Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic administration of ursodeoxycholic acid (UDCA) has recently been suggested as a potential treatment for cholestatic liver disease. The purpose of this study was to examine the effects of chronic oral administration of UDCA on the histological, biochemical, and hemodynamic abnormalities induced by bile duct ligation in the rat. Fifty-one rats with ligation-section of the common bile duct were randomly and blindly assigned to receive UDCA (25 mg/kg each day) or placebo by gavage for 4 weeks. At the end of the treatment period, morphometric analysis showed that in rats treated with UDCA, hepatocyte and sinusoidal volume fractions were significantly higher than in rats receiving placebo [41.9 +/- 3.2% vs. 28.1 +/- 1.8%, (mean +/- SE) and 7.4 +/- 0.1% vs. 4.3 +/- 0.3%, respectively], whereas bile duct volume fraction (reflecting bile ductular proliferation) and connective tissue fraction were significantly lower in rats treated with UDCA than in rats receiving placebo (14.2 +/- 1.5% vs. 20.0 +/- 1.0% and 35.4 +/- 2.4% vs. 47.6 +/- 1.7%, respectively). Serum aminotransferase and alkaline phosphatase activities, and total serum bile acids and individual bile acid concentrations were not significantly different between the two groups. Portal pressure (12.7 +/- 0.5 mm Hg vs. 17.1 +/- 0.5 mm Hg), portal tributary blood flow (5.7 +/- 0.4 vs. 9.3 +/- 0.4 mL.min-1.100 g-1 body weight), and cardiac index (41.1 +/- 1.8 vs. 50.6 +/- 1.4 mL.min-1.100 g-1 body weight) were significantly lower in UDCA-treated rats than in placebo-treated animals. In portal vein stenosed rats, chronic administration of UDCA had no hemodynamic effects, a finding that suggests UDCA has no direct vasoactive effect on splanchnic circulation. It is concluded that in rats with bile duct ligation UDCA limits the severity of liver disease and consequently of portal hypertension and hyperkinetic circulation.
 ...
PMID:Ursodeoxycholic acid limits liver histologic alterations and portal hypertension induced by bile duct ligation in the rat. 156 85

To test further the competence of the cirrhotic liver to metabolize xenobiotics, hepatocytes were isolated from control and CCl4-induced cirrhotic male or female rats. Histologically micronodular cirrhosis was present in all CCl4-treated rats, while control rats had normal livers. Portal perfusion pressure and intrahepatic collagen content were also significantly increased by CCl4 administration. In male rats, no significant differences in levels of circulating transaminases nor in alkaline phosphatase was observed between cirrhotic and control rats, while CCl4-treated females had slightly higher than normal serum transaminase levels at the time of the studies. Hepatocytic cytochrome P-450 and basal xenobiotic biotransformation were unaffected by micronodular cirrhosis in both genders; calculation of the aminopyrine and 7-ethoxycoumarin intrinsic clearances (Cli) revealed, however, a slightly decreased transformation potential in hepatocytes obtained from cirrhotic females, a phenomenon not observed in cirrhotic male rats. It is speculated that the observed reduction in Cli may have been independent of cirrhosis per se, owing to the perduring cytotoxic effect of CCl4 as evidenced by the higher than normal level of transaminases in female rats. Finally, male rats were subjected to in vivo administration of phenobarbital or 3-methylcholanthrene; both compounds led to significant induction of the mixed-function oxidase system, which was similar in magnitude and in selectivity in control and cirrhotic rats as illustrated by calculation of the Michaelis-Menten kinetic parameters for aniline p-hydroxylation, aminopyrine-N-demethylation, 7-ethoxycoumarin-O-deethylation, and p-nitrophenol UDP-glucuronyl transferase. We conclude that in well-established but compensated and hepatolysis-free micronodular cirrhosis, hepatocytes are fully able to transform xenobiotics and to respond normally and selectively to inducers of drug metabolism.
 ...
PMID:Unimpaired induction of drug-metabolizing enzymes in hepatocytes isolated from rats with micronodular cirrhosis. 205 6

The elevation of serum alkaline phosphatase (ALP) that develops in the dog after 24 hours of colon ischemia was studied to determine its tissue origin. Portal, hepatic, and aortic blood were sampled but no difference in ALP level among these sites was found. In sera shown to have a significant rise in ALP, other tests of liver function were unchanged from normal, suggesting the ALP did not originate from the liver. On electrophoresis the "ischemic ALP" migrated faster than a known liver ALP standard but more slowly than an intestinal ALP sample.
 ...
PMID:Studies on the alkaline phosphatase rise following colon ischemia. 746 48

We studied portal hemodynamic changes by using duplex Doppler in 10 pigs with hepatic artery embolization (HAE) and hepatic artery ligation (HAL) and in 5 with HAL only. Serum concentration of alkaline phosphatase, ALT, direct and indirect bilirubin were determined simultaneously. Hepatic angiography and hepatic vascular cast were performed in the 5 pigs, and pathological examination in others. Portal venous velocity (PVV) and portal blood flow (PBF) increased after HAE, ALP, ALT, direct indirect bilirubin slightly elevated (P > 0.05) in the two groups after operation and most of them decreased subsequently within 7 days. Linear regression of PBF with ALP, ALT, direct and indirect bilirubin occurred in the experimental group. Liver necrosis was seen in all pigs of the experimental group and only one in the control group. Angiography and vascular cast showed that hepatic artery collaterals occurred at the portal hilus in the two groups and were more rich in the control group. Extrahepatic and intrahepatic arterial collaterals were seen from 1 to 3 weeks after HAE. The estimation of PVV and PBF by duplex Doppler may reflect the development of collaterals indirectly and is helpful in assessing the effect of HAE.
 ...
PMID:[Experimental study of portal hemodynamic changes after hepatic artery embolization]. 825 4

Among 211 patients who, between 1985 and 1990, underwent liver resection in Kyushu University Hospital, uncontrollable ascites occurred in 53 (25%). A univariate analysis revealed that postoperative death with liver failure occurred more frequently in patients with intractable ascites (p < 0.05). Alanine amino transferase levels were significantly higher in patients with intractable ascites (p < 0.05), but serum bilirubin, alkaline phosphatase and serum albumin levels did not differ significantly. Portal pressure (p < 0.05), the operation time (p < 0.01) and blood loss (p < 0.01) were significantly higher in patients with intractable postoperative ascites. A multiple analysis showed a correlation between the operation time, portal hypertension and postoperative intractable ascites. Postoperative histology revealed that a larger number of patients with cirrhosis had intractable ascites (p < 0.05). We conclude that cirrhosis, portal pressure and operating time are the most important factors related to intractable ascites in the case of hepatectomy. Areas of the liver to be resected should be limited in cirrhotic patients with portal hypertension.
 ...
PMID:Liver resection and intractable postoperative ascites. 846 21

In patients with portal hypertension, particularly with extrahepatic portal vein obstruction, portal biliopathy producing biliary ductal and gallbladder wall abnormalities are common. Portal cavernoma formation, choledochal varices and ischemic injury of the bile duct have been implicated as causes of these morphological alterations. While a majority of the patients are asymptomatic, some present with a raised alkaline phosphatase level, abdominal pain, fever and cholangitis. Choledocholithiasis may develop as a complication and manifest as obstructive jaundice with or without cholangitis. Endoscopic sphincterotomy and stone extraction can effectively treat cholangitis when jaundice is associated with common bile duct stone(s). Definitive decompressive shunt surgery is sometimes required when biliary obstruction is recurrent and progressive.
 ...
PMID:Portal biliopathy. 1168 33

Criteria for histologic diagnosis of chronic rejection (CR) are based on changes seen late in the disease process that are likely to be irreversible and unresponsive to treatment. Changes occurring during the evolution of CR are less clearly defined. The serial biopsy specimens, failed allografts, and biochemical profiles of 28 patients who underwent retransplantation for CR were examined with the aim of identifying histologic and biochemical features that were present during the early stages of CR. For each case, a point of acute deterioration in liver function tests (LFTs) was identified ("start time" [ST]) that subsequently progressed to graft failure. Biopsy specimens before, at the time of ("start biopsy" [SB]), and after the ST were assessed histologically, and findings were correlated with the biochemical changes. CR resulted from acute rejection (AR) that did not resolve. Centrilobular necroinflammation (CLNI) associated with an elevated aspartate transaminase (AST) level and portal tract features of AR were present at the start. Portal AR features resolved, CLNI persisted, AST level remained elevated, and bilirubin and alkaline phosphatase levels progressively increased throughout the evolution of CR. Portal tracts also showed a loss of small arterial and bile duct branches, with arterial loss occurring early and bile duct loss as a later progressive lesion. Foam cell arteriopathy was rarely seen in needle biopsy specimens. In conclusion, findings from this study may help identify patients at risk of progressing to graft loss from CR at a stage when the disease process is potentially reversible and amenable to treatment.
 ...
PMID:Histologic and biochemical changes during the evolution of chronic rejection of liver allografts. 1187 Mar 79

Impairment of venous outflow from the liver manifests as zone 3 sinusoidal dilatation and congestion (SDC) in liver biopsy. The spectrum of histologic changes in portal tracts has not been described. We studied liver biopsies from 34 patients with a confirmed diagnosis of venous outflow impairment (VOI). Liver transplant recipients and biopsies with cirrhosis and hepatic neoplasms were excluded. Clinical records were reviewed for laboratory tests and radiographic findings. In all, 19 patients had right heart disease, 13 had classic Budd-Chiari syndrome and two had veno-occlusive disease. Liver chemistry tests showed elevated liver transaminases (n=21; 61.8%), elevated alkaline phosphatase (n=31; 91.2%) and GGT (all 13 cases tested). The elevation in ALT and AST was mild (below 200 U/l in all cases), while alkaline phosphatase (ALP) was elevated above 500 U/l in nine (26.5%) patients and above 1000 U/l in three cases. On biopsy, all cases showed SDC. The portal tracts showed (a) portal expansion with bile ductular proliferation (n=16; 47.1%) accompanied by lymphoplasmacytic infiltrate (n=10), lymphocytic cholangitis (n=3) and portal or periportal fibrosis (n=11), (b) Portal and/or periportal fibrosis without ductular proliferation (n=3; 8.8%) or (c) Normal portal tracts (n=15; 44.1%). The combination of elevated ALP and bile ductular changes on biopsy suggested chronic bile duct disease. Ultrasound/CT scan evaluation of bile ducts in 26 patients showed no biliary tree abnormality. Antimitochondrial antibody testing in eight cases also yielded negative results. In conclusion, bile ductular proliferation, portal inflammation and portal-based fibrosis are commonly seen in liver biopsies of patients with VOI even in the absence of bile duct disease. These changes are often accompanied by elevated ALP and GGT and can lead to the suspicion of chronic biliary disease. In the absence of demonstrable abnormalities in the biliary tree, these changes can be attributed to venous outflow impairment.
 ...
PMID:Histologic changes mimicking biliary disease in liver biopsies with venous outflow impairment. 1509 6

The present study was designed to investigate the effects of quercetin on oxidative stress and activation of nuclear factor kappa B (NF-kappaB) in an experimental model of portal hypertensive gastropathy induced by partial portal vein ligation (PPVL). Portal pressure was significantly elevated in PPVL rats. Transaminase and alkaline phosphatase activities were not significantly modified, indicating absence of liver injury. Histological analysis of gastric sections showed a lost of normal architecture, with edema and vasodilatation. The cytosolic concentration of thiobarbituric acid reactive substances and the lipoperoxidation measurement by chemiluminiscence were significantly increased. Superoxide dismutase activity in gastric mucosa was significantly reduced. Portal hypertensive gastropathy induced a marked activation of NF-kappaB, accompanied by a decrease in IkappaB protein levels and a significant induction of nitric oxide synthase (iNOS) protein. Administration of quercetin markedly alleviated histological abnormalities and inhibited oxidative stress and NF-kappaB activation. IkappaB decrease and induction of iNOS protein were partially prevented by quercetin. Quercetin treatment, by abolishing the NF-kappaB signal transduction pathway, may block the production of noxious mediators involved in the pathogenesis of portal hypertensive gastropathy.
 ...
PMID:Quercetin prevents oxidative stress and NF-kappaB activation in gastric mucosa of portal hypertensive rats. 1547 65

Bile duct invasion is rare in patients with hepatocellular carcinoma (HCC). We show the usefulness of selective transcatheter hepatic arterial embolization (TAE) followed by microwave coagulation therapy (MCT) in a case of HCC with portal and biliary tumor thrombi that ruptured into the biliary system. A 70-year-old man with HCC was admitted because of melena and postprandial abdominal pain. Four years earlier, he had undergone posterior segmentectomy of the liver for HCC. Portal venous thrombus was detected on computed tomography (CT) 3 months earlier. On admission laboratory tests revealed the following values: serum alkaline phosphatase, 760 IU/L; total serum bilirubin, 11.9 mg/dL; direct bilirubin, 9.8 mg/dL; serum hemoglobin, 7.7 g/dL; alpha-fetoprotein 103.9 ng/mL; and PIVKA-2, 52,655 mAU/mL. Serum examinations were positive for anti-hepatitis C virus antibody but negative for hepatitis B surface antigens. Ultrasonography revealed a hypoechoic mass in the right branch of the bile duct at the hepatic hilum. Doppler ultrasonography showed blood flow in the mass. CT showed diffuse tumor involvement throughout the liver parenchyma and the presence of a high-density substance in the right intrahepatic bile duct. The diagnosis was hemobilia secondary to HCC in the right hepatic lobe. The symptoms recurred, and emergency TAE was performed 5 days after the onset of hemobilia. The symptoms subsided, and liver function improved. Endoscopic retrograde cholangiography revealed obstruction of the right intrahepatic bile duct. Surgery was performed 15 days after TAE, and MCT of the right hepatic hilum was performed. After MCT, CT revealed necrosis of the right hepatic hilum. Seven months after TAE, the patient died of liver failure with no recurrence of hemobilia.
 ...
PMID:Transcatheter hepatic arterial embolization followed by microwave ablation for hemobilia from hepatocellular carcinoma. 1902 68


1 2 Next >>