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Immunoglobulin D multiple myeloma (IgD MM) is a rare isotype of multiple myeloma (MM), comprising less than 2% of all cases. It is often associated with advanced disease at the time of diagnosis, an aggressive clinical course, and shorter overall survival (OS) than other subtypes of MM. There is an increased frequency of undetectable or small monoclonal (M-) protein levels on electrophoresis, hypercalcemia, anemia, lytic bony lesions, and renal failure. However, given the rarity of the disease, there are few cases of IgD MM described in the literature. Given the very small amount of IgD immunoglobulins, they may form very small or undetectable M spike on electrophoresis, making the diagnostic error in diagnosing this specific subgroup very easy. Treatment for MM has seen significant advancement, especially over the last decade, with the advent of medications such as proteasome inhibitors, immunomodulatory agents, and monoclonal antibodies. It is important to understand how IgD MM responds to these newer agents and why this disease continues to be associated with poor outcomes despite advancements in treatment. Small clinical studies on patients with IgD MM show better outcomes following a combination of high-dose chemotherapy (HDCT) and autologous stem cell transplant (ASCT) compared to standard chemotherapy. Given the rarity of the disease, there are no large studies done to see the effectiveness of these treatments, and most of the data are derived from small case series. We report a case of IgD kappa MM that was incidentally discovered following a traumatic bicycle accident. The patient started treatment with bortezomib and dexamethasone (Vd) as an inpatient while he was in the rehabilitation unit and was later switched to bortezomib, dexamethasone, and lenalidomide (VRd) as an outpatient. He has now completed seven cycles and successfully underwent autologous hematopoietic stem cell transplantation., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2022, MacDougall et al.)

Paraneoplastic neurological syndromes (PNS) are a group of rare immune-mediated disorders with neurological sequela in cancer patients. It usually occurs when an immune response against a systemic tumor is incorrectly directed to the nervous system. Compared to other reported manifestations of PNS in breast cancer, Guillain Barre syndrome (GBS) is exceedingly rare. There is only one other reported case in the literature of GBS that was diagnosed in a breast cancer patient. We report the second recorded case of a 61-year-old female with a history of early-stage breast cancer, who presented with symptoms of lower extremity weakness initially suspected to be GBS but later found to have been recurrent breast cancer. No specific guidelines are available for the treatment of PNS. Treatment of underlying malignancy with chemotherapy and immunotherapies are usually recommended., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2021, Madala et al.)

A 47-year-old male with stage IV pancreatic cancer developed gemcitabine-induced thrombotic microangiopathy (GiTMA) after treatment with gemcitabine and nab-paclitaxel. GiTMA is a rare and life-threatening complication with an incidence ranging from 0.015% to 1.4% and reported mortality rate ranging from 50% to 90%. Clinically, GiTMA manifests as microangiopathic hemolytic anemia, thrombocytopenia, and renal failure. Early identification of GiTMA is essential to initiate early treatment and improve survival. Treatment of GiTMA includes discontinuation of gemcitabine, along with initiation of steroids, therapeutic plasma exchange (TPE), rituximab, and eculizumab. To our knowledge, this is the first case of GiTMA treated with ravulizumab, a long-acting complement inhibitor. Given the increasing number of patients treated with gemcitabine and seriousness of this complication, it is important for physicians to be aware of this disease entity and maintain a high index of suspicion when evaluating patients with microangiopathic hemolytic anemia, thrombocytopenia, and renal failure., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2021, MacDougall et al.)

Vancomycin-induced immune thrombocytopenia (ITP) is a rare, potentially life-threatening complication from an antibiotic frequently used in medical practice. We report a case of an 81-year-old male with recent removal of an infected right knee prosthesis and insertion of an articulating antibiotic spacer, presenting from rehabilitation for severe thrombocytopenia (1 X 10 3 /µL). The patient's thrombocytopenia was initially falsely attributed to rifampin-induced ITP, a much more common cause of drug-induced thrombocytopenia. Only later, after a second precipitous drop in platelet count, vancomycin was correctly identified as the culprit. The patient's serum was tested for drug-dependent platelet antibodies with and without vancomycin. A positive reaction for IgG was detected by flow cytometry in the absence of vancomycin, which was potentiated in the presence of vancomycin. The result indicated the presence of vancomycin-dependent and nondrug-dependent platelet reactive antibodies and confirmed the diagnosis of vancomycin-induced ITP. In this case, the correct diagnosis was masked by the simultaneous administration of two drugs that cause drug-induced ITP and highlights the importance of early recognition of rare, vancomycin-induced ITP., Competing Interests: The authors have declared that no competing interests exist., (Copyright © 2020, MacDougall et al.)