Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Information from 72 patients from 7 families in England and Wales confirms that hereditary pancreatitis is inherited as an autosomal dominant conditions with limited penetrance. The degree of penetrance is approximately 80%. These patients have had recurrent attacks of abdominal pain starting from childhood or young adult life. The mean age of onset in the 7 families studied was 13.6 years. There were two peaks, with maximum numbers at 5 years and 17 years. The second peak was thought to represent genetically susceptible individuals having pain brought on by alcohol rather than representing evidence of genetic heterogeneity. Five of the 7 families had members with both childhood and adult ages of onset. Only 4 patients out of 72 had life-threatening disease and in the majority of cases the attacks of pain were of nuisance value only. Hereditary pancreatitis was implicated in only 1 patient's death and this was not definite. Patients appear to get better after a period of symptoms usually as they approach middle age, or after a severe attack. In older patients alcohol, emotional upsets, and fatty food appear to precipitate attacks. Pancreatic insufficiency (5.5%), diabetes mellitus (12.5%), pseudocysts (5.5%), and haemorrhagic pleural effusion are uncommon complications. Portal vein thrombosis occurred definitely in 2 patients and was suspected in 3 others. Carcinoma of the pancreas was not found in any of 72 patients studied in detail; however, 2 members from a family not visited personally had chronic pancreatitis and malabsorption going on to carcinoma. They may have suffered from a different disease. Genetic linkage information was too slight for many definite conclusions. However, there was no suggestion of linkage with any of the markers tested.
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PMID:Hereditary pancreatitis in England and Wales. 67 83

One hundred and fourteen consecutive patients with unresectable hepatocellular carcinoma were treated by chemoembolization using ethiodized oil (Lipiodol), anticancer agents. Ninety patients had concomitant chronic liver disease. Hepatocellular carcinoma (HCC) was diagnosed by US, contrast enhanced CT, fine needle biopsy and alpha-feto-protein level. Admission criteria were as follows: tumor confined to the liver with or without hilar nodal involvement, Child class A or B, white blood cell count above 2.000/mmc and platelet count above 75,000/mmc. All the patients underwent angiographic chemoembolization with Lipiodol and anticancer agents. In 98 patients we performed transcatheter hepatic arterial embolization (TAE) with Gelfoam or for Ivalon sponge. In 16 patients TAE was not performed because of portal thrombosis (7 cases) or technical reasons (9 cases). Mitomycin was used in 40 patients and dihydroxyanthracenedione (DADH) in 58 patients. In the TAE group 83 patients were Child A and 15 Child B. In 27 patients HCC was mononodular whereas in 71 it was multinodular. In 41 patients the tumor was more than 5 cm in diameter (in multinodular tumors only the larger lesion was taken into account). In 56 patients chemoembolization plus TAE was repeated. Seven patients died within one month after treatment: two from myocardial infarction, two from liver failure, two from digestive haemorrhage and one from necrotizing pancreatitis. Long-term survival rates were investigated in relation to prognostic factors: anti-cancer agent, number of nodes, tumor size and Child stage using Kaplan-Meier method. Survival rate at 12, 24 and 36 months are 64%, 38%, and 30% respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The treatment of hepatocellular carcinoma by chemoembolization]. 802 66

Portal vein thrombosis (PVT) is usually a complication of pre-existing cirrhosis, abdominal malignancy (e.g., pancreatic or hepatocellular carcinoma), or abdominal inflammation (e.g., appendicitis, diverticulitis, pancreatitis). Less frequently, PVT can be associated with myeloproliferative or connective tissue disorders or inflammatory bowel disease [1]. PVT can cause or exacerbate portal hypertension; variceal bleeding or hypersplenism may then develop acutely or several years later. PVT also complicates portosystemic shunt surgery or hepatic transplantation. Unfortunately, the signs and symptoms of PVT can be subtle or nonspecific and can be overshadowed by the underlying illness. The radiologist may be the only physician to suggest the preoperative or premortem diagnosis of PVT. Familiarity with the imaging findings of PVT, therefore, is imperative.
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PMID:Portal vein thrombosis: imaging findings. 827 95

We describe seven cases of thrombosis of the portal and splenic vein after elective splenectomy. The diagnosis was initially unrecognized in all patients and was confused with biliary sepsis (three cases), postoperative pancreatitis (three cases), or pulmonary emboli (one case). Two patients in whom the diagnosis of portal vein thrombosis was not made within 3 days of disease onset died. In the five survivors, the diagnosis was based on clinical suspicion, confirmed with color flow Doppler ultrasonography or computed tomography with intravenous contrast material, and treated with thrombolytic agents, anticoagulants, and antibiotics. In two patients, splenic vein thrombus was visualized on initial postoperative imaging studies and the thrombus subsequently extended into the portal vein. Portal vein thrombosis should be considered in patients with fever and abdominal complaints after splenectomy. Urgent treatment with thrombolysis and anticoagulants may preserve bowel integrity and be lifesaving.
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PMID:Portal vein thrombosis after elective splenectomy. An underappreciated, potentially lethal syndrome. 848 90

Accidental hypothermia has been described in the forensic literature but reports of occurrence in hospitalized patients are rare. Associated anatomic lesions include acute hemorrhagic pancreatitis and characteristic acute gastric ulcers termed Wischnewski ulcers. We report here two patients with cirrhosis and ascites; one also had hepatocellular carcinoma. Portal vein thrombosis, acute hemorrhagic pancreatitis and Wischnewski ulcers were present in both. The clinical records documented hypothermia that progressed over several days. Temperature nadirs of 31.0 degrees C (87.8 degrees F) and 32.2 degrees C (90.0 degrees F) were recorded in each patient, respectively, one day before death, although each transiently reached temperatures that did not register on standard monitoring devices. This is the first report that chronicles antemortem body temperatures in hypothermic patients with Wischnewski ulcers and pancreatitis at autopsy. Also, the association of these findings with portal vein thrombosis and cirrhosis has not been previously described. We discuss this constellation of findings with regard to possible mechanistic interrelations.
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PMID:Wischnewski ulcers and acute pancreatitis in two hospitalized patients with cirrhosis, portal vein thrombosis, and hypothermia. 1048 64

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

Portal vein thrombosis is a rare complication accompanied with acute pancreatitis or cholangitis/cholecystitis. The main pathogenesis of portal vein thrombosis in pancreatitis or cholangitis/cholecystitis are suggested to be venous compression by pseudocyst and an imbalance between the blood coagulation and fibrinolysis. In this case report, we experienced a 63 year old male who developed portal vein thrombosis later in the course of the treatment of acute gallstone pancreatitis with cholangitis/cholecystitis without any symptom or sign. The diagnosis of portal vein thrombosis was given on follow up CT scan and serum protein S activity was decreased to 27% in laboratory study. Immediate anticoagulation therapy with heparin and thrombolytic therapy with urokinase and balloon dilatation were performed. Despite the aggressive treatment, complete reperfusion could not be obtained. With oral warfarin anticoagulation, the patient showed no disease progression and was discharged. We report a case of portal vein thrombosis as a complication of acute pancreatitis and cholangitis/cholecystitis with a review of literatures.
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PMID:[A case of portal vein thrombosis associated with acute pancreatitis and cholangitis]. 1603 Apr 6

Acute pancreatitis is a multisystem disorder which can result in a variety of complications. Vascular complications can occur commonly in acute pancreatitis. Splenic artery rupture, aneurysms; gastro duodenal artery aneurysms; splenic venous thrombosis; portal venous thrombosis and rarely, superior mesenteric venous thrombosis, are the vascular complications of pancreatitis. Ischaemic stricture of the small bowel can occur secondary to pancreatitis, but it is extremely rare. Hence, we are reporting this case of a proximal jejunal stricture which occurred secondary to the pancreatitis which was caused by a superior mesenteric thrombosis.
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PMID:Bowel block in pancreatitis. 2390 21

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 (PVT) is a relatively common complication in patients with liver cirrhosis, but several other causes might play an important role in PVT pathogenesis. We present a case of alcoholic chronic pancreatitis complicated by acute extensive PVT. The patient was managed conservatively with danaparoid sodium at first, but the thrombosis gradually extended. We then tried radiological intervention using the direct transhepatic and transjugular intrahepatic postsystemic shunt approaches. Although we were able to successfully catheterize the percutaneous transhepatic portal vein (PTP), we could not achieve recanalization of the portal vein. Therefore, PTP catheterization and systemic intravenous infusion of urokinase and heparin was performed to prevent further progression of the thrombosis and cavernous transformation was finally achieved. Computed tomography (CT) and magnetic resonance cholangiopancreatography revealed a pancreatic stone which had possibly induced dilatation of the tail duct and formation of a pancreatic pseudocyst and caused intractable pancreatitis. We performed endoscopic retrograde cholangiopancreatography and placed a stent in the pancreatic duct, which completely cured the pancreatitis. Retrospectively, the previous CT with curved multi-planar reconstruction was reviewed and a fistula was detected between the pancreatic pseudocyst and splenic vein. We concluded that the etiology of the PVT was not only inflammatory extension from pancreatitis but also a fistula between the pancreatic duct and the splenic vein.
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PMID:Acute portal vein thrombosis due to chronic relapsing pancreatitis: a fistula between a pancreatic pseudocyst and the splenic vein. 2618 9


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