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AA (Inflammatory) Amyloidosis Treatment & Management

  • Author: Richa Dhawan, MD, CCD; Chief Editor: Herbert S Diamond, MD  more...
 
Updated: Dec 06, 2015
 

Medical Care

At present, the major therapeutic strategy in amyloid A (AA) amyloidosis is treatment of the primary inflammatory disease in order to reduce the circulating levels of the amyloid precursor protein, serum amyloid A (SAA). Intensive treatment that lowers SAA levels to less than 10 mg/L may halt disease progression and induce a slow progressive recovery of renal function. The minority of patients in whom the underlying inflammatory disease cannot be identified are a serious management challenge, and the therapy in these cases has to be empirical, guided by frequent assays of SAA.

Accounts exist of the disappearance of the amyloid deposits associated with tuberculosis or chronically infected burns with appropriate treatment of the infection. Similarly, case reports exist of the disappearance of amyloid deposition associated with chronic inflammatory bowel disease after resection of the affected section of bowel.

Data from a randomized prospective series of patients with juvenile chronic arthritis who were treated with chlorambucil or cyclophosphamide show that the occurrence of amyloidosis is markedly reduced.[28] The tradeoff for the aggressive use of alkylating agents is an increased incidence of leukemia.

Treatment with tumor necrosis factor–α (TNF-α) inhibitors and interleukin-1 (IL-1) inhibitors has proved effective in controlling the progression of renal amyloid in patients with inflammatory arthritides and hereditary periodic fevers. The application of these agents possibly achieve similar therapeutic effects without the additional risk, thus lowering the incidence of amyloidosis without increasing mortality.

The rationale for using TNF inhibitors in secondary amyloidosis comes from the fact that these medications lower levels of serum IL-6, which is an important mediator of the acute phase inflammatory response. By reducing IL-6, synthesis of acute-phase proteins is reduced, systemic inflammation suppressed, and SAA levels are lowered, leading to reduction of amyloid deposits.[29]

Biologic agents such tocilizumab (an anti–IL-6 receptor antibody) used in juvenile idiopathic arthritis, and infliximab, an anti-TNF antibody, have been used to successfully reduce inflammation and thereby induce SAA reduction in AA amyloidosis.[30]

A case report described combination therapy with steroids, methotrexate, and intravenous hyperalimentation benefiting GI symptoms in a patient with rheumatoid arthritis (RA) and intestinal AA amyloidosis.[31]

Castelman disease, a rare IL-6–secreting tumor, can sometimes be completely excised. In those cases where surgery is not feasible or curative, evidence suggests benefit with anti-IL-6 therapies.[23]

The use of colchicine (0.6 mg tid) by patients with familial Mediterranean fever (FMF) has been shown to reduce or eliminate the febrile episodes and to prevent the appearance of renal amyloidosis.[32] The mechanism of action is not clear, although the elimination of AA deposition is likely mediated through the suppression of the inflammatory response and SAA production, rather than having a primary effect on amyloidogenesis.

Based on observations of people with FMF and mice with experimental AA amyloidosis, individual patients with the nephrotic syndrome secondary to renal AA amyloidosis in the course of inflammatory bowel disease, ankylosing spondylitis, and psoriatic arthritis were treated with colchicine and had clinical pictures consistent with the resolution of the nephrotic syndrome.

Although none of these reports contained follow-up renal biopsies, the clinical information supports the conclusion; however, many unreported instances in which colchicine has been used unsuccessfully in similar circumstances also are likely to exist. The only attempt at a randomized prospective trial of colchicine has been carried out in AL disease, and it showed no effect on that process.

Anakinra, a recombinant form of IL-1 receptor antagonist, has shown favorable effects on dermatologic and rheumatic manifestations in patients with Muckle–Wells syndrome and familial cold autoinflammatory syndrome. This treatment also resulted in the resolution of AA amyloidosis in these patients.[33]

The following are new approaches to the treatment of AA amyloidosis that are currently undergoing clinical trials:

  • A low–molecular-weight sulfonated molecule has been developed that interferes with fibril formation and deposition of amyloid by inhibiting interaction of SAA with glycosaminoglycans. In experimentally induced murine AA amyloidosis, this drug (NC-503) has been shown to reduce the amount of amyloid deposits.
  • Dimerization of human SAP molecules in vivo with a palindromic compound (CPHPC) triggers very rapid clearance of the complexed protein by the liver, depleting SAP from the circulation within a few hours of drug administration.
  • A case report describes severe protein-losing enteropathy with intractable diarrhea due to systemic AA amyloidosis successfully treated with corticosteroids and octreotide. [34]
  • A single patient with AA amyloidosis secondary to Hodgkin lymphoma was administered 4'-iodo-4'deoxydoxorubicin as antitumor therapy (see the treatment section in Amyloidosis, Immunoglobulin-Related); this patient has been reported to show a reduction in proteinuria and the liver amyloid burden on biopsy. The response was not complete and the resolution on liver biopsy may have been the result of sampling differentially infiltrated portions of tissue; nonetheless, the result is potentially exciting. [35]
  • A more experimentally and theoretically based approach uses the observation that anionic sulphonates interfere with the deposition of AA fibrils in a murine model of inflammatory amyloidosis. Little or no toxicity was shown in the preclinical testing.
  • The plasma glycoprotein serum amyloid P component (SAP) is a universal constituent of all types of amyloid plaques, and potentiates the amyloidogenic process. A study by Bodin and colleagues tested a two-step therapeutic strategy for amyloidosis that targeted SAP by first pharmacologically depleting circulating levels of SAP with the bivalent crosslinker CPHPC, and then subsequently administering anti-human-SAP antibodies. In mice transgenic for human SAP, an experimental model of systemic AA amyloidosis, this treatment regimen produced almost complete regression of hepatic and splenic amyloid deposits 4 weeks after anti-SAP treatment. [36] In a phase I trial in 15 patients, this treatment safely triggered clearance of amyloid deposits from the liver and some other tissues. [37]
  • Interactions between heparan-sulfate and dermatan-sulfate glycosaminoglycan (GAG)-containing proteoglycans and the misfolded amyloid precursor protein are also considered important for amyloidogenesis and the stabilization of amyloid. This insight has been used in a clinical trial to destabilize amyloid deposits with eprodisate, a negatively charged, sulfonated GAG analog, which binds to GAG-binding sites of the amyloid fibrils. [38]
  • Experiments have shown that a number of agents appear to retard AA amyloidosis in animal models. These include fenofibrate, FK506, and lovastatin, inhibition of interactions between SAA and the receptor for advanced glycation end-products (RAGE). [39, 40]
  • A study demonstrated the efficacy of pegylated INF-alpha once a week in FMF in the induction of a durable disease remission and the almost complete reversal of secondary renal AA amyloidosis. [41]

Renal replacement therapy

In patients with AA amyloidosis who were treated before 1990, the major cause of death was renal failure, generally accounting for 35-70% of mortality, with infection responsible for an additional 10-20%. The mean survival was 2-4 years, with the degree of renal insufficiency present at the time of diagnosis correlating with longevity. In a series of patients with AA amyloidosis presenting from 1985-1999, the median survival was 53 months, and the median renal survival (time alive and independent of renal replacement) was 18 months.[42] Because of the increased availability of renal replacement, renal failure was the cause of death in only 12.5% of patients, and infection became dominant (42%). Nonetheless, the results of dialysis in patients with renal amyloid and an underlying inflammatory disease are worse than the results in those undergoing dialysis for other chronic renal diseases.

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Surgical Care

Renal transplantation is an option in these patients, with some successes reported; however, data suggest that patients who have amyloidosis do not have as favorable a prognosis as patients transplanted for other forms of renal failure. Nonetheless, results have been improving, and transplantation is a reasonable option, particularly if the primary inflammatory disease has been treated successfully.

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Consultations

See the list below:

  • Because AA amyloidosis is usually a complication of a primary chronic infectious or inflammatory disease, consultations with specialists in infectious diseases concerning antibiotics, surgical resection, and other diagnostic and therapeutic modalities are appropriate.
    • Consult a rheumatologist with regard to newer modes of anti-inflammatory treatment before assuming that the patient will inevitably follow a downhill course.
    • Nephrologic and surgical management of the chronic renal failure also requires a coordinated team approach for an optimal outcome.
    • Cardiac complications at the time of transplantation seem to be more common in patients with amyloidosis than in those with other forms of renal failure.
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Diet

No specific dietary recommendations for patients with amyloid disease exist. Patients with chronic kidney disease should be managed by a nutritionist who has experience with such patients, maintaining appropriate levels of sodium and protein intake.

Occasionally, patients have significant gastrointestinal symptoms. In these cases, attention should be paid to maintaining caloric intake with minimal gastrointestinal distress.

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Activity

Encourage as much activity as the patient can tolerate in order to maintain muscle mass and a positive outlook.

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Contributor Information and Disclosures
Author

Richa Dhawan, MD, CCD Associate Professor, Director of Osteoporosis Clinic, Center of Excellence for Arthritis and Rheumatology, Louisiana State University Health Science Center at Shreveport

Richa Dhawan, MD, CCD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American College of Rheumatology, American Association of Physicians of Indian Origin

Disclosure: Nothing to disclose.

Coauthor(s)

Joel N Buxbaum, MD Professor, Department of Molecular and Experimental Medicine, The Scripps Research Institute

Joel N Buxbaum, MD is a member of the following medical societies: American Association for the Advancement of Science, American Society for Clinical Investigation, American Society of Human Genetics, Association of American Physicians, Association of Black Cardiologists, Henry Kunkel Society

Disclosure: Received consulting fee from Foldrx pharmaceuticals for consulting; Received consulting fee from Isis pharmaceuticals for consulting; Received consulting fee from alnylam pharmaceutical for consulting; Received consulting fee from Pfizer Pharmaceuticals for consulting.

Eisha Mubashir, MD Fellow in Rheumatology, Department of Medicine, Center of Excellence for Arthritis and Rheumatology, Louisiana State University School of Medicine in Shreveport

Disclosure: Nothing to disclose.

Mohammed Mubashir Ahmed, MD Associate Professor, Department of Medicine, Division of Rheumatology, University of Toledo College of Medicine

Mohammed Mubashir Ahmed, MD is a member of the following medical societies: American College of Physicians, American College of Rheumatology, American Federation for Medical Research

Disclosure: Nothing to disclose.

Ratinder J Kaur, MD Fellow, Department of Rheumatology, Louisiana State University School of Medicine in Shreveport

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Elliot Goldberg, MD Dean of the Western Pennsylvania Clinical Campus, Professor, Department of Medicine, Temple University School of Medicine

Elliot Goldberg, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD Visiting Professor of Medicine, Division of Rheumatology, State University of New York Downstate Medical Center; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

Robert E Wolf, MD, PhD Professor Emeritus, Department of Medicine, Louisiana State University School of Medicine in Shreveport; Chief, Rheumatology Section, Medical Service, Overton Brooks Veterans Affairs Medical Center

Robert E Wolf, MD, PhD is a member of the following medical societies: American College of Rheumatology, Arthritis Foundation, Society for Leukocyte Biology

Disclosure: Nothing to disclose.

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