Primary ciliary dyskinesia (PCD) is a rare disease, predominantly inherited as an autosomal recessive, with ciliary dysfunction leading to impaired mucociliary clearance, chronic airway infection and inflammation. Situs inversus totalis occurs in ~50 % of PCD patients and it is known as Kartagener syndome. Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent attacks of fever and peritonitis, pleuritis, arthritis, or erysipelas-like skin disease. FMF is caused by mutations in the MEFV gene which is located on chromosome 16p13.3. p.M680I, p.M694 V, p.M694I, p.V726A on exon 10 and p.E148Q on exon 2 are the most common mutations among FMF patients and these constitute 85 % of all. Homozygosity of R202Q polymorphism is strongly associated with FMF. We would like to present a case of Kartagener syndrome accompanied by FMF with R202Q polymorphism. Our case is the first in the literature indicating the accidental coexistence of FMF and Kartagener syndrome.

Primary ciliary dyskinesia (PCD) is a rare disease, predominantly inherited as an autosomal recessive, with ciliary dysfunction leading to impaired mucociliary clearance, chronic airway infection and inflammation. Situs inversus totalis occurs in *50 % of PCD patients and it is known as Kartagener syndome. Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent attacks of fever and peritonitis, pleuritis, arthritis, or erysipelas-like skin disease. FMF is caused by mutations in the MEFV gene which is located on chromosome 16p13.3. p.M680I, p.M694 V, p.M694I, p.V726A on exon 10 and p.E148Q on exon 2 are the most common mutations among FMF patients and these constitute 85 % of all. Homozygosity of R202Q polymorphism is strongly associated with FMF. We would like to present a case of Kartagener syndrome accompanied by FMF with R202Q polymorphism. Our case is the first in the literature indicating the accidental coexistence of FMF and Kartagener syndrome.

Introduction: Systemic lupus erythematosus (SLE) is a multisystemic, autoimmune connective tissue disease characterized by a variable course and prognosis. We aimed to determine IL-10, IL-17 and IL-23 cytokines and vitamin D levels in SLE patients, which we think play role in the pathogenesis of the disease. Material and Method: Forty SLE patients and 20 healthy controls were included in our study. Levels of IL-10, IL-17 and IL-23 were measured by sandwich ELISA method. Quantitative data are expressed as mean ± standard deviation and median range (maximum-minimum) values. The data were analyzed at 95% confidence interval, and cases where the p value was less than 0.05 were considered statistically significant. Results: IL-10 and IL-17 levels of the control and patient groups were compared and no statistically significant difference was found (p=0.333, p=0.99). IL-23 levels of the patient group were found to be higher than the control group and were found to be statistically significant (p<0.001). No statistically significant relationship was found between disease duration or SLEDAI score and IL-23 levels (p=0.476). 25 (OH) vitamin D levels of the patient group were found to be lower than the control group and were statistically significant (p=0.003). No significant relationship was found between IL-10 and IL-17 levels and vitamin D. Significant relationship was found between IL-23 and vitamin D levels (p=0.019). Discussion: In our study, there was no significant difference between the groups in terms of IL-10 or IL-17, while IL-23 levels were found to be significantly higher in SLE patients. Vitamin D levels were found to be lower in the patient group with SLE compared to the control group, and a negative correlation was found between the disease duration and IL-23. Specific blocking of the IL-23 immune pathway can be an effective and safe treatment option in the treatment of SLE.