Pulmonary apical fibrocystic disease. A serologic study.
Common aetiopathogenic factors were sought in 12 patients with progressive pulmonary apical fibrocystic changes, active human-type tuberculosis excluded. HLA-typing did not reveal any clear-cut trends; only the three patients with ankylosing spondylitis or Reiter's disease were HLA-B27 positive. Six patients had HLA-Cw3, which exceeds the prevalence in referents, antibodies, as well as other tissue antibodies, were mainly negative so that autoimmune aetiology is not likely. Similarly, antimicrobial antibodies were found occasionally, while low-titred influenza antibodies were positive in all patients. Serum proteins, immunoglobulins, rheumatoid factor and C-reactive protein were suggestive of chronic inflammation, as were low positive titres of smooth muscle antibodies in nine patients. In spite of the uniform clinical picture and course of the disease, no uniform aetiopathogenic factors were found, but possible unidentified slow- and low-grade viral or fungal infection is discussed.
D000328:Adult; D000368:Aged; D000974:Antibodies, Antinuclear / Q000032:analysis; D000907:Antibodies, Bacterial / Q000032:analysis; D000914:Antibodies, Viral / Q000032:analysis; D001798:Blood Proteins / Q000032:analysis; D005260:Female; D006680:HLA Antigens / Q000032:analysis; D006801:Humans; D008297:Male; D008875:Middle Aged; D011658:Pulmonary Fibrosis / Q000097:blood / Q000276:immunology*
D000974:Antibodies, Antinuclear; D000907:Antibodies, Bacterial; D000914:Antibodies, Viral; D001798:Blood Proteins; D006680:HLA Antigens