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Background & aims: The rate of mortality from Spontaneous Peritonitis (SP) in cirrhotic patients is still high despite the development of new antibiotic treatments and intensive hospital care. The coexistence of spontaneous fungal peritonitis (SFP) is almost entirely ignored health problem, because it is difficult to be diagnosed at an early stage by conventional culture-based methods. Therefore, this study was designed to employ PCR-based method in evaluating the prevalence of fungal infection in cirrhotic patients with peritonitis who failed to respond to the recommended therapy and to determine its association with in-hospital mortality. Subjects and Methods: A total of 80 cirrhotic patients admitted to the hospital with ascitis (June-2013 to April-2015) were followed in this study. Results: During hospitalization, 23 (42%) of patients had died although they received guideline-driven treatment. The demographics, clinical, hematological, and biochemical data were similar in both mortality and survival groups. However, the incidence of fungus infection was the only significantly elevated parameter in the mortality group than in the survival group (7/23;30% vs.0/32;0%, P = 0.0012). This fungal infection was significantly associated with SP drug resistance development (P = 0.007). Intriguingly, all the cases of fungal infection were detected by PCR-based method while culture-based diagnosis was able to detect the fungal infection in only 4 of these cases indicating a diagnostic sensitivity of 57%. Conclusion: Our results reflect a strong association between SFP and in-hospital mortality in cirrhotic patients with SP that may offer a coherent explanation for the antibiotic treatment failure in such patients. Prompt PCR-detection and antifungal coverage is warranted in these cases.

Objective MicroRNAs are large family clusters of small noncoding RNAs that implicated in genetic and epigenetic regulation of several immunological processes and pathways. As an epigenetic modifier, the microRNA 17‐92 cluster host gene (MIR17HG) has been shown to regulate the expression of genes involved in systemic lupus erythematosus (SLE) pathway. This study aimed to explore the association of MIR17HG (rs4284505; A>G) variant with SLE development and phenotype in a sample of the Eastern Mediterranean population. Methods A total of 326 participants (163 patients with SLE and 163 healthy controls) were enrolled in this study. The different genotypes of the MIR17HG (rs4284505) variant were characterized using the TaqMan real‐time polymerase chain reaction technique. Association with the available clinical and laboratory data, including the systemic lupus erythematosus disease activity index (SLEDAI), was also executed. Results The MIR17HG (rs4284505) variant showed a protective effect against developing SLE under heterozygote (A/G vs A/A; odds ratio [OR] = 0.10, 95% confidence interval [CI] = 0.05‐0.20, P < 0.001) and dominant (A/G+G/G vs A/A; OR = 0.39, 95% CI = 0.25‐0.61, P < .001) models. This association was consistent even after SLE stratified by lupus nephritis. In contrast, rs4284505 (G/G) genotype conferred increased susceptibility to SLE (G/G vs A/A+A/G; OR = 2.15, 95% CI = 1.31‐3.53, P = .002). Moreover, the rs4284505 variant showed a statistically significant association with mucocutaneous lesions and SLEDAI scores (all P < .05). Conclusion This study is the first one to explore that the MIR17HG rs4284505 is associated with SLE risk; (A/G) genotype conferred a protective effect, while the (G/G) genotype showed increased susceptibility to SLE and association with the disease severity in the study population.

Toll-like receptor (TLR) family signature has been implicated in sepsis etiopathology. We aimed to evaluate the genetic profile of TLR pathway-related key genes; the myeloid differentiation protein 88 (MYD88), IL1 receptor-associated kinase 1 (IRAK1), the nuclear factor kappa-B1 (NFKB1), and interleukin 6 (IL6) in the blood of neonates with sepsis at the time of admission and post-treatment for the available paired-samples. This case–control study included 124 infants with sepsis admitted to the neonatal intensive care unit and 17 controls. The relative gene expressions were quantified by TaqMan Real-Time qPCR and correlated to the clinic-laboratory data. MYD88, NFKB1, and IL6 relative expressions were significantly higher in sepsis cases than controls. Higher levels of MYD88 and IL6 were found in male neonates and contributed to the sex-based separation of the cases by the principal component analysis. ROC analysis revealed MYD88 and NFKB1 transcripts to be good biomarkers for sepsis. Furthermore, patients with high circulatory MYD88 levels were associated with poor survival, as revealed by Kaplan–Meier curves analysis. MYD88, NFKB1, and IL6 transcripts showed association with different poor-outcome manifestations. Clustering analysis split the patient cohort into three distinct groups according to their transcriptomic signature and CRP levels. In conclusion, the study TLR pathway-related transcripts have a gender-specific signature, diagnostic, and prognostic clinical utility in neonatal sepsis.