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Sexual Precocity in a 16-Month-Old
3 S: H- {9 q' i6 R/ _Boy Induced by Indirect Topical
8 q4 }$ q9 i. L0 }' ^6 HExposure to Testosterone
7 H2 j. ?8 g$ L: LSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
) A( o$ x/ x% J* b- h% Q' m5 nand Kenneth R. Rettig, MD1
) @! {2 p0 A6 w2 k( {" T( MClinical Pediatrics  Y) X6 l$ F2 u# B
Volume 46 Number 6
" r# k- D3 {- q: |- A) }  qJuly 2007 540-543) E4 F5 j' m( N1 N( w' d
© 2007 Sage Publications
& M# R* @) F  n5 L0 h10.1177/00099228062966510 [6 F; Z7 z4 O% V+ \
http://clp.sagepub.com* e8 F0 K% {! z; S# L3 v; l) q
hosted at# A+ Y+ k0 `9 |. k
http://online.sagepub.com8 c0 T4 e) {5 E1 i! E6 G6 v
Precocious puberty in boys, central or peripheral,- q9 C) C8 ~0 I& q. _: ~
is a significant concern for physicians. Central% O$ C+ s/ o0 u
precocious puberty (CPP), which is mediated
% \% F4 G& G; V  J" K$ j' Rthrough the hypothalamic pituitary gonadal axis, has0 \$ m# V* k% P+ Z
a higher incidence of organic central nervous system
( }; r1 b' A4 n" hlesions in boys.1,2 Virilization in boys, as manifested: p* a- j4 W6 M# L+ N6 O
by enlargement of the penis, development of pubic4 w- A$ C- Z; L) ?( H
hair, and facial acne without enlargement of testi-- x) Q4 `) k4 ?. P; a- [
cles, suggests peripheral or pseudopuberty.1-3 We$ e3 N) P, Q. k) K* `
report a 16-month-old boy who presented with the8 B; ?+ x/ w4 {& @0 Z, @% @
enlargement of the phallus and pubic hair develop-
1 @; \6 Q8 ]# H; c3 \* D$ P5 C# zment without testicular enlargement, which was due
7 d! H1 M! j. q8 |to the unintentional exposure to androgen gel used by
6 e/ i3 ^" `  g2 T  H+ k. G$ _the father. The family initially concealed this infor-- t8 ?5 F. [/ C) |
mation, resulting in an extensive work-up for this8 |9 {% W9 y* a3 x1 C' H* P6 g. G
child. Given the widespread and easy availability of
& T5 w1 \1 `$ Ptestosterone gel and cream, we believe this is proba-
: G5 }+ {8 c) L, k" @# N; zbly more common than the rare case report in the1 v; Y. v4 s0 _. k" Q: d% d
literature.4
8 E7 u: Y: e1 m: K4 UPatient Report
' h& k+ O5 F/ S, eA 16-month-old white child was referred to the
# j! P% I' H5 i2 o7 g. s8 J: jendocrine clinic by his pediatrician with the concern6 \- F! c8 E. F* O3 S  N9 Q
of early sexual development. His mother noticed
$ Z4 E6 @# ~0 ^$ ^$ Klight colored pubic hair development when he was
' g+ I( E0 t0 V% P" pFrom the 1Division of Pediatric Endocrinology, 2University of$ ]5 j( n0 y7 u3 t- ^/ T' E
South Alabama Medical Center, Mobile, Alabama.
( g3 b3 t" O2 x0 v9 rAddress correspondence to: Samar K. Bhowmick, MD, FACE,  T' E: c; t/ ]2 ^8 f; [
Professor of Pediatrics, University of South Alabama, College of
5 l1 a* w) y3 z0 LMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. J7 Q/ {# Z8 F$ D
e-mail: [email protected].# s( e# t. b1 @$ t3 O/ n
about 6 to 7 months old, which progressively became
/ h* i/ H; @8 |! r  w* u7 h' xdarker. She was also concerned about the enlarge-
0 a) l2 K) J3 g2 s* Sment of his penis and frequent erections. The child
0 n' \+ ^, T3 A0 ?2 r8 Wwas the product of a full-term normal delivery, with
% E% z, a- P* i2 h. e$ ua birth weight of 7 lb 14 oz, and birth length of
( t' o( K2 \% P# ]0 j20 inches. He was breast-fed throughout the first year
8 B: L' A2 M3 [: d/ X3 pof life and was still receiving breast milk along with! M# g# d' v! _: ~! M# r3 {, `
solid food. He had no hospitalizations or surgery,
3 J) R  L# q- w( c$ f  Qand his psychosocial and psychomotor development
0 _0 x+ s9 j& I2 S$ Y* _5 c9 z  i# J, \was age appropriate.+ F- w" f3 w5 |4 e
The family history was remarkable for the father,# U7 t" j+ Y+ v2 F+ \9 M! a
who was diagnosed with hypothyroidism at age 16,
6 y; j9 U  a' N$ g5 zwhich was treated with thyroxine. The father’s  A" C* p8 t; k+ C6 p
height was 6 feet, and he went through a somewhat. f- S6 u; s+ I, l" s+ A
early puberty and had stopped growing by age 14.% ?; C/ Y6 |' I0 K4 i9 m
The father denied taking any other medication. The1 l" l& Q- Y  r' D& h& U2 U8 v0 ^, z
child’s mother was in good health. Her menarche3 G+ p  o* s+ n: l9 A/ ]: w1 K
was at 11 years of age, and her height was at 5 feet
+ A! e/ d: R+ z0 b, D# K5 inches. There was no other family history of pre-1 S3 q- x4 N2 o3 t
cocious sexual development in the first-degree rela-
% N3 |. C' x: |$ `& Ktives. There were no siblings.: U- S# ~, N7 u8 H" X( C1 Q
Physical Examination. J# Q, N! p# L4 |7 v2 o$ P" @
The physical examination revealed a very active,7 v5 X: s- @6 u4 ]& x% h1 l6 \
playful, and healthy boy. The vital signs documented" @% T. R& a  A. y* m+ Y9 g  N
a blood pressure of 85/50 mm Hg, his length was0 q: t4 j( F; j8 A- I
90 cm (>97th percentile), and his weight was 14.4 kg
3 G6 E7 q9 l% s; u1 B(also >97th percentile). The observed yearly growth5 A$ Z1 z& j* E5 v( ~" e6 a7 S4 z# Y
velocity was 30 cm (12 inches). The examination of4 l$ e& _# V& [$ o: H
the neck revealed no thyroid enlargement.
1 T  d# W% J$ d3 b- v2 K1 KThe genitourinary examination was remarkable for
7 M, {  k" a' e* ~) oenlargement of the penis, with a stretched length of
# v4 T3 }% ~/ w) ~# Q8 cm and a width of 2 cm. The glans penis was very well
* c& C3 q1 t3 S- i; [: `developed. The pubic hair was Tanner II, mostly around
: L) d3 l' `" y. X540/ @3 G; I" f$ ]; r' ^
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ @9 f( v1 t( Y3 C% f% H; ^the base of the phallus and was dark and curled. The
: k/ h' K/ W4 V* f. ntesticular volume was prepubertal at 2 mL each.
$ A% {# k6 d+ R1 n% N. w! r4 QThe skin was moist and smooth and somewhat
4 u5 b& a( D$ `+ Hoily. No axillary hair was noted. There were no' h" F' k  o: o4 Y5 e$ }" s
abnormal skin pigmentations or café-au-lait spots.+ |$ L3 G: l. ~  z8 S& T
Neurologic evaluation showed deep tendon reflex 2+
" D& ^. x8 I& \7 ebilateral and symmetrical. There was no suggestion' F: P3 h3 X: ^' d: e
of papilledema.
& h( l3 ]* I/ B- dLaboratory Evaluation
8 S( N/ F8 a& G( u$ M8 P8 `5 vThe bone age was consistent with 28 months by- b& ?+ v1 g! O7 Q( f  d
using the standard of Greulich and Pyle at a chrono-
+ l" [! W. l2 Y0 vlogic age of 16 months (advanced).5 Chromosomal5 C/ A( T1 `; T& U" H5 c0 b
karyotype was 46XY. The thyroid function test
7 z3 R# _$ W- d6 Y9 x4 Eshowed a free T4 of 1.69 ng/dL, and thyroid stimu-) D( x( ]! r. g( y4 M* [3 _1 y) k
lating hormone level was 1.3 µIU/mL (both normal).' D7 \& d. d# v" z+ i7 K
The concentrations of serum electrolytes, blood4 w; M& G3 G; {' B! a7 c, I( L
urea nitrogen, creatinine, and calcium all were) S1 b7 h4 @# i. g, X* b4 \/ D
within normal range for his age. The concentration
; S. l* p4 X! u5 W! J. Nof serum 17-hydroxyprogesterone was 16 ng/dL
8 C5 ?" v0 \5 R: Q6 K" m) R(normal, 3 to 90 ng/dL), androstenedione was 20* @* `% k* g$ u1 [) p' }
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
' I; [( |5 ]) j1 U" {9 iterone was 38 ng/dL (normal, 50 to 760 ng/dL),
: ]! ?7 b9 l# N7 F0 rdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
( ^+ S* n+ m* w% I49ng/dL), 11-desoxycortisol (specific compound S)
7 O' r& x8 M, L- C1 ~! a9 kwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
; u% L' R( x8 M; T, c2 b% Rtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total$ ^2 l  x( {4 ?
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),8 p2 A; R5 d, I+ b
and β-human chorionic gonadotropin was less than; `; e: }! F+ n) s. R0 c
5 mIU/mL (normal <5 mIU/mL). Serum follicular
: j1 e5 ]3 }! V& M( fstimulating hormone and leuteinizing hormone0 p2 @# u+ O' u) ~2 X! ]
concentrations were less than 0.05 mIU/mL
1 C( X5 y& D" X( J0 J. E(prepubertal).4 o+ D/ `5 S+ n' N7 `2 @
The parents were notified about the laboratory3 V( K4 l1 q2 ?! o, Q& I
results and were informed that all of the tests were
9 Z6 H& I9 v8 c( |0 Lnormal except the testosterone level was high. The8 z; y% Y! w% U
follow-up visit was arranged within a few weeks to
- R" ]* v+ x6 Wobtain testicular and abdominal sonograms; how-
1 E* M! [* j; i8 Never, the family did not return for 4 months.9 m7 p1 h) i: y
Physical examination at this time revealed that the
2 D: s. \) H# K( h! G/ z/ kchild had grown 2.5 cm in 4 months and had gained; v. G" Z/ \8 O9 d* R
2 kg of weight. Physical examination remained
, J- Z1 j; R4 Z& Z$ \3 I5 r% Hunchanged. Surprisingly, the pubic hair almost com-0 K0 H' L( W/ L
pletely disappeared except for a few vellous hairs at
3 W4 N5 i8 _" u% g* Gthe base of the phallus. Testicular volume was still 28 c( ?0 }& W% S' A" ]
mL, and the size of the penis remained unchanged.
; e" k7 ?6 @/ e, L2 R5 |The mother also said that the boy was no longer hav-
6 F$ [. Z, K' s0 Ning frequent erections.; {3 `. `6 l( [- f! q# A/ {6 m7 b
Both parents were again questioned about use of; j$ t4 l6 o& O/ h2 Z8 Y9 r
any ointment/creams that they may have applied to; n4 X- ^) F" a6 j1 A' [8 ?6 p
the child’s skin. This time the father admitted the
, X% T1 r6 ]$ A7 nTopical Testosterone Exposure / Bhowmick et al 541
) ?, f) E) q% \+ Wuse of testosterone gel twice daily that he was apply-6 n2 a/ G- T. l# p2 j
ing over his own shoulders, chest, and back area for
; c- p( v( v# k6 h) _  Q- {a year. The father also revealed he was embarrassed' n- M5 I, ]" i9 ?
to disclose that he was using a testosterone gel pre-" `& H9 N: [7 g1 M
scribed by his family physician for decreased libido
( e4 F- |  e2 i# Y' y5 r+ esecondary to depression.9 _0 @& A8 a/ k+ v0 f4 ~% p' Y
The child slept in the same bed with parents.5 Q( [& g2 p7 W) }( u0 n
The father would hug the baby and hold him on his
& [& O$ H4 J6 B/ S& hchest for a considerable period of time, causing sig-) t2 l; S1 ~# q
nificant bare skin contact between baby and father.4 y' Y+ i8 F! F( `# _
The father also admitted that after the phone call,
6 l$ S9 o3 F. U1 awhen he learned the testosterone level in the baby  H* ]9 K4 }& Y5 U0 c- g) n1 S
was high, he then read the product information! h( J0 m! }4 x# y. n; G
packet and concluded that it was most likely the rea-
5 A& n% ^& K) V: y/ uson for the child’s virilization. At that time, they
. C4 B! A' |5 }decided to put the baby in a separate bed, and the4 t6 I$ o; h: o; W" K
father was not hugging him with bare skin and had8 x5 w# i( l8 w" B5 F0 A
been using protective clothing. A repeat testosterone" i3 w1 R; |# y4 Y+ z& S* q
test was ordered, but the family did not go to the
7 o; H2 x1 R; A9 p5 V- tlaboratory to obtain the test.
) }) ]! V* a( z3 b1 A  h9 wDiscussion5 R5 d4 \% d, L8 E( o
Precocious puberty in boys is defined as secondary
5 ], ^' E6 d3 n4 Fsexual development before 9 years of age.1,44 K2 N7 q4 i6 c5 p8 b; g
Precocious puberty is termed as central (true) when
$ Y! c. Z6 R' i5 K& C0 ?( |; Jit is caused by the premature activation of hypo-7 V$ X4 i' y% H' f+ \* I) W- w/ e6 i
thalamic pituitary gonadal axis. CPP is more com-
4 y3 O7 h. J5 M7 {" {$ wmon in girls than in boys.1,3 Most boys with CPP/ t) F  K* A; t2 w' v! J! m. c6 j
may have a central nervous system lesion that is7 r2 F' l0 W% y( L
responsible for the early activation of the hypothal-  R4 b" `8 c, z/ W* W, T
amic pituitary gonadal axis.1-3 Thus, greater empha-
4 y3 D) H$ M7 J" Bsis has been given to neuroradiologic imaging in! a+ s! F9 d7 R! T. _
boys with precocious puberty. In addition to viril-" i8 V% `' m# f2 i$ F, C& |1 p
ization, the clinical hallmark of CPP is the symmet-
( y* ]; i9 O; q- P6 m% hrical testicular growth secondary to stimulation by( ]: T, h0 N2 I: O4 b$ n; ^
gonadotropins.1,3
* i0 A' z$ v6 _5 e) E% `Gonadotropin-independent peripheral preco-
- T; l% p: ^* I( t; d" B6 ncious puberty in boys also results from inappropriate+ n7 B3 F7 n$ _: {0 m/ f; e
androgenic stimulation from either endogenous or
3 {6 m( b2 v) o4 }+ bexogenous sources, nonpituitary gonadotropin stim-
9 m: k. w/ x. _' W  u1 k' dulation, and rare activating mutations.3 Virilizing
9 [7 z; K6 v& T- {) `9 D: Icongenital adrenal hyperplasia producing excessive
8 d. K3 X0 H3 O1 s0 padrenal androgens is a common cause of precocious# k& F0 H+ H* l  d& K4 _
puberty in boys.3,4
7 v, \2 N$ t5 N, x( ?/ bThe most common form of congenital adrenal
6 P" M& o0 G2 T0 p3 d: Uhyperplasia is the 21-hydroxylase enzyme deficiency.6 s+ F1 K9 J  f0 ?: z  V$ Q
The 11-β hydroxylase deficiency may also result in  i3 ]& V& ?% o7 d+ B1 ~$ d
excessive adrenal androgen production, and rarely,
3 m  Z* \7 A/ x7 ?6 M+ X1 Oan adrenal tumor may also cause adrenal androgen9 J. X7 p6 q3 A: Y/ W
excess.1,3' R, t- R) l1 N" R6 y
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! U0 T" S. A9 E+ U- j" J" z
542 Clinical Pediatrics / Vol. 46, No. 6, July 20074 B. m9 s. ]3 K" [
A unique entity of male-limited gonadotropin-
) v4 L" \7 H) B4 t7 {independent precocious puberty, which is also known
0 S2 m9 k) g9 ?as testotoxicosis, may cause precocious puberty at a# H# `  N4 n  f& R" W) p% h
very young age. The physical findings in these boys
/ S& Z! k4 y- J: b7 K3 i1 M* V3 rwith this disorder are full pubertal development,
) g7 J6 [! q) A2 kincluding bilateral testicular growth, similar to boys, n2 O! Z) o2 j8 T0 j' v' K- _
with CPP. The gonadotropin levels in this disorder
9 q! G, L3 R- c, K& zare suppressed to prepubertal levels and do not show
. a  x9 R* r! Y  Zpubertal response of gonadotropin after gonadotropin-
9 Z9 b8 P4 ]# ?2 O6 }releasing hormone stimulation. This is a sex-linked, y) X* w* `+ s! o
autosomal dominant disorder that affects only+ r5 A8 l$ h2 X) Z! l# [
males; therefore, other male members of the family1 H7 ]% N: L( }. i7 t' V' H7 P
may have similar precocious puberty.34 F# m, ]& i# {0 k
In our patient, physical examination was incon-
1 C1 N% J2 l, h- Y3 Hsistent with true precocious puberty since his testi-
' d1 y. h5 x% d  }cles were prepubertal in size. However, testotoxicosis1 D. L* }( Z  X" U& n+ K& H( x
was in the differential diagnosis because his father
# ?& k9 ~9 r9 M( o4 J  vstarted puberty somewhat early, and occasionally,5 z3 w( q0 `. f6 q& @3 j6 I9 q
testicular enlargement is not that evident in the4 o: b3 P! r6 i5 J5 z
beginning of this process.1 In the absence of a neg-
# T7 `- U' D  ?6 N: P; Yative initial history of androgen exposure, our2 F4 y! l7 t: }" ^# B! A( `! K; M0 e0 p
biggest concern was virilizing adrenal hyperplasia,
9 ?+ X6 V! y' {% teither 21-hydroxylase deficiency or 11-β hydroxylase$ |+ V9 f" Y5 a, [, t: ^& N3 L$ b1 @
deficiency. Those diagnoses were excluded by find-
# e2 t1 F" i# Y$ m' t4 K* T' c: n7 xing the normal level of adrenal steroids.
% a7 x* G% h, N  j; uThe diagnosis of exogenous androgens was strongly! R- e" ^* R4 N, M' R1 o/ C# a3 B3 E
suspected in a follow-up visit after 4 months because- {; M% m* X9 ^5 @
the physical examination revealed the complete disap-1 }! M' m9 F* k- D' D1 [
pearance of pubic hair, normal growth velocity, and
- a- f( Y! t5 Rdecreased erections. The father admitted using a testos-2 F; f6 ?4 V3 q: w
terone gel, which he concealed at first visit. He was
0 M0 U  N) u$ ?; ^6 vusing it rather frequently, twice a day. The Physicians’8 Q- {3 j. N4 m# U( [
Desk Reference, or package insert of this product, gel or" G) Q- @- \0 G: w8 J1 r* M
cream, cautions about dermal testosterone transfer to3 K" S; D3 U+ g( S" Q3 R
unprotected females through direct skin exposure./ r; i4 j. q- L% k9 c  E7 j
Serum testosterone level was found to be 2 times the! X: c/ N- @7 @% f: a8 E6 t0 a
baseline value in those females who were exposed to1 X7 X5 ?6 M+ f7 b
even 15 minutes of direct skin contact with their male
9 Y. R9 z3 g1 K) e. l+ H" v$ ?* @  j& ypartners.6 However, when a shirt covered the applica-' f: d+ @) S/ H3 V7 M" Q) l
tion site, this testosterone transfer was prevented.! q# H' M- k: W. o
Our patient’s testosterone level was 60 ng/mL,1 \/ P. v# m2 q
which was clearly high. Some studies suggest that
( n5 G: w  C+ C# ]. G5 I. ydermal conversion of testosterone to dihydrotestos-
; D- H( D2 i$ N- V* H& Fterone, which is a more potent metabolite, is more
0 J$ s0 d4 \1 z8 mactive in young children exposed to testosterone! y. ~/ S" E& M# S  F1 o; Y* p8 j
exogenously7; however, we did not measure a dihy-3 L8 X! w; z" c" U" L' Y
drotestosterone level in our patient. In addition to
) V0 [/ Q* {! Q$ U+ Rvirilization, exposure to exogenous testosterone in
5 v3 q) p5 k& pchildren results in an increase in growth velocity and$ r7 e9 `! F9 Q' g  h6 v
advanced bone age, as seen in our patient.+ f; u6 P  {0 ]. m7 X) G& e# s& O
The long-term effect of androgen exposure during
" ?5 x3 P3 x/ j8 h0 f3 Kearly childhood on pubertal development and final& Q( q; v* I$ {, l" _7 I  K- G
adult height are not fully known and always remain" G& v5 M& I0 P
a concern. Children treated with short-term testos-
" c3 [2 W. G+ n3 C1 c5 x3 H6 ~8 t# cterone injection or topical androgen may exhibit some  j! d' z1 |0 Z
acceleration of the skeletal maturation; however, after
4 L4 }* I& l: ^' {% E3 H8 v# |cessation of treatment, the rate of bone maturation
+ d! k- I! P  K! d; H/ Ydecelerates and gradually returns to normal.8,9
5 R: c4 p. k+ S7 h( @There are conflicting reports and controversy/ z, y( t% Z2 R2 u: a9 a& A
over the effect of early androgen exposure on adult
$ @/ v& b6 N* T( s, Q5 apenile length.10,11 Some reports suggest subnormal9 Y$ O  O+ {0 G7 J
adult penile length, apparently because of downreg-1 d8 s( u; A1 |. h
ulation of androgen receptor number.10,12 However,( A& R* _5 V' W+ Y
Sutherland et al13 did not find a correlation between
% Z- o/ O4 k5 A: Z4 o5 t9 @! Bchildhood testosterone exposure and reduced adult3 l7 P: p' M( l7 I  y+ O& A1 G
penile length in clinical studies.: ?9 J* P+ W5 p1 U& c% i
Nonetheless, we do not believe our patient is
' \# `( b9 ~9 F) N8 c7 |6 u' Cgoing to experience any of the untoward effects from9 _7 k$ C7 o6 z+ ?) u. `/ ~$ Z+ q- P
testosterone exposure as mentioned earlier because
" k" P# n# X- qthe exposure was not for a prolonged period of time.% Q; |" m0 S9 Q* F6 ?0 }% ^5 a- W8 N
Although the bone age was advanced at the time of0 E! u2 d; q0 ^' @- y/ b: K
diagnosis, the child had a normal growth velocity at6 O2 g1 V4 Y1 M
the follow-up visit. It is hoped that his final adult
) u# K" q' z2 d& u& Z6 Jheight will not be affected.* q6 h- m6 [  D, d$ m
Although rarely reported, the widespread avail-+ ~& b, b& Y4 P( K1 _  P% T" r# i
ability of androgen products in our society may
, ~1 F3 }; y+ a$ a5 nindeed cause more virilization in male or female! e4 q' ~, W+ J0 @& F* }
children than one would realize. Exposure to andro-
$ R8 J8 ?5 S. P1 }4 }. Agen products must be considered and specific ques-
( Y) W3 L0 N0 Qtioning about the use of a testosterone product or
$ g2 t$ {" E& H! e" T) R* d3 l0 x3 W. @gel should be asked of the family members during
$ Y1 d! J# f. W/ K6 l  _5 Zthe evaluation of any children who present with vir-
' h. k6 _. H9 O9 G* W0 Cilization or peripheral precocious puberty. The diag-
) R  ^9 ^3 L% U3 ^# l- `nosis can be established by just a few tests and by+ X  p: l# Y2 b) j. B* W: B
appropriate history. The inability to obtain such a
: I/ G' X4 }5 l4 ~history, or failure to ask the specific questions, may5 u8 d6 q' {8 ^; |
result in extensive, unnecessary, and expensive
: s, U& a2 }9 finvestigation. The primary care physician should be5 X+ r/ j9 x/ P2 a) I4 O" {% a1 U
aware of this fact, because most of these children
% y- m. D  K: v- M  \may initially present in their practice. The Physicians’
! `; p+ T, o6 VDesk Reference and package insert should also put a
" x, L) m0 o# o1 j  U0 c2 u( Zwarning about the virilizing effect on a male or7 x. W5 {6 r, E; R/ Z1 u: p
female child who might come in contact with some-5 y2 R' g) _$ x1 z8 S3 @) S
one using any of these products.' w3 h: R- O2 E+ e& v
References
1 i7 C+ @& g6 [+ f& _1. Styne DM. The testes: disorder of sexual differentiation
5 w3 [" l! S4 _; P% Z8 L* ~and puberty in the male. In: Sperling MA, ed. Pediatric
- @) W5 A. o6 A! e8 N4 X% C) UEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;3 K/ U4 Z) K7 U1 B2 Z" s8 Q
2002: 565-628.
: J5 Y% Z. ~! y" a2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
% k7 U9 X3 [1 k( Mpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
; O6 ~9 O; Y# N% @  m# q+ VBoy Induced by Indirect Topical
9 _; ]: e, O: n  A. N- VExposure to Testosterone( z8 i& l0 v  X$ q; F7 ]
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
; ^& ]' y8 A+ V; c, z' T1 o: Pand Kenneth R. Rettig, MD10 S% x. Z3 ], S
Clinical Pediatrics- r% A9 N  S' V
Volume 46 Number 6
& D% J7 H6 ^3 R  T! YJuly 2007 540-5432 m  t  G% D. _# }, D
© 2007 Sage Publications
" y! D- L# ]3 }6 ]9 F4 ^10.1177/0009922806296651: ~, ^$ l) J/ l9 ~
http://clp.sagepub.com
" `' I, p. y* I' N  K. Jhosted at8 Z% \) [7 @  c* U; Q, i# Q
http://online.sagepub.com0 D  d! j' r) H' e- I9 b
Precocious puberty in boys, central or peripheral,1 b: N, I2 M. y
is a significant concern for physicians. Central2 r* B0 h  J! N
precocious puberty (CPP), which is mediated; R! @" X! x; }/ I4 n
through the hypothalamic pituitary gonadal axis, has6 I8 S( Y% N, g) t$ ?
a higher incidence of organic central nervous system
* b% Y* ?  o$ N& f: glesions in boys.1,2 Virilization in boys, as manifested
5 z* Q, q! o- X7 [3 gby enlargement of the penis, development of pubic$ ?) f7 `: S) S0 q
hair, and facial acne without enlargement of testi-, N/ ^1 V+ u; f  N& i& x
cles, suggests peripheral or pseudopuberty.1-3 We
& D) F5 {7 M# H+ A- a2 `& kreport a 16-month-old boy who presented with the( P9 l$ E: M- A( t9 L; ?
enlargement of the phallus and pubic hair develop-5 D9 v: [7 f" e+ ~
ment without testicular enlargement, which was due
# x+ m4 ]" S# Wto the unintentional exposure to androgen gel used by0 Y. p$ n! B9 s; n
the father. The family initially concealed this infor-- J2 ^; x. t6 j! q9 U# f1 d# r
mation, resulting in an extensive work-up for this; o) v9 i2 i8 F) e# C& Z" t- @3 `
child. Given the widespread and easy availability of
- u# {) x& H- z* m1 q6 h5 f& Ttestosterone gel and cream, we believe this is proba-* P6 u! _! y  ^# d2 U5 z! B
bly more common than the rare case report in the0 U. X* W9 Y4 t' d: k
literature.4
/ Z3 q; R* E8 k" n  N- _* a' q. C. hPatient Report
+ w9 e% ~" n! g$ L( o: }A 16-month-old white child was referred to the( q8 {$ y, `$ t. O
endocrine clinic by his pediatrician with the concern0 Y" t, h# X3 |4 O1 z
of early sexual development. His mother noticed
# w9 A" T: I1 P# P! Y- clight colored pubic hair development when he was2 x- r2 Z3 s  u+ K# u; q
From the 1Division of Pediatric Endocrinology, 2University of
" l7 I; i# e/ s0 ^South Alabama Medical Center, Mobile, Alabama.
( T7 R. V  i' f1 K: [Address correspondence to: Samar K. Bhowmick, MD, FACE,
' l9 }1 b! J- H* pProfessor of Pediatrics, University of South Alabama, College of
* T% o, o! S; Q, k0 M( ^' q, qMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
" U0 I2 [6 a' he-mail: [email protected].# g. |* z8 m+ @: u$ R0 M- F  j0 [
about 6 to 7 months old, which progressively became
' _) D/ f5 F( ~+ odarker. She was also concerned about the enlarge-
4 A  {! v! a+ I/ R# Nment of his penis and frequent erections. The child, t+ `! h5 d* H/ _
was the product of a full-term normal delivery, with8 T/ z0 \) ~, u% O
a birth weight of 7 lb 14 oz, and birth length of
. Y' z8 N$ V, i5 ^0 ]20 inches. He was breast-fed throughout the first year9 }0 u- x" k+ }  P
of life and was still receiving breast milk along with+ a: j" z8 x! I) V4 r1 Z
solid food. He had no hospitalizations or surgery,1 }0 a5 U# w" N0 ], ^4 y
and his psychosocial and psychomotor development
* k8 U$ o+ t2 A' i$ d1 S8 ~' pwas age appropriate.4 g5 ^$ N% R# z) C0 M
The family history was remarkable for the father,
/ `+ Z! N. H3 d  K, {who was diagnosed with hypothyroidism at age 16,8 w( X+ t2 j$ u1 @/ _1 y
which was treated with thyroxine. The father’s
* E  ~( K9 t: p1 Z2 ?; _height was 6 feet, and he went through a somewhat6 P6 N) v0 G! h; e6 b
early puberty and had stopped growing by age 14.
# v, S! y9 J$ M. p" ]& ^The father denied taking any other medication. The
$ d; o2 ^' r: s  E& H7 O: a  ~! ]. }2 mchild’s mother was in good health. Her menarche, ^/ g& x4 _& G- Y) G
was at 11 years of age, and her height was at 5 feet, ~; S) _  S0 j. E! v6 v" d
5 inches. There was no other family history of pre-6 W7 O- T% m$ }
cocious sexual development in the first-degree rela-  a7 }. M" U" R9 ?8 t5 V
tives. There were no siblings.
3 d9 z% Y0 H3 ]3 u$ d- yPhysical Examination
+ }: C0 \9 C% {/ U; bThe physical examination revealed a very active,+ |0 b% f2 J! s! F5 W1 l0 a1 S
playful, and healthy boy. The vital signs documented5 x3 X& H- Z* l$ d- ?( Q
a blood pressure of 85/50 mm Hg, his length was
7 V1 v1 D/ J% J' H1 g; h90 cm (>97th percentile), and his weight was 14.4 kg" a5 |) E) `- W4 a
(also >97th percentile). The observed yearly growth
8 G1 p5 H4 g  L+ ~# Wvelocity was 30 cm (12 inches). The examination of5 Y: C0 `  t5 e& n
the neck revealed no thyroid enlargement., `2 w0 j% _; F& D8 \
The genitourinary examination was remarkable for9 ~5 ~' y0 `& \( N4 ?- o0 }1 G8 S
enlargement of the penis, with a stretched length of5 ~- [* F$ c1 [/ h9 i9 R/ s
8 cm and a width of 2 cm. The glans penis was very well$ T- V8 ^2 c; [# Y( {: \
developed. The pubic hair was Tanner II, mostly around
8 `" _. z7 Y& R6 p( N540
3 Q9 `9 S( ]* z. C, K: _& z5 Y* [0 D6 Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 k8 `% j* h& w+ P$ R, d+ nthe base of the phallus and was dark and curled. The- W: b% g; p- h, W& `* s# k$ E+ K
testicular volume was prepubertal at 2 mL each.- c; O8 H$ R8 I; {: @6 d
The skin was moist and smooth and somewhat
/ M2 O/ e) {( N' h' H+ x  R! moily. No axillary hair was noted. There were no
) u( w4 j" j; d, r! v0 N' babnormal skin pigmentations or café-au-lait spots.
: c( P3 R2 a" U% `- uNeurologic evaluation showed deep tendon reflex 2+
: P/ E. V7 a* U- b6 g; O/ E1 ?bilateral and symmetrical. There was no suggestion
' x- Z: W- E" H' M9 r4 `: ]  ?$ Hof papilledema.
7 }' u8 L0 ^" B5 M, |- @& TLaboratory Evaluation
7 V  `( V! }7 I* d) Y* i! NThe bone age was consistent with 28 months by
) d# j: w# e: u& |% j0 Zusing the standard of Greulich and Pyle at a chrono-
$ c+ S  x" W1 [6 e" m+ V; @logic age of 16 months (advanced).5 Chromosomal" r8 \5 `4 a) Q
karyotype was 46XY. The thyroid function test4 @! h+ u# Z/ N  J5 K) |0 ~9 I
showed a free T4 of 1.69 ng/dL, and thyroid stimu-9 L4 d* s( O/ R) B) x/ `6 Q) w
lating hormone level was 1.3 µIU/mL (both normal).
& Y) m5 z% t" `2 C% eThe concentrations of serum electrolytes, blood# U, _. |- E: z! w
urea nitrogen, creatinine, and calcium all were% E/ p: x6 q4 \9 t! g
within normal range for his age. The concentration
! N+ E/ X+ s, X1 [: c7 ?, Gof serum 17-hydroxyprogesterone was 16 ng/dL: G; I! a9 }  l0 y
(normal, 3 to 90 ng/dL), androstenedione was 20
' z. [$ v; K  I) B9 fng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
0 m' i6 D+ `. @: }; i* X+ N: Mterone was 38 ng/dL (normal, 50 to 760 ng/dL),
/ O6 u# N  R% t- Q4 w# sdesoxycorticosterone was 4.3 ng/dL (normal, 7 to/ q0 Y3 Q6 B( m
49ng/dL), 11-desoxycortisol (specific compound S)8 m9 j8 W  E) V: R# W
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) P0 j1 A. ?2 K- Z% P  L
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total- C3 T, w8 Z$ w/ F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! B( z6 W1 z* {+ v4 vand β-human chorionic gonadotropin was less than
7 @5 ?; _+ s  }& x* ^# E5 mIU/mL (normal <5 mIU/mL). Serum follicular
# X, c: q. Q# r- N" K) ostimulating hormone and leuteinizing hormone3 B. j+ B4 n" N( j4 z+ I7 @6 K, P3 C
concentrations were less than 0.05 mIU/mL
% A" N- G+ R9 j+ l2 I1 H(prepubertal).
" T+ f5 ^" g7 d$ xThe parents were notified about the laboratory
. g! K& ]- r4 f! S2 N$ Aresults and were informed that all of the tests were
* O, l' h3 h' z% k4 Onormal except the testosterone level was high. The
  Y0 h% G# e9 T$ T) bfollow-up visit was arranged within a few weeks to
+ Y3 G9 N8 Q# ]  Fobtain testicular and abdominal sonograms; how-
+ N; j7 n; b2 J$ o: z! z" Tever, the family did not return for 4 months.
4 q. J2 z" W6 B. t3 }0 M, @. xPhysical examination at this time revealed that the
: Z9 _3 k% H9 \6 [: t, _4 [child had grown 2.5 cm in 4 months and had gained
8 b% z$ W: b* b  k1 P2 kg of weight. Physical examination remained9 O  E3 b4 t3 E3 q4 M7 ?8 ^9 {
unchanged. Surprisingly, the pubic hair almost com-
+ f9 a+ D4 e- u- p: p* [pletely disappeared except for a few vellous hairs at
6 S7 b1 K4 j/ A' y+ _the base of the phallus. Testicular volume was still 2
6 T/ K' W7 c( z; ]1 y$ V; vmL, and the size of the penis remained unchanged.  q; D5 |( y8 o& ]( ]
The mother also said that the boy was no longer hav-
* m# t  ]" e2 _; O- sing frequent erections.4 e: B' [" A+ \3 s0 _, ~
Both parents were again questioned about use of
  I# ]2 |8 [8 [. A2 b5 Y2 d  b+ oany ointment/creams that they may have applied to5 _6 U# u' n* b6 ~3 t. B
the child’s skin. This time the father admitted the
( G* C# L0 P& w6 d1 g; dTopical Testosterone Exposure / Bhowmick et al 541* d- V8 X, \- v. p
use of testosterone gel twice daily that he was apply-3 [$ x1 e/ Q5 p4 h% ~
ing over his own shoulders, chest, and back area for
7 h! H* e' h5 A" d6 A& P# B# a/ aa year. The father also revealed he was embarrassed
9 O1 J! d" _1 F& Zto disclose that he was using a testosterone gel pre-0 L, D( u6 F5 L
scribed by his family physician for decreased libido
$ l! Y$ c' s+ ^$ i1 ysecondary to depression.
# E) B4 c' ?  B* @; n# PThe child slept in the same bed with parents.
( B6 K% g& Q' V8 \3 ^! e8 LThe father would hug the baby and hold him on his* G- _3 m7 m  p6 Q
chest for a considerable period of time, causing sig-
" z+ J0 Q; M0 T9 ~nificant bare skin contact between baby and father.
5 w+ b4 p( A. P: N& KThe father also admitted that after the phone call,* c# w6 K( w: C" u4 D7 `
when he learned the testosterone level in the baby
7 M" y( ?* z) M( R& uwas high, he then read the product information
+ o/ F+ ^0 M- X" ]packet and concluded that it was most likely the rea-) ~7 D; R7 h. Z0 S) B# D" l
son for the child’s virilization. At that time, they
8 u1 [& b5 w9 a& T2 ]decided to put the baby in a separate bed, and the  m. A. T- l% M( s) w: ~
father was not hugging him with bare skin and had
( M0 }) }7 H) v4 b4 S+ {; wbeen using protective clothing. A repeat testosterone  y! s* l: Q, ?0 U
test was ordered, but the family did not go to the
3 q! r+ J9 p" ?2 C& j6 R' Mlaboratory to obtain the test.
+ s1 }$ q2 q% M1 e% k! rDiscussion
5 S0 z, W* W% _- F% E' LPrecocious puberty in boys is defined as secondary
: W; j5 J: y9 e7 k6 |. X2 S( ?sexual development before 9 years of age.1,4" L! S. A# p' _1 G: t( M# r# p
Precocious puberty is termed as central (true) when" r. D0 K$ C+ W5 B/ x- T
it is caused by the premature activation of hypo-; x2 T# o0 t3 s/ Z3 S' O
thalamic pituitary gonadal axis. CPP is more com-% E7 n* U5 W. x$ M" k. }; e. {
mon in girls than in boys.1,3 Most boys with CPP
; W$ n- q0 d( [, q) y/ hmay have a central nervous system lesion that is
" u  A0 N6 F' P, zresponsible for the early activation of the hypothal-; }( z( @* o4 Y/ ]& o) G
amic pituitary gonadal axis.1-3 Thus, greater empha-$ L6 g8 Q2 l* W5 v* E. O
sis has been given to neuroradiologic imaging in7 K  O2 V3 @1 m- t/ E; N7 T
boys with precocious puberty. In addition to viril-4 l' ]/ G& i! N* l
ization, the clinical hallmark of CPP is the symmet-
3 ~0 a( |( `/ C% ~rical testicular growth secondary to stimulation by
; K) M; T  m- B' m- E$ igonadotropins.1,3, l$ y4 i2 @' R, P9 k# r
Gonadotropin-independent peripheral preco-% H% E5 m7 _0 W) g2 q; q; F
cious puberty in boys also results from inappropriate# o/ i% v- L0 [- _4 @5 d% z
androgenic stimulation from either endogenous or
% f5 H. u# G4 N9 p* Gexogenous sources, nonpituitary gonadotropin stim-
, \7 C$ T0 [- j) bulation, and rare activating mutations.3 Virilizing- o; B. b5 F; P4 V6 j0 j$ `  z" P
congenital adrenal hyperplasia producing excessive' c/ }& L! P; \( i
adrenal androgens is a common cause of precocious( \( N; ~/ C# i# j0 W- h
puberty in boys.3,4
" [8 b+ s, p2 a9 a9 bThe most common form of congenital adrenal
! D) [7 C- t/ v# _+ Z8 w9 ]hyperplasia is the 21-hydroxylase enzyme deficiency.
; f* P. H* U( SThe 11-β hydroxylase deficiency may also result in/ \1 V7 U" e0 V! j2 l' ]
excessive adrenal androgen production, and rarely,: Q1 x+ S" H( V( Y( D" S+ y. i
an adrenal tumor may also cause adrenal androgen, x5 U! X' `8 g
excess.1,3
0 f/ c. w" r, L7 E" iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
4 Y9 ~6 I/ A: g6 y- d1 f7 Q: ]542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
6 S; l: x  p7 q' K5 n! XA unique entity of male-limited gonadotropin-1 e3 p1 K# m' n5 [& _
independent precocious puberty, which is also known/ [$ o# \1 d4 p0 O4 ]" X8 h
as testotoxicosis, may cause precocious puberty at a  k& H# O' t9 x" Q3 \: E2 R
very young age. The physical findings in these boys
1 u% g% Z) n) ]$ j' {6 u3 N* Ywith this disorder are full pubertal development,) P1 p: e  M' e) w+ ~6 Y
including bilateral testicular growth, similar to boys
6 C  m* l# z6 ?& @, E0 i5 s/ uwith CPP. The gonadotropin levels in this disorder& }0 _4 G5 b( k. B
are suppressed to prepubertal levels and do not show- @7 k; G! ]' A& R5 B
pubertal response of gonadotropin after gonadotropin-  J1 H0 ]; K2 B1 c3 j7 N/ e
releasing hormone stimulation. This is a sex-linked1 E$ c+ \) U* T" G
autosomal dominant disorder that affects only+ R/ v0 C6 }7 m' q5 ~, W3 s5 z
males; therefore, other male members of the family
# }) J$ G, ]: U! h- qmay have similar precocious puberty.3
" k+ k& U( p' B3 \: M  `/ Y* iIn our patient, physical examination was incon-8 B5 N) a, c; z, ]; W  N* T
sistent with true precocious puberty since his testi-1 q  s( G6 |9 i4 G/ X
cles were prepubertal in size. However, testotoxicosis
1 B9 J/ P- C, H$ r( A2 `( Bwas in the differential diagnosis because his father
/ l2 j3 f6 g! a3 M6 T7 `1 q5 S' d. o" }started puberty somewhat early, and occasionally,$ G) F9 N3 f3 a
testicular enlargement is not that evident in the* e9 y4 G3 B* V& Y$ L3 ~
beginning of this process.1 In the absence of a neg-
" ^* @" b& t( ]% Q1 c% Y* fative initial history of androgen exposure, our5 q' ?: A9 q" k+ c+ w/ i" l$ e0 s
biggest concern was virilizing adrenal hyperplasia,; D: D; _3 |" _0 H* v
either 21-hydroxylase deficiency or 11-β hydroxylase
2 y& O# S9 t  [  g2 rdeficiency. Those diagnoses were excluded by find-
) W/ c) Q/ E% M  hing the normal level of adrenal steroids.( B+ Y+ J- v+ w5 U; H% @
The diagnosis of exogenous androgens was strongly) C& {' p, r; D. g& j# y4 _' r7 B
suspected in a follow-up visit after 4 months because
2 k6 _* x4 i6 u1 O4 @the physical examination revealed the complete disap-: p* s! b- i+ j) W2 p
pearance of pubic hair, normal growth velocity, and& \& q2 |; _9 z- k6 v
decreased erections. The father admitted using a testos-
: r  L% |9 C6 s. k. ~7 Nterone gel, which he concealed at first visit. He was/ J+ v, ^' t( w$ l) {# G" W
using it rather frequently, twice a day. The Physicians’1 c$ L: I5 W* G5 y9 }
Desk Reference, or package insert of this product, gel or. c* Z2 i/ g" B6 l: A8 M( H5 P8 K
cream, cautions about dermal testosterone transfer to& w' a: J' k6 b+ a- F) F; e
unprotected females through direct skin exposure./ ]* s( C! z8 `
Serum testosterone level was found to be 2 times the1 c# F/ A' s1 L' ^
baseline value in those females who were exposed to( ?0 F* o1 [0 a: T1 }% j
even 15 minutes of direct skin contact with their male
1 u) p1 M' N: q) F% l) V" B2 Bpartners.6 However, when a shirt covered the applica-
& ]  w, e6 x# [, X2 v1 Ttion site, this testosterone transfer was prevented.
2 f; }+ q- O$ ^" X5 I$ O5 [Our patient’s testosterone level was 60 ng/mL,4 u5 v: A0 u9 N2 v* f; u0 c! g2 b
which was clearly high. Some studies suggest that( d3 n. w5 c9 b9 C' P
dermal conversion of testosterone to dihydrotestos-+ I" O# P* [* |# d( f1 J
terone, which is a more potent metabolite, is more9 p0 T1 {$ E; Q2 ?( v/ P
active in young children exposed to testosterone5 _9 k0 C2 r& ~* d
exogenously7; however, we did not measure a dihy-6 f8 V4 ~9 [$ k$ w  w
drotestosterone level in our patient. In addition to
- C* t+ w, o% Y& ^. Hvirilization, exposure to exogenous testosterone in
7 y1 |% R* H/ b3 K) b* K$ Ychildren results in an increase in growth velocity and' ~% O! s, i' W3 ~% Q/ P
advanced bone age, as seen in our patient., V; ?& i3 G+ w4 W) Y  M' v: G4 R
The long-term effect of androgen exposure during
6 ~+ B6 ?$ i- ~2 h% C% p7 \- S! A( Qearly childhood on pubertal development and final
! w* b2 x$ L2 ~7 {0 r  ?( {+ }adult height are not fully known and always remain& J) ^- @" U4 h" q% s% t6 Y
a concern. Children treated with short-term testos-
, D) }! v% R6 z0 b: ~- |terone injection or topical androgen may exhibit some
7 s/ r& I2 l) S4 D2 Y) w: o  u  yacceleration of the skeletal maturation; however, after
( A: ]7 S- ]) z! D$ q$ \( acessation of treatment, the rate of bone maturation2 ^9 Z/ u6 {* R' C1 L. `
decelerates and gradually returns to normal.8,96 z$ ~8 S$ |6 `% T, c  D7 C8 L
There are conflicting reports and controversy
- u8 U: H( {, C2 @over the effect of early androgen exposure on adult
4 j  ~, r- N* A9 f* Jpenile length.10,11 Some reports suggest subnormal5 T( P  g( v& z5 c# y1 v' T: d
adult penile length, apparently because of downreg-
# E  |6 ?$ Z# M# a/ H3 d% ]ulation of androgen receptor number.10,12 However,+ T. p" j8 [. O1 |/ |- r
Sutherland et al13 did not find a correlation between
2 D( {/ a! x: {9 G3 ochildhood testosterone exposure and reduced adult
: B7 e- a9 w; |7 o6 i6 L. Q! U! Apenile length in clinical studies.& f* z( \! N1 Z! ]
Nonetheless, we do not believe our patient is
) Q4 U5 H" ~" `going to experience any of the untoward effects from
( o! A5 Q% W6 c# e# y8 n, f1 Ktestosterone exposure as mentioned earlier because  t2 u: U, E/ z2 w4 @& a6 K; H- j
the exposure was not for a prolonged period of time.
9 w* g& ?" o$ V+ DAlthough the bone age was advanced at the time of( N4 w, ~, \4 ]
diagnosis, the child had a normal growth velocity at
7 ~! F" \' w0 ^/ a8 l6 Xthe follow-up visit. It is hoped that his final adult, l/ {9 U: W8 o; `. k5 i7 ~
height will not be affected.' i  l1 \, h% a' H) h* q  a5 S, r
Although rarely reported, the widespread avail-4 d9 ]' j7 R1 }% ]
ability of androgen products in our society may
* B" M6 i6 [' d# u% y* Z- K; Eindeed cause more virilization in male or female% y  ?: I) T8 b$ U1 r4 u8 H
children than one would realize. Exposure to andro-$ ?* r; ^/ E5 x
gen products must be considered and specific ques-
# L1 S) [4 ?0 D- e# a; f2 Wtioning about the use of a testosterone product or
" W# [! H4 D. Y- r! Ygel should be asked of the family members during' ^: q) `( c# f! q
the evaluation of any children who present with vir-
& k* |* F" x6 Q- ?: M" V9 Pilization or peripheral precocious puberty. The diag-
  c# b5 c+ _9 v! q2 C1 W9 D2 h8 qnosis can be established by just a few tests and by7 {$ }: A" d1 r) N1 m8 x$ \
appropriate history. The inability to obtain such a8 n  p. z" J$ a# i$ @4 |
history, or failure to ask the specific questions, may
4 G2 r( }0 E/ r- k0 @& ~result in extensive, unnecessary, and expensive
/ V2 C( u; D1 a  G4 r. l5 u% {investigation. The primary care physician should be
* }9 l  |' c0 e( A, saware of this fact, because most of these children, O5 @( g% }. D( x, O& O' i1 a
may initially present in their practice. The Physicians’
! o" }' q8 {+ ~# t2 fDesk Reference and package insert should also put a8 e* q  K4 r3 s/ }4 p# k
warning about the virilizing effect on a male or& n( O! E% U( g3 n
female child who might come in contact with some-
4 U, |1 o, O6 _one using any of these products.
& g$ W0 }2 v6 U$ j% g# wReferences$ p8 W+ C* p" O) u
1. Styne DM. The testes: disorder of sexual differentiation. ^. q2 j+ `3 I* e$ O7 \' C9 c: ~
and puberty in the male. In: Sperling MA, ed. Pediatric4 Q* J& s% H# f2 h1 C5 z4 {
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
* C0 v4 r8 o% ]3 p8 h! M* B2002: 565-628.
. M  i- v/ p1 G3 V2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
1 U, Q+ {  k: g- Spuberty 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

! k9 E( q- h! \% C) 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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