Amyloidosis - Other Illnesses

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What is amyloidosis?

Amyloidosis is a group of diseases that are a consequence of abnormal protein deposits in various tissues of the body. These abnormal proteins are called amyloid. Depending on the structure of the particular amyloid, the protein can accumulate in an isolated tissue or be widespread, affecting numerous organs and tissues. There are over 30 different amyloid proteins.

Amyloid protein can be deposited in a localized area and may not be harmful or only affect a single tissue of the body impairing its function. This form of amyloidosis is called localized amyloidosis. Amyloidosis that affects many tissues throughout the body is referred to as systemic amyloidosis. Systemic amyloidosis can cause serious changes in virtually any organ of the body, including the kidneys, heart, and lungs.

Systemic amyloidosis has been classified into three major types that are very different from each other. These are distinguished by a two-letter code that begins with an A (for amyloid). The second letter of the code stands for the protein that accumulates in the tissues in that particular type of amyloidosis. The types of systemic amyloidosis are currently categorized as primary (AL), secondary (AA), and hereditary (ATTR, amyloid apolipoprotein A1 or AApoAI, amyloid apolipoprotein A2 or AApoAII, AGel, ALys, AFib).

Amyloidosis that occurs as its own entity is called primary amyloidosis. Secondary amyloidosis is amyloidosis that occurs as a byproduct of another illness, including chronic infections (such as tuberculosis or osteomyelitis), or chronic inflammatory diseases (such as rheumatoid arthritis, ankylosing spondylitis, and inflammatory bowel disease). Other forms of amyloidosis include beta-2 microglobulin amyloidosis from chronic kidney dialysis and localized amyloidoses. Amyloidosis that is localized to a specific body area from aging does not have systemic implications for the rest of the body. The protein that deposits in the brain of patients with Alzheimer's disease is a form of amyloid.

Primary amyloidosis

Primary amyloidosis, or AL, occurs when a specialized cell in the bone marrow (plasma cell) spontaneously overproduces a particular protein portion of an antibody called the light chain. (This is why it is coded as AL.) The deposits in the tissues of people with primary amyloidosis are AL proteins. Primary amyloidosis can occur with a bone marrow cancer of plasma cells called multiple myeloma (fewer than 20% of AL patients). Primary amyloid is not associated with any other diseases but is a disease entity of its own, conventionally requiring chemotherapy treatment. Researchers at the Mayo Clinic in Rochester, Minn., and Boston University in Boston, Mass., have demonstrated the benefits of stem-cell transplantation for primary amyloidosis. In stem-cell transplantation, the patients' own stem cells are harvested to treat primary amyloidosis by replacing abnormal plasma cells in the bone marrow.

Secondary amyloidosis

When amyloidosis occurs secondarily as a result of another illness, such as chronic infections (for example, tuberculosis or osteomyelitis) or chronic inflammatory diseases (for example, rheumatoid arthritis and ankylosing spondylitis), the condition is referred to as secondary amyloidosis or AA. The amyloid tissue deposits in secondary amyloidosis are AA proteins. The treatment of patients' secondary amyloidosis is directed at treating the underlying illness in that particular patient.

Familial amyloidosis (hereditary amyloidosis)

Familial amyloidosis (ATTR, AApoAI, AApoAII, AGel, ALys, AFib) is a rare form of inherited amyloidosis. The amyloid deposits in most familial amyloidosis are composed of the protein transthyretin, or TTR, which is made in the liver. Familial amyloidosis is an inherited autosomal dominant in genetics terminology. This means that for the offspring of a person with the condition, there is a 50% chance of inheriting it. This form of amyloidosis is also referred to as hereditary amyloidosis.

Beta-2 microglobulin amyloidosis (dialysis amyloidosis)

Beta-2 microglobulin amyloidosis occurs when amyloid deposits develop in patients on dialysis with longstanding kidney failure. The amyloid deposits are composed of beta-2 microglobulin protein and are often found around joints.

Localized amyloidoses

The many forms of localized amyloidosis are a result of amyloid deposits in specific areas of the body and are distinct from systemic forms of amyloidosis that deposit amyloid throughout the body. Localized amyloid deposits occur in the brain from Alzheimer's disease. In various tissues, often with aging (senile amyloidosis), amyloid can be locally produced and deposited to cause tissue injury. Prions are infectious amyloid proteins that transmit the diseases kuru, Creutzfeldt-Jakob disease, fatal familial insomnia, and Gerstmann-Straussler-Scheinker syndrome.

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See what others are saying

Comment from: berrypicker, 55-64 Female (Patient) Published: February 28

I was diagnosed in 2012 with amyloidosis. I thought I was having heart problems but that turned out to be acid reflux and the amyloid deposit was found in my stomach when they did the scope for the reflux. I also have an ulcer found at that time. I have Sjogren's syndrome and sub-acute cutaneous lupus. I take clobetasol for the plaques from the lupus, and Nexium for the reflux. I have no pain, but find I am often more tired than I was. I have read that reducing or eliminating gluten from the diet may help prevent some of the buildup of amyloid chains, and that there are some essential oils that may be of benefit. I am trying to structure my diet to remove refined sugar, gluten, red meat, caffeine, and all processed and deep fried foods. I'm also am adding omega 3, turmeric and probiotics along with my regular vitamins. I read that bromelain helps as well, and will add that when I check with my doctor.

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Comment from: Casey, 55-64 Male (Patient) Published: August 15

My father died of familial amyloidosis in 1987. I was diagnosed in 3/12 when I was 62 years old, I have type Thr60Ala. I have autonomic and peripheral nerve damage, and had cardiac amyloidosis as well. This type requires a heart/liver transplant from the same donor, I was on the waiting lists. I received the dual transplants in 12/13. I am now 8 months out, transplants are doing good, still have to contend with my transthyretin polyneuropathy symptoms. I may go on drug therapy soon, once my immunosuppressants go to lower maintenance dosages.

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