ReviewHemaSphere2020
Systemic AL Amyloidosis: Current Approaches to Diagnosis and Management.
Review in HemaSphere, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Mexican position paper for the diagnosis and treatment of cardiac amyloidosis.Archivos de cardiologia de Mexico · 2024Guideline
- Mechanisms of damage and therapies for cardiac amyloidosis: a role for inflammation?Clinical research in cardiology : official journal of the German Cardiac Society · 2026Review
- Concurrence of renal amyloidosis and membranous nephropathy: a case series and literature review.BMC nephrology · 2026Review
- Diagnostic challenge of systemic amyloidosis mimicking EGFR-TKI toxicity in lung adenocarcinoma: a case report.Translational lung cancer research · 2025Article
- Proving Bone Marrow Plasma Cell Clonality by Flow Cytometry: An Important Tool in the Diagnosis of Immunoglobulin Light-Chain Amyloidosis.Biomedicines · 2025Article
- Beyond NT-proBNP and troponin: How machine learning redefines light-chain cardiac amyloidosis risk assessment.BMC medical informatics and decision making · 2025Article
- Article
- Light Chain (AL) Amyloidosis Masquerading as Scleroderma: A Diagnostic Challenge.Journal of hematology · 2025Article
- Diagnostic pathways, cardiac manifestations and outcomes in light chain amyloidosis: analysis of a US claims database.Open heart · 2025Article
- Hepatic amyloidosis in a patient with chronic liver failure: A case report.World journal of clinical cases · 2024Article
- A review of recent clinical trials to evaluate disease-modifying therapies in the treatment of cardiac amyloidosis.Frontiers in medicine · 2024Review
- Diagnosis for Chinese patients with light chain amyloidosis: a scoping review.Annals of medicine · 2023Article
- Proteinase 3 Antibody and Anti-Double-Stranded DNA in a Patient With Immunoglobin Light Chain Amyloidosis.Cureus · 2023Article
- Article
- Clinical effects of tranexamic acid on bleeding tendency due to fibrinolytic activation of AL amyloidosis.BMJ case reports · 2023Article
- Diagnostic Challenges and Solutions in Systemic Amyloidosis.International journal of molecular sciences · 2023Review
- Bad players in AL amyloidosis in the current era of treatment.Expert review of hematology · 2023Article
- Article
- AL Amyloidosis for Cardiologists: Awareness, Diagnosis, and Future Prospects:JACC. CardioOncology · 2022Review
- Practice of Multidisciplinary Collaborative Chain Management Model in Constructing Nursing Path for Acute Trauma Treatment.Emergency medicine international · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AL amyloidosis is characterized by a low-level expansion of an indolent, small plasma cell clone that produces amyloidogenic light chains. Amyloid aggregates or preceding intermediaries cause direct cell damage through their proteotoxicity, and amyloid deposits distort tissue architecture, and, eventually, lead to organ impairment. It is a rare, underdiagnosed disease with a diverse clinical presentation depending on the organ tropism of the amyloid fibrils; cardiac and renal involvement is most common, but any organ can be affected, excluding the central nervous system. A high level of awareness and a systematic approach using newly emerging screening biomarkers is required to achieve early diagnosis. Management should be multidisciplinary as supportive management tailored to management of organ dysfunction is paramount to survival and minimization of treatment-associated toxicity. The initial therapeutic aim is to rapidly eliminate the clonal plasma cell that produces the circulating amyloid precursor and achieve a complete hematologic response, and if possible with undetectable minimal residual disease as assessed by next-generation methods (flow and sequencing), with minimal toxicity. Treatment is tailored to the initial risk assessment of the patients. Treatments are based on regimens adapted from the expanding options that are available for multiple myeloma patients and hematological response rates have improved. Organ response rates are strongly associated with deeper hematologic response but usually lag behind hematological response and are also dependent on the initial organ function reserve. Agents directed against the amyloid deposits have been explored to aid amyloid clearance and improve organ function, but data are still negative.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.