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

Twenty-four patients with biguanide-induced lactic acidosis were reported to the Adverse Drug Reaction Register of the Finnish National Board of Health from 1974-1977. Of them, 23 had been treated with phenformin and one with metformin. The mean age of the patients was 71 years, and all but one were more than 65 years of age. The mortality rate was 63%. One patient had cirrhosis of the liver and one was already known tohave had impaired renal function. Fourteen of the patients had a normal serum creatinine concentration either before or after the development of lactic acidosis. Thus, in most patients it had not been possible to prevent development of lactic acidosis by observing the contraindications to biguanide therapy. Most patients had some form of co-existing cardiovascular disease. Tetracycline therapy was a probable precipitating factor in three cases. Based on the statistics of biguanide consumption in Finland, the annual incidence of biguanide-induced lactic acidosis in 1976 and 1977 was between 1/2000 and 1/3000 and that of fatal lactic acidosis was 1/4000.
 ...
PMID:Biguanide-induced lactic acidosis in Finland. 49 89

Acid-base status was determined in 86 patients with cirrhosis of the liver. Group I comprised 55 patients living more than 3 months after examination (stable). Another 18 stable patients with a surgical porta-caval shunt (p.c.a.) formed group II. Group III consisted of 12 terminal patients without p.c.a. examined within the last week of life. With respect to liver function group II was intermediate between I and III. The most common acid-base disturbance in group I was compensated respiratory alkalosis (20%) followed by compensated metabolic alkalosis (15%). 50% of group II presented compensated respiratory alkalosis. 85% of group III showed metabolic acidosis, which was compensated in only half of the patients. Respiratory alkalosis seemed more related to impairment of liver function than to portasystemic shunting. The genesis of the terminal metabolic acidosis was complex. Renal function was reduced in 92% of group III, and lactic acidosis was found in 36%. In this group hepatic function was most severely impaired, and 60% were hypotensive. These disturbances were not related to aetiology or treatment of the liver disease.
 ...
PMID:Acid-base status in liver cirrhosis. Disturbances in stable, terminal and portal-caval shunted patients. 127 3

Disorders of acid-base balance are frequently encountered in fulminant hepatic failure, liver cirrhosis and autoimmune liver diseases. The disorders per se except lactic acidosis rarely poses serious clinical problems. However metabolic alkalosis induced by administration of diuretics and hypokalemia in renal tubular acidosis are risk factors for hepatic encephalopathy.
 ...
PMID:[Disorders of acid-base balance in liver disease]. 143 10

This study examined the acid base disturbances in 18 adults with acute renal failure (ARF) from one of new aspects, which is lactate metabolism and pathophysiology. 10 patients (55%) of them were accompanied by lactic acidosis and 9 patients (90%) of those with lactic acidosis also had severe hepatic failure. Mortality of patients with lactic acidosis was 80%, and much higher than that of ARF (66.7%). Lactate, pyruvate, lactate-to-pyruvate ratio (L/P) were 76.7 +/- 15.66 mg/dl, 3.30 +/- 0.74 mg/dl and 19.9 +/- 1.41, respectively. All of them significantly raised, compared to values of healthy adults, patients with liver cirrhosis, chronic renal failure and diabetes mellitus. Arterial pH and HCO3- levels were 7.20 +/- 0.04 and 10.6 +/- 1.20 mEq/l. Anion gap (AG) was 30.0 +/- 3.66 mEq/l. Significant correlations of lactate with pH, HCO3-, AG and L/P were demonstrated, while correlations of lactate with BUN, CR and prothrombin time were not significantly observed. Lactic acidosis results from two mechanisms. One is lactate overproduction (e.g tissue hypoxia) and the other is lactate underutilization (e.g severe liver and/or renal failure). Whenever lactic acidosis occurred, both mechanisms were present simultaneously and continuously. Especially, the latter mechanism had a very important role on it, and seemed to decide the prognosis of the patients with lactic acidosis. Therapy of lactic acidosis was very difficult. First of all, we tried to improve the circulatory failure and severe acidemia (pH less than 7.20) not to fall into vicious cycle. Then, CAVH, if combined with alkali infusion, seemed to be the most useful technique in managing lactic acidosis with ARF.
 ...
PMID:[Acute renal failure with lactic acidosis]. 221 21

A patient with cirrhosis developed hemoperitoneum, lactic acidosis, and hyperphosphatemia in the absence of shock. At post-mortem examination occult multicentric hepatocellular carcinoma eroding the liver capsule was present. The case emphasizes the central role of the liver in lactic acidosis, indicates that hemoperitoneum may precipitate this complication, and documents the association of lactic acidosis and hyperphosphatemia.
 ...
PMID:Lactic acidosis associated with cirrhosis, hepatoma, hemoperitoneum, and hyperphosphatemia. 301 70

In western industrialized countries ethanol is an important etiologic factor in the development of cirrhosis of the liver. Metabolic, immunologic and physico-chemical alterations of the hepatocyte due to ethanol are involved in the pathogenesis of alcoholic liver disease. However, the mechanisms by which ethanol damages the liver are far from clear. During the last two decades, the effect of ethanol on multiple biochemical pathways of the hepatocyte has been investigated intensively. The present paper is focusing on the metabolic aspects of alcoholic liver disease. In the first part of the review, special emphasis has been led on the metabolites of ethanol oxidation, while in the second part microsomal enzyme induction due to alcohol has been discussed. More than 90% of ethanol metabolism takes place in the liver via cytoplasmic alcoholdehydrogenase (ADH) and via a microsomal ethanol oxidizing system (MEOS). The products of these reactions are reduced nicotinadenine dinucleotide phosphate (NADH), acetaldehyde and acetate. NADH alters the redox state of the liver cell favouring all reductive processes. This shift in metabolic pathways results in hyperlactacidaemia, lactacidosis, ketosis and hyperuricaemia. Disturbances of the carbohydrate metabolism may lead either to hypo- or hyperglycaemia. The altered redox state also influences the metabolic pathways of lipid metabolism leading to lipid accumulation within the hepatocyte which can be morphologically observed as alcoholic fatty liver. In addition, porphyrin and collagen metabolism is also affected by the increased NADH/NAD+ ratio. On the other hand, acetaldehyde damages the microtubular system and the mitochondria. Acetaldehyde may also be responsible for the increased lipidperoxidation after chronic ethanol ingestion.
 ...
PMID:[Metabolic aspects of alcoholic liver damage: 1984/5 update. 1. Epidemiology and alcohol metabolism]. 639 85

Basic caloric needs of patients with compensated liver cirrhosis and healthy controls were supplied for 48 h with mixtures of glucose, fructose, sorbite, and xylit. Mixed solutions (20% w/v) containing glucose + fructose (n = 6), glucose + sorbite (n = 36), glucose + xylit (n = 37) in a 1:1 ratio, and glucose + fructose + xylit (n = 6) in a 1:2:1 ratio as well as glucose alone (n = 6) were administered in a dosage of 0.25 g/kg/h each. Utilization of the monosubstances, corresponding blood levels, and the effects on parameters of carbohydrate and lipid metabolism were frequently controlled. In contrast to mixed solutions, infusion of glucose alone caused a pronounced increase of the insulin levels and hyperglycemia in some patients suffering from liver cirrhosis. In both groups infusion of glucose + xylit was accompanied by a rise of uric acid levels. In liver cirrhotics a permanent decrease of phosphate as well as an increase of xylit concentrations were observed. These changes were not seen with xylit lowered to 50%, in glucose + fructose + xylit infusion. Therefore, we recommend to restrict xylit in liver cirrhotics to 100/24 h. No significant changes of blood gas measurements, ph values, hyperlactatemia, or lactic acidosis were seen. There was no difference in the anticatabolic, antilipolytic, and antiketogenic effect of the solutions. The least changes of all controlled parameters were observed with glucose + fructose and glucose + fructose + xylit infusions.
 ...
PMID:[Carbohydrate infusions in internal diseases. A comparative study in metabolically healthy, liver diseased and diabetic patients. VIII. Continuous infusions of low dosage carbohydrate mixtures in patients with liver cirrhosis]. 681 63

Lactic acidosis has been described in patients with liver disease. Hyperlactacidaemia results from an imbalance in lactate production versus lactate utilization. It is estimated that the liver utilizes approximately 30 percent of the total lactate produced in the body under basal conditions, primarily by gluconeogenesis. The gluconeogenesis from lactate 10 mM and lactacidaemia were determined in order to investigate the effects of CCl4+ethanol administration in liver injury and, the possible effect of colchicine in our experimental fibrosis model. The tests were determined after 15, 30 or 45 days of treatment. The results indicate that the gluconeogenesis was significantly inhibited in both CCl4+ethanol groups and CCl4+ethanol+colchicine groups. By contrast, the lactacidaemia levels were much higher in the CCl4+ethanol groups than the colchicine groups. Summarising, we have documented that hyperlactacidaemia is due to the inhibition of lactate utilization by the isolated hepatocytes in experimental cirrhosis, and that the improvement in lactacidaemia caused by colchicine is not primarily due to an increase in hepatic lactate utilization.
 ...
PMID:Colchicine alters lactate utilization in isolated hepatocytes of rats treated with CCl4 and ethanol. 842 5

Chronic hepatitis B is a widespread viral illness with the serious sequelae of cirrhosis and hepatocellular carcinoma. Current therapy with interferon is not universally efficacious, and this has led to the evaluation of other antiviral agents. A recent Phase II trial of the nucleoside analogue, fluoroiodoarabinofuranosyluracil (fialuridine, FIAU) was halted because of the sudden development of severe multisystem toxicity characterized by hepatic failure, lactic acidosis, and pancreatitis, which resulted in the deaths of five patients. We systematically evaluated pre- and post-therapy biopsy, explant, and autopsy specimens from the 15 patients involved in this trial to define the hepatic changes of fialuridine toxicity and to determine whether the degree of pre-existing hepatitis contributed to the severity of toxicity. Severe hepatotoxicity from fialuridine was characterized by hepatomegaly with diffuse, predominantly microvesicular steatosis, hepatocellular glycogen depletion, marked bile ductular proliferation, and cholestasis. Ultrastructural examination revealed intracytoplasmic lipid droplets and marked mitochondrial injury. Patients in whom severe toxicity did not develop mainly showed changes caused by the underlying chronic hepatitis B alone. There was a subtle increase in the amount of microvesicular steatosis in two of six patients with mild or no symptoms of toxicity. The microscopic and ultrastructural pattern of injury and systemic symptoms in patients with fialuridine toxicity are consistent with severe mitochondrial and metabolic derangements. Similar hepatic pathologic findings have been reported rarely for other antiviral nucleoside analogues, which suggests that the mechanisms of toxicity might be related.
 ...
PMID:Histopathologic changes associated with fialuridine hepatotoxicity. 907 26

Since ethanol metabolism predominantly takes place in the liver it is not surprising that hepatic intermediary metabolism is strikingly influenced. Alcohol is metabolized via three enzyme systems: alcohol dehydrogenase (ADH), microsome ethanol oxidizing system (MEOS) and catalase. The ADH reaction produces reducing equivalents as NADH which results in various metabolic disorders such as hyperproteinemia IV and V, hypoglycaemia, lactacidosis, hyperuricaemia, and certain forms of porphyria. The metabolism of hormones is also disturbed. Alcohol fatty liver is a direct consequence of NADH production. Alcoholic liver disease comprises of fatty liver, alcoholic hepatitis and cirrhosis. Risk factors of alcoholic liver disease are the amount of alcohol consumed, drinking pattern, female gender and certain genetic predispositions. Alcoholic hepatitis is characterized by a typical clinical and laboratory feature, and specific heaptic morphology. Poor prognostic factors are continuous alcohol consumption, cholestatis and perivenular fibrosis. Alcoholic cirrhosis has similar complications as cirrhosis of other etiology. Therapy includes abstinence, antioxidative drugs, steroids, and S-adenosylmethionine. Liver transplantation is of long-term benefit.
 ...
PMID:[Alcohol and the liver]. 1080 81


1 2 3 4 5 Next >>