The frequent occurrence of both rheumatoid arthritis and autoimmune thyroiditis was already investigated with in part many conflicting results. We investigated a number of 792 patients (383 of them suffering from rheumatoid arthritis and 409 with osteoarthritis). In all patients antithyroid peroxidase and antithyroglobulin antibodies were determined. Patients with rheumatoid arthritis showed a significantly higher occurrence of circulating thyroid antibodies than those with osteoarthritis (9.1% versus 3.7%, p = 0.0016). We conclude that there exists a cumulate coincidence of both diseases. Patients suffering from rheumatoid arthritis should undergo a thyroid examination especially for the presence of autoimmune thyroiditis.

Familial Mediterranean fever (FMF) is an autosomal recessive hereditary disease. FMF-related arthritis affects large joints, especially in the lower extremities. It starts with acute pain and swelling and affects one joint at a time. Fever is the most common symptom in FMF. Monoarthritis as the sole symptom is relatively rare and thus delayed diagnosis of the disease in a patient who had been suffering from monoarthritis for several years. Genetic analysis showing typical mutations in the patient eventually resulted in correct diagnosis, although classical clinical diagnostic criteria were not met. The patient received appropriate therapy with colchicine, which led to remission of the symptoms.

The frequent occurrence of both rheumatoid arthritis and autoimmune thyroiditis was already investigated with in part many conflicting results. We investigated a number of 792 patients (383 of them suffering from rheumatoid arthritis and 409 with osteoarthritis). In all patients antithyroid peroxidase and antithyroglobulin antibodies were determined. Patients with rheumatoid arthritis showed a significantly higher occurrence of circulating thyroid antibodies than those with osteoarthritis (9.1% versus 3.7%, p = 0.0016). We conclude that there exists a cumulate coincidence of both diseases. Patients suffering from rheumatoid arthritis should undergo a thyroid examination especially for the presence of autoimmune thyroiditis.

Influences of non-steroidal anti-inflammatory drugs (NSAID) on concentrations of thyroid hormones are known for a long time. These effects could be explained with interference between NSAIDs and thyroid hormone binding. We investigated the effects of a single dose of aceclofenac on thyroid function and thyroid hormone binding in 18 healthy volunteers. Serum levels of free thyroid hormones (FT3, FT4) and thyrotropin (TSH) were measured with commercial available kids and thyroid hormone binding was estimated with a specially modified horizontal argarose-gel-electrophoresis prior to and 2 hours after receiving a single dose of aceclofenac. We found a significant decrease in T3 binding on TBG and a significant increase of albumin-bound T3. All other investigated thyroid hormone binding parameters, FT3 and FT4, showed no significant changes. We conclude that aceclofenac leads to a significant redistribution of T3 protein binding. These effects seem to be explained by T3 displacement from TBG induced by aceclofenac.

Influences of non-steroidal anti-inflammatory drugs (NSAID) on concentrations of thyroid hormones are known for a long time. These effects could be explained with interference between NSAIDs and thyroid hormone binding. We investigated the effects of a single dose of aceclofenac on thyroid function and thyroid hormone binding in 18 healthy volunteers. Serum levels of free thyroid hormones (FT3, FT4) and thyrotropin (TSH) were measured with commercial available kids and thyroid hormone binding was estimated with a specially modified horizontal argarose-gel-electrophoresis prior to and 2 hours after receiving a single dose of aceclofenac. We found a significant decrease in T3 binding on TBG and a significant increase of albumin-bound T3. All other investigated thyroid hormone binding parameters, FT3 and FT4, showed no significant changes. We conclude that aceclofenac leads to a significant redistribution of T3 protein binding. These effects seem to be explained by T3 displacement from TBG induced by aceclofenac.