Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020500 (hyperoxaluria)
 912 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

143 patients (70 patients with Crohn's disease, 11 with ulcerative colitis, 40 with an intestinal by-pass operation, 9 with non-tropical sprue, 10 with short bowel syndrome, and 3 with other gastrointestinal disease) were studied during a metabolic regime including a fixed oral supply of 70 g fat, 800 mg calcium, and 200 mg oxalate. Faecal fat, 47Ca-absorption, 14C-oxalate absorption, and renal oxalate excretion were measured, and in the majority of patients a 14C-glyco-cholic acid breath test was also performed. 14Ca-absorption was practically identical (r = 0.92), whether determined by whole-body counting or from the accumulation of absorbed 47Ca in the skeleton of the underarm. 14C-oxalate absorption and renal oxalate excretion agreed well (r = 0.85). Steatorrhoea correlated weakly with renal oxalate excretion (r = 0.63, p less than 0.001), whereas no correlation was present between faecal fat and calcium absorption or between oxalate and calcium absorption under the constant conditions prevailing during the study. It is recommended that a "trifixed" regime with absorption studies of fat, calcium, and oxalate be undertaken previous to therapy that aims at a reduction of steatorrhoea or hyperoxaluria or an improvement of calcium absorption in chronic malabsorption syndromes, not least because therapy of these categories of patients most often continues for years.
 ...
PMID:Standardized ("trifixed") diet in the study of chronic malabsorption syndromes. 67 51

Evidence is presented that many of the enteric and systemic manifestations after jejunoileal bypass can be related to an inflammatory process within the bypassed small bowel rather than to the surgically induced sequelae of a short bowel syndrome with malabsorption. Invasion of the excluded segment by fecal flora was associated with a histologically demonstrable inflammatory response of the mucosa. The disorder was of variable severity and duration and occurred in the majority of 28 bypass patients. Progression to a clinical syndrome resembling an acute abdomen occurred in about 15% of the patients. Small bowel ileus and, in some patients, obstruction of the colon were suggested by physical signs and x-ray findings. Surgical exploration in such instances demonstrated an inflammaotry process of the excluded small bowel loops with severe distention of this segment and of the colon, but not organic obstruction. Pneumatosis cystoides intestinalis was a sequal in two patients. Exudative protein loss was documented in the severe cases. Most of the systemic sequelae are comparable to those seen with inflammatory diseases of the bowel such as Crohn's disease. Fever, excessive weight and lean tissue loss, and the involvement of skin, blood vessels, joints and possibly, the liver suggest an immune response as a common factor in the pathogenesis. The clinical improvement with antibiotics such as metronidazole or with restitution of normal bowel continuity indicates that the bacterial flora in the excluded small bowel segment or its byproducts are causally related to the systemic complications. Hyperoxaluria may be primarily the sequela of steatorrhea and not of the inflammatory process.
 ...
PMID:Bypass enteropathy: an inflammatory process in the excluded segment with systemic complications. 83 42

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.
 ...
PMID:[Long-term TPN for short bowel syndrome]. 314 68

We report a case of urolithiasis associated with short bowel syndrome. A 56-year-old woman was admitted to our hospital for asymptomatic bilateral renal stones. She had received extensive resection of small intestine due to strangulating obstructive ileus 7 years ago (residual intestine, only 20 cm). Subsequently, she was in a state of short bowel syndrome. Plain film of kidney, uteter, bladder and computed tomography revealed bilateral renal stones (right 4 mm, left 10 mm). The left renal stone was successfully treated by extracorporeal shock wave lithotripsy. Since the right renal stone was small, no treatment was performed. The stone fragments were composed of calcium oxalate and calcium phosphate, and excessive urinary excretion of oxalate (103.8 mg/day) was observed. In this patient, urolithiasis was diagnosed to be due to enteric hyperoxaluria caused by short bowel syndrome. To prevent the recurrence of stone formation, she was treated with oral administration of calcium lactate, sodium/potassium citrate and magnesium oxide. We review the Japanese literatures on urolithiasis with short bowel syndrome.
 ...
PMID:[A case of urolithiasis associated with short bowel syndrome]. 1263 4

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

The formation of renal calculi secondary to enteric hyperoxaluria is rare in the paediatric population. We present the case of an 8-year-old boy who had short bowel syndrome resulting in enteric hyperoxaluria which led to the development of urolithiasis and bilateral ureteric strictures, both of which resolved with medical management. We also review the literature on enteric hyperoxaluria.
 ...
PMID:Case report of paediatric oxalate urolithiasis and a review of enteric hyperoxaluria. 1966 61

Acute oxalate nephropathy can occur due to primary hyperoxaluria and secondary hyperoxaluria. The primary hyperoxalurias are a group of autosomal recessive disorders of endogenous oxalate overproduction. Secondary hyperoxaluria may occur as a result of excess dietary intake, poisoning with oxalate precursors (ethylene glycol), or enteric hyperoxaluria. The differential diagnosis of enteric hyperoxaluria includes inflammatory bowel disease, short bowel syndrome, bariatric surgery (with jejunoileal bypass or Roux-en-Y gastric bypass), celiac disease, partial colectomy, and chronic pancreatitis. The common etiology in all these processes is fat malabsorption, steatorrhea, saponification of calcium, and absorption of free oxalate. Hyperoxaluria causes increased urinary oxalate excretion, urolithiasis (promoted by hypovolemia, decreased urinary pH caused by metabolic acidosis, and decreased citrate and magnesium concentrations in urine), tubulointerstitial oxalate deposits, and tubulointerstitial nephritis. We report a rare case of acute oxalate nephropathy due to pancreatic atrophy and exocrine insufficiency caused by newly diagnosed pancreatic cancer.
...
PMID:Acute oxalate nephropathy due to pancreatic atrophy in newly diagnosed pancreatic carcinoma. 2661 99