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Warm Autoimmune Hemolytic Anemia (WAIHA)

by | Mar 9, 2021 | News Releases | 0 comments

Bay Biosciences provides high quality, clinical grade bio-specimens, cryogenically preserved sera (serum), plasma and peripheral blood mononuclear cells (PBMC) biofluid samples from patients diagnosed with warm autoimmune hemolytic anemia (WAIHA).

The sera (serum), plasma and PBMC biofluid specimens are processed from patient’s peripheral whole-blood using customized collection and processing protocols. The warm autoimmune hemolytic anemia (WAIHA) bio-specimens are collected from unique patients diagnosed with warm autoimmune hemolytic anemia (WAIHA) disease and are provided to a valued pharmaceutical customer for research, diagnostics, discovery and drug development.

Detailed clinical data, cold agglutinin disease patients history, symptoms, complete blood count (CBC), elevated biomarker levels, genetic and metabolic information, histopathological findings, annotations associated with warm autoimmune hemolytic anemia (WAIHA) patient’s specimens is provided to a valued customer for research, development and drug discovery. The warm autoimmune hemolytic anemia (WAIHA) sera (serum), plasma and peripheral blood mononuclear cells (PBMC) biofluid are processed from patients peripheral whole-blood using customized collection and processing protocols.

Warm Autoimmune Hemolytic Anemia (WAIHA) Overview

Warm antibody autoimmune hemolytic anemia (WAIHA) is an autoimmune disorder characterized by the premature destruction of healthy red blood cells (hemolysis). Autoimmune diseases occur when the body’s own immune system attacks healthy tissue. In the case of WAIHA and other types of autoimmune hemolytic anemia, red blood cells are “tagged” by antibodies and are then destroyed by other types of immune cells. Warm autoimmune hemolytic anemia (WAIHA) is defined as the destruction of circulating red blood cells (RBCs) in the setting of anti-RBC autoantibodies that optimally react at 37°C to 40°C.

Warm antibody autoimmune hemolytic anemia (WAIHA) is the most common form of autoimmune hemolytic anemia. Autoimmune hemolytic anemia (WAIHA) is caused by autoantibodies that react with self red blood cells (RBCs) and cause them to be destroyed. Warm AIHA, due to antibodies that are active at body temperature, is the most common type of WAIHA. About half of the cases are of unknown cause, with the other half attributable to a predisposing condition or medications being taken.

 Autoimmune hemolytic anemia (AIHA) is a rare and heterogeneous disease that affects 1 to 3 patients among 100 000 per year in the United States, warm auto-antibodies are responsible for 60 to 70% of WAIHA, this diseases can occur in patients at any age. The disease is termed “warm” because the antibodies are active and cause hemolysis at body temperature, which is not necessarily the case in other types of autoimmune hemolytic anemia. Normally, the red blood cells have a life span of approximately 120 days before they are destroyed by the spleen. In patients with WAIHA, the red blood cells are destroyed prematurely and the rate of production of new cells in the bone marrow can no longer compensate for their loss.

Patients of any age, including children, may develop WAIHA, but it is more common among adults, with a peak incidence between 50 to 70 years. The median age at onset is 52 years. It is possibly slightly more common in women compared to men. Secondary WAIHA is more common in people with predisposing conditions, such as those with lymphomas and leukemias or those with a disease affecting the immune system.

Causes of Warm Autoimmune Hemolytic Anemia (WAIHA)

Warm autoimmune hemolytic anemia (WAIHA) occurs when antibodies produced by the immune system bind to red blood cells and identify them as targets to be attacked. Most of the “tagged” red blood cells are transported to the spleen, where they are destroyed by different types of immune cells. Antibodies are specialized proteins that usually bind to invading organisms and lead to their destruction. There are five main classes of antibodies: IgA, IgD, IgE, IgG, and IgM. Most cases of WAIHA are due to IgG antibodies. Less often, IgM or IgA antibodies cause the disorder. When antibodies attack healthy tissue, they may be referred to as autoantibodies. In the case of WAIHA, these autoantibodies are active and can trigger hemolysis when they are at body temperature.

The trigger leading to the development of autoantibodies against red blood cells is usually unknown. These cases may be referred to as primary or idiopathic WAIHA. The disorder may also have a clear trigger in the case of secondary WAIHA. The list of causes of secondary WAIHA is extensive but notably includes medications, autoimmune diseases such as Systemic Lupus Erythematosus and rheumatoid arthritis, deficiency of the immune system (immunodeficiency), leukemias and lymphomas, infections, and pregnancy. Identifying the cause of secondary WAHIA is important, as it might influence treatment and management of the underlying condition.

Causes of Warm Autoimmune Hemolytic Anemia WAIHA

Warm autoimmune hemolytic anemia (WAIHA) can develop at any age, but the median age of onset is 52 years. This means that one half of affected individuals will be younger than 52 years of age when the disease begins and that the other half will be above the age of 52. The symptoms of WAIHA usually develop slowly over a period of several weeks to months, but in some patients can develop suddenly over a few days.

Specific symptoms that occur may vary from one person to another and depend on the rate of onset, the degree of hemolysis, and the presence of an underlying disorder. Some individuals, especially those with a gradual onset of anemia, may not have any obvious symptoms (asymptomatic).

Symptoms of anemia include paleness of the skin (pallor), fatigue, shortness of breath (dyspnea), dizziness and palpitations. In cases of brisk and severe hemolysis, chest pain, decreased alertness (lethargy), confusion, transient loss of consciousness (syncope), and deregulation of heart rate and blood pressure (hemodynamic instability) might occur.

Hemolysis also leads to increased release of hemoglobin (an oxygen-carrying protein) in the blood and urine, which can result in darkly pigmented urine. Hemoglobin is degraded into a yellow compound called bilirubin, which can accumulate and lead to yellowing of the skin and whites of the eyes (jaundice). An enlarged spleen (splenomegaly) can also be seen. Splenomegaly may cause an affected individual to have a bloated or full feeling in the abdomen. WAIHA is also associated with an increased risk of blood clots in the veins (venous thromboembolism). These clots can notably develop in the legs (deep vein thrombosis) and have the potential to detach, circulate in the blood, and occlude the veins of the lungs (pulmonary embolism). Thromboembolisms typically occur in the weeks after diagnosis and are more common in patients with more severe hemolysis and in those that are treated with surgical removal of the spleen (splenectomy). Rarely, clots can form in the arteries feeding the heart (coronary arteries) and lead to a heart attack (myocardial infarction) or in the arteries of the brain (cerebral arteries) and lead to a stroke. Patients that require a splenectomy are also at a higher rate of developing infections. After being treated, 30% of patients will be cured, and the rest are at risk of developing recurrent episodes of hemolysis. The majority of patients with WAIHA survive, although a mortality rate of about 5% is seen. Mortality is mainly attributed to thromboembolisms and infections, and the risk depends on many factors, notably the cause of WAIHA and the overall health of the affected individual.

Signs and Symptoms of Warm Autoimmune Hemolytic
Anemia (WAIHA)

Following are some of the common signs and symptoms of warm autoimmune hemolytic anemia:

Diagnosis of Warm Autoimmune Hemolytic Anemia (WAIHA)

A diagnosis of hemolytic anemia may be suspected based on a thorough clinical evaluation, a detailed patient history, identification of characteristic symptoms and a variety of tests such as blood tests that measure values of hemoglobin and the percentage of the total blood volume occupied by red blood cells (hematocrit). Blood tests may also show an elevated value of immature red blood cells (reticulocytes), which occurs when the body is forced to produce extra red blood cells to make up for those that are destroyed prematurely. Some individuals with hemolytic anemia have elevated values of bilirubin in the blood (hyperbilirubinemia). Hemolytic anemia also leads to increased values of lactate dehydrogenase (LDH) in the blood, as it is released from destroyed red blood cells. Haptoglobin is a hemoglobin scavenger that gets consumed when increased values of hemoglobin are released in the blood due to hemolysis. Haptoglobin values are therefore low in hemolytic anemia. When hemolytic anemia is suspected to be autoimmune in origin, specialized tests such as a Coombs test may be performed. This test is used to detect antibodies that act against red blood cells. A sample of blood is taken and then exposed to the Coombs reagent. A positive test is indicated when the red blood cells clump in the presence of the reagent. The autoantibodies seen in WAIHA are notable for being of the IgG subtype in most cases and being active at body temperature.

Depending on the case, further testing might be performed to attempt to identify a cause of secondary WAIHA. In summary, the following sequence allows the diagnosis of WAIHA:

1). Detection of anemia with increased reticulocyte counts

2). Determination that the anemia is caused by hemolysis, based on elevated bilirubin and LDH and low haptoglobin

3). Determination that WAIHA is the cause of hemolytic anemia with a Coombs test and

4). possible investigation for a secondary cause of WAIHA.

 

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