Liver Messages for use on World Liver Day

Today is world liver day: Liver Messages for use

Dr K K Aggarwal

1. Many drugs, NSAIDs, paracetamol, anti-diabetics, anti-epileptic drugs, Anti TB drugs can raise liver enzymes.
2. Many herbs can also raise liver enzymes.
3. SGOT/SGPT > 2 suggests alcoholic liver disease [[Cohen, JA, Kaplan, MM. The SGOT/SGPT ratio — an indicator of alcoholic liver disease. Dig Dis Sci 1979; 24:835.]
4.  SGOT can be more than SGPT in NASH, hepatitis C Cirrhosis, Dengue, acute muscle injury, H1N1 flu, Wilson’s disease.
5. 2 fold rise of Gama GT with SGOT/SGPT 2:1 unless proved otherwise is alcoholic liver disease. [Moussavian, SN, Becker, RC, Piepmeyer, JL, et al. Serum gamma-glutamyl transpeptidase and chronic alcoholism. Influence of alcohol ingestion and liver disease. Dig Dis Sci 1985; 30:211.]
6. In Alcoholic Hepatitis SGOT is never more than 8 fold elevated. {uptodate: http://www.uptodate.com/online/content/topic.do?topicKey=hep_dis/14684&selectedTitle=3%7E150&source=search_result} “It is rare for the SGOT/ AST to be greater than eightfold elevated and even less common for the SGPT /ALT to be greater than fivefold elevated. The ALT may even be normal even in patients with severe alcoholic liver disease.”
   
   
7. Positive HBsAg and core antibody means chronic infection. Go for e-antigen, e-antibody, and Hepatitis B DNA test.
8. Positive HBsAg & surface antibodies means immunity to Hepatitis B.
9. Positive HBV DNA & positive e antigen indicates viral replication.
10. Positive HBsAg & negative HBV DNA & negative e-antigen suggests carrier state.
11. Serum Fe /TIBC > 45%, ferritin of > 400 mg/ml in man (300 in women) suggest hereditary hemochorotosis.
12. Immediately after muscle injury, SGOT, SGPT may rise with SGOT/SGPT ratio of more than 3.  
13. In muscle injury CPK & LDH rises in proportion with rise in SGOT and SGPT.
14. SGOT & SGPT may be high in thyroid disorders.
15. Auto-immune Hepatitis will always have hyper gama globulimia.
16. Persistently high SGOT & SGPT more than two times normal require liver biopsy. http://www.uptodate.com/online/content/topic.do?topicKey=hep_dis/14684&selectedTitle=3%7E150&source=search_result
    
    
17. Over 2-fold polyclonal elevation of immunuglobin suggest auto-immune Hepatitis.
18. An elevated Gama GT with otherwise normal liver test should not warrant further liver workup.  [http://www.uptodate.com/online/content/topic.do?topicKey=hep_dis/14684&selectedTitle=3%7E150&source=search_result
19.  Gama GT may be high in patients taking anti-epileptic drugs.
20. Approximately 70 to 80 percent of patients with hepatic encephalopathy improve after correction of precipitating factors.
21. Minimal hepatic encephalopathy can alone be treated with lactulose.
22. Zinc deficiency is common in patients with cirrhosis and in those with hepatic encephalopathy
23. hypokalemia increases renal ammonia production
24. Cleansing of the colon is a rapid and effective method to remove ammoniagenic substrates.
25. There is no good clinical evidence supporting protein restriction in patients with acute hepatic encephalopathy.
26. Ammonia is the best characterized neurotoxin that precipitates hepatic encephalopathy.
27. Only 50 percent of patients with variceal hemorrhage stop bleeding spontaneously.
28. There is more than 90% spontaneous bleeding cessation rate in patients with other forms of upper gastrointestinal hemorrhage.
29. In variceal bleed, after active bleeding stops, there is a high risk of recurrent bleed for the next 6 weeks.
30. The greatest risk or variceal re-bleed is within the first 48 to 72 hours
31. Over 50 percent of all early variceal re-bleeding episodes occur within the first 10 days.
32.  Bacterial infections are present in up to 20 percent of patients with cirrhosis who are hospitalized with gastrointestinal bleeding; up to an additional 50 percent develop an infection while hospitalized.
33. Short-term (maximum 7 days) antibiotic prophylaxis should be instituted in any patient with cirrhosis and GI hemorrhage.
34. Elective surgery is contraindicated in patients with histologic evidence of alcoholic hepatitis.
35.  The MELD score is a statistical model predicting survival in patients with cirrhosis.
36. Anesthesia mortality in cirrhosis at 30 days range from 6 percent (MELD score, <8) to more than 50 percent (MELD score, >20).
37. Patients with mild to moderate chronic liver disease without cirrhosis usually tolerate surgery well
38. Patients with NASH do not appear to have excessive mortality following elective surgery.
39. Moderate to severe steatosis means more than 30 percent of hepatocytes contain fat.
40. Following any surgery, patients with liver disease should be observed closely for hepatic decompensation.
41. Asymptomatic patients with mild chronic hepatitis are at low risk for complications during any surgery
42. Infection with the hepatitis C virus (HCV) can result in both acute and chronic hepatitis.
43. HCV accounts for approximately one-third of HCC cases
44. Most patients with chronic infection are asymptomatic or have only mild nonspecific symptoms.
45. Alcohol promotes the progression of chronic HCV even in patients with a relatively low alcohol intake.
46. High risk patients testing should include HBsAg and anti-HBs. Patients who are negative for these markers should be vaccinated.
47.  Type 1 classic autoimmune hepatitis: + ve antibodies to nuclei (ANA) and/or smooth muscle (ASMA) and antiactin antibodies (AAA).
48.  Type 2 autoimmune hepatitis: + ve antibodies to liver/kidney microsomes (ALKM-1), and/or antibodies to a liver cytosol antigen (ALC-1 or LC1).
49. Fulminant E hepatitis is more likely in those who are pregnant and in those who are malnourished or have preexisting liver disease.
50. An effective vaccine against HEV has been developed but is not yet commercially available.
51.  The degree of liver enzymes can help in differentiating between hepatocellular and cholestatic processes.
52. SGOT, SGPT values less than eight times normal may be seen in either hepatocellular or cholestatic liver disease.
53. SGOT, SGPT values 25 times normal or higher are seen primarily in hepatocellular diseases.
54. The SGOT rarely exceeds 300 U/L in alcoholic hepatitis.
55. Patients with acute hepatitis C are usually asymptomatic.
56.  While SGOT, SGPT values less than eight times normal may be seen in either hepatocellular or cholestatic liver disease, values 25 times normal or higher are seen primarily in hepatocellular diseases. Patients with jaundice from cirrhosis may have normal or only slight elevations of the liver enzymes.
57. Wilson disease (Serum aminotransferases typically less than 2,000 IU/L (AST often greater than ALT) Roberts, EA, Schilsky, ML. A practice guideline on Wilson disease. Hepatology 2003; 37:1475.
58. Muscle disorders — Elevated serum aminotransferases may be caused by disorders that affect organs other than the liver, most commonly striated muscle. Serum AST and ALT may both be elevated with muscle injury. Their ratio depends in part upon when they are assessed relative to the muscle injury. Immediately after muscle injury, the AST/ALT ratio is generally greater than three, but approaches one within a few days because of a faster decline in the serum AST. Peak AST and ALT levels are variable. In one series, peak AST levels range from as low as 235 IU to as high as 10,000 IU while peak ALT ratios range from as low as 115 IU/L to as high as 850 IU/L [Nathwani, RA, Pais, S, Reynolds, TB, Kaplowitz, N. Serum alanine aminotransferase in skeletal muscle diseases. Hepatology 2005; 41:380.]
59. NASH: Hepatic steatosis and an associated condition, non-alcoholic steatohepatitis (NASH), may present solely with mild elevations of the serum aminotransferases, which are usually less than fourfold elevated. NASH is a condition more common in women and associated with obesity and type 2 diabetes mellitus. (See "Nonalcoholic steatohepatitis".) In contrast to alcohol related liver disease, the ratio of AST to ALT is usually less than one.
60. Dengue SGOT > SGPT [J Clin Virol. 2007 Mar;38(3):265-8. Epub 2007 Feb 15.] [January 2008, Vol. 37 No. 1 http://www.annals.edu.sg/PDF/37VolNo1Jan2008/V37N1p82.pdf]