Introduction: Hepatitis B virus (HBV) reactivation (so-called reverse seroconversion) is a rare but known complication of hematopoietic stem cell transplantation, immunosuppressive therapy, or high-dose chemotherapy plus rituximab. This event is linked to a treatment-related fall in titers of antibodies to hepatitis B surface antigen (HBsAb) below the protective threshold level.
Case Presentation: A 77-year-old Korean man diagnosed with primary amyloidosis was started on melphalan/dexamethasone combination therapy. During treatment, laboratory indices of hepatic function suddenly deteriorated, and he developed acute hepatitis through reverse HBV seroconversion, becoming positive for hepatitis B surface antigen (HBsAg) and negative for HBsAb. HBV DNA was also detectable in serum to a profound extent. Normal liver function was gradually restored during the course of antiviral therapy (entecavir).
Conclusions: HBV reactivation may lead to fatal liver disease in a significant percentage of patients. As a result, physicians often screen for HBsAg and HBsAb prior to initiating chemotherapy, advising antiviral treatment in patients seropositive for HBsAg, even in the absence of hepatitis B e antigen. Here, a case of HBV reactivation is described, involving a patient given relatively low-dose chemotherapy (melphalan/dexamethasone) for primary amyloidosis.
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http://dx.doi.org/10.1186/s13256-015-0610-z | DOI Listing |
Nat Commun
January 2025
Center for Early Detection and Interception of Blood Cancers, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Early therapeutic intervention in high-risk smoldering multiple myeloma (HR-SMM) has shown benefits, however, no studies have assessed whether biochemical progression or response depth predicts long-term outcomes. The single-arm I-PRISM phase II trial (NCT02916771) evaluated ixazomib, lenalidomide, and dexamethasone in 55 patients with HR-SMM. The primary endpoint, median progression-free survival (PFS), was not reached (NR) (95% CI: 57.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Wollongong, Wollongong, NSW, Australia.
Background: Brain iron dyshomeostasis has been observed in behavioral deficits relevant to neurodegenerative diseases such as Alzheimer's disease (AD), but it remains unclear whether it is a primary cause or an epiphenomenon of disease.
Method: We assessed the effects of brain iron dyshomeostasis on spatial cognition and cognitive flexibility using the IntelliCage system, recognition memory using novel object recognition tasks and anxiety-like behavior using the open field and elevated plus maze tests. We investigated these phenotypes in a HfexTfr2 mouse model of brain iron dyshomeostasis alone (Iron) or combined with an APP/PS1 model of Alzheimer's Aβ amyloidosis (Aβ+Iron), compared with APP/PS1 mice with Aβ amyloidosis alone (Aβ) or wildtype controls.
Alzheimers Dement
December 2024
Institute for Memory Impairments and Neurological Disorders (MIND), Irvine, CA, USA.
Background: Several variants have been identified that protect against the development of Alzheimer's disease (AD). Understanding how these alleles convey protection inform us not only about the disease pathogenesis, but also guide therapeutic strategies. The UCI MODEL-AD consortium has developed several protective alleles including a putative gain of function variant of ABCA7, and the APOE Christchurch variant.
View Article and Find Full Text PDFBMC Cardiovasc Disord
January 2025
Department of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai, 200092, China.
Background: Systemic light chain amyloidosis is a rare and debilitating disease, especially for which initially presented with digestive tract involvement. Myocardial amyloidosis is highly aggressive with generally poor prognosis and often resulted in missed diagnosis or misdiagnosis with routine examination tools. Multimodality imaging play an important role in diagnosing the amyloidosis effect on multiple organs.
View Article and Find Full Text PDFBr J Haematol
January 2025
Department of Haematology, University College London Hospital, London, UK.
Systemic light chain (AL) amyloidosis is a rare clonal plasma cell disorder characterized by the production of amyloidogenic immunoglobulin light chains, which causes the formation and deposition of amyloid fibrils, leading to multi-organ dysfunction. Current treatment is directed at the underlying plasma cell clone to achieve a profound reduction in the monoclonal free light chain production. The standard-of-care first-line therapy is a combination of daratumumab, cyclophosphamide, bortezomib and dexamethasone (D-VCd regimen), resulting in high rates of haematological and organ responses.
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