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

We report the case of a young HIV seropositive patient with severe hemophilia A who presented rapid liver failure related to his chronic C hepatitis. The patient had been receiving factor VIII:C clotting factor concentrates (mean 60,000 U/year) since 1975. In 1984 alanine aminotransferase presented abnormal levels. The CD4 lymphocyte count in 1991 was normal and ultrasonographic scan showed normal liver morphology. In 1991 the patient were found to be seropositive for HCV antibodies as detected by the ELISA method and confirmed by the RIBA method. One year later, a progressive increase in policlonal gamma-globulin and a decrease in the CD4+ lymphocyte count to below 500/muL were detected in concomitance with ultrasonographic evidence of a progressive increase in the longitudinal diameters of the liver and spleen and signs of liver inhomogeneity. A significant inverse correlation was observed between the increase in the longitudinal diameter of the liver and the decline in albumin levels, and between the increase in the longitudinal diameter of the liver and the drop in platelet count. Elevated levels of ammonemia, gamma-glutamyl transpeptidase, alkaline phosphatase and IgA were detected. Moreover, decreased levels of the C4 and C3 complement fractions were documented. At this time (1994), esophagogram and esophagogastroscopy evidenced varicosities in the lower esophageal section (stage F1). The patient died in 1995 March at the age of 29 years of sudden septic shock related to Pseudomonas aeruginosa infection.
 ...
PMID:Rapid liver failure related to chronic C hepatitis in an HIV seropositive hemophilic patient with severe immunodepression. 887 Mar 78

To quarantine human tumor samples for transplantation into immune deficient mice or tumor xenograft lines established and introduced from other institutions, we performed isolated implantation and passaging of tumors in a vinyl isolator, and microbiological examinations of sentinel mice kept together with tumor bearing mice. We examined 105 pairs of sentinel mice used to quarantine 907 tumors, and found six cases of contamination or infection with Staphylococcus aureus, 20 cases with Pseudomonas aeruginosa and one case with mouse hepatitis virus (MHV). It was, however, possible that Mycoplasma pulmonis contamination was overlooked because the microbe had been isolated from tumors passaged after quarantine, even though the results of the quarantine of these tumors showed no sign of pathogens. Direct culture of tumors for the microbe was recommended to improve the quarantine system.
 ...
PMID:Quarantine for contaminated pathogens in transplantable human tumors or infections in tumor bearing mice. 914 98

A 34-year-old man diagnosed with fulminant hepatitis, caused by hepatitis B virus, and acute renal failure was referred to our hospital. After admission to the intensive care unit, the liver and renal failure were ameliorated. Melena requiring transfusion occurred during the course of his illness. Endoscopic examination demonstrated pseudomembranes, erosions, ulcers, and hemorrhage in the duodenum, the upper jejunum, and the terminal ileum, suggesting widespread lesions throughout the small intestine. Pseudomonas putida, Xanthomonas maltophilia, and Candida glabrata were cultured from ileal fluid. Candida glabrata was also detected in sputum, feces, and on an intravenous catheter tip. The patient was treated with amphotericin B and miconazole. The melena was ameliorated, but inflammation of the small intestine persisted. Although we had difficulty in treating the enteritis, the patient survived, and 1 year later colonoscopic examination demonstrated no abnormalities. The small intestine is a difficult site to examine, but endoscopic examination of this site is important when massive hemorrhage develops.
 ...
PMID:Fulminant hepatitis complicated by small intestine infection and massive hemorrhage. 965 23

Pseudomonas luteola is an aerobic, Gram negative rod, formerly classified as CDC group Ve-1 and Chryseomonas luteola. It is an uncommon clinical isolate. A previously healthy 59-year-old homosexual man with facial cellulitis and Pseudomonas luteola bacteremia is reported. Previously reported cases of P. luteola bacteremia have occurred in association with pancreatic abscess, prosthetic valve endocarditis, cardiac surgery, granulomatous hepatitis, peritonitis, and indwelling vascular catheters. This case suggests that the spectrum of disease caused by this bacteria may continue to expand.
 ...
PMID:Facial cellulitis and Pseudomonas luteola bacteremia in an otherwise healthy patient. 993 47

A new system designed for cell surface display of recombinant proteins on Escherichia coli was evaluated for expression of eukaryotic viral antigens. The major surface antigen of hepatitis B virus (HBsAg) was fused to the ice nucleation protein (INP), an outer membrane protein of Pseudomonas syringae. Western blotting, immunofluorescence microscopy, whole-cell ELISA, and ice nucleation activity assay confirmed expression of recombinant proteins on the surface of Escherichia coli. This study indicated that INP-based cell surface display can be used for epitope mapping and recombinant bacteria expressing hepatitis viral antigens may be used for developing live vaccines.
 ...
PMID:Cell surface display of hepatitis B virus surface antigen by using Pseudomonas syringae ice nucleation protein. 1066 68

The role of leptin was investigated in two models of T cell-mediated hepatitis: the administration of Con A or of Pseudomonas aeruginosa exotoxin A (PEA). In both models, leptin-deficient (ob/ob) mice were protected from liver damage and showed lower induction of tumor necrosis factor (TNF) alpha and IL-18 compared with their lean littermates. Neutralization of TNF-alpha reduced induction of IL-18 by either Con A (70% reduction) or PEA (40% reduction). Pretreatment of lean mice with either soluble TNF receptors or with an anti-IL-18 antiserum significantly reduced Con A- and PEA-induced liver damage. The simultaneous neutralization of TNF-alpha and IL-18 fully protected the mice against liver toxicity. However, neutralization of either IL-18 or TNF-alpha did not inhibit Con A-induced production of IFN-gamma. Thymus atrophy and alterations in the number of circulating lymphocytes and monocytes were observed in ob/ob mice. Exogenous leptin replacement restored the responsiveness of ob/ob mice to Con A and normalized their lymphocyte and monocyte populations. These results demonstrate that leptin deficiency leads to reduced production of TNF-alpha and IL-18 associated with reduced T cell-mediated hepatotoxicity. In addition, both TNF-alpha and IL-18 appear to be essential mediators of T cell-mediated liver injury.
 ...
PMID:Leptin-deficient (ob/ob) mice are protected from T cell-mediated hepatotoxicity: role of tumor necrosis factor alpha and IL-18. 1068 32

Infection is a major complication and the leading cause of death in thalassemia, especially E-beta thalassemia. The spectrum of infections in E-beta thalassemia include mild and severe infections, therapy-related infections such as Yersinia enterocolitica infection associated with desferrioxamine (DFO) therapy, and transfusion-transmitted disease, as well as unique infections such as with pythiosis. Prospective studies in Thailand indicate that patients with E-beta thalassemia had more frequent episodes of both mild and severe infections. The former included upper respiratory tract infection, acute gastroenteritis, cutaneous abscess, and gingivitis. Severe infections occurred more commonly in patients with splenectomy and included septicemia, pneumonia, biliary tract infection, salmonellosis, and urinary tract infection. Responsible organisms were Escherichia coli (26%), Klebsiella pneumoniae (23%), Salmonella (15%), and Streptococcus pneumoniae (13%). Other organisms included Pseudomonas, Staphylococci, Burkholderia pseudomallei (melioidosis), and Aeromonas. Patients undergoing DFO therapy are at risk for Y. enterocolitica infection which may be localized to mesenteric nodes and tonsils or occur as a generalized form such as septicemia. Recently, we have seen a unique infection so-called vascular pythiosis. Patients usually presented with clinical features of vascular occlusion of lower limbs from ascending arteritis and thrombosis. The causative organism, Pythium insidiosum, is fungus-like, in the kingdom Stramenopila, and in the class Oomycetes. The mortality rate is high and the only effective treatment has been early amputation or possibly immunotherapy. The predisposing factors of infections in thalassemia include splenectomy, iron overload, anemia, and granulocyte dysfunctions. General management of infections in thalassemia consist of prevention, i.e., immunization with pneumococcal and hepatitis vaccines, oral penicillins especially in patients with splenectomy, removal of predisposing factors such as gallstones, iron overload, and appropriate antibiotics.
 ...
PMID:Infections in E-beta thalassemia. 1113 34

CHARACTERISTIC FEATURES: Piercing, an act that modifies the body, has progressed considerably in France over the last few years. The population involved has grown and become more diversified. Performed with a solid needle or a catheter, a wide variety of anatomic localizations are concerned, particularly the nose, ears, and navel. The shape of the "rings", generally made of surgical steel, niobium or titanium, varies greatly. Wound healing by epithelialisation can take up to several months. INFECTIOUS RISK: Between 10% and 20% of all piercings lead to a local infection. The most commonly found causal agests are Staphylococcus aureus, group A Streptococcus and Pseudomonas sp. These germs can cause severe life-threatening complications even in common localizations (earlobe). Viral transmission is another risk (hepatitis B, hepatitis C, hepatitis delta, HIV). A few cases of fatal fulminant hepatitis have been described immediately after piercing. SAFETY MEASURES: Generally performed under less than desirable sanitary conditions, safety measures are needed for piercing. Among professional "piercers", a certain number have emphasized the need for providing their clients with safer services. The prevention of infection risk should be a priority for all. Work along this line has been done in the United States and Canada. In light of the impact on public health, it is important to rapidly develop guidelines and regulations for piercing in France. Both professional piercers and health care workers should participate in developing these safety measures in order to assure their implementation.
 ...
PMID:[Piercing and its infectious complications. A public health issue in France]. 1124 29

Liver resident NK1.1+ T cells are supposed to play a pivotal role in the onset of inflammatory liver injury in experimental mouse models such as concanavalin A (Con A)-induced hepatitis. These cells, expressing the adhesion receptor, CD44, are largely depleted from the liver by a single intravenous injection of low-molecular-weight fragments of hyaluronic acid (LMW-HA). Here, we report that LMW-HA pretreatment protected mice from liver injury in several models of T-cell- and macrophage-dependent, tumor necrosis factor alpha (TNF-alpha)-mediated inflammatory liver injury, i.e., from liver injury induced by either Con A or Pseudomonas exotoxin A (PEA) or PEA/lipopolysaccharide (LPS). Interestingly, apart from inhibition of cellular adhesion, pretreatment of mice with LMW-HA was also capable of preventing hepatocellular apoptosis and activation of caspase-3 induced by direct administration of recombinant murine (rmu) TNF-alpha to D-galactosamine (GalN)-sensitized mice. LMW-HA-induced hepatoprotection could be neutralized by pretreatment with the nuclear factor-kappaB (NF-kappaB) inhibitor, pyrrolidine dithiocarbamate (PDTC), demonstrating the involvement of NF-kappaB in the observed protective mechanism. Indeed, injection of LMW-HA rapidly induced the production of TNF-alpha by Kupffer cells and the translocation of NF-kappaB into hepatocellular nuclei. Both LMW-HA-induced TNF-alpha production and NF-kappaB translocation were blocked by pretreatment with PDTC. Our findings provide evidence for an unknown mechanism of LMW-HA-dependent protection from inflammatory liver disease, i.e., induction of TNF-alpha- and NF-kappaB-dependent cytoprotective proteins within the target parenchymal liver cells.
 ...
PMID:Low-molecular-weight hyaluronic acid induces nuclear factor-kappaB-dependent resistance against tumor necrosis factor alpha-mediated liver injury in mice. 1152 40

TNF-alpha is a central mediator of T cell activation-induced hepatitis in mice, e.g., induced by Pseudomonas exotoxin A (PEA). In this in vivo mouse model of T cell-dependent hepatitis, liver injury depends on both TNFRs. Whereas TNFR1 can directly mediate hepatocyte death, the in vivo functions of TNFR2 in pathophysiology remained unclear. TNFR2 has been implicated in deleterious leukocyte activation in a transgenic mouse model and in enhancement of TNFR1-mediated cell death in cell lines. In this study, we clarify the role of hepatocyte- vs leukocyte-expressed TNFR2 in T cell-dependent liver injury in vivo, using the PEA-induced hepatitis model. Several types of TNFR2-expressing leukocytes, especially neutrophils and NK cells, accumulated within the liver throughout the pathogenic process. Surprisingly, only parenchymal TNFR2 expression, but not the TNFR2 expression on leukocytes, contributed to PEA-induced hepatitis, as shown by analysis of wild-type --> tnfr2 degrees and the reciprocal mouse bone marrow chimeras. Furthermore, PEA induced NF-kappaB activation and cytokine production in the livers of both wild-type and tnfr2 degrees mice, whereas only primary mouse hepatocytes from wild-type, but not from tnfr2 degrees, mice were susceptible to cell death induced by a combination of agonistic anti-TNFR1 and anti-TNFR2 Abs. Our results suggest that parenchymal, but not leukocyte, TNFR2 mediates T cell-dependent hepatitis in vivo. The activation of leukocytes does not appear to be disturbed by the absence of TNFR2.
 ...
PMID:Parenchymal, but not leukocyte, TNF receptor 2 mediates T cell-dependent hepatitis in mice. 1257 85


<< Previous 1 2 3 Next >>