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Updated: Feb 13, 2026

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Light Chain Amyloidosis.

Paolo Milani1, Giampaolo Merlini1, Giovanni Palladini1

  • 1Amyloidosis Research and Treatment Center, Foundation "Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Policlinico San Matteo" and Department of Molecular Medicine, University of Pavia, Pavia, Italy.

Mediterranean Journal of Hematology and Infectious Diseases
|March 14, 2018
PubMed
Summary
This summary is machine-generated.

Light chain (AL) amyloidosis involves amyloidogenic light chains misfolding and damaging organs. Risk-adapted chemotherapy and novel therapies offer improved treatment strategies for this plasma cell disorder.

Keywords:
amyloidosisdiagnosislight chainsresponsetherapy

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Area of Science:

  • Hematology
  • Oncology
  • Nephrology

Background:

  • Light chain (AL) amyloidosis stems from plasma cell clones producing amyloidogenic light chains.
  • These proteins misfold, aggregate into amyloid fibrils, and deposit in tissues, causing irreversible organ damage.
  • Cardiac involvement is a critical determinant of prognosis in AL amyloidosis.

Purpose of the Study:

  • To review current treatment strategies for light chain (AL) amyloidosis.
  • To discuss risk-adapted therapies based on organ involvement and patient risk stratification.
  • To highlight emerging therapeutic approaches targeting amyloid deposits and the underlying plasma cell clone.

Main Methods:

  • Review of current chemotherapy regimens, including bortezomib-based treatments and autologous stem cell transplant.
  • Evaluation of novel agents in the relapsed/refractory setting and their move to upfront therapy.
  • Exploration of antibody-based and small molecule therapies targeting amyloidogenesis.

Main Results:

  • Risk-adapted chemotherapy is essential, with autologous stem cell transplant for low-risk patients.
  • Bortezomib-based regimens are standard for intermediate and high-risk patients.
  • Emerging therapies show promise as complements to standard chemotherapy, with ongoing clinical trials.

Conclusions:

  • Treatment for AL amyloidosis requires a risk-adapted approach targeting the plasma cell clone.
  • Novel therapeutic strategies, including antibodies and small molecules, are expanding treatment options.
  • Advances in understanding cardiac damage and clone characteristics pave the way for potential cures.