41.   A thorough interview revealed no symptoms suggestive of inflammatory bowel disease in the healthy twins.

42.   They were, however, included in the analysis because, being monozygotic, these twins are genetically identical with those who ultimately developed inflammatory bowel disease.

43.   In general, there were large variations in cellular subclass distribution among individuals, in the inflammatory bowel disease twins and normal controls.

44.   There is no doubt that genetic factors are involved in inflammatory bowel disease, although the influence of heredity might be different in the two diseases.

45.   The latter antibodies have also been detected in serum of non-affected family members of inflammatory bowel disease patients.

46.   Serum antineutrophil cytoplasmic autoantibodies in inflammatory bowel disease are mainly associated with ulcerative colitis.

47.   Perinuclear antineutrophil cytoplasmic antibodies have recently been demonstrated in the seaa of patients with inflammatory bowel disease.

48.   Also in patients with inflammatory bowel disease antineutrophil cytoplasmic antibodies have been detected.

49.   The fluorescence pattern of inflammatory bowel disease associated antineutrophil cytoplasmic antibodies is characteristically perinuclear.

50.   Control subjects were patients from the same outpatient clinics, matched for sex and age to the inflammatory bowel disease patients without evidence of inflammatory bowel disease.