[Hyperaggregation syndrome in patients with osteolytic psoriatic arthritis]. / Giperagregatsionnyi sindrom u bol'nykh s osteoliticheskim variantom psoriaticheskogo artrita.

AIM: To study blood rheology in patients with psoriatic arthritis (PA) having local or advanced osteolysis. MATERIALS AND METHODS: The trial included 16 patients with significant PA and clinical and x-ray symptoms of joint surface osteolysis. Kinetics of red cell aggregation and disaggregation was studied in specially designed erythroagregometer. RESULTS: The assessment of red cell aggregation indicated the presence of hyperaggregation syndrome in the majority of PA patients with associated osteolysis. CONCLUSION: Hyperaggregation may contribute to bone destruction. Its onset can be reviewed as a risk factor for serious destructive changes in the joints.

[Alterations of rheological properties of blood in systemic sclerodermia]. / Narusheniia reologicheskikh svoistv krovi pri sistemnoi sklerodermii.

AIM: To study hemorheological status in systemic sclerosis (SS) patients. MATERIAL AND METHODS: Macro- and microrheology of blood were investigated in 70 SS patients. The rate of spontaneous aggregation of red blood cells [T1(s)], durability of the largest units [Ia2.5(%)], general hydrodynamic durability of units [beta(s-1)], limit of fluidity [tau 0 (mPa)], Casson viscosity K (mPa/s) were determined. RESULTS: The total severity of hemorheological disturbances was 1.90 +/- 0.07 with T1 = 4.98 +/- 1.52s, beta = 62.76 +/- 19.32s, Ia 2.5 = -0.78 +/- 12.83%, tau 0 = 7.00 +/- 0.45 mPa. The Casson viscosity did not differ from normal levels. Plasma viscosity was 1.71 +/- 0.18 rel units, viscosity of sera 1.55 +/- 0.14 rel.units. The severity of hemorheological disturbances did not differ in cute and chronic courses but the parameter beta (72.0 +/- 4.5) was significantly higher (p < 0.05) in the acute course. The severity of hemorheological disturbances was highest in SS patients with cardiac disease (p < 0.05) and in 10 year SS duration. CONCLUSION: The course of SS is complicated by progressive hyperaggregation syndrome promoting development of visceral pathology. Active correction of hemorheology is pathogenetically validated in SS.