What drugs cause TMA?

What drugs cause TMA?

Antineoplastic therapy may induce TMA. Most of the cases reported are associated with mitomycin. TMA has also been associated with cyclosporin, tacrolimus, muromonab-CD3 (OKT3) and other drugs such as interferon, anti-aggregating agents (ticlopidine, clopidogrel) and quinine.

How do you treat TMA?

For example, infectious causes of TMA might be treated with antibiotics and supportive care. At times, plasma exchange, immune suppression, and/or complement blocking therapies may be used to treat other causes of TMA. Individuals with severe kidney injury may require dialysis.

What is the Plasmic score?

PLASMIC score identifies a subgroup of patients lacking significant response to plasma exchange. Summary: Background The PLASMIC score was recently published to distinguish patients with severe ADAMTS-13 deficiency from those without for early identification of thrombotic thrombocytopenia purpura (TTP).

What medications cause TTP?

In this review, five drugs that have been the subject of the most and the most recent reports of drug-associated TTP-HUS are discussed: mitomycin C, cyclosporine, quinine, ticlopidine, and clopidogrel.

What causes TMA?

The specific cause is dependent of the type of TMA that is presented, but the two main pathways that lead to TMA are external triggers of vascular injury, such as viruses, bacterial Shiga toxins or endotoxins, antibodies, and drugs; and congenital predisposing conditions, including decreased levels of tissue factors …

What are the symptoms of TMA?

Signs and symptoms The clinical presentation of TMA, although dependent on the type, typically includes: fever, microangiopathic hemolytic anemia (see schistocytes in a blood smear), kidney failure, thrombocytopenia and neurological manifestations.

What is Upshaw Schulman syndrome?

Hereditary thrombotic thrombocytopenic purpura (Upshaw-Schulman syndrome) is a rare disorder characterized by thrombocytopenia as a result of platelet consumption, microangiopathic hemolytic anemia, occlusion of the microvasculature with von Willebrand factor-platelet-thrombic and ischemic end organ damage.

How long can you live with TTP?

The most striking evidence for the impact of morbidities following recovery from TTP is decreased survival. Among the 77 patients who survived their initial episode of TTP (1995-2017), 16 (21%) have subsequently died, all before their expected age of death (median difference, 22 years; range 4-55 years).

What triggers TTP?

A lack of activity in the ADAMTS13 enzyme (a type of protein in the blood) causes TTP. The ADAMTS13 gene controls the enzyme, which is involved in blood clotting. The enzyme breaks up a large protein called von Willebrand factor that clumps together with platelets to form blood clots.