Neomycin and plasma lipoproteins in type II hyperlipoproteinemia

Hoeg, Jeffrey M.; Schaefer, Ernst J.; Romano, Carol A.; Bou, Ernestina; Pikus, Anita; Zech, Loren A.; Bailey, Kent R.; Gregg, Richard E.; Wilson, Peter W.F.; Sprecher, Dennis L.; Grimes, Alison; Sebring, Nancy G.; Ayres, E. J.; Jahn, Christine; Brewer, H. Bryan

doi:10.1038/clpt.1984.219

Cited by 27 publications

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“…Lipid and lipoprotein concentrations were determined on EDTA plasma samples obtained after 12-to 24-hr fasts before and after 8 to 14 mo of lovastatin therapy. The cholesterol and triglyceride concentrations in the different lipoprotein fractions were determined as previously described (5).…”

Section: Methodsmentioning

confidence: 99%

Cholesteryl Ester Storage Disease: Hepatopathology and Effects of Therapy With Lovastatin

et al. 1990

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We describe three patients with cholesteryl ester storage disease. Diagnosis was confirmed by demonstrating a deficiency in lysosomal acid cholesteryl hydrolase activity in cultured skin fibroblasts from each of these patients. All had hepatomegaly, elevated serum aminotransferase activities and hyperlipoproteinemia. Histological examination of liver biopsy specimens before treatment revealed accumulation of fat within hepatocytes, bile duct epithelium and endothelial and Kupffer cells. Cholesterol crystals were recognized by their birefringence in frozen sections. A striking feature was the presence of markedly hypertrophied Kupffer cells and portal macrophages with foamy, tan-colored cytoplasm that stained readily with the periodic acid-Schiff reagent and aldehyde fuchsin. Periportal fibrosis was noted in all cases; incomplete cirrhosis was present in one case. Distinctive and hitherto undescribed lysosomal accumulations of triglyceride and cholesterol crystals were noted. The patients were treated with lovastatin, a cholesterol-lowering agent, for at least 12 mo. No significant changes were seen in serum lipoprotein concentrations or liver histopathology after therapy. Thus lovastatin did not have an obviously beneficial effect on abnormal lipid metabolism in these patients.

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Section: Methodsmentioning

confidence: 99%

Cholesteryl Ester Storage Disease: Hepatopathology and Effects of Therapy With Lovastatin

et al. 1990

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“…Triglyceride and cholesterol assays were performed using the enzymatic production of a formazan or quinoneimine dye, followed by absorbance measurement at 500 nm (21,22) and HDL cholesterol levels were determined after dextran sulfate precipitation (23). The lipoprotein cholesterol levels were then calculated as previously outlined (24). Control values are those established by the Lipid Research Clinics (25).…”

Section: Methodsmentioning

confidence: 99%

Oral carnitine therapy in children with cystinosis and renal Fanconi syndrome.

Gahl¹,

Bernardini

Dalakas

et al. 1988

J. Clin. Invest.

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11 children with either cystinosis or Lowe's syndrome had a reduced content of plasma and muscle carnitine due to renal Fanconi syndrome. After treatment with oral L-carnitine, 100 mg/kg per d divided every 6 h, plasma carnitine concentrations became normal in all subjects within 2 d. Initial plasma free fatty acid concentrations, inversely related to free carnitine concentrations, were reduced after 7-20 mo of carnitine therapy. Muscle lipid accumulation, which varied directly with duration of carnitine deficiency (r = 0.73), improved significantly in three of seven rebiopsied patients after carnitine therapy.

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“…Only 5 % of orally administered neomycin is absorbed and the drug does not accumulate. However, small quantities of neomycin can be found in plasma 3 months after its discontinuation [17,18]. Long- 40 40 term use of neomycin has been shown to be safe when pretreatment renal function is normal and treatment is followed up later [9,18].…”

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confidence: 99%

“…However, small quantities of neomycin can be found in plasma 3 months after its discontinuation [17,18]. Long- 40 40 term use of neomycin has been shown to be safe when pretreatment renal function is normal and treatment is followed up later [9,18]. Possible adverse changes in the intestinal microflora and high frequency of diarrhoea [18] are also concerns.…”

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Cholesterol malabsorption caused by sitostanol ester feeding and neomycin in pravastatin-treated hypercholesterolaemic patients

Vanhanen

1994

Eur J Clin Pharmacol

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Serum cholesterol values were insufficiently reduced by pravastatin in two different patient populations. Therefore, we studied whether further cholesterol reduction could be achieved by inhibiting both cholesterol synthesis (by pravastatin) and absorption (by neomycin or sitostanol ester). Thus, we measured serum cholesterol, cholesterol precursors (reflecting cholesterol synthesis), cholestanol and plant sterols (reflecting cholesterol absorption and biliary secretion) for up to 6 weeks in pravastatin-treated patients with familial hypercholesterolaemia (FH, n = 13) and with and without ileal bypass during addition of neomycin (1.5 g per day) and in another patient population of non-FH (n = 14) subjects during addition of sitostanol ester (1.5 g per day). Addition of neomycin lowered serum total, LDL and HDL cholesterol by a further 20%, and increased the pravastatin-lowered precursor:cholesterol ratios by 20% (irrespective of ileal bypass). It also reduced by 20% the plant sterol:cholesterol ratio (irrespective of ileal bypass) which was markedly increased by pravastatin alone. Pravastatin and neomycin in combination lowered total, LDL and HDL cholesterol by 45%, 53% and 17%, respectively. This combined regimen reduced the serum lathosterol:cholesterol ratio to about half of the reduction caused by pravastatin, while the elevation of the plant sterols:cholesterol ratio was less with the combination than with pravastatin alone. Changes in serum cholesterol precursor:cholesterol and plant sterol:cholesterol ratios during the combined treatment were smaller in the subgroup with ileal bypass. Addition of sitostanol ester did not lower serum total or LDL cholesterol nor the precursor:cholesterol ratios significantly, while the reduction observed in the plant sterols:cholesterol ratios was similar to that achieved with neomycin addition.(ABSTRACT TRUNCATED AT 250 WORDS)

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Neomycin and plasma lipoproteins in type II hyperlipoproteinemia

Cited by 27 publications

References 0 publications

Cholesteryl Ester Storage Disease: Hepatopathology and Effects of Therapy With Lovastatin

Cholesteryl Ester Storage Disease: Hepatopathology and Effects of Therapy With Lovastatin

Oral carnitine therapy in children with cystinosis and renal Fanconi syndrome.

Cholesterol malabsorption caused by sitostanol ester feeding and neomycin in pravastatin-treated hypercholesterolaemic patients

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