The current COVID-19 pandemic caused by SARS-CoV-2 has become a global health emergency. Treatment of chronic inflammatory bowel disease (CIBD) according to the standards includes the use of 5-aminosalicylic acid (5-ASA), corticosteroids, cytostatics, and biological therapy. However, these treatments can weaken the immune system, which potentially puts COPD patients at increased risk of infections and infectious diseases, including COVID-19. Therefore, patients with CVD have a greater risk of developing COVID-19 and more severe clinical course, or even death, compared to the general population.
The first and mandatory step in the treatment of hypertension is lifestyle modification (LS), which is aimed at correcting the above risk factors, primarily modifiable ones. A big problem is the choice of the most optimal treatment for hypertension, which can slow down the progression of lesions of the heart, blood vessels, kidneys, brain and eyes. The vast majority of hypertensive patients who seek medical help require combination antihypertensive therapy. At the same time, the most appropriate at the present level is the use of fixed combinations of such drugs.
Skin lesions in coronavirus infection caused by the SARS-CoV-2 virus are divided into seven categories. The first category includes skin angiitis caused directly by COVID-19 infection, against which the walls of small vessels of the dermis are damaged by immune complexes circulating in the blood. Angiitis is localized on the skin of the upper and lower extremities. They look like frostbite, painful, itchy. Such manifestations usually occur in young patients with a mild course of the disease, appear in the late stages and last about 12 days. The second category includes papular-vesicular rashes, which are characterized by acute clinical manifestations in the form of chickenpox, more similar to prickly heat, occurring against a background of high fever and increased sweating.
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