A guide to acquired vitamin K coagulophathy diagnosis and treatment: the Russian perspective.

Physicians often come across with cases of vitamin K antagonists-dependent coagulopathy for reasons such as accidental use of the vitamin K antagonists (VKA), excessive administration of prescribed anticoagulants of indirect action or not reported administration of vitamin K antagonists due to memory impairment and/or other mental disorders, even deliberate use thereof (attempt to murder or suicide). Rodenticide-poisoning (coumarins, warfarins) via food or occupational accidents are difficult to diagnose. This article discusses different types of acquired vitamin K-dependent coagulopathy. Differential diagnosis is primarily based on patient statements before additional causes of vitamin K deficiency are explored. Even when pathological vitamin K deficiency is not determined, appropriate and urgent medical treatment is necessary: administration of fresh frozen plasma or concentrated factors of the prothrombin complex, administration of vitamin K remedies along with symptomatic therapy. With early diagnosis and prescription of appropriate therapy, prognosis is favorable. Reasons for vitamin K antagonists-dependent coagulopathy cases.

Interrelations between Immunogenetic Factors (HLA antigens) and Lymphocyte Subset Quantitative Rearrangements in Hodgkin's Disease Patients.

In this report we analyzed interrelations between cell quantity in lymphocyte subsets and lymphocyte immunogenetic (HLA) markers in 30 untreated patients with Hodgkin's disease (HD). We defined percentage and the absolute number of peripheral blood lymphocyte subsets expressing CD3, CD4, CD8, CD16, CD25 and CD72 markers for HD patients referring to their HLA phenotype (A, B, Cw loci and DRB1). HD patients had decreased absolute number of all the lymphocyte subsets. This was apparently associated with reduced number of peripheral blood lymphocytes, since their subset shares remained similar to those of healthy volunteers. HD patients had different HLA repertoire: some displayed simultaneous exertion of four antigens in A and B loci ("full house" patients) and others - reduced HLA repertoire ("non-full house" patients). Simultaneous analysis of lymphocyte subset rearrangements and HLA expression revealed that "full house" patients had no significant rearrangements in lymphocyte subsets, except reduced CD4(+) and increased CD25(+) lymphocytes. The reduction of expressed HLA alleles interrelated with reliable decrease of CD3(+), CD4(+), CD16(+) cells. Expression of such HLA alleles as A1, A2, B13, B16, B17, B21, B27, DR2 and DR4 also interrelated with significant decrease in some lymphocyte subsets, of which CD4(+) cells prevailed. The most distinct reduction of lymphocyte subsets interrelated with expression of B17 and DR2 HLA loci. Hence, in HD patients pathological rearrangements of lymphocyte subsets are strictly associated with their HLA expression.