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Sexual Precocity in a 16-Month-Old
! g- K# D8 t5 aBoy Induced by Indirect Topical( J. T( k( n' }, d6 o
Exposure to Testosterone7 G" q. O9 j; T9 Z
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ H  r9 O. m- I. eand Kenneth R. Rettig, MD1
$ G# a0 o4 Q8 T" V4 b9 @8 O8 MClinical Pediatrics! b0 d1 u: H" L4 ~! j3 a" w8 q
Volume 46 Number 6
1 J0 r! m" u4 J7 h5 BJuly 2007 540-5433 k' _- I0 k/ Z2 E) O# t7 S4 D
© 2007 Sage Publications$ ^9 I+ A% |: s* ~! y
10.1177/0009922806296651/ K; j  q& a9 ^
http://clp.sagepub.com) H$ r+ @  F- E) Q
hosted at2 K1 U' u/ _- T2 a% ^) m' ~
http://online.sagepub.com/ F( d  ~0 R- ?4 u$ l" K1 T
Precocious puberty in boys, central or peripheral,$ h, l& i  B# A4 @& `4 {6 X4 G! F( f
is a significant concern for physicians. Central- K4 A1 w8 Q0 F
precocious puberty (CPP), which is mediated* h3 g8 {3 G0 j# I
through the hypothalamic pituitary gonadal axis, has
( [* a. o9 P6 ~% ya higher incidence of organic central nervous system0 L4 H6 E2 d7 F: f; w1 c
lesions in boys.1,2 Virilization in boys, as manifested% N' f3 @: f- l" _( D) s
by enlargement of the penis, development of pubic4 v( b# }* M0 J' k: _: R, b/ d
hair, and facial acne without enlargement of testi-  }1 R+ X+ ~7 o$ x
cles, suggests peripheral or pseudopuberty.1-3 We* K1 u9 _/ @3 m! L3 h0 ?
report a 16-month-old boy who presented with the7 N3 J( H2 _! ]  M
enlargement of the phallus and pubic hair develop-
2 Q& X8 \1 ?6 dment without testicular enlargement, which was due+ `  Q3 d+ l6 a# J
to the unintentional exposure to androgen gel used by- u2 }+ j* M# }2 ?6 ]5 {- i
the father. The family initially concealed this infor-% l, u& J6 {' A+ z+ R
mation, resulting in an extensive work-up for this
. b% Q: J7 P( ], m+ w" S* Schild. Given the widespread and easy availability of
9 P" u. m' r# q, n# V% q! vtestosterone gel and cream, we believe this is proba-
" H  o7 Y* H  ^: p( a" L# y6 zbly more common than the rare case report in the
: t9 m* V7 b* x+ \& X2 ^9 W+ zliterature.4
6 u0 Q+ G7 Z$ e; m+ cPatient Report
( Z. [' l4 N8 E; j' DA 16-month-old white child was referred to the
" K; ]5 @. O- b+ G7 ?* {) }endocrine clinic by his pediatrician with the concern8 j; S; n/ O% b& @/ G
of early sexual development. His mother noticed
6 F& }5 f" T) m( slight colored pubic hair development when he was
9 B$ s$ `6 o0 U- s! SFrom the 1Division of Pediatric Endocrinology, 2University of
; F1 f- o- i9 K/ pSouth Alabama Medical Center, Mobile, Alabama.
" T$ {4 M5 ]' r# Q8 P: ?( VAddress correspondence to: Samar K. Bhowmick, MD, FACE,' h& ?& ~0 ]; \4 @. u; V' L5 g: w* ~
Professor of Pediatrics, University of South Alabama, College of
# p6 i6 H: J" `Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
. z0 y4 q0 [4 _0 Z" ee-mail: [email protected]., f: m$ c9 Q: h% y
about 6 to 7 months old, which progressively became1 H2 K2 {6 b. U( c: ?6 P
darker. She was also concerned about the enlarge-% J9 b3 x% S: {6 s4 E
ment of his penis and frequent erections. The child
0 i4 a/ s. E! ]+ Dwas the product of a full-term normal delivery, with
9 `8 i/ `4 c( `+ T" B0 {a birth weight of 7 lb 14 oz, and birth length of
6 O- `9 |) P6 Z! o5 k20 inches. He was breast-fed throughout the first year
& D5 m  V) E5 |0 j6 T- K; ^' {of life and was still receiving breast milk along with
6 Q& ^( W- ]5 k; \8 B4 N" gsolid food. He had no hospitalizations or surgery,
/ n) q& p& L6 q4 @1 o8 iand his psychosocial and psychomotor development
, o" o6 d5 T( c4 z0 }, P; Qwas age appropriate.7 _4 l$ A6 D* V& f2 s/ M3 u/ O
The family history was remarkable for the father,
% o0 @" o- Y5 m: c, N5 A; G- Y( Rwho was diagnosed with hypothyroidism at age 16,: |) _, z$ B1 q3 w& d, J
which was treated with thyroxine. The father’s
# d  a5 I8 E8 Hheight was 6 feet, and he went through a somewhat
. a6 |/ T) ?7 v  Jearly puberty and had stopped growing by age 14.( q) {) R- B/ f
The father denied taking any other medication. The
9 [! c& q! E: g2 Bchild’s mother was in good health. Her menarche
9 t/ j% M2 @% a1 c8 z4 }; d" pwas at 11 years of age, and her height was at 5 feet
$ E0 |# X; K# ^" ^3 m8 d5 inches. There was no other family history of pre-
. i7 u# {) C+ icocious sexual development in the first-degree rela-
0 \& u- O' F* `tives. There were no siblings.2 O* \9 L( R& ?- G
Physical Examination2 H  `) w1 G( Y# U; \5 T+ N& k1 W
The physical examination revealed a very active,/ w1 ]9 O5 z: m
playful, and healthy boy. The vital signs documented
6 R3 p9 L6 E3 T  x; }$ p$ a' Ka blood pressure of 85/50 mm Hg, his length was
" B+ F& W2 Z1 x6 ?' |9 D90 cm (>97th percentile), and his weight was 14.4 kg
+ N$ w7 y5 i( O, I0 k(also >97th percentile). The observed yearly growth
* Y& z7 t' |: e$ ?- Wvelocity was 30 cm (12 inches). The examination of
) ]( r$ {/ o  B2 d# ythe neck revealed no thyroid enlargement.
* a3 D0 B5 M! J9 W7 Z' \! v3 sThe genitourinary examination was remarkable for6 R; n, s# x* U  V2 y7 z* c; D
enlargement of the penis, with a stretched length of, Q, I7 q- n; ?7 B
8 cm and a width of 2 cm. The glans penis was very well0 ^9 ]% o8 L* Y
developed. The pubic hair was Tanner II, mostly around$ \3 b* f$ x# }
540# i. P; v2 S5 v
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from1 l8 I! D+ m( N2 ?' A, U# M, `
the base of the phallus and was dark and curled. The2 R, m$ c2 a' R, b9 X
testicular volume was prepubertal at 2 mL each.3 N  S* u! |. S3 \% W
The skin was moist and smooth and somewhat% X. x7 P1 B9 H! b. O& y
oily. No axillary hair was noted. There were no
. j. G4 S+ T* h4 {& D* C! uabnormal skin pigmentations or café-au-lait spots.
8 M5 l9 ^7 z7 ]# S: x( FNeurologic evaluation showed deep tendon reflex 2+
) i$ ^+ A4 v6 W% m6 h1 Bbilateral and symmetrical. There was no suggestion: t; |9 s% C7 P) d; ~
of papilledema.+ M: J; z; F% B- l+ I: c: q; z
Laboratory Evaluation8 i2 \2 D8 v) S" e5 l
The bone age was consistent with 28 months by
/ _6 H+ U3 `# @+ `: g) Xusing the standard of Greulich and Pyle at a chrono-
" S  e; ^' Z7 o  J' {; plogic age of 16 months (advanced).5 Chromosomal; n) J. F+ a( b% {2 k* ^! C/ P
karyotype was 46XY. The thyroid function test- A$ {* n' e8 \4 i# U
showed a free T4 of 1.69 ng/dL, and thyroid stimu-$ U4 G3 i) Z7 ~+ y7 A
lating hormone level was 1.3 µIU/mL (both normal).3 `9 l; S. x( ]& |7 {- x* B
The concentrations of serum electrolytes, blood% F2 G% ~- H9 f, Z9 [
urea nitrogen, creatinine, and calcium all were
- ~6 U( K$ J! S$ K& V/ R6 gwithin normal range for his age. The concentration: A9 Q4 \; @6 T" f
of serum 17-hydroxyprogesterone was 16 ng/dL
! V5 g/ c6 o* M. }(normal, 3 to 90 ng/dL), androstenedione was 20' ?" }0 o+ i3 u9 x& Z/ e
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
# M: x: I; @2 w# Eterone was 38 ng/dL (normal, 50 to 760 ng/dL),( u# E7 j% o; Z" X, p
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
. r2 u2 l* F$ X- d4 B- l8 k: E) [49ng/dL), 11-desoxycortisol (specific compound S)
4 E# G$ J9 n! h0 C3 ~8 Xwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-% G& M8 U9 J+ _
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
/ C# j2 `1 I4 A/ q3 Utestosterone was 60 ng/dL (normal <3 to 10 ng/dL),, |. C9 H# ]% v4 ?
and β-human chorionic gonadotropin was less than
$ V/ S9 i/ d. X) n5 mIU/mL (normal <5 mIU/mL). Serum follicular1 k/ v% }( P1 w$ c7 [6 J" ?5 c
stimulating hormone and leuteinizing hormone
7 G- N& c! i, ~concentrations were less than 0.05 mIU/mL$ P/ s4 H6 D! ]4 V) K) c% q- _+ V) M
(prepubertal).
, {. O" M! _5 n8 f" hThe parents were notified about the laboratory
7 T: n; V! u! J7 N% gresults and were informed that all of the tests were0 U" D$ D3 u2 r, B6 s6 x" q& i
normal except the testosterone level was high. The
  V) k+ w5 N: `+ P9 ?" n$ b8 }follow-up visit was arranged within a few weeks to1 `& }; l* X+ v
obtain testicular and abdominal sonograms; how-
9 L: c' c7 c" R$ J# Q' g" kever, the family did not return for 4 months.; q* y+ s. P; F% S
Physical examination at this time revealed that the) `# C% [: ?4 L+ x9 Z" ~
child had grown 2.5 cm in 4 months and had gained1 m5 e" k+ E, y
2 kg of weight. Physical examination remained3 e+ p6 y9 F3 i
unchanged. Surprisingly, the pubic hair almost com-
, [# [7 `; l/ K4 ^$ ~- d) B0 m, wpletely disappeared except for a few vellous hairs at
& k: _9 f9 J, `5 E; K8 Nthe base of the phallus. Testicular volume was still 2- e0 B, w! J  ^; H: o
mL, and the size of the penis remained unchanged.
8 X* E0 A. V, j1 |- W$ J( ]The mother also said that the boy was no longer hav-" N2 k& m4 u3 ]- B- R
ing frequent erections.+ h* ~$ J4 p! Q4 `* w
Both parents were again questioned about use of
6 @) _& J2 P1 ~3 E! w) U& J( `any ointment/creams that they may have applied to
! k) Y  x/ N2 K0 H; U) Q& v: q- Tthe child’s skin. This time the father admitted the1 ^9 n8 c. @3 \  [- Y% E( n  R8 z
Topical Testosterone Exposure / Bhowmick et al 541" t9 p& l6 Q7 c4 m
use of testosterone gel twice daily that he was apply-6 P2 H5 E& }2 O% f, C
ing over his own shoulders, chest, and back area for
4 w* Y' J, b4 D* s- i8 ga year. The father also revealed he was embarrassed
$ n$ |  _, D$ P. ?; u9 d& p- Z2 ^to disclose that he was using a testosterone gel pre-4 M1 \" W3 Y# ?. P0 i  u
scribed by his family physician for decreased libido2 {1 W6 i3 P% u6 q$ X: {9 D
secondary to depression.
' e0 N4 |1 e& c/ B- AThe child slept in the same bed with parents.
8 E# A$ L5 e1 H* V1 d0 YThe father would hug the baby and hold him on his
/ e% H! C, t2 g7 {* W) Fchest for a considerable period of time, causing sig-
8 X* @: U+ J) ^+ M0 D0 znificant bare skin contact between baby and father.! [' A& I$ c/ v) i" T8 z
The father also admitted that after the phone call,
/ J9 w$ n- w" ^when he learned the testosterone level in the baby
# F  j* o! [; n+ @3 v2 ~. G2 ^- R" nwas high, he then read the product information
" X, F& O% l, z# v; Q  tpacket and concluded that it was most likely the rea-
: o! ^+ X& m% a, h7 ]3 Sson for the child’s virilization. At that time, they
4 x% J8 Q7 J7 T7 _+ P, [' f' B7 Rdecided to put the baby in a separate bed, and the; A% l% q: F' \3 m; h& g
father was not hugging him with bare skin and had6 y! B# n6 V4 H1 \1 @* z' o& n/ W
been using protective clothing. A repeat testosterone/ A( ^1 T) A2 ?
test was ordered, but the family did not go to the
# |3 x: P$ {6 elaboratory to obtain the test.
7 m/ }0 b7 x+ r% q3 kDiscussion
- O0 K  t4 w8 B! MPrecocious puberty in boys is defined as secondary
) K& j9 @6 K+ @5 j" Bsexual development before 9 years of age.1,4
: B, [/ I% R' q  v! c. }6 DPrecocious puberty is termed as central (true) when
& D& ^' y) ^( e6 t1 G. _it is caused by the premature activation of hypo-
3 N+ W: G5 {: G4 k' K' I1 tthalamic pituitary gonadal axis. CPP is more com-
! m3 j  X6 ~; O# K# a3 t- smon in girls than in boys.1,3 Most boys with CPP
  z0 [2 e9 m0 V" a' [- t1 ?may have a central nervous system lesion that is$ Q' A3 H: W3 x
responsible for the early activation of the hypothal-; f9 [+ e$ R  h) q3 n- U
amic pituitary gonadal axis.1-3 Thus, greater empha-
7 ]) d/ }( g! L: A# fsis has been given to neuroradiologic imaging in
$ i# }- Q4 q/ i+ |0 K' I( Sboys with precocious puberty. In addition to viril-
2 Z( F" q" f* }5 Xization, the clinical hallmark of CPP is the symmet-
; n7 q) g" t6 h' [6 l4 _. Xrical testicular growth secondary to stimulation by
; j3 U4 F( i7 X/ M0 A- @gonadotropins.1,3; b: W; }' b3 o+ Q5 F, t% N% i
Gonadotropin-independent peripheral preco-/ Y; P1 O  D$ H% A
cious puberty in boys also results from inappropriate
5 g# C2 H$ P6 B, d( Z) Qandrogenic stimulation from either endogenous or
* c. N9 i; ?$ E: `9 Qexogenous sources, nonpituitary gonadotropin stim-! Z5 b6 m7 E+ K
ulation, and rare activating mutations.3 Virilizing
5 D+ G, `: R- O$ h, @congenital adrenal hyperplasia producing excessive, ~$ t3 X# a6 G
adrenal androgens is a common cause of precocious
$ D. X' l4 Z: X5 H) apuberty in boys.3,4  Q: S! F8 f. U, j/ g6 w
The most common form of congenital adrenal( {' F- y* b: ^
hyperplasia is the 21-hydroxylase enzyme deficiency.: ]2 B- j* M5 @1 G& G. X
The 11-β hydroxylase deficiency may also result in4 x* Q1 n( h8 e) f4 C  E
excessive adrenal androgen production, and rarely,+ a0 o- `- b4 [1 |& R
an adrenal tumor may also cause adrenal androgen
! o7 c; I4 ]% L" Y( N: c. y6 }excess.1,3  x, t7 k- v# |3 n& s- }5 ^' B' |
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 K  d: F# l" c3 }5 n9 y" a( p542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
( u# o- b6 t" t' M$ i% SA unique entity of male-limited gonadotropin-
  C, F' C3 z0 tindependent precocious puberty, which is also known( p1 z: J: L- N  {+ O. m
as testotoxicosis, may cause precocious puberty at a
: w! l: H) O& i/ b, Dvery young age. The physical findings in these boys; _4 J" O, A/ V  W  t1 n, V
with this disorder are full pubertal development,
) }  g6 y* X6 K. K) m5 [/ L2 @including bilateral testicular growth, similar to boys
) Y* m0 |* ~' V( bwith CPP. The gonadotropin levels in this disorder. C4 ~4 G7 C. \$ v% X4 T0 O
are suppressed to prepubertal levels and do not show  s* Q# @- ^5 d0 b& B2 e
pubertal response of gonadotropin after gonadotropin-/ f7 o/ B8 m2 I: J1 @- x8 w/ u
releasing hormone stimulation. This is a sex-linked% Q( i+ [: {8 r% U# Z) h
autosomal dominant disorder that affects only9 }( L6 }6 Z- l8 B6 y
males; therefore, other male members of the family8 w& a/ P9 J, V& d2 m' ~1 _
may have similar precocious puberty.3* j, h' w3 F9 x; K" I# T8 R
In our patient, physical examination was incon-
8 U( ]3 b# u+ T7 s- W& Usistent with true precocious puberty since his testi-
5 Z* j+ y$ m' b- ?. \0 ~cles were prepubertal in size. However, testotoxicosis
# e# W5 h/ g; h( H: Kwas in the differential diagnosis because his father# b8 Y7 O! I+ a  u; B( A: Y
started puberty somewhat early, and occasionally,. H# k: O  t; m9 Z5 O7 W% Q
testicular enlargement is not that evident in the9 D0 G7 O! L+ s" B9 }
beginning of this process.1 In the absence of a neg-5 ]  U) `4 v  K: v. q( D5 L
ative initial history of androgen exposure, our$ H' ]# I. B( J2 w: @" Z
biggest concern was virilizing adrenal hyperplasia,
% E" k! k/ K+ X2 W& j2 qeither 21-hydroxylase deficiency or 11-β hydroxylase
4 a# h# s7 m3 o) V' [deficiency. Those diagnoses were excluded by find-
) o6 ~, }7 T+ Z/ P9 Jing the normal level of adrenal steroids.
, E) H4 b1 x3 v0 X* QThe diagnosis of exogenous androgens was strongly
, Z# N( d7 p9 |3 |/ m! g* Ususpected in a follow-up visit after 4 months because
% g! A1 G4 d2 V! f* y9 Z; I( Kthe physical examination revealed the complete disap-
8 x: E3 L3 |  S, R3 @' \7 B# ]0 Vpearance of pubic hair, normal growth velocity, and
- C/ U) _# F: o! }7 ^decreased erections. The father admitted using a testos-
. H! H9 V, }7 A( _8 d) m/ @terone gel, which he concealed at first visit. He was5 G0 ]/ V- x+ F- m0 D( J# _
using it rather frequently, twice a day. The Physicians’' R1 W* a8 H8 x6 V. G0 E
Desk Reference, or package insert of this product, gel or
  @7 E4 p0 a) I; Q4 ?cream, cautions about dermal testosterone transfer to  {& d% e  d! m3 u2 w: e% H6 \1 G
unprotected females through direct skin exposure.
+ r* S: M, F$ b& ~. _4 ^# s" KSerum testosterone level was found to be 2 times the
7 L3 U2 X/ c5 w5 |  y$ \baseline value in those females who were exposed to
- a: U$ y% f: o) `  C+ r8 d, Leven 15 minutes of direct skin contact with their male
! _( U! w$ X6 B& F, m  j* O+ i7 zpartners.6 However, when a shirt covered the applica-" r7 W' R. ]7 F3 Y/ v; }9 C
tion site, this testosterone transfer was prevented.
; {  d/ y) A5 \2 e* \3 TOur patient’s testosterone level was 60 ng/mL,- h' f* J6 t  Q) g* y
which was clearly high. Some studies suggest that
8 c* ^: f( c  V$ }% C6 n7 L2 n* ]dermal conversion of testosterone to dihydrotestos-
7 T) j2 B) W7 S8 Y' ~, i1 o) tterone, which is a more potent metabolite, is more- u  {, g& @8 V1 [: ~& `, G5 z- p
active in young children exposed to testosterone
/ ]9 c9 G. R5 W6 W' d# nexogenously7; however, we did not measure a dihy-7 c6 l& g  S/ m7 K$ y
drotestosterone level in our patient. In addition to0 p) q0 c& e, k: Q
virilization, exposure to exogenous testosterone in
0 B  ?" ]5 s8 b0 E% p5 nchildren results in an increase in growth velocity and" w- t# O+ j0 Z1 G. M
advanced bone age, as seen in our patient.
+ t; k! r: _+ S- [9 ]& `8 lThe long-term effect of androgen exposure during
( t/ t& Z9 x; w7 c1 F4 Wearly childhood on pubertal development and final. e* d: M! l% f- o
adult height are not fully known and always remain
% N' A; O# U6 o- Ya concern. Children treated with short-term testos-
8 r, A9 w( o; [( k' Qterone injection or topical androgen may exhibit some
# h5 v8 K8 Z% Q# R( a+ V& Wacceleration of the skeletal maturation; however, after- x; B- f# }; g- J, L
cessation of treatment, the rate of bone maturation# I+ j8 _9 {# v8 c) c
decelerates and gradually returns to normal.8,9. e% v7 T. |- y/ q3 Z4 Q* ~
There are conflicting reports and controversy
0 W3 v- V+ S+ |" V- qover the effect of early androgen exposure on adult" P8 A1 e" G, s" x( Q& p  O( M
penile length.10,11 Some reports suggest subnormal; x$ q9 l3 T0 @) @9 B
adult penile length, apparently because of downreg-5 |  K. N/ U: M* L$ V
ulation of androgen receptor number.10,12 However,
/ X6 c+ X. P1 }$ }# \Sutherland et al13 did not find a correlation between# A6 G! N, B# g+ N0 K, ~' J) I. {
childhood testosterone exposure and reduced adult
  W. I* P" D9 ^+ k2 r) S; B2 npenile length in clinical studies.
# r/ {+ o% |' x* GNonetheless, we do not believe our patient is8 U1 |3 a) X! {% O2 k! f0 }& D9 Y
going to experience any of the untoward effects from; K, b, r0 Y2 i7 G' H- d5 E1 g& y
testosterone exposure as mentioned earlier because
7 L( c0 L# w1 ~% }$ Ethe exposure was not for a prolonged period of time.6 d! V3 S5 X" r/ t3 X
Although the bone age was advanced at the time of
2 e$ p$ _* a5 @- N2 g; l* Ldiagnosis, the child had a normal growth velocity at
9 i- d! D  C4 zthe follow-up visit. It is hoped that his final adult
1 e) a  H8 f2 dheight will not be affected.
. k0 G7 N0 ?9 I, n- R# w1 WAlthough rarely reported, the widespread avail-9 M- ~  ]& V* ^- E3 h+ S
ability of androgen products in our society may1 {! F3 \" t: E% F: ]1 x6 N* N
indeed cause more virilization in male or female' \( O: h, [# t5 C
children than one would realize. Exposure to andro-
! X9 _" @) Q' R- Ogen products must be considered and specific ques-
& y4 {1 n$ X$ N/ \1 q9 |* s* t! Itioning about the use of a testosterone product or
& Q" y" ]0 j0 l: M7 b6 fgel should be asked of the family members during
* R* D% ?. S# L- N7 z3 {9 Pthe evaluation of any children who present with vir-
! a9 x( E/ z) [1 y9 r* d* ^ilization or peripheral precocious puberty. The diag-+ o& x0 D5 W. b8 N. \. C' N
nosis can be established by just a few tests and by
' E( n; M, c: @6 e0 ?$ qappropriate history. The inability to obtain such a
* m6 ]& F; O5 s: _8 Nhistory, or failure to ask the specific questions, may; ]: h2 O- ^' b3 h
result in extensive, unnecessary, and expensive$ R0 e0 x- y) c! m) v& `# d* P5 }
investigation. The primary care physician should be
* t# b* Y& K4 L7 \, N1 h3 Aaware of this fact, because most of these children2 W1 ^- _9 g2 r, j! @7 `8 I& [
may initially present in their practice. The Physicians’
' K9 h3 L7 R' {; SDesk Reference and package insert should also put a6 Z8 I+ i3 E7 `, K, z' X
warning about the virilizing effect on a male or4 }2 W, G- O7 L' @
female child who might come in contact with some-. t# Z% k* h$ r
one using any of these products.
- W0 ~8 H9 b( i& {' m' o7 ]References  J" g" j4 v/ c( r
1. Styne DM. The testes: disorder of sexual differentiation5 {! g0 F. ]6 O
and puberty in the male. In: Sperling MA, ed. Pediatric
) I! @5 \  I( n1 ~" A7 `3 L+ TEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;1 A6 E3 a$ Z3 i3 n
2002: 565-628.
" c) Y9 l) y5 S; a1 [9 J* f( {2 n2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious( X! m) P) @, f4 U
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old2 l9 a" L$ D. h4 _6 I- i. Q; R( I& L
Boy Induced by Indirect Topical  Q2 Y- \/ [2 b( e
Exposure to Testosterone
8 z' J  e) {- Z6 C% iSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2! H4 h! N$ D  v2 E$ |
and Kenneth R. Rettig, MD1
& W$ [/ @/ p) C/ P0 y% m, ^Clinical Pediatrics
- L3 }3 X4 E) G8 a* rVolume 46 Number 6* |( t- M& s) I7 {* f
July 2007 540-5436 w2 Q& s: G9 J: g3 m* s
© 2007 Sage Publications
( @5 e/ Z! J. A* i8 m$ {" I10.1177/0009922806296651
) x+ Y' `5 D- `$ c: Q4 G" e; Jhttp://clp.sagepub.com
8 o7 T, N4 t( z8 m8 Y, U  X2 ?hosted at5 u/ j9 i" ?8 M" ^( D9 \
http://online.sagepub.com9 ]  Q% ?: |2 N3 |8 d  c
Precocious puberty in boys, central or peripheral,! C% U# ]; b4 O% P& V
is a significant concern for physicians. Central
! B! v( {$ K. h4 H# Xprecocious puberty (CPP), which is mediated
7 {8 G' y& N! l3 t+ t8 \  hthrough the hypothalamic pituitary gonadal axis, has
  x+ e, ?/ H- Sa higher incidence of organic central nervous system
# v9 T7 R3 m: s* `: A- V8 I/ S: Q& elesions in boys.1,2 Virilization in boys, as manifested# A7 I; A- l2 [
by enlargement of the penis, development of pubic5 V1 S/ }. o5 W9 j
hair, and facial acne without enlargement of testi-1 W' N. ?5 P: U' B2 c& H
cles, suggests peripheral or pseudopuberty.1-3 We
* l) M$ R- p6 X# b" O% I  p3 h$ |# Oreport a 16-month-old boy who presented with the! D' w8 q) E# y& @& E
enlargement of the phallus and pubic hair develop-' l+ _; s& m4 ^' _% x  \: _+ x, e
ment without testicular enlargement, which was due
2 [6 Y; }) Q6 Z4 b' \to the unintentional exposure to androgen gel used by
& u. P; W7 {7 c; Vthe father. The family initially concealed this infor-3 `+ g- q- m5 q2 d
mation, resulting in an extensive work-up for this
4 P2 v9 v1 J" r6 t- \; Dchild. Given the widespread and easy availability of
& i% M0 n; k4 l8 _2 htestosterone gel and cream, we believe this is proba-
# X  y$ }0 h0 J0 X# y: A# gbly more common than the rare case report in the4 p9 ?- z9 ^8 p5 C
literature.4( n! X* _; j7 k& q- M+ |8 |
Patient Report
0 R- P: d) Y1 O9 RA 16-month-old white child was referred to the/ f: g5 b: {) Y
endocrine clinic by his pediatrician with the concern
' m1 T/ F' s# [3 hof early sexual development. His mother noticed
0 L6 d7 `/ J  l. a* r3 _# clight colored pubic hair development when he was
8 j% d2 Z' i% L4 @/ e- eFrom the 1Division of Pediatric Endocrinology, 2University of
6 @. Y1 ]) X7 sSouth Alabama Medical Center, Mobile, Alabama.
5 f% k9 @" {* |3 qAddress correspondence to: Samar K. Bhowmick, MD, FACE,' m& s% p% B: l! [* }4 K; P. ^
Professor of Pediatrics, University of South Alabama, College of
1 X; k1 S+ y  b$ t, `$ E& \Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
) s: z7 ?( A) y5 ?" |- m7 ge-mail: [email protected].
/ a4 h& s9 C+ l* p" s' _6 h% Habout 6 to 7 months old, which progressively became
6 d* T4 N$ V' O* y3 o: f  ?. Q, Edarker. She was also concerned about the enlarge-8 e8 X' `4 X0 A
ment of his penis and frequent erections. The child6 S* y+ G; w# O  u9 L, u# O
was the product of a full-term normal delivery, with5 r; z4 x2 K5 i- r+ l1 E+ g4 S6 {2 H
a birth weight of 7 lb 14 oz, and birth length of% g4 L7 L' G; ]
20 inches. He was breast-fed throughout the first year
% ]6 ?5 V) K+ i; d8 Z- nof life and was still receiving breast milk along with4 U; J( U7 r! c% M: k$ ]4 B- y
solid food. He had no hospitalizations or surgery,2 \* j* `0 O$ Q# K% X' S* {/ H
and his psychosocial and psychomotor development! |+ `2 A; S9 ?. ~2 K3 I3 o
was age appropriate.) V$ f' z- Z# \- W
The family history was remarkable for the father,
9 t) m5 }4 I8 i- `2 T2 A5 vwho was diagnosed with hypothyroidism at age 16,. t: r* o' Z- L
which was treated with thyroxine. The father’s# _, H& Y2 S# c4 k# L5 T; S! T
height was 6 feet, and he went through a somewhat
3 o( O7 M* d+ ?1 g9 \# y! t5 ~; ~early puberty and had stopped growing by age 14.' P% b, d: u% _: H" \( Q
The father denied taking any other medication. The* ?6 k. {' e( I/ \) x# x9 F
child’s mother was in good health. Her menarche
: i  y3 Y! H% ]( U. kwas at 11 years of age, and her height was at 5 feet
9 N+ A8 @0 Y& ?; J+ C: j5 E5 inches. There was no other family history of pre-& o- q. e8 Q" k& M/ V- }+ G9 v7 h) Q
cocious sexual development in the first-degree rela-
- {. O, e2 R5 mtives. There were no siblings.6 R. M  c" z$ c# r( S& r! w) }* @" }& L
Physical Examination
4 p3 R3 r" o% m: GThe physical examination revealed a very active,$ q9 r& |* O6 p$ _5 r
playful, and healthy boy. The vital signs documented
  L. f5 F/ l# z" G4 G0 Pa blood pressure of 85/50 mm Hg, his length was
5 s, G! c1 I% J% |; ]/ z1 g90 cm (>97th percentile), and his weight was 14.4 kg: x! G! }% k9 K" n
(also >97th percentile). The observed yearly growth
3 h3 ?2 t0 ~! V  Nvelocity was 30 cm (12 inches). The examination of, X$ I" I9 s# S/ L2 g
the neck revealed no thyroid enlargement.
8 S0 X( j. x3 ?  }" n+ E6 DThe genitourinary examination was remarkable for
  _1 F- y3 r: e# E9 Y" f3 k% Ienlargement of the penis, with a stretched length of. N6 w: C+ g* \0 a: A
8 cm and a width of 2 cm. The glans penis was very well9 J; N; W. l9 _- v1 u
developed. The pubic hair was Tanner II, mostly around, _' B/ l$ Z) E
540
5 I0 X) G% R  [1 N% \( i1 b9 z. xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from0 D. q9 x' f7 y& F, P1 i
the base of the phallus and was dark and curled. The% H8 F2 [: f6 ^
testicular volume was prepubertal at 2 mL each.
4 Q* N2 m. ]$ m# AThe skin was moist and smooth and somewhat6 E7 v! ?# U  l) w( s
oily. No axillary hair was noted. There were no, P; x! U* T' O% L+ W; U, I
abnormal skin pigmentations or café-au-lait spots.
$ Q$ e) q7 I+ Z; d. A8 _) Y1 i3 }Neurologic evaluation showed deep tendon reflex 2+% }# k' [6 O  S* @1 |
bilateral and symmetrical. There was no suggestion
( j6 {* J( w8 E  m4 `' Zof papilledema.
! p5 _9 W& s4 t' pLaboratory Evaluation/ l$ t' n+ i; L5 K1 e& [6 [* n6 }
The bone age was consistent with 28 months by
5 R& `6 \+ _+ Ausing the standard of Greulich and Pyle at a chrono-
: R& s: e" x9 Z9 {$ W9 }6 T0 o, ologic age of 16 months (advanced).5 Chromosomal/ L2 m+ @+ N* ^+ i9 n6 o( k( c: D  L
karyotype was 46XY. The thyroid function test5 H8 R. c$ W0 Y. G' w8 g4 L1 a; ]
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
( N  t" `0 n5 x3 K0 |, E+ Tlating hormone level was 1.3 µIU/mL (both normal).; [* q0 W9 @: x+ d5 o7 Q8 `3 J/ x& m% e
The concentrations of serum electrolytes, blood7 z! [0 J0 t" U; i: g( w
urea nitrogen, creatinine, and calcium all were
" q8 p' g2 r8 Swithin normal range for his age. The concentration. M% V- t0 R0 b% @
of serum 17-hydroxyprogesterone was 16 ng/dL8 J& T( M! n" H, ]% x
(normal, 3 to 90 ng/dL), androstenedione was 20
, }0 l8 B& v- y. l  ^/ X7 ?ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
$ g3 `; o3 Z' e- V7 v5 p% c: vterone was 38 ng/dL (normal, 50 to 760 ng/dL),
9 }$ z) R( P; a& u$ fdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
) ]0 Z: e) W1 {! F" m0 ?49ng/dL), 11-desoxycortisol (specific compound S)
1 j7 {0 q! d7 b4 w: Z5 W5 _was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
4 V" {$ g- h( a# V  A# p* T  Otisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total4 x- y1 L2 ~5 x- C
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),, ]4 L& @7 Q0 I5 t& g4 |$ T
and β-human chorionic gonadotropin was less than# U! ?6 z! ~, V+ y( g+ {$ G/ Q
5 mIU/mL (normal <5 mIU/mL). Serum follicular( i8 w2 Q) @( ]
stimulating hormone and leuteinizing hormone+ g" h% Z0 c4 P* J4 S
concentrations were less than 0.05 mIU/mL
3 T; q' u+ X" N% z* P; d8 M(prepubertal).9 G& a9 j" Q9 `. T+ v
The parents were notified about the laboratory, e6 B, {* |1 [* h5 W$ ]/ x
results and were informed that all of the tests were% d  K; b+ |$ l- \2 C% P
normal except the testosterone level was high. The% p6 S* x+ E7 h( R3 t
follow-up visit was arranged within a few weeks to
) E1 V' |, C( ^' n. Y- Zobtain testicular and abdominal sonograms; how-
7 o8 z( p  L( P: }ever, the family did not return for 4 months.+ y6 G3 x1 m/ l7 L3 `
Physical examination at this time revealed that the
# W' [! M$ R# u0 L! D  L" rchild had grown 2.5 cm in 4 months and had gained- P2 m/ e6 x) H0 D0 ?" d, a1 h+ y9 ?
2 kg of weight. Physical examination remained; \9 g# b% v; M5 C# \# C' T
unchanged. Surprisingly, the pubic hair almost com-
" n+ X. b- N$ y: H7 vpletely disappeared except for a few vellous hairs at
2 ^$ @7 A$ M/ |the base of the phallus. Testicular volume was still 2$ B5 J- `1 l* D9 e; b
mL, and the size of the penis remained unchanged.. ]1 F2 a4 i! j/ ^1 a
The mother also said that the boy was no longer hav-" {/ I8 v5 \* v6 ~3 e9 `3 L
ing frequent erections.2 C4 E! W0 h; R+ i% Q1 m& ~
Both parents were again questioned about use of
# o; u7 J, Z* N9 A' x+ g6 Xany ointment/creams that they may have applied to
& f% [# P7 S. [the child’s skin. This time the father admitted the6 q; x  o& T' ^- u
Topical Testosterone Exposure / Bhowmick et al 541
' m8 r% T9 V. A( K+ @use of testosterone gel twice daily that he was apply-
! M5 `* t3 \6 V7 u) a1 s/ Cing over his own shoulders, chest, and back area for
( ~1 U+ Y5 C8 w- Q% l. Y% i" i0 La year. The father also revealed he was embarrassed
; ~3 D' T  F  J% C/ k3 x* ~to disclose that he was using a testosterone gel pre-; s& e$ x- p9 F
scribed by his family physician for decreased libido
: H6 H! |7 D$ \3 M4 jsecondary to depression.- Q; Q, W% @! I& u% K
The child slept in the same bed with parents.
$ x! L5 T) S/ m$ q3 hThe father would hug the baby and hold him on his4 ~& j- g9 k+ y. V
chest for a considerable period of time, causing sig-; V  R5 m6 K- N) y( m
nificant bare skin contact between baby and father.) C0 ]6 ^! G8 Z
The father also admitted that after the phone call,: R+ f- P* D4 A' X) D. O$ z9 G
when he learned the testosterone level in the baby
- [6 o8 g8 r/ ?4 Xwas high, he then read the product information
9 q8 e' ~1 B0 N3 }5 B, Rpacket and concluded that it was most likely the rea-, y) W( ?0 ]' M# O2 F3 E  J4 [
son for the child’s virilization. At that time, they
2 n0 P- {! u. ^decided to put the baby in a separate bed, and the# v9 w) h6 |9 D7 y+ e& D
father was not hugging him with bare skin and had4 L: c5 V  `: d( n
been using protective clothing. A repeat testosterone
! e/ O. U- Z% Btest was ordered, but the family did not go to the
# P7 O" m; A( D. f) {! {# _0 n+ S7 claboratory to obtain the test.9 D$ T, p- d6 Q* F; m( a
Discussion
, H3 m9 d, [, r9 H- N2 f5 RPrecocious puberty in boys is defined as secondary2 |' N8 m- M, P9 `3 z4 g
sexual development before 9 years of age.1,4
4 @) S% A0 s% c$ IPrecocious puberty is termed as central (true) when$ u8 l& B; O0 Y
it is caused by the premature activation of hypo-6 w! z5 P) a/ ^$ w1 O2 L6 {6 x5 O
thalamic pituitary gonadal axis. CPP is more com-8 r1 h' W8 f1 Z" F' G, w+ d1 X% y
mon in girls than in boys.1,3 Most boys with CPP3 B. w: X1 b2 e/ c! B) z
may have a central nervous system lesion that is+ P" }" V9 G) C3 A9 d
responsible for the early activation of the hypothal-
0 ~  q, h( N. H$ P, O! Famic pituitary gonadal axis.1-3 Thus, greater empha-
8 @9 ~. ], y# M" B' asis has been given to neuroradiologic imaging in
8 e0 w4 a6 c) K% r0 Oboys with precocious puberty. In addition to viril-, S/ h- E( ~6 `% s- Y7 y) K
ization, the clinical hallmark of CPP is the symmet-
, f3 B7 h+ `$ m% L4 J% hrical testicular growth secondary to stimulation by
1 L0 |4 Q* ~! a5 Agonadotropins.1,3
0 H0 u. n( q/ m( b# tGonadotropin-independent peripheral preco-' C$ G8 S: b% W' J5 n' k
cious puberty in boys also results from inappropriate$ j$ _  D' E: k5 r5 N& T
androgenic stimulation from either endogenous or
8 a5 P' E8 ]3 X1 E  M" cexogenous sources, nonpituitary gonadotropin stim-! b- q! l/ O3 n" \1 E
ulation, and rare activating mutations.3 Virilizing7 g( e) S6 l6 b
congenital adrenal hyperplasia producing excessive, B3 F! m+ A5 C; I: ^1 k! S! x
adrenal androgens is a common cause of precocious
2 F6 e1 P1 k8 v5 ^# ^) ~$ Opuberty in boys.3,4
: s' L# N5 ^0 X+ n  H$ Z8 uThe most common form of congenital adrenal
+ e0 ~; V! R1 l) jhyperplasia is the 21-hydroxylase enzyme deficiency.
9 U  Q2 S, q' k3 n% W' fThe 11-β hydroxylase deficiency may also result in6 `/ _3 {) R; N# e! P
excessive adrenal androgen production, and rarely,
' m. W) ]- i& \6 J, I; I( j! R$ Xan adrenal tumor may also cause adrenal androgen: e/ X( M" C( j& P& s- D
excess.1,3
' x0 D" L) Y; Q4 B8 tat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 B8 w4 [- ]2 H3 X/ Z$ @8 N542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
8 t$ y$ m: x6 j, M+ C: {# I+ OA unique entity of male-limited gonadotropin-
5 c) B  Y9 C* Y3 q8 d& E* ]8 bindependent precocious puberty, which is also known
7 R; E' K/ O: f) H  uas testotoxicosis, may cause precocious puberty at a0 Y4 ?2 K, m% Y5 Y' t! {$ W
very young age. The physical findings in these boys( U; W( w/ ~( Q0 m
with this disorder are full pubertal development,
8 D: f5 H- G  E; Z" ?2 qincluding bilateral testicular growth, similar to boys# j1 b' u& q" i6 B
with CPP. The gonadotropin levels in this disorder
$ Q  w6 {9 o. ?8 T3 Yare suppressed to prepubertal levels and do not show7 f! M4 l% `6 @$ W$ M! r
pubertal response of gonadotropin after gonadotropin-% k  R9 r$ c  |9 S# A
releasing hormone stimulation. This is a sex-linked! C8 g% k$ R$ A- U# t6 [) `' b) v
autosomal dominant disorder that affects only/ d  _) C; H) _9 }
males; therefore, other male members of the family2 \4 N$ y# _: G8 z6 i4 `4 L
may have similar precocious puberty.3+ F) ?( V$ ^! [
In our patient, physical examination was incon-! i7 y4 O' F' }5 x  v/ M- J- c
sistent with true precocious puberty since his testi-
' Z4 S: V  R- W) m* t! W5 ccles were prepubertal in size. However, testotoxicosis1 Y: V9 t) U; j6 `* g
was in the differential diagnosis because his father
" ~* H3 W6 f4 Bstarted puberty somewhat early, and occasionally,
* p. a3 P# `% j- D, Btesticular enlargement is not that evident in the" F( G6 i' a6 {! f" I! d; |* T8 M1 G5 `
beginning of this process.1 In the absence of a neg-5 k4 D2 P" g" N* L, m
ative initial history of androgen exposure, our
3 p! q8 O; s4 ~$ `% I# S& n0 n6 Abiggest concern was virilizing adrenal hyperplasia,7 B4 m% y/ y4 }' V; r
either 21-hydroxylase deficiency or 11-β hydroxylase
, j( P* _' u5 b8 c+ l' j, mdeficiency. Those diagnoses were excluded by find-
" Y1 U0 y4 Q& E$ Hing the normal level of adrenal steroids.. Y0 w4 w4 \6 Z) W  u
The diagnosis of exogenous androgens was strongly
9 R) z1 b! ?' e- \- t2 ^- J+ lsuspected in a follow-up visit after 4 months because8 a5 S7 i* @; l6 L
the physical examination revealed the complete disap-
+ z. b/ b* Y( l8 y8 {/ }* n, epearance of pubic hair, normal growth velocity, and3 U2 c) \4 c4 K/ \, Q
decreased erections. The father admitted using a testos-
6 I4 E0 k3 p0 ?2 Mterone gel, which he concealed at first visit. He was& |8 f, `( c7 o) x; \6 z
using it rather frequently, twice a day. The Physicians’
7 |8 d. A& g/ ?- {9 T* mDesk Reference, or package insert of this product, gel or4 s/ n+ l( J0 A3 l$ Z! v
cream, cautions about dermal testosterone transfer to+ {  c8 n1 a  A
unprotected females through direct skin exposure." u% d: _7 \4 @* M  Y$ C
Serum testosterone level was found to be 2 times the8 o2 v3 b/ W6 ^% ^9 G
baseline value in those females who were exposed to; G: x& `: O/ O$ j3 K' U2 ^1 j- |, d
even 15 minutes of direct skin contact with their male' \- Z4 r. w2 P4 A
partners.6 However, when a shirt covered the applica-; I/ F( u5 W) \0 Q
tion site, this testosterone transfer was prevented.
/ d8 e- }/ N: R% e* t: oOur patient’s testosterone level was 60 ng/mL,
7 o$ C+ I% F5 `( Swhich was clearly high. Some studies suggest that% a3 M# D( k& t+ ~; @
dermal conversion of testosterone to dihydrotestos-
9 N$ |; ]+ x. ^) oterone, which is a more potent metabolite, is more" d5 s# z! T7 r( {! y; M
active in young children exposed to testosterone
# [1 Y" J( @4 [3 }exogenously7; however, we did not measure a dihy-7 f7 Z4 d% f. n
drotestosterone level in our patient. In addition to1 l- l% {$ G$ _5 f
virilization, exposure to exogenous testosterone in
2 K5 X- L9 B# ~- H" n" ^" Achildren results in an increase in growth velocity and/ {9 ]0 ?4 ?; ?# [
advanced bone age, as seen in our patient.9 _% Y  p( ^1 t
The long-term effect of androgen exposure during+ Y% D2 B7 p+ m( d) X) a
early childhood on pubertal development and final
$ g7 M) a( `) Y5 ~" a6 _! W: p- \# padult height are not fully known and always remain: n3 d7 k: H+ I/ Y* _# m8 Z
a concern. Children treated with short-term testos-
: h, D) ^5 x( E& t4 s: G7 S: Zterone injection or topical androgen may exhibit some3 ?$ \4 t: y& X
acceleration of the skeletal maturation; however, after
' i( {: O. B( x% f' ?cessation of treatment, the rate of bone maturation' S9 D) r7 a; k& h# `
decelerates and gradually returns to normal.8,9) |+ f) h- K2 m
There are conflicting reports and controversy5 K  e8 s; R2 a" O0 H) u9 x% o1 h& E
over the effect of early androgen exposure on adult
# }4 T5 b3 |( g. F) \* p' W) t  Xpenile length.10,11 Some reports suggest subnormal/ S& l" w0 Y6 y2 S" w* s
adult penile length, apparently because of downreg-5 \2 U# W7 c, z$ J: n- G; `: X
ulation of androgen receptor number.10,12 However,
  F( j& B8 S$ Y5 k" ~Sutherland et al13 did not find a correlation between: b9 c! _+ S8 Z+ m2 g/ h7 D+ n
childhood testosterone exposure and reduced adult
( E4 i1 ?* w. N0 Dpenile length in clinical studies.
" e! |( q7 V* j7 O/ b8 y: ^Nonetheless, we do not believe our patient is
2 J' A8 i' {6 r" K# bgoing to experience any of the untoward effects from
. h: b8 n$ S/ g' F5 q) J9 e! Otestosterone exposure as mentioned earlier because& D3 D8 W/ e3 g, Z* N0 g
the exposure was not for a prolonged period of time./ S4 v$ Q) `. ~9 U
Although the bone age was advanced at the time of
6 W$ W+ ?6 J* y4 P  F; Z9 adiagnosis, the child had a normal growth velocity at
/ s; D; b4 Q3 i. f8 Qthe follow-up visit. It is hoped that his final adult/ w7 a1 V$ Y) Y: |
height will not be affected.. d# o! x( [& \8 F
Although rarely reported, the widespread avail-
5 l; |" W- U* `. ?! z, G. h7 tability of androgen products in our society may8 `- e9 Y6 v5 h2 w. X
indeed cause more virilization in male or female
4 H3 Q& P: B" u6 J3 m4 i7 |! ychildren than one would realize. Exposure to andro-
# A8 b. X) o4 _& P/ Ngen products must be considered and specific ques-
' O, r/ X) }* V7 u# K% E4 y2 gtioning about the use of a testosterone product or: a) i0 Q2 h- ~: L
gel should be asked of the family members during
2 P8 k* l& F$ [, ?2 Vthe evaluation of any children who present with vir-, p+ h3 O# `- \6 Z0 q: ~
ilization or peripheral precocious puberty. The diag-
! O5 s! T0 U/ q! J% ^- l/ Gnosis can be established by just a few tests and by
3 Y( b' `8 v: p) ~6 v; p" _appropriate history. The inability to obtain such a
" |# [( b0 I4 V4 h: B- |history, or failure to ask the specific questions, may
3 v% |" h( y' \) w( N$ h, e- O( nresult in extensive, unnecessary, and expensive1 n1 R# z. K0 Y$ v; R$ X' v
investigation. The primary care physician should be
, `7 k; u& ]# w% ?aware of this fact, because most of these children! E8 u" j! r" K: u. h
may initially present in their practice. The Physicians’
2 q3 M; x' L0 V0 a) J. E9 Y( CDesk Reference and package insert should also put a
* y6 U. L9 ^3 a( H7 ]warning about the virilizing effect on a male or$ u$ q( C) M) I* X' j+ f
female child who might come in contact with some-
( M) _0 t2 ]  m3 N* I5 |one using any of these products.& V: i8 V% N( L  X# ]8 v
References
) q1 Q0 E# K2 g8 {9 t7 |1. Styne DM. The testes: disorder of sexual differentiation" @1 s7 }/ u# i* A) U- g
and puberty in the male. In: Sperling MA, ed. Pediatric5 H2 [* w9 F/ f
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;. m8 c8 i, X& O; t" d
2002: 565-628.
: |& f& P( ]) j1 e2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 Q; l% @/ T( z. ]0 P/ W: c8 upuberty in children with tumours of the suprasellar pineal
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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
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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
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
& u4 m, w/ ]0 n% o
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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