What is the cause and treatment of amyloidosis?

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I went through your query and understand your concern.

Amyloids are made up of protein and glycogen.

Cofactors, such as glycosaminoglycans and SAP, may play a role in predisposition to amyloid formation via one or more of the following effects:

1. Modulation of fibrillogenesis by direct binding to specific domains of subunit proteins or their precursors.

2. Stabilization of the fibril and protection from degradation.

3. Localization to specific organs or tissue sites by binding to matrix components or receptor molecules.

4. Secondary effects on the metabolism of precursor protein, leading to the accumulation of degradation products with amyloidogenic potential.

5. Modulation of proteolytic events that may facilitate fibril formation.

Major forms of amyloidosis include:

1. AL amyloidosis – Due to deposition of protein derived from immunoglobulin light chain fragments. It is a potential complication of any plasma cell dyscrasia that produces monoclonal immunoglobulin.

2. Transthyretin amyloidosis (ATTR) – Due to either specific heritable mutations, which are associated with familial amyloid polyneuropathy (FAP) and/or familial amyloid cardiomyopathy, or which more often may occur in a nonfamilial form as a concomitant of aging without apparent mutations (wild-type transthyretin [TTR] amyloidosis.

3. AA amyloidosis – The most common form in resource-limited countries. It may complicate chronic diseases associated with ongoing or recurring inflammation, such as chronic infections; rheumatoid arthritis (RA), spondyloarthritis, inflammatory bowel disease; or periodic fever syndromes.

Typical organs involved include the kidney, liver, and spleen. Some of the conditions associated with AA include the following:

1. Rheumatoid arthritis (RA).

2. Alzheimer's disease.

3. Multiple myeloma.

4. Juvenile idiopathic arthritis.

5. Ankylosing spondylitis.

6. Psoriasis and psoriatic arthritis.

7. Still disease.

8. Familial Mediterranean fever.

9. Crohn's disease.

10. Leprosy.

11. Osteomyelitis.

12. Tuberculosis.

13. Chronic bronchiectasis.

14. Castleman disease.

15. Hodgkin and non-Hodgkin lymphoma.

16. Renal cell carcinoma.

17. Gastrointestinal, lung, or urogenital carcinoma.

18. Cryopyrin-associated periodic syndromes (CAPS).

Diagnosis by:

1. Stains for Congo red (apple-green birefringence).

2. Hematoxylin and eosin stains for amorphous material.

3. Kappa and lambda light chains.

4. Beta-amyloid A4 protein.

5. Transthyretin.

6. Beta 2-microglobulin.

7. Cystatin C.

8. Gelsolin.

9. Immunoreactivity with anti-amyloid AA antibody.

Treatment by

1. Tafamidis ( transthyretin stabilizer).

2. Vutrisiran (RNA interference therapeutic).

3. Patisiran (RNA interference therapeutic).

4. Doxycycline (tetracycline).

A pilot study demonstrated a reduction in arthralgia and increased range of motion with Doxycycline treatment. The authors theorize that Doxycycline inhibits β2-microglobulin fibrillogenesis and inhibits the accumulation in bone architecture. Their trial monitored long-term dialysis patients with severe amyloid arthropathy.

Kindly consult a specialist, talk with them, and take medications with their consent.

Hope it helps.

Thank you.