Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three residents of New Jersey suddenly developed vomiting, abdominal pain, and watery diarrhea 12 h after ingesting five to 13 hand-picked Amanita phalloides-type mushrooms. The group was led by an amateur mycologist who had been eating hand-picked mushrooms without complications for 20 years. The patients developed mild to severe acute hepatic injury, with a peak serum aspartate aminotransferase level ranging from 133 to 826 Karmen U/L, and a peak serum alanine amino-transferase level ranging from 163 to 1176 Karmen U/L. One of the patients developed a transient severe coagulopathy, but no one developed renal failure or hepatic coma, and all rapidly improved. These three cases demonstrate that mycetismus can occur in the heavily urbanized northeastern United States, that consuming hand-picked mushrooms even under the guidance of an experienced amateur may be dangerous, and that Amanita phalloides ingestion produces a biphasic illness with early gastrointestinal symptoms and subsequent hepatic injury.
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PMID:Gastrointestinal and hepatic effects of Amanita phalloides ingestion. 147 67

T-2 toxin was given as a single intravascular dose at either 0.6 or 4.8 mg/kg to different groups of 50-kg female swine. Blood samples were taken at hourly intervals for determination of concentrations or activities of the following substances in serum or plasma: creatinine, blood urea nitrogen, inorganic phosphorus, total calcium, ultrafilterable calcium, magnesium, sodium, potassium, chloride, total protein, albumin, cholesterol, glucose, alkaline phosphatase, aspartate aminotransferase, and total bilirubin. Coagulation analyses included prothrombin time, partial thromboplastin time, activated coagulation time, and fibrin degradation products. Red blood cell, white blood cell, and platelet counts, hemoglobin concentrations, and hematocrits were determined from whole blood samples. An initial leukocytosis was followed by a leukopenia. The numbers of red cells, the hemoglobin concentration, and the hematocrit were increased. Nucleated red blood cells were seen in the blood smears. The serum concentration of bound calcium decreased, while phosphorus, magnesium, and potassium increased. Clinical screening tests detected no evidence of a coagulopathy in swine given T-2 toxin intravascularly.
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PMID:Experimental T-2 toxicosis in swine. II. Effect of intravascular T-2 toxin on serum enzymes and biochemistry, blood coagulation, and hematology. 406 62

The major causes of liver graft failure are acute rejection, technical failure, and primary nonfunction (PNF). This study was undertaken to determine whether delayed return of neuromuscular function correlates with allograft primary dysfunction in humans given vecuronium. Twenty-two adult patients undergoing orthotopic liver transplantation were given an initial dose of vecuronium, 0.1 mg/kg intravenously (i.v.). All patients recovered from vecuronium-induced neuromuscular block prior to explantation. No additional neuromuscular blocker was given until the liver graft was implanted and reperfused. Fifteen minutes after reperfusion another 0.1 mg/kg vecuronium was given IV and recovery time from attaining complete neuromuscular block to return of the fourth twitch of a train-of-four was recorded. Patients were divided into three groups according to postoperative liver function. Group I consisted of 17 patients with immediate normal liver graft function. Group II consisted of four patients with primary dysfunction (PDF) [peak aspartate aminotransferase (AST) and alanine aminotransferase (ALT) > 2000 U/L, prothrombin time > 16 s, and poor quality and quantity of bile within 3 days postoperatively] which eventually recovered normal function. Group III consisted of one patient with PNF (uncorrectable coagulopathy, severe metabolic acidosis, rising AST and ALT, and minimal or no bile output), whose graft never recovered. Recovery time in Groups II and III was prolonged compared to Group I (P < 0.05). Recovery time in Group III was prolonged compared to Group II (P < 0.05). A test based on these results using a recovery time of > 135 min as a predictor of PDF has a sensitivity and specificity of 80% and 76%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Duration of vecuronium-induced neuromuscular block as a predictor of liver allograft dysfunction. 786 19

Postoperative thrombocytopenia following hepatic cryotherapy has been well documented and shown to be significantly greater than in control patients who had an identical incision or major laparotomy. Serum aspartate transaminase (AST) levels have been used as a reliable indicator of hepatocellular destruction. This study reviews 65 consecutive hepatic cryotherapy operations. We have excluded all patients who had repeat cryotherapy to lesions (n = 6), all who had a colonic or hepatic resection procedure (n = 7), all who had tumors other than colorectal metastases (n = 5), patients with inadequate data (n = 9), and those who were asplenic (n = 2). Of the remaining 36 patients, 14 were treated with a single freeze/thaw cycle, 12 were treated with a double freeze/thaw cycle, and 10 were treated with mixed single and double freezes. The most common platelet nadir was day 3 (n = 21) followed by day 2 (n = 11), with the remaining platelet nadirs being day 1 or 4 (n = 4). The percentage fall in platelet count was found to correlate with the rise in day 1 AST level (r2 = 0.74, least squares linear regression). The double freeze/thaw cycle patients had a significantly greater fall in platelet count (p = 0.01, Mann-Whitney two sample test). Another institution has reported three deaths due to multiple problems, including coagulopathy in patients treated with double freeze/thaw cycle cryotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thrombocytopenia after hepatic cryotherapy for colorectal metastases: correlates with hepatocellular injury. 797 99

Death from ferric chloride poisoning has never been reported in Taiwan. We report a fatality from the suicidal ingestion of ferric chloride solution used as an etching agent for printed circuitry. A 25-y-old woman presented with vomiting after ingestion of 200 ml ferric chloride solution (pH 1.0). She had hypoxemia and severe metabolic acidosis with respiratory alkalosis initially. Three hours after her ingestion she presented with drowsy consciousness, tachycardia, tachypnea and protracted vomiting. Laboratory studies showed leukocytosis, elevated glucose, aspartate aminotransferase, amylase, lactate dehydrogenase, and total bilirubin, coagulation defect and hemolysis. Aspiration pneumonia and vision loss were also noted. Four hours after ingestion cardiopulmonary arrest suddenly occurred after severe vomiting and she expired. Toxicological studies showed marked elevation of serum iron (2440 micrograms/dl); the estimated oral dose of ferric chloride was equivalent to 11.52 g (230 mg/kg) of elemental iron. This patient did not receive deferoxamine due to rapid deterioration and a late diagnosis. Deferoxamine should be given in any symptomatic patient or in the presence of anion gap metabolic acidosis with a history of ferric chloride ingestion.
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PMID:A fatal case of acute ferric chloride poisoning. 946 7

Cryoshock is a syndrome of coagulopathy, renal, and pulmonary injury following cryotherapy, and its etiology is unknown. The aim of this study was to assess the impact of hepatic cryotherapy on renal function, and whether this effect is related to volume of cryotherapy, and to identify any predictors of renal impairment in patients who undergo cryotherapy. A retrospective analysis of all patients with primary or secondary hepatic malignancy treated with cryotherapy from April 1990 to October 1996 was conducted. Ten of 204 patients with renal impairment (elevation in creatinine of greater than 0.02 mmol/L for more than 2 days postprocedure) were identified. One patient has postoperative pancreatitis with late renal impairment (20 days) and was excluded. The severity of renal impairment was usually modest (mean rise in creatinine of 0.31 mmol/L; SD, 0.19). Two patients required temporary hemodialysis. Only one patient, who had significant cardiac disease, had associated pulmonary injury and shock. Demographic data in both groups were comparable, except for a trend toward more noncolorectal cancer patients in the renal impairment group (4/9 vs 33/194). Patients in the renal impairment group had a greater number of lesions than those of the nonrenal impairment group (3.4 vs 2.1, p < 0.01), as well as larger lesion diameter (2.9 vs 1.9, p < 0.01), increased freezing time (74.7 vs 44.3, p < 0.01), and a higher aspartate transaminase (AST) (2254 vs 1157, p < 0.01). This study suggests that renal impairment is more likely to be seen in patients undergoing more extensive cryotherapy. The number and diameter of lesions together with AST data link renal injury with magnitude of liver injury--all renal impairment patients had an AST > 1000, compared with only 28% of patients who did not.
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PMID:Renal impairment in hepatic cryotherapy. 965 30

Actinomycin-D (Act-D) is a rare cause of veno-occlusive disease (VOD). Between 1993 and 1998, we managed 6 patients, all male, median age 19 months (range 6-48 months) who received Act-D for Wilms' tumour (n=4), clear cell sarcoma (n=1) or rhabdomyosarcoma (n=1). VOD presented with a median platelet count of 12 x 10(9)/l, INR 3.8, fibrinogen 16 mg/l, fibrinogen degradation products (FDPs) > or =80 microg/l, aspartate aminotransferase (AST) 6922 IU/l, bilirubin 47 micromol/l. In 3 cases, transient liver dysfunction and thrombocytopenia without neutropenia had been observed after a previous course of Act-D. All six children developed encephalopathy, hepatomegaly, ascites, reversed portal flow and renal impairment. All received mechanical ventilation and two required haemofiltration. The treatment was supportive. Severe Adult Respiratory Distress Syndrome developed in 3 patients, all of whom died. 3 patients recovered. The outcome of VOD with multi-organ failure is poor. Intravascular coagulopathy precedes and characterises severe VOD during Act-D treatment.
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PMID:Veno-occlusive disease with multi-organ involvement following actinomycin-D. 1137 45

Although cryotherapy of liver tumors is generally considered a safe procedure, a syndrome of coagulopathy and fatal multiorgan failure has been observed in some patients and is called the cryoshock phenomenon. Our aim was to establish an animal model of this phenomenon and examine the effects of the basic parameters of freezing or cryotherapy on it. A group of 75 female Sprague-Dawley rats were allocated randomly to five groups: (1) sham laparotomy (n = 15); (2) small (25% liver volume) single freeze (n = 15); (3) small (25% liver volume) double freeze (n = 15); (4) large (50% liver volume) single freeze (n = 15); (5) large (50% liver volume) double freeze (n = 15). Blood samples were collected at different postoperative times, and organs were harvested for histopathology. There was a significant release of tumor necrosis factor-a (TNFa) and interleukin 6 (IL-6) following hepatic freezing, which was greatest in group 5. Postoperative serum cytokine levels were significantly associated with hepatocellular injury, as measured by postoperative serum aspartate transaminase (AST) concentrations. Severe hemoglobinuria and renal injury, as demonstrated by the serum creatinine level and the glomerular neutrophil count, were observed and were greatest in group 5. Hepatic cryosurgery is associated with release of IL-6 and TNFa and renal injury in a rat model. It is likely that the cryoshock phenomenon is another form of the systemic inflammatory response syndrome. Based on the results of this study, it is possibly mediated by cytokines released from the frozen liver tissue. We therefore caution against cryotherapy of large tumor volumes.
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PMID:Large volume hepatic freezing: association with significant release of the cytokines interleukin-6 and tumor necrosis factor a in a rat model. 1229 23

For the development of an artificial liver support system, a clinically relevant large-animal model of fulminant hepatic failure (FHF) is indispensable. Although several large-animal models have been reported so far, they have not been entirely satisfactory. Recently, we have developed a new porcine model of FHF by means of intraportal administration of 0.1 mg/kg of alpha-amanitin and 1 microg/kg of lipopolysaccharide (LPS). This model has the following superior features: 100% mortality within 5 days along with a marked elevation of aspartate transaminase (AST) levels to around 10,000 IU/l, and severe metabolic disorders such as serum lactate accumulation, hypoglycemia, coagulopathy, plasma amino acid imbalance, and hyperammonemia; an onset of hepatic encephalopathy and a significant increase in intracranial pressure immediately before death; a reversal of FHF by orthotopic liver transplantation, proving that the toxicity is liver-specific and that the graft liver is unaffected; and the capability of the damaged liver to recover and achieve both morphological and functional regeneration in 1 week if supported by an efficient auxiliary graft. Because this porcine model satisfies many of the required criteria of an optimal FHF model, it is expected to provide a useful tool for the study of FHF and the development of new therapies.
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PMID:Large-animal models of fulminant hepatic failure. 1459 18

Several reports claim that portal hypertension after living-donor liver transplantation (LDLT) adversely affects graft function, but few have assessed the impact of portal venous pressure (PVP) on graft regeneration. We divided 32 adult LDLT recipients based on mean PVP during the 1st 3 days after LDLT into a group with a PVP > or = 20 mm of Hg (H Group; n = 17), and a group with a PVP < 20 mm of Hg (L Group; n = 15). Outcome in the H Group was poorer than in the L Group (58.8 vs. 92.9% at 1 year). Peak peripheral hepatocyte growth factor (HGF) during the 1st 2 weeks was higher in the H Group (L: 1,730 pg/mL, H: 3,696 pg/mL; P < .01), whereas peak portal vascular endothelial growth factor (VEGF) level during the 1st week was higher in the L Group (L: 433 pg/mL, H: 92 pg/mL; P < .05). Graft volume (GV) / standard liver volume (SLV) was higher in the H Group (L / H, at 2, 3, and 4 weeks, and at 3 months: 1.02 / 1.24, .916 / 1.16, .98 / 1.27, and .94 / 1.29, respectively; P < .05). Peak serum aspartate aminotransferase, bilirubin levels, and international normalized ratio after LDLT were significantly higher in the H Group, as was mean ascitic fluid volume. In conclusion, early postoperative PVP elevation to 20 mm of Hg or more was associated with rapid graft hypertrophy, higher peripheral blood HGF levels, and lower portal VEGF levels; and with a poor outcome, graft dysfunction with hyperbilirubinemia, coagulopathy, and severe ascites. Adequate liver regeneration requires an adequate increase in portal venous pressure and flow reflected by clearance of HGF and elevated VEGF levels.
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PMID:Impact of portal venous pressure on regeneration and graft damage after living-donor liver transplantation. 1569 May 38


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