Biomedical subjects

Naila Arebi

Publications and source records attributed to Naila Arebi.

4 recordsLinked to original sources

PubMed2007

Medium-term results of oral tacrolimus treatment in refractory inflammatory bowel disease.

BACKGROUND: This study aimed to evaluate the efficacy of oral tacrolimus in patients with inflammatory bowel disease (IBD) refractory to conventional therapy, including azathioprine, 6-mercaptopurine, and infliximab. METHODS: Retrospective review of all patients with IBD treated with oral tacrolimus was undertaken. Tacrolimus was administered t an initial dose of 0.05 mg/kg twice daily, aiming for serum trough levels of 5-10 ng/mL. We evaluated clinical response, a retrospective estimated Crohn's disease activity index (CDAI) for Crohn's disease (CD), modified Truelove-Witts index for ulcerative colitis (UC), and modified pouch disease activity index (mPDAI) for pouchitis. Patients had been monitored clinically for benefit and side effects and by whole blood tacrolimus level approximately every 4 weeks for the duration of treatment. Clinical remission was defined as an estimated CDAI <150 (CD), an inactive disease score on the Truelove-Witts index (UC), and mPDAI <5 (pouchitis). RESULTS: Twelve patients with CD, six with UC, and one with pouchitis, all resistant to previous therapies, were treated for a median of 5 months. After 4 weeks 10 CD (83%), four UC (67%) patients, and one pouchitis patient had a clinical response. There was a median reduction of the estimated CDAI of 108 points (range 35-203; P = 0.002) and stool frequency of three per day at week 4. Remission was achieved in 42% (5/12) of CD and 50% (3/6) of UC patients at the end of follow-up. Side effects included temporary elevated creatinine (n = 1), tremor (n = 3), arthralgia (n = 1), insomnia (n = 1), and malaise (n = 1). Four patients discontinued treatment due to side effects. CONCLUSION-: Oral tacrolimus is well tolerated and effective in patients with refractory IBD in the short- to medium-term. Further controlled, long-term evaluation is warranted.

Administration, Oral↗

PubMed2006

Position changes improve visibility during colonoscope withdrawal: a randomized, blinded, crossover trial.

BACKGROUND: Adequate distension is essential to maximize neoplasia detection during colonoscope withdrawal. Position changes may improve distension but are often not performed in routine practice. OBJECTIVE: To assess whether routine position changes improve luminal distension during colonoscope withdrawal. DESIGN: Randomized, blinded, crossover trial. SETTING: Single tertiary-referral center, United Kingdom. PATIENTS: Fourteen patients attending for routine colonoscopy. INTERVENTIONS: Videotaped, back-to-back examination of colon proximal to rectosigmoid junction in left lateral position only, then with position changes: left lateral for the cecum to the hepatic flexure, supine for the transverse colon, and right lateral for the splenic flexure and the descending colon, or vice versa. MAIN OUTCOME MEASUREMENTS: Luminal distension as scored by a blinded video reviewer. Luminal distension was scored on a scale of 1 to 5 for each colonic area: 1, complete collapse; 5, widely distended to limit of view. A score of 2 or less was considered inadequate for diagnosis. RESULTS: Scores for the 2 examinations from the blinded video reviewer were significantly higher in the transverse, the splenic flexure, and the descending colon, P = .02, .002, and <.001, respectively. Without position changes, 6 of 14 of patients (43%) would have had a nondiagnostic distension score (1 or 2) in at least 1 colonic area, P = .03. LIMITATIONS: Nonvalidated scoring system for luminal distension, however, good agreement between endoscopist and blinded reviewer, weighted kappa 0.53, 95% confidence interval 0.38-0.69. CONCLUSIONS: Position change, a cost-neutral intervention, during colonoscope withdrawal improved luminal distension between hepatic flexure and sigmoid-descending junction and has the potential to reduce adenoma and early cancer miss rates.

Colon↗

PubMed2006

A novel method of treating colonic angiodysplasia.

BACKGROUND: Colonic angiodysplasia is responsible for up to a third of lower-GI bleeding cases. Argon plasma coagulation (APC) is a recognized treatment modality, but active bleeding decreases the ablative efficacy of APC by dissipation of the energy. APC has been associated with colonic perforation. OBJECTIVES: We propose a novel and safe method for the treatment of colonic angiodysplasia by a submucosal injection of a saline epinephrine solution followed by the application of APC. PATIENTS: Three patients with a total of 10 colonic angiodysplasias were treated with this injection-APC method. INTERVENTIONS: Saline adrenaline solution (1:200,000) 2 to 3 mL was injected beneath the angiodysplasia before application of APC. APC 50 W and gas flow 2 L were applied onto the vascular lesion until the sufficient thermal effect was observed. RESULTS: There were no procedure-related complications. CONCLUSIONS: This new injection-APC method was safe for the treatment of colonic angiodysplasia. This may be useful in treating right-sided colonic lesions where the risks of perforation are greater than for the rest of the colon.

Aged↗

PubMed2002

Nitric oxide regulates the release of somatostatin from cultured gastric rabbit primary D-cells.

BACKGROUND & AIMS: Neuronal nitric oxide synthase (nNOS) is present in gastric D-cells. Mucosal somatostatin is diminished in H. pylori gastritis, where production of nitric oxide (NO) is increased. Therefore, we investigated the role of NO in D-cell function and the effects of prolonged exposure of D-cells to NO. METHODS: Rabbit gastric D-cells were cultured. Somatostatin-14 was measured after 2 hours to examine the effects of arginine, nitric oxide sythase (NOS) inhibitors, and NO donors. Some cells were preincubated with a slow releasing NO donor for 12 hours. Results are expressed as percentage of total cell content. Nitrate content was measured by chemiluminescent assay. RESULTS: L-arginine increased somatostatin-14 release in the presence of CCK8 from 4.4% +/- 0.5% to 6.4% +/- 0.4% (P < 0.02), and this was accompanied by NO release from 27 +/- 7 micromol/L to 86 +/- 12 micromol/L (P = 0.001). D-arginine and L-lysine had no effect. NOS inhibitors LNNA, SMT, and 7NI significantly attenuated the stimulatory response to L-arginine. NO donors sodium nitroprusside (SNP), 1 mmol/L, and S-nitroso-N-acetyl-D-L-penicillamine, 0.1 mmol/L, significantly increased basal and cholecystokinin-8 (CCK8) stimulated somatostatin release. Oxyhemoglobin attenuated the effect of SNP but not of L-arginine. Neither cyclic guanosine monophosphate nor guanylate cyclase were involved in the response to NO. However, inhibition of adenosine diphosphate (ADP) ribosyltransferase significantly decreased the response to L-arginine. Preincubation for 12 hours with 150 micromol/L (Z)-1-[(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate; IP3, inositol triphosphate decreased the 2-hour cellular response to CCK8 and SNP. CONCLUSIONS: NO regulates rabbit D-cells. Acute exposure stimulates somatostatin mediated by ADP ribosylation, whereas long-term exposure reduces cellular responses to stimuli. The latter pathway may be responsible for the suppression of somatostatin in H. pylori gastritis.

Adenosine Diphosphate Ribose↗