LETTERS AND CORRESPONDENCE Letters and correspondence submitted for possible publication must be identified as such. Text length must not exceed 500 words and five bibliographic references. A single concise figure or table may be included if it is essential to support the communication. Letters not typed double-spaced will not be considered for publication. Letters not meeting these specifications will not be returned to authors. Letters to the Editor are utilized to communicate a single novel observation or finding. Correspondence is to be used to supplement or constructively comment on the contents of a publication in the journal and cannot exceed the restrictions for Letters to the Editor. The Editor reserves the right to shorten text, delete objectional comments, and make other changes to comply with the style of the journal. Permission for publication must be appended as a postscript. Submissions must be sent to Marcel E. Conrad, M.D., Associate Editor, American Journal of Hematology, USA Cancer Center, Mobile, Alabama 36688 to permit rapid consideration for publication. Interferon-Alpha 2b Interaction With Acenocoumarol To the Editor: Several well-described side effects are ubiquitous among patients receiving interferon-alpha [1]. A possible interaction between in- terferon and warfarin increasing the prothrombin time has been recently reported [2]. We report the first case of potentiation of acenocoumarol by interferon. A 46-year-old-woman was admitted for treatment of chronic C hepatitis. She had received acenocoumarol since 1979 after a mitral valve replace- ment. Her maintenance dose alternated between 2 and 1 mg daily. Throm- botest was stable between 30 and 35%. In February 1995, thrombotest was 35%. Six weeks after she was given interferon-alpha 2b, 3 million units three times a week, we observed increased anticoagulation with a throm- botest of 19% and gingival bleeding. The patient required a reduction dose of acenocoumarol to achieve appropriate prolongation of the prothrombin time. She was prescribed acenocoumarol 1 mg daily, as opposed to an alternating schedule required before admission. Subsequent thrombotests have remained between 25 and 40%. In October, as hepatitis C virus infection was in remission, interferon was tapered to 3 million units twice a week. Three weeks later we observed decrease anticoagulation with a thrombotest of 69%. Anticoagulation returned to its initial value after the patient was given a dose alternated between 2 and 1 mg daily. However, when prothrombin time was controlled at a different time after interferon therapy, we observed differences in the degree of anticoagulation. Throm- botest increased from 27 and 35% one day after the injection of interferon to 64 and 72% two or three days later. Liver function tests were normal, except for mild cytolysis, and no other therapy than interferon can account for the fluctuation of anticoagulation observed in this patient. Potentiation of oral anticoagulant by interferon has been reported recently in 5 patients receiving warfarin, resulting in in- creased anticoagulation with an increased serum warfarin concentration necessitating a reduction in dose [2]. Our observation suggests that poten- tiation can also occur with acenocoumarol. An inhibition of hepatic mi- crosomial enzymes by interferon can be suspected [3]. Indeed, interferon depresses cytochrome P-450 in mice [4], and has been shown to reduce the activity of drug-metabolizing enzymes in the human liver [3]. When interferon is given to patients receiving oral anticoagulant, the degree of anticoagulation should be carefully monitored. JACQUES SERRATRICE JEAN-MARC DURAND SOPHIE MORANGE Department of Internal Medicine and Toxicology, CHU Sainte Marguerite, Marseille, France REFERENCES 1. Quesada JR, Talpaz M, Rios A, Kurzrock R, Gutterman JU: Clinical toxicity of interferons in cancer patients: a review. J Clin Oncol 234–243, 1986. 2. Adachi Y, Yokoyama Y, Nanno T, Yamamoto T: Potentiation of warfarin by interferon. Br Med J 311:292, 1995. 3. Okuno H, Kitao Y, Takasu M, et al: Depression of drug metabolizing activity in the human liver by interferon-a. Eur J Clin Pharmacol 39:365–367, 1990. 4. Renton KW, Singh G, Stebbing N: Relationship between the antiviral effects of interferons and their abilities to depress cytochrome P-450. Biochem Pharmacol 33:3899–3902, 1984. Atypical Presentation of Post-Partum Visceral Leishmaniasis To the Editor: A thirty-one-year-old woman was referred because of fever, anorexia, and malaise of fifteen days’ duration. Fever was double quotid- ian, and was accompanied by profuse sweating. Twenty days before ad- mission she had given birth to a healthy child. Her husband was a military officer and they lived across the Greek-Albanian border the last 20 months. On admission temperature was 37.6°C, blood pressure 110/70 mmHg, pulse rate 90 per min, and respiration rate 18 per min. Physical examination revealed a palpable spleen 3 to 4 cm below the left subcostal margin. There was neither lymphadenopathy nor hepatomegaly. On complete blood count she proved to be pancytopenic: the hematocrit was 29%, the white cell count 3,450/L (with neurtophils 44%, lympho- cytes 38%, monocytes 15%, and eosinophils 3%), and the platelet count 110,000/L. C-reactive protein was 32 mg/dL, and erythrocyte sedimen- tation rate 55 mm per hour. There was a polyclonal hypergammaglobu- linemia on protein electrophoresis. Biochemical tests and urinalysis were within normal limits except for an increase in lactic dehydrogenase (560 IU/L, with an upper limit of 450 IU/L). A chest X-ray and an electrocar- diogram were normal. An abdominal ultrasound confirmed the splenomeg- aly. Tuberculin skin test and serological tests for syphilis, brucella, CMV, EBV, HIV, and hepatitis viruses were negative. Serum direct agglutination test for Leishmania was also negative. American Journal of Hematology 57:89–92 (1998) © 1998 Wiley-Liss, Inc.