[Clinical manifestations of APS-nephropathy in primary antiphospholipid syndrome]. / Klinicheskie proiavleniia nefropatii, sviazannoi s antifosfolipidnym sindromom, pri pervichnom antifosfolipidnom sindrome.

AIM: To elicit clinical features of nephropathy associated with antiphospholipid syndrome (APSN) in patients with primary antiphospholipid syndrome (PAPS). MATERIAL AND METHODS: The analysis of clinical characteristics and course of APSN has covered 24 patients with PAPS (16 females and 8 males, mean age 34.3 years). Renal damage was represented by arterial hypertension (AH), urinary syndrome, functional decline. All the patients were tested for anticardiolipin antibodies and/or lupus anticoagulant. Renal biopsy was made in 7 patients. RESULTS: PAPS patients developed renal affection in the onset of APS or within the first 5 years of its course. In the majority of patients APSN combined with abnormalities of CNS, heart and skin. Arterial/arteriolar thromboses prevailed. APSN manifested with: AH (n = 23, severe AH in 11), abnormal renal filtration (n = 17, creatinine rise in 8), urinary syndrome with proteinuria (n = 23, in 14 with hematuria). The following clinical variants of APSN were proposed: urinary syndrome with AH (n = 16; 67%), acute nephritic syndrome (n = 7; 29%), nephrotic syndrome (n = 1). Morphological studies of biopsies from APSN patients have revealed sclerotic changes, thrombotic microangiopathy, nonspecific alterations in the glomeruli. CONCLUSION: APSN is a variant of microvascular renal affection caused by thrombotic processes in intra-organ microcirculation. It is an early clinical marker of APS. Clinically, APSN manifests with vascular renal affection, the earliest symptom being inhibition of glomerular filtration. Clinical combinations of the symptoms allow to distinguish variant of APSN suggesting the existence of acute and chronic APSN. Combination of APSN with affection of the CNS, heart and skin points to a special PAPS subtype characterized by generalized ischemic damage to the organs as a result of intraorganic arterial and/or arteriolar thromboses.

[Use of plasmapheresis in the treatment of drug-resistant cardiac arrhythmias]. / Ispol'zovanie plazmafereza pri lechenii narushenii ritma serdtsa, rezistentnykh k lekarstvennoi terapii.

AIM: To study the therapeutical efficiency of plasmapheresis (PA) in patients with drug-resistant cardiac arrhythmias (CA) and its mechanisms. MATERIALS AND METHODS: Discrete PA sessions were carried out in 56 patients with drug-resistant CA: paroxysmal atrial arrhythmia (AA), ventricular and supraventricular premature contractions, supraventricular tachycardia of various etiology. Biochemical blood values, coagulographic parameters, lipid peroxidation (LPO), the spectrum of nonesterified fatty acids (NEFA), the level of medium-sized molecules were determined, ECG monitoring, EchoCG, and left ventricular radioisotope computed tomography were performed before and after a PA session. RESULTS: PA was effective in 50% of cases. The duration of its effect averaged 3.0 (1.25-5.0) months. PA was more beneficial for patients with IHD, AA with normal left atrial dimensions, and hyperlipidemia. The duration of the effect was significantly higher when antiarrhythmic drug therapy was continued after PA. Due to PA, there were significant decreases in the blood concentrations of cholesterol, medium-sized molecules, malonic dialdehyde (MDA) and in the proportion of polyunsaturated NEFA. The antiarrhythmic effect was associated with the decreases in MDA and NEFA, with a tendency for a reduction in the rate of chemiluminescence. CONCLUSION: PA may be used in the treatment of drug-resistant CA. The most significant mechanism of its antiarrhythmic activity is to recover sensitivity to antiarrhythmics. The intrinsic antiarrhythmic activity may be associated with its effect on NEFA metabolism and LPO; however, its mechanisms await further studies.

[The heparin and trental treatment of patients with the hemorrhagic form of erysipelas]. / Lechenie bol'nykh s gemorragicheskoi formoi rozhi geparinom i trentalom.

Activation of procoagulant hemostasis and signs of increased consumption of thrombocytes were indications for the treatment of patients with hemorrhagic erysipelas by means of heparine (60 patients) and trental (30 patients). Heparine was introduced subcutaneously as "minidoses" by means of electrophoresis into the inflammation focus. Heparine produced a positive effect on hemostasis and fibrinolysis, favoured rapid disappearance of the hemorrhagic syndrome, prevention of complications of erysipelas. Trental effected positively thrombocytic hemostasis, local manifestations of the hemorrhagic syndrome but did not prevent the development of thrombophlebitis as complication of the disease.

[The use of Soviet substitutes for batroxobin in the determination of fibrinogen]. / Ispol'zovanie otechestvennykh zamenitelei batroksobina pri opredelenii fibrinogena.

Plasma fibrinogen was measured by kinetic photometry with two Soviet analogs of the foreign agent batroxobin: ancistron-N and agichal, obtained from Central Asian Aspidelaps lubricus venom by different techniques. Both the preparations of thrombin-like enzyme from the venom have proved to be adequate substituents of batroxobin; the optimal concentration of ancistron-N for this test was found to be 20 micrograms/ml or 0.04 U/ml, that of agichal 0.5 micrograms/ml.

[Changes in various hemostasis indices during transient coronary insufficiency with different durations of myocardial ischemia]. / Osobennosti dinamiki nekotorykh pokazatelei gemostaza pri transitornoi koronarnoi nedastatochnosti s razlichnoi dlitel'nost'iu perioda ishemii miokarda.

Experiments on 93 white random-bred male rats weighing 200 +/- 10 g have shown that during myocardial ischemia under transitory coronary insufficiency, there is an increase in platelet adhesive capacity, acceleration of fibrinogenesis, staged time course of formation of the fibrin-platelet structure of the blood clot, depression of its velocity and lysis degree, as well as of fibrin polymerization. Postischemic reperfusion of the coronary blood flow is not followed by normalization of all the hemostatic indicators under study even after a short-term (10 min) myocardial ischemia. Reperfusion after a long-term (40 min) ischemia gives rise to depression of coagulation and fibrinolytic activity, while that after a still longer ischemia (120 min) is characterized by discordant changes in the parameters of the systems indicated. It is assumed that similar shifts in hemostasis can be observed in patients with different patterns of coronary insufficiency.