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Biomedical subjects

G Ziegler

Publications and source records attributed to G Ziegler.

At least 55 records · Page 3Linked to original sources

[Systematic study of various tumoral markers in prevalent bone metastasis].

In the presence of prevalent bone metastases, the precise histo-pathological diagnosis of the primary tumor is often difficult. The authors study the diagnostic value of systematic serum assay of a series of tumoral tracers (ACE, AFP, PAP and PSA, SCC, CA 19:9, CA 15:3, CA 125) which until now were used in evolutive and therapeutic monitoring. 34 patients were selected for this preliminary retrospective study (including 20 with a demonstrated histopathological diagnosis). 70 p. cent of prevalent bone metastases express a target tracer corresponding to the initial location. In some cases, an elevated tracer, because of its specificity, may bring about a diagnostic or therapeutic decision (always according to the context). No conclusion may currently be drawn in case of discordance between the anatomo-clinical context and the "profile" of the markers (1 case in our series).

Biomarkers, Tumor↗

Lack of effect of nitrendipine on the pharmacokinetics and pharmacodynamics of midazolam during steady state.

1. The possible interaction (as indicated by rat experiments) between calcium channel blocking agents and benzodiazepines has been evaluated in nine healthy subjects. 2. Subsequently to an intravenous loading dose (0.07 mg kg-1) midazolam was infused for 6 h (0.035 mg kg-1 h-1) and steady state plasma levels between 54 to 114 micrograms l-1 were achieved. Two hours after the bolus of midazolam a solution of 20 mg nitrendipine or placebo was administered in a randomized, double-blind crossover fashion. 3. The marked sedative-hypnotic effects of midazolam as assessed by visual analogue scales (about four fold increase in the sedation index) and choice reaction time (100% prolongation) indicated some form of adaptation or tolerance towards the end of the infusion. However, the midazolam-induced impairments were not affected by nitrendipine. 4. EEG-data indicated stabile benzodiazepine-like effects during the complete infusion period of midazolam (e.g. decrease in alpha activity, increase in sigma, delta 2 and beta 1 activity). Again, these alterations were not modified by nitrendipine. 5. There was also no pharmacokinetic interaction between both agents, since elimination of midazolam (t 1/2 = 2.5 +/- 0.8 h; CL = 548 +/- 143 ml min-1) was in close agreement with control values (t 1/2 = 2.4 +/- 0.6 h; CL = 512 +/- 102 ml min-1). Likewise, plasma levels of nitrendipine were comparable to literature data. 6. Thus, it could be concluded that nitrendipine does not affect the action of midazolam and therefore a direct involvement of calcium at the benzodiazepine receptor site is unlikely under our clinical conditions.

Adult↗

Intravertebral vacuum phenomenon in multiple myeloma.

Authors report one case of intravertebral vacuum phenomenon associated with a multiple myeloma. Initially, there occurred a collapse and a lysis of the L4 vertebral body. Two months later, after chemotherapy and cobalt-therapy, X-ray examination showed a vacuum cleft phenomenon within the body of L4 and a backward displacement of the L4 posterior wall. At the same time the patient complained of a cruralgia. Recovery occurred after decompression surgery. Histologic sampling of the L4 vertebral body revealed bone necrosis without any abnormal plasmocytosis. Authors draw attention to the neurological complications occurring in the course of the vertebral necrosis and to the fact that, even in case of multiple myeloma, the occurrence of a transverse vacuum cleft may result from osteonecrosis.

Aged↗

Does the benzodiazepine antagonist Ro 15-1788 antagonize the action of ethanol?

Ethanol aggravates benzodiazepine-induced central nervous depression by pharmacokinetic and/or pharmacodynamic interactions and Ro 15-1788 reverses promptly the hypnotic effects of benzodiazepines. We therefore studied the acute effects of Ro 15-1788 on the ethanol-induced sedation in six healthy male subjects. Subsequently to an oral loading dose (0.54 g ethanol kg-1) ethanol was infused for 4 h (0.15 g ethanol kg-1 h-1) and steady state blood levels between 0.9 to 1.2 g l-1 were reached within 2 h. At steady state and during the elimination phase of ethanol an intravenous bolus of 0.5 mg Ro 15-1788 or placebo was administered in a randomized, double-blind crossover fashion. The marked sedative effects of ethanol as assessed by visual analogue scales (2 to 6 fold increase in the sedation index), and choice reaction time (25 to 40% prolongation) were not affected by Ro 15-1788. However, the pharmaco-EEG indicated that Ro 15-1788 seems to reverse transiently the ethanol-induced changes in total alpha, delta, and slow alpha bands. There was no pharmacokinetic interaction between both agents since elimination of Ro 15-1788 (t1/2 = 1.2 +/- 0.7 h) and of ethanol (0.17 +/- 0.02 g l-1 h-1) were in good agreement with control values. Thus, it could be concluded that Ro 15-1788 might affect for a short while the action of ethanol by interfering with the benzodiazepine receptors.

Adult↗

[Prevalence and etiology of mental problems in tumor patients].

Data obtained from a questionnaire completed by 177 cancer patients were analyzed for prevalence of depressive and anxiety disorders and aspects of coping behavior. We found a high correlation between frequency of depressive symptoms and the period time after which cancer was diagnosed. According to data reported by other authors, prevalence of depression ranged between 21% and 32%. Anxiety disorders were found in about 40% of all cancer patients. Chemotherapy seems to be very stressing: During the course of therapy, we found a duplication of depressive symptoms, severe depression increases from 0% to 17%. Personality-traits possibly predict anticipated nausea and vomiting (ANV). Patients with ANV show higher values in depression, anxiety, fatalism, but lower ones in internal control measured before chemotherapy.

Adaptation, Psychological↗

Central and autonomic nervous system side effects of ketanserin.

A placebo controlled, randomized, double-blind cross-over study was carried out in 7 healthy volunteers in order to study the central and autonomic nervous system side effects of ketanserin in comparison to clonidine. Psychometric performance was assessed as well as electroencephalographic recordings (EEG), saliva production, mean arterial blood pressure (MAP) and pulse rate under placebo conditions (P, 10 ml saline), following 0.15 mg/kg ketanserin or 2 micrograms/kg clonidine i.v. administration. The sedation index as well as the deceleration of EEG frequencies clearly expressed sedation following both, ketanserin and clonidine. Saliva production was significantly decreased by ketanserin (p less than 0.05) and clonidine (p less than 0.01), respectively. MAP was only very slightly reduced by ketanserin, while clonidine caused a small but significant decrease (p less than 0.0001). The pulse rate changes did not reach a clinically important extent. Thus, sedation as main central nervous system side effect and reduction in salivation as autonomic nervous system side effect of ketanserin could be clearly quantified in comparison to placebo and clonidine.

Adult↗