Marta Kumor
Medical University of Warsaw
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Marta Kumor.
Chest | 2014
Brian D. Kent; Ludger Grote; Silke Ryan; Jean-Louis Pépin; Maria Rosaria Bonsignore; Ruzena Tkacova; Tarja Saaresranta; Johan Verbraecken; Patrick Levy; Jan Hedner; Walter T. McNicholas; Ulla Anttalainen; Ferran Barbé; Ozen K. Basoglu; Piotr Bielicki; Pierre Escourrou; Cristina Esquinas; Ingo Fietze; Lynda Hayes; Marta Kumor; John A. Kvamme; Lena Lavie; Peretz Lavie; Carolina Lombardi; Oreste Marrone; Juan F. Masa; Josep M. Montserrat; Gianfranco Parati; Athanasia Pataka; Thomas Penzel
BACKGROUND OSA is associated with an increased risk of cardiovascular morbidity. A driver of this is metabolic dysfunction and in particular type 2 diabetes mellitus (T2DM). Prior studies identifying a link between OSA and T2DM have excluded subjects with undiagnosed T2DM, and there is a lack of population-level data on the interaction between OSA and glycemic control among patients with diabetes. We assessed the relationship between OSA severity and T2DM prevalence and control in a large multinational population. METHODS We performed a cross-sectional analysis of 6,616 participants in the European Sleep Apnea Cohort (ESADA) study, using multivariate regression analysis to assess T2DM prevalence according to OSA severity, as measured by the oxyhemoglobin desaturation index. Patients with diabetes were identified by previous history and medication prescription, and by screening for undiagnosed diabetes with glycosylated hemoglobin (HbA1c) measurement. The relationship of OSA severity with glycemic control was assessed in diabetic subjects. RESULTS T2DM prevalence increased with OSA severity, from 6.6% in subjects without OSA to 28.9% in those with severe OSA. Despite adjustment for obesity and other confounding factors, in comparison with subjects free of OSA, patients with mild, moderate, or severe disease had an OR (95% CI) of 1.33 (1.04-1.72), 1.73 (1.33-2.25), and 1.87 (1.45-2.42) (P < .001), respectively, for prevalent T2DM. Diabetic subjects with more severe OSA had worse glycemic control, with adjusted mean HbA1c levels 0.72% higher in patients with severe OSA than in those without sleep-disordered breathing (analysis of covariance, P < .001). CONCLUSIONS Increasing OSA severity is associated with increased likelihood of concomitant T2DM and worse diabetic control in patients with T2DM.
Advances in Experimental Medicine and Biology | 2015
Piotr Bielicki; Tadeusz Przybyłowski; Marta Kumor; M. Barnaś; M. Wiercioch; Ryszarda Chazan
Obstructive sleep apnea syndrome (OSAS) is characterized by complete cessation of inspiratory flow (apnea) or upper airway airflow limitation (hypopnea) with increased respiratory muscle activity, which is repeatedly observed during sleep. Hypothyroidism has been described as a rare cause of OSAS, but it is considered to be the main cause of breathing disorders during sleep in patients in whom an improvement of OSAS is observed after thyroid hormone replacement therapy. Nevertheless, euthyreosis due to thyroxine replacement in patients with OSAS often does not improve the breathing disorder and treatment with continuous positive airway pressure is usually applied. The aim of this study was to assess thyroid function in patients with OSAS. We studied 813 patients in whom severe OSAS was diagnosed; the mean apnea-hypopnea index was 44.0. Most of the patients were obese (mean BMI 33.1 ± 6.6 kg/m2) and had excessive daytime sleepiness (ESS 12.8 ± 6.6). With the thyroid stimulating hormone (TSH) concentration as the major criterion, hypothyroidism was diagnosed in 38 (4.7%) and hyperthyroidism was diagnosed in 31 (3.8%) patients. Analysis of basic anthropometric data, selected polysomnography results, and TSH, fT3, and fT4 values did not reveal any significant correlations. In conclusion, the incidence of thyroid function disorders seems to be no different in OSAS than that in the general population. We did not find correlations between TSH activity and the severity of breathing disorders during sleep.
Chest | 2018
Oreste Marrone; Fabio Cibella; Jean-Louis Pépin; Ludger Grote; Johan Verbraecken; Tarja Saaresranta; John A. Kvamme; Ozen K. Basoglu; Carolina Lombardi; Walter T. McNicholas; Jan Hedner; Maria Rosaria Bonsignore; Ulla Anttalainen; Ferran Barbé; Sezai Tasbakan; Piotr Bielicki; Marta Kumor; Izolde Bouloukaki; Sophia E. Schiza; Pierre Escourrou; Gabriel Roisman; Ingo Fietze; Thomas Penzel; Brian D. Kent; Silke Ryan; Patrick Levy; Renaud Tamisier; Gianfranco Parati; Juan F. Masa; Josep M. Montserrat
Background The impact of treating OSA on renal function decline is controversial. Previous studies usually included small samples and did not consider specific effects of different CPAP modalities. The aim of this study was to evaluate the respective influence of fixed and autoadjusting CPAP modes on estimated glomerular filtration rate (eGFR) in a large sample of patients derived from the prospective European Sleep Apnea Database cohort. Methods In patients of the European Sleep Apnea Database, eGFR prior to and after follow‐up was calculated by using the Chronic Kidney Disease‐Epidemiology Collaboration equation. Three study groups were investigated: untreated patients (n = 144), patients receiving fixed CPAP (fCPAP) (n = 1,178), and patients on autoadjusting CPAP (APAP) (n = 485). Results In the whole sample, eGFR decreased over time. The rate of eGFR decline was significantly higher in the subgroup with eGFR above median (91.42 mL/min/1.73 m2) at baseline (P < .0001 for effect of baseline eGFR). This decline was attenuated or absent (P < .0001 for effect of treatment) in the subgroup of patients with OSA treated by using fCPAP. A follow‐up duration exceeding the median (541 days) was associated with eGFR decline in the untreated and APAP groups but not in the fCPAP group (P < .0001 by two‐way ANOVA for interaction between treatment and follow‐up length). In multiple regression analysis, eGFR decline was accentuated by advanced age, female sex, cardiac failure, higher baseline eGFR, and longer follow‐up duration, whereas there was a protective effect of fCPAP. Conclusions fCPAP but not APAP may prevent eGFR decline in OSA.
Polish archives of internal medicine | 2017
Małgorzata Barnaś; Marta Maskey-Warzęchowska; Piotr Bielicki; Marta Kumor; Ryszarda Chazan
INTRODUCTION Melatonin secretion, one of the main factors controlling the sleep-wake rhythm, may be disrupted in patients with sleep disorders. OBJECTIVES The aim of the study was to evaluate the profile of circadian melatonin secretion in patients with obstructive sleep apnea (OSA) and to assess the impact of 2-day and 3-month treatment with continuous airway pressure (CPAP) on diurnal and nocturnal serum melatonin levels. PATIENTS AND METHODS Serum melatonin levels were evaluated in 71 untreated patients with OSA and 18 healthy controls at 6 time points: 10 AM, 2 PM, 6 PM, 10 PM, 2 AM, and 6 AM. The measurements were repeated after 2 days and 3 months of CPAP treatment. RESULTS Melatonin secretion rhythm was altered in 25.4% of the patients with OSA. In patients with preserved secretion rhythm, the serum melatonin level was significantly lower at 2 AM and 6 AM, compared with healthy controls: 68.2 pg/ml (interquartile range [IQR], 30.1-109.8 pg/ml) vs 109.1 pg/ml (IQR, 63-167.9 pg/ml), P = 0.02 and 40.8 pg/ml (IQR, 20.8-73.2 pg/ml) vs 67.7 pg/ml (IQR, 32.7-131.7 pg/ml), P = 0.04, respectively. Melatonin levels did not change significantly after the 2-day and 3-month CPAP treatment. However, at 3 months, a shift of the peak melatonin concentration to 2 AM was observed in patients with an altered secretion rhythm. CONCLUSIONS OSA has a significant effect on serum melatonin levels. Neither short-term nor long-term CPAP treatment significantly changes melatonin concentrations; however, our results seem to indicate that a 3-month CPAP treatment may be helpful in restoring the physiological rhythm of melatonin secretion in patients with OSA.
Advances in respiratory medicine | 2006
Tadeusz Przybyłowski; Piotr Bielecki; Marta Kumor; Katarzyna Hildebrand; Marta Maskey-Warzęchowska; Joanna Wiwała; Justyna Kościuch; Piotr Korczynski; Ryszarda Chazan
Advances in respiratory medicine | 2011
Marta Kumor; Piotr Bielicki; Tadeusz Przybyłowski; Renata Rubinsztajn; Jan Zieliński; Ryszarda Chazan
Advances in respiratory medicine | 2006
Renata Rubinsztajn; Marta Kumor; Krzysztof Byśkiniewicz; Ryszarda Chazan
Advances in respiratory medicine | 2004
Marta Maskey-Warzęchowska; Tadeusz Przybyłowski; Katarzyna Hildebrand; Marta Kumor; Katarzyna Górska; Adam Frangrat; Joanna Kucińska; Justyna Kościuch; Ryszarda Chazan
Advances in respiratory medicine | 2006
Marta Kumor; Renata Rubinsztajn; Krzysztof Byskiniewicz; Piotr Bielicki; Ryszarda Chazan
Advances in respiratory medicine | 2004
Marta Kumor; Tadeusz Przybyłowski; Marta Maskey-Warzęchowska; Katarzyna Hildebrand; Adam Fangrat; Piotr Bielecki; Katarzyna Górska; Justyna Kościuch; Joanna Kucińska; Ryszarda Chazan