Placebo-controlled trial of ulcerative colitis with oral 4-aminosalicylic acid.

Forty patients with active ulcerative colitis were randomly assigned to receive either 4 g of oral enterically coated 4-aminosalicylic acid (para-aminosalicylic acid) or placebo. The duration of treatment was 12 weeks. Disease activity was assessed by grading clinical symptoms of blood, mucus, urgency, sigmoidoscopic findings, and degree of histological inflammation in rectal biopsy specimens. At 12 weeks, 11 of 20 patients (55%) who received 4-aminosalicylic acid showed improvement in clinical and sigmoidoscopic variables. In contrast, only 1 of 20 patients (5%) who had received placebo showed improvement (P less than 0.005). Eighteen of the 19 patients in the placebo group who showed no improvement were treated subsequently with open-label 4-aminosalicylic acid. Of the 18, 11 showed clinical and sigmoidoscopic improvement. Patients allergic or intolerant to sulfasalazine with extensive disease were more likely to respond to 4-aminosalicylic acid.

Predictive value of a low serum trypsinogen.

Previous studies, in selected populations, have determined that a low serum trypsinogen can be seen in chronic exocrine pancreatic disorders (CP) and primary diabetes mellitus (DM). In this study, we investigated the predictive value of a low serum trypsinogen. The study population consisted of 488 consecutive emergency room patients admitted to our hospital on whom a serum amylase was drawn by the emergency room staff. Of the sera drawn, 418 were saved and tested for immunoassayable trypsinogen. Ten of 418 (2.4%), had a low level of this marker (less than 10 ng/ml). Of these 10, four had obvious historical or clinical evidence of CP during their initial hospitalization. Six patients, however, had no initial evidence of CP. Follow-up was obtained in three of the six, and all three had evidence of CP despite absence of symptoms. Of the 418 patients, 37 had DM. A low trypsinogen was found in three of these 37, and all three had concomitant CP. We conclude that this new assay has excellent predictive value in diagnosing chronic exocrine pancreatic disorders.

Effects of purified aflatoxin on broiler chickens.

Purified aflatoxin B1 (AFB1) or AFB1 plus aflatoxin B2 (AFB2) was given daily for 5 weeks in gelatin capsules to 2-week-old feather-sexed broilers. In Experiment 1, pure AFB1 was given in doses equivalent to the quantity of toxin received, if diets containing either 0, 200, 500 or 1000 ppb of AFB1 were consumed. In Experiment 2, pure AFB1 or AFB1 plus B2 was administered in capsules in doses equivalent to the quantity of toxin received, if diets containing either 0, 100, 200, or 400 ppb of AFB1 were consumed. In Experiment 1, pure AFB1 greater than or equal to 500 ppb was only mildly toxic. These levels produced a significant decrease in the 5-week weight gain and microscopic lesions indicative of alfatoxicosis. No morbidity, mortality, or effects on feed conversion or immune responses, however, were noted in birds given pure AFB1 at these levels. Gross liver lesions indicative of aflatoxin toxicity occurred at the 1000 ppb only. Results of Experiment 2 were similar to the first. Weight gain and feed conversion were not affected for broilers receiving pure AFB1 as low as 200 ppb. No morbidity, mortality, or gross lesions were evident in birds given either pure AFB1 or AFB1 plus AFB2 as high as 400 ppb. However, cell-mediated immunity as measured by a delayed hypersensitive skin test was significantly affected in birds receiving 400 ppb AFB1 plus AFB2. No effects on humoral immunity or the development of acquired immunity to Newcastle disease or fowl cholera vaccination were noted.

Effect of purified aflatoxin on turkeys.

Purified aflatoxin B1 (AFB1) or AFB1 plus aflatoxin B2 (AFB2) was given daily for 5 weeks in gelatin capsules to 2-week-old Nicholas X Nicholas turkeys. In Experiment 1, pure AFB1 was given in dosages equivalent to the quantity of toxin received if diets containing either 0, 200, 500, or 1000 ppb of AFB1 were consumed. In Experiment 2, either pure AFB1 or AFB1 plus AFB2 was given in capsules equal to the quantity of toxin received if a diet containing either 0, 100, 150, or 200 ppb of AFB1 was consumed. In Experiment 1, pure AFB1 administered by capsule equal to 500 and 1000 ppb was highly toxic and by the second week, it resulted in 100% morbidity, mortality, and gross and microscopic lesions. Aflatoxin B1 at 200 ppb caused none of these changes. However, it did cause a significant depression in feed conversion, but not weight gain, during all weeks and also a reduction in cell-mediated immunity (CMI) as measured by a delayed hypersensitive skin test to mycobacterium. Results in Experiment 2 were similar to the first. Aflatoxin B1 and AFB1 plus AFB2 as high as 200 ppb resulted in no morbidity, mortality, or gross or microscopic lesions. Also, no significant reductions in either weight gain or feed conversion were evident in any level of either AFB1 or AFB1 plus AFB2. However, numerical, but not statistically significant, dose-related reductions in all CMI tests were noted in birds receiving either AFB1 or AFB1 plus B2 at as low as 100 ppb.

Effect of zinc, copper, and iron on ochratoxin A production.

The effect of zinc, copper, and iron levels on production of ochratoxin A by Aspergillus ochraceus Wilhelm in a synthetic medium in a shake culture was investigated. Optimal concentrations of ZnSO(4), CuSO(4), and FeCl(3) for ochratoxin A production were 0.055 to 2.2 mg/liter, 0.004 to 0.04 mg/liter, and 1.2 to 24 mg/liter, respectively. Zinc and copper levels greater than optimum reduced the rate of ochratoxin accumulation without altering either glutamate or sucrose utilization. Ochratoxin A production was correlated with rapid utilization of sucrose by the fungus and decreasing pH of the medium. Most of the glutamic acid was removed from the medium prior to ochratoxin production. There was no correlation between mycelial dry weight and ochratoxin A production.