Amyloidosis

IBD patients have a higher level of serum amyloid-A (SAA), an acute phase protein which is the precursor of tissue amyloid. This is probably related to chronic inflammation and to the duration and extension of the disease [32, 33], although other studies have not supported this hypothesis [34-36]. Long-term steroids therapy has also been advocated [37].

Amyloidosis may involve different organs but there is a clear predilection for renal parenchyma. This condition usually manifests with asymptomatic proteinuria, but the evolution to a nephritic syndrome is not rare, and eventually can lead to death. According to the largest reported series [33], the true incidence of amyloidosis is less than 1% in patients with CD and 0.07% in those with UC. Patients with both ileitis and colitis have the highest risk (1.3-1.6%) [32-34].

The most effective way to stop amyloidosis is resection of the affected bowel [35, 38]. However, surgery in these patients suffers from a higher rate of morbidity and mortality [32-37,39] and is often ineffective when a nephritic syndrome has already developed [33, 34].

Success of medical treatment with colchicine (0.6-1.5 mg/day) has been reported in small series [33, 40-42], but its mechanism of action is not clear. End-stage disease can be managed with plasmapheresis and azathioprine [43], but it eventually requires a renal transplant [44].

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