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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thiamine, an essential co-enzyme, improves glucose utilization. Thiamine hydrochloride (50 mg per capita per day for 30 days), given to 25 patients with liver cirrhosis who had hyperglycaemia, produced a significant reduction (P less than 0.001) in blood glucose levels. It is therefore suggested that thiamine supplements be given to cirrhotics with hyperglycaemia, to improve glucose utilization.
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PMID:Effect of thiamine on glucose utilization in hepatic cirrhosis. 188 79

Altered metabolism has been shown to exist in the settings of surgical stress, cancer, cirrhosis, sepsis, and trauma. Each condition is characterized by varying degrees of alteration in metabolic processes, and within a given patient, these metabolic alterations will change as the patient's status changes. Nutrition support is an integral part of the metabolic management of critically ill patients. Metabolic changes impact nutritional substrate requirements and utilization. As the patient's clinical condition deteriorates, clinical signs and symptoms become less reliable in predicting or assessing the existing physiologic state. Objective measurements are needed to define the metabolic status during these physiologic changes. The purpose of this article is to review selected indices that have been used to identify abnormalities in nutritional substrate metabolism. Although some of these tests are readily available and inexpensive, many have not been used outside of the research setting and, therefore, their clinical utility has yet to be determined. However, their use as research tools for defining metabolism warrants their inclusion in order to assist the clinician in interpreting research studies. The biochemical markers discussed include glucose, lactate, pyruvate, triglycerides, beta-hydroxybutyrate, acetoacetate, urinary nitrogen, acute phase proteins, visceral proteins, 3-methylhistidine, plasma amino acids, oxygen consumption, and resting energy expenditure. Each marker is defined in terms of its biochemical significance, and the literature describing changes that occur in various stress states is cited.
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PMID:Overview of biochemical markers used for nutrition support. 190 7

Pancreatic secretion and hepatic removal of insulin have been measured in thioacetamide (TAA)-induced compensated rat liver cirrhosis in perfusion experiments. Peripheral plasma concentrations of glucose and insulin were slightly decreased in TAA-treated rats. Pancreatic secretion and hepatic removal of insulin remained unchanged by the TAA-treatment. Thus, even in morphologically and biochemically proven experimental liver cirrhosis, insulin secretion and removal may not be disturbed.
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PMID:Secretion and elimination of insulin by the in vitro perfused pancreas and liver of rats with thioacetamide-induced liver cirrhosis. 191 35

We performed 93 sclerotherapy sessions on liver cirrhosis patients with recurrent variceal bleedings. In each session, hypertonic glucose, thrombin and 1% polidocanol were consecutively injected into the varices, and changes in the hemostatic system were examined in relation to the symptoms observed during the treatment. Patients underwent sclerotherapy with no complaints in 62 (67%) sessions, and complained of slight symptoms of general fatigue and headache in 19 (20%). In the other 12 (13%) sessions, the procedure was discontinued due to marked manifestations of these symptoms. All symptoms were temporary and disappeared completely after the procedure. These temporary symptoms were closely related to changes in coagulation tests similar to those of disseminated intravascular coagulation, which were observed just after the treatment. Possible activation of the renal kallikrein-kinin system following injection sclerotherapy was also demonstrated.
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PMID:Manifestations of temporary symptoms during endoscopic variceal sclerotherapy using thrombin as a sclerosant. 192 Sep 57

Hepatic parenchymal tissue is known to be one of the major sites of thyroid hormone metabolism as well as glucagon action. Alterations in circulating thyroid hormone concentrations, as well as hyperglucagonemia, are well documented in subjects with hepatic cirrhosis and advanced liver dysfunction. Also, we have documented recently that hyperglucagonemia induced in normal subjects alters thyroid hormone metabolism, with lowering of serum T3 and a rise in serum reverse T3 (rT3) levels. Thus, it is conceivable that rising glucagon concentrations are responsible for altered thyroid hormone levels in hepatic cirrhosis. To examine this hypothesis, this study determined relationships between plasma glucose, glucagon, insulin, and insulin:glucagon ratio on one hand, and thyroid hormone concentrations on the other, in 51 subjects with hepatic cirrhosis. Significant negative correlations were noted between plasma glucagon and serum T3 (r = -0.418, p less than 0.001) as well as T3:T4 ratio (r = -0.627, p less than 0.0001), whereas significant positive correlations were observed between plasma glucagon and serum rT3 (r = 0.504, p less than 0.001) as well as rT3:T4 ratio (r = 0.644, p less than 0.0001). No such significant relationships were noted between either insulin, glucose and insulin:glucagon ratio on one hand and any of thyroid hormone indices on the other. Therefore, this study indicates that, in hepatic cirrhosis, circulating glucagon concentrations may play a major contributing role in induction of altered serum thyroid hormone concentration by influencing thyroid hormone metabolism.
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PMID:Low serum T3 and raised reverse T3 levels in hepatic cirrhosis: role of glucagon. 192 46

Twenty uncomplicated cases of cirrhosis of liver, proved by liver biopsy, and free from other systemic diseases were studied. Glucose (pre- and postprandial) and electrolytes (Na+, K+, Cl-) values were compared to those of systemic and portal venous blood. Chloride level in ascitic fluid was found to be significantly high in cirrhosis, as compared to portal and systemic venous blood. Sodium and glucose levels were similar in ascitic fluid and portal venous blood except in two cases complicated with tuberculous peritonitis, where pre- and postprandial glucose levels were considerably low. In 55% cases, there was impaired glucose tolerance, as measured by pre- and postprandial glucose levels in systemic venous blood.
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PMID:Study of ascitic fluid in relation to systemic and portal venous blood in hepatic cirrhosis. 194 Apr 16

Glucose homeostasis and fatty acid metabolism are abnormal in patients with cirrhosis. To assess the metabolic response to starvation in an animal model of cirrhosis, glycogen and fuel metabolism were characterized in rats with CCl4-induced cirrhosis studied 2 wk after 10 weekly doses of CCl4. Plasma concentrations of glucose and beta-hydroxybutyrate were not different between fed CCl4-treated and control rats, but plasma nonesterified fatty acid concentrations were higher in cirrhotic animals (0.25 +/- 0.01 vs. 0.39 +/- 0.04 mmol/L; p less than 0.05). After 12 hr of starvation, the plasma nonesterified fatty acid concentration had reached 0.58 +/- 0.04 mmol/L in CCl4-treated rats, compared with 0.38 +/- 0.04 mmol/L in control rats (p less than 0.05). The redistribution of the hepatic carnitine pool toward acylcarnitines, which is characteristic of starvation, was complete after fasting for 12 hr in the CCl4-treated rats, compared with the 24 hr required in control rats. In fed cirrhotic rats, liver glycogen content per gram liver was decreased by 64% compared with control rats (30.0 +/- 5.1 vs. 10.8 +/- 1.1 mg/gm liver wet wt; p less than 0.05). After 12-hr fasting, hepatic glycogen content had fallen to 14.3 +/- 3.9 and 4.8 +/- 0.4 mg/gm liver wet wt (p less than 0.05) in control and cirrhotic animals, respectively. To further characterize the status of glycogen metabolism in cirrhotic livers, activities of glycogen synthase and glycogen phosphorylase were determined. Hepatic active and total glycogen phosphorylase activities normalized to hepatocellular content were unaffected by CCl4 treatment, whereas total glycogen synthase activity was increased by 45%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased hepatic glycogen content and accelerated response to starvation in rats with carbon tetrachloride-induced cirrhosis. 195 69

Ten patients with chronic hepatic disease (CHD) were compared with 34 non-CHD (N) pts. All patients underwent a peritoneal equilibration test; the asymptotic curves for small solutes transport were transformed into straight lines; protein transport was also expressed as a straight line; the slopes of these linear functions were used as index of solute transfer. CHD patients showed increased UF and transport of all solutes. The well-known relationships between UF and glucose absorption and between UF and dialysate sodium concentration were observed in N, but not in CHD patients. In patients without hepatic disease there was also a relationship between UF and the glucose transport slope, which was not observed in CHD pts. These results are probably due to the influence of hepatic lymph production plus increased lymphatic removal, observed in non uremic patients affected by cirrhosis, on the mechanisms of water and solute transport in CAPD. CHD patients can be managed either with CAPD or with short frequent exchanges. Ascites production can be evaluated by the difference between the observed UF in a patient with CHD and the expected UF in N patients.
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PMID:Transport of water and solutes in uremic patients with chronic hepatic disease in CAPD. 198 13

To explore further the pathogenesis of glucose intolerance and insulin resistance observed in patients with cirrhosis and portal hypertension, we studied a 35-year-old woman with presinusoidal portal hypertension without cirrhosis due to nodular regenerative hyperplasia of the liver. After oral glucose ingestion, glucose tolerance remained normal; however, this occurred at the expense of a markedly hyperinsulinemic plasma response, suggesting the presence of insulin resistance. To examine this question more directly, we performed a stepwise euglycemic insulin clamp study in combination with an infusion of [6-3H]glucose and [1-14C]palmitate and indirect calorimetry. The ability of insulin to promote total body (primarily muscle) glucose uptake was markedly impaired, whereas its effect to suppress hepatic glucose production was normal compared with results obtained in nine healthy subjects. Moreover, insulin failed to normally suppress plasma free fatty acid turnover and oxidation in this patient. This informative case demonstrates that portal hypertension alone, without hepatic dysfunction from cirrhosis, is associated with impaired insulin-mediated glucose and plasma free fatty acid metabolism and may also play a predominant role in the development of insulin resistance in many cirrhotic patients.
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PMID:Insulin resistance in noncirrhotic idiopathic portal hypertension. 198 28

Porcine gastric inhibitory polypeptide (GIP) was infused iv (120 micrograms in 60 min) in seven patients with biopsy-proven hepatic cirrhosis who had surgical porta-caval anastomoses and hyperglucagonemia in the postabsorptive state. The infusions resulted in elevation of blood levels of immunoreactive GIP into the upper range of those observed after ingestion of large mixed meals. This was accompanied by significant increments in immunoreactive glucagon (IRG) in the plasma. Similar infusions in two cirrhotic patients with surgical porta-caval anastomoses who had normal plasma IRG levels in the postabsorptive state had no effect on the plasma IRG level. Ingestion of triglyceride (60 g) in hyperglucagonemic cirrhotic patients with porta-caval anastomoses also resulted in elevation of plasma immunoreactive GIP, and this was again associated with significant elevation of the plasma IRG level. Chromatography studies showed that the increments in plasma IRG after the administration of GIP or triglyceride were largely accounted for by increases in pancreatic-type glucagon. There were no significant effects of administration of GIP or triglyceride on the blood levels of glucose or immunoreactive insulin. It is concluded that porcine GIP is glucagonotropic in patients with cirrhosis of the liver who show elevated levels of IRG in the plasma in the postabsorptive state. This effect is not due to diversion of portal blood to the systemic circulation and may be attributable to hypersensitivity of the alpha-cells to stimulation by GIP.
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PMID:Stimulation of glucagon secretion by gastric inhibitory polypeptide in patients with hepatic cirrhosis and hyperglucagonemia. 198 10


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