The diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer. In some cases, doctors may treat ulcers without diagnosing them with specific tests and observe whether the symptoms resolve, thus indicating that their primary diagnosis was accurate.

More specifically, peptic ulcers erode the muscularis mucosae, at minimum reaching to the level of the submucosa (contrast with erosions, which do not involve the muscularis mucosae).

Confirmation of the diagnosis is made with the help of tests such as endoscopies or barium contrast x-rays. The tests are typically ordered if the symptoms do not resolve after a few weeks of treatment, or when they first appear in a person who is over age 45 or who has other symptoms such as weight loss, because stomach cancer can cause similar symptoms. Also, when severe ulcers resist treatment, particularly if a person has several ulcers or the ulcers are in unusual places, a doctor may suspect an underlying condition that causes the stomach to overproduce acid.

An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on people in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.

One of the reasons that blood tests are not reliable for accurate peptic ulcer diagnosis on their own is their inability to differentiate between past exposure to the bacteria and current infection. Additionally, a false negative result is possible with a blood test if the person has recently been taking certain drugs, such as antibiotics or proton-pump inhibitors.

The diagnosis of "Helicobacter pylori" can be made by:

- Urea breath test (noninvasive and does not require EGD);

- Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive. Most labs are not set up to perform "H. pylori" cultures;

- Direct detection of urease activity in a biopsy specimen by rapid urease test;

- Measurement of antibody levels in the blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;

- Stool antigen test;

- Histological examination and staining of an EGD biopsy.

The breath test uses radioactive carbon to detect H. pylori. To perform this exam the person will be asked to drink a tasteless liquid which contains the carbon as part of the substance that the bacteria breaks down. After an hour, the person will be asked to blow into a bag that is sealed. If the person is infected with H. pylori, the breath sample will contain radioactive carbon dioxide. This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria.

The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be kept in mind. This is especially true in ulcers of the "greater (large) curvature" of the stomach; most are also a consequence of chronic "H. pylori" infection.

If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the person stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.

Other radiological studies frequently used to assess patients with chronic stomach problems include a barium swallow, where a dye is consumed and pictures of the esophagus and stomach are obtained every few minutes. Other tests include a 24-hour pH study, CT scans or MRI.

A gastroenterologist is a medical professional that can diagnose esophagitis. To diagnose esophagitis, the doctor will interview the patient regarding their signs and symptoms. If the doctor suspects esophagitis, tests can be ordered. Esophagitis can be diagnosed by an upper endoscopy, biopsy, upper GI series (or barium swallow), and laboratory tests.

An upper endoscopy is a procedure to look at the esophagus by using an endoscope. While looking at the esophagus, the doctor is able to take a small biopsy. The biopsy can be used to confirm inflammation of the esophagus.

An upper GI series uses a barium contrast, fluoroscopy, and an X-ray. During a barium X-ray, a solution with barium or pill is taken before getting an X-ray. The barium makes the organs more visible and can detect if there is any narrowing, inflammation, or other abnormalities that can be causing the disease. The upper GI series can be used to find the cause of GI symptoms. An esophagram is if only the throat and esophagus are looked at.

Laboratory tests can be done on biopsies removed from the esophagus and can help determine the cause of the esophagitis. Laboratory tests can help diagnose a fungal, viral, or bacterial infection. Scanning for white blood cells can help diagnose eosinophil esophagitis.

Some lifestyle indicators for this disease include: stress, unhealthy eating, smoking, drinking, family history, allergies, and an immunodeficiency. It is important for the doctor to review the patient's medical history before diagnosing with esophagitis. Specific subtypes and other causes should be taken into account when making the final diagnosis.

The diagnosis of GERD is usually made when typical symptoms are present. Reflux can be present in people without symptoms and the diagnosis requires both symptoms or complications and reflux of stomach content.

Other investigations may include esophagogastroduodenoscopy (EGD). Barium swallow X-rays should not be used for diagnosis. Esophageal manometry is not recommended for use in diagnosis, being recommended only prior to surgery. Ambulatory esophageal pH monitoring may be useful in those who do not improve after PPIs and is not needed in those in whom Barrett's esophagus is seen. Investigation for H. pylori is not usually needed.

The current gold standard for diagnosis of GERD is esophageal pH monitoring. It is the most objective test to diagnose the reflux disease and allows monitoring GERD patients in their response to medical or surgical treatment. One practice for diagnosis of GERD is a short-term treatment with proton-pump inhibitors, with improvement in symptoms suggesting a positive diagnosis. Short-term treatment with proton-pump inhibitors may help predict abnormal 24-hr pH monitoring results among patients with symptoms suggestive of GERD.

Younger people with ulcer-like symptoms are often treated with antacids or H2 antagonists before endoscopy is undertaken.

People who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue (misoprostol) in order to help prevent peptic ulcers.

There are many tools for investigating stomach problems. The most common is endoscopy. This procedure is performed as an outpatient and utilizes a small flexible camera. The procedure does require intravenous sedation and takes about 30–45 minutes; the endoscope is inserted via the mouth and can visualize the entire swallowing tube, stomach and duodenum. The procedure also allows the physician to obtain biopsy samples. In many cases of bleeding, the surgeon can use the endoscope to treat the source of bleeding with laser, clips or other injectable drugs.

Often, a diagnosis can be made based on the patient's description of their symptoms, but other methods which may be used to verify gastritis include:

- Blood tests:

- Blood cell count

- Presence of "H. pylori"

- Liver, kidney, gallbladder, or pancreas functions

- Urinalysis

- Stool sample, to look for blood in the stool

- X-rays

- ECGs

- Endoscopy, to check for stomach lining inflammation and mucous erosion

- Stomach biopsy, to test for gastritis and other conditions

Treatments for esophagitis include medications to block acid production, to manage pain, and to reduce inflammation. Other treatments include antibiotics and intravenous nutrition.

To treat reflux esophagitis, over the counter antacids, medications that reduce acid production (H-2 receptor blockers), and proton pump inhibitors are recommended to help block acid production and to let the esophagus heal. Some prescription medications to treat reflux esophagitis include higher dose H-2 receptor blockers, proton pump inhibitors, and prokinetics, which help with the emptying of the stomach.

To treat eosinophilic esophagitis, avoiding any allergens that may be stimulating the eosinophils is recommended. As for medications, proton pump inhibitors and steroids can be prescribed. Steroids that are used to treat asthma can be swallowed to treat eosinophil esophagitis due to nonfood allergens. The removal of food allergens from the diet is included to help treat eosinophilic esophagitis.

For infectious esophagitis, a medicine is prescribed based on what type of infection is causing the esophagitis. These medicines are prescribed to treat bacterial, fungal, viral, and/or parasitic infections.

An endoscopy can be used to remove ill fragments. Surgery can be done to remove the damaged part of the esophagus. For reflux esophagitis, a fundooplication can be done to help strengthen the lower esophageal sphincter from allowing backflow of the stomach into the esophagus. As for patients that have a narrowing esophagus, a gastroenterologist can perform a procedure to dilate the esophagus.

Some home remedies and lifestyle changes to help with esophagitis include losing weight, stop smoking, lowering stress, avoid sleeping/lying down after eating, raise your head while laying down, taking medicines correctly, avoiding certain medications, and avoiding foods that cause the reflux that might be causing the esophagitis.

If the disease remains untreated, it can cause scarring and discomfort in the esophagus. If the irritation is not allowed to heal, esophagitis can result in esophageal ulcers. Esophagitis can develop into Barrett's esophagus and can increase the risk of esophageal cancer.

The prognosis for a person with esophagitis depends on the underlying causes and conditions. If a patient has a more serious underlying cause such as a digestive system or immune system issue, it may be more difficult to treat. Normally, the prognosis would be good with no serious illnesses. If there are more causes than one, the prognosis could move to fair.

Endoscopy, the looking down into the stomach with a fibre-optic scope, is not routinely needed if the case is typical and responds to treatment. It is recommended when people either do not respond well to treatment or have alarm symptoms, including dysphagia, anemia, blood in the stool (detected chemically), wheezing, weight loss, or voice changes. Some physicians advocate either once-in-a-lifetime or 5- to 10-yearly endoscopy for people with longstanding GERD, to evaluate the possible presence of dysplasia or Barrett's esophagus.

Biopsies performed during gastroscopy may show:

- Edema and basal hyperplasia (nonspecific inflammatory changes)

- Lymphocytic inflammation (nonspecific)

- Neutrophilic inflammation (usually due to reflux or "Helicobacter" gastritis)

- Eosinophilic inflammation (usually due to reflux): The presence of intraepithelial eosinophils may suggest a diagnosis of eosinophilic esophagitis (EE) if eosinophils are present in high enough numbers. Less than 20 eosinophils per high-power microscopic field in the distal esophagus, in the presence of other histologic features of GERD, is more consistent with GERD than EE.

- Goblet cell intestinal metaplasia or Barrett's esophagus

- Elongation of the papillae

- Thinning of the squamous cell layer

- Dysplasia

- Carcinoma

Reflux changes may not be erosive in nature, leading to "nonerosive reflux disease".

Once a patient complains of dysphagia they should have an "upper endoscopy" (EGD). Commonly patients are found to have esophagitis and may have an esophageal stricture. Biopsies are usually done to look for evidence of esophagitis even if the EGD is normal. Usually no further testing is required if the diagnosis is established on EGD. Repeat endoscopy may be needed for follow up.

If there is a suspicion of a proximal lesion such as:

- history of surgery for laryngeal or esophageal cancer

- history of radiation or irritating injury

- achalasia

- Zenker's diverticulum

a "barium swallow" may be performed before endoscopy to help identify abnormalities that might increase the risk of perforation at the time of endoscopy.

If achalasia suspected an upper endoscopy is required to exclude a malignancy as a cause of the findings on barium swallow. Manometry is performed next to confirm. A normal endoscopy should be followed by manometry, and if manometry is also normal, the diagnosis is functional dysphagia.

The patient is generally sent for a GI, pulmonary, or ENT, depending on the suspected underlying cause. Consultations with a speech therapist and registered dietitian nutritionist (RDN) are also needed, as many patients may need dietary modifications such as thickened fluids.

The most confirmatory investigation is endoscopy of upper gastrointestinal tract.

Laboratory

- Individuals with gastric outlet obstruction are often hypochloremic, hypokalemic, and alkalotic due to loss of hydrogen chloride and potassium. High urea and creatinine levels may also be observed if the patient is dehydrated.

Abdominal X-ray

- A gastric fluid level may be seen which would support the diagnosis.

Barium meal and follow through

- May show an enlarged stomach and pyloroduodenal stenosis.

Gastroscopy

- May help with cause and can be used therapeutically.

The differential diagnosis of gastric outlet obstruction may include: early gastric carcinoma hiatal hernia, gastroesophageal reflux, adrenal insufficiency, and inborn errors of metabolism.

A diagnosis of gastric dilatation-volvulus is made by several factors. The breed and history will often give a significant suspicion of gastric dilatation-volvulus, and the physical exam will often reveal the telltale sign of a distended abdomen with abdominal tympany. Shock is diagnosed by the presence of pale mucous membranes with poor capillary refill, increased heart rate, and poor pulse quality. Radiographs (x-rays), usually taken after decompression of the stomach if the dog is unstable, will show a stomach distended with gas. The pylorus, which normally is ventral and to the right of the body of the stomach, will be cranial to the body of the stomach and left of the midline, often separated on the x-ray by soft tissue and giving the appearance of a separate gas filled pocket (double bubble sign).

The treatment for bile reflux is the same as the treatment for acidic reflux. In general, everything that can

reduce acidic reflux can reduce bile reflux. Examples include lifestyle modification, weight reduction, and the avoidance of eating immediately before sleep or being in the supine position immediately after meals. In addition, smoking has been found to be a factor in the development of acidic reflux. Thus, all of these factors should be applied to bile reflux as well.

Likewise, drugs that reduce the secretion of gastric acid (e.g., proton pump inhibitors)

or that reduce gastric contents or volume can be used to treat acidic bile reflux. Because prokinetic drugs increase the motility of the stomach and accelerate gastric emptying, they can also reduce bile reflux. Other drugs that reduce the relaxations of the lower esophageal sphincter, such as baclofen, have also proven to reduce bile reflux, particularly in patients who are refractory to (medically unresponsive to) proton pump inhibitor therapy.

Medications used in managing biliary reflux include bile acid sequestrants, particularly cholestyramine, which disrupt the circulation of bile in the digestive tract and sequester bile that would otherwise cause symptoms when refluxed; and prokinetic agents, to move material from the stomach to the small bowel more rapidly and prevent reflux.

Biliary reflux may also be treated surgically, if medications are ineffective or if precancerous tissue is present in the esophagus.

Antacids are a common treatment for mild to medium gastritis. When antacids do not provide enough relief, medications such as H blockers and proton-pump inhibitors that help reduce the amount of acid are often prescribed.

Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. They include the medications sucralfate and misoprostol. If NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate.

Several regimens are used to treat "H. pylori" infection. Most use a combination of two antibiotics and a proton pump inhibitor. Sometimes bismuth is added to the regimen.

LPR presents with non-specific symptoms and signs that make differential diagnosis difficult to achieve. Furthermore, symptoms of the disorder overlap greatly with symptoms of other disorders. Therefore, LPR is under-diagnosed and under-treated. As there are multiple potential etiologies for the respiratory and laryngeal symptoms of LPR, diagnosing LPR based on symptoms alone is unreliable. Laryngoscopic findings such as erythema, edema, laryngeal granulomas, and interarytenoid hypertrophy have been used to establish the diagnosis; however, these findings are nonspecific and have been described in the majority of asymptomatic subjects undergoing laryngoscopy. Response to acid-suppression therapy has been suggested as a diagnostic tool for confirming diagnosis of LPR, but studies have shown that the response to empirical trials of such therapy (as with proton-pump inhibitors) in these patients is often disappointing. Several studies have emphasized the importance of measuring proximal esophageal, or ideally pharyngeal acid exposure, in patients with clinical symptoms of LPR to document reflux as the cause of the symptoms.

Additionally, several potential biomarkers of LPR have been investigated. These include inflammatory cytokines, carbonic anyhydrase, E-cadherin and mucins; however, their direct implications in LPR are still being established. The presence of pepsin, an enzyme produced in the stomach, in the hypopharynx has also become an increasingly researched biomarker for LPR. Research suggests that the stomach enzyme pepsin plays a crucial role in the complex mechanism behind LPR.

Before a diagnosis can be made, a physician will need to record the patient’s medical history and ask for details about the presenting symptoms. Questionnaires such as the Reflux Symptom Index (RSI), Quality-of-Life Index (QLI) for LPR, Glottal Closure/Function Index (GCI) and Voice Handicap Index (VHI) can be administered to gain information about the patient's medical history as well as their symptomatology. A physical examination will then need to be performed with particular concentration around the head and neck. A scope with a specialized camera lens made of fiber optic strands is gently fed down the throat and feeds back images to a monitor. This provides a clear view of the throat and larynx. Signs of LPR include redness, swelling, and obvious irritation. Other, more invasive tests, such as fibre-optic transnasal laryngoscopy, 24-hour ambulatory dual probe pHmetry, pharyngeal pHmetry, transnasal esophagoscopy (TNE) and biopsy may be used. A noninvasive test for diagnosis of LPR is the collection of refluxate where the refluxed material is collected and analyzed. Another noninvasive diagnostic test that can be used is an empirical trial of proton-pump inhibitor therapy; however, this test is mostly successful in diagnosing GERD.

There is no agreed-upon assessment technique to identify LPR in children. Of the debated diagnostic tools, multichannel intraluminal impedance with pH monitoring (MII-pH) is used as it recognizes both acid and non-acid reflux. A more common technique that is used is 24-hour dual probe pH monitoring. Both of these tools are expensive and are therefore not widely used.

Gastric dilatation volvulus is an emergency medical condition: having the animal examined by a veterinarian is imperative. GDV can become fatal within a matter of minutes.

Treatment usually involves resuscitation with intravenous fluid therapy, usually a combination of isotonic fluids and hypertonic saline or a colloidal solution such as hetastarch, and emergency surgery. The stomach is initially decompressed by passing a stomach tube, or if that is not possible, trocars can be passed through the skin into the stomach to remove the gas, alternatively the trocars may be inserted directly into the stomach following anaesthesia in order to reduce the chances of infection. During surgery, the stomach is placed back into its correct position, the abdomen is examined for any devitalized tissue (especially the stomach and spleen). A partial gastrectomy may be necessary if there is any necrosis of the stomach wall.

On chest radiography, a retrocardiac, gas-filled viscus may be seen in cases of intrathoracic stomach, which confirms the diagnosis. Plain abdominal radiography reveals a massively distended viscus in the upper abdomen. In organoaxial volvulus, plain films may show a horizontally oriented stomach with a single air-fluid level and a paucity of distal gas. In mesenteroaxial volvulus, plain abdominal radiographic findings include a spherical stomach on supine images and 2 air-fluid levels on erect images, with the antrum positioned superior to the fundus.

- Upper GI contrast studies:

The diagnosis of gastric volvulus is usually based on barium studies; however, some authors recommend computed tomography (CT) scanning as the imaging modality of choice.

Upper gastrointestinal (GI) contrast radiographic studies (using barium or Gastrografin) are sensitive and specific if performed with the stomach in the "twisted" state and may show an upside-down stomach. Contrast studies have been reported to have a diagnostic yield in 81–84% of patients.

Often performed for an evaluation of acute abdominal pain, a computed tomography (CT) scan can offer immediate diagnosis by showing two bubbles with a transition line. Proponents of CT scanning in the diagnosis of gastric volvulus report several benefits, including:

1. the ability to rapidly diagnose the condition based on a few coronal reconstructed images,

2. the ability to detect the presence or absence of gastric pneumatosis and free air,

3. the detection of predisposing factors (i.e., diaphragmatic or hiatal hernias), and

4. the exclusion of other abdominal pathology.

- Endoscopy:

Upper gastrointestinal (GI) endoscopy may be helpful in the diagnosis of gastric volvulus. When this procedure reveals distortion of the gastric anatomy with difficulty intubating the stomach or pylorus, it can be highly suggestive of gastric volvulus. In the late stage of gastric volvulus, strangulation of the blood supply can result in progressive ischemic ulceration or mucosal fissuring.

The nonoperative mortality rate for gastric volvulus is reportedly as high as 80%. Historically, mortality rates of 30–50% have been reported for acute gastric volvulus, with the major cause of death being strangulation, which can lead to necrosis and perforation. With advances in diagnosis and management, the mortality rate from acute gastric volvulus is 15–20% and that for chronic gastric volvulus is 0–13%.

Most damage to the pyloric valve occurs as a complication of gastric surgery. Other causes of biliary reflux may be:

- Peptic ulcer

- Gallbladder surgery (cholecystectomy)

A significant fraction of cases are idiopathic, with no identified specific etiology.

A health care provider will diagnose dumping syndrome primarily on the basis of symptoms. The following tests may also help confirm dumping syndrome and exclude other conditions with similar symptoms:

- A modified oral glucose tolerance test checks how well insulin works with tissues to absorb glucose. A health care provider often confirms dumping syndrome in people with:

- low blood sugar between 120 and 180 minutes after drinking the solution

- an increase in hematocrit of more than 3 percent at 30 minutes

- a rise in pulse rate of more than 10 beats per minute after 30 minutes

- A gastric emptying scintigraphy test involves eating a bland meal that contains a small amount of radioactive material. An external camera scans the abdomen to locate the radioactive material. The radiologist measures the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal. The test can help confirm a diagnosis of dumping syndrome.

The health care provider may also examine the structure of the esophagus, stomach, and upper small intestine with the following tests:

- An upper GI endoscopy to see the upper GI tract. A gastroenterologist carefully feeds the endoscope down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining.

- An upper GI series examines the small intestine. During the procedure, the person will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Barium coats the small intestine, making signs of a blockage or other complications of gastric surgery show up more clearly on x rays.

For practical purposes, gastric pH an endoscopy should be done in someone with suspected achlorhydria. Older testing methods using fluid aspiration through a nasogastric tube can be done, but these procedures can cause significant discomfort and are less efficient ways to obtain a diagnosis.

A complete 24-hour profile of gastric acid secretion is best obtained during an esophageal pH monitoring study.

Achlorhydria may also be documented by measurements of extremely low levels of pepsinogen A (PgA) () in blood serum. The diagnosis may be supported by high serum gastrin levels ().

The "Heidelberg test" is an alternative way to measure stomach acid and diagnose hypochlorhydria/achlorhydria.

A check can exclude deficiencies in iron, calcium, prothrombin time, vitamin B-12, vitamin D, and thiamine. Complete blood count with indices and peripheral smears can be examined to exclude anemia. Elevation of serum folate is suggestive of small bowel bacterial overgrowth. Bacterial folate can be absorbed into the circulation.

Once achlorhydria is confirmed, a hydrogen breath test can check for bacterial overgrowth.

On x-rays, gas may be visible in the abdominal cavity. Gas is easily visualized on x-ray while the patient is in an upright position. The perforation can often be visualised using computed tomography. White blood cells are often elevated.

Management of symptoms for patients within this subgroup of the GERD spectrum is difficult. Once these patients are identified, behavioural and dietary changes are advised. Dietary modifications may include limiting the intake of chocolate, caffeine, acidic food and liquids, gaseous beverages and foods high in fat. Behavioral changes may include weight loss, cessation of smoking, limiting alcohol consumption and avoiding the ingestion of food shortly before bed. Lifestyle changes in children diagnosed with LPR include dietary modifications to avoid foods that will aggravate reflux (e.g., chocolate or acidic and spicy food), altering positioning (e.g., sleeping on your side), modifying the textures of foods (e.g., thickening feeds to heighten awareness of the passing bolus), and eliminating the intake of food before bed.

Proton pump inhibitors (PPIs) are the leading pharmaceutical intervention chosen for the relief and reduction of LPR and are typically recommended for ongoing use twice a day for a period of 3–6 months. PPIs have been shown to be ineffective in very young children and are of uncertain efficacy in older children, for whom their use has been discouraged. While PPIs may provide limited clinical benefits in some adults, there is insufficient evidence to support routine use. Many studies show that PPIs are not more effective than placebos in treating LPR.

When medical management fails, Nissen fundoplication can be offered. However, patients should be advised that surgery may not result in complete elimination of LPR symptoms and even with immediate success, recurrence of symptoms later on is still possible.

One way to assess treatment outcomes for LPR is through the use of voice quality measures. Both subjective and objective measures of voice quality can be used to assess treatment outcomes. Subjective measures include scales such as the Grade, Roughness, Breathiness, Asthenia, Strain Scale (GRBAS); the Reflux Symptom Index; the Voice Handicap Index (VHI); and a voice symptom scale. Objective measures often rely on acoustic parameters such as jitter, shimmer, signal-to-noise ratio, and fundamental frequency, among others. Aerodynamic measures such as vital capacity and maximum phonation time (MPT) have also been used as an objective measure. However, there is not yet a consensus on how best to use the measures or which measures are best to assess treatment outcomes for LPR.

Gastroparesis can be diagnosed with tests such as x-rays, manometry, and gastric emptying scans. The clinical definition for gastroparesis is based solely on the emptying time of the stomach (and not on other symptoms), and severity of symptoms does not necessarily correlate with the severity of gastroparesis. Therefore, some patients may have marked gastroparesis with few, if any, serious complications.