IntroductionCoronaviruses (CoVs), mainly targeting human respiratory system, are responsible for health-threatening outbreaks including severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS) and lastly coronavirus disease 2019 (COVID-19) [1]. In December 2019, in the Chinese Province of Wuhan the novel coronavirus has been identified in patients with atypical pneumonia characterized by fever, dry cough and progressive dyspnea [2]. Rapidly, this coronavirus, namely SARS-CoV-2 1 , has spread worldwide, leading to a serious lung inflammation, acute respiratory distress syndrome (ARDS), cardiac and renal injury, especially in patients with older age and comorbidities (diabetes mellitus, hypertension, and heart failure) [3][4][5]. According to disease progression, patients may be roughly divided into two groups; asymptomatic or mild cases that usually 2.The origin and structural features of SARS-CoV2CoVs belong to big family Coronaviridae which consists of two subfamilies: Orthocoronavirinae and Torovirinae.

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Objective Persistent inflammation is an insidious and less studied feature of FMF. We investigated clinical determinants of persistent inflammation and its associations with individual damage items. Methods This is a cross-sectional analysis of 917 FMF patients, who fulfilled the Tel Hashomer criteria and had at least 6 months’ follow-up. Patients were stratified based on whether they had persistent inflammation. We used logistic regression analysis to investigate independent predictors of persistent inflammation and the associated individual damage items. Results One hundred and forty-two (15%) patients had persistent inflammation. Active FMF (54%) was the most prominent reason for the persistent inflammation. Spondylarthritis (16%), other inflammatory arthritis (8%) and IBD (2%) were other frequent reasons. Male gender, history of exertional leg pain, inflammatory comorbidities, M694V homozygosity, colchicine resistance, lower education levels and musculoskeletal attack dominance were found to be the independent predictors of persistent inflammation. Earlier disease onset led to a tendency towards persistent inflammation. Patients with persistent inflammation were more likely to suffer damage. There is an increased risk of developing proteinuria, amyloidosis and renal insufficiency. Conclusion We identified, for the first time, the predictors of persistent inflammation in adult FMF patients and related individual damage items of the Autoinflammatory Disease Damage Index. Persistent inflammation is insidious and one of the chief causes of damage; therefore, especially patients with these predictors should be followed up more closely. If detected, underlying inflammatory comorbidities should be assessed meticulously as early detection and proper treatment strategies may favourably impact the natural history of the disease.

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.

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Introduction Systemic lupus erythematosus (SLE) is associated with an increased risk of pulmonary infections, as well as a rare condition known as shrinking lung syndrome (SLS). The diaphragm has an important role to play in lung physiology and might also play a role in these adverse events. Here, we aimed to investigate whether SLE patients have impairment in their diaphragmatic muscle thickness and function with respect to another connective-tissue disease: primary Sjögren’s syndrome (pSS). Method Patients diagnosed with SLE who were in remission or who had minimal disease activity and had at least one year of follow-up were included in this study. Patients with known lung pathology and smokers were excluded. Patients with pSS constituted the second experimental group. Ultrasonographic evaluation of the diaphragmatic muscle was conducted by an experienced independent sonographer at three time points, diaphragmatic thickness during deep and quiet inspiration and maximum expiration being measured. Diaphragmatic muscle function was evaluated with maximum expiratory pressure (MEP) and maximum inspiratory pressure (MIP). Results A total of 115 patients were studied ( n = 39 SLE; n = 76 pSS). The mean ±  standard deviation ( SD) thickness of the diaphragmatic muscles during quiet inspiration was significantly reduced in patients with SLE compared to patients with pSS (2.32 mm vs. 2.81 mm; p < 0.05). Similarly, the thickness during deep inspiration and at maximum deep expiration were significantly lower in SLE patients (2.88 mm vs. 3.29 mm and 1.92 mm vs. 2.33 mm, respectively; p < 0.01). MIPs and MEPs, defined as the percentages of expected values, were significantly lower in patients with SLE compared to those with pSS (80% vs. 92% and 76% vs. 120%, respectively; p < 0.05). Diaphragmatic muscle thickness during deep inspiration demonstrated a moderate correlation with MIP ( r = 0.434; p = 0.001). Conclusion SLE patients had reduced diaphragmatic muscle thickness compared to those with pSS, which was associated with impaired functional tests. Further prospective studies are needed to investigate whether structural and functional impairments in diaphragmatic muscle play a role in an increased risk of pulmonary infections and SLS in patients with SLE.

Background/Objective: Core muscle endurance (CME), which is the ability of sustaining the activity of trunk muscles, has been shown to be lower in patients with ankylosing spondylitis (AS). The aim was to investigate the possible relationship between CME times and balance, fatigue, physical activity (PA) level, and thoracic kyphosis angle.Methods: Fifty-one patients with AS with a mean age of 41.0 years (interquartile range, 25/75 years; 29.0/51.0 years) were included in the study. Core muscle endurance times were assessed by using trunk extension, trunk flexion, and side bridge tests. Overall stability index, anteroposterior stability index, mediolateral stability index, and limits of stability were evaluated with the Biodex Balance System. Fatigue and PA levels were surveyed using Fatigue Severity Scale and International Physical Activity Questionnaire, respectively. Thoracic kyphosis angle was measured by using a digital inclinometer. Additionally, CME times were compared for "high-fatigue" versus "low-fatigue" and as "low PA" versus "moderate/high PA" groups. Spearman correlation coefficients and Mann-Whitney U test were used for statistical analysis.Results: Significant correlations were detected between overall stability index, anteroposterior stability index, Fatigue Severity Scale, International Physical Activity Questionnaire, and all CME tests (p < 0.05) and between mediolateral stability index and side bridge test (p < 0.05). Limits of stability correlated only with side bridge test (p < 0.05). Core muscle endurance significantly differed between high-fatigue and low-fatigue groups (p < 0.05), except trunk flexor test (p > 0.05). No significant differences were observed between low PA and moderate/high PA groups (p > 0.05), except side bridge test (p < 0.05).Conclusions: Core muscle endurance times seem to be related to PA level, fatigue, and balance but not with thoracic kyphosis angle. Assessing CME in patients with AS might help in planning individualized exercise programs.

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