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Results for “JAUNDICE, OBSTRUCTIVE”

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At least 19 recordsLinked to original sources
PubMed2006

[Neuroblastoma presenting as obstructive jaundice].

Obstructive jaundice as a presentation of abdominal tumors in childhood is extremely rare. To date, only 4 cases of neuroblastoma causing obstructive jaundice at diagnosis have been reported in children. We report a 4-year-old boy who presented to the emergency department with abdominal pain, jaundice, choluria and acholia. A diagnosis of unresectable, nonmetastatic neuroblastoma was made. Chemotherapy reduced the size of the tumor and relieved the symptoms of obstructive jaundice without the need for decompressive surgery. Abdominal tumors should be included in the differential diagnoses of obstructive jaundice in childhood.

Abdominal Neoplasms↗
PubMed1996

Vascular smooth muscle reactivity and endothelium derived relaxing factor in experimental obstructive jaundice.

Obstructive jaundice is associated with a predisposition to systemic hypotension and acute renal failure. Altered vascular reactivity may contribute to the development of hypotension. In this experimental study on dogs, alterations in vascular contractile responses to noradrenaline, serotonin and KCl were investigated. Contractile responses to noradrenaline, serotonin,,, KCL and relaxation responses to papaverin and acetylcholine were provoked in isolated femoral arteries of both control dogs and animals with obstructive jaundice. In this situation concentration-response curves of noradrenaline and serotonin were blunted when compared with controls. This blunting disappeared when endothelium was removed. In rings precontracted with phenylephrine, EDRF relaxation responses to acetylcholine were increased significantly as compared to controls: at lower concentrations maximal relaxation response occurred. Contractile responses to KCl and relaxation responses to papaverin did not differ between the groups, endothelium present or removed. These results indicate that obstructive jaundice induces a decrease in vascular contractile responses and an increased EDRF relaxation response. We suggest that an excess in the amount of released EDRF may be one of the causes inducing systemic hypotension in obstructive jaundice.

Animals↗
PubMedDate not supplied

Role of oxygen free radical scavengers in acute renal failure complicating obstructive jaundice.

Obstructive jaundice is associated with high morbidity and mortality. Major complications such as pulmonary dysfunction, renal failure and sepsis are frequently encountered. Recent studies and observations suggest that the free oxygen radicals (FORs) produced in obstructive jaundice may play a significant role in the etiopathogenesis of acute renal failure (ARF). Thirty rats were divided into three groups, as sham, control and treatment groups containing 10 rats each. Laparatomy was performed on each animal in the control and treatment groups and common bile ducts were ligated. Common bile duct was observed but was not ligated for the rats in the sham group. Saline solution injection was begun on the first day of surgical procedure and repeated once a day during the following 5 days. The same procedure was performed with oxygen radical scavenger dimethyl sulfoxide (1.5 mg/kg/day i.p.) instead of saline in the treatment group. The rats were sacrificed on the 7th postoperative day. On the 7th postoperative day, the bilirubin, urea and creatinine levels of the control and treatment groups were significantly higher in comparison with the sham group (p < 0.01). Although there was no statistically significant difference between the bilirubin levels of the control and treatment groups (p > 0.05), the urea and creatinine levels in the treatment group were significantly lower (p < 0.01). On the 7th postoperative day, the erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels of the control and treatment groups were significantly lower than those of the sham group (p < 0.01), whereas renal and erythrocyte malondialdehyde (MDA) levels were significantly higher (p < 0.01). Although SOD and GSH-Px levels did not differ significantly between the treatment and control groups (p > 0.05), renal and erythrocyte MDA levels of the treatment group were significantly lower than those of the control group (p < 0.01). The histopathological scores were significantly higher in the control and treatment groups (p < 0.01); there was no significant difference between the control and treatment groups (p > 0.05). FORs seem to play a significant role in the etiopathogenesis of renal failure in obstructive jaundice. Antioxidant treatment may decrease oxidative damage due to FORs and may prevent renal failure.

Acute Kidney Injury↗
PubMedDate not supplied

Effect of different enteral nutrients on bacterial translocation in experimental obstructive jaundice.

Obstructive jaundice leads to bacterial translocation (BT) by disruption of the gut barrier, intestinal microecology, and impaired host immune defence. The objective of the present study is to investigate the effects of different enteral nutrients on BT that is induced by obstructive jaundice in rats. Eighty male Wistar-Albino rats were randomly assigned into 4 groups. Group 1: 20 rats underwent laparotomy, common bile duct (CBD) was not actually ligated and transected, but sham ligation of CBD was performed. Groups 2-4: 60 rats underwent laparotomy, CBD ligation and transection. Group 1 and 2 rats were given rat chow, group 3 rats were fed a glutamine and arginine supplemented enteral diet, and group 4 rats were fed an arginine, m-RNA and omega-3 supplemented enteral diet, an immunonutrient. Rats in groups 3 and 4 had significantly less BT to mesenteric lymph nodes compared to rats in group 2 (p = 0.001). These findings suggest that oral administration of an arginine and glutamine supplemented diet and immunonutrition reduce BT in rats with obstructive jaundice.

Animals↗
PubMed1991

Induction of DNA replication and cell growth in rat liver by obstructive jaundice.

Obstructive jaundice, produced by ligating the common bile duct, induced a transient DNA replication followed by cell proliferation in rat liver. At 48 h after the operation, DNA polymerase alpha activity started to increase and reached its maximum level (more than twice the control) at day 4. At day 7, the enzyme level had decreased to the control level. Pulse-labeling experiment using radioactive thymidine showed that the rate of DNA synthesis increased approximately 2.5-fold in the same pattern as that of DNA polymerase alpha. The mitotic index in hepatocytes also increased 10-fold at day 4 and then decreased. The proliferation of liver cells induced by obstructive jaundice mimics the regeneration of partially hepatectomized liver, although the response was slightly delayed and the proliferation was transient.

Alanine Transaminase↗
PubMed1998

[Diagnosis and therapy of obstructive jaundice].

Obstructive jaundice is a sign of intra- or posthepatic blockage of bile flow. This diagnosis has to be differentiated from various other diagnoses such as disorders of bilirubin metabolism or hepatocellular causes of jaundice. An accurate evaluation of the past medical history and clinical examination of the patient can already establish obstruction as the cause of jaundice in most cases. For prevention of a cholangitis further imaging procedures should focus on rapidly establishing the cause and the location of obstruction. Further therapeutic procedures are dependent on the type of obstruction and the condition of the patient. Most importantly there should be a decompression of the biliary tree with ES or PTBD.

Cholestasis, Extrahepatic↗
PubMed1989

Hepatic recovery after biliary decompression of experimental obstructive jaundice.

Obstructive jaundice was produced in 11 dogs by common bile duct ligation for 4 weeks, then biliary decompression was performed by bilioenteric anastomosis. Animals were regularly studied over the 2 months after decompression by the following methods: (1) serum biochemistry was monitored; (2) light microscopic changes in serial liver biopsies were graded; (3) the respiratory characteristics of isolated hepatic mitochondria, obtained by open liver biopsy, were studied using an oxygen micro-electrode system; (4) in vivo handling of an hepatobiliary imaging agent (diisopropyl iminodiacetic acid) was studied by dynamic liver scintiscanning. None of these liver assessments were normalized after 7 to 10 days of biliary decompression. Our study suggests that biliary decompression of patients with extrahepatic biliary obstruction requires long periods of time to enable major recovery of the abnormal liver function induced by biliary obstruction.

Anastomosis, Surgical↗
PubMed1990

Adult hepatic fibropolycystic disease presenting as obstructive jaundice.

Obstructive jaundice caused by compression of the common hepatic duct by a simple hepatic cyst in a 31 year old Europid man is reported. The jaundice and duct compression resolved after percutaneous aspiration of the cyst under ultrasound direction and the patient has been well for 12 months.

Adult↗
PubMed1988

[Respiratory function of mitochondria fractionated from isolated hepatocytes of rats with obstructive jaundice].

Obstructive jaundice model was created using rats by the ligation of bile duct. One, 2, 3 weeks later, the respiratory function and morphology of the hepatic mitochondria were comparatively evaluated between mitochondria directly fractionated from liver tissue and mitochondria from isolated hepatocytes. Respiratory function of the former deteriorated with the duration of jaundice. ATP synthesis decreased to 75% of the control at 1 and 2 weeks, and 58% at 3 weeks after ligation. On the contrary, it was 97%, 88% and 87% of the control. On the contrary, it was 97%, 88% and 87% of the control at 1, 2 and 3 weeks in the latter. By electron microscopic examination, the size of mitochondria of the jaundiced liver is inconsistent and smaller in general than the control. These data suggest that the deterioration of mitochondrial function in the jaundiced liver is not caused mainly by the disturbance of mitochondria themselves, but caused by the respiratory inhibitory factors which exist around the mitochondria.

Animals↗
PubMed2002

Increased nitric oxide production in hepatocytes is involved in liver dysfunction following obstructive jaundice.

BACKGROUND: Obstructive jaundice damages critical functions in the liver. However, the mechanisms involved in hepatic dysfunction are obscure. Nitric oxide is implicated in liver injury under various pathological conditions. We previously reported that proinflammatory cytokine interleukin-1beta (IL-1beta) stimulated the production of nitric oxide in hepatocytes, which was associated with mitochondrial dysfunction. Studies were performed to examine whether obstructive jaundice influences the production of nitric oxide in hepatocytes and alters hepatic energy metabolism. MATERIAL AND METHODS: Hepatocytes were isolated and cultured from a rat model of obstructive jaundice or sham control. Nitric oxide production, ATP content, and ketone body ratio (acetoacetate/beta-hydroxybutyrate; KBR) were compared between the two groups in the presence of IL-1beta. RESULTS: Hepatocytes obtained from obstructive jaundice rats markedly increased the levels of nitric oxide production stimulated by IL-1beta compared with those from sham control. Western blot analysis revealed that the enhancement of nitric oxide production was a posttranslational event, since protein levels of inducible nitric oxide synthase (NOS) were unchanged between the two groups. IL-1beta decreased cellular ATP content in obstructive jaundice but not in sham control. Further, the KBR, which is a marker of mitochondrial redox state, was lower in obstructive jaundice than in sham control. Addition of N(G)-monomethyl-L-arginine, an inhibitor of NOS, abolished the decreases in ATP content and KBR as well as the nitric oxide production. CONCLUSIONS: These results indicate that a priming of nitric oxide production following obstructive jaundice is associated with the alteration of hepatic energy metabolism in part through mitochondrial dysfunction. Regulation of nitric oxide production may be a useful therapy for preventing liver dysfunction in obstructive jaundice.

Adenosine Triphosphate↗
PubMed2006

Evidence for intestinal oxidative stress in patients with obstructive jaundice.

BACKGROUND: Obstructive jaundice results in failure of the intestinal barrier with consequent systemic endotoxemia associated with septic complications. We have recently shown that gut barrier failure in experimental obstructive jaundice is associated with high intestinal oxidative stress. This study was undertaken to investigate whether oxidative alterations occur in the intestinal mucosa of patients with obstructive jaundice. PATIENTS AND METHODS: Fifteen patients with malignant biliary obstruction and no signs of cholangitis and 15 control patients were subjected to duodenal biopsy to assess intestinal oxidative stress, estimated by lipid peroxidation (malondialdehyde - MDA) and glutathione redox state [reduced glutathione (GSH), glutathione disulphide (GSSG) and GSH/GSSG ratio]. In addition, mucosal biopsies were examined histologically and intestinal mucosal protein content was determined biochemically as an index of intestinal trophic state. RESULTS: Patients with obstructive jaundice presented high levels of intestinal oxidative stress, with significantly increased lipid peroxidation (P < 0.001). Glutathione redox state was also suggestive of high intestinal oxidative stress in jaundiced patients, indicated by significantly decreased GSH (P = 0.001) and GSH/GSSG ratio (P = 0.006) and increased GSSG (P = 0.026). Histological examination showed a mild infiltration of the lamina propria by chronic inflammatory cells in obstructive jaundice, whereas duodenal architecture remained intact and epithelial continuity was retained. Duodenal mucosa was atrophic in jaundiced patients as indicated by a significant reduction of mucosal protein content compared with controls (P = 0.001). Among oxidative stress parameters, intestinal GSH exhibited a significant positive correlation with mucosal protein content (r = 0.588, P = 0.021). CONCLUSIONS: Obstructive jaundice in humans induces intestinal oxidative stress, which may be a key factor contributing to intestinal barrier failure and the development of septic complications in this patient population.

Aged↗
PubMedDate not supplied

Effect of N-acetylcysteine on blood and tissue lipid peroxidation in lipopolysaccharide-induced obstructive jaundice.

In obstructive jaundice, free radical production is increased and antioxidative activity is reduced. N-Acetylcysteine (NAC) has a beneficial effect with anti-inflammatory and antioxidant activity, acting as a free radical scavenger. NAC inhibits inducible nitric oxide synthase, suppresses cytokine expression/release, and inhibits adhesion molecule expression and nuclear factor kappa B. The aim of this study was to investigate the effects of NAC on liver/renal tissue and serum lipid peroxidation in lipopolysaccharide (LPS)-induced obstructive jaundice. We randomized 60 rats into 6 groups: group 1, Sham; group 2, obstructive jaundice (OJ) induced after bile-duct ligation; group 3, OJ + NAC (100 mg kg- 1 subcutaneously); group 4, OJ + LPS (10 mg kg-1); group 5, OJ + NAC + LPS; and group 6, OJ + LPS + NAC. For each group, the biochemical markers of lipid peroxidation and the antioxidant products were measured in serum and liver/renal tissue after sacrifice. Almost all lipid peroxidation products levels were increased and antioxidant products levels were decreased in groups who received LPS (groups 4, 5, and 6), but the effect was less remarkable when NAC was administered before LPS (group 5). The same trend was seen for groups with OJ +/- LPS who did not received NAC or received it after induced toxemia (groups 2, 4, and 6) as compared to groups 1 and 3. Moreover, in the case of OJ + LPS, rats treated with NAC before LPS (group 5) had lower lipid peroxidation products levels and higher antioxidant products levels as compared to those who did not received NAC (group 4). This phenomenon was not reproducible with NAC administered after LPS (group 6). Thus, results of this study showed that NAC prevents the deleterious effects of LPS in obstructive jaundice by reducing lipid peroxidation in serum and liver/renal tissue if administered before LPS. Nonetheless, NAC failed to prevent the lipid peroxidation in the case of established endotoxemia in obstructive jaundice.

Acetylcysteine↗
PubMed2000

Impaired Kupffer cell function and effect of immunotherapy in obstructive jaundice.

BACKGROUND: Obstructive jaundice is frequently associated with septic complications. This study examined the influence of biliary obstruction on bacterial clearance and translocation. The study focused on the phagocytic and killing activities of Kupffer cells and the preventive effect on bacterial translocation of OK-432, which is a hemolytic streptococcal preparation developed as a biological response modifier. METHODS: To study the mechanism of sepsis in obstructive jaundice, two groups of Wistar rats were examined: rats subjected to common bile duct ligation (CBDL) and rats subjected to a sham operation. Bacterial clearance, organ distribution, hepatic blood flow, and phagocytic function of Kupffer cells were examined. To evaluate the effect of OK-432 on bacterial translocation, rats were divided into three groups: sham operation + phosphate-buffered saline (PBS), CBDL + PBS, and CBDL + OK-432. RESULTS: In this study, clearance of Escherichia coli. from the peripheral blood in CBDL rats was decreased significantly compared with that in sham-operated rats. Significant decreases in E.coli trapped in the liver and in hepatic blood flow were observed in CBDL rats compared with sham-operated rats. Phagocytic activity and superoxide production of Kupffer cells isolated from CBDL rats were significantly lower than in sham-operated rats. The incidence of bacterial translocation in CBDL rats was increased significantly, and oral administration of OK-432 prevented it. CONCLUSION: The results suggest that susceptibility to infection in obstructive jaundice is due to impaired phagocytic function of Kupffer cells. Furthermore, obstructive jaundice promotes bacterial translocation, and OK-432 may be useful in preventing this translocation.

Animals↗
PubMed2003

Non-Hodgkin lymphoma presenting with obstructive jaundice.

BACKGROUND: Obstructive jaundice is a rare presenting feature of non-Hodgkin lymphoma (NHL). Lymphomatous masses in the peripancreatic and hepatic hilar regions are potentially difficult to diagnose. METHODS: A retrospective analysis was undertaken of patients presenting with obstructive jaundice secondary to NHL at a tertiary care hepatobiliary unit. RESULTS: Over a 7-year period, six adults and three children with NHL were managed. The site of the lymphomatous mass was at the hepatic hilum in six patients and the peripancreatic area in three. Diagnostic procedures included a laparotomy and biopsy in four patients, hepatic trisectionectomy in two, percutaneous biopsy in two and lymph node biopsy in one patient. Percutaneous biopsy confirmed the diagnosis in both the patients in whom it was attempted. One patient died following liver resection. Chemotherapy was the mainstay of treatment and achieved complete remission in four patients, partial remission in three and no response in one patient. Two patients subsequently required operation for a benign biliary stricture after achieving complete remission. CONCLUSION: NHL must be considered in the differential diagnosis of obstructive jaundice in adults and children. Attempts must be made to diagnose the condition using non-operative techniques. Chemotherapy is the mainstay of treatment. Late benign strictures of the bile duct requiring operation may develop.

Adolescent↗
PubMed2000

External and internal-external biliary drainage in children with malignant obstructive jaundice.

BACKGROUND: Obstructive jaundice is an uncommon but important clinical problem in children with cancer. Percutaneous transhepatic biliary drainage is widely used to relieve malignant biliary obstruction in adults, but its use in children has not been well described. MATERIALS AND METHODS: Six patients aged between 1 and 17 years underwent external or internal-external biliary drainage to relieve malignant obstructive jaundice. Biochemical, haematological and microbiological parameters were measured before the procedure and repeated 7-9 days later. RESULTS: External or internal-external biliary drainage was technically successful in all patients. No patient developed clinically significant biliary sepsis. Asymptomatic duodenal perforation occurred in one patient with bulky duodenal tumour following conversion from external to internal-external drainage. CONCLUSIONS: External biliary drainage may be successfully performed in children with malignant obstructive jaundice.

Adolescent↗