However, the lesion criteria for the use of ESD, rather than strip biopsy, remain to be elucidated. Methods:  On the basis of reviews of literature and our observations concerning the outcome of strip biopsy, we set the criteria for selecting strip biopsy and ESD as follows. The indications for strip biopsy were lesions less than 10 mm in size and located in the anterior wall or greater curvature of the lower and middle stomach. ESD was indicated for all other lesions. The validity of the criteria was then analyzed prospectively in 156 patients. The rate of en bloc R0 resection and local recurrence were evaluated.

Results:  Subsequently, 156 lesions were divided according to the criteria and were endoscopically Selisistat supplier resected by strip biopsy (n = 13) or ESD (n = 143). The en bloc R0 resection rates for the whole group and MG-132 in vitro the strip biopsy and ESD groups was 93.5% (146/156), 92.3% (12/13), and 93.7% (134/143), respectively. None of the patients had suffered from local recurrence in either the strip biopsy or ESD groups. Conclusion:  The validity of our criteria for selecting strip biopsy and ESD was verified. Our criteria exploit the advantages of both procedures and obtain better endoscopic therapy outcomes for EGC. “
“Adult patients with cystic fibrosis (CF) have an increased risk of gastrointestinal malignancies.

We hypothesized that increased intestinal cell turnover beginning in childhood may explain the increased risk of malignancy in early adulthood.

Therefore we aimed to measure faecal M2-pyruvate kinase (M2-PK), a biomarker of intestinal cell turnover, in children with CF. To assess whether the increased cell turnover is secondary to intestinal inflammation, the secondary aims were to measure faecal calprotectin and evaluate its association with faecal M2-PK. Faecal samples, for 上海皓元医药股份有限公司 M2-PK and calprotectin measurements, were prospectively collected from children with CF and healthy controls (HC). Thirty-three children with CF (mean (SD) 7.3 (3.8) years old; 29 pancreatic insufficient (PI)) were enrolled and compared to 33 age-matched HC. Faecal M2-PK in CF patients (median (interquartile range (IQR)): 4.7 (1.5 – 9.7)) was greater than HC (1.0 (1.0 – 1.0) U/ml; P < 0.0001), and higher in PI (median (IQR): 5.1 (1.8 – 13.7)) than pancreatic sufficient patients (1.0 (1.0 – 1.0) U/ml; P = 0.002). Faecal calprotectin was significantly elevated in CF than HC (median (IQR) 61.3 (43.8 – 143.8) vs. 19.5 (19.5 – 35.1) mg/kg; P < 0.0001). However, there was no correlation between faecal M2-PK and faecal calprotectin levels among subjects with CF (r = 0.29; P = 0.1). Increased intestinal cell turnover is present in children with PI CF. The lack of relationship between faecal M2-PK and calprotectin suggests contributing factor(s) other than inflammation may be present.

However, the lesion criteria for the use of ESD, rather than strip biopsy, remain to be elucidated. Methods:  On the basis of reviews of literature and our observations concerning the outcome of strip biopsy, we set the criteria for selecting strip biopsy and ESD as follows. The indications for strip biopsy were lesions less than 10 mm in size and located in the anterior wall or greater curvature of the lower and middle stomach. ESD was indicated for all other lesions. The validity of the criteria was then analyzed prospectively in 156 patients. The rate of en bloc R0 resection and local recurrence were evaluated.

Results:  Subsequently, 156 lesions were divided according to the criteria and were endoscopically selleck chemical resected by strip biopsy (n = 13) or ESD (n = 143). The en bloc R0 resection rates for the whole group and buy MAPK Inhibitor Library the strip biopsy and ESD groups was 93.5% (146/156), 92.3% (12/13), and 93.7% (134/143), respectively. None of the patients had suffered from local recurrence in either the strip biopsy or ESD groups. Conclusion:  The validity of our criteria for selecting strip biopsy and ESD was verified. Our criteria exploit the advantages of both procedures and obtain better endoscopic therapy outcomes for EGC. “
“Adult patients with cystic fibrosis (CF) have an increased risk of gastrointestinal malignancies.

We hypothesized that increased intestinal cell turnover beginning in childhood may explain the increased risk of malignancy in early adulthood.

Therefore we aimed to measure faecal M2-pyruvate kinase (M2-PK), a biomarker of intestinal cell turnover, in children with CF. To assess whether the increased cell turnover is secondary to intestinal inflammation, the secondary aims were to measure faecal calprotectin and evaluate its association with faecal M2-PK. Faecal samples, for 上海皓元医药股份有限公司 M2-PK and calprotectin measurements, were prospectively collected from children with CF and healthy controls (HC). Thirty-three children with CF (mean (SD) 7.3 (3.8) years old; 29 pancreatic insufficient (PI)) were enrolled and compared to 33 age-matched HC. Faecal M2-PK in CF patients (median (interquartile range (IQR)): 4.7 (1.5 – 9.7)) was greater than HC (1.0 (1.0 – 1.0) U/ml; P < 0.0001), and higher in PI (median (IQR): 5.1 (1.8 – 13.7)) than pancreatic sufficient patients (1.0 (1.0 – 1.0) U/ml; P = 0.002). Faecal calprotectin was significantly elevated in CF than HC (median (IQR) 61.3 (43.8 – 143.8) vs. 19.5 (19.5 – 35.1) mg/kg; P < 0.0001). However, there was no correlation between faecal M2-PK and faecal calprotectin levels among subjects with CF (r = 0.29; P = 0.1). Increased intestinal cell turnover is present in children with PI CF. The lack of relationship between faecal M2-PK and calprotectin suggests contributing factor(s) other than inflammation may be present.

Double-balloon enteroscopy: input loop to the duodenum and distal stomach through the afferent loop, we found antrum scattered ulcers and old blood about the size of0.4 cm*0.3 cm, XL765 in vivo coated with white fur, bled when biopsy was performed around the ulcer. Diagnostic conclusions: distal gastric ulcers, A2 period. Conclusion: The patient underwent PPI treatment and followed-up six months. His stool was normal and fecal occult blood was negative. Key Word(s): 1. Double-balloon; 2. enteroscopy; 3. gastric bypass; Presenting Author: ZHANYUE NIU Additional

Authors: LIYA ZHOU Corresponding Author: LIYA ZHOU Affiliations: Peking University Third Hospital, Department of Gastroenterology Objective: Treatment of moderate gastric dysplasia is debated. This retrospective study investigates the developing time of moderate gastric dysplasia, focus on the find more risks of the moderate

gastric dysplasia development, and the characters of severe dysplasia or cancer. Based on the progression time and risk factors, guidelines on endoscopic surveillance or treatment strategies can be indicated. Methods: Patients who received endoscopic surveillance with diagnosis of gastric moderate dysplasia in Peking University Third Hospital from January 2006 to December 2012 were investigated. The patients who got severe dysplasia or gastric cancer were defined as positive ends, and assigned to the case group. Other patients without progression were assigned to the control group. Chi-square analysis and binary logistic regression analysis were used to analyze the location, the size, the endoscopic performance

and infection of Helicobacter pylori of the lesions between the two groups. Results: 107 patients with 135 gastric moderate dysplasia lesions were investigated. There were 20 patients with 22 lesions in the case group, while 87 patients with 113 lesions in the control group. In patients with severe dysplasia or gastric cancer, progression time medchemexpress during first 3 months after the discovering of gastric moderate dysplasia was 40%(8/20), 50%(10/20) during the fires half a year, 55%(11/20) during the first year and 90%(18/20) during the first 3 years. Congestive gastric mucosal lesions were more likely to progress. The severe dysplasia or cancer Showed the characteristics for ulcer or bulge, and the longest diameter was more than 2.5 cm (Chi-square analysis, P < 0.05). Conclusion: Moderate dysplasia for congestion performance was more likely to progress. Ulcer, bulge and lesions in the longest diameter greater than 2.5 cm were the characteristics of severe hyperplasia or cancer. The interval time of endoscopic surveillance was no more than 3 months. Key Word(s): 1. gastric dysplasia; 2. cancer; 3. endoscopic; 4.

Furthermore, the diagnostic performance of immunostaining for integrins and laminin was evaluated using highly positive groups for integrins and positive groups for laminin and selleck chemical calculating the sensitivity, specificity, positive predictive value and negative predictive value to differentiate CoCC from CCC. The following cell lines were used: five human CCC cell lines, HuCCT1 and HuH28 (Human Science Research Resources

Bank, Osaka, Japan) and RBE, SSP-25 and TKKK (RIKEN BioResource Center, Tsukuba, Japan); six HCC cell lines, Hep G2, HLF and Li-7 (RIKEN BioResource Center), and HuH-6, HuH-7 and PLC/PRF/5 (Human Science Research Resources Bank); Saracatinib in vitro and two CHC cell lines, KMCH-1 and KMCH-2 (H. Yano, Kurume University, Kurume, Japan).[27, 28] The HuCCT1, HuH28, RBE, SSP-25 and Li-7 cells were cultured in RPMI-1640 (Life Technologies, Carlsbad, CA, USA) and 10% fetal bovine serum (FBS) (Life Technologies) supplemented with penicillin and streptomycin in 100-mm dishes at 37°C with 5% CO2. Similarly, the TKKK, PLC/PRF/5, HuH-6, HuH-7 and KMCH-1

cells were cultured with 10% FBS, and the HLF and KMCH-2 cells were cultured with 5% FBS in Dulbecco’s modified Eagle’s medium (DMEM; Life Technologies). The Hep G2 cells were grown in modified Eagle’s medium (Life Technologies) with 10% FBS and 0.1 mM non-essential amino acids. A solution of trypsin-ethylenediaminetetraacetic acid was used for subculturing. Moreover, KMCH-2 was cultured in a collagen gel matrix (Cell matrix TypeI-A, pH 3.0; Nitta Gelatin, Osaka, Japan) following the method of Yano et al.[28] To collect the cells, the gel was dissolved with 0.02% collagenase on day 10. KMCH-2 cells cultured in the conventional medium to confluent or subconfluent condition

or for 10 days in collagen gel matrix in each of three dishes were used for the ITGB6, B4 and A3 mRNA assays. Total RNA was extracted from the 13 medchemexpress cell lines using an AllPrep DNA/RNA/Protein Mini Kit (Qiagen, Hilden, Germany) according to the manufacturer’s instructions. One microgram of total RNA was reverse transcribed to cDNA using a QuantiTect RT Kit (Qiagen) with oligo (dT) and random hexamers in accordance with the manufacturer’s instructions. The quantitative reverse transcription polymerase chain reaction (PCR) was performed using Power SYBR Green Master Mix (Life Technologies) and 1 μg of cDNA as the template, as previously described.[29] The following primer sets for the detection of ITGB6, B4, and A3 and the housekeeping genes B2M (β2-microglobulin) and TBP (TATA box-binding protein) were designed using Primer3Plus (http://primer3plus.

Furthermore, the diagnostic performance of immunostaining for integrins and laminin was evaluated using highly positive groups for integrins and positive groups for laminin and selleck compound calculating the sensitivity, specificity, positive predictive value and negative predictive value to differentiate CoCC from CCC. The following cell lines were used: five human CCC cell lines, HuCCT1 and HuH28 (Human Science Research Resources

Bank, Osaka, Japan) and RBE, SSP-25 and TKKK (RIKEN BioResource Center, Tsukuba, Japan); six HCC cell lines, Hep G2, HLF and Li-7 (RIKEN BioResource Center), and HuH-6, HuH-7 and PLC/PRF/5 (Human Science Research Resources Bank); BVD-523 and two CHC cell lines, KMCH-1 and KMCH-2 (H. Yano, Kurume University, Kurume, Japan).[27, 28] The HuCCT1, HuH28, RBE, SSP-25 and Li-7 cells were cultured in RPMI-1640 (Life Technologies, Carlsbad, CA, USA) and 10% fetal bovine serum (FBS) (Life Technologies) supplemented with penicillin and streptomycin in 100-mm dishes at 37°C with 5% CO2. Similarly, the TKKK, PLC/PRF/5, HuH-6, HuH-7 and KMCH-1

cells were cultured with 10% FBS, and the HLF and KMCH-2 cells were cultured with 5% FBS in Dulbecco’s modified Eagle’s medium (DMEM; Life Technologies). The Hep G2 cells were grown in modified Eagle’s medium (Life Technologies) with 10% FBS and 0.1 mM non-essential amino acids. A solution of trypsin-ethylenediaminetetraacetic acid was used for subculturing. Moreover, KMCH-2 was cultured in a collagen gel matrix (Cell matrix TypeI-A, pH 3.0; Nitta Gelatin, Osaka, Japan) following the method of Yano et al.[28] To collect the cells, the gel was dissolved with 0.02% collagenase on day 10. KMCH-2 cells cultured in the conventional medium to confluent or subconfluent condition

or for 10 days in collagen gel matrix in each of three dishes were used for the ITGB6, B4 and A3 mRNA assays. Total RNA was extracted from the 13 MCE cell lines using an AllPrep DNA/RNA/Protein Mini Kit (Qiagen, Hilden, Germany) according to the manufacturer’s instructions. One microgram of total RNA was reverse transcribed to cDNA using a QuantiTect RT Kit (Qiagen) with oligo (dT) and random hexamers in accordance with the manufacturer’s instructions. The quantitative reverse transcription polymerase chain reaction (PCR) was performed using Power SYBR Green Master Mix (Life Technologies) and 1 μg of cDNA as the template, as previously described.[29] The following primer sets for the detection of ITGB6, B4, and A3 and the housekeeping genes B2M (β2-microglobulin) and TBP (TATA box-binding protein) were designed using Primer3Plus (http://primer3plus.

Most of the IL-22 transgenic mice died within the first few days after birth. In addition, Savan et al.19 developed transgenic mice in which IL-22R1 was expressed

on lymphocytes. These mice died of inflammation 6-8 weeks after birth and also showed high levels of circulating IL-22, thus demonstrating that aberrant expression of IL-22R1 was sufficient to drive IL-22 production by lymphocytes. In this study, we demonstrate that a high percentage of inflammatory cells in patients with chronic hepatitis B virus (HBV) MK-8669 in vitro or hepatitis C virus (HCV) expressed IL-22 and that the number of IL-22–positive cells correlates positively with the grade of liver inflammation and serum levels of aspartate aminotransferase, thus implicating IL-22–expressing lymphocytes as mediators of pathogenesis in these diseases. At present, there are no small animal models available with chronic viral hepatitis and liver inflammation that are associated with elevation of IL-22 in the liver. As mentioned above, transgenic mice with IL-22 overexpression in lymphoid cells died within the first few days after birth.18 Thus, in order to define the role of elevated

IL-22 in the pathogenesis of liver disease, we developed transgenic mice with overexpression of IL-22 in the liver under the control of the albumin promoter to imitate mTOR inhibitor the situation in viral hepatitis patients with high levels of IL-22 in the liver. In contrast to EμLCK promoter–driven or the rat insulin II promoter–driven IL-22TG mice,18 liver-specific IL-22TG had no obvious adverse phenotypes and no overt inflammation, but were completely resistant to T cell hepatitis, had 上海皓元 accelerated liver regeneration after partial hepatectomy, and showed increased sensitivity to diethylnitrosamine (DEN)-induced liver cancer. ALT, alanine aminotransferase; AST, aspartate aminotransferase; ConA, concanavalin A; DEN, diethylnitrosamine; HBV, hepatitis B virus; HCV, hepatitis C virus; IL-22, interleukin-22; PCR, polymerase chain reaction; PHx, partial

hepatectomy; pSTAT, phosphorylated signal transducer and activator of transcription; SAA, serum amyloid A; STAT, signal transducer and activator of transcription; TG, transgenic; WT, wild-type. Most human cirrhotic liver samples were obtained from recipient livers after transplantation; some liver samples from patients with chronic HBV or HCV were obtained by way of biopsy (Supporting Information Table 1). Evaluation of severity of disease followed the Scheuer criterion. The degree of inflammatory infiltration was defined as grade (G), and the degree of fibrosis was defined as stage (S). Normal healthy liver samples were obtained from normal healthy donors for liver transplantation. The study protocol involved in human samples was approved by the local ethics committee, and all patients provided written informed consent.

Most of the IL-22 transgenic mice died within the first few days after birth. In addition, Savan et al.19 developed transgenic mice in which IL-22R1 was expressed

on lymphocytes. These mice died of inflammation 6-8 weeks after birth and also showed high levels of circulating IL-22, thus demonstrating that aberrant expression of IL-22R1 was sufficient to drive IL-22 production by lymphocytes. In this study, we demonstrate that a high percentage of inflammatory cells in patients with chronic hepatitis B virus (HBV) find more or hepatitis C virus (HCV) expressed IL-22 and that the number of IL-22–positive cells correlates positively with the grade of liver inflammation and serum levels of aspartate aminotransferase, thus implicating IL-22–expressing lymphocytes as mediators of pathogenesis in these diseases. At present, there are no small animal models available with chronic viral hepatitis and liver inflammation that are associated with elevation of IL-22 in the liver. As mentioned above, transgenic mice with IL-22 overexpression in lymphoid cells died within the first few days after birth.18 Thus, in order to define the role of elevated

IL-22 in the pathogenesis of liver disease, we developed transgenic mice with overexpression of IL-22 in the liver under the control of the albumin promoter to imitate selleck products the situation in viral hepatitis patients with high levels of IL-22 in the liver. In contrast to EμLCK promoter–driven or the rat insulin II promoter–driven IL-22TG mice,18 liver-specific IL-22TG had no obvious adverse phenotypes and no overt inflammation, but were completely resistant to T cell hepatitis, had medchemexpress accelerated liver regeneration after partial hepatectomy, and showed increased sensitivity to diethylnitrosamine (DEN)-induced liver cancer. ALT, alanine aminotransferase; AST, aspartate aminotransferase; ConA, concanavalin A; DEN, diethylnitrosamine; HBV, hepatitis B virus; HCV, hepatitis C virus; IL-22, interleukin-22; PCR, polymerase chain reaction; PHx, partial

hepatectomy; pSTAT, phosphorylated signal transducer and activator of transcription; SAA, serum amyloid A; STAT, signal transducer and activator of transcription; TG, transgenic; WT, wild-type. Most human cirrhotic liver samples were obtained from recipient livers after transplantation; some liver samples from patients with chronic HBV or HCV were obtained by way of biopsy (Supporting Information Table 1). Evaluation of severity of disease followed the Scheuer criterion. The degree of inflammatory infiltration was defined as grade (G), and the degree of fibrosis was defined as stage (S). Normal healthy liver samples were obtained from normal healthy donors for liver transplantation. The study protocol involved in human samples was approved by the local ethics committee, and all patients provided written informed consent.

On the other hand, H. pylori prevalence among HIV-infected children from Uganda was surprisingly low, only 22.5% compared to the prevalence in healthy African children which is much higher [10]. The explanation for significantly lower prevalence in HIV-infected children is accidental eradication with frequent antibiotic therapy used for the treatment of infectious comorbidity. Muhsen et al.[11] studied the prevalence of H. pylori infection in different ethnic groups within the same geographic area and found

22.9% seropositivity among Jewish children and significantly higher 45.6% in Arab children in Israel. JNK inhibitor This difference was explained by different socioeconomic status, cultural habits and family size [11]. In an another study, risk factors for the acquisition and maintenance of the H. pylori infection were more than three siblings in the family, the use of well water for drinking, and male gender [12]. Conditions and clinical presentations selleck products indicating or precluding search for H. pylori infection have been extensively reviewed in the recently published guidelines [13] and are summarized in the Table 1. Testing for H. pylori in children should be performed in properly

selected patients (Table 1) and with an adequate diagnostic procedure. Current recommendations do not approve a “test and treat” approach, but to select a patient in whom organic disease is expected based on detailed medical history and physical examination [13]. Therefore, diagnostic procedures should aim to determine underlying disease and not to detect H. pylori [13]. Although noninvasive tests yield high sensitivity and specificity, endoscopy with histopathology remains the only method that can detect

lesions associated with the infection, but also other possible causes of the patient’s symptoms [14]. As no single test is accurate enough for detection of H. pylori, current guidelines recommend medchemexpress endoscopy with gastric biopsies and confirmation of infection with two different tests: either histopathology and rapid urease test or a culture [13]. Regarding noninvasive tests, recently published meta-analysis on the performance of the 13C-urea breath test (13C-UBT) showed relatively good accuracy especially in children older than 6 years of age (sensitivity 96.6%, specificity 97.7%) [15]. However, stool antigen-detection test do not depend on the age and has similar accuracy; meta-analysis on stool antigen-detection tests revealed that enzyme-linked immunosorbent assay (ELISA) monoclonal antibodies have the best performance, with sensitivity and specificity of 97% compared to ELISA polyclonal antibodies (sensitivity of 92%, specificity of 93%), and to one-step monoclonal antibody tests (sensitivity of 88%, specificity of 93%) [16]. Therefore, both of noninvasive tests, 13C-UBT and the accurate stool antigen-detection test, are recommended as reliable methods for evaluation of eradication rate in children [13].

The presence of a membrane in the inferior vena cava also influences therapy as many of these patients are treated by dilatation of the inferior vena cava rather than surgical shunts or transjugular intrahepatic portosystemic shunts (TIPS). In the patient illustrated below, membranous obstruction of the inferior vena cava was associated with vascular collaterals that resulted in an unusual appearance on a chest radiograph. A 42-year-old woman was investigated because of fatigue, mild dyspnea

and a 3-month history of peripheral edema. Physical examination revealed two varicose vessels on her left back. A chest radiograph showed an abnormality in the left lower lobe of her lung that raised the possibility of lung cancer (Figure 1). However, a Doppler ultrasound study and an abdominal computed tomography scan showed a narrow segment between the inferior DNA Synthesis inhibitor vena cava and the right atrium consistent with a Budd-Chiari syndrome. The diagnosis was confirmed by angiography that demonstrated complete

obstruction of the inferior vena cava (arrowhead) and Selleck Paclitaxel the formation of numerous collateral vessels (1 represents the inferior vena cava; 2, left renal vein; 3, ascending lumbar vein; 4, left subphrenic vein; 5, right subphrenic vein) as shown in Figure 2. A dilated cardiac septal vein (arrow) created the abnormality on the chest radiograph. This vein was linked to the left subphrenic vein in the cardiac septum and entered into the superior vena cava through the left brachiocephalic vein. After balloon dilatation of the inferior vena cava, blood was shown to enter the right atrium and pressure in the inferior vena cava fell from 16 mmHg to 9 mmHg. Various investigations did not reveal a hypercoagulable state. Treatment resulted in improvement in symptoms and a reduction in the size of the abnormality on the chest radiograph. Contributed by “
“To the Editor: We read with great interest the practice guidelines for the diagnosis and MCE公司 management of autoimmune hepatitis recently issued by the American Association for the Study of Liver Diseases

(AASLD).1 In particular, we appreciate the new definition of biochemical remission, which now requires not only normal bilirubin and gamma-globulin levels but also normal serum aminotransferases; this is at variance with the 2002 definition,2 which considers aminotransferase levels lower than twice the upper limits of normal to be sufficient. According to the 2002 criteria, nearly 80% of patients with autoimmune hepatitis enter remission within 3 years. The recently coined new definition will result in a tremendous change in the rate of response to immunosuppressive treatment for autoimmune hepatitis. Here we present our own experience, which has already been published in part,3 and compare the different response rates according to the 2002 and 2010 definitions of remission.

The presence of a membrane in the inferior vena cava also influences therapy as many of these patients are treated by dilatation of the inferior vena cava rather than surgical shunts or transjugular intrahepatic portosystemic shunts (TIPS). In the patient illustrated below, membranous obstruction of the inferior vena cava was associated with vascular collaterals that resulted in an unusual appearance on a chest radiograph. A 42-year-old woman was investigated because of fatigue, mild dyspnea

and a 3-month history of peripheral edema. Physical examination revealed two varicose vessels on her left back. A chest radiograph showed an abnormality in the left lower lobe of her lung that raised the possibility of lung cancer (Figure 1). However, a Doppler ultrasound study and an abdominal computed tomography scan showed a narrow segment between the inferior Dabrafenib vena cava and the right atrium consistent with a Budd-Chiari syndrome. The diagnosis was confirmed by angiography that demonstrated complete

obstruction of the inferior vena cava (arrowhead) and HCS assay the formation of numerous collateral vessels (1 represents the inferior vena cava; 2, left renal vein; 3, ascending lumbar vein; 4, left subphrenic vein; 5, right subphrenic vein) as shown in Figure 2. A dilated cardiac septal vein (arrow) created the abnormality on the chest radiograph. This vein was linked to the left subphrenic vein in the cardiac septum and entered into the superior vena cava through the left brachiocephalic vein. After balloon dilatation of the inferior vena cava, blood was shown to enter the right atrium and pressure in the inferior vena cava fell from 16 mmHg to 9 mmHg. Various investigations did not reveal a hypercoagulable state. Treatment resulted in improvement in symptoms and a reduction in the size of the abnormality on the chest radiograph. Contributed by “
“To the Editor: We read with great interest the practice guidelines for the diagnosis and MCE management of autoimmune hepatitis recently issued by the American Association for the Study of Liver Diseases

(AASLD).1 In particular, we appreciate the new definition of biochemical remission, which now requires not only normal bilirubin and gamma-globulin levels but also normal serum aminotransferases; this is at variance with the 2002 definition,2 which considers aminotransferase levels lower than twice the upper limits of normal to be sufficient. According to the 2002 criteria, nearly 80% of patients with autoimmune hepatitis enter remission within 3 years. The recently coined new definition will result in a tremendous change in the rate of response to immunosuppressive treatment for autoimmune hepatitis. Here we present our own experience, which has already been published in part,3 and compare the different response rates according to the 2002 and 2010 definitions of remission.