Bitterness in the mouth: why it occurs and how to get rid of it

How does a bitter taste in the mouth occur?

The taste in your mouth doesn't have to be overtly bitter; it can feel metallic, sour, or just plain unpleasant. Usually its appearance is associated with certain conditions:

• immediately after eating (if you overeat or eat certain foods);
• after taking medications, especially if a person takes them on an empty stomach;
• after physical activity;
• immediately after waking up.

Bitterness is felt as a foreign, strong, unpleasant taste that comes from the oropharynx or has no obvious source. It may be part of a symptom complex. Along with a bitter taste, the following may appear:

• heaviness in the side;
• abdominal pain;
• white coating on the tongue;
• nausea, vomiting;
• heartburn;
• belching;
• dry mouth or, on the contrary, excessive salivation;
• dizziness;
• bloating;
• bleeding gums;
• cold symptoms (sore throat, cough, fever, weakness);
• decreased appetite;
• deterioration of smell and other symptoms.

By exactly when bitterness appears and what other symptoms arise, one can judge the causes of the condition. To make a diagnosis, you need to see a doctor and describe to him in detail how you feel.

Causes of bitter taste in mouth

Bitterness in the mouth can appear due to diseases of the digestive system, teeth and gums, due to changes in hormonal levels, taking certain medications and for other reasons (Fig. 1). At the same time, the accompanying symptoms and conditions under which a person feels a bitter taste in the mouth will be different.

Figure 1. Some causes of bitterness in the mouth. Source: MedPortal

Poor quality food

Foods cooked with a lot of oil, fat or burnt can cause a bitter taste in the mouth. Sometimes the bitter taste is associated with drinking black coffee or very strong tea. It can also appear if a person has eaten sunflower seeds or nuts. The bitterness will go away if you drink cool water, but a slight unpleasant aftertaste may persist for a while. If the bitter taste comes from food, there will be no other symptoms (pain, indigestion).

Age-related changes

With age, a person's taste perception gradually changes. Older people are less able to discern tastes, but may still experience bitterness. This is associated with a number of other health changes, for example, decreased saliva production, dry mucous membranes, and a gradual deterioration in oral health.

Smoking

If a person smokes frequently, they perceive the taste of food less well, and this can increase the bitter taste in the mouth. Also, bitterness in the mouth of smokers may be associated with the taste and smell of tobacco smoke. The resins contained in it linger on the mucous membrane of the oral cavity and settle on the surface of the tooth enamel. This is the cause of bad breath, deteriorating dental health and the associated persistent bitter taste. You can beat it with chewing gum or mints, but it is better to quit smoking or at least reduce the number of cigarettes you smoke.

Pregnancy

In the first trimester, bitterness in the mouth may appear along with other symptoms of toxicosis. It usually worsens with nausea or after vomiting. Fluctuations in estrogen levels can affect the perception of tastes. Cholestasis of pregnancy can also cause bitterness. This is a relatively rare syndrome that develops in the third trimester and is characterized by pruritus and cholestatic jaundice. Cholestasis in pregnancy resolves after childbirth and is considered a relatively harmless condition, but if symptoms appear, you should inform your obstetrician-gynecologist.

Functional dyspepsia

Functional dyspepsia is a disorder in which a person does not have severe diseases of the digestive system, but experiences pain, early satiety and a feeling of fullness after eating, and a burning sensation in the upper abdomen. In this condition, the feeling of bitterness occurs due to slow digestion of food. It may be accompanied by abdominal cramps and other unpleasant sensations. Functional dyspepsia is associated with a number of factors, including stress, smoking, heredity, and recent infectious diseases. You can relieve the bitter taste in your mouth by drinking water with lemon juice. If the condition does not go away or the pain intensifies, diarrhea, vomiting or other severe symptoms appear, you should immediately consult a doctor.

Hepatitis

Bitterness in the mouth is the initial symptom of hepatitis and accompanies liver inflammation. In this case, the bitter taste appears in the morning, immediately after waking up or 30-60 minutes after eating. This is accompanied by heaviness in the right hypochondrium, pain, nausea and vomiting containing bile. With toxic hepatitis, symptoms appear for a short time and disappear after starting treatment. With viral hepatitis, bitterness in the mouth persists almost constantly.

Pathologies of the gastrointestinal tract

If food digestion is impaired, an unpleasant taste appears in the mouth. The sensation of bitterness may occur due to a change in taste perception. It occurs, for example, with pancreatitis and may be accompanied by vomiting and the appearance of a yellow or grayish coating on the tongue. A common cause of bitterness in the mouth is gastroesophageal reflux disease (GERD). In this disease, stomach contents (stomach juice and food particles) regularly back up into the esophagus, causing heartburn and a bitter taste in the mouth (video 1).

Video 1. Symptoms of gastroesophageal reflux disease.

If a person has chronic gastritis or duodenitis, a bitter taste appears when he violates the recommended diet. In diseases of the digestive system, a feeling of bitterness in the mouth is always associated with food intake (appears some time after it).

Biliary system damage

A bitter taste may appear in the mouth due to cholelithiasis, cholecystitis, cholangitis and other diseases of the biliary system (gall bladder and bile ducts). At first, bitterness may appear only after drinking alcohol, fatty or fried foods.

“Burning in the mouth, tongue covered with a yellow coating, discomfort, and so on. In 95% of cases, this is due to the reflux of bile from the duodenum into the stomach. In the stomach, this bile is mixed with hydrochloric acid, thrown into the esophagus and then into the oral cavity.”

Karasev I. A., candidate of medical sciences, gastroenterologist, surgeon, endoscopist.

Without treatment, the condition will gradually worsen. The bitter taste will bother you more often and last longer. Along with it, nausea, pain in the hypochondrium on the right side, and stool disorders may occur. The feeling of bitterness becomes permanent if a severe inflammatory disease of the gallbladder or bile ducts develops (cholangitis, cholecystocholangitis, cholecystitis and others). Also among the possible causes are biliary dyskinesia, due to which the outflow of bile is disrupted, and cholelithiasis. Less commonly, the disorder is associated with parasitic liver disease (giardiasis, opisthorchiasis or echinococcosis).

Dental diseases

The feeling of bitterness can be caused by the presence of tartar, caries, gingivitis or other dental problems. There are usually other symptoms:

• toothache;
• enamel sensitivity (reaction to cold or hot, sweet, sour);
• bleeding gums;
• tooth mobility;
• gums look red or swollen;
• There is a noticeable plaque on the enamel that cannot be removed by regular teeth brushing.

Problems with the health of teeth and gums may be associated with xerostomia, a condition in which insufficient saliva is produced and the mouth constantly feels dry. This increases the risk of tooth decay and gum disease, and causes an unpleasant odor in the mouth, which is perceived as bitter. Xerostomia can occur due to smoking, mouth breathing, aging, diabetes, or autoimmune diseases. This condition requires consultation with a dentist.

Sometimes bitterness in the mouth appears after dental treatment. This may be due to the use of certain medications or materials, or the installation of dentures, braces and other structures in the mouth. If the bitter taste does not go away or persists for several days, you should contact your dentist.

Neurological disorders

The mouth may taste bitter due to damage to the brain structures that process taste information. In this case, taste perception is disrupted: for example, sour foods may seem sweet, salty foods may seem sour, and a person may not perceive some tastes. This can occur after a traumatic brain injury or stroke. Sometimes taste disturbances are associated with Alzheimer's disease and other age-related diseases in which neurodegenerative processes occur.

Complications of pharmacotherapy

There are more than 250 types of medications that can cause taste disturbances, including the appearance of bitterness in the mouth. This can happen if the drug affects the taste buds of the brain, if part of it remains in the saliva and changes its taste, if the drug suppresses the microflora, which is why fungal diseases develop. Among the drugs that can cause a bitter taste in the mouth:

• antibiotics;
• medications for arrhythmia, diuretics, statins and other drugs used for cardiovascular diseases;
• drugs used in chemotherapy;
• muscle relaxants, migraine medications and other neurological drugs;
• neuroleptics, sedatives, hypnotics, antidepressants;
• non-steroidal anti-inflammatory drugs;
• bronchodilators;
• antihistamines;
• antiviral drugs;
• nicotine replacement therapy products.

Rare causes

Sometimes bitterness in the mouth becomes a symptom of endocrine disorders: diabetes mellitus, hypothyroidism, hypocortisolism and others. It can accompany some cancers and respiratory diseases. Rarely, the cause is an infection of the salivary glands. A bitter taste may occur in cases of poisoning due to accidental ingestion of a toxic substance. In all these cases, the appearance of bitterness is accompanied by other symptoms of the underlying disease.

Laryngopharyngeal reflux in gastroenterological practice

Gastroesophageal reflux disease (GERD) is one of the most common pathologies of the gastrointestinal tract. At the International Congress of Gastroenterology, held in Montreal in 2005, a unified definition of the disease, a description of symptoms and a classification of the disease were developed, which formed the basis of the Montreal Consensus [1]. The Consensus divides the clinical manifestations of GERD into esophageal and extraesophageal syndromes. The presence of reflux-associated symptoms in the absence of damage to the esophageal mucosa is regarded as esophageal syndrome, manifested solely by symptoms, and in the presence of damage to the esophageal mucosa - as esophageal syndromes with damage to the esophagus (complications). Extraesophageal syndromes were divided, in turn, into syndromes whose connection with GERD has been established, and syndromes whose connection with GERD is suspected. Extraesophageal syndromes with an established connection with GERD include reflux cough, reflux laryngitis, reflux asthma and reflux-induced destruction of tooth enamel, and syndromes with a presumptive connection with GERD include pharyngitis, sinusitis, pulmonary idiopathic fibrosis and recurrent otitis media [ 2, 3].

The word “reflux” itself literally means “reverse flow”. GERD is detected in many patients with chronic laryngitis. Otorhinolaryngologists often refer to this condition as laryngopharyngeal reflux (LPR), which represents the retrograde entry of stomach contents - acid and pepsin, as well as bile acids into the laryngopharynx [4, 5]. There are a number of synonyms for LPR, such as extraesophageal reflux, reflux laryngitis and laryngeal reflux. There is currently no gold standard for diagnosing LPR, and therefore data on its epidemiology are limited. In one study of 105 normal healthy volunteers, 86% had laryngopharyngeal reflux during laryngoscopy [6]. In a meta-analysis by AL Merati et al. analyzed data from pH probe readings in 264 patients with LPR; as a result, gastroesophageal reflux was detected in 10–60% of patients [7]. Studies such as these show that LPR is common in the general population, but needs to be diagnosed in some patients before adequate treatment can be given.

Normally, the upper esophageal sphincter and, to some extent, the larynx protect the lower respiratory tract from the entry of contents from the esophagus and stomach. The larynx is very well innervated and any esophageal reflux in a normal person will cause a protective cough. In patients with LPR, this “safety mechanism” may fail. For example, JE Aviv et al. The study showed that sensory deficits may play a role in the formation of LPR. The authors found a decrease in the laryngeal reflex in response to endoscopic air insufflation in patients with documented LPR [8]. Most researchers propose two main pathophysiological mechanisms for LPR, which directly or indirectly cause damage to the larynx by the contents of the esophagus and stomach. The direct mechanism is the result of the action of gastric contents (acid, pepsin and/or bile acids) acting directly on the mucous membrane of the hypopharynx. The indirect mechanism manifests itself as a result of the effect of reflux on the reflex structures of the larynx. This irritation is thought to cause bronchospasm, which in turn stimulates the vagal response, usually resulting in a nonproductive cough. The delicate ciliated epithelium of the posterior wall of the larynx, which normally evacuates mucus from the trachea, is significantly damaged by contact with gastroduodenal chemical agents, which can lead to mucous stasis in the larynx and discomfort [9]. Recently, it has been suggested that the enzyme carbonic anhydrase, which stimulates bicarbonate secretion, protects laryngeal tissues from reflux and that this protective mechanism may be impaired in the larynx of patients with LPR [10].

Most patients diagnosed with LPR may not have the classic symptoms of GERD. The main symptoms of LPR are respiratory complaints such as pain or burning in the throat, chronic cough (51%), excessive expectoration of mucus (42%), dysphonia (71%), dysphagia (35%), lump in the throat (47%), vertical (daytime) reflux, laryngospasm [11]. Researchers estimate that up to 50% of patients with laryngeal and voice disorders have reflux [12]. Based on laryngoscopy data, a special scale of “reflux signs” (SRS) was developed in 2001, which included 8 characteristic laryngoscopic symptoms with a general assessment of their severity from 0 to 26 points, which are presented in table. 1 [13]. Conducted by MF Vaezi et al. studies have shown that the presence of more than 7 points on the SRS correlated by 95% with positive data from 24-hour esophageal pH monitoring and suggested the presence of LPR [14]. Many patients with LPR often turn to a phoniatrist because they do not have pathognomonic complaints. If a patient’s dysphonia continues for more than three months, he or she should be screened to detect LPR [15].

Unfortunately, the specificity of laryngoscopic findings and their assessment using the presented SRS is not very high [6]. In 2002, the authors who developed the SRS also proposed the “Reflux Symptoms Index” (RSI) questionnaire, recommended for assessing the effectiveness of LPR treatment with proton pump inhibitors (PPIs), which consists of 9 questions and includes a dynamic assessment of a number of indicators (Table 2). Each IRS symptom is rated over the past month on a scale from 0 (no problems) to 5 (severe problems). A score of more than 13 correlates with a positive result of pH monitoring [13]. It is a self-administered tool that helps clinicians assess the clinical severity of LPR symptoms at diagnosis and then over time after treatment. The IRS is significantly higher in patients with LPR than in healthy controls (21.2 vs. 11.6, p < 0.001). However, this indicator is rarely used by general practitioners and otolaryngologists [16]. In 2004, R. Williams et al. proposed a scale for assessing the severity of chronic laryngitis in otorhinolaryngological manifestations of the extraesophageal form of GERD: degree 0 - no signs of inflammation, degree I (mild) hyperemia and/or swelling in the area of ​​the arytenoid cartilages and interarytenoid space, degree II (moderate) - distribution of hyperemia and/ or edema beyond the area of ​​the arytenoid cartilages and the interarytenoid space to the vocal folds, degree III (severe) - the presence of ulcerations in the area of ​​the arytenoid cartilages and the interarytenoid space or the spread of the inflammatory process to the subvocal part of the larynx [17].

As is known, the most sensitive test for practical diagnosis of pathological acid gastroesophageal reflux is daily intraesophageal pH monitoring, when intraesophageal pH is continuously recorded at a distance of 5 cm above the lower esophageal sphincter. As a standard test for diagnosing LPR, ambulatory 24-hour intraesophageal hypopharyngeal pH monitoring using two pH sensors is proposed, with the second (proximal) pH sensor for fixing supraesophageal reflux as a cause of ENT disorders installed 5 cm above the upper alimentary sphincter (VPS) [18]. Unfortunately, although hypopharyngeal pH monitoring is a more sensitive test for identifying patients with GERD-induced ENT disorders, negative results cannot exclude LPR due to the intermittent nature of the disease and variability. Currently, a more accurate and patient-friendly method for diagnosing LPR has been developed by measuring naso- and oropharyngeal pH using a special Restech's Dx-pH measurement system, which allows recording pH fluctuations in the oral cavity and nasopharynx every 1/2 s for 48 hours [14 , 19].

Treatment of patients with LPR should include diet, lifestyle modifications, physical therapies, and pharmacotherapy. Modification of diet and lifestyle involves the patient following the following recommendations:

• after eating, you should avoid bending forward, you should go to bed with your head elevated;
• do not wear tight clothes and tight belts;
• avoid large meals;
• do not eat at night;
• limit the consumption of foods that cause a decrease in the pressure of the lower alimentary sphincter (LES) and have an irritating effect (fats, alcohol, coffee, chocolate, citrus fruits);
• stop smoking;
• normalize body weight.

Foods and drinks containing caffeine, alcohol, chocolate and mint relax the lower esophageal sphincter and increase stomach acid production, while carbonated drinks with/or without caffeine increase reflux and belching. In addition, the intake of acidic foods (with a pH below 4.6), such as citrus fruits and other sour fruits, tomatoes, dry wines and some others, should be limited. Lifestyle modifications that can reduce symptoms of LPR, as well as other manifestations of extraesophageal reflux, include smoking cessation and weight loss. A study by DL Steward et al. [20] showed that lifestyle changes for 2 months or more, with or without PPI therapy, significantly reduced the symptoms of chronic laryngitis.

Drug therapy usually includes PPIs, H2 receptor agonists, prokinetics, and cryoprotectants for the laryngeal mucosa. Empirical therapy with PPIs is justified because it can help in the diagnosis ex juvantibus (from the Latin ex - based on, juvanus - helping), i.e. treatment carried out in order to clarify the diagnosis. To date, studies of the effectiveness of PPIs in the treatment of LPR patients have produced a wide range of responses [21].

Studies evaluating the effectiveness of PPIs in LPR show results ranging from very good, with response rates reaching 70%, to no difference with placebo [22]. A controlled trial using lansoprazole 30 mg twice daily for three months in 22 patients with idiopathic chronic laryngitis found that 50% of patients in the treatment group had a complete response compared with 10% in the control group [23]. However, another study using lansoprazole at a similar dosage and regimen found no difference in response rates in patients with laryngopharyngitis [24]. A large multicenter study involving 145 patients with suspected LPR showed no benefit of esomeprazole 40 mg twice daily for four months compared with placebo [25]. One recent study of 85 patients with LPR found that PPI twice daily was more effective than once daily and that extending the course of treatment from two to four months resulted in more positive responses [26]. In general, for LPR, the use of a standard dose of PPI twice daily for two to three months is justified. Current recommendations do not suggest the use of H2-blockers in combination with PPIs in patients with suspected LPR [27, 28]. To achieve the best results, PPIs should be taken on an empty stomach 30 minutes before meals, with a course of treatment of 2–6 months until complete histological remission of laryngitis is achieved [29]. Patients whose quality of life and symptoms do not improve after two to three months of therapy most likely do not have GERD as a cause of LPR, but they should be evaluated for the presence of mixed reflux using manometry and pH monitoring [30]. If there is no effect from taking a PPI, a reassessment of symptoms with the participation of specialists from a pulmonologist and an allergist is necessary [31, 32].

The necessary comprehensive diagnosis and treatment of LPR was demonstrated by E. F. Kokorina, who assessed, in addition to endoscopic signs of esophagitis, the severity of chronic laryngitis in otorhinolaryngological manifestations of the extraesophageal form of GERD using the Williams scale, the level of dysphonia was assessed using the Consensus Auditory-Perceptual Evaluation of Voice (CAPE) scoring scale. V), proposed by the American Speech-Language Hearing Association, 2003. All patients underwent correction of GERD using PPI drugs; for the treatment of LPR in the main group of patients, the drug Erespal was added according to the standard regimen for 3 weeks. The duration of standard antireflux therapy was 3 months. Dynamic assessment of LPR was carried out several times up to 6 months after treatment; a statistically significant acceleration in the regression of reflux-induced changes in the larynx in patients of the main group was revealed [33]. I. L. Klyaritskaya, A. P. Balabantseva in their study showed that the use of double doses of PPI (pantoprazole) for 12 weeks leads to a significant reduction in symptoms of LPR compared to the control group. The optimal duration of treatment is 6–12 months, and after stopping the medication after 6 weeks it leads to an increase in scores on the Reflux Symptom Index questionnaire [34].

It is necessary to consider the use of prokinetics in the complex treatment of both GERD and LPR, which is a manifestation of GERD. Drugs such as metoclopramide, domperidone, cisapride and tegaserod have been used in patients with GERD in the past, but regular use of these drugs is not recommended by current standards due to limited indications and a high side effect profile [35]. In the treatment of GERD today, according to indications, the prokinetic agents itopride and mosapride are used; unfortunately, the latter is not registered in Russia. Itopride, registered in Russia since 2007, is used in patients with LPR as an adjuvant together with PPIs, as well as for other extraesophageal syndromes, accelerating the rate of reduction of symptoms [36, 37]. E. P. Oleinik et al. recommend the use of itopride, based on their own experience of using it in almost 1000 patients, in the complex treatment of all types of voice disorders due to GERD and LPR [38]. F.V. Semenov et al. A study involving 200 patients with LPR assessed the effectiveness of a two-week course of itopride in the treatment of otolaryngological manifestations of LPR. Its use led to a decrease in subjective complaints of patients and a weakening of the severity of laryngoscopic signs such as hyperemia and swelling of the mucous membrane of the arytenoid cartilages [39].

There are several scientific publications in the literature regarding rehabilitation speech therapy treatment of LPR with special voice exercises that strengthen the muscles of the larynx, and in some centers such therapy is carried out empirically without medical evidence-based support. A report on laryngeal rehabilitation in the treatment of chronic cough associated with GERD was recently published with significant improvement in symptoms [40].

The role of surgical fundoplication in patients refractory to even high (double) doses of PPI remains controversial. In a study by J. Swoger et al. evaluated symptoms in 10 PPI-resistant patients after fundoplication compared with 12 PPI-resistant patients who continued conservative treatment with double doses of PPI, showing that only 1 patient (10%) benefited from fundoplication, which was no different from the group comparison (7%) [41]. However, the role of surgery in PPI-resistant patients who have abnormal non-acid reflux remains important. They can be successfully treated with laparoscopic Nissen fundoplication [42]. Today, the Society of American Gastrointestinal and Endoscopic Surgeons clinical guidelines recommend antireflux surgery for patients who: have failed or are intolerant to medications; have significant extraesophageal manifestations such as aspiration, asthma, or cough; have ulcerative strictures as a complication of GERD [43].

Thus, there are no specific lesions of the larynx with laryngopharyngeal reflux, so the diagnosis of this pathology should be comprehensive and include both ENT and gastroenterological examination methods. Treatment of laryngopharyngeal reflux should also be comprehensive, from lifestyle modification and the use of local remedies to a long course of proton pump inhibitors and prokinetics in adequate dosage, and if they are ineffective, surgical treatment methods should be used.

Literature

1. Vakil, N. van Zanden S.V., Kahrilas P. et al. The Montreal definition and classification of gastroesophageal reflux disease: A global evidence-based consensus // Am. J. Gastroenterol. 2006. Vol. 101. P. 1900–1920.
2. Katz PO, Gerson LB, Vela MF Diagnosis and Management of Gastroesophageal Reflux Disease // Am J Gastroenterol. 2013. Vol. 108. R. 308–328.
3. Lazebnik L. B., Bordin D. S., Masharova A. A. Modern understanding of gastroesophageal reflux disease: from Genval to Montreal // Experimental and clinical gastroenterology. 2007. No. 5. P. 4–10.
4. Koufman JA, Aviv JE, Casiano RR, Shaw GY Laryngopharyngeal reflux: position statement of the committee on speech, voice, and swallowing disorders of the American Academy of OtolaryngologyHead and Neck Surgery // Otolaryngol Head Neck Surg. 2002. Vol. 127. R. 32–35.
5. Ford CN Evaluation and management of laryngopharyngeal reflux // JAMA. 2005. Vol. 294. R. 1534–1540.
6. Hicks DM, Ours TM, Abelson TI et al. The prevalence of hypopharynx findings associated with gastroesophageal reflux in normal volunteers // J Voice. 2002. Vol. 16. R. 564–579.
7. Merati AL, Lim HJ, Ulualp SO, Toohill RJ Meta-analysis of upper probe measurements in normal subjects and patients with laryngopharyngeal reflux // Ann Otol Rhinol Laryngol. 2005. Vol. 114. R. 177–182.
8. Aviv JE, Liu H, Parides M et al. Laryngopharyngeal sensory deficits in patients with laryngopharyngeal reflux and dysphagia // Ann Otol Rhinol Laryngol. 2000. Vol. 109. R. 1000–1006.
9. Hanson DG, Jiang JJ Diagnosis and management of chronic laryngitis associated with reflux // Am J Med. 2000. Vol. 108. R. 112S–119S.
10. Johnston N., Bulmer D., Gill GA et al. Cell biology of laryngeal epithelial defenses in health and disease: further studies // Ann Otol Rhinol Laryngol. 2003. Vol. 112. R. 481–491.
11. Koufman JA The otolaryngologic manifestations of gastroesophageal reflux disease (GERD): a clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an experimental investigation of the role of acid and pepsin in the development of laryngeal injury // Laryngoscope. 1991. Vol. 101. R. 1–78.
12. Koufman JA, Amin MR, Panetti M. Prevalence of reflux in 113 consecutive patients with laryngeal and voice disorders // Otolaryngol Head Neck Surg. 2000. Vol. 123. R. 385–388.
13. Belafsky PC, Postma GN, Koufman JA The validity and reliability of the reflux finding score (RFS) // Laryngoscope. 2001. Vol. 111. P. 1313–1317.
14. Vaezi MF Sensitivity and specificity of reflux-attributed laryngeal lesions: experimental and clinical evidence // Am. J. Med. 2003. Vol. 115, (Suppl. 3 A). P. 97 S-104.
15. Karkos PD, Yates PD, Carding PN, Wilson JA Is laryngopharyngeal reflux related to functional dysphonia? // Ann Otol Rhinol Laryngol. 2007. Vol. 116, No. 1. P. 24–29.
16. Ahmed TF, Khandwala F, Abelson TI et al. Chronic laryngitis associated with gastroesophageal reflux: prospective assessment of differences in practice patterns between gastroenterologists and ENT physicians // Am J Gastroenterol. 2006. Vol. 101. R. 470–478.
17. Williams RB, Szczesniak MM, Maklean HM et al. Predictors of Outcome in an Open Label, Therapeutic Trial of High-Dose Omeprazol in Laryngitis // Am J Gastroenterol. 2004. Vol. 42. R. 776–785.
18. Vincent DA Jr., Garrett JD, Radionoff SL et al. The proximal probe in oesophageal pH monitoring: development of a normative database // J. Voice. 2000. Vol. 14. P. 247–254.
19. Ayazi S., Lipham J., Hagen G. et al. A new technique for measurement of pharyngeal pH: normal values ​​and discriminating pH threshold // J. Gastroenterol. Surg. 2009. Vol. 13 (8). P. 1422–1429.
20. Steward DL, Wilson KM, Kelly DH et al. Proton pump inhibitor therapy for chronic laryngopharyngitis: a randomized placebo-control trial // Otolaryngol Head Neck Surg. 2004. Vol. 131. R. 342–350.
21. Martinucci I., de Bortoli N., Savarino E. et al. Optimal treatment of laryngopharyngeal reflux disease // Ther Adv Chronic Dis. 2013. Nov. Vol. 4 (6). R. 287–301.
22. Vaezi MF Extraesophageal manifestations of gastroesophageal reflux disease // Clin Cornerstone. 2003. Vol. 5. R. 32–38.
23. El-Serag HB, Lee P, Buchner A et al. Lansoprazole treatment of patients with chronic idiopathic laryngitis: a placebo-controlled trial // Am J Gastroenterol. 2006. Vol. 96. R. 979–983.
24. Havas T. et al. Posterior pharyngolaryngitis: double blind randomized placebo controlled trial of proton pump inhibitor therapy // Aust J Otolaryngol. 1999. Vol. 3. R. 243–246.
25. Vaezi MF, Richter JE, Stasney CR et al. Treatment of chronic posterior laryngitis with esomeprazole // Laryngoscope. 2006. Vol. 116. R. 254–260.
26. Park W., Hicks DM, Khandwala F. et al. Laryngopharyngeal reflux: prospective cohort study evaluating optimal dose of proton-pump inhibitor therapy and pretherapy predictors of response // Laryngoscope. 2005. Vol. 115. R. 1230–1238.
27. Peghini PL, Katz PO, Castell DO Ranitidine controls nocturnal gastric acid breakthrough on omeprazole: a controlled study in normal subjects // Gastroenterology. 1998. Vol. 115. R. 1335–1339.
28. Fackler WK, Ours TM, Vaezi MF, Richter JE Long-term effect of H2 RA therapy on nocturnal gastric acid breakthrough // Gastroenterology. 2002. Vol. 122. R. 625–632.
29. Belafsky PC, Postma GN, Koufman JA Validity and reliability of the reflux symptom index (RSI) // J Voice. 2002. Vol. 16. R. 274–277.
30. Yuksel ES, Vaezi MF Extraesophageal manifestations of gastroesophageal reflux disease: cough, asthma, laryngitis, chest pain // Swiss Med Wkly. 2012. Vol. 142. R. l35–44.
31. Kahrilas P., Shaheen N., Vaezi M. et al. American Gastroenterological Association Medical Position Statement on the management of gastroesophageal reflux disease // Gastroenterology. 2008. Vol. 135(4). R. 1383–1391, e1381–e1385.
32. Zerbib F., Stoll D. Management of laryngopharyngeal reflux: an unmet medical need // Neurogastroenterol Moti. 2010. Vol. l22. R. 109–112.
33. Kokorina V. E. Use of the drug erespal in schemes for the correction of reflux-induced laryngitis // Bulletin of Otorhinolaryngology. 2010. No. 6. pp. 61–63.
34. Klyaritskaya I. L., Balabantseva A. P. Comparative effectiveness of high daily doses of proton pump inhibitors for laryngopharyngeal reflux // Ukrainian Therapeutic Journal. 2012. No. 1. pp. 21–27.
35. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease // American Journal of Gastroenterology. 2005. Vol. 100 (1). R. 190–200.
36. Ezzat WF, Fawaz SA, Fathey H., El Demerdash A. Virtue of adding prokinetics to proton pump inhibitors in the treatment of laryngopharyngeal reflux disease: prospective study // Journal of Otolaryngology. 2011. Vol. 40 (4). 350–356.
37. Chun BJ, Lee DS The effect of itopride combined with lansoprazole in patients with laryngopharyngeal reflux disease // European Archives of Oto-Rhino-Laryngology. 2013. Vol. 270(4). 1385–1390.
38. Oleynik E. P., Kochesokova E. A., Ivanchenko G. F., Demchenko E. V. Treatment of patients with dysphonia with gastroesophageal reflux disease // Treating Physician. 2010. No. 9. pp. 7–10.
39. Semenov F.V., Gorbonosov I.V., Vartanyan M.S. Experience with the use of itopride for the treatment of otorhinolaryngological manifestations of laryngopharyngeal reflux // Farmateka. 2011. No. 2. pp. 91–95.
40. Pacheco A., Cobeta I., Wagner C. Refractory chronic cough: new perspectives in diagnosis and treatment // Arch Bronconeumo. 2013. Vol. l49. R. 151–157.
41. Swoger J., Ponsky J., Hicks DM et al. Surgical fundoplication in laryngopharyngeal reflux unresponsive to aggressive acid suppression: a controlled study // Clin Gastroenterol Hepatol. 2006. Vol. 4. R. 433–441.
42. Mainie I., Tutuian R., Agrawal A. et al. Combined multichannel intraluminal impedance-pH monitoring to select patients with persistent gastro-oesophageal reflux for laparoscopic Nissen fundoplication // Br J Surg. 2006. Vol. 93. R. 1483–1487.
43. Zerbib F., Sifrim D., Tutuian R. et al. Modern medical and surgical management of difficult-to-treat GORD // United Eur Gastroenterol J. 2013. Vol. 1. R. 21–31.

E. Yu. Plotnikova*, 1, Doctor of Medical Sciences, Professor M. V. Krasnova**, Candidate of Medical Sciences K. A. Krasnov**, Candidate of Medical Sciences E. N. Baranova*

* State Budgetary Educational Institution of Higher Professional Education Kemerovo State Medical Academy of the Ministry of Health of the Russian Federation, Kemerovo ** Municipal Budgetary Healthcare Institution City Clinical Hospital No. 3 named after. M. A. Podgorbunsky, Kemerovo

1 Contact information

Abstract. Ethiopathogenetic mechanisms, clinical indicators and diagnostic methods of laryngopharyngital reflux. Modern treatment methods are described that presumably diet, changing of the mode of life, physical treatment methods and drug therapy as well as indications for surgery.

Help before diagnosis

Even if a diagnosis has not yet been made, several measures can be taken to alleviate the condition:

• Adjust your diet, remove fatty and fried foods, eat more often and in small portions.
• Stop smoking or reduce the number of cigarettes you smoke.
• Limit alcohol consumption.
• Drink more water.

Monitor the quality of oral hygiene. You should brush your teeth twice a day, as well as use mouthwash and floss. If you have problems with your teeth, you need to visit a dentist.

Photo: goffkein/freepik.com

Important! You should not try to use folk remedies or treat yourself - this can be dangerous. If a bitter taste in your mouth appears regularly, you should consult a doctor and get recommendations for treatment.

When to see a doctor?

If the appearance of bitterness in the mouth is not associated with drinking coffee, burnt or poor-quality food, if the bitter taste appears regularly or persists for a long time, if it is accompanied by other symptoms, you should consult a doctor. This could be a dentist, if the bitterness in the mouth is associated with diseases of the teeth and gums, a gastroenterologist, if the cause may be diseases of the digestive organs or biliary tract, a hepatologist, if there are symptoms of liver disease.

Important! In some cases, you need to urgently seek medical help. If bitterness in the mouth is associated with accidental ingestion of poison, if it appears along with other severe symptoms (difficulty breathing, swelling of the tongue, lips, difficulty swallowing, paralysis, changes in consciousness), you should immediately call emergency medical help.

Methods for treating bitterness in the mouth

To treat this disease, you can use freshly squeezed juices.

In all cases, treatment of bitterness in the mouth should begin with a visit to a specialist and a comprehensive examination.

This symptom indicates various pathologies in the body, so it is important to accurately determine the cause of the disorders so that the treatment is effective.

In almost all cases, the success of treatment largely depends on the efforts of the patient himself. First of all, you will need to adjust your diet: you will need to exclude any hard-to-digest food and alcoholic drinks from your diet, and you will need to follow a diet.

Compliance with the diet also requires stopping smoking and consuming any substances that can irritate the mucous membranes. In addition to the medications that the doctor will prescribe to treat the identified disease, it will be useful to use the following folk remedies:

• Constantly drinking plenty of fluids helps improve the functioning of the digestive system. You need to drink at least 2-2.5 liters of water per day; in addition, drinking rosehip or currant decoction is beneficial.
• Drinking freshly squeezed vegetable and fruit juices - carrot, orange, apple, etc.
• Natural juices help improve appetite, provoke salivation, and in addition, the body receives a sufficient amount of vitamins.
• Use of sedatives. Many digestive disorders occur against the background of a constant remedy, so the use of sedatives will be required. This is an infusion of valerian, motherwort decoctions, and also the use of sedative tea.
• It is also necessary to normalize the functioning of the intestines: for this it is necessary to consume sorbents, as well as foods rich in fiber to get rid of constipation.

It is important to remember that bitterness in the mouth is not an independent disease, but only one of the alarming signs that requires mandatory diagnosis and correction of the diet. Only with an integrated approach will treatment be successful and avoid possible complications.

Diagnostics

You can start diagnosing with a consultation and examination with a doctor. To do this, you need to contact a therapist, gastroenterologist, hepatologist or dentist. The doctor will conduct a survey and refer the patient for examination.

Photo: okfoto / freepik.com

During the consultation, the doctor needs to describe in detail the existing symptoms, tell how often and under what circumstances bitterness appears. Information about lifestyle, diet, and existing diseases will be useful.

For diagnosis, the following studies are carried out:

• Duodenal sounding. If a malfunction of the biliary tract is suspected, portions of bile are taken using a probe for bacteriological examination, and the rate of excretion of bile into the duodenum is also assessed.
• Gastroscopy (EGDS, FGDS) is a study using a gastroscope. Allows you to examine the mucous membrane of the digestive organs and do a biopsy (take tissue samples for laboratory testing).
• Ultrasound of the liver, gall bladder and other organs. It is carried out to assess the size and presence of changes in internal organs.
• Lab tests. If diseases of the digestive organs or biliary tract are suspected, a stool test is prescribed. A biochemical blood test is performed if cholecystitis is suspected. A test for hCG and sex hormones, as well as a serological test if viral hepatitis is suspected, can also be performed.

Treatment

Treatment is prescribed based on diagnostic results, taking into account the causes of bitterness in the mouth.

Conservative therapy

Photo: freepik.com
A doctor may prescribe the following medications:

• Choleretics and cholekinetics. These are choleretic drugs that are prescribed for cholangitis and cholecystitis.
• Enzymes that stimulate digestion. They can be used not only for diseases of the digestive organs, but also for liver damage (in combination with hepatoprotectors).
• Antispasmodics. They are prescribed if bitterness in the mouth appears along with abdominal pain and is associated with gastritis or other diseases of the digestive system. Antispasmodic drugs relieve pain and relax the smooth muscles of the stomach.

If the appearance of bitterness is associated with viral hepatitis, the doctor will prescribe complex therapy for the underlying disease. In case of parasitic infection, anthelmintic drugs are prescribed. Additionally, it is recommended to follow a diet, frequent, small meals and control the drinking regime.

Surgery

Surgical treatment is carried out for gallstone disease to remove and remove stones - calculi. If the gallstones are small, the ESWL (extracorporeal shock wave lithotripsy) technique is used, crushing the stones with a shock wave. In more severe cases, open or laparoscopic cholecystectomy is prescribed. It is carried out if neither diet nor ultrasound methods improve the condition. A cholecystectomy involves removing the gallbladder.

Stones extracted from the gallbladder. Photo: Alena1919 / Depositphotos

What complications does bitterness in the mouth lead to?

Bitterness in the mouth may indicate serious inflammatory processes in the digestive tract.

If you ignore an alarming sign, you may soon encounter very unpleasant consequences of the development of pathology.

Bitterness in the mouth may indicate serious inflammatory processes in the digestive tract: cholecystitis, gastritis, pancreatitis, etc.

Lack of timely treatment leads to the fact that the disease becomes chronic, and it becomes much more difficult to cope with it.

A constant bitter taste leads to loss of appetite, which results in weight loss to the point of exhaustion. Eating habits change; over time, a person may almost completely lose the ability to taste food. All this, in combination with other symptoms of the disease, leads to the development of depression and a general deterioration in well-being.