In the Wuhan Province of China, in December 2019, the novel coronavirus 2019 (COVID-19) has caused a severe involvement of the lower respiratory tract leading to an acute respiratory syndrome. Subsequently, coronavirus 2 (SARS-CoV-2) provoked a pandemic which is considered a life-threatening disease. The SARS-CoV-2, a family member of betacoronaviruses, possesses single-stranded positive-sense RNA with typical structural proteins, involving the envelope, membrane, nucleocapsid and spike proteins that are responsible for the viral infectivity, and nonstructural proteins. The effectual host immune response including innate and adaptive immunity against SARS-Cov-2 seems crucial to control and resolve the viral infection. However, the severity and outcome of the COVID-19 might be associated with the excessive production of proinflammatory cytokines “cytokine storm” leading to an acute respiratory distress syndrome. Regretfully, the exact pathophysiology and treatment, especially for the severe COVID-19, is still uncertain. The results of preliminary studies have shown that immune-modulatory or immune-suppressive treatments such as hydroxychloroquine, interleukin (IL)-6 and IL-1 antagonists, commonly used in rheumatology, might be considered as treatment choices for COVID-19, particularly in severe disease. In this review, to gain better information about appropriate anti-inflammatory treatments, mostly used in rheumatology for COVID-19, we have focused the attention on the structural features of SARS-CoV-2, the host immune response against SARS-CoV-2 and its association with the cytokine storm.
Angiotensin-converting enzyme (ACE)/Angiotensin (Ang) II pathway has crucial regulatory effects on circulatory hemostasis and immune responses. This pathway has a major role in the development of acute lung injury and acute respiratory distress syndrome (ARDS), which is a devastating complication of SARS-CoV-2 infection. The aim of this study is to investigate the serum ACE activity and its correlation with clinical features and the disease severity in patients with COVID-19. Patients with confirmed COVID-19 by detecting SARS-CoV-2 nucleic acid RT-PCR were included in the study. Demographic data, clinical features, laboratory and radiologic investigations were recorded. Patients were classified by disease severity; asymptomatic, mild, and severe pneumonia. The serum ACE activity was evaluated with an autoanalyzer based on a spectrophotometric method. Fifty-five patients (50.9% female) and 18 healthy subjects (33.3 % female) were enrolled in the study. The median age of patients was 40 years, ranging from 22 to 81 years. Eighteen healthy subjects were served as the control group. The baseline characteristics were comparable between groups. The median serum ACE activity of patients and controls (38.00 [IQR 21] U/L and 32.00 [IQR 24] U/L, respectively) and of between patients grouped by disease severity (38.5 [IQR 19], 36 [IQR 25], and 38 [IQR 22] U/L, asymptomatic, mild and severe pneumonia group, respectively) were similar. There was no correlation between the serum ACE activity and conventional inflammatory markers. In this study, we did not find an association between serum ACE activity and COVID-19 and serum ACE activity on admission did not reflect disease severity.
Dear Editor, VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is an often fatal, X-linked disease characterized by haematological dysplasia overlapping with severe autoinflammatory manifestations. Acquired somatic mutations of the ubiquitin-like modifier activating enzyme (UBA1) gene impairs ubiquitylation, causing activation of the innate immune system and release of pro-inflammatory cytokines, TNF-α, IL-8, IL-6, IFN-γ and IFN-inducible protein-10 (IP-10) that culminate in severe systemic inflammation [ 1]. VEXAS syndrome patients present with protean clinical manifestations, including fever, chondritis, neutrophilic dermatosis, arthritis, pulmonary infiltrate and systemic vasculitis [ 1]. Thrombosis, predominantly as unprovoked venous thrombosis, has been reported in up to 56% of VEXAS syndrome patients [ 2]. Although chronic inflammation, vasculitis, endothelial dysfunction, disrupted anticoagulant mechanisms and prothrombotic antibodies are suggested mechanisms, the exact pathogenesis of thrombosis is yet to be elucidated [ 2].
Objective: Behçet’s disease (BD) is a chronic, multisystem disorder that can cause severe morbidity and mortality. Monitoring tools that measure disease activity are required for effective management of BD. We aimed to investigate the association of prognostic nutritional index (PNI) with disease activity in BD. Methods: In this cross-sectional study, we enrolled 88 adult patients with BD and 51 healthy controls. The patients were divided into patients with active and inactive BD according to their disease activities. PNI was calculated using the following formula: 10×serum albumin (g/dL)+0.005×peripheral lymphocyte count (per mm3). To evaluate BD activity, the Behçet Disease Current Activity Form was used. The relations of BD activity with PNI, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, erythrocyte sedimentation rate, and C-reactive protein were investigated. A receiver operator characteristic curve analysis was used to define the optimum cutoff value of PNI for active BD. Results: A total of 48 patients were classified as having active BD and 40 as having inactive BD. Patients with active BD had lower mean PNI than patients with inactive BD and healthy controls (51.8±4.2, 57.4±2.9, and 56.6±3.6, respectively; p<0.001). In multivariate analysis, PNI was the only independent predictor of BD activity (odds ratio, -0.687; 95% confidence interval 0.548-0.861; p=0.001). The optimum cutoff of PNI for active BD was 55.35 with 79.2% sensitivity and 77.75% specificity. Conclusion: PNI was significantly associated with BD activity. PNI may be a useful tool for the assessment of disease activity in BD. Cite this article as: Ataş N, Babaoğlu H, Demirel E, Çelik B, Bilici Salman R, Satış H, et al. Use of prognostic nutritional index in the evaluation of disease activity in patients with Behçet’s disease. Eur J Rheumatol 2020; 7(3): 99-104.