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)

Dantrolene sodium or dantrolene1 is 1([5-(nitrophenyl)furfurylidend] amino) hydantoin sodium hydrate. It is indicated for use in chronic disorders characterised by skeletal muscle spasticity, such as spinal cord injury, stroke, cerebral palsy and multiple sclerosis. Dantrolene is believed to act directly on the contractile mechanism of skeletal muscle to decrease the force of contraction in the absence of any demonstrated effects on neural pathways, on the neuromuscular junction, or on the excitable properties of the muscle fibre membranes. Controlled trials have demonstrated that dantrolene is superior to placebo in adults or children with spasticity from various causes, as evidenced by clinical assessments of disability and daily activities, and by muscle and reflex responses to mechanical and electrical stimulation. It is somewhat less effective in patients with multiple sclerosis than in those with spasticity from other causes. There has been a general clinical impression in controlled trials that dantrolene caused less sedation than would have been expected from therapeutically comparable doses of diazepam. In 2 controlled trials, there was no significant difference between dantrolene and diazepam in terms of reductions in spasticity, clonus, and hyperreflexia, but side-effects such as drowsiness and inco-ordination occurred significantly more frequently on diazepam. Long-term studies have indicated continuing benefit for patients taking dantrolene, though the incidence of side-effects has often been high and there has been a suggestion of exacerbation of seizures in children with cerebral palsy. Dantrolene may be of value in the medical treatment of spasm of the external urethral sphincter due to neurological and non-neurological disease, and animal studies suggest a potential use in the management of malignant hyperpyrexia. Chemical evidence of liver dysfunction may occur in 0.7 to 1% of patients on long-term treatment with dantrolene, with symptomatic hepatitis in 0.35 to 0.5% and fatal hepatitis in 0.1 to 0.2%. The drug commonly causes transient drowsiness, dizziness, weakness, general malaise, fatigue and diarrhoea at the start of therapy. Muscle weakness may be the principal limiting side-effect in ambulant patients, particularly in those with multiple sclerosis, and therapy could be hazardous in patients with pre-existing bulbar or respiratory weakness. The dosage of dantrolene has been fixed in most controlled trials, though long-term studies have indicated the need for individualisation of dosage. The initial dose is usually 25mg once daily, increasing to 25mg two, three or four times daily, and then by increments of 25mg up to as high as 100mg two, three or four times daily. The lowest dose compatible with optimal response is recommended.
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PMID:Dantrolene sodium: a review of its pharmacological properties and therapeutic efficacy in spasticity. 31 89

Clostridium septicum infection causing 5.0 to 5.2% mortality is reported for the first time in the literature from six-week-old growing geese in three flocks comprising 5,200, 5,500 and 5,900 geese, respectively. The affected birds exhibited weakness, uncoordinated movement, ataxia and, frequently, oblique position of the head and neck (torticollis) as well as signs indicative of dysequilibrium. The affected birds died within 18-24 h. Gross pathological examination revealed anaemia, hepatitis with map-like necroses of irregular outline (Fig. 1), acute enteritis, pulmonary oedema and cardiac dilatation. Light and electron-microscopic examination showed that the sinusoids of the liver were markedly dilated (Fig. 2) and filled with serous exudate and gas (Figs 2 and 3), and the hepatocytes surrounding them exhibited severe oedema (Fig. 4). Among the hepatocytes, ciliated bacteria 7-10 mu in length and 1-3 mu in width, bounded by a well-defined cell wall and often showing signs of spore formation were observed (Figs 5 and 6). By bacteriological examination the pathogen was isolated, its properties were studied, and the clinical entity of malignant oedema was experimentally reproduced by intramuscular injection of guinea-pigs and rabbits. The applied antibiotic (oxytetracycline) and furazolidone therapy proved effective.
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PMID:Demonstration of Clostridium septicum infection in a goose flock. 147 92

A 62-year-old woman with hepatitis-B-surface-antigen-positive hepatic cirrhosis presented with weakness and paresthesias over the distal part of the limbs in the course of adenine arabinoside 5'-monophosphate (ARA-AMP) treatment, and recovered spontaneously after several weeks of drug withdrawal. Electrophysiological and histological studies demonstrated axonal neuropathy. Although the patient received a relatively low total dose (120 mg/kg), her age and advanced liver disease may have played a role in the ARA-AMP neurotoxicity.
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PMID:Toxic neuropathy after adenine arabinoside treatment in chronic HBsAg-positive liver disease. 168 32

After intranasal inoculation, mouse hepatitis virus (MHV) gains entry into the central nervous system (CNS) via the olfactory and trigeminal nerves. Under the appropriate conditions, some mice develop clinically apparent demyelinating encephalomyelitis several weeks later, with virus always present in the spinal cord. To determine the pathway by which virus reaches the cord, brains and spinal cords of infected, asymptomatic mice were analyzed by in situ hybridization. Viral RNA was always detected in the anterior part of the upper spinal cord. A similar analysis of mice with the recent onset of hindlimb weakness showed that viral RNA was detected in the same location. The results suggest that MHV is transported to the spinal cord via well-defined neuroanatomic pathways and that viral amplification with resultant clinical disease occurs from this site of persistence in the anterior spinal cord. This process of viral amplification may involve the generation of viral variants as has been described for MHV-infected rats. No major changes in viral RNA or protein could be detected when MHV isolated from mice with hindlimb paralysis was analyzed. The data suggest that the generation of viral variants is not important in the pathogenesis of the late onset of neurological disease induced by MHV in mice.
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PMID:Identification of the spinal cord as a major site of persistence during chronic infection with a murine coronavirus. 215 80

A case of polymyositis associated with chronic active hepatitis was reported. A 53-year-old man, who had no previous history of blood transfusion nor hepatitis, noticed proximal dominant muscle weakness on January 29, 1985. He was admitted to Kyoto National Hospital on February 7, and laboratory studies disclosed the elevation of serum enzyme levels; creatine kinase (CK) 9845 IU/L (normal 54-263), glutamate oxaloacetate transaminase (GOT) 834 IU/L (9-31), glutamate pyruvate transaminase (GPT) 491 IU/L (4-34), lactate dehydrogenase (LDH) 2135 IU/L (248-464). Also serum gamma globulin was high (1.8 g/dl) and LE-like cell was found. The diagnosis of polymyositis was made and prednisolone therapy (60 mg/day) was started on February 23. The elevated serum enzymes decreased gradually, but severe muscle weakness persisted for about one month. On April 3, he was admitted to our hospital. Physical examination revealed moderate proximal dominant muscle weakness without skin eruption, jaundice or hepatosplenomegaly. The serum enzymes were still high; CK 1826, GOT 173, GPT 232 (GOT less than GPT), LDH 1548. However, alkaline phosphatase (ALP) and bilirubin were normal. Hepatitis B surface antigen (HBsAg) was not detected. Antinuclear antibody was positive. The electromyogram study showed myopathic change, and the muscle biopsy demonstrated myopathic change and cell infiltration, compatible with polymyositis. These results suggested liver dysfunction associated with polymyositis. Prednisolone therapy was continued and muscle weakness decreased. From December, 1985, serum enzymes (CK, GOT, GPT, LDH) elevated again and muscle weakness also slightly increased. Anti-smooth muscle antibody was positive. It was suggested that both polymyositis and liver dysfunction deteriorated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of polymyositis associated with chronic active hepatitis]. 218 64

A deficiency of exogenous and endogenous carnitine is present in those pathologies in which the most important clinical sign is represented by weakness and steatosis. We have studied the serum levels of carnitine in 14 children with hepatic disease (8 with acute HAV hepatitis, 2 with acute HBV hepatitis, 2 with toxic hepatitis, 2 with chronic hepatitis). In patients with acute, infective and toxic hepatitis we have found levels of carnitine (25.71 +/- 2.14 nM/ml) below normal (50.87 +/- 1.46 nM/ml). In 5 cases we have performed two blood tests, at admittance to the hospital and at the end of the illness. The variability in carnitine levels in these two blood exams shows a clear correlation with clinical improvement, decrease in aminotransferase and increase in serum carnitine. In chronic hepatitis we have found normal levels of carnitine. Probably it is correlated with the absence of steatosis seen at hepatic biopsy.
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PMID:[Preliminary results on blood carnitine levels in children with hepatic pathology]. 279 79

Geotropic direction-changing nystagmus in lateral body positions was observed in 4-week-old BALB/c mice after intracerebral injection with a temperature-sensitive mutant of mouse hepatitis virus. The positional nystagmus was detected already 2 days after infection and it lasted half a year at least. The nystagmic responses of the semicircular canals were also evaluated before and after infection. They were unaltered during the disease, which was clinically manifested by general weakness, ataxia and tremor. Histopathological examination 2 weeks after infection revealed demyelination in various parts of the CNS.
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PMID:Virus-induced central positional nystagmus in mice. 299 48

Psittacine inclusion body hepatitis (also known as Pacheco's parrot disease) was believed to be responsible for fatal necrotizing hepatitis and splenitis in a variety of psittacine birds from a private aviary. Splenic cells and degenerative hepatocytes around the outer zone of necrotic areas had margination of nuclear material and large intranuclear inclusion bodies. Clinical signs consisted of weakness, anorexia, vomiting, loose feces, and slight ruffling of feathers. The source of the infection was undetermined, but could have been associated with 3 Patagonian conures within the aviary. Patagonian conures are well-recognized as clinically normal carriers. The outbreak was limited by strict quarantine and disinfection of the aviary for 14 days.
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PMID:Psittacine inclusion body hepatitis in an aviary. 299 45

A case of chronic polyneuropathy associated with chronic type B hepatitis was described. A 31 year-old male was admitted to our hospital with a 2-year history of progressive weakness and sensory disturbances of all limbs. There was past history of acute type B post-transfusion hepatitis after subtotal gastrectomy. On examination there was generalized muscle weakness, particularly in movements of the hands and feet with areflexia. He had a steppage gait. Sensory examination revealed moderately decreased pinprick, light touch, vibration and position sense in the distal portion of all extremities. On admission, hepatitis associated antigen and antibody were negative and positive, respectively. The level of circulating immune complexes was high with the titer of 6.6 micrograms/ml by Clq assay and 16X by Raji cell assay. Liver biopsy revealed fibrosis and periportal inflammatory infiltrate compatible with the diagnosis of chronic viral hepatitis. Sural nerve biopsy showed marked loss of large myelinated fibers and epineural vasculitis with the thickened blood vessel wall and mononuclear cell infiltrates. There have been increasing evidences that extrahepatic manifestations are caused by vasculitis due to HBs antigen-antibody immune complex deposits. On the basis of findings in the literature it seems possible that chronic polyneuropathy may be related to the vasculitis due to HBs antigen-antibody complex deposits after hepatitis B virus infection.
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PMID:[A case of chronic polyneuropathy associated with chronic type B hepatitis]. 317 85

Patients with agammaglobulinemia are particularly susceptible to chronic enteroviral infections of the central nervous system. Data on 42 patients were obtained by literature review, communications with other physicians, and personal experiences. Thirty-eight patients had congenital immunodeficiencies, most frequently X-linked agammaglobulinemia. Most patients who could be assessed were receiving maintenance therapy with intramuscular gamma-globulin before their enteroviral infection. Seven patients had not been recognized as hypogammaglobulinemic before the onset of infection. The commonest pathogens were echoviruses (37 of 41 cases), especially type 11 (11 cases). Thus far, four patients have had sequential or simultaneous infections with a second enteroviral serotype. Other features of the disease have included weakness, lethargy or coma, headaches, hearing loss, seizures, ataxia, and paresthesias. Some patients have also had nonneurologic manifestations of chronic enteroviral infection, including fever, the dermatomyositis-like syndrome, edema, rashes, and hepatitis. Treatment has consisted primarily of antibody administration, either in intravenous immunoglobulin preparations or in immune plasma. Twelve patients have received intraventricular immunoglobulin through reservoir devices; six of these 12 have improved substantially, as judged by clinical criteria.
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PMID:Chronic enteroviral meningoencephalitis in agammaglobulinemic patients. 329


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