Read ahead to learn about what PUD is, how it’s diagnosed, and what the latest peptic ulcer treatment guidelines recommend.

What is peptic ulcer disease (PUD)?

PUD is a common gastrointestinal disorder that occurs when stomach acid and digestive enzymes erode the lining of the stomach or the duodenum.

The duodenum is the first part of the small intestine, and its closeness to the stomach makes it vulnerable to damage by stomach acid.

When acid damages the lining of the stomach or duodenum, patients may experience:

• Burning pain in the upper abdomen
• Belching
• Indigestion
• Nausea
• Vomiting
• Bloating — or a feeling of excessive gas in the digestive tract 

It’s important to note that 70% of patients with gastric and duodenal ulcers don’t experience any symptoms.

Instead, they may only be diagnosed incidentally through an endoscopic procedure for another problem. In other cases, they may present with a complication of PUD, such as perforation or a bleeding peptic ulcer.

Perforation refers to a tear in the stomach or duodenum, which can cause a severe abdominal infection. Peptic ulcer bleeding means that blood vessels have been damaged and leak blood into the digestive tract. Bleeding ulcers can show up as black-colored (or tarry) stools. 

In both these cases, the condition is known as complicated peptic ulcer disease.

What causes peptic ulcer disease?

A Helicobacter Pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the two major causes of PUD.

1. pylori is a type of bacteria that can survive in the acidic environment of the stomach. It’s estimated that up to 70% of duodenal ulcers and 50% of gastric ulcers are caused by H. pylori. 

When this bacterium infects the stomach lining, it leads to the production of excess acid, leading to the formation of an ulcer.

On the other hand, NSAIDs reduce the production of prostaglandins, which are protective compounds that help keep the stomach lining healthy. 

When these compounds aren’t produced in large enough quantities, the stomach lining is left vulnerable to damage from excessive acid.

Keep in mind that H. pylori and NSAIDs don’t cause peptic ulcers on their own. Instead, they combine with other risk factors, such as smoking and alcohol use, to create an environment in which PUD can occur.

In addition, there are many other rarer causes of PUD, including:

• Non-NSAID drugs like acetaminophen, steroids, and antidepressants
• Infections like cytomegalovirus (CMV), herpes simplex virus (HSV-1), and Epstein-Barr virus (EBV)
• Radiation
• Illicit drugs like cocaine
• Surgery

How to diagnose peptic ulcer disease?

PUD can be diagnosed with history taking and investigations.

During history-taking, your healthcare provider will ask you about your symptoms as well as any risk factors for PUD you may have. 

They will also ask you about any alarm symptoms — such as weight loss, difficulty in swallowing, and a family history of gastric cancer.

If you’re under 60 years of age and don’t have any alarm symptoms, your doctor may order a test for determining your H. pylori infection status. This can include:

• A urea breath test, where you drink a liquid containing urea and then your breath is tested for molecules that indicate the presence of H. pylori.
• Fecal antigen test, where a stool sample is tested for the presence of H. pylori antigens.

On the other hand, if you’re over 60 years of age or have any alarm symptoms, regardless of age, your healthcare provider will refer you for an endoscopy. This is where a camera is inserted down your throat to look at the lining of the stomach and duodenum.

It’s important to note that endoscopy is the only way to definitively diagnose PUD (just like a colonoscopy is the only way to diagnose colon cancer). The other tests can only tell you if you have an H. pylori infection or not.

In addition, your doctor may take a biopsy during the endoscopy procedure to rule out cancer. 

A biopsy removes a small piece of tissue from the lining of the stomach or duodenum, which is then analyzed under a microscope. This is important because ulcers can also cause cancer.

What are the treatment options for peptic ulcer disease?

There are three main treatment options for PUD, including lifestyle changes, medication, and surgery.

Lifestyle changes

Making changes to your lifestyle is an important — and often the first — part of managing PUD. 

This can include quitting smoking, stopping NSAIDs or steroids, avoiding alcohol, and reducing stress levels. 

It’s also important to eat a balanced diet that is low in fat and processed foods while still providing adequate nutrition.

Medication

If lifestyle changes don’t work, drugs are the next step. If your doctor finds you have an H. pylori infection, they will give you drugs to eradicate these bacteria. This is called Helicobacter Pylori eradication therapy and usually includes 3 drugs:

• A proton pump inhibitor, such as omeprazole, to reduce stomach acid production
• Two antibiotics, such as clarithromycin and amoxicillin

The antibiotics you get can vary depending on how resistant H. pylori is in your area, but the duration of treatment usually remains constant at 10-14 days.

If you test negative for H. pylori, your doctor may prescribe you only an acid-suppressing drug (like a PPI) for 4-8 weeks, depending on the location of your ulcer.

In addition, you might also be asked to use antacids and cytoprotective agents like sucralfate, which promote ulcer healing and prevent further damage.

Surgery

In rare cases, surgical treatment may be needed if the ulcer doesn’t respond to lifestyle changes and medications. Surgery is usually only considered if:

• PUD leads to complications, such as recurrent bleeding or a perforated peptic ulcer
• You have a disease that requires you to keep taking NSAIDs, such as ankylosing spondylitis
• You can’t tolerate medications like proton pump inhibitors

In all these cases, you may have to undergo one of these procedures:

• Vagotomy: This is a procedure to remove the nerve in your stomach that’s responsible for producing acid. It can be done either as an open surgery or laparoscopically.
• Partial gastrectomy: This involves removing part of your stomach that has the ulcer. You may get a Billroth 1 operation (for duodenal ulcers) or Billroth 2 operation (for gastric ulcers).
• Total gastrectomy: This is when the entire stomach is removed. This procedure is usually only done if you have cancer.

The type of procedure you get will depend on factors such as the location of your ulcer and your overall health. 

Your doctor will discuss these options with you to help you decide which one is best for you. But most cases of PUD respond to medical treatment, so there’s no need to worry.

FAQ

Below is a list of the common questions we hear on this topic.

What foods to avoid with peptic ulcer disease?

It’s best to avoid high-fat, processed, and fried foods, as well as spicy, acidic, or fatty items. You should also limit your intake of caffeine and alcohol, as these substances can irritate the lining of your stomach.

Can peptic ulcer disease cause diarrhea?

Yes, PUD can cause diarrhea in some cases. This is usually due to the irritation of the lining of your digestive tract by stomach acid, which can lead to inflammation and irritation in the intestines. 

If you experience any changes in your bowel habits, it’s important to talk to your doctor to determine the cause.

Can peptic ulcer disease be cured?

Yes, PUD can often be cured with lifestyle changes and medications. If lifestyle changes and medications don’t work, surgery may be necessary. 

However, it’s important to note that no matter what treatment you receive, it’s important to follow up with your doctor to ensure the ulcer has healed and there are no further complications.

How common is peptic ulcer disease?

PUD affects 6 million people in the US each year. Fortunately, the number of people affected by this disease is decreasing, as we can now easily diagnose and treat H. pylori infections.

Does peptic ulcer disease go away on its own?

No, peptic ulcer disease usually doesn’t go away on its own. That’s why it’s important to seek medical attention if you are experiencing any symptoms. Remember, PUD is usually caused by an infection (H. Pylori), which will need antibiotics to cure.

How to prevent peptic ulcer disease?

Peptic ulcer disease can be prevented by practicing good hygiene. That’s because H. pylori, the bacteria that cause the infection, can be passed on through contaminated food and water. 

So it’s best to wash your hands often and avoid eating food from places that aren’t hygienic. Avoiding certain medications, such as NSAIDs and steroids, can also help reduce your risk of developing PUD.

Is peptic ulcer disease hereditary?

Yes, there is a genetic element to PUD. Although a bacterial infection causes it, people with certain genes are more likely to develop an ulcer due to the way their body reacts to H. pylori.

The post Peptic Ulcer Disease Treatment Guidelines appeared first on LAcolon.

In this post, we’ll discuss the following:

• What GOO is
• The symptoms of GOO
• The causes of GOO
• How GOO is diagnosed
• How GOO is treated

Let’s begin!.

What is gastric outlet obstruction?

Gastric outlet obstruction is a condition characterized by a blockage at the lower end of the stomach, which delays gastric emptying.

This blockage is usually caused by a cancerous mass, but you also have gastric outlet obstruction secondary to non-cancerous causes like a helicobacter pylori infection, volvulus, foreign bodies, and strictures.

H.pylori is a common infection worldwide, and it is the most common cause of peptic ulcer disease. This is where patients develop ulcers near the end of the stomach, which can lead to scarring and benign gastric outlet obstruction.

On the other hand, volvulus occurs when the gut twists around itself for one reason or another. This can also block the lower end of the stomach, leading to GOO.

What are gastric outlet obstruction (GOO) symptoms?

The most common symptom of GOO is post-prandial vomiting. This vomiting occurs 1-2 hours after a meal and contains foodstuffs because of delayed gastric emptying.

Other symptoms can include:

• Weight loss
• Abdominal pain
• Dilated abdomen
• Feeling full after eating just a little
• Succussion splash, which is a splashing sound that is heard when you shake the patient’s belly. This sound is usually found in healthy individuals immediately after eating a meal. However, if it’s heard more than 3 hours after a meal, it indicates GOO.

Some patients with GOO might also have symptoms related to electrolyte imbalance. That’s because when you vomit constantly, you lose potassium from the body. This can result in symptoms like:

• Nausea
• Fatigue
• Palpitations
• Muscle weakness
• Low blood pressure

It’s important to note that vomiting after eating food can also occur in other conditions. For example, if you vomit immediately after a meal, you may have a problem with the esophagus (and not the stomach).

Similarly, if the color of your vomit is green, then you may have duodenal obstruction, an obstruction in the small intestine instead of the stomach.

This is why it’s important to present an accurate account of your symptoms to your doctor so they rule out other conditions that mimic GOO, such as pyloric stenosis.

What is the most common cause of gastric outlet obstruction in adults?

The most common cause of gastric outlet obstruction in adults is cancer. This is called malignant gastric outlet obstruction, and it can be both intrinsic and extrinsic to the stomach.

Intrinsic obstruction is caused by cancers of the stomach and duodenum (the small intestine), while extrinsic compression can occur from pancreatic cancer, lymphoma, or biliary tract cancer.

Interestingly, the most common cause of GOO was H.pylori before it was displaced by cancer. This happened because we can now prevent, diagnose, and treat H.pylori infections very well, which has reduced the number of patients that get GOO because of it.

Which diagnostic test is best suited to help identify gastric outlet obstruction?

The best test to diagnose gastric outlet obstruction is an esophagogastroduodenoscopy, which is also called an upper gastrointestinal endoscopy.

During an endoscopy, a doctor inserts a long, flexible tube with a camera attached to your mouth and down your gastrointestinal tract. 

This helps them directly look at the obstruction. It also allows them to take a small piece of the obstructing tissue and send it to the lab for cancer testing. This procedure is called a biopsy, and it’s the only way to diagnose cancer, the most common cause of GOO.

How is gastric outlet obstruction diagnosed?

Gastric outlet obstruction is diagnosed by a combination of history, physical examination, and investigations.

During history taking, your healthcare provider will ask you questions about your symptoms. Next, they will conduct a physical exam, where they will listen for the succussion splash and look for any abdominal distention.

If they think your history and physical exam point towards GOO, they will ask you to undergo certain investigations to confirm the diagnosis. These include:

• Upper GI series, where you have to swallow a fluid. Next, the healthcare provider takes images of your gut, which is clearly visible due to the fluid you swallowed. This helps doctors identify the site and size of the obstruction.
• CT scan or MRI
• Upper gastrointestinal endoscopy, which is the confirmatory test as discussed above
• Lab investigations support the diagnosis by revealing low potassium and chloride levels.

How do you treat a gastric outlet obstruction?

Gastric outlet obstruction is treated with a combination of supportive care and definitive treatment.

Supportive care aims to keep the patient comfortable while the doctor determines the exact cause of their gastric outlet obstruction and plans treatment. It involves:

• Stopping all oral intake
• Passing a nasogastric tube, which starts at the nose and ends at the stomach. This can be used to decompress the stomach if the pressure is too high.
• Giving IV fluids and electrolytes
• Giving IV proton pump inhibitors reduces acid production and prevents further damage to the stomach’s lining.
• Drugs for relieving pain and vomiting

Once the patient has been stabilized through supportive care, the doctor then provides definitive treatment for GOO. This involves reliving the obstruction and treating its underlying cause.

For example, if the cause of GOO is peptic ulcer disease, treatment will involve acid-suppressing drugs and antibiotics against H.pylori (which is the main cause of peptic ulcer disease).

But at the same time, you might also have to undergo a surgical procedure to relieve the obstruction. This can include:

• Endoscopic stenting
• Endoscopic balloon dilation
• Gastrojejunostomy, where the surgeon bypasses the obstruction and creates a new connection between the stomach and the small intestine. This is a major operation, so it’s a good idea to read our post on leaving the hospital after a major surgery.
• Gastrectomy, where a part of the stomach is removed
• Radiation and chemotherapy in case of malignant obstruction

The exact procedure you get for gastric outlet obstruction depends on the cause of your obstruction and your overall health status.

Gastric outlet obstruction overview

Gastric outlet obstruction is a blockage that prevents food from passing into the small intestine. It can occur due to various causes, such as tumors, inflammation, or scarring. The most common symptom is nausea and vomiting after having meals.

If you suspect you may have GOO, your doctor will likely conduct various tests to diagnose the condition. These include an upper GI series, CT scan, MRI, and endoscopy.

Finally, treatment will involve supportive care and definitive treatment. Supportive care is aimed at making the patient more comfortable while they are being worked up, while definitive treatment is aimed at relieving the obstruction and treating its underlying cause.

Depending on the cause of the obstruction, definitive treatment could include stent placement, gastrojejunostomy, gastrectomy, radiation, and chemotherapy.

The post Gastric Outlet Obstruction (GOO): Symptoms, Management, & Treatment appeared first on LAcolon.

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FECAL MICROBIAL TRANSPLANTATION: IT WORKS!

NO GOOD DEED GOES UNPUNISHED

Everything comes at a cost. Not uncommonly, patients who have been treated with antibiotics for one type of infection, develop a second, opportunistic infection. When a majority of normal or pathogenic bacteria are removed by antibiotics used to treat an active infection, there may be an overgrowth of previously dormant and harmless bacteria, which now have the “opportunity” to wreak their own brand of havoc. This first unintended consequence has led to a second unintended consequence, the emergence of new resistant strains of opportunistic bacteria such as the commensal Clostridium difficile (C. diff.)

In the gastrointestinal tract, the opportunistic Clostridium difficile, an anaerobic, spore-forming, Gram-positive bacillus, is the potential culprit which may produce toxins that cause abdominal discomfort and diarrhea. C. diff. is the most common cause of pseudomembranous colitis, a term which refers to the membranes seen in an infected, inflamed colon. The membranes are thick collections of inflammatory cells, fibrin and necrotic debris. Pseudomembranous colitis can progress to toxic megacolon, which is a life threatening, acute colonic distention. Each year, fifteen thousand hospitalized patients die as a result of toxic megacolon, an unintended result of antibiotic usage.

Pseudomembranous colitis may affect outpatients or inpatients. The infection rate increases with the length of inpatient hospitalization. The most common symptoms are abdominal pain and bloating and a profuse watery diarrhea in an individual who has been treated with antibiotics or chemotherapeutic drugs. Almost any antibiotic can cause a Clostridium difficile infection with the most common offender being the cephalosporins and the fluoroquinolones. Symptoms are often accompanied by lethargy, fever and an elevated white blood cell count.

ROW, ROW, ROW YOUR BOAT. HAPPY BIRTHDAY TO YOU

When present outside of the body, the bacteria exist as heat-resistant spores, which are viable for long periods of time and are resistant to the majority of the commercially available alcohol-based disinfectants. The commonly used hand gels, so often found in dispensers throughout hospitals, are likewise ineffective. Soaps and bleach-based products can eradicate the spores. For the average person, the most reliable method of killing these spores is good, ole fashioned, thorough hand washing with soap and water. Hand washing while twice, very slowly singing Row, Row, Row Your Boat, or Happy Birthday To You, should do the job. C. diff. does not routinely infect all who come in contact with it. Nevertheless, please continue washing and singing while visiting in the hospital.

If ingested, the acid-resistant spores pass undigested through the stomach and arrive in the colon, where, when exposed to bile acids, they resume bacterial growth and reproduction, and produce disease-causing cytotoxins and enterotoxins. It is these toxins which are responsible for the colonic inflammation and pseumembranes seen in pseudomembranous colitis.

FIRST, DO NO HARM.

Does all of this vexation and brouhaha revolve around simple diarrhea? Unfortunately, simple diarrhea can rapidly become complicated diarrhea. C. diff diarrhea and pseudomembranous colitis can progress quickly beyond Row, Row, Row Your Boat. Most surgeons know of at least one patient who has succumbed to this disease.

Accurate and timely diagnosis is imperative in preventing the spread of the infection and ensuring that the treatment is directed toward the correct disease. As not all diarrhea is caused by C. diff., it is important that treating physicians embark on a protocol which is based on a correct diagnosis.

In the past, toxin identification required the collection of three stool samples. Each sample took unduly long to analyze for the presence of the toxin. This was problematic as antibiotic therapy was delayed pending collection and analysis of multiple diarrheal samples Today, testing is performed on one fresh, liquid stool and the C. diff. toxin can be identified within six hours of collection.

TREATMENT: PRONE TO COSTLY FAILURE. WOULD VEGAS LIKE THESE ODDS?

The treatment of a mild C. diff. infection begins with one of two antibiotics, metronidazole (Flagyl®) or vancomycin. The treating physician chooses the appropriate drug after considering many variables related to the patient’s health. A cure is achieved in up to 75% of cases. However, treatment fails in the remaining 25% of patients. Those at risk for failure include the elderly, those with other medical conditions such as diabetes or cardiopulmonary diseases, and those requiring ongoing antibiotic treatment. Recurrence is associated with a 50% to 60% chance of experiencing another recurrence. These are not great odds.

Metronidazole is usually used as the first line antibiotic and vancomycin is used in case of a metronidazole failure, allergy, disease recurrence or other concerns. Metronidazole has the added benefit that it can be delivered orally or by intravenous infusion. Vancomycin is effective only if delivered orally or by enema. Hospitalized patients who respond appropriately to antibiotics may be discharged home and followed on an outpatient basis.

Some patients have resistant disease or develop recurrent disease despite antibiotic treatment. They may develop chronic or refractory C. diff colitis. These patients pose a major dilemma. Prior to the advent of fecal microbial transplantation, the only other management option that could be offered was an operation to remove the entire colon- a total abdominal colectomy eradicated the disease.

FECAL MICROBIAL TRANSPLANTATION: THE YELLOW BRICK ROAD IS COVERED WITH STOOL. “ICK” AND “GROSS”

Fecal transplantation involves obtaining stool from a healthy donor, and transferring it into the colon of the patient with the stubborn infection. The rationale is that the reintroduced “good” bacteria will replace the “bad” bacteria and allow for a full and complete recovery. And it does just that. It works! However, many respond with an “ick” or a “gross” when FMT is discussed as a treatment option. The desire to overcome a noxious disease eventually triumphs over “ick”, and patients readily accept FMT as a life saving alternative.

How is the transplant performed? The recipient undergoes a standard colonoscopy preparation. This is safe in the usual patient with chronic C. diff. The donated stool is converted into a thick liquid solution. Under inpatient or outpatient anesthesia, the solution of “good” stool is placed through the side channel of a colonoscope and into the colon of the recipient.

BETTER ODDS.

While this procedure is still new and more FMT treatment data remains to be collected, there are several hundred patients reported in the medical literature who have shown cure rates of greater than 95%. Rare recurrences usually resolve after a repeat stool transfer.

While there are medical centers that use stool banks to store frozen donor feces for future use, there does not appear to be a shortage of donor stool at this time. Research has shown that using donor stool from an intimate partner of the recipient makes the most sense. The logic is that the recipient has already been exposed to any potential donor infections. There has not been a single case report of a donor-to-recipient infection transmitted by this procedure. However, stool is a bodily fluid, and recipient infection remains a theoretical potential risk. Absent having a related donor, it does not really matter who donates the stool. Importantly, donors should not have taken antibiotics or have been hospitalized within six months prior to the donation, and the donor should not work or have worked in a health care facility which might have the potential for harboring an occult C. diff. colonization. It is important that the stool donor be tested for an asymptomatic Clostridium difficile infection. The testing protocol for other transmissible diseases is complex and should be undertaken by a physician with diagnostic experience and an established protocol. The final decision as to the extent of donor testing is undertaken after a thorough discussion with the donor and the recipient.

THE END OF THE ROAD.

Symptoms often disappear immediately after the transplant. If patients remain disease-free for at least as long as their prior disease-free period, the treatment is considered to have been curative.

With or without “ick”, fecal microbial transplantation, in the hands of an experienced specialist, can cure a “gross” disease.

The post Fecal Microbial Transplantation (FMT) appeared first on LAcolon.

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Tailoring Management Strategies to H. pylori Status

Treatment for all peptic ulcer patient infected with H. pylori was strongly recommended by the 1994 National Institute of Health (NIH) Consensus Development Conference and the 1997 American Digestive Health Foundation (ADHF) International Update Conference on H. pylori. Recommended as appropriate goals for success of an eradication regimen were more than 90% on a “per-protocol” (PP) analysis and more than 80% on an “intent-to-treat” (ITT) analysis.

Bismuth-based triple therapy (BTT: bismuth subsalicylate 2 tablets qid, metronidazole 250 mg qid, and tetracycline 500 mg qid for 2 weeks, accompanied by a H2RA for 4 weeks) produced eradication rates of 77% and 82% in historical trials reviewed by the FDA for approval. BTT has had more limited success in clinical practice because of the regimen’s complexity, metronidazole resistance, and adverse effects. Compliance with BTT needs to be high; the chance of success is greatly reduced in patients who take 60% or less of the prescribed medication. Rates of metronidazole resistance vary widely among different countries and different regions of the same country. They are currently about 50% in the United States and are rapidly increasing.

The combination of omeprazole 40 mg qd and clarithromycin 500 mg tid for 2 weeks, followed by omeprazole 20 mg qd for a further 2 weeks, was the first regimen to the FDA-approved. In FDA pivotal trials, eradication rates were 64% and 74%. Ranitidine bismuth citrate (RBC) is a new chemical entity that is also
FDA-approved as part of the treatment of H. pylori infection in patients with peptic ulcer. RBC 400 mg bid with clarithromycin 500 mg tid for 2 weeks, followed by RBC 400 mg bid alone for a further 2 weeks, produced eradication rates of 73% and 84% in FDA pivotal trials.

Increasing evidence suggests that a PPI or RBC plus two antibiotics (i.e., clarithromycin plus either amoxicillin or metronidazole) for 1 to 2 weeks is the best treatment for H. pylori infection. The first PPI-based triple combination to be FDA-approved is lansoprazole 30 mg bid with clarithromycin 500 mg bid and amoxicillin 1000 mg bid for 2 weeks. Eradication rates in a large US-based multicenter trial were 94% (PP) and 86% (ITT).

Although H. pylori infection is the single most common cause of peptic ulceration, it is not the sole cause – particularly in the United States. Recent reports have documented absence of H. pylori infection in up to 42% of patients with peptic
ulcer. Some of these cases may be explicable on the basis of false-negative tests for H. pylori infection, the surreptitious or overuse use of aspirin or NSAIDs, or Zollinger-Ellison syndrome. However, some patients have truly “idiopathic” H. pylori-negative peptic ulcer disease. These patients may have a particularly severe ulcer diathesis characterized by refractoriness to 2RAs, rapid recurrence after healing, and a high incidence of complications. Long-term medical treatment with a PPI is the most appropriate form of management. The FDA has approved omeprazole 20 mg qd and lansoprazole 15 mg qd for the short-term treatment of active duodenal ulcer to produce healing. Lansoprazole 15 mg qd is also FDA-approved as maintenance therapy of healed duodenal ulcer.

There is overwhelming evidence that cure of H. pylori infection eliminates the probability of recurrence of duodenal or gastric ulcer in those patients in whom the ulcer was truly H. pylori-related. True reinfection after cure of H. pylori infection is rare in adults but more frequent in very young children. A number of studies have shown substantial reduction in the rates of recurrent duodenal ulcer hemorrhage 1 to 2 years after cure of H. pylori infection. In patients found to have bleeding from a peptic ulcer, and in whom there is evidence of H. pylori infection, treatment for the infection should be started prior to hospital discharge.

The cumulative costs of different forms of therapy for duodenal ulcer have been modeled over a 15-year period. The total costs of elective surgery or either the continuous or intermittent use of an H2RA were considerably greater than those of antimicrobial treatment for H. pylori infection. Recent studies have also focused on the cost-effectiveness of different methods of diagnosing the presence of peptic ulcer and/or H. pylori infection. In general, treatment of H. pylori infection with some combination of antimicrobial agents and an antisecretory drug, as endorsed by the 1994 NIH conference and the 1997 ADHF conference, has been associated with the lowest cost per ulcer cured. Prompt, effective treatment of H. pylori infection in patients with peptic ulcer makes sound economic sense.

QUESTION:
What is the status of breath tests for diagnosing H. pylori infection?
In the urea breath tests, urea in which carbon 12 has been substituted with carbon 13 or 14 is given by mouth. In the presence of H. pylori infection, the urease of the bacterium splits the urea to produce ammonia and labeled carbon dioxide, which is detected in a breath sample. These commercially available tests are simple to perform and have excellent operating characteristics. They may be used either before or after treatment. Sensitivity of the urea breath tests may be
reduced in patients recently taking antibiotics, bismuth compounds, or acid-suppressing medicines.

QUESTIONS

We hear much about metronidazole resistance, but what is the impact of resistance on therapy?

The impact is considerable. Eradication rates for otherwise effective regimens drop to 65% in the presence of metronidazole resistance. A realistic approach is to promote use of the regimens that are effective regardless of the problem of resistance. Adding a PPI to BMT therapy might suffice because with this quadruple regimen the mean eradication rate was reduced by only 2% in patients with resistance to metronidazole. A better and more cost effective approach is the use of PPI, amoxicillin, and clarithromycin. This combination was effective in more than 90% of patients with metronidazole resistance in a recent European trial.

If a patient has a duodenal ulcer, is it necessary to test for H. pylori?

Although it has been argued that confirmation of H. pylori infection is unnecessary in patients with an endoscopic diagnosis of duodenal
Ulcer, H. pylori-negative duodenal ulceration is a definite phenomenon in the United States that requires accurate diagnosis and evaluation. Routine treatment of patients with duodenal ulcer for H. pylori infection is not recommended without prior documentation of infection.

What is the best way to test for H. pylori?

This method of testing for H. pylori infection depends on the clinical situation. If an ulcer is detected at upper gastrointestinal endoscopy, some form of biopsy urease test is recommended, with the potential caveat that the result may be false-negative. The urea breath test is the method of choice for diagnosing infection when endoscopy is not indicated and for documenting cure of infection after treatment. Serologic analysis may be used for confirming the presence of infection in patients with a previous diagnosis of peptic ulcer and in whom endoscopy is not otherwise necessary.

What is the status of an H. pylori vaccine?

Vaccination against H. pylori infection is a possibility for the future. There are a number of potential H. pylori antigens that may be used for the purposes of vaccination, particularly urease and heat-shock proteins. These will have to be administered orally with a suitable and safe adjuvant. Preliminary trials of the use of a vaccine therapeutically (rather than prophylactically) have produced reduced colonization with H. pylori in some patients.

The post Peptic Ulcer (Helicobacter) appeared first on LAcolon.

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(BLASS-toe-SIS-tiss HOM-in-iss)

What is Blastocystis hominis?

Blastocystis hominis is a common microscopic parasitic organism found throughout the world. Infection with Blastocystis hominis is called blastocystosis (BLASS-toe-SIS-toe-sis.)

What are the symptoms of infection with Blastocystis?

Watery or loose stools, diarrhea, abdominal pain, anal itching, weight loss, and excess gas have all been reported in persons with Blastocystis infection. Many people have no symptoms at all.

How long will I be infected?

Blastocystis can remain in the intestines for weeks, months, or years.

Is Blastocystis hominis the cause of my symptoms?

It is hard to be sure, and experts disagree on this point. Whether or not B. hominis is the primary cause of your symptoms is unknown. Finding Blastocystis in stool samples should be followed up with a careful search for other possible causes of your symptoms.

Symptoms may be caused by infection with other parasitic organisms, bacteria, or viruses. Often, B. hominis is found along with other such organisms that are more likely to be the cause of your symptoms. Sometimes symptoms are not caused by an infection at all. Antibiotics, some cancer drugs, and medications used to control high blood pressure may be causing your symptoms. Hormone or endocrine diseases, diseases like Crohn’s, colitis, or hereditary factors may be the cause of illness. Food additives or food allergies may also be a cause of abdominal discomfort.

Is having blastocystosis common?

Yes; in fact many people have Blastocystis, some without ever having symptoms.

What should I do if I think I have blastocystosis?

See your health care provider who will ask you to provide stool samples for testing. Diagnosis may be difficult, so you may be asked to submit several stool samples.

Is medication available to treat blastocystosis?

Yes; drugs are available by prescription to treat blastocystosis; however, sometimes medication is not effective.

How did I get blastocystosis?

It’s hard to say. How Blastocystis is transmitted is unknown, although the number of people infected seems to increase in areas where sanitation and personal hygiene is inadequate.

How can I prevent infection with Blastocystis?

• Wash hands with soap and water after using the toilet and before handling food. Avoid water or food that may be contaminated.
• Wash and peel all raw vegetables and fruits before eating.
• When traveling in countries where the water supply may be unsafe, avoid drinking unboiled tap water and avoid uncooked foods washed with unboiled tap water. Bottled or canned carbonated beverages, seltzers, pasteurized fruit drinks, and steaming hot coffee and tea are safe to drink.
• If you work in a child care center where you change diapers, be sure to wash your hands thoroughly with plenty of soap and warm water after every diaper change, even if you wear gloves.

Should I be concerned about spreading infection to the rest of my household?

No. If you practice adequate personal hygiene, including thorough hand washing with soap and warm water after using the toilet and before handling food, there is little risk of spreading infection.

Causal Agent:

The taxonomic classification of Blastocystis hominis is mired in controversy. It has been previously considered as yeasts, fungi, or ameboid, flagellated, or sporozoan protozoa. Recently, however, based on molecular studies, especially dealing with the sequence information on the complete SSUrRNA gene, B. hominis has been placed within an informal group, the stramenoiles (Silberman et al. 1996). Stramenopiles are defined, based on molecular phylogenies, as a heterogeneous evolutionary assemblage of unicellular and multicellular protests including brown algae, diatoms, chrysophytes, water molds, slime nets, etc. (Patterson, 1994).

Cavalier-Smith (1998) considers stramenopiles to be identical to his infrakingdom Heterokonta under the kingdom Chromista. Therefore, according to Cavalier-Smith, B. hominis is a heterokontid chromista.

Life Cycle:

Clinical Features:

Whether Blastocystis hominis can cause symptomatic infection in humans is a point of active debate. This is because of the common occurrence of the organism in both asymptomatic and symptomatic persons. Those who believe symptoms could be related to infection with this parasite have described a spectrum of illness including watery diarrhea, abdominal pain, perianal pruritus, and excessive flatulence.

Laboratory Diagnosis:

Diagnosis is based on finding the cyst-like stage in feces. Permanently stained smears are preferred over wet mount preparations because fecal debris may be mistaken for the organisms in the latter. Do not wash specimens in water (e.g., during concentration procedures) as this will lyse the organisms, resulting in false negatives.

Diagnostic findings

• Microscopy
• Morphologic comparison with other intestinal parasites
• Bench aid for Blastocystis

Treatment:

Despite the controversial clinical significance of this organism, metronidazole or iodoquinol has been reported to be effective. See recommendations in The Medical Letter (Drugs for Parasitic Infections) for complete information.

(This fact sheet is for information only and is not meant to be used for self-diagnosis or as a substitute for consultation with a health care provider. If you have any questions about the disease described above or think that you may have a parasitic infection, consult a health care provider.)

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Common Infections. Many Symptoms.

“…gonorrhea, chlamydia, syphilis, herpes simplex virus and cytomegalovirus are all part of the differential diagnosis…”

The anorectum is a specialized region of the gastrointestinal tract, performing sensory, storage and elimination functions. The mucosal lining in the rectum is columnar. It transitions to a squamous mucosa in the anal canal. It is richly endowed with discriminatory nerve endings to allow the body to distinguish between flatus, liquid and solid waste. While sturdy, the mucosal surfaces are vulnerable to trauma and infections. With or without an anal or rectal injury, sexually transmitted disease may be the source of considerable morbidity. While symptoms may be found in patients with normal immune systems, they are found in increasing frequency in the immunocompromised population. In patients with pre-existing systemic conditions such as AIDS or HIV, common pathogens may take on an even more ominous clinical significance. Part I of this two-part article contains a discussion of the anorectal manifestations of the most common sexually transmitted diseases.

ANAL INFECTIONS

Anal infections are common and the frequency of these infections are increasing. Diagnosis has become more difficult in recent years owing to the complexity of the pathogens. Diagnosis and treatment has become even more challenging in the HIV+ patient population. There are many coexisting variables in the HIV+ population, with the potential for several asymptomatic co-existing infections in the anorectum. These may alter the integrity of the mucosa, thus decreasing the effectiveness of the natural mucosal barrier. Sexually transmitted diseases, such as gonorrhea, chlamydia, syphilis, herpes simplex virus, and cytomegalovirus are all part of the differential diagnosis in the symptomatic HIV+ patient. Counseling and prolonged follow up is necessary in all patients.

A thorough history accompanied by a focused physical examination will usually yield the cause of an anorectal infection in most patients. Laboratory studies (serological, bacteriological or pathological with tissue biopsy and examination) are confirmatory.

GONORRHEA

Gonorrhea is the most common sexually transmitted infection in the homosexual male. It is caused by Neisseria Gonorrhoeae, a Gram-negative intracellular diplococcus.

It is often seen in conjunction with a chlamydia infection. Symptoms include tenesmus, pruritus and proctitis with a thick yellow mucopurulent discharge. Gram negative intracellular diplococci seen on a Gram stain and subsequently grown on a Thayer-Martin plate confirm the diagnosis. A single, 125mg intramuscular dose of ceftriaxone may be given empirically before culture results are received. Follow up examination with cultures should be performed to confirm the eradication of the disease. Partners should also be evaluated and treated if necessary, as there is increased risk of re-infection from an untreated partner.

CHLAMYDIA

Chlamydia trachomatis is the most commonly reported bacterial sexually transmitted disease in the United States. Chlamydia often coexists with gonorrhea, and treatment should be geared towards both infections. Pain, tenesmus, and proctitis are the typical symptoms. These symptoms often progress to lymphogranuloma venereum, with painful lymphadenopathy, perirectal abscesses and stricture formation. Diagnosis is confirmed by complement fixation testing or urinary polymerase chain reaction tests. Either a single, one-gram oral dose of azithromycin, or 100 mg of oral doxycycline taken twice daily for one week are the preferred treatments. However, because of the high relapse rate, many practitioners recommend a two to three week course of doxycycline.

SYPHILIS

Syphilis has often been called “the great imitator”, because so many of the signs and symptoms are indistinguishable from those of other diseases. Syphilis is caused by the bacterium Treponema pallidum. Anal syphilis manifests as a chancre, or highly infectious ulcer, during the first stage of the disease. Chancres are painless in other sites but cause severe pain in the anal region. The disease progresses to the second-stage, condyloma lata, in one-third of patients. Condyloma lata may appear as smooth painless warts, or raised, red painful warts and may be accompanied by fever, malaise, and a maculopapular rash on the palms and soles of the feet. Serological diagnosis is confirmed by V.D.R.L. (Venereal Disease Research Laboratory) assay. Initial treatment consists of 1-gram intramuscular benzathine penicillin-LA (long acting). Benzathine penicillin-LA is in short supply and the treatment may need to be changed to doxycycline, 100mg orally, taken twice daily for three weeks. Additionally, the treatment regimen may need to be altered or intensified in the HIV+ patient.

ANAL ULCERS

Herpes Simplex Virus type II is the causative factor in 90% of cases of anal herpes and may be a cofactor in the transmission of HIV by causing breaks in the anorectal epithelial barrier. Cytomegalovirus also causes ulceration and may be a coexisting factor with other anorectal infections. Herpetic ulcers are normally present for ten days. Persistence of herpetic ulcers and vesicles beyond one month is an AIDS-defining condition. Anorectal pain and tenesmus can progress to systemic signs of fever, malaise, and inguinal lymphadenopathy. Biopsy of the ulcer base reveals multinucleated giant cells or intranuclear inclusion bodies. Biopsy sensitivity declines with the progression of healing. Empiric treatment is recommended with 400-800mg of oral acyclovir taken five times daily for one week. Topical acyclovir does not prevent the recurrence of sores, but may decrease pain and itching if applied when the earliest symptoms first appear.

Idiopathic AIDS-related ulcers are usually seen in advanced disease with CD4 T-cell counts less than 200 cells/microliter. These ulcers are differentiated from benign anal fissures in that they occur more proximally and are associated with a hypotonic rather than a hypertonic anal sphincter. AIDS-related ulcers may burrow through the submucosa into the intersphincteric plane, potentially pocketing into the deep post-anal space. This pocketing can cause a sensation of pressure as well as a deep-seated pain. A course of Flagyl and acyclovir may improve symptoms in some patients, but debridement and injection of a depot steroid into the base and sides of the ulcer may be necessary. Often these ulcers are resistant to treatment and can become a considerable source of morbidity.

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Human Papillomavirus and Squamous Cell Carcinoma of the Anus.

A Major Nuisance and Growing Menace.

“Prevention of disease transmission is the goal in any illness… Many people have a genital HPV infection without exhibiting any signs or symptoms.”

At any given time in the United States, twenty million men and women have an active Human papillomavirus (HPV) infection. Five million new cases are diagnosed each year. These represent one third of all cases of newly diagnosed sexually transmitted infections. In addition to the morbidity of the disease itself, HPV is strongly associated with the development of squamous cell carcinoma of the anus. Hence, this ubiquitous virus has taken on a more menacing significance than simply that of an inconvenient sexually transmitted disease.

Human papillomavirus is a small double-stranded DNA virus with a diameter
of 55 nm. It is encased in a protein capsid with the viral genome existing in a circular or epitomal configuration. An intact capsid is necessary for HPV to be infectious. The viral genome is divided into 3 regions. The Upstream Regulatory Region (URR), the Early Region (E) and the Late Region (L). Each region is responsible for a part of the transcription, replication or capsid production process.

Many people have a genital HPV infection without exhibiting any signs or symptoms. Even without signs or symptoms however, the disease can be transmitted sexually and complications of the infection may become manifest.

A Major nuisance

The most common clinical manifestation of HPV is that of genital warts. Sometimes called condyloma accuminata or venereal warts, these lesions are the most easily recognized sign of a genital HPV infection. Human papillomavirus types 1, 2, and 4 together comprise the major cause of cutaneous papillomas in the general population.
Genital warts are soft, moist, or flesh colored and appear in the genital area within weeks or months after infection. They sometimes appear in clusters that resemble cauliflower-like bumps, and can be either raised or flat, small or large. Genital warts may be found in women on the vulva and cervix, inside and surrounding the vagina, or around the anus. In men, genital warts may appear on the scrotum or penis or in and around the anus. There are cases where genital warts have been found on the thigh and groin.

Oftentimes, patients are unable to relate the appearance of genital warts with any specific activity. However, genital warts are very contagious and may be spread during oral, vaginal, or anal sex with an infected partner. They may be transmitted by
skin-to-skin contact during sexual activity. About two-thirds of people who have sexual contact with a partner with genital warts will develop warts, usually within 3 months of contact.

The diagnosis of warts is easily made by visual inspection. Topically applied disclosing agents such as acetic acid (vinegar) will sometimes show otherwise invisible lesions.

There are many forms of treatment for anal warts. These include chemical methods such as 20 percent podophyllin antimitotic solution, Trichloroacetic acid (TCA), 0.5 percent podofilox solution, and 5 percent imiquimod cream (Aldara®). Common side effects of treatment include burning, redness and itching. These medications should be utilized only by physicians trained in their use. Podophyllin, podofilox and 5-FU should not be used during pregnancy.

While chemical methods may be curative, treatment may ultimately require some form of physical removal or destruction. This can be accomplished through freezing,
electrodessication (cautery) or laser ablation. Surgical excision offers the most thorough and complete means of eradication. Subdermal injection of Interferon, more commonly used in the past, may be used to augment the treatment. Even with the best of treatments, recurrence is common, and focused long-term surveillance is necessary in order to
spot recurrences as soon as they arise.

A growning menace

Genital warts are strongly associated with the development of squamous cell carcinoma of the anal canal. Integration of the Human papillomavirus DNA into the host cell genome is believed to be essential for malignant progression. Human papillomavirus type 16 is present in 30-75% of cases of anal cancer. Additionally, types 6, 11, and 18 are present in an additional 10% of cases. HPV appears to play a central yet unknown role in the development of the disease.

Recently, many physicians have begun to use cytological testing to aid in the early diagnosis of pre-malignant or malignant changes in the anal epithelium. The anal area is brushed with a small brush and the specimen is sent for cytological evaluation. This is similar to Pap smear testing for pre-malignant changes of the cervical epithelium in women. The results may be normal or may show atypia or any of the three grades of Anal Intraepithelial Neoplasia (AIN). AIN I is the earliest manifestation of dysplasia, while
AIN III is associated with severe dysplasia (Bowen’s disease). It is not yet clear that
progression of AIN necessarily leads to carcinoma of the anus. It is also unclear as to whether or not eradication of these affected areas of the anal canal will lead to the prevention of carcinoma. Extrapolation from the gynecological literature and cervical dysplasia studies has prompted further research into evaluating the natural history of Anal Intrapithelial Neoplasia.

If anal carcinoma is diagnosed, the standard treatment of 5-FU, mitomycin-C and radiation is used. Five-year cure rates approach 84%. Follow up biopsies may be used to examine the treated area. In patients experiencing an incomplete response, or in those patients exhibiting a recurrence of the disease, an abdominoperineal resection may be used as a salvage technique.

Prevention of disease transmission is the goal in any illness. Latex condoms are helpful but not completely protective as lesions may arise in covered areas. Misuse or failure to cover all exposed areas can also lead to the spread of disease. Regular examinations of susceptible individuals may aid in the control of early disease. The larger the load of condyloma, the more difficult is the treatment. Cytological swabbing and testing with early diagnosis may one day enable the practitioner to treat HPV while it is in the microscopic stages. Further research is necessary to clarify this issue.

As of now, HPV vaccines are still in the experimental stages and prevention remains the best cure.

“Cytological swabbing and testing with early diagnosis may one day enable the practitioner to treat HPV while it is in the microscopic stages.”

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Human Papilloma Virus–HPV

An alphabet of diseases – some bothersome and some ominous

“Prevention of disease transmission is the goal in any illness… Many people have a genital HPV infection without exhibiting any signs
or symptoms.”

The term Anal Intraepithelial Neoplasia (AIN) describes the microscopic finding of dysplastic, non-malignant cells in the anal canal. AIN has been subdivided into AIN I, II, and III, representing low, moderate, and high-grade dysplasia. This dysplasia has been thought to arise as a result of local infection with the Human papillomavirus. The Human papillomavirus is a small double-stranded DNA virus with a diameter of 55 nm. and is encased in a protein capsid. The term AIN has gradually replaced other descriptive terminology such as atypical squamous cells of indeterminate significance (ASCUS), low-grade squamous intraepithelial lesions (LSIL), or high-grade squamous intraepithelial lesions (HSIL).

One third of all cases of newly diagnosed sexually transmitted infections are related to HPV. Five million new cases of HPV are diagnosed each year, and at any given time in the United States, twenty million men and women have an active infection. Many patients will progress to the development of anal condyloma acuminata (genital warts). In addition, HPV is strongly associated with the development of squamous cell carcinoma of the anus. Hence, this ubiquitous virus has taken on a more menacing significance. It is no longer considered to be simply an inconvenient sexually transmitted disease. Many people have a genital HPV infection without exhibiting any signs or symptoms. Even when asymptomatic, the disease can be transmitted and complications of the infection may become manifest.

THE MICROSCOPIC PROBLEM:

Anal Intraepithelial Neoplasia (AIN)
With the development of cervical PAP smears, the relationship between cervical HPV and cervical cancer has become well established. The relationship between anal HPV and the development of anal cancer from AIN is less well defined. The anal canal, like the cervix, is a transition zone, transitioning from a squamous epithelium to a columnar epithelium. Anal cytology, via anal PAP smears, has been accepted as a screening tool to identify patients with anal dysplasia. There is no widespread acceptance of a particular specific screening algorithm however. This is due to variability in interpretation of AIN and limitations of our understanding of the exact relationship between HPV, AIN, and anal cancer.
Serotypes 16, 18, 31, 33, and 35 are associated with malignant potential. Transmission most commonly occurs as a result of anoreceptive intercourse. However, the virus can pool at the base of the penis, scrotum, or vagina and extend to the anal area. Infection with oncogenic serotypes can persist and result in a progression from low- to high-grade dysplasia and anal cancer.

While non-HIV infected individuals may harbor HPV and be at risk for the development of anal squamous cell carcinoma, recent studies have suggested a permissive role of HIV infection in the development of anal cancerin HIV-infected men and women. HIV-positive patients are more likely to have AIN III and are more likely to progress from AIN I to AIN III, especially with CD4 counts <200 cells/mm. With the widespread use of highly active antiretroviral therapy (HAART) in increasing the length of survival of HIV-positive individuals, we may soon see an increase in the rate of development of anal cancer in outwardly healthy but immunocompromised individuals.

The anal pap smear

Many physicians have begun to use cytological testing to aid in the early diagnosis of pre-malignant or malignant changes in the anal epithelium. The anal area is brushed and the specimen is sent for cytological evaluation. This is similar to Pap smear testing for pre-malignant changes of the cervical epithelium in women. The results may be normal or may show any of the three grades of Anal Intraepithelial Neoplasia. AIN I is the earliest manifestation of dysplasia, while AIN III is associated with severe dysplasia (Bowen’s disease). It is not yet clear that progression of AIN necessarily leads to carcinoma of the anus, and, it is also unclear as to whether or not eradication of these affected areas of the anal canal will lead to the prevention of carcinoma. Extrapolation from the gynecological literature and cervical dysplasia studies has prompted further research into evaluating the natural history of Anal Intraepithelial Neoplasia.

If squamous cell carcinoma of the anus is diagnosed, the standard treatment of intravenous 5-FU, mitomycin-C and radiation is used. Five-year cure rates approach 84%. Follow up biopsies may be used to examine the treated area. In patients experiencing an incomplete response, or in those patients exhibiting a recurrence of the disease, an abdominoperineal resection may be used as a salvage technique.

THE MACROSCOPIC PROBLEM:

Condyloma Acuminata, A Major Nuisance
The most common clinical manifestation of HPV is that of genital warts. Sometimes called condyloma acuminata or venereal warts, these lesions are the most easily recognized sign of a genital HPV infection. Human papillomavirus serotypes 6, and 11 comprise the major cause of cutaneous papillomas in the general population.

Genital warts are soft, moist, flesh colored and appear in the genital area within weeks or months after infection. They sometimes appear in clusters that resemble cauliflower-like bumps, and are raised or flat. In women, genital warts may present on the vulva or cervix, and inside the vagina or anus.

In men, genital warts may appear on the scrotum, penis or in and around the anus. There are cases where genital warts have been found on the thigh and groin.

Oftentimes, patients are unable to relate the appearance of genital warts to any specific activity. However, genital warts are contagious and may be spread during oral, vaginal or anal sexual contact with an infected partner. They may be transmitted by skin-to-skin contact during sexual activity. Two-thirds of people who have sexual contact with a partner with genital warts will develop warts, usually within 3 months of contact.
The diagnosis of warts is easily made by visual inspection. Topically applied disclosing agents such as acetic acid may disclose otherwise invisible lesions.

There are many forms of treatment for anal warts. These include chemical methods such as podophyllin ointment, trichloroacetic acid, 0.5% podofilox solution (Condylox®), and 5% imiquimod cream (Aldara®). Common side effects of treatment include burning, redness and itching. These medications should be utilized only by physicians trained in their use. Podophyllin, podofilox and 5-FU should not be used during pregnancy.

While chemical methods may be curative, treatment may ultimately require some form of physical removal or destruction. This can be accomplished through freezing, electrodessication (cautery) or laser ablation. Surgical excision offers the most thorough and complete means of eradication. Subdermal injection of Interferon, more commonly used in the past, may be used to augment the treatment. Even with the best of treatments, recurrence is common and long-term surveillance is necessary in order to spot recurrences as soon as they arise.

Prevention is the cure

Prevention of disease transmission is the goal in any illness. Latex condoms are helpful but not completely protective as lesions may arise in covered areas. Misuse or failure to cover all exposed areas can also lead to the spread of disease. Regular examinations of susceptible individuals may aid in the control of early disease. The larger the load of condyloma, the more difficult is the treatment. Cytological swabbing and testing with early diagnosis may one day enable the practitioner to treat HPV while it is in the microscopic stages. Further research is necessary to clarify this issue.
Prevention remains the best cure.

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