Duodenal Ulcer: Causes

Pathogenesis (development of disease)

In duodenal ulcer, damage to the mucosa of the duodenum occurs, usually due to infection with the bacterium Helicobacter pylori (>90% of cases). Duodenal ulcers (duodenal ulcers) are located in the anterior wall of the bulbus duodeni (first, ampullary part of the duodenum) in 90 % of cases. The majority of ulcers are localized in the anterior wall. In 10-20% of cases, two opposite ulcers are detected (kissing ulcers). Secretion of gastric acid is usually increased but may be normal.

Etiology (causes)

Biographic causes

  • Genetic burden from parents, grandparents
    • Genetic diseases
      • Alpha-1-antitrypsin deficiency (AATD; α1-antitrypsin deficiency; synonyms: Laurell-Eriksson syndrome, protease inhibitor deficiency, AAT deficiency) – relatively common genetic disorder with autosomal recessive inheritance in which too little alpha-1-antitrypsin is produced because of a polymorphism (occurrence of multiple gene variants). A deficiency of protease inhibitors is manifested by a lack of inhibition of elastase, which causes the elastin of the pulmonary alveoli to degrade. As a result, chronic obstructive bronchitis with emphysema (COPD, progressive airway obstruction that is not fully reversible) occurs. In the liver, the lack of protease inhibitors leads to chronic hepatitis (liver inflammation) with transition to liver cirrhosis (non-reversible damage to the liver with pronounced remodeling of the liver tissue). The prevalence (disease frequency) of homozygous alpha-1 antitrypsin deficiency is estimated at 0.01-0.02 percent in the European population.
  • Blood group – blood group 0 (↑)
  • Factor HLA-B5 (↑)

Behavioral causes

  • Nutrition
    • High consumption of mono- and disaccharides such as white flour products and confectionery products
    • Rare intake of omega-3 and -6 fatty acids.
    • Excessive intake of table salt
    • Micronutrient deficiency (vital substances) – see Prevention with micronutrients.
  • Consumption of stimulants
    • Coffee (high consumption)
    • Alcohol
    • Tobacco (smoking)
  • Drug use
    • Cocaine
  • Psycho-social situation
    • Psychological stress – increase in the incidence (frequency of new cases) of peptic ulcers (presence of acid as a prerequisite for the development of the ulcer).

Causes related to disease

  • Alpha-1-antitrypsin deficiency – common, genetic disorder. Diagnosis is to be made by determination of alpha-1-antitrypsin serum level. The disease can manifest in the lungs in the form of chronic obstructive bronchitis with emphysema (COPD) and in the liver in the form of chronic hepatitis with transition to cirrhosis.
  • Chronic lung disease – such as chronic obstructive pulmonary disease (COPD).
  • Chronic renal insufficiency
  • Chronic pancreatitis (inflammation of the pancreas) – relationship not yet clearly established.
  • Duodenal stenosis – narrowing of the duodenum.
  • Hyperparathyroidism (parathyroid hyperfunction) – connection not clearly established.
  • Infection with other pathogens such as cytomegalovirus (CMV) or herpes simplex virus (HSV).
  • Infection with Helicobacter pylori – in > 90% of cases.
  • Coronary artery disease (coronary artery disease) – connection not clearly established.
  • Liver cirrhosis (liver shrinkage) – connective tissue remodeling of the liver associated with functional impairment.
  • Mastocytosis – two main forms: cutaneous mastocytosis (skin mastocytosis) and systemic mastocytosis (whole body mastocytosis); clinical picture of cutaneous mastocytosis: Yellowish-brown spots of varying size (urticaria pigmentosa); in systemic mastocytosis, there are also episodic gastrointestinal complaints (gastrointestinal complaints), (nausea (nausea), burning abdominal pain and diarrhea (diarrhea)), ulcer disease, and gastrointestinal bleeding (gastrointestinal bleeding) and malabsorption (disorder of food absorption); In systemic mastocytosis, there is an accumulation of mast cells (cell type that is involved in, among other things, allergic reactions). Among other things, involved in allergic reactions) in the bone marrow, where they are formed, as well as accumulation in the skin, bones, liver, spleen and gastrointestinal tract (GIT; gastrointestinal tract); mastocytosis is not curable; course usually benign (benign) and life expectancy normal; extremely rare degeneration mast cells (= mast cell leukemia (blood cancer)).
  • Crohn’s disease – chronic inflammatory bowel disease (CED); usually runs in relapses and can affect the entire digestive tract; characteristic is the segmental affection of the intestinal mucosa (intestinal mucosa), that is, it may be affected several intestinal sections that are separated from each other by healthy sections.
  • Nephrolithiasis (kidney stones).
  • Polycythaemia vera – pathological multiplication of blood cells (particularly affected are: especially erythrocytes/red blood cells, to a lesser extent also platelets (blood platelets) and leukocytes/white blood cells); stinging itching after contact with water (aquagenic pruritus).
  • Sarcoidosis (synonyms: Boeck’s disease; Schaumann-Besnier’s disease) – systemic disease of connective tissue with granuloma formation (skin, lungs and lymph nodes).
  • Systemic mastocytosis – disease characterized by excessive proliferation of mast cells in internal organs/bone marrow.
  • Zollinger-Ellison syndrome – benign or malignant (benign or malignant) tumor, usually located in the pancreas (pancreas), leading to increased gastrin production.

Medication

Other causes