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Biomedical subjects

G Pöllmann

Publications and source records attributed to G Pöllmann.

7 recordsLinked to original sources
PubMed1999

Association between serum pepsinogen A and C levels, serum gastrin concentrations and Helicobacter pylori antibodies.

Pepsinogen A and C as well as gastrin were measured in the serum of 117 patients with rheumatic diseases. Moreover, the patients were divided up in groups by aids of a semiquantitative, rapid enzyme immunoassay for detection of Helicobacter pylori: 20 patients without H. pylori antibodies (AB) negative, 18 positive + (= weak AB-titre), 21 positive +2 (medium AB-titre), and 58 positive +3 (high AB-titre). The semiquantitative determinations of H. pylori-AB correlated with pepsinogen A, C and gastrin. Patients with H. pylori-AB positive +3 showed significantly higher values of pepsinogen C (p < or = 0.01) as well as pepsinogen A and gastrin (p < or = 0.05) than H. pylori-AB negative patients. Significantly increased levels of pepsinogen A (> 150 ng/ml) and C (> 25 ng/ml) were found to occur in 39% and 100% of patients with high H. pylori-AB titres. The measurement of serum pepsinogen C concentrations may provide additional diagnostic information of the extent of mucosal lesions in patients with positive H. pylori-AB titres treated with antirheumatic drugs. Our findings suggest that the semi-quantitative classification of positive AB-results can be useful in cases determining H. pylori infection and mucosal irritation if other investigations are not available.

Adult↗
PubMed1999

[Adhesion molecule ICAM-1 in patients with chronic polyarthritis--effects of inpatient rehabilitation].

In rheumatoid arthritis (RA) the adhesion molecule ICAM-1 mediates the adhesion of leucocytes following subsequent transendothelial migration including interactions and adhesion of several cell types such as fibroblasts, T-lymphocytes and synoviocytes. Significantly increased ICAM-1 levels were measured in the acute phase of RA. The correlation of ICAM-1 levels with the pteridine neopterin (p < or = 0.01) may reflect the role of this adhesion molecule in modulation of immune responses. Despite the significantly higher levels of acute phase reactions parallel to the elevated ICAM-1 levels, no correlations were found between ICAM-1 and erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and serum-Amyloid A (SAA). During an in-patient multidisciplinary rehabilitation programme the levels of ICAM-1 in serum and the majority of all investigated laboratory and clinical parameters such as ESR, CRP, SAA, fibrinogen, pain, swollen and painful joint count, morning stiffness and health assessment questionnaire improved.

Acute-Phase Proteins↗
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↗