Antibiotic Prescription and In-Hospital Mortality in COVID-19: A Prospective Multicentre Cohort Study.

BACKGROUND: Since the beginning of the COVID-19 pandemic, empiric antibiotics (ATBs) have been prescribed on a large scale in both in- and outpatients. We aimed to assess the impact of antibiotic treatment on the outcomes of hospitalised patients with moderate and severe coronavirus disease 2019 (COVID-19). METHODS: We conducted a prospective multicentre cohort study in six clinical hospitals, between January 2021 and May 2021. RESULTS: We included 553 hospitalised COVID-19 patients, of whom 58% (311/553) were prescribed antibiotics, while bacteriological tests were performed in 57% (178/311) of them. Death was the outcome in 48 patients-39 from the ATBs group and 9 from the non-ATBs group. The patients who received antibiotics during hospitalisation had a higher mortality (RR = 3.37, CI 95%: 1.7-6.8), and this association was stronger in the subgroup of patients without reasons for antimicrobial treatment (RR = 6.1, CI 95%: 1.9-19.1), while in the subgroup with reasons for antimicrobial therapy the association was not statistically significant (OR = 2.33, CI 95%: 0.76-7.17). After adjusting for the confounders, receiving antibiotics remained associated with a higher mortality only in the subgroup of patients without criteria for antibiotic prescription (OR = 10.3, CI 95%: 2-52). CONCLUSIONS: In our study, antibiotic treatment did not decrease the risk of death in the patients with mild and severe COVID-19, but was associated with a higher risk of death in the subgroup of patients without reasons for it.

Anticoagulant protein S in COVID-19: low activity, and associated with outcome.

Introduction. COVID-19 disease was associated with both thrombo-embolic events and in-situ thrombi formation in small vessels. Antiphospholipidic antibodies were found in some studies.Aim. Assessment of protein S activity in patients with COVID-19 as a cause of this prothrombotic state, and of the association of protein S activity with worse outcome.Methods. All patients admitted for COVID-19 disease in a university hospital between 15th of May and 15th of July 2020 were prospectively enrolled into this cohort study. Patients treated with antivitamin K anticoagulants and with liver disease were excluded. All patients had protein S activity determined at admission. The main outcome was survival, while secondary outcomes were clinical severity and lung damage.Results. 91 patients were included, of which 21 (23.3%) died. Protein S activity was decreased in 65% of the patients. Death was associated with lower activity of protein S (median 42% vs. 58%, p < 0.001), and the association remained after adjustment for age, inflammation markers and ALAT. There was a dose-response relationship between protein S activity and clinical severity (Kendall_tau coefficient = -0.320, p < 0.001; Jonckheere-Terpstra for trend: p < 0.001) or pulmonary damage on CT scan (Kendall_tau coefficient = -0.290, p < 0.001; Jonckheere-Terpstra for trend: p < 0.001). High neutrophil count was also independently associated with death (p = 0.002).Conclusion. Protein S activity was lower in COVID-19 patients, and its level was associated with survival and disease severity, suggesting that it may have a role in the thrombotic manifestations of the disease.

Acute Bilateral Phrenic Neuropathy: from Diabetes Mellitus to Focal Guillain-Barré Syndrome.

Bilateral phrenic neuropathy is a rare cause of acute ventilatory failure posing both diagnostic and therapeutic difficulties. We report the case of a 55-years-old diabetic male presenting with acute onset orthopnea. Clinical and radioscopic evaluations suggested bilateral diaphragmatic paralysis, electroneuromyographic studies revealed bilateral acute phrenic neuropathy, and cerebrospinal fluid examination found albuminocytologic dissociation. The administration of high-dose intravenous immunoglobulin was followed by prompt improvement. During the next months the symptoms continued to regress. There were no recurrences. We consider the patient had a spatially limited form of acute inflammatory demyelinating polyradiculoneuropathy. The case underlies the importance of considering an immune mediated etiology in patients with acute bilateral phrenic neuropathy. To the best of our knowledge no similar case has been reported.