Hyperlipidemic state and cardiovascular risk in course of primary biliary cirrhosis

Longo, Matteo; Crosignani, Andrea; Battezzati, Pier Maria; Invernizzi, Pietro; Squarcia, C.; Pipia, Cristina; Colombo, L; Colombo, Alessandro; Dosio, Sabina; Perego, Francesca; Meda, Francesca; Podda, Mauro

doi:10.1016/s0016-5085(00)86184-3

Cited by 3 publications

(2 citation statements)

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“…Furthermore, in a recent prospective study from our group [6] the incidence of nonfatal cardiovascular events did not differ from general population, and a relationship between hypercholesterolemia and cardiovascular disease was not observed. These results may be explained partially by the particular lipoprotein pattern observed during chronic cholestasis, characterized by elevated levels of circu-…”

Section: Introductionmentioning

confidence: 54%

Hyperlipidemia in chronic cholestatic liver disease

Longo

Crosignani

Podda

2001

Curr Treat Options Gastro

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Hyperlipidemia with a marked increase of low-density lipoprotein (LDL) and high- density lipoprotein (HDL) cholesterol levels is a common feature in patients with chronic cholestatic liver disease. Excess morbidity and mortality from cardiovascular disease has not been reported in these patients. This may be due to the particular lipoprotein pattern observed during chronic cholestasis, characterized by elevated serum HDL cholesterol, which may have a cardioprotective effect. However, in a subgroup of patients with chronic cholestasis, hyperlipidemia is characterized by markedly elevated LDL levels with normal or low HDL levels, probably reflecting hypercholesterolemia with coexisting familial and nutritional origins. Ursodeoxycholic acid, the only drug approved for the treatment of chronic cholestatic liver diseases, has been shown to slightly decrease serum cholesterol concentrations. However, the extent of LDL reduction by ursodeoxycholic acid may be insufficient to protect this subgroup of patients from increased cardiovascular risk. Patients in this subgroup probably would benefit from dietary modification, weight loss, and the administration of specific lipid-lowering drugs. Cholestyramine, which is the first-line treatment for pruritus in chronic cholestasis, may be also indicated for its cholesterol-lowering capacity in patients with hypercholesterolemia who complain of pruritus. Administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (simvastatin or pravastatin, 20 mg/d) should be limited to hypercholesterolemic patients with mild chronic cholestatic liver diseases in whom HDL serum levels are below the protective range or if additional risk factors for cardiovascular diseases are present.

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Section: Introductionmentioning

confidence: 54%

Hyperlipidemia in chronic cholestatic liver disease

Longo

Crosignani

Podda

2001

Curr Treat Options Gastro

Self Cite

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“…Insulin resistance was considered to be responsible for the development of coronary disease in patients with systemic lupus erythematosus [13,14], and it has been observed in patients with autoimmune hepatitis [15]. However, previous articles failed to demonstrate the increase in the risk of cardiovascular mortality in patients with PBC [16,17], who often exhibited hypercholesterolemia secondary to cholestasis.…”

Section: Introductionmentioning

confidence: 99%

Contribution of Zinc Deficiency to Insulin Resistance in Patients with Primary Biliary Cirrhosis

Himoto

Yoneyama

Kurokochi

et al. 2011

Biol Trace Elem Res

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The relationship between metabolic abnormalities of trace elements and insulin resistance has been established. Recent studies have revealed that insulin resistance is associated with autoimmune responses. The purpose of this study was to examine the correlation between zinc or copper metabolism and insulin resistance in patients with primary biliary cirrhosis (PBC). Sixteen patients with PBC were divided into two groups: early and advanced stage disease. The overall value of the homeostasis model assessment of insulin resistance (HOMA-IR) in patients with advanced stage PBC was significantly higher than that in patients with early stage PBC, although the mean value in advanced stage PBC was significantly lower than that in hepatitis C virus (HCV)-related liver cirrhosis. There was an inverse correlation between serum zinc concentrations and HOMA-IR values in patients with PBC, while we found no correlation between serum copper levels and HOMA-IR values. HOMA-IR values were inversely associated with peripheral platelet counts, indicating the relationship between insulin resistance and hepatic fibrosis. These results suggest that zinc deficiency plays important roles of insulin resistance and subsequent hepatic fibrosis in patients with PBC, although insulin resistance in advanced stage PBC was significantly milder than that in HCV-related liver cirrhosis.

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