Temporal Artery Amyloidosis (TAA)

Temporal artery amyloidosis means “amyloid” protein has been laid down in the wall of the superficial temporal artery (the vessel your doctor sometimes biopsies when giant cell arteritis is suspected). It can look like temporal arteritis on symptoms, but under the microscope it is amyloid, not vasculitis, and care focuses on finding the amyloid type and treating the underlying disease. Lippincott JournalsPubMed

Temporal artery amyloidosis happens when misfolded proteins called “amyloid” build up in the walls of the temporal artery, a medium-sized artery that runs just under the skin at your temples. The abnormal protein sits in the artery wall like grit in a pipe. Over time, it stiffens and narrows the vessel, and the artery cannot bring normal blood flow to nearby tissues. This buildup can look and feel like giant cell arteritis (GCA) because both can cause headache, jaw pain while chewing, scalp tenderness, and even sudden vision loss. But the cause is different: GCA is an inflammatory disease, while amyloidosis is a protein-deposit disease. The definite way to tell them apart is to look at a biopsy of the temporal artery under the microscope and use a special stain called Congo red. Congo red makes amyloid glow apple-green under polarized light, which is a classic clue. In most reports, amyloid found in the temporal artery comes from light-chain (AL) amyloidosis, and less commonly from transthyretin (ATTR) amyloidosis; ATTR can be hereditary or age-related. Because the symptoms can mimic GCA, doctors should consider amyloidosis when a biopsy for suspected GCA shows no vasculitis but does show the Congo-red signal for amyloid. EyeWiki+1PubMed

Amyloidosis is a condition in which certain proteins misfold, stick together, and form stiff, waxy fibers called amyloid. These fibers build up outside cells and crowd normal tissues. When amyloid settles in a blood vessel such as the temporal artery, it can make the wall thick and inflexible. This may reduce blood flow or irritate nearby nerves and tissues, causing head or temple pain, scalp tenderness, or jaw tiredness when chewing—symptoms that can mimic giant cell arteritis. The only way to be sure is to look at a biopsy of the artery. Special stains—especially Congo red—make amyloid glow apple-green under polarized light, which is a classic sign. After amyloid is confirmed, doctors use additional tests to identify the amyloid type (for example, AL from light chains, ATTR from transthyretin, or AA from serum amyloid A). Treatment is not one-size-fits-all: it depends on the type of amyloid and which organs are involved (heart, kidneys, nerves, etc.). PMCNCBIMSD Manuals

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Types

1. AL (light-chain) amyloidosis
   This type comes from abnormal fragments of antibodies (light chains) made by a small clone of plasma cells in the bone marrow. These fragments misfold and deposit as amyloid in many organs. The temporal artery can be involved and mimic GCA. Congo red on temporal-artery biopsy can reveal the diagnosis. PubMedUCL Discovery

2. ATTR amyloidosis
   This type comes from the transthyretin (TTR) protein made by the liver. It has two forms:
   • Hereditary (ATTRv/hATTR) due to a gene mutation.
   • Wild-type (ATTRwt) due to age-related misfolding without a mutation.
   Temporal-artery ATTR is uncommon, but it is reported. When it occurs, it may imitate GCA, and tissue typing identifies TTR. PubMedOxford Academic

3. AA amyloidosis (secondary)
   This type comes from long-standing inflammation in the body (for example, chronic infections or certain rheumatic diseases). It rarely shows up in the temporal artery, but cases exist—sometimes in the setting of temporal arteritis itself. PubMedEJCRIM

Key point: Type-specific testing is essential because treatments differ for AL, ATTR, and AA amyloidosis. Congo red tells you “it’s amyloid,” but mass spectrometry or immunohistochemistry tells you which type. EyeWiki

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Causes

These are underlying conditions that can produce amyloid in the body and, rarely, lead to deposits in the temporal artery. Each item includes a simple “why.”

1. AL amyloidosis from MGUS (monoclonal gammopathy of undetermined significance).
   A small plasma-cell clone makes abnormal light chains that misfold and deposit. UCL Discovery

2. AL amyloidosis from smoldering myeloma.
   A larger but still “smoldering” clone produces more light chains, raising amyloid risk. UCL Discovery

3. AL amyloidosis from multiple myeloma.
   A malignant plasma-cell clone overproduces light chains that become amyloid. UCL Discovery

4. Hereditary ATTR (ATTRv/hATTR).
   A TTR gene mutation makes the TTR protein unstable, so it misfolds and deposits. Amyloidosis Research Consortium

5. Wild-type ATTR (ATTRwt).
   Aging alone can make TTR misfold in some people; deposits often prefer the heart and tendons, and rarely arteries like the temporal artery. ScienceDirect

6. Rheumatoid arthritis → AA amyloidosis.
   Chronic inflammation drives excess serum amyloid A protein that misfolds and deposits. Frontiers

7. Ankylosing spondylitis → AA amyloidosis.
   Long-standing inflammation can lead to SAA overproduction and amyloid. Frontiers

8. Inflammatory bowel disease (Crohn’s/ulcerative colitis) → AA amyloidosis.
   Chronic gut inflammation can generate AA amyloid. Frontiers

9. Chronic infections (such as tuberculosis, bronchiectasis, osteomyelitis) → AA amyloidosis.
   Persistent infection fuels SAA and amyloid. Frontiers

10. Familial Mediterranean fever → AA amyloidosis.
    Recurrent inflammatory flares raise SAA and amyloid risk. Frontiers

11. Castleman disease → AA amyloidosis.
    A cytokine-rich inflammatory state can drive AA deposits. Frontiers

12. Chronic skin inflammatory diseases (severe hidradenitis suppurativa, psoriasis) → AA amyloidosis.
    Years of inflammation may produce AA amyloid. Frontiers

13. Untreated autoinflammatory syndromes (e.g., TRAPS) → AA amyloidosis.
    Inherited over-inflammation escalates SAA production. Frontiers

14. Poorly controlled chronic lung infection (e.g., non-tuberculous mycobacteria) → AA amyloidosis.
    Ongoing airway inflammation sustains SAA elevation. Frontiers

15. Long-term hemodialysis → β2-microglobulin amyloidosis.
    β2-microglobulin can deposit in tissues; vascular involvement is less typical but reflects systemic amyloidosis biology. amyloidosissupport.org

16. Chronic osteomyelitis → AA amyloidosis.
    Bone infection keeps inflammation high for years. Frontiers

17. Recurrent abdominal infections or bronchiectasis exacerbations → AA amyloidosis.
    Frequent flares raise SAA and deposit risk. Frontiers

18. Temporal arteritis (GCA) with prolonged severe inflammation → AA amyloidosis as a complication.
    Inflammatory load can secondarily trigger AA amyloid. PubMedEJCRIM

19. Monoclonal light-chain production without overt myeloma (evolving AL).
    Even small clones can seed amyloid if produced long enough. UCL Discovery

20. Systemic amyloidosis of mixed or rare types (e.g., apolipoprotein AI, fibrinogen Aα).
    These are uncommon but show that multiple proteins can rarely form amyloid. amyloidosissupport.org

Take-home: these causes do not “target” the temporal artery on purpose. They create amyloid in the body, and the temporal artery is one of the possible, rare landing places. The biopsy proves it when present. EyeWiki

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Symptoms

Each symptom is written in one or two simple sentences and linked to why it happens.

1. New headache at the temples.
   The artery wall is stiff and thick, so the vessel does not flex well. That irritates nearby tissues and causes pain, much like GCA. EyeWiki

2. Scalp tenderness or soreness when combing hair.
   The skin over the artery is sensitive because the vessel underneath is rigid and inflamed by deposits. EyeWiki

3. Jaw pain while chewing (jaw claudication).
   Blood to chewing muscles is not enough during effort, so the muscle aches. This is a classic GCA-like symptom that can appear in TAA. PubMed

4. Tender, thick, or cord-like temporal artery.
   Deposits make the artery feel hard or knotted under the skin. EyeWiki

5. Sudden vision loss or blurry vision.
   If blood flow to the optic nerve or retina drops, vision can fall quickly. This is a medical emergency in any GCA-like picture. EyeWiki

6. Fatigue and low energy.
   Systemic amyloidosis often causes whole-body tiredness. EyeWiki

7. Unintended weight loss.
   Chronic disease and poor appetite can lead to weight loss. EyeWiki

8. Numbness, tingling, or burning in feet or hands.
   Some amyloidosis types injure nerves (peripheral neuropathy). Amyloidosis Research Consortium

9. Dizziness when standing (orthostatic symptoms).
   Autonomic nerves controlling blood pressure may be affected. Amyloidosis Research Consortium

10. Carpal tunnel symptoms (hand numbness at night).
    ATTR often deposits around the wrist tendons and ligaments. ScienceDirect

11. Shortness of breath or leg swelling.
    Cardiac amyloid stiffens the heart muscle and can lead to heart failure signs. ScienceDirect

12. Irregular heartbeat or palpitations.
    Amyloid in the heart can disturb rhythm. ScienceDirect

13. Easy bruising or waxy skin change.
    Amyloid can deposit in skin and small vessels, making skin fragile. (Described across systemic AL.) AHA Journals

14. Tongue enlargement or mouth soreness (macroglossia, AL).
    Some AL patients develop a large, stiff tongue that feels awkward. AHA Journals

15. Poor response to steroids that would usually help GCA.
    If symptoms look like GCA but steroids do not work as expected, amyloidosis should be checked. UCL Discovery

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Diagnostic tests

Important idea: Doctors often start with a GCA work-up because the symptoms overlap. If the temporal artery biopsy does not show vasculitis but does show Congo-red-positive material, amyloidosis becomes the answer. The tests below help prove amyloid and identify the type (AL vs ATTR vs AA), which guides treatment.

A) Physical exam

1. Careful palpation of the temporal arteries.
   The doctor feels for a thick, beaded, or tender artery and checks the pulse there. A hard, knobbly artery suggests a structural wall problem like amyloid or arteritis. EyeWiki

2. Visual acuity and visual-field check.
   Any drop may suggest optic nerve or retinal ischemia. This flags urgency. EyeWiki

3. Scalp and jaw exam during chewing.
   Localized scalp soreness and provoked jaw pain point toward a flow-limitation problem at the temple area. PubMed

4. Whole-body exam for systemic amyloid signs.
   Cardiac congestion, neuropathy, carpal tunnel scars, or macroglossia push suspicion toward AL or ATTR. ScienceDirectAHA Journals

B) Manual/bedside maneuvers

5. “Chew test” for jaw claudication.
   Gentle, repeated chewing of soft food can reproduce pain if flow is poor. It is not a formal test but helps triage what to do next. PubMed

6. Orthostatic vital signs.
   Measuring blood pressure lying and standing can detect autonomic nerve involvement, common in some amyloid types. Amyloidosis Research Consortium

7. Tinel’s sign at the wrist.
   Tapping over the carpal tunnel may reproduce tingling if ATTR-related tendon deposits compress the median nerve. ScienceDirect

C) Laboratory & pathological tests

8. ESR and CRP.
   In GCA these are usually very high. In TAA, they may be normal or only mildly raised, so a mismatch raises suspicion for amyloid instead of arteritis. (Clinical reasoning supported by case series). PubMed

9. Serum and urine protein electrophoresis with immunofixation + serum free light chains.
   These detect a light-chain clone for AL amyloidosis. This is essential when Congo red is positive. UCL Discovery

10. Temporal artery biopsy with Congo red staining.
    This is the key test when GCA is suspected. Congo red shows apple-green birefringence under polarized light, proving amyloid in the artery wall. EyeWiki

11. Amyloid typing by mass spectrometry (or immunohistochemistry).
    Typing tells you AL vs ATTR vs AA and directly drives therapy choices. EyeWiki

12. Abdominal fat-pad biopsy (or fine-needle aspiration).
    A simple, office-based way to look for systemic amyloid. It can be quite sensitive in ATTRv and many AL cases, though not perfect, so a negative test does not rule it out. PMC+1AHA Journals

13. Cardiac biomarkers (NT-proBNP, troponin).
    If elevated with suggestive imaging, they support cardiac involvement by amyloid (important for staging and treatment decisions). AHA Journals

14. Urinalysis and kidney function.
    Protein leakage and kidney impairment can signal systemic amyloid burden. AHA Journals

D) Electrodiagnostic tests

15. 12-lead electrocardiogram (ECG).
    Low voltages or conduction blocks can point to cardiac amyloid involvement, often seen in ATTR or AL. AHA Journals

16. Holter or event monitor.
    Checks for arrhythmias that amyloid can trigger. Helpful for symptoms like palpitations or fainting. AHA Journals

17. Nerve conduction studies / autonomic reflex testing.
    Document peripheral or autonomic neuropathy, which is common in AL and hereditary ATTR. Amyloidosis Research Consortium

E) Imaging tests

18. Temporal artery ultrasound (Doppler).
    In GCA, a “halo sign” is classic. In TAA the picture may not match classic GCA, nudging the team toward biopsy and Congo red. (Used adjunctively in the GCA vs amyloid distinction.) EyeWiki

19. Cardiac scintigraphy with 99mTc-PYP (or DPD/HMDP outside the U.S.).
    Strong heart uptake on these scans with no monoclonal light-chain signal supports ATTR amyloidosis and can avoid heart biopsy. This is now a standard pathway for ATTR work-up. ASNC+1AHA Journals

20. Echocardiography and/or cardiac MRI.
    These show a stiff, thick-looking heart and distinctive MRI patterns when amyloid infiltrates the heart; they help stage disease and guide care. AHA Journals

Non-pharmacological treatments

These measures do not dissolve amyloid, but they reduce symptom burden, protect organs, and prepare you for disease-modifying therapy. Each item includes a simple description, purpose, and mechanism.

1. Structured diagnosis pathway
   What: Ensure biopsy with Congo red and arrange formal amyloid typing (immunohistochemistry/mass spectrometry) plus organ assessment (heart, kidneys, nerves).
   Purpose: Get the right type and full organ map so treatment matches the biology.
   How it helps: Correct typing unlocks specific therapy (e.g., D-VCd for AL; tafamidis or gene-silencers for ATTR). MSD Manuals

2. Family history & genetic counseling (for suspected ATTR)
   What: Ask about cardiomyopathy/neuropathy; consider TTR gene testing if ATTR is on the table.
   Purpose: Distinguish hereditary ATTR from wild-type.
   How: Genetic testing guides therapy choice and helps relatives. MSD Manuals

3. Cardiac self-care with daily weights & sodium restriction
   What: Weigh yourself daily and limit salt (~2 g/day if your clinician agrees).
   Purpose: Prevent fluid overload in amyloid cardiomyopathy.
   How: Less sodium → less water retention → easier breathing and less swelling (edema). (General heart-failure best practice.)

4. Fluid management education
   What: Recognize early signs of congestion (rapid weight gain, ankle swelling) and dehydration (dizziness, low urine).
   Purpose: Keep a narrow, safe fluid balance.
   How: Practical tips reduce ER visits. (General heart-failure/CKD care.)

5. Compression therapy for edema
   What: Graduated compression stockings if approved by your cardiology team.
   Purpose: Move fluid back into circulation; reduce leg heaviness.
   How: External pressure assists venous/lymphatic return.

6. Orthostatic hypotension strategies
   What: Rise slowly, elevate head of bed, small frequent meals; abdominal binders if advised.
   Purpose: Reduce dizziness/falls when autonomic nerves are affected.
   How: Mechanical maneuvers aid blood pressure maintenance.

7. Neuropathy-friendly footwear & skin care
   What: Cushioned shoes, daily foot checks.
   Purpose: Prevent ulcers/infections in sensory neuropathy.
   How: Protects insensate areas from pressure and trauma.

8. Targeted physical therapy
   What: Gentle aerobic + resistance program supervised by a therapist.
   Purpose: Maintain stamina without overexertion.
   How: Conserves function in muscle/nerve involvement.

9. Energy budgeting & activity pacing
   What: Plan tasks around best energy periods; rest before you feel spent.
   Purpose: Reduce post-exertional crashes.
   How: Pacing keeps symptoms manageable.

10. Sleep optimization & CPAP screening
    What: Screen for sleep apnea; practice good sleep hygiene.
    Purpose: Improve daytime energy and heart strain.
    How: Better oxygenation reduces stress on sick organs.

11. Vaccination plan (influenza, pneumococcal, COVID-19 as locally recommended)
    What: Stay current with non-live vaccines.
    Purpose: Prevent infections that can worsen AA amyloidosis or derail AL/ATTR care.
    How: Fewer infections = less inflammation/reserve loss. (General guidance.)

12. Dental and oral health
    What: Regular dental care and mouth hygiene.
    Purpose: Reduce infection and bleeding risk (macroglossia/soft-tissue amyloid may complicate care).
    How: Lower bacterial load; easier nutrition.

13. Safe nutrition with small, frequent, protein-rich meals
    What: 4–6 smaller meals with adequate protein if kidneys allow.
    Purpose: Support weight and healing; avoid hypotension after large meals.
    How: Smooth calorie intake; limits post-prandial BP drop in autonomic neuropathy.

14. Iodinated contrast caution & kidney protection
    What: Alert radiology if kidneys are involved; consider alternative imaging or hydration protocols.
    Purpose: Prevent contrast-induced kidney hits.
    How: Risk–benefit planning preserves renal function. (General nephrology practice.)

15. Medication reconciliation
    What: Review NSAIDs, certain calcium-channel blockers, and other drugs that can worsen edema or kidneys.
    Purpose: Avoid iatrogenic harm.
    How: Choose kidney- and heart-friendly options.

16. Fall-prevention home review
    What: Remove trip hazards, improve lighting, use handrails.
    Purpose: Reduce fracture/bleed risk in orthostatic hypotension or neuropathy.
    How: Safer environment lowers injury risk.

17. Heat/cold exposure moderation
    What: Dress in layers; avoid extremes.
    Purpose: Autonomic dysfunction can impair temperature control.
    How: Keeps symptoms and blood pressure steadier.

18. Psychological support & peer groups
    What: Counseling; patient organizations for AL/ATTR.
    Purpose: Coping skills and practical tips from others.
    How: Better adherence and quality of life.

19. Travel planning
    What: Break long trips; keep meds/summary letter handy; compression on flights.
    Purpose: Reduce clot, edema, and stress.
    How: Structured pacing and hydration.

20. Care coordination with an amyloidosis center
    What: Seek input from a specialist center (hematology/cardiology/neurology).
    Purpose: Access to up-to-date, type-specific care and trials.
    How: Multidisciplinary oversight improves outcomes. (See modern AL/ATTR updates.) ASCO PublicationsWiley Online Library

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Drug treatments

Important: Doses below are typical references; your clinicians tailor these to you based on organs, weight, and other medicines. Always follow your care team’s exact prescription.

A) For AL (light-chain) amyloidosis

1. Daratumumab + Bortezomib + Cyclophosphamide + Dexamethasone (D-VCd)
   Class: Anti-CD38 mAb + proteasome inhibitor + alkylator + steroid.
   Typical dosing (example): daratumumab (often subcutaneous 1,800 mg weekly then spaced), bortezomib ~1.3 mg/m² weekly, cyclophosphamide ~300 mg/m² weekly, dexamethasone 20–40 mg weekly—per protocol.
   When: First-line for most newly diagnosed AL without prohibitive cardiac stage.
   Purpose/Mechanism: Rapidly suppresses the plasma-cell clone so light chains drop fast and organ injury slows.
   Key evidence/notes: The ANDROMEDA trial established D-VCd as a frontline standard, producing high complete/very good partial response rates. Common side effects: cytopenias, infections, neuropathy (from bortezomib), steroid effects. ASH PublicationsNatureASH Confex

2. Bortezomib + Cyclophosphamide + Dexamethasone (VCd)
   Class: PI + alkylator + steroid.
   When: Alternative where daratumumab isn’t suitable.
   Purpose: Plasma-cell kill; light-chain reduction.
   Side effects: Neuropathy, cytopenias, GI upset. ASH Publications

3. High-dose Melphalan with Autologous Stem Cell Transplant (ASCT)
   Class: Alkylator + rescue stem cells.
   When: Fit, carefully selected patients (cardiac/renal criteria).
   Purpose: Deep, durable hematologic responses.
   Side effects: Transplant toxicities; requires experienced center. (Consensus practice.) ASCO Publications

4. Daratumumab (maintenance or relapse)
   Class: Anti-CD38 monoclonal antibody.
   When: As part of induction/maintenance or at relapse; IV 16 mg/kg or SC formulations per schedule.
   Mechanism: Immune-mediated plasma-cell depletion.
   Side effects: Infusion reactions (less with SC), infections. ASCO Publications

5. Lenalidomide (± dexamethasone)
   Class: IMiD.
   When: Selected relapsed/refractory AL; use cautiously in cardiac disease.
   Mechanism: Anti-plasma-cell and immune modulation.
   Side effects: Cytopenias, rash, edema.

B) For ATTR (transthyretin) amyloidosis

6. Tafamidis (61 mg free-acid once daily, bioequivalent to 80 mg meglumine)
   Class: TTR stabilizer.
   When: ATTR-CM (cardiomyopathy) with NYHA I–III; improves survival and reduces hospitalizations.
   Mechanism: Stabilizes TTR tetramer → fewer misfolded monomers → less amyloid.
   Side effects: Generally well tolerated. PMC+1Pfizer

7. Patisiran (IV q3 weeks), Inotersen (SC weekly), or Vutrisiran (SC q3 months)
   Class: Gene silencers (siRNA/antisense) that reduce hepatic TTR production.
   When: ATTR polyneuropathy; patisiran/vutrisiran also show cardiac parameter benefits in some studies.
   Side effects: Patisiran—infusion-related; Inotersen—thrombocytopenia/renal monitoring; Vutrisiran—generally favorable. (Contemporary data.)

8. Diflunisal (250 mg twice daily)
   Class: NSAID that stabilizes TTR at higher affinity sites.
   When: Off-label in some centers when other options are unavailable/tolerability allows.
   Side effects: Typical NSAID risks (GI bleed, kidneys); requires careful selection.

C) For AA amyloidosis

9. Control of the driving inflammation
   Examples: Colchicine 0.6 mg 1–2×/day for FMF; IL-6 blockade (tocilizumab) for RA/systemic inflammation; disease-specific biologics for IBD, etc.
   Mechanism: Lowering serum amyloid A levels slows AA fibril formation.
   Side effects: Drug-specific (e.g., infection risk with biologics). MSD Manuals

D) Supportive agents used across types (symptom/organ support)

10. Diuretic-based edema control (e.g., furosemide ± spironolactone)
    Class: Loop ± mineralocorticoid antagonist.
    Purpose: Symptom relief in congestion; not disease-modifying.
    Side effects: Electrolyte shifts, kidney effects; dosing is individualized. (Standard heart-failure practice.)

Other organ-support medications (midodrine/droxidopa for orthostatic hypotension, neuropathic-pain agents, anticoagulation in atrial arrhythmias, etc.) are prescribed case-by-case by your clinicians.

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Dietary “molecular” supplements

Supplements do not replace disease-modifying therapy. Evidence in amyloidosis is limited; always clear these with your care team to avoid interactions.

1. Vitamin D (e.g., 800–2000 IU/day as advised): supports bone/muscle; low levels are common.

2. Thiamine (B1, clinician-guided): supports nerve/energy, especially with diuretic use.

3. Vitamin B12 (as needed for deficiency): helps neuropathy and blood health.

4. Omega-3 fatty acids (per label): general cardiovascular support; may help triglycerides.

5. Magnesium (if low): supports rhythm/neuropathy symptoms; avoid excess in CKD.

6. Coenzyme Q10: energy metabolism support; evidence in amyloid is sparse—use cautiously.

7. EGCG (green tea extract): has anti-amyloid lab signals; clinical benefit unproven; monitor for liver effects.

8. Curcumin: anti-inflammatory/anti-aggregation signals in models; evidence in humans is limited.

9. Taurine: membrane stabilization/energy roles; human data in amyloidosis lacking.

10. Probiotics (food-based): gut health during immunosuppression—choose pasteurized products and review with your team.

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Regenerative / stem-cell–type” therapies

There are no over-the-counter “immunity boosters” proven to treat amyloidosis. The real “regenerative” options are advanced medical and surgical therapies used selectively.

1. Autologous Stem Cell Transplant (ASCT) for AL
   Dose/How: High-dose melphalan followed by reinfusion of your stem cells.
   Function: Allows stronger chemo to reset plasma-cell production.
   Mechanism: Eliminates the clone making toxic light chains; organs sometimes recover partially. ASCO Publications

2. Heart Transplant (advanced amyloid cardiomyopathy)
   Function: Replaces end-stage amyloid heart when otherwise eligible.
   Mechanism: Restores pump function; in ATTRv, may be combined with liver transplant to reduce further TTR production. (Specialist-center practice.)

3. Liver Transplant (selected hereditary ATTR variants)
   Function: Removes the main source of mutant TTR.
   Mechanism: New liver makes wild-type TTR, slowing new amyloid seeding (nerve benefit > established heart deposits).

4. Combined Heart–Liver Transplant (ATTRv with severe heart disease)
   Function: Addresses both pump failure and mutant TTR source at once.
   Mechanism: Comprehensive reset in ultra-selected patients.

5. Kidney Transplant (end-stage renal disease from amyloid)
   Function: Restores kidney function after disease control.
   Mechanism: Replaces damaged organ after hematologic/inflammatory control.

6. Clinical-trial biologics and gene-targeted therapies
   Function: Next-generation TTR silencers/stabilizers or novel anti-amyloid strategies.
   Mechanism: Lower production, stabilize protein, or enhance clearance; ask an amyloidosis center about active trials. (Ongoing 2024–2025 research.) ScienceDirectOnline JCF

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Procedures/surgeries

1. Temporal artery biopsy (diagnostic, not curative)
   Procedure: Small segment of artery is removed under local anesthesia.
   Why: Distinguish amyloid from giant cell arteritis; guides life-saving therapy choices. EyeWiki

2. Autologous stem cell transplant (ASCT) — see above
   Why: Pursue deep hematologic response in fit AL patients. ASCO Publications

3. Heart transplant (± LVAD bridge)
   Why: End-stage cardiac failure from amyloid unresponsive to medical therapy.

4. Liver transplant (± combined heart–liver in ATTRv)
   Why: Remove the source of mutant TTR in hereditary ATTR.

5. Kidney transplant
   Why: End-stage renal failure after disease control to restore independence from dialysis.

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Prevention

You cannot “prevent” a genetic or plasma-cell disorder by lifestyle alone, but you can reduce complications and avoid delays in diagnosis.

1. Seek early evaluation for new temple pain, scalp tenderness, or jaw claudication—especially if you’re older—so biopsy can separate GCA from amyloidosis. Lippincott Journals

2. Keep inflammation diseases (RA, IBD, FMF) under tight control to lower AA amyloid risk. MSD Manuals

3. Maintain regular follow-up if you have a monoclonal gammopathy (MGUS) or plasma-cell disorder.

4. Vaccinate per guidelines to avoid infection-triggered setbacks.

5. Limit sodium to protect heart/kidneys when involved.

6. Avoid NSAIDs unless advised (kidney/edema risks).

7. Medication checkups to avoid drug interactions (e.g., with tafamidis or gene silencers).

8. Foot care and fall-prevention if you have neuropathy or orthostatic symptoms.

9. Genetic counseling for families with ATTR variants.

10. Center-of-excellence care to stay aligned with evolving evidence. ASCO Publications

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When to see a doctor

• Sudden vision changes, one-sided vision loss, or new jaw pain with chewing.

• New or worsening temple/scalp pain or tenderness.

• Shortness of breath, rapid weight gain, or swelling of legs/abdomen.

• Fainting, chest pain, or irregular heartbeat.

• Foamy urine, swelling around eyes, or sharp drop in urine output.

• Numbness, burning feet, dizziness on standing, or severe fatigue.

• Unintended weight loss, tongue enlargement, easy bruising, or purpura.
  (These can reflect organ involvement or a competing diagnosis like GCA; prompt evaluation matters.) Lippincott Journals

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What to eat and what to avoid

Eat more of:

• Low-salt, fresh foods: steamed vegetables, fruits, lean proteins (fish, poultry, tofu), whole grains.

• Protein at each meal (as allowed by your kidney team) to maintain muscle.

• Potassium-rich foods only if your labs allow; otherwise follow renal guidance.

• Fluids to thirst unless you have a heart-failure fluid limit—follow your plan.

Limit/Avoid:

• High-sodium processed foods (canned soups, deli meats, fast food).

• Alcohol (can worsen cardiomyopathy and neuropathy).

• NSAIDs without clinician approval (kidney/edema risk).

• Grapefruit if any of your medicines interact (check labels).

• Raw/unpasteurized foods if immunosuppressed (infection risk).

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Frequently asked questions

1. Is temporal artery amyloidosis the same as giant cell arteritis (GCA)?
   No. They can look alike clinically, but biopsy distinguishes them: GCA shows vasculitis; amyloidosis shows Congo red–positive deposits with apple-green birefringence. EyeWiki

2. How rare is amyloid in the temporal artery?
   It’s uncommon, usually discovered on biopsy done for suspected GCA; several case reports describe AL amyloid mimicking GCA. PubMedBioMed Central

3. Does temporal artery amyloid mean I have systemic amyloidosis?
   Often it prompts a full work-up to check for systemic involvement and type. Some patients do have systemic disease (AL, ATTR, or AA). MSD Manuals

4. What tests confirm amyloidosis?
   Congo red staining of tissue with apple-green birefringence, then typing by immunohistochemistry or mass spectrometry; blood/urine and organ imaging follow. PMCMSD Manuals

5. What symptoms suggest heart involvement?
   Breathlessness, ankle swelling, low blood pressure, fainting, or abnormal rhythms—seek cardiology input promptly.

6. What’s the first-line treatment for AL amyloidosis now?
   D-VCd (daratumumab + bortezomib + cyclophosphamide + dexamethasone) in most newly diagnosed patients, based on high response rates. ASH PublicationsNature

7. Is there a pill for ATTR amyloid heart disease?
   Yes: tafamidis (61 mg free-acid once daily) improves survival and reduces hospitalizations; gene-silencing therapies are used mainly for neuropathy and are evolving. PMC+1Pfizer

8. Can AA amyloidosis be reversed?
   Controlling the underlying inflammation can stabilize or improve organ function by reducing new amyloid formation. MSD Manuals

9. Do supplements cure amyloidosis?
   No. They may support nutrition or symptoms but do not replace disease-modifying therapy.

10. Is surgery needed for the temporal artery itself?
    Usually only for biopsy. Surgery does not remove systemic amyloid. EyeWiki

11. Can I exercise?
    Yes—gentle, supervised exercise is helpful. Avoid overexertion and follow cardiac guidance.

12. What about pregnancy?
    Discuss early with specialists; decisions depend on organ involvement and therapy plans.

13. Will I need lifelong treatment?
    Many patients need ongoing monitoring; the exact plan depends on the amyloid type and organ response.

14. What if my biopsy was negative but symptoms persist?
    Temporal artery biopsy can miss lesions. Your team may pursue further testing (imaging, repeat or contralateral biopsy) depending on suspicion.

15. Where should I be treated?
    Whenever possible, at or in consultation with an amyloidosis-experienced center to access up-to-date protocols and trials. ASCO Publications

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

Last Updated: August 28, 2025.