After each “voluntary famine” or “weight reducing” diet medicine x topol 2015 order lamictal visa, your body will put on weight much faster than it did before treatment yeast infection discount lamictal 25mg amex. Under normal circumstances symptoms 8 days after conception order lamictal line, the body converts calories into heat medicine sans frontiers lamictal 50mg amex, which then simply evaporates. Well circulated brown fat tissue, which is located near the large arteries and in the underarms, is the main source of this energy. New research suggests that in some obese people this mechanism may be disturbed and that the best dietary rules would be of no avail. Abusing the body’s digestive system through frequent strict dieting may be the main cause of this problem. Because artificial sweeteners are low-energy foods and non-physiological, the body deals with them in the same way as described above. This principle is a well-known and commonly applied practice, both in the food industry and in animal feeding. Animal feeds contain highly concentrated saccharin to stimulate the animal’s appetite so that they eat more frequently and grow fat faster. Children eating diet foods in lieu of the full-calorie versions may lead to overeating and obesity when they grow up, according to a 2007 report from the University of Alberta, Canada. Lead researcher Professor David Pierce stated, "Based on what we’ve learned, it is better for children to eat healthy, well balanced diets with sufficient calories for their daily activities rather than low-calorie snacks or meals. Because sugar can move straight through the stomach walls, it will appear in the bloodstream within 3-5 minutes. However, the body has to keep the blood sugar level in check since too little or too much sugar can be dangerous. When sugar touches the 451 Timeless Secrets of Health and Rejuvenation taste buds for the sweet taste on the tongue, the pancreas is given the instruction to secrete insulin, which is required to make it (the sugar) available to the cells. If you eat artificial sweeteners, the body naturally responds to their sweet taste by secreting insulin. Rather than receiving sugar in the blood as expected, however, it receives a combination of protein compounds. Doing its normal job, the pancreas has already prepared a portion of insulin that now floats about in the bloodstream searching for the expected sugar. However, since this situation can be life endangering, your body quickly signals “hunger” which becomes a sudden, strong “craving. Instead of saving the calories that are contained in ordinary sugar, you have artificially increased your need and appetite for more sweet food. If you try to satisfy this desire by eating more foods containing artificial sweeteners (without calories), the urge to eat will become even stronger than before and you will start overeating. Researchers have found that the urge to eat more food after ingesting artificial sweeteners in a drink can last up to 90 minutes, even when all blood tests show normal values. A more serious situation arises when the body is given artificial sweeteners on an ongoing basis. Since the sweeteners repeatedly stimulate the taste buds responsible for detecting sugar, the brain maintains an almost continuous urge to eat. At the same time, the liver is instructed by the brain to store sugar supplies rather than to release them, which causes chronic fatigue. The pancreas, which had wrongly assumed that real sugar was entering the bloodstream, eventually realizes that it has been cheated. Sweeteners Cause Obesity, Depression, Brain Damage Sugar is known to “improve” moods for relatively short periods of time. With the help of insulin, sugar increases the secretion of serotonin in the brain. The only way to get out of this situation, it seems, is to eat sugar so that the body can secrete insulin again. But food manufactures know that the more artificially sweetened foods and beverages you consume, the more you will want their normal sugar-containing foods and beverages as well. Diet foods and diet beverages have not only contributed to a massive increase in sugar consumption and obesity but also led to an epidemic of depression. I have seen numerous depressed people over the years, a large percentage of whom regularly used artificial sweeteners. By cutting out diet foods and "light" products, they have returned to their normal moods, and they have lost excess weight, too. Apart from causing obesity and depression, sweeteners have been linked to insomnia, headaches, giddiness, loss of memory, nausea, pre-menstrual syndrome, panic attacks, epileptic fits, and even overstimulation of breast glands leading to breast cancer. Once it has entered the intestinal tract, aspartame is converted into two highly excitatory neurotransmitter amino acids, aspartic acid and phenylalinine, as well as into methyl alcohol (wood-grain alcohol) and formaldehyde (embalming fluid). Wood alcohol is one of the most dangerous substances that result from eating artificial sweeteners. It may directly enter the bloodstream and move through the brain barrier into the central nervous system where it can influence the neurotransmitters, alter brain function, and cause brain damage. According 452 Timeless Secrets of Health and Rejuvenation to Consumer Reports, aspartame has a shelf life of between two and three months. Aspartame accounts for more than 75 percent of the total adverse reactions to food reported to the U. Hundreds of airline pilots have reported symptoms of memory loss and confusion, headaches, seizures, visual disturbances and gastrointestinal reactions as a result of consuming sweeteners. If pregnant women consume large quantities of diet sodas to avoid weight gain, their placenta may accumulate methyl alcohol, causing mental retardation in the fetus. They also risk maternal malnutrition because of the gastrointestinal problems and diarrhea associated with sweeteners. Added to soft drinks, they are now even linked with testicular damage and other key areas of the body. Stimulating the brain of a child with these “pleasure-enhancing” chemicals in beverages will, in some cases, program their senses to look for and use stronger addictive substances such as hard drugs or large amounts of alcohol later in life. To avoid serious health problems, it is best to stick to foods and beverages that come from purely natural sources. A sugar called tagatose is one of the next sweeteners that will be appearing on products labeled under the pseudo-hygienic appellations of “Light”, “Lite”, “Low Calorie”, “Sugar Free”, “Sugarless", “Low Fat”, or “Low Sodium, ” “etc. Some researchers believe hyperuricemia is a risk factor for ischemic heart disease, and it has been associated with lipid abnormalities, hypertension, stroke, and preeclampsia. It is an especially hazardous effect with regards to diabetes because hyperuricemia is damaging to the pancreas as well as possibly causing major harm to other organs and systems in the body. Having too much uric acid in the blood predisposes you to developing gout, a painful joint condition. If you wish to protect yourself and your family from the dreadful consequences of universal deceit and actually benefit from the foods you eat, start with fruit, vegetables, grains, nuts, seeds, and legumes. Light-Food—A Weight Booster “Foolproof” Slimming Diets Most dietary approaches in the past were based on the simple mathematical concept that, because 1 kg of body fat contains 7, 000 calories, taking in 1, 000 calories less each day would cause a person to lose 1 kg of body fat a week. Since this equation sounded so logical and convincing, many people tried to shed the undesirable weight by controlling their daily intake of calories. Actually, the more people reduced their calorie intake, the faster they put on weight. When you analyze the results of all the prominent slimming techniques and dietary plans, you face the following facts. Of those who continue, only a few lose weight and most of those people put the weight back on again. The biggest craze on the slimming market concerns the consumption of “light” food. You can eat as much as you like and will not put on weight because the products contain few or no fattening substances at all. With these, you supposedly don’t have to restrict yourself or curb your appetite any longer, and at the same time you become slim. At last, food manufacturers have complied with the demands made by nutritional scientists and dieticians to produce foods with fewer calories. Consumers feel relieved that the new food is fat-free and without sugar, and instead contains fat substitutes, water and artificial sweeteners. And by adding artificial flavors to the food and using other forms of chemical manipulation, the taste buds believe that it is the real thing.
Because of this self-regulating mechanism schedule 6 medications buy lamictal in india, we are able to medicine used to treat chlamydia purchase lamictal 100 mg with mastercard survive even extremely poor diets with very little calcium intake treatment 1st degree burns cheap lamictal 200mg line. We can even fast on distilled water for several weeks without developing a calcium deficiency (distilled water removes calcium from the body) 911 treatment buy cheap lamictal 200 mg on line. Yet if the consumption of dairy foods continues for a long time, the calcium reserves get depleted faster than they can be replenished, leading to damage of the bone tissue. Regular consumption of milk and dairy products would turn the blood acidic and kill it if the body didn’t mobilize large amounts of minerals to save itself from acid death. Yet, in the long term, this emergency measure leads to demineralization of the tissues and organs, and subsequent acidosis. This causes a depletion of nutrients in the tissues, especially of those that form the bones and joints. Cows maintain strong and hardy bones and teeth throughout their lives and get most of their calcium from the greens they eat. Occasionally they lick on limestone, but this is certainly not enough to supply the large quantities of calcium they require to build and rebuild their heavy skeletons. If milk were the most useful and 443 Timeless Secrets of Health and Rejuvenation important source of calcium for grown animals then nature would certainly have designed ways of supplying them with milk throughout their lives. But as it turns out, they have access to milk only at the beginning stages of their lives. Drinking whole milk regularly can eventually exhaust the liver’s bile-producing capacity. Low fat milk requires less bile to digest the fat contained in the milk, yet milk protein cannot be digested without the naturally high concentrations of milk fat. Added to that, without sufficient bile, calcium cannot be properly digested or absorbed either. The large amounts of undigested milk protein increase acidity in the body and the unused crude milk calcium can cause calcification of joints, arteries and kidneys. There is also plenty of calcium in almonds, black molasses, sesame seeds, broccoli, Brazil nuts, millet, oats and citrus fruits. The calcium contained in these foods is readily absorbed by the human digestive system, provided the digestive system functions efficiently. Osteoporosis and osteoarthritis are basically metabolic disorders that are caused by severe congestion and an unbalanced diet/lifestyle, and almost never by insufficient calcium intake. Osteoporosis is virtually unknown in such places as Africa where people eat far fewer proteins than those living in developed countries. Milk Consumption Linked to Diabetes and Allergies Initial studies on diabetes revealed that the frequency of insulin dependent diabetes is linked to breast feeding. The longer children were breastfed by their mothers, the less was their risk of developing diabetes later in life. The interpretation of this finding was revised, however, after it was found that children who are fed with cow’s milk formula rather than with mother’s milk were the most likely candidates for diabetes. More precise studies revealed that diabetics have a striking number of antibodies against a particular protein in their blood. Diabetes is considered an “autoimmune disease” which means that the body supposedly directs its defenses against itself. The particular protein that the body tries to combat here comes from the whey of cow’s milk. If the milk protein becomes lodged in the body’s connective tissues, it is only natural for the body’s immune cells (white cells) to attack and remove it. The fact that this response by the immune system inflames the cells surrounding these tissues (which is essential for healing) should not be misconstrued to be an autoimmune disease. Ever since cows milk has been used to make cheese, whey, which is a waste product of cheese production, has been fed to pigs. This practice continued even after scientists attributed great nutritional value to whey. Since nobody really liked drinking this “precious” ingredient of milk it was mixed in with foods. Scientists have discovered that the beta-casein (a particular protein) in cow’s milk can trigger an immune response that may, in turn, cross-react with an antigen to cause an allergic reaction. An allergy is the body’s response to fight a substance that it considers dangerous to its health and survival. Today, millions of people in the Western Hemisphere are suffering from allergies caused by milk or products that contain milk powder or whey. Perhaps this is the reason most populations in the world avoid drinking cow’s milk. The current “allergy epidemic” in developed countries may have well been caused by the “miracle food” whey which is added to so many food products, including children’s foods, fresh cheese, ready-made soups, diet foods, etc. We are practically infested by this milk protein unless we live off purely natural foods. This effectively gave farmers the legal permission to treat their herds with the controversial hormone. The license was accompanied with a new labeling policy, previously unheard of in the United States. The granting of a license to increase milk production through hormones comes at a time when milk production is already much higher than is milk consumption. Most industrialized nations destroy enormous quantities of milk and butter to manipulate the prices with no regard to the cows’ health. Cows are naturally made to produce a certain amount of milk according to the demand from their offspring. The hormone-induced artificial increase of milk yield causes a number of cow’s diseases that are met by administering large quantities of antibiotics. How much a cow must be suffering when its udder is being extended to beyond it natural capacity is not even considered an issue. Under normal circumstances, you will not find young animals going around and begging other animals to give them some of their milk. Any adverse reactions to partaking of the milk of another species are to be expected. However, if milk causes allergies or other diseases why doesn’t everyone who regularly consumes cows milk suffer from the same problems Left unaltered, cows milk is completely balanced regarding its natural ingredients. By removing one essential part of the milk, that is, fat, the milk protein can no longer be digested completely, hence there will be a “leftover” of undigested and irritating proteins that the body’s immune system begins to combat and get rid of. In my practice I have found that persons who are of Vata constitution seem to digest and metabolize milk much better than Kapha types, provided it is fresh, whole fat and boiled before consumption (Pasteurizing of milk differs from boiling it in that is uses an extremely high temperature, namely, 285 degrees F (141 degrees C). The mucus producing effect of milk may help lubricate their intestinal lining, which has the tendency to be dry. The milk’s heavy and warming qualities may pacify Vata and thereby outweigh some negative effects that milk may have for other body types. Healthy Vata types and, to a certain extent, healthy Pitta types seem to produce more of the specific digestive enzymes, which are used to break down milk proteins, than Kapha types. In Kapha types, milk protein remains undigested and can trigger allergic reactions with intense mucus irritation and sinus congestion. The Kapha’s blood vessel walls tend to clog up quickly with excessive proteins as a result of overeating dairy foods or meat. This may explain why this particular body type is more prone to obesity and congestive heart failure than the Vata type. Yet the enzymes are needed to make the milk nutrients available to the body cells. Newly born calves die within 445 Timeless Secrets of Health and Rejuvenation six months when fed with pasteurized cow’s milk. One can only imagine the turmoil that must be going on in the tiny intestinal tract of a baby who is fed with pasteurized milk or sterilized milk formula. As mentioned before, such babies usually develop colic, become bloated and chubby, discharge mucus, catch colds frequently, are restless, and cry a lot. The best advise is to breastfeed as long as is possible, avoid dairy-based formulas altogether, use alternatives such as coconut milk (the closest to human milk) as well as some almond milk, hemp milk or rice milk; and give freshly mashed fruits, vegetables and rice when the baby is ready to eat solids.
Aside from alcohol medicine man movie cheap 50 mg lamictal amex, another addictive substance often mentioned in association with acute pancreatitis is marijuana in treatment buy lamictal 25 mg with amex, abused by smoking medicine interactions purchase lamictal with visa. A smaller series of marijuana-induced pancreatitis cases was reported by Wargo et al symptoms lactose intolerance lamictal 100mg fast delivery. Interestingly, stimulation of cannabinoid receptors was found to be a protective mechanism during experimental pancreatitis. This is yet another example of ambivalent behavior of some xenobiotics towards the pancreatic tissue. Diagnostics, disease course and management Among the reasons why the real incidence of drug-induced acute pancreatitis is still not known, the difficulties in diagnosis are probably most important. Milder cases of pancreatic injury are often missed because serum amylase and lipase estimations are not part of the metabolic profile obtained during a routine health checkup and abdominal pain is often attributed to underlying diseases. The first criterion seems to be easy to achieve until we remember that monotherapy in our patients becomes more and more scarce. Use of the classification systems mentioned above may be very useful for that purpose. Excluding all other causes of the disease is also not so straightforward in many cases of acute pancreatitis. The validity of diagnosis may depend on the equipment available and even more on the experience of the medical staff. Discontinuation of oral therapy is a natural part of any management of acute pancreatitis. In patients treated by multiple pharmacotherapy, it is impossible to decide which medication withdrawal led to a resolution of the symptoms and laboratory findings. In these cases, acute pancreatitis is usually diagnosed within several days from drug administration. Due to the character of the disease and ethical considerations, deliberate, repeated administration of suspect drug to induce a new episode of acute pancreatitis is not possible. An exception is the use of essential drugs in cases where the benefits outweigh the risks. A simplified algorithm for diagnosing drug-induced pancreatitis is given in Figure 1. The suspected drug etiology should be considered after the exclusion of more common causes of illness. A detailed medication history documentation is obvious as well as the determination of suspicious substances. There is no evidence for preferring one of these systems, so it is possible to use both, mainly if there is a difference between them in classifying a specific suspicious agent. Using these classification systems may improve the quality of information for further patient treatment and further processing of the event for scientific or pharmacovigilance purposes. Level of Characteristics probability Certain A clinical event, including a laboratory test abnormality, that occurs in a plausible time relation to drug administration, and which cannot be explained by concurrent disease or other drugs or chemicals the response to withdrawal of the drug (dechallenge) should be clinically plausible the event must be definitive pharmacologically or phenomenologically using a satisfactory rechallenge procedure if necessary Probable A clinical event, including a laboratory test abnormality, with a reasonable time relation to administration of the drug, unlikely to be attributed to concurrent disease or other drugs or chemicals, and which follows a clinically reasonable response on withdrawal (dechallenge) Rechallenge information is not required to fulfill this definition Possible A clinical event, including a laboratory test abnormality, with a reasonable time relation to administration of the drug, but which could also be explained by concurrent disease or other drugs or chemicals Information on drug withdrawal may be lacking or unclear Unlikely A clinical event, including a laboratory test abnormality, with a temporal relation to administration of the drug, which makes a causal relation improbable, and in which other drugs, chemicals, or underlying disease provide plausible explanations Conditional / A clinical event, including a laboratory test abnormality, reported as an unclassified adverse reaction, about which more data are essential for a proper assessment or the additional data are being examined Unassessable / A report suggesting an adverse reaction that cannot be judged, because unclassifiable information is insufficient or contradictory and cannot be supplemented or verified Table 3. Of course, severe cases tend to be more often 30 Acute Pancreatitis reported both in the literature and in spontaneous pharmacovigilance reports. In the disease management, there are no specific issues concerning drug-induced pancreatitis, with an exception of an immediate withdrawal of the suspected drug. A difficult question is how to reintroduce medication if the causative agent is not unambiguously identified. We recommend not introducing all withdrawn drugs at the same time to distinguish the cause of a possible flare-up. The most suspected drugs should be substituted by their analogs with a different chemical structure. Secondary prevention consists of avoiding the drug which caused the episode of acute pancreatitis. Rechallenge of such an agent is justified only if its benefits outweigh the risks, as discussed above. Future research Given how inadequate the current state of knowledge on drug-induced pancreatic injury is, the area for further research in this field is remarkably wide. The majority of the knowledge on the topic has been obtained from case reports or their series. These will remain a major source of information, so it is necessary to improve their informative value substantially. Provide the age and sex of the patient, along with the indication for treatment with a drug; provide the dose and frequency of medication; b. Document a definite case of pancreatitis based on current diagnostic guidelines; c. Provide information on the time course between initiation of drug and onset of pancreatitis; d. Exclude the most common causes of pancreatitis; document a positive response to withdrawal of medication;. Higher level of knowledge may be obtained by performing multicenter studies targeted at the etiology of non-alcoholic, non-biliary pancreatitis. Several thousands of acute pancreatitis cases must be involved in these studies to reveal the actual occurrence of drug induced pancreatitis. Any new pharmacoepidemiological study on this topic would be useful, but to improve the validity of its outcomes, substantially better input data are required. For this purpose, it would be optimal that each single case of acute pancreatitis included in such a study be documented according to the above principles. An obvious field for this research is the issue of diseases with a high Acute Pancreatitis Induced by Drugs 31 incidence of this disorder. Another issue is the experimental pharmacological research of mechanisms by which xenobiotics can damage the pancreatic tissue as well as the common mechanisms of immune-mediated tissue injury caused by drugs. Any substantial progress in this research can contribute to a progress in two scientific challenges: recognizing the nature of more frequent causes of acute pancreatitis and also recognizing the cause and pathogenesis of idiosyncratic adverse drug reaction. Epidemiological studies show a very wide range of its incidence, but at least the absolute number of its cases is undoubtedly increasing. We are able to identify the drugs with the greatest risk and populations at risk, but the absolute risk for medication users is still very low. A better understanding of drug mediated pancreatic injury can also help to understand the etiology of more common types of acute pancreatitis. Research in drug-induced acute pancreatitis is both a challenge and an opportunity to improve the collaboration of gastroenterology and clinical pharmacology. Introduction Evidence accumulated for the past two decades leads to the conclusion that obesity enhances the development of acute pancreatitis and worsens its clinical course. We will try to give an answer to this issue by presenting the scientific data accumulated thus far. According to the definition, one should calculate the total amount of body fat a person has and deduct the “normal” amount of fat from it. The method is based on the presumption that a person’s excess weight predominantly consists of fat. The advantage of this method is its application simplicity, namely the lack of complicated procedures needed to determine it as well as the fact that it has been globally accepted. Other methods used to determine obesity measure the amount of subcutaneous fat tissue. These methods are based on the fact that the amount of subcutaneous fat tissue correlates well with the amount of excess fat tissue. The methods include the measurement of skin fold thickness, waist diameter and waist-to-hip ratio. The limiting factor for these methods is the presence of edema in the investigated areas (liver cirrhosis, heart and kidney diseases). It is used to measure body composition based on the difference in the absorption of X-rays in different types of tissues (bone, fat, muscle, water). After two decades of tedious work in finding the best method for estimating the amount of body fat in acute pancreatitis, scientists offer no clear answers. The following sections offer a detailed insight into the best methods for estimating the amount of body fat in acute pancreatitis. Only few epidemiological studies have tried to establish a direct link between obesity and the onset of acute pancreatitis, but the studies’ findings are contradictory. Therefore, it is hard to determine whether or not obesity has a direct impact on the onset of acute pancreatitis. Another factor taken into consideration when analyzing obesity’s effect on the onset of acute pancreatitis is weight distribution.
Does it only happen along with other symptoms, such as palpitations?
Nausea or vomiting
Too much salt or sodium bicarbonate in your diet
Learning how to test and record blood glucose (see: blood glucose monitoring) and urine ketones
Allergic reaction to a drug (acute interstitial allergic nephritis)
Immunoglobulin A anti-tissue transglutaminase antibody deposits in the small intestinal mucosa of children with no villous atrophy symptoms rsv buy 200 mg lamictal free shipping. A modified extraction protocol enables detection and quantification of celiac disease related gluten proteins from wheat treatment wasp stings purchase genuine lamictal on line. Journal of Chromatography B medications hyperthyroidism discount 200mg lamictal amex, Analytical Technologies in the Biomedical Life Sciences 2009;877(10):975-982 van Dommelen P treatment 3rd degree hemorrhoids buy discount lamictal 50mg online, et al. Screening rules for growth to detect celiac disease: a case-control simulation study. Incidence of enteropathy-associated T-cell lymphoma: a nation-wide study of a population based registry in the Netherlands. The presence of small intestinal intraepithelial gamma/delta T-lymphocytes is inversely correlated with lymphoma development in refractory celiac disease. Age-related clinical, serological, and histopathological features of celiac disease. Detection of celiac disease and lymphocytic enteropathy by parallel serology and histopathology in a population based study. Prospective human leukocyte antigen, endomysium immunoglobulin A antibodies, and transglutaminase antibodies testing for celiac disease in children with Down syndrome. The evidence base for interventions used to maintain remissions in Crohn’s Disease. How long is it advisable to prolong maintenance treatment of patients with ulcerative colitis Genome-wide association defines more than 30 distinct susceptibility loci for Crohn’s disease. Inflammatory bowel disease: clinical aspects and established and evolving therapies. Blood-based biomarkers can differentiate ulcerative colitis from crohn’s disease and noninflammatory diarrhea. Aspirin in the aetiology of Crohn’s disease and ulcerative colitis: a European prospective cohort study. The Safety Profile of Infliximab in Patients with Crohn’s Disease: the Mayo Clinic Experience in 500 Patients. Advanced age is an independent risk factor for severe infections and mortality in patients given anti tumor necrosis factor therapy for inflammatory bowel disease. Health care resource use and costs for Crohn’s disease before and after infliximab therapy. Early Combined immunosuppression or conventional management in patients with newly diagnosed Crohn’s disease: an open randomized trial. Prospective study of the effects of concomitant medications on thiopurine metabolism in inflammatory bowel disease. Psychosocial features of inflammatory bowel disease in the pediatric age group: acceptance of and adaptation to the disease. Gastrointestinal sensory and motoro disturbances in inflammatory bowel disease—clinical relevance and pathophysiological mechanisms. Guidelines for screening and surveillance of asymptomatic colorectal cancer in patients with inflammatory bowel disease. Increased Risks of Developing Anxiety and Depression in Young Patients With Crohn’s Disease. Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel disease. Proceedings of the National Academy of Sciences of the United States of America 2007;104(34):13780-5. Application of the Montreal classification for Crohn’s disease to a single clinician database of 1015 patients. Application of the Vienna classification for Crohn’s disease to a single clinician database of 877 patients. Natural history and clinical behaviour of Crohn’s disease extending beyond two decades. Temporal and geographic evolution of longstanding Crohn’s disease over more than 50 years. Medical therapy and birth outcomes in women with Crohn’s disease: what should we tell our patients Mucosal healing in inflammatory bowel disease: results from a Norwegina-based cohort. What Histologic Features Best Differentiate Crohn’s Disease from Ulcerative Colitis Inflammatory bowel disease: Current insights into pathogenesis and new therapeutic options; probiotics, prebiotics and synbiotics. Prevalence and management of anemia in children, adolescents, and adults with inflammatory bowel disease. Molecular pathogenesis of inflammatory bowel disease: genotypes, phenotypes and personalized medicine. A population-based study of fatigue and sleep difficulties in inflammatory bowel disease. Venous thromboembolism during active disease and remission in inflammatory bowel disease: a cohort study. A meta-analysis review of the psychosocial adjustment of youth with inflammatory bowel disease. Suicide risk in adolescents with chronic illness: implications for primary care and specialty pediatric practice: a review. European evidence-based consensus on the diagnosis and management of Crohn’s Disease. Inflammatory bowel disease: Epidemiology, pathogenesis, and therapeutic opportunities. Consensus conference: colorectal cancer screening and surveillance in inflammation bowel disease. Interleukin-23 restrains regulatory T cell activity to Drive T cell-dependent colitis. Safety of Immunomodulators and Biologics for the Treatment of Inflammatory Bowel Disease During Pregnancy and Breast-feeding. Early Mucosal Healing With Infliximab Is Associated With Improved Long-term Clinical Outcomes in Ulcerative Colitis. Feacal calprotectin: a noninvasive diagnostic tool and marker of severity in pouchitis. Increased risk of lymphoma among inflammatory bowel disease patients treated with azathioprine and 6-mercaptopurine. The role of breastfeeding in postpartum disease activity in women with inflammatory bowel disease, the American Journal of Gastroenterology 2005; 100:102-105. Autophagy, microbial sensing, endoplasmic reticulum stress, and epithelial function in inflammatory bowel disease. Chromoscopy-guided endomicroscopy increases the diagnostic yield of intraepithelial neoplasia in ulcerative colitis. A systematic review of factors that contribute to hepatosplenic T cell lymphoma in patients with inflammatory bowel disease. A retrospective analysis of the efficacy and safety of infliximab as rescue therapy in acute severe ulcerative colitis. American Gastroenterological Association Institute Technical Review on Corticosteroids, Immunomodulators, and Infliximab in Inflammatory Bowel Disease. The choice trial: adalimumab demonstrates safety, fistula healing, improved quality of life and increased work productivity in patients with Crohn’s disease who failed prior infliximab therapy. The front line of enteric host defense against unwelcome intrusion of harmful microorganisms: Mucins, antimicrobial peptides, and microbiota. Current Strategies in the Management of Intra-abdominal Abscesses in Crohn’s Disease. Systematic review: the short term and long term efficacy of adalimumab following discontinuation of infliximab.
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