Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over the past decade we have reported excellent outcomes in pediatric living-donor liver transplantation (LDLT) with recipient survival exceeding 90%. Principles established in these patients were extended to LDLT in adults. To compare outcomes in donors and recipients between adult and pediatric LDLT in a single center, we reviewed patient records of 45 LDLT performed between 1/98 and 2/01: 23 adult LDLT (54 +/- 6.5 yr) and 22 pediatric LDLT (33.7 +/- 53.5 months). Preoperative liver function was worse in adults (International Normalized Ratio [INR] 1.5 +/- 0.4 vs. INR 1.2 +/- 0.5; p = 0.032). 4 adults (17%) met criteria for status 1 or 2A. Only 1 child was transplanted urgently. Analysis included descriptive statistics and Kaplan-Meier estimation. Donor mortality was 0% with 1 re-exploration, 2.4%. Median hospital stay (LOS) was 6.0 days (range, 4-12 days). Donor morbidity and LOS did not differ by sex, extent of hepatectomy, or adult and pediatric LDLT ( p = 0.49). In contrast, recipient outcomes were worse for adults. Adult 1 year graft survival was 65% (3 retransplants [ReTx], 5 deaths) vs. 91% for children (1 ReTx, 1 death) p = 0.02. Graft losses in adults were due to sepsis (n = 3), small for size (n = 2), suicide, and hepatic artery thrombosis (HAT), whereas in children graft losses were due to portal thrombosis and total parenteral nutrition (TPN) liver failure. Biliary leaks occurred in 22% of adults and 9% of children. Hepatic vein obstruction occurred in 17% of adults and in none of the children. Median LOS was comparable (adult, 16.5 days (range, 7-149 days); child, 17 days (range, 10-56 days), p = 0.2). Graft function (total bilirubin (TBili) < 5mg/dl, INR < 1.2, aspartate aminotransferase (AST) < 100 U/l) normalizing by day 4 in children and by day 14 in adults. Adults fared worse, with an array of problems not seen in children, in particular, hepatic vein obstruction and small-for-size syndrome. Biliary leaks were diagnosed later in adults and were lethal in 3 cases; this was later avoided with biliary drainage in adult recipients. Finally, use of LDLT in decompensated adults led to death in 3 of 4 patients, and should be restricted to elective use.
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PMID:Analysis of failure in living donor liver transplantation: differential outcomes in children and adults. 1260 66

We report the case of a 18-year-old woman with portal vein thrombosis and chronic hepatitis C virus. Portal vein thrombosis was diagnosed by chance on ultrasound examination during initial hepatitis C virus-positive patient screening. The patient interview revealed a history including exchange transfusion at birth, followed by necrotising ulcerocolitis and septicemia. The investigation of general factors favoring thrombosis showed acquired protein S deficiency and heterozygous factor V Leiden mutation. This case demonstrates the value of systematic investigations for general thrombophilic factors in cases of portal vein thrombosis even when a local cause is found.
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PMID:[Portal vein thrombosis associated with factor V Leiden mutation in a woman who underwent exchange transfusion at birth]. 1291 Feb 30

DIAGNOSTIC CIRCUMSTANCES: Portal vein thrombosis is the second cause of portal hypertension after cirrhosis in Western countries. Diagnosis can be either made at the acute stage in the context of abdominal pain or after appearance of a porto-portal collateral venous circulation leading to the formation of a portal cavernoma, the diagnosis being made in the circumstance of rupture of oesophageal varicose veins or manifestations of hypersplenism. AETIOLOGICAL SURVEY: In the absence of hepatocellular carcinoma, causes that need to be investigated are cirrhosis, local factors (intra-abdominal sepsis, abdominal surgery, splenectomy or pancreatitis), and one or several prothrombotic affections (acquired or inherited prothrombotic states are present in 70% of cases, with myeloproliferative disease ranking first). REGARDING TREATMENT: Anticoagulant therapy generally allows recanalisation of the thombosed veins in recently constituted thrombosis. Some patients at the portal cavernoma stage can also benefit from anticoagulant therapy: patients with a prothrombotic state without large oesophageal-gastric varicose veins. In the case of large oesophageal-gastric varicose veins that have never bled, treatment to prevent haemorrhages due to portal hypertension according to the same modalities as in cirrhosis must be associated with the prescription of an anticoagulant. In the absence of prothrombotic affection or in patients having already suffered from haemorrhages due to portal hypertension, the benefit of anticoagulant therapy is less clearly established.
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PMID:[Portal vein thrombosis]. 1453 80

A 42-year old man, 1 year previously diagnosed with ulcerative colitis after an emergency subtotal colectomy with formation of an ileostomy because of severe colitis with perforation, was admitted with sepsis and jaundice. The liver enzymes were elevated and blood cultures were positive for Streptococcus milleri. Magnetic resonance imaging showed a complete thrombosis of the main stem of the portal vein with occlusion of the left branch. Intravenous antibiotic therapy combined with heparinisation led to complete recanalisation of the thrombus. Portal vein thrombosis is a rare complication of inflammatory bowel disease and has been described in only 10 patients thus far. Multiple aetiologic factors may be responsible in relation to inflammatory bowel disease, such as hypercoagulability, thrombocytosis and abdominal sepsis. In patients with inflammatory bowel disease, unexplained sepsis and abnormal liver function tests, the possibility of an acute portal vein thrombosis should be considered and investigated, because unrecognised it may have serious long-term complications.
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PMID:Sepsis and elevated liver enzymes in a patient with inflammatory bowel disease: think of portal vein thrombosis. 1511 44

Liver abscess is a rare condition in neonates and its diagnosis requires a high degree of suspicion. CT scan and ultrasound are the most sensitive diagnostic modalities for detecting hepatic abscess. Portal vein thrombosis and cavernoma formation are rare complications following neonatal liver abscess and sepsis. We describe the case of two neonates with hepatic abscess following umblical vein catheterisation, with rare complications of portal vein thrombosis and portal vein cavernoma formation. Therefore, unreserved caution should be exercised in performing umbilical cannulation in neonates due to the inherent risks involved with this procedure.
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PMID:Liver abscess, portal vein thrombosis and cavernoma formation following umbilical vein catherisation in two neonates. 1805 Aug 47

Portal vein thrombosis is a rare but well-known complication after abdominal surgery. To our knowledge, there have been no reports about this complication after cardiopulmonary bypass surgery. This can probably be explained by the variety of clinical pictures and difficulties in the establishment of a diagnosis of portal vein thrombosis. Among the possible trigger factors, bacteremia, that is usually caused by Bacteroides fragilis or by Escherichia coli, has been assessed. In this case, several blood culture specimens and fluid from abdominal paracentesis consistently grew coagulase-negative staphylococci which have been proved to be one of the most common pathogens in postoperative infection after cardiac surgery. The patient received clopidogrel before and after coronary artery bypass grafting. We speculate that in this clinical situation associated with coagulase-negative staphylococcal bacteremia, clopidogrel resistance may play an important role. The natural history of portal vein thrombosis in this case is complicated by massive fatal gastrointestinal bleeding from rupture of the esophageal varices. Emergency endoscopic therapy with esophageal variceal ligation, injection of a sclerosing solution and using of vasoconstrictive agents helped only in the first episode of bleeding. Portal vein thrombosis after coronary artery bypass grafting is a serious complication. The clinical picture of portal vein thrombosis may vary greatly and the presence of this condition should be suspected when faced with abdominal pain with gastrointestinal bleeding of unknown origin and sepsis.
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PMID:Portal vein thrombosis associated with coronary artery bypass surgery. 1821 99

Portal vein thrombosis is a fairly common clinical condition that is usually not fatal but may give rise to serious complications. We report the case of a woman who was always in good health until the age of 50, when she developed acute gastroenterocolitis with inflammation of the portal vein (pylephlebitis or septic portal thrombophlebitis), resulting in thrombus formation, rupture of the vascular wall and exsanguination. At autopsy, no signs of thrombosis or inflammation were found elsewhere in the body and there was no evidence of any other disease or abnormality. Pylephlebitis may occur following intra-abdominal sepsis from any source. It is a rare condition that carries a high mortality. Rupture of the inflamed portal vein and possibly the adjacent artery is an extremely rare complication.
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PMID:Fatal hemorrhage due to thrombosis and rupture of the portal vein and hepatic artery. 1978 25

Portal vein thrombosis is an uncommon but an important cause of portal hypertension. The most common etiological factors of portal vein thrombosis are liver cirrhosis and malignancy. Albeit rare, portal vein thrombosis can also occur in the presence of local infection and inflammation such as pancreatitis or cholecystitis. A 52-year-old male was admitted because of general weakness and poor oral intake. He had an operation for colon cancer 18 months ago. However, colonic stent had to be inserted afterwards because stricture developed at anastomosis site. Computed tomography taken at admission revealed portal vein thrombosis and inflammation at colonic stent insertion site. Blood culture was positive for Escherichia coli. After antibiotic therapy, portal vein thrombosis resolved. Herein, we report a case of portal vein thrombosis with sepsis caused by inflammation at colonic stent insertion site which was successfully treated with antibiotics.
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PMID:[Portal vein thrombosis with sepsis caused by inflammation at colonic stent insertion site]. 2599 79

Portal vein thrombosis is an uncommon finding that typically arises in the context of cirrhosis. In the acute setting, it may present with abdominal pain, portal hypertension, ascites, gastrointestinal bleeding, or mesenteric ischemia. Local risk factors that predispose its formation include: cirrhosis, hepatocellular carcinoma, pancreatitis, and intraabdominal infection. Systemic factors, including hypercoagulable states and sepsis, also pose an increased risk. JAK2 V617F positive myeloproliferative disorders are associated with systemic prothrombotic states and are a less frequently identified cause of portal vein thrombosis. We present a case of acute unprovoked portal vein thrombosis diagnosed in a 59-year-old male without local disease factors. Computed tomography, magnetic resonance cholangiopancreatography, and ultrasound demonstrated the presence of portal vein thrombosis with neighboring periportal and pancreatic head edema. Peripheral blood testing detected the presence of JAK2 V617F mutation. The patient was discharged on 6-month anticoagulation therapy and outpatient follow-up.
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PMID:Acute portal vein thrombosis in a 59-year-old male with JAK2 V617F mutation. 3025 17


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