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PubMed2006

[Hepatic infarction following prolonged prone position].

A 61-year-old woman with chronic renal failure was scheduled for posterior spinal fusion. The duration of surgery was over ten hours and the patient was placed on prone position almost whole period of surgery. Although the surgery was finished without any obvious complications, laboratory examinations revealed marked liver dysfunction the day after the surgery. On the third postoperative day, computed tomography examination strongly suggested the liver infarction. Liver infarction has been considered as a rare complication because of two kinds of blood streams, the hepatic artery and the portal vein, but we should suspect the liver dysfunction from ischemia after the surgery of prolonged prone position.

Female↗
PubMed1983

An intensive drug monitoring study suggesting possible clinical irrelevance of impaired drug disposition in liver disease.

1 Liver disease can alter the disposition and clinical effects of drugs. However, even though altered drug disposition occurs, there is no clinical evidence relating it to an increased susceptibility to adverse drug reactions (ADRs). 2 An intensive prospective drug monitoring study of 2,582 hospitalized patients was conducted. The adverse drug reactions probability scale (APS) was used to assess ADRs. Only non-mild, definite or probable ADRs (APS greater than or equal to 5) were included. Severity of liver dysfunction was assessed by a composite clinical and laboratory index (CCLI). 3 The frequency of ADRs was higher in 402 patients with cirrhosis (27.4%) than in 661 with renal dysfunction (22.8%) and in 249 with other parenchymatous liver diseases (13.7%) or in 1,270 patients with neither liver diseases nor renal dysfunction (10.9%) (chi 2 3 = 85.53, P less than 0.001). The frequency of ADRs in cirrhotics was highly correlated with the severity of the liver dysfunction measured by CCLI (r = 0.82, P less than 0.001). 4 Drugs predominantly eliminated by liver metabolism were not among those most commonly inducing ADRs or those causing severe reactions in cirrhotics. Thus, frusemide caused the most common and the most severe ADRs, whereas reactions induced by sedatives were uncommon. Drug-induced hepatic encephalopathy was more common in cirrhotics receiving diuretics (13.3%) than in those receiving sedatives (1.8%) (chi 2 y.c. = 5.29, P less than 0.025). Patients with alcoholic liver disease had more drug-induced hepatic encephalopathy (7.7%) than those with non-alcoholic liver disease (1.2%) (chi 2 y.c. = 11.86, P less than 0.001). 5 These results indicate that susceptibility to ADRs is increased only in severe cirrhosis and that the most common and severe ADRs seem more likely related to enhanced pharmacodynamic action than to impaired drug disposition.

Brain Diseases↗
PubMed1997

Graft dysfunction following liver transplantation: role of free radicals.

BACKGROUND/AIMS: Following orthotopic liver transplantation primary graft non-function occurs in about 10% of patients, and survival depends on early retransplantation. The aetiology has yet to be defined, but reperfusion injury as a result of free radical production has been considered as a possible mechanism. In this study we looked for evidence of free radical generation intraoperatively and assessed the relationship between free radical production and graft function. METHODS/RESULTS: Twenty-one patients (M:F 10:11, mean age; 53 +/- 3.8 years) who underwent liver transplantation for end-stage liver disease were studied. Free radical activity increased significantly following reperfusion, as shown by: (i) the diene conjugated method, where the percentage molar ratio increased from a baseline of 10.87 +/- 0.78% to 24.42 +/- 7.8% (p < 0.01), and (ii) by electron paramagnetic resonance, where a more than a twofold rise in radical concentration was detected (p < 0.05). The increase in free radical activity detected by the diene conjugated method was significantly higher in patients with poor outcome as compared with those who had uneventful recovery (p < 0.01). CONCLUSION: Free radical activity is increased following reperfusion of liver graft during transplantation, and the magnitude of the rise is related to the severity of graft dysfunction.

Biomarkers↗
PubMed1999

Plasma fatty acids concentrations in postoperative patients with biliary atresia.

The concentrations of plasma fatty acids in postoperative patients with biliary atresia (BA) were measured to clarify whether they had essential fatty acid deficiency. Thirty-eight fasting blood samples from 14 postoperative patients with BA were studied. All of them had the hepatic portoenterostomy without any stoma. Samples were divided into three groups on the basis of liver function. The concentrations of fatty acids in the plasma fat were measured quantitatively. Non-essential fatty acids levels were increased and omega-3 fatty acids levels were decreased with the progress of deterioration of hepatic function. Regarding omega-6 fatty acids, C18:2 and 20:4 did not show any significant difference between the three groups and the control, and only C20:3 increased with the deterioration of liver dysfunction. The ratio of C20:3 (omega-6) to C20:4 (omega-6) was increased significantly with the progress of liver dysfunction. The activity of delta-5 desaturase was suspected to be suppressed in BA patients with poor liver function. The BA patients with poor bile flow did not show any decrease of omega-6 fatty acids in the plasma, but were at risk of developing omega-3 fatty acid deficiency.

Biliary Atresia↗
PubMed2000

Antiphospholipid antibodies are related to portal vein thrombosis in patients with liver cirrhosis.

The pathogenesis of portal vein thrombosis (PVT) in cirrhotic liver patients is not known. PVT has been related to liver dysfunction, neoplasm, hemodynamic factors, and hypercoagulability states. PVT has been reported in patients with antiphospholipid syndrome without liver cirrhosis. Our aim was to find the role of antiphospholipid antibodies (APAs) and coagulation inhibitors in PVT in patients with liver cirrhosis. We present a case-controlled study, matched by age, liver function, and etiology, to discover the role of APAs and anticoagulant protein activity in PVT in cirrhotic patients. We studied 30 cirrhotic patients: 6 of 10 (60%) patients with PVT were APA-positive, whereas only 2 of 20 (10%) in the cirrhotic control group were APA-positive (p < 0.005). Low serum levels of protein C, protein S antithrombin III, and plasminogen were found in cirrhotic patients; and, no differences were found between patients with and without PVT. Significantly lower protein S and antithrombin III levels were found in patients with Child-Pugh class C. Therefore, APAs were related to PVT in cirrhotic patients; but, a lower concentration of coagulation inhibitors was associated with liver dysfunction alone.

Antibodies, Antiphospholipid↗
PubMed1988

Thyroid hormones and thyroxine-binding globulin in relation to liver function and serum testosterone in men with alcoholic cirrhosis.

In 73 euthyroid male patients with histologically verified alcoholic cirrhosis, thyroid hormones, thyroxine-binding globulin (TBG) and testosterone concentrations (total, non-protein- and non-SHBG-bound) were studied in relation to each other and to the degree of liver dysfunction. Serum concentrations of triiodothyronine (T3) decreased significantly (p less than 0.05) and thyroid-stimulating hormone (TSH) increased with progressing liver dysfunction. Serum concentrations of tetraiodothyronine (T4), TBG and T4/TBG ratio did not correlate significantly with liver function. Serum T3 concentrations correlated significantly (Kendall Tau-beta = -0.33, p = 0.001) with total serum testosterone concentrations, while there was a negative correlation (Kendall Tau-beta = -0.20, p = 0.025) between testosterone and TSH values. No correlation was found between testosterone concentrations and serum levels of TBG. It is proposed that the association between T3 and TSH on one hand and testosterone concentrations on the other reflects a covariation of these variables with liver function. The TBG level was normal in most patients and was not correlated to testosterone concentrations.

Adult↗
PubMed1990

Extrahepatic cell membrane lipid abnormalities and cellular dysfunction in liver disease.

Liver disease is associated with characteristic changes in the lipid composition of the surface coat of plasma lipoprotein particles. Cholesterol and lecithin molecules accumulate as hepatic secretion of lecithin-cholesterol acyltransferase decreases, and the arachidonate content, the precursor for eicosanoid production, is also reduced. By exchange and equilibration processes, such abnormal circulating lipoproteins should tend to induce corresponding changes in cell membrane lipid composition; studies in both human and experimental liver disease confirm that this does occur and that it is wide-spread. The correct functioning of membrane proteins, which serve as receptors or are responsible for enzymatic and transport processes, is most commonly dependent on the fluidity of their lipid bilayer matrix. Because cholesterol enrichment of biomembranes reduces bulk lipid fluidity, it can be predicted that extrahepatic membrane dysfunction might be a general feature of severe liver disease. This concept is supported by increasing experimental evidence and, as a consequence, it is proposed that many of the cellular disturbances and metabolic abnormalities accompanying hepatic disease result from, or are exacerbated by, lipoprotein-induced changes in membrane lipid composition and function. Importantly, this mechanism also suggests that drugs which can fluidise membranes, such as S-adenosyl-L-methionine (SAMe), might help ameliorate cellular dysfunction.

Humans↗
PubMed1992

Thyroid dysfunction in multi-transfused iron loaded thalassemia patients.

Seventy-two transfusion-dependent iron loaded thalassemia patients were investigated for thyroid dysfunction by estimating circulating thyroid hormones (T4 and T3) and basal thyroid stimulating hormone (TSH). They were also evaluated for their liver function (biochemically) and iron overload by estimating serum ferritin. Thyroid failure (hypothyroidism) was documented in 14 patients (19.4%). In all, 3 groups were seen, i.e. Group 1: Normal T4, T3, TSH (58 patients: 80.6%); Group 2: Compensated hypothyroidism characterized by normal T4, T3 and raised TSH (9 patients: 12.5%); Group 3: Decompensated hypothyroidism characterized by decreased T4 and increased TSH (5 patients: 6.9%). Interestingly, impaired thyroid function could not be correlated with age, amount of blood transfused, liver dysfunction or degree of iron overload. It is postulated that an inter-play between chronic hypoxia, liver dysfunction and iron overload may be responsible for the thyroid damage.

Body Height↗
PubMedDate not supplied

Pathologic changes in pigeons infected with a virulent Trichomonas gallinae strain (Eiberg).

Trichomonas gallinae, Eiberg strain, is a virulent hepatotropic flagellate parasite of pigeons. The parasite initially infects the upper digestive tract, causing the formation of ulcers, which allow it to enter the circulatory system. The trichomonads later gain access to the liver, where they cause the formation of caseous lesions. Vascular congestion and perivascular cuffing in the liver were seen as early as 4 days postinfection (PI). By day 7 PI, a marked reduction in abdominal fat and hepatosplenomegaly was evident. Hepatocytes underwent fatty degeneration (seen by day 7 PI) before total necrosis set in. On day 8 PI, trichomonads could be found among the necrotic hepatocytes in caseous lesions. These lesions were delineated by a wall of leukocytes and occasional giant cells. Nonimmune pigeons died within 14 to 17 days PI of liver dysfunction. Other organs (kidney and genitalia) were also seen to undergo degeneration. These manifestations probably reflect the progression of liver dysfunction.

Adipose Tissue↗
PubMed1995

Serum glutathione S-transferase B1 activity as an index of liver function in cystic fibrosis.

AIMS: To evaluate serum glutathione S-transferase B1 (GST B1), a highly sensitive test of hepatocellular function, as a means of identifying liver disease in patients with cystic fibrosis (CF). METHODS: The presence of liver disease was sought over a three year period in 60 children with CF, using a combination of clinical assessment, ultrasound examination, conventional biochemical tests of liver function (LFTs), and measurement of GST B1. RESULTS: Reference ranges for serum GST B1 were established in a paediatric control population. The 95% value (4.55 micrograms/l) was similar to the upper limit of normal previously derived in adults. Mean (SE) serum GST B1 activities were higher in the CF population (9.0 (1.14) micrograms/l) than in age matched controls (2.4 (0.15) micrograms/l). Ten patients with CF showed clinical signs of liver dysfunction. All but one had a serum GST B1 > 4.55 micrograms/l. Twelve other patients had elevated LFTs without clinically evident liver dysfunction, six had abnormal ultrasound scans and two showed both of these anomalies. Thirty patients with CF had neither biochemical, ultrasonographic nor clinical signs of liver disease. On review three years later, clinically important liver disease was reaffirmed in eight of the 10 index cases and had become apparent in a further eight, all of whom had elevated GST B1 activities. Five (36%) of the patients with elevated LFTs and two (33%) with isolated ultrasound changes continued to show these abnormalities. CONCLUSIONS: The limitations of conventional LFTs and ultrasound scans were evident from this study. The results suggest that elevated GST B1 activities may be a better predictor of hepatic dysfunction in CF than conventional LFTs.

Adolescent↗
PubMed2001

Staphylococcal enterotoxin B potentiates LPS-induced hepatic dysfunction in chronically catheterized rats.

Most models of liver dysfunction in sepsis use endotoxin (lipopolysaccharide; LPS) to induce a pathophysiological response. In our study published in this issue (Beno DWA, Uhing MR, Goto M, Chen Y, Jiyamapa-Serna VA, and Kimura RE. Am J Physiol Gastrointest Liver Physiol 280: G858-G865, 2001), the adverse effect of LPS on hepatic function in vivo was only significant at relatively high LPS doses despite high tumor necrosis factor-alpha concentrations. However, many patients with sepsis are exposed to multiple bacterial toxins that may augment the immune response, resulting in increased hepatic dysfunction. We have developed a model of polymicrobial sepsis by parentally administering a combination of staphylococcal enterotoxin B (SEB) and LPS. Using this model, we demonstrate that SEB (50 microg/kg) potentiates the effect of LPS-induced hepatic dysfunction as measured by decreased rates of biliary indocyanine green clearance and bile flow. These increases were most pronounced with doses of 10 and 100 microg/kg LPS, doses that by themselves do not induce hepatic dysfunction. This may explain the seemingly increased incidence and severity of liver dysfunction in sepsis, and it suggests that the exclusive use of LPS for replicating septic shock may not be relevant for studies of hepatic dysfunction.

Animals↗
PubMed2003

A new dimension of 1H-NMR spectroscopy in assessment of liver graft dysfunction.

High-resolution 1H-NMR spectroscopy of serum and urine samples of an 11-year-old male living related orthotopic liver transplant recipient is reported. Serum glutamine increased to abnormal levels along with simultaneous abnormal excretion of urinary glutamine post-transplantation. High levels of glutamine in both blood and urine and concomitant reduced urea levels in urine were found to be evidence of impairment in urea cycle and compatible with persistently abnormal graft function. Thus glutamine levels in serum and urine, and urea in the urine as observed by 1H-NMR spectroscopy highlight their important roles in monitoring liver graft function; increased glutamine levels lead to brain damage, if untreated.

Adult↗
PubMed2003

Mechanism of primary Cd2+-induced rat liver mitochondria dysfunction: discrete modes of Cd2+ action on calcium and thiol-dependent domains.

We attempted to discern discrete sites of Cd2+ deleterious action on rat liver mitochondrial function. In particular, EGTA, ADP, and cyclosporin A (potent mitochondrial permeability transition antagonists) affected mainly Cd2+-induced changes in resting state respiration, eliminating its stimulation in KCl medium, while dithiothreitol (DTT, a dithiol reductant) produced its effect both on Cd2+ activation of the basal respiration and Cd2+ depression of uncoupler-stimulated respiration, evoking its restoration. Substantial differences in DTT influence on mitochondrial respiration at low and high [Cd2+] were revealed, namely, an enhanced mitochondrial permeabilization in the presence of saturated [DTT] at high [Cd2+] took place. Besides, DTT only partially reversed Cd2+-induced swelling in NH4NO3 medium when glutamate plus malate or succinate without rotenone was used. Contrarily, DTT produced complete reversal of the swelling of succinate-energized mitochondria when rotenone was present in the medium. In addition, in the presence of rotenone both Cd2+-produced activation of the resting state respiration in KCl medium and Cd2+-induced swelling in sucrose medium of succinate-energized mitochondria were more sensitive to cyclosporin A than the same Cd2+ effects obtained on mitochondria oxidizing succinate (without rotenone) or glutamate plus malate. We have concluded that Cd2+, producing primary mitochondrial dysfunction, acts both as a thiol and Me2+ binding site reagent. Suppositions about possible localization of separate sites of direct Cd2+ effects on mitochondrial function were made.

Adenosine Diphosphate↗
PubMed2005

Excessive portal flow causes graft failure in extremely small-for-size liver transplantation in pigs.

AIM: To evaluate the effects of a portocaval shunt on the decrease of excessive portal flow for the prevention of sinusoidal microcirculatory injury in extremely small-for-size liver transplantation in pigs. METHODS: The right lateral lobe of pigs, i.e. the 25% of the liver, was transplanted orthotopically. The pigs were divided into two groups: graft without portocaval shunt (n = 11) and graft with portocaval shunt (n = 11). Survival rate, portal flow, hepatic arterial flow, and histological findings were investigated. RESULTS: In the group without portocaval shunt, all pigs except one died of liver dysfunction within 24 h after transplantation. In the group with portocaval shunt, eight pigs survived for more than 4 d. The portal flow volumes before and after transplantation in the group without portocaval shunt were 118.2+/-26.9 mL/min/100 g liver tissue and 270.5+/-72.9 mL/min/100 g liver tissue, respectively. On the other hand, in the group with portocaval shunt, those volumes were 124.2+/-27.8 mL/min/100 g liver tissue and 42.7+/-32.3 mL/min/100 g liver tissue, respectively (P<0.01). As for histological findings in the group without portocaval shunt, destruction of the sinusoidal lining and bleeding in the peri-portal areas were observed after reperfusion, but these findings were not recognized in the group with portocaval shunt. CONCLUSION: These results suggest that excessive portal flow is attributed to post transplant liver dysfunction after extreme small-for-size liver transplantation caused by sinusoidal microcirculatory injury.

Animals↗
PubMed2002

Neonatal cholestatic hepatitis from carbamazepine exposure during pregnancy and breast feeding.

OBJECTIVE: To report a case of transient cholestatic hepatitis occurring in an infant between the third and seventh weeks of life, most likely due to carbamazepine exposure during pregnancy and breast feeding. CASE SUMMARY: A boy, born to an epileptic mother who had been treated with carbamazepine monotherapy throughout pregnancy and breast feeding, experienced asphyxia at birth with transient hepatic dysfunction in the first week of life. After full recovery from asphyxia, he experienced a second period of liver dysfunction, presenting as cholestatic hepatitis that lasted approximately 5 weeks. Infectious and metabolic etiologies as well as extrahepatic biliary atresia were excluded. DISCUSSION: Carbamazepine is known to induce hepatic damage in children and adults. As the drug crosses the placenta and is excreted into breast milk, infants of mothers taking carbamazepine might also develop liver dysfunction. In addition to the present case, there are 2 well-documented case reports of cholestasis in association with transplacental and transmammary carbamazepine exposure. CONCLUSIONS: Carbamazepine-induced hepatitis may occur in association with prenatal exposure and breast feeding. This may expose infants to unnecessary diagnostic procedures, and should therefore be mentioned in the company's product information.

Breast Feeding↗
PubMed2002

Application of preoperative portal vein embolization before major hepatic resection in patients with normal or abnormal liver parenchyma.

BACKGROUND: Clinical parameters influencing the effect of preoperative portal vein embolization (PVE) in hypertrophying the nonembolized lobe of patients with either normal or abnormal liver parenchyma and its effect upon portal pressure were examined to identify the patient population for whom this approach is most suited. METHODS: The study population included 43 patients undergoing major hepatectomy after PVE. Patients were divided into 2 groups according to their liver parenchyma: 17 patients with normal liver parenchyma (N group) and 26 patients with damaged liver parenchyma due to viral hepatitis (D group). We calculated the correlation between volumetric increases in the nonembolized (left) lobe after PVE (hypertrophic ratio = post-PVE left lobe volume/pre-PVE left lobe volume) using computed tomography volumetry before and 2 weeks after PVE. Clinical parameters also were examined to identify those parameters modifying the hypertrophic ratio in each group, and changes in portal pressure by PVE and the subsequent hepatectomy were recorded. Finally, by comparing patients with or without postoperative liver failure after hepatectomy, the influence of the hypertrophic ratio and portal pressure on the outcome of subsequent hepatectomy was examined. RESULTS: The hypertrophic ratio was 1.34 +/- 0.23 in the N group, and 1.25 +/- 0.21 in the D group. This difference was not significant. Multiple regression analysis revealed that the parenchymal volumetric rate of the right lobe (PVR) in the D group and both PVR and prothrombin time in the N group were independent parameters predicting the hypertrophic ratio. The portal pressure increased immediately after PVE and was similar in both groups to levels after hepatectomy. Six patients in the D group experienced postoperative liver dysfunction. In 5 of these 6 patients, the hypertrophic ratio was below 1.2, and the portal pressure was higher than that in patients without liver dysfunction. CONCLUSIONS: PVE induces hypertrophy of the nonembolized lobe of both abnormal and normal liver parenchyma, and the effect was predictable. Postoperative liver failure appeared to be more severe in patients having a lower hypertrophic ratio and higher portal pressure in abnormal liver parenchyma, however. PVE also may have diagnostic use in predicting portal pressure after hepatectomy, which may be associated with surgical outcome.

Adult↗
PubMed1994

[Changes in plasma concentrations of human hepatocyte growth factor before and after major intra-abdominal surgery under nitrous oxide-sevoflurane anesthesia].

The measurements of human hepatocyte growth factor (hHGF) in plasma and liver function tests were performed in 23 patients before and after major intra-abdominal surgery under nitrous oxide-sevoflurane anesthesia. Plasma concentrations of hHGF in 12 patients with normal liver function (Group 1) and in 11 patients with liver dysfunction (Group 2) were 0.34 +/- 0.07 and 0.44 +/- 0.12 ng.ml-1 (mean +/- SD) before the surgery, respectively. After the surgery, plasma concentration of hHGF remained unchanged in Group 1, but significantly increased to 0.61 +/- 0.32 ng.ml-1 in Group 2. Other routine laboratory data reflecting hepatic functions remained unchanged in both groups. These results suggest that liver damage during surgery and anesthesia occurs more likely in patients with liver dysfunction than in patients with normal liver function, and hHGF can be a more sensitive indicator of hepatic damage than conventional liver function tests.

Abdomen↗