Dapsone-induced haemolytic anaemia, hepatitis and agranulocytosis in a leprosy patient with normal glucose-6-phosphate-dehydrogenase activity
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1 Lepr Rev (2008) 79, CASE REPORT Dapsone-induced haemolytic anaemia, hepatitis and agranulocytosis in a leprosy patient with normal glucose-6-phosphate-dehydrogenase activity RANTHILAKA R. RANAWAKA, SURESH MENDIS & HEMA S. WEERAKOON Teaching Hospital Anuradhapura, Sri Lanka Accepted for publication 11 September 2008 Summary A 21 year old boy with borderline lepromatous leprosy and normal glucose-6-phosphate-dehydrogenase activity developed haemolytic anaemia, hepatitis and agranulocytosis following 19 weeks of multi-bacillary multi-drug therapy. With early administration of antibiotics and G-CSF our patient recovered without residual complications. All patients taking dapsone should be warned to discontinue the drug immediately in the event of fever, chills and sore throat occurring within the treatment period until further investigations are performed. Introduction Dapsone is used as a primary drug for leprosy. The adverse effects of dapsone include haemolysis, methaemoglobinaemia and hepatitis. Agranulocytosis is rare; this severe and unpredictable idiosyncratic reaction has been reported to occur in % of patients treated with dapsone. 1 5 Agranulocytosis is a fatal complication, which is characterised by a decrease in peripheral neutrophil count to less than cells/l, where other cell populations remain relatively normal. Case Report A 21 year old boy presented with six hypopigmented, anaesthetic macules on the back of the trunk of 1 year s duration. Borderline lepromatous leprosy was diagnosed and was started on Correspondence to: Dr Ranthilaka R. Ranawaka, No: 310/4 Kulasiri Kumarage Mawatha, Katuwana, Homagama, Sri Lanka (Tel: þ ; ranthilaka37@yahoo.com) /08/ $1.00 q Lepra
2 Table 1. Monitoring of the leprosy patient during MB therapy Date Prior to Rx December 07 and January Presented with fever and sore throat for 6 days 139th day (19 weeks and 6 days) after recovery Period treatment 1st day 22nd day 38th day 56th day Haemoglobin (g/dl) Total WBC count ( 10 9 /L) Investigations Neutrophils (%) were not Lymphocytes (%) performed Eosinophils (%) 2 Monocytes (%) Platelet count ( 10 9 /L) Retic count (%) Haematocrit (%) On rifampicin and clofazimine Glucose-6-phosphatedehydrogenase(G6PD) activity Within normal limits Normal limits Serum bilirubin(0 2-2 mg/dl) 2 4 Indirect fraction (mg/dl) 1 5 Direct fraction (mg/dl) 0 9 SGPT(4 27 IU/L at 37 8C) SGOT (4 42 IU/L at 37 8C) Dapsone-induced agranulocytosis in leprosy 437
3 438 R. R. Ranawaka et al. multibacillary multi-drug therapy (MB-MDT) which consists of a monthly dose of 600 mg rifampicin and 300 mg clofazimine, a daily dose of 100 mg dapsone and 50 mg clofazimine. Routine screening tests were done prior to treatment (Table 1). Since his haemoglobin was 17 g/dl and haematocrit 52%, he was investigated for polycythaemia. He was an ex-smoker who stopped smoking one month ago. There were no symptoms related to polycythaemia. On examination there was no lymphadenopathy or hepatospleenomegaly. Chest X-ray, blood gas analysis, abdominal and pelvic ultrasonography and lung spirometry were within normal limits. Blood picture showed normocytic normochromic red cells with mild polychromasia, bite cells and occasional blast cells. White cells and platelets were normal in number and morphology. It was concluded that his haemoglobin was in upper normal range; therefore bone marrow test was not performed. After 2 weeks -MDT treatment repeat haemoglobin was 16 3 g/dl and reticulocyte count was 9%. In spite of a normal repeat glucose-6-phosphate-dehydrogenase (G6PD) test, evidence of oxidative haemolysis was seen in the blood picture with polychromasia. Since his haemoglobin was within normal limits we continued MB-MDT treatment with close monitoring. After 19 weeks -MDT he presented to a physician with a history of fever for 6 days and sore throat for 3 days. Full blood count (FBC) showed a total white cell count (WBC) of /L with a differential count of zero neutrophils and 100% lymphocytes. He was mildly icteric with elevated liver enzymes (Table 1). He was diagnosed as having agranulocytosis, haemolytic anaemia and hepatitis following MB therapy. MB-MDT therapy was stopped immediately. At the intensive care unit he was treated with broad spectrum antibiotics and monitored for neutrophil counts. Blood cultures and urine cultures were negative. Although WBC count gradually improved over five days, persistent high fever warranted treatment with recombinant human granulocyte-colony stimulating factor; rhg-csf (Filgrastim). Following 10 days of intravenous antibiotics and 5 days of rhg-csf he was cured without residual complications. After 4 weeks when his FBC was within normal limits he was re-started on rifampicin 600 mg monthly and clofazimine 100 mg daily. Patient s liver enzymes and FBC are monitored monthly, and are within normal range at the 9th month of treatment. Our plan is to continue rifampicin and clofazimine for a total of 12 months. Discussion The current prevalence of leprosy in Sri Lanka is 0 6 per population. Most leprosy patients are treated at the dermatology clinics throughout the country. This is the first case of dapsone induced agranulocytosis reported from the Teaching Hospital Anuradhapura. There were 78 new patients registered for leprosy treatment at the Teaching Hospital Anuradhapura in 2007, the year in which this case was reported. Since this patient was apparently healthy and was not on any other drugs in the previous 3 months which could have caused agranulocytosis; such as chloramphenicol or exposure to radiation, we concluded that his agranulocytosis, haemolysis and hepatitis were due to dapsone. Two weeks after the initial screening tests, his reticulocytes increased to 9% from 0 2%. There is therefore evidence of active regeneration of bone marrow in response to a stimulus. As the G6PD was normal no other investigations were done. However, acute haemolysis and agranulocytosis can also occur in persons with normal G6PD activity. 4
4 Dapsone-induced agranulocytosis in leprosy 439 Dapsone induced agranulocytosis is an idiosyncratic reaction and may occur well within the intended dosage range, when severe, can also involve platelets. Usually, once the drug is withdrawn blood counts return to normal within days. Sudden drop in white cell production leaves the body susceptible to bacterial infections and septicemia. Though reversible, the condition can be fatal. According to literature immunocompromised leprosy patients exhibit virtually zero risk of developing agranulocytosis, while patients not otherwise ill and taking the drug as an antimalarial in combination with pyrimethamine are at 1: risk. However, patients taking dapsone to control dermatitis herpetiformis are at a fold greater risk than normal. 2,3,5 In the majority of cases, its occurrence is due to sensitisation to the drug which depresses the formation of granulocytes in the bone marrow. The mechanism postulated for the sensitisation is the formation of hydroxylamine, the toxic metabolite of dapsone which is also responsible for methaemoglobinaemia and haemolysis. 2 Another possible mechanism is the formation of antibodies for neutrophil progenitors in the bone marrow and the resultant destruction producing agranulocytosis. 2 Neutropenia is noticed earliest at 3 weeks and the onset almost always occurs within 3 months. 1,2 Therefore some authors suggest monitoring leukocyte count with a differential and haemoglobin levels weekly for the first month of therapy, twice monthly for the next 2 months and periodically thereafter in order to detect complication early. Except for screening investigations blood tests are not routinely done on leprosy patients in the local setting. Drugs are issued from nearest anti-leprosy clinics and patients are seen at the dermatology unit at the end of the therapy. But in this patient we have been monitoring his blood counts every 2 weeks for 2 months and then monthly once since he showed evidence of polycythaemia. After conclusion of upper normal range haemoglobin we did not follow him up in our clinic and he was issued drugs as an out-patient for 2 months. After 19 weeks -MDT therapy and normal WBC for 12 weeks, he developed agranulocytosis acutely within 2 months. We doubt whether monitoring blood counts during the first 3 months would have helped to detect agranulocytosis in this case. We suggest that monitoring blood counts serially in high risk patients (elderly.60 years of age, patients with dermatitis herpetiformis, linear IgA disease, coeliac disease) would help to detect this fatal complication early. We suggest that all patients taking dapsone should be warned to discontinue the drug immediately in the event of fever, chills and sore throat occurring within total treatment period until further investigations are performed. Also, since hydroxylamine, the toxic metabolite of dapsone is responsible for both haemolysis and agranulocytosis, close monitoring of patients with haemolysis who are continuing dapsone may help to detect agranulocytosis early. We believe that in our patient, early treatment with antibiotics and G-CSF accounted for his survival. References 1 Bhat RM, Radhakrishnan K. A case report of dapsone induced agranulocytosis in an Indian mid-borderline leprosy patient. Lepr Rev, 2003; 74: Coleman MD. Dapsone-mediated agranulocytosis: risks, possible mechanisms and prevention. Toxicology, 2001; 162:
5 440 R. R. Ranawaka et al. 3 Anderson F, Konzen C, Garbe E. Systematic review: Agranulocytosis induced by non-chemotherapy drugs. Ann Intern Med, 2007; 146: Figueiredo MS, Pinto BO, Zago MA. Dapsone-induced haemolytic anaemia and agranulocytosis in a patient with normal glucose-6-phosphate-dehydrogenase activity. Acta Haematol, 1989; 82: Hornsten P, Keisu M, Wiholm BE. The incidence of agranulocytosis during treatment of dermatitis herpetiformis with dapsone as reported in Sweden, 1972 through Arch Dermatol, 1990; 126:
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