Cleveland Clinic journal of medicine
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At present, there are no firm guidelines for the treatment of COVID-19-related emotional distress. The current approach is based on our knowledge of how to manage anxiety in medically ill patients, taking into consideration all associated medical comorbidities, drug-drug interactions, and the patient's specific needs and preexisting mental illness. Interventions should be implemented at the bedside to augment the patient's own resiliency in coping with these stressful events. A targeted combination of psychopharmacology (targeting acute anxiety and panic symptoms) and psychotherapy (relaxation techniques, breathing exercises, and encouragement) is recommended.
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The COVID-19 pandemic has caused a sense of unease in the rheumatology community about the risk to patients with immune-mediated diseases, given their predisposition to infection due to underlying disease states and immunosuppressive therapies. Thus far, there have been few cases of COVID-19 reported in patients with immune-mediated diseases and there have been no formal guidelines released on the management of patients with immune-mediated diseases in the setting of COVID-19. Results of clinical trials and data from the Global Rheumatology Alliance registry are eagerly awaited to gain further insight into the impact of this novel infection on our vulnerable patient population.
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Cutaneous manifestations, a well-known effect of viral infections, are beginning to be reported in patients with COVID-19 disease. These manifestations most often are morbilliform rash, urticaria, vesicular eruptions, acral lesions, and livedoid eruptions. ⋯ With COVID-19, although we are at a relatively early point in the pandemic, cutaneous manifestations in infected patients are beginning to emerge from around the world. In this article, we describe some of the current cutaneous abnormalities observed in patients with COVID-19.
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Concerns have been raised about the potential for renin-angiotensin system (RAS) inhibitors to upregulate expression of angiotensin-converting enzyme 2 (ACE2) and thus increase susceptibility to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) entry. Currently, there is no evidence that even if RAS inhibitors increase expression and activity of ACE2, that they would increase the risk of SARS-CoV-2 infection by facilitating greater viral entry or worsen outcomes in patients with COVID-19. At this time, there is no clinical evidence to suggest that treatment with RAS inhibitors should be discontinued in stable patients with COVID-19. In hospitalized patients with severe COVID-19, decisions about these medications should be based on clinical condition, including hemodynamic status and renal function.
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SARS-CoV-2, the virus that causes COVID-19, is transmitted through respiratory secretions and saliva. The virus can also live for short periods of time (1 to several hours) on fomites such as doorknobs, handrails, and tables. ⋯ Asymptomatic shedding of the virus does occur and may account for up to 60% of cases. Risk factors for a more severe course of COVID-19 include age 65 and older, living in a nursing home or long term care facility, chronic lung disease, and others.