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Sexual Precocity in a 16-Month-Old- |0 n, [- s/ m2 x: t3 {: m
Boy Induced by Indirect Topical
, \1 ^' _1 S( V- k2 g0 \Exposure to Testosterone4 N8 [4 ?7 v( z) I# p) H) n& z/ A4 b
Samar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
0 n7 d6 T4 ~# K! _and Kenneth R. Rettig, MD1  A& h4 R3 b7 ?% r9 I: s8 @
Clinical Pediatrics
) t6 ~" a8 F- L; x7 N3 v" h) jVolume 46 Number 60 Y( s; B0 c. m9 F% W4 d' d( C
July 2007 540-5437 z! f8 q( _# K! n9 O
© 2007 Sage Publications5 N! g( G% R' c% z
10.1177/00099228062966511 u5 Z' H! r* ^7 f
http://clp.sagepub.com7 t5 H5 o% r: B) _# f; b, F9 a! P
hosted at
, x; n7 |7 j. J2 _http://online.sagepub.com
3 V- o$ a  K; ~. N0 g4 n: I* cPrecocious puberty in boys, central or peripheral,5 I# [8 O- g- ~* _# B- w  d# {
is a significant concern for physicians. Central
4 s3 C. d6 f# Mprecocious puberty (CPP), which is mediated
$ \+ @1 j# M4 V3 m3 E0 nthrough the hypothalamic pituitary gonadal axis, has
: P* U8 X  M) d/ j" w  t( Qa higher incidence of organic central nervous system5 J5 a/ x8 q& U; D& b
lesions in boys.1,2 Virilization in boys, as manifested
8 c3 j; r) x* Z2 }by enlargement of the penis, development of pubic8 n% U2 K5 l; ]
hair, and facial acne without enlargement of testi-
9 W4 f, ~% J( O. H* {7 hcles, suggests peripheral or pseudopuberty.1-3 We
' Y' M) R4 B5 V" Q) t0 hreport a 16-month-old boy who presented with the
2 |. W: ], D. I- r1 fenlargement of the phallus and pubic hair develop-" x+ T; y* i( u5 y2 f
ment without testicular enlargement, which was due! i5 A3 M' z' h6 c0 {; T
to the unintentional exposure to androgen gel used by4 K: ~+ Y  z+ Y3 v, s; ^
the father. The family initially concealed this infor-8 y+ q6 o% B- B
mation, resulting in an extensive work-up for this
% ^- Y# @' Y; M: v7 jchild. Given the widespread and easy availability of, k8 ?6 J, D  D4 T" d/ |" e5 h+ p: r; e
testosterone gel and cream, we believe this is proba-5 V) @, ^! D. v# n1 l0 ~# @& `
bly more common than the rare case report in the
& @2 z7 e4 T0 k7 U. Uliterature.4
. e6 {8 F6 Z1 D2 z  {2 }Patient Report1 l8 O( j0 L1 m, S& W
A 16-month-old white child was referred to the
5 ?# o: H7 Y% N* S- g6 q; y* Pendocrine clinic by his pediatrician with the concern# p* Z$ M3 ~( A$ H) Y+ G% l
of early sexual development. His mother noticed* [1 ~' I3 }# R
light colored pubic hair development when he was
7 _$ T- J! m0 L7 W. w+ n& c; i3 yFrom the 1Division of Pediatric Endocrinology, 2University of
1 R% i, T5 k5 J% o2 O( n$ q' XSouth Alabama Medical Center, Mobile, Alabama.. L- r" s' O5 I2 @& y
Address correspondence to: Samar K. Bhowmick, MD, FACE,8 c+ n0 }. V0 w" a9 `) v
Professor of Pediatrics, University of South Alabama, College of
- t* e" z* ]( J) {( F" `1 D$ I2 z' r6 fMedicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;" U2 W/ j# F1 c" P  V$ Q
e-mail: [email protected].8 \3 @9 f( f5 P/ k' {+ }( y7 o
about 6 to 7 months old, which progressively became
5 _/ ^( P- G" J+ w. [darker. She was also concerned about the enlarge-( e3 W& }6 R0 t6 {" ^, |
ment of his penis and frequent erections. The child# [' H: Y  \6 Y! S/ _7 W
was the product of a full-term normal delivery, with
9 c0 ~- I4 a- k1 x5 h: F; x1 la birth weight of 7 lb 14 oz, and birth length of
+ w. c3 T( F4 ]8 V* }- L20 inches. He was breast-fed throughout the first year
! w) Z( W( n. C6 O( C& C1 Pof life and was still receiving breast milk along with+ C7 t4 {% J3 Y5 J* Z0 n
solid food. He had no hospitalizations or surgery,: Y. n& P% L) O" H- ~( P
and his psychosocial and psychomotor development/ K# _* f9 q  L7 x2 Q+ F
was age appropriate.
+ E' Q; T- V, C5 `7 s& ^The family history was remarkable for the father,) \; b( B$ m! n, H; _* |5 r3 {
who was diagnosed with hypothyroidism at age 16,1 U* s6 Z  z4 [# y+ L  b
which was treated with thyroxine. The father’s8 D2 D, F) @, p6 ?- \+ r
height was 6 feet, and he went through a somewhat
! n$ I# t/ Z6 mearly puberty and had stopped growing by age 14.
2 U& _1 a+ `/ RThe father denied taking any other medication. The1 G2 U/ Q$ j' W: M
child’s mother was in good health. Her menarche# H* }: Z* `+ b9 [, V7 @: d' h
was at 11 years of age, and her height was at 5 feet) g# q7 q& c. J2 I
5 inches. There was no other family history of pre-
: Y. A4 P7 ^3 Mcocious sexual development in the first-degree rela-& ^9 ?' ?* O3 f& L. u2 u9 W
tives. There were no siblings.4 _- U! ]$ j. n4 Y) |
Physical Examination
1 ^7 r; u. L2 {3 f8 Q# E7 q0 uThe physical examination revealed a very active,
  a0 h- i+ w( [. Z: l) v% Dplayful, and healthy boy. The vital signs documented
0 U2 @% T; Z6 H1 j. p7 k2 ua blood pressure of 85/50 mm Hg, his length was! v- {# _2 h% V7 a+ U( ~
90 cm (>97th percentile), and his weight was 14.4 kg
1 J5 ]1 U! G5 U3 P5 a# ]* {(also >97th percentile). The observed yearly growth) R6 v8 _  V& t( p% s# l! Q
velocity was 30 cm (12 inches). The examination of
5 _/ L" _1 t. bthe neck revealed no thyroid enlargement.) f2 ~$ }6 D4 ^% H' Q9 d
The genitourinary examination was remarkable for/ O$ ]7 J+ v' g& H% x! |7 O1 e/ N
enlargement of the penis, with a stretched length of, ^/ d, Y* X* V. [9 A" b
8 cm and a width of 2 cm. The glans penis was very well
1 y5 p. P% D3 \( S) _" Mdeveloped. The pubic hair was Tanner II, mostly around; o9 c* X  x* S$ N; b$ }
5409 B7 b# W9 }  V2 o, T. q
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
6 R& q5 l6 v6 `( D; Rthe base of the phallus and was dark and curled. The
. Z. \* M( s: h8 ]3 h4 g) n* Vtesticular volume was prepubertal at 2 mL each.# z" C6 n% Y' I* x% h. N( x( _
The skin was moist and smooth and somewhat' {4 c8 p$ K- j) X, g
oily. No axillary hair was noted. There were no
. S* s9 z- K; n  A" }" i6 Habnormal skin pigmentations or café-au-lait spots.& F& L$ ~% i' t. y
Neurologic evaluation showed deep tendon reflex 2+2 f/ j. C% E8 p3 Q: n) S, j* x
bilateral and symmetrical. There was no suggestion4 A# k3 q- t7 u/ s
of papilledema.
1 ~4 g4 d  {7 c  D* E4 E! u3 VLaboratory Evaluation. E% ~1 Z! ^7 C+ z. _2 r
The bone age was consistent with 28 months by: s5 y5 r) h4 {/ w
using the standard of Greulich and Pyle at a chrono-$ C* V7 C2 Z6 g. z, U8 ~6 z
logic age of 16 months (advanced).5 Chromosomal$ p5 `3 E8 A0 r) R" _  f% W$ L
karyotype was 46XY. The thyroid function test
- F% r9 E, @  F& zshowed a free T4 of 1.69 ng/dL, and thyroid stimu-+ q1 }( I  c, T8 Z
lating hormone level was 1.3 µIU/mL (both normal).
( x3 x& G7 R$ s1 M7 k3 XThe concentrations of serum electrolytes, blood  j0 t# l- z8 h" g- J, P
urea nitrogen, creatinine, and calcium all were6 t6 G/ b# G  a7 l3 x$ g1 a
within normal range for his age. The concentration% G3 ~; P; G0 C$ G; U. k( X% \# ?
of serum 17-hydroxyprogesterone was 16 ng/dL- G/ D+ n  [4 x8 {' c5 X+ y/ r
(normal, 3 to 90 ng/dL), androstenedione was 20
  r2 T# K: j) }6 m/ }2 [% {* a0 zng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-) }  k6 p- H2 P: ~7 p
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
1 L$ W0 |$ B! [! T4 l5 Ddesoxycorticosterone was 4.3 ng/dL (normal, 7 to
2 p( e& l# i! z: {  Y0 k+ O49ng/dL), 11-desoxycortisol (specific compound S)
" O$ f; x4 r) n$ t0 @/ R( Mwas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-
! p: E1 ]& N- ^# E' Ytisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total
8 r$ ^* P$ {9 W2 W3 V& _1 Htestosterone was 60 ng/dL (normal <3 to 10 ng/dL),
4 |! y  D, C2 |+ D. f8 r7 Jand β-human chorionic gonadotropin was less than8 M8 F2 B  l9 P8 K
5 mIU/mL (normal <5 mIU/mL). Serum follicular
3 T5 S+ U3 z  F3 ~stimulating hormone and leuteinizing hormone3 O+ N2 c! v8 t% {! [  \
concentrations were less than 0.05 mIU/mL
2 Z% f7 o8 A  k! e. W# f5 Y(prepubertal).
5 p/ [5 j% p/ EThe parents were notified about the laboratory
  F7 z) d* n3 S2 Aresults and were informed that all of the tests were) u/ m3 j& x' i# J( ?# F4 z
normal except the testosterone level was high. The
$ R/ O$ f* Y& v3 ]8 sfollow-up visit was arranged within a few weeks to
3 q6 S- M& D3 }obtain testicular and abdominal sonograms; how-
* s2 [+ z( R& ^3 d% ]ever, the family did not return for 4 months.
8 E: w- ]$ T' |- qPhysical examination at this time revealed that the: K+ _% D2 q4 K$ W
child had grown 2.5 cm in 4 months and had gained
; G& B2 X5 s) |' K4 k/ G9 x$ [  Z2 kg of weight. Physical examination remained# a2 f3 B& j. P9 F6 }
unchanged. Surprisingly, the pubic hair almost com-9 Z. [9 ]1 K0 n, Y; @' R
pletely disappeared except for a few vellous hairs at
+ S! \0 I# d1 @! r- hthe base of the phallus. Testicular volume was still 2
8 U5 Q/ |# x, M  O( J0 n; z- c' d( amL, and the size of the penis remained unchanged.
" T1 T/ J4 ?. N+ Q$ t' JThe mother also said that the boy was no longer hav-
9 u4 B$ \  r9 d- Y. P# h4 a$ Sing frequent erections.! u4 m* R+ I) ^6 a% J+ r# J
Both parents were again questioned about use of
1 W) g) Z: ^% C+ @any ointment/creams that they may have applied to+ |, j2 {- U! ]
the child’s skin. This time the father admitted the) F- b8 ^% }5 d7 j) y
Topical Testosterone Exposure / Bhowmick et al 5416 n# W: W: _1 ]% L
use of testosterone gel twice daily that he was apply-
/ M$ @4 f, v( x  A0 A& b- J$ aing over his own shoulders, chest, and back area for
. t; o1 A' x$ l5 z3 ?+ @$ N, d  ia year. The father also revealed he was embarrassed/ y" {# U& @% j1 d  v5 B6 S8 ]' A
to disclose that he was using a testosterone gel pre-
, w, s) T, V  v; ^" Kscribed by his family physician for decreased libido
3 b8 }7 s4 O( E; Q, T/ Xsecondary to depression.
& ?) i2 ], P5 M' r2 D. G: VThe child slept in the same bed with parents.
& Q1 X8 g) V+ t& q3 R: zThe father would hug the baby and hold him on his+ f4 X& f1 ]- f5 z
chest for a considerable period of time, causing sig-3 ^. J- X7 S' \' w% g
nificant bare skin contact between baby and father.. f5 p' Z/ b% `& P6 N  E
The father also admitted that after the phone call,. m$ c- Q: N2 f' e7 L9 q+ d' r
when he learned the testosterone level in the baby
7 N2 Z2 w. c' T. s6 h/ O8 Q" dwas high, he then read the product information/ G: [+ z4 B: `/ z: {7 I* K& z
packet and concluded that it was most likely the rea-
( J" P( h9 \/ A2 `% wson for the child’s virilization. At that time, they1 M0 z/ R; S3 }# [: O
decided to put the baby in a separate bed, and the
/ [% I# k$ a- N7 ifather was not hugging him with bare skin and had$ c0 w7 S1 k& |4 |4 v- n/ Q) s8 R
been using protective clothing. A repeat testosterone5 G& R% u% B2 _: W0 @3 \' Q" l) f6 M" ^0 H
test was ordered, but the family did not go to the$ @( R! k! p1 R$ @. t
laboratory to obtain the test.
+ J- T- Z8 Q' ^) B  }5 bDiscussion
: Z% `& B" u0 s! G9 g% ePrecocious puberty in boys is defined as secondary
+ Z( j0 ]! u+ w2 [7 V- v! }sexual development before 9 years of age.1,4, F% j6 a  ^' B; m
Precocious puberty is termed as central (true) when
# X! k+ C% F: j0 X* Kit is caused by the premature activation of hypo-* i8 @+ A  d: l0 ]/ o
thalamic pituitary gonadal axis. CPP is more com-
% _# \& _* ?6 h% Xmon in girls than in boys.1,3 Most boys with CPP8 f' a# e* c( C% l
may have a central nervous system lesion that is
( r$ r% h" ]8 k% X' M" \responsible for the early activation of the hypothal-
$ k' A0 I& y: Lamic pituitary gonadal axis.1-3 Thus, greater empha-( j' [$ Z. D& l5 Z. h7 s9 P
sis has been given to neuroradiologic imaging in
& p& R5 e$ i- X! W: ~2 b9 U2 h0 Wboys with precocious puberty. In addition to viril-
$ H$ e1 |  m- m2 r+ {ization, the clinical hallmark of CPP is the symmet-+ F% J( B2 ^8 e0 t
rical testicular growth secondary to stimulation by
- y1 D! Z) b$ d8 igonadotropins.1,3. l1 ]* R& s8 F' Y) ~
Gonadotropin-independent peripheral preco-
7 }2 R* ^8 c# H8 b/ |+ scious puberty in boys also results from inappropriate  P$ H& r- m$ h2 ~; A
androgenic stimulation from either endogenous or
+ D$ Y' S9 k5 ]% `exogenous sources, nonpituitary gonadotropin stim-
1 S- V0 e1 W2 \& Wulation, and rare activating mutations.3 Virilizing
: A" N4 g9 _3 w% ycongenital adrenal hyperplasia producing excessive
6 k2 q( B9 G- m8 W2 x, [adrenal androgens is a common cause of precocious
4 r4 k3 E+ h# o$ T# y# ^$ spuberty in boys.3,4. _' S" t; w$ N) S; X  }& _
The most common form of congenital adrenal
1 C# P% m, G. B* lhyperplasia is the 21-hydroxylase enzyme deficiency.
# u( o1 Y' v% w- `The 11-β hydroxylase deficiency may also result in  ], g3 S4 n: F! f1 d5 `2 n+ h, g
excessive adrenal androgen production, and rarely,( T; K( r; ]! Q( {0 v+ Z
an adrenal tumor may also cause adrenal androgen
8 w& F$ M9 h! f1 ~excess.1,3
2 o+ x) j* @* aat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ V8 f. L% R+ E1 R8 S
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007
' e! T  F8 j* B5 AA unique entity of male-limited gonadotropin-! z2 ~% }' C8 a4 R! q5 }
independent precocious puberty, which is also known7 e- A  S6 Z4 z* }
as testotoxicosis, may cause precocious puberty at a
' H/ g& X% `% G8 y+ t; pvery young age. The physical findings in these boys
* |4 x8 B/ F4 w, |  F' H! H: X6 fwith this disorder are full pubertal development,* q! ]* b* T, q
including bilateral testicular growth, similar to boys! e% ~( j  C/ I
with CPP. The gonadotropin levels in this disorder: s. j% Y2 G8 d. d; n
are suppressed to prepubertal levels and do not show7 E7 b& P- c. m- v3 m' d
pubertal response of gonadotropin after gonadotropin-
9 |  {+ p# W7 L* V7 D% x! N8 kreleasing hormone stimulation. This is a sex-linked
; C1 m) h. H5 s. Vautosomal dominant disorder that affects only
) \. L! D- u* m; J; B' M! nmales; therefore, other male members of the family7 v6 X1 l% r5 c
may have similar precocious puberty.3$ H. Y) H* w. s1 t0 q
In our patient, physical examination was incon-7 t% }5 T- f2 E4 W
sistent with true precocious puberty since his testi-( P2 q) p0 T) x; p" a0 ~0 K
cles were prepubertal in size. However, testotoxicosis3 s1 {1 M' H6 y% D; \3 C" M* c
was in the differential diagnosis because his father  J- z1 C7 D+ }% O0 x* K6 f9 m
started puberty somewhat early, and occasionally,2 I) D5 Z5 E# ^6 B0 m
testicular enlargement is not that evident in the8 b/ T0 W' B* g8 r( D- ~' e' a" R
beginning of this process.1 In the absence of a neg-8 I2 S# z2 \, P8 }" O
ative initial history of androgen exposure, our
! p8 `  z7 S' z6 q# G. }+ b  Obiggest concern was virilizing adrenal hyperplasia,0 ^) `+ Y& q; ^) u: p
either 21-hydroxylase deficiency or 11-β hydroxylase
4 @8 z* l8 I% o! Q- f1 ldeficiency. Those diagnoses were excluded by find-
" `* w6 G6 K. c1 f* Q# s+ b6 ping the normal level of adrenal steroids.
0 g+ g! K1 B$ w; dThe diagnosis of exogenous androgens was strongly  s9 T" D: V* {/ }" W3 H# J: b
suspected in a follow-up visit after 4 months because
" u, S% ~/ Z3 y& k* J9 e. r0 R7 x" }$ {the physical examination revealed the complete disap-
% U$ U8 ]( M1 N0 xpearance of pubic hair, normal growth velocity, and
, o; b. d; O! n3 p6 Z" t9 x* wdecreased erections. The father admitted using a testos-# v. M2 Y! o& [! V. V* _
terone gel, which he concealed at first visit. He was
5 p7 W; H9 j) h/ n4 M2 Ousing it rather frequently, twice a day. The Physicians’9 h8 J9 I  B) L+ M( m# m
Desk Reference, or package insert of this product, gel or
- t! a; b5 o! A2 L: D$ J+ E0 Zcream, cautions about dermal testosterone transfer to+ a: l# u' f" b8 s' v
unprotected females through direct skin exposure.
6 z5 s- k& [2 r% \2 d+ R- x+ C# D: I9 gSerum testosterone level was found to be 2 times the
  f7 L  u1 [  u! q; K, Ybaseline value in those females who were exposed to1 e1 {9 W& W4 ?; `5 V0 |
even 15 minutes of direct skin contact with their male5 E9 h1 G" ~6 m% q: M( F
partners.6 However, when a shirt covered the applica-
/ l/ |" i' D1 [) Ktion site, this testosterone transfer was prevented.0 V5 g4 P- j5 {! g+ x
Our patient’s testosterone level was 60 ng/mL,7 ]) C8 d6 t' i+ b5 R
which was clearly high. Some studies suggest that2 D+ |1 M% i. ^  V
dermal conversion of testosterone to dihydrotestos-
( J) o0 \1 U0 w, p' R) {. D$ [terone, which is a more potent metabolite, is more
" j- E( y# y# R8 w  lactive in young children exposed to testosterone
, F9 U/ [4 m* C9 [7 J( p4 n" Bexogenously7; however, we did not measure a dihy-
6 [% O  A4 @8 Z1 gdrotestosterone level in our patient. In addition to
4 z5 A) r' l# L, l, Qvirilization, exposure to exogenous testosterone in' M  @. X" O6 O: t
children results in an increase in growth velocity and
3 |- v3 t1 [/ Z% _% z9 Tadvanced bone age, as seen in our patient.+ V0 ^$ N3 g) E' `
The long-term effect of androgen exposure during
; E& K4 m, T3 V  n9 h. @' Dearly childhood on pubertal development and final
7 @" s" [3 j, ^. S* z, Uadult height are not fully known and always remain6 J5 p& }) T9 Y. v" w5 ?+ F
a concern. Children treated with short-term testos-7 C/ [  t9 z5 _5 F3 H3 @' c
terone injection or topical androgen may exhibit some: T; V  s: o' y6 Q5 f: P0 O
acceleration of the skeletal maturation; however, after
' L+ E& A& y- J6 ?7 U! S! kcessation of treatment, the rate of bone maturation
( ]2 o- q3 R8 Cdecelerates and gradually returns to normal.8,9
8 q9 K" \3 f' f" sThere are conflicting reports and controversy6 O. D7 h( i2 I' z  x
over the effect of early androgen exposure on adult' d! ?% r8 I- ?
penile length.10,11 Some reports suggest subnormal! u  U4 S( p- V% C) z
adult penile length, apparently because of downreg-; c; f1 G/ `. _- v" M" s$ b
ulation of androgen receptor number.10,12 However,6 T% K: N9 C* l
Sutherland et al13 did not find a correlation between+ P$ B, U. H! B3 X" ~/ k
childhood testosterone exposure and reduced adult" k6 E( s. q. j; q. b" T, E
penile length in clinical studies.8 W+ S0 \1 Q0 F* X3 @0 H# d' i
Nonetheless, we do not believe our patient is
9 ?9 Z; H2 a$ w6 j# hgoing to experience any of the untoward effects from
; f. x0 A2 R9 }' O! Vtestosterone exposure as mentioned earlier because" ^& C6 N! G+ F- U
the exposure was not for a prolonged period of time.
  y% t* r3 L! {3 m5 ZAlthough the bone age was advanced at the time of" W; n" z+ `' D; C' i
diagnosis, the child had a normal growth velocity at
! K9 d) V3 \: w# ythe follow-up visit. It is hoped that his final adult2 ~" s! y, h$ P% n
height will not be affected.. a, a% Z* k8 D; h5 A
Although rarely reported, the widespread avail-
9 G4 R2 R, X5 t% fability of androgen products in our society may$ U; i' }7 u, f7 D2 e
indeed cause more virilization in male or female3 w' U+ X5 E' t) c& Y
children than one would realize. Exposure to andro-
1 m4 B+ |4 e/ P7 ]$ `- c% C" Z. @! Fgen products must be considered and specific ques-
0 W: W: r8 a) Y" }' Vtioning about the use of a testosterone product or
& W) T' U6 m* t- C  [  O  c! K3 e3 Igel should be asked of the family members during
  E" t) W& x. `the evaluation of any children who present with vir-, X, d/ w$ h2 ^- }. z$ x8 @
ilization or peripheral precocious puberty. The diag-
& [9 k; y) D& n1 a9 Fnosis can be established by just a few tests and by
# B0 ]; K( g! m$ v3 sappropriate history. The inability to obtain such a$ j1 I: P% H% e! T# X' @
history, or failure to ask the specific questions, may
" |1 ?  D( W  |1 n  Yresult in extensive, unnecessary, and expensive
# O/ E& o$ s( _$ I6 p+ einvestigation. The primary care physician should be
+ B$ v! L+ k; W: ~& Waware of this fact, because most of these children9 u+ K$ Q$ f* U3 h( r* c# h' a0 z
may initially present in their practice. The Physicians’
- s* @- F4 u4 CDesk Reference and package insert should also put a
( }( j6 _* i- Ywarning about the virilizing effect on a male or& L6 [% i9 l' d3 _+ X  K
female child who might come in contact with some-
8 S/ n7 ~  A* Y8 Zone using any of these products.
' |2 A% F( o) {0 Z& n( tReferences
8 e' ~& h2 n; t/ E7 z1. Styne DM. The testes: disorder of sexual differentiation
! s% w) ^1 S. ~( Y( W& l* w4 ]0 mand puberty in the male. In: Sperling MA, ed. Pediatric; H5 t! g; ^/ o3 D+ O4 p  g  S& }
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
8 E3 R% D) b+ h' {2002: 565-628.
6 K0 }' O+ y% L5 B, V3 L3 m' v+ @2 j2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious" _9 u/ S* Z# o' X8 t
puberty in children with tumours of the suprasellar pineal
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Sexual Precocity in a 16-Month-Old) B: k! W& c  j( }2 l
Boy Induced by Indirect Topical
+ D& h7 s" a5 }" r* x: |Exposure to Testosterone
. s" c, I3 G) X* d# m7 ~/ V1 C* dSamar K. Bhowmick, MD, FACE,1 Tracy Ricke, MD,2
1 c8 P/ `/ d- q6 l+ [8 ?+ k8 rand Kenneth R. Rettig, MD1; Y1 p0 o5 z8 w5 l, D& {6 \
Clinical Pediatrics* P& T4 _* j% s
Volume 46 Number 6+ K# i7 l7 b" X+ E5 a( h  C4 Q
July 2007 540-543
/ z  U6 ]- Y& T# K© 2007 Sage Publications
( N" [. J8 R! T7 X10.1177/0009922806296651. Y/ N' K3 \' Q! u
http://clp.sagepub.com, s) i$ K9 G3 b4 p% R
hosted at
$ S/ \( }6 U/ h2 }, uhttp://online.sagepub.com
9 l% f( I3 T1 a1 {: sPrecocious puberty in boys, central or peripheral,& E7 q9 _0 g$ r3 y
is a significant concern for physicians. Central
, L3 n! Z& b- j8 fprecocious puberty (CPP), which is mediated2 f6 O$ _8 D: ]: e( ]) Y
through the hypothalamic pituitary gonadal axis, has
7 _+ T; H3 u, B8 H1 U" W. Ha higher incidence of organic central nervous system
  i' B5 r$ H3 |* M7 @" D) }, \lesions in boys.1,2 Virilization in boys, as manifested
: W( @  }7 X( L& e; |, ?' dby enlargement of the penis, development of pubic
/ ~& t- Y; S7 T) [% _% c3 Y5 bhair, and facial acne without enlargement of testi-
4 b; {. \, a2 A8 K% I0 _. Tcles, suggests peripheral or pseudopuberty.1-3 We" ]7 g: k. O- m: T
report a 16-month-old boy who presented with the8 J* j: P6 `& I6 ]: c! @9 X0 U) V
enlargement of the phallus and pubic hair develop-
2 P- X& X" s, `ment without testicular enlargement, which was due- i0 l/ C: s- [! q5 R6 ^! o
to the unintentional exposure to androgen gel used by
% `% B0 s+ e5 E$ m) v1 ethe father. The family initially concealed this infor-
& S/ J$ E3 _  X$ u0 ]0 `' O$ X) Imation, resulting in an extensive work-up for this2 o/ a4 Q( a& @
child. Given the widespread and easy availability of
8 E4 d* q! J/ v( X- q7 J7 t) y8 [" etestosterone gel and cream, we believe this is proba-' U* }, x- p9 w" d
bly more common than the rare case report in the
8 T4 P/ b; m) A9 Q8 uliterature.4
3 s# G% D% q% }2 `. ^% ]Patient Report7 g. k' P( C% D9 v2 C
A 16-month-old white child was referred to the
8 K' V& e3 d/ dendocrine clinic by his pediatrician with the concern
, `7 n, L1 H/ a8 dof early sexual development. His mother noticed
- ]  H4 @2 B6 g! @5 klight colored pubic hair development when he was2 W: d- r* z# i8 g& \3 `
From the 1Division of Pediatric Endocrinology, 2University of; g) [7 l# G' ]
South Alabama Medical Center, Mobile, Alabama.# [$ A8 g0 ~# B* @8 w
Address correspondence to: Samar K. Bhowmick, MD, FACE,  K5 i: x. J: A. z0 w2 m' p
Professor of Pediatrics, University of South Alabama, College of
3 L3 B' E% d/ j6 ]Medicine, 2451 Fillingim St. Mastin 212, Mobile, AL 36617-2297;
/ E: B  L: w! Me-mail: [email protected].- R0 O1 a/ N7 T2 d
about 6 to 7 months old, which progressively became
, s% y. f, \4 w- c* k2 I1 `6 adarker. She was also concerned about the enlarge-
/ S2 b* B5 X7 i3 {9 Vment of his penis and frequent erections. The child
5 T$ k7 u7 g: W: L. xwas the product of a full-term normal delivery, with
/ m; B' i$ P- O- h0 s0 Ga birth weight of 7 lb 14 oz, and birth length of! R; R+ z- y/ Q: d- A* I% w: ^
20 inches. He was breast-fed throughout the first year
. b$ Z; Y3 k1 f; i0 bof life and was still receiving breast milk along with7 X& H6 F3 N, ~, ?4 u
solid food. He had no hospitalizations or surgery,
1 W7 p+ P+ ~  ^' B1 [) ]0 wand his psychosocial and psychomotor development
: m1 X, |: b# ~1 Z8 J% Ywas age appropriate.
8 G& `7 e  c; n  U- R& hThe family history was remarkable for the father,  ^& F4 P/ h% I6 e( R. y$ t
who was diagnosed with hypothyroidism at age 16,
$ D8 f3 A  Z! ?) ~which was treated with thyroxine. The father’s" L7 L0 [& @/ O; R3 g' _4 q$ K$ j9 M
height was 6 feet, and he went through a somewhat2 Q$ _0 l) ^5 O$ G
early puberty and had stopped growing by age 14.4 H  r& T* h. D+ r' U; A) K* n
The father denied taking any other medication. The
, _  [+ Z" R/ j# Dchild’s mother was in good health. Her menarche! `3 _$ D  L% Q$ b, @
was at 11 years of age, and her height was at 5 feet; f) F& ?4 n" l7 s# A, _
5 inches. There was no other family history of pre-' V8 k" O: D7 W+ ]6 ^3 q
cocious sexual development in the first-degree rela-
% V* ~) i: a+ r: q! Htives. There were no siblings.$ J5 g  I7 L& ?, l9 c& s
Physical Examination- |1 G( ^7 w; j5 r9 y" ~/ @
The physical examination revealed a very active,
& [+ d* B" @% M, \% Gplayful, and healthy boy. The vital signs documented
$ T" V. h/ ?2 C9 Z7 Ja blood pressure of 85/50 mm Hg, his length was: h" Q, @7 }8 V
90 cm (>97th percentile), and his weight was 14.4 kg
& b3 u) L+ }2 l(also >97th percentile). The observed yearly growth
. z  ?% ^: c4 \" uvelocity was 30 cm (12 inches). The examination of- r  I- k1 i4 S+ S) j
the neck revealed no thyroid enlargement." F1 T7 ]7 Z" `) D* x/ V* t
The genitourinary examination was remarkable for3 q5 Z, {: ?; R: r% u! G0 n! p
enlargement of the penis, with a stretched length of7 f8 d# E9 B6 S8 J6 C6 x
8 cm and a width of 2 cm. The glans penis was very well
5 |5 h' B# ?( J$ X+ Adeveloped. The pubic hair was Tanner II, mostly around& I+ t! F" b; T" C4 _% E' e
540" V# `/ n, {. r! W6 V) D! F
at University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from
; N* {4 ~) y* ]3 [! uthe base of the phallus and was dark and curled. The
) Y; y) T: b* Y  Ntesticular volume was prepubertal at 2 mL each.
. }/ I& x2 s% ]- v* R6 YThe skin was moist and smooth and somewhat
' L7 F7 ^8 |& e% j5 b0 f7 Ioily. No axillary hair was noted. There were no6 T5 M2 l  q8 b4 w+ y
abnormal skin pigmentations or café-au-lait spots.) k  l+ O3 v: Z$ _2 D, `, Z% p
Neurologic evaluation showed deep tendon reflex 2+0 k# j- }4 I' u0 G6 t
bilateral and symmetrical. There was no suggestion* N, L3 R& q1 E$ Y
of papilledema.
2 q# ^: O  i( p( yLaboratory Evaluation
6 ]0 B, i6 ]- b, rThe bone age was consistent with 28 months by
1 V+ ]5 J4 J0 O7 e! A# @using the standard of Greulich and Pyle at a chrono-' k$ ^0 @: J4 r
logic age of 16 months (advanced).5 Chromosomal
- _/ X" k' ]; y$ x' v( ckaryotype was 46XY. The thyroid function test
, o' \# J9 a  p0 Y- j' L/ wshowed a free T4 of 1.69 ng/dL, and thyroid stimu-
! {5 U5 ]' U$ ^lating hormone level was 1.3 µIU/mL (both normal).! }& o7 x: L$ F5 L  q
The concentrations of serum electrolytes, blood
) O# Y& G( [  {5 L1 wurea nitrogen, creatinine, and calcium all were
- i  X9 j2 Q* W' A- t" v  z, Cwithin normal range for his age. The concentration, @; a, e3 c9 S: s/ T; @
of serum 17-hydroxyprogesterone was 16 ng/dL
7 g( D, ~3 Z3 W, z; {& O4 p- x(normal, 3 to 90 ng/dL), androstenedione was 203 P- E& m$ l' f4 w
ng/dL (normal, 18 to 80 ng/dL), dehydroepiandros-/ h9 o6 U. Q6 I0 w
terone was 38 ng/dL (normal, 50 to 760 ng/dL),
. M& s1 W7 x2 i" r) W  mdesoxycorticosterone was 4.3 ng/dL (normal, 7 to
* ^/ v8 a5 |# o" I8 {; K49ng/dL), 11-desoxycortisol (specific compound S)
" M- p/ G+ s% {& f* N2 R1 o. Ywas 43 ng/dL (normal, 10 to 156 ng/dL), serum cor-) H5 f+ E9 b! a
tisol was 7.6 µg/dL (normal, 2.8 to 23 µg/dL), total* h- O' h: E. z$ j
testosterone was 60 ng/dL (normal <3 to 10 ng/dL),
' `6 _4 d# G! }3 y" y1 H- Dand β-human chorionic gonadotropin was less than& e$ W, x9 k$ j' N
5 mIU/mL (normal <5 mIU/mL). Serum follicular5 y$ g' M- t- \
stimulating hormone and leuteinizing hormone
" j5 w( \; Z7 B; B# E$ D2 dconcentrations were less than 0.05 mIU/mL8 b+ }1 P5 r8 {; @5 k$ A) X
(prepubertal).
" l% F8 E; U/ {1 \+ ^The parents were notified about the laboratory
; a- \" y! ]" i; K' C, |1 Sresults and were informed that all of the tests were# p6 p5 q0 `) k" }% j2 p
normal except the testosterone level was high. The
& B# K, x4 Z3 Z" Rfollow-up visit was arranged within a few weeks to' Q/ {" G' b; T& w( x2 h
obtain testicular and abdominal sonograms; how-
) \/ Q: N- @" N. b- ~% g$ uever, the family did not return for 4 months.
5 ~6 _* \% H8 v+ |: @9 L: ~& ?Physical examination at this time revealed that the/ X$ y1 a* M/ B0 ~, t. |* M
child had grown 2.5 cm in 4 months and had gained
2 H! ^/ h2 ~/ b4 x5 c2 kg of weight. Physical examination remained
1 E; P4 ^4 S; y; E- |5 r6 Eunchanged. Surprisingly, the pubic hair almost com-
! U! C2 Z- A$ d( A, u4 i( mpletely disappeared except for a few vellous hairs at
$ |6 S2 e7 |# ^/ c$ K; zthe base of the phallus. Testicular volume was still 2; x* I  `- o/ f( c, F
mL, and the size of the penis remained unchanged.  |- e3 a' X  S2 x. @& {" n
The mother also said that the boy was no longer hav-# D0 N4 c6 J0 F6 x+ z+ v3 `& f; l
ing frequent erections.
2 r9 i" {5 S9 o& [0 V  IBoth parents were again questioned about use of
/ H) \! j' f  n5 p' f1 hany ointment/creams that they may have applied to! Z0 d4 ?# ]/ `* S8 ], f0 E
the child’s skin. This time the father admitted the
" ~; v9 X$ B1 o; t9 A0 ^! E) TTopical Testosterone Exposure / Bhowmick et al 541, G: A+ K7 y/ j+ L8 A6 V
use of testosterone gel twice daily that he was apply-
: }9 m2 y  b$ z, x7 c: ming over his own shoulders, chest, and back area for9 v9 E: S$ _# i5 D; i
a year. The father also revealed he was embarrassed" E- c2 o' P- e& P) Q2 u
to disclose that he was using a testosterone gel pre-9 C* m2 r0 `$ W; q
scribed by his family physician for decreased libido
6 D+ n; R# Z( D& Y: p4 y- Ssecondary to depression.) p; j3 `" ]) V% X; b1 ]
The child slept in the same bed with parents.
4 ?" g( o' c+ B/ AThe father would hug the baby and hold him on his
  _- A4 |1 f, z( jchest for a considerable period of time, causing sig-6 R3 s$ p) i9 B3 W7 _% N9 P" t
nificant bare skin contact between baby and father.
! u* {* s- z+ ~The father also admitted that after the phone call,
- F, a3 r4 q* W& l; [when he learned the testosterone level in the baby/ v8 g3 w- A# N# g/ E* r4 q5 I; q
was high, he then read the product information$ C; Z3 r( ?$ [8 Y
packet and concluded that it was most likely the rea-8 x1 Y, a$ n% u; Z$ ]
son for the child’s virilization. At that time, they
2 K; m* U0 K1 T4 c2 ~decided to put the baby in a separate bed, and the
" {0 v) l  j) `0 W5 U! Ifather was not hugging him with bare skin and had
2 _* n! J/ K- m$ ^: y; N  B0 }- ^been using protective clothing. A repeat testosterone0 w! {' K: j9 y; u9 ~6 u# f
test was ordered, but the family did not go to the
! J# O/ c4 n- \* b8 @; [1 jlaboratory to obtain the test.
. C+ h6 F4 k" n1 ~- C; I  T9 sDiscussion
# O) b$ J" S6 m. @Precocious puberty in boys is defined as secondary
6 Z4 g; A. Z3 s2 J* K  Zsexual development before 9 years of age.1,4
5 b! f0 x' Z; f8 N6 s) bPrecocious puberty is termed as central (true) when
' h* z& ]) H7 i, b) i1 zit is caused by the premature activation of hypo-* ?' a) |4 T* ]/ K2 `$ b
thalamic pituitary gonadal axis. CPP is more com-
* k, [; ]0 r' c( I) }. ^& |mon in girls than in boys.1,3 Most boys with CPP
3 ]4 D* l" G* e1 u$ i) `may have a central nervous system lesion that is
2 [& i, r$ \; tresponsible for the early activation of the hypothal-
5 I/ X4 m' E  O# X3 i) M9 ~amic pituitary gonadal axis.1-3 Thus, greater empha-
$ ~9 B+ O$ O/ bsis has been given to neuroradiologic imaging in
( S  W! P( I7 p# `- v! ]boys with precocious puberty. In addition to viril-
' g$ d6 ]! u6 b4 S, Jization, the clinical hallmark of CPP is the symmet-" w% O2 m6 n, V* U
rical testicular growth secondary to stimulation by% H- E' ]$ H: S4 T* y7 c
gonadotropins.1,3' J8 ~0 x) Y/ u: w& C
Gonadotropin-independent peripheral preco-
! d. j5 Y7 H  a5 K9 D" @& u5 @cious puberty in boys also results from inappropriate
/ l1 t, ~7 j7 w5 K$ _. A8 aandrogenic stimulation from either endogenous or4 m$ y2 i9 \$ ~; H! \9 J. h
exogenous sources, nonpituitary gonadotropin stim-0 }  y: J9 Y+ z8 t6 B
ulation, and rare activating mutations.3 Virilizing9 r# R' _4 q' {9 G$ X! w" ^% c, l, z: V
congenital adrenal hyperplasia producing excessive
  h; r( h  L- H* ^2 ~4 _5 tadrenal androgens is a common cause of precocious/ T+ f" C; B! X1 Q
puberty in boys.3,4
. |2 u) V: b  G$ v2 iThe most common form of congenital adrenal0 R# a7 Y+ a' q) B. F8 r3 y' w' o8 [
hyperplasia is the 21-hydroxylase enzyme deficiency.
% `  H) p1 a4 J, }4 X* E0 sThe 11-β hydroxylase deficiency may also result in5 Y: u6 x2 f& F' U! S9 O
excessive adrenal androgen production, and rarely,
/ V/ K8 D7 T1 f! J4 S* ?$ zan adrenal tumor may also cause adrenal androgen- x6 v. X: g3 A$ W0 P
excess.1,3
0 h! L, X& K% Hat University of Manchester Library on May 25, 2015 cpj.sagepub.com Downloaded from+ s' R6 N' }+ Y: \0 U6 p
542 Clinical Pediatrics / Vol. 46, No. 6, July 2007& |# \" j6 b, _! m' k
A unique entity of male-limited gonadotropin-8 E5 G  L* E2 p* H; ^$ v
independent precocious puberty, which is also known% H/ c, i( K& u% f( j* V. w
as testotoxicosis, may cause precocious puberty at a5 ]8 O6 u9 t7 U9 l. f/ E
very young age. The physical findings in these boys* e; [( e9 D9 Q. w! H' k
with this disorder are full pubertal development,
* b1 }% \$ ~, I" Q( q- cincluding bilateral testicular growth, similar to boys0 o4 {1 D1 b4 I1 z) W* `$ I
with CPP. The gonadotropin levels in this disorder
* L" V3 g# F' vare suppressed to prepubertal levels and do not show( l; Y+ S  P  R& v# c8 k' C2 q* M
pubertal response of gonadotropin after gonadotropin-4 Q6 [- w+ x; v$ Y; r" v  j* B$ d+ b
releasing hormone stimulation. This is a sex-linked$ G- {4 s, V* l
autosomal dominant disorder that affects only
2 S, Y. G( r0 w- J8 ~males; therefore, other male members of the family
& a2 O& E) R& X+ o. Tmay have similar precocious puberty.3
3 P, p- C5 k* C4 K9 v! K5 K2 d6 jIn our patient, physical examination was incon-
1 f. Q2 _3 F, t/ o6 Y  P3 M2 [sistent with true precocious puberty since his testi-
4 c5 c" u& W: h0 _0 [cles were prepubertal in size. However, testotoxicosis
7 d4 ^4 H- d, d0 i# Z3 f& owas in the differential diagnosis because his father
  |  `) A$ Q# u5 X4 l1 b2 ^" lstarted puberty somewhat early, and occasionally,! Q2 T( l# i1 F+ i
testicular enlargement is not that evident in the, v4 f6 ~9 l2 e* \* f; W
beginning of this process.1 In the absence of a neg-, p5 U: y: \. q% R4 ^9 Q
ative initial history of androgen exposure, our* ]4 F3 P5 A: X+ v8 [' `
biggest concern was virilizing adrenal hyperplasia,$ [; M, o: d$ D6 G
either 21-hydroxylase deficiency or 11-β hydroxylase3 F! o. [7 j9 w& ]6 a
deficiency. Those diagnoses were excluded by find-
6 z' @3 l9 R5 O% N2 ?ing the normal level of adrenal steroids.
' C' n- X, B. X/ Y5 R! S# ZThe diagnosis of exogenous androgens was strongly
* w: @. \9 w: Z  i6 w  R9 bsuspected in a follow-up visit after 4 months because8 {0 W% G# `, _& V* w; f: m
the physical examination revealed the complete disap-1 x; x; j0 M" L/ W( f. }
pearance of pubic hair, normal growth velocity, and
& \6 {/ K9 l$ c8 Wdecreased erections. The father admitted using a testos-- Y, z! E. {2 ~( t
terone gel, which he concealed at first visit. He was
4 p5 S" V8 G' d; u( M9 V) ausing it rather frequently, twice a day. The Physicians’' `: i# u# M9 a+ @4 l3 m* ~
Desk Reference, or package insert of this product, gel or/ y, V6 h. g4 F5 r( V, v
cream, cautions about dermal testosterone transfer to; J8 C% e; W$ ~. P' Z* @
unprotected females through direct skin exposure.2 ^& Z7 m6 ?' h* t  y" G2 u
Serum testosterone level was found to be 2 times the
+ ?  `+ E( j8 Obaseline value in those females who were exposed to2 H0 Z' G# [) ?. e
even 15 minutes of direct skin contact with their male* C. B- u& ^/ x! W* O
partners.6 However, when a shirt covered the applica-
+ U9 c0 x, H9 h7 M- _) v& Ytion site, this testosterone transfer was prevented." i6 Y0 G# a3 s$ \  i, H: {* r
Our patient’s testosterone level was 60 ng/mL,
: S4 @% I) T9 [5 P9 [which was clearly high. Some studies suggest that4 G3 I; ^7 M5 C- ^. \' X
dermal conversion of testosterone to dihydrotestos-0 u4 c: ~% t& i( [( H9 G4 C
terone, which is a more potent metabolite, is more
: e8 @5 S; W* q& S- ~active in young children exposed to testosterone3 |9 n+ Q  r/ c* s% O) d
exogenously7; however, we did not measure a dihy-
4 I! k! M# l: |" A2 a& edrotestosterone level in our patient. In addition to# w( G# z5 n! ~3 g- H
virilization, exposure to exogenous testosterone in
1 U3 `& _' c2 N' G; fchildren results in an increase in growth velocity and
7 k$ L# ~" E9 k0 @5 ^: jadvanced bone age, as seen in our patient.' E2 C% F' H( N, V9 ]; @
The long-term effect of androgen exposure during
' S  h$ j, m$ C4 g$ X% z- uearly childhood on pubertal development and final
$ p! z0 p( J" h: c; jadult height are not fully known and always remain
0 C/ G+ ^+ E$ F: ja concern. Children treated with short-term testos-9 d2 ~' C* d0 f8 b- f- Z- p
terone injection or topical androgen may exhibit some0 o: _: \5 |3 e* p
acceleration of the skeletal maturation; however, after
1 C$ C$ [- T+ N; Ccessation of treatment, the rate of bone maturation0 V- b! z/ d4 T8 ~$ o! a& ?& K  R/ B
decelerates and gradually returns to normal.8,9; a( {: H& q( D
There are conflicting reports and controversy
, g, y* w1 J3 i; [over the effect of early androgen exposure on adult1 B0 m8 ]( A0 H: ]( y9 p
penile length.10,11 Some reports suggest subnormal0 J& S  q. I- X- q" j( p
adult penile length, apparently because of downreg-
5 P. C5 k, w( a* m. E* Aulation of androgen receptor number.10,12 However,: |* f' \- b% N( o" o1 D
Sutherland et al13 did not find a correlation between
0 K3 M0 a, {+ k$ u' Ochildhood testosterone exposure and reduced adult) h7 o8 f& ~  i+ @
penile length in clinical studies.. B# ]+ @& r+ b* O7 x9 K
Nonetheless, we do not believe our patient is
4 }8 Z, v5 b. |" r7 }going to experience any of the untoward effects from
; |! Y# e: r5 S/ q: a$ _, |( ktestosterone exposure as mentioned earlier because- c; V# B  T7 ?: H
the exposure was not for a prolonged period of time.
* h* L4 T! I* n+ c1 gAlthough the bone age was advanced at the time of
) N2 p: F1 f! ]& s3 [- L3 M- W$ h0 e& Qdiagnosis, the child had a normal growth velocity at
$ F1 H7 C9 ^! Hthe follow-up visit. It is hoped that his final adult
% B9 u6 B: ]; ~1 ?, jheight will not be affected.4 s, c0 m2 ^+ I7 q  j$ v+ ]
Although rarely reported, the widespread avail-' R* m" a" b4 [! z9 @& @9 x- K
ability of androgen products in our society may$ {  b2 c4 l& {2 O3 L6 p
indeed cause more virilization in male or female" j, i# p) E, J& G# P3 f# z
children than one would realize. Exposure to andro-* I# {! }- O- ^* ^
gen products must be considered and specific ques-
0 M; N2 Z4 B2 ^: Rtioning about the use of a testosterone product or/ N! t; _& w, I. c7 \& Z
gel should be asked of the family members during
+ S9 I& O" m* S. }$ Hthe evaluation of any children who present with vir-, C2 ~% o' g: `) t; M
ilization or peripheral precocious puberty. The diag-
* y7 \& a( G- w, p1 _1 w  Bnosis can be established by just a few tests and by& u! B2 [: B% ]9 i( j) q
appropriate history. The inability to obtain such a
( F  R* k! ], H5 P8 w' |% W( y& Whistory, or failure to ask the specific questions, may
8 Z( U) y9 y8 J/ X& Iresult in extensive, unnecessary, and expensive9 f# F# A' w5 [( x5 d+ q# z
investigation. The primary care physician should be
) B6 |1 ^' t- V5 v) w( B$ K2 i" h( Saware of this fact, because most of these children
0 Z) o' J& R$ J+ r, pmay initially present in their practice. The Physicians’
; h3 X4 V& n# ^5 W% y  }Desk Reference and package insert should also put a8 m9 d1 J% _% z8 ]8 O* W
warning about the virilizing effect on a male or' z7 |) W) f4 R1 Q1 I8 k
female child who might come in contact with some-
! q' s1 F, ~( v6 w6 q1 rone using any of these products.9 k) k6 E3 E  [* t
References) [% a" f3 m5 X% V6 \, e" _' s
1. Styne DM. The testes: disorder of sexual differentiation
( L- Y& l) L0 D. aand puberty in the male. In: Sperling MA, ed. Pediatric1 e3 ?0 X4 \% ]) X. Q
Endocrinology. 2nd ed. Philadelphia, PA: WB Saunders;
" X! U; r9 a. Q' c% g; T2002: 565-628.- N+ L. S: K) |
2. Rivarola M, Belgorosky A, Mendilaharzu H, et al. Precocious4 N! c2 B# C: w
puberty in children with tumours of the suprasellar pineal
發表於 2025-1-7 21:59:43 | 顯示全部樓層
這個我收藏了!謝謝分享!WK的資源越來越豐富,這少不了大大的辛勞!
發表於 2025-1-10 10:43:39 | 顯示全部樓層
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

) a) L3 `: G& r; m. N* y& I( \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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