Microvesicular Steatosis of the Liver

Hautekèete, M.; Degott, Claude; Benhamou, J P

doi:10.1080/17843286.1990.11718105

Cited by 73 publications

(46 citation statements)

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“…Since it may be associated with different risk factors, we included in this study only overweight individuals who did not present significant variation in body weight during the last three months. These patients presented a high NAFLD prevalence (23)(24)(25), often associated with the presence of fibrosis (7).…”

Section: Discussionmentioning

confidence: 99%

Serum laminin, type IV collagen and hyaluronan as fibrosis markers in non-alcoholic fatty liver disease

Santos

Leite-Mor

Kondo

et al. 2005

Braz J Med Biol Res

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Hepatic fibrosis in patients with non-alcoholic fatty liver disease is associated with progression of the disease. In the present study, we analyzed the discriminative ability of serum laminin, type IV collagen and hyaluronan levels to predict the presence of fibrosis in these patients. In this preliminary report, we studied 30 overweight patients divided into two groups according to the absence (group I, N = 19) or presence (group II, N = 11) of fibrosis in a liver biopsy. Triglycerides, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltranspeptidade, hyaluronan (noncompetitive fluoroassay), type IV collagen, and laminin (ELISA) were determined. Group II presented significantly higher mean laminin, hyaluronan, type IV collagen, and aspartate aminotransferase values, which were due to the correlation between these parameters and the stage of fibrosis in the biopsy (Spearman's correlation coefficient, rS = 0.65, 0.62, 0.53, and 0.49, respectively). Analysis of the ROC curve showed that laminin values >282 ng/ml were those with the best diagnostic performance, with 87% accuracy. Association of laminin with type IV collagen showed improvement in the positive predictive value (100%), but with reduction in diagnostic sensitivity (64%). When compared with the criteria of Ratziu et al. [Gastroenterology (2000) 118: 1117-1123] for the diagnosis of septal fibrosis, laminin values presented a better diagnostic accuracy (83 vs 70%). Determination of extracellular matrix components in serum, especially of laminin, may identify patients with non-alcoholic fatty liver disease and fibrosis and these components may be used as indicators for liver biopsy in these patients

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Section: Discussionmentioning

confidence: 99%

Serum laminin, type IV collagen and hyaluronan as fibrosis markers in non-alcoholic fatty liver disease

Santos

Leite-Mor

Kondo

et al. 2005

Braz J Med Biol Res

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“…Therefore, maintaining the concept of microsteatosis as a unique entity is no longer justified. 5 Macrosteatosis is a feature of nonalcoholic fatty liver disease that is characterized by accumulation of triglycerides in the liver, 26 depletion in n-3 long chain PUFAs and enhancement of n-6:n-3 PUFA ratio. This is associated with changes in gene expression, with decreased fatty acid oxidation and triacylglycerol export, and enhanced lipid synthesis, leading to fat accumulation in the liver.…”

Section: Discussionmentioning

confidence: 99%

“…4 The histological lesion in microsteatosis consists of fatty microvesicles, measuring less than 1 m, filling the hepatocyte cytoplasm, whereas the nucleus remains centrally located. 5 In contrast, in macrosteatosis, hepatocytes contain one single large vacuole of fat, which displaces the nucleus to the periphery of the cell. 4,6 High degrees of macrosteatosis are known risk factors of primary nonfunction; grafts with severe macrosteatosis are no longer recommended to be used, 7 whereas a safe use of microsteatotic organs has been reported.…”

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confidence: 99%

Prevention of reperfusion injury and microcirculatory failure in macrosteatotic mouse liver by omega‐3 fatty acids†‡

et al. 2007

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Macrovesicular hepatic steatosis has a lower tolerance to reperfusion injury than microvesicular steatosis with an abnormally high ratio of omega-6 (n-6): omega-3 (n-3) polyunsaturated fatty acids (PUFAs). We investigated the influence of PUFAs on microcirculation in steatotic livers and the potential to minimize reperfusion injury in the macrosteatotic liver by normalization of PUFAs. Ob/ob mice were used as a model of macrovesicular hepatic steatosis and C57/Bl6 mice fed a choline-deficient diet for microvesicular steatosis. Steatotic and lean livers were subjected to 45 minutes of ischemia and 3 hours of reperfusion. Hepatic content of omega-3 and omega-6 PUFAs was determined. Microcirculation was investigated using intravital fluorescence microscopy. A second group of ob/ob mice was supplemented with dietary omega-3 PUFAs and compared with the control diet-fed group. Microcirculation, AST, and Kupffer cell activity were assessed. Macrosteatotic livers had significant microcirculatory dysfunction correlating with high omega-6: omega-3 PUFA ratio. Dietary omega-3 PUFA resulted in normalization of this ratio, reduction of intrahepatic lipids, and decrease in the extent of macrosteatosis. Defective microcirculation was dramatically ameliorated with significant reduction in Kupffer cell activity and protection against hepatocellular injury both before ischemia and after reperfusion. Conclusion: Macrosteatotic livers disclosed an abnormal omega-6: omega-3 PUFA ratio that correlates with a microcirculatory defect that enhanced reperfusion injury. Thus, protective strategies applied during or after ischemia are unlikely to be useful. Preoperative dietary omega-3 PUFAs protect macrosteatotic livers against reperfusion injury and might represent a valuable method to expand the live liver donor pool. (

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“…18,19 This is in contrast to fatty liver associated with microvesicular steatosis in which the clinical implications are usually more serious. 1,2,20,21 In addition, microvesicular steatosis is often accompanied by severe hepatic dysfunction and systemic derangements such as cerebral edema seen in Reye' s syndrome. 21 At the other end of the nutritional spectrum, fatty liver is also seen in states of extreme malnutrition.…”

mentioning

confidence: 99%

“…It is observed in a variety of genetic and acquired conditions including congenital metabolic conditions, fatty liver of pregnancy, Reye' s syndrome, and hepatotoxic reactions secondary to drugs and toxins. [1][2][3][4] These conditions appear to share a common mechanistic feature in that they are often characterized by an impairment in mitochondrial ␤-oxidation. 3,4 Macrovesicular steatosis, on the other hand, is the most common histologic pattern in triglyceride-related steatosis and has been observed in a broad range of clinical conditions including nutritional, metabolic, and drug-induced processes.…”

mentioning

confidence: 99%