Clin J Gastroenterol (2012) 5:127–130 DOI 10.1007/s12328-012-0289-2
CASE REPORT
Eosinophilic gastroenteritis in a patient with chronic hepatitis C who received treatment with pegylated interferon Genryu Hirano • Atsushi Fukunaga • Tetsuro Sohda • Hideo Kunimoto • Kaoru Yotsumoto • Kunitoshi Sakurai • Hideyuki Iwashita • Shuichi Ueda • Keiji Yokoyama • Daisuke Morihara • Yoshitaka Tomioka • Akira Anan • Masashi Yamaguchi • Yasuaki Takeyama • Kouichi Eguchi • Masaharu Sakamoto • Makoto Irie • Kaoru Iwata • Satoshi Shakado • Kunihiko Aoyagi • Shotaro Sakisaka
Received: 14 October 2011 / Accepted: 4 February 2012 / Published online: 24 February 2012 Ó Springer 2012
Abstract A 54-year-old male was treated for chronic hepatitis C with pegylated interferon (PEG-IFN) a-2a administered for 24 weeks. HCV-RNA was negative at 24 weeks after treatment, showing sustained virological response (SVR). Abdominal distention and diarrhea were observed 28 weeks after commencing the treatment, i.e., 4 weeks after completing treatment. The elevation of eosinophil count was observed in blood tests and ascites, and because eosinophilic infiltration was also observed on gastrointestinal histopathology, the patient was diagnosed with eosinophilic enteritis. As the eosinophil count spontaneously improved and abdominal symptoms disappeared, the patient was not treated with steroids. The onset of eosinophilic enteritis during interferon therapy is comparatively rare. In this case, PEG-IFN was considered to be the causative factor. Furthermore, we suggested that subserosal eosinophilic enteritis may have characteristic symptoms in patients having hepatic diseases treated with interferon.
This case study was presented at the 96th Kyushu branch meeting of the Japanese Society of Gastroenterology (November 2010, Okinawa). G. Hirano (&) A. Fukunaga T. Sohda H. Kunimoto K. Yotsumoto K. Sakurai H. Iwashita S. Ueda K. Yokoyama D. Morihara Y. Tomioka A. Anan M. Yamaguchi Y. Takeyama K. Eguchi M. Sakamoto M. Irie K. Iwata S. Shakado K. Aoyagi S. Sakisaka Department of Gastroenterology and Medicine, Fukuoka University Faculty of Medicine, 7-45-1 Nanakuma, Jonan, Fukuoka 814-0180, Japan e-mail: [email protected] S. Ueda D. Morihara M. Sakamoto S. Sakisaka The Division of Advanced Clinical Research for Viral Hepatitis and Liver Cancer, Fukuoka University Faculty of Medicine, Fukuoka, Japan
Keywords Chronic hepatitis C Eosinophilic gastroenteritis Pegylated interferon (PEG-IFN) Predominant subserosal layer disease
Introduction The treatment rate of chronic hepatitis C has dramatically improved because of interferon therapy [1]. When considering the overall long-term prognosis and the risk of progression to hepatic cirrhosis and hepatocellular carcinoma for patients with chronic hepatitis C, interferon therapy has yielded an improvement in quality of life and prognosis. This therapy is also cost-effective [2]. However, numerous issues still remain, such as elderly patients with hepatitis C, groups who are refractory to genotype 1 antiviral treatment, and the influence of various side effects. In the present case, interferon therapy was used for a chronic hepatitis C patient and brought about a reduction in the viral load. This is the first case report in which PEG-IFN administration was involved in the onset of eosinophilic gastroenteritis.
Case report The patient was a 54-year-old male. Liver function abnormality had been observed when he was in his 20s, and he was later diagnosed with chronic hepatitis C. The hepatitis C virus (HCV) was of serotype 1, and serum HCV RNA was 4.9 log IU/ml. Interferon therapy (PEG-IFN a-2a once weekly) was commenced in early September 2009. He was treated for 24 weeks, and HCV-RNA was negative at 24 weeks after treatment, showing SVR. However, he presented with loss of appetite, abdominal distention, and
123
128
diarrhea from late April of the same year, and he was admitted for observation, examinations, and treatment. The previous medical history revealed treatment for bronchial asthma and chronic sinusitis, and fenestration had been performed for the chronic sinusitis when he was 48 years old. No notable findings in his family history or lifestyle history were identified. He was not taking any medicines or dietary supplements before the onset of this disease. Abdominal distension was confirmed at the time of admission. Findings from blood tests showed a white blood cell count of 4,800/ll, which was within normal values, but the eosinophil count was elevated by 46.5%. Biochemical tests showed slightly elevated aspartate aminotransferase of 42 IU/l (normal \33 IU/ml) and alanine aminotransferase of 39 IU/l (normal value \30 IU/ml). Serum HCV RNA was negative. Abdominal contrast-enhanced CT examinations confirmed ascites around the liver, the intestinal tract, and in the abdomen. Thickening of the intestinal tract wall was observed along the upper gastrointestinal tract (Fig. 1). The ascitic sample was straw colored with an increased cell count of 5,400/ll, of which eosinophils accounted for 95%. Allergic tests showed non-specific IgE elevation of 642 IU/ml (normal \400 IU/ml). Specific IgE was negative for dietary antigens. It was also negative for other infectious diseases Fig. 1 a Abdominal contrastenhanced CT examinations confirmed ascites around the liver, the digestive tract, and in the abdomen. b Thickening of the intestinal wall was mainly confirmed in the upper gastrointestinal tract
Fig. 2 a Upper gastrointestinal tract endoscopy confirmed edematous changes in the gastric mucosa. b Colonoscopy confirmed edematous changes throughout the entire colon and loss of the vascular appearance of the colon
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such as parasitosis (Ascaris lumbricoides, Echinococcus granulosus, Strongyloides stercoralis, etc.) and Helicobacter pylori. Upper gastrointestinal endoscopy confirmed edematous changes in the gastric mucosa. Colonoscopy confirmed edematous changes throughout the entire colon and loss of the vascular appearance in it (Fig. 2). Upper gastrointestinal barium study of the small intestine did not show mucosal edema of the duodenum and jejunum. The results of histopathological findings confirmed eosinophilic infiltration of the mucosal lamina propria (Fig. 3). We excluded hypereosinophilic syndrome and the vasculitis syndromes (polyarteritis nodosa, Churg-Strauss syndrome, Wegener’s granulomatosis, etc.). As the diagnostic criteria defined by Talley et al. [3] were met, the patient was diagnosed with eosinophilic gastroenteritis. Clinical management, including treating without the use of steroids, improved the eosinophil count as well as ascites, and the gastrointestinal symptoms also disappeared (Fig. 4).
Discussion Eosinophilic gastroenteritis is a disorder of unknown etiology, first reported by Kaijser in 1937 [4], and
Clin J Gastroenterol (2012) 5:127–130
129
Fig. 3 The results of histopathological findings confirmed eosinophilic infiltration of the mucosal lamina propria (arrow) /µ l 2500
LogIU/ml 6
PEG-IFNα α-2a
5
2000
HCV -RNA
4
1500
3 1000 2 500
eosinophil count
1
0
0 2009 6 9
2010 year 2
3
4
5
6
7
month
Fig. 4 Clinical course of the patient
characterized by edematous tissue and eosinophilic infiltration without vasculitis in the gastrointestinal tract wall. In the Klein et al. classification [5], eosinophilic gastroenteritis is classified into three types, namely predominant mucosal layer disease, predominant muscle layer disease, and predominant subserosal layer disease, depending on the degree of eosinophilic infiltration, with the predominant mucosal type having the highest incidence. The present case was considered to be of the predominant subserosal layer type as the symptom of abdominal distention with eosinophilic ascites was more obvious than gastrointestinal symptoms. The diagnostic criteria for eosinophlic gastroenteritis by Talley et al. are as follows: eosinophilia in the peripheral blood; eosinophilic infiltration proven by biopsies in more than one place in the gastrointestinal tract or characteristic X-ray findings with eosinophilia in the peripheral blood; the ability to rule out parasitic diseases and pathological changes outside the gastrointestinal tract.
If the above three criteria are met, eosinophilic gastroenteritis is diagnosed, and in the present case the diagnostic criteria were met. Eosinophilic gastroenteritis has already been reported as a complication after interferon-a therapy for renal cancer and during interferon a-2b therapy for chronic hepatitis C [6, 7], but the present case is the first report where PEG-IFN was considered to be the cause of eosinophilic gastroenteritis. Various complications during interferon treatment are often reported. Furthermore, as for the complications that occur after interferon treatment, thyroid disease and diabetes mellitus have been widely reported [8, 9]. In diseases caused by eosinophilic proliferation, there is proliferation in the marrow and release to the periphery mediated by Th2 lymphocyte-derived IL-5, resulting in eosinophilic induction and infiltration, and it has been suggested that eotaxins are involved in the migration of eosinophils to inflamed tissues and other regions [10]. Changes in the white blood cell count and various cytokines caused by interferon treatment vary among individuals. The present patient originally had a history of treatment for bronchial asthma and chronic sinusitis, and the eosinophil count had trended to slightly higher values as compared with reference values. We consider that the cytokine IL-5 and chemokine eotaxin were activated by PEG-IFN, and an increase in the eosinophil count was provoked, resulting in the onset of eosinophilic enteritis. However, it is difficult to determine whether PEG-IFN induced gastroenteritis or termination of PEG-IFN resulted in gastroenteritis. The eosinophil count decreases slightly during interferon administration (Fig. 4) as interferon may inhibit eosinophils, and therefore we hypothesize that eosinophilic gastroenteritis developed after interferon treatment. Interferon inhibits the production of eotaxin, and it has also been reported that eosinophils are controlled [11]. Regarding the critical time lag, as there are no past reports, the origin is unknown. A time lag may have occurred in an immune response due to the stable serum concentration, which is a characteristic of PEG-IFN. This is a complication that occurs after interferon treatment. PEG-INF is suggested as a possible trigger in the onset of eosinophilic gastroenteritis, but its role either as an inducer or an inhibitor remains unclear. In the previous and present reports [7], a high eosinophil count was present in the ascitic fluid; hence, it was believed that predominantly subserosal eosinophilic enteritis may have characteristic findings in patients with pre-existing hepatic disease who are being treated by interferon. It has been reported that steroids, the first choice drug therapy for eosinophilic enteritis, have a response rate of higher than 90% [12]. Although steroids have high efficacy, there have been several reports of relapse on discontinuation. Treatment with antihistamines is also
123
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reported to be effective for relapsed cases, with comparatively fewer side effects, and antihistamines are prescribed as maintenance therapy after discontinuing steroid treatment. Although there have been many cases of relapse, approximately 5% of cases spontaneously improve or enter remission. Spontaneously improved cases have also been reported in the elderly [13], but there are no predictable prognostic factors. In the present case, because the effects of interferon were reduced and activation of various cytokines was decreased, a lowered eosinophil count was confirmed, and the symptoms were considered to have gradually entered remission. We encountered eosinophilic gastroenteritis in a patient with chronic hepatitis C who received treatment with PEGIFN. We suggested that subserosal eosinophilic enteritis may have characteristic symptoms in patients having hepatic diseases treated with interferon.
4.
5. 6.
7.
8.
9.
10. Conflict of interest of interest.
The authors declare that they have no conflict 11.
References 1. Hayashi N, Takehara T. Antiviral therapy for chronic hepatitis C: past, present, and future. J Gastroenterol. 2006;41:17–27. 2. Hino K, Ishida H, Inoue Y, Okita K. Cost of effectiveness in the treatment for hepatocellular carcinoma. Nippon Rinsho. 2009;67: 664–7. 3. Talley NJ, Shorter RG, Phillips SF, Zinsmeister AR. Eosinophilic gastroenteritis: a clinicopathological study of patients with
123
12.
13.
disease of the mucosa, muscle layer, and subserosal tissues. Gut. 1990;31:54–8. Kaijser R. Zur Kenntis der allegischen Affektionen des verdauugskannals vom standpunkt des chirurgen aus. Arch Klin Chir. 1937;188:36–64. Klein NC, Hargrove RL, Sleisenger MH, Jeffries GH. Eosinophilic gastroenteritis. Medicine. 1970;49:299–319. Hirano M, Mori S, Higa I. A case of eosinophilic enteritis considered to be induced by interferon-a. Urol Surg Dept. 2003;16: 262. Kakumitsu S, Shijo H, Akiyoshi N, Seo M, Okada M. Eosinophilic enteritis observed during alpha-interferon therapy for chronic hepatitis C. J Gastroenterol. 2000;35:548–51. Tran HA, Reeves GE, Ianna EA, Leembruggen N. Thyroid function outcomes after pegylated interferon-a and ribavirin therapy for chronic hepatitis C. Endocr Pract. 2010;16: 934–9. Yamazaki M, Sato A, Takeda T, Komatsu M. Distinct clinical courses in type 1 diabetes mellitus induced by peg-interferonalpha treatment for chronic hepatitis C. Intern Med. 2010;49: 403–7. Ogbogu PU, Bochner BS, Butterfield JH, Gleich GJ, Huss-Marp J, Kahn JE, et al. Hypereosinophilic syndrome: a multicenter, retrospective analysis of clinical characteristics and response to therapy. J Allergy Clin Immunol. 2009;124:1319–25. Miyamasu M, Yamaguchi M, Nakajima T, Misaki Y, Morita Y, Matsushima K, Yamamoto K, Hirai K. Th1-derived cytokine IFN-gamma is a potent inhibitor of eotaxin synthesis in vitro. Int Immunol. 1999;11(6):1001–4. Lee CM, Changchien CS, Chen PC, Lin DY, Sheen IS, Wang CS, et al. Eosinophilic gastroenteritis: 10 year experience. Am J Gastroenterol. 1993;88:70–4. Ohira G, Matsui Y, Urashima T, Usui A, Taniguchi T, Ochiai T. A case of eosinophilic enteritis requiring emergency surgery. Jpn J Gastroenterol Surg. 2006;39:1534–9.
CASE REPORT
Eosinophilic gastroenteritis in a patient with chronic hepatitis C who received treatment with pegylated interferon Genryu Hirano • Atsushi Fukunaga • Tetsuro Sohda • Hideo Kunimoto • Kaoru Yotsumoto • Kunitoshi Sakurai • Hideyuki Iwashita • Shuichi Ueda • Keiji Yokoyama • Daisuke Morihara • Yoshitaka Tomioka • Akira Anan • Masashi Yamaguchi • Yasuaki Takeyama • Kouichi Eguchi • Masaharu Sakamoto • Makoto Irie • Kaoru Iwata • Satoshi Shakado • Kunihiko Aoyagi • Shotaro Sakisaka
Received: 14 October 2011 / Accepted: 4 February 2012 / Published online: 24 February 2012 Ó Springer 2012
Abstract A 54-year-old male was treated for chronic hepatitis C with pegylated interferon (PEG-IFN) a-2a administered for 24 weeks. HCV-RNA was negative at 24 weeks after treatment, showing sustained virological response (SVR). Abdominal distention and diarrhea were observed 28 weeks after commencing the treatment, i.e., 4 weeks after completing treatment. The elevation of eosinophil count was observed in blood tests and ascites, and because eosinophilic infiltration was also observed on gastrointestinal histopathology, the patient was diagnosed with eosinophilic enteritis. As the eosinophil count spontaneously improved and abdominal symptoms disappeared, the patient was not treated with steroids. The onset of eosinophilic enteritis during interferon therapy is comparatively rare. In this case, PEG-IFN was considered to be the causative factor. Furthermore, we suggested that subserosal eosinophilic enteritis may have characteristic symptoms in patients having hepatic diseases treated with interferon.
This case study was presented at the 96th Kyushu branch meeting of the Japanese Society of Gastroenterology (November 2010, Okinawa). G. Hirano (&) A. Fukunaga T. Sohda H. Kunimoto K. Yotsumoto K. Sakurai H. Iwashita S. Ueda K. Yokoyama D. Morihara Y. Tomioka A. Anan M. Yamaguchi Y. Takeyama K. Eguchi M. Sakamoto M. Irie K. Iwata S. Shakado K. Aoyagi S. Sakisaka Department of Gastroenterology and Medicine, Fukuoka University Faculty of Medicine, 7-45-1 Nanakuma, Jonan, Fukuoka 814-0180, Japan e-mail: [email protected] S. Ueda D. Morihara M. Sakamoto S. Sakisaka The Division of Advanced Clinical Research for Viral Hepatitis and Liver Cancer, Fukuoka University Faculty of Medicine, Fukuoka, Japan
Keywords Chronic hepatitis C Eosinophilic gastroenteritis Pegylated interferon (PEG-IFN) Predominant subserosal layer disease
Introduction The treatment rate of chronic hepatitis C has dramatically improved because of interferon therapy [1]. When considering the overall long-term prognosis and the risk of progression to hepatic cirrhosis and hepatocellular carcinoma for patients with chronic hepatitis C, interferon therapy has yielded an improvement in quality of life and prognosis. This therapy is also cost-effective [2]. However, numerous issues still remain, such as elderly patients with hepatitis C, groups who are refractory to genotype 1 antiviral treatment, and the influence of various side effects. In the present case, interferon therapy was used for a chronic hepatitis C patient and brought about a reduction in the viral load. This is the first case report in which PEG-IFN administration was involved in the onset of eosinophilic gastroenteritis.
Case report The patient was a 54-year-old male. Liver function abnormality had been observed when he was in his 20s, and he was later diagnosed with chronic hepatitis C. The hepatitis C virus (HCV) was of serotype 1, and serum HCV RNA was 4.9 log IU/ml. Interferon therapy (PEG-IFN a-2a once weekly) was commenced in early September 2009. He was treated for 24 weeks, and HCV-RNA was negative at 24 weeks after treatment, showing SVR. However, he presented with loss of appetite, abdominal distention, and
123
128
diarrhea from late April of the same year, and he was admitted for observation, examinations, and treatment. The previous medical history revealed treatment for bronchial asthma and chronic sinusitis, and fenestration had been performed for the chronic sinusitis when he was 48 years old. No notable findings in his family history or lifestyle history were identified. He was not taking any medicines or dietary supplements before the onset of this disease. Abdominal distension was confirmed at the time of admission. Findings from blood tests showed a white blood cell count of 4,800/ll, which was within normal values, but the eosinophil count was elevated by 46.5%. Biochemical tests showed slightly elevated aspartate aminotransferase of 42 IU/l (normal \33 IU/ml) and alanine aminotransferase of 39 IU/l (normal value \30 IU/ml). Serum HCV RNA was negative. Abdominal contrast-enhanced CT examinations confirmed ascites around the liver, the intestinal tract, and in the abdomen. Thickening of the intestinal tract wall was observed along the upper gastrointestinal tract (Fig. 1). The ascitic sample was straw colored with an increased cell count of 5,400/ll, of which eosinophils accounted for 95%. Allergic tests showed non-specific IgE elevation of 642 IU/ml (normal \400 IU/ml). Specific IgE was negative for dietary antigens. It was also negative for other infectious diseases Fig. 1 a Abdominal contrastenhanced CT examinations confirmed ascites around the liver, the digestive tract, and in the abdomen. b Thickening of the intestinal wall was mainly confirmed in the upper gastrointestinal tract
Fig. 2 a Upper gastrointestinal tract endoscopy confirmed edematous changes in the gastric mucosa. b Colonoscopy confirmed edematous changes throughout the entire colon and loss of the vascular appearance of the colon
123
Clin J Gastroenterol (2012) 5:127–130
such as parasitosis (Ascaris lumbricoides, Echinococcus granulosus, Strongyloides stercoralis, etc.) and Helicobacter pylori. Upper gastrointestinal endoscopy confirmed edematous changes in the gastric mucosa. Colonoscopy confirmed edematous changes throughout the entire colon and loss of the vascular appearance in it (Fig. 2). Upper gastrointestinal barium study of the small intestine did not show mucosal edema of the duodenum and jejunum. The results of histopathological findings confirmed eosinophilic infiltration of the mucosal lamina propria (Fig. 3). We excluded hypereosinophilic syndrome and the vasculitis syndromes (polyarteritis nodosa, Churg-Strauss syndrome, Wegener’s granulomatosis, etc.). As the diagnostic criteria defined by Talley et al. [3] were met, the patient was diagnosed with eosinophilic gastroenteritis. Clinical management, including treating without the use of steroids, improved the eosinophil count as well as ascites, and the gastrointestinal symptoms also disappeared (Fig. 4).
Discussion Eosinophilic gastroenteritis is a disorder of unknown etiology, first reported by Kaijser in 1937 [4], and
Clin J Gastroenterol (2012) 5:127–130
129
Fig. 3 The results of histopathological findings confirmed eosinophilic infiltration of the mucosal lamina propria (arrow) /µ l 2500
LogIU/ml 6
PEG-IFNα α-2a
5
2000
HCV -RNA
4
1500
3 1000 2 500
eosinophil count
1
0
0 2009 6 9
2010 year 2
3
4
5
6
7
month
Fig. 4 Clinical course of the patient
characterized by edematous tissue and eosinophilic infiltration without vasculitis in the gastrointestinal tract wall. In the Klein et al. classification [5], eosinophilic gastroenteritis is classified into three types, namely predominant mucosal layer disease, predominant muscle layer disease, and predominant subserosal layer disease, depending on the degree of eosinophilic infiltration, with the predominant mucosal type having the highest incidence. The present case was considered to be of the predominant subserosal layer type as the symptom of abdominal distention with eosinophilic ascites was more obvious than gastrointestinal symptoms. The diagnostic criteria for eosinophlic gastroenteritis by Talley et al. are as follows: eosinophilia in the peripheral blood; eosinophilic infiltration proven by biopsies in more than one place in the gastrointestinal tract or characteristic X-ray findings with eosinophilia in the peripheral blood; the ability to rule out parasitic diseases and pathological changes outside the gastrointestinal tract.
If the above three criteria are met, eosinophilic gastroenteritis is diagnosed, and in the present case the diagnostic criteria were met. Eosinophilic gastroenteritis has already been reported as a complication after interferon-a therapy for renal cancer and during interferon a-2b therapy for chronic hepatitis C [6, 7], but the present case is the first report where PEG-IFN was considered to be the cause of eosinophilic gastroenteritis. Various complications during interferon treatment are often reported. Furthermore, as for the complications that occur after interferon treatment, thyroid disease and diabetes mellitus have been widely reported [8, 9]. In diseases caused by eosinophilic proliferation, there is proliferation in the marrow and release to the periphery mediated by Th2 lymphocyte-derived IL-5, resulting in eosinophilic induction and infiltration, and it has been suggested that eotaxins are involved in the migration of eosinophils to inflamed tissues and other regions [10]. Changes in the white blood cell count and various cytokines caused by interferon treatment vary among individuals. The present patient originally had a history of treatment for bronchial asthma and chronic sinusitis, and the eosinophil count had trended to slightly higher values as compared with reference values. We consider that the cytokine IL-5 and chemokine eotaxin were activated by PEG-IFN, and an increase in the eosinophil count was provoked, resulting in the onset of eosinophilic enteritis. However, it is difficult to determine whether PEG-IFN induced gastroenteritis or termination of PEG-IFN resulted in gastroenteritis. The eosinophil count decreases slightly during interferon administration (Fig. 4) as interferon may inhibit eosinophils, and therefore we hypothesize that eosinophilic gastroenteritis developed after interferon treatment. Interferon inhibits the production of eotaxin, and it has also been reported that eosinophils are controlled [11]. Regarding the critical time lag, as there are no past reports, the origin is unknown. A time lag may have occurred in an immune response due to the stable serum concentration, which is a characteristic of PEG-IFN. This is a complication that occurs after interferon treatment. PEG-INF is suggested as a possible trigger in the onset of eosinophilic gastroenteritis, but its role either as an inducer or an inhibitor remains unclear. In the previous and present reports [7], a high eosinophil count was present in the ascitic fluid; hence, it was believed that predominantly subserosal eosinophilic enteritis may have characteristic findings in patients with pre-existing hepatic disease who are being treated by interferon. It has been reported that steroids, the first choice drug therapy for eosinophilic enteritis, have a response rate of higher than 90% [12]. Although steroids have high efficacy, there have been several reports of relapse on discontinuation. Treatment with antihistamines is also
123
130
Clin J Gastroenterol (2012) 5:127–130
reported to be effective for relapsed cases, with comparatively fewer side effects, and antihistamines are prescribed as maintenance therapy after discontinuing steroid treatment. Although there have been many cases of relapse, approximately 5% of cases spontaneously improve or enter remission. Spontaneously improved cases have also been reported in the elderly [13], but there are no predictable prognostic factors. In the present case, because the effects of interferon were reduced and activation of various cytokines was decreased, a lowered eosinophil count was confirmed, and the symptoms were considered to have gradually entered remission. We encountered eosinophilic gastroenteritis in a patient with chronic hepatitis C who received treatment with PEGIFN. We suggested that subserosal eosinophilic enteritis may have characteristic symptoms in patients having hepatic diseases treated with interferon.
4.
5. 6.
7.
8.
9.
10. Conflict of interest of interest.
The authors declare that they have no conflict 11.
References 1. Hayashi N, Takehara T. Antiviral therapy for chronic hepatitis C: past, present, and future. J Gastroenterol. 2006;41:17–27. 2. Hino K, Ishida H, Inoue Y, Okita K. Cost of effectiveness in the treatment for hepatocellular carcinoma. Nippon Rinsho. 2009;67: 664–7. 3. Talley NJ, Shorter RG, Phillips SF, Zinsmeister AR. Eosinophilic gastroenteritis: a clinicopathological study of patients with
123
12.
13.
disease of the mucosa, muscle layer, and subserosal tissues. Gut. 1990;31:54–8. Kaijser R. Zur Kenntis der allegischen Affektionen des verdauugskannals vom standpunkt des chirurgen aus. Arch Klin Chir. 1937;188:36–64. Klein NC, Hargrove RL, Sleisenger MH, Jeffries GH. Eosinophilic gastroenteritis. Medicine. 1970;49:299–319. Hirano M, Mori S, Higa I. A case of eosinophilic enteritis considered to be induced by interferon-a. Urol Surg Dept. 2003;16: 262. Kakumitsu S, Shijo H, Akiyoshi N, Seo M, Okada M. Eosinophilic enteritis observed during alpha-interferon therapy for chronic hepatitis C. J Gastroenterol. 2000;35:548–51. Tran HA, Reeves GE, Ianna EA, Leembruggen N. Thyroid function outcomes after pegylated interferon-a and ribavirin therapy for chronic hepatitis C. Endocr Pract. 2010;16: 934–9. Yamazaki M, Sato A, Takeda T, Komatsu M. Distinct clinical courses in type 1 diabetes mellitus induced by peg-interferonalpha treatment for chronic hepatitis C. Intern Med. 2010;49: 403–7. Ogbogu PU, Bochner BS, Butterfield JH, Gleich GJ, Huss-Marp J, Kahn JE, et al. Hypereosinophilic syndrome: a multicenter, retrospective analysis of clinical characteristics and response to therapy. J Allergy Clin Immunol. 2009;124:1319–25. Miyamasu M, Yamaguchi M, Nakajima T, Misaki Y, Morita Y, Matsushima K, Yamamoto K, Hirai K. Th1-derived cytokine IFN-gamma is a potent inhibitor of eotaxin synthesis in vitro. Int Immunol. 1999;11(6):1001–4. Lee CM, Changchien CS, Chen PC, Lin DY, Sheen IS, Wang CS, et al. Eosinophilic gastroenteritis: 10 year experience. Am J Gastroenterol. 1993;88:70–4. Ohira G, Matsui Y, Urashima T, Usui A, Taniguchi T, Ochiai T. A case of eosinophilic enteritis requiring emergency surgery. Jpn J Gastroenterol Surg. 2006;39:1534–9.
