Apolipoprotein and lipid abnormalities in chronic liver failure

Spósito, Andrei C.; Vinagre, C.G.; Pandullo, Fernando Luis; Mies, Suzette; S, Raia; Ramires, José Antônio Franchini

doi:10.1590/s0100-879x1997001100004

Cited by 14 publications

(11 citation statements)

References 13 publications

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“…This again supports the finding of this study, showing a decline in HDL level in these disease groups. Sposito et al [16] further reported that ApoA and ApoB were reduced in chronic liver failure. A differential reduction in ApoA and ApoB levels in different disease groups was noted in this study.…”

Section: Discussionmentioning

confidence: 94%

Impact of Viral Hepatitis on Apo- and Lipoprotein Status in Blood

Irshad

Dube²,

Joshi³

2007

Med Princ Pract

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Objectives:To investigate the effect of viral hepatitis on serum levels of apo- and lipoproteins in different forms of liver diseases. Materials and Methods: One hundred and thirty adult patients and 100 healthy age- and gender-matched control individuals participated in this study. Patients were grouped according to four types of liver disease: acute viral hepatitis, chronic active hepatitis (CAH), cirrhosis of the liver and fulminant hepatic failure. Results: Hepatitis B virus, C virus and E virus (HEV) infections were recorded in different combinations in these patients, but viral infections of hepatitis A and D were not seen in any of the patient groups. The results of lipo- and apoprotein analysis showed different patterns. The low-density lipoprotein value was high in the CAH group. In the other three groups, low-density lipoprotein level was comparable to the control value. The high-density lipoprotein level (p = 0.02) was significantly low in all groups except in the cirrhosis group. Apo-A was significantly reduced in the acute viral hepatitis and fulminant hepatic failure groups, whereas Apo-B level was low in the CAH and cirrhosis groups. The lipoprotein (a) level in these groups was low, compared to control. Conclusion: No apparent relationship was observed between etiological viruses and ensuing changes in lipid/lipoprotein profile.

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Section: Discussionmentioning

confidence: 94%

Impact of Viral Hepatitis on Apo- and Lipoprotein Status in Blood

Irshad

Dube²,

Joshi³

2007

Med Princ Pract

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“…ApoA‐I and ApoB levels have been found to be low in patients with liver failure and cirrhosis but few studies have reported on the association between ApoA‐I and ApoB with PLC. The liver is involved in the synthesis of ApoA‐I and ApoB polypeptides present in HDL and LDL fractions .…”

Section: Discussionmentioning

confidence: 99%

The association between individual metabolic syndrome components, primary liver cancer and cirrhosis: A study in the Swedish AMORIS cohort

et al. 2017

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Metabolic syndrome (MetS) is associated with non-alcoholic fatty liver disease, which may progress to cirrhosis, a significant risk factor of hepatocellular carcinoma (HCC), the commonest malignant primary liver cancer (PLC). We investigated the association between the individual components of MetS (lipids, apolipoproteins, raised glucose, diabetes and obesity), PLC and cirrhosis. A total of 509,436 participants from the Swedish AMORIS cohort, recruited between January 1985 and December 1996 (end-date December 2011), aged ≥20 with baseline triglycerides (TG), total cholesterol (TC), glucose and liver enzymes were included. Those with baseline benign liver tumours, PLC or cirrhosis were excluded. Multivariate Cox regression, adjusted for age, gender, socio-economic status, liver disease (excluding cirrhosis) and MetS factors were used to estimate the association with PLC and cirrhosis. There were 766 PLC and 2,775 cirrhosis cases over 13 years. Raised TG, low TC, raised glucose, diabetes and low HDL were associated with an increased risk of developing PLC and cirrhosis. ApoB/ApoA-I ratio were also associated with PLC, whilst low LDL, raised TG/HDL, low ApoA-I and low ApoB were associated with cirrhosis. Obesity was significantly associated with PLC but not cirrhosis. Raised TG, low TC, raised glucose and diabetes showed stronger associations with PLC in participants with cirrhosis but many participants developed PLC without cirrhosis. Individual components of MetS (lipids, apolipoproteins, raised glucose, diabetes and obesity) were associated with an increased risk of developing PLC or cirrhosis. MetS components were more strongly associated with PLC with preceding cirrhosis history but many participants developed PLC without cirrhosis.

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“…22 In a study of 74 patients with chronic liver failure, HDL lipid fractions were reduced by 46% overall, and the HDL-C:ApoA-I ratio was inversely correlated with severity of liver failure. 40 In older studies in which HDL-C was not measured chemically but was quantified using electrophoresis, ␣-lipoprotein was absent in 41 of 46 subjects with acute viral hepatitis and its return appeared to be a prognostic indicator of recovery. 41 LCAT activity in a small group of children with acute hepatitis appeared to correlate with the quantity of HDL present, although electrophoretic absence of ␣-lipoprotein was seen in subjects with normal amounts of LCAT.…”

Section: Acquired Severe Lcat Activitymentioning

confidence: 99%