Named after William M. Ord (1834-1902)
Synonymes: Autoimmune thyroiditis type 1B, Autoimmune thyroiditis type Typ 2B, Atrophic Thyroiditis
2 Etiology and Pathogenesis
The disease is characterized by a destruction of thyroid tissue that is caused by different cellular and humoral immune processes. While detailled trigger mechanisms are still unknown, it has become clear that formation of microsomal antibodies against thyroid peroxidase (TPO-AB) and of antibodies against thyroglobulin (Tg-AB) plays a critical role. These antibodies precipitate impaired thyroid function.
A small percentage of Ord patients seems to be antibody negative, but this subpopulation may be difficult to separate from patients with elapsed silent thyroiditis.
Diagnostical criteria for Ord's disease are:
- Decreased thyroid volume (normal: 15 to 18 mL in females, 20 to 25 mL in males)
- hypoechogenic pattern in ultrasonography
- Reduced Technetium-Uptake (TcTU) in thyroid scintigraphy
- Positive Tg-AB and/or TPO-AB.
Symptoms of Ord's disease are varying and ambiguous. Most cases show abortive course or proceed with very few symptoms being easily treated by substituting thyroid hormones.
There is no evidence for an effective activity of immunosuppressive angents.
Ord's disease doesn't heal up why it requires life-long substitution with T4. The disease may sometimes be associated with cervical lymphomas. Therefore regular investigation of neck and thyroid via ultrasonography is recommended.
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