Therapeutic effects of nandrolone decanoate, tibolone, lynestrenol and ethylestrenol on Sjogren's syndrome-like disorder in NZB/W mice. (1/4)

Growth of mononuclear cell infiltration in submandibular glands is significantly inhibited by Org OD14 (tibolone), lynestrenol and ethylestrenol given orally to New Zealand Black/White (NZB/W) mice from 26 weeks of age onwards. In addition, the extent of already established mononuclear cell infiltrations is significantly inhibited and reduced by nandrolone decanoate injected from 43 weeks of age onwards. Tibolone and nandrolone decanoate are the most potent of the four drugs. The therapeutic effect of these four steroids on the Sjogren's syndrome-like disorder in NZB/W mice is not related to their endocrine activities.  (+info)

Clinical and laboratory double-blind investigation on effect of fibrinolytic therapy in patients with cutaneous vasculitis. (2/4)

The effects of phenformin and ethyloestrenol and phenformin and stanozolol on the clinical state, plasma fibrinolytic activity, and fibrinogen-fibrin-related antigen (F.R.-antigen) were compared with placebo in 13 patients with cutaneous vasculitis. Eight patients showed considerable clinical improvement when taking phenformin and an anabolic steroid; an impaired fibrinolytic activity before treatment favoured clinical improvement.  (+info)

Pharmacological enhancement of fibrinolytic activity and 125I-fibrinogen survival. (3/4)

Studies with (125)I-fibrinogen after the administration of phenformin plus ethyloestrenol in five subjects showed no evidence of enhanced catabolism of fibrinogen despite a fall in plasma fibrinogen concentration and shortened clot lysis time. It seems probable that the fall in plasma fibrinogen concentration after the administration of these drugs is related to diminished hepatic synthesis of fibrinogen and is independent of the induction of plasminogen activator release.  (+info)

Effect of ethyloestrenol on fibrinolysis in the vessel wall. (4/4)

Forty-nine patients with decreased fibrinolytic activity in the vessel walls or a decreased release mechanism, or both, were treated with ethyloestrenol for three to 17 months. Forty-five of the patients had had recurrent, phlebographically verified, deep venous thrombosis (DVT) and four had arterial thrombosis. Ethyloestrenol 8 mg/day was given to 31 patients and 4 mg/day was given to 12. The remaining six patients had been treated with a combination of phenformin and ethloestrenol. The phenformin was withdrawn but they were kept on ethyloestrenol 8 mg/day. Another 15 patients with a normal fibrinolytic system--four with recurrent DVT and 11 with severe arteriosclerosis--were given ethyloestrenol 8 mg/day. The spontaneous fibrinolytic activity, local fibrinolytic activity during standardised venous occlusion of the arms, and fibrinolytic activity of the vessel walls increased significantly after treatment with ethyloestrenol 8 mg/day for three months. No further increase occurred after three months, and ethyloestrenol 4 mg/day had no effect. No values rose significantly in the patients with a normal fibrinolytic system. One patient suffered a recurrence within three months of treatment, before the fibrinolytic system became normal. In one patient the fibrinolytic defect reappeared after 10 months in spite of continued treatment. Two of the three women of fertile age developed irregular cycles and intermenstrual bleeding, which disappeared when the treatment was withdrawn. No other side effects were observed.  (+info)