[The indices of cellular-vascular, coagulatory haemostasis and fibrinolysis in arterial hypertension of patients of different age groups].

The contrastive analysis of the indices of cellular and vascular, coagulatory haemostasis and fibrinolysis in arterial hypertension (AH) was held among the patients of different age groups. 69 patients with AH were researched. The average age of afflicted people in the first blockette is 50,9+/-0,7 years, in the second blockette - 70,7+/-1,5. In order to evaluate the condition of haemostasis the afflicted people were researched in the following indices: amount of thrombocytes, hemolysate-aggregative test (HAT), leukocytic-thrombocytic aggregation (LTA), activity of Villebrand factor (FV), inactivation index of thrombin (IIT), activated partial thromboplastin time (APTT), prothrombin index (PTI), fibrinogen, antithrombin III (AIII), Hageman-dependent fibrinolysis (HDF), lupous anticoagulants (LA), autocoagulatory test (ACT). All the examined patients with AH showed considerable abnormalities in cellular and vascular and coagulatory links of haemostasis and the system of fibrinolysis. It is observed, that aged afflected people with AH have progressive hyperaggregation of thrombocytes, the activity of Villebrand factor increases, the rise of coagulatory link activity of haemostasis and the exhaustion of anticoagulants' products is more considerable, the subsequent fibrinolysis depression is observed, but hyperfibrinogenemia accrues. The received results show the heterogeneity of AH in different age groups.

[Combination of Libman-Sacks endocarditis with infectious endocarditis]. / Sochetanie éndokardita Libmana-Saksa i infektsionnogo éndokardita.

Out of 242 patients treated for systemic lupus erythematosus (SLE) in Novosibirsk for 15 years, valvular lesions and endocarditis were diagnosed in 41(16.9%) patients. Combination of Libman-Sax endocarditis (LSE) with infectious endocarditis (IE) was observed in three patients (two women, one man, age 18-40 year). SLE ran a subacute course in one woman, an acute one--in the other. LSE emerged early in SLE in two patients. All the patients had polyorganic lupus pathology, lupus nephritis with nephrotic syndrome (morphological class IV). Two patients had mitral valve disease, one patient--mitral-aortic disease. The rise of secondary IE was seen after massive immunosuppressive therapy. The diagnosis of secondary IE was made after SLE duration for 10-36 months. At IE diagnosis, all the patients had high titers of blood antiphospholipid antibodies. IE was of staphylococcal origin in two patients and candidosis-induced in one patient. In SLE with IE there was thromboembolic syndrome. LSE and IE have related aspects which should be regarded in clinical practice: possible "IE mask" in LSE, risk of secondary IE in about 10% of LSE patients, prophylactic measures necessary to prevent IE in hemodynamically prominent forms of LSE.

[Synchronizing therapy with plasmapheresis and cyclophosphamide in rapidly progressing systemic lupus erythematosis with kidney involvement]. / Sinkhroniziruiushchaia terapiia plazmaferezom i tsiklofosfamidom bystroprogressiruiushchei sistemnoi krasnoi volchanki s porazheniem pochek.

12 patients with rapidly progressive systemic lupus erythematosus (SLE) combined with renal failure were treated for 6 months according to the following scheme: 3 consecutive procedures of plasmapheresis (60 ml/kg x 3), 3 consecutive pulse doses of cyclophosphamide (400 mg/m2 x 3), 3 prednisolone infusions (2 mg/kg x 3), oral cyclophosphamide (100-250 mg/day) and prednisolone (0.5 mg/kg with subsequent dose reduction). Dose of the drugs was controlled by blood leukocyte count and creatinine clearance. The patients were included in the trial in the preset time. All the patients had active SLE (33.5 +/- 2.7 U according to SLAM). 75, 25, 58.3, 33.4, 8.3% of patients had mixed, nephrotic, mesangiocapillary, mesangioproliferative, membraneous nephritis, respectively. 26 weeks of the treatment produced a response in 83.3% of the patients. The disease activity lowered to 12.8 +/- 2.9 U. Four-year survival reached 81%. Cytopenia developed in 25% of patients, deep hemopoiesis depression was not observed. Septic candidiasis arose in one woman on the third year of the follow-up. Clinical validity of the above method is stated in severe SLE.

[Myocardial infarction in systemic lupus erythematosus]. / Infarkt miokarda pri sistemnoi krasnoi volchanke.

Six patients under 50 with confirmed systemic lupus erythematosus (SLE) developed myocardial infarction at different intervals from the disease onset (1-21 years). Five of them had chronic disease, one suffered from acute SLE. The analysis of clinical findings identified myocardial infarction risk factors in SLE (chronic course of the disease, long-term glucocorticosteroid treatment, hypercholesterolemia, persistent nephrotic syndrome, arterial hypertension, vasculitis, hypercoagulation, antiphospholipid antigens) and provided a basis for prevention of this severe SLE complication.

[Amyloidosis in systemic lupus erythematosus]. / Amiloidoz pri sistemnoi krasnoi volchanke.

Based on the authors' experience from 1982 to 1990 it was noted that out of 26 cases of renal amyloidosis in the presence of nonpurulent and purulent conditions 2 patients (7%) demonstrated the association with systemic lupus erythematosus (SLE). It was also noted that amyloidosis developed in the patients with a long history of the disease. Long-course immunosuppression treatment could be regarded as the other factor-of-risk for amyloidosis development. Histochemical examination of both patients demonstrated that amyloid deposits in the renal glomeruli were resistant to the potassium permanganate effect and consisted of AL-protein. The results obtained indicated the possibility of appearance of immunoglobulins AL--the proteins of the primary amyloidosis--synthesized in the spectrum in the SLE presence as well as their deposition in the renal glomeruli. As a possible cause of proteinuria and the nephrotic syndrome in SLE patients amyloidosis should be diagnosed in the life time and be regarded in the choice of therapeutic policy as well as in the assessment of pulse immunosuppressive therapy practicability.