Pathogenesis (development of disease)
True and pseudodiverticula can be distinguished. Diverticula are frequently located in the sigmoid colon (sigmoid diverticulosis). The cause for the formation of diverticula is probably excessive intraluminal pressure (increased intestinal pressure) and increased intestinal motility (→ diverticulosis/change of the colon in the form of small protrusions of the intestinal wall). In old age, this is compounded by decreasing intestinal wall elasticity (weakness of the connective tissue). In diverticulosis, no inflammatory markers (cytokine TNF-alpha; cell surface markers CD4, CD8 and CD57) can be detected in the mucosa. CONCLUSION: Colonic diverticulosis is not a chronic inflammation (inflammation). Diverticulitis is inflammation of the wall of the diverticulum. If the area surrounding the diverticulum is also involved in the inflammation, it is called peridiverticulitis. The inflammation results from the retention of stool in the diverticula (fecal calculus). This can also lead to perforation (breakthrough). Arrosion (“gnawing”, “gnawing”) of the adjacent supplying vessels may cause bleeding.
Etiology (causes)
Biographic causes
- Genetic burden
- Disease runs in families; twin studies estimate heredity at 40% to 53%; genome-wide association study (GWAS) has identified 39 additional single nucleotide polymorphisms (SNP); an earlier smaller GWAS already found 3 risk genes
- Genetic diseases
- Coffin-Lowry syndrome – genetic disorder that is X-linked dominant; physical features, such as a widened nose and enlarged lips, and limitation of mental development.
- Ehlers-Danlos syndrome (EDS) – genetic disorders that are both autosomal dominant and autosomal recessive; heterogeneous group caused by a disorder of collagen synthesis; characterized by increased elasticity of the skin and unusual tearability of the same (habitus of the “rubber man”)
- Marfan syndrome – genetic disease that can be inherited both autosomal dominant or isolated (as a new mutation); systemic connective tissue disease, which is characterized mainly by tall stature, spider-limbedness and hyperextensibility of the joints; 75% of these patients have an aneurysm (pathological (pathological) bulge of the arterial wall).
- Polycystic kidney disease – kidney disease due to multiple cysts (fluid-filled cavities) in the kidneys.
- Partly with autosomal dominant as well as autosomal recessive inheritance (see below Cystic Kidney Disease).
- Williams-Beuren syndrome (WBS; synonyms: Williams syndrome, Fanconi-Schlesinger syndrome, idiopathic hypercalcemia or Elfin-face syndrome) – genetic disorder with autosomal dominant inheritance; with symptoms such as cognitive impairment of varying severity, growth retardation (even intrauterine), hypercalcemia (excess calcium) in the first years of life, microencephaly (abnormally small head), facial shape abnormalities, etc.
- Age – increasing age
Behavioral causes
- Nutrition
- Low fiber diet
- High-fat diet and low fiber intake at the same time
- Consumption of red meat, i.e., muscle meat of pork, beef, lamb, veal, mutton, horse, sheep, goat (1.58 times the risk of diverticulitis in men)
- Micronutrient deficiency (vital substances) – see prevention with micronutrients.
- Consumption of stimulants
- Alcohol (> 30 g/day)
- Tobacco (smoking)
- Physical activity
- Physical inactivity
- Sitting activity
- Overweight (BMI ≥ 25; obesity).
Disease-related causes
- Dysbiosis (imbalance of the intestinal flora).
- Constipation (constipation)
Medication
- Calcium antagonists – a phenome-wide association study indicates that individuals with the variants in the genes that affect the action of calcium antagonists are more likely than others to develop diverticulosis. However, the probability of disease is very low, and was just 1.02 (95% confidence interval 1.01 to 1.04), indicating an increase of 2%.Glucocorticoids* .
- Immunosuppressants*
- Non-steroidal anti-inflammatory drugs (NSAID)* : Acetylsalicylic acid
- Opioids*
* Drugs that have a negative effect on the progression of diverticular disease.
