Lipid metabolism in Bilharzial cirrhosis

Ghanem, M. H.; Fahmy, M. H.; Aboul-Kheir, F; Mikhail, M.N.; Guirgis, F. K.

doi:10.1016/0021-9150(70)90083-3

Cited by 4 publications

(3 citation statements)

References 16 publications

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“…Although TC and LDL-C were decreased in SM patients, we noted increased levels of HDL-C, consistent with an early report that alpha-lipoproteins were significantly higher in patients with Bilharzial hepatic fibrosis [6]. By contrast, infection of ApoE-deficient mice with S. mansoni cercariae resulted in reduced HDL-C [11], although levels do not change during chronic exposure to schistosome eggs [12].…”

Section: Discussionsupporting

confidence: 90%

“…We, and others, have previously reported low plasma total cholesterol in human studies [6], [7] and in infected animals [11]–[13], [41]. Doenhoff et al [11] have shown that when fat-fed ApoE-deficient mice are infected with S. mansoni the decrease in plasma cholesterol is associated with a 50% reduction in atherosclerotic plaque progression, consistent with the low frequency of atherosclerosis noted in schistosomiasis patients [6], [42].…”

Section: Discussionsupporting

confidence: 72%

“…Previous studies have reported that human schistosomiasis alters plasma lipid composition [6]–[9] and metabolism [10]. From animal model studies, it is generally agreed that S. mansoni infection reduces levels of plasma cholesterol and triglycerides in both rodents [11], [12] and non-human primates [13], [14].…”

Section: Introductionmentioning

confidence: 99%

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Human Plasma Lipid Modulation in Schistosomiasis Mansoni Depends on Apolipoprotein E Polymorphism

et al. 2014

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BackgroundSchistosomiasis mansoni is a parasitic liver disease, which causes several metabolic disturbances. Here, we evaluate the influence of Apolipoprotein E (APOE) gene polymorphism, a known modulator of lipid metabolism, on plasma lipid levels in patients with hepatosplenic schistosomiasis.Methodology/Principal FindingsBlood samples were used for APOE genotyping and to measure total cholesterol (TC), LDL-C, HDL-C and triglycerides. Schistosomiasis patients had reduced TC, LDL-C and triglycerides (25%, 38% and 32% lower, respectively; P<0.0001) compared to control individuals, whereas HDL-C was increased (10% higher; P = 0.0136). Frequency of the common alleles, ε2, ε3 and ε4, was similar (P = 0.3568) between controls (n = 108) and patients (n = 84), implying that APOE genotype did not affect susceptibility to the advanced stage of schistosomiasis. Nevertheless, while patient TC and LDL-C levels were significantly reduced for each allele (except TC in ε2 patients), changes in HDL-C and triglycerides were noted only for the less common ε2 and ε4 alleles. The most striking finding, however, was that accepted regulation of plasma lipid levels by APOE genotype was disrupted by schistosomiasis. Thus, while ε2 controls had higher TC and LDL-C than ε3 carriers, these parameters were lower in ε2 versus ε3 patients. Similarly, the inverse relationship of TG levels in controls (ε2>ε3>ε4) was absent in patients (ε2 or ε4>ε3), and the increase in HDL-C of ε2 or ε4 patients compared to ε3 patients was not seen in the control groups.Conclusion/SignificanceWe confirm that human schistosomiasis causes dyslipidemia and report for the first time that certain changes in plasma lipid and lipoprotein levels depend on APOE gene polymorphism. Importantly, we also concluded that S. mansoni disrupts the expected regulation of plasma lipids by the different ApoE isoforms. This finding suggests ways to identify new metabolic pathways affected by schistosomiasis and also potential molecular targets to treat associated morbidities.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 72%

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Human Plasma Lipid Modulation in Schistosomiasis Mansoni Depends on Apolipoprotein E Polymorphism

et al. 2014

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Serum and urinary ribonuclease in children with schistosomal hepatic fibrosis

Zeitoun¹,

Hamam²,

M³

et al. 1978

Transactions of the Royal Society of Tropical Medicine and Hygi

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Serum and urinary RNase activity was determined in 15 normal children and in 52 children in various clinical stages of schistosomal hepatic fibrosis. The activity of serum RNase was compared with that of serum GOT, GPT and AP. The activity of serum and urinary RNase in the different schistosomal groups was significantly higher than in healthy children. The elevated levels of serum and urinary RNase activity were possibly due to malnutrition with tissue catabolism, zinc-deficiency and liver cell injury. Treatment with Astiban and protein-rich diet resulted in a significant decrease in serum and urinary RNase activity and an in significant drop in serum GOT, GPT and AP. Serum and urinary RNase appear to be more sensitive indices for evaluating the early metabolic disturbances in schistosomal patients than GOT, GPT or AP. Our findings also showed that the severity of cases could be graded according to the level of urinary RNase.

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