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Introduction: Migraine is a highly prevalent neurological disease and the search for an effective treatment to improve the patient's quality of life is essential. In 2018, anti-CGRP monoclonal antibodies were approved in Spain as a preventive treatment, and have proved to be effective in reducing the number of migraine crisis per month compared to placebo., Patients and Methods: We conducted a descriptive and retrospective study of 14 patients suffering from high-frequency or chronic episodic migraine, under follow-up in our headache unit, in whom an anti-CGRP monoclonal was changed due to its ineffectiveness. Epidemiological data and variables related to the response to both drugs were collected, such as headache days per month and migraine days per month, as well as validated quality of life scales (Migraine Disability Assessment Scale and Headache Impact Test-6)., Results: 50% of patients were males, with a median age of 46.5 years and 92% were diagnosed with chronic migraine. A follow-up of 6 to 12 months after the change of treatment was performed in 91.6% and significant improvement was observed in 33% of the patients. In addition, 50% had an initial response after three doses of the first monoclonal drug., Conclusions: In our series, 66% of patients who did not respond to a first drug responded initially to the switch and this improvement was maintained in 36% of them. Larger studies are needed to clarify this difference in response to different anti-CGRP monoclonal antibodies.

Killer cell immunoglobulin-like receptors (KIRs) are regulators of cytolytic activity of natural killer and certain T cells through interactions with human leukocyte antigen (HLA) class I ligands. KIRs have been shown to contribute to the pathogenesis of several autoimmune diseases, but their role in multiple sclerosis (MS) is still unclear. Here we determined the influence of KIR genes and their HLA class I ligands on susceptibility to MS and on the response to interferon-beta treatment in a Spanish population. KIR and HLA genotyping were performed in 200 MS patients and 200 controls. Significantly higher frequencies were found for KIR2DL5 and KIR3DS1 genes in MS patients and the carriage of the KIR2DL1 gene was associated with a higher progression index. Moreover, the frequency of the HLA-Bw4 motif was significantly reduced in MS patients. The KIR2DL1 and HLA-C2 matches were more frequent in MS patients, whereas the KIR3DL1 and HLA-Bw4 matches were more frequent in healthy controls. Nevertheless, non significant associations were found between all the KIR genes and therapeutic response to interferon-beta. Our results confirm that the carriage of HLA-Bw4 is a protective factor in MS and suggest that KIR2DL5 and KIR3DS1 may have a predisposing role in the disease., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

The TNF-related apoptosis inducing ligand (TRAIL)/TRAIL receptor system participates in crucial steps in immune cell activation or differentiation. It is able to inhibit proliferation and activation of T cells and to induce apoptosis of neurons and oligodendrocytes, and seems to be implicated in autoimmune diseases. Thus, TRAIL and TRAIL receptor genes are potential candidates for involvement in susceptibility to multiple sclerosis (MS). To test whether single-nucleotide polymorphisms (SNPs) in the human genes encoding TRAIL, TRAILR-1, TRAILR-2, TRAILR-3 and TRAILR-4 are associated with MS susceptibility, we performed a candidate gene case-control study in the Spanish population. 59 SNPs in the TRAIL and TRAIL receptor genes were analysed in 628 MS patients and 660 controls, and validated in an additional cohort of 295 MS patients and 233 controls. Despite none of the SNPs withstood the highly conservative Bonferroni correction, three SNPs showing uncorrected p values<0.05 were successfully replicated: rs4894559 in TRAIL gene, p = 9.8×10(-4), OR = 1.34; rs4872077, in TRAILR-1 gene, p = 0.005, OR = 1.72; and rs1001793 in TRAILR-2 gene, p = 0.012, OR = 0.84. The combination of the alleles G/T/A in these SNPs appears to be associated with a reduced risk of developing MS (p = 2.12×10(-5), OR = 0.59). These results suggest that genes of the TRAIL/TRAIL receptor system exerts a genetic influence on MS.