ArticleClinical case reports2026
Primary (AL) Amyloidosis Following COVID-19 Infection: A Case Report.
Article in Clinical case reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Primary (AL) Amyloidosis Following COVID-19 Infection: A Case Report.Clinical case reports · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary (AL) amyloidosis is a rare systemic disorder caused by extracellular deposition of monoclonal immunoglobulin light chains, resulting in multi-organ dysfunction. SARS-CoV-2 infection may induce persistent inflammatory and immune dysregulation, potentially promoting amyloid formation, although clinical evidence is limited, making the recognition of post-COVID-19 amyloidosis clinically relevant and potentially novel. A 39-year-old Caucasian male presented with progressive weight loss (18 kg over 6 months), epigastric pain, early satiety, and hepatosplenomegaly. Ten months prior, he had recovered from COVID-19 with mild pulmonary involvement. Initial ultrasonography and endoscopy were unremarkable except for mild gastritis. Subsequent imaging revealed hepatosplenomegaly (liver: 200 mm; spleen: 157 mm) and cholestatic liver enzyme elevation. Investigations for sclerosing cholangitis were negative. Liver biopsy with Congo red staining confirmed amyloid deposition, and bone marrow analysis revealed clonal plasma cells, establishing primary (AL) amyloidosis. Echocardiography showed left ventricular hypertrophy (LVH) due to amyloid infiltration. This case underscores a possible association between SARS-CoV-2 infection and primary amyloidosis. Post-COVID inflammatory responses, elevated serum amyloid A, oxidative stress, and hypercoagulability may collectively facilitate amyloidogenic peptide formation and tissue deposition. Molecular dynamics studies further support the plausibility of SARS-CoV-2-induced amyloidogenesis. Primary amyloidosis may develop following COVID-19. Clinicians should consider amyloidosis in patients with unexplained weight loss, hepatosplenomegaly, or cholestatic liver enzyme abnormalities after SARS-CoV-2 infection. Early biopsy and type-specific diagnosis are essential for timely management. This case highlights the potential clinical significance of a post-COVID-19 association, as primary amyloidosis may develop following COVID-19.
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