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PubMedDate not supplied

[Obstructive jaundice caused by hepatocellular carcinoma].

The Authors take a hint from recent observation of two patients with hepatocellular carcinoma presenting with obstructive jaundice to analyse the litterature and their clinical cases. They conclude that in the evolution of hepatocellular carcinoma can be found "early" or "late" jaundice. The latest is hepatocellular and/or obstructive jaundice and it is harbinger of fatal prognosis because of a big hepatocelluar carcinoma that has invaded biliary tree and/or liver failure by concomitant cirrhosis. The "early" jaundice appears when the tumor is still small and it is always obstructive due to intrabile duct tumor growth. This kind of jaundice has a good prognostic meaning because, together with imaging techniques, permits an early diagnosis of the hepatocellular carcinoma necessary for satisfactory palliation or occasional cure.

Adult↗
PubMedDate not supplied

Predictive value of risk factors in patients with obstructive jaundice.

Clinical and laboratory parameters that may affect post-operative mortality and morbidity were studied in 215 patients operated on for obstructive jaundice. The cause of the bile duct obstruction was benign disease in 56.7% of patients and malignant disease in 43.3%. Overall postoperative mortality and morbidity rates were 21.9% and 33.5%, respectively. Eight risk factors were shown to be associated with increased mortality: age > 70 years; malignancy; leucocytosis > 15 000 cells/microl and fever > 38.5 degrees C; haematocrit < or = 30%; creatinine > 1.3 mg/dl; albumin < or = 3 g/dl; bilirubin > 20 mg/dl; and serum alkaline phosphatase > 100 IU/l. The simultaneous presence of less than three risk factors was always associated with post-operative survival, but concomitant existence of seven or more risk factors indicated 100% mortality. Understanding the factors related to post-operative morbidity and mortality in patients with obstructive jaundice will better guide appropriate surgical or non-surgical management and lead to improved survival.

Adult↗
PubMed2003

The effect of immunonutrition on bacterial translocation, and intestinal villus atrophy in experimental obstructive jaundice.

BACKGROUND & AIMS: Spontaneous bacterial infection and septicemia due to increased bacterial translocation (BT) in patients with obstructive jaundice result in significant morbidity and mortality. The present study evaluates the effects of enteral nutrition with immune enhancing feeds on BT and intestinal villus histopathology promoted by obstructive jaundice. METHODS: Fifty male Wistar-albino rats weighing 250-300g were assigned into five equal groups of 10. Animals in Groups I, II, and III were fed with standard chow, those in Group IV were given glutamine 1g/kg/day and the remaining 10 animals in Group V were fed with an arginine, omega-3 fatty acids, and RNA-supplemented enteral diet for (1g/kg/day amino acid and 230 kcal/kg) 7 days preoperatively. Group I underwent sham operation and the remaining animals in all other groups underwent common bile duct ligation. After operation, Group I had standard chow, Groups II and IV had glutamine, Groups III and V had an arginine omega-3 fatty acids, and RNA-supplemented enteral diet for 7 days. All animals were sacrificed on the 8th postoperative day and evaluated both biochemically and histopathologically. Samples from blood, liver, mesenteric lymph nodes and spleen were cultured under aerobic conditions. RESULTS: Significantly less BT was observed in groups fed with an arginine, omega-3 fatty acids, and RNA-supplemented enteral diet or glutamine in pre-and postoperative periods as compared to others (P<0.001). Histologic evaluation also showed significant reduction in villus atrophy in these groups. CONCLUSIONS: Enteral immunonutrition using glutamine or arginine, omega-3 fatty acids, and RNA-supplemented enteral diet during both pre-and postoperative periods seems to reduce BT and decrease atrophy of intestinal mucosal villi in rats with obstructive jaundice.

Animals↗
PubMed1988

Impaired immune function in obstructive jaundice.

Sepsis is a common and occasionally lethal complication of obstructive jaundice. The reasons for this increased susceptibility to infection are unknown. This study examines lymphocyte and reticuloendothelial (RES) function in animals with obstructive jaundice. Twelve New Zealand white rabbits (3-4 kg) were studied. Lymphocyte function was evaluated in six rabbits by phytohemagglutinin (PHA), concanavalin A (Con A), and pokeweed mitogen (PWM) stimulation. In six animals, hepatic RES function was assessed by calculating the phagocytic index (PI) using the disappearance of 99Tc sulfacolloid (5 mg/kg) iv. After baseline studies, the common bile duct was divided and ligated. The above studies and serum bilirubin were repeated at 3 weeks. Obstruction was then relieved by cholecystojejunostomy (CJ) and RES studies repeated monthly x 6. Preobstructive lymphocyte function showed a stimulation index ratio (log) of 0.85 +/- 0.25 for PHA, 0.75 +/- 0.3 for Con A, and 0.71 +/- 0.25 for PWM. With biliary obstruction, the values fell to -0.23 +/- 15 (P less than 0.006), -0.31 +/- 0.12 (P less than 0.006), and -0.29 (P less than 0.006), demonstrating impaired lymphocyte function. When tested lymphocytes were mixed with control pooled rabbit serum, however, no lymphocyte impairment was noted. Baseline hepatic PI was 6.02 +/- 0.18 and fell to 3.79 +/- 0.33 with obstruction (P less than .01) and remained low at (3.20 +/- 0.14) 1 month (P less than 0.01) and (3.33 +/- 0.23) at 3 months (P less than .01), after CJ but returned to normal (8.04 +/- 0.97) at 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Glomerular alterations associated with obstructive jaundice.

An immunohistochemical and clinicopathologic analysis of glomerular alterations was carried out in 20 autopsy cases with obstructive jaundice. The 20 cases without clinical nephritis had primary carcinoma of various locations, including the stomach, rectum, pancreas, and biliary tract. Mesangial IgA deposition was present on immunofluorescence staining in four cases, IgG in two cases, IgM in five cases, and C3 in four cases. Glomerular polymeric IgA containing A1, A2, and J chain was considered to originate from the gastrointestinal tract. All immunofluorescence-positive cases except one had electron-dense deposits in mesangial regions. These findings suggest that glomerular IgA deposition develops in a handful of patients suffering from obstructive jaundice, presumably due to the passive trapping of circulating immune complexes. Furthermore, glomerular IgA deposition in patients with obstructive jaundice is not influenced by duration or intensity of jaundice, and it unlikely induces clinical nephritis.

Aged↗
PubMed1989

Endotoxaemia and hepatic injury in obstructive jaundice.

To examine whether endotoxaemia contributes to the development of bile infarction and whether obstructive jaundice enhances endotoxin hepatotoxicity, the present study was undertaken in rats. The development of bile infarction and the elevation of serum transaminase activities in rats following ligation of the common bile duct were not prevented by administration of polymyxin B, neomycin, or lactulose, which have anti-endotoxin properties. Moreover, the morphological and functional changes in obstructive jaundice were not enhanced by administration of endotoxin. These data indicate that endotoxaemia does not contribute to the development of bile infarction. On the other hand, the administration of a small dose of endotoxin to rats with biliary obstruction--a dose which does not induce abnormalities of liver function tests or any morphological changes in the liver in non-jaundiced rats--led to focal hepatocellular coagulative necrosis and elevation of serum transaminase levels. These data indicate that endotoxin-induced hepatic injury is potentiated in obstructive jaundice.

Animals↗