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Sexual Precocity in a 16-Month-Old( }) h% Z+ m5 m' s+ \7 ~
Boy Induced by Indirect Topical
1 T9 i' c* H: d1 M# l/ i1 OExposure to Testosterone
/ y9 K0 G) O1 @& R. n# m7 I  }Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
! U. P+ C& z0 jand Kenneth R. Rettig, MD1
/ Z* k% f9 |# ?7 N2 Q, [Clinical Pediatrics5 z. s! t: ~0 S' x
Volume 46 Number 6
; @0 w3 L) t' `9 KJuly 2007 540-543- x& c2 t7 @4 y2 P2 d
© 2007 Sage Publications
2 m* [" M' h' H, X, i10.1177/0009922806296651
* h6 o+ c5 [) ^1 ehttp://clp.sagepub.com( y) ?; b$ P2 @5 n% Y
hosted at
) R- A# f% s, i& n% L. X# Ghttp://online.sagepub.com
- f  q5 Z3 J1 V2 w8 H. l/ s7 ]2 QPrecocious puberty in boys, central or peripheral,
6 I0 \, R- A' I# b4 Vis a significant concern for physicians. Central
: p% }) b; s2 j; Pprecocious puberty (CPP), which is mediated
, j% j1 g% h" g- Q2 l0 bthrough the hypothalamic pituitary gonadal axis, has( A$ N. a9 I8 m0 E
a higher incidence of organic central nervous system- ^$ z* ]. t9 ^' H  V
lesions in boys.1,2 Virilization in boys, as manifested! |9 k, P3 R1 e) ?
by enlargement of the penis, development of pubic
) O1 c' z+ a) D; ?$ Z8 r7 J. whair, and facial acne without enlargement of testi-
. q; W. b+ T8 z* ^( k' c/ t8 w9 rcles, suggests peripheral or pseudopuberty.1-3 We
" \9 i5 f3 L) e- d9 {  \! }. ?report a 16-month-old boy who presented with the
1 ]: f% ]0 t0 C* ?7 lenlargement of the phallus and pubic hair develop-  O( B/ O+ r0 x: t1 X! j
ment without testicular enlargement, which was due
% Y" f# _3 `' C! x4 R6 e% wto the unintentional exposure to androgen gel used by& y0 O  T( J, A: C& A: O0 t
the father. The family initially concealed this infor-
0 ?6 ]; K2 S: F3 R  X0 nmation, resulting in an extensive work-up for this) x: {" ]9 U- U
child. Given the widespread and easy availability of- Y7 f# \1 p. b1 X
testosterone gel and cream, we believe this is proba-
" A+ h) Z: o# A- u; o! O; ~bly more common than the rare case report in the
  X) _8 \: c& `% |7 Jliterature.4
% T2 t. h# c; j# K, kPatient Report/ B7 ?& R+ z4 `2 C8 _6 ?8 v# D
A 16-month-old white child was referred to the
' P3 u: I" k1 c8 ~+ M# x$ @9 @endocrine clinic by his pediatrician with the concern/ J. [4 c% r0 n7 P8 z
of early sexual development. His mother noticed
/ _9 _/ ]. ~, x+ Flight colored pubic hair development when he was0 \$ ^8 I+ o: R+ ^- Y0 B! {' E
From the 1Division of Pediatric Endocrinology, 2University of7 P+ V) z' N7 D8 D5 r& o6 U1 {/ y
South Alabama Medical Center, Mobile, Alabama.
, O: W3 W+ J' s! u; eAddress correspondence to: Samar K. Bhowmick, MD, FACE,1 x5 G8 C5 |  H+ h
Professor of Pediatrics, University of South Alabama, College of2 m7 Q3 Q/ j! H5 r# f, P
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" {6 |# H% T+ v0 `/ X
e-mail: [email protected].
- ?* D1 Z6 E5 g" y6 {about 6 to 7 months old, which progressively became
* o5 ?5 D. T$ m8 K. N& sdarker. She was also concerned about the enlarge-. i3 H8 B2 A  V  {
ment of his penis and frequent erections. The child2 @; V  x2 G, _5 ^2 L) |, f
was the product of a full-term normal delivery, with
& J: h! J2 f6 |1 d2 Ba birth weight of 7 lb 14 oz, and birth length of- n# e# h9 Z: E5 X! t
20 inches. He was breast-fed throughout the first year
# F2 R, w1 V6 D# |8 iof life and was still receiving breast milk along with
% M* _5 T& H% {8 h* lsolid food. He had no hospitalizations or surgery,) T# G4 X7 a5 z* ]0 J# j
and his psychosocial and psychomotor development
2 J/ ~$ J( N+ G0 M" vwas age appropriate./ e5 L- L6 N9 t, w. i
The family history was remarkable for the father,6 Z  ]1 h" }0 N7 D
who was diagnosed with hypothyroidism at age 16,
. T8 Q; Z0 G  `9 T3 N. Gwhich was treated with thyroxine. The father’s2 o* |" {/ ]+ y
height was 6 feet, and he went through a somewhat! X$ Y- ?" S' M! C" y1 \3 o; `
early puberty and had stopped growing by age 14.
2 h! t" N$ j8 u" n" L4 b( kThe father denied taking any other medication. The/ j( L6 p! N3 x8 A6 \  S9 X# m" X- d
child’s mother was in good health. Her menarche2 P8 L0 s, L" U; Z( _0 M% B# @
was at 11 years of age, and her height was at 5 feet( h$ K1 y0 f: N6 J$ s* `" |8 @
5 inches. There was no other family history of pre-
; }' w' j6 g/ e5 G3 b: X/ ^$ b6 _- fcocious sexual development in the first-degree rela-
& ]- f9 L# C, q& t0 z" w- Ftives. There were no siblings.
9 A4 J) K6 C0 q- J, \0 OPhysical Examination8 J4 I0 i4 n6 q9 j1 p1 S8 G. h
The physical examination revealed a very active,
0 s0 U2 [) p" X$ Wplayful, and healthy boy. The vital signs documented! ]! ]6 S) f# ~( b9 d: s
a blood pressure of 85/50 mm Hg, his length was$ J- I2 t: M- B, A
90 cm (>97th percentile), and his weight was 14.4 kg- _- r/ i+ d' p& h! U' H5 D
(also >97th percentile). The observed yearly growth
, C# ]6 g! y0 O' v- t8 ~$ ?velocity was 30 cm (12 inches). The examination of# g5 \- _- Z, n: F* C- \
the neck revealed no thyroid enlargement.! f1 D% u; f* C' \+ V
The genitourinary examination was remarkable for0 b3 z. P4 Q, k  Q  b
enlargement of the penis, with a stretched length of
0 u/ F' o  J/ Q: e, O, y, M8 cm and a width of 2 cm. The glans penis was very well
* k# W9 u+ m( {) O  F* ]) {8 u% H. Jdeveloped. The pubic hair was Tanner II, mostly around
7 s3 `) S* Z2 R' i- t% d+ T5403 m3 J8 U* ^/ u" @: u) q1 m  @
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
( n' g$ d+ h% A1 O8 A2 ethe base of the phallus and was dark and curled. The
) `9 W% z& S  ~3 M$ |. `, |testicular volume was prepubertal at 2 mL each./ |. Q( r& o) f* Z* \6 K6 w+ _2 z
The skin was moist and smooth and somewhat) q) z& S) J$ n  u6 j
oily. No axillary hair was noted. There were no8 X4 G/ ?4 e# o- I/ c& C
abnormal skin pigmentations or café-au-lait spots.
7 q5 l) b: L6 A& g3 L: K. p: \0 MNeurologic evaluation showed deep tendon reflex 2+
- T3 I& E3 ~; V$ I' Mbilateral and symmetrical. There was no suggestion! d/ K7 K( b8 Q
of papilledema./ P* u( m) V' W& A+ u5 {
Laboratory Evaluation) a2 z1 q) g9 s1 |
The bone age was consistent with 28 months by. ~/ {* M9 k# \+ H+ A" z
using the standard of Greulich and Pyle at a chrono-# s' p6 [/ ~9 R5 V* K# b  l- J
logic age of 16 months (advanced).5 Chromosomal/ ^$ T/ ]$ |* }9 u
karyotype was 46XY. The thyroid function test7 `; Y4 X$ q# }
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
: L4 }" B9 s) T) y2 Z4 S9 ^" olating hormone level was 1.3 µIU/mL (both normal).. y& t; W: }* M. F- e
The concentrations of serum electrolytes, blood
9 ?4 Q; m! `8 ~$ i, H1 b% D5 G, ^, Zurea nitrogen, creatinine, and calcium all were
8 @" ]+ t4 `& w5 gwithin normal range for his age. The concentration
/ P( L5 ~. W; G. a# Xof serum 17-hydroxyprogesterone was 16 ng/dL
; B% M0 T% C- C5 B& L: R, g: p(normal, 3 to 90 ng/dL), androstenedione was 20
4 L/ [+ F; x7 y( i# f( ?2 F8 W0 rng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
! ^9 H4 @* _7 i- H7 g8 B# Dterone was 38 ng/dL (normal, 50 to 760 ng/dL),: p3 D; w. E/ D" i5 T9 l
desoxycorticosterone was 4.3 ng/dL (normal, 7 to% a+ N6 u% D; k$ E$ Q+ B0 G
49ng/dL), 11-desoxycortisol (specific compound S)3 b8 s5 a' i8 t$ p
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-8 d' D; S& U0 c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total% n- ?2 [& c4 h. x' _; k) n" F
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),  h, }' _7 E2 Y
and β-human chorionic gonadotropin was less than- t1 C& R& Z. \" V
5 mIU/mL (normal <5 mIU/mL). Serum follicular
  G' X; y& \/ R. zstimulating hormone and leuteinizing hormone$ _$ @! x0 c4 q# O6 v, [5 B
concentrations were less than 0.05 mIU/mL9 P/ M3 t3 ~. y/ i7 r9 n5 g4 |. a5 V
(prepubertal).
- O2 E& e& m0 `  B% Y7 sThe parents were notified about the laboratory* W$ P5 E" a5 B2 [; {
results and were informed that all of the tests were& N7 B! y7 r( e9 ~. U* M  J% u
normal except the testosterone level was high. The, M# J. f6 I+ ?. X+ O$ t
follow-up visit was arranged within a few weeks to
$ a) J# C6 W" X: s6 H# e) [obtain testicular and abdominal sonograms; how-
: R1 c! @5 \1 ?( P3 Jever, the family did not return for 4 months.2 p- \1 n5 ~6 O' K9 n
Physical examination at this time revealed that the5 u6 o8 z. I1 ~" Q: L3 B2 O$ B3 Q# `
child had grown 2.5 cm in 4 months and had gained! p5 r* ]7 _+ N  b- v2 V/ t5 M9 n
2 kg of weight. Physical examination remained. F# X; `+ z5 v9 |% z
unchanged. Surprisingly, the pubic hair almost com-
( ~6 z/ N2 s3 vpletely disappeared except for a few vellous hairs at
# b) D/ \1 H8 i1 e# @; ?the base of the phallus. Testicular volume was still 20 v8 ^. [) P" W$ m
mL, and the size of the penis remained unchanged.( q8 C* p4 }1 o9 Z+ Y: ]; b
The mother also said that the boy was no longer hav-1 M6 X  c+ S7 B* y) L
ing frequent erections.6 K! F$ X* a$ W5 H; A+ z
Both parents were again questioned about use of
9 s2 q5 N# O" R* v( z2 v. `6 Bany ointment/creams that they may have applied to
! R3 c( W3 k  u! Q9 e: G7 V% M/ Xthe child’s skin. This time the father admitted the
# c4 C0 O, _( `0 U  W- k5 Z) [( {Topical Testosterone Exposure / Bhowmick et al 5410 m" h. R; v8 u; R
use of testosterone gel twice daily that he was apply-8 ^+ k9 X8 b3 m: J4 l1 u
ing over his own shoulders, chest, and back area for+ p6 s! ]- X2 A8 G$ b3 i2 m
a year. The father also revealed he was embarrassed. v/ N9 f' U3 O2 ^
to disclose that he was using a testosterone gel pre-
+ e# r) L) `# X) ]3 Dscribed by his family physician for decreased libido( k! p7 ^/ g/ n3 \: }+ Z% M# f
secondary to depression.
; R. A1 ^. l% m3 R. {) c, yThe child slept in the same bed with parents.
1 Z. J1 }- q7 e) c+ n+ r, n- y' sThe father would hug the baby and hold him on his
5 s! o: U$ l, R; t# zchest for a considerable period of time, causing sig-: @+ U8 g8 i1 j, h" ~
nificant bare skin contact between baby and father.
0 B; Y; p/ h% h0 Y( iThe father also admitted that after the phone call,  t* B# J) X* x/ r& S
when he learned the testosterone level in the baby
) m. e8 s* y5 Nwas high, he then read the product information8 ~, p8 \* }/ o3 Q7 k: p
packet and concluded that it was most likely the rea-2 p) u! T2 t. e
son for the child’s virilization. At that time, they
$ p. v5 j3 g3 f. Edecided to put the baby in a separate bed, and the+ ?, P) L  f" ]& ?) a
father was not hugging him with bare skin and had' R; u) ^4 h8 M5 s
been using protective clothing. A repeat testosterone
" ?8 `' F# t5 L0 z7 Z# Stest was ordered, but the family did not go to the
1 Z6 c& u/ ?0 S( l' Claboratory to obtain the test.
% g, c! j: X! n6 t# B6 YDiscussion
# O6 g! Q& L8 O8 nPrecocious puberty in boys is defined as secondary
3 O4 l9 ^) l$ X% p. qsexual development before 9 years of age.1,4) b4 s, D$ c8 m
Precocious puberty is termed as central (true) when
9 [, e# R; M; A: lit is caused by the premature activation of hypo-
' R+ \  \2 D' Vthalamic pituitary gonadal axis. CPP is more com-
- V/ K4 Z# j2 bmon in girls than in boys.1,3 Most boys with CPP1 Z6 g, A' T0 `! d
may have a central nervous system lesion that is
+ a( v1 ~7 Q# [6 j/ F$ Xresponsible for the early activation of the hypothal-$ W# `/ m( ^. }' B; j
amic pituitary gonadal axis.1-3 Thus, greater empha-! }  L4 I0 y0 a5 h* t
sis has been given to neuroradiologic imaging in4 s2 e$ v" a' @" ^
boys with precocious puberty. In addition to viril-
/ J7 k0 |& [, E  \- t& E' u/ Lization, the clinical hallmark of CPP is the symmet-/ d$ ~* \" a8 `8 C
rical testicular growth secondary to stimulation by
6 A0 b) G& o3 M+ I% Egonadotropins.1,3  Q( g+ k$ |& q9 p  o+ ?
Gonadotropin-independent peripheral preco-, a7 z% R3 Y/ }% q
cious puberty in boys also results from inappropriate
; S$ f/ r8 a0 Q/ handrogenic stimulation from either endogenous or
6 H/ E6 R8 r# B. V0 T; X% b; {: z' sexogenous sources, nonpituitary gonadotropin stim-
5 N% ^7 M" I) I4 F# O  N" R! A  gulation, and rare activating mutations.3 Virilizing' B& z+ Q! }. @2 d, [+ `+ V% }
congenital adrenal hyperplasia producing excessive
0 r$ Q! ~! @* @, i) K3 L) ?adrenal androgens is a common cause of precocious
5 \5 [  [) f& d7 [' C# v9 G) epuberty in boys.3,40 a7 s! L$ ^- @- Z. @. b
The most common form of congenital adrenal% m# a+ J5 ]; F* ]6 l8 {
hyperplasia is the 21-hydroxylase enzyme deficiency.9 {% F! ]# {( J
The 11-β hydroxylase deficiency may also result in
2 [% ]) Q6 J) R' B- n" Gexcessive adrenal androgen production, and rarely,
9 d, W' D7 ~5 R# |- @an adrenal tumor may also cause adrenal androgen& m5 u% `, M* {* [( \) S
excess.1,3
' k* R6 d) e, _0 J0 zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 g* c2 p1 m; H( m
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
! t1 |, e6 U+ ^$ |2 m  O( TA unique entity of male-limited gonadotropin-
% v  b: l7 y8 ?9 V2 Sindependent precocious puberty, which is also known
. x: I6 E6 A$ {" las testotoxicosis, may cause precocious puberty at a0 v/ e) o6 ^: s2 N5 |
very young age. The physical findings in these boys. _- G) ~0 H" e" [3 |
with this disorder are full pubertal development,& b' H! |  T4 t6 O) f
including bilateral testicular growth, similar to boys
& `; S. ^4 p$ v" W0 b7 Mwith CPP. The gonadotropin levels in this disorder' p: x* F  ?% C% {$ O
are suppressed to prepubertal levels and do not show8 `4 o" @7 \/ {* d7 y+ L
pubertal response of gonadotropin after gonadotropin-0 o* k! @6 p2 {" y" u& s
releasing hormone stimulation. This is a sex-linked3 {" a8 `7 i( w: n* J" |/ _
autosomal dominant disorder that affects only
$ d! b& Q, M  w+ N% G2 c( V  K( nmales; therefore, other male members of the family8 ^! Q8 S/ R& a3 g2 c  }, m
may have similar precocious puberty.32 @0 i5 O" s( ~( W; G7 @5 e3 ]
In our patient, physical examination was incon-6 v2 a, x- ^0 H, f0 U
sistent with true precocious puberty since his testi-* L8 i: l/ R, R
cles were prepubertal in size. However, testotoxicosis; B2 a: O6 z3 A1 m
was in the differential diagnosis because his father) N2 \% J7 X; n1 g; P
started puberty somewhat early, and occasionally,5 j  p0 u0 V& n8 @+ ]
testicular enlargement is not that evident in the
7 e  m7 A5 B+ ^6 l7 d1 Mbeginning of this process.1 In the absence of a neg-& O, e2 Q3 t4 |4 i0 n0 E8 x
ative initial history of androgen exposure, our
$ r' H9 @! s: f9 o6 x4 z$ j4 g3 W0 |biggest concern was virilizing adrenal hyperplasia,
: Y0 ?% B( r9 G! U, xeither 21-hydroxylase deficiency or 11-β hydroxylase
' L# c- p; `: F8 Udeficiency. Those diagnoses were excluded by find-
( s! N9 p! J3 T2 }% j( n2 Xing the normal level of adrenal steroids.
* L' e; a) M5 ]( P# a9 {The diagnosis of exogenous androgens was strongly
. w/ B4 ^; t6 D5 k1 p& Lsuspected in a follow-up visit after 4 months because
$ ]! w* r3 E# }# V8 s% kthe physical examination revealed the complete disap-% z4 G; u$ Z' F/ c1 j9 u5 r
pearance of pubic hair, normal growth velocity, and  T. t% T- _/ {' {' k) y5 r2 t
decreased erections. The father admitted using a testos-
$ S3 V/ L8 C* E  {" h6 ~- {terone gel, which he concealed at first visit. He was( Q' }% J$ ^' A( \* U" L
using it rather frequently, twice a day. The Physicians’
4 }/ D2 @- u* [' H# D% G9 ?Desk Reference, or package insert of this product, gel or
$ j# u( m- l0 p" O" \cream, cautions about dermal testosterone transfer to. b- z6 \" }5 Y& ~6 E7 G# q
unprotected females through direct skin exposure.; `: l: e9 ?& x5 W  O6 G: ]7 p
Serum testosterone level was found to be 2 times the+ |/ j0 H2 d- C# h, h" N5 u
baseline value in those females who were exposed to
3 t4 N5 |- D- K' Z# w" G; u' y# peven 15 minutes of direct skin contact with their male+ e# j( t- }) ~  X. z
partners.6 However, when a shirt covered the applica-
5 W% r5 X* B; ~tion site, this testosterone transfer was prevented.9 U+ J- S5 f. l6 A
Our patient’s testosterone level was 60 ng/mL,+ w) X+ Z( L" I$ m! G% a  v
which was clearly high. Some studies suggest that$ L- q( L  d9 C" r* L/ v
dermal conversion of testosterone to dihydrotestos-
' O& z3 I, g; X, W" n) zterone, which is a more potent metabolite, is more
- M2 s- S# d1 x" p/ y" E; Aactive in young children exposed to testosterone
; V, i4 p5 t" Fexogenously7; however, we did not measure a dihy-# v+ T' L1 ^# \0 T
drotestosterone level in our patient. In addition to7 Q8 e( P# G  U4 ~% C+ w& S
virilization, exposure to exogenous testosterone in
; _$ e2 M0 A; h; ]children results in an increase in growth velocity and
, n7 a3 \, C) q9 h4 M) fadvanced bone age, as seen in our patient.
- M7 d; Y2 ?- Z& @6 PThe long-term effect of androgen exposure during7 {7 _2 Y4 [  Z% l1 i- m: d
early childhood on pubertal development and final
' R, I" X  U' H4 U, w& G; N, M' hadult height are not fully known and always remain, D- z6 s7 g, E
a concern. Children treated with short-term testos-; ?$ g0 G0 @9 t& ^  w
terone injection or topical androgen may exhibit some
9 B7 h- N% x7 I# n2 H( m. Tacceleration of the skeletal maturation; however, after
1 b* ?/ P# g: _6 H- z+ ?* }1 ?cessation of treatment, the rate of bone maturation
6 y$ n8 I8 H7 k3 ~8 ~decelerates and gradually returns to normal.8,98 u; W2 c7 g( T1 {2 n( c
There are conflicting reports and controversy
/ ^0 x! u+ e# ?' S; o. G2 H: N; oover the effect of early androgen exposure on adult( L& A9 @) H) q5 x0 \. S
penile length.10,11 Some reports suggest subnormal& u1 @3 @  G0 r: L
adult penile length, apparently because of downreg-
6 W  ?. N' P7 x; g0 s" k/ Iulation of androgen receptor number.10,12 However,
9 K0 [) N) [8 o; rSutherland et al13 did not find a correlation between8 ~, q% u: \8 W' D( H# C  J
childhood testosterone exposure and reduced adult1 D, c- t2 ~' ]* K* }% |( t
penile length in clinical studies.2 B2 A- i% m. [2 |* N% C
Nonetheless, we do not believe our patient is7 b8 S" a1 k/ ?5 V& }
going to experience any of the untoward effects from7 r7 ]8 x! }3 y% ~1 |; c: ?$ W
testosterone exposure as mentioned earlier because) E7 b" {! I% t1 B: |8 ~
the exposure was not for a prolonged period of time.
7 \1 m; t7 b( b( iAlthough the bone age was advanced at the time of
( u9 s* q  k+ Y, ~* e2 f) _3 _0 mdiagnosis, the child had a normal growth velocity at
' Z# v# j. e9 L, L) W/ ^. `the follow-up visit. It is hoped that his final adult
4 K6 F7 a" L5 ~  }' b( o, Theight will not be affected.
- @3 m( l' U9 `4 O) SAlthough rarely reported, the widespread avail-& U3 J& O, f( _/ `. C
ability of androgen products in our society may
& f. g1 C& [- v# \% @! O- I. o1 Y4 Gindeed cause more virilization in male or female
3 y6 Z  _7 I. P5 d# h/ V: c( V9 fchildren than one would realize. Exposure to andro-
2 n* N: l9 I  p4 `5 ~9 i+ y/ |gen products must be considered and specific ques-7 f. l( h- T  g$ R0 W: U9 D
tioning about the use of a testosterone product or
) w' z+ O8 V" g7 Z  Bgel should be asked of the family members during8 d+ M: x3 O* H1 A" h% o
the evaluation of any children who present with vir-) q, z; \6 N+ W* h1 t- ^6 A- k
ilization or peripheral precocious puberty. The diag-
* x. e/ Y- j9 m, u& l* W3 F; rnosis can be established by just a few tests and by
/ P! w" j' _+ ]4 s$ g) H5 j" Vappropriate history. The inability to obtain such a: I' n6 Y* E8 C+ i7 g$ P8 y! g
history, or failure to ask the specific questions, may4 {- m8 x: b( O* t4 q4 f2 w
result in extensive, unnecessary, and expensive
5 Y/ t/ [3 ^( e% j- Dinvestigation. The primary care physician should be
) B* J% {' Q9 m" l# D3 i6 Haware of this fact, because most of these children
0 G6 q0 `. C# v' b# M3 Smay initially present in their practice. The Physicians’# ~  f/ }0 f. O) q% O1 Q& B
Desk Reference and package insert should also put a
' n! J! F: e5 E7 Q  W. Cwarning about the virilizing effect on a male or& [6 B, q+ |- H  v- X% R6 \
female child who might come in contact with some-. `; g9 G6 i  T9 W) \  o# J8 G  `" i' R
one using any of these products.5 p5 |6 @0 b( m9 q9 S; W% l
References
7 j/ Z4 K: \" ^, q( o5 @* l1. Styne DM. The testes: disorder of sexual differentiation" \6 y* @8 G, \( B
and puberty in the male. In: Sperling MA, ed. Pediatric: j0 {/ I2 d0 p
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. S: v& M) l$ S3 q, {+ P: F' Q2002: 565-628.
5 `8 Z! F7 p" `6 f' f2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious7 o9 S7 w; i' R7 u
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
9 m# y( l! R3 OBoy Induced by Indirect Topical! J% o6 m/ F$ A5 l% `- G
Exposure to Testosterone/ C  [% g9 S6 _, d* V
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2* j/ q! u" f3 g: b: S( r
and Kenneth R. Rettig, MD10 D/ @% {% o# B4 E
Clinical Pediatrics
4 d8 Z+ v; D+ [. B1 A+ UVolume 46 Number 6
  f) U/ k$ i1 c/ H. E0 G. q2 D/ i; _) e8 M- oJuly 2007 540-543
! @1 ?& K' L9 b* Z! ]' k# t: o© 2007 Sage Publications
2 k; c1 f0 n& t/ R$ M  N* `10.1177/00099228062966511 F$ X' f3 h6 R
http://clp.sagepub.com
& G1 g/ L0 s( E2 H6 ~hosted at
/ m0 u7 n8 W: L% ?5 \8 z2 phttp://online.sagepub.com0 Q% v" z% S# k; Z
Precocious puberty in boys, central or peripheral,
( w" c- U- |$ H2 I1 j( C3 j% Z$ pis a significant concern for physicians. Central
4 I* x# S8 p# ]2 Y! A* vprecocious puberty (CPP), which is mediated
1 t; C, X* o" u; [% B* u2 N. Fthrough the hypothalamic pituitary gonadal axis, has
9 {0 _+ e; h, K8 W/ Ia higher incidence of organic central nervous system
2 h! y+ ^9 l. ?lesions in boys.1,2 Virilization in boys, as manifested
% D6 C$ s+ v) Aby enlargement of the penis, development of pubic
. ^7 G+ c8 \. N! xhair, and facial acne without enlargement of testi-2 K* x, X/ @1 q" W; ?" h  D
cles, suggests peripheral or pseudopuberty.1-3 We
: l0 r+ X1 r% I" [# k1 f' ^) [report a 16-month-old boy who presented with the4 e' y4 X# ^- g. g3 c7 i- U. I0 S
enlargement of the phallus and pubic hair develop-
1 L9 t4 h! ?8 L; E2 f+ D3 m: ]7 I; G! ement without testicular enlargement, which was due
8 V0 X- i3 D; h) d9 W* A  C1 Mto the unintentional exposure to androgen gel used by2 u8 G2 f# }( H) {# `. Y
the father. The family initially concealed this infor-
+ Q" Z; v0 D8 o  r0 r# z+ Kmation, resulting in an extensive work-up for this
/ c" q4 K9 D9 Q* F2 A0 u" Schild. Given the widespread and easy availability of$ j* J- r, }6 n$ c, ?; c
testosterone gel and cream, we believe this is proba-( F: s# P  s! B
bly more common than the rare case report in the
2 u; e8 g- X* c) ]1 j2 H1 a) Yliterature.4
( x: Z) c; F* Z1 B& rPatient Report
' h+ J7 y1 w* I  p  BA 16-month-old white child was referred to the& S1 F, c( l5 A% ^+ e
endocrine clinic by his pediatrician with the concern
0 [  c% G+ c7 ~8 m5 E" Pof early sexual development. His mother noticed
7 z' t1 L; O5 f" olight colored pubic hair development when he was) y6 G& U" E/ g6 p4 G
From the 1Division of Pediatric Endocrinology, 2University of; {7 G- [2 l- \; ]6 o! [
South Alabama Medical Center, Mobile, Alabama.1 h# L1 v& ^: @+ a" `4 A  ~% P. F
Address correspondence to: Samar K. Bhowmick, MD, FACE,4 A; I# G8 ]6 t3 r" k
Professor of Pediatrics, University of South Alabama, College of0 d" l3 y2 K2 }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;. H$ w! N5 Y0 w8 z9 d; I
e-mail: [email protected].
) h4 A, p3 {: _9 m- x- J5 Vabout 6 to 7 months old, which progressively became
0 W9 p2 X0 T2 J  k; m; {9 Mdarker. She was also concerned about the enlarge-
. v: ]( j- v0 e7 oment of his penis and frequent erections. The child" C3 J2 N3 o( z; l6 C" M7 r1 {) e& H
was the product of a full-term normal delivery, with+ S3 S0 g* u) C
a birth weight of 7 lb 14 oz, and birth length of
; E) ]4 E2 {: b, R1 l; ]& `20 inches. He was breast-fed throughout the first year% G1 x8 G$ p9 s6 Y1 n
of life and was still receiving breast milk along with
8 K( P( s, X; hsolid food. He had no hospitalizations or surgery,# N7 f: L) g2 [) Q# {* d' c$ F4 _
and his psychosocial and psychomotor development# G+ W/ |: Y9 a# f' p
was age appropriate." O: f7 R6 R1 S# c7 S
The family history was remarkable for the father,
; Y6 h+ c1 s9 a# m/ u3 U% iwho was diagnosed with hypothyroidism at age 16,
$ x7 U" ]# i: c2 L% ]/ r9 u. ]which was treated with thyroxine. The father’s
( X; Z+ J5 J/ q0 qheight was 6 feet, and he went through a somewhat- [' X1 ~# p- R' R) }) ^) _! ^) _
early puberty and had stopped growing by age 14.8 E) P2 t3 D! b/ z' _- f! Q
The father denied taking any other medication. The
! i# ^$ h& {& _4 }7 g* U; G0 bchild’s mother was in good health. Her menarche
: ]: Q) f0 i# I- N/ X3 j- r: Dwas at 11 years of age, and her height was at 5 feet) g9 S4 J( F$ m) K" P0 G: \
5 inches. There was no other family history of pre-
" {4 v. W2 L/ u$ T/ vcocious sexual development in the first-degree rela-
" W6 I7 g1 x$ y% A& b7 s4 y0 Ltives. There were no siblings.
+ P# c+ u: ~3 N% U- `/ u  UPhysical Examination
. f! y3 K, {7 d" iThe physical examination revealed a very active,
; l" e( w/ c$ m" C! i- P* v* Bplayful, and healthy boy. The vital signs documented& T" A$ F5 F0 r! u' ]9 z
a blood pressure of 85/50 mm Hg, his length was
" M, q0 }2 u) \0 C90 cm (>97th percentile), and his weight was 14.4 kg2 G' c  _( r9 p2 v4 r9 V
(also >97th percentile). The observed yearly growth# Q+ N) e6 t* w$ b
velocity was 30 cm (12 inches). The examination of
2 b( M/ A" \$ D9 Q0 i# qthe neck revealed no thyroid enlargement.  l# {% N, h3 d3 H# \) b
The genitourinary examination was remarkable for8 ?* M8 [' H; P- J, [
enlargement of the penis, with a stretched length of
, ^# f4 i( h/ W2 h. K) ?5 |  I1 j8 cm and a width of 2 cm. The glans penis was very well; J( u, G+ A2 y) }6 `
developed. The pubic hair was Tanner II, mostly around7 C/ ^2 ]) \  [: c, u: L
5407 }0 O+ i+ P; ~
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the base of the phallus and was dark and curled. The0 t$ O/ t2 H" q; i
testicular volume was prepubertal at 2 mL each.+ [- P# m. e) [& E
The skin was moist and smooth and somewhat
# o! T2 `0 u0 R+ q& ~; h: Joily. No axillary hair was noted. There were no' r6 D7 z' G" q& L  M
abnormal skin pigmentations or café-au-lait spots.) p3 {- ?8 y; @4 q9 D& I
Neurologic evaluation showed deep tendon reflex 2+; |- P/ r- ?- Q# K, k/ {* F
bilateral and symmetrical. There was no suggestion% p; x; H) W3 h# N/ t  x2 _
of papilledema.' N% N1 g1 Q; S/ W( d
Laboratory Evaluation% m+ X6 m9 A9 c0 N
The bone age was consistent with 28 months by8 z- B& l% K0 a% p
using the standard of Greulich and Pyle at a chrono-2 V: O+ y' v3 v) Q- l
logic age of 16 months (advanced).5 Chromosomal8 \6 P% n4 ^3 P: f- L4 t
karyotype was 46XY. The thyroid function test
+ L& B( P$ Y0 u, u* ashowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! g7 g$ e7 z7 n6 L0 l5 Wlating hormone level was 1.3 µIU/mL (both normal).& }: d4 ~$ @- |' F
The concentrations of serum electrolytes, blood+ ]7 g: X( ^4 F" i& H* v# H
urea nitrogen, creatinine, and calcium all were
2 n! ^  u) @) Ywithin normal range for his age. The concentration9 R% j6 @( @$ l/ q+ W3 K
of serum 17-hydroxyprogesterone was 16 ng/dL
: O4 W- M+ F2 z# e(normal, 3 to 90 ng/dL), androstenedione was 20
/ Z: U' Q0 x6 D- Zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-7 E2 F9 U# w& V3 j( C' ^: N
terone was 38 ng/dL (normal, 50 to 760 ng/dL),5 m" m% D) B$ {
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 h4 |% F$ [& @5 l/ s49ng/dL), 11-desoxycortisol (specific compound S). `5 ]& b! t7 U/ @9 Q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 o0 ~1 K5 o8 _: g+ u: J1 l; c
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
& `0 H  Q& K% q, Y  T# Vtestosterone was 60 ng/dL (normal <3 to 10 ng/dL),; g- Y! P& ?8 M# ^
and β-human chorionic gonadotropin was less than
' w' L. @: Q$ n$ m- ^5 n5 mIU/mL (normal <5 mIU/mL). Serum follicular- n7 r5 C) U9 _! N  T
stimulating hormone and leuteinizing hormone5 n4 a! [# E. q
concentrations were less than 0.05 mIU/mL5 L" E' n( |; }: f: D$ U
(prepubertal)." [) K1 H7 }2 O  m: S
The parents were notified about the laboratory$ U6 b0 p' ~" Y3 A# L! T
results and were informed that all of the tests were) Y6 X' L  t; h' X9 B& W
normal except the testosterone level was high. The& b8 y2 U8 G6 R9 L
follow-up visit was arranged within a few weeks to. O& _3 n/ ~$ t5 r% Z0 c1 A+ G
obtain testicular and abdominal sonograms; how-+ d' d* b# t/ v! u# u' N. P7 h: r
ever, the family did not return for 4 months.
- F- ~1 ?& D7 P* y) o6 hPhysical examination at this time revealed that the
% V- x3 o  @! p1 [9 K% \8 {8 Zchild had grown 2.5 cm in 4 months and had gained
  M7 C5 X2 o7 H) M" U2 kg of weight. Physical examination remained0 z4 t& v) B9 p; H' ^: c; e
unchanged. Surprisingly, the pubic hair almost com-2 W( I- [7 [; Q9 ^2 c5 c; o
pletely disappeared except for a few vellous hairs at& ]6 D( k% o, l' R9 A; C) h
the base of the phallus. Testicular volume was still 2/ [# E* g4 T4 Q. r0 K3 Y' j
mL, and the size of the penis remained unchanged.
/ p" r$ D) b# i4 N* K2 Z: m* |The mother also said that the boy was no longer hav-
) |  G4 a* V) P9 h9 Iing frequent erections.
% _9 E( ]9 I# i, ~Both parents were again questioned about use of
/ M. r! y& r6 ~* Xany ointment/creams that they may have applied to
+ y, F& @: V* R0 k' r5 kthe child’s skin. This time the father admitted the4 p9 J& r2 S5 z' \2 r8 A- S
Topical Testosterone Exposure / Bhowmick et al 541. t; M5 W( O& T# h$ R2 W) X
use of testosterone gel twice daily that he was apply-2 }  R+ ~) q4 v( O; ?9 _
ing over his own shoulders, chest, and back area for
% P9 t0 k( T1 G3 Aa year. The father also revealed he was embarrassed7 s) L# m: m) `
to disclose that he was using a testosterone gel pre-
+ |; B* R# R' E& R+ x+ D6 o4 _. gscribed by his family physician for decreased libido
; ]& N! M8 N4 E  F& z2 ^3 Vsecondary to depression.. e& ^. }) x* F9 E* y
The child slept in the same bed with parents.
4 x0 }6 P$ H; ^  f6 WThe father would hug the baby and hold him on his0 {" ]0 P$ Q0 x' Q
chest for a considerable period of time, causing sig-) i' ]# Q  h4 F0 v4 ]
nificant bare skin contact between baby and father.$ d. o) w5 q# ]7 m9 I1 p
The father also admitted that after the phone call,
2 U! Q9 S8 N  ~3 Bwhen he learned the testosterone level in the baby
2 n- o. y& b' B( W' `5 Wwas high, he then read the product information
3 ]& a" A3 j; v- n& C0 V9 Ppacket and concluded that it was most likely the rea-
  s. z9 D- m8 tson for the child’s virilization. At that time, they
8 F! X* Y2 O  ydecided to put the baby in a separate bed, and the# F% e7 f: t) k! B8 O
father was not hugging him with bare skin and had! |2 d; b/ {" W: e; |
been using protective clothing. A repeat testosterone
5 F7 }( v* p& i4 @) Wtest was ordered, but the family did not go to the) n( d" U0 D' q/ O0 `& Q
laboratory to obtain the test.
% \  j' t$ m6 `8 jDiscussion  v. v) p. U" w/ P
Precocious puberty in boys is defined as secondary
: q! K4 V# I% k2 }' W- W7 asexual development before 9 years of age.1,47 R, s; m$ j" b1 Q; L  Y/ n
Precocious puberty is termed as central (true) when
! b2 Y2 M* Z9 y" iit is caused by the premature activation of hypo-
' K" m1 d9 z( m4 ^- N: Vthalamic pituitary gonadal axis. CPP is more com-8 i& d0 I6 h# |3 }% t7 z3 ~
mon in girls than in boys.1,3 Most boys with CPP  r& Z: z! r0 y) u
may have a central nervous system lesion that is' p& P- d) H6 Z5 w
responsible for the early activation of the hypothal-
- V/ t# u6 e: Bamic pituitary gonadal axis.1-3 Thus, greater empha-
+ Z% ~- G; a! w+ M: Q- \) Y. Dsis has been given to neuroradiologic imaging in2 x" r( i; I/ q5 r
boys with precocious puberty. In addition to viril-: Q6 J/ X$ l5 p$ _# z' s
ization, the clinical hallmark of CPP is the symmet-
' m9 @- N: i) k% ?4 f9 R. Mrical testicular growth secondary to stimulation by
8 \+ t! B( P/ T1 n; \/ ogonadotropins.1,39 i9 C8 u* X. _* C6 @9 j: x/ v
Gonadotropin-independent peripheral preco-
8 O, x. f" Q9 jcious puberty in boys also results from inappropriate% Y! P4 A# W: A: j
androgenic stimulation from either endogenous or
$ p& F. z( t9 ]; Eexogenous sources, nonpituitary gonadotropin stim-5 E- H" {  {  V  a  F( H
ulation, and rare activating mutations.3 Virilizing
& p: A3 X& q2 A7 B+ s& z7 X7 \congenital adrenal hyperplasia producing excessive, Q0 p+ Q; [8 W0 N9 s
adrenal androgens is a common cause of precocious& w3 l$ I& ^! W) X
puberty in boys.3,4; V5 e' z5 e2 O, V( L
The most common form of congenital adrenal. N- W) s) y$ @2 G! i' w  S7 h
hyperplasia is the 21-hydroxylase enzyme deficiency.+ b7 l* N- y$ D0 N5 K; k. Q
The 11-β hydroxylase deficiency may also result in" h* Z8 r  P" \) Q1 U0 Y$ U
excessive adrenal androgen production, and rarely,
: e+ j3 a* ^: c% Lan adrenal tumor may also cause adrenal androgen8 h2 h- \" V" J" ?+ V/ D+ c6 H* `2 }
excess.1,3
5 {. V& `& y1 Lat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# N) h( L- O$ T6 Q6 Q2 D1 D
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007$ d0 d4 g1 r( H  r  x
A unique entity of male-limited gonadotropin-" _: u# ?. f# M  V, x
independent precocious puberty, which is also known
3 m( X; C# o9 V% d# f: W" zas testotoxicosis, may cause precocious puberty at a
+ d4 f7 q1 @  g: ^  t* A$ Ivery young age. The physical findings in these boys7 C  P5 I$ b, H6 [" m+ R7 f
with this disorder are full pubertal development,
* _) S+ L- p- |1 R6 ?. uincluding bilateral testicular growth, similar to boys( E- @: \" ^/ T
with CPP. The gonadotropin levels in this disorder' e2 M( B6 g7 e) x1 d! n7 E2 ?
are suppressed to prepubertal levels and do not show! ^/ }7 m6 t" J0 n
pubertal response of gonadotropin after gonadotropin-
# D- K6 W! U, c6 X) t! [7 xreleasing hormone stimulation. This is a sex-linked6 j5 X9 M( p5 p/ N* Z8 s1 n
autosomal dominant disorder that affects only) n% D/ @) Q( O4 J
males; therefore, other male members of the family- t$ T' q$ A% N
may have similar precocious puberty.3
- @8 o. r5 j: u9 p0 x! x9 u. X5 ZIn our patient, physical examination was incon-
3 d/ C* j! f# Z: x) l5 qsistent with true precocious puberty since his testi-
: i4 x8 Y+ P1 D3 E, T- S3 A* ]cles were prepubertal in size. However, testotoxicosis
! w5 {- x5 }4 [6 E4 wwas in the differential diagnosis because his father
, [: P7 F/ _  ~8 f5 U6 ystarted puberty somewhat early, and occasionally,2 T' @4 w* G' w9 p: r+ [1 `4 n
testicular enlargement is not that evident in the
9 L6 ~  g7 {9 Z$ h  D% C4 Jbeginning of this process.1 In the absence of a neg-, O& e0 J5 N8 H. r% n+ D5 q' N
ative initial history of androgen exposure, our
& v" K4 P- _% W. Y0 Kbiggest concern was virilizing adrenal hyperplasia,* b  w* M* x, u8 J7 y9 P/ B
either 21-hydroxylase deficiency or 11-β hydroxylase
3 c% C0 P0 F  m! l# Mdeficiency. Those diagnoses were excluded by find-5 z2 L3 _. M0 N9 x' @. y9 D
ing the normal level of adrenal steroids.
8 j) @  G+ t% a/ d# jThe diagnosis of exogenous androgens was strongly
7 W: ^9 @/ h' N9 ?# ?suspected in a follow-up visit after 4 months because4 |1 ?8 H7 \3 J2 y0 m1 I
the physical examination revealed the complete disap-
; W, S; I* z# {" @. `pearance of pubic hair, normal growth velocity, and& O2 G6 A4 X% c
decreased erections. The father admitted using a testos-7 R1 g/ o- X! o- _6 K* u$ m
terone gel, which he concealed at first visit. He was! x: J" o7 \/ o7 z3 J
using it rather frequently, twice a day. The Physicians’
+ U" s. C  b! O0 KDesk Reference, or package insert of this product, gel or5 D* I9 d/ f" }- @( q
cream, cautions about dermal testosterone transfer to
* J: G7 `) s3 O5 F. d/ E. I" Y; {unprotected females through direct skin exposure.
1 I0 T. \! X0 WSerum testosterone level was found to be 2 times the
! N9 I$ {. S* `1 ~baseline value in those females who were exposed to
# U" k6 T2 O# |6 deven 15 minutes of direct skin contact with their male
( G* ], @/ \0 N% ]partners.6 However, when a shirt covered the applica-& i3 S1 P7 E6 o
tion site, this testosterone transfer was prevented.# Z' C2 C4 x* \) l5 F1 B4 O
Our patient’s testosterone level was 60 ng/mL,3 W6 w  f1 U/ Z  V' }8 d. l" H9 T+ R
which was clearly high. Some studies suggest that
- Q+ F- o* d% i( x0 odermal conversion of testosterone to dihydrotestos-4 f* w# U  R* e6 j
terone, which is a more potent metabolite, is more6 b  t: d; t! w. d
active in young children exposed to testosterone
  q0 s: K( `- ]/ ~, gexogenously7; however, we did not measure a dihy-, A, K- n" J% ]9 r/ O
drotestosterone level in our patient. In addition to' @4 E- \# S: p" U, P/ T
virilization, exposure to exogenous testosterone in
$ c! {, z0 d$ |0 w) S) b- ochildren results in an increase in growth velocity and1 I, _& a0 U2 @9 q8 W) G
advanced bone age, as seen in our patient.
, ]4 @4 g& z: P3 s  H8 ?" ?The long-term effect of androgen exposure during
" ?7 @4 @0 ?- m6 w" `( m* U  ?early childhood on pubertal development and final0 `8 \1 h7 {% K# w6 E
adult height are not fully known and always remain0 f" Z  ?6 q# `7 |) T2 X( P( K! `" R
a concern. Children treated with short-term testos-
# @7 d( Z$ a- v( o6 o. Z; cterone injection or topical androgen may exhibit some
2 @: @) A2 Y  C* h5 m/ S$ A( X( g: ?acceleration of the skeletal maturation; however, after
$ x/ _% I! S, h' r; B0 Ocessation of treatment, the rate of bone maturation
* I4 @: P8 e' E" c" sdecelerates and gradually returns to normal.8,9
2 ~3 \+ t1 @. qThere are conflicting reports and controversy
. m8 o7 h- W( c9 z' N/ J, Aover the effect of early androgen exposure on adult& t( B$ _& M& H
penile length.10,11 Some reports suggest subnormal
! ?: w/ T. x  ~# x; I) m5 L0 Cadult penile length, apparently because of downreg-
# V4 M. D) [9 _1 Julation of androgen receptor number.10,12 However,8 k3 m. m  a/ j3 z& k; {# @$ f
Sutherland et al13 did not find a correlation between" U) x6 w$ k- X! W7 H
childhood testosterone exposure and reduced adult
9 s, G" }( H# X7 L+ [1 {$ upenile length in clinical studies.
! @& F1 U1 T' B$ M) Z8 C6 VNonetheless, we do not believe our patient is# o& A: F' i" z( H5 {
going to experience any of the untoward effects from
6 J% \' w/ Z8 K0 A% ~+ L9 Etestosterone exposure as mentioned earlier because
  H3 [, ^/ \/ a1 D7 fthe exposure was not for a prolonged period of time.. G8 O, b+ h/ A8 K
Although the bone age was advanced at the time of
; v! `: y. R$ R) K6 P) f8 ndiagnosis, the child had a normal growth velocity at
" a4 L$ B( S' Q8 h; B) f7 r3 Cthe follow-up visit. It is hoped that his final adult  r9 x  {: b: b! C& q
height will not be affected.
6 s. V* H# q, Q2 E3 d. fAlthough rarely reported, the widespread avail-
& V& _- v% f/ P* Y$ o* C5 d* ?# nability of androgen products in our society may- z6 K! s* ~) {  m
indeed cause more virilization in male or female# w, ^# X5 i- ^$ j& q  p
children than one would realize. Exposure to andro-# I- b, |7 Z" Q4 [
gen products must be considered and specific ques-9 q9 o2 E. O" o5 `
tioning about the use of a testosterone product or
/ N2 E# s6 e3 I  ~* R6 O; Dgel should be asked of the family members during
! a3 c3 Z9 D' a' ^. N2 k$ dthe evaluation of any children who present with vir-) U' x. |7 D" h4 h) |. @
ilization or peripheral precocious puberty. The diag-
. U" F7 a& `8 R6 pnosis can be established by just a few tests and by
& `% W- p1 N6 s3 ]- D0 N. wappropriate history. The inability to obtain such a
. l. F/ S+ a; ~; Whistory, or failure to ask the specific questions, may
' P* q( x: w1 h, D: Oresult in extensive, unnecessary, and expensive- V2 k8 U- G: t+ F% H' [
investigation. The primary care physician should be% V. t4 p  \, J1 }9 y; ^8 T/ q
aware of this fact, because most of these children
7 @' u5 q0 r2 ^& e% @may initially present in their practice. The Physicians’
7 `5 j* r' c* z7 F7 iDesk Reference and package insert should also put a
1 W2 G7 w) n  b* }4 @9 J' p6 lwarning about the virilizing effect on a male or
2 p  v7 t3 c! q( P: z+ c2 r9 Zfemale child who might come in contact with some-
  M+ _8 Z, s& y" K6 rone using any of these products.( ]& C% c+ N1 A9 H' w  R
References
" A- f# m3 f* x* i: J7 v1. Styne DM. The testes: disorder of sexual differentiation, r- m  g* C' @3 \4 I
and puberty in the male. In: Sperling MA, ed. Pediatric0 b8 A5 R" Q& B  X. j
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
. Z8 Z  o4 U% @2002: 565-628.
( v! r7 a$ v3 E8 ~2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
$ `7 r+ {* y6 _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
- y% O7 L2 b8 x. O2 R' A
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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