Up-To-Date View on the Clinical Manifestations and Complications of Chronic Pancreatitis
Chronic pancreatitis is an inflammatory disease that causes irreversible anatomical changes including infiltration of inflammatory cells, fibrosis and pancreatic calcification with destruction of the structure of the gland, leading to abdominal pain, endocrine and exocrine dysfunction. Pancreatic exocrine insufficiency (PEI) prevalence in chronic pancreatitis varies between 40 and 94%. PEI is diagnosed by direct and indirect tests. Nutritional status is assessed by anthropometric indicators; laboratory tests—hemoglobin, plasma proteins (albumin, prealbumin, retinol-binding protein, transferrin), fat-soluble vitamins A, D, E, K; micronutrients. Pancreatic enzyme replacement therapy (PERT) is a fundamental part of PEI treatment. An optimal PERT could prevent serious PEI complications such as metabolic bone disease, adverse cardiovascular events, cachexia, poor quality of life and mortality. A periodic screening for PEI complications with a respect to their primary and secondary prophylaxis is mandatory. Diabetes mellitus secondary to pancreatic disease is defined as pancreatogenic diabetes or type 3c diabetes mellitus. Patients with chronic pancreatitis are at increased risk for pancreatic cancer influenced by smoking, alcohol abuse, chronic inflammation and pancreatic stellate cells over-proliferation. However, chronic pancreatitis could be further complicated with splenic vein thrombosis, pseudocysts, duodenal or biliary obstruction, pseudoaneurysm and pancreatic duct stones which might require endoscopic or surgical treatment.
Part of the book: Pancreatitis
Gastric Microbiota: Between Health and Disease
The etiologic link between H. pylori infection and gastric chronic inflammation and related complications has been well established, but pathogenic pathways are still widely discussed and not sufficiently clear. The introduction of culture-independent molecular techniques has allowed better understanding of the gastric microbiota and has revealed that, when present, H. pylori represents the main colonizer but is part of a far more complex and dynamic microbiota than previously thought. This conceptual shift has made way for new pathogenic theories, focused on the interrelations between H. pylori and other gastric microbiota. Main factors that affect the gastric microbiota are gastric acidity, inflammation, and environmental factors, such as diet and drugs. Previous studies have made progress in explaining the complex interactions between gastric microorganisms in healthy individuals and their role in the development of related gastroduodenal (peptic ulcers and gastric cancer (GC)) and extraintestinal diseases, but more scientific proof is needed. This review presents current knowledge on gastric microbiota and its role in health and in the development of gastroduodenal diseases.
Part of the book: Gastrointestinal Stomas
Current View on Autoimmune Gastritis
Autoimmune gastritis (AIG) is a chronic inflammatory disease of the gastric corpus and fundus. Although still unclear, genetic and environmental factors, antigenic mimicry or cross-reactivity are proposed pathogenic mechanisms. Parietal cells destruction results in loss of intrinsic factor and increased gastric pH due to hypochlorhydria and G-cell proliferation. Furthermore, atrophy, intestinal, pancreatic and spasmolytic polypeptide-expressing metaplasia are observed. AIG is underdiagnosed, however, proper diagnostic approach, including endoscopic, serological and histopathological assessment, is required. Gastroscopy with corpus and fundus biopsies is a gold standard. A serological combination of anti-parietal cell antibodies, intrinsic factor antibody, anti-Helicobacter pylori IgG, gastrin, pepsinogen I and pepsinogen I/II ratio improves the diagnostic sensitivity and specificity and allows atrophy level prediction. AIG might manifest with multifactorial iron deficiency anemia, vitamin B12 deficiency (pernicious anemia), neurological and neuropsychiatric conditions, small intestinal bacterial overgrowth and gastrointestinal infections. AIG association with other autoimmune diseases is well-established. Gastric cancer and gastric carcinoid are neoplastic transformations of a continuous chronic inflammation. Patients with AIG should be carefully monitored as no specific AIG therapy is available and disease complication could be fatal.
Part of the book: Gastritis
Helicobacter pylori Infection
Helicobacter pylori (H. pylori) is a Gram-negative spiral bacterium commonly found in the stomach. Major part of the world’s population is infected with H. pylori and is at increased risk of severe gastritis, peptic ulcer disease, and gastric cancer. Most studied virulence factors of the bacterium are the cytotoxin-associated gene (CagA) and the vacuolating cytotoxin A (VacA). The H. pylori infection is diagnosed by invasive (histological examination, culture, and rapid urease test, which require endoscopy and biopsy) and noninvasive methods (serology, urea breath test, and stool antigen test). H. pylori eradication is preferred for a long-term prevention of complications. Current treatments consist of antibiotics and adequate PPI dose and can be divided into two strands—with or without bismuth. Achieving an eradication rate of >90% is an indicator for effective treatment. Due to the increasing levels of antibiotic resistance, the standard triple therapy is largely replaced with a quadruple therapy, especially in countries with high resistance rates. Antimicrobial susceptibility testing should be performed after the second-line treatment failure, leading to an individualized patient treatment. Clear explanations and patients’ compliance are of great importance for a better outcome.
Part of the book: Gastritis