1. The serum lipoproteins, apoproteins and lecithin-cholesterol acyltransferase activity of three patients with abetalipoproteinaemia have been studied.2. Concentration of lipoproteins with a density of less than 1-063 was found to be 5-6 mg/lOO ml of plasma. The protein part consisted only of apoAI polypeptides.3. Concentration of total serum high-density lipoproteins was 90-100 mg/lOO ml. After total delipidization of this fraction, apoproteins were separated by column chromatography. All apoA and most of the apoC peptides could be demonstrated by immunochemical methods and polyacrylamide gel electrophoresis.4. Quantification of individual polypeptides indicated that the proportions apoAI : apoAII :apoAIII in high-density lipoproteins were not different from those observed in normal subjects. ApoCIII, was absent in the patients' serum. In the remaining apoC peptides differences in the distribution compared with normal subjects could be demonstrated.
5.With antibodies to lipoprotein B, acetylated lipoprotein B or apolipoprotein B no reaction could be observed with abetalipoproteinaemic serum or any density fraction tested including density 1.23 infranate.6. Isoelectric focussing of prestained lipoproteins in complete patients' serum revealed the absence of four major lipoprotein families present in normal serum.7. Lecithin-cholesterol acyltransferase activity of abetalipoproteinaemic serum was reduced to a value of about 50% of normal but lipoproteins of patients' serum could be utilized as a substrate only to a minor degree. The maximum activity was observed only if lipoproteins of normal serum were added to the assay system.
The catechol-O-methyltransferase inhibitors entacapone and opicapone prolong the efficacy of conventional oral levodopa/dopa decarboxylase inhibitor formulations through an increase in levodopa plasma bioavailability. Catechol-O-methyltransferase inhibitors influence the homocysteine metabolism associated with levodopa/dopa decarboxylase application. The objectives of this study were to compare the impact of additional single-day entacapone or opicapone intake on the pharmacokinetic plasma behaviour of levodopa, 3-O-methyldopa and total homocysteine in 15 Parkinson’s disease patients, with concomitant scoring of motor symptoms, under standardized conditions. The patients received opicapone plus two doses of 100 mg levodopa/carbidopa and, one week later, two doses of levodopa/carbidopa/entacapone or vice versa. Levodopa, 3-O-methyldopa and total homocysteine were determined with reversed-phase high-performance liquid chromatography. Levodopa bioavailability and its maximum concentration were higher with opicapone. The computed peak-to-trough difference was lower after the second levodopa administration with entacapone. The fluctuation index of levodopa did not differ between both conditions. 3-O-methyldopa decreased on both days. Homocysteine levels did not significantly vary between both conditions. A significant homocysteine decrease occurred with entacapone, but not with opicapone. Motor behaviour improved with entacapone, but not with opicapone. Opicapone baseline scores were significantly better, and thus the potential for the improvement in motor symptoms was lower compared with the entacapone condition. The higher levodopa bioavailability with opicapone suggests that it is more efficacious than entacapone for the amelioration of “off” phenomena in fluctuating patients when co-administered with a levodopa/dopa decarboxylase inhibitor regimen. Both compounds prevented an increase in homocysteine, which is a metabolic marker for an impaired capacity in the performance of methylation processes.
In a 21-year-old Caucasian woman with von Hippel-Lindau disease, norepinephrine-producing adrenal pheochromocytoma was identified as the underlying cause of severe hypertension. She was found to have extremely elevated levels of circulating renin and aldosterone, and she was markedly hypokalemic. Administration of captopril further enhanced renin secretion, while her blood pressure improved. The patient became normokalemic following tumor removal, and her blood pressure decreased to normal levels with reestablishment of normal circadian blood pressure rhythm. This case demonstrates that, in the absence of renovascular or malignant hypertension, pheochromocytoma can be the underlying cause for the clinical syndrome of hypertension associated with severe hypokalemia and hyperreninemic hyperaldosteronism.
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