Gastritis with high acidity: symptoms and treatment

Gastritis is one of the most common diseases among all pathologies of the digestive system. This disease is observed in 80-90% of the population. Its main danger is the transition to peptic ulcer disease and the possibility of malignancy.

Gastritis is a specific disease of inflammatory-dystrophic origin of the stomach, in which structural changes occur in its mucous membrane, leading to dystrophy, atrophy or dysregeneration. In the process of these changes, the secretion functions of digestive enzymes (hydrochloric acid and pepsin), synthesis and motility processes of gastrointestinal hormones are disrupted.

Epidemiology

According to statistics, gastritis is registered in 80-90% of adults. Helicobacter pylori associated is recognized as the most common; it accounts for 90% of all diagnoses of chronic hepatitis. The most dangerous form with a high percentage of malignancy is atrophic, occurring in 5% of cases in people under 30 years of age, in 35% in patients 30-50 years of age, in 70% in patients over 50 years of age.

In children, the disease most often develops during puberty and at the age of 4-7 years, when the child is most susceptible to infectious and viral diseases.

Salivary glands – increased salivation and dry mouth

There are a number of tips to help keep
your salivary glands healthy:
First, you need to drink plenty of water. Secondly, you should use chewing gum that does not contain sugar. And thirdly, it is necessary to suck on lollipops, which also do not contain sugar.

In certain cases, your dentist may recommend gargling with artificial saliva. The above drug is sold in spray or liquid form. You do not need a prescription to purchase it, but use it several times a day. However, artificial saliva does not contain proteins, minerals and other necessary elements that are contained in natural salivary fluid. Thus, the above drug will simply be useless for digestion.

Etiology

The development of gastritis is caused by the influence of many factors on gastric tissue. Among the reasons, exogenous and endogenous factors are distinguished.

Exogenous factors include:

• eating disorders;
• bacterial colonization by Helicobacter pylori, less commonly by other bacteria or fungi;
• radiation exposure, chemical damage;
• long-term use of medications that irritate the mucous membrane (the most aggressive are glucocorticosteroids, anti-inflammatory drugs, acetylsalicylic acid, etc.);
• parasitic infestations;
• bad habits (especially alcohol and smoking);
• chronic stress.

Among the endogenous factors are:

• genetic predisposition;
• autoimmune processes;
• duodenogastric reflux;
• metabolic disorders;
• endogenous intoxications;
• endocrine dysfunctions;
• hypoxemia;
• avitaminosis;
• chronic infectious diseases;

Also, the development of gastritis is promoted by various reflex effects from other affected organs.

Excess saliva, or how to prevent it

By and large, there are three types of therapy that are used to treat increased salivation. These include Botox injections, surgical treatment and medications that are available only by prescription. It all depends on the factors that caused the disease. It is clear that the simplest thing will be to prescribe certain medications. Typically, the above drugs will include scopolamine and glycopyrrolate. Side effects include increased heart rate, trouble urinating, drowsiness, and blurred vision.

For severe forms of drooling, specialists resort to Botox injections into the salivary glands (one or more). The treatment is considered safe, but its effect only lasts for several months. And only in very severe cases do doctors resort to surgery. During surgery, the salivary glands are removed or the direction of the excretory ducts is changed.
With the help of surgery, you can permanently get rid of increased salivation. Salivary glands – increased salivation and dry mouth

Pathogenesis

The mechanism of pathogenesis is based on characteristic inflammation of the mucous membrane, which leads to its structural restructuring. If predisposing factors and the active influence of causes are present, the process of inflammation begins, which is characterized by a long course.

Chronitization is based on round cell inflammatory infiltration by neutrophils and other cells of the autoimmune system of the mucosa. Under the influence of the inflammatory reaction, the links in the restructuring of the shell structure and the development of active dysregenerative processes in it are triggered with a further transition to dystrophy and atrophy. The result of these processes is a quantitative change in hydrochloric acid.

The leading role is occupied by associated Helicobacter pylori, the second most common is drug-induced gastritis, and then atrophic.

Signs, symptoms and treatment of gastritis

Gastritis is an inflammatory process in the gastric mucosa. This disease provokes a violation of the absorption of food and digestion. This is the most common disease among others in the digestive system. Most often, gastritis occurs in elderly and middle-aged individuals. It comes in acute and chronic forms. Acute appears when the disease progresses for the first time, and chronic is present on an ongoing basis in the patient’s life. If acute gastritis is not treated in time, it will gradually turn into chronic.

Symptoms of the disease

Clinical symptoms can be divided into pain, dyspeptic disorders, and general symptoms of malaise.

Pain syndrome

Quite often it is the leading link in the clinical picture of the disease, since it is with this that patients seek help.

As a rule, pain is localized in the epigastrium, in other parts of the abdomen much less often. With gastritis with high acidity, a typical pain syndrome develops 1-2 hours after eating, the pain is acute and cutting in nature.

Dyspeptic manifestations

This syndrome is characterized by a violation of the digestion process, which is manifested by the following symptoms:

• decreased appetite;
• discomfort after eating;
• heartburn (may worsen when changing position);
• nausea;
• belching, flatulence;
• gagging - sometimes vomiting;
• sour or metallic taste.

With gastritis with high acidity, the symptoms are most often mildly expressed and become more active in combination with provoking factors (significant pauses between meals, severe stress, overeating, violation of the temperature regime of food, etc.).

General symptoms of illness

As a rule, with uncomplicated forms of pathology, the general condition changes to an insignificant extent. As the inflammatory process increases, changes can be quite pronounced. The most commonly observed symptoms are:

• severe general weakness;
• hypotension, dizziness;
• irritability;
• increased sweating;
• intolerance to certain foods;
• reduction in body weight by more than 5% of total weight within six months;
• hypovitaminosis.

Patients with Helicobacter pylori with hyperacidity may develop ulcer-like symptoms, which indicate a probable pre-ulcerative condition.

In general, the clinical picture is determined by the specificity of gastric secretion disorders and the degree of motor-evacuation dysfunction. The initial period is characterized by symptom-free symptoms, then, as the inflammatory process progresses, a pain syndrome develops with the addition of dyspepsia.

Gastritis or functional dyspepsia?

The term “gastritis” is usually used to refer to various inflammatory and degenerative changes in the gastric mucosa. But in fact, the disease itself is quite rare and can only be diagnosed using a biopsy during a gastroscopy procedure.

Often what is called gastritis is functional dyspepsia (a set of disorders of the digestive system). The term “gastritis” is also mistakenly used to mean gastroesophageal reflux disease (GERD) or irritable bowel syndrome (IBS).

Currently, the diagnosis of “gastritis” is usually made in the presence of morphological signs discovered after undergoing a series of medical examinations, in particular, after laboratory identification of the main causative agent of the disease - the bacterium Helicobacter pylori (H. Pilory), histological studies and FGDS.

Classification, stages of the disease

In clinical practice in Russia, the working classification based on the developments of S. M. Ryss and the Sydney classification is most often used.

Working classification

According to etiology and pathogenesis:

1. Type A

   : characterized by autoimmune fundic atrophic processes, including those associated with Addison-Bearman anemia;

2. Type B

   : specific bacterial antral non-atrophic process associated with Hp;

3. Type C

   : a chemical form associated with reflux of lysolecithin, duodenogastric reflux, and also due to the use of medications;

   Read also:  Leukoplakia: what is it and how is it treated in dentistry
4. Type AB

   : characteristic combined atrophic pangastritis, characterized by the involvement of all parts of the stomach in the process.

In addition, there are alcoholic, drug, radiation, lymphocytic, granulomatous eosinophilic and other forms of the disease.

According to topographer-morphological features

By localization:

• fundal;
• astral;
• pangastritis.

According to morphological criteria:

• surface form;
• interstitial;
• atrophic (mild, moderate or severe);
• with complete or partial intestinal metaplasia (small or large intestine).

According to specific morphological characteristics

According to the severity of inflammation:

• minimum;
• insignificant level;
• moderate;
• expressed.

By degree of activity:

• not active;
• mild;
• average;
• heavy.

According to the severity of coolant contamination:

• not expressed;
• lungs;
• average;
• tall.

According to the features of the clinic:

• with a predominance of pain (type B);
• with a predominance of dyspeptic disorders (type A);
• latent (asymptomatic).

According to functional criteria:

• with preserved secretion;
• with increased;
• with secretory insufficiency.

According to endoscopic criteria:

• erythematous (exudative);
• with flat (sharp) erosions;
• rising erosions (chronic);
• hemorrhagic;
• complicated by reflux gastritis;
• hyperplastic.

Separately, gastritis of unknown origin is distinguished, as well as of mixed origin.

The course of chronic hepatitis is characterized by two stages: relapse (exacerbation) and remission, gradually replacing each other.

specialist

Our doctors will answer any questions you may have

Tumasova Anna Valerievna Gastroenterologist

Stages of the disease

The disease occurs in 4 main stages:

1. Hyperemic.

   At the initial stage, the mucous membrane acquires a reddish color, and slight swelling appears.

2. Hypertrophic.

   At this stage, thickening of the mucosa occurs with a parallel decrease in hydrochloric acid. Changes are likely both in tissues and at the cellular level (dysplasia), as well as the accumulation of leukocytes (metaplasia).

3. Atrophic.

   As a result of a long-term ongoing process of inflammation, the mucous membrane becomes thinner, regenerative capacity decreases, and epithelial cells die off and are subsequently replaced by scar tissue.

4. Erosive and/or ulcerative.

   Due to thinning of the mucous membrane, focal lesions of varying depths form on the inner surface of the stomach.

With each subsequent exacerbation, these lesions deepen and grow, and the symptoms increase accordingly.

Excess saliva in the mouth

By and large, a large amount of saliva is not a problem if the condition is not systemic. Typically, the amount of saliva you produce depends on what you drink or eat. In a healthy person, the body easily eliminates excess salivation. In general, excessive salivation is caused by overactivity of the salivary glands, as well as if a person has a disturbed swallowing process.

If you eat a spicy dish during your lunch break, your body will begin to intensively secrete saliva. This is because the taste buds on the tongue help increase the volume of fluid produced. For a visual example, you can put something sharp on your tongue. After a few moments, you will be able to feel a rush of saliva into your mouth. Also, sour foods affect excessive salivation. Accordingly, you can reconsider your diet if you are concerned about excess salivary secretion. In addition, the above symptom may occur as a result of certain diseases and abnormalities, as well as due to the use of special medications.

Possible complications

If the doctor’s recommendations are not followed or therapy is inadequate, gastritis can be complicated by the following pathological conditions:

• digestive disorders in the form of malabsorption and dyspepsia;
• vitamin B deficiency;
• peptic ulcer: most often develops with the erosive form of gastritis;
• gastric bleeding: occurs with ulcers and erosions. Clinical signs will include pallor, weakness, cold and sticky sweat, shortness of breath, tachycardia, the presence of blood in the vomit, black stools. This condition requires immediate hospitalization;
• atrophic gastritis: the glands of the mucous membrane almost completely stop producing secretions, the process of replacement with scar tissue begins, it refers to a prenatal condition, the likelihood of malignancy is extremely high;
• iron deficiency anemia (develops with low production of Castle factor);
• stomach cancer.

During an exacerbation, severe complications can develop within several days, and sometimes even one day.

Treatment

Basic treatment is based on the complete or maximum possible exclusion of “aggression” factors that negatively affect the gastric mucosa. Therapy during an exacerbation period begins with following a gentle diet according to Pevzner (table No. 1 and No. 2).

Diet for gastritis

In case of relapse of the disease, a gentle diet is used, and the preparation option is pureed. The basic principles of therapeutic nutrition include:

• mechanical sparing:

  is carried out thanks to the choice of products according to the degree of coarse fiber content, digestion time in the stomach, as well as through the process of thorough culinary processing (steam cooking, stewing, giving food the consistency of puree);

• thermal sparing:

  is ensured by the exclusion of excessively hot and cold foods that can injure the mucous membrane. The most optimal temperature for hot dishes should be in the range of +30-40 degrees;

• chemical sparing:

  consists of increasing vegetable fats and animal proteins against the background of the physiological norm of vitamins, microelements, and all carbohydrates. This is due to the ability of fats to slow down gastric secretion, and on the part of proteins - inactivation of hydrochloric acid;

• limiting the amount of food taken at one time (the “often, but little” principle):

  Meals should be 5-6 times a day, in small portions. The best option would be to match food intake with the process of activating the production of hydrochloric acid.

In addition, foods that have a medium and low level of stimulation of acid production are excluded from the diet: berries, fruits, meat, soft-boiled eggs, white bread crackers, cereals, sweet fruits and vegetables.

During a gentle diet, the range includes:

• pureed vegetable soups (excluding cabbage soup and borscht), milk and cereal or noodle soups;
• unleavened cottage cheese, low-fat and non-spicy varieties of cheese;
• boiled pureed vegetables: Brussels sprouts and cauliflower (white cabbage is prohibited), zucchini, carrots, beets, tomatoes;
• compotes with pureed dried fruits;
• dried wheat bread.

All dishes are cooked strictly by steaming, boiling until soft, grinding and serving warm.

During the period of remission, it is advisable to adhere to the principles of a healthy diet. It is important to exclude spices, spicy foods, smoked meats and marinades, and strong meat broths. You should limit pastry, tea, drinks with a high carbon dioxide content, and chewing gum. It is strictly forbidden to drink alcoholic beverages, coffee, and smoking is also prohibited.

Drug treatment

The use of medications is aimed at reducing the active production of hydrochloric acid, regenerating the mucosa and increasing the protective functions of the mucous-bicarbonate barrier. The main groups of drugs used include:

• proton pump inhibitors: the principle of action is based on reducing the formation of hydrochloric acid, they are not addictive (omeprazole, pantoprazole, esomeprazole, etc.);
• H2-histamine receptor blockers: drugs block the effect of histamine on the parietal and parietal cells, resulting in a decrease in the synthesis of pepsin and hydrochloric acid. There is also an increase in the formation of prostaglandins, which increases the protective properties of the mucosa and stimulates regenerative processes. With prolonged use, addiction occurs;
• cytoprotectors: bismuth preparations, sucralfate, misoprostol are prescribed;
• antibacterial therapy: used in a combination of 2-3 drugs, the goal is eradication of Helicobacter pylori (penicillins, niroimidazole derivatives, macrolides);
• prokinetics: prescribed to reduce the frequency of reflexes (itopride hydrochloride, cerucal, domperidone);
• antispasmodics: the mechanism of action is to relieve spasticity (mebeverine, no-spa, hyoscine butyl bromide);
• replacement therapy: prescribed for the atrophic form and achlorhydria (enzymes and gastric juice drugs).

Other groups of drugs are prescribed for the treatment of concomitant pathologies and complications.

Drooling (sialorrhea, hypersalivation, ptyalism) is characterized by an increase in the amount of saliva with its flow from the oral cavity through the border of the lips in such a volume that it negatively affects the social and domestic activities and daily life of the patient, leading to damage to the soft tissues of the oral cavity, lips and chin . Parkinson's disease (PD) is the most common cause of sialorrhea in adults. The incidence of this suffering in PD varies from 45 to 80% [1, 2]. Some researchers note a lower prevalence of sialorrhea - 10%. Initially, drooling only bothers you at night, but later, as the disease progresses, it also occurs during the day. Although the association of sialorrhea with PD has been known since the time of J. Parkinson's classic monograph, the pathophysiology of sialorrhea has not been sufficiently studied.

Functioning of the salivary glands under physiological conditions

Depending on the size, small and large salivary glands are distinguished. The minor salivary glands are localized in the mucous membrane of the lips, cheeks, tongue, hard and soft palate. The large salivary glands are located outside the mouth. Three pairs of major salivary glands (parotid, submandibular, sublingual) produce and secrete saliva. Parotid glands ( glandula parotidea

) are located directly under the skin, in front and downward from the auricle, on the lower jaw, at the posterior edge of the masticatory muscle.

The external carotid artery and its branches pass through the parotid gland. Per day, the parotid glands secrete about 1/3 of the volume secreted by all salivary glands (approximately 0.2-0.7 liters of saliva).

Submandibular salivary gland ( glandula submandibularis

) is located superficially, under the cervical fascia and skin. Medially it borders with the styloglossus and hyoglossus muscles, above with the lower jaw, and below it emerges from under its lower edge. In front, the gland is in contact with the posterior edge of the mylohyoid muscle, and laterally it is adjacent to the facial artery and vein. The submandibular gland secretes saliva containing both mucous and serous (protein) secretions.

Sublingual gland ( glandula sublingualis

) is located immediately under the mucous membrane of the floor of the mouth, on both sides of the tongue, on the upper surface of the mylohyoid muscle. Laterally it comes into contact with the inner surface of the body of the lower jaw, medially with the genioglossus, geniohyoid, and hyoid-glossus muscles. The sublingual glands secrete saliva containing a serous (protein) secretion. It is richer in mucin than the saliva of the parotid and submandibular glands, has a pronounced alkaline reaction and high phosphatase activity [3].

The secretory activity of the salivary glands is regulated by the salivary zone of the cerebral cortex and the nuclei of the brain stem. This zone is excited by signals coming from taste buds. Next, the cortical zones interact with the upper (in the region of the parvocellular reticular nucleus) and lower (in the lateral part of the reticular formation) salivary centers of the brain stem.

The secretory activity of the salivary glands is provided by sympathetic and parasympathetic innervation. However, when eating and swallowing, the activity of parasympathetic innervation is mainly activated. Parasympathetic afferent pathways, receiving a signal from the receptors of the pharynx and esophagus, reach the salivary center located in the medulla oblongata through the system of the vagus nerve and visceral nerves [2–4].

Parasympathetic efferentation occurs through two pathways. The glossopharyngeal nerve innervates the auricular ganglia and subsequently the parotid gland via the auriculotemporal nerve. The facial nerve innervates the submandibular ganglia through the chorda tympani and then through the lingual nerve ensures the functioning of the submandibular and sublingual glands [5] .

The process of salivation is inextricably linked with swallowing. The act of swallowing consists of three phases: oral, pharyngeal and esophageal. The oral phase is voluntary, while the pharyngeal and esophageal phases are involuntary. The act of swallowing begins with the involvement of more than 30 different muscles of the oropharynx to form and move the bolus of food into the esophagus. Subsequently, the upper esophageal sphincter (EES) opens and the food bolus passes from the pharynx into the esophagus and then into the stomach [2, 6]. Central motor control of swallowing function is provided by the premotor cortex, primary motor cortex, basal ganglia, pedunculopontine nucleus, and cerebellum. Central neurons project to the stem swallowing centers, in particular the nuclei of the solitary tract (common to the facial, glossopharyngeal and vagus nerves, providing taste sensitivity). These centers further regulate the functions of structures involved in the swallowing process, such as the tongue, muscles of the larynx, pharynx and upper esophagus. At the same time, the muscles of the tongue are controlled by the nucleus of the hypoglossal nerve; the muscles of the larynx, pharynx and upper esophagus are controlled by n . a mbiguous

(common to the vagus and glossopharyngeal nerves) [4, 7]. In patients with PD, the oropharyngeal phase of swallowing is predominantly affected.

Function of the salivary glands in PD

Two causes of drooling in BP are actively debated. One of them is a violation of saliva production, and the other reason may be insufficient saliva utilization. Overproduction of saliva can certainly cause drooling. However, many studies have shown [8, 9] that patients with PD produce even less saliva than healthy people. The exact mechanisms causing the decrease in salivation remain unknown [10].

A decrease in salivary secretion in PD may reflect the involvement of the stem salivary nucleus and cranial autonomic ganglia. One possible explanation is a dopamine deficiency. Experimental studies in animal models have shown that dopamine modulates salivary secretion [11, 12]. Studies in rats have demonstrated that activation of central and peripheral dopamine receptors induces salivation [11]. It is known that damage to the striatum, globus pallidus and the descending pathway to the lateral part of the reticular formation of the midbrain can significantly reduce salivation [13]. Pathological studies have revealed the presence of Lewy bodies in patients with PD both in autonomic formations (in the superior cervical ganglion, sympathetic trunk of the cervix, peripheral vagus nerve) and in the submandibular gland [14]. Although Lewy bodies are found in peripheral ganglia, involvement of the cranial parasympathetic ganglia in the degeneration process has not been established. Dopamine has been confirmed to stimulate salivation, even with the administration of the peripheral D2 receptor blocker domperidone, which is indirect evidence of the involvement of higher levels of regulation in this system, including the basal ganglia and brainstem, which may be responsible for reducing salivation in these patients [15]. .

Studies assessing the intensity of production and rate of salivary excretion of the parotid glands using scintigraphy did not show a difference in saliva production, but the rate of saliva excretion to discrete stimuli was significantly higher in patients with PD compared to healthy controls [16, 17]. Thus, increased salivary flow is not a major contributor to the pathophysiology of drooling in BP. However, increasing the excretion rate partially increases sialorrhea.

In PD, the function of the blood-salivary barrier is disrupted, its permeability to calcium, magnesium and zinc increases and the concentration of copper in saliva decreases. Taking levodopa brings the permeability of the blood-salivar barrier closer to functional compliance with healthy ones [18]. Thus, dopamine regulation of not only the volume of saliva secreted, but also the ratio of its mucosal and serous components and elemental composition is not excluded.

Swallowing dysfunction may be one of the leading causes of drooling in patients with BP. It is known that the dorsal motor nucleus of the vagus nerve is affected already in the early stages of PD, although other central regulators of swallowing remain intact for a long time. At the same time, the pedunculopontine tegmental nucleus, which modulates the activity of the medulla oblongata nuclei, is also affected quite early in PD.

The nucleus ambiguus regulates the function of the striatal muscles of the pharynx and upper esophagus. The dorsal motor nucleus of the vagus nerve controls the intermuscular nerve plexuses of the smooth muscles of the esophagus. While the myenteric plexus and dorsal nucleus are affected in the early stages of PD, the pathology of the oral and pharyngeal stages in patients with PD at the onset of the disease is associated not with the involvement of the nucleus ambiguus, but with a violation of the supramedullary control of swallowing.

Oropharyngeal phase disruption found in PD may contribute to the accumulation of saliva in the oral cavity. Oropharyngeal dysphagia is thought to result from bradykinesia. Animal studies have shown that after injection of 6-hydroxydopamine (6-OHDA), the rate of tongue protrusion slows down in experimental rats, and the average duration of tongue pressure becomes significantly longer compared to the control group [19]. Another study [20] showed that the maximum tongue pressure in patients with severe stages of PD was weaker compared to patients with early or moderate stages, and the transit time of the bolus in the oropharynx was negatively correlated with the speed of tongue movement. Both studies reflect the fact that patients with PD have bradykinesia of the oropharyngeal phase of swallowing and impaired tongue muscle function.

Thus, dysfunction of tongue control contributes to dysphagia and may be a cause of drooling. A videofluorographic study in a model of parkinsonism in rats (after injection of 6-OHDA) showed a slower progression of the food bolus compared to the control group [21].

A study using barium in patients with drooling in PD demonstrated a direct correlation between the severity of dysphagia and the severity of sialorrhea [22]. Scintigraphy showed the presence of subclinical manifestations of dysphagia in all patients with sialorrhea. Patient complaints of drooling aggravated swallowing disorders [17]. Thus, oropharyngeal dysphagia may be a major pathophysiological factor in drooling in PD.

Another cause of drooling may be impaired motility of the upper esophagus. Data from manometric studies provided evidence of impaired EEC relaxation in patients with PD compared with controls.

Often, a manifestation of PD is a dystonic swallowing disorder [23]. In this case, dysfunction of the pharyngo-cricoid muscles leads to dysphagia. The pharyngo-cricoid muscles are the upper sphincters of the esophagus. Accordingly, impairment of their ability to adequately relax during swallowing can lead to impairment of the ability to swallow solid food. This condition is often called crico-pharyngeal achalasia and is characterized by insufficient relaxation of the upper esophageal sphincter in duration and severity.

However, this factor cannot be the only cause of dysphagia, and if the patient has sufficient pharyngeal propulsive force, swallowing will not be significantly affected [24, 25]. There is probably a combination of disturbances in the oropharyngeal and esophageal phases of swallowing.

Hypomimia, involuntary opening of the mouth, slouching or drooping head can also lead to inability to retain saliva in the mouth [26]. At the same time, there is no evidence that drug-induced dyskinesias can cause drooling. Thus, today three main mechanisms of sialorrhea in PD are considered: increased secretion of saliva, inability to retain saliva in the oral cavity (hypomimia, involuntary opening of the mouth, stooping or drooping head), deterioration of salivary clearance (lingual bradykinesia, oropharyngeal dysphagia, upper sphincter dysfunction esophagus).

Epidemiology and maladjustment

On average, 50% of patients with PD complain of drooling, subclinical sialorrhea is objectified (videofluoroscopy) in 90% [2, 7]. Drooling is present in 86% of patients with dysphagia and only 40% without it [27].

Patients suffering from excessive salivation experience difficulty articulating speech and swallowing, and have bad breath. Constant leakage of saliva from the oral cavity forces one to resort to the use of handkerchiefs or towels, leading to perioral cracking, irritation, and maceration of the skin. Wetness and soiling of clothes and bedding increases the burden on caregivers. Psychologically, excessive drooling can lead to decreased self-esteem and social isolation.

Treatment methods

Treatment of sialorrhea in PD includes methods aimed at reducing saliva production with the prescription of acetylcholine transport blockers, cholinesterase inhibitors; use of clozapine and quetiapine; improvement of motor symptoms of PD with dopaminergic agents and surgical neuromodulation. However, the effectiveness of these methods is only partial, and new pharmacological and non-pharmacological approaches to the treatment of sialorrhea are needed. For this purpose, various groups of drugs are being studied, including anticholinergic drugs, adrenergic receptor antagonists, and botulinum toxins (BTX).

Anticholinergic drugs.

For selective action, blockers of M3-cholinergic receptors, predominantly localized in the salivary glands, are required. This way you can avoid side effects such as confusion, hallucinations, constipation, urinary retention, and drowsiness. For this purpose, the following were studied: sublingual atropine [28], sublingual ipratropine bromide spray [29], oral glycopyrrolate [30], and oral tropical tropamide [31]. Current MDS guidelines for the use of anticholinergic drugs for the treatment of drooling in PD indicate that glycopyrrolate is effective, but proven efficacy lasts for 1 week and there is insufficient information on its tolerability. There is also insufficient information on the effectiveness and tolerability of ipratropine.

Adrenergic receptor agonists

may partially reduce sialorrhea. Clozapine, yohimbine, and α2-adrenergic receptor antagonists have been reported in the literature as having drooling as a side effect. Based on this, α-2-adrenergic receptor agonists should reduce salivation. Specifically, clonidine reduced sialorrhea in a small, randomized, double-blind, placebo-controlled trial of 32 patients [32]. Oral modafinil 100 mg daily also reduces drooling. However, modafinil is an α-1-adrenergic receptor agonist, and the reduction in sialorrhea is most likely due to a reduction in dysphagia rather than suppression of salivary production [32]. Thus, there are currently no recommendations for the use of α2-adrenergic receptor agonists in the treatment of hypersalivation, but clonidine and modafinil may be considered promising agents.

Botulinum therapy

The main mechanism of action of BTX is inhibition of acetylcholine release. Local injections into the salivary glands inhibit cholinergic parasympathetic and postganglionic sympathetic activity, causing a decrease in salivary secretion. Two serotypes of BTX are being studied to reduce sialorrhea: serotype A and serotype B. Two types of BTX type A, onabotulinumtoxin and abobotulinumtoxin, are used in the treatment of sialorrhea.

Studies have been conducted to study onabotulinumtoxin of various designs (observational, open, open case-control, randomized placebo-controlled) [33-38]. In all of these studies, injections were made into the parotid gland. One of them [37] included patients not only with PD, but also with multiple system atrophy and dementia with Lewy bodies. Two studies [33, 36] used ultrasound guidance. One study [33] showed no difference in the effectiveness of injections with and without ultrasound guidance. The therapeutic effect was assessed after 1–16 weeks. BTX was administered in doses of 5 to 50 units into the parotid gland and 5 units into the submandibular gland with a significant reduction in salivation and a duration of effect of up to 4 months.

Abobotulinum toxin (Dysport) was injected into the parotid gland in all studies. In some of them [39], BTX was additionally injected into the submandibular salivary gland. Most studies did not use additional injection control methods. Only two of them [39, 40] used ultrasound guidance. The duration of outcome assessment ranged from 1 to 4 weeks. All studies demonstrated the effectiveness of abobotulinumtoxin in doses of 75-146.2 units when injected into each parotid gland and 78.7 units into each submandibular salivary gland. Salivation was significantly reduced in patients not only with PD, but also with multiple system atrophy, corticobasal degeneration, and amyotrophic lateral sclerosis [41]. Both according to objective assessment methods and according to the subjective feelings of patients, the therapeutic effect persisted for 1-4 months. Additionally, it was found that there are no significant differences in therapeutic effects between injections of the drug into the parotid or submandibular glands [26].

BTX type B (rimabotulinumtoxin, not registered in Russia) was also injected mainly into the parotid salivary gland [42–47], two studies used ultrasound guidance [31, 45]. All studies demonstrated the effectiveness of BTX type B in doses of 500-2000 and 250 units when injected into the parotid and submandibular glands, respectively, with an average duration of effect of 4.8 months.

The objective of one of the studies was to compare BTX types B and A (randomized, placebo-controlled, crossover, ultrasound-guided) [48]. Either 100 units of abobotulinumtoxin or 1000 units of rimabotulinumtoxin were injected into the parotid gland; either 25 units of abobotulinumtoxin or 250 units of rimabotulinumtoxin were injected into the submandibular gland. When assessing salivation using the DSFS (Drooling Severity Scale and Frequency Scale) and DRS (Drooling Rating Scale) methods 1 month after the injection, the result was better in the group that received BTX type B, but after 2 months the results were equal.

According to MDS recommendations, BTX are effective in the symptomatic treatment of sialorrhea in PD [49]. The therapeutic effect begins 1 week after the injection and lasts 3-5 months. Ultrasound-guided injections may be more accurate. There were no differences in the effectiveness of BTX types A and B. Typical side effects such as dry mouth are mild.

Pharyngeal-cricoid dysphagia can also be successfully compensated with BTX injections. Several injection techniques have been described, including both percutaneous and endoscopic techniques [50, 51]. Administration of BTX type A 30 IU for dysphagia into the pharyngo-cricoid muscle under the control of electromyography and esophagoscopy leads to a decrease in swallowing disorders after 48 hours: swallowing function improves, hyperactivity of the pharyngo-cricoid muscle decreases according to electromyography [52]. Dysphagia usually returns 22 weeks after injection. During these weeks of swallowing improvement, patients regain lost body weight [51, 53]. This fact is important in improving the quality of life of patients.

Non-pharmacological treatments

Various non-pharmacological treatments are offered, such as chewing gum, behavior modification, radiation therapy, and surgical methods. However, only 2 studies on this topic have been published. L. Marks et al. [54] conducted a randomized placebo-controlled trial in 6 patients with PD. Patients were required to voluntarily swallow each time they heard a sound. This modified behavior resulted in a significant reduction in sialorrhea as assessed by DRS. At the same time, the results that reached their maximum 1 month after training turned out to be minimal after 3 months. The authors concluded that patient motivation and voluntary control of swallowing should be considered and used in the treatment of patients with sialorrhea.

Another study used bilateral 12 Gy radiotherapy to the parotid and superior submandibular glands [5]. Hypersalivation decreased significantly after 1 month after radiotherapy, and the effect persisted for up to 1 year. The most common adverse events were decreased taste and dry mouth. However, 75% of adverse events were transient.

We have not found any studies in the literature regarding the effect of surgical neuromodulation. It is possible that in some cases, when chronic stimulation of the basal ganglia causes deterioration in swallowing, drooling may increase [56]. A recent study [57] showed an adverse effect of bilateral stimulation of the subthalamic nucleus.

The bottom line is that there are no current recommendations for the use of non-pharmacological methods in the treatment of sialorrhea in BP. However, behavior modification and, in refractory cases, radiotherapy can be considered as additional components of the overall treatment package.

In conclusion, drooling has negative consequences on the lives of both patients with PD and their caregivers. While the leading role in sialorrhea is probably not overproduction of saliva, but swallowing disorders, most treatment methods are aimed at reducing secretion. Currently, injections of botulinum toxins into the major salivary glands are the most effective treatment. The pathophysiology of ptyalism, standardization of diagnostic criteria, methods for assessing severity, and development of treatment strategies for sialorrhea in PD require further study.

Prognosis and prevention

The prognosis is usually favorable. Complications, especially bleeding and malignancy, pose a danger.

To prevent the occurrence and progression of gastritis, it is necessary:

• maintain an optimal diet;
• to refuse from bad habits;
• carry out regular sanitation of the oral cavity;
• promptly identify and treat other pathologies of the digestive system.

Patients with a severe course and atrophic form should be registered at the dispensary with annual endoscopic monitoring, and also undergo anti-relapse treatment in the fall and spring.