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Sexual Precocity in a 16-Month-Old+ w2 z' ?1 i% ^2 L- j
Boy Induced by Indirect Topical$ f8 ]3 O# u/ A$ s
Exposure to Testosterone
/ o2 H, X7 S3 k6 mSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2( S8 K# _' S% d- f. V
and Kenneth R. Rettig, MD14 Z! B& ~% ~" x5 V3 _2 d7 H& W
Clinical Pediatrics
. y* f3 P7 e, G; c9 `0 NVolume 46 Number 63 I1 Q3 ]5 _2 U2 M  v: s; c+ I$ H
July 2007 540-543
) Y) T9 o4 \$ r& s4 Y0 P© 2007 Sage Publications2 a5 t2 Z) j; B' O2 ^& a& Y* B" q
10.1177/0009922806296651
! h% U1 Z) J/ mhttp://clp.sagepub.com
' v% I" N3 c2 J7 {hosted at
7 M( O" s3 q4 W! t$ F  P1 _+ e7 Whttp://online.sagepub.com4 y2 K/ g7 J  v$ _
Precocious puberty in boys, central or peripheral,
. B# O# L! z$ A3 his a significant concern for physicians. Central
+ Y6 y' l1 a$ q) M3 B2 q8 kprecocious puberty (CPP), which is mediated0 R% y( X0 K( W" a; b6 g$ ]
through the hypothalamic pituitary gonadal axis, has
( S+ d/ n& z+ ]1 E. Ha higher incidence of organic central nervous system
2 a% C& K& |0 Z) jlesions in boys.1,2 Virilization in boys, as manifested
7 H' D$ @) [' r5 m: I4 [; kby enlargement of the penis, development of pubic6 Y9 F8 M! e. D, X9 c
hair, and facial acne without enlargement of testi-
% [6 D9 l. Z% e4 I$ z! G  G7 K; Tcles, suggests peripheral or pseudopuberty.1-3 We
3 n4 B- Y- G5 d; ]! \& v/ o3 jreport a 16-month-old boy who presented with the* O/ t+ Y0 ^* Z, k
enlargement of the phallus and pubic hair develop-, S) G' `# [& [9 X! b- `
ment without testicular enlargement, which was due
2 D5 q3 t0 I: ?# V% [# Jto the unintentional exposure to androgen gel used by
( v3 Z3 h8 z: E# \* X! xthe father. The family initially concealed this infor-
$ E+ F  J( v. t3 y% v5 Fmation, resulting in an extensive work-up for this: \. g: [' Q0 ~+ z8 o
child. Given the widespread and easy availability of
- q. g) W9 N3 q. Y% J/ C, Ytestosterone gel and cream, we believe this is proba-
- `0 |# q1 @) _9 y1 |$ Ably more common than the rare case report in the
) @' ?0 t% U8 x6 u# c/ w3 Zliterature.4
' n3 n* g& h2 N4 r; }; dPatient Report
) y, ^4 o( S; t# ?6 K$ B  a. u& Y& CA 16-month-old white child was referred to the. q% ^' n: D+ x+ A1 ~3 X
endocrine clinic by his pediatrician with the concern
1 W1 V* M, _2 B3 F; L9 dof early sexual development. His mother noticed, j* S/ D, H- ?/ i
light colored pubic hair development when he was
5 k! S: G" @7 zFrom the 1Division of Pediatric Endocrinology, 2University of9 }5 G4 @# B/ T2 a. V# ~
South Alabama Medical Center, Mobile, Alabama.
, \/ |  c- I) `2 lAddress correspondence to: Samar K. Bhowmick, MD, FACE,
7 o' n/ ]( ]4 Q- F; PProfessor of Pediatrics, University of South Alabama, College of! M+ k9 ?, M+ n5 T# x0 o; O2 c* O
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;7 f  G' @& ?6 s4 w( A
e-mail: [email protected].
1 L, n$ g0 Y; [1 `2 vabout 6 to 7 months old, which progressively became9 V7 U! I* c9 L3 A1 A; D% q: o
darker. She was also concerned about the enlarge-$ P8 }- y2 i" {5 n& c: Z( K
ment of his penis and frequent erections. The child
2 r# V# B/ U) Q2 A8 ?& n, ?, fwas the product of a full-term normal delivery, with9 U1 Y6 k7 f2 {$ G) V0 r% O1 F7 s
a birth weight of 7 lb 14 oz, and birth length of" o8 W3 l( P  `
20 inches. He was breast-fed throughout the first year
0 [! u; a9 [  yof life and was still receiving breast milk along with$ [! k$ k! g9 V1 [$ l9 u
solid food. He had no hospitalizations or surgery,# \% M( o; c. f4 ^( k, r
and his psychosocial and psychomotor development/ C  _  v8 c- J, ?* t
was age appropriate.
' w/ _" B* }7 i: RThe family history was remarkable for the father,
/ }4 t' I3 Z2 Owho was diagnosed with hypothyroidism at age 16,
+ \: `8 g& k0 w( o$ O9 \( |4 |which was treated with thyroxine. The father’s' [/ c0 @/ F9 f2 a$ U) W
height was 6 feet, and he went through a somewhat
( }6 S6 j7 h1 Oearly puberty and had stopped growing by age 14.
: z* W2 h5 x* }/ ~3 FThe father denied taking any other medication. The
9 k& \, A  g6 J. P9 S2 ~4 i. Uchild’s mother was in good health. Her menarche
# s3 ]) s$ a* Q1 G9 Fwas at 11 years of age, and her height was at 5 feet% E7 `' u, z: Z: q3 ]: {3 m1 c
5 inches. There was no other family history of pre-& d& F" x. @( J0 v# k
cocious sexual development in the first-degree rela-
7 n. k) d( h1 Itives. There were no siblings., u: X* K, Q' K3 {% M7 \% \0 X
Physical Examination4 a5 p% t9 P! r  c
The physical examination revealed a very active,
3 A( p5 j/ m  wplayful, and healthy boy. The vital signs documented
: U: S7 W0 f4 q; ~a blood pressure of 85/50 mm Hg, his length was
" m* o: R8 @  g$ c  A90 cm (>97th percentile), and his weight was 14.4 kg" N6 X* ^3 X0 Q- v8 k7 t5 i5 O5 z
(also >97th percentile). The observed yearly growth
* p! j( I3 P9 H! y9 f0 X, d8 `velocity was 30 cm (12 inches). The examination of+ p6 Z$ I, d7 g
the neck revealed no thyroid enlargement./ G" M  ~$ d; T5 ~: h; E
The genitourinary examination was remarkable for
: t; ]% S* z  I" ~. ?3 [, ?( nenlargement of the penis, with a stretched length of
0 j, L$ \& v& t  e% W8 cm and a width of 2 cm. The glans penis was very well
# a% Q& H# l$ ~9 r8 Gdeveloped. The pubic hair was Tanner II, mostly around6 r* N$ G) Y  m. f. p; s
5400 j$ z7 L! w  @  a4 E, W
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the base of the phallus and was dark and curled. The
8 u; I6 i- z: ]% a- w2 Ntesticular volume was prepubertal at 2 mL each.2 B5 [; Z7 g+ b0 ~# r  M
The skin was moist and smooth and somewhat
8 f& ~$ i( Q& F2 A# A/ Koily. No axillary hair was noted. There were no
2 f) C( Y5 F3 X  T6 |abnormal skin pigmentations or café-au-lait spots.
. I' O8 @! [8 {" L9 I" a" T/ {% `Neurologic evaluation showed deep tendon reflex 2+* ~7 h* o' Y( y+ |0 Q  T
bilateral and symmetrical. There was no suggestion
: L  \- z! s. @3 w6 s5 A- Mof papilledema.& u0 W$ l$ n7 `3 @5 K: D( v5 J
Laboratory Evaluation
5 @/ M$ t5 J. J2 D$ A. zThe bone age was consistent with 28 months by
  `; a' K# P" Z6 @using the standard of Greulich and Pyle at a chrono-
0 X8 F6 R* [" e! C+ m1 U; {logic age of 16 months (advanced).5 Chromosomal  \" O- e7 e, _7 z+ {
karyotype was 46XY. The thyroid function test; f$ k  \' e0 g
showed a free T4 of 1.69 ng/dL, and thyroid stimu-# r9 l- |' [2 c3 ~! ~% j
lating hormone level was 1.3 µIU/mL (both normal).& A) _' n& Y3 }+ j+ \$ S8 u
The concentrations of serum electrolytes, blood
2 k6 ~0 F: w! ]% Zurea nitrogen, creatinine, and calcium all were2 O% Q" U# [5 j; N; |" _
within normal range for his age. The concentration
3 n+ O# I) n% b, s2 cof serum 17-hydroxyprogesterone was 16 ng/dL: D( U4 C: j% v/ R2 v( g9 i
(normal, 3 to 90 ng/dL), androstenedione was 20
8 G5 R+ q# q$ u" p/ W  w+ Mng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
9 v4 |! A& `7 Fterone was 38 ng/dL (normal, 50 to 760 ng/dL),  S, `2 [8 V3 @: e  U9 J
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
6 x9 C" x* E4 x4 n  }* f% h49ng/dL), 11-desoxycortisol (specific compound S)
* n6 U# _' L2 K, E$ {/ S. ~was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
( w! L; z9 N9 A. n7 f" D9 d/ B( Etisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total0 F7 c$ X7 @" t6 R2 ~
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
  K$ @3 i" R& @. d! [* \: q; P7 `( pand β-human chorionic gonadotropin was less than
# v5 @8 e0 F0 `% e& K! A5 mIU/mL (normal <5 mIU/mL). Serum follicular
& [$ p7 D. }9 X1 D5 x- G5 B, rstimulating hormone and leuteinizing hormone
# `/ V5 @% J# Fconcentrations were less than 0.05 mIU/mL
4 Q) F& K0 z: \- m. d(prepubertal).9 q. a) C4 I8 B' I. r8 Y' f: A
The parents were notified about the laboratory+ d; B/ S4 v# ^5 C/ C* Q
results and were informed that all of the tests were! \8 z9 ]% ^: ]) B# j$ q- {7 Z
normal except the testosterone level was high. The* E3 U9 H1 ~+ o- K: N
follow-up visit was arranged within a few weeks to
' d8 X1 S* t/ \+ P$ \obtain testicular and abdominal sonograms; how-
% [) o$ o+ A: q# {. [9 ^6 d7 Cever, the family did not return for 4 months.
. O! }- f2 Y% S1 }Physical examination at this time revealed that the; v5 U) F- J- ^
child had grown 2.5 cm in 4 months and had gained, N. T. r4 V6 t5 x# ~4 ]' s: V0 A' U
2 kg of weight. Physical examination remained
0 Y' ?( {$ m# D2 qunchanged. Surprisingly, the pubic hair almost com-
% k4 P' S$ H# P) y! W/ {4 ?pletely disappeared except for a few vellous hairs at! X2 ^. Q! T- ?, f. F
the base of the phallus. Testicular volume was still 2+ G. f1 W; M, C2 H: q# g
mL, and the size of the penis remained unchanged.
/ f: o' b" ?2 ?( @. n; j/ d3 xThe mother also said that the boy was no longer hav-* v, l  I& }% \0 K% a- c8 G+ H% u
ing frequent erections.
  k5 Z+ z6 H* e7 o6 O7 iBoth parents were again questioned about use of
0 p8 m2 b" ?* F4 U9 ~6 }8 E" Fany ointment/creams that they may have applied to; M& b2 e3 o/ P9 I
the child’s skin. This time the father admitted the) T& S5 H0 Q  E, y2 j
Topical Testosterone Exposure / Bhowmick et al 541
% v! Q  R8 ]( U/ ~7 W+ m5 g, v; fuse of testosterone gel twice daily that he was apply-
( X& ^  G0 J3 J- r& Eing over his own shoulders, chest, and back area for- U' x" A9 e3 ]' [- H* o
a year. The father also revealed he was embarrassed
4 {" S7 Q0 ]% @; R+ Lto disclose that he was using a testosterone gel pre-
* @; w, K) K+ _  Q: E6 b# Uscribed by his family physician for decreased libido
: r7 N3 v' @4 g; q: ssecondary to depression.
+ d. n/ Q2 w3 ~2 F+ {1 x9 fThe child slept in the same bed with parents., T! S" Z  a$ a" o  h
The father would hug the baby and hold him on his
& y3 {5 O7 M0 {2 s, r5 r2 T/ [1 Hchest for a considerable period of time, causing sig-
% L8 R9 r5 C) f, vnificant bare skin contact between baby and father.
; d; \& f. M5 @; d4 N1 c3 }The father also admitted that after the phone call,. r& n2 N" A0 [0 c- {* v
when he learned the testosterone level in the baby
" E4 B3 D6 I! d4 }8 r, }7 lwas high, he then read the product information) `) o" D: T5 F( f8 p
packet and concluded that it was most likely the rea-
( U( ~+ I! P& f, h- lson for the child’s virilization. At that time, they
/ ?; M6 @1 i! ~2 A% T0 x+ Zdecided to put the baby in a separate bed, and the
0 z+ y) w+ C5 s) o0 Gfather was not hugging him with bare skin and had
* k0 b2 d: B, Z$ Y9 l0 v* S5 Pbeen using protective clothing. A repeat testosterone
7 u& u  }! i  T% b$ vtest was ordered, but the family did not go to the
' P( H3 M2 v& \  mlaboratory to obtain the test.- q5 K+ Y% F/ Y0 g
Discussion2 H" ~2 M- l6 `- B
Precocious puberty in boys is defined as secondary
0 n  e# I* E5 p: Csexual development before 9 years of age.1,4
' {; X. a0 Y' \" l1 j7 u  U) H8 rPrecocious puberty is termed as central (true) when
: D# e  Q; P3 y; zit is caused by the premature activation of hypo-
0 q3 ?9 W. \( }6 Q6 [8 Bthalamic pituitary gonadal axis. CPP is more com-( f5 v- h: w9 L9 q' A
mon in girls than in boys.1,3 Most boys with CPP) r" s/ z# V& t, u
may have a central nervous system lesion that is
4 }* a. R+ F, N: Tresponsible for the early activation of the hypothal-
5 j% K; z3 Y6 ]1 ]' ~/ O. b" m: Pamic pituitary gonadal axis.1-3 Thus, greater empha-! t  u% n& ]  \& U! W8 S- b! A
sis has been given to neuroradiologic imaging in
$ |8 R/ e" D# M$ {5 Jboys with precocious puberty. In addition to viril-! ^# q$ p5 j) ?, |: @. m
ization, the clinical hallmark of CPP is the symmet-7 _# ^, P) K" r: i* E" m- H
rical testicular growth secondary to stimulation by
9 W% i% X3 L8 k3 s: N  cgonadotropins.1,3  V2 D. m' L) E* i# g9 I
Gonadotropin-independent peripheral preco-: ?9 q1 {3 F, A3 E" T
cious puberty in boys also results from inappropriate9 }7 c; q* K# ?/ P! H( j$ U0 f, K1 y
androgenic stimulation from either endogenous or: Y: f# T8 F- J+ |5 q% g; {% D* s
exogenous sources, nonpituitary gonadotropin stim-' ~6 m3 y+ \: a$ k# F( [
ulation, and rare activating mutations.3 Virilizing
  u4 K% z! u* e* Econgenital adrenal hyperplasia producing excessive% N# `9 y6 n1 a/ S: O* t+ B& i7 d
adrenal androgens is a common cause of precocious
1 @8 H2 w: Y2 R7 X+ V) {2 _puberty in boys.3,42 T2 R* c% Q/ k0 x* \  n
The most common form of congenital adrenal
- C; i+ G0 M6 Z! chyperplasia is the 21-hydroxylase enzyme deficiency.
9 B8 x  J3 O0 }" F8 S/ sThe 11-β hydroxylase deficiency may also result in+ q# d8 C/ k4 W- Q" S
excessive adrenal androgen production, and rarely,. N2 o6 u" Z5 x7 o8 m% R  G: r
an adrenal tumor may also cause adrenal androgen9 V* V6 K" S1 L
excess.1,3
6 j% D3 N( f  Zat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
9 d/ e5 g% k, j# n542 Clinical Pediatrics / Vol. 46, No. 6, July 2007* g2 x% T! s5 u# U( m+ |
A unique entity of male-limited gonadotropin-
. d3 ~8 T9 B7 g; m& hindependent precocious puberty, which is also known" Z; S: C' J! c3 g+ g& A( v
as testotoxicosis, may cause precocious puberty at a
3 y7 z2 ^' Z" U# j4 Z6 ?9 V- V0 qvery young age. The physical findings in these boys1 }+ @* O. j6 H( d& f0 D
with this disorder are full pubertal development,
% x& h, [& ?# l/ h( ~including bilateral testicular growth, similar to boys
0 C* T0 {! d' o. Jwith CPP. The gonadotropin levels in this disorder
3 W# c4 S; V. l( ?; Mare suppressed to prepubertal levels and do not show
: B0 M9 [2 ?5 u/ zpubertal response of gonadotropin after gonadotropin-
$ H7 g* ^+ d& h. areleasing hormone stimulation. This is a sex-linked
4 V8 Q7 v; z8 Gautosomal dominant disorder that affects only
( o% v4 ~* M6 Q5 r1 I3 Wmales; therefore, other male members of the family: c+ M" @. T# W
may have similar precocious puberty.3' \! V: Y/ @% [9 d8 I" h2 ]9 H# K
In our patient, physical examination was incon-
( u; s$ i2 F' x3 |3 c3 p. ^sistent with true precocious puberty since his testi-3 O) G4 X! i- s) t# h
cles were prepubertal in size. However, testotoxicosis; u" N- _7 c& h
was in the differential diagnosis because his father
+ v3 J$ D1 E8 z' x$ Hstarted puberty somewhat early, and occasionally,
) _" ]; k- a' Y  ltesticular enlargement is not that evident in the% i% Z0 }+ \0 f+ z* l2 b3 P2 _
beginning of this process.1 In the absence of a neg-
3 B$ j: P. o& y: |ative initial history of androgen exposure, our
* r% [3 J& K. ?4 L1 g/ H0 t4 r$ ~biggest concern was virilizing adrenal hyperplasia,
# I) ^. x3 p) T$ }) ?either 21-hydroxylase deficiency or 11-β hydroxylase4 b$ o  W+ V: u& r
deficiency. Those diagnoses were excluded by find-* \4 v% m  A+ B6 _$ B
ing the normal level of adrenal steroids.) J8 }: o3 ~. l( o
The diagnosis of exogenous androgens was strongly& l$ q+ Q# C, `* _' g
suspected in a follow-up visit after 4 months because$ b/ V8 W3 A& \* N: a3 A" ~' A
the physical examination revealed the complete disap-( ]7 _, ^  h6 G! m$ M. N0 ?' b' m
pearance of pubic hair, normal growth velocity, and
2 w  n. L' J  O5 m8 |decreased erections. The father admitted using a testos-
2 t* h" L& G3 M0 Z1 P( Pterone gel, which he concealed at first visit. He was
' `% W2 Y2 _7 x7 C' b3 e" b. tusing it rather frequently, twice a day. The Physicians’5 g6 l9 d% d/ V0 v
Desk Reference, or package insert of this product, gel or5 @# P; g! e* @4 C
cream, cautions about dermal testosterone transfer to
  B( o1 x6 m0 {3 w" k2 uunprotected females through direct skin exposure./ C5 i( q# Z; T* D
Serum testosterone level was found to be 2 times the* K  U+ o8 U% ?" h
baseline value in those females who were exposed to' n% @8 f9 r) M8 R; r
even 15 minutes of direct skin contact with their male
' x& M' N: ?& C3 P$ Q! fpartners.6 However, when a shirt covered the applica-
! g6 C! U. D% Q0 Ition site, this testosterone transfer was prevented.2 P% ?+ `; T% q  L/ ^1 G, Z) z4 o9 o
Our patient’s testosterone level was 60 ng/mL,
8 w: b+ ?1 K, g. L! Z7 F( ^" ]$ Owhich was clearly high. Some studies suggest that
# N$ c. @8 ]: s+ Y7 edermal conversion of testosterone to dihydrotestos-
  ~* _: U3 v6 I4 e4 O  W$ m! c' E$ Wterone, which is a more potent metabolite, is more
; T3 F& B! z) p8 P( q: Sactive in young children exposed to testosterone* d) h) d1 F1 N+ _5 {
exogenously7; however, we did not measure a dihy-
" ?- e4 n+ ^0 l4 W' j  Y& Tdrotestosterone level in our patient. In addition to
: N2 z5 w: t$ \; k/ L$ svirilization, exposure to exogenous testosterone in1 |* ~5 g5 {  k
children results in an increase in growth velocity and" B" G/ ]( Z* Y3 a6 M5 h
advanced bone age, as seen in our patient.5 _2 t2 u  I9 P
The long-term effect of androgen exposure during
! o3 J+ i* b$ wearly childhood on pubertal development and final. N- ^  q& V  ]( v0 u
adult height are not fully known and always remain
& u" ?' V+ U8 x3 h7 W7 ra concern. Children treated with short-term testos-# W! [+ i* p% c' t- s  S
terone injection or topical androgen may exhibit some
! X& L9 r9 e" {' U. t" z; sacceleration of the skeletal maturation; however, after+ i) E* x( P% a  I  z* p
cessation of treatment, the rate of bone maturation
: z4 z1 N/ |0 ~0 x- bdecelerates and gradually returns to normal.8,9
: W; R2 f) T2 ^9 V0 F# o* SThere are conflicting reports and controversy8 `+ m, P2 L! Z: r$ q
over the effect of early androgen exposure on adult
% F$ s" @; `9 C* u/ N4 y5 n( ^penile length.10,11 Some reports suggest subnormal4 ^5 c" F# J0 h8 m# h8 y$ I, t
adult penile length, apparently because of downreg-% D& o0 Y# S5 ]& X$ z2 K
ulation of androgen receptor number.10,12 However,, H: b. l0 L( B( E5 L# h
Sutherland et al13 did not find a correlation between
  |8 h# w& ~: q6 z$ H. tchildhood testosterone exposure and reduced adult
" v, ?1 L/ N7 v3 y  r- Bpenile length in clinical studies.: h. M; n; L  v5 c& ]; a3 y
Nonetheless, we do not believe our patient is* y" c5 L- E2 R( L0 U6 A
going to experience any of the untoward effects from
" Q6 j, F+ g* k/ H; ?testosterone exposure as mentioned earlier because$ H* y/ v% m0 m5 A+ d$ `
the exposure was not for a prolonged period of time.1 k/ U6 @7 G0 W
Although the bone age was advanced at the time of# E( T1 F: X; G- M. G
diagnosis, the child had a normal growth velocity at5 {) m& n1 i. _6 O3 p$ ]! r
the follow-up visit. It is hoped that his final adult
5 B, r' ?" \8 o9 U8 l: L1 {1 kheight will not be affected.. K- c# g9 r% @. U
Although rarely reported, the widespread avail-
* ]$ R+ I% ~4 ~( r4 A/ X" mability of androgen products in our society may
1 k% G% Y/ p  x' xindeed cause more virilization in male or female2 {: h1 N+ H' |, S& u
children than one would realize. Exposure to andro-8 R# e. T9 O1 G4 U4 y. S
gen products must be considered and specific ques-
+ H0 }! A2 H3 q; ^' U2 p2 q. Ationing about the use of a testosterone product or
6 E# m: R0 |& H0 {gel should be asked of the family members during# z9 Q0 m4 O1 t+ ?
the evaluation of any children who present with vir-! |. ~+ `1 j6 o# f4 x5 S: F
ilization or peripheral precocious puberty. The diag-6 K: u3 h9 Z" G2 s- r3 ~' y3 q
nosis can be established by just a few tests and by
  T4 o  A0 L; n6 R2 happropriate history. The inability to obtain such a! a- f8 h# L3 u4 F: e+ g
history, or failure to ask the specific questions, may
+ E$ }0 }0 J# V' ?) d" ^result in extensive, unnecessary, and expensive
. g# s) q) U+ y9 Uinvestigation. The primary care physician should be" o" X7 \. M5 J7 u" p/ U4 a
aware of this fact, because most of these children7 \$ x* x. d9 s' X# }
may initially present in their practice. The Physicians’2 y6 |5 z+ d4 u  u6 K3 N' h2 n8 a
Desk Reference and package insert should also put a
# u8 Z0 a/ t4 p- ^. ?# V- Swarning about the virilizing effect on a male or
2 O8 K; D+ I$ H8 `: h3 g% @female child who might come in contact with some-6 b7 w: G5 Z! v& |6 Q/ O0 d+ M
one using any of these products.
2 M/ I/ G& X. D; i5 mReferences' h; ~" ]0 j7 i; i2 _
1. Styne DM. The testes: disorder of sexual differentiation
' {% d% j1 a' E2 sand puberty in the male. In: Sperling MA, ed. Pediatric+ {: v6 d1 J  n2 j( |
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
; X' p# ?& C: A& N4 L9 B: w2002: 565-628." H- N: j4 J: c1 F
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious; k  C2 q9 C2 A$ v( m# O( a
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old* d8 z5 X+ P, L* H
Boy Induced by Indirect Topical
9 Q: d1 l, b9 q2 ?- }* E) f2 zExposure to Testosterone
) L4 f+ W; S7 U* J. c5 DSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,24 I+ h" l$ a3 H4 U6 y
and Kenneth R. Rettig, MD1
2 }* @9 o& A! R% IClinical Pediatrics
1 A- S( r; s1 J, I- k1 T; T( DVolume 46 Number 63 F) z; o) I- D! w! b. O$ i$ Z: i/ y8 k
July 2007 540-543
- R0 b6 O$ z% _" W© 2007 Sage Publications  y8 A) ]" S, c$ W4 _; k
10.1177/0009922806296651$ K& t! i: y3 B
http://clp.sagepub.com3 e2 Z$ ^6 |( g2 ]2 Z8 r4 ^
hosted at0 i7 X# o" \. C+ @: @' K
http://online.sagepub.com
  u4 g2 @% C- f: E: yPrecocious puberty in boys, central or peripheral,
3 s" S7 e1 B/ n& G& k& ?- zis a significant concern for physicians. Central; [6 g. J  @+ Y* S# H6 L
precocious puberty (CPP), which is mediated
  h! x6 j4 P2 B" k* {& T: Wthrough the hypothalamic pituitary gonadal axis, has
1 A2 x! j' t6 p+ Ea higher incidence of organic central nervous system
  u+ H0 p4 J; n9 K) Glesions in boys.1,2 Virilization in boys, as manifested5 u9 T' u0 l+ f2 R
by enlargement of the penis, development of pubic
7 W0 T9 }3 @# B. T6 O" Hhair, and facial acne without enlargement of testi-
  g5 \; {, n: @, K9 i/ q4 @cles, suggests peripheral or pseudopuberty.1-3 We
7 r  m& e( A+ A  d; ^( {& C! _report a 16-month-old boy who presented with the5 w3 v* ]2 `. g/ z. ~( [! d
enlargement of the phallus and pubic hair develop-
4 U5 R( D0 u: ~) i6 zment without testicular enlargement, which was due' o  V* ^) @/ l( V7 D( e0 e; o
to the unintentional exposure to androgen gel used by
+ k& p# y6 A5 ~the father. The family initially concealed this infor-
+ p' G# d' h) k* q" {mation, resulting in an extensive work-up for this" S: g2 a# o8 Z
child. Given the widespread and easy availability of2 R5 i) ~/ I  D
testosterone gel and cream, we believe this is proba-, K0 V4 k  \! B" `# j) T; u5 Q
bly more common than the rare case report in the
2 R; p' C: @- r0 Nliterature.4" @0 E% Z7 [( b# {+ a" E8 P
Patient Report
; p- v0 `2 g1 xA 16-month-old white child was referred to the8 _; Z9 E) w$ j! \
endocrine clinic by his pediatrician with the concern7 W" D2 e6 i1 s$ _/ @
of early sexual development. His mother noticed
6 \( Z6 Q+ B# R% A5 C! @4 P% H( h8 Dlight colored pubic hair development when he was! j) J/ f. o' _& j/ J& y
From the 1Division of Pediatric Endocrinology, 2University of
: e) R! V$ T- K- F4 P: z7 oSouth Alabama Medical Center, Mobile, Alabama.
2 r8 c) R5 w3 |1 o; x( L/ C/ fAddress correspondence to: Samar K. Bhowmick, MD, FACE,2 M+ C* U6 }1 ^: J& G7 ?- X7 w: W( A
Professor of Pediatrics, University of South Alabama, College of
2 o3 e2 q2 ]2 ~$ \# g( C7 yMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;8 G; v# ^2 t% _& w& H% Q
e-mail: [email protected].
0 T3 `9 ~3 u, p; {% T. rabout 6 to 7 months old, which progressively became
4 @! n; A& L, G, Ldarker. She was also concerned about the enlarge-) K- ]5 @, E1 w; b* c3 ?2 m1 g
ment of his penis and frequent erections. The child
: I- s& i) i: g7 g; awas the product of a full-term normal delivery, with
$ y3 q5 h; m. S9 p/ {( S$ ga birth weight of 7 lb 14 oz, and birth length of
3 m5 _6 B" K! D9 }20 inches. He was breast-fed throughout the first year% X  L& R9 U7 s/ d2 g
of life and was still receiving breast milk along with5 ]$ l$ ?- D! N; z
solid food. He had no hospitalizations or surgery,8 D; h" A( z- m* f6 l0 R( U2 C
and his psychosocial and psychomotor development
4 z  Y3 g  b' C" V2 v4 twas age appropriate.
+ N7 W3 y" l3 y+ m; pThe family history was remarkable for the father,# j% t5 D9 |, u5 n; a0 B
who was diagnosed with hypothyroidism at age 16,
/ ?# T, g7 L! f2 B- awhich was treated with thyroxine. The father’s
5 _' S) r& A$ u- l, L( iheight was 6 feet, and he went through a somewhat
) @+ A7 h3 T. ?: W6 {$ L' k) Cearly puberty and had stopped growing by age 14.1 }9 b! I: t! e1 i/ S: t
The father denied taking any other medication. The8 B# B7 O, q  y* \6 W2 Q0 p
child’s mother was in good health. Her menarche
7 J$ d$ N) X! I& r# @2 @was at 11 years of age, and her height was at 5 feet
1 {$ I' `' }4 V& e( Z) ?' O+ _5 inches. There was no other family history of pre-9 Z3 `/ s4 H% W: ~+ o' J+ @
cocious sexual development in the first-degree rela-
. j$ q$ V# J. V7 ?: U+ ztives. There were no siblings.) T& a* d3 f- c
Physical Examination
7 p4 \% R& w8 EThe physical examination revealed a very active,3 j9 _# H# z' I, K# c( T* y9 K+ l) i
playful, and healthy boy. The vital signs documented7 l# _2 A2 F9 o" n- W' b
a blood pressure of 85/50 mm Hg, his length was& B0 J7 a! t2 @; u
90 cm (>97th percentile), and his weight was 14.4 kg
; e# U- `3 m0 [2 |- b(also >97th percentile). The observed yearly growth" W0 ~+ G# K, _0 h& r+ w5 ~
velocity was 30 cm (12 inches). The examination of
) n- X( ]- v$ k  Tthe neck revealed no thyroid enlargement.* O& @( v! o: D' x& U4 R0 J7 r, R
The genitourinary examination was remarkable for- h& w8 w% B3 J' j, {/ q' i. n
enlargement of the penis, with a stretched length of: C# Q7 b% e( i- q$ f5 @8 v
8 cm and a width of 2 cm. The glans penis was very well
  O  N1 j; A. @: ydeveloped. The pubic hair was Tanner II, mostly around
+ Q4 L+ n- i2 L- M540" v- R" P2 u0 H7 X( M
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, v5 D0 T6 M- ]  w& W$ ithe base of the phallus and was dark and curled. The
; C2 h$ g8 S8 m: e7 @6 U( h  d7 ktesticular volume was prepubertal at 2 mL each." t- ~* _4 E1 h
The skin was moist and smooth and somewhat' R) @7 u7 ?+ R( W" l7 {
oily. No axillary hair was noted. There were no
& r  N' B' u. G; I. A+ mabnormal skin pigmentations or café-au-lait spots.( x  ?9 p9 M9 k/ B' N
Neurologic evaluation showed deep tendon reflex 2+
1 @3 \' u+ Z- U& q) n) vbilateral and symmetrical. There was no suggestion" q; j8 |" L& U* Q
of papilledema.! G: m) `- G' Y, c3 B- p
Laboratory Evaluation
5 X, u* g, ]- qThe bone age was consistent with 28 months by8 l6 Y( p: G9 |; H" h6 R
using the standard of Greulich and Pyle at a chrono-
' f6 C$ ]3 v2 G, F# i- qlogic age of 16 months (advanced).5 Chromosomal- }# i- N1 U8 a6 Q% F* p; r8 q! N
karyotype was 46XY. The thyroid function test4 H6 N1 C3 a. u6 D/ T
showed a free T4 of 1.69 ng/dL, and thyroid stimu-; u4 A) m5 \9 H! a4 Y/ {4 g9 U
lating hormone level was 1.3 µIU/mL (both normal).
. J! l& v& h2 s: o" V2 h: _% W+ aThe concentrations of serum electrolytes, blood
+ u- l3 y. w8 eurea nitrogen, creatinine, and calcium all were' w, K  q0 E; O  r8 c
within normal range for his age. The concentration
( `- o+ Q1 g+ C7 m) K1 Yof serum 17-hydroxyprogesterone was 16 ng/dL
' D6 V5 |0 W8 G, @" e+ j0 }2 X(normal, 3 to 90 ng/dL), androstenedione was 201 z9 J7 u8 @7 ]3 z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
" G  L8 G! E2 Kterone was 38 ng/dL (normal, 50 to 760 ng/dL),! ?' G& d/ N- M. N0 `1 ]  X+ Y
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
+ N5 ~& ^; t* f' B- b1 h49ng/dL), 11-desoxycortisol (specific compound S)
* n$ @2 V+ u3 E, J/ c; S5 l2 Pwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-( e3 ?8 _* J1 F, d; O! h
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total8 ?9 `  U# j3 i) b% h
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
9 [( J. d# x9 F4 z8 zand β-human chorionic gonadotropin was less than% H1 P7 T9 E+ h. v
5 mIU/mL (normal <5 mIU/mL). Serum follicular, `$ i0 K  z0 x3 J
stimulating hormone and leuteinizing hormone8 m4 j  M2 b2 M+ n9 V" A7 t7 H
concentrations were less than 0.05 mIU/mL
  k) Z  Y7 I1 W! P! V! N; O(prepubertal).# U0 }, N3 q! Q
The parents were notified about the laboratory( X1 ?0 a; k$ Y' ]* ~. G; ^) h5 P
results and were informed that all of the tests were
6 X2 L) F& o0 j6 c& l: P3 ]normal except the testosterone level was high. The
  [9 N! l4 P: @* R8 Cfollow-up visit was arranged within a few weeks to1 }3 N6 s5 @: _
obtain testicular and abdominal sonograms; how-* }9 O5 B2 m& p
ever, the family did not return for 4 months.+ ?5 \# o$ ~/ e2 n( P9 V1 ]5 M$ _3 z
Physical examination at this time revealed that the0 x4 ^" o* d7 q$ \
child had grown 2.5 cm in 4 months and had gained
& O2 I# h- j! S: ^  }4 I# x2 _2 kg of weight. Physical examination remained2 p  _. n, F0 I+ S, t8 q
unchanged. Surprisingly, the pubic hair almost com-, `$ Q+ {$ @7 I" c
pletely disappeared except for a few vellous hairs at. O- G4 u% E4 C* d% M/ ^
the base of the phallus. Testicular volume was still 2) b" C, A3 i( v8 c
mL, and the size of the penis remained unchanged.
) ~2 u# Q3 S2 x% n, ]The mother also said that the boy was no longer hav-+ O5 f' Q; X4 V' l; ~
ing frequent erections.0 A% j/ t8 c# U7 v2 q8 v
Both parents were again questioned about use of' Q, a: u- b7 ~
any ointment/creams that they may have applied to; w% U& P: z" s( s9 K$ g! Q* ?
the child’s skin. This time the father admitted the, h) f/ j, v+ d) }
Topical Testosterone Exposure / Bhowmick et al 541
9 b8 _7 ~1 d' E2 Z1 L2 guse of testosterone gel twice daily that he was apply-
0 W! C2 L; J. `6 r$ L5 d6 t9 I7 Jing over his own shoulders, chest, and back area for; d' E. f9 `8 [4 y3 F$ }
a year. The father also revealed he was embarrassed
, n% w5 y4 \8 H7 cto disclose that he was using a testosterone gel pre-' @0 W* q- N$ C/ _( T0 H
scribed by his family physician for decreased libido  }; U: Z; y! \3 @$ e- l/ k: }; C
secondary to depression.
6 ]' q4 k" r  J$ \The child slept in the same bed with parents.+ c  k9 a( [+ |2 D* x
The father would hug the baby and hold him on his
; q- ]! [! y$ e) j- {chest for a considerable period of time, causing sig-9 |. f/ @& M, p" B2 C8 e1 y
nificant bare skin contact between baby and father.
8 w! v+ y9 v; X! `2 ?' oThe father also admitted that after the phone call," {, c4 [5 c2 x, R" h4 Y
when he learned the testosterone level in the baby; B: Y4 J$ T: `9 x
was high, he then read the product information
8 j, E7 K( N# ~: x; M5 C7 Gpacket and concluded that it was most likely the rea-, Z9 I; C; H( b5 k. g
son for the child’s virilization. At that time, they
/ ~& b- p2 m  Q, T' k2 Xdecided to put the baby in a separate bed, and the
1 C" @. H" ?' G$ C; E# Pfather was not hugging him with bare skin and had- L: l1 ~7 H/ I5 h' p# V! |- o
been using protective clothing. A repeat testosterone* N# X& Y1 m; N( f/ b
test was ordered, but the family did not go to the! ^" @' O3 m/ c4 Y9 e# x# w
laboratory to obtain the test.+ O  U( N0 B" Y# |" c
Discussion
' m$ V0 R" j  ]& g  S+ YPrecocious puberty in boys is defined as secondary; M4 d0 ^2 F7 s. N# A8 K% Z/ `  P
sexual development before 9 years of age.1,4
- H, E6 c8 c6 e' x2 O3 x# ~Precocious puberty is termed as central (true) when1 U. p- W' A0 n: a
it is caused by the premature activation of hypo-- \' W8 k8 Q$ C( X# e( s4 W
thalamic pituitary gonadal axis. CPP is more com-1 v/ @; v0 g- d2 D9 S4 m7 W
mon in girls than in boys.1,3 Most boys with CPP# `1 u2 g9 ?3 a) ^7 P9 ]
may have a central nervous system lesion that is
5 r9 b# o$ I; Q7 W& Oresponsible for the early activation of the hypothal-% _0 Y- i, m" V; G6 R
amic pituitary gonadal axis.1-3 Thus, greater empha-  l# ?1 y# m# I! b( v' W
sis has been given to neuroradiologic imaging in
2 k. \0 ]8 r' O9 j8 \boys with precocious puberty. In addition to viril-9 q* p, F# J3 @8 m
ization, the clinical hallmark of CPP is the symmet-
/ O, P, z8 h# E3 C: Crical testicular growth secondary to stimulation by
; Z) Y" r6 a1 j/ }0 lgonadotropins.1,3
' c$ K1 \! ]3 l& M0 NGonadotropin-independent peripheral preco-
7 i+ A0 Q7 Z. Zcious puberty in boys also results from inappropriate
' }# l& x1 X6 K2 F5 }" |androgenic stimulation from either endogenous or
; B0 _  A3 H% J; |exogenous sources, nonpituitary gonadotropin stim-8 _8 `* Q4 S: ~% b/ S
ulation, and rare activating mutations.3 Virilizing
+ d  U- B+ B6 |) W8 ~- p  Icongenital adrenal hyperplasia producing excessive
" \' {, B% j- o- l6 r5 `' Oadrenal androgens is a common cause of precocious
4 Q# N3 s3 B2 y# bpuberty in boys.3,4
9 o2 C2 f$ Z! W5 QThe most common form of congenital adrenal
+ X4 o! b& B  _& ?0 Hhyperplasia is the 21-hydroxylase enzyme deficiency.
% ~* H7 ^' Y, sThe 11-β hydroxylase deficiency may also result in
' A: \5 R; Q, [' l; @8 J$ j: iexcessive adrenal androgen production, and rarely,
+ E& m# Y+ p# p/ S& w7 n3 F" jan adrenal tumor may also cause adrenal androgen
1 r  y2 f3 X/ G, a3 L! ^5 `( X1 @excess.1,3$ o, m& h8 Q) Y! A$ W( a: q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
5 g8 w; v2 N$ B+ }( R$ U6 B542 Clinical Pediatrics / Vol. 46, No. 6, July 2007) z1 i2 Y. R9 i+ o2 X- V2 u& u
A unique entity of male-limited gonadotropin-
+ F* L: |% r  bindependent precocious puberty, which is also known
9 h! [/ b1 f: [7 Ias testotoxicosis, may cause precocious puberty at a
" i; T' G- @$ dvery young age. The physical findings in these boys
1 ]& R, u" j! C9 y$ rwith this disorder are full pubertal development,$ H/ c/ C! o) {5 q8 z$ j! }3 ?7 s
including bilateral testicular growth, similar to boys
' A, y7 [, ?/ c- q8 q) H2 Iwith CPP. The gonadotropin levels in this disorder: c$ E5 P1 N4 o( f5 v! m
are suppressed to prepubertal levels and do not show
& Y  B9 F- _/ p0 upubertal response of gonadotropin after gonadotropin-/ }9 e" s7 c- {  _! a6 P
releasing hormone stimulation. This is a sex-linked& F% E0 \6 K3 o/ I
autosomal dominant disorder that affects only3 G: {6 H! {0 P  D1 g$ u8 r
males; therefore, other male members of the family
8 p1 y( S; j  D: k1 F9 W, c- M% Pmay have similar precocious puberty.3* H# a5 O# R- A6 ~
In our patient, physical examination was incon-
% _3 c8 L4 G/ {; O: s- A+ Fsistent with true precocious puberty since his testi-2 B: T: _- u; `- a
cles were prepubertal in size. However, testotoxicosis: @- b& e5 `7 P' f
was in the differential diagnosis because his father
8 B4 B5 D: o4 ], e1 Dstarted puberty somewhat early, and occasionally,: T+ |% E) Q- G5 y9 d7 A
testicular enlargement is not that evident in the
, {3 \! Z; i% X& p& tbeginning of this process.1 In the absence of a neg-: E& V9 o8 Z" h# {
ative initial history of androgen exposure, our
5 r! i( ?# ]  Z9 P6 X+ U4 Rbiggest concern was virilizing adrenal hyperplasia,
/ V9 ?$ c8 U- j$ _- \either 21-hydroxylase deficiency or 11-β hydroxylase
4 n+ u% y. ]) v0 z6 k! Pdeficiency. Those diagnoses were excluded by find-
% S& ~2 U6 X5 d3 A8 L+ oing the normal level of adrenal steroids.
5 y+ z% b: U$ ]: _The diagnosis of exogenous androgens was strongly! B( L* {, w+ J1 b, ^
suspected in a follow-up visit after 4 months because9 M/ d/ R; H/ c  N3 `" o7 l
the physical examination revealed the complete disap-) L: h. U- V6 W, m% F9 z
pearance of pubic hair, normal growth velocity, and! k! {- E# _6 Y
decreased erections. The father admitted using a testos-
' w  t5 Q4 e; k7 J- M, z' d; |6 Oterone gel, which he concealed at first visit. He was, P! l5 U' _7 D. I3 A
using it rather frequently, twice a day. The Physicians’
5 d+ Z( J! W8 t/ T# ?Desk Reference, or package insert of this product, gel or
9 W! `+ j. G" }cream, cautions about dermal testosterone transfer to: H0 e2 U6 N, {$ ]6 S% n
unprotected females through direct skin exposure.$ u* R: v' h1 U- e/ H. N
Serum testosterone level was found to be 2 times the
' S, z1 B  b- `baseline value in those females who were exposed to, O- G; J5 r1 v6 }( w8 I
even 15 minutes of direct skin contact with their male
/ z9 C( @1 Z" I8 t$ Vpartners.6 However, when a shirt covered the applica-
4 G' q# o( O4 L$ {/ W" L6 Ktion site, this testosterone transfer was prevented.1 A$ }# O/ ]. I) n6 ^  A
Our patient’s testosterone level was 60 ng/mL,9 l% z( W, ^2 ]% g- m3 p
which was clearly high. Some studies suggest that# ]- J& T' J7 ^
dermal conversion of testosterone to dihydrotestos-/ I+ `6 Z5 ?4 ?/ y8 }: U: v3 u8 Y
terone, which is a more potent metabolite, is more4 d+ z) _% e% }" m  {7 }# I
active in young children exposed to testosterone( s; N2 q2 K/ D7 D
exogenously7; however, we did not measure a dihy-7 p% s) z: W) ^, @( B, e+ ]; ~+ j- I
drotestosterone level in our patient. In addition to2 R$ @1 B, V4 @) E
virilization, exposure to exogenous testosterone in7 ]' [" d; ]& m/ b# q3 i
children results in an increase in growth velocity and+ H! X6 z3 d0 k& m, O4 M3 q
advanced bone age, as seen in our patient.' d4 Q$ A$ j$ A' d& H- J! Q
The long-term effect of androgen exposure during
8 v3 @, ~1 X3 L5 B: G( {: _' V4 zearly childhood on pubertal development and final
: V; v: ]' d" m# v2 Vadult height are not fully known and always remain
6 b* i* O' K' k* [7 g$ @a concern. Children treated with short-term testos-: Z0 M. u9 U4 b3 t0 @
terone injection or topical androgen may exhibit some7 P% B4 f8 W/ b8 q
acceleration of the skeletal maturation; however, after
; W, ?+ A3 E7 ecessation of treatment, the rate of bone maturation, D3 v* n7 \7 l; t5 l* a3 {
decelerates and gradually returns to normal.8,9
8 k- `+ E" d% ^+ s! O, SThere are conflicting reports and controversy8 S  t3 i' ]$ d9 N: j9 l2 d
over the effect of early androgen exposure on adult
- v& j, G( v2 n: C( H/ w) Q0 Bpenile length.10,11 Some reports suggest subnormal/ U3 n2 W3 y: Z9 S+ `1 J) `" X3 d  p5 s
adult penile length, apparently because of downreg-; f2 ^" v) U$ M; G: C  M8 p
ulation of androgen receptor number.10,12 However,; O( y, s. p1 t0 E3 H# O" z$ `
Sutherland et al13 did not find a correlation between
: ~) h1 j- M/ Q4 ]5 lchildhood testosterone exposure and reduced adult
( l& Q+ R) V+ Spenile length in clinical studies.
7 v( T/ S- D8 b7 n  CNonetheless, we do not believe our patient is
" y, l  q) m- x6 [( {going to experience any of the untoward effects from
. x  V0 |: C1 o/ Ctestosterone exposure as mentioned earlier because3 f- L* G" m5 y% u' K* {
the exposure was not for a prolonged period of time.# U. \8 I' \( x3 n( @
Although the bone age was advanced at the time of  f, `1 F/ @* H, w
diagnosis, the child had a normal growth velocity at$ O9 ]0 W9 ~9 H& K9 m
the follow-up visit. It is hoped that his final adult
3 M) V6 u1 Z0 r+ a% ^, n, x# Y) rheight will not be affected.
  P0 k" ~" u' M/ |' i+ X) p: \Although rarely reported, the widespread avail-
! V! B6 S/ I: hability of androgen products in our society may
, P8 g8 {! F9 ?. J7 ^9 Windeed cause more virilization in male or female
! y/ R8 U+ d! n3 `8 _' fchildren than one would realize. Exposure to andro-8 t% g4 R$ S$ C" K8 v
gen products must be considered and specific ques-1 Z2 _1 e3 |. o- d2 @% |
tioning about the use of a testosterone product or
5 f) b4 |' i3 U+ m9 jgel should be asked of the family members during
4 ]3 T$ n/ c& W' \2 N" l4 X* zthe evaluation of any children who present with vir-# ?" `0 {7 [) l9 ^3 G* k5 A9 d0 T
ilization or peripheral precocious puberty. The diag-
+ g7 i9 H/ Q2 R$ ?0 j6 lnosis can be established by just a few tests and by
7 H2 ~1 V* D. \! z" w% Rappropriate history. The inability to obtain such a
5 m4 Q# S0 Z3 h. z) Z- Xhistory, or failure to ask the specific questions, may2 T9 b4 b: B; |7 B0 X" k
result in extensive, unnecessary, and expensive
8 U5 E6 ?! r1 L, L  r) j' q, Yinvestigation. The primary care physician should be
/ V. l- W. X. Qaware of this fact, because most of these children
! M# R* N1 h+ ~* i, S- ^may initially present in their practice. The Physicians’
$ F& \# [* J. k1 a1 x6 _6 MDesk Reference and package insert should also put a+ E; x. v3 g; B6 Z7 h
warning about the virilizing effect on a male or9 r8 L) O+ q8 U: c7 ^, o
female child who might come in contact with some-
% A& \/ w7 p: a' Rone using any of these products.4 A# S" i# I$ s/ h: F! t: {- q
References; W9 W; P. G5 o9 t
1. Styne DM. The testes: disorder of sexual differentiation0 h4 i4 M( H3 V" _, T/ {
and puberty in the male. In: Sperling MA, ed. Pediatric
+ I, @. y* l. z" N* ?7 sEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
+ T: L6 L! O# A6 V( ]) D2002: 565-628.
- Q; ~' ^' Y$ Q8 ~2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious% J8 l$ r6 C6 N% h' W- {) k
puberty in children with tumours of the suprasellar pineal
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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
1 Y0 Y9 ^! l: g4 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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