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Sexual Precocity in a 16-Month-Old8 Z+ b1 E1 Q% v+ O% V8 J
Boy Induced by Indirect Topical" K* r* s( l- s1 n
Exposure to Testosterone
, O$ U8 x2 e- m: s( GSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,25 [, H. l2 U- |8 P* b
and Kenneth R. Rettig, MD1! l% _* y$ C+ d5 p; g- R
Clinical Pediatrics9 @# x7 \6 V! U- X! x0 C2 y1 ~* H9 T
Volume 46 Number 6
( f1 C0 F) m5 _) R5 x2 ZJuly 2007 540-543, A6 C% {3 j. T2 l; C
© 2007 Sage Publications
* x. |" @. U: q& @10.1177/0009922806296651- e( s. q/ r- b
http://clp.sagepub.com9 Q1 g3 y1 V3 }: j/ D- j" v0 H
hosted at1 J0 O# y0 p: `8 _% _
http://online.sagepub.com
) l- J+ b- I4 m$ QPrecocious puberty in boys, central or peripheral,  z; g" J! Q8 h, k7 _8 w7 r! b& q
is a significant concern for physicians. Central
- c- E  Z6 ?: `) {; hprecocious puberty (CPP), which is mediated
% \1 T2 t+ I2 Y( T) Tthrough the hypothalamic pituitary gonadal axis, has7 H; n" ^, ^6 N0 q0 Z) b0 h9 C' J( B
a higher incidence of organic central nervous system
2 n. ]. [' `. [: Q% ilesions in boys.1,2 Virilization in boys, as manifested
' ?2 l. F, I! O3 Fby enlargement of the penis, development of pubic
9 q. _( V( o: I- A2 Dhair, and facial acne without enlargement of testi-
& f4 B9 K1 z; x9 j; V( L+ v) wcles, suggests peripheral or pseudopuberty.1-3 We
: W- c' C6 v) u+ Ereport a 16-month-old boy who presented with the+ m8 l: o- ~5 U6 \( \& N7 I
enlargement of the phallus and pubic hair develop-
& V+ i5 d, _4 |" P! G5 Rment without testicular enlargement, which was due
$ A2 `$ m$ x, J5 Cto the unintentional exposure to androgen gel used by  ~* i" l/ E7 b5 D
the father. The family initially concealed this infor-  G' B/ s9 D* H. g! `: ^
mation, resulting in an extensive work-up for this
4 \& `7 z8 ~; u$ \5 Schild. Given the widespread and easy availability of6 a  Q% l9 `. u, o; {2 f$ Y! j
testosterone gel and cream, we believe this is proba-
7 G0 O& C: U/ N/ S3 sbly more common than the rare case report in the7 I4 ^) x9 k. }! r. j1 _
literature.4
9 R+ B5 F" c; J. @" m. hPatient Report
" Q; P6 o: f8 ?% e$ o; g; y/ xA 16-month-old white child was referred to the
! R9 E9 t  Q) E. Z4 i, @% U# A. [endocrine clinic by his pediatrician with the concern
$ I7 C2 v$ Z0 v2 ^8 c5 u& rof early sexual development. His mother noticed" [8 a& s! U4 ]  r
light colored pubic hair development when he was
) U3 Z( D" Z3 N  J/ r% t" {From the 1Division of Pediatric Endocrinology, 2University of
# I9 R, ?: O$ I- L" V0 ?% oSouth Alabama Medical Center, Mobile, Alabama.% ~2 _% G9 ]% C: o5 c% U
Address correspondence to: Samar K. Bhowmick, MD, FACE,
. S/ \4 w# R7 M7 b/ |Professor of Pediatrics, University of South Alabama, College of
2 b) J- U1 r, ~6 `Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
, {! ?: L: f7 P' v1 z6 U# me-mail: [email protected].
. s7 k# e2 _$ j( I) V0 a( r8 y0 N" uabout 6 to 7 months old, which progressively became
! U" ], F' C) t2 d9 {- `darker. She was also concerned about the enlarge-- S- m+ e; W$ _9 b7 ^: _0 Z! {
ment of his penis and frequent erections. The child. Y* I4 q: A$ S8 M
was the product of a full-term normal delivery, with1 ^2 H* @/ v# v2 w' p7 p
a birth weight of 7 lb 14 oz, and birth length of
6 e2 T( r% o3 I* a' M20 inches. He was breast-fed throughout the first year
% t# c2 Q" D- j5 m& K' Yof life and was still receiving breast milk along with
  m' }1 J+ N9 k1 m9 O/ S/ J- I8 u0 \solid food. He had no hospitalizations or surgery," r0 I. t4 I9 W9 z" t$ R! _6 U
and his psychosocial and psychomotor development
! O, O/ D" i! k% Mwas age appropriate.
' U! K0 [# q$ W: yThe family history was remarkable for the father,2 U( [/ v- c" z$ ]
who was diagnosed with hypothyroidism at age 16,
4 i" O7 e& Q( u0 I+ F# V! X1 }which was treated with thyroxine. The father’s, T7 ^1 @' W  Y/ |# q' W8 [% w
height was 6 feet, and he went through a somewhat
- k1 M. _) t  C& M. Vearly puberty and had stopped growing by age 14.. }# {: g1 L+ n3 A
The father denied taking any other medication. The$ Y5 \* O/ q: K9 S/ Q/ o+ G1 f# I
child’s mother was in good health. Her menarche
' i. ?0 Y, C* E( V1 [' xwas at 11 years of age, and her height was at 5 feet4 u8 b4 x* d" j' l& H3 [6 F5 ?
5 inches. There was no other family history of pre-9 l4 J# E- q4 l/ J
cocious sexual development in the first-degree rela-! v$ d% F+ U8 U; s, A
tives. There were no siblings.3 ~$ M. L; s; E1 Y  f
Physical Examination
+ H! |' @3 o6 Z5 N* w4 ~The physical examination revealed a very active,7 O  Y$ n4 j/ J) n# X6 O( h
playful, and healthy boy. The vital signs documented* M2 i% Q3 V$ Q9 k' @
a blood pressure of 85/50 mm Hg, his length was- A3 E+ t6 L' B+ H: z
90 cm (>97th percentile), and his weight was 14.4 kg( T( @' O' _# u+ S" v
(also >97th percentile). The observed yearly growth
8 U1 @, T" M1 x; ^* Ivelocity was 30 cm (12 inches). The examination of
3 V6 M7 _$ O- d1 ^+ Kthe neck revealed no thyroid enlargement.' {9 k8 z5 u1 |; ?7 `
The genitourinary examination was remarkable for
1 }4 d' A$ Z1 w8 Penlargement of the penis, with a stretched length of
1 ~! |0 m; d# |( k8 p$ ~# c8 cm and a width of 2 cm. The glans penis was very well
+ a' x& H& X' `6 m3 F" ^developed. The pubic hair was Tanner II, mostly around
7 y: h  z: m2 a9 i/ B- }540
8 ?) g3 o% V5 @4 m1 Uat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from5 @9 ?) Z6 g$ Z& x# N$ k  _
the base of the phallus and was dark and curled. The
9 T) O9 n: D$ Ktesticular volume was prepubertal at 2 mL each.
+ Y0 R  M/ o5 t: lThe skin was moist and smooth and somewhat
$ e! W$ g! C& R" U4 u2 G2 c8 Voily. No axillary hair was noted. There were no
. u* o4 W- y) c8 I- F1 k$ n2 m- @abnormal skin pigmentations or café-au-lait spots.
8 X; B: [/ J, b$ HNeurologic evaluation showed deep tendon reflex 2+
5 B1 S3 g' S5 E0 t/ Ibilateral and symmetrical. There was no suggestion% P6 s+ F' h$ J+ o
of papilledema.2 v+ Z; j6 M7 p" r/ {" J. [! C- o) W  L
Laboratory Evaluation
3 E: i. w- X9 ZThe bone age was consistent with 28 months by) ]  p- W5 O  m* D$ s9 W: b
using the standard of Greulich and Pyle at a chrono-
7 I8 _. M- l& E* S0 f/ V1 q, ?logic age of 16 months (advanced).5 Chromosomal! d6 V! Z* ]0 c" p- z( g
karyotype was 46XY. The thyroid function test' s; h4 {  p5 M) p8 @
showed a free T4 of 1.69 ng/dL, and thyroid stimu-% H8 E$ P1 S, C" f4 N
lating hormone level was 1.3 µIU/mL (both normal).4 @5 w  u% ]; L4 Z, [
The concentrations of serum electrolytes, blood
' D) \' Q8 V" ?" uurea nitrogen, creatinine, and calcium all were
9 W1 O! U- j! Y" c, f, y7 nwithin normal range for his age. The concentration& L. K" f% \- L- |3 [
of serum 17-hydroxyprogesterone was 16 ng/dL8 r) {$ n6 h2 h# ^6 U" Z
(normal, 3 to 90 ng/dL), androstenedione was 20
* J& \% g" P; S) e& s$ j8 i) |ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
; _$ z4 t- @. d# M3 bterone was 38 ng/dL (normal, 50 to 760 ng/dL),9 {. S8 q# K( G# H! Y
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 F4 J/ A: m! w: I1 _7 i6 }49ng/dL), 11-desoxycortisol (specific compound S)
5 o3 ^* ^9 z6 s4 D; mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
2 ]; S8 f4 g4 L2 y) F4 A9 b* wtisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total3 q9 f( R% n3 i
testosterone was 60 ng/dL (normal <3 to 10 ng/dL)," h* F4 ]) N: |
and β-human chorionic gonadotropin was less than+ ?( W( L) ~$ @+ F, Z( e
5 mIU/mL (normal <5 mIU/mL). Serum follicular* A% s9 l# X4 @; N2 G1 T: i/ O; n  _
stimulating hormone and leuteinizing hormone
2 x+ l9 y9 c. pconcentrations were less than 0.05 mIU/mL9 b# K& V) P% j) O8 l( M
(prepubertal).5 x" h, G7 V2 E3 l( d' _2 x
The parents were notified about the laboratory
; \1 a: b7 G+ |* M- x2 o1 Aresults and were informed that all of the tests were
) R" m- s& P& D, ~1 w* |. u) Nnormal except the testosterone level was high. The1 U6 P% B$ c; {6 I2 X, Z3 Z
follow-up visit was arranged within a few weeks to
* s# N3 y  F' r5 Z6 j/ d& F) Uobtain testicular and abdominal sonograms; how-! Q0 s: p* z2 y0 K5 p& i0 S" w5 R
ever, the family did not return for 4 months.
$ l, g- y1 h' r3 v, B8 O1 Y: XPhysical examination at this time revealed that the2 I2 J& k/ n  X/ t! L' x  s- L) n
child had grown 2.5 cm in 4 months and had gained
) T5 w) ^) N. g' i, c- o) h2 kg of weight. Physical examination remained
8 m$ O' l, t  i  ^unchanged. Surprisingly, the pubic hair almost com-, Z# j( Z! @# l
pletely disappeared except for a few vellous hairs at( P; t+ L; a+ E, ]! C3 j6 w# M
the base of the phallus. Testicular volume was still 2
) V2 X0 V! I  N  G9 bmL, and the size of the penis remained unchanged.% R8 C$ g% ~3 C2 I- G2 M
The mother also said that the boy was no longer hav-; x- b7 C: ?+ n: E
ing frequent erections.
. @0 x$ N4 t+ t/ Z; S& w6 WBoth parents were again questioned about use of
  E$ |7 d7 a8 S9 t( x+ ]) w$ Many ointment/creams that they may have applied to' o# h  ?6 c. W0 c- D: H6 ~
the child’s skin. This time the father admitted the6 S8 K& v$ _' w# z# v
Topical Testosterone Exposure / Bhowmick et al 5414 A7 |5 t4 d; I7 \; |/ \3 J  R
use of testosterone gel twice daily that he was apply-9 k. ]" s3 x/ @/ p# t3 _: V3 Q
ing over his own shoulders, chest, and back area for1 F) L; ~8 A# z# Z7 M( y1 R* y4 M4 m! }% J
a year. The father also revealed he was embarrassed
$ d1 m7 y% l0 h4 ]* i% uto disclose that he was using a testosterone gel pre-
( n& V) u2 k; `% i: p6 B0 qscribed by his family physician for decreased libido
' G* `, c5 M" Qsecondary to depression.* P0 B& K0 a6 X4 e3 M# O3 F
The child slept in the same bed with parents.
. e- x( j6 h: R  xThe father would hug the baby and hold him on his
; f& V& t; f6 l+ Y8 Qchest for a considerable period of time, causing sig-( x. e" h- _! A1 g9 S% O
nificant bare skin contact between baby and father.% w4 t8 n8 I' E+ t/ h
The father also admitted that after the phone call,
. q1 L/ X( m8 T" G. Xwhen he learned the testosterone level in the baby  w) V; l3 t! G4 H* ?
was high, he then read the product information
1 X) d# \' q) \0 n) Fpacket and concluded that it was most likely the rea-. \$ b9 b5 v4 V" P  D0 I% r# Q
son for the child’s virilization. At that time, they! A% }  _) v5 y7 ~
decided to put the baby in a separate bed, and the
( ?0 J7 B" G4 h8 Q* ]; rfather was not hugging him with bare skin and had0 k8 Y+ ^/ r( U0 j6 I, ~9 S* |! S/ A
been using protective clothing. A repeat testosterone
3 Q: H; J' e# k; t1 p( ttest was ordered, but the family did not go to the0 j% @" \' l+ q" i# h' C# i
laboratory to obtain the test.
6 r! \, {7 `- X1 CDiscussion
3 [6 `) P0 l3 Y4 C0 }Precocious puberty in boys is defined as secondary
8 a( p1 m: H8 `- q9 @" H. Rsexual development before 9 years of age.1,4
- a3 `) e% f7 |. cPrecocious puberty is termed as central (true) when5 ~% r% H2 i2 i+ |
it is caused by the premature activation of hypo-
; g7 b3 H! C/ r! R- ?" nthalamic pituitary gonadal axis. CPP is more com-
1 z& A0 [6 ~5 n1 @7 xmon in girls than in boys.1,3 Most boys with CPP7 J. `- \/ P) q
may have a central nervous system lesion that is) ?% j+ v( r$ I
responsible for the early activation of the hypothal-/ Z! D+ S. Y- b9 m9 N4 T- H5 I& C
amic pituitary gonadal axis.1-3 Thus, greater empha-
" j, c7 ~) C! }5 psis has been given to neuroradiologic imaging in, k4 {. S9 r  N4 S# g  ~: A9 U
boys with precocious puberty. In addition to viril-
4 _+ e% l! a' z. Cization, the clinical hallmark of CPP is the symmet-
( z9 V* m4 m: l$ |/ ^& s. ^rical testicular growth secondary to stimulation by# _% b6 T1 L& Z1 T. j0 z6 X
gonadotropins.1,3; d4 w* l5 L  c
Gonadotropin-independent peripheral preco-
# m. `" Q/ J0 \  F6 [& ?3 Qcious puberty in boys also results from inappropriate7 t$ t  _9 v/ ~; n
androgenic stimulation from either endogenous or
2 h& ^" N5 v1 Xexogenous sources, nonpituitary gonadotropin stim-
0 O; \4 g  w2 R9 f# mulation, and rare activating mutations.3 Virilizing, j  `" A- B' N, U* I- F6 z1 |
congenital adrenal hyperplasia producing excessive
  p) t' {2 v! \1 P. [adrenal androgens is a common cause of precocious
0 y* J# y- a8 |5 n3 ]puberty in boys.3,4) i1 s+ L$ v' V; w
The most common form of congenital adrenal
1 u9 R2 R% ~. B1 {/ F2 i' o6 Rhyperplasia is the 21-hydroxylase enzyme deficiency.
- ^- N. S/ ]3 c8 V+ X+ A0 `The 11-β hydroxylase deficiency may also result in
  I) H* m/ |! J+ u1 Q0 p) j% H( vexcessive adrenal androgen production, and rarely,
7 E4 _$ D3 S5 d5 Y6 Lan adrenal tumor may also cause adrenal androgen
4 Z5 r/ i; q1 C! @, }excess.1,31 q2 E: d- Z) N. w: y* c; g
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from$ l: U7 @4 A5 j/ }! J% ~6 e
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007" s! N! p8 ~0 G6 ^
A unique entity of male-limited gonadotropin-: h9 S# w$ x" D0 w. T/ \$ a8 C. G
independent precocious puberty, which is also known
  {9 ~9 m3 i8 C5 B" ?4 D/ Z* Kas testotoxicosis, may cause precocious puberty at a+ R8 Y% _' g& H( J5 K/ i( M( i
very young age. The physical findings in these boys
/ C  C( c& K+ A1 u' @# Ywith this disorder are full pubertal development,
5 |2 ?8 c8 f# }/ qincluding bilateral testicular growth, similar to boys( V  s5 H" D2 K! ]; x( F
with CPP. The gonadotropin levels in this disorder
; ]4 P1 }: X7 M" l( |1 Rare suppressed to prepubertal levels and do not show
7 g& `. p; E$ p2 h" z! ppubertal response of gonadotropin after gonadotropin-5 h7 k% E9 G7 P6 J9 k
releasing hormone stimulation. This is a sex-linked
& X' Q0 Z* o9 [! E0 }" z6 x& }autosomal dominant disorder that affects only; X) ]- v$ i& T
males; therefore, other male members of the family
5 x7 o" s  A# f8 v( kmay have similar precocious puberty.3& p1 ?# m1 p  Z0 P
In our patient, physical examination was incon-
# I) `! u0 m# L. m  B2 p0 j8 Isistent with true precocious puberty since his testi-
( E& i5 m$ j0 q. \$ w" x3 f) H) y- kcles were prepubertal in size. However, testotoxicosis
" F1 M$ L/ l9 V- _3 {( X, \9 ~was in the differential diagnosis because his father! P2 q* w) Y* M; p/ m" W
started puberty somewhat early, and occasionally,: N! p( ]2 C, K. D+ G/ z9 C
testicular enlargement is not that evident in the8 u9 P8 m0 T0 |6 H! i. m
beginning of this process.1 In the absence of a neg-* ?1 h2 x/ ~7 I  ~& i9 i
ative initial history of androgen exposure, our$ ^  Q1 R" y  I/ U5 J+ h
biggest concern was virilizing adrenal hyperplasia,
7 ^7 b7 \2 O& E1 I6 K( }4 }) L3 K& aeither 21-hydroxylase deficiency or 11-β hydroxylase
2 ]  {# l6 U: L8 S! ]deficiency. Those diagnoses were excluded by find-
4 U, T4 m# [" G$ E2 Z# Xing the normal level of adrenal steroids.
/ V, g4 }- V( A. h- p* ?4 yThe diagnosis of exogenous androgens was strongly3 T3 w4 K1 ]4 M: _6 B7 s
suspected in a follow-up visit after 4 months because/ ]  ?1 s! T/ A' j
the physical examination revealed the complete disap-, ?; {/ W$ G0 a! h5 g3 E2 b
pearance of pubic hair, normal growth velocity, and
6 f: i$ `( p) q: ^" [7 Kdecreased erections. The father admitted using a testos-( w$ e3 A% D/ C( v  d/ h# u
terone gel, which he concealed at first visit. He was
9 }' l) i. i" Jusing it rather frequently, twice a day. The Physicians’) |1 h# m1 t. B# c* C" g4 k+ n* W
Desk Reference, or package insert of this product, gel or
6 [" \* F, n/ V1 C/ ?! Hcream, cautions about dermal testosterone transfer to
  N- q+ Q- j/ q" gunprotected females through direct skin exposure.
3 ~+ c+ k7 O6 A' i( aSerum testosterone level was found to be 2 times the
, X! {8 z! j; ~3 v7 N: i: h: rbaseline value in those females who were exposed to) `9 R2 ?. e- b% M( N3 A
even 15 minutes of direct skin contact with their male
2 I2 s# |9 r. B& ?partners.6 However, when a shirt covered the applica-& K" O4 q/ z6 @3 m( ^
tion site, this testosterone transfer was prevented.
0 T4 k/ d& D9 f+ h# N" b+ S7 ~, fOur patient’s testosterone level was 60 ng/mL,/ j0 _* s; a- o7 S1 [) T6 b
which was clearly high. Some studies suggest that
1 a& N6 U) z, J3 qdermal conversion of testosterone to dihydrotestos-
; k7 Z( m! ^# S! A' _terone, which is a more potent metabolite, is more
; Q1 @9 v9 B) d- o% q- E) Dactive in young children exposed to testosterone: g/ r  I1 C- j; `3 P5 x4 o) N
exogenously7; however, we did not measure a dihy-7 O) B! o7 |4 v
drotestosterone level in our patient. In addition to
" E$ O: Z. U; U1 d' ^; _# w5 Gvirilization, exposure to exogenous testosterone in
( }1 Y$ S6 t# {/ i9 v) N( ?$ R5 Rchildren results in an increase in growth velocity and; P/ s0 m& J& n2 x. @
advanced bone age, as seen in our patient.8 y" O! w7 P+ `$ t( f! e
The long-term effect of androgen exposure during: H7 k) Q" C. g5 ?2 n! O
early childhood on pubertal development and final) O, `1 K3 P3 E9 h( C
adult height are not fully known and always remain% ]+ f. w% D! ?. T% X+ M
a concern. Children treated with short-term testos-+ f3 M9 O. ]  [3 z. n, a
terone injection or topical androgen may exhibit some% y& [- \$ ^4 Y
acceleration of the skeletal maturation; however, after- g1 H. ?- g) \4 w+ }. n, c
cessation of treatment, the rate of bone maturation6 P# ^6 D, ?- d0 Z( Y. |& g3 n* c& d
decelerates and gradually returns to normal.8,9
1 r% w/ m" B6 t1 c* d2 zThere are conflicting reports and controversy0 M# f- v- C& W) n$ ~% c. N+ a
over the effect of early androgen exposure on adult
& R% k& f/ C. u8 E* l0 j/ N3 Ypenile length.10,11 Some reports suggest subnormal
2 j3 G+ u+ s$ s# l* d7 ~! U" Yadult penile length, apparently because of downreg-, Q6 [. z  z/ c- g3 O0 e* a
ulation of androgen receptor number.10,12 However,, m, r* e( ]3 |+ m: h; J
Sutherland et al13 did not find a correlation between. _# I0 _9 \- J4 y* {3 p& m, J' U
childhood testosterone exposure and reduced adult
0 p, y8 K  z7 }& J5 [; jpenile length in clinical studies.
( [) i7 `$ s! `, V3 W$ E& }Nonetheless, we do not believe our patient is& R* K, |. F2 D' J; @5 j
going to experience any of the untoward effects from9 U0 u! {' p. W
testosterone exposure as mentioned earlier because: C- s8 u( `$ Z& z
the exposure was not for a prolonged period of time.4 t+ m9 P  ?. w1 k$ T; L( o/ D
Although the bone age was advanced at the time of: s# N. H- E+ G9 h) V8 X
diagnosis, the child had a normal growth velocity at
1 s' P5 j% N3 n& Q$ r+ zthe follow-up visit. It is hoped that his final adult" b; U8 k8 A) b# I( V, J8 y1 I
height will not be affected.
* a& j! B0 X$ V' [3 }Although rarely reported, the widespread avail-4 ?3 p3 w2 ~; ]5 |" {& G
ability of androgen products in our society may
) m- E$ C4 J. n1 G: Findeed cause more virilization in male or female8 p# ~7 ]8 k9 ^0 b2 M2 @; \3 c
children than one would realize. Exposure to andro-
4 I# ^  s2 f* ngen products must be considered and specific ques-! ]. y$ H9 @7 i" k2 z% e
tioning about the use of a testosterone product or5 r' Q, f/ z& s4 n1 _# d
gel should be asked of the family members during
% m. D. T! m4 O" {& ]the evaluation of any children who present with vir-
. j6 |1 L" Z/ ?+ p5 Dilization or peripheral precocious puberty. The diag-
  l/ o$ I, ]  B. w, Anosis can be established by just a few tests and by
9 u3 b, S$ ^. k, Pappropriate history. The inability to obtain such a7 G' E3 Y% T& j' S1 w" R
history, or failure to ask the specific questions, may, |7 |9 q4 O2 ?) c* w# A
result in extensive, unnecessary, and expensive1 a  H) o2 a3 r
investigation. The primary care physician should be2 f% z4 [. Y- c4 ^! M
aware of this fact, because most of these children
& ~8 p3 X, J- T6 [4 Wmay initially present in their practice. The Physicians’" ~2 w- T7 @( |# q  A3 K8 h/ k
Desk Reference and package insert should also put a3 w& Z1 T8 T( V, u
warning about the virilizing effect on a male or5 u5 G' v/ \' V$ G4 R. H& w. d
female child who might come in contact with some-
) L! F4 x5 F$ yone using any of these products.6 t, b  K* U: R1 e$ U& I
References
2 o: [& b6 p5 L' R  m1. Styne DM. The testes: disorder of sexual differentiation
, B4 Q8 d2 n: O5 [0 a" f% Z  }# Hand puberty in the male. In: Sperling MA, ed. Pediatric  ]6 M3 _) v6 D& i- e9 o
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 d) g! ]2 w6 m" n8 A2002: 565-628.
3 c% n/ O! j2 l/ o2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious- Q9 r  @2 d: V
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
# w" ^6 O% f# l/ c1 hBoy Induced by Indirect Topical
1 @1 P8 ?/ ?: X4 B, t% x! jExposure to Testosterone3 f0 e3 D7 p7 r  _; H& F
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. H" {/ m7 D" j
and Kenneth R. Rettig, MD1
, ]$ ~4 {- ~) R* TClinical Pediatrics& I$ I# X1 E& M; j- n. j
Volume 46 Number 6
  |- K  A2 s2 J6 U' RJuly 2007 540-543. V% _+ a6 A# \+ K4 X# Y4 T
© 2007 Sage Publications
& z( z* D  P- L, j10.1177/0009922806296651. ]6 P1 C" \7 X
http://clp.sagepub.com( f, X( |9 q% W. P8 W( J
hosted at
$ o, i+ u) m9 Z  M$ |. P6 @http://online.sagepub.com
: E4 s! a+ X' f. V3 ^Precocious puberty in boys, central or peripheral,; q4 C6 ^* z1 @& C, Z
is a significant concern for physicians. Central, n4 D) q( {! A0 W7 \
precocious puberty (CPP), which is mediated
+ O; G! [8 v6 L7 m4 x* X3 nthrough the hypothalamic pituitary gonadal axis, has
; J/ P4 {( g8 M4 t. \: l, D- Xa higher incidence of organic central nervous system
" E- v, ~& R  _5 d2 Mlesions in boys.1,2 Virilization in boys, as manifested/ ^) g  a, T$ m4 H5 `2 ]4 ]
by enlargement of the penis, development of pubic
  l+ X: w6 N4 R8 q* thair, and facial acne without enlargement of testi-% K! h# {# I' Y# z
cles, suggests peripheral or pseudopuberty.1-3 We
1 @, ]& L: z% r1 U* F# k. ?report a 16-month-old boy who presented with the
' P/ G; b8 _# o1 }' Genlargement of the phallus and pubic hair develop-
& _3 `$ m3 W4 Xment without testicular enlargement, which was due
8 ^  j2 d8 I! O+ `to the unintentional exposure to androgen gel used by' {$ C  z& Q1 n5 [1 j3 [! N
the father. The family initially concealed this infor-
# ?$ }$ t2 U) @; u8 a3 p$ Cmation, resulting in an extensive work-up for this
$ e3 r4 q; e! w5 W/ Ychild. Given the widespread and easy availability of
( S5 J: q3 p, b0 D" Z9 @testosterone gel and cream, we believe this is proba-
! o$ Z2 t: ^, X( q) w4 X; L" lbly more common than the rare case report in the
8 Z$ x/ g; k  U4 I& i. B7 Nliterature.4+ o9 h! @% R$ T$ u2 \8 ^
Patient Report1 `& B0 y! n( M$ K5 t
A 16-month-old white child was referred to the5 q' A% S$ F: @0 a+ `9 Y
endocrine clinic by his pediatrician with the concern1 N0 T& ]2 z2 v& @
of early sexual development. His mother noticed5 k: o! l4 z" @: E, n
light colored pubic hair development when he was
$ j* Q+ S3 G& Q  e+ A5 iFrom the 1Division of Pediatric Endocrinology, 2University of2 ~8 \# U4 n+ i
South Alabama Medical Center, Mobile, Alabama.
- L7 f6 S. |/ SAddress correspondence to: Samar K. Bhowmick, MD, FACE,
0 m2 L1 {( _2 e" C5 M% F/ |5 m0 XProfessor of Pediatrics, University of South Alabama, College of1 B# q7 p: L' B% f9 i2 V; L3 @% }
Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
6 [9 K* c5 ~* g& }e-mail: [email protected].
0 s2 y/ u( J) X/ Jabout 6 to 7 months old, which progressively became4 Z- r. Y* y9 K
darker. She was also concerned about the enlarge-: C* c2 m* I3 H
ment of his penis and frequent erections. The child
) Q! L% v& F$ R7 Z. Z7 f7 z1 ]was the product of a full-term normal delivery, with* j; w3 _4 f; ?& y0 H6 r
a birth weight of 7 lb 14 oz, and birth length of. q2 a3 W7 g/ h8 X" N; j4 R* F) [
20 inches. He was breast-fed throughout the first year/ ^" h; }7 W+ M; r6 h3 u
of life and was still receiving breast milk along with
, g: n- r6 l4 Z) g4 gsolid food. He had no hospitalizations or surgery,
$ u  q( w" L' X9 r6 k5 ~and his psychosocial and psychomotor development6 S; `5 i& V2 C% s; k* Q
was age appropriate.
1 P8 ?& @* `6 `6 c  i9 rThe family history was remarkable for the father,+ n' y& f* x& P  {2 r& Y' Y# I2 _" P
who was diagnosed with hypothyroidism at age 16,
8 B9 P2 J8 V% B7 q: j( Jwhich was treated with thyroxine. The father’s
. b6 e$ h9 O2 Z7 @height was 6 feet, and he went through a somewhat
, H& q! c7 f; {( fearly puberty and had stopped growing by age 14.8 R+ |( }, t0 [  s
The father denied taking any other medication. The
" D0 Y/ d* H) h/ mchild’s mother was in good health. Her menarche
8 o5 `- n* C. |# Z- l. _4 r7 Gwas at 11 years of age, and her height was at 5 feet' _. S2 l+ ^, Z
5 inches. There was no other family history of pre-
  R0 W/ q9 h- d* G3 b9 m! ^cocious sexual development in the first-degree rela-
, f$ D7 k- ~& n7 R8 w" Stives. There were no siblings./ ?  l( \8 M, N: p! V' q1 J- v% x/ _- r
Physical Examination
5 K* ]; ^6 o( `4 ^. ~The physical examination revealed a very active,
% c( s' S5 W* R0 x; O, V4 T4 oplayful, and healthy boy. The vital signs documented
, k* ]5 a. A5 Ka blood pressure of 85/50 mm Hg, his length was. C5 |# |, I3 R; ~
90 cm (>97th percentile), and his weight was 14.4 kg
; U" i) D1 @' e' G/ E# C(also >97th percentile). The observed yearly growth
6 O0 z( a' `9 gvelocity was 30 cm (12 inches). The examination of- X5 z7 k' D7 g% o7 V$ n" P
the neck revealed no thyroid enlargement.
) R. j% q) x4 r7 s0 `3 U: o. YThe genitourinary examination was remarkable for
* p4 P! s& v4 E: q3 n: Lenlargement of the penis, with a stretched length of$ Z3 L& P+ ?# o7 ?/ r# P
8 cm and a width of 2 cm. The glans penis was very well
# N; C3 L4 R2 hdeveloped. The pubic hair was Tanner II, mostly around2 f: H8 [/ m4 l# W+ s% r: T
5404 j0 Z4 {% L  j. ~
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
" T. J1 F) ^( E5 s! T* n5 sthe base of the phallus and was dark and curled. The( |* [4 c4 A, j0 w3 R7 Q; t
testicular volume was prepubertal at 2 mL each.( |# ]' o7 k/ d" P' Y; V# B
The skin was moist and smooth and somewhat
3 p% S! k% e( r9 l' [oily. No axillary hair was noted. There were no
4 B9 ]( J6 ]$ W, t4 p, k3 V- labnormal skin pigmentations or café-au-lait spots.
- V! o; f* J( n2 t3 gNeurologic evaluation showed deep tendon reflex 2+
2 _" A9 Q# x+ _7 O6 \1 D% s4 ?bilateral and symmetrical. There was no suggestion
/ x6 ?5 n% n! xof papilledema.- L4 u/ Z* P" l& J7 V1 a1 G, ~, L
Laboratory Evaluation$ D* i" W) ^! K  p% a
The bone age was consistent with 28 months by
# G5 e6 P: n0 Musing the standard of Greulich and Pyle at a chrono-
7 x1 h* t9 T. \- h9 Y, k* H/ j& ^: o' Flogic age of 16 months (advanced).5 Chromosomal/ v2 |9 _; m: Z2 m- N4 }
karyotype was 46XY. The thyroid function test
" W4 Y6 m0 Q* u1 W( D. `showed a free T4 of 1.69 ng/dL, and thyroid stimu-* J' J, Q6 c' g: f$ L$ x
lating hormone level was 1.3 µIU/mL (both normal).
& E9 I0 [; `+ m5 j% ^: F7 WThe concentrations of serum electrolytes, blood  C5 X; c7 T: K8 ~8 X* B8 J
urea nitrogen, creatinine, and calcium all were$ B8 q7 n& v; ~$ o" z2 I2 i- B
within normal range for his age. The concentration
8 n2 ?6 P0 M. T' {& Nof serum 17-hydroxyprogesterone was 16 ng/dL
; |& h( G3 S' D0 w" q0 _" @(normal, 3 to 90 ng/dL), androstenedione was 201 I' C+ B9 p- u% ?* Y3 t
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
; d6 W# _& g6 q5 h* @terone was 38 ng/dL (normal, 50 to 760 ng/dL),% I6 n6 `9 ], G6 ]9 v
desoxycorticosterone was 4.3 ng/dL (normal, 7 to
! f. I% {' E' Z7 k- E1 m0 Q! y  p$ b2 F49ng/dL), 11-desoxycortisol (specific compound S)0 w9 p2 F; W( d0 w4 X8 L" @5 e& [
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-2 y1 V4 Q5 `. O2 W2 ~( ^! ^
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* \: M1 L4 ^+ U" b2 O
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
0 o% _' V/ A$ v) e3 _8 Mand β-human chorionic gonadotropin was less than
! K# D( x; M/ i$ U8 C$ V1 s+ W3 M5 mIU/mL (normal <5 mIU/mL). Serum follicular9 H! {! N% x5 |2 Y+ a1 k
stimulating hormone and leuteinizing hormone4 U' v# C, @' w+ P( `
concentrations were less than 0.05 mIU/mL9 z2 Y4 X4 S5 D" C
(prepubertal).9 c: W" X6 N. x- s$ p. ]
The parents were notified about the laboratory8 d3 U7 N( g5 \* T9 }
results and were informed that all of the tests were
: R) r. \% S5 c' @0 z' U8 X6 anormal except the testosterone level was high. The
+ o  ^1 H5 {9 o" Hfollow-up visit was arranged within a few weeks to9 }) C, i3 A/ Z
obtain testicular and abdominal sonograms; how-3 k  {7 g) C- h4 ]- Y* c+ B
ever, the family did not return for 4 months.
0 _! L7 U$ E7 `Physical examination at this time revealed that the9 y1 R% x" }1 C  l9 I# R; \' Z
child had grown 2.5 cm in 4 months and had gained. v  @* E, o: p, M' l$ D
2 kg of weight. Physical examination remained/ I: g6 c1 g6 J. r
unchanged. Surprisingly, the pubic hair almost com-
9 G" z/ F1 @0 n/ u7 {* }pletely disappeared except for a few vellous hairs at6 ?1 {1 y4 b/ d) u% `6 F' |
the base of the phallus. Testicular volume was still 2( j( [; J, A" G; l1 g
mL, and the size of the penis remained unchanged.+ H+ ^4 d5 v: y6 j; Z+ h
The mother also said that the boy was no longer hav-
# k* j& v# I+ y; O' X/ ling frequent erections.( p9 v/ h% H7 I, Y( y
Both parents were again questioned about use of
4 J* G( n: F( m& ~6 Z* B' K) B3 sany ointment/creams that they may have applied to
8 ?0 u& r# f/ [8 @the child’s skin. This time the father admitted the
& e' |# Q; Q: {* OTopical Testosterone Exposure / Bhowmick et al 541% |# b  I  I& w+ ~: H& z
use of testosterone gel twice daily that he was apply-' X1 W9 Z# ]  ]2 s1 e
ing over his own shoulders, chest, and back area for4 n, L* j& n+ m( z
a year. The father also revealed he was embarrassed- V* `; R. u+ H/ Q) |" A! f# O
to disclose that he was using a testosterone gel pre-6 ~, ^  x. A$ u! G
scribed by his family physician for decreased libido+ A5 J( O1 H0 q' J; h( y
secondary to depression.0 T) ]6 n. B) z) `6 U
The child slept in the same bed with parents.: X& L/ G' G  J4 x1 J: J
The father would hug the baby and hold him on his8 g& p, {; k; P- J: }* A! d
chest for a considerable period of time, causing sig-
9 h' O% p; s" Znificant bare skin contact between baby and father.
$ k* d: q4 f" F, cThe father also admitted that after the phone call,3 F% H6 j4 A6 u. `4 m3 M
when he learned the testosterone level in the baby$ ?0 W% X+ U5 {& @5 G1 O% M9 \
was high, he then read the product information
4 m0 r7 f$ f5 k5 U" V  o/ spacket and concluded that it was most likely the rea-9 y& H+ `5 I5 {; F% _
son for the child’s virilization. At that time, they: q6 P0 Z: y7 B/ I
decided to put the baby in a separate bed, and the
9 [( ]$ t# F5 U& X& a0 e! Ofather was not hugging him with bare skin and had' D( k% ]& T) Y6 |, P. Y! _1 j
been using protective clothing. A repeat testosterone/ q" P2 Y# H. V0 f9 T
test was ordered, but the family did not go to the
" R% |# b; Y. o* s, J$ elaboratory to obtain the test.+ v& Q: v6 E7 {* u, K' A  E
Discussion
: F4 ]* w6 l( j* j0 s" H+ p6 u% {Precocious puberty in boys is defined as secondary
0 n# B5 A  y) tsexual development before 9 years of age.1,4
8 x) O" \4 t) RPrecocious puberty is termed as central (true) when8 G: [9 a2 W. ~7 ?2 w# D
it is caused by the premature activation of hypo-: u+ \2 }/ ^' r' K2 r8 ~- e8 I8 p
thalamic pituitary gonadal axis. CPP is more com-
3 ]1 A7 I6 T! m" Mmon in girls than in boys.1,3 Most boys with CPP  O% k  v' s/ C$ \0 L& V
may have a central nervous system lesion that is; w5 F! F3 J% {0 n
responsible for the early activation of the hypothal-5 E8 m* b1 S' H7 n6 w
amic pituitary gonadal axis.1-3 Thus, greater empha-5 u) i. K) l2 U) z/ `
sis has been given to neuroradiologic imaging in
( j1 i! {: G) L! y! W/ zboys with precocious puberty. In addition to viril-& E, q$ [- y1 s! R3 J9 D
ization, the clinical hallmark of CPP is the symmet-
" j8 E, G, ?( U6 h0 F! M1 D  @rical testicular growth secondary to stimulation by
1 x; j% Z0 X; igonadotropins.1,3; m3 l8 y; H1 a; m! Y1 r
Gonadotropin-independent peripheral preco-
9 K& B0 Y0 }8 i# g$ kcious puberty in boys also results from inappropriate. d* k4 \7 @  Y' D9 _) }! S4 o3 v
androgenic stimulation from either endogenous or
2 }) x$ Q* p7 S" R! Sexogenous sources, nonpituitary gonadotropin stim-1 j: e) z+ T0 t3 B" i( X! c
ulation, and rare activating mutations.3 Virilizing  }- Y, s* v( ~0 _8 J* h5 q
congenital adrenal hyperplasia producing excessive
, d- ^( X9 E# l0 V" d# i2 Xadrenal androgens is a common cause of precocious# u3 f9 e2 a7 f, F- g( J
puberty in boys.3,4) |/ k8 S5 M: ]) c% D! Q
The most common form of congenital adrenal. H8 P) \+ ^  C2 ?# y
hyperplasia is the 21-hydroxylase enzyme deficiency.
7 |3 Q" F* v* E; QThe 11-β hydroxylase deficiency may also result in; m  d! ]% [2 h5 V* s" x" n
excessive adrenal androgen production, and rarely,
5 O& d, p2 W( m3 P! z" Lan adrenal tumor may also cause adrenal androgen
1 \, ^7 Y4 }4 I7 c* A8 `excess.1,3% [. V+ E/ b& k
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
3 @+ w2 r  ?2 A; i# _- o542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
1 l! g( U" ]2 e( o$ _A unique entity of male-limited gonadotropin-
4 u4 `. u! M' F, Qindependent precocious puberty, which is also known* m; l2 S2 B' I' G
as testotoxicosis, may cause precocious puberty at a
/ u. `6 Z. F& y( E( Wvery young age. The physical findings in these boys. s+ }& i: w1 m, {- R
with this disorder are full pubertal development,
& t" Z' R' V  qincluding bilateral testicular growth, similar to boys
! x8 t* s: r: ]8 Z- Mwith CPP. The gonadotropin levels in this disorder; @. {! ?4 s  p% e# C& U8 R7 H
are suppressed to prepubertal levels and do not show5 p9 O0 A" q' c- y# V2 }. M
pubertal response of gonadotropin after gonadotropin-
0 N% k9 \8 a" _8 b, C( ?& Zreleasing hormone stimulation. This is a sex-linked/ ?9 Z; f) O9 T
autosomal dominant disorder that affects only
, f; T5 k- l/ X3 j4 t$ ~males; therefore, other male members of the family$ _5 }  {- M* d! y) T
may have similar precocious puberty.3
: ~" i- T$ B8 }: }( LIn our patient, physical examination was incon-# j1 F: U7 X$ H
sistent with true precocious puberty since his testi-
  N1 `1 {5 O" rcles were prepubertal in size. However, testotoxicosis" G/ o4 [- d* X3 K( M7 V
was in the differential diagnosis because his father0 C! V+ x1 \9 l: K
started puberty somewhat early, and occasionally,
, n% }. M( H! qtesticular enlargement is not that evident in the- A  L$ g6 K! z: M* p
beginning of this process.1 In the absence of a neg-  O+ y$ ?( y: v- }
ative initial history of androgen exposure, our' E! Q6 {# i0 M3 u  T) S
biggest concern was virilizing adrenal hyperplasia,) {! m; a, B$ ~
either 21-hydroxylase deficiency or 11-β hydroxylase
+ t, ]& \! L; R: Ddeficiency. Those diagnoses were excluded by find-) K9 |6 K; {# O# S+ q$ Z# {4 G8 H" `
ing the normal level of adrenal steroids.
" `7 V' H4 t) Y4 y, vThe diagnosis of exogenous androgens was strongly2 N1 c& k, Y6 G' {
suspected in a follow-up visit after 4 months because
9 ?; {5 A8 \& P" E$ o  d+ Kthe physical examination revealed the complete disap-
9 E* u; i1 Z; S" w# I5 ]pearance of pubic hair, normal growth velocity, and
  I6 M- P1 u& {$ bdecreased erections. The father admitted using a testos-
9 ^$ M: Q, p/ s5 W& eterone gel, which he concealed at first visit. He was; A3 T  a5 _  ~2 L6 P
using it rather frequently, twice a day. The Physicians’& a& T; ]1 R  D7 ^5 J
Desk Reference, or package insert of this product, gel or
8 N  ?, @) Z! O, v# x: ~cream, cautions about dermal testosterone transfer to( n% w. d5 r6 U6 J4 ?  ]" d1 U
unprotected females through direct skin exposure.
) [5 `9 g# z# ISerum testosterone level was found to be 2 times the3 ~' F# h0 u$ \
baseline value in those females who were exposed to* _' ^6 E. \2 c# e5 l$ T; \
even 15 minutes of direct skin contact with their male7 d7 m; R8 \3 I
partners.6 However, when a shirt covered the applica-$ N( P8 |9 u" B  D/ m2 T
tion site, this testosterone transfer was prevented.' V; V* W. K' o# o! X% A
Our patient’s testosterone level was 60 ng/mL,7 N4 u- M- k  q( \5 y6 c. p- R( T
which was clearly high. Some studies suggest that* M6 I6 u( Z% j
dermal conversion of testosterone to dihydrotestos-
; g; T) U. I5 fterone, which is a more potent metabolite, is more# D8 ?* D( L( J2 u8 p
active in young children exposed to testosterone
( Q8 m/ Z/ P! h- F: yexogenously7; however, we did not measure a dihy-
: _+ x4 P0 P( M; e0 I6 a) `drotestosterone level in our patient. In addition to' _; s, n: H! K. q+ Z, X$ D4 L
virilization, exposure to exogenous testosterone in( K) ~& R& s- P. u2 A
children results in an increase in growth velocity and5 \0 N% o  ~0 e. A3 N7 g7 a; y
advanced bone age, as seen in our patient.
. i& M$ J6 ^8 W6 mThe long-term effect of androgen exposure during
0 [, Z) K% q1 Xearly childhood on pubertal development and final
& ~7 w$ J8 c5 E6 v3 r# J& D& C5 Badult height are not fully known and always remain
( a) W$ J2 j1 xa concern. Children treated with short-term testos-
) J- v7 ~/ {9 u' G$ n& w. jterone injection or topical androgen may exhibit some% h3 k9 ]% ^8 `5 U( @* t, k3 J
acceleration of the skeletal maturation; however, after# J6 C. K3 _6 Q
cessation of treatment, the rate of bone maturation
# G9 q! D8 k( ldecelerates and gradually returns to normal.8,9; x% P% b! t7 }3 Y" T' E) x8 k
There are conflicting reports and controversy# ]! j! H& j. B, e* ?
over the effect of early androgen exposure on adult; @) T# Z3 G! J9 n( p/ F( _
penile length.10,11 Some reports suggest subnormal
; ~# p. w5 p- s6 R4 fadult penile length, apparently because of downreg-8 y  W4 E/ Y  x2 E5 g$ p
ulation of androgen receptor number.10,12 However,- t3 ^: {" M5 f& a  T
Sutherland et al13 did not find a correlation between
$ L" \4 g0 t7 k7 V2 r/ h, S: ichildhood testosterone exposure and reduced adult
0 g6 C* u1 G2 `  F& upenile length in clinical studies.
  i/ K& j! ]* `9 jNonetheless, we do not believe our patient is. x+ b; t- ]+ }+ u) T; K
going to experience any of the untoward effects from% D5 {5 d; ^; I9 G. j
testosterone exposure as mentioned earlier because
! }/ w% K4 S8 R. c3 gthe exposure was not for a prolonged period of time.8 ^/ S# i6 k# k) ^* J8 D8 ?
Although the bone age was advanced at the time of6 D: ^+ o* c; S0 G3 b
diagnosis, the child had a normal growth velocity at8 H1 ^3 L' f8 n: P! N
the follow-up visit. It is hoped that his final adult# ]! a: d' k) z8 N; K6 {0 z7 r9 N
height will not be affected.4 U( a# z- M6 Z* e2 u
Although rarely reported, the widespread avail-" c) y8 }8 q: m, `" s
ability of androgen products in our society may% a% j; S7 I0 v$ I% a4 @) V# d9 t
indeed cause more virilization in male or female
, D. G) f# Q+ }" k! wchildren than one would realize. Exposure to andro-
5 E' d1 A" _  N/ s& e+ e% K( _- Qgen products must be considered and specific ques-
8 T6 p5 r0 |1 e% P% N5 z6 v4 c# Ntioning about the use of a testosterone product or& O: ]8 n( I" T5 P" J6 w7 |
gel should be asked of the family members during
! Q2 j: a3 r$ K& zthe evaluation of any children who present with vir-: y6 ?( p7 {# P; f4 P
ilization or peripheral precocious puberty. The diag-. O2 S5 h1 W' C! U4 _  c/ u
nosis can be established by just a few tests and by+ W8 [* s8 \: ^. j0 Z, U
appropriate history. The inability to obtain such a- v% ]; F3 {4 p: z2 e, X3 B
history, or failure to ask the specific questions, may
, @  v7 M- E8 \result in extensive, unnecessary, and expensive, G7 ?. t  N& a; X
investigation. The primary care physician should be+ M1 c: ?; Z% i8 w8 @; g; O* a
aware of this fact, because most of these children
1 F! s5 e+ X8 Hmay initially present in their practice. The Physicians’8 Y  o# r6 V- ^& [# x% x
Desk Reference and package insert should also put a! O5 p3 o7 X% R0 D
warning about the virilizing effect on a male or
- o( z. z1 Y+ \) A$ A) dfemale child who might come in contact with some-" D* d4 a6 ~7 c
one using any of these products., ]: e  Z$ d, c  |! a3 `8 z
References& i0 j0 ]; P( b6 r* U# u( L$ K, J# N
1. Styne DM. The testes: disorder of sexual differentiation
; L$ ~. `; z# m" J. n) E5 jand puberty in the male. In: Sperling MA, ed. Pediatric$ P- A2 L/ B2 @* F/ n. f
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: l" w/ A+ X- D, }+ ]2002: 565-628.* w) e: T" \1 m& x3 _- s
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious* q3 l9 Z, h; X% N) R0 E* P* G
puberty in children with tumours of the suprasellar pineal
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這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
VIP精品區,資源無限好賺金任務區,輕松賺金幣
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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
VIP精品區,資源無限好賺金任務區,輕松賺金幣
加入VIP,享受高級特權宣傳賺金又升級,超級棒
4个什么样的?
發表於 2025-1-19 02:41:05 | 顯示全部樓層

; z2 A# K; S  S8 n  O. U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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