Lamictal counseling

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Attending1985

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Do you guys routinely discuss hlh when starting lamictal?

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I had to look that up. So my answer is no.
Maybe this would be a good question for a poll.
 
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Straight from the FDA:

"A diagnosis of HLH can be established if a patient has at least five of the following eight signs or symptoms:
• Fever and rash
• Enlarged spleen
• Cytopenias
• Elevated levels of triglycerides or low blood levels of fibrinogen
• High levels of blood ferritin
• Hemophagocytosis identified through bone marrow, spleen, or lymph node biopsy
• Decreased or absent Natural Killer (NK) Cell activity
• Elevated blood levels of CD25 showing prolonged immune cell activation"

AKA, completely useless criteria for the outpatient provider. I just counsel for fever/rash as normal, and warn that if not caught, these could lead to death. This covers SJS/TEN as well as HLH - and I instruct to have them reach out to me if they notice anything unusual.
 
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I don't, just on SJS/TEN as it's black box. If they've got early symptoms I tell them to stop and monitor and if symptoms persist or worsen go to the ER where the docs can work up whatever is necessary.

I just looked up the prevalence. As of 2018 there were 8 cases worldwide of identified lamotrigine-induced HLH. It's unreasonable to expect us to counsel patients on every possible side effect of every med we start, especially if it's not even on the FDA packet inserts.
 
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You can steal my smartphrase.

Start Lamotrigine at 25 mg by mouth daily for 2 weeks, then raise to 50 mg by mouth daily for 2 weeks, then raise to 100 mg by mouth daily. I explained the risks of the medication including the need to take as prescribed, possible rash, and Stevens-Johnson Syndrome. The patient knows if the medication is not taken consistently it cannot simply be resumed at the prior dosage and to call me to see if it can be restarted.

Whenever I start someone on Lamotrigine this is put on their plan and I text this to the patient's phone. I have a medical texting system that keeps a permanent record of texts so I can always prove later it was sent to them.
 
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I am sure to tell women it may render birth control pills less effective.
So my understanding of this is that coadministration of HCP with lamotrigine reduces effective lamotrigine serum levels, but the contraceptive efficacy is not meaningfully affected.


Ltg levels, with and without coadministration of HCP

1691003105556.png


Estrogen and progestin levels, with and without coadministration with ltg:

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" For all subjects studied, and in both pill cycles, serum progesterone values remained well below 5.1 nmol l−1, indicating maintenance of contraceptive efficacy during the period of co-administration."
 
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So my understanding of this is that coadministration of HCP with lamotrigine reduces effective lamotrigine serum levels, but the contraceptive efficacy is not meaningfully affected.


Ltg levels, with and without coadministration of HCP

View attachment 375145

Estrogen and progestin levels, with and without coadministration with ltg:

View attachment 375144


" For all subjects studied, and in both pill cycles, serum progesterone values remained well below 5.1 nmol l−1, indicating maintenance of contraceptive efficacy during the period of co-administration."

This is correct. OCPs generally decrease serum lamotrigine levels up to 50% and those levels can spike during the "off" week of many OCPs, but lamotrigine doesn't generally change the efficacy of OCPs despite a mild decrease in progestin/levonorgestrel levels (up to 20%). Part of why I generally don't like using lamictal for patients I suspect have PMDD and want on OCPs. Same thing with depakote. Other anticonvulsants we use that are enzyme-inducing (carbamazepine, oxcarb, topiramate for example) may decrease efficacy of contraceptives, but it depends on the MOA and formulation of the contraceptive. Also, OCPs also have some funky interactions with benzos and may increase serum concentrations of valium and clonazepam and increase clearance of ativan, so may need dose adjustments depending on what benzo you're using.
 
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Back to HLH, no, I do not and I also had to look up what it was. There are many, many much more likely adverse reactions. Also, the patient is more likely to win the lottery and not just a regular state lottery, but some sort of interstate mega millions thing. Honestly if the patient somehow developed this...it would be hard to tie it back to the lamotrigine even playing a part since it is usually a genetic condition of some sort.
 
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This is correct. OCPs generally decrease serum lamotrigine levels up to 50% and those levels can spike during the "off" week of many OCPs, but lamotrigine doesn't generally change the efficacy of OCPs despite a mild decrease in progestin/levonorgestrel levels (up to 20%). Part of why I generally don't like using lamictal for patients I suspect have PMDD and want on OCPs. Same thing with depakote. Other anticonvulsants we use that are enzyme-inducing (carbamazepine, oxcarb, topiramate for example) may decrease efficacy of contraceptives, but it depends on the MOA and formulation of the contraceptive. Also, OCPs also have some funky interactions with benzos and may increase serum concentrations of valium and clonazepam and increase clearance of ativan, so may need dose adjustments depending on what benzo you're using.
Oh okay I’m not crazy

But the benzos? These are the helpful tidbits I wish we got in didactics
 
I had a patient with HLH once. ICU rotation as an M4. Was not related to Lamictal. We spent some time gawking at the record-setting ferritin results and promptly deferred all decision making to heme.

Like others, I counsel on fever and rash and the potentially life threatening nature of them, and the need for retitration if they stop the med or miss too many doses. No need to get into the weeds.
 
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