Do high-dose corticosteroids improve outcomes in hospitalized COVID-19 patients?

Coronavirus disease 2019 (COVID-19) is characterized by dysregulated hyperimmune response and steroids have been shown to decrease mortality. However, whether higher dosing of steroids results in better outcomes has been debated. This was a retrospective observation of COVID-19 admissions between March 1, 2020, and March 10, 2021. Adult patients (≥18 years) who received more than 10 mg daily methylprednisolone equivalent dosing (MED) within the first 14 days were included. We excluded patients who were discharged or died within 7 days of admission. We compared the standard dose of steroids (<40 mg MED) versus the high dose of steroids (>40 mg MED). Inverse probability weighted regression adjustment (IPWRA) was used to examine whether higher dose steroids resulted in improved outcomes. The outcomes studied were in-hospital mortality, rate of acute kidney injury (AKI) requiring hemodialysis, invasive mechanical ventilation (IMV), hospital-associated infections (HAI), and readmissions. Of the 1379 patients meeting study criteria, 506 received less than 40 mg of MED (median dose 30 mg MED) and 873 received more than or equal to 40 mg of MED (median dose 78 mg MED). Unadjusted in-hospital mortality was higher in patients who received high-dose corticosteroids (40.7% vs. 18.6%, p < 0.001). On IPWRA, the use of high-dose corticosteroids was associated with higher odds of death (odds ratio [OR] 2.14; 95% confidence interval [CI] 1.45-3.14, p < 0.001) but not with the development of HAI, readmissions, or requirement of IMV. High-dose corticosteroids were associated with lower rates of AKI requiring hemodialysis (OR 0.33; 95% CI 0.18-0.63). In COVID-19, corticosteroids more than or equal to 40 mg MED were associated with higher in-hospital mortality.

Differences in metabolic parameters and gene expression related to osteochondrosis/osteoarthrosis in pigs fed 25-hydroxyvitamin D3.

Osteochondrosis/osteoarthrosis (OC/OA) are common terms for various joint pathologies that occur in pigs. Pathologies that may contribute to these disorders have been described, but the primary cause(s) remain unknown. We hypothesised that as OC has some similarities to dyschondroplasia, which involves a failure of growth plate chondrocytes to fully differentiate and hypertrophy, treatment with 25-hydroxyvitamin D3 (25-D) might reduce the incidence and/or severity of lesions in pigs, as it does in chickens with dyschondroplasia. Control pigs were fed a commercial diet ad libitum. In the treated group this diet was supplemented with 25-D at 0.1 mg/kg. Ten pigs from each of the control and treated groups were sampled at 7, 12, 16 and 21 weeks. Treatment with 25-D had no effect on the incidence or severity of OC/OA lesions. Cartilage dry weight, total collagen content and proteoglycan content, and plasma levels oftotal calcium, inorganic phosphorous, vitamin C, insuline-like growth factor-I, parathyroid hormone and tumour necrosis factor alpha were unaffected by treatment. In addition, none of these parameters were correlated with the incidence or severity of OC/OA lesions. The mRNA expression levels of 21 out of 23 genes assayed by RT-PCR were unaltered in articular cartilage from OA lesion samples as compared to normal articular cartilage. However, collagen type II was reduced and collagen type X increased in OA lesion and near lesion samples. These results suggest that OA in pigs may share some features of osteoarthritis in other mammalian species.