Background: There is a lack of information about the course of coronavirus disease 2019 (COVID-19) in patients with severe asthma who were treated with biologics. Some reports indicated that treatment with benralizumab, dupilumab, and omalizumab in patients with severe asthma was not associated with significant adverse effects during COVID-19.Methods: Asthma itself or the biologic agents used to treat asthma can have a positive effect on the course of COVID-19.There seem not to be any cases that specifically reported the use of mepolizumab in a patient who was infected with COVID.Results: We reported of a 55-year-old woman with a diagnosis of severe asthma for; 3 years and who was being treated withmepolizumab, with no evidence of loss of asthma control, at the time of contracting COVID-19 and who had been followed up inthe allergy clinic. In addition, there are no data on mepolizumab therapy in patients with elevated liver enzyme levels.Conclusion: With this case, we also reported that no adverse effects were observed during mepolizumab treatment in a patient with elevated liver enzyme levels.
Based on these results, we ascertain that sTWEAK has a role in etiopathogenesis of IBD. In addition, we believe that sTWEAK could be used as a marker for both disease activity criteria and treatment monitoring.
Because of similar clinical manifestations and laboratory findings, differential diagnosis of pulmonary embolism and community-acquired pneumonia (CAP) is generally difficult. Therefore, this study was conducted to find good markers for the easy, cheap, and fast differential diagnosis of pulmonary embolism and CAP. Thirty-four patients diagnosed with pulmonary embolism and 38 patients with CAP who were admitted to either emergency department or chest diseases outpatient clinic were included in this study. On admission and third day, complete blood count, C-reactive protein (CRP), erythrocyte sedimentation rate, procalcitonin (PCT), and D-dimer levels of each patient were measured. Neutrophil-to-lymphocyte ratio (NLR) was calculated using the formula NLR = neutrophil count/lymphocyte count. NLR/D-dimer and PCT/D-dimer ratios were also calculated. First day neutrophil count (P = 0.005), NLR (P = 0.002), CRP (P < 0.001), erythrocyte sedimentation rate (P < 0.001), PCT (P < 0.001), NLR/D-dimer (P < 0.001), and PCT/D-dimer (P < 0.001) levels were higher in patients with CAP compared with patients with pulmonary embolism. In stepwise logistic regression analysis done with all the parameters used for the differential diagnosis of pulmonary embolism and CAP, CRP, PCT/D-dimer, and NLR/D-dimer were found to be independent predictive factors for the presence of CAP. Among these factors, NLR/D-dimer ratio was found to be the most sensitive (97.4%) to have the highest negative predictive value 96.7% and to be the most accurate (area under curve = 0.921) (91.7%) parameter for the differential diagnosis of pulmonary embolism and CAP. In this study, NLR/D-dimer ratio was found to be more sensitive and more selective with negative predictive value and area under curve for the differential diagnosis of pulmonary embolism and CAP compared with other laboratory tests.
The aims of this study were to measure the levels of interleukin-33 (IL-33) and soluble Suppression of Tumorigenicity 2 (sST2) in patients with newly diagnosed primary hypertension (HT) and to determine the relationship between carotid intima-media thickness (CIMT) and IL-33/sST2. Eighty-two patients with newly diagnosed primary HT and ninety healthy volunteers were included in the study. CIMT ⩾0.9 mm was considered as significant for subclinical atherosclerosis. The sST2 levels of patients with primary HT were higher than those of the control group, whereas the IL-33 levels of these patients were much lower than those of the control group. The sST2 levels were higher in patients with subclinical atherosclerosis than in control subjects or patients with primary HT but not with subclinical atherosclerosis. In the primary HT group, sST2 had a positive correlation with CIMT, 24-h systolic-diastolic blood pressure, low-density lipoprotein and C-reactive protein, whereas sST2 had a negative correlation with the IL-33 level. A stepwise multivariable logistic regression analysis revealed that sST2 is an independent risk factor for subclinical atherosclerosis. Although the diagnostic predictive value of HT risk was determined as >51.8 pg l(-1) in the receiver operating characteristic curve analysis in respect of the sST2 level, the diagnostic predictive value for subclinical atherosclerosis risk was determined to be >107.2 pg l(-1). The sST2 level displays a positive correlation with atherosclerotic changes, and is an independent risk factor for subclinical atherosclerosis expressed as increased CIMT.
Background
In this study, we aimed to evaluate the sleep quality among chronic urticaria patients using the Chronic Urticaria Quality‐of‐Life Questionnaire (CU–Q2oL), sleep quality assessment tools, and polysomnography and to investigate any relationships between the obtained results.
Methods
The study included 21 patients diagnosed with chronic spontaneous urticaria and 19 healthy controls. We recorded the patients' sleep quality data, including CU–Q2oL, Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), and polysomnography results.
Result
Patients in the chronic urticaria group were more likely to have an ESS score of ≥10 (52.4% vs. 5.3%, p = 0.004) and an apnea‐hypopnea index of ≥5 (44.4% vs. 5.3%, p = 0.017) compared to the control group. In the patient group, the CU–Q2oL total score was positively correlated with sleep latency (r = 0.713, p = 0.004) and PSQI–C1 score (r = 0.726, p = 0.005), while it was negatively correlated with urticaria duration (r = −0.579, p = 0.015), apnea‐hypopnea index (r = −0.607, p = 0.021), longest apnea duration (r = −0.583, p = 0.029), total number of respiratory events (r = −0.618, p = 0.018), and apnea count (r = −0.686, p = 0.007).
Conclusion
We conclude that sleep‐related problems exist among a considerably large proportion of patients with chronic spontaneous urticaria.
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