Case Report: The entanglement of infection and autoimmunity: a case of Caplan syndrome

TL;DR

This case report describes a rare condition where lung disease and rheumatoid arthritis coexist, emphasizing the role of infections in triggering immune issues.

Contribution

The report highlights the interplay between infections and autoimmunity in Caplan syndrome, advocating for early monitoring and comprehensive care.

Findings

Elevated rheumatoid factor and ACPA levels preceded visible lung changes in the patient.

Inflammatory markers increased despite controlled infections and limited immunosuppressive therapy.

Infections may act as triggers for immune dysregulation in autoimmune conditions like Caplan syndrome.

Abstract

Caplan syndrome is a rare disorder characterized by the coexistence of pneumoconiosis and rheumatoid arthritis (RA), primarily observed in individuals with silica or coal dust exposure. Data on disease behavior in the context of incomplete or irregular immunosuppressive therapy remain limited. This case report describes a 56-year-old man with a history of mixed dust exposure and smoking who presented with recurrent fever, chest pain, and polyarthralgia. Despite being diagnosed and treated for pulmonary tuberculosis and cryptococcosis, his respiratory and articular symptoms persisted. Serological tests revealed persistently elevated rheumatoid factor (RF) and anticitrullinated peptide antibody (ACPA), while a lung biopsy demonstrated chronic inflammation with carbon deposition, confirming Caplan syndrome. Retrospective analysis indicated that elevations of RF and ACPA preceded observable radiological and pathological changes. Notably, inflammatory markers continued to rise significantly even after infections were controlled and despite only episodic glucocorticoid use. This case highlights the importance of early serological monitoring and comprehensive management in high-risk patients and underscores that, rather than being viewed merely as complications, infections in autoimmune contexts should be recognized as potential triggers and aggravators of immune dysregulation, warranting heightened vigilance in both diagnosis and management.

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