Advanced Therapy in Gastroenterology and Liver Disease - part 5 ppsx

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Calcium-activated potassium channels in basolateral membranes of colon epithelial cells; reconstitution and functional properties. Wien Klin Wochenschr 1990;102:622–8. 339 CHAPTER 56 DIETARY-INDUCED SYMPTOMS LAWRENCE R. SCHILLER,MD ESOPHAGUS In the esophagus, the repeated swallows associated with eating and the postprandial rise in serum gastrin levels decrease lower esophageal sphincter (LES) tone. In addition, gastric distention due to ingested food and intragastric gas production as acid is neutralized by food increase the number of transient LES relaxations (the “belching reflex”) and per- mit gastroesophageal reflux to occur. Patients with gastroesophageal reflux disease often note a distinct increase in symptoms postprandially. Fatty foods and hypertonic beverages may be particular problems (see later in chapter). S TOMACH Eating stimulates gastric acid secretion, increasing the vol- ume of material in the stomach. The ability of the stomach to hold the additional fluid and the meal is due to gastric accommodation, which allows the gastric wall to relax. This vagally mediated reflex is disturbed in some patients with FD and in patients after vagotomy, who cannot accommodate large volumes in the stomach. This may aggravate gastroesophageal reflux, speed gastric emptying of liquids, and trigger sensations of bloating or early satiety. Antral motility also is stimulated by eating. S MALL BOWEL In the small bowel, ingestion of food rapidly converts the fasting pattern of motility, which features cyclical migrating motor complexes, into the more chaotic postprandial pattern. Chyme emptied from the stomach is joined by pancreatic and biliary secretions, which distend the small bowel and stimulate peristalsis. The bowel wall is sensitive to distention and eating acti- vates afferent nerves that may produce painful sensations in some individuals. The entry of chyme into the duodenum also results in release of many peptides and other sig- naling s ubstances that p roduce effects elsewhere in the gut and even outside the GI tract. COL ON F ood residues enter the c olon hour s after ingestion. Carbohydrate that is not absorbed in the small intestine Most patients with gastrointestinal (GI) symptoms attribute their symptoms to “something”they ate and want advice from the doctor about what to eat to minimize their symptoms. Symptoms after food ingestion most often are due to normal food-induced physiological changes, such as the gastrocolic reflex, or to the effects of food digestion, such as the generation of gas. They rarely are due to food allergy or to immunologic reactions to food breakdown products, such as in celiac disease. Specific problems will not be discussed further in this chapter. There are separate chapters on food allergies (Chapter 57, “Gastrointestinal Food Allergy”), celiac disease (Chapter 61, “Celiac Sprue and Related Problems”), and lactose intolerance (Chapter 62, “Lactose Intolerance”). Food-related symptoms often occur when organic problems are present, but probably occur most often in patients with common functional bowel disorders, such as functional dyspepsia (FD) or irritable bowel syndrome (IBS). Patients with organic problems, such as short bowel syndrome, will have exacerbation of symptoms like diarrhea when eating, with some foods producing more problems than others. Patients with functional problems tend to be unusually sensitive to distention and other digestive events, and, therefore, may have aggravation of their basic symptoms when ingesting any foods. However some foods may be more problematic than others. It is not that these foods cause the fundamental functional problem, only that the offending foods aggravate the symptoms of those conditions (O’Sullivan and O’Morain, 2003). Meal-Related Physiological Changes Response to a Meal Intestinal fluid and electrolyte transport and motility con- tinue during fasting, but ingestion of a meal results in a prompt alteration of activity. This is not different conceptually than what happens to the cardiovascular system with exercise, but it typically involves changes that are an order of magnitude greater. Thus salivary, gastric, biliary, and pancreatic secretion increase 10-fold or more over basal levels, and motility patterns abruptly change from fasting to fed patterns. 340 / Advanced Therapy in Gastroenterology and Liver Disease (poorly absorbed carbohydrate and fiber) enters the right colon and is fermented by the colonic bacterial flora. The products of fermentation are short chain fatty acids—up to 80 g of which can be produced by the colonic flora— a nd voluminous amounts of gas (carbon dioxide and hydrogen gas) (Hammer et al, 1989; Hammer et al,1990). Every 10 g of carbohydrate can yield about 1 L of gas. Gas can distend the colon, stimulating motility and causing bloating, cramps and pain in some people. Effects of Specific Foods and Food Additives People ingest a variety of substances that consist of mixtures of chemicals that can have specific effects on the body.These chemicals include primary macronutrients, such as carbohydrates, fats, and proteins; micronutrients, such as vitamins and minerals; and incidental chemicals that have no nutritive value,but are part of the animals and plants that we eat, such as caffeine in coffee or theobromine in chocolate. These incidental chemicals may be biologically active in the gut and elsewhere in the body and may produce symptoms. Carbohydrates Carbohydrates are responsible for a variety of food-induced symptoms (Table 56-1). These symptoms can be due to hypertonicity or to malabsorption of carbohydrate. Ingestion of hypertonic carbohydrate solutions results in entry of water into the gut lumen to produce osmotic equilibration. This is mostly a problem for individuals with unregulated gastric emptying, such as those who have had g astric surgery, and can produce a dumping syndrome with bloating, nausea, diarrhea, flushing, and hypotension. Hypertonic carbohydrate solutions, such as fruit juices, also can produce dyspepsia, probably by stimulation of receptors in the esophagus and stomach. Malabsorption of carbohydrate in the small intestine results in delivery of excess fermentable substrate to the colon. This can be due to generalized malabsorption (eg, celiac disease or short bowel syndrome) or to malabsorption of specific carbohydrate moieties. In addition, excess dietary fiber ingestion will load the colon with additional carbohydrate. When smaller amounts of carbohydrate are delivered to the colon, excess gas, bloating and cramps develop as gas is produced as a byproduct of fermentation. Diarrhea is produced when larger amounts are ingested or insufficient time is allowed for absorption due to accelerated transit. Symptoms can develop with as little as 5 to 10 g of excess carbohydrate entering the colon. Symptoms relate more to the total amount of fermentable carbohydrate entering the colon than to the specific type of carbohydrate that is malabsorbed. In some cases, “tolerance” to gradually increasing amounts of carbohydrate develops, which is probably related to changes in bacterial metabolism. Specific carbohydrates may be incompletely absorbed by the small intestine in certain individuals. These include fructose, sucrose, lactose, and the sugar alcohols: mannitol and sorbitol. MANNITOL AND SORBITOL A bso rption of mannit o l and s or bitol is int r insically limited by the absence of carriers or pores in the intestine that per- mit their transport. Thus, everyone malabsorbs these substances. These agents are used as non-nutritive sweeteners in a variety of dietetic foods and as sweeteners in “sugar- free” chewing gum (Carefree, Dentyne, Extra) and medicines. Sorbitol is also a natural component of some fruits and fruit juices, such as apple juice and pear juice (Rumessen and Gudmand-Hoyer, 1988; Perman, 1996). FRUCTOSE Fructose absorption is mediated by facilitated diffusion across the brush border, but the capacity for transport is limited. Thus, symptoms of fructose malabsorption will develop when the amount ingested is greater than a thresh- old amount. Fructose is found naturally in many fruits and vegetables, and high fructose corn syrup is a popular sweet- ener in soft drinks and processed foods (Rumessen and G udmand-Hoyer, 1988; Perman, 1996; Ravich et al, 1983). TABLE 56-1. Carbohydrate-Induced Symptoms in Specific Situations Symptoms Situations Due to hypertonicity Dumping syndrome Gastric surgery Bloating Vagotomy Nausea Pylor oplasty Diarrhea Antrectomy Flushing Gastrojejunostomy Hypotension Bariatric pr ocedur es Dyspepsia after fr uit juice Gastr oesophageal r eflux disease Due to malabsorption or ingestion of poorly absorbed carbohydrates Gas, bloating, diar r hea, pain Generalized malabsorption Celiac disease Short bowel syndrome Specifi c malabsorption Fructose Sucrose Lactose Poorly absorbed substances Mannitol, sorbitol Dietar y fi ber Dietary-Induced Symptoms / 341 Sucrose is rarely malabsorbed, but some individuals have an inherited defect in sucrase-isomaltase, the brush border enzyme necessary for its absorption. Individuals with vil- lous atrophy may have an acquired enzyme deficiency. LACTOSE There is a separate chapter on lactose intolerance (see Chapter 62,“Lactose Intolerance”). The most common carbohydrate that is malabsorbed is lactose or milk sugar (Vesa et al, 2000). Lactose is the primary carbohydrate in milk, and all mammals depend on lactase activity in the intestine to digest and absorb this substrate in infancy. Most mammals retain lactase activity until weaning and then turn off production of this enzyme, because milk is no longer a part of the diet. Most human populations retain lactase expression through adolescence and then become lactase insufficient. In some populations (particularly the individuals in the Northern European gene pool), lactase activity is main- tained into adulthood, but is typically lost gradually, producing some degree of lactose intolerance with aging. The degree of lactose intolerance is highly variable and the development of symptoms depends not only on the amount consumed (eg, 12.5 g per glass of milk), but also on such factors as the amount of other fermentable sub- strates ingested with the meal, coexisting mucosal disease, and the rate of transit through the intestine. Lactose tolerance can be tested by assessing symptoms after ingestion of 1 to 2 cups of milk (240 to 480 mL) or, more formally, by breath hydrogen testing after a lactose load (typically 25 g). Use of milk that has been treated to hydrolyze the lactose can reduce symptoms. In sensitive individuals, care must also be taken with the ingestion of processed foods that ha v e been fortified with nonfat dry milk to improve their nutritional characteristics (Paige et al, 1975). Fats Fats also can produce a number of symptoms (Table 56-2). Fat digestion is a complex process and the GI tract is orga- nized to slow the movement of fats through the intestine to allow sufficient time for fat digestion to occur. Thus fatty meals slow gastric emptying and intestinal transit and, ulti- mately, induce satiety and stop food intake. This is mediated by duodenal receptors that recognize the presence of fat within the lumen, cause the release of cholecystokinin (CCK) into the blood, and set off neural reflexes. The consequences of reduced gastric emptying may include exacerbation of gastroesophageal reflux, bloating, and early s atiety. However, as shown by Lin and colleagues (1999), fat intolerance is associated with rapid gastric emptying. Most fat is absorbed in the jejunum and fat entering the lower ileum triggers the “ileal brake”by release of peptide YY, which inhibits gastric emptying and proximal small bowel transit. Patients who have had substantial ileal resections lack this mechanism and may flood the colon with unabsorbed nutrients after meals, producing diarrhea, gas, and cramps. Dietary fat also has an effect on colonic motility. One of the key activators of the gastrocolic reflex is fat entering the duodenum. Because of this many patients with diarrhea have bowel movements after meals and soon learn to restrict their food intake to avoid diarrhea. This promotes development of food aversions and weight loss in patients with chronic diarrhea. An exaggerated gastrocolic reflex may also play a role in postprandial urgency in patients with IBS.* Proteins Proteins are less likely than other macronutrients to cause the kind of GI symptoms that we are discussing (nonim- munologically mediated symptoms) because they are ingested as large polymers that do not exert much osmotic activity, and they are efficiently digested and absorbed by the intestine. Some foods, however, contain bioactive amines and peptides that may influence gut activity. An example is coffee, which, in addition to caffeine, contains dozens of peptides that may influence gastric acid secretion and other GI events. Amino acids stimulate CCK secretion and may induce abdominal pain by stimulation of pan- cr eat ic exocrine secretion if the pancreatic duct is struc- turally or functionally obstructed. Capsaisin, Caffeine, and Others Other dietary components that may induce GI symptoms include capsaisin, caffeine, and various minerals. Capsaisin is the “active”ingredient in hot peppers and reacts with specific receptors in the mucosa that activate enteric sensory nerves. The physiological “purpose”of these receptors is not clear at the present time. Caffeine and other bioactive amines have pharmacological effects when ingested in milligram amounts. In addition to central nervous system effects, the co-editor of this text and his colleagues have shown that caffeine can increase intestinal chloride secretion by inhibiting phosphodiesterase, which may exaggerate diarrhea in pat ients with ileostomies and in those with IBS (Wald et al, 1976). Minerals such as calcium, aluminum, and iron tend TABLE 56-2. Fat-Associated Symptoms and Situations Symptoms Situations Dyspepsia Gastroesophageal reflux disease Bloating, early satiety Gastric surgery Postprandial urgency of defecation Irritable bowel syndrome Distension Postprandial upper abdominal pain *Editor’s Note: Patients learn to eat grilled chicken breast rather than hamb urg e r at fast food restaurants. (TMB) 342 / Advanced Therapy in Gastroenterology and Liver Disease to be constipating, whereas magnesium may cause diarrhea. Many patients ingest dietary supplements containing these elements and may not be aware of their effects on bowel function. Finally, many patients ingest “health foods”which o ften contain herbal products, including senna and aloe, which can have profound effects on gut function. Every patient needs to be asked about ingestion of these products. There is a separate chapter on alternative medicines (Chapter 58, “Complementary and Alternative Medicines in Gastrointestinal Disease”).* Impact of Food Intolerances in Specific Conditions Symptoms in many GI conditions may be aggravated by food intolerance. Several disorders in which dietary factors should be explored by the physician are discussed below and summarized in Table 56-3. Functional Syndromes Functional syndromes, such as IBS, FD, chronic diarrhea, and chronic constipation are common disorders, affecting up to 20% of the US population. Although their pathophysiology is gradually being unraveled, management is still based on symptom control. Food intolerance may play an important role in aggravating symptoms and should be probed. Motility Disorders M otility disorders , such as gastroparesis and chronic intestinal pseudo-obstruction, can also be affected by diet. Although controlled clinical studies to prove efficacy have not been conducted, dietary management is key to the long term treatment of these conditions. Post-Surgery Syndromes Post-surgery syndromes are another fruitful area for dietary therapy. No surgical intervention on the gut is without the potential for disturbing function, and when the distur- bance is severe enough to produce symptoms, careful dietary management can improve matters substantially. Conditions in which food intolerance may aggravate symptoms include postvagotomy or postgastrectomy dumping syndrome, short bowel syndrome, ileostomy diarrhea, postresection diarrhea, and ileoanal pouch dysfunction. There are separate chapters on some of those situations. Evaluation of Symptoms That May Be Related to Food Ingestion Many different symptoms may be due to food ingestion and its consequences. These include abdominal pain in any area, heartburn, bloating, nausea, abdominal distention, *Editor’s Note: Garlic is widely touted as a health food. However, there are numerous biologically active amines in garlic that are used as vermifuges in animals and children. Some individuals, including the aforementioned editor are, as adults, highly sensitive to an alcohol soluble fraction of garlic with a cramping laxative effect. (TMB) TABLE 56-3. Potential Food Intolerance in Clinical Conditions Condition Potential Food Intolerance Mechanism Gastroesophageal reflux disease Hypertonic, carbohydrate-rich liquids Osmoreceptors Fatty foods Delayed gastric emptying, reduced LES pressure Gastroparesis Hypertonic beverages Delayed gastric emptying Fatty foods Delayed gastric emptying Raw fr uits, vegetables Impaired trituration Dumping syndr ome Hypertonic carbohydrate Intestinal hormone release, osmotic fluid shifts Functional dyspepsia Many Gastric distention, delayed gastric emptying, abnormal gastric motility, hypersensitivity to distention Chronic intestinal pseudo-obstruction Fiber Potential substrate for bacterial overgrowth Short bowel syndrome Caffeine Increased secretion, motility Carbohydrate Fermentation Fatty foods Accentuated gastrocolic reflex Irritable bowel syndrome Carbohydrate (lactose, sorbitol, fructose) Osmotic diarrhea, fermentation Fatty foods Accentuated gastr ocolic r efl ex Chr onic diarrhea (including functional, postresection, and ileostomy diarrhea) Fatty foods Accentuated gastrocolic reflex Chronic constipation Fiber Fermentation Ileal pouch–anal anastomosis Carbohydrate (lactose, sorbitol, fructose) Osmotic diarrhea, fermentation LES = lower esophageal sphincter . Dietary-Induced Symptoms / 343 gas, and diarrhea. The physician needs to establish the tim- ing of the symptoms in relation to a meal and should try to establish a link between specific foods and the present- ing symptoms. This can be done best by a diet and symp- t om diary in which the temporal relation between ingestion of certain foods and the onset of symptoms can be deter- mined. However, bacterial fermentation of unabsorbed carbohydrates may occur many hours after ingestion. Reproducibility of symptom induction by specific foods should be the basis for trial of an elimination diet. Registered dietitians can be a valuable help in sorting through the patient’s history and recommending alternative diets.* *Editor’s Note: The careful reader who employs the concepts nicely demonstrated in this chapter will help a lot of patients obtain significant relief. As stated in the first sentence of this chapter, many patients do attribute some of their symptoms to “something they ate!” (TMB) Supplemental Reading Burden S. Dietary treatment of irritable bowel syndrome: cur- rent evidence and guidelines for future practice. J Hum Nutr Diet 2001;14:231–41. H ammer HF, Fine KD, Santa Ana CA, et al. Carbohydrate malabsorption. Its measurement and its contribution to diarrhea. J Clin Invest 1990;86:1936–44. Hammer HF, Santa Ana CA, Schiller LR, Fordtrans JS. Studies o f osmotic diarrhea induced in normal subjects by ingestion o f polyethylene glycol and lactulose. J Clin Invest 1989;84:1056–62. Lin HC, Van Citters GW, Zhao XT, Waxman A. Fat intolerance depends on rapid gastric emptying. Dig Dis Sci 1999;44:330–5. O ’Sullivan M, O’Morain C. Food intolerance: dietary treatments in functional bowel disorders. Curr Treat Options Gastroenterology 2003;6:339–45. Paige DM, Bayless TM, Huang SS,Wextner R. Lactose hydrolyzed milk. Am J Clin Nutr 1975;28:898–22. Perman JA. Digestion and absorption of fruit juice carbohydrate. J Am Coll Nutr 1996;15Suppl 5:12–17S. Ravich WJ, Bayless TM, Thomas M. Fructose: incomplete intestinal absorption in humans. Gastroenterology 1983;84:26–9. Rumessen JJ, Gudmand-Hoyer E. Functional bowel disease: malabsorption and abdominal distress after ingestion of fructose, sorbitol, and fructose–sorbitol mixtures. Gastroenterology 1988;95:694–700. Vesa TH, Marteau P, Korpela R. Lactose intolerance. J Am Coll Nutr 2000;19Suppl 2:165–75S. Wald A, Back C, Bayless TM. Effect of caffeine on the human small intestine. Gastroenterology 1976;71:738–42. Gastrointestinal Food Allergy / 345 is the major cause of anaphylactic reactions in industrial- ized societies including the United States, Australia, and Europe. The prevalence of peanut allergy (0.5 to 7% of adults in the United States and the United Kingdom) and i ts potentially fatal consequences has had significant effect on the operational policies of groups ranging from school districts to the airline industry. Fatal anaphylaxis can result from exposure to minute amounts of antigen such as that imparted by a kiss. Food-associated exercise-induced anaphylaxis is a rare type of anaphylaxis in which the food only elicits an anaphylactic reaction when the subject exercises within several hours of ingesting that food. Acetylsalicylic acid can also augment type I allergic symptoms when com- bined with food and exercise in such individuals. Pollen-Food Allergy Syndrome The oral allergy syndrome or pollen-food allergy syndrome results from various plant proteins that cross-react with certain inhalant antigens, particularly birch, ragweed, and mug- wort (Sloane and Sheffer, 2001). Exposure to the cross-reacting foods may lead to pruritis, tingling and/or swelling of the tongue, lips, palate, or oropharynx, and, occasionally, to bronchospasm or more systemic reactions. Foods that cross-react with birch include raw potatoes, car- rots, celery, apples, pears, hazelnuts, and kiwi. Those individuals that are allergic to ragweed may react to fresh melons and to bananas. It is important to educate patients with inhalant allergies about potential cross-reacting foods. Latex-Food Allergy Syndrome Latex-food allergy syndrome, also referred to as the latex-fruit syndrome,is a specific form of food allergy in which food antigens cross-react with various latex antigens (Blanco, 2003). Natural rubber latex contains over 200 proteins, 10 of which bind IgE Hevea brasiliensis latex protein allergens (HEV b 1 to 10) and cross-react with a variety of food antigens including kiwi (HEV b 5), potato and tomato (HEV b 7), and avocado, chestnut, and banana (HEV b 6). In latex-sensitive individuals exposure to these foods can result in the same symptoms as if exposed to latex ranging from pruritis, eczema,oral-facial swelling, asthma, GI complaints, and anaphylaxis. A large number of studies from around the world indicate that the natural rubber latex allergy is increasing in prevalence and that the frequency of associated food allergy varies from 21 to 58% (Blanco, 2003). Worldwide, banana, avocado, chestnut and kiwi are the most common causes of food-induced symptoms associated with latex allergy. Other Immune-Mediated GI Adverse Reactions to Food Immunologic reactions to foods involving mechanisms other than immediate hypersensitivity,such as cell-mediated immunity (see Table 57-2), play a role in food protein- induced enterocolitis syndromes (FPIES),such as cow’s milk protein enteropathy, and also celiac disease. FPIES also known as food protein-induced enteropathies, present in infancy or e arly childhood and are most commonly due to cow’s milk protein followed by soy protein and less commonly, egg, fish, and other food antigens (Nowak-Wegrzyn et al, 2003). Clinical manifestations include diarrhea, vomiting, anemia, bleeding, and failure to thrive. As with many other food allergies, such cases are managed by elimination of the specific food antigen until the disease resolves with age. It is common practice to switch infants with enterocolitis from a cow’s milk-based formula to a soy-protein derived formula, but because over half will react to soy protein, continued problems may result from the development of soy–protein- induced enterocolitis. Hypoallergenic or elemental feeds are often necessary in such cases. Celiac Disease Celiac disease is one of the best-recognized diseases resulting from an immunologic reaction to food. Dietary ingestion of gliadin found in wheat, hordelein in rye, and secalin on barley, induces an enteropathy in genetically suscepti- ble individuals. Removal of the offending grains from the diet restores normal small bowel function and appearance, with improvement in symptoms that can range from diarrhea, weight loss, and failure to thrive, to the more common but less often recognized complaints of fatigue, dyspepsia, neurological dysfunction, and musculoskeletal problems.As with other immune-mediated ARF, elimination of the offending food substance (gluten) is the primary method of management in celiac disease. However, unlike most other food protein-induced enteropathies, g l uten must be eliminated from the diet on a lifelong basis in celiac disease. See Chapter 61,“Celiac Sprue and Related Problems” for a more complete discussion of celiac-sprue. Eosinophilic Gastroenteritis Food allergy is thought to play a role in some cases of eosinophilic gastroenteritis, a relatively rare condition characterized by eosinophilic infiltration of the gut and, often, peripheral eosinophilia. Approximately half the patients with eosinophilic gastroenteritis have atopic features, including food allergy. Strategies to identify and eliminate food antigens should be followed as in other food allergic conditions, but often other measures, particularly corticosteroids, are necessary to manage patients with eosinophilic gastroenteritis. Even after thorough evalua- t ion for parasites, an e mpiric course o f ant ihelminthic therapy may be given before embarking on a course of corticosteroids. Allergic eosinophilic esophagitis presents in infancy thr ough adolescence and manifests with symptoms of gastroesophageal reflux that are often refractory 346 / Advanced Therapy in Gastroenterology and Liver Disease to typical antisecretory therapy (Hill et al, 2000). As with lower GI presentations of allergic eosinophilic conditions, this disorder is characterized by eosinophilic infiltration of the mucosa, but also the histologic hallmarks of gastro- e sophageal reflux disease (GERD) and abnormal 24-hour pH monitoring. Young children with this diagnosis usually have a clinical and histologic benefit from eliminating specific foods. Nonimmune Adverse Reactions to Food The vast majority of ARF are not immunologic in origin (see Table 57-1) and by virtue of their prevalence, are important considerations in the examination of patients complaining of ARF. Food toxicity or food poisoning results from microbial contamination of food causing pri- marily GI manifestations due to preformed toxins (eg, staphylococcal enterotoxin) or replication of enteric pathogens ( Campylobacter, Salmonella, Shigella, Escherichia coli). These reactions can be distinguished from other ARF because they usually do not recur and have fairly characteristic presentations. Occasionally, a self-limited infection may result in a postinfectious irritable bowel syndrome (IBS). This is discussed in the chapter on IBS (see Chapter 39, “Irritable Bowel Syndrome”) and the chapter on traveler’s diarrhea (see Chapter 50,“Traveler’s Diarrhea”). Anaphylactoid or Pseudoallergic Anaphylactoid or pseudoallergic reactions to food result from foods that mimic the effects of mast cell degranula- tion but do not involve IgE antibodies. Strawberries and shellfish may cause this type of ARF. Certain food ingredi- ents, including additives such as salicylates, benzoates, and tar t razine , ind uce pseudoallergic reactions. As with true food allergy, patients exhibiting such reactions should be instructed to avoid the offending food substance if iden- tifiable. Pharmacological reactions to food or food additives represent a relatively common type of ARF, although most of these reactions cause symptoms outside of the GI tract. Histamine found in certain cheeses or in scrombroid fish, such as tuna, can cause headaches and diffuse ery- thema of the skin. Certain individuals develop migraine headaches to various foodstuffs, including those rich in amines. Sulfites, tartrazine and monosodium glutamate (MSG) have all been associated with asthma, and MSG can cause a characteristic syndrome consisting of a burning or warm sensation, chest tightness, headache, and gastric dis- c omfort shortly after its ingestion. Lactose Intolerance Globally, lactose intolerance is the most common adverse reaction to a specific food, with most cases the result of declining levels of intestinal lactase activity in later childhood and adult life, although rare congenital deficiencies can occur. Symptoms of lactase insufficiency are usually dose related and include bloating, flatulence, and diarrhea. Secondary lactase deficiency can result from viral gastroenteritis, radiation e nteritis, Crohn’s disease (CD), and celiac sprue. It is important from a management standpoint to understand that individuals with constitutive lactose intolerance (1) do not suffer severe and potentially life-threatening complications of ingesting lactose and (2) are able to consume naturally lactose free diary products including most cheeses and yogurts. This contrasts with cow’s milk allergic individuals who may suffer anaphylactic or asthmatic reactions to dairy products and must avoid all foods containing the culprit cow’s milk protein allergen, usually casein or β-lactoglobulin. There is a chapter on carbohydrate intolerance (see Chapter 62, “Lactose Intolerance”). Psychological Reactions In certain individuals, reactions to food may be psychological (Kelsay, 2003). This is a difficult type of ARF to diag- nose because the mechanisms giving rise to such reactions are poorly understood. Individuals who are not confirmed to have ARF have higher rates of hypochondria, hysteria, somatization, and anxiety than those with ARF confirmed by food challenge. An individual who experienced a severe ARF may avoid the culprit food for fear of further reactions, and there is also some evidence that hypersensitivity reactions to food may be triggered through central neural mechanisms so that, eventually, just the thought of ingesting the food can trigger allergic symptoms in the absence of antigen. Food allergy itself may lead to psychological distress, and studies of food allergic subjects report an altered quality of life for the individual and their fam- il y , with severe manifestations such as anaphylaxis resulting in a post-traumatic stress situation. Physiologic Reactions Perhaps the most common form of ARF results from physiologic reactions to food components or additives. It is well known that starches found in legumes serve as substrate for gas production by colonic flora and many other foods are associated with “gas,” including onions, cabbage, bran fiber, and other vegetables and grains. Certain foods and food additives affect the lower esophageal sphincter, whereas foods high in fat delay gastric emptying, resulting in symptoms of heartburn and dyspepsia. These physiologic reactions to foods are typically noted by patients with functional bowel disease, many of whom exhibit height- e ned endocrine, motor and sensory responses to normal digestive events. Because elimination of the offending food(s) may provide some benefit in select patients, it is imp ortant to determine whether specific food intolerances exist in this group of patients. The reader is referred to evaluation of food allergies have recently been published as a medical position statement by the American Gastro- enterological Association (Sampson et al, 2001). It is essen- tial to obtain a careful history correlating symptoms with s pecific foods. Most immediate hypersensitivity reactions to food include a set of symptoms that consistently occur minutes to hours after ingesting certain foods. In some individuals, other factors, such as medications or exercise, may modulate the reaction to a specific food. Specificity of the reaction does not always imply a food allergy because patients with anaphylactoid reactions or lactose intolerance report defined reactions to specific foods. However, the nature of the reaction will help differentiate lactose intolerance (gas, bloating, diarrhea) from an allergy to cow’s milk protein (often urticaria, swelling of the lips and oral mucosa, and/or asthmatic symptoms occur in addition to GI symptoms). Dairy, Elimination, Challenge If a specific food or group of foods cannot be identified by the initial history,the patient should keep a diet diary for several weeks in an attempt to correlate foods with GI and other symptoms. After certain foods are identified as possible cul- prits by history or a diet diary, these items should be eliminated from the diet for several weeks to determine the effect on symptoms. If a benefit is seen, the patient may reintro- duce the putative allergen(s) in an attempt to prove the association. Such open food challenges are subject to bias and should be corroborated by another more objective method before permanent elimination from the diet, particularly if the patient is young and the food(s) in question represent a major component of the diet (eg, eggs, milk, wheat). Skin testing, in vitro testing and blinded oral challenges may be he lp ful in this regard and are briefly discussed below. T ABLE 57-3. Approach to Patient With Suspected F ood Allergies as a Cause of Gastrointestinal Symptoms 1. Establish foods and food additives that r epr oducibly cause symptoms • Careful history • Diet diary • Elimination diet • Skin testing and/or RAST • Food antigen challenge 2. Exclude and manage other disorders that may mimic GI food allergy • CBC, peripheral blood eosinophil count • Celiac serology • Lactose hydr ogen br eath test • Stool studies • Endoscopy and biopsy 3. Initiate tr eatment for food aller gy • Avoidance of specific foods • Medications for after accidental exposure (antihistamines, epinephrine, corticosteroids) • Preventive measures (Oral cromoglycate, avoid co-precipitating factors, eg, medications) • Education about hidden sour ces of antigens and cross-reacting foods CBC = complete blood count; GI = gastrointestinal; RAST = radioallergosorbent test. Gastrointestinal Food Allergy / 347 Chapter 56,“Dietary-Induced Symptoms”for a further discussion of dietary-induced GI symptoms. GI Disorders and ARF Functional Disorders It is human nature for patients with GI disorders to believe that something in their diet has caused their condition even in the absence of a history of food intolerance. A significant number of GI conditions are associated with ARF but food plays a causal role in only some of these disorders. For patients with GERD, nonulcer dyspepsia, IBS, and other functional conditions, nonspecific physiological reactions to food can provoke symptoms. It is generally advisable to instruct these patients to avoid foods that cause symptoms, but nondietary measures are usually also necessary to manage their complaints. However, food protein intolerance or allergy may play a role in infants with GERD symptoms. There is no generalized role for hypoallergenic diets in IBS, although a few studies report benefit from such diets (reviewed by Spanier et al, 2003) and, in some instances, instituting a rigorous diet is helpful in convinc- ing patients that specific dietary factors are not the sole cause of their illness. I NFLAMMATORY BOWEL DISEASE There are many studies that have examined the role of diet in inflammatory bowel disease (IBD) but there is no evidence that specific immune-mediated reactions to food play a role in the majority of patients with either CD or ulcerative colitis. Elemental enteral feeding and parenteral nutrition can assist in the management of IBD patients with benefits that appear related to improved nutrition and bowel rest (and decreased fecal flow) rather than removal of specific allergens from the diet. Patients in remission should be encouraged to eat a nutritionally balanced diet without restrictions unless they experience intolerance to specific foods. It is typical for IBD patients to be instructed to avoid dairy products but this is unnecessary in most cases. Apart from those with symptomatic lactose intolerance (in which case they should still be able to eat most cheeses and yogurts) or rare instances of cow’s milk protein allergy, IBD patients should be encouraged to consume dairy products because they are excellent sources of biologically available calcium in a population at increased risk of osteoporosis. Approach to Patients Complaining of ARF A significant component of the difficulty in managing food allergy is determining whether the patient has food allergy or another form of ARF (Table 57-3). Guidelines for the [...]... (Chapter 60, “Nonsteroidal Antiinflammatory DrugInduced Small and large Intestinaal Injury”) on NSAIDinduced injury to the small and large intestine 357 358 / Advanced Therapy in Gastroenterology and Liver Disease A family history may reveal hereditary disorders resulting in OGIB, including hereditary hemorrhagic telangectasias (HHT), Osler-Weber-Rendu disease (OWR) and polyposis syndromes Patients... COX-1 and 2, intestinal integrity, and pathogenesis of nonsteroidal anti -in ammatory drug enteropathy in mice Gastroenterol 2002;122:1913–23 Tibble J, Sigthorsson G, Foster R, et al Faecal calprotectin: a simple method for the diagnosis of NSAID-induced enteropathy Gut 1999; 45: 362–6 368 / Advanced Therapy in Gastroenterology and Liver Disease TABLE 6 1-1 Relationship of the Major Grains Family Gramineae... of nonsteroidal anti -in ammatory drugs on the small and large intestine Gastroenterol 1993;104:1832–7 Hayllar J, Price AB, Smith T, et al Nonsteroidal antiinflammatory drug-induced small intestinal in ammation and blood loss: effect of sulphasalazine and other disease modifying drugs Arthr Rheum 1994;37:1146 50 Laine L, Connors LG, Reicin A, et al Serious lower gastrointestinal clinical events with nonselective... Drug-induced small bowel injury Dieulafoy’s malformation Amyloidosis von Willebrand’s disease Portal hypertensive intestinal “opathy” Pancreatic hemosuccus Osler-Weber-Rendu Adapted from Mujica and Barkin, 1996 AVM = arteriovenous malformations; GAVE = gastric antral vascular ectasias 362 / Advanced Therapy in Gastroenterology and Liver Disease rather ineffective Hemostasis can be achieved in 50 to 85% ... propagation and/ or configuration of interdigestive migrating motor complexes 2 Bursts of nonpropagated phasic pressure activity in the fasting and fed states 3 Sustained (> 30 min) and intense phasic pressure activity occurring in a segment of intestine while normal or reduced activity is noted simultaneously at other levels of the intestine 4 Inability of the ingested meal to change fasting intestinal activity... gastrointestinal bleeding Gastroenterology 2000;118:197–200 Barkin JS, Friedman S Wireless capsule endoscopy requiring surgical intervention: the world’s experience Am J Gastroenterol 2002;97:S298 Barkin JS, Ross BS Medical therapy for chronic gastrointestinal bleeding of obscure origin Am J Gastroenterol 1998;93:1 250 –4 Bashir RM, Al-Kawas FH Rare causes of occult small intestinal bleeding, including... in the irritable bowel syndrome Arch Intern Med 2003;163:2 65 74 Complementary and Alternative Medicine in Gastrointestinal Disease / 353 early during the course of their disease (Astin, 1998) Others may be comfortable with conventional medicine and only seek out CAM when they believe they have seen the limitations of conventional medicine In general, patients do not abandon conventional medicine in. .. medicine use by patients with inflammatory bowel disease Am J Gastroenterol 1998;93:697–701 356 / Advanced Therapy in Gastroenterology and Liver Disease Hilsden RJ, Meddings JB, Verhoef MJ Complementary and alternative medicine use by patients with in ammatory bowel disease: an internet survey Can J Gastroenterol 1999;13:327–32 Hilsden RJ,Verhoef MJ Complementary and alternative medicine: evaluating... with both suspected and verified AVMs and OGIB (Barkin and Ross, 1998) Treatment courses are recommended in six-month intervals to minimize side effects, including breast tenderness and vaginal bleeding in woman and gynecomastia and decreased libido in men Summary Until recently the approach to diagnosis of OGIB has been fairly standardized, and for many physicians, often frustrating Patients are subjected... interferon-γ, or strategies to antagonize the actions of Th2 cytokines, such as IL-4 and Il -5 The benefit of such approaches in food allergy was recently documented in a double blind randomized, placebo controlled, dose-ranging trial, in which a humanized monoclonal IgG1 antibody against IgE that recognizes and masks an epitope in the CH3 region of IgE responsible for binding to the FcRεI on mast cells and . syndrome in osteoporotic women. J Intern Med 2001; 250 :361–6. Ormarsdottir S, Ljunggren O, Mallmin H, et al. Circulating levels of insulin-like growth factors and their binding proteins in patients. skin testing by injecting the GI mucosa with a panel of antigens and observing for a wheal -and- flare response by endoscopy but this form of testing has not been incorporated into routine clinical. origin. There is a separate chapter (C hapter 60, “Nonsteroidal Antiinflammatory Drug- Induced Small and large Intestinaal Injury”) on NSAID- induced injury to the small and large intestine. A

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