Abstract.
We describe a 58-year-old patient with relapsing high-grade non-Hodgkin’s lymphoma who exhibited exacerbation of posthypoxic action myoclonus during high-dose intravenous trimethoprim-sulfamethoxazole (TMP-SMX) treatment for highly suspicious Pneumocystis jiroveci pneumonia (PCP). Three months previously the patient had experienced a hypoxic insult caused by respiratory arrest due to an anaphylactic reaction to antibiotic therapy. He had developed posthypoxic action myoclonus (Lance-Adams syndrome), which was well controlled by oral treatment with piracetam. However, after TMP-SMX therapy (115 mg/kg daily) was started for suspicion of newly developed PCP, posthypoxic action myoclonus worsened dramatically resulting in complete disability. Anti-myoclonic therapy with increased doses of piracetam and valproic acid did not significantly improve his clinical condition. Only when TMPSMX doses were reduced (38 mg/kg daily) on day 12 did action myoclonus cease within 2 to 3 days. We suggest that TMP-SMX can exacerbate posthypoxic action myoclonus.
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Jundt, F., Lempert, T., Dörken, B. et al. Trimethoprim-Sulfamethoxazole Exacerbates Posthypoxic Action Myoclonus in a Patient with Suspicion of Pneumocystis jiroveci Infection. Infection 32, 176–178 (2004). https://doi.org/10.1007/s15010-004-3011-6
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DOI: https://doi.org/10.1007/s15010-004-3011-6