Journal of the Louisiana State Medical Society
Table 1. 18 And, for the risk of alcohol-related liver disease, recent studies have shown that the risk begins at 30 grams of ethanol per day. 19 By report, the decedent in the current case ingested “a pint of gin” each day. With conversion, this translates into roughly 16 ounces of liquor of daily use or 10 times the amount that defines moderate drinking. Diagnosing alcoholic liver disease can be a challenge for clinicians. Physical and laboratory findings are often nondiagnostic, especially in patients with early alcoholic liver disease. Patients commonly deny alcohol abuse and frequently underreport alcohol consumption. Therefore, clinicians must have a low threshold of suspicion for alcohol abuse and rely on indirect evidence such as information from family, questionnaires, or observation of physical, social, and psychological consequences of abuse. 5 As clini- cians may utilize liver biopsy information to help make clinicopathologic correlates about patients, it is important for them to consider whether or not MDBs were demonstrated along with steatosis, whether histologic staining was via the customary H&E or required use of immunohistochemical modalities, and whether there were an abundance of or a paucity of either vague or well-established forms of intra- cytoplasmic MBDs. By not only adding these descriptive features to the pathologist’s report, but also by increasing the clinician’s awareness of their meaning, the level of index of suspicion for whether chronic alcohol usage has served to play a role in the liver derangement being demonstrated may effectively be enhanced. ACKNOWLEDGEMENTS The authors would like to gratefully acknowledge the support of the Orleans Parish Coroner’s Office: Dr. Frank Minyard and Chief Investigator JohnGagliano for providing the case material for this report. REFERENCES 1. FrankeWW, DenkH, SchmidMet al. Ultrastructural, biochemical and immunologic characterization of Mallory bodies in livers of griseofulvin treated mice. Lab Invest 1979;40:207-220. 2. Denk H, Krepler E, Lackinger U, et al. Immunological and biochemical characterization of the keratin related component of Mallory bodies: a pathological pattern of hepatocytic cytokeratins. Liver 1982;2:165-175. 3. Strnad P, Zatloukal K, Stumptner C et al. Mallory Denk bodies: lessons learned from keratin containing hepatic inclusion bodies. Bio Biophsy Acta 2008;1782:764-774. 4. Crawford JM. Histologic findings in alcoholic liver disease. Clin Liver Dis 2012;16: 699. 5. O’Shea RS, Dasarathy S, McCullough AJ, et al. Alcoholic liver disease. Hepatology 2010; 51:307. 6. Zatloukal K, French SW, Stumptner C et al. From Mallory to Mallory-Denk bodies: what, how and why? Exper Cell Res 2007:2033-2049. 7. Mallory F. Cirrhosis of the liver. Five different types of lesions from which it may arise. Bul Johns Hopkins Hosp 1911;22:69-75. 8. Jenson K, Gluud C. The Mallory body: morphological, clinical and experimental studies (Part 1 of a literature survey). Hepatology
1994; 20:1061-1077. 9. RayMB. Distribution patterns of cytokeratin antigen determinants in alcoholic and nonalcoholic liver diseases. HumPathol 1987;18:61- 66. 10. Brunt EM. Nonalcoholic steatohepatitis. Semin Liver Dis 2004;24:3- 20. 11. Brunt EM. Non alcoholic fatty liver disease in: AD Burt, BC Portmann, LD Farrell (Eds.), McSween’s Pathology of the Liver , Churchill Livingstone Elsevier, 2007 12. Wanless IR, Lentz JS. Fatty liver hepatitis (steatohepatitis) and obesity: an autopsy study with analysis of risk factors. Hepatology 1990;12:1106-1110. 13. Denk H, Frank WW, Kerkaschki D et al. Mallory bodies in experimental animals and man. Int Rev Exper Pathol 1979; 20:77- 121. 14. Peters M, Liebman HA, Tong MJ et al. Alcoholic hepatitis: granulocyte chemotactic factor form Mallory body stimulated human peripheral blood mononuclear cells. Clin Immunol Immunopathol 1983; 28:418-430. 15. Denk H, Franke WW. Rearrangement of the hepatocyte cytoskeleton after toxic damage: involution, dispersal and peripheral accumulation of Mallory body material after drug withdrawl. Dur J Cell Biol 1981;23:241-249 16. http://www.cdc.gov/injuryresponse/alcohol-screening (Accessed on October 26, 2013). 17. U.S. Department of Agriculture and U.S. Department of Health and Human Services. Dietary Guidelines for Americans, 7th Edition, Washington, DC: US Government Printing Office; 2010, p. 30–32. 18. http://pubs.niaaa.nih.gov/publications/ RethinkingDrinking (Accessed on October 26, 2013). 19. Bellentani S, Saccoccio G, Costa G, et al. Drinking habits as cofactors of risk for alcohol induced liver damage. The Dionysos Study Group. Gut . 1997;41:845–850.
In the Department of Pathology at Louisiana State University School of Medicine in New Orleans, Dr. Nuttli is a third-year Pathology Resident and Dr. McGoey is an Associate Professor of Pathology and Residency Program Director.
48 J La State Med Soc VOL 166 January/February 2014
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