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Sexual Precocity in a 16-Month-Old
  N2 R$ p% |( S/ qBoy Induced by Indirect Topical
$ C( m7 E9 a0 w: k) \Exposure to Testosterone
- U  w8 a# F& h; q- _6 T4 V6 MSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2$ i5 f9 w4 C6 w5 c1 N
and Kenneth R. Rettig, MD1$ y9 c: e: o6 T
Clinical Pediatrics5 p8 Q2 p: \# M5 U, Q9 Z3 x" h
Volume 46 Number 6
8 o" W& o: T: sJuly 2007 540-5434 \$ i$ N/ L8 _, J  z; b
© 2007 Sage Publications$ X1 a' |  c5 T7 C
10.1177/00099228062966513 _# \6 ~9 ]8 Y- V& y
http://clp.sagepub.com; l3 D& K6 K& L8 w
hosted at
- W$ V. R: E  U: j/ f+ _http://online.sagepub.com
% i& h0 d8 G) @( I  B" M" MPrecocious puberty in boys, central or peripheral,2 \$ d! a5 m! D& L' [& W9 A5 F
is a significant concern for physicians. Central
& ^' d& r3 n6 A1 g0 V9 G3 ~, w5 c: pprecocious puberty (CPP), which is mediated
. c) {# L: f) Uthrough the hypothalamic pituitary gonadal axis, has
7 o  `$ b  k( N& }& [/ J( A/ e, sa higher incidence of organic central nervous system
8 H5 R, c* }' }" d* ~; S2 jlesions in boys.1,2 Virilization in boys, as manifested4 H% V) g7 X  C1 V8 y0 J- B) O1 }6 _
by enlargement of the penis, development of pubic
: H* S. }4 H' T5 K3 Khair, and facial acne without enlargement of testi-
9 s, |" a& h. M3 l! I- ^cles, suggests peripheral or pseudopuberty.1-3 We
! _+ \- b* O9 X' |7 yreport a 16-month-old boy who presented with the
0 U+ W2 D! `% x3 n% `9 Y  f6 |enlargement of the phallus and pubic hair develop-
. L6 s% J' M' o& Vment without testicular enlargement, which was due
7 F/ P& ~1 U7 \1 L2 L; jto the unintentional exposure to androgen gel used by
8 S' Z/ P6 d4 z( \! m( J+ ]the father. The family initially concealed this infor-3 P8 A6 F8 B( B' v, I3 F
mation, resulting in an extensive work-up for this& h4 w" X7 s+ L! j9 Y+ E. B) o
child. Given the widespread and easy availability of
; @$ p' O& Q; K. V! gtestosterone gel and cream, we believe this is proba-
- _9 N; A" Y' F4 r7 x; _! Ebly more common than the rare case report in the
  m* p: T4 a; z% o, V2 aliterature.4- I' X2 p, z4 H- O* }
Patient Report9 \+ z- d, X4 _8 f  n7 M
A 16-month-old white child was referred to the
/ y$ N- k8 b4 c$ P2 |! s% o7 qendocrine clinic by his pediatrician with the concern
$ B  c- }7 R/ C( bof early sexual development. His mother noticed
% h* i5 n" l/ [( T1 b& j. _+ k7 Glight colored pubic hair development when he was. {6 h. ]5 Z1 o# J
From the 1Division of Pediatric Endocrinology, 2University of
6 F3 k  E- G2 x: ~1 u0 uSouth Alabama Medical Center, Mobile, Alabama.
/ E0 e* F1 w$ E+ x. E: bAddress correspondence to: Samar K. Bhowmick, MD, FACE,
( R1 G5 A0 z2 X3 ^! R2 T1 `Professor of Pediatrics, University of South Alabama, College of
/ d1 `3 p4 W2 QMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;/ i5 Y; t# r+ C! m; F" R9 B$ k2 y
e-mail: [email protected].
/ E) p$ i, V5 ]: b7 g* T  Pabout 6 to 7 months old, which progressively became
1 V2 g, o' e! {2 z2 \darker. She was also concerned about the enlarge-# |6 |7 G! P/ E4 e) X- \
ment of his penis and frequent erections. The child8 H9 O2 B, Z3 o3 T/ A5 v
was the product of a full-term normal delivery, with
4 o% M- X4 @5 T1 p7 |8 P" m# |# i7 ra birth weight of 7 lb 14 oz, and birth length of
2 X# }! Y- h& R# @& _+ s20 inches. He was breast-fed throughout the first year7 v9 l. o# A' j) h3 a, \4 V
of life and was still receiving breast milk along with
3 a$ Q/ `9 i2 S2 |& x& V0 @solid food. He had no hospitalizations or surgery,
3 u4 }* _; P- d& q! band his psychosocial and psychomotor development
7 I/ N- S! D* g& g$ e+ {5 B: ]was age appropriate.3 c( A7 h+ `- t, x- _; Y
The family history was remarkable for the father,7 L* P6 A' B3 M6 W# F
who was diagnosed with hypothyroidism at age 16,6 p: O8 C5 G# a' u* m/ C, p
which was treated with thyroxine. The father’s
% B1 N( x9 g5 J! \2 K3 g! r( Dheight was 6 feet, and he went through a somewhat0 h. b4 O5 U, L  X3 I( y0 ~1 M
early puberty and had stopped growing by age 14.& Z# J) o4 T; v* L+ m+ M+ b9 o
The father denied taking any other medication. The
. I) M+ D" ]9 J5 r  e3 Kchild’s mother was in good health. Her menarche
- W/ @/ G- K4 E7 x+ H- ]was at 11 years of age, and her height was at 5 feet
+ x- {+ f3 E: y7 w- x- v9 c5 inches. There was no other family history of pre-, Y+ |* J* \. ^
cocious sexual development in the first-degree rela-
" E2 a4 b1 `- E3 Y/ W% L8 v% gtives. There were no siblings.
0 z: d; f7 [" s) s( IPhysical Examination
1 r5 R6 `( w; T2 c7 D: LThe physical examination revealed a very active,
4 h! C, ]- B4 O3 j& L: o8 uplayful, and healthy boy. The vital signs documented
8 T, g/ Y* r- X; F5 H8 }a blood pressure of 85/50 mm Hg, his length was
+ h1 V/ g3 E3 {2 D7 o0 U# ~/ T$ L0 @90 cm (>97th percentile), and his weight was 14.4 kg1 s9 d6 t. o; |. Y6 j: r1 y
(also >97th percentile). The observed yearly growth
4 u( g) L* I$ w# t' T0 e) }velocity was 30 cm (12 inches). The examination of& m8 z+ i+ H9 |$ Z, z. P2 n% R
the neck revealed no thyroid enlargement.6 r" I7 Z" g( b9 M* O! o$ L
The genitourinary examination was remarkable for, }) S/ @' k+ U+ _5 i8 o; G2 Z
enlargement of the penis, with a stretched length of
# S: E  S2 X4 K- P8 cm and a width of 2 cm. The glans penis was very well
8 }% K$ l- I9 p3 D: Rdeveloped. The pubic hair was Tanner II, mostly around
0 z  s5 {3 I. G) q3 y1 w5 t2 C540
8 o! l8 T- W7 O& P% mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
' O5 E% V5 j0 A$ ~* I: ^the base of the phallus and was dark and curled. The" Z' Z0 G6 Y7 S# m
testicular volume was prepubertal at 2 mL each.' J  }. ]. _2 X0 T0 S) K0 S
The skin was moist and smooth and somewhat) @$ E' V/ q( p0 ~% a
oily. No axillary hair was noted. There were no
/ F3 o& r. b! A$ b) C. F$ Eabnormal skin pigmentations or café-au-lait spots.9 B) q1 C% e9 M* x
Neurologic evaluation showed deep tendon reflex 2+
) x7 C8 Y/ Z+ W; k0 wbilateral and symmetrical. There was no suggestion
/ l) n: ^# z) jof papilledema.
7 |/ d9 y0 C5 X% JLaboratory Evaluation
4 l( E. f( C9 h7 \" i* rThe bone age was consistent with 28 months by
9 n' ~: @4 e9 M9 m: R/ `using the standard of Greulich and Pyle at a chrono-9 u' G3 s: }( Y9 h0 J1 T
logic age of 16 months (advanced).5 Chromosomal
, R3 [" T3 o' v( F" Wkaryotype was 46XY. The thyroid function test0 ~3 [; N, ?: M! E, G3 Y# D7 k& a2 K
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
$ \; t- {% [3 a% ^lating hormone level was 1.3 µIU/mL (both normal).
& b. O9 s6 a0 g, J$ S2 M1 cThe concentrations of serum electrolytes, blood" G7 V0 |& N( c
urea nitrogen, creatinine, and calcium all were
, S! ^% e. O6 a' X7 u4 f; F9 Twithin normal range for his age. The concentration% g* \4 b" _, ]( c+ k+ h) y
of serum 17-hydroxyprogesterone was 16 ng/dL
, w" P% {1 A" `& T" I# Z+ _( G2 K(normal, 3 to 90 ng/dL), androstenedione was 200 p; l; r4 L1 O. T$ P! R
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
- ?: ?* L  X! `7 M2 Uterone was 38 ng/dL (normal, 50 to 760 ng/dL),
7 K9 k2 A$ o2 U8 ]9 Idesoxycorticosterone was 4.3 ng/dL (normal, 7 to  `+ u* f5 T& ~# e, ^
49ng/dL), 11-desoxycortisol (specific compound S)
; @/ j5 S8 w# K; wwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
: q) K( G2 E8 |" f) l# y( Gtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total' V, W" C1 v$ r! O$ f- ?/ P7 T
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
# }: v) G, ~2 N, E8 V& \and β-human chorionic gonadotropin was less than
5 Y0 Q9 \7 n4 w) a; E; l% N5 mIU/mL (normal <5 mIU/mL). Serum follicular0 {9 ^6 s4 C! g+ B( m8 i, s/ j" d9 C  r
stimulating hormone and leuteinizing hormone" ?! o) s2 w2 L* H- j9 t' B
concentrations were less than 0.05 mIU/mL& _7 s- L" |8 ^% a
(prepubertal).+ U- g. W. d# J7 U9 Q3 a9 e5 W- K
The parents were notified about the laboratory5 j6 S) Y! k9 Y, E/ G; h
results and were informed that all of the tests were
3 Q' B1 I+ j" z( N. f- q0 j( N4 Cnormal except the testosterone level was high. The
' E( j9 W1 |7 {/ Pfollow-up visit was arranged within a few weeks to
! @; v  a3 |  ^* f- tobtain testicular and abdominal sonograms; how-
  S- D7 N1 T/ h( }ever, the family did not return for 4 months.
+ ^& l6 u. Q6 v! \" |$ b$ cPhysical examination at this time revealed that the6 m; h: B0 Q/ w$ `0 A3 ~; Z, q8 U
child had grown 2.5 cm in 4 months and had gained
& o* V0 W' ]# k% Z2 kg of weight. Physical examination remained
# Z& F3 X- Z, Munchanged. Surprisingly, the pubic hair almost com-
& _$ s6 S+ p" }# ]) z, Gpletely disappeared except for a few vellous hairs at
4 s* I( U$ b" C0 }" x$ i# l  Athe base of the phallus. Testicular volume was still 2
3 o5 `3 {. E) }: t% kmL, and the size of the penis remained unchanged.) U3 O% r$ e2 f2 [
The mother also said that the boy was no longer hav-) S5 Y) O4 `4 O3 ?2 }6 N, W: T. j
ing frequent erections.
! ]' E8 P; V( D8 B+ \Both parents were again questioned about use of* Q- ~1 ?! ^9 R. C7 w
any ointment/creams that they may have applied to) d& \- N6 s2 y8 a6 ?. c
the child’s skin. This time the father admitted the- o: W% w9 S- t' c: G" W  m
Topical Testosterone Exposure / Bhowmick et al 541! _# M/ }" Y5 p0 P! g
use of testosterone gel twice daily that he was apply-4 b' a/ @- P- b6 p* x7 X
ing over his own shoulders, chest, and back area for
7 Z9 x- i5 f+ @: G( n& M) y8 Oa year. The father also revealed he was embarrassed, g5 j5 J/ @) T; B- q9 ^4 ]0 E, w& ^$ d
to disclose that he was using a testosterone gel pre-: o# i& b; \9 n1 m4 ^/ d
scribed by his family physician for decreased libido
: n+ B' U8 {* L; `; |7 Wsecondary to depression.: L- g6 d8 w+ {) f, U' |* Y
The child slept in the same bed with parents.
$ r* U9 e) E4 gThe father would hug the baby and hold him on his
0 Z0 n1 |- Z3 Vchest for a considerable period of time, causing sig-
) H" ~/ u  w' u# E+ jnificant bare skin contact between baby and father.. p- G# ]" ~9 F
The father also admitted that after the phone call,5 w+ a% K  D3 \( k/ f2 B; g
when he learned the testosterone level in the baby; R8 x$ }8 h1 L- ^
was high, he then read the product information$ x! ~5 ]* X" a4 G' A
packet and concluded that it was most likely the rea-
" }( t1 @6 n7 b  N& G$ dson for the child’s virilization. At that time, they
% s- ^  A$ {1 Y7 K% @( E. u1 Mdecided to put the baby in a separate bed, and the; C7 u4 [% M$ V4 w) r) f& S
father was not hugging him with bare skin and had) v, _0 }( a6 o- v
been using protective clothing. A repeat testosterone
5 w6 `, I# m" Y' R3 f+ btest was ordered, but the family did not go to the
4 a* g  Q9 C9 z% ?* i7 claboratory to obtain the test.
& F* f7 C2 g2 p3 ?; cDiscussion
' I3 @, R  e- {( l# ~Precocious puberty in boys is defined as secondary+ k6 K6 o! i; L" D( h
sexual development before 9 years of age.1,4: O$ c5 U6 N: E' d: M; A
Precocious puberty is termed as central (true) when
" w  G  k/ v, w/ J+ Mit is caused by the premature activation of hypo-1 S% q3 s* l2 _1 `) g* C# n
thalamic pituitary gonadal axis. CPP is more com-. U/ u/ ~$ P2 l( I3 i
mon in girls than in boys.1,3 Most boys with CPP6 T: v* p: g4 p$ n; p7 H
may have a central nervous system lesion that is# j) B, C) h5 H, q! a# K
responsible for the early activation of the hypothal-
$ l1 U/ A0 F9 X7 `6 V, h1 q8 Xamic pituitary gonadal axis.1-3 Thus, greater empha-/ T( ~% y# o. F, d, m
sis has been given to neuroradiologic imaging in9 R4 B9 V0 |7 d. }7 b
boys with precocious puberty. In addition to viril-
. U/ n% h9 @' `- Rization, the clinical hallmark of CPP is the symmet-' d& D* r( s* e6 T, t+ c3 K
rical testicular growth secondary to stimulation by$ ?5 i  ?/ C; v) o
gonadotropins.1,3
8 i2 s  [7 |) }5 ^Gonadotropin-independent peripheral preco-+ ?; @' L# ]2 ?& r8 b6 B) w$ T8 h
cious puberty in boys also results from inappropriate
. U$ D- h2 Q9 J+ j, s, L9 candrogenic stimulation from either endogenous or
; `2 n' R5 p1 b* x2 e. Cexogenous sources, nonpituitary gonadotropin stim-4 [. o9 g- a2 N6 N, E% a  j
ulation, and rare activating mutations.3 Virilizing
. b  D9 o/ |9 N' M: mcongenital adrenal hyperplasia producing excessive
% C) w' }& w$ J9 C3 X+ {- v% aadrenal androgens is a common cause of precocious
; {" p" @% f5 K; `2 Mpuberty in boys.3,4+ n3 D6 `$ a# }1 [7 C. M+ Z6 V3 v! T
The most common form of congenital adrenal
6 Q. \7 `( }" O& Y. j- T/ \2 x; Nhyperplasia is the 21-hydroxylase enzyme deficiency./ I7 G  l( J. O" G. [, \" e; B
The 11-β hydroxylase deficiency may also result in
/ ~8 N+ V9 E& s3 U/ Y7 [: @& Yexcessive adrenal androgen production, and rarely,$ B1 c, V3 T" ]5 j0 @# U  S3 Y7 C
an adrenal tumor may also cause adrenal androgen/ V$ a7 N  c" E: r( g
excess.1,34 `, V( \9 T5 g4 l# u! n
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; C+ S+ m6 N, F( p+ m5 c542 Clinical Pediatrics / Vol. 46, No. 6, July 2007! r, O. D+ n& Q+ V& n& i- f
A unique entity of male-limited gonadotropin-
5 w# n& M! B' w) E* l2 xindependent precocious puberty, which is also known; W' r8 p! T! m0 K
as testotoxicosis, may cause precocious puberty at a
: i- N0 R. w! z4 _/ \4 qvery young age. The physical findings in these boys  |  n! ?) @4 s0 Z( ^
with this disorder are full pubertal development,3 ~/ V) k+ F  `# L
including bilateral testicular growth, similar to boys
( d2 o6 k7 @/ K9 Y$ ?) fwith CPP. The gonadotropin levels in this disorder0 I7 S% i& Y; N  i
are suppressed to prepubertal levels and do not show
4 f1 p+ N- w/ v5 h' W) Z1 u4 ypubertal response of gonadotropin after gonadotropin-
' W) X1 ^( k/ X  T' M1 Yreleasing hormone stimulation. This is a sex-linked2 ~5 q& G4 \1 e" b4 R6 ^' u
autosomal dominant disorder that affects only
: D$ P( z* C; C& E1 Y$ U1 D7 Umales; therefore, other male members of the family
' _$ O0 I$ p- x1 K$ Jmay have similar precocious puberty.31 H! H# H* q, h0 E# H
In our patient, physical examination was incon-2 {8 T- Z# R! k* X' w6 \! W$ E( K: W
sistent with true precocious puberty since his testi-) g7 a# L/ _, Z/ i
cles were prepubertal in size. However, testotoxicosis
( |! b( n$ V! B' D0 T( A" Ywas in the differential diagnosis because his father
4 K5 X6 q+ V/ R1 W+ k9 D5 \started puberty somewhat early, and occasionally,  j/ ~$ }1 a. u, W% J, p
testicular enlargement is not that evident in the- e7 ?$ k% h5 C; a3 s* c! T1 ?! ]
beginning of this process.1 In the absence of a neg-8 |2 F. F1 V4 G/ K
ative initial history of androgen exposure, our
' `; O' m5 }$ ]/ h+ ~* xbiggest concern was virilizing adrenal hyperplasia,- }! s  b6 h9 o, C+ F
either 21-hydroxylase deficiency or 11-β hydroxylase: Y6 j  w. C- n+ U5 i# F% \& z
deficiency. Those diagnoses were excluded by find-
) H( [5 T" b% N4 b7 \1 ]) q% Iing the normal level of adrenal steroids.1 R5 m" z; `: ?/ l1 L
The diagnosis of exogenous androgens was strongly
: q# C! T4 S3 \suspected in a follow-up visit after 4 months because
5 \' `; b. H% ^# l7 p- U& d" t1 Athe physical examination revealed the complete disap-
" g& I% m! }' W3 Q+ X; Apearance of pubic hair, normal growth velocity, and# v: I, ~8 q2 n$ k4 q1 j
decreased erections. The father admitted using a testos-$ R+ ~& N7 s7 f1 _5 U4 V  ?8 F8 _
terone gel, which he concealed at first visit. He was
# m2 L0 t) P9 \$ {8 Ousing it rather frequently, twice a day. The Physicians’
; R- L1 ^4 ^7 [Desk Reference, or package insert of this product, gel or
9 ~7 M; n0 @: |, d+ Mcream, cautions about dermal testosterone transfer to
8 q& h2 j) D- p8 Punprotected females through direct skin exposure.
) Z: x# I# w& ZSerum testosterone level was found to be 2 times the
$ l. E# U3 ~" r9 ~" F5 Vbaseline value in those females who were exposed to1 [/ p* `; {& q9 H* i( d
even 15 minutes of direct skin contact with their male$ u0 }! W( Z$ g! q
partners.6 However, when a shirt covered the applica-
9 ]# l3 S+ [" e/ ~tion site, this testosterone transfer was prevented.
! |% \& J( k2 R9 K. u( \/ t8 OOur patient’s testosterone level was 60 ng/mL,
% m9 U( S8 W; D% I9 t% z, r  b! xwhich was clearly high. Some studies suggest that
1 d  D% X7 ~/ Ddermal conversion of testosterone to dihydrotestos-
& v0 j. k# }4 sterone, which is a more potent metabolite, is more
8 c- }1 C+ R7 Q7 a& b& S0 d4 ~2 Pactive in young children exposed to testosterone2 f0 ^" b6 ]/ `: ?8 R
exogenously7; however, we did not measure a dihy-
) X0 M- G, }/ A- W/ j/ x" Odrotestosterone level in our patient. In addition to
2 p/ v' ~6 n1 ?virilization, exposure to exogenous testosterone in
0 W  {7 o. `! i+ Hchildren results in an increase in growth velocity and
. M9 ]; u  a8 V( ~advanced bone age, as seen in our patient.5 b' d: k" r  q4 G5 e1 z' `
The long-term effect of androgen exposure during
, q6 l9 R& B/ @0 u- oearly childhood on pubertal development and final
0 a! F: e& _9 l& ~% b% m! tadult height are not fully known and always remain
; s7 {9 Y7 P' H/ y* ua concern. Children treated with short-term testos-
. @8 X5 w* B/ c9 p6 w! O, fterone injection or topical androgen may exhibit some
9 Z; R% r' W/ h$ n7 A+ Macceleration of the skeletal maturation; however, after* m( v8 ]1 F+ v5 y" ~5 V
cessation of treatment, the rate of bone maturation
( e, g! j1 l& p6 J. s/ S5 p9 sdecelerates and gradually returns to normal.8,9
) ~; q. X5 c- E1 ]0 i* O" M, m1 {/ vThere are conflicting reports and controversy
7 k* E& i* ]2 P( l$ _' s/ U, }over the effect of early androgen exposure on adult: x0 [" n& q6 x8 u/ C5 m
penile length.10,11 Some reports suggest subnormal
3 B! `! {4 I8 c7 radult penile length, apparently because of downreg-
8 d' J6 j, G; P2 O- {( S2 H2 Fulation of androgen receptor number.10,12 However,
: i6 l& Z4 L6 h. R' M1 O' ^. |Sutherland et al13 did not find a correlation between) c! B% n2 n: n$ d4 |
childhood testosterone exposure and reduced adult
2 I( x1 d2 C( V& v, lpenile length in clinical studies., J# y. p) D% {
Nonetheless, we do not believe our patient is
3 h% B8 s$ w- Z3 F: Cgoing to experience any of the untoward effects from2 U$ |- F+ E1 T8 n, m
testosterone exposure as mentioned earlier because
, |; f; |  N7 X' V' Mthe exposure was not for a prolonged period of time.& Q6 i6 m+ b& B  I( Q5 v- G
Although the bone age was advanced at the time of
. ~: Q7 ^- I  r, V4 V2 adiagnosis, the child had a normal growth velocity at  m. N4 d) p2 i% P( X- l
the follow-up visit. It is hoped that his final adult
% p% y4 u2 }3 O$ i; H1 Yheight will not be affected.8 d" F" m' y( A1 Y2 `# p4 f
Although rarely reported, the widespread avail-  N  b) `8 d9 ^. n
ability of androgen products in our society may) ^# x  |( ]9 l4 O8 i0 H/ ~
indeed cause more virilization in male or female/ C( n1 _8 _$ |1 A
children than one would realize. Exposure to andro-
8 H5 Z; \! x( R' bgen products must be considered and specific ques-! v1 T( M9 w( ^& A' X/ z- B
tioning about the use of a testosterone product or! S, O% b- Q3 D& [# e6 f9 N8 Z
gel should be asked of the family members during8 u; t! w9 W1 h" f% N1 S2 ?* j% Z
the evaluation of any children who present with vir-
: q. B0 m* ~/ y- y( l+ Y6 Bilization or peripheral precocious puberty. The diag-6 W- T: |) ]% e# G8 \% T
nosis can be established by just a few tests and by3 @, M6 m! H# g0 p
appropriate history. The inability to obtain such a& ~. E" J. y& ^
history, or failure to ask the specific questions, may
2 v8 T+ U# l" {' ~8 ?result in extensive, unnecessary, and expensive5 z& a+ U" l7 B5 E" f* @, G
investigation. The primary care physician should be
; F; @: R  y; X0 D' V) gaware of this fact, because most of these children
, A1 B& P) ~" {' a. |! Amay initially present in their practice. The Physicians’/ S, I( T( U: M3 {& \2 F
Desk Reference and package insert should also put a; g3 A1 _( f/ q7 Y0 \/ t  i5 L0 I
warning about the virilizing effect on a male or, l4 @# x# d: O* L, y
female child who might come in contact with some-
" J1 _" o2 v& Z& s4 z0 r; ~one using any of these products./ y( B( q( w+ G' T+ s2 W) f" Q0 i
References) o4 Q1 B1 Q) x7 G3 v4 l* u
1. Styne DM. The testes: disorder of sexual differentiation
8 u# B# \: i- B' t* Yand puberty in the male. In: Sperling MA, ed. Pediatric
% B2 D8 O! b) w" x& z0 P+ W$ O1 JEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;2 ]0 m# O7 g2 q
2002: 565-628.
+ C& _% J, P  B+ x* `2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- R5 s' H4 e6 \6 j- o. k
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old# G9 m6 F5 @" b
Boy Induced by Indirect Topical# `9 n1 {: T+ y/ V! z! R% X
Exposure to Testosterone! o  l7 |1 R0 A. x. o# f
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,29 z9 a6 |6 }7 A# |
and Kenneth R. Rettig, MD1- y  F, ]4 l; z3 ]( Z( D
Clinical Pediatrics
" P0 B& _, x0 x5 x3 PVolume 46 Number 65 @( z) W# m- T8 C/ z9 h3 ?
July 2007 540-543
8 B, |6 F8 i& h( f2 i0 i+ J( k© 2007 Sage Publications  `3 @. x) E# m# `
10.1177/0009922806296651. h/ k* a  H  h: l  u( I2 `
http://clp.sagepub.com
! x5 ]6 b! {: A" Y* shosted at/ L- s$ \. D- S. X
http://online.sagepub.com8 F! v' r" [* |$ h2 f" x# ]
Precocious puberty in boys, central or peripheral,% M/ q" X3 e" s1 {( F' G# [
is a significant concern for physicians. Central
7 G5 Y1 P7 m4 o. Q4 H$ Hprecocious puberty (CPP), which is mediated$ h- N, f. ~: ]& Y% l
through the hypothalamic pituitary gonadal axis, has: y  H4 T0 D, |1 z3 Y
a higher incidence of organic central nervous system( D% s7 U' Z8 K( q7 D# X
lesions in boys.1,2 Virilization in boys, as manifested% t, g5 s3 o5 z
by enlargement of the penis, development of pubic5 F! k- J& C/ [( n
hair, and facial acne without enlargement of testi-
1 O( s  n. I4 {; p( ucles, suggests peripheral or pseudopuberty.1-3 We' Z# X& ~8 w, X! }3 O) ?; A" B6 X. {
report a 16-month-old boy who presented with the8 k; Y* i2 ?0 x
enlargement of the phallus and pubic hair develop-% d  L; O' j9 ]0 b
ment without testicular enlargement, which was due8 G" F. L/ E% m
to the unintentional exposure to androgen gel used by! A9 H. J; q, |! p% f
the father. The family initially concealed this infor-, b5 b# q2 g* I; t  c5 Z" c' J
mation, resulting in an extensive work-up for this
& |9 h' ~9 @( Qchild. Given the widespread and easy availability of2 U) @" n3 h* T! \0 H
testosterone gel and cream, we believe this is proba-7 S) ^& Q8 P) i3 W
bly more common than the rare case report in the3 I9 `* O1 B2 h7 K
literature.48 Y3 l  f' i) g  e2 C. e- g5 y
Patient Report4 G" G  V7 ~: Y4 z
A 16-month-old white child was referred to the
8 P+ ^( G* I# n: t* h) J, A# dendocrine clinic by his pediatrician with the concern# I6 E9 h$ B- O* N4 ^
of early sexual development. His mother noticed
+ g2 s6 V# z: P* W' alight colored pubic hair development when he was6 l# W' S; F3 A0 P
From the 1Division of Pediatric Endocrinology, 2University of
7 H7 ^  `. c8 f" ]  ^/ M1 j6 fSouth Alabama Medical Center, Mobile, Alabama.
% p% a' y9 M8 j' vAddress correspondence to: Samar K. Bhowmick, MD, FACE,
" K9 u5 Y. v6 a" r. o* xProfessor of Pediatrics, University of South Alabama, College of  m( P; c6 J0 R, P; K/ H* `& J
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;2 a: G' H* M( F  }
e-mail: [email protected].
0 y$ s# B' b# G5 Z3 Y8 R6 Sabout 6 to 7 months old, which progressively became7 i0 Z3 C$ t" p' |. c! v/ P
darker. She was also concerned about the enlarge-" G+ v' |! \. L8 m
ment of his penis and frequent erections. The child
" l2 d) D6 Q5 Y' p' gwas the product of a full-term normal delivery, with  c" h" [! L" X+ e
a birth weight of 7 lb 14 oz, and birth length of& v; z! a  O( n0 u* d& X2 p
20 inches. He was breast-fed throughout the first year* Y  v# F+ s- o9 Z+ Q
of life and was still receiving breast milk along with  e$ W1 u( ~! Z! Y  ]* }
solid food. He had no hospitalizations or surgery,: Q0 u3 p6 a; z& v: Q8 ?+ ~
and his psychosocial and psychomotor development0 E* F9 a. F: L
was age appropriate.* ]( i9 d9 Q  k
The family history was remarkable for the father,% z; J. ~6 U% m  H* I1 ?% R: z
who was diagnosed with hypothyroidism at age 16,
- {; n3 L) G2 v+ w+ ewhich was treated with thyroxine. The father’s
# Z9 x5 S/ v, s  \; Mheight was 6 feet, and he went through a somewhat$ {, Q  j, y5 [5 t( r
early puberty and had stopped growing by age 14.! j: V$ I. I$ j# O$ A& Z, q$ k* Q& E! d
The father denied taking any other medication. The
  i9 S. D5 T8 ochild’s mother was in good health. Her menarche9 c" A" t3 |! Z' m& f4 R
was at 11 years of age, and her height was at 5 feet
1 Q: r: p+ g3 g3 w5 inches. There was no other family history of pre-
% J/ u9 V" f2 `$ `* z9 Q9 F! b" Qcocious sexual development in the first-degree rela-
' q# {# n( n8 Dtives. There were no siblings.
$ s  }5 g# S! ]Physical Examination2 X9 c% l5 R' m3 G( j
The physical examination revealed a very active,
* w8 W6 D; o. S; z" ~# u1 u0 dplayful, and healthy boy. The vital signs documented. Y2 f/ u% G4 z1 a9 r8 s% X
a blood pressure of 85/50 mm Hg, his length was
: M! T* k9 ]3 t4 Z* I7 o" y% y90 cm (>97th percentile), and his weight was 14.4 kg
% t  H4 ]9 z( T) L3 G- n(also >97th percentile). The observed yearly growth
. [4 S: P: b" r' r5 dvelocity was 30 cm (12 inches). The examination of+ l8 w% F& R; ^! P+ s6 E3 r5 r, [6 i- T7 Z
the neck revealed no thyroid enlargement.6 ^. m# r) {  C+ B  d1 ?
The genitourinary examination was remarkable for
, o' B8 b- a. ~enlargement of the penis, with a stretched length of
8 Y! ^" C" K' s) y: l+ i8 cm and a width of 2 cm. The glans penis was very well
8 \4 F4 T1 D5 X$ `1 \! Zdeveloped. The pubic hair was Tanner II, mostly around) N4 g7 \* j. s
540
( }1 o4 n) \; ]1 mat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from& e, h, H# @, J0 Q5 K6 p
the base of the phallus and was dark and curled. The
& V# h3 S; s# ?4 Btesticular volume was prepubertal at 2 mL each.1 e9 R9 p+ I, r' }
The skin was moist and smooth and somewhat
/ R4 c- s. G6 k. roily. No axillary hair was noted. There were no
; _2 V4 {* p% D$ ~* Wabnormal skin pigmentations or café-au-lait spots.7 G0 h7 O% x6 S" @; b) y& v! _
Neurologic evaluation showed deep tendon reflex 2+% T0 v  X  w1 X, R; X% e
bilateral and symmetrical. There was no suggestion
) e% K$ F) S( ^of papilledema.) _" I6 p$ a% S
Laboratory Evaluation; A/ M! l$ A/ q2 w6 U
The bone age was consistent with 28 months by0 ~0 G- X2 t6 h- x; h
using the standard of Greulich and Pyle at a chrono-
7 m4 k! ~6 r, ]/ B8 Xlogic age of 16 months (advanced).5 Chromosomal2 y! |9 @' @+ {6 d; \. |$ B+ E
karyotype was 46XY. The thyroid function test4 S1 f6 j( M( v' a
showed a free T4 of 1.69 ng/dL, and thyroid stimu-8 p4 a: `, F  h6 \1 X$ S1 h. m
lating hormone level was 1.3 µIU/mL (both normal).- ]# D: _# R2 E* Y* [
The concentrations of serum electrolytes, blood6 ?9 O" f1 X& {" i) @1 q  n1 l
urea nitrogen, creatinine, and calcium all were9 b$ f; m. q& E! {  f8 u
within normal range for his age. The concentration% Z( v' x; m! {) y: R- N! }3 Y- W
of serum 17-hydroxyprogesterone was 16 ng/dL0 a% v/ f5 f" w2 f  @
(normal, 3 to 90 ng/dL), androstenedione was 20
3 F" z: K# ^8 L7 a: D+ Vng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-3 c% B2 O& n) |2 [& P- X$ O( g
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
, [1 `) d* X4 f8 Y6 _desoxycorticosterone was 4.3 ng/dL (normal, 7 to, s* Q# ^1 u# T, g' R: }0 u: Y3 d. f  Q
49ng/dL), 11-desoxycortisol (specific compound S)
7 J" M( P+ H" Bwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 y: A8 K( e, S  r3 Q
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total7 _* `6 [( ~* K4 i
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
! s8 }9 c5 r. U9 b# }and β-human chorionic gonadotropin was less than4 V" k) Z, r; l2 A& o& @1 X
5 mIU/mL (normal <5 mIU/mL). Serum follicular
* ^; L' ~% `' h  }8 ?2 t3 Sstimulating hormone and leuteinizing hormone; B; t* L8 o; w( t
concentrations were less than 0.05 mIU/mL
5 I$ c7 N6 h4 M- B; D(prepubertal).1 @" C) J6 `3 X; C
The parents were notified about the laboratory
2 B% `$ T1 T0 w0 c& p  Jresults and were informed that all of the tests were8 |% b7 F# v" K' x
normal except the testosterone level was high. The
+ s' S" {6 W# M& y. l, Dfollow-up visit was arranged within a few weeks to+ @# }' Y) ], k6 ]3 J
obtain testicular and abdominal sonograms; how-( K3 h* k$ J6 R
ever, the family did not return for 4 months.9 t+ J' Y6 g, n. f% w  b
Physical examination at this time revealed that the+ g. ?! {3 L  T5 }6 ?
child had grown 2.5 cm in 4 months and had gained
. n" D1 P6 w8 a: ]) [% Z2 kg of weight. Physical examination remained- v# L& d5 f/ z) P
unchanged. Surprisingly, the pubic hair almost com-
$ h% f4 ?/ ~) Y; |7 Hpletely disappeared except for a few vellous hairs at
. o4 }* g- T  w' V  `( vthe base of the phallus. Testicular volume was still 2
- T$ A! _. r& S( pmL, and the size of the penis remained unchanged./ t$ z7 J; X( {
The mother also said that the boy was no longer hav-8 i& e% U% C8 K8 d
ing frequent erections.! i8 ^  g6 Z  _1 c# Y/ U6 K2 z
Both parents were again questioned about use of0 a  e* G  i* w& T, D8 Q+ E
any ointment/creams that they may have applied to( ^! d' P# e5 w8 R/ x. ^7 W0 P- E
the child’s skin. This time the father admitted the5 u7 p, m7 c  p
Topical Testosterone Exposure / Bhowmick et al 541
) K* [# A7 f0 F# W8 guse of testosterone gel twice daily that he was apply-+ u1 }. S( t6 U1 Y) p: U
ing over his own shoulders, chest, and back area for
( A: k5 Q; H! Y8 {7 @& W* ]" w) E4 _a year. The father also revealed he was embarrassed
8 S, l$ Y0 d9 {5 ato disclose that he was using a testosterone gel pre-; x* u' x( I# r/ b$ X
scribed by his family physician for decreased libido
. F; {( m- I& _' q& y% Q4 ]secondary to depression.& l9 l- ^4 Z4 w4 b
The child slept in the same bed with parents.0 b. ?# i* k6 V( Z
The father would hug the baby and hold him on his# x+ {) A3 K: G2 i' ~) P( `
chest for a considerable period of time, causing sig-
9 ^" S9 {4 i1 b8 R/ R3 j; }# dnificant bare skin contact between baby and father.! P" u0 |5 R. M2 }8 I- ~) D8 W
The father also admitted that after the phone call,
, e' S- l4 f/ Y0 Uwhen he learned the testosterone level in the baby$ U0 U* ]* S% o7 N
was high, he then read the product information. y, D% I7 H, }$ b! Q! Q6 W: P
packet and concluded that it was most likely the rea-4 ?: o% f& G0 v  u
son for the child’s virilization. At that time, they  ^2 b& Z) }- d# X6 K
decided to put the baby in a separate bed, and the0 |- X! }  z0 v0 A  @
father was not hugging him with bare skin and had
( z9 H5 N! w  kbeen using protective clothing. A repeat testosterone& d2 V( m! ?5 C- y  P, u/ q' i$ J
test was ordered, but the family did not go to the$ J: \% ^$ J5 o. r- s% j
laboratory to obtain the test.% }! P2 @( p6 u, D; ^
Discussion
4 q1 m4 @9 h1 U4 ?( F8 C) g) WPrecocious puberty in boys is defined as secondary/ F# x% J  t" H
sexual development before 9 years of age.1,4- X" @. g2 Y9 O4 V) x. P
Precocious puberty is termed as central (true) when
2 J6 E$ @3 L) ~9 t& i6 N2 Jit is caused by the premature activation of hypo-$ |  T4 x; P% h2 a& a; m$ d. z
thalamic pituitary gonadal axis. CPP is more com-
5 g6 [1 s3 p- }mon in girls than in boys.1,3 Most boys with CPP
3 q: ~9 ]" g8 Z1 O; v; d3 i. S2 [may have a central nervous system lesion that is" y7 G5 e% ]3 U* B
responsible for the early activation of the hypothal-
4 t% W( _, t' t7 Z/ Q/ Zamic pituitary gonadal axis.1-3 Thus, greater empha-+ d) D/ u+ l1 }( I
sis has been given to neuroradiologic imaging in# k1 `& h1 C3 }: N
boys with precocious puberty. In addition to viril-
0 n# T. m3 i. g3 uization, the clinical hallmark of CPP is the symmet-
4 t3 [' |4 Z" Trical testicular growth secondary to stimulation by) x5 K9 }2 Q5 p/ {7 E
gonadotropins.1,3( r1 Y; s7 a6 Y( ^
Gonadotropin-independent peripheral preco-
$ \4 B5 `# A& e6 U: R; ycious puberty in boys also results from inappropriate
5 D4 `0 f8 g- H! \, q# Qandrogenic stimulation from either endogenous or! h  F5 V4 t# X8 w+ d
exogenous sources, nonpituitary gonadotropin stim-
2 O! L$ v$ R' r  julation, and rare activating mutations.3 Virilizing
& _& d5 ~; a' t% q& l/ \% |congenital adrenal hyperplasia producing excessive
2 m9 \% A5 v* o5 c5 B% j+ B2 H2 D4 yadrenal androgens is a common cause of precocious
$ m  H- m2 Q3 A- `0 N6 [  @puberty in boys.3,4
5 j& c2 k' j" b3 Y/ G$ CThe most common form of congenital adrenal
$ e; p: q! L/ thyperplasia is the 21-hydroxylase enzyme deficiency.; m. V8 o0 |/ L; t  E9 |5 y+ S! A
The 11-β hydroxylase deficiency may also result in( @% e0 b8 N/ W0 W5 l
excessive adrenal androgen production, and rarely,
  y) J( J8 ?+ @4 van adrenal tumor may also cause adrenal androgen
9 {9 Y; x) M8 Y8 F/ h* Z1 Uexcess.1,3
  D/ g- A3 ~' K) o; q3 yat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from! M! K  K% r/ F0 j3 O: Q2 M
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
- u+ h9 @" K; ^5 h5 t$ AA unique entity of male-limited gonadotropin-
. w, f$ u9 Z+ W* B, q; F/ dindependent precocious puberty, which is also known
7 ]' R, L6 j; Q* ]3 S; gas testotoxicosis, may cause precocious puberty at a! z4 s3 X" r% D7 X
very young age. The physical findings in these boys" ^3 i% j* x- d) k6 y1 i3 d
with this disorder are full pubertal development,7 x& X  u* e5 z; ^: a4 }8 ]
including bilateral testicular growth, similar to boys
) D+ }4 A! N+ b& m5 @6 ?with CPP. The gonadotropin levels in this disorder, S% Y  h4 h/ s) `
are suppressed to prepubertal levels and do not show" c) n* P7 ?  v0 o
pubertal response of gonadotropin after gonadotropin-
, Y4 V9 w  w) ~6 Q, ]0 A1 j  T! Dreleasing hormone stimulation. This is a sex-linked6 L# L2 W8 q/ `. Z6 g; {
autosomal dominant disorder that affects only$ P- k* a6 b0 E) I: \5 l
males; therefore, other male members of the family
& p/ Q& g/ b9 q  omay have similar precocious puberty.3( n/ `! @! _4 m9 o0 u
In our patient, physical examination was incon-
: W: e4 h# _+ a- f! usistent with true precocious puberty since his testi-
, I6 L+ @/ J* O) m  A) Pcles were prepubertal in size. However, testotoxicosis1 Q% T, s: ?3 R
was in the differential diagnosis because his father
  v6 s/ l8 A8 x' U* Fstarted puberty somewhat early, and occasionally,$ a2 V9 z" S8 ~
testicular enlargement is not that evident in the8 \/ N! j1 @  G( A$ F# p2 h% Q
beginning of this process.1 In the absence of a neg-
2 x4 q1 M/ N( X% z% y! Y) J+ Aative initial history of androgen exposure, our
) _& t. [/ |% k7 ^1 Sbiggest concern was virilizing adrenal hyperplasia,
- x" c2 |. I  E! e+ O/ C" {either 21-hydroxylase deficiency or 11-β hydroxylase
2 |& f: N. }) p# v# Q; Ldeficiency. Those diagnoses were excluded by find-
: N# a0 s: @/ ying the normal level of adrenal steroids.) H! m( ^/ k$ K' B( z
The diagnosis of exogenous androgens was strongly$ f' A# F2 D3 _$ g" A
suspected in a follow-up visit after 4 months because0 j! b  k) [6 @' U
the physical examination revealed the complete disap-
8 K8 k  j# V! E1 mpearance of pubic hair, normal growth velocity, and
" y( h+ t5 G) x) G( @decreased erections. The father admitted using a testos-* P$ G% m' l5 b  N" G. P3 f  D
terone gel, which he concealed at first visit. He was( |" n- W6 G9 |1 v2 J
using it rather frequently, twice a day. The Physicians’
) L8 z$ `4 w  l5 z3 i! J) P& }# CDesk Reference, or package insert of this product, gel or$ F: s0 g8 D% p' n+ ]& @2 h/ G
cream, cautions about dermal testosterone transfer to
+ r- j5 i& G3 |unprotected females through direct skin exposure.; ^! t; W. _; Z; j/ m- I2 V& Z) h
Serum testosterone level was found to be 2 times the( u( g# X4 i# M1 _  U9 y
baseline value in those females who were exposed to
* |" |3 K- d' K7 x) jeven 15 minutes of direct skin contact with their male
& q3 R4 A" G) L: zpartners.6 However, when a shirt covered the applica-
3 G/ K6 @( N) Z9 {4 c$ Otion site, this testosterone transfer was prevented.1 Z' H1 u! I' _5 `
Our patient’s testosterone level was 60 ng/mL,
8 N: O8 c; y, [! a( B7 ?( Qwhich was clearly high. Some studies suggest that( x& ?* d4 Z9 r' _! Q2 z
dermal conversion of testosterone to dihydrotestos-* S- O  o& ~6 N( ~! Y% J
terone, which is a more potent metabolite, is more9 ]0 n6 i; ~! G. Y. N# F6 D
active in young children exposed to testosterone
' W2 p+ {& i8 F* |2 b& d: fexogenously7; however, we did not measure a dihy-1 Q; M) T: p/ y& A( w4 n
drotestosterone level in our patient. In addition to
& z7 e2 L" w4 k3 @virilization, exposure to exogenous testosterone in
+ e, w: m' M  `% a+ h; m+ C" dchildren results in an increase in growth velocity and
' k1 d8 \: n1 N# s5 f0 \advanced bone age, as seen in our patient.8 d. B8 F2 y( ?
The long-term effect of androgen exposure during4 S$ k# K9 Q% N7 a
early childhood on pubertal development and final' \# [, o/ N3 M, y1 {% t- n: j6 ^
adult height are not fully known and always remain. e- l+ }) t( p5 J: b7 e) s
a concern. Children treated with short-term testos-
% i3 ]' p3 H* g* R' {% J, x& H$ |  f6 _terone injection or topical androgen may exhibit some
& c& L7 J7 Y8 Q9 Aacceleration of the skeletal maturation; however, after
! P% U7 f: ?! L. _$ |cessation of treatment, the rate of bone maturation  g. x. M- O9 P/ w9 o
decelerates and gradually returns to normal.8,9
1 s% Q$ m, b, ~There are conflicting reports and controversy6 a* x; ]9 k2 K$ y5 ]: a5 l
over the effect of early androgen exposure on adult
+ K' I# @, q. q. [penile length.10,11 Some reports suggest subnormal
& X; p! `: A" n" `. S* q2 q0 Badult penile length, apparently because of downreg-
, g2 @/ q' _: b" d8 d" E+ C( ?: Dulation of androgen receptor number.10,12 However,2 F* C7 J1 z" m9 j
Sutherland et al13 did not find a correlation between4 O  _# N5 g, |7 P: ~- |
childhood testosterone exposure and reduced adult
4 Z2 j2 k& c' W4 ]1 mpenile length in clinical studies.
% m" i1 A% n4 X( r" \" s8 k. M! aNonetheless, we do not believe our patient is8 ]9 `! L5 b1 r$ E+ ~' r; N  @
going to experience any of the untoward effects from. v2 ~3 b8 e0 J2 G
testosterone exposure as mentioned earlier because% ?( C4 F7 p1 C, ]) y: h
the exposure was not for a prolonged period of time.
; U7 l# q' h! W: _  D0 tAlthough the bone age was advanced at the time of
  R/ m6 Q6 Q! s1 Q' A3 {diagnosis, the child had a normal growth velocity at: [( M4 ^1 d/ ~( J$ I' e
the follow-up visit. It is hoped that his final adult
$ O8 V" f7 B( e: Xheight will not be affected.0 H% j$ w/ q! O5 W) d/ F7 w( j
Although rarely reported, the widespread avail-
$ F  G$ |$ U' ^: q( X: B) Iability of androgen products in our society may* B, P1 J5 s% s0 Z# ?
indeed cause more virilization in male or female
. n1 Y' s/ Q& s& K2 |6 Rchildren than one would realize. Exposure to andro-
, g3 r3 R8 `" X7 f- {! t% tgen products must be considered and specific ques-1 ?& D: v; C7 A% V) u
tioning about the use of a testosterone product or
7 m( ?8 i$ H+ g0 A" \' b2 ~4 Sgel should be asked of the family members during" C3 u+ x7 r, r" ?; \5 l
the evaluation of any children who present with vir-
+ M: p$ \1 q& w) y0 G6 _ilization or peripheral precocious puberty. The diag-
/ |; W9 h6 e* pnosis can be established by just a few tests and by' k3 m) K  }: N" s& i5 i/ d* W$ {
appropriate history. The inability to obtain such a
0 O! j6 J1 S0 j( p& Hhistory, or failure to ask the specific questions, may: C7 i, i' X+ u7 o
result in extensive, unnecessary, and expensive
, c% B; w" A9 B6 ?investigation. The primary care physician should be% `$ p" `% v; a4 g& L, w
aware of this fact, because most of these children
% C8 V" I/ x$ D9 c  p4 Amay initially present in their practice. The Physicians’9 ~# h6 m/ b1 _! u* H* [
Desk Reference and package insert should also put a
( l* n+ [* H0 b# Y; q' \warning about the virilizing effect on a male or
* Y2 t5 l# K, W( G9 i0 }( M+ _female child who might come in contact with some-) n# B9 h" c* q& ^" a/ D8 q7 ]
one using any of these products.
, e! A, J" Y5 r6 }8 JReferences* E6 e& |3 c1 _0 z; d2 z
1. Styne DM. The testes: disorder of sexual differentiation# X' W7 q  f, i$ g9 c& {% e- T, x) @
and puberty in the male. In: Sperling MA, ed. Pediatric2 C9 C  n# ?* A# n9 a
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;% s# `2 }; B) W7 L3 O
2002: 565-628./ U6 }9 g+ F3 H1 ?# P
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; }$ H. ?. d. ^' Q: N
puberty 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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
感謝大大的辛勞分享!我會繼續在WK關注大大的文章!
發表於 2025-1-11 22:18:01 | 顯示全部樓層
女厕偷拍辅导班主任尿尿老师的逼很嫩还有一点
發表於 2025-1-17 16:31:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層
1 U& T8 j, v# P9 Z# J
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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