Therapeutic drug monitoring of cyclosporin (CsA) has been established as part of the routine clinical treatment of patients following organ transplantation for more than 20 years, and based on contemporary knowledge, many consensus guidelines have been published to assist clinics and laboratories attain optimal strategies for patient care. This article addresses the newer directions in CsA monitoring, with particular reference to the Australasian situation that has evolved since the 1993 Australasian guideline. These changes have included the introduction of alternative assay methodologies, changed CsA formulation from Sandimmun to Neoral throughout Australasia, and alternatives to trough concentration (C0) monitoring, especially 2-hour concentration (C2) monitoring and associated validated dilution protocols to accurately quantitate the higher whole blood CsA concentrations. The revision was prepared following a recent survey of all Australasian CsA-monitoring laboratories where discordant practices were evident.

暂无摘要。

Forty-seven patients with primary pulmonary hypertension were evaluated with a dose titration protocol utilizing nifedipine (20 mg orally) or diltiazem (60 mg orally) given every hour until maximal effectiveness was achieved. Of the patients tested, 15 (32%) had a greater than 20% reduction in pulmonary artery pressure (mean 36.2 +/- 8%, p less than 0.01) and pulmonary vascular resistance (mean 50.2 +/- 7%, p less than 0.01) (pressure responders). Nineteen (40%) had a greater than 20% reduction in pulmonary vascular resistance (mean 25.2 +/- 12%, p less than 0.01), with less than a 20% decrease in pulmonary artery pressure (resistance responders). Ten had no significant change in pulmonary artery pressure or pulmonary vascular resistance (nonresponders), and three were unable to tolerate the calcium channel blocking agents. No hemodynamic profile allowed prediction of the type of response to these agents. No mortality or serious morbidity was associated with the drug testing. These findings indicate that calcium channel blockers, when titrated to maximally effective doses, may cause substantial reductions in pulmonary artery pressure and pulmonary vascular resistance in patients with primary pulmonary hypertension. Testing with hemodynamic monitoring is necessary to ascertain which patients will respond. Patients with primary pulmonary hypertension are able to tolerate short-term administration of high doses of calcium channel blockers.