ABSTRACT
BACKGROUND AND PURPOSE: Extensive brainstem diffusion-weighted imaging (DWI) hyperintensity has been associated with poor outcomes. We aim at documenting a series of patients with extensive DWI pontine lesions who achieved independence following endovascular therapy and aggressive medical therapy in the setting of posterior circulation basilar artery occlusion (BAO). METHODS: This is a retrospective endovascular database review of a single-operator experience over a 9-year period for patients with (1) complete BAO, (2) extensive bilateral pontine DWI changes and (3) 90-day modified Rankin scale 0-2. RESULTS: Three out of a total of 40 patients met the inclusion criteria. Case 1 was an 18-year-old male with National Institutes of Health Stroke Scale (NIHSS) 32 on admission, treated 25 h after symptom onset. Case 2 was a 56-year-old male with NIHSS 19, treated 10 h after onset. Case 3 was a 73-year-old male with NIHSS 29, treated 6 h after onset. Full endovascular reperfusion was achieved in all 3 patients. A literature review identified 9 additional cases of extensive pontine DWI changes and good outcome. These patients were young (32 ± 22 years), mostly males (69%), presented with a relatively low posterior circulation Acute Stroke Prognosis Early CT Score (6 ± 1), were treated relatively late from last known normal (13 ± 10 h) and were mostly (84%) treated with endovascular intervention. CONCLUSION: Extensive bilateral pontine DWI lesions among patients with BAO are not an unequivocal indicator of poor prognosis. We advise strong caution when considering these findings in the treatment decision algorithm.
ABSTRACT
BACKGROUND: Clostridium difficile is an anaerobic bacterium that causes antibiotic-associated diarrhea. It produces toxin A and toxin B (TcdB), which cause injury to the gut epithelium. Glutamine is a fundamental fuel for enterocytes, maintaining intestinal mucosal health. Alanyl-glutamine (AQ) is a highly soluble dipeptide derivative of glutamine. We studied whether administration of AQ ameliorates the effects of TcdB in the intestinal cells and improves the outcome of C. difficile infection in mice. METHODS: WST-1 proliferation and cell-wounding-migration assays were assessed in IEC-6 cells exposed to TcdB, with or without AQ. Apoptosis and necrosis were assessed using Annexin V and flow cytometry. C57BL/6 mice were infected with VPI 10463 and treated with either vancomycin, AQ, or vancomycin with AQ. Intestinal tissues were collected for histopathologic analysis, apoptosis staining, and determination of myeloperoxidase activity. RESULTS: AQ increased proliferation in intestinal cells exposed to TcdB, improved migration at 24 and 48 hours, and reduced apoptosis in intestinal cells challenged with TcdB. Infected mice treated with vancomycin and AQ had better survival and histopathologic findings than mice treated with vancomycin alone. CONCLUSIONS: AQ may reduce intestinal mucosal injury in C. difficile-infected mice by partially reversing the effects of TcdB on enterocyte proliferation, migration, and apoptosis, thereby improving survival from C. difficile infection.
