PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Blind Loop Syndrome”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1975

Small intestinal mucosal injury in the experimental blind loop syndrome. Light- and electron-microscopic and histochemical studies.

Microscopic (light and electron) and histochemical abnormalities have been demonstrated in the jejunum of rats with the blind loop syndrome. Three groups of animals were studied: normal control animals, and animals with either self-filling (SF) or self-emptying (SE) blind loops. Vitamin B12 malabsorption and bacterial overgrowth occurred only in those animals with SF blind loops. Three jejunal segments were studied: the blind loop segment and the jejunal segments proximal and distal to the blind loop. In the animals with the blind loop syndrome, those with SF blind loops, the most striking findings occurred in the blind loop itself, with similar but less marked changes in the jejunum distal but not proximal to the blind loop segment. Hypertrophy of both crypts and villi was evident with focal abnormalities of villus architecture. Approximately 10 to 20% of the columnar cells in the upper half of the villi were swollen and vesiculated. By electron microscopy microvilli demonstrated a variety of degeneration changes and the glycocalyx and terminal web were disrupted. Mitochondria and endoplasmic reticulum (ER), both smooth and rough, were swollen. Concentric whorls of parallel membranes and long, curvilinear rough ER were present in the cytoplasm. Histochemically, there was loss of enzymatic activity in the epithelial brush border, mitochondria and ER. Inasmuch as bacterial invasion of the jejunal mucosa was not seen, the etiology of these changes is not known but may involve bacterial "toxins" or products of bacterial metabolism. These morphological observations demonstrate that both brush border and intracellular injury occur in the jejunal epithelial cell of rats with the experimental blind loop syndrome.

Animals↗
PubMed1977

Brush border peptidases and arylamidases in the experimental blind loop syndrome of the rat.

Peptidase and arylamidase activities were assessed in purified brush borders from jejunum of rats with surgically created blind loops. The blind loop segment and the jejunum proximal and distal to the blind loop were studied. Comparable jejunal segments from control rats were also studied. The blind loop syndrome was documented by presence of macrocytic anemia. Enzyme activities were determined on purified brush borders. In rats with the blind loop syndromes enzymatic activities hydrolizing sucrose, L-Leucyl-beta-naphthylamide, L-lysyl-beta-naphthylamide, alpha-L-glutamyl-beta-naphthylamide, L-phenylalanyl-alanine and L-leucyl-glycine were significantly reduced as compared to controls (P less than 0.001). After a short course of antibiotic therapy enzymatic activities returned to normal. Our findings suggest a reversible intestinal mucosa damage in the rat with blind loop syndrome.

Aminopeptidases↗
PubMed1989

The deconjugation ability of bacteria isolated from the jejunal fluids in the blind loop syndrome with high 14CO2 excretion--using the breath analysis technique and thin-layer chromatography.

Five patients with blind loop syndrome (Billroth II) were examined by measuring 14CO2 specific activity of expired breath samples taken at intervals after a meal containing glycine-1-14C cholate. The 5 patients tested showed a marked increase of 14CO2 specific activity. Furthermore, the ability of deconjugation of bacteria isolated from the jejunal fluids in the efferent loop of these patients was tested by thin layer chromatography. The bacterial species identified from the samples were as follows: enterococcus, Lactobacillus (L) buchneri, L. bifidus, L. brevis, Eubacterium (E) lentum, Bacteroides (B) vulgaricus, B. filamentosum, Corynebacterium (C) granulosum, Escherichia (E) coli, Staphylococcus (S) epidermidis, and Aerobacter (A) aerogenes. These species of bacteria, except E. coli and A. aerogenes, showed the deconjugation ability by which conjugated bile acids in ox gall was hydrolyzed. Administration of chloramphenicol (1g per day for 14 days orally divided doses) to the 5 patients reduced 14CO2 specific activity significantly. On the other hand, 9 healthy men (control subjects) who were tested showed a flat curve, and 8 of the 9 had no growth of bacteria isolated from the jejunal fluids. The remaining healthy man showed an overgrowth of E. coli and Pseudomonas (P) aeruginosa, but the species did not have the ability of deconjugation. Thus, we concluded that the patients with blind loop syndrome(Billroth II) had the bacterial overgrowth in the efferent loop that contained species with deconjugation ability, and, as a result the bacterial overgrowth contributed to causing abnormalities (increased deconjugation) in the metabolism of bile acids in the small intestine. When the concentration of conjugated bile acids in the small intestine was reduced to levels below the critical micellar concentration by several factors, fat malabsorption and subsequent steatorrhea were induced (1,-4). Furthermore, H. Fromm and A. F. Hofmann presented in vivo that the patients with blind loop syndrome had fat malabsorption and the patients who had a high 14CO2 output after oral administration of glycine-1-14C cholate showed a low 14CO2 output after oral administration of antibiotic drug (5,6). However, there has been no report on the deconjugation ability of bile acids of bacteria isolated from the jejunal fluids in the efferent loop of patients with Billroth II who had positive breath tests.(ABSTRACT TRUNCATED AT 400 WORDS)

Bacteria↗
PubMed1975

Functional, biochemical and morphological alterations in the intestines of rats with an experimental blind-loop syndrome.

In rat self-filling blind loops and in the contiguous regions of the intestinal tract, considerable functional impairment, accompanied by pronounced morphological transformations of the mucosa, has been observed. The histological alterations consist of mucosal hypertrophy and a reduction in the villus height: crypt length ratio, which is indicative of a hyper-regenerative change. Various enzyme activities of the epithelial cells are reduced and the absorption otinal juices is greatly altered in favour of the free acids. Two mec,anisms have 0een dicids, or meta0olites from bacterial degradation, on the absorptive epithelium; 2. Reduced cellular maturity in response to the effect of bile acids and/or bacteria on the lifespan of the cells.

Animals↗
PubMed1981

Protein-losing enteropathy in the human and experimental rat blind-loop syndrome.

Protein-losing enteropathy in 2 human subjects with small intestine bacterial overgrowth is reported. Partial improvement in 1 and complete normalization in the 2nd, during long-term antibiotic therapy, demonstrate for the first time antibiotic reversibility of protein-losing enteropathy in the human blind-loop syndrome. Studies in rats with experimental jejunal blind loops revealed depressed serum protein levels and excessive fecal excretion of intravenously administered 51Cr as compared with nonoperated and surgical controls. Comparison of protein loss of rats with blind loops present for varying lengths of time and paired comparison of rats tested for protein loss at two different times revealed a relatively stable degree of protein loss once it was manifest. Reversal of protein loss with antibiotic therapy was accomplished in only a small percentage of rats, and in those only after prolonged therapy. Surgical extirpation of the blind loop from rats with protein-losing enteropathy consistently corrected the protein loss, although this correction was delayed up to 9 wk from the time of corrective surgery. These studies demonstrate (a) significant protein loss as one etiologic factor for protein metabolic disturbances in the human and experimental rat blind-loop syndrome, (b) the occurrence of intestinal protein loss as a manifestation of functionally significant mucosal injury in the contaminated nonstagnant small bowel as well as the stagnant part of the small intestine affected by bacterial overgrowth, and (c) the difficulty of reversing functionally significant mucosal injury in the blind-loop syndrome once it has been manifest.

Animals↗
PubMed1997

Blind loop syndrome: an unusual cause of panniculitis.

We describe a 52-year-old woman with panniculitis and blind loop syndrome. She had undergone a gastrectomy for peptic ulcer 4 years before. Tender erythematous nodules on her palms and soles were associated with diarrhea and weight loss. A biopsy specimen revealed septal and lobular panniculitis. A glucose hydrogen breath test was consistent with bacterial overgrowth. These results were consistent with panniculitis associated with a blind loop syndrome. Only four cases of this association have been reported previously.

Animals↗
PubMed1975

The uptake of vitamin B12 by the sediment of jejunal contents in patients with the blind-loop syndrome.

Following preincubation of intrinsic factor- (IF-) bound 57CoB12 with the jejunal sediments of 6 patients with the blind-loop syndrome, the mean uptake by the sediments of IF-57CoB12 (28.1 percent plus or minus 4.2 percent S,E.M.) was significantly higher than the mean uptake by jejunal sediments from 5 control patients (5.8 per cent plus or minus 3.5 percent) (p smaller than 0.01). The uptake by the sediments significantly decreased when the incubations were carried out in the presence of lincomycin and neomycin. The jejunal sediments from the patients with the blind-loop syndrome inhibited the uptake of IF-57CoB12 by perfused rat intestinal segments (p smaller than 0.01), whereas the sediments from the control patients had no such inhibitory effect (p smaller than 0.5).

Aged↗
PubMed1978

Enterotoxigenicity of colonising coliform bacteria in tropical sprue and blind-loop syndrome.

The enterotoxigenicity of strains of Klebsiella pneumoniae, Enterobacter cloacae, and Escherichia coli, which represented the predominant coliform species isolated from the jejunum of 12 patients with tropical sprue and 5 with the blind-loop syndrome, was quantitatively assessed in terms of the ability of toxin preparations to induce water secretion as assayed by in-vivo perfusion in the rat jejunum. All 12 patients with sprue harboured 1 or more highly toxigenic strains--14 of the 16 strains isolated from this group produced heat-labile and/or heat-stable toxins which were as potent as toxins derived from strains isolated from persons with acute diarrhoea and documented as toxigenic. None of the 9 strains isolated from patients with the blind-loop syndrome produced potent toxins. This difference between the coliform bacteria in sprue and the blind-loop syndrome probably accounts, at least partly, for the different intestinal response in these two disorders to contamination by these organisms.

Acute Disease↗
PubMed1978

Pathogenesis of mucosal injury in the blind loop syndrome.

Bacterial extracts were prepared from cultures originating in chronic self-filling intestinal blind loops in rats. Their ability to remove active maltase molecules from isolated brush border membranes was studied in vitro. Twelve strains in 51 tested, belonging to one of three species, Bacteroides fragilis, Clostridium perfringens, and Streptococcus fecalis, possessed maltase-releasing activity. The ability to remove maltase correlated well with the ability to hydrolyze p-nitrophenyl-tert-butyloxycarbonyl-l-alaninate (NBA), an ester substrate rapidly hydrolyzed by elastase, but not with substrated favored by tryhsin and chymotrypsin. Maltase-releasing activity from C. perfringens was strongly inhibited by soybean trypsin inhibitor and to a lesser extent by lima bean trypsin inhibitor. Of four chloromethylketone active-site directed inhibitors tested with specificities for elastase, trypsin, and chymotrypsin, inhibition was maximal with elastase-specific inhibitors. In two species, activity was shown to be heat sensitive, and to be inhibited by concentration of the extract. In one species maltase-releasing activity was shown to be due to an enzyme of molecular weight at least 66,000 with the capacity to remove lactase, sucrase, and alkaline phosphatase, as well as maltase. The results indicate that anaerobic or facultatively anaerobic species, previously identified with the pathology of of the blind loop syndrome, contain proteases which are capable of removing components of the intestinal surface membrane. These proteases appear to have elastase-like substrate specificity and may be involved in the etiology of disaccharidase deficiency in bacterial overgrowth syndromes.

Animals↗
PubMed1979

Sensitivity of bile acid breath test in the diagnosis of bacterial overgrowth in the small intestine with and without the stagnant (blind) loop syndrome.

The bile acid breath test was studied to examine its sensitivity for establishing the diagnosis of bacterial overgrowth in comparison to that of the Schilling test and small-intestinal cultures in 12 patients with a stagnant (blind) loop syndrome, as well as in 38 patients who had other conditions with suspected bacterial contamination of the small intestine. The presence of bile acid malabsorption was excluded in all 50 patients by studies of fecal excretion of radioactively labeled bile acids. The bile acid breath test was positive in 100% (12/12) of the patients with a stagnant (blind) loop syndrome, whereas 92% (11/12) had a positive Schilling test and 75% (9/12) a positive small-intestinal culture. The abnormal tests improved only in 2 of 4 patients treated with tetracycline. In the group of 38 patients without demonstrable dilated or blind loops of small bowel who were suspected of having bacterial contamination of small bowel, the bile acid breath test was positive in 53% (20/38), the Schilling test in 39% (15/38), and the small-intestinal culture in 45% (17/38). The difference in the incidence of positive results between the tests in the two patient groups was statistically not significant. The findings of these studies have the following diagnostic implications: (1) Bile acid breath test, Schilling test, and cultures of aspirates from the upper small bowel are of comparable sensitivity in the detection of bacterial overgrowth in the small intestine. (2) A negative bile acid breath test makes the diagnosis of a stagnant (blind) loop syndrome very unlikely.

Bacteria↗
PubMedDate not supplied

Osteomalacia complicating a blind loop syndrome from congenital megaesophagus-megaduodenum.

A young female with osteomalacia complicating a blind loop syndrome associated with congenital megaduodenum is described. In this case, the correction of vitamin D malabsorption by administration of antibiotics highlights the role of massive intraluminal bacterial overgrowth from destruction of vitamin D, or decreased unicellar solubilization due to deconjugation of biliary acids. The importance of cutaneous vitamin D synthesis in patients with osteomalacia of gastrointestinal origin is emphasized. The detection of megaduodenum and megaesophagus in the patient's father may be the first report of a familial association of these gastrointestinal abnormalities.

Abnormalities, Multiple↗
PubMed2001

Blind loop syndrome after biliopancreatic diversion: a diagnostic challenge.

BACKGROUND: Biliopancreatic diversion (BPD) according to Scopinaro's method is a safe and effective technique for treatment of morbid obesity. In this operation a side-to-side enteroenterostomy is created 60 cm proximal to the ileocecal valve. Malabsorption of fat and starch is one of the main goals of the BPD. Ingestion of an excess of fat leads to steatorrhea. As a side-effect, malabsorption of iron, calcium and other elements can occur causing anemia and hypocalcemia. The blind loop syndrome gives the same symptoms. METHODS: A lady was admitted with a long history of steatorrhea, anemia and hypocalcemia due to a blind loop syndrome after a BPD. The diagnostic problem in this patient is illustrated. RESULTS: The diagnosis was only made at exploratory laparotomy. CONCLUSION: The blind loop syndrome was then treated with resection of the blind loop and antibiotics.

Adult↗
PubMed1979

Protein digestion and absorption in the blind loop syndrome.

Protein digestion and absorption was studied in rats with 6-week-old surgically constructed self-filling intestinal blind loops and steatorrhea, ie, blind-loop animals and controls were fed a 14C-labeled protein meal containing a nonabsorbable marker, 51CrCl3, and sacrificed 1 or 2 hr later. Intestinal contents were analyzed for 14C, 51Cr, protein, trypsin, and the products of digestion. At 1 hr, 14C absorption was greater in controls, but at 2 hr there was no difference in absorption between the two groups. Marker studies showed that blind-loop filling resulted in a delay of the progression of intestinal contents distally. Intraluminal trypsin and porteolysis were similar in the two groups. Endogenous protein was greater in the blind-loop animals. The early stages of the blind-loop syndrome may be characterized by delayed protein absorption secondary to blind-loop filling, which is compensated for by the distal gut resulting in an absence of overall protein malabsorption.

Animals↗