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)

A 55-year-old female was admitted to our hospital because of high fever, nonproductive cough and dyspnea. Initially she had been treated with cephem antibiotics by a local doctor. However, acute respiratory failure due to severe pneumonia developed. The partial pressure of oxygen in arterial blood was 55.5 Torr. Her chest X-ray revealed wide-spread infiltrates with air bronchograms throughout the entire left lung, and pleural effusions were also present in the chest CT scan. Because the patient had a history of the contact with birds, we suspected psittacosis and administered Minocycline immediately. As a result, her clinical condition improved and the abnormal shadow on the chest X-ray film improved markedly in three days. Because the serum titer of a complement fixation test against Chlamydia rose to 1:512, we made the diagnosis of psittacosis. In addition, femoral muscle pain, and a high level of serum GOT, GPT, CK, Aldolase and Myoglobin indicated hepatitis and myositis. In the lung tissue specimens obtained by TBLB performed on the 10th hospital day, slight interstitial pneumonia and intracellular inclusion bodies were found by light microscopy and Chlamydial agents were found electron microscopically.
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PMID:[A case of fulminant psittacosis showing Chlamydia in TBLB specimens]. 204 Dec 51

We report two cases of aluminium phosphide poisoning who presented with rare manifestations, one with bleeding diathesis, hepatitis and acute tubular necrosis and the other with acute respiratory failure.
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PMID:Aluminium phosphide poisoning. Two cases with rare presentation. 229 63

Review of the 70 transfusion-associated fatalities reported to the Bureau of Biologics (BOB) between 1976 and 1978 revealed 44 acute hemolytic reactions, two delayed hemolytic reactions, five fatalities associated with acute respiratory failure, two cases of bacterial contamination, one graft-versus-host reaction (GVHR), ten cases of hepatitis, and six fatalities not associated with transfusion. Thirty-eight of 44 acute hemolytic reactions were due to ABO incompatibility. Clerical confusion was the cause of 33 of 37 cases in which error could be defined.
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PMID:Transfusion-associated fatalities: review of Bureau of Biologics reports 1976-1978. 689 37

In ischemic hepatitis, which is not rare, there is a marked but transient increase in serum aminotransferase activity to at least 20 times the upper limit of normal, without any other cause for hepatic necrosis. It is generally preceded by an acute cardiac complication, usually pulmonary edema or a tachyarrhythmia, causing decrease in cardiac output, or may follow acute respiratory failure. The typical histological lesion is centrilobular hepatic necrosis. We present 2 cases of ischemic hepatitis due to hypotension following rapid atrial fibrillation, sepsis and acute respiratory failure, highlighting the different etiologies, laboratories results, and the relative benign course, described in the literature. The patients were a woman aged 80 and a man aged 76. Awareness of the place of this disorder in the differential diagnosis of acute hepatitis may save needless, dangerous investigations.
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PMID:[Ischemic hepatitis]. 884 54

Out of a prospective series of 142 consecutive episodes of hypoxic (ischemic) hepatitis (HH), we identified 17 episodes associated with an acute exacerbation of chronic respiratory failure (CRF) without left cardiac failure. In the aim to evaluate the role of arterial hypoxemia in the pathogenesis of HH associated with respiratory failure, these 17 episodes of HH (study group) were hemodynamically compared with a control group of 17 episodes of HH associated with congestive heart failure (CHF) (control group 1) and a group of 16 episodes of acute respiratory failure (ARF) not complicated by HH (control group 2). Arterial hypoxemia was significantly more severe in the study group (arterial blood tension in O2 [PaO2], 34 mm Hg) than in control group 1 (PaO2, 70 mm Hg; P <.0001) and control group 2 (PaO2, 45.5 mm Hg; P =.002). The role of arterial hypoxemia, however, appeared weakened by comparable degrees of systemic hypotension and liver passive congestion in episodes of HH associated with CRF and episodes of HH associated with CHF. Finally, the causative role of arterial hypoxemia emerged from hemodynamic measurements of cardiac index (CI), systemic vascular resistances (SVR), and oxygen transport: systemic hypotension in HH associated with CHF (control group 1) was the result of a fall in CI (median, 2. 33 L/min. m2; range, 1.21-3.14 L/min. m2) associated with high SVR (median, 2,492 dyn. s/cm5. m2; range, 1,382-4,053 dyn. s/cm5. m2), whereas in HH associated with respiratory failure (study group), systemic hypotension was the result of a fall in SVR (median, 1,053 dyn. s/cm5. m2; range, 646-3,148 dyn. s/cm5. m2), resulting in high CI (median, 4.23 L/min. m2; range, 1.9-5.32 L/min. m2) (P =.0087 and. 0038 for cardiac index and SVR, respectively). Moreover, measurements of oxygen transport in patients with HH associated with respiratory failure showed low values of O2 delivery (DO2) (median, 376 mL/min. m2; range, 253-427 mL/min. m2) as a result of extreme arterial hypoxemia despite high CI. In conclusion, these hemodynamic results and additional measurements of hepatic blood flow (HBF) by the method of galactose clearance at a low concentration suggest that in the setting of HH associated with respiratory failure, the liver is not "ischemic," despite hypotension, but rather "hypoxic" as a result of the combination of severe arterial hypoxemia and elevated central venous pressure (CVP).
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PMID:Hypoxic hepatitis caused by acute exacerbation of chronic respiratory failure: a case-controlled, hemodynamic study of 17 consecutive cases. 991 19

Transgenic mice expressing the c-Myc oncogene driven by woodchuck hepatitis virus (WHV) regulatory sequences develop hepatocellular carcinoma with a high frequency. To investigate genetic lesions that cooperate with Myc in liver carcinogenesis, we conducted a genome-wide scan for loss of heterozygosity (LOH) and mutational analysis of beta-catenin in 37 hepatocellular adenomas and carcinomas from C57BL/6 x castaneus F1 transgenic mice. In a subset of these tumors, chromosome imbalances were examined by comparative genomic hybridization (CGH). Allelotyping with 99 microsatellite markers spanning all autosomes revealed allelic imbalances at one or more chromosomes in 83.8% of cases. The overall fractional allelic loss was rather low, with a mean index of 0.066. However, significant LOH rates involved chromosomes 4 (21.6% of tumors), 14, 9 and 1 (11 to 16%). Interstitial LOH on chromosome 4 was mapped at band C4-C7 that contains the INK4a/ARF and INK4b loci, and on chromosome 14 at band B-D including the RB locus. In man, the homologous chromosomal regions 9p21, 13q14 and 8p21-23 are frequently deleted in liver cancer. LOH at chromosomes 1 and 14, and beta-catenin mutations (12.5% of cases) were seen only in HCCs. All tumors examined were found to be aneuploid. CGH analysis of 10 representative cases revealed recurrent gains at chromosomes 16 and 19, but losses or deletions involving mostly chromosomes 4 and 14 generally prevailed over gains. Thus, Myc activation in the liver might select for inactivation of tumor suppressor genes on regions of chromosomes 4 and 14 in a context of low genomic instability. Myc transgenic mice provide a useful model for better defining crosstalks between oncogene and tumor suppressor pathways in liver tumorigenesis.
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PMID:Recurrent allelic deletions at mouse chromosomes 4 and 14 in Myc-induced liver tumors. 1189 80

The molecular mechanisms of acute hepatitis C virus (HCV) infection, end-stage hepatitis (cirrhosis), and hepatocellular carcinoma have been extensively studied, but little is known of the changes in liver gene expression during the early stages of liver fibrosis associated with chronic HCV infection, that is, the transition from normal liver (NL) of uninfected patients to the first stage of liver fibrosis (F1-CH-C). To obtain insight into the molecular pathogenesis of F1-CH-C, we used real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) to study the mRNA expression of 240 selected genes in liver tissue with F1-CH-C, in comparison with NL. The expression of 54 (22.5%) of the 240 genes was significantly different between F1-CH-C and NL; 46 genes were upregulated and 8 were downregulated in F1-CH-C. The most noteworthy changes in gene expression mainly affected the transcriptional network regulated by interferons (IFNs), including both IFN-alpha/beta-inducible genes (STAT1, STAT2, ISGF3G/IRF9, IFI27, G1P3, G1P2, OAS2, MX1) and IFN-gamma-inducible genes (CXCL9, CXCL10, CXCL11). Interesting, upregulation of IFN-alpha/beta-inducible genes (but not IFN-gamma-inducible genes) was independent of histological scores (grade and stage of fibrosis) and HCV characteristics (hepatic HCV mRNA levels and the HCV genotype), and was specific to HCV (as compared to hepatitis B virus (HBV)). Other genes dysregulated in F1-CH-C, albeit less markedly than IFN-alpha/beta- and IFN-gamma-inducible genes, were mainly involved in the activation of lymphocytes infiltrating the liver (IFNG, TNF, CXCL6, IL6, CCL8, CXCR3, CXCR4, CCR2), cell proliferation (p16/CDKN2A, MKI67, p14/ARF), extracellular matrix remodeling (MMP9, ITGA2), lymphangiogenesis (XLKD1/LYVE), oxidative stress (CYP2E1), and cytoskeleton microtubule organization (STMN2/SCG10). Thus, a limited number of signaling pathways, and particularly the transcriptional network regulated by interferons, are dysregulated in the first stage of HCV-induced liver fibrosis. Some of the genes identified here could form the basis for new approaches aimed at refining IFN-based therapies for chronic HCV infection.
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PMID:Molecular profiling of early stage liver fibrosis in patients with chronic hepatitis C virus infection. 1566 Nov 46

Diffuse pulmonary hemorrhage leading to death is a syndrome which may develop in leptospirosis, but its pathophysiology is not well documented. We report an autopsy case of leptospirosis. A healthy 41-year-old man presented with low back myalgia, dry cough and fever for 4 days and a normal chest X-ray on admission. Acute respiratory failure developed hours later. Profuse bloody fluid appeared in the endotracheal tube immediately after intubation. Chest X-ray showed whiteness across all lung fields. He died of persistent shock 16 h after the onset of acute respiratory failure. Autopsy revealed diffuse pulmonary hemorrhage with hyaline-membrane formation, myocarditis, interstitial nephritis and hepatitis. Silver stain of lung and kidney tissue demonstrated leptospires. Immunohistochemical staining showed inducible nitric oxide synthase in alveolar macrophages. Immunofluorescein staining showed immunoglobulin in alveolar septum and alveolar space. This case suggests that hemorrhagic diffuse alveolar damage with persistent shock is related to over-production of nitric oxide and immunoglobulin deposition in fatal leptospirosis.
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PMID:Nitric oxide production and immunoglobulin deposition in leptospiral hemorrhagic respiratory failure. 1638 81

Bentazone is a herbicide widely used in the agrochemical field and acts by interference in photosynthesis in plants. Case reports of bentazone poisoning in humans are rare, but hepatorenal damage and death have been described, though the mechanism of toxicity remains speculative. We describe 2 cases of acute bentazone poisoning and compare these with other literature reports. The clinical picture included nausea, vomiting, diarrhea, abdominal pain with gastrointestinal corrosive injury, dyspnea and acute hepatorenal dysfunction. Respiratory failure, acute hepatitis, acute renal failure requiring hemodialysis, and death occurred following a large ingested dose of 1,764 mg/kg. Bentazone may have direct organ toxicity, especially in liver and kidney, in subjects with renal hypoperfusion, rhabdomyolysis, preexisting renal disease or concomitant nephrotoxic drug consumption. Aggressive supportive therapy, hydration and measures to prevent renal hypoperfusion are essential to reverse acute renal failure.
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PMID:Acute renal failure induced by bentazone: 2 case reports and a comprehensive review. 1844 22

We report the clinical and radiological central nervous system manifestations of a 27-year-old man with Q fever who subsequently developed acute disseminated encephalomyelitis and showed a significant response to steroids. The patient presented with headache and fever and quickly progressed to develop acute respiratory failure and hepatitis. A prompt evaluation revealed positive serology for Q fever and doxycycline was initiated. Approximately 1 week into his illness he was noted to be profoundly weak. Neuroimaging with magnetic resonance imaging (MRI) revealed diffuse white matter T2/FLAIR hyperintensities, with evidence of restricted diffusion. He was given high-dose steroids for a presumed diagnosis of acute disseminated encephalomyelitis (ADEM) and within days he had both clinical and MRI improvement. In addition to well-described meningitis and encephalitis, Q fever may also be associated with diffuse CNS lesions that may be demyelinating inflammatory in pathophysiology, and therefore responsive to high-dose steroids.
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PMID:Central nervous system manifestations of Q fever responsive to steroids. 1974 43


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