Celiac Disease Symptoms and Gluten-Free Diet Information
One of the major controversies of the treatment of celiac disease relates to the amount of gluten allowed in the diet of celiac disease patients. The National Food Authority has redefined the term gluten-free. Previously, 0.02 gluten was acceptable as being gluten-free, but now gluten-free means no gluten and 0.02 is currently labeled as low gluten. However, the stringency of gluten restriction (zero tolerance versus low gluten ingestion) is an issue that is far from being resolved, as the opinions differ among scientists and celiac disease support groups worldwide. These controversies are due to a lack of solid scientific evidence for a threshold of gluten consumption that does cause intestinal damage. Common Name In Celiac Disease TABLE 61-2. Diet in Celiac Disease *The coat of some cheeses may contain gluten.
The association between celiac disease and diabetes is well recognized (Walsh et al, 1978, Talal et al, 1997). Celiac disease is more prevalent in patients with diabetes than in the general population. A common underlying immunogenetic predisposition has been identified (HLA DQ2). Conversely, the proportion of subjects with endoscopically confirmed celiac disease and concomitant diabetes mellitus is about 8 . Hence, this association with celiac disease may explain diarrhea in a small proportion of patients with diabetes.
Medications and vitamin and mineral supplements may also contain gluten as an inactive ingredient. The manufacturers can change the inactive ingredients of these products without warning, because there are no regulations on the formulation of inactive drug components. Vegetable gum and modified food starch can contain gluten. All medications should be checked for nebulous ingredients, especially if they are to be taken for a long period of time. It is imperative to know the lot number of nonprescription medications when contacting the manufacturer for clarification of the inactive ingredients. Prescription medications purchased through a pharmacy come with an ingredient list on the package insert. Different batches of medications may, however, contain different ingredients.
If the clinical examination or routine laboratory tests are suggestive of malabsorption, further testing should be undertaken to identify potentially relevant conditions, specifically celiac sprue, bacterial overgrowth, and pancreatic exocrine insufficiency. Anti-endomysial and antitissue transglutaminase antibodies should be sought, and, eventually, a jejunal biopsy will be needed to confirm any positive serological findings. In patients with concomitant diabetes and celiac disease confirmed by jejunal biopsy, the institution of a gluten-free diet leads to the regression of mucosal abnormalities and typically normalizes bowel habits. There is a separate chapter on celiac sprue (see Chapter 61, Celiac Sprue and Related Problems ).
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 susceptible 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, gluten 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.
American Gastroenterological Association medical position statement celiac sprue. Gastroenterology 2001 120 1522-5. Barucha AE. Fecal incontinence. Gastroenterology 2003 124 1672-85. Talal AH, Murray JA, Goeken JA, Sivitz WI. Celiac disease in an adult population with insulin-dependent diabetes mellitus use of endomysial antibody testing. Am J Gastroenterol 1997 92 1280-4. Walsh CH, Cooper BT, Wright AD, et al, Diabetes mellitus and coeliac disease a clinical study. Q J Med 1978 47 89-100.
Celiac disease is characterized by the damage of the small intestinal mucosa caused by prolamins (alcohol-soluble fractions) of wheat, barley and rye in genetically susceptible subjects. It is the gliadin fraction of wheat gluten that is associated with the development of the intestinal damage. The disease is strongly associated with certain human lymphocyte antigen alleles, particularly DQA1*0501 DQB1*0201. The presence of gluten in the intestine leads to a self-perpetuating mucosal damage, whereas the elimination of gluten results in a full mucosal recovery. The keystone treatment of celiac disease patients is a lifelong elimination diet in which food products containing wheat, rye, and barley are avoided. Both in vivo challenges and in vitro immunologic studies support the possibility that oat (once considered toxic for celiac disease patients) can be safely ingested. However, because of the uncontrolled harvesting and milling procedures, a cross contamination of oat with gluten is...
Exocrine pancreatic insufficiency Celiac sprue SB bacterial overgrowth Bile acid malabsorption encountered mechanisms for diarrhea in patients with diabetes should be considered. Diarrhea may result from intake of medications or the excessive use of dietetic foods that contain sorbitol as a sweetener. Autonomic neuropathy (Vinik et al, 2003) or diseases associated with diabetes, such as celiac disease, may be the underlying causes of chronic diarrhea.
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 ).
A minority of adult patients with celiac disease fail to respond to treatment with a gluten-free diet (Table 61-3). The most likely cause of nonresponsiveness is continued gluten ingestion, which can be voluntary or inadvertent. Other causes of nonresponsiveness are other food intolerance diseases (eg, milk, soy), pancreatic insufficiency, enteropathy-associated T-cell lymphoma, refractory sprue, and ulcerative jejunitis. TABLE 61-3. Drug Therapies in Celiac Disease
The most frequent disaccharidase deficiency associated with untreated celiac disease is a low or missing intestinal lactase activity. It can be treated with lactase enzyme supplements or lactose-free milk. This deficit typically resolves within 2 to 3 months on a gluten-free diet, unless the patients have permanent adult-type hypolactasia. The necessity of a long term lactose-free diet should be assessed individually. Roggero and colleagues (1989) used the breath hydrogen test to estimate the lactose absorption capacity of 42 infants and children who had flat small intestinal mucosa. All patients had positive tests when using the standard challenge dose of 2 g kg body weight. However, most of the subjects tolerated the 0.5 to 1.5 g kg doses. If a patient on gluten-free diet still experiences gaseousness, the possibility of lactose malabsorption should be considered.
In North America the Food Allergy and Anaphylaxis Network (1-800-929-4040, ) is a source of valuable information for those with various types of food allergy. Similarly, it is important for celiac patients to join local celiac disease foundations and support groups that can provide valuable information used to determine sources of gluten free foods and medications.
Several lines of evidence suggest that factors other than glucocorticoids contribute to bone loss in inflammatory conditions of the bowel. Patients with recently diagnosed inflammatory bowel disease (IBD) do not have decreased bone mass density compared with age-matched controls however, those with symptoms of 6 months duration have lower bone mass density than age-matched controls (Stockbrugger et al, 2002). A variety of cytokines are overproduced in IBDs and celiac disease and may have detrimental effects on BMD. The inflammatory cytokines IL-1 p, IL-6 and TNF-a are elevated in the systemic circulation of patients with CD. In patients with celiac disease, there is increased IL-1p and IL-6 in the systemic circulation which correlates with osteopenia. TNF-a expression is also increased in the mucosa of celiac patients, and, recently, treatment with infliximab has been shown beneficial in a patient with gluten-insensitive, refractory disease (Gillett et al, 2002).
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 early 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.
The mechanism of metabolic bone disease in patients with liver disease is multifactorial. The liver is a source of factors involved in bone remodeling and these factors are reduced in chronic liver disease. Patients with liver disease have impaired osteoblast proliferation and thus decreased bone formation. The liver is a source of insulin-like growth factor (IGF)-1, which is important in bone remodeling. Animal data suggest that the decrease in IGF-1 in cirrhosis results in decreased bone formation. In humans, however, the correlation between IGF-1 and osteopenia is less clear. OPG is also produced by the liver, and reductions in this may result in increased osteoclast activity. In general cholestatic liver diseases are associated with lower BMD than noncholestatic liver diseases. In particular patients with PBC appear to have decreased BMD but this may also occur because patients are generally older, postmenopausal women. There are also data to suggest that patients with PBC or...
The majority of the clinically useful autoantibody tests have been cleared by the FDA for in vitro use to help diagnose autoimmune diseases. These include those to help diagnose connective tissue diseases such as RA, SLE, SS, SSc, and PM DM gastrointestinal diseases such as celiac disease, Crohn's disease, and ulcerative colitis autoimmune liver diseases such as PBC and autoimmune hepatitis types I and II autoimmune vasculitides such as Wegener's granuloma-tosis and Goodpasture's syndrome autoimmune endocrine diseases such as Hashimoto's thyroiditis and Graves' disease and autoimmune coagulation disorders such as antiphospholipid syndrome. Examples of clinically useful autoantibody tests that have not been cleared by the FDA include antibodies to help diagnose pernicious anemia, autoimmune skin-blistering diseases such as pemphigus and pemphigoid, and some autoimmune neurological diseases. Auto-
On calreticulin, Ku70, and Ku80 antigens, 60S ribosomal protein P2, filaggrin, histidyl-tRNA synthetase, and PM Scl 100 antigen. The examples we have selected are (1) proteinase-3, a 29-32-kDa serine proteinase recognized by antibodies from patients with Wegener's granulomatosis (for a review on proteinase-3 epitopes, see 215 ) (2) calreticulin, a 46-kDa calcium-binding protein with multiple regulatory functions that is targeted by autoantibodies in various diseases, including SLE, subacute and neonatal lupus, SS, RA, MCTD, hepatic and celiac disease, and hepatocellular carcinoma, as well as some parasitic diseases and (3) DNA topoisomerase I, a 100-110-kDa nuclear protein that relaxes super-coiled DNA for cellular functions such as replication, recombination, transcription, and DNA repair. Anti-DNA topoisomerase I antibodies are disease-specific diagnostic marker antibodies for SSc. Figure 9.3 presents the results obtained in humans by using synthetic peptides in different test...
Possible gluten contamination of products that are presumed to be gluten free is a recurrent problem. This cross contamination can occur on farms where the grains are grown and harvested, on mills where grains are processed into flours, or on food processing lines where one line produces a food that includes gluten and the line next to it produces a gluten-free product. Contamination might also occur in stores where grains are available from open bins, in restaurants, at salad bars, or any place where a variety of different meals are produced or different ingredients come together.
Thus, any of the infectious diarrheas must always be considered and excluded in patients with IPAA diarrhea. Moreover, patients lacking a colon are more sensitive to the fluid losses that accompany any common infectious diarrhea which increase fecal volumes. Thus, consideration must always be given to small bowel diseases, such as celiac sprue, lactase deficiency, CD of the proximal bowel, and bacterial overgrowth. If a positive diagnosis of a pouch-related cause cannot be made, etiologies outside the pouch must be sought. Chapter 56, Dietary-Induced Symptoms, has additional clues.
Given this background, it is clear that GI diseases resulting in inflammation or pathology of the upper small bowel are particularly susceptible to osteoporosis. Examples of these include celiac sprue, Crohn's disease (CD), pancreatic insufficiency (PI) (Moran et al, 1997) and postgastrectomy (Vestergaard, 2003). CD patients are especially at risk if they have had extensive surgical resections or have diffuse intestinal disease. With improved medical and surgical therapy for CD, extensive surgical resections are thankfully the exception. Patients with jejuno-ileal bypass are also at risk for osteoporosis. It remains to be seen whether less drastic weight loss surgeries, such as gastric banding, will contribute to decreased BMD over time. In chronic cholesta-tic liver disease, vitamin D and calcium are malabsorbed and should be supplemented. Celiac sprue
The diagnosis is confirmed by demonstration of an increased serum VIP level by radioimmunoassay. An increased a-chorionic gonadotropin suggests malignancy.42 The differential diagnosis should include villous adenoma, inflammatory bowel disease, infectious diarrhea, celiac sprue, surreptitious laxative abuse, and other endocrine tumors such as gastrinoma, somatostatinoma, medullary thyroid carcinoma, and carcinoid tumors. At present, there are no known provocative or inhibitory agents to secure an otherwise equivocal diagnosis.
Lymphocytic gastritis (LG) is associated with celiac disease and has been reported in as many as 33 of adult patients with celiac disease. Lymphocytic colitis seems to be more common (38 ) in celiac disease affected by LG (Wu and Hamilton, 19990). The treatment of the colitis involves the use of antiinflammmatory agents, including mesalamine and steroids. There is a separate chapter on collagenous and lymphocytic colitis (see Chapter 87, Microscopic Colitis Collagenous, Lymphocytic, and Eosinophilic Colitis ).
Twenty four to 40 of patients with untreated celiac disease have temporary pancreatic hypofunction. Carroccio and colleagues (1995) performed a double-blind, placebo-controlled study on 40 patients. Half of the patients received pancreatic enzyme supplementation, while the control group was treated with placebo. After 30 days of treatment, the increase in height Z score, weight-for-height, arm circumference, and subscapular and triceps fold measurements were greater in the study group.
Successful management of patients with complex aphthosis requires an accurate diagnosis, classification of the disease, and recognition of causal or associated conditions. It is incumbent on the clinician to evaluate the patient with complex aphthosis for these conditions. Correction of the underlying condition such as gluten-sensitive enteropathy (GSE) by a gluten-free diet can result in a substantial diminution of disease activity or a remission11. Gastrointestinal diseases have been associated with lesions of RAS for many years. Indeed, according to DuBois and van den Berghe15, the word sprue, signifying the gastrointestinal disease, is derived from the Dutch word spruw which means aphthosis. The association of lesions of RAS with GSE sprue has been recognized previously11. The malabsorption associated with GSE can lead to deficiencies of B vitamins and folate. Some authors report that both oral and gut lesions resolve with a gluten-free diet. Furthermore, some patients with...
The diseases discussed in this chapter are all associated with inappropriately low BMD resulting from a variety of distinct mechanisms. Given that the causes of bone loss are distinct, the examination of the patient with GI-related metabolic bone disease should be tailored to the particular situation. Figure 55-2 presents an algorithm that is useful in various scenarios. Diseases such as celiac disease commonly cause osteoporosis. Indeed, in studies of asymptomatic osteoporotic women, 10 demonstrate antitissue transglutaminase antibodies suggesting that celiac disease may be a contributing factor for osteoporosis in the general population (Nuti et al, 2001). Diseases such as UC and, to a lesser extent, CD result in decreased BMD because of cumulative corticosteroid use therefore tests of BMD such as dual-energy x-ray absorptiometry (DXA) are more important following steroid exposure. In addition to DXA testing, other tests such as quantitative (usually calcaneal) Crohn's disease...
Myoclonus in the context of cerebellar ataxia is often part of a progressive disorder, such as ataxia-telangiectasia (AT), in which case other dyskinesias may be present, or spinocerebellar ataxia (SCA). Progressive myoclonus ataxia (PMA) can be associated with celiac disease (Bhatia et al., 1995), but in many instances a more specific diagnosis cannot be made (Marsden et al., 1990).
The practicing gastroenterologist is frequently confronted with immune-related diseases, such as Crohn's disease (CD), ulcerative colitis (UC), celiac sprue, and pernicious anemia (PA). However, the role of the gastrointestinal (GI) tract as the body's largest lymphoid organ is often overlooked. In fact, the surface area of the GI tract could cover two tennis courts, and within that surface is a rich supply of B- and T-lymphocytes, macrophages, and dendritic cells. The number of lymphocytes in the GI tract exceeds that in the spleen, but unlike other lymphoid organs, immune-associated cells in the GI tract are constantly confronted with antigen (mainly in the form of bacteria and food). Gut-associated lymphoid tissue, generally known as mucosa-associated lymphoid tissue (MALT), regulates immune responses in the gut to maintain homeostasis. Without this tight regulation, inflammation would predominate in the GI tract. Therefore, it is not difficult to imagine how disease can result in...
Villous atrophy of the small bowel has been documented in some cases of lymphocytic and collagenous colitis. This probably represents another entity rather than concomitant celiac disease because several of these patients with collagenous colitis have been given gluten-free diets without improvement. Consequently, the possibility of small bowel disease should be investigated in a medically unresponsive patient with collagenous lymphocytic colitis. Conversely, collagenous lymphocytic colitis should be considered in a patient with refractory malabsorption and or diarrhea and small bowel villous atrophy. This is discussed in the chapter on celiac disease (Chapter 61, Celiac Sprue and Related Problems ).
Celiac disease patients are at high risk for developing a low bone mineral density and bone turnover impairment. Persistent villous atrophy is associated with low bone mineral density. Of 86 consecutive newly diagnosed, biopsy confirmed celiac disease patients, 40 had osteopenia and 26 osteoporosis (Mora et al, 1999). There were no differences between males and females, or fertile and postmenopausal women. Bone mineral density in adult patients responsive to diet did not differ from that in healthy controls. Children maintained on a gluten-free diet for at least 5 years had nor mal bone mineralization and bone turnover. Even in postmenopausal women, a gluten-free diet led to a significant improvement in bone mineral density. In these cases, supplement treatment with vitamin D and calcium is indicated.
Collagenous and lymphocytic colitis are clinicopatho-logic syndromes that represent distinct, possibly autoimmune, forms of idiopathic inflammatory colonic bowel disease. Both disorders present as chronic, watery, noninfectious diarrhea in middle-aged patients with negative radiographic and endoscopic studies. Collagenous colitis predominantly occurs in women lymphocytic colitis is found equally in both genders. Often there is intermittent, diffuse abdominal pain, and, not surprisingly, some patients have a previous diagnosis of irritable bowel syndrome (IBS). Routine blood studies generally show normal results, but elevations in the Westergren sedimentation rate and eosinophil count are not uncommon. Abnormalities in complement levels, serum immunoglobulins (Igs), and pANCA (antineutrophil cytoplasmic antibodies) may be found. Although stool studies are negative for pathogens and blood, up to 55 of patients have white blood cells in stool samples. Other medical conditions reported to...
Celiac disease patients in whom the lack of compliance to a gluten-free diet has been ruled out belong to the refractory sprue category. These patients typically undergo pharma-cologic therapies, including steroids or immunosuppressants such as azathioprine and cyclosporin. If patients do not respond to these managements, the ultimate treatment is total parenteral nutrition. None of these therapies have been subjected to rigorous controlled studies (Horvath and Fasano, 2001). In young children with villus atrophy who do not respond to a gluten-free diet, diseases that must be considered include the following (1) tufting enteropathy, (2) pancreatic insufficiency, and (3) unrecognized chronic giardiasis.
The spectrum of GI disease in IgA deficiency is similar to CVID, but is in general less severe. As in CVID, giardiasis, NLH, IBD, and celiac disease occur with increased frequency. These diseases occur almost exclusively in IgA-deficient patients with concomitant IgG2 subclass deficiency, which we and others consider a disease distinct from selective IgA deficiency and more akin to CVID. Celiac disease in IgA deficient individuals shares some features with the sprue-like illness in CVID, including no evidence of antibodies to gliadin and endomysium, and no evidence of IgA-secreting plasma cells on small bowel biopsy. otherwise, the clinical response in IgA-deficient patients with celiac disease differs in that many IgA deficient patients with celiac disease will respond to a gluten-free diet. Giardiasis and NLH occur at a lower rate in IgA-deficient patients than in CVID patients. Management for giardiasis and IBD in IgA deficiency is subject to the same caveats noted for CVID...
Ing celiac diet, as well as the absence of federal regulations for accurate food and drug labeling, represent significant challenges for newly diagnosed patients. Despite the efforts of celiac disease support groups there are still no laws regulating gluten-free labeling in the United States. The American Dietetic Association's National Center for Nutrition and Dietetics Consumer Nutrition Hotline at 1-800-366-1655 is a valuable source of updated information on the treatment of celiac disease. One of the functions of the Consumer Nutrition Hotline is to refer consumers and health care professionals to registered dietitians who have expertise in special diseases. The Consumer Nutrition Hotline can also provide phone numbers and addresses of companies within the food industry to help to clarify the ingredients of a given food product and how it has been processed.
Fat malabsorption can accompany chronic liver disease but the degree of steatorrhea is modest, with over 70 of the ingested fat being absorbed. In patients with PBC, an association with celiac disease has been reported. Thus, in patients with PBC and suggestion of malabsorption of fat or other specific deficiencies (eg, magnesium, iron) celiac disease should be excluded because the treatment for this condition is specific (ie, gluten-free diet). Screening for celiac disease in patients with PBC and vice versa is a topic of current discussion that will not be addressed in this chapter.
Therapy for secondary causes of CIP should focus on the underlying disorder. This often includes correcting electrolytes, managing dehydration, treating infections, using immunosuppressants for patients with collagen vascular diseases, initiating a gluten-free diet for pseudo-obstruction associated with celiac disease, or treating the underlying cancer that has caused a paraneoplastic syndrome. Treating idiopathic or primary CIP, however, is often quite difficult. One important lesson to remember is the adage of primum no nocere. Ill-planned or repeated surgeries, radical treatments, and injudicious use of narcotics will make the patient worse. Although several large, double blind, placebo controlled studies were performed to evaluate the efficacy of medications for the treatment of CIP in the past, these agents are either no longer available (cisapride) or they
In both children and adults, iron-deficient anemia represents the most frequent extraintestinal symptom of subclinical celiac disease. Malabsorption of iron in the duodendum, as well as occult blood loss, can contribute to iron deficiency. The majority (51 to 84 ) of children have iron deficiency at the time of diagnosis. The prevalence of celiac disease in adult patients with sideropenic anemia is 5 to 6 , whereas in the group not responding to iron therapy it can reach 20 . Iron replacement therapy, in addition to diet, should be considered in most patients with celiac disease.
In spite of the variety of mechanisms leading to metabolic bone disease, there are several treatment strategies that are broadly applicable. The best strategy is prevention (eg, avoidance of glucocorticoids to treat IBD whenever possible). Effective treatment of the underlying GI disease (eg, gluten-free diet in celiac disease) can improve BMD within a year (Mora et al, 1998 Szathmari et al, 2001 McFarlane et al, 1995). Of course, even at the time of diagnosis, bone loss may be well on its way. Low BMD is a result of decreased bone formation and or increased bone resorption. Most therapies for osteoporosis aim to inhibit bone resorption (eg, bisphosphonates Table 55-4 ). Bisphosphonates are highly effective for both prevention (Saag et al, 1998 Cohen et al, 1999 Reid et al, 1998) and treatment of glucocorti-coid and postmenopausal osteoporosis (Reid et al, 1998 Adachi et al, 1996) (see Table 55-4). As a class of drugs they are more effective than vitamin D, fluoride or calcitonin for...
Recent advances in molecular biology and genetic engineering and a better understanding of the immune mechanisms involved in celiac disease pathogenesis, represent solid bases for future alternative approaches to the treatment of the disease. It is conceivable to project innovative treatments based on either the engineering of grains that lack the toxic domains that trigger the autoimmune process or the development of vaccines that will prevent the onset of disease in genetically predisposed individuals.
An under-appreciated cause ofosteoporosis in patients with GI or liver disease is hypogonadism. Patients treated with glucocorticoids for any reason suppress gonadal and adrenal sex hormone production via suppression of the hypothalamic-pituitary axis. Women with CD, celiac disease or severe weight loss from any cause often do not menstruate and must be treated as if postmenopausal (Sher et al, 1994). Women that are postmenopausal and have coexistent GI diseases such as CD or celiac disease are at very high risk for osteoporosis and fractures (Clements et al, 1993). Similarly women with primary biliary cirrhosis (PBC) who are postmenopausal are at significantly higher risk than younger women for osteoporosis and fractures (Solerio et al, 2003). Estrogen replacement, especially in younger women who are not postmenopausal, should be considered. Estrogen replacement therapy has been shown to be safe and effective in patients with PBC (Monegal et al, 1997). Men with CD, celiac disease,...
Diagnostic tests for non-IgE-mediated food allergies include food allergy patch testing, T-cell cytokine assays, and measurements of markers of eosinophil activation. Conventional patch testing is used to diagnose contact hypersensitivity reactions involving T cells and has been applied to the evaluation of food allergy in the setting of atopic dermatitis and allergic eosinophilic esophagitis, primarily to cow's milk proteins (De Boissieu et al, 2003). Other tests may be useful in specific conditions, such as 24hour pH monitoring in eosinophilic esophagitis. Occult parasitic infections should be excluded in order to diagnose idiopathic or allergic eosinophilic syndromes and, occasionally, a course of empiric antihelminthic therapy may be indicated. Histological analysis is important in many presentations of food allergy including eosinophilic esophagitis, food protein-induced enterocolitis and proc-tocolitis, and celiac disease.
The role of the cerebellum in myoclonus has been debated, but the increased association of ataxia with myoclonus compared to other dyskinesias is inescapable. The cerebellar dentate nucleus was found to be abnormal in Alzheimer disease with myoclonus, due to an increase in the mean volume of large over small neurons in the dentate (Fukutani et al., 1999). Selective degeneration of the dentate nucleus and dentatorubrothalamic pathway was found in Gaucher type 3 with myoclonus (Verghese et al., 2000). In progressive myoclonus ataxia associated with celiac disease, the myoclonus is of cortical origin but the pathology is in the cerebellum, with Purkinje cell loss and Bergmann astro-cytosis (Bhatia et al., 1995). Purkinje cell loss also occurs in post-anoxic myoclonus and could lead to myoclonus by causing thalamo-cortical and reticular hyperexcitability (Welsh et al., 2002).
Malabsorption Celiac disease Short bowel syndrome Specific malabsorption Fructose Sucrose Lactose Poorly absorbed substances Mannitol, sorbitol Dietary fiber 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...
Prolamins are found in a variety of widely used grains. Patients should be aware that products labeled wheat free, are not necessarily gluten free. They may contain gluten as well as other grains that are not allowed. Wheat, rye, and barley are the predominant grains containing toxic peptides. However, triticale (a combination of wheat and rye), kamut, and spelt (sometimes called farro) are also toxic.
This is a catastrophic watery diarrhoea with severe nocturnal exacerbations and faecal incontinence, preceded momentarily by characteristic abdominal rumblings. Malabsorption does not normally occur. The symptoms are intermittent, with normal bowel actions in between, and sometimes even constipation. These features persist for months or years, rarely disappearing altogether. The diagnosis is made, firstly, by excluding other causes of diarrhoea such as coeliac disease or pancreatic malfunction, and secondly, by establishing the presence of peripheral and autonomic neuropathy. The diarrhoea may be treated with any antidiarrhoeal agent, the best of which is codeine phosphate. Tetracycline in two or three doses of 250 mg has a dramatic effect in about half of patients it should only be used at the onset of an attack. Some authorities suggest the use of tetracycline or metronidazole for two to three weeks but long-term antibiotics are not indicated. Clonidine can be tried but is of little...
The treatment of CD and DH should always include a gluten-free diet. Since most patients with DH do not suffer from gastrointestinal symptoms and skin lesions can be controlled by dapsone, it is important to carefully inform the patient of the necessity to maintain a gluten-free diet for a lifetime. Since such a diet is difficult to maintain, patients need to be motivated and carefully educated, and the support of a dietitian is essential. In addition, in many countries, self-support groups have been established to aid the patient in dealing with the diet. Gluten is present in most common grains (wheat, rye, barley) but not in rice and corn. It was believed that oats also contain gluten and play a role in inducing DH, but recently oats have been shown to be devoid of toxicity in DH patients (Hardman et al. 1997 Reunala et al. 1998). Patients benefit from a gluten-free diet in different respects. Though only 5-10 of DH patients have gastrointestinal symptoms such as diarrhea, bloating...
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 enteritis, 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 p-lactoglobulin. There is a chapter on carbohydrate intolerance (see Chapter 62, Lactose Intolerance ).
Plain meat, fish, beans, legumes, eggs, and nuts are allowed in the gluten-free diet. Other safe foods include plain veg etables, fruits, and plain peanut butter. Although dairy products and cheeses are allowed, patients should be aware that the coat of certain cheeses may contain gluten. Also acquired live lactase levels are common in active celiac disease leading to lactose intolerance. Rice can be ingested in all its varieties including white rice, brown rice, rice bran, rice polish, sweet rice, and wild rice. Rice is the basis of many safe cereals and pastas. Different rice flours are often used in gluten-free baking and are usually combined with other gluten-free flours or baking ingredients. Also, acquired live lactase levels are common in active celiac disease leading to lactose intolerance. buckwheat seed is called kasha. Pure buckwheat flour has a very strong taste therefore, it is only used in small quantities. Although buckwheat itself is gluten-free, the buckwheat wheat...
Living Gluten Free
A beginners guide that will reveal how living "G" free can help you lose weight today! This is not a fad diet, or short term weight loss program that sometimes makes you worse off than before you started. This is a necessity for some people and is prescribed to 1 out of every 100 people on earth by doctors and health professionals.