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101
Vol. 35, pp. 101ῒ107, 2007
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F C B!/GHIJ"KLM+ C B!/GH?#N* 2005
8 * 15 01O;CP:Q9RῌST$%&'I()NM+ U&VWX 3 Y*
Z hepatitis C virus ῌHCV῍ RNA +/,[/\]^M+ U&VWX 8 Y*01_,-`ab
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? 14 Yq2r3Is^@$%&'It\N* uX+c,vwNM+ O;CP:Q9R
ῌST$%&'xyt?4z{5`|6KLM`* $%&'tXs HCV RNA
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C B!/GH* O;CP:Q9RῌST$% &'* xyt* 4CDE89€
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89€`GmLM Genotype 1b Bl‚4CD
C B!/GH?6j Genotype 1 Bl‚4C
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C B!/GHF 1 I¢£NM+ 4CDED
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6@sU&yˆAŽ`§HZijk\`¨©KL
j1*2῏+ Œ>* ?/U\KLj Genotype 2 B
M+
M,@4CDE
F+Z,U&yˆAŽ`BK
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Table 1. Laboratory Findings
῍ 1')‚ƒῌ„…†‡0Q 8 - 15
ῌ 4ˆ'()*ῌ+,
!
"῍ C #$%
5
ῌ ‰Š‹Œ 3 9 HCV RNA &'()*ῌ+,
FŽ012
ῌ ‰Š‹Œ 8 Q 10 -
2005 8 - 10 ./012
ῌ
‘4’^6“”
ῌ _$aK`•_$a6
: 49 34
`&5Š‹
῍ ’^6F
predonisolone, bucillamine 5 ῌ ‰Š‹Œ 13 ˆ'()*
ῌ 51 34678 losartan potassium 5
+,=–5—M
῍ ’^6Fb˜™
9:2
ῌ
š5›῍ Qœcd‡“”
ῌ ežŸZ9
: 71ῌ ;<1ῌ
:&@0 ¡῍ ¢ž£¤f5gh 14 ¥iœ
: =%>?@01ῌ
jQ 11 - 16 5‡25¦0
153.3 cm, !A 53.0 kg, !B 35.6ῌCῌ
ῌ dŒ’^6cdF§
ῌ ˆ'
78 140ῐ80 mmHg, "# 56 Cῐ$῎%῏ῌ DEF&
()*ῌ+,k¦l¨
'ῌ G(H)*71I῍ GJH)K+1ῌ G
} \ © m  \ ῍ ¦ Œ ‡ HCV
JH)LM,)N-1ῌ .OPQ
RNA Žª῎'gh«n¬῏o¡\
OR/50"Sῌ 12F34ῌ59861I῍ & ῌFigure 2῍ῌ p‰9n¬o¡\
q­
7589TSῌ UV:WW;1ῌ <X
k®
"Š‹rsHt7&5u>
0
YF89TSῌ =Z[>\]0=?2
@¯῍ HCV-RNA MF 31 KIUῐml 0—v
ῌ6:4ῌ
4῍ HCV w°xyz 5A {n῎non-structural re-
: : @ABC0^_^!6D50"
ῌ
gion 5A; NS5A῍ Interferon sensitivity determin-
EFGFH
\4῍ IJ`aKFbcDd
ing region ῌISDR῍ ±²³´|R5 7 µv0"
U9:2
ῌ HCV eLf#F Genotype 1b #9
ῌFigure 3῏ῌ
'ghMF 450 KIUῐml 9:2
ῌTable 1῍ῌ
: $iNCOPj
Q 8 - 11 RSk5lm
ῌ T"n
C #$%&'()*‰
UopVF9῍ qrWFH
\
ῌ X
¬¶5·
%&­f0¸s}­f'
_ J 5 s! 0 $ t Y Z u50 "
gh}­f'¡ 12&7ῑ9῏ῌ 'gh
hepatitis C virus ῌHCV῍ &$9 A1ῐF1
}­f9:&'gheLf#'ghMF
vw9:2
ῌFigure 1῍ῌ '()*
‰¬¶E~0\47῍8῏῍ ”X€
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46
D
EF^G SVR N? CH-C 1 103
Figure 1. Liver needle biopsy was carried out to evaluate histological activity and degree of fibrosis῍ the tissue showed
mild fibrosis of the periportal areas ῌarrow῍ and mild infiltration of inflammatory cells mainly composed of
mononuclear cells. Limiting plate was maintained ῌarrowheads῍. These findings correspond to chronic active
hepatitis, A1῏F1. ῌa: Masson-trichrome stain, b: hematoxylin-eosin stain῍.
Figure 2. Clinical course.
Figure 3. Amino acid substitution in ISDR.
῍ Geno-
HI?JK/LMN?O0P5ῌ
type 1b 6G Genotype 1b QRE HCV RNA !
"#$%&!ῌ'()'! 48 *+,-.
?CS14ῌ 6
/0123145 ῌ 67894:
!ῌ'()'!+,TU
EFCG
!"#$%&!ῌ'()'!+,;<
I?JK/LMN?VW01῍
,0=>?5@ABC5+,D
EFCG
XYZ[ HCV RNA 31 KIU῏ml 0\]
10῎
47
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·¸¹ab
104
º»c¼
ῌ Martinot-Peignoux q&'> ISDR ?@AB5F—"M
HCV-RNA ˜?.17῏m NS5B .18῏?@AB5
ῌ
)*
d&'(+,01!
!
" Genotype 1b #"$%῍ 23῍ HIUEB
"2™Kv
&'()*
+, HCV
JK"L‘’„<L+>H
ῌ
11῏
- 5A . ῌnon-structural region 5A; NS5
opῌqrsq&'M
A῍ Interferon sensitivity determining region
FNšO›'œžŸ
19῍ῌ ῌISDR῍ /01!23῍ 456
>yz! P;¡Sd¢£Qv¤
789
Rv¥¦2LRCS1m§"
W>ῌ
ῌ Enomoto Genotype 1b #
T¨"2opῌqrsq&
C #9:; 82 <=> ISDR ?@AB
'! 50 U©"O›'Vª
56 0῎C#῏> 0ῐ῍ 1ῑ3 D῎E#῏
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> 14ῐ῍ 4 DFG῎5#῏> 100ῐ >HI
¢£Qv¤X¬eY>H3῍ Uv"L3
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12ΐ14῏
S20῏ῌ
23 ῍ JK Pascu "LIM
­Zi4>H῍ L®"R¯C°d
N0!14῏ῌ ±w῍ ²°[\³;3x]´
OP<=> ISDR ?@AB" 7 QR5
µ!i49HS῍ "^_(
S 5# > H ! " ῌ >
O›'"Ud‚ƒ`"L+>H
13῏
ISDR 5#>H3῍ &'(#$%
ῌ
TU"&'( 14 VE)U
῍
UE"MWWX
Y&'(Z*(
῏
++
ῌ [,῍ \])*
+
™¶n῎῍ O›'œS"&'
,:-^_`."/a0b9#
:Ux"MWWX
Y&'(Z*(
cd"
WI239῏῍ >:-
Genotype1b Wj&'( C #9:
^_ F1 e1>HIM2f3g"h
; 1 yzῌ &'()*
+,
i4901!ῌ Zeuzem Genotype
‚ƒ"|}d>;"2MUE
1 #Wj#&'( C #9:;"2k
)…i4>H01!ῌ
24 V&'"2῍ l5 48 V67
& ' ( Z* (
ῌῑῐ῎
15῏ῌ m῍ n῎opῌqrs
1῏ Berg T, von Wagner M, Nssser S, Sarrazin C,
q&'"tu8O9vw&῍ Heintges T, Gerlach T, Buggisch P, Goeser T,
:UxK"&'(Z*0 C #9
Rasenack J, Page GR, Schmidt WE, Kalli-
:; 1 yz16῏ῌ vM Genotype
nowski B, Klinker H, Spengler U, Martus P,
1b #Wj&'(;y{|}!
Alshuth U and Zeuzem S. Extended treatment
῍ &'( 93 KIUῒml
duration for hepatitis C virus type 1: compar-
~€023῍ ISDR ?@AB5
ing 48 versus 72 weeks of peginterferon-alfa-2a
5 QR"
plus ribavirin. Gastroenterology 2006; 130:
S5#>HIῌ \]2
L&'()*
+,‚ƒ„<"L
1086ΐ1097.
3opῌqrsq&'U
2῏ Sanchez-Tapias JM, Diago M, Escartin P, En-
E)…i4>H01!ῌ
riquez J, Romero-Gomez M, Barcena R, Cre-
UE)…†‡ˆ=*῍ ‰Š*2Ly
spo J, Andrade R, Martinez-Bauer E, Perez R,
‹*>?e~M
῍ Œy‹)(
Testillano M, Planas R, Sola R, Garcia-
i4>Hῌ [,>῍ @AUEB
Bengoechea M, Garcia-Samaniego J, Munoz-
ŽCK:;DE!‘’"„<d
Sanchez M and Moreno-Otero R; TeraVIC-4
“”•F>Hῌ –G῍ ῌqrs
Study Group. Peginterferon-alfa2a plus ribavi48
&$_/'(`a SVR bc,de CH-C 3 1 *
rin for 48 versus 72 weeks in patients with
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9῏ Moussalli J, Opollon P and Poynard T. Man-
detectable hepatitis C virus RNA at week 4 of
agement of hepatitis C. J Viral Hepat. 1998; 5:
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73ῑ82.
Gastroenterology
2006;
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10῏ 789:῍ ;
451ῑ460.
<῍ =>?@῍ AB῍ C
DE῍ FGῌ Genotype 1 +HIJKL
3῏ Dalgard O, Bjøro K, Hellum KB, Myrvang B,
Ritland S, Skaug K, Raknerud N and Bell H.
M3 C Treatment with pegylated interferon and ri-
PQN a-2b RSTUSN 48 V"#$%3W
! PEG- N O
bavirin in HCV infection with genotype 2 or 3
#ῒNOPQN a-2b RSTUSN 6
for 14 weeks: A pilot study. Hepatology 2004;
XY"#$%R3 retrospective Z[\ῒῌ ]^ 2004; 49: 1099ῑ1121.
40: 1260ῑ1265.
4῏ Mangia A, Santoro R, Minerva N, Ricci GL,
11῏ Martinot-Peignoux M, Boyer N, Pouteau M,
Carretta V, Persico M, Vinelli F, Scotto G,
Castelnau C, Giuly N, Duchatelle V, Auperin
Bacca D, Annese M, Romano M, Zechini F,
A, Degott C, Benhamou JP, Erlinger S and
Sogari F, Spirito F and Andriulli A. Peginter-
Marcellin P. Predictoes of sustained response
feron alfa-2b and ribavirin for 12 vs. 24 weeks
to alpha interferon therapy in chronic hepatitis
in HCV genotype 2 or 3. N Engl J Med 2005;
C. J Hepatol. 1998; 29: 214ῑ223.
352: 2609ῑ2617.
12῏ Enomoto N, Sakuma I, Asahina Y, Kurosaki
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M, Murakami T, Yamamoto C, Izumi N, Ma-
H, Rasenack J, Heintges T, Bergk A, Berns-
rumo F and Sato C. Comparison of full-length
meier C, Häussinger D, Herrmann E and Zeu-
sequences of interferon-sensitive and resistant
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6῏ ῍ 13῏ Enomoto N, Sakuma I, Asahina Y, Kurosaki
῍ ῍ ῍ ῌ C ῎ 2῏
M, Murakami T, Yamamoto C, Ogura Y,
!
Izumi N, Marumo F and Sato C. Mutations in
IFN-a-2bῐribavirin "#$% ῒ&$'()*
the nonstructural protein 5A gene and response
+,-./012345ῒῌ 6 2005; 47:
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240ῑ244.
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7῏ Shiratori Y, Kato N, Yokosuka O, Imazeki F,
77ῑ81.
Hashimoto E, Hayashi N, Nakamura A,
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Asada M, Kuroda H, Tanaka N, Arakawa Y
B, Hopf U, Schreier E and Berg T. Sustained
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interferon therapy in chronic hepatitis C virus
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8῏ Yoshioka K, Kobayashi M, Orito E, Watan-
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15῏ Zeuzem S, Buti M, Ferenci P, Horsmans Y,
Hirofuji H, Fuji A, Kuriki J, Arao M, Murase
Cianciara J, Ibranyi E, Weilamd O, Noviello
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49
abcde
106
./01
f
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N, Asahina Y, Kurosaki M, Ueda E, Tanabe
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῍ ῎ῌ
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ῌ ῌ 2004ῌ 523῍527
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ῌ !"
ῌ ,)-
of amino acid substitution pattern in Core pro-
ῌ #$%&'ῌ ()*+
ῌ ./01ῌ 23
4ῌ 567
tein of hepatitis C virus genotype 1b high viral
8ῌ !9:;ῌ <=>?῍ @ABCDEFG
load and non-virological response to inter-
HIJKLMNEOPQMῌRSTRMUH
feron-ribavirin combination therapy. Intervi-
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18ῌ Hamano K, Sakamoto N, Enomoto N, Izumi
50
SVR CH-C 1 107
Abstract
A Case of Chronic Hepatitis C Obtained Sustained Virological
Response Regardless of Premature Discontinuation of
Peg-IFN a2b Plus Ribavirin Treatment
Kotaro Matsunaga1, Chiaki Okuse1, Kayo Adachi1, Masaru Okamoto1,
Minoru Kobayashi1, Hiroki Ikeda1, Hideaki Takahashi1, Yoshiki Katakura1,
Toshiya Ishii1, Nobuyuki Matsumoto1, Junki Koike2, Hiroshi Yotsuyanagi3,
Shiro Iino4, Michihiro Suzuki1, and Fumio Itoh1
A 54-year-old woman, who had been under treatment for rheumatoid arthritis and Sjögren’s syndrome,
was diagnosed as having chronic hepatitis C ῌCH-C῍ with genotype 1b and high load viremia. She was
admitted to our hospital for pegylated interferon ῌPeg-IFN῍ a2b plus ribavirin treatment for chronic
hepatitis C. Her serum hepatitis C virus ῌHCV῍-RNA level became undetectable 3 weeks after the initiation
of peg-IFN a2b plus ribavirin treatment. She su#ered from severe sore throat 8 weeks after the initiation of
peg-IFN a2b plus ribavirin treatment. Despite symptomatic medications, sore throat continued. Peg-IFN
a2b plus ribavirin treatment was discontinued because a causal relationship between sore throat and
Peg-IFN a2b plus ribavirin treatment was suspected. Sore throat improved after discontinuation of Peg-IFN
a2b plus ribavirin treatment. Although recurrence of hepatitis and viremia was predisposed because of
premature discontinuation of the peg-IFN a2b plus ribavirin treatment, she has remained HCV-RNA
negative, subsequently.
1 Division of Gastroenterology and Hepatology, Department of Internal Medicine, St. Marianna University School of
Medicine, Kawasaki, Japan
2 Department of Pathology, St. Marianna University School of Medicine, Kawasaki, Japan
3 Division of Infectious Diseases, Department of Internal Medicine, University of Tokyo, Tokyo, Japan
4 Research Center for Liver Disease, Kiyokawa Medical Center, Tokyo, Japan
51
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