A novel coronavirus termed as COVID-19 by WHO has been the causative agent of an unprecedented pandemic in the history of humanity. The global burden of mortality and morbidity associated with this pandemic continues to increase with each passing day as it is progressively leading to multiorgan dysfunction. In most cases, the cause of death has been attributed to respiratory failure, sepsis, cardiac failure, kidney injury, or coagulopathy. As more knowledge is being unfolded, an in-depth understanding of various systemic manifestations and complications of SARS-CoV2 is vital for optimum management of these patients. This novel virus is known to spread faster than its two ancestors, the SARS-CoV and Middle East respiratory syndrome coronavirus (MERS-CoV), demonstrating a case fatality ranging from 5 to 8% [ 1 ]. Hematological abnormalities such as lymphopenia, thrombocytopenia, elevated D-Dimer, elevated fibrinogen, elevated fibrinogen degradation products as well as cytokines such as IL-6 are emerging as important prognostic marker for worse outcome of COVID-19. Among various systemic manifestations, hematological complications such as venous thrombosis causing pulmonary embolism or deep vein thrombosis, and arterial thrombosis causing myocardial infarction, strokes or limb ischemia are being noted to be directly linked to high mortality from COVID-19. An attempt to understand the pathophysiology of various hematological abnormalities including cytokine storm, hypercoagulable state and some rare presentations of this disease hence becomes imperative. Through this review, we aim to provide an up-to-date summary of current evidence-based literature of hematological manifestations, their consequences and management including role of anticoagulation and drugs targeting cytokine storm in patients with SARS-CoV-2.
Tumor lysis syndrome (TLS) is a constellation of metabolic derangements that occur as a consequence of rapid cell turnover in malignancy and the release of intracellular solutes-potassium, phosphate, and nucleic acid metabolites. TLS classically occurs following chemotherapy, with severe renal failure. However, the entity referred to as spontaneous TLS occurs without a precipitating factor of chemotherapy, radiotherapy, steroid therapy, or immunotherapy and can develop in both hematologic and solid malignancies. Here, we report a rare case of a patient who presented with nonspecific symptoms, hyperphosphatemia, hyperuricemia, but hypercalcemia, resultant acute renal failure, with a large mediastinal mass and a pericardial effusion, who was later found to have spontaneous TLS. The workup led to the diagnosis of T-cell leukemia. Spontaneous TLS is often the first manifestation of occult or undetected malignancy, making this oncologic emergency a challenge to manage. The early diagnosis and prompt treatment of spontaneous TLS can reduce morbidity and mortality for patients with an otherwise curable disease.
Acinetobacter genus includes multiple species, most notably A. baumanii that constitutes a common cause of nosocomial infections worldwide, particularly in patients with underlying immunodeficiency and risk factors (e.g., prior broad-spectrum antibiotic therapy, central venous catheter, mechanical ventilation). A. junii is a very rare human pathogen that is particularly associated with outbreaks of sepsis in immunocompromised neonates and pediatric oncology patients and rarely in immunocompromised adults. To our knowledge, this is the first case report of cavitary pneumonia with bacteremia secondary to A. junii in a patient with systemic lupus erythematosus (SLE).
Peritumoral light chain (AL) amyloidosis secondary to lymphoid malignancies is a rare but well-described entity. Peritumoral deposition of amyloid without systemic amyloidosis has been described in mucosaassociated lymphoid tissue (MALT) lymphomas; however, there are no reported cases of follicular lymphoma with localized peritumoral AL amyloidosis without systemic involvement of amyloidosis. We present a rare case of a patient with advanced follicular lymphoma with peritumoral lymph node IgM lambda light chain amyloidosis without an underlying monoclonal gammopathy or plasma cell dyscrasia.
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