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Query: UMLS:C0042961 (volvulus)
 4,305 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Conditions which resulted in colonic preservation such as strangulated hernia, intestinal volvulus, and mesenteric infarction were once the main reasons for a major intestinal resection leading to the short bowel syndrome. Now Crohn's disease is the most common underlying diagnosis; such patients often have a jejunostomy. A measurement of the residual jejunal length from the duodenojejunal flexure makes possible predictions of patient outcome. Patients with a jejunostomy and less than 100 cm jejunum usually need long-term parenteral support, whereas 50 cm or more of jejunum usually suffices for adequate oral nutrition if the colon is preserved. While patients with and without a colon have problems with nutrient absorption, those with a jejunostomy also have problems of water, sodium and magnesium losses. Stomal losses may exceed oral intake and all such patients ('secretors') need parenteral supplements. Fluid and sodium losses can be reduced by octreotide, omeprazole or H2 blockers but not sufficiently to avoid the need for intravenous supplements. Colonic preservation increases the incidence of calcium oxalate renal stones (20%). Patients with and without a colon have a high prevalence of gallstones (40%). Clinically important intestinal adaptation occurs in those with a colon but not in those with a jejunostomy. Many surgical techniques, including small bowel transplantation, have been suggested to improve absorption, but as the quality of life of most patients with a short bowel is good with current treatments, they are not at present recommended.
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PMID:The short bowel syndrome: what's new and old? 844 53

Although urolithiasis is common in spinal cord injury patients, it is presumed that the predisposing factors for urinary stones in spinal cord injury patients are immobilization-induced hypercalciuria in the initial period after spinal injury and, in later stages, urine infection by urease-producing micro-organisms, e.g., Proteus sp., which cause struvite stones. We describe a patient who sustained C-7 complete tetraplegia in a road traffic accident in 1970, when he was 16 years old. Left ureterolithotomy was performed in 1971 followed by left nephrectomy in 1972. Probably due to adhesions, this patient developed volvulus of the intestine in 1974. As he had complete tetraplegia, he did not feel pain in the abdomen and there was a delay in the diagnosis of volvulus, which led to ischemia of a large segment of the small bowel. All but 1 ft of jejunum and 1 ft of ileum were resected leaving the large bowel intact. In 1998, suprapubic cystostomy was performed. In 2004, this patient developed calculus in the solitary right kidney. Complete stone clearance was achieved by extracorporeal shock wave lithotripsy. Stone analysis: calcium oxalate 60% and calcium phosphate 40%. Metabolic evaluation revealed hyperoxaluria, hypocitraturia, and hypomagnesiuria. Since this patient had hyperoxaluria, the stool was tested for Oxalobacter formigenes, a specific oxalate-degrading, anerobic bacterium inhabiting the gastrointestinal tracts of humans; absence of this bacterium appears to be a risk factor for development of hyperoxaluria and, subsequently, calcium oxalate kidney stone disease. DNA from the stool was extracted using the QIAamp DNA stool Mini Kit (Qiagen, Chatsworth, CA). The genomic DNA was amplified by polymerase chain reaction using specific primers for oxc gene (developed by Sidhu and associates). The stool sample tested negative for O. formigenes. The patient was prescribed potassium citrate mixture; he was advised to avoid oxalate-rich food, maintain recommended levels of calcium in his diet, and take live bio-yogurt. Two months later, 24-h urinary oxalate decreased from 0.618 to 0.411 mmol/day; 24-h urine citrate increased from 0.58 to 1.10 mmol/day. Six months later, an oxalate absorption test was performed. The patient swallowed a capsule, soluble in gastric juice, containing 50 mg (0.37 mmol) sodium [13C2]oxalate corresponding to 33.8 mg of [13C2]oxalic acid. The amount of labeled oxalate, excreted in urine, was measured by a gas chromatographic-mass spectrometric assay. Oxalate absorption, expressed as the percentage of the labeled dose recovered in the 24-h urine after dosing, was 8.3% (reference range: 2.3-17.5%). In addition to other conventional measures, oral administration of O. formigenes or lactic acid bacteria mixture to promote bacterial degradation of oxalate in the gut, and thus combat hyperoxaluria, may play a role in prevention of calcium oxalate kidney stones.
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PMID:Hyperoxaluria, hypocitraturia, hypomagnesiuria, and lack of intestinal colonization by Oxalobacter formigenes in a cervical spinal cord injury patient with suprapubic cystostomy, short bowel, and nephrolithiasis. 1761 9