Gas and Bloating
Gas and bloating are common complaints for many patients, often quite bothersome and difficult to treat. Associated symptoms include belching, bloating, abdominal pain, constipation and flatulence, yet these are usually not due to “excess gas” production as commonly assumed.
A variety of diseases must be considered as a cause or contributing factor such as:
- Irritable Bowel Syndrome,
- Inflammatory Bowel Disease
- Celiac Disease
- Gastroparesis
- Superior Mesenteric Artery Syndrome
- Small Bowel Intestinal Overgrowth
- Disaccharide Deficiencies (i.e. Lactose Intolerance)
- Gastric Outlet Obstruction
- Post-Surgical States (i.e. Whipple, Roux-en-Y, ileo-colonic surgeries and anastomosis)
- Pancreatic Disases
- Aerophagia
- Rumination Syndrome
Complaints
If excessive gas is present, it may be due to swallowed air (aerophagia), increased intra-luminal gas production, decreased gas absorption (due to obstruction), or excessive gas intake such as with carbonated drinks.
- Aerophagia occurs if abnormal amounts of air are swallowed i.e. with food intake (due to poor dentures or rushed eating habits), due to anxiety, chewing gum and even due to smoking. Burping or belching is the way most swallowed air is expelled. The remaining gas moves into the small intestine where it is partially absorbed, while a small amount is released through the rectum. Studies have suggested that air may be swallowed into the esophagus rather than the stomach, resulting in excessive belching. This esophageal air can then easily be expelled, resulting in excessive belching.
- Increased intestinal gas can occur due to bacterial fermentation of non-digestible carbohydrates in the small bowel (small bowel bacterial overgrowth) or in the colon. Bacterial fermentation of ingested carbohydrates or proteins leads to hydrogen production, causing excessive gas. High concentrations of oligosaccharides or difficult to digest starches (flours made from wheat, oats, potatoes, and corn) lead to increased hydrogen production. This mechanism is the basis of the FODMAP diet, as malabsorption or maldigestion of carbohydrates may lead to increased intraluminal gas, complaints of abdominal pain and flatulence. These unabsorbed carbohydrates provide a substrate for rapid bacterial fermentation and lead to an increased osmotic load, altered gastrointestinal motility and a change in the profile of the bacterial flora. Furthermore patients with functional bowel disease (such as irritable bowel syndrome) may have a heightened sensitivity to the effects of malabsorbed carbohydrates, even though the rates of carbohydrate malabsorption may not differ from healthy subjects.
- To see a list of foods low and high FODMAP, visit the Australian-based MONASH University website, where this diet originated.
Diagnosis
Patients with bloating often lack an identifiable cause and can be classified as having a functional disorder.
- A careful history, physical exam and possibly a food diary review are the first important steps towards a diagnosis.
- Warning signs such as diarrhea, weight loss, abdominal pain, distention, anorexia or nutritional deficiency should prompt evaluation for other conditions such as inflammatory bowel disease, celiac disease or structural abnormalities as discussed above.
- Work up may include baseline laboratory testing, stool examination (fat, Giardia), a lactose tolerance test, celiac serology, and a small bowel radiograph vs. CT, an upper endoscopy and possibly a colonoscopy.
- Hydrogen breath testing may be used to assess for specific food issues and to test for small bowel bacterial overgrowth.
- Although abdominal distension is seen in patients with irritable bowel syndrome, an obstructing lesion should be considered.
- Pancreatic disease and cancer are in the differential, especially if malabsorption or steatorrhea are noted.
- Post surgical changes (i.e. Roux-en-Y, Whipple resection, ileo-colonic anastomoses etc) can lead to small bowel dysmotility as well as small bowel bacterial overgrowth. A cholecystectomy may lead to fat malabsorption due to lack of adequate bile presence, if larger fat-rich meals are consumed.
- Aerophagia can be diagnosed if troublesome repetitive belching at least several times a week is observed and/or if air swallowing is objectively noted.
Treatment
Treatment requires a multifactorial and often emperic approach.
- If aerophagia is suspected, then explaining this process to the patient may be beneficial.
- Discontinuation of habits such as gum chewing, smoking, drinking carbonated beverages, and gulping food and liquids as well as stress management may reduce the amount of ingested air. Eating at a slow pace and checking with a dentist to make sure dentures fit properly should also help.
- Avoidance of foods that may contribute to gas production is an initial step. This includes a temporary trial of lactose and fructose avoidance, avoidance of sorbitol (contained in diet foods and chewing gum), and avoidance of other gas-producing foods such as cabbage, onions, broccoli, brussel sprouts, wheat, and potatoes. This recommendation is part of the FODMAP diet (FODMAPs stands for Fermentable Oligo-, Di- and Mono-saccharides, and Polyols). FODMAPs include lactose in milk products, fructose and polyols found in fruits, fructans in wheat, onion or garlic, and galacto-oligosaccharides in beans and lentils. .
High FODMAP foods include
- fruits such as apples, apricots, cherries, mango, pears, nectarines, peaches, pears, plums, prunes, watermelon
- certain grains when consumed in large amounts such as rye, wheat
- lactose-containing foods such as custard, ice cream, margarine, milk (cow, goat, sheep), soft cheese, including cottage cheese and ricotta, yogurt
- legumes such as baked beans, chickpeas, lentils, kidney beans
- sweeteners such as fructose, high fructose corn syrup, isomalt, maltitol, mannitol, sorbitol, xylitol
- vegetables such as artichokes, asparagus, avocado, beets, broccoli, brussel sprouts, cabbage, cauliflower, garlic (with large consumption), fennel, leeks, mushrooms, okra, onions, peas, radiccio lettuce, scallions (white parts), shallots, sugar snap peas, snow peas
Simethicone (e.g., Gas-X, Mylanta Gas, Phazyme) is a foaming agent active in the stomach so that gas is more easily belched up. However, simethicone has no effect on intestinal gas. Simethicone preparations are widely used but have not proven clinical benefit.
Beano™, an alpha-galactosidase over-the-counter agent may reduce gas production in subjects taking non-digestable fibers, but its clinical value is questionable. Beano comes in liquid or tablet form. Beano has no effect on gas caused by lactose or fiber. Heat degrades the enzyme in Beano so it cannot be added to food while it is being cooked. Since Beano is made from an enzyme (alpha-galactosidase) extracted from a food-grade mold, patients with allergies to molds may react to Beano. Those with galactosemia (an inherited disorder characterized by the inability to metabolize galactose) should not use Beano.
The enzyme lactase, which aids with lactose digestion, is available in liquid and tablet form without a prescription (e.g., Dairy Ease, Lactaid). Adding a few drops of liquid lactase to milk before drinking it or chewing lactase tablets just before eating helps digest foods that contain lactose. Also, lactose-reduced milk and other products are available at many grocery stores.
If bacterial overgrowth or an altered flora are strongly suspected (best confirmed by breath-testing), a two-week trial of an antibiotic treatment may be helpful (i.e. Xifaxan® – rifaximin, a nonabsorbable antibiotic).
Probiotics such as ALIGN® – bifidobacterium infantis have been tried with varied success.
Smaller more frequent meals, less fatty foods and a trial of digestive pancreatic enzymes may all be of value.
Summary
In summary gas and bloating are difficult to treat symptoms which require vigilance and close cooperation between patients and providers in hope of partial or complete symptom relief. I typically approach this in a stepwise fashion. Laboratory testing will be used to screen for inflammation and celiac disease, while a trial of ALIGN may be initiated. If warning signs such as weight loss are present, aggressive work-up is immediately warranted. Otherwise a more conservative approach can be tried. Breath testing for lactose intolerance and work-up for small bowel overgrowth should be done. Dietary modifications will always be stressed and the FODMAP diet be reviewed.
You might find more info regarding functional gastrointestinal and motility disorders at the IFFGD website.
Gastroparesis
The current guidelines as published by the American College of Gastroenterology (ACG) on the management of gastroparesis are summarized below.
Gastroparesis is a common disorder that produces symptoms of gastric retention in the absence of physical obstruction. Patients report nausea, vomiting, early satiety, and fullness. These symptoms may be intermittent or continuous. Less recognized symptoms include pain and bloating. Gastroparesis may cause diminished caloric intake as well as vitamin (A, B6, C, K) and mineral (iron, potassium, zinc) deficiencies. Management of gastroparesis includes correction of these nutritional deficiencies, relief of symptoms of gastric emptying and, in diabetics, improvement of glycemic control. If oral intake is not adequate, enteral nutrition via jejunostomy tube needs to be considered. Medical therapy uses prokinetic and antiemetic drugs (i.e. metoclopramide, domperidone, erythromycin), as well as centrally acting antidepressants (used as symptom modulators). Gastric electrical stimulation (GES) may relieve symptoms, such as vomiting. Surgical approaches include a venting gastrostomy and feeding jejunostomy. Partial gastrectomy and pyloroplasty should be used only in carefully selected patients.
DEFINITION
- The diagnosis of gastroparesis is based on the combination of symptoms, absence of gastric outlet obstruction or gastric ulceration, and delay in gastric emptying.
- Accelerated gastric emptying and functional dyspepsia can present with similar symptoms to those of gastroparesis; documentation of delayed gastric emptying is recommended before selecting therapy with prokinetic agents or gastric electrical stimulation (GES).
CAUSE OF GASTROPARESIS
- Patients should be screened for diabetes mellitus, thyroid dysfunction, neurological disease, a history of prior gastric or bariatric surgery, and autoimmune disorders.
- A prodrome suggesting viral illness may lead to gastroparesis (postviral gastroparesis).
- Uncontrolled ( > 200 mg/dl) glucose levels may aggravate symptoms of gastroparesis and delay gastric emptying. Optimization of glycemic control may improve symptoms of delayed gastric emptying.
- Medication-induced delay in gastric emptying (i.e. from narcotic and anticholinergic agents) should be considered.
- Gastroparesis can be associated with gastroesophageal reflux disease (GERD) and should be considered in patients with refractory GERD.
DIAGNOSIS
- Delay in gastric emptying is required for the diagnosis of gastroparesis. Scintigraphic gastric emptying of solids is the standard for a diagnosis of gastroparesis. The most reliable method is gastric retention of solids at 4 h measured by scintigraphy. Medications that affect gastric emptying should be stopped at least 48 h before diagnostic testing and patients with diabetes should have blood glucose <275mg/d before starting the gastric emptying test.
DIFFERENTIAL DIAGNOSIS
- The presence of rumination syndrome, cyclic vomiting syndrome (CVS) or eating disorders (anorexia nervosa, bulimia) should be considered.
- Chronic cannabinoid agent usage may cause a CVS like syndrome.
MANAGEMENT
I. NUTRITIONAL THERAPY
- Management includes restoration of fluids and electrolytes, nutritional support and optimization of glycemic control in diabetics.
- Oral intake is preferable for nutrition and hydration.
- Patients should receive dietician counseling regarding frequent small low fat, low fiber meals.
- Enteral nasoenteric or jejunostomy tube feeding should be pursued, if oral intake is insufficient, especially if unintentional weight loss of 10% during a period of 3–6 months or repeated hospitalizations occur.
- Enteral postpyloric feeding is preferable to gastric feeding and preferable to parenteral nutrition.
II. GLYCEMIC CONTROL
- Good glycemic control should be the goal as hyperglycemia inhibits gastric emptying.
- Pramlintide and GLP-1 analogs may delay gastric emptying in diabetics. Cessation of these treatments should be considered before initiation of therapy for gastroparesis.
III. PHARMACOLOGIC THERAPY
- Prokinetic therapy should be used to improve gastric emptying and gastroparesis symptoms.
- Metoclopramide is the first line therapy and should be administered at the lowest effective dose (in a liquid formation to facilitate absorption). The risk of tardive dyskinesia is estimated to be <1%. Discontinue therapy if involuntary movements develop.
- Domperidone can be prescribed with investigational new drug (IND) clearance from the Food and Drug Administration (FDA). It appears as effective as metoclopramide without causing central nervous system side effects. Domperidone may prolong the corrected QT interval on electrocardiogram; a baseline electrocardiogram is recommended and treatment withheld if the corrected QT is >470ms in male and 450ms in female patients. Follow-up electrocardiogram on treatment with domperidone is advised. Erythromycin improves gastric emptying. Erythromycin should be given iv in hospitalized patients. Oral treatment with erythromycin improves gastric emptying, however, effectiveness of oral therapy is limited by tachyphylaxis.
- Treatment with antiemetic agents will improve nausea and vomiting but not improve gastric emptying.
- Tricyclic antidepressants (TCA) can be considered for refractory nausea and vomiting in gastroparesis but will not result in improved gastric emptying and may even worsen gastric emptying.
IV. INTRAPYLORIC BOTULINUM TOXIN INJECTION
- Intrapyloric botulinum toxin injection is not recommended.
V. GASTRIC ELECTRICAL STIMULATION
- GES may be considered for compassionate treatment in patients with refractory symptoms, particularly nausea and vomiting. Symptom severity and gastric emptying have been shown to improve in patients with diabetic gastroparesis (DG), but not in idiopathic (IG) or postsurgical gastroparesis (PSG).
VI. SURGICAL TREATMENTS: VENTING GASTROSTOMY, GASTROJEUNOSTOMY, PYLOROPLASTY, AND GASTRECTOMY
- A venting gastrostomy and feeding jejunostomy may be performed for symptom relief.
- Completion gastrectomy could be considered in patients with PSG who remain markedly symptomatic and fail medical therapy.
- Surgical pyloroplasty or gastrojejunosotomy have been performed for treatment for refractory gastroparesis, but further studies are needed before advocating this treatment.
- Partial gastrectomy and pyloroplasty should only be used in carefully selected patients.
VII. ALTERNATIVE MEDICINES
- Acupuncture has been associated with improved rates of gastric emptying and reduction of symptoms.
UG’s addendum to these guidelines: Some of our patients have also responded well to Iberogast, an OTC herbal preparation.
Celiac Disease
Celiac Disease is a disorder of the gut that results from damage to the small intestine and causes many non-specific symptoms. The damage is caused by the immune system which becomes misdirected after activation by a protein called gluten in genetically pre-disposed persons. Gluten is found naturally in wheat, barley and rye. It is also used in many processed foods as a binder or filler.
The symptoms of Celiac Disease are varied and can be seen in many other disorders. Because of this overlap, Celiac Disease is severely under diagnosed, with patients’ symptoms being potentially misattributed to some other process. There is tremendous variability across patients in severity of presentation and some patients have no symptoms at all. Some of the “classic” signs or symptoms include:
- Abdominal pain in the upper or mid abdomen
- Weight loss
- Diarrhea, specifically very foul-smelling, bulky, greasy diarrhea
- Anemia from iron deficiency
- Bloating
- Growth retardation in children
However, not all patients have all or even any of the classic findings. Other possible less common presentations include:
- Constipation
- Infertility
- Osteoporosis, especially in young people or men
- Mild elevations in liver tests
- Folic acid or vitamin B12 deficiency
- Recurrent fetal loss
- Non-hereditary cerebellar ataxia
- Dental enamel problems
- Delayed puberty
- Recurrent migraines
- Many of the signs and symptoms are related to malabsorption of various nutrients.
As noted, many patients are misdiagnosed. A common misdiagnosis is Irritable Bowel Syndrome. This is understandable as so many of the hallmark symptoms of both diseases are so similar.
Research – based estimates of the incidence of Celiac Disease indicate it afflicts nearly 1% of the general U.S. population. It is seen most frequently (but not exclusively) in people of northern European ancestry. There are certain situations or diseases that are associated with a higher risk of having Celiac Disease, including having a first degree relative with the disease (increases risk 10 fold to a total risk of 10%), Type 1 Diabetes, Primary Biliary Cirrhosis, and certain genetic syndromes such as Down, Turner, and Williams Syndromes (Down Syndrome confers the highest risk at up to 16%). Microscopic colitis is sometimes seen along-side Celiac Disease. Dermatitis Herpetiformis is a very itchy rash that looks like chicken pox, typically occurring on the extensor surfaces of the elbows and knees. It is gluten sensitive and is only seen in Celiac Disease patients (although only a small minority of celiac patients have it).
Diagnosis is based on a combination of laboratory findings and biopsy findings. The best labs at present include the Tissue Transglutaminase (TTG) IgA and IgG antibodies, and Deamidated Gliadin Peptide (DGP) IgA and IgG Antibodies. Many labs offer these tests, along with a total serum IgA level (due to the high prevalence of IgA deficiency in celiac patients) as a panel (the so-called “Celiac Reflexive Panel”). This panel has an accuracy that is in the 95% range, so it is very reliable whether it is positive or negative. Biopsy confirmation is important to be sure of the diagnosis. Biopsies are obtained at the time of upper GI endoscopy from the duodenum (the upper portion of the small intestine, just after the stomach. Typical hallmark findings of Celiac Disease on biopsy include villous atrophy (villi are the small finger-like projections in the small intestine that increase surface area); infiltration of the surface cells by immune cells called lymphocytes (“intraepithelial lymphocytosis”) and deepening of pits in the small bowel lining (“crypt hyperplasia”). There are other diseases that can cause similar appearance on biopsy, so the combination of labs and biopsy findings is important to make the diagnosis.
It is important to note that a person must be ingesting gluten for the labs and biopsies to be reliable.
Treatment is strict and absolute adherence to a gluten free diet. This is easier said than done due to the ubiquitous nature of gluten, especially in processed foods. It is much easier, however, now that manufacturers are required by law to list any wheat or gluten contents prominently on their labels. There are many resources in the community and online for following a gluten free diet. We have a packet of information that our patients receive at the time of diagnosis. Successful treatment is patient driven and knowledge based.
- Gluten-free baked goods are very different from gluten containing ones, since gluten is the ingredient which gives bread the smooth somewhat rubbery texture. There are many different types of gluten-free baked goods available, however these gluten-free baked require an “acquired taste”. Patients generally find options that work for them.
- Safe foods include meats, fruits and vegetables and nuts.
- Spices and other cooking adjuncts are potential sources of contamination but gluten-free spices should be pretty easily available.
- Any processed foods are suspect until proven gluten free. Again, this is easier to figure out since the laws require listing of gluten content (or even potential content) on the label. I often joke with my patients the they just need to avoid the center of the grocery store.
- Celiacs struggle with going out to eat at restaurants and at parties because there is such a high risk of contamination.
- Medications are also potential sources of contamination.
- Patients need to maintain separate toasters at home, but I do not recommend entirely separate sets of pots and pans, as long as there is good cleaning between cooking episodes.
With a gluten-free diet, the laboratory and biopsy abnormalities discussed above eventually (over 3-6 months) revert to normal and symptoms go away in almost all patients.
A well-controlled celiac patient should enjoy a normal life expectancy.
Uncontrolled Celiac Disease is a risk factor for malnutrition, osteoporosis, anemia, failure to thrive, and also confers a low but increase risk of small intestinal lymphomas.
- If the symptoms do not go away, or come back despite a gluten-free diet, the possible causes include inadvertent contamination, microscopic colitis, refractory celiac disease, or some other intercurrent disease such as an infection or inflammatory process.
Gluten Sensitivity or Intolerance: There are many people who feel much better when they eat gluten free. I consider these people to probably have gluten-responsive irritable bowel syndrome, of wheat/gluten sensitivity. Gluten is a difficult molecule to digest and many people respond to it poorly. However, as noted above, if you are concerned you may have Celiac Disease, I strongly believe you should be formally tested before embarking on a gluten-free diet trial. I feel this is especially true for parents considering the diagnosis for their children.
Clinical Follow-up: Typically I see my patients with Celiac Disease about 3 and maybe 6 months after the diagnosis to be sure their labs are improving and try to answer any questions they may have regarding the gluten free diet. We typically offer a referral to a dietician early on. I recommend yearly monitoring visits for my Celiac Disease patients. We check labs, including the specific celiac serology that was most abnormal on their initial evaluation, as well as other labs, including especially labs that were abnormal at the time of diagnosis such as a blood count, chemistries and liver tests, iron studies, vitamin D level, other vitamins such as B12 and folic acid, and maybe a test of bleeding time, called a protime (PT).
A diagnosis of Celiac Disease is a life altering experience. Eating is obviously a basic function and a great joy of life. Many patients are initially overwhelmed by the diagnosis and have a hard time believing they will ever be able to figure out, much less survive and even enjoy eating a gluten-free diet. However, it can be done. There are many resources available and more and more options for eating well come to market every day. Restaurants and grocery stores increasingly appreciate the economic engine that 1% of the population represents, and so gluten free menus are becoming more common.
Finally, at its core, a gluten-free diet is a very healthy diet. It is macrobiotic and full of unprocessed “real” food: fruit from the tree, vegetables from the vine, meat off the hoof. Celiac patients generally feel much better when they are finally gluten free. Often, they do not realize just how poorly they were feeling. With a gluten free diet and the resulting normalization of the small bowel, the discomfort, gaseousness, diarrhea and other symptoms, which patients just considered “normal” for them, resolve and they feel truly healthy for the first time in years.
Colonoscopy Surveillance
Guidelines for Colonoscopy Surveillance After Screening and Polypectomy:
A Consensus Update by the US Multi-Society Task Force on Colorectal Cancer
Often patients ask the important question when they should have a repeat colonoscopy done. The US Multi-Society Task Force (MSTF) guidelines attempt to address this important question and warrant a review on this education blog. When doing so one must recall that these guidelines do not apply to patients with a family history of colon cancer, or other genetic syndromes such as FAP or HNPCC.
In general a simple rule applies to surveillance colonoscopies:
- If no polyps are found at the initial exam, then a 10 year follow-up is appropriate.
- If small (<10 mm) rectal or sigmoid colonic hyperplastic polyps are found at the initial exam, then a 10 year follow-up is appropriate.
- If 1-2 small (<10 mm) tubular adenomas are found at the initial exam, then a 5-10 year follow-up is appropriate.
- If 3 or more tubular adenomas are noted at the initial exam, if a tubular adenoma is larger that 10mm, or if a villous component is noted on histology, then a 3 year follow-up is appropriate.
- If more than 10 adenomas are noted at the initial exam, then a less than 3 year follow-up may be advised.
- If an adenoma with high-grade dysplasia was noted at the initial exam and complete excision has been accomplished, then a 3 year follow-up is appropriate.
- Serrated lesions are followed according to these above discussed principles.
- Sessile serrated polyp(s) <10 mm with no dysplasia: 5 year follow-up is appropriate.
- Sessile serrated polyp(s) >10 mm or a sessile serrated polyp(s) with dysplasia or a traditional serrated adenoma: 3 year follow-up is appropriate.
- A serrated polyposis syndrome requires a more aggressive surveillance protocol with likely yearly colonoscopies (i.e. similar to aFAP – attenuated familial adenomatous polyposis)
Current guidelines factor in that important lesions may be missed at baseline colonoscopy. While the risk of having an advanced adenoma on the initial screening colonoscopy is estimated at 4-10%, several prospective studies have shown that the risk of having advanced adenomas within 5 years after a negative screening colonoscopy is low at 1.3–2.4%. This evidence supports the 10-year interval recommendation after a negative screening colonoscopy for average-risk individuals, as long as the baseline colonoscopy was complete, thorough and with a good bowel preparation. Evidence suggests that size (>10 mm), histology (tubular adenoma, sessile serrated polyp, villous histology, high-grade dysplasia) and location (proximal to the sigmoid colon) are risk factors that might be associated with higher risk of CRC.
Ongoing surveillance after the first follow-up colonoscopy
The appropriate ongoing follow-up interval after the initial screening colonoscopy and first follow-up surveillance colonoscopy is being better defined. Data suggest that the detection of an advanced adenoma is an important risk factor for finding further advanced adenomas at the next examination. Otherwise, if patients had no adenomas or only a low-risk lesion, the risk of advanced neoplasia at the next examination is low. Patients with only a low-risk lesion at baseline and no adenomas at the first follow-up surveillance colonoscopy appear to have a very low risk (2.8%- 4.9%) of having advanced adenomas at the second surveillance examination 3–5 years later.
It is therefore recommended that patients with a negative or low risk baseline study and a negative study at the first surveillance interval study can have their next surveillance examination at 10 years.
Patients with high risk lesions at any examination appear to remain at high risk and should have shorter follow-up intervals for surveillance.
Age specific guidelines: When should surveillance stop?
Given considerable evidence of increased procedural risk of colonoscopy (complications) at an advanced age, surveillance and screening should not be continued if the risk outweighs the benefit.
- The United States Preventive Services Task Force (USPSTF) does not recommend screening after age 85.
- Patients with high risk lesions may still benefit from surveillance, given the higher risk for developing advanced neoplasia.
- The USPSTF recommends against routine screening for patients aged 75–85 years but allows for individualization. The US Multi-Society Task Force (MSTF) recognizes that this age group (75–85) may benefit from surveillance, depending on life expectancy.
How about the question of a poor prep, guaiac positive stool or a new symptom – what to do?
- Given that a poor-quality bowel preparation may obscure visualization of the colon and allow for missed lesions, the MSTF recommends that the examination be repeated within 1 year.
- If a positive fecal occult test, positive guaiac test, or positive fecal immunochemical test is obtained before the scheduled surveillance colonoscopy, no change in interval appears needed, as long as patients have had an adequate baseline colonoscopy. The MSTF recommends against interval fecal testing within the first 5 years after a colonoscopy, as the likelihood of a false-positive test is high, resulting in unnecessary early colonoscopies.
- If a patient develops new symptoms during the surveillance interval (i.e. minor rectal bleeding, diarrhea, constipation), a colonoscopy should only be repeated if the colonoscopy would answer important clinical questions (i.e. IBD, ischemic colitis, microscopic colitis etc.). The likelihood of finding significant pathology (regarding colon cancer risk) after a prior adequate colonoscopy is low.
Eosinophilic Esophagitis
The current clinical guidelines as published by the American College of Gastroenterology (ACG) on the diagnosis and management of Eosinophilic Esophagitis (EoE) are summarized below:
EoE is an increasingly recognized and prevalent condition and important cause of esophageal symptoms. It is presumed to result from eosinophilic activation to dietary antigens, which is limited to the esophagus. Inflammatory strictures, secondary dysmotility and resulting dysphagia are common problems. Current management includes food exclusion diets, swallowed topical steroids and proton pump inhibitors. Strictures may require endoscopic dilatation. Relapse is common and strategies for maintaining remission are being developed.
Definition and Causes of Esophageal Eosinophilia
- Esophageal eosinophilia, the finding of eosinophils in the squamous epithelium of the esophagus, is abnormal and the underlying cause should be identified.
- EoE is clinicopathologic disorder diagnosed by clinicians taking into consideration both clinical and pathologic information without either of these parameters interpreted in isolation, and defined by the following criteria:
- Symptoms related to esophageal dysfunction.
- Eosinophil-predominant inflammation on esophageal biopsy; peak value of ≥15 eosinophils per high-power field (eos/hpf).
- Mucosal eosinophilia is isolated to the esophagus and persists after a PPI trial.
- Secondary causes of esophageal eosinophilia excluded.
- A response to treatment (dietary elimination; topical corticosteroids) supports the diagnosis.
- Esophageal biopsies are required to diagnose EoE. 2-4 biopsies should be obtained from both the proximal and distal esophagus to maximize the likelihood of detecting esophageal eosinophilia in all patients in whom EoE is being considered.
- At the time of initial diagnosis, biopsies should be obtained from the antrum and/or duodenum to rule out other causes of esophageal eosinophilia in all children and in adults with gastric or small intestinal symptoms or endoscopic abnormalities.
Diagnostic Challenges: PPI-responsive esophageal eosinophilia and GERD
- Proton-pump inhibitor esophageal eosinophilia (PPI-REE) should be diagnosed when patients have esophageal symptoms and histologic findings of esophageal eosinophilia, but demonstrate symptomatic and histologic response to proton-pump inhibition.
- At this time, the entity is considered distinct from EoE, but not necessarily a manifestation of GERD.
- To exclude PPI-REE, patients with suspected EoE should be given a 2-month course of a PPI followed by endoscopy with biopsies.
- A clinical, endoscopic and/or histologic response to a PPI does not establish gastroesophageal reflux as the cause of esophageal eosinophilia. To determine whether reflux is contributing to esophageal eosinophilia, additional evaluation for GERD, as per standard clinical practice, is recommended. This may include ambulatory pH testing in selected cases.
Pharmacologic Treatments
- Topical steroids (i.e., fluticasone or budesonide, swallowed rather than inhaled, for an initial duration of 8 weeks) are a first-line pharmacologic therapy for treatment of EoE.
- Prednisone may be useful to treat EoE if topical steroids are not effective or in patients who require rapid improvement in symptoms. Patients without symptomatic and histologic improvement after topical steroids might benefit from a longer course of topical steroids, higher doses of topical steroids, systemic steroids, elimination diet, or esophageal dilation.
- There are few data to support the use of mast cell stabilizers or leukotriene inhibitors, and biologic therapies remain experimental at this time.
Fluticasone
- Children b 88 – 440 mcg / day in a divided dose
- Adults 880 – 1760 mcg / day in a divided dose
Budesonide
- Children 1 mg/day
- Adults 2 mg day, typically in a divided dose
Dietary Treatments
- Dietary elimination can be considered as an initial therapy in the treatment of EoE in both children and adults.
- The decision to use a specific dietary approach (elemental, empiric, or targeted elimination diet) should be tailored to individual patient needs and available resources.
- Clinical improvement and endoscopy with esophageal biopsy should be used to assess response to dietary treatment when food antigens are either being withdrawn from or reintroduced to the patient.
- Gastroenterologists should consider consultation with an allergist to identify and treat extraesophageal atopic conditions, assist with treatment of EoE, and to help guide elemental and elimination diets.
Strategies for Dietary Elimination
- Total elimination of all food allergens with elemental or amino-acid-based formula.
- Targeted elimination diet guided by allergy testing, typically skin prick testing or patch testing.
- Empiric six-food elimination diet: soy, egg, milk, wheat, nuts, and seafood.
- The duration of the treatment is usually 4-8 weeks, followed by a reintroduction period once remission has been achieved. One food or food group can be introduced every 2-4-6 weeks with observation of clinical symptoms and a subsequent endoscopy if no change in symptoms occur. A food trigger is identified based on the recurrence of symptoms and esophageal eosinophilia. Because patients typically have more than one food trigger, the process is continued until all foods have been added or an acceptable diet is reached. Patients who are treated with an elemental formula undergo a substantially longer reintroduction process. Once food triggers are identified, patients are advised to eliminate these agents from their diet completely.
Endoscopic Treatment
- Esophageal dilation may be used as an effective therapy in symptomatic patients with strictures that persist in spite of medical or dietary therapy. Patients should be well informed of the risks of esophageal dilation in EoE including post-dilation chest pain (up to 75% of patients), bleeding, and esophageal perforation.
Maintenance Therapy
- While knowledge of the natural history of EoE is limited, patients should be counseled about the high likelihood of symptom recurrence after discontinuing treatment due to the chronic nature of this disease.
- The overall goal of maintenance therapy is to minimize symptoms and prevent complications of EoE, preserve quality of life, with minimal long-term adverse effects of treatments.
- Maintenance therapy with topical steroids and/or dietary restriction should be considered for all patients, but particularly in those with severe dysphagia or food impaction, high-grade esophageal stricture and rapid symptomatic/histologic relapse following initial therapy.
- The endpoints of therapy of EoE include improvements in clinical symptoms and esophageal eosinophilic inflammation. While complete resolution of symptoms and pathology is an ideal endpoint, acceptance of a range of reductions in symptoms and histology is a more realistic and practical goal in clinical practice. Symptoms are an important parameter of response in EoE, but cannot be used alone as a reliable determinant of disease activity and response to therapy, given that compensatory dietary and lifestyle factors can mask symptoms.
Diseases Associated with Esophageal Eosinophilia
- Eosinophilic gastrointestinal diseases
- PPI-responsive esophageal eosinophilia
- Celiac disease
- Crohn’s disease
- Infection
- Hypereosinophilic syndrome
- Achalasia
- Drug hypersensitivity
- Vasculitis
- Pemphigus
- Connective tissue diseases
- Graft vs. host disease
- PPI, proton-pump inhibitor.
Proposed Classification/Grading System for the Endoscopic Assessment of Esophageal Features of EoE
Major features
Edema (decreased vascular markings, mucosal pallor)
- Grade 0: Absent. Distinct vascularity present
- Grade 1: Loss of clarity or absence of vascular markings
Fixed rings (concentric rings, corrugated esophagus, corrugated rings, ringed esophagus, trachealization)
- Grade 0: None
- Grade 1: Mild-subtle circumferential ridges
- Grade 2: Moderate-distinct rings that do not impair passage of a standard diagnostic adult endoscope (outer diameter 8 – 9.5 mm)
- Grade 3: Severe-distinct rings that do not permit passage of a diagnostic endoscope
Exudates (white spots, plaques)
- Grade 0: None
- Grade 1: Mild-lesions involving less than 10 % of the esophageal
- surface area
- Grade 2: Severe-lesions involving greater than 10 % of the esophagealsurface area
Furrows (vertical lines, longitudinal furrows)
- Grade 0: Absent
- Grade 1: Vertical lines present
Stricture
- Grade 0: Absent
- Grade 1: Present (specify estimated luminal diameter)
Minor features
Crepe paper esophagus (mucosal fragility or laceration upon passage of endoscope, not after esophageal dilation)
- Grade 0: Absent
- Grade 1: Present
Narrow-caliber esophagus (reduced luminal diameter of the majority of the tubular esophagus)
- Grade 0: Absent
- Grade 1: Present
Antibiotic Prophylaxis For Endoscopic Procedures
By Dr. Michael Sossenheimer
An important topic and often asked question must be reviewed on this site: Whether to use antibiotics for procedures? The science and guidelines of antibiotic prophylaxis for gastrointestinal endoscopic procedures have changed over the years, causing some general misinformation and confusion. Although bacteremia can occur after endoscopic procedures, this is no longer considered a marker for endocarditis risk, as significant infections are extremely rare. Furthermore, there is no evidence that antibiotic prophylaxis before endoscopic procedures would protect against endocarditis.
Current American Heart Association (AHA) as well as American Society of Gastrointestinal Endoscopy (ASGE) guidelines no longer consider gastrointestinal procedures high risk for bacterial endocarditis and do not recommend routine use of endocarditis prophylaxis. Yet the ASGE revised guidelines from November 2014 now specifically state that patients with high risk cardiac conditions (such as prosthetic valves or prior endocarditis) may benefit from prophylactic antibiotics.
In addition certain high-risk procedures and high-risk patients may still pose an exception, as some patients with established enterococci GI-tract infections i.e. cholangitis and significant cardiac issues associated with the highest risk of an adverse outcome may benefit from antibiotics.
High-risk procedures:
The following endoscopic procedures are still considered high-risk for bacteremia:
- Endoscopic retrograde cholangiopancreatography (ERCP) in an obstructed bile duct which can not be adequately drained.
- Endoscopic ultrasound with fine-needle aspiration (EUS-FNA) in a pancreatic cystic lesions.
- Percutaneous endoscopic gastrostomy (PEG)
Low-risk endoscopic procedures:
- Routine diagnostic or therapeutic upper endoscopy
- Routine diagnostic or therapeutic colonoscopy
- Routine diagnostic or therapeutic flexible sigmoidoscopy
So what procedures or patients should be considered for antibiotic prophylaxis?
- ERCP in an obstructed bile duct which is anticipated not to be drained successfully.
- ERCP or EUS-FNA for pancreatic cystic lesions.
- Any cirrhotic patient with acute gastrointestinal bleeding even if not being treated with endoscopic procedures.
- Percutaneous endoscopic gastrostomy feeding tube placement (PEG).
- For patients with vascular grafts the guidelines disagree as the AHA recommends antibiotics within 6 months of a graft procedure while the ASGE does not.
- For any prosthetic joint patient antibiotics are not recommended.
Please remember that these guidelines DO NOT APPLY TO DENTAL WORK or DENTAL PROCEDURES as the oral flora and associated infectious risks are significantly different.
Diagnosis & Management of Celiac Disease
The American College of Gastroenterology (ACG) published recent clinical guidelines on the diagnosis and management of Celiac Disease (CD).
CD is one of the most common causes of chronic malabsorption. Symptoms can include diarrhea, weight loss, abdominal pain and bloating. CD remains under diagnosed in the United States. To allow for a quick overview of this challenging yet important paper, UG has posted the listed recommendations:
Glossary: CD – Celiac Disease, GFD – Gluten Free Diet, NRCD – Non-Responsive or Refractory Celiac Disease
SUMMARY OF RECOMMENDATIONS
Diagnosis of CD
- Patients with symptoms, signs, or laboratory evidence suggestive of malabsorption, such as chronic diarrhea with weight loss, steatorrhea, postprandial abdominal pain, and bloating, should be tested for CD.
- Patients with symptoms, signs, or laboratory evidence for which CD is a treatable cause should be considered for testing for CD.
- Patients with a first-degree family member who has a confirmed diagnosis of CD should be tested if they show possible signs or symptoms or laboratory evidence of CD.
- Consider testing of asymptomatic relatives with a first degree family member who has a confirmed diagnosis of CD.
- CD should be sought among the explanations for elevated serum aminotransferase levels when no other etiology is found.
- Patients with Type I DM should be tested for CD if there are any digestive symptoms, or signs, or laboratory evidence suggestive of CD.
- IgA anti-TTG antibody is the preferred single test for detection of CD in individuals over the age of 2 years.
- When there exists a high probability of CD wherein the possibility of IgA deficiency is considered, total IgA should be measured. An alternative approach is to include both IgA and IgG-based testing, such as IgG DGPs, in these high-probability patients.
- In patients in whom low IgA or selective IgA deficiency is identified, IgG-based testing (IgG DGPs and IgG TTG) should be performed.
- If the suspicion of CD is high, intestinal biopsy should be pursued even if serologies are negative.
- All diagnostic serologic testing should be done with patients on a gluten-containing diet.
- Antibodies directed against native gliadin are not recommended for the primary detection of CD.
- Combining several tests for CD in lieu of TTG IgA alone may marginally increase the sensitivity for CD but reduces specificity and therefore are not recommended in low-risk populations.
- When screening children younger than 2 years of age for CD, the IgA TTG test should be combined with DGPs (IgA and IgG).
Confirmatory testing in CD
- The confirmation of a diagnosis of CD should be based on a combination of findings from the medical history, physical examination, serology, and upper endoscopy with histological analysis of multiple biopsies of the duodenum.
- Upper endoscopy with small-bowel biopsy is a critical component of the diagnostic evaluation for persons with suspected CD and is recommended to confirm the diagnosis.
- Multiple biopsies of the duodenum (one or two biopsies of the bulb and at least four biopsies of the distal duodenum) are recommended to confirm the diagnosis of CD.
- Lymphocytic infiltration of the intestinal epithelium in the absence of villous atrophy is not specific for CD and other causes should also be considered.
Ancillary testing in CD
- HLA-DQ2 / DQ8 testing should not be used routinely in the initial diagnosis of CD. HLA-DQ2 / DQ8 genotyping testing should be used to effectively rule out the disease in selected clinical situations. Examples of such clinical situations include but are not limited to:
- Equivocal small-bowel histological finding (Marsh I-II) in seronegative patients
- Evaluation of patients on a GFD in whom no testing for CD was done before GFD
- Patients with discrepant celiac-specific serology and histology
- Patients with suspicion of refractory CD where the original diagnosis of celiac remains in question
- Patients with Down’ s syndrome
- Capsule endoscopy should not be used for initial diagnosis except for patients with positive celiac-specific serology who are unwilling or unable to undergo upper endoscopy with biopsy. Capsule endoscopy should be considered for the evaluation of small-bowel mucosa in patients with complicated CD.
- Intestinal permeability tests, D-xylose, and small-bowel follow-through are neither specific nor sensitive and are not recommended for CD diagnosis.
- Stool studies or salivary tests are neither validated nor recommended for use in the diagnosis of CD.
- Symptoms or symptom response to a GFD alone should not be used to diagnose CD, as these do not differentiate CD from non-celiac gluten sensitivity.
- A diagnosis of non-celiac gluten sensitivity should be considered only after CD has been excluded with appropriate testing.
Diagnosis of patients on a GFD
- While standard diagnostic tests (specific serology and intestinal biopsy) have a high PPV for CD, they should not be relied upon to exclude CD in patients already adhering to a GFD.
- HLA-DQ2 / DQ8 genotyping should be used to try to exclude CD prior to embarking on a formal gluten challenge.
- CD should be differentiated from non-celiac gluten sensitivity in order to identify the risk for nutritional deficiency states, complications of CD, risk for CD and associated disorders in family members, and to influence the degree and duration of adherence to the GFD.
- Formal gluten challenge should be considered, where necessary, to diagnose or exclude CD in patients already adhering to a GFD.
- Despite the disadvantages of neither confirming nor excluding a diagnosis of CD, some patients will opt to continue on a strict GFD without undergoing formal gluten challenge; such patients should be managed in a similar fashion to those with known CD.
Treatment/Management of CD
- People with CD should adhere to a GFD for life. A GFD entails strict avoidance of all products containing the proteins from wheat, barley, and rye.
- While pure oats appear to be safely tolerated by the majority of people with CD, oats should be introduced into the diet with caution and patients should be monitored closely for evidence of adverse reaction.
- People with CD should be referred to a registered dietitian who is knowledgeable about CD in order to receive a thorough nutritional assessment and education on the GFD.
- People with newly diagnosed CD should undergo testing and treatment for micronutrient deficiencies. Deficiencies to be considered for testing should include, but not be limited to, iron, folic acid, vitamin D, and vitamin B12.
Monitoring of CD
- People with CD should be monitored regularly for residual or new symptoms, adherence to GFD, and assessment for complications. In children, special attention to assure normal growth and development is recommended.
- Periodic medical follow-up should be performed by a health-care practitioner with knowledge of CD. Consultation with a dietitian should be offered if gluten contamination is suspected.
- Monitoring of adherence to GFD should be based on a combination of history and serology (IgA TTG or IgA (or IgG) DGP antibodies).
- Upper endoscopy with intestinal biopsies is recommended for monitoring in cases with lack of clinical response or relapse of symptoms despite a GFD.
- Monitoring of people with CD should include verification of normalization of laboratory abnormalities detected during initial laboratory investigation.
Non-resonsve or refractory CD
- Patients with NRCD should be evaluated carefully to identify and treat the specific etiology in each patient.
- Early steps in the evaluation should include measurement of celiac serologies and a thorough review of the patient’s diet by a dietitian who is experienced in CD management.
- Differentiation should be made between Type I and Type II refractory CD as this is important for management and prognosis.
- Treatment with medication, as an adjunct to the GFD, should be considered in refractory CD.
- Patients with RCD should be monitored closely and receive aggressive nutritional support, including parenteral nutrition whenever indicated.
Conditions in which CD occurs more frequently and/or for whom a GFD may be beneficial
- Symptomatic malabsorption
- Diarrhea with weight loss
- Chronic diarrhea with or without abdominal pain
- Chronic iron deficiency and anemia
- Metabolic bone disease and premature osteoporosis
- Postprandial bloating and gaseousness
- Unexplained weight loss
- Abnormal elevated liver enzymes
- Incidental discovery of villous atrophy endoscopically or histologically
- Dermatitis herpetiformis
- Peripheral neuropathy
- Oral aphthous ulcers
- Growth failure
- Discolored teeth or developmentally synchronous enamel loss
- Thyroid disease
- Irritable bowel syndrome
- Down’s and Turner’s syndromes
CD less common but treatable
- Pulmonary hemosiderosis
- Unexplained male or female infertility
- Dyspepsia
- Amenorrhea
- Chronic fatigue
- Apparent malabsorption of thyroid replacement medication
- Epilepsy or ataxia
- Constipation
- Recurrent abdominal pain
Other causes of villous atrophy in duodenum
- Tropical sprue
- Small-bowel bacterial overgrowth
- Autoimmune enteropathy
- Hypogammaglobulinemic sprue
- Drug-associated enteropathy (e.g., olmesartan)
- Whipple disease
- Collagenous sprue
- Crohn’s disease
- Eosinophilic enteritis
- Intestinal lymphoma
- Intestinal tuberculosis
- Infectious enteritis (e.g., giardiasis)
- Graft versus host disease
- Malnutrition
- Acquired immune deficiency syndrome enteropathy
Inflammatory Bowel Disease – Introduction and Overview
To write about Inflammatory Bowel Disease (IBD) for our UG patient information blog is a daunting task and this blog can at best provide a general overview as a starting point for an educated open discussion between patients and providers. Certain internet-sites will also give guidance, such as the Crohn’s and Colitis Foundation of America (CCFA) or the patient education portals of the American College of Gastroenterology (ACG) and the American Gastroenterological Association (AGA).
When talking about IBD, one refers to two inflammatory conditions of the gut, either Ulcerative Colitis (UC) or Crohn’s Disease (CD). While UC will only affect the large intestine (colon) and does not skip lesions (always starting at the anus/rectum), CD can involve the entire GI tract from mouth to anus, may skip areas of the gut, and often involves the terminal ileum. Extraintestinal manifestations of IBD include joints (IBD related arthritis), eye problems (iritis) and skin lesions (such as erythema nodosum or pyoderma gangrenosum). In addition, IBD can be associated with a liver condition called primary sclerosing cholangitis (PSC), a related autoimmune disorder of the bile ducts.
A clear cause of IBD has not yet been discovered, with multifactorial genetic and environmental influences being investigated. While significant research is being conducted and multiple gene loci have been found, a definitive cure is not yet in sight. IBD is felt to be an autoimmune disorder with abnormal immune response and inflammation arising from a pathologic response to a viral, bacterial, or possibly allergic intestinal injury in genetic susceptible individuals. Since about 10% of IBD patients have affected family members, a genetic predisposition is indeed likely. UC occurs more frequently in younger individuals (15 to 40 years old); CD can have a bimodal distribution, affecting the young and old. Indeed reports of newly diagnosed CD in 80 year olds are not uncommon. While an estimated 130-240 per 100,000 people may be affected, there appears to be neither male nor female predominance.
UC will typically only affect the lining (mucosa) of the large intestine, but CD (potentially affecting the entire GI-tract) can be a transmural illness, involving the entire thickness of the bowel wall. This difference in mucosal and transmural inflammation also affects the varying presentations of these similar yet different diseases. While both may present with pain, diarrhea, bleeding (both diseases may at times only be limited to the large intestine), patients with CD are more likely to develop abscesses and/or fistulas to the abdominal wall, anus and perineum, or other organs (i.e. bowel, bladder, vagina). Due to the transmural inflammation of CD, strictures and obstructions can form, leading to possible bowel obstructions. While both UC and CD can present with periods of remission and relapse, only UC can be “cured” with surgery.
Trigger factors of these diseases are being debated. Stress may have a negative influence but this is difficult to measure or prove. Nicotine use is of grave concern, especially in CD and smoking must be stopped if at all possible. NSAIDs may trigger a flare and should be avoided.
Diagnosis: Given a great variety of symptoms and a possible overlap with the Irritable Bowel Syndrome, a diagnosis can be difficult to make or confirm. Symptoms such as abdominal pain, diarrhea, weight loss, rectal bleeding, or fever should be taken seriously and should be worked up by a health care provider. Other issues such as fatigue, loss of appetite, joint pains, liver disease, unexplained anemia, aphthous oral ulcers and iritis (redness and swelling of the eyes) should also raise concerns.
In order to make a diagnosis, multiple modalities may be used such as laboratory work-up, stool samples (to rule out infections), cross-sectional x-ray images (CT-enteroclysis or MR-enteroclysis) and endoscopic work up (EGD, Colonoscopy, Enteroscopy, Camera-Pill Endoscopy). There is no single test that can definitively diagnose or exclude IBD. A detailed patient history and physical exam as well as an established “time-line” of symptoms and findings can be useful to establish a diagnosis of IBD.
Treatment: The medical treatment of IBD (UC and CD) is very similar for both conditions; drugs approved for one disease will often be used for the other.
- 5-ASA formulations [aminosalicylates: sulfasalazine (Azulfidine®), balsalazide (Colazal®), mesalamine (Delzicol®, Asacol HD®, Lialda®, Pentasa®, Apriso®, Rowasa® enema, Canasa®), olsalazine (Dipentum®)] have been used for decades and are available as oral medications, suppositories, or enemas. It is understood that 5-ASA molecules affect the disease process on an intraluminal-local mucosal level. They are usually well tolerated, but like any medications can have serious side effects and should be discussed with and monitored by the treating provider.
- Corticosteroids, such as prednisone/hydrocortisone, are often used if 5-ASA products are insufficient to control inflammation. While steroids can be given iv, orally, as suppositories, or as enemas, the long-term side effect profile (infections, cataract formation, bone-loss, weight gain, fat redistribution, skin break-down) is unfavorable and therefore steroids should be avoided if possible. Furthermore steroids may alter the natural history or CD, changing the disease from a fibrostenotic stricturing process to a fistulizing process. Newer steroid preparations such as budesonide (Entocort®, Uceris®) may have a more favorable side effect profile but must still be viewed with caution.
- Immunomodulating medications such as azathioprine (Imuran®), 6-mercaptopurine (Purinethol®), or methotrexate (Trexall®) are used for more advanced disease states. These drugs, although well tolerated, must be monitored carefully as they can increase infectious complications, bone marrow suppression, liver injury and even cancer. METHOTREXATE MAY NEVER BE USED DURING PREGNANCY.
- Biologic treatments like infliximab (Remicade®), adalimumab (Humira®) and certolizumab pegol (Cimzia®) have traditionally been used for patients with moderate to severe CD. Infliximab (Remicade®) and adalimumab (Humira®) are also indicated and approved for UC. There drugs target specific proteins in the immune system to control inflammation. These anti-tumor necrosis factor (Anti-TNF) medications recognize, attach to and block certain actions of the immune system. Like all other drugs, they do not cure IBD, but reduce the level of inflammation. Like immunomodulators, these drugs can cause rare but serious side effects such as infections or cancer, and must be closely monitored by the treating provider.
- Natalizumab (Tysabri®) may be used in CD patients who have failed two biologics.
Step-Up vs. Step-Down Therapy: Traditionally, a step-up approach was used, i.e. mesalamine and steroid preparations to be used first, followed by immunomodulators and then “topped-off” by biologic agents, as these were initially only used for the treatment of moderate to severe CD if not responding to the standard step-up approach (aminosalicylates, corticosteroids or immunosuppressive agents). Given the severe potential complications of CD, a step-down approach is now being considered in CD, where early initiation of immunomodulator and biologic therapy is recommended to prevent fistulizing or fibrostenotic disease.
Diet: No single diet is uniformly recommended by the US GI-societies; a well-balanced healthy diet is still the best option. A low-roughage diet is suggested during disease activity; lactose intolerance may develop due to small bowel inflammation. Given concerns for potential bone loss, calcium supplementation can be considered with 400-800 IU Vitamin D and 800-1000 mg calcium as a daily dose being preferred. Too much calcium supplementation may be of concern as cardiac and overall morbidity and mortality may increase if over 1400 mg calcium is taken daily. A multi-vitamin may be of benefit to address micronutrient losses. Although we do not endorse a specific product, Forvia appears to address potential losses in IBD patients and it may be worthwhile for our patients to research that product and compare it to other MVI brands.
General Health Management: Regular provider follow-up is key to good health and disease control. In general all IBD patients should follow routine health maintenance protocols (i.e. management of screening, hypertension etc), routine vaccinations are advised; LIVE VACCINATIONS MUST BE AVOIDED, if patients are on biologics and/or immunomodulators. Yearly Dermatology visits are advised for those on biologics and/or immunomodulators to minimize skin cancer risks; women should see their OBGYNs regularly (including routine pap-smears etc.).
Surgery in IBD: Surgeons and Gastroenterologists work closely together for patients with IBD. A multi-specialty approach offers the best overall outcome for fistulizing as well as fibrostenotic CD. While surgery can not cure CD, significant positive impact can be expected for appropriately selected patients (ie complications of obstruction, abscess, fistula, failure to respond to medical treatment). Surgery can “cure” UC by removing the entire colon. This is usually done in a two-stage operation, creating first an “ileostomy” (the ileum is attached to the abdominal wall) while creating an ileal pouch; in a second operation the ileostomy is then “taken down” and the pouch is attached to the anus.
Utah Gastroenterology Blog 