Функциональная диспепсия: причины, симптомы и методы лечения.

Functional dyspepsia (FD) is a common gastrointestinal disorder defined by symptoms emanating from the gastroduodenal region in the absence of an underlying organic disease that may easily explain the symptoms. Characteristic symptoms include epigastric burning, epigastric pain, postprandial fullness, and early satiety. FD was formerly known as non ulcer dyspepsia, as opposed to "organic dyspepsia" with underlying conditions of gastritis, peptic ulcer disease, or cancer. The exact cause of functional dyspepsia is unknown however there has been many theories regarding the mechanisms. Risk factors for developing functional dyspepsia include female sex, smoking, non steroidal anti inflammatory medication use, and H pylori infection. Gastrointestinal infections can trigger the onset of functional dyspepsia. Theories behind the pathophysiology of functional dyspepsia include gastroduodenal motility, gastroduodenal sensitivity, intestinal microbiota, immune dysfunction, gut brain axis dysfunction, abnormalities of gastric electrical rhythm, and autonomic nervous system/central nervous system dysregulation. Functional dyspepsia is diagnosed based on clinical criteria and symptoms. Depending on the symptoms present patients may need blood work, imaging, or endoscopies to confirm the diagnosis of functional dyspepsia. Functional dyspepsia is further classified into two subtypes, postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS). Functional dyspepsia can be managed with medications such as prokinetic agents, fundus relaxing drugs, centrally acting neuromodulators, and proton pump inhibitors. Up to 15 20% of patients with functional dyspepsia experience persistent symptoms. Functional dyspepsia is more common in women than men. In Western nations the prevalence is believed to be 10 40% and 5 30% in Asian nations.

Symptoms of functional dyspepsia include epigastric burning, epigastric pain, postprandial fullness (often described as bloating by patients), and early satiety. Although functional dyspepsia is typically chronic, the symptoms are generally sporadic, even during periods of severe symptoms. Patients typically refer to early satiety as a vague abundance of gas after eating or discomfort, but in reality, what they truly mean is that they find it difficult to finish a normal sized meal because they are uncomfortable or feel full.

Functional dyspepsia has a wide range of complex etiologies. Gastric motor function abnormalities have long been linked to functional dyspepsia. However, a study revealed that there was no relationship between symptoms and stomach physiological abnormalities. The symptoms are significantly modulated by meal consumption, and genetic factors may also play a part.

Several epidemiological studies have demonstrated a moderate correlation between dyspepsia in the general population and female sex, smoking, non steroidal anti inflammatory medication use, and H pylori infection. On the other hand, the Kyoto consensus indicates that H pylori infection is an organic cause of dyspepsia, sometimes known as H pylori associated dyspepsia. However, this phrase is controversial because the general consensus also indicates that the patient should be diagnosed with functional dyspepsia if symptoms continue or return following successful elimination. In one long term investigation, a high body mass index was an independent predictor of the emergence of functional dyspepsia. Since the brain and gut communicate through the hypothalamic pituitary adrenal axis and the enteric nerve system, psychological comorbidity plays a significant influence in the development of functional dyspepsia. Anxious participants had an eight fold increased risk of developing functional dyspepsia compared to those without anxiety in a population based survey conducted in Sweden. According to two Australian longitudinal investigations, there are reciprocal effects between the stomach and the brain. Specifically, people who had functional dyspepsia at baseline were more likely than those who did not experience anxiety or depression during follow up.

Acute gastroenteritis can lead to the development of post infection functional dyspepsia.

Because functional dyspepsia symptoms are complicated and heterogeneous, the underlying pathophysiology of the disorder is still unknown despite a great deal of research. One of the main pathophysiologic mechanisms thought to underlie the symptoms of functional dyspepsia is delayed stomach emptying. Several studies have looked into the connection between the pattern and intensity of symptoms and delayed stomach emptying. The proportion of dyspeptic individuals with delayed stomach emptying varies from 20% to 50%, depending on the study. In response to gastric balloon distension during fasting and following meal intake, patients with functional dyspepsia demonstrate impaired proximal stomach accommodation. Due to the poor accommodation, there is a disproportional volume distribution, with the fundus volume being less and the antral volume being bigger than usual. Furthermore, individuals suffering from functional dyspepsia exhibit compromised fundus accommodation in reaction to duodenal distension.

In functional dyspepsia, the stomach's sensitivity to chemical and mechanical stimuli is changed. Following stomach distension, even patients with normal accommodation experience discomfort. Additionally, some individuals exhibit hypersensitivity to distension of the duodenum, jejunum, indicating a more widespread sensitization of the central and autonomic nervous systems. The bile acid pool may vary as a result of microbiome modifications brought on by small intestine inflammation. On the other hand, a decrease in primary bile acid levels may have an impact on the small intestine's microbial diversity, which may promote the proliferation of proinflammatory bacteria and low grade inflammation, both of which may result in the breakdown of the epithelial barrier. A shift in the ratio of main to secondary bile acids and decreased amounts of total bile acids in certain patients with functional dyspepsia during fasting further suggest the involvement of gastrointestinal microbes.

Some other functional gastrointestinal disorders have been linked to low grade mucosal inflammation and elevated quantities of inflammatory cells, such as intraepithelial lymphocytes and mast cells. The quantity of cell surface markers needed for more proliferation or differentiation of specialized cells, however, does not increase in functional dyspepsia; rather, it indicates the active state of these cells. Reduced expression of two markers—FAS, which is involved in lymphocyte homoeostasis and cell apoptosis, and HLA DRA, which is involved in B cell proliferation—has been linked to functional dyspepsia and is thought to reflect changes in duodenal lymphocyte populations. Moreover, duodenal eosinophilia has been linked to symptoms of postprandial distress syndrome, as opposed to an increase in mast cells.

There is a subpopulation of people with functional dyspepsia who have involvement in the gut brain axis. Through the hypothalamic pituitary adrenal axis, changes in epithelial barrier function brought on by immune system and gastrointestinal microbiota disruptions can control gut brain connections. This impact has been demonstrated in controlled trials including healthy volunteers under stress as well as in animal models of functional dyspepsia. Anatomical and functional connectivity impairments were observed in brain regions important for processing visceral afferent information in patients with functional dyspepsia, according to MRI results.

Additionally, there is proof that up to two thirds of patients with functional dyspepsia have anomalies in the underlying stomach myoelectrical activity, as determined by cutaneous electrogastrography. It is yet unknown how this discovery relates to stomach emptying and symptom patterns. There was no association discovered between the pattern of dyspeptic symptoms and the existence of electrogastrography results. There has been good evidence of a relationship between aberrant gastric electrical rhythm and delayed stomach emptying.

It has been proposed that certain patients with functional dyspepsia may have anomalies in their autonomic nervous system. Particularly, it has been suggested that efferent vagal dysfunction may be the cause of antral hypomotility and poor adaption to a meal. Additionally, there is proof that psychological variables and both stomach functionality and symptoms of functional dyspepsia are related to psychopathology. Low vagal activity has been suggested as the mediating mechanism in these relationships.

Functional dyspepsia is diagnosed using clinical symptoms and Rome IV criteria, which were recently revised. The clinical examination and patient history should look for alarm symptoms. Alarm symptoms include dysphagia, especially if progressive, or odynophagia, overt gastrointestinal bleeding, such as melena or hematemesis, persistent vomiting, unintentional weight loss, family history of gastric or esophageal cancer, palpable abdominal or epigastric mass or abdominal adenopathy, and signs of iron deficiency anemia. At least one of the following: There is no validated diagnostic algorithm, and current guidelines and the Rome committee oppose routine laboratory testing in all patients. Requesting a complete blood count is probably a good idea because anemia diagnosis could alter the final diagnosis. Liver function tests are needed if there is concern regarding a potential hepatobiliary cause of severe episodic epigastric discomfort. While a negative endoscopy is strictly necessary to validate a functional dyspepsia diagnosis, The most recent guidelines for managing dyspepsia prohibit endoscopic use in patients under 60 years of age because its low yield, even in cases where alarm symptoms are present. Because of the low yield, routinely requesting an abdominal ultrasound or CT scan in the absence of alarm symptoms or signs is not advised. Up to 25% of individuals with functional dyspepsia display delayed stomach emptying, making gastric emptying investigations of little benefit despite the significant symptom overlap and diagnostic confusion between gastroparesis and functional dyspepsia.

Treatment for functional dyspepsia involves addressing the predominant symptom or symptoms with a realistic discussion of the limitations of available therapies to manage expectations, as well as providing reassurance that there is no structural cause for the symptoms and an explanation of the pathophysiology and natural history of the disorder. Although they haven't been thoroughly investigated, dietary and lifestyle changes are typically advised. It makes sense to advise patients to eat smaller, more frequent meals and to steer clear of foods that worsen their symptoms. Although there is no proof connecting coffee and spicy meals high in capsaicin to symptoms, they are generally avoided. Prokinetic medications are effective in treating functional dyspepsia by stimulating the contractions of the stomach's smooth muscle and have been suggested as initial treatments for PDS. Prokinetics include agonists of the 5 HT receptor 4 (5 HT4), antagonists of the D(2) dopamine receptor, and agonists of the motilin receptor, such erythromycin. There aren't many high quality trials and there's frequently little evidence in the literature supporting their symptomatic benefit. 5 HT1A agonists, muscarinic auto receptor antagonists, and acetylcholinesterase inhibitors, such as acotiamide, can all target impaired stomach accommodation. tandospirone, and acotiamide are beneficial for PDS symptoms. Numerous, frequently tiny, investigations have assessed centrally acting neuromodulators in the context of functional dyspepsia. Its reasoning stems from the common occurrence of psychiatric comorbidity and the theory that visceral hypersensitivity may react to centrally active neuromodulators and play a role in the development of symptoms. These medications are most likely the most helpful for EPS. However, similar to 5 HT1A agonists that act on stomach accommodation, they may also have therapeutic effects in PDS through their effects on gastrointestinal motility. The most widely utilized first line therapy for functional dyspepsia is inhibition of acid secretion. Compared to people with PDS, those with EPS are more likely to respond.

The natural history of most people with functional dyspepsia is chronic and variable, consisting of periods during which the patient has no symptoms at all interspersed with phases of symptom return. According to data from population based studies, during an extended period of follow up, 15–20% of patients with functional dyspepsia may experience persistent symptoms, and 50–35% may experience a resolution of symptoms; the remaining 30–35% of patients may experience fluctuating symptoms that meet the criteria for another functional gastrointestinal disorder. Functional dyspepsia is a chronic condition, although there is no proof that it is linked to a lower chance of survival.

Regardless of the various functional dyspepsia criteria, the population prevalence of the disorder varies greatly around the world, with high overall rates (10–40%) in Western nations and low overall rates (5–30%) in Asian nations. Women are more likely than males to experience functional dyspepsia.