Transcript:
John L. Reagan, MD: I’m John Reagan. I’m an associate professor of medicine at The [Warren] Alpert Medical School at Brown University [in Providence, Rhode Island] and the director of hematology at Lifespan Cancer Institute at Rhode Island Hospital.

Nicholas James Short, MD: I’m Nicholas Short from [The University of Texas] MD Anderson Cancer Center in Houston, Texas. I specialize in acute leukemia, AML [acute myeloid leukemia] and ALL [acute lymphocytic leukemia]. We’re here to talk about tumor lysis syndrome. John, start with an overview of what tumor lysis syndrome is.

John L. Reagan, MD: Tumor lysis syndrome is the destruction and release of whatever is within the cell into the blood stream. If you think about your regular chemistry panels, [let’s say] your potassium levels are very low and your sodium levels are very high. That’s because there’s a lot of intracellular potassium. One thing we find with tumor lysis syndrome is that you get release of this potassium within the cells, nucleic acids, phosphorus, and uric acid. Anything within the cell gets released out. The problem with phosphorus is that it sometimes ends up binding to that calcium and lowers your calcium levels. That’s the hallmark problem with tumor lysis syndrome: what’s inside is suddenly released and brought outside. There are some questions and risk factors that happen with tumor lysis syndrome. Nick, can you go into a little more detail in terms of those risk factors?

Nicholas James Short, MD: Some patients have what we call spontaneous tumor lysis syndrome. Oftentimes in the setting of a hematologic malignancy-leukemia or lymphoma, patients can present with these processes ongoing. The cells may be dying because they’re rapidly dividing, but tumor lysis treatment is also something that we give to patients. We give some therapy, which is a sign in some cases that it’s effective, which is good. But these cells then die as a result.

Some of the main risk factors are those hematologic malignancies, particularly leukemias and lymphomas. In general, the more aggressive you think of the malignancy, the more likely it is to cause tumor lysis syndrome. The acute leukemias—AML, ALL—are more likely than the chronic leukemias to cause tumor lysis syndrome. It’s the same for the more aggressive B-cell lymphoma, particularly Burkitt lymphoma. Those are more likely to cause it. Those can all be spontaneous. Of course, when we give treatment, 1 factor is how sensitive the underlying disease is to the treatments we’re giving. If we’re giving a very effective treatment to a very chemotherapy-sensitive leukemia or lymphoma, then that patient may be more likely to develop tumor lysis syndrome.

In 1 example, we can see what that is—for example, venetoclax in CLL [chronic lymphocytic leukemia]. This is a very effective therapy. Historically, we didn’t think CLL caused tumor lysis as much as some of these more aggressive forms of leukemia. But because venetoclax is so effective in treating CLL, we can see that. That’s why there are strategies in place when you’re treating a patient with CLL with venetoclax to do a very slow ramp-up of this.

There are other characteristics that can be associated with the development of tumor lysis syndrome. For example, if the patient has a very high LDH [lactate dehydrogenase], this is a sign of rapid cell turnover. That goes along with the more aggressive malignancies. Patients with baseline renal dysfunction are more likely to get what we would call a clinical tumor lysis syndrome and worsening renal dysfunction. We have to be very cognizant of that. In general, it’s more common when we give treatment to patients with newly diagnosed disease because they’re generally going to be more likely to have chemotherapy-sensitive disease. Unfortunately, as patients go through treatment, their disease often becomes less sensitive to the treatments that we give, and we don’t see as much tumor lysis syndrome in those cases.

Transcript edited for clarity.