Bilirubin hepatitis

Conditicms that increase direct bilirubin Hepatic damage Bile duct obstruction... 

Adverse effects include nausea, vomiting, diarrhoea, abdominal discomfort, dry mouth, taste disturbances headache, dizziness, insomnia myalgia, rash, pruritus, dry skin, hyperpigmentation, nephrolithiasis, dysuria, haematuria, crystalluria, proteinuria elevated liver enzymes and bilirubin, hepatitis neutropenia, haemolytic anaemia and hyperglycaemia etc. 

Methotrexate Oral or IM 7.5-15 mg per week Baseline AST, ALT, ALK-P, albumin, total bilirubin, hepatitis B and C studies, CBC with platelets, Scr CBC with platelets, AST, albumin every 1 -2 months... 

Infusion reactions fevers, chills, nausea, vomiting, hypotension, dyspnea myelosuppression may be severe and prolonged tumor lysis syndrome WBCs should be reduced to <30,000/mm prior to administration if possible, to decrease risk increased liver function tests and bilirubin, hepatic veno-occlusive disease... 

Older adults are particularly susceptible to a potentially fatal hepatitis when taking isoniazd, especially if they consume alcohol on a regular basis. Two other antitubercular drugs rifampin and pyrazinamide, can cause liver dysfunction in the older adult. Careful observation and monitoring for signs of liver impairment are necessary (eg, increased serum aspartate transaminase, increased serum alanine transferase, increased serum bilirubin, and jaundice). 

Knowledge of the biochemistry of the porphyrins and of heme is basic to understanding the varied functions of hemoproteins (see below) in the body. The porphyrias are a group of diseases caused by abnormalities in the pathway of biosynthesis of the various porphyrins. Although porphyrias are not very prevalent, physicians must be aware of them. A much more prevalent clinical condition is jaundice, due to elevation of bilirubin in the plasma. This elevation is due to overproduction of bilirubin or to failure of its excretion and is seen in numerous diseases ranging from hemolytic anemias to viral hepatitis and to cancer of the pancreas. 

When bifimbin in the blood exceeds 1 mg/dL (17.1 lmol/L), hyperbifimbinemia exists. Hyperbilirubinemia may be due to the production of more bilirubin than the normal fiver can excrete, or it may result from the failure of a damaged fiver to excrete bilirubin produced in normal amounts. In the absence of hepatic damage, obstmction of the excretory ducts of the fiver—by preventing the excretion of bilirubin—will also cause hyperbilirubinemia. In all these situations, bifimbin accumulates in the blood, and when it reaches a certain concentration (approximately 2-2.5 mg/dL),... 

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. 

Conjugated hyperbilirubinemia commonly results from blockage of the hepatic or common bile ducts, most often due to a gallstone or to cancer of the head of the pancreas. Because of the obstruction, bilirubin diglu-curonide cannot be excreted. It thus regurgitates into the hepatic veins and lymphatics, and conjugated bilirubin appears in the blood and urine (choluric jaundice). 

The commonest causes of obstructive (posthepatic) jaundice are cancer of the head of the pancreas and a gallstone lodged in the common bile duct. The presence of bilirubin in the urine is sometimes referred to as choluria—therefore, hepatitis and obstruction of the common bile duct cause choluric Jaundice, whereas the Jaundice of hemolytic anemia is referred to as acholuric. The laboratory results in patients with hepatitis are variable, depending on the extent of damage to parenchymal cells and the extent of micro-obstruction to bile ductules. Serum levels of ALT and AST are usually markedly elevated in hepatitis, whereas serum levels of alkaline phosphatase are elevated in obstructive liver disease. 

The Group II (biliary tract) enzymes are abnormal usually when the serum bilirubin concentration is also abnormal. Most commonly used is alkaline phosphatase which is a highly sensitive indicator of biliary tract obstruction, perhaps because the enzyme is synthesized as an induced response to obstruction of even small bile ducts. Most techniques used to identify the origin of an elevated serum alkaline phosphatase are not very useful from a clinical viewpoint (23). The simultaneous measurement of GMT activity has been found to be useful in differentiating between the hepatic and bony origin of alkaline phosphatase. An increased GMT activity in a patient with an increased ALP activity is a good indication that there is biliary biliary tract disease (62,63). 

Solberg and co-workers have applied discriminate analysis of clinical laboratory tests combined with careful clinical and anatomic diagnoses of liver disease in order to determine which combinations of the many dozen liver diagnostic tests available are the bes t ( ). These authors found that the measurement of GPT, GMT, GOT, ALP and ceruloplasmin were the most useful enzymatic tests, when combined with other non-enzymatic tests such as the measurement of bilirubin, cholesterol, hepatitis-B associated Australian antigen, etc. Another group of highly useful enzymes, not discussed in this review, are those clotting factors and the enzyme cholinesterase which are synthesized by the liver cells. 

In the bile-duct-ligated rat, hepatic mitochondrial lipid peroxides are increased and correlate with serum levels of alkaline phosphatase, bilirubin and alanine aminotransferase (Sokol et al., 1991). Dietary vitamin E deficiency resulted in relatively higher lipid peroxide and bilirubin... 

Host factors can help to ensure selection of the most appropriate antimicrobial agent. Age is an important factor in antimicrobial selection. With regard to dose and interval, renal and hepatic function varies with age. Populations with diminished renal function include neonates and the elderly. Hepatic function in the neonate is not fully developed, and drugs that are metabolized or eliminated by this route may produce adverse effects. For example, sulfonamides and ceftriaxone may compete with bilirubin for binding sites and may result in hyperbilirubinemia and kernicterus. Gastric acidity also depends on... 

Elevated hepatic transaminases (greater than 5 times upper limit of normal) or bilirubin (greater than 2.5 upper limit of normal)... 

TC, lamivudine ABC, abacavir APV, amprenavir AST, aspartate aminotransferase ALT, alanine aminotransferase ATV, atazanavir CBC, complete blood cell count D/C, discontinue ddl, didano-sine d4T, stavudine EFV, efavirenz FTC, emtricitabine P1BV, hepatitis B virus F1CV, hepatitis C vims HIV, human immunodeficiency virus IDV, indinavir IV, intravenous LFT, liver function tests LPV/r, lopinavir + ritonavir NNRTI, nonnucleoside reverse transcriptase inhibitor NRTI, nucleoside reverse transcriptase inhibitor NVP, nevirapine PI, protease inhibitor PT, prothrombin time T.bili, total bilirubin TDF, tenofovir disoproxiI fumarate TPV, tipranavir ULN, upper limit of normal ZDV, zidovudine. 

Cui, Y., et al. Hepatic uptake of bilirubin and its conjugates by the human organic anion transporter SLC21A6J. Biol. Chem. 2001, 276, 9626-9630. 

Progressive liver damage (shock liver) manifests as elevated serum hepatic transaminases and unconjugated bilirubin. Impaired synthesis of clotting factors may increase prothrombin time (PT), international normalized ratio, and activated partial thromboplastin time (aPTT). 

Routine liver assessment tests include alkaline phosphatase, bilirubin, aspartate transaminase, alanine transaminase, and y-glutamyl transpeptidase (GGT). Additional markers of hepatic synthetic activity include albumin and prothrombin time. The substances are typically elevated in chronic inflammatory liver diseases such as hepatitis C, but may be normal in others with resolved infectious processes. 

Mild elevations of serum bilirubin, /globulin, and hepatic transaminase (alanine transaminase and aspartate transaminase) values to about twice normal in acute anicteric disease. 

Hepatic Effects. Liver function tests (serum bilirubin, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transferase) completed in 11 hexachloroethane workers were within the normal range (Selden et al. 1994). Plasma hexachloroethane levels in these workers, who wore protective equipment, were 7.3 + 6.04 pg/L at the time of the tests (Selden et al. 1993). Mild skin and mucous membrane irritation were reported in the exposed group, suggesting that exposure may have been through either the inhalation or dermal routes of exposure. 

Hepatic Effects. Liver function tests (serum bilirubin, alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase) were not affected in 11 hexachloroethane-exposed workers who wore protective clothing (Selden et al. 1993). 

Litwack G, Ketterer B, Arias IM (1971) Ligandin a hepatic protein which binds steroids, bilirubin, carcinogens and a number of exogenous organic anions. Nature 234 466 167 Lubchenco J, Gaines SD (1981) A unified approach to marine plant-herbivore interactions. 

Hepatic Effects. An increase in serum alkaline phosphatase was noted in workers exposed to unspecified levels of cyanide however, serum bilirubin was found to be within the normal range in these workers (Kumar et al. 1992). 

Enhanced bilirubin level may suggest drug toxicity, bile-tract obstruction, hepatitis and hepatic dysfunction,... 

Increased bilirubin levels are caused due to the intake of large doses of such drugs as chloroquine, vitamin K, sulpha-drugs, tetracyclines, paracetamol, nicotinic acid and monoamine oxidase inhibitors (e.g., iproniazid RP 1.0 nialamide RP 1.8 isocarboxazid RP 3.1 phenelzine RP 18 pheniprazine RP31 and tranylcypromine RP 45), where RP designates the Relative Potency based on the tiyptamine potentiation test. The elevated levels are due to hepatic injury, and... 

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