No abstract

Addition of AZA to glucocorticoids for the induction of remission of nonsevere SNVs does not improve remission rates, lower relapse risk, spare steroids, or diminish the EGPA asthma/rhinosinusitis exacerbation rate.

ABSTRACT— Although it has been established that liver failure is associated with arterial hypocapnia and alkalaemia (i.e., respiratory alkalosis), the influence of liver failure on mixed venous acid‐base status has not yet been studied. Thus, arterial and mixed venous acid‐base status were simultaneously measured in controls and in a large series of patients with cirrhosis. Grade B patients (n = 28) or Grade C patients (n = 21) had significantly lower arterial and mixed venous carbon dioxide tensions than controls (n = 29). Grade B or Grade C patients also had significantly higher arterial, mixed venous pH, and lower mixed venous bicarbonate concentrations than controls. Among Grade A patients (n = 27), those with the lowest Pugh's score (i.e., equal to five) had significantly lower mixed venous carbon dioxide tension than controls. The other arterial and mixed venous acid‐base values did not differ significantly between Grade A patients with the lowest Pugh's score and controls. Grade A patients with a Pugh's score equal to six and Grade B patients had similar acid‐base disorders. No significant differences were found between groups concerning the anion gap and plasma chloride concentrations. In conclusion, this study shows that in Grade B or C patients, respiratory alkalosis was responsible for mixed venous hypocapnia, alkalaemia and hypobicar‐bonataemia. In addition, in Grade A patients with the lowest Pugh's score (equal to five), analysis of arterial and mixed venous blood revealed that mixed venous hypocapnia was the sole anomaly of the acid‐base status. This last finding suggests that mixed venous hypocapnia might be an early event preceding the onset of arterial hypocapnia.