Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Jaundice is a disorder of bilirubin metabolism and has many causes. History and physical examination help establish the diagnosis in 70 to 80 percent of patients. Elevation of alkaline phosphatase and gamma-glutamyl transpeptidase suggests cholestasis, either intrahepatic (e.g., medication reactions) or extrahepatic (e.g., choledocholithiasis), whereas markedly elevated serum aminotransferases are indicative of hepatocellular damage from infection, toxins or ischemia. Ultrasound examination is a useful initial procedure when extrahepatic obstruction is suspected. Endoscopic retrograde cholangiopancreatography and computed tomography may be better used to diagnose obstruction at the level of the pancreas or distal common bile duct. The treatment is based on the etiology of jaundice and includes removal of offending medications or toxins, therapy for underlying liver disease or surgery for extrahepatic obstruction.
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PMID:Jaundice. 154 99

Nonanastomotic biliary strictures that involve only the biliary tree of the graft occur after orthotopic liver transplantation in patients with hepatic artery thrombosis, chronic ductopenic rejection and ABO blood group incompatibility. This complication may also occur in the absence of these known risk factors. The major focus of our study was to evaluate the risk factors for nonanastomotic biliary stricturing of unknown cause after orthotopic liver transplantation. Results demonstrate that the development of biliary strictures is strongly associated with the duration of cold ischemic storage of allografts in both Euro-Collins solution and University of Wisconsin solution. Results also demonstrate that strictures are not associated with the type of biliary reconstruction, the primary liver disease, cytomegalovirus infection, allograft rejection or the presence of a positive lymphocytotoxic crossmatch. More recently, we have markedly reduced the occurrence of nonanastomotic biliary stricturing by decreasing the ischemia time of our allografts. Thus nonanastomotic biliary strictures appear to be the result of the ischemia/reperfusion-induced tissue injury associated with the harvest and implantation of allografts.
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PMID:Ischemic-type biliary complications after orthotopic liver transplantation. 161 82

The novel tissue-specific contrast agent, Gd-BOPTA/Dimeg, was tested in MR imaging of experimental focal liver disease and of acute myocardial ischemia in rats. Directly implanted liver tumors and blood-borne metastases were used as models for focal liver disease and occlusion of the lower anterior descending coronary artery as model for acute ischemia. The studies with implanted tumors, at a dose level of 250 mumol/kg, showed a very high (370%) and persistent (greater than 2 h) increase in the tumor-liver contrast-to-noise ratio (CNR), owing to selective enhancement of normal liver parenchyma signal intensity. While all blood-borne metastases showed a similar late CNR enhancement, some of them experienced early contrast loss due to transient signal intensity enhancement. In myocardial imaging, Gd-BOPTA/Dimeg produced a signal intensity enhancement in normal myocardium and an injured area-normal area CNR enhancement which were both much stronger and more persistent than those produced by Gd-DTPA/Dimeg.
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PMID:Gd-BOPTA/Dimeg: experimental disease imaging. 181 66

Drugs containing ergotamine are commonly used in the treatment of migraine. Hypersensitivity to these drugs may be triggered off even with intake of recommended doses, inducing peripheral ischemia. Contributing factors to ergotism are concurrent fever, liver disease and drugs such as erythromycin or propranolol. We present a case history and different methods of treatment.
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PMID:[Ergotamine induced ischemia]. 212 Jul 88

We describe a patient who developed progressive hepatic failure one year after pancreatoduodenectomy for pancreatic carcinoma and died of gastrointestinal bleeding. He suffered from progressive weight loss after surgery, even though obstruction or stenosis of the gastrointestinal tract was excluded. At autopsy, the liver showed extensive perivenular fibrosis associated with variable loss of hepatocytes, perisinusoidal fibrosis, alcoholic hyalin and a lack of parenchymal regenerative activity, all of which closely resembled severe alcoholic liver disease. Stricture of both the main pancreatic duct and the pancreaticojejunostomy with almost complete loss of exocrine acini was also found, and the recurrent tumor was seen to have caused portal venous obstruction and hepatic arterial stenosis. A combination of these nutritionally unfavorable circumstances and prolonged ischemia appeared to have been responsible for the liver injury in this non-alcoholic patient.
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PMID:Liver injury with perivenular fibrosis and alcoholic hyalin after pancreatoduodenectomy for pancreatic carcinoma. 245 95

Liver biopsy results and clinical records from 13 patients with sickle cell anemia were reviewed to assess the relative importance of local ischemia or of factors unrelated to sickling as a cause of their liver disease. Two of the biopsy specimens were normal and one showed cirrhosis. Nine patients had received multiple blood transfusions and nine had cholelithiasis, of whom two also had choledocholithiasis. Seven had both risk factors. Five had lobular cholestasis and four had acute or chronic hepatitis. One biopsy specimen showed changes of the Budd-Chiari syndrome. Another showed clear portal tract changes of large bile duct obstruction but no mechanical blockage of the biliary system; this suggests the thickened bile as postulated by Muirhead. Otherwise the changes observed were those to be expected in a heavily transfused population with a high prevalence of gallstones.
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PMID:Histopathologic features of liver biopsy specimens in sickle cell disease. 334 26

An enhanced frequency and morbidity of urinary tract infections (UTI) have been observed in association with alcoholism and liver disease. The causes of these phenomena may relate, in part, to the defects in humoral and cellular immune mechanisms that occur in alcoholism. Urinary catheterization is the most common cause of UTI in hospitalized alcoholics. The severity of the sequelae of UTI in alcoholism is demonstrated by the unusually frequent occurrence of renal papillary necrosis (RPN) in conjunction with pyelonephritis in these patients. Indeed, in over 90% of the reported cases of RPN occurring with alcoholism or liver disease, pyelonephritis has been a contributing factor. The proclivity to medullary ischemia and RPN in this patient group may be, at least in part, a result of interstitial renal edema secondary both to infection and the effect of ethanol per se and to renal arterial vasoconstriction that occurs in cirrhosis. The frequency with which death due to sepsis or renal failure occurs in association with UTI in alcoholics obliges the physician to exercise caution in the prevention and treatment of UTI in these patients.
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PMID:Urinary tract infections and renal papillary necrosis in alcoholism. 370 22

The case of an obese patient who developed massive centrilobular liver cell necrosis, severe coagulopathy, acute renal failure, and encephalopathy is presented. Hypovolemia and heart failure were absent, but the acute liver disease was associated with severe arterial hypoxemia due to obstructive sleep apnea that was shown by the nocturnal blood oxygen desaturation, the results of the polysomnographic study, and normal baseline pulmonary function tests. In this obese patient, liver cell necrosis was caused by severe liver cell hypoxia secondary to severe arterial hypoxemia as a consequence of obstructive sleep apnea associated with a Pickwickian syndrome. This observation is consistent with the hypothesis that liver ischemia was directly related to severe arterial hypoxemia.
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PMID:Ischemic hepatitis due to obstructive sleep apnea. 755 54

Hepatectomy was performed under in situ right lobar hypothermic perfusion combined with hepatoprotective agents in six patients who had hepatocellular carcinoma and coexisting liver disease. Following occlusion of the right hepatic vein and the right portal pedicle, in situ cold perfusion was initiated using chilled Ringer's lactate infused through a cannula placed in the right main portal vein. The right superior segments were resected in a bloodless field. The liver was cooled to 22-26 degrees C for 40 to 80 minutes with no significant changes in systemic hemodynamics or body temperature. Postoperative liver functions showed no marked derangement; the mean peak GPT was 221 U and the mean peak total bilirubin 2.3 mg d/l. Local cooling minimizes the risk of ischemia/reperfusion injury in this very vulnerable population, yet gives the surgeon adequate time to perform a challenging resection in a bloodless field.
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PMID:Hepatic resection under in situ hemihepatic hypothermic perfusion with hepatoprotective agents. 778 26

An increasing number of patients with severe liver dysfunction are admitted to the ICU for stabilization and organ-specific support, including liver transplantation. Global impairment of hepatic performance frequently results in pathologic organ interactions that limit the potential for recovery. One of the most notable of these interactions is the hepatorenal syndrome, an otherwise uniformly fatal complication of end-stage liver disease characterized by the progressive development of oliguria and low urine sodium excretion. The syndrome can occur in the setting of either acute or chronic liver disease, and portal hypertension may be important in the pathogenesis. The patient with the hepatorenal syndrome also has a number of systemic circulatory abnormalities induced by liver disease and/or portal hypertension, but the exact pathologic role of these abnormalities in the development of oliguria is uncertain. It is reasonably well established that diminished systemic BP characteristic of liver failure is not the primary cause of renal insufficiency. Rather, intrarenal preglomerular vasoconstriction mediated by unknown stimuli is the major defect in the hepatorenal syndrome, manifested by relative ischemia. Current data point to abnormal renal sympathetic innervation as one of the more likely major causes of this vasoconstriction. After exclusion of systemic intravascular volume depletion and other causes of oliguria, dialytic therapy is indicated when liver transplantation or recovery of liver function is anticipated; terminal supportive care is appropriate when these outcomes are not options.
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PMID:Organ interactions in the hepatorenal syndrome. 780 2


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