The Intern At Work: Internal Medicine
Jun 14, 2026 · 18 min · 8 segments
Send us Fan Mail In this episode, we discuss how to recognize and manage Behçet Disease. Written by Dr. Oswald Chan (Internal Medicine Resident). Reviewed by Dr. Alexa Smith, (Rheumatologist) and Dr…
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Oswald ChanHost
Bichette disease is a chronic, relapsing, and remitting systemic inflammatory disorder with vasculitis that can affect all types and sizes of arteries and veins.
While the exact cause of Bichette is not known, it is believed to occur in genetically predisposed individuals who are exposed to an environmental or infectious trigger, leading to a dysregulated autoimmune response.
Prevalence of Bichette disease has increased along the ancient Silk Road, extending from the Mediterranean to East Asia.
Individuals carrying the HLA-B51 gene are at a greater risk of developing the disease, although genetic contribution is estimated at less than 20%.
Infectious antigens such as streptococcal species are believed to exhibit molecular mimicry, a process by which microbial proteins that closely resemble the body's own proteins trigger a response from both the innate and adaptive immune system.
Bichette disease is thought to influence innate immunity through changes in neutrophil activity, particularly increased neutrophil motility, endothelial binding and oxidation.
Adaptive immunity may be affected through alterations in T-cell and cytokine activation.
Studies have observed elevated levels of T helper 1, 2, and 17 lymphocytes in individuals with active disease along with increased production of pro-inflammatory cytokines such as TNF-alpha, IL-6, IL-8, and IL-17.
Endothelial cell dysfunction is another associated feature, with studies exploring the possible role of impaired nitric oxide activity and presence of anti-endothelial antibodies.
In addition, researchers investigating the prothrombotic state seen in Bichette have reported increased thrombin formation and decreased levels of activated protein C in individuals with the disease.
This hypercoagulability is felt to be driven by the combination of endothelial dysfunction and vascular injury stemming from inflammation.
Overall, the interaction between genetic, environmental, and immunologic factors result in the wide-ranging clinical manifestations of Bichette disease.
Bichette disease is a chronic, relapsing, and remitting systemic inflammatory disorder with vasculitis that can affect all types and sizes of arteries and veins.
While the exact cause of Bichette is not known, it is believed to occur in genetically predisposed individuals who are exposed to an environmental or infectious trigger, leading to a dysregulated autoimmune response.
Prevalence of Bichette disease has increased along the ancient Silk Road, extending from the Mediterranean to East Asia.
Individuals carrying the HLA-B51 gene are at a greater risk of developing the disease, although genetic contribution is estimated at less than 20%.
Infectious antigens such as streptococcal species are believed to exhibit molecular mimicry, a process by which microbial proteins that closely resemble the body's own proteins trigger a response from both the innate and adaptive immune system.
Bichette disease is thought to influence innate immunity through changes in neutrophil activity, particularly increased neutrophil motility, endothelial binding and oxidation.
Adaptive immunity may be affected through alterations in T-cell and cytokine activation.
Studies have observed elevated levels of T helper 1, 2, and 17 lymphocytes in individuals with active disease along with increased production of pro-inflammatory cytokines such as TNF-alpha, IL-6, IL-8, and IL-17.
Endothelial cell dysfunction is another associated feature, with studies exploring the possible role of impaired nitric oxide activity and presence of anti-endothelial antibodies.
In addition, researchers investigating the prothrombotic state seen in Bichette have reported increased thrombin formation and decreased levels of activated protein C in individuals with the disease.
This hypercoagulability is felt to be driven by the combination of endothelial dysfunction and vascular injury stemming from inflammation.
Overall, the interaction between genetic, environmental, and immunologic factors result in the wide-ranging clinical manifestations of Bichette disease.
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