ArticleArchives of dermatological research1991
In vivo and in vitro effects of glucocorticoids on lectin-induced blastogenesis in atopic dermatitis.
Article in Archives of dermatological research, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Lectins Are the Sparkle of Hope for Combating Coronaviruses and the Global COVID-19.Advanced pharmaceutical bulletin · 2022Review
- Inhibition of rat splenocyte proliferation with methylprednisolone: in vivo effect of liposomal formulation.Pharmaceutical research · 1994Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of glucocorticoids administered in vivo and in vitro on lectin-induced proliferation of lymphocytes sampled from venous blood were investigated in patients with atopic dermatitis (AD) and in normal controls. Stimulation by concanavalin A (Con A), phytohaemagglutinin A (PHA) and pokeweed mitogen (PWM) in patients and controls did not differ significantly under baseline conditions. After in vivo administration of methylprednisolone the decline of Con A-induced blastogenesis of leucocytes was similar in both groups, whereas PHA stimulation caused a significant reduction in the controls only. In vitro addition of different dexamethasone concentrations had a pronounced suppressive effect on Con A- and PHA-induced blastogenesis in both groups, whereas PWM stimulation was unaffected. Pretreatment in vivo with methylprednisolone further decreased the suppression of the Con A and PHA lymphocyte proliferation rate by dexamethasone added in vitro in controls but not in patients. With regard to B-cell proliferation generated by PWM, no consistent glucocorticoid effect could be observed. The impaired effect on lymphocyte blastogenesis of glucocorticoids administered in vivo, in contrast to a normal in vitro reaction to dexamethasone, together with recent findings of an altered glucocorticoid receptor pharmacology in AD, points to a decreased biological in vivo efficiency of methylprednisolone in atopic dermatitis.
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Registered trials
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