Long-term efficacy of infliximab treatment for AA-amyloidosis secondary to chronic inflammatory arthritis

Classic Autoinflammatory Diseases

“…Lachmann et al reported an improvement in renal function in patients with a median SAA concentration of 6 mg/l and deterioration in patients with a median SAA concentration of 28 mg/l, 186 confirming that regression of amyloid deposits in these patients is dependent upon successful treatment with immunosuppressive strategies or biological agents, such as anti-TNF therapies or interleukin-1 blockers, that lower SAA levels significantly. 187,188 A potential treatment currently in phase III trials is eprodisate, a sulfonated molecule that competitively binds to the glycosaminoglycan-binding sites on SAA and inhibits fibril polymerization and thus further amyloid deposition/accumulation. A recent randomized clinical trial in 183 patients with amyloidosis showed that, at doses between 800 and 2400 mg total daily dose, depending on renal function, active treatment slowed down progressive renal failure in patients with AA amyloidosis in the treatment but not placebo arm.…”

A man with generalised lymphadenopathy

“…[10][11][12] In AL amyloidosis, chemotherapy reduces the production of amyloid precursor proteins, thereby improving target organ function and survival. Therapeutic strategies include high dose melphalan followed by autologous stem cell transplantation; the combination of melphalan and corticosteroids; thalidomide; the new and less toxic thalidomide analogue, lenalidomide; and the proteasome inhibitor bortezomib, which can be combined with dexamethasone.…”

Review of eprodisate for the treatment of renal disease in AA amyloidosis

“…Regression of amyloid deposits in these patients is dependent upon successful treatment with immunosuppressive strategies or biological agents such as anti-TNF therapies or interleukin-1 receptor antagonists. 38,39 The increase in use of disease-modifying agents and biological treatments for rheumatic diseases has led to a subsequent decline in the incidence of patients requiring renal replacement therapy for amyloid. 40 Targeting the production of amyloidogenic proteins is a potentially effective strategy, but achieving adequate control of protein production can prove difficult.…”