British]ournalo/ Hatrnatologu, 1992. 81, 131-139
Correspondence PLATELET GLYCOPROTEIN Ib IN A PATIENT WITH CHRONIC RENAL FAILURE AND GLANZMANN’S THROMBASTHENIA We read with interest the recent paper by Sloand et a1 (199 1) on glycoprotein Ib (GPIb) and plasma von Willebrand factor (vWF) in uraemic patients. They found that platelets from many uraemic patients on maintenance haemodialysis showed a decreased responsiveness to ristocetin and a reduced platelet GPIb content. We recently investigated a patient with Glanzmann’s thrombasthenia (GT) who had chronic renal failure and was on haemodialysis. The GPIb content of the patient’s platelets was determined by flow cytometry and ristocetin-induced agglutination was also assessed. The patient was a 44-year-old woman who had previously been diagnosed as having type I GT (Yasunaga. 1986). Her platelet count was normal, the bleeding time was prolonged, and clot retraction was abnormal. Platelet aggregation induced by ADP, collagen, epinephrine or thrombin was absent or extremely weak. She had suffered from chronic renal failure for about 4 years and also had hypermenorrhoea. Her renal failure progressed to uraemia with a marked increase of the potassium, creatinine and blood urea nitrogen levels. Emergency haemodialysis was carried out and she subsequently continued on maintenance haemodialysis. Using the slope of the agglutination curve of formalin-fixed platelets as a n index of the response to ristocetin according to the method of Sloand et a1 (19 9 1 ), we found a significant difference between platelets from uraemic patients without GT ( 5 . 2 f 5 . 5 , n = 13) and platelets from normal controls (15.3 f 4 . 0 . n = 10). although four of the uraemic patients showed a normal platelet response. However, we did not find any significant difference in the response to ristocetin between the GT patient’s platelets either before (1 5.9 f 9.3. n = 3 ) or after dialysis (18.8 f 6.1. n = 3 ) and platelets from normal controls. Furthermore, we could not find a reduction of GPIb in the GT patient’s platelets using flow cytometry (Nomura & Kokawa. 1990). although we confirmed a reduction of platelet GPIb in all the uraemic patients without GT. Although the reason for the decrease in platelet GPIb in uraemic patients is unclear, Sloand et a1 (1991) have
suggested that the action of plasmin on this glycoprotein may be a contributing factor. On the other hand, Adelman et a1 (1 988) investigated the binding to platelets of plasminogen (the precursor of plasmin), and reported that plasminogen may bind to GPIIb/IIIa on resting or stimulated platelets and thus interact with fibrinogen. It is known that vWF (which binds to GPIb) can also bind to GPIIb/IIIa (Sakariassen et al. 1986). Thus, some factors related to GPIIb/IIIa. which is a multifunctional GP, may participate in the reduction of GPIb levels in uraemic platelets. Platelet function in haemodialysis patients with GT has rarely been reported previously and we hope to make a more detailed study of such cases. First Department 01 Internal Medicine, *Emergency Care Unit. tSecond Department of Internal Medicine, Kansai Medical University, Osaka. Japan
SHOSAKU NOMURA HIROKOKAWAMURA* AKIRASHOUZUt TERUTOSHI KOKAWA KOJIRO YASUNACA
REFERENCES Adelman. B.. Rizk. A. & Hanners, E. ( 1988)Plasminogeninteractions with platelets in plasma. Blood, 72, 1530-1 5 3 5 . Nomura. S. & Kokawa. T. ( I 990) Recent advance on analysis of antiplatelet antibody-special reference to application of flow cytometry. Automation and New Technology in the Clinical Laborutory (ed. by K. Okuda).pp. 287-294. Blackwell Scientific Publications, Oxford. Sakariassen. K.S.. Nievelstein. P.F.E.M.. Coller, B.S. & Sixrna. J.J. (1986)The role of platelet membrane glycoprotein Ib and IIb-IIIa in platelet adherence to human artery subendothelium. British Journal ojHaernatology. 63, 681-691. Sloand, E.M., Sloand, J.A.. Prodouz. K., Klein. H.G.. Yu. M.W.. Harvath. L. & Fricke. W. (1991)Reduction of platelet glycoprotein Ib in uraemia. British Journal of Huematology. 77, 375-381. Yasunaga. K. ( 1 986) Congenital platelet function disorder: survey and pathophysiology. Acta Haematologica japonicu. 49, 14991508.
AMYLASE PRODUCTION I N MONOCLONAL GAMMOPATHY OF UNDETERMINED SIGNIFICANCE bone marrow, absence of osteolytic lesions, and stability of the M-protein during 1 5 years of observation. A 58-year-old Japanese man referred to our hospital in September 1976 was diagnosed as having IgG-K-type MGUS. Laboratory investigation revealed: Hb 13.2 g/dl: WBC 2 . 3 x 10y/l.platelets 110 x 10y/l. creatinine 0.8 mg/dl: total
We present a patient with monoclonal gammopathy of undetermined significance (MGUS) with hyperamylasaemia. While the patient was suspected to be in a n early stage of multiple myeloma from pancytopenia. clinically we could not reach a diagnosis of multiple myeloma because of a serum Mprotein concentration < 3 0 g/l, < 5 % plasma cells in the
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Correspondence PLATELET GLYCOPROTEIN Ib IN A PATIENT WITH CHRONIC RENAL FAILURE AND GLANZMANN’S THROMBASTHENIA We read with interest the recent paper by Sloand et a1 (199 1) on glycoprotein Ib (GPIb) and plasma von Willebrand factor (vWF) in uraemic patients. They found that platelets from many uraemic patients on maintenance haemodialysis showed a decreased responsiveness to ristocetin and a reduced platelet GPIb content. We recently investigated a patient with Glanzmann’s thrombasthenia (GT) who had chronic renal failure and was on haemodialysis. The GPIb content of the patient’s platelets was determined by flow cytometry and ristocetin-induced agglutination was also assessed. The patient was a 44-year-old woman who had previously been diagnosed as having type I GT (Yasunaga. 1986). Her platelet count was normal, the bleeding time was prolonged, and clot retraction was abnormal. Platelet aggregation induced by ADP, collagen, epinephrine or thrombin was absent or extremely weak. She had suffered from chronic renal failure for about 4 years and also had hypermenorrhoea. Her renal failure progressed to uraemia with a marked increase of the potassium, creatinine and blood urea nitrogen levels. Emergency haemodialysis was carried out and she subsequently continued on maintenance haemodialysis. Using the slope of the agglutination curve of formalin-fixed platelets as a n index of the response to ristocetin according to the method of Sloand et a1 (19 9 1 ), we found a significant difference between platelets from uraemic patients without GT ( 5 . 2 f 5 . 5 , n = 13) and platelets from normal controls (15.3 f 4 . 0 . n = 10). although four of the uraemic patients showed a normal platelet response. However, we did not find any significant difference in the response to ristocetin between the GT patient’s platelets either before (1 5.9 f 9.3. n = 3 ) or after dialysis (18.8 f 6.1. n = 3 ) and platelets from normal controls. Furthermore, we could not find a reduction of GPIb in the GT patient’s platelets using flow cytometry (Nomura & Kokawa. 1990). although we confirmed a reduction of platelet GPIb in all the uraemic patients without GT. Although the reason for the decrease in platelet GPIb in uraemic patients is unclear, Sloand et a1 (1991) have
suggested that the action of plasmin on this glycoprotein may be a contributing factor. On the other hand, Adelman et a1 (1 988) investigated the binding to platelets of plasminogen (the precursor of plasmin), and reported that plasminogen may bind to GPIIb/IIIa on resting or stimulated platelets and thus interact with fibrinogen. It is known that vWF (which binds to GPIb) can also bind to GPIIb/IIIa (Sakariassen et al. 1986). Thus, some factors related to GPIIb/IIIa. which is a multifunctional GP, may participate in the reduction of GPIb levels in uraemic platelets. Platelet function in haemodialysis patients with GT has rarely been reported previously and we hope to make a more detailed study of such cases. First Department 01 Internal Medicine, *Emergency Care Unit. tSecond Department of Internal Medicine, Kansai Medical University, Osaka. Japan
SHOSAKU NOMURA HIROKOKAWAMURA* AKIRASHOUZUt TERUTOSHI KOKAWA KOJIRO YASUNACA
REFERENCES Adelman. B.. Rizk. A. & Hanners, E. ( 1988)Plasminogeninteractions with platelets in plasma. Blood, 72, 1530-1 5 3 5 . Nomura. S. & Kokawa. T. ( I 990) Recent advance on analysis of antiplatelet antibody-special reference to application of flow cytometry. Automation and New Technology in the Clinical Laborutory (ed. by K. Okuda).pp. 287-294. Blackwell Scientific Publications, Oxford. Sakariassen. K.S.. Nievelstein. P.F.E.M.. Coller, B.S. & Sixrna. J.J. (1986)The role of platelet membrane glycoprotein Ib and IIb-IIIa in platelet adherence to human artery subendothelium. British Journal ojHaernatology. 63, 681-691. Sloand, E.M., Sloand, J.A.. Prodouz. K., Klein. H.G.. Yu. M.W.. Harvath. L. & Fricke. W. (1991)Reduction of platelet glycoprotein Ib in uraemia. British Journal of Huematology. 77, 375-381. Yasunaga. K. ( 1 986) Congenital platelet function disorder: survey and pathophysiology. Acta Haematologica japonicu. 49, 14991508.
AMYLASE PRODUCTION I N MONOCLONAL GAMMOPATHY OF UNDETERMINED SIGNIFICANCE bone marrow, absence of osteolytic lesions, and stability of the M-protein during 1 5 years of observation. A 58-year-old Japanese man referred to our hospital in September 1976 was diagnosed as having IgG-K-type MGUS. Laboratory investigation revealed: Hb 13.2 g/dl: WBC 2 . 3 x 10y/l.platelets 110 x 10y/l. creatinine 0.8 mg/dl: total
We present a patient with monoclonal gammopathy of undetermined significance (MGUS) with hyperamylasaemia. While the patient was suspected to be in a n early stage of multiple myeloma from pancytopenia. clinically we could not reach a diagnosis of multiple myeloma because of a serum Mprotein concentration < 3 0 g/l, < 5 % plasma cells in the
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