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)

Cardiac and circulatory failure are the main causes of hypoxic hepatitis. In a prospective study of 142 cases of hypoxic hepatitis collected during a 10-year period, we encountered two cases resulting from extreme arterial hypoxemia without congestive heart failure, cor pulmonale, or circulatory failure. Both patients were morbidly obese women admitted to the intensive care unit for carbonarcosis. Oxygen arterial saturation was very low, less than 35% in both patients, but there was no history of cardiac or respiratory failure and no clinical evidence of circulatory failure. Cardiac function, evaluated by isotopic scintigraphy, was normal. After the episode of hypoxic hepatitis, a diagnosis of obstructive sleep apnea was made clinically and confirmed by performing nocturnal oximetry, which showed multiple episodes of oxygen desaturation in both patients. Polysonography could be performed in one case and was typical of obstructive sleep apnea. Liver ischemia is the main mechanism leading to hypoxic hepatitis. More recently, the role of passive congestion of the liver has been emphasized. Arterial hypoxemia, however, is generally considered to be a minor factor. Our two cases support the hypothesis that severe arterial hypoxemia may lead to hypoxic hepatitis even in the absence of cardiac and circulatory failure.
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PMID:Hypoxic hepatitis caused by severe hypoxemia from obstructive sleep apnea. 925 50

We present a case of an obese young man who developed ischemic hepatitis, severe coagulopathy, acute renal failure, and encephalopathy. Heart failure and hypovolemia were absent. Oxygen arterial saturation was very low, between 77% and 99% during the day, with no history of respiratory failure. A diagnosis of obstructive sleep apnea was made clinically and confirmed by performing formal polysomnography. The polysomnographic study showed multiple episodes of apneas and hypopneas with severe oxygen desaturation. The patient was treated with continuous positive airway pressure through a nose mask and clinical manifestations related to profound nocturnal desaturation were ameliorated. He was discharged 32 days after admission with normal results of laboratory tests. This case report is presented to support the hypothesis that hypoxic hepatitis was directly related to severe arterial hypoxemia.
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PMID:A case of ischemic hepatitis. 1538 90

Patients with obstructive sleep apnea (OSA) are at risk for the development of fatty liver as a result of being overweight. Several data suggest that OSA per se could be a risk factor of liver injury; ischemic hepatitis during OSA has been reported, and OSA is an independent risk factor for insulin resistance. Therefore, we investigated liver damage and potential mechanisms in 163 consecutive nondrinking patients with nocturnal polysomnographic recording for clinical suspicion of OSA. Serum levels of liver enzymes were measured in all patients. Liver biopsy was offered to patients with elevated liver enzymes. Intrahepatic hypoxia was assessed by the expression of vascular endothelial growth factor (VEGF) on liver biopsy specimens. Severe OSA (apnea-hypopnea index [AHI] > 50/hr) was seen in 27% of patients; 52% had moderate OSA (AHI 10-50/hr), and 21% had no OSA. Overall, 20% had elevated liver enzymes. Independent parameters associated with elevated liver enzymes were body mass index (BMI) (OR: 1.13; CI: 1.03-1.2) and severe OSA (OR: 5.9; CI: 1.2-29). Liver biopsy was performed in 18 of 32 patients with elevated liver enzymes and showed steatohepatitis in 12 cases, associated with fibrosis in 7 cases. Patients with severe OSA were more insulin-resistant according to homeostasis model assessment, had higher percentage of steatosis as well as scores of necrosis and fibrosis, despite similar BMI. Hepatic immunostaining used as an indirect marker of hypoxia was not different between patients with or without severe OSA. In conclusion, severe OSA is a risk factor for elevated liver enzymes and steatohepatitis independent of body weight. Promotion of insulin resistance is probably involved. Further studies are needed to determine whether hypoxia contributes directly to liver injury.
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PMID:Chronic liver injury during obstructive sleep apnea. 1591 59

Chronic intermittent hypoxia, a characteristic of obstructive sleep apnea (OSA), is associated with the progression of simple hepatic steatosis to necroinflammatory hepatitis. We determined whether inhibition of a hypoxia-induced signaling pathway could attenuate hypoxia-exacerbated lipoapoptosis in human hepatocytes. The human hepatocellular carcinoma cell line (HepG2) was used in this study. Palmitic acid (PA)-treated groups were used for two environmental conditions: Hypoxia (1% O2) and normoxia (20% O2). Following the treatment, the cell viability was determined by the 3,4-(5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt (MTS) assay, and the mechanism of lipoapoptosis was evaluated by Western blotting. Hypoxia exacerbated the suppression of hepatocyte growth induced by palmitic acid via activation of mitochondrial apoptotic pathways as a result of endoplasmic reticulum (ER) and oxidative stresses. Ammonium pyrrolidine dithiocarbamate, a scavenger of reactive oxygen species, attenuated the hypoxia-exacerbated lipoapoptosis in hepatocytes, whereas glycerol, which reduces ER stress, did not. This may have been because inhibition of oxidative stress decreases the expression of pro-apoptotic proteins, such as caspase 9 and cytochrome c. These results suggested that modulation of apoptotic signaling pathways activated by oxidative stress can aid in identifying novel therapeutic strategies for the treatment of nonalcoholic steatohepatitis (NASH) with OSA. Further in vivo studies are necessary to understand the pathophysiologic mechanism of NASH with OSA and to prove the therapeutic effect of the modulation of the signaling pathways.
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PMID:Reduction of oxidative stress attenuates lipoapoptosis exacerbated by hypoxia in human hepatocytes. 2565 28

Cardiovascular (CV) disease is the most common cause of morbidity and mortality worldwide, particularly in the presence of the metabolic syndrome (MetS). Classifications and treatment of the MetS have recently been redefined. While the majority of the cardiac components such as hypertension, diabetes mellitus (DM) and dyslipidemia (DLD) are objectively measurable elements, a few disparities among the definitions have to be considered that can variably modify diagnosis, treatment and prevention. Non-cardiac factors such as liver disease (including, but not limited to, alcoholic and non-alcoholic steatosis/hepatitis), renal disease, severe obesity, polycystic ovarian syndrome and obstructive sleep apnea (OSA), may have independent or synergistic relationship with complementary cardiac MetS elements, and these additional risk factors may have an incremental adverse impact on CV outcome. The combination of all these factors potentiates the adverse significance on CV events. MetS not only increases morbidity and mortality but also has economic ramifications for the healthcare system. Prevention of CV disease includes primary and secondary aspects. Besides overall advances to provide optimal care for hypertension, diabetes, and dyslipidemia, early-targeted inventions to diagnose, treat and prevent OSA, and severe obesity, are needed.
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PMID:Interrelationships with Metabolic Syndrome, Obesity and Cardiovascular Risk. 2745 5