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C Erhardt

Publications and source records attributed to C Erhardt.

5 recordsLinked to original sources
PubMed2004

Prostaglandin-mediated control of rat brain kynurenic acid synthesis--opposite actions by COX-1 and COX-2 isoforms.

Kynurenic acid (KYNA), an endogenous glutamate-receptor antagonist preferentially blocking NMDA-receptors, has analgesic properties and has also been implicated in the pathophysiology of schizophrenia. Recently, the non-steroid anti-inflammatory drug (NSAID) diclofenac was found to increase rat brain KYNA. Here, we analyze whether cyclooxygenase (COX)-1 or COX-2 modulate the levels of rat brain KYNA. The non-selective COX-inhibitor diclofenac (50 mg/kg, i.p.) or indomethacin (50 mg/kg, i.p.), a non-selective inhibitor with a preferential selectivity for COX-1, produced an elevation in brain KYNA. In contrast, the COX-2 selective inhibitors parecoxib (25 mg/kg, i.p.) or meloxicam (5 mg/kg, i.p.) decreased brain KYNA. Both elevation and lowering of brain KYNA by indomethacin or parecoxib, respectively, were prevented by the prostaglandin E1/E2 agonist misoprostol (1 mg/kg, s.c.). It is proposed that increased brain KYNA formation induced by NSAIDs displaying an inhibitory action on COX-1 contribute to their analgesic efficacy as well as to their psychiatric side effects.

Animals↗
PubMed2003

[Cortical arousal, autonomic arousal. Evaluation techniques and clinical importance].

The respiratory disorders expressed by obstructive hypopneas and apneas during sleep, as well as the sequences of crescendo in respiratory effort without hypopneas or apneas which define the upper airway resistance syndrome, terminate with (thanks to) an arousal, defined by EEG changes. In some cases, the activation of the central nervous system is restricted to a sympathetic activation, which has been mainly studied in the cardiovascular area, and is not always accompanied by a cortical arousal. Various approaches (heart rate, blood pressure, pulse transit time, peripheral arterial tonometry) make the identification of sympathetic activation possible. Sympathetic activation seems to be more sensitive than cortical arousal to the stimulations generated by the respiratory system via an activation of mechanoreceptors stimulated by the increased respiratory effort in response to total or partial occlusion of the upper airway. The mechanisms of the cortical or autonomic arousal are not fully understood, but their detection could be a diagnostic tool for the identification of such disorders. Such tools are currently under validation.

Airway Obstruction↗
PubMed1981

Alterations in T gamma cells in patients with chronic idiopathic thrombocytopenic purpura.

The number and percentage of T cells bearing Fc gamma receptors (T gamma) was quantitated in peripheral blood of patients with the autoimmune disease chronic ITP. In over half the patients, low initial percentages were obtained, the great majority of which returned to within the normal range after incubation under capping conditions. The phenomenon could be reproduced by pretreating normal T cells with immune complex containing sera or aggregated HGG. Furthermore, a reversible reduction in T gamma cells was observed in control patients with nonimmune thrombocytopenia and in pregnancy. In each case an association was observed between the reduced T gamma cell levels and the presence of circulating immune complexes, which suggested that the results could be explained by masking of Fc gamma receptors with preformed IgG-containing complexes. By contrast, patients with other autoimmune diseases such as scleroderma and rheumatoid arthritis had high or normal numbers of T gamma cells, respectively. Taken together, the findings do not support the existence of a gross deficiency of suppressor cells in patients with autoimmune disease and emphasize the need for caution in selection of markers for identification of T cell subsets.

Animals↗
PubMedDate not supplied

Treating rheumatoid arthritis early with disease modifying drugs reduces joint damage: a randomised double blind trial of sulphasalazine vs diclofenac sodium.

BACKGROUND: Current disease management in rheumatoid arthritis (RA) has moved towards "inverting the therapeutic pyramid" by introducing disease-modifying anti-rheumatic drugs (DMARDs) early. Despite the logic of early DMARD therapy, there is a dearth of supportive evidence for this approach. We report a randomised controlled trial comparing sulphasalazine monotherapy with diclofenac monotherapy in early RA. The primary aim was to provide unequivocal evidence that early DMARDs prevent erosive damage. The secondary aim was to evaluate if sulphasalazine used alone has comparable symptomatic benefits to NSAIDs. METHODS: 117 patients with RA for under 12 months of diagnosis (mean 2 months) were randomised (62 sulphasalazine; 55 diclofenac). Sulphasalazine patients comprised 76% women, and 58% were rheumatoidfactor positive. Diclofenac patients comprised 74% women, and 54% were seropositive. 36% completed 12 months of therapy (16 sulphasalazine; 26 diclofenac); sulphasalazine was given for a mean period of 21 weeks and diclofenac for a mean period of 33 weeks. Results were analysed on an intention to treat basis. RESULTS: After 12 months the mean number of new erosions in patients randomised to receive sulphasalazine was 2.0 (95%CI 0.9, 3.1) and in patients randomised to receive diclofenac was 7.5 (95%CI 4.1, 10.9; p = 0.002 by Student's unpaired t-test). An analysis of valid compliant completers showed the mean number of new erosions in patients who received 12 months therapy with sulphasalazine was 2.3 (95%CI 0.6, 4.0) and in patients who received 12 months diclofenac was 10.5 (95%CI 5.0, 15.9; p = 0.018 by Student's unpaired t-test). The Ritchie articular index, swollen joint counts and pain scores decreased with both sulphasalazine and diclofenac, with mean falls in both groups of 15-20% at 2 weeks and 30-40% at 4 and 8 weeks. There were no differences between treatments. Disease activity scores showed similar highly significant mean decreases within both treatment groups (P < 0.001 in all cases) of 0.5 at 2 weeks and 1.0 at 4 weeks; at 12 and 26 weeks they were significantly lower with sulphasalazine (p = 0.036 and 0.045). 75% of the patients given sulphasalazine and 65% of those given diclofenac had one or more adverse events with no major differences between treatments. CONCLUSIONS: These results show that an accelerated dosing schedule of sulphasalazine has identical effects to diclofenac in reducing symptoms, indicating it is a rapidly effective DMARD. They also provide unequivocal evidence, analysed on an intention to treat basis, that early treatment with sulphasalazine significantly reduces the extent of radiological progression in active RA.

Anti-Inflammatory Agents, Non-Steroidal↗