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Pulmonary apical fibrocystic disease. A serologic study
European Journal of Respiratory Diseases
|February 1, 1981
Summary
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.