Anthony Perissinotti, PharmD, BCOP: Tumor lysis syndrome [TLS] is an oncologic emergency that can be life threatening. It's an urgent diagnosis that we have to monitor for when patients are getting chemotherapy. Essentially what happens is when malignant cells that respond to therapy and the intracellular contents get released into the blood stream. The intracellular contents are generally potassium, phosphorus, and then nucleic acids, which can turn into uric acid. There are 2 general definitions that we use, 1 is the Cairo-Bishop criteria and the other is the Howard criteria.

The signs and symptoms of tumor lysis syndrome, I like to break them down into either laboratory or clinical. Laboratory tumor lysis syndrome is characterized by hyperkalemia, hypophosphatemia, hyperuricemia. You see a secondary hypo-low calcium, and this is because the calcium ends up binding with the phosphorus and the phosphorus just overwhelms the calcium and the calcium drops. So those are some of the laboratory findings. We also have the clinical tumor lysis syndrome signs and symptoms which is what we're trying to prevent. The laboratory abnormalities often are OK, but we really want to try to prevent clinical tumor lysis syndrome because this is where things can become more life threatening and cause end-organ damage. So some things that we can see are cardiac arrhythmias, we can see hypotension, heart failure, and renal failure that leads to oliguria, muscle cramps, tetany seizures, syncope and sudden death.

The malignancies that tend to cause tumor lysis syndromes are those that are fast dividing or rapidly growing malignancies or very high bulk tumors. Also disease states that are very responsive to therapy. Some examples are going to be our acute leukemias, acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL). Then some of our lymphoid tumors such as Burkitt lymphoma, a very fast dividing, very responsive disease state. Diffuse large B-cell lymphomas, especially the more aggressive one like double-hit which have rearrangement in MYC and BCL2. We can see also some of our T-cell lymphomas that can be proliferative and very responsive and thus cause tumor lysis syndrome. There is some that believe that some of our solid tumor malignancies can also cause tumor lysis syndrome because there are again some things that are very responsive and fast dividing like our small cell lung cancers. Also our germ cell tumors.

Within pediatrics indeed they also see acute leukemias, but they can also see neuroblastoma, which is again, quite proliferative and responsive to therapy. Actually pediatrics, for whatever reason, their TLS tends to be a little bit more robust. Probably due to the fact that their malignancies are rapidly responsive to therapy as opposed to adults. Besides disease states we do worry about some drugs that can increase patients risk for tumor lysis. I think one of the newest drugs that should be implicated with TLS is venetoclax. This is especially true when we use venetoclax for lymphoid disease states, specifically chronic lymphocytic leukemia [CLL]. Our patients with CLL, cells are primed for death because they have an overactivation of BCL2. And when you add a BCL2 inhibitor like venetoclax you can see profound and robust tumor lysis syndrome. So we have many mitigation strategies to help prevent that from happening.

Transcript edited for clarity.