There are numerous studies showing the role of human leukocyte antigens (HLAs) related with susceptibility or resistance to certain diseases. The aim of this study was to determine the association of HLA-B27 with ankylosing spondylitis (AS), polyarthralgia, lumboishialgia, acute anterior uveitis (AAU), psoriatic arthritis (PA), synovitis coxae and rheumatoid arthritis (RA) in patients from Vojvodina, Serbia. An HLA I class typing was performed by the serological immunomagnetic two-color fluorescence method using peripheral blood T lymphocytes in 97 patients and 224 healthy controls from the population of Vojvodina, Serbia. We calculated HLA-B27 frequencies, relative risk (RR), ethiologic fraction (EF), e.g., population attributive risk, when RR was greater than 1, while, preventive fraction (PF) was calculated when RR was lower than 1. This study revealed the strongest association of AS with HLAB27 antigen: RR = 25.0, while the EF was greater than 0.15, respectively. The χ2 test showed the significant difference (p <0.05) in HLA-B27 in patients with AS in comparison to controls (χ2 = 52.5). It was concluded that there is a positive association of HLA-B27 with AS and that HLA-B27 can serve as a marker for predisposition to diseases.
Major histocompatibility complex (MHC) genes are involved in various mechanisms of pathogenesis and immunoediting of hematological diseases. This study aimed to investigate the association between HLA -A, -B and -DRB1 alleles with hematological diseases. In this study, we performed DNA-based HLA typing by polymerase chain reaction analysis with sequence-specific primers (PCR-SSP) to distinguish HLA-A, -B, and -DRB1 alleles. Eighty-two patients with hematological diseases (29 with acute lymphoblastic leukemia (ALL), 19 with acute nonlymphoblastic leukemia (ANLL), 5 with chronic myelogenous leukemia (CML), 2 with chronic lymphocytic leukemia (CLL), 9 with myelodysplastic syndrome (MDS), 9 with lymphomas (M.Hodgkin (HL) and non-Hodgkin (NHL)), 7 with aplastic anemia (AA) and 2 with multiple myeloma (MM)), were included in the study and compared with 111 healthy blood donors, residents from Vojvodina, evaluating the strength of the observed associations by measuring the aetiologic and preventive fractions. Among the alleles significantly associated with hematological diseases, HLA-A24 showed an aetiologic fraction higher than those of HLA-A26 and A25 (RR=1.027, EF=1.233, RR=1.047, EF=1.141 and RR=1.213, EF=0.910).Negative association with significant preventive fraction was observed with HLA-B18 and HLA-DRB111 alleles, with RR=0.400, PF=0.179 and RR=0.587, PF=0.176. Our results suggest that HLA-A24, A26 and A25 as associated more frequently than other specificities with a hypothetical disease predisposing genes, may play a role in the pathogenesis of hematological diseases
Introduction. Acute pancreatitis is usually caused by biliary lithiasis and alcohol consumption. Pancreatitis in the elderly is a problem of increasing occurrence. Anatomic abnormalities may represent a less frequent, but important etiological factor. The duodenal diverticula rarely produce signs of inflammation, obstruction, hemorrhage or perforation. In some cases secondary biliary-pancreatic complications are found when a diverticulum originates from the papilla of Vater. Case Report. This case report describes a patient diagnosed with duodenal diverticulum who developed a framework of abdominal pain and laboratory findings compatible with acute pancreatitis which occurred two times in a short period of time. Conclusion. The association of duodenal diverticulum and acute pancreatitis has been reported, but it is important to point out that anatomic abnormalities may represent a less frequent but important etiological factor for acute pancreatitis.
The classical paradigm of autoimmune pathogenesis involving specific genetic makeup and exposure to environmental triggers has been challenged recently by the addition of a third element, the loss of intestinal barrier function. Regardless of HLA B27 phenotype or gastrointestinal symptoms, evidence of ileitis, ileocolitis or colitis exists in patients with spondyloarthropathy. The FUT2 secretory gene is a strong candidate for Crohn's susceptibility by shaping the functional states of mucosal microbiota and may thus have influence on the release of zonulin, the main regulator of gut permeability. Gram negative bacteria precipitate and may be involved in the pathogenesis of spondyloarthropathies. Susceptibility to many infectious agents is associated with ABO blood group or secretor state. Patients who cannot secrete ABO and Lewis blood group antigens into body fluids, an ability controlled by a single gene on chromosome 19, are known to be at increased risk of certain autoimmune diseases associated with human leukocyte antigen (HLA) markers. Lewis (Le) blood group phenotype can be used to infer secretor status. The objective of this study was to determine the distribution of secretor state and Lewis blood group phenotype in patients with seronegative spondyloarthropathies and healthy control subjects. Hundred and ten (110) patients with seronegative spondyloarthropathies (58 females and 52 males) and 103 control (74 males and 29 females) subjects participated in this study. Samples of saliva and blood were subjected to haemagglutination inhibition tests for determination of secretor status and Lewis phenotype. A total of 92(84%) patients and 92 (89%) control subjects were secretors while 18 (16%) patients and 11 (11%) control subjects were non-secretors. There was no statistically significant difference (?2 1,461 p<0,05 and degrees of freedom 1) in distribution of secretor status in comparison to seronegative spondyloarthropathies by comparing two observed populations. Seven patients had modified (reduced) expression of Lewis b antigen on their erythrocytes. Reduction of Lewis b antigen expression was not observed on erythrocytes of healthy subjects. Reduced expression of Lewis b antigen could be a consequence of the inflammatory process within the gut and it also suggests several pathogenic mechanisms which may be relevant to the synthesis of Lewis antigens inside the gut or its absorption on erythrocytes in patients with spondyloarthropathy.
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