Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Brucella infection is a systemic disease, but the microorganism rarely causes infections in the gastrointestinal system such as hepatitis, cholecystitis, colitis and pancreatitis. Spontaneous bacterial peritonitis due to Brucella is extremely rare. Herein, we report a case of cirrhosis complicated with nongranulomatous hepatitis and peritonitis, both due to Brucella. A 63 year-old man with diabetes mellitus was admitted to hospital with complaints of weakness, backache, abdominal pain and abdominal swelling. On the basis of physical examination and laboratory findings, cryptogenic cirrhosis and spontaneous bacterial peritonitis were diagnosed. Due to persistent fever and backache, serum Brucella agglutination test was performed and found to be positive. Brucella melitensis was isolated from ascitic fluid culture. Liver biopsy findings revealed cirrhosis and a nongranulomatous hepatitis which was thought might be due to Brucella infection. Doxycycline and rifampicin, in addition to diuretics were administered for spontaneous ascites infection due to Brucella. A week later, the patient's condition improved and he became afebrile. After two months of therapy, the ascites had almost disappeared.
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PMID:Spontaneous bacterial peritonitis due to Brucella infection. 1461 44

The authors present case of patient with biliary stent dislocation after chest injury and fracture of VIII. rib. Polymorbid patient with cirrhosis, chronic pancreatitis, portal hypertension (Child Plugh B) and biliary stent insertion came with acute abdominal pain and inflammatory signs. Progressive signs of acute abdomen have led to laparotomy. Perforation of duodeno-jejunal-loop due to dislocated biliary stent, small loop adhesions and thickened intestine wall were found. Postsurgical period was complicated with obstructive ileus, cholecystitis and cholangiolitis and the second biliary stent was inserted. Present-day status of the patient is satisfactory.
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PMID:[Jejunal perforation by a plastic biliary stent after injury]. 1508 18

At present there is no established therapy for treating patients with hereditary hemorrhagic telangiectasia (HHT) and symptomatic hepatic involvement. We present the results of a prospective study with 15 consecutive patients who were treated with staged hepatic artery embolization (HAE). Branches of the hepatic artery were selectively catheterized and embolized in stages using polyvinyl alcohol particles (PVA) and platinum microcoils or steel macrocoils. Prophylactic antibiotics, analgesics and anti-emetics were administered after every embolization. Clinical symptomatology and cardiac output were assessed before and after therapy as well as at the end of follow-up (median 28 months; range 10-136 months). Five patients had abdominal pain and four patients had symptoms of portal hypertension. The cardiac output was raised in all patients, with cardiac failure being present in 11 patients. After treatment, pain resolved in all five patients, and portal hypertension improved in two of the four patients. The mean cardiac output decreased significantly ( P<0.001) from 12.57+/-3.27 l/min pre-treatment to 8.36+/-2.60 l/min at the end of follow-up. Symptoms arising from cardiac failure resolved or improved markedly in all but one patient. Cholangitis and/or cholecystitis occurred in three patients of whom two required a cholecystectomy. One patient with pre-existent hepatic cirrhosis died as a complication of the procedure. Staged HAE yields long-term relief of clinical symptoms in patients with HHT and hepatic involvement. Patients with pre-existing hepatic cirrhosis may be poor candidates for HAE.
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PMID:Hepatic artery embolization for treatment of patients with hereditary hemorrhagic telangiectasia and symptomatic hepatic vascular malformations. 1531 41

Juvenile haemochromatosis is an autosomal, recessive inherited iron metabolism disorder. The rapid deterioration and malignant prognosis differentiate juvenile haemochromatosis from hereditary haemochromatosis. The authors summarize the history of a 25 year old man, who worked in Hungary as a guest worker living in Romania. No significant illness has occurred in his previous history. The abdominal pain was his first symptom and he was treated in different institutions, where cholecystitis, alcoholic hepatic disease, hepatic cirrhosis were considered as a cause of his symptoms. Some weeks later atrial tachycardia, and congestive heart failure were observed and he was sent to our Cardiology Department. The echocardiography revealed diffuse hypokinesis, serious systolic dysfunction (ejection fraction: 21%), grade II mitral and tricuspid insufficiency with pulmonary hypertension. Considering the rapid deterioration of his cardiac function, myocarditis was suspected. Myocardial biopsy and coronary arteriography were performed. Coronary arteries were normal. Ventricular fibrillation occurred during coronary arteriography. Myocardial biopsy revealed juvenile haemochromatosis. Special laboratory examinations (transferrin saturation) were made after biopsy, that also confirmed the diagnosis of juvenile haemochromatosis. Cardiac transplantation was planned. Some days after the diagnosis was made the patient died of cardiogenic shock and intractable heart failure. Autopsy revealed hypogonadism and serious haemochromatosis in different parenchymal organs. Juvenile haemochromatosis should be considered in every young patient with congestive heart failure of unknown etiology.
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PMID:[Juvenile haemochromatosis presenting as intractable congestive heart failure]. 1646 15

Intrahepatic cholestasis of pregnancy (ICP) is a liver disorder, thought to be specific for pregnancy and to spontaneously resolve after delivery. Increased rates of gallstone formation and hepatitis C have previously been associated with ICP. However, there are no longitudinal studies to determine its significance as an indicator of subsequent liver or biliary diseases. In this retrospective cohort study with cases and controls we assessed the risk of liver and biliary diseases in 21,008 women, 10,504 with a history of ICP during the years 1972-2000 (cases) and 10,504 with a normal pregnancy (controls). Cases and controls were matched for age, time of delivery, and place of delivery. The diagnoses of liver and biliary disease were traced from the Finnish Hospital Discharge Register with an almost 100% coverage. Several liver and biliary diseases were found to have a significantly higher incidence in patients with ICP than in controls. The rate ratio for hepatitis C was 3.5 (CI 1.6-7.6; P < .001), for nonalcoholic liver cirrhosis 8.2 (CI 1.9-35.5; P < .05), for gallstones and cholecystitis 3.7 (CI 3.2-4.2; P < .001) and for nonalcoholic pancreatitis 3.2 (CI 1.7-5.7; P < .001). In conclusion, there is an association of ICP with several liver and biliary diseases. Some patients with ICP are at risk of the subsequent development of cirrhosis and other severe chronic diseases. Contrary to what has been previously thought, follow-up may need to be considered for these patients.
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PMID:Intrahepatic cholestasis of pregnancy as an indicator of liver and biliary diseases: a population-based study. 1655 65

Operative interventions in the patients suffering calculous cholecystitis on the hepatic cirrhosis background are accompanied by multiple complications. During ten year period laparoscopic cholecystectomy was conducted in the clinics in 138 patients suffering hepatic cirrhosis. In 12 patients, admitted to the hospital for obturation jaundice, endoscopic retrograde cholangiopancreaticography and endoscopic papillotomy were primarily done. In 3-7 days after successful removal of calculi from the ducts the laparoscopic cholecystectomy was performed. In 39 (28.3%) of patients complications had occurred, the most frequent of which was intraabdominal hemorrhage, as well as gastrointestinal bleeding from the varicosely changed esophageal veins in the early postoperative period--in 15 (10.8%). Two patients died as a consequence of postoperative hemorrhage occurring from varicosely changed esophageal veins, developed on the hepatocellular insufficiency background.
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PMID:[Characteristics of laparoscopic interventions in the patients with calculous cholecystitis complicated with hepatic cirrhosis]. 1743 18

An analysis of surgical treatment of 124 patients with "difficult" gallbladder has shown that in most cases (59.7%) the causes impeding surgical procedures were massive commissural processes in the gallbladder zone and stony infiltrates of the hepato-duodenal ligament with shrunken or sclerosed gallbladder as well as earlier operations on the gallbladder, a combination of echinococcosis and liver cirrhosis with acute calculous cholecystitis, cholecystodigestive fistulas, Mirizzi syndrome and intrahepatic location of the gallbladder. Videolaparoscopic operations in such cases are extremely difficult, so open laparotomic operations should be preferred.
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PMID:[Surgical treatment of patients with complicated forms of cholelithiasis]. 1766 81

Obesity has become epidemic in the United States, in Europe, and in many urban areas in the developing world. The globalization of certain 'fast foods' and 'soft drinks' may, in part, be contributing to this epidemic. Diets high in saturated fatty acids and trans fats as well as drinks that have high fructose corn syrup levels may be particularly harmful. Recent research suggests that fat is a dynamic endocrine organ and that visceral fat is associated with the metabolic syndrome. Central obesity leads to organ steatosis and altered serum adipokines including reduced adiponectin and markedly elevated leptin. This abnormal adipokine milieu results in increased tissue infiltration of monocytes and macrophages which produce proinflammatory cytokines that alter organ function. Over many years, the combination of steatosis and local inflammation leads to fibrosis and eventually to cancer. Nonalcoholic fatty liver disease (NAFLD) is a precursor for nonalcoholic steatohepatitis (NASH). NAFLD and NASH (1) lead to cirrhosis and hepatocellular carcinoma, (2) increase the risk of liver resection, and (3) compromise the outcome of liver transplantation. Similarly, in the pancreas nonalcoholic fatty pancreas disease (NAFPD) may lead to nonalcoholic steatopancreatitis (NASP). NAFPD and NASP may (1) promote the development of chronic pancreatitis and pancreatic cancer, (2) exacerbate the severity of acute pancreatitis, and (3) increase the risk of pancreatic surgery. In the gallbladder nonalcoholic fatty gallbladder disease (NAFGBD, cholecystosteatosis) may lead to steatocholecystitis. Cholecystosteatosis may be an explanation for (1) the increased incidence of chronic acalculous cholecystitis and (2) the increased number of cholecystectomies.
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PMID:Hepato-pancreato-biliary fat: the good, the bad and the ugly. 1833 22

The significance of gallbladder wall thickness (GBWT) in regard to gallbladder disease (GBD) is not completely understood. Thickening of the gallbladder wall has been observed in patients with acute calculous and acalculous cholecystitis and chronic cholecystitis. However, various pathologic processes, such as gallbladder cancer and nonbiliary disorders such as liver cirrhosis and viral hepatitis, could also cause thickening of the gallbladder wall. To date, there is no report available on the genetic factors influencing GBWT. Therefore we sought to estimate the heritability (h2) of GBWT and to perform a genome-wide search to identify the susceptibility genes for GBWT, using data from the San Antonio Family Diabetes/Gallbladder Study (SAFDGS), a family study of Mexican Americans. GBWT was measured by ultrasound. After adjusting for the significant effects of age, sex, GBD (i.e., asymptomatic gallstones), metabolic syndrome, and duration of type 2 diabetes (T2DM), GBWT was found to be under significant and appreciable additive genetic influences (h2 +/- SE = 0.38 +/- 0.09, P < 0.0001). The strongest evidence for linkage occurred between markers D11S912 and D11S968 on chromosome 11q24-q25 (LOD = 2.7), where we have already shown suggestive evidence for linkage of GBD (LOD = 2.7) in a subset of our SAFDGS data. Potential evidence for linkage occurred at markers D1S1728 (1p31.1; LOD = 1.4) and D16S748 (16p13.1; LOD = 1.4), respectively. In conclusion, our study provides suggestive evidence for linkage of GBWT on chromosome 11q in Mexican Americans, and future tasks of mapping susceptibility gene(s) for GBD and its related traits, such as GBWT, in this chromosomal region can be fruitful.
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PMID:Autosomal genome-wide linkage analysis to identify loci for gallbladder wall thickness in Mexican Americans. 1850 42

A 63-year-old woman was admitted for cholecystitis and underwent a laparoscopic cholecystectomy (LC). She experienced abdominal pain and hemobilia 11 days after the LC. Angiography was performed but it did not show any source of bleeding. Thereafter, at 27 days after LC, a repeat angiogram was performed which revealed a pseudoaneurysm (PA) arising from a cystic artery stump and an embolized PA sack. However, another PA arising from near the embolized PA and liver abscess was observed 4 days after embolization. The arterial collateral flow was evaluated by endovascular balloon occlusion of the right hepatic artery and it was embolized proximal and distal to the bleeding point. The embolization of the partial hepatic artery was effective for PA when packing the PA sack proved to be insufficient. In patients with liver cirrhosis or liver abscess who require an adequate arterial liver flow, it is important to evaluate the collateral arterial flow before hepatic artery embolization.
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PMID:Hemobilia and cystic artery stump pseudoaneurysm associated with liver abscess after a laparoscopic cholecystectomy: report of a case. 1851 42


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