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• W2021197533 abstract "Objective To evaluate a possible etiologic role of a α-antitrypsin deficiency (α1AD), most frequently caused by a Z allele mutation, in ulcerative colitis (UC) and Crohn disease (CD). Patients and Methods This retrospective study included 10 patients diagnosed with and/or treated for inflammatory bowel disease (IBD) between 1976 and 1997 and identified from the Mayo Clinic Medical Index System. All 10 patients had either α1 AD and CD or α1AD and UC. The α1-antitrypsin (α1AT)types and levels were determined with isoelectric focusing testing. The allele types, representing genotypes, were designated PiZZ (or ZZ) for homozygotes and PiMZ (or MZ) for heterozygotes. Results Seven patients had UC: 4 were genotype ZZ and 3 MZ. Four of these 7 patients had emphysema, 2 had asthma, and 1 had chronic bronchitis. Five were cigarette smokers, but only 1 had smoked coincident with activity of her UC. Two of the UC patients never smoked, and 1 of these 2 had asthma. Three of the 10 patients had CD, 2 genotype ZZ and 1 MZ. Two of the 3 patients were longterm cigarette smokers, and both had emphysema. Nine of the 10 patients with UC and α1 AD required surgery. Conclusions The need for surgery in patients with UC and α1-AD may point to a unique phenotypic subgroup of patients with α1AD and severe UC. Further studies are required to substantiate the etiologic role of α1AD in IBD. Our observations, if confirmed by future studies, suggest that in patients with both IBD and chronic obstructive pulmonary disease, α1AD testing should be considered. To evaluate a possible etiologic role of a α-antitrypsin deficiency (α1AD), most frequently caused by a Z allele mutation, in ulcerative colitis (UC) and Crohn disease (CD). This retrospective study included 10 patients diagnosed with and/or treated for inflammatory bowel disease (IBD) between 1976 and 1997 and identified from the Mayo Clinic Medical Index System. All 10 patients had either α1 AD and CD or α1AD and UC. The α1-antitrypsin (α1AT)types and levels were determined with isoelectric focusing testing. The allele types, representing genotypes, were designated PiZZ (or ZZ) for homozygotes and PiMZ (or MZ) for heterozygotes. Seven patients had UC: 4 were genotype ZZ and 3 MZ. Four of these 7 patients had emphysema, 2 had asthma, and 1 had chronic bronchitis. Five were cigarette smokers, but only 1 had smoked coincident with activity of her UC. Two of the UC patients never smoked, and 1 of these 2 had asthma. Three of the 10 patients had CD, 2 genotype ZZ and 1 MZ. Two of the 3 patients were longterm cigarette smokers, and both had emphysema. Nine of the 10 patients with UC and α1 AD required surgery. The need for surgery in patients with UC and α1-AD may point to a unique phenotypic subgroup of patients with α1AD and severe UC. Further studies are required to substantiate the etiologic role of α1AD in IBD. Our observations, if confirmed by future studies, suggest that in patients with both IBD and chronic obstructive pulmonary disease, α1AD testing should be considered." @default.
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• W2021197533 date "2000-05-01" @default.
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• W2021197533 title "α1-Antitrypsin Deficiency and Inflammatory Bowel Diseases" @default.
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• W2021197533 doi "https://doi.org/10.4065/75.5.450" @default.
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