Subjects:
BloodWork, Free Research Articles, Lymphoid Neoplasia
Topics:
malaria, vivax, pancytopenia
Routine blood counts in a 65-year-old man revealed marked lymphocytosis (hemoglobin, 115 g/L; total leukocyte count [TLC], 70.2 × 109/L; absolute lymphocyte count [ALC], 65.5 × 109/L; platelets, 142 × 109/L). Examination revealed enlarged cervical lymph nodes and hepatomegaly 2 cm below costal margin without splenomegaly. A week later, without any therapy/intervention, he developed high-grade fever, breathlessness, and diarrhea over 3 to 4 days. Hemograms revealed pancytopenia (hemoglobin, 95 g/L; TLC, 3.3 × 109/L; ALC, 1.8 × 109/L; platelets, 30 × 109/L). Bone marrow showed 86% lymphoid cells with typical chronic lymphocytic leukemia (CLL) immunophenotype (CD19+/CD5+/CD23+/CD20dim/κdim). Additionally, blood and marrow films showed amoeboid trophozoites and schizonts of Plasmodium vivax (see inset), confirmed on immunochromatographic testing. Many red blood cells contained multiple rings. Hemophagocytosis was inconspicuous. Serum urea was 110 mg% (preinfection result, 44 mg%), creatinine was 2.4 mg%, and lactate dehydrogenase (LDH) was 1050 IU/L, with normal sodium and potassium levels. Artesunate therapy cleared the parasite. Five days later, TLC was 16.2 × 109/L and after 11 days was 47.7 × 109/L. The typical CLL blood picture returned. LDH was 880 IU/L. Urea, creatinine, and uric acid normalized. Hemoglobin and platelets returned slowly to pretherapy levels. / Vivax malaria may cause pancytopenia via hemophagocytic lymphohistiocytosis, myelosuppression, hypersplenism (all clinically/morphologically unlikely in our case), or tumor lysis by infection-related steroid release. Implications of infection-lowered counts remain open to exploration by future clinical/therapeutic mechanistic studies.
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Routine blood counts in a 65-year-old man revealed marked lymphocytosis (hemoglobin, 115 g/L; total leukocyte count [TLC], 70.2 × 109/L; absolute lymphocyte count [ALC], 65.5 × 109/L; platelets, 142 × 109/L). Examination revealed enlarged cervical lymph nodes and hepatomegaly 2 cm below costal margin without splenomegaly. A week later, without any therapy/intervention, he developed high-grade fever, breathlessness, and diarrhea over 3 to 4 days. Hemograms revealed pancytopenia (hemoglobin, 95 g/L; TLC, 3.3 × 109/L; ALC, 1.8 × 109/L; platelets, 30 × 109/L). Bone marrow showed 86% lymphoid cells with typical chronic lymphocytic leukemia (CLL) immunophenotype (CD19+/CD5+/CD23+/CD20dim/κdim). Additionally, blood and marrow films showed amoeboid trophozoites and schizonts of Plasmodium vivax (see inset), confirmed on immunochromatographic testing. Many red blood cells contained multiple rings. Hemophagocytosis was inconspicuous. Serum urea was 110 mg% (preinfection result, 44 mg%), creatinine was 2.4 mg%, and lactate dehydrogenase (LDH) was 1050 IU/L, with normal sodium and potassium levels. Artesunate therapy cleared the parasite. Five days later, TLC was 16.2 × 109/L and after 11 days was 47.7 × 109/L. The typical CLL blood picture returned. LDH was 880 IU/L. Urea, creatinine, and uric acid normalized. Hemoglobin and platelets returned slowly to pretherapy levels.

Vivax malaria may cause pancytopenia via hemophagocytic lymphohistiocytosis, myelosuppression, hypersplenism (all clinically/morphologically unlikely in our case), or tumor lysis by infection-related steroid release. Implications of infection-lowered counts remain open to exploration by future clinical/therapeutic mechanistic studies.

Routine blood counts in a 65-year-old man revealed marked lymphocytosis (hemoglobin, 115 g/L; total leukocyte count [TLC], 70.2 × 109/L; absolute lymphocyte count [ALC], 65.5 × 109/L; platelets, 142 × 109/L). Examination revealed enlarged cervical lymph nodes and hepatomegaly 2 cm below costal margin without splenomegaly. A week later, without any therapy/intervention, he developed high-grade fever, breathlessness, and diarrhea over 3 to 4 days. Hemograms revealed pancytopenia (hemoglobin, 95 g/L; TLC, 3.3 × 109/L; ALC, 1.8 × 109/L; platelets, 30 × 109/L). Bone marrow showed 86% lymphoid cells with typical chronic lymphocytic leukemia (CLL) immunophenotype (CD19+/CD5+/CD23+/CD20dim/κdim). Additionally, blood and marrow films showed amoeboid trophozoites and schizonts of Plasmodium vivax (see inset), confirmed on immunochromatographic testing. Many red blood cells contained multiple rings. Hemophagocytosis was inconspicuous. Serum urea was 110 mg% (preinfection result, 44 mg%), creatinine was 2.4 mg%, and lactate dehydrogenase (LDH) was 1050 IU/L, with normal sodium and potassium levels. Artesunate therapy cleared the parasite. Five days later, TLC was 16.2 × 109/L and after 11 days was 47.7 × 109/L. The typical CLL blood picture returned. LDH was 880 IU/L. Urea, creatinine, and uric acid normalized. Hemoglobin and platelets returned slowly to pretherapy levels. / Vivax malaria may cause pancytopenia via hemophagocytic lymphohistiocytosis, myelosuppression, hypersplenism (all clinically/morphologically unlikely in our case), or tumor lysis by infection-related steroid release. Implications of infection-lowered counts remain open to exploration by future clinical/therapeutic mechanistic studies.
View largeDownload PPT

Routine blood counts in a 65-year-old man revealed marked lymphocytosis (hemoglobin, 115 g/L; total leukocyte count [TLC], 70.2 × 109/L; absolute lymphocyte count [ALC], 65.5 × 109/L; platelets, 142 × 109/L). Examination revealed enlarged cervical lymph nodes and hepatomegaly 2 cm below costal margin without splenomegaly. A week later, without any therapy/intervention, he developed high-grade fever, breathlessness, and diarrhea over 3 to 4 days. Hemograms revealed pancytopenia (hemoglobin, 95 g/L; TLC, 3.3 × 109/L; ALC, 1.8 × 109/L; platelets, 30 × 109/L). Bone marrow showed 86% lymphoid cells with typical chronic lymphocytic leukemia (CLL) immunophenotype (CD19+/CD5+/CD23+/CD20dim/κdim). Additionally, blood and marrow films showed amoeboid trophozoites and schizonts of Plasmodium vivax (see inset), confirmed on immunochromatographic testing. Many red blood cells contained multiple rings. Hemophagocytosis was inconspicuous. Serum urea was 110 mg% (preinfection result, 44 mg%), creatinine was 2.4 mg%, and lactate dehydrogenase (LDH) was 1050 IU/L, with normal sodium and potassium levels. Artesunate therapy cleared the parasite. Five days later, TLC was 16.2 × 109/L and after 11 days was 47.7 × 109/L. The typical CLL blood picture returned. LDH was 880 IU/L. Urea, creatinine, and uric acid normalized. Hemoglobin and platelets returned slowly to pretherapy levels.

Vivax malaria may cause pancytopenia via hemophagocytic lymphohistiocytosis, myelosuppression, hypersplenism (all clinically/morphologically unlikely in our case), or tumor lysis by infection-related steroid release. Implications of infection-lowered counts remain open to exploration by future clinical/therapeutic mechanistic studies.

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© 2013 by The American Society of Hematology
2013
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