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Neurology India, Vol. 57, No. 4, July-August, 2009, pp. 424-425 Invited Commentary Invited commentary Lekha Pandit Department of Neurology, KS Hegde Medical Academy, Mangalore, India Correspondence Address: Dr. Lekha Pandit, Department of Neurology, KS Hegde Medical Academy, Mangalore 575018, Karnataka, India, Panditmng@gmail.com Date of Acceptance: 11-Aug-2009 Code Number: ni09122 Multiple sclerosis (MS) is a chronic and relentlessly progressive disorder, in the vast majority of patients affected worldwide. The data available from long-term follow-up of patients with an initial benign presentation has shown that a significant number of patients develop disabling deficits especially involving cognitive functions. There are no reliable clinical or radiological predictors of disease course in MS. In addition, pathological evidence exists of irreversible brain damage very early on in the course of disease. Therefore, there is no doubt that a disease modifying agent is needed; this agent should have an acceptable safety profile and should not only reduce relapses but also delay the progression of disease. In developing countries such as India, another factor would be affordability of this medication which has to be taken very often for indefinite periods of time. In this context, a report by Singhal et al. , [1] on the use of mitoxantrone as an initial agent in the treatment of MS, is interesting. The authors have shown reasonably good response to the treatment in a significant number of patients. They have, however, treated their patients, who had varying duaration and stage of disease, unblinded. Mitoxantrone, though more affordable in comparison to interferon and glatiramir acetate, does not share the safety profile of the latter. In view of potentially fatal cardio toxicity, frequent cardiological evaluations are required during the course of medications. Therapy related leukemia is another concern which has been reported up to as much as five years after treatment. Therefore, the actual benefit will fall on a select minority of patients who can be kept under stringent follow-up and are willing to consider alternative and costly disease modifying drugs (DMD) after the initial therapy with mitoxantrone. The authors have left this intriguing question unanswered. Mitoxantrone is not a 'stand alone' treatment modality in MS. Initial benefit with mitoxantrone is not necessarily sustained, and therefore, subjecting a patient to a drug which is cheaper but has safety issues must be carefully considered while selecting patients for this form of therapy. However, it must be acknowledged that mitoxantrone along with newer molecules such as monoclonal antibodies are being increasingly recognized as drugs which induce a quick remission. The role of combination therapy with mitoxantrone is being explored through several trials at the moment. This paper brings to focus the growing recognition that MS is not uncommon in India and that there is a real need for a safe and affordable treatment. Extending this study to include larger and more homogenous group of patients and combing with relatively less expensive disease modifying agents such as azathioprine may be worth considering in the future. References
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