Abstract

Background

SARS‐COV‐2 infection reframed medical knowledge in many aspects, yet there is still a lot to be discovered. Coronavirus disease 19 (COVID-19) can cause neuropsychiatric, psychological, and psychosocial impairments. Literature regarding the cognitive impact of COVID-19 is still limited.

This study aims to evaluate cognitive function, anxiety, and depression among patients with coronavirus disease 19.

Methods

Sixty COVID-19 patients were recruited and sub-grouped according to the site of care into three groups, home isolation, ward, and RICU, and compared with 60 matched control participants. Entire clinical history, O₂ saturation, mini-mental state examination (MMSE), Hamilton’s anxiety (HAM-A), and depression rating scales (HAM-D) were assessed.

Results

MMSE showed significantly lowest results for the ICU group, with a value of 21.65 ± 3.52. Anxiety levels were the highest for the ICU group, with a highly significant difference vs. the home isolation group (42.45 ± 4.85 vs. 27.05 ± 9.52; p< 0.001). Depression values assessed showed a highly significant difference in intergroup comparison (44.8 ± 6.64 vs. 28.7 ± 7.54 vs. 31.25 ± 8.89; p<0.001, for ICU vs. ward vs. home group, respectively).

MMSE revealed a significant negative correlation with age and education level, anxiety level had significant negative correlations with severity of illness and male gender, and depression level had highly significant negative correlations with severity of illness and male gender.

Conclusion

Both cognitive and neuropsychiatric symptoms were affected in COVID-19 cases, especially in ICU-admitted patients. The impact of these disorders was significant in older age, lower oxygen saturation, and severe disease.

Abstract

Background 

Chronic obstructive pulmonary disease (COPD) is ordinarily associated with social and economic burden. Pulmonary hypertension attributed to COPD varies greatly among studies; and accounts for worse quality of life and hence increased morbidity and mortality.

Aim

This study aimed to evaluate impact of pulmonary hypertension on exercise capacity, and possible predictors for exercise intolerance among COPD patients.

Methods 

Patients suffering from COPD (73 patients) were grouped according to echocardiographic assessment for the presence of pulmonary hypertension into two groups. The assessment included full clinical history, mMRC dyspnea scale, COPD assessment test, arterial blood gases before and after exercise testing, and assessment of resting pulmonary function test. Also transthoracic echocardiography, cardiopulmonary exercise testing (CPET) using incremental treadmill exercises protocol was done for all participants.

Results 

A total of 39 (53.4%) COPD patients have pulmonary hypertension. COPD patients with pulmonary hypertension had significantly lower parameters of pulmonary function tests either pre or postbronchodilator; significantly lower pH, PaO₂ and SaO₂ either before or after CPET. It was found that all parameters of metabolic response during exercise were significantly lower among COPD-PH patients (P<0.001). Pulmonary artery systolic pressure (PASP) showed significant negative correlations with peak VO₂ (r=−0.514, P<0.001), VO₂/kg (r=−0.443, P<0.001), oxygen pulse (% predicted) (r=−0.459, P<0.001), oxygen saturation post exercise (r=−0.427, P<0.001). Also PASP showed significant positive correlation with VE/VO₂ (at peak) (r=0.374, P=0.001), VE/VCO₂ (at peak) (r=0.609, P<0.001). Predictors of poor exercise capacity among COPD patients included in the study were COPD-PH group (OR=8.84, 95%CI= 1.79–43.65), PASP (OR=1.11, 95% CI=1.02–1.15), forced expiratory volume (FEV₁)% (OR=0.89, 95% CI=0.84–0.95) and mMRC (OR=3.10, 95% CI=1.13–8.47), CAT assessment (OR=1.37, 95% CI=1.14–1.65), MVV L/min (OR=0.91, 95% CI=0.86–0.96) and mean PAP (OR=1.16, 95% CI=1.11–1.29).

Conclusion 

Pulmonary hypertension in patients with COPD is negatively correlated with exercise capacity, specifically peak VO₂ percent predicted. Furthermore, pulmonary hypertension had a significant impact on gas exchange. Assessment of pulmonary hypertension using echocardiography among COPD patients is a valuable tool for predicting exercise impairment.

Abstract

Background

Behçet’s disease (BD) is a multi-organ disease with different systemic manifestations. While rare in the United States and Europe, it is more common in the Middle East and Asia. BD is one of the commonest encountered vasculitis in Egypt. This study aims to evaluate BD patients' sleep patterns, quality of life, and psychological aspects.

Methods

Patients suffering from Behçet’s disease (thirty patients) and 30 matched age and sex-healthy control participants were recruited in our study. The assessment included the entire clinical history and laboratory investigations, including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and Oxygen saturation level. Evaluation of sleep quality and presence of sleep-disordered breathing was done using the Pittsburgh Sleep Quality Index (PSQI), Insomnia severity index (ISI), and Epworth sleepiness scale (ESS). Hamilton’s anxiety (HAM-A) and depression rating scales (HAM-D) were used for psychological assessment. The Short Form 36 Quality Of Life Scale (SF-36 QOL) assessed participants' quality of life.

Results

Behçet’s disease patients suffered significantly higher levels of anxiety and depression compared to the control group. The prevalence of insomnia and daytime sleepiness was significantly higher among BD patients. All components of PSQI, including the global score, were significantly higher among the BD group. Physical functioning, role limitation due to physical health, and emotional problems; also, general health indices were significantly lower for the BD group. Patients with active BD showed significantly higher levels of anxiety, depression, insomnia, day time dysfunction and significantly lower all domains of the SF-36 QOL Scale.

Conclusions

BD is associated with low sleep quality and high levels of anxiety and depression.

Disease activity directly impacts anxiety, depression levels, lower sleep quality, and lower quality of life among BD patients.

Abstract

Background

Severe asthma exacerbation can be a frightening experience to the patient and physician. Despite continuous efforts to frame management guidelines and advances in treatment, severe exacerbations still occur. In order to prevent and judicious management of asthma exacerbations, we should predict them first. This study aims to evaluate distinct clinical trajectories and management outcome of patients with severe asthma exacerbations and also evaluate predictors for poor outcome.

Methods

Patients suffering from acute asthma exacerbation and presented to emergency room (forty patients) were grouped into 2 groups (groups A and B) according to severity of exacerbation. Assessment included full clinical history, laboratory investigations (including eosinophil cell count and serum IgE level), Beck’s anxiety and depression inventory scales, assessment of asthma medication adherence and control level, and peak expiratory flow measurement (at presentation, 1 and 6 h after).

Results

Fifty-five percent of patients suffered from severe and life-threatening asthma exacerbations, 63.6% of them were females. The most important predictors for severe exacerbations were SO2 < 90% at baseline (OR = 4.56; 95% CI = 3.45–7.56; P < 0.001), PEFR after 1 h (OR= 3.34; 95%CI = 1.90–4.90; P < 0.001), and uncontrolled asthma (OR= 3.33; 95%CI = 2.50–5.05; P < 0.001). Predictors for hospitalization were old age (OR = 1.11; 95%CI = 1.09–2.11; P < 0.001), uncontrolled asthma (OR = 2.34; 95%CI = 2.01–4.40; P < 0.001), PEFR after 1 h (OR= 4.44; 95%CI= 3.24–7.68; P < 0.001), and SO2 <90% at baseline (OR= 5.67; 95%CI= 3.98–8.50; P < 0.001).

Conclusions

Severe asthma exacerbations can be predicted by old age, previous history of mechanical ventilation, obstructive sleep apnea, overuse of SABA, uncontrolled asthma, moderate to severe depression, eosinophilia, SO₂ <90%, and low peak expiratory flow rates.

 can be identified with simple biomarkers. Studies are needed to validate the use of these biomarkers to direct therapy for AECOPD.

Aim of this study

to evaluate the use of blood eosinophilia (>2%) in directing steroids therapy in AE-COPD.

Patients and methods

In the preliminary retrospective analysis of 13297 admissions (2010-2014), AECOPD was the cause in 5016 events, COPD with bronchiectasis (1386) and α1 antitrypsin deficiency (264) were excluded and data of 3366 exacerbations were revised. 2442 (72.5%) were bacterial and 924 (27.5%) Eosinophilic ( Eosinophils>2%). All patients received standard therapy according to GOLD Guidelines. The baseline clinical, functional characteristics, days of hospital stay, side effects, treatment failure, number of exacerbation, need for ICU were recorded. The second phas

Background: Proprotein convertase subtilisin/kexin type 9 (PCSK-9) is a circulating protein that plays an important role in lipid metabolism and is linked to inflammation, which has implications for atherosclerosis and its severe cardiac effects. We studied the potential association of the PCSK-9 gene single nucleotide polymorphism (SNP), Oxidized low-density lipoprotein receptor 1- (OLR-1), and caspase-3 serum levels with the risk and severity of premature coronary artery disease (PCAD). The potential contribution of PCSK-9 serum level to the severity of PCAD patients was also assessed. Method: This case-control study included 120 PCAD patients (age < 45), and 60 age matched healthy controls. Serum PCSK-9 and caspase-3 levels and clinical characteristics were recorded. SYNTAX score was calculated to estimate the severity of the coronary artery lesions. The SNP rs2483205 of the PCSK-9 gene and the rs11053646 of the OLR-1gene were genotyped in all participants. Results: Serum PCSK-9 levels were higher in PCAD patients and were significantly different among the three SYNTAX score groups (SS ≤ 12, 12 < SS ≤ 21.5, and SS > 21.5). The diagnostic cutoff values of PCSK-9 and caspase-3 levels for PCAD were > 3.2 ng/mL for both, yielding an area under the curve (AUC) of 0.98 and 0.92, sensitivity of 85 %, 98 %, and specificity of 99.5 %, 93 % for PCSK-9 and caspase-3, respectively. The genotypes TT + CT vs. CC of PCSK-9′s rs2483205 SNP presented a higher risk for PCAD and higher SYNTAX scores. Furthermore, the rs11053646 SNP of OLR-1 presented the CG genotype as more risky and having higher SYNTAX scores. Conclusion: Circulating PCSK9 and caspase-3 concentrations were higher in PCAD patients and were associated with CAD severity. The SNPs of PCSK-9 (rs2483205) and OLR-1 (rs11053646) were associated with PCAD and its severity.

the use of objective measures in CI process is very important to set the dynamic range especially in cases of infants and young children. some examples of theses measures are ESRT, EABR, ECAP.so this study designed to use objective measures in programming CI especially when the child is unable to provide reliable behavioral response.