Platelet Activation in Psoriasis

Summary

Recent epidemiological studies have suggested that psoriasis represents a risk factor for thrombotic vascular diseases. In order to evaluate the possible role of hemostatic changes in the development of thrombotic episodes in psoriasis, some parameters of the hemostatic “balance” were investigated in 22 male psoriatic patients and compared to those of 22 male control subjects. Incidence of known risk factors for vascular diseases (diabetes, hypertension, smoking, dyslipidemia) was comparable in the two study groups. There were no statistically significant differences in platelet count, circulating platelet aggregates, platelet production of malondialdehyde (MDA), total plasma anti thrombin and fibrinolytic activities. In patients with psoriasis the incidence of spontaneous platelet hyperaggregability and plasma levels of β-thromboglobulin were significantly higher than in control subjects. Platelet regeneration time, measured as MDA recovery after aspirin ingestion, was significantly shorter in psoriatic patients. These data suggest that an in vivo platelet activation occurs in patients with psoriasis and could contribute to the development of thrombotic complications. The release of mitogenic and inflammatory substances by activated platelets may play a role in the histogenesis of psoriatic lesions.

Keywords

Platelet - Vascular disease - Psoriasis

• References

• 1 McDonald CJ, Calabresi P. Psoriasis and occlusive vascular disease. Br J Dermatol 1978; 99: 469-475
• 2 Lane JL, Bird P, Rizza CR. A new assay for the measurement of total progressive antithrombin. Br J Haematol 1975; 30: 103-115
• 3 Astrup T, Müllertz S. The fibrin plate method for estimating fibrinolytic activity. Arch Biochem Biophys 1952; 40: 346-351
• 4 Nenci GG, Agnelli G, Berrettini M, Parise P, Ballatori E. Inhibition of spontaneous platelet aggregation by sulfinpyrazone. Thromb Haemostas 1979; 42: 621-625
• 5 Breddin K, Krzywanek HJ, Bald M, Kutschera J. Is enhanced platelet aggregation a risk factor for thromboembolic complication in atherosclerosis. In Platelet aggregation and drugs Caprino L, Rossi EC. (Eds) Academic Press; London: 1974. pp 197-212
• 6 Wu KK, Hoak JC. A new method for the quantitative detection of platelet aggregates in patients with arterial insufficiency. Lancet 1974; 2: 924-926
• 7 Stuart MJ, Murphy S, Oski FA. A simple nonradioisotope technique for the determination of platelet life span. N Engl J Med 1975; 292: 1310-1313
• 8 Nenci GG, Parise P, Capodicasa E, Berrettini M. Platelet malondialdehyde production kinetics after cyclooxygenase block. Haemostasis 1983; 13: 53-60
• 9 Schafer AI, Handin RI. The role of platelets in thrombotic and vascular disease. Prog Cardiovasc Dis 1979; 22: 31-52
• 10 Ludlam CA, Moore S, Bolton AE, Pepper DS, Cash JD. The release of a human platelet specific protein measured by a radioimmunoassay. Thromb Res 1975; 6: 543-548
• 11 Harker LA. Platelet survival time: its measurement and use. In Progress in hemostasis and thrombosis Spaet HT. (Ed.) Grune & Stratton; New York: 1978. 4 321-347
• 12 Davi G, Reni GB. et al Enhanced platelet release reaction in insulin-dependent and insulin-independent diabetic patients. Haemostasis 1982; 12: 275-281
• 13 Lentini S, Bologna E. Hypertension and platelet aggregation. In Platelet aggregation and drugs Caprino L, Rossi EC. (Eds) Academic Press; London: 1974. pp 63-76
• 14 Carvalho AC A, Colman RW, Lees RS. Platelet function in hyperlipoproteinemia. N Engl J Med 1974; 290: 434-438
• 15 Levine PH. An acute effect of cigarette smoking on platelet function. A possible link between smoking and arterial thrombosis Circulation 1973; 48: 619-623
• 16 Braverman IM. Electron microscopic studies of the microcirculation in psoriasis. J Invest Dermatol 1972; 59: 91-98
• 17 Braverman IM. Microcirculation in psoriasis. In Psoriasis; Proc. II International Symposium Farber ME, Cox AJ. (Eds) Yorke Medical Books; New York: 1976. pp 28-35
• 18 Hammarrstrøm S, Hamberg M, Samuelsson B, Duell EA, Stawiski M, Voorhees JJ. Increased concentrations of free arachidonic acid, prostaglandins E₂ and F_2α, and of 12L-hydroxy-5,8,10,14-eicosatetraenoic acid (HETE) in epidermis of psoriasis: evidence for pertur- o bated regulation of arachidonic acid levels in psoriasis. Proc Natl Acad Sci USA 1975; 72: 5130-5134
• 19 Hammarrstrøm S, Lindgren JA, Marcelo C, Cuell EA, Anderson TF, Voorhees JJ. Arachidonic acid transformations in normal and psoriatic skin. J Invest Dermatol 1979; 73: 180-183
• 20 Moncada S, Gryglewski RI, Bunting S, Vane JR. A lipid peroxide inhibits the enzyme in blood vessel microsomes that generates from prostaglandin endoperoxides the substance (prostaglandin X) which prevents platelet aggregation. Prostaglandins 1976; 12: 715-737
• 21 Nachman RL, Weksler B, Ferris B. Increased vascular permeability produced by human platelet granule cationic extract. J Clin Invest 1970; 49: 274-281
• 22 Kepner N, Creasy G, Lipton A. Platelets as a source of cellproliferating activity. In Platelets: a multidisciplinary approach. de Gaetano G, Garattini S. (Eds) Raven Press; New York: 1978. pp 205-212