Pathogenesis Of Inflammation In Patients Research Articles

Mean Neutrophils to Lymphocytes Ratio in Patients with Coronary Artery Ectasia

Background: The Neutrophil to Lymphocyte (N/L) ratio has appeared as a novel marker of inflammation for cardiac as well as vascular diseases. Atherosclerosis and inflammatory markers shows a major role in the etiology as well as pathogenesis of coronary artery ectasia (CAE). Objective: This study objective was to know about the mean neutrophils to lymphocytes ratio (NLR) in patients who are known to have Coronary artery ectasia (CAE). Study Design: This study was a Cross Sectional Study. Methodology: Total 60 patients with diagnosis of CAE presenting in cardiac emergency or cardiac OPD and admitted in CCU were enrolled. Coronary angiogram was performed to look for evidence of coronary artery ectasia. A blood sample of 5ml was taken and sent to hospital laboratory to find NLR ratio as per operational definition. All collected data was entered and evaluated in SPSS v23.0. It was stratified for gender, age, BMI, DM (200mg/dl) and HTN (>160/90mmHg) to address effect modifiers. Post stratified, t-test was used to rule out these effect modifiers by taking p-value ≤0.05 as significant. Results: In this study, 60 patients who had Coronary artery ectasia (CAE) fulfilling selection criteria were included from Department of Cardiology, Gulab Devi Hospital, Lahore. In these patients, 37(61.7%) were males and 23(38.3%) were females. Mean age of the patients were 40.5±14.8 years with 18 and 70 as minimum and maximum ages. Mean NLR of the patients were 2.4±1.2 with 0.72 and 4.98 as minimum and maximum values. Conclusion: Elevated Neutrophil to Lymphocyte ratio (NLR) plays a significant role in the pathogenesis of inflammation in patients with coronary artery ectasia (CAE). Key Words: Coronary artery ectasia, Neutrophils to Lymphocytes ratio.

Systemic and local cytokine profile and risk factors for persistent allergic airway inflammation in patients sensitised to house dust mite allergens

ObjectiveTo evaluate cytokine profile, vitamin D status, symptom score and quality of life in patients with persistent allergic airway diseases sensitised to house dust mites (HDM) in comparison with healthy individuals.Material and methodsPatients sensitized to HDM with persistent AR and having symptoms for at least 2 years with or without AA were involved into the study. Measurements of vitamin D level in serum and IL-10, IL-13, IL-17, IL-22, IL-33 and IFN-gamma in serum and nasal lavage were performed by ELISA.ResultsEighty-one subjects were involved into the study. Serum IL-10 concentration was higher in patients with AR than in patients with AR and AA (6.71 ± 1.73 vs. 1.98 ± 0.24, p < 0.05). IFN-gamma level in nasal lavage was higher in patients with AR and AA than in patients with AR (p < 0.01) and healthy individuals (p < 0.05) (7.50 ± 0.37 vs. 6.80 ± 0.99 vs. 6.50 ± 0.22). Serum IL-22 negatively correlated with IL-22 in nasal lavage, whereas serum IFN-gamma positively correlated with IFN-gamma in nasal lavage. Positive correlation between serum IL-17 and total IgE and negative correlation between IL-17 in nasal lavage and eosinophils in nasal smear were found in patients with AR and AA. Serum IFN-gamma decreased the risk of AR for healthy individuals. Serum IL-10 and vitamin D decreased risk for development of AA for patients with AR. IL-22 in serum and IL-10 and IL-33 in nasal lavage increased this risk.ConclusionNovel cytokines such as IL-22, IL-17 and IL-33 and vitamin D may be involved in pathogenesis of persistent airway inflammation in patients sensitized to HDM.

Роль лейкотриенов в патогенезе воспаления у больных с различным фенотипом бронхиальной астмы и хронической обструктивной болезнью легких

Роль лейкотриенов в патогенезе воспаления у больных с различным фенотипом бронхиальной астмы и хронической обструктивной болезнью легких

Review article: the role of the autonomic nervous system in the pathogenesis and therapy of IBD.

There is a growing body of evidence implicating a role for the brain-gut axis in the pathogenesis of inflammation in patients with IBD. To perform a narrative review of published literature regarding the association of the autonomic nervous system and intestinal inflammation and to describe the rationale for and emerging use of autonomic manipulation as a therapeutic agent METHODS: Current relevant literature was summarised and critically examined. There is substantial pre-clinical and clinical evidence for a multifaceted anti-inflammatory effect of the vagus at both systemic and local intestinal levels. It acts via acetylcholine-mediated activation of α-7-acetylcholine receptors involving multiple cell types in innate and adaptive immunity and the enteric nervous system with subsequent protective influences on the intestinal barrier, inflammatory mechanisms and the microbiome. In patients with IBD, there is evidence for a sympatho-vagal imbalance, functional enteric neuronal depletion and hyporeactivity of the hypothalamic-pituitary-adrenal axis. Direct or transcutaneous vagal neuromodulation up-regulates the cholinergic anti-inflammatory pathway in pre-clinical and clinical models with down-regulation of systemic and local intestinal inflammation. This is supported by two small studies in Crohn's disease although remains to be investigated in ulcerative colitis. Modulating the cholinergic anti-inflammatory pathway influences inflammation both systemically and at a local intestinal level. It represents a potentially underutilised anti-inflammatory therapeutic strategy. Given the likely pathogenic role of the autonomic nervous system in patients with IBD, vagal neuromodulation, an apparently safe and successful means of increasing vagal tone, warrants further clinical exploration.

The Role of Innate Lymphoid Cells in the Pathogenesis of Immune Inflammation in Patients with Ulcerative Colitis

The Role of Innate Lymphoid Cells in the Pathogenesis of Immune Inflammation in Patients with Ulcerative Colitis

Endotoxemia in end-stage kidney disease.

Chronic unexplained inflammation remains a prevalent and clinically significant problem for patients with end-stage kidney disease (ESKD), especially in the dialysis population. The causes of persistent inflammation are likely to be multifactorial, but the underlying mechanisms remain to be elucidated. Endotoxins are reported to play a significant role in the pathogenesis of inflammation in patients with ESKD. However, blood endotoxin measurement with the Limulus amoebocyte lysate (LAL) assay is difficult with current detection systems. The reported degree and prevalence of endotoxemia varies in the literature. There are questions as to whether endotoxemia is truly present; whether the varied findings are due to methodological issues with the LAL assay and whether any endotoxemia that might be present plays a role in chronic inflammation frequently observed in ESKD patients. This review will discuss the challenges of accurate blood endotoxin detection, the potential source of blood endotoxins, and the significance of endotoxemia to patient with ESKD.