Light-Chain Amyloidosis

Other names
Types
Causes
Common symptoms
Diagnostic tests
Non-pharmacological treatments
Drug treatments
Dietary molecular supplements
Regenerative / stem-cell–related
Surgeries / procedures
Preventions
When to see doctors urgently
What to eat — and what to avoid
FAQs

Light-chain amyloidosis—often shortened to AL amyloidosis—is a disease where abnormal proteins called light chains are made by a small group of blood cells (plasma cells or some B-cells). These light chains misfold. When they misfold, they stick together and form long fibers called amyloid. The amyloid fibers deposit in body tissues—for example in the heart, kidneys, nerves, liver, gut, skin, and tongue. These deposits do not belong there. They stiffen and damage the organ. Over time, the organ cannot work well.

Light-chain amyloidosis is a disease in which an abnormal group of plasma cells in the bone marrow makes misfolded immunoglobulin light chains. These light chains circulate in the blood, then stick together as amyloid fibrils and deposit in organs such as the heart, kidneys, liver, nerves, and gut. The deposits make organs stiff and weak, so they cannot do their jobs well. Because the source is a small plasma-cell clone, modern therapy targets both the clone (to stop new amyloid) and the organs (to protect and support them). ASH Publications

AL amyloidosis is not an infection. It is not “just inflammation.” It happens because there is a clone (a small group) of cells in the bone marrow that makes too many abnormal light chains. Sometimes that clone is related to multiple myeloma or another B-cell blood disease, but in many people it is smaller and only shows up as an abnormal protein in the blood or urine.

Doctors confirm AL amyloidosis by taking a tiny piece of tissue (often belly fat, sometimes the affected organ), staining it with Congo red dye, and looking under a special light (polarized light). True amyloid shows a green glow (called apple-green birefringence). Then the lab must type the amyloid to prove it is light-chain type (and not another kind like ATTR). Correct typing guides treatment.

This disease often involves more than one organ, but one organ may dominate (for example, heart-dominant or kidney-dominant disease). Symptoms build slowly at first (tiredness, swelling), and later can become serious (heart failure, kidney failure, nerve damage). Early diagnosis and treatment of the plasma-cell clone can slow or stop new amyloid from forming and improve outcomes.

Other names

AL amyloidosis
Primary systemic amyloidosis (older term)
Immunoglobulin light-chain amyloidosis
Monoclonal light-chain amyloidosis

(All of these mean the same core problem: misfolded immunoglobulin light chains forming amyloid deposits.)

Types

By the protein subtype
The light chain can be lambda (λ) or kappa (κ). Lambda is more common in AL. This detail matters for lab tests and sometimes for biology, but treatment targets the cell clone, not a specific letter.
By how widespread it is
- Systemic AL amyloidosis: Most people have this. Amyloid deposits are found in more than one organ.
- Localized AL amyloid: Rare. Deposits are limited to a single area (for example, the larynx, airway, or skin). Localized disease behaves differently and is often treated locally.
By the main organ involved
- Cardiac-dominant AL: Heart walls get stiff; people get shortness of breath, leg swelling, low blood pressure, and abnormal heart rhythms.
- Renal-dominant AL: Kidneys leak protein (foamy urine) and cause swelling; kidney function may drop.
- Neuropathy-dominant AL: Numbness, tingling, pain, and autonomic symptoms like dizziness on standing or gut problems.
- Hepatic-dominant AL: Liver enlargement, abnormal liver tests, and fullness.
- Gastrointestinal/soft-tissue AL: Diarrhea or constipation, weight loss, macroglossia (big tongue), bruising, carpal tunnel.
By the associated clone
- Non-IgM AL (plasma-cell clone): The commonest form; related to MGUS, smoldering myeloma, or myeloma.
- IgM AL (B-cell/LPL/WM clone): Less common; the abnormal cell is a lymphoplasmacytic cell (seen in Waldenström macroglobulinemia-type biology).
By treatment status
- Newly diagnosed
- Relapsed or refractory (the clone returns or does not respond; doctors then change therapy)

Causes

Important note: In AL amyloidosis the true “cause” is a monoclonal clone making misfolded light chains. Many items below are underlying conditions or risk contributors that lead to or are associated with that clone. I list them plainly so the pathway is easy to understand.

Monoclonal gammopathy of undetermined significance (MGUS)
A small plasma-cell clone makes a monoclonal protein without symptoms. In a small share of people, this clone evolves and begins to produce amyloid-forming light chains, leading to AL.
Smoldering multiple myeloma (SMM)
A larger plasma-cell clone than MGUS, but still without classic myeloma organ damage. The clone can produce abundant light chains that form amyloid.
Multiple myeloma (MM)
A cancer of plasma cells. Some patients with myeloma produce amyloidogenic light chains, so AL and myeloma can co-exist.
Waldenström macroglobulinemia / lymphoplasmacytic lymphoma (IgM clones)
Less common, but IgM-related clones can secrete light chains that cause AL, often with somewhat different organ patterns.
Other B-cell non-Hodgkin lymphomas that secrete light chains
Rarely, a B-cell lymphoma (such as marginal zone lymphoma or CLL) can produce a monoclonal light chain that forms amyloid.
Solitary plasmacytoma (secretory)
A single plasma-cell tumor may secrete light chains. If those light chains are amyloid-forming, AL can occur.
Post-transplant lymphoproliferative disorders (PTLD)
After solid-organ or stem-cell transplant, immunosuppression can allow a B-cell clone to expand and secrete monoclonal light chains, rarely causing AL.
Chronic antigen stimulation driving B-cell clones
Long-standing stimulation (from chronic infection or immune activation) can select for a clone that makes a monoclonal light chain. This is uncommon, but it explains some cases.
Hepatitis C-associated monoclonal gammopathy (rare link)
Hepatitis C can drive B-cell clones and cryoglobulins. In rare cases, a light-chain monoclonal protein emerges and may lead to AL.
Age-related clonal hematopoiesis and plasma-cell expansion
With older age, small clones are more common. This increases the chance that a clone will produce amyloid-forming light chains.
Genetic features of the light chain
Some light-chain variable region sequences are more amyloid-prone. This is a molecular cause inside the protein itself.
Family history of plasma-cell disorders
Families with more MGUS/myeloma suggest inherited susceptibility to clonal plasma-cell growth, which can raise AL risk indirectly.
Male sex (epidemiologic pattern)
AL is more common in men. This is a population pattern, not a direct cause, but it reflects how plasma-cell clones are distributed.
African or African-diaspora ancestry (risk of plasma-cell disorders)
Some groups have a higher baseline rate of MGUS/myeloma, which can increase the pool of people at risk for AL. (This is about population risk, not destiny.)
Radiation or certain chemical exposures (limited evidence)
Studies suggest possible links between occupational exposures (like certain solvents) and plasma-cell disorders, which could indirectly raise AL risk.
Obesity and metabolic factors (population association)
Obesity has been tied to higher myeloma risk in population data. By increasing plasma-cell disorders, it may indirectly raise AL risk.
Long-term immunosuppression
Suppressed immune surveillance can permit clonal B-cell/plasma-cell growth, increasing the chance of a monoclonal light chain.
Autoimmune diseases with secondary clonal expansions
Some autoimmune settings are associated with MGUS or lymphomas. Very rarely, the resulting light chain is amyloid-forming.
Chronic kidney disease (CKD) with reduced light-chain clearance
CKD does not cause AL, but reduced clearance can raise circulating light-chain levels, which may worsen amyloid deposition when a clone is present.
Prior plasma-cell disorder therapy with surviving resistant clones
After treatment for a plasma-cell disease, resistant subclones can remain and later produce amyloid-forming light chains, leading to relapsed AL.

Common symptoms

Tiredness and low energy
The body spends energy fighting organ stress. Anemia and heart or kidney strain also cause fatigue.
Unintentional weight loss
People may lose weight because the body is under stress, appetite is low, or the gut does not absorb food well.
Swelling of feet and ankles
Kidneys leak protein into urine. Low blood protein lets fluid move into tissues, causing pitting edema.
Foamy urine
Extra protein in urine makes bubbles or foam. This is a classic kidney sign.
Shortness of breath on effort
Stiff heart muscle fills poorly and pumps less forward blood. Lungs can also collect fluid, making breathing hard.
Dizziness or fainting when standing
Amyloid can damage autonomic nerves. Blood pressure drops when standing (orthostatic hypotension).
Numbness, tingling, or burning pain in feet and hands
Peripheral nerves are injured by amyloid, causing neuropathy that often starts in the feet.
Wrist pain or nighttime hand tingling (carpal tunnel)
Amyloid in the wrist tunnel squeezes the median nerve, causing numbness and weak grip.
Irregular heartbeat or palpitations
The heart’s electrical system can be disturbed, causing skipped beats or fast rhythms.
Large tongue (macroglossia)
The tongue can enlarge and feel firm. People may snore, lisp, or have bite marks on the sides.
Easy bruising, especially around the eyes
Weak blood vessel support from amyloid leads to purpura, often in the eyelids (“raccoon eyes”).
Early fullness, bloating, or bowel changes
Amyloid can stiffen the stomach and intestines, slowing movement and causing diarrhea or constipation.
Loss of appetite and nausea
Gut involvement, liver stress, or medicines can reduce appetite and cause nausea.
Right upper belly fullness from liver enlargement
The liver may grow and feel heavy or uncomfortable, and lab tests may rise.
Sexual dysfunction
Autonomic nerve damage can lead to erectile dysfunction or less arousal.

Diagnostic tests

A) Physical examination

General exam for weight, color, and muscle bulk
Doctors look for weight loss, pale skin (anemia), and muscle wasting, which suggest chronic illness.
Skin and eyelid check for easy bruising and “pinch purpura”
Gentle pressure may cause purple spots. This happens because amyloid weakens small vessels.
Tongue and mouth inspection
A firm, enlarged tongue with tooth indentations suggests macroglossia, a classic AL sign.
Heart and fluid status exam
A raised neck vein, soft heart sounds, leg edema, and lung crackles point to stiff-heart failure from cardiac amyloid.

B) Manual/bedside tests

Orthostatic blood pressure test
Measure BP lying down and then standing. A drop with symptoms means autonomic neuropathy.
Pitting-edema check at the ankles
Press the skin over the shin or ankle. A lasting dent shows fluid overload, often from kidney or heart involvement.
Phalen and Tinel maneuvers for carpal tunnel
Wrist bending or tapping causes tingling in the fingers if the median nerve is compressed by amyloid.

C) Laboratory and pathological tests

Serum protein electrophoresis with immunofixation (SPEP/IFE)
Finds a monoclonal protein (“M-spike”) or a faint band. Immunofixation tells which immunoglobulin and light chain.
Urine protein electrophoresis with immunofixation (UPEP/IFE)
Detects light chains in urine (Bence Jones protein). Important when the blood test looks normal but urine is positive.
Serum free light-chain (sFLC) assay and κ/λ ratio
Measures free κ and λ light chains. An abnormal ratio supports a light-chain-secreting clone.
24-hour urine protein (or spot albumin/creatinine ratio)
Quantifies how much protein the kidneys are losing, which helps stage kidney involvement.
Basic labs: CBC, kidney and liver panels, electrolytes, albumin
Show anemia, creatinine rise, liver test changes, and low albumin from heavy protein loss.
Cardiac biomarkers: NT-proBNP and troponin
These rise when the heart is stressed or damaged. They help stage cardiac AL and track response.
Abdominal fat-pad fine-needle aspirate with Congo red stain
A quick, low-risk test that often shows amyloid with apple-green birefringence under polarized light.
Bone-marrow biopsy with plasma-cell studies
Measures percent plasma cells, looks for clonal markers, and may show Congo-red-positive deposits. FISH/genetic studies help risk-stratify the clone.
Definitive amyloid typing (mass spectrometry or immunohistochemistry)
Proves the amyloid is AL (light chain) and not another type (like ATTR). Correct typing is essential before treatment.

D) Electrodiagnostic tests

12-lead electrocardiogram (ECG)
May show low voltage, pseudoinfarct patterns, conduction blocks, or atrial fibrillation. These patterns hint at cardiac amyloid.
Nerve conduction studies and EMG
Confirm length-dependent neuropathy and carpal-tunnel involvement. Helpful when numbness or pain is a major complaint.

E) Imaging tests

Transthoracic echocardiography (heart ultrasound)
Shows thick but stiff heart walls, small cavity, diastolic dysfunction, and sometimes speckled appearance. Strain imaging may show apical sparing, a clue to amyloid.
Cardiac MRI with late gadolinium enhancement and T1 mapping
Very sensitive for infiltrative cardiomyopathy. It shows diffuse uptake and abnormal tissue signals consistent with amyloid infiltration.

Non-pharmacological treatments

Each item lists a brief description, purpose, and mechanism/how it helps.

Salt restriction & fluid awareness
Description: Limit salt (often 1.5–2 g/day) and watch daily fluid intake if you have heart or kidney involvement.
Purpose: Reduce swelling and breathlessness.
Mechanism: Less sodium lowers water retention and venous congestion, easing strain on the heart and kidneys. jhltopen.org
Daily weights & edema self-check
Description: Weigh yourself at the same time daily; track ankle/abdominal swelling.
Purpose: Catch fluid build-up early.
Mechanism: Small weight jumps often mean fluid retention; early diuretic adjustment can prevent admissions. jhltopen.org
Compression stockings (class II–III) & leg elevation
Description: Wear graded stockings; elevate legs above heart when resting.
Purpose: Reduce edema and orthostatic symptoms.
Mechanism: Improves venous return and reduces pooling in the legs. AAFP
Slow postural changes & counter-maneuvers
Description: Rise slowly; perform calf pumps or leg-cross/hand-grip before standing.
Purpose: Ease orthostatic hypotension (drop in BP on standing).
Mechanism: Increases venous return and autonomic compensation. Cleveland Clinic Journal of Medicine
Small, frequent meals
Description: Eat smaller portions more often; avoid large, high-carb meals.
Purpose: Prevent post-meal blood-pressure drops and bloating.
Mechanism: Large meals divert blood to the gut and worsen hypotension. AAFP
Exercise that is symptom-guided
Description: Gentle aerobic activity and light resistance, supervised when cardiac involvement exists.
Purpose: Maintain strength without overtaxing the heart.
Mechanism: Preserves conditioning and reduces deconditioning; avoid strain in restrictive cardiomyopathy. jhltopen.org
Sleep with head-of-bed elevation
Description: Raise the head of your bed 10–20 cm.
Purpose: Reduce nocturnal cough, reflux, and nocturnal hypertension in autonomic dysfunction.
Mechanism: Decreases venous return and reflux at night. AHA Journals
Medication review to avoid problematic drugs
Description: Avoid or minimize digoxin and most non-dihydropyridine calcium-channel blockers in cardiac AL; avoid NSAIDs if kidneys are involved.
Purpose: Prevent toxicity and worsening heart/kidney function.
Mechanism: Amyloid binds digoxin (risk of toxicity); CCBs often poorly tolerated in amyloid hearts; NSAIDs reduce renal blood flow. jhltopen.org
Vaccinations (flu, COVID-19, pneumococcal, shingles when appropriate)
Description: Keep up to date per CDC/ACIP guidance; ideally before or between chemo cycles.
Purpose: Lower infection risk while immunosuppressed.
Mechanism: Promotes protective antibodies against respiratory and VZV infections. CDC+2CDC+2
Antiviral prevention with certain therapies
Description: If you receive bortezomib-based therapy, your team often prescribes low-dose acyclovir/valacyclovir.
Purpose: Prevent shingles.
Mechanism: Suppresses varicella-zoster reactivation during proteasome-inhibitor therapy. PMC+1
Foot care and nerve protection
Description: Check feet daily; wear cushioned shoes; protect from burns.
Purpose: Limit injury if you have numbness/neuropathy.
Mechanism: Prevents ulcers and infections while sensation is reduced. Myeloma UK
Dietary pattern rich in plants, lean protein, and adequate calories
Description: Focus on fresh foods; avoid ultra-processed, very salty items.
Purpose: Maintain weight and muscle; support healing.
Mechanism: Adequate protein/energy counters catabolism from illness/therapy. jhltopen.org
Anemia & bone-health support (as advised by your team)
Description: Correct iron/B12/folate/Vit-D deficiencies when present.
Purpose: Improve energy and reduce fracture risk.
Mechanism: Replacing true deficiencies improves oxygen delivery and bone strength. (General hematology guidance.)
Sleep apnea screening
Description: If snoring/daytime sleepiness occur, get tested.
Purpose: Reduce nightly hypoxia and cardiac strain.
Mechanism: Treating OSA improves quality of life and heart outcomes. (General cardiology guidance.)
Fall-prevention plan
Description: Remove trip hazards; use night lights; physical therapy for balance.
Purpose: Reduce injury with neuropathy or orthostatic hypotension.
Mechanism: Lowers fall and fracture risk. AAFP
Palliative care early (symptom-focused)
Description: Add a symptom-care team alongside active treatment.
Purpose: Control breathlessness, pain, anxiety; plan goals.
Mechanism: Multidisciplinary support improves comfort and decision-making. (Oncology best practice.)
Stress, mood, and social-support therapy
Description: Counseling, support groups, mindfulness.
Purpose: Ease distress from a chronic, multi-organ disease.
Mechanism: Reduces sympathetic overdrive; improves adherence and coping. (Oncology best practice.)
Careful travel and heat planning
Description: Avoid prolonged standing/heat; hydrate wisely.
Purpose: Prevent hypotension episodes.
Mechanism: Heat and dehydration worsen pooling and low BP. AAFP
Regular dental and skin care
Description: Keep mucosa/skin healthy during steroid/chemo therapy.
Purpose: Reduce infections.
Mechanism: Fewer portals for bacteria when immune defenses are low. (Oncology best practice.)
Written action plan
Description: Know when to call for weight gain, low BP, fever, chest pain, shortness of breath, or new swelling.
Purpose: Speedy care for flares or complications.
Mechanism: Early intervention prevents severe decompensation. (Oncology/cardiology best practice.)

Drug treatments

Below are the commonly used, evidence-supported options. Exact choices, doses, and timing are individualized by your hematology/amyloidosis team.

Daratumumab + CyBorD (cyclophosphamide–bortezomib–dexamethasone)
Class: Anti-CD38 monoclonal antibody + chemotherapy/proteasome inhibitor/steroid.
Typical schedule: Daratumumab SC 1,800 mg: weekly (cycles 1–2), every 2 weeks (cycles 3–6), then every 4 weeks up to ~2 years; bortezomib 1.3 mg/m² SC + cyclophosphamide 300 mg/m² weekly + dexamethasone weekly for 6 cycles (28-day cycles).
Purpose: Current standard of care for most newly diagnosed patients not going directly to transplant; rapidly shuts down the light-chain–producing clone and improves organ responses.
Mechanism: Daratumumab kills CD38-positive plasma cells; bortezomib blocks the proteasome; cyclophosphamide is cytotoxic; dexamethasone is lymphotoxic/anti-inflammatory.
Key side effects: infusion-related reactions (less with SC), infections, neuropathy (bortezomib), cytopenias, fluid retention (steroids). New England Journal of Medicine+2PMC+2
High-dose melphalan with autologous stem-cell transplant (ASCT)
Class: Alkylating agent + stem-cell rescue (a procedure with chemotherapy).
Dose: Melphalan 200 mg/m² (often reduced to 140 mg/m² in older/frailer or organ-involved patients).
Purpose: Deep, durable clonal responses in carefully selected, fit patients (often younger, limited cardiac involvement).
Mechanism: High-dose cytotoxic therapy wipes out the clone; reinfused stem cells restore marrow function.
Side effects: Mucositis, cytopenias, infection risk; transplant-related morbidity requires expert center. ASTCT Journal+2ASH Publications+2
Bortezomib–cyclophosphamide–dexamethasone (CyBorD) without daratumumab
Class: PI + alkylator + steroid.
Use: Alternative frontline when anti-CD38 cannot be used.
Notes: Add antiviral prophylaxis to prevent shingles during PI therapy. PMC
Lenalidomide-based regimens (e.g., Rd or with cyclophosphamide/bortezomib)
Class: IMiD (immunomodulatory drug).
Use: Relapsed disease or intolerance to first-line; slower organ responses and more fluid retention—used carefully in cardiac AL.
Mechanism/side effects: Immune and anti-angiogenic effects; cytopenias, rash, VTE risk (consider anticoagulation prophylaxis as appropriate). (Hematology reviews.)
Pomalidomide-based regimens
Class: IMiD (later generation).
Use: Relapsed/refractory AL after lenalidomide/bortezomib; monitor for edema and cytopenias. (Hematology reviews.)
Ixazomib-based therapy
Class: Oral proteasome inhibitor.
Use: Selected relapsed patients; oral option where bortezomib neuropathy is problematic. (Hematology reviews.)
Carfilzomib combinations (careful in cardiac AL)
Class: PI (epoxyketone).
Use: Later-line; may cause/worsen cardiac events—used with caution in amyloid cardiomyopathy. (Hematology reviews.)
Dexamethasone (as a core component)
Class: Corticosteroid.
Use: Part of most regimens.
Notes: Can cause fluid retention, mood changes, high glucose; doses often adjusted in cardiac involvement. (Hematology practice.)
Alkylators beyond melphalan (e.g., bendamustine)
Use: Relapsed disease options; dose-adjust in organ dysfunction. (Hematology reviews.)
Venetoclax (especially for t(11;14) AL)
Class: BCL-2 inhibitor (targeted therapy).
Use: Off-label but increasingly used in t(11;14) AL with strong activity; often 200–400 mg/day with careful step-up and monitoring, in combination regimens; infection prophylaxis is important.
Evidence: Multiple series and conference updates show deep hematologic responses in t(11;14) AL. PMC+2PMC+2
Doxycycline (adjunct, case-based)
Class: Tetracycline antibiotic used off-label as fibril-disrupting adjunct.
Use: Sometimes added after transplant or with chemotherapy in cardiac AL; evidence mixed; best within trials/center protocols.
Mechanism: May help disaggregate amyloid fibrils in vitro; clinical data are suggestive but not definitive. Nature+1
Amiodarone for atrial arrhythmias
Class: Antiarrhythmic.
Use: Rhythm control in cardiac AL when needed; monitor thyroid/liver.
Note: Anticoagulation is usually recommended if AF occurs because thrombus risk is high in amyloidosis, even when CHA₂DS₂-VASc is low. American College of Cardiology+1
Diuretics (e.g., loop diuretics ± spironolactone)
Class: Heart-failure symptom control.
Use: Treat congestion/edema; careful dose titration with daily weights.
Mechanism: Increase salt and water excretion; cornerstone for cardiac/renal involvement. jhltopen.org
Midodrine
Class: Alpha-agonist for orthostatic hypotension.
Use: Raises standing BP and reduces dizziness; risk of supine hypertension. AAFP+1
Droxidopa
Class: Norepinephrine pro-drug.
Use: Alternative to midodrine; improves standing BP with lower risk of supine hypertension in meta-analyses. PMC+1
Fludrocortisone (select cases)
Class: Mineralocorticoid.
Use: Expands plasma volume in autonomic failure; watch for edema, low potassium. AAFP
Neuropathic-pain agents (duloxetine, gabapentin/pregabalin)
Class: SNRI/anticonvulsants.
Use: Relieve burning/numb pain from small-fiber or axonal neuropathy.
Evidence: First-line for neuropathic pain in general; choice guided by comorbidities. ScienceDirect
Anticoagulants (DOACs or VKAs) when AF or atrial thrombus risk is present
Use: Stroke prevention; amyloidosis carries high thrombus risk, and DOACs perform at least as well as warfarin in analyses.
Mechanism/notes: Prevent clots in low-flow, stiff atria; consider TEE if rhythm control; follow bleeding risk carefully. PMC+1
Prophylactic antivirals with proteasome inhibitors
Class: Acyclovir/valacyclovir.
Use: Prevent shingles during bortezomib therapy. PMC
Infection prophylaxis as indicated (e.g., PJP prophylaxis with high-dose steroids, vaccines as above)
Use: Reduce serious infections while on therapy. ASCO Publications

Important cautions in cardiac AL: Avoid digoxin and most non-dihydropyridine calcium-channel blockers when possible; they may be poorly tolerated or risky in amyloid hearts. Manage heart failure mainly with diuretics; ACE/ARB/β-blockers are often less helpful due to low stroke volume and hypotension. jhltopen.org

Dietary molecular supplements

These do not treat the plasma-cell clone. They may support general health or specific symptoms; use only with your clinicians, because interactions with chemo can be serious.

Vitamin D (e.g., 800–2,000 IU/day if deficient)
Function: Bone and muscle support; fracture prevention with steroids/immobility.
Mechanism: Improves calcium balance and bone mineralization. (General endocrine consensus.)
Omega-3 fish oil (e.g., 1 g/day EPA+DHA)
Function: Heart and lipid support; anti-inflammatory effects.
Mechanism: Modulates eicosanoids and membrane function. (Cardio-metabolic data.)
Thiamine (vitamin B1) if low or on high-dose diuretics
Function: Energy metabolism.
Mechanism: Repletes water-soluble vitamin lost with diuresis. (Heart-failure nutrition guidance.)
Vitamin B12 (per deficiency)
Function: Nerve health and red-cell production.
Mechanism: Cofactor for myelin and DNA synthesis. (Neurology/hematology guidance.)
Magnesium (for cramps; adjust for kidney function)
Function: Muscle/nerve stability.
Mechanism: Normalizes neuromuscular excitability. (General.)
Alpha-lipoic acid (e.g., 300–600 mg/day) — for neuropathic symptoms
Function: Antioxidant; used in diabetic neuropathy; evidence in AL is extrapolated.
Mechanism: Redox modulation; may reduce burning pain. (Neuropathy literature.)
Coenzyme Q10 (e.g., 100–200 mg/day) — optional
Function: Mitochondrial cofactor; sometimes used in heart failure; evidence is limited in AL.
Mechanism: Electron transport support. (Cardiology supplements literature.)
Probiotic foods (yogurt/kefir) if tolerated
Function: Gut health during antibiotics/chemo.
Mechanism: Supports microbiome balance. (GI supportive care.)
Protein supplement if under-nourished
Function: Maintain lean mass during therapy.
Mechanism: Provides essential amino acids for repair. (Oncology nutrition.)
Electrolyte solutions (low-sugar) during diuretic titration/heat
Function: Prevent symptomatic hypotension/dehydration.
Mechanism: Replenishes sodium/potassium thoughtfully. (Orthostatic hypotension care.)

Avoid green-tea extracts (EGCG) and certain flavonoid megadoses around bortezomib, because they can chemically block the drug’s proteasome-inhibiting action. Also avoid grapefruit products with many cancer drugs due to CYP interactions. Always run supplements by your team. PMC+2Drugs.com+2

Regenerative / stem-cell–related

These are not miracle regeneration pills. In AL, “regenerative/stem-cell” therapy mainly refers to mobilizing your own stem cells and supporting blood-cell recovery around transplant or chemotherapy.

Filgrastim (G-CSF)
Dose: Typical mobilization 10 µg/kg/day SC for several days (center-specific).
Function: Mobilizes stem cells from marrow to blood for collection; speeds neutrophil recovery.
Mechanism: Stimulates neutrophil/precursor proliferation and release. (Transplant standards.)
Plerixafor
Dose: Often 0.24 mg/kg SC before apheresis (center protocol).
Function: Boosts stem-cell mobilization when G-CSF alone is inadequate.
Mechanism: CXCR4 antagonist releases stem cells from marrow niches. (Transplant standards.)
High-dose melphalan (conditioning) before ASCT
Function: Eradicates plasma-cell clone; “makes space” for stem-cell rescue.
Mechanism: Alkylates DNA; the reinfused autologous stem cells then re-seed healthy marrow. ASTCT Journal
Erythropoiesis-stimulating agents (epoetin/darbepoetin) — selective use
Function: Help symptomatic chemotherapy-related anemia when appropriate.
Mechanism: Stimulates RBC production; use per oncology guidelines (after correcting iron/B12/folate). (Oncology guidance.)
IVIG (intravenous immunoglobulin) — in hypogammaglobulinemia with recurrent infections
Function: Passive antibody replacement if serious infections occur, usually post-therapy.
Mechanism: Provides broad IgG pool. (Hematology practice.)
Thrombopoietin-receptor agonists (eltrombopag/romiplostim) — selected cases
Function: Support platelets if severe, persistent thrombocytopenia limits therapy (specialist decision).
Mechanism: Stimulates megakaryocytes; used cautiously. (Hematology practice.)

Surgeries / procedures

Autologous Stem-Cell Transplant (ASCT)
Procedure: Collect your stem cells (apheresis) after G-CSF ± plerixafor; give high-dose melphalan; reinfuse stem cells.
Why: Offers deep clonal responses and can extend survival in carefully selected patients treated at experienced centers. ASTCT Journal
Heart transplantation (selected patients with advanced cardiac AL)
Procedure: Orthotopic heart transplant at expert centers, often followed by anti-plasma-cell therapy (and sometimes later ASCT) to control the clone.
Why: For end-stage restrictive cardiomyopathy when other options cannot stabilize the patient; chosen centers report improved survival in selected cases. ScienceDirect
Kidney transplantation
Procedure: Deceased or living-donor transplant when renal failure occurs and the plasma-cell clone is well controlled.
Why: Restores kidney function and quality of life; recurrence risk exists but is acceptable with good hematologic control. AMJ Transplant
Permanent pacemaker
Procedure: Device implanted for conduction disease (e.g., AV block) causing bradycardia/syncope.
Why: Conduction problems are common in cardiac amyloidosis; pacemakers treat slow rhythms, though they don’t cure amyloid. PubMed+1
(Selected) Implantable cardioverter-defibrillator (ICD)
Procedure: Shock device for dangerous ventricular arrhythmias.
Why: Considered for standard indications, but overall survival benefit is uncertain in amyloidosis because many deaths are not due to shockable rhythms. Decision is individualized. JACC+1

Preventions

Control salt, track weight, and act early on fluid gain. jhltopen.org
Keep vaccines current (flu, COVID-19, pneumococcal; shingles as appropriate). CDC+1
Use antiviral prophylaxis during proteasome-inhibitor therapy. PMC
Prevent falls: slow standing, handrails, good lighting, stable shoes. AAFP
Review meds for amyloid-unsafe drugs (digoxin, some CCBs) and for interactions. jhltopen.org
Avoid green-tea extracts and grapefruit when on bortezomib-based therapy unless your team says it’s safe. PMC+1
Treat sleep apnea if present; protect sleep. (Cardiology best practice.)
Practice meticulous foot/skin care to prevent infections. Myeloma UK
Manage stress and maintain social support; consider counseling. (Oncology best practice.)
Keep a written plan for when to call your team (fever, chest pain, rapid weight gain, fainting, new swelling). (Oncology best practice.)

When to see doctors urgently

New or worsening shortness of breath, chest pain, fainting, or palpitations.
Rapid weight gain (e.g., >1 kg in 24 hours) or sudden leg/abdominal swelling.
Fever ≥38°C, chills, or suspected infection during treatment.
Severe dizziness on standing that does not improve with simple measures.
New numbness/weakness, sudden vision or speech changes.
Any bleeding you cannot easily stop or black/tarry stools.
In amyloidosis—especially with heart involvement—problems escalate fast, so low-threshold contact with your team is wise. (Standard oncology/cardiology safety guidance.)

What to eat — and what to avoid

Eat more of:

Fresh, low-salt foods: home-cooked vegetables, fruits, whole grains.
Lean protein: fish, poultry, eggs, tofu, lentils—support healing.
Healthy fats: olive oil; nuts/seeds (portion-controlled).
Adequate fluids (as advised by your team), distributed through the day.
Probiotic foods (yogurt/kefir) if tolerated.

Avoid or limit:

High-salt/processed foods (chips, instant noodles, canned soups, deli meats).
Very large meals (favor smaller, frequent meals to protect BP). AAFP
Alcohol (can worsen hypotension and interact with medicines).
Green-tea extracts and grapefruit during certain therapies (see interaction warning). PMC+1
Unproven “cure” supplements—always clear any supplement with your oncology team first.

FAQs

1) Is AL amyloidosis a cancer?
It comes from a small clone of plasma cells, similar to myeloma but usually smaller. We treat it with anti-myeloma–type drugs and sometimes stem-cell transplant. ASH Publications

2) What is the main goal of treatment?
Two goals: stop new amyloid by turning off the plasma-cell clone, and support/repair organs so they can work better. ASH Publications

3) What is the current first-line regimen?
Most patients receive daratumumab + CyBorD, which improved responses and outcomes compared with CyBorD alone. New England Journal of Medicine+1

4) Who should get a transplant (ASCT)?
Fit patients with limited cardiac involvement may benefit. Transplant decisions are made at experienced centers after careful risk assessment. ASTCT Journal

5) If I have heart involvement, which heart drugs work best?
Diuretics are the cornerstone. Digoxin and some calcium-channel blockers can be risky and are often avoided. jhltopen.org

6) Do I need blood thinners if I have AF?
Amyloidosis increases atrial-thrombus risk, so anticoagulation is usually recommended with AF and may be considered based on imaging/risk even when scores look low. DOACs perform at least as well as warfarin in analyses. PMC+1

7) Can amyloid deposits be removed from organs?
Some investigational antibodies (e.g., CAEL-101) aim to clear deposits; phase 3 trials are ongoing. Today’s routine care focuses on stopping new amyloid and letting organs recover. MedPath

8) Is there a targeted pill for my specific genetics?
If your plasma cells carry t(11;14), venetoclax (off-label) may work well; ask about trials or specialist use. PMC

9) Will nerves get better?
If treatment stops new amyloid, nerve symptoms may stabilize or slowly improve; pain medicines and safety steps help in the meantime. Myeloma UK

10) Are “natural” supplements safe?
Not always. Green-tea extracts (EGCG) can block bortezomib, and grapefruit alters many drug levels. Always discuss supplements with your team. PMC+1

11) Why do doctors insist on antivirals with bortezomib?
To prevent shingles; it’s a known risk with proteasome inhibitors. PMC

12) Can large meals make me dizzy?
Yes. Big meals can drop blood pressure in autonomic dysfunction—use small, frequent meals. AAFP

13) Will I need devices like a pacemaker or ICD?
Pacemakers help slow-rhythm/conduction disease. ICD benefit is uncertain in amyloidosis; decisions are individualized. PubMed+1

14) How long will I stay on daratumumab?
In trials, daratumumab continued every 4 weeks for up to ~2 years after the initial weekly/biweekly phases, if tolerated and effective. Your plan may differ. PMC

15) Is doxycycline a cure?
No. It’s sometimes used as an adjunct; evidence is mixed, and it should not replace standard anti-plasma-cell therapy. Nature

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: September 11, 2025.

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