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Different course of reactive arthritis in two HLA-B27 positive brothers with fatal outcome in one
T Yli-Kerttula1, T Möttönen, A Toivanen
1Department of Medicine, Turku University, Finland.
Abstract:
During an outbreak of Yersinia pseudotuberculosis III, one of two HLA-B27 positive brothers developed reactive arthritis (ReA), mild at first, but later severely destructive and ultimately fatal. The reactivation of ReA was possibly triggered by an oral polio vaccine. The cause of death was severe secondary amyloidosis. The other brother was exposed to the same Y. pseudotuberculosis strain but did not develop any disease during or after the outbreak. However, he later developed ReA due to a Salmonella infection, with a benign course.
Insights
Human leukocyte antigen B27 (HLA-B27) positive individuals can develop severe reactive arthritis (ReA) following infections. Genetic predisposition and triggers like vaccines may influence disease severity and outcomes in ReA.
Area of Science:
- Immunogenetics
- Rheumatology
- Infectious Diseases
Background:
- Reactive arthritis (ReA) is an inflammatory condition often triggered by bacterial infections.
- The human leukocyte antigen B27 (HLA-B27) gene is strongly associated with ReA development and severity.
- Understanding the interplay between genetics, infection, and immune response is crucial for ReA pathogenesis.
Observation:
- Two HLA-B27 positive brothers were exposed to Yersinia pseudotuberculosis III.
- One brother developed severe, destructive, and fatal reactive arthritis, potentially reactivated by an oral polio vaccine, leading to death from secondary amyloidosis.
- The other brother, despite exposure to the same pathogen, experienced a mild, benign course of reactive arthritis following a subsequent Salmonella infection.
Findings:
- HLA-B27 positivity alone does not guarantee disease development after infection.
- Disease severity in ReA can vary significantly, even among genetically similar individuals.
- External factors, such as vaccination, may influence disease reactivation and progression in genetically susceptible individuals.
Implications:
- This case highlights the complex factors influencing reactive arthritis severity, including genetic predisposition and environmental triggers.
- Further research into HLA-B27 associated diseases and potential therapeutic targets for managing severe ReA and secondary amyloidosis is warranted.
- The findings underscore the importance of considering individual immune responses in infectious disease outbreaks and vaccination strategies.