OCD tx after SJS on sertraline?

[Penguin10]

Does anyone know of papers/guidance on SSRI or TCA use for patient with history of stevens johnson syndrome after starting sertraline?

I could only find a couple of case reports in languages I am not fluent in regarding antidepressant rechallenge.

Tried memantine monotherapy with limited response, pt hesitant about SGAs and asked to reconsider antidepressants, but I can't locate any very specific discussion about risk of recurrence with various options, just vague 'avoid class' stuff (which given the literature on rechallenge with lamotrogine seems a little hand wavey).

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[wolfvgang22]

Did the patient have SJS from Sertraline? Or did the patient have SJS from lamotrigine?

 

[clausewitz2]

Does anyone know of papers/guidance on SSRI or TCA use for patient with history of stevens johnson syndrome after starting sertraline?

I could only find a couple of case reports in languages I am not fluent in regarding antidepressant rechallenge.

Tried memantine monotherapy with limited response, pt hesitant about SGAs and asked to reconsider antidepressants, but I can't locate any very specific discussion about risk of recurrence with various options, just vague 'avoid class' stuff (which given the literature on rechallenge with lamotrogine seems a little hand wavey).

This paper I found in what looks like probably not the highest impact factor journal suggests that sertraline is probably uniquely bad in terms of propensity for causing SJS among common antidepressants:

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: Assessment of Medication Risks with Emphasis on Recently Marketed Drugs. The EuroSCAR-Study

Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but severe cutaneous adverse reactions (SCAR) related to a variety of med…

www.sciencedirect.com

In general more of the literature supports the idea that cross-reactivity really shouldn't be the default assumption for SRIs (that is, SSRIs or TCAs) because their chemical structures are not tremendously similar. SJS is not a neurotransmitter driven reaction but an autoimmune one, so the function of the molecule is very much beside the point compared to the conformation of the molecule.

 

[Penguin10]

Did the patient have SJS from Sertraline? Or did the patient have SJS from lamotrigine?

The patient's SJS was to sertraline. Thanks for clarifying, I should type slower.

This paper I found in what looks like probably not the highest impact factor journal suggests that sertraline is probably uniquely bad in terms of propensity for causing SJS among common antidepressants:

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: Assessment of Medication Risks with Emphasis on Recently Marketed Drugs. The EuroSCAR-Study

Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but severe cutaneous adverse reactions (SCAR) related to a variety of med…

www.sciencedirect.com

In general more of the literature supports the idea that cross-reactivity really shouldn't be the default assumption for SRIs (that is, SSRIs or TCAs) because their chemical structures are not tremendously similar. SJS is not a neurotransmitter driven reaction but an autoimmune one, so the function of the molecule is very much beside the point compared to the conformation of the molecule.

Thanks, this is helpful. I will check out the paper. Your second point affirms my general understanding, which is validating. Intellectually, I think it's probably very reasonable to rechallenge with a different SSRI, but I guess that emotionally I would prefer to having something saying someone else tried it first...

 

[hebel]

This paper I found in what looks like probably not the highest impact factor journal suggests that sertraline is probably uniquely bad in terms of propensity for causing SJS among common antidepressants:

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: Assessment of Medication Risks with Emphasis on Recently Marketed Drugs. The EuroSCAR-Study

Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare but severe cutaneous adverse reactions (SCAR) related to a variety of med…

www.sciencedirect.com

In general more of the literature supports the idea that cross-reactivity really shouldn't be the default assumption for SRIs (that is, SSRIs or TCAs) because their chemical structures are not tremendously similar. SJS is not a neurotransmitter driven reaction but an autoimmune one, so the function of the molecule is very much beside the point compared to the conformation of the molecule.

You think this would apply to colitis as well? Either collagenous or lymphocytic.

 

[robellis]

Clomipramine

 

[clozareal]

I'm not familiar with SJS/TEN on SSRIs/TCAs. How was the diagnosis of SJS made in this patient?

This goes without saying, but make sure they have high quality exposure and response prevention.

You can also consider TMS.

 

[Mass Effect]

Why not try TMS? Has the patient failed CBT?

 

[futureapppsy2]

Why not try TMS? Has the patient failed CBT?

Also curious why CBT (particularly exposure response prevention) hasn't been tried here (if it hasn't), given it's high level of effectiveness with OCD and previous medication failures and adverse reactions in this patient.

 

[Penguin10]

I'm not familiar with SJS/TEN on SSRIs/TCAs. How was the diagnosis of SJS made in this patient?

This goes without saying, but make sure they have high quality exposure and response prevention.

You can also consider TMS.

Initial event was in childhood (15+ years ago) so I don't have records, but good reminder to question chart lore.

Extensive therapy with OCD focused therapists without adequate response.

Sertraline has post-marketing SJS reports apparently, it seems to be most commonly implicated SSRI, clomipramine seems to get a bit more press than average too, but this DermNet article reference duloxetine and alprazolam as other known precipitants. Definitely low frequency, high risk.

I offered TMS during intial conversations, but good point to circle back now

Thanks for all the input, appreciate it.

 

[clozareal]

Ah I see. I'm just wondering if it was truly SJS vs DRESS (I think SSRIs may have higher risk for this) vs benign rash, which would have different management strategies. It might be worth it get a dermatology consultation and see what they say. Perhaps they'll suggest testing for HLA-B*58:01 (for DRESS) or HLA-B*1502 (for SJS) testing or something else.

 

[clausewitz2]

I am really hoping nobody is diagnosing SJS without a dermatologist laying eyes on the person somewhere in the tempor vicinity.

Re: other pharmacological treatments if you are dead set on avoiding SRIs for whatever reason, next step is abilify/risperidone at low dose v. memantine. Beyond that you are getting into ondansetron or, hilariously enough, lamotrigine.

If there have really been repeated failures of E/RP and multiple med trials may also be a surgical candidate.

 

[Penguin10]

Ah I see. I'm just wondering if it was truly SJS vs DRESS (I think SSRIs may have higher risk for this) vs benign rash, which would have different management strategies. It might be worth it get a dermatology consultation and see what they say. Perhaps they'll suggest testing for HLA-B*58:01 (for DRESS) or HLA-B*1502 (for SJS) testing or something else.

Interesting thanks!

 

[Penguin10]

I appreciated the input to my question and wanted to share a bit more literature I ran across after posting here:

Byrne, A., Arkell, S., Bandi, P. Progress in Neurology and Psychiatry Vol. 21 Iss. 4, 2017, pages 9-12 (www.progressnp.com)

This case report describes a patient who developed drug-induced hypersensitivity syndrome (which their derm consultant said could have progressed to DRESS).

They identified several other cases in their literature review in which patients developed a severe cutaneous reaction to an SSRI and then went on to have recurrent reactions to other SSRIs.

Jan, V., Toledano, C., Machet, L., Machet, M.C., Vaillant, L., Lorette, G. Stevens Johnson Syndrome after sertraline. Acta Derm Venereol. 1999 Sep; 79(5): 401. doi: 10.1080/000155599750010472. PMID 10494732

This case reports describes an episode of SJS after sertraline and in their lit review cites another paper published in French which they say described cross reactivity with multiple SSRIs in two cases:

Beauquier B, Fahs H. Effets secondaires dermatologiques des
antidepresseurs inhibiteurs de la recapture de la serotonine :
hypothese d'une allergie croisee. A propos de deux cas. Encephale
1998; 24: 62 ± 4.

Obviously a very limited evidence base, but seems to be a pattern that suggests it may be wise to switch classes if someone has a severe skin reaction to an SSRI.

 

[coyotelime]

Curious what you ended up doing in this case given concern for cross reactivity with other SRIs, pt reluctance to try SGAs, and lack of response to glutamatergic therapy. Clomipramine? NAC? TMS (is there good evidence for this?)?

 

[ObsequiousAplomb]

Admittedly, I didn't read what you linked. Did the sources indicate that the risk of SJS is particular to the SSRI class, or does it not make a distinction among classes?

Said in a different way, does the SJS from SSRIs indicate that the person is susceptible to SJS in general, and the other SSRI is merely another medication given to someone sensitive to SJS reactions? Or does the data seem to indicate that structurally unrelated compounds with similar mechanism actually have similar SJS risks, and that this risk is related to the putative MOA?

 

[Penguin10]

Curious what you ended up doing in this case given concern for cross reactivity with other SRIs, pt reluctance to try SGAs, and lack of response to glutamatergic therapy. Clomipramine? NAC? TMS (is there good evidence for this?)?

Talked about all of those, went with clompiramine. I don't know how good TMS looks, but locally more programs are offering it. Curious about insurance coverage too.

 

[Penguin10]

Admittedly, I didn't read what you linked. Did the sources indicate that the risk of SJS is particular to the SSRI class, or does it not make a distinction among classes?

Said in a different way, does the SJS from SSRIs indicate that the person is susceptible to SJS in general, and the other SSRI is merely another medication given to someone sensitive to SJS reactions? Or does the data seem to indicate that structurally unrelated compounds with similar mechanism actually have similar SJS risks, and that this risk is related to the putative MOA?

I don't think there is support for people having general susceptibility to SJS, so I would imagine it's something common to the specific agents, but there's nothing definitive about mechanism from those case reports.

The consensus clinical intuition here, which fit my thinking, was that another SSRI was probably reasonable given the structural differences. I later found case reports of significant skin reactions, not all of which were SJS, with SSRI switches. My takeaway was to remember that lots of things that seem to 'make sense' when reasoning from a physiology/pathophysiology perspective don't hold up in clinical practice and that I need to get better at lit search strategies...