Persistent airway inflammation may require the use of different markers for monitoring airway inflammation. In this study, the authors investigated whether adenosine, which may be produced in allergic inflammatory conditions, could be measured with good reproducibility in exhaled breath condensate (EBC), and whether its concentration was elevated in patients with asthma.EBC adenosine and exhaled nitric oxide (eNO), a noninvasive marker of asthmatic airway inflammation, were measured in 40 healthy volunteers and 43 patients with allergic bronchial asthma. Repeatability of adenosine measurement was checked in 20 pairs of samples collected from healthy control subjects.Adenosine was detectable in all EBC samples by the applied high-performance liquid chromatographic method. The mean difference between repeated measurements of adenosine was -0.1 nM and all differences were within the coefficient of repeatability. Adenosine concentration was higher in steroid-naive patients (n=23) compared with healthy control subjects and steroid-treated patients (n=20). In patients with worsening symptoms of asthma (n=23), adenosine concentration was elevated compared with those in a stable condition (n=20). Furthermore, adenosine concentrations were related to eNO levels in asthmatic patients.These results, showing good reproducibility of adenosine measurements and increased adenosine concentrations in steroid-naive patients and in patients with worsening of asthmatic symptoms, indicate that adenosine measurement in exhaled breath condensate might be an acceptable novel method to investigate the role of local production of adenosine in the airways.
In asthmatic patients, airway obstruction provoked by exercise challenge is accompanied by an increase in plasma adenosine level. In this study, the current authors investigated if exercise-induced bronchoconstriction was associated with local changes of adenosine concentration in the airways.Oral exhaled breath condensate (EBC) collection (5-min duration) and forced expiratory volume in one second (FEV1) measurements were performed at rest (baseline) and 4-8 times after treadmill exercise challenge in healthy and asthmatic subjects. Adenosine concentration in EBC was determined by HPLC.Observations indicated that physical exercise results in bronchoconstriction together with a significant increase of adenosine level in EBC in asthmatic patients (mean¡SD maximal fall in FEV1 27¡13%; associated increase in adenosine 110¡76% as compared to baseline), but not in healthy control subjects. Exercise-induced changes in adenosine concentration correlated significantly with the fall in FEV1 values in asthmatic patients.In conclusion, the observed increase in adenosine concentration of oral exhaled breath condensate most probably reflects changes in the airways during exercise-induced bronchoconstriction. Due to its known bronchoconstrictor property in asthma, adenosine may contribute to the development of bronchospasm.
Continuous positive airway pressure (CPAP) provides a well‐documented symptomatic relief for most patients with obstructive sleep apnea (OSA); however, its effect on dyslipidaemia remains contradictory. The aim of this longitudinal pilot study was to investigate the effect of long‐term CPAP treatment on the lipid profile of patients with severe OSA. Fasting serum levels of total cholesterol (TC), low‐ and high‐density lipoprotein cholesterol (LDL‐C and HDL‐C) and triglyceride (TG) were longitudinally measured in 33 OSA patients with an apnea‐hypopnea index (AHI) of ≥30 events/hr, at the time of diagnosis (baseline) and at control visits following fixed‐pressure CPAP treatment. Compared to baseline values, even as short as a 2‐month CPAP therapy resulted in a significant decrease of both TC and LDL‐C levels (TC, 5.62 ± 0.22 vs. 5.18 ± 0.21 mmol/L; LDL‐C, 3.52 ± 0.19 vs. 3.19 ± 0.2 mmol/L; p < 0.05 for each). These lipid fractions exhibited similar improvements at 6 months and after 5 years of CPAP treatment (TC, 5.1 ± 0.17 mmol/L; LDL‐C, 2.86 ± 0.16 mmol/L; p < 0.01 for each). The reduction in lipid levels was greater in younger patients and/or in those who had higher body mass index (BMI) (p < 0.05). There were no significant correlations between AHI and lipid levels (p > 0.05); BMI showed a weak negative association with HDL‐C fraction (BMI, r = −0.263, p < 0.05). CPAP therapy had neither short‐ nor long‐term effects on TG and HDL‐C levels (p > 0.05). CPAP therapy has a rapid and long‐lasting beneficial effect on the lipid profile of patients with severe OSA.
Bevezetés: A SARS-CoV-2 által okozott fertőzés az elmúlt három évben meghatározta mindennapi életünket, és nem várt terhet rótt az egészségügyi ellátórendszerre, többek között azáltal, hogy komoly kockázati tényezőt jelenthet a már meglévő, különböző légzőszervi megbetegedésekkel küzdő betegek számára is. Célkitűzés: A COVID–19 és a fertőzéskor már fennálló légzőszervi megbetegedések, elsősorban a krónikus obstruktív tüdőbetegség (COPD), valamint az asztma összefüggéseinek feltárása. Módszer: Hazai vizsgálatunkban közel 29 000 beteg adatait dolgoztuk fel retrospektíven. Eredmények: Eredményeink alapján elmondható, hogy a COPD mint társbetegség megléte a nemzetközi megállapítással egybehangzóan összefüggést mutat a COVID–19-fertőzés súlyosságával, illetve enyhén növeli az intenzív osztályos kezelés és a gépi lélegeztetés szükségességének kockázatát a SARS-CoV-2 okozta megbetegedés során. Asztma esetében mindezt nem sikerült kimutatnunk, vagyis sem a SARS-CoV-2-fertőzés súlyosságát, sem az intenzív osztályos kezelés és a gépi lélegeztetés szükségességét nem befolyásolta jelentősen az asztma mint társbetegség megléte. Megbeszélés: Ahogy nemzetközi tanulmányokban is olvasható, a COPD mint társbetegség megléte nem növeli jelentős mértékben a SARS-CoV-2-fertőzés kockázatát. Ugyanakkor kijelenthető, hogy a COPD növeli a COVID–19-pozitív betegek kórházba kerülésének esélyét, és emeli a megbetegedés súlyosabb lefolyásának valószínűségét. Tekintettel a COPD-betegekben a tüdő károsodása során végbemenő szerkezeti átépülésre és rendellenes regenerálódási folyamatokra, e betegek a vírusfertőzés lezajlása után fokozott odafigyelést, valamint személyre szabott rehabilitációt igényelnek. Következtetés: Összességében elmondható, hogy a jövőben a személyre szabott terápiás megközelítés bevezetéséhez elengedhetetlen a különböző COPD-s fenotípusok (valamint egyéb krónikus tüdőbetegségek) és a SARS-CoV-2-fertőzés klinikai megnyilvánulásainak mélyreható vizsgálata. Orv Hetil. 2023; 164(2): 51–56.
Continuous positive airway pressure (CPAP) treatment results in nearly complete remission of symptoms of obstructive sleep apnoea (OSA); however, its effect on OSA comorbidities including cardiovascular diseases remains contradictory. Here we investigated the short-and long-term effect of CPAP treatment on matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) in patients with severe OSA. Serum levels of 7 MMPs and 3 TIMPs were followed in OSA patients (n = 28) with an apnoea-hypopnoea index of ≥30 events/h at the time of diagnosis and at control visits (2 months, 6 months and 5 years) after initiation of fixed-pressure CPAP treatment. The first few months of CPAP therapy resulted in significant decrease of MMP-8 and MMP-9 levels (MMP-8: 146 (79-237) vs. 287 (170-560) pg/mL; MMP
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