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

The relationship between the impairment in hepatic and renal function in cirrhosis has not been well established. This study investigated urinary sodium excretion in comparison with quantitative parameters of liver function in 75 patients with various degrees of cirrhosis kept on a constant salt diet of 120 mmol/d for 5 days before the start of the study. The aminopyrine breath test (ABT), indocyanine green (ICG) elimination, galactose elimination capacity (GEC), and hepatic sorbitol elimination (HSE) served as quantitative parameters of liver function. Results for the quantitative tests were compared with those for the Child-Pugh score. Urinary sodium excretion showed a significant nonlinear relationship to ABT (r = .70; P < .0001). Less-significant correlations were observed for ICG (r = .60), the Child-Pugh score (r = -.57), GEC (r = .44), and HSE (r = .34). Because a number of significant correlations were observed between the different liver function tests, multivariate analysis was used to further elucidate the relationship between hepatic function and sodium excretion. Only one independent predictor of urinary sodium excretion could be identified, and that was the ABT (P < .02). More than half of the nonascitic patients showed a urinary sodium excretion of less than 80% of dietary sodium intake, indicating impaired renal sodium handling in preascitic cirrhosis. Based on the 95% confidence interval (CI) for ABT of nonascitic patients with normal (mean ABT 0.56% dose x kg/mmol CO2; 95% CI: 0.44 to 0.69) and reduced urinary sodium excretion (mean ABT 0.26% dose x kg/mmol CO2; 95% CI: 0.18 to 0.35), a threshold level of ABT of about 0.4 (% dose x kg/mmol CO2) for conservation of normal urinary sodium excretion in cirrhosis can be defined. This ABT value reflects an approximate 50% reduction in function compared with the mean of cirrhotic patients with normal liver and kidney function (0.81% dose x kg/mmol CO2). The presence of ascites was also associated with a reduction in ABT to below 0.4 (% dose x kg/mmol CO2), while, for all other parameters, either the cut-off point was close to the lower limit of normal or no cut-off level could be detected. In conclusion, the results of the present study provide further evidence that the impairment in urinary sodium excretion in cirrhosis is related to hepatic function. The data suggest a nonlinear relationship. Because ABT has been shown to reflect functional hepatocellular mass, the occurrence of sodium retention and ascites appears to be related to a threshold of an approximate 50% reduction in functional liver cell mass.
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PMID:Urinary sodium balance in patients with cirrhosis: relationship to quantitative parameters of liver function. 936 55

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 shown that administration of inorganic potassium phosphates (Pi) to patients with severe diabetic ketoacidosis was able to increase the P50 (the PO2 necessary to achieve a hemoglobin saturation of 50%) by a non diphosphoglycerate (DPG) mediated effect. This suggests that the oxyhemoglobin dissociation curve (ODC) may be determined not only by pH, temperature, CO2 content and DPG but also by plasmatic ions. In order to test this hypothesis we have determined the ODC on whole blood in two groups of subjects, 49 control subjects with matching age and sex and 49 patients suffering from liver cirrhosis, acute pancreatitis, septic shock and acute respiratory distress syndrome. The patients had many ionic disorders induced either by their diseases or by the applied treatment. The mean ODC of the patients did not differ from the normal values. In contrast, the dispersion of PO2 around the saturations values was increased from 5 to 80% saturation. A forward regression analysis showed that the DPG level and the levels of inorganic phosphates and natrium (Na+) played a significant role in determining the position of the ODC according to the following equation: P50 (mmHg) = 34.5 + 0.225 DPG + 0.62 Pi-0.09 Na+, where DPG is in micromol.gHb-1 and Pi and Na+ in mEq.l-1. In separate experiments we showed that the Bohr effect as expressed in d (log PO2)/dpH amounted to -0.53, -0.46 and -0.42 for SO2 equal to 5%, 50% and 95%, respectively. The corresponding values for the temperature effect was expressed in d (log PO2)/dT amounted to 0.028, 0.024, and 0.020 respectively. The fact that ions play an role in regulating the position of the ODC of patients with ionic disorders may have therapeutical implications, preventive or curative.
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PMID:Effect of inorganic ions on the oxyhemoglobin dissociation curve of severely ill patients. 976 30

We evaluated the hypothesis that venous congestion (increased venous volume), as reflected by venous hypertension (increased venous pressure), can arise when the right ventricle is unable to elevate the pulmonary arterial pressure sufficiently to propel the cardiac output through an anatomically inadequate or inappropriately constricted pulmonary vasculature. Changes in venous pressure were evaluated in clinically healthy broilers during modest increases in pulmonary vascular resistance induced by inhalation of 5% CO2 and during large increases in pulmonary vascular resistance accomplished by acutely tightening a snare around one pulmonary artery. Inhalation of 5% CO2 induced a pronounced respiratory acidosis, as reflected by increases the partial pressure of CO2 and the hydrogen ion concentration in arterial blood. Inhalation of 5% CO2 also increased pulmonary arterial pressure by approximately 3 mm Hg and increased venous pressure by approximately 1 mm Hg when compared with the pre-inhalation venous pressure. Tightening the pulmonary artery snare increased the pulmonary arterial pressure by approximately 10 mm Hg, and this degree of pulmonary hypertension was sustained until the snare was released. When compared with the pre- and post-snare intervals, tightening of the pulmonary artery snare induced a sustained increase in venous pressure of > or = 1 mm Hg. Veins have highly compliant walls that permit an approximate doubling in volume with only small (4 to 6 mm Hg) increases in central venous pressure. Presumably the apparently modest 1 mm Hg increase in venous pressure measured after CO2 inhalation or unilateral pulmonary artery occlusion reflects a large increase in venous volume and, thus, substantial venous congestion. These observations support the hypothesis that increases in pulmonary vascular resistance can initiate increases in venous pressure by challenging the capacity of the right ventricle to propel all of the returning venous blood through the lungs. Central venous congestion predisposes broilers to the onset of cirrhosis and ascites by impeding the outflow of hepatic venous blood and increasing the hydrostatic pressure within hepatic sinusoids.
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PMID:Venous blood pressure in broilers during acute inhalation of five percent carbon dioxide or unilateral pulmonary artery occlusion. 1053 94

The Giant Panda is an endangered species that would benefit from biotechnological assistance in reproduction. However, because there are only a few of these animals left in the world, scientists hesitate to use them for research procedures. We were fortunate to obtain ovaries from a Giant Panda that died of hepatic cirrhosis during the nonbreeding season. Oocytes were harvested within 4 h of death by dissecting the ovarian cortex in physiological saline and collecting the cumulus-oocyte complexes from the fluid, and then were classified into large (> 125 microns) and small (100 to 124 microns) follicular oocytes and placed in TCM199 supplemented with FSH (10 micrograms/mL) and LH (20 micrograms/mL). After culture for 22 h at 37 degrees C in air with 5% CO2, response was evaluated by growth of oocytes and presence of the first polar body. Of the 26 large follicular oocytes that were harvested, 12 were considered suitable for IVM, and 14 were degenerated, had a broken zona pellucida or had lost some cytoplasm. Of the 12 cultured oocytes, all grew to a mean diameter of 141.1(SD = +/- 6.7, n = 12), and 4 released the first polar body. None of the small follicular oocytes showed growth or other signs of maturation. We conclude from our preliminary results that it is possible to obtain functional Giant Panda oocytes from ovaries obtained post mortem during the nonbreeding season.
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PMID:In vitro maturation of follicular oocytes of the Giant Panda (Ailuropoda melanoleuca): a case report. 1073 62

Disadvantages related to CO2 pneumoperitoneum in high risk patients (anesthesiologic classification in III and IV ASA), have led to the development of the abdominal wall retractor, a device designed to facilitate laparoscopic surgery without conventional pneumoperitoneum. A case of a patient with acute cholecystitis, well-compensated liver cirrhosis, and high respiratory and cardiologic risk (ASA III class), submitted to laparoscopic cholecystectomy with gasless technique is reported.
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PMID:[Gasless laparoscopic cholecystectomy. Selective intervention in a high surgical risk patient]. 1083 83

The derangement of sex hormone serum levels in cirrhotic patients is well-delineated, and increased levels of progesterone and estradiol have been associated to hyperventilation in cirrhotic patients. These hormones have a well-known role in the regulation of vascular tone. The aim of this study was to evaluate whether sex hormone levels contribute to pulmonary vasodilatation (PV) and gas exchange abnormalities in cirrhosis. Contrast transesophageal echocardiography, arterial blood gases, parameters of liver function, pulmonary function test, estradiol and progesterone levels were determined in 45 male cirrhotic patients. Nineteen of 45 patients (42.2%) presented PV. Hyperventilation (pressure arterial of CO2< or =35 mmHg) was correlated to progesterone levels (p<0.05) and pressure arterial of CO2 was high in patients with PV (p<0.005) and Child class B and C (p<0.01). Hypoxemia (pressure arterial of O2<80 mmHg) had inverse correlation with progesterone (p<0.05) and estradiol (p<0.05) levels and pressure arterial of O2 was low in patients with Child class B and C (p<0.05). PV was present in patients with high estradiol levels (p<0.05), high progesterone levels (p<0.005) and Pugh class B and C (p<0.05). Logistic regression analysis identified progesterone as the sole independent factor associated to PV (p<0.0005). Multivariate linear regression showed that PV was the sole independent factor related to both pressure arterial of CO2 (p<0.05) and pressure arterial of O2 (p<0.01) levels. PV was independently associated to gas exchange abnormalities in cirrhosis. Progesterone and estradiol were related with PV in cirrhotic patients.
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PMID:Implications of estradiol and progesterone in pulmonary vasodilatation in cirrhotic patients. 1188 76

Dichloroacetate (DCA) has been used as an experimental treatment for lactic acidosis because it lowers plasma lactic acid concentration. Three potential mechanisms could underlie the hypolactatemic action of DCA, but the dominant mechanism in vivo remains unclear. This study tested whether DCA-induced hypolactatemia occurs via decreased lactate production, increased lactate clearance, or decreased rate of glycolysis in healthy humans and in patients with end-stage cirrhosis. Cirrhosis is associated with decreased hepatic pyruvate dehydrogenase (PDH) content. Six healthy volunteers and 7 cirrhotic patients received a primed, constant infusion of 1-13C-pyruvate and 15N-alanine for 5 hours. DCA (35 mg/kg intravenously) was administered at 2 hours. Plasma isotopic enrichment was measured by gas chromatography/mass spectrometry (GC/MS), and exhaled CO2 enrichment by isotope ratio mass spectrometry. Pyruvate and alanine production rates (Ra) were determined by isotope dilution, and pyruvate oxidation calculated as 13CO2 production from 13C-pyruvate. Ra lactate was calculated as the difference between Ra pyruvate and its disposal by oxidation to CO2 and conversion to alanine. Baseline plasma lactate kinetics in cirrhotic patients did not differ from controls. DCA decreased lactate concentration in both groups by approximately 53%. DCA decreased glycolysis (Ra pyruvate) by 24%, increased the fraction of pyruvate oxidized to CO2 by 26%, and decreased pyruvate transamination to alanine by 25%. DCA also inhibited lactate production by 85%, but decreased plasma lactate clearance by 60% in both groups. DCA reduces plasma lactic acid concentration by inhibiting production, via stimulating pyruvate oxidation and inhibiting glycolysis, rather than increasing clearance. In addition, end-stage cirrhosis does not alter either the mechanism or the magnitude of the metabolic response to DCA.
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PMID:Mechanism of dichloroacetate-induced hypolactatemia in humans with or without cirrhosis. 1528 Oct 24

In the belief that the advantages stemming from a minimally invasive approach are significant, particularly in cirrhosis patients, we decided to apply this technique in the treatment of a group of patients suffering from HCC associated with cirrhosis. Sixteen patients (10 men, 6 women; mean age 60.1 years) underwent laparoscopic surgery for HCC associated with well compensated HCV-related liver cirrhosis (Child-Pugh class A; mean tumour size 2.9 cm). Seven of these lesions were located in the left liver and 9 in the right lobe. Laparoscopy was performed with a CO2 pneumoperitoneum (12-14 mmHg). The Pringle manoeuvre was not used. There was one conversion to laparotomy due to inadequate exposure. We performed 13 non-anatomical resections, 1 VI segmentectomy and 1 anatomical left lobectomy. None of the patients required blood transfusions. One patient died of severe respiratory distress syndrome on postoperative day 3. Major morbidity included 2 moderate postoperative ascites successfully resolved with conservative treatment. To date (mean follow-up: 18 months) no recurrences at the resection site or port-site metastases have been observed. Limited laparoscopic liver resections for HCC in cirrhotic patients are technically feasible and safe when careful selection criteria are adopted (hepatic involvement limited and located in the left or anterior right segments, tumour size smaller than 5 cm, Child-Pugh class A).
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PMID:[Laparoscopic liver resection without a Pringle maneuver for HCC in cirrhotic patients]. 1583 34

The incidence of hepatocellular carcinoma (HCC) in cirrhotic patients is increasing. Despite advances in imaging and laboratory screening which allow earlier diagnosis, the surgeon is all too often confronted with an HCC of advanced stage or arising in the setting of severe cirrhosis. Hepatic resection is still considered the treatment of choice for hepatocellular carcinoma in patients with liver cirrhosis. From 1998 to 2005, 6 patients (5 males, 1 female, age 52-70 years, mean age 64.1 years) with HCC associated severe, but well compensated liver cirrhosis (Child A-- 4 patients, Child B--2 patients) underwent 9 hepatic resection in our department. Mean tumor size was 56 mm (range 23-86 mm). Two of these lesions were in the left liver and four in the right lobe. Doppler ultrasonography was performed in all cases and CT in 3 cases to confirm the extension of the lesions. Laparoscopy was performed in 3 patients under CO2 pneumoperitoneum. The Pringle maneuver was not used. The transection of the liver parenchyma was obtained by the use of Ligasure and harmonic scalpel. Nine hepatic resections were performed: 7 segmentectomy and 2 non-anatomical resections. The resection margin was 1 cm. The mean operative time was 90 minutes (range 60-120). Mean blood loss was 250 ml and 2 patients required blood transfusion. One patient died on the tenth postoperative day from a severe respiratory distress syndrome and hepatic failure. Major morbidities occurred in three patients who developed moderate postoperative ascites, which resolved successfully with conservative treatment in two patients. Limited liver resection in cirrhotic patients with HCC is feasible with a low complication rate when careful selection criteria are followed (tumor size smaller than 8 cm, Child-Pugh A class and the good general conditions of the patients). Other medical and interventional treatments (chemoembolization, chemotherapy) can only slow the progress of HCC.
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PMID:[Liver resection for hepatocellular carcinoma in cirrhotic patients]. 1661 Jan 75


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