In an attempt to verify whether the periodicity of ulcer-related symptoms would be confirmed by a spring and fall exacerbation of peptic ulcers, we have analyzed the monthly variation of active duodenal ulcers found at endoscopy of the upper gastrointestinal tract in the years 1979-1981. Control diagnoses were active gastric ulcers, gastric and rectal adenocarcinomas, and rheumatoid arthritis. Data were also available on hospital admission for perforated ulcers. The calendar fluctuation of active duodenal ulcer is characterized by a significant fall in August which is associated with July and fall peaks. This pattern of variation for duodenal ulcer was evident in both sexes and across the different decades of age. Duodenal ulcer diagnosis and hospitalization for perforated ulcer fluctuated in a similar way. The shape of monthly variation for active duodenal ulcer was not paralleled by similar changes in gastric ulcers and in the control diagnoses, gastric and rectal carcinomas, and rheumatoid arthritis.
Candida overgrowth in gastric juice of peptic ulcer subjects under therapy with H2-receptor (H2-R) antagonists has been detected in 21.4 and 53.8% of cases after short- and long-term treatment respectively, and in 8 % of controls. Both types of H2-R antagonists, ranitidine and cimetidine, were equally associated with production of yeasts. The location of ulcers, whether gastric or duodenal, seems to have no influence on fungal growth. Females were more susceptible than males to develop Candida in gastric juice. In the short-term course with H2-R blockers fungal colonization of gastric juice was associated with delay of the rate of ulcer healing. Fungal detection in gastric juice was not associated with mucosal invasion by Candida since in none of the patients who had a biopsy for gastric ulcer was Candida detected by histology.
Treatment with recombinant IFN-beta, at doses of up to 18 MIU for 6 months, is safe and well tolerated. However, the results of the trial do not support the use of IFN-beta monotherapy in patients with chronic hepatitis C that is resistant to IFN-alpha.
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