The recently published manuscript entitled “Epigenetically Altered T Cells Contribute to Lupus Flares” summarizes recent advances in our understanding of how the environment alters the immune system to cause flares of systemic lupus erythematosus (SLE) in genetically predisposed people, and why it affects women approximately 9 times more often than men

Systemic Lupus Erythematosus (SLE) is a devastating autoimmune disease that affects women to men at a ratio of 9:1 and is predominant in those of African ancestry. In SLE, the presence of autoantigens results in aberrant immune activation leading to systemic inflammation that predominantly affects the brain, kidneys, blood, and skin. Current guidelines recommend treatment with immunosuppressive drugs like prednisone, cyclophosphamide, azathioprine, and even some antimalarial drugs

We present two unique cases in which two HIV positive patients with generalized lymphadenopathy and pancytopenia without any skin lesions were diagnosed with primary lymph node Kaposi´s Sarcoma after excisional biopsy of an inguinal lymph node. 

Peripheral pancytopenia is not a disease by itself; rather it describes simultaneous presence of anemia, leucopenia and thrombocytopenia resulting from a number of disease processes.

The incidence of thromboembolic events in COVID-19 is reportedly higher in intensive care unit (ICU) patients (29.4%) as compared to non-ICU patients (11.5%), while data on thromboembolic events in non-hospitalized, self-limiting COVID-19 is unavailable. Renal infarction with COVID-19 has only been reported in three patients who had severe infection, multiple comorbidities, and/or immuno-compromised state post kidney transplantation. Since the onset of the SARS-CoV-2 pandemic, guidelines for the prophylaxis and treatment of COVID- 19-related hypercoagulability have only been focused on hospitalized patients. Concurrently, risk factors and management guidelines for thromboembolic events in mild COVID-19 have remained unidentified. In this report, we describe a case of a 38-year-old male–with no medical history pertinent to hypercoagulability–who developed an isolated renal infarction one week after being diagnosed with mild COVID-19.