ABSTRACT
Encephalopathy is a disorder characterized by altered brain function, which can be attributed to various causes. Encephalopathy associated with metronidazole administration occurs rarely and depends on the cumulative metronidazole dose, and most patients with this condition recover rapidly after discontinuation of therapy. Because metronidazole is metabolized in the liver and can be transported by the cerebrospinal fluid and cross the blood-brain barrier, it may induce encephalopathy even at a low cumulative dose in patients with hepatic dysfunction. We experienced a patient who showed ataxic gait and dysarthric speech after receiving metronidazole for the treatment of hepatic encephalopathy that was not controlled by the administration of lactulose. The patient was diagnosed as metronidazole-induced encephalopathy, and stopping drug administration resulted in a complete recovery from encephalopathy. This case shows that caution should be exercised when administering metronidazole because even a low dose can induce encephalopathy in patients with liver cirrhosis.
Subject(s)
Anti-Infective Agents/adverse effects , Brain Diseases/chemically induced , Hepatic Encephalopathy/drug therapy , Liver Cirrhosis/complications , Metronidazole/adverse effects , Anti-Infective Agents/therapeutic use , Brain Diseases/diagnosis , Hepatic Encephalopathy/etiology , Humans , Magnetic Resonance Imaging , Male , Metronidazole/therapeutic use , Middle Aged , Tomography, X-Ray ComputedABSTRACT
Solitary necrotic nodules of the liver occur rarely. Although these nodules are usually benign, they are surgically removed in most cases because they cannot be differentiated from malignant lesions. To date, the natural history of solitary fibrous nodules remains unclear. We present the case of an incidentally detected hepatic mass (diameter 2 cm) in a 35-year-old man. The hepatic mass was diagnosed as a solitary necrotic nodule by liver biopsy. Follow-up radiologic examination revealed that the solitary necrotic nodule had spontaneously regressed. This is the first report on the natural course history of a solitary necrotic nodule.
ABSTRACT
A previous report by this laboratory demonstrated that bacterial iron chelator (siderophore) triggers inflammatory signals, including the production of CXC chemokine IL-8, in human intestinal epithelial cells (IECs). Microarray-based gene expression profiling revealed that iron chelator also induces macrophage inflammatory protein 3 alpha (MIP-3alpha)/CC chemokine-ligand 20 (CCL20). As CCL20 is chemotactic for the cells involved in host adaptive immunity, this suggests that iron chelator may stimulate IECs to have the capacity to link mucosal innate and adaptive immunity. The basal medium from iron chelator deferoxamine (DFO)-treated HT-29 monolayers was as chemotactic as recombinant human CCL20 at equivalent concentrations to attract CCR6(+) cells. The increase of CCL20 protein secretion appeared to correspond to that of CCL20 mRNA levels, as determined by real-time quantitative RT-PCR. The efficacy of DFO at inducing CCL20 mRNA was also observed in human PBMCs and in THP-1 cells, but not in human umbilical vein endothelial cells. Interestingly, unlike other proinflammatory cytokines, such as TNF-alpha and IL-1beta, a time-dependent experiment revealed that DFO slowly induces CCL20, suggesting a novel mechanism of action. A pharmacologic study also revealed that multiple signaling pathways are differentially involved in CCL20 production by DFO, while some of those pathways are not involved in TNF-alpha-induced CCL20 production. Collectively, these results demonstrate that, in addition to some bacterial products known to induce host adaptive immune responses, direct chelation of host iron by infected bacteria may also contribute to the initiation of host adaptive immunity in the intestinal mucosa.
