HLA typing in Vogt-Koyanagi-Harada syndrome in North Indian patients.

PURPOSE: To report the HLA profile of VKH patients from India. METHOD: Forty-one patients and 50 controls were studied. Phenotyping using a lymphocytotoxicity assay was done for HLA-A and -B. DNA-based sequence-specific low resolution typing was done for HLA-DR and -DQ loci. RESULTS: HLA-A9 was over-represented in the patient population (p = 0.01), whereas HLA-A11 (p = 0.03) and HLA-DRB1*13 (p = 0.007) were found to be underrepresented. The frequency of HLA-DRB1*04 was 14.6% and 10% in the patient population and controls, respectively. The HLA-DQ frequencies did not differ significantly between patients and controls. CONCLUSION: Unlike that reported in most populations, we did not find a significant association between HLA-DRB1*04 and our patient population.

Platelet alloimmunization in multitransfused patients with haemato-oncological disorders.

BACKGROUND: We studied the incidence of platelet alloimmunization in multitransfused patients with haemato-oncological disorders and determined the factors influencing alloimmunization. We also assessed the effect of alloimmunization on response to platelet transfusion. METHODS: Fifty patients with haemato-oncological disorders who received multiple transfusions were included. The patients were tested for antibodies before they received any transfusion and then after 3-4 weeks of transfusion. Lymphocytotoxicity and platelet immunofluorescence suspension tests were used to detect antiplatelet antibodies. Symptomatic improvement was used to assess the response to platelet transfusions. RESULTS: Thirty patients were positive by the lymphocytotoxicity test, giving an incidence of 60% for anti-HLA antibodies. The panel reactivity of the antibodies ranged from 3% to 100%. Nineteen patients were positive by the platelet immunofluorescence suspension test, 16 of whom were also positive by the lymphocytotoxicity test. The overall incidence of antiplatelet antibodies was 66%. The number of transfusions received and the underlying haemato-oncological disorder were not risk factors for the development of antibodies. Patients with a past history of transfusions and those with a positive obstetric history had a significantly higher incidence of antibodies. The response to transfusion therapy was poor in patients with antibodies, as 71.4% of patients with antibodies were nonresponsive compared to only 26.6% of antibody-negative patients. CONCLUSION: A high percentage of multitransfused patients developed antiplatelet antibodies. Previous sensitization was an important risk factor for the development of antibodies. Patients with high panel reactivity (HLA) showed non-responsiveness to platelet transfusions. Testing for the presence of antiplatelet antibodies and provision of compatible platelets should be important components in the management of patients with platelet transfusion refractoriness.

Evaluation of the Pyruvate Kinase isoenzyme tumor (Tu M2-PK) as a tumor marker for cervical carcinoma.

Various isoforms of the glycolytic enzyme pyruvate kinase are expressed in different cell types. One of these isoforms, Tu M2-PK, is over-expressed in tumor cells and released into body fluids. Plasma determination of Tu M2-PK has been shown to discriminate between benign and malignant lesions. Tu M2-PK was quantitated in the plasma of 50 patients with cervical carcinoma, 10 patients with chronic cervicitis and 10 healthy controls. The concentration of Tu M2-PK was determined by commercial kits using a sandwich enzyme linked immunosorbent assay based on two monoclonal antibodies (clone I and II) specific for Tu M2-PK. The sensitivity of the test for discrimination of malignant from non-malignant condition was 82% with a specificity of 60%. Highly significant statistical difference was found in the means of three groups (P = 0.0002). The present results indicate that Tu M2-PK can be used as a tumor marker in follow-up of patients with cervical carcinoma.