[Degradation of purine nucleotides in patients with chronic obstruction to airflow].
ABSTRACT The increase in hypoxanthine (Hx), xanthine (X), uric acid (VA) and total purines (TP) that may be found in several clinical conditions associated with tissue hypoxia has been attributed to an increase in adenine nucleotides degradation by a reduced ATP synthesis caused by oxygen deprivation. To test this hypothesis we have investigated the urinary excretion of Hx, X, VA, TP and radioactivity elimination after labeling the adenine nucleotides with adenine (8-14C) in 5 patients with chronic airflow obstruction (CAFO), in the basal state and after oxygen therapy (FiO2, 24%). The results were compared with those from 4 normal individuals. Patients with COFA showed an increase of the renal elimination of Hx, X, VA, TP and radioactivity, which was significantly different from the control group (p less than 0.05). Oxygen administration was associated with a significant reduction in the excretion of purines and radioactivity (p less than 0.01), which decreased to values similar to those found in normal individuals. These findings suggest that in patients with COFA and severe hypoxemia there is a marked increase in the degradation of adenine nucleotides. The normalization of the purine and radioactivity excretion after oxygen therapy points to a basic role of oxygen in the catabolism of adenine nucleotides.
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ABSTRACT: Pulmonary arterial hypertension is a malignant disease with a median survival of 3 years. Uric acid levels are elevated in severe heart failure and in states of hypoxemia. Early data suggest a correlation between hyperuricemia and severe pulmonary arterial hypertension. We studied 29 patients with pulmonary arterial hypertension diagnosed and treated between 1998 and 2001. Clinical characteristics (6 min walk test and New York Heart Association class) and hemodynamic parameters (pulmonary artery pressure, pulmonary vascular resistance and cardiac output) were evaluated and correlated to uric acid level in a retrospective study. Uric acid levels correlated positively with New York Heart Association class (r=0.66, P<0.001) and negatively with 6 min walk test (r=-0.35, P=0.03). Uric acid levels were higher in patients who died than in patients who survived at the end ofthe follow-up period (8.8 vs. 5.7 mg/dl, P=0.001). This study shows that uric acid levels are elevated in severe pulmonary arterial hypertension and can be used as a prognostic marker of disease severity.Respiratory Medicine 02/2003; 97(2):130-3. DOI:10.1053/rmed.2003.1440 · 2.92 Impact Factor
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ABSTRACT: Serum uric acid (UA), the final product of purine degradation, has been shown to be increased in the hypoxic state. We assessed whether the presence of higher values of serum UA and serum UA to creatinine ratio is associated with clinical or functional characteristics in patients with chronic obstructive pulmonary disease (COPD). Fifty-nine consecutive stable patients with COPD, without comorbid conditions, were included. Clinical and functional characteristics were compared between patients with levels below and above the median values of serum UA and serum UA to creatinine ratio. Patients with serum UA levels above the median value differed significantly from the group with levels below this value only in FVC (p=0.04), and serum UA did not correlate significantly with the parameters analyzed. Patients with the serum UA to creatinine ratio above the median value had lower FVC (63 +/- 18 vs. 73 +/- 15 percentage of predicted, p=0.028), lower FEV(1) (43 +/- 19 vs. 55 +/- 18 percentage of predicted, p=0.019), and a higher level of dyspnea (MRC scale, 1.5 +/- 1.1 vs. 0.8 +/- 1.0, p=0.011). The serum UA to creatinine ratio correlated with FVC (r=-0.27), with FEV(1) (r=-0.31), and with dyspnea (r=0.29). In view of these results, we consider that the serum UA to creatinine ratio warrants evaluation as an additional parameter for predicting outcome in COPD.Beiträge zur Klinik der Tuberkulose 02/2007; 185(1):21-4. DOI:10.1007/s00408-006-0076-2 · 2.17 Impact Factor
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ABSTRACT: This report describes a 75-year-old Caucasian man with extensive urate deposits and severe gouty arthropathy that confined him to a wheelchair. Since age 50, he suffered multiple acute gout flares and progressive deformities in his hands, feet, knees, and elbows (tophi). Serum creatinine was 1.4 mg/dL and serum urate 9.4 mg/dL. Conditions known to increase uric acid production (psoriasis, chronic bronchitis) and to decrease uric acid excretion (hypothyroidism, metabolic syndrome, and nephroangiosclerosis) may operate in a single patient, illustrating the dramatic clinical course of untreated gout.Nucleosides Nucleotides & Nucleic Acids 07/2008; 27(6):604-7. DOI:10.1080/15257770802138418 · 0.89 Impact Factor