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J L Beaumont

Publications and source records attributed to J L Beaumont.

At least 19 recordsLinked to original sources
PubMed1992

Hyperhomocyst(e)inemia, anti-estrogen antibodies and other risk factors for thrombosis in women on oral contraceptives.

Hyperhomocyst(e)inemia was shown to be associated with vascular occlusion in atherosclerotic patients. We have conducted a study to determine if hyperhomocyst(e)inemia was also related to the vascular events observed in women on oral contraceptives, presumably having little or no atherosclerosis. Two hundred women receiving oral contraceptives were included in the study: 100 were healthy controls and 100 had documented vascular occlusion. Determination of serum homocyst(e)ine and anti-estrogen antibody levels wore performed under blind conditions. They were evaluated in logistic regression models in which age and smoking were also included. Women with vascular occlusion had higher levels of homocyst(e)ine (P less than 0.001) and of anti-estrogen antibodies (P less than 0.001) when compared to controls. They were also older (P less than 0.001) and more frequently smokers (P less than 0.05). The above mentioned variables were, in isolation, independent predictors of vascular occlusion. Moreover, a model assessing those variables and their interactions indicated that the levels of anti-estrogen antibodies and smoking increased the predictability in older women, as well as the levels of age-adjusted homocyst(e)ine. The study suggests that the above factors can identify women at risk and that determination of anti-estrogen antibodies and homocyst(e)ine levels may help to detect women predisposed to vascular occlusions when taking oral contraceptives.

Adult↗
PubMed1991

Oral contraceptives, sex steroid-induced antibodies and vascular thrombosis: results from 1318 cases.

The role of antiethinyl estradiol antibodies (anti EE Ab) and associated risk factors was evaluated in 1318 cases of venous or arterial thrombosis in oral contraceptives (OC) users, and compared to 61 non-users and 124 healthy current users. Anti EE Ab were absent in non-users and present in 33% of healthy users and 72% of those with thrombosis, either arterial or venous. Age, duration of use, hyperlipidaemia and smoking were factors associated with thrombosis only in women with an arterial disease. While the two predominant factors, anti EE Ab and smoking may be risk factors in their own right, the combination of both was found in 47.7% of women with thrombosis. It is proposed that thrombosis associated with OC use may be explained by an immunological disease in which anti EE Ab and their complexes with the circulating synthetic hormones may be harmful to the vessels, as also suggested by the type of lesions already described in OC users. The determination of anti EE Ab in healthy users may identify a group at risk of thrombosis.

Adult↗
PubMed1990

Circulating IgA-Lp complexes in Watanabe heritable hyperlipidemic and cholesterol fed NZW rabbits.

Auto-immune immunoglobulin-lipoprotein complexes (Ig-Lp), as well as other modified lipoproteins, are activators of the transformation of macrophages into foam cells which may be the first step in atherogenesis. In humans circulating Ig-Lp have been demonstrated in autoimmune hyper- or dyslipidemia (AIH, DIH) and found to be associated with conditions related to atherosclerosis. Thus Ig-Lps may be significant and potentially primary atherogenic factors. In order to test this hypothesis we compared the distribution of Ig-Lps in 14 WHHL homozygote rabbits and in 15 normal fed and 8 cholesterol-fed NZW rabbits, all males aged 4-6 months. The Ig-Lps were detected by ELISA using 2 different capture anti-Lp and 4 indicator antibodies specific for either total Igs or the IgA, IgM or IgG classes. Some Ig-Lp of all classes were found in normal fed NZW. As compared with these normal levels, IgA-Lp are increased 2.5-fold in both the WHHL and the cholesterol-fed NZW rabbits (P = 0.0002). During cholesterol feeding the increase of IgA-Lp and total cholesterol and their decrease after returning to a normal diet were parallel in NZW rabbits, but their variation was mainly independent. IgM-Lp was also increased, but to a much lesser extent, in WHHL and in cholesterol-fed NZW. IgG-Lp was not increased in WHHL and only moderately increased in some of the cholesterol-fed NZW. The WHHL and the cholesterol-fed NZW rabbits did not differ by the IgA-Lp content of the serum, but the level of IgM-Lp was higher in the former.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Retinyl palmitate labeled intestinally derived lipoproteins accumulate in the circulation of WHHL rabbits.

The behavior of native retinyl palmitate labeled intestinally derived lipoproteins and their remnants was studied in 8 NZW and 8 WHHL (5 homo- and 3 heterozygote) normal-fed rabbits and in 3 cholesterol-fed NZW, after 1 month of cholesterol feeding, and 3 and 5 months after resuming normal feeding. Palmitate labeled lipoproteins were produced by the intestine after administration of 50,000 IU of Vitamin A, together with olive oil via gastric intubation. Blood was drawn before and 3,6,9,12,24, and in some instances, 48 h later. Retinol (R) and retinyl palmitate (RP) were measured in whole serum and in the chylomicron, d less than 1006, d greater than 1006 less than 1019, d greater than 1019 less than 1063, d greater than 1063 less than 1210 g/ml lipoprotein fractions and in the infranatant. The R content of the serum was almost all concentrated in the infranatant, it did not change during the vitamin A test and was similar in WHHL, and normal- or cholesterol-fed NZW rabbits. In the normal-fed NZW the RP content of the serum increased within 6 h after giving the vitamin A fat meal (peak value less than 200 microgram/100 ml) and then decreased. In the WHHL homozygotes, the RP increased to a much greater degree (peak value 600-1820 micrograms) and for a much longer time, as it was still increased in the 5 cases studied after 24 h, and in 3 cases studied after 48 h. Similar RP curves were obtained in NZW rabbits, after 1 month of cholesterol feeding.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Vascular risk of oral contraceptive agents: realities and mechanisms. II. Mechanisms of vascular accidents: their prevention].

The mechanism of the vascular complications related to oral contraception is still unclear. In the present paper are discussed: (a) the possibility of accelerated atherosclerosis, suggested by the presence of a number of risk factors, a hypothesis which is not confirmed by pathological findings; (b) the possibility of a coagulation disease leading to thrombosis; (c) the arguments in favor of an immunological mechanism. This hypothesis is supported by the strong correlation between vascular complications and presence of antibodies against the synthetic hormones contained in the drug. It is also consistent with the aspect of the lesions, which might be induced by circulating immune complexes and antibodies. It is proposed that women at risk should be detected by systematic determination of antiethinylestradiol antibodies.

Adult↗
PubMed1989

[Vascular risk of oral contraceptive agents: realities and mechanisms. I. Risk evaluation].

The suspected risk of oral contraception was confirmed when large scale epidemiological studies became available. The present work recalls the methodology of a good evaluation, the pros and cons of retrospective and prospective studies, the different appreciations provided by measuring "relative risk" or "attributable risk". In terms of public health, the data obtained supported the necessity to include mortality related to oral contraception in an evaluation of reproductive mortality. This work compares the incidence of vascular complications evaluated through different studies, according to the criteria selected and the type of vascular disease. The advantage of lowering estrogen content is considered.

Abortion, Spontaneous↗
PubMed1979

[A method of separation of antilipoprotein immunoglobulins by chromatography on glass beads (author's transl)].

In this method, under certain experimental conditions, the use of calibrated glass beads permitted the separation of lg with antilipoprotein antibody activity (HLAA). The sera are first precipitated on ammorium sulphate at 25 per cent, 30 per cent and 40 per cent saturation. The precipitates are then submitted to short ultracentrifugation and the product of ultra-entrifugation is fractionnated on a glass bead column, balanced then eluted with an acetate veronal buffer at pH 9. The eluted fraction in peak 1 contains antibodies (IgG or IgA) and albumin. Passive hemagglutination with red cells covered with beta and alpha-lipoproteins, through chromium chloride, together with inhibition of the reaction show that the activity of these Ig antibodies is directed against lipoprotein antigens.

Chromatography, Affinity↗
PubMed1979

Cholesterol synthesis by human fibroblasts in the presence of LDL and anti-LDL IgA.

LDL interact with fibroblasts through specific membrane sites. This reaction is the first step of a mechanism which leads to the regulation of intracellular cholesterol synthesis. When LDL form a complex with an IgA from a myeloma serum with mixed hyperlipidemia and xanthomatosis, they no longer function as a regulator, and the result is excess production of free intracellular cholesterol. No excess cholesterol production is observed when myeloma IgA is replaced by control IgG and IgA.

Cholesterol↗
PubMed1978

In vitro interaction of LDL, anti-lipoprotein IgA and human fibroblasts.

Human LDL were bound and internalized by cultured human fibroblasts. When an antilipoprotein IgA kappa from a case of myeloma with hyperlipidemia and xanthomatosis was introduced into the system, LDL uptake dropped by 50% but LDL binding to fibroblasts was unchanged. In the same system, IgG and IgA controls were inactive.

Adult↗