Background: Studies with latest technologies such as endoscopy with magnification and chromoendoscopy showed that various endoscopic aspects are clearly related to infection by Helicobacter pylori (HP). The description of different patterns of erythema in gastric body under magnification of images revived interest in identifying these patterns by standard endoscopy. Aim:To validate the morphologic features of gastric mucosa related to H. pylori infection gastritis allowing predictability of their diagnosis as well as proper targeting biopsies. Methods: Prospective study of 339 consecutive patients with the standard videoendoscope image analysis were obtained, recorded and stored in a program database. These images were studied with respect to the presence or absence of H. pylori, diagnosed by rapid urease test and/or by histological analysis. Were studied: a) normal mucosa appearance; b) mucosal nodularity; c) diffuse nonspecific erythema or redness (with or without edema of folds and exudate) of antrum and body; d) mosaic pattern with focal area of hyperemia; e) erythema in streaks or bands (red streak); f) elevated (raised) erosion; g) flat erosions; h) fundic gland polyps. The main exclusion criteria were the use of drugs, HP pre-treatment and other entities that could affect results. Results: Applying the exclusion criteria, were included 170 of the 339 patients, of which 52 (30.58%) were positive for HP and 118 negative. On the positive findings, the most associated with infection were: nodularity in the antrum (26.92%); presence of raised erosion (15.38%) and mosaic mucosa in the body (21.15%). On the negative group the normal appearance of the mucosa was 66.94%; erythema in streaks or bands in 9.32%; flat erosions 11.86%; and fundic gland polyps 11.86%. Conclusion: Endoscopic findings are useful in the predictability of the result and in directing biopsies. The most representative form of HP related gastritis was the nodularity of the antral mucosa. The raised erosion and mucosa in mosaic in the body are suggestive but not specific to the infection. The other forms were not conclusive of the presence of HP.

Mannose binding lectin is a lectin instrumental in the innate immunity. It recognizes carbohydrate patterns found on the surface of a large number of pathogenic micro-organisms, activating the complement system. However, this protein seems to increase the tissue damage after ischemia. In this paper is reviewed some aspects of harmful role of the mannose binding lectin in ischemia/reperfusion injury.

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BackgroundMannose binding lectin (MBL) appears to be involved in susceptibility to rheumatoid arthritis (RA), in the inflammatory process and in the genesis of atherosclerotic disease.ObjectiveTo study the association of MBL serum levels and its genotypic variation with carotid arteries intimal thickness (IMT) in RA patients from Southern Brazil.MethodsMBL serum levels, MBL2 genotyping and IMT were investigated in 90 RA patients along with their demographic, clinical and laboratory profile. MBL levels and MBL2 genotyping were evaluated in 90 healthy controls.ResultsA significant lower MBL serum concentration was observed in patients with RA in relation to controls (528 ng/mL vs 937.5 ng/mL, p = 0.05, respectively). The median IMT in RA patients was 0.59 mm (0.51 to 0.85 mm). There was no correlation between levels of MBL with disease activity, erythrocyte sedimentation rate, autoantibodies presence or IMT (p = NS). A weak and negative correlation was found between MBL and CRP levels (Rho = −0.24; p = 0.02;). The MBL2 variant at codon 54 (variant B) and HYPA haplotype were the most frequently observed in the RA sample (67.5% and 31.7%). MBL2 wild type (A/A) were associated with lower IMT when compared with heterozygotes (A/O; p = 0.04) and low producers (O/O; p = 0.05). In addition, high producers genotypes had lower levels of CRP when compared with medium (p = 0.04) or with low producers (p = 0.05).ConclusionRA patients had lower MBL levels than controls. MBL were negatively associated with CRP serum levels; low MBL genotypes producers increased thickness of the IMT than high producers.

BackgroundThe binding lectin mannose (MBL) is a serum protein of collectin family that appears to be involved in the inflammatory process and in the genesis of atherosclerotic disease.ObjectivesTo study the association of serum levels of MBL and its genotypic variation with carotid arteries intimal thickness (IMT) in rheumatoid arthritis (RA) patients from Southern Brazil.MethodsSerum level, MBL genotyping and IMT were studied in 90 RA patients along with their demographic, clinical and laboratory profile. MBL levels were measured in 90 healthy controls.ResultsThere was significant difference between mean serum levels of MBL in patients with RA and controls (528 ng/mL vs 937.5 ng/mL, p=0.05, respectively). The median IMT in RA patients was 0.59 mm (0.51 to 0.85 mm). There was no correlation between levels of MBL with disease activity measured by DAS-28 (disease activity score-28), erythrocyte sedimentation rate (ESR), autoantibodies presence or IMT (p=NS). A negative correlation was found between MBL levels with CRP levels (p=0.02). The mutation vat codon 54 (variant B) and HYPA haplotype were the most frequent (67.5% and 31.7%, respectively) in the RA sample. Dominant genotypes (A/A) are associated with lower IMT when compared with heterozygotes (A/O; p=0.04) and homozygous recessive (O/O; p=0.05). Also dominant genotypes had lower CRP when compared with heterozygous (p=0.04) or with recessive genotypes (p=0.05).ConclusionsRA patients had lower MBL levels than controls. MBL serum levels are negatively associated with CRP; low producers of MBL had increased thickness of the IMT than high producers.References Scarno A, Perrotta FM, Cardini F, Carboni A, Annibali G, Lubrano E, et al. Beyond the joint: Subclinical atherosclerosis in rheumatoid arthritis. World J Orthop [Internet]. 2014;5(3):328–35. Available from: Ip WK, Lau YL, Chan SY, Mok CC, Chan D, Tong KK, et al. Mannose-binding lectin and rheumatoid arthritis in southern Chinese. Arthritis Rheum. 2000;43(8):1679–87.J Maury CP, Aittoniemi J, Tiitinen S, Laiho K, Kaarela K, Hurme M, et al. Variant mannose-binding lectin 2 genotype is a risk factor for reactive systemic amyloidosis in rheumatoid arthritis. Jounal Intern Med. 2007;262:466–9.Graudal NA, Homann C, Madsen HO, Svejgaard A, Jurik AG, Graudal HK, et al. Mannan Binding Lectin in Rheumatoid Arthritis. A Longitudinal Study. J Rheumatol. 1998;25(4):629–35.Carvalho EG, Utiyama SRR, Kotze LMS, Reason ITM. Lectina ligante de manose (MBL): características biolόgicas e associação com doenças. Res bras alerg imunopatol. 2007;30(5):187–93. Disclosure of InterestNone declared