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This case highlights the importance of considering tuberculosis as an underlying cause of gastrointestinal amyloidosis, even in patients previously treated for the infection. Clinicians should maintain a high index of suspicion for atypical presentations of amyloidosis, especially in individuals with chronic inflammation, enabling early diagnosis and tailored management for improved patient outcomes. Abstract: Gastrointestinal amyloidosis is a rare condition often associated with chronic inflammation. We present a unique case of a 50-year-old female with a history of miliary tuberculosis who developed gastrointestinal amyloidosis. The patient exhibited chronic loose stools, weight loss, abdominal pain, and urinary incontinence symptoms. Diagnostic workup revealed characteristic findings of amyloidosis on biopsy. Despite treatment for tuberculosis, her symptoms persisted, highlighting the challenging nature of managing this condition. This case underscores the importance of considering tuberculosis as a potential cause of secondary amyloidosis in patients with ongoing symptoms of inflammation and infection. Early recognition and tailored management are crucial in optimizing patient outcomes.
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PURPOSE: Aurora A kinase (AAK) is upregulated in highly proliferative lymphomas, suggesting its potential as a therapeutic target. Alisertib is a novel oral AAK inhibitor without adverse safety signals in early-phase studies that demonstrated preliminary activity in T-cell lymphoma. This phase II study was conducted to further investigate the efficacy of alisertib in relapsed or refractory peripheral T-cell non-Hodgkin lymphoma (PTCL). PATIENTS AND METHODS: Eligible patients with histologically confirmed relapsed/refractory PTCL or transformed Mycosis fungoides (tMF) received alisertib 50 mg twice a day for 7 days on 21-day cycles. RESULTS: Of 37 eligible patients, the histologic subtypes enrolled included PTCL not otherwise specified (n = 13), angioimmunoblastic T-cell lymphoma (n = 9), tMF (n = 7), adult T-cell lymphoma/leukemia (n = 4), anaplastic large-cell lymphoma (n = 2), and extranodal natural killer/T-cell lymphoma (n = 2). Grade 3 and 4 adverse events in ≥ 5% of patients included neutropenia (32%), anemia (30%), thrombocytopenia (24%), febrile neutropenia (14%), mucositis (11%), and rash (5%). Treatment was discontinued most commonly for disease progression. Among the PTCL subtypes, the overall response rate was 30%, whereas no responses were observed in tMF. Aurora B kinase was more commonly overexpressed than AAK in tumor specimens. Analysis of AAK, Aurora B kinase, MYC, BCL-2, phosphatidylinositol 3-kinase γ, and Notch1 expression revealed no association with response. CONCLUSION: Alisertib has antitumor activity in PTCL, including heavily pretreated patients. These promising results are being further investigated in an ongoing international, randomized phase III trial comparing alisertib with investigator's choice in PTCL.