Many drugs influence the severity of WED symptoms; some drugs alleviate, whereas others aggravate them. A study of pharmacological profiles suggests that drugs that alleviate WED tend to reduce TH activity, whereas drugs that aggravate WED tend to augment TH. One of these effects may actually be secondary to the diverse actions these drugs have on the Cytochrome P450 system (CYP450): the first induces the system (e.g., dopamine agonists), and the second inhibits it. Sequential deiodination degrades approximately 80% of the circulating pool of TH, and the remainder is mainly metabolized within the cytochrome P450 system, where TH is conjugated with glucuronides and sulfates. Glucuronides are then excreted into bile, where they participate as intermediates in the enterohepatic cycle and fecal excretion of TH. As TH may inhibit sleep, we believe that one of the mechanisms by which an elevated sympathetic nervous tonus system hampers sleep is through releasing TH directly from the thyroid gland via its fibers directed to the gland. Willis-Ekbom disease (Restless Legs Syndrome) Pathophysiology: The Imbalance Between Dopamine and Thyroid Hormone Theory: José Carlos Pereira Jr, Marcia Pradella-Hallinan
Last date updated on April, 2024