Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four children had progressive degeneration of the cerebral cortex, with hepatic cirrhosis. They and four previously described ones, are representative of a distinct form of hepatocerebral degeneration. Onset of the neurological disorder is between ages 1 and 3 years, at times with mild developmental delay. Explosive onset of intractable convulsions, leaving the child in a stuporous and demented state, is characteristic. Generalized hypotonia or hemiparesis were observed in several affected children. Clinical evidences of hepatic disease, including ascites and jaundice, occurred late, if at all. The illness ended fatally within ten months of onset of convulsions. Pathological findings in the brain are neuronal loss and gliosis, in a pattern that is indistinguishable from that in degeneration of the cerebral gray matter in infancy (Alpers disease). The hepatic lesions consist of cirrhosis or of subacute hepatitis, with superimposed fatty infiltration of hepatocytes. The disorder is genetically determined, with recessive inheritance.
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PMID:Infantile diffuse cerebral degeneration with hepatic cirrhosis. 125 62

A 29-year-old man with quiescent multiple sclerosis had hemiparesis during the prodrome of serologically confirmed type A hepatitis. After neurological symptoms and acute hepatitis had abated, hemiparesis again developed when skin tests were applied. While he was receiving prednisone, skin test inflammation and neurological signs cleared. One year later, lymphocyte stimulation, which had been noticeably elevated during his exacerbations, returned to low normal. Both hepatitis A and skin test antigens produced immunostimulation that resulted in exacerbation of multiple sclerosis.
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PMID:Immunologic mechanisms in multiple sclerosis. Exacerbation by type A hepatitis and skin test antigens. 743 54

Epidural abscess is an uncommon infectious disease. The cervical spine is the least frequent site of spinal epidural abscess. It has been reported that early diagnosis and surgical treatment prevent neurological deficit, but it is difficult to diagnose this disease clinically. We presented a rare case of cervical epidural abscess caused by MRSA. A 54-year-old man was admitted to our hospital because of acute renal failure and hepatitis. He was treated with hemodialysis via the femoral route. His renal function recovered but high fever continued. MRSA was identified from the AV shunt catheter. He noted pain and dysesthesia on his left shoulder one month after admission. He was transferred to our department with suspect of spinal tumor. Neurological examination demonstrated left hemiparesis with superficial sensory disturbance between C8 and Th2. Cervical CT scan showed osteomyelitis at the left C7 lamina and facet. MR imaging disclosed that an epidural mass at C7 had low signal intensity on T1 weighted and high signal intensity on T2 weighted and ring-like enhancement with gadolinium. He was treated conservatively for a month. Sequential MR imaging showed the mass had homogeneous enhancement at C7 epidural space extending to the left intervertebral foramen. Laboratory examination showed normal. The patient was diagnosed as having cervical epidural abscess. A C6 through Th2 laminectomy and C8 foraminotomy were performed and an encapsulated abscess including yellowish pus was totally removed. The pathological diagnosis was non-specific abscess in the subacute stage. MRSA was identified by the intraoperative pus culture. After the surgery, antibiotics were administered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cervical spinal epidural abscess caused by methicillin-resistant Staphylococcus aureus (MRSA)]. 796 65

We report the case of a patient with corticosteroid-responsive giant cell hepatitis associated with typical manifestations and changes of polyarteritis nodosa from the kidney and central nervous system. Initially, the patient presented with transient right hemiparesis, followed by spontaneous remission without any abnormalities on computed tomography scan, magnetic resonance imaging and cerebrospinal fluid examination. A few months later he was admitted to our clinic because of icterus, peripheral oedema and abdominal distension. He was found to have clinical signs of active cirrhosis. Serological tests for hepatitis B, C and HIV virus were negative. Serum ceruloplasmin. a1-AT and ferritin levels were within normal limits. Antinuclear antibodies were positive (1: 160). Liver biopsy showed micronodular cirrhosis with many eosinophils in the portal tracts and giant hepatocytes with multiple nucleoli in the lobule. Fulfilling the diagnostic criteria for autoimmune hepatitis, he was started on treatment with prednisolone and azathioprine, resulting in both clinical and biochemical responses. Four years later he presented with severe pain at the right costovertebral angle. Ultrasonography revealed a haematoma at the right kidney, and selective angiography of the abdominal aorta, renal arteries and hepatic artery documented microaneurysms in both kidney and liver arteries. Because of severe haemorrhage, right nephrectomy was performed. Histology of kidney specimen showed characteristic lesions of polyarteritis nodosa. Several months later, while on treatment with prednisolone and cyclophosphamide, the patient experienced a fatal episode of brain haemorrhage. An association between autoimmune hepatitis, polyarteritis nodosa and postinfantile giant cell hepatitis has not been reported previously.
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PMID:Post-infantile giant cell hepatitis associated with autoimmune hepatitis and polyarteritis nodosa. 1184 28

We report a 6-year-old Iranian boy with silvery-gray hair, eyelashes and the eyebrows who was admitted because of seizures and subsequent stupor. He had previous history of acute hemiparesis at 1 year of age and hepatitis-like syndrome 3 months ago. Microscopic examination of the patient's hair shaft revealed different sized clumps of melanin seen in the center of the shafts. Bone marrow aspiration revealed erythroid hyperplasia and erythrophagocytic cells. Bilateral frontal cortical and subcortical high signal lesions, dirty white matter, high signal areas in the upper pons and in both caudates and lentiform nuclei in T2 WI were the brain MRI findings of the patient. He died in the accelerated phase of Griscelli Syndrome (GS) type 2. To our knowledge we report the first case of GS from Iran.
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PMID:Bilateral basal ganglia involvement in a patient with Griscelli syndrome. 1695 71

The authors described three groups of patients after acute poisonings. In the first group were 60 patients after carbon tetrachioride poisoning, the second group consisted of 81 patients after mushroom poisoning and 20 patients after ethylene glycol poisoning were in the third group. Besides two patients with rare poisonings after potassium dichromate and after paraquat poisoning were analysed. All groups of patients with the kidney damage were presented from the diagnostic, differential diagnostic, conservative, ntra- and extracorporeal elimination treatment point of view. In the group of patients suffering from acute carbon tetrachloride poisoning and with acute renal failure following therapy was used: conservative treatment, exchange blood transfusion--in 4 patients in hepatic coma, renal replacement therapy (peritoneal dialysis, haemodialysis, plasmapheresis). From the total number of 60 patients 58 survived and 2 patients died in liver coma. Survival of patients after mushroom poisoning depended on amount of oral use of mushroom (Amanita phalloides), on early admission in dialysis centre and on early beginning of renal replacement therapy within 24 hr after acute poisoning. Twenty four patients from 81 patients of this group died. Main clinical signs of ethylene glycol poisoning were various neurological symptoms (cramps, hemiparesis, coma), severe metabolic acidosis (pH = 7.06 +/- 0.14), leucocytosis (26.4 +/- 5.5x 10(9)/L) and the signs of acute toxic hepatitis and of acute renal failure. Calcium oxalic crystals in urine were present in 17 patients and leucocytosis was observed in every patient. In the first 4 patients we administered intravenously ethylalcohol as an antidotum and later in other patients we used ethylalcohol in dialysis solution. The concentration of ethylalcohol in dialysis solution was 100 mg%. Severe metabolic acidosis improved in 17 patients using bicarbonate haemodialysis and 3 patients died before the possibility to use bicarbonate haemodialysis. Eighty-four hours after acute potassium dichromate poisoning and 24 hours after exchange blood transfusion during haemodialysis a 41-year old man died in haemorhagic shock, which developed after the extensive chemical burns of mucous membrane of gastrointestinal tract caused by this poison. Our patient after paraquat poisoning was treated by repeated charcoal haemoperfusion and haemodialysis. Despite of that therapy the patient died in severe respiratory insufficiency.
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PMID:Renal replacement therapy in acute poisonings--one center experience. 2405 74