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Biomedical subjects

I Biemond

Publications and source records attributed to I Biemond.

112 records · Page 7Linked to original sources
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Therapy and prevention of gastric ulcer.

After establishing the benign nature of a gastric ulcer, the treatment is primarily medical. This medical therapy is aimed to alleviate symptoms, to heal the ulcer and to prevent relapses. Based on the history of non-steroidal anti-inflammatory drugs (NSAIDs) and the Helicobacter pylori-status, gastric ulcer patients can be divided into four categories (1) H. pylori positive plus NSAID-use, (2) H. pylori positive without NSAID use, (3) NSAID use with negative H. pylori-status, (4) Negative H. pylori-status and no NSAID use. Patients taking NSAIDs should stop this therapy if possible. Patients with gastric H. pylori infection should be treated by a regimen of a proton pump inhibitor with at least two appropriate antibiotics. This treatment will result in early alleviation of symptoms, rapid healing of the ulcer and prophylaxis of ulcer relapse. In patients with gastric ulcer who cannot stop NSAIDs, maintenance therapy with prostaglandins or potent antisecretory drugs should be considered. The few patients with gastric ulcer who do not take NSAIDs and do not have gastric H. pylori infection should be treated by antisecretory drugs, and they should be carefully followed endoscopically to exclude malignant (carcinoma, lymphoma) or non-peptic (Crohn's disease) disease. All patients with gastric ulcer should be re-endoscoped to verify complete ulcer healing. Surgery may be considered in gastric ulcer patients with complications, in those with severe dysplasia of the gastric mucosa, and in those who are not able or willing to take the medication.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMedDate not supplied

Levels of circulating cellular fibronectin are increased in patients with rheumatoid vasculitis.

OBJECTIVE: To investigate whether serum levels of circulating cellular fibronectin (cFN) are increased in patients with rheumatoid arthritis (RA) complicated by vasculitis. METHODS: Levels of serum cFN were determined by an enzyme-linked immunosorbent assay (ELISA) in 26 RA patients with histologically proven vasculitis of recent onset (RV) and were compared to the levels in 47 RA patients with extraarticular manifestations of recent onset but no histological evidence of vasculitis (RA+), 43 patients with uncomplicated RA (RA-), 16 patients with systemic lupus erythematosus and active disease (SLE), 30 patients with active Crohn's disease (CD), 21 young healthy controls (yHC) and 17 elderly healthy controls (eHC). Plasma levels of cFN and von Willebrand factor antigen were also determined in the RA patients. RESULTS: In RV patients, the median cFN level was significantly (P = 0.01) higher compared to that of RA+ patients, and was also significantly (P < 0.0000) higher compared to the cFN level in the RA-, SLE, CD, yHC and eHC groups. When compared to eHC, the cFN level was significantly higher in RA+ (P = 0.008); it was also higher in RA-, although not significantly (P = 0.42). 77% of the RV patients, 55% of the RA+ patients, and 37% of the RA-patients had a cFN level > 2 SD above the mean level for eHC. At an optimal cut-off titre the sensitivity of the cFN ELISA in discriminating RV patients from RA+ patients was 90%, the specificity was 46% and the accuracy was 68%. Plasma levels of cFN correlated significantly (r = 0.62; P < 0.001) with the von Willebrand factor antigen levels. CONCLUSIONS: Increased levels of serum cFN are present in patients with RA, and are frequently found in RA patients with extraarticular manifestations, particularly in those with vasculitis.

Adolescent↗