Abstract Middle East Respiratory Syndrome (MERS), Severe Acute Respiratory Syndrome (SARS) and Coronavirus Disease 2019 (COVID-19) are caused by three distinct coronaviruses belonging to the same genus. COVID-19 and its two predecessors share many important features in their clinical presentations, and in their propensity for progression to severe disease which is marked by high rates of morbidity and mortality. However, comparison of the three viral illnesses also reveals a number of specific differences in clinical manifestations and complications, which suggest variability in the disease process. This narrative review delineates the pulmonary, cardiac, renal, gastrointestinal, hepatic, neurological, and hematologic complications associated with these three respiratory coronaviruses. It further describes the mechanisms of immune hyperactivation—particularly cytokine release syndrome—implicated in the multi-organ system injury seen in severe cases of MERS, SARS, and COVID-19.

The different presentations, comorbidities, and outcomes of COVID-19 highlight the importance of early identification and proper triage of patients. High-risk patients can be divided into patients with common comorbidities and patients with special categories. Common comorbidities include, but are not limited to, Cardiovascular Disease (CVD), Diabetes Mellitus (DM), immunosuppression, underlying respiratory disease, and obesity. Certain categories of COVID-19 patients are also at increased risk, including neonates and pregnant women.  In the present article, we delineate the reported risk factors for acquisition of infection, and for increased severity of the clinical disease. We also comparatively analyze those risk factors associated with COVID-19 and with the antecedent human acute respiratory syndrome-causing viruses, SARS-CoV-1 and MERS-CoV. We hypothesize that the structural similarities of the three viruses predict a similarity in the profile of high-risk patients. Several pathophysiological patterns have been detected to support this theory.

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Highlights Involvement of the pancreas is exceedingly rare in sarcoidosis. Pancreatitis in a patient with pulmonary sarcoidosis can be secondary to a sarcoid inflammatory process. Pancreatic sarcoidosis can be discovered incidentally on radiography and may mimic neoplasia. Pancreatic sarcoidosis can be found concomitantly with more than one type of neoplastic lesion. Histopathologic assessment is required for definitive diagnosis.

Background: COVID-19 is an infection secondary to the novel SARS-COV-2 virus with a well-established increased risk for thrombotic events. However, the interaction between COVID-19 and other patient-specific hereditary or acquired thrombophilias remains a poorly explored area. Case Presentation: We herein report a case of a 23-year-old Caucasian female with known risk factors for coagulopathy (smoking, oral contraceptives, anti-phospholipid (aPL) antibodies, heterozygous Factor V Leiden mutation, and homozygous methylenetetrahydrofolate reductase (MTHFR) mutation) who developed a Budd-Chiari syndrome after testing positive for COVID-19. To our knowledge, this is the first report of a case of splanchnic vein thrombosis in a COVID-19 patient with the above risk factors. Conclusion: Such a presentation underscores the additional increased thrombotic risk attributed to COVID-19 infections in the setting of underlying hereditary or acquired thrombophilias.