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Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study
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| Zeitschriftentitel: | Journal of Pediatric Gastroenterology and Nutrition |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , |
| In: | Journal of Pediatric Gastroenterology and Nutrition, 43, 2006, S1 |
| Format: | E-Article |
| Sprache: | Englisch |
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Wiley
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| Schlagwörter: |
| author_facet |
Regev, Arie Guaqueta, Constanza Molina, Enrique G. Conrad, Andrew Mishra, Vishnu Brantly, Mark L. Torres, Maria De Medina, Maria Tzakis, Andreas G. Schiff, Eugene R. Regev, Arie Guaqueta, Constanza Molina, Enrique G. Conrad, Andrew Mishra, Vishnu Brantly, Mark L. Torres, Maria De Medina, Maria Tzakis, Andreas G. Schiff, Eugene R. |
|---|---|
| author |
Regev, Arie Guaqueta, Constanza Molina, Enrique G. Conrad, Andrew Mishra, Vishnu Brantly, Mark L. Torres, Maria De Medina, Maria Tzakis, Andreas G. Schiff, Eugene R. |
| spellingShingle |
Regev, Arie Guaqueta, Constanza Molina, Enrique G. Conrad, Andrew Mishra, Vishnu Brantly, Mark L. Torres, Maria De Medina, Maria Tzakis, Andreas G. Schiff, Eugene R. Journal of Pediatric Gastroenterology and Nutrition Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study Gastroenterology Pediatrics, Perinatology and Child Health |
| author_sort |
regev, arie |
| spelling |
Regev, Arie Guaqueta, Constanza Molina, Enrique G. Conrad, Andrew Mishra, Vishnu Brantly, Mark L. Torres, Maria De Medina, Maria Tzakis, Andreas G. Schiff, Eugene R. 0277-2116 1536-4801 Wiley Gastroenterology Pediatrics, Perinatology and Child Health http://dx.doi.org/10.1097/01.mpg.0000226387.56612.1e <jats:title>ABSTRACT</jats:title><jats:sec><jats:title>Background:</jats:title><jats:p>The role of the heterozygous PiZ state of alpha‐1 antitrypsin deficiency (α<jats:sub>1</jats:sub>ATD) in the pathogenesis of chronic liver disease (LD) is still a matter of controversy.</jats:p></jats:sec><jats:sec><jats:title>Aim:</jats:title><jats:p>To determine the prevalence of α<jats:sub>1</jats:sub>ATD heterozygote states in a large population of patients with established LD compared with individuals with no LD, and to determine whether the prevalence of PiZ is increased in patients with more severe LD.</jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p>A cross sectional case‐control study among patients with and without LD. Blood samples were tested for α<jats:sub>1</jats:sub>AT levels and α<jats:sub>1</jats:sub>AT phenotype. The severity of LD was determined by clinical evaluation, lab tests, imaging studies and histopathology.</jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p>In total, 1405 patients were enrolled; 651 with, and 754 without LD. Out of them, 173 patients had decompensated cirrhosis requiring liver transplantation. PiMZ was significantly more prevalent in White patients (3.5%) compared with Hispanics (1.7%; <jats:italic>P</jats:italic> = 0.029). There was no difference in PiMZ prevalence between the total LD group and the group with no LD (2.1% vs. 1.7%; <jats:italic>P</jats:italic> = 0.64). Within the LD group, 5.7% of 173 patients with decompensated LD, listed for liver transplantation, had PiMZ, compared with 2.1% of 478 patients with less severe LD (<jats:italic>P</jats:italic> = 0.016). Similarly, there was a disproportionately higher prevalence of PiZ among hepatitis C virus (HCV) patients (5.6%) and patients with nonalcoholic fatty liver disease (NAFLD) (5.0%) with decompensated LD, compared with HCV patients (1.2%) and NAFLD patients (1.9%) with less severe LD (<jats:italic>P</jats:italic> = 0.044 and 0.017, respectively). Patients with cryptogenic cirrhosis, who were not considered NAFLD patients, did not have a higher prevalence of PiMZ compared with patients with LD of known etiologies (1.9% vs. 2.3%; <jats:italic>P</jats:italic> = 0.12).</jats:p></jats:sec><jats:sec><jats:title>Conclusions:</jats:title><jats:p>We found no association between the heterozygous PiZ state of α<jats:sub>1</jats:sub>ATD and the presence of chronic LD in‐general or the presence of cryptogenic cirrhosis. In contrast, patients with decompensated LD of any etiology had a significantly higher prevalence of PiMZ compared with patients with compensated LD. Furthermore, in patients with chronic LD due to HCV or NAFLD there was a significant association between the PiMZ heterozygous state and increased severity of LD and the need for liver transplantation. These interim results suggest that the PiMZ α<jats:sub>1</jats:sub>ATD heterozygous state may have a role in worsening LD due to HCV or NAFLD.</jats:p></jats:sec> Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study Journal of Pediatric Gastroenterology and Nutrition |
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2006 |
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Journal of Pediatric Gastroenterology and Nutrition |
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49 |
| title |
Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_unstemmed |
Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_full |
Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_fullStr |
Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_full_unstemmed |
Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_short |
Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_sort |
does the heterozygous state of alpha‐1 antitrypsin deficiency have a role in chronic liver diseases? interim results of a large case‐control study |
| topic |
Gastroenterology Pediatrics, Perinatology and Child Health |
| url |
http://dx.doi.org/10.1097/01.mpg.0000226387.56612.1e |
| publishDate |
2006 |
| physical |
|
| description |
<jats:title>ABSTRACT</jats:title><jats:sec><jats:title>Background:</jats:title><jats:p>The role of the heterozygous PiZ state of alpha‐1 antitrypsin deficiency (α<jats:sub>1</jats:sub>ATD) in the pathogenesis of chronic liver disease (LD) is still a matter of controversy.</jats:p></jats:sec><jats:sec><jats:title>Aim:</jats:title><jats:p>To determine the prevalence of α<jats:sub>1</jats:sub>ATD heterozygote states in a large population of patients with established LD compared with individuals with no LD, and to determine whether the prevalence of PiZ is increased in patients with more severe LD.</jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p>A cross sectional case‐control study among patients with and without LD. Blood samples were tested for α<jats:sub>1</jats:sub>AT levels and α<jats:sub>1</jats:sub>AT phenotype. The severity of LD was determined by clinical evaluation, lab tests, imaging studies and histopathology.</jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p>In total, 1405 patients were enrolled; 651 with, and 754 without LD. Out of them, 173 patients had decompensated cirrhosis requiring liver transplantation. PiMZ was significantly more prevalent in White patients (3.5%) compared with Hispanics (1.7%; <jats:italic>P</jats:italic> = 0.029). There was no difference in PiMZ prevalence between the total LD group and the group with no LD (2.1% vs. 1.7%; <jats:italic>P</jats:italic> = 0.64). Within the LD group, 5.7% of 173 patients with decompensated LD, listed for liver transplantation, had PiMZ, compared with 2.1% of 478 patients with less severe LD (<jats:italic>P</jats:italic> = 0.016). Similarly, there was a disproportionately higher prevalence of PiZ among hepatitis C virus (HCV) patients (5.6%) and patients with nonalcoholic fatty liver disease (NAFLD) (5.0%) with decompensated LD, compared with HCV patients (1.2%) and NAFLD patients (1.9%) with less severe LD (<jats:italic>P</jats:italic> = 0.044 and 0.017, respectively). Patients with cryptogenic cirrhosis, who were not considered NAFLD patients, did not have a higher prevalence of PiMZ compared with patients with LD of known etiologies (1.9% vs. 2.3%; <jats:italic>P</jats:italic> = 0.12).</jats:p></jats:sec><jats:sec><jats:title>Conclusions:</jats:title><jats:p>We found no association between the heterozygous PiZ state of α<jats:sub>1</jats:sub>ATD and the presence of chronic LD in‐general or the presence of cryptogenic cirrhosis. In contrast, patients with decompensated LD of any etiology had a significantly higher prevalence of PiMZ compared with patients with compensated LD. Furthermore, in patients with chronic LD due to HCV or NAFLD there was a significant association between the PiMZ heterozygous state and increased severity of LD and the need for liver transplantation. These interim results suggest that the PiMZ α<jats:sub>1</jats:sub>ATD heterozygous state may have a role in worsening LD due to HCV or NAFLD.</jats:p></jats:sec> |
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| author | Regev, Arie, Guaqueta, Constanza, Molina, Enrique G., Conrad, Andrew, Mishra, Vishnu, Brantly, Mark L., Torres, Maria, De Medina, Maria, Tzakis, Andreas G., Schiff, Eugene R. |
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| description | <jats:title>ABSTRACT</jats:title><jats:sec><jats:title>Background:</jats:title><jats:p>The role of the heterozygous PiZ state of alpha‐1 antitrypsin deficiency (α<jats:sub>1</jats:sub>ATD) in the pathogenesis of chronic liver disease (LD) is still a matter of controversy.</jats:p></jats:sec><jats:sec><jats:title>Aim:</jats:title><jats:p>To determine the prevalence of α<jats:sub>1</jats:sub>ATD heterozygote states in a large population of patients with established LD compared with individuals with no LD, and to determine whether the prevalence of PiZ is increased in patients with more severe LD.</jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p>A cross sectional case‐control study among patients with and without LD. Blood samples were tested for α<jats:sub>1</jats:sub>AT levels and α<jats:sub>1</jats:sub>AT phenotype. The severity of LD was determined by clinical evaluation, lab tests, imaging studies and histopathology.</jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p>In total, 1405 patients were enrolled; 651 with, and 754 without LD. Out of them, 173 patients had decompensated cirrhosis requiring liver transplantation. PiMZ was significantly more prevalent in White patients (3.5%) compared with Hispanics (1.7%; <jats:italic>P</jats:italic> = 0.029). There was no difference in PiMZ prevalence between the total LD group and the group with no LD (2.1% vs. 1.7%; <jats:italic>P</jats:italic> = 0.64). Within the LD group, 5.7% of 173 patients with decompensated LD, listed for liver transplantation, had PiMZ, compared with 2.1% of 478 patients with less severe LD (<jats:italic>P</jats:italic> = 0.016). Similarly, there was a disproportionately higher prevalence of PiZ among hepatitis C virus (HCV) patients (5.6%) and patients with nonalcoholic fatty liver disease (NAFLD) (5.0%) with decompensated LD, compared with HCV patients (1.2%) and NAFLD patients (1.9%) with less severe LD (<jats:italic>P</jats:italic> = 0.044 and 0.017, respectively). Patients with cryptogenic cirrhosis, who were not considered NAFLD patients, did not have a higher prevalence of PiMZ compared with patients with LD of known etiologies (1.9% vs. 2.3%; <jats:italic>P</jats:italic> = 0.12).</jats:p></jats:sec><jats:sec><jats:title>Conclusions:</jats:title><jats:p>We found no association between the heterozygous PiZ state of α<jats:sub>1</jats:sub>ATD and the presence of chronic LD in‐general or the presence of cryptogenic cirrhosis. In contrast, patients with decompensated LD of any etiology had a significantly higher prevalence of PiMZ compared with patients with compensated LD. Furthermore, in patients with chronic LD due to HCV or NAFLD there was a significant association between the PiMZ heterozygous state and increased severity of LD and the need for liver transplantation. These interim results suggest that the PiMZ α<jats:sub>1</jats:sub>ATD heterozygous state may have a role in worsening LD due to HCV or NAFLD.</jats:p></jats:sec> |
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| spelling | Regev, Arie Guaqueta, Constanza Molina, Enrique G. Conrad, Andrew Mishra, Vishnu Brantly, Mark L. Torres, Maria De Medina, Maria Tzakis, Andreas G. Schiff, Eugene R. 0277-2116 1536-4801 Wiley Gastroenterology Pediatrics, Perinatology and Child Health http://dx.doi.org/10.1097/01.mpg.0000226387.56612.1e <jats:title>ABSTRACT</jats:title><jats:sec><jats:title>Background:</jats:title><jats:p>The role of the heterozygous PiZ state of alpha‐1 antitrypsin deficiency (α<jats:sub>1</jats:sub>ATD) in the pathogenesis of chronic liver disease (LD) is still a matter of controversy.</jats:p></jats:sec><jats:sec><jats:title>Aim:</jats:title><jats:p>To determine the prevalence of α<jats:sub>1</jats:sub>ATD heterozygote states in a large population of patients with established LD compared with individuals with no LD, and to determine whether the prevalence of PiZ is increased in patients with more severe LD.</jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p>A cross sectional case‐control study among patients with and without LD. Blood samples were tested for α<jats:sub>1</jats:sub>AT levels and α<jats:sub>1</jats:sub>AT phenotype. The severity of LD was determined by clinical evaluation, lab tests, imaging studies and histopathology.</jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p>In total, 1405 patients were enrolled; 651 with, and 754 without LD. Out of them, 173 patients had decompensated cirrhosis requiring liver transplantation. PiMZ was significantly more prevalent in White patients (3.5%) compared with Hispanics (1.7%; <jats:italic>P</jats:italic> = 0.029). There was no difference in PiMZ prevalence between the total LD group and the group with no LD (2.1% vs. 1.7%; <jats:italic>P</jats:italic> = 0.64). Within the LD group, 5.7% of 173 patients with decompensated LD, listed for liver transplantation, had PiMZ, compared with 2.1% of 478 patients with less severe LD (<jats:italic>P</jats:italic> = 0.016). Similarly, there was a disproportionately higher prevalence of PiZ among hepatitis C virus (HCV) patients (5.6%) and patients with nonalcoholic fatty liver disease (NAFLD) (5.0%) with decompensated LD, compared with HCV patients (1.2%) and NAFLD patients (1.9%) with less severe LD (<jats:italic>P</jats:italic> = 0.044 and 0.017, respectively). Patients with cryptogenic cirrhosis, who were not considered NAFLD patients, did not have a higher prevalence of PiMZ compared with patients with LD of known etiologies (1.9% vs. 2.3%; <jats:italic>P</jats:italic> = 0.12).</jats:p></jats:sec><jats:sec><jats:title>Conclusions:</jats:title><jats:p>We found no association between the heterozygous PiZ state of α<jats:sub>1</jats:sub>ATD and the presence of chronic LD in‐general or the presence of cryptogenic cirrhosis. In contrast, patients with decompensated LD of any etiology had a significantly higher prevalence of PiMZ compared with patients with compensated LD. Furthermore, in patients with chronic LD due to HCV or NAFLD there was a significant association between the PiMZ heterozygous state and increased severity of LD and the need for liver transplantation. These interim results suggest that the PiMZ α<jats:sub>1</jats:sub>ATD heterozygous state may have a role in worsening LD due to HCV or NAFLD.</jats:p></jats:sec> Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study Journal of Pediatric Gastroenterology and Nutrition |
| spellingShingle | Regev, Arie, Guaqueta, Constanza, Molina, Enrique G., Conrad, Andrew, Mishra, Vishnu, Brantly, Mark L., Torres, Maria, De Medina, Maria, Tzakis, Andreas G., Schiff, Eugene R., Journal of Pediatric Gastroenterology and Nutrition, Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study, Gastroenterology, Pediatrics, Perinatology and Child Health |
| title | Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_full | Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_fullStr | Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_full_unstemmed | Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_short | Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| title_sort | does the heterozygous state of alpha‐1 antitrypsin deficiency have a role in chronic liver diseases? interim results of a large case‐control study |
| title_unstemmed | Does the Heterozygous State of Alpha‐1 Antitrypsin Deficiency Have a Role in Chronic Liver Diseases? Interim Results of a Large Case‐Control Study |
| topic | Gastroenterology, Pediatrics, Perinatology and Child Health |
| url | http://dx.doi.org/10.1097/01.mpg.0000226387.56612.1e |