Ibrutinib/rituximab interaction
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Disseminated enterovirus infection: case report A 57-year-old man developed disseminated enterovirus infection following combined treatment with ibrutinib and rituximab for Mantle cell lymphoma (MCL). The man was diagnosed with MCL in July 2017. He also had a history of arterial hypertension and mild neuropathy. He was initiated on treatment with alternate R-CHOP/R-DHAP regimens consisting of rituximab, dexamethasone, cytarabine and cisplatin, as a part of clinical trial. After achieving complete remission, he was initiated on maintenance therapy from February 2018 with ibrutinib 560mg once daily and SC rituximab 1400mg every 8 weeks [not all routes stated]. In August 2018 at the age of 57 years, he developed a painful swelling of his calves. A subsequent examination did not reveal deep venous thrombosis or soft tissue infection. He revealed that he had also previously developed a short episode of gastroenteritis. The man was treated with unspecified diuretics, however, the treatment only showed temporary improvement. Over the following weeks, his symptoms worsened and spread to the upper extremity and proximal trunk muscles. He was treated with steroids. Additionally, ibrutinib was discontinued transiently, but discontinuation showed no effect. In November 2018, the swelling in his calves worsened. He did not show new physical findings except a single, slightly enlarged lymph node of the right groin. Laboratory examinations showed increased levels of creatine kinase and lactate dehydrogenase; further testing was negative for autoimmune serology. Treatment with dipyrone [metamizole] and tilidine showed only limited effect. A CT scan in January 2019 showed diffuse subcutaneous oedema, but there were no signs of lymphoma relapse. His condition deteriorated and he had difficulty walking. His limb swelling progressed and he was hospitalised. Upon admission, he reported generalised pain and his performance score deteriorated further. Examination showed significant generalised oedema prominently in lower extremities and slight erythema. The muscles of his extremities and trunk were sensitive to palpitation and painful. He did not show neurological deficit, but weak symmetric fist closure and shoulder lift were noted. He was diagnosed with myositis of an unknown cause. His differential diagnoses included autoimmune myositis, therapy-related side effects or neurological disease or infectious disease. Suspecting therapy-related side effects, ibrutinib and rituximab were discontinued. Initial laboratory analysis was significant for inflammatory constellation and slightly elevated transaminases. His immunoglobulin G levels, plasma protein and albumin levels were decreased. He showed elevated creatine kinase. Further analysis only confirmed mild neuropathy. An MRI exam of the thighs showed myositis, which was confirmed by a muscle biopsy. He further developed acute kidney injury with further increase in uric acid, lactate dehydrogenase, creatine kinase, leukocyte count and myoglobin. Hence, a diagnosis of rhabdomyolysis
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