Report of nomenclature meeting for α1-antitrypsin

Dw, Cox; Am, Johnson; Fagerhol, Magne K.

doi:10.1007/bf00287070

Cited by 150 publications

(58 citation statements)

References 11 publications

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“…Alpha-I-antitrypsin phenotyping was performed by one of us (A. Myron Johnson, MD) at the University of North Carolina School of Medicine through the use of isoelectric focusing and acid starch gel electrophoresis followed by crossed immunoelectrophoresis, as recommended by the International Pi Committee (7).…”

Section: Methodsmentioning

confidence: 99%

Genetic predictors of patient response and side effects in the treatment of rheumatoid arthritis with a high dose nonsteroidal antiinflammatory drug regimen

Semble

Metcalf

Turner

et al. 1982

Arthritis & Rheumatism

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Clinical, laboratory, genetic, and radiologic studies were evaluated for 18 patients with rheumatoid arthritis who were treated for a mean of 16.6 months with a regimen involving supplementary aspirin and piroxicam, an investigational, nonsteroidal antiinflammatory agent. Although improvement in disease activity was seen, progression was evident on successive radiographs. Disease activity was not associated with the presence of any of the genetic markers. Peptic ulcers developed in 33% of patients, all of whom had type 0 blood. ABO blood typing may therefore be useful in patients with rheumatoid arthritis before consideration of therapy with potentially ulcerogenic drugs.In rheumatoid arthritis, recent evidence has suggested that the characterization of certain genetic factors, such as human leukocyte antigens (HLA), A 3 0 blood groups, and alpha-I-antitrypsin phenotypes, may be useful in predicting the severity of PATIENTS AND METHODSIn an open-label study, 45 patients, ages 21-65 years, with rheumatoid arthritis categorized as functional class I1 or 111 according to criteria of the American Rheumatism Association (4), took between 20 and 40 mg of piroxicam daily for up to 946 days (5). Patients with active ulcer disease were excluded by a preliminary upper gastrointestinal barium roentgenogram. Patients who developed gastrointestinal symptoms suggestive of ulcer disease underwent additional radiologic study. Maintenance doses of gold, prednisone (510 mg/day), and small doses of aspirin were allowed but carefully recorded. For 3 months, patients were evaluated with safety and articular checks every 2 weeks; thereafter, the checks were at monthly intervals. Patient and observer assessments, the latex agglutination test, grip strength, joint count, and the Westergren erythrocyte sedimentation rate comprised a cumulative grading method, the Modified Rheumatoid Activity Index (6). This index was calculated by expressing the raw scores of the 6 parameters as percentages, adding them together, and multiplying the sum by y6.The minimum score possible was 0, the maximum, 245 (6). Joint counts were graded 1 (subjective tenderness only), 2 (wincing), and 3 (wincing plus withdrawal) in 76 joints; the maximum possible score was 228.

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Section: Methodsmentioning

confidence: 99%

Genetic predictors of patient response and side effects in the treatment of rheumatoid arthritis with a high dose nonsteroidal antiinflammatory drug regimen

Semble

Metcalf

Turner

et al. 1982

Arthritis & Rheumatism

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show abstract

“…As detection techniques advanced and proteins began to be separated on the basis of their isoelectric point (for AAT between pH 4 -5), the nomenclature system was revised so AAT variants were designated with earlier letters of the alphabet if exhibiting anodal migration and later letters of the alphabet if exhibiting cathodal migration. Furthermore, as the letters of the alphabet were exhausted, place of origin names are used in addition to the letter of the closest anodal allele (Cox, Johnson, and Fagerhol 1980). More precisely the birthplace of the first described individual to carry a novel allele is used, for example Q0cairo was used to describe a novel Null mutation found in the first recognised case whose birthplace was Cairo .…”

Section: Molecular Pathophysiologymentioning

confidence: 99%

Alpha-1 Antitrypsin Deficiency – A Genetic Risk Factor for COPD

Carroll¹,

O’Connor²,

Reeves³

et al. 2012

Chronic Obstructive Pulmonary Disease - Current Concepts and Practice

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“…AAT is produced in the liver, released into the circulation and enters the lungs by diffusion, where it inhibits neutrophil elastase [3]. AAT is a 394 amino acid, 52 kDa acute phase glycoprotein encoded on the long distal arm of the chromosome 14 (14q32.1) [4].…”

Section: Introductionmentioning

confidence: 99%