We present the case of a healthy 38-year-old male who developed parosmia following a second dose of AstraZeneca with a negative nasal swab of coronavirus disease 2019 (COVID-19) infection. The patient noted parosmia that started suddenly after one week of receiving the second dose of AstraZeneca with no association with other symptoms. The patient has still not recovered from his parosmia until the publication of this article. The olfactory disorder was confirmed using a validated questionnaire for parosmia assessment and examination by rhinoscopy. Parosmia is a rare side effect of COVID-19, and its pathophysiological mechanism is still unknown. More research in the future is needed to know the association of parosmia with COVID-19 vaccine.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with unpredictable course and flares. The clinical manifestation can vary from mild to severe and life-threatening disease. Infection is the primary cause of mortality in hospitalized SLE patients. There is a paucity of evidence to support the co-management of SLE with major organ involvement and sepsis. We describe the clinical response of a 35-year-old male diagnosed with SLE; then, he developed severe sepsis and a flare of SLE with major organ involvement including lupus nephritis (LN), myocarditis, and neuropsychiatric systemic lupus erythematosus (NPSLE). Based on the patient’s condition, a treatment dilemma was encountered, and after a multidisciplinary meeting, the decision was made to use a combination of rituximab (RTX), intravenous immunoglobulin (IVIG), and pulse steroid. Shortly, the patient’s condition started to improve, and his symptoms were resolved. In conclusion, our clinical case suggests that combined RTX, IVIG, and pulse steroid seem to be effective and safe in achieving clinical response, thus representing a good choice for managing severe SLE flares in sepsis.

Critical care knowledge constitutes an essential component in medicine. Unfortunately, ICU knowledge acquisition is limited in many medical schools. This study is intended to measure the knowledge background, gaps, and the confidence toward critical care concepts among final year medical students and interns at

Hereditary hemochromatosis (HH) is a multisystem disease characterized by iron overload and various clinical presentations, including cirrhosis, diabetes mellitus, and heart failure. HH can be caused by the human homeostatic iron regulator (HFE) and non-HFE gene mutations. Aplastic anemia is a rare, lifethreatening bone marrow failure in which fat replaces pluripotent stem cells, resulting in pancytopenia and hypoplasia of bone marrow. We present a case of a five-year-old-boy who initially presented with a large ecchymosis located at the right side of the chest and abdomen. These started suddenly after minor trauma. Later, he was diagnosed with idiopathic aplastic anemia and treated with immunosuppressive therapy (IST). As part of the workup for pancytopenia, we ordered whole exome sequencing (WES) and diagnosed the patient with autosomal recessive hereditary hemochromatosis (ARHH). The ARHH is caused by HFE pathogenic gene mutation variant (c.187C>G p homozygous genotype). After six months of IST, he still had persistent disease. Human leukocyte antigen (HLA) typing showed he has a sister who is a full match but also has ARHH. Because of this, a haploidentical hematopoietic stem cell transplantation (hHSCT) from the father was performed. The hHSCT had a successful outcome. We suggest that in children with idiopathic aplastic anemia, physicians should be aware of the possibility of co-existing hereditary hemochromatosis or secondary hemochromatosis. Serum ferritin and transferrin saturation should also be measured regularly in order to detect early hemochromatosis.

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