Multiple drugs

Abstract

Various toxicites: case report The man in his 50s developed kidney failure and ischaemic brain damage during treatment with sodium picosulfate and magnesium oxide. He developed hypomanic symptoms secondary to prednisolone. Additionally, he exhibited lack of efficacy during treatment with methylprednisolone, metronidazole and tetracycline [duration of treatments to reaction onsets not stated]. The man was hospitalised due to a 3-week history of frequent voluminous bowel movements. He had a history of myocardial and brain infarction in his 20s. He had been receiving aspirin [acetylsalicylic acid] and simvastatin. Following admission, he started receiving treatment with sodium picosulfate [sodium picosulphate] and magnesium oxide [routes and dosages not stated]. After a week, improvement was noted, and he was discharged with an outpatient clinic appointment for colonoscopy. However, after a month, his condition relapsed, and he was admitted again. At this time, reduced body weight (from 104kg to 82kg) was noted along with acute renal failure (with creatinine value of 115 mmol/L) and acute metabolic acidosis. Thus, the man’s treatment was started with an unspecified fluid infusion. On the following day, dysarthria and ataxia were noted leading to the suspicion of stroke. Thus, he was transferred to the neurology department at a regional hospital for assessment for thrombectomy. He was noted to have a recent infarction in the small brain and brain stem, a thrombus in the left subclavian artery and occlusion of the distal left vertebral artery. Eventually, his neurological symptoms improved and a complete remission was achieved. He received dalteparin, and was transferred back to the local hospital. After haematological assessment, he received clopidogrel in favour of aspirin in order to optimise stroke prophylaxis. Later, the dose of dalteparin was reduced for inpatient thromboprophylaxis. Based on examinations, it was considered that his prerenal kidney failure and ischaemic brain damage were associated with the combined treatment with sodium picosulfate and magnesium oxide. Over the following two months, chronic active inflammation with cryptitis and total toteatrophy [Sic.] in all small intestine segments was observed. The picture showed microscopic atrophy of intestinal tumours and diffuse inflammation. Testing for antibodies against cardiolipin was transiently positive. An examination showed small intestine anaerobic bacterial overgrowth. Subsequently, he received treatment with oral metronidazole 400mg×2 [Sic.] and oral tetracycline 250mg×4 [Sic.] for over 2 weeks, but no effect was noted. He also received multiple medications; however, they did not provide sufficient efficacy. He received oral high-dose prednisolone 30 mg/day treatment for suspected Crohn’s disease that resulted in a temporary good effect; however, the treatment lead to the development of hypomanic symptoms. After steroid tapering, the symptoms relapsed. There was a lack of sufficient effect with azathioprine. He was transferred to bed ward at a regional hospital. Steroids and azathioprine were stopped, he was treated with vedolizumab. After a few months, his condition deteriorated further. After further investigations, he was diagnosed with autoimmune enteropathy. Thus, he received IV methylprednisolone 40mg daily for 2 weeks. After no clinical or endoscopic response, methylprednisolone was stopped. Later, he was treated with infliximab and budesonide, and improvement was noted. He received azathioprine to prevent the formation of antibodies to infliximab. After discharge, he was hospitalised once due to diarrhoea and elevated gall stasis parameters. During a 10-month follow-up, a clear improvement was noted. The treatment regimen consisting of infliximab and budesonide, was tapered down and was later stopped [not all outcomes stated].