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PubMed1994

[Humoral autoimmunity markers in autoimmune endocrine diseases].

To clarify the value of autoantibodies as risk factors of complications in various endocrine abnormalities, the incidence of autoantibodies to thyroid microsomal antigen (ATMA), thyroglobulin, and the surface antigens of the rat islet, adrenal cortex, adenohypophyseal cells and human skin fibroblasts was studied in patients with insulin-dependent mellitus (IDDM), at the onset of the disease and during one-year insulin therapy, non-insulin-dependent diabetes mellitus (NIDDM), Hashimoto thyroiditis, Graves' disease, diabetes associated with thyroidal dysfunction, euthyroid polynodular goiter, Schmidt and polyglandular syndromes and in the population. The antibodies were determined by ELISA. Polyclonal activation of the immune system was found in all abnormalities, except in polyglandular in children. The proportion of patients with more than one type of antibodies was minimal (26.4%) in IDDM and maximal (62.0%) in Graves' disease. Among IDDM patients, polyclonal activation of the immune system was observed more often in women than in men (48.5 vs 8.5%). The persistence of antibodies to fibroblasts in IDDM patients was associated with the development of vascular complications. The latter were observed in 4 of 7 patients who had these antibodies during a year and in none of negative patients. Thus, fibroblast antibodies may have a predicative significance for the development of late diabetic complications. The highest prevalence of these antibodies was discovered in Graves' disease (37.9%) wherein the antibodies may be involved in the development of exophthalmus and pretibial mixedema. Thyroidal dysfunction developed in all IDDM patients with ATMA preserved during a year and in none ATMA-negative patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Effectiveness of radioiodine (131-I) as definitive therapy in patients with autoimmune and non-autoimmune hyperthyroidism.

We evaluated the outcome of radioiodine (RAI) therapy in 100 consecutive patients treated in the period 2000-2001 for hyperthyroidism due to Graves' disease (GD), toxic adenoma (TA) and toxic multinodular goiter (TMG). Thyroid function was measured before and after therapy every 3-6 months up to 3 yr. Three years after therapy, 75% of TA patients were euthyroid, 18.7% were hypothyroid and 6.3% hyperthyroid. Of the TMG patients, 62.2% were euthyroid, 18.9% were hypothyroid and 18.9% hyperthyroid. In GD patients euthyroidism was achieved in 12.9% of the patients, hypothyroidism in 74.2% and hyperthyroidism persisted in 12.9%. Definitive hypothyroidism was significantly higher in GD (p<0.0001) than in TA and TMG patients. Overall, positive effect of RAI (definitive hypothyroidism or euthyroidism) was very high: 93.7% in TA, 81.1% in TMG and 87.1% in GD patients. Thyroid volume reduction was observed in all patients, but was higher in GD patients (mean reduction of 76%) and in TA patients (mean nodule reduction of 69%). In TMG, mean reduction was of 32%. The median activity of RAI received by the 86 cured patients was 555 MBq (15 mCi) compared to 407 Mbq (11 mCi) received by the 14 patients who remained hyperthyroid. No influence was found between outcome and clinical parameters at the moment of 131-I therapy. In conclusion, our results indicate that RAI therapy is highly effective and safe for the control of hyperthyroidism.

Adult↗
PubMed1988

Autoimmune effector cells. Part 10: Effector cells of autoimmune encephalomyelitis in healthy nonimmune rats.

This paper describes our ongoing investigation of the activation of effector cells of experimental allergic encephalomyelitis (EAE) from nonimmune Lewis rats by sequential culture of spleen cells (SpC) with myelin basic protein (BP) and transfer to syngeneic recipients. We show that SpC initiate the effector cell activation process, whereas thymocytes (Thy) are ineffective. Intermediary recipients of BP-cultured SpC are 'primed' for EAE, but do not develop the disease; this primed state persists for at least 2 months. No evidence was found that suppressor cells account for the failure of the intermediary recipients to develop EAE. The activation process can be inhibited by including monoclonal anti-Ia antibody in the primary culture, indicating that multiple triggering signals are involved in the activation of autoreactive T cells.

Animals↗