Letters and Corrections1 May 1987Type V Hyperlipoproteinemia and PlasmapheresisWERNER O. RICHTER, M.D., GERD BREHM, M.D., PETER SCHWANDT, M.D.WERNER O. RICHTER, M.D.Search for more papers by this author, GERD BREHM, M.D.Search for more papers by this author, PETER SCHWANDT, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-106-5-779_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Patients with excessive type V hyperlipoproteinemia develop several forms of abdominal pain that can be caused by three mechanisms: painful and tender spleen and liver, intestinal dysfunction, and pancreatitis (1-3). Pancreatitis is the most serious complication and can result in death (4). High serum levels of chylomicrons (triglycerides in concentrations greater than 1000 mg/dL) cause these complications through an increase in plasma viscosity (5); therefore, severe pancreatitis, intractable abdominal pain, and other complications such as seizures or gastrointestinal hemorrhage need to be treated by the induction of a rapid decrease in the level of chylomicrons in blood....References1. FALLATGLUECK RC. Familial and acquired type V hyperlipoproteinemia. Atherosclerosis. 1976;23:41-62. CrossrefMedlineGoogle Scholar2. GREENBERGBLACKWELDERLEVY BWR. Primary type V hyperlipoproteinemia: a descriptive study in 32 families. Ann Intern Med. 1977;87:526-34. LinkGoogle Scholar3. BROWNBAGINSKYEHNHOLM WMC. Primary type I and type V hyperlipoproteinemia. In: Hyperlipidemia: Diagnosis and Therapy. RIFKIND BM, LEVY RI, eds. New York: Grune & Stratton; 1977:93-112. Google Scholar4. FREDRICKSONLEVY DR. Familial hyperlipoproteinemia. In: The Metabolic Base of Inherited Disease. STANBURY JB, WYNGAARDEN JB, FREDRICKSON DS, eds. New York: McGraw-Hill; 1972:545-614. Google Scholar5. SEPLOWITZCHIENSMITH ASF. Effects of lipoproteins on plasma viscosity. Atherosclerosis. 1981;38:89-95. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: University of Munich, Klinikum Grosshadern D-8000 Munich 70 West Germany PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByPlasma Exchange for Dramatic Gestational Hyperlipidemic PancreatitisTreatment of severe familial hypertriglyceridemia during pregnancy with very-low-fat diet and n-3 fatty acidsRole of LDL apheresis in the management of hypercholesterolaemiaPrognosis of DyslipoproteinemiaPlasmafiltration als Akuttherapie der exzessiven Hyperlipoproteinämie 1 May 1987Volume 106, Issue 5Page: 779-779KeywordsAbdominal painAttentionBlood plasmaEpileptic seizuresGastrointestinal hemorrhageLiverPancreatitisSpleen Issue Published: 1 May 1987 PDF DownloadLoading ...
A statistical survey about the results of treatment of Pentoxifyllin (Trental) in acute and long-standing sensorineural hearing losses is given. The pharmacological effect of viscosity lowering in such patients is demonstrated. The role of erythrocytes and their behaviour in relation to the viscosity of blood its showed by means of literature.
Combinations of DHA and EPA have been shown to effectively reduce cardiovascular death in patients with coronary heart disease.Occlusions of coronary arteries in dogs lead to ventricular fibrillation which could be avoided by concomitant infusion of free EPA and DHA.Obviously local lipases in the myocardium are not able to release n-3 fatty acids acutely from cell membranes.Further in vitro studies have shown that only free n-3 fatty acids are able to suppress fibrillation.Therefore it may be an option to maintain higher free n-3 fatty acid levels in serum to claim more efficacy in reduc-ing dangerous arrhythmias.To clarify whether a daily intake of 0.85 grams or a once weekly intake (5.95 grams) of ethyl esters of EPA and DHA (ratio 1.25 to 1.00) is superior in maintaining higher free serum levels 12 healthy probands (33 + 8 years old, 10 women, 2 men) were included in a cross-over study.During the whole study period they were not allowed to eat fish.After a run-in period of two weeks subjects were randomly allocated either to receive 1 capsule per day (0.85 g) or 7 capsules once a week for six weeks, followed by a four-week wash-out period.Then the probands received the other regime for six weeks followed by four weeks of wash-out.Blood samples were taken at weekly intervals -24 hours after intake of one capsule and 7 days after intake of 7 capsules.Furthermore, blood samples were obtained on four consecutive days at week 5 to follow the increase and decrease after high dose supplementation.Free and total serum n-3 fatty acids were determined as methyl esters by gaschromatography.The determination of EPA and DHA serum concentration in weekly intervals (at trough levels) showed significantly higher levels on the daily regime for free EPA and DHA as well as for total EPA and DHA.The daily determinations at week five showed that the once-week high dose supplementation resulted in lower serum concentrations 48 -72 hours after intake than the daily regime.Therefore a daily supplementation of a smaller amount of n-3 fatty acids seems to be superior to a once weekly intake of a high dose regarding free and total EPA and DHA concentrations in serum.
Atherosclerosis is the main cause of death in diabetes mellitus. This may at least in part be due to lipoprotein abnormalities which have been described in these patients. Apolipoprotein-E is a component of most lipoprotein fractions and plays an important role in the catabolism of VLDL. The different apolipoprotein-E phenotypes determined genetically are associated with certain hyperlipoproteinemias in a various degree in nondiabetic patients. In most cases apolipoprotein-E phenotype E2/2 is characteristic for familial dysbetalipoproteinemia. Phenotype E3/2 was found to be more frequent in hypertriglyceridemia while phenotype E4/3 was associated with hypercholesterolemia as well as with type V hyperlipoproteinemia. We studied apolipoprotein-E phenotypes and serum lipids in 141 type II diabetic patients (36 normolipidemic 41 type IIa hyperlipidemic, 32 type IIb hyperlipidemic, 24 type II hyperlipidemic, 8 type V hyperlipidemic). the phenotype E3/3 was more common in normolipidemic diabetic (77.8%) than in hyperlipoproteinemic diabetic patients (42.9%) or in the control group (57.5%). On the other hand phenotype E3/2 was more frequent in hypertriglyceridemic (50%) than in normolipidemic (5.6%) or hypercholesterolemic (hyperlipoproteinemia IIa: 4.9%, IIb: 9.4%) diabetic patients. The phenotype E4/3 was more frequent in all hyperlipoproteinemic diabetic patients, especially in those having hypercholesterolemia (34.2%) or mixed hyperlipidemia (50%). In conclusion we found a strong association between apo-E2 and hypertriglyceridemia in diabetic patients. This association was stronger than the one found in the general population. The association between apo-E4 and hypercholesterolemia in diabetic patients was similar to the one described in non-diabetic patients. We therefore conclude that type II diabetes mellitus is a possible cofactor in the apolipoprotein-E2 associated hyperlipoproteinemia.
