Peptic ulcers: digesting more than food – includes information on who’s at risk, drugs and diets used as treatment, etc
Peptic ulcers plague about one in 10 North Americans but new treatments can now prevent many of the more serious complications.
Although the subject of many a joke, ulcers are no laughing matter. One of the world’s most common maladies, peptic ulcers make life miserable for 10 per cent of Canadians at some point in their lives. While ulcers can also occur in other parts of the body, the popular term refers primarily to peptic ulcers in the duodenum first part of the small intestine leading out of the stomach) or in the stomach itself (SEE DIAGRAM). Misconceptions abound Many people falsely refer to bouts of indigestion as an ulcer acting up.” A recent nation-wide survey revealed how amazingly ill-informed Canadians are about ulcers, most believing stress to be the main cause. Almost 90 per cent hold to the outmoded idea that milk and bland diets are the best ulcer cures. Contrary to long-standing myths, new studies show no evidence that stress causes ulcers. Easy-going people are as likely to get them as hard-driving workaholics. Althouth stress may aggravate an existing ulcer, there is no evidence that it causes one. And milk or bland diets are no longer considered effective ulcer cures. Most startling of all is the fact that half of the people surveyed who’d already had an ulcer thought that aspirin (ASA) is the best treatment. “Incredible!” comments one University of Toronto expert, “because aspirin, along with other non-steroidal anti-inflammatory drugs is a prime ulcer-provoker.” What exactly is an ulcer? Peptic ulcer is an umbrella term for certain lesions (sores) in the lining of the stomach and duodenum – top part of the small intestine. The word “peptic” comes from pepsin, the enzyme that normally helps to break down food and contributes to the erosion that produces an ulcer. Ulcers are small pits or craters in parts of the gastrointestinal tract’s surface lining. They develop in the mucous membrane which lines the digestive tract, often appearing as white or pale yellow spots due to surrounding inflammation. Peptic ulcers occur most often in the duodenum (duodenal ulcers) less commonly in the stomach itself gastric ulcers). Occasionally ulcers arise in the esophagus or in the small bowel (Meckel’s diverticulosis).
In the past, peptic ulcer disease, especially duodenal ulcers, afflicted mainly men, but nowadays many women are also affected (particularly the elderly and those who take antiinflammatory drugs to relieve conditions such as arthritis). Although ulcers vary in size from a pin hole to one inch or larger, size has little to do with the intensity of pain experienced. While some ulcers heal spontaneously on their own, others persist for months despite treatment. About three quarters of those with duodenal ulcers have a relapse or repeat ulcer within a year of having treated one. The digestive tract’s natural defences normally protect it from destruction One University of Toronto expert remarks that “it’s a wonder the stomach doesn’t self-destruct, considering the strong acid it contains – powerful enough to destroy most tissues.” The stomach and duodenum have several lines of defence with which to withstand the corrosive action of acidic secretions. What causes ulcers? The exact cause(s) of peptic ulcer disease remain uncertain. Nobody knows why certain people get ulcers, why some flare up time and again while others heal themselves. However, it’s now generally believed that peptic ulcers develop when the aggressive forces in the digestive tract (the acid and pepsin) overwhelm its defensive elements (the mucosal lining and its protective mechanisms). While formerly blamed almost entirely on “too much acid,” recent studies show that although duodenal ulcer patients may have excess acid (up to double normal values) gastric ulcers develop more because of alterations in the mucosal defences than owing to high acid levels. Recent evidence suggests that ulcers form when there’s a flaw in the mechanism that normally shields the gastrointestinal lining from corrosion. If something goes out of kilter and excess acid is secreted or the mucosal lining is weakened, the strong digestive juices overpower the defences and penetrate surrounding tissues, literally “eating them up.” Scientists don’t know why the mucosal lining becomes weakened, although they suspect it may be linked to inadequate prostaglandin activity. Recent research also implicates a spiral bacterium, Helicobacter pylori, first observed in the gastric mucosa during the 19th century, as a factor in ulcer formation. This infection has only recently been linked to peptic ulcers, a surprising connection since stomach acid is normally a bacterial killer. However, H. pylori bacteria appear to have adapted well to the stomach’s hostile acidic environment and may promote ulcer formation by invading the cells and undermining the defense mechanisms. Studies show that 84 per cent of patients with duodenal ulcers, 57 per cent of ulcer-free patients with dyspepsia (indigestion) and 21 per cent of normal subjects harbour H. pylori infections, the incidence increasing with age. Treatment with bismuth salts and antibiotics may help to eliminate H. pylori infections. However, the role of H. pylori remains controversial and some researchers suggest that these infections probably do not cause peptic ulcers, claiming instead that overlapping risk factors (such as smoking and other diseases) may precipitate them. Aspirin (ASA) and other nonsteroidal anti-inflammatory drugs (NSAIDs) have recently emerged as a significant risk factor in ulcer formation, especially gastric ulcers. These drugs injure the stomach lining and suppress its defense mechanisms, largely by blocking the production of prostaglandins. Hard to differentiate duodenal from gastric ulcers Gastric and duodenal ulcers have broadly overlapping symptoms, making it difficult to tell them apart without doing X-ray or endoscopic tests. For example, while food often brings rapid relief for duodenal ulcers (in 20-65 per cent of sufferers), it tends to worsen the gastric type. Yet a fair number (two to 50 per cent) of those with gastric ulcers also find that food soothes the discomfort. Nonetheless, there are a few clues to help distinguish the two forms. Duodenal ulcers typically affect people under age 50, mostly men. And because duodenal ulcers are often linked to excess acid, the pain generally hits when the stomach is empty and has nothing with which to buffer it. The pain of duodenal ulcers is usually worst between meals (one to three hours after eating) and at night, often sending sufferers to the fridge for a “midnight” snack, sometimes between one and three a.m! The irresistible urge to reach for a soda cracker in the wee morning hours may signal a peptic ulcer of the duodenal variety. Eating can stop the pain within minutes. Gastric or stomach ulcers – less common than the duodenal variety – typically afflict middle-aged and older people, men and women alike. Gastric ulcer pain, not usually linked to excess acid, tends to come and go, sometimes being worst soon after eating (although, depending on the ulcer’s location in the stomach, eating may relieve the discomfort). NSAIDs (anti-inflammatory drugs) are major culprits in gastric ulcer formation. Sufferers may have occasional nausea and appetite loss. Some people have both duodenal and gastric ulcers. Silent ulcers Not all peptic ulcers herald their presence by pain. Some produce little or no pain and people don’t know they have an ulcer until it bleeds or causes other trouble. About 10 to 25 per cent of those with peptic ulcer disease have “silent ulcers” which give no warning symptoms regardless of severity. Complications such as severe bleeding and/or perforation may be the first sign of a silent ulcer in someone with no previous pain and no history of peptic ulcer disease. Studies show that those particularly prone to silent ulcers include smokers, the elderly, those with a history of peptic ulcers, those on ulcer therapy who stop taking the medication too soon and people on NSAIDs. Studies suggest that up to 90 per cent of ulcers due to NSAIDs are silent and hard to detect until complications occur. Diagnosis Most peptic ulcers herald their presence by abdominal pain sometimes described as “bad indigestion.” A peptic ulcer typically produces a dull, gnawing ache or hunger pain in the pit of the stomach – often relieved in short order by eating, drinking or taking an antacid. “Pain is the most distinctive feature of ulcers,” wrote the renowned Canadian physician Dr. William Osler in 1892. “The attacks may occur at intervals with great intensity for weeks or months at a time…” Nowadays, given a set of symptoms suggestive of ulcers, physicians may first treat with medication, and order diagnostic tests only if the pain persists. The barium X-ray, once the standard test, has now been largely supplanted by endoscopy – using a fibreoptic tube or endoscope, inserted via the mouth, to look inside the GI tract and identify any abnormalities present. lf the initial examination reveals a duodenal ulcer, the patient is usually treated with medication (e.g., H2-blockers). However, if the examination indicates the presence of a gastric ulcer, the person is generally sent for further tests because about four per cent of gastric ulcers are malignant. Endoscopy is usually recommended for all gastric ulcer sufferers (to take biopsy samples and test for cancer) and for those with complicated or severe peptic ulcer disease- bleeding or scarring from previous ulcers. NB: The endoscope, a long, narrow, flexible tube with a light at the end, permits physicians to directly view the gut lining, revealing any small changes in its surface – not generally visible by X-ray. An endoscopic exam also permits a biopsy to be done, collecting tissue samples for examination by a pathologist. Treatment: what brings relief? Before effective modem medications appeared on the scene, serious peptic ulcer disease was usually treated by surgery. However, the past 15 years have seen dramatic improvements in ulcer management. Drug therapy can now heal many ulcers and helps to prevent repeat attacks. The key lies in recognizing the symptoms, making a correct diagnosis and prescribing drugs before serious damage is done. Current medical treatment aims to relieve the pain, heal the ulcer and prevent complications. Physicians generally prescribe one of the new ulcer medications to protect the lining from further attack while the ulcer heals. Used appropriately, these medications can stop ulcer symptoms within days and heal them in four to eight weeks. But even if symptoms abate, drug therapy should be continued for the full period presribed. Although the pain may vanish within days, the medication should not be stopped until the ulcer has fully healed. Occasionally, multiple drug courses are needed to complete healing. Ulcers in smokers are harder to treat because tobacco smoke stimulates stomach acid secretion and inhibits healing. Bleeding ulcers can now be treated by adrenaline injections (via an endoscope), hypertonic saline or thermocoagulation using heater-probes or lasers. Surgery is a last resort. While 20 years ago operations were widely used to cure and prevent ulcers, by cutting out bits of the stomach to curb acid production, gastrectomy (removing part of the stomach) is now generally performed only for those with severe complications or if ulcers refuse to heal. Preventing repeat ulcers Unfortunately, ulcers tend to recur, especially in smokers, and multiple drug courses may be necessary. People who have illnesses that call for NSAIDs therapy may require a maintenance or preventive dose of anti-ulcer drugs, or better still might try alternative medication. To prevent ulcer recurrence, people prone to them are urged to:
stop taking NSAIDs and use alternative therapy – perhaps try analgesics (painkillers)
possibly take a small maintenance dose of H2- receptor blockers or other medication controversial). In conclusion.- With the advent of effective anti-ulcer medication, surgery for this condition is on the wane and hopefully in future even better medications will completely eliminate the need for surgical remedies. However, to make sure their ulcers heal, people are urged to take the full course of medication prescribed. Drugs used to treat e tic ulcer disease Antacids Still of value in ulcer treatment, (mostly for duodenal ulcers) antacids neutralize the acid, relieve pain and promote mucosal healing. Antacids come in tablet or liquid form – liquids being the mosteffective. They are best taken one to three hours after meals and at bedtime. Their appeal is limited by rather short-lasting action. Aluminium hydroxide and magnesium hydroxide are the longest acting forms. Calcium carbonate (found in Tums and Rolaids) gives rapid relief but is apt to trigger “acid rebound” – a surge of acid after two or three hours. One big problem with antacids is failure to take the right amount: people often self-medicate without advice and stop taking the medication as soon as the pain vanishes, rather than continuing until the ulcer heals. Most antacids have some side effects – varying with the type chosen. Magnesium-containing brands commonly cause diarrhea. Aluminum compounds may cause constipation and prolonged therapy can disrupt mineral metabolism (possibly also contributing to the risks of Alzheimer’s disease). Antacids rich in sodium should be avoided by people with high blood pressure and kidney or heart disease. Some antacids interfere with the action of other drugs notably warfarin, digoxin, anticonvulsants, some antibiotics and anti-inflammatories. Gastric acid suppressors (that reduce or arrest gastric acid secretion) * Histamine H2-receptor blockers (acid-reducing drugs) have transformed ulcer management. Taken as tablets, H2-blockers act on the stomach’s surface “receptors” and prevent release of histamine, one of the substances that stimulates hydrochloric acid secretion, inhibiting acid build-up. (Histamine is also involved in allergic reactions, but the receptors are different: ulcer drugs don’t cure allergies.) The end result of H2-blocker treatment is less stomach acid which permits healing. These drugs can reduce ulcer pain within hours of the first dose, allowing ulcers to heal in a few weeks. The first of the H2-blockers on the market, cimetidine, introduced in the early 1970s, revolutionized ulcer treatment. Besides cimetidine (Tagamet) and ranitidine (Zantac), acid-suppressing drugs include the more recent famotidine (Pepcid) and nizatidine (Axid) – a single bedtime dose healing a duodenal ulcer in four weeks and a gastric ulcer in six to eight weeks. Side-effects of H2-blockers, especially cimetidine, include dizziness, mental confusion and sleepiness (especially frequent in the elderly). They can also cause impotence in men and breast enlargement. The H2-blockers may also interact with other drugs (such as warfarin, theophylline and Valium). * Proton-pump Inhibitors. The recently approved and now available drug, omeprazole, is 10 times more powerful in suppressing stomach acid production than the H2-blockers, able to promote duodenal ulcer healing in two to four weeks, not necessarily as swift with gastric ulcers. This potent acid-inhibitor can suppress about 95 per cent of stomach acid production. it is especially useful for treating people whose ulcers fail to respond to H2receptor blockers or other medications and those with Zollinger-Ellison syndrome. Side effects include diarrhea, cramps, indigestion, gas (bloating) in some people. Anti-cholinergics (inhibitors of acetylcholine) In wide use before the arrival of H2-receptor blockers but now mainly of historical interest, these drugs are still occasionally used in conjunction with new medications to treat stubborn ulcers and for the Zollinger-Ellison syndrome. Gut lining protectors or barrier shields (ulcer-coating, “cytoprotective ” agents) *Sucralfate (Sulcrate or Carafate) – an aluminium salt of sucrose – doesn’t alter stomach acid levels, but coats the ulcer (crater), forming a barrier across which hydrochloric acid and pepsin cannot pass, permitting it to heal. Taken two to four times a day and at bedtime, sucralfate has fewer side effects than H2-blockers. However, about five per cent of those on it report nausea, constipation or a metallic taste in the mouth. No clinically significant drug interactions have been reported. Prostaglandin-like medications (a new class of synthetic prostaglandins with potent anti-ulcer properties) * Misoprostol (Cytotec), a synthetic prostaglandin-E, is especially valuable for people such as arthritics who take ASA/aspirin or other NSAIDs that suppress natural prostaglandin production. Newly available in Canada, misoprostoldecreases acid production and enhances the mucosal defences. Healing rates roughly parallel those with H2-receptor blockers, but one big advantage of the synthetic prostaglandins is their ability to combat the damaging effects of NSAIDS. (Misoprostol is highly effective in healing aspirin-induced ulcers.) Moreover, the latest studies suggest it can also protect against NSAID induced kidney damage (a recently reported adverse effect of these anti-inflammatory drugs). Misoprostol may be prescribed together with anti-inflammatories for arthritics. However, misoprostol’s side effects – experienced by nine to 13 per cent of patients – may limit its use, especially diarrhea, abdominal cramps and menstrual disturbances. Used inappropriately, it may cause uterine contractions and spontaneous abortion, so should never be prescribed to childbearing women. Other occasional adverse effects are headache, dizziness, fever and flushing. The long term effects are unknown. Antibacterials * Colloidal bismuth suspensions such as Pepto-Bismol (bismuth subsalicylate) might promote ulcer healing not by influencing gastric acid levels but by increasing prostaglandin secretion and suppressing H. pylori infections. Combination therapy with bismuth plus antibiotics may help to eradicate intestinal infections therapy that’s still experimental. The digestive tract’s normal lines of defence include: * The structure of its lining or mucosa – with columnar cells
that form a physical barrier. * Secretion of mucus – which provides lubrication and a gel
coating to combat acidic corrosion. * Production of bicarbonate – which buffers the gastric acid. * Release of prostaglandins – hormone-like chemicals – that
protect the mucosa from damage in several ways. Prostaglandins
stimulate or turn on mucus and bicarbonate
secretion, increase cell renewal, act on the smooth muscle to
dilate blood vessels and increase blood flow. * An epidermal (growth) factor- also present in the saliva of
many other animals, which aids cell regeneration. Who’s most at risk? Known risk factors for peptic ulcer disease include: * Heredity. Close relatives of ulcer patients are three times more likely than others to develop peptic ulcers. * Smoking. A major contributor and one reason why women (of whom increasing numbers are now smoking) develop ulcers more often than previously. Smoking doubles the chances of getting an ulcer, increases their severity, slows healing and enhances the risk of recurrence and complications. Clinical studies show that smokers have a 72 per cent ulcer recurrence rate compared to 21 per cent in nonsmokers. in one study, 87 per cent of all patients with perforated duodenal ulcers were smokers. * Regular consumption of nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Advil, Motrin) naproxen (Naprosyn), piroxicam (Feldene) ranks high among the causes of peptic ulcer disease. The incidence of ulcers increases by five to 10 per cent in those who take NSAIDs – substances that damage the digestive tract lining and disrupt its defenses also raising the risk of complications, especially bleeding and perforation, more with gastric than duodenal ulcers. The use of NSAIDs increases the risk of peptic ulcer disease in anyone, but the elderly – women in particular – are at greatest risk. Ulcers due to NSAIDs pose a sizeable problem because almost 50 per cent of arthritics (two million Canadians) regularly take these drugs. * Caffeine, not necessarily a risk factor, stimulates gastric acid secretion. Coffee should not be taken on an empty stomach in ulcer-prone people. * Spicy diets aren’t usually ulcer-provokers. The texture and amount of food are no longer considered key players in ulcer formation. No particular food leads to ulcers, although the mere act of eating can aggravate or relieve ulcer pain. Nor does the old dietary standby of eating frequent small, bland meals combat an ulcer. Scientists now know that eating frequent small meals simply switches on the stomach’s digestive acid secretions more often, leading to greater destruction of the mucosal lining. * Milk may aggravate rather than relieve ulcer pain! Although it can temporarily relieve the discomfort of an ulcer, milk promotes the release of more gastric acid than it can counteract. 9 Alcohol may be a risk factor. While pure ethanol alcohol) decreases gastric acid production, the protein content of beer or wine may promote acid secretion and increase ulcer risks. Excessive alcohol consumption is inadvisable for those prone to ulcers (for others too!) * The role of stress. While it was formerly believed that hardworking “type A,” stressed-out people were most prone to ulcers, the link remains unproven. Studies indicate no greater psychological stress in those with ulcers than in the general population. However, the inability to cope well with stress may play a role. While ulcer patients don’t necessarily experience more stress than others, they may perceive more stress in their lives and handle it less effectively. Zollinger-Ellison Syndrome: a special case In this uncommon, sometimes inherited syndrome, multiple duodenal ulcers form because a tumour in the duodenum or pancreas induces over-secretion of the hormone gastrin, which in turn triggers excess acid production, The natural defense mechanisms of the gut are then overwhelmed allowing ulcers to develop and recur, increasing the likelihood of severe complications. Patients with Zollinger-Ellison syndrome don’t usually respond well to anti-ulcer medications except to the recently released, very potent acid-suppressor, omeprazole. Complications of untreated peptic ulcers can be severe Up to 20 per cent of peptic ulcer sufferers may develop complications which include: A bleeding ulcer – found in 15-20 per cent of ulcer patients is caused by digestive juices corroding an artery, an event that can be frightening cause the ulcer may have given no previous hint of its existence until all acute bleed shown by bloody vomit and/or black, tarry stools, signals its presence. Slow-bleeding ulcers may cause anemia (dizziness and fatigue) due to unnoticed internal blood loss. Ulcer bleeding is often intermittent and stops spontaneously in 90 per cent of cases. The remainder may need surgery, although injection therapy has recently shown promise in hatting thee bleeding. A perforated ulcer – which eats into and penetrates the stomach or duodenal wall – affects five to 10 per cent of sufferers. more commonly men than women. An obstructive ulcer – perhaps due to chronic scar formation – blocks the passage of- food through the gastric outlent and may cause sudden nausea and vomiting, often late in the day.
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