[Pregnancy in the premorbid period and during systemic lupus erythematosus].
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Biomedical subjects
Publications and source records attributed to D Zitnan.
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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.
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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.
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