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Cause And Symptoms

Complications

Diagnosis And Treatment

Overview

Prevention

References

acquired-thrombotic-thrombocytopenia-purpura-attp

Acquired Thrombotic Thrombocytopenia Purpura aTTP

<h2>What is TTP?</h2>
Thrombotic thrombocytopenic purpura (TTP)— A rare, life-threatening medical emergency
TTP is a rare, life-threatening thrombotic microangiopathy (TMA). There are approximately 3 cases per million people.1,2 
 The name thrombotic thrombocytopenic purpura describes the 3 main characteristics of the disease.

Thrombotic:&nbsp;characterized by the formation of microthrombi (blood clots) within a blood vessel, which clog the vessel and prevent blood circulation.

Thrombocytopenic:&nbsp;a lower-than-normal platelet count due to the consumption of platelets during microthrombi formation, which causes occlusion of microvasculature.

Purpura:&nbsp;spots of variable size on the skin or in the mucous membranes, due to small hemorrhages; they can be dark red and as small as a pinhead (petechiae) or purplish and 2 to 3 cm in diameter (ecchymosis).

<h2>Types of TTP</h2>

<h2>Primary aTTP vs secondary aTTP2,6,7</h2>

<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="background-color: rgb(241, 135, 0);">
 TTP causes systemic microthrombi and consequent thrombocytopenia, hemolytic anemia, and organ ischemia. These symptoms—coupled with TTP’s rarity—can cause confusion with other TMAs, making TTP a challenge to diagnose.8-10</td>
 </tr>
 </tbody>
</table>

<h2>Signs and symptoms of aTTP include1,7-10</h2>

Petechiae, purpura, bruising (skin)

Headache, confusion, seizures, coma 
 (neurological)

Abdominal pain, diarrhea 
 (gastrointestinal)

Suspect aTTP?

<h2 style="text-align: center;">The incidence of TTP is 2 to 6 per million individuals4</h2>

<h2 style="text-align: center;">aTTP primarily affects young, healthy adults13,14</h2>

years of age on average

of people affected are women

higher aTTP incidence 
 in the Black population

<h2 style="text-align: center;">If left untreated, TTP is rapidly fatal8,15-17</h2>

acute mortality rate16,17

of TTP deaths occur within 24 hours of presentation8

<h3 style="text-align: center;">Even with plasma exchange therapy (PEX), mortality risk persists15,16,18</h3>

<h2>The burden of thrombotic thrombocytopenic purpura (TTP)</h2>
Short- and long-term implications threaten patients with aTTP
<h3>Short-term implications</h3>

An increased time at risk of microvascular thrombosis can lead to irreversible organ damage to the heart, brain, and kidneys16

<h3>Long-term implications</h3>

<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="background-color: rgb(241, 135, 0); text-align: center;">Long-term morbidity leads to suboptimal health-related quality of life, in both mental (anxiety, depression) and physical functioning, and potentially reduces life expectancy8-20</td>
 </tr>
 </tbody>
</table>

Abbreviations

<h2>The pathophysiology of thrombotic thrombocytopenic purpura (TTP)</h2>
<h3>TTP is characterized by potentially fatal systemic microthrombi1,2</h3>
TTP is caused by severely decreased activity of the ADAMTS13&nbsp;enzyme. ADAMTS13 is the protease that cleaves von Willebrand factor (vWF). In patients with acquired TTP (aTTP), this deficiency is immune mediated.1
Decreased ADAMTS13 activity leads to an accumulation of ultra-large von Willebrand factor (ULvWF) multimers, which spontaneously bind to platelets and induce aggregation. This results in dangerous microthrombi that drive severe thrombocytopenia, microangiopathic hemolytic anemia, and organ ischemia.2
ADAMTS13=a disintegrin and metalloproteinase with thrombospondin type 1 motif, 13.
<h4>TTP pathophysiology</h4>
An in-depth exploration of the causes of TTP and the severe consequences of the disease.

TTP is a life-threatening thrombotic microangiopathy (TMA) that requires quick diagnosis and urgent treatment.&nbsp;1,2

Understanding TTP

<h2>What is the pathophysiology of aTTP?</h2>
<h3>3 Key mechanisms drive the pathophysiology of aTTP2</h3>

Auto antibody formation 
 Autoantibodies to ADAMTS13 inhibit its activity or enhance clearance of the enzyme.

ADAMTS13 deficiency causes&nbsp;uncleaved ULvWF 
 ADAMTS13 (the enzyme responsible for cleaving vWF in the blood-clotting process) is deficient, leaving platelet-hyperadhesive ULvWF strands intact to circulate without being cleaved.

Microthrombi formation 
 ULvWF accumulates and spontaneously binds to platelets, forming microthrombi.

<h3>Normal Physiology2,3</h3>

<h3>Thrombotic Thrombocytopenic Purpura2,3</h3>

Adapted from Joly B et al.&nbsp;Blood&nbsp;2017 and Saad J &amp; Schoenberger L 2018.

<h2>Formation of microthrombi causes2</h2>

<h4>Severe thrombocytopenia</h4>
(often platelets &lt;30 × 109/L)

<h4>Microangiopathic hemolytic anemia 
 (MAHA)</h4>
characterized by the presence of schistocytes in blood smear

<h4>Organ ischemia</h4>
(lesions can occur in any organ, but they most frequently affect the heart, brain, gastrointestinal tract, and kidney)

<table border="1" cellpadding="1" cellspacing="1" style="width:100%;">
 <tbody>
 <tr>
 <td style="text-align: center; background-color: rgb(241, 135, 0);">Platelet aggregation leads to microthrombi formation, which can have fatal consequences.1,2</td>
 </tr>
 </tbody>
</table>

<h2>Signs and symptoms of aTTP</h2>
The symptoms of aTTP are driven by microthrombi, which are unpredictable and potentially fatal1,2
Microthrombi can have serious acute and chronic consequences in TTP—putting patients at risk for devastating effects and death without urgent treatment.

<h3 style="text-align: center;">Microthrombi can occur in any organ with microvessels, but the most commonly affected are3</h3>

Tissue and organ damage resulting from ischemia leads to increased levels of lactate dehydrogenase (LDH), troponins (heart), and creatinine (kidney).¹,⁴

<h2>Expert Opinion About aTTP</h2>

<h2>Signs and symptoms of acquired thrombotic thrombocytopenic purpura (aTTP) include1,4,5</h2>

of TTP episodes result in ischemia due to platelet aggregation in the microcirculation of the brain.3

<h2>The consequences of microthrombi can be severe, with TTP potentially resulting in acute thromboembolic events such as1,2,4</h2>

<h4>&nbsp;</h4>
<h4>Arterial thrombosis</h4>

<h2>Consequences can also be long term</h2>

TTP is a life-threatening thrombotic microangiopathy (TMA) that requires quick diagnosis and urgent treatment. 1,2

ACQUIRED-THROMBOTIC-THROMBOCYTOPENIA-PURPURA-ATTP

RARE-BLOOD-DISORDERS

Acquired

Thrombotic

Thrombocytopenic

Purpura

Acquired or immune-mediated thrombotic thrombocytopenic purpura (aTTP) is a rare blood disorder that develops when the immune system stops ADAMTS13 from working properly. This syndrome is characterized by anemia caused by damage to red blood cells accompanied by a low platelet count, neurologic symptoms, and renal disease.1
<table border="1" cellpadding="1" cellspacing="1" style="height: 120px; width: 700px;">
 <tbody>
 <tr>
 <td>aTTP share many similarities with other blood diseases, whose treatment algorithms are different from aTTP. Thus, accurate diagnosis is an essential step to accurately prescribe an effective treatment. To do so, ADAMTS13 activity testing should be done.1</td>
 </tr>
 </tbody>
</table>
<table border="1" cellpadding="1" cellspacing="1" style="width:700px;">
 <tbody>
 <tr>
 <td style="text-align: center; background-color: rgb(68, 11, 18);">Your role is crucial to the diagnosis and speed of appropriate treatment for aTTP</td>
 </tr>
 </tbody>
</table>

ADAMTS13 Activity testing will help confirm or exclude your patient’s TTP disease diagnosis. In addition, the test results may assist clinical decision making in the treatment of aTTP.2

The management of exacerbations and disease relapse is an important aspect of treatment and follow-up of patients with immune-mediated thrombotic thrombocytopenic purpura (iTTP), also known as acquired TTP. Severe ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) deficiency during clinical remission is associated with risk of relapse and may guide prophylactic immunemodulatory therapy.

black

Patients with TTP in remission should have regular ADAMTS13 activity measurements during follow- up. Although not based on a formal review of published evidence, it is suggested that ADAMTS13 levels should be assessed monthly for the first 3 months, every 3 months through the first year, and every 6–12 months thereafter.1 A decline in ADAMTS13 activity might warrant more frequent measurements, as persistently low levels may increase the risk for relapse.4,5

A blood sample for ADAMTS13 testing (ADAMTS13 activity and inhibitors or anti-ADAMTS13 IgG) should be obtained prior to initiation of therapeutic plasma exchange (TPE) or any blood product in a patient with clinical suspicion of TTP.4

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aTTP is a Medical Emergency With Long Term Consequences

The ISTH TTP Guidelines are the first evidence-based, international guidelines on the diagnosis, treatment, and management of TTP. The guidelines emphasize the importance of diagnosis through clinical assessment or risk assessment tools, such as the French or PLASMIC score. Clinical assessment can help predict the likelihood of severe ADAMTS13 deficiency in a patient with suspected TTP and guide treatment decisions.1
Inform your approach to thrombotic thrombocytopenic purpura (TTP) treatment by understanding key clinical considerations and therapeutic options.

The International Society on Thrombosis and Haemostasis (ISTH) TTP Guideline

TTP is a life-threatening thrombotic microangiopathy (TMA) that requires quick diagnosis and urgent treatment. 1,2

Resources

TTP is a life-threatening thrombotic microangiopathy (TMA) that requires quick diagnosis and urgent treatment. 1,2

Acquired Thrombotic Thrombocytopenia Purpura aTTP

Latest Articles

Understanding TTP

aTTP is a Medical Emergency With Long Term Consequences

Resources