Acetaldehyde alters coagulation protein function

Basista, Michael H.; Joseph, Attaya; Smolen, Steve; Koterba, Alan; Brecher, Arthur S.

doi:10.1007/bf02087660

Cited by 29 publications

(16 citation statements)

References 12 publications

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“…Hence, free acetaldehyde in the blood plasma would not be anticipated in quantity. The potential of fibrinogen to be clotted is also diminished by acetaldehyde [9], as is thrombin [12]. Prior thrombin and fibrinogen studies both utilized thrombin-fibrinogen interactions in the absence of plasma.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Acetaldehyde on Human Plasma Factor XIII Function

Suchocki

Brecher

2007

Dig Dis Sci

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The effect of acetaldehyde on the transglutaminase activity in pooled normal human plasma has been investigated. In this study, 0.05, 0.2, and 0.7 ml of pooled human plasma were preincubated for 30 min. at room temperature with buffer or acetaldehyde at final concentrations of 40.6, 22.4, and 11.2 mM before being utilized for Factor XIIIa assay with fibrinogen and thrombin which had been preheated at 40 degrees C to destroy endogenous Factor XIII/XIIIa activity. At all concentrations of acetaldehyde and all concentrations of plasma-containing Factor XIII which were employed, prolongation of both clotting time and stabilization time was observed. The 11.2 mM acetaldehyde is within the range of daily acetaldehyde production to be predicted in severe alcoholics as a consequence of imbibing alcohol. The stabilization times measured for Factor XIIIa activity appear to be the most sensitive to acetaldehyde compared to acetaldehyde effects on thrombin, Factor Xa, and fibrinogen studied earlier in this laboratory, as well as Factors II, VII, and X.

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Section: Discussionmentioning

confidence: 99%

The Effect of Acetaldehyde on Human Plasma Factor XIII Function

Suchocki

Brecher

2007

Dig Dis Sci

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“…The prolonged clotting times are attributed to a deficiency of vitamin K and a subsequent varying degrees of the production of coagulation factors [17]. Also acetaldehyde (ACH), the primary metabolic product of ethanol can contribute to this failure by inactivating the coagulation system [18][19][20][21][22] through the interaction with coagulation proteins at high concentrations [23].…”

Section: Discussionmentioning

confidence: 99%

“…-Group 1: asphyxial deaths with BAL>1‰ (N=69, 18 females, 51 males; mean age, 46.5 years); in all cases, the cause of death was asphyxia. The minimum BAL was 1.04‰, the highest 4.11‰ with a mean value of 2.37‰.…”

Section: Methodsmentioning

confidence: 99%

Clotted blood as sign of alcohol intoxication: a retrospective study

et al. 2007

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A total of 138 autopsies performed at the Institute of Legal Medicine of the University of Münster between 1994 and 2006 were subdivided into two groups: (1) 69 asphyxial deaths with a blood alcohol level (BAL) > 1 per thousand and (2) 69 asphyxial deaths with a BAL of 0.00 per thousand. The coagulation state in the central vessels was registered in all cases as fluid, compactly clotted or loosely clotted, and the post-mortem interval was recorded. Histology investigations were performed on the liver to analyze the incidence of hepatic fibrosis/cirrhosis. Fisher's exact test was performed to check for statistical significance. The blood was found to be clotted in 49.3% of the cases of group (1) and in 5.8% of group (2) (p < 0.01). The post-mortem interval did not have any influence on the coagulation state as observed in both groups. Liver fibrosis/cirrhosis was a rare finding detected in three cases in group 1 and in two cases in the control group 2 and, therefore, not relative to our observations. A distinctly positive BAL is often associated with heavy stages of blood coagulation as observed during autopsy. Distinctly positive alcohol concentrations have an influence on the fibrinolytic process and, hence, on the coagulation status.

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“…Acetaldehyde, one of the products of alcohol metabolism, could react with coagulation proteins to alter their function (Basista et al 1994) or form adducts with platelets which may interfere with their activation and aggregation (Spertini et al 1992). Another possibility is that ethanol inhibits secretion of phospholipase A2 (EC 3.1.1.4) with resultant suppressed arachidonic acid release from platelet membranes, and decreased prostanoid formation and aggregation responses (Stubbs & Rubin, 1992).…”

Section: Effects Of Alcohol Intakementioning

confidence: 99%

Diet and haemostatic processes

Vorster

Jerling

1997

Nutr. Res. Rev.

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Diet plays an important role in the primary and secondary prevention of cardiovascular disease. The growing perception that abnormal haemostatic processes of coagulation, platelet aggregation and fibrinolysis contribute to cardiovascular disease aetiology motivated this review on the relationships of diet, specific foods and nutrients with haemostatic function. Functional endpoints that reflect the function and status of some of these processes and which can be measured in dietary trials are identified. The effects of energy intake and expenditure, alcohol, total fat and specific fatty acids, non-starch polysaccharides (dietary fibre), antioxidant nutrients and some foods on a variety of haemostatic markers are reviewed. The results indicate that the prudent low-fat, high-fibre diet and maintenance of ideal body weight recommended to protect against and treat hyperlipidaemia and coronary heart disease will also benefit haemostatic profiles. It is concluded that more research on specific effects is needed for improved recommendations on a population level for prevention of cardiovascular disease.

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Acetaldehyde alters coagulation protein function

Cited by 29 publications

References 12 publications

The Effect of Acetaldehyde on Human Plasma Factor XIII Function

The Effect of Acetaldehyde on Human Plasma Factor XIII Function

Clotted blood as sign of alcohol intoxication: a retrospective study

Diet and haemostatic processes

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