Evaluation of acid-base status in patients admitted to ED-physicochemical vs traditional approaches.

BACKGROUND: The aim of this study is to evaluate the value of physicochemical, base excess (BE), and plasma bicarbonate concentration ([HCO3(-)]) approaches on the assessment of acid-base status in patients presented to the emergency department (ED). METHODS: Upon presentation at ED, patients whose arterial blood was deemed in need of analysis were studied. Arterial blood gases, serum electrolytes, and proteins were measured and used to derive [HCO3(-)], BE, anion gap (AG), AG adjusted for albumin (AGadj), strong ion difference, strong ion gap (SIG) and SIG corrected for water excess/deficit (SIGcor). In each patient the acid-base status was evaluated using the BE, [HCO3(-)], and physicochemical approaches. RESULTS: A total of 365 patients were studied. Compared with BE (n = 202) and [HCO3(-)] (n = 151), physicochemical approach (n = 279) identified significantly more patients with metabolic acid-base disturbances (P < .0001). Significantly fewer patients with unmeasured anions acidosis were identified with AGadj than with SIGcor (164 vs 230; P < .0001). On the basis of BE, 75 patients had normal acid-base balance, and 65 (87%) of them exhibited at least 1 hidden acid-base disturbance, identified by the physicochemical approach. The corresponding values with [HCO3(-)] approach were 108 and 95 (88%) patients. When patients with high AGadj were excluded, 44 patients with BE and 67 with [HCO3(-)] approach had normal acid-base status, and most of them exhibited at least 1 acid-base disturbance with the physicochemical approach, whereas 12 and 21 patients, respectively, had high SIGcor. CONCLUSION: Compared with the BE and [HCO3(-)] methods, the physicochemical approach has a better diagnostic accuracy to identify metabolic acid-base disturbances.

Oxidative DNA damage and somatic mutations: a link to the molecular pathogenesis of chronic inflammatory airway diseases.

BACKGROUND: Acquired somatic mutations induced by oxidative stress may contribute to the molecular pathogenesis of chronic inflammatory airway diseases. The objective of this study was to assess the intensity of oxidative DNA damage and the presence of microsatellite DNA instability (MSI), a marker of acquired somatic mutations, in patients with COPD, patients with noncystic fibrosis bronchiectasis, and control subjects. METHODS: Induced sputum and peripheral blood from 97 subjects were analyzed; 36 patients with COPD, 36 patients with bronchiectasis, 15 smokers without COPD, and 10 healthy control subjects. DNA was extracted and analyzed for MSI. 8-hydroxy-2'-deoxyguanosine (8-OHdG), a specific marker of oxidant-induced DNA damage, was measured in serum and sputum supernatants. RESULTS: None of the patients with bronchiectasis or control subjects (non-COPD smokers, healthy subjects) exhibited any genetic alteration. In contrast, MSI was found in 38% of COPD specimens. Sputum 8-OHdG was statistically significantly increased in COPD when compared with subjects with bronchiectasis (P = .0002), smokers without COPD (P = .0056), and healthy subjects (P = .0003). Sputum 8-OHdG in MSI-positive patients with COPD differed significantly from that of MSI-negative patients with COPD (P = .04) and smokers without COPD (P = .008), but was not statistically different (P = .07) among MSI-negative patients with COPD and smokers without COPD. Serum 8-OHdG was significantly increased in MSI-positive compared with MSI-negative patients with COPD (P = .001), but was not statistically significant in smokers without COPD (P = .09). Serum 8-OHdG was increased in smokers without COPD compared with MSI-negative patients with COPD (P = .009). CONCLUSIONS: There is a clear disparity in COPD regarding oxidant-induced DNA damage and somatic mutations. This may reflect a difference in the oxidative stress per se or a deficient antioxidant and/or repair capacity in the lungs of patients with COPD.