Therapeutic effects of Ginkgo biloba extract against acute ischemic colitis.

Ginkgo biloba extract (GBE) is a plant extract obtained from the leaves of G biloba tree. The aim of this study was to evaluate the clinicopathologic characteristics and therapeutic effects of GBE on ischemic colitis (IC).Forty-seven patients with IC were divided as GBE group (n = 30) and routine group (n = 17). The routine group was given routine therapy, and the GBE group was given routine therapies plus GBE intravenous injection. Clinicopathologic characteristics, endoscopy findings, serum antioxidant enzymes, and inflammatory mediators were evaluated.About 89.3% initial symptom was acute-onset abdominal cramping and abdominal pain followed with hematochezia. The lesions were mainly located in sigmoid colon (80.8%). Serum level of superoxide dismutase (SOD) in patients with IC was significantly decreased (P < .05), while methane dicarboxylic aldehyde (MDA), tumor necrosis factor alpha (TNF-α), and interleukin-6 (IL-6) levels were significantly increased (P < .05). However, serum procalcitonin (PCT) level showed no significant change. Treatment of GBE resulted in quick remittance of abdominal pain and hematochezia, and significant attenuation of colon macroscopic and histologic damage in all patients. Furthermore, the treatment also significantly increased SOD levels, decreased MDA, TNF-α, and IL-6 levels (P < .05).Acute-onset abdominal cramping or abdominal pain followed with hematochezia was the mainly initial symptom of IC, and sigmoid and descending colons were the common vulnerable sites. GBE exerted a beneficial effect on IC with faster symptom relief and better mucosal healing, possibly through scavenging oxidative-free radicals and downregulating inflammatory mediators. GBE may be a promising candidate for protection against IC.

Stercoral colitis complicated with ischemic colitis: a double-edge sword.

BACKGROUND: Stercoral colitis is a rare inflammatory process involving the colonic wall secondary to fecal impaction with high morbidity and mortality; especially if complicated with ischemic colitis, stercoral ulcer formation and subsequent perforation. There are several case reports published on abdominal perforation resulting from stercoral colitis. However, stercoral colitis complicated by ischemic colitis is rare. The purpose of this case report is to describe the potential challenges in the diagnosis and management of stercoral colitis with ischemic colitis. CASE PRESENTATION: An 87 years old male with history of chronic constipation presents with severe abdominal pain to the emergency department. The patient was hemodynamically stable. On physical examination, the abdomen was mildly distended with moderate tenderness. Lab work was significant for leukocytosis and lactic acidosis. Abdominal CT scan revealed large amount of retained stool in the colon, bowel wall thickening and infiltration of peri-colonic fat, which were suggestive for stercoral colitis. Patient was started on IV fluids and antibiotics. He was given an enema, followed by laxative and manual disimpaction of stool. Colonoscopy was performed and biopsies were obtained. Tissue biopsy was significant for focal active colitis with regenerative glandular changes and neural hyperplasia. CONCLUSION: Elevated lactic acid level secondary to ischemia of the bowel wall with CT scan findings aid in establishing the diagnosis of stercoral colitis complicated with ischemic colitis. Urgent treatment with laxatives and fecal disimpaction is indicated to prevent perforation and peritonitis.

Rebamipide enema therapy for left-sided ischemic colitis patients accompanied by ulcers: open label study.

AIM: To attempt rectal administration of rebamipide in the treatment of ischemic colitis patients with ulcers, and evaluate its effects. METHODS: We compared 9 ischemic colitis patients (2 men, 7 women) with ulcers treated by bowel rest only from 2000 to 2005 (conventional therapy group), with 6 patients (2 men, 4 women) treated by rebamipide enema therapy in 2006 (rebamipide enema therapy group) and analyzed the mean duration of fasting and hospitalization, degree of ulcer healing, and decrease in WBC count for the two groups. RESULTS: The mean duration of fasting and hospitalization were 2.7+/-1.8 d and 9.2+/-1.5 d in the rebamipide group and 7.9+/-4.1 d and 17.9+/-6.8 d in the control group, respectively, and significantly reduced in the rebamipide group (t= -2.915; P=0.0121 and t= -3.054; P=0.0092). As for the degree of ulcer healing at 7 d after admission, the ulcer score was reduced by 3.5+/-0.5 (points) in the rebamipide group and 2.8+/-0.5 (points) in the control group (t=1.975; P=0.0797), while the decrease in WBC count was 120.0+/-55.8 (x 10(2)/microL) in the rebamipide group and 85.9+/-56.8 (x 10(2)/microL) in the control group (t=1.006; P=0.3360). CONCLUSION: In left-sided ischemic colitis patients with ulcers, rebamipide enema therapy significantly reduced the duration of fasting and hospitalization, recommending its use as a new and effective therapeutic alternative.

Membrane permeability and antipyrine absorption in a rat model of ischemic colitis.

The aim of this study was to determine whether the duration of ischemia affects antipyrine absorption in the large intestine. This was carried out in a rat model of ischemic colitis in which ischemia and associated inflammation was induced by marginal vessel ligation. Blood flow was disrupted by positioning an o-ring around the distal rectum and ligating the marginal vessel at two locations in the hind-gut ligament artery region. Ligation was performed for 1, 2, 3, and 5h. We assessed large intestine damage by measuring key indicators of inflammation, myeloperoxidase (MPO) activity and thiobarbituric acid reactant substrates (TBARS) in the mucosa and by histological staining with hematoxylin-eosin stain. Antipyrine membrane permeability was assessed in Ussing-type diffusion chambers, and related pharmacokinetics were calculated from antipyrine plasma concentration measurements following colon administration of the drug. Vessel ligation caused some sloughing of epithelial cells and elevated the MPO and TBARS levels. Prolonged ligation failed to affect the apparent permeability coefficient (P(app)) of antipyrine. Prolonged ligation, however, gradually increased plasma antipyrine concentrations to near control levels. This increase was paralleled by increases in the absorption rate constant AUC and antipyrine bioavailability. Taken together, these results suggest that the absorption kinetics of antipyrine may depend on blood flow changes in the large intestine that occur with inflammation.