Causes

Esophagitis cannot be spread. However, infections can be spread by those who have infectious esophagitis. Esophagitis can develop due to many causes. GERD is the most common cause of esophagitis because of the backflow of acid from the stomach, which can irritate the lining of the esophagus.

Other causes include:

- Medicines- Can cause esophageal damage that can lead to esophageal ulcers

- Nonsteroidal anti-inflammatory drugs (NSAIDS)-aspirin, naproxen sodium, and ibuprofen. Known to irritate the GI tract.

- Antibiotics- doxycycline and tetracycline

- Quinidine

- Biphosphonates- used to treat osteoporosis

- Steroids

- Potassium chloride

- Chemical injury by alkaline or acid solutions

- Physical injury resulting from nasogastric tubes.

- Alcohol abuse- Can wear down the lining of the esophagus.

- Crohn's disease – a type of IBD and an autoimmune disease that can cause esophagitis if it attacks the esophagus.

- Stress- Can cause higher levels of acid reflux

- Radiation therapy-Can affect the immune system.

- Allergies (food, inhalants)- Allergies can stimulate eosinophilic esophagitis.

- Infection-People with an immunodeficiencies have a higher chance of developing esophagitis.

- Vitamins and supplements (iron, Vitamin C, and potassium)-Supplements and minerals can be hard on the GI tract.

- Vomiting- Acid can irritate esophagus.

- Hernias-A hernia can poke through the diaphragm muscle and can inhibit the stomach acid and food from draining quickly.

- Surgery

Prevention

Since there can be many causes underlying esophagitis, it is important to try to find the cause to help to prevent esophagitis. To prevent reflux esophagitis, avoid acidic foods, caffeine, eating before going to bed, alcohol, fatty meals, and smoking. To prevent drug-induced esophagitis, drink plenty of liquids when taking medicines, take an alternative drug, and do not take medicines while lying down, before sleeping, or too many at one time. Esophagitis is more prevalent in adults and does not discriminate.

Reflux esophagitis

A backflow of stomach acids into the esophagus that causes irritation, chronic inflammation, and tissue damage in the esophagus.

Infectious esophagitis

Esophagitis that happens due to a viral, fungal, parasitic or bacterial infection. More likely to happen to people who have an immunodeficiency. Types include:

Fungal

- Candida (Esophageal candidiasis)

Viral

- Herpes simplex (Herpes esophagitis)

- Cytomegalovirus

Drug-induced esophagitis

Damage to the esophagus due to medications. If the esophagus is not coated or if the medicine is not taken with enough liquid, it can damage the tissues.

Eosinophilic esophagitis

This esophagitis is caused by a high concentration of eosinophils in the esophagus. The presence of eosinophils in the esophagus may be due to an allergen or acid reflux. This esophagitis can be triggered by allergies to food or to inhaled allergens. This type is still poorly understood.

Lymphocytic esophagitis

Lymphocytic esophagitis is when there is an increased amount of lymphocytes in the lining of the esophagus. It is a rare condition. It could be connected to eosinophilic esophagitis.

Herpes esophagitis is a viral infection of the esophagus caused by "Herpes simplex virus" (HSV).

While the disease most often occurs in immunocompromised patients, including post-chemotherapy, immunosuppression with organ transplants and in AIDS, herpes esophagitis can also occur in immunocompetent individuals.

Herpes simplex virus is commonly found in humans, yet uncommonly results in systemic manifestations. Suppression of HIV with antiretroviral medications, careful monitoring of immunosuppressive medications are important means of prevention. Antiviral prophylaxis such as daily acyclovir in immunocompromised individuals may be considered.

Cytomegalovirus esophagitis is a form of esophagitis associated with cytomegalovirus.

It is likely to present with a single, deep ulcer as opposed to the multiple shallow ulcers seen in herpes esophagitis.

Cytomegalovirus colitis, also known as CMV colitis, is an inflammation of the colon

Causes

The infection is spread by saliva, urine, respiratory droplets, sexual contact, and blood transfusions. Most people are exposed to the virus in their lifetime, but it usually produces mild or no symptoms in healthy people.

However, serious CMV infections can occur in people with weakened immune systems. This includes patients receiving chemotherapy for cancer and patients on immune-suppressing medicines following an organ transplant.

In rare instances, more severe CMV infection involving the GI tract has been reported in people with a healthy immune system.

The systemic use of corticosteroids in the context of inflammatory bowel disease.

Esophageal candidiasis is an opportunistic infection of the esophagus by "Candida albicans". The disease usually occurs in patients in immunocompromised states, including post-chemotherapy and in AIDS. However, it can also occur in patients with no predisposing risk factors, and is more likely to be asymptomatic in those patients. It is also known as candidal esophagitis or monilial esophagitis.

The current first-line treatment is fluconazole, 200 mg. on the first day, followed by daily dosing of 100 mg. for at least 21 days total. Treatment should continue for 14 days after relief of symptoms.

Other therapy options include:

- nystatin is not an effective treatment for esophageal candidiasis. It can be used as (swish, do not swallow) treatment for oral candidiasis that occurs with the use of asthma pumps.

- other oral triazoles, such as itraconazole

- caspofungin, used in refractory or systemic cases

- amphotericin, used in refractory or systemic cases

Among individuals being treated in intensive care units, the mortality rate is about 30-50% when systemic candidiasis develops.

Recommendations for pregnant women with regard to CMV infection:

- Throughout the pregnancy, practice good personal hygiene, especially handwashing with soap and water, after contact with diapers or oral secretions (particularly with a child who is in day care). Sharing of food, eating and drinking utensils, and contact with toddlers' saliva should be avoided.

- Women who develop a mononucleosis-like illness during pregnancy should be evaluated for CMV infection and counseled about the possible risks to the unborn child.

- Laboratory testing for antibody to CMV can be performed to determine if a woman has already had CMV infection.

- Recovery of CMV from the cervix or urine of women at or before the time of delivery does not warrant a cesarean section.

- The demonstrated benefits of breast-feeding outweigh the minimal risk of acquiring CMV from the breast-feeding mother.

- There is no need to either screen for CMV or exclude CMV-excreting children from schools or institutions because the virus is frequently found in many healthy children and adults.

Treatment with hyperimmune globulin in mothers with primary CMV infection has been shown to be effective in preventing congenital disease in several studies. One study did not show significant decrease in the risk of congenital cytomegalovirus infection.

Most healthy people working with infants and children face no special risk from CMV infection. However, for women of child-bearing age who previously have not been infected with CMV, there is a potential risk to the developing unborn child (the risk is described above in the Pregnancy section). Contact with children who are in day care, where CMV infection is commonly transmitted among young children (particularly toddlers), may be a source of exposure to CMV. Since CMV is transmitted through contact with infected body fluids, including urine and saliva, child care providers (meaning day care workers, special education teachers, as well as mothers) should be educated about the risks of CMV infection and the precautions they can take. Day care workers appear to be at a greater risk than hospital and other health care providers, and this may be due in part to the increased emphasis on personal hygiene in the health care setting.

Recommendations for individuals providing care for infants and children:

- Employees should be educated concerning CMV, its transmission, and hygienic practices, such as handwashing, which minimize the risk of infection.

- Susceptible nonpregnant women working with infants and children should not routinely be transferred to other work situations.

- Pregnant women working with infants and children should be informed of the risk of acquiring CMV infection and the possible effects on the unborn child.

- Routine laboratory testing for CMV antibody in female workers is not specifically recommended due to its high occurrence, but can be performed to determine their immune status.

"Candida" yeasts are generally present in healthy humans, frequently part of the human body's normal oral and intestinal flora, and particularly on the skin; however, their growth is normally limited by the human immune system and by competition of other microorganisms, such as bacteria occupying the same locations in the human body.

"Candida" requires moisture for growth, notably on the skin. For example, wearing wet swimwear for long periods of time is believed to be a risk factor. In extreme cases, superficial infections of the skin or mucous membranes may enter into the bloodstream and cause systemic "Candida" infections.

Factors that increase the risk of candidiasis include HIV/AIDS, mononucleosis, cancer treatments, steroids, stress, antibiotic usage, diabetes, and nutrient deficiency. Hormone replacement therapy and infertility treatments may also be predisposing factors. Treatment with antibiotics can lead to eliminating the yeast's natural competitors for resources in the oral and intestinal flora; thereby increasing the severity of the condition. A weakened or undeveloped immune system or metabolic illnesses are significant predisposing factors of candidiasis. Almost 15% of people with weakened immune systems develop a systemic illness caused by "Candida" species. Diets high in simple carbohydrates have been found to affect rates of oral candidiases.

"C. albicans" was isolated from the vaginas of 19% of apparently healthy women, i.e., those who experienced few or no symptoms of infection. External use of detergents or douches or internal disturbances (hormonal or physiological) can perturb the normal vaginal flora, consisting of lactic acid bacteria, such as lactobacilli, and result in an overgrowth of "Candida" cells, causing symptoms of infection, such as local inflammation. Pregnancy and the use of oral contraceptives have been reported as risk factors. Diabetes mellitus and the use of antibiotics are also linked to increased rates of yeast infections.

In penile candidiasis, the causes include sexual intercourse with an infected individual, low immunity, antibiotics, and diabetes. Male genital yeast infections are less common, but a yeast infection on the penis caused from direct contact via sexual intercourse with an infected partner is not uncommon.

GERD is caused by a failure of the lower esophageal sphincter. In healthy patients, the "Angle of His"—the angle at which the esophagus enters the stomach—creates a valve that prevents duodenal bile, enzymes, and stomach acid from traveling back into the esophagus where they can cause burning and inflammation of sensitive esophageal tissue.

Factors that can contribute to GERD:

- Hiatal hernia, which increases the likelihood of GERD due to mechanical and motility factors.

- Obesity: increasing body mass index is associated with more severe GERD. In a large series of 2,000 patients with symptomatic reflux disease, it has been shown that 13% of changes in esophageal acid exposure is attributable to changes in body mass index.

- Zollinger-Ellison syndrome, which can be present with increased gastric acidity due to gastrin production.

- A high blood calcium level, which can increase gastrin production, leading to increased acidity.

- Scleroderma and systemic sclerosis, which can feature esophageal dysmotility.

- The use of medicines such as prednisolone.

- Visceroptosis or Glénard syndrome, in which the stomach has sunk in the abdomen upsetting the motility and acid secretion of the stomach.

GERD has been linked to a variety of respiratory and laryngeal complaints such as laryngitis, chronic cough, pulmonary fibrosis, earache, and asthma, even when not clinically apparent. These atypical manifestations of GERD are commonly referred to as laryngopharyngeal reflux (LPR) or as extraesophageal reflux disease (EERD).

Factors that have been linked with GERD, but not conclusively:

- Obstructive sleep apnea

- Gallstones, which can impede the flow of bile into the duodenum, which can affect the ability to neutralize gastric acid

In 1999, a review of existing studies found that, on average, 40% of GERD patients also had "H. pylori" infection. The eradication of "H. pylori" can lead to an increase in acid secretion, leading to the question of whether "H. pylori"-infected GERD patients are any different than non-infected GERD patients. A double-blind study, reported in 2004, found no clinically significant difference between these two types of patients with regard to the subjective or objective measures of disease severity.

Sixty percent of mothers of preterm infants are infected with cytomegalovirus (CMV). Infection is asymptomatic in most instances but 9% to 12% of postnatally infected low birth weight, preterm infants have severe, sepsis-like infection. CMV infection duration can be long and result in pneumonitis in association with fibrosis. CMV infection in infants has an unexpected effect on the white blood cells of the immune system causing them to prematurely age. This leads to a reduced immune response similar to that found in the elderly.

GERD may lead to Barrett's esophagus, a type of intestinal metaplasia, which is in turn a precursor condition for esophageal cancer. The risk of progression from Barrett's to dysplasia is uncertain, but is estimated at about 20% of cases. Due to the risk of chronic heartburn progressing to Barrett's, EGD every five years is recommended for people with chronic heartburn, or who take drugs for chronic GERD.

Congential rubella is still a risk with higher risk among immigrant women from countries without adequate vaccination programs.

Gastroesophageal reflux disease (GERD) affects approximately 40% of adults. Strictures occur in 7 to 23% of patients with GERD who are untreated.

EoE is a relatively poorly understood disease of which awareness is rising.

At a tissue level, EoE is characterized by a dense infiltrate with white blood cells of the eosinophil type into the epithelial lining of the esophagus. This is thought to be an allergic reaction against ingested food, based on the important role eosinophils play in allergic reactions. Eosinophils are inflammatory cells that release a variety of chemical signals which inflame the surrounding esophageal tissue. This results in the signs and symptoms of pain, visible redness on endoscopy, and a natural history that may include stricturing.

Treatment strategies may include medication, dietary modification to exclude food allergens, and mechanical dilatation of the esophagus.

The current recommendation for first line treatment is PPI in lieu of diet as more than half of people with EOE respond to this, and it is a low risk, low cost treatment. The next step treatment is topical corticosteroids (topical viscous budesonide or fluticasone).

Dietary treatment can be effective, as there does appear to be a role of allergy in the development of EOE. Allergy testing is not particularly effective in predicting which foods are driving the disease process. Various approaches have been tried, where either six food groups (cow´s milk, wheat, egg, soy, nuts and fish/seafood), four groups (animal milk, gluten-containing cereals, egg, legumes) or two groups (animal milk and gluten-containing cereals) are excluded for a period of time, usually six weeks. Endoscopy is required to measure the response to the dietary measure. A "top down" (starting with six foods, then reintroducing) approach may be very restrictive. Four- or even two-group exclusion diets may be less difficult to follow and reduce the need for many endoscopies if the response to the limited restriction is good.

Endoscopic dilatation is sometimes required if there is significant narrowing of the esophagus. This is effective in 84% of people who require this procedure.

Barrett's esophagus is a premalignant condition. Its malignant sequela, oesophagogastric junctional adenocarcinoma, has a mortality rate of over 85%. The risk of developing esophageal adenocarcinoma in people who have Barrett's esophagus has been estimated to be 6–7 per 1000 person-years, however a cohort study of 11,028 patients from Denmark published in 2011 showed an incidence of only 1.2 per 1000 person-years (5.1 per 1000 person-years in patients with dysplasia, 1.0 per 1000 person-years in patients without dysplasia). The relative risk of esophageal adenocarcinoma is approximately 10 in those with Barret's esophagus, compared to the general population. Most patients with esophageal carcinoma survive less than one year.

The role of "Helicobacter pylori" in functional dyspepsia is controversial, and no clear causal relationship has been established. This is true for both the symptom profile and pathophysiology of functional dyspepsia. Although some epidemiologic studies have suggested an association between "H. pylori" infection and functional dyspepsia, others have not. The discrepancy may stem in part from differences in methodology and lack of adequate consideration of confounding factors such as past history of peptic ulcer disease and socioeconomic status. Controlled trials disagree about whether or not "H. pylori" eradication is beneficial in functional dyspepsia, with roughly half of the trials showing improvement and the other half no improvement. In a recent multicenter U.S. trial that randomized 240 patients to treatment or placebo, and followed patients for 12 months, 28% of treated patients versus 23% of those receiving placebo reported relief of symptoms at the 12-month follow-up. Similarly, recent European trials have not shown significant differences in symptoms after "H. pylori" eradication as compared with controls. Systematic reviews of eradication have been conducted, with varying results. A systematic review in the Annals of Internal Medicine suggested no statistically significant effect, with an odds ratio (OR) for treatment success versus control of 1.29 (95% CI, 0.89–1.89; P = 0.18). Still, no effect was seen after adjusting for heterogeneity and for cure of "H. pylori". In contrast, a Cochrane review found a small but statistically significant effect in curing symptoms ("H. pylori" cure vs placebo, 36% vs 30%, respectively).

Acute, self-limited "dyspepsia" may be caused by overeating, eating too quickly, eating high-fat foods, eating during stressful situations, or drinking too much alcohol or coffee. Many medications cause dyspepsia, including aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics (metronidazole, macrolides), diabetes drugs (metformin, Alpha-glucosidase inhibitor, amylin analogs, GLP-1 receptor antagonists), antihypertensive medications (angiotensin converting enzyme [ACE] inhibitors, Angiotensin II receptor antagonist), cholesterol-lowering agents (niacin, fibrates), neuropsychiatric medications (cholinesterase inhibitors [donepezil, rivastigmine]), SSRIs (fluoxetine, sertraline), serotonin-norepinephrine-reuptake inhibitors (venlafaxine, duloxetine), Parkinson drugs (Dopamine agonist, monoamine oxidase [MAO]-B inhibitors), corticosteroids, estrogens, digoxin, iron, and opioids.

It can also be caused by certain medical conditions, such as:

- Ulcers

- Abscesses

- Upper respiratory tract infections

- Inflammation or infection of the mouth, tongue, or throat (esophagitis, pharyngitis, tonsillitis, epiglottitis)

- Immune disorders

- Oral or throat cancer

Barrett's esophagus occurs due to chronic inflammation. The principal cause of the chronic inflammation is gastroesophageal reflux disease, GERD (UK: GORD). In this disease, acidic stomach, bile, and small intestine and pancreatic contents cause damage to the cells of the lower esophagus. Recently, bile acids were shown to be able to induce intestinal differentiation, in gastroesophageal junction cells, through inhibition of the epidermal growth factor receptor (EGFR) and the protein kinase enzyme Akt. This results in the eventual up-regulation of the p50 subunit of protein complex NF-κB ("NFKB1"), and ultimately activation of the homeobox gene "CDX2", which is responsible for the expression of intestinal enzymes such as guanylate cyclase 2C. This mechanism also explains the selection of HER2/neu (also called ERBB2) and the overexpressing (lineage-addicted) cancer cells during the process of carcinogenesis, and the efficacy of targeted therapy against the Her-2 receptor with trastuzumab (Herceptin) in the treatment of adenocarcinomas at the gastroesophageal junction.

Researchers are unable to predict who with heartburn will develop Barrett's esophagus. While no relationship exists between the severity of heartburn and the development of Barrett's esophagus, a relationship does exist between chronic heartburn and the development of Barrett's esophagus. Sometimes, people with Barrett's esophagus have no heartburn symptoms at all. In rare cases, damage to the esophagus may be caused by swallowing a corrosive substance such as lye.