Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013395 (dyspepsia)
 4,879 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 58-year-old woman with erythropoietic protoporphyria, asymptomatic liver involvement had been diagnosed 12 years earlier. For more than 20 years the patient had been known to have symptomatic gallstones. A mild polyneuropathy of the lower limbs had been diagnosed several years ago. In December 1992, she presented with colicky upper abdominal pain, dyspepsia and mild jaundice. Diagnosis of beginning cholestasis in erythrohepatic protoporphyria and coincidental choledocholithiasis was made. A causal relation between choledocholithiasis and deterioration of liver function was assumed. Endoscopic extraction of the bile duct stones, however, could not prevent the development of terminal hepatic failure. Biochemically, an excessive protoporphyrinemia and coproporphyrinuria were found. Five weeks after presentation, the patient underwent orthotopic liver transplantation. Immediately after the operation she developed a severe axonal neuropathy with cranial nerve involvement. One year after transplantation, her general condition has markedly improved, but there is still a disabling polyneuropathy. Recently, there were single reports on patients with very similar neurological symptoms following liver transplantation in erythropoietic protoporphyria. This case supports the assumption of a distinct protoporphyrin-induced neural damage in severe hepatic failure.
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PMID:Liver failure in erythropoietic protoporphyria associated with choledocholithiasis and severe post-transplantation polyneuropathy. 887 10

The study focuses on evaluation of the Default Mode Network (DMN) activity in functional magnetic resonance imaging (fMRI) in resting state in patients with functional dyspepsia (FD) and irritable bowel syndrome (IBS), Crohn's disease and colitis ulcerosa (IBD) in comparison to healthy volunteers. We assume that etiology of both functional and non-specific inflammatory bowel diseases is correlated with disrupted structure of axonal connections. We would like to identify the network of neuronal connections responsible for presentation of symptoms in these diseases. 56 patients (functional dyspepsia, 18; Crohn's disease and colitis ulcerosa, 18; irritable bowel syndrome, 20) and 18 healthy volunteers underwent examination in MRI of the brain with assessment of brain morphology and central nervous system activity in functional imaging in resting state performed in 3T scanner. Compared to healthy controls' DMN in patients with non-specific digestive tract diseases comprised additional areas in superior frontal gyrus of left hemisphere, in left cingulum and in the left supplementary motor area. Discovered differences in the DMNs can be interpreted as altered processing of homeostatic stimuli. Our study group involved patients suffering from both functional and non-specific inflammatory bowel diseases. Nevertheless a spectrum of changes in the study group (superior frontal gyrus of the left hemisphere, in the left cingulum and in the left supplementary motor area) we were able to find common features, differentiating the whole study group from the healthy controls.
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PMID:Imaging of Morphological Background in Selected Functional and Inflammatory Gastrointestinal Diseases in fMRI. 3250 92