588
Correspondence
activity of platelet-derived growth factor(s) in patients with myeloproliferativedisease. Acta Haonatologica, 8 1, 1 3 1-1 3 5. Katoh. 0.. Kimura, A.. Itoh. T. & Kuramoto. A. (1990) Plateletderived growth factor messenger RNA is increased in bone marrow megakaryocytes in patients with myeloproliferative disorders. American journal of Hematology. 3 5 , 1 4 5 - 1 50. Katoh. 0.. Kimura. A. & Kuramoto. A. (1988) Platelet-derived growth factor is decreased in patients with myelofibrosisdisorders. American journal of Hematology. 27, 276-280. Marcus, R.E.. Hibbin. J.A.,Matutes. E., Whittle, N.. Waterfield. M.D. & Goldman, J.M. ( 1 986) Megakaryoblastic transformation of myelofibrosis with expression of the c-sis oncogene. Scandinavian journal of Haematology, 36, 186-1 93.
Martyre. M.C.. Magdelenat, H.. Bryckaert. M.C.. Laine-Bidron. C. & Calvo. F. ( 1 991 a) Increased intraplatelet levels of platelet-derived growth factor and transforming growth factor-/3 in patients with myelofibrosis with myeloid metaplasia. British journal o/ Haematology. 77, 80-86. Martyre, M.C.. Magdelenat. H. & Calvo. F. (1991 b) Interferon-? in vivo reverses the increased platelet levels of platelet-derivedgrowth factor and transforming growth factor-/3in patients with myelotibrosis with myeloid metaplasia. British journal of HaenintologU. 77, 4 3 1 - 4 3 5. Romano. M.. Poggi. A.. Donati. M.B.. Cortelazzo. S.. Vicro. P. & Barbui.T. ( 1 9 8 6 ) Reduced platelet mitogenic activity in myeloproliferative disorders. Lancet. ii, 3 4 5 .
MONOCYTE MONOLAYER ASSAY, AUTOANALYSER VALUES, AND HAEMOLYTIC DISEASE OF THE NEWBORN We read with interest the communication by Hadley et a1 (199 1 ) regarding correlation of serological, quantitative and cell mediated functional assays of maternal alloantibodies with the severity of haemolytic disease of the newborn. We have recently undertaken a similar study attempting to correlate a monocyte monolayer assay with indirect antiglobulin antibody titres, autoanalyser quantitation values and the subsequent occurrence of haemolytic disease of the newborn. We retrospectively tested previously frozen sera from 9 6 pregnant women found to have identifiable clinically significant red cell antibodies by our routine serological techniques. Clinical outcome of 75 of these pregnancies was obtained retrospectively. Antibodies investigated included anti-D ( 4 2 ) , anti-c (14). anti-E ( 3 ) , anti-Ce ( 3 ) , anti-e (1). anti-K ( 1 2 ) . anti-k (1). anti-Fya (1 l ) ,a n t i 8 ( 3 ) . anti-Jk" ( 2 ) . anti-Jkb (1). The occurrence and severity of haemolytic disease of the newborn was assessed and classified from questionnaires completed by referring obstetricians. Monocyte monolayer assay was found to be a poor positive predictor of haemolytic disease of the newborn as has been reported elsewhere (Garratty. 1990). In our laboratory monocyte monolayer assay proved to be 60% predictive for haemolytic disease of the newborn requiring transfusion therapy but was, however, 97%predictive for non-affected or mildly affected infants. Monocyte monolayer assay did not correlate well with IAT titres ( r , = 0 . 3 ) or with anti-D quantitation ( r , = 0 . 5 ) . However, for anti-c quantitation correlation was surprisingly good ( rp= 0.9) (Spearman Rank Correlation).
Monocyte monolayer assay in this laboratory was found to be labour intensive, subjective and costly. Hadley et a1 comment that monocyte based functional assays may best predict the severity of haemolytic disease of the newborn. This may well be true if a monocyte-based chemiluminescence test or antibody dependent cell mediated cytotoxicity assay is used. Our results would, however, confirm that a monocyte monolayer assay despite its good negative predictive value, is a poor positive predictor for haemolytic disease of the newborn. We agree with Hadley et a1 that prospective studies using more reliable functional assays to predict haemolytic disease of the newborn non-invasively are needed. Regional Transfusion Centre, West Derby Street, Liverpool L7 8TW
I. M. BROMILOW J. K. M. DUGUID
REFERENCES Garratty. G. (1990) Predicting the clinical significance of red cell antibodies with in vitro cellular assays. Transfusion Medicine Reviews, 4. 297-312. Hadley. A.G., Kumpel. B.M.. Leader. K.A.. Poole. G.D. & Fraser, I.D. ( 1 9 9 1 ) Correlation of serological, quantitative and cell mediated functional assays of maternal alloantibodies with the severity of haemolytic disease of the newborn. British journal ofHaematolog!j. 77,221-228.
NITRENDIPINE TREATMENT AND BLOOD RHEOLOGY IN PATIENTS WITH SICKLE CELL DISEASE We have previously reported that nitrendipine inhibits formation of dense sickle cells in a n in vitro model in which red blood cells are exposed to cycles of deoxygenation and reoxygenation (Nash et a!, 1989). Dense sickle cells (including irreversibly sickled cells, ISC) are thought to be important mediators of vascular obstructive pathology for two main reasons: their inherently poor deformability and their tendency to undergo haemoglobin S (HbS) polymerization more rapidly and at higher pOr compared to less dense cells. The number of ISC has also been linked with the rate of
intravascular haemolysis (Serjeant et al, 1969). We therefore carried out a small-sca!e. open trial of nitrendipine. to test whether treatment would improve blood rheology or alter haematological indices reflecting red cell destruction. Seven subjects with homozygous (HbSS) sickle cell disease were studied (four female and three male, age 22-3 5 years). They had not had a crisis within the previous 4 weeks or a blood transfusion within 3 months. Each received 5 mg nitrendipine twice daily for 1 week, then 10 mg twice daily for 5 weeks. Nitrendipine is a dihydropyridine Ca-entry
Correspondence
activity of platelet-derived growth factor(s) in patients with myeloproliferativedisease. Acta Haonatologica, 8 1, 1 3 1-1 3 5. Katoh. 0.. Kimura, A.. Itoh. T. & Kuramoto. A. (1990) Plateletderived growth factor messenger RNA is increased in bone marrow megakaryocytes in patients with myeloproliferative disorders. American journal of Hematology. 3 5 , 1 4 5 - 1 50. Katoh. 0.. Kimura. A. & Kuramoto. A. (1988) Platelet-derived growth factor is decreased in patients with myelofibrosisdisorders. American journal of Hematology. 27, 276-280. Marcus, R.E.. Hibbin. J.A.,Matutes. E., Whittle, N.. Waterfield. M.D. & Goldman, J.M. ( 1 986) Megakaryoblastic transformation of myelofibrosis with expression of the c-sis oncogene. Scandinavian journal of Haematology, 36, 186-1 93.
Martyre. M.C.. Magdelenat, H.. Bryckaert. M.C.. Laine-Bidron. C. & Calvo. F. ( 1 991 a) Increased intraplatelet levels of platelet-derived growth factor and transforming growth factor-/3 in patients with myelofibrosis with myeloid metaplasia. British journal o/ Haematology. 77, 80-86. Martyre, M.C.. Magdelenat. H. & Calvo. F. (1991 b) Interferon-? in vivo reverses the increased platelet levels of platelet-derivedgrowth factor and transforming growth factor-/3in patients with myelotibrosis with myeloid metaplasia. British journal of HaenintologU. 77, 4 3 1 - 4 3 5. Romano. M.. Poggi. A.. Donati. M.B.. Cortelazzo. S.. Vicro. P. & Barbui.T. ( 1 9 8 6 ) Reduced platelet mitogenic activity in myeloproliferative disorders. Lancet. ii, 3 4 5 .
MONOCYTE MONOLAYER ASSAY, AUTOANALYSER VALUES, AND HAEMOLYTIC DISEASE OF THE NEWBORN We read with interest the communication by Hadley et a1 (199 1 ) regarding correlation of serological, quantitative and cell mediated functional assays of maternal alloantibodies with the severity of haemolytic disease of the newborn. We have recently undertaken a similar study attempting to correlate a monocyte monolayer assay with indirect antiglobulin antibody titres, autoanalyser quantitation values and the subsequent occurrence of haemolytic disease of the newborn. We retrospectively tested previously frozen sera from 9 6 pregnant women found to have identifiable clinically significant red cell antibodies by our routine serological techniques. Clinical outcome of 75 of these pregnancies was obtained retrospectively. Antibodies investigated included anti-D ( 4 2 ) , anti-c (14). anti-E ( 3 ) , anti-Ce ( 3 ) , anti-e (1). anti-K ( 1 2 ) . anti-k (1). anti-Fya (1 l ) ,a n t i 8 ( 3 ) . anti-Jk" ( 2 ) . anti-Jkb (1). The occurrence and severity of haemolytic disease of the newborn was assessed and classified from questionnaires completed by referring obstetricians. Monocyte monolayer assay was found to be a poor positive predictor of haemolytic disease of the newborn as has been reported elsewhere (Garratty. 1990). In our laboratory monocyte monolayer assay proved to be 60% predictive for haemolytic disease of the newborn requiring transfusion therapy but was, however, 97%predictive for non-affected or mildly affected infants. Monocyte monolayer assay did not correlate well with IAT titres ( r , = 0 . 3 ) or with anti-D quantitation ( r , = 0 . 5 ) . However, for anti-c quantitation correlation was surprisingly good ( rp= 0.9) (Spearman Rank Correlation).
Monocyte monolayer assay in this laboratory was found to be labour intensive, subjective and costly. Hadley et a1 comment that monocyte based functional assays may best predict the severity of haemolytic disease of the newborn. This may well be true if a monocyte-based chemiluminescence test or antibody dependent cell mediated cytotoxicity assay is used. Our results would, however, confirm that a monocyte monolayer assay despite its good negative predictive value, is a poor positive predictor for haemolytic disease of the newborn. We agree with Hadley et a1 that prospective studies using more reliable functional assays to predict haemolytic disease of the newborn non-invasively are needed. Regional Transfusion Centre, West Derby Street, Liverpool L7 8TW
I. M. BROMILOW J. K. M. DUGUID
REFERENCES Garratty. G. (1990) Predicting the clinical significance of red cell antibodies with in vitro cellular assays. Transfusion Medicine Reviews, 4. 297-312. Hadley. A.G., Kumpel. B.M.. Leader. K.A.. Poole. G.D. & Fraser, I.D. ( 1 9 9 1 ) Correlation of serological, quantitative and cell mediated functional assays of maternal alloantibodies with the severity of haemolytic disease of the newborn. British journal ofHaematolog!j. 77,221-228.
NITRENDIPINE TREATMENT AND BLOOD RHEOLOGY IN PATIENTS WITH SICKLE CELL DISEASE We have previously reported that nitrendipine inhibits formation of dense sickle cells in a n in vitro model in which red blood cells are exposed to cycles of deoxygenation and reoxygenation (Nash et a!, 1989). Dense sickle cells (including irreversibly sickled cells, ISC) are thought to be important mediators of vascular obstructive pathology for two main reasons: their inherently poor deformability and their tendency to undergo haemoglobin S (HbS) polymerization more rapidly and at higher pOr compared to less dense cells. The number of ISC has also been linked with the rate of
intravascular haemolysis (Serjeant et al, 1969). We therefore carried out a small-sca!e. open trial of nitrendipine. to test whether treatment would improve blood rheology or alter haematological indices reflecting red cell destruction. Seven subjects with homozygous (HbSS) sickle cell disease were studied (four female and three male, age 22-3 5 years). They had not had a crisis within the previous 4 weeks or a blood transfusion within 3 months. Each received 5 mg nitrendipine twice daily for 1 week, then 10 mg twice daily for 5 weeks. Nitrendipine is a dihydropyridine Ca-entry
