<p>Azathioprine (AZA), a prodrug of 6 mercaptopurine, is an immunosuppressant that can be used as adjunctive therapy with corticosteroids in the treatment of arteritic form of ischemic optic neuropathy. Although myelotoxicity is known to occur while using azathioprine, severe pancytopenia is rarely seen. Patients with thiopurine methyltransferase (TPMT) deficiency are at high risk of developing severe myelosuppression. A 63 year* old female with ischemic optic neuropathy was initiated treatment with oral methylprednisone. As two courses of oral steroids showed no significant improvement, oral azathioprine 25 mg twice daily was added and gradually increased to 50 mg twice daily with relief of symptoms. 6 mo later, she was admitted with acute stroke and lab reports showed low levels of total blood counts or pancytopenia. The patient was put on broad spectrum antibiotics; given injection of granulocyte colony stimulating factor 300 mcg subcutaneously and blood transfusion as correction till counts normalised. She improved over 14 d and on next follow-up counts were in normal range. Causality was assessed by Naranjo causality assessment scale and a probable relationship was obtained between azathioprine and pancytopenia with a score of 6. Variations in TPMT activity occurs due to genetic polymorphism. Physicians should be aware of the possibility of myelosuppression while prescribing azathioprine. Frequent blood count monitoring is the most convenient way to avoid this problem where testing for TPMT deficiency is not possible.</p>
Objective: To report a case of lithium induced bilateral nonpitting pedal edema. Methods:The clinical data of a bipolar affective disorder patient with current episode of mania and psychotic symptoms who experienced bilateral non pitting pedal edema with lithium. Results:The patient was a 29 yr old female who developed bilateral non-pitting type pedal edema with lithium therapy with normal plasma lithium level (0.72mEq/l). She is a known case of bipolar affective disorder (BPAD) was admitted to psychiatry department with episode of mania with psychotic symptoms. She had history of drug induced hypersensitivity reaction with eosinophilia and systemic symptoms (DRESS) with oxcarbazepine and so the drug was discontinued and was started on tablet lithium 400 mg twice daily. On admission here, the dose of lithium was increased to 1200 mg/day. The patient gradually improved but she developed bilateral non-pitting pedal edema. Serum lithium concentration was normal and there were no other early symptoms of lithium toxicity. But as the patient's distress further increased with increasing pedal edema, it was decided to stop lithium altogether and to maintain the patient on tablet quetiapine 800 mg therapy for BPAD. Within one week of stopping lithium the edema on both her feet decreased significantly. Causality was assessed by naranjo causality assessment scale and a probable relationship was obtained between lithium and pedal edema with a score of 6. Conclusion:This case emphasises that regular physical examination and laboratory investigations are important for patients who are on lithium therapy. Clinicians should always be careful while initiating lithium treatment in a patient with respect to the initial dose and dose escalation even after a period of successful therapy with lithium, as minor dose escalation can cause major changes in the serum lithium concentration and thereby the patient's tolerability to lithium.
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