Treatment depends on the type of<unk>  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<unk> <unk> . However, only 20–25% of people are eligible for stem cell transplant. Chemotherapy treatment including cyclophosphamide-bortezomib-dexamethasone is currently the recommended treatment option for people with<unk> <unk>  not eligible for transplant. In AA, symptoms may improve if the underlying condition is treated. In people who have inflammation caused by AA<unk> , tumour necrosis factor (TNF)-alpha inhibitors such as infliximab and etanercept are used for an average duration of 20 months. If TNF-alpha inhibitors are not effective, Interleukin-1 inhibitors (e.g. anakinra, canakinumab, rilonacept) and interleukin-6 inhibitors (e.g. tocilizumab) may be considered. Management of ATTR<unk>  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. Previously, for variant ATTR<unk> , liver transplant was the only effective treatment. New therapies include diflunisal, inotersen, and patisiran. Diflunisal binds to misfolded mutant TTR protein to prevent its buildup, like how tafamidis works. Low-certainty evidence indicates that it mitigates worsening of peripheral neuropathy and disability from disease progression. Inotersen blocks gene expression of both wild-type and mutant TTR, reducing amyloid precursor. Moderate-certainty evidence suggests that it mitigates worsening of peripheral neuropathy. Long-term efficacy and safety of inotersen use in people with mutant TTR-related<unk>  is still be evaluated in a phase-III clinical trial as of 2021. Both diflunisal and inotersen may<unk> so mitigate declines in quality-of-life, though the evidence for this effect is unclear. For people with cardiac ATTR the effect of inotersen use is inconclusive and requires further investigation. In 2018, inotersen was approved by the European Medicines Agency to treat polyneuropathy in adults with hereditary transthyretin<unk> . It has since been approved for use in Canada, the European Union and in the USA. Patisiran functions similarly to inotersen. Moderate-certainty evidence suggests that patisiran mitigates worsening of peripheral neuropathy and disability from disease progression. Additionally, low-certainty evidence suggests that patisiran mitigates decreases in quality-of-life and slightly reduces the rate of adverse events versus placebo. There is no evidence of an effect on mortality rate. A review of early data from use of patisiran in people with variant cardiac ATTR suggests that it may reduce mortality and hospitalization, however this is still being investigated and requires further investigation. In 2018, patisiran was not recommended by NICE in the UK for hereditary transthyretin-related<unk> . As of July 2019 further review however is occurring. It was approved for this use in the United States, however. The roles of inotersen and patisiran in cardiac ATTR<unk>  are still being investigated. In 2021, in a clinical trial using the CRISPR gene-editing technique, several participants had an "80% to 96% drop in TTR levels, on par or better than the average of 81%" who were given patisiran. Support groups People affected by<unk>  are supported by organizations, including the<unk>  Research Consortium,<unk>  Foundation,<unk>  Support Groups, and<unk>  Australia.
Amyloidosis
Sjögren syndrome  Sjögren syndrome  1
Gamasoidosis
Melioidosis
Sarcoidosis
Amyloid cardiomyopathy
Neurosarcoidosis
Cardiac amyloidosis