Conversion to Sandimmun Neoral in stable renal transplant recipients over 1 year: hepatitis, liver dysfunction, dosing intervals, and therapeutic ranges.
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Administration, Oral↗
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Measurement of serum bile alcohol levels in liver dysfunction, using isotope dilution-mass spectrometry.
We determined the concentration of two major serum bile alcohols, 27-nor-5 beta-cholestane-3 alpha,7 alpha,12 alpha,24,25-pentol and 5 beta-cholestane-3 alpha,7 alpha,12 alpha,25,26-pentol, in healthy controls and patients with acute hepatitis, chronic hepatitis, and cirrhosis, using isotope dilution-mass spectrometry. In healthy controls the mean total amount of the two major bile alcohols was 9.6 +/- 3.4 ng/ml (mean +/- SD). In patients with liver diseases the mean values were as follows: acute hepatitis, 44.8 +/- 18.2 ng/ml; chronic hepatitis, 18.2 +/- 5.6 ng/ml; Child grade A cirrhosis, 37.9 +/- 26.0 ng/ml; Child grade B, 42.7 +/- 22.0 ng/ml; and Child grade C, 71.2 +/- 24.2 ng/ml. The mean ratio of 5 beta-cholestane-3 alpha,7 alpha,12 alpha,25,26-pentol to 27-nor-5 beta-cholestane-3 alpha,7 alpha,12 alpha,24,25-pentol in patients with Child grade C cirrhosis was significantly higher than that in healthy controls (1.42 +/- 0.92 versus 0.61 +/- 0.11; p less than 0.05).
Adult↗
Escherichia coli-induced lung and liver dysfunction in dogs: effects of flunixin meglumine treatment.
Twelve dogs were infused with 10(10) Escherichia coli/kg of body weight through a portal vein catheter over a 1-hour period; 6 dogs were treated with flunixin meglumine (1 mg/kg) 15 minutes after the infusion had begun. Six dogs (controls) were infused with a comparable volume of sterile saline solution over the same period. Over a 4-hour monitoring period, nontreated septicemic dogs developed systemic hypotension, decreased cardiac output, increased portal pressure, increased serum alanine transaminase values, increased extravascular liver water, increased liver glycogen depletion, and decreased arterial oxygen tension compared with control dogs. Accumulations of polymorphonuclear leukocytes and E coli were found in the livers and lungs of septicemic dogs. Flunixin meglumine treatment prevented systemic hypotension and hypoxemia, reversed the early but not the late stages of portal hypertension, and decreased E coli concentrations in the lungs. Other effects of treatment were not noticed.
Animals↗
Liver disease in patients with liver dysfunction prior to bone marrow transplantation.
Twenty-two patients with previous hepatic compromise who underwent allogeneic bone marrow transplant (BMT) for treatment of hematologic malignancy or other hematologic disease between 1984 and 1990 were chosen for the present study. After transplant, 19 (86.4%) of the patients developed hepatitis, including six cases (27.3%) of acute hepatitis, 12 (54.6%) of chronic hepatitis and one uncharacterized hepatitis. Nine chronic hepatitis patients were followed-up for 7-56.5 months (medium 35.5 months) with biochemistry studies and ultrasonography. Throughout the observation period, liver cirrhosis or hepatoma were not detected and no patients developed veno-occlusive disease. Furthermore patients who developed hepatitis after transplant had worse prognoses. Based on serial serological survey of the various hepatitis B virus (HBV) antigens and antibodies, we have found that most of the recurrent viral hepatitis in transplant patients could be attributed to the reactivation of the virus. In addition, the use of immunosuppressive drugs, persisting infection by HCV and the development of graft-versus-host disease may also play a role in modulating the course of viral hepatitis in BMT patients.
Adolescent↗
Liver dysfunction and parenteral nutritional therapies.
Hepatobiliary dysfunction associated with the use of total parenteral nutrition is a commonly recognized phenomenon occurring in up to 90% of patients on long-term therapy. Reasons for these abnormalities, both supported by research as well as theoretical possibilities are explored. Practical guidelines considered useful in documenting, preventing and treating serious hepatic consequences of total parenteral nutrition are discussed. The role of combined liver and small bowel transplantation as treatment for select patients is also reviewed.
Alanine Transaminase↗
How does liver dysfunction influence serum CA 19-9 in pancreatic cancer?
Serum CA 19-9 was determined in 83 control subjects, 99 patients with pancreatic cancer, 104 with chronic pancreatitis and 137 with extra-pancreatic diseases mainly of gastrointestinal origin in order to evaluate whether hepatic factors can influence circulating CA 19-9 in pancreatic cancer. Sensitivity, specificity and accuracy of this test in determining pancreatic malignancy were: 74%, 83% and 57%. We divided patients into two groups: group A (159 cases) and group B (181 cases) with and without anatomical liver damage (presence of primary or metastatic cancer, cirrhosis, hepatitis, steatofibrosis, cholangitis). Group A presented higher CA 19-9 values as compared to group B. Significant correlations were found in group B but not in group A between CA 19-9 and ALT, ALP and total bilirubin. Multiple regression analysis (CA 19-9 dependent and ALT, ALP and total bilirubin predictor variables) was significant only in group B. The standardized partial regression coefficients found to be significant were those of ALP and total bilirubin. We can conclude that CA 19-9 is an index of pancreatic cancer with satisfactory sensitivity and specificity. The presence of anatomical liver damage seems to increase the value of this index, probably releasing CA 19-9 into the bloodstream. Extra-hepatic cholestasis may also be an important factor in elevating CA 19-9 probably by reducing the hepatic catabolism of this glycoprotein.
Adult↗
S-adenosyl-L-methionine. A review of its pharmacological properties and therapeutic potential in liver dysfunction and affective disorders in relation to its physiological role in cell metabolism.
S-Adenosyl-L-methionine (SAMe) is a naturally occurring molecule distributed to virtually all body tissues and fluids. It is of fundamental importance in a number of biochemical reactions involving enzymatic transmethylation, contributing to the synthesis, activation and/or metabolism of such compounds as hormones, neurotransmitters, nucleic acids, proteins, phospholipids and certain drugs. The administration of a stable salt of SAMe, either orally or parenterally, has been shown to restore normal hepatic function in the presence of various chronic liver diseases (including alcoholic and non-alcoholic cirrhosis, oestrogen-induced and other forms of cholestasis), to prevent or reverse hepatotoxicity due to several drugs and chemicals such as alcohol, paracetamol (acetaminophen), steroids and lead, and to have antidepressant properties. In all of these studies SAMe has been very well tolerated, a finding of great potential benefit given the well-known adverse effects of tricyclic antidepressants with which it has been compared in a few trials. Thus, with its novel mechanisms of action and good tolerability, SAMe is an interesting new therapeutic agent in several diverse disease conditions, but its relative value remains to be determined in appropriate comparisons with other treatment modalities in current use.
Animals↗
Erythrocytes with T-state-stabilized hemoglobin as a therapeutic tool for postischemic liver dysfunction.
This study aimed to examine if T-state stabilization of hemoglobin in erythrocytes could protect against postischemic organ injury. Human erythrocytes containing three different states of Hb allostery were prepared: control Hb (hRBC), CO-Hb that is stabilized under R-state with the 6-coordinated prosthetic heme (CO-hRBC), and alpha-NO-deoxyHb stabilized under T-state (alpha-NO-hRBC). To prepare alpha-NO-RBC, deoxygenated RBC was treated with FK409, a thiol-free NO donor, at its half molar concentration to that of Hb; this procedure resulted in the 5-coordinated NO binding on the alpha-subunit heme, as judged by electron spin resonance spectrometry. Rats were subject to 20 min systemic hemorrhage to maintain mean arterial pressure at 40 mm Hg, and reperfused with one of hRBCs. This protocol for ischemia, followed by 60 min reperfusion with physiological saline, caused modest metabolic acidosis and cholestasis. Administration of hRBC or COhRBC significantly attenuated cholestasis and improved acidosis. Rats treated with alpha-NO-hRBC exhibited greater recovery of metabolic acidosis and bile excretion than those treated with hRBC or CO-hRBC, displaying the best outcome of local oxygen utilization in hepatic lobules. Half-life time of alpha-NO-RBC administered in vivo was approximately 60 min. These results suggest that T-state Hb stabilization by NO serves as a stratagem to treat postischemic organ dysfunction.
Acidosis↗
The impact of liver dysfunction on outcome in patients with multiple injuries.
Multiple organ dysfunction syndrome (MODS) is the leading cause of late deaths after traumatic injury. The relative importance of dysfunction of individual organ systems in determining outcome from MODS has not been clearly defined. Some studies have suggested that hepatic dysfunction associated with MODS increases mortality, whereas others have suggested that it contributes little to outcome in trauma patients. To clarify the role of the hepatic dysfunction after traumatic injury we retrospectively reviewed all trauma patients with an Injury Severity Score > or = 14 admitted from January 1, 1994 through June 30, 1997 for the presence of hepatic dysfunction defined as a serum bilirubin > or = 2.0 mg/dL. Of the 1962 patients who met the entry criteria 154 developed hepatic dysfunction during their hospital stay. Patients with hepatic dysfunction were older (46 +/- 2 versus 41 +/- 1 years), were more severely injured (Injury Severity Score 31.5 +/- 0.9 versus 23.3 + 0.2), and had a lower prehospital blood pressure (102 +/- 3 versus 117 +/- 1 mm Hg) compared with patients who did not develop hepatic dysfunction. Patients with hepatic dysfunction were more likely to present with shock as reflected in a lower initial emergency room blood pressure (109 +/- 3 versus 128 +/- 1 mm Hg) and base deficit (-6.9 +/- 0.6 versus -3.5 +/- 0.1 mEq/L). Patients who developed hyperbilirubinemia had longer lengths of stay in the intensive care unit (15.8 +/- 1.2 versus 3.4 +/- 0.2 days) and the hospital (27.4 +/- 1.7 versus 11.1 +/- 0.2 days) and a higher in-hospital mortality (16.2% versus 2.5%). These data demonstrate that the development of hepatic dysfunction reflects the severity of injury and is associated with a significantly worse outcome after traumatic injury.
Adult↗
Acute hyperphosphatemia caused by sodium phosphate enema in a patient with liver dysfunction and chronic renal failure.
We report a case of acute hyperphosphatemia secondary to rectal administration of sodium phosphate and sodium biphosphate (Fleet enema). Parathyroid hormone and calcitonin levels were measured along with phosphate clearance and the tubular reabsorption of phosphate.
Acute Disease↗
Hepatic venous hemoglobin oxygen saturation predicts liver dysfunction after hepatectomy.
A fiberoptic flow-directed catheter inserted into the hepatic vein continuously measures hepatic venous oxygen hemoglobin saturation (ShvO2). This study determined whether intraoperatively measured ShvO2 could predict postoperative serum activities of aminotransferases and patient outcome in 83 patients undergoing hepatectomy. The duration of intraoperative ShvO2 less than or equal to 10, 20, 30, 40, and 50% was calculated in each case. Significant increases in postoperative serum aminotransferases were associated with more than 1, 11, 31, 51, and 181 min of duration of ShvO2 less than or equal to 10, 20, 30, 40, and 50%, respectively. The incidence of postoperative liver failure significantly increased when the duration of ShvO2 less than or equal to 20, 30, and 40% exceeded 11, 31, and 51 min, respectively. The mortality from liver failure was significantly higher when the duration of ShvO2 less than or equal to 30 and 40% exceeded 31 and 51 min, respectively. Therefore, intraoperative monitoring of ShvO2 may predict not only the increase in postoperative serum aminotransferases but also patient outcome in terms of postoperative liver failure after hepatectomy.
Adult↗
A syndrome of lipoatrophy, lactic acidaemia and liver dysfunction associated with HIV nucleoside analogue therapy: contribution to protease inhibitor-related lipodystrophy syndrome.
BACKGROUND: Lipodystrophy (LD; peripheral lipoatrophy, central adiposity) hyperlipidaemia and insulin resistance often complicate protease inhibitor-containing antiretroviral therapy. Lipoatrophy and abdominal distension were observed in protease inhibitor-naive nucleoside analogue reverse transcriptase inhibitor (NRTI) recipients with lactic acidaemia and hepatic impairment, which are known NRTI-induced mitochondrial toxicities. DESIGN AND SETTING: Case-control study in a university-based outpatient clinic. PATIENTS AND METHODS: The patients studied included 14 NRTI recipients with lipoatrophy, 32 antiretroviral-naive patients without LD, 28 NRTI recipients without LD, 44 combined NRTI-protease inhibitor recipients without LD, and 102 NRTI-protease inhibitor recipients with LD. Data was obtained on body composition (questionnaire, physical examination, dual-energy x-ray absorptiometry and abdominal computerized tomography), with biochemical, lipid and glycaemic parameters. RESULTS: The NRTI-LD syndrome was characterized by recent onset fatigue and nausea, peripheral lipoatrophy (6 kg loss over 4 months), abdominal distension (ascites +/- hepatomegaly) and elevated lactate (4.6, 1.1, 1.2, 1.4 and 1.7 mmol/l, respectively; P< 0.0001) and liver enzymes. Cases without hepatic involvement also had lower body fat and greater lactate than unaffected controls. Metabolic disturbances and weight improved after cessation. The NRTI-LD syndrome differed from protease inhibitor-related LD syndrome by the presence of recent onset symptoms and weight loss, higher lactate and alanine aminotransferase, and lower albumin, cholesterol, triglycerides, glucose and insulin. In treated controls, current stavudine therapy, protease inhibitor duration, and lactic acidaemia were independently associated with both lipoatrophy and abdominal obesity; total NRTI duration was also associated with lipoatrophy, and lamivudine and protease inhibitor duration with buffalo hump. CONCLUSIONS: A syndrome of lipoatrophy, constitutional illness, lactic acidaemia and hepatic dysfunction can complicate NRTI therapy. Both protease inhibitor and NRTI therapies, particularly if associated with lactic acidaemia, contribute to LD syndrome, but have some distinguishable clinical and metabolic effects.
Acidosis, Lactic↗
Acute megakaryoblastic leukemia with t(17;22)(q21;q13) and liver dysfunction.
The t(1;22)(p13;q13) is associated with acute megakaryoblastic leukemia (AMKL) seen mostly in young infants and known to have a poor prognosis. A 5-year-old child had prolonged prothrombin and partial thromboplastin times, low albumin, and decreased vitamin K-dependent coagulation factors and factor V activities at the time of AMKL diagnosis. All of these factors normalized following chemotherapy when remission was achieved. Cytogenetic analysis revealed a female karyotype with a balanced t(17;22)(q21;q13). Here, we present an AMKL pediatric case with a novel translocation and significant hepatocellular dysfunction that resolved with chemotherapy. The t(17;22) (q21;q13) may represent a variant of t(1;22)(p13;q13).
Antineoplastic Combined Chemotherapy Protocols↗
Liver dysfunction in patients bitten by Crotalus Durissus terrificus (Laurenti, 1768) snakes in Botucatu (State of São Paulo, Brazil).
Thirty-two patients bitten by venomous snakes sixteen by Bothrops spp. and sixteen by Crotalus durissus terrificus were studied. The group comprised thirty males and two females, aged eight to sixty-three years (mean 33 +/- 15). Bromsulphalein tests were increased in the majority of patients bitten by Crotalus durissus terrificus. The correlation coefficient of Spearman was positive between bromsulphalein tests and alanine aminotransferase levels, and between alanine aminotransferase and aspartate aminotransferase levels only in the Crotalus group. The only patient who died was bitten by Crotalus durissus terrificus and showed hydropic degeneration and mitochondrial injury in the liver. It was concluded that the hepatic damage might have been caused by at least two possible mechanisms: venom effect on liver mitochondria and cytokine effects on hepatocyte, specially interleukin-6.
Adolescent↗
Liver dysfunction rather than intravascular coagulation as the main cause of low protein C and antithrombin III in acute leukemia.
Protein C, a newly identified inhibitor of blood coagulation, was measured immunologically in 58 patients with untreated acute leukemias and compared with that of normal subjects. On the average, slightly lower values were found. However, the 17 patients with overt laboratory pictures of decompensated disseminated intravascular coagulation (DIC), including 11 cases with acute promyelocytic leukemia, had protein C concentrations no lower than those of the remaining 41 patients without DIC. Antithrombin III activity and antigen were normal and, like protein C, not lowered in DIC. The concentrations of both proteins were closely correlated with changes in the indexes for liver synthetic function. A subgroup of 13 patients with hyperleukocytic leukemias had lower protein C and antithrombin III, in line with the more compromised synthetic function of their livers. Our findings indicate that liver impairment rather than DIC is the main cause of the changes in the two naturally occurring inhibitors of blood coagulation.
Adult↗
[An autopsy case of intravascular malignant lymphomatosis with hemophagocytic syndrome, mental confusion and liver dysfunction].
A 66-year-old Japanese man was admitted to Hitachi General Hospital because of fatigue, fever, edema, and icterus. A blood examination showed anemia, leukocytosis, and hyperbilirubinemia. Antibiotics did not alleviate the inflammatory symptoms. On the 13th hospital day, the patient demonstrated mental confusion, with progressive anemia and thrombocytopenia. Bone marrow aspiration revealed an increase of macrophages showing erythrophagocytosis. A diagnosis of hemophagocytic syndrome was made, but no viral infection or hematological malignancy could be detected. The patient was treated with gamma-globulin and methylprednisolone for hemophagocytic syndrome, but died of respiratory insufficiency with progressive hyperbilirubinemia and trombocytopenia on the 29th hospital day, A postmortem examination showed proliferation of lymphoma cells within the small blood vessels of the brain, lungs, liver, and many other organs, but the bone marrow was not involved. An immunohistochemical examination resulted in a diagnosis of intravascular malignant lymphomatosis (IML) of B cell origin. No viral infection was detected with in situ hybridization methods. Although IML occasionally accompanies thrombocytopenia, infiltration of lymphoma cells in the bone marrow is rare. Lymphoma associated hemophagocytic syndrome may cause cytopenia in some patients with IML, as indicated in this case.
Aged↗
Decreased serum selenium in alcoholics--a consequence of liver dysfunction.
The serum concentration of selenium was decreased by 17 and 48% in non-cirrhotic and cirrhotic alcoholics, respectively, as compared to healthy controls. In these alcoholics the serum selenium correlated positively with the serum albumin and plasma prothrombin time and inversely with the serum bilirubin, alkaline phosphatase and gamma-glutamyl transpeptidase. Abstinence from ethanol for two weeks was without effect on the serum selenium level in non-cirrhotic alcoholics and acute alcohol intake did not change the serum selenium concentration in non-alcoholic volunteers. In patients with primary biliary cirrhosis the serum concentration of selenium was similar to that in the alcoholic cirrhotics. In patients with hypoalbuminaemia of renal origin the serum selenium was normal. In conclusion our results show that the deterioration of liver function, irrespective of its aetiology, leads to the decrease in serum selenium levels. Whether a defect in removal of lipoperoxides is associated with this decrease in serum selenium concentration remains to be decided by further studies.
Adult↗
Prolonged fasting in humans results in diminished plasma choline concentrations but does not cause liver dysfunction.
Choline is a major donor of methyl groups, a precursor for membrane synthesis, and a component of the neurotransmitter acetylcholine. Choline-deficient diets deplete humans of choline and cause hepatic dysfunction and steatosis. In this study we determined whether acute starvation also depletes choline, as indicated by changes in plasma choline or phosphatidylcholine. Healthy humans (n = 10) fasted for 7 d, ingesting only water and mineral-vitamin supplements. Their mean (+/- SEM) plasma choline concentration was 9.5 +/- 0.5 micromol/L at the start of the study and dropped to 7.8 +/- 0.3 micromol/L after 1 wk of fasting (P < 0.01). The plasma phosphatidylcholine concentration did not change significantly (2.2 +/- 0.1 mmol/L at the start of the study and 2.4 +/- 0.2 mmol/L after 1 wk of fasting). Capacity of the liver to secrete lipoproteins was not affected by prolonged fasting. The mean plasma concentration of low-density-lipoprotein cholesterol was 3.3 +/- 0.2 mmol/L (126 +/- 8 mg/dL) at the start of the study and 4.9 +/- 0.5 mmol/L (188 +/- 19 mg/dL) after 1 wk of fasting. Liver damage assessed by serum alanine aminotransferase activity occurred in only 1 of 10 subjects. We conclude that prolonged fasting in humans modestly diminished plasma choline but was not associated with signs of choline deficiency, such as perturbed lipoprotein secretion and liver damage.
Adult↗