Initiation of fingolimod treatment results in a transient decrease in heart rate and may also be associated with atrioventricular conduction delays (all patients should be observed for a period of 6 hours for signs and symptoms of bradycardia). Has not been studied in patients with sitting heart rate less than 55 beats per minute, patients receiving concurrent therapy with β-blockers or in those with a history of syncope. Has also not been studied in patients with second-degree or higher AV block, sick-sinus syndrome, ischemic cardiac disease, congestive heart failure or significant cardiovascular disease (use in such patients should be based on overall benefit-risk assessment and careful observation during initiation of therapy is recommended due to the potential for serious rhythm disturbances). Has not been studied in patients with arrhythmias requiring treatment with class Ia (e.g. quinidine, disopyramide) or class III (e.g. amiodarone, sotalol) antiarrhythmic medicinal products (since initiation of fingolimod treatment results in decreased heart rate, should not be co-administered with these medicinal products). At treatment initiation in patients receiving β-blockers, or other substances which may decrease heart rate (e.g. verapamil, digoxin, anticholinesteratic agents or pilocarpine), caution should be exercised because of the additive effects on heart rate. Fingolimod treatment resulted in a prolongation of QTcI, with the upper limit of the 90% CI ≤13.0 ms (medicinal products that may prolong QTc interval are best avoided in patients with relevant risk factors, e.g. hypokalemia, congenital QT prolongation, congestive heart failure, concomitant administration of antiarrhythmic medicinal products in class Ia (e.g. quinidine, disopyramide), or class III (e.g. amiodarone, sotalol)). Fingolimod presents a dose-dependent reduction of the peripheral lymphocyte count to 20-30% of baseline values, due to the reversible sequestration of lymphocytes in lymphoid tissues. Absolute lymphocyte count <0.2 10^9^/L or serious infections, should lead to treatment interruption; the immune system effects of fingolimod may increase the risk of infections. Since fingolimod reduces blood lymphocyte counts, peripheral blood lymphocyte counts cannot be utilized to evaluate the lymphocyte subset status of a patient treated with fingolimod. Macular edema with or without visual symptoms has been reported, occurring predominantly in the first 3-4 months of therapy (ophthalmological evaluation is recommended, specially in patients with uveitis and concomitant diabetes mellitus; discontinue treatment if a patient develops macular edema). Elevations in liver transaminases occurred in patients treated with fingolimod (recent (e.g. within last 6 months) transaminase and bilirubin levels should be available before initiation of treatment; liver transaminases should be monitored at months 1, 3 and 6 on therapy and periodically thereafter). If liver transaminases rise above 5 times the ULN, more frequent monitoring should be instituted, including serum bilirubin and alkaline phosphatase (ALP) measurement and the treatment with fingolimod should be interrupted and only re-commenced once liver transaminase values have normalized. Patients treated with fingolimod presented an increase in systolic and diastolic pressure (blood pressure should be regularly monitored during treatment). Respiratory effects can occur (should be used with caution in severe respiratory disease, pulmonary fibrosis and chronic obstructive pulmonary disease). When switching from other immunosuppressive medications, the duration and mode of action of such substances must be considered when initiating fingolimod, to avoid additive immune suppressive effects. If a decision is made to stop treatment, a 6 week interval without therapy is needed, based on half-life, to clear fingolimod from the circulation.