Liver in obesity.

Abstract

SUMMARY We report on clinical, nutritional, and hepatic histological findings in 50 non-selected obese subjects (mean overweight +74%; range +21-138%). The pathogenesis of the liver damage was assessed with the help of multidimensional analysis of a number of clinical variables. According to the severity of the hepatic lesions, the patients have been ranged in five groups: 0 (normal liver) 10%; I (fatty liver) 48%; II (fatty hepatitis) 26%; III (fatty fibrosis) 8%; IV (fatty cirrhosis) 8%. The more severe changes (groups III and IV) were constantly associated with excessive alcohol intake. The multidimensional analysis was unable to find a relationship between obesity and the development of fibrosis and cirrhosis whereas it showed that: (a) there was a highly significant correlation between the daily ethanol intake and the degree of overweight, (b) severe fatty metamorphosis was significantly associated with the degree of overweight, the existence of diabetes mellitus, and the amount of alcohol and fat intake, (c) nutritional factors, in particular deficient protein intake, have only an accessory effect in the development of mild inflammation and fibrosis, (d) the consumption of potentially hepatotoxic drugs, very high in the obese (about five drugs per day) could have a role in the development of cirrhosis. In conclusion in our study, there was no evidence that obesity per se could result in severe liver damage.Controversy exists in the literature about the incidence and nature of liver lesions in obese patients. In most studies fatty liver was the only significant abnormality,1-4 but recent reports have suggested that severe liver damage, sometimes mimicking the entire histological spectrum of alcoholic liver disease, could be found in obesity.512In most of these studies, however, information on the potential hepatotoxic factors occuring in obesity was usually lacking. Thus, we undertook a crosssectional study of the liver histology in 50 nonselected obese patients with the aims: (a) to define precisely the prevalence, the nature, and the severity of the liver lesions in obesity; (b) to determine, by the multidimensional analysis, the quantitative and/or qualitative clinical variables which were related to the observed histological abnormalities. Methods PATIENTSFifty obese patients, consecutively hospitalised in a

Liver steatosis in juvenile obesity: correlations with lipid profile, hepatic biochemical parameters and glycemic and insulinemic responses to an oral glucose tolerance test

“…In fact, we have not considered as steatosis the pattern of slight increase of the liver echogenicity and echo discrepancy between liver and kidney that other authors have classi®ed as mild steatosis, 3 because this ®gure may be equivocal in obesity. The present data show a direct although weak correlation between the degree of obesity and that of steatosis, according with several observations, 8,21,23,24,36,37 but opposite results are reported, 6,38 possibly related to the minor severity of weight excess of the subjects. On the other hand, as far as the Table 3 The biochemical parameters in the subjects, grouped according to the pubertal stage and to the presence (S) or not (N) of steatosis (* P`0.001 vs stages II ± III; **P`0.001 vs stages IV ± V; {P`0.05, {P`0.01, §P`0.001, N vs S) Liver steatosis in juvenile obesity G Guzzaloni et al duration of obesity is concerned, which we have not considered for the lack of reliable data, there are many concerns in the literature: in fact it has been suggested that both a long, 19,20,23,24,36,38 and a shorter duration 22 could be independent cofactors for determining steatosis, and also that no correlation exists with the duration as such, at least in adults.…”

“…3,4 In adults the severity of steatosis has been correlated with the degree of obesity, 5 ± 8 although opposite results have been reported, 9 ± 11 and with the serum levels of free fatty acids, as well as glycemia and insulinemia. 6,12,13 However, no correlation with liver biochemical abnormalities was found. 10,12,14 ± 16 In childhood and adolescent obesity the fatty change of the liver has also been well documented, although with different values of prevalence, and correlated with duration and degree of obesity and with serum levels of transaminases.…”

Liver abnormalities in severely obese subjects: Effect of drastic weight loss after gastroplasty

“…This suggests that the rapid mobilization of intra-and extrahepatic fat stores, probably associated in some cases with de®cient protein diet during weight loss, may contribute to the aggravation of preexistent liver steatosis in these subjects. 20,24 Liver insults by hepatotoxic drugs, moderate alcohol intake or viral infections are retrospectively dif®cult to exclude and may explain part of the in¯ammatory changes observed in the second liver biopsy. Nevertheless, when hepatitis was present, a further investigation was performed on the liver fragment in most cases.…”

Obesity and liver disease

“…As recently reviewed 55 , these findings were confirmed in further studies. 44,56,57 In an autopsy study, steatohepatitis was found in 18.5% of markedly obese patients in contrast to only 2.7% of lean patients, while severe fibrosis was found in 13.8% versus 6.6% respectively. 58 Large series of liver biposies performed in severely obese subjects submitted to bariatric surgery have been recently published.…”

“…The observation that some obese individuals presented a liver disease histologically indistinguishable from alcoholic liver disease itself had long been recognized. [42][43][44][45][46][47][48][49] Interestingly, it has been recently demonstrated that obesity also increases the risk of liver disease induced by either alcohol 50 or chronic hepatitis C. [51][52][53] In a literature survey of 41 original articles comprising information on liver morphology in 1515 morbidly obese patients, liver biopsy was considered as normal in only 12% of the cases. 54 The most frequent abnormality reported was fatty changes present in 80% of the biopsies; portal inflammation was also common (33%) while portal or periportal fibrosis was observed in 29%.…”