ArticleSleep & breathing = Schlaf & Atmung2025
Reduction of carbonic anhydrase activity is associated with amelioration of obstructive sleep apnea.
Article in Sleep & breathing = Schlaf & Atmung, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Carbonic Anhydrase I and II as Biomarkers and Therapeutic Targets in Human Disease: From Physiology to Clinical Translation.International journal of molecular sciences · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe carbonic anhydrase (CA) enzyme plays an important role in the equilibration of carbon dioxide and bicarbonate (HCO
methodsData from three separate cohorts of healthy volunteers and patients with OSA were used to quantify CA activity in whole blood and cerebrospinal fluid (CSF). The influence of the CA inhibitory drugs acetazolamide and sulthiame, on CA activity in-vitro/in-vivo, was assessed. The association between CA-inhibitor plasma concentration and HCO
resultsStability of CA activity in stored blood was high. CA activity in whole blood contained five times higher activity compared with CSF. The CA-inhibitory drugs dose-dependently reduced CA activity in-vitro/in-vivo. The CA inhibitor sulthiame reduced venous HCO
conclusionsCA-inhibitory drugs reduced CA activity in whole blood suggesting a therapeutic role of CA inhibition in OSA. The findings also suggest that an activated CA system may constitute a pathophysiological mechanism in some forms of OSA. CLINICAL
trial registrationN/A.
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