Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present here thirteen patients (5 men and 8 women, aged 31 to 73, mean 55 years) with spastic paraparesis who showed clinical features similar to those of HTLV-1 associated myelopathy without HTLV-1 antibody, but with positive antibody to hepatitis B virus (HBV). All of these patients showed slowly progressive difficulty in walking. Five patients had previous histories of blood transfusion, of these one with history of B hepatitis. Neurologically, muscle weakness, spasticity and exaggerated deep tendon reflexes in the lower extremities were common to all the patients. Seven patients showed Babinski's reflex. Disturbance of micturition was noted in 3 patients. None showed organic changes of the spine on magnetic resonance image (MRI). None was serologically positive for syphilis and had cryoglobulin and hypergammaglobulinemia. Elevated levels of the liver enzymes were noted in two patients. All patients were positive for hepatitis B surface antibody (HBs-Ab) (EIA) but negative for hepatitis B surface antigen (HBs-Ag) (EIA). Five patients were seropositive for hepatitis C virus (HCV) (PHA). In 3 of them, reverse transcriptase polymerase chain reaction was performed but failed to detect HCV-RNA. All patients underwent spinal tap, and showed normal cell count and protein concentration in their cerebrospinal fluid (CSF). Atypical cells were not observed in all the patients. The CSFs from three patients were tested for HBs-Ag and HBs-Ab. HBs-Ag was negative in all three patients, but HBs-Ab was positive in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hepatitis B virus antibody positive spastic paraparesis]. 795 26

A 56-year old man was hospitalized for spasmodic paraparesis with sphincter disorders. After exclusion of spinal cord compression and all other inflammatory, infectious or neoplastic causes, the possibility of a connexion with an hepatitis B vaccination performed with a recumbent vaccine three weeks before the neurological disorders appeared was considered. The pathogenesis of such a myelitis remains uncertain. It is based on the possible reactivation of a dormant virus or a crossed antigenic reaction between a protein of the vaccine and the nervous system. The course of the disease is usually favourable. The frequency of this complication would be more accurately determined if all neurological manifestations occurring after hepatitis B vaccination were reported.
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PMID:[Acute myelitis after vaccination against hepatitis B]. 812 2

We investigated clinical features and immunological parameters in 40 patients with slowly progressive spastic paraparesis including 13 cases (4 men and 9 women, aged 43 to 71, mean 61 years) with positive antibody to hepatitis B virus (HBV), 13 (6 men and 7 women, aged 39 to 75, mean 63 years) with positive antibody to HBV and HTLV-I, and 14 (3 men and 11 women, aged 33 to 71, mean 55 years) with positive antibody to HTLV-I (HAM). None showed obviously organic changes of the spine on magnetic resonance image. Patients with positive antibody to HBV (hepatitis B virus associated myelopathy, HBM) were significantly lower in disability grade and had a fewer incidence of micturition than in the HAM. Furthermore, natural killer (NK) activities were in normal range and peripheral blood lymphocytes did not show autologous proliferation response (APR). Patients with positive antibody to both HBV and HTLV-I showed APR similar to HAM, but in most patients NK activities were within normal range. These results suggest that the mechanism of myelopathy in HBM may be different from that in HAM, and HBV infection may play a role as a cofactor in HAM.
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PMID:[Clinical and immunological findings of hepatitis B virus associated spastic paraparesis--a comparison with HAM]. 924 35

Portosystemic encephalopathy (PSE) is a well-known, common complication of portal hypertension. It is thought to be caused by nitrogenous substances such as ammonia, which are normally cleared from the blood stream by the liver. In cirrhosis and other hepatic disorders with portosystemic shunting (PSS)-- either surgical portosystemic anastomoses (PSA) or spontaneous PSS-- the collateral vessels bypass the liver allowing the accumulation of toxic, ammoniacal substances in the blood and tissues. PSE is characterized by encephalopathy; portosystemic myelopathy (PSM) is characterized by paresis of the extremities, Babinski signs and muscle spasticity in patients with cirrhosis and/or PSS. Usually only the lower extremities are involved. This report presents the first case of this syndrome observed 5 years after a transjugular intrahepatic portosystemic shunt. The 31 year old man with chronic Hepatitis B developed complete spastic paraparesis within 4 weeks after onset of clinical/neurological symptoms, accompanied by an episode of severe hepatic encephalopathy. The transcortical magnetic stimulation showed normal motoric stimulation times to the abductor digiti minimi muscles but no stimulation to the tibialis muscles was seen. Lumbar stimulation to the tibialis muscles, however, was normal. This indicates loss of motor neurons in the spinal cord, a characteristic finding in patients with portosystemic myelopathy. We performed a search of the literature for all reported cases of cirrhosis and/or PSS that developed PSM. However, the intervals between the construction of a shunt and the diagnosis of portosystemic myelopathy were shorter in total portacaval shunts (median 16 months) than in partial, non-portacaval shunts (median 60 months, p < 0.01). This suggests that not only the shunt itself but also the shunted volume contributes to the development of the syndrome Sixty-one patients with PSM have been reported in the literature since 1944. PSE had developed before PSM in almost all cases. PSM occurred from 1 month to 10 years after the creation of portacaval anastomoses (PCA) or splenorenal shunts (SRS) or in cirrhotic patients without shunts. No one type of liver disease or type of shunt appears to predispose to PSM. The mechanisms of PSE and PSM are thought to be similar and of nitrogenous origin, but their pathogenesis remains unknown. Lathyrism, a toxic syndrome with similar symptoms and signs, is caused by the ingestion of a legume, Lathyrus sativa, which contains beta-N-oxalo-L amino-L-alanine (BOAA). This animal model with or without BOAA appears to offer a reliable way of studying PSM experimentally.
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PMID:Portosystemic myelopathy: spastic paraparesis after portosystemic shunting. 1663 7

Human T-cell lymphotropic virus type-1 (HTLV-1) has a large global burden and in some key communities, such as Indigenous Australians living in remote areas, greater than 45% of people are infected. Despite HTLV-1 causing serious malignancy and myelopathic paraparesis, and a significant association with a range of inflammatory comorbidities and secondary infections that shorten lifespan, few biomedical interventions are available. HTLV-1 starkly contrasts with other blood-borne sexually transmitted viral infections, such as, HIV, hepatitis B virus, and hepatitis C virus, with no antiviral treatments that reduce virus-infected cells, no rapid diagnostics or biomarker assays suitable for use in remote settings, and no effective vaccine. We review how the replication strategies and molecular properties of HTLV-1 establish a long-term stealthy viral pathogenesis through a fine-tuned balance of persistence, immune cell dysfunction, and proliferation of proviral infected cells that collectively present robust barriers to treatment and prevention. An understanding of the nature of the HTLV-1 provirus and opposing actions of viral-coded negative-sense HBZ and positive-sense regulatory proteins Tax, p12 and its cleaved product p8, and p30, is needed to improve the biomedical tools for preventing transmission and improving the long-term health of people with this lifelong infection.
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PMID:Human T-cell lymphotropic virus type-1: a lifelong persistent infection, yet never truly silent. 3298 97