Abnormality of the immune system may play an important role in the pathogenesis of schizophrenia (SCZ). We aim to investigate the relationship between clinical features of SCZ and tumor necrosis factor-alpha (TNF-α) −238 G/A, −308 G/A polymorphisms in SCZ patients by comparing genotype distributions of TNF-α gene polymorphisms between patients and healthy controls. A sample of 113 patients with SCZ and 104 healthy volunteers was included in the study. SCID-I was used to confirming the diagnosis according to DSM-IV-TR criteria. We evaluated the patients with some scales and data forms in terms of clinical features, symptom severity, level of insight, suicidal behavior, and treatment response. PCR-RFLP was used to determine TNF-α gene polymorphisms from DNA material. The distributions of TNF-α − 238 G/A and TNF-α − 308 G/A polymorphisms of the patients diagnosed with SCZ were not significantly different from the control group. There was a significant difference in the TNF-α − 238 G/A genotype distributions between treatment-resistant and treatment-responsive SCZ patients. Again, the distributions of TNF-α − 238 G/A genotype of attempted suicide patients in SCZ were significantly different from the non-attempted suicide of SCZ patients. Whereas TNF-α − 238 G/A and −308 G/A polymorphisms were not associated with SCZ, TNF-α − 238 G/A polymorphism may be related to treatment resistance and attempted suicide in SCZ patients in the Turkish population.

Background: Pro-inflammatory/anti-inflammatory cytokine imbalance in cerebrospinal fluid or plasma of schizophrenia (SCZ) and bipolar disorder (BD) patients has been documented over the last decade. We aim to examine the interleukin-1 receptor antagonist(IL-1RA)andIL-4variable number of tandem repeat (VNTR) polymorphisms in SCZ and BD patients by comparing them with healthy controls.Methods: Two hundred and thirty-four unrelated patients (127 patients with SCZ, 107 patients with BD) and 204 healthy controls were included. The Structured Clinical Interview for DSM-IV Axis I Disorders was used to confirm the diagnosis. In addition, the polymerase chain reaction technique was used to investigateIL-1RAandIL-4VNTR polymorphisms.Results: Our results showed that the distributions ofIL-1RAandIL-4genotype and the allele frequencies of SCZ or BD patients were not significantly different from the healthy control group.IL-1RAallele 2 homozygous genotype andIL-1RAallele 2 frequencies were non-significantly higher among SCZ patients than in controls.Conclusions: Our study indicates that theIL-1RA and IL-4VNTR polymorphisms are not considered risk factors for developing SCZ and BD among Turkish patients.

Background/Objectives: Growing evidence suggests that disruption of circadian rhythms contributes to the pathogenesis of inflammation and inflammatory bowel disease; however, clinical data linking circadian gene variants to ulcerative colitis remain limited. In this study, we aimed to investigate associations between key circadian rhythm gene polymorphisms and clinical and treatment-related characteristics in ulcerative colitis. Methods: A total of 107 patients with ulcerative colitis and 80 healthy controls were included in this single-center cross-sectional study. The BMAL1 rs7950226, CLOCK rs1801260, and CRY1 rs2287161 polymorphisms were analyzed using the polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) method. Genotype and allele frequency distributions were compared between patients and controls, and associations with clinical characteristics were evaluated within the ulcerative colitis cohort. Results: Genotype distributions of BMAL1 rs7950226 and CLOCK rs1801260 were similar between patients with ulcerative colitis and healthy controls; however, the G allele of BMAL1 was more frequent in patients (p = 0.028). Within the ulcerative colitis cohort, CLOCK rs1801260 genotypes were significantly associated with inflammatory and treatment-related characteristics, with the CC genotype linked to higher C-reactive protein levels (p = 0.021) and the TT genotype associated with increased azathioprine use (p = 0.006). Conclusions: These findings suggest a potential association between circadian rhythm gene variants and clinical features of ulcerative colitis, particularly in relation to inflammatory activity and treatment requirements, and provide preliminary clinical insight that warrants further investigation in larger and longitudinal studies.

Background/Objectives: Interleukin-6 is a key proinflammatory cytokine involved in the pathophysiology of Familial Mediterranean Fever (FMF). This study aimed to evaluate interleukin-6 levels and the interleukin-6 rs1800795 variant in pediatric FMF participants and to investigate their associations with clinical manifestations, laboratory findings, and Mediterranean fever (MEFV) mutation status. Methods: The research involved 69 pediatric FMF participants and 50 healthy children. Interleukin-6 levels, laboratory findings, and genotype distributions of the interleukin-6 rs1800795 variant were compared between FMF and control groups. Moreover, the relationship between interleukin-6 levels and clinical findings, MEFV mutation status, and laboratory parameters were evaluated in the FMF group. Results: In the FMF group, interleukin-6, serum amyloid-A (SAA), white blood cell count (WBC), neutrophil, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) levels were higher compared to the control group. In the FMF group, interleukin-6 levels showed a positive correlation with ISSF score, annual attack frequency, the number of concomitant symptoms, disease duration, SAA, CRP, and ESR. The allele and genotype distribution of the interleukin-6 rs1800795 variant was similar to those in the control and FMF groups. In the FMF group, interleukin-6 values were higher in patients with abdominal pain, fever, chest pain, or arthralgia compared to those without these symptoms. Interleukin-6 levels were higher in both homozygous and compound heterozygous subgroups compared to the heterozygous subgroup. Conclusions: Elevated interleukin-6 levels in symptomatic pediatric FMF patients and those with homozygous or compound heterozygous MEFV mutations suggest that interleukin-6 may reflect both clinical disease severity and MEFV mutation status.