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       #Post#: 5042--------------------------------------------------
       (Abst.) Cardiogenic shock after ocrelizumab infusion in RRMS (MS
        Journal)
       By: agate Date: January 2, 2026, 1:55 am
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       This article was "restricted access" but through an
       institutional affiliation (University of Chicago alumni access)
       I was able to get it and will see if a link to it will work
       here.
       From Multiple Sclerosis Journal (December 31, 2025):
       Cardiogenic shock after ocrelizumab infusion in
       relapsing-remitting multiple sclerosis
  HTML https://journals.sagepub.com/doi/10.1177/13524585251407501?_gl=1*1hyni0n*_up*MQ..*_ga*MTEyOTkwMjA0Ni4xNzY3MzM5ODk5*_ga_60R758KFDG*czE3NjczMzk4OTgkbzEkZzEkdDE3NjczMzk5OTckajYwJGwwJGg2Mjk2NzgzMDE.
       EDITED TO ADD: Apparently access to the full article will be
       denied using that link but at least the abstract is viewable.
       #Post#: 5043--------------------------------------------------
       Excerpt from article on cardiogenic shock after ocrelizumab infu
       sion
       By: agate Date: January 3, 2026, 1:29 am
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       This article contains some observations about ocrelizumab,
       rituximab, and ofatumumab (reference notes omitted):
       [quote]
       The temporal relationship with drug administration, in
       combination with the reversibility of left ventricular
       dysfunction and the exclusion of alternative causes in a
       previous healthy patient, suggests a causal association with
       ocrelizumab, which was rated as “probable” according to the
       Naranjo scale. Further support for a potential role of
       ocrelizumab comes from the recognized cardiotoxicity of
       Rituximab, a chimeric anti-CD20 antibody, which has been
       associated with myocardial infarction, arrhythmias, and
       cardiogenic shock. A pharmacovigilance analysis of the US Food
       and Drug Administration Adverse Events Reporting System (FAERS)
       database in 2022 revealed an increased risk of major
       cardiovascular complications in patients taking ocrelizumab or
       ofatumumab (subcutaneously administered fully human anti-CD20
       monoclonal antibody) for MS. Acute coronary syndromes and heart
       failure were more frequently reported with ocrelizumab, whereas
       atrial fibrillation was more commonly reported with ofatumumab.
       Since FAERS is a spontaneous reporting system, complete
       information on patients' cardiovascular risk factors,
       co-morbidities and concomitant medications is often lacking, and
       a causal link between the cardiac events and the drugs cannot be
       established. To date, no consistent or confirmed safety signals
       have been formally recognized by regulatory authorities (FDA and
       EMA).
       The mechanisms behind anti-CD20-related cardiac toxicity are
       unknown, but a dysregulation of the immune system can be
       hypothesized. In our case, given the lack of systemic allergic
       symptoms and the gradual onset, an acute coronary syndrome in
       the context of a type I hypersensitivity reaction (named Kounis
       syndrome) can be excluded. Instead, the temporal course of
       symptoms suggests a delayed immune-mediated reaction. Many
       cardiac adverse events reported with rituximab occurred during
       or soon after the first infusion, likely due to cytokine release
       syndrome. Still, reports of heart failure with a more subacute
       onset (>24 hours) or after subsequent infusions also exist.
       Kanamori et al. described three cases of delayed and progressive
       reduction in left ventricular function following rituximab
       administration. In these patients, increased serum levels of
       transforming growth factor- (TGF-β) and accumulation of
       reticulin fiber in cardiomyocytes were observed after infusion,
       potentially contributing to impaired myocardial contractility
       and conduction. Histological analysis in our patient excluded
       significant interstitial myocardial fibrosis. Nonetheless,
       experimental studies in animal models demonstrated that B-cell
       depletion may up-regulate proinflammatory cytokines in the
       serum; in this light, it is possible that transient
       cytokine-mediated effects may have contributed to the reversible
       cardiac dysfunction observed. Additional plausible contributors
       include disturbances in intracellular calcium homeostasis,
       possibly linked to CD20 ion channel function, and increased
       oxidative stress, supported by experimental data showing
       increased ROS production and mitochondrial alterations after
       B-cell depletion and cytokine release.[/quote]
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