OBJECTIVE To compare the complication rates and outcomes in cats with ureteral obstruction treated by placement of double-pigtail ureteral stents or ureteral bypass (UB) devices. DESIGN Retrospective cohort study. ANIMALS Cats with unilateral or bilateral ureterolithiasis that received double-pigtail ureteral stents (30 stents in 27 cats; stent group) or UB devices (30 devices in 23 cats; UB group). PROCEDURES Medical records were reviewed to collect data on signalment, clinical signs, serum biochemical data, surgical procedure, duration of hospitalization, complications, and follow-up (≥ 6 months after placement) information. Outcomes were compared between device types. RESULTS Median durations of surgery and hospitalization were significantly longer in the stent versus UB group. Perioperative mortality rate was 18% (5/27) in the stent group and 13% (3/23) in the UB group. Median survival time was shorter in the stent versus UB group. Stent placement was associated with a greater risk of lower urinary tract-related signs, such as hematuria (52% [14/27]) and pollakiuria or stranguria (48% [13/27]). The risk of device occlusion was also greater in the stent (26% [7/27]) versus UB (4% [1/23]) group. The percentage of cats requiring additional procedures to treat complications was greater in the stent (44%; complications included uroabdomen, stent occlusion, and refractory cystitis) versus UB (9%; complications included UB occlusion and urethral obstruction) group. CONCLUSIONS AND CLINICAL RELEVANCE Although the benefits of stent placement in the treatment of ureteral obstruction in cats have been established, results suggested that cats treated with UB devices had a lower risk of complications and a longer survival time than those treated with double-pigtail ureteral stents.
Lymphoma may be a frequent cause of spontaneous perforation in cats. Therefore, histological examination of ulceration is essential in all cases. The direct and sole implication of anti-inflammatory administration in a gastrointestinal perforation is not clearly established in this study.
Increased consumption of energy-rich foods is a key factor in overweight, obesity, and associated metabolic disorders. This would be, at least in part, related to microbiota disturbance. In rodent models of obesity, microbiota disruption has been associated with alteration of the intestinal barrier, endotoxemia, inflammation grade, and insulin sensitivity. The aim of the present study was to assess the effects of a high-fat diet (HFD), fed at two energetic levels, on microbiota, intestinal barrier, and inflammatory and metabolic parameters in dogs. A HFD (33% fat as fed, 4,830 kcal/kg) was given to 24 healthy Beagle dogs at 100% (HF-100; n = 8) and at 150% (HF-150; n = 16) of their maintenance energy requirements for 8 weeks. Analysis of similarity revealed a significant difference in gut microbiota β-diversity following the diet compared to week 0 in both groups while α-diversity was lower only in the HF-150 group. Firmicutes/Bacteroidetes ratio was higher in the HF-150 group compared to the HF-100 group at weeks 2 and 8. A reduction in insulin sensitivity was observed over time in the HF150 group. Neither endotoxemia nor inflammation was observed in either group, did not find supporting data for the hypothesis that the microbiota is involved in the decline of insulin sensitivity through metabolic endotoxemia and low-grade inflammation. Colonic permeability was increased at week 4 in both groups and returned to initial levels at week 8, and was associated with modifications to the expression of genes involved in colonic barrier function. The increase in intestinal permeability may have been caused by the altered intestinal microbiota and increased expression of genes encoding tight junction proteins might indicate a compensatory mechanism to restore normal permeability. Although simultaneous changes to the microbiota, barrier permeability, inflammatory, and metabolic status have not been observed, such a causal link cannot be excluded in dogs overfed on a HFD. Further studies are necessary to better understand the link between HFD, intestinal microbiota and the host.
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