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Sexual Precocity in a 16-Month-Old
# T( s) |+ {8 I: wBoy Induced by Indirect Topical
  s5 o% H2 J8 m  \Exposure to Testosterone* M. L- F# C( n' N
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
2 T) L  m* I! _( |and Kenneth R. Rettig, MD1
9 F8 Q" n5 K5 B2 _/ D/ cClinical Pediatrics
, f. Z/ P. _' [Volume 46 Number 6
$ r8 B  E# y- ]. E1 BJuly 2007 540-543
5 k8 P- J! R; N5 C' M% q& D8 N© 2007 Sage Publications0 [0 ]9 H( |" @% K
10.1177/0009922806296651% n( K3 z. E  U
http://clp.sagepub.com
% B  w& m0 T5 _5 C6 Q5 h2 \hosted at/ E. S7 M9 }) s8 M
http://online.sagepub.com
( H9 a9 y8 L4 O8 }2 n" ?" zPrecocious puberty in boys, central or peripheral,; n1 z- T% c  Y1 f1 b1 G8 Q" K
is a significant concern for physicians. Central" w- l4 s; G/ V% X/ |( ?  A, v
precocious puberty (CPP), which is mediated7 A+ g/ p5 s  c4 L; ?# c( Z4 u
through the hypothalamic pituitary gonadal axis, has! W8 H7 J- K! s
a higher incidence of organic central nervous system
) A( ^1 _: ^" m- A9 z( C& ^/ O1 hlesions in boys.1,2 Virilization in boys, as manifested. M, ]4 p* ?0 a& u
by enlargement of the penis, development of pubic
; d: R  k/ Y7 A( B7 dhair, and facial acne without enlargement of testi-2 i0 W! `/ o+ A9 w
cles, suggests peripheral or pseudopuberty.1-3 We
2 C9 F6 g/ j0 B' x" W4 e$ D% qreport a 16-month-old boy who presented with the
( T3 J0 X& V6 [1 B1 ]* penlargement of the phallus and pubic hair develop-
; Y9 C: u  p# w6 s0 ement without testicular enlargement, which was due
8 i7 R7 N& [3 \to the unintentional exposure to androgen gel used by
- x! Q0 ^* V' h" _, e7 Tthe father. The family initially concealed this infor-
! C+ c: m8 f9 Y1 cmation, resulting in an extensive work-up for this& T" R7 W0 {2 p8 s* n
child. Given the widespread and easy availability of
. w' S5 i1 G+ ]testosterone gel and cream, we believe this is proba-
( R6 c, G3 q% M0 Q& B" b( Lbly more common than the rare case report in the
6 e1 ]% ?: a( F, `+ |8 ]8 d8 Lliterature.4
7 Y- j, _: @; [" q5 U5 i3 ?Patient Report
7 X+ _4 ^4 `; C- B' K# w8 J! w3 w+ {A 16-month-old white child was referred to the) i4 F( f# j5 g' O
endocrine clinic by his pediatrician with the concern4 C* z$ F2 g5 ~# ^5 y5 y( W7 S
of early sexual development. His mother noticed- h: m9 f3 c( F' v% ^
light colored pubic hair development when he was3 @) A* e8 v8 U& l9 U" D
From the 1Division of Pediatric Endocrinology, 2University of
2 h8 a! ~; G  R( R' }& B% ^South Alabama Medical Center, Mobile, Alabama.
0 q5 J' g( T5 \% I) z0 i* k9 Y8 @Address correspondence to: Samar K. Bhowmick, MD, FACE,
! K! O1 Y* I$ f( qProfessor of Pediatrics, University of South Alabama, College of: [  |& e* Q9 |: |
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 t% T6 Z. t; m
e-mail: [email protected].3 @/ U# Z9 ~2 r# A0 x! q
about 6 to 7 months old, which progressively became$ i! k& l# J+ A
darker. She was also concerned about the enlarge-1 Y) v( B- [6 S8 J# j
ment of his penis and frequent erections. The child$ o" r! S5 y8 ^/ i5 ?3 W
was the product of a full-term normal delivery, with# X$ T1 }4 T( Q1 r
a birth weight of 7 lb 14 oz, and birth length of
1 Q2 F: Y3 A- f, Z6 n  k20 inches. He was breast-fed throughout the first year" R; g3 q/ N( k) a
of life and was still receiving breast milk along with
' P3 m# ^0 K9 P, p; msolid food. He had no hospitalizations or surgery,
& n2 I; P' }- t; K$ {and his psychosocial and psychomotor development1 s7 q4 a# J9 {7 e! z' H3 z; W3 m
was age appropriate.7 m) [: v; a/ c" H3 p7 ]
The family history was remarkable for the father,1 g) p9 e  P' n$ q  y* l
who was diagnosed with hypothyroidism at age 16,
% Y, Z/ U2 K" f& c( ]which was treated with thyroxine. The father’s) U7 G2 ~! o# D! j( d. ?9 U
height was 6 feet, and he went through a somewhat1 J& r& \  k8 @( O
early puberty and had stopped growing by age 14.0 q7 P5 x/ P7 L
The father denied taking any other medication. The5 N0 }3 p( |. f# [5 X
child’s mother was in good health. Her menarche
# E# M! m" T9 M3 D* S, x& Vwas at 11 years of age, and her height was at 5 feet+ z0 }9 Y( @! E8 `$ |3 F6 `3 t
5 inches. There was no other family history of pre-
4 n( Q+ s3 B/ Q; e2 @8 o! x% X# `cocious sexual development in the first-degree rela-) e+ I( Y9 t$ w) }) J& ], H3 w
tives. There were no siblings.
8 J9 U1 b) K* w' G) F7 ~- VPhysical Examination' i7 s. N' `6 z6 V/ f' Q% `' i) f
The physical examination revealed a very active,
( [5 K9 o' ^/ Lplayful, and healthy boy. The vital signs documented; V. y* F5 m4 Y# [9 }* R, o
a blood pressure of 85/50 mm Hg, his length was
0 U5 q: X1 M* {90 cm (>97th percentile), and his weight was 14.4 kg' i$ r; I4 v, m' R8 a/ r8 S
(also >97th percentile). The observed yearly growth
, ~8 o8 y% _; J7 nvelocity was 30 cm (12 inches). The examination of; b( t7 r, f4 x% L) k* A. B
the neck revealed no thyroid enlargement.9 I2 c0 a! R3 k- @+ B) v# e- B
The genitourinary examination was remarkable for
5 U" s/ F+ ^) f( j) h% Y& Fenlargement of the penis, with a stretched length of
% b1 b  _4 R% p% M' }) N3 ?8 p8 cm and a width of 2 cm. The glans penis was very well
- D, z& ~8 W, \# k6 G, |2 edeveloped. The pubic hair was Tanner II, mostly around
0 c. o0 Z1 F: C; A540
/ ^. M* r/ ?2 Pat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
+ h8 P8 [0 a9 I0 R! ^/ othe base of the phallus and was dark and curled. The
( T6 c, ]3 K6 V5 R0 N2 |testicular volume was prepubertal at 2 mL each.
) b" f2 G( {+ A/ @6 DThe skin was moist and smooth and somewhat
- @8 i' {/ c; U( ~' O4 Aoily. No axillary hair was noted. There were no
( [( V" K7 i- T" B0 R4 {1 ?abnormal skin pigmentations or café-au-lait spots.
+ }/ g* i9 g. A$ u, r1 I7 R/ }3 VNeurologic evaluation showed deep tendon reflex 2+! }7 k, ^0 b. ]1 s1 I
bilateral and symmetrical. There was no suggestion" |  b5 q) V6 |4 R  L4 A
of papilledema.
2 f: `" \* h4 p4 cLaboratory Evaluation
- F) t* ?5 t. g+ b! o, ~! L( oThe bone age was consistent with 28 months by
; g% Q) v* D. musing the standard of Greulich and Pyle at a chrono-
& O- a6 y& @+ n% ^" v" N2 P7 t  ^logic age of 16 months (advanced).5 Chromosomal$ \1 i; ~7 v& q3 F# W9 F$ ~2 A
karyotype was 46XY. The thyroid function test
( ^$ s: E* Y$ w/ C7 A$ sshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
9 g9 b$ H4 X: Z4 Plating hormone level was 1.3 µIU/mL (both normal).( {& }  @, g% A( o$ B: d5 `
The concentrations of serum electrolytes, blood
1 K) q2 Y  y! i! l% B8 Ourea nitrogen, creatinine, and calcium all were
9 R) K7 K7 K' z  b( H8 n3 k1 twithin normal range for his age. The concentration
. ]' r! O. b* o: }of serum 17-hydroxyprogesterone was 16 ng/dL' E; k  c5 H4 E+ f0 M
(normal, 3 to 90 ng/dL), androstenedione was 204 h& E4 g! F9 w# C
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
& t& B' G. V0 m! T- r' yterone was 38 ng/dL (normal, 50 to 760 ng/dL),
4 ?. }$ l7 ~9 [/ E+ `desoxycorticosterone was 4.3 ng/dL (normal, 7 to
1 [5 B5 T3 o$ W; v0 a7 k( y: E( V49ng/dL), 11-desoxycortisol (specific compound S)
$ ]$ {+ i9 Z  ]' f; {was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 f; Y+ D! j! v, @' ~# V! V) f( O+ c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total" k# R/ Z/ u0 d9 [! }! M; c& N
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ ]( k+ g1 [" b: m1 {) Kand β-human chorionic gonadotropin was less than# T7 r# K3 F2 F. Q$ z& n
5 mIU/mL (normal <5 mIU/mL). Serum follicular
; y4 v# b8 U9 o1 f' N: q7 [stimulating hormone and leuteinizing hormone
4 `1 `2 f2 @# tconcentrations were less than 0.05 mIU/mL) O& }5 ]( c& Y" X0 u
(prepubertal).
/ L4 H$ q! e$ r- [The parents were notified about the laboratory
7 y: E1 @4 v' q( U6 J9 Aresults and were informed that all of the tests were' o  _+ }5 N- Z$ ~4 Z: G9 x
normal except the testosterone level was high. The# I- N; i: x  c/ D  M8 g8 m
follow-up visit was arranged within a few weeks to8 ]  O, ]9 z6 j1 C. r5 _
obtain testicular and abdominal sonograms; how-
, W1 y+ O2 s$ a" ^  ?% I$ Tever, the family did not return for 4 months.
/ m" d" _7 f1 I+ j- y. z3 pPhysical examination at this time revealed that the
, P/ \2 C$ J% q3 T, F2 V: Xchild had grown 2.5 cm in 4 months and had gained  n: z, o4 E7 z8 e! U) r% u
2 kg of weight. Physical examination remained+ z6 E7 {$ C2 w( L& h
unchanged. Surprisingly, the pubic hair almost com-
% R3 ~3 @1 h, A3 x# R2 |) l3 ]6 Upletely disappeared except for a few vellous hairs at' c3 _, h( O5 X! a: w* ?, H5 j
the base of the phallus. Testicular volume was still 2
& S  M; E. R; j7 ~# {  F$ n0 ^9 ]8 amL, and the size of the penis remained unchanged.; F! x8 [3 g# t0 F$ O( y, A1 J
The mother also said that the boy was no longer hav-! e, l; X/ ]0 n
ing frequent erections.$ P, f3 d& \3 k; c
Both parents were again questioned about use of1 s# L6 d( P! j6 s6 e) h: T% D# H1 E
any ointment/creams that they may have applied to0 m6 R2 }' G/ f' V( A
the child’s skin. This time the father admitted the
+ c! f# Y0 o! L# P' w. dTopical Testosterone Exposure / Bhowmick et al 541
( P* K9 X0 m! luse of testosterone gel twice daily that he was apply-
: v6 B7 |# l! |' ^! P7 t1 V  Y  F$ sing over his own shoulders, chest, and back area for& V/ z* t1 B! W- N  e( B2 j3 n9 b& q
a year. The father also revealed he was embarrassed9 y, ~" C! [9 X" p  C
to disclose that he was using a testosterone gel pre-
/ u. @' K! w: [% u& j. Yscribed by his family physician for decreased libido
7 a) r9 S" o5 Nsecondary to depression.- N6 g: |2 {) p: F
The child slept in the same bed with parents.
$ V0 v$ k" c% @# U* r9 @: ~The father would hug the baby and hold him on his5 A7 s" [# ^. }  @! H6 G
chest for a considerable period of time, causing sig-/ F, Y+ q. H. {" r' I9 p2 @4 Z
nificant bare skin contact between baby and father.# O7 m, A- r$ E! s' g
The father also admitted that after the phone call,$ ^: U! z/ D$ \( v8 X
when he learned the testosterone level in the baby
5 q1 g2 k5 S& Vwas high, he then read the product information
" T  `) C# M# {. d; C9 \packet and concluded that it was most likely the rea-
0 k& |$ @- F! u9 Vson for the child’s virilization. At that time, they: a+ Y5 Q" L" h* L0 c9 P4 [4 c' w
decided to put the baby in a separate bed, and the
2 B' _4 t% J  d/ d6 Q  Sfather was not hugging him with bare skin and had6 |5 X# J" ]0 Z! v, I5 V% h* y
been using protective clothing. A repeat testosterone$ X6 i1 i" _: F# F* o4 v4 f* f
test was ordered, but the family did not go to the
, C5 C4 q% }( t3 ]1 `1 R' Flaboratory to obtain the test.
4 ^4 _+ D' y" y( ~  }Discussion
7 S4 u' Q1 z, I" RPrecocious puberty in boys is defined as secondary8 T+ f( F2 W( ?% L
sexual development before 9 years of age.1,4' F* J; r/ O) M# W
Precocious puberty is termed as central (true) when
9 p/ z: f& `- c/ Q: b7 m. Vit is caused by the premature activation of hypo-
" g" |: [) g5 U: \* `6 _# R* @thalamic pituitary gonadal axis. CPP is more com-( B+ Q' ?! L0 u2 Q. J
mon in girls than in boys.1,3 Most boys with CPP. D  F: d* U$ P3 F2 h2 ~
may have a central nervous system lesion that is6 d& R- v% G2 b% H; p# G9 l% f
responsible for the early activation of the hypothal-
" ^# |* A% A) L$ H. lamic pituitary gonadal axis.1-3 Thus, greater empha-. u: Q, z( t3 p' M( I% O* ]
sis has been given to neuroradiologic imaging in) b* ]6 z$ {( S( ~7 q
boys with precocious puberty. In addition to viril-% y% [! {" P$ ?4 F
ization, the clinical hallmark of CPP is the symmet-
6 [+ T) y4 D3 Z# z0 prical testicular growth secondary to stimulation by  a4 T% g8 e3 l2 K" Q
gonadotropins.1,3
3 Q$ g+ U) i6 w3 z) H/ y: _Gonadotropin-independent peripheral preco-
$ L, d8 n: F; X5 h) M9 C8 F! Ucious puberty in boys also results from inappropriate
/ S8 y5 n, t3 v) ^androgenic stimulation from either endogenous or8 o( R* w, T- k; N8 b
exogenous sources, nonpituitary gonadotropin stim-
0 H. a& j6 R) c- p, zulation, and rare activating mutations.3 Virilizing0 W1 [- P# h. {3 v/ P8 b
congenital adrenal hyperplasia producing excessive
* {. q+ B, V+ `# D2 H4 A  [8 Oadrenal androgens is a common cause of precocious
( v' u7 r# p5 }% _0 z8 C- W8 G8 Ppuberty in boys.3,4, \, E1 d3 J7 c8 v7 Z$ V
The most common form of congenital adrenal
/ \1 s; P7 r  `2 u* Y5 Mhyperplasia is the 21-hydroxylase enzyme deficiency.4 T% r' x+ |' T4 u8 L& K
The 11-β hydroxylase deficiency may also result in4 g* P2 o9 _7 H
excessive adrenal androgen production, and rarely,; D& E5 a2 h1 h6 t+ W- S3 N) Z
an adrenal tumor may also cause adrenal androgen: S0 t+ x' m1 X2 F4 Q
excess.1,3
+ |6 U3 Q( u$ f; Rat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 k- c) Y* m4 C( y/ x: w' t, t542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" Y* @1 l( o- x' ]  I7 M0 m$ Z: `( `
A unique entity of male-limited gonadotropin-2 x7 o+ q9 E* ]& s8 A. o) S
independent precocious puberty, which is also known: Y  I, a5 n( }5 o+ U+ T
as testotoxicosis, may cause precocious puberty at a  J% p/ ^8 ]% X2 Q/ P, {
very young age. The physical findings in these boys' p: S4 ^3 o0 p) J( p* ?
with this disorder are full pubertal development,8 n: M1 y2 n) `
including bilateral testicular growth, similar to boys! u$ O+ w0 s; \/ p  [+ O
with CPP. The gonadotropin levels in this disorder
* B' d4 S8 o( ^1 y+ Z( y) ]2 g" ^8 gare suppressed to prepubertal levels and do not show
% M2 n  O" K' C( q: \% N, z3 ~8 epubertal response of gonadotropin after gonadotropin-: \) S9 y5 _3 c
releasing hormone stimulation. This is a sex-linked, B! H2 U) N! |9 V' v2 I
autosomal dominant disorder that affects only9 E3 Y) w7 A7 d
males; therefore, other male members of the family
. L; Q) E6 U* |6 O- n5 ^may have similar precocious puberty.3" O* }" j4 r$ L7 c- A$ I, Z
In our patient, physical examination was incon-
% y) U( q! h2 Nsistent with true precocious puberty since his testi-
1 c; |0 N9 J+ Ncles were prepubertal in size. However, testotoxicosis
! v6 O( D/ g- a% rwas in the differential diagnosis because his father8 l0 i& W, C2 C: w  J- @
started puberty somewhat early, and occasionally,& k8 W% c9 c! ?  S
testicular enlargement is not that evident in the0 I) P, |6 y2 G) x1 z# a
beginning of this process.1 In the absence of a neg-
2 c. `. z( L: l/ V7 L9 Native initial history of androgen exposure, our
/ x& U, C3 d' e  @- ?3 xbiggest concern was virilizing adrenal hyperplasia,
" h' Q% O/ t! n- }either 21-hydroxylase deficiency or 11-β hydroxylase8 O6 z0 W0 j2 o9 `- e9 |$ P. Y
deficiency. Those diagnoses were excluded by find-
1 x% Q8 f+ P6 f. xing the normal level of adrenal steroids.
8 l$ t: z7 k5 W5 z) @The diagnosis of exogenous androgens was strongly
* Y& w6 t8 F9 dsuspected in a follow-up visit after 4 months because1 }, ]2 R0 [% ]9 k9 x$ L7 ~: s. m
the physical examination revealed the complete disap-
6 g1 s% k! o8 T9 `/ W  rpearance of pubic hair, normal growth velocity, and- w" n4 Z; @- @& ^& d
decreased erections. The father admitted using a testos-
/ U8 N3 T. {2 h, iterone gel, which he concealed at first visit. He was
$ W0 G! G% p! n- x; w4 B% v( Wusing it rather frequently, twice a day. The Physicians’# }( s5 p4 C% W( M9 j# D
Desk Reference, or package insert of this product, gel or
& F7 u' m  V* F% y+ n% ccream, cautions about dermal testosterone transfer to
/ g! G9 X+ ~( runprotected females through direct skin exposure.
6 `6 T7 {) R  c, \! g( N0 ASerum testosterone level was found to be 2 times the9 B+ g. c2 B5 P1 N/ M# F& _. U
baseline value in those females who were exposed to6 f% i( i/ o" ~2 N& w
even 15 minutes of direct skin contact with their male6 K! D1 x. N# l% ~: k+ q. H
partners.6 However, when a shirt covered the applica-; N: {/ p) `# H& \0 |1 j
tion site, this testosterone transfer was prevented.6 o! n# G& d+ t* u7 N& p8 Z
Our patient’s testosterone level was 60 ng/mL,) |) n; j3 h) X( f; @
which was clearly high. Some studies suggest that  n0 c/ T5 ?* Y9 i% f
dermal conversion of testosterone to dihydrotestos-5 H4 J9 Y4 L/ J4 E5 c- g# Z
terone, which is a more potent metabolite, is more
0 z" W7 o/ g% u: I$ H, @active in young children exposed to testosterone+ G* m& p! ?8 a, a
exogenously7; however, we did not measure a dihy-+ \! [. Y* n' f; ~: o
drotestosterone level in our patient. In addition to& Q8 ~( R6 [. T
virilization, exposure to exogenous testosterone in
! Y+ g! X( f6 N7 p! K# Y6 V6 k, achildren results in an increase in growth velocity and
1 o6 ^9 x' G. X* W1 X+ h1 p5 m+ sadvanced bone age, as seen in our patient.+ F8 a! B  k) o7 H  \+ N" A
The long-term effect of androgen exposure during
( l! ~7 Z+ ~! |4 J9 a, z2 dearly childhood on pubertal development and final" X* m) P1 M* Z# G& ]/ M
adult height are not fully known and always remain4 C3 S" i5 K3 X' u" Q, x
a concern. Children treated with short-term testos-4 r- N' o  a% D; M' D
terone injection or topical androgen may exhibit some8 p  k$ E" K  y3 b. c
acceleration of the skeletal maturation; however, after
6 a, E0 b+ R, V& }- ?9 Acessation of treatment, the rate of bone maturation1 `4 l2 j+ e1 v! ?" Z* J( r
decelerates and gradually returns to normal.8,9
0 A! s& {" A; A* Q4 r8 oThere are conflicting reports and controversy
, l- h+ `, \0 e$ Z, `- P4 }# j, R  jover the effect of early androgen exposure on adult
$ h! {- ?% f/ T. P$ upenile length.10,11 Some reports suggest subnormal
& h# e; J" C. w( @' Ladult penile length, apparently because of downreg-
& l! C' O$ o  d& A0 Oulation of androgen receptor number.10,12 However,
# L+ n, H9 o- vSutherland et al13 did not find a correlation between2 u/ r* n, ~8 P, h0 ]& k2 ?2 g
childhood testosterone exposure and reduced adult. R0 q( B; [; {3 @/ L# ?
penile length in clinical studies.1 l& P' Z  _' h9 F/ f& Y. Y2 K
Nonetheless, we do not believe our patient is
3 A; Z5 O' W& v$ }( S- Ugoing to experience any of the untoward effects from
$ @4 H) N1 P# X  \$ Ytestosterone exposure as mentioned earlier because
1 G2 C6 Q/ J, M" Nthe exposure was not for a prolonged period of time.) J; l: _! D% l4 H
Although the bone age was advanced at the time of
( k* @! z* E% Zdiagnosis, the child had a normal growth velocity at
" S( w+ y3 K* D* i+ r' Ithe follow-up visit. It is hoped that his final adult
! I* C% ]* `0 W, L2 u8 g, Uheight will not be affected." x# ?$ z; D, p3 r) I! u- C
Although rarely reported, the widespread avail-
: Z/ c$ x% S, @( fability of androgen products in our society may
) D  V) v: r# u1 h1 p9 Zindeed cause more virilization in male or female4 e0 R# p* F) h) \0 v( d) h
children than one would realize. Exposure to andro-- v5 x4 e' V$ O2 F* T1 N: I
gen products must be considered and specific ques-/ o% d/ ^, Z; _6 A
tioning about the use of a testosterone product or* Z$ {4 x# g% i; j0 B4 h
gel should be asked of the family members during
) T- }+ v7 U+ Q' qthe evaluation of any children who present with vir-$ u9 f$ f6 V) [" Y# X$ Z! ]0 V
ilization or peripheral precocious puberty. The diag-
) _8 _9 o/ C2 A. dnosis can be established by just a few tests and by
7 D7 W  g" f/ |! W6 I' Z- ^appropriate history. The inability to obtain such a
* E4 O' ?" O: d7 p, ?history, or failure to ask the specific questions, may# k$ U  ?# z) C% Y" K1 B* e9 @& I
result in extensive, unnecessary, and expensive
- k: l2 p$ L- r4 uinvestigation. The primary care physician should be
, d9 L5 @2 w: I4 k4 p& naware of this fact, because most of these children5 h' x% v9 Y7 _! T. ?/ V
may initially present in their practice. The Physicians’1 R+ x( W/ @6 {; x. X) _
Desk Reference and package insert should also put a) T0 a$ D7 _% m- ^4 [' G) ]1 \  a
warning about the virilizing effect on a male or# l- `4 q2 w; c9 i- J
female child who might come in contact with some-7 Y' b! X& _" s: _
one using any of these products.- m6 A3 `, s- s' [( x4 [
References
! W6 ~6 H/ u3 v$ V" l1. Styne DM. The testes: disorder of sexual differentiation' }3 `6 Z3 E. t6 W8 z8 G( `! ~
and puberty in the male. In: Sperling MA, ed. Pediatric
5 G9 {5 G3 M3 b9 R7 h* q/ IEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
6 k* Y! z- U" P3 E- M, ^2002: 565-628.
: b& q% r( [' N$ Z& }2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
" k( z% x) ~6 U- s1 Cpuberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old. T5 \: L, ?0 Q
Boy Induced by Indirect Topical# e+ c  C9 P: m: L% c( @
Exposure to Testosterone- \9 T- v: w: `% T
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2% W- }7 `. t8 Y% d6 U5 \
and Kenneth R. Rettig, MD1  M5 w/ H" f7 v
Clinical Pediatrics
: _  ^0 c  k" [/ [0 _Volume 46 Number 6* d, g, r- w  z5 X
July 2007 540-5437 g. k! z! M, ?7 M( ]
© 2007 Sage Publications6 n7 p$ a& @: n, g, ]
10.1177/0009922806296651
# h7 e0 W; C5 ]2 s. \+ ]http://clp.sagepub.com& g7 f- N3 _$ |+ ]
hosted at
* b& ^9 K! y* M' Ehttp://online.sagepub.com4 ?4 L6 I' {) L
Precocious puberty in boys, central or peripheral,. o6 A# \" i$ `& s: |
is a significant concern for physicians. Central( C; ~4 {  P! a( |3 h7 E
precocious puberty (CPP), which is mediated/ y+ s( k$ _# f
through the hypothalamic pituitary gonadal axis, has
. t# D0 J& C1 |; C; S* k6 d* ]2 @a higher incidence of organic central nervous system# u0 ]' {& ^3 H% Y* e9 o
lesions in boys.1,2 Virilization in boys, as manifested
9 J$ N# D* Y- j; b8 Vby enlargement of the penis, development of pubic
3 Z. n2 N) ^6 h& b0 jhair, and facial acne without enlargement of testi-4 \1 V7 |$ l3 j
cles, suggests peripheral or pseudopuberty.1-3 We8 a3 [2 O9 E8 K- i. G5 t# R+ D
report a 16-month-old boy who presented with the
4 r: b: w2 l& }/ Zenlargement of the phallus and pubic hair develop-9 P' n. O4 x! Q5 O: y+ B
ment without testicular enlargement, which was due
# j% {* g- a/ H' bto the unintentional exposure to androgen gel used by$ A/ t1 F2 D7 }3 }1 A
the father. The family initially concealed this infor-1 h/ m0 }. E" q" f3 J& j
mation, resulting in an extensive work-up for this: e6 t# {* V6 R; B
child. Given the widespread and easy availability of9 M* H1 a% K/ I) P3 N$ \
testosterone gel and cream, we believe this is proba-+ d+ T( ?4 b' A
bly more common than the rare case report in the
  B8 X+ A9 u9 Q$ |9 v6 fliterature.4
- L$ L, i" E$ d/ B5 M  uPatient Report
6 ?2 _# w! x7 R& MA 16-month-old white child was referred to the0 J1 L. h6 w5 v6 _- {
endocrine clinic by his pediatrician with the concern
' X% \- ]$ \8 _+ @9 M" pof early sexual development. His mother noticed
; J6 s0 {, o/ Hlight colored pubic hair development when he was
1 A/ J8 s) G- e8 ^3 N( g$ C& wFrom the 1Division of Pediatric Endocrinology, 2University of, E8 V6 e$ \3 Z& c$ `4 G1 t
South Alabama Medical Center, Mobile, Alabama.
" n# i+ F/ E9 ]0 S  H: kAddress correspondence to: Samar K. Bhowmick, MD, FACE,
+ P+ d; O/ h' y  H! r" f) RProfessor of Pediatrics, University of South Alabama, College of
8 i# L! ?$ M+ yMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
1 w# v1 h) u$ H  O5 `" Xe-mail: [email protected]./ y  A8 o  l: p7 m. {  X  j8 N
about 6 to 7 months old, which progressively became
/ r% M1 Y& x9 H" x$ `! {" o& Gdarker. She was also concerned about the enlarge-& X, h0 v5 R$ U+ o
ment of his penis and frequent erections. The child4 z- M8 r& M6 z6 L3 Q3 ?9 p8 D! s
was the product of a full-term normal delivery, with# b* g/ y" ~) [1 \2 {  ~, a
a birth weight of 7 lb 14 oz, and birth length of
6 H4 Y' O8 `0 x% F3 J) `. n20 inches. He was breast-fed throughout the first year
( Z- o1 j- m6 rof life and was still receiving breast milk along with
# O) U9 E6 ]% `; x6 S- Msolid food. He had no hospitalizations or surgery,
4 D" j! y6 Q5 l" Zand his psychosocial and psychomotor development
& _! O9 w3 V8 }" T  \" _# Jwas age appropriate.; G5 X& [3 ^. ^5 f' f" V$ P
The family history was remarkable for the father,$ e5 a2 A2 q: s4 I
who was diagnosed with hypothyroidism at age 16,4 U( \7 }6 t7 S+ M8 g0 ]. ^
which was treated with thyroxine. The father’s8 ?- z; H! o+ x4 @
height was 6 feet, and he went through a somewhat, D$ f5 Z3 r+ W% V% d, i" O; K8 y
early puberty and had stopped growing by age 14.
8 _/ x) G& N& B- mThe father denied taking any other medication. The: o0 w2 e5 m# W
child’s mother was in good health. Her menarche
% C$ Q/ O; U, E4 ?; c. Qwas at 11 years of age, and her height was at 5 feet7 }! e) r7 V- {8 j4 J6 W
5 inches. There was no other family history of pre-
# \# e5 |7 y  ]% k6 W. ?; ]cocious sexual development in the first-degree rela-9 @+ I1 W" D' \! \" u4 W# y
tives. There were no siblings.
+ Q, d# x/ {% B& \5 F, sPhysical Examination
' l! l, ?8 s' h% |$ ~/ bThe physical examination revealed a very active,
# ]% B3 V" x/ P) Q3 y" rplayful, and healthy boy. The vital signs documented5 ], X2 O4 D0 p4 s( s; g% C  g
a blood pressure of 85/50 mm Hg, his length was
) A- P2 `- J5 L+ |  m5 Z+ f" ^90 cm (>97th percentile), and his weight was 14.4 kg
1 H. G8 P$ e& `4 g- E' i+ D(also >97th percentile). The observed yearly growth1 U6 d, o6 H7 y! l: R
velocity was 30 cm (12 inches). The examination of
. q0 l4 Q9 G1 g9 n! s* I' qthe neck revealed no thyroid enlargement.( S! q2 j. n5 [8 I
The genitourinary examination was remarkable for0 y3 ]* [  ?3 w" I' t) ^$ O
enlargement of the penis, with a stretched length of
$ S5 X7 L/ ]9 y+ _& |! {" y8 cm and a width of 2 cm. The glans penis was very well
. [* A. r9 W: S7 L% A' X4 w) fdeveloped. The pubic hair was Tanner II, mostly around
/ W4 I' @! J9 a) ~7 j540
2 \/ w- S7 z2 T, u( Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from2 p) r) [  t  y- C" N
the base of the phallus and was dark and curled. The: i# Y) G" ^- A3 ^6 A2 @  }, ?
testicular volume was prepubertal at 2 mL each.: h) D4 \6 G! [& K' v( L1 g5 {
The skin was moist and smooth and somewhat1 v) D" ~) l$ V* n
oily. No axillary hair was noted. There were no/ W8 r1 [! K2 V8 H3 @+ D" F
abnormal skin pigmentations or café-au-lait spots.) M0 z3 D) G6 K2 V0 t; t
Neurologic evaluation showed deep tendon reflex 2+( A4 p8 |& v, m' [5 H6 Q2 o
bilateral and symmetrical. There was no suggestion
/ f! X' q. B- C( q: Tof papilledema.1 j9 U+ j: k$ a5 S& `" r- R
Laboratory Evaluation& l  L, u7 u' F
The bone age was consistent with 28 months by. s0 r( u& {0 ]3 b9 F
using the standard of Greulich and Pyle at a chrono-1 j) W  j3 {1 u6 \3 ^9 u
logic age of 16 months (advanced).5 Chromosomal
8 I* K0 t6 T" ^8 U8 Bkaryotype was 46XY. The thyroid function test) R& O/ z3 S: I$ L0 P
showed a free T4 of 1.69 ng/dL, and thyroid stimu-) D( l) i! J0 @5 G
lating hormone level was 1.3 µIU/mL (both normal).
+ O0 B+ X4 `) o6 J; O+ [0 d1 bThe concentrations of serum electrolytes, blood" m: J) n) j8 T
urea nitrogen, creatinine, and calcium all were
! G) D3 Q5 `: k: }, }5 f) R; Pwithin normal range for his age. The concentration
: M: K# N' G$ T; [9 G3 yof serum 17-hydroxyprogesterone was 16 ng/dL
" b$ Q; `4 L0 i% ?5 M- w; b1 c(normal, 3 to 90 ng/dL), androstenedione was 20' B; a7 k9 W8 V; E8 q+ ?
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  M. Q4 M) y3 \$ @9 ?! w
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
3 d; H9 y6 H7 l6 Zdesoxycorticosterone was 4.3 ng/dL (normal, 7 to2 `) v* x" m; H0 h0 R5 q
49ng/dL), 11-desoxycortisol (specific compound S)
( m6 A. v2 {4 [# bwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 O2 |1 m6 M2 B. D# K) @# b8 p7 Z
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total) ^$ ?( _: Z- A
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
+ ~9 a- N- S- i6 E' oand β-human chorionic gonadotropin was less than
. v' S) B; n: ]/ O2 m5 mIU/mL (normal <5 mIU/mL). Serum follicular
/ T' m- D* g! Z" S4 T- ystimulating hormone and leuteinizing hormone. K+ H6 b0 j  L% H/ D9 a
concentrations were less than 0.05 mIU/mL
% q# L9 f" [2 W7 \(prepubertal)., j% ^! J5 m2 {$ P  X
The parents were notified about the laboratory
4 |/ a$ s- {8 G* Vresults and were informed that all of the tests were
/ c6 g2 L$ A! S" z0 T+ xnormal except the testosterone level was high. The
% X# R6 ^. }. w. g% b0 Rfollow-up visit was arranged within a few weeks to
4 g9 G- |' g! Bobtain testicular and abdominal sonograms; how-" [8 c  b7 N8 M
ever, the family did not return for 4 months.
1 X5 z" o4 X7 S6 e7 A( K9 UPhysical examination at this time revealed that the
. {4 Z. a4 T7 J0 q) y3 ]child had grown 2.5 cm in 4 months and had gained
% a0 r7 e7 D7 I# ]/ |2 K+ S. o2 kg of weight. Physical examination remained
% t  z0 ^4 u# }, R/ C: |/ iunchanged. Surprisingly, the pubic hair almost com-7 A; [/ F3 S8 i& L% L" `
pletely disappeared except for a few vellous hairs at2 e! j$ S9 G4 I2 i
the base of the phallus. Testicular volume was still 27 D" g- W) W0 m; N* T- q
mL, and the size of the penis remained unchanged.' I& |( K* O) d  V0 n9 _
The mother also said that the boy was no longer hav-( y# E9 j* U* B. V" m
ing frequent erections.5 F0 n& {0 C+ p5 [5 Q1 ?
Both parents were again questioned about use of9 s2 ?2 I- u5 J; y
any ointment/creams that they may have applied to; B/ V& o" l( b4 D" D2 ?* M- q' z% N
the child’s skin. This time the father admitted the# }3 ]4 Y5 u- M& u1 z( s
Topical Testosterone Exposure / Bhowmick et al 541
5 r4 C4 C6 M9 T/ L7 L4 D6 Y7 P* juse of testosterone gel twice daily that he was apply-
% _4 B' o9 m% u5 f8 ging over his own shoulders, chest, and back area for
1 H: f. g3 M, B. Z+ ba year. The father also revealed he was embarrassed: C* ~; S: \/ _8 g& Y- i
to disclose that he was using a testosterone gel pre-, n7 ^7 s& H4 ^7 a
scribed by his family physician for decreased libido
2 C  F2 k8 w1 q% R1 u1 F5 msecondary to depression.
) a& _% q: P( ?, W! G& oThe child slept in the same bed with parents.! H5 X8 l, X3 V0 N! L
The father would hug the baby and hold him on his
" J, H8 r9 w+ u0 b0 echest for a considerable period of time, causing sig-; e9 y0 I' Z/ L' t' o
nificant bare skin contact between baby and father.
* r2 g0 R+ x* M9 q6 [! k- h2 B) {The father also admitted that after the phone call,
) D1 @5 I8 _- dwhen he learned the testosterone level in the baby- n, c+ r! e. s" p
was high, he then read the product information. l9 h" V# v. @, I0 N; t% X* `
packet and concluded that it was most likely the rea-. w9 R- g% K, S* y
son for the child’s virilization. At that time, they+ x0 I) V9 d0 C$ p) d( H8 m: ?
decided to put the baby in a separate bed, and the7 D9 U  g4 Q) F' ?* R$ d" c
father was not hugging him with bare skin and had: _* x1 w$ x( _" j( h0 i* v& f
been using protective clothing. A repeat testosterone2 m7 N7 W7 a( m& v" j% \
test was ordered, but the family did not go to the3 U' m2 m5 M# N! \' Q% y6 b
laboratory to obtain the test.
7 Q& h' L% }8 V8 i* VDiscussion
- a" M* u0 q  w; GPrecocious puberty in boys is defined as secondary2 q# |" v" z+ \: t
sexual development before 9 years of age.1,4$ k$ [6 V" R8 f8 Z, r3 V' J/ ~
Precocious puberty is termed as central (true) when, B2 k) J/ d8 g- A3 l
it is caused by the premature activation of hypo-% x& p( E. b' r/ \
thalamic pituitary gonadal axis. CPP is more com-0 b: \0 X+ \- H( @
mon in girls than in boys.1,3 Most boys with CPP
8 b. S+ |5 }2 ~3 \0 x+ W- b7 I/ Smay have a central nervous system lesion that is8 Y. b# W3 t/ K8 k8 o! x7 b5 }, ]) O# I
responsible for the early activation of the hypothal-4 b( S/ q) [# b$ Z4 l! Y$ [
amic pituitary gonadal axis.1-3 Thus, greater empha-* {0 e# N. ^# \; x
sis has been given to neuroradiologic imaging in
& v: R8 [2 C$ m  Dboys with precocious puberty. In addition to viril-$ N! t. h5 `8 }6 j" N
ization, the clinical hallmark of CPP is the symmet-
3 n5 p5 ]6 [4 L4 m7 |1 k7 frical testicular growth secondary to stimulation by
6 h3 @8 g) \2 o, S8 ogonadotropins.1,3# v# _" ]1 U$ c! z/ L, [! d1 G
Gonadotropin-independent peripheral preco-
% z: e" L. r  bcious puberty in boys also results from inappropriate
! }4 b+ K7 W& t# y# g. nandrogenic stimulation from either endogenous or
( p% o4 O) N- z$ }5 U  sexogenous sources, nonpituitary gonadotropin stim-
" s- \9 ?4 m# eulation, and rare activating mutations.3 Virilizing
3 [, k5 Z" ]5 |  A2 q: r5 scongenital adrenal hyperplasia producing excessive
' R% x4 j' [1 N( L3 m, ?adrenal androgens is a common cause of precocious2 D$ i! X' n; H8 O
puberty in boys.3,4) V. `+ f3 L8 M% ]( l' o5 c
The most common form of congenital adrenal
6 }4 ^1 \7 Q1 X; x2 F) z: I$ [hyperplasia is the 21-hydroxylase enzyme deficiency.
/ ?$ d2 F- G8 A, q" bThe 11-β hydroxylase deficiency may also result in$ o3 F* H+ c7 O! S6 s
excessive adrenal androgen production, and rarely,* X2 i# u0 a9 F7 ]1 y+ c
an adrenal tumor may also cause adrenal androgen
; l% Z" J+ a" U' }: A. [excess.1,3
0 G8 S9 b- }8 G# J/ |at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from' }3 F3 Z9 F# {& P$ |) f
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007: y' _8 q. h, ^( t. v8 x
A unique entity of male-limited gonadotropin-8 I* c6 G% _9 \( g. i
independent precocious puberty, which is also known
9 O" X( {# E/ S" n: E6 ]3 b' C0 Mas testotoxicosis, may cause precocious puberty at a
, W2 q# ?1 a- M9 `  l6 @- V& z6 tvery young age. The physical findings in these boys
/ t( h9 \) d8 [; Rwith this disorder are full pubertal development,
& y& S: _$ Y$ f4 V: O; j/ sincluding bilateral testicular growth, similar to boys
& f( v6 |6 i8 e: ]) Awith CPP. The gonadotropin levels in this disorder* h) x: x* x2 O- E8 x4 ~
are suppressed to prepubertal levels and do not show
% @$ q- u) W' Q& o0 x1 w# w2 }pubertal response of gonadotropin after gonadotropin-
7 @1 r  ~; }. Ireleasing hormone stimulation. This is a sex-linked7 [- L; R3 f0 P
autosomal dominant disorder that affects only6 {& [4 a2 M) Y7 P8 a
males; therefore, other male members of the family4 T" n  B( W" S4 f" ?
may have similar precocious puberty.35 k0 ^/ ?0 ^7 @7 p
In our patient, physical examination was incon-
! O; d! z( l7 Z2 C4 Hsistent with true precocious puberty since his testi-) `; ~5 j0 h+ _
cles were prepubertal in size. However, testotoxicosis
1 ~$ l9 x& Q  K' v" u8 pwas in the differential diagnosis because his father
& ~% U5 S2 ~$ \; n* a8 l  P& W7 ostarted puberty somewhat early, and occasionally,; \! l  @) B2 i: Q# f
testicular enlargement is not that evident in the- K. P* Q( g+ M. q2 [& X
beginning of this process.1 In the absence of a neg-! ?/ k& q+ b6 g3 h1 N
ative initial history of androgen exposure, our7 P/ X7 e; x: v+ a; j2 A+ b8 Q
biggest concern was virilizing adrenal hyperplasia,% b  H; }. y: t. W6 }* h
either 21-hydroxylase deficiency or 11-β hydroxylase
/ d& g6 g1 P0 J1 ?* y: [deficiency. Those diagnoses were excluded by find-
+ E1 }( ~* {$ k+ ]- o% u& ]8 ding the normal level of adrenal steroids.0 _5 v& ~8 i( _, ?9 O- m
The diagnosis of exogenous androgens was strongly" v( V3 q* l, L7 B* X1 [
suspected in a follow-up visit after 4 months because6 e3 x7 @1 F' M* J( f$ M
the physical examination revealed the complete disap-( y3 _( A& N* V! X, V7 z! x8 o8 T
pearance of pubic hair, normal growth velocity, and  @/ @, l& k  H; E& W) v% U  r
decreased erections. The father admitted using a testos-! R! v& ?: c% }2 I$ T4 U1 v
terone gel, which he concealed at first visit. He was+ j2 V2 s; ~9 e* O% Y' E8 F
using it rather frequently, twice a day. The Physicians’
' s- c; j2 N1 e1 l: \2 nDesk Reference, or package insert of this product, gel or+ O+ P8 X3 y  \- D" E
cream, cautions about dermal testosterone transfer to/ }3 Y) Z& d( b9 Q6 Y; B% m
unprotected females through direct skin exposure.
! ?3 |9 m4 I5 {$ ]: P1 RSerum testosterone level was found to be 2 times the& I7 _, N- |+ E  b- f: r* h. t) \
baseline value in those females who were exposed to0 Y" a5 \, p+ K, c2 Q2 h
even 15 minutes of direct skin contact with their male) C; k6 @' N. A0 s- U1 o$ ]7 g: `
partners.6 However, when a shirt covered the applica-
/ c9 X. L6 t5 }9 o: Y! ition site, this testosterone transfer was prevented.
4 r+ l) |' K( f. }% T+ v8 w5 vOur patient’s testosterone level was 60 ng/mL,; |. v) Z( d1 W- p$ K9 z2 f
which was clearly high. Some studies suggest that
  }# m; o4 K7 S. C" @* zdermal conversion of testosterone to dihydrotestos-9 x! T$ \8 v: a! P. x' z
terone, which is a more potent metabolite, is more/ y- |1 _+ Q& U
active in young children exposed to testosterone
$ C- `, J% j: ?- ]2 c. s+ {exogenously7; however, we did not measure a dihy-
! Y# g- V; }% j9 z: B! Ndrotestosterone level in our patient. In addition to1 a8 y9 Q. W( [5 z/ n
virilization, exposure to exogenous testosterone in
1 W# `" d0 M' t# u! f: S9 W2 Kchildren results in an increase in growth velocity and( J% a, z7 S" E0 ^! I
advanced bone age, as seen in our patient.3 B( U  ]8 b% D. W0 {
The long-term effect of androgen exposure during- q$ n6 _( f. u& |/ B& J4 o6 L1 A+ X
early childhood on pubertal development and final  P! O4 V7 \! m, ]& Y
adult height are not fully known and always remain+ j8 L$ r9 f! l& o( f
a concern. Children treated with short-term testos-9 z4 i- b, `8 q3 I
terone injection or topical androgen may exhibit some
6 c# T; @9 V6 ~$ qacceleration of the skeletal maturation; however, after; H, G$ A2 [" t! d3 }. F. v. z
cessation of treatment, the rate of bone maturation
. @# B) A4 y$ h* q3 S3 ndecelerates and gradually returns to normal.8,9
2 r' z$ M9 Y6 KThere are conflicting reports and controversy
( T* z) S+ i; ~$ [: Z4 N& Jover the effect of early androgen exposure on adult
! j1 c* f2 M7 Y% [: ?3 k- l* N- npenile length.10,11 Some reports suggest subnormal$ d) o4 h. R3 w4 [6 z2 `4 g
adult penile length, apparently because of downreg-
; {2 f# n6 x6 S$ ]ulation of androgen receptor number.10,12 However,- a$ d, K1 F# y* k1 R$ h& }# N6 {
Sutherland et al13 did not find a correlation between9 z% h7 e" f( c& h& `7 w
childhood testosterone exposure and reduced adult4 @( ~( i. a' l- C1 l+ l
penile length in clinical studies.
) Z$ Y3 j# r/ vNonetheless, we do not believe our patient is# f9 S# y7 V1 ^
going to experience any of the untoward effects from& F9 d( d! L1 `9 ~: [) Z
testosterone exposure as mentioned earlier because
7 _; ?7 N2 v6 b4 _the exposure was not for a prolonged period of time.  `. N7 v+ L' m  [1 E- f4 f9 }
Although the bone age was advanced at the time of& ~. k3 U! y) U0 @8 F& h
diagnosis, the child had a normal growth velocity at) ^# b1 Z  c! d4 x4 W
the follow-up visit. It is hoped that his final adult2 p  d+ P7 [* Q' D3 q  I
height will not be affected., }; p4 J  x+ d' @& k
Although rarely reported, the widespread avail-6 O6 h1 C3 ~" v. z
ability of androgen products in our society may
+ @9 _' Z3 U2 \/ r1 g6 zindeed cause more virilization in male or female! D6 `3 J; D- p
children than one would realize. Exposure to andro-
& @" ]- z2 X! m7 Z9 y2 `gen products must be considered and specific ques-( T# ^5 H5 S. }1 G7 O
tioning about the use of a testosterone product or' ~$ K; O' J% I" i
gel should be asked of the family members during% e0 ]% v/ q. Q& c& Y
the evaluation of any children who present with vir-  L3 h- ]  ^9 z
ilization or peripheral precocious puberty. The diag-( X7 Z. j7 s8 K7 [
nosis can be established by just a few tests and by
; Q9 V# Y/ I4 z/ d9 s7 _appropriate history. The inability to obtain such a  S0 O$ q# `6 h
history, or failure to ask the specific questions, may# S& K5 E5 L3 k; f
result in extensive, unnecessary, and expensive" w1 c1 K; U9 C, n
investigation. The primary care physician should be
7 S6 d1 Y. u/ e* d$ e) iaware of this fact, because most of these children
7 i( K9 i: c) _0 q% Cmay initially present in their practice. The Physicians’
/ @7 O' }+ y! J: M! a6 o$ qDesk Reference and package insert should also put a) v( d! \5 a7 C4 y# [3 O
warning about the virilizing effect on a male or
" e  W4 a( o3 ]7 y# ^6 efemale child who might come in contact with some-5 S! f+ `7 E: H  B
one using any of these products.+ d# ]# z& e2 T8 P  B
References) Q% j1 e0 z' w* I  D! V
1. Styne DM. The testes: disorder of sexual differentiation
3 i* I7 }9 O. F& Band puberty in the male. In: Sperling MA, ed. Pediatric
+ r8 J: W5 U, Y9 Z* B3 K  E5 PEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
( h+ K8 T) _  C) `( w  j) k! M2002: 565-628.+ g% Z6 p7 Q3 \) t. d
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; T+ z% ^2 M6 `1 W' t, |" p
puberty in children with tumours of the suprasellar pineal
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發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
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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

  c1 _, B! u) g+ n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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