Introduction: Obesity and type 2 diabetes mellitus have reached epidemic proportions worldwide. Abnormal sleep has been linked to both incident and prevalent obesity and type 2 diabetes. We aimed to characterize abnormal sleep patterns [ASP's] in patients with obesity, type 2 diabetes, or both. Subjects: The study included 92 subjects divided into four groups: Group 1, 23 obese patients (BMI > 30) with type 2 diabetes mellitus; Group 2, 23 non-obese diabetic patients; group 3, 23 obese subjects without diabetes; group 4, 23 matched healthy control subjects. Methods: Waist circumference and BMI [body mass index] estimation, fasting and post challenge plasma glucose ''groups 2 & 4", HOMA-IR [Homeostatic model assessment-Insulin resistance] estimation, and finally evaluation for ASP's using a CDC [Centers for Disease Control and prevention] validated questionnaire. Results: Post-prandial glucose and BMI significantly predicted Sleep latency and sleep hours at night respectively. Both group 1 and 3 compared to group 4 showed higher prevalence of: Insomnia [p < .01], snoring [p < .01], fragmented sleep [p < .05], excessive day time sleepiness [p < .001], and daytime dysfunction [p < .001]. Group 2 compared to group 4 showed higher prevalence of: Insomnia, snoring, fragmented sleep, and finally, daytime dysfunction [All p < .01]. Group 1 compared to groups 3 and 4 had significantly less hours of sleep at night [p < .01]. Group 1 compared to group 2 showed higher prevalence of: Insomnia, fragmented sleep, excessive day time sleepiness, and daytime dysfunction [All p < .05]. Finally, group 3 compared to group 2 showed higher prevalence of: Excessive day time sleepiness, and daytime dysfunction [p < .01]. Conclusion: The combination of obesity and diabetes mellitus is associated with poor quality and quantity of sleep with resultant significant daytime dysfunction. Glycemic, and adiposity measures predicted sleep latency and hours.

Background:Fatigue is a prevalent and fundamental phenomenon in psoriatic arthritis (PsA) patients. It often interferes with physical and social functions and may lead to social withdrawal, long-standing sick leave, disability and loss of work productivity. Fatigue is a prevalent symptom in patients with chronic rheumatic diseases. Cytokines as interleukin IL-23/17 play a pivotal role in the pathogenesis of PsA.Objectives:To assess fatigue in PsA patients and determine its relation to serum IL 23 levels, disease activity, Skin severity, physical function and quality of life (QoL).Methods:Fifty PsA patients and 46 matched healthy controls were included in this study. Skin severity based on the Psoriasis Area and Severity Index (PASI), the Disease Activity index for Psoriatic Arthritis (DAPSA) and the Functional Assessment of Chronic Illness Therapy (FACIT-F) were assessed. Physical function was assessed by the Health Assessment Questionnaire Disability Index (HAQ-DI) and health-related QoL was assessed using the Short Form Health Survey (SF-36), Psoriatic Arthritis QoL (PsAQoL) and the Dermatology Life Quality Index (DLQI). Serum IL-23 levels were measured in the studied groups.Results:The study included 23 (46%) females and 27 (54%) males with a mean age of 42.78±12.33 years. The mean serum IL-23 level was significantly higher in PsA patients (50.89 ±13.86 pg/ml) than in controls (43.88 ± 6.34 pg/ml) (p=0.006). The FACIT score ranged from 2-41. Severe fatigue (score <30) was reported in 27 (54%) PsA patients. There were significant correlations between FACIT-F and (DAPSA, PASI, HAQ-DI, PsAQoL, DLQI and SF-36). No significant correlations could be detected between FACIT-F and serum levels of IL-23 and CRP.Conclusion:Fatigue was a frequent complaint in PsA patients. There was a mutual negative impact between fatigue and each of PsA joint disease activity and physical function and it worsened the QoL. Fatigue was worsened with increased severity of skin PsO. Although serum level of IL-23 was significantly elevated in PsA patients than the controls, it wasn’t correlated with fatigue score. Hence IL-23 can’t be considered a biomarker for fatigue severity.References:[1]Chandran V, Bhella S, Schentag C, Gladman DD. Functional Assessment of Chronic Illness Therapy-Fatigue Scale is valid in patients with psoriatic arthritis. Ann Rheum Dis 2007; 66(7):936.[2]Mortada M, Abdul-Sattar A, Gossec L. Fatigue in Egyptian patients with rheumatic diseases: a qualitative study. Health Qual Life Outcomes 2015; 13:134.[3]Krajewska-Wlodarczyk M, Owczarczyk-Saczonek A, Placek W. Fatigue - an underestimated symptom in psoriatic arthritis. Reumatologia 2017; 55(3):125-30.[4]Strand V, Mease P, Gossec L, Elkayam O, van den Bosch F, Zuazo J, et al. Secukinumab improves patient-reported outcomes in subjects with active psoriatic arthritis: results from a randomised phase III trial (FUTURE 1). Ann Rheum Dis 2017; 76(1):203-7.[5]Reygaerts T, Mitrovic S, Fautrel B, Gossec L. Effect of biologics on fatigue in psoriatic arthritis: A systematic literature review with meta-analysis. Joint Bone Spine 2018; 85(4):405-10.Table.Correlation between FACIT-F score and different parameters in patients groupFACIT-FrspDAPSA-0.365*0.009*PASI-0.424*0.002*HAQ-DI-0.464*0.001*PsAQoL-0.633*<0.001*DLQI-0.492*<0.001*SF-360.600*<0.001*CRP-0.1670.247Serum IL-23 levels-0.1830.204rs: Spearman coefficient, *: Statistically significant at p ≤ 0.05Figure. Correlation between FACIT-F and DAPSA in the studied PsA patients.Acknowledgments:I am deeply indebted to my late Professor Abdelmoniem Helal for his expert guidance and keen interest throughout the work.Thanks to My parents and Husband.Disclosure of Interests:None declared

Objectives It is not known why only some hepatitis C virus (HCV) infected patients develop glomerulonephritis (GN). Therefore, we investigated the role of soluble complement regulators in the development of HCV associated GN. Methods Patients with HCV associated GN who were admitted to our nephrology unit between July 2016 and July 2018 were recruited to the study (group 1). Two other age and sex matched groups were studied as control groups: patients with HCV without GN (group 2) and healthy HCV negative volunteers (group 3). There were 26 participants in each of the three groups at the end of the recruitment period. An assay of serum fluid-phase complement regulators was performed using enzyme linked immunosorbent assay technique. Three complement single nucleotide polymorphisms (SNPs) were analyzed using real time polymerase chain reaction (Taqman; thermo fisher scientific): rs2230199 and rs1047286 for complement 3 (C3) and rs800292 for complement factor H (CFH). Results Serum levels of complement 4 binding protein (C4BP) were significantly lower in group 1 (median 70 ng/ml) than in groups 2 (median 88.8 ng/ml) and 3 (median 82.8 ng/ml) with p value of 0.007. The minor allele (allele A) of rs800292 for CFH was significantly higher in group 2 and group 3 (G 54% and A 46%) than in group 1 (G 73% and A 27%), p = 0.04. Conclusions Low C4BP levels are associated with GN in HCV infected patients. In addition, rs800292 SNP in CFH protects against GN in patients with HCV.

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Chimerism analysis is an important method for monitoring outcome of allogenic hematopoietic stem cell transplantation. Variable number tandem (VNTR) analysis is considered an informative technique to follow up chimerism state. The aim of the work is to study certain number of VNTRs to identify their potential value in the detection of chimerism in transplanted patients in conventional ablative transplants. Also to demonstrate the value of T cells subset analysis in detecting transplantation outcomes. This study included 17 pairs undergoing HSCT. Informative loci pre-transplantation using five VNTR loci and two gene loci were identified. After transplantation the informative loci were used to detect chimerism status. After DNA extraction from blood samples, amplification of VNTR loci was performed using a conventional PCR protocol. Extra sample post transplantation was collected and pre-treated with resetting technique in order to separate T cells, its product was subjected to DNA extraction then amplification of informative loci was done. Amplified product of DNA samples was run on 2% agarose gel stained using ethidium bromide. Fourteen recipients showed full done chimerism in both whole blood and T cells separated cells, one recipient died after HSCT, one recipient showed split chimerism and one pair failed to detect informative locus. VNTR analysis using a panel of five loci is suitable to detect state of chimerism after HSCT.