Complement c4b–null alleles in felty's syndrome
Wendy Thomson BSc
Research Assistant
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Search for more papers by this authorPaul A. Sanders MB, MRCP
Senior Registrar in Rheumatology
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Search for more papers by this authorMartin Davis MB, MRCP
Tutor in Rheumatology
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Search for more papers by this authorJudith Davidson MSc
Senior Scientific Officer
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Search for more papers by this authorPhilip A. Dyer PhD
Top Grade Scientific Officer
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Search for more papers by this authorCorresponding Author
David M. Grennan MD, Phd, FRCP
Consultant and Senior Lecturer in Rheumatology
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Rheumatic Diseases Centre, Hope Hospital, Salford, M6.8HD, UKSearch for more papers by this authorWendy Thomson BSc
Research Assistant
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Search for more papers by this authorPaul A. Sanders MB, MRCP
Senior Registrar in Rheumatology
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Search for more papers by this authorMartin Davis MB, MRCP
Tutor in Rheumatology
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Search for more papers by this authorJudith Davidson MSc
Senior Scientific Officer
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Search for more papers by this authorPhilip A. Dyer PhD
Top Grade Scientific Officer
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Search for more papers by this authorCorresponding Author
David M. Grennan MD, Phd, FRCP
Consultant and Senior Lecturer in Rheumatology
University of Manchester, Rheumatic Diseases Centre, Hope Hospital, Salford, and the North West Tissue Typing Laboratory, St. Mary's Hospital, Manchester, United Kingdom.
Rheumatic Diseases Centre, Hope Hospital, Salford, M6.8HD, UKSearch for more papers by this authorAbstract
C4A and C4B allotypes were compared in 20 patients with Felty's syndrome (FS), 52 patients with rheumatoid arthritis (RA), and 55 control subjects. Nineteen of the FS patients had HLA–DR4. A C4B-null allele was more frequent in the patients with FS (60%) than in either the RA patients (15%) or the control subjects (26%). Only the differences between patients with FS and those with RA remained statistically significant when DR4 positive subjects were compared. The C4B null allele may identify individuals within the rheumatoid population who are at risk of developing particular systemic complications.
Reference
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