Causes of achalasia of cardia
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The causes of achalasia of cardia have not been clarified to the present day.
In the etiology of cardiac achalasia, two factors are of primary interest at the present time:
- Histologically, the degenerative changes in the intramural nerve plexuses of the esophagus are almost always found. (Similar changes were described in Chagas disease and therefore trypanosomiasis was recognized as one of the possible causes of mega-esophagus, as with the megacolon). But it remains a question. Whether these changes are consequences, for example, of necrosis from pressure during congestion in the enlarged esophagus.
- Psychogenesis is evident in most patients.
A certain role is played by psychoemotional stressful situations and the use of very cold food.
In the initial stages of cardiac achalasia, esophagoscopy and biopsy specimens of the mucous membrane do not show organic changes. However, in a number of works devoted to a detailed histological study of the esophageal wall, persistent changes in the intramural nervous system have been established. At present, it is established that the basis for such a violation is the deficit of a specific neurotransmitter - nitrogen oxide (NO), formed from L-arginine with the participation of the NO synthetase enzyme. NO effects are realized through cyclic guanosine monophosphate. NO leads to relaxation of the smooth muscle cell. In recent years, patients with achalasia of cardia showed a significant decrease in the content of the NO synthetase enzyme in the tissues of the lower esophageal sphincter. This leads to a decrease in the formation of NO and a loss of ability to relax the lower esophageal sphincter. As the disease progresses, there are changes in the muscular fibers of the esophagus (proliferation of collagen fibers between myofiobilli). With the help of electron microscopy, degenerative changes in the branches of the vagus nerve were also revealed.
Probably, violations of the innervation of the esophagus are the main mechanism for the development of cardiac achalasia. Along with the violation of relaxation of the lower esophageal sphincter, the contractility of the thoracic esophagus also decreases, due to the presence of an obstruction to the passage of food in the form of a non-loosening lower esophageal sphincter.
[Pathogenesis of achalasia of cardia
The pathogenesis of cardiac achalasia is associated with a congenital or acquired lesion of the intramural neural plexus of the esophagus (intermuscular - Auerbachian) with a decrease in the number of ganglion cells. As a result, the peristaltic activity of the esophageal wall is broken and there is no relaxation of the lower esophageal sphincter in response to swallowing (which served as the basis for the introduction of the term "achalasia": Greek a - absence, chalasis - relaxation). It is most likely that this is due to a deficiency of inhibitory neurotransmitters, primarily nitric oxide (N0). Thus, in the way of the food lump appears an obstacle in the form of an unshaken sphincter and food intake in the stomach is difficult: for example, it can occur only with additional filling of the esophagus with liquid, when the mass of the column has a mechanical effect on the cardiac sphincter.