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Sexual Precocity in a 16-Month-Old
* J- d; G  A# y6 S5 W' J/ w" b3 b5 Z3 wBoy Induced by Indirect Topical
$ p' I0 \9 D1 h8 _$ h  KExposure to Testosterone
6 K+ I/ p  s0 f0 i" s5 n! MSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
' b2 i& ?, S: M; ^' |and Kenneth R. Rettig, MD1" |0 L( U, S; r/ b0 K8 N- O7 @8 G
Clinical Pediatrics7 R' P2 S, x2 f# d
Volume 46 Number 6) T* \/ K; h/ I
July 2007 540-543
- N/ e  t) k9 ^2 R5 f, q/ D7 ?( p© 2007 Sage Publications7 u+ E1 }- K# |8 v
10.1177/0009922806296651- P1 G$ A/ b7 O6 s" U% U5 K& Z4 A7 m
http://clp.sagepub.com
3 A) o- c, p8 Z* W* Khosted at- W+ |8 `8 @. L  c9 a$ }, h4 \
http://online.sagepub.com
. M9 s8 ~( S7 O; M  m) TPrecocious puberty in boys, central or peripheral,0 ~" B( N! y1 D) s' K3 G0 j: _" u
is a significant concern for physicians. Central
2 r- j, d; j: a/ z: S  Wprecocious puberty (CPP), which is mediated
, c/ k. R2 H6 K, v5 {- ithrough the hypothalamic pituitary gonadal axis, has
5 ?3 E5 v8 B3 p( J8 m9 W/ ~a higher incidence of organic central nervous system
4 W5 p5 x& H0 _* t! ulesions in boys.1,2 Virilization in boys, as manifested
! e( a2 u9 O( rby enlargement of the penis, development of pubic
" j0 R5 l0 r& Vhair, and facial acne without enlargement of testi-5 |8 H1 I) B6 i8 P/ X+ C
cles, suggests peripheral or pseudopuberty.1-3 We/ J( `: g5 w5 r$ d9 F6 o
report a 16-month-old boy who presented with the
! u  x8 `) k! v/ a+ Z5 Jenlargement of the phallus and pubic hair develop-7 z8 x; {8 H  f
ment without testicular enlargement, which was due6 L% v" d9 d; V0 w; T/ \
to the unintentional exposure to androgen gel used by
8 d6 t3 z; t8 wthe father. The family initially concealed this infor-- a, g, z5 g4 X
mation, resulting in an extensive work-up for this
4 F8 `; U2 p: U$ q* Xchild. Given the widespread and easy availability of3 Y2 e& Y" C( Y4 V  n
testosterone gel and cream, we believe this is proba-
7 F3 @4 c0 `4 n+ W( N% ]# dbly more common than the rare case report in the2 J& x0 a& M& J
literature.4. k$ E5 s% G, q/ B+ K" E
Patient Report
/ I) k% s8 Z! i4 IA 16-month-old white child was referred to the# `) W* Z8 z% Q, n" a
endocrine clinic by his pediatrician with the concern! T9 V! F. _* U$ \: `8 I5 O
of early sexual development. His mother noticed( B  ~1 x4 Q3 k9 M& }8 v
light colored pubic hair development when he was  P' G8 q' s- ]( O
From the 1Division of Pediatric Endocrinology, 2University of
3 G( i" e; A" t6 i& w9 u6 WSouth Alabama Medical Center, Mobile, Alabama.) p0 I1 u# r) V. l' m
Address correspondence to: Samar K. Bhowmick, MD, FACE,3 w! r; t1 B: c
Professor of Pediatrics, University of South Alabama, College of
' s) v( _9 K! d& e# {Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;* j/ z% ~9 W' a
e-mail: [email protected].
% j. L" H$ @: I: v! ]* B$ T. Kabout 6 to 7 months old, which progressively became
; Z  s" P" P: D. s1 j- v, ~darker. She was also concerned about the enlarge-
8 F5 Z* s1 O1 c2 |: y2 Q  nment of his penis and frequent erections. The child7 m- ]7 c6 w$ O' y, i& t
was the product of a full-term normal delivery, with
! Z* x5 r. z& a% w6 |a birth weight of 7 lb 14 oz, and birth length of
8 f9 R* N) W& n. Q20 inches. He was breast-fed throughout the first year
' Z/ C3 _: d( _1 ~of life and was still receiving breast milk along with
+ B+ H7 }2 s4 H! Rsolid food. He had no hospitalizations or surgery,9 s- W# z# J* C, f* @( F6 k5 H
and his psychosocial and psychomotor development; u3 G9 O  L0 D$ t
was age appropriate.
4 }+ p( X1 h6 D* rThe family history was remarkable for the father,
" _4 K' n' Q" d0 m% `1 X! _- Awho was diagnosed with hypothyroidism at age 16,
( F7 E$ O3 G* o7 m2 S9 _6 N! Z9 Kwhich was treated with thyroxine. The father’s* `0 g1 s9 [1 A
height was 6 feet, and he went through a somewhat
2 P1 c- x+ f+ m- b+ eearly puberty and had stopped growing by age 14.
/ j  X' H& G& E. U8 N, ~4 E. @, RThe father denied taking any other medication. The+ ]6 n& u5 k& D7 u% x# K5 h) u
child’s mother was in good health. Her menarche
. C) g3 u& f6 hwas at 11 years of age, and her height was at 5 feet
) }4 c- L( k. w$ T/ K5 inches. There was no other family history of pre-
2 W) s; h# N1 H+ O2 y- h# mcocious sexual development in the first-degree rela-0 o5 e( P* {: z3 ~1 J: V5 P
tives. There were no siblings.# r% U+ j3 o. X- W$ V8 u
Physical Examination5 Z. n# y7 n$ W2 d2 q9 q
The physical examination revealed a very active,
8 ~+ _. E% P9 q- V8 m' mplayful, and healthy boy. The vital signs documented8 @  ~$ V" w0 {& b6 j$ T
a blood pressure of 85/50 mm Hg, his length was
& L  H8 w' Q7 L2 \1 W90 cm (>97th percentile), and his weight was 14.4 kg
4 e( I& ^0 I9 m# A# N/ f(also >97th percentile). The observed yearly growth) W; @: O1 b# Q
velocity was 30 cm (12 inches). The examination of. G+ G& d" v  H1 `
the neck revealed no thyroid enlargement.
5 C3 w8 e- a7 l$ h% eThe genitourinary examination was remarkable for6 T- Q  S( f" `( \
enlargement of the penis, with a stretched length of
3 \! G' u" C- v2 `8 cm and a width of 2 cm. The glans penis was very well
6 |8 d1 e* l" X* Z, ]. z0 r" pdeveloped. The pubic hair was Tanner II, mostly around
% [* G1 j0 L. y( y5 c540
+ r+ m3 `# z7 f! ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; {0 \$ C: v0 D; Ethe base of the phallus and was dark and curled. The
5 C  S# j1 _' d3 H/ v) {0 I" Ztesticular volume was prepubertal at 2 mL each.- Q2 s1 }$ s9 t# \4 i3 E
The skin was moist and smooth and somewhat; ?. y. k9 }8 G' q  y! b' f
oily. No axillary hair was noted. There were no/ ~# _8 i+ }! f0 z# f$ w) d
abnormal skin pigmentations or café-au-lait spots.! S9 \  r" ~4 ]8 M& a
Neurologic evaluation showed deep tendon reflex 2+
% d# a# ]' a) @bilateral and symmetrical. There was no suggestion& p1 @6 Z6 |+ H; ^) R7 T
of papilledema.
- w, W" j- [3 S# ~2 }8 E$ tLaboratory Evaluation
3 y: a( c5 i( F0 }  aThe bone age was consistent with 28 months by# {* Q: g$ [: U( n( ^$ Q
using the standard of Greulich and Pyle at a chrono-
! P: Y7 U" Z6 v6 N  a$ i% v+ O+ L8 Elogic age of 16 months (advanced).5 Chromosomal- o! P; l5 n7 e1 X% v; X! Q# n, y! a
karyotype was 46XY. The thyroid function test
4 f9 m6 m% }4 n6 p8 X% s2 a6 W  cshowed a free T4 of 1.69 ng/dL, and thyroid stimu-! r" p: Q3 K, D2 u" \" O
lating hormone level was 1.3 µIU/mL (both normal).
$ y) g1 b; L  S; B$ a! _4 n3 aThe concentrations of serum electrolytes, blood: N4 X3 s! Y, k/ r* c: @6 ^
urea nitrogen, creatinine, and calcium all were
2 c* u. s6 h- D2 v% m- lwithin normal range for his age. The concentration+ q. ^; t% P& W% p( a9 K
of serum 17-hydroxyprogesterone was 16 ng/dL  J( u7 K# j: v% [
(normal, 3 to 90 ng/dL), androstenedione was 20
% f( B  S4 f8 I$ f4 sng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! Z) f) L0 t; Y6 Lterone was 38 ng/dL (normal, 50 to 760 ng/dL),1 @5 {1 S' V2 Z/ l2 g
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 [  g: e0 z( o8 S  w+ \: j7 q49ng/dL), 11-desoxycortisol (specific compound S); G! z8 n" J4 x. W
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-6 v% l) H. X9 w
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# I: f6 x# Q$ x8 X3 }- s* b
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
6 {0 h% l8 \2 N* R& i  Mand β-human chorionic gonadotropin was less than
! `) I; t( _3 h+ R2 J! w/ Y) ^1 ^6 H5 mIU/mL (normal <5 mIU/mL). Serum follicular, h% m( ~( @8 @7 y1 K0 {+ H) C
stimulating hormone and leuteinizing hormone
- P' l9 L* `+ i- i0 w( P8 zconcentrations were less than 0.05 mIU/mL2 a: }$ k) ]4 W. G( G; ]! b9 @
(prepubertal).
: |) E8 G( f: B  j8 K5 i( KThe parents were notified about the laboratory
! R, r9 u+ O' f; ~+ Q+ t+ d3 N8 @results and were informed that all of the tests were( u" E6 D: G3 \/ A3 B- Y* `
normal except the testosterone level was high. The
( x2 `# z  k5 P6 Z* Tfollow-up visit was arranged within a few weeks to3 W2 H' \1 F% h2 M
obtain testicular and abdominal sonograms; how-0 {1 b6 B: \0 w( `
ever, the family did not return for 4 months./ l; L! A# K: c; E5 @4 N! `
Physical examination at this time revealed that the3 a5 I- M: `1 I8 Y0 ^9 x3 O( H
child had grown 2.5 cm in 4 months and had gained
- ?, i4 r9 v% z/ Y& Q2 kg of weight. Physical examination remained
; k. s( t: R) X. S4 H% Iunchanged. Surprisingly, the pubic hair almost com-; O1 Y; y( P, Q$ c
pletely disappeared except for a few vellous hairs at0 y- e' U/ k; g1 j8 N6 X7 _7 c
the base of the phallus. Testicular volume was still 2
1 ~! I8 h$ B. S7 F% q5 KmL, and the size of the penis remained unchanged.
1 N% e+ \8 f$ ?. \The mother also said that the boy was no longer hav-: R* a. f5 P7 A" [3 X
ing frequent erections., J$ R5 P7 u3 x: S" Q
Both parents were again questioned about use of0 ?+ j& p! ^4 n/ \6 I
any ointment/creams that they may have applied to' V. i) n( ~& @4 ^2 M0 @5 n2 m
the child’s skin. This time the father admitted the
; N6 q& h5 V( c8 JTopical Testosterone Exposure / Bhowmick et al 541" c/ c4 z% l2 w7 h8 U4 n, j+ N
use of testosterone gel twice daily that he was apply-) D0 Z3 v$ [6 N* |5 {
ing over his own shoulders, chest, and back area for/ O7 q: r: h: g( K% N
a year. The father also revealed he was embarrassed
* Q6 `, \9 m" S# e9 _1 l6 _4 mto disclose that he was using a testosterone gel pre-; k/ u$ [. f& ?# g5 j7 g
scribed by his family physician for decreased libido
. A1 `% c6 }7 ^secondary to depression.
8 j+ K7 f  E5 Q/ {6 yThe child slept in the same bed with parents.
- G! l1 ^* A" {  G+ CThe father would hug the baby and hold him on his
+ Q1 [# g+ `* z8 \chest for a considerable period of time, causing sig-
0 T- M- q% N  K5 [nificant bare skin contact between baby and father.
- F# Y2 W% V# T' a7 ZThe father also admitted that after the phone call,
! ?* Z% \1 u3 G" z2 P, W8 ?5 Twhen he learned the testosterone level in the baby9 c. J; `4 N6 y0 S$ V2 h" ^
was high, he then read the product information
: d  d1 E4 B( b* h* `! c! @( }packet and concluded that it was most likely the rea-
  D8 G- ]& [* k7 oson for the child’s virilization. At that time, they4 }7 o  o& ~; j% @8 s
decided to put the baby in a separate bed, and the
1 Y9 _! X4 ^9 r( e7 qfather was not hugging him with bare skin and had( n% t8 x$ y" G3 ]
been using protective clothing. A repeat testosterone
; h6 Z2 g% a% i# L( T, B+ j) Dtest was ordered, but the family did not go to the
; \+ [0 l, a' D1 _laboratory to obtain the test.5 @5 b# P6 u$ ?- }3 e4 L
Discussion* H( @6 P7 W8 B+ ^
Precocious puberty in boys is defined as secondary7 P( q1 F/ [' I" U5 p
sexual development before 9 years of age.1,4( N1 ~, M. c  q" Z4 x
Precocious puberty is termed as central (true) when
. F0 d! F) k9 }# yit is caused by the premature activation of hypo-- R! U0 R0 }  R- N) ^% D* U
thalamic pituitary gonadal axis. CPP is more com-, Q( D9 B; Y" `! V* ~
mon in girls than in boys.1,3 Most boys with CPP) J' V& Q3 t. h. m! A
may have a central nervous system lesion that is
: m, W. o. z9 H. vresponsible for the early activation of the hypothal-  X3 s# ]: u) C3 ]0 z; S
amic pituitary gonadal axis.1-3 Thus, greater empha-4 H2 M/ W+ V, B/ l( r! I
sis has been given to neuroradiologic imaging in" q8 W# ^# Q2 b3 F1 u
boys with precocious puberty. In addition to viril-. n) `$ l; E: {+ s
ization, the clinical hallmark of CPP is the symmet-1 f& i# u9 U7 M" [/ \/ p9 |. E
rical testicular growth secondary to stimulation by! Y2 ^+ o3 K% r4 E7 R6 h+ H2 F4 D
gonadotropins.1,3
) H  j8 c4 C' U: Y% C( ZGonadotropin-independent peripheral preco-# z% `) Y, Y$ o8 t! z# E+ w
cious puberty in boys also results from inappropriate
6 [/ I8 j3 N6 J) a1 h# X" Fandrogenic stimulation from either endogenous or
- V/ `9 |7 ]2 F: x2 e0 a, eexogenous sources, nonpituitary gonadotropin stim-
* |/ T/ V/ V3 z) \+ [: oulation, and rare activating mutations.3 Virilizing" D3 Y! `1 F6 p
congenital adrenal hyperplasia producing excessive' U& p3 t: |' i6 D6 ^/ M6 K" h. N- p
adrenal androgens is a common cause of precocious
# v; _9 f. b. H( G8 b. fpuberty in boys.3,4
  o5 ]: f; i" r8 c. }. @' Z1 U6 f! EThe most common form of congenital adrenal
8 j3 R4 j% G& |; L) p' |hyperplasia is the 21-hydroxylase enzyme deficiency.0 L: [) W9 ]' P' q
The 11-β hydroxylase deficiency may also result in
. e  n, v2 S2 Q, S2 ~( g& t/ [excessive adrenal androgen production, and rarely,0 ^# p6 i% L; B: z6 u
an adrenal tumor may also cause adrenal androgen
& D% K; r( E9 g* K: P4 F/ rexcess.1,3" E% O. Z; d% U8 j6 n
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& z9 Y  D$ g. h% x9 ?$ l, D
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
: D' g2 L( |7 `A unique entity of male-limited gonadotropin-
/ s# L: k5 X9 h: O7 Kindependent precocious puberty, which is also known
- a' i! I4 P" s: f/ Mas testotoxicosis, may cause precocious puberty at a3 V5 R# o. M; Q$ j4 K% X# `7 }2 |
very young age. The physical findings in these boys) @5 K3 f! \, B: w1 O) S
with this disorder are full pubertal development,
. M5 f# n$ l1 }  p# }7 H/ i7 f! @including bilateral testicular growth, similar to boys; g3 Z! p, I* O" U( g7 N1 n2 @
with CPP. The gonadotropin levels in this disorder- J7 {, T2 U% Z" t
are suppressed to prepubertal levels and do not show
: u) h. B/ s! ?pubertal response of gonadotropin after gonadotropin-5 C) C4 h8 ?5 N' Y8 t. Q7 l9 E
releasing hormone stimulation. This is a sex-linked
$ J; L. ^2 q6 ?% ^  \0 |autosomal dominant disorder that affects only, w) r2 g4 P' g7 K
males; therefore, other male members of the family
- U( ~* f8 }; qmay have similar precocious puberty.3$ s( [; F' }. F0 l0 E  {+ t+ ?: N
In our patient, physical examination was incon-
) o" Z# f) w, P  h8 N) d* ~# zsistent with true precocious puberty since his testi-
5 s; Y0 {2 Y  Y; M6 Vcles were prepubertal in size. However, testotoxicosis& U4 M/ L3 D0 ~
was in the differential diagnosis because his father3 m5 i. y7 }4 O1 M2 D% |+ w0 N; }
started puberty somewhat early, and occasionally,$ H. n9 E0 _; ^* V' b5 d
testicular enlargement is not that evident in the
9 e* Y/ `: Q5 Z- |beginning of this process.1 In the absence of a neg-. l' O& a' v+ A7 z
ative initial history of androgen exposure, our0 G* P, ]. k" c
biggest concern was virilizing adrenal hyperplasia,9 T- V! q9 y% Y9 X3 V+ c
either 21-hydroxylase deficiency or 11-β hydroxylase& G% t2 z  ~8 ~/ M
deficiency. Those diagnoses were excluded by find-) |  \+ h3 m) C; k" i
ing the normal level of adrenal steroids.
3 N( b* R. s! O' X, t0 p" H: u( pThe diagnosis of exogenous androgens was strongly
/ m( e  D0 a+ u, T2 [9 R4 B% b2 p# qsuspected in a follow-up visit after 4 months because! \" _2 W% Z6 w. j$ `. ^
the physical examination revealed the complete disap-
* S- Z# e- W  g9 apearance of pubic hair, normal growth velocity, and: ]4 x) J; [+ G! ^8 q% c, p, g% ~
decreased erections. The father admitted using a testos-
4 h- D5 }, |3 c0 Q4 bterone gel, which he concealed at first visit. He was! y4 X3 B+ ~3 H1 ^: n
using it rather frequently, twice a day. The Physicians’
) R) J! v/ f" i# w7 |9 pDesk Reference, or package insert of this product, gel or: X9 @4 _$ c8 K; D5 u! N4 B
cream, cautions about dermal testosterone transfer to
7 c: _' _5 z) S# Z7 _" k! Dunprotected females through direct skin exposure.
# i" K. }/ z( r9 |9 c5 ^; ISerum testosterone level was found to be 2 times the! N& b- F8 `' z9 O
baseline value in those females who were exposed to+ [( p2 U+ R- f
even 15 minutes of direct skin contact with their male
  A8 _3 C: E2 X- tpartners.6 However, when a shirt covered the applica-
; f. c- W( Q8 Y' o2 b9 _- Ation site, this testosterone transfer was prevented.
7 \7 Q- ]+ [* D/ w" _Our patient’s testosterone level was 60 ng/mL,
; _7 v- R1 t: G' h7 Iwhich was clearly high. Some studies suggest that
0 w! S7 H: \; C( X) i, h* [dermal conversion of testosterone to dihydrotestos-/ T( R3 I# w/ a
terone, which is a more potent metabolite, is more; W0 h2 L/ T0 a6 j$ @3 w
active in young children exposed to testosterone0 p! z- l* N$ k# Z. O+ s
exogenously7; however, we did not measure a dihy-
& i/ m7 ]/ I6 Q0 {' e# ldrotestosterone level in our patient. In addition to
/ E# j6 b& u3 t1 E$ vvirilization, exposure to exogenous testosterone in0 h3 C1 H% y) b$ x7 N
children results in an increase in growth velocity and
& M  }3 [, l. G/ A$ aadvanced bone age, as seen in our patient.  |( }. Z/ _, p0 e
The long-term effect of androgen exposure during
: @- v1 `5 `( Y3 s7 h1 P* bearly childhood on pubertal development and final( U) ?4 x& [# M- @4 \& u9 X% u# o
adult height are not fully known and always remain
- ^( f* R" [9 p6 e; Y  O& ga concern. Children treated with short-term testos-. z/ X$ x9 b) K0 m* z: I9 f" a
terone injection or topical androgen may exhibit some0 l) G6 \" {; G' e9 w) A
acceleration of the skeletal maturation; however, after
7 t, a" l5 n, ]9 i! p3 I" s' jcessation of treatment, the rate of bone maturation
* o% d  L" y( Rdecelerates and gradually returns to normal.8,9
3 Y7 v+ j  J5 T& A1 v7 n9 AThere are conflicting reports and controversy
+ r' H. O$ F& c# r7 \% c# D7 _: Nover the effect of early androgen exposure on adult  _8 w" N/ s& R3 T5 ]8 ^0 g
penile length.10,11 Some reports suggest subnormal/ T' p! u5 Q8 [( ~% S
adult penile length, apparently because of downreg-8 [' v7 h/ K4 s) V2 b8 `3 L
ulation of androgen receptor number.10,12 However,. [/ Q# N8 r$ l' C: o0 B; k  c
Sutherland et al13 did not find a correlation between/ g9 L/ J+ z2 f+ b( g3 [4 @
childhood testosterone exposure and reduced adult
2 k* n+ E% N0 K8 H* T& F  Zpenile length in clinical studies.0 p3 A- ^4 K; \
Nonetheless, we do not believe our patient is4 a8 v9 M/ E1 J, o1 }8 h
going to experience any of the untoward effects from' V5 A7 ^; U8 q  r4 R, T* _" K
testosterone exposure as mentioned earlier because
, v2 u4 Q9 n" U8 pthe exposure was not for a prolonged period of time.6 s. @# z4 g+ x* y2 V
Although the bone age was advanced at the time of. w1 |* P" H$ \& h0 w# |
diagnosis, the child had a normal growth velocity at
% a, B, Q1 a0 {  Fthe follow-up visit. It is hoped that his final adult- N1 d, C/ ?/ a( ?! X% _2 u
height will not be affected.1 T0 a" k* J: J8 u8 Q. o9 g8 s
Although rarely reported, the widespread avail-
, }. ^" o! K0 c! I; Q1 a/ L4 r  @. mability of androgen products in our society may
: L. j% \' r, sindeed cause more virilization in male or female
& I# _8 m0 o0 t3 F  |% i' zchildren than one would realize. Exposure to andro-4 R/ E6 J3 I2 u8 q) \3 L
gen products must be considered and specific ques-
2 @; s& X6 m& R. [* xtioning about the use of a testosterone product or$ d+ L: G5 s8 P$ A% N. |
gel should be asked of the family members during1 I0 V1 U, F+ _& }$ d
the evaluation of any children who present with vir-
: N3 Q8 u1 I. eilization or peripheral precocious puberty. The diag-
4 N5 s8 _$ h- r2 dnosis can be established by just a few tests and by; q' a7 J" y/ v5 ]% z. @
appropriate history. The inability to obtain such a
6 v4 j7 h& d& {3 a7 g5 rhistory, or failure to ask the specific questions, may! ]! A4 Z1 T. ~' x0 z; W
result in extensive, unnecessary, and expensive  G) K7 z/ `$ T" s+ K7 d4 d5 m
investigation. The primary care physician should be: o! v; X, n; [, V# y7 x- O4 E
aware of this fact, because most of these children5 l* Y' G- c' p4 G# r& K
may initially present in their practice. The Physicians’
- l) A/ o; L/ ?+ ~! R  }0 o) x3 Q  xDesk Reference and package insert should also put a% s. l  [/ U" g$ q, j3 C
warning about the virilizing effect on a male or1 [6 F" X2 ^, J0 v( Y" Y" z, w* y
female child who might come in contact with some-- O$ W; i% ~/ Z% R9 I/ |
one using any of these products.; Q( i  y; w. ~2 U9 L; P; L
References
/ `' t+ n& K+ V4 U- R1. Styne DM. The testes: disorder of sexual differentiation2 r% K( L- f8 W* I6 Q- j5 V* e3 d, q
and puberty in the male. In: Sperling MA, ed. Pediatric
/ ^' i! j& M* M9 v- o) EEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" H) q2 j) E: v: X, ~( L# X: f" K0 [2002: 565-628.. W: h$ b2 n- P( j8 Z' ]
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
* Y+ h7 y) G, M; K( W! j# }7 opuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old: ?# o! n. B% G+ r
Boy Induced by Indirect Topical, Q! B# S" g9 u
Exposure to Testosterone
- b4 }! v" |( \% NSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,22 b2 p  F' r4 p; W( d& w- z- G. m  y
and Kenneth R. Rettig, MD1& K# m! j" E+ s& P. ^% C9 E: G. i" O
Clinical Pediatrics
  m6 D, \. H8 K7 z0 E3 dVolume 46 Number 67 G' R7 }" m9 o
July 2007 540-543
9 O" b, m# G0 T: W7 {© 2007 Sage Publications( l* X7 n/ [0 v
10.1177/0009922806296651
1 ^9 j5 g* c: w& I/ R1 B( v0 ?: Fhttp://clp.sagepub.com6 V( G/ F" X' d5 E
hosted at
6 ^& |1 n2 ~  V: s4 Z, Thttp://online.sagepub.com# }+ w# X5 P& |; r
Precocious puberty in boys, central or peripheral,3 R" @0 N4 p1 Z) `) e+ v7 j
is a significant concern for physicians. Central
# R( u- {3 u% j6 cprecocious puberty (CPP), which is mediated
$ ?0 i/ j/ \' a( F" q: bthrough the hypothalamic pituitary gonadal axis, has
: W% T8 T' y) z. t; ^1 L* o1 A0 |8 xa higher incidence of organic central nervous system
1 ]5 g& q" [& i# l, glesions in boys.1,2 Virilization in boys, as manifested# ]- {7 r4 D$ G6 B, {
by enlargement of the penis, development of pubic: `8 l7 j3 C/ I" p: C! B: g. K, V( Z
hair, and facial acne without enlargement of testi-! H/ D( x1 ?9 J; _/ q$ _* B
cles, suggests peripheral or pseudopuberty.1-3 We
, J8 B* P$ Z- s5 Z* B/ V( Rreport a 16-month-old boy who presented with the
  x# j6 y4 }  V4 t! Y& P6 \  ^enlargement of the phallus and pubic hair develop-& g& N1 O0 }" ^
ment without testicular enlargement, which was due! [, ^! J6 o" p' N
to the unintentional exposure to androgen gel used by
+ @! S2 b6 c5 K$ h! E& gthe father. The family initially concealed this infor-. |% i, q! u1 Z9 \
mation, resulting in an extensive work-up for this& V  Q9 p& c: S( n4 j5 D
child. Given the widespread and easy availability of
$ d% P+ }+ [8 Z3 t; V2 K' _testosterone gel and cream, we believe this is proba-2 _- ]0 A2 K) ^3 Z1 ~5 J
bly more common than the rare case report in the" {( o$ d3 S! ]7 a
literature.4, m8 u9 O$ A7 C
Patient Report5 j3 @$ L2 b9 X$ ?3 U
A 16-month-old white child was referred to the
' a' X) t$ q8 I8 ~* s  X. Jendocrine clinic by his pediatrician with the concern- g% n* t- U. O4 v
of early sexual development. His mother noticed% Q, j1 n# w$ F8 ?+ \$ A
light colored pubic hair development when he was
; `( d- x) U+ z) eFrom the 1Division of Pediatric Endocrinology, 2University of) A, V+ S5 j  ?8 V" g  d$ x0 Z
South Alabama Medical Center, Mobile, Alabama.
# r' C# o' T. @Address correspondence to: Samar K. Bhowmick, MD, FACE,6 o+ b+ R: w* \
Professor of Pediatrics, University of South Alabama, College of2 i; l, w' |6 s* A# ?; ^+ s
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" |5 t- G( s$ F- n# {6 {4 l
e-mail: [email protected].
2 N! Z( z2 y8 z! j1 n- cabout 6 to 7 months old, which progressively became
" L) _: [5 [$ y) m* N4 O$ q9 p# wdarker. She was also concerned about the enlarge-/ T$ M7 X( |1 c# ^
ment of his penis and frequent erections. The child3 C# I, S; N0 b) I+ m
was the product of a full-term normal delivery, with9 K. B. H, F( K5 ?0 v  Y
a birth weight of 7 lb 14 oz, and birth length of) c% I' I+ E& X2 l4 \
20 inches. He was breast-fed throughout the first year
! F+ ]3 y1 T# s- F+ ?( {of life and was still receiving breast milk along with; A& }; v5 b/ G) n3 {6 w
solid food. He had no hospitalizations or surgery,
2 y0 ]% k1 R: Tand his psychosocial and psychomotor development& {/ i6 b# D( K+ V7 E2 Y
was age appropriate.
/ D4 O: N) V7 e- w3 v7 T1 wThe family history was remarkable for the father,
" Y+ _0 J, n! `# r& f+ xwho was diagnosed with hypothyroidism at age 16,* x  O+ ]1 t& k; C
which was treated with thyroxine. The father’s3 g! `' S* a! n8 X: ?" g9 q
height was 6 feet, and he went through a somewhat4 W6 _4 b% B% U+ m( S
early puberty and had stopped growing by age 14.
8 _9 a3 K) C$ E7 v2 I) G& PThe father denied taking any other medication. The1 R/ \7 x8 b  @5 m& H3 ^
child’s mother was in good health. Her menarche
$ l) q  Z0 l0 L2 N2 C+ vwas at 11 years of age, and her height was at 5 feet2 j! h9 U  d4 q6 z) k
5 inches. There was no other family history of pre-
8 A% O# q7 `$ O; o& \* tcocious sexual development in the first-degree rela-: q. X0 l; I* y2 p8 O1 Y
tives. There were no siblings.4 J4 \& Q9 W0 ~0 S8 k$ d$ q% X
Physical Examination
' q9 o0 n  [! z6 I4 T4 c: \The physical examination revealed a very active,
9 U; a" K; `! X: ?! ?$ kplayful, and healthy boy. The vital signs documented* k( [: G# X9 @: Y% ~
a blood pressure of 85/50 mm Hg, his length was
1 J) o' Y7 ]! n90 cm (>97th percentile), and his weight was 14.4 kg
2 U  K# j: g8 Z& v! `# L3 w(also >97th percentile). The observed yearly growth
. T# q& X" A& k0 i8 K( hvelocity was 30 cm (12 inches). The examination of+ ^5 {$ l/ `! \0 ~+ C
the neck revealed no thyroid enlargement.4 P$ l! n. U9 B! X, o. p+ K
The genitourinary examination was remarkable for
; _$ M/ Q+ `! Q* m2 r- }enlargement of the penis, with a stretched length of
( F- Z1 Q" l. d: c: k8 cm and a width of 2 cm. The glans penis was very well" S# q* ], i- K; |/ M5 p
developed. The pubic hair was Tanner II, mostly around
. {9 H/ [/ s, e: x9 _( E; x+ S4 y540
9 I. w  w. ?. o: R2 o; k0 Bat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from7 X) B/ o' K1 [# N1 h; o/ r
the base of the phallus and was dark and curled. The/ q' W3 V$ a* p' N7 i" P6 z
testicular volume was prepubertal at 2 mL each.4 i; O# @# H4 O
The skin was moist and smooth and somewhat
, G1 s8 b3 z0 M: g, Uoily. No axillary hair was noted. There were no. f; l% k7 q. o2 c8 M! h/ I: }
abnormal skin pigmentations or café-au-lait spots.
$ j7 \9 A' S4 }. z# sNeurologic evaluation showed deep tendon reflex 2+2 ]0 X% e& o6 |; n8 }* T
bilateral and symmetrical. There was no suggestion; _; _: {7 {2 c, O/ @
of papilledema., l  V7 ?% C: |8 X
Laboratory Evaluation
7 A+ X+ t. g$ U" U0 y# B8 ]* i/ eThe bone age was consistent with 28 months by
! w8 I0 f$ s' t4 |7 p1 xusing the standard of Greulich and Pyle at a chrono-
  w' O( J0 ~3 e# vlogic age of 16 months (advanced).5 Chromosomal
3 ]1 ?. J, v$ S9 i1 f; r) akaryotype was 46XY. The thyroid function test
5 j; H* J9 V8 [$ n8 [% I! U+ t; D3 qshowed a free T4 of 1.69 ng/dL, and thyroid stimu-, ]/ d  |& @/ F6 `% ^7 K
lating hormone level was 1.3 µIU/mL (both normal).5 s9 I2 u4 ^; w, D
The concentrations of serum electrolytes, blood# k9 m/ x8 G) v4 l
urea nitrogen, creatinine, and calcium all were
5 s, n$ ?' X! H* b' Cwithin normal range for his age. The concentration$ h6 X$ j8 C% u( N* Q8 m" v
of serum 17-hydroxyprogesterone was 16 ng/dL
% w( j& _$ P+ ]2 h2 s) y  C5 n(normal, 3 to 90 ng/dL), androstenedione was 20% U8 {( o  h9 F
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
8 I" c& I7 @/ z# t: z3 Rterone was 38 ng/dL (normal, 50 to 760 ng/dL),1 W0 ?; z$ A) q' {9 L
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 s( G+ J# S' m! V' w- n* w49ng/dL), 11-desoxycortisol (specific compound S)
5 A- ]% o: L- b) Owas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& i3 \2 h- g. X7 K/ {; r. vtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 r  W4 ?0 p- T5 X" X( {8 {: s6 gtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),3 o: h  H& C0 k* |6 ]
and β-human chorionic gonadotropin was less than9 R: ?$ J3 M: V- a0 X/ h7 V
5 mIU/mL (normal <5 mIU/mL). Serum follicular3 p3 C; h$ S/ s( n$ Y
stimulating hormone and leuteinizing hormone
) r7 O( E1 E/ C% Y7 J' f  sconcentrations were less than 0.05 mIU/mL, @; M, ^: M& _2 ]; d- y- b3 Z
(prepubertal).
) w3 L$ A2 D  L. _8 R1 b, wThe parents were notified about the laboratory! D% n* l$ E1 V( ]
results and were informed that all of the tests were% S$ L9 Y; W+ X
normal except the testosterone level was high. The
2 k7 q* U: C- _( F, s9 H; g' Ofollow-up visit was arranged within a few weeks to6 H' `8 y  Q  @' S1 ~6 \
obtain testicular and abdominal sonograms; how-
; M8 G) f6 K  C( F' H3 Aever, the family did not return for 4 months.7 Q$ r# w0 O8 e% s9 [3 k" B$ ?
Physical examination at this time revealed that the. i: i/ l1 U$ q3 \9 `
child had grown 2.5 cm in 4 months and had gained- ?. [- L' c7 ~. Y$ v" X8 \/ D' y3 ~: j
2 kg of weight. Physical examination remained- |+ V/ A* K5 I/ R& F  e! ]
unchanged. Surprisingly, the pubic hair almost com-3 J( @0 S1 u. Z( E; ?# {1 l
pletely disappeared except for a few vellous hairs at/ q# P& S6 Y! M
the base of the phallus. Testicular volume was still 2
2 g8 ?0 g, n0 `7 p# e8 ~# UmL, and the size of the penis remained unchanged.
+ k, A* q  e; L* YThe mother also said that the boy was no longer hav-' ^; F; K  ?2 m; k) J( x
ing frequent erections.6 B* K2 M3 Z. j0 h' d; y" W8 f
Both parents were again questioned about use of5 R. ~# R* \! k& d2 I
any ointment/creams that they may have applied to/ R' T: N9 a* O
the child’s skin. This time the father admitted the
7 j7 A5 }1 `- {/ s; w8 r$ i0 HTopical Testosterone Exposure / Bhowmick et al 541
9 S0 k/ T3 R- R6 X! O& Cuse of testosterone gel twice daily that he was apply-
8 i( ^: T0 E5 Z6 Ving over his own shoulders, chest, and back area for' ^2 X, P, i! S6 _
a year. The father also revealed he was embarrassed
( z5 \' ]% h3 D+ N3 Kto disclose that he was using a testosterone gel pre-
5 u& ]" p" N! S( [' {scribed by his family physician for decreased libido3 k- @% m6 ]! y# s
secondary to depression.
" s! z0 j' P2 U8 \0 PThe child slept in the same bed with parents.5 ?# C9 m8 E) [/ h
The father would hug the baby and hold him on his  A0 H% R9 {7 G- i0 s$ |+ C# J
chest for a considerable period of time, causing sig-
9 T& @% A; r; y6 h+ n# hnificant bare skin contact between baby and father.* M( ?9 A" v- j2 v% [
The father also admitted that after the phone call,$ v1 e0 O( S- Y, a" I; U, I8 g1 `
when he learned the testosterone level in the baby
# V/ D/ Q! `$ ?0 o' Rwas high, he then read the product information
3 E/ @  M! H* i+ Qpacket and concluded that it was most likely the rea-" N: K% v. D0 v# F" M
son for the child’s virilization. At that time, they
/ A* E/ \0 U; \2 ~* B& pdecided to put the baby in a separate bed, and the& _$ |5 J1 y, {7 i. x
father was not hugging him with bare skin and had
( h# a: k  A' n( C7 i1 H2 C( R# f: Tbeen using protective clothing. A repeat testosterone
- @0 {, v, ?! D- G* ptest was ordered, but the family did not go to the7 d' U% C! @: F0 U! E3 P
laboratory to obtain the test., ]3 ]* S6 P: X7 W8 R0 p- L6 X9 p7 g
Discussion9 s+ H- M! [) o# ?
Precocious puberty in boys is defined as secondary
0 S0 ?# I9 h8 _2 k. M& ksexual development before 9 years of age.1,4
6 w  n9 K# J: T( V. O% zPrecocious puberty is termed as central (true) when
" O* W9 x# u* n! W1 v$ xit is caused by the premature activation of hypo-8 G' [* H+ Y& @8 e9 M
thalamic pituitary gonadal axis. CPP is more com-
4 [; y8 V4 ^% p' X7 u" T$ Ymon in girls than in boys.1,3 Most boys with CPP
! f2 U3 \/ j; D; q) m( Kmay have a central nervous system lesion that is
- q8 U' W! |8 ]$ C) e6 tresponsible for the early activation of the hypothal-
4 w4 B! \- c4 ^5 z6 U( ramic pituitary gonadal axis.1-3 Thus, greater empha-
' n$ }" l% S$ B) Z$ v* ssis has been given to neuroradiologic imaging in7 W! I$ v. |5 G* k* v
boys with precocious puberty. In addition to viril-- j* Z# U4 |# h! x
ization, the clinical hallmark of CPP is the symmet-
; Y* j9 w6 S8 X$ x( i2 p! W# _: srical testicular growth secondary to stimulation by
$ }. s0 E& V3 ]gonadotropins.1,32 ]0 s0 @/ J: }) o6 p
Gonadotropin-independent peripheral preco-* ?3 {4 d: `- x3 U2 s$ F8 x. _1 A
cious puberty in boys also results from inappropriate8 @/ o6 i; L6 T# z( i1 @
androgenic stimulation from either endogenous or, Z% K! _, `2 @  d4 N+ U
exogenous sources, nonpituitary gonadotropin stim-4 M/ {% K& ~+ y
ulation, and rare activating mutations.3 Virilizing& O4 _; U: P5 R  t) ~
congenital adrenal hyperplasia producing excessive
, u% e# B/ j4 q2 padrenal androgens is a common cause of precocious8 v, d! R+ Q! k5 o) V9 I8 [
puberty in boys.3,4
5 z$ u/ Y& g" l% lThe most common form of congenital adrenal
! }8 V, x. [4 ]# N) Bhyperplasia is the 21-hydroxylase enzyme deficiency.
) u2 M  @5 w1 E2 NThe 11-β hydroxylase deficiency may also result in
& Q, Y9 R9 J, h5 j# q0 b( L/ uexcessive adrenal androgen production, and rarely,
5 D8 P6 r2 Z' K8 ~) r4 Ran adrenal tumor may also cause adrenal androgen8 S/ a. e" j' i
excess.1,3
: v: L6 C, x+ eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ X2 N8 g9 E7 @' z3 l  y# y, n' b542 Clinical Pediatrics / Vol. 46, No. 6, July 2007( t, C+ ?$ }: [
A unique entity of male-limited gonadotropin-
0 I" ]+ r. c, Y4 N, ], pindependent precocious puberty, which is also known
5 y5 C+ v# J/ }$ y. E8 tas testotoxicosis, may cause precocious puberty at a+ j, i1 H& Q! y( r0 R: l+ U; m: w, x
very young age. The physical findings in these boys4 d7 A2 b5 z( n( E5 @
with this disorder are full pubertal development,
5 X; e% h2 F) M2 `1 ~& b( mincluding bilateral testicular growth, similar to boys
2 Q9 Y( x5 e; R% iwith CPP. The gonadotropin levels in this disorder
. Q6 C  T: M4 R$ `7 vare suppressed to prepubertal levels and do not show
1 Z; R  ~6 P# h" Spubertal response of gonadotropin after gonadotropin-
  t8 y8 p- M7 Freleasing hormone stimulation. This is a sex-linked4 A3 t, S7 U+ d, u1 k0 {
autosomal dominant disorder that affects only
  v2 E3 R6 N  d' w" K3 ^males; therefore, other male members of the family
5 S6 H1 `3 [3 i' f% D  Z( Bmay have similar precocious puberty.3! a$ e9 z6 ?4 j. I& a
In our patient, physical examination was incon-) i+ |! g& n# ?6 P; [: d
sistent with true precocious puberty since his testi-5 e' S3 J. d7 y5 d& Z5 x, X
cles were prepubertal in size. However, testotoxicosis. K1 s, w8 h' W) s$ x( J) O
was in the differential diagnosis because his father) }0 b( w& ~5 ^& i: i. n3 a0 U
started puberty somewhat early, and occasionally,( ?) v# ?1 J. s9 m0 G, U. v
testicular enlargement is not that evident in the
) R9 P* {2 h  T/ c+ b* l# p" Pbeginning of this process.1 In the absence of a neg-
# _5 C9 I( Q4 B: J4 uative initial history of androgen exposure, our
' ~' h$ [+ x7 u2 dbiggest concern was virilizing adrenal hyperplasia," B- I# \# x. P, |  r
either 21-hydroxylase deficiency or 11-β hydroxylase" L4 e& e% }0 j: W
deficiency. Those diagnoses were excluded by find-8 Y. j# S9 C) b/ R5 x  n3 q  K2 ]
ing the normal level of adrenal steroids.+ M# e2 f' R; Q' X  Z* Q
The diagnosis of exogenous androgens was strongly
) |- D2 K9 o, T7 i* X" msuspected in a follow-up visit after 4 months because0 t5 t9 N: c3 ~. @+ I
the physical examination revealed the complete disap-6 M5 ~1 J$ v" \7 z7 T
pearance of pubic hair, normal growth velocity, and
! i) |4 V, z8 R7 Gdecreased erections. The father admitted using a testos-) L3 [: g6 B7 p5 s
terone gel, which he concealed at first visit. He was) `8 h) |$ ^# D
using it rather frequently, twice a day. The Physicians’( ^% b' _* J  E% D0 F/ m5 U& M
Desk Reference, or package insert of this product, gel or" P' S2 t9 o! N* L& X  o
cream, cautions about dermal testosterone transfer to
4 i; I) u& W! Xunprotected females through direct skin exposure., G' \5 R0 B! A. G) B6 R
Serum testosterone level was found to be 2 times the
& g' A+ {% ]$ g- g+ kbaseline value in those females who were exposed to
5 Q( P$ s+ u$ x8 O, @- j# l. ?even 15 minutes of direct skin contact with their male
! {8 b- L- J, ^: H  B; o0 opartners.6 However, when a shirt covered the applica-5 R* v+ p7 k1 H8 r0 R
tion site, this testosterone transfer was prevented.
$ ^; w$ G5 l$ X( \# W7 qOur patient’s testosterone level was 60 ng/mL,  j$ \5 B+ ]7 I; Z+ }  h4 t
which was clearly high. Some studies suggest that5 G; l$ c& n" v1 y/ Y
dermal conversion of testosterone to dihydrotestos-
8 F2 n6 h& T& P2 Yterone, which is a more potent metabolite, is more) d: ~  [- {1 m" }$ k
active in young children exposed to testosterone
1 a, W) V: v, f$ n- y( h; M. @1 r/ u( {exogenously7; however, we did not measure a dihy-. s. o- }* ~8 o% L4 r3 }
drotestosterone level in our patient. In addition to
3 i# b$ V2 Z. D; `+ f, jvirilization, exposure to exogenous testosterone in
$ C# ~: z0 I# q6 m' m) f# j7 Echildren results in an increase in growth velocity and
2 A0 _/ ]3 u6 P, padvanced bone age, as seen in our patient.& {  Y4 M% ~. ]  g4 ]/ u
The long-term effect of androgen exposure during9 z+ k9 g) i  Y5 X5 \1 j
early childhood on pubertal development and final4 H" P. e5 G/ e  T: `! U" {
adult height are not fully known and always remain
; a2 f# _+ h  u! t  s! d2 g( \a concern. Children treated with short-term testos-- N- W" ~  e8 x! ^1 M9 b" r, M% M
terone injection or topical androgen may exhibit some9 t" y( X& s. J2 n3 D5 F) D( B
acceleration of the skeletal maturation; however, after4 ~; Q8 n0 [3 f/ H% m2 Q% R
cessation of treatment, the rate of bone maturation
" I7 W7 z$ W% x% j: ydecelerates and gradually returns to normal.8,9
. b( ]( G- x+ F7 K. R, C0 lThere are conflicting reports and controversy& F# p! i- }9 _$ k- r  W
over the effect of early androgen exposure on adult
1 u. y9 }! |$ n4 k, tpenile length.10,11 Some reports suggest subnormal% b( @2 f$ N1 `; _  {& ~$ t
adult penile length, apparently because of downreg-( i; L/ u. W2 l. B
ulation of androgen receptor number.10,12 However,+ y% N( w& r; M8 S- t7 @' M, G
Sutherland et al13 did not find a correlation between
7 n6 Q* q7 A1 R6 ~' schildhood testosterone exposure and reduced adult
) |+ r" R( \# Z& Jpenile length in clinical studies.1 |: }5 ?) n. C
Nonetheless, we do not believe our patient is
1 d! F9 t' ^( ?$ k' ^going to experience any of the untoward effects from
) |* _- v: H' R% S2 Ftestosterone exposure as mentioned earlier because
2 l9 I* i' {" Z& V  a( C5 cthe exposure was not for a prolonged period of time.4 m) X  ?+ L: v6 a
Although the bone age was advanced at the time of) z) V6 Z- O& i1 m. U1 |
diagnosis, the child had a normal growth velocity at
) Q0 V1 X( c. x! k" Fthe follow-up visit. It is hoped that his final adult
* P  C! Y0 q4 J: iheight will not be affected.; M( t8 l. g+ K* I2 c3 x1 S6 r
Although rarely reported, the widespread avail-
. D* q0 y4 x- {. S# f; Wability of androgen products in our society may
9 X  u: V/ Q# Y6 @0 D  m# I5 Dindeed cause more virilization in male or female; L; I* m! J9 J
children than one would realize. Exposure to andro-
+ c) |3 l& Z, S4 J& n4 Pgen products must be considered and specific ques-0 b0 v3 m1 p, m  B# ^$ x* [
tioning about the use of a testosterone product or
) y; d8 ~. t, J; N: t% {* O6 Egel should be asked of the family members during
7 H4 J! n8 }" \8 c+ ]  t# k$ tthe evaluation of any children who present with vir-
! ^, d$ y; y( x4 q% dilization or peripheral precocious puberty. The diag-
1 o; f- B% l7 b1 O# `6 Z$ U( Tnosis can be established by just a few tests and by
4 l! t  A# y  z) G# S+ rappropriate history. The inability to obtain such a* ]3 a2 \: Y. V" W* d  S, |
history, or failure to ask the specific questions, may
- @5 i  p5 r# `, Eresult in extensive, unnecessary, and expensive3 U; T, @* j- @$ }
investigation. The primary care physician should be  v" S  Z! A. l# W
aware of this fact, because most of these children2 I5 y; `! S" ]* w% R+ p$ ]* H
may initially present in their practice. The Physicians’: V# l6 H5 b' o  k0 L
Desk Reference and package insert should also put a
; ~2 m6 `- v9 O) o  q* J- _$ k7 j! \3 pwarning about the virilizing effect on a male or
2 d' R' D0 R1 V* k; Cfemale child who might come in contact with some-
2 i$ b8 `5 `2 b2 m6 \( J8 {+ @one using any of these products.
; j% H. Z8 G2 s( f7 TReferences
& V5 S% Q7 I& t: }( [# t2 J! c1. Styne DM. The testes: disorder of sexual differentiation1 _9 U7 f. L; ~- \5 L7 Z* k
and puberty in the male. In: Sperling MA, ed. Pediatric
3 i: ]/ [, u. U7 w* \3 }  Y2 ~! BEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;9 V9 O! `. v8 ^! x5 H
2002: 565-628.
/ O- Q) v* M1 o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
- {6 Q& M/ |: ~3 Y" @3 xpuberty 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
2 Q, [' L, x: m: q. n5 F4 a( @
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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