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J Lukác

Publications and source records attributed to J Lukác.

At least 37 records · Page 2Linked to original sources
PubMed1995

[General therapeutic approaches in systemic vasculitides].

The paper presents general therapeutic principles applied in systemic vasculitis. Several factors may help to contain the clinical activity, such as the location and extent of the inflammatory process affecting the vascular system, the ultimate narrowing of the vascular lumen with subsequent ischemia of the affected tissue and organ. Treatment of vasculitis involves besides glucocorticoids not only cytotoxic drugs (cyclophosphamide, chlorambucil, methotrexate), and immunomodulatory therapeutic agents with immunosuppressive action (cyclosporin A) but also other immunomodulatory drugs, as e.g. dialyzed homogenate of leukocytes (DHL), pentoxyphylline, hydrolytic enzymes, and monoclonal antibodies. The authors emphasize the importance of a complex approach in the management of systemic vasculitis. (Tab. 1, Ref. 36.).

Humans↗
PubMed1991

[Increased numbers of large granular lymphocytes in the peripheral blood in selected inflammatory rheumatic diseases].

In six patients with selected inflammatory rheumatic diseases the authors found increased numbers of LGL in the peripheral blood. Concurrently in these patients an increase of lymphocytes with the CD57 sign was found. In one patient with rheumatoid arthritis more detailed analysis revealed a reduced number of lymphocytes with sign CD16. In this patient in the peripheral blood cells with signs CD3+ and CD57 were found and the function of NK cells was markedly reduced. The clinical course of the disease in the patients was severe, in particular in SLE, where in three patients the disease was associated with the development of lupus glomerulonephritis. The patients were treated by immunosuppressive therapy. The authors reflect on the causes of the increase of LGL cells and do not rule out the possible presence of a serious immunoregulatory disorder between T and B lymphocytes.

Adult↗
PubMed1989

[The effect of colchicine and its derivatives on the activity of enzyme markers of T-lymphocytes].

Colchicine and its less toxic derivatives (demecolcine and deacetyl colchicine), in dependence on the concentration in the incubation medium, inhibited the activity of adenosine deaminase in the lymphocytes. All the three substances increased the level of cyclic adenosine monophosphate which has the ability of influencing the proliferation of T-lymphocytes. Colchicine and its derivates also inhibited the activity of purine nucleooxidophosphorylase, which, similarly as adenosine deaminase, is a marker enzyme of T-lymphocytes. The results obtained lead to the assumption that the mentioned preparations inhibit the function of T-lymphocytes.

Adenosine Deaminase↗
PubMed1989

[Evaluation of long-term immunotherapy in patients with lupus nephritis].

In 177 patients with lupus nephritis in the course of three decades three methods of immunotherapy were used the effect of which was evaluated retrospectively. When the criterium of the survival period was used, it was revealed that from a group of 66 patients treated only with glucocorticoids (mainly prednisone by the oral route) less than 60% survived five years the onset of lupus nephritis, only 33% survived 10 years. From a group of 81 patients treated with glucocorticoids and cytostatics (mostly cyclophosphamide by the oral route) 80% survived five years and 50% ten years, while in a group of 30 patients treated with glucocorticoids, cyclophosphamide and levamisole 90% survive five years and as many as 70% ten years from the onset of lupus nephritis. From the onset of SLE however as many as 80% survived ten years in all three analyzed groups, which provides evidence that lupus nephritis accounts for the greatest mortality in patients with SLE, as renal failure was the cause of death in one third of the patients. As to complications, secondary infections were recorded in almost 30% of the patients, incl. 9% lethal ones, non-infections complications less than 5%. The authors discuss assumed mechanism of the action of combined immunotherapy, which holds a priority position, as compared with glucocorticoid monotherapy.

Cyclophosphamide↗
PubMed1987

Deficiency of C2, the second complement component, in the family of a patient with SLE-like syndrome: the first case of hereditary C2 deficiency in Czechoslovakia.

A family with hereditary C2 deficiency was discovered in Czechoslovakia. The proband is a 47-year-old female with a SLE-like syndrome and zero activity of the classical complement pathway. Functional CH50, C1, C2, and C4 estimations for all family members revealed a homozygous C2 deficiency in both the proband and her elder sister, and several heterozygotic C2-deficient individuals. The defect segregates with haplo-type HLA A25, B18, DR2.

Adult↗
PubMed1985

Effect of ketanserin on Raynaud's phenomenon in progressive systemic sclerosis: a double-blind trial.

Ketanserin was used in a randomized double-blind trial in 15 patients with Raynaud's phenomenon in progressive systemic sclerosis (PSS). Its effect on Raynaud's phenomenon was evaluated by IR-radiometry, Doppler ultrasound, nailfold capillaroscopy, frequency of finger ulcerations and patient complaints before and after a 3-month course of treatment with oral ketanserin in the dosage of 60 mg daily in the first month and 120 mg in the second and third months. Of the 8 patients treated with ketanserin, 5 showed improvement. In the other 2 patients with progression of skin sclerosis and multiorgan involvement, the peripheral vascular disorder was unchanged. Ketanserin treatment was discontinued in one patient owing to dizziness and anxiety. In one patient ketanserin was reduced to 60 mg daily because of fluid retention. There were no other adverse effects. In 7 control patients on placebo there was no significant improvement in Raynaud's phenomenon. Ketanserin, a selective, specific and pure antagonist of 5-hydroxytryptamine (serotonin) appears to be an effective agent in the treatment of Raynaud's phenomenon and digital ischaemic ulcers in PSS. Moreover, ketanserin could contribute to the understanding of the role of 5-hydroxytryptamine in PSS pathogenesis.

Adult↗
PubMed1984

Clinical and immunological characterization of systemic lupus erythematosus in patients with circulating interferon and migration inhibitory factor.

The simultaneous occurrence of interferon and migration inhibitory factor was found in sera from 9 patients with systemic lupus erythematosus (SLE). Their clinical picture was characterized by a moderate course of the disease. In 7 patients the inflammatory tendoarticular manifestations were accentuated. Glomerulonephritis was found only in 3 patients and was successfully suppressed by immunosuppressive therapy. In the peripheral blood of most of these patients, normal or moderately increased levels of active E-rosettes were found. Therefore we consider these SLE patients as a group with characteristic signs of activated cell-mediated immunity (lymphokine release, active E-rosettes). Although the reason for this activation remains unknown, we suppose that some concomitant bacterial infection, perhaps mycobacterial, may contribute to this immunological phenomenon.

Adult↗