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Sexual Precocity in a 16-Month-Old" p0 N  X9 D6 L3 B! E2 F
Boy Induced by Indirect Topical8 _& c7 e( ]! F* i# ]$ W
Exposure to Testosterone
4 N; m2 F% N; k5 o; [- w$ m; z: ^Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
/ {: P6 ?0 d/ Aand Kenneth R. Rettig, MD1
0 s0 i. _5 R; D) {/ }Clinical Pediatrics
3 y  Z3 W* k0 h! oVolume 46 Number 6' p7 F" _; B: i, |- E. U+ s: I
July 2007 540-543
# _" O5 K% E; H' }" u/ k© 2007 Sage Publications
4 r! c  z5 r" w% O! y10.1177/0009922806296651& B, O! r' F; J- o' F
http://clp.sagepub.com4 O0 [9 |) B9 y: {# w0 z
hosted at
2 I% y  O# z& D& R8 R+ Khttp://online.sagepub.com; |$ A3 ]4 h! C4 K! Y% h" g
Precocious puberty in boys, central or peripheral,
( u, \" u9 k2 w/ R4 V/ ]is a significant concern for physicians. Central
  p. V% m1 h3 ]( vprecocious puberty (CPP), which is mediated: C3 o# ^% [9 f# W( ?
through the hypothalamic pituitary gonadal axis, has
+ E+ q, \" c5 q9 E  W" m! L* p/ Va higher incidence of organic central nervous system7 q, ~+ ~. o) B
lesions in boys.1,2 Virilization in boys, as manifested* x  \, |& Z, Q" H
by enlargement of the penis, development of pubic5 A. D8 m: x2 {% I' W; h
hair, and facial acne without enlargement of testi-( w3 q* O( j* J: j. r& p# \3 C
cles, suggests peripheral or pseudopuberty.1-3 We  O, E  f9 ^, D8 f* `6 \9 v: p
report a 16-month-old boy who presented with the0 \% h0 h6 a* V: E
enlargement of the phallus and pubic hair develop-' W( M. n6 P3 X# q5 H
ment without testicular enlargement, which was due- H/ _8 {0 c- j3 t2 c
to the unintentional exposure to androgen gel used by
5 q+ T& v# G* l5 Y3 sthe father. The family initially concealed this infor-
9 }7 F# l5 i; v5 q7 Hmation, resulting in an extensive work-up for this/ X) s! i% `+ T* u. F' M& l$ w! D
child. Given the widespread and easy availability of
% `6 w' C8 F8 Wtestosterone gel and cream, we believe this is proba-
- `: G5 {6 ~4 v1 hbly more common than the rare case report in the
- P  d0 B) B. x; v4 g6 D  \9 xliterature.4
$ Z) T9 t: b5 qPatient Report5 Q1 S. ^) [: s! h
A 16-month-old white child was referred to the7 f9 R$ V5 B: \7 l4 Y6 d' E' a0 c
endocrine clinic by his pediatrician with the concern" S/ e4 Q2 v; ^, Y9 j
of early sexual development. His mother noticed6 E' `, l9 G' C+ x) G7 N8 x
light colored pubic hair development when he was
- A( y& q* y# y6 BFrom the 1Division of Pediatric Endocrinology, 2University of$ {! N" E/ t) d1 G' L8 d. {
South Alabama Medical Center, Mobile, Alabama., |4 x  y3 l0 k  A. N0 L& I5 W
Address correspondence to: Samar K. Bhowmick, MD, FACE,7 a3 L4 l/ q- M- I0 V% n
Professor of Pediatrics, University of South Alabama, College of
4 [; D, X) k; x% fMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
, p8 ~* K3 v; V# x) C+ v% Ge-mail: [email protected].
8 c$ Z8 f/ a) Z, A) E3 \. Tabout 6 to 7 months old, which progressively became9 J' Q5 D- `: c; n8 A/ d  S
darker. She was also concerned about the enlarge-
* p- k: x, Z9 a5 Wment of his penis and frequent erections. The child
# i7 [; B0 y9 [6 T  g1 fwas the product of a full-term normal delivery, with$ T2 U% N+ N1 s- t! P
a birth weight of 7 lb 14 oz, and birth length of
% t3 E: c5 W' f20 inches. He was breast-fed throughout the first year
: ~/ G2 o0 v) b( S/ t0 N  _of life and was still receiving breast milk along with1 L" S9 e  V$ O5 o3 W/ J& `& L( c0 i! `
solid food. He had no hospitalizations or surgery,% {- k! t4 Y# v  ]9 ?
and his psychosocial and psychomotor development- _; i' T& W, l! |- e! q. J* g
was age appropriate./ E# p2 X' \2 k; d5 ^9 `
The family history was remarkable for the father,& I$ B& R# V7 C5 G2 Y
who was diagnosed with hypothyroidism at age 16,
( C( V0 \+ X8 z9 n: {; @5 n. i; ^& Pwhich was treated with thyroxine. The father’s% {' J3 ?  Q9 }$ ^/ m
height was 6 feet, and he went through a somewhat2 D/ D0 ]9 q% h2 G+ f  X. \
early puberty and had stopped growing by age 14.. s7 E& G& D' K' F# w
The father denied taking any other medication. The
2 @! b' ?% j8 v: z/ vchild’s mother was in good health. Her menarche& o. n* N- S2 }7 }" @$ Z; K, _4 d
was at 11 years of age, and her height was at 5 feet2 T# `! j" o: S8 ~) O
5 inches. There was no other family history of pre-* [( e4 B" L8 d0 G! w8 X
cocious sexual development in the first-degree rela-8 t: F- x5 C9 @
tives. There were no siblings.
: E6 r2 ?" ?# h7 |7 \( rPhysical Examination" j* M$ \7 L7 m' ?0 x8 d
The physical examination revealed a very active,
# p4 z' W3 Q; q# rplayful, and healthy boy. The vital signs documented
: m+ l& i  h0 w- @a blood pressure of 85/50 mm Hg, his length was+ S: `8 T' f; W+ a  M. u4 }9 A
90 cm (>97th percentile), and his weight was 14.4 kg# R" K9 B$ [) s6 ^
(also >97th percentile). The observed yearly growth1 i5 n& @# P; `, c+ s
velocity was 30 cm (12 inches). The examination of
6 I1 L% w" ?$ a1 c# Jthe neck revealed no thyroid enlargement.
( r- J% {! z% M: O+ U  KThe genitourinary examination was remarkable for
: n; g6 T# [1 Eenlargement of the penis, with a stretched length of  V1 A: |9 c* l4 D7 W
8 cm and a width of 2 cm. The glans penis was very well
: q, q% {/ A( r. fdeveloped. The pubic hair was Tanner II, mostly around! r" H. h! c" b) V* P" e& z
540: r" j1 f. K- Q7 V# n! g/ A
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
* k  p8 K" i! i+ Q* o6 {" }7 athe base of the phallus and was dark and curled. The
0 `5 a5 @6 A: wtesticular volume was prepubertal at 2 mL each.
, J" B4 e$ B+ \: N: AThe skin was moist and smooth and somewhat+ P  V5 R& F1 k* }: i+ i
oily. No axillary hair was noted. There were no
2 l: r3 f% h' f9 eabnormal skin pigmentations or café-au-lait spots.
) d$ I1 H; |4 t$ ]Neurologic evaluation showed deep tendon reflex 2+
" G* K( x0 B. c6 P! U5 Cbilateral and symmetrical. There was no suggestion
* {  e8 \- A7 N( Tof papilledema.
( `9 c2 Q' @2 j6 s' t0 f* y4 ~Laboratory Evaluation! ]. u% s) F' h7 ~+ s2 U
The bone age was consistent with 28 months by
0 q7 \0 u' d6 \7 y" S0 z  Rusing the standard of Greulich and Pyle at a chrono-  s( F# k% \6 H- t, p/ n& z
logic age of 16 months (advanced).5 Chromosomal
# r* p( U9 t8 `( T5 k& l  Bkaryotype was 46XY. The thyroid function test4 w! ~& ^: c4 ~5 M  k& G5 k' e
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
0 [  z, h' ~: o# R  y, qlating hormone level was 1.3 µIU/mL (both normal).& s. |, \! q7 o$ A. j2 g
The concentrations of serum electrolytes, blood
6 b+ j8 W7 U, R4 ^! M, p! C: W6 [urea nitrogen, creatinine, and calcium all were+ L( g( y: G$ H3 a# _
within normal range for his age. The concentration, U$ C& j# H7 P; a0 N6 u6 ~  F
of serum 17-hydroxyprogesterone was 16 ng/dL: q3 N' Z( n# V! v8 h% S: u
(normal, 3 to 90 ng/dL), androstenedione was 20
* }- Q7 v* F2 v( jng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-  j8 A* u0 x7 ?& p& T7 k
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
: R* Z% |7 ]/ p) Q" n/ a4 ^5 jdesoxycorticosterone was 4.3 ng/dL (normal, 7 to+ c! A9 e7 ?; s: K+ a$ X. q
49ng/dL), 11-desoxycortisol (specific compound S)
1 P. D9 m/ f2 {2 d( p1 m3 ?was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-7 {. N' r5 P$ P' m; C# O  `8 O, L# O5 a
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total+ k. O% K0 h  _, j2 D7 d2 n/ H' K' X
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),/ {' C3 n6 Z( t1 N7 v3 n
and β-human chorionic gonadotropin was less than' T3 m6 Z/ Y! j8 o  w2 Q) h
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  |/ K. c% w4 o( e" _stimulating hormone and leuteinizing hormone4 k, v& M, E) t8 _5 O
concentrations were less than 0.05 mIU/mL  j4 S" }/ f; g# N) U5 p
(prepubertal).
+ E- g7 e  |, w5 E  m+ f3 G* PThe parents were notified about the laboratory) M/ H- l( D- B3 t: I. ?2 v
results and were informed that all of the tests were8 z% G' i: e% B6 n. ?1 B
normal except the testosterone level was high. The. H( [1 ~* G" W) L
follow-up visit was arranged within a few weeks to
, y+ e' P- G% i' v: d- iobtain testicular and abdominal sonograms; how-
1 K4 i! E- k' t; r1 Tever, the family did not return for 4 months.( U: O) L% U3 j0 I1 g& `6 ~, g) H
Physical examination at this time revealed that the/ j1 K" @8 m4 {1 b) i: `, D
child had grown 2.5 cm in 4 months and had gained
) }9 g& N) ^4 z2 r# X2 kg of weight. Physical examination remained
" s- y$ X( [" O7 Tunchanged. Surprisingly, the pubic hair almost com-
9 X* c* _( I# x& f2 v5 ?7 qpletely disappeared except for a few vellous hairs at
( D8 v( R: o- s6 D  _' z. f( C0 mthe base of the phallus. Testicular volume was still 2
5 J! u' _% T0 Y% H$ l, pmL, and the size of the penis remained unchanged.6 a! r, c: n1 G
The mother also said that the boy was no longer hav-+ z1 ^* E: Z  M9 z
ing frequent erections.. r# y  K( h6 O; n
Both parents were again questioned about use of
" P* l5 y5 f: O. }any ointment/creams that they may have applied to
2 p2 a+ W! O6 Q; L, @1 o, xthe child’s skin. This time the father admitted the
- Z& z" M0 V" R' m7 ]2 iTopical Testosterone Exposure / Bhowmick et al 541
" B- B5 T! @2 `( y- uuse of testosterone gel twice daily that he was apply-
+ V, J4 c$ N5 H& Ting over his own shoulders, chest, and back area for
) `5 ^( D1 i8 L( a/ B# sa year. The father also revealed he was embarrassed: E7 @+ _9 Q& R  Q4 A3 L
to disclose that he was using a testosterone gel pre-
" N% P: u9 A# T+ ]2 |  `) G7 Escribed by his family physician for decreased libido
% X/ m- [; r# G$ B  Ssecondary to depression.
4 T+ n3 i, d! U0 O- |The child slept in the same bed with parents.$ V. `4 w2 U, [8 M; U4 Q, a5 `3 [
The father would hug the baby and hold him on his2 q; {1 r  v0 t- F' d/ G
chest for a considerable period of time, causing sig-! A0 Z: v. P: }& `; \5 U! Z; \: D* Z
nificant bare skin contact between baby and father.
. E* g: b; {, K+ s; O& PThe father also admitted that after the phone call,5 a# P; |+ U, K7 v& X1 ?; D
when he learned the testosterone level in the baby
0 i; g3 P; W7 _3 _was high, he then read the product information
7 u8 J: y% ~0 c: Jpacket and concluded that it was most likely the rea-7 `6 F/ r7 e3 D
son for the child’s virilization. At that time, they
  R" b9 b; [: u" I" g0 sdecided to put the baby in a separate bed, and the" E/ Z8 w+ A/ }* }
father was not hugging him with bare skin and had6 C7 w1 Z* j" j7 M2 _2 @: W
been using protective clothing. A repeat testosterone
: J! h6 s- v/ F2 `test was ordered, but the family did not go to the
, M  l8 Q. Z- ~5 A/ G4 F+ Jlaboratory to obtain the test.
$ G$ K+ M# ]$ t' V. I1 f0 `+ d& ^; C( sDiscussion
' V  Y& f* l- [0 k9 F8 ^" T8 jPrecocious puberty in boys is defined as secondary& H5 J9 J' f# M/ w* K- e
sexual development before 9 years of age.1,4
5 T5 D! ]/ p& N$ P( g7 R" I. H6 \) lPrecocious puberty is termed as central (true) when
" B; F$ C# }3 U( @it is caused by the premature activation of hypo-4 y1 U* H+ j0 M# Y  z8 T1 ]& e
thalamic pituitary gonadal axis. CPP is more com-' S9 L5 F' L7 n4 [2 i
mon in girls than in boys.1,3 Most boys with CPP0 \8 h( ?! n. s* R) r' W# H1 B
may have a central nervous system lesion that is" o/ e) K2 i4 T7 r
responsible for the early activation of the hypothal-
# \( ], S& O; \+ P+ o! yamic pituitary gonadal axis.1-3 Thus, greater empha-! S# ^8 p- W, T5 D
sis has been given to neuroradiologic imaging in% \  d" C4 V0 r- t4 ^
boys with precocious puberty. In addition to viril-
7 O0 h* y- A, k, k* P/ O7 b- Vization, the clinical hallmark of CPP is the symmet-
! A" Z8 v8 m! Brical testicular growth secondary to stimulation by
$ e2 M3 U0 j+ K/ s2 z' ?gonadotropins.1,3
; I& f5 b0 p8 [9 E1 mGonadotropin-independent peripheral preco-' s, Q5 U# O' H, c
cious puberty in boys also results from inappropriate3 z, L/ U; I4 C6 o' J$ }0 ~. {
androgenic stimulation from either endogenous or6 r* \# Q: [8 }1 O  t* L8 [- L; D, v
exogenous sources, nonpituitary gonadotropin stim-$ ?, _9 M3 k+ h2 p2 H
ulation, and rare activating mutations.3 Virilizing
1 [& D7 H" B" e2 c  |. _congenital adrenal hyperplasia producing excessive
6 i  @) K+ n2 [: _; `adrenal androgens is a common cause of precocious
% I: H$ M) q9 Y. D! p. q8 mpuberty in boys.3,4
4 O1 _* p' A# u1 O" zThe most common form of congenital adrenal! ?' c3 T7 d# C% J. V
hyperplasia is the 21-hydroxylase enzyme deficiency.
, P; y, k# i# t4 b8 B9 TThe 11-β hydroxylase deficiency may also result in: v0 D) u  c& j+ n  I, J, k' z
excessive adrenal androgen production, and rarely,
7 p2 p7 Z9 b$ q9 C9 @7 M+ g4 \& z, san adrenal tumor may also cause adrenal androgen
, @# a7 o; Q7 zexcess.1,34 I7 i2 X$ Z9 L2 p! v
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from% a7 {) L) m* h; g0 M& p
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
3 \6 U, V9 \: e& aA unique entity of male-limited gonadotropin-
- c- F5 f5 U, t0 O) @+ iindependent precocious puberty, which is also known$ A7 a# o, g, w6 x0 m
as testotoxicosis, may cause precocious puberty at a
4 w* p/ }  j6 F/ k; G, i; svery young age. The physical findings in these boys
& q5 o% x% v. Ywith this disorder are full pubertal development,
4 |! X$ f, a1 n! j2 f5 zincluding bilateral testicular growth, similar to boys8 T' O% p  K- l* V9 P9 n4 Y6 Z
with CPP. The gonadotropin levels in this disorder
( z; M" M8 o$ S$ dare suppressed to prepubertal levels and do not show
+ m6 j0 B4 d) Qpubertal response of gonadotropin after gonadotropin-
) }: S; b! C1 b# v1 d, Qreleasing hormone stimulation. This is a sex-linked7 A0 C; _8 t6 ^# C/ s6 e
autosomal dominant disorder that affects only
. F- o0 ^. b( d$ Y1 L2 ^males; therefore, other male members of the family
5 E# G% u# Y; \may have similar precocious puberty.3" q9 f- L2 x* f3 I* C6 G
In our patient, physical examination was incon-
, C  e5 E$ r5 V5 q/ n8 Rsistent with true precocious puberty since his testi-
1 P+ U' O$ h/ U1 x/ K: u% Vcles were prepubertal in size. However, testotoxicosis3 w* u3 K& Z2 R0 ^$ O. h0 f  T
was in the differential diagnosis because his father2 U3 H' ?* a; a& T  u9 ~
started puberty somewhat early, and occasionally,
" z4 h( {4 W! N/ Ltesticular enlargement is not that evident in the
3 e6 a. m  Z. O. a7 ?  ~7 {' Jbeginning of this process.1 In the absence of a neg-
, x  \0 C' m8 W, ~; w& Y4 xative initial history of androgen exposure, our
7 Q( g# E, m4 k* [0 `3 ibiggest concern was virilizing adrenal hyperplasia,
9 d) k; W  t6 aeither 21-hydroxylase deficiency or 11-β hydroxylase
% u  o; ~# z# {* h; Mdeficiency. Those diagnoses were excluded by find-2 z$ M* z( {5 z% J
ing the normal level of adrenal steroids.
1 M  U5 e8 [' S2 _) VThe diagnosis of exogenous androgens was strongly5 A, ^9 ?8 k- i. V2 X# X: S
suspected in a follow-up visit after 4 months because) `6 y, |# u, ?. Q( ]7 R8 K; S
the physical examination revealed the complete disap-6 [7 C/ N6 R* u+ b8 _0 h
pearance of pubic hair, normal growth velocity, and! c& W( m: a4 K$ x
decreased erections. The father admitted using a testos-
% X; N9 r: C- r% Y0 i' M; b* q2 Hterone gel, which he concealed at first visit. He was
9 Z9 ^- O" f, f" rusing it rather frequently, twice a day. The Physicians’" i/ J/ \/ B7 \0 X0 q3 A1 _, M7 Z
Desk Reference, or package insert of this product, gel or
, P5 _" E, h7 H, e" S! m* jcream, cautions about dermal testosterone transfer to
' C; `; Z0 I* |  z/ e( f! `$ Aunprotected females through direct skin exposure.
( G5 g. v0 b& j; J1 r! l+ QSerum testosterone level was found to be 2 times the
# E, S- j* \. X$ B6 Y- _* Pbaseline value in those females who were exposed to0 Q5 h9 P' n4 |& `) h, m" t
even 15 minutes of direct skin contact with their male5 j% Y2 h+ M. y9 H# p0 P
partners.6 However, when a shirt covered the applica-% Z9 I7 p2 I! j7 ]: g: p
tion site, this testosterone transfer was prevented.4 s% L) f3 R/ i- ~
Our patient’s testosterone level was 60 ng/mL,1 O6 N2 Z; r# a2 ~
which was clearly high. Some studies suggest that
6 r! M/ D. N2 G& z& r5 g/ Z/ qdermal conversion of testosterone to dihydrotestos-
5 \) F3 u+ W% H! d$ f, iterone, which is a more potent metabolite, is more
  m8 o& X5 B: _1 F  U0 @active in young children exposed to testosterone
$ ~$ M7 |( W$ N7 D/ S; Cexogenously7; however, we did not measure a dihy-
6 _7 C% s" E! j" h8 F2 K1 U( [2 c+ kdrotestosterone level in our patient. In addition to
% L6 o* J; ^! \3 t" M9 gvirilization, exposure to exogenous testosterone in
) M2 j& q$ g" ?" z# Q3 V2 r+ zchildren results in an increase in growth velocity and
  M6 ?/ K) m: n. d  A% y  vadvanced bone age, as seen in our patient., E! }* x: ^- r, C+ ]
The long-term effect of androgen exposure during4 n9 |/ c, G$ ~( v4 G2 w
early childhood on pubertal development and final
: c, w* ]( x7 X% U3 J! ]adult height are not fully known and always remain
* m1 ]7 p% O4 B; i4 O& D# F! ua concern. Children treated with short-term testos-* v$ X7 u/ b& t1 k& \9 [
terone injection or topical androgen may exhibit some  V* q! t% O* g
acceleration of the skeletal maturation; however, after
, G& t& S) \4 Jcessation of treatment, the rate of bone maturation! E* e4 r3 o" p; s& D
decelerates and gradually returns to normal.8,9
/ |6 d" X+ t5 P9 n6 ~; `3 K* x1 MThere are conflicting reports and controversy# P+ p/ D9 Y& ]8 j$ R, \- [4 l' R
over the effect of early androgen exposure on adult5 ^: z- Z3 t: S2 d6 g2 u2 R3 ~
penile length.10,11 Some reports suggest subnormal
. K! _) M; |9 Ladult penile length, apparently because of downreg-
6 }- F* O: d- \ulation of androgen receptor number.10,12 However,7 l, v# a8 F3 ^2 Y/ C3 `
Sutherland et al13 did not find a correlation between# M+ K3 x& A0 R- c' Z
childhood testosterone exposure and reduced adult. f  A8 y5 c' @+ ~! a9 R
penile length in clinical studies.
, Y5 o) b" ?/ U  ?6 l8 X' `Nonetheless, we do not believe our patient is
7 W8 @$ g" M* [' A4 e( `going to experience any of the untoward effects from
" r7 o, ]2 v9 l# m1 b# V0 k6 d; Utestosterone exposure as mentioned earlier because
+ N0 X9 g. ^4 [2 `the exposure was not for a prolonged period of time.
" Y& d1 Z/ U) |( j* vAlthough the bone age was advanced at the time of
, u0 d: ~  C% hdiagnosis, the child had a normal growth velocity at
* R9 ]+ ~! h1 W% o2 k4 Q  \) ~the follow-up visit. It is hoped that his final adult
3 J& r' X3 d; {- B* j( g4 T4 xheight will not be affected.& ]" Y" E3 G3 ^. ^. \( [
Although rarely reported, the widespread avail-, x$ {  K$ x. @$ O2 Z9 D( Z; k) H) Y
ability of androgen products in our society may) o  W7 q6 h( e+ x' O$ I
indeed cause more virilization in male or female8 q* s  g/ W+ T* X
children than one would realize. Exposure to andro-) q! B/ G- Q$ ?7 t* Q, E
gen products must be considered and specific ques-3 g/ W! R4 Y3 ]
tioning about the use of a testosterone product or
. Y* ]6 M$ E$ ~( B% lgel should be asked of the family members during, @6 P. ~9 X9 ]! J& M5 ]( K6 s7 i
the evaluation of any children who present with vir-
( v5 i% r( O) ^ilization or peripheral precocious puberty. The diag-1 _& z$ x% i- d) K& z% Q9 Z
nosis can be established by just a few tests and by9 K* F2 r. O+ A8 k# U0 X
appropriate history. The inability to obtain such a
( O' t6 ^3 K( O' ?1 V! Z1 xhistory, or failure to ask the specific questions, may
* R) ~+ j! e/ i4 C+ nresult in extensive, unnecessary, and expensive2 K3 s8 u: L3 {4 t! ]* a
investigation. The primary care physician should be# }3 Q" \8 D. w3 ]5 m
aware of this fact, because most of these children8 W- {  V. h6 t7 f0 D
may initially present in their practice. The Physicians’
3 Y0 @1 F6 ^) N4 J! Y" d; wDesk Reference and package insert should also put a
1 J+ h4 v, Y( F  L9 X5 D1 Fwarning about the virilizing effect on a male or
' B, U* q: l6 ?6 {# o7 u; Q! V+ Vfemale child who might come in contact with some-- T2 j! j% H" N! Y
one using any of these products.
) U1 ?- r, s* l/ Y- ^References
+ {6 x' O! m. b" o2 ?; X/ Z1. Styne DM. The testes: disorder of sexual differentiation* `8 P( `! d0 G' r$ I
and puberty in the male. In: Sperling MA, ed. Pediatric
0 H/ w8 {1 G$ z: M* Y* ^Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 c! s5 }* r( r" @' O+ l2 I2002: 565-628.
0 k' B  H' c, I2 W2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious  @6 }( U6 s8 v! T2 Z' h& Y0 s
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old* B* v4 [' I' [5 J6 s; P
Boy Induced by Indirect Topical+ d; H' o+ {1 K/ N/ Z" ?" x4 e
Exposure to Testosterone
( A. ~$ e/ ]7 j' l5 C) @Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
+ [  w3 G1 ]" [; Kand Kenneth R. Rettig, MD11 m, q" ~; T# ?( Q5 k
Clinical Pediatrics
  j. n) W# m; ^" x. dVolume 46 Number 6
! u8 W5 T. K3 sJuly 2007 540-543, B2 v. g9 ^1 \0 S; M/ T- q# t
© 2007 Sage Publications+ C$ Q( y2 J3 c
10.1177/0009922806296651
$ f( O; C7 T, d& X3 \  E8 j/ Uhttp://clp.sagepub.com+ q7 U6 ?  X% ?
hosted at  H% t4 S, d1 I+ q( S
http://online.sagepub.com+ R0 v. t5 F( ~9 @# l
Precocious puberty in boys, central or peripheral,
! [  Q' w- T  T* ~4 ris a significant concern for physicians. Central
# P% G  Q- @& Sprecocious puberty (CPP), which is mediated% [9 k0 l( S$ v; n- |
through the hypothalamic pituitary gonadal axis, has$ b: C  D4 F( [' ^$ \% t
a higher incidence of organic central nervous system! P5 `% z8 }* R( d- q+ u
lesions in boys.1,2 Virilization in boys, as manifested. A  l4 E% r7 b5 Y
by enlargement of the penis, development of pubic! t1 G& Z9 M) H3 b$ G; S
hair, and facial acne without enlargement of testi-
* `1 ^9 _* D4 o! ?cles, suggests peripheral or pseudopuberty.1-3 We
: B9 y% u6 r$ R$ C* @9 vreport a 16-month-old boy who presented with the2 B% V& m$ d7 ?* D
enlargement of the phallus and pubic hair develop-% Q* u6 R0 ^7 i0 L3 Y4 b
ment without testicular enlargement, which was due
9 v+ N6 ?" t* ^  s1 R% j5 a! k. Fto the unintentional exposure to androgen gel used by. @1 Y5 |9 `# D7 g3 x
the father. The family initially concealed this infor-! E& O) w8 O9 q6 E5 e
mation, resulting in an extensive work-up for this
7 c% z" J) r( z3 i4 Kchild. Given the widespread and easy availability of2 i+ T4 g7 l5 X& v' O: t9 y
testosterone gel and cream, we believe this is proba-2 B; I2 v# ?8 c. K, N
bly more common than the rare case report in the
) K( y/ T! F6 R, D% Iliterature.46 n1 @, g7 o5 _$ Q  C) f
Patient Report
8 s$ E3 P4 q. z: `# GA 16-month-old white child was referred to the
# b3 l3 B$ H6 o% z, q! D4 Wendocrine clinic by his pediatrician with the concern
+ {( G1 M/ k% E4 Tof early sexual development. His mother noticed
; a5 R. ~: D5 H$ V" G& f% Tlight colored pubic hair development when he was# e7 D3 s9 ^9 Y. W# {  I! t2 e
From the 1Division of Pediatric Endocrinology, 2University of# q  `: D( c5 [+ ]# \
South Alabama Medical Center, Mobile, Alabama.
" t) e, G' O, bAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 M7 s0 b7 h2 ]5 U
Professor of Pediatrics, University of South Alabama, College of
; C7 k4 b8 d* w& ^3 gMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
5 Y% \* u$ y, ^; b, y0 c/ h! De-mail: [email protected].: F; O2 F8 o& _- ^/ L: X
about 6 to 7 months old, which progressively became
4 P; G* v* h2 Hdarker. She was also concerned about the enlarge-2 F  H5 _( b8 W+ ?
ment of his penis and frequent erections. The child
0 _2 Y* ?% ?: }( _was the product of a full-term normal delivery, with9 c0 D" n4 P$ H% r( P& g
a birth weight of 7 lb 14 oz, and birth length of0 \# {% u1 }1 P# T* ]7 g
20 inches. He was breast-fed throughout the first year
9 _0 h' m4 l/ `of life and was still receiving breast milk along with
7 o" r$ A2 J3 P7 N9 I( q* Z% Jsolid food. He had no hospitalizations or surgery,
! a& _. `$ a6 c4 v+ Xand his psychosocial and psychomotor development4 N: D5 m3 ]+ p, a* ]' R
was age appropriate.' c4 o' K! {7 |
The family history was remarkable for the father,! d  Y" {2 Q- o2 U/ Y5 N
who was diagnosed with hypothyroidism at age 16,9 n8 s0 ?4 w5 A
which was treated with thyroxine. The father’s: y# Z. ^, q' w3 Y
height was 6 feet, and he went through a somewhat
4 b% L/ z- J+ I# n& [1 }8 nearly puberty and had stopped growing by age 14., @" P- [' F. O6 G) e2 h1 o  O
The father denied taking any other medication. The& j! Y& ]9 O. a: v
child’s mother was in good health. Her menarche
% W. J6 o" e+ t' H6 ^; j& rwas at 11 years of age, and her height was at 5 feet! o& @5 X: c+ f9 z" e2 I
5 inches. There was no other family history of pre-$ B7 [: E$ {1 h: x( P( s, ^  W$ f
cocious sexual development in the first-degree rela-
: ?) f3 m4 s) I. _) x4 Ftives. There were no siblings.
  O* @; s) A& T+ CPhysical Examination; Z4 r% {4 @* v4 D
The physical examination revealed a very active,
; r" i1 ?* O3 z1 \! r( p, }playful, and healthy boy. The vital signs documented
5 y8 @) I$ g' ^& b" ?a blood pressure of 85/50 mm Hg, his length was1 n" k! }5 `7 u5 i. M
90 cm (>97th percentile), and his weight was 14.4 kg8 C4 O7 }6 k5 t, N5 X9 P" k
(also >97th percentile). The observed yearly growth* N/ {  e0 |) M, }+ H. X; M
velocity was 30 cm (12 inches). The examination of
+ N1 |: ]) Y7 g& D4 o( m' fthe neck revealed no thyroid enlargement.7 Z2 ^9 `0 V5 h# D$ P2 Z: \- S
The genitourinary examination was remarkable for" z, \4 H& f% a0 L+ V: u% t- F
enlargement of the penis, with a stretched length of* j2 R9 ?' j$ e# {+ a; O( c% F
8 cm and a width of 2 cm. The glans penis was very well
' I# ^& g, _; pdeveloped. The pubic hair was Tanner II, mostly around
  J; Q+ J9 I# c" S540+ M( `& \6 u4 y, Z
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# c+ `/ Z3 i% d( t% w* t, v
the base of the phallus and was dark and curled. The4 @3 t8 v8 o0 M
testicular volume was prepubertal at 2 mL each.
/ C7 C; r1 l2 B% X8 e- zThe skin was moist and smooth and somewhat
; z; q: m& k1 T- ?oily. No axillary hair was noted. There were no
' U  x  i$ u! ]% wabnormal skin pigmentations or café-au-lait spots.! B+ u9 v6 y( z! Q8 ^$ D# t
Neurologic evaluation showed deep tendon reflex 2+, g" n8 y5 ?' t2 d5 ~9 I: y5 k. b
bilateral and symmetrical. There was no suggestion
4 R- G; |, Y7 Y5 {of papilledema.! P& m( E3 C/ P5 @7 d* s+ p
Laboratory Evaluation# C0 S. V; y2 w8 ?6 {
The bone age was consistent with 28 months by
: w5 J6 z0 o) W( P  ~1 q, @& v  }using the standard of Greulich and Pyle at a chrono-
9 b8 a7 m% I" H1 P) alogic age of 16 months (advanced).5 Chromosomal
2 _1 J: y4 p  n( s' i5 s$ Kkaryotype was 46XY. The thyroid function test
9 ]( R+ T& w2 o* W1 f5 P- g0 z( pshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
3 N3 L: P  V! u$ ^lating hormone level was 1.3 µIU/mL (both normal).8 A0 ^' _1 j' Z# ]
The concentrations of serum electrolytes, blood
4 c& g. M* L" ~( j( Rurea nitrogen, creatinine, and calcium all were  e* R% c6 v6 C3 q
within normal range for his age. The concentration+ b5 s% S- n% e) C9 ]3 ]* k
of serum 17-hydroxyprogesterone was 16 ng/dL6 |8 \+ t5 a5 d) ]- f
(normal, 3 to 90 ng/dL), androstenedione was 20
: q* N. b. T* ~- s. A6 B2 Ing/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
7 n0 ~( G: x3 N7 Z( fterone was 38 ng/dL (normal, 50 to 760 ng/dL),& f! J# k; A% D: i) w: S0 v
desoxycorticosterone was 4.3 ng/dL (normal, 7 to8 n/ z9 T, w# C! l; L+ }6 H
49ng/dL), 11-desoxycortisol (specific compound S): \' E" }/ a0 A( I
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-- q& p/ S3 J% D" Q, [6 L% i
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total# e2 Z4 o5 _# K
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ S! N& a9 P2 |7 m4 ]3 ?and β-human chorionic gonadotropin was less than
: P; I; O. @0 F& w$ K5 mIU/mL (normal <5 mIU/mL). Serum follicular0 s2 d& Y6 N, b% o9 q+ L
stimulating hormone and leuteinizing hormone
- d1 s: G- u+ Rconcentrations were less than 0.05 mIU/mL$ z- N! H) U/ W% h+ C8 K# @
(prepubertal).+ X. W/ P/ ^$ [6 E% p& k2 j% c8 g! d
The parents were notified about the laboratory  T! V7 \& Z' k7 \# R- a/ S
results and were informed that all of the tests were
7 f4 ]1 `) x$ L8 B6 `/ O' A$ w  F9 f* lnormal except the testosterone level was high. The
( o4 Z5 K" C* @* z9 T3 vfollow-up visit was arranged within a few weeks to* ?: C& b- s# C: w
obtain testicular and abdominal sonograms; how-
. K, r4 r6 B4 |5 L; Jever, the family did not return for 4 months.
$ M5 F+ @( [- q) [6 ^' fPhysical examination at this time revealed that the( f* ^) O4 k3 E9 U8 t5 k
child had grown 2.5 cm in 4 months and had gained
  |# F' M. q, h1 ~$ a2 G8 t' M  ?9 M2 kg of weight. Physical examination remained& }+ P. v# |1 V( t$ }
unchanged. Surprisingly, the pubic hair almost com-, i* D; o6 E1 i
pletely disappeared except for a few vellous hairs at
& ]2 K8 v7 U" ithe base of the phallus. Testicular volume was still 2
# R  }- ]1 ]2 m% p0 E- ?7 QmL, and the size of the penis remained unchanged.  r* `& o% ]& ^- X5 @8 v
The mother also said that the boy was no longer hav-; [7 n( x* L% T: ^0 B% \1 G
ing frequent erections.
4 r5 \* k) I. B, z! q- |5 d5 pBoth parents were again questioned about use of
/ W* h* a. a& \; s) L0 Yany ointment/creams that they may have applied to# [0 K9 z4 l" b1 {0 c' r" j
the child’s skin. This time the father admitted the* c7 R! K8 g7 {1 M
Topical Testosterone Exposure / Bhowmick et al 541
: |. a/ ]- G- d5 L, euse of testosterone gel twice daily that he was apply-
& D- B6 _7 P* Z# b8 ping over his own shoulders, chest, and back area for
4 L  h5 {3 N& L# c2 ba year. The father also revealed he was embarrassed# U# r) ]2 K0 r# }3 S
to disclose that he was using a testosterone gel pre-
  f% y0 ]* M- e! E! K4 l- ~0 \scribed by his family physician for decreased libido; v: k$ I8 n' p* e0 _
secondary to depression.5 x. D9 c5 i% e8 h7 }# @$ f: q
The child slept in the same bed with parents.: x7 M) E+ e# g% l5 U2 p" z
The father would hug the baby and hold him on his4 T* O4 P3 s" c7 T0 G
chest for a considerable period of time, causing sig-
* W% V: P) t8 p- @& }nificant bare skin contact between baby and father.8 J# t$ e7 K! s+ ], p
The father also admitted that after the phone call,
1 @; A7 h; s# [% k- u- |0 S; bwhen he learned the testosterone level in the baby
9 Y1 i9 h& v3 W0 G5 U" z9 ]  pwas high, he then read the product information
# O. M* k& ?* E, n' I' a1 xpacket and concluded that it was most likely the rea-
, k; O$ Y. \8 e/ n7 ason for the child’s virilization. At that time, they
1 M( d2 d  k! @  Idecided to put the baby in a separate bed, and the
7 V0 v1 @8 a2 c( |& ^/ p3 efather was not hugging him with bare skin and had: x1 U- S# e8 J/ c& r0 R
been using protective clothing. A repeat testosterone% Q3 C/ r! l) D! Q0 k
test was ordered, but the family did not go to the3 E1 \: f6 U& ~/ G
laboratory to obtain the test.! o3 l# F" A. v6 |+ v, H" W& h
Discussion
3 y2 ]( `( b; M9 p' W8 c! O$ n( OPrecocious puberty in boys is defined as secondary* G! K( i4 b  x/ |3 f- W! n& D
sexual development before 9 years of age.1,44 J9 F+ k% o. \8 S* j
Precocious puberty is termed as central (true) when
- R! C$ j( `, Z, S# v1 _5 nit is caused by the premature activation of hypo-! T. o5 s& W6 h7 x
thalamic pituitary gonadal axis. CPP is more com-
) P" k) a) @8 v1 Rmon in girls than in boys.1,3 Most boys with CPP: {, l7 D: {4 j* O+ \- W& _6 A
may have a central nervous system lesion that is
  T+ |9 K% L5 w2 \' U5 r9 lresponsible for the early activation of the hypothal-/ V% ?) A8 @( L1 o6 W/ K0 i5 R$ }
amic pituitary gonadal axis.1-3 Thus, greater empha-
. Q) n$ `2 s( _( S# i' ^sis has been given to neuroradiologic imaging in! G8 V0 c) m2 b- V
boys with precocious puberty. In addition to viril-
% x8 b/ e& f/ c9 o. \* i; rization, the clinical hallmark of CPP is the symmet-
! l+ q+ k0 f  J- Zrical testicular growth secondary to stimulation by2 ]9 l2 S5 ]- A5 P( v2 q
gonadotropins.1,3
. ~: H: Z% g, V  E3 IGonadotropin-independent peripheral preco-
0 [$ U6 ]% e0 P% h- z( Y* @* z* Gcious puberty in boys also results from inappropriate5 M: i6 [" O$ ^7 a; }
androgenic stimulation from either endogenous or
5 i: g; d& b2 j/ S) Y) Pexogenous sources, nonpituitary gonadotropin stim-
" @3 Z: z4 c1 d  U+ Uulation, and rare activating mutations.3 Virilizing+ S. z, k: @; L) K5 @9 p
congenital adrenal hyperplasia producing excessive
! b) k1 P0 I6 R1 l0 b+ W8 Hadrenal androgens is a common cause of precocious4 {8 R- M% i, G# F2 E3 H6 v
puberty in boys.3,4
% W$ j8 c8 p( }' Z  ~! ~' KThe most common form of congenital adrenal' s0 q6 i) h- Y. @5 V" E
hyperplasia is the 21-hydroxylase enzyme deficiency.
  d! p& H) G) U3 {The 11-β hydroxylase deficiency may also result in
: m1 A- d+ S2 cexcessive adrenal androgen production, and rarely,
: n, d$ y0 @! E5 c7 d' Qan adrenal tumor may also cause adrenal androgen
4 C! P8 z3 A* g$ Pexcess.1,3! {4 K4 A3 }# u# W9 j
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from; h/ f, J' g# ]! A& u/ _
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
& N. h2 D4 d& L% K/ mA unique entity of male-limited gonadotropin-
8 l+ ^4 V9 |4 K# k) S8 V' |- k$ _7 Hindependent precocious puberty, which is also known
$ P# V- ^+ a5 mas testotoxicosis, may cause precocious puberty at a
, C5 i# K" H2 H' T! m: V9 [' d6 kvery young age. The physical findings in these boys9 J' l, k  P! t6 E7 _
with this disorder are full pubertal development,8 m# n# b& ]' Y
including bilateral testicular growth, similar to boys9 A$ U4 j' F* \; K+ i# Z% o0 F8 E
with CPP. The gonadotropin levels in this disorder
. u( m. j8 @! r5 M; n- nare suppressed to prepubertal levels and do not show
% N8 D& `' Y4 |3 A3 T6 c. i  ^$ j8 Mpubertal response of gonadotropin after gonadotropin-
* W! Y! i1 K1 k, R& O. nreleasing hormone stimulation. This is a sex-linked, W& h& \! S7 r
autosomal dominant disorder that affects only
- _* H! P" K+ a! c$ L# Z4 m9 q7 @0 s* Cmales; therefore, other male members of the family
/ J( Q9 R. V2 X+ Z7 n# jmay have similar precocious puberty.39 k, f' u% d7 K! e/ }* `' Y0 `- Y
In our patient, physical examination was incon-
" O% c* V5 X! p0 T. zsistent with true precocious puberty since his testi-
' q( N" d, @, Q5 ]cles were prepubertal in size. However, testotoxicosis0 h! R- ?1 _! m# w2 I4 V4 l3 p: r
was in the differential diagnosis because his father
9 }  y6 M, {9 w6 w& w( {+ Rstarted puberty somewhat early, and occasionally,% e2 O% T5 l* x7 B+ m
testicular enlargement is not that evident in the
+ j; G$ R# l/ I3 n' j1 N9 F! kbeginning of this process.1 In the absence of a neg-
! g, _, V% K+ K* b4 Z" p! r2 |ative initial history of androgen exposure, our" |' `; G, \8 u3 N$ C
biggest concern was virilizing adrenal hyperplasia,2 e, K- e# N0 i: t+ }4 z  A
either 21-hydroxylase deficiency or 11-β hydroxylase
3 U1 E* P" z  h4 Z, H5 \deficiency. Those diagnoses were excluded by find-
, Z$ P- ?# }4 }- ?  j" U+ k* a9 }6 Qing the normal level of adrenal steroids.
( {, K9 C0 H& R. X. vThe diagnosis of exogenous androgens was strongly0 O- k- w: W$ s6 _$ F" [3 c
suspected in a follow-up visit after 4 months because
7 n. k  d4 m; ^( G2 P& Rthe physical examination revealed the complete disap-* A3 n: S; D5 l0 W& t% b8 ~
pearance of pubic hair, normal growth velocity, and
% x% A! H0 \2 {/ M! ~# k) K% mdecreased erections. The father admitted using a testos-4 Q" ]+ H" Y) X' M
terone gel, which he concealed at first visit. He was# p; a1 E5 G* p! {$ C& u! l' E
using it rather frequently, twice a day. The Physicians’
9 |, G# b8 l5 R; j! z0 ^Desk Reference, or package insert of this product, gel or
( u% o0 L/ V. R2 v# O" W+ [& bcream, cautions about dermal testosterone transfer to
  P: o* [, T4 a  Z3 n* Kunprotected females through direct skin exposure./ e% O# {$ J! s8 f6 D  W
Serum testosterone level was found to be 2 times the) ]$ ~9 U0 W& f
baseline value in those females who were exposed to1 a$ R( r6 j' g  g. j
even 15 minutes of direct skin contact with their male
( x( ~3 u2 _3 O( P4 ~0 _partners.6 However, when a shirt covered the applica-
# s' T  f; I* g+ W2 g& Q3 ~9 y" rtion site, this testosterone transfer was prevented.) u/ J2 v+ g+ \: S: E
Our patient’s testosterone level was 60 ng/mL,
$ Q9 x& {7 d$ G/ Rwhich was clearly high. Some studies suggest that) r8 r; @- _6 u3 _: T" k- \( s" H
dermal conversion of testosterone to dihydrotestos-8 ?' [& ^) N; r6 d1 }. y
terone, which is a more potent metabolite, is more/ ]) a4 S  `1 @. `) O" M2 z5 m# w
active in young children exposed to testosterone7 y" C! e: O5 ~1 m4 V0 x9 \
exogenously7; however, we did not measure a dihy-
. O& r! [3 s' e. s  _drotestosterone level in our patient. In addition to* g5 E! E3 k$ {$ I# O
virilization, exposure to exogenous testosterone in
2 z. c' T4 D$ T' b# R: tchildren results in an increase in growth velocity and( _1 s) r9 |  ?; C
advanced bone age, as seen in our patient.% i, n7 }5 C  N# w$ `- U: i$ a
The long-term effect of androgen exposure during
9 p7 F+ y5 N: c( Rearly childhood on pubertal development and final9 x$ l' U; F8 L3 u
adult height are not fully known and always remain8 k. c3 J- _1 b5 V  i
a concern. Children treated with short-term testos-- I( M% L) }  \% A. x0 ~
terone injection or topical androgen may exhibit some# r3 o1 M3 @4 _
acceleration of the skeletal maturation; however, after
5 w+ h$ A/ p: Acessation of treatment, the rate of bone maturation
( y9 U  N% l, @0 K# |$ a: B3 xdecelerates and gradually returns to normal.8,9
  y- D7 ^* I+ w, M9 M/ P, IThere are conflicting reports and controversy
: g) }8 K7 u8 j& h4 O/ {8 U; dover the effect of early androgen exposure on adult
' {% i) M1 K/ a& O: G; c: J& ipenile length.10,11 Some reports suggest subnormal
/ L, c. a- k  |  s6 ]adult penile length, apparently because of downreg-
; X' i7 O8 x) c2 kulation of androgen receptor number.10,12 However,2 C7 @6 P0 c: G7 h  Q3 ]
Sutherland et al13 did not find a correlation between
" [* ]( H( _1 ?8 i) M9 R" mchildhood testosterone exposure and reduced adult
2 {! t3 e2 r1 vpenile length in clinical studies.
! ]1 z' t) x# |% X$ j+ D  @* J5 Z( wNonetheless, we do not believe our patient is
& }* E4 g. i' I9 R, i& _: n, Agoing to experience any of the untoward effects from: |, V( [, }0 g: f' _3 ?* p' q
testosterone exposure as mentioned earlier because! ?! n' n: ?! S  m$ i) c
the exposure was not for a prolonged period of time.8 V, e( T1 T1 `, h* L+ e
Although the bone age was advanced at the time of
2 S, O9 v. j1 l5 O- A( g  tdiagnosis, the child had a normal growth velocity at
& G1 O. V5 L& v+ {, ?the follow-up visit. It is hoped that his final adult3 p& J7 @  H7 O3 S7 A! `
height will not be affected.4 C, I& X- \5 p8 @
Although rarely reported, the widespread avail-) Y9 G/ p. g& y' w0 g" h
ability of androgen products in our society may, B+ n& A! K# R; F; W
indeed cause more virilization in male or female/ y* W  C; i' q' G1 K
children than one would realize. Exposure to andro-! I4 B9 P% _1 {2 m
gen products must be considered and specific ques-; ?! J4 c. ~" W2 p  J4 D5 K
tioning about the use of a testosterone product or; n  ?4 t. ?' H- X
gel should be asked of the family members during
. G  K" o+ r$ Y+ z) i4 t4 o9 ~% mthe evaluation of any children who present with vir-
, C) j, }, |. w5 h! V7 a" dilization or peripheral precocious puberty. The diag-# |+ M0 d$ I( Y; l- t. Q
nosis can be established by just a few tests and by
3 p8 s. T. G% H! Qappropriate history. The inability to obtain such a
4 p, r5 q! h9 B5 K# Whistory, or failure to ask the specific questions, may
9 j: h% U3 b% A) L3 Y+ Eresult in extensive, unnecessary, and expensive
" l) ^5 U6 s7 Q7 u0 F+ n! x+ I: {7 ~investigation. The primary care physician should be
2 e2 k4 l! g4 _5 o) _2 g4 x$ _( |aware of this fact, because most of these children
' [! S% B! i: n* Lmay initially present in their practice. The Physicians’
8 m: B9 ?9 U* b; y+ iDesk Reference and package insert should also put a
$ Y3 S8 Z5 D6 Y1 A* ]warning about the virilizing effect on a male or5 J! N! ?1 I- u9 A; x2 W$ ?: w0 ]
female child who might come in contact with some-* p3 E" L# H7 E! d% g, I
one using any of these products.7 o4 A$ `) c5 n% F0 `0 f8 ?, `+ H1 h
References
. U& R& H8 o! J1. Styne DM. The testes: disorder of sexual differentiation7 f; a, Q8 B1 C" y
and puberty in the male. In: Sperling MA, ed. Pediatric- b  `+ s6 L3 x# O6 U; Z& Y& @
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;7 k8 }# f0 j7 `  |+ @
2002: 565-628.. \1 M# ?' p) c* i3 ?# f
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# B  ~, ^% }8 \& B
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
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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
! C& q" T. a8 l! e7 Z( D
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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