Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 1 MAC of either halothane, enflurane or isoflurane on splanchnic haemodynamics were studied in cirrhotic rats that were either normovolaemic or hypovolaemic from haemorrhage. A group of conscious rats acted as the control group. Bile duct ligation had been carried out in all the rats four weeks previously to induce cirrhosis. At the time of the study, all the rats were anaesthetized with ether for catheterization of the left femoral artery and vein, and the left ventricle via the right carotid. The control group was allowed to awake. When the other rats started to recover, they were artificially ventilated with room air and 1 MAC of the halogenated agent. Heart rate and mean arterial blood pressure were monitored continuously. Once the animals had remained steady for one hour, 1.25 ml of blood for 100 g body weight was removed over a 10 min period. PaO2, PaCO2, arterial pH, heart rate, mean arterial blood pressure, cardiac index and regional blood flows (RBF) were measured before, and thirty minutes after the haemorrhage. Cardiac output and RBF were measured using the radioactive-labelled microsphere method. Only 32 animals were finally included, eight in each group. Splanchnic, portal and hepatic arterial blood flows were similar in conscious rats and in those receiving isoflurane or halothane, and were higher than in those receiving enflurane. The lowest splanchnic and portal venous blood flows were found in those rats receiving enflurane. After haemorrhage, these RBF decreased significantly in all groups except in the enflurane group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of halogenated anesthetics on splanchnic hemodynamic in normo- and hypovolemic cirrhotic rats]. 144 14

The effects of ketamine, halothane, enflurane, and isoflurane on systemic and splanchnic hemodynamics in cirrhotic rats that were either normovolemic or hypovolemic following hemorrhage were characterized. Rats received at random either ketamine (30 mg/kg iv, 1.5 mg.kg-1.min-1 iv), halothane, enflurane, or isoflurane (1 MAC). Conscious rats were considered the control group. Four weeks before hemodynamic studies bile duct ligation was performed in all rats to induce cirrhosis. Hemodynamic measurements were performed using the radioactive microsphere method 1 h after the onset of anesthesia and 30 min after hemorrhage. Anesthetized rat lungs were mechanically ventilated with room air. Before hemorrhage cardiac index was higher in conscious rats and in rats receiving isoflurane than in the other groups (P less than 0.001). Hepatic arterial blood flow was similar in conscious rats and in those receiving isoflurane or halothane and was higher than in those receiving ketamine or enflurane. The lowest splanchnic and portal venous tributary blood flows were observed in rats receiving enflurane. After hemorrhage cardiac index was significantly less than before hemorrhage in all groups, except in rats receiving enflurane. After hemorrhage portal venous tributary blood flow decreased significantly in all groups except in enflurane group. During halothane and enflurane anesthesia hepatic arterial blood flow and hepatic arterial fraction of cardiac output decreased (P less than 0.01) and they were maintained in the other groups. After hemorrhage hepatic arterial fraction of cardiac output in conscious rats was higher than in those receiving ketamine, halothane, or enflurane (P less than 0.05) and was similar to those receiving isoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of ketamine, halothane, enflurane, and isoflurane on systemic and splanchnic hemodynamics in normovolemic and hypovolemic cirrhotic rats. 236 Jul 21

Previous studies indicated decreased numbers and depressed clearance function of hepatic macrophages in alcoholic liver disease (ALD). We examined hepatic macrophages by immunohistochemical techniques in 45 liver biopsies from patients with a spectrum of ALD and compared them with 20 histologically normal biopsies from non-alcoholic patients. Antisera against lysozyme, alpha 1-antitrypsin (alpha 1AT) and a cytoplasmic molecule on macrophages (MAC-387) were used and the number of positively staining hepatic sinusoidal macrophages and portal tract macrophages assessed separately. Portal tract macrophage numbers were increased with all three markers in biopsies exhibiting only fatty change (P less than 0.05) and with MAC-387 in all ALD groups. In agreement with previous studies, lysozyme positive hepatic sinusoidal macrophages were decreased in all ALD groups. However, the other markers did not show any significant decrease and MAC-387 positive macrophages were increased in livers with cirrhosis plus hepatitis (P less than 0.01). The use of three markers revealed phenotypic heterogeneity of hepatic macrophages with antibodies to lysozyme and alpha 1 AT staining more hepatic sinusoidal macrophages than MAC-387, but MAC-387 and anti-lysozyme staining more portal tract macrophages than anti-alpha 1AT. Since hepatic macrophages appear to be heterogeneous and capable of diverse functions including the release of cytotoxic mediators, the finding of increased numbers, even in early ALD, suggests they may contribute to the increased numbers, even in early ALD, suggests they may contribute to the tissue damage.
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PMID:Portal tract macrophages are increased in alcoholic liver disease. 278 81

A rat model was used to determine whether isoflurane exacerbates liver dysfunction and whether its metabolism is changed in the presence of cirrhosis. Male Wistar rats were gavaged weekly with carbon tetrachloride until cirrhosis was well advanced. They and control rats without pretreatment with carbon tetrachloride and without cirrhosis were then exposed to 1.45% (1 MAC) isoflurane for 3 hours. Blood and urine samples were taken before, immediately, as well as 4, 24, 48, and 72 hours after anesthesia to measure liver function and isoflurane defluorination. After the last samples had been obtained, the rats were sacrificed and the liver removed for histologic examination and in vitro metabolic studies. Serum levels of SGOT and SGPT and inorganic fluoride production in rats with cirrhosis were similar to those in control rats without cirrhosis. Concentrations of cytochromes b5 and p-450 and specific activities of microsomal defluorinase and several cytosolic enzymes were significantly lower in cirrhotic than in noncirrhotic liver, but their total amounts in whole liver were the same. The results imply that cirrhosis does not increase the risk of acute hepatotoxicity of isoflurane. They also demonstrate that metabolism of isoflurane and perhaps other volatile anesthetics may be unaffected in rats with cirrhosis, even though liver architecture is severely disrupted.
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PMID:Hepatotoxicity and metabolism of isoflurane in rats with cirrhosis. 291 55

Halothane, enflurane, isoflurane, and fentanyl were examined for their potential to exacerbate liver dysfunction in rats with preexisting cirrhosis. Male Wistar rats given sodium phenobarbital for 2 weeks are assigned randomly to two groups. One group (cirrhotic) was exposed by inhalation to carbon tetrachloride (CCl4) in air at weekly intervals for 12 weeks to induce cirrhosis. The other group (noncirrhotic) was handled similarly but received air only. Five weeks after the last exposure to CCl4, cirrhotic and noncirrhotic rats were given three hours of 1 MAC halothane, enflurane, or isoflurane in 50% oxygen, or 350 micrograms fentanyl per kg of body weight and 50% oxygen, or 50% oxygen only. Blood gas tensions and blood glucose levels were measured before, during, and at the end of exposure. Forty-eight hours after exposure, serum chemistries were measured in each rat for comparison with preexposure values. Rats were then killed by CO2 overdose, and liver, kidney, and testis were prepared for microscopic examination. Enflurane, isoflurane, and halothane, but not fentanyl, produced mild respiratory acidosis and no change in serum glucose levels. All anesthetics resulted in a mild but similar degree of acute liver dysfunction as indicated by small increases in SGOT or SGPT in both cirrhotic and noncirrhotic rats. Liver histology revealed mild to moderate portal cirrhosis with fibrosis and well-developed micronodules in rats exposed to CCl4, but no superimposed acute hepatocellular damage was noted. It is concluded that all the anesthetics used in this study were associated with the same minimal degree of postanesthetic hepatic dysfunction and that the dysfunction was similar in both cirrhotic and noncirrhotic rats.
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PMID:Effects of volatile anesthetics or fentanyl on hepatic function in cirrhotic rats. 406

We identified 54 patients with AIDS and ascites seen over a 4.5-year period at a university hospital. This retrospective study is the largest reported series of patients with AIDS and ascites. Patients with AIDS who are evaluated for ascites should be stratified by the CD4 + cell count and the presence or absence of portal hypertension based upon the serum-ascites albumin gradient and clinical presentation. Awareness of possible surgery-related causes of ascites is crucial, as these patients may not manifest the usual signs and symptoms of peritonitis or abdominal catastrophes seen in immunocompetent hosts. Patients with evidence of portal hypertension due to hepatic cirrhosis and an elevated ascitic neutrophil count should be suspected to be infected with common bacterial pathogens associated with peritonitis unless the CD4 + cell count is below 50 cells/mm3. When the CD4 + cell count declines below this threshold, infections due to Mycobacterium avium complex, cytomegalovirus, and other opportunistic infections should be considered.
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PMID:Ascites and the acquired immunodeficiency syndrome. Report of 54 cases. 896 82

Abnormalities in iron metabolism have been reported in patients with acquired immunodeficiency syndrome (AIDS). To assess the frequency of abnormal hepatic iron deposition in these patients and to examine potential causes of iron overload, we analyzed the amount of iron at different cellular sites in liver sections obtained at autopsy of 78 patients with AIDS. Quantitation of serum iron and transferrin levels and estimation of total iron binding capacity was obtained using serum from 63 patients. The number of whole blood/packed red blood cell transfusions and opportunistic infections was recorded. Of the 78 patients, 25 (32%) showed a Grade 3 or 4 (0-4 scale) iron level, distributed in three patterns, i.e., in hepatocytes only, in hepatocytes and Kupffer cells, and in Kupffer cells only. In these 25 livers, 4 had cirrhosis, with no documented cause; the mean number of transfusions was 12.5; and 16 (64%) had Mycobacterium avium-Mycobacterium intracellulare infection. In the 53 livers with little or no iron, 5 had cirrhosis, with 3 of those 5 listing alcoholic liver disease or hepatitis as the cause; the mean number of transfusions was 1.4; and 18 (34%) had Mycobacterium avium-Mycobacterium intracellulare infection. Transferrin saturation was more than 50% in 6 (29%) of 21 cases with increased hepatic iron levels and in 6 (14%) of 42 cases with little or no hepatic iron. These results indicate that hepatic iron overload in patients with AIDS is associated with blood transfusions, an elevated transferrin saturation, and Mycobacterium avium-Mycobacterium intracellulare infection. Significant hepatic iron deposition in patients with AIDS with no other apparent cause of cirrhosis suggests an etiologic role for iron in hepatic injury. The increase in hepatic iron levels in these patients has potentially adverse clinical effects related to the use of transfusions, iron supplements, and iron-containing drugs.
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PMID:Increased hepatic iron in the acquired immunodeficiency syndrome: an autopsy study. 938 70

90K/MAC-2BP glycoprotein is a serum tumour marker, member of the scavenger receptor cysteine rich (SRCR) protein superfamily, involved in different immunological mechanisms. In the present study, we determined 90K serum levels by a sandwich enzyme immunoassay using the same monoclonal antibody in 11 chronic active hepatitis (CAH), 48 liver cirrhosis and 36 hepatocellular carcinoma (HCC). In comparison, the same samples were also tested for AFP. According to a cut-off point of 14 micrograms/mL for the 90K, established as 100% of specificity in 50 controls, we observed increasing positivities from CAH to cirrhosis and then to HCC (27%, 50% and 78%, respectively). In cirrhotic patients 90K levels were associated with the presence of anti-HCV antibodies, but not with the degree of liver compromise. Finally, 90K sensitivity was higher than AIFP in all groups of hepatic patients. However, further investigations are needed before proposing 90K as a clinical useful tumour marker in the progression from cirrhosis to HCC.
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PMID:Serum 90K/MAC-2BP glycoprotein levels in hepatocellular carcinoma and cirrhosis. 1062 37

Glycoprotein 90K/MAC-2BP is a member of the scavenger receptor cystein-rich protein superfamily, which is thought to be involved in immune surveillance, defending the body against pathogens and cancer. 90K serum levels are elevated in patients with cancer of various origins and in viral infections, such as human immunodeficiency virus and hepatitis C virus (HCV). Because in patients with HCV-related cirrhosis the incidence of hepatocellular carcinoma (HCC) is high, in the present paper we examined, by means of an enzyme-linked immunosorbent assay, the 90K serum levels in 103 patients with liver cirrhosis, and in 69 with HCC, and compared them to alpha-fetoprotein, the reference tumor marker for this neoplasm. Serum levels of 90K (cut-off 14 microg/ml) were elevated both in cirrhosis (39%) and HCC (46%) compared to controls (14.1 microg/ml vs. 10.6 microg/ml in cirrhosis, and 14.8 microg/ml vs. 9.1 microg/ml in HCC, p < or = 0.001). There was a significant association with the presence of anti-HCV antibodies. 90K was found to be a non-specific tumor marker which is complementary to alpha-fetoprotein on the basis of its probable different biological significance. In fact, 74% of HCC patients had at least one positive marker. Combined use of 90K and alpha-fetoprotein could improve the sensitivity of a single test in the diagnosis of HCC.
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PMID:Serum 90K/MAC-2BP glycoprotein in patients with liver cirrhosis and hepatocellular carcinoma: a comparison with alpha-fetoprotein. 1175 11

Mycobacterium avium complex (MAC) frequently disseminates in AIDS patients, where the gastrointestinal tract is a major target organ. While ascites in AIDS patients is common, peritonitis secondary to MAC is rare. We describe the first case of MAC peritonitis in an AIDS patient without underlying cirrhosis, portal hypertension, chylous ascites or peritoneal dialysis. This case highlights the need to be aware of atypical presentations of MAC disease in AIDS patients with a history of disseminated MAC, even those who compliantly take highly active antiretroviral therapy.
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PMID:Mycobacterium avium complex peritonitis in an AIDS patient. 1186 72


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