Familial Mediterranean Fever and Multiple Sclerosis Successfully Treated With Interferon Beta-1a: A Case Report

Abstract

Familial Mediterranean fever (FMF) is an autosomal recessive autoinflammatory disorder. It is characterized by recurrent attacks of fever, peritonitis, pleuritis, and synovitis and common in Mediterranean people including Turks, Arabs, Armenians, and non-Ashkenazi Jews. 1 The responsible gene for FMF is MEFV located on chromosome 16p. Multiple sclerosis (MS) is the most common demyelinating disease of central nervous system. MS is characterized by inflammation and demyelination and caused by several environmental and genetic factors. Patients with FMF have a susceptibility to develop MS. Mutations of genes like MEFV encoding pyrin protein may promote development of MS disease. 2 Akman-Demir et al. 3 suggested a four-fold increased rate of FMF among MS patients. Currently, there is no curative treatment for both diseases. Immunomodulatory drugs display beneficial effects by decreasing severity and frequency of MS attacks. CASE REPORT A 37-year-old male patient was admitted to our department with numbness of lower extremities and difficulty in walking in September 2017. He had been suffering from numbness for more than three months and from gait disturbance for the last month. A few years before, he had numbness on lower extremities but he did not admit to any hospital and his complaints were completely resolved within two weeks. In his neurological examination, hypoesthesia in right ABSTRACT Multiple sclerosis (MS) is the most common demyelinating disease in Turkey while familial Mediterranean fever (FMF) is the most common periodic fever syndrome worldwide. In this article, we report a 37-year-old male patient admitted with complaint of difficulty in walking. He had been taking colchicine at admission for 27 years. Despite this therapy, he had been experiencing twice monthly severe FMF attacks. After systemic and neurological examinations, laboratory tests and cranial and spinal magnetic resonance imaging, he was diagnosed as MS. Interferon (IFN) beta-1a was initiated three times/weekly subcutaneously for MS treatment. He stopped colchicine treatment after five months of IFN treatment because he did not suffer from any FMF attacks. He is still attack free for both diseases for a follow-up duration of 12 months. IFN beta is one of the most preferred agents for MS treatment but not one of the agents used for the treatment of FMF. Interferon beta can be a treatment of choice in patients with coincident FMF and MS and can be used in colchicine-resistant patients after being studied in systematic clinical studies.

Solving a diagnostic dilemma in a patient with periodic fever—When the pieces of the puzzle finally fit

“…IL‐1 targeting therapy (anakinra or canakinumab) has been successful in managing both overlap conditions in two case reports, while a third report described relapse freedom on colchicine and rituximab using clinical and MRI follow‐up data. 11 , 12 , 13 A case series of ocrelizumab treatment for 18 months in 11 people with secondary progressive MS showed reduction in both FMF and MS attacks. 14 …”

A Hepatitis B Virus-Derived Peptide Can Inhibit Infection of Human Lung Cells with SARS-CoV-2 in a Type-1 Interferon-Dependent Manner

“…Paradoxically, in addition to its antiviral effect, IFN-I, particularly IFN-β, can also exert anti-inflammatory effects by enhancing the production of immunosuppressive cytokine IL-10, enhancing the expression of SOCS-1, downregulating matrix metalloproteinase–9 (MMP-9), or inducing IFI16-mediated inflammasome inhibition [ 26 ] (graphical abstract). Therefore, IFN-Is have been widely applied to treat autoimmune and inflammatory diseases, such as multiple sclerosis (MS) [ 5 ], familial Mediterranean fever (FMF) [ 43 ], and Behcet’s syndrome [ 44 ]. In this study, our transcription profile assay indicated that Poly6 treatment of SARS-CoV-2-infected Calu-3 cells led to the upregulation of the genes STAT1 , IRF3 , IRF9 , JAK1 , and IFI16 ( Figure 4 D and Figure S4 ) and of two immunosuppressive molecules, IL-10 and SOCS-1, but to the downregulation of pro-inflammatory genes such as IL-6 and IL-1β .…”