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Sexual Precocity in a 16-Month-Old, s, |) y' P. h$ Z3 f9 t4 P, N: K6 y
Boy Induced by Indirect Topical
: r) z2 j( `+ @; P4 D1 [% F2 NExposure to Testosterone
9 y# g2 [9 a1 l' p) m/ i9 }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
( p. o( T: a9 h- p) d% E1 v( uand Kenneth R. Rettig, MD1& V" V8 y; d' k3 c
Clinical Pediatrics
1 V; n2 W# p2 o# M& C8 mVolume 46 Number 63 K- o" F. O- a# E
July 2007 540-543* B& Z7 u* u+ ]" {# F  Q; s! ]
© 2007 Sage Publications
% ~( l! c# `, C  u6 F2 a6 W( _5 [10.1177/00099228062966514 s1 W0 e" e0 f/ y9 F! ]
http://clp.sagepub.com. T+ f: v  L+ t8 l
hosted at1 y1 E3 F8 |+ ~& [2 f* k. b
http://online.sagepub.com4 o- p& X/ c& F
Precocious puberty in boys, central or peripheral,- `7 `- H* N+ d% C( Y! _2 w
is a significant concern for physicians. Central' _2 e& l$ u( B# w
precocious puberty (CPP), which is mediated3 Y& W" w0 U+ M
through the hypothalamic pituitary gonadal axis, has8 f& v9 C/ l* N4 @! x8 [# {  E
a higher incidence of organic central nervous system" _7 U8 R8 G& m2 @
lesions in boys.1,2 Virilization in boys, as manifested
; q2 J( P% w% {) L+ [( }by enlargement of the penis, development of pubic
' Y' l0 b, A  y3 b6 C/ `hair, and facial acne without enlargement of testi-
3 z5 ^; y2 m3 g/ kcles, suggests peripheral or pseudopuberty.1-3 We
4 O6 K" w. |2 e" [( Freport a 16-month-old boy who presented with the' ?* n4 e: `8 O3 t% W3 K: a& }
enlargement of the phallus and pubic hair develop-* q! P2 l0 ]( s3 P/ Y+ N
ment without testicular enlargement, which was due2 r+ O) [' ?) [* ^+ I# @: }8 Q
to the unintentional exposure to androgen gel used by
$ q  F: @. }5 f% V$ ?+ c4 [, R5 cthe father. The family initially concealed this infor-2 d! \4 }7 c' I: O
mation, resulting in an extensive work-up for this
7 F/ @  H7 N/ v1 \/ h4 X* P" Ochild. Given the widespread and easy availability of
' Y9 r/ U4 F: R0 G  D/ O/ |testosterone gel and cream, we believe this is proba-
4 b6 b, e1 N! m, K9 c% Ybly more common than the rare case report in the
% d) G0 t3 q% a6 W# ?5 r1 Oliterature.4: ~, [7 k6 o. Q6 z$ u
Patient Report
" C# j7 w. c; fA 16-month-old white child was referred to the
' b$ X  p$ n( @endocrine clinic by his pediatrician with the concern
: O  G& P: F+ v6 pof early sexual development. His mother noticed( L0 D4 b" J% e) J: H# @
light colored pubic hair development when he was, ]/ v6 _" ?: K
From the 1Division of Pediatric Endocrinology, 2University of: i; _: O9 h/ T  E& P1 p8 |) l
South Alabama Medical Center, Mobile, Alabama.
) T# B4 H. I1 K. p* P, M9 dAddress correspondence to: Samar K. Bhowmick, MD, FACE,
! o: x0 J4 |' {# t+ t1 eProfessor of Pediatrics, University of South Alabama, College of' z) _2 K5 B* f% v: ^- {" }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
$ e) u. v) S. v9 X. S& We-mail: [email protected].
/ P2 Q. h9 @8 [, eabout 6 to 7 months old, which progressively became
& ]! H+ x5 a, kdarker. She was also concerned about the enlarge-
$ C: C" |0 K# T+ b4 K7 Xment of his penis and frequent erections. The child
; P# E9 \5 z# D! u9 D2 zwas the product of a full-term normal delivery, with
% @7 G, S2 Q( R4 ]a birth weight of 7 lb 14 oz, and birth length of
4 ^- C! Y$ z. B! b2 `20 inches. He was breast-fed throughout the first year
& g4 x! [- ?6 b  g- P; Y) q5 _of life and was still receiving breast milk along with
8 O: X. |5 f2 z( {solid food. He had no hospitalizations or surgery,% l3 }- e% O* y3 X
and his psychosocial and psychomotor development
1 m( T( p" T" t/ D5 D' t- qwas age appropriate.
9 K. }- y( c3 O. b: s! e7 IThe family history was remarkable for the father,+ ]- @* e' `! I3 a5 c, ?2 k4 g$ h
who was diagnosed with hypothyroidism at age 16,
6 u7 U1 Q8 d) c% r3 fwhich was treated with thyroxine. The father’s
3 T: F3 d9 J( s+ y  p4 L- I  m% F5 \, Xheight was 6 feet, and he went through a somewhat7 ]1 h0 C# ~( p4 X( q0 C
early puberty and had stopped growing by age 14.* `: W. ~* @& C' U
The father denied taking any other medication. The: K" x# ^. Y( z
child’s mother was in good health. Her menarche* N9 \* z' U7 ?4 p* W9 N
was at 11 years of age, and her height was at 5 feet2 g# r" t' g) _- Q3 W5 K/ D0 D
5 inches. There was no other family history of pre-
7 i8 ~4 I' ^/ {: C. G# g' Icocious sexual development in the first-degree rela-! N. y0 g1 Q, n; t) D" N9 S' |- T
tives. There were no siblings.
! n" G7 ~$ f4 A: h/ p1 GPhysical Examination: @6 |" F4 }9 A( B0 M$ D7 f- {
The physical examination revealed a very active,
+ L0 P7 l! d+ E9 x8 V# p) vplayful, and healthy boy. The vital signs documented
: v* y; I( y4 F9 K# m' Ea blood pressure of 85/50 mm Hg, his length was
/ [. C3 d) J5 J& N. X5 @90 cm (>97th percentile), and his weight was 14.4 kg- I- ^% F4 h- }1 I0 U2 g
(also >97th percentile). The observed yearly growth& C5 \" \% M7 i5 Q! s1 s
velocity was 30 cm (12 inches). The examination of
* O+ v9 \- `8 V4 h$ R6 }the neck revealed no thyroid enlargement.
, A+ h2 h4 [# X, E' _The genitourinary examination was remarkable for# {6 I7 E+ H0 I9 c
enlargement of the penis, with a stretched length of2 ~( ~. P/ x' D
8 cm and a width of 2 cm. The glans penis was very well2 C8 t; K) {6 v5 s6 F( y5 {
developed. The pubic hair was Tanner II, mostly around7 m% }- j5 q( M6 [  @5 K
540
' Q$ N3 U2 s% m9 z8 p( f2 _% I* ^at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' R' V; O6 W2 }  k  o0 vthe base of the phallus and was dark and curled. The& o% Z% e! k: Y( b1 d
testicular volume was prepubertal at 2 mL each.: V3 L$ X& ]3 U4 m+ `
The skin was moist and smooth and somewhat
9 e! A" v. p/ Z2 _) W* Q2 |  ooily. No axillary hair was noted. There were no2 W7 u# S7 A! e' N! k
abnormal skin pigmentations or café-au-lait spots.
  x1 p/ S- _1 m; ]* SNeurologic evaluation showed deep tendon reflex 2+8 I* q, A* c1 H6 I. K  k2 S2 k) Q7 _
bilateral and symmetrical. There was no suggestion
9 x4 t% L" f/ p- S0 a2 Q& Dof papilledema.
8 b8 x, G' Q* Z4 DLaboratory Evaluation
4 l2 f* @7 f* J, ^  `The bone age was consistent with 28 months by
9 k$ _1 Q( H( Y  `using the standard of Greulich and Pyle at a chrono-
* V# k% g( }# d+ @7 A8 ?logic age of 16 months (advanced).5 Chromosomal6 F% V2 l, v: u/ d3 K7 k
karyotype was 46XY. The thyroid function test
" W- q8 J# \( s( vshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
' U  M1 m  n2 {5 q/ S3 Zlating hormone level was 1.3 µIU/mL (both normal)./ H% |% Z: G) v7 t: I+ K' S
The concentrations of serum electrolytes, blood1 k$ _+ W2 f* Z7 l( `. h5 _- g
urea nitrogen, creatinine, and calcium all were
" E- g) d5 O2 T. I% Fwithin normal range for his age. The concentration& g* M3 B) G7 R5 g8 |8 u4 l
of serum 17-hydroxyprogesterone was 16 ng/dL
8 H; A# _5 e4 u) ~6 v(normal, 3 to 90 ng/dL), androstenedione was 208 ?& v) w0 o7 M$ b. A/ @% B
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' d6 d/ _. S6 d2 T7 K. _# Fterone was 38 ng/dL (normal, 50 to 760 ng/dL),
) g  f- t( x/ Mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
8 z) l: q  S. \2 K49ng/dL), 11-desoxycortisol (specific compound S)0 j: _& ^8 X* t; A$ k  F% F9 `# |, ^
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
' g1 c7 C3 r9 `tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
1 l, k$ f, D+ m: ^4 e! r# Stestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' A9 w4 |: M0 k: O" K5 u! ?: x$ Aand β-human chorionic gonadotropin was less than
0 G0 J* T# o. r! d  m% |5 mIU/mL (normal <5 mIU/mL). Serum follicular
$ r" \- K/ X' R. S. h+ L: J6 P' W+ bstimulating hormone and leuteinizing hormone  h( w; \9 s+ L/ ]# l
concentrations were less than 0.05 mIU/mL3 G! L: K' x  Z) P
(prepubertal).' G. c$ O7 l* e7 f# ]) X
The parents were notified about the laboratory
) P1 r7 C4 ^: T: [$ Sresults and were informed that all of the tests were% x5 d& A5 R; M8 z! `3 U
normal except the testosterone level was high. The! ]  M1 Y+ m4 o4 _- V
follow-up visit was arranged within a few weeks to4 _5 ?, A% o3 _2 V$ C! R& f9 K/ a
obtain testicular and abdominal sonograms; how-
( Y, W: G' Z& K8 z; ^/ o! ^. P, Iever, the family did not return for 4 months.& B3 M! x& H, p! a
Physical examination at this time revealed that the' I4 B2 F: K1 S. Z* h8 y' p+ T
child had grown 2.5 cm in 4 months and had gained
2 I7 {* |% B1 r; G5 B2 kg of weight. Physical examination remained8 y0 \* L4 `' C9 M9 K; ^8 ~
unchanged. Surprisingly, the pubic hair almost com-
/ V/ X3 o8 f6 c" a$ K- ppletely disappeared except for a few vellous hairs at& J& `3 X# z( ^, L/ Q1 m# p- L
the base of the phallus. Testicular volume was still 2# P. Y/ m6 _# S$ x" f$ V
mL, and the size of the penis remained unchanged.6 X  \0 [6 }' ?) p  x
The mother also said that the boy was no longer hav-$ z; T; A' [- L6 g. |% j: e% b
ing frequent erections.  f% ?( h9 ], t7 A- I: i0 N8 H; c
Both parents were again questioned about use of
$ e6 r% |6 D; X: W: qany ointment/creams that they may have applied to1 Z3 C4 G+ w  i2 A1 Y
the child’s skin. This time the father admitted the4 ^, a# I, U2 `8 r
Topical Testosterone Exposure / Bhowmick et al 541. h% K0 v2 s3 P- t# g0 [
use of testosterone gel twice daily that he was apply-* }! F- T7 ~$ I! m
ing over his own shoulders, chest, and back area for% ~/ R9 n( y5 K% B4 m
a year. The father also revealed he was embarrassed* c$ @1 G9 A1 j, g% G4 d
to disclose that he was using a testosterone gel pre-/ F7 p  P2 s9 I7 W5 R. F
scribed by his family physician for decreased libido) F2 u: Y  e3 \7 K
secondary to depression.
- ?( D+ Y+ l6 P0 TThe child slept in the same bed with parents.
% t: H, R4 ~* p) h1 YThe father would hug the baby and hold him on his1 n" i/ o8 L% k" t. d
chest for a considerable period of time, causing sig-
$ v; A2 d8 B+ F" c& ]0 H% z4 Gnificant bare skin contact between baby and father.0 I0 q' N- s+ G) e" N+ G
The father also admitted that after the phone call,/ g4 u; f% N( R; I% p' t9 Z. V
when he learned the testosterone level in the baby
$ `& d& t# l" t6 |# @% rwas high, he then read the product information5 W5 ~, R5 y# f& P9 g' K
packet and concluded that it was most likely the rea-  Z; ^/ k: f  k: `1 p+ I/ J
son for the child’s virilization. At that time, they
+ a$ A9 K; H1 D7 k# W' K3 Zdecided to put the baby in a separate bed, and the! y$ w1 g& [  l' i
father was not hugging him with bare skin and had0 m- F; y. p( L4 F
been using protective clothing. A repeat testosterone
. _# U4 u0 C* Q- etest was ordered, but the family did not go to the
- o1 A# O2 Z9 S. Y! [# ulaboratory to obtain the test.
# N, A7 Q$ X$ C6 e) b3 k0 K7 p+ KDiscussion
8 w: b  `4 e, m9 s% e$ B2 p  X/ LPrecocious puberty in boys is defined as secondary+ D$ a) A: e' o$ m2 r5 e- X$ Y1 Z
sexual development before 9 years of age.1,40 |# b% m) H1 ]
Precocious puberty is termed as central (true) when7 M5 `9 \8 \$ M  O- F/ {" M
it is caused by the premature activation of hypo-$ N% O: x7 C, ]6 r) V
thalamic pituitary gonadal axis. CPP is more com-
- B, P3 w7 A1 Dmon in girls than in boys.1,3 Most boys with CPP/ Z2 {( w( [6 e+ g6 c6 O5 ~# y
may have a central nervous system lesion that is
" Q% t: Q' N9 m# r1 \+ f) zresponsible for the early activation of the hypothal-
4 }0 S" V9 v# B3 U, }  }amic pituitary gonadal axis.1-3 Thus, greater empha-8 G" U1 Q& I% `: q+ b
sis has been given to neuroradiologic imaging in. x- t" I* V5 `
boys with precocious puberty. In addition to viril-$ y; D, x" T4 {( K8 V; p4 z: s
ization, the clinical hallmark of CPP is the symmet-; u" S% P6 W" L! ^
rical testicular growth secondary to stimulation by
& A$ D  E# ^5 N/ E3 [0 U' g1 Ngonadotropins.1,3
" k% M! `6 M  iGonadotropin-independent peripheral preco-4 \: t" I# A/ m* J# G1 `- a
cious puberty in boys also results from inappropriate2 ?- q4 D# g1 E  J9 w
androgenic stimulation from either endogenous or
* M! d% ?. c" [5 p* Nexogenous sources, nonpituitary gonadotropin stim-/ D' p  q! p, q+ H' G8 R" z" _
ulation, and rare activating mutations.3 Virilizing0 T1 _! P7 S8 L4 v4 W" y
congenital adrenal hyperplasia producing excessive3 B- A3 E% i( Y6 s8 O  C( j- Y, k
adrenal androgens is a common cause of precocious* n& k( e, M! c
puberty in boys.3,4
; `+ L+ g: ~, W5 V5 x) K: S4 DThe most common form of congenital adrenal
9 P% i2 q0 t. N0 g: ~; e! s4 Vhyperplasia is the 21-hydroxylase enzyme deficiency.
3 J' e- a3 s! DThe 11-β hydroxylase deficiency may also result in' A) \/ \& a4 a2 V. s
excessive adrenal androgen production, and rarely,
. L3 g7 @1 e* q, q1 Wan adrenal tumor may also cause adrenal androgen: D# E1 J7 r) [  F( `/ ^0 p  H0 d! {
excess.1,3; f. n# S% W" t8 O
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 P2 I; J  v7 S! W' y* b542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
) ~  h& \* @5 {, MA unique entity of male-limited gonadotropin-
$ g+ o6 q8 M/ K  Oindependent precocious puberty, which is also known
5 ~' h/ C* M) Z* O& G4 J5 x& zas testotoxicosis, may cause precocious puberty at a
  w4 J0 c/ H/ Overy young age. The physical findings in these boys
0 ?7 I; C, l; ^, f. R7 @with this disorder are full pubertal development,! _, \. D* ]" ?: j6 v; ~' [' W
including bilateral testicular growth, similar to boys7 x2 Y4 I0 r# f' }7 S* O6 ~
with CPP. The gonadotropin levels in this disorder
' Y) h) c1 T  g; S; Y- eare suppressed to prepubertal levels and do not show( G# k/ w% x$ a5 M! t2 Q4 I& R! S
pubertal response of gonadotropin after gonadotropin-0 U8 o9 F0 F* K4 ~: v2 P
releasing hormone stimulation. This is a sex-linked
9 ~( V: C1 G! Q7 a* f' Z  Kautosomal dominant disorder that affects only
4 q8 S  X, w0 Z1 l0 X) \males; therefore, other male members of the family
, H$ L3 \( r8 m! B- k6 l0 G: E; cmay have similar precocious puberty.3' q5 A, U$ H# i7 r2 \
In our patient, physical examination was incon-. A3 G1 R; ]% Z5 s' q
sistent with true precocious puberty since his testi-- E5 w  ]1 I* s3 M
cles were prepubertal in size. However, testotoxicosis
5 t1 d- Q7 [8 |$ Pwas in the differential diagnosis because his father
" G0 d4 a! V' k9 \- Nstarted puberty somewhat early, and occasionally,
* r/ p4 K3 s( p  s) v. Itesticular enlargement is not that evident in the  q$ J8 e, R) Y5 p
beginning of this process.1 In the absence of a neg-' j$ c2 q- Y7 i& G
ative initial history of androgen exposure, our- p! y! M: l' E. ?# W" b, a
biggest concern was virilizing adrenal hyperplasia,- G" b  E) Y8 @
either 21-hydroxylase deficiency or 11-β hydroxylase3 I' ~" z) h5 A& P. _+ E  S
deficiency. Those diagnoses were excluded by find-
/ t/ C8 j8 B  x4 j" Q' ?! p* [ing the normal level of adrenal steroids.
" o7 j) W3 p" J  E' e0 GThe diagnosis of exogenous androgens was strongly
, Z0 @" P# ?# Y7 Ssuspected in a follow-up visit after 4 months because8 _0 `" R- v% k" o- W* b8 l0 Y
the physical examination revealed the complete disap-
0 o0 R& J6 v8 C- n7 ipearance of pubic hair, normal growth velocity, and3 g* ^5 Y& H  b
decreased erections. The father admitted using a testos-- k& Y& Y, z5 y0 c* e+ x
terone gel, which he concealed at first visit. He was( j* ~' h( y. b/ @* A! Y
using it rather frequently, twice a day. The Physicians’& |# C8 j; q* ~0 J9 q
Desk Reference, or package insert of this product, gel or
5 \' M# s+ Q8 w1 G! U0 Dcream, cautions about dermal testosterone transfer to
' @. L4 D& _1 ~. Z9 _5 F9 Runprotected females through direct skin exposure.
( k+ w! u# P. _) g4 mSerum testosterone level was found to be 2 times the! Y/ O5 m4 k* R* T; g9 Y; j3 X2 x
baseline value in those females who were exposed to8 X# M- x; `! G! k" q
even 15 minutes of direct skin contact with their male
3 e. U1 C1 `% U1 qpartners.6 However, when a shirt covered the applica-
% D6 K( l. T* O& Ption site, this testosterone transfer was prevented.3 @: h, A, V- w$ ?+ ~3 \
Our patient’s testosterone level was 60 ng/mL,
/ u6 m6 V; j% O2 ^# J5 e  gwhich was clearly high. Some studies suggest that
5 w; P+ y  \/ c, \& b: s8 kdermal conversion of testosterone to dihydrotestos-
; _/ `1 F8 ?+ N& j. c) Jterone, which is a more potent metabolite, is more
! h. E* |4 c2 X+ i! o! ?) S' K+ D) Aactive in young children exposed to testosterone
9 I3 S/ e3 A( fexogenously7; however, we did not measure a dihy-* L! |. Q' x. O
drotestosterone level in our patient. In addition to7 ?: K( O( ]; D) [# z, G+ m
virilization, exposure to exogenous testosterone in  d% L. J- P( H4 H/ f' ?5 n; P# r
children results in an increase in growth velocity and$ m: r: B7 i% F* O* m$ E& s
advanced bone age, as seen in our patient.
3 \0 v6 Z' i0 ^The long-term effect of androgen exposure during
" Y& Z% z# n# @% y& Hearly childhood on pubertal development and final
9 Q+ |- U) X, radult height are not fully known and always remain; h% `/ J6 r* @/ _6 }
a concern. Children treated with short-term testos-/ n6 p$ w" E$ k! A$ G, Q
terone injection or topical androgen may exhibit some
+ G8 g: z- ^$ g' _1 O4 f* o0 I; iacceleration of the skeletal maturation; however, after
2 z; C0 {4 E; s- ocessation of treatment, the rate of bone maturation( M/ m; c: r4 [6 ~! d
decelerates and gradually returns to normal.8,9
: H$ [# ^  o& T, x8 Y5 cThere are conflicting reports and controversy
$ o+ s* p* z8 x* ~! uover the effect of early androgen exposure on adult% j' s6 y$ a' |! ?
penile length.10,11 Some reports suggest subnormal7 x: ?" m1 N! b, B8 E
adult penile length, apparently because of downreg-
: y  P! S8 `7 ~* ]4 x: }* ^ulation of androgen receptor number.10,12 However,
9 `* `- R! i0 z; FSutherland et al13 did not find a correlation between
8 o) @0 I+ _' f7 D) E1 o3 `childhood testosterone exposure and reduced adult) t' l, j, {4 e/ W+ u. g! x0 g
penile length in clinical studies.
! g/ P  G- Z7 v$ I0 F9 aNonetheless, we do not believe our patient is2 j( {# O" Q  O$ m! q* t
going to experience any of the untoward effects from8 W0 Y/ ?1 s6 n
testosterone exposure as mentioned earlier because
( F, L& @0 ^# n0 dthe exposure was not for a prolonged period of time.
4 b7 X9 i$ b- N3 E0 Q# n$ qAlthough the bone age was advanced at the time of5 n& w1 v6 V1 ]+ A: g
diagnosis, the child had a normal growth velocity at' e4 G/ c0 f$ e# @2 n/ R; `
the follow-up visit. It is hoped that his final adult
5 ?5 s8 j' q# a8 T6 `# gheight will not be affected.( }7 q' R: n- b
Although rarely reported, the widespread avail-
4 F; N8 B/ G9 q: j3 @ability of androgen products in our society may
- Q& k; Z; e. T2 u7 g( g% ~indeed cause more virilization in male or female: d0 m4 E4 L; `# @. b' v# c+ W- |
children than one would realize. Exposure to andro-0 f0 f" {, R2 Q7 F* ]3 g
gen products must be considered and specific ques-
0 c8 d1 y! j; T. b9 htioning about the use of a testosterone product or
: [0 ^7 p0 P5 A8 P4 D3 D  ]) t6 Xgel should be asked of the family members during
% c& l1 b9 M! J" h; K+ _: Sthe evaluation of any children who present with vir-; v9 T9 O  M1 E7 x; B( r& i
ilization or peripheral precocious puberty. The diag-7 g7 N4 A$ L9 s2 G
nosis can be established by just a few tests and by- A, D' t+ b, A, P& [- t0 Y* g9 P
appropriate history. The inability to obtain such a  K' i! O3 X1 O( q  W. W5 j
history, or failure to ask the specific questions, may
5 q' p( {7 S0 \; \" b) U5 o" wresult in extensive, unnecessary, and expensive+ c: ~8 [# m' W' k; I" V
investigation. The primary care physician should be
+ Q* a7 l3 j! I; y0 u6 kaware of this fact, because most of these children/ Q2 V5 V# K% J2 W" E
may initially present in their practice. The Physicians’! l( Y0 D9 V8 _1 l8 U+ a: c" d8 h
Desk Reference and package insert should also put a& F& I2 @1 H1 ^7 n
warning about the virilizing effect on a male or  K3 q" }2 w1 o& h
female child who might come in contact with some-: l6 p. b, L" o1 g1 P
one using any of these products.% {  d8 j: Q- a5 ]; U( T
References
3 V6 x5 z  G9 c1. Styne DM. The testes: disorder of sexual differentiation" F$ \1 h. b4 b/ Y% \
and puberty in the male. In: Sperling MA, ed. Pediatric! f8 ]* Z: b! l! B8 Y
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;- w1 N9 K5 j  k$ o
2002: 565-628.7 \, Y% q, J) X3 N' m7 S
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: m+ p# H. s3 O9 `. U" }+ u. Y  upuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old: H' Y$ p) o1 H/ I2 b8 v
Boy Induced by Indirect Topical
8 u: i6 l( h/ _8 v& bExposure to Testosterone7 H, [; c" `! P/ {' f5 j
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
% B) Y9 j8 L, O# fand Kenneth R. Rettig, MD11 O; ?3 {0 Z+ [9 U4 b# E
Clinical Pediatrics
. ^  x$ B  _* v. @Volume 46 Number 6" m. l) t2 C. @( J: L  l; u7 S! `
July 2007 540-543( m5 B( e" f$ l7 U
© 2007 Sage Publications
8 D4 Q, z* t+ e1 ?# l10.1177/0009922806296651
, k* Z$ w9 ?) Q; q! j# ?http://clp.sagepub.com, A& x6 V+ G$ b) h6 g
hosted at
; r6 b0 i* Z5 ?% A& m, P2 G( whttp://online.sagepub.com) x" A5 A$ m2 x4 ?9 y  x+ H; _
Precocious puberty in boys, central or peripheral,8 T. U8 z7 _% o+ o' f
is a significant concern for physicians. Central( r- {' H: l; u2 c
precocious puberty (CPP), which is mediated. M* F6 v* L/ F
through the hypothalamic pituitary gonadal axis, has, t6 X  U) x/ d% x( X8 N
a higher incidence of organic central nervous system% `: Z8 W, v2 O; N( Q2 S
lesions in boys.1,2 Virilization in boys, as manifested
, O$ `5 l/ O0 K, t0 Xby enlargement of the penis, development of pubic
' Z$ Y% h( q4 p5 ehair, and facial acne without enlargement of testi-8 L( m" v% Y/ i! h4 Q% N* x
cles, suggests peripheral or pseudopuberty.1-3 We
, f$ a! C2 }1 U% N$ J* N  Creport a 16-month-old boy who presented with the
3 A: L2 S5 K6 ?7 B# u- R( D% Y, senlargement of the phallus and pubic hair develop-0 k$ q5 ~+ u$ s, V  O
ment without testicular enlargement, which was due
1 W0 M' j& G# b6 N9 n9 v5 n: Xto the unintentional exposure to androgen gel used by
, B! }' w4 V+ M; K$ A2 Gthe father. The family initially concealed this infor-
! z" a1 y4 v/ |. E: S- \% I2 ymation, resulting in an extensive work-up for this3 _% M; g/ K5 k5 B" i6 r
child. Given the widespread and easy availability of- V7 @$ J& H% e( I. X8 A
testosterone gel and cream, we believe this is proba-
. G$ S/ Y) q! a) z1 b  hbly more common than the rare case report in the1 I( @& p; `6 b3 K% J4 `
literature.4
3 M$ x4 I- i/ j7 S7 r% HPatient Report
4 T& d8 m- _9 w1 YA 16-month-old white child was referred to the
4 d( t# q9 H& F4 Mendocrine clinic by his pediatrician with the concern
$ v8 S. e9 G; f, ?8 R8 G' p' Nof early sexual development. His mother noticed
6 B& I9 S( A6 [  O6 ^# Glight colored pubic hair development when he was& T9 s: A# b/ Q' M
From the 1Division of Pediatric Endocrinology, 2University of0 j- `7 Y- ?: v' a4 d. B
South Alabama Medical Center, Mobile, Alabama.
2 z# d7 @& `" D+ ]8 |# Z0 M1 jAddress correspondence to: Samar K. Bhowmick, MD, FACE,; j! t8 g4 i5 E% W' y4 ]
Professor of Pediatrics, University of South Alabama, College of
* ^% q' B0 T8 ~' R  |0 ~5 f. VMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
+ ~( W: u, w. a8 S+ y# le-mail: [email protected].4 M, _# a5 ^# }" x+ s. u
about 6 to 7 months old, which progressively became( G$ j/ K9 f; o8 [) B6 q& @
darker. She was also concerned about the enlarge-7 k! T; g+ t( Y: z( k
ment of his penis and frequent erections. The child5 z% s& T: A" d! C8 u9 t
was the product of a full-term normal delivery, with
7 Z7 a# `+ n, j0 Qa birth weight of 7 lb 14 oz, and birth length of
# C2 ^( x% Q0 b4 c0 ~20 inches. He was breast-fed throughout the first year' e4 W9 ^' n( F. `# @
of life and was still receiving breast milk along with0 J% H1 s" |6 p/ _; C
solid food. He had no hospitalizations or surgery,
" Z6 s) y" r8 K, n! Band his psychosocial and psychomotor development
' q) y5 ~$ E3 `' i8 m9 ~was age appropriate.. f1 q- [, ?0 L8 X- @/ ~, H1 D4 Z, b/ h
The family history was remarkable for the father,- H# u$ D1 O; B0 V6 u
who was diagnosed with hypothyroidism at age 16,8 E1 N& k: b; d/ N( P
which was treated with thyroxine. The father’s
8 w5 \$ {2 h3 xheight was 6 feet, and he went through a somewhat
- B5 h) C# `) G) L7 s( f# learly puberty and had stopped growing by age 14." _4 m0 }/ x* {* R2 n6 A
The father denied taking any other medication. The
, {- F$ |; N5 `& G8 Y( w# i+ ychild’s mother was in good health. Her menarche  M' V; |9 x1 c/ ^/ J
was at 11 years of age, and her height was at 5 feet8 y" W7 a8 H; S- [/ t$ h2 _
5 inches. There was no other family history of pre-( K3 S* O- I( u5 U
cocious sexual development in the first-degree rela-! A7 m  B5 R. c) L1 T; T3 P5 f/ ]
tives. There were no siblings.
' f! T9 V; B$ Y; g& bPhysical Examination
; E. K5 W+ @& r) j- A' w9 wThe physical examination revealed a very active,2 L& s2 p9 V8 z0 Z" F+ M. h
playful, and healthy boy. The vital signs documented
# G" P+ b( R  k/ c+ Fa blood pressure of 85/50 mm Hg, his length was* r; s: [- `: H3 @' `
90 cm (>97th percentile), and his weight was 14.4 kg
" Z* t/ H2 @+ f0 V0 H' c(also >97th percentile). The observed yearly growth
4 y4 b' B' k( O& i/ r8 Kvelocity was 30 cm (12 inches). The examination of& f. W6 u5 Y+ n5 X6 h
the neck revealed no thyroid enlargement.% e0 L7 c. n* Y# p! ]& s, S5 G
The genitourinary examination was remarkable for: V# P6 Q. [+ T7 A: u7 S3 I# S
enlargement of the penis, with a stretched length of
% Z% r' H2 _+ q' {4 v% O) E8 cm and a width of 2 cm. The glans penis was very well1 M6 X, m6 I1 k6 q9 J! @0 z6 ]
developed. The pubic hair was Tanner II, mostly around. v4 D4 J6 s$ P; i# `, D( o
5403 e& z" h2 F6 z  {& K. W
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from: }3 s  _7 k3 T9 [' T
the base of the phallus and was dark and curled. The
$ Q$ c. B) Z; |7 R& }1 l3 @# Stesticular volume was prepubertal at 2 mL each.
! \4 S  ]5 b# U( n: `1 }4 N0 ]5 U/ J; V1 FThe skin was moist and smooth and somewhat* J+ L( \) N3 a; y
oily. No axillary hair was noted. There were no& n# e! J% C  L8 \6 \" L- `) Z
abnormal skin pigmentations or café-au-lait spots.
! B4 A7 j+ p" {* ENeurologic evaluation showed deep tendon reflex 2+
9 g, c! B$ W% C  Gbilateral and symmetrical. There was no suggestion$ k  z4 F! u6 B0 E, \+ I
of papilledema.
) o& b6 ~2 ]" B7 P* g* zLaboratory Evaluation+ }% s3 o0 S$ U9 n9 x. t: ]9 f6 g$ L
The bone age was consistent with 28 months by
) ~) s2 \* V" ^2 f* R; t. Dusing the standard of Greulich and Pyle at a chrono-/ l0 r+ q/ `5 T5 f+ p
logic age of 16 months (advanced).5 Chromosomal
% l: A0 y$ k4 {( U/ F6 akaryotype was 46XY. The thyroid function test
2 A8 K; s+ M# S/ h3 v) }showed a free T4 of 1.69 ng/dL, and thyroid stimu-) l" `1 Q9 R; a2 n1 K
lating hormone level was 1.3 µIU/mL (both normal).6 B& C: W7 n8 ]3 O8 l
The concentrations of serum electrolytes, blood
' x9 {( j. q, T2 B4 f( A2 Surea nitrogen, creatinine, and calcium all were
$ j; q4 c" ]) F4 _0 C3 zwithin normal range for his age. The concentration
# Y2 Q4 K, Y3 e# {of serum 17-hydroxyprogesterone was 16 ng/dL
0 K( n+ U4 h* s/ p" {0 L& W# b(normal, 3 to 90 ng/dL), androstenedione was 205 S8 }9 M5 c, Q; x5 [, L) w, h
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-. o) Z* i6 H8 |; T3 p
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
* Y, p7 ?8 x% Sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to4 @  [. N2 ~6 Q* k" f+ @
49ng/dL), 11-desoxycortisol (specific compound S)2 O+ b5 I3 u5 O. }3 `
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
, l; G3 T, @% F* c0 Wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total, A* i( I  Q1 S9 F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),) e3 w, a- o) C4 z$ M& q
and β-human chorionic gonadotropin was less than* [- v' E( B8 c2 V
5 mIU/mL (normal <5 mIU/mL). Serum follicular" [( k+ }/ ?# O3 T. o  S
stimulating hormone and leuteinizing hormone8 I& ?7 r$ H( [4 {! i
concentrations were less than 0.05 mIU/mL
# t0 N9 a! ^/ \7 N- m9 |+ D1 B- V(prepubertal).
* X8 S, Z# S5 }  t+ M3 i! bThe parents were notified about the laboratory8 u/ t9 H- i: X6 d* n! o! H6 Q
results and were informed that all of the tests were& T7 H# ?4 l3 q# a1 j
normal except the testosterone level was high. The
- _3 b% I# k) E& s# C5 T6 i5 g2 vfollow-up visit was arranged within a few weeks to
6 P/ _' ~/ S4 A: x+ ^9 G& o1 x: Kobtain testicular and abdominal sonograms; how-
+ ~( Z2 j0 V" Vever, the family did not return for 4 months.$ U5 ]4 J- b8 n: G. S: p% G  d
Physical examination at this time revealed that the( ~6 W' P8 D0 `% g
child had grown 2.5 cm in 4 months and had gained
. b0 g. W4 r+ m, Y5 _6 e2 kg of weight. Physical examination remained
# t! L2 n* X  f/ @5 K! ^, ~( Vunchanged. Surprisingly, the pubic hair almost com-& z+ n- v/ a. t, I# E
pletely disappeared except for a few vellous hairs at
- j, y$ G& Y4 g5 y7 Dthe base of the phallus. Testicular volume was still 2. w3 w0 v, V& Y- @  Y
mL, and the size of the penis remained unchanged.% J! e! T- X% z' ~) T
The mother also said that the boy was no longer hav-
% A& J8 V: Q* [. ying frequent erections.
7 I) c' H3 s, Z3 T+ u" [Both parents were again questioned about use of6 w  Q- R0 B: [0 k/ \5 `1 \, ^
any ointment/creams that they may have applied to. `- k- W* \0 j" q. L) ]
the child’s skin. This time the father admitted the
5 g4 P; o' S6 ~) q% q. bTopical Testosterone Exposure / Bhowmick et al 541
: w# P8 Z, i& z- luse of testosterone gel twice daily that he was apply-! f8 h/ |8 U) |4 D0 O4 C
ing over his own shoulders, chest, and back area for, X! l, U0 F$ L  t* B% V
a year. The father also revealed he was embarrassed
' {* l$ d) s4 F9 g- U8 _7 fto disclose that he was using a testosterone gel pre-2 }( p/ T6 z$ ?; z0 \) A. \
scribed by his family physician for decreased libido- v8 Z+ B5 T% {2 Y
secondary to depression.
/ H, X% [) Z4 R2 eThe child slept in the same bed with parents.5 E( V5 |/ r% x' t' |/ ^: M
The father would hug the baby and hold him on his" q8 P2 A& y0 X+ h3 X
chest for a considerable period of time, causing sig-
4 t" R+ ~$ B) ^: a$ {* Anificant bare skin contact between baby and father.' `( @; }' ?7 Z4 t* z
The father also admitted that after the phone call,6 R/ s/ Z5 R/ ]4 g3 \, R( B7 Y
when he learned the testosterone level in the baby9 r. b  [( k5 Q0 t7 s2 v2 V
was high, he then read the product information  C1 f7 g# `+ [2 @
packet and concluded that it was most likely the rea-1 t8 e" n$ ]6 E) y$ t8 e# P* H
son for the child’s virilization. At that time, they
4 `* r) {- a5 M$ tdecided to put the baby in a separate bed, and the- i  z, j, j$ k" {1 G
father was not hugging him with bare skin and had
3 D* f. K3 G9 B: \8 n7 xbeen using protective clothing. A repeat testosterone4 E' `- k! j, E" w% w* D7 j( O
test was ordered, but the family did not go to the: |7 [7 C2 X( G' ?# a
laboratory to obtain the test.
6 t; X% d0 ^* g) M6 V' n0 }9 |" D$ s8 Y/ ZDiscussion
$ o) T% c" z( U9 J- @: T7 e& ^Precocious puberty in boys is defined as secondary
4 k2 D- F  Z0 y( O1 a# X( Fsexual development before 9 years of age.1,4
# {! K) H/ J  A8 l6 S9 {Precocious puberty is termed as central (true) when
6 d6 Y( Z7 {: u4 C: J$ Q' Oit is caused by the premature activation of hypo-
/ |% B! T& ~0 ^5 Z' D% X- ?8 Y& Ethalamic pituitary gonadal axis. CPP is more com-/ L  ~" x5 Z% Z9 i( e! F) \; f
mon in girls than in boys.1,3 Most boys with CPP& `# @, U, G$ a1 m! @0 n
may have a central nervous system lesion that is
. a4 i1 o' G& f6 {1 \responsible for the early activation of the hypothal-
' O5 q% ~+ h: g  s7 x8 _amic pituitary gonadal axis.1-3 Thus, greater empha-- r' G4 @( u7 u. r5 U' Q
sis has been given to neuroradiologic imaging in- b0 I2 L% s9 }3 e# D8 d
boys with precocious puberty. In addition to viril-1 W5 S/ R1 E) x) O: l6 S
ization, the clinical hallmark of CPP is the symmet-
5 U% p3 A5 w5 Arical testicular growth secondary to stimulation by
! p4 E2 v& b6 z9 vgonadotropins.1,3
# q3 t5 O4 x+ {. m2 B7 f$ vGonadotropin-independent peripheral preco-
( \9 U* |6 C! n! Hcious puberty in boys also results from inappropriate8 v+ K4 L% M$ f! R2 `6 z: X* f( l
androgenic stimulation from either endogenous or
/ b8 U( j2 G4 ?" G5 |exogenous sources, nonpituitary gonadotropin stim-
$ g! T% ]9 o+ b9 I# b. ]; Vulation, and rare activating mutations.3 Virilizing
! G5 M2 T% u! f8 \8 B0 G" G& h; @" Icongenital adrenal hyperplasia producing excessive
2 |1 t: |- S6 L5 h2 C2 Y% ^/ Kadrenal androgens is a common cause of precocious
4 c3 {5 w% F- c# z7 vpuberty in boys.3,4
: ^; z# J/ t8 u! s9 mThe most common form of congenital adrenal
* q9 V3 P- }" Y3 E/ rhyperplasia is the 21-hydroxylase enzyme deficiency.$ l1 \/ W; e; }+ n
The 11-β hydroxylase deficiency may also result in
+ L9 ]( \8 G9 O$ X0 Gexcessive adrenal androgen production, and rarely," e. O$ }- W; y4 ^1 x( r
an adrenal tumor may also cause adrenal androgen
- j" d( o/ I) o8 hexcess.1,3
7 z$ _# q/ z: T# n" G( Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ N) w0 W. D2 l) q
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& U8 U* [( W- [# fA unique entity of male-limited gonadotropin-' K0 X1 B/ ^8 e8 a
independent precocious puberty, which is also known: U2 q9 S' F6 j) G
as testotoxicosis, may cause precocious puberty at a
. b* h; j( Z: m. Gvery young age. The physical findings in these boys
; a1 P: F/ f0 I8 Twith this disorder are full pubertal development,
8 `7 ~8 W6 L+ G8 q9 b+ @/ Q8 H' Jincluding bilateral testicular growth, similar to boys
& P# ?7 C6 Y" swith CPP. The gonadotropin levels in this disorder9 E: p5 D+ p' D0 c
are suppressed to prepubertal levels and do not show- _& j+ _1 ^6 X3 M8 }( y
pubertal response of gonadotropin after gonadotropin-2 t" ^: l' L6 h5 v( {
releasing hormone stimulation. This is a sex-linked
! o3 E3 w! `/ r9 F3 Wautosomal dominant disorder that affects only
& j9 C) N& J& J+ C. Y( k; j* B, Jmales; therefore, other male members of the family# _0 s- S4 ]1 w1 V; k5 h5 m
may have similar precocious puberty.3  M* p* [  z1 \$ F
In our patient, physical examination was incon-
/ G1 l* h3 H! I7 _/ y8 Ysistent with true precocious puberty since his testi-
  i$ R. ~! b* ]5 M! @! jcles were prepubertal in size. However, testotoxicosis
# m4 T: O% Y, t( hwas in the differential diagnosis because his father0 K, K5 z# S5 ~" Q* e1 P; _8 Q
started puberty somewhat early, and occasionally,
( ^$ `* L. f; K: Ktesticular enlargement is not that evident in the( @3 A0 X0 X, `3 n
beginning of this process.1 In the absence of a neg-
: E# V& c' W% Q9 F! mative initial history of androgen exposure, our
5 a4 p) G: i1 ]. k7 k" xbiggest concern was virilizing adrenal hyperplasia,
. b# t& u0 W  G8 {6 h  U2 zeither 21-hydroxylase deficiency or 11-β hydroxylase( `7 z% j. g0 s% J" P( k& ?. d
deficiency. Those diagnoses were excluded by find-
" d3 z/ _) U6 ^ing the normal level of adrenal steroids.
$ Z" F0 \. G2 Z+ Z; V7 l1 p# b7 eThe diagnosis of exogenous androgens was strongly
& z! j+ R! t4 ?suspected in a follow-up visit after 4 months because" N2 U9 F; t3 H! Q  e  C. U
the physical examination revealed the complete disap-
( z9 {4 A) d* N7 [9 ^/ g# p3 ipearance of pubic hair, normal growth velocity, and
& }6 N& s  d; Pdecreased erections. The father admitted using a testos-
* d. _. y9 f! K* Eterone gel, which he concealed at first visit. He was1 V( x# }8 [% u, E" B$ |% b2 b
using it rather frequently, twice a day. The Physicians’( ~! Z1 [* d# M8 G# \: y  @: m
Desk Reference, or package insert of this product, gel or+ ^5 v) L6 \- S" @0 Q* p; `: t3 C* X
cream, cautions about dermal testosterone transfer to
3 m  F# b: C# d( t' \3 dunprotected females through direct skin exposure.
% _, }# v; ~! j! j; G+ u4 PSerum testosterone level was found to be 2 times the) Q) ?* W, ~! R# L; G
baseline value in those females who were exposed to2 J9 t- u7 C8 H) Z6 C, d# \
even 15 minutes of direct skin contact with their male# F9 Y$ d* G2 v& M% Y# ]: O
partners.6 However, when a shirt covered the applica-
+ M" `( @0 G' G8 |4 ?1 _tion site, this testosterone transfer was prevented.$ W3 _9 @3 |9 u4 U6 W( e
Our patient’s testosterone level was 60 ng/mL,
5 m% E6 q+ X. l8 K1 N3 g' o0 T6 owhich was clearly high. Some studies suggest that. [3 @% e9 i2 B: X4 d4 I9 O4 N
dermal conversion of testosterone to dihydrotestos-
6 m$ C5 r4 U' n1 }terone, which is a more potent metabolite, is more3 P4 o5 P' q2 \9 R) a
active in young children exposed to testosterone4 |5 x2 T  L0 W# M& d: f
exogenously7; however, we did not measure a dihy-
3 L3 I. U& f, s! K# e: I) Q7 Vdrotestosterone level in our patient. In addition to
* _2 B: P5 }0 e8 c6 E# S5 w% Xvirilization, exposure to exogenous testosterone in( ]! A& A+ O/ n: m, {3 g- y
children results in an increase in growth velocity and4 F1 G( [3 j4 `: t: y8 U/ j
advanced bone age, as seen in our patient.
  \( Y: t$ {) xThe long-term effect of androgen exposure during
& `! R5 O; @. pearly childhood on pubertal development and final: A. h) \0 f0 I! }) Y- T+ X
adult height are not fully known and always remain: c1 w1 _# K0 e2 b. P3 \
a concern. Children treated with short-term testos-
* L; Y# O8 ]6 e" [; m/ kterone injection or topical androgen may exhibit some
6 ]5 Y, H2 G8 D8 a9 C; l: l/ E3 V! vacceleration of the skeletal maturation; however, after& F4 U2 i8 ~9 P! S7 S
cessation of treatment, the rate of bone maturation7 k3 @  [% e9 K1 k4 ]% [
decelerates and gradually returns to normal.8,9
, z" r' ?# Z( |& G) d% rThere are conflicting reports and controversy6 [* `4 P) W% d9 l# [. X
over the effect of early androgen exposure on adult
: h, O( v* g4 A5 E3 L3 Z1 X: wpenile length.10,11 Some reports suggest subnormal2 M/ \. `  @5 o* i
adult penile length, apparently because of downreg-
0 {" [. q$ q& w  u; Q0 \6 tulation of androgen receptor number.10,12 However,' N2 O- o0 Y, N* B0 m3 A& h
Sutherland et al13 did not find a correlation between9 V' D" k( r3 D- u4 x# i
childhood testosterone exposure and reduced adult$ C0 w" y& C& Z: f* ?+ }6 k- w0 y/ ]
penile length in clinical studies.) u' O. ?  O, k# W7 S5 m
Nonetheless, we do not believe our patient is
' B# p/ @' q1 j! a) Hgoing to experience any of the untoward effects from" }- ?0 ]: u4 O0 f
testosterone exposure as mentioned earlier because, `" @# ?( ^5 j( z7 o
the exposure was not for a prolonged period of time.! r) |2 O% J" Q7 f0 D, f& s
Although the bone age was advanced at the time of# t8 w4 t$ Q- v) n( Y8 U/ E
diagnosis, the child had a normal growth velocity at, N# j, a" L9 X* b) V3 z
the follow-up visit. It is hoped that his final adult+ U6 o3 w1 L+ o7 z2 }; {4 v
height will not be affected.
# z7 n$ M% r9 g' q: _9 U4 mAlthough rarely reported, the widespread avail-  i5 K4 I/ c; g/ b* Q: r, _
ability of androgen products in our society may
7 H- h% i' ^- R8 {6 h- x- \( Uindeed cause more virilization in male or female% d3 m& |% }2 s* {8 _$ K7 P
children than one would realize. Exposure to andro-
4 k4 ]! B/ i5 O# @) h+ Ngen products must be considered and specific ques-* Q  [. A8 M" E9 ?
tioning about the use of a testosterone product or6 O* u9 F# K2 a  x# l9 f
gel should be asked of the family members during: o$ c# d) L3 I
the evaluation of any children who present with vir-: O1 `) y' b/ g  a; U6 d- [
ilization or peripheral precocious puberty. The diag-
3 G! q9 m: P8 W# S9 E' _; hnosis can be established by just a few tests and by  `# Y" j% ^2 u7 _
appropriate history. The inability to obtain such a
. [5 }6 ]2 D7 w* H, Ohistory, or failure to ask the specific questions, may
( v" |, o- u) S! ^- m) tresult in extensive, unnecessary, and expensive9 _+ C& e" m0 J( H
investigation. The primary care physician should be
! x6 P7 W  x" s+ faware of this fact, because most of these children
, |- |7 J9 C' ]; d0 _; Imay initially present in their practice. The Physicians’' x2 M  X% Q; I& I6 k" m
Desk Reference and package insert should also put a
2 t8 h0 ~! k% M3 ^. Ewarning about the virilizing effect on a male or
+ E3 Y6 I0 V! }/ L. W1 Ufemale child who might come in contact with some-
; P, v0 y% s; V% s9 Q4 M" Aone using any of these products.. Y) b/ u0 O- m% U' @0 z/ t2 y
References
+ N2 t. F8 h- u3 E8 b1. Styne DM. The testes: disorder of sexual differentiation1 U0 v9 B3 n: i# C. J
and puberty in the male. In: Sperling MA, ed. Pediatric5 I" `, M4 c: n- Q# |
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  z6 h- `/ B2 i' L9 C* i2002: 565-628.
" q9 C, V% d( E8 \" U2 e0 Y* D5 y2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
: [& L$ C7 M; O/ ~% _5 jpuberty 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
; O9 ~: X: W, _: e/ I& |0 B
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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