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Sexual Precocity in a 16-Month-Old" a% {" G* @' [7 p  g% e
Boy Induced by Indirect Topical
$ ]5 n! f) ]9 ]! J- dExposure to Testosterone
$ }) y# a+ B6 R4 LSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2  M( D. ~1 M  A6 a: v  A
and Kenneth R. Rettig, MD12 P( y$ a5 t+ F  ~* P8 x
Clinical Pediatrics! `: r5 t5 T9 `. w' @) \% m
Volume 46 Number 6
* w/ J4 _% Q* h, O0 d6 x" mJuly 2007 540-543
/ z3 Q2 z5 Q5 ]# S. P© 2007 Sage Publications- G" i, [$ r2 f# w+ K, h1 S
10.1177/0009922806296651
" v% b0 E% X$ J- |  Dhttp://clp.sagepub.com
% J; o/ W$ @3 N# I; t4 z$ S# Ehosted at' T. ]. y' a/ B
http://online.sagepub.com; ]% @& e8 d6 z4 I" b: C$ Y
Precocious puberty in boys, central or peripheral,
' n  w/ m: a' ~$ i% ^( Wis a significant concern for physicians. Central
5 g/ y* o" Y5 x# Kprecocious puberty (CPP), which is mediated7 ~- o: X9 A( N% n
through the hypothalamic pituitary gonadal axis, has
  ]* u/ E' D+ I% b3 V$ [+ g; k7 aa higher incidence of organic central nervous system8 j% b; t3 p; r$ N8 [
lesions in boys.1,2 Virilization in boys, as manifested
! Q: P( x$ _; h/ m! sby enlargement of the penis, development of pubic
' Q# W% h+ I) L, R+ |3 jhair, and facial acne without enlargement of testi-
8 g3 l4 h6 m8 t" b- h' L; ^- {) ^cles, suggests peripheral or pseudopuberty.1-3 We% A  `) N+ Q- x# X' r; I
report a 16-month-old boy who presented with the
' [) p4 f$ X0 W7 E  Fenlargement of the phallus and pubic hair develop-
( j  x3 H  B" R: tment without testicular enlargement, which was due
& Y$ }+ a0 d" ~9 jto the unintentional exposure to androgen gel used by5 J  |9 |6 F1 f0 t3 i  ?( E. H
the father. The family initially concealed this infor-7 ^5 j- o* X+ p& H4 D
mation, resulting in an extensive work-up for this5 i, C" B5 E# q% [5 S6 h, P  {
child. Given the widespread and easy availability of
$ T/ w9 ?% m7 g! g+ z* gtestosterone gel and cream, we believe this is proba-2 Z7 L% J4 u2 q9 e4 C
bly more common than the rare case report in the5 v- z  U/ I/ A0 E. O8 W8 |3 ?
literature.4" L8 V% [4 Z. J; |( `/ W0 {' s. [+ a
Patient Report
4 ~) w0 B& c7 t1 g8 ?: GA 16-month-old white child was referred to the
  M: A, R# R" q1 W# D$ Yendocrine clinic by his pediatrician with the concern( h0 O) x0 a3 z3 y" m% Q# f! n+ B: P
of early sexual development. His mother noticed
  B$ G9 W8 N; U! ]8 e3 _light colored pubic hair development when he was
1 J7 i3 j: a- ]- H7 }$ I/ q" ]/ nFrom the 1Division of Pediatric Endocrinology, 2University of
1 b! w8 |' p2 m/ L# j+ U* i, p' OSouth Alabama Medical Center, Mobile, Alabama.$ ]: Q8 N# S8 O  M3 b
Address correspondence to: Samar K. Bhowmick, MD, FACE,
6 ?8 }7 q: ?! Z7 U% A% y  [7 hProfessor of Pediatrics, University of South Alabama, College of5 L2 z( i$ c' U! Y' M' i1 _
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
0 A* O+ ~: `1 k+ x( J' Ce-mail: [email protected].6 D$ i+ z5 @! H  `5 {( R
about 6 to 7 months old, which progressively became+ ^0 t0 Q+ o- C) D7 x" c
darker. She was also concerned about the enlarge-) M5 h1 {! G' l" N: H: A, L
ment of his penis and frequent erections. The child
3 \( ~% h3 @0 B; a+ L2 ?& J3 lwas the product of a full-term normal delivery, with
- [" P9 q( `# I3 P% q. `) n* H7 p. m* {a birth weight of 7 lb 14 oz, and birth length of
! z* `2 D! j8 @& H1 W. H20 inches. He was breast-fed throughout the first year
, M1 _9 B) K6 v1 \; R& oof life and was still receiving breast milk along with/ \0 I/ ]. J% Q+ N! I7 g) x' B
solid food. He had no hospitalizations or surgery,* O: x1 L( A9 p- S, h
and his psychosocial and psychomotor development) `8 T8 N7 O5 ~: i% ^0 X. _0 ^3 y
was age appropriate.
" ]8 p$ l' L6 F. ?( K6 DThe family history was remarkable for the father,- F( ?2 V; P8 A) G( q8 e8 @; |6 f
who was diagnosed with hypothyroidism at age 16,# j: l" z; K# b+ i5 U$ d2 u
which was treated with thyroxine. The father’s; y: h8 n/ |) N: f" r
height was 6 feet, and he went through a somewhat- f& i; G* L7 `" ]% P. ^+ y
early puberty and had stopped growing by age 14.4 H& k3 ?# Y# m7 r
The father denied taking any other medication. The
) c) z1 m$ F3 W* v5 v- @child’s mother was in good health. Her menarche
. M" u! [" T: [* u/ Twas at 11 years of age, and her height was at 5 feet& w) {, Z; M2 J* e' I8 d! Q5 C  Y
5 inches. There was no other family history of pre-
- e1 r3 q/ r- \8 Y  P/ d, l8 k8 V! Qcocious sexual development in the first-degree rela-
. y; |% O, ]- O: ~. U) X; Ttives. There were no siblings.3 ^! j  U8 F  @8 p' J: ?$ p
Physical Examination
" D8 U2 w9 `& ?4 _3 n0 rThe physical examination revealed a very active,
' r  V9 c+ }9 |/ I0 Qplayful, and healthy boy. The vital signs documented; @2 B+ u  v, n% }: B
a blood pressure of 85/50 mm Hg, his length was
# a( j3 m* A& L2 G3 g; J90 cm (>97th percentile), and his weight was 14.4 kg5 H1 K. v  z( @' S& x5 i/ |
(also >97th percentile). The observed yearly growth+ E+ H: S" g  g! o$ L8 n/ P6 t
velocity was 30 cm (12 inches). The examination of! O* y) [- @0 L, B3 ?+ s
the neck revealed no thyroid enlargement.
; m9 V0 ~( Q1 P' q( {# y# |% ZThe genitourinary examination was remarkable for: p' y. {7 S5 N% u$ I0 O
enlargement of the penis, with a stretched length of) b( r& G6 d3 [, Y
8 cm and a width of 2 cm. The glans penis was very well5 p  M' O! _5 G" j* M- t
developed. The pubic hair was Tanner II, mostly around
3 r7 ^2 j% `. v% Z2 Z0 x1 E540
' q, c& o( O' |3 eat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
8 a3 P) A( Y5 U8 ^. w2 athe base of the phallus and was dark and curled. The( s, H5 n9 V8 G# y$ q: X' u5 a
testicular volume was prepubertal at 2 mL each.
8 d- n/ F4 R; ~  f& k$ tThe skin was moist and smooth and somewhat* c( T* A/ }5 l4 L' v
oily. No axillary hair was noted. There were no
. H& R8 \" n0 K/ [abnormal skin pigmentations or café-au-lait spots., O* o2 s( [8 l2 s
Neurologic evaluation showed deep tendon reflex 2+
7 N' G8 @* C# x, T$ T; o+ z& @# Vbilateral and symmetrical. There was no suggestion; r/ {5 C( N( V, E# \# v2 @9 V( A$ L
of papilledema.2 l8 k" c% }; C: L: d
Laboratory Evaluation; U# a& q3 _! A, O. j  {! c3 a
The bone age was consistent with 28 months by# n. T/ R0 O$ ^) }8 J
using the standard of Greulich and Pyle at a chrono-
7 p1 O% q/ w) n) plogic age of 16 months (advanced).5 Chromosomal, x3 m  ?" n! s# `: y
karyotype was 46XY. The thyroid function test
. S/ ^. n( d) \9 Oshowed a free T4 of 1.69 ng/dL, and thyroid stimu-7 _$ v7 X+ v5 J/ @" ~
lating hormone level was 1.3 µIU/mL (both normal).
# |' _7 M- n. B4 W, |The concentrations of serum electrolytes, blood5 F. o! T) W. u2 ~/ @8 v! N
urea nitrogen, creatinine, and calcium all were6 \' {% v, E& k8 N
within normal range for his age. The concentration- D$ q8 H) _/ p
of serum 17-hydroxyprogesterone was 16 ng/dL
7 f$ J/ P. n& y' E(normal, 3 to 90 ng/dL), androstenedione was 20/ b8 x) k' i) ^+ U
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ ^& L/ x$ p- c2 p$ j3 t. d1 d
terone was 38 ng/dL (normal, 50 to 760 ng/dL),' [" d/ n  `. w$ O: d# g
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
% j5 [5 }% X; R. e& Z3 s. b49ng/dL), 11-desoxycortisol (specific compound S)7 l7 X, i  U8 ~9 G7 n% z/ q
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-9 m8 k* n. t& o8 t: w& `+ w, s
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
7 q: _4 ?" i* [/ [' @0 Ktestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
$ O/ z6 @/ r9 Y% f# q: Gand β-human chorionic gonadotropin was less than
) W& ?1 e7 p: Q# S% O8 V, E5 mIU/mL (normal <5 mIU/mL). Serum follicular
0 `) ^+ z3 A. M8 }  M/ {# zstimulating hormone and leuteinizing hormone
9 I9 j/ X" U7 `6 e; oconcentrations were less than 0.05 mIU/mL6 t) u; {$ C- O% F6 o# l$ p
(prepubertal).
3 I% g) u4 c, X6 \# u/ u! IThe parents were notified about the laboratory) j" {6 K  i+ ^. }5 {6 k2 ~, R/ C
results and were informed that all of the tests were( G" W4 F2 v6 X; d4 u9 K
normal except the testosterone level was high. The
/ c% K# S4 ~" g" Q* ?) kfollow-up visit was arranged within a few weeks to
7 N- a: t1 R' O0 y6 x" l- ]obtain testicular and abdominal sonograms; how-# j4 b9 y  X; X& C5 N3 P
ever, the family did not return for 4 months.
, z' H! U% S5 ~* Z9 CPhysical examination at this time revealed that the
- C- G  K2 L. X5 P- ychild had grown 2.5 cm in 4 months and had gained+ V* r) H! t2 T+ `1 |
2 kg of weight. Physical examination remained0 l) f+ o* X" h7 x& b2 L/ D
unchanged. Surprisingly, the pubic hair almost com-
# V9 n: `' \: x% X/ mpletely disappeared except for a few vellous hairs at
7 \6 R5 |% ^3 V# O/ A4 }0 d( V" N( r6 Dthe base of the phallus. Testicular volume was still 2& j! V, o5 L' I6 C) D& l
mL, and the size of the penis remained unchanged.% z& m4 }. q4 Y/ P- @5 B
The mother also said that the boy was no longer hav-8 y! o6 e7 f$ f+ h6 }! ^8 a
ing frequent erections.
0 e# V: b7 N. z/ |Both parents were again questioned about use of5 n# K; Q7 y+ @1 ^9 |) R7 [
any ointment/creams that they may have applied to
! p' z! ]1 g, Tthe child’s skin. This time the father admitted the
6 ?) l7 m- c1 L2 L% G/ S5 ~5 I: ^Topical Testosterone Exposure / Bhowmick et al 541
( z. u9 \. k# C  U0 a! B8 muse of testosterone gel twice daily that he was apply-) `' q! ], }2 g: |/ D+ D
ing over his own shoulders, chest, and back area for
5 O; q9 r$ |: L6 H, \# ja year. The father also revealed he was embarrassed
7 c9 o5 O$ X! y; M+ _% u$ dto disclose that he was using a testosterone gel pre-
& {4 X1 b3 q  Bscribed by his family physician for decreased libido
: E/ ]/ n1 ?* S& K" }" Z' Bsecondary to depression.) G6 Z0 v' C& Y+ E" G
The child slept in the same bed with parents.' y, ~$ h# g  \8 Y
The father would hug the baby and hold him on his
6 z) J4 J0 p0 H5 hchest for a considerable period of time, causing sig-/ o5 f3 D2 r0 `& x: u
nificant bare skin contact between baby and father.
( A& H% o9 z2 D) w( iThe father also admitted that after the phone call,1 D" G+ t/ w1 ]+ t, s2 t5 _
when he learned the testosterone level in the baby5 N9 A# K# b$ H% H2 i
was high, he then read the product information
2 T* T$ h! F. v, m3 s2 Qpacket and concluded that it was most likely the rea-4 d, m7 W+ C, E/ h! i! Z+ ^
son for the child’s virilization. At that time, they
" a4 m  H9 K* d; P& B$ L0 G$ odecided to put the baby in a separate bed, and the
) r/ B: w, L2 t( U. tfather was not hugging him with bare skin and had
% E- \% k& g4 E" e* o3 w! c) [been using protective clothing. A repeat testosterone1 B" W4 h% M7 s3 e1 K
test was ordered, but the family did not go to the
$ A) I' n4 o" ~5 D: zlaboratory to obtain the test.! @9 H8 G6 F/ v! D7 E5 T
Discussion3 [4 S* J7 e  I8 g0 D' D
Precocious puberty in boys is defined as secondary
% D$ z9 x/ Y- j6 Isexual development before 9 years of age.1,4
% C! B4 [" D% X3 d: {* ?6 hPrecocious puberty is termed as central (true) when
9 n' ^! p$ I% Z# v( K  S; t( Zit is caused by the premature activation of hypo-
5 ^3 S4 K  z% K/ Z$ |5 H5 Z/ hthalamic pituitary gonadal axis. CPP is more com-' U$ u0 Z: H6 T9 T  i+ x% g" _( o
mon in girls than in boys.1,3 Most boys with CPP
- J  n/ \4 n% J" x8 n& V9 q5 F6 M# T5 Mmay have a central nervous system lesion that is
1 S5 \7 C4 i8 ]1 @7 y/ k1 qresponsible for the early activation of the hypothal-0 y. D* `6 Y* T  s& h8 m' m5 m5 A
amic pituitary gonadal axis.1-3 Thus, greater empha-% v" [3 K- w  r0 i* O
sis has been given to neuroradiologic imaging in$ f; V7 ]# T0 _2 X# s2 {
boys with precocious puberty. In addition to viril-
2 B  A3 L( Z8 F! m8 \% ~# V: Pization, the clinical hallmark of CPP is the symmet-
$ Y, w( z8 {8 o! Erical testicular growth secondary to stimulation by
! h3 c; t  _# W% ugonadotropins.1,3" s% B2 w) I* [2 E) k3 G
Gonadotropin-independent peripheral preco-
, b/ N5 r3 K' s2 a- Pcious puberty in boys also results from inappropriate% N) h* B% ]; _4 a+ E
androgenic stimulation from either endogenous or
; i) v$ U# K$ j" Z4 Aexogenous sources, nonpituitary gonadotropin stim-( q9 C$ h/ D1 Q- _1 S3 n
ulation, and rare activating mutations.3 Virilizing8 f' l2 h' \0 W( ?/ d
congenital adrenal hyperplasia producing excessive8 m3 ]  D$ J  u* z3 j; X2 I
adrenal androgens is a common cause of precocious; L9 z: R+ `* X4 [, F2 w, f) V0 }
puberty in boys.3,4
% ?8 i. L3 @! M: e% [+ OThe most common form of congenital adrenal# d  N; `/ E+ T0 L1 f
hyperplasia is the 21-hydroxylase enzyme deficiency.. v3 t0 r9 W5 _( W: r
The 11-β hydroxylase deficiency may also result in
$ z8 m- A- |2 c9 y" ]- aexcessive adrenal androgen production, and rarely,0 v- E; }% }4 j# j) j+ Q
an adrenal tumor may also cause adrenal androgen6 U$ q, \7 T/ F
excess.1,3
) ~4 g! R9 d3 I& b3 `at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
, j6 m4 K3 c, f' ^542 Clinical Pediatrics / Vol. 46, No. 6, July 20078 K2 I8 P0 m7 g8 H
A unique entity of male-limited gonadotropin-4 J1 ?9 w1 c% @
independent precocious puberty, which is also known
) B7 o) S6 G: J6 k, A6 Tas testotoxicosis, may cause precocious puberty at a" l2 V* b. f5 t2 \& a: h: E
very young age. The physical findings in these boys- g8 x3 i/ z) P' ^+ |2 a* k
with this disorder are full pubertal development,. w. Z  d7 x2 o! w% \2 [
including bilateral testicular growth, similar to boys
: X" d8 s( }* U: ywith CPP. The gonadotropin levels in this disorder
5 R3 y4 T7 M4 L7 D$ s* Pare suppressed to prepubertal levels and do not show  v( y& c+ y' ?8 w+ x0 S7 q4 B
pubertal response of gonadotropin after gonadotropin-
4 ^/ g7 \3 S/ Areleasing hormone stimulation. This is a sex-linked0 ~9 ~* j! w$ K$ J2 D  O+ D* a% v
autosomal dominant disorder that affects only
1 f, M7 z# ?7 q" i8 C; F- Gmales; therefore, other male members of the family5 [6 Y5 `: s6 ~# L# S; T
may have similar precocious puberty.3
9 U& Y% t" z  ?- TIn our patient, physical examination was incon-- @' d7 x+ ]$ v9 w' e7 @. Y$ i' ]
sistent with true precocious puberty since his testi-1 m+ K" s- Q1 u% W$ [
cles were prepubertal in size. However, testotoxicosis) j+ c! d# _! g1 s
was in the differential diagnosis because his father, f  w" v" ]; ]
started puberty somewhat early, and occasionally,
/ _: V! ]4 x% S, i: C  gtesticular enlargement is not that evident in the
( _- n. K! b+ t% Q) Tbeginning of this process.1 In the absence of a neg-
# F( u! A( i) r6 ?. }# j' Tative initial history of androgen exposure, our
* r- j; T! y+ _0 r! c/ l- S! s7 Xbiggest concern was virilizing adrenal hyperplasia,) k- A, m8 X. C1 j
either 21-hydroxylase deficiency or 11-β hydroxylase: \1 K+ J; F" G' ?% }
deficiency. Those diagnoses were excluded by find-
3 o0 b( g+ R8 R2 Uing the normal level of adrenal steroids.
+ n, B" ^) G$ w% `The diagnosis of exogenous androgens was strongly7 m! t" J2 D* \( ]8 n
suspected in a follow-up visit after 4 months because' R1 L8 E5 V+ m1 g/ ^5 Y
the physical examination revealed the complete disap-  q" P9 w/ H3 D# m: s1 o
pearance of pubic hair, normal growth velocity, and- t9 m+ u* E4 c0 ~& n
decreased erections. The father admitted using a testos-
+ V2 b1 o4 V& p2 vterone gel, which he concealed at first visit. He was
' T  @1 f5 a0 s; ]+ f. `1 Yusing it rather frequently, twice a day. The Physicians’
# K) c9 P/ V3 ^5 B* ^Desk Reference, or package insert of this product, gel or! E- ]) g3 B. ~) M: B
cream, cautions about dermal testosterone transfer to
+ U$ U6 \( z' T; yunprotected females through direct skin exposure.
: L: j! Q$ i( R! f8 uSerum testosterone level was found to be 2 times the3 D# l$ `! Z) W; _% o/ _# {
baseline value in those females who were exposed to: _  @) ?/ d* U+ y: u! N
even 15 minutes of direct skin contact with their male
1 e) p; ~' I3 R. D& Gpartners.6 However, when a shirt covered the applica-
$ W1 G, O- U4 Ztion site, this testosterone transfer was prevented.' j) A& c: a+ T* i  `
Our patient’s testosterone level was 60 ng/mL,% e+ s7 d! J5 A; t, A& Y- _
which was clearly high. Some studies suggest that
" z9 n2 R8 j' q5 odermal conversion of testosterone to dihydrotestos-8 r2 D! Q" O2 u' d, n+ I; d% \- _
terone, which is a more potent metabolite, is more
3 S; J" z( i* zactive in young children exposed to testosterone
$ a6 X5 k( ~* U2 H' Bexogenously7; however, we did not measure a dihy-9 d& M& X3 d) P% h6 c0 F, ?9 G( R
drotestosterone level in our patient. In addition to: G1 |1 X$ D* Y7 N
virilization, exposure to exogenous testosterone in
( q. z  W- d$ H, B3 Echildren results in an increase in growth velocity and
1 j; ?) ^, r% T, B% \0 d6 |advanced bone age, as seen in our patient.
4 m+ v( f9 y5 h3 r# `2 ?The long-term effect of androgen exposure during
& s3 ]1 v; @$ u( |* uearly childhood on pubertal development and final
) y. u9 c/ e" s2 e9 M0 s7 T- e! radult height are not fully known and always remain
8 O# h. ]1 `: t( m" ?9 F1 H; }a concern. Children treated with short-term testos-
1 Q0 a* U1 Q5 R0 N* V8 Qterone injection or topical androgen may exhibit some
8 A3 U  H, s" Macceleration of the skeletal maturation; however, after; S4 K1 I) j% X& l- j  ]
cessation of treatment, the rate of bone maturation
8 p2 P+ ?& M2 }! N# \decelerates and gradually returns to normal.8,9
+ ~: T( v7 d7 X1 ~- Q8 cThere are conflicting reports and controversy1 ?; R, e, U0 c: m
over the effect of early androgen exposure on adult
7 A/ X- @0 Y2 n2 u& T6 K0 spenile length.10,11 Some reports suggest subnormal
+ N3 i  m7 k2 ]( Q" ]$ U7 |. Fadult penile length, apparently because of downreg-
2 Q5 ?, s5 l: [3 t& }9 V3 M) e2 {+ ?ulation of androgen receptor number.10,12 However,
' k) f1 o& s5 i& m7 RSutherland et al13 did not find a correlation between3 u! E# o2 r" f% p0 \( ^
childhood testosterone exposure and reduced adult
- {  f: Q+ D! o. c% v& r% Epenile length in clinical studies.8 Y- U7 r# n% b
Nonetheless, we do not believe our patient is. M8 O; F* F+ D% P
going to experience any of the untoward effects from" }& }2 s9 T) \; b5 K" j$ W
testosterone exposure as mentioned earlier because
" {/ N% {: a) }- [9 f; ~9 \the exposure was not for a prolonged period of time.8 \& F) x' k4 J8 S- w: T) `
Although the bone age was advanced at the time of& G0 q1 M1 x8 ^& h0 n  |1 V1 D
diagnosis, the child had a normal growth velocity at
3 A$ p% t$ M6 H2 N# ythe follow-up visit. It is hoped that his final adult
) m$ b1 d+ a1 t  A( c2 h5 E" lheight will not be affected.
3 Q- f7 b9 T  x: c8 ]Although rarely reported, the widespread avail-* t" P. J. R7 p+ N
ability of androgen products in our society may* @( V' S! G  K: M+ @" Q/ A
indeed cause more virilization in male or female. O+ p, U, w1 w& C; p# ]
children than one would realize. Exposure to andro-
( p! G4 E. J6 u( @gen products must be considered and specific ques-
/ d2 ?, u" P' V: f9 [! ytioning about the use of a testosterone product or
3 j" ^: ]8 q; ?5 b% Z# D: p) bgel should be asked of the family members during
; x" S+ W; T5 N0 s3 \+ G; f% C- ?the evaluation of any children who present with vir-
7 N* J0 |# G5 U% gilization or peripheral precocious puberty. The diag-
$ L$ P. P$ `6 k# inosis can be established by just a few tests and by
+ t2 \0 @2 s- e3 P  aappropriate history. The inability to obtain such a
* i  y1 z: p" _8 O$ D0 U6 ~: e: _history, or failure to ask the specific questions, may3 y8 G$ k5 G& `* P9 q
result in extensive, unnecessary, and expensive
+ d; k$ \- ^1 j  W3 d  _; Uinvestigation. The primary care physician should be8 |7 v) c* Y$ @0 K
aware of this fact, because most of these children
. b" Z+ F' R4 a7 k! l2 Zmay initially present in their practice. The Physicians’
3 s' o. e* Q+ N& y1 jDesk Reference and package insert should also put a3 Q) P! \% C1 ?9 [* e
warning about the virilizing effect on a male or
) w3 P# U3 Q0 H1 [female child who might come in contact with some-' P( M; f. F9 v' Z7 r. m, ]. g4 |8 j
one using any of these products.
5 m: x6 P/ a6 L# NReferences! L% H8 Y! b1 v/ a, A$ Z
1. Styne DM. The testes: disorder of sexual differentiation
7 ~0 B* o/ I- zand puberty in the male. In: Sperling MA, ed. Pediatric7 V+ g  |2 C, Q/ C4 j% C7 D
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;7 ?3 q7 I$ a! c! Y0 ?. g
2002: 565-628.* G3 f$ U& I+ ?5 G5 S# a2 e
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious. V( F' K7 c. F* y
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old( \- [6 Z4 _0 Y# H' m& }; o+ W
Boy Induced by Indirect Topical
& V  Y: K& @3 M- \# R# P$ x8 S7 jExposure to Testosterone
# K/ ]9 v* I! n  L, w9 ?$ z: n7 QSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
, F4 J0 s: v6 v( n7 E' `and Kenneth R. Rettig, MD1
6 l) e: ]9 @7 ]+ J* z! DClinical Pediatrics) x' W# _0 Q/ j2 r' T. f
Volume 46 Number 6
% ^, u# q( |0 t1 R" [: @1 _July 2007 540-543+ q% {' Z8 E( l* l' W
© 2007 Sage Publications/ ~) R# p/ M" H
10.1177/0009922806296651
/ R0 @. |2 b0 N1 h  A+ Khttp://clp.sagepub.com
- r! f5 }' W9 C; f% _hosted at
5 V8 i/ N& ^% u  dhttp://online.sagepub.com
* `* z  ]9 o- ~- J5 x( v; _2 JPrecocious puberty in boys, central or peripheral,) h  A5 x! C- D6 Z  A3 V$ h
is a significant concern for physicians. Central! R5 _/ t6 P" s+ S( E# r
precocious puberty (CPP), which is mediated
* m+ f' m( J% [through the hypothalamic pituitary gonadal axis, has
1 P6 V: Q5 v, a" Ga higher incidence of organic central nervous system: }" o. U5 b3 G# h: I
lesions in boys.1,2 Virilization in boys, as manifested+ z/ ?1 u* z1 W( t* b7 ]: w; g$ J
by enlargement of the penis, development of pubic
& L& s7 ^- G( S3 C/ E* lhair, and facial acne without enlargement of testi-
* `5 u" N" P5 _' fcles, suggests peripheral or pseudopuberty.1-3 We
- x, ?3 k; X, [1 l+ _2 freport a 16-month-old boy who presented with the6 R" O- {7 t4 ~* @
enlargement of the phallus and pubic hair develop-/ {; W# e- Z' z! o( T
ment without testicular enlargement, which was due
7 P+ L4 j4 V: Q/ p. Y9 Jto the unintentional exposure to androgen gel used by; c4 ~: n# W9 O+ \8 ^
the father. The family initially concealed this infor-
" s0 f- U2 _- X6 t7 f4 hmation, resulting in an extensive work-up for this' |6 s9 x4 n$ m; t  S& `( g
child. Given the widespread and easy availability of
. ?0 x- {5 q) @testosterone gel and cream, we believe this is proba-0 X$ Z0 z5 Z; X  Q! f& j. ]; L; y
bly more common than the rare case report in the
4 o4 k  v, E. `' _, Kliterature.4
; f# }, @7 ?- ?% DPatient Report+ D3 v0 R7 s& Q6 N, G3 Y- h# K
A 16-month-old white child was referred to the
! R( j/ h# @+ e  l% a9 _$ q2 z3 Fendocrine clinic by his pediatrician with the concern
+ V$ x" L& i' H8 x; k! F4 Qof early sexual development. His mother noticed+ K! ]8 m; {9 H" l; l
light colored pubic hair development when he was" v! K7 |9 u9 ?8 ^
From the 1Division of Pediatric Endocrinology, 2University of5 n8 F' |) d+ @( `* A$ r
South Alabama Medical Center, Mobile, Alabama.
9 G: j* I7 Z4 fAddress correspondence to: Samar K. Bhowmick, MD, FACE,7 [# b* P: C# R- n
Professor of Pediatrics, University of South Alabama, College of
6 R( S+ V) b- z5 h/ h2 bMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;9 z* m3 v# k. V; N0 M1 t8 T% M
e-mail: [email protected]." K& E8 l8 a0 @+ w9 Y8 y
about 6 to 7 months old, which progressively became
% J9 T7 @; ?% P: Y& W* Jdarker. She was also concerned about the enlarge-
1 c3 i/ n9 c' W1 H3 C8 O( Mment of his penis and frequent erections. The child
1 \3 V8 C& G9 U, v5 k. s/ Vwas the product of a full-term normal delivery, with
+ ^/ L2 r6 _9 Q1 X! ?a birth weight of 7 lb 14 oz, and birth length of0 _; a. b4 n: O; m
20 inches. He was breast-fed throughout the first year
; X' G3 B( j5 Cof life and was still receiving breast milk along with' M& L5 v* y& p3 ~
solid food. He had no hospitalizations or surgery,! i  v$ Q# |+ y8 h
and his psychosocial and psychomotor development
. N5 ~- t* P- v: z  R7 e: Pwas age appropriate.
# F  g; \2 N2 P7 W9 T& NThe family history was remarkable for the father,
9 y) M& x0 t. G& U; B  p" k/ q& {. G) Owho was diagnosed with hypothyroidism at age 16,  D) T$ h/ M/ V" K2 E" P3 y. m: ]
which was treated with thyroxine. The father’s
, }/ k- D7 {7 C) |$ pheight was 6 feet, and he went through a somewhat
* m  W2 @3 c5 ^early puberty and had stopped growing by age 14.
( u6 m( R, F  R/ gThe father denied taking any other medication. The
/ V/ g5 t9 E: b! u3 Lchild’s mother was in good health. Her menarche: [- q) }$ j. u9 e
was at 11 years of age, and her height was at 5 feet- e9 P! k  J) @# D7 p! d1 Q* K
5 inches. There was no other family history of pre-2 H. s* e7 M6 H$ h. |* Q
cocious sexual development in the first-degree rela-4 r; l- G  u/ a
tives. There were no siblings.6 O3 m& D9 Z3 i: o
Physical Examination
3 l" G5 F3 u, C- z1 |The physical examination revealed a very active,5 m; R$ z2 E+ @: f0 t; J
playful, and healthy boy. The vital signs documented
* g: s0 ?# p, W' Q4 ba blood pressure of 85/50 mm Hg, his length was
7 d! D7 d1 t7 v+ r; F. D2 Z# |- @90 cm (>97th percentile), and his weight was 14.4 kg
& [. H6 n( _/ z  }2 F! h(also >97th percentile). The observed yearly growth
4 |0 k* w  M8 P+ m2 |$ Z* hvelocity was 30 cm (12 inches). The examination of
, S8 |% L) }, k4 R; t/ b9 D! Y. fthe neck revealed no thyroid enlargement.% `% k3 M8 L  b1 W1 x
The genitourinary examination was remarkable for
" _% U! X8 q2 z! L! {# p  G% Jenlargement of the penis, with a stretched length of3 ?/ l# E8 r! V* W
8 cm and a width of 2 cm. The glans penis was very well& j3 D0 h/ h4 S, C* e% ~1 x. i# h
developed. The pubic hair was Tanner II, mostly around* B6 n; l% R( f) k( m, {
540( j! {" g) A$ @$ P$ u3 R
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
  N: l+ y  q  V8 p" kthe base of the phallus and was dark and curled. The' v$ `# I6 t+ V
testicular volume was prepubertal at 2 mL each.
7 X& y* @  a9 Q; _The skin was moist and smooth and somewhat
1 M4 q* P5 H$ o2 E3 Zoily. No axillary hair was noted. There were no
) c7 p4 x( D' Y2 t1 qabnormal skin pigmentations or café-au-lait spots.
7 P4 C& y  @8 M' @* nNeurologic evaluation showed deep tendon reflex 2+
7 p, V3 X$ R9 X, ibilateral and symmetrical. There was no suggestion
# l( @! ?* r* J9 Z5 L/ d! nof papilledema.  x) p+ }" s% S: |4 i8 O' ?
Laboratory Evaluation. A$ w4 _) N/ r
The bone age was consistent with 28 months by
5 c; g7 D& z' h% B# f, d- n* w5 dusing the standard of Greulich and Pyle at a chrono-
6 ?% Z4 E2 X  W1 Slogic age of 16 months (advanced).5 Chromosomal
1 a6 l) A0 b; akaryotype was 46XY. The thyroid function test+ k  l9 H8 u6 C" X* [$ Q: U0 v
showed a free T4 of 1.69 ng/dL, and thyroid stimu-
4 l- |- ?5 ~; I/ _; Llating hormone level was 1.3 µIU/mL (both normal).  s( Y' X# R+ L/ n. s  U- w
The concentrations of serum electrolytes, blood) n' B" F' }% g' t/ n; P- X0 \
urea nitrogen, creatinine, and calcium all were7 U; `' M; {2 x5 @  `. `' C/ i2 V
within normal range for his age. The concentration5 ?6 o, ^, J' C+ u" Q2 Q
of serum 17-hydroxyprogesterone was 16 ng/dL* V! f  }8 r& O9 {" H# T
(normal, 3 to 90 ng/dL), androstenedione was 207 h: s5 F2 q. P5 Z
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ o, y6 w. R% e- I$ S9 T; |
terone was 38 ng/dL (normal, 50 to 760 ng/dL),- ^' t3 Z. V! ^) |
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
9 F# k* A# N! C, V1 l8 J' f49ng/dL), 11-desoxycortisol (specific compound S)5 N, n3 @8 p( Q! Z/ G0 ?
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
9 s" {* |/ y! R8 K9 y# Ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total: }  i& [1 o: B" i6 D8 Y- x
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),0 f0 |; `: n$ Q/ f' ~' c. s6 D
and β-human chorionic gonadotropin was less than" N, Z1 H- N! T' l
5 mIU/mL (normal <5 mIU/mL). Serum follicular/ \3 r. x2 n& k- }
stimulating hormone and leuteinizing hormone. H& A4 V8 A/ J/ j6 z
concentrations were less than 0.05 mIU/mL
+ f# U8 A% p: a1 }2 X) U(prepubertal).& ~- R' l, \# q' M: m3 J& [
The parents were notified about the laboratory( X  v5 C/ G3 j7 U+ a, N
results and were informed that all of the tests were
' F7 C. A  Y1 H/ g+ ]7 Jnormal except the testosterone level was high. The& t( G5 K; D" c1 O% ]1 U/ F
follow-up visit was arranged within a few weeks to
% k. o9 U6 {: b$ P# i7 e; aobtain testicular and abdominal sonograms; how-5 `$ _* O$ Z# }" M" w2 j$ [" V& T
ever, the family did not return for 4 months.7 x6 [7 D7 l- F0 C" e% E
Physical examination at this time revealed that the
; {" _. z2 {4 b  d8 ?( f6 Wchild had grown 2.5 cm in 4 months and had gained
4 D2 j5 d& b, V7 Q6 s% P7 g1 I; i2 kg of weight. Physical examination remained
; ~) y* u0 G" R  ]' qunchanged. Surprisingly, the pubic hair almost com-- @  s6 F6 J& ^2 M9 o  B; m1 A
pletely disappeared except for a few vellous hairs at) t; B: n8 g% l1 T- V2 l" j8 R* ?: ?
the base of the phallus. Testicular volume was still 29 }3 G4 O) D& g
mL, and the size of the penis remained unchanged./ L: C7 h6 b5 ~/ q. k' x1 g
The mother also said that the boy was no longer hav-
4 n7 z2 U" d  ying frequent erections.) _6 c& y8 c5 \8 C% \$ S
Both parents were again questioned about use of6 R" x( ~0 K: n' o  N* i! m
any ointment/creams that they may have applied to
3 e% N4 Z( [4 p, Kthe child’s skin. This time the father admitted the
5 {9 P3 Y+ ]2 ^0 F5 y1 LTopical Testosterone Exposure / Bhowmick et al 541
6 U: _# C2 ~; K1 r% I; j4 Huse of testosterone gel twice daily that he was apply-: y! G4 |& w8 k
ing over his own shoulders, chest, and back area for, ~7 S& i) e  Z" U- l
a year. The father also revealed he was embarrassed
3 U- M& M' U; H' ?. g% l6 e5 A0 Jto disclose that he was using a testosterone gel pre-$ C7 i" y; u3 u, i9 S; l, k
scribed by his family physician for decreased libido
6 w: K& v3 r' a3 s/ l9 usecondary to depression.
( h5 ?# ^* J$ A  e5 Y3 N9 BThe child slept in the same bed with parents.
( s1 ?) l( x$ {( mThe father would hug the baby and hold him on his
+ W. @4 [8 g; s8 P6 @- B- ochest for a considerable period of time, causing sig-
; `8 k8 Z* L  u' knificant bare skin contact between baby and father.6 j6 [- u# V3 }8 P( P% U
The father also admitted that after the phone call,
7 ?: o" L7 T7 A/ z# R! I( vwhen he learned the testosterone level in the baby
7 Z0 F) L3 M8 F* g. q* `9 uwas high, he then read the product information4 {( p4 E+ p- M3 G& y1 f
packet and concluded that it was most likely the rea-9 l& M4 y# t! F# E
son for the child’s virilization. At that time, they! |) u# n8 c! y3 A" U1 G
decided to put the baby in a separate bed, and the# `# E, @$ H' U0 |; i, r2 x
father was not hugging him with bare skin and had; Q4 A0 v  s  D' D$ ~" L& ?
been using protective clothing. A repeat testosterone
: t9 [( C1 Z  J! Z/ E6 utest was ordered, but the family did not go to the7 s! L- V, Q" H. |; |
laboratory to obtain the test.
# z6 U& E3 r# YDiscussion
0 _/ B4 F3 ]# w- a) B+ FPrecocious puberty in boys is defined as secondary
" U, b5 U& ^. \9 E1 i* ~. [sexual development before 9 years of age.1,4% |3 t6 K# ?+ s$ e7 Z# b
Precocious puberty is termed as central (true) when
' v  u6 h; N$ eit is caused by the premature activation of hypo-! ]# B: P1 ^' ]. W; V; r
thalamic pituitary gonadal axis. CPP is more com-5 ^5 R/ ?4 z3 ~6 H  G
mon in girls than in boys.1,3 Most boys with CPP$ ]# ^& X) g4 D
may have a central nervous system lesion that is
( w8 f. K5 _4 P( `1 i1 zresponsible for the early activation of the hypothal-8 y$ r5 I. C: g/ e4 s* [+ {: g: ]
amic pituitary gonadal axis.1-3 Thus, greater empha-( |" d7 X1 C: Y+ a6 |* u
sis has been given to neuroradiologic imaging in
6 X9 }0 o1 K3 z* nboys with precocious puberty. In addition to viril-
8 t8 J: @. e* M% n' d% L7 S8 Mization, the clinical hallmark of CPP is the symmet-
8 ^+ \  v: T3 Q+ G' Zrical testicular growth secondary to stimulation by
. j2 V  m' }9 t' h* O1 Fgonadotropins.1,37 _& {2 ~# n8 X4 ~& S
Gonadotropin-independent peripheral preco-
- d, m% R; c: o: k0 ?% C; Ccious puberty in boys also results from inappropriate
! A: }$ \" J% m/ eandrogenic stimulation from either endogenous or" Q) ~, L: G8 i) u' L0 A. T
exogenous sources, nonpituitary gonadotropin stim-
" s* B0 |* P7 Z$ o3 D5 lulation, and rare activating mutations.3 Virilizing: N- B9 e: o. W' h
congenital adrenal hyperplasia producing excessive
+ ^7 t0 c8 R" V: B2 a+ Q; {  }7 [adrenal androgens is a common cause of precocious* ]1 Q+ |8 a2 M
puberty in boys.3,4' k4 r! Y! k' }) m7 x
The most common form of congenital adrenal% N: p, p- R0 P5 _( a0 i- _4 d
hyperplasia is the 21-hydroxylase enzyme deficiency.
3 h9 {9 [- F% G8 I1 s' HThe 11-β hydroxylase deficiency may also result in0 k; Y9 a- S' _. D/ w
excessive adrenal androgen production, and rarely,
! d. H, J( ~1 r4 c( ?5 {an adrenal tumor may also cause adrenal androgen. @# m' H( g- V. a2 Z& q2 Q
excess.1,3
$ J& s- S! D; _) Cat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from# p. Z3 ~3 v& k& [+ m; I: y( P
542 Clinical Pediatrics / Vol. 46, No. 6, July 20072 u  {8 U4 Z2 U) U
A unique entity of male-limited gonadotropin-6 }1 [) ]" D0 b, E- B
independent precocious puberty, which is also known8 u& q4 |/ Z  B  y
as testotoxicosis, may cause precocious puberty at a
9 x$ X* l) t) w+ Z3 M! n- @% pvery young age. The physical findings in these boys0 _, }3 Z8 N6 G# g; s# E7 e5 G
with this disorder are full pubertal development,
6 Y- z( n, k4 _5 B. t" jincluding bilateral testicular growth, similar to boys- s) |1 u( Y- `) u- e+ A
with CPP. The gonadotropin levels in this disorder
  N9 B; x0 ]. n: dare suppressed to prepubertal levels and do not show
& U* E. T8 o) h: ~5 bpubertal response of gonadotropin after gonadotropin-
5 J) J* C7 A$ V* xreleasing hormone stimulation. This is a sex-linked
5 h! v/ n, e; s$ }autosomal dominant disorder that affects only& G' [" P3 v, I1 p2 {
males; therefore, other male members of the family
% d3 I& Q& j, `may have similar precocious puberty.3
* Z8 ~% s" A0 g1 dIn our patient, physical examination was incon-0 p! c# k1 o( v) ]  ~
sistent with true precocious puberty since his testi-
* r* {$ }/ f% e- @9 U  ]cles were prepubertal in size. However, testotoxicosis. h- {6 O& `: j" A. n/ c4 ]
was in the differential diagnosis because his father
, c; t2 j$ g) Z5 O9 H8 sstarted puberty somewhat early, and occasionally,1 T$ G* B  P" T7 d* J$ u- ^
testicular enlargement is not that evident in the
5 z! N2 n. C6 s3 Y8 X4 n6 Tbeginning of this process.1 In the absence of a neg-
7 |0 C; `* K7 B/ {4 K$ E; A' vative initial history of androgen exposure, our$ g' z1 T% y( t$ h. v
biggest concern was virilizing adrenal hyperplasia,
4 ~; x1 Z) Z) X5 z+ Qeither 21-hydroxylase deficiency or 11-β hydroxylase
1 O( M/ @- R0 O, e* H2 i8 ?deficiency. Those diagnoses were excluded by find-
, O- a# Y: b" M/ b+ ding the normal level of adrenal steroids.  Y1 Q/ X) y9 d- ^  z, X
The diagnosis of exogenous androgens was strongly
2 Q+ U6 O6 a$ b+ w% Vsuspected in a follow-up visit after 4 months because/ D! Q. \  Z! K2 {& O
the physical examination revealed the complete disap-
7 e, x5 I, O) `3 qpearance of pubic hair, normal growth velocity, and% @- i! Z1 ^' y% h. T3 {+ `& F- p
decreased erections. The father admitted using a testos-
% z9 l8 j6 h" O7 W' r3 H* z8 zterone gel, which he concealed at first visit. He was4 ]* u$ L3 D: Z( d* u1 r9 Z
using it rather frequently, twice a day. The Physicians’
5 }  K4 f$ M2 K9 q8 B/ n0 ~Desk Reference, or package insert of this product, gel or
  Q  K# G- f# u7 f$ ucream, cautions about dermal testosterone transfer to4 s6 q; B, p8 X' L! A
unprotected females through direct skin exposure.
* b! Z+ e6 T! Z0 V0 f) x1 z2 {2 a% xSerum testosterone level was found to be 2 times the) ~% Z: U& a! D- Z4 ?
baseline value in those females who were exposed to
& r% `7 O; S1 [* i9 f/ Weven 15 minutes of direct skin contact with their male; R7 c  e% U- n9 E5 p$ b* V6 Z& ~
partners.6 However, when a shirt covered the applica-6 r5 ^, a( E' i5 w7 q4 Q
tion site, this testosterone transfer was prevented.  [0 k. m. w! }7 _" _: ]
Our patient’s testosterone level was 60 ng/mL,1 c1 L' A: H  r2 C" t4 |! ^
which was clearly high. Some studies suggest that4 o4 y+ e! g7 K! p9 w; M6 J
dermal conversion of testosterone to dihydrotestos-. e4 f$ H2 z: P5 A8 T
terone, which is a more potent metabolite, is more$ F; Y3 w9 f/ g: \, [
active in young children exposed to testosterone( U% N9 ?( h2 V9 F- @- Z3 b
exogenously7; however, we did not measure a dihy-5 V; l& D8 f. e* P$ z8 B' D4 B
drotestosterone level in our patient. In addition to
% A1 J0 z- J0 {: B. M2 i2 Cvirilization, exposure to exogenous testosterone in3 M3 }6 G( e1 M! Y& W
children results in an increase in growth velocity and
, {1 k# y, p  G2 h! t1 uadvanced bone age, as seen in our patient.
# h6 ]' Y2 Z4 g$ o! V1 {/ H6 `The long-term effect of androgen exposure during) \8 ~: Q9 G( C1 d$ `) U1 p
early childhood on pubertal development and final
, K+ t& E6 \1 f: r$ ]. Tadult height are not fully known and always remain: w9 Z) _" x+ f3 y# i0 s/ o
a concern. Children treated with short-term testos-3 c; b( l2 W! e0 W8 _. X1 o
terone injection or topical androgen may exhibit some; i' Z1 W# f2 s8 U$ A) g
acceleration of the skeletal maturation; however, after
4 E7 e2 s, W6 O. \5 M7 A; w2 jcessation of treatment, the rate of bone maturation
( J0 d( S! D/ b/ qdecelerates and gradually returns to normal.8,9
% `) ^5 c9 g& q" f* ~- tThere are conflicting reports and controversy
' X/ U: ~6 h4 q$ ?+ L% nover the effect of early androgen exposure on adult
) o7 y  O$ _4 I1 {3 ipenile length.10,11 Some reports suggest subnormal3 @5 {7 \! F# M9 ~5 F
adult penile length, apparently because of downreg-, z1 }8 }$ p# F2 L
ulation of androgen receptor number.10,12 However,4 O; b" Y, U- J* `3 n
Sutherland et al13 did not find a correlation between
; ~& o' c- j. w+ I. b0 J7 ^  ^childhood testosterone exposure and reduced adult
0 i; w4 s1 L- s9 V) apenile length in clinical studies.
" [7 K" ]* T2 i0 E9 S4 L0 T- ANonetheless, we do not believe our patient is
' _# l; r/ W! d# _- R7 o9 Igoing to experience any of the untoward effects from  s- k+ B) k6 ]" @) }
testosterone exposure as mentioned earlier because9 G8 o4 M4 _# K% }  p+ t0 A
the exposure was not for a prolonged period of time.6 S2 _1 p1 M: W1 s9 m4 `
Although the bone age was advanced at the time of6 g5 ]# j  T$ S: G6 P) b4 z
diagnosis, the child had a normal growth velocity at
  U0 |4 e) M7 p- p  pthe follow-up visit. It is hoped that his final adult; s9 a3 Y: I% E- m; m" o5 L
height will not be affected.
' N7 v3 R4 S8 e+ Z0 oAlthough rarely reported, the widespread avail-
: ?* w7 c' f0 f; rability of androgen products in our society may
3 T) [8 z5 b8 J% sindeed cause more virilization in male or female$ s$ x+ H  G* O# W
children than one would realize. Exposure to andro-
4 i" l) O% N( B% m- F$ hgen products must be considered and specific ques-
  z/ t2 |9 G. \5 N5 E) ntioning about the use of a testosterone product or
3 H' C9 i* u& Ugel should be asked of the family members during
$ q" k" `: t+ D0 L: b% Wthe evaluation of any children who present with vir-
+ y  k3 D6 w) X6 Pilization or peripheral precocious puberty. The diag-
1 ~: V0 z, V4 U) M9 S8 ?* Fnosis can be established by just a few tests and by
/ Z* I) w9 E6 [1 Eappropriate history. The inability to obtain such a
% W; a$ }3 h; U8 ]% e7 U5 dhistory, or failure to ask the specific questions, may
; N0 Y9 M6 C' X! lresult in extensive, unnecessary, and expensive
! t( N$ Y8 B, M+ Y- i& N& rinvestigation. The primary care physician should be- W, }# n6 r- Q% x1 E# B
aware of this fact, because most of these children
. V+ o1 p" I( P9 b7 Nmay initially present in their practice. The Physicians’
$ `: _. J" J4 N  y6 oDesk Reference and package insert should also put a) E! e0 }+ Z% i
warning about the virilizing effect on a male or
6 Y9 p& a9 Z+ d6 ^female child who might come in contact with some-8 J4 t7 [1 |+ F" g0 }# T1 `
one using any of these products.5 B. F9 c/ ]. o1 B; Y: k
References' O( S! M- d- _) G, X% h# u* Z" o
1. Styne DM. The testes: disorder of sexual differentiation+ P% t1 [8 g0 b% p! n0 H
and puberty in the male. In: Sperling MA, ed. Pediatric  ~/ }' H( P. [
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
  v& u6 k- Y$ k2002: 565-628.
# d- g' D! ~' y9 b  o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious
9 |! E$ C; S8 c6 |! p8 }8 r, Fpuberty 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

. z% L  @" P* d! g9 q& f" B4 ]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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