Does Angiotensin II receptor blockers increase the risk of SARS-CoV-2 infection? A real-life experience.

OBJECTIVE: Since the start of the COVID-19 pandemic, millions of people have been infected with thousands of deaths. Few data regarding factors that increase the risk of infection are available. Our study aimed to evaluate all people living in retirement homes (PLRNH) and identify factors that could increase infection risk in a close community. MATERIALS AND METHODS: We conducted a retrospective study enrolling all PLRNH, where at least one SARS-CoV-2 infected person was present. Variables were compared with Student's t-test or Pearson chi-square test as appropriate. Uni- and multivariate analyses were conducted to evaluate variables' influence on the infection. RESULTS: We included 452 PLRNH; 144 (31.7%) were male, with a mean age of 82.2±8.6 years. People with a positive swab for SARS-CoV-2 were 306 (67.4%). A significant difference between SARS-CoV-2 infected and not infected was observed in the percentage of those receiving chronic treatment with Angiotensin II receptor blockers (ARBs) (18.6% vs. 9.5%, p=0.012). On the contrary, there was no difference in the proportion of those receiving ACE inhibitors (ACE-I) (21.2% vs. 23.6%, p=0.562). At multivariate analysis, people with mental illness and cancer had an increased risk of being infected. Furthermore, receiving ARBs as a chronic treatment was an independent predictor of infection risk [OR 1.95 (95% CI 1.03-3.72) p=0.041]. CONCLUSIONS: Our data suggest that, in close communities, such as retirement nursing homes, the receipt of ARBs increased the risk of acquiring SARS-CoV-2 infection. However, before changing an important chronic treatment in a fragile population, such as the elderly living in retirement nursing homes, clinicians should carefully evaluate the risk-benefit ratio.

Clinical features, laboratory findings and predictors of death in hospitalized patients with COVID-19 in Sardinia, Italy.

OBJECTIVE: Since December 2019, when the first SARS-CoV2 infections have been reported, the number of cases has increased exponentially. In our University Hospital Unit, the first patient with COVID-19 was admitted on the 8th of March 2020. We aimed to investigate the predictors of death among inpatients with COVID-19. MATERIALS AND METHODS: We performed a retrospective, monocentric study, consecutively enrolling patients with SARS-CoV2 infection. Clinical, laboratory, and radiological data were collected from the 8th of March to the 8th of April 2020. We aimed to describe the most frequent clinical and laboratory features and predictors of death among patients admitted to our Unit. RESULTS: 87 patients were enrolled, 56 (64.4%) were male, with a median age of 72 (IQR 62.5-83.5) years. The majority of our population had at least one comorbidity in their medical anamnesis. Hypertension and cardiovascular disease were the most frequent, followed by obesity. Eighty (92%) patients had at least one symptom, whereas 7 (8%) were asymptomatic. The most common symptoms were fever and dyspnoea. Overall, 53 patients had lung disease confirmed at CT scan (60.9%). Twenty-five (28.7%) deaths occurred. Statistically significant predictors of death at multivariate analysis were lymphocytes count <900 cells/mm3, moderate ARDS, and lack of compliance at baseline. CONCLUSIONS: This is the first Italian experience available. Our results seem to be in line with international literature. As highlighted by our data, more studies are needed to investigate the role of lymphocytes subsets, CT scan values. Furthermore, therapy choice and timing in this challenging setting should be urgently investigated in randomized clinical trials.

The effectiveness of the anti-CD11d treatment is reduced in rat models of spinal cord injury that produce significant levels of intraspinal hemorrhage.

We have previously reported that administration of a CD11d monoclonal antibody (mAb) improves recovery in a clip-compression model of SCI. In this model the CD11d mAb reduces the infiltration of activated leukocytes into the injured spinal cord (as indicated by reduced intraspinal MPO). However not all anti-inflammatory strategies have reported beneficial results, suggesting that success of the CD11d mAb treatment may depend on the type or severity of the injury. We therefore tested the CD11d mAb treatment in a rat hemi-contusion model of cervical SCI. In contrast to its effects in the clip-compression model, the CD11d mAb treatment did not improve forelimb function nor did it significantly reduce MPO levels in the hemi-contused cord. To determine if the disparate results using the CD11d mAb were due to the biomechanical nature of the cord injury (compression SCI versus contusion SCI) or to the spinal level of the injury (12th thoracic level versus cervical) we further evaluated the CD11d mAb treatment after a T12 contusion SCI. In contrast to the T12 clip compression SCI, the CD11d mAb treatment did not improve locomotor recovery or significantly reduce MPO levels after T12 contusion SCI. Lesion analyses revealed increased levels of hemorrhage after contusion SCI compared to clip-compression SCI. SCI that is accompanied by increased intraspinal hemorrhage would be predicted to be refractory to the CD11d mAb therapy as this approach targets leukocyte diapedesis through the intact vasculature. These results suggest that the disparate results of the anti-CD11d treatment in contusion and clip-compression models of SCI are due to the different pathophysiological mechanisms that dominate these two types of spinal cord injuries.