Pentoxifylline Explores New Horizons in Treatment of Hashimoto Thyroiditis

Abstract

Hashimoto Thyroiditis is an autoimmune disease and the most common cause of hypothyroidism in developed countries. As the disease initiates unusual thyroidal antigens are exposed to the immune system. The immune system sensitizes to those antigens and creates a cell mediated autoimmune response against thyroid gland. Inflammatory cells infiltrate within thyroid follicles and destruct the follicles by inflicting oxidative stress and inducing apoptosis. The inflammatory process also reduces sensitivity of thyrocytes to Thyroid Stimulating Hormone (TSH). As the disease progresses and the follicles degrade, fibrotic tissue replaces the follicles until the whole gland becomes fibrotic. Pentoxiflline could inhibit autoimmune destruction of thyrocytes, suppress cell mediated immune response against thyroid, decrease oxidative damage to thyrocytes, increase sensitivity of thyrocytes to TSH and hinder fibrotic degeneration of thyroid. Thereby PTX could cure HT and alleviate symptoms of hypothyroidism.

The Use of Pentoxifylline Topical in the Treatment of Alopecia in Rats

“…These can be seen to be modified by the increase of cAMP. Eventually, Neuner et al also showed in vivo and in vitro whereby PTX decrease intercellular adhesion molecule (I CAM)-1 production on individual monocytes controlled by TNF-α inhibition 26 .…”

TGF-β Physiology as a Novel Therapeutic Target Regarding Autoimmune Thyroid Diseases: Where Do We Stand and What to Expect

“…In many diseases such as alcoholic steatohepatitis, sarcoidosis, post-radiation fibrosis, and various types of neuropathy, the suppressed expression of TGF-β restores the disturbed Th1/Th2 equilibrium and limits Th1-regulated immune responses. Pentoxifylline (PTX) has been therapeutically used to effectively suppress TGF-β activation and prevent the detrimental autoimmune responses associated with this growth factor [61]. -Treatment strategies based on progesterone had been effective in treating preterm infants suffering from bronchopulmonary dysplasia via dose-dependent suppression of TGF-β-mediated activation and ensuing transcription of the Smad2/3 complex [33].…”