NURSING PATIENTS UNDERGOING SURGERY FOR ULCERATIVE COLITIS.
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A case of thrombophlebitis migrans in ulcerative colitis in a Maltese housewife is reported. The association of thrombo-embolic disease and ulcerative colitis is reviewed.
BACKGROUND AND PURPOSE: Patients with ulcerative colitis have a higher rate of tubular nephropathies. Data concerning the cause of these lesions is rare and inconsistent, the occurrence may be part of the disease itself or a side effect of 5-aminosalicylates (5-ASA). This study investigated proteinuria and eosinophiluria in patients with moderate ulcerative colitis under treatment with 5-ASA. PATIENTS AND METHODS: Urine specimens (microelectrophoresis and eosinophiluria) of 34 patients with acute onset of moderate ulcerative colitis who were treated only with 5-ASA as active drug were analyzed. RESULTS: Data of 27 patients could be evaluated. Twelve patients had tubular proteinuria previous to treatment. By the end of the study, urine specimens normalized in six, in further six the proteinuria remained unaltered, two patients developed proteinuria under treatment. In 14 patients, proteinuria was not detectable at any time. Eosinophiluria was found in none of the specimens. CONCLUSION: Under treatment with 5-ASA no toxic or allergic nephropathy developed. One initially pathologic urine specimen normalized under treatment coming along with remission of the intestinal symptoms and histological findings. This indicates an association between the activity of the ulcerative colitis and might be caused by renal excretion of pro-inflammatory cytokines.
BACKGROUND: The aetiology of bone loss in ulcerative colitis is multifactorial, but corticosteroid treatment is an important risk factor. A novel formulation of Eudragit-L-coated prednisolone metasulphobenzoate (Predocol) has been developed, in order to deliver high mucosal levels of prednisolone within the colon but with little systemic absorption. The aim of this study was to investigate its efficacy, and short-term effects on bone formation and bone mineral density. METHODS: In a 12-week longitudinal study 13 patients with active colitis were treated with a reducing dose of Predocol. Disease activity scores were recorded and the bone formation marker osteocalcin was measured before, during and after treatment, with hip and spine bone mineral density assessed at baseline and after treatment. RESULTS: Eleven of the 13 patients completed the study. Compared with baseline, disease activity scores improved significantly after 4 weeks [difference in means, 6.9; 95% confidence interval (CI), 5.2, 8.7; P < 0.0001] and 12 weeks (difference in means, 5.7; 95% CI, 3.3, 8.2; P < 0.0001) of treatment. Osteocalcin did not fall compared with baseline [16.91 mg/l (95% CI, 12.70, 21.12)], after 4 weeks [13.67 mg/l (95% CI, 8.72, 18.60)] (difference in means, 3.25; 95% CI, 2.37, 8.87; P = 0.23) or 12 weeks [23.91 mg/l (95% CI, 16.10, 31.74)] (difference in means, 13.23; 95% CI, 2.45, 16.48; P = 0.13) of treatment. Similarly, bone mineral density at the hip [0.99 g/cm (95% CI, 0.90, 1.09)] did not change after 12 weeks of treatment [1.00 g/cm (95% CI, 0.89, 1.11)] (difference in means, 0.01; 95% CI, 0.25, 0.34; P = 0.74). Spine bone mineral density did not fall from pre-treatment levels [1.20 g/cm (95% CI, 1.11, 1.30)] after 12 weeks [1.19 g/cm (95% CI, 1.10, 1.29)] (difference in means, 0.01; 95% CI, 0.004, 0.01; P = 0.26). CONCLUSIONS: These results confirm that Predocol is effective treatment for acute ulcerative colitis and short courses of the steroid have no adverse effects on bone formation and bone mineral density. The encouraging results from this study suggest that Predocol may be a significant advance in preventing corticosteroid induced bone loss in ulcerative colitis.
A 27-year-old woman with a 9-year history of ulcerative colitis involving the entire colon was admitted to our hospital in August 1992 because of bloody stools and left lower abdominal pain. She had been treated with sulfasalazine since 1983 and the colitis had been clinically quiescent or mild for 7 years. She had also been diagnosed as having primary sclerosing cholangitis (PSC) 4 years prior to this admission, based on the clinical, laboratory, and cholangiographic findings. A barium enema and colonoscopy showed an irregular mass obstructing the bowel lumen in the distal portion of the descending colon. Biopsy specimens taken from the mass revealed moderately differentiated adenocarcinoma, and a subtotal colectomy was performed. Histologic examination of the mass lesion showed moderately differentiated adenocarcinoma invading the pericolic adipose tissue. She is currently alive 3 years after surgery. PSC has recently been reported as a risk factor for colonic neoplasia in patients with long-standing ulcerative colitis. In Japan, however, colorectal cancer associated with PSC and ulcerative colitis has rarely been reported. The present case suggests that the risk of colonic cancer is higher in patients with ulcerative colitis and PSC than in patients with ulcerative colitis alone.
Ulcerative colitis and obesity share a systemic chronic inflammatory response manifested by increased inflammatory markers. There are data suggesting a benefit in both diseases after inflammatory markers are decreased. We present a 39-year-old morbidly obese male with a history of ulcerative colitis who manifested significant symptomatic improvement after an 86.8% excess weight loss following gastric bypass surgery. We believe that this result may have been due to a reduction of inflammatory markers secondary to considerable weight loss. Although to our knowledge there are no publications showing a direct relationship between symptomatic improvement of ulcerative colitis and weight loss in the obese patient, we believe that weight loss surgery could become a promising tool in the treatment of ulcerative colitis when associated with morbid obesity.
BACKGROUND: Probiotics are efficacious for treating and maintaining remission of ulcerative colitis. AIM: To conduct a randomized placebo-controlled trial of bifidobacteria-fermented milk supplementation as a dietary adjunct in treating active ulcerative colitis. METHODS: Twenty patients with mild to moderate, active, ulcerative colitis randomly received 100 mL/day of bifidobacteria-fermented milk or placebo for 12 weeks with conventional treatment. RESULTS: Clinical and endoscopic activity indices and histological scores were similar in the two groups before treatment. Although improvements were significant in both groups, the clinical activity index was significantly lower in the bifidobacteria-fermented milk than in the placebo group after treatment. The post-treatment endoscopic activity index and histological score were significantly reduced in the bifidobacteria-fermented milk, but not the placebo group. Increases in faecal butyrate, propionate and short-chain fatty acid concentrations were significant in the bifidobacteria-fermented milk, but not the placebo group. No adverse effects were observed in either group. CONCLUSION: Supplementation with this bifidobacteria-fermented milk product is safe and more effective than conventional treatment alone, suggesting possible beneficial effects in managing active ulcerative colitis. This is a pilot study and further larger studies are required to confirm the result these preliminary results.
BACKGROUND: Butyrate oxidation within the colonocyte is selectively inhibited by hydrogen sulphide, reproducing the metabolic lesion observed in active ulcerative colitis. AIMS: To study generation of hydrogen sulphide by sulphate reducing bacteria (SRB) and the effects of 5-aminosalicylic acid (5-ASA) in patients with ulcerative colitis in order to identify a role of this noxious agent in pathogenesis. PATIENTS: Fresh faeces were obtained from 37 patients with ulcerative colitis (23 with active disease) and 16 healthy controls. METHODS: SRB were enumerated from fresh faecal slurries and measurements made of sulphate reducing activity, and sulphate and hydrogen sulphide concentrations. The effect of 5-ASA on hydrogen sulphide production was studied in vitro. RESULTS: All controls and patients with active ulcerative colitis carried SRB and total viable counts were significantly related to the clinical severity grade. SRB were of two distinct types: rapidly growing strains (desulfovibrios) which showed high sulphate reduction rates, present in 30% of patients with ulcerative colitis and 44% of controls; and slow growing strains which had little activity. In vitro, 5-ASA inhibited sulphide production in a dose dependent manner; in patients with ulcerative colitis not on these drugs faecal sulphide was significantly higher than in controls (0.55 versus 0.25 mM, p=0.027). CONCLUSIONS: Counts and carriage rates of SRB in faeces of patients with ulcerative colitis are not significantly different from those in controls. SRB metabolism is not uniform between strains and alternative sources of hydrogen sulphide production exist in the colonic lumen which may be similarly inhibited by 5-ASA. The evidence for hydrogen sulphide as a metabolic toxin in ulcerative colitis remains circumstantial.
Colorectal strictures, either benign or malignant, are not uncommon in ulcerative colitis. Fifty nine of 1156 ulcerative colitis patients (5%) admitted to this hospital between 1959 and 1983 developed 70 separate colorectal strictures. Seventeen of the 70 strictures (24%) proved to be malignant and the other 53 benign. Nine patients developed more than one stricture. Three principal features distinguished the 17 malignant from the 53 benign strictures in this series: (1) appearance late in the course of ulcerative colitis (61% probability of malignancy in strictures that develop after 20 years of disease v 0% probability in those occurring before 10 years); (2) location proximal to the splenic flexure (86% probability of malignancy v 47% in sigmoid, 10% in rectum, and 0% in splenic flexure and descending colon); and (3) symptomatic large bowel obstruction (100% probability of malignancy v only 14% in the absence of obstruction or constipation). Moreover, cancer associated with strictures tends to be more advanced (76% stage D, 24% A and B) than that which does not produce strictures (18% stage D, 59% A and B).
BACKGROUND & AIMS: Mechanisms of diarrhea in ulcerative colitis (UC) are still unknown. Functional and structural characterization of epithelial barrier and transport properties in ulcerative colitis (UC) was performed. METHODS: Inflamed sigmoid colon epithelium from UC patients was studied by alternating current impedance analysis to determine the pure epithelial resistance as a measure of intestinal barrier function. Tight junction (TJ) structure was investigated by freeze-fracture electron microscopy. RESULTS: Although total wall resistance was reduced in UC by 50%, impedance analysis uncovered a much more pronounced barrier defect. Epithelial resistance decreased from 95 +/- 5 to 20 +/- 3 omega3. cm2, which in conventional analysis is masked by an increase in subepithelial resistance from 14 +/- 1 to 36 +/- 3 omega3. cm2 caused by inflammation. This was paralleled by a change in epithelial cell TJ structure in UC. Strand count decreased from 6.94 +/- 0.25 to 4.76 +/- 0.47 at the surface and from 7.26 +/- 0.31 to 5.46 +/- 0.37 in the crypts. CONCLUSIONS: The inflamed colonic mucosa in UC has an impaired barrier function that is much more pronounced than previously assumed. An altered TJ structure contributes to this barrier defect which, because of increased back leak, can reduce net ion transport. Thus, a leak-flux mechanism contributes to the diarrhea in UC.
Inspite of a higher prevalence of ulcerative colitis complications of Crohn's disease make a surgical intervention more often necessary. Emergent operations of ulcerative colitis confront with minimal surgery of Crohn's disease. Today the basic treatment of both diseases is conservative; an elective operation at the right moment may reduce on the other hand the number of emergency cases.
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