A condition in which there is a change of one adult cell type to another similar adult cell type.
A condition with damage to the lining of the lower ESOPHAGUS resulting from chronic acid reflux (ESOPHAGITIS, REFLUX). Through the process of metaplasia, the squamous cells are replaced by a columnar epithelium with cells resembling those of the INTESTINE or the salmon-pink mucosa of the STOMACH. Barrett's columnar epithelium is a marker for severe reflux and precursor to ADENOCARCINOMA of the esophagus.
Pathological processes that tend eventually to become malignant. (From Dorland, 27th ed)
Lining of the STOMACH, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. The surface cells produce MUCUS that protects the stomach from attack by digestive acid and enzymes. When the epithelium invaginates into the LAMINA PROPRIA at various region of the stomach (CARDIA; GASTRIC FUNDUS; and PYLORUS), different tubular gastric glands are formed. These glands consist of cells that secrete mucus, enzymes, HYDROCHLORIC ACID, or hormones.
Inflammation of the GASTRIC MUCOSA, a lesion observed in a number of unrelated disorders.
GASTRITIS with atrophy of the GASTRIC MUCOSA, the GASTRIC PARIETAL CELLS, and the mucosal glands leading to ACHLORHYDRIA. Atrophic gastritis usually progresses from chronic gastritis.
A glandular epithelial cell or a unicellular gland. Goblet cells secrete MUCUS. They are scattered in the epithelial linings of many organs, especially the SMALL INTESTINE and the RESPIRATORY TRACT.
Tumors or cancer of the STOMACH.
The muscular membranous segment between the PHARYNX and the STOMACH in the UPPER GASTROINTESTINAL TRACT.
A de novo myeloproliferation arising from an abnormal stem cell. It is characterized by the replacement of bone marrow by fibrous tissue, a process that is mediated by CYTOKINES arising from the abnormal clone.
Infections with organisms of the genus HELICOBACTER, particularly, in humans, HELICOBACTER PYLORI. The clinical manifestations are focused in the stomach, usually the gastric mucosa and antrum, and the upper duodenum. This infection plays a major role in the pathogenesis of type B gastritis and peptic ulcer disease.
An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the ESOPHAGUS and the beginning of the DUODENUM.
A spiral bacterium active as a human gastric pathogen. It is a gram-negative, urease-positive, curved or slightly spiral organism initially isolated in 1982 from patients with lesions of gastritis or peptic ulcers in Western Australia. Helicobacter pylori was originally classified in the genus CAMPYLOBACTER, but RNA sequencing, cellular fatty acid profiles, growth patterns, and other taxonomic characteristics indicate that the micro-organism should be included in the genus HELICOBACTER. It has been officially transferred to Helicobacter gen. nov. (see Int J Syst Bacteriol 1989 Oct;39(4):297-405).
That part of the STOMACH close to the opening from ESOPHAGUS into the stomach (cardiac orifice), the ESOPHAGOGASTRIC JUNCTION. The cardia is so named because of its closeness to the HEART. Cardia is characterized by the lack of acid-forming cells (GASTRIC PARIETAL CELLS).
High molecular weight mucoproteins that protect the surface of EPITHELIAL CELLS by providing a barrier to particulate matter and microorganisms. Membrane-anchored mucins may have additional roles concerned with protein interactions at the cell surface.
Inflammation of the DUODENUM section of the small intestine (INTESTINE, SMALL). Erosive duodenitis may cause bleeding in the UPPER GI TRACT and PEPTIC ULCER.
A gel-forming mucin that is primarily found on the surface of gastric epithelium and in the RESPIRATORY TRACT. Mucin 5AC was originally identified as two distinct proteins, however a single gene encodes the protein which gives rise to the mucin 5A and mucin 5C variants.
The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.
Endoscopic examination, therapy or surgery of the esophagus.
The development of bony substance in normally soft structures.
An EPITHELIUM with MUCUS-secreting cells, such as GOBLET CELLS. It forms the lining of many body cavities, such as the DIGESTIVE TRACT, the RESPIRATORY TRACT, and the reproductive tract. Mucosa, rich in blood and lymph vessels, comprises an inner epithelium, a middle layer (lamina propria) of loose CONNECTIVE TISSUE, and an outer layer (muscularis mucosae) of SMOOTH MUSCLE CELLS that separates the mucosa from submucosa.
Endoscopic examination, therapy or surgery of the interior of the stomach.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
A gel-forming mucin found predominantly in SMALL INTESTINE and variety of mucous membrane-containing organs. It provides a protective, lubricating barrier against particles and infectious agents.
A malignant epithelial tumor with a glandular organization.
A gel-forming mucin that is predominantly associated with the gastric epithelium.
The region between the sharp indentation at the lower third of the STOMACH (incisura angularis) and the junction of the PYLORUS with the DUODENUM. Pyloric antral glands contain mucus-secreting cells and gastrin-secreting endocrine cells (G CELLS).
Epithelial cells that line the basal half of the GASTRIC GLANDS. Chief cells synthesize and export an inactive enzyme PEPSINOGEN which is converted into the highly proteolytic enzyme PEPSIN in the acid environment of the STOMACH.
Tumors or cancer of the ESOPHAGUS.
The area covering the terminal portion of ESOPHAGUS and the beginning of STOMACH at the cardiac orifice.
One or more layers of EPITHELIAL CELLS, supported by the basal lamina, which covers the inner or outer surfaces of the body.
The viscous secretion of mucous membranes. It contains mucin, white blood cells, water, inorganic salts, and exfoliated cells.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Retrograde flow of gastric juice (GASTRIC ACID) and/or duodenal contents (BILE ACIDS; PANCREATIC JUICE) into the distal ESOPHAGUS, commonly due to incompetence of the LOWER ESOPHAGEAL SPHINCTER.
Mucins that are found on the surface of the gastric epithelium. They play a role in protecting the epithelial layer from mechanical and chemical damage.
The shortest and widest portion of the SMALL INTESTINE adjacent to the PYLORUS of the STOMACH. It is named for having the length equal to about the width of 12 fingers.
Pathological processes involving the STOMACH.
Ulceration of the GASTRIC MUCOSA due to contact with GASTRIC JUICE. It is often associated with HELICOBACTER PYLORI infection or consumption of nonsteroidal anti-inflammatory drugs (NSAIDS).
A type II keratin found associated with KERATIN-19 in ductal epithelia and gastrointestinal epithelia.
An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.
The mucous membrane lining the RESPIRATORY TRACT, including the NASAL CAVITY; the LARYNX; the TRACHEA; and the BRONCHI tree. The respiratory mucosa consists of various types of epithelial cells ranging from ciliated columnar to simple squamous, mucous GOBLET CELLS, and glands containing both mucous and serous cells.
A type I keratin expressed predominately in gastrointestinal epithelia, MERKEL CELLS, and the TASTE BUDS of the oral mucosa.
Large, branched, specialized sweat glands that empty into the upper portion of a HAIR FOLLICLE instead of directly onto the SKIN.
A species of HELICOBACTER that colonizes in the STOMACH of laboratory MICE; CATS; and DOGS. It is associated with lymphoid follicular hyperplasia and mild GASTRITIS in CATS.
A PEPTIC ULCER located in the DUODENUM.
Endoscopic examination, therapy or surgery of the gastrointestinal tract.
Retrograde bile flow. Reflux of bile can be from the duodenum to the stomach (DUODENOGASTRIC REFLUX); to the esophagus (GASTROESOPHAGEAL REFLUX); or to the PANCREAS.
A class of fibrous proteins or scleroproteins that represents the principal constituent of EPIDERMIS; HAIR; NAILS; horny tissues, and the organic matrix of tooth ENAMEL. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms a coiled-coil alpha helical structure consisting of TYPE I KERATIN and a TYPE II KERATIN, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. alpha-Keratins have been classified into at least 20 subtypes. In addition multiple isoforms of subtypes have been found which may be due to GENE DUPLICATION.
The larger air passages of the lungs arising from the terminal bifurcation of the TRACHEA. They include the largest two primary bronchi which branch out into secondary bronchi, and tertiary bronchi which extend into BRONCHIOLES and PULMONARY ALVEOLI.

Hybrid capture II, a new sensitive test for human papillomavirus detection. Comparison with hybrid capture I and PCR results in cervical lesions. (1/1094)

AIM: To test a new assay for the detection of human papillomavirus (HPV) DNA, hybrid capture II (HC II), compared with the previous commercialized hybrid capture I (HC I) and polymerase chain reaction (PCR) results on cervical scrapes from fresh cone excision biopsy samples. METHODS: The three methods were used on cervical scrapes from 42 fresh cone excision biopsy samples. There were nine metaplastic and inflammatory lesions, five low grade lesions, and 28 high grade lesions. PCR was performed using the general primers GP5+/GP6+. The viral load of high risk HPV DNA was estimated by the ratio of relative light units to positive control values in the samples. RESULTS: The sensitivity of HC I for the detection of high grade lesions was 71.4%, while it was 92.8% for HC II and 96.4% for the PCR. Considering only the absence of detectable cervical in situ neoplasia, the specificity was 88.9% for HC I, 66.7% for HC II, and 66.7% for PCR. With HC II, for a ratio of cervical sample to normal control of > 200, the sensitivity for the detection of high grade lesion was only 34.6% with a specificity of 66.7%. CONCLUSIONS: HPV detection with the HC II assay is more sensitive than the previous HC I and represents a more convenient and easier test than PCR for routine use. Nevertheless the viral load estimated with this test cannot be a reliable predictive indicator of high grade lesions.  (+info)

Precancerous lesions in two counties of China with contrasting gastric cancer risk. (2/1094)

BACKGROUND: Gastric cancer (GC) is one of the most common cancers worldwide and shows remarkable geographical variation even within countries such as China. Linqu County in Shandong Province of northeast China has a GC rate that is 15 times higher than that of Cangshan County in Shandong, even though these counties are within 200 miles of each other. METHOD: In order to evaluate the frequency of precancerous gastric lesions in Linqu and Cangshan Counties we examined 3400 adults in Linqu County and 224 adults in Cangshan County. An endoscopic examination with four biopsies was performed in each individual of the two populations. RESULTS: The prevalence of intestinal metaplasia (IM) and dysplasia (DYS) was 30% and 15.1%, respectively, in Linqu compared to 7.9% and 5.6% in Cangshan (P < 0.01). Within these histological categories, advanced grades were found more often in Linqu than in Cangshan. The prevalences of IM and DYS were more common at each biopsy site in Linqu, where the lesions also tended to affect multiple sites. CONCLUSIONS: The findings of this study support the concept that IM and DYS are closely correlated with risks of GC and represent late stages in the multistep process of gastric carcinogenesis.  (+info)

KRAS mutations predict progression of preneoplastic gastric lesions. (3/1094)

Eight hundred sixty-three subjects with atrophic gastritis were recruited to participate in an ongoing chemoprevention trial in Narino, Colombia. The participants were randomly assigned to intervention therapies, which included treatment to eradicate Helicobacter pylori infection followed by daily dietary supplementation with antioxidant micronutrients in a 2 x 2 x 2 factorial design. A series of biopsies of gastric mucosa were obtained according to a specified protocol from designated locations in the stomach for each participant at baseline (before intervention therapy) and at year three. A systematic sample of 160 participants was selected from each of the eight treatment combinations. DNA was isolated from each of these biopsies (n = 320), and the first exon of KRAS was amplified using PCR. Mutations in the KRAS gene were detected using denaturing gradient gel electrophoresis and confirmed by sequence analysis. Of all baseline biopsies, 14.4% (23 of 160) contained KRAS mutations. Among those participants with atrophic gastritis without metaplasia, 19.4% (6 of 25) contained KRAS mutations, indicating that mutation of this important gene is likely an early event in the etiology of gastric carcinoma. An important association was found between the presence of KRAS mutations in baseline biopsies and the progression of preneoplastic lesions. Only 14.6% (20 of 137) of participants without baseline KRAS mutations progressed from atrophic gastritis to intestinal metaplasia or from small intestinal metaplasia to colonic metaplasia; however, 39.1% (9 of 23) with baseline KRAS mutations progressed to a more advanced lesion after 3 years [univariate odds ratio (OR), 3.76 (P = 0.05); multivariate OR adjusted for treatment, 3.74 (P = 0.04)]. In addition, the specificity of the KRAS mutation predicted progression. For those participants with G-->T transversions at position 1 of codon 12 (GGT-->TGT), 19.4% (5 of 17) progressed (univariate OR, 2.4); however, 60.0% (3 of 5) of participants with G-->A transitions at position 1 of codon 12 (GGT-->AGT) progressed (univariate OR, 8.7; P = 0.004 using chi2 test).  (+info)

Apoptotic activity is increased in parallel with the metaplasia-dysplasia-carcinoma sequence of the bronchial epithelium. (4/1094)

A high level of apoptotic activity and an independence of apoptosis from the expression of p53 and bcl-2 have been observed in non-small-cell lung carcinoma. We examined 44 samples of normal, metaplastic and premalignant (i.e. mild, moderate and severe dysplasias and carcinoma in situ) bronchial epithelia to evaluate whether differences in the apoptotic activity could already be seen in the stages preceding squamous cell carcinoma of the lung (SQCLC). Apoptotic cells and bodies were visualized by 3' end labelling. The expression of p53 and members of the bcl-2 gene family, such as bcl-2, bax and mcl-1, were determined immunohistochemically with specific antibodies. The relative number of apoptotic cells and bodies [apoptotic index (AI%)] was already increased threefold as the normal bronchial epithelium changed to squamous metaplasia, and the AIs of the dysplastic lesions were about four times higher than those of the normal epithelium. Apoptosis was significantly associated with cell proliferation, as determined by proliferating cell nuclear antigen (PCNA) immunohistochemistry. However, the extent of apoptosis did not correlate with the expression of p53, bcl-2, bax and mcl-1. We conclude that, in the metaplasia-dysplasia-carcinoma sequence in the lung, the elevation of the AI% is an early event associated with cell proliferation activity, but is independent of the expression of p53, bcl-2, mcl-1 and bax.  (+info)

Intestinal metaplasia of human stomach displays distinct patterns of mucin (MUC1, MUC2, MUC5AC, and MUC6) expression. (5/1094)

Intestinal metaplasia is a well-established premalignant condition of the stomach that is characterized by mucin carbohydrate modifications defined by histochemical methods. The purpose of the present study was to see whether the expression of mucin core proteins was modified in the different types of intestinal metaplasia and to evaluate the putative usefulness of mucins as "molecular markers" in this setting. We used a panel of monoclonal antibodies with well-defined specificities to MUC1, MUC2, MUC5AC, and MUC6 to characterize the expression pattern of mucins. In contrast to normal gastric mucosa, the complete form or type I intestinal metaplasia (n = 20) displayed little or no expression of MUC1, MUC5AC, or MUC6 in the metaplastic cells and strong expression of the intestinal mucin MUC2 in the goblet cells of all cases. The incomplete forms of intestinal metaplasia, type II (n = 25) and type III (n = 16), expressed MUC1 and MUC5AC in every case, both in goblet and in columnar cells. MUC6 was also expressed in 16 cases of type II intestinal metaplasia and in 11 cases of type III intestinal metaplasia. The intestinal mucin MUC2 was expressed in every case of incomplete intestinal metaplasia, mostly in goblet cells. The mucin expression profile in the different types of intestinal metaplasia allows the identification of two patterns: one defined by decreased levels of expression of "gastric" mucins (MUC1, MUC5AC, and MUC6) and expression of MUC2 intestinal mucin, which corresponds to type I intestinal metaplasia, and the other defined by coexpression of "gastric mucins" (MUC1, MUC5AC, and MUC6) together with the MUC2 mucin, encompassing types II and III intestinal metaplasia. Our results challenge the classical sequential pathway of intestinal metaplasia (from type I to type III via a type II intermediate step).  (+info)

Helicobacter pylori-induced chronic active gastritis, intestinal metaplasia, and gastric ulcer in Mongolian gerbils. (6/1094)

The establishment of persisting Helicobacter pylori infection in laboratory animals has been difficult, but in 1996 Hirayama reported the development of a successful Mongolian gerbil model. The present study was undertaken with two aims: to better characterize the normal histological structure and histochemical properties of the gastric mucosa of the Mongolian gerbil; and to evaluate the progression of the histopathological features of H. pylori-induced gastritis in this animal model for one year after the experimental infection. Seventy-five Mongolian gerbils were used. Mongolian gerbils were sacrificed at 2, 4, 8, 12, 26, 38, and 52 weeks after H. pylori inoculation. Sections prepared from stomachs immediately fixed in Carnoy's solution were stained with hematoxylin and eosin and Alcian blue at pH 2.5/periodic acid-Schiff, a dual staining consisting of the galactose oxidase-cold thionin Schiff reaction and paradoxical Concanavalin A staining, and with immunostaining for H. pylori and BrdU. H. pylori infection induced in the Mongolian gerbil a chronic active gastritis, in which a marked mucosal infiltration of neutrophils on a background of chronic inflammation became detectable 4 weeks after inoculation and continued up to 52 weeks. Intestinal metaplasia and gastric ulcers appeared after 26 weeks in some of the animals, whereas others developed multiple hyperplastic polyps. The Mongolian gerbil represents a novel and useful model for the study of H. pylori-induced chronic active gastritis and may lend itself to the investigation of the epithelial alterations that lead to intestinal metaplasia and gastric neoplasia.  (+info)

Pathologic changes induced in respiratory tract mucosa by polycyclic hydrocarbons of differing carcinogenic activity. (7/1094)

Seven aromatic polycyclic hydrocarbons (PCHs) were investigated for their toxic effects on respiratory mucosa: benzo(e)pyrene (BeP), pyrene, anthracene, benz(a)anthracene(BaA), dibenz(a,c)anthracene(DBacA), benzo (a)pyrene (BaP), and dimethylbenz(a)anthracene (DMBA). The compounds were chosen because they comprise a spectrum of PCHs ranging from noncarcinogens, to initiators, to weak and strong carcinogens. All of them except DMBA are environmentally relevant chemicals. The chemicals were tested over an 8-week period. Heterotopic tracheal transplants were continously exposed and the histopathologic effects induced by the various PCHs were periodically assessed semiquantitatively. All PCHs exhibited varying degrees of toxicity for respiratory epithelium and submucosa. BeP clearly showed the least toxicity followed by pyrene and anthracene. BaA and DBacA caused marked epithelial and submucosal changes. In addition to epithelial hyperplasia, undifferentiated epithelium and squamous metaplasia developed. Marked mononuclear infiltration occurred in the subepithelial connective tissue. With BaP the epithelial and submucosal changes were similar but were much stronger. DMBA was the most toxic substance, causing epithelial necrosis followed by generalized keratinizing squamous metaplasia; the subepithelial changes consisted of an early acellular exudate and, later (at 8 weeks), marked condensation and hyalinization of the lamina propria. The toxic response pattern of the tracheal mucosa to carcinogenic agents was characterized by the chronicity of epithelial and connective tissue damage, as opposed to the short-lived hyperplastic and inflammatory response elicited by the noncarcinogens and weak initiators.  (+info)

Helicobacter pylori infection enhances glandular stomach carcinogenesis in Mongolian gerbils treated with chemical carcinogens. (8/1094)

Helicobacter pylori (Hp) is thought to be a stomach carcinogen from epidemiological findings. To determine the effects of infection with the bacteria on experimental carcinogenesis, a study of the glandular stomach of Mongolian gerbils (MGs) was performed. Male MGs were treated with N-methyl-N'-nitro-N-nitrosoguanidine followed by inoculation with Hp or infected with Hp followed by N-methyl-N'-nitro-N-nitrosoguanidine administration. Animals were killed at week 50, and their excised stomachs underwent microbiological and histopathological examinations. In addition, a serological investigation was performed. The incidences of adenocarcinomas were significantly higher in animals treated with 60 or 300 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine for 10 weeks followed by Hp inoculation or Hp followed by 20 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine for 30 weeks than in the respective controls. Moreover, tumour-bearing animals had higher titres of anti-Hp antibodies than tumour-free animals. Of interest was the finding that a dose of 100 p.p.m. N-methyl-N'-nitro-N-nitrosoguanidine given to infected gerbils eradicated the Hp in about half the animals, with a concomitant reduction in the promoting effect. No tumours were found in animals infected with Hp without N-methyl-N'-nitro-N-nitrosoguanidine or non-treated gerbils. Hp infection enhances glandular stomach carcinogenesis in MGs treated with N-methyl-N'-nitro-N-nitrosoguanidine. Animals with high titres of anti-Hp antibodies are at greatest risk of developing neoplasms.  (+info)

Examples and Observations:

1. Gastric metaplasia: This is a condition where the stomach lining is replaced by cells that are similar to those found in the esophagus. This can occur as a result of chronic acid reflux, leading to an increased risk of developing esophageal cancer.
2. Bronchial metaplasia: This is a condition where the airways in the lungs are replaced by cells that are similar to those found in the trachea. This can occur as a result of chronic inflammation, leading to an increased risk of developing lung cancer.
3. Pancreatic metaplasia: This is a condition where the pancreas is replaced by cells that are similar to those found in the ducts of the pancreas. This can occur as a result of chronic inflammation, leading to an increased risk of developing pancreatic cancer.
4. Breast metaplasia: This is a condition where the breast tissue is replaced by cells that are similar to those found in the salivary glands. This can occur as a result of chronic inflammation, leading to an increased risk of developing salivary gland cancer.

Etiology and Pathophysiology:

Metaplasia is thought to be caused by chronic inflammation, which can lead to the replacement of one type of cell or tissue with another. This can occur as a result of a variety of factors, including infection, injury, or exposure to carcinogens. Once the metaplastic changes have occurred, there is an increased risk of developing cancer if the underlying cause is not addressed.

Clinical Presentation:

Patients with metaplasia may present with a variety of symptoms, depending on the location and extent of the condition. These can include pain, difficulty swallowing or breathing, coughing up blood, and weight loss. In some cases, patients may be asymptomatic and the condition may be detected incidentally during diagnostic testing for another condition.

Diagnosis:

The diagnosis of metaplasia is typically made based on a combination of clinical findings, radiologic imaging (such as CT scans or endoscopies), and histopathological examination of biopsy specimens. Imaging studies can help to identify the location and extent of the metaplastic changes, while histopathology can confirm the presence of the metaplastic cells and rule out other potential diagnoses.

Treatment:

Treatment for metaplasia depends on the underlying cause and the severity of the condition. In some cases, treatment may involve addressing the underlying cause, such as removing a tumor or treating an infection. In other cases, treatment may be directed at managing symptoms and preventing complications. This can include medications to reduce inflammation and pain, as well as surgery to remove affected tissue.

Prognosis:

The prognosis for metaplasia varies depending on the underlying cause and the severity of the condition. In general, the prognosis is good for patients with benign metaplastic changes, while those with malignant changes may have a poorer prognosis if the cancer is not treated promptly and effectively.

Complications:

Metaplasia can lead to a number of complications, including:

1. Cancer: Metaplastic changes can sometimes progress to cancer, which can be life-threatening.
2. Obstruction: The growth of metaplastic cells can block the normal functioning of the organ or gland, leading to obstruction and potentially life-threatening complications.
3. Inflammation: Metaplasia can lead to chronic inflammation, which can cause scarring and further damage to the affected tissue.
4. Bleeding: Metaplastic changes can increase the risk of bleeding, particularly if they occur in the digestive tract or other organs.

The condition is named after Dr. Norman Barrett, who first described it in 1956. It is a precancerous condition, meaning that if left untreated, it can progress to esophageal cancer over time. The exact cause of Barrett esophagus is not fully understood, but chronic acid reflux is thought to play a role in its development.

The symptoms of Barrett esophagus are similar to those of GERD and may include heartburn, difficulty swallowing, chest pain, and regurgitation of food. The condition can be diagnosed through an endoscopy, which involves inserting a flexible tube with a camera into the esophagus to visualize the cells lining the esophagus.

Treatment for Barrett esophagus typically involves controlling the underlying acid reflux through lifestyle changes and medications. In some cases, surgery may be necessary to repair any damage to the esophageal lining or to strengthen the lower esophageal sphincter (LES), which is the muscle that separates the esophagus from the stomach and prevents acid reflux.

It's important for individuals with chronic acid reflux to be screened regularly for Barrett esophagus, as early detection and treatment can help prevent the development of esophageal cancer.

Examples of precancerous conditions include:

1. Dysplasia: This is a condition where abnormal cells are present in the tissue, but have not yet invaded surrounding tissues. Dysplasia can be found in organs such as the cervix, colon, and breast.
2. Carcinoma in situ (CIS): This is a condition where cancer cells are present in the tissue, but have not yet invaded surrounding tissues. CIS is often found in organs such as the breast, prostate, and cervix.
3. Atypical hyperplasia: This is a condition where abnormal cells are present in the tissue, but they are not yet cancerous. Atypical hyperplasia can be found in organs such as the breast and uterus.
4. Lobular carcinoma in situ (LCIS): This is a condition where cancer cells are present in the milk-producing glands of the breasts, but have not yet invaded surrounding tissues. LCIS is often found in both breasts and can increase the risk of developing breast cancer.
5. Adenomas: These are small growths on the surface of the colon that can become malignant over time if left untreated.
6. Leukoplakia: This is a condition where thick, white patches develop on the tongue or inside the mouth. Leukoplakia can be a precancerous condition and may increase the risk of developing oral cancer.
7. Oral subsquamous carcinoma: This is a type of precancerous lesion that develops in the mouth and can progress to squamous cell carcinoma if left untreated.
8. Cervical intraepithelial neoplasia (CIN): This is a condition where abnormal cells are present on the surface of the cervix, but have not yet invaded surrounding tissues. CIN can progress to cancer over time if left untreated.
9. Vulvar intraepithelial neoplasia (VIN): This is a condition where abnormal cells are present on the vulva, but have not yet invaded surrounding tissues. VIN can progress to cancer over time if left untreated.
10. Penile intraepithelial neoplasia (PIN): This is a condition where abnormal cells are present on the penis, but have not yet invaded surrounding tissues. PIN can progress to cancer over time if left untreated.

It is important to note that not all precancerous conditions will develop into cancer, and some may resolve on their own without treatment. However, it is important to follow up with a healthcare provider to monitor any changes and determine the best course of treatment.

Symptoms of gastritis may include abdominal pain, nausea, vomiting, loss of appetite, and difficulty swallowing. In severe cases, bleeding may occur in the stomach and black tarry stools may be present.

Diagnosis of gastritis is typically made through endoscopy, during which a flexible tube with a camera and light on the end is inserted through the mouth to visualize the inside of the stomach. Biopsies may also be taken during this procedure to examine the stomach tissue under a microscope for signs of inflammation or infection.

Treatment of gastritis depends on the underlying cause, but may include antibiotics for bacterial infections, anti-inflammatory medications, and lifestyle modifications such as avoiding alcohol, losing weight, and eating smaller more frequent meals. In severe cases, surgery may be necessary to remove damaged tissue or repair any ulcers that have developed.

This definition is based on the data provided by the Healthcare Common Procedure Coding System (HCPCS) and the American Medical Association (AMA).

It's important to note that there may be other definitions or meanings of "Gastritis, Atrophic" in the medical field, and this definition is not intended to be an exhaustive or definitive one.

The information provided herein is only for informational purposes, and it should not be relied upon as medical advice or a substitute for professional medical care. If you have any specific questions or concerns about your health, or if you are seeking medical attention, you should consult with a qualified healthcare provider who can provide personalized and appropriate care based on your individual needs.

There are several types of stomach neoplasms, including:

1. Adenocarcinoma: This is the most common type of stomach cancer, accounting for approximately 90% of all cases. It begins in the glandular cells that line the stomach and can spread to other parts of the body.
2. Squamous cell carcinoma: This type of cancer begins in the squamous cells that cover the outer layer of the stomach. It is less common than adenocarcinoma but more likely to be found in the upper part of the stomach.
3. Gastric mixed adenocarcinomasquamous cell carcinoma: This type of cancer is a combination of adenocarcinoma and squamous cell carcinoma.
4. Lymphoma: This is a cancer of the immune system that can occur in the stomach. It is less common than other types of stomach cancer but can be more aggressive.
5. Carcinomas of the stomach: These are malignant tumors that arise from the epithelial cells lining the stomach. They can be subdivided into adenocarcinoma, squamous cell carcinoma, and others.
6. Gastric brunner's gland adenoma: This is a rare type of benign tumor that arises from the Brunner's glands in the stomach.
7. Gastric polyps: These are growths that occur on the lining of the stomach and can be either benign or malignant.

The symptoms of stomach neoplasms vary depending on the location, size, and type of tumor. Common symptoms include abdominal pain, nausea, vomiting, weight loss, and difficulty swallowing. Diagnosis is usually made through a combination of endoscopy, imaging studies (such as CT or PET scans), and biopsy. Treatment depends on the type and stage of the tumor and may include surgery, chemotherapy, radiation therapy, or a combination of these. The prognosis for stomach neoplasms varies depending on the type and stage of the tumor, but early detection and treatment can improve outcomes.

PMF is a chronic disease that worsens over time, and it can lead to complications such as bleeding, infection, and bone damage. Treatment options include medications to reduce symptoms and slow the progression of the disease, as well as blood transfusions and splenectomy (removal of the spleen) in severe cases. The median age at diagnosis is around 60 years old, and the disease affects approximately 2-5 cases per million people per year.

Sources:

* American Cancer Society. (2019). What is primary myelofibrosis? Retrieved from
* Leukemia and Lymphoma Society. (n.d.). Primary Myelofibrosis. Retrieved from

1. Gastritis: Inflammation of the stomach lining, which can be acute or chronic.
2. Peptic ulcer disease: Ulcers in the stomach or duodenum (the first part of the small intestine) that are caused by H. pylori infection.
3. Gastric adenocarcinoma: A type of stomach cancer that is associated with long-term H. pylori infection.
4. Mucosa-associated lymphoid tissue (MALT) lymphoma: A rare type of cancer that affects the immune cells in the stomach and small intestine.
5. Gastroesophageal reflux disease (GERD): A condition in which stomach acid flows back up into the esophagus, causing symptoms such as heartburn and regurgitation.
6. Helicobacter pylori-associated chronic atrophic gastritis: A type of chronic inflammation of the stomach lining that can lead to stomach ulcers and stomach cancer.
7. Post-infectious irritable bowel syndrome (PI-IBS): A condition that develops after a gastrointestinal infection, characterized by persistent symptoms such as abdominal pain, bloating, and changes in bowel habits.

Helicobacter infections are typically diagnosed through endoscopy, where a flexible tube with a camera and light on the end is inserted into the stomach and small intestine to visualize the mucosa and look for signs of inflammation or ulcers. Laboratory tests such as breath tests and stool tests may also be used to detect the presence of H. pylori bacteria in the body. Treatment typically involves a combination of antibiotics and acid-suppressing medications to eradicate the infection and reduce symptoms.

Preventing Helicobacter Infections:

While it is not possible to completely prevent Helicobacter infections, there are several measures that can be taken to reduce the risk of developing these conditions:

1. Practice good hygiene: Wash your hands regularly, especially before eating and after using the bathroom.
2. Avoid close contact with people who have Helicobacter infections.
3. Avoid sharing food, drinks, or utensils with people who have Helicobacter infections.
4. Avoid consuming undercooked meat, especially pork and lamb.
5. Avoid consuming raw shellfish, especially oysters.
6. Avoid consuming unpasteurized dairy products.
7. Avoid alcohol and caffeine, which can irritate the stomach lining and increase the risk of developing Helicobacter infections.
8. Maintain a healthy diet that is high in fiber and low in fat.
9. Manage stress, as stress can exacerbate symptoms of Helicobacter infections.
10. Practice good oral hygiene to prevent gum disease and other oral infections that can increase the risk of developing Helicobacter infections.

Conclusion:

Helicobacter infections are a common cause of stomach ulcers, gastritis, and other gastrointestinal disorders. These infections are caused by the bacteria Helicobacter pylori, which can be found in the stomach lining and small intestine. While these infections can be difficult to diagnose, a combination of endoscopy, blood tests, and stool tests can help confirm the presence of Helicobacter bacteria. Treatment typically involves a combination of antibiotics and acid-suppressing medications to eradicate the infection and reduce symptoms. Preventive measures include practicing good hygiene, avoiding close contact with people who have Helicobacter infections, and maintaining a healthy diet.

In medical terminology, "itis" is a suffix that indicates inflammation or infection. Therefore, duodenitis specifically refers to the inflammation of the duodenum.

Examples of medical conditions that may cause duodenitis include:

* Viral or bacterial infections
* Autoimmune disorders such as Crohn's disease or ulcerative colitis
* Gut injury due to trauma, surgery, or burns
* Radiation therapy or chemotherapy

Duodenitis can be diagnosed through various medical tests such as:

* Endoscopy: A flexible tube with a camera and light on the end is inserted through the mouth and into the duodenum to visualize the inside of the digestive tract.
* Biopsy: A small sample of tissue is taken from the duodenum for examination under a microscope.
* Blood tests: To check for signs of infection or inflammation, such as elevated white blood cell count or liver enzymes.

Treatment options for duodenitis depend on the underlying cause and severity of the condition. Some possible treatment options include:

* Antibiotics to treat bacterial infections
* Anti-inflammatory medications such as corticosteroids or nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce inflammation and pain.
* Dietary modifications, such as avoiding trigger foods or taking probiotics to promote gut health.
* Stress management techniques, such as relaxation exercises or cognitive behavioral therapy, to help manage symptoms of stress-related duodenitis.
* Surgery may be necessary in severe cases or if other treatments are not effective.

It is important to seek medical attention if you experience persistent or severe abdominal pain, as duodenitis can be a sign of a more serious underlying condition. A healthcare professional can help determine the cause and develop an appropriate treatment plan.

Heterotopic ossification can cause a range of symptoms depending on its location and severity, including pain, stiffness, limited mobility, and difficulty moving the affected limb or joint. Treatment options for heterotopic ossification include medications to reduce inflammation and pain, physical therapy to maintain range of motion, and in severe cases, surgical removal of the abnormal bone growth.

In medical imaging, heterotopic ossification is often diagnosed using X-rays or other imaging techniques such as CT or MRI scans. These tests can help identify the presence of bone growth in an abnormal location and determine the extent of the condition.

Overall, heterotopic ossification is a relatively rare condition that can have a significant impact on a person's quality of life if left untreated. Prompt medical attention and appropriate treatment can help manage symptoms and prevent long-term complications.

Adenocarcinoma is a term used to describe a variety of different types of cancer that arise in glandular tissue, including:

1. Colorectal adenocarcinoma (cancer of the colon or rectum)
2. Breast adenocarcinoma (cancer of the breast)
3. Prostate adenocarcinoma (cancer of the prostate gland)
4. Pancreatic adenocarcinoma (cancer of the pancreas)
5. Lung adenocarcinoma (cancer of the lung)
6. Thyroid adenocarcinoma (cancer of the thyroid gland)
7. Skin adenocarcinoma (cancer of the skin)

The symptoms of adenocarcinoma depend on the location of the cancer and can include:

1. Blood in the stool or urine
2. Abdominal pain or discomfort
3. Changes in bowel habits
4. Unusual vaginal bleeding (in the case of endometrial adenocarcinoma)
5. A lump or thickening in the breast or elsewhere
6. Weight loss
7. Fatigue
8. Coughing up blood (in the case of lung adenocarcinoma)

The diagnosis of adenocarcinoma is typically made through a combination of imaging tests, such as CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a sample of tissue from the affected area and examining it under a microscope for cancer cells.

Treatment options for adenocarcinoma depend on the location of the cancer and can include:

1. Surgery to remove the tumor
2. Chemotherapy, which involves using drugs to kill cancer cells
3. Radiation therapy, which involves using high-energy X-rays or other particles to kill cancer cells
4. Targeted therapy, which involves using drugs that target specific molecules on cancer cells to kill them
5. Immunotherapy, which involves using drugs that stimulate the immune system to fight cancer cells.

The prognosis for adenocarcinoma is generally good if the cancer is detected and treated early, but it can be more challenging to treat if the cancer has spread to other parts of the body.

Types of Esophageal Neoplasms:

1. Barrett's Esophagus: This is a precancerous condition that occurs when the cells lining the esophagus undergo abnormal changes, increasing the risk of developing esophageal cancer.
2. Adenocarcinoma: This is the most common type of esophageal cancer, accounting for approximately 70% of all cases. It originates in the glands that line the esophagus.
3. Squamous Cell Carcinoma: This type of cancer accounts for about 20% of all esophageal cancers and originates in the squamous cells that line the esophagus.
4. Other rare types: Other rare types of esophageal neoplasms include lymphomas, sarcomas, and carcinoid tumors.

Causes and Risk Factors:

1. Gastroesophageal reflux disease (GERD): Long-standing GERD can lead to the development of Barrett's esophagus, which is a precancerous condition that increases the risk of developing esophageal cancer.
2. Obesity: Excess body weight is associated with an increased risk of developing esophageal cancer.
3. Diet: A diet high in processed meats and low in fruits and vegetables may increase the risk of developing esophageal cancer.
4. Alcohol consumption: Heavy alcohol consumption is a known risk factor for esophageal cancer.
5. Smoking: Cigarette smoking is a major risk factor for esophageal cancer.
6. Family history: Having a family history of esophageal cancer or other cancers may increase an individual's risk.
7. Age: The risk of developing esophageal cancer increases with age, with most cases occurring in people over the age of 50.
8. Other medical conditions: Certain medical conditions, such as achalasia, may increase the risk of developing esophageal cancer.

Symptoms and Diagnosis:

1. Dysphagia (difficulty swallowing): This is the most common symptom of esophageal cancer, and can be caused by a narrowing or blockage of the esophagus due to the tumor.
2. Chest pain or discomfort: Pain in the chest or upper back can be a symptom of esophageal cancer.
3. Weight loss: Losing weight without trying can be a symptom of esophageal cancer.
4. Coughing or hoarseness: If the tumor is obstructing the airway, it can cause coughing or hoarseness.
5. Fatigue: Feeling tired or weak can be a symptom of esophageal cancer.
6. Diagnosis: A diagnosis of esophageal cancer is typically made through a combination of endoscopy, imaging tests (such as CT scans), and biopsies.

Treatment Options:

1. Surgery: Surgery is the primary treatment for esophageal cancer, and can involve removing the tumor and some surrounding tissue, or removing the entire esophagus and replacing it with a section of stomach or intestine.
2. Chemotherapy: Chemotherapy involves using drugs to kill cancer cells, and is often used in combination with surgery to treat esophageal cancer.
3. Radiation therapy: Radiation therapy uses high-energy X-rays to kill cancer cells, and can be used alone or in combination with surgery or chemotherapy.
4. Targeted therapy: Targeted therapy drugs are designed to target specific molecules that are involved in the growth and spread of cancer cells, and can be used in combination with other treatments.

Prognosis and Survival Rate:

1. The prognosis for esophageal cancer is generally poor, with a five-year survival rate of around 20%.
2. Factors that can improve the prognosis include early detection, small tumor size, and absence of spread to lymph nodes or other organs.
3. The overall survival rate for esophageal cancer has not improved much over the past few decades, but advances in treatment have led to a slight increase in survival time for some patients.

Lifestyle Changes and Prevention:

1. Avoiding tobacco and alcohol: Tobacco and alcohol are major risk factors for esophageal cancer, so avoiding them can help reduce the risk of developing the disease.
2. Maintaining a healthy diet: Eating a balanced diet that is high in fruits, vegetables, and whole grains can help protect against esophageal cancer.
3. Managing obesity: Obesity is a risk factor for esophageal cancer, so maintaining a healthy weight through diet and exercise can help reduce the risk of developing the disease.
4. Reducing exposure to pollutants: Exposure to certain chemicals and pollutants, such as pesticides and asbestos, has been linked to an increased risk of esophageal cancer. Avoiding these substances can help reduce the risk of developing the disease.
5. Getting regular screening: Regular screening for Barrett's esophagus, a precancerous condition that can develop in people with gastroesophageal reflux disease (GERD), can help detect and treat esophageal cancer early, when it is most treatable.

Current Research and Future Directions:

1. Targeted therapies: Researchers are working on developing targeted therapies that can specifically target the genetic mutations that drive the growth of esophageal cancer cells. These therapies may be more effective and have fewer side effects than traditional chemotherapy.
2. Immunotherapy: Immunotherapy, which uses the body's immune system to fight cancer, is being studied as a potential treatment for esophageal cancer. Researchers are working on developing vaccines and other immunotherapies that can help the body recognize and attack cancer cells.
3. Precision medicine: With the help of advanced genomics and precision medicine, researchers are working to identify specific genetic mutations that drive the growth of esophageal cancer in each patient. This information can be used to develop personalized treatment plans that are tailored to the individual patient's needs.
4. Early detection: Researchers are working on developing new methods for early detection of esophageal cancer, such as using machine learning algorithms to analyze medical images and detect signs of cancer at an early stage.
5. Lifestyle modifications: Studies have shown that lifestyle modifications, such as quitting smoking and maintaining a healthy diet, can help reduce the risk of developing esophageal cancer. Researchers are working on understanding the specific mechanisms by which these modifications can help prevent the disease.

In conclusion, esophageal cancer is a complex and aggressive disease that is often diagnosed at an advanced stage. However, with advances in technology, research, and treatment options, there is hope for improving outcomes for patients with this disease. By understanding the risk factors, early detection methods, and current treatments, as well as ongoing research and future directions, we can work towards a future where esophageal cancer is more manageable and less deadly.

GER can be caused by a variety of factors, including:

* Weakening of the lower esophageal sphincter (LES), which allows stomach acid to flow back up into the esophagus.
* Delayed gastric emptying, which can cause food and stomach acid to remain in the stomach for longer periods of time and increase the risk of reflux.
* Obesity, which can put pressure on the stomach and cause the LES to weaken.

Symptoms of GER can include:

* Heartburn: a burning sensation in the chest that can radiate to the throat and neck.
* Regurgitation: the sensation of food coming back up into the mouth.
* Difficulty swallowing.
* Chest pain or tightness.
* Hoarseness or laryngitis.

If left untreated, GER can lead to complications such as esophagitis (inflammation of the esophagus), strictures (narrowing of the esophagus), and barrett's esophagus (precancerous changes in the esophageal lining).

Treatment options for GER include:

* Lifestyle modifications, such as losing weight, avoiding trigger foods, and elevating the head of the bed.
* Medications, such as antacids, H2 blockers, and proton pump inhibitors, to reduce acid production and relax the LES.
* Surgical procedures, such as fundoplication (a procedure that strengthens the LES) and laparoscopic adjustable gastric banding (a procedure that reduces the size of the stomach).

It is important to seek medical attention if symptoms persist or worsen over time, as GER can have serious complications if left untreated.

There are many different types of stomach diseases, some of which include:

1. Gastritis: This is inflammation of the stomach lining, which can be caused by infection, autoimmune disorders, or excessive alcohol consumption.
2. Peptic ulcer: This is a sore on the lining of the stomach or duodenum (the first part of the small intestine). Peptic ulcers are often caused by infection with the bacterium Helicobacter pylori, but they can also be caused by excessive acid production.
3. Gastroesophageal reflux disease (GERD): This is a condition in which stomach acid flows back up into the esophagus, causing symptoms such as heartburn and difficulty swallowing.
4. Stomach cancer: This is a type of cancer that affects the stomach lining, and it can be caused by a variety of factors including age, diet, and family history.
5. Inflammatory bowel disease (IBD): This is a chronic condition that causes inflammation in the digestive tract, including the stomach. Crohn's disease and ulcerative colitis are examples of IBD.
6. Gastrointestinal motility disorders: These are conditions that affect the muscles and nerves of the digestive system, causing problems with movement and contraction of the stomach and intestines.
7. Stomach polyps: These are growths on the lining of the stomach that can be benign or cancerous.
8. Hiatal hernia: This is a condition in which part of the stomach bulges up into the chest through a hole in the diaphragm, which can cause symptoms such as heartburn and difficulty swallowing.
9. Gastroesophageal reflux disease (GERD): This is a chronic form of acid reflux that can cause symptoms such as heartburn and difficulty swallowing.
10. Zollinger-Ellison syndrome: This is a rare condition that causes the stomach to produce too much acid, leading to symptoms such as heartburn, nausea, and vomiting.

These are just some of the many possible causes of stomach pain. It's important to see a doctor if you experience persistent or severe stomach pain, especially if it is accompanied by other symptoms such as fever, bleeding, or difficulty swallowing. Your doctor can perform tests and examinations to determine the cause of your stomach pain and recommend appropriate treatment.

Stomach ulcers are caused by an imbalance between the acid and mucus in the stomach, which can lead to inflammation and damage to the stomach lining. Factors that can contribute to the development of a stomach ulcer include:

* Infection with the bacterium Helicobacter pylori (H. pylori)
* Overuse of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen
* Excessive alcohol consumption
* Smoking
* Stress
* Zollinger-Ellison syndrome, a rare condition that causes the stomach to produce too much acid.

Symptoms of a stomach ulcer may include:

* Pain in the upper abdomen, often described as a burning or gnawing sensation
* Nausea and vomiting
* Bloating and gas
* Abdominal tenderness
* Loss of appetite
* Weight loss

Treatment for stomach ulcers typically involves antibiotics to kill H. pylori, if present, and acid-suppressing medications to reduce the amount of acid in the stomach. In severe cases, surgery may be necessary. Lifestyle changes, such as avoiding NSAIDs, alcohol, and smoking, can also help manage symptoms and prevent recurrence.

Preventive measures for stomach ulcers include:

* Avoiding NSAIDs and other irritating substances
* Using acid-suppressing medications as needed
* Maintaining a healthy diet and lifestyle
* Managing stress
* Avoiding excessive alcohol consumption

It is important to seek medical attention if symptoms persist or worsen over time, as stomach ulcers can lead to complications such as bleeding, perforation, and obstruction. Early diagnosis and treatment can help prevent these complications and improve outcomes.

There are different types of hyperplasia, depending on the location and cause of the condition. Some examples include:

1. Benign hyperplasia: This type of hyperplasia is non-cancerous and does not spread to other parts of the body. It can occur in various tissues and organs, such as the uterus (fibroids), breast tissue (fibrocystic changes), or prostate gland (benign prostatic hyperplasia).
2. Malignant hyperplasia: This type of hyperplasia is cancerous and can invade nearby tissues and organs, leading to serious health problems. Examples include skin cancer, breast cancer, and colon cancer.
3. Hyperplastic polyps: These are abnormal growths that occur in the gastrointestinal tract and can be precancerous.
4. Adenomatous hyperplasia: This type of hyperplasia is characterized by an increase in the number of glandular cells in a specific organ, such as the colon or breast. It can be a precursor to cancer.

The symptoms of hyperplasia depend on the location and severity of the condition. In general, they may include:

* Enlargement or swelling of the affected tissue or organ
* Pain or discomfort in the affected area
* Abnormal bleeding or discharge
* Changes in bowel or bladder habits
* Unexplained weight loss or gain

Hyperplasia is diagnosed through a combination of physical examination, imaging tests such as ultrasound or MRI, and biopsy. Treatment options depend on the underlying cause and severity of the condition, and may include medication, surgery, or other interventions.

The main causes of duodenal ulcers are:

1. Infection with the bacterium Helicobacter pylori (H. pylori)
2. Overuse of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen
3. Excessive alcohol consumption
4. Smoking
5. Zollinger-Ellison syndrome, a rare condition that causes the stomach to produce too much acid

Symptoms of duodenal ulcers may include:

1. Abdominal pain, which can be worse when eating or at night
2. Nausea and vomiting
3. Bloating and gas
4. Acid reflux
5. Weight loss

Diagnosis of a duodenal ulcer typically involves a combination of endoscopy, where a flexible tube with a camera is inserted through the mouth to visualize the inside of the digestive tract, and breath tests to detect H. pylori infection.

Treatment for duodenal ulcers usually involves eradication of H. pylori infection, if present, and avoidance of NSAIDs and other irritants. Antacids or acid-suppressing medications may also be prescribed to help reduce symptoms and allow the ulcer to heal. In severe cases, surgery may be necessary.

Prevention of duodenal ulcers includes:

1. Avoiding NSAIDs and other irritants
2. Eradicating H. pylori infection
3. Quitting smoking and excessive alcohol consumption
4. Managing stress
5. Eating a healthy diet with plenty of fruits, vegetables, and whole grains

Prognosis for duodenal ulcers is generally good if treated promptly and effectively. However, complications such as bleeding, perforation, and obstruction can be serious and potentially life-threatening. It is important to seek medical attention if symptoms persist or worsen over time.

In conclusion, duodenal ulcers are a common condition that can cause significant discomfort and disrupt daily life. While they can be caused by a variety of factors, H. pylori infection is the most common underlying cause. Treatment typically involves eradication of H. pylori infection, avoidance of NSAIDs and other irritants, and management of symptoms with antacids or acid-suppressing medications. Prevention includes avoiding risk factors and managing stress. With prompt and effective treatment, the prognosis for duodenal ulcers is generally good. However, complications can be serious and potentially life-threatening, so it is important to seek medical attention if symptoms persist or worsen over time.

Learn More:

Bile Reflux | Symptoms, Causes, Treatments | American ...
https://www.gi.org/topics/bile-reflux/

Normal physiological metaplasia, such as that of the endocervix, is highly desirable. The medical significance of metaplasia is ... If the stimulus causing metaplasia is removed or ceases, tissues return to their normal pattern of differentiation. Metaplasia ... squamous metaplasia). Metaplasia is an adaptation that replaces one type of epithelium with another that is more likely to be ... Metaplasia (Greek: "change in form") is the transformation of one differentiated cell type to another differentiated cell type ...
Intestinal metaplasia Squamous metaplasia Micrograph of Barrett's esophagus, an example of glandular metaplasia. "Metaplasia". ... Glandular metaplasia is a type of metaplasia where irritated tissue converts to a glandular form. An example occurs in the ... Ward AM (July 1971). "Glandular metaplasia and mucin production in transitional cell carcinomas of bladder". J. Clin. Pathol. ...
... is a condition affecting the epithelial surfaces of the body. It is caused by a dietary deficiency of ...
... is a benign non-cancerous change (metaplasia) of surfacing lining cells (epithelium) to a squamous ... Metaplasia Dysplasia Barrett esophagus - a columnar cell metaplasia of squamous epithelium Subareolar abscess Goralczyk, R ( ... Vitamin A deficiency or overdose can also lead to squamous metaplasia. In regard to the cervix, squamous metaplasia can ... Common sites for squamous metaplasia include the bladder and cervix. Smokers often exhibit squamous metaplasia in the linings ...
... is the transformation (metaplasia) of epithelium (usually of the stomach or the esophagus) into a type of ... AGA Clinical Practice Guidelines on Management of Gastric Intestinal Metaplasia Intestinal metaplasia (definition) - mondofacto ... Risk factors for progression of gastric intestinal metaplasia to full blown cancer are smoking and family history. Choi, AY; ... Although it was originally reported that people of East Asian ethnicity with gastric intestinal metaplasia are at increased ...
Metaplasia Johansson J, Håkansson HO, Mellblom L, et al. (March 2010). "Pancreatic acinar metaplasia in the distal oesophagus ... as may be seen in a true metaplasia. The histopathologic features of pancreatic acinar metaplasia are: (1) the presence of cell ... Pancreatic acinar metaplasia (PAM) is a common incidental histopathologic finding present in approximately 20-25% of patients ... "Prevalence and significance of pancreatic acinar metaplasia at the gastroesophageal junction". Am. J. Surg. Pathol. 20 (12): ...
"Nephrogenic metaplasia". Pathology Outlines. Retrieved 22 October 2016. Peeker R Aldenborg F Fall M: Nephrogenic adenoma: A ...
"Intraocular osseous metaplasia. A clinico-pathological study". Indian J Ophthalmol. 50 (3): 183-8. PMID 12355691.{{cite journal ...
Endometriosis Metaplasia Bermejo, Rosa; Gómez, Alicia; Galiana, Nuria; Campos, Antonio; Puente, Rebeca; Bas, Ernesto; Díaz- ...
The reversible transformation of cells of one differentiated cell type to another is called metaplasia. This transition can be ... Slack JM (January 2009). "Metaplasia and somatic cell reprogramming". The Journal of Pathology. 217 (2): 161-8. doi:10.1002/ ...
An example of PAS-D in use is in showing gastric/duodenal metaplasia in duodenal adenomas. PAS diastase stain is also used to ... Periodic acid-Schiff stain Diastase Rubio CA (2007). "Gastric duodenal metaplasia in duodenal adenomas". J. Clin. Pathol. 60 (6 ...
Fukunaga M(2000). Smooth muscle metaplasia in ovarian endometriosis. Histopathology 36(4):348-352. Fujii S, Konishi I, Mori T ( ... Anyway, the phenomenon of smooth muscle cell metaplasia occurring in association with endometriosis (endomyometriosis), as well ...
The disease was also known as myelofibrosis with myeloid metaplasia and agnogenic myeloid metaplasia The World Health ... Tefferi A (2003). "The forgotten myeloproliferative disorder: myeloid metaplasia". The Oncologist. 8 (3): 225-231. doi:10.1634/ ... Lichtman MA (July 2005). "Is it chronic idiopathic myelofibrosis, myelofibrosis with myeloid metaplasia, chronic megakaryocytic ... "The role of splenectomy in myelofibrosis with myeloid metaplasia". Minerva Chirurgica. 65 (6): 619-625. PMID 21224796. "FDA ...
Retrieved 2016-06-07 Definition of metaplasia. Merriam-Webster Online Dictionary. Retrieved 2016-06-07 Definition of ...
Metaplasia, however, aligns more closely with transdifferentiation, because metaplasia refers more to the idea of a phenotypic ... Metaplasia refers to the change from a fully differentiated cell type to another. This implies that the cell is able to adapt ... The idea of metaplasia depends on the ability for a cell to dedifferentiate. This definition is important to consider when ... Metaplasia [13] is not another definition of dedifferentiation, but the two words have very similar implications for cells. ...
Squamous metaplasia of breast epithelia is known to be more prevalent in postmenopausal women (where it does not cause any ... Squamous metaplasia of lactiferous ducts - abbreviated SMOLD is a change where the normal double layer cuboid epithelium of the ... Further uncertainty in the relation of SMOLD and the subareolar abscess is that squamous metaplasia is very often caused by ... It is a frequently aseptic inflammation and has been associated with squamous metaplasia of lactiferous ducts. The term is ...
Adenocarcinoma of the stomach and intestinal metaplasia. H&E stain. If cancer cells are found in the tissue sample, the next ... Tsukamoto T, Mizoshita T, Tatematsu M (2006). "Gastric-and-intestinal mixed-type intestinal metaplasia: aberrant expression of ... and intestinal metaplasia. In addition, Foxp3 polymorphism (rs3761548) might contribute to gastric cancer development through ... it associates intestinal metaplasia in neighbouring mucosa. Depending on glandular architecture, cellular pleomorphism and ...
"Visceral Nodular Cartilaginous Metaplasia in Rockfishes (Sebastes Spp.) in the Eastern North Pacific Ocean." Journal of ... discrete nodules of cartilaginous metaplasia. Like other rockfish, yellowmouth rockfish have swim bladders that are unable to ...
The presence of intestinal metaplasia in Barrett's esophagus represents a marker for the progression of metaplasia towards ... The metaplasia is grossly visible through a gastroscope, but biopsy specimens must be examined under a microscope to determine ... Colonic metaplasia is usually identified by finding goblet cells in the epithelium and is necessary for the true diagnosis.[ ... The presence of goblet cells, called intestinal metaplasia, is necessary to make a diagnosis of Barrett's esophagus. This ...
Spechler SJ, Goyal RK (February 1996). "The columnar-lined esophagus, intestinal metaplasia, and Norman Barrett". ...
In 2018, Merchant was awarded additional NIH funding to study "MDSC Polarization and Helicobacter-Induced Gastric Metaplasia;" ... "1R01DK118563-01, MDSC POLARIZATION AND HELICOBACTER-INDUCED GASTRIC METAPLASIA". projectreporter.nih.gov. Retrieved 2020-06-10 ...
Slack, J.M.W. (2007). "Metaplasia and transdifferentiation: from pure biology to the clinic". Nature Reviews Molecular Cell ... Casimir CM, Gates PB, Patient RK, Brockes JP (1988-12-01). "Evidence for dedifferentiation and metaplasia in amphibian limb ...
"CDX1 is an important molecular mediator of Barrett's metaplasia". Proceedings of the National Academy of Sciences of the United ... with special emphasis on participation in intestinal metaplasia of the human stomach". Gastric Cancer. 4 (4): 185-91. doi: ...
Slack, J.M.W. (2007). "Metaplasia and transdifferentiation: from pure biology to the clinic". Nature Reviews Molecular Cell ...
Intestinal metaplasia is classified histologically as complete or incomplete. With complete metaplasia, gastric mucosa is ... Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum and may extend to the body. Gastric ... Mucous gland metaplasia, the reversible replacement of differentiated cells, occurs in the setting of severe damage of the ... In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently ...
This mode of bone formation is identified as metaplasia. Osteoderms are not historically uniform but include a mix of tissues, ...
Yadav UC, Aguilera-Aguirre L, Ramana KV, Boldogh I, Srivastava SK (2010). "Aldose reductase inhibition prevents metaplasia of ... root pathology modulating treatment for asthma and COPD since it has been shown that they inhibit goblet cell metaplasia in the ...
Interleukin-13 has a critical role in goblet cell metaplasia. Goblet cells are filled with mucin (MUC). MUC5AC Mucin 5AC is a ... goblet cell metaplasia, mucus hypersecretion and airway remodelling which all contribute to airway obstruction. murine studies ...
2001). "LI-cadherin: a marker of gastric metaplasia and neoplasia". Gut. 49 (1): 73-81. doi:10.1136/gut.49.1.73. PMC 1728355. ...
Areas of squamous metaplasia and epithelial pearls may be present. The tumor is not enveloped, but it is surrounded by a ...
Lewis, secretor, and ABO phenotypes, and sulfomucin expression in gastric intestinal metaplasia. J Torrado; J Torrado ... We explored the association between the expression of sulfomucins in gastric intestinal metaplasia, a known marker of ... and sulfomucin expression in gastric intestinal metaplasia.. Cancer Epidemiol Biomarkers Prev 1 April 1997; 6 (4): 287-289. ...
Maxwell, P. (2002). bcl-2 and p21 immunostaining of cervical tubo-endometrial metaplasia. Histopathology, 40(1)(1), 107-108. ... Maxwell, P 2002, bcl-2 and p21 immunostaining of cervical tubo-endometrial metaplasia., Histopathology, vol. 40(1), no. 1, pp ... bcl-2 and p21 immunostaining of cervical tubo-endometrial metaplasia. In: Histopathology. 2002 ; Vol. 40(1), No. 1. pp. 107-108 ... bcl-2 and p21 immunostaining of cervical tubo-endometrial metaplasia. Histopathology. 2002;40(1)(1):107-108. ...
Three types of metaplasia model through Kras activation, Pten deletion, or Cdh1 deletion in the gastric epithelium. ... Three types of metaplasia model through Kras activation, Pten deletion, or Cdh1 deletion i ... Chronic inflammation and intestinal metaplasia are strongly associated with gastric carcinogenesis. Kras activation and Pten ... Metaplasia; Camundongos Transgênicos; PTEN Fosfo-Hidrolase/genética; Fenótipo; Proteínas Proto-Oncogênicas p21(ras)/genética; ...
Metaplasia. Abnormal replacement of cells.. Methemoglobinemia. Excessive accumulation of an inactive form of hemoglobin in the ...
Squamous metaplasia. +. -. -. +. -. -. -. +. Atypical pneumocytes. +++. -. -. +. -. -. -. +. Interstitial pneumonitis. +. -. - ...
This page includes the following topics and synonyms: AGUS Pap Smear, Atypical Glandular Cells of Undetermined Significance.
Myeloid metaplasia (see the image below). Peripheral smear from a patient with agnogenic myeloid metaplasia. This image shows ... Peripheral smear from a patient with agnogenic myeloid metaplasia. This image shows the presence of teardrop red blood cells ( ...
Another possible pre-cancerous change is intestinal metaplasia. In this condition, the cells that normally line the stomach are ... Both atrophic gastritis and intestinal metaplasia can lead to having too few gland cells, which would normally secrete ...
Myeloid metaplasia (see the image below). Peripheral smear from a patient with agnogenic myeloid metaplasia. This image shows ... Peripheral smear from a patient with agnogenic myeloid metaplasia. This image shows the presence of teardrop red blood cells ( ...
Idiopathic myelofibrosis; Myeloid metaplasia; Agnogenic myeloid metaplasia; Primary myelofibrosis; Secondary myelofibrosis; ...
The FOXM1 inhibitor RCM-1 suppresses goblet cell metaplasia and prevents IL-13 and STAT6 signaling in allergen-exposed mice. ... FOXM1 promotes allergen-induced goblet cell metaplasia and pulmonary inflammation. Ren, X; Shah, TA; Ustiyan, V; Zhang, Y; ... Small molecule compound RCM-1, which inhibits goblet cell metaplasia and lung inflammation in asthma (Sun et al, Science ...
b) Pseudopyloric glandular metaplasia in the terminal ileum (×400 magnification). (c) Longitudinal ulcer with luminal stenosis ...
... squamous metaplasia). The cord had no twists but contained numerous smaller blood vessels, some of which surrounded the ...
Epithelial squamous metaplasia: can be confused for carcinoma in situ * Bronchial mural destruction ... Usual respiratory type epithelium may be ulcerated and replaced by granulation tissue or squamous metaplasia * Chronic ... More eosinophils, goblet cell hyperplasia and metaplasia, Charcot-Leyden crystals, smooth muscle hypertrophy * Aspiration ...
Categories: Metaplasia Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, CopyrightRestricted 5 images ...
Oral and gastric microbiome in relation to gastric intestinal metaplasia. Opens in a new tab ...
Muc-5/5ac mucin messenger RNA and protein expression is a marker of goblet cell metaplasia in murine airways. Am J Respir Cell ... IL-4 induces mucin gene expression and goblet cell metaplasia in vitro and in vivo. J Immunol 1999. 162:6233-6237. View this ... An important result coming from our in vitro studies is that IL-13 may both induce mucus metaplasia and alteration of ciliated ... In animal models of asthma, interleukin-13 (IL-13) induces goblet cell metaplasia, eosinophil infiltration of the bronchial ...
Non-neoplastic effects included inflammation of the nose and lungs, metaplasia of the olfactory epithelium and hyperplasia of ... olfactory epithelium metaplasia, respiratory epithelium hyperplasia; no NOAEC as LOAEC is lowest exposure level tested in the ... squamous metaplasia, hyaline degeneration, goblet cell hyperplasia and glandular hyperplasia of the respiratory epithelium (NTP ... squamous metaplasia, hyaline degeneration, goblet cell hyperplasia, glandular hyperplasia of the respiratory epithelium); no ...
Myelosclerosis with myeloid metaplasia. 9962/3. Essential thrombocythemia. 9963/3. Chronic neutrophilic leukemia. ...
Squamous metaplasia and ectropion Ectropion Metaplasia Inflammation and cervicitis Candidiasis Trichomonas vaginalis ...
Glew, R.H., Haese, W.H. and McIntyre, P.A. (1973) Myeloid metaplasia with myelofibrosis. The clinical spectrum of ...
This abnormal tissue in the esophagus is known as "intestinal metaplasia." If left untreated, over time the intestinal ... The pathologist confirms the presence or absence of intestinal metaplasia and determines the degree of dysplasia (low, ... metaplasia can turn into more severely abnormal tissue, termed "esophageal dysplasia.". At the Center for Advanced Digestive ...
2005) Osseous metaplasia in the setting of nephrogenic fibrosing dermopathy. J Cutan Pathol 32: 172-175 ...
  • We explored the association between the expression of sulfomucins in gastric intestinal metaplasia, a known marker of preneoplastic progression, and the expression of Lewis, secretor, and ABO phenotypes, in 523 subjects from Nariño, Colombia, and 856 subjects from northern Spain. (aacrjournals.org)
  • Chronic inflammation and intestinal metaplasia are strongly associated with gastric carcinogenesis . (bvsalud.org)
  • Both atrophic gastritis and intestinal metaplasia can lead to having too few gland cells, which would normally secrete substances that help protect the cells in the stomach's inner lining. (cancer.org)
  • atrophy 8% and intestinal metaplasia in 6% of the cases. (who.int)
  • Helicobacter pylori infection causes chronic active gastritis and it has a role in the development of lym- phoid follicles, intestinal metaplasia, atrophy and dysplasia. (who.int)
  • However, in few cases some strains duced acid secretion, intestinal metaplasia, and in- are capable of attacking the mucosa. (who.int)
  • This abnormal tissue in the esophagus is known as "intestinal metaplasia. (nyp.org)
  • If left untreated, over time the intestinal metaplasia can turn into more severely abnormal tissue, termed "esophageal dysplasia. (nyp.org)
  • The pathologist confirms the presence or absence of intestinal metaplasia and determines the degree of dysplasia (low, intermediate, or high grade). (nyp.org)
  • Gastric cancer is the fourth commonest ently reported that H. pylori eradication were subjected to routine history and malignant disorder and the second com- can lead to a regression of acute gastritis clinical examination, fol owed by an monest cause of cancer-related death and intestinal metaplasia, and that such upper gastrointestinal endoscopic ex- worldwide [1]. (who.int)
  • Original research: Endoscopic grading of gastric intestinal metaplasia on risk assessment for early gastric neoplasia: can we replace histology assessment also in the West? (bmj.com)
  • intestinal metaplasia and atrophy. (bvsalud.org)
  • Three types of metaplasia model through Kras activation, Pten deletion, or Cdh1 deletion in the gastric epithelium. (bvsalud.org)
  • bcl-2 and p21 immunostaining of cervical tubo-endometrial metaplasia. (qub.ac.uk)
  • 2022 DDIT4 Licenses Only Healthy Cells to Proliferate During Injury-induced Metaplasia. (wustl.edu)
  • however, biopsy of tic revealed squamous metaplasia with keratinization and negative cytology. (medscape.com)
  • Keratinizing squamous metaplasia in and of itself is not a worrisome finding. (medscape.com)
  • Some studies have shown that concurrent carcinoma (transitional cell carcinoma, squamous cell carcinoma, or adenocarcinoma) of the bladder was found in 10% to 20% of patients with squamous metaplasia, but the malignant lesion was usually noted to arise in the nonmetaplastic portions of the epithelium. (medscape.com)
  • Because both squamous metaplasia and certain types of bladder cancer can be caused by chronic inflammation, it is not surprising that these 2 entities may occur in the same patient. (medscape.com)
  • However, the way to lower the patient's risk of developing cancer is not to remove the squamous metaplasia, but to eliminate the source of the chronic inflammation. (medscape.com)
  • Keratinizing Squamous Metaplasia - Medscape - Feb 14, 2006. (medscape.com)
  • Widran J, Sanchez R, Gruhn J. Squamous metaplasia of the bladder: a study of 450 patients. (medscape.com)
  • Mechanisms of asbestos-induced squamous metaplasia in tracheobronchial epithelial cells. (nih.gov)
  • PURPOSE The intent of this solicitation is to promote research on the molecular and cellular mechanisms involved in hypersecretion of mucus and mucous cell metaplasia in human airway diseases. (nih.gov)
  • This Request for Applications (RFA), Molecular Mechanisms of Mucous Cell Metaplasia and Excess Mucous Secretion In Airway Diseases, is related to one or more of the priority areas. (nih.gov)
  • RESEARCH OBJECTIVES Background Mucous cell metaplasia with mucous hypersecretion is a prominent manifestation of many common inflammatory diseases of the upper and lower airways. (nih.gov)
  • In doing so, ApoE attenuates airway remodeling (mucous cell metaplasia) and airway hyperreactivity. (nih.gov)
  • Typically, as vascular inflammation progresses, vessels may undergo mineralization, leading to cartilage formation and ultimately osseous metaplasia. (nih.gov)
  • 1. Endocervical adenocarcinoma in situ of tubal type and its relation to atypical tubal metaplasia. (nih.gov)
  • 11. Endocervical tubal metaplasia and adenocarcinoma in situ: role of immunohistochemistry for carcinoembryonic antigen and vimentin in differential diagnosis. (nih.gov)
  • Knowledge of the molecular pathways that regulate secretion and metaplasia in the pulmonary mucous cells of individuals with airway diseases might aid the rational development of new drugs for the control of mucous function. (nih.gov)
  • Figure Legend: Figure 1 Brain, Artery - Metaplasia, Osseous in an F344/N male rat from a chronic study. (nih.gov)
  • Metaplasia occurs rarely as a spontaneous lesion but, rather, as part of the progression of mineralization or atherosclerotic lesions. (nih.gov)
  • In Smad6-knockout mice, cartilaginous metaplasia and trabecular bone formation containing marrow elements have been noted in the aorta and around the outflow track of the heart. (nih.gov)
  • Cartilaginous metaplasia and calcification in aortic allograft is associated with transforming growth factor 1 expression. (nih.gov)
  • Figure 3 Aorta - Metaplasia, Osseous in a female B6C3F1/N mouse from a subchronic study. (nih.gov)
  • 5. Tubal metaplasia of the uterine cervix: a prevalence study in patients with gynecologic pathologic findings. (nih.gov)