Blood-Groups and Blood-Clotting

Mourant, A. E.; Kopeć, AdaC.; Domaniewska-Sobczak, Kazimiera

doi:10.1016/s0140-6736(71)90961-5

Cited by 61 publications

(15 citation statements)

References 9 publications

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“…Whether these lower VIIIC and vWF levels may account for our observed higher APTT values in O subjects is unknown. The ABO blood group influence on APTT values would fit an observed significant excess of non-0 blood group patients relative to O patients among population with thromboembolic dis ease [21][22][23].…”

Section: Discussionmentioning

confidence: 96%

Influence of Age, Sex and ABO Blood Group on Activated Partial Thromboplastin Time

Fourel

Gabastou²,

Roure³

et al. 1993

Pathophysiol Haemos Thromb

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To evaluate the influence of age, sex and ABO blood group on the activated partial thromboplastin time (APTT), we performed this test in 642 preoperative ambulant adult subjects. There was a significant negative correlation (R = 0.31, p < 0.001) between age and APTT. Sex and ABO blood group had a significant influence on APTT, with lower mean in females (30.9 s) and non-0 subjects (30.7 s) than in males (31.6 s) and·subjects (32.0 s) (p = 0.015 and < 0.001, respectively). The largest difference between the upper cut-off values of APTT determined in patient subgroups defined on age, sex and ABO blood group is observed for non-O females over 40 years (36.9 s) and·males under 40 years (41.1 s). These results emphasize the laboratory’s difficulties to define valid APTT normal range and thus to detect true mild coagulation disorders in preoperative asymptomatic patients.

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Section: Discussionmentioning

confidence: 96%

Influence of Age, Sex and ABO Blood Group on Activated Partial Thromboplastin Time

Fourel

Gabastou²,

Roure³

et al. 1993

Pathophysiol Haemos Thromb

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“…Rh -ve 4/6 0-67 0/9 0 < 0-02 patients stronger antibody producers (Ichikawa, 1959) more prone to most autoimmune diseases (Mourant et al, 1978), more at risk from haemorrhage (Mourant et al, 1971), and J perhaps more cancer resistant (Mourant, 1976) *Conversion factor for mg%, x 6. tBy x2 for difference between proportions of non-cancer deaths in levamisole and placebo groups without correction for multiple comparisons.…”

Section: Resultsmentioning

confidence: 99%

Levamisole and surgery in bronchial carcinoma patients: increase in deaths from cardiorespiratory failure.

Anthony¹,

Mearns²,

Mason³

et al. 1979

Thorax

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Life table analysis of early entry to this randomised blind trial of 318 patients has shown a significantly poorer survival for resected lung cancer patients treated with levamisole for three days before operation and three days a fortnight thereafter than for placebo-treated controls. This excess was largely due to deaths that had been attributed to operation or other causes (non-cancer deaths), most occurring in the six weeks after operation. In the 99 resected patients treated with levamisole there was a 15% excess of deaths in this category, compared with the placebo-treated controls. Extensive analysis excluded maldistribution of patients between the groups as a cause of this difference.Many more died in respiratory distress, mostly without clear cause, in the levamisole group. Antibody (lgG) reacting with myocardial sarcolemma or sarcoplasm was found in the only serum samples available for testing which were drawn from patients during the syndrome. The findings are in keeping with a primary effect on the heart, possibly involving an autoimmune mechanism. The effect has not been noted in other trials.

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“…Almost invariably, an excess of either A or B blood groups, or both, and a deficit of O were found among subjects with Ml, as compared to controls. Most of these findings have been summarized by Mourant et al 43 The mean pooled relative incidence of A compared with O was 1.30.…”

Section: Genetic Markers and Coronary Heart Diseasementioning

confidence: 87%

Genetic aspects of arteriosclerosis.

Goldbourt¹,

Neufeld²

1986

Arteriosclerosis

110

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Conclusions 372uals to CHD or atherosclerosis have not been defined. Current methods fall short of an ideal, but unfeasible, experimental set-up in which the results of genetic manipulation could be observed. Still, recent developments have augmented our knowledge to an important degree. During the past decade the discovery of restriction endonucleases and molecular cloning are revolutionizing gene mapping and the understanding of human anatomy and pathology at the DNA level. A recent interdisciplinary approach involving geneticists, epidemiologists, and clinicians has been instrumental in advancing our knowledge. In this review, we will assess the different types of evidence for the genetic determination of indicators of arteriosclerosis. We shall also discuss avenues of investigation that might lead us closer to the formidable, and so far elusive, task of disentangling the contributions of genetic and environmental causes of arteriosclerosis, its precursors, and its sequelae. Familial Aggregation of Coronary Heart DiseaseThe initial suggestion of genetic factors in the etiology of CHD came from findings of familial aggregation of the disease in a number of studies over the past 35 years. 8 ' 9 Research either centered around defined pedigrees or involved the large scale investigation of total communities including core families. One such example is the Tecumseh Study. 10 A significant early observation was made by Slack and Evans 11 who showed that among the relatives of 121 men and 96 women with CHD there was a sevenfold increase in mortality compared with the relatives of 104 male and 105 female controls.Other studies have also examined the risk factors among the first-degree relatives of persons afflicted with CHD in an effort to segregate the risk factors from the familial effect. An important study of familial aggregation was conducted by Rissanen 12 in North Karelia, Finland, and in a southern Finnish population. In North Karelia the CHD risk ratio was 3.5 for brothers of CHD index patients. The form of CHD in the proband brothers resembled that in the patients themselves, in both severity and in fatality. Among 1387 first-degree relatives of 203 male probands with confirmed myocardial infarction (Ml) and 692 relatives of 106 age-matched healthy controls, Rissanen 13 also showed that, for brothers of probands with early diagnosed Ml, a greater risk of CHD by age 55 years (elevenfold if Ml in the proband was established at or earlier than age 45I) was found in subjects from North Karelia than in those from the south (which was sevenfold). This was an important point in light of the notorious regional differences in CHD in Finland. The risk of the probands' brothers increased sharply with decreasing age at onset of disease in the probands. In addition to this most impressive familial aggregation of the disease, Rissanen also showed that hypertension and hyperiipidemia were most common among the relatives of the younger patients, although the contribution of these risk factors diminished with the advan...

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Blood-Groups and Blood-Clotting

Cited by 61 publications

References 9 publications

Influence of Age, Sex and ABO Blood Group on Activated Partial Thromboplastin Time

Influence of Age, Sex and ABO Blood Group on Activated Partial Thromboplastin Time

Levamisole and surgery in bronchial carcinoma patients: increase in deaths from cardiorespiratory failure.

Genetic aspects of arteriosclerosis.

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