We provide clear evidence that hepcidin-25 is present in bile, saliva, pleural and ascitic fluids. Hepcidin is likely to play a role here in innate immunity.
COVID-19 is a disease caused by the SARS-CoV-2 virus, characterized by an early mild to moderate viral syndrome of fever, tiredness, cough, and headache. 1 Over 80% of patients have a self-limiting illness not requiring hospital admission and show clear improvement in two weeks. A minority of COVID-19 patients progress through a transition phase around days 7-11 of worsening pulmonary complications. 1 These manifest as breathlessness, acute lung injury and respiratory failure, and often progress to require mechanical ventilation with subsequent high mortality. This deterioration appears to be driven by lung host responses including a cytokine storm of inflammation leading to severe tissue damage and irreversible organ failure likened to acute respiratory
We propose a new hypothesis that the established drug pentoxifylline deserves attention as a potential repurposed therapeutic for COVID-19. Pentoxifylline is an anti-inflammatory agent that suppresses adenosine responses, reduces Tumour Necrosis Factor alpha, Interleukin 1, Interleukin 6 and Interferon gamma and may act to reduce tissue damage during the cytokine storm response to SARS-CoV-2 infection. This agent has been used clinically for many years and has a favourable profile of safety and tolerability. Pre-clinical data support pentoxifylline as effective in cytokine-driven lung damage. Clinical studies of pentoxifylline in radiation and cytokine-induced lung damage in humans are positive and consistent with anti-inflammatory efficacy. Pentoxifylline is a readily available, off-patent, inexpensive drug suitable for large scale use, including in resourcelimited countries. Current trials of therapeutics are largely focussed on the inhibition of viral processes. We advocate urgent randomised trials of pentoxifylline for COVID-19 as a complementary approach to target the host responses.
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