Genetic variants IL1B +3954C>T and -511C>T associated with incapacity and allodynia in migraine

IntroductionThe main mechanisms in the physiopathology of migraine are cortical spreading depression and trigeminal activation with release CGRP. Neurogenic inflammation neuroinflammation can exert an influence over both these mechanisms, but there still a number gaps our understanding. Interleukin (IL)- 1β is pro-inflammatory cytokine whose levels plasma increase during attack phase migraine. Thus far, its genetic variants have not been well studied. ObjectiveTo investigate association between IL1B +3954C>T (rs1143634) -511C>T (rs16944) susceptibility to clinical characteristics. Subjects MethodsCase control study comprising 307 participants, whom 152 had diagnosis 155 were healthy controls, paired by sex, age, ethnicity BMI. The demographic data evaluated. patients interviewed using structured form containing information about type (with or without aura, episodic chronic), age at onset disease, frequency attacks, accompanying symptoms that triggered headaches. also answered validated questionnaires evaluate incapacity (Migraine Disability Assessment - MIDAS) impact (Headache Impact Test HIT-6) for migraine, presence allodynia (ASC-12), as anxiety (State Anxiety Inventory STAI 1 2), (Beck Depression Inventory) hyperacusis scale.The identified polymerase chain reaction (PCR) fluorescence PCR products evaluated Step One thermocycler (Applied Biosystems). analyses conducted dominant, codominant, recessive over- dominant models. Categorical via chi-squared test Fisher’s exact test, continuous Mann-Whitney test. (To see complete abstract, please, check out PDF).