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Colchicine-Resistant Familial Mediterranean Fever With Depressive State Successfully Treated With Escitalopram
Masamitsu Toshida1, Yuki Konishi1, Atsuko Ikenouchi1
1Psychiatry, University of Occupational and Environmental Health, Kitakyushu, JPN.
Abstract:
Familial Mediterranean fever (FMF) is a hereditary autoinflammatory disease associated with the Mediterranean fever (MEFV) gene and is mainly characterized by periodic fever and serositis. Colchicine has been used to prevent FMF episodes and reduce the frequency of attacks. We report the case of a 64-year-old man who presented with depressive symptoms and was resistant to colchicine treatment. Adding escitalopram to the ongoing colchicine regimen dramatically improved his fever, abdominal pain, and depressive symptoms. The change in cytokines, ABCB1 effects, and increased serotonin were related to these mechanisms. This case suggested that adding escitalopram to colchicine is a viable treatment option for colchicine-resistant FMF.
Insights
Familial Mediterranean Fever (FMF) is an autoinflammatory disease. Adding escitalopram to colchicine improved symptoms in a colchicine-resistant FMF patient, suggesting a new treatment approach.
Area of Science:
- Genetics and Immunology
- Pharmacology
Background:
- Familial Mediterranean Fever (FMF) is a hereditary autoinflammatory disorder linked to the MEFV gene.
- Characterized by recurrent fever and serositis, FMF is typically managed with colchicine to prevent attacks.
Observation:
- A 64-year-old male patient with FMF exhibited resistance to colchicine treatment.
- He also presented with significant depressive symptoms.
Findings:
- Co-administration of escitalopram with colchicine led to a marked improvement in FMF symptoms, including fever and abdominal pain.
- The patient's depressive symptoms also resolved with the combined treatment.
Implications:
- This case suggests that combining escitalopram with colchicine is a potential therapeutic strategy for colchicine-resistant FMF.
- Potential mechanisms involve modulation of cytokines, ABCB1 transporter activity, and serotonin pathways.
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