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Infection of the stomach lining: Gastritis – Symptoms and causes


Gastritis | Cedars-Sinai

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What is gastritis?

Gastritis is when your stomach lining gets red and swollen (inflamed).

stomach lining is strong. In most cases, acid does not hurt it. But it can get inflamed
and irritated if you drink too much alcohol, eat spicy foods, have damage from pain
relievers called NSAIDs, or smoke.

What causes gastritis?

Gastritis may be caused by many things. It can be caused by diet and lifestyle habits
such as:

  • Drinking too much alcohol
  • Eating spicy foods
  • Smoking
  • Extreme
    stress. This can be from serious or life-threatening health problems.
  • Long-term use of aspirin and over-the-counter pain and fever medicines

Health issues that can lead to gastritis include:

  • Infections caused by bacteria and viruses
  • Major surgery
  • Traumatic injury or burns

Some diseases can also cause gastritis. These include:

  • Autoimmune
    This is when your immune system attacks your body’s healthy cells
    by mistake.
  • Chronic bile
    This is when bile backs up into your stomach and food pipe
    (esophagus). Bile is a fluid that helps you digest food.
  • Pernicious
    . This is a form of anemia that happens when your stomach can;t digest
    vitamin B-12.

What are the symptoms of gastritis?

Each person’s symptoms may vary. The most common symptoms of gastritis include:

  • Stomach upset or pain
  • Belching and hiccups
  • Belly
    (abdominal) bleeding
  • Nausea and vomiting
  • Feeling of fullness or burning in your stomach
  • Loss of appetite
  • Blood
    in your vomit or stool. This is a sign that your stomach lining may be bleeding.

symptoms of gastritis may look like other health problems. Always see your healthcare
provider for a diagnosis.

How is gastritis diagnosed?

Your healthcare provider will give you a physical exam and ask about your past health.
You may also have tests including:

  • Upper GI
    (gastrointestinal) series or barium swallow.
    This X-ray checks the organs of
    the top part of your digestive system. It checks the esophagus, stomach, and the
    first part of your small intestine (duodenum). You will swallow a metallic fluid
    called barium. Barium coats the organs so that they can be seen on the X-ray. 
  • Upper
    endoscopy (EGD.
    This test looks at  the inside of your esophagus, stomach,
    and duodenum. It uses a thin, lighted tube, called an endoscope. The tube has a
    camera at one end. Your healthcare provider puts the tube into your mouth and throat.
    Then the provider moves it into your esophagus, stomach, and duodenum. Your provider
    can see the inside of these organs. He or she can also take a small tissue sample
    (biopsy) if needed.
  • Blood
    You will have a test for H. pylori, a type of bacteria that may be in
    your stomach. Another test will check for anemia. You can get anemia when you don’t
    have enough red blood cells. Sometimes you may have low levels of certain vitamins
    and need to take a dietary supplements.
  • Stool sample
    This test checks to see if you have stomach bacteria that can cause
    gastritis. A small sample of your stool is collected and sent to a lab. Another stool
    test can check for blood in your stool. This may be a sign of gastritis if you have
  • Breath
    You may have a test where your breath is collected and analyzed for a
    stomach bacteria.

How is gastritis treated?

Treatment will depend on your symptoms, age, and general health. It
will also depend on how severe the condition is.

most cases, you will be given antacids and other medicines to reduce your stomach
This will help ease your symptoms and heal your stomach lining.

your gastritis is caused by an illness or infection, your provider will also treat
health problem.

your gastritis is caused by the H. pylori bacteria, you will be given medicines to
kill the bacteria. In most cases, you will take more than 1 antibiotic and a proton
inhibitor. A PPI is medicine that reduces the amount of acid in your stomach. You
also be given a medicine for diarrhea.

Don’t have any foods, drinks, or medicines that cause symptoms or irritate your
stomach. If you smoke, it is best to quit. If you take aspirin or NSAIDs often, talk
with your healthcare provider about other options.

What are possible complications of

Chronic gastritis hurts your stomach lining. It can raise your risk for other health
problems. These include:

  • Peptic
    ulcer disease. This causes painful sores in your upper digestive tract.
  • Gastric
    polyps. These are small masses of cells that form on the inside lining of your
  • Stomach
    tumors. These can be cancer or not cancer (benign).

may also get atrophic gastritis. This can happen if your gastritis is caused by the
pylori bacteria or by an autoimmune disorder. Atrophic gastritis destroys the stomach
lining cells that make your digestive juices. This raises your risk for getting stomach
cancer. It can also cause low levels of certain vitamins in your blood.

Can gastritis be prevented?

Experts don’t know to stop gastritis from happening. But you may lower your risk of
getting the disease by:

  • Having good hygiene habits, especially washing your hands. This can keep you from
    getting the H. pylori bacteria.
  • Not eating or drinking things that can irritate your stomach lining. This includes
    alcohol, caffeine, and spicy foods.
  • Not
    taking medicines such as aspirin and over-the-counter pain and fever medicines. These
    include NSAIDs (nonsteroidal anti-inflammatory medicines.

When should I call my healthcare provider?

Call your healthcare provider if your symptoms get worse or if you have new symptoms.
Call right away if you have bloody vomit, blood in your stools, or black, tarry-looking

Key points about gastritis

  • Gastritis is a redness and swelling (inflammation) of the stomach lining.
  • It can be caused by drinking too much alcohol, eating spicy foods, or smoking.
  • Some diseases and other health issues can also cause gastritis.
  • Symptoms may include stomach pain, belching, nausea, vomiting, abdominal bleeding,
    feeling full, and blood in vomit or stool.
  • In most
    cases, you will be given antacids and other medicines to reduce your stomach
  • Don’t
    have foods or drinks that irritate your stomach lining.
  • Stop smoking.

Next steps

Tips to help you get the most from a
visit to your healthcare provider:

  • Know the reason for your visit and what you want to happen.
  • Before your visit, write down questions you want answered.
  • Bring someone with you to help you ask questions and remember what your provider
    tells you.
  • At the visit, write down the name of a new diagnosis, and any new medicines,
    treatments, or tests. Also write down any new instructions your provider gives
  • Know why a new medicine or treatment is prescribed, and how it will help you.
    Also know what the side effects are.
  • Ask if your condition can be treated in other ways.
  • Know why a test or procedure is recommended and what the results could mean.
  • Know what to expect if you do not take the medicine or have the test or
  • If you have a follow-up appointment, write down the date, time, and purpose for
    that visit.
  • Know how you can contact your provider if you have questions.

Medical Reviewer: Raymond Kent Turley BSN MSN RN

Medical Reviewer: John Hanrahan MD

Medical Reviewer: L Renee Watson MSN RN

© 2000-2021 The StayWell Company, LLC. All rights reserved. This information is not intended as a substitute for professional medical care. Always follow your healthcare professional’s instructions.

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Helicobacter pylori infection


Helicobacter pylori (H pylori) is a type of bacteria that infects the stomach. It is very common, affecting about two thirds of the world’s population and about 30% to 40% of people in the United States. H pylori infection is the most common cause of peptic ulcers. However, the infection does not cause problems for most people.

Alternative Names

H pylori infection


H pylori bacteria are most likely passed directly from person to person. This tends to happen during childhood. The infection remains throughout life if not treated.

It’s not clear how the bacteria are passed from one person to another. The bacteria may spread from:

  • Mouth-to-mouth contact
  • GI tract illness (particularly when vomiting occurs)
  • Contact with stool (fecal material)
  • Contaminated food and water

The bacteria may trigger ulcers in the following way:

  • H pylori enters the mucus layer of the stomach and attaches to the stomach lining.
  • H pylori cause the stomach to produce more stomach acid. This damages the stomach lining, leading to ulcers in some people.

Besides ulcers, H pylori bacteria can also cause a chronic inflammation in the stomach (gastritis) or the upper part of the small intestine (duodenitis).

H pylori can also sometimes lead to stomach cancer or a rare type of stomach lymphoma.


About 10% to 15% of people infected with H pylori develop peptic ulcer disease. Small ulcers may not cause any symptoms. Some ulcers can cause serious bleeding.

An aching or burning pain in your abdomen is a common symptom. The pain may be worse with an empty stomach. The pain can differ from person to person, and some people have no pain.

Other symptoms include:

  • Feeling of fullness or bloating and problems drinking as much fluid as usual
  • Hunger and an empty feeling in the stomach, often 1 to 3 hours after a meal
  • Mild nausea that may go away with vomiting
  • Loss of appetite
  • Weight loss without trying
  • Burping
  • Bloody or dark, tarry stools or bloody vomit

Exams and Tests

  • Have peptic ulcers or a history of ulcers
  • Have discomfort and pain in the stomach lasting more than a month
  • Tell your provider about the medicines you take. The nonsteroidal anti-inflammatory drugs (NSAIDs) can also cause ulcers. If you show the symptoms of infection, the provider may perform following tests for H pylori. These include:

    • Breath test — urea breath test (Carbon Isotope-urea Breath Test, or UBT). Your provider will make you swallow a special substance that has urea. If H pylori are present, the bacteria turn the urea into carbon dioxide. This is detected and recorded in your exhaled breath after 10 minutes.
    • Blood test — measures antibodies to H pylori in your blood.
    • Stool test — detects the presence of bacteria in the stool.
    • Biopsy — tests a tissue sample taken from the stomach lining using endoscopy. The sample is checked for bacterial infection.


    In order for your ulcer to heal and to reduce the chance it will come back, you will be given medicines to:

    • Kill the H pylori bacteria (if present)
    • Reduce acid levels in the stomach

    Take all of your medicines as you have been told. Other lifestyle changes can also help.

    If you have a peptic ulcer and an H pylori infection, treatment is recommended. The standard treatment involves different combinations of the following medicines for 10 to 14 days:

    • Antibiotics to kill H pylori
    • Proton pump inhibitors to help lower acid levels in the stomach
    • Bismuth (the main ingredient in Pepto-Bismol) may be added to help kill the bacteria

    Outlook (Prognosis)

    If you take your medicines, there is a good chance that the H pylori infection will be cured. You will be much less likely to get another ulcer.

    Sometimes, H pylori can be hard to fully cure. Repeated courses of different treatments may be needed. A stomach biopsy will sometimes be done to test the germ to see which antibiotic might work best. This can help guide future treatment. In some cases, H pylori can’t be cured with any therapy, though the symptoms may be able to be reduced.

    If cured, reinfection may occur in areas where sanitary conditions are poor.

    Posssible Complications

    A long-term (chronic) infection with H pylori may lead to:

      Complications may include:

      • Severe blood loss
      • Scarring from an ulcer may make it harder for the stomach to empty
      • Perforation or hole of the stomach and intestines

      When to Contact a Medical Professional

      Severe symptoms that begin suddenly may indicate a blockage in the intestine, perforation, or hemorrhage, all of which are emergencies. Symptoms may include:

      • Tarry, black, or bloody stools
      • Severe vomiting, which may include blood or a substance with the appearance of coffee grounds (a sign of a serious hemorrhage) or the entire stomach contents (a sign of intestinal obstruction)
      • Severe abdominal pain, with or without vomiting or evidence of blood


      Morgan DR, Crowe SE. Helicobacter pylori infection. In: Feldman M, Friedman LS, Brandt LJ, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease. 10th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 51.

      National Cancer Institute website. Helicobacter pylori and cancer. www.cancer.gov/about-cancer/causes-prevention/risk/infectious-agents/h-pylori-fact-sheet. Updated September 5, 2013. Accessed April 3, 2017.

      Teitelbaum EN, Hungness ES, Mahvi DM. Stomach. In: Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston Textbook of Surgery. 20th ed. Philadelphia, PA: Elsevier; 2017:chap 48.

      Peptic Ulcers, Gastritis & Helicobacter…

      Most ulcers are caused by bacteria called Helicobacter pylori (H. pylori), which are believed to be transmitted from person to person through close contact and exposure to fecal matter or vomit. The bacteria cause an infection that weakens the protective mucus in the stomach and duodenum, allowing acid to get through to the sensitive lining beneath. Both the acid and bacteria irritate the lining and cause an ulcer to form.

      If left untreated, a H. pylori infection can cause gastritis (inflammation of the lining of the stomach). Gastritis can occur suddenly (acute gastritis) or gradually (chronic gastritis). An untreated H. pylori infection may also progress into peptic ulcer disease or stomach cancer later in life. Another common cause of gastritis is long-term use of aspirin, ibuprofen and other anti-inflammatory drugs.

      In the past, children with peptic ulcers lived with the chronic condition for several years or even a lifetime. Today, we have a better understanding of what causes peptic ulcers and how to treat them, meaning most children can be cured.

      Symptoms of peptic ulcers, gastritis and H. pylori infection can be very mild in some children.

      Abdominal discomfort is the most common symptom of peptic ulcers and usually feels like a dull, gnawing ache. The pain often occurs two or three hours after a meal or in the middle of the night when the stomach is empty. The pain may come and go for several days or weeks. Eating and taking antacid medicine helps relieve the discomfort. It is not clear if H. pylori infection without ulcers causes abdominal pain.

      Other symptoms include:

      • Bloating
      • Burping
      • Dark stool (with gastritis or an ulcer)
      • Nausea
      • Poor appetite
      • Vomiting
      • Weight loss

      Diagnosis of Peptic Ulcers, Gastritis & Helicobacter Pylori

      If your child experiences symptoms of peptic ulcers, gastritis or H. pylori infection, a pediatric gastroenterologist can perform the following exams and tests to make a diagnosis:

      • Physical exam. A physician will examine the abdomen for signs of bloating and can track your child’s weight loss.
      • Complete medical history. Your child’s physician will review your child’s health records and family health history.
      • Upper gastrointestinal (GI) endoscopy. Your child’s doctor can perform an upper gastrointestinal (GI) endoscopy to examine the esophagus, stomach and duodenum.
      • Biopsy. A pediatric gastroenterologist may take a stomach tissue sample to study the cells for signs of damage or infection.
      • Blood tests. A variety of blood tests can indicate the presence of other reasons for abdominal pain.
      • Breath tests. Breath tests measure the amount of gases, such as hydrogen, in the breath which can be a sign of bacterial overgrowth in the intestines or lactose intolerance.
      • Stool tests. By studying the contents of your child’s stool, the physician can get information about infections that may be upsetting the digestive tract.

      H. Pylori Transmission and Spread of Infection


      H. pylori is commonly transmitted person-to-person by saliva. The bacteria can also be spread by fecal contamination of food or water. In developing countries, a combination of untreated water, crowded conditions, and poor hygiene contributes to higher H. pylori prevalence. Most people become infected as children, and parents and siblings seem to play a primary role in transmission.

      Spread of Infection

      H. pylori enters the body through the mouth, moves through the digestive system, and infects the stomach or the first part of the small intestine. The spiral-shaped bacterium uses its tail-like flagella to move around and burrow into the stomach lining, which causes inflammation.

      Unlike other bacteria, H. pylori bacteria can survive in the harsh acidic environment of the stomach because they produce a substance that neutralizes stomach acid. This substance, urease, reacts with urea to form ammonia, which is toxic to human cells. Depending on where the infection occurs in the stomach, H. pylori can also cause overproduction of stomach acid.

      Diagram of H. Pylori Infection

      Source: Y_tambe, dual-license with GFDL and CC-by-SA, http://upload.wikimedia.org/wikipedia/commons/5/51/H_pylori_ulcer_diagram_en.png


      While there is no formal progression of the H. pylori infection, several steps are well documented. This process is very slow, taking decades, and may stop at any step because gastric cancers probably require several other factors to develop in addition H. pylori infection.

      Stage 1:
      Normal stomach lining (mucosa)
      Stage 2:
      Inflammation of the stomach lining (chronic gastritis)
      Stage 3:
      Loss of stomach cells and impaired digestive system (atrophic gastritis)
      Stage 4:
      Transformation of the stomach lining (intestinal metaplasia)
      Stage 5:
      Beginning stages of stomach cancer (dysplasia)
      Stage 6:
      Stomach cancer (gastric adenocarcinoma)


      pylori, Helicobacter pylori infection and skin diseases

      Author: Dr Eugene Tan, Dermatology Registrar, Waikato Hospital, Hamilton, New Zealand, 2009.

      What are Helicobacter pylori?

      Helicobacter pylori (H. pylori) are bacteria found in the stomach that are responsible for most cases of peptic ulcer. About half of the world’s population has the bacteria making it the most common bacterial infection in humans [1].

      H. pylori infection is more common in developing nations. The risk of contracting H. pylori is related to socioeconomic status and poor living conditions such as overcrowding, lack of clean, running water and a higher number of siblings. As a result, most children in developing nations are infected before the age of 10.

      In New Zealand, there is a higher prevalence amongst Maori and Polynesians. Studies show that about 5% of European children become infected with H. pylori by the age of 20 years, in contrast to 50% of Polynesian children [2].

      The exact route of infection remains unknown, but person-to-person transmission through oral/oral or faecal/oral exposure is the most likely cause. Activities such as sharing food, cutlery or poor toilet hygiene can result in the transmission of H. pylori to another individual.

      What diseases are linked to

      H. pylori infection?

      H. pylori cause direct disease of the stomach. Other conditions are probably related to the body’s immune response to the bacteria.

      • Chronic gastritis (inflammation of the stomach lining)
      • Peptic ulcers
      • Stomach cancers
      • Certain types of lymphomas (cancers of lymphoid tissue)

      What are the symptoms of H. pylori infection?

      Most individuals with H. pylori infection have no symptoms. Symptoms arise if infection with H. pylori causes peptic ulcers or gastritis. These symptoms can be non-specific and may include:

      • Abdominal pain (usually in the upper abdomen)
      • Nausea
      • Vomiting
      • Bloating
      • Red or tar-coloured stools (indicating bleeding in the intestine)
      • Low blood count (anaemia).

      How do H. pylori damage the stomach?

      The damage to the lining of the stomach is due to a complex interaction of the bacteria and the host’s immune response. H. pylori release several enzymes and microbial products that directly damage the lining of the stomach. The immune system reacts by mounting a florid inflammatory response in an attempt to eradicate the bacteria. As a consequence of this inflammatory response, the stomach lining is unintentionally damaged.

      What investigations are there for H. pylori?

      There are several tests available to detect the presence of H. pylori in the stomach:

      • Blood test – This detects specific antibodies against H. pylori bacterium.
      • Breath test – This involves drinking a solution of carbon labelled urea. This solution is broken down by H. pylori, and its breakdown products can be detected in the breath.
      • Stool test – This detects H. pylori proteins in the faeces.
      • Endoscopic testing – This involves the use of optical instruments for the visual examination of interior parts of the body. A flexible tube is inserted through the mouth into the stomach and upper regions of the small intestine. Small tissue samples can be taken from the stomach wall, which is then tested for H. pylori.

      Blood test and breath test are often the first line approach to testing for H. pylori. Endoscopic biopsy is a relatively invasive procedure and is often reserved for patients who require endoscopy for another reason.

      Who should be tested?

      The American College of Gastroenterology recommends testing in the following situations [3]:

      • Patients with active peptic ulcer disease
      • A history of documented peptic ulcer
      • Gastric MALT (Mucosa Associated Lymphoid Tissue) lymphoma
      • Patients who have undergone resection of early gastric cancer.

      Testing is not recommended for people who are asymptomatic (no symptoms) or who have no history of peptic ulcer disease. However, certain population groups who are at risk for developing ulcers or stomach cancers may be considered for asymptomatic testing.

      What is the treatment?

      Treatment of H. pylori infection involves taking several medications for 7 to 14 days (“Triple therapy”), for example, a proton-pump inhibitor (inhibitor of stomach acid secretion) such as omeprazole 40mg once daily, amoxicillin 1g twice daily and clarithromycin 500mg twice daily.

      Treatment cures up to 90% of individuals.

      What is the relationship of H. pylori to diseases of the skin?

      H. pylori have been implicated in a variety of diseases that are not related to the gastrointestinal tract. The skin is an example, and several studies have suggested an association with the following conditions [4,5]:

      Does the treatment of H. pylori affect skin disease?

      Several small studies have suggested that eradicating H. pylori has a positive outcome on certain skin diseases such as urticaria, Behçet disease, lichen planus, atopic dermatitis, Sweet disease and systemic sclerosis. Conditions which may not benefit are psoriasis and rosacea.

      These studies are not randomised and involve small numbers of patients so no definitive conclusion can be drawn about the eradication of H. pylori in skin diseases at present.



      1. Cover TL, Blaser MJ. Helicobacter pylori in health and disease. Gastroenterology 2009; 136: 1863-73. Medline.
      2. Fraser A. Helicobacter pylori: a historical perspective 1983-2003. N Z Med J 2004; 117: 1194. U896. Fulltext.
      3. Chey WD, Wong BC. American College of Gastroenterology guideline on the management of Helicobacter pylori infection. Am J Gastroenterol 2007; 102: 1808-25. Medline.
      4. Hernando-Harder AC, Booken N, Goerdt S et al. Helicobacter pylori infection and dermatologic diseases. Eur J Dermatol 2009. Medline.
      5. Wedi B, Kapp A. Helicobacter pylori infection in skin diseases: a critical appraisal. Am J Clin Dermatol 2002; 3: 273-82. Medline.

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      H. pylori Bacteria » Palmer General Surgeon

      H. pylori is a common type of bacteria that grows in the digestive tract and has a tendency to attack the stomach lining. It infects the stomachs of roughly 60 percent of the world’s adult population. H. pylori infections are usually harmless, but they’re responsible for the majority of ulcers in the stomach and small intestine.

      The “H” in the name is short for Helicobacter. “Helico” means spiral, which indicates that the bacteria are spiral shaped.

      H. pylori often infect your stomach during childhood. While infections with this strain of bacteria typically don’t cause symptoms, they can lead to diseases in some people, including peptic ulcers, and an inflammatory condition inside your stomach known as gastritis.

      H. pylori are adapted to live in the harsh, acidic environment of the stomach. These bacteria can change the environment around them and reduce its acidity so they can survive. The spiral shape of H. pylori allows them to penetrate your stomach lining, where they’re protected by mucus and your body’s immune cells are not able to reach them. The bacteria can interfere with your immune response and ensure that they’re not destroyed. This can lead to stomach problems.

      What causes H. pylori infections?

      It’s still not known exactly how H. pylori infections spread. The bacteria have coexisted with humans for many thousands of years. The infections are thought to spread from one person’s mouth to another. They may also be transferred from feces to the mouth. This can happen when a person does not wash their hands thoroughly after using the bathroom. H. pylori can also spread through contact with contaminated water or food.

      The bacteria are believed to cause stomach problems when they penetrate the stomach’s mucous lining and generate substances that neutralize stomach acids. This makes the stomach cells more vulnerable to the harsh acids. Stomach acid and H. pylori together irritate the stomach lining and may cause ulcers in your stomach or duodenum, which is the first part of your small intestine.

      What are the symptoms of H. pylori infection?

      Most people with H. pylori don’t have any symptoms.

      When the infection leads to an ulcer, symptoms may include abdominal pain, especially when your stomach is empty at night or a few hours after meals. The pain is usually described as a gnawing pain, and it may come and go. Eating or taking antacid drugs may relieve this pain.

      If you have this type of pain or a strong pain that doesn’t seem to go away, you should visit your doctor.

      A number of other symptoms may be associated with H. pylori  infection, including:

      • excessive burping
      • feeling bloated
      • nausea
      • heartburn
      • fever
      • lack of appetite, or anorexia
      • unexplained weight loss

      See your doctor immediately if you experience:

      • trouble swallowing
      • anemia
      • blood in the stool

      However, these are common symptoms that could be caused by other conditions. Some of the symptoms of H. pylori infection are also experienced by healthy people. If any of these symptoms persist or you’re concerned about them, it’s always best to see your doctor. If you notice blood or a black color in your feces or vomit, you should consult your doctor.

      How are H. pylori infections diagnosed?

      Your doctor will ask about your medical history and family history of disease. Be sure to tell your doctor about any medications you’re taking, including any vitamins or supplements. If you’re experiencing symptoms of a peptic ulcer, your doctor will likely ask you specifically about your use of NSAIDs, such as ibuprofen.

      Your doctor may also perform many other tests and procedures to help confirm their diagnosis:

      Physical exam

      During a physical exam, your doctor will examine your stomach to check for signs of bloating, tenderness, or pain. They’ll also listen for any sounds within the abdomen.

      Blood test

      You may need to give blood samples, which will be used to look for antibodies against H. pylori. For a blood test, a healthcare provider will draw a small amount of blood from your arm or hand. The blood will then be sent to a laboratory for analysis. This is only helpful if you have never been treated for H. pylori before.

      Stool test

      A stool sample may be needed to check for signs of H. pylori in your feces. Your doctor will give you a container to take home with you to catch and store a sample of your stool. Once you return the container to your healthcare provider, they will send the sample to a laboratory for analysis. This and the breath tests usually will require you to stop medications such as antibiotics and proton pump inhibitors (PPIs) before the test.

      Breath test

      If you have a breath test, you’ll swallow a preparation containing urea. If H. pylori bacteria are present, they will release an enzyme that breaks down this combination and will release carbon dioxide, which a special device then detects.


      If you have an endoscopy, your doctor will insert a long, thin instrument called an endoscope into your mouth and down into your stomach and duodenum. An attached camera will send back images on a monitor for your doctor to view. Any abnormal areas will be inspected. If necessary, special tools used with the endoscope will allow your doctor to take samples from these areas.

      What are the complications of H. pylori infections?

      • Inflammation of the stomach lining. H. pylori infection can irritate your stomach, causing inflammation (gastritis).
      • Stomach cancer. H. pylori infection is a strong risk factor for certain types of stomach cancer.

      How are H. pylori infections treated?

      If you have an H. pylori infection that isn’t causing you any problems and you aren’t at increased risk of stomach cancer, treatment may not offer any benefits.

      Stomach cancer, along with duodenal and stomach ulcers, is associated with H. pylori infection. If you have close relatives with stomach cancer or a problem such as a stomach or duodenal ulcer, your doctor may want you to have treatment. Treatment can cure an ulcer, and it may reduce your risk of developing stomach cancer.


      You will normally need to take a combination of two different antibiotics, together with another drug, such as a proton-pump inhibitor, that reduces your stomach acid. Lowering stomach acid helps the antibiotics work more effectively. This treatment is sometimes referred to as triple therapy.

      Treatment may vary depending on your past medical history and if you have allergies to any of these medications.

      After treatment, you will have a follow-up test for H. pylori. In most cases, only one round of antibiotics is needed to clear the infection, but you might need to take more, using different drugs.



      In areas of the world where H. pylori infection and its complications are common, doctors sometimes test healthy people for H. pylori.

      If you’re concerned about H. pylori infection or think you may have a high risk of stomach cancer, talk to your doctor. Together you can decide whether you may benefit from H. pylori screening.

      Lifestyle and diet

      There’s no evidence that food and nutrition play a role in preventing or causing peptic ulcer disease in people infected with H. pylori. However, spicy foods, alcohol, and smoking may worsen a peptic ulcer and prevent it from healing properly.

      Gastritis is when the lining of the stomach becomes inflamed or swollen.

      What is Gastritis?

      Gastritis is a condition where infections and conditions cause inflammation in the lining of your stomach. The stomach lining becomes inflamed or swollen and can have a variety of warning symptoms.

      • Indigestion
      • A burning or gnawing feeling in the stomach
      • Feeling full or bloated after eating
      • Nausea and vomiting
      • Belching
      • Loss of appetite
      • Upper abdominal pain or discomfort

      Causes of Gastritis:

      • Infection from bacteria such as Helicobacter pylori (H, pylori)
      • Excessive use of alcohol
      • Frequent use of pain relievers such as aspirin, ibuprofen, and naproxen
      • Long-term use of medications for acid reflux and indigestion
      • Chronic stress
      • Autoimmune disorders
      • Cocaine use
      • Recurring bile reflux from the small intestine
      • Diets high in fat and oil, especially saturated and trans fat
      • Smoking
      • Age – Your stomach lining thins as you age, making you more vulnerable to inflammatory infections

      Diagnosis of Gastritis

      If you are experiencing symptoms of gastritis for more than a week, you should seek help from one of the doctors at Digestive Care Physicians in Cumming, Alpharetta, Lawrenceville, or Johns Creek, GA. It could be possible that you are having internal bleeding if you experience dizziness, unexplained weakness, plaeness, black, tarring stools, red, fresh-looking blood in the stool, red blood in vomit or vomiting blood.

      One of the gastroenterologists at Digestive Care Physicians can use a wide range of tests and tools to give you an accurate diagnosis of your condition:


      Most gastritis medications focus on reducing the amount of acid in the stomach. Common acid reducing medications include:

      • Antacids. Antacids typically contain magnesium, calcium, sodium, or aluminum salts that can help neutralize stomach acids. Antacids can sometimes cause constipation or diarrhea and other side effects.
      • Proton-pump inhibitors (PPIs). These reduce the amount of acid the stomach produces. People can buy low-strength versions of lansoprazole and omeprazole over the counter, but most PPIs are only available on prescription.
      • h3 blockers. h3 blockers are antihistamines that can help reduce stomach acid production. Most types of h3 blockers are available in both over-the-counter and prescription strengths.

      Regardless of the cause or severity of symptoms, making dietary and lifestyle changes may help treat or reduce the symptoms.

      • Avoid or reduce alcohol consumption
      • Avoid spicy foods
      • Avoid rich, oily, or fried foods
      • Avoid acidic foods, especially citrus fruits and juices
      • Eat smaller meals but more frequently
      • Reduce salt consumption
      • Eat less red meat
      • quitting smoking
      • Drink lots of water and stay hydrated
      • Manage stress

      Chronic gastritis can cause pain and discomfort and lead to serious complications if left untreated. People should seek help from one of our board certified gastroenterologists at Digestive Care Physicians if they have symptoms of chronic gastritis. They have 4 locations north of Atlanta in Cumming, Alpharetta, Johns Creek, and Lawrenceville, GA.



      90,000 symptoms and treatment in adults, price in St. Petersburg

      In the absence of adequate treatment, gastritis adversely affects the patient’s quality of life. The digestion of food and the absorption of nutrients deteriorate, which affects the general condition of the body, the efficiency and activity of the patient. In severe cases, complications may develop (peptic ulcer, profuse bleeding, cicatricial deformities, fistulas, megaloblastic anemia, cachexia). Metaplasia of the epithelium is fraught with the formation of a malignant tumor (adenocarcinoma of the stomach).

      Causes of gastritis

      Gastritis develops as a result of exposure to several damaging factors at once. These include tissue ischemia, disorders of the motor and secretory functions of the stomach, contact of mucous membranes with aggressive substances. The following factors are capable of provoking active inflammation of the mucous layer:

      • Infections. 90% of gastritis cases are associated with Helicobacter pylori infection. Less commonly, inflammation occurs as a result of the activation of opportunistic microorganisms.
      • Chemicals. The gastric mucosa can become inflamed upon contact with toxic compounds, as well as while taking medications with ulcerogenic properties.
      • Chronic diseases of other organs of the digestive tract. In some cases, gastritis develops due to retrograde reflux of the contents of the duodenum and irritation with bile.
      • Neurohumoral disorders. The most striking example is the inflammation of the gastric mucosa due to microcirculatory disorders against the background of chronic stress.

      Predisposing factors are bad habits (smoking, alcohol consumption), systematic errors in nutrition (consumption of hot, sour, spicy foods, foods with extractive substances, soda), old age (due to thinning of the stomach walls).

      Symptoms of gastritis

      The main manifestation of inflammation of the gastric mucosa is pain. Unpleasant sensations are localized in the epigastric region, but can be given to the back and hypochondrium.The intensity of the pain syndrome depends on the activity of inflammation and the degree of destructive changes. So, with acute gastritis, the pain is bright, cutting. With chronic – dull, aching, pressing. Unbearable stabbing or burning pains indicate the development of complications.

      Acute inflammation is characterized by increased pain after a considerable time after eating. These are the so-called “hungry” and “night” pains. Chronic gastritis is characterized by increased pain immediately after eating. Other signs of gastritis are dyspepsia (heaviness, bitterness in the mouth, flatulence, stool disturbances), nausea, vomiting, lack of appetite, and aversion to certain foods.

      Types of gastritis

      Taking into account the clinical and morphological features of the course of the disease, the following forms of gastritis are distinguished:

      • By the nature of the flow. Gastritis is acute (bright manifestations, pronounced changes in the mucous membranes) and chronic (erased symptoms, sluggish inflammation).
      • By type of inflammatory reaction. Inflammation can be lymphocytic, allergic, granulomatous, hypertrophic, atypical.
      • By localization of inflammatory changes.Antral, fundic or pangastritis (extensive inflammation of the entire organ).
      • By origin. With an unclear etiology, a mixed origin of gastritis is most likely. With an autoimmune process, they speak of type A gastritis, with an infectious – type B, chemical – type C.
      • For the safety of the secretory function. Hyperacid, hypoacid or normacid form.
      • By morphological changes in the mucosa. Gastritis can be catarrhal (the most common variant), fibrinous, erosive, phlegmonous, atrophic.

      Diagnostics of gastritis

      With signs of gastritis, you should consult a gastroenterologist. Diagnosis begins with collecting complaints, medical history and physical examination. To assess the general condition of the body and identify possible causes of the disease, general clinical laboratory tests are prescribed. To examine the gastric mucosa and accurately diagnose, an endoscopic examination of the stomach and duodenum (EGD) is performed, and a biopsy of the mucosa is performed. Without fail, the patient takes a test for Helicobacter pylori (respiratory urease test).

      How is the treatment for gastritis of the stomach?

      Depending on the form of the disease and the risk of complications, gastritis is treated in a hospital or on an outpatient basis. An integrated approach implies giving up bad habits, correcting diet. Drug therapy includes antibacterial drugs, antisecretory drugs, drugs to restore the mucous membrane and its protective properties, as well as drugs to correct symptoms.

      In the treatment of chronic gastritis, diet and lifestyle play a special role.It is advisable to exclude stress, bad habits, to normalize the qualitative and quantitative composition of the diet, taking into account the activity of the secretory function of the stomach. With a lack of hydrochloric acid, replacement therapy is indicated.

      Which clinic should I go to for the treatment of gastritis?

      Gastroenterologists of the MEDIONA PARNAS Medical Center successfully diagnose and treat all clinical forms of gastritis. The center has advanced equipment for a comprehensive examination of patients in the shortest possible time.The tactics of treating gastritis and preventing relapse are selected strictly on an individual basis.

      How much does gastritis treatment cost?

      Prices for the treatment of gastritis and other medical services in the multidisciplinary center “MEDIONA PARNAS” can be found by phone, during a personal visit to the clinic, or viewed on the website.

      Get rid of stomach pain – sign up for a consultation with the gastroenterologists of the MEDIONA PARNAS center at your convenience!

      H.pylori as a major cause of gastric carcinogenesis

      CM. Tkach, MD, DSc, Professor, National Medical University named after V.I. A.A. Bogomolets, Kiev

      One of the most common sites of cancer in both men and
      women is the stomach. Among all malignant neoplasms, stomach cancer
      (RJ) ranks second in frequency of occurrence in the world.

      In 2002, the number of new cases and deaths from gastric cancer, according to the database
      International Agency for Research
      on Cancer, IARC) Globocan, was estimated at 933 thousand and 699 thousand, respectively. By
      Gastrointestinal cancers in Europe (M.R. Keighley, 2003), annually
      in Europe, about 200 thousand new cases of gastric cancer are diagnosed, which are responsible
      for almost 150 thousand deaths a year. In Ukraine, RJ for the first time every year
      diagnosed in about 13 thousandpatients, and in 61.8% of them – in III and IV
      stages; within a year, 58.1% of patients with newly diagnosed gastric cancer die.
      In total, about 34 thousand patients with gastric cancer are registered in Ukraine.
      It has now been proven that the most important risk factor for gastric cancer and one of the main
      factors of gastric carcinogenesis is H. pylori infection. Frequency
      H. pylori infection of the population is 74% of the population in developing and
      58% in developed countries. In 2002, 590 thousand people were recorded.cases of gastric cancer,
      caused by H. pylori infection (5.5% of all cancers in the world), that is
      it is the most common malignant tumor caused by an infectious factor
      (slightly more than the number of malignant tumors arising from
      exposure to human papillomavirus). H. pylori infection is practically
      the only risk factor, the impact on which can actually reduce
      risk of developing noncardiac gastric cancer.
      H. pylori is the first bacterium to be classified by the International
      by the WHO Cancer Research Agency as a definite carcinogen due to its
      epidemiological relationship with gastric adenocarcinoma and gastric MALT lymphoma (mucosa-associated
      lymphoid tissue lyphoma). H. pylori infection refers to “slow” infections,
      that is, there are many years before it leads to the development of atrophic
      gastritis and intestinal metaplasia, which increase the likelihood of developing cancer or lymphoma
      stomach. The results of prospective studies indicate that in patients
      infected with H. pylori, the risk of gastric cancer is increased by 3-6 times. Hypothetical
      cascade of a sequence of events leading ultimately to development
      adenocarcinoma of the stomach, proposed by R.Correa about 15 years ago, now
      time is generally accepted. According to him, within 30 years, 50%
      those infected with H. pylori will develop atrophy of the gastric mucosa, 40% –
      intestinal metaplasia, 8% – dysplasia and 1-2% – gastric adenocarcinoma.
      The likelihood that an infected subject will develop gastric cancer depends on the whole
      a number of factors (Fig.). In deciphering the molecular genetic basis of these factors
      significant progress has been made in recent years.

      Phenotypes of those infected with H. pylori
      Based on clinical positions, the probability of developing H. pylori-induced gastric cancer
      largely depends on the phenotype of the lesion of the gastric mucosa
      develops in an infected subject. Currently identified three
      the main phenotype of H. pylori-induced gastritis, each of which is associated with
      a number of pathophysiological abnormalities that can explain why there is
      one or another clinical outcome.
      The most common phenotype that can be called simple, or
      benign, gastritis, characterized by moderate pangastritis with
      a slight violation of the secretion of gastric acid. This phenotype is usually
      observed in patients in whom the disease is asymptomatic and for
      life does not develop any serious pathology of the stomach.
      The second phenotype is the so-called duodenal ulcer phenotype, which is observed in
      about 15% of infected patients.Patients with this phenotype are characterized by
      severe inflammation in the antrum of the stomach, high levels of gastrin,
      relatively healthy gastric body mucosa and very high production
      of hydrochloric acid. This combination of pathophysiological abnormalities contributes to
      the development of peptic ulcers, especially duodenal and prepyloric.
      The third and prognostically most serious phenotype is the gastric cancer phenotype, which
      characterized by the predominance of gastritis of the body of the stomach, multifocal
      gastric atrophy, hypo- or achlorhydria.These deviations that take place
      in about 1% of infected patients, develop as a direct result
      chronic inflammation caused by infection and increase the risk of gastric cancer. Phenotype of gastric cancer
      especially common in certain regions of Asia where this malignant
      swelling is a common condition. Physiologically, it is characterized by low
      acid secretion, high gastrin and low
      pepsinogen I and pepsinogen I / pepsinogen II ratios.The most intriguing
      aspect is that patients who develop duodenal ulcers,
      are actually protected from the development of gastric cancer, that is, these two outcomes are mutually
      exclusive. Thus, H. pylori infection can result in several
      different clinical outcomes. An explanation of this paradox is necessary for
      understanding the pathogenesis of H. pylori-associated diseases in general and stomach cancer
      in particular.

      Main factors of H. pylori virulence
      Complete decoding of the H. pylori genome.pylori has shown that for different strains of this
      bacteria are characterized by specific regions of DNA. Therefore, some
      strains may be more oncogenic than others. Genetic polymorphism
      includes the islet of pathogenicity cag and its effector CagA, which improves adhesion
      bacterial agent with cells containing Lewis antigen, and enhances
      tissue damage. CagA-protein introduced into the cell by the bacterial agent
      triggers inflammation and is associated with the VacA cytotoxin.Among the sick
      infected with a CagA-positive strain, atrophic gastritis is more common,
      they have a higher level of IgG antibodies against H. pylori than CagA-negative
      VacA is a pore-forming cytotoxin. As with most H. pylori factors,
      there is significant genetic diversity in the VacA gene, and therefore
      the activity of different alleles of the toxin differs in their cytotoxicity. Recent
      studies examining the potential effects of VacA on the immune system,
      showed that in vitro VacA is a very potent inhibitor of activation
      T cells.The role of VacA in vivo is not fully understood. VacA is thought to help H.
      pylori receive nutrients by damaging the epithelial barrier or causing
      passage of small molecules through cell membranes. It is also possible that his
      the main role is to suppress the T-cell immune response, although there was no
      it has been reliably established whether VacA penetrates sufficiently for this purpose

      CagA and cag – an islet of pathogenicity of the type 4 secretory system
      CagA is a protein from H.pylori, which was originally identified as a marker
      diseases, since in part of the population with antibodies to this protein,
      a higher prevalence of both peptic ulcer and
      adenocarcinoma of the stomach. Most of the studies carried out have shown that when
      the presence of this protein in H. pylori, the relative risk of such diseases
      increases 2-3 times, and some data indicate an increased risk of cancer
      stomach with CagA + H. pylori infection by 28.4 times.CagA + strains of H. pylori also
      associated with more severe inflammation, cell proliferation, metaplasia
      gastric mucosa.
      The first significant breakthrough in the study of CagA was the realization that its gene
      is part of a large so-called pathogenicity island (cag PAI) –
      the region of horizontally acquired DNA, which is embedded in the genome more
      virulent strains of H. pylori. It is hypothesized that H. pylori PAI cag may
      serve as a new transport system for the secretion of virulent factors.Next
      an important breakthrough in understanding the function of CagA came when researchers noted
      that, upon contact with gastric cancer cells in culture, some H.
      pylori are capable of causing significant cytoskeletal rearrangements and changes
      cell shapes, and these changes are associated with tyrosine phosphorylation of some
      proteins. This was a surprising find as it implied that CagA could
      be transferred into the cytoplasm of the host cell and can interact with
      tyrosine kinases inside them. Interestingly, the cellular enzymes responsible for
      phosphorylation of CagA are known oncogenes. CagA also affects
      control of the cell cycle and stimulates the invasive ability of epithelial
      cells by activating the matrix of metalloproteinases. All of these phenotypic effects
      CagA and the molecules with which it interacts are associated with carcinogenesis and
      transmission of impulses during wound healing, which suggests numerous
      mechanisms of realization of the role of CagA in the development of peptic ulcer disease and gastric cancer.
      In addition to the direct effect of CagA on epithelial synapses, factor impulse transmission
      growth and cytoskeleton, CagA also has a pronounced pro-inflammatory effect.
      H. pylori infection has been found to induce a strong inflammatory response,
      which is accompanied by the expression of chemokines that attract neutrophils (in
      in particular, IL-8). It has also been shown that the CagA protein can activate nuclear
      transcription factor kB (NF-kB) through independent mechanisms leading to activation
      pro-inflammatory signals and secretion of IL-8. An intriguing recent find consists of
      in that cag PAI by activating NF-kB can also cause cumulation of mutations.
      In studies on cell cultures, it was shown that cag PAI + strains of H. pylori
      cause the expression of a DNA-transformed enzyme, which leads to the accumulation
      mutations in the p53 tumor suppressor.
      Thus, the detection of CagA, a factor of H. pylori pathogenicity,
      a pronounced effect on the epithelium is, of course, an outstanding discovery.
      However, despite all the pathogenic properties of CagA, in most people,
      the epithelium of the digestive tract which is daily exposed to
      CagA + strains of H.pylori do not develop clinical manifestations of the disease, and those who
      for whom this actually occurs, the effects of CagA “accumulate” over the course of
      long period. Therefore, we still have to understand under what conditions
      CagA signals become pathogenic. Given the link between CagA and cancer development,
      of considerable interest is the question of whether CagA is delivered to
      precursor cells in the mucous membrane, in which processes are then disrupted
      differentiation. It is also important to investigate how exposure to CagA can change
      epithelium at different stages of infection.For example, what effect does
      CagA on the mucous membrane of the stomach of a healthy person and the stomach of a patient with
      atrophic gastritis, where there are already changes in the cellular composition of the glands?
      Many important questions still await study.

      Role of host genetic factors in H.
      As noted above, H. pylori causes damage, initiating chronic
      inflammation in the stomach lining. This inflammation is mediated by many
      pro- and anti-inflammatory cytokines.Genetic polymorphism directly
      affects changes in the intensity of the cytokine response, and depend on this
      definitive clinical consequences in humans. It is assumed that in the case
      H. pylori infections, the most relevant candidate genes are those
      whose products are involved in the management of innate and acquired immune
      responses to H. pylori infection and which mediate subsequent inflammation.
      Since this list of candidate genes is extensive, the initial search focused on
      on genes that were most related to the physiology of the stomach, in particular to
      secretion of gastric acid.
      As previously mentioned, H. pylori gastritis is associated with three
      the main phenotypes that are closely correlated with clinical outcomes:
      phenotype of duodenal ulcer, benign phenotype and phenotype of gastric cancer.
      Studies have shown that pharmacological inhibition of hydrochloric acid production
      acid in the stomach can lead to a change from the predominance of antrum
      gastritis (duodenal ulcer phenotype) to the prevalence of fundic gastritis with
      the development of gastric atrophy (gastric cancer phenotype).Thus, it became clear that
      there is a regulated endogenous agent that, in the presence of H. pylori
      has a pronounced pro-inflammatory effect, and is also an inhibitor
      acid production and the most appropriate host genetic factor,
      to be learned. The IL-1β gene is one of the earliest and most important
      proinflammatory cytokines in the context of H. pylori infection, it is also the most
      a strong known inhibitor of acid production.

      Role of IL-1 gene cluster polymorphism in H.pylori

      El-Omar et al. showed that the proinflammatory polymorphism of the IL-1 gene cluster
      (IL-1B encodes IL-1β, and IL-1RN encodes its receptor antagonists) increases
      risk of gastric cancer and precancerous changes in the presence of H. pylori. People with
      genotypes IL-1B-31 * C or 511 * T and IL-1RN * 2 / * 2 are at higher risk
      development of hypochlorhydria and gastric atrophy in response to H. pylori infection. For them
      also characterized by a 2-3-fold increase in the risk of malignancy compared with
      patients who have fewer pro-inflammatory genotypes.
      In addition, pro-inflammatory IL-1 genotypes increase the risk of intestinal and
      diffuse types of gastric cancer, but this risk is limited to noncardiac localization of the tumor.
      Indeed, IL-1 markers do not affect the risk of developing adenocarcinoma of the cardia.
      stomach, esophageal adenocarcinoma or esophageal squamous cell carcinoma.
      The latest data are fully consistent with the proposed mechanism of influence of this
      polymorphism on the development of gastric cancer, namely, a decrease in the secretion of gastric acid.A high level of the IL-1β genotype increases the risk of noncardiac gastric cancer – a disease,
      characterized by hypochlorhydria, but does not affect cancers associated with
      exposure to high levels of acidity, such as esophageal adenocarcinoma
      and some types of cardia cancer. Interestingly, a high level of pro-inflammatory
      genotypes IL-1β “protects” against the development of erosive and non-erosive esophagitis:
      suggest that this effect is realized by reducing acidity
      gastric juice due to the induction of atrophy of the mucous membrane of the body of the stomach.
      Association between IL-1 and GC gene cluster polymorphism and precancerous
      conditions has been independently confirmed by other studies including individuals
      Caucasians, Asians and Hispanics.
      Three meta-analyzes published to date indicate a role for IL-1
      proinflammatory genotype in the development of gastric cancer. The authors of two of them concluded that
      proinflammatory IL-1 genotypes increase the risk of this
      diseases.These results indicate that IL-1β is a key
      cytokine in the pathogenesis of H. pylori-induced gastric cancer and precancerous conditions, and
      changes in its genotype act as genetic factors of the host organism,
      mediating this effect.

      Role of other cytokine gene polymorphisms
      Soon after it was identified that the accumulation of polymorphisms
      genes IL-1 is a risk factor for gastric cancer, have been identified
      pro-inflammatory genotypes of tumor necrosis factor a (TNFα) and IL-10 as
      independent additional risk factors for noncardinal gastric cancer.
      TNFα is another potent pro-inflammatory cytokine that is produced in
      gastric mucosa in response to H. pylori infection. Like IL-1β, it has
      acid-lowering effect, but weaker. It is known that TNFα-308 polymorphism G> A
      involved in many stages of inflammation. Transfer of the pro-inflammatory TNFα allele
      increases the risk of noncardiac gastric cancer by 2. 2 times. The role of TNFα G> A polymorphism in gastric cancer
      was independently confirmed by the study by Machado et al.
      IL-10 is an anti-inflammatory cytokine that reduces the level of IL-1β, TNFα,
      interferon-7 and other pro-inflammatory cytokines.Relative deficiency of IL-10
      can lead to a hyperinflammatory Th2 response when infected with H. pylori,
      which is accompanied by severe damage to the gastric mucosa and
      increases the risk of noncardiac gastric cancer by 2.5 times.
      El-Omar et al. studied the effect of increasing the number of pro-inflammatory
      genotypes (IL-1β-511 * T, IL-1RN * 2 * 2, TNFα-308 * A and IL-10 ATA / ATA) for the risk of developing
      RJ. The risk progressively increased in such a way that the presence of three or
      four of these polymorphisms increased the likelihood of gastric cancer by 27 times.The fact that H.
      pylori is a prerequisite for the association of these polymorphisms with
      malignancy, demonstrates that in this situation, inflammation really leads
      to carcinogenesis.
      Another important cytokine that plays a central role in pathogenesis
      disease caused by H. pylori is IL-8. This chemokine is powerful
      chemoattractive agent for neutrophils and lymphocytes. It also provides
      impact on cell proliferation, migration and tumor angiogenesis.The gene has
      well-established polymorphism of the promoter at position 251 (IL-8-251 T> A).
      Allele A is associated with increased IL-8 production in H. pylori infected
      the mucous membrane of the stomach. Its role in increasing risk has also been identified.
      severe inflammation and precancerous gastric changes in Caucasian and
      Asian race. However, the same polymorphisms could increase the risk of gastric cancer in some
      Asian populations and have no effect on Caucasians at all.

      The role of innate immune response gene polymorphism
      Genetic polymorphism of inflammatory cytokines plays an important role in
      development of H. pylori-induced gastric adenocarcinoma. However, initially
      the innate immune system responds to H. pylori infection. It is likely that
      functionally significant polymorphism in the genes of this part of the immune system can
      influence the magnitude and subsequent direction of the immune response
      host against infection.Most H. pylori cells do not invade the mucosa
      the lining of the stomach. In this case, the inflammatory response is caused by the addition of H. pylori
      to the epithelium of the stomach. Toll-like receptor type 4 (TLR4) that binds to
      the lipopolysaccharide component of the cell wall of gram-negative bacteria was
      originally identified as a potential signaling receptor for H.
      pylori on gastric epithelial cells.
      Hold et al. hypothesized that the TLR4 + 896A> G polymorphism is associated with
      excessive and destructive chronic inflammatory phenotype in subjects,
      infected with H.pylori. This phenotype is characterized by gastric atrophy and
      hypochlorhydria – signs of an increased risk of gastric cancer. In a recent study by Hold
      et al. tested the effect of this polymorphism on H. pylori-induced
      gastric phenotype and risk of developing precancerous and cancerous conditions. Authors
      assessed the relationship of precancerous changes in the stomach in relatives of patients with gastric cancer,
      including those diagnosed with hypochlorhydria and gastric atrophy.
      Currently, there is a widespread point of view that subjects with full
      pro-inflammatory genetic structure based on a combination of markers
      adaptive and innate immune systems (such as IL-1β, TNFα, IL-10, IL-8,
      TLR4) respond to H.pylori, creating an environment inside the stomach,
      which is characterized by chronic inflammation and low acidity. This
      the environment promotes the growth of other bacteria within the stomach, maintaining
      inflammation and oxidative / genotoxic stress. Subjects with such
      proinflammatory polymorphisms can respond in the same way to others (non-H.
      pylori) bacteria, thus supporting the neoplastic process. It may
      explain why the last stages of gastric carcinogenesis do not require
      presence of H. pylori and why this microorganism is absent in tumor tissue

      Thus, numerous studies of recent years are convincing
      indicates that H. pylori infection, especially cytotoxic strains,
      is one of the leading causes of the development of noncardiac gastric cancer. In the presence of
      certain genetic factors of the host H. pylori triggers a cascade of reactions,
      initiating acute and chronic inflammation followed by atrophic
      gastritis, hypochlorhydria and continuous genotoxic stress.Enhancement
      Intraluminal gastric pH and emerging intragastric alkaline shift
      promote overgrowth in the stomach of anaerobic bacteria producing
      nitrosocomponents with pro-carcinogenic activity. Under the influence
      induced by NO synthase, nitrites (NO2) are transformed into NO with the formation
      potential N-nitroso mutagens. This chain reaction leading to
      endoluminal formation of carcinogens and disruption in the cellular genome,
      inhibited by antioxidants; in particular, it explains the preventive action
      ascorbic acid.
      As noted above, H. pylori infection is now practically
      the only risk factor, the impact on which can actually reduce
      risk of developing noncardiac gastric cancer. It is believed that H. pylori eradication with early
      detection of atrophy of the gastric mucosa can subsequently significantly
      reduce the risk of developing gastric cancer. Several controlled studies have already
      demonstrated that eradication of H. pylori can lead to regression of atrophy
      and intestinal metaplasia, although publications remain controversial.Given the very
      close correlation between H. pylori atrophic gastritis and gastric cancer, the latter
      European guidelines for the management of H. pylori-infected patients
      (Maastricht Consensus 2-2000 and 3-2005) still consider atrophic
      gastritis is among the definitively proven indications for the eradication of this
      microorganism. In the Maastricht Consensus 3-2005 on the prevention of gastric cancer
      a whole section is devoted to the eradication of H. pylori. It is noted that H. pylori –
      it is the most proven risk factor for noncardiac gastric cancer (evidence level
      A).Noncardiac adenocarcinoma is associated with H. pylori on average in 71%
      cases, and H. pylori eradication prevents the development of preneoplastic
      changes in the gastric mucosa, if it is reached to the hypothetical “point
      no return ”, which appears to be dysplasia (level A).
      Eradication of H. pylori for the prevention of gastric cancer can be economically beneficial
      (Level B) although further global research is required. Anyway
      it is necessary to develop new strategies for screening for gastric cancer and to look for new drugs.
      Of course, the Screen & treat strategy of screening tests
      large populations of people (usually by serological diagnosis of H. pylori),
      could provide more benefits for all mankind if its application
      today would not be limited by the existing disadvantages of eradication therapy
      and financial capabilities. The most important obstacle to strategy implementation
      universal screening and treatment is a rather complex standard regimen
      eradication with a significant possibility of failure in treatment, the development of side
      effects and resistance of H. pylori infection to antibacterial drugs.
      Two experimental H. pylori vaccines have been developed: one with
      using recombinant produced genetically modified E. coli,
      the other with VacA toxin. It is possible that large-scale vaccination against
      H. pylori could be a cost-effective strategy for the prevention of gastric cancer.
      In conclusion, we emphasize once again that the majority of scientists around the world recognize H.
      pylori as a cardinal factor in gastric carcinogenesis and are unanimous in their
      opinion that further research in this area will help to destroy
      such a global lethal malignant tumor as gastric cancer.



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      General description

      Gastritis is an inflammation of the gastric mucosa, leading to a violation of its function, especially secretory. If a person has gastritis, the incoming food is poorly processed, which leads to a violation of the absorption of nutrients for the human body.

      About 60-85% of the world’s population suffers from chronic gastritis, especially at a young age from 18 to 35 years. In connection with the modern rate of urbanization, gastritis began to occur more often in children from 8 to 13 years old.

      Gastritis is also divided in relation to the secretion of hydrochloric acid into:

      • Gastritis with hypoacid stomach
      • Gastritis with normal stomach acidity
      • Gastritis with increased acidity of the stomach

      Due to the presence of a certain type of gastritis in a person, different groups of drugs will be prescribed.

      Causes of gastritis of the stomach

      Due to the occurrence, they are divided: acute and chronic gastritis.

      Acute gastritis is an acute inflammation of the gastric mucosa when exposed to an irritant, that is, the ingestion of chemically active substances (acids, alkalis) into the stomach, taking medications (NSAIDs), poisoning with poor-quality food and / or contaminated with infected microorganisms.

      The emergence and development of chronic gastritis is influenced by many factors.The main ones are exogenous.

      Exogenous factors are:

      • The presence in the stomach of bacteria such as Helicobacter pylori, which are the main etiological factor in the onset of chronic gastritis. Influence of other bacteria not proven
      • Violation of power supply
      • Alcohol and tobacco abuse
      • Long-term use of drugs affecting the gastric mucosa, the main of them: NSAIDs and glucocorticosteroids (prednisolone)
      • Emotional stress, stress

      Along with exogenous factors, there are also internal factors (endogenous) that contribute to the onset of chronic gastritis:

      • Genetic predisposition
      • Duodenogastric reflux
      • Endogenous intoxication
      • Chronic infectious diseases
      • Metabolic disorders
      • Hypoavitaminosis
      • For other diseases of the gastrointestinal tract, for example, chronic pancreatitis, chronic cholecystitis, which reflexively affect the gastric mucosa

      Symptoms of gastritis

      • Aching or cramping pains of low intensity in the epigastric region, more often occurring on an empty stomach or immediately after eating
      • Constant heartburn, especially at night and morning hours, sour belching
      • Nausea, rarely vomiting of gastric contents
      • Belching air, sour or bitter taste
      • Severity in the epigastric region after eating, a feeling of rapid filling of the stomach
      • Bad taste in the mouth, bitterness
      • Decreased appetite


      • General clinical analysis of blood, urine
      • Analysis of feces for coprogram
      • Biochemical blood test (liver function tests, cholesterol, alkaline phosphatase)
      • ECG
      • X-ray of the chest organs in 2 projections
      • X-ray of the esophagus, stomach with barium mixture
      • Ultrasound of the hepatobiliary system
      • Daily monitoring of pH in the lower part of the esophagus and stomach
      • EGDS
      • Non-invasive tests for the determination of Helicobacter pylori (respiratory)

      Treatment of gastritis

      The main treatment for chronic gastritis consists of adhering to a healthy lifestyle and proper balanced nutrition.

      Maintaining a healthy lifestyle and proper rational nutrition consists of:

      • Refusal to consume alcoholic, strongly carbonated drinks
      • Weight loss with obesity
      • Quitting smoking
      • Avoiding large meals and late hours

      If these non-drug treatments do not bring relief, drugs are used.

      It is recommended to start treatment already at the first signs of inflammation in the stomach.

      The following drugs are used:

      • Prokenetics (help accelerate the movement of the food bolus from the esophagus into the stomach, then into the duodenum, increase the tone of the lower esophageal sphincter) – Domperidone (Motilak, Motilium), Itoprid (Ganaton)
      • Antisecretory drugs (help suppress the secretion of hydrochloric acid) – proton pump inhibitors (Omeprazole, Pantoprazole, Esomeprazole, Rabeprazole)
      • Antacids (Phospholugel, Almagel, Gaviscon)
      • Belching air, sour or bitter taste

      In case of detected contamination of the gastric mucosa H. pylory, an antibacterial regimen is used.

      The treatment regimen is selected individually in accordance with the patient’s condition and concomitant diseases.

      There are several standard treatment regimens:

      • Antibiotics (penicillin series: amoxicillin, macrolides – clarithromycin).
      • Proton pump inhibitors (omeprazole, rabeprazole, esomeprazole, pantoprazole)
      • Bismuth preparations (novobismol, de-nol)

      Chronic gastritis and the risk of developing stomach cancer

      Stomach cancer is one of the diseases arising from chronic gastritis – inflammation of the stomach lining.The most common cause of chronic gastritis is infection with the bacteria Helicobacter pylori (hereinafter, H. pylori). In turn, the incidence of cancer of the gastric mucosa, which is not affected by H. pylori, is only 1% or less. Therefore, if these harmful bacteria are eliminated, the incidence of stomach cancer will decrease. That is why, in February 2013, within the framework of medical insurance in Japan, a program of eradication therapy (i. e. treatment aimed at eliminating harmful bacteria) began, which began to be used in people with chronic gastritis caused by H.pylori. Prior to the introduction of this program, eradication therapy under health insurance was carried out only in patients with stomach cancer, gastric and duodenal ulcers, and in people with blood disease associated with infection with Helicobacter pylori.

      Therefore, those people who underwent a physical examination or simply EGD in the past, especially those who were diagnosed with atrophic or chronic gastritis, are recommended to be checked for the presence of Helicobacter pylori, since it is possible that at that time the diagnosis of this infection was not yet included in the examination program …

      Chronic gastritis caused by Helicobacter pylori is also called atrophic gastritis. Atrophy (thinning) of the gastric mucosa can begin at the age of 20 and in a few years will spread to the entire mucous membrane. Approximately 10% of people with atrophy have a risk of developing stomach cancer after 10 years, which increases over the years. That is why such an examination as EGD is an extremely important diagnostic method, which allows not only detecting cancer, but predicting the risk of developing cancer based on the degree of atrophy of the gastric mucosa.With a high degree of atrophy of the gastric mucosa, it is important to be observed with EGD once a year, so that it is possible to detect cancer at the earliest stage.

      In addition, H. pylori eradication therapy has the potential to reduce the risk of stomach cancer. The reports state that “in patients who received eradication therapy after treatment for early gastric cancer, compared with patients who did not receive this therapy, only 1/3 of patients developed a relapse of gastric cancer within 3 years. “.Unfortunately, it is impossible to reduce the risk of developing stomach cancer to 0% by just killing the pylori bacteria, but it is possible to prevent the disease, so we urge you to actively use this type of treatment as a preventive measure.

      Source: Raffles Japanese Clinic


      Gastritis is a group of diseases, the common feature of which is inflammation of the gastric mucosa.

      This is most often associated with an infection with the bacterium Helicobacter pylori, which is also the cause of stomach ulcers.Alcohol abuse or prolonged use of pain relievers can contribute to the development of gastritis.

      Gastritis can occur suddenly and pass quickly (acute gastritis) or develop gradually and persist for a long time (chronic gastritis). In rare cases, it leads to ulcers and is a factor that increases the risk of stomach cancer. However, it is usually asymptomatic and does not require treatment.

      Synonyms Russian

      Acute gastritis, chronic gastritis.

      English synonyms

      Chronic gastritis, acute gastritis.


      Chronic gastritis is most often asymptomatic, but sometimes it manifests itself as follows:

      • pain or discomfort in the upper abdomen,
      • nausea, vomiting,
      • burning or aching pain in the upper abdomen, heaviness, bloating,
      • a feeling of fullness in the abdomen, quick satiety.

      In most cases, these symptoms should be regarded as manifestations of functional dyspepsia in the absence of organic diseases of the gastrointestinal tract.

      Acute gastritis is usually accompanied by severe abdominal pain, nausea and vomiting.

      General information about the disease

      Gastritis is a group of diseases, the common feature of which is inflammation of the gastric mucosa.

      The stomach is a sac-shaped organ located in the upper abdomen behind the lower ribs.It serves as a “reservoir” for incoming food and produces juice for digestion.

      Gastritis occurs when the balance between the effects of hydrochloric acid and the protective factors of the mucous membrane is disturbed. This is due to various reasons: the presence of bacteria and toxins secreted by them, alcohol intake, pain relievers. As a result, inflammation of the gastric mucosa develops.

      Gastritis is acute and chronic.

      1. Acute gastritis is a rapidly developing inflammation that resolves within a short period of time.Most often it is caused by infection with the bacterium Helicobacter pylori and is asymptomatic, sometimes becoming chronic.

      Also a common cause of acute gastritis is the consumption of large amounts of alcohol, the abuse of painkillers (aspirin, ibuprofen, etc.).

      2. Chronic gastritis develops gradually. It affects about 80-90% of the adult population.

      Chronic gastritis is characterized by inflammation of the gastric mucosa at the cellular level, which can only be established under a microscope.Over time, the mucous membrane becomes thinner (atrophies), as a result of which the production of gastric juice decreases.

      There are two main forms of chronic gastritis.

      1. Gastritis caused by the bacterium Helicobacter pylori (95% of all cases of chronic gastritis). Once in the stomach, it contributes to the development of chronic inflammation, eventually leading to thinning of the mucous membrane. However, in most people, the H. pylori bacteria does not cause any symptoms.

      2. Autoimmune gastritis.Its development is associated with autoimmune mechanisms. In this case, the body produces antibodies to its own cells of the gastric mucosa, which leads to their damage. As a result, the production of hydrochloric acid decreases and the gastric mucosa becomes thinner.

      In a healthy body, the gastric mucosa produces a protein necessary for the absorption of vitamin B12, which plays an important role in the formation of red blood cells. With a lack of B 12 , B 12 develops – deficient anemia.

      Autoimmune gastritis develops very slowly and is usually detected in old age.

      Who is at risk?

      • Helicobacter pylori infected with the bacterium make up more than half of the world’s population.

      It should be noted that this bacterium is only one of the causes of gastritis; additional factors are often decisive: smoking, alcohol consumption, painkillers.

      • Those who regularly use pain relievers: aspirin, analgin, nise, ibuprofen, etc.
      • Alcohol abusers.
      • Those who have undergone severe stress, for example, after undergoing surgery, trauma, burns and severe infections.
      1. Patients with autoimmune diseases such as B 12 – deficiency anemia, inflammatory bowel disease, autoimmune thyroiditis.


      The diagnosis of “chronic gastritis” can be made only on the basis of the results of examining a piece of the gastric mucosa under a microscope.

      Since the most common cause of gastritis is the bacterium Helicobacter pylori, first of all, its presence in the body is determined.

      Detection of Helicobacter pylori infection

      • Helicobacter pylori, IgA, Helicobacter pylori, IgG – detection of antibodies to this bacterium. The results of this study are highly reliable, however, it is not used to assess the effectiveness of treatment, since antibodies to Helicobacter pylori persist for a long time after getting rid of it.
      • Helicobacter pylori, DNA, – determination of bacterial DNA in feces.
      • Respiratory urease test. This study is highly sensitive and specific. Helicobacter pylori in the process of life forms a lot of urease (a special enzyme). During the test, the subject drinks a liquid containing radioactive carbon. Helicobacter breaks down the substances contained in the liquid, forming carbon dioxide exhaled by a person. Accordingly, the presence of labeled carbon in the exhaled carbon dioxide indicates that a person is infected with the Helicobacter bacterium.

      A negative test result for Helicobacter may indicate that a person is not infected. With additional symptoms, endoscopy is prescribed.

      • Endoscopy (FGDS – fibrogastroduodenoscopy). A hollow tube equipped with a lens is inserted through the esophagus into the stomach. During the EGD, a biopsy is performed – taking pieces of tissue from the gastric mucosa for subsequent study, during which Helicobacter can be identified, in addition, the nature of the inflammation and the type of gastritis can be determined.

      Tests confirming the diagnosis of autoimmune gastritis

      • Complete blood count. For gastritis caused by Helicobacter pylori, changes in the general blood count are uncommon. With autoimmune gastritis associated with B 12 deficiency anemia, the hemoglobin level can be reduced, the average erythrocyte volume (MCV) increased, and the hemoglobin content in the erythrocyte (MCN) increased.
      • Pepsinogen I, pepsinogen II. Pepsinogen is produced by the cells of the gastric mucosa.A decrease in its level indicates atrophy (thinning) of the gastric mucosa, which is typical for advanced cases of chronic gastritis.
      • Gastrin is a hormone produced by stomach cells to stimulate the production of gastric juice by mucosal cells. With autoimmune gastritis, its concentration increases significantly.
      • Antibodies to parietal cells of the stomach. In autoimmune diseases, antibodies to parietal cells damage the stomach lining. Their level in autoimmune gastritis rises almost always.
      • Vitamin B 12 . A decreased level of vitamin B 12 in the blood indicates B 12 – deficiency anemia associated with autoimmune gastritis.
      • Endoscopy (FGDS) with biopsy. In the course of examining the cells of the gastric mucosa under a microscope, changes characteristic of chronic autoimmune gastritis are revealed.


      Treatment of gastritis depends on its cause.

      In case of acute gastritis caused by alcohol abuse or pain relievers, it is necessary to give them up.

      Chronic gastritis caused by the bacterium Helicobacter can be cured by killing the bacteria when:

      • There are symptoms of illness that cause discomfort,
      • there is a hereditary predisposition to the development of stomach cancer,
      • the patient is forced to regularly take painkillers and anti-inflammatory drugs.

      The bacterium is destroyed by a course of antibiotics within 10-14 days. To assess the success of therapy, a repeated analysis for the Helicobacter bacterium is required.

      In most cases, gastritis treatment also involves taking medications that reduce the production of hydrochloric acid and help heal the stomach lining.


      At the moment, no methods have been developed to prevent gastritis.

      Recommended analyzes

      90,000 Chronic gastritis – MyPathologyReport.ca

      What is chronic gastritis?

      Chronic gastritis means inflammation of the stomach lining.The inflammation damages the foveolar cells in the epithelium, which interferes with the normal functioning of the stomach.


      The stomach is part of the gastrointestinal tract. When we eat, food enters the mouth and travels down the esophagus to the stomach. Once in the stomach, food mixes with strong acid, which breaks down the food into very small particles. This process is called digestion. The digested food particles are then either absorbed into the bloodstream or removed from the body as waste.

      The tissue on the inside of the stomach is made up of specialized epithelial cells that form a barrier called the epithelium. Cells at the top of the epithelium, called foveolar cells, protect the stomach from strong acid used to break down food. Beneath the superficial epithelium is a thin layer of tissue called the Lamina Propria that supports the superficial cells. Together, the superficial epithelium and the lamina propria are called the mucosa.

      Symptoms of chronic gastritis

      The most common symptoms of chronic gastritis are abdominal pain (aching or burning) that worsens with an empty stomach, nausea, bloating, and loss of appetite.

      What causes chronic gastritis?

      The most common cause of chronic gastritis is infection of the stomach with a bacteria called Helicobacter pylori. The infection is more common in rural areas and in the developing world. Chronic gastritis can also be seen in people who have previously been treated for Helicobacter pylori.Chronic gastritis can persist for months or even years after successful treatment.

      Other causes of chronic gastritis include:

      • Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and advil.
      • Excessive alcohol consumption.
      • Reflux of bile.
      • Autoimmune diseases.
      How do pathologists make this diagnosis?

      Diagnosis is usually made after a small sample of tissue is removed in a procedure called a biopsy.The tissue is then examined by a pathologist under a microscope. Your pathologist may order additional tests such as immunohistochemistry or specific spots to look for Helicobacter pylori.

      Chronic gastritis means that your pathologist has noticed an increased number of specialized immune cells called plasma cells inside the lamina propria. Pathologists describe this change as chronic inflammation.

      What to look for in a chronic gastritis pathology report
      Active gastritis

      Active gastritis means that, in addition to chronic inflammation, your pathologist saw ongoing tissue damage or damage.Another term for active gastritis is acute gastritis. To make this diagnosis, your pathologist must examine specialized immune cells called neutrophils in the epithelium.

      Active gastritis may be seen shortly after the onset of the injury or injury, or even later if you have not yet received treatment. The most common cause of active gastritis is Helicobacter Pylori infection. Neutrophils in the epithelium protect the body from bacteria, but also damage epithelial cells.

      Active gastritis due to Helicobacter pylori infection should be treated with antibiotics. If left untreated, a Helicobacter infection can cause stomach ulcers. Untreated Helicobacter infection also increases the risk of stomach cancer.

      Inactive gastritis

      Some pathology reports describe chronic gastritis as chronic inactive gastritis. The addition of the word “inactive” to the diagnosis means that no specialized immune cells, called neutrophils, were found to damage the epithelium.Neutrophils are usually found shortly after the onset of injury and are a sign of ongoing damage (see Active gastritis above).

      Intestinal metaplasia

      Chronic gastritis that is not treated can damage the foveolar process. epithelium. If damage continues over many years, the foveolar epithelium is slowly replaced by a new type of epithelium, similar to the epithelium of the small intestine.

      The transition from foveolar epithelium to the epithelium of the small intestine is an example of metaplasia and pathologists describe a specific type of metaplasia in the stomach as intestinal metaplasia.If your pathologist finds intestinal metaplasia in the tissue sample, this will be described in your report.

      Intestinal metaplasia is a non-malignant change that develops after many years of trauma. Although not cancer in and of itself, it increases the risk of developing stomach cancer, called adenocarcinoma, over time. The risk increases when a different type of change is triggered. dysplasia is also seen (see Dysplasia below).


      dysplasia is the word pathologists use to describe abnormal growth.Like intestinal metaplasia, dysplasia can develop in patients suffering from chronic gastritis for many years.

      Most patients with chronic gastritis do not have dysplasia, but if found, it will be reported on. Pathologists divide dysplasia into low and high. nets depending on how abnormal the tissue looks when examined under a microscope.

      Dysplasia is a non-malignant change. However, it is considered a precancerous condition because it increases the risk of developing stomach cancer, called adenocarcinoma, over time.The risk of cancer is higher with high-grade dysplasia.

      Jason Wasserman MD, FRCPC (updated Sep 18, 2021)

      Candidiasis | Dentistry Mitino

      Oral candidiasis is a specific infection provoked by opportunistic yeast-like fungi Candida ablicans. The patient’s mucous membrane of the mouth swells, dense plaques with a white coating appear. You can often feel a strong burning sensation in the affected areas, dry mouth, pain when eating.Often there are seizures, lips peeling and cracking. Timely treatment allows you to completely get rid of candidiasis.

      What is oral candidiasis

      Oral candidiasis affects the mucous membrane of the mouth. In fact, it looks like a strong white coating on a certain area.

      Important! Candida fungi, appearing in the mouth, may in the future cause such pathological processes as vaginal candidiasis, skin candidiasis, sepsis.

      Most often, candidiasis occurs in infancy and young age. It often affects the elderly over 60 years of age.

      There are four stages in the development of candidiasis:

      1. Adhesion. At this stage, a harmful microorganism is attached to the mucous membrane.

      2. Colonization. The fungus is actively multiplying in the attachment area.

      3. Invasive growth. Candidiasis becomes evident, the barrier and protective functions of the oral mucosa are impaired, so the fungi multiply even faster.

      4. Distribution. The fungus spreads through the circulatory system through tissue penetration.

      How does the disease proceed

      Candidiasis has two forms of its course: acute and chronic.Options for the acute form:

      1. The appearance of a whitish bloom. White masses, often of a curdled consistency, appear on the mucous membrane in the mouth. The plaque is easily removed, but forms again. Under the removed plaque, you can notice severe redness and slight swelling.

      2. Atrophic candidiasis. In this case, the mucous membrane, on the contrary, dries up, and plaque does not appear.Redness quickly forms, the reed papillae begin to atrophy and the roughness of the tongue gradually smoothes out.

      The chronic form has such manifestations:

      1. Hyperplastic candidiasis. The mucous membrane becomes red and swollen, and white or gray plaques form on it.

      2. Chronic atrophic candidiasis. Appears in the mouth of those who wear dentures.

      Both of these forms proceed in different ways:

      Symptoms of the disease

      The symptomatology of the disease is associated with its localization:

      • Candidiasis of the tongue. In this case, a yellow coating appears, sometimes the tongue becomes grayish. Local inflammations and dull yellow films may form. If candidiasis is atrophic, then the back of the tongue becomes purple and dry.A white bloom appears in the center and on the sides.

      • Area of ​​the corners of the mouth and the red border of the lips. Often appears simultaneously with candidiasis of the tongue. The corners of the mouth swell from the influx of moisture, become inflamed, and a white coating appears on them, which is easy to remove. The affected areas quickly turn red, “smoothed”. The red border of the lips is the rarest area of ​​infection by fungi.

      • Candidiasis of the tonsils. The area of ​​the pharynx, arches and tonsils reddens a little, there is a slight swelling and white spots of plaque. There is no discomfort with meals.

      Causes of candidiasis

      The disease provokes a fungus. More than half of all people on the planet are carriers of candida, but they do not experience any inconvenience. Symptoms can only appear when the host’s general or local immunity is reduced or the chemical balance of the oral cavity is disturbed.

      Factors provoking candidiasis:

      • Pregnancy. Carrying a child is always associated with disruptions in hormonal levels and metabolism, a decrease in immunity.

      • General diseases. For example, diseases of the gastrointestinal tract, adrenal glands, HIV and others. Often, oral candidiasis can be used to diagnose diabetes.

      • Side effects of drugs. If the patient takes corticosteroids and cytostatics, then his immunity decreases. Also, the cause of oral candidiasis can be a long course of antibiotics.

      • Avitaminosis, especially the lack of vitamins of groups B, C, PP.

      • Addictions, especially alcoholism and drug addiction, which disrupt the chemical balance of all body systems.

      • Use of prostheses. Candidiasis can occur if the prosthetics was performed poorly: the prostheses are not “fitted” perfectly and leave wounds on the mucous membrane when worn. Moreover, dentures can cause allergies, and due to mechanical damage, the fungus will spread throughout the body faster.

      Another common route of infection is from another person. Most often, fungi are transmitted through unprotected sexual intercourse, the use of the same dishes or hygiene items, during childbirth.Less commonly, infection occurs after contact with infected animals.

      Diagnosis of the disease

      The doctor conducts a survey and examination of the patient. The parameters for assessing the oral mucosa are as follows:

      • color: white or red,

      • structure: smooth or rough,

      • location of infected areas: on the tongue, palate, floor of the mouth, gums, lips,

      • the depth of the lesion,

      • contours of white spots and the total area of ​​the lesion.

      One of the most significant parameters is the color of the infected tissue:

      1. Red indicates inflammation, but no mechanical damage. Relevant for the erythematous form.

      2. White can denote keratic infection, that is, keratinization of the mucous membrane, or necrotic form of candidiasis – destruction of the epithelium, which is important for the erosive and ulcerative form.

      If during a standard examination the doctor could not determine the nature of the disease, he takes a smear and sends it for laboratory tests (most often – microscopic analysis, sowing of Candida on Sabouraud’s medium, serological reactions).

      Treatment and prevention of candidiasis

      Treatment of candidiasis involves local and general interventions:

      • oral cavity treatment,

      • treatment in parallel with current diseases,

      • strengthening of immunity.

      Most often, the doctor prescribes rinsing with special solutions (soda, boric acid, etc.), the use of antifungal ointments. Several antimycotics are also prescribed.

      Approximately on the 5th day of treatment, keratoplastic drugs are prescribed. The patient should carefully monitor oral hygiene. Physiotherapy is especially effective, for example, laser therapy, ultraviolet irradiation, electrophoresis.Rarely when general immunotherapy is required. Vitamins are often prescribed to patients.

      Important! On average, treatment lasts about 10 days after symptom elimination. The first improvement occurs in about 4–5 days. The general period of treatment depends on the form and manifestation of the disease.

      Predictions for candidiasis depend on its form:

      • with mild course the prognosis is favorable, and relapses are rare;

      • with a moderate variant of candidiasis, there is a likelihood of a recurrence of the pathology;

      • in severe form , chronic infection and candidal sepsis are possible.

      The main preventive measures for candidiasis are as follows:

      1. Meticulous oral hygiene. It is necessary to properly brush your teeth, avoid injuries to soft tissues, use rinse aid and dental floss.

      2. Competent selection of a toothbrush. First, the toothbrush should not be too soft or too hard. Secondly, it is changed every 2-3 months.Thirdly, you need to rinse it well after each cleaning, preferably with antibacterial soap.

      3. Denture care. After each meal, they need to be washed well with a special detergent, and also properly stored.

      4. Healthy lifestyle: balanced diet, moderate and regular physical activity, no bad habits.

      5. Regular dental visits – at least every six months.

      6. Breast hygiene. If a woman is breastfeeding, she must maintain nipple hygiene, observe and heal cracks and other injuries that often accompany feeding.

      Complications of candidiasis

      Complications of candidiasis can follow if medical assistance was not provided in a timely manner, or if the patient did not follow all the doctor’s prescriptions.

      In medical practice, there are the following main complications after candidiasis:

      • Candidal esophagitis. This is an inflammation of the esophagus. The patient feels bloating, heartburn, discomfort in the throat, often difficulty swallowing solid food, bitterness or sour taste in the mouth. In advanced forms, the disease leads to an ulcer, rupture of the esophageal tube, narrowing of the lumen of the esophagus.

      • Candidal tracheitis, that is, inflammation of the trachea. The patient’s temperature quickly rises to 37 degrees, he experiences chest pain, and shortness of breath begins. When coughing, there is a feeling of suffocation and burning.A person may experience pain in the area of ​​the shoulder blades and sternum. Sometimes pustules appear on the skin. If the disease is left unattended, it will provoke sepsis.

      • Gastrointestinal candidiasis. The gastric mucosa is especially confirmed to be a disease. Dysbiosis occurs in severe form. The patient experiences constant nausea, vomiting is observed, often with blood and white blotches. The temperature is stable (37–38 degrees). Stomach hurts, diarrhea occurs.

      • Secondary infection. Since candidiasis lowers immunity, and organs and tissues become very susceptible, there is a high probability of contracting a third-party infection.

      • Sepsis. This is one of the most severe complications of candidiasis. It appears due to the entry of fungi into all organs. The patient experiences constant nausea, vomiting, painful sensations in the abdomen.Tachycardia and a temperature rise of more than 38 degrees are often observed. In case of untimely assistance, such a complication can be fatal.

      It is not difficult to prevent candidiasis – it is enough to observe oral hygiene, lead an active and healthy lifestyle, and consume enough vegetables and fermented milk products.