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Autoimmune Hemolytic Anemia

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Following specialists treat  Autoimmune Hemolytic Anemia.

Overview

Autoimmune hemolytic anemia is a condition characterized by the body’s production of proteins known as antibodies, which attack the person’s own normal red blood cells causing them to rupture. The result is that the affected individual’s red blood cell levels decreases, and this leads to reduced oxygen supply to the organs and tissues of the body.

The normal life cycle of red blood cells is around 120 days, and with autoimmune hemolytic anemia this number can decrease down to a few days in severe cases.

Autoimmune hemolytic anemia can be classified as either warm or cold subtypes, with the latter including conditions such as paroxysmal cold hemoglobinuria and cold agglutinin disease. Each of these diseases has different causes and management protocols, so it’s very important to correctly classify the condition.

Prevalence of autoimmune hemolytic anemia

Autoimmune hemolytic anemia is a rare condition which affects one to three people in every 100,000 individuals annually.

What causes autoimmune hemolytic anemia?

The causes of autoimmune hemolytic anemia aren’t clearly understood, and researchers think that the condition may have primary causes or may be secondary to other underlying diseases.

In 50 percent of cases the cause of autoimmune hemolytic anemia is idiopathic, which means that there is no direct known cause of the condition.

Warm autoimmune hemolytic anemia is due to secondary causes which include other autoimmune conditions such as lupus, rheumatoid arthritis, Crohn’s disease, scleroderma, and ulcerative colitis, and lymphoproliferative conditions such as lymphoma and chronic lymphocytic leukemia. Rare causes include infections and non-lymphoid cancers.

Rarely, certain medications such as penicillin and alpha-methyldopa can also cause autoimmune hemolytic anemia.

Cold agglutinin disease is typically classified as primary (unknown cause) or secondary (caused by an underlying condition). Secondary cold agglutinin disease may be associated with:

Signs and Symptoms

The signs and symptoms of autoimmune hemolytic anemia commonly include paleness of the skin, fatigue, dizziness, lightheadedness, and generalized weakness.

Less common clinical features may include an increased heart rate which may or may not have an irregular rhythm, chest palpitations, yellowing of the skin and/or white of the eyes (jaundice), and dark urine.

Diagnosis

The diagnosis of autoimmune hemolytic anemia is suspected on the medical history given by the patient and the clinical findings made on examination. Other causes of decreased red blood cell levels also need to be excluded to reach the diagnosis of autoimmune hemolytic anemia.

A complete blood count with a peripheral smear of the affected blood will demonstrate the hemolysis (blood cell destruction) caused by the condition. Bilirubin and lactate dehydrogenase levels will also be elevated as these are contents of the red blood cells which are released. Urine tests will demonstrate increased levels of urobilinogen, too.

A positive direct Coombs test in the presence of the above-mentioned serum and urinary results will confirm the diagnosis of the condition.

Management

The management of autoimmune hemolytic anemia will depend on the type of blood disorder present in the affected individual.

Warm-type autoimmune hemolytic anemia is managed by first reducing the inflammation cause by the autoimmune reaction with corticosteroids. If this fails, then surgical removal of the spleen (splenectomy) is indicated. Medications that can be used include those that suppress the immune system such as danazol, cyclosporine, cyclophosphamide and rituximab.

Cold agglutinin disease is managed by avoiding cold temperatures, which is the trigger for the condition. Patients with a more severe case of this subtype may be managed with rituximab.

Is autoimmune hemolytic anemia inherited?

In many cases, the cause of autoimmune hemolytic anemia remains unknown. Some researchers believe that there are multiple factors involved, including genetic and environmental influences (multifactorial). In a very small number of cases, autoimmune hemolytic anemia appears to run in families. In these cases, it appears to follow an autosomal recessive pattern of inheritance.

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Treatment of autoimmune hemolytic anemia

An autoimmune disease is one where antibodies are produced which attack an element of our own body. Antibodies are the molecules produced by our immune system which are designed to recognize and destroy ‘foreign’ material. For example, we normally make antibodies to recognize bacteria or viruses, a crucial step in allowing our immune system to identify and destroy the disease. However, if the body ‘incorrectly’ makes antibodies against cells or molecules which belong to us then that part of the body is attacked, leading to an auto-immune disease.  More well-known autoimmune diseases include rheumatoid arthritis or inflammatory bowel disease. However, auto-immune diseases can also attack the skin, the thyroid gland and even the blood cells. Autoimmune hemolytic anemia (AIHA) occur when the body produces antibodies which recognize our own red blood cells. These antibodies then attach to the red blood cells and ‘burst’ (or hemolyse) them. As the body cannot keep up with the rate of destruction of red blood cells, the patient becomes anemic – and may suffer with symptoms including shortness of breath, fatigue and fainting. In the most severe cases, there may not be sufficient red cells to transport oxygen to the tissues and the person becomes critically unwell.

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Research

Recent research related to Autoimmune Hemolytic Anemia