PubMed · 6628247
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T Risler, L Seipel. 1983-11-04. [Controlled digitalis therapy].. https://doi.org/10.1055/s-2008-1069808
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Numerous studies involving patients with hypercholesterolemia have demonstrated that reduction of lipid levels markedly reduces morbidity and mortality from cardiovascular disease. Diet alone may enable patients without established disease to attain target lipid levels, but pharmacotherapy generally is necessary for those with coronary artery disease. Choice of a suitable agent for monotherapy--a bile acid resin, niacin, or an HMG-CoA reductase inhibitor--may be determined by patient phenotype. For resistant cases, therapy combining an HMG-CoA reductase inhibitor with another agent generally is effective and well tolerated.
Cholestyramine resin in a bile acid sequestrant which binds with bile salts in the intestinal lumen to increase the fecal excretion of bile salts and, thus, lower blood serum cholesterol. In order to gain a better understanding of the low in vivo potency of cholestyramine, in vitro equilibrium binding studies, water sorption studies, and resin capacity measurements were performed using cholestyramine and the bile salt sodium glycocholate. Equilibrium binding and water sorption studies entailed equilibrating cholestyramine (1.0-20 mg/mL) with solutions which varied in glycocholate anion concentration (0.20-16.5 mM) and chloride anion concentration (15-150 mM). The resin's practical specific capacity for glycocholate was lower than the practical specific capacity for chloride. This difference suggests that the rigid, bulky bile salt was pore excluded from 10% of the resin's ionogentic sites. A fundamental parameter called the capacity-corrected molar selectivity coefficient, KGC-Cl-, was postulated to describe the underlying binding phenomena and was determined by measuring the free glycocholate and chloride anion concentrations; KGC-Cl- ranged from 9.8 (+/- 0.7) to 18.6 (+/- 0.2) and depended on the square of the free chloride concentration. The capacity-corrected molar selectivity coefficient was larger than the molar selectivity coefficient due to pore exclusion of glycocholate. A more simple method to calculate the capacity-corrected molar selectivity coefficient which required less data gave similar values to the more rigorous method (r2 = 0.955).
A 51-year-old man had for 5 years been known to have erythropoietic protoporphyria. GPT levels were raised up to 40 U/l, gamma-GT up to 120 U/l. After lengthy exposure to sun radiation an erythema with blisters, abdominal discomfort and jaundice developed (total bilirubin 7.3 mg/dl) and biliary liver cirrhosis with portal hypertension and splenomegaly were diagnosed. Because the acute hepatobiliary complications were not improved by conservative treatment (daily 750 mg ursodeoxycholic acid and 12 g colestyramine), an orthotopic liver transplantation was performed without complication. The excised liver showed small nodular parenchymal transformation and contained reddish brown protoporphyrin pigment in the hepatocellular cytoplasm, the Kupffer cells, the canaliculi and in some biliary ducts. Bilirubin and transaminase levels in blood became normal after the transplantation, as did the urinary excretion of coproporphyrin. However, isomer I was still dominant. The protoporphyrin level in erythrocytes and plasma remained elevated. After a symptom-free interval of one year biochemical and histological tests demonstrated protoporphyrin-induced damage in the transplanted liver.