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1.
Medicina (B Aires) ; 58(3): 271-6, 1998.
Artigo em Espanhol | MEDLINE | ID: mdl-9713095

RESUMO

In our country, patients with congestive heart failure who are treated chronically with digoxin are usually advised by their physicians to stop taking the medication two days a week. This is probably aimed at decreasing digitalis toxicity. Based on digoxin pharmacokinetics we assumed that the drug plasmatic level should diminish by 40 to 50%, below the therapeutic concentration of 0.8 to 2 milligrams, after two days of suspension. The objectives of this study were: a) to analyze the reduction of the plasmatic concentration of digoxin after a two day interruption of treatment, b) to compare the plasmatic levels of the drug between patients who received continuous and discontinuous treatment. A prospective, randomized and simple blind trial was designed. A total of 36 patients with congestive heart failure and systolic dysfunction with atrial fibrillation or sinus rythm were included. Group 1 (19 patients) received continuous treatment and Group 2 (17 patients) took the drug from Monday to Friday. In the continuous treatment group there was no significant difference between the Monday (1.06 +/- 0.55 milligrams) and the Friday (1.1 +/- 0.57 milligrams) digoxin concentrations. In the discontinuous treatment group the Monday digoxin concentration (0.611 +/- 0.396 milligrams) was lower than the Friday one (1.04 +/- 0.58 milligrams). The difference was statistically significant with a p = 0.000002. In conclusion, the two days a week suspension schedule reduces the plasmatic concentration of digoxin to subtherapeutic levels while the continuous regime maintains stable concentrations within the therapeutic range. Adjusting the dose to the creatinine clearance, average concentrations of 1 milligram are obtained. These results suggest that digitalis intoxication could be prevented by adjusting the dose according to renal function rather than interrupting the treatment as it is usually done in our country.


Assuntos
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico , Digoxina/uso terapêutico , Insuficiência Cardíaca/tratamento farmacológico , Adolescente , Adulto , Idoso , Inibidores da Enzima Conversora de Angiotensina/sangue , Inibidores da Enzima Conversora de Angiotensina/farmacocinética , Digoxina/sangue , Digoxina/farmacocinética , Feminino , Insuficiência Cardíaca/sangue , Humanos , Masculino , Pessoa de Meia-Idade
2.
Medicina (B Aires) ; 57(2): 200-4, 1997.
Artigo em Espanhol | MEDLINE | ID: mdl-9532830

RESUMO

A 22 year-old woman with a seven year history of (SLE) was readmitted because of oliguria, edema, dyspnea and arterial hypertension. She had a previous biopsy diagnosis of focal glomerulonephritis, (WHO III b), and had been treated with immunosuppressors and steroids. Laboratory data showed lupus activity, AHM with thrombocytopenia, nephrotic-range proteinuria and renal failure. A second renal biopsy was performed showing diffuse proliferative nephritis, (WHO IV), in association with noninflammatory necrotizing vasculopathy with luminal obliteration. She started with hemodialysis and was subsequently treated with methylprednisolone pulses, plasmapheresis, cyclophosphamide and oral steroids. During the inpatient period, she had generalized seizures, acute lung injury and pulmonary hemorrhage. These complications, the AHM and the thrombocytopenia receded totally. Renal function was never resumed. We emphasize that this association of diffuse proliferative nephritis with noninflammatory necrotizing vasculopathy is not infrequent and has a poor renal prognosis. The AHM with thrombocytopenia was interpreted as secondary to endothelial cell damage due to vasculopathy.


Assuntos
Anemia Hemolítica/etiologia , Rim/irrigação sanguínea , Rim/patologia , Lúpus Eritematoso Sistêmico/complicações , Obstrução da Artéria Renal/etiologia , Trombose/etiologia , Adulto , Feminino , Glomerulosclerose Segmentar e Focal/etiologia , Humanos , Hipertensão Renovascular/etiologia , Nefrite Lúpica/etiologia , Insuficiência Respiratória/etiologia , Trombocitopenia/etiologia
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