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)

The formalin-inactivated Rift Valley fever virus (RVFV) vaccine, TSI-GSD-200, was administered subcutaneously to highly susceptible adult Wistar-Furth rats (LD50-1 p.f.u., ZH501 strain). Vaccine was administered on days 0, 7 and 28, the same time course used for at-risk personnel. Six months postimmunization, when the serum plaque-reduction neutralization titre (PRNT)80 had declined to low or undetectable levels, rats were challenged with 4.4 log10 p.f.u. of the virulent ZH501 strain in a nose-only dynamic aerosol apparatus. Ninety-seven per cent (33/34) of the non-vaccinated control rats died. In contrast, only 32% (33/105) of the vaccinated animals died. In vaccinated rats that succumbed, there was a doubling of the mean time to death and the cause of death shifted from hepatitis to encephalitis. Rats with a PRNT80 of greater than or equal to 1:40 were protected from clinical disease and histological evidence of hepatic or encephalitic lesions. While the precise mechanisms of immunity against aerosol challenge remain unresolved, here the serum PRNT titre correlated with protection.
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PMID:Efficacy of a Rift Valley fever virus vaccine against an aerosol infection in rats. 175 89

The apoprotein and lipid composition and the morphology of lipoproteins was determined in rats with D-(+)-galactosamine (GalN) hepatitis. Single intraperitoneal injections of GalN at several dose levels and postinjection exsanguination times resulted in depressed levels of cholesteryl esters, an index of plasma lecithin:cholesterol acyltransferase (LCAT) activity, and increased levels of phospholipids, unesterified cholesterol, and triglycerides. Plasma withdrawn from rats 24 hr after injection of 1000 mg/kg GalN was most deficient in cholesteryl ester and was studied further by sequential isolation of VLDL, LDL, HDL1, HDL2, and HDL3. The increased plasma triglyceride (TG) after GalN treatment accumulated in TG-rich VLDL which contained two types of particles: a large (mean diameter 193.6 +/- 48.3 nm) and rough-edged particle, and a smooth one with a mean diameter (63.4 +/- 13.2 nm) similar to control VLDL (69.4 +/- 20.2 nm). The increased phospholiThe increased plasma triglyceride (TG) after GalN treatment accumulated in TG-rich VLDL which contained two types of particles: a large (mean diameter 193.6 +/- 48.3 nm) and rough-edged particle, and a smooth one with a mean diameter (63.4 +/- 13.2 nm) similar to control VLDL (69.4 +/- 20.2 nm). The increased phospholiThe increased plasma triglyceride (TG) after GalN treatment accumulated in TG-rich VLDL which contained two types of particles: a large (mean diameter 193.6 +/- 48.3 nm) and rough-edged particle, and a smooth one with a mean diameter (63.4 +/- 13.2 nm) similar to control VLDL (69.4 +/- 20.2 nm). The increased phospholipids and unesterified cholesterol were predominantly in LDL, HDL1, and HDL2 which were largely rouleaux of flattened vesicles. Density gradient ultracentrifugation of d greater than 1.006 g/ml lipoproteins confirmed these results. GalN hepatitis appeared to decrease the larger apoB335K subspecies and the apoC-III0 and apoC-III2 content of VLDL. However, total apoB concentration as GalN VLDL was increased 2.6-fold over control. LDL and HDL were markedly enriched in apoE. LDL apoB concentration was decreased by 41% while HDL was deficient in apoA-I, A-II and A-IV, and C. These results demonstrate association of increased plasma triglycerides with particles of grossly abnormal apoprotein composition, and the association of increased plasma phospholipids and unesterified cholesterol with apoE-rich lipoproteins during the LCAT defect produced by GalN hepatitis. These abnormal lipoproteins may represent an abnormal level of normal LCAT substrates important in the transport and esterification of plasma cholesterol.
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PMID:Alterations in lipoprotein composition associated with galactosamine-induced rat liver injury. 711 68

During the past decades major improvements in blood safety have been achieved, both in developed and developing countries. The introduction of donor counseling and screening for different pathogens has made blood a very safe product, especially in developed countries. However, even in these countries, there is still a residual risk for the transmission of several pathogens. For viruses such as the human immunodeficiency virus (HIV), and the hepatitis viruses B and C, this is due mainly to window-period donations. Furthermore, the threat of newly emerging pathogens which can affect blood safety is always present. For example, the implications of the agent causing new variant Creutzfeld-Jakob disease for transfusion practice are not yet clear. Finally, there are several pathogens, e.g. CMV and parvo B19, which are common in the general donor population, and might pose a serious threat in selected groups of immunosuppressed patients. In the future, further improvements in blood safety are expected from the introduction of polymerase chain reaction for testing and from the implementation of photochemical decontamination for cellular blood products. The situation in transfusion medicine in the developing world is much less favorable, due mainly to a higher incidence and prevalence of infectious diseases.
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PMID:Transfusion-transmitted diseases: risks, prevention and perspectives. 991 6

Three categories of emerging risks are studied: 1) A new variant of Creutzfeld-Jakob disease, different from its sporadic form; limited to the British isles (48 of 51 cases), it affects younger patients, and has a higher duration with a predominance of psychiatric symptoms. Environmental risk factors include a previous stay in the British isles and oral transmission via contaminated food. No link has been made evident between blood component (BC) transfusion and occurrence of the disease. A potential risk exists if its agent is found in blood and peripheral lymphoid tissues and if buffy coat from infected animals has been inoculated intracerebrally. Since 1993, prevention measures have been taken: exclusion of donors with a potential risk as well as transfused donors, systematic leukocyte reduction and implementation of disease surveillance. Excluding donors after a several month-stay in the British Isles is being discussed. 2) Novel hepatitis viruses. Hepatitis G virus (HGV) has been detected in 2-4% of blood donors. Ten percent of patients with chronic non-A-E hepatitis are HGV RNA positive. The incidence of HGV infection is higher than expected from PCR studies. HGV has a high prevalence in the world. Novel DNA non-enveloped virus (TTV) has a normal distribution. Its prevalence varies from 2 to 80%, depending on the country. Although it has not been shown to be aggressive for the liver, prolonged follow-up is required. 3) Human herpes virus 8 (HHV8) is associated with Kaposi's sarcoma in 80% of cases. Its prevalence (0-20%) varies depending on the country. Kaposi's sarcoma has never been reported after BC transfusion. PCR-based viral DNA searches have yielded negative results in 19 poly-transfused subjects. Continuous monitoring is required for recipients at risk (e.g., immunosuppressed). In response to a possible health risk, emerging risks govern the "Precaution Principle", so difficult to implement.
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PMID:[Transfusion safety: emergent or hypothetical risks]. 1073 Mar 44

We present a series of 8 patients (6 males, 2 females) with hepatocellular carcinoma (HCC) and glycogen storage disease type Ia (GSD Ia). In this group, the age at which treatment was initiated ranged from birth to 39 years (mean 9.9 years). All patients but one were noncompliant with treatment. Hepatic masses were first detected at an age range of 13-45 years (mean 28.1 years). Age at diagnosis of HCC ranged from 19 to 49 years (mean 36.9 years). Duration between the diagnosis of liver adenomas and the diagnosis of HCC ranged from 0 to 28 years (mean 8.8 years, SD = 11.5). Two patients had positive hepatitis serologies (one hepatitis B, one hepatitis C). Alpha-fetoprotein (AFP) was normal in 6 of the 8 patients. Carcinoembryonic antigen (CEA) was normal in the 5 patients in which it was measured. Current guidelines recommend abdominal ultrasonography with AFP and CEA levels every 3 months once patients develop hepatic lesions. Abdominal CT or MRI is advised when the lesions are large or poorly defined or are growing larger. We question the reliability of AFP and CEA as markers for HCC in GSD Ia. Aggressive interventional management of masses with rapid growth or poorly defined margins may be necessary to prevent the development of HCC in this patient population.
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PMID:Hepatocellular carcinoma in glycogen storage disease type Ia: a case series. 1587 4

While transfusion of blood components is usually safe, there are risks of adverse effects that can have immunologic, nonimmunologic, or infectious causes. In patients, the fear of infectious disease transmission predominates, although the risk has been extremely low since the introduction of reliable serologic and molecular biological testing methods. This article addresses the incidence, clinical picture, and etiology of adverse effects of transfusion. It also reports on current knowledge concerning transfusion-associated acute lung injury, which has gained much attention in the last few years. Besides hepatitis and human immunodeficiency viruses, cytomegalovirus, parvovirus B19, prion transmission, and the risk of variant Creutzfeld-Jakob disease are also discussed.
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PMID:[Risks and side effects of blood transfusion]. 1975 92

Glycogen storage disease type Ia (GSD-Ia; also called von Gierke disease) is an autosomal recessive disorder of carbohydrate metabolism caused by glucose-6-phosphatase deficiency. There have been many reports describing hepatic tumors in GSD patients; however, most of these reports were of hepatocellular adenomas, whereas there are only few reports describing focal nodular hyperplasia (FNH) or hepatocellular carcinoma (HCC). We report a case with GSD-Ia who had undergone a partial resection of the liver for FNH at 18 years of age and in whom moderately differentiated HCC had developed. Preoperative imaging studies, including ultrasonography, dynamic computer tomography (CT) and magnetic resonance imaging, revealed benign and malignant features. In particular, fluorodeoxyglucose-positron emission tomography (FDG-PET)/CT revealed the atypical findings that FDG accumulated at high levels in the non-tumorous hepatic parenchyma and low levels in the tumor. Right hemihepatectomy was performed. During the perioperative period, high-dose glucose and sodium bicarbonate were administered to control metabolic acidosis. He had multiple recurrences of HCC at 10 mo after surgery and was followed-up with transcatheter arterial chemoembolization. The tumor was already highly advanced when it was found by chance; therefore, a careful follow-up should be mandatory for GSD-I patients as they are at a high risk for HCC, similar to hepatitis patients.
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PMID:Hepatocellular carcinoma and focal nodular hyperplasia of the liver in a glycogen storage disease patient. 2276 70