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Results for “Bilirubinemia”

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At least 19 recordsLinked to original sources
PubMed2005

[Survival of patients with malignant biliary stricture based on endoscopic brushing and on bilirubinemia].

BACKGROUND: Pancreatic cancer and cholangiocarcinoma are the main causes of malignant biliary stricture. Both types of cancers have dismal survival rates, and treatment has little or no effect on prolonging the patients lives. Prognostic definition at initial endoscopic retrograde cholangiopancreatography is important to choose the most suitable management. AIM: To analyse endoscopic brushing and bilirubinemia importance in determination of the survival of patients with malignant biliary stricture. METHODS: Patients with biliary strictures diagnosed during endoscopic retrograde cholangiopancreatography were submitted to double brushing cytology. Serum samples were taken from all patients for bilirubinemia assay. Patients were followed to determine the final diagnosis and survival rates. RESULTS: A total of 50 patients with biliary stricture underwent endoscopic retrograde cholangiopancreatography (40 ultimately found to have a final diagnosis of malignant disease). Hyperbilirubinemia or cytology brushing positive for malignancy was related to a shorter survival rate. CONCLUSION: This research data demonstrate the possibility of determining the prognosis of patients with malignant biliary stricture using endoscopic brushing results and bilirubinemia levels.

Adult↗
PubMedDate not supplied

[Computed tomographic cholangiography in the diagnosis of choledocholithiasis in severe bilirubinemia].

Cholangiography used with oral or intravenous contrast agents has gained wide acceptance as the most objective preoperative diagnostic technique for choledocholithiasis. However, an indirect contrasting technique has been found quite unfit in patients with severe bilirubinemia. Despite this, the authors employed indirect contrasting of the bile ducts in 104 patients with severe bilirubinemia in combination with computed tomographic cholangiography. Contrasting took place in 90 (86.5%) patients. In complete obstruction of the choledochus (10 patients), intraductal hypertension prevents the contrast agent and bile from entering the hepatic ducts and the contrast agent is excreted by the kidneys. Thus, the use of the latest equipment and computers allows one to detect minor biliary contrast concentrations during indirect contrasting of the biliary tract in severe bilirubinemia.

Aged↗
PubMed2001

Differing pathogenesis of perinatal bilirubinemia in glucose-6-phosphate dehydrogenase-deficient versus-normal neonates.

The objective was to compare the contribution to perinatal bilirubinemia of hemolysis and UDP-glucuronosyltransferase (UGT) gene promoter polymorphism, seen in Gilbert's syndrome, between glucose-6-phosphate dehydrogenase (G-6-PD)-deficient and -normal neonates. Serum total bilirubin (STB) values from 52 G-6-PD-deficient and 166 G-6-PD-normal term, male neonates, sampled within 3 h of delivery (first sample) and on d 3 (second sample), were analyzed in relation to blood carboxyhemoglobin corrected for inspired CO (COHbc), an accurate index of hemolysis, and UGT promoter genotype. COHbc values (% total Hb) were greater in G-6-PD-deficient neonates than controls: first sample 1.00 +/- 0.25% versus 0.84 +/- 0.24%, p < 0.0001; second sample 0.83 +/- 0.20% versus 0.76 +/- 0.19%, p = 0.002. First sample COHbc and STB values did not correlate in either the G-6-PD-deficient or control groups, whereas second sample COHbc values correlated significantly with corresponding STB values in the control population only (r = 0.28, p = 0.0007). At second sampling, there was a higher allele frequency of the variant UGT promoter among those with STB values > or =75th percentile than those <75th among the G-6-PD-deficient neonates (0.60 versus 0.33, respectively, p = 0.025), but not controls (0.31 versus 0.40, respectively, p = 0.24). Among those infants with at least one variant UGT promoter allele, STB values were higher in the G-6-PD-deficient neonates than controls at second sampling only (181 +/- 56 microM versus 149 +/- 46 microM, respectively, p = 0.03). Both within and between the G-6-PD-deficient and control groups, our data demonstrate changing and differing contributions of hemolysis and UGT promoter polymorphism to bilirubinemia during the first 3 d of life.

Base Sequence↗
PubMed1992

Micro-invasive management of neonatal bilirubinemia.

The present study aims at analyzing the suitability of transcutaneous approach and filter paper technique using Minolta Jaundicemeter in the management of neonatal bilirubinemia. I compared serially measured values of Serum Bilirubin Index (SBI) by using filter paper technique and transcutaneous bilirubin index (TcBI) with serum bilirubin level determined by Diazo Method in 100 clinically jaundiced newborns and in 25 neonates at birth. The estimation of TcBI is simple, quick, reliable and non-traumatic to the newborn with no workload on the laboratory and technician. However, different nomograms are to be prepared for different laboratories, as also for the newborns with difference in skin pigmentation, gestational age and after phototherapy. SBI determined by filter paper technique eliminates these limitations. Moreover, the linear correlation was stronger between SBI and Diazo values (r = 0.9343, p < 0.001) in comparison to TcBI with Diazo values (r = 0.9090, p < 0.001). Further SBI readings almost correspond with actual serum bilirubin levels while corresponding TcBI values were much higher especially at higher diazo values. Thus TcBI can be used routinely for the surveillance of neonatal jaundice till it reaches a level corresponding to critical serum bilirubin level at which active management is required. At this point, serum bilirubin level may be confirmed by SBI.

Bilirubin↗
PubMed1979

Vitamin E and neonatal bilirubinemia.

A study was designed to determine the effect of vitamin E on bilirubinemia in the preterm infant. Twenty infants with birth weight between 1,000 and 1,500 gm and 20 infants with birth weights between 1,501 and 2,000 gm were studied. Half the infants in each birth weight group received vitamin E administered intramuscularly in a total dose of 50 mg/kg during days 1 to 3 of life; the remaining infants served as controls. The administration of vitamin E produced significantly increased plasma tocopherol concentrations and normal hydrogen peroxide hemolysis tests by the end of the first week of life. Infants with birthweights less than or equal to 1500 gm who received vitamin E demonstrated a significant decrease in serum bilirubin on day 3 of life (6.5 +/- 2.2 vs 8.8 +/- 2.2 mg/dl) as well as a significant decrease in peak serum bilirubin during the first week of life (8.3 +/- 2.2 vs 10.6 +/- 2.6 mg/dl). The duration of phototherapy also was significantly less in the vitamin E-supplemented group (48 +/- 18 vs 107 +/- 31 hours). These differences were less pronounced in infants with birth weights more than 1,500 gm.

Bilirubin↗
PubMed1994

Fetal cocaine exposure and neonatal bilirubinemia.

To assess the effect of fetal exposure to cocaine on neonatal serum bilirubin values, we compared 17 infants whose cocaine exposure was confirmed by urine toxicology studies, with no evidence of other drug exposure by history or urinalysis, with 31 sequentially born healthy term infants without evidence of maternal drug use. The mean (+/- SD) bilirubin concentration in control infants was 110 +/- 32 mumol/L (6.5 +/- 1.9 mg/dl) at 30.5 +/- 5.4 hours of age, compared with 55 +/- 26 mumol/L (3.2 +/- 1.5 mg/dl) at 30.8 +/- 5.3 hours in cocaine-exposed infants (p < 0.001). We also compared the abilities of cocaine and clofibrate, a known inducer of bilirubin uridine diphosphate-glucuronosyl transferase (BGT), to induce drug and bilirubin metabolizing pathways in young male Sprague-Dawley rats. Animals received drugs or saline solution for 7 days, and livers were assayed for cytochrome P-450, peroxisomal beta-oxidase, delta 5-3-ketosteroid isomerase (KSI), glutathione-S-transferase (GST), and BGT. Cocaine was a weak inducer of GST but a strong inducer of KSI, a member of the GST family of enzymes that is closely associated with bilirubin transport (ligandin) in liver, and a moderately strong inducer of BGT. Neither drug increased cytochrome P-450 levels, and only clofibrate induced peroxisomal beta-oxidase. We conclude that cocaine appears to induce bilirubin metabolizing pathways, resulting in a lower risk of neonatal hyperbilirubinemia.

Animals↗