Prostate specific antigen production by breast tumors after induction with oral contraceptives.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
The use of oral contraceptives have been shown to produce alterations in the normal physiology of many organ systems. However, little is known as to the effect of oral contraceptives on the immune response. The current study was undertaken to determine if women on low dose oral contraceptives show alterations in their initial immune response. An in vitro assay stimulating human peripheral lymphocytes was used. No differences were found in the proliferative immune response of B- or T-cells in women taking low dose oral contraceptives as compared to controls. This study suggests that the initial immune response of lymphocytes in patients on low dose oral contraceptives remains intact.
Explore the source record for details and available documents.
Eighty-one women with a history of thrombosis were classified into three groups: group I (n = 29), women in whom thrombosis developed during oral contraception; group II (n = 33), those who used oral contraceptives (OC) without complications but experienced vascular occlusion in other risk situations; group III (n = 19), women who never used OC. The level of antibodies to anionic phospholipids (PLa), a response to activated protein C (APC), and the presence for the mutation in the coagulation factor V gene causing APC resistance were studied. In the studied groups, APC resistance was present in 14% to 42% of patients. PLa were elevated in about half of APC-resistant patients. The incidence of APC resistance correlated with the recurrency of the thrombotic events within the groups. In most cases it was tightly connected to the mutation in the factor V gene. Women in whom thrombosis developed while they were taking OC (group I) differed from the others, having a remarkable disagreement between the lowest incidence of APC resistance and a relatively increased number of the mutation (14% vs 38%, p < 0.025). This finding suggested that the APC response is flexible. An influence of OC that predisposes a reduction in APC response is discussed.
Explore the source record for details and available documents.
QUESTION: In the "Journal of the American Medical Association" editorial "Oral contraceptives and immune responses" (209: 410, 1969) the following statement appears: "Other reactions of delayed hypersensitivity, such as the tuberculin response, are similarly suppressed by estrogens and presumably by oral contraceptives also." Does this mean that women taking birth control pills may have a false-negative tuberculin skin test reaction? ANSWER: I am not aware of any studies of tuberculin skin test reaction in women taking birth control pills. However, in the immunologic studies which have been done, the birth control pills have had primarily the same effect as estrogen. There are experiemntal studies in animals in which the findings point to a considerable reduction, though not an abolition, of tuberculin skin test sensitivity in animals given estrogen. It seems likely, therefore, that the tuberculin sensitivity in the skin may well be somewhat reduced in women taking oral contraceptives, though direct evidence is lacking.
During the past decade, family-planning programmes have been conducted on the assumption that developments in the field of contraception (e.g., hormonal contraceptives and intra-uterine devices) had reached a stage of considerable technical perfection. Enough information has now been accumulated, however, to indicate that this assumption was not fully justified; the high drop-out rates from these programmes observed under different conditions indicate that there is an urgent need for further improvements of the existing methods and for the development of new methods based on different approaches. A prerequisite for the development of such methods is a greatly improved knowledge of the physiological factors influencing the various steps of the reproductive processes in the human species.In an attempt to focus attention on the various steps which are susceptible to controlled interference, a brief review is given of some of the present concepts of the regulation of spermiogenesis, ovulation and the menstrual cycle, sperm capacitation, fertilization, tubal passage, zygote and blastocyst formation, implantation and early embryonic development. It is concluded that the reproductive processes are indeed subject to intricate biochemical and hormonal regulatory mechanisms and that the different phases of these processes do offer a variety of possibilities for hormonal, pharmacological and perhaps also immunological interference.
Three types of data are presented which suggest that sperm receptor activity is associated with a 58,000 Mr acidic glycoprotein (PPZA) isolated from pig zonae: (1) boar sperm fail to bind to pig zonae pretreated with univalent antibody to PPZA; (2) boar sperm pretreated with PPZA are inhibited in binding to intact pig zonae; (3) binding studies utilizing boar sperm and radiolabeled PPZA indicate an inhibition of radiolabeled PPZA binding to sperm by non-labeled PPZA in a dose-related manner. Collectively these data suggest that, at least in the pig system, the contraceptive action of zona antibodies is accomplished by a specific immunologic reaction between antibody and the zona sperm receptor site rather than to a non-specific blockage of this receptor.
The ability of condoms to retain all elements of semen during intercourse has been assessed by postcoital visual inspection and in vitro permeability studies. Yet, these observations may not be sufficiently precise or realistic. This pilot study evaluated prostate-specific antigen (PSA) as a semen marker of inapparent failure of the condom barrier under conditions of actual use. Twelve couples collected samples from the vagina and surfaces of the condom using sterile cotton swabs. We obtained precoital and postcoital samples for 24 acts of unprotected intercourse, 54 acts of intercourse using intact condoms, and 40 acts of intercourse using condoms that had been deliberately punctured. We used electrophoresis to determine the amount of PSA present in the samples. PSA was detected in 100% (24/24) of vaginal samples collected immediately after unprotected intercourse and in none of the vaginal samples collected more than 24 h after intercourse (0/90). PSA was also present in 98% (83/85) of the samples collected from the inside of the condom that had failed during intercourse. Excluding uses where the condom failed during intercourse, PSA was detected in 2% (1/47) of the postcoital vaginal samples collected after use of intact condoms and in 41% (14/34) of the samples collected after use of condoms with known 1-mm punctures. We conclude that PSA shows great promise as a semen biomarker in clinical trials of barrier methods. We recommend that future studies further investigate the ability of this biomarker to identify condom failures and quantify the extent of semen exposure associated with various types of condom failures.
A significant increase in the number of old people in the populations of developed countries was followed by an increase in morbidity and mortality resulting from main age-related diseases -- cardiovascular, cancer, neurodegenerative, diabetes mellitus, decrease in resistance to infections. Obviously, the development of the means of prevention of the premature aging of humans is crucial for the realization of this program. However, data available on such kind of means are rather scarce, contradictory and are often not reliable from the points of view of the adequacy of the experiments to current scientific requirements as well as the interpretation of the results and safety. Data available on the increase in life span and the adverse effects of the following geroprotectors were critically analyzed: antioxidants, chelate agents and lathyrogens, succinate, adaptogens and herbs, neurotropic drugs, inhibitors of monoamine oxidase, glucocorticoids, dehydroepiandrosterone, sex and growth hormones, melatonin, pineal peptide preparations, protein inhibitors, antidiabetic biguanides, thymic hormones and peptides, immunomodulators, enteroadsorbents, lypofuscin inhibitors, as well as calorie intake restriction and special diets. Most of the available results were insufficient and could not provide convincing evidence for the life span extension and the safety of the suggested geroprotectors. Drugs and means prolonging the life span could be subdivided into three groups: (a) geroprotectors prolonging the life span equally in all the members of the population: these postponed the beginning of the population's aging; (b) geroprotectors decreasing the mortality rate in a long-lived subpopulation, which raised their maximal life span: these slowed down the population's aging rate; (c) geroprotectors increasing the survival rate in a short-lived subpopulation without changes in the maximal life span: in this case, the aging rate increased. There was a high positive correlation between the type of geroprotector-induced aging delay and the pattern of tumour development in the same population of animals. The first type of geroprotectors did not influence the incidence of tumour but increased tumour latency. The second type of geroprotectors was effective both in the inhibition of spontaneous carcinogenesis and the increase in tumour latency. Certain drugs of the third type raised tumour incidence in the exposed populations. According to the multistage model, geroprotectors either inhibit or accelerate the passage of carcinogen-exposed cells form one stage to another. Thus, the efficacy of geroprotectors as preventive means of cancer development will decrease with respect to the age of exposure onset. Recommendations of the available drugs and means of life span increase should be carefully reconsidered under the international scientific control.
Rabbit polyclonal antibodies to the idiotype of murine monoclonal anti-sperm antibodies were developed and characterized. M29.6 and M42.15 are monoclonal antibodies (mAbs) that inhibit fertilization in vivo and in vitro. Sera from rabbits inoculated with purified mAbs (Ab1) were absorbed with normal mouse and isotype-specific immunoglobulin (Ig); the anti-idiotype Ig fraction (Ab2) was isolated by protein A-chromatography or by chromatography on the corresponding idiotype column. Binding specificity of Ab2 was confirmed by measuring the reactivity of Ab2 with homologous and heterologous mAbs. Ab2 competitively inhibited 125I-labeled Ab1 binding to mouse sperm, suggesting that the Ab2 preparation possessed subpopulations directed against idiotopes similar or adjacent to the antigen-binding site of the mAb. Anti-idiotype antibodies reactive with the antigen-combining site of the anti-sperm mAb may contain subpopulations that mimic the mouse sperm epitope recognized by Ab1. Immunization with Ab2 induced anti-(anti-idiotype) antibodies (Ab3), which competitively inhibited binding of 125I-labeled Ab1 to immobilized Ab2. These results are consistent with the hypothesis that immunization of mice with antibodies to the idiotype of sperm-specific mAbs can induce antibodies that share structural similarities with the anti-sperm mAb used for their induction. Immunization with anti-idiotype antibodies that mimic sperm antigen structure represents a possible strategy for induction of immunity to sperm.
Sperm antigens were assessed for their ability to induce cell-mediated immune (CMI) responses. Purified fertilization antigen (FA-1), protamine, and the lithium diiodosalicylate (LIS)-solubilized sperm preparation activated presensitized lymphocytes to secrete soluble mediators that activated macrophages and significantly inhibited sperm motility and embryonic development. The FA-1, however, was the most potent antigen in inducing proliferative response as well as the release of soluble mediators. LIS-sperm preparation, which contained numerous antigens, showed the least activity. The unsensitized control spleen cells did not secrete any factor(s) when activated with the antigen. In conclusion, these results indicate that sperm antigens can specifically induce (CMI) factors that have detrimental effects on sperm motility and preimplantation embryos. These findings may have potential clinical implications for humans, especially in immunologic and unexplained infertility, recurrent abortions, and development of antisperm contraceptive vaccines.
The frequency of genital Herpes simplex type 2 infections in a group of twenty adult Costa Rican women was studied by isolation of the virus and the measurement of neutralizing antibody activity in sera. The virus could not be isolated in any of the vaginal secretions. Neutralizing antibody activity to herpes virus types 1 and 2 was found in sera from sixteen subjects. An antibody II/I index equal to or larger than 87, indicative of infection with Herpes simplex type 2 was found in fifty per cent of the population studied, a second segment was composed by the subjects with indices below 87. Evaluation of antibody activity to Herpes simplex type 2 revealed that: a) only a small percentage of the women lacked detectable antibody activity to the virus; b) there is a significant difference (p < 0.005) between the mean number of years of sexual experience among the two population segments; and c) there is a positive correlation (p < 0.05) between II/I index values and age among the women of the population segment with a II/I index equal to or larger than 87.
A 26 year-old woman presented with a left hemichorea while taking oral contraceptives (a combination of ethinyl-estradiol and norethisterone). There was marked improvement of the choreic movements after discontinuation of the oral contraceptive and complete resolution by 6 weeks. Induction of chorea is a rare complication of oral contraceptives. The possible mechanisms are briefly reviewed.
OBJECTIVE: To investigate the influence of breast feeding, use of the oral contraceptive pill (OCP), and parity on rheumatoid arthritis (RA). METHODS: One hundred and seventy six women with RA were compared with 145 control subjects; all had at least one child. RA patients were classified as having severe (n = 82) or mild disease (n = 89) according to clinical joint evaluation, radiological score, biological inflammation, and the presence of HLA-DR1 or -DR4 alleles. RESULTS: The mean age of RA patients was 58 years, and the mean age at the time of diagnosis of RA was 46 years. The mean time between onset of RA and the first birth was 23.6 (SD 3.8) years. The OCP user rates were 33% in the RA group and 47.6% in the control group (p < 0.02). OCP use was related to the mother's year of birth. The relative risk for developing RA was 0.598 (95% confidence interval (CI) 0.33 to 1.1) in women who had used OCP for more than five years compared with those who had never used OCPs. In contrast, the age at which the first pregnancy occurred, the number of children breast fed, and the duration of breast feeding were comparable in RA patients and healthy subjects. Among the RA patients, parity, duration of breast feeding, and the number of breast fed children were significantly increased in those with severe disease. Having more than three children increased the risk of developing severe disease 4.8-fold when adjusted for age and OCP use. Forty six percent of women with severe RA had a history of breast feeding duration greater than six months before disease onset, compared with 26% of patients with mild disease (p < 0.008). Having more than three breast fed children increased the risk of poor disease prognosis 3.7-fold. In contrast, OCP use had a protective role in the course of RA (44% of RA patients with mild disease were OCP users, compared with 21.7% of those with severe RA; p < 0.001). Among those using OCP for more than five years, the relative risk of developing severe disease was 0.1 (95% CI 0.01 to 0.6), after adjustment for age, parity, and breast feeding. CONCLUSION: Our results suggest that parity, and to a lesser extent breast feeding, before RA onset worsened RA prognosis, whereas OCP use had a protective role. Prolactin and oestrogen may have a role in these effects.
Previous reports speculated that vascular events could be related to the development of antibodies against synthetic steroids contained in oral contraceptives or other hormonal treatments. This study describes original immunoassays designed to detect antisynthetic steroid antibodies. In a first step, the assays were characterized and validated using animal-raised antisteroid antibodies. In a second step, a population of 88 oral contraceptive users, 47 of them having developed a vascular thrombosis during synthetic steroid use and 41 serving as healthy control users, were tested. Detection of antibodies against ethinylestradiol, levonorgestrel, norethisterone, cyproterone acetate, and gestodene showed that the values obtained in normal oral contraceptive users as well as thrombosis patients are very low, and show no statistically significant difference between the two groups tested. Taken together, these data indicate that the "immunological hypothesis" related to antisteroid antibodies is unlikely to explain the pathogenesis of vascular events in oral contraceptive users.
Explore the source record for details and available documents.
Explore the source record for details and available documents.