Jaundice Enzymes

DIDANOSINE Although rare, pancreatitis and peripheral neuropathy are possible adverse reactions seen with didanosine The nurse must be alert for symptoms of pancreatitis (nausea, vomiting, abdominal pain, jaundice, elevated enzymes) and for signs of peripheral neuropathy (numbness, tingling, or pain in the feet or hands). It is important to immediately report these signs to the primary health care provider. 

HDL is synthesized and secreted from both liver and intestine (Figure 25—5). However, apo C and apo E are synthesized in the liver and transferred from fiver HDL to intestinal HDL when the latter enters the plasma. A major function of HDL is to act as a repository for the apo C and apo E required in the metabohsm of chylomicrons and VLDL. Nascent HDL consists of discoid phosphohpid bilayers containing apo A and free cholesterol. These hpoproteins are similar to the particles found in the plasma of patients with a deficiency of the plasma enzyme lecithimcholesterol acyltransferase (LCAT) and in the plasma of patients with obstructive jaundice. LCAT—and the LCAT activator apo A-I— bind to the disk, and the surface phosphohpid and free cholesterol are converted into cholesteryl esters and... 

Table 32-3 summarizes laboratory results obtained on patients with three different causes of jaundice—hemolytic anemia (a prehepatic cause), hepatitis (a hepatic cause), and obstruction of the common bile duct (a posthepatic cause). Laboratory tests on blood (evaluation of the possibihty of a hemolytic anemia and measurement of prothrombin time) and on semm (eg, electrophoresis of proteins activities of the enzymes ALT, AST, and alkahne phosphatase) are also important in helping to distinguish between prehepatic, hepatic, and posthepatic causes of jaundice. 

The variant was found In a 22 year old woman with chronic hemolytic anemia characterized by a persistent retlculocytosls, development of gallstones requiring cholecystectomy, frequent episodes of jaundice, dark urine, and falling PCV value. Her mother, maternal grandfather, and sister have a similar clinical picture In all patients red cell enzymes are elevated with a retlculocytosls of about 10%, and 2,3-DPG levels are normal ... 

Herbal remedies that have been reported to be he-patotoxic include chaparral (Larrea tridentata), germander (Teucrium chamaedrys), and life root (Senecio aureus) [18]. Cases reported patients developing jaundice, fatigue, pruritus, markedly elevated serum liver enzyme levels, severe cholestasis, hepatitis, and hepatocellular injury or necrosis documented by serial liver biopsies [19-21]. Signs and symptoms may occur as early as 3 weeks to as late as 7 months following ingestion [20,21]. 

Some liver damage has been reported in humans after acute exposure to high doses. In workers exposed to high levels of acrylonitrile vapors, mild jaundice was diagnosed (Wilson 1944). In a case of an accidental dermal exposure of a man, enzyme levels in the blood suggestive of liver injury were reported for several days (Vogel and Kirkendall 1984). These effects appeared to be fully reversible. 

Several other metal complexes have promising photodynamic activity and are currently under development (248). Metalloporphyrins inhibit the enzyme heme oxygenase for example, chromium porphyrin and mesoporphyrin are potent inhibitors of heme oxygenase both in vitro and in vivo (249, 250) and are being used for the treatment of the neonatal jaundice. 

Physiologic jaundice in the newborn, especially premature infimts (enzymes may not be fuUy induced)... 

Hepatomegaly, jaundice, and altered liver function tests have been reported in accidental poisonings with DME An outbreak of toxic liver disease was associated with DME exposure at a fabric coating factory. Thirty-six of 58 workers had elevations of either aspartate aminotransferase or alanine aminotransferase. Serological tests excluded known infectious causes of hepatitis in all but two cases. After modification of work practices and removal of the most severely affected from exposure, improvement in liver enzyme abnormalities and symptoms occurred in most patients. Medical surveillance of the working population for 14 months revealed no further cases of toxic liver... 

If any patient develops symptoms suggesting hepatic dysfunction, check liver enzymes. If jaundice is observed, discontinue therapy. 

Diarrhea nausea vomiting jaundice liver enzyme abnormalities. Azotemia elevated BUN/creatinine increased serum uric acid levels (in patients predisposed to gouty arthritis) thrombocytopenia megaloblastic anemia weakness dizziness Hypokalemia headache dry mouth anaphylaxis. ... 

Hepatic Hepatic cholestasis, hepatic toxicity, hepatitis, hyperbilirubinemia, increased liver enzymes, jaundice, liver failure. 

Renal/Hepatic function impairment Hepatic dysfunction, including increased liver enzymes and hepatitis, with or without jaundice, has been reported with the use of telithromycin. In the presence of severe renal impairment (Ccr less than 30 mL/min), including patients who need dialysis, the dose of telithromycin has not been established. 

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). 

Hepatic Effects. Human and animals studies of carbon tetrachloride toxicity reveal that the principal adverse systemic effect in injury to the liver, as evidenced by clinical signs jaundice, swollen and tender liver), biochemical alterations (elevated levels of hepatic enzymes in the blood, loss of... 

Four weeks after receiving a bone marrow transplant, Mary Smith developed jaundice and a skin rash on her hands, feet, and face. She also had occasional episodes of vomiting and diarrhea. Qtnical chemistry results showed her serum hver enzymes (LDH, ALT) and bUirubin level to be elevated. What is the most likely cause of Mary s symptoms and what is the best therapy ... 

Pruritus, rash, photosensitivity, dizziness, drowsiness, headache, diarrhea, nausea, vomiting, abdominal pain, increased liver enzymes, jaundice, increased BUN and creatinine, weakness, hearing loss... 

The most frequently reported side effects are Gl-related complaints i.e. nausea, dyspepsia, abdominal pain and diarrhoea. Other side effects include headache, skin rash and transient elevation of liver enzymes, hepatic dysfunction with or without jaundice and psychosis. 

The appearance of laboratory abnormalities does not require cessation of treatment however, if enzyme levels do not stabilize or return to normal, VPA should be discontinued and an alternate mood-stabilizing agent such as lithium used in its place. Liver function tests should be monitored more often during the first several weeks of therapy and every 6 to 12 months afterward. Routine liver function testing probably does not significantly prevent the occurrence of these unpredictable drug effects. Therefore, patients should be cautioned to immediately report symptoms of possible early hepatotoxicity such as easy bruising, decreased appetite, malaise, jaundice, and periorbital or dependent edema. In summary ... 

Ingestion of copper sulfate by humans causes vomiting, cramps, convulsions, and as little as 27 grams of the compound may cause deulh. An important part of the toxicity of copper to both plants and animals is probably due to its combination with thiol groups of certain enzymes, thereby inactivating them. The effects ol chronic exposure to copper in animals are cirrhosis of the liver, failure of growth, and jaundice. 

In a retrospective review of 497 patients taking propylthiouracil for hyperthyroidism, clinically overt hepatitis developed in six patients at 12-49 days after starting the drug (50). Jaundice and itching were present in five, fever in two, rash in two, and arthralgia in one. Serum bilirubin, alanine transaminase, and alkaline phosphatase were increased in five, four, and six patients respectively. The type of hepatic injury was cholestatic in three, hepatocellular in one, and mixed in two. There were no differences in age, sex, drug dose, or serum thyroid hormone concentrations at time of diagnosis in those with hepatic injury compared with those without. Liver function normalized in all patients at 16-145 days after withdrawal of propylthiouracil. In addition to these cases of overt liver injury, 14% of the cohort had mild asymptomatic liver enzyme rises at a mean of 75 days after the start of treatment. 

A 74-year-old woman who had used acarbose for 3 months developed progressive weakness and jaundice (60). Her bilirubin was 152 pmol/l (direct bilirubin 96 pmol/1). All of her liver enzymes were substantially raised. All other investigations were normal, except that she was positive for hepatitis C antigen. After withdrawal of acarbose everything became normal within 1 month. 

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