The effect of nedocromil on weal reactions in human skin.

Humphreys, F.; Shuster, Sam

doi:10.1111/j.1365-2125.1987.tb03191.x

Cited by 11 publications

(4 citation statements)

References 10 publications

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“…Also, the drug did not inhibit the weal response as would have been expected if it had antihistaminic effects. Indeed, with the higher concentration of histamine, there was a statistically significant increase in the area of the weal, an observation similar to that previously reported ( Humphreys et al ., 1987 ).…”

Section: Discussionsupporting

confidence: 91%

Nedocromil sodium inhibits histamine‐induced itch and flare in human skin

Ahluwalia

McGill

Church

2001

British J Pharmacology

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This study was designed to test the hypothesis that nedocromil sodium inhibits sensory nerve function to reduce¯are and itch in human skin. Nedocromil sodium (2%) or water (control) was introduced into the volar forearm skin of eight non-atopic volunteers by iontophoresis (8 mC) and histamine (20 ml of 1 mM and 300 nM) injected intradermally 10 min later at the same site. Itch was assessed on a visual analogue scale every 20 s for 5 min. Weal and¯are areas and mean blood¯ux within the¯are were assessed by scanning laser Doppler imaging at 10 min. The results showed that nedocromil sodium reduced itch scores, totalled over 5 min, by *74.0% (P50.005) and¯are areas by *65% (P50.03). Neither weal areas nor blood¯ux within were reduced. These data demonstrate that nedocromil sodium is e ective in reducing neurogenic itch and¯are in the skin. We suggest that its mechanism of action is modulation of sensory neurone activation or conduction in the skin.

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Section: Discussionsupporting

confidence: 91%

Nedocromil sodium inhibits histamine‐induced itch and flare in human skin

Ahluwalia

McGill

Church

2001

British J Pharmacology

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“…Nedo also has no effect on mediator release from skin mast cells. This failure to inhibit IgE-dependeni mediator release supports the findings of Humphreys and Shuster [24] that this drug iontophoresed into human skin had no effect on wealing produced by intradermal histamine, 48/80 or house dust mite antigen. This failure clearly distinguishes human skin mast cells from the other mast cells examined.…”

Section: Discussionsupporting

confidence: 86%

Inhibition profiles of sodium cromoglycate and nedocromil sodium on mediator release from mast cells of human skin, lung, tonsil, adenoid and intestine

Okayama¹,

Benyon²,

Rees³

et al. 1992

Clin Experimental Allergy

108

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We have studied an aspect of the functional heterogeneity of human mast cells, namely responsiveness to the inhibitory effects of sodium cromoglycate and nedocromil sodium. The effects of these drugs were examined on the release of histamine and PGD2 from mast cells of human skin, lung, tonsils, adenoids and intestine. A high concentration, 1000 microM, of sodium cromoglycate was required to significantly inhibit histamine release from lung and tonsillar mast cells. Nedocromil sodium, 1000 microM, was more effective than sodium cromoglycate against histamine release from lung, tonsillar and adenoidal cells. Both compounds showed tachyphylaxis in lung and tonsillar mast cells but not in adenoidal and intestinal mast cells. In contrast, in intestinal mast cells, the effect of nedocromil sodium was weaker and more variable than sodium cromoglycate. Skin mast cells differed from mast cells of the other anatomical sites in being unresponsive to sodium cromoglycate and nedocromil sodium. Our results confirm that high concentrations of sodium cromoglycate and nedocromil sodium are required to achieve even modest inhibition of mediator release from human mast cells under in vitro conditions. Notwithstanding this, the results also indicate that differences exist among skin, lung, tonsillar, adenoidal and intestinal mast cells with respect to their sensitivity to sodium cromoglycate and nedocromil sodium, thus extending our knowledge of functional heterogeneity within the human mast cell populations.

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“…Following astemizole treatment, HUMPHREYS et al (1987) found a 47% inhibition ofwealing with house dust mite and 68% inhibition of compound 48/80 wealing while histamine wealing was inhibited by 83%; these observations might imply that while histamine has a role in mediating the weal and flare reaction, other mediators are also involved, as suggested by KRAUSE and SHUSTER (1984). However, HUMPHREYS et al (1987) showed that topical indomethacin did not affect the rate of formation, the magnitude, or the rate of disappearance of weals induced by histamine, compound 48/80, or house dust mite extract. Indomethacin has been said to attenuate the late skin response with allergen challenge, implying that cyclo-oxygenase products of arachidonic acid, possibly prostaglandin D 2 , are important in this response also (GRONNENBERG and ZETTER-STROM 1985).…”

Section: G Pharmacological Modulation Of Mediator Secretion From Skimentioning

confidence: 71%

“…In chopped human skin, P2-agonists are at least 100 times less efficacious in inhibiting IgE-dependent histamine secretion compared with their effects on dispersed lung mast cells (CLEGG et al 1985), supporting the findings in vivo. Furthermore the more recently introduced sodium nedecromil, which inhibits release from lung mast cells, causes histamine release in skin (HUMPHREYS and SHUSTER 1987). This chromone has a potent activity in inhibiting mediator secretion from isolated rat peritoneal mast cells (ORR 1975), though it is less active on histamine secretion from either chopped human lung fragments (CHURCH and YOUNG 1983) of dispersed human lung mast cells (CHURCH and HIROI 1987).…”

Section: G Pharmacological Modulation Of Mediator Secretion From Skimentioning

confidence: 99%