Paulina Krawiec

Dr. Paulina Krawiec

Medical University of Lublin
orcid

Research Focus & Metrics

Academic Career Length

14Years (2013-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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21 July 2022 in Nutrients
Verified
Journal Article
Open access
PDF file
ARAgata Rocka
Agata Rocka
FJFaustyna Jasielska
Faustyna Jasielska
DMDominika Madras
Dominika Madras
PKPaulina Krawiec
Paulina Krawiec
EPElżbieta Pac-Kożuchowska
Elżbieta Pac-Kożuchowska
Background: Over the last few decades, the time children spend using electronic devices has increased significantly. The aim of the study was to evaluate the impact of screen time on dietary behaviors and physical activity in children and adolescents. Methods: An online survey was conducted among parents of preschool and school-aged children during the COVID-19 lockdown in Poland. There were 3127 surveys used in the analysis. Results: Survey responses referred to 1662 (53%) boys and 1465 (47%) girls, with a mean age of 12.1 ± 3.4 years. During a routine weekday, most children (71%) spent >4 h on educational activities using electronic devices, and 43% of children spent 1–2 h using devices for recreational purposes. The majority of children (89%) were exposed to screens during meals, and ate snacks between main meals (77%). There was an association between screen time and the exposure to screens during meals, and between screen time and time spent performing physical activity. Conclusions: This study revealed that the majority of children were exposed to screens during meals, which is a risk factor of obesity. The promotion of the judicious use of digital devices and healthy dietary habits associated with the use of screens may be an important component of obesity prevention strategies.

23 December 2023 in Nutrients
Verified
Journal Article
Open access
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IPIwona Piątkowska-Chmiel
Iwona Piątkowska-Chmiel
PKPaulina Krawiec
Paulina Krawiec
KZKarolina Joanna Ziętara
Karolina Joanna Ziętara
PPPiotr Pawłowski
Piotr Pawłowski
MSMarzena Samardakiewicz
Marzena Samardakiewicz
Mariola HerbetMariola Herbet
Mariola Herbet
During the COVID-19 pandemic, an increase in the incidence of overweight and obesity in children was observed. It appears that unhealthy food choices, an unbalanced diet, and a sedentary lifestyle, as well as experiencing stress related to the pandemic, may be contributing to this disturbing trend. Chronic stress is a significant factor contributing to eating disorders and obesity in youngsters, involving medical, molecular, and psychological elements. Individuals under chronic stress often focus on appearance and weight, leading to negative body image and disrupted relationships with food, resulting in unhealthy eating behaviors. Chronic stress also impacts hormonal balance, reducing the satiety hormone leptin and elevating the appetite-stimulating hormone ghrelin, fostering increased hunger and uncontrolled snacking. Two systems, the hypothalamic–pituitary–adrenal axis and the sympathetic system with the adrenal medulla, are activated in response to stress, causing impaired secretion of noradrenaline and cortisol. Stress-related obesity mechanisms encompass oxidative stress, neuroinflammation, insulin resistance, and neurohormonal and neurotransmission disorders. Stress induces insulin resistance, elevating obesity risk by disrupting blood sugar regulation and fat storage. Stress also affects the gut microbiome, potentially influencing chronic inflammation and metabolic processes linked to obesity. In conclusion, chronic stress is a multifaceted risk factor for eating disorders and obesity in children, necessitating a comprehensive understanding of effective preventive and intervention strategies amid the escalating prevalence of childhood overweight and obesity.

10 March 2021 in Journal of Inflammation
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Journal Article
Open access
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PKPaulina Krawiec
Paulina Krawiec
APAgnieszka Pawłowska-Kamieniak
Agnieszka Pawłowska-Kamieniak
EPElżbieta Pac-Kożuchowska
Elżbieta Pac-Kożuchowska
Background: The differences between adults and children in inflammatory bowel disease (IBD) phenotype, severity, complications, co-morbidities, and response to the therapy resulted in the extraction of paediatric IBD. It has been revealed that the substantial role in the development of IBD in children under 6 years of age plays a single genetic mutation (monogenic IBD). On the other hand, in older children and adolescents IBD is usually associated with number of interactions between susceptibility loci (polygenic IBD). Main body: Until now there have been described about 60 monogenic defects which affect the variety of immune mechanisms in IBD pathogenesis including epithelial barrier, function of neutrophil granulocytes and phagocytes, T- and B-cell selection and activation, immune inhibitory mechanisms, or apoptosis. Il-10 is an anti-inflammatory cytokine which modulates innate and adaptive immunity affecting expression of pro-inflammatory molecules and function of the variety of immune cells. Patients with identified defects in Il-10 pathway manifest with life-threating colitis with perianal lesions which occurs within first months of life. Allogenic hematopoietic stem cell transplantation is curative therapy in children with Il-10 signalling defects. Conclusion: Clinical awareness of Il-10 signalling defects enables early recognition and prompt management of the disease.

28 April 2021 in Advances in Clinical and Experimental Medicine
Verified
Journal Article
Open access
APAgnieszka Pawłowska-Kamieniak
Agnieszka Pawłowska-Kamieniak
PKPaulina Krawiec
Paulina Krawiec
EPElżbieta Pac-Kożuchowska
Elżbieta Pac-Kożuchowska
Cytokines affect a number of processes in the living body. Interleukin 6 (IL-6) is a cytokine involved in inflammation, infection response and also regulation of metabolism. It stimulates target cells through a membrane-bound IL-6 receptor. Inflammatory bowel diseases (IBD) are autoimmune diseases whose incidence and prevalence are increasing worldwide. It is a group of chronic gastrointestinal disorders characterized by multifactorial, still unknown pathogenesis, varied symptomatology, course with periods of exacerbation and remission, and polymorphic infiltration in histopathological examination. As it is known, pro-inflammatory cytokines, including IL-6, in IBD initiate, intensify and support the development of the inflammatory process in the intestine. Our knowledge of IL-6 biology has important consequences for therapeutic strategies. Elevation of IL-6 concentration can be considered as an early and sensitive, although non-specific marker for various inflammatory conditions and may be used in the diagnosis and monitoring of patients with IBD.

28 July 2020 in Scientific Reports
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Journal Article
Open access
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PKPaulina Krawiec
Paulina Krawiec
EPElżbieta Pac-Kożuchowska
Elżbieta Pac-Kożuchowska
Interleukin 17A (IL-17A) and interleukin 17F (IL-17F) appear to play important role in pathogenesis of some autoimmune diseases. However, their role in inflammatory bowel disease (IBD) has not been yet fully elucidated. We aimed to determine serum IL-17A and IL-17F in children with IBD and to assess their association with IBD activity. Recruited children underwent blood tests including complete blood count, C-reactive protein, erythrocyte sedimentation rate, IL-17A and IL-17F and stool sampling for calprotectin. The study group comprised 68 children with IBD, including 43 with ulcerative colitis and 25 with Crohn’s disease. Control group included 20 healthy children. IL-17A was significantly increased in children with IBD (median: 10.95 pg/ml; range: 0.65–200.54 pg/ml) compared to controls (median: 4.09 pg/ml; range: 0.67–26.20 pg/ml) (p = 0.002). IL-17A was significantly increased in patients with active phase of ulcerative colitis (median: 14.58 pg/ml; range: 0.65–200.54 pg/ml) compared to those in ulcerative colitis remission (median: 8.13 pg/ml; range: 1.61–58.56 pg/ml) (p = 0.04). There were no significant differences in IL-17A among patients with active and inactive Crohn’s disease (p = 0.18). IL-17F did not differ significantly between children with IBD (median: 15.11 pg/ml; range: 0.09–189.84 pg/ml) and controls (median: 11.56 pg/ml; range: 0.19–32.49 pg/ml) (p = 0.33). Our study suggests that interleukin 17A may diverse active phase from remission only in ulcerative colitis but not in Crohn’s disease.

1 March 2019 in Digestive and Liver Disease
Verified
Journal Article
Open access
PKPaulina Krawiec
Paulina Krawiec
EPElżbieta Pac-Kożuchowska
Elżbieta Pac-Kożuchowska
There is no single reliable marker of iron homeostasis in inflammatory bowel disease. To determine diagnostic usefulness of soluble transferrin receptor and soluble transferrin receptor/log ferritin index in iron deficiency anemia in children with inflammatory bowel disease. We assessed soluble transferrin receptor in serum and calculated soluble transferrin receptor/log ferritin index in 75 children with inflammatory bowel disease. Diagnostic ability to identify iron deficiency anemia was examined by receiver operating characteristic analysis. Study group comprised 27 cases of iron deficiency anemia, 6 anemia of chronic disease with iron deficiency, 5 anemia of chronic disease. Soluble transferrin receptor was significantly increased in children with iron deficiency anemia (median: 1.63 μg/ml) compared to non-anemic children (median: 1.02 μg/ml). Soluble transferrin receptor/log ferritin index was significantly higher in iron deficiency anemia (median: 1.76) than in anemia of chronic disease (median: 0.55), anemia of chronic disease with iron deficiency (median: 0.68) or patients without anemia (median: 0.72). Soluble transferrin receptor and its index were not correlated with disease activity or inflammatory markers. Diagnostic power for soluble transferrin receptor/log ferritin index (0.864) was superior to soluble transferrin receptor (0.768) in iron deficiency anemia recognition. Soluble transferrin receptor/log ferritin index has better diagnostic utility than soluble transferrin receptor for iron deficiency anemia detection in pediatric inflammatory bowel disease.