Patient: Gender, 26-year-old Final Diagnosis: COVID-19 Symptoms: Cough • fever Medication:— Clinical Procedure: — Specialty: Hematology Objective: Rare co-existance of disease or pathology Background: Beta-hemoglobinopathies and glucose-6-phosphate dehydrogenase (G6PD) deficiency are genetic disorders that cause hemolytic anemia when exposed to oxidative stress. Their co-existence is, however, not proven to enhance the severity of anemia. Case Report: We report the case of a young man with no known co-morbidities, who came with fever and cough and was diagnosed with COVID-19 pneumonia. He was found to have hemoglobin D thalassemia and G6PD deficiency during further evaluation. Hydroxychloroquine therapy started initially, was discontinued after 3 doses once the G6PD deficiency was diagnosed. His hospital course showed a mild drop in hemoglobin with evidence of hemolysis on peripheral smear. However, the hemoglobin improved without any need for transfusion. Conclusions: Hydroxychloroquine therapy can induce hemolytic crises in patients with underlying G6PD deficiency or hemoglobinopathies and should be avoided or closely monitored. Immediate intervention to stop hydroxychloroquine after 3 doses saved our patient from a major hemolytic crisis. The significance of this case report is that it is the first report that outlines the clinic course of COVID-19 pneumonia in a patient with underlying hemoglobin D disease and G6PD deficiency.

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COVID-19 has surfaced as a multi-organ disease predominantly affecting the respiratory system. Detection of the viral RNA through reverse transcriptase–PCR (RT-PCR) from a nasopharyngeal or throat sample is the preferred method of diagnosis. Recent evidence has suggested that COVID-19 patients can shed the SARS-CoV-2 for several weeks. Herein, we report six cases of COVID-19 who had persistently positive SARS-CoV-2 on repeat RT-PCR testing reaching up to 9 weeks. The spectrum of cases described ranges from asymptomatic infection to severe COVID-19 pneumonia. A full understanding of the virus’s transmission dynamics needs further research. Prolonged viral shedding currently has unclear implications on the management and isolation decisions—the role of the cycle threshold (Ct) value in guiding therapeutic decisions is yet to be clarified. More data on the relationship between Ct values and viral cultivation are needed, especially in patients with prolonged viral shedding, to understand the virus’s viability and infectivity.

The commonest etiologies of new-onset pancytopenia are congenital bone marrow failure syndromes, marrow space-occupying lesions, infections, and peripheral destruction. Nutritional deficiencies, including folate and vitamin B12, can occasionally cause pancytopenia. We report a 48-year-old gentleman who presented with a 1-week history of dizziness and upper gastrointestinal bleeding. Laboratory evaluation revealed pancytopenia, macrocytosis, toxic neutrophils, hemolysis, suppressed reticulocyte count, positive direct anti-globulin test (DAT), severely reduced B12 levels, and positive anti-intrinsic factor and anti-parietal cell antibodies. He was started on weekly intramuscular B12 supplementation and showed improvement in blood cell counts during follow-up. Recognition of B12 deficiency as a cause of pancytopenia and DAT-positive autoimmune hemolytic anemia can help to avoid unwanted investigations and aid in early diagnosis and treatment.

Artery of Percheron (AOP) is an abnormal variant of the arterial supply of the thalamus. AOP occlusion can lead to bilateral thalamic and rostral midbrain infarct presenting as memory loss, fluctuating levels of consciousness, and altered mental status. A 43-year-old woman with a history of antiphospholipid syndrome (APS), managed on dabigatran, presented with acute confusion and drowsiness. She had slurred and slowed speech, disorientation in time and place, left-sided facial droop, decreased power of the left side (4/5), and was unable to walk due to generalized weakness. Labs showed a prolonged prothrombin time and activated partial thromboplastin time, positive lupus anticoagulant, anti-cardiolipin, beta-2 glycoprotein, anti-nuclear and anti-dsDNA antibodies. Contrast-enhanced CT perfusion showed ischemic changes in the bilateral thalami, suggesting infarct along the AOP territory. AOP infarcts are scarce and the presenting complaints are unusual of cerebrovascular accidents. It requires a high index of suspicion to detect. There are no other reports in the literature of patients with

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Tuberculosis (TB) is a common post-transplant infection with high prevalence in developing countries due to reactivation. Post-transplant TB involves the respiratory system in 50% of patients, followed by disseminated involvement in 30%. The risk of tuberculosis of renal allograft post-transplantation is determined by disease endemicity in the donor population and the immunosuppressant regimen. TB can cause allograft rejection and graft loss due to delayed diagnosis or reduced immunosuppressant drug efficacy. A 23-year-old lady was seen 40 days after cadaveric unrelated renal transplantation from China. She was on immunosuppression with tacrolimus, mycophenolate, and prednisolone. Examination showed lowgrade fever and infected surgical site in the right iliac fossa draining pus. Imaging showed fluid pockets, parenchymal micro-abscesses, and perinephric collections in the right iliac fossa communicating with skin. A diagnosis of renal allograft TB without dissemination was made after TB polymerase chain reaction (PCR) from early morning urine was positive. She was started on anti-TB therapy. The sinus tract healed, and renal parameters improved after six months of therapy. Follow-up magnetic resonance imaging (MRI) showed resolution of the micro-abscesses as well as the surrounding fluid collection. Renal angiogram demonstrated well-perfused, normally functioning, non-obstructed renal transplant. Tuberculosis of renal allograft should be considered in a transplant recipient with pyrexia of unknown origin and persistent discharge from the surgical site, not responding to antimicrobials. Tuberculosis of transplant kidney can cause graft loss due to allograft rejection when there is a delayed diagnosis, or as anti-TB drugs reduce the efficacy of immunosuppressant medications. The index of suspicion should be high when donor status is unknown or if the donor is from an endemic tuberculosis area. Timely diagnosis and treatment helped to save the transplanted kidney of our patient without rejection.

Acquired von Willebrand Disease (AVWD) is a rare disorder in which qualitative or quantitative defects in von Willebrand factor (VWF) occur secondary to other conditions. AVWD occurs in patients with myeloproliferative disorders due to formation of autoantibodies against VWF and development of excessive shear stress causing disruption of VWF multimers. AVWD is different from congenital VWD in its acute onset and absence of family history. We report a 42-year-old gentleman with essential thrombocythemia, who was on cytoreductive therapy with hydroxyurea, and presented with an acute history of gum bleeding with hemoptysis, without any antecedent trauma or infections. His platelet count was very high, and prothrombin time and activated partial thromboplastin time were prolonged. The VWF ristocetin cofactor assay (VWF: RCo) was low, but VWF antigen level (VWF: Ag) was normal. Their ratio (VWF: RCo/VWF: Ag) was much lower than the acceptable lower limit. Treatment in AVWD is focused on addressing the underlying disorder. Early recognition of AVWD and its primary cause is mandatory in providing adequate therapy and achieving a cure.