Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Crohn's disease involves a great risk of malnutrition. Malabsorption, bacterial contamination, frequent abdominal surgery, meal-related pain, protein loss through the damaged mucosa contribute to creating nutritional problems. Malnutrition can worsen the outcome, both in medical and surgical patients, and deteriorate an often already altered immune response. Weight loss, low levels of blood protein, electrolytes, micronutrients and vitamins are usually related to the extension of the mucosal damage. Nutritional assessment can be difficult due to oedema and bleeding, who interfere with both clinical and laboratory evaluation. The exact amount of nitrogen, lipids, minerals stool loss can be useful. It is widely accepted the use of nutritional support in Crohn's disease, but many Authors do not agree concerning the route (enteral or parenteral) and the kind of nutrient to be used. Still controversial is the role of nutrition: just support or real therapy? Most recent hypothesis concerning the pathogenesis of Crohn's disease indicate food and/or bacterial antigens as involved in determining the pathology. The "bowel rest", considered for many years as a fasting period necessarily supported by parenteral nutrition, can also be obtained by the temporarily reduction or stop in presenting those antigens to the bowel mucosa. This new concept can be achieved not only by parenteral nutrition, but with an enteral elemental diet as well. The elemental diet contains all nutrients in the simplest way and thus succeeds in lowering or eliminating the antigenic power. The reported results seem to indicate an equivalence of enteral and parenteral nutrition; anyway enteral is advisable when feasible, being more physiological and less expensive and involving a lower risk of serious complications.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Possibilities and limitations of nutritional support in Crohn disease]. 129 38

Malabsorption due to severe pancreatic exocrine insufficiency is one of the most important late features of chronic pancreatitis. Generally, steatorrhea is more severe and occurs several years prior to malabsorption of other nutrients because synthesis and secretion of lipase are impaired more rapidly, its intraluminal survival is shorter, and the lack of pancreatic lipase activity is not compensated for by nonpancreatic mechanisms. Patients suffer not only from nutritional deficiencies but also from increased nutrient delivery to distal intestinal sites, causing symptoms by profound alteration of upper gastrointestinal secretory and motor functions. Adequate nutrient absorption requires delivery of sufficient enzymatic activity into the duodenal lumen simultaneously with meal nutrients. The following recommendations are based on modern therapeutic concepts: 25,000 to 40,000 units of lipase per meal using pH-sensitive pancreatin microspheres, with dosage increases, compliance checks, and differential diagnosis in case of treatment failure. Still, in most patients, lipid digestion cannot be completely normalized by current standard therapy, and future developments are needed to optimize treatment.
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PMID:Pancreatic enzyme replacement therapy. 1127 76

Treatment of steatorrhea by lipase supplementation therapy has become more successful in the last decade due to better understanding of the physiology and pathophysiology of the digestive process. Porcine lipase has been the therapeutic standard for several decades and will continue to be the treatment of choice in pancreatic exocrine insufficiency. Modern therapeutic concepts recommend administration of 25,000-40,000 units of porcine lipase per meal using pH-sensitive pancreatin microspheres. In case of treatment failure, the dose should be increased, compliance should be checked, and other reasons for malabsorption should be excluded. Still, in most patients, lipid digestion cannot be completely normalized by current standard therapy, and future developments are needed for optimizing treatment. In this article, pathophysiologic characteristics of pancreatic exocrine insufficiency, prerequisites for use of alternative lipase sources as well as currently available lipases of nonporcine origin, and new developments are discussed. Current literature suggests that bovine lipase products present a theoretical alternative but play no major role in the western world. Fungal lipase has inferior properties compared with conventional products. Bacterial lipase products show promising potential and offer future therapeutic alternatives. Moreover, human pancreatic lipase gene transfer and application of bioengineered human gastric lipase appear on the horizon.
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PMID:Lipase supplementation therapy: standards, alternatives, and perspectives. 1249 9

Effective treatment of malabsorption due to severe pancreatic exocrine insufficiency requires delivery of sufficient enzymatic activity into the duodenal lumen simultaneously with meal nutrients. To achieve this, modern therapeutic concepts recommend administration of 25,000 to 40,000 units of lipase per meal using pH-sensitive pancreatin microspheres. In case of treatment failure, dosage should be increased two to three times. If this still is not successful, compliance may be checked by measurement of fecal chymotrypsin, although this is not a standardized procedure. In the compliant patient, diagnosis of pancreatic exocrine insufficiency needs to be reviewed, particularly cases of celiac disease, (concomitant) bacterial overgrowth, and blind loop syndrome, as well as giardiasis, which need to be excluded or otherwise be treated specifically. Finally, additional acid suppression with application of unprotected pancreatin and/or reduced fat intake may help to control malabsorption. Still, in most patients, lipid digestion cannot be completely normalized by current standard therapy. On the one hand, this leads to loss of energy that may only partly be compensated for by increased nutrient intake. On the other hand, increased nutrient exposition of distal intestinal sites may release excessive amounts of mostly inhibitory distal intestinal neurohumoral mediators, and thereby disturb gastrointestinal secretory and motor functions. Consequently, future developments are needed for optimizing treatment.
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PMID:Pancreatic Enzyme Supplementation Therapy. 1295 43

Short bowel syndrome (SBS) is a global malabsorption syndrome that results from extensive intestinal resections. It used to be a typical complication of repetitive bowel resections in patients with Crohn's disease. However, due to improved medical and surgical therapies for these patients it currently occurs more frequently as a consequence of vascular disorders in adults (intestinal infarction) and congenital aberrations in children, respectively. Adequate therapy depends on the degree of (small) bowel losses and on resulting functional disturbances. Moreover, it must be adjusted to the postoperative adaptation process, which consists of three phases: The immediate acute phase lasts less than 4 weeks and serves to stabilise the patient. The subsequent year should be used to induce maximal adaptation by gradually increasing nutrient exposure. When maximal stimulation of nutrient absorption has been achieved, permanent maintenance nutrition treatment should be defined individually, dependent on extent and quality of nutritive deficits. In patients with Crohn's disease, optimal treatment of the underlying disease is of pivotal importance in order to avoid a further reduction of absorptive capacity or other complications. Current investigations aim at improving the adaptation process by administration of specific diets and growth hormones. With these, it appears possible to treat even some patients with very short bowel, i.e. less than 50 cm of small intestine left, with oral nutrition, only. Still, a considerable proportion of patients will need long-term parenteral nutrition. If young patients experience intolerable complications of parenteral nutrition, intestinal transplantation may be considered as a high risk therapy of last choice.
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PMID:Management of the short bowel syndrome after extensive small bowel resection. 1549 90

Growth retardation is one of the most prominent consequences of childhood cholestatic liver diseases. The pathogenesis of malnutrition is multifactorial and includes reduced calorie intake, fat malabsorption, abnormal protein metabolism, and increased energy expenditure. Poor growth is a typical feature of biliary atresia, cystic fibrosis, progressive familial intrahepatic cholestasis and Alagille syndrome. In some of these features it is not only directly related to impaired nutrient absorption. Liver transplantation is required if liver disease progresses to liver failure - improved nutritional status is achieved within weeks after surgery. Still, patients with Alagille syndrome present with only slight catch-up growth after transplantation, while patients with PFIC and biliary atresia grow significantly.<br />
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PMID:Factors affecting catch-up growth after liver transplantation in children with cholestatic liver diseases. 2030 23

Chronic diarrhea, defined as a decrease in stool consistency for more than four weeks, is a common but challenging clinical scenario. It can be divided into three basic categories: watery, fatty (malabsorption), and inflammatory. Watery diarrhea may be subdivided into osmotic, secretory, and functional types. Watery diarrhea includes irritable bowel syndrome, which is the most common cause of functional diarrhea. Another example of watery diarrhea is microscopic colitis, which is a secretory diarrhea affecting older persons. Laxative-induced diarrhea is often osmotic. Malabsorptive diarrhea is characterized by excess gas, steatorrhea, or weight loss; giardiasis is a classic infectious example. Celiac disease (gluten-sensitive enteropathy) is also malabsorptive, and typically results in weight loss and iron deficiency anemia. Inflammatory diarrhea, such as ulcerative colitis or Crohn disease, is characterized by blood and pus in the stool and an elevated fecal calprotectin level. Invasive bacteria and parasites also produce inflammation. Infections caused by Clostridium difficile subsequent to antibiotic use have become increasingly common and virulent. Not all chronic diarrhea is strictly watery, malabsorptive, or inflammatory, because some categories overlap. Still, the most practical diagnostic approach is to attempt to categorize the diarrhea by type before testing and treating. This narrows the list of diagnostic possibilities and reduces unnecessary testing. Empiric therapy is justified when a specific diagnosis is strongly suspected and follow-up is available.
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PMID:Evaluation of chronic diarrhea. 2208 67

The patient was a 77-year-old woman. She was diagnosed as intraducal papillary mucinous neoplasms (IPMN). She refused an operation for 3 years. After all, a nodule in the main pancreatic duct was pointed out, she agreed and was referred to us. Her past history showed pacemaker implantation for third-degree atrioventricular block, and no impaired glucose tolerance. Abdominal CT showed a dilated whole pancreatic duct and a multilocular cystic tumor. Endoscopic retrograde pancreatography showed a marked dilation of the main pancreatic duct. We diagnosed as main duct IPMN. Intraoperative US showed no nodule in pancreatic duct, and there was no suspicious lesion of invasive cancer. We performed segmental pancreatectomy between the left side of common bile duct and the pancreas tail. The tumor was resected with clear margins. Both cut-ends of the main pancreatic duct were anastomosed to a jejunal loop. The postoperative course was excellent. She was discharged on day 16. The glycemic control was good, she needed no treatment for diabetes. Total pancreatectomy has many problems such as insulin and pancreatic polypeptide deficiency, hypoglycemia, malabsorption, diarrhea and liver dysfunction. We avoided total pancreatectomy so that her quality of life was maintained. Still a careful follow -up is required.
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PMID:[A case of intraductal mucinous neoplasms with the whole main pancreatic duct dilation treated via segment pancreatectomy]. 2220 12

Establishing the diagnosis of cystic fibrosis (CF) is straight forward in the majority of patients: they present with a clear clinical picture (most frequently chronic respiratory symptoms plus malabsorption), the sweat chloride value is>60mmol/L and two known disease causing CFTR mutations are identified. In less than 5% of subjects, mainly those with a milder or limited phenotype, the diagnostic process is more complex, because initial diagnostic test results are inconclusive: sweat chloride concentration in the intermediate range, less than 2 CF causing mutations identified or both. These patients should be referred to expert centers where bioassays of CFTR function like nasal potential difference measurement or intestinal current measurement can be done. Still, in some patients, despite symptoms compatible with CF and some indication of CFTR dysfunction (e.g. only intermediate sweat chloride value), diagnostic criteria are not met (e.g. only 1 CFTR mutation identified). For these subjects, the term CFTR related disorder (CFTR-RD) is used. Patients with disseminated bronchiectasis, congenital bilateral absence of the vas deferens and acute or recurrent pancreatitis may fall in this category. CF has a very wide disease spectrum and increasingly the diagnosis is being made during adult life, mainly in subjects with milder phenotypes. In many countries, nationwide CF newborn screening (NBS) has been introduced. In screen positive babies, the diagnosis of CF must be confirmed by a sweat test demonstrating a sweat chloride concentration above 60mmol/L. To achieve the benefit of NBS, every baby in whom the diagnosis of CF is confirmed must receive immediate follow-up and treatment in a CF reference center. CF NBS is not full proof: some diagnoses will be missed and in some babies the diagnosis cannot be confirmed nor ruled out with certainty. Screening algorithms that include gene sequencing will detect a high number of such babies that are screen positive with an inconclusive diagnosis (CFSPID). Even in 2016, the most reliable and widely available diagnostic test for CF is the measurement of chloride concentration in sweat. The method of choice is sweat induction by pilocarpine iontophoresis, followed by sweat collection on a gauze or filter paper or in a Macroduct coil. Since mutation specific therapies have become available, it is important to identify the mutations responsible for CF in each individual patient.
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PMID:The diagnosis of cystic fibrosis. 2857 37