donderdag 3 maart 2016

Over herstel (remissie) bij de behandeling met schildklierremmers

Als je schildklier te veel hormoon maakt door de ziekte van Graves kan gekozen worden voor een behandeling met schildklier remmende medicijnen. De behandeling duurt 1 à 1½ jaar. Hierna is de ziekte bij minder dan de helft van de patiënten genezen. Je noemt zo’n genezing een remissie. In de praktijk blijkt dat bij ongeveer 50-70% van de Gravespatiënten de hyperthyreoïdie weer terugkeert (= relapse).

Doel van de onderzoeken is om meer inzicht te krijgen in dat mechanisme van het ontstaan van een remissie. Wat zou er kunnen gebeuren?

Remission of Graves’ disease during anti-thyroid drug therapy. Time to reconsider the mechanism?
Peter Laurberg

Antithyroid drug therapy of Graves’ hyperthyroidism: realistic goals and focus on evidence
Peter Laurberg, Stig Andersen, Jesper Karmisholt

Therapy of Graves’ hyperthyroidism with thionamide anti-thyroid drugs is accompanied by a gradual remission of the autoimmune aberration in the majority of patients. The most likely mechanism behind this remission has been considered to be a direct immunosuppressive effect of thionamide drugs.

However, a number of findings in clinical studies of patients with Graves’ disease indicate that remission is probably not caused by a special effect of thionamide drugs. Many studies have shown that remission is linked to restoration of the euthyroid state, and that it is independent of drug dose and type. Moreover, similar remission is observed when patients become euthyroid after thyroid surgery.

Patients may become ill by the running of a vicious cycle of hyperthyroidism worsening the autoimmunity, and autoimmunity worsening the hyperthyroidism. Once patients are made euthyroid by one or the other drug or by thyroid surgery, the majority of patients will gradually enter remission of the disease.

The conclusion that remission is associated with restoration of the euthyroid state, and that it is not a special drug effect, highlights the importance of making and keeping patients with Graves’ disease euthyroid.

Acceptance of the mechanism highlights the importance of making and keeping the patient with Graves’ disease euthyroid. This may occasionally include more prolonged use of MMI. To minimize the risk of side effects, the lowest possible dose of the drug should be used. Several investigators have reported that such therapy may prevent relapse of overt Graves’ disease. One mechanism behind such a protective effect of low dose MMI therapy may be a decrease in the risk of reactivation of the vicious cycle. An additional possibility would be that the risk of relapse is diminished by keeping thyroid iodine content low.

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