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Biomedical subjects

G Pöllmann

Publications and source records attributed to G Pöllmann.

5 recordsLinked to original sources
PubMed1997

[Therapy of hyperuricemia and gout].

Therapy of hyperuricemia and gout has to depend on pathogenesis and stage of the disease. Dietary regimen are in the forefront in treatment of asymptomatic hyperuricemia. Uric acid lowering drugs can only be supported in repeated serum-measures from 9 mg/dl up. The therapy of an acute attack of gout primarily is done with non-steroidal antiinflammatory drugs, in rare cases with colchicine or corticoids. Gouty arthritis in intermission, independent of the extent of hyperuricemia, as well as chronic gout are indications for an uric acid lowering pharmacotherapy, usually for life. A special therapeutic challenge arises out of renal complications and the frequent association with the metabolic syndrome.

Acute Disease↗
PubMed1990

Influence of lornoxicam on serum pepsinogen levels.

Serum pepsinogen I was determined radioimmunologically in 18 patients suffering from lumbar backache syndromes. These patients were then treated with lornoxicam 4 mg twice daily over a period of 2 weeks. No significant increase in the serum pepsinogen I level was found in 17 (94.4%) of cases. Using the serum pepsinogen I as a parameter for the integrity of the gastric mucosa, this suggests good gastric tolerance of lornoxicam.

Adult↗
PubMedDate not supplied

[Helicobacter pylori associated gastrointestinal mucosal lesions: is there an increased risk during therapy with nonsteroidal antirheumatic agents?].

ENDPOINTS: Are there connections between Helicobacter pylori-induced and NSAID-induced gastrointestinal mucosal lesions leading to an increased risk? Are there any diagnostic or therapeutic consequences? METHODS: Evaluation of H.P. infection, NSAID medication and mucosal lesions in 303 patients with rheumatic diseases. RESULTS: The prevalence of H.P. infection was 67.7%. Positive H.P. antibodies were found in 96.2% of patients with mucosal lesions, confirmed by endoscopy. There was no statistically significant increase of mucosal lesions in patients with both H.P.-infection and NSAID therapy. CONCLUSIONS: The main cause for gastrointestinal mucosal lesions is H.P. infection (> 90%). A general mucoprotective therapy in patients with H.P. infection and NSAID therapy cannot be supported. It may be supposed that a part of mucosal lesions connected to NSAID-therapy in recent decades probably was the consequence of H.P. infections. Eradication of H.P. might be of higher importance in the future.

Adult↗
PubMedDate not supplied

[Value of pepsinogen I in serum as a screening method for early detection of gastroduodenal lesions and follow-up in therapy with non-steroidal antirheumatic drugs].

Gastroduodenal lesions of the mucosa are known to be the most frequent side effect during therapy with non-steroidal antiinflammatory drugs (NSAIDs). We investigated the radioimmunological determination of serum-pepsinogen I as an indicator for the quality of the gastroduodenal mucosa. A good correlation was found between the endoscopy findings of 78 patients and contemporary determinations of serum-pepsinogen. Further, a follow-up of pepsinogen I was made during the treatment of 107 patients with degenerative rheumatic diseases with eight different NSAIDs. The results recommend the determination of pepsinogen I as an indicator of gastroduodenal mucosal changes under therapy with NSAIDs; this determination gives a deciding factor for the gastrolesive potency of an NSAID.

Adult↗