C-Kit Immunohistochemical Expression as a Complementary Method to Assess Mast Cell Density in Helicobacter pylori-Mediated Gastritis.

INTRODUCTION: Chronic gastritis is a group of conditions commonly characterized by stomach lining inflammation. The study aimed to investigate the clinical and pathological aspects that play a role in its development. Additionally, the study examines the use of CD117 as an immunohistochemistry marker in evaluating mast cell density (MCD). METHODS: This retrospective, cross-sectional study was conducted in Iraqi Kurdistan with a sample size of 380 patients. Patient data included gastritis type, neutrophil infiltration severity, mononuclear cell infiltration within the lamina propria, intestinal metaplasia, and glandular atrophy, which were categorized and given a score. The CD117 level was identified using an anti-human rabbit polyclonal antibody. RESULTS: A statistically significant association was revealed between Helicobacter pylori-mediated gastritis and non-specific gastritis with age, activity, H. pylori and MCD, dysplasia, and malignancy. Meanwhile, no association was found with gender, inflammatory infiltrate, intestinal metaplasia, and glandular atrophy. C-Kit exhibited a marked increase in MCD in patients with H. pylori-mediated gastritis, intestinal metaplasia, atrophy, and gastric carcinoma. However, a significant decrease in MCD was observed on repeating endoscopy evaluations for patients after treatment. CONCLUSION: Regions that exhibit severe inflammation, metaplasia, atrophy, and carcinoma demonstrated an increase in MCD with H. pylori-mediated gastritis. A detailed investigation in clinical practice to screen early diagnosis and treatment needs to be performed in high H. pylori prevalence.

Expression of cytokeratin 7/20 and Ki67 in Helicobacter pylori-associated gastritis and intestinal metaplasia.

INTRODUCTION: Cytokeratins (CKs) have been associated with precancerous and cancerous gastric lesions in patients with Helicobacter pylori-associated chronic gastritis, making them useful for diagnosing epithelial tumors. METHODOLOGY: A retrospective study was conducted utilizing 200 formalin-fixed paraffin-embedded gastric biopsy samples collected from the lesser curvature of the stomach. Samples from the control group, patients with H. pylori infection, and patients with H. pylori-associated gastritis, with complete and incomplete intestinal metaplasia (IM) were immunostained. Monoclonal antibodies were utilized to determine the expression of CK7, CK20, and Ki-67. RESULTS: Patients infected with H. pylori had strong CK20 expression on the surface, and weak CK7 expression on the surface and deep glands; while non-specific chronic gastritis patients had weak focal CK7 expression and strong CK20 expression. The normal gastric mucosa of patients in the control group had relatively weak CK7 expression, restricted to a few cells in the neck and deep glands. CK20 showed diffuse strong reactivity on the surface. On the other hand, patients with complete IM showed a CK7 staining pattern that was either negative or weakly focal on the surface and crypts associated with diffuse surface CK20 and focal crypt staining corresponding to gastric type IM. The Ki67 proliferating index was low (≤ 15%) in H. pylori infected patients, high (> 30%) in patients with incomplete IM, and intermediate (16-30%) in patients with complete IM. CONCLUSIONS: These results indicate a significant link between the expressions of CK7/CK20 and Ki67 in patients afflicted with H. pylori and IM.

Correlation between the insertion-deletion variant of the angiotensin-converting enzyme gene and various classes of heart failure.

The angiotensin-converting enzyme (ACE) genetic variation for insertion/deletion (I/D) is located at the 16th intron of the ACE gene. A number of studies investigated the homozygous deletion genotype of ACE and its association with cardiovascular diseases. However, ACE's genetic variation and its association with heart failure (HF) is yet to be confirmed. We examined the possibility of the association between the ACE I/D gene variant with the severity of HF. The ACE genotypes were determined by polymerase chain reactions using samples derived from 150 patients with HF and 90 healthy subjects which were age and gender-matched. These patients included those of all four of the New York Heart Association (NYHA) classes. Echocardiography was performed on all HF patients and ejection fraction (EF), left ventricular systolic and diastolic diameters were measured. The HF patients were redistributed to systolic where EF is equal and less than 45% and non-systolic HF where EF is more than 45%. We demonstrate a statistically significant difference in DD genotype in NYHA class IV in comparison to the control group. The values of odds ratio (OR) (95%CI) of the DD genotype (DD vs ID and II) were 3.37 (1.01-11.19) (p value = 0.039) and the OR (95%CI) of the D allele (D vs I) was 2.55 (0.98-6.65) (p value = 0.049). Higher frequencies of D allele compared to I allele is linked to severity of HF. DD variant of the ACE gene is associated with NYHA class IV heart failure. This could have a profound impact on risk stratification and prognosis of HF in the management of this condition.

The impact of COVID-19 on BNP, NT-proBNP and ANP in heart failure.

Extensive research has been conducted on biomarkers associated with coronavirus disease 2019 (COVID-19) in both healthy individuals and those with various conditions, particularly heart diseases. However, there is a limited investigation into the relationship between widely used cardiac biomarkers known as natriuretic peptides, including Brain natriuretic peptide (BNP), N-Terminal Pro-B-Type Natriuretic Peptide (NT-proBNP), and Atrial natriuretic peptide (ANP), and COVID-19 infection specifically in patients with heart failure. These natriuretic peptides assess the hemodynamic stress on the heart wall and have the potential to serve as biomarkers for evaluating the severity of COVID-19 infection in heart failure patients. Therefore, this study aimed to assess the plasma concentration of BNP, NT-proBNP, and ANP in a medium-sized cross-sectional case-control study involving 360 heart failure patients, both infected and uninfected with COVID-19. The heart failure patients were categorized into subgroups based on their Ejection Fraction (EF) percentage, namely heart failure with reduced EF (HFrEF), heart failure with mid-range EF (HFmrEF), and heart failure with preserved EF (HFpEF). Our findings demonstrate a significant increase in plasma levels of BNP and NT-proBNP in all heart failure patients, as well as in each subgroup (HFrEF, HFmrEF, and HFpEF) when infected with COVID-19, compared to uninfected heart failure patients. These established cardiac biomarkers have the potential to be utilized as future indicators for assessing the severity of COVID-19 infection in heart failure patients, thereby enhancing heart failure management and reducing irreversible cardiac damage.