No abstract

The underlying cause of many complications associated with severe COVID-19 is attributed to the inflammatory cytokine storm that leads to acute respiratory distress syndrome (ARDS), which appears to be the leading cause of death in COVID-19. Systemic corticosteroids have anti-inflammatory activity through repression of pro-inflammatory genes and inhibition of inflammatory cytokines, which makes them a potential medical intervention to diminish the upregulated inflammatory response. Early in the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, the role of corticosteroids was unclear. Corticosteroid use in other indications such as ARDS and septic shock has proven benefit while its use in other respiratory viral pneumonias is associated with reduced viral clearance and increased secondary infections. This review article evaluates the benefits and harms of systemic corticosteroids in patients with COVID-19 to assist clinicians in improving patient outcomes, including patient safety. Dexamethasone up to 10 days is the preferred regimen to reduce mortality risk in COVID-19 patients requiring oxygen support, mechanical ventilation, or extracorporeal membrane oxygenation. If dexamethasone is unavailable, other corticosteroids can be substituted at equivalent doses. Higher doses of corticosteroids may be beneficial in patients who develop ARDS. Corticosteroids should be avoided early in the disease course when patients do not require oxygen support because of potential harms.

Two experiments with broiler chicks and one experiment with laying hens were conducted to determine the MEn value of conjugated linoleic acid (CLA). In Experiment 1, for 8 d, 16-d-old chicks were fed diets in which 4, 8, or 12% of CLA Source A or 4, 8, or 12% of soybean oil (SO) was substituted for glucose. Dietary MEn increased linearly (P < or = 0.001) with increments of CLA Source A or SO. Regression analysis relating increases in dietary MEn and increments of the dietary fat sources showed that the MEn values of CLA Source A and SO, when evaluated separately, were 7,419 and 8,429 kcal/kg, respectively. In Experiment 2, feed was withheld from laying hens for 38 h and then the hens were force-fed diets containing 15% glucose, 15% CLA Source A, or 15% SO (two feedings of 30 g each). Excreta samples were collected for 36 h after the last feeding. The MEn values obtained for CLA Source A and SO were 8,517 and 8,437 kcal/kg, respectively. The MEn of CLA Source B (higher in unsaturated fatty acids than CLA Source A) was determined in Experiment 3 by feeding diets containing 4, 8, or 12% CLA Source B to 14-d-old chicks. Increases in dietary MEn with increments of CLA Source B were curvilinear, with resulting MEn of 9,375 to 9,588 kcal/kg of fat when CLA Source B was fed at 4 or 8% of the diet and 7,917 kcal/kg when fed at 12% of the diet. Results of this research show that CLA sources can contribute substantial energy to diets, but the MEn value of CLA sources for young chicks varies with fatty acid composition and dietary concentration.

Three experiments were conducted to determine the effect of dietary vitamin K1 (K1) on selected plasma characteristics and bone ash in poults. In Experiment 1, diets were supplemented with 0, 0.5, 1.0, or 2.0 mg of K1/kg. All diets contained 1,650 IU of vitamin D3 (D3)/kg. Dietary K1 had no effect on tibia ash at 7 d or incidence of a severe, rickets-like condition. Tibia ash of poults fed 2.0 mg of K1/kg, however, was greater at 14 d of age than that of poults fed the basal diet. Dietary inclusion of 0.5 mg of K1/kg was as effective as 1 or 2 mg of K1/kg in reducing plasma prothrombin time. In Experiment 2, a 2 x 4 factorial arrangement was used consisting of 1,650 or 550 IU of D3/kg and 0.1, 0.45, 1.0, and 2.0 mg of K1/kg. Dietary D3 and K1 had no effect on bone ash. Dietary inclusion of 0.1 mg of K1/kg seemed to be enough to minimize plasma prothrombin time. In Experiment 3, dietary treatments consisted of a control (1,650 IU of D3 and 2.0 mg of K1/kg) and K1 concentrations of 0, 0.37, 2.28, or 5.33 mg/kg in diets containing 275 IU of D3/kg. Poults fed the low-D3 diet without K1 consumed less feed, gained less weight, and had increased plasma alkaline phosphatase activity, decreased inorganic phosphorus level, and decreased tibia ash (P < 0.05) compared with those of poults fed the control diet. Feed intake and body weight gain were improved, plasma alkaline phosphatase activity decreased, and plasma inorganic phosphorus increased or tended to increase when poults were fed the low-D3 diet supplemented with 0.37 or 2.88 mg of K1/kg compared with poults fed the low-D3 diet without K1 supplementation. Tibia ash of poults fed the low-D3 diet was not affected by K1 supplementation. The results of this research show that dietary K1 concentration had little, if any, effect on bone development in 1- to 14-d-old turkeys.

In a preliminary experiment, the inclusion of vitamin K1 (K1) at a dietary level of 0.1 mg/kg was as effective as 1 or 2 mg/kg in reducing plasma prothrombin time (PT). To obtain an estimate of the dietary K1 requirement and to compare the biopotency of different vitamin K sources for poults, three additional experiments were conducted. In Experiment 1, an incomplete factorial arrangement of treatments was used in which five dietary concentrations of K1 (0, 0.1, 0.25, 0.5, or 2.0 mg/kg) were tested and two concentrations of neomycin (0 or 75 mg/L) in drinking water were used in conjunction with 0, 0.1, and 0.5 mg of K1/kg of diet. Thus, we used a total of eight treatments. Each treatment was given to two pens of poults, with eight poults per pen. Prothrombin time and prothrombin concentration (PC) in plasma were not influenced by inclusion of neomycin in drinking water. The K1 requirement was estimated, on the basis of PT and PC, to be 0.099 and 0.13 mg/kg, respectively, in Experiment 1. Dietary K1 concentrations tested in Experiment 2 were 0, 0.08, 0.31, or 0.44 mg/kg. A similar protocol to that of Experiment 1 was used in this experiment. The results of Experiment 2 indicated that the dietary K1 requirement was 0.079 mg, based on the influence of dietary K1 on PT. In Experiment 3, dietary treatments consisted of the equivalent of 0.22, 0.55, or 1.11 microM of menadione equivalent/kg from vitamin K1, menadione dimethypyrimidinol bisulfite (MPB) or menadione nicotinamide bisulfite (MNB), respectively, and a control without supplementation of any vitamin K source. The results of Experiment 3 showed that the biopotency of K1 was greater than that of MPB or MNB. The biopotencies of MPB and MNB were similar, although MNB was more potent in reducing plasma PT when supplemented at the level of 0.1 mg of menadione/kg. A nadir of PT and a plateau of PC were evident with a dietary supplementation of MPB or MNB at a level of 0.25 mg of menadione/kg. Results of this research show that the dietary K1 requirement of young turkeys is in the range of 0.079 to 0.13 mg/kg, and ingestion of neomycin did not affect estimates of the requirement. The biopotency of vitamin K1 in reducing plasma PT and increasing plasma PC was greater than that of MPB or MNB. The biopotency of MNB was greater than that of MPB when menadione supplementation was equivalent to 0.10 mg of K1/kg.