[Retrospective Analysis of Bortezomib or Lenalidomide for Very Elderly Patients with Newly Diagnosed Multiple Myeloma].

In elderly patients aged≥80 with newly diagnosed multiple myeloma(NDMM), the optimal initial doses of bortezomib (Bor)and lenalidomide(Len)remain unclear. We performed a retrospective analysis that included 20 patients with NDMM aged≥80 years who underwent treatment with Bor or Len at our hospital from July 2010 to December 2019. Among the patients treated with Bor, the median time to next treatment(TTNT)was 4.2 months, and the median dose was 1.0 mg/m2 per injection. While patients with International Staging System(ISS)Ⅲ or an estimated glomerular filtration rate of < 40 mL/ min/1.73 m2 required dose reductions, dose intensity did not significantly affect TTNT. Among the patients treated with Len, the median TTNT was 14.6 months, and the median dose of Len was 10.0 mg/day. All patients who started with6le;10 mg Len continued the initial dose; the others required a dose reduction. Treatment was discontinued in 2 patients because of disease progression and in other 15 patients because of adverse events(AEs). In conclusion, initial doses of Bor at 1.0 mg/ m2 per injection and Len at 10 mg per day may provide potent disease control and permit continuing treatment with few AEs in elderly patients with MM.

Efficacy and safety of low-dose imatinib in an elderly patient with mixed phenotype acute leukemia with t(9;22)(q34;q11.2);BCR-ABL1.

Low-dose imatinib with monitoring of drug concentrations in blood may successfully control Philadelphia chromosome-positive mixed phenotype acute leukemia (Ph+MPAL), particularly in elderly patients with comorbidities.

[Spontaneous Splenic Rupture with Angioimmunoblastic T-Cell Lymphoma Successfully Treated Using Transcatheter Arterial Embolization].

A 75-year-old woman presented to our hospital with a history of fever, cervical lymphadenopathy, and fatigue. Computed tomography(CT)revealed systemic lymphadenopathy with prominent splenomegaly. Axillary lymph node biopsy results revealed diffuse proliferation of atypical lymphoid cells with arborizing high endothelial venules. Immunohistochemical staining was positive for CD3, CD5, and CD10, but negative for CD20 and CD79a. Given these findings, a diagnosis of angioimmunoblastic T-cell lymphoma(AITL)was made. Due to the extremely high tumor burden, pre-therapy with corticosteroids was initiated. However, the patient suddenly went into hemorrhagic shock. Contrast-enhanced CT revealed abdominal bleeding due to splenic rupture. Bleeding was rapidly controlled using transcatheter arterial embolization(TAE). Five days after TAE, mini-CHOP therapy was initiated. Splenomegaly is common in hematologic disease. Owing to the lethality of the condition, in cases of progressive anemia with splenomegaly in patients with hematologic disease, the possibility of splenic rupture should be considered. Since TAE carries no risk of post-splenectomy infection and allows timely resumption of chemotherapy, it could be considered as one of the preferred treatment choices for splenic rupture in hemodynamically unstable patients.

The First Autopsy Case of Fatal Acute Cardiac Failure after Administration of Carfilzomib in a Patient with Multiple Myeloma.

Carfilzomib (CFZ) improves progression-free survival for patients with relapsed or refractory multiple myeloma (MM) but has shown higher frequency of cardiovascular adverse events (CVAEs) than other proteasome inhibitors. We report the first autopsy case of acute death from cardiac failure shortly after administration of carfilzomib. A 74-year-old female was diagnosed with IgA MM after a 2-year period of smoldering MM. She was refractory to both bortezomib plus dexamethasone and lenalidomide plus dexamethasone therapies, so she subsequently received CFZ in combination with lenalidomide and dexamethasone. The day after the start of the therapy, she complained of severe dyspnea with a significant decline in left ventricular ejection fraction. Her acute cardiac failure rapidly progressed, and she died on day 7 of the start of CFZ. The autopsy showed invasion of inflammatory cells between the myocardial cells and very little myocardial necrosis. There was no obvious thrombus in the coronary artery of the heart, and no infarction or amyloid deposition was observed in the myocardium. Pathological findings of hypersensitivity myocarditis, a drug-induced cardiomyopathy, appeared to agree with this case except for absence of an eosinophilic infiltration of the myocardium. A CFZ-induced CVAE is generally considered reversible. However, rapidly progressing fatal heart failure like in our case is rare. To characterize CFZ-associated CVAE, further case collection is needed.