Erythrocyte membrane lipids and serum selenium in post-viral and alcoholic cirrhosis

Erythrocyte-membrane fatty acid composition and cholesterol content were evaluated along with serum selenium in 33 patients with liver cirrhosis and in 40 normal subjects. Thirteen patients were suffering from post-viral (group V) and 20 from alcoholic (group A) cirrhosis. The aim of the study was to elucidate whether membrane lipid abnormalities in cirrhosis were linked to the aetiology of the disease or whether they were the results of the cirrhotic process itself. The patients presented a significant increase in membrane cholesterol, palmitic acid (C16:0) and saturated fatty acids (SFA), and a decrease in polyunsaturated fatty acids (PUFA) and polyunsaturated/saturated fatty acids ratio (P/S) compared with the control group. Serum selenium levels were significantly reduced. When patients were subdivided according to aetiology, the alcoholic patients showed greater lipid composition abnormalities than the viral cirrhotics (higher levels of SFA and lower PUFA and P/S), while pathologic palmitic acid, membrane cholesterol and serum selenium values were confirmed in both groups of patients.

In conclusion, low serum selenium and a series of erythrocyte membrane lipid composition abnormalities would appear to be features peculiar to cirrhosis. Alcoholic cirrhotics, on the other hand, show a more deranged erythrocyte membrane lipid profile.     

Plasma and red cell lipids in alcoholics with macrocytosis

The cholesterol and phospholipid content and the fatty acid composition in plasma and red cell membranes was determined in 10 alcoholics with macrocytic erythrocytes. None of the patients had anemia. Red cells exhibited macrocytosis up to 108 fl in all patients. Bilirubin, albumin, prothrombin, and cholinesterase were in the normal range, whereas transaminases and gamma-glutamyl transpeptidase activities in serum were elevated in most of the patients. The molar ratio cholesterol/phospholipids in red cells was not altered in alcoholics. An abnormally high ratio of saturated/unsaturated fatty acids was found in plasma as well as in red cell phospholipids from alcoholics. Linoleic acid was substantially decreased in plasma of alcoholics (controls 32.3%, alcoholics 21.8%). This fatty acid abnormality was reflected by a decrease of linoleic acid in red cell phosphatidylcholine. The present data may suggest that fatty acid changes taking place in membranes of macrocytes were a consequence of changes in the plasma and reflect plasma/membrane exchanges rather than direct effects of ethanol on red cell membranes. Lipid alterations of red cell membranes may be involved in the development of macrocytosis in chronic alcoholism.     

Erythrocyte damage and leukocyte activation in ischemic stroke

Background: The traditional lipid risk factors can only predict some of the cardiovascular events. Our work has focused on new potential biological markers of risk, namely leukocyte activation and erythrocyte membrane damage, in ischemic stroke cases. Methods: Besides the traditional lipid profile, we evaluated the plasma levels of elastase and lactoferrin as markers of leukocyte activation, and membrane band 3 protein profile and membrane bound hemoglobin as markers of erythrocyte damage. Total and differential leukocyte counts and erythrocyte counts, hematocrit and hemoglobin concentrations were also evaluated. The lipid study included the evaluation of triglycerides, total cholesterol, high-density lipoprotein cholesterol (HDLc), low-density lipoprotein cholesterol (LDLc), apolipoprotein AI (Apo AI) and B (Apo B), and lipoprotein (a) (Lp(a)). The work was performed in a control group (n=29) with no history of cardiovascular events, presenting normal hematological and lipid values, and in a pathologic group (n=21) of ischemic stroke cases diagnosed by computed tomographic imaging. Results: We found that ischemic stroke was associated with significantly higher values of leukocytes, which seem to be activated, as shown by significant higher levels of elastase and lactoferrin. This activation seems to impose erythrocyte damage, as suggested by a significant increase in membrane bound hemoglobin and by a different band 3 profile. Conclusions: Our data suggest that plasma levels of elastase and lactoferrin, together with levels of erythrocyte membrane bound hemoglobin and band 3 profile, could be used as powerful new markers of risk for cardiovascular events.     

Erythrocyte membrane alterations and plasma lipids in patients with chylomicronemia and in Tangier disease

The relationship between erythrocyte membrane structural and functional alterations and plasma lipids was studied in three patients with chylomicronemia due to either lipoprotein lipase (LPL) deficiency, apo C-II deficiency (in an individual who also suffers from thalassemia minor) or coexistent diabetes mellitus (and decreased LPL activity) and in a patient with Tangier disease. All of the patients' erythrocytes had significantly elevated phosphatidyl-choline (PC): sphingomyelin (Sph) ratios (most marked in the patient with Tangier disease). Major differences were observed in the PC: Sph ratios of erythrocytes and plasma. The pattern of changes in erythrocyte membrane enzyme activities differed despite similarities in the lipid composition of the erythrocytes. The changes in osmotic fragility (OF) were inversely related to the membrane cholesterol:phospholipid ratio. An even stronger negative correlation was found between OF at the lowest NaCl concentrations and the activities of both Na+,K+- and Mg++-ATPases. The ratio of total: surface sulfhydryl titres also correlated significantly with OF.     

A cytochemical study of leukocyte lipids in patients with viral hepatitis

The lipid content of the neutrophilic leukocytes has been measured in 64 patients with viral hepatitides by the cytochemical methods over the course of the disease. The studies have revealed a regular depression of the lipid content in the leukocytes, depending on the disease stage and severity as well as on the treatment administered. This fact evidences the tension of the defense mechanisms of the body. Studies on the leukocytic intracellular lipids in viral hepatitis display the pattern of the pathochemical changes in the body and show the defense potential of the body in this disease.     

Cell-mediated immunity to acetaldehyde in alcoholic liver disease demonstrated by leukocyte migration test.

To determine whether a sensitization to ethanol metabolites occurs in alcoholic liver disease, reactivity of lymphocytes to nontoxic amounts of acetaldehyde was studied by direct elaboration of migration inhibitory factor (MIF) production. Eighteen alcoholics with various degrees of biopsy-proven liver damage showed increased MIF production in response to acetaldehyde; the mean value of the group differed significantly from 15 healthy controls, 15 subjects with nonalcoholic liver disease, and 15 alcoholics without liver involvement (P less than 0.001, P less than 0.001, P less than 0.02, respectively). Among the alcoholics with liver disease, none individuals (50%) with histological signs of advanced alcoholic hepatitis showed the highest percentage of inhibition of migration; the value differed significantly from the remaining patients with lesser degrees of hyaline necrosis in liver biopsies (P less than 0.005). These results indicate that acetaldehyde is involved in the pathogenesis of alcoholic hepatitis. Clinically, this test might facilitate the selection of patients with alcoholic hyaline necrosis.     

Serum lipids as biochemical manifestations of hepatic alcoholic, viral, and mixed viral-and-alcoholic lesion

The parameters of lipids, which reflect the morphological manifestations of hepatic damages of alcoholic, viral, and mixed viral-and-alcoholic genesis, were determined. The serum lipid spectrum was studied in 50 alcoholic patients without viral hepatitis markers, in 30 patients with chronic viral hepatitis B (CVHB), and in 40 with CVHB concurrent with alcoholism. Puncture biopsy of the liver and a histological study of its biopsy specimen were made in 47 patients. Total lipid levels above 9.0 g/l were the most typical biochemical marker of alcoholic damage to the liver; lysophosphatidylcholine (LPC) levels below 7% were a marker of its viral damage; total lipid levels above 9.5 g/l and LPC levels below 5% were a marker of its viral-and-alcoholic damage. Thus, serum lipids may be used as biochemical markers of the morphological manifestations of hepatic damages of various genesis.     

Long-term ethanol consumption and macrocytosis: diagnostic and pathogenic implications

Although excessive alcohol consumption is known to elevate the mean cell volume (MCV) of erythrocytes, the relationships among the intensity of ethanol exposure, the generation of abnormal red blood cell indices, and the underlying pathogenic mechanisms have remained unclear. The authors examined 105 alcoholics with a wide range of ethanol consumption (40-500 g of ethanol/day), 62 moderate drinkers (mean consumption 1-40 g/day), and 24 abstainers, who underwent detailed interviews, measurements of blood cell counts, markers of liver status, and circulating antibodies against ethanol-derived protein modifications. Follow-up information was collected from healthy volunteers with detailed records on drinking habits. Data from the NORIP project for laboratory parameters in apparently healthy moderate drinkers or abstainers (n = 845) were used for reference interval comparisons. The highest MCV (P < 0.001) and mean cell hemoglobin (MCH) (P < 0.01) occurred in the alcoholics. However, the values in the moderate drinkers also responded to ethanol intake such that the upper normal limit for MCV based on the data from moderate drinkers was 98 fl, as compared with 96 fl from abstainers. Follow-up cases with carefully registered drinking habits showed parallel changes in MCV and ethanol intake. Anti-adduct IgA and IgM against acetaldehyde-induced protein modifications were elevated in 94% and 64% of patients with high MCV, respectively, the former being significantly less frequent in the alcoholics with normal MCV (63%) (P < 0.05). The data indicate dose-related responses in red blood indices upon chronic ethanol consumption, which may also be reflected in reference intervals for hematological parameters in health care. Generation of immune responses against acetaldehyde-modified erythrocyte proteins may be associated with the appearance of such abnormalities.     

血脂、胆红素、尿酸及不同炎性细胞与冠心病的相关性分析

目的探讨血脂、胆红素、尿酸及不同炎性细胞变化在冠状动脉粥样硬化性心脏病患者中的临床意义。方法选择142例经冠脉造影证实为冠状动脉粥样硬化性心脏病的患者,按造影结果分为单支病变组(58例),双支病变组(46例)和多支病变组(38例),并设60例冠脉造影正常患者为对照组,按照SYNTAX评分系统衡量冠脉造影结果。入院时测其白细胞计数、白细胞亚型计数及比例、中性粒细胞计数/淋巴细胞计数比值(NLR)及血脂、胆红素和尿酸,分析患者血脂、胆红素、尿酸及不同炎性细胞变化的临床意义及其与SYNTAX评分的相关性。结果随着冠脉病变支数增加,TG、LDL-C及UA水平升高(P<0.05),而TBiL、IBiL水平明显降低(P<0.05);白细胞计数、单核细胞计数及NLR值升高(P<0.05),而淋巴细胞计数降低(P<0.05);多元线性回归分析提示TG、HDL-C及UA与冠状动脉造影SYNTAX评分独立相关(其偏相关系数分别为0.264、-0.275、0.205,P<0.05),白细胞计数和NLR与SYNTAX评分独立相关(偏相关系数分别为0.587、0.342,P<0.05)。结论随着冠脉病变程度和范围进展,TG和UA水平升高而HDL-C降低;白细胞计数和NLR值升高,提示血脂和尿酸及不同炎性细胞与冠脉病变相关。     

Erythrocyte aldehyde dehydrogenase activity in alcoholic subjects and its value as a marker for hepatic aldehyde dehydrogenase in subjects with and without liver disease

Erythrocyte aldehyde dehydrogenase activity was assayed in actively drinking alcoholics, patients with alcoholic liver disease who claimed to be abstaining, patients with non-alcoholic liver disorders and normal controls. Hepatic cytosolic aldehyde dehydrogenase was also assayed in the majority of the subjects. Actively drinking alcoholics had significantly lower erythrocyte aldehyde dehydrogenase activity than controls (P less than 0.01) but abstaining alcoholic liver disease and non-alcoholic liver disorder subjects did not. There was a significant correlation between erythrocyte and hepatic cytosolic aldehyde dehydrogenase activity in the control group (r = 0.94, P less than 0.05) but not in the other study groups.     

红细胞免疫系统研究进展

1930年Duke发现锥虫在抗血清及补体存在时可黏附到人类红细胞膜上,并发现不同人红细胞对锥虫的黏附能力不同。1953年Nelson发现调理过的梅毒螺旋体及肺炎双球菌也可结合到人类红细胞膜上,并称之为免疫黏附。1963年Nishioka证实这种免疫黏附现象是通过人红细胞膜C_3受体(补体受体Ⅰ型,CR1)而实现的。1981年美国生殖免疫学家     

Erythrocyte transketolase activity in uremia

We performed a study concerning the activity of erythrocyte transketolase and thiamine metabolism in 73 uremic patients with or without neuropathy and 67 normal control subjects. Although the total vitamin B1 level in whole blood was high in the uremic patients, the transketolase activity in the hemolysate and the thiamine pyrophosphate effect on it were lower than those of normal subjects. The values of the transketolase activity of the two groups were statistically correlated with the levels of the thiamine pyrophosphate effect and the vitamin B1 content of the blood. Inhibition of transketolase activity was apparent in the uremic patients. However, this inhibition did not seem to be the only cause for the development of uremic neuropathy since no significant difference in these activities was observed among uremic patients with and without neuropathy. Moreover, a direct correlation could not be confirmed between transketolase activity and motor nerve conduction velocity.