Annals of
Ann Hematol (1992) 64:43-45
Hematology 9 Springer-Verlag 1992
Case report Acute parvovirus B 19 infection mimicking myelodysplastic syndrome of the bone marrow H. Baurmann 1, 17. E Schwarz 2, J. Oertel 1, S. Serke 1, M. Roggendorf 2, and D. Hulln 1 1 Abteilung for Innere Medizin mit Schwerpunkt H~imatologie und Onkologie, Universit~itsklinikum Rudolf Virchow, Standort Charlottenburg, Freie Universit~it Berlin, Spandauer Datum 130, W-1000 Berlin 19, FRG z Max yon Pettenkofer Institut ftir Hygiene und Medizinische Mikrobiologie, Ludwig-Maximilians-Universit~it, Pettenkoferstrasse 9a, W-8000 Munich 2, FRG Received July 29, 1991/Accepted October 28, 1991
Summary. A 36-year-old, previously h e a l t h y w o m a n was referred to o u r i n s t i t u t i o n with p a n c y t o p e n i a a n d splenom e g a l y for suspected acute leukemia. Bone m a r r o w aspiration showed m a r k e d dysplastic changes, excess o f blasts, a n d o n l y s p u r i o u s red b l o o d cell precursors. A c t i o n was t a k e n to p r e p a r e allogeneic b o n e m a r r o w t r a n s p l a n t a t i o n f r o m an H L A i d e n t i c a l sibling for m y e l o d y s p l a s t i c syndrome. R e p e a t cytological e x a m i n a t i o n o f the b o n e m a r row revealed striking h y p e r p l a s i a o f the red cell line with presence o f a b n o r m a l giant proerythroblasts. A c u t e parvovirus B19 infection was suspected a n d c o n f i r m e d by d e t e c t i o n o f anti-B 19 I g M a n d B 19 D N A . T h e u n d e r l y ing disease for this t r a n s i e n t a p l a s t i c crisis was a f o r m e r l y u n k n o w n h e r e d i t a r y spherocytosis. Key words: Parvovirus B 19 - M y e l o d y s p l a s t i c s y n d r o m e - H e r e d i t a r y spherocytosis
Introduction M y e l o d y s p l a s t i c s y n d r o m e s as c l o n a l diseases o f the b o n e m a r r o w are being increasingly recognized as an i m p o r t a n t cause o f p e r i p h e r a l b l o o d cytopenia. B o n e m a r r o w aspirates show v a r i o u s degrees o f dysplastic changes in different cell lines. Blast cell excess is c o r r e l a t e d with risk o f leukemic t r a n s f o r m a t i o n a n d overall p r o g n o s i s [1, 9]. I n 1981, p a r v o v i r u s B 19 (B 19) was i d e n t i f i e d as the etiologic agent o f transient e r y t h r o b l a s t o p e n i a in p a t i e n t s with u n d e r l y i n g h e m o l y t i c disease [10, 13]. B 19 is k n o w n for its p r o n o u n c e d t r o p i s m to e r y t h r o i d p r o g e n i t o r cells, l e a d i n g to i n h i b i t i o n o f erythropoiesis. However, transient d r o p s in leukocyte a n d platelet counts have also been r e p o r t e d [15]. H e r e we show t h a t b o n e m a r r o w infection by p a r v o v i r u s B 19 can closely m i m i c m y e l o d y s -
Address for correspondence: H. Baurmann, Service Clinique des Maladies du Sang, Hematologie Adulte, Hopital Saint-Louis, 1, Avenue Claude Vellefaux, F-75010 Paris, France
p l a s i a a n d s h o u l d be considered as a differential d i a g n o sis early on in the d i a g n o s t i c pathway.
Case report In March 1991, a 36-year-old woman was admitted to a community hospital because of fever and pancytopenia. Four months previously she had had an uneventful delivery of her second child. No blood disorders were known in the family, and her former medical history was unremarkable until she developed high-grade temperature (39~176 myalgia, and general malaise 3 days prior to admission. Blood count at presentation showed hemoglobin 59 g/l, platelets 70 x 109/1, and leukocytes 1.8 • 109/1 with a differential count of 32~ neutrophils, 3~ monocytes, 2070 eosinophils, 1% basophils, 54~ lymphocytes, and 8~ atypical lymphoid cells with marked plasma basophilia and a less mature chromatin pattern. Four units of packed red blood cells were given, with little effect on hemoglobin values. The patient was transferred to our institution 1 day after initial presentation for suspected acute leukemia. On admission the patient was afebrile. Physical findings were normal except for frank splenomegaly confirmed by ultrasound examination. Blood count values were identical to previous results. No peripheral blasts were seen. Slight elevation of serum bilirubin (27 pg/1) and lactate dehydrogenase levels (330 U/I) were noted. The Coombs' test was negative. The bone marrow aspirate was hypocellular, showing multiple abnormal megacaryocytes, almost complete absence of erythropoiesis, and, among the myeloid series, an excess of blastic cells. These blasts accounted for 15070 of bone marrow cells, were largely myeloperoxydase positive, and had in part monocytic/histiocytic features (Fig. 1). Iron staining revealed no ring sideroblasts. A preliminary diagnosis of refractory anemia with excess of blasts (RAEB) was made, and a search for an HLA identical bone marrow donor among the siblings of the patient was started. During the next few days the patient remained well but required transfusion of seven more packed red blood cell units. Six days after her referral to our hospital (day 10 after onset of symptoms), a second bone marrow aspiration was done for diagnostic confirmation. Surprisingly, the picture had considerably changed. Bone marrow this time was hypercellular; there was no longer an excess of blasts but marked hyperplasia of erythropoiesis with presence of giant forms of abnormal proerythroblasts. Megacaryocytes still showed dysplastic features but were found in normal amounts (Fig. 2). Reticulocyte counts of the same day and 1 day later were 2.9x109/1 and 22.8x109/1, respectively. Serological examination revealed acute parvovirus B19 infection, detecting anti-B 19 IgM and anti-B 19 IgG by enzyme linked immunoassay
44
Fig. 1 A, B. Bone marrow aspirate, day 5. A Myeloid blast cell excess (arrow heads upper left), one of the rare pronormoblasts (middle), and a rnononucleated megakaryocyte (lower right). • 1000. B Myeloblastic and monocytic/ histiocytic cells, x 1575
Fig. 2 A, B. Bone marrow aspirate, day 10. A Erythroid hyperplasia and a binucleated pronormoblast. • 1000. B Giant trinucleated pronormoblast. )
Ann Hematol (1992) 64:43-45
Hematology 9 Springer-Verlag 1992
Case report Acute parvovirus B 19 infection mimicking myelodysplastic syndrome of the bone marrow H. Baurmann 1, 17. E Schwarz 2, J. Oertel 1, S. Serke 1, M. Roggendorf 2, and D. Hulln 1 1 Abteilung for Innere Medizin mit Schwerpunkt H~imatologie und Onkologie, Universit~itsklinikum Rudolf Virchow, Standort Charlottenburg, Freie Universit~it Berlin, Spandauer Datum 130, W-1000 Berlin 19, FRG z Max yon Pettenkofer Institut ftir Hygiene und Medizinische Mikrobiologie, Ludwig-Maximilians-Universit~it, Pettenkoferstrasse 9a, W-8000 Munich 2, FRG Received July 29, 1991/Accepted October 28, 1991
Summary. A 36-year-old, previously h e a l t h y w o m a n was referred to o u r i n s t i t u t i o n with p a n c y t o p e n i a a n d splenom e g a l y for suspected acute leukemia. Bone m a r r o w aspiration showed m a r k e d dysplastic changes, excess o f blasts, a n d o n l y s p u r i o u s red b l o o d cell precursors. A c t i o n was t a k e n to p r e p a r e allogeneic b o n e m a r r o w t r a n s p l a n t a t i o n f r o m an H L A i d e n t i c a l sibling for m y e l o d y s p l a s t i c syndrome. R e p e a t cytological e x a m i n a t i o n o f the b o n e m a r row revealed striking h y p e r p l a s i a o f the red cell line with presence o f a b n o r m a l giant proerythroblasts. A c u t e parvovirus B19 infection was suspected a n d c o n f i r m e d by d e t e c t i o n o f anti-B 19 I g M a n d B 19 D N A . T h e u n d e r l y ing disease for this t r a n s i e n t a p l a s t i c crisis was a f o r m e r l y u n k n o w n h e r e d i t a r y spherocytosis. Key words: Parvovirus B 19 - M y e l o d y s p l a s t i c s y n d r o m e - H e r e d i t a r y spherocytosis
Introduction M y e l o d y s p l a s t i c s y n d r o m e s as c l o n a l diseases o f the b o n e m a r r o w are being increasingly recognized as an i m p o r t a n t cause o f p e r i p h e r a l b l o o d cytopenia. B o n e m a r r o w aspirates show v a r i o u s degrees o f dysplastic changes in different cell lines. Blast cell excess is c o r r e l a t e d with risk o f leukemic t r a n s f o r m a t i o n a n d overall p r o g n o s i s [1, 9]. I n 1981, p a r v o v i r u s B 19 (B 19) was i d e n t i f i e d as the etiologic agent o f transient e r y t h r o b l a s t o p e n i a in p a t i e n t s with u n d e r l y i n g h e m o l y t i c disease [10, 13]. B 19 is k n o w n for its p r o n o u n c e d t r o p i s m to e r y t h r o i d p r o g e n i t o r cells, l e a d i n g to i n h i b i t i o n o f erythropoiesis. However, transient d r o p s in leukocyte a n d platelet counts have also been r e p o r t e d [15]. H e r e we show t h a t b o n e m a r r o w infection by p a r v o v i r u s B 19 can closely m i m i c m y e l o d y s -
Address for correspondence: H. Baurmann, Service Clinique des Maladies du Sang, Hematologie Adulte, Hopital Saint-Louis, 1, Avenue Claude Vellefaux, F-75010 Paris, France
p l a s i a a n d s h o u l d be considered as a differential d i a g n o sis early on in the d i a g n o s t i c pathway.
Case report In March 1991, a 36-year-old woman was admitted to a community hospital because of fever and pancytopenia. Four months previously she had had an uneventful delivery of her second child. No blood disorders were known in the family, and her former medical history was unremarkable until she developed high-grade temperature (39~176 myalgia, and general malaise 3 days prior to admission. Blood count at presentation showed hemoglobin 59 g/l, platelets 70 x 109/1, and leukocytes 1.8 • 109/1 with a differential count of 32~ neutrophils, 3~ monocytes, 2070 eosinophils, 1% basophils, 54~ lymphocytes, and 8~ atypical lymphoid cells with marked plasma basophilia and a less mature chromatin pattern. Four units of packed red blood cells were given, with little effect on hemoglobin values. The patient was transferred to our institution 1 day after initial presentation for suspected acute leukemia. On admission the patient was afebrile. Physical findings were normal except for frank splenomegaly confirmed by ultrasound examination. Blood count values were identical to previous results. No peripheral blasts were seen. Slight elevation of serum bilirubin (27 pg/1) and lactate dehydrogenase levels (330 U/I) were noted. The Coombs' test was negative. The bone marrow aspirate was hypocellular, showing multiple abnormal megacaryocytes, almost complete absence of erythropoiesis, and, among the myeloid series, an excess of blastic cells. These blasts accounted for 15070 of bone marrow cells, were largely myeloperoxydase positive, and had in part monocytic/histiocytic features (Fig. 1). Iron staining revealed no ring sideroblasts. A preliminary diagnosis of refractory anemia with excess of blasts (RAEB) was made, and a search for an HLA identical bone marrow donor among the siblings of the patient was started. During the next few days the patient remained well but required transfusion of seven more packed red blood cell units. Six days after her referral to our hospital (day 10 after onset of symptoms), a second bone marrow aspiration was done for diagnostic confirmation. Surprisingly, the picture had considerably changed. Bone marrow this time was hypercellular; there was no longer an excess of blasts but marked hyperplasia of erythropoiesis with presence of giant forms of abnormal proerythroblasts. Megacaryocytes still showed dysplastic features but were found in normal amounts (Fig. 2). Reticulocyte counts of the same day and 1 day later were 2.9x109/1 and 22.8x109/1, respectively. Serological examination revealed acute parvovirus B19 infection, detecting anti-B 19 IgM and anti-B 19 IgG by enzyme linked immunoassay
44
Fig. 1 A, B. Bone marrow aspirate, day 5. A Myeloid blast cell excess (arrow heads upper left), one of the rare pronormoblasts (middle), and a rnononucleated megakaryocyte (lower right). • 1000. B Myeloblastic and monocytic/ histiocytic cells, x 1575
Fig. 2 A, B. Bone marrow aspirate, day 10. A Erythroid hyperplasia and a binucleated pronormoblast. • 1000. B Giant trinucleated pronormoblast. )
