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IDA patients have a high frequency of migraine headache. The presence of anxiety and depression have great influence on the presence of migraine in IDA patients.

Carotid artery stenosis (CAS) is primarily caused by atherosclerotic plaque. Progressive inflammation may contribute to the rupture of an atherosclerotic plaque. The platelet-to-lymphocyte ratio (PLR) is a new and simple marker that indicates inflammation. In this study, we aimed to investigate the use of the PLR to determine the severity of CAS. One hundred forty patients were chosen from among patients who underwent carotid angiography in our institution. Symptomatic patients with stenosis >50% in the carotid arteries and asymptomatic patients with stenosis >80% were diagnosed via carotid angiography as having critical stenosis. Patients were classified into two groups. Group 1 included patients who had critical CAS, whereas Group 2 included patients with noncritical CAS, as determined by carotid angiography. Correlations between the PLR and the severity of CAS were analyzed. There were no significant differences in sex and age between the two groups. The PLR was 162.5 ± 84.7 in the noncritical CAS group patients and 94.9 ± 60.3 in the critical CAS group patients (p < 0.0001). The PLR value of 117.1 had 89% sensitivity and 68% specificity for CAS [95% confidence interval, 0.043-0.159; area under the curve, 0.101 ± 0.03)]. In this study, we have shown that PLR values may be associated with critical stenosis in at least one of the carotid arteries. Furthermore, PLR values may be used to predict critical stenosis in the carotid arteries.

In this study, the prevalence and characteristics of definite migraine in primary restless legs syndrome (pRLS) patients and matched control patients (CPs) were investigated. We evaluated 63 consecutive adult pRLS patients and 141 age- and sex-matched controls in this case-control study. The diagnosis of migraine and its subtypes were defined based on The International Classification of Headache Disorders-II. Only those with "definite" migraine were included in the study. The mean age of 63 adult pRLS patients (15 men and 48 women) who participated in the study was 49.4 years. A total of 27 patients (42.9%) had definite migraine. Of these migraineurs, seven (11.1%) were without aura and 20 (31.8%) were with aura. The mean age of the 141 matched CPs was 48.7 years. A total of 32 CPs (22.7%) experienced migraine. Among these 32 migraineurs, 28 (19.9%) were without aura and four (2.8%) were with aura. Migraine and migraine with aura were significantly more common in pRLS patients than in CPs. pRLS patients with migraine were more anxious and experienced a shorter duration of RLS symptoms than pRLS patients without migraine. Migraineurs in the pRLS group tended to have high scores for severity of migraine headache by Visual Analog Scale score and high levels of disability by Migraine Disability Assessment grading than those in the control group. pRLS patients showed a positive association with definite migraine headaches. In contrast to results highlighted in recent studies, we found a strong link between migraine with aura and pRLS.

Natural killer (NK) cell killer immunoglobulin-like receptors (KIRs) contribute to the pathogenesis of many diseases. We determined the association between polymorphisms of KIR and their ligands and susceptibility to non-Hodgkin lymphoma (NHL), clinical features and prognosis. We included 90 patients with NHL and 94 controls. In the NHL group, KIR2DS1, HLA-Bw4 (Thr80) and HLA-Bw4 (Thr80)+/Bw4 (Iso80)- ligands were significantly more frequent. Patients with early-stage NHL had more frequent KIR2DL5 and KIR2DL5B than patients with advanced-stage NHL. During a median follow-up of 27 months, 26 patients with NHL died. Poor prognostic factors in univariate analysis were KIR2DL5A, KIR2DS1 and KIR3DS1 genotypes. In multivariate Cox regression analysis, advanced age and early relapse were poor prognostic factors. KIR genes and ligands had no significant effect on survival. The activating KIR2DS1 gene might activate NK cells, contributing to the production of more lymphoma cells. In addition, KIR2DS1, KIR2DL5A and KIR3DS1 might also be associated with a poor prognosis in NHL.

Genetic polymorphisms of platelet endothelial cell adhesion molecule-1 (PECAM-1) were found to play roles in atherosclerotic events. We determined PECAM-1 polymorphisms, soluble PECAM-1, and CD40L levels in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and evaluated their associations with clinical atherosclerotic complications. We included 100 RA patients, 81 SLE patients, and 94 healthy controls. The clinical features about the patients were obtained from medical records. Past cardiovascular complications were recorded. The most frequent gene polymorphisms of PECAM-1 were studied in our genetics laboratory. Soluble PECAM-1 and CD40L levels in serum were determined with ELISA. The frequencies of 373C (rs668) and 1688A (rs12953) alleles were higher in RA patients when compared to controls (p values, 0.028 and 0.016). RA and SLE patients had significantly higher allele frequencies for 2008A (rs1131012) when compared to controls (p values, 0.016 and 0.001). SLE patients had significantly more frequent AA genotype for rs1131012 polymorphism than RA patients and controls (p values, 0.007 and <0.001). Soluble PECAM-1 level was significantly higher in RA patients than in SLE patients and healthy controls (p values <0.001). Atherosclerotic complications were more frequent in SLE patients with AG genotype (rs12953) than those with AA genotype (p = 0.021). SLE patients with CC genotype (rs668) had a significantly lower frequency of atherosclerotic complications than those with CG genotype (p = 0.045). Nevertheless, in multivariate analysis, there was no association between genotype and atherosclerotic complications. We found associations between various PECAM-1 polymorphisms in RA and SLE; PECAM-1 and soluble CD40 ligand (sCD40L) levels were significantly higher in RA patients than in SLE and control groups. PECAM-1 polymorphisms in SLE were protective against atherosclerotic complications.