Health Update

by Tyrone M. Reyes, M.D.

Peptic ulcers have plagued human beings throughout the centuries, but the exact cause of the condition was uncertain. In 1940, Dr. A. Stone Freedberg of Harvard Medical School identified unusual curved bacteria in the stomachs of ulcer victims. He suspected that they might be responsible for ulcers but abandoned the research when his team was unable to grow the bacteria in the lab.

Doctors went on treating patients with diet modifications, antacids, and operations for the next 40 years. But, in the early 1980s, two Australian physicians, Dr. Barry J. Marshall and Dr. J. Robin Warren, discovered how to culture the bacterium in the laboratory. Next, they tried to infect experimental animals. It’s a traditional step in microbiological research, but it failed because their bacterium, now called Helicobacter pylori (HP), can infect only humans. Dr. Marshall responded to two years of scientific frustration by taking the dramatic step of drinking a vial of fluid laced with about a billion bacteria. A week later, he developed stomach symptoms; after another 10 days, a gastroscopy showed that his stomach tissue was actually inflamed and teeming with HP. Fortunately, Dr. Marshall recovered fully and continued his research. And both men were alive and well on October 3, 2005, when this pioneering research was rewarded with the Nobel Prize in Medicine.

Meet The Ulcer Bug

Your stomach may be hospitable to rice, but it’s hostile to bacteria. In fact, HP is the only bacterium that can survive — and thrive — in the stomach. The bug has several properties that explain its unique adaptation.

First, it needs only a tiny amount of oxygen, about a fifth of the amounts humans need. Second, its spiral shape allows it to burrow through the mucus that covers the stomach lining. Third, it has up to seven whip-like proteins that project from the end of the bug and propel it through the mucus. Fourth, it has special receptors that permit it to latch onto stomach cells once it makes its way through the mucus (see figure).

HP has another property that is the most important of all. It can split molecules of urea, a chemical that’s present in human tissues and fluids. The process releases ammonia and carbon dioxide, which form a cloudlike mantle around the bacterium, protecting it from the stomach acid that kills ordinary bacteria. This ability to split urea is a big plus for HP, but doctors have turned it to their own advantage by developing the urea breath test to diagnose the infection.

Who gets hp?

According to the best estimate, about half the world’s population is infected with HP, making it the most common bacterial infection of humans. Because the organism spreads only in food or water that has been contaminated by infected human fecal material, HP infection is most common in regions with crowded living conditions, poor hygiene, and inadequate sanitation. In some developing countries, the prevalence could approach 80 percent. The rate could also vary with socioeconomic status and age.

How HP Harms

Unlike strep or staph, which are often carried in the skin or in the throat without causing inflammation, HP always triggers inflammation, in this case, stomach inflammation or gastritis. The bacterium produces a variety of toxins that stimulate white blood cells to produce small proteins (cytokines) that perpetuate the inflammatory cycle. Strains of HP that contain a specific gene, cag A, are the most virulent. However, not even this nasty strain ever spreads from the stomach lining to other parts of the body.

Although everyone who harbors HP has at least some degree of gastritis, the great majority have no symptoms and remain well. But in the course of a lifetime, up to three percent of people with HP go on to develop peptic ulcers in the stomach or duodenum (the portion of the intestines just beyond the stomach) and a much lower percentage develop stomach cancer or the low-grade stomach lymphoma known as MALT. Smoking increases the risk of ulcers and cancers related to HP, and it also makes antibiotic treatment more difficult. Diets high in salt, smoked foods, and preserved foods boost the risk of cancer, but foods that provide vitamin C and other antioxidants appear to reduce the risk.

Doctors agree that HP does not cause gastroesophageal reflux disease (GERD; “heartburn”). Some evidence has also linked HP to other disorders, ranging from iron deficiency anemia to skin and blood problems, low levels of HDL (“good”) cholesterol and atherosclerosis. More research is needed to determine if any of these associations are valid.

Diagnosis

The easiest way to diagnose HP is with a blood test that can detect the antibodies that form in response to the infection. It has, however, two drawbacks. First, it cannot discriminate between an active infection that is causing disease and a simmering infection that is not producing symptoms. Second, the blood test cannot tell if treatment has produced a cure, since antibiotics linger in the blood long after HP has been eradicated. Still, if antibody levels are very high before the treatment, they suggest active infection, while a sharp reduction after therapy suggests success.

The old standby is a test that depends on HP’s ability to split urea. The urea breath test is safe, accurate, and quick — and since it detects only active bacteria, it can be used to test for cure. A newer test detects bacterial proteins in stools. About 94 percent of patients with active HP infection have a positive stool test – and if treatment is successful, nearly all will have a negative test one to four weeks after therapy.

The “gold standard” test, however, requires an endosocopy and stomach biopsy. It involves passing a fiberoptic tube through the mouth into the stomach. Sedation and spraying a local anesthetic in the patient’s throat is usually done before the procedure. Indeed, endoscopy was used to document Dr. Marshall’s self-induced infection in 1984.

Treatment

Get an infection, take an antibiotic, and enjoy the cure. That’s the way it works for many bacteria — but not for HP, which has the nasty ability to become resistant to antibiotics. Fortunately, doctors can outwit their adversary by using combination therapy. Many programs are available; all require two antibiotics plus one or two acid-neutralizing drugs. Here are some of the medications commonly recommended:

• Amoxicillin (many brands). This penicillin derivative is more active than similar medications because it is secreted into the gastric fluid.

• Clarithromycin (Klaricid, Klarmyn, Onexid). This member of the erythromycin family is one of the most effective drugs for HP.

• Metronidazole (Flagyl, Anerobia, others). Once uniformly effective against HP, emerging bacterial resistance has led many doctors to use it only for patients who cannot take amoxicillin.

• Tetraycline (many brands). This antibiotic is most often used in combination with other drugs for patients who have failed first-line treatment.

• Omeprazole (Losec). The first proton-pump inhibitor, omeprazole dramatically reduces stomach acid. It has no direct effect on HP, but it increases the efficacy of antibiotics. Many newer proton-pump inhibitors are available and can be substituted for omeprazole in appropriate doses.

• Bismuth subsalicyclate (available in the US as Pepto-Bismol). Although not an antibiotic, bismuth is able to kill HP in the stomach. This is always used in combination with two antibiotics.

• Ranitidine bismuth citrate. This newer drug combines ranitidine (Zantac), which has been used for years to reduce stomach acid, with bismuth, which has antibacterial property. This drug cannot eradicate HP on its own and is prescribed with other medications.

Many treatment combinations are available. The most popular one administers amoxicillin, clarithromycin, and omeprazole for seven to 14 days. But many other regimens have been advocated.

Evidence suggests that HP has coexisted with humans for thousands of years, but doctors have known about it for a scant quarter-century. Scientists have learned a lot more since the pioneering research of Dr. Marshall and Dr. Warren, though many questions remain unanswered. But at least, you no longer have to be concerned that worry and stress will give you an ulcer.

Source: Philippine Star