ABSTRACT
Packaging materials intended for direct food contact were acquired on the Brazilian retail market and analysed for their plasticizer content. Analyses were carried out by gas chromatography with flame ionization detection. Di-2-ethyl-hexyl adipate (DEHA), di-2-ethyl-hexyl phthalate (DEHP) and di-iso-decyl phthalate (DIDP) plasticizers were identified in films and closure seals in concentrations ranging from 12 to 19% (w/w), 15 to 44% (w/w) and 10 to 11% (w/w), respectively. Brazilian regulations state that for use with foods with a fat content above 5%, the levels of DEHP and DIDP in the plastic material should be no greater than 3%. The results obtained demonstrate a lack of conformity. It would be advisable to include information on the labels of packaging materials about their restrictions of use in order to advise manufacturers and consumers about their proper usage.
Subject(s)
Food Packaging/standards , Plasticizers/analysis , Adipates/analysis , Chromatography, Gas , Diethylhexyl Phthalate/analysis , Humans , Phthalic Acids/analysis , Polyvinyl Chloride/chemistryABSTRACT
The effects of bedtime 70 micrograms and twice daily 35 micrograms doses of enprostil on 24-hour intragastric acidity were investigated in nine duodenal ulcer patients in remission. Median nocturnal acidity decreased significantly by 30% with 35 micrograms twice daily, and by 48% with 70 micrograms at bedtime. In a clinical trial using bedtime dosing, 102 duodenal ulcer patients randomly received either ranitidine 300 mg or enprostil 70 micrograms. More ulcers healed after 4 and 8 weeks treatment with ranitidine than with enprostil (76% ranitidine vs 52% enprostil, at 4 weeks p = 0.0065 and 94% vs 68%, respectively at 8 weeks, P = 0.0007). However, 6 months after cessation of treatment there was no material difference in overall outcome. Despite combining mucosal protection with acid inhibition enprostil treatment conferred no advantage over simple acid inhibition.
Subject(s)
Duodenal Ulcer/drug therapy , Enprostil/therapeutic use , Gastric Acid/metabolism , Ranitidine/therapeutic use , Adult , Aged , Circadian Rhythm , Duodenal Ulcer/physiopathology , Female , Follow-Up Studies , Gastric Acidity Determination , Humans , Male , Middle AgedABSTRACT
Twenty-four hour intragastric acidity was measured in nine volunteer subjects in a single-blind placebo-controlled cross-over study comparing the effects of famotidine with ranitidine. The volunteer subjects received famotidine (40 mg at night), famotidine (20 mg at night), ranitidine (300 mg at night) or placebo in a predetermined random order. Twenty-four hour intragastric acidity was measured after the seventh dose of each drug or placebo. Famotidine (20 mg), famotidine (40 mg) and ranitidine, all caused a significant decrease of intragastric nocturnal acidity when compared with placebo (P less than 0.01), with no effect during the daytime (P greater than 0.05). Treatment with all the drugs caused a significant rise of fasting plasma gastrin concentration compared with placebo (P less than 0.05).
Subject(s)
Gastric Acid/metabolism , Histamine H2 Antagonists/pharmacology , Thiazoles/pharmacology , Administration, Oral , Adult , Aged , Dose-Response Relationship, Drug , Drug Evaluation , Duodenal Ulcer/blood , Duodenal Ulcer/physiopathology , Famotidine , Gastric Acidity Determination , Gastrins/blood , Humans , Male , Middle Aged , Random Allocation , Ranitidine/pharmacology , Secretory Rate/drug effects , Time FactorsABSTRACT
Ten healthy volunteers were studied before, during, and after treatment with omeprazole 30 mg daily for two weeks. On the 14th night mean nocturnal (2100-0700) intragastric acidity was significantly decreased by 75% (p less than 0.001). At 0700, 22 hours after the last dose of omeprazole, there were significant increases in the bacterial count and the nitrite and N-nitrosamine concentrations in the gastric juice (p less than 0.001). Three days later these changes had resolved. Short term treatment of healthy volunteers with omeprazole is associated with a short lived increase in the gastric bacterial flora, with endogenous production of N-nitroso compounds.
