Who is most susceptible to peptic ulcers

In most persons infected with H. The supernatants of gastric mucosal biopsy specimens from persons with H. Because the ABO blood group antigens are also major histocompatibility antigens, the aim of this study was to assess the effect of ABO blood group on inflammatory responses of human leukocytes exposed to H. Outer membrane preparations were isolated, as described elsewhere [ 6 ], from the following strains of H.

One-day-old human buffy coat samples 50 mL were obtained from the Scottish National Blood Transfusion Service and were diluted 1: 2 in sterile pyrogen-free PBS under aseptic conditions. Diluted blood 15 mL was layered carefully on Histopaque 5 mL containing 5. Louis in sterile plastic centrifuge tubes and was centrifuged for 30 min at g. Leukocytes were collected from the interface and were washed twice with pyrogen-free PBS Life Technologies Gibco BRL, Gaithersburg, MD , and the leukocytes were enumerated microscopically by the trypan blue exclusion method.

Cells from 40 donors were examined, 10 from each ABO blood group. Differential counts for the cell preparations were within normal ranges. These samples were used in the binding assays.

All cell samples were tested against all 4 strains at the same time. Binding of fluorescein isothiocyanate—labeled H. The results for each sample were expressed as binding index, calculated by multiplying the percentage of cells with fluorescence greater than the control, to which no bacteria were added by the mean fluorescence of the positive cell population [ 6 ]. The bacteria or antigens were suspended in DMEM without antibiotics, and control wells contained only medium with cells.

After 18 h of incubation, the viability of the cells was determined by the trypan blue exclusion method. To determine whether leukocytes from persons of blood group O exhibited responses to other antigens, the experiments were repeated with sterile culture filtrates of Escherichia coli O The filtrates were prepared in a category III containment facility and were filter sterilized.

No viable organisms were cultured from the preparations. The antibody was diluted in coating buffer consisting of sodium carbonate 15 m M , sodium bicarbonate 35 m M , and sodium azide 3 m M ; pH 9. The plates were washed 6 times with washing buffer consisting of 0. The blocking buffer was removed, and supernatant samples mL were added to duplicate wells. The substrate mL was added to the wells; it contained 40 mg of O -phenylenediamine in mLof 0. The color change was stopped after 10—20 min by addition of mL of The absorbance at nm was determined by an ELISA plate reader Dynatech Laboratories, Chantilly, VA and corrected by subtracting the absorbance of the corresponding blank well containing each of the components except the cell supernatant.

The significance levels for differences between groups were examined with the Kruskal-Wallis test, and correlations between the bacterial binding and inflammatory responses were made with Spearman's correlation coefficient.

Binding of different isolates of H. The mean binding indices of the 4 H. Mean of binding indices for 4 strains of Helicobacter pylori to leukocytes from donors of different ABO blood groups. There was no significant difference in binding of any of the 4 isolates of H. Among 3 experiments with leukocytes from blood group O donors, the responses were dose-dependent for the bacteria and for the antigen preparations. OMP preparations were used to compare differences in response of leukocytes from donors of different ABO blood groups.

Results obtained with cells of 40 different persons 10 donors of each ABO group are summarized in tables 2—4. Mean levels of interleukin IL —6 released from leukocytes of different ABO blood groups in response to outer membrane protein prepared from 4 different Helicobacter pylori strains.

Mean levels of interleukin IL —10 released from leukocytes of different ABO blood groups in response to outer membrane protein prepared from 4 different Helicobacter pylori strains. Although the highest levels were elicited from cells of group A donors in response to strain GC, there were no significant differences associated with ABO blood group or for the individual strains of H.

There were significant correlations between binding of H. There was no significant correlation between bacterial binding and detection of IL A previous study of cytokines released from human leukocytes stimulated by H.

It has been suggested that development of more serious gastroduodenal disease might be related to infection with ulcerogenic or carcinogenic strains of H. An increased prevalence of antibodies to the cagA protein has been reported for patients with peptic ulcer disease or gastric cancer [ 16—18 ]. Studies that make use of polymerase chain reaction amplification and DNA hybridization found that cagA in clinical isolates was not significantly associated with duodenal ulcer disease [ 19 ].

A study of an Australian population reported that the prevalence of antibodies to the cagA protein in the duodenal ulcer group was higher than that found in the control group; however, in a Chinese population, no significant difference was found between the prevalence of antibodies to the cagA antigen in asymptomatic subjects and that in gastric cancer patients [ 20 ].

Analysis of the antibody responses to other H. Density of colonization is associated with inflammatory response [ 9 ]. The results of the binding studies do not support this hypothesis. Persons of blood group O are significantly overrepresented among patients with gastric or duodenal ulcers, compared with patients of the other blood groups [ 4 , 7 , 21—24 ]. Another study found a correlation between ABO blood group and H.

Blood group O patients had H. Other studies failed to find an association between H. A peptic ulcer is a sore on the lining of your stomach or the first part of your small intestine duodenum.

If the ulcer is in your stomach, it is called a gastric ulcer. If the ulcer is in your duodenum, it is called a duodenal ulcer. In the past, experts thought lifestyle factors such as stress and diet caused ulcers. Today we know that stomach acids and other digestive juices help create ulcers. These fluids burn the linings of your organs. The most common ulcer symptom is a dull or burning pain in your belly between your breastbone and your belly button navel.

This pain often occurs around meal times and may wake you up at night. It can last from a few minutes to a few hours. Peptic ulcer symptoms may look like other health problems. Always see your healthcare provider to be sure.

Your healthcare provider will look at your past health and give you a physical exam. You may also have some tests. Treatment will depend on the type of ulcer you have. Your healthcare provider will create a care plan for you based on what is causing your ulcer. Treatment can include making lifestyle changes, taking medicines, or in some cases having surgery. In most cases, medicines can heal ulcers quickly. Once the H. You may also need surgery if your ulcer causes other medical problems.

Untreated peptic ulcers may cause other health problems. Sometimes they bleed. If they become too deep, they can break through your stomach. Health Home Conditions and Diseases. Ulcers are fairly common. What causes peptic ulcers? Causes of peptic ulcers include: H. Most ulcers are caused by an infection from a bacteria or germ called H. This bacteria hurts the mucus that protects the lining of your stomach and the first part of your small intestine the duodenum.

Stomach acid then gets through to the lining. NSAIDs nonsteroidal anti-inflammatory drugs. These are over-the-counter pain and fever medicines such as aspirin, ibuprofen, and naproxen. Over time they can damage the mucus that protects the lining of your stomach. What are the symptoms of peptic ulcers? Less common ulcer symptoms may include: Feeling full after eating a small amount of food Burping Nausea Vomiting Not feeling hungry Losing weight without trying Bloody or black stool Vomiting blood Peptic ulcer symptoms may look like other health problems.

How are peptic ulcers diagnosed? Imaging tests used to diagnose ulcers include: Upper GI gastrointestinal series or barium swallow. This test looks at the organs of the top part of your digestive system. It checks your food pipe esophagus , stomach, and the first part of the small intestine the duodenum. Drinking alcohol can increase discomfort when you have an ulcer. Spicy foods, caffeine, and acidic juices do not cause peptic ulcers, and a bland diet is no longer recommended for people with ulcers.

However, you may find there are things that aggravate your symptoms and you can choose to avoid them while your ulcer is being treated and healing. Emotional stress is no longer thought to be a cause of ulcers, but people who are experiencing it often report increased pain of existing ulcers. The discovery of the true causes of most peptic ulcers has reduced the stigma that it is primarily caused by stress or diet. While you may still need lifestyle adjustments to relieve symptoms, effective treatments can mean being cured rather than having to manage peptic ulcer disease for the rest of your life.

If you have a history of heavy drinking, you may be more likely to develop ulcers. Drinking alcohol can also cause ulcer symptoms to flare up, but researchers say that even people without ulcers can have similar symptoms if they drink excessively. Possibly, people who are stressed are more likely to learn they have ulcers because they see a doctor for issues related to stress.

They may also increase their risk because of stress-related behaviors like drinking and smoking. Stomach cancer does not cause ulcers. However, the same bacteria that put you at risk for ulcers, Helicobacter pylori , may over time damage the lining of your gastrointestinal system and lead to lymphoma of the stomach. Gas pain? Stool issues? Sign up for the best tips to take care of your stomach.

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