Search PubMed⌕ Search

Biomedical subjects

C L Burek

Publications and source records attributed to C L Burek.

At least 55 records · Page 3Linked to original sources
PubMed1990

Thyroid autoantibodies in black and in white children and adolescents with type 1 diabetes mellitus and their first degree relatives.

Genetic susceptibility is an important issue in understanding the mechanism of the autoimmune endocrinopathies and in assessing the risk of these conditions in pediatric patients. To this end, we evaluated autoantibodies to thyroid antigens, thyroglobulin (TgA) and microsomal antigen (TMA), in white and in American black juvenile patients with Type I diabetes mellitus (DM) to determine the predictive value of thyroid autoantibodies for the development of autoimmune thyroid disease. Sera from 159 patients (77 black and 82 white) with Type I DM were evaluated. A greater number of whites (41/82 or 50%) than blacks (12/72 or 16%) had thyroid autoantibodies (p less than 0.01). Fourteen patients (4 black and 10 white) exhibited hypothyroidism, and all had both TgA and TMA. Three patients (all black) had Graves' disease, one of whom had both TgA and TMA. Families of each racial group that had a diabetic child (proband) with thyroid autoantibodies (seropositive) or without thyroid autoantibodies (seronegative) were assessed for TgA and TMA as well as autoimmune thyroid disease. The prevalence of thyroid autoantibodies among siblings of seropositive probands was significantly greater than among the siblings of seronegative probands (p less than 0.01). The white sibling population showed a closer association of thyroid autoantibody prevalence with increasing age (p less than 0.05) than the blacks. Significantly more parents of probands than control parents exhibited thyroid autoantibodies (p less than 0.01). The general pattern of inheritance of either racial group showed that if one or both parents had thyroid autoantibodies, their progeny developed a significantly higher prevalence of thyroid autoantibodies than those of the seronegative parents. While there was no increase in overt thyroid disease among siblings of seropositive probands, a risk of developing autoimmune thyroid disease is probably imparted to these siblings by virtue of the thyroid autoantibodies.

Adolescent↗
PubMed1990

Mapping the autoepitopes of thyroglobulin.

Chronic thyroiditis is currently the best available model of an organ-restricted autoimmune disease, because the principle antigen Tg is a well-characterized protein and the disease can be reproduced by experimental immunization. The pattern of autoantigenic determinants of Tg that is recognized by sera from subjects without detectable thyroid disease is clearly different from that seen with thyroiditis patients. Both sets of sera react with the evolutionary conserved portions, the hormonogenic regions containing the T3 and T4 moieties. Sera of thyroiditis patients, however, also react with the evolutionary variable, species-specific portions of the Tg molecule. Mice immunized with human Tg respond to the same, immunodominant sites. Mice injected with mouse Tg preferentially recognize the analogous, mouse-specific sites of Tg. Mice are not restricted, however, in their use of V-(D)-J genes for Ig production, even when the same antigenic determinant is involved.

Animals↗
PubMed1990

Human autoimmune thyroid disease: risk factors.

Genetics sets the groundwork for the predisposition to autoimmune thyroid disease, and in certain individuals, such as the juveniles presented here, very little impetus is needed to push normal immune reactions to autoimmune disease. However, in individuals who inherit only a few of these traits, the accumulation of many developmental and environmental insults may promote the development of disease.

Animals↗
PubMed1989

Type I diabetes in an adolescent with common variable immunodeficiency.

A male adolescent with common variable immunodeficiency developed type I diabetes approximately 1 year after the initiation of immunoglobulin therapy. Immunologic evaluation revealed decreased numbers of T cells and an intrinsic B cell defect in immunoglobulin production. Lymphocytes from the patient failed to generate normal suppressor activity. There were no insulin or islet cell antibodies present in the patient's serum or in the commercial immunoglobulin preparations he received. The patient's HLA phenotype included HLA-DR3 and 4, placing him genetically at high risk for type I diabetes.

Adolescent↗
PubMed1986

Cell-mediated immunity in autoimmune thyroid disease.

The initiation of an autoimmune response requires the establishment of an appropriate microenvironment. This, in turn, involves several requirements, including antigen expression on the membrane surface of the target cells, class II antigen expression on the antigen-presenting cell or target cell, a relative systemic or local increase in the helper/inducer subset of T cells, and/or a relative decrease in the suppressor subset of T cells. All of these conditions have been described in the thyroid gland. Appropriate cellular interactions result in the appearance of activated T cells and the generation of cytotoxic T cells. The pathologic alterations may be produced by the local production of antibody and subsequent formation of immune complexes, by direct lymphocyte damage, or by lymphokine production. Autoimmune thyroid disease remains, to our minds, the most instructive paradigm of the organ-specific autoimmune endocrinopathies.

Animals↗
PubMed1985

The genetics of thyroiditis as a prototype of human autoimmune disease.

The predisposition to autoimmune disease has been termed an autoimmune diathesis. The genetic basis for this predisposition has been analyzed, using three different models: juvenile thyroiditis in humans, spontaneous thyroiditis in chickens, and experimental thyroiditis in mice. At least three different categories of genetic factors contribute to the development of autoimmunity. They include an increased immune response due to immunoregulatory genes associated with the major histocompatibility complex, the balance of thymus-derived lymphocyte population with helper/inducer vs suppressor properties, and intrinsic metabolic abnormalities of the target thyroid cells.

Adolescent↗
PubMed1983

An enzyme-linked immunosorbent assay for antibody against acetylcholine receptor.

An enzyme-linked immunosorbent assay is described for measurement of antibody against Torpedo acetylcholine receptor. As here developed, the assay is highly sensitive, reproducible, and requires small quantities of immunological reagents. Relative measurements of antibody concentration by this method are proportional to those determined by radioimmunoassay.

Animals↗
PubMed1983

Profile of autoantibodies in human diseases.

Testing for autoantibodies has an important place in the clinical immunodiagnostic laboratory. The presence of autoantibodies can aid in the diagnosis or confirmation of AID, as in the case of chronic thyroiditis, which is invariably associated with thyroid antibodies. Conversely the lack of antibody can help exclude the diagnosis of disease. The diagnosis of SLE can virtually be ruled out in patients who do not have ANA. Finding autoantibodies may help in difficult differential diagnosis, such as in those patients with liver disorders. Sometimes the type of autoantibody may be an indicator of prognosis. An example is in those SLE patients who develop anti-DNA antibodies, as mentioned previously. Along the same line, monitoring ANA has been of value in establishing effective treatment in SLE patients, as ANA disappear upon therapy and recur with return of active disease. The detection of autoantibodies may also be used for the identification of other family members of patients with AID who may have a greater risk of developing the disease. Finally, autoantibody detection has provided a tool for basic research which has aided both in classification of disease and increased our understanding of the normal control of immune regulation.

Adrenal Cortex↗
PubMed1982

Transient thyrotoxicosis in an infant delivered to a long-acting thyroid stimulator (LATS)- and LATS protector-negative, thyroid-stimulating antibody-positive woman with Hashimoto's thyroiditis.

A thyrotoxic infant was delivered to a woman with a long-standing history of Hashimoto's thyroiditis, but with no evidence of Graves' disease. Long-acting thyroid stimulator (LATS) and LATS protector were absent, but thyroid-stimulating antibody was transiently present in the infant and markedly and persistently elevated in the mother. It is concluded that the maternal level of thyroid-stimulating immunoglobulins determines the presence and duration of transient neonatal thyrotoxicosis, and that thyroid-stimulating antibody is distinct from LATS and LATS protector.

Adult↗
PubMed1982

Autoimmunity in endocrine diseases.

The realization that autoimmunity underlies many endocrine disorders of previously unknown etiology has greatly broadened our understanding of the pathogenesis of these diseases. It has provided new explanations for their heredity and their association with particular HLA haplotypes. It has also offered new tools for diagnosing these diseases as well as monitoring their course or predicting their outcome. Finally, establishing the autoimmune basis of these diseases offers new potential for their treatment. The next quarter century of research into immunologic aspects of endocrine diseases promises to be as fruitful as the last.

Animals↗
PubMed1981

Impaired antibody responses to a pneumococcal polysaccharide vaccine in patients with non-Hodgkin's lymphoma in remission.

Eight patients with non-Hodgkin's lymphoma who have been in complete clinical remission for the mean of 23.3 months were evaluated for their antibody responses to a pneumococcal vaccine. The results were correlated with lymphocyte subpopulations, serum immunoglobulin levels, and in vitro mitogenic responses to phytohemagglutinin, concanavalin and pokeweed mitogen. Two patients with normal antibody responses had immunoglobulin levels and mitogenesis within the range of controls. Impaired antibody responses in the remaining six patients were correlated either with marked depressed mitogenesis to phytohemagglutinin or with low levels of IgA. Impaired humoral immune responses seem to persist in these patients even after several months of sustained clinical remission.

Antibodies, Bacterial↗
PubMedDate not supplied

Macroorchidism and testicular fibrosis associated with autoimmune thyroiditis.

A 16-year-old male with long-standing atrophic chronic lymphocytic thyroiditis was evaluated for macroorchidism. A testicular biopsy prior to treatment revealed peritubular and interstitial fibrosis, reduced spermatogenesis and sparse Leydig cells with nonprominent smooth endoplasmic reticulum. Biological/immunological LH and FSH ratios were reduced, I-LH and FSH response to GnRH was blunted, and levels of testosterone and androstenedione were low. Twenty-two months after thyroid treatment, the testicular size was unchanged, and the degree of fibrosis showed minimal regression. Spermatogenesis with normal morphology was present, Leydig cells with Reinke crystals were present, and surface area and diameter of the seminiferous tubules had increased only slightly. There was a normal I-LH and FSH response to GnRH, and normal levels of testosterone and androstenedione. This study, along with previous reports, suggests that the etiology of the hypothyroid state may influence the development of testicular fibrosis.

Adolescent↗