Bilateral Deep Vein Thrombosis and Pulmonary Embolism Due to Right Common Iliac Artery Aneurysm with a Contained Rupture

Venous thromboembolism (comprising deep venous thrombosis and/or pulmonary embolism) is a common disease, often of multifactorial cause. Focal iliac artery aneurysms are relatively rare, and only a few reports exist in the literature describing patients with venous thromboembolism resulting from venous floe disruption due to iliac artery aneurysm. Thus, we report a case of a 65-year-old male presenting with pulmonary embolism and bilateral deep vein thrombosis associated with a contained rupture of the right common iliac artery aneurysm

Predictors of SARS-CoV-2 IgG Spike Antibody Responses on Admission and Clinical Outcomes of COVID-19 Disease in Fully Vaccinated Inpatients: The CoVax Study

Background: SARS-CoV-2 vaccines have shown high efficacy in protecting against COVID-19, although the determinants of vaccine effectiveness and breakthrough rates are yet to be determined. We aimed at investigating several factors affecting the SARS-CoV-2 IgG Spike (S) antibody responses on admission and clinical outcomes of COVID-19 disease in fully vaccinated, hospitalized patients. Methods: 102 subjects were enrolled in the study. Blood serum samples were collected from each patient upon admission for the semiquantitative determination of the SARS-CoV-2 IgG S levels with lateral flow assays. Factors influencing vaccine responses were documented. Results: 27 subjects had a negative antibody test upon hospital admission. Out of the 102 patients admitted to the hospital, 88 were discharged and 14 died. Both the absence of anti-S SARS-CoV-2 antibodies and poor clinical outcomes of COVID-19 disease were associated with older age, lower Ct values, and a shorter period between symptom onset and hospital admission. Ct values and time between symptom onset and hospitalization were independently associated with SARS-CoV-2 IgG S responses upon admission. The PaO2/FiO2 ratio was identified as an independent predictor of in-hospital mortality. Conclusions: Host- and disease-associated factors can predict SARS-CoV-2 IgG S responses and mortality in hospitalized patients with breakthrough SARS-CoV-2 Infection

Eight Weeks Unsupervised Pulmonary Rehabilitation in Previously Hospitalized of SARS-CoV-2 Infection

The aim of our study was to determine the impact of unsupervised Pulmonary Rehabilitation (uns-PR) on patients recovering from COVID-19, and determine its anthropometric, biological, demographic and fitness correlates. All patients (n = 20, age: 64.1 ± 9.9 years, 75% male) participated in unsupervised Pulmonary Rehabilitation program for eight weeks. We recorded anthropometric characteristics, pulmonary function parameters, while we performed 6 min walk test (6 MWT) and blood sampling for oxidative stress measurement before and after uns-PR. We observed differences before and after uns-PR during 6 MWT in hemodynamic parameters [systolic blood pressure in resting (138.7 ± 16.3 vs. 128.8 ± 8.6 mmHg, p = 0.005) and end of test (159.8 ± 13.5 vs. 152.0 ± 12.2 mmHg, p = 0.025), heart rate (5th min: 111.6 ± 16.9 vs. 105.4 ± 15.9 bpm, p = 0.049 and 6th min: 112.5 ± 18.3 vs. 106.9 ± 17.9 bpm, p = 0.039)], in oxygen saturation (4th min: 94.6 ± 2.9 vs. 95.8 ± 3.2%, p = 0.013 and 1st min of recovery: 97.8 ± 0.9 vs. 97.3 ± 0.9%), in dyspnea at the end of 6 MWT (1.3 ± 1.5 vs. 0.6 ± 0.9 score, p = 0.005), in distance (433.8 ± 102.2 vs. 519.2 ± 95.4 m, p < 0.001), in estimated O2 uptake (14.9 ± 2.4 vs. 16.9 ± 2.2 mL/min/kg, p < 0.001) in 30 s sit to stand (11.4 ± 3.2 vs. 14.1 ± 2.7 repetitions, p < 0.001)] Moreover, in plasma antioxidant capacity (2528.3 ± 303.2 vs. 2864.7 ± 574.8 U.cor., p = 0.027), in body composition parameters [body fat (32.2 ± 9.4 vs. 29.5 ± 8.2%, p = 0.003), visceral fat (14.0 ± 4.4 vs. 13.3 ± 4.2 score, p = 0.021), neck circumference (39.9 ± 3.4 vs. 37.8 ± 4.2 cm, p = 0.006) and muscle mass (30.1 ± 4.6 vs. 34.6 ± 7.4 kg, p = 0.030)] and sleep quality (6.7 ± 3.9 vs. 5.6 ± 3.3 score, p = 0.036) we observed differences before and after uns-PR. Our findings support the implementation of unsupervised pulmonary rehabilitation programs in patients following COVID-19 recovery, targeting the improvement of many aspects of long COVID-19 syndrome

Genotype-Phenotype Relationships in Inheritable Idiopathic Pulmonary Fibrosis: A Greek National Cohort Study

International audienceBackground: Monogenic and polygenic inheritances are evidenced for idiopathic pulmonary fibrosis (IPF). Pathogenic variations in surfactant protein-related genes, telomere-related genes (TRGs), and a single-nucleotide polymorphism in the promoter of MUC5B gene encoding mucin 5B (rs35705950 T risk allele) are reported. This French-Greek collaborative study, Gen-Phen-Re-GreekS in inheritable IPF (iIPF), aimed to investigate genetic components and patients' characteristics in the Greek national IPF cohort with suspected heritability.Patients and methods: 150 patients with familial PF, personal-family extrapulmonary disease suggesting short telomere syndrome, and/or young age IPF were analyzed.Results: MUC5B rs35705950 T risk allele was detected in 103 patients (90 heterozygous, 13 homozygous, allelic frequency of 39%), monoallelic TRG pathogenic variations in 19 patients (8 TERT, 5 TERC, 2 RTEL1, 2 PARN, 1 NOP10, and 1 NHP2), and biallelic ABCA3 pathogenic variations in 3. Overlapping MUC5B rs35705950 T risk allele and TRG pathogenic variations were shown in 11 patients (5 TERT, 3 TERC, 1 PARN, 1 NOP10, and 1 NHP2), MUC5B rs35705950 T risk allele, and biallelic ABCA3 pathogenic variations in 2. In 38 patients, neither MUC5B rs35705950 T risk allele nor TRG pathogenic variations were detectable. Kaplan-Meier curves showed differences in time-to-death (p = 0.025) where patients with MUC5B rs35705950 T risk allele alone or in combination with TRG pathogenic variations presented better prognosis.Conclusion: The Gen-Phen-Re-GreekS in iIPF identified multiple and overlapping genetic components including the rarest, underlying disease's genetic "richesse," complexity and heterogeneity. Time-to-death differences may relate to diverse IPF pathogenetic mechanisms implicating "personalized" medical care driven by genotypes in the near futur

Genotype-Phenotype Relationships in Inheritable Idiopathic Pulmonary Fibrosis: A Greek National Cohort Study

Background: Monogenic and polygenic inheritances are evidenced for idiopathic pulmonary fibrosis (IPF). Pathogenic variations in surfactant protein-related genes, telomere-related genes (TRGs), and a single-nucleotide polymorphism in the promoter of MUC5B gene encoding mucin 5B (rs35705950 T risk allele) are reported. This French-Greek collaborative study, Gen-Phen-Re-GreekS in inheritable IPF (iIPF), aimed to investigate genetic components and patients’ characteristics in the Greek national IPF cohort with suspected heritability. Patients and Methods: 150 patients with familial PF, personal-family extrapulmonary disease suggesting short telomere syndrome, and/or young age IPF were analyzed. Results: MUC5B rs35705950 T risk allele was detected in 103 patients (90 heterozygous, 13 homozygous, allelic frequency of 39%), monoallelic TRG pathogenic variations in 19 patients (8 TERT, 5 TERC, 2 RTEL1, 2 PARN, 1 NOP10, and 1 NHP2), and biallelic ABCA3 pathogenic variations in 3. Overlapping MUC5B rs35705950 T risk allele and TRG pathogenic variations were shown in 11 patients (5 TERT, 3 TERC, 1 PARN, 1 NOP10, and 1 NHP2), MUC5B rs35705950 T risk allele, and biallelic ABCA3 pathogenic variations in 2. In 38 patients, neither MUC5B rs35705950 T risk allele nor TRG pathogenic variations were detectable. Kaplan-Meier curves showed differences in time-to-death (p = 0.025) where patients with MUC5B rs35705950 T risk allele alone or in combination with TRG pathogenic variations presented better prognosis. Conclusion: The Gen-Phen-Re-GreekS in iIPF identified multiple and overlapping genetic components including the rarest, underlying disease’s genetic “richesse,” complexity and heterogeneity. Time-to-death differences may relate to diverse IPF pathogenetic mechanisms implicating “personalized” medical care driven by genotypes in the near future