Verfahren zur Photometrischen Bestimmung des Blutbilirubins

Jendrassik, L.; Cleghorn, R. A.

doi:10.1007/bf01779503

Cited by 107 publications

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“…17,21 Both total and nonabsorbable suture, a double ligation separated by approximately 2 mm was performed. The common bile duct was conjugated plasma bilirubin were measured by an adaptation of the diazo method of Jendrassik and Grof 22 for total bilirudivided between the ligations. The abdominal incision was then closed.…”

Section: Methodsmentioning

confidence: 99%

Reversible impairment of neonatal hepatobiliary function by maternal cholestasis

et al. 1996

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importance of the implications derived from these findThe effect of total blockage of maternal biliary excreings both in the nutrition and management of human tion during the last third of the pregnancy on the matuneonates demands further evaluation of the hepatobiliration of hepatobiliary function was investigated in neoary function of babies born after alterations of fetal-manatal rats. Extrahepatic obstruction of the common bile ternal bile acid homeostasis, such as in maternal obstetduct on day 14 of pregnancy induced a marked enhanceric cholestasis. (HEPATOLOGY 1996;23:1208-1217.) ment in serum bilirubin-mainly conjugated bilirubinand bile acid concentrations as compared with shamoperated pregnant rats. Excretion of bile acids by the Normal fetal development requires efficient transfer kidney was significantly increased, whereas fecal elimi-across the placenta. Nutrients are supplied by the nation of these compounds was almost abolished. Most mother while certain potentially toxic compounds cross of the cholestatic mothers (CMs) (77%) were able to carry the placenta, mainly in the fetus-to-mother direction. pregnancy to term and lactation until weaning (21 days Among the latter are bile acids. Both in humans and after birth). The body and liver weights of their offspring experimental animals, the onset of bile acid biosynthewere lower than for offspring of control healthy mothers sis precedes the development of efficient mechanisms in all postnatal periods considered. Serum bile acid concentrations were higher in the fetuses and neonates of involved in enterohepatic circulation.1 Hepatic insuffiCMs. This difference was evident up to 1 week after ciency with respect to bile acid secretion is found in weaning and disappeared in young adult animals (8 both premature and full-term infants.2 This is accomweeks old). When the bile secretion rate was investi-panied by a marked immaturity of small intestinal gated in these animals at 4 or 8 weeks of age, no signifi-transport of bile acids. [3][4][5] Because the accumulation of cant difference was found as far as nonstimulated bile bile acids within the fetus can seriously challenge the flow and bile acid output was concerned. However, the viability of pregnancy, such compounds must be transbiliary response to stepwise sodium taurocholate (TC) ferred to the mother, whose liver is able to excrete them intravenous infusion showed that 4-week-old neonates into bile. Therefore, fetal-maternal bile acid homeostaof CMs had impaired bile acid secretion. Moreover, the sis requires both functional placental transfer and normaximal secretion rate (SR max ) for TC was significantly reduced (030%), whereas the choleretic ability of tauro-mal maternal hepatobiliary function. cholate was not modified. This alteration was not selec-Obstetric cholestasis is a pathological situation chartive for bile acids. The SR max for bromosulfophthalein acterized by a 10-to 100-fold increase in postprandial (BSP) was also significantly lowered (040%). These dys-bile acid concentrations in the m...

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Section: Methodsmentioning

confidence: 99%

Reversible impairment of neonatal hepatobiliary function by maternal cholestasis

et al. 1996

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“…The activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) were analyzed using the methods described by Reitman and Frankel [16] and Kind and King [17], respectively, using Randox kits (Randox Laboratories, UK); serum albumin was estimated using the methods described by Northam and Widdowson [18]; total bilirubin was determined colorimetrically using the method described by Jendrassik and Grof [19], while the total protein was assayed by the direct Biuret method as described by Gornall, Bardawill and David [20].…”

Section: Liver Function Testsmentioning

confidence: 99%

Acute and sub-chronic oral toxicity studies on the methanol leaf extract of Gnetum africanum Welw in wistar rats.

Udeh¹,

Anaga²,

Asuzu³

2018

Am J Res Med Sci

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Aim: Acute and subchronic toxicity studies were performed on Gnetum africanum Welw leaves using well-established guidelines and methods. In spite of its use as a herbal remedy, there is a dearth of data on toxicity studies of the plant extract. Method: Gnetum africanum leaves were identified by a plant taxonomist, air-dried, pulverized, and extracted with 80% methanol for 48 hours in July 2015. The extract was concentrated in-vacuo and stored as Gnetum africanum extract (GAE) at 4°C. Thirty-five male albino rats randomly divided into seven groups (n = 5) were used for acute toxicity test, which was done in August 2015. Rats in groups 1-6 were given GAE at 500, 1,000, 2,000, 3,000, 4,000 and 5,000 mg/kg, respectively, while group 7 rats received 10 ml/ kg distilled water. Feed and water were provided and they were observed for signs of toxicity for 48 hours. A 90-day subchronic toxicity study was conducted using 56 rats of four groups (n = 14) in December 2015-March, 2016. Group 1 received feed without GAE, while groups 2-4 were given feed with GAE at 10, 20 and 40 mg/kg respectively. Four rats from each group were bled on days 30, 60, and 90 for clinical biochemistry and sacrificed for histopathological examination. Result: The median lethal dose (LD 50 ) was greater than 5,000 mg/kg while no-observed-adverse-effect-level was 40 mg/kg. Serum marker enzymes and creatinine were not increased in rats given extract in feed, while there were no histopathological lesions in the organs studied. Conclusions: The extract is safe at both the acute and subchronic levels. ARTICLE HISTORY

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“…The CN patient in family D was not considered further because he required chronic therapy with high-dose phenobarbital, which decreases plasma bilirubin levels by increasing hepatic clearance of UCB. 28 In each subject, after an overnight fast, serum levels of total bilirubin (TB) and direct-reacting bilirubin were determined by diazo methods 29,30 at least 3 times within 6 months prior to the BSP study; the upper normal limit for TB (mean ϩ 2 SD) was 20 mol/L. The early fractional plasma disappearance rate (K 1 ) of BSP (E. Merck, Darmstadt, Germany) at the low dose of 0.59 mol/kg body weight was determined after an overnight fast, as described previously.…”

Section: Methodsmentioning

confidence: 99%

Hepatic uptake of organic anions affects the plasma bilirubin level in subjects with Gilbert's syndrome mutations in UGT1A1

Persico¹

2001

Hepatology

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Although in Gilbert's syndrome (GS), bilirubin glucuronidation is impaired due to an extra TA in the TATA box of the promoter of the gene for bilirubin UDP-glucuronosyltransferase 1 (UGT1A1), many GS homozygotes lack unconjugated hyperbilirubinemia. Accordingly, an additional defect in bilirubin transport might be required for phenotypic expression. Plasma bilirubin and the early fractional hepatic uptake rate (BSP K 1 ) of a low dose of tetrabromosulfophthalein (0.59 mol/kg) were determined in (1) 15 unrelated patients with unconjugated hyperbilirubinemia plus 12 random controls; (2) 4 unrelated GS probands and 15 of their first-degree relatives; (3) 7 unrelated patients with hemolysis due to ␤-Thalassemia minor. Subjects were classified by DNA sequencing of the promoter region of both UGT1A1 alleles. In group 1, GS homozygotes showed a highly significant negative linear correlation between plasma bilirubin levels and BSP K 1 . BSP K 1 values overlapped considerably between GS and normal subjects, whereas, in group 2, they were clustered within, and sharply segregated among, families. Patients with hemolysis, despite elevated plasma bilirubin levels, had mean BSP K 1 values similar to the normal subjects. Within each GS subgroup with defined UGT1A1 mutations, the plasma bilirubin level is in part determined by the organic anion uptake rate, assessed by early plasma disappearance of low-dose BSP. The lower BSP uptake in GS is not secondary to the hyperbilirubinemia, but probably caused by (an) independent, genetically determined defect ( Gilbert's Syndrome (GS) is an inherited form of mild, chronic, unconjugated hyperbilirubinemia, 1-3 which is associated with an extra TA in the promoter region of both alleles for bilirubin UDP-glucuronosyltransferase 1 (UGT1A1). [4][5][6][7][8] The resultant 65% decrease in transcription of the (TA) 7 TAA mutant alleles explains the impaired conjugation of bilirubin found in all GS patients. 9,10 The abnormal (TA) 7 TAA allele has a reported prevalence of 34% to 40% in white adults 4,5 and Sephardic Jewish neonates. 11 Thus, 12% to 16% should be and are homozygous for this abnormality, 4-8 yet only 3% to 9% of such populations, or less than half the expected proportion of homozygotes, have an increased level of unconjugated bilirubin (UCB) in plasma. 7,8,[12][13][14] This suggests that additional steps in bilirubin metabolism and/or transport must be impaired for hyperbilirubinemia to be manifested in (TA) 7 TAA homozygotes with reduced expression of UGT1A1.Thus far, both increased bilirubin production (from hemolysis, 1-3,11,15,16 which may not be overt [16][17][18] ) and/or decreased hepatic uptake of UCB have been documented in many presumed GS subjects. Some also exhibit decreased plasma clearance of tetrabromosulfophthalein (BSP) 20-22 and other organic anions, 20,23,24 including several therapeutic agents, [24][25][26] which appear to share hepatic uptake mechanisms with UCB. 27 With BSP, impaired uptake may be unmasked in GS patients if the administered dose is reduced ...

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Verfahren zur Photometrischen Bestimmung des Blutbilirubins

Cited by 107 publications

References 0 publications

Reversible impairment of neonatal hepatobiliary function by maternal cholestasis

Reversible impairment of neonatal hepatobiliary function by maternal cholestasis

Acute and sub-chronic oral toxicity studies on the methanol leaf extract of Gnetum africanum Welw in wistar rats.

Hepatic uptake of organic anions affects the plasma bilirubin level in subjects with Gilbert's syndrome mutations in UGT1A1

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