1 t0 n
advanced bone age, as seen in our patient.  l! l) S! m* `: z: _. c
The long-term effect of androgen exposure during2 ~, ~6 ?; n* I3 s" k9 z
early childhood on pubertal development and final
8 i; ~- @+ E! w# U6 Gadult height are not fully known and always remain
/ T6 u# Q! n3 ?a concern. Children treated with short-term testos-& A- N  V  E# L$ V
terone injection or topical androgen may exhibit some
8 v' m1 D9 s5 }& g% kacceleration of the skeletal maturation; however, after
5 u/ L& ~2 w* A" {' G8 g3 ^cessation of treatment, the rate of bone maturation* Q7 [; l( v3 h; e! T
decelerates and gradually returns to normal.8,98 v, O  I; Q6 k; l8 i  C
There are conflicting reports and controversy' |9 O7 }" s9 u0 v' {1 q, K
over the effect of early androgen exposure on adult
, L. L1 v& b! x" g) Y; A3 c) l) Apenile length.10,11 Some reports suggest subnormal0 y9 \  e" k+ K( m/ ]  a
adult penile length, apparently because of downreg-% A# y5 }( D% M1 n' e
ulation of androgen receptor number.10,12 However,4 n( i' {7 O4 ^2 J  T" l
Sutherland et al13 did not find a correlation between
: L/ z8 n2 j5 W" w' B7 ^; echildhood testosterone exposure and reduced adult
+ W$ x0 k! K8 {8 V5 G$ hpenile length in clinical studies.
0 L/ v7 f) H( S0 @' ZNonetheless, we do not believe our patient is
! d4 e9 e; U4 u5 W, Ygoing to experience any of the untoward effects from3 _' N( F6 J. K  F  M
testosterone exposure as mentioned earlier because
2 E4 p3 k2 T- [' ~7 {the exposure was not for a prolonged period of time.+ s2 U+ `. }  j! g" r
Although the bone age was advanced at the time of/ I6 p! f2 P  v' t
diagnosis, the child had a normal growth velocity at
  M. `; R( [& W+ u9 x. Qthe follow-up visit. It is hoped that his final adult: }& ]2 s1 M( J: B* C" j
height will not be affected.
. q! P+ N* O- [2 x- D" L0 B: lAlthough rarely reported, the widespread avail-- @5 P1 n! Y: u2 d8 S  M# X
ability of androgen products in our society may
5 K, {/ P( H# X  b! m' y5 Q' Kindeed cause more virilization in male or female+ [) A7 U/ C. x' r
children than one would realize. Exposure to andro-2 X. ~; h/ ~% M: t* [
gen products must be considered and specific ques-4 i$ ^6 p0 S" z, Z/ U
tioning about the use of a testosterone product or
4 z7 U: u  g* P1 ]9 r  K. pgel should be asked of the family members during
: a# L  ~" ]2 d, i4 f* kthe evaluation of any children who present with vir-
/ o: f4 y1 U; X& b% Y6 c; k' E; uilization or peripheral precocious puberty. The diag-
& U9 b0 _9 l1 Q* e* lnosis can be established by just a few tests and by
7 M& @1 U; v$ K7 q" F# Tappropriate history. The inability to obtain such a
3 v$ H- v% e' uhistory, or failure to ask the specific questions, may' z( A$ d) p$ I# R# U+ `* |
result in extensive, unnecessary, and expensive
3 K% I. U% W& I' s' x, e% M) d0 Oinvestigation. The primary care physician should be
' n  \) p8 g+ V; i" Naware of this fact, because most of these children; }4 Y) [8 m- p2 C+ ^% J( i  o
may initially present in their practice. The Physicians’# ]1 a9 D) g/ x. B
Desk Reference and package insert should also put a
/ h, d! ~' V. l% jwarning about the virilizing effect on a male or
8 O7 O" m$ B2 \8 M5 O" I  vfemale child who might come in contact with some-
( P7 s: P# M# I+ m! V& m% {# Kone using any of these products.7 K1 }% X" u: g( A$ {* Y
References, B8 N. Q0 ~, G- V
1. Styne DM. The testes: disorder of sexual differentiation( O' q! O4 p; c. o% h
and puberty in the male. In: Sperling MA, ed. Pediatric; K1 [* T; a; R% O' e7 E) f7 M% U
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
- E/ D( D2 p. g6 g6 n2002: 565-628.+ a! N/ ^: \; W& t' d
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
7 M  g6 e+ b1 }5 r1 [) A2 {puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
. ]* Y! k6 r3 H8 H3 \; EBoy Induced by Indirect Topical, N8 E" b! q! X! e. D$ K
Exposure to Testosterone
$ v/ c/ i: j6 j" W: [Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,27 Y+ a5 N1 n# k- _
and Kenneth R. Rettig, MD1, q: t$ @. B( f' @1 v+ a! q$ f+ T: _( w
Clinical Pediatrics4 n& p7 O2 A- ?, {7 c
Volume 46 Number 68 V" ]" f9 f; K7 F7 F# `* J5 E
July 2007 540-543
; a7 l: A5 y$ u# ]: h- D6 d© 2007 Sage Publications/ n$ l' [+ E: ?# B
10.1177/00099228062966518 ~+ c/ \; h  c, T
http://clp.sagepub.com
; p! {! K$ b( g  \" W& f% K  mhosted at
/ ^/ B$ Y7 ~/ X" @6 }6 E) A- m+ qhttp://online.sagepub.com4 p4 i9 G/ V9 |3 c
Precocious puberty in boys, central or peripheral,5 D4 A0 V9 e: j$ ~+ i/ r8 t. S
is a significant concern for physicians. Central# s* |0 D$ h- A; K6 M+ w4 v
precocious puberty (CPP), which is mediated% `1 ~! Y, i& H7 H! e0 y# c
through the hypothalamic pituitary gonadal axis, has
. Y. i8 L5 j- u4 Ga higher incidence of organic central nervous system
+ v: |/ Y+ k: @4 I* k8 F, Tlesions in boys.1,2 Virilization in boys, as manifested
9 l) d$ c# L" jby enlargement of the penis, development of pubic1 y, o; {' C, R% u: q! j# Z
hair, and facial acne without enlargement of testi-
$ g) `, x5 b2 ~cles, suggests peripheral or pseudopuberty.1-3 We
$ j' ]8 ?2 [" |8 Treport a 16-month-old boy who presented with the
) K- j: K" D* Z2 ~enlargement of the phallus and pubic hair develop-
4 T: W( I: F9 Gment without testicular enlargement, which was due4 j5 }0 L2 F* q- L( a% f  D" A" ~6 Y
to the unintentional exposure to androgen gel used by
& U, R. D, B0 j! R# Q) ?9 T1 Ethe father. The family initially concealed this infor-
9 a( c4 H4 m3 `# F. ~# Z9 omation, resulting in an extensive work-up for this9 L( b4 D% L3 @
child. Given the widespread and easy availability of
; W8 l% Z0 i( O8 W* E( u9 xtestosterone gel and cream, we believe this is proba-
' w1 I/ H* D$ `& Lbly more common than the rare case report in the3 {  B( \2 B. m8 s& C! n
literature.4
2 C) d0 r, f: d& qPatient Report
# J3 N0 F& `% w3 oA 16-month-old white child was referred to the6 m) Y2 M1 i" N7 R/ Q: x* A
endocrine clinic by his pediatrician with the concern8 S6 L- Z, V% R" @' ]9 @* b
of early sexual development. His mother noticed
; \/ d# Z/ ?3 G2 i' I- N, a9 rlight colored pubic hair development when he was
" Z4 {% s( v; r3 q) D* ^From the 1Division of Pediatric Endocrinology, 2University of+ E7 r+ P/ U6 P% W
South Alabama Medical Center, Mobile, Alabama.( A* k3 w4 h; R  ]
Address correspondence to: Samar K. Bhowmick, MD, FACE,
  o7 f8 Z, L. X3 [1 T3 x# BProfessor of Pediatrics, University of South Alabama, College of
! P: y2 o5 w! ?' g$ y& y0 j3 FMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 P' Y* O$ h' L. Z
e-mail: [email protected].
* m8 I# J% m! Mabout 6 to 7 months old, which progressively became' B8 I. k: c' k+ x
darker. She was also concerned about the enlarge-' q3 A1 H. W8 E8 k* L% J$ U/ l( W: b
ment of his penis and frequent erections. The child0 `* r6 W& C. b. ^5 N
was the product of a full-term normal delivery, with
2 {" ^  f- d) A! S% g* fa birth weight of 7 lb 14 oz, and birth length of0 C9 P6 W) A$ e! R7 r! y
20 inches. He was breast-fed throughout the first year0 i! _, D4 |, v# R/ E) L
of life and was still receiving breast milk along with
, Y2 r3 T+ r  Y3 Z% \solid food. He had no hospitalizations or surgery,
' w2 g- G2 A1 Wand his psychosocial and psychomotor development
1 p& e' _! a' z3 j4 J; z: P" V: r3 Uwas age appropriate.
$ O& n5 ?4 H. w, ]4 q$ vThe family history was remarkable for the father,
" ?. [2 m5 ^! K! A1 pwho was diagnosed with hypothyroidism at age 16,9 v. K/ v0 Z- `) K; }. M
which was treated with thyroxine. The father’s6 F8 [% ?* p; G1 D' |; U+ ^
height was 6 feet, and he went through a somewhat
( |/ e! s" {0 k) K( l% m( U- Learly puberty and had stopped growing by age 14.* j$ i3 o5 V6 u
The father denied taking any other medication. The
$ D0 X) K/ Y! n) j6 M5 w2 P' [child’s mother was in good health. Her menarche
# O( V" }* \4 G- @7 Ewas at 11 years of age, and her height was at 5 feet
; V+ e6 r9 }6 M, A" C3 }5 inches. There was no other family history of pre-
$ e+ }0 `) l3 t! Ycocious sexual development in the first-degree rela-, V/ |4 v1 }9 Z4 V( d# X) P
tives. There were no siblings.
/ u% [" r" b$ h! v" e! nPhysical Examination0 G! i5 z4 m2 j4 l! O
The physical examination revealed a very active,
- ?3 [4 l# L$ x7 w1 y" S: ~2 {  }playful, and healthy boy. The vital signs documented
0 n5 b5 t& A5 J: N& `- X  }a blood pressure of 85/50 mm Hg, his length was% B/ ^3 s2 |) j' F# m0 F1 S2 ^& _
90 cm (>97th percentile), and his weight was 14.4 kg
6 j' L9 j! d! q$ y% ](also >97th percentile). The observed yearly growth
: M" {8 g5 i3 a' A( Ovelocity was 30 cm (12 inches). The examination of1 X+ `( T& u5 l  d  c
the neck revealed no thyroid enlargement." A% P3 l( s# m% f
The genitourinary examination was remarkable for1 u" ~+ l" T* s  [! B
enlargement of the penis, with a stretched length of
+ D6 }' |0 }% {8 cm and a width of 2 cm. The glans penis was very well) h: A# \0 S9 g8 c1 D
developed. The pubic hair was Tanner II, mostly around- i+ W' X0 }; V
540
- P: \+ Z: Y$ }" C1 lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 T7 \& c1 ?2 r/ gthe base of the phallus and was dark and curled. The
) Z7 b* B2 h+ G1 ]testicular volume was prepubertal at 2 mL each.
% _; S* Z8 m1 g" qThe skin was moist and smooth and somewhat  ~" a0 v, E5 f2 h
oily. No axillary hair was noted. There were no0 y: z: O8 j7 H4 j+ E! m
abnormal skin pigmentations or café-au-lait spots.
* q+ s1 Z  Q0 ~5 [' ?; a; aNeurologic evaluation showed deep tendon reflex 2+- L9 [* B% W3 }
bilateral and symmetrical. There was no suggestion. B8 ~6 V1 y' R; c
of papilledema.
' z* p" P7 ?. k! oLaboratory Evaluation
3 I6 @  i7 c0 |2 @8 b, hThe bone age was consistent with 28 months by2 B5 C- y, \3 G: A7 ?( c- [2 J
using the standard of Greulich and Pyle at a chrono-3 a- |8 q8 H; R; k
logic age of 16 months (advanced).5 Chromosomal% r; C0 X* w: z* w) V+ v9 m
karyotype was 46XY. The thyroid function test; T+ Q7 j! C. {$ _1 ~5 N: F
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 h2 @3 y! H  }$ K$ N) Olating hormone level was 1.3 µIU/mL (both normal).0 J7 }" ^; `5 h* z. }
The concentrations of serum electrolytes, blood
8 q0 d4 F( j; P5 Y& p- W& U! Durea nitrogen, creatinine, and calcium all were
+ i8 y4 z) L8 T- H' ]7 s7 D* I1 ?within normal range for his age. The concentration
- G$ l1 ^" S$ V6 q, @# H; n9 f7 ?of serum 17-hydroxyprogesterone was 16 ng/dL+ q* M. a/ G6 R5 y' b" M* ?( V& g1 d
(normal, 3 to 90 ng/dL), androstenedione was 20
' D& n0 j4 j# a: V$ m' m. g1 Xng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
. d/ p5 g9 d& q& z6 @7 aterone was 38 ng/dL (normal, 50 to 760 ng/dL),
+ R  B% ^+ a1 R( ~desoxycorticosterone was 4.3 ng/dL (normal, 7 to
  ~2 W4 T; k& H, l; U  m0 f49ng/dL), 11-desoxycortisol (specific compound S)
7 |. g7 ?# ?8 ^5 c) w; g8 Hwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
1 P- G6 p% U* X2 P0 ^tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total( _' r, w6 e" U6 r. _) X- Q8 J
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
; \4 Q$ Y4 B0 s( b* h4 xand β-human chorionic gonadotropin was less than. R' j/ }5 b1 S5 i5 @( C
5 mIU/mL (normal <5 mIU/mL). Serum follicular
' M# d" m. w/ }+ G  hstimulating hormone and leuteinizing hormone! D* Z, A5 A2 U: R0 u, W
concentrations were less than 0.05 mIU/mL
) E9 \$ M' l! `(prepubertal).6 O" X, ]* |5 J4 E2 i
The parents were notified about the laboratory0 A- i" _) L  p9 L
results and were informed that all of the tests were
  s$ D, V/ v5 B  H9 p$ Znormal except the testosterone level was high. The/ o; j, _0 p& V
follow-up visit was arranged within a few weeks to
8 ]- c1 Q  ^2 q( I! yobtain testicular and abdominal sonograms; how-
3 ~9 N% a# u/ s# S( Hever, the family did not return for 4 months., A0 `( A+ h0 o) j6 H: k2 V
Physical examination at this time revealed that the1 B8 W" w/ X6 X6 [& P2 {
child had grown 2.5 cm in 4 months and had gained
; o0 K' F" v$ M% Y2 kg of weight. Physical examination remained* D. H) c# Y( T1 C
unchanged. Surprisingly, the pubic hair almost com-) J2 z- m# g$ m; Q8 ^
pletely disappeared except for a few vellous hairs at
+ n4 c, u; @" A; Sthe base of the phallus. Testicular volume was still 2
7 U2 ]$ D: s' |9 k: E+ emL, and the size of the penis remained unchanged.4 [) M& j7 I" o. o+ s. }1 x
The mother also said that the boy was no longer hav-
9 i- P( R6 A* s; q; m) ging frequent erections.$ P$ e5 b3 U: f
Both parents were again questioned about use of
; c9 }5 ?8 V; \5 uany ointment/creams that they may have applied to8 d8 F5 _4 m" x  M
the child’s skin. This time the father admitted the) M9 D8 P. ?# q7 L. a
Topical Testosterone Exposure / Bhowmick et al 541
/ o  M( j3 f) [5 \$ A3 R8 a1 Muse of testosterone gel twice daily that he was apply-
4 l% p) w% B/ }7 ving over his own shoulders, chest, and back area for3 ^7 p5 _0 c4 h$ e- B
a year. The father also revealed he was embarrassed. K0 C, }+ e9 j- Z0 F. z
to disclose that he was using a testosterone gel pre-8 o' Y5 [& K& C. j
scribed by his family physician for decreased libido
7 F4 u' v& P5 m9 L# H. u. y7 isecondary to depression.
# I: B& m0 X* bThe child slept in the same bed with parents.
) k' U( ^1 o: s6 l  lThe father would hug the baby and hold him on his: T+ n: d1 `3 d! c6 O
chest for a considerable period of time, causing sig-
& t' g$ i! ~1 e/ O& E2 `nificant bare skin contact between baby and father.* `) |- Q' n( f: x+ t. m
The father also admitted that after the phone call,  I( e; N- l' N; S$ i
when he learned the testosterone level in the baby
' N  |% H1 E& D+ U& Vwas high, he then read the product information
5 a# H/ K9 \! s) T( _, A' ?packet and concluded that it was most likely the rea-
! d6 K! }* X: B% d! Uson for the child’s virilization. At that time, they
( ~* E# ?; _+ z. p: _, Ndecided to put the baby in a separate bed, and the
, M0 ~3 B  E! Jfather was not hugging him with bare skin and had
' q3 R! ?: A, i. M3 c2 @+ X. g. w' Dbeen using protective clothing. A repeat testosterone
# T* S2 R- B7 n$ V1 l; }test was ordered, but the family did not go to the
1 e3 b, @# X! c% c* n% L/ Y3 B! ]9 |laboratory to obtain the test.# R3 w  L& F2 _, z
Discussion
' l8 i' J, ^! _8 J2 r6 C& PPrecocious puberty in boys is defined as secondary  I, Y6 Q9 B& f' b& j+ Q( k
sexual development before 9 years of age.1,46 M9 H( |3 F, M6 y( G$ v2 h
Precocious puberty is termed as central (true) when: w8 }2 N& r5 Y$ @% ^! x
it is caused by the premature activation of hypo-
/ p# G/ X$ x* }thalamic pituitary gonadal axis. CPP is more com-
6 U% d$ E) n" j: ~) T& o! m" Fmon in girls than in boys.1,3 Most boys with CPP6 \3 Q) ^) C1 O6 R) l
may have a central nervous system lesion that is9 [) r1 z! n0 ^& `" d" z
responsible for the early activation of the hypothal-5 @5 x! K; h6 S" g( o4 t2 ^
amic pituitary gonadal axis.1-3 Thus, greater empha-% [  h9 a9 w$ r2 F9 i9 |
sis has been given to neuroradiologic imaging in
$ k- ]/ a, v# Y) a; [# r: D' r' pboys with precocious puberty. In addition to viril-& k* t, d5 G# C: R9 f+ S
ization, the clinical hallmark of CPP is the symmet-
( i0 n: s; J! Z$ nrical testicular growth secondary to stimulation by
/ }& V3 U4 `+ `4 f, D( rgonadotropins.1,33 A, e3 T7 W9 w" m) b% r
Gonadotropin-independent peripheral preco-
) }% ~% W  ^7 d% R; q& t7 S! Lcious puberty in boys also results from inappropriate
1 ?- D0 w: ?  u( S3 }androgenic stimulation from either endogenous or+ @3 M) l7 P, b# {( o
exogenous sources, nonpituitary gonadotropin stim-8 ?0 B4 n! j! Y2 B: C
ulation, and rare activating mutations.3 Virilizing( X' b+ W, j0 a2 d; ]- O% O
congenital adrenal hyperplasia producing excessive
2 G( K- \$ z$ F; s% e1 dadrenal androgens is a common cause of precocious
' V. X$ b- R- bpuberty in boys.3,4
2 e: A3 {9 G  a5 B  m0 B9 F& ~2 PThe most common form of congenital adrenal. C- m$ U1 Y# s8 N8 i; L, S
hyperplasia is the 21-hydroxylase enzyme deficiency.$ T3 i3 K0 F5 w
The 11-β hydroxylase deficiency may also result in3 y' k! v: X1 D8 V' u; L( k
excessive adrenal androgen production, and rarely,
1 w& ^8 ]* K+ m; [% T7 ^/ ~* j+ aan adrenal tumor may also cause adrenal androgen2 g. I0 y- m' m% A* B
excess.1,3% v; A6 ]! H5 w: c
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
# p+ d  u! O6 u+ V2 X542 Clinical Pediatrics / Vol. 46, No. 6, July 20076 y9 _$ h/ j6 ?4 ^5 s" |
A unique entity of male-limited gonadotropin-2 b, d. @1 W* [% I% H- A9 D8 X
independent precocious puberty, which is also known; f. c, U, g# D9 N
as testotoxicosis, may cause precocious puberty at a
0 p- ?: k5 A0 x+ y7 ]very young age. The physical findings in these boys
& g! x# X5 f( g8 f$ q# r* T& Jwith this disorder are full pubertal development,# C. t- u  p+ I, h& Y
including bilateral testicular growth, similar to boys
( U7 z, U  j3 ^* Q6 U# uwith CPP. The gonadotropin levels in this disorder
* V) j+ G2 ~2 ]* z( N# h/ Iare suppressed to prepubertal levels and do not show
9 J  R6 j  w4 u  C2 z6 z8 j* spubertal response of gonadotropin after gonadotropin-3 ]6 }) f" ^" {& ^& O3 L, b% t
releasing hormone stimulation. This is a sex-linked+ B' p, W0 X7 N# T& W. W; m
autosomal dominant disorder that affects only6 ]1 E& }$ @, i" y5 A7 n, K
males; therefore, other male members of the family* Q  X3 n& k, Y" A) l! M
may have similar precocious puberty.3  d8 h' a$ `  W0 L- C% \
In our patient, physical examination was incon-
3 N6 i  y* F$ L6 w7 Y! nsistent with true precocious puberty since his testi-
- I- W$ A5 {9 v' P( pcles were prepubertal in size. However, testotoxicosis
, z& T2 j% j: F4 Mwas in the differential diagnosis because his father
% o. e* a" N) M# r  k; dstarted puberty somewhat early, and occasionally," {: [4 g; g& o4 v4 ?% e
testicular enlargement is not that evident in the
9 c$ v2 s+ w* x, n! S  fbeginning of this process.1 In the absence of a neg-+ Y' ~* ~' w% E
ative initial history of androgen exposure, our
1 N8 d0 a3 X5 Y* g+ \biggest concern was virilizing adrenal hyperplasia,
# `$ ^/ n! z1 _# [either 21-hydroxylase deficiency or 11-β hydroxylase
" }% J* P0 q7 L; R$ O# s# Odeficiency. Those diagnoses were excluded by find-
5 Q$ @/ c9 R/ k* ting the normal level of adrenal steroids.: i3 l: }" r( a  E8 d3 B
The diagnosis of exogenous androgens was strongly3 W3 v* t. S4 `$ e. G
suspected in a follow-up visit after 4 months because
: }2 v, y% g5 U3 g/ a0 I/ m3 a2 U8 _9 athe physical examination revealed the complete disap-* k8 c; E$ L! f; [
pearance of pubic hair, normal growth velocity, and0 S) l# {+ e3 [- \) S3 M' d, A: k
decreased erections. The father admitted using a testos-! {  q: d4 J/ C' W; `1 x  Q8 j
terone gel, which he concealed at first visit. He was
1 m7 [, O2 E( v/ @3 f7 ?% Qusing it rather frequently, twice a day. The Physicians’( y+ I9 P& [# w+ |0 Q# p' `
Desk Reference, or package insert of this product, gel or/ H8 Q' `! S1 d* n4 e3 Z, @7 M
cream, cautions about dermal testosterone transfer to
3 w6 a# O. L* T% P$ Kunprotected females through direct skin exposure.. t/ O: ~+ M7 T7 K
Serum testosterone level was found to be 2 times the  G% i' |. ^& {
baseline value in those females who were exposed to
+ c& m! B7 u% F3 z  G) h0 t/ W" veven 15 minutes of direct skin contact with their male7 d& X! r/ l4 Y$ e: A+ a. ^
partners.6 However, when a shirt covered the applica-
: N4 ~5 \# Y4 F0 o% r! L. z: P4 qtion site, this testosterone transfer was prevented.
& I& Q6 |0 \+ G7 aOur patient’s testosterone level was 60 ng/mL,# w! B  j# Z$ Q
which was clearly high. Some studies suggest that
( C% V1 t! u5 o: X, E$ K  X/ ldermal conversion of testosterone to dihydrotestos-7 p* s  v3 T; P2 X: ?% _
terone, which is a more potent metabolite, is more
# U2 l2 O0 W; |1 n) M5 M9 \active in young children exposed to testosterone) r4 n0 J) ?9 z+ ~0 t
exogenously7; however, we did not measure a dihy-: `& k$ P. X' l1 y2 j/ t+ x( F
drotestosterone level in our patient. In addition to
9 u; {) b- J% s4 Q& mvirilization, exposure to exogenous testosterone in
2 D& P3 j& p& ?' Nchildren results in an increase in growth velocity and; `' v$ _  O& ^- t5 b* a
advanced bone age, as seen in our patient.
6 n1 M9 n" ~5 O0 s7 M" r- i2 kThe long-term effect of androgen exposure during. F; M$ O# l7 C- m
early childhood on pubertal development and final
$ w# ^9 e- p# A  k0 f$ xadult height are not fully known and always remain
0 l3 x5 l# ~  G4 na concern. Children treated with short-term testos-( r  u2 g* y- H, t( D. E
terone injection or topical androgen may exhibit some+ T1 s/ Q! e, A2 r. s5 ]+ E* f1 ~
acceleration of the skeletal maturation; however, after4 x% w; `* c& ?. Y* Q# s; \
cessation of treatment, the rate of bone maturation
% B! t2 v7 [* ~6 f$ a& M3 ]* Mdecelerates and gradually returns to normal.8,9
+ d2 v" A& O/ T9 ]1 V" FThere are conflicting reports and controversy  R5 i4 Y4 P3 e/ j
over the effect of early androgen exposure on adult
$ f1 W- d* C9 W) l6 s, p: e4 Hpenile length.10,11 Some reports suggest subnormal
7 f" W3 @, m- @8 |7 l  P8 Eadult penile length, apparently because of downreg-
! `  D) g8 \! M$ Z8 Y% @ulation of androgen receptor number.10,12 However,
0 C+ w. T- ^, @; @/ iSutherland et al13 did not find a correlation between0 T: l$ v% F) y  }6 i
childhood testosterone exposure and reduced adult
& N& k5 W5 b) E1 p4 B' Y* Hpenile length in clinical studies., C+ T& {9 E2 S1 H, P
Nonetheless, we do not believe our patient is
$ ], |5 L5 q: V3 J( B3 G7 B( [going to experience any of the untoward effects from: `) T' c  K3 {; t7 s) r
testosterone exposure as mentioned earlier because1 M4 a/ Q$ m  u9 |$ l6 p. i
the exposure was not for a prolonged period of time.: A# _2 q) N8 }3 R( @' S% C
Although the bone age was advanced at the time of
2 H0 U2 N1 |! F4 Ediagnosis, the child had a normal growth velocity at
% t3 S. }- d- @( ]; K) Jthe follow-up visit. It is hoped that his final adult6 i6 S( S, Q& Q- x. K) W, F
height will not be affected.
$ P: p8 |4 K' g0 ]7 m! DAlthough rarely reported, the widespread avail-
& `" |$ R6 L& ]; @; g5 vability of androgen products in our society may; C$ ?* F0 M7 Z2 u/ x- @0 O6 B
indeed cause more virilization in male or female! K- j% q) c  W$ v3 Q9 m- G' L( ~# c
children than one would realize. Exposure to andro-) N9 H( h% x9 d! \6 q8 {! K
gen products must be considered and specific ques-* n* F2 }7 t" H& T* G" w% C2 ]$ d
tioning about the use of a testosterone product or, g; |: H5 {0 x0 h0 J
gel should be asked of the family members during
5 C1 p4 y- }! M) jthe evaluation of any children who present with vir-
$ `& z, D+ L; d2 r" A* E, Milization or peripheral precocious puberty. The diag-* h  A' C$ ?  y- E2 @- x) b4 q* z
nosis can be established by just a few tests and by
+ r* ~; N0 A! x  R( yappropriate history. The inability to obtain such a
) [# V& y+ t5 Z3 m7 thistory, or failure to ask the specific questions, may9 L. K- T, p0 ~6 E/ {
result in extensive, unnecessary, and expensive9 b! Y; G4 x# _0 Y0 s9 }1 z. j% ]
investigation. The primary care physician should be
; F# \5 \! p, w) M& oaware of this fact, because most of these children
/ Z9 w( ^" B+ |may initially present in their practice. The Physicians’& ^3 H* [( W" z; V' e% [3 s
Desk Reference and package insert should also put a
6 m" R5 t6 x* Rwarning about the virilizing effect on a male or. D( D" G5 A" F6 g+ ]+ R
female child who might come in contact with some-$ E" \' \' H( w7 I0 P5 T
one using any of these products.- G8 t  N* }- J: b. ?: O
References6 M2 n  l9 X6 W! J2 Z: M. J& j% B. ]3 O
1. Styne DM. The testes: disorder of sexual differentiation
$ T$ s/ x# |, X: uand puberty in the male. In: Sperling MA, ed. Pediatric1 v- ]. C) l7 q' k! O9 E3 F
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
# ^# u. V# T- v1 W+ L) V4 t2002: 565-628.( {# G( v$ b9 m6 u
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious9 D6 `2 J, O. {' }
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
# F% c' B+ }+ l# t0 F
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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