The Liver in Morbid Obesity and Following Bypass Surgery for Obesity

Marubbio, A.T.; Rucker, Richard D.; Schneider, Philip D.; Horstmann, Joseph P.; Varco, Richard L.; Buchwald, Hēnry

doi:10.1016/s0039-6109(16)41986-9

Cited by 27 publications

(9 citation statements)

References 45 publications

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“…Indeed, steatosis has been reported in NANBH [23,24]. Concomitant inflammatory changes are prominent in NANBH, although one group claims that fatty changes may be more prominent [25], Mild to moderate portal round cell infiltration have also been reported in approx imately 20-40% of obese patients [26][27][28], In our report, inflammatory cells were infrequent and the correlation between overweight and raised ALT further diminishes the possibility of NANBH in these obese blood donors. From most of these studies, together with our report one must conclude that in apparently healthy individuals with persistently raised ALT overweight and liver steatosis is the most common cause.…”

Section: Liver Morphologymentioning

confidence: 46%

Persistent Alanine Aminotransferase Elevation in Healthy Swedish Blood Donors - Mainly Caused by Obesity

Wejstål¹,

Hansson²,

Lindholm³

et al. 1988

Vox Sanguinis

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Five hundred consecutive healthy blood donors were tested for serum alanine aminotransferase (ALT) and 44 (8.8%) had increased levels. Donors with and without raised ALT were compared in several aspects but only weight (expressed as percentage of ideal body weight) and sex differed significantly (119.1 ± 14.5 and 106.3 ± 12.8%, respectively; p<0.001 and males 97.7 and 77.1%, respectively; p<0.01). The 44 donors with raised ALT were followed up and in 13 out of 15 donors with persistently raised ALT without obvious reason, a liver biopsy was performed. Ten donors had various degrees of liver steatosis, 2 had normal liver morphology and in 1 donor chronic hepatitis could not be ruled out. If ALT screening is introduced as a surrogate test for non-A, non-B hepatitis in Swedish blood donors, we suggest that a correction for overweight must be considered in order to minimize donor loss.

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Section: Liver Morphologymentioning

confidence: 46%

Persistent Alanine Aminotransferase Elevation in Healthy Swedish Blood Donors - Mainly Caused by Obesity

Wejstål¹,

Hansson²,

Lindholm³

et al. 1988

Vox Sanguinis

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“…Of the several series of patients who had serial liver biopsies following JIB, most report some incidence of increased steatosis and fibrosis at follow-up, and some even report hepatic failure leading to death or transplant. [174][175][176][177][178][179][180] Several explanations have been proposed, including rapid, profound weight loss following JIB and the subsequent massive mobilization of visceral adipocyte LCFAs into the portal circulation and hepatic parenchyma. Though few studies have looked at liver histology in a period of rapid weight loss from any intervention, one study of diet-induced weight loss found that the rate of weight loss achieved predicted severity of liver histology to the extent that increased steatosis was only seen in patients who lost more than 1.6 kg/week.…”

Section: Impact Of Bariatric Surgery On Nafldmentioning

confidence: 99%

Role of Fatty Acids in the Pathogenesis of Obesity and Fatty Liver: Impact of Bariatric Surgery

Verna

Berk

2008

Semin Liver Dis

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Nonalcoholic fatty liver disease (NAFLD) spans a spectrum from simple steatosis to nonalcoholic steatohepatitis (NASH) to cirrhosis. Simple steatosis is the substrate upon which the more serious entities in the spectrum develop; it is the first ''hit'' in the multistep pathogenesis of NASH, which is considered the hepatic manifestation of the metabolic syndrome. Demonstration of the existence of regulatable fatty acid transport mechanisms has contributed to clarifying the role of fatty acid disposition in obesity, the various components of NAFLD, and the metabolic syndrome. Hepatic steatosis is closely linked to obesity. This linkage is based on the fact that obesity results in marked enlargement of the intraabdominal visceral fat depots. The eventual development of insulin resistance leads to continuous lipolysis within these depots, releasing fatty acids into the portal circulation, where they are rapidly translocated to the liver and reassembled into triglycerides. Reactive oxygen species, generated in the liver from oxidation of fatty acids, are precipitating factors in the cascade of events leading from simple steatosis to NASH. Dysregulation of fatty acid disposition, with ectopic lipid accumulation in other tissues, is a major contributing factor to other components of the metabolic syndrome. Bariatric surgery is an effective treatment for severe obesity, but its role in the management of the various forms of fatty liver disease is unclear. Our review of the literature that includes both initial and follow-up liver biopsies suggests that most obese patients with simple steatosis and NASH who undergo bariatric surgery will achieve improvement in hepatic histology, but that occasional patients, especially those who lose weight very rapidly, may show worsening of either fibrosis or steatohepatitis.

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“…Precisely relating these findings to LFT changes is somewhat difficult and speculative. Several studies, however, have demonstrated hepatocyte changes after PIB [20] and after the far more extensive jejunoileal bypass for obesity [21,22].…”

Section: Discussionmentioning

confidence: 99%

Lipid Modulation and Liver Function Tests: A Report of the Program on the Surgical Control of the Hyperlipidemias (POSCH)

Buchwald¹,

Williams²,

Matts

et al. 2002

European Journal of Cardiovascular Prevention & Rehabilitat

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Background Statin drugs are known to cause dosedependent abnormalities in liver function tests (LFTs), with elevations three times the upper limits of normal of the aminotransferase enzymes in up to 2.5% of patients on the highest prescribable doses. The Program on the Surgical Control of the Hyperlipidemias (POSCH) trial employed no hypocholesterolaemic drugs and used a surgical procedure, partial ileal bypass, as the intervention modality.Methods Serum total bilirubin, alkaline phosphatase and serum glutamic-oxaloacetic transaminase (SGOT) (equivalent to aspartate aminotransferase [AST]), were the LFTs obtained in POSCH at baseline, 3 months, annually for 5 years, and at 7 or 10 years postrandomization.Results Abnormal values were found for total bilirubin in seven of 416 control group (CG) patients (1.68%) and in 34 of 373 intervention group (IG) patients (9.16%) (P ¼ 0.001); for alkaline phosphatase, in 28 of 378 (7.41%) and in 41 of 326 (12.58%) (P ¼ 0.0214); and for SGOT, in 102 of 412 (24.76%) and in 161 of 372 (43.28%) (P ¼ 0.001). Values twice the upper limit of normal occurred in 1 CG and 1 IG patient for total bilirubin and for alkaline phosphatase, and in 11 CG and 7 IG patients for SGOT (NS). Values three times the upper limit of normal did not occur in any patient for total bilirubin or alkaline phosphatase, and occurred in 3 CG and 5 IG patients for SGOT (NS). ConclusionsIn POSCH, the IG demonstrated statistically significant mild increases for total bilirubin, alkaline phosphatase and SGOT levels, with no significant increases in values twice or greater the upper limits of normal.

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The Liver in Morbid Obesity and Following Bypass Surgery for Obesity

Cited by 27 publications

References 45 publications

Persistent Alanine Aminotransferase Elevation in Healthy Swedish Blood Donors - Mainly Caused by Obesity

Persistent Alanine Aminotransferase Elevation in Healthy Swedish Blood Donors - Mainly Caused by Obesity

Role of Fatty Acids in the Pathogenesis of Obesity and Fatty Liver: Impact of Bariatric Surgery

Lipid Modulation and Liver Function Tests: A Report of the Program on the Surgical Control of the Hyperlipidemias (POSCH)

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