RESUMO
Large cell neuroendocrine carcinoma (LCNEC) constitutes a rare subset of highly undifferentiated malignancies known for their aggressive nature. Although these tumors commonly originate in the lungs and gastrointestinal tract, their potential occurrence is not restricted to specific anatomical sites, giving rise to a variety of symptoms. Notably, cases of neuroendocrine tumors (NETs) with an unidentified primary source exhibit a graver prognosis and shorter survival periods compared to those with clearly identified origins. NETs frequently demonstrate a propensity to metastasize, spreading to diverse anatomical regions such as the liver, lungs, lymph nodes, and bones, illustrating their aggressive nature and the complexity of their management. In this context, we present the case of a 59-year-old male who sought medical attention in the emergency department due to right upper quadrant (RUQ) abdominal pain. Initial diagnostic assessments revealed significantly elevated liver function tests and severe hypercalcemia. A right upper quadrant ultrasound (RUQ US) was subsequently performed, which revealed heterogeneous hepatic echotexture with innumerable echogenic masses, suggesting a metastatic process. A computed tomography (CT) scan was then ordered to evaluate further the RUQ US findings, which showed numerous hypovascular liver masses, raising concerns of malignancy. A liver biopsy confirmed a diagnosis of LCNEC with an unidentified primary source.
RESUMO
Introduction: During treatment for malignant lymphoma, cytopenia can develop for several reasons. This can range from mild cytopenias leading to infection and bleeding to full-blown drug-induced aplastic anaemia. While aplastic anaemia affects individuals of all genders and ages, here, we describe aplastic anaemia after chemotherapy exposure to bendamustine in a 65-year-old female with non-Hodgkin's lymphoma. Case description: A 65-year-old woman with recurrent indolent marginal zone lymphoma and post-chemotherapy with bendamustine and rituximab, presented with a neutropenic fever and was admitted with a leading diagnosis of sepsis. In the previous two weeks, the patient required regular transfusions of packed red blood cells and platelets and maintained a daily ZARXIO® regimen. Laboratory results revealed pancytopenia, and broad-spectrum antibiotics (cefepime/vancomycin) were given. The patient was subsequently admitted to the hospital under the care of the haematology/oncology team and was ultimately diagnosed with aplastic anaemia, likely as a consequence of bendamustine chemoimmunotherapy. She elicited a positive response to the triple immunosuppressive therapy (IST) regimen (two immunotherapeutic agents plus one anti-thymocyte globulin (ATG), after which her cell counts returned to normal. Conclusions: This case underscores the importance of recognising haematologic complications linked to bendamustine and advocates for further research to increase the understanding among healthcare professionals of drug-induced aplastic anaemia. Bendamustine can cause severe autoimmune haemolytic anaemia and aplastic anaemia and may require multiple transfusions and a multidrug regimen for treatment. The use of ATG as a therapeutic intervention is appropriate because it has been effective in treating aplastic anaemia. LEARNING POINTS: Bendamustine can cause severe autoimmune haemolytic anaemia and aplastic anaemia, a side effect which has rarely been reported but is of significant clinical importance.Drug-induced aplastic anaemia is a complex, potentially devastating consequence of treating blood cancers and is a relatively unexplored area that requires further understanding.Anti-thymocyte globulin is effective in treating bendamustine-induced aplastic anaemia as it degrades lymphocytes that destroy the bone marrow.