title: Platelet-activating factor and arachidonic acid metabolites in psoriatic inflammation.
abstract: Platelet-activating factor (PAF), as well as PAF acetylhydrolase (PAF-AH) activity in the peripheral blood plasma of patients with psoriasis and palmoplantar pustolosis, was measured with a radioimmunoassay technique, and compared with leukotriene (LT) B4, LTC4, LTD4 and E4 (LTD4/E4), thromboxane (TX) B2 and prostaglandin (PG) E2 levels. In a normal healthy group (n = 12) PAF level was 25.9 +/- 6.5 pg/0.1 ml plasma (mean +/- standard error of the mean: SEM), and this was elevated in patients with psoriasis (68.1 +/- 11.8, n = 25, P < 0.01), without a change in the PAF-AH level. LTB4 showed a similar increase (115.0 +/- 21.6 pg/ml vs. 68.2 +/- 11.8 pg/ml, P < 0.05), while TXB2 and PGE2 showed insignificant (P > 0.05) changes. LTC4 and LTD4/E4 were around the level of the limit of detection. Patients with palmoplantar pustulosis (n = 33) demonstrated similar, but milder and statistically insignificant, increases in PAF, LTB4, TXB2 and PGE2 levels. Modulation of the mediator levels before and after treatment was compared in 16 patients with psoriasis and 11 with palmoplantar pustulosis. PAF in psoriasis significantly decreased after treatment (70.9 +/- 17.1 to 25.1 +/- 5.5, P < 0.05) and this was moderately correlated (r = 0.298) with clinical improvement as indicated by the psoriasis area and severity index (38.5 +/- 7.5 to 10.9 +/- 4.2, P < 0.01). TXB2 (180.2 +/- 100.4 to 34.1 +/- 13.5), PGE2 (3.7 +/- 0.7 to 2.9 +/- 0.5) and LTB4 (120.1 +/- 31.1 to 84.2 +/- 8.2), in psoriasis, mildly decreased without statistical significance. Patients with palmoplantar pustulosis demonstrated a similar decrease in all mediators without statistical significance. The results obtained suggest a role of PAF in psoriasis. As the priming effects of PAF have been shown, for leucocytes and endothelial cells, to enhance their inflammatory response, we assume that PAF has roles in the acute phase of psoriatic and leucotactic inflammation.
authors.affiliation: Department of Dermatology, Saitama Medical School, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Izaki
authors.forename: T
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Goto
authors.forename: S
authors.initials: S
authors.lastname: Ishimaru
authors.forename: F
authors.initials: F
authors.lastname: Yudate
authors.forename: K
authors.initials: K
authors.lastname: Kitamura
authors.forename: M
authors.initials: M
authors.lastname: Matsuzaki
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D000293:Adolescent; D000328:Adult; D000368:Aged; D016718:Arachidonic Acid / Q000378:metabolism*; D002648:Child; D015232:Dinoprostone / Q000097:blood; D005260:Female; D006801:Humans; D015289:Leukotrienes / Q000097:blood; D008297:Male; D008875:Middle Aged; D010741:Phospholipases A / Q000097:blood; D010972:Platelet Activating Factor / Q000378:metabolism*; D011565:Psoriasis / Q000097:blood* / Q000188:drug therapy; D013929:Thromboxane B2 / Q000097:blood
chemical_list: D015289:Leukotrienes; D010972:Platelet Activating Factor; D016718:Arachidonic Acid; D013929:Thromboxane B2; D010741:Phospholipases A; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase; D015232:Dinoprostone