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Pulmonary apical fibrocystic disease. A serologic study
Abstract:
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.
Insights
This study investigated 12 patients with progressive pulmonary fibrocystic changes, excluding tuberculosis. No uniform cause was found, but slow-acting viral or fungal infections are suggested as potential factors.
Area of Science:
- Pulmonary Medicine
- Immunology
- Infectious Diseases
Background:
- Progressive pulmonary apical fibrocystic changes present a diagnostic challenge.
- Exclusion of active tuberculosis is crucial in differential diagnosis.
Purpose of the Study:
- To identify common aetiopathogenic factors in patients with progressive pulmonary apical fibrocystic changes.
- To explore potential autoimmune, infectious, or genetic links.
Main Methods:
- Human leukocyte antigen (HLA) typing was performed.
- Analysis of various antibodies including tissue, antimicrobial, influenza, and smooth muscle antibodies.
- Assessment of serum proteins, immunoglobulins, rheumatoid factor, and C-reactive protein.
Main Results:
- No clear HLA trends were observed, except for HLA-B27 positivity in patients with spondylitis.
- Autoimmune markers and most antimicrobial antibodies were negative.
- All patients had low-titred influenza antibodies; nine showed low positive smooth muscle antibodies.
- Biochemical markers indicated chronic inflammation.
Conclusions:
- No single aetiopathogenic factor was identified for the observed pulmonary fibrocystic changes.
- The findings suggest a possible role for unidentified slow-acting viral or fungal infections.
- Further research is warranted to elucidate the etiology of this condition.