
16.01.2006, 22:48
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Registriert seit: 01.03.2005
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@streetiswatching:
Zitat:
H2-antagonists and possibilities for their therapeutic use in dermatology]
[Article in German]
Diller G, Orfanos CE.
H2-antagonists differ from the commonly applied antihistamines (H1-antagonists) by blocking a different spectrum of histamine-mediated pharmacologic reactions. Their effects on the skin as the target organ may be stronger, weaker, or even reverse. The main representative of this group of drugs is cimetidine. Other compounds are still in experimental stages. Some controversial effects were reported in urticaria, pruritus, atopic dermatitis, mastocytosis of the skin, and also in acne and psoriasis. With polyetiologic symptoms, as are manifested in cases of urticaria and pruritus, the efficacy of the drug may depend on the underlying disease. In acne and psoriasis, the clinical type and stage of the disease may also play a major role in the outcome of such studies. Experimental and clinical findings suggest that cimetidine has some immunomodulating effect in terms of influencing the delayed type skin hypersensitivity. The intake of cimetidine should be registered in patch testing. Application of H2-antagonists may be beneficial in diseases with reduced immune resistance (generalized mycotic infections). Serious group-specific side-effects of H2-antagonists are not yet known. Several side-effects have been reported following oral intake of cimetidine; however, their frequency seems rather low.
This study suggests that h2 receptor blockade reduce the delayed type hypersenstivity of the the skin to antigens (toxins, foods etc). So acne sufferers in addition to them producing more toxins (possibly through an effect of histamine-via h2 recpetors- on cellular metabolic rate), also catabolising carbohydrates more rapidly (leading to hyperglyceamia and insulin resistance) ALSO have increased inflammatory sensitivity to antigens, which manifests as acne.
NOW i have some interesting supportive research....This could be very important.
1. Histamine potently suppresses human IL-12 and stimulates IL-10 production via H2 receptors.
J Immunol 1998 Sep 1;161(5):2586-93 (ISSN: 0022-1767)
Elenkov IJ; Webster E; Papanicolaou DA; Fleisher TA; Chrousos GP; Wilder RL
Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, Bethesda, MD 20892, USA. ElenkovI@cc1.nichd.nih.gov.
IL-12 and IL-10, respectively, stimulate Th1 and Th2 immune responses. The development of some allergic reactions, infections, and tumors are associated with excessive histamine production and a shift toward Th2 responses. Here we address the possibility that this association is causally linked, at least in part, to modulation of IL-12 and IL-10 production by histamine. We report that histamine dose-dependently inhibited the secretion of human IL-12 (p70) and increased the production of IL-10 in LPS-stimulated whole blood cultures. These effects of histamine were antagonized by cimetidine, an H2 receptor antagonist, but not by selective H1 and H3 receptor blockers, and were mimicked by an H2 receptor agonist.
The effects of histamine on IL-12 and IL-10 secretion were independent of endogenous secretion of IL-10 or exogenous addition of IL-12, while Ro 20-1724, a phosphodiesterase inhibitor, potentiated the effects of histamine on IL-12 and IL-10 production, implicating cAMP in its actions. Similar modulatory effects of histamine on IL-12 and IL-10 production, which were reversed by the H2 antagonist cimetidine, were observed in PBMC and isolated monocytes stimulated by Staphylococcus aureus Cowan strain 1 and LPS, respectively. Thus, histamine, via stimulation of H2 receptors on peripheral monocytes and subsequent elevation of cAMP, suppresses IL-12 and stimulates IL-10 secretion, changes that may result in a shift of Th1/Th2 balance toward Th2-dominance. This may represent a novel mechanism by which excessive secretion of histamine potentiates Th2-mediated allergic reactions and contributes to the development of certain infections and tumors normally eliminated by Th1-dependent immune mechanisms.
To summerize..chronically raised histamine levels (histadelia), cause increased release of IL-10 by white blood cells (called monocytes) which is a chemical messenger in the immune system. This IL-10 then activates T-Helper cells (Th2 cells) and suppresses Th1 cells.
The whole immune system function depends on the relative balance in activity of Th1 and Th2 cells. If there is an overactivity in Th2 then the person is more prone to certain conditions, and allergies etc.
The following artical explains the relevance of this much better...
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