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Biomedical subjects

A Wehmeier

Publications and source records attributed to A Wehmeier.

41 records · Page 3Linked to original sources
PubMed1988

Drugs or diet: do they protect against degenerative cardiovascular disease?

Early observations that the regular use of aspirin (acetylsalicylic acid, ASA), a nonsteroidal anti-inflammatory agent, seemed to protect against myocardial infarction and reduce platelet aggregation made this substance the most frequently used drug in large clinical trials. The objectives of these studies were to reduce thromboembolic complications in arterial cardiovascular diseases (prevention of myocardial infarction in unstable angina, secondary prevention of acute myocardial infarction, and increased patency of aortocoronary bypass grafts) and to reduce platelet deposition on artificial surfaces (artificial heart valves and hemodialysis shunts). Despite the recent synthesis of more selective inhibitors of arachidonic acid metabolism in blood platelets, and a multitude of questions concerning optimal dose, schedule, and mode of action that still remain open, ASA continues to be the most frequently used drug in arterial vascular disorders. Because of the frequent and potentially serious side effects of aspirin, mainly on the gastrointestinal tract, less toxic ways of inhibiting eicosanoid metabolism in blood platelets are attracting more and more interest. Among these, the alimentary substitution of omega-3 fatty acids for a competitive inhibition of the omega-6-arachidonic acid metabolism seems the most promising. Results with fish-oil diet raise the question of whether substitution of polyunsaturated lipid acids influence only platelet metabolism, or whether the action of "anti-platelet" drugs or diet in cardiovascular disorders is mediated primarily by leukocytes or monocytes. This new dietary principle, which possibly corrects only a poor alimentary habit of civilization, could open simple and adequate ways for even a primary prophylaxis of vascular disease by diet alone or, at least for therapeutic aims, in combination with drugs.

Cardiovascular Agents↗
PubMed1987

Polychemotherapy of acute myelogenous leukemia in a patient with acute intermittent porphyria.

The safety of drugs in hepatic porphyrias has largely been established by clinical experience, which is very limited in the case of antineoplastic agents. We administered three cycles of polychemotherapy consisting of daunorubicin, cytarabine and 6-thioguanine, and modified supportive care to a 33-year-old Turkish woman suffering from acute myelogenous leukemia. The urinary excretion of total porphyrins, porphobilinogen, and aminolevulinic acid was continuously monitored. Excretion of these metabolites was permanently elevated, but the values were comparatively low during cytotoxic therapy while peak values were recorded at the onset of fever during bone marrow aplasia; yet there were no clinical signs of porphyritic attacks at that time. A few potentially unsafe drugs were tolerated without an increase in porphyrin excretion. Although the susceptibility to drugs is highly variable in patients with hepatic porphyrias, the treatment of malignancy in these patients seems justified as long as porphyrin excretion under therapy is not grossly elevated over baseline values and appropriately modified supportive care is administered.

Acute Disease↗
PubMed1979

Inhibition of platelet thrombus formation by chlorpromazine acting to diminish haemolysis.

There is increasing evidence that the sudden, unpredicatable event initiating myocardial infarction is fissuring of an atherosclerotic plaque. The resulting haemorrhage into the arterial wall produces obstructive platelet thrombi, just as arterial haemorrhages elsewhere produce haemostatic platelet plugs. It has been suggested that such platelet aggregation depends on ADP originating in red cells which are subjected to excessive haemodynamic stress at the site of haemorrhage. The release of ADP from red cells has been demonstrated in vitro in equivalent condtions of shear stress; and other mechansims, such as activation by collagen, cannot account for the rapidity with which the platelets react. One of us (G.V.R.B.) has suggested that drugs capable of counteracting haemolysis might diminish the activating effect of erythrocytes on platelets and so inhibit their aggregation as thrombi. Thus, chlorpromazine, added to human blood at concentrations which diminish haemoylsis but do not directly affect platelet aggregation, prolonged the 'bleeding time' from small holes in artificial vessels where extravasation is terminated, as in living arterioles, by aggregated platelets. The bleeding time was also prolonged by apyrase, consistent with the conclusion that the chlorpromazine acted through decreasing plasma ADP. We show here that this occurs through the anti-haemolytic action of chlorpromazine.

Adenosine Diphosphate↗
PubMedDate not supplied

Infusion-related toxicity of three different amphotericin B formulations and its relation to cytokine plasma levels.

A prospective study was performed to compare the infusion-associated toxicity of three different amphotericin B preparations and to correlate acute side-effects with plasma levels of tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-1 receptor antagonist (IL-1-RA) during and after the infusions. Six adult neutropenic patients with acute leukaemia suffering from suspected or documented systemic fungal infections were treated on three consecutive days with conventional amphotericin B (AmB), liposomal AmB (AmBisome) and AmB mixed in lipid emulsion (AmB/lipid). Drugs were given over 1-2 h. Drug-induced toxicity was monitored every 30 min for 4 h. Plasma levels of the three cytokines were determined using commercially available enzyme-linked immunosorbent assay (ELISA) techniques. Four of six patients showed toxicity after AmB and AmB/lipid infusions; only one patient reacted to liposomal AmB. Clinical toxicity was associated with increases in TNF-alpha plasma levels during two of four infusions of AmB and three of four infusions of AmB/lipid. Major increases in IL-6 occurred during three of four infusions of AmB and during all four AmB/lipid infusions associated with clinical toxicity. Three of four AmB infusions and all four AmB/lipid infusions accompanied by clinical toxicity were associated with major increases in IL-1-RA plasma concentrations. Liposomal AmB was better tolerated than AmB and AmB/lipid. This formulation also caused the lowest liberation of all three cytokines tested. The severity of clinical symptoms did not correlate closely with absolute cytokine plasma levels. The findings provide further evidence that expression of TNF-alpha, IL-6 and IL-1-RA plays an important role in mediating AmB-related acute toxicity in vivo.

Adult↗