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)

Orlistat (Xenical, Hoffmann-La Roche) is a powerful inhibitor of gastrointestinal lipase and as such, reduces fat absorption. Unlike other weight-reducing drugs it is minimally absorbed and has no effects in the CNS. Orlistat is indicated for patients with a body mass index (BMI) of at least 30 kg/m2 or 28 kg/m2 in the presence of obesity-associated complications, such as hypertension, diabetes mellitus, hyperlipidaemia and obstructive sleep apnoea. In clinical trials, orlistat (120 mg t.i.d.) in combination with life-style modification and a hypocaloric diet (30% of energy from fat) induced significantly more weight loss and improved health complications of obesity (diabetes, hypertension, hyperlipidaemia) compared to patients treated with diet alone. Side effects related to fat malabsorption, occurred in more than 20% of subjects during the first year of treatment and included oily faecal spotting, abdominal pain, flatus with discharge and fatty/oily stool. Side effects from orlistat diminished in the second year of treatment. Plasma concentrations of fat soluble vitamins decreased in orlistat-treated patients but did not usually fall below the normal range. No studies have evaluated the efficacy of orlistat or side effect profile beyond two years.
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PMID:Orlistat in the treatment of obesity. 2694 9

Carbohydrates are hydrolyzed in the intestinal lumen by specific enzymes to monosaccharides before transport across the brush border membrane of epithelial cells into the cell interior. The enzymes implicated in the digestion of carbohydrates in the intestinal lumen are membrane-bound glycoproteins that are expressed at the apical domain of the enterocytes. Absent or reduced activity of one of these enzymes is the cause of disaccharide intolerance and malabsorption, the symptoms of which are abdominal pain, cramps or distention, flatulence, nausea and osmotic diarrhea. Lactose intolerance is the most common intestinal disorder that is associated with an absence or drastically reduced levels of an intestinal enzyme, in this case lactase-phlorizin hydrolase (LPH). The pattern of reduction of activity has been termed late onset of lactase deficiency or adult type hypolactasia. It was thought that the regulation of LPH was post-translational and was associated with altered structural features of the enzyme. Recent studies, however, suggest that the major mechanism of regulation of LPH is transcriptional. Other forms of lactose intolerance include the rare congenital lactase deficiency and secondary forms, such as those caused by mucosal injury, due to infectious gastroenteritis, celiac disease, parasitic infection, drug-induced enteritis and Crohn's disease. This review will shed light on important strucural and biosynthetic aspects of LPH, the role played by particular regions of the LPH protein in its transport, polarized sorting, and function, as well as on the gene expession and regulation of the activity of the enzyme.
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PMID:Molecular and cellular aspects and regulation of intestinal lactase-phlorizin hydrolase. 1133 11

Specific malabsorption of carbohydrate is related to the lack or decrease in enzymatic activity needed for its hydrolysis; seldom, it is related to the lack or overloading in transport mechanism of monosaccharide. Ingestion of unabsorbed carbohydrate may induce digestive symptoms due to its colonic fermentation (borborygmus, bloating, pain, and flatus) or its osmotic activity (diarrhoea). In a patient consuming at least a bowl of milk per day and suffering of functional digestive symptoms, intolerance to lactose must be ruled out because its treatment is easy and efficient, i.e. to put fermented dairy products in place of milk.
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PMID:[Specific carbohydrate malabsorption]. 1145 11

Persons with lactose intolerance are unable to digest significant amounts of lactose because of a genetically inadequate amount of the enzyme lactase. Common symptoms include abdominal pain and bloating, excessive flatus, and watery stool following the ingestion of foods containing lactose. Lactase deficiency is present in up to 15 percent of persons of northern European descent, up to 80 percent of blacks and Latinos, and up to 100 percent of American Indians and Asians. A sizable number of adults believe they are lactose intolerant but do not actually have impaired lactose digestion, and some persons with lactase deficiency can tolerate moderate amounts of ingested lactose. A diagnosis of lactose intolerance can usually be made with a careful history supported by dietary manipulation. If necessary, diagnosis can be confirmed by using a breath hydrogen or lactose tolerance test. Treatment consists primarily of avoiding lactose-containing foods. Lactase enzyme supplements may be helpful. The degree of lactose malabsorption varies greatly among patients with lactose intolerance, but most of them can ingest up to 12 oz of milk daily without symptoms. Lactose-intolerant patients must ensure adequate calcium intake.
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PMID:Lactose intolerance. 1250 58

Small bowel diverticulosis (SBD) is a rare entity. Most cases of diverticulosis are asymptomatic. SBD is often discovered incidentally during contrast studies and endoscopy. When patients report chronic gastrointestinal symptoms such as abdominal pain, bloating, flatulence, and anemia, SBD is often an overlooked diagnosis. Patients requiring treatment for SBD are those with complications such as malabsorption, hemorrhage, obstruction, and acute inflammation with abscess or rarely perforation. Malabsorption can be managed with broad-spectrum antibiotics and vitamin supplementation. Hemorrhage is treated conservatively with resuscitation efforts, but recurrent bleeding requires surgery. Enteroliths causing obstruction in the duodenum can be relieved by endoscopy, that is, by manipulation, but jejunoileal obstruction requires a resection. Pseudo- obstruction may be managed with prokinetics such as metoclopramide, erythromycin, and the 5-hydroxytryptamine 4 agonist tegaserod. Uncomplicated cases of SBD are treated with bowel rest and antibiotics. However, perforation or abscess formation not amenable to percutaneous drainage mandates surgical resection. Any patient with a triad of anemia, abdominal pain, and an abdominal radiograph with dilated loops of small bowel merits SBD in the differential diagnosis.
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PMID:Small Bowel Diverticulosis: An Overlooked Entity. 1252 66

Orlistat, a potent gastrointestinal lipase inhibitor, is a member of a new class of drugs designed for the long-term treatment of obesity. When given with a fat-containing meal, orlistat reduces dietary fat absorption by approximately 30%, which equates to a decrease in caloric absorption of approximately 200 kilocalories per day. A 2-year European study found a mean decrease in body weight of 10.2% (10.3 kg) in the orlistat group compared to 6.1% (6.1 kg) in the placebo group at 1 year. Additionally, 9.3% of the orlistat group versus 2.1% of the placebo group lost >20% of their initial weight. Serum lipids and diabetes control are also improved by orlistat. Related to orlistat's mechanism of action, side effects include oily spotting, flatulence and frequent loose stools, but not frank diarrhea or intestinal malabsorption. Vitamin D and beta-carotene levels decreased, but remained within the normal range. In summary, orlistat is the first example of a new class of antiobesity drugs that enhances weight loss and weight maintenance by interfering with dietary fat absorption. Orlistat has tolerable gastrointestinal side effects and no major drug toxicity. Orlistat is a viable adjunct to lifestyle interventions used in the long-term management of obesity.
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PMID:Orlistat for the long-term treatment of obesity. 1297 16

The maturational decline in lactase activity renders most of the world's adult human population intolerant of excessive consumption of milk and other dairy products. In conditions of primary or secondary lactase deficiency, the lactose sugars in milk pass through the gastrointestinal tract undigested or are partially digested by enzymes produced by intestinal bacterial flora to yield short chain fatty acids, hydrogen, carbon dioxide, and methane. The undigested lactose molecules and products of bacterial digestion can result in symptoms of lactose intolerance, diarrhea, gas bloat, flatulence, and abdominal pain. Diagnosis of lactose intolerance is often made on clinical grounds and response to an empiric trail of dietary lactose avoidance. Biochemical methods for assessing lactose malabsorption in the form of the lactose breath hydrogen test and direct lactase enzyme activity performed on small intestinal tissue biopsy samples may also be utilized. In some adults, however, high levels of lactase activity persist into adulthood. This hereditary persistence of lactase is common primarily in people of northern European descent and is attributed to inheritance of an autosomal-dominant mutation that prevents the maturational decline in lactase expression. Recent reports have identified genetic polymorphisms that are closely associated with lactase persistence and nonpersistence phenotypes. The identification of genetic variants associated with lactase persistence or nonpersistence allows for molecular detection of the genetic predisposition towards adult-onset hypolactasia by DNA sequencing or restriction fragment length polymorphism analysis. The role for such genetic detection in clinical practice seems limited to ruling out adult-onset hypolactasia as a cause of intolerance symptoms but remains to be fully defined. Attention should be paid to appropriate interpretation of genetic detection in order to avoid potentially harmful reduction in dairy intake or misdiagnosis of secondary lactase deficiency.
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PMID:Genetic variation and lactose intolerance: detection methods and clinical implications. 1528 17

Celiac disease (CD) is characterized by malabsorption of nutrients in the small intestine. The availability of highly specific and sensitive serologic tests has facilitated its diagnosis, increasing the disease prevalence. The aim of this study was to determine the clinical, laboratory, and histopathological features of CD in Turkish adults. Between 1968 and 2002, CD patients presenting to the Gastroenterology Unit were evaluated retrospectively. From 2002, newly diagnosed patients were prospectively followed up. Sixty patients (39 female, 21 male) were included in the study. Mean body mass index was 22.2 +/- 5.4 kg/m2. The most common symptoms were diarrhea, weight loss, and flatulence. Most common comorbidities were anemia, osteoporosis, type 1 diabetes mellitus, and steatohepatitis. Six (10.0%) patients had a family history of diabetes mellitus; one (1.7%) patient had a family history of CD. Plasma glucose and serum gamma-glutamyltransferase levels were significantly higher in females than males. Most common histopathological findings were increased lymphocytes in the lamina propria (76.2%) and villus epithelium (59.5%). Over the years, the cumulative frequency of CD increased more in females than males. This is the first study in the literature showing the characteristics of CD in Turkish adults. In our previous recent study, the prevalence of tissue transglutaminase antibody positivity in Turkish healthy blood donors was 1.3%, indicating a high prevalence of CD in our population. In this study, the cumulative frequency of CD increased more in females than males. With the better understanding and increased suspicion of the disease, more patients are being diagnosed in our population.
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PMID:Celiac disease in the Turkish population. 1571 51

Lactose intolerance is common in Thai adults who ingest cow's milk but its incidence has not been clearly defined The authors evaluated 45 volunteers (15 males, 35 females), aged 21-31 yrs old, who drank one 240-ml box of milk daily. A Lactose tolerance test was performed using a breath-hydrogen test (BHT) after oral intake of 25 g of lactose dissolved in 250 ml of water The presence of gastrointestinal symptoms of lactose intolerance, flatulence, abdominal pain and diarrhea, were recorded Twenty-one subjects (47%) were categorized as lactose malabsorbers and intolerant, two subjects (4%) were malabsorbers but tolerant, and 22 of 45 (49%) were absorbers and tolerant. The incidence of lactose malabsorption was, thus, 51%; symptoms of intolerance were found in 21 of the 23 malabsorbers, making the incidence of lactose intolerance 47%. In the lactose malabsorbant and intolerant group, the more breath-hydrogen (H) the more symptoms observed All subjects who had a negative breath-H2 test had no symptoms. The breath-H2 test should be used as a standard method to evaluate lactose absorption and lactose tolerance. The incidence of lactose intolerance has decreased from the past and the symptoms are not so severe that the people limit the consumption of milk since it is a major source of food containing good quality of protein and calcium.
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PMID:Lactose intolerance in Thai adults. 1582 48

Sugars normally are absorbed in the small intestine. When carbohydrates are malabsorbed, the osmotic load produced by the high amount of low molecular weight sugars and partially digested starches in the small intestine can cause symptoms of intestinal distention, rapid peristalsis, and diarrhea. Colonic bacteria normally metabolize proximally malabsorbed dietary carbohydrate through fermentation to small fatty acids and gases (ie, hydrogen, methane, and carbon dioxide). When present in large amounts, the malabsorbed sugars and starches can be excreted in the stool. Sugar intolerance is the presence of abdominal symptoms related to the proximal or distal malabsorption of dietary carbohydrates. The symptoms consist of meal-related abdominal cramps and distention, increased flatulence, borborygmus, and diarrhea. Infants and young children with carbohydrate malabsorption show more intense symptoms than adults; the passage of undigested carbohydrates through the colon is more rapid and is associated with detectable carbohydrates in copious watery acid stools. Dehydration often follows feeding of the offending sugar. In this review we present the clinical and current molecular aspects of disaccharidase digestion.
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PMID:Disaccharide digestion: clinical and molecular aspects. 1652 88


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