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Sexual Precocity in a 16-Month-Old& n! |& l" \8 `# v5 d8 @3 u
Boy Induced by Indirect Topical* h' P: l. M: j+ D+ T- p
Exposure to Testosterone" c5 e" J: V) l$ E/ J$ G8 o
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
7 b# }+ f# ~$ z7 ^7 \$ w& V  Aand Kenneth R. Rettig, MD1
% b3 x+ ~2 |) q4 F' V5 L9 D$ DClinical Pediatrics7 `" j/ d  V, F& k
Volume 46 Number 6
0 V, O1 Y" @( K; P8 j4 fJuly 2007 540-543* y9 w% X, r) U5 G1 d
© 2007 Sage Publications
- q$ i! L. |9 Z& G10.1177/0009922806296651
" B( T, F3 f$ m# `' C* k5 Ahttp://clp.sagepub.com
* r+ K5 A7 K7 ]! w6 c: J5 \* rhosted at0 C6 a1 w: _6 |" I
http://online.sagepub.com
/ w) I4 k' R- ?6 b: ~) l1 MPrecocious puberty in boys, central or peripheral,- ~* }3 l9 X8 z+ R0 D
is a significant concern for physicians. Central
, `# N! H- p; Y' L, ~2 `" c5 Rprecocious puberty (CPP), which is mediated! c; B+ m! I0 Y0 v' n8 p' H9 S  U4 E
through the hypothalamic pituitary gonadal axis, has% o& k$ v5 H. W9 v5 F# p
a higher incidence of organic central nervous system
8 u1 ?$ y8 k( Y* y; {$ d3 Jlesions in boys.1,2 Virilization in boys, as manifested
, z7 c2 d) y0 u0 B4 Z: D( d- M8 pby enlargement of the penis, development of pubic/ b& C/ m4 a2 `) j# ]
hair, and facial acne without enlargement of testi-
1 z" t: @2 M* ]; Bcles, suggests peripheral or pseudopuberty.1-3 We( E- a, q7 S. Z% }4 h7 E/ L4 V
report a 16-month-old boy who presented with the; X! S, p0 M8 n3 v! M
enlargement of the phallus and pubic hair develop-
/ Q# f. f) |6 ~2 M+ r6 Cment without testicular enlargement, which was due( E% l0 @& j" v0 F+ _3 E) x+ e
to the unintentional exposure to androgen gel used by
0 W0 i) l; \! r# ?$ zthe father. The family initially concealed this infor-
. {( j8 Z, u0 g: O+ f+ y2 {mation, resulting in an extensive work-up for this
; @% @2 R8 h9 v( \% Zchild. Given the widespread and easy availability of2 o( h: M/ f) J8 Q' H
testosterone gel and cream, we believe this is proba-
6 U( Y, I2 v7 e2 M4 ?bly more common than the rare case report in the9 ?: e$ _" @: I: w  H/ q7 a
literature.4
: z. j2 p# ~9 C+ DPatient Report& a3 e7 l+ o9 B- Y0 Z# C
A 16-month-old white child was referred to the9 B/ H5 o# y# H0 [1 y
endocrine clinic by his pediatrician with the concern
9 G" f/ e+ C) T( hof early sexual development. His mother noticed
  @! x' \; p) o* L+ B8 n, s; |* Flight colored pubic hair development when he was+ t# H4 L1 W1 X' D$ o* U7 ?( p
From the 1Division of Pediatric Endocrinology, 2University of# ^0 u9 S& ^- `% m: e8 H4 C
South Alabama Medical Center, Mobile, Alabama.% ]' y. d! Z# s5 e# g: R7 h
Address correspondence to: Samar K. Bhowmick, MD, FACE,
( ?# D' M! O' yProfessor of Pediatrics, University of South Alabama, College of
! l4 ^1 W  \( X% ^+ {/ ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 k  i4 s/ }8 z# T
e-mail: [email protected].
& c$ ]' Q7 c# aabout 6 to 7 months old, which progressively became+ P* {. b! n7 [; G6 J  l
darker. She was also concerned about the enlarge-' e! y: D8 `6 o# k8 ^5 O
ment of his penis and frequent erections. The child
0 b' q+ x  z8 {0 m; [was the product of a full-term normal delivery, with4 ~6 _  R6 P) H. y7 @" C
a birth weight of 7 lb 14 oz, and birth length of6 I# Q- [  h& k  A
20 inches. He was breast-fed throughout the first year
. u( D3 I$ J  d" c/ Z) F% \/ C) ?of life and was still receiving breast milk along with
: g$ [( i7 D1 J1 K4 P0 N* }solid food. He had no hospitalizations or surgery,
6 e) [* X4 L$ G9 v! F9 Fand his psychosocial and psychomotor development
1 j) ]3 l. k4 q; Ywas age appropriate.
% Q8 I& a4 s' }% u2 ^The family history was remarkable for the father,/ n7 d" s1 A8 R/ P
who was diagnosed with hypothyroidism at age 16,
: c  m; [7 r7 L. |  Dwhich was treated with thyroxine. The father’s+ I3 V" Q7 c  X
height was 6 feet, and he went through a somewhat0 z. r# I% Y% |2 \) g# i5 R
early puberty and had stopped growing by age 14./ Q7 G# _) D# f7 N: G
The father denied taking any other medication. The
) K( q$ F. k2 c1 ?child’s mother was in good health. Her menarche
+ H' p. H+ h, O, l! lwas at 11 years of age, and her height was at 5 feet) G% H! u+ V3 m$ J& H: {' t3 |
5 inches. There was no other family history of pre-
' k, _1 U0 J; y7 ?6 R2 g& ^cocious sexual development in the first-degree rela-/ m' b; a7 ^; d+ k& M) E+ P
tives. There were no siblings.; A) R4 c' e& s8 }0 G
Physical Examination
$ ~( C1 Q9 H. s; d1 B0 b- wThe physical examination revealed a very active,
" q9 M4 H& l4 z% |* @/ V% x4 Rplayful, and healthy boy. The vital signs documented
% @0 I% ^- U% \4 U3 g+ l6 Ya blood pressure of 85/50 mm Hg, his length was
; {  ~- V) r" G( j90 cm (>97th percentile), and his weight was 14.4 kg5 b, Z: {$ E0 i) v5 F; }  M, s( |
(also >97th percentile). The observed yearly growth& @" z% z0 v# ]. |5 s
velocity was 30 cm (12 inches). The examination of: [. J5 m$ [/ {& ~) h
the neck revealed no thyroid enlargement.6 v( r9 l' _' i# j7 V9 U8 R) T
The genitourinary examination was remarkable for+ r- \3 ?5 R$ |3 Q
enlargement of the penis, with a stretched length of  o4 j* O) s6 T: ]% O# k
8 cm and a width of 2 cm. The glans penis was very well
4 X0 a; z$ F/ j2 Rdeveloped. The pubic hair was Tanner II, mostly around/ @% Z5 N5 h6 y
540
0 r# r# P+ l# G5 w1 lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, a1 T/ C0 A" m" t2 X! Q3 i% gthe base of the phallus and was dark and curled. The+ g; w( }! _" d& L
testicular volume was prepubertal at 2 mL each.& g  @1 G- Q* J4 k* @4 a; ~
The skin was moist and smooth and somewhat( u& ]* C0 e9 z, t& y# M4 j# _
oily. No axillary hair was noted. There were no  m8 S/ @0 F% l9 {, S
abnormal skin pigmentations or café-au-lait spots.
: ~" o! o7 v# g7 ^& d' pNeurologic evaluation showed deep tendon reflex 2+: W% W9 z4 s; x: B3 ?. V+ x
bilateral and symmetrical. There was no suggestion7 ^: K* f) s, `
of papilledema.6 |3 j. F( d9 ?9 I$ n( P' P# V8 n
Laboratory Evaluation
: I( Z2 q* z9 p) m, z. s9 cThe bone age was consistent with 28 months by
( J' n" ?1 u7 U: G' _6 |using the standard of Greulich and Pyle at a chrono-" [. ]  w0 d; k; Y
logic age of 16 months (advanced).5 Chromosomal/ X3 ?* s$ Z  ]7 b
karyotype was 46XY. The thyroid function test- c+ A: ^; d2 X/ ~, ~9 g9 m
showed a free T4 of 1.69 ng/dL, and thyroid stimu-5 k* K1 Q) \) M3 b5 m7 y! Q
lating hormone level was 1.3 µIU/mL (both normal).8 J& n7 Q/ A/ B1 ?
The concentrations of serum electrolytes, blood
/ L0 Y- W% c3 ]' Y3 v5 z4 N, surea nitrogen, creatinine, and calcium all were
- c3 a% F3 k2 e$ N4 Jwithin normal range for his age. The concentration! }+ c* k/ q! g/ j4 q$ F$ h
of serum 17-hydroxyprogesterone was 16 ng/dL
) g5 l7 y2 Y, D' j- t8 c( R(normal, 3 to 90 ng/dL), androstenedione was 20' n5 U4 Z9 X; x+ J$ U; c8 M5 [! E
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-1 R7 I( k9 N& o) u8 S, H* R* g
terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 M$ S- e1 W' s+ W9 m& T2 _8 {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 p. F4 k' P3 y* `49ng/dL), 11-desoxycortisol (specific compound S)2 C( y3 u5 w, J4 U) V+ Q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
* r% S( @  v. d) K. p9 jtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* v* G( k& I8 G/ s
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),5 O6 L! n! b1 L$ R# v, x4 v
and β-human chorionic gonadotropin was less than: h: j$ Z% }8 P! Y0 ~
5 mIU/mL (normal <5 mIU/mL). Serum follicular5 [1 c; F* H, b/ s4 s
stimulating hormone and leuteinizing hormone
! y+ C7 _5 K) Yconcentrations were less than 0.05 mIU/mL
' |3 z  J- g. R' D2 n7 v(prepubertal).1 R2 w7 }& E- l" b9 e
The parents were notified about the laboratory9 `  ^. M' Y5 Q
results and were informed that all of the tests were
( ?, U, ~7 e! V8 R9 onormal except the testosterone level was high. The6 U8 H; ~) b! ^/ ]" g
follow-up visit was arranged within a few weeks to
' H  H+ C$ f% D0 @( x6 ~obtain testicular and abdominal sonograms; how-
# V, z& W7 @4 R% @: pever, the family did not return for 4 months.
! n  e3 w, z9 xPhysical examination at this time revealed that the
; t. }9 |+ k: Z; pchild had grown 2.5 cm in 4 months and had gained& k- A9 x% N4 O7 d
2 kg of weight. Physical examination remained* |: l5 y( ?) h
unchanged. Surprisingly, the pubic hair almost com-0 B7 O4 t- ^1 f) F) ?% ~9 F" E
pletely disappeared except for a few vellous hairs at
5 v% }: ]% j0 k% e' H7 zthe base of the phallus. Testicular volume was still 2
1 o, @2 ^+ H3 Y1 ]2 [mL, and the size of the penis remained unchanged.
' m$ h) E3 s; Z, D8 fThe mother also said that the boy was no longer hav-
) Z" R2 m5 d8 b* D. g, Xing frequent erections.4 b, W/ g& m1 c3 e: H
Both parents were again questioned about use of
* _2 m; A) V9 N- z% I4 Lany ointment/creams that they may have applied to% m/ [& F; D, r$ b4 D0 j* c% Y, F
the child’s skin. This time the father admitted the
1 ^/ K$ A$ P0 U$ XTopical Testosterone Exposure / Bhowmick et al 541
$ `: t& k2 K, T3 j* A5 W$ T  ause of testosterone gel twice daily that he was apply-
! N7 y- n# q8 F; q6 [- Y1 M8 A& }$ \ing over his own shoulders, chest, and back area for
3 X, ~7 E* E! f8 J: q/ A/ ma year. The father also revealed he was embarrassed( U7 c0 s  q1 ~/ B2 o7 d0 m
to disclose that he was using a testosterone gel pre-! [. {% f8 d0 ]: N2 o
scribed by his family physician for decreased libido
6 {% B, g0 T7 w) K5 Isecondary to depression.
/ v* ^2 h' H( e8 [- P0 B5 dThe child slept in the same bed with parents.
9 k5 x+ d5 \. f2 BThe father would hug the baby and hold him on his
0 Y- R  }! ?- f) |# E* ychest for a considerable period of time, causing sig-+ v1 T' V* ?' G$ _# ~4 K
nificant bare skin contact between baby and father.9 T' r: \  }: P4 y( k1 M6 E9 p3 ]
The father also admitted that after the phone call,7 A* W, V8 d) @4 y+ s7 A
when he learned the testosterone level in the baby
5 M' c, d% k4 g/ W" V; q; ~was high, he then read the product information
% g. S6 W* ?5 N1 M3 Q) z$ H& zpacket and concluded that it was most likely the rea-! H, S/ R9 j7 e0 [$ [% k# p. U
son for the child’s virilization. At that time, they
( V/ l+ F9 @. B, _2 M* i& edecided to put the baby in a separate bed, and the9 Y+ F9 S( i+ ?# j# ~" C* |; k
father was not hugging him with bare skin and had5 r* W: X' x& k2 E. W3 o! a8 P- |+ A
been using protective clothing. A repeat testosterone( L3 n( R6 o8 V/ w
test was ordered, but the family did not go to the3 u! i. S: y- E1 J( f9 |( D
laboratory to obtain the test." J0 m& O% Y! ^5 D8 p- F
Discussion
/ a3 }/ @; H" j& Y5 VPrecocious puberty in boys is defined as secondary
* ?' O' {' V6 @) s. I) {' Wsexual development before 9 years of age.1,4
  g2 C4 A) j1 u$ W: t+ z+ TPrecocious puberty is termed as central (true) when
' G8 h. q8 A% ]2 q; Cit is caused by the premature activation of hypo-
/ @, P$ Z0 x! g: a. hthalamic pituitary gonadal axis. CPP is more com-, Q/ B4 j% O( c* m: y. J. t& a9 r
mon in girls than in boys.1,3 Most boys with CPP
. ?) w9 U  c! Y2 |; d! vmay have a central nervous system lesion that is' k* m- i  I( ^
responsible for the early activation of the hypothal-0 X7 q1 L" {% C- [3 R4 p3 D* Y
amic pituitary gonadal axis.1-3 Thus, greater empha-
5 B8 H+ }: |  l3 z/ zsis has been given to neuroradiologic imaging in
+ C8 _) V7 a$ Kboys with precocious puberty. In addition to viril-
* }* `! m4 ]$ t( Wization, the clinical hallmark of CPP is the symmet-) M# t$ C- x6 N  Y
rical testicular growth secondary to stimulation by
" T8 Z. ~. C$ {gonadotropins.1,3
% k5 u( G3 z" H" w5 RGonadotropin-independent peripheral preco-: U9 R5 h/ W. w% W
cious puberty in boys also results from inappropriate
: O, S3 i) N6 m* M4 @5 `; ~androgenic stimulation from either endogenous or  W! p; ?' L6 U
exogenous sources, nonpituitary gonadotropin stim-
7 f# x& [  U' k" R/ _& Z1 gulation, and rare activating mutations.3 Virilizing9 p% ?# s9 R1 L. ?3 h# L, N
congenital adrenal hyperplasia producing excessive- `* v* p* F7 O: {
adrenal androgens is a common cause of precocious. g; b1 U: r# D3 J. s
puberty in boys.3,4( }, b5 ?8 ]8 |0 F* I7 V5 l
The most common form of congenital adrenal& t& n* y' u0 B/ O
hyperplasia is the 21-hydroxylase enzyme deficiency.
+ @( {0 u1 q$ q. r0 QThe 11-β hydroxylase deficiency may also result in, d' ~. H/ C& G1 @8 C1 d
excessive adrenal androgen production, and rarely,
! p; }% E6 D$ i7 {  y; _an adrenal tumor may also cause adrenal androgen
' a/ I. r2 A- K: P9 Pexcess.1,3# E3 c6 S, F5 L: |* [/ j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# k" T- b$ i9 w- I
542 Clinical Pediatrics / Vol. 46, No. 6, July 20071 [( z: [  o: J- p/ `
A unique entity of male-limited gonadotropin-
5 ?/ x; |' h5 c. B0 e4 pindependent precocious puberty, which is also known
; A2 J: X+ z' v3 v; Fas testotoxicosis, may cause precocious puberty at a4 P# S* D% H( ~3 P3 T. _9 b$ M
very young age. The physical findings in these boys9 t5 f& W+ z: A2 \; V! V$ l
with this disorder are full pubertal development,7 A! S7 A5 v" A! t! K
including bilateral testicular growth, similar to boys
1 t5 t# I: a( f$ x" nwith CPP. The gonadotropin levels in this disorder
9 B- X" V9 I! f; Mare suppressed to prepubertal levels and do not show# h& S/ l# j8 P  Y& S
pubertal response of gonadotropin after gonadotropin-
8 k' Y. K! N- Y7 i. zreleasing hormone stimulation. This is a sex-linked+ X4 R% {5 B0 _) W/ J0 H
autosomal dominant disorder that affects only
. I8 _: t2 {" _4 _* Xmales; therefore, other male members of the family
7 P4 S: t, m- h  G% L, Tmay have similar precocious puberty.39 w- k7 W: {0 T* L% K0 C) A( h3 t
In our patient, physical examination was incon-9 r' `8 P6 H2 b: Q: f3 s
sistent with true precocious puberty since his testi-
. t) R* Y  E- j  C) Scles were prepubertal in size. However, testotoxicosis; y. `  C' p: k5 S! c
was in the differential diagnosis because his father  @  C  R) a7 N' @
started puberty somewhat early, and occasionally,
. d; S" i- _" P1 p9 [testicular enlargement is not that evident in the7 B& S7 X$ Q6 Q0 u: T* |
beginning of this process.1 In the absence of a neg-
/ W5 J* i1 \" z; o+ L) Rative initial history of androgen exposure, our
7 f- p6 ~7 o, }biggest concern was virilizing adrenal hyperplasia,
& b" M+ Y6 B- v! n+ i8 _9 peither 21-hydroxylase deficiency or 11-β hydroxylase# S' z5 J2 z6 U3 K
deficiency. Those diagnoses were excluded by find-4 c8 \: q) m: N, }) m, y. l0 M
ing the normal level of adrenal steroids.
, [) F  n9 @) m0 EThe diagnosis of exogenous androgens was strongly
9 y8 N5 e1 W4 E9 p1 `8 @+ q" w- wsuspected in a follow-up visit after 4 months because
: N* b  `0 I/ J6 f( U4 _- ?the physical examination revealed the complete disap-
, S: D% f- O. s1 I! Bpearance of pubic hair, normal growth velocity, and
- a; L1 p) V7 o3 K# m. Ddecreased erections. The father admitted using a testos-4 ]" g; Y; \0 S$ q3 u& O( M
terone gel, which he concealed at first visit. He was
  R8 l  g6 w  f8 F. F  ?using it rather frequently, twice a day. The Physicians’0 R( W: F7 X( Z' E
Desk Reference, or package insert of this product, gel or
: R  J. U3 k+ x6 ]  u2 acream, cautions about dermal testosterone transfer to6 p9 q, Y& W  F2 Z' j
unprotected females through direct skin exposure., s$ H' z4 M; R% z0 `! t
Serum testosterone level was found to be 2 times the8 w; T- }+ d/ y4 X
baseline value in those females who were exposed to
/ G7 U, q9 j5 Y( \+ Eeven 15 minutes of direct skin contact with their male
4 e8 A3 _# v+ Y! e/ zpartners.6 However, when a shirt covered the applica-
& O6 b2 v& }- z2 rtion site, this testosterone transfer was prevented.
( ?; u7 p. O2 L. dOur patient’s testosterone level was 60 ng/mL,
# L& Q: @* c- K) c; Fwhich was clearly high. Some studies suggest that
4 ~! {: x& m& Y. A0 tdermal conversion of testosterone to dihydrotestos-# [, ^  j9 P) G% J
terone, which is a more potent metabolite, is more
  r9 z1 k/ h: q, `0 D" ~3 Uactive in young children exposed to testosterone
( {0 V3 K5 Z0 n- f9 s8 W+ {# S0 Lexogenously7; however, we did not measure a dihy-; `: @# y# ~, B! Y
drotestosterone level in our patient. In addition to; ]2 A; d- |0 F" b* s
virilization, exposure to exogenous testosterone in# G- T5 h7 m1 c+ Q; E
children results in an increase in growth velocity and. W8 i: h! s! U' |
advanced bone age, as seen in our patient.
8 K8 c1 e/ e1 E# z2 dThe long-term effect of androgen exposure during
* {# A, b0 k9 Tearly childhood on pubertal development and final
) ~; l( A3 Q; n/ A* wadult height are not fully known and always remain( U& O& l8 x" r/ ^. M. a
a concern. Children treated with short-term testos-
6 s( O! Q) K5 K/ z; Rterone injection or topical androgen may exhibit some# P" S, A4 x: S6 t4 x; ?
acceleration of the skeletal maturation; however, after
# f7 q( s& s( `5 ccessation of treatment, the rate of bone maturation
* B. T3 G* f2 L4 O. K1 ^' ^! sdecelerates and gradually returns to normal.8,9
6 W4 f+ w7 z+ v9 {' E6 U# o% _! OThere are conflicting reports and controversy- B3 z, v8 d9 Z1 K
over the effect of early androgen exposure on adult5 ^& Z2 Z, |( L2 j* ]) E( ~" A
penile length.10,11 Some reports suggest subnormal2 \4 D6 M) h" v- D( V
adult penile length, apparently because of downreg-1 C) {# V, U$ \2 }
ulation of androgen receptor number.10,12 However,6 |  G- E4 i# x
Sutherland et al13 did not find a correlation between
6 u- j0 f4 b4 @8 u* C, Ochildhood testosterone exposure and reduced adult# [; V/ k3 D- `- \% K# |" E  w
penile length in clinical studies.6 F: F& R2 L+ k" r1 E3 ~0 K
Nonetheless, we do not believe our patient is7 t9 Y: n4 X6 }6 z7 ?, l+ ~
going to experience any of the untoward effects from
4 c2 j6 |# K( z8 q8 X3 m2 ~+ l- Gtestosterone exposure as mentioned earlier because  J& p/ N5 C, ^
the exposure was not for a prolonged period of time.
  C& Z8 z4 O0 y  L' fAlthough the bone age was advanced at the time of( j1 U0 N1 A: x' _' H9 H
diagnosis, the child had a normal growth velocity at
0 M  t* V7 ^, H5 M# {) b2 fthe follow-up visit. It is hoped that his final adult
$ p+ c( [5 Q. V" B; qheight will not be affected.
( w; l. Z6 w8 ^" J+ s6 y" xAlthough rarely reported, the widespread avail-/ v6 p! ?, H! E. u' F* G
ability of androgen products in our society may
3 t9 `/ W, ]6 O# `2 Eindeed cause more virilization in male or female2 U  X7 A/ g5 v
children than one would realize. Exposure to andro-" t2 U8 f; e8 v% y8 y* p
gen products must be considered and specific ques-
' f' }/ [! E" }( l" K2 Utioning about the use of a testosterone product or
! `# t  s% B: U3 X3 T7 Ygel should be asked of the family members during
2 A2 T' `2 T* W% o$ z8 X* G, ]  `1 dthe evaluation of any children who present with vir-3 a. b) c; c& E* |) B& F) T
ilization or peripheral precocious puberty. The diag-* \" F0 U3 G: s1 {+ i, c
nosis can be established by just a few tests and by- [0 b- P1 J, I$ M
appropriate history. The inability to obtain such a( P8 W0 Y3 }# t! n0 u
history, or failure to ask the specific questions, may
" X. l& z# M; v( F3 D+ X& [) xresult in extensive, unnecessary, and expensive/ }) j8 \# n) r, R" M7 }/ w7 |. D, q
investigation. The primary care physician should be# M; x2 B  ?+ }) |
aware of this fact, because most of these children
  ]) `/ R' g, l0 F6 d: z( nmay initially present in their practice. The Physicians’& ^  e- L4 N3 F4 u- D) }
Desk Reference and package insert should also put a. m0 X7 z' D) X. x3 I  B0 m
warning about the virilizing effect on a male or+ R8 h( Z1 V8 Z0 ]* b
female child who might come in contact with some-
+ V  g7 E3 L" Tone using any of these products.- C; ?' _: ]- m( j
References0 X. t0 e' z. [$ ~4 e( f: [9 e# Q
1. Styne DM. The testes: disorder of sexual differentiation# }+ W9 _) B% @* L( o
and puberty in the male. In: Sperling MA, ed. Pediatric
% z; y7 h/ e" \( uEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;4 j" I( C! Z$ S* ?! D
2002: 565-628.6 e: A' j- y/ o! D! G4 z
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ K- ^0 `2 Z$ `  X, y6 f: fpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
1 I' |: `- S8 `& X3 r8 \Boy Induced by Indirect Topical
8 P. ~3 D! b: WExposure to Testosterone
/ M! T3 m" O- E* G$ J% x: RSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 W0 `# k& W- g7 q& {
and Kenneth R. Rettig, MD1
! D' m( G: m& H( m9 pClinical Pediatrics3 K' [# U8 `4 c# {. S
Volume 46 Number 64 _! s  V$ Z9 `; t' g/ \
July 2007 540-543
) ~9 G- w2 x0 |© 2007 Sage Publications" d. F7 K1 u+ q) U( E
10.1177/00099228062966513 j% l) Q5 F' N! }1 y
http://clp.sagepub.com
, {5 `, h  h0 C+ dhosted at
* L5 B) K0 b1 v+ e8 h0 k9 W6 M/ shttp://online.sagepub.com6 C6 L" ?# B) X+ w* _) a; p
Precocious puberty in boys, central or peripheral,4 s; \' X! W/ a- [* L
is a significant concern for physicians. Central
9 z6 C* X; M6 t2 ^$ Sprecocious puberty (CPP), which is mediated  _4 Q% I0 g# [& L. t/ j
through the hypothalamic pituitary gonadal axis, has1 F# ]1 {% p2 u( s* ]$ W
a higher incidence of organic central nervous system
9 F" j7 Z; a4 m" d6 jlesions in boys.1,2 Virilization in boys, as manifested; d+ C, x* l# b/ C# ?7 Q, j* T
by enlargement of the penis, development of pubic- G* Q8 E& H: R2 L3 `/ G. ?
hair, and facial acne without enlargement of testi-5 d! y5 d% f: S5 Y4 N; F
cles, suggests peripheral or pseudopuberty.1-3 We
0 z8 B: F5 G/ ]report a 16-month-old boy who presented with the
2 o* }* T6 \3 H$ |) r' w& I8 fenlargement of the phallus and pubic hair develop-
" a  a! T! \) I( @0 kment without testicular enlargement, which was due2 K7 v; U- }. M( f2 f$ ~, `( D
to the unintentional exposure to androgen gel used by
6 \% R# I& M/ p; |) F6 D+ Ythe father. The family initially concealed this infor-
+ Y6 F. K& r) t0 u% ^1 ?+ B, ~3 f$ E* C* Wmation, resulting in an extensive work-up for this
6 |# P, x3 T: _/ \' f: bchild. Given the widespread and easy availability of
4 E* s" `/ f  x' P- V' c, `" }testosterone gel and cream, we believe this is proba-
* X6 D2 `2 E0 F4 kbly more common than the rare case report in the/ G6 H- U; ]$ @' j: P6 L
literature.47 q3 R( n9 O6 u
Patient Report
9 E; y4 d) c9 s+ {A 16-month-old white child was referred to the/ `4 N$ Z) g9 u  @
endocrine clinic by his pediatrician with the concern
  e$ n6 ]! s( hof early sexual development. His mother noticed" p1 m, ]1 n2 F
light colored pubic hair development when he was
  E+ `* j( Q: R$ ]0 sFrom the 1Division of Pediatric Endocrinology, 2University of" Y2 R9 T" P1 R( l. h# y8 l
South Alabama Medical Center, Mobile, Alabama.
6 v, Y6 b. K* F2 w" r2 `4 MAddress correspondence to: Samar K. Bhowmick, MD, FACE,5 z; X& t0 [! ?! x
Professor of Pediatrics, University of South Alabama, College of
0 ]% {. j' ~& S0 xMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" Y( ]: |  j/ ]. d
e-mail: [email protected].
9 S" V, ], U  V+ T# ^! f4 Nabout 6 to 7 months old, which progressively became. [- F" y1 H  w# `' ~
darker. She was also concerned about the enlarge-: S1 d) r4 E9 F2 R
ment of his penis and frequent erections. The child0 A9 Q) I$ g& a( O9 ]
was the product of a full-term normal delivery, with! y% }: d  E. S: |
a birth weight of 7 lb 14 oz, and birth length of
7 n. f% u) M  d+ y2 a20 inches. He was breast-fed throughout the first year. F5 m4 W/ j2 _7 w; g8 v
of life and was still receiving breast milk along with
9 t, i8 z1 Q; y2 f$ psolid food. He had no hospitalizations or surgery,
1 w6 I. ^& @& `+ D5 u6 y; nand his psychosocial and psychomotor development
$ e7 m$ G2 n9 c2 q" O) i4 Awas age appropriate.
3 v0 P2 D6 U& u5 k& x9 i: GThe family history was remarkable for the father,
$ l; B# f0 L1 {- r, h5 z5 a1 hwho was diagnosed with hypothyroidism at age 16,& Z, _* W( `+ |& \
which was treated with thyroxine. The father’s1 d: [" S* R" |0 Y5 R0 [/ e
height was 6 feet, and he went through a somewhat& k5 ]  ]: g/ J; M& J1 W! n: _: G
early puberty and had stopped growing by age 14.
1 m1 N1 ]/ x6 C/ Z, XThe father denied taking any other medication. The  ?& i4 j% q' }9 j* T. b0 h
child’s mother was in good health. Her menarche! _1 Z2 a( I5 d0 B1 @5 ^) Y
was at 11 years of age, and her height was at 5 feet
# N3 c2 G$ d' p2 Y5 inches. There was no other family history of pre-( M5 Z$ X; ?, X9 |. x; p
cocious sexual development in the first-degree rela-! o+ P) {7 e" L/ W3 e/ @5 J: o; v# F: s
tives. There were no siblings.( @( g: B! x+ X7 k0 @% V
Physical Examination0 z1 ^5 \) d* Y  P" s% r; [
The physical examination revealed a very active,2 _# w) e+ y3 ~  D# b. q/ o0 `8 W; T  k
playful, and healthy boy. The vital signs documented" q3 f8 n9 f6 p) ?  h4 P
a blood pressure of 85/50 mm Hg, his length was
& j1 x( w9 z! O7 x4 W1 J90 cm (>97th percentile), and his weight was 14.4 kg
6 J" k: D5 o& ]6 e* J+ K8 R; e(also >97th percentile). The observed yearly growth
' x1 B2 M3 Y0 t+ ~velocity was 30 cm (12 inches). The examination of
/ e/ T/ @9 f: J0 X& U% g" ~the neck revealed no thyroid enlargement.
) N  d: W, U" x/ m( f: y8 }The genitourinary examination was remarkable for+ s2 l2 W- c( B9 J0 H3 `
enlargement of the penis, with a stretched length of
- }+ c! g: G; F4 }2 u8 cm and a width of 2 cm. The glans penis was very well0 i4 L3 f+ L' D5 A4 G
developed. The pubic hair was Tanner II, mostly around
5 p$ X- e" k6 ^$ i6 j2 n540, ^" }# ]6 Y- h) V. g: ~0 e4 {* `
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( o, G: l( }8 q# w4 `* `the base of the phallus and was dark and curled. The
2 A+ X3 p. W9 y& vtesticular volume was prepubertal at 2 mL each.
4 S3 G, r- k  eThe skin was moist and smooth and somewhat& Q7 T, d2 @  P
oily. No axillary hair was noted. There were no" r' C/ l% H) S) ?5 z, Y
abnormal skin pigmentations or café-au-lait spots.5 H4 A/ f( ?$ L
Neurologic evaluation showed deep tendon reflex 2+8 T; r- b. j1 Q
bilateral and symmetrical. There was no suggestion# Z% ^  k% n0 [# U4 }/ A3 h
of papilledema.
# T7 D! }6 X5 d. A, sLaboratory Evaluation
. D. P& B2 i8 U( }  }( E+ _The bone age was consistent with 28 months by  z1 y0 w6 y, `; J1 l# {
using the standard of Greulich and Pyle at a chrono-! @- a" h. p* P8 H( Z3 x
logic age of 16 months (advanced).5 Chromosomal" i8 h; e) J* _2 z
karyotype was 46XY. The thyroid function test9 Y1 q6 S3 n8 \5 Z& w
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
8 {& `& U) A8 H/ flating hormone level was 1.3 µIU/mL (both normal).
, k  t% |! }, z) F# m0 @The concentrations of serum electrolytes, blood  w, ]2 F* \) m% }7 r
urea nitrogen, creatinine, and calcium all were% h8 K1 i! l( [0 D
within normal range for his age. The concentration
6 h# b' ]( D6 _% m# Q7 Jof serum 17-hydroxyprogesterone was 16 ng/dL
( d1 R6 B0 V, _2 ]; W(normal, 3 to 90 ng/dL), androstenedione was 20
4 L, D( j& n! {/ j0 N4 ?ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
5 q3 p% S. b6 K" B3 U2 {" \terone was 38 ng/dL (normal, 50 to 760 ng/dL),
- \4 d; R( F7 P3 X/ [7 x. ]desoxycorticosterone was 4.3 ng/dL (normal, 7 to* d: }5 l  {! n. B: N% C+ `
49ng/dL), 11-desoxycortisol (specific compound S)
6 @0 E' p- `2 Pwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- ^8 k9 E# u: N: W4 R1 p! \1 E8 f
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: [& e* A5 Z6 F/ l! Y3 J
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),4 I! P* d  g- j# p1 ]
and β-human chorionic gonadotropin was less than
4 @+ h- K8 E. P% \2 @9 M( P7 b4 l5 mIU/mL (normal <5 mIU/mL). Serum follicular
( |1 w, \9 H9 w* _5 s4 @7 Gstimulating hormone and leuteinizing hormone$ j' q; A, }% e0 k- h$ g: v
concentrations were less than 0.05 mIU/mL
5 E3 ], F' J. F1 D3 u4 k: ~(prepubertal).$ |2 s% [3 \$ G# d/ o
The parents were notified about the laboratory
$ W& C. Y2 \1 b- |" g3 q( Jresults and were informed that all of the tests were, v# x, ~  F3 ~3 R1 k- _& }; h
normal except the testosterone level was high. The
/ K$ K4 N4 ]' Afollow-up visit was arranged within a few weeks to
6 x5 v0 e7 v1 y, U+ hobtain testicular and abdominal sonograms; how-7 i3 l  F" A) X$ o/ l2 r3 V
ever, the family did not return for 4 months.
0 `% Q% o& A/ v- m# h- SPhysical examination at this time revealed that the* ^/ t1 h; ^* m5 t% C
child had grown 2.5 cm in 4 months and had gained5 f: {* D' o$ h4 @2 {5 h' U$ t5 y
2 kg of weight. Physical examination remained% U! d/ J/ z/ Q" n+ S4 v
unchanged. Surprisingly, the pubic hair almost com-- ]; J4 ?6 z  q& p7 a
pletely disappeared except for a few vellous hairs at
4 y2 T8 `/ G5 k' ^the base of the phallus. Testicular volume was still 2
' T7 e. u: |# v1 F; `, v' ?mL, and the size of the penis remained unchanged.1 k5 b/ \5 n  M0 B4 C
The mother also said that the boy was no longer hav-
3 @+ X9 u5 q7 e$ ^/ }- j1 Hing frequent erections.
; Q0 h$ e3 ]  u+ |Both parents were again questioned about use of
/ V, J) H7 J4 Z, ^3 nany ointment/creams that they may have applied to) S2 G# {) ]! ~& K* U3 D
the child’s skin. This time the father admitted the. x  r8 C  ]9 C
Topical Testosterone Exposure / Bhowmick et al 5410 c1 v1 y5 ~1 u2 L
use of testosterone gel twice daily that he was apply-- H& O% _. w8 k
ing over his own shoulders, chest, and back area for7 {: M8 ~/ Q" r1 X7 U/ V
a year. The father also revealed he was embarrassed) l; W+ I, z% u) ], H
to disclose that he was using a testosterone gel pre-0 o+ O/ [- j$ [* @1 a  C: g1 N8 b
scribed by his family physician for decreased libido, h) i& x; Q. u/ ]
secondary to depression.
7 z8 i8 c0 m3 L( |; D4 e  bThe child slept in the same bed with parents.
; Y& x) j& c# E0 G7 T! x8 eThe father would hug the baby and hold him on his
# S4 J3 l8 G0 h8 O4 ?9 zchest for a considerable period of time, causing sig-# {2 E$ y- N# H  I6 \
nificant bare skin contact between baby and father.
. D' K: O! N& n9 XThe father also admitted that after the phone call,
8 _+ h3 O8 W2 x* J! z5 lwhen he learned the testosterone level in the baby
' F% C  v) P$ k1 M5 [1 ]was high, he then read the product information3 Q6 A1 F4 v& k$ ~( U
packet and concluded that it was most likely the rea-: G' ^. t) s! X) l/ ~
son for the child’s virilization. At that time, they
( ]. j( H$ \: q) E; e, ddecided to put the baby in a separate bed, and the
- Q3 f, `; B! j1 J" dfather was not hugging him with bare skin and had) X( X% s8 L( m# r, r9 K
been using protective clothing. A repeat testosterone
7 b# j: r. N+ }8 h) e0 n- J; {test was ordered, but the family did not go to the
, p! \6 }$ A% p' Q: m" nlaboratory to obtain the test." r8 Q# y1 P, I  [6 A7 @
Discussion
& P3 _* ~' Q, d" WPrecocious puberty in boys is defined as secondary& ?8 D/ _. l: z' p) M8 Z0 W* h
sexual development before 9 years of age.1,4
$ S- n2 ?' B/ B! s' @7 D0 ZPrecocious puberty is termed as central (true) when
/ V2 B8 L' l  C3 C) ?. _it is caused by the premature activation of hypo-
% ^' d1 p) g+ ^6 P$ ~1 ?* |% I5 c& gthalamic pituitary gonadal axis. CPP is more com-/ D( U! P+ j2 a; Y4 `3 z
mon in girls than in boys.1,3 Most boys with CPP
& G" U3 u/ x# s+ Rmay have a central nervous system lesion that is
' T6 s6 y: e" U! e6 o# h. F2 e2 lresponsible for the early activation of the hypothal-$ k% ?( D  e( P
amic pituitary gonadal axis.1-3 Thus, greater empha-4 H- i* |$ G3 {* S/ l) ~9 V
sis has been given to neuroradiologic imaging in2 P, T: D9 u, t, `
boys with precocious puberty. In addition to viril-
8 v, a& T8 H: }4 q4 R+ F- U# Jization, the clinical hallmark of CPP is the symmet-: q$ E% b! X2 U. f4 \( E
rical testicular growth secondary to stimulation by
  q$ o6 I+ z" @: D! p. P( J, egonadotropins.1,3
  i, n0 U& s: {1 qGonadotropin-independent peripheral preco-
6 W8 j, P" k* C$ j4 }$ E6 Pcious puberty in boys also results from inappropriate) U- l6 M" X" ~, I: D! w* d7 c
androgenic stimulation from either endogenous or8 C# ~, ^/ _: c0 A4 R
exogenous sources, nonpituitary gonadotropin stim-
9 b" M/ G5 t4 j+ I7 Tulation, and rare activating mutations.3 Virilizing2 R) s7 z4 Q* n- w
congenital adrenal hyperplasia producing excessive9 B! k; K7 m( w
adrenal androgens is a common cause of precocious/ z/ _6 p' R  ^, o5 X
puberty in boys.3,4
- A$ L9 p5 e9 o1 a$ d+ E. x. F6 MThe most common form of congenital adrenal% n2 O) K* p1 H
hyperplasia is the 21-hydroxylase enzyme deficiency.3 N0 j, S+ J& k% A+ P4 e9 K. c
The 11-β hydroxylase deficiency may also result in
% W4 U% f) s( n& `# rexcessive adrenal androgen production, and rarely,' F4 T: Z8 D7 ?) Y2 M
an adrenal tumor may also cause adrenal androgen
. r5 t/ d2 e1 ~3 p  J7 fexcess.1,30 F3 @- Z! {$ ^4 _3 T* @/ k' b
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' M. R  s$ V6 k* ?542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* e9 ?; q" O5 Z, X
A unique entity of male-limited gonadotropin-
6 X1 G+ V- [$ z& A0 Cindependent precocious puberty, which is also known4 K) r0 v) |/ v  b
as testotoxicosis, may cause precocious puberty at a6 i; d+ D' u& J9 |) @4 f
very young age. The physical findings in these boys
4 k# k8 O; r# ?4 G0 H) C! N% ~with this disorder are full pubertal development,
8 v1 O' ]$ u( m  mincluding bilateral testicular growth, similar to boys7 o6 ~; U+ c% v' W
with CPP. The gonadotropin levels in this disorder
2 b1 O  |7 b' x) Jare suppressed to prepubertal levels and do not show
5 k8 M' P, b' e+ g- t" Qpubertal response of gonadotropin after gonadotropin-
8 n: I% i/ ^/ O- `releasing hormone stimulation. This is a sex-linked
; V' ^7 ?; j7 Y6 P6 A3 eautosomal dominant disorder that affects only
) G+ }+ O4 t+ h! |- ~! \0 imales; therefore, other male members of the family9 O* _- t4 x/ P1 p, a
may have similar precocious puberty.3- Q8 j$ `. e/ |- \
In our patient, physical examination was incon-* k2 v' s# K; z2 {( ^
sistent with true precocious puberty since his testi-
! ?" o+ K) X" }cles were prepubertal in size. However, testotoxicosis1 K, e/ m; |+ R5 D! r6 w# ?& ?/ C
was in the differential diagnosis because his father1 }) g' z. m+ F  n# h
started puberty somewhat early, and occasionally,
5 @6 Q0 F# I% M0 i- d3 Q2 Wtesticular enlargement is not that evident in the2 T, ~! A' w, X# ^/ B- a1 s
beginning of this process.1 In the absence of a neg-
3 ]: B+ v* j* `3 }7 f  p% eative initial history of androgen exposure, our" x8 U$ t; ]% f4 V$ r$ p% J% n( k7 t
biggest concern was virilizing adrenal hyperplasia,
: M6 s$ G: B& e* ]) T$ a5 ^either 21-hydroxylase deficiency or 11-β hydroxylase5 E# U: v8 m* @& |% m  n" c
deficiency. Those diagnoses were excluded by find-. D0 ], B; C. o% L8 G
ing the normal level of adrenal steroids.4 R; _2 A8 F; j' S
The diagnosis of exogenous androgens was strongly7 i+ `" G. i. A9 C, Z* W% M
suspected in a follow-up visit after 4 months because. m; e) b" \+ v6 c8 M
the physical examination revealed the complete disap-
; ~  v2 r$ N; g% O/ cpearance of pubic hair, normal growth velocity, and: A" V: {) g, B4 [2 W; e
decreased erections. The father admitted using a testos-5 T3 n2 L) a) S7 B9 f5 D
terone gel, which he concealed at first visit. He was
8 U# g" p9 T: J. {+ Eusing it rather frequently, twice a day. The Physicians’
$ k( ]9 g. k) g+ G% W4 R, ?Desk Reference, or package insert of this product, gel or0 m% l" x$ w/ T/ S/ T
cream, cautions about dermal testosterone transfer to
& b- D: T" ], Uunprotected females through direct skin exposure.; C; c, q' ?* G
Serum testosterone level was found to be 2 times the
4 g5 v7 |4 O4 Ibaseline value in those females who were exposed to# N4 M7 \+ ~$ j) j7 v$ j+ Z1 u
even 15 minutes of direct skin contact with their male) A& _, M2 A2 [' q+ M$ @' ]. u
partners.6 However, when a shirt covered the applica-
, t4 x( m& Q! a. Ption site, this testosterone transfer was prevented.
: e# S1 H: C% ]/ f3 o# NOur patient’s testosterone level was 60 ng/mL,- `1 }, K/ e/ T8 D  C% q
which was clearly high. Some studies suggest that
& v$ l3 \6 Y3 W4 Mdermal conversion of testosterone to dihydrotestos-
1 q" h: B# G+ d7 T1 s  I- E2 r; _terone, which is a more potent metabolite, is more
: s6 _! J! g9 y) n: }- W. E: _active in young children exposed to testosterone3 A6 l% |8 ?/ o5 L( ?7 \/ I1 T; s
exogenously7; however, we did not measure a dihy-
' B5 y* s0 p: ?& }6 y1 T* V0 ldrotestosterone level in our patient. In addition to( I. c& G5 z/ m5 Y' G5 t2 t. q
virilization, exposure to exogenous testosterone in$ J' D+ H$ |, s1 ?
children results in an increase in growth velocity and/ y! \9 J- X5 t' b9 O
advanced bone age, as seen in our patient.; W1 x7 `; e$ y+ ]
The long-term effect of androgen exposure during
0 X5 T' M! m/ s8 a/ o" V2 f: B- ~early childhood on pubertal development and final
- ]( }, J2 n- Qadult height are not fully known and always remain6 a& h/ M* L& D5 L
a concern. Children treated with short-term testos-1 N/ N6 l/ _  U) Q3 t8 v, @/ B" l8 b
terone injection or topical androgen may exhibit some& Q. X6 h6 O4 F1 j
acceleration of the skeletal maturation; however, after
% F: P$ t$ Z( _6 @2 j- Y( {! |6 Hcessation of treatment, the rate of bone maturation
$ a" e5 X, o$ W( w0 _' ^- r2 l( ndecelerates and gradually returns to normal.8,9
# n7 a( H2 h! B( hThere are conflicting reports and controversy) L! y( c. Y; Q1 Q; q' O4 @" J
over the effect of early androgen exposure on adult1 u+ G4 h% m9 u7 ?- V+ ^, B
penile length.10,11 Some reports suggest subnormal
  S- t+ S' z1 s! F( C6 x1 T0 N& {/ hadult penile length, apparently because of downreg-1 @4 r8 v) M, V. C+ F: Y" n
ulation of androgen receptor number.10,12 However,& j7 j( U$ X* u( W- K8 C
Sutherland et al13 did not find a correlation between4 c% c, H) C5 s9 [. c
childhood testosterone exposure and reduced adult/ ]/ A3 V$ i" a$ I
penile length in clinical studies.8 L" v$ {8 r# z3 ^4 o
Nonetheless, we do not believe our patient is3 a2 t8 x% N$ F8 j# ], Y3 B" f
going to experience any of the untoward effects from0 S' h0 |- s# u+ f) T0 {; A+ w& X
testosterone exposure as mentioned earlier because$ J: ^8 C  u) \# ~. b, K+ X, J
the exposure was not for a prolonged period of time.
% q: [# E1 J6 F; RAlthough the bone age was advanced at the time of
. B) r3 }' f, h/ Q% U: a+ n: m4 o& |% y  Adiagnosis, the child had a normal growth velocity at
! a3 r' I/ O) I) }1 Ethe follow-up visit. It is hoped that his final adult
6 ^5 w0 ?  [0 s2 ~7 ?3 |/ @. dheight will not be affected.
( s- A5 Y& a2 Q% M) M& [& eAlthough rarely reported, the widespread avail-8 G5 \8 \0 q4 m! n; y  |( F& r
ability of androgen products in our society may( B9 B. i4 e4 X
indeed cause more virilization in male or female
( i8 K# m" l1 }: L& x8 @children than one would realize. Exposure to andro-
: u1 U+ k; R5 ?( Y. sgen products must be considered and specific ques-$ L) ]. R/ [) T) ~$ [
tioning about the use of a testosterone product or
0 Y) K4 U! u9 M/ e; o8 ogel should be asked of the family members during
# r5 }- x5 c3 s, n5 athe evaluation of any children who present with vir-6 z- q. P/ w: Y- G* m0 D2 o
ilization or peripheral precocious puberty. The diag-7 G  x; ^8 M" j( ?0 h) R9 H# `
nosis can be established by just a few tests and by
7 I. L8 c# E' q. B2 c; Tappropriate history. The inability to obtain such a1 X  S& P* V' r9 Y' d
history, or failure to ask the specific questions, may  J6 E1 M5 F" S/ p1 e( F
result in extensive, unnecessary, and expensive: I* z7 a$ b0 o4 a& F& _
investigation. The primary care physician should be
  B, N! h* F! ^5 Qaware of this fact, because most of these children0 F9 E5 V7 L9 W5 N; D- G
may initially present in their practice. The Physicians’
) l( H- O4 f3 _( I( g9 C& c; dDesk Reference and package insert should also put a
3 C3 B2 S. G5 b, s9 `  wwarning about the virilizing effect on a male or
$ `3 T4 h: Z( Ofemale child who might come in contact with some-
" H+ `) E0 {' S8 m8 h5 tone using any of these products.
' _7 m% K$ ^- f- p5 k5 p. w* uReferences$ I( m" ~" T  a5 f6 x3 ^2 M$ L: \
1. Styne DM. The testes: disorder of sexual differentiation
4 \, ?# K( _) Hand puberty in the male. In: Sperling MA, ed. Pediatric
$ ^  ?+ b* p1 G, |& ]3 a( QEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
, U! W8 j9 M3 j, j2002: 565-628.2 g1 ?* X. v9 i4 ?2 \, \3 Q
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
) A" I  ~- W1 _$ l* ypuberty 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
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
- j: N' P% O0 w8 h) d
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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