Background Lower muscle mass is a known predictor of unfavorable outcome, but its prognostic impact on COVID-19 patients is unknown. Purpose To investigate the contribution of CT-derived muscle status in predicting clinical outcomes in COVID-19 patients. Materials and Methods Clinical/laboratory data and outcomes (intensive care unit [ICU] admission and death) were retrospectively retrieved for patients with reverse transcriptase polymerase chain reaction-confirmed COVID-19, who underwent chest CT on admission in four hospitals in Northern Italy from February 21 to April 30, 2020. Extent and type of pulmonary involvement, mediastinal lymphadenopathy, and pleural effusion were assessed. Cross-sectional areas and attenuation of paravertebral muscles were measured on axial CT images at T5 and T12 vertebral level. Multivariable linear and binary logistic regression, including calculation odds ratios (OR) with 95% confidence intervals (CIs), were used to build four models to predict ICU admission and death, tested and compared using receiver operating characteristic curve (ROC) analysis. Results A total 552 patients (364 men; median age 65 years, interquartile range 54–75) were included. In a CT-based model, lower-than-median T5 paravertebral muscle area showed the highest ORs for ICU admission (OR 4.8, 95% CI 2.7–8.5; P <.001) and death (OR 2.3, 95% CI 1.0–2.9; P =.027). When clinical variables were included in the model, lower-than-median T5 paravertebral muscle area still showed the highest ORs both for ICU admission (OR 4.3; 95% CI 2.5–7.7; P <.001) and death (OR 2.3, 95% CI 1.3–3.7; P =.001). At ROC analysis, the CT-based model and the model including clinical variables showed the same area under the curve (AUC) for ICU admission prediction (AUC 0.83, P =.380) and were not different in predicting death (AUC 0.86 versus AUC 0.87, respectively, P =.282). Conclusion In hospitalized patients with COVID-19, lower muscle mass on CT was independently associated with ICU admission and hospital mortality.

Anti-Ro/SSA antibodies are associated with neonatal lupus but are also considered a possible cause for unexplained pregnancy loss and adverse pregnancy outcome. In a large multicentres cohort study we have prospectively followed 100 anti-Ro/SSA positive women (53 systemic lupus erythematosus (SLE)) during their 122 pregnancies and 107 anti-Ro/SSA negative women (58 SLE) (140 pregnancies). Anti-Ro/SSA antibodies were tested by immunoblot and counterimunoelectrophoresis. Mean gestational age at delivery (38 vs 37.9 weeks), prevalence of pregnancy loss (9.9 vs 18.6%), preterm birth (21.3 vs 13.9%), cesarean sections (49.2 vs 53.4%), premature rupture of membranes (4.9 vs 8.1%), preeclampsia (6.6 vs 8%), intrauterine growth retardation (0 vs 2.3%)and newborns small for gestational age (11.5 vs 5.8%) were similar in anti-Ro/SSA positive and negative SLE mothers; findings were similar in non-SLE women. Two cases of congenital heart block were observed out of 100 anti-Ro/SSA positive women. In conclusion, anti-Ro/SSA antibodies are responsible for congenital heart block but do not affect other pregnancy outcomes, both in SLE and in non-SLE women. The general outcome of these pregnancies is now very good, ifprospectively followed by multidisciplinary teams with ample experience in this field.

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Pulmonary parenchymal and vascular damage are frequently reported in COVID-19 patients and can be assessed with unenhanced chest computed tomography (CT), widely used as a triaging exam. Integrating clinical data, chest CT features, and CT-derived vascular metrics, we aimed to build a predictive model of in-hospital mortality using univariate analysis (Mann–Whitney U test) and machine learning models (support vectors machines (SVM) and multilayer perceptrons (MLP)). Patients with RT-PCR-confirmed SARS-CoV-2 infection and unenhanced chest CT performed on emergency department admission were included after retrieving their outcome (discharge or death), with an 85/15% training/test dataset split. Out of 897 patients, the 229 (26%) patients who died during hospitalization had higher median pulmonary artery diameter (29.0 mm) than patients who survived (27.0 mm, p < 0.001) and higher median ascending aortic diameter (36.6 mm versus 34.0 mm, p < 0.001). SVM and MLP best models considered the same ten input features, yielding a 0.747 (precision 0.522, recall 0.800) and 0.844 (precision 0.680, recall 0.567) area under the curve, respectively. In this model integrating clinical and radiological data, pulmonary artery diameter was the third most important predictor after age and parenchymal involvement extent, contributing to reliable in-hospital mortality prediction, highlighting the value of vascular metrics in improving patient stratification.

Idiopathic recurrent acute pericarditis (IRAP) is suspected to be an autoimmune phenomenon. We studied 46 consecutive patients. We looked for: 1) the occurrence of new diagnoses of autoimmune diseases during our follow up; 2) HLA typing; and 3) the presence of the most frequent mutations linked to familial Mediterranean fever (FMF gene or MEFV). HLA typing was done in 21 patients at loci B, DRB1, DQA1 and DQB1. MEFV gene was looked in 23 patients using specific primers. During the follow-up we made a new diagnosis of primary Sjögren's syndrome in four patients (8.7%) and of rheumatoid arthritis in one patient (2.2%). HLA B14, DRB1*01 and DQB1*0202 were significantly more prevalent, but we did not find a typical HLA typing. MEFV gene was searched: exon 10 was checked by sequence and the E148Q mutation by restriction site analysis. No mutations were found. In conclusion, the prevalence of definite immunorheumatological diseases and the absence of the mutations linked to FMF reinforce the notion that idiopathic acute recurrent pericarditis is an autoimmune condition.