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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During the past several years there has been increasing interest in refunctionalizing patients who have undergone radical extirpative surgery for pelvic malignancies and patients with dysfunctional bladders. To accomplish this, intestinal segments have been successfully employed in a variety of configurations. Independent of their optimal urosurgical implementation these procedures are not without potential complications, a significant portion of which involve metabolic derangements. Besides first follow-up results of patients with bladder substitution or continent urinary diversion, analysis of experimental investigations and functionally comparable clinical conditions enables an insight into potential following physiopathological interrelationships. These concern, besides the problem of chronic metabolic acidosis, disorders of bile acid and vitamin B12 metabolism as well as the potential induction of a secondary hyperoxaluria with subsequent oxalate concrement diathesis. Furthermore, there may be a malabsorption of calcium and vitamin D with development of intestinal osteopathy due to the reduction of absorptive surface. Apart from these problems of enteral loss and deficiency manifestations, several case reports and investigations suggest that bone demineralization can occur as a consequence of chronic metabolic acidosis and patients are at risk of skeletal demineralization. The pathogenesis of this association has yet to be clarified. These physiopathological interrelationships must be considered in medical attendance of patients with intestinal substitute bladders and continent supravesical pouch systems over many years. As these procedures become more popular, it becomes important to identify any metabolic changes that may occur as their consequence.
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PMID:[Bladder replacement and continent diversion: what about metabolic complications?]. 184 45

The active transport of conjugated bile acids by the ileum is responsible for the enterohepatic circulation of bile acids, a physiological process that ensures an ample supply to the intestine of these key biological surfactants, irrespective of the rate of their biosynthesis from cholesterol. The ileal bile acid transport system is a high capacity, low affinity secondary active Na+ co-transport system that differs in substrate specificity from that present in the hepatocyte. Ileal transport is homeostatically regulated by feedback inhibition of the bile acids that are transported. The enterohepatic circulation is responsible for the concentration profile present in the intestine--high concentrations in the small intestine and low concentrations in the large intestine. Loss of ileal absorption, when mild, leads to a sequence of events that result in increased concentrations in the large intestine causing diarrhea. Severe bile acid malabsorption causes decreased concentrations in the small intestine which in turn lead to fat maldigestion and fat malabsorption. The increased passage of fatty acids into the colon contributes to diarrhea. Fat maldigestion and malabsorption also causes increased absorption of dietary oxalate from the colon which causes hyperoxaluria and contributes to nephrolithiasis. In cholestatic liver disease, inappropriate upregulation of ileal bile acid transport is likely to cause retention of hepatotoxic endogenous bile acids. In familial hypercholesterolemia, efficient bile acid absorption contributes to downregulation of LDL receptors and the maintenance of elevated plasma cholesterol levels; upregulation of bile acid transport during bile acid sequestrant therapy could diminish its efficacy. Efforts are in progress to develop a suitable bile acid analogue to be administered orally for conditions of bile acid deficiency in the small intestine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biological and medical aspects of active ileal transport of bile acids. 206 93

The role of the kidney in states of hyperoxaluria and hypercalciuria was investigated in seven patients with hyperoxaluria after jejunoileal bypass (JIB) and six patients with idiopathic hypercalciuria (IHC). Eight apparently healthy persons formed a control group. Besides hyperoxaluria, the patients with JIB displayed an elevated plasma concentration of oxalate and the oxalate clearance was increased and higher than creatinine clearance, indicating a net tubular secretion of oxalate. The JIB patients had lower 24-h urinary excretions of calcium, phosphate, magnesium and citrate and higher serum parathyroid hormone (PTH) than controls, indicating increased secretion of PTH to compensate for calcium malabsorption. IHC patients exhibited increased fasting urinary calcium even though their serum values were similar to those in the controls. These results indicate a reduced tubular calcium reabsorption, which was most pronounced in patients with highest PTH values. We conclude that hyperoxaluria in JIB patients is associated both with intestinal hyperabsorption and with enhanced tubular secretion of oxalate, and that in some patients with IHC hypercalciuria is due to reduced tubular reabsorption of calcium.
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PMID:Hyperoxaluria or hypercalciuria in nephrolithiasis: the importance of renal tubular functions. 212 87

Enteric hyperoxaluria due to malabsorption syndromes has been well documented to cause renal calculi and chronic tubulointerstitial renal damage. Rarely, in the setting of intestinal bypass operations for morbid obesity, enteric hyperoxaluria has produced acute renal failure. We report two patients who suffered acute deterioration of renal function associated with increased intestinal absorption and renal excretion of oxalate associated with steatorrhea. One patient had a large portion of his small bowel resected many years prior to the onset of the renal failure and the second patient had chronic pancreatitis causing steatorrhea. Both patients had renal biopsy documentation of the acute nature of the tubular damage produced by oxalate deposition. The mechanisms of their deterioration of renal function may relate to sudden increases in steatorrhea in association with episodes of volume depletion. Enteric hyperoxaluria may be an easily overlooked and potentially preventable etiology of acute renal dysfunction.
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PMID:Acute deterioration of renal function associated with enteric hyperoxaluria. 222 62

Jejunoileal bypass (JIB) has been widely performed for treatment of excessive obesity. Formation of calcium oxalate stones is a common side effect. Since, under physiological conditions, the intestinal absorption of calcium and that of oxalate are interrelated, intestinal oxalate and calcium absorption were measured in the present study by isotope techniques in 19 JIB patients and 20 healthy controls. The JIB patients showed pronounced hyperoxaluria and markedly increased absorption of oxalate, with a urinary excretion of 14C-oxalate of 29 +/- 19% (controls 6.2 +/- 3.7%; p less than 0.001). There was a strong correlation between the intestinal absorption and urinary excretion of oxalate in the JIB patients (r = 0.72; p less than 0.001). Furthermore, their oxalate kinetics was altered, with continued urinary excretion of 14C-oxalate for up to 48 hours. The JIB patients also had reduced calcium absorption (36 +/- 9.1% vs. 47 +/- 9.0%; p less than 0.001) and patients with malabsorption of calcium and low urinary calcium had the highest intestinal absorption and urinary excretion of oxalate. It is concluded that hyperoxaluria in JIB patients is due to a significant extent to hyperabsorption of oxalate.
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PMID:Intestinal absorption of oxalate and calcium in patients with jejunoileal bypass. 259 24

Urinary oxalate concentrations were measured in 45 patients with quiescent Crohn's disease, four patients with chronic pancreatitis and five healthy subjects after a normal oxalate (150 g/day) diet, after a high-fat (150 g/day), normal oxalate diet and after and after a high-oxalate (500 mg/day) diet. Urinary oxalate concentrations were significantly (P less than 0.05) higher in patients with Crohn's disease and steatorrhoea, but not in those with chronic pancreatitis, after administrating a high-oxalate diet compared with healthy subjects. Mean oxalate values were 19.1 mg/24 h in controls compared with 65.8 mg/24 h in Crohn's disease patients. A direct correlation (r = 0.37, P less than 0.01) was established between faecal rats and urinary oxalate after oval oxalate load: this correlation (r = 0.43, P less than 0.01) is closer when only patients with Crohn's disease are considered. The study, therefore, confirmed a correlation between steatorrhoea and hyperoxaluria in patients with Crohn's disease; however, the high percentage of false positive results limits the use of urinary oxalate concentrations as a reliable indicator of lipid malabsorption. It is concluded that, at present, measurement of urinary oxalate cannot be recommended as a valid alternative to the Van de Kamer method for diagnosing lipid malabsorption.
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PMID:Urinary oxalate recovery after oral oxalic load: an alternative method to the quantitative determination of stool fat for the diagnosis of lipid malabsorption. 262 29

Hyperoxaluria and hypercalciuria are common features of renal calcium stone disease. The purpose of the present investigation was to examine the relationships between the intestinal absorption and the renal handling of oxalate and calcium in patients with idiopathic renal stone disease and in patients with enteric hyperoxaluria following jejunoileal bypass (JIB), in comparison with healthy controls. Hyperoxaluria was associated with a higher frequency of both stone episodes and stone operations than a lower urinary oxalate concentration. Patients with idiopathic stone disease showed increased intestinal uptake of both oxalate and calcium, which was probably of importance for their propensity to form calcium oxalate-containing stones. Hyperoxaluria in patients with JIB was found to be a result of hyperabsorption of oxalate, and these patients displayed altered oxalate kinetics with continued urinary excretion of orally administered 14C-oxalate for more than 48 hours. The prolonged excretion is assumed to be due to a prolonged absorption and/or an increased oxalate pool. Malabsorption of calcium and low fasting urinary calcium excretion in the JIB patients were associated with high tubular reabsorption of calcium, the latter presumably attributable to a compensatory increase in circulating parathyroid hormone (PTH). In most recurrent renal stone formers the urinary calcium concentration was increased, with an inverse relationship to serum PTH, indicating intestinal hyperabsorption of calcium. A subgroup of hypercalciuric patients showed increased urinary calcium due to reduced tubular reabsorption of calcium. It is suggested that this is a renal defect resulting in a compensatory rise in PTH. Two different mechanisms of similar prevalence might explain enhanced secretion of PTH in normocalcaemic stone disease, namely reduced calcium absorption and a renal defect in the form of reduced tubular reabsorption of calcium. Glycosaminoglycans efficiently inhibit calcium oxalate crystal growth by binding to the surface of calcium oxalate crystals. In this study the binding was dependent on ionic strength. Higher affinity to the crystals may be the reason why highly charged glycosaminoglycans were more efficient inhibitors of calcium oxalate crystal growth. A calcium-containing organic marine hydrocolloid with the capacity to bind oxalate in vitro was shown to reduce enteric hyperoxaluria. In addition to biochemical effects considerable improvements in diarrhoeal symptoms were reported.
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PMID:Oxalate metabolism in renal stone disease with special reference to calcium metabolism and intestinal absorption. 266 21

The formation of a neobladder by the transformation of sections of the terminal ileum has become an important alternative to supravesical urinary diversion. The discussion about the optimal urosurgical technique however has, so far ignored the problems of consecutive enteric defunctionalization and deficiency symptoms resulting from the anatomical shortening of the ileum. The analysis of experimental investigations and functionally comparable syndromes, such as Crohn's disease, permits an insight into the pathophysiological consequences. These relate to disorders in the bile acid and vitamin B12 metabolism and to the potential induction of a secondary hyperoxaluria, with a subsequent oxalate calculus diathesis. Further more, the reduction of the absorption area in the ileum can lead to calcium and vitamin D malabsorption with the development of intestinal osteopathy. These pathophysiological relationships must be taken into account in the long-term medical care of patients with ileal neobladder. The preventive and therapeutic measures are described.
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PMID:[Ileocystoplasty and enteropathies]. 276 94

One hundred and sixty three children who received total parenteral nutrition (TPN), including 7 cases of short bowel syndrome, were studied to evaluate the role of TPN in the management of infants with extremely short bowel. Three of the seven were died of sepsis related with central venous catheter (CV catheter) during the period of malabsorption when TPN was necessary. Two children of other diseases were died of catheter sepsis, 5 out of 163 in total, making the mortality late of TPN 3%. Incidence of CV catheter related complications was significantly less frequent in Broviac catheter when compared with conventional Silastic catheter (p less than 0.01). Another significant complication of TPN in cases of short bowel syndrome was hepatic dysfunction. Cholestatic liver dysfunction seemed to be cleared when enteral feeding was started even with TPN going on. Oral feeding should be started in the early postoperative period with concomitant TPN covering the fluid loss. A case of copper deficiency with high output jejunostomy and a case of urolithiasis with hyperoxaluria complicated with short bowel were reported.
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PMID:[Long-term TPN for short bowel syndrome]. 314 68

The increased oxalic acid absorption is a well documented finding in gastroenterological diseases. The malabsorption of bile acids and fat is important in the pathogenesis of the hyperoxaluria. The enteric absorption of 14C-labelled oxalic acid was measured in 49 patients with different diseases. The dihydroxy-trihydroxy-ratio of bile acids is significantly decreased in patients with hyperoxaluria over 20% of the ingested dosage. We didn't find any correlation between the excretion of oxalic acid and the intraduodenal pancreatic lipase activity.
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PMID:[Pancreatico-biliary secretion in enteral hyperoxaluria]. 325 36


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