Video
Case 2: Prescribing Intranasal Esketamine
Two psychiatrists review the case of 42-year-old female patient with a treatment resistant depression diagnosis that was prescribed intranasal esketamine.
Lisa Harding, MD: We’re going to answer some of these questions as well as we move on to the second case scenario. This is a patient who’s been diagnosed with treatment-resistant depression and has been prescribed intranasal esketamine. This patient is a 42-year-old woman with long-standing MDD [major depressive disorder] and chronic anxiety who was diagnosed in her 20s. She’s now referred with complaints of anxiety, hedonia, and boredom. The patient has tried several treatments over the course of her illness, such as quetiapine, citalopram, paroxetine, and lithium, without complete relief of symptoms. Blood levels were checked regularly and found to be within therapeutic range. She has since developed chronic kidney disease. The patient has a BMI [body mass index] of 30 and severe scoliosis. She was subsequently started on intranasal esketamine.
Angelos, my overall impression of this patient is pretty similar to the first one. When she presented with anxiety, hedonia, and boredom, were those symptoms the beginning of the chronic kidney failure that was found later on? With what frequency were her laboratory tests being drawn? It’s really interesting that this patient was on quetiapine as well. In thinking through where that fit into her treatment regimen, what line of treatment was that? What symptoms was that helping with? In terms of the paroxetine, how much of her symptoms did it even help with? By the blood draws, we know they’re referring to the lithium. The intranasal esketamine was a really good choice in this patient given that if we look at the second-generation augmentation with antipsychotics in a patient who already has a BMI of 30 and looking at the possible auctions of metabolic syndrome vs trying a medication that doesn’t have those effects. What are your thoughts?
Angelos Halaris, MD, PhD, APA, ACNP, CINP: My thoughts are similar to what I shared with you in regard to the first case. But this case is also complicated in its own right because of the concomitant serious medical condition, kidney disease, which could lead to kidney failure and even death. The question is how much of that is in reaction to the physical debilitation. How extensive is the medical problem? Is it being addressed successfully? Is this patient receiving any supportive therapy to help her accept and live with the debilitation from the physical point of view?
I’d like to add another thought that applies to the first case as well. With respect to the selection of a pharmacotherapeutic agent, there are tests on the market that we refer to summarily as pharmacogenomic testing. There are a handful of products marketed, most of them are approved by the FDA, and these tests allow the prescribing provider to ascertain whether the pharmacogenomic profile of the patient will allow us to select a medication that’s congruent. For example, some patients have a pharmacogenomic profile with a variant of the serotonin transporter gene that indicates an SSRI [selective serotonin reuptake inhibitors] wouldn’t be the best choice. Additionally, the test results of such testing allow the provider to determine how to dose the medication. Some people are rapid metabolizers, in which case a higher dose may be OK to achieve response. The reverse can also be true. We could have slow metabolizers with a specific cytochrome P450 enzyme, in which case even conventional doses could lead to adverse effects and lack of tolerability. These are important pieces of information that we can now obtain with a simple test that’s generally covered by insurance with affordable co-pay and can turn people’s lives around.
Lisa Harding, MD: Science has given us many advantages. But my aspirational hope is that litmus tests will come. It’s amazing to know whether they’re fast metabolizers or slow metabolizers, because we know that attrition occurs. When patients get lost to follow-up, they stop medications because of the adverse effects. That is an amazing tool. But stretching beyond that, how do we measure response? We don’t have that litmus test yet to say. Even though they can metabolize the drug, are they going to respond to it?
This transcript has been edited for clarity.
