Hypoxia is an important topic both physiologically and clinically in obstructive sleep apnea syndrome (OSAS) and chronic obstructive pulmonary disease (COPD). Uric acid (UA) is the end product of adenosine triphosphate (ATP) degradation, which it has been suggested, correlates with acute and long term effects of hypoxia.1,2 The potential application of this metabolite in patients who suffer nocturnal hypoxemia could be a useful marker for nocturnal hypoxemia follow-up.

We read with great interest the article by Ozanturk et al.3 and congratulate the authors on their study. The authors investigated the association of UA metabolites with nocturnal hypoxemia, apnea–hypopnea index, noninvasive mechanical ventilation (NIMV) usage, and five-year mortality in COPD and OSAS patients. We are in agreement that UA excretion is a practical marker of tissue hypoxia and could be useful in the management of OSAS and COPD patients. However, we think that there are some additional factors during this long term observation that could have influenced the performance of UA metabolism described by Ozanturk et al.3

First, the mechanism of nocturnal hypoxemia within COPD and OSAS patients is not the same. Although these two diseases develop hypoxemia, they do not have a similar pattern and compensatory mechanism. For example, COPD hypoxemia is progressive, worsening mainly by inflammatory exacerbations, while OSAS hypoxemia is nocturnal and intermittent, without inflammatory exacerbations. We consider that this is a controversial aspect worth discussing, which may influence UA metabolism.

Second, the criterion for nocturnal hypoxemia was defined by the authors as a percentage of time spent below oxyhemoglobin saturation of 90% for >10% of sleep time. Although, there is no universal definition in the grading of nocturnal intermittent hypoxemia,2 we feel the level used by the authors needs more precise definition. Additionally, OSAS and COPD laboratory protocols vary greatly in the duration of hypoxia exposure, number of hypoxia episodes per day, and the total number of days of exposure.2

Third, patients were contacted after 5 years by the authors with a questionnaire, including information on the NIMV treatment used. But we have no information of long-term adherence to PAP. In relation to COPD patients, this article does not mention the need for long-term oxygen therapy, and if the patients were on maximal pharmacological and non-pharmacological therapy according to disease severity. Additionally, in the literature there was evidence that UA levels were higher in COPD patients with more severe airflow limitation and frequent exacerbations. It would be interesting to include a subgroup analysis of COPD patients using the current GOLD classification in a future study.

Finally, we think that it is essential to consider some additional cofactors that may have influenced these results, including cardiovascular factors control, such as hypertension, which may differ among groups over the 5 years of study.4 Also the impact of long-term dietary factors on UA metabolism needs to be taken into account.5

The complexity of UA metabolism and its association with nocturnal intermittent hypoxemia and non-intermittent hypoxemia represent an original approach, but further prospective clinical trials are needed to confirm these results.