Objectives: The aim of study was to compare salivary and serum concentrations of interleukin 1 beta (IL-1β), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α) in patients with oral leukoplakia, oral cancer and healthy controls. Study design: Eighty eight patients (28 with oral cancer, 29 leukoplakia, and 31 healthy controls) were included in this study. Cytokine concentrations were measured by commercial enzyme linked immunoassay. Results: Salivary IL-1β and IL-6 were significantly higher in oral cancer patients than in patients with leukoplakia and control group (p<0.05). No differences in concentrations of salivary TNF-α between either of the groups were observed. Serum concentrations of IL-1β were below level of detection in all but two participants. No significant differences between the groups were observed in serum concentrations of IL-6. Serum TNF-α was significantly higher in control subjects than in oral cancer patients. Conclusions: Patients with oral cancer have elevated levels of inflammatory cytokines in their saliva. Whether this elevation can be used for monitoring the malignant transformation of oral leukoplakia remains to be answered by further follow up studies. Key words: Cytokines, oral, leukoplakia, cancer.

No abstract

No abstract

No abstract

Dear Sir,The Rh blood group system is determined by the highly homologous RHD and RHCE genes located on the first chromosome, which encode for the RhD and RhCE polypeptides. D antigen is of special clinical relevance in the fields of transfusion medicine and obstetrics. Owing to its high immunogenicity, D antigen can induce the production of alloantibodies and thus cause posttransfusion haemolytic reaction and haemolytic disease of the newborn (Wagner et al., 2000).About 0·2-1% of the European population are carriers of structurally altered RHD alleles encoding for various types of weak D proteins. At the molecular level, point mutations resulting in amino acid substitutions in the intracellular or transmembranous segments of RhD protein are causing weak D phenotypes. More than 170 different RHD alleles closely related to the expression of the respective D phenotype, including more than 70 weak D types, have been discovered to date (Flegel, 2007). Some weak D types (types 1, 2 and 3) are not associated with the development of alloantibodies; however, alloimmunisation in weak D types 4·2, 11 and 15 carriers have been reported (Flegel, 2006). Owing to the extremely small phenotypic variation, particular weak D types are very difficult to differentiate by serology and can only be identified by molecular methods, thus enabling definitive decision on the mode of transfusion treatment and the need of anti-D prophylaxis in pregnant women. The individuals who are carriers of weak D types 1, 2 and 3 can receive transfusion of D+ red blood cell (RBC) units, although such pregnant women do not require anti-D prophylaxis. Thus, the unnecessary utilisation of D− RBC units and RhIg is avoided (Flegel and Wagner, 2002).Particular segments of the RHD gene sequence are multiplied by RHD genotyping using primers specific for the known mutations characterising particular weak D types by use of the polymerase chain reaction with sequence-specific priming (PCR-SSP). This procedure is employed to determine polymorphism of the weak D types.