Search PubMed⌕ Search

Biomedical subjects

U Armbrecht

Publications and source records attributed to U Armbrecht.

41 records · Page 3Linked to original sources

Analytical and clinical evaluation of a radioimmunoassay for gastrin.

Prior to a study of the pathophysiological significance of chronic atrophic gastritis and hypergastrinemia, we evaluated a new radioimmunoassay kit for serum total gastrin (Diagnostic Products Corp.). The mean intra-assay CV ranged from 2 to 5% (2386 patients' samples in 47 assay runs done during four months). Total CVs for two controls ranged from 4 to 10%. Within-assay bias was 5%. Oleate decreased the values, indicating that intravenous heparin, which releases endothelial lipase, causing in vitro lipolysis, should be avoided if indwelling catheters are used for sampling, e.g., during provocation tests for gastrin release. Of three other commercial kits examined, two were affected by oleate. Other anions such as heparin and EDTA also affected the assay. Values for gastrin in heparinized plasma from surgical patients representing a variety of disorders agreed well with results obtained by a reference laboratory. We confirm the usefulness of this assay for discriminating clinical situations and conclude that ligand assays, besides those for thyroid assessment, should be assessed for interference from nonesterified fatty acids. Preliminary data also suggest a marked age dependence of serum gastrin concentration.

Adult↗

[Diagnostic significance of heat-induced inhibition of erythrocyte sedimentation (author's transl)].

Heat-induced inhibition of erythrocyte sedimentation (HIES) was examined in 158 cases. HIES is significantly lower in patients with a liver cell damage isolated or due to metastases of a neoplastic process in comparison to that in patients suffering from inflammation or malign tumor not involving the liver. Generally, HIES depends upon the concentration of lysophosphatidyl choline (lysolecithin) which is set free in plasma by lecithin-cholesterol-acyltransferase (LCAT) during incubation. In patients with lever cell damage, LCAT is diminished. HIES is being influenced by several factors: Lysophosphatidyl choline is bound to albumin, and this prevents its reaction on the erythrocyte surface. Lysophospholipase reduces the concentration of lysophosphatidyl choline in the plasma by splitting off its fatty acid in the alpha-position. Specific serum proteins, the so-called agglomerines, which are responsible for the acceleration of erythrocyte sedimentation, are counteracting the HIES. The concentration of albumin and agglomerines in plasma and the activity of lysophospholipase are subject to physiologically and pathologically caused deviations. Thereby, HIES is being influenced individually at varying degrees. This makes it difficult to estimate the LCAT activity which represents the principal cause of HIES. As a consequence, HIES seems not to be suitable for clinical diagnostics.

Blood Proteins↗