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Results for “Liver Dysfunction”

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At least 109 records · Page 6Linked to original sources

PubMed1983

Disopyramide-associated liver dysfunction.

A case of disopyramide-associated cholestatic jaundice is presented, and all reported cases of disopyramide-associated liver dysfunction are reviewed. Manifestations of liver dysfunction usually appear during the first week of treatment. Discontinuing administration of the drug often results in prompt clinical resolution, although in rare instances, laboratory abnormalities persist up to 18 months. Physicians should be aware of this rare but serious complication of disopyramide therapy.

Adult↗

PubMed1977

Acute encephalopathy with liver dysfunction, chylous ascites and cytomegalovirus infection.

A child with acute encephalopathy and liver dysfunction subsequently developed acute chylous ascites. Titers for cytomegalovirus increased from less than 1:2 to 1:32 during the illness, and cytomegalovirus was isolated from the urine. The case is the first one possibly linking cytomegalovirus and acute encephalopathy and liver dysfunction in a child. In our patient, enlargement of the abdominal lymph nodes, as seen on a lymphangiogram, resulted in a severe obstruction of abdominal lymphatic flow, producing a transudation of lymph into the peritoneal cavity. The acute chylous ascites associated with mesenteric lymphadenitis was likely caused by the cytomegalovirus infection.

Brain Diseases↗

PubMed2000

Altered pharmacokinetics and metabolism of CPT-11 in liver dysfunction: a need for guidelines.

Metabolic conversion of CPT-11 is a major route of elimination of this new topoisomerase 1 inhibitor. Presently, recommendations for dose adjustments of CPT-11 in patients with liver dysfunction are lacking. We describe the case of a patient with metastatic colon cancer with liver dysfunction treated with CPT-11 at two different dose levels (100 mg/m2 and 30 mg/m2, single dose, administered as a 90-min i.v. infusion). The lactones and carboxylates of CPT-11 and SN-38 were determined by high-performance liquid chromatography. SN-38 glucuronide was determined after deglucuronidation. The procedures allowed intrapatient comparison of pharmacokinetics and metabolism of the drug. Severe side effects were encountered, which could be explained by the reduced clearance of CPT-11 and its metabolites. These included neutropenic fever with culture-proven septicemia, thrombocytopenia, somnolence, diarrhea, and signs and symptoms of transient hepatic failure. Our findings offer important data for the further development of guidelines for dose reduction of CPT-11 in patients with liver dysfunction.

Antineoplastic Agents, Phytogenic↗

PubMed1999

Pretreatment with soluble thrombomodulin prevents intrasinusoidal coagulation and liver dysfunction following extensive hepatectomy in cirrhotic rats.

The major cause of posthepatectomy liver dysfunction is supposed to be microcirculatory disturbance caused by imbalance of intrasinusoidal coagulation equilibrium. Thrombomodulin (TM) is a potent anticoagulant expressed on the endothelial cell surface that regulates the coagulation system by binding thrombin and accelerating the thrombin-catalyzed activation of protein C. Therefore, we examined the effect of soluble TM purified from human urine (UTM) on intrasinusoidal coagulation in cirrhotic rats. Dimethylnitrosamine-induced cirrhotic rats underwent 70% hepatectomy and received endotoxin 48 h after. UTM or vehicle alone was intravenously administered to each rat 30 min before endotoxin injection. UTM treatment attenuated the increases in cytosolic enzymes and serum hyaluronic acid level. The UTM supply improved the survival rate of the rats at 12 h after endotoxin challenge. Histologically, intrasinusoidal fibrin depositions and massive hepatocellular necrosis observed in control rats were scarcely found in UTM-treated rats. Immunohistochemical examination revealed that marked TM stains in sinusoidal endothelial cells were well preserved in UTM-treated rats. In conclusion, UTM administration prevented intrasinusoidal fibrin depositions and attenuated posthepatectomy liver dysfunction in cirrhotic rats.

Animals↗

PubMed1992

Liver dysfunction and acute cardiocirculatory failure in children.

We report 15 children who developed transient liver dysfunction related to hepatic ischaemia. All patients had cardiocirculatory failure 24 h before the onset of liver injury (day 1). Peak serum values of transaminases occurred between day 1 and day 3: SGOT (mean: 759 IU/l, range: 150-4400); SGPT (418 IU/l, 95-2547). Transaminase values decreased rapidly and normalised from day 6 to day 10. Minimum values of prothrombin test (PT) occurred on day 1 (31%, 10-70) and 13/15 patients had a PT less than 50% (27%, 10-44). PT values normalized from day 3 to day 10. Hypoglycaemia was present in 8/15 patients on day 1. Liver dysfunction improved after correction of the circulatory failure. These results confirm that transient hepatic dysfunction, probably as a consequence of hepatic hypoperfusion, may occur frequently in children after acute circulatory failure. We conclude that the diagnosis of ischaemic liver injury or shock liver syndrome in children can be made on clinical and biochemical criteria, and that liver biopsy is unnecessary.

Acute Disease↗

PubMed1992

Gut ischemia/reperfusion-induced liver dysfunction occurs despite sustained oxygen consumption.

We have previously shown that gut ischemia/reperfusion (I/R) causes liver dysfunction in vivo (increased [I125]albumin leak, decreased mitochondrial redox potential). Our purpose was to investigate liver dysfunction due to gut I/R in an ex vivo model where oxygen delivery (DO2) could be controlled. Rats underwent laparotomy (sham) or 45 min of superior mesenteric artery (SMA) occlusion (I/R) and 6 hr later the gut and liver were isolated in situ. Pressures were monitored while recirculating blood was perfused via the hepatic artery (2.5 ml/min) for 90 min and the SMA (7.5 ml/min) for the first 30 min, then the portal vein (7.5 ml/min) for 60 min. Both gut and liver DO2 and VO2 (Fick method) were maintained throughout the study period in the gut I/R as well as sham groups. Despite maintenance of liver VO2, however, gut I/R resulted in a marked and persistent reduction in bile flow. In conclusion, dysfunctional bile production after gut I/R is not due to impaired VO2, but rather gut-liver signaling yet to be defined.

Animals↗

PubMed1977

Liver dysfunction in patients with hemophilia.

The incidence of post-transfusion hepatitis and liver dysfunction is presented in fifty-four patients with classical hemophilia who received episodic and/or prophylactic Factor VIII concentrate. 42.5% had persistent biochemical evidence of liver dysfunction with elevated SGOT and SGPT; 3.8% have persistent (HBs) antigenicity and 90% have (HBsAb) antibodies. The results are the same for those who were treated episodically and received an average of 753 units Factor VIII per week as those treated prophylactically who received an average of 686 Factor VIII units per week. The incidence of clinical and/or subclinical disease is unaffected by the transfusion regimen or the amount of concentrate used. The necessity for close follow is emphasized for determination of chronic liver disease and its further therapy.

Adolescent↗

PubMed1983

Protein-energy malnutrition and liver dysfunction limit the usefulness of the relative dose response (RDR) test for predicting vitamin A deficiency.

The relative dose response (RDR) test was examined for its value in predicting vitamin A nutriture among chronically ill patients with protein-energy malnutrition and among patients with varying degrees of liver dysfunction. The RDR test was elevated (ie greater than 14 per cent) and, thus, predictive of vitamin A deficiency in only 4 out of 9 patients with combined vitamin A deficiency and protein-energy malnutrition. Among 27 patients with liver dysfunction who had vitamin A determinations performed on liver biopsy material, there was no correlation found between the RDR response and the hepatic vitamin A level. Of 12 patients with low hepatic vitamin A levels (less than 100 micrograms/g wet weight), the RDR test was normal in 9 (75 per cent). Inability of the RDR test to predict vitamin A nutriture in patients with protein-energy malnutrition and in patients with liver dysfunction may, in part, be due to inadequate synthesis or release of retinol-binding protein.

Aged↗

PubMed2004

Serum hyaluronate level for predicting subclinical liver dysfunction after hepatectomy.

The serum hyaluronate (HA) level reflects sinusoidal endothelial cell function correlated with liver function. We have reviewed multiple liver function indicators from 37 patients who underwent hepatectomy for various liver diseases. The serum HA level was well correlated with the indocyanine green retention rate at 15 minutes (ICGR15), lectin-cholesterol (LCAT), hepatocyte growth factor (HGF), liver uptake ratio of technetium-99m galactosyl human serum albumin (99mTc-GSA) at 15 minutes (HH15), prealbumin, and hepatic uptake ratio of 99mTc-GSA at 15 minutes (LHL15). In addition, the model for end-stage liver disease (MELD) score at 7 days after operation was well correlated with serum HA, ICGR15, HH15, and LHL15. In patients who showed serum an HA level of = 100 ng/ml before hepatectomy, the MELD score had significantly deteriorated by 7 days after hepatectomy. Of the 20 patients who showed a serum HA level < 100 ng/ml before hepatectomy, 11 had high serum HA after hepatectomy. The bilirubin level 7 days after operation in this group was much higher than that for patients who maintained a serum HA level < 100 ng/ml after hepatectomy. In addition, the serum HGF level before hepatectomy in this group was significantly lower. We concluded that the serum HA level is a reliable indicator when evaluating liver function and predicting liver dysfunction after hepatectomy. Furthermore, patients with a significantly low HGF level who have a normal HA level are susceptible to liver dysfunction after hepatectomy.

Aged↗

PubMed1991

Chronic liver dysfunction in heart transplant recipients, with special reference to viral B, C, and non-A, non-B, non-C hepatitis. A retrospective study in 80 patients with follow-up of 60 months.

In order to assess the prevalence, causes, and severity of chronic liver dysfunction (LD) in heart transplant patients, 80 transplanted patients followed for 60 months (median; range, 1.5-98 months) were reviewed. Sustained liver dysfunction was found in 50 patients, occurring during the first year after heart transplantation in 42 (84%) of them. Most patients were asymptomatic (80%). Causes for the liver dysfunction included non-A, non-B hepatitis in 16 cases (32%), viral B hepatitis in 13 (26%), delta hepatitis in one (2%), drug-induced hepatitis in six (12%), and cardiac failure in seven (14%). Anti-HCV antibodies were found in 56.2% of patients with non-A, non-B hepatitis and in 22% of patients with HBV hepatitis. It was found neither in patients with drug-induced hepatitis cardiac failure nor in patients with normal liver tests. This study outlines a high prevalence of LD (62.5%) in heart transplant patients, the high frequency of viral-related chronic LD (usually of moderate severity), and high incidence of HCV and HBV hepatitis.

Adolescent↗

PubMed2002

Inborn errors presenting with liver dysfunction.

In neonates, inborn errors of metabolism can produce all the major signs of liver dysfunction - jaundice, coagulopathy, hepatomegaly, splenomegaly, ascites and encephalopathy. The significance of encephalopathy in the neonate is different from that in older patients; it is usually due to a specific abnormality such as hypoglycaemia rather than being a non-specific indicator of liver failure. Attention is focused on five neonatal presentations: unconjugated hyperbilirubinaemia, cholestatic jaundice with otherwise good liver function, severe liver dysfunction (jaundice, coagulopathy persisting after vitamin K, and ascites), hepatomegaly with hypotonia+/- cardiomyopathy; and hepatosplenomegaly. The metabolic disorders presenting in these ways are listed alongside specific clinical features that can aid differential diagnosis and tests that can be used to confirm or refute the diagnosis. Diagnosis is important because treatment can be dramatically effective, e.g. withdrawal of galactose in galactosaemia. Even when treatment is not effective it is often possible to offer prenatal diagnosis for future pregnancies.

Diagnosis, Differential↗

PubMed2004

5-fluorouracil leucovorin and oxaliplatin (FOLFOX) in the treatment of metastatic colon cancer with severe liver dysfunction.

Colon cancer patients with severe hepatic dysfunction secondary to liver metastases have limited treatment options. 5-Fluorouracil (5-FU) infusional therapy has been attempted, but data suggesting significant clinical benefit are lacking. Although both 5-FU and oxaliplatin have been well tolerated as single agents in patients with severe hepatic dysfunction, the combination of these drugs in this setting has not been investigated. We report on three patients with severe liver dysfunction secondary to metastatic colon cancer treated with a combination of 5-FU, oxaliplatin, and leucovorin (FOLFOX). All three patients tolerated chemotherapy well without any significant toxicity. Liver function tests improved within 2 weeks from the start of treatment. Clinical outcomes consisted of two partial responses and one disease stabilization. Two patients progressed after 4 and 7 months from FOLFOX initiation while treatment is ongoing in the third patient. FOLFOX chemotherapy is feasible and can be associated with positive outcomes in patients with metastatic colon cancer and severe hepatic dysfunction. This regimen should be investigated further in similar clinical settings.

Adult↗

PubMed2006

Prevalence of amiodarone-related hepatotoxicity in 720 Chinese patients with or without baseline liver dysfunction.

BACKGROUND: The prevalence of hepatotoxicity after longterm oral amiodarone therapy in Chinese patients with or without elevated liver enzymes at baseline is unknown. HYPOTHESIS: Amiodarone may still be safely prescribed for Chinese patients who have baseline liver dysfunction. METHODS: This is a retrospective cross-sectional study. Significant liver dysfunction (SLD) was defined as alanine aminotransferase (ALT) > 2 times upper limit of normal range. RESULTS: Baseline liver function was checked in 628 of the 720 Chinese patients identified. The mean duration of amiodarone use was 615.9 +/- 703.1 days. Ninety patients (14.3%) had elevated baseline ALT. The prevalence of SLD was 3.7% (confidence interval [CI] 2.1-5.3%) and 4.4% (CI 0.2-8.6%) in patients with normal (n = 538) and elevated (n = 90) baseline ALT, respectively (p = 0.765). Therapy was continued in 42 patients with elevated baseline ALT until final follow-up. Eight of these (19.0%) had elevated ALT upon final follow-up, but the derangement was mild (mean ALT 134.8 +/- 145.9 IU/l, median 76 IU/l). During follow up, 24 patients developed SLD and half of these subsequently withdrew from therapy. The ALT levels at final follow-up had improved over time in both groups, but the mean difference was not significant (255.1 +/- 706.4 vs. 131.0 +/- 207.5 IU/l, p = 0.312). CONCLUSION: The prevalence of SLD in Chinese patients taking oral amiodarone with or without elevated baseline ALT was similar (4.4 vs. 3.7%). It seems that amiodarone may be safely prescribed in patients with elevated baseline ALT.

Alanine Transaminase↗

PubMed1996

Role of non-transferrin bound iron in iron overload and liver dysfunction in long term survivors of acute leukaemia and bone marrow transplantation.

AIMS: To determine whether nontransferrin bound iron is present in the serum of long term survivors of acute leukaemia and bone marrow transplantation who have liver dysfunction as indicated by consistently raised serum aspartate aminotransferase (AST) activities. METHODS: Thirty eight patients, who were at least three years from the end of treatment, were studied. Serum samples were analysed for hepatitis C, hepatitis B, AST, ferritin, and non-transferrin bound iron. A bleomycin based assay was used to detect non-transferrin bound iron. Patient and blood bank records were examined to determine the number of units of transfused blood received by each patient. RESULTS: Ten patients had consistently raised serum AST activities. Of these, two had evidence of hepatitis C infection, one had chronic hepatitis B infection and one had chronic graft versus host disease affecting the liver. None of these four patients had detectable non-transferrin bound iron. The remaining six patients had no obvious reason for raised AST activities, but four had non-transferrin bound iron detectable in their serum as compared with only two out of 28 patients with normal AST activities. Patients with abnormal AST activities had higher serum ferritin concentrations than those with normal AST, though serum ferritin was raised in 21 of 28 patients without liver dysfunction. CONCLUSION: Non-transferrin bound iron may be found in this group of patients, suggesting that iron overload is the cause of the observed liver dysfunction. Non-transferrin bound iron may also be a more specific indicator of iron overload than the serum ferritin concentrations.

Adult↗

PubMed2002

Development of liver dysfunction after delivery is possibly due to postpartum autoimmune hepatitis. A report of three cases.

Autoimmune diseases, especially autoimmune thyroid disease, frequently develop after delivery due to the immune rebound mechanism. Most cases involve transient dysfunction of affected organs. We examined three patients who developed liver dysfunction after delivery. They were all diagnosed with definite or probable autoimmune hepatitis using the scoring system of the International Autoimmune Hepatitis Group. Moreover, all of them had anti-CYP2D6 antibodies detected by a sensitive radioligand assay. Our findings strongly suggest that liver dysfunction is induced by postpartum autoimmune hepatitis, and clinicians should be aware of this disease.

Adult↗

PubMed2000

Relationships of serum pro-inflammatory cytokines and vascular endothelial growth factor with liver dysfunction in severe ovarian hyperstimulation syndrome.

The aims of this study were to determine if differences in serum pro-inflammatory cytokines, vascular endothelial growth factor (VEGF) and clinical pregnancy rate, could be observed in women with severe ovarian hyperstimulation syndrome (OHSS) in those who did and did not have liver dysfunction. Twenty-nine in-vitro fertilization patients with severe OHSS were included. The patients were divided into the normal liver function tests (LFT) group (n = 14) and the abnormal LFT group (n = 15) according to the LFT on day of admission. Periodic measurements of serum interleukin (IL)-6, IL-8, tumour necrosis factor-alpha (TNF-alpha), VEGF, oestradiol, progesterone concentrations, and LFT were performed during hospitalization. Concentrations of IL-6 in the active phase of OHSS were significantly higher in the abnormal LFT group than in the normal LFT group (19.7 +/- 15.7 versus 8.1 +/- 7.0 pg/ml, respectively). The severity of liver dysfunction was not correlated with concentrations of oestradiol, progesterone, haematocrit, white blood cell counts, or any studied cytokine. The clinical pregnancy rate was significantly lower in the abnormal LFT group (46.7%) than in the normal LFT group (85.7%). These results suggest that IL-6 cytokine system may play a role in the pathogenesis of liver dysfunction in severe OHSS. Abnormal LFT were associated with lower clinical pregnancy rates.

Adult↗

PubMed1980

Effect of improved absorption on development of jejunoileal bypass-induced liver dysfunction in rats.

Jejunoileal bypasses were performed in rats to determine the effect of improved absorption on the development of liver dysfunction occurring after this procedure. Several parameters of liver function were measured in rats 7 weeks after both the standard 85% small-bowel bypass and an 80% bypass in which an extra 5 cm of intact bowel was retained. Animals having undergone 80% bypass had a lesser degree of lowering of serum protein and triglyceride levels, hepatic cytochrome P-450 content, and hepatic glucose-6-phosphatase activity than did the animals undergoing 85% bypass. Abnormalities found in 85% bypass animals were only partially reproduced by reducing food intake in another group of 80% bypassed animals. These findings emphasize the importance of nutritional factors in the etiology of bypass-induced liver disease and militate against toxin production in the defunctionalized bowel as the sole cause of liver dysfunction following bypass.

Animals↗

PubMed2004

Argatroban dosing in intensive care patients with acute renal failure and liver dysfunction.

STUDY OBJECTIVE: To demonstrate dosing adjustment difficulties of argatroban encountered in critically ill patients with acute liver dysfunction who are receiving continuous renal replacement therapy. DESIGN: Case description. SETTING: Medical and surgical intensive care unit in a tertiary care, university-affiliated hospital. PATIENTS: Four consecutive patients with proven heparin-induced thrombocytopenia (HIT), acute renal failure requiring continuous renal replacement therapy, and various levels of transient hepatic impairment. INTERVENTION: Argatroban, a direct synthetic thrombin inhibitor, was given continuously and stabilized at 0.125-0.85 microg/kg/minute to attain an activated partial thromboplastin time (aPTT) 1.5-2.5 times the normal value for periods of 6-36 days. MEASUREMENTS AND RESULTS: Argatroban was started at the usual dosage of 2 microg/kg/minute, which resulted in significant overshooting of the aPTT and international normalized ratio (INR). No patient experienced bleeding or thrombotic complications. All patients were stabilized with reduced dosages such as those recommended for patients with chronic hepatic impairment. CONCLUSION: We recommend argatroban therapy for intensive care patients with HIT, especially those with renal failure. However, in all patients with suspected liver dysfunction due to recent elevation of liver transaminase levels and combined renal failure, a decrease in the initial dosage and careful titration of the infusion are mandatory. Further studies are needed to fully elucidate argatroban elimination and dosage adjustments for intensive care patients.

Acute Kidney Injury↗