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      Chronic Gastritis Is Associated with a Decreased High-Density Lipid Level: Histological Features of Gastritis Based on the Updated Sydney System

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          Abstract

          Chronic gastritis could activate a systemic inflammatory response that could result in adverse lipid profiles. To determine the severity of chronic gastritis, Helicobacter pylori (HP), mononuclear cell (lymphocytes and plasma cells), and neutrophil scores were assessed on the basis of the updated Sydney system (USS), which is widely used for histological grading. The aim of this study was to assess the relationships between gastric histological features and lipid profile levels. This study included 15,322 males and 5929 females who underwent a health checkup and gastric biopsy at the Kangbuk Samsung Medical Center (KBSMC). We analyzed whether the HP, mononuclear cell, and neutrophil grades according to the USS were related to serum leukocyte count, unhealthy behaviors, and lipid profile levels. Gastritis with HP, neutrophils, or moderate to severe mononuclear cells was associated with an elevated serum leukocyte count. A high leukocyte count was related to increased low-density lipoproteins (LDL) and triglycerides/very-low-density lipoprotein (VLDL) and decreased high-density lipoproteins (HDL). In multivariate analyses, chronic gastritis with HP or moderate to severe mononuclear cells was significantly associated with decreased HDL in males, while mononuclear cells were significantly related to decreased HDL in females. Chronic gastritis was associated with an increased systemic inflammatory response, which was associated with unfavorable lipid profiles, especially low HDL levels.

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          Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994.

          The Sydney System for the classification of gastritis emphasized the importance of combining topographical, morphological, and etiological information into a schema that would help to generate reproducible and clinically useful diagnoses. To reappraise the Sydney System 4 years after its introduction, a group of gastrointestinal pathologists from various parts of the world met in Houston, Texas, in September 1994. The aims of the workshop were (a) to establish an agreed terminology of gastritis; (b) to identify, define, and attempt to resolve some of the problems associated with the Sydney System. This article introduces the Sydney System as it was revised at the Houston Gastritis Workshop and represents the consensus of the participants. Overall, the principles and grading of the Sydney System were only slightly modified, the grading being aided by the provision of a visual analogue scale. The terminology of the final classification has been improved to emphasize the distinction between the atrophic and nonatrophic stomach; the names used for each entity were selected because they are generally acceptable to both pathologists and gastroenterologists. In addition to the main categories and atrophic and nonatrophic gastritis, the special or distinctive forms are described and their respective diagnostic criteria are provided. The article includes practical guidelines for optimal biopsy sampling of the stomach, for the use of the visual analogue scales for grading the histopathologic features, and for the formulation of a comprehensive standardized diagnosis. A glossary of gastritis-related terms as used in this article is provided.
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            Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary heart disease: meta-analyses of prospective studies.

            A large number of epidemiologic studies have reported on associations between various "inflammatory" factors and coronary heart disease (CHD). To assess the associations of blood levels of fibrinogen, C-reactive protein (CRP), and albumin and leukocyte count with the subsequent risk of CHD. Meta-analyses of any long-term prospective studies of CHD published before 1998 on any of these 4 factors. Studies were identified by MEDLINE searches, scanning of relevant reference lists, hand searching of cardiology, epidemiology, and other relevant journals, and discussions with authors of relevant reports. All relevant studies identified were included. The following information was abstracted from published reports (supplemented, in several cases, by the authors): size and type of cohort, mean age, mean duration of follow-up, assay methods, degree of adjustment for confounders, and relationship of CHD risk to the baseline assay results. For fibrinogen, with 4018 CHD cases in 18 studies, comparison of individuals in the top third with those in the bottom third of the baseline measurements yielded a combined risk ratio of 1.8 (95% confidence interval [CI], 1.6-2.0) associated with a difference in long-term usual mean fibrinogen levels of 2.9 pmol/L (0.1 g/dL) between the top and bottom thirds (10.3 vs 7.4 pmol/L [0.35 vs 0.25 g/dL]). For CRP, with 1053 CHD cases in 7 studies, the combined risk ratio of 1.7 (95% CI, 1.4-2.1) was associated with a difference of 1.4 mg/L (2.4 vs 1.0 mg/L). For albumin, with 3770 CHD cases in 8 studies, the combined risk ratio of 1.5 (95% CI, 1.3-1.7) was associated with a difference of 4 g/L (38 vs 42 g/L, ie, an inverse association). For leukocyte count, with 5337 CHD cases in the 7 largest studies, the combined risk ratio of 1.4 (95% CI, 1.3-1.5) was associated with a difference of 2.8 x 10(9)/L (8.4 vs 5.6 x 10(9)/L). Each of these overall results was highly significant (P<.0001). The published results from these prospective studies are remarkably consistent for each factor, indicating moderate but highly statistically significant associations with CHD. Hence, even though mechanisms that might account for these associations are not clear, further study of the relevance of these factors to the causation of CHD is warranted.
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              Atherogenesis in perspective: hypercholesterolemia and inflammation as partners in crime.

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                Author and article information

                Journal
                J Clin Med
                J Clin Med
                jcm
                Journal of Clinical Medicine
                MDPI
                2077-0383
                14 June 2020
                June 2020
                : 9
                : 6
                : 1856
                Affiliations
                [1 ]Departments of Pathology, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul 03181, Korea; idavid.kim@ 123456samsung.com
                [2 ]Department of Internal Medicine, Eulji Hospital, Eulji University School of Medicine, Seoul 01830, Korea; sbk1026@ 123456eulji.ac.kr
                [3 ]Department of Pathology, Hanyang University Guri Hospital, Hanyang University College of Medicine, Guri-si, Gyeonggi-do 11923, Korea; yhoh@ 123456hanyang.ac.kr (Y.H.O.); pathjwy@ 123456gmail.com (W.Y.J.)
                [4 ]Departments of Emergency Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul 03181, Korea; jiung.na@ 123456samsung.com (J.U.N.); pcmd.choi@ 123456samsung.com (P.C.C.)
                [5 ]Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul National University Boramae Medical Center, Seoul 07061, Korea; khl2876@ 123456gmail.com
                [6 ]Department of Pathology, Hallym University Sacred Heart Hospital, Hallym University College of Medicine, Anyang-si, Gyeonggi-do 14068, Korea; mulank@ 123456hanmail.net
                [7 ]Department of Internal Medicine, Hanyang University Guri Hospital, Hanyang University College of Medicine, Guri-si, Gyeonggi-do 11923, Korea; moonji@ 123456hanyang.ac.kr
                [8 ]Division of Endocrinology, Department of Internal Medicine, Hanyang University Guri Hospital, Hanyang University College of Medicine, Guri-si, Gyeonggi-do 11923, Korea; lanugo@ 123456hanyang.ac.kr
                [9 ]Department of Neurology, Hanyang University College of Medicine, Seoul 04763, Korea; kiwook-oh@ 123456hanyang.ac.kr (K.-W.O.); aescula@ 123456hanmail.net (Y.S.K.)
                Author notes
                [* ]Correspondence: kyueng@ 123456gmail.com (K.-W.M.); emking@ 123456hanmail.net (S.K.H.); Tel.: +82-31-560-2496 (K.-W.M); +82-02-2001-2591 (S.K.H.); Fax: +82-31-560-2339 (K.-W.M.); +82-02-2220-2891 (S.K.H.)
                Author information
                https://orcid.org/0000-0002-9299-5476
                https://orcid.org/0000-0002-4757-9211
                https://orcid.org/0000-0003-0983-707X
                https://orcid.org/0000-0003-4786-2823
                https://orcid.org/0000-0002-8535-0565
                https://orcid.org/0000-0001-6011-629X
                Article
                jcm-09-01856
                10.3390/jcm9061856
                7355915
                32545889
                cf1cbec0-7b71-433b-8504-86fb065ab35c
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 10 April 2020
                : 07 June 2020
                Categories
                Article

                helicobacter,cholesterol,gastritis,cardiovascular diseases

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