The efficacy of levofloxacin-based triple therapy for first-line helicobacter pylori eradication.
Forty malnourished patients, 20 with benign disease and 20 with malignancy, were administered a 'home-brew' enteral diet (1140 calories and 60 g protein per litre) perioperatively for 14 days. They received 2500 to 4000 calories per day according to their requirement. Weight, triceps skinfold thickness, midarm circumference, serum albumin and transferrin, absolute lymphocyte count and creatinine-height index were monitored on days 0, 7 and 14. Nitrogen balance was estimated on alternate days and the results of the two groups were compared.
The patient was treated with oral hypotonic fluid restriction (0.5 l/day), 2 l of oral glucose-saline solution per day, high-dose oral antimotility agents (loperamide and codeine phosphate), a proton-pump inhibitor (omeprazole) and oral magnesium replacement. A year later, the patient's loop jejunostomy was closed and an end ileostomy fashioned, bringing an additional 35 cm of small bowel into continuity; macronutrient absorption improved but her problem of dehydration was only slightly reduced. She was stabilized on a twice-weekly subcutaneous magnesium and saline infusion and daily oral 1alpha-hydroxycholecalciferol.
The whole plant of L. indica was extracted using methanol and then subjected to preliminary chemical screening. The in vitro antibacterial screening on two Gram-positive and two Gram-negative bacteria as well as three Shigella species of which two bacteria were antibiotic-resistant were evaluated by disc diffusion method. Castor oil-induced diarrhoea on Wistar albino rats was performed by using loperamide as a standard control. The in vitro antacid activity was tested by artificial stomach model. The neutralization efficiency, capacity, volume and hydrogen ions consumed were also evaluated.
The effects of KW-5092, [1-[2-[[[5-(piperidinomethyl)-2- furanyl]methyl]amino]ethyl]-2-imidazolidinylidene]propanedinitr ile fumarate, on the loperamide- or clonidine-induced delayed propulsion were determined in rats and compared with those of other gastroprokinetic agents. Administration of loperamide (0.3 mg/kg, s.c.) or clonidine (0.01 mg/kg, s.c.) induced delay of the evacuation time of the teflon ball, which had been inserted into the distal colon. The delayed evacuation was improved dose-dependently by KW-5092 at 3 to 10 mg/kg (p.o.) or higher. Neostigmine at 0.3 to 3 mg/kg (p.o.) and T-1815 at 1 to 100 mg/kg (p.o.) also improved the delayed ball evacuation. These results suggest that KW-5092 stimulates the delayed colonic propulsion.
The median sedation scores for ABCB1 mut/mut dogs were higher than nor/nor dogs at all time points and were higher in mut/nor dogs for the first 2 hours. These differences were not found to be significant for any individual time point (P > .05). The median sedation score AUC for mut/mut dogs was significantly higher than nor/nor dogs (P = .028), but the AUC for mut/nor dogs was not (P = .45). There were no significant differences between groups for heart rate, respiratory rate, and blood pressure (P > .05).
The analgesic properties and mechanisms of loperamide hydrochloride, a peripherally acting opioid receptor agonist, in neuropathic pain warrant further investigation.
To evaluate whether low DHEA-S levels are predictors of cortical origin, benignity and hormonal activity in incidentally detected adrenal masses, thirty-five patients with adrenal incidentalomas were studied. All patients were operated on and the diagnosis was histologically confirmed. Basal endocrine workup included plasma determination of cortisol before and after dexamethasone (1 mg overnight), plasma ACTH (08:00 h), 17-OH-progesterone, testosterone and potassium, standing plasma renin activity and aldosterone, supine and standing plasma noradrenaline and adrenaline. If necessary, we performed dexamethasone suppression tests at low (2 mg) and high (8 mg) doses, or the loperamide test (16 mg os) for evaluation of glucocorticoid activity and the glucagon test (1 mg i.v.) for exploring adrenal medulla function. Plasma DHEA-S was measured in all patients and the results were compared to those obtained in controls matched for age, sex and menopausal status. Suppression of DHEA-S was found in 11 out of 35 patients (31.5%). However, this hormonal finding occurred in 50% of the extracortical adrenal lesions, while in proven cortical adenomas (no. = 19) it was detected in only 5 patients (26.3%). Sensitivity, specificity, diagnostic accuracy and positive predictive value of low DHEA-S in indicating a cortical origin of the mass were 0.27, 0.0, 0.25, and 0.80. In malignancies (no. = 6) low DHEA-S levels were found in 1 out of 2 metastases and never in cortical carcinomas. Sensitivity, specificity, diagnostic accuracy and positive predictive value of low DHEA-S in indicating a benign form were 0.34, 0.83, 0.42, and 0.91. Six out of 19 patients with cortical adenomas showed signs of hypothalamic-pituitary adrenal (HPA)-axis dysfunction. Low DHEA-S levels were found in 50% of adenomas with HPA-axis abnormality and in 15.3% of adenomas without hormonal activity. Sensitivity, specificity, diagnostic accuracy, and positive predictive value of low DHEA-S levels in indicating hormonal activity of the mass were 0.50, 0.84, 0.73, and 0.60. Our data indicate that the association between low DHEA-S levels and adrenal incidentalomas is frequent. Low DHEA-S appears to be a poor predictor of hormonal activity with low sensitivity and specificity in respect of cortical origin and benignity of the mass. In conclusion, our results show that DHEA-S measurement does not offer relevant clinical information in the management of adrenal incidentalomas.