Background-Because serious adverse reactions to allopurinol have been related to a reduce creatinine clearance rate and prolonged half life of oxypurinol, it has been recommended that the dose should be adjusted according to the rate of creatinine clearance. However, in some patients with gout the dose is not suYcient to reduce serum levels of uric acid (<390 µmol/l) and to halt disease progression. Objective-To determine the prevalence of adverse reactions attributable to allopurinol in patients with primary gout according to dose and creatinine clearance rate. Methods-Data on 120 patients with gout receiving allopurinol, in whom the starting dose was adjusted according to creatinine clearance rate and later increased in some patients to control the disease, were retrospectively reviewed. Two groups were compared: group A, 52 patients receiving creatinine clearance adjusted maintenance doses of allopurinol and group B, 68 patients receiving non-adjusted higher maintenance doses of allopurinol. Results-During follow up 57% required higher allopurinol doses than those recommended according to their creatinine clearance rate. Only five (4%) of 120 consecutive patients developed allopurinol related adverse reactions: four minor skin reactions and one allopurinol hypersensitivity syndrome (AHS). Three of these (including the case of AHS) occurred in group A and two in group B (p=NS). The duration of allopurinol treatment was the same in both groups (group A: 2.3 (3.3) years; group B: 3.7 (4.8) years). No patient in group A, but 44% in group B had a creatinine clearance rate of <50 ml/ min. None of the patients received concomitant diuretics, ampicillin, or azathioprine. Conclusions-No increase was seen in the prevalence of adverse reactions to allopurinol in patients who received higher allopurinol maintenance doses than those recommended according to creatinine clearance rate. (Ann Rheum Dis 2001;60:981-983) Allopurinol is the urate lowering drug most frequently used in patients with gout and other hyperuricaemic conditions. It has been estimated that approximately 2% of patients treated with allopurinol develop minor adverse reactions which often disappear after stopping the drug. Serious and life threatening adverse events such as the allopurinol hypersensitivity syndrome (AHS) are rare.

Cyclooxygenase (COX)-2 inhibitors are widely prescribed for their antiinflammatory and analgesic effects. The potential for COX-2 inhibitors to exert deleterious effects on renal function similar to those of traditional nonsteroidal antiinflammatory drugs is not well defined. Until recently, COX-1 was considered responsible for the synthesis of renal prostaglandins. However, COX-2 is also constitutively expressed in the human kidney Clinical studies have reported a significant decrease in glomerular filtration rate in young and elderly sodium-depleted volunteers given COX-2 inhibitors. We describe the case of a 71-year-old woman who developed acute renal failure after receiving a 50-mg dose of the selective COX-2 inhibitor rofecoxib.

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To measure the amount of tissue factor released during specimen collection and its potential effect of shortening the prothrombin time, we measured tissue factor and pro-thrombin time in twenty-three paired venous and capillary blood samples from antico-agulated patients and in ten paired samples from controls. We also compared venous prothrombin time determined by a plasma-based assay with venous and capillary pro-thrombin time determined with a whole blood assay. Venous specimens were obtained using a two-syringe technique; capillary specimens were obtained by fingerstick after wiping the first drop of blood. Plasma tissue factor was determined by an enzyme-linked immunoabsorbant assay. The patients' mean venous tissue factor (235 ± 101 pg/ml) and capillary tissue factor (268 ± 106 pg/ml) were higher than those of the controls (161 ± 42 pg/ml and 187 ± 63 pg/ml, respectively, P < 0.05). These differences disappeared after adjusting for age. Capillary tissue factor levels were higher than venous tissue factor (244 ± 102 pg/ml vs. 213 ± 93 pg/ml), with a mean difference of 31 pg/ml (P = 0.0001). In addition, whole blood prothrombin time was lower in the capillary than in the venous samples (17.7 ± 5 sec vs. 18.3 ± 5.4 sec, P = 0.004). However, there was no correlation between capillary-venous differences in tissue factor and capillary-venous differences in the whole blood prothrombin time. Whole blood capillary and venous prothrombin times highly correlated with the plasma-based venous prothrombin time (r = 0.98, P < 0.0001). These results demonstrate that obtaining blood by fingerstick does not result in a clinically significant release of tissue factor. In addition, we did not observe any interference of plasma tissue factor with the whole blood prothrombin time assay. A direct relationship between tissue factor and age was observed. Am.

To measure the amount of tissue factor released during specimen collection and its potential effect of shortening the prothrombin time, we measured tissue factor and prothrombin time in twenty-three paired venous and capillary blood samples from anticoagulated patients and in ten paired samples from controls. We also compared venous prothrombin time determined by a plasma-based assay with venous and capillary prothrombin time determined with a whole blood assay. Venous specimens were obtained using a two-syringe technique; capillary specimens were obtained by fingerstick after wiping the first drop of blood. Plasma tissue factor was determined by an enzyme-linked immunoabsorbant assay. The patients' mean venous tissue factor (235 ± 101 pg/ml) and capillary tissue factor (268 ± 106 pg/ml) were higher than those of the controls (161 ± 42 pg/ml and 187 ± 63 pg/ml, respectively, P < 0.05). These differences disappeared after adjusting for age. Capillary tissue factor levels were higher than venous tissue factor (244 ± 102 pg/ml vs. 213 ± 93 pg/ml), with a mean difference of 31 pg/ml (P = 0.0001). In addition, whole blood prothrombin time was lower in the capillary than in the venous samples (17.7 ± 5 sec vs. 18.3 ± 5.4 sec, P = 0.004). However, there was no correlation between capillary-venous differences in tissue factor and capillary-venous differences in the whole blood prothrombin time. Whole blood capillary and venous prothrombin times highly correlated with the plasma-based venous prothrombin time (r = 0.98, P < 0.0001). These results demonstrate that obtaining blood by fingerstick does not result in a clinically significant release of tissue factor. In addition, we did not observe any interference of plasma tissue factor with the whole blood prothrombin time assay. A direct relationship between tissue factor and age was observed. Am.