HİPOTANSİYONUN YOL AÇTIĞI BİR İSKEMİK HEPATİT OLGUSU
İskemik hepatit, karaciğerde dolaşım yetmezliği sonucu, 24 saat içinde serum transaminaz ve laktik dehidrogenaz seviyelerinin normale göre 75-100 katı kadar yükselip, 7-10 gün içinde tekrar normale dönmesi ile karakterize klinik bir tablodur. İskemik hepatite hipotansiyon, hipoksi veya her ikisi birlikte öncülük edebilir ve bu olgularda hipotansiyonun en sık nedeni kardiyovasküler hastalıklardır. Histopatolojik olarak karaciğer biyopsisinde sentrilobüler nekrozun görülmesi tipiktir. Bu makalede miyokard infaktüsü sonrası gelişen hipotansiyon sonucunda karaciğer enzimlerinde ani ve belirgin yükselme ve sonrasında hızlı düşme ile ortaya çıkan iskemik hepatitli bir olguyu sunduk ve hastalığın özelliklerini tartıştık
A Case of Hypotension Induced Ischemic Hepatitis
Ischemic hepatitis is a disease clinically characterized by a sudden rise in serum transaminases and lactic dehydrogenase levels to 75- to 100-fold normal levels, followed by resolution to near normal levels within 7 to 10 days as a result of an acute circulatory failure due to cardiovascular disease in most of the reported cases. Such impairment of liver function tests is due to haemodynamic hepatocyte injury that results from failure of hepatic perfusion. Liver biopsy shows focal centrilobular necrosis. Ischemic hepatitis should be anticipated in all patients with a recent history of systemic hypotension. In this paper we describe a case of ischemic hepatitis, in which an acute derangement of liver function tests occurred as a consequence of myocardial infarction and discuss features of this disease.
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- 1. Fuchs S, Bogomolski-Yahalom V, Paltiel O, Ackerman
Z. Ischemic hepatitis: clinical and laboratory
observations of 34 patients. J Clin Gastroenterology
1998; 26:183-6.
- 2. Lefkovitch JH, Mendez L. Morphologic features of
hepatic injury in cardiac disease and shock. J Hepatol
1986; 2 : 313-327.
- 3. Gitlin NG, Serio KM. Ishemic hepatitis: Widening
horizons.Am J Gastroenterol 1992; 7 : 831.
- 4. Johnson RD, O'Connor ML, Kerr RM. Extreme serum
elevations of aspartate aminotransferase. Am J
Gastroenterol 1995; 90 : 1244.
- 5. Seeto RK, Fenn B, Rockey DC. Ischemic hepatitis:
clinical presentation and pathogenesis. Am J Med
2000; 109: 109-13.
- 6. Henrion J, Luwaert R, Colin L, Shimtz A, Scharipa M,
Heller FR. Hypoxic hepatitis. A propective, clinical
and hemodynamic study of 45 episodes. Gastroentrol
Clin Biol 1990; 14 : 836-841.
- 7. Dunn GD, Hayes P, Breen KJ, Schenker S. The liver in
conjestive heart failure. A review Am J Med Sci 1973 ;
265 : 174-189.
- 8. Schafer DF, Sorrell MF. Vascular disease of the liver,
ischemic hepatitis. In: Feldman M, Scharschmidt BF,
Sleisenger MH (eds). Sleisenger&Fordtran's
Gastrointestinal and Liver Disease, 6 edition, WB
Saunders Company, Philadelphia, 1998 ;p:1194.
- 9. Naschitz JE , Slobodin G, Lewis R J, Zuckerman E,
Yeshurun D. Heart diseases affecting the liver
and liver diseases affecting the heart. Am Heart J.
2000: 140(1) : 111-20.
- 10. Potter JM, Hickman PE. Cardiodepressant drugs and
the high mortality rate associated with ischemic
hepatitis Critical Care Medicine 1992; 20: 474-478.
- 11. Mathurin P, Durand F, Ganne N, Mollo JL, Lebrec D,
Degott C, Erlinger S, BenhamouJP, Bernuau J.
Ischemic hepatitis due to obstructive sleep apnea
Gastroenterology 1995; 109 : 1682-1684.
- 12. Holland SM, Gallin JI. Disorders of granulocytes and
monocytes. In: FauciAS, Braunwald E, Isselbacher KJ,
Wilson JD, Martin JB, Kasper DL, Hauser SL, Longo
DL. Harrison's Principles of internal medicine, 14th
edition, NewYork, McGraw-Hill, 1998; p: 355.
- 13. Cassidy WM, Reynolds TB. Serum lactic
dehydrogenase in the differential diagnosis of acute
hepatocellular injury. J Clin Gastroenterol 1994; 19:
118-21.