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Bilirubin serum levels

Type I Crigler-Najjar syndrome is a rare autosomal recessive disorder. It is characterized by severe congenital jaundice (serum bilirubin usually exceeds 20 mg/dL) due to mutations in the gene encoding bilirubin-UGT activity in hepatic tissues. The disease is often fatal within the first 15 months of life. Children with this condition have been treated with phototherapy, resulting in some reduction in plasma bilirubin levels. Phenobarbital has no effect on the formation of bilirubin glucuronides in patients with type I Crigler-Najjar syndrome. A liver transplant may be curative. [Pg.283]

Results are means of duplicate determinations. Serums are from the routine laboratory. Bilirubin levels are assayed values. [Pg.119]

Hyperbilirubinemia Abnormally high concentrations of the bile pigment bilirubin in the bloodstream. Hyperbilirubinemia is defined as a total serum bilirubin level greater than 5 mg/dL. [Pg.1568]

Bilirubin is diazotized with para-sulphonyl benzene diazonium compound and the absorbance of the resulting azobilirubin is measured at 600 nm to determine bilirubin level in the biological fluid e.g., blood serum. In usual practice, a serum blank is run simultaneously by reacting the serum with caffeine, sulphanilic acid and tartaric acid, and the absorbance of the blank is measured at 600 nm which is subsequently subtracted from the azobilirubin absorbance initially obtained before the bilirubin level is finally determined. [Pg.57]

Orotic acid and aspartic acid, when given orally to full-term, healthy newborn infants for the first 4 days of life, can significantly lower their serum bilirubin level [187]. The effect of aspartic acid is immediate, whereas that of orotic acid is delayed [187]. [Pg.291]

Bilirubin effects depend on the method used for analysis. Interferences in direct serum protein methods are observed at bilirubin levels greater than 5 mg/100 ml (K7). A sample containing 20 mg of bilirubin per 100 ml increased the apparent total protein by 0.2 g/100 ml. Concentrations of bilirubin as high as 20 mg/ml do not effect albumin assays using bromocresol green binding (D12), but have a marked effect on these assays when [2-(p-hydroxyphenylazo)-benzoic acid] (HABA) dye is used (A7b). [Pg.7]

Drug/Lab test interactions Thiazides may decrease serum PBI levels without signs of thyroid disturbance. Thiazides also may cause diagnostic interference of serum electrolyte, blood, and urine glucose levels (usually only in patients with a predisposition to glucose intolerance), serum bilirubin levels, and serum uric acid levels. In uremic patients, serum magnesium levels may be increased. Bendroflumethiazide may interfere with the phenolsulfonphthalein test due to decreased excretion. In the phentolamine and tyramine tests, bendroflumethiazide... [Pg.679]

Hepatic Effects. An animal study revealed that hexachlorobutadiene can affect the liver. However, the effects were less serious compared to effects in the kidney at the same dose. Liver weights were decreased in female rats fed 5 mg/kg/day or greater hexachlorobutadiene for 4 weeks (Jonker et al. 1993b). Histological examinations were not performed. However, evaluation of serum biochemical parameters in males revealed increased enzyme activity (aspartate aminotransferase, p <0.02) and total bilirubin levels (p<0.02) at doses of 20 mg/kg/day (highest dose tested). [Pg.36]

Liver injury is clinically defined as an increase of serum alanine amino transferase (ALT) levels of more than three times the upper limit of normal and a total bilirubin level of more than twice the upper limit of normal [4]. The clinical patterns of liver injury can be characterized as hepatocellular (with a predominant initial elevation of ALT), cholestatic (with an initial elevation of alkaline phosphatase) or mixed. The mechanisms of drug-induced hepatotoxicity include excessive generation of reactive metabolites, mitochondrial dysfunction, oxidative stress and inhibition of bile salt efflux protein [5]. Better understandings of these mechanisms in the past decades led to the development of assays and models suitable for studying such toxic mechanisms and for selecting better leads in the drug discovery stage. [Pg.345]

Hepatic Effects. Carbon tetrachloride has been known for many years to be a powerful hepatotoxic agent in humans and in animals. The principal clinical signs of liver injury in humans who inhale carbon tetrachloride are a swollen and tender liver, elevated levels of hepatic enzyme (aspartate aminotransferase) in the serum, elevated serum bilirubin levels and the appearance of jaundice, and decreased serum levels of proteins such as albumin and fibrinogen (Ashe and Sailer 1942 McGuire 1932 New et al. 1962 Norwood et al. 1950 Straus 1954). In cases of acute lethal exposures, autopsy generally reveals marked liver necrosis with pronounced steatosis (Jennings 1955 Markham 1967 Smetana 1939), and repeated or chronic exposures leads in some cases to fibrosis or cirrhosis (McDermott and Hardy 1963). [Pg.31]

Detection of liver injury has commonly been associated with alternations in serum levels of certain hepatic enzymes and proteins. Elevation in bilirubin levels following exposure (Barnes and Jones 1967) has been detected in humans, as have decreased serum levels of secreted liver proteins (e.g., albumin and fibrinogen) (Ashe and Sailer 1942 McGuire 1932 New et al. 1962 Norwood et al. 1950 Straus 1954). Elevations in serum levels of enzymes (e.g., ALT, AST, LDFI, OCT) have been reported following acute- and intermediate-duration exposures to carbon tetrachloride in animals (Bruckner et al. 1986 FI ayes et al. 1986 Sakata et al. 1987). [Pg.87]

In die peripheral blood system, crocetin derivatives prevent an elevation in bilirubin levels [3] and also reduce elevated levels of serum cholesterol and triglyceride [4]. Anti-tumor activity of saffron is observed in mice transplanted with several types of tumor cell lines including sarcoma 180, Ehrlich ascites carcinoma, and Dalton s lymphoma ascites... [Pg.314]

Treatment of male Charles-Foster rats with sublethal doses of xylene (0.2 mL of 5 mmol/L extra-pure xylene solution on alternate days for 30 days isomeric composition not indicated) resulted in slight increases of serum aspartate and alanine aminotransferase and alkaline phosphatase activities and bilirubin concentration (Rana Kumar, 1993). A slight increase in alanine aminotransferase activity was also observed after a 3.5-week treatment of male Wistar rats with zneto-xylene (800 mg/kg bw per day on five days per week, by gavage) (Elovaara et al., 1989). Inhalation exposure of C3H/HeJ mice to /jora-xylenc (1200 ppm [5200 mg/m ], 6 h per day for four days) did not affect the serum alanine or aspartate aminotransferase or lactate dehydrogenase activities, or bilirubin level (Selgrade et al., 1993). [Pg.1195]

He suggested that the effect may be due to an interference in enterohepatic circulation and/or an inhibition of the absorption of dietary cholesterol. The latter hypothesis is likely the more accurate explanation, as we found no other evidence of an interference in enterohepatic circulation, such as changes in serum bilirubin levels. [Pg.475]

The liver is the principal metabolic organ, and hepatic disease or dysfunction may impair drug elimination. Any alteration in the serum albumin or bilirubin levels and in the prothrombin time indicates impaired liver function. Similarly, skin bruising and bleeding tendency indicate decreased production of clotting factors by the liver. [Pg.20]

Hepatic Effects. Jaundice, hepatomegaly, and increased serum bilirubin levels have been observed in humans with white phosphorus-induced bums (Song et al. 1985 Summerlin et al. 1967 Walker et al. 1947). [Pg.91]

Unfortunately, visual assessment has not been correlated with actual bilirubin levels. Therefore, laboratory measurement of the actual total serum bilirubin levels is mandatory. The timing of these measurements becomes important because of the bilirubin load and level of maturation of bilirubin-UDP-glucuronyltransferase. [Pg.241]

A serum total bilirubin level in excess of 50 pmol/L can produce clinical jaundice in adults. In neonates a level of 80 pmol/L or above... [Pg.77]

In adults, yellowing of the skin or jaundice usually occur when serum bilirubin is higher than 50 pmol/L. In neonates, a bilirubin level in... [Pg.89]

The effect of ethinylestradiol 50 pg daily on liver function tests was examined in five women with PBC. These patients had been previously exposed to various HRT preparations (oestrogen or an oestrogen-progestogen combination). Three of the women, who had normal or near-normal serum bilirubin before treatment, tolerated HRT well. However, the remaining two, who were profoundly jaundiced (with serum bilirubins of 193 pmol/L and 365 pmol/L, respectively) before treatment, experienced a further increase in serum bilirubin levels two to three months after starting treatment. A decrease in bilirubin levels occurred in both patients upon withdrawal of ethinylestradiol [18]. [Pg.266]

Scleral icterus occurs from a serum bilirubin level of 1.6-1.8 mg/dl upwards. At the same time, the conjunctiva is icterially discoloured. Jaundice is based on the affinity of the elastic fibres for bilirubin. [Pg.85]

Differentiation between obstructive and parenchymatous cholestasis is possible in > 90% of cases. A serum bilirubin level of up to 30 mg/dl is not seen as a methodological impediment to sequential scintigraphy. In incomplete obstruction with nondilated bile ducts, this technique provides more information than can be obtained using ultrasound. (17, 18)... [Pg.194]

In about 90% of all neonates, jaundice occurs after the first 2-5 days of life and rarely exceeds 6 mg/dl serum bilirubin. In premature infants, bilirubin levels can rise to 10-12 mg/dl. The cause is related to a number of factors .) reinforced degradation of haemoglobin as a result of the short erythrocyte survival span of 70-90 days (120 days in adults), (2.) reduction in cellular transport proteins, above all ligandin, (i.) deficiency of uri-dyltransferase and glucuronosyltransferase, and (4.) increasing intestinal absorption of meconium bilirubin. [Pg.219]


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See also in sourсe #XX -- [ Pg.695 ]




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