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

Short bowel syndrome (SBS) comprises the sequelae of nutrient, fluid, and weight loss that occurs subsequent to greatly reduced functional surface area of the small intestine. Signs and symptoms of SBS include electrolyte disturbances; deficiencies of calcium, magnesium, zinc, iron, vitamin B12, or fat-soluble vitamin deficiency; malabsorption of carbohydrates, lactose, and protein; metabolic acidosis, gastric acid hypersecretion; formation of cholesterol biliary calculi and renal oxalate calculi; and dehydration, steatorrhea, diarrhea, and weight loss. Thorough nutritional management is the key factor in achieving an optimal outcome in SBS. Total parenteral nutrition is necessary in the early stages, as is replacement of excess fluid and electrolyte losses. Nutritional management of SBS has traditionally been divided into three phases: an acute phase when total parenteral nutrition is usually begun, an adaptation phase, and a maintenance phase. Recommendations regarding the need for parenteral nutrition vary depending on the presence or absence of certain factors: the ileocecal valve, jejunum, and functional colon. Patients with residual small bowel length of 100 cm or less usually require the administration of parenteral nutrition at home with good results. The total parenteral nutrition diet should consist of a majority of calories from fat, followed by protein, and the remaining as carbohydrates. Vitamins, minerals, and trace elements should also be added accordingly. Although total parenteral nutrition is initially necessary, treatment goals should focus on early transition to enteral nutrition followed by oral feeds. Other recent advances in the medical management of SBS include pharmacologic treatment and the use of specific nutrients and growth factors to stimulate intestinal absorption and adaptation. Both animal studies and clinical trials in humans have shown much promise in supplementation with growth factors and hormones. This strategy is likely to play a greater role in the treatment of SBS in the future.
 ...
PMID:Nutritional management of short bowel syndrome in adults. 1187 98

Hyperoxaluria is rarely considered as a cause of rapidly progressive renal failure. A case is reported of a patient in whom rapidly renal failure developed after subtotal small bowel resection. A diagnosis of calcium oxalate deposits nephropathy was confirmed by renal biopsy. This cause of renal failure may be underestimated and should be systematically searched for in all patients with malabsorption.
 ...
PMID:Hyperoxaluria: an underestimated cause of rapidly progressive renal failure. 1188 21

Short bowel syndrome is an uncommon disease that results from extensive intestinal resection. Short bowel patients develop severe malabsorption of macronutrients, micronutrients, electrolytes and water, and pose difficult management problems. This report describes a typical patient with the short bowel syndrome and how each component of the malabsorption syndrome is managed to maintain nutritional, electrolyte, and water balance. In practice, some short bowel patients become dependent on parenteral nutrition for life, while others become independent with time due to intestinal adaptation and can be managed on oral intake and supplementations. Short bowel patients are at risk of developing gallstones, oxalate kidney stones and, rarely, d-lactic acidosis, and the pathophysiology of these disease processes is outlined. A minority of short bowel patients may ultimately require intestinal transplantation due to irreversible complications, and the current status of this intervention is reviewed. Finally, growth factors that stimulate intestinal growth and, thus, enhance absorptive capacity, are currently being identified and may eventually be introduced in the treatment of these patients.
 ...
PMID:Short bowel syndrome. 1246 7

Secondary hyperoxaluria is due either to increased intestinal oxalate absorption or to excessive dietary oxalate intake. Certain intestinal diseases like short bowel syndrome, chronic inflammatory bowel disease or cystic fibrosis and other malabsorption syndromes are known to increase the risk of secondary hyperoxaluria. Although the urinary oxalate excretion is usually lower than in primary hyperoxaluria, it may still lead to significant morbidity by recurrent urolithiasis or progressive nephrocalcinosis. A clear distinction between primary and secondary hyperoxalurias is important. As correct classification may be difficult, appropriate diagnostic tools are needed to delineate the metabolic background as a basis for optimal treatment. We developed an individual approach for the evaluation of patients with suspected secondary hyperoxaluria. First, 24 h urines are examined repeatedly for lithogenic (e.g. calcium, oxalate, uric acid) and stone-inhibitory (e.g. citrate, magnesium) substances, and the patients are asked to fill in a dietary survey form. Urinary saturation is calculated using the computer based program EQUIL2, and the BONN-Risk-index is determined. The measurement of plasma oxalate and of urinary glycolate helps to distinguish between primary and secondary hyperoxalurias. If secondary hyperoxaluria is suspected, the stool is examined for Oxalobacter formigenes, an intestinal oxalate degrading bacterium, as lack or absence may lead to increased intestinal oxalate absorption. The last diagnostic step is to study the intestinal oxalate absorption using [13C2]oxalate. Depending on the results, various therapeutic options are available: 1) a diet low in oxalate, but normal or high in calcium, 2) a high fluid intake (>1.5 L/m2/d), 3) medications to increase the urinary solubility, 4) specific therapeutic measures in patients with malabsorption syndromes, depending on the underlying pathology, and 5) intestinal recolonization of Oxalobacter formigenes or the treatment with other oxalate degrading bacteria.
 ...
PMID:Diagnostic and therapeutic approaches in patients with secondary hyperoxaluria. 1295 11

Diarrhoea, malabsorption and malnutrition characterise the short bowel syndrome. The underlying gastrointestinal disorders, the types of intestinal resections performed and the subsequent pathophysiological situations are reviewed. Recommended therapeutic measures in the postoperative period as well as in the rehabilitation of patients with short bowel syndrome are discussed in more detail. In the postoperative period, parenteral nutrition is essential followed by an enteral diet to stimulate bowel adaptation, reduce fluid loss and increase nutrient absorption. The final diet should be based on the anatomy of the retained bowel (presence or absence of a colon and ileum). The importance of the colon as a digestive organ in patients with short bowel and the need of a low-oxalate diet are underlined. The possible benefit of new treatment options (glutamine, growth hormone and glucagon-like peptide 2) is discussed. Both typical complications of the short bowel syndrome and management of these complications are presented.
 ...
PMID:[Clinical management of patients with short bowel syndrome]. 1600 49

Orlistat is an oral inhibitor of gastrointestinal lipase used for weight reduction in obese patients. Although most adverse drug effects manifest in the gastrointestinal tract, this is the first reported case of orlistat-induced acute kidney injury secondary to acute oxalate nephropathy in a white woman with underlying chronic kidney disease. Acute kidney injury was associated temporally with an increased dose of orlistat and the development of increased fat malabsorption (more frequent loose oily stools). Urine sediment showed abundant calcium oxalate crystals and increased 24-hour urine oxalate concentration. Kidney biopsy showed deposition of calcium oxalate crystals within tubular lumens, consistent with acute oxalate nephropathy. Orlistat therapy was discontinued, and oral fluid intake was increased. A second kidney biopsy performed 1 month later to evaluate the slow resolution of kidney failure did not show calcium oxalate crystals within tubules. A steady improvement in renal function subsequently was observed. Results of a repeated 24-hour urine oxalate collection performed 3 weeks later when kidney function had improved were within normal limits.
 ...
PMID:Acute oxalate nephropathy associated with orlistat, a gastrointestinal lipase inhibitor. 1718 56

Orlistat, an anti-obesity drug, is a potent and specific inhibitor of intestinal lipases. In light of the recent US FDA approval of the over-the-counter sale of orlistat (60 mg three times daily), clinicians need to be aware that its use may be associated with less well known, but sometimes clinically relevant, adverse effects. More specifically, the use of orlistat has been associated with several mild-to-moderate gastrointestinal adverse effects, such as oily stools, diarrhoea, abdominal pain and faecal spotting. A few cases of serious hepatic adverse effects (cholelithiasis, cholostatic hepatitis and subacute liver failure) have been reported. However, the effects of orlistat on non-alcoholic fatty liver disease are beneficial. Orlistat-induced weight loss seems to have beneficial effects on blood pressure. No effect has been observed on calcium, phosphorus, magnesium, iron, copper or zinc balance or on bone biomarkers. Interestingly, the use of orlistat has been associated with rare cases of acute kidney injury, possibly due to the increased fat malabsorption resulting from the inhibition of pancreatic and gastric lipase by orlistat, leading to the formation of soaps with calcium and resulting in increased free oxalate absorption and enteric hyperoxaluria. Orlistat has a beneficial effect on carbohydrate metabolism. No significant effect on cancer risk has been reported with orlistat.Orlistat interferes with the absorption of many drugs (such as warfarin, amiodarone, ciclosporin and thyroxine as well as fat-soluble vitamins), affecting their bioavailability and effectiveness. This review considers orlistat-related adverse effects and drug interactions. The clinical relevance and pathogenesis of these effects is also discussed.
 ...
PMID:Orlistat-associated adverse effects and drug interactions: a critical review. 1809 46

Surgical intervention has become an accepted therapeutic alternative for the patient with medically complicated obesity. Multiple investigators have reported significant and sustained weight loss after bariatric surgery that is associated with improvement of many weight-related medical comorbidities, and statistically significant decreased overall mortality for surgically treated as compared with medically treated subjects. Although the Roux-en-Y gastric bypass (RYGB) is considered an acceptably safe treatment, an increasing number of patients are being recognized with nephrolithiasis after this, the most common bariatric surgery currently performed. The main risk factor appears to be hyperoxaluria, although low urine volume and citrate concentrations may contribute. The incidence of these urinary risk factors among the total post-RYGB population is unknown, but may be more than previously suspected based on small pilot studies. The etiology of the hyperoxaluria is unknown, but may be related to subtle and seemingly subclinical fat malabsorption. Clearly, further study is needed, especially to define better treatment options than the standard advice for a low-fat, low-oxalate diet, and use of calcium as an oxalate binder.
 ...
PMID:Nephrolithiasis after bariatric surgery for obesity. 1835 97

Calcium oxalate (CaOx) deposition in the renal allograft is an under recognized and important cause of acute tubular injury and early allograft dysfunction. We present a case of late transplant dysfunction due to acute oxalate nephropathy. The patient presented with diarrhea and deteriorating graft function, and a diagnosis of enteric hyperoxaluria secondary to pancreatic insufficiency was made. This had occurred, as the patient had been noncompliant with his pancreatic enzyme replacement therapy. Treatment to reduce his circulating oxalate load was initiated, including twice-daily hemodialysis, low fat and oxalate diet and appropriate administration of pancreatic enzyme supplements. Graft function subsequently recovered. The possibility of fat malabsorption leading to enteric hyperoxaluria should be considered in renal graft recipients presenting with loose stools and graft dysfunction.
 ...
PMID:Acute oxalate nephropathy causing late renal transplant dysfunction due to enteric hyperoxaluria. 1855 38

Bariatric surgery is now recognized as a sure and effective way for weight reduction in morbid obesity. However some procedures induce intestinal malabsorption leading to enteric hyperoxaluria. So bariatric surgery could place these patients not only at risk for nephrolithiasis but also for oxalate induced nephropathy and chronic renal failure. Because of the growing incidence of obesity worldwide, physicians and patients should be aware of such potential complications. There is no mean to discuss this treatment because of its spectacular efficiency on obesity and its comorbidities. But it is necessary to choose the surgical technique according to the risk factors of the patients. Following surgery, preventive treatment strategies are indicated, such as modified dietary lifestyle and specific drugs as we suggested to limit or even avoid these complications. However observance could fail in the long term. In case of oxalate nephropathy, surgery may be proposed to restore the intestinal tract but with the risk of overweight relapse. To illustrate this matter, we report here significant observations of three patients, which, having successfully benefited from the same bariatric surgery, have presented lithiasic complications for two of them and oxalate nephropathy leading to chronic renal failure and hemodialysis for the third.
 ...
PMID:[Bariatric surgery, calcium oxalate urinary stones and oxalate nephropathy]. 2113 57


<< Previous 1 2 3 4 5 6 7 8 Next >>