1.
[The use of fenazid in patients with pulmonary tuberculosis with poor isoniazid tolerance].
Borisova, MI, Stakhanov, VA, Sharkova, TI, Ivashchenko, NA
Problemy tuberkuleza i boleznei legkikh. 2003;(7):34-7
Abstract
The paper shows the experience gained in the use of the new Russian antituberculous drug fenazid in patients with different forms of active pulmonary tuberculosis and with neuro- and angiotoxic reactions to isoniazid. The study group comprised 25 patients aged 23 to 70 years who received fenazid as tablets in a daily dose of 0.5 g for 2 months at the first stage of the basic course of chemotherapy. The control group including 24 patients of the same age was given the routine antituberculous chemotherapy regimen, including isoniazid. The use of fenazid permits adequate therapy in patients with poor isoniazid tolerance, which may recommend fenazid to individuals at high risk for adverse reactions as their prevention.
2.
Iron chelation improves endothelial function in patients with coronary artery disease.
Duffy, SJ, Biegelsen, ES, Holbrook, M, Russell, JD, Gokce, N, Keaney, JF, Vita, JA
Circulation. 2001;(23):2799-804
Abstract
BACKGROUND Some epidemiological studies have shown that increased iron stores are associated with increased cardiovascular events. Redox-active iron may contribute to lipid peroxidation, endothelial cell activation, and generation of reactive oxygen species (especially hydroxyl radical, via Fenton chemistry). Increased oxidative stress is associated with impaired action of endothelium-derived nitric oxide in patients with atherosclerosis. METHODS AND RESULTS To test the hypothesis that reducing vascular iron stores would reverse endothelial dysfunction, we examined the effects of the iron chelator deferoxamine (500 mg intra-arterially over 1 hour) on vasomotor function in forearm resistance vessels of patients with coronary artery disease by venous occlusion plethysmography. Patients with coronary artery disease had impaired endothelium-dependent vasodilation in response to methacholine compared with healthy control subjects (P<0.001). Deferoxamine infusion decreased serum iron levels (P<0.001). Deferoxamine improved the blood flow response to methacholine in patients with coronary artery disease (P<0.01 by 2-way repeated-measures ANOVA) but had no effect on the response to sodium nitroprusside. In normal volunteers, deferoxamine had no effect on the response to methacholine. The nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine abolished augmentation of the methacholine response associated with deferoxamine. The hydroxyl radical scavenger mannitol had no effect on the methacholine response. CONCLUSIONS Deferoxamine improved nitric oxide-mediated, endothelium-dependent vasodilation in patients with coronary artery disease. These results suggest that iron availability contributes to impaired nitric oxide action in atherosclerosis.