[HLA haplotypes in Itsenko-Cushing disease].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R P Manishkina.
Explore the source record for details and available documents.
Ninety-seven patients suffering from Itsenko [correction of Icenko]-Cushing disease were examined. Analysis was made first of all of the clinical and laboratory signs pointing to the presence of other endocrine diseases to distinguish two groups of patients. The first group included subjects who did not manifest any concomitant diseases. The number of men and women was the same. The second group was made up of patients with associated Itsenko [correction of Icenko]-Cushing disease and other endocrine diseases. In this particular group, women were predominant. The first group patients demonstrated the predominance of the DR7 incidence, the second group that of the DR5. The method of estimating HLA associations identified is proposed. It allows distinguishing specific and nonspecific associations. In Itsenko [correction of Icenko]-Cushing disease, DR7 association is specific, whereas B8 and DR5 associations are unspecific. A specific polyendocrine autoimmune syndrome associated with Itsenko [correction of Icenko]-Cushing disease was revealed. A concept of the pathogenesis of Itsenko [correction of Icenko]-Cushing disease is advanced.
The data of HLA-haplotyping were used as an allele marker controlling hereditary hemochromatosis in 23 patients with beta-thalassemia. The results obtained have permitted a conclusion that hemosiderosis in patients with beta-thalassemia may be caused by association of beta-thalassemia gene with hereditary hemochromatosis. Early diagnosis of hyperferremia is of great prognostic importance as the adequate treatment timely conducted can prevent the development of irreversible changes in the patients.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The determination of HLA antigens in 54 patients with Icenko-Cushing's disease demonstrated the high rate of AIO antigens (50.7%), B8 (27.3%) and B27 (26.2%) antigens. In the control group, the rate of the same antigens amounted to 17.8, 16.3 and 7.4%, respectively. Specific features were also revealed in the rate of individual HLA haplotypes. The rate of A X IO, B8; A X IO, B27 haplotypes occurring relatively rarely in normal subjects was high in patients with Icenko-Cushing's disease. The high rate of AIO, B8 and B27 antigens may attest to the high risk of the development of Icenko-Cushing's disease in subjects carrying these antigens.
Natural cold isolymphocytotoxins (NCILCT) were studied in sera of patients with chronic renal insufficiency who had undergone 3-200 hemodialyses, in sera of healthy subjects before and after intramuscular injections of 5-9 ml of whole autologous blood, and in sera of hemophilia patients before and after a transfusion of 130-250 ml of freshly drawn donor plasma concentrate. It was noted NCILCT activity rose from 20-50% to 50-100% dead cells after injections of autologous blood and plasma transfusions in the majority of cases. In subjects who had undergone hemodialysis from 50 to 200 time NCILCT activity was considerably higher (50-80% dead cells) compared to patients with 3-10 hemodialyses (20-30% dead cells). It was suggested that the graft protection effect of blood transfusions and hemodialysis on kidney graft may be associated with an increase in NCILCT activity.
Explore the source record for details and available documents.
Activity of natural cold isolymphocytotoxins (NCILCT) was studied in the serum of 16 volunteers who received whole auto blood injections. Autohemostimulation was shown to result in the increased activity of NCILCT. The evidence obtained allowed the conclusion that autohemostimulation can be used for preparation of active NCILCT test sera.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.