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A Vojdani

Publications and source records attributed to A Vojdani.

34 records · Page 2Linked to original sources
PubMed1995

Silicone breast implants and autoimmunity: causation, association, or myth?

In vivo and in vitro studies, case reports and population studies show that: (1) silicone is immunogenic; (2) silicone is biodegradable and transported via the reticuloendothelial system to distant locations; (3) silicone breast implants "leak" and in turn silicone migrates outside the breast tissue; (4) case reports and population studies document an autoimmune reaction and immunological dysfunction in patients with silicone breast implants; (5) these immunological abnormalities and symptoms are reversible upon removal of the breast implants (in 50-70% of cases). The criteria to establish medical causation are defined, and based on those criteria it is concluded that silicone breast implants cause immunological disease.

Animals↗
PubMed1994

Antibody to silicone and native macromolecules in women with silicone breast implants.

Silicone implants have been associated with the development of multiple organ system abnormalities, including rheumatic disorders, nervous system, pulmonary dysfunction associated with autoantibodies and abnormalities of cellular immunity. In this regards a number of case reports and series of articles have been described. We hypothesized that an immune reaction to silicone breast implants would include the host reactivity against silicone and the macromolecules within the microenvironment of the implant, and these autoantibodies may react with other tissue antigens far from the site of the implant. To test this hypothesis 520 Symptomatic women with Silicone Implants which have developed Silicone related Immunological disorders and have typically complained of breast pain, Myalgia-Arthralgia, fatigue, or generalized pain, were examined by their physician. Blood samples were obtained and examined for the presence of Silicone antibodies, Myelin Basic Protein and human serum albumin antibodies. These samples were then compared to 520 matched controls without implants. At least at the level of two standard deviation silicone specific antibodies, IgG, IgA IgM, IgE and IgG+IgA+IgM antibodies were detected above the mean of normal controls. When these antibodies were classified based on the specialty of the examining physician, the % of patients with Silicone Antibodies were varied; general practice 51.6, Rheumatology 58.7, and Plastic Surgery 83.3, which may relate to the severeness of the disease. Being that a large % of patients demonstrated very high levels of Myelin Basic Protein Antibodies, possible cross reactive antibodies were sought. However, absorption of highly positive sera for Silicone Antibodies with MBP did not change the levels of Silicone Antibodies. On the other hand, Silicone-HSA was able to reduce the antibody values significantly. This reduction in antibody levels by Silicone is the best indication for the specificity of these antibodies. Moreover when data for silicone antibodies and MBP antibodies was analyzed in patients some with high and others with medium or low levels of silicone antibodies, MBP antibodies did not correspond to the silicone antibody levels. Similarly human serum albumin antibodies which was significantly higher in patients with silicone implants did not correlate with levels of silicone antibodies. These results indicate that immune reaction to silicone and different tissue antigens do occur and they are initiated through different mechanisms. And since predominant antibody class against silicone, MBP and HSA was IgM, clonal activation of IgM is possible which certainly warrants further investigation.

Adult↗
PubMed1977

The concept of orthodontic treatment for the adult.

Through our experience gained with adult patients during the last ten years we have found it useful to divide them into three groups:- 1--Those who are very strongly motivated to accept orthodontic treatment for cosmetic purposes and with whom treatment will usually be satisfactory. 2--Those who are suffering from anxiety states and who have developed a fixation on a dental fault and with whom it is very unwise to begin treatment before a favourable psychiatric report is obtained. 3--Those patients who need treatment before prosthetic rehabilitation or for other physical disorders and in whom treatment may or may not be successful, depending on the degree of co-operation shown by the patient and on good teamwork between dental specialists.

Adult↗
PubMedDate not supplied

Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism.

Similar to many complex autoimmune diseases, genetic and environmental factors including diet, infection and xenobiotics play a critical role in the development of autism. In this study, we postulated that infectious agent antigens such as streptokinase, dietary peptides (gliadin and casein) and ethyl mercury (xenobiotic) bind to different lymphocyte receptors and tissue enzyme (DPP IV or CD26). We assessed this hypothesis first by measuring IgG, IgM and IgA antibodies against CD26, CD69, streptokinase (SK), gliadin and casein peptides and against ethyl mercury bound to human serum albumin in patients with autism. A significant percentage of children with autism developed anti-SK, anti-gliadin and casein peptides and anti-ethyl mercury antibodies, concomitant with the appearance of anti-CD26 and anti-CD69 autoantibodies. These antibodies are synthesized as a result of SK, gliadin, casein and ethyl mercury binding to CD26 and CD69, indicating that they are specific. Immune absorption demonstrated that only specific antigens, like CD26, were capable of significantly reducing serum anti-CD26 levels. However, for direct demonstration of SK, gliadin, casein and ethyl mercury to CD26 or CD69, microtiter wells were coated with CD26 or CD69 alone or in combination with SK, gliadin, casein or ethyl mercury and then reacted with enzyme labeled rabbit anti-CD26 or anti-CD69. Adding these molecules to CD26 or CD69 resulted in 28-86% inhibition of CD26 or CD69 binding to anti-CD26 or anti-CD69 antibodies. The highest % binding of these antigens or peptides to CD26 or CD69 was attributed to SK and the lowest to casein peptides. We, therefore, propose that bacterial antigens (SK), dietary peptides (gliadin, casein) and Thimerosal (ethyl mercury) in individuals with pre-disposing HLA molecules, bind to CD26 or CD69 and induce antibodies against these molecules. In conclusion, this study is apparently the first to demonstrate that dietary peptides, bacterial toxins and xenobiotics bind to lymphocyte receptors and/or tissue enzymes, resulting in autoimmune reaction in children with autism.

Adolescent↗
PubMedDate not supplied

Suppressed natural killer cell activity in patients with silicone breast implants: reversal upon explantation.

We have previously shown that natural killer (NK) cell activity is significantly suppressed in patients with silicone breast implants. These patients were symptomatic and the suppression of natural killer cell activity was associated with additional significant immunological abnormalities (Vojdani et al., 1992a). Our studies have recently been confirmed by Smith et al. (1994), who described natural killer cell activity suppression following exposure to silicone gel, and reversal upon removal of the gel. This study has been designed to evaluate natural killer cell activities in symptomatic women with silicone breast implants and again after explantation of the implants. Each patient served as her own control. Our findings show a marked significant increase in previously suppressed natural killer cell activity in 50% of the patients. In the other 50%, no change or suppressed NK activity was observed. These findings are compatible with recent studies in experimental animals, which show that administration of silicone reduces natural killer cell activity, and that this is reversible upon removal of the silicone. Since NK cells are important in the control of tumor cell growth, we propose here that patients with reduced NK cell activity are at a higher risk of developing cancer, a concept recently described in experimental animals (Potter et al., 1994; Salhon et al., 1994).

Breast Implants↗
PubMedDate not supplied

Minimizing cancer risk using molecular techniques: a review.

This review article summarizes molecular markers that can signal enhanced risk of cancer and provide clinicians with these clues in order to attempt the use of natural and synthetic compounds to intervene in the early precancerous stages of carcinogenesis before invasive disease begins. With an aim such as this in mind, we have begun to apply molecular techniques based on many research articles to look for biomarkers capable of signaling a greater risk of cancer. It is possible to attain relatively quick answers by monitoring selected signs and damage in the body which provide the environment for abnormal cell growth and differentiation. These molecular techniques aim to uncover critical precancerous events taking place inside the body and identify measurable biologic flags signaling their occurrence. For years now, scientists have understood that the onset of cancer is a gradual, step-wise process that may unfold over the course of decades, rather than a single, fixed event that can be dated in a pathologist's report. Carcinogenesis usually encompasses the prolonged accumulation of injuries at several different biological levels and includes both genetic and biochemical changes in cells. At each of these levels there is an opportunity for intervention-a chance to prevent, slow or even halt the gradual march of healthy cells toward malignancy. It is estimated that 75% of cancers are induced by chemicals; thus, if exposure to chemicals is avoided, cancer can be prevented. Also, depending on the individual's genetic background, the ability to metabolize chemicals is different among the population. This means that, "you and I can be exposed to exactly the same amount of a chemical," yet our response will differ because we metabolize carcinogens differently due to different rates of deoxyribonucleic acid (DNA) repair, apoptosis, and mitosis or different levels of Phase I and Phase II detoxification enzymes. This, along with a more or less efficient immune system, may promote tumor formation or destroy a cancer cell at its earliest stage of development. Therefore, measurement of the biologic markers such as DNA and protein adducts, DNA damage, programmed cell death, DNA repair system, mitosis, gene activation, levels of antioxidants and efficient immune function described in this chapter and summarized in Figures 2 and 10, are biological clues indicating that the body has been assaulted by toxic (or cancer-causing) agents. This early identification of biomarkers for special vulnerability to the effects of chemicals and detection of selected signs of precancerous damage in the body may culminate preventive measures and the saving of lives.

Apoptosis↗
PubMedDate not supplied

The effects of carcinogenic methylcholanthrene on carbohydrate residues of NK cells.

The present study examines the effect of methylcholanthrene (MCA), a a carcinogenic polycyclic hydrocarbon, on the carbohydrate receptor determinants (RD) on natural killer (NK) cell surface using the bead-coupled lectin assay. Murine NK cells exhibited different degrees of preferential binding to the specific lectins tested. Of the ten lectins tested, five exhibited a positive binding affinity while the remaining five exhibited no or insignificant binding. NK cells bind to beads derivatized with mannose specific lectins: Concanavalin A (Con A), Lens culinaris, and Pisum sativum. NK cells also bind to other lectin beads such as Triticum vulgaris (GalNac) and Vicia villosa (D-GlcNAc). All these lectin beads exhibited greater than 90% adhesion. The underivatized control beads exhibited no NK binding. The NK cells that were exposed to MCA for 2 h demonstrated a significant decrease in lectin bead-cell coupling in a dose dependent manner. MCA (10 micrograms/mL) caused a 17.8%, 40% and 4.7% decrease in binding affinity when introduced to the mannose specific lectins; Con A, L. culinaris and P. sativum beads, respectively. The binding of T. vulgaris and V. villosa to NK cells was inhibited (23.4% and 28%) by MCA treatment. An increase in the dose to 20 micrograms/mL resulted in a greater inhibition in binding affinity towards lectin beads. Con A, 35.3%, L. culinaris, 62.6%, P. sativum, 30.9%, T. vulgaris, 44.2% and V. villosa, 46.2%. The effect of MCA activation and cytotoxic response. Hydrolysis of PI metabolites (PIP and PIP2) cause generation of secondary messenger: inositol-1,4,5-triphosphate and diacylglycerol, both of which elicit an immune response through their products (Ca2+ and PKC) respectively. Identification of the relationship between receptor level, induction of second messenger and cytotoxic activity may resolve the molecular basis of suppression of NK cytotoxicity by MCA and other PAH compounds.

Animals↗
PubMedDate not supplied

A practical approach to orthodontic treatment for the adult patient.

The possibilities of treating malocclusions in adults are discussed and four cases of orthodontic treatment undergone by adults are described. Proper treatment can bring about improvements in most cases but it is neither necessary nor advisable to attempt a complete correction of all irregularities.

Adult↗
PubMedDate not supplied

Silicone implants and systemic immunological disease: review of the literature and preliminary results.

Silicone has been utilized as an implant in reconstructive surgery. For years, silicone has been considered to be biologically inert and essentially harmless. Several studies and case reports show that female patients treated with silicone implants developed a systemic disease associated with immunological abnormalities. Removal of the silicone implants was associated with recovery and resolution of the immune abnormalities. Recently, specific antibodies to silicone have been isolated in children with silicone implants. Additionally, immunological abnormalities and high incidence of systemic progressive sclerosis in patients with silicone implants or injections further support the notion that silicone is not biologically inert, and can cause a syndrome of a systemic disease and immunological abnormalities. The specific mechanisms and duration of the latency period is not yet fully understood.

Adult↗
PubMedDate not supplied

Immune alteration associated with exposure to toxic chemicals.

Immunological abnormalities including lymphocyte subset, lymphocyte immune functional assays, chemical antibodies, and different markers for autoimmune response were examined in individuals exposed to a variety of chemicals in computer manufacturing plants. A comparison of 289 individuals exposed to chemicals to 120 controls revealed that exposed individuals had a significantly higher percentage with either increased or decreased T helper/T suppressor ratios. In addition, the individuals with abnormal T4/T8 ratios demonstrated significant elevation in chemical-hapten antibodies. Therefore, 87 exposed subjects with abnormal T4/T8 ratios were selected for further evaluation by lymphocyte phenotypic expression and T cell, B cell, NK activity, and autoimmune markers, and were compared to 60 controls. The comparison of exposed individuals with controls indicated elevation of T cell (CD3), B cell (CD19), and activated T cell (CD10, CD15, CD26, CD38), suppressed T cell and B cell function decreased or increased NK cell cytotoxic activity. Autoimmunity due to chemical exposure was evidenced by elevation of TA1 phenotype frequencies and presence of rheumatoid factor, immune complexes, ANA, and anti myelin basic protein antibodies. We conclude that chemical exposure may induce immune abnormalities including immune suppression and autoimmunity.

Adult↗
PubMedDate not supplied

Immune functional impairment in patients with clinical abnormalities and silicone breast implants.

Silicone, previously thought to be a biologically inert and harmless material, has now been reported to elicit antibody response and to be responsible for adjuvant disease in humans. The present study was designed to evaluate the immune function of forty individuals who had undergone silicone breast augmentation for a period of longer than ten years and who were compared with 40 sex and age-matched controls. The following immunological functions were studied: lymphocyte subset analysis, lymphocyte mitogenic response, NK cytotoxic activity and markers for autoimmunity such as ANA, rheumatoid factor immune complexes such as smooth muscle, myelin, and thyroid, and tissue antibodies. Results of lymphocyte subpopulation analysis showed significantly elevated T helper/suppressor ratio in 60% and significantly decreased T helper/suppressor ratio in 7.5% of the silicone implant group, while the control group showed increased helper/suppressor ratio only in 10% of tested individuals and no significant decrease in the T helper/suppressor ratio. There was 20% inhibition in T cell mitogenic responses in the silicone implant group, which is significant when compared to the controls. When NK cytotoxic activity was compared between the two groups, significant inhibition in the ability of lymphocytes to kill tumor target cells was observed in the silicone implant group. This inability of target cell lysis was attributed to the demonstrated lack of granularity of NK cells from the silicone implant group. There was significant increase in: immune complexes, anti-nuclear antibodies, anti-thyroid antibodies, anti-striated muscle cell antibody, and anti-myelin basic protein antibodies. These immunological abnormalities in individuals who underwent silicone breast augmentation indicate a mechanism of tissue injury to these patients, causing autoimmune diseases or syndromes. Since autoimmunity in some other conditions is associated with abnormalities in the HLA serotyping system, and since some collagen vascular diseases have been associated with a higher incidence of the HLA serotyping system, it is recommended that HLA studies be included in future investigations of immune-mediated abnormalities associated with silicone breast augmentation. Our findings here show definite abnormalities of the T helper/suppressor ratio, increased autoimmunity, as well as increased production of immune complexes. Silicone implants have been used in cosmetic and reconstructive surgery more than 30 years (Brown et al., 1960). The gel used in the implant is produced from silicone, which is then related with methyl chloride and polymerized to form stable polydimethylsiloxane (Brown, et al., 1960). There have been a number of reports describing the occurrence of connective tissue disease in patients after the implantation of silicone.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗