Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Posterior reversible encephalopathy syndrome (PRES) is characterized by a clinical and radiological entity with the sudden onset of seizures, headache, altered consciousness, and visual disturbances in patients with the findings of reversible vasogenic subcortical edema without infarction. Hypertension, renal disease, and autoimmune disease are co-morbid conditions of PRES. Nevertheless, there have only been a few case reports of PRES in a patient with anti-glomerular basement membrane antibody glomerulonephritis (anti-GBM GN). This paper presents the possible first Korean case of a 36-year-old woman with the striking features of PRES. She presented with a sudden onset of visual blindness, headache, and seizure. The brain MRI images revealed hyperintense lesions in both the occipital and parietal lobes, which suggested vasogenic edema. Three months before this presentation, she was diagnosed with anti-GBM GN. Since then, she underwent immunosuppression with cyclophosphamide and steroid, and hemodialysis for renal failure with a treatment of anti-GBM GN.
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PMID:Unusual Case of Posterior Reversible Encephalopathy Syndrome in a Patient with Anti-glomerular Basement Membrane Antibody Glomerulonephritis: A Case Report and Review of the Literature. 2904 2

Small and medium vessel vasculitides, either ANCA-associated or caused by anti-GBM antibodies, are multisystemic diseases with predominantly renal involvement that often require dialysis support; clinical remission can be induced with immunosuppressive therapies including apheretic treatments, high doses of steroids, and immune suppressants. In addition to the complications resulting from the primary pathological process, those associated with the immunosuppressive therapies are not negligible. Reversible Posterior Encephalopathy Syndrome (PRES) is a clinical condition with a hyperacute onset, which can complicate the evolution of vasculitides while treated by immunosuppressive therapy. Relevant pathogenic factors are represented by alterations of the cerebral blood-brain barrier or vasogenic and/or brain edema phenomena, also related to uncontrolled hypertension. We describe two cases of patients with systemic vasculitides, rapidly progressive renal failure (RPGN) requiring dialysis, and poor response to the initial immunosuppressive therapy who were treated subsequently with rituximab. PRES developed immediately after administration of the drug, which, however resulted effective on the course of the vasculitis in one case and not effective in the other. In both cases, the subsequent radiological controls showed a total resolution of the encephalic alterations observed during the acute phase.
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PMID:[Posterior Reversible Encephalopathy Syndrome (PRES) induced by Rituximab in two patients with vasculitis, and treated by hemodialysis]. 3003 47

Anti-glomerular basement membrane (anti-GBM) antibody disease is a rare type of small-vessel vasculitis. Posterior reversible encephalopathy syndrome (PRES) is a syndrome of heterogeneous aetiologies grouped together based on similar neuroimaging findings. We report a rare case of a patient who received treatment for anti-GBM antibody disease who developed PRES. A 33-year-old woman presented with severe generalised oedema, proteinuria, haematuria, and cylindruria. She was diagnosed with anti-GBM antibody disease based on positive findings for anti-GBM antibodies and urinalysis. Haemodialysis was eventually required. She received steroid therapy, plasma exchange therapy, and intravenous cyclophosphamide, along with a red blood cell transfusion for progressive anaemia. After the transfusion, she experienced nausea, severe headache, visual hallucinations, and agitation followed by seizures and a rapid increase in blood pressure. Imaging studies led to a diagnosis of PRES. Renal failure improved with the decrease in anti-GBM antibodies, and haemodialysis was discontinued. Phenytoin was administered, and seizures disappeared. Although we cannot rule out the possibility that the treatment this patient underwent for anti-GBM antibody disease led to the development of PRES, we speculate that endothelial dysfunction leading to the development of PRES is caused not only by known risk factors such as cytotoxic agents, blood transfusions, or renal failure, but also by immunological abnormalities and subsequent inflammatory reactions due to anti-GBM antibody disease. These factors may be shared pathophysiologic mechanisms of PRES and anti-GBM antibody disease.
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PMID:Anti-glomerular basement membrane antibody disease complicated by posterior reversible encephalopathy syndrome. 3286 22