[Mike Mercury]

from Wikipee:

There are about 30 different types of amyloidosis, each due to a specific protein misfolding. Some are genetic while others are acquired. They are grouped into localized forms, and systemic ones.

The four most common types of systemic amyloidosis are light chain (AL), inflammation (AA), dialysis-related (Aβ2M), and hereditary and old age (ATTR and familial amyloid polyneuropathy.

Treatment

Treatment is geared towards decreasing the amount of the involved protein.

Treatment depends on the type of amyloidosis that is present. Treatment with high dose melphalan, a chemotherapy agent, followed by stem cell transplantation has shown promise in early studies and is recommended for stage I and II AL amyloidosis. However, only 20–25% of people are eligible for stem cell transplant. Chemotherapy and steroids, with melphalan plus dexamethasone, is mainstay treatment in AL people not eligible for transplant.

In AA, symptoms may improve if the underlying condition is treated; eprodisate has been shown to slow renal impairment by inhibiting polymerization of amyloid fibrils.

Management of ATTR amyloidosis will depend on its classification as wild type or variant. Both may be treated with tafamidis, a low toxicity oral agent that prevents destabilization of correctly folded protein. Studies showed tafamidis reduced mortality and hospitalization due to heart failure.[28] Previously, for variant ATTR amyloidosis, liver transplant was the only effective treatment. However, newer therapies including diflunisal, an anti-inflammatory drug, and inotersen and patisiran, drugs which prevent misfolded protein formation, have shown early promises in slowing disease progression. The latter two drugs have shown their benefit in neurological impairment scores and quality of life measures. However, their role in cardiac ATTR amyloidosis is still being investigated