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)

Distal renal tubular acidosis (dRTA) may complicate renal transplantation, liver cirrhosis, and obstructive uropathy. Indeed, its occurrence may be an early clue to an episode of rejection of the graft or to obstructive uropathy. The mechanism in most patients with dRTA is impaired distal secretion of protons. In some patients, however, back leak of protons from tubular lumen to blood may abolish distal tubular ability to maintain urine to blood proton gradients. In patients with obstructive uropathy the spectrum of tubular acidosis is widened by the occurrence of additional defects in tubular secretion of potassium and impairment of hydrogen ion secretion secondary to hypoaldosteronism. Hyperkalemia is also seen in "voltage dependent" states such as following the administration of lithium and amiloride. Hyperkalemia per se is conducive to acidosis by a combination of extrarenal and several intrarenal mechanisms.
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PMID:Acquired distal renal tubular acidosis in man. 675 51

The reduced hepatic blood flow calculated from hepatic scintigram with 198Au colloid was elucidated as the primary responsible factor for postoperative hepatic insufficiency. However 198Au colloid is no longer in use because of the high levels of radiation. Although 99mTc-phytate behaves similarly to 198Au on imaging, there were discrepancies between the hepatic blood flow index (KL) value and the severity of cirrhosis determined by laboratory data or by histology. In the measurement of hepatic blood flow using a radioactive colloid, factors like organ distribution, stability and uniformity of the colloid particles influence the values. In the present study, a 111In colloid was prepared and administered to rats to investigate the usefulness: as much as 95.4 (0.8) [Mean (+/- SD)]% of the colloid accumulated in the liver at pH 6.8. The distribution of particle diameter was within a relatively narrow range with the peak at 0.2 to 0.4 microns. Moreover, the KL values were not affected by condition of the reticuloendothelial system. The values showed a significant correlation with the measurements of the hepatic tissue blood flow obtained by the hydrogen gas clearance method (gamma = 0.83, P < 0.001). Thus, the 111In colloid can be clinically used as a substitute for 198Au colloid in the preoperative examination for estimation of the limit of resection.
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PMID:Measurement of hepatic blood flow using 111In colloid. 761 93

Gastric lesion was induced by the oral administration of acidified aspirin in rats with hepatic cirrhosis produced by N-nitrosodiethylamine (NDA) or carbon tetrachloride (CCl4). Gastric lesion by acidified aspirin was aggravated in NDA-induced cirrhosis, but not in CCl4-cirrhotic rats. To clarify this difference in the susceptibility of the gastric mucosa, gastric mucosal blood flow and gastric emptying were measured by the hydrogen gas clearance method and beads method, respectively. Gastric mucosal blood flow was lower and gastric emptying was significantly delayed in NDA-induced cirrhotic rats as compared with the controls, but not in CCl4-induced cirrhotic rats. Gastric mucosal blood flow in NDA-induced cirrhotic rats was significantly decreased by the oral administration of acidified aspirin as compared with the controls. Aldioxa dose-dependently inhibited the gastric lesion formation by acidified aspirin and inhibited the decrease of gastric mucosal blood flow in NDA-induced cirrhotic rats. These results suggest that aggravation of gastric lesion induced by acidified aspirin in NDA-induced cirrhotic rats would be due to the decrease of gastric mucosal blood flow and delay of gastric emptying. In addition, aldioxa showed a protective effect against gastric lesions induced by acidified aspirin in NDA-induced cirrhotic rats, suggesting that this compound would have an inhibitory effect on gastric lesions that are accompanied by hepatic cirrhosis.
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PMID:[Acidified aspirin-induced gastric lesion in rats with hepatic cirrhosis produced by N-nitrosodiethylamine or carbon tetrachloride. Effect of aldioxa on gastric lesions]. 814 3

The hydrogen breath test has been used to investigate the incidence of small-bowel bacterial overgrowth in 45 chronic alcoholics and in 60 controls with no history of alcohol abuse. In the group of patients with alcoholic liver disease, the percentage of cases with bacterial overgrowth was almost three times (37.8%) that of controls not abusing alcohol (13.3%; p < 0.001). A separate evaluation of alcoholics with cirrhosis in comparison with those without cirrhosis, revealed no significant difference in the incidence of bacterial overgrowth (42.9% and 33.3%; p > 0.05). Some 16.7% of the controls and 8.9% of the patients with alcoholic liver disease were classified as "non-excreters". Among patients with alcoholic liver disease, the mouth-to-caecum transit time was prolonged by 21.5% in comparison with the controls not abusing alcohol (p < 0.025). The results suggest that bacterial overgrowth might contribute to the functional and/or morphological abnormalities of the small intestine commonly found in patients with chronic alcohol abuse.
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PMID:Breath hydrogen excretion in patients with alcoholic liver disease--evidence of small intestinal bacterial overgrowth. 844 53

Gallstones form as a result of many disorders. Unphysiologic supersaturation, generally from hypersecretion of cholesterol, is essential for the formation of cholesterol gallstones. The other common abnormalities of the hepatobiliary system in gallstone patients are accelerated nucleation, gallbladder hypomotility, and the accumulation of mucin gel. An attempt is made here to relate hypersecretion of cholesterol and biliary supersaturation to the molecular basis of the associated phenomena. Supersaturation of bile with calcium hydrogen bilirubinate, the acid calcium salt of unconjugated bilirubin, is essential for pigment gallstone formation, but its magnitude remains undefined in model systems. Nucleation and the precipitation of calcium hydrogen bilirubinate with the polymerization of the pigment in the gallbladder, together with the deposition of the inorganic salts, calcium carbonate and phosphate, result in black pigment gallstone formation. On the basis of ex vivo muscle studies, gallbladder hypomotility is unlikely in patients with black pigment stones but is invariably present in patients with cholesterol stones. Pigment supersaturation in the gallbladder is the result of hepatic hypersecretion of bilirubin conjugates in hemolytic disorders and possibly enterohepatic cycling of unconjugated bilirubin in nonhemolytic states. Less common is bile salt hyposecretion from impaired synthesis in constitutional disorders and cirrhosis, and uncompensated interruption of the enterohepatic circulation in ileal dysfunction syndromes. Bile salt deficiency causes incomplete solubilization of unconjugated bilirubin and impaired binding of calcium ions. Stasis and anaerobic bacterial infection are responsible for brown pigment stones, which usually form in the bile ducts. In addition to the precipitation of calcium hydrogen bilirubinate that remains unpolymerized, there is also the deposition of the calcium salts of saturated fatty acids and free bile acids, both of which are the result of bacterial enzymatic hydrolysis of biliary lipids.
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PMID:Pathogenesis of gallstones. 848 Aug 73

Interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) are major proinflammatory cytokines inducing the synthesis and release of many inflammatory mediators. They are involved in immune regulation, autoimmune diseases, and inflammation. Acanthoic acid, (-)-pimara-9(11),15-dien-19-oic acid, is a pimaradiene diterpene isolated from the Korean medicinal plant, Acanthopanax koreanum. When human monocytes/macrophages stimulated with silica were treated with 0.1-10 microg/ml acanthoic acid, the production of IL-1 and TNF-alpha was inhibited up to 90%, but the production of interleukin-6 (IL-6) was not inhibited at all. At these concentrations, it had no cytotoxic effect on human monocytes/macrophages. It also suppressed the production of TNF-alpha by alveolar macrophages and lymphocytes stimulated with silica. In addition, acanthoic acid inhibited the release of superoxide anion and hydrogen peroxide from human monocytes/macrophages and neutrophils. To know the antifibrotic effects of acanthoic acid, its effects on fibroblast proliferation and collagen synthesis were tested. The proliferation of NIH3T3 cells was inhibited almost completely by the addition of the culture supernatants of human monocytes/macrophages treated with acanthoic acid, but not by the addition of acanthoic acid only. In vitro and in vivo treatment with acanthoic acid reduced collagen production by rat lung fibroblasts and lung tissue. Furthermore, acanthoic acid suppressed granuloma formation and fibrosis in the experimental silicosis. Acanthoic acid reduced serum GOT and GPT in the rats with cirrhosis induced by CCl4, and it was effective in reducing hepatic fibrosis and nodular formation. Taken together, these data indicate that acanthoic acid has a potent anti-inflammatory and antifibrosis effect by reducing IL-1 and TNF-alpha production.
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PMID:Suppression of interleukin-1 and tumor necrosis factor-alpha production by acanthoic acid, (-)-pimara-9(11),15-dien-19-oic acid, and it antifibrotic effects in vivo. 866 Aug 20

The purpose of this study was to correlate the hyperintensity in the globus pallidus seen on T1-weighted magnetic resonance imaging (MRI) of the brain in chronic liver disease with changes in metabolite ratios measured from both proton and phosphorus-31 magnetic resonance spectroscopy (MRS) localised to the basal ganglia. T1-weighted spin echo (T1WSE) images were obtained in 21 patients with biopsy-proven cirrhosis (nine Child's grade A, eight Child's grade B and four Child's grade C). Four subjects showed no evidence of neuropsychiatric impairment on clinical, psychometric and electrophysiological testing, four showed evidence of subclinical hepatic encephalopathy and 13 had overt hepatic encephalopathy. Signal intensities of the globus pallidus and adjacent brain parenchyma were measured and contrast calculated, which correlated with the severity of the underlying liver disease, when graded according to the Pugh's score (p < 0.05). Proton MRS of the basal ganglia was performed in 12 patients and 14 healthy volunteers. Peak area ratios of choline (Cho), glutamine and glutamate (Glx) and N-acetylaspartate relative to creatine (Cr) were measured. Significant reductions in mean Cho/Cr and elevations in mean Glx/Cr ratios were observed in the patient population. Phosphorus-31 MRS of the basal ganglia was performed in the remaining nine patients and in 15 healthy volunteers. Peak area ratios of phosphomonoesters (PME), inorganic phosphate, phosphodiesters (PDE) and phosphocreatine relative to beta ATP (ATP) were then measured. Mean values of PME/ATP and PDE/ATP were significantly lower in the patient population. No correlation was found between the T1WSE MRI contrast measurements of the globus pallidus and the abnormalities in the metabolite ratios measured from either proton or phosphorus-31 MR spectra. Our results suggest that pallidal hyperintensity seen on T1WSE MR imaging of patients with chronic liver disease is not related to the functional abnormalities of the brain observed in hepatic encephalopathy.
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PMID:MR imaging and spectroscopy of the basal ganglia in chronic liver disease: correlation of T1-weighted contrast measurements with abnormalities in proton and phosphorus-31 MR spectra. 886 45

Changes in cerebral hemodynamics and metabolism associated with anesthesia and liver transplantation may present particular hazards for patients with cirrhosis. Fifteen patients undergoing liver transplantation were studied, 7 of whom had encephalopathy. Cerebral blood flow (CBF) was measured at the start of surgery, during veno-venous bypass and post reperfusion, using a method based on the Kety-Schmidt method. Cerebral metabolism was assessed by measuring the cerebral metabolic rate for oxygen (CMRO2) and the lactate oxygen index (LOI). The cerebral vascular reactivity to carbon dioxide (CO2) was studied during the preanhepatic and post reperfusion phases. During the preanhepatic period, the median CBF was 44 mL/100 g/min at an arterial carbon dioxide tension (PaCO2) of 3.8 kPa. After reperfusion the CBF increased (P < .02) to 102 mL/100 g/min, the arterial hydrogen ion concentration increased from 39 nmol/L to 53 nmol/L (P < .02) and the jugular venous oxygen saturation from 74% to 89% (P < .02). CBF was similar in patients with and without encephalopathy. The cerebral vascular reactivity to CO2 remained intact, although after reperfusion, the CBF for a given PaCO2 was greater, and the slope of the CBF/CO2 response curve diminished. The CMRO2 was normal in patients without encephalopathy. In the encephalopathic patients, the CMRO2 was low during all stages of transplantation (0.54, 0.86, 1.24 mL/100 g/min, respectively). Patients with encephalopathy may be at increased risk of hypoxemic brain injury during transplantation. To minimize this possibility, more detailed neurological monitoring may be useful.
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PMID:Cerebral blood flow and metabolism in patients with chronic liver disease undergoing orthotopic liver transplantation. 946 33

We have postulated that reduced hepatic blood flow is the primary factor responsible for postoperative hepatic insufficiency, and have shown the usefulness of the hepatic blood flow index (KL) estimated by 198Au colloid. However, 198Au colloid has became unavailable due to its intense exposure activity. Therefore, we prepared 111In colloid as a substitute for 198Au colloid to evaluate hepatic functional reserve. In the present study, a 111In colloid was administered to rats to investigate the possibility of clinical application. First, liver cirrhosis was induced in rats using CCl4 Changes in KL and hepatic tissue blood flow were measured by hydrogen gas clearance (HL) after CCl4 injection, and was shown to correlates well with it. The correlation between KL and HL, together with normal and cirrhotic liver, was significant (r = 0.83, p < 0.01) Second, reticuloendothelial function was modulated with Zymosan A (stimulation) and Silica (suppression). The KL value remained unchanged in spite of the addition of an activator or suppressor to the reticuloendothelial system. Third, 30% and 70% hepatectomy models were studied according to the method of Higgins-Anderson. KL and HL was measured before and 1, 3 and 7 days after hepatectomy. KL and HL after 30% and 70% hepatectomy showed similar changes. These results indicate that the clearance of 111In colloid can be used clinically as an index of the hepatic blood flow.
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PMID:Experimental evaluation of hepatic functional reserve using 111In colloid for clinical application. 970 77

As altered gastrointestinal motility could be involved in the pathogenesis of small intestinal bacterial overgrowth observed in liver cirrhosis, we investigated mouth to caecum transit time (MCTT) and solid meal gastric emptying (SMGE) in patients with cirrhosis. MCTT was estimated in 20 cirrhotics and 12 healthy controls using lactulose hydrogen breath test. SMGE was measured in 12 patients with cirrhosis and 27 controls by means of 99-m Tc-sulphur colloid labelling egg albumin and gamma scintigraphy. T1/2 and percentage of marker remaining in stomach (MRS) at 60, 90, and 120 min were calculated. MCTT was prolonged in patients with cirrhosis (111 +/- 7 min) compared to controls (83 +/- 6 min; p < 0.02). No significant differences were demonstrated in SMGE t1/2 between controls (84 +/- 5 min) and cirrhotics (91 +/- 6 min). Also, MRS was similar in patients with cirrhosis and healthy controls at 60, 90 and 120 min. We conclude that MCTT is prolonged in patients with cirrhosis. In addition, our data suggest that pyloruscaecum component plays the main role in delaying orocaecal transit time in cirrhosis.
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PMID:[Patients with liver cirrhosis: mouth-cecum transit time and gastric emptying of solid foods]. 972 75


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