Thesis supervisor: Andrea Párniczky
Location of studies (in Hungarian): Semmelweis Egyetem Abbreviation of location of studies: SE
Description of the research topic:
Cystic fibrosis (CF) is an autosomal recessive disorder, caused by mutations leading to abnormalities in the cystic fibrosis transmembrane conductance regulator (CFTR)—a chloride channel involved in electrolyte and water movement across cell membranes. CFTR dysfunction leads to multisystem disease, but cystic fibrosis related lung disease is the primary cause of morbidity and death in people with CF. Improved life expectancy of people with CF has led to increase prevalence of other complications. Cystic fibrosis-related diabetes (CFRD) is the most common extrapulmonary complication of CF. Around 40% of patients with CF above age 20 and 50% above age 30 have CFRD. Exocrine insufficiency of the pancreas is the most common gastroinestinal manifestaion of CF. Two third of the CF patients have exocrine pancreatic dysfunction at birth. Protein and fat malabsorption, failure to thrive, poor weight gain, deficiency of macro-and micronutrients resulted by the lack of pancreatic enzymes. Both the pancreas exocrin insufficiency and CFRD are associated with increased morbidity and mortality, related to their negative impact on nutritional status and lung function.
The aims of the Cystic Fibrosis Related Pancreatic Disorder Registry (CFRPDR) are 1) better awareness and increased screening for cystic fibrosis related exocrine and endocrine pancreatic disfunction 2) recognition of early predictor markers for CFRD 3) focus on early treatment of CFRD 4) get more knowledge about the effect of CFRD on the course of CF 5) elucidating the assocition between the exocrin pancreatic disfunction and the onset of CRFD 6) improved nutritional status and 7) survival in people with CFRD.
Deadline for application: 2021-10-18
2024. IV. 17. ODT ülés Az ODT következő ülésére 2024. június 14-én, pénteken 10.00 órakor kerül sor a Semmelweis Egyetem Szenátusi termében (Bp. Üllői út 26. I. emelet).
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