Summary OBJECTIVE In recent years anti‐phospholipid antibodies have gained much attention since they are frequently associated with thrombosis, recurrent abortion, and thrombocytopenia. Besides disease‐specific autoantibodies, other autoantibodies reactive with both organ and non‐organ specific autoantigens have been found in patients with autoimmune thyroid diseases. Therefore the objective of this study was to evaluate the presence and significance of anti‐phospholipid antibodies in untreated patients with different forms of autoimmune thyroid diseases. PATIENTS AND METHODS Thirty‐one patients (26 females, five males; mean age 42.5 years) affected by different autoimmune thyroid diseases were studied. Fourteen patients were affected by Graves' disease, eight by silent thyroiditis, five by Hashimoto's thyroiditis. Four patients with Graves' disease in remission were also evaluated. Anti‐cardiolipin antibodies were detected by enzyme linked immunosorbent assay. In five Graves' disease patients anti‐cardiolipin antibodies were evaluated before and after 3 months of therapy with methimazole. RESULTS Seventeen out of 31 patients were positive for IgG and/or IgM anti‐cardiolipin antibodies, the highest levels occurring in three Graves' disease patients with severe thyrotoxicosis. In four of five Graves' patients evaluated before and after methimazole therapy, anti‐cardiolipin antibodies decreased following treatment. None of the patients with increased IgG and/or IgM anti‐cardiolipin antibodies showed clinical manifestations of the anti‐phospholipid syndrome during our observation which ranged from 1 to 5 years. CONCLUSIONS Our results showed an increased incidence of anti‐cardiolipin antibodies in patients affected by autoimmune thyroid diseases. However, these autoantibodies seem merely to represent a non‐specific marker of immune dysregulation.
Primary hypothyroidism is a chronic and insidious disease caused by failure of thyroid hormone production. We observed a 38-year-old woman admitted to our hospital due to progressive proximal weakness, muscle pain and fatigue during mild exercise. Laboratory tests showed features of rhabdomyolysis and hypothyroidism. After examination of the thyroid, we reached a diagnosis of Hashimoto’s thyroiditis and hypothyroid myopathy. Hypothyroidism should be considered as a differential diagnosis of creatine kinase elevation; actually, neuromuscular symptoms and signs occur in most newly diagnosed patients with thyroid diseases. Hypothyroidism presenting as muscle stiffness and pseudohypertrophy is called ‘Hoffman’s syndrome’.
Fifteen patients affected by new-onset Graves' disease with ophthalmopathy have been examined for lymphocyte subset phenotypes by two-colour cytometric analysis. CD5+ B cells were significantly increased in comparison to the normal population (43.2 +/- 20.6% versus 19.5 +/- 6.9%; p < 0.0009); total T cells showed a normal amount (70.4 +/- 9.6%), but the levels of THLADR+ cells were significantly increased in comparison to the control group (13.7 +/- 10.5% versus 4.7 +/- 3.2%; p < 0.007). The characterization of the subset suppressor-inducer CD4+ CD45RA+, evaluated as percentage of the total CD4+ T cells, showed a significant decrease in comparison with the control group (43.8 +/- 13.5% versus 52.3 +/- 6.5%; p < 0.03). Serum immunoglobulin evaluation showed a statistically significant increase of IgM (p < 0.05) and a significant decrease of IgA (p < 0.02). A statistical correlation between IgM levels and percentage of CD5+ B cells has been found (p < 0.04). The defect of suppressor-inducer T cell subset, along with the increase of CD5+ B cells may contribute to the pathogenetic mechanism of the disease in patients with a genetically-induced aberrant immune response.
Different antibodies against both organ- and non-organ-specific autoantigens have been found in patients with autoimmune thyroid diseases. The aim of our study was to evaluate the presence of antineutrophil cytoplasmic antibodies (ANCA) in sera of patients affected by Graves' disease (GD) and Hashimoto's thyroiditis (HT). These antibodies were investigated by indirect immunofluorescence; the reactivity against myeloperoxidase and lactoferrin was assessed by ELISA. ANCA were detected by immunofluorescence in 28.5% of patients with GD and 9% of patients with HT. Anti-lactoferrin antibodies were found in 3 of 21 (14.2%) patients affected by GD and in 2 of 11 (18.1%) cases of HT. Anti-myeloperoxidase antibodies were detected only in one (4.7%) patient with GD.
Twenty eight patients (25F, 3M) affected by autoimmune and non-autoimmune thyroid diseases were studied. HSP 70 antibodies were present in 21.4% of patients. Five of them were affected by Graves' disease and one by De Quervain's thyroiditis. The HSP 70 antibodies mean values of patients were significantly higher than the normals (p < 0.05). This datum was confirmed by Western blotting. The presence of HSP 70 antibodies in the sera of those patients may support the link between the protein and the thyroid autoimmune processes.
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