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Sexual Precocity in a 16-Month-Old* l/ R6 S' n. P) F
Boy Induced by Indirect Topical7 ~* z0 ~$ m/ L0 r
Exposure to Testosterone! g+ ^7 `3 L1 h; a/ I& w$ G
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,26 I9 v( B3 E3 H
and Kenneth R. Rettig, MD1- V) r: t) e1 o
Clinical Pediatrics, Y; c7 g3 ~; u+ E
Volume 46 Number 60 r- L. W. k3 k4 I
July 2007 540-543# Q9 j3 u, L! a6 E# _
© 2007 Sage Publications; d( x  _9 C) u4 N
10.1177/00099228062966516 u, W! v" Y4 L& l( A* Q+ M2 E
http://clp.sagepub.com
0 q) U. v0 o4 c+ }. [- x. c5 X$ z8 Ahosted at3 G' w+ d- J5 @3 Y. r5 J
http://online.sagepub.com& ^* }# Q3 ?+ I. t# n
Precocious puberty in boys, central or peripheral,, ?" N: U0 P0 o. h8 e! {; ]
is a significant concern for physicians. Central8 n! q% g0 M5 D
precocious puberty (CPP), which is mediated
+ z1 K- O7 J$ T3 w+ Dthrough the hypothalamic pituitary gonadal axis, has
8 G' G) D! v' t# k4 e5 R& A3 a# ]a higher incidence of organic central nervous system, E. [, L- ~: X; u- L0 ?
lesions in boys.1,2 Virilization in boys, as manifested6 K- L& F2 x; d+ s! e; {9 z
by enlargement of the penis, development of pubic$ e3 S/ m: e% T( i- }9 d
hair, and facial acne without enlargement of testi-3 v. E* N7 K% ], b' L2 G: f- O. ^
cles, suggests peripheral or pseudopuberty.1-3 We0 U5 [: H( ~7 h& K( C/ ~+ A
report a 16-month-old boy who presented with the, \+ i1 i" z4 g& L8 L# b! ^. i" H2 z
enlargement of the phallus and pubic hair develop-( q/ U) v# L* _
ment without testicular enlargement, which was due- p% n" I8 {+ z" _6 L
to the unintentional exposure to androgen gel used by$ l* }( T: g2 d5 P2 ]! s8 e
the father. The family initially concealed this infor-
' L$ \+ z" B! k: z5 w. b1 J$ Amation, resulting in an extensive work-up for this
, z) ~) N" ^# t. f  n+ D# pchild. Given the widespread and easy availability of/ L7 W+ Q* `/ m
testosterone gel and cream, we believe this is proba-
" w; ^, @! L" T; wbly more common than the rare case report in the1 w8 j, b6 F; r3 [2 O  ?6 [
literature.42 I+ [0 H( K. e# R/ H" X. S
Patient Report
2 g7 s$ _4 ?; h7 y. F* uA 16-month-old white child was referred to the
8 c- A+ U: R% E  Gendocrine clinic by his pediatrician with the concern
8 q# G; F+ Y" _7 T+ r8 J! W; Eof early sexual development. His mother noticed
# v9 r, {6 H( o' h  k7 glight colored pubic hair development when he was
4 t+ ~8 l1 G* N: Z. oFrom the 1Division of Pediatric Endocrinology, 2University of
- I: D9 p/ x  a0 |/ Y$ _8 uSouth Alabama Medical Center, Mobile, Alabama.
! I0 \" \" c- ^8 `Address correspondence to: Samar K. Bhowmick, MD, FACE,$ P+ }. x; L" _6 t
Professor of Pediatrics, University of South Alabama, College of
& z8 L/ K; t" e$ IMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ e3 V, z5 ?; T" u; d8 d  Y4 me-mail: [email protected].' }0 ~4 i2 |$ ]4 G. u9 x* o. C
about 6 to 7 months old, which progressively became
* t7 w( X$ W! W$ {; ~6 t' X5 Udarker. She was also concerned about the enlarge-
, h9 C9 v& d( @ment of his penis and frequent erections. The child* N1 o1 J. b& w- W
was the product of a full-term normal delivery, with7 z5 R" N& A0 i5 l) r
a birth weight of 7 lb 14 oz, and birth length of
( `- }4 S7 a6 g! }. r20 inches. He was breast-fed throughout the first year
" Q2 l- f  r. c5 yof life and was still receiving breast milk along with
/ j1 N' ?2 D0 P, [+ T( [9 G# Xsolid food. He had no hospitalizations or surgery,
) k! D' D9 h9 j9 Oand his psychosocial and psychomotor development
. B. t9 m5 q* h6 n' O/ D! Y# H& wwas age appropriate., O7 @% m2 b% e% Y9 h
The family history was remarkable for the father,
4 {1 K+ S4 K% B6 r% t9 C/ ]who was diagnosed with hypothyroidism at age 16,
  H" s( S) ]- p8 D+ H6 I8 T# Z# s. x" cwhich was treated with thyroxine. The father’s
- r9 G1 C: z3 s) @; ]- ?height was 6 feet, and he went through a somewhat
8 H; ~- M' G% t* `: Z6 yearly puberty and had stopped growing by age 14.
" ^2 n6 e1 k" u. P. O7 }9 dThe father denied taking any other medication. The2 ]  F2 q* c5 m2 T& Y1 a
child’s mother was in good health. Her menarche
0 F+ o* n) [+ c8 swas at 11 years of age, and her height was at 5 feet
; m% b* c, e* ^$ k% h* x5 inches. There was no other family history of pre-
* J& b: |" s# Ncocious sexual development in the first-degree rela-
) ^7 L$ f3 B  Z4 g' F1 Ntives. There were no siblings.
* f% Z6 L' Y# [+ c% K: OPhysical Examination
* d5 {+ Z0 i7 ~& C: yThe physical examination revealed a very active,; i. _3 Y+ \$ s) d0 S
playful, and healthy boy. The vital signs documented; j" ^) ^6 t0 p, u$ L6 p' m
a blood pressure of 85/50 mm Hg, his length was' X# g1 a; p4 j& T  D* ~  i- X
90 cm (>97th percentile), and his weight was 14.4 kg
8 E- j4 Z% F- P7 N& n(also >97th percentile). The observed yearly growth: u0 H4 h% W8 Q/ w0 x
velocity was 30 cm (12 inches). The examination of
" k+ d( n4 Y7 J* D5 kthe neck revealed no thyroid enlargement.
& n0 N& [# `" V* q/ V0 _The genitourinary examination was remarkable for% g" J( L8 T5 }, ]" H
enlargement of the penis, with a stretched length of3 B! H" c1 }7 C7 J
8 cm and a width of 2 cm. The glans penis was very well) O! E0 ]0 E3 X) I. p2 Z7 d' x2 M& _
developed. The pubic hair was Tanner II, mostly around( X: `- c& j7 x  @7 j5 N0 I
5402 t2 ?0 K6 X: N6 _
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" i# G0 @3 {  Y4 z* ^0 q0 n! M
the base of the phallus and was dark and curled. The. S! \: w1 y% ~) I# v; c1 H  P! |
testicular volume was prepubertal at 2 mL each.
% U, v& V' V3 dThe skin was moist and smooth and somewhat/ e( q  A7 m0 b% W/ w3 l) T3 z
oily. No axillary hair was noted. There were no. L' \8 m8 o1 |, _. \
abnormal skin pigmentations or café-au-lait spots.# x0 `# ?5 |* {9 E8 b
Neurologic evaluation showed deep tendon reflex 2+
0 O! f7 e- G9 [" s% Xbilateral and symmetrical. There was no suggestion
8 U. O0 g& W7 k0 T8 Jof papilledema.: h2 k* x- u0 l8 s
Laboratory Evaluation3 B/ h, d0 K( ~; @- _9 H1 J' S/ O
The bone age was consistent with 28 months by2 j1 J1 r  }' z
using the standard of Greulich and Pyle at a chrono-9 I7 j( n! m+ T+ H3 p4 E* ?5 c8 n
logic age of 16 months (advanced).5 Chromosomal3 y4 O  F* b; u+ L  E
karyotype was 46XY. The thyroid function test
! h0 I" ^3 f, X* L  S# m/ P. y' B; bshowed a free T4 of 1.69 ng/dL, and thyroid stimu-" Q* `8 L$ g* l# P
lating hormone level was 1.3 µIU/mL (both normal)./ N# ~: l7 ]% y2 J: {8 @  d& P6 g
The concentrations of serum electrolytes, blood0 k% @* {) U) ~5 b# b3 ~4 ?
urea nitrogen, creatinine, and calcium all were+ W& N7 w2 B. n
within normal range for his age. The concentration" [$ Y9 v1 q" J2 G3 W4 a$ d1 D. E
of serum 17-hydroxyprogesterone was 16 ng/dL
" p' y! d% v# m# U4 L(normal, 3 to 90 ng/dL), androstenedione was 20& B0 \: E/ k( C1 M' `
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-$ d4 |/ T- c2 H6 i3 {
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
0 d$ h$ f! ?* U" b) M) vdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
5 V# f7 Z) K( c49ng/dL), 11-desoxycortisol (specific compound S)* s0 l; k5 T8 h  r% R6 G; w
was 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
& r; d; F7 t) _" ptisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total  b) S5 F( L! G0 N1 H
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
- {/ C# h, o# Y/ [3 n$ m3 zand β-human chorionic gonadotropin was less than
5 |: ~) s0 d+ _5 mIU/mL (normal <5 mIU/mL). Serum follicular9 x6 K/ C; g  p$ s4 Z6 u% ~
stimulating hormone and leuteinizing hormone
) D5 e$ T1 M5 }% }% B0 U- Lconcentrations were less than 0.05 mIU/mL3 |3 |: `' y0 j& N  A
(prepubertal).
; n/ A6 ~  x3 ]" T, h. ]( FThe parents were notified about the laboratory( w$ w& i* L# Z' _: W- w
results and were informed that all of the tests were- k" J4 A, A6 S$ K% Z
normal except the testosterone level was high. The
( [" i8 A. p: S% Mfollow-up visit was arranged within a few weeks to8 Y& n" E/ G% X( h6 N( T
obtain testicular and abdominal sonograms; how-
+ v, {. {: t9 T/ f5 E+ C: G, w0 gever, the family did not return for 4 months.6 S' ^1 H6 B  L7 G7 \
Physical examination at this time revealed that the
& G' T4 a& O/ Q+ S# M+ Zchild had grown 2.5 cm in 4 months and had gained
* r* A7 Q0 [0 F0 X+ \5 s8 [2 kg of weight. Physical examination remained
) y( Y, b6 Q7 l* munchanged. Surprisingly, the pubic hair almost com-
- w7 y# W/ k0 z6 V9 n' |& epletely disappeared except for a few vellous hairs at
, ^$ |& u9 t2 ~6 t2 G9 othe base of the phallus. Testicular volume was still 2
. j( r% _$ ^8 vmL, and the size of the penis remained unchanged.+ N" y$ \. B: G& n: ]6 z. l5 v
The mother also said that the boy was no longer hav-
: F- s6 W0 @9 v6 O. ~0 Ling frequent erections.# s9 z3 l9 C1 e/ S& X8 O
Both parents were again questioned about use of+ P! [" T- o: G
any ointment/creams that they may have applied to
" d" T$ {& c; vthe child’s skin. This time the father admitted the
4 [& y# p; c  d+ h1 MTopical Testosterone Exposure / Bhowmick et al 541' u' B) e/ Q" l. k) C
use of testosterone gel twice daily that he was apply-5 F% j( Q8 q/ w" H
ing over his own shoulders, chest, and back area for
& o& v$ A+ p6 O/ ea year. The father also revealed he was embarrassed
  \" J! [0 r- H1 ?3 w& Vto disclose that he was using a testosterone gel pre-
* o* ?" s. v+ Xscribed by his family physician for decreased libido
- p* w! M" _- m5 U5 d4 rsecondary to depression.( G2 F- \2 K1 L
The child slept in the same bed with parents.
, g* @7 U5 [. d" f+ E4 [- ?: tThe father would hug the baby and hold him on his
' {; a8 V* p* a. K- F* ]: E+ A  h' Xchest for a considerable period of time, causing sig-
2 `6 q* p, x8 P6 K8 I3 }nificant bare skin contact between baby and father.
0 y$ E+ p2 n$ z' D% D7 TThe father also admitted that after the phone call,( X& T$ X- u: ~: }2 b6 d  H
when he learned the testosterone level in the baby
8 f/ [/ l, q4 E2 z0 ~2 z- V1 ?9 xwas high, he then read the product information
0 M  _% p9 m% dpacket and concluded that it was most likely the rea-6 g" D( v9 x( M# L
son for the child’s virilization. At that time, they
. t1 _" @1 L& |& I& N" H# E) mdecided to put the baby in a separate bed, and the  b4 f( O8 y) W- g4 M5 @: p; P" V
father was not hugging him with bare skin and had- t8 `" L3 ?, r2 @' n
been using protective clothing. A repeat testosterone
: g2 S' N1 Q8 |  B: qtest was ordered, but the family did not go to the; l/ a6 d4 z* x
laboratory to obtain the test.
& h* _$ k) P% _4 t4 G7 sDiscussion
: p2 Z( T" N9 sPrecocious puberty in boys is defined as secondary  W$ n' w* R2 t8 t$ f  G
sexual development before 9 years of age.1,4
% h4 [" t3 V/ d2 l: qPrecocious puberty is termed as central (true) when
% g9 u7 g2 L# g. D8 I9 |it is caused by the premature activation of hypo-3 `% Z9 e# o# I  V! P
thalamic pituitary gonadal axis. CPP is more com-+ ]" W4 d3 P9 z
mon in girls than in boys.1,3 Most boys with CPP1 Y+ F5 Z* z, P# t% ]0 T, L
may have a central nervous system lesion that is
% ^/ Z; _2 v2 n, u4 D6 p2 Zresponsible for the early activation of the hypothal-- N# z7 A! r# t  U9 q, ^7 c) g
amic pituitary gonadal axis.1-3 Thus, greater empha-2 T, I; q* R: S8 m2 ~( ?: l4 E
sis has been given to neuroradiologic imaging in
8 n/ K$ C+ K& Tboys with precocious puberty. In addition to viril-
( C6 V8 U  l+ l- mization, the clinical hallmark of CPP is the symmet-
7 m$ [; i$ t9 \5 Mrical testicular growth secondary to stimulation by5 z* H' T* d6 h( ]5 R9 e- G
gonadotropins.1,3
7 q, }; I7 K! k3 [6 x. \( GGonadotropin-independent peripheral preco-
; }) |1 E, e9 Q/ q" W5 h6 W! Bcious puberty in boys also results from inappropriate
5 {. U* g7 S* p( e+ C( Sandrogenic stimulation from either endogenous or
* \. i. N3 x# b, bexogenous sources, nonpituitary gonadotropin stim-" G: K  g6 W2 ]; X* A3 Z5 A% e: p+ S) ~
ulation, and rare activating mutations.3 Virilizing. z" u1 ]+ h4 Q' j+ G# [+ p
congenital adrenal hyperplasia producing excessive$ M6 l$ p/ l2 x* y$ q
adrenal androgens is a common cause of precocious
, }+ t! X# n: @" {% ^& |puberty in boys.3,4& V2 P) S9 f$ a# M
The most common form of congenital adrenal
0 W5 \# w0 I' S* Zhyperplasia is the 21-hydroxylase enzyme deficiency.
$ @( w2 u+ E3 K" I- M0 X6 k1 y1 MThe 11-β hydroxylase deficiency may also result in
2 t. J- _& j9 Z$ Oexcessive adrenal androgen production, and rarely,
+ a  \0 v9 Z: n  K% O$ oan adrenal tumor may also cause adrenal androgen
0 ^8 Y( |1 F( s; {, }) q/ L$ Lexcess.1,3
/ E8 }6 w, I; g" O0 c/ Iat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
! N8 ]# T6 d" {8 P542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' x8 n) a/ _6 l& `9 TA unique entity of male-limited gonadotropin-! L2 }6 x9 o  E. j+ x
independent precocious puberty, which is also known
8 i4 T7 h& {7 _& X4 H8 Yas testotoxicosis, may cause precocious puberty at a
6 `' R+ y# q/ F1 J+ [very young age. The physical findings in these boys' J( L+ B$ p% U- s/ H* v5 Y1 j" W0 w
with this disorder are full pubertal development," ?6 z% a( C& p- ^8 F, Q
including bilateral testicular growth, similar to boys  M" p( v0 ]3 s7 V! T4 R! m7 i: M% O
with CPP. The gonadotropin levels in this disorder
% Q* H. F& B8 P* r0 @are suppressed to prepubertal levels and do not show
8 t9 n- @# B7 M& K% ^- n6 I8 _3 Z: |pubertal response of gonadotropin after gonadotropin-
6 Y" T8 b  B2 C- f. U/ Q. w& T2 t& Areleasing hormone stimulation. This is a sex-linked5 v2 s7 }/ ~* x  h! V
autosomal dominant disorder that affects only3 C0 Z7 x  A, b- D% B8 L  j* w6 C) ?
males; therefore, other male members of the family0 l3 i& B3 N  a/ u7 p' W# C' T2 K3 [
may have similar precocious puberty.39 x5 D# R* M4 k+ d, [/ \7 g$ @5 @6 k
In our patient, physical examination was incon-
! T" }) ?' }% I/ }6 g) b% s; G; _6 Hsistent with true precocious puberty since his testi-
; E) K2 c' X! A8 O5 ucles were prepubertal in size. However, testotoxicosis5 C- U. N+ o; t! G! l# j0 n8 N
was in the differential diagnosis because his father
9 |. J  O" J7 p8 cstarted puberty somewhat early, and occasionally,
' D2 p7 D) X; F: l* m4 B0 ?' ?" etesticular enlargement is not that evident in the
- ]! i; ?8 m6 k3 c5 ybeginning of this process.1 In the absence of a neg-
- E) C* j# Y: F/ o3 f7 Wative initial history of androgen exposure, our
- l+ s/ l6 v3 J! e$ qbiggest concern was virilizing adrenal hyperplasia,
% w1 {  U1 }1 D5 f+ I: I/ \either 21-hydroxylase deficiency or 11-β hydroxylase
+ W, t! ~  f; Z0 Ddeficiency. Those diagnoses were excluded by find-
- Q! ]) P4 ^* `( u* y, v4 k9 Ving the normal level of adrenal steroids.% m$ j1 p9 v# D0 N
The diagnosis of exogenous androgens was strongly
3 W& f& f. v6 k! G" ?- z: xsuspected in a follow-up visit after 4 months because6 V6 |  b  E- {/ U! W' D
the physical examination revealed the complete disap-
7 Q9 F# l! u; H* x" q- Zpearance of pubic hair, normal growth velocity, and* {# C$ q7 Q& I$ _6 X& i7 m. Z
decreased erections. The father admitted using a testos-' U1 `% r# z, `3 u1 V
terone gel, which he concealed at first visit. He was
. V# ]# Y' [/ S/ k9 T% `* dusing it rather frequently, twice a day. The Physicians’$ m3 f+ k. i8 B( C9 C! z" e( T
Desk Reference, or package insert of this product, gel or
) W7 x: N9 f( t1 j! \1 s' Ecream, cautions about dermal testosterone transfer to' Y. C5 h+ q0 g$ a0 [
unprotected females through direct skin exposure.
7 a# o+ ?8 h6 |$ x  ]+ CSerum testosterone level was found to be 2 times the
% G; V) {; s3 G2 C- H0 ]+ |baseline value in those females who were exposed to, ?0 E% i. Q' c
even 15 minutes of direct skin contact with their male
$ P" t* \( W6 p+ t, t) F. Mpartners.6 However, when a shirt covered the applica-
6 n, w* u6 w# p& xtion site, this testosterone transfer was prevented.
4 [, k9 `9 h9 cOur patient’s testosterone level was 60 ng/mL,$ B9 c( K, b& W! H
which was clearly high. Some studies suggest that
$ W/ s2 B) R* C6 Fdermal conversion of testosterone to dihydrotestos-
' e/ i& L8 m. [! cterone, which is a more potent metabolite, is more. \3 u3 z$ r4 Z( i3 ^& S
active in young children exposed to testosterone% ~5 b8 H8 i# z* ]" K
exogenously7; however, we did not measure a dihy-& G) ?. J; D' O1 |1 U
drotestosterone level in our patient. In addition to
2 ^0 X$ Z+ x* m+ a- F. Ovirilization, exposure to exogenous testosterone in
* p6 F2 t+ j! N8 ~- Vchildren results in an increase in growth velocity and% i6 h  n# W  o& |/ ?
advanced bone age, as seen in our patient.. w6 L) ^: X: v9 s: ]
The long-term effect of androgen exposure during4 R( T- i5 r1 p
early childhood on pubertal development and final
9 d. ?+ A8 ]' L/ w0 X5 K8 h1 W! Vadult height are not fully known and always remain. F9 C* s; r) i2 n& D
a concern. Children treated with short-term testos-
6 ^; U6 `; W& Z. P8 ~& dterone injection or topical androgen may exhibit some* C: J" C: z8 g9 _* m
acceleration of the skeletal maturation; however, after
/ Z! `9 H! {, I+ [8 W3 rcessation of treatment, the rate of bone maturation$ y$ E& w1 u, H& m3 Y- Y0 _1 `
decelerates and gradually returns to normal.8,9. ?7 W/ ^/ F% E; j" j* j4 s2 A4 M; c
There are conflicting reports and controversy
% {. p: ?* c8 \: K8 yover the effect of early androgen exposure on adult. |  V# h7 z. P( l' n6 r/ I2 W2 H
penile length.10,11 Some reports suggest subnormal# p+ R& a' N0 L: z6 C- C
adult penile length, apparently because of downreg-
' h" m0 g# {* U0 L* [+ R# Gulation of androgen receptor number.10,12 However,5 `) A0 Z2 A3 i" k  g% ?% d" V
Sutherland et al13 did not find a correlation between
* C/ W3 S% {5 |' `; f+ }$ ]childhood testosterone exposure and reduced adult
; ?) Y& V) ?" V& epenile length in clinical studies.
  m5 r* n3 ], [0 r3 N6 _. W% [9 qNonetheless, we do not believe our patient is
5 ~6 n7 a/ r( ]' o. Ggoing to experience any of the untoward effects from: e4 p& j. l4 q% z. @; P6 C( T
testosterone exposure as mentioned earlier because
4 G2 [( r  g  a8 @& }the exposure was not for a prolonged period of time.% r' i6 |! }! `' v6 I2 Y
Although the bone age was advanced at the time of
: m/ \; g5 i. D( w$ B* ldiagnosis, the child had a normal growth velocity at' F/ ^* K$ P* j7 W: @" ^. k$ z
the follow-up visit. It is hoped that his final adult% @0 C7 {6 N: W- t" S
height will not be affected.
# B- v6 ]' D6 {, \3 B) ~Although rarely reported, the widespread avail-/ h7 \" a+ ]  m  \
ability of androgen products in our society may! t8 {+ U; T$ y. M
indeed cause more virilization in male or female
4 C8 G( K" L- ~0 t( Tchildren than one would realize. Exposure to andro-
( K! l! e3 b! Y9 Agen products must be considered and specific ques-" ]# a# V/ Y8 h+ \, G* ]4 F* N# |1 c
tioning about the use of a testosterone product or+ `  @$ E9 q( a3 R& V' c
gel should be asked of the family members during3 |2 I) V0 l5 a8 C' n
the evaluation of any children who present with vir-
- i# }, Q8 e  B: L7 \1 Nilization or peripheral precocious puberty. The diag-0 M) R! a6 x6 G
nosis can be established by just a few tests and by$ G5 O) E6 Q8 `8 W% o
appropriate history. The inability to obtain such a
* E0 H8 N* E5 Lhistory, or failure to ask the specific questions, may
( x# X  O) O7 v  w' N' ?( ?) Zresult in extensive, unnecessary, and expensive
3 U$ C, ]' U$ e2 Qinvestigation. The primary care physician should be
) c8 W) O' w2 }. V6 t/ vaware of this fact, because most of these children- h% N: U) s' g  {9 C
may initially present in their practice. The Physicians’' r8 T- I9 A8 ^3 }) U/ C
Desk Reference and package insert should also put a7 ?8 G; }5 N, C; x6 a
warning about the virilizing effect on a male or
$ E) N, }8 [! f3 i' Lfemale child who might come in contact with some-
* K$ M% q  B0 f# G$ H8 @4 }one using any of these products.  _1 ~  h  u: Z# w2 U8 m
References
( W  ?6 u/ W: h6 K1. Styne DM. The testes: disorder of sexual differentiation2 q  M) h& J+ X% k, J7 c
and puberty in the male. In: Sperling MA, ed. Pediatric
" K) @3 c# k4 h- [3 yEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;# j  }% w* O0 }5 z* R
2002: 565-628.7 P9 K+ v/ t2 c. T1 ^% H& s
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious0 s# g' @- }1 X4 V5 G
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old
/ S3 |4 @. |+ N2 }Boy Induced by Indirect Topical' V' k6 n3 C" X1 c. o
Exposure to Testosterone
5 u6 {/ g& F  n( Z) s6 C: ~Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2. p. C% s" J( j( C
and Kenneth R. Rettig, MD1
: H; @( {; o+ K) m2 t- {) r8 L; qClinical Pediatrics
, Z7 G8 G, C" Q+ ]Volume 46 Number 6. W) q' f( c2 K7 d
July 2007 540-543
. S9 a% r9 X5 \( W2 v0 ], W" K© 2007 Sage Publications
# s% K( ^/ F& p& U: N" n10.1177/0009922806296651
) S" [* O' U8 C" _http://clp.sagepub.com
) |; J: E9 ~8 M+ Y: J8 `* ~hosted at
# u0 o: |7 u) a) y: ~+ Nhttp://online.sagepub.com+ \) q7 x3 ?+ c( h
Precocious puberty in boys, central or peripheral,
% R) R$ X/ \5 R5 Q) v2 Tis a significant concern for physicians. Central
3 n" i# ?: i3 yprecocious puberty (CPP), which is mediated
& b: p, N, a/ t9 ~7 Cthrough the hypothalamic pituitary gonadal axis, has
; G7 M- \6 X( i. U5 Ta higher incidence of organic central nervous system/ a- F% K9 ?# U8 y: F
lesions in boys.1,2 Virilization in boys, as manifested( Y9 m$ p( [$ G
by enlargement of the penis, development of pubic* h1 i/ ~( I3 s/ }
hair, and facial acne without enlargement of testi-
0 f9 R* [# N7 X4 _6 U4 bcles, suggests peripheral or pseudopuberty.1-3 We; L1 G7 Z. v( [# {* t! f
report a 16-month-old boy who presented with the
' z$ y. f8 E; ?; Z$ Penlargement of the phallus and pubic hair develop-* \& Y4 `# N# ?) T' P
ment without testicular enlargement, which was due
3 d# m: _- k8 G8 G! g/ @to the unintentional exposure to androgen gel used by% l/ B5 q; O7 Q) D6 B8 c1 l
the father. The family initially concealed this infor-
8 ?+ w7 w2 j, S- Mmation, resulting in an extensive work-up for this0 v/ ?' }& h% r3 V1 @. K1 n% A
child. Given the widespread and easy availability of) V* c" a$ j# a0 X: J& d% O, U  [
testosterone gel and cream, we believe this is proba-; F9 ?) f& B$ x+ m: F+ y
bly more common than the rare case report in the0 |$ V: S& _4 R& \) o6 z# h
literature.4
$ t6 [; _! I  `. s6 _* X: D+ `Patient Report
/ Q7 T" R, g  S6 j1 w/ R0 O4 ^2 B0 J% wA 16-month-old white child was referred to the: U9 Q2 W7 d+ S& I
endocrine clinic by his pediatrician with the concern
' }6 g7 M1 o2 L' H" n; l' oof early sexual development. His mother noticed) W7 R& i2 ?3 s
light colored pubic hair development when he was
( p  j/ j5 E6 c; e$ q0 ZFrom the 1Division of Pediatric Endocrinology, 2University of8 j" p) \. j1 y1 F) H% a4 }
South Alabama Medical Center, Mobile, Alabama.* i. w) {  T! I# R
Address correspondence to: Samar K. Bhowmick, MD, FACE,
) e  a0 m" b1 m* J- U, y# uProfessor of Pediatrics, University of South Alabama, College of
( P0 `/ B/ E+ t7 kMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;6 @: Z7 Y+ i$ Z! `/ |" a
e-mail: [email protected].
% u5 b: c; w9 t3 P2 b8 Sabout 6 to 7 months old, which progressively became6 @/ _: E: U! B( v
darker. She was also concerned about the enlarge-
! o  R5 O8 L# j" ?+ s) z6 I0 ?ment of his penis and frequent erections. The child
) \7 g  e6 e3 D3 f2 j! iwas the product of a full-term normal delivery, with9 r% S% z1 ^* \* A
a birth weight of 7 lb 14 oz, and birth length of/ t; W  z+ r2 B1 s8 G* B
20 inches. He was breast-fed throughout the first year
) Z$ ]$ ?6 J( P: u7 `2 g) Lof life and was still receiving breast milk along with$ J) r. v1 h" a( c$ _
solid food. He had no hospitalizations or surgery,. _: K7 @" d% K; `0 |% ]
and his psychosocial and psychomotor development
. p1 T5 [$ Y( o- Rwas age appropriate.
8 w0 D, W/ d; ]5 ]# e6 v8 bThe family history was remarkable for the father,6 ]  l2 A; d. u! A2 ~. v
who was diagnosed with hypothyroidism at age 16,
9 u. {6 B: W& F1 V: u: m6 ^which was treated with thyroxine. The father’s
) ]- s. ?4 Y9 v) G2 t' r8 S  ?6 F, C/ eheight was 6 feet, and he went through a somewhat
( ?9 {/ d& ]! v% {+ Aearly puberty and had stopped growing by age 14.
" R: t* }$ w* X! A# g& v5 CThe father denied taking any other medication. The
8 |# s" X4 M& uchild’s mother was in good health. Her menarche
2 M/ J, U7 q" W- m1 Wwas at 11 years of age, and her height was at 5 feet
8 j7 Q( s, Z! Z0 k' @& A5 ?5 inches. There was no other family history of pre-
6 }1 r0 b" c6 @cocious sexual development in the first-degree rela-6 H; o" [+ l% k8 t4 [0 k
tives. There were no siblings.4 a; X" R/ I/ f! H' W5 w1 C
Physical Examination" Q/ y5 ?  [/ S+ M
The physical examination revealed a very active,
/ o6 O6 R# h1 Zplayful, and healthy boy. The vital signs documented
& l* r  B" L6 @. R3 y, \/ [, za blood pressure of 85/50 mm Hg, his length was' d; \- [# F: R; w% O. ?" I
90 cm (>97th percentile), and his weight was 14.4 kg# D% Y2 q! i2 }: ^' n+ C: u+ H
(also >97th percentile). The observed yearly growth( W6 ~, ]2 ~- E+ p2 f( k
velocity was 30 cm (12 inches). The examination of
, s4 g" X7 w+ U$ _6 Xthe neck revealed no thyroid enlargement.8 C3 w* J- B& D) l
The genitourinary examination was remarkable for0 @1 `0 V& ?3 ~0 c* {4 O
enlargement of the penis, with a stretched length of
0 ]. ]+ V3 a1 e& r3 }8 cm and a width of 2 cm. The glans penis was very well
0 `  g9 G5 K6 O6 t$ ddeveloped. The pubic hair was Tanner II, mostly around
: r2 O8 W+ D/ V; Z  R% x; O540
1 O9 P; P# K& }3 x1 W5 aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from* l6 A4 _! S' I% t8 J  v2 h* x6 k3 k
the base of the phallus and was dark and curled. The
/ {2 F: r. g+ T! U) H& ]. o5 Ntesticular volume was prepubertal at 2 mL each.) q$ C! p/ E: H# l
The skin was moist and smooth and somewhat( i$ a0 q0 ]" u9 W. O/ e
oily. No axillary hair was noted. There were no5 A! S( A& V8 J1 N) Z* v, \3 `
abnormal skin pigmentations or café-au-lait spots.* M' ~+ {* S1 @# i/ M
Neurologic evaluation showed deep tendon reflex 2+9 d* P! ]  {+ K9 T5 v+ c8 v% A
bilateral and symmetrical. There was no suggestion$ J- O! P5 Z1 Q
of papilledema.6 L- h" \/ d' M+ `0 {, }
Laboratory Evaluation
( r# U4 s; }; y- ^( I: iThe bone age was consistent with 28 months by
) }3 u  ^4 B; [' {% A1 e2 Rusing the standard of Greulich and Pyle at a chrono-# t+ l4 ~  F1 Y" a
logic age of 16 months (advanced).5 Chromosomal
# L; u( W+ f; V# @( w' f9 s- mkaryotype was 46XY. The thyroid function test
( r# L9 W0 d6 Q& wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
+ _: z( C) z3 h4 v; r% klating hormone level was 1.3 µIU/mL (both normal).
% [3 d, O! k+ H$ v, O0 Y) t9 YThe concentrations of serum electrolytes, blood
2 M' F. u2 Y( V/ K" P3 Nurea nitrogen, creatinine, and calcium all were
2 L0 }2 z6 h6 Owithin normal range for his age. The concentration
8 o3 p. g3 r3 r- E+ O- f1 M8 xof serum 17-hydroxyprogesterone was 16 ng/dL
2 H) L. l6 M* k(normal, 3 to 90 ng/dL), androstenedione was 20
% x+ _; K1 }. ong/dL (normal, 18 to 80 ng/dL), dehydroepiandros-
6 t' z" u4 ]% X8 `, D5 Rterone was 38 ng/dL (normal, 50 to 760 ng/dL),
6 o4 w) M9 j* w( [& L8 kdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
0 j- H8 q4 R' l49ng/dL), 11-desoxycortisol (specific compound S)
% k; A+ x- j( S) V) ywas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-0 I5 R4 |! O3 e$ A
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
3 [6 I2 C/ ]/ h6 e+ I) ttestosterone was 60 ng/dL (normal <3 to 10 ng/dL),- ]1 \9 Z% a1 o- z; X; [: b! M& A/ M
and β-human chorionic gonadotropin was less than  I! _" \" P% ]) e' w+ \
5 mIU/mL (normal <5 mIU/mL). Serum follicular% P' j# K( ~7 q5 N
stimulating hormone and leuteinizing hormone2 w3 \, v; w0 K4 w0 L
concentrations were less than 0.05 mIU/mL
, \- {- b( |. A7 ?- Q% n0 U(prepubertal).
8 S5 H; Q' b- i* F( L2 fThe parents were notified about the laboratory) {' V0 _0 F; N2 Q( U1 ]# T
results and were informed that all of the tests were* C$ T  |; Z% J9 D
normal except the testosterone level was high. The+ K1 u+ o  |$ J7 W; C
follow-up visit was arranged within a few weeks to
1 `8 @$ f; j4 w5 A; x# s( Aobtain testicular and abdominal sonograms; how-. K2 ]" n' x% @: @' d$ \
ever, the family did not return for 4 months.( r7 {+ t: e8 ^' l! {
Physical examination at this time revealed that the' |; s" e/ u3 Y1 T1 Q
child had grown 2.5 cm in 4 months and had gained9 x+ U6 u9 y4 H
2 kg of weight. Physical examination remained& S) ?7 @/ o! P5 P6 |7 h
unchanged. Surprisingly, the pubic hair almost com-" b6 ~( a* d  P; W$ M( Q
pletely disappeared except for a few vellous hairs at
1 b7 p: e, `& z* Z5 S- Y! ?" A; y1 mthe base of the phallus. Testicular volume was still 2
! O8 W4 z. F: V0 i; LmL, and the size of the penis remained unchanged.4 G5 p% E( q& o/ ]2 \3 h  a- ^
The mother also said that the boy was no longer hav-5 G. v- y; _3 S$ O* U5 s
ing frequent erections.
0 [" M7 G  |1 m& z9 EBoth parents were again questioned about use of/ t) M+ C5 E3 \
any ointment/creams that they may have applied to! z  d7 ^9 z/ @2 D* k" [
the child’s skin. This time the father admitted the
; m3 \# y& V$ L" FTopical Testosterone Exposure / Bhowmick et al 541
' {! B- X6 a0 Yuse of testosterone gel twice daily that he was apply-
9 l- n) a9 S4 ^+ }! r" C; Ting over his own shoulders, chest, and back area for; G8 Y( a2 X, S# n" e" G
a year. The father also revealed he was embarrassed0 Z( j8 G" V, v  t$ W
to disclose that he was using a testosterone gel pre-
, x$ a5 g% Z; a$ R, ?scribed by his family physician for decreased libido& G2 x: Y. f9 s/ q% R6 }
secondary to depression.0 e6 {5 h; K% |& s1 K
The child slept in the same bed with parents.* h5 E! {4 \; q# n0 X
The father would hug the baby and hold him on his  P' E+ F& @  T
chest for a considerable period of time, causing sig-- X/ ?% ~3 p+ W9 k( ?% N
nificant bare skin contact between baby and father.9 T$ I* G* `' _  P
The father also admitted that after the phone call,
1 J2 h; Y8 Z: i8 r9 ?when he learned the testosterone level in the baby
1 {, N' ?" a; y, Q3 Twas high, he then read the product information8 r2 |+ i- T# B9 r
packet and concluded that it was most likely the rea-
" x' f- n7 n9 _$ ?% E6 \8 t! }/ |  Bson for the child’s virilization. At that time, they9 r0 y# Z6 J# T4 ~0 |. F0 c  b
decided to put the baby in a separate bed, and the
) o% N6 r4 D- M: p$ Hfather was not hugging him with bare skin and had5 f9 {3 S0 l  b# g/ ^6 Y
been using protective clothing. A repeat testosterone& x  D+ r! B& i$ N0 M; u% Q
test was ordered, but the family did not go to the0 h* q" H" {) K" |
laboratory to obtain the test.
( e7 L% |  z: H$ ?0 z7 cDiscussion! v2 A+ Z4 v# n  \  S3 w: `
Precocious puberty in boys is defined as secondary: K. \& [$ T1 R' J3 i! n
sexual development before 9 years of age.1,4
4 z, L0 p' ^4 k  X2 {& ?- OPrecocious puberty is termed as central (true) when
( K9 m4 Q' ~; K. {& Nit is caused by the premature activation of hypo-( k- A0 S/ t$ K( }9 k0 h: A
thalamic pituitary gonadal axis. CPP is more com-( ^  X  I; c9 a
mon in girls than in boys.1,3 Most boys with CPP
) ~, m+ w. N; Q8 F/ L* D4 imay have a central nervous system lesion that is
5 h# o; F, `$ P, T( b7 k+ b3 Cresponsible for the early activation of the hypothal-3 Y% R2 W3 k$ d- g
amic pituitary gonadal axis.1-3 Thus, greater empha-1 j$ U# B2 d) o" ^) F0 z
sis has been given to neuroradiologic imaging in$ p1 S/ B" O+ F8 W
boys with precocious puberty. In addition to viril-
5 x$ c3 a" p: k1 |  t8 |" \ization, the clinical hallmark of CPP is the symmet-
; V. w2 i# ~7 J: }8 e) prical testicular growth secondary to stimulation by
9 l$ U5 S/ ^) M: bgonadotropins.1,3
# r- \$ G3 _' `0 K9 h! ?Gonadotropin-independent peripheral preco-. y: c+ \5 v1 f
cious puberty in boys also results from inappropriate
  n8 }1 C9 s% x. randrogenic stimulation from either endogenous or7 Z7 \- b4 g2 w" |" L: G  ~/ i- |. {
exogenous sources, nonpituitary gonadotropin stim-9 p1 f  c, O/ c
ulation, and rare activating mutations.3 Virilizing
8 K) O  a# O, p  h% Z$ qcongenital adrenal hyperplasia producing excessive5 k1 t% z+ U: B
adrenal androgens is a common cause of precocious* \8 L" ~" c, O# ^& y2 i
puberty in boys.3,4
* I7 u/ F/ t2 m* aThe most common form of congenital adrenal
' Q( ?% Q$ s( H+ E: }hyperplasia is the 21-hydroxylase enzyme deficiency.
0 I7 Y- m* z; L, {The 11-β hydroxylase deficiency may also result in  K9 t- p, y4 l3 K# a5 g
excessive adrenal androgen production, and rarely,4 U7 N" L+ A) D6 v2 L5 |6 f& b
an adrenal tumor may also cause adrenal androgen8 R. O! z  A2 r% `' g9 G1 x
excess.1,3
- y. p8 i* u! N( B" xat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from" ~! r  C4 |2 A# a4 N  s
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
/ \* I$ E' H+ x: U9 ~. G- Y) rA unique entity of male-limited gonadotropin-
2 t0 F9 _. }4 _3 v) ~independent precocious puberty, which is also known
; D3 N# G. a$ Z0 sas testotoxicosis, may cause precocious puberty at a
: e; L9 o& ^8 o- R* Dvery young age. The physical findings in these boys
1 d% N( V* `( A% }6 x7 Mwith this disorder are full pubertal development,
5 a6 t; _: e# E# A4 h$ o1 k" Yincluding bilateral testicular growth, similar to boys
# Q9 s/ Q& f- B4 P3 Lwith CPP. The gonadotropin levels in this disorder
1 g3 Z8 L$ F4 j- Y/ D  oare suppressed to prepubertal levels and do not show
6 z! o  v) F) U8 Zpubertal response of gonadotropin after gonadotropin-
% `9 o  p0 `- m4 Greleasing hormone stimulation. This is a sex-linked1 N! ?" M  i+ n) V; A  G6 i
autosomal dominant disorder that affects only$ u+ P* {1 N5 K, V; g' {2 T
males; therefore, other male members of the family% t, @' b% j! g/ t! a
may have similar precocious puberty.3
, p, y% j- n( _: l! L7 L' T8 pIn our patient, physical examination was incon-
7 m$ w# _; G* q+ tsistent with true precocious puberty since his testi-- M" R( ^* I& |' m3 O6 s
cles were prepubertal in size. However, testotoxicosis
* C2 N# ?. I( K" k5 Hwas in the differential diagnosis because his father% \9 W1 S$ f5 p0 r8 n
started puberty somewhat early, and occasionally,
  t3 L  A4 F1 t' {/ ptesticular enlargement is not that evident in the
" D% K1 {% }9 |; g. s/ W7 Qbeginning of this process.1 In the absence of a neg-1 G! E6 Z  W6 H
ative initial history of androgen exposure, our
0 d# `/ A: u5 Jbiggest concern was virilizing adrenal hyperplasia,9 v% Z- Z6 k) v2 [3 D1 Q
either 21-hydroxylase deficiency or 11-β hydroxylase9 e, O! s& p" a
deficiency. Those diagnoses were excluded by find-+ a4 w' J. L# G
ing the normal level of adrenal steroids.
) }% I' |( B* {% @6 EThe diagnosis of exogenous androgens was strongly
7 m& ^8 V  k" @* Lsuspected in a follow-up visit after 4 months because
$ v! X1 A6 I! w' G5 b, Ythe physical examination revealed the complete disap-
0 v  y9 b& G/ C! I5 }pearance of pubic hair, normal growth velocity, and3 @4 s: |4 M& \2 d# O9 w
decreased erections. The father admitted using a testos-
0 b: z5 G+ T6 q1 @& V4 _terone gel, which he concealed at first visit. He was+ {/ _% N" A  A9 I9 r1 d# A
using it rather frequently, twice a day. The Physicians’8 y1 K1 |2 z' m" a( i( n
Desk Reference, or package insert of this product, gel or  F2 u3 }8 Z% A3 `; e
cream, cautions about dermal testosterone transfer to
% P, w) B/ o* c7 V& B% q4 S2 k$ @unprotected females through direct skin exposure.3 M7 L- C; w) o7 E3 C$ E
Serum testosterone level was found to be 2 times the; @, s) e2 H. j! M; J6 i2 l
baseline value in those females who were exposed to
, W+ ~3 m+ a1 B9 |- \4 _: [; qeven 15 minutes of direct skin contact with their male
2 \4 B0 @  B3 C; n0 Q/ n, m/ c: epartners.6 However, when a shirt covered the applica-
7 y( n; v4 T+ l/ F4 F# ^6 l- Ption site, this testosterone transfer was prevented.
6 ^9 S7 e; {" Z( b. Z+ S! s4 b" z1 wOur patient’s testosterone level was 60 ng/mL,( K; I* r( c. N
which was clearly high. Some studies suggest that8 `# d$ U' Q8 X
dermal conversion of testosterone to dihydrotestos-% K  Y2 \3 o; h7 J4 c
terone, which is a more potent metabolite, is more: c# C7 t+ L8 R0 @! [1 H
active in young children exposed to testosterone
8 x! W" x8 E3 m$ P& H/ N& [exogenously7; however, we did not measure a dihy-
# S7 D" y- l5 B) L$ kdrotestosterone level in our patient. In addition to
! Z# d/ p* L4 V8 C4 m, V3 i; Z5 Ovirilization, exposure to exogenous testosterone in
2 e4 Q; e+ N. T6 A" T3 H7 uchildren results in an increase in growth velocity and
/ c+ V( k% X6 z6 s7 }advanced bone age, as seen in our patient.
* Q# m  a8 Z* gThe long-term effect of androgen exposure during
' L0 _4 q: j" B/ M7 ?early childhood on pubertal development and final
. n6 p7 ?- m6 x$ v) |8 aadult height are not fully known and always remain. t, v2 |$ B6 G
a concern. Children treated with short-term testos-
$ f+ s( \" z  dterone injection or topical androgen may exhibit some7 G" H2 V3 R- l5 X
acceleration of the skeletal maturation; however, after
1 d0 X# T2 O  i2 z! T, mcessation of treatment, the rate of bone maturation3 O! @# {: ~9 q1 `9 ]
decelerates and gradually returns to normal.8,9! Y) u* q* n) a1 a' f
There are conflicting reports and controversy
% E9 V" p9 v; cover the effect of early androgen exposure on adult% P8 ]% `4 c) x; t9 A. f
penile length.10,11 Some reports suggest subnormal
* M9 x: Q. V9 uadult penile length, apparently because of downreg-0 Z" V5 U8 x* W( @$ ^0 e
ulation of androgen receptor number.10,12 However,
( y- l  i+ L( k1 P# o0 D$ W. Z1 xSutherland et al13 did not find a correlation between% S( [; ^2 Y, e5 P: N4 C1 b
childhood testosterone exposure and reduced adult
9 `0 Y4 ~- ^1 L- u1 I9 W0 Qpenile length in clinical studies.7 \) o2 a# e$ r  N) v
Nonetheless, we do not believe our patient is
( W& p! q6 `1 l9 S8 a( _1 dgoing to experience any of the untoward effects from
7 F% s" Z: _% Btestosterone exposure as mentioned earlier because1 J/ Q9 ?3 @) d5 Z
the exposure was not for a prolonged period of time.6 U0 y# U$ T( K4 p
Although the bone age was advanced at the time of
# I: u& g! U- K( P: hdiagnosis, the child had a normal growth velocity at
1 j& b% ?  _8 Pthe follow-up visit. It is hoped that his final adult
2 N! x* A" R! i6 ]" Zheight will not be affected., I+ {# G: ~& G3 ~
Although rarely reported, the widespread avail-! J1 b, ^2 J4 Z1 V+ n; e. l' U
ability of androgen products in our society may
+ u6 p; o9 Y# g/ V3 O5 xindeed cause more virilization in male or female6 x  A/ c4 s3 f  L
children than one would realize. Exposure to andro-
+ j& d" P* ?1 w$ f% egen products must be considered and specific ques-& d! A$ X4 e, x1 j3 Q: v! o
tioning about the use of a testosterone product or
# _& K; t9 b! `5 \; Agel should be asked of the family members during& w  I7 e3 b0 S% [6 C
the evaluation of any children who present with vir-! L9 n4 \/ r+ R% b
ilization or peripheral precocious puberty. The diag-
& t' Z! n; h8 ~5 K/ N; rnosis can be established by just a few tests and by1 x1 y0 H) O+ @  Z& x# e* S. |
appropriate history. The inability to obtain such a( i3 u2 R$ K& ^" {1 p5 E% r
history, or failure to ask the specific questions, may
0 ~+ e5 O( U  N- q( ]" V" d$ r* iresult in extensive, unnecessary, and expensive
+ {7 L, j' G! U4 O7 ?! O* zinvestigation. The primary care physician should be
8 Q  U% H: D& u  S8 oaware of this fact, because most of these children
0 A8 a# x* Q! x3 h  _may initially present in their practice. The Physicians’, z5 a5 R) s, r0 _/ S/ y1 G2 {
Desk Reference and package insert should also put a
  `6 r$ Z9 Y; rwarning about the virilizing effect on a male or
4 Q& D9 D( D+ y4 Ffemale child who might come in contact with some-+ S$ P0 A# [* u% U' t
one using any of these products.
0 T" ~4 f+ \  j* \7 X. eReferences5 v. s, }9 ], r$ b/ w, F: N
1. Styne DM. The testes: disorder of sexual differentiation
( M* z0 k# @. L) @# O$ b3 ]and puberty in the male. In: Sperling MA, ed. Pediatric
7 K( E6 D* `: R7 \" U$ }2 H6 a$ A5 lEndocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
: l6 C0 p0 R& @, J! Y9 V* }2002: 565-628.
3 G) Z: T1 Y* z+ P4 U7 z2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious# p- c' r  |$ Z% z; \
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
2 w& o" X- [9 h5 a% ]5 v8 d
精妙絕倫的精品,感謝啊!期待你更多更好的創作哦!
發表於 2025-3-8 22:04:50 | 顯示全部樓層
絕對的好貼!謝謝啊!逐字逐圖地看完這個帖子以後,我的心久久不能平靜,感恩啊!
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