We present a case of a male patient in his mid-30s with COVID-19-induced lung failure requiring extracorporeal membrane oxygenation, who needed an emergency oesophagogastroduodenoscopy due to major upper gastrointestinal bleeding. Endoscopy exposed severe ulcerative duodenitis with diffuse mucosal bleeding. While CT angiography did not show any signs of ischaemia, histopathology revealed duodenitis with substantial inflammatory cell infiltrates consisting of neutrophils and CD3+ T lymphocytes with equal CD4+/CD8+ distribution. Since the composition of cell infiltrates coincides with changes in inflammatory patterns of the respiratory mucosa from patients with COVID-19 and in COVID-19-associated enterocolitis, and systemic dexamethasone treatment became standard of care in ventilated intensive care unit patients with COVID-19 infection, we initiated an individualised therapeutic attempt to treat the duodenitis with topical enteral budesonide. Follow-up oesophagogastroduodenoscopies within 4 weeks of enteral budesonide administration revealed a full clinical and histological healing of the duodenal mucosa with marked reduction of neutrophilic and lymphocytic infiltrates.To our knowledge, the current report is the first description of enteral budesonide treatment of duodenitis in a patient with COVID-19 infection and warrants further investigation, whether budesonide might constitute a novel therapeutic strategy for the management of COVID-19-related intestinal mucosal damage.

Growth hormone (GH) is required to maintain normal cardiac structure and function and has a positive effect on cardiac remodeling in experimental and possibly human disease. Cardiac resistance to GH develops in the uremic state, perhaps predisposing to the characteristic cardiomyopathy associated with uremia. It was hypothesized that administration of low-dosage GH may have a salutary effect on the cardiac remodeling process in uremia, but because high levels of GH have adverse cardiac effects, administration of high-dosage GH may worsen uremic cardiomyopathy. In rats with chronic renal failure, quantitative cardiac morphology revealed a decrease in total capillary length and capillary length density and an increase in mean intercapillary distance and fibroblast volume density evident. Low-dosage GH prevented these changes. Collagen and TGF-␤ immunostaining, increased in chronic renal failure, were also reduced by GH, suggesting a mechanism for its salutary action. Low-dosage GH also prevented thickening of the carotid artery but did not affect aortic pathology. In contrast, high-dosage GH worsened several of these variables. These results suggest that low-dosage GH may benefit the heart and possibly the carotid arteries in chronic renal failure.

Ginger is a world known food plant which is equally reputed for its medicinal properties. The aim of the work is to study the acute and subacute cardiovascular toxicity of ginger in adult male albino rats and its possible mechanisms of action. The in-vivo studies included eighty four adult male albino rats for the acute and subacute toxicity experiments. The rats were divided into 7 groups each one consisted of 12 rats. All rats received ginger orally in saline. Each of the in-vivo studies included 2 control groups, the negative and positive control rats. In the acute toxicity study, rats received ginger in a single dose of 2500 mg/ kg. In the subacute toxicity study group VI and VII received ginger in a daily dose of 50 mg/ kg and 500 mg/ kg respectively for 28 days. After 24 hours of the acute toxicity and 28 days of the subacute experiments six rats of each group were used for blood pressure and heart rate recording. The other 6 rats were used for histopathological study of the cardiac tissue. The in-vitro experiments included 6 rabbits each weighing 1.5-2 kg. Ginger (5mg/ml) was incubated with the aortic spiral strip of each rabbit to investigate the possible mechanisms of action of Ginger. It was concluded that; single dose of 2500 mg/ kg ginger can be a toxic by causing severe hypotension and bradycardia with induction of prenecrotic changes in cardiac tissue. The administration of ginger in a dose of 50 mg/ kg for 28 days produced bradycaria with waviness in cardiac muscle fibers. Ginger in a dose of 500 mg/ kg produced both hypotension and bradycardia with degenerative changes in cardiac myocyte tissue. The hypotensive and bradycardic effects of ginger may be partially due to induction of vasodilatation by increasing nitric oxide release or synthesis and partially due to a calcium channel blocking effect. Also, a cholino-mimetic effect could be contributed in the cardiovascular effects of ginger. While the In-vitro results revealed that ginger is a partial vasorelaxant as it produced a relaxant effect on rabbit's aortic strip procontracted with phenylephrine, while preincubation with L-nitroarginine methyl ester (L-NAME) significantly attenuated the ginger-induced relaxation indicating that the vasodilator effect of ginger is partially mediated through nitric oxide synthesis or release from L-NAME.

No abstract

No abstract