- Email: [email protected]
Antibodies to nuclear antigens in patients undergoing long-term hemodialysis
factor Leukocyte
Endotoxin chemotaxis
DNA antibodies
Colt dialyzers
undergoing long-term hemodialysis. Am J Med 60: 673-676,
1976.
Free nuclei of damaged leukocytes adhere to hemodialysis membranes. To see if the incidence of antibodies to nuclear antigens is increased in patients receiving hemodialysis. serums from 77 patients undergoing long-term dialysis for one to 66 months were assayed for antibodies to extractable nuclear antigen and native deoxyribonucleic acid (DNA) by hemagglutination technics. Serums from 300 other hospital patients (who did not have diseases known to be associated with antibodies to nuclear antigens) were assayed concurrently. Of the 77 dialysis patients, serums from 19 (25 per cent) were positive for one or both antibodies. Serums from only three (1 per cent) of the 300 other patients had detectable antibodies. The incidence was significantly higher (p < 0.001) in dialysis patients suggesting the possibility of sensitization to nuclear antigens during hemodialysis.
tientS
Mph KD, l-lustedFC, Sharp GC, Siemsen AW: Antibodies to nuclear anttgens in pa-
Nuclear antigens
Two siblings with hereditary Fletcher factor (prekallikrein) deficiency were studied for alterations of fibrinolysis, platelet function, skin inflammatory responses, permeability factor (PF/dil) formation and leukocyte chemotaxis. PFldil caused increased vessel permeability in human skin; in vitro generation of PFldil required both the Hageman factor and prekallikrein. The Fletcher factor-deficient subjects responded in a normal manner to PF/diI. Etased on the Fletcher factor-coagulation assay, the biologic halfdisappearance tlme of prekallikretn (after the transfusion of normal plasma in one of the subjects) was estimated at 35 hours. Therefore, these studies suggest that severe prekallikrein (Fletcher factor) deficiency in man is not associated with any clinically significant impairment in hemostasis, fibrinolysis, inflammatory responses or leukocyte function.
Hathaway WE, Wuspper KD, Weston WL, Humbert JR, Rivers RPA. Genton E, August CS, Montgomery RR, Mass MF: Clinical and physiologic studies of two siblings with prekallikrein (Fletcher factor) deficiency. Am J Med 60: 654-664, 1976.
Permeability Prekallikrein
Fletcher factor deficiency
Flbrinolytic actlvlty
Hereditary
nephritis Renal involvement
Deafness Megakaryocytes
effusion
Mitral Insufficiency
Cardiomyopathy
Echocardiography is an extremely useful noninvasive technic in the differential diagnosis of a large heart. It may show whether a large heart is due to left ventricular hypet-trophy or dllatation, or if it is due to a pericardial effusion. The hypertrophied heart may be further characterized by determining whether it is symmetrical, as caused by aortic stenosls or hypertension, or whether it is asymmetrical, which is characteristic of hypertrophic cardiomyopathy. These and other conditions can be distinguished by echocardiography. Finally, mediastinal tumors may simulate a large heart, and demonstration Of normal cardiac dimensions and wall motion can exclude a cardiac etiology for the “large heart.”
in the differential diagnosis of the large heart. Am J
heart
tumors Hypertrophlc
Medlastlnal
Abbasl AS: Echocardiography Med 60: 677-666.1976.
Perlcardlal
Echocardiography
A fourth kindred displaying the triad of hereditary nephritis, deafness and-thrombocytopenia with giant platelets is described. Renal involvement, a common cause of death amongst afflitted subjects, appears to have a better prognosis in the affected members of this family. Although the electron microscopic appearance of the megakaryocytes in the present case appears similar to that in previously reported cases, we suggest that the “giant” platelets may result from a degenerative process of megakaryocytes leading to nuclear regression and cytoplasmic fragmentation, rather than the usual blebbing process.
Parsa KP. Lee DEN, Zamboni L, Glasaock RJ: Hereditary nephritis, deafness and abnormal thrombopoiesis. Study of a new kindred. Am J Mecl60: 665-672, 1976.
Abnormal thrombopolesis
Endotoxin chemotaxis
DNA antibodies
Colt dialyzers
undergoing long-term hemodialysis. Am J Med 60: 673-676,
1976.
Free nuclei of damaged leukocytes adhere to hemodialysis membranes. To see if the incidence of antibodies to nuclear antigens is increased in patients receiving hemodialysis. serums from 77 patients undergoing long-term dialysis for one to 66 months were assayed for antibodies to extractable nuclear antigen and native deoxyribonucleic acid (DNA) by hemagglutination technics. Serums from 300 other hospital patients (who did not have diseases known to be associated with antibodies to nuclear antigens) were assayed concurrently. Of the 77 dialysis patients, serums from 19 (25 per cent) were positive for one or both antibodies. Serums from only three (1 per cent) of the 300 other patients had detectable antibodies. The incidence was significantly higher (p < 0.001) in dialysis patients suggesting the possibility of sensitization to nuclear antigens during hemodialysis.
tientS
Mph KD, l-lustedFC, Sharp GC, Siemsen AW: Antibodies to nuclear anttgens in pa-
Nuclear antigens
Two siblings with hereditary Fletcher factor (prekallikrein) deficiency were studied for alterations of fibrinolysis, platelet function, skin inflammatory responses, permeability factor (PF/dil) formation and leukocyte chemotaxis. PFldil caused increased vessel permeability in human skin; in vitro generation of PFldil required both the Hageman factor and prekallikrein. The Fletcher factor-deficient subjects responded in a normal manner to PF/diI. Etased on the Fletcher factor-coagulation assay, the biologic halfdisappearance tlme of prekallikretn (after the transfusion of normal plasma in one of the subjects) was estimated at 35 hours. Therefore, these studies suggest that severe prekallikrein (Fletcher factor) deficiency in man is not associated with any clinically significant impairment in hemostasis, fibrinolysis, inflammatory responses or leukocyte function.
Hathaway WE, Wuspper KD, Weston WL, Humbert JR, Rivers RPA. Genton E, August CS, Montgomery RR, Mass MF: Clinical and physiologic studies of two siblings with prekallikrein (Fletcher factor) deficiency. Am J Med 60: 654-664, 1976.
Permeability Prekallikrein
Fletcher factor deficiency
Flbrinolytic actlvlty
Hereditary
nephritis Renal involvement
Deafness Megakaryocytes
effusion
Mitral Insufficiency
Cardiomyopathy
Echocardiography is an extremely useful noninvasive technic in the differential diagnosis of a large heart. It may show whether a large heart is due to left ventricular hypet-trophy or dllatation, or if it is due to a pericardial effusion. The hypertrophied heart may be further characterized by determining whether it is symmetrical, as caused by aortic stenosls or hypertension, or whether it is asymmetrical, which is characteristic of hypertrophic cardiomyopathy. These and other conditions can be distinguished by echocardiography. Finally, mediastinal tumors may simulate a large heart, and demonstration Of normal cardiac dimensions and wall motion can exclude a cardiac etiology for the “large heart.”
in the differential diagnosis of the large heart. Am J
heart
tumors Hypertrophlc
Medlastlnal
Abbasl AS: Echocardiography Med 60: 677-666.1976.
Perlcardlal
Echocardiography
A fourth kindred displaying the triad of hereditary nephritis, deafness and-thrombocytopenia with giant platelets is described. Renal involvement, a common cause of death amongst afflitted subjects, appears to have a better prognosis in the affected members of this family. Although the electron microscopic appearance of the megakaryocytes in the present case appears similar to that in previously reported cases, we suggest that the “giant” platelets may result from a degenerative process of megakaryocytes leading to nuclear regression and cytoplasmic fragmentation, rather than the usual blebbing process.
Parsa KP. Lee DEN, Zamboni L, Glasaock RJ: Hereditary nephritis, deafness and abnormal thrombopoiesis. Study of a new kindred. Am J Mecl60: 665-672, 1976.
Abnormal thrombopolesis