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Experts refer to the third category of skin manifestations as pink lichen and papulosquamous rashes, which are infectious-allergic skin lesions associated with COVID-19 infection. The clinical feature of pink lichen in this case is the absence of maternal plaque. The fourth category includes a measles rash. To the fifth - toxicodermia. This rash is associated with individual intolerance of patients of certain groups of drugs. The sixth category of skin manifestations of coronavirus infection, scientists include urticaria, which in some cases may be a harbinger of the onset of COVID-19.

Moreover, low vitamin D levels common in patients with CVD may increase the risk and severity of COVID-19. This is because vitamin D increases levels of anti-inflammatory cytokines and reduces viral replication, which in turn can reduce pro-inflammatory cytokines that contribute to lung damage. Despite the lack of evidence demonstrating increased susceptibility to COVID-19, drugs used in the treatment of COPD increase the risk of respiratory tract infections to varying degrees. However, theoretically, some immunosuppressive drugs may have beneficial effects, given that the cause of death in COVID-19 is a cytokine storm leading to acute respiratory failure.

5-ASA preparations have very weak immunosuppressive activity. There are no reports that these drugs are associated with an increased risk of infection, and studies evaluating the safety profile of 5-ASA do not show an increased risk of serious or opportunistic infections. Treatment with 5-ASA should be continued without concern for an increased risk of infection or severe COVID-19. If the patient is in contact with a patient with COVID-19 or develops COVID-19, treatment with 5-ASA should be continued.

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If a patient tests positive for SARS-CoV-2 and/or develops COVID-19, discontinuation of biologics should be considered until the patient clears the infection. JAK inhibitors (tofacitinib and others) selectively affect the intracellular JAK/STAT signaling system, which mediates the action of many cytokines involved in the pathogenesis of ulcerative colitis. Unlike genetically engineered biological drugs, inhibition


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