Fat digestion and exocrine pancreatic function in primary biliary cirrhosis

Ros, Emilio; García-Pugés, A; Reixach, María; Cusó, Eulalia; Rodés, Joan

doi:10.1016/0016-5085(84)90142-2

Cited by 46 publications

(9 citation statements)

References 35 publications

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“…The importance of this phase is underscored by a 30% reduction in dietary lipid absorption in patients with biliary atresia [136]. Similarly, rats with biliary drainage displayed reduced linoleic acid absorption [137]. …”

Section: Intraluminal Abnormalitiesmentioning

confidence: 99%

Mechanisms of lipid malabsorption in Cystic Fibrosis: the impact of essential fatty acids deficiency

et al. 2005

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Transport mechanisms, whereby alimentary lipids are digested and packaged into small emulsion particles that enter intestinal cells to be translocated to the plasma in the form of chylomicrons, are impaired in cystic fibrosis. The purpose of this paper is to focus on defects that are related to intraluminal and intracellular events in this life-limiting genetic disorder. Specific evidence is presented to highlight the relationship between fat malabsorption and essential fatty acid deficiency commonly found in patients with cystic fibrosis that are often related to the genotype. Given the interdependency of pulmonary disease, pancreatic insufficiency and nutritional status, greater attention should be paid to the optimal correction of fat malabsorption and essential fatty acid deficiency in order to improve the quality of life and extend the life span of patients with cystic fibrosis.

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Section: Intraluminal Abnormalitiesmentioning

confidence: 99%

Mechanisms of lipid malabsorption in Cystic Fibrosis: the impact of essential fatty acids deficiency

et al. 2005

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“…The lipases synthesized by the pancreas are involved in the hydrolysis of insufficiently emulsified fats, which slows down the rate of their splitting. The results obtained by Ross et al indicate that pancreatic synthesis of lipases and their entry into the duodenum in PBC is not impaired and is not the cause of steatorrhea development [ 10 ]. The activity of pancreatic amylase in patients with PBC is within the normal range [ 10 , 11 ].…”

Section: The Mechanism Of Dietary Lipid Metabolism Disorders In Pbcmentioning

confidence: 99%

“…The results obtained by Ross et al indicate that pancreatic synthesis of lipases and their entry into the duodenum in PBC is not impaired and is not the cause of steatorrhea development [ 10 ]. The activity of pancreatic amylase in patients with PBC is within the normal range [ 10 , 11 ]. The severity of steatorrhea also does not correlate with the increased activity of alkaline phosphatase in these patients [ 10 , 11 ].…”

Section: The Mechanism Of Dietary Lipid Metabolism Disorders In Pbcmentioning

confidence: 99%

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Features of Lipid Metabolism Disorders in Primary Biliary Cholangitis

Reshetnyak

Маев

2022

Biomedicines

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Primary biliary cholangitis (PBC), previously known as primary biliary cirrhosis, is an autoimmune liver disease that mostly affects women. A progressive disorder in the processes of bile secretion and enterohepatic bile salts circulation in patients with PBC already in its early stages, leading to an insufficient release of bile acids into the bowel and their entry into the systemic circulation. Insufficient bile acids released into the duodenum contributes to the development of malabsorption, energy malnutrition, and slowly progressive weight loss. The pathophysiological mechanisms of weight loss and its slow progression are associated with the deterioration of the fat emulsification processes and with the reduced absorption of hydrolyzed products, such as fatty acids and monoglycerides, with steatorrhea in patients with PBC, as well as in those with gut dysbiosis. Just in the early stages of the disease, this results in accelerated fatty acid β-oxidation that is aimed at compensating for progressive energy malnutrition. The entry of bile acids into the systemic circulation in PBC is accompanied by dyslipidemia. The mechanism of hyperlipidemia in patients with PBC differs from that in other conditions because along with an increase in total cholesterol (TC), there are elevated high-density lipoprotein levels and the appearance of unusual lipoprotein X (Lp-X). The appearance of Lp-X is most likely to be the body’s protective reaction to inactivate the detergent effect of bile acids on the membrane structures of blood corpuscles and vascular endothelial cells. It is bile acids, rather than TC levels, that correlate with the content of Lp-X and determine its formation. Concomitant hypercholesterolemia in patients with PBC is also aimed at neutralizing the detergent effect of bile acids that have entered the systemic circulation and is most likely a compensatory reaction of the body. “Anomalous” hypercholesterolemia in PBC can serve as a model system for the search and development of new methods for the treatment of dyslipidemia since it occurs without an increase in the incidence of cardiovascular events.

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“…Περίπου 30% των ασθενών παρουσιάζει έλλειψη βιταμίνης Α η οποία σπάνια είναι συμπτωματική και αντιμετωπίζεται με εξωγενή χορήγηση 15000 iu/day 169,170 .…”

Section: θεραπείαunclassified

Παράγοντες Κινδύνου Για Θρόμβωση Σε Ασθενείς Με Πρωτοπαθή Χολική Κίρρωση Και Μη Αλκοολική Στεατοηπατίτιδα

Chrysanthos¹,

Χρύσανθος²

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Σεμινάριο για τη σημασία της κλινικής αντοχής και της φαρμακοκινητικής των νουκλεοτιδικών αναλόγων στην αντιική θεραπεία 4/04 3.3.2.1.2. Πολυθεματική εκπαιδευτική διημερίδα Ελληνικής εταιρείας μελέτης του ήπατος (ΕΕΜΗ) 5/04 3.3.2.1.3. Μετεκπαιδευτικό σεμινάριο Ελληνικής Γαστρεντερολογικής εταιρείας (ΕΓΕ) 11/04 3.3.2.1.4. Μετεκπαιδευτικό σεμινάριο ΕΕΜΗ 6/5/05 3.3.2.1.5. Εκπαιδευτικό σεμινάριο <<Ηπατολογία>> Ελληνική εταιρεία έρευνας και εκπαίδευσης στη πρωτοβάθμια φροντίδα υγείας (ΕΕΕΕΠ) 30/9-2/10/05 (5 CME) 3.3.2.1.6. Μετεκπαιδευτικό σεμινάριο ΕΓΕ 6/10/05 (5 CME) 3.3.2.1.7. Εκπαιδευτική διημερίδα <<Ηπατολογικά θέματα για τον Γαστρεντερολόγο>> επαγγελματική ένωση γαστρεντερολόγων Ελλάδος (ΕΠΕΓΕ) 5-6/11/05 (5 CME) 3.3.2.1.8. 5 η Διημερίδα ιογενούς ηπατίτιδας Β και C 28-29/1/06 (12 CME) 3.3.2.1.9. 1 η εκπαιδευτική ημερίδα <<εξελίξεις στη γαστρεντερολογία και ηπατολογία>> Ελληνικό ίδρυμα Γαστρεντερολογίας και Διατροφής (ΕΛΙΓΑΣΤ) 18/2/06 3.3.2.1.10. 1 ο Μετεκπαιδευτικό σεμινάριο των ενόπλων δυνάμεων στην ενδοσκόπηση του πεπτικού 8-9/12/06 (8 CME) 3.3.2.1.11. 6 η Διημερίδα ιογενούς ηπατίτιδας Β και C 27-28/1/07 (12 CME) 3.3.2.1.12. 2 η εκπαιδευτική διημερίδα <<εξελίξεις στη γαστρεντερολογία και ηπατολογία>> ΕΛΙΓΑΣΤ 23-24/2/07 (6 CME) 3.3.2.1.13. Μετεκπαιδευτικό σεμινάριο ΕΕΜΗ 28/4/07 3.3.2.1.14. Μετεκπαιδευτικό σεμινάριο ΕΓΕ 7/10/07 (3 CME) 3.3.2.1.15. 2 ο Μετεκπαιδευτικό σεμινάριο των ενόπλων δυνάμεων στην ενδοσκόπηση του πεπτικού 25-26/1/08 (8 CME) 3.3.2.1.16. 7 η Διημερίδα ιογενούς ηπατίτιδας Β και C 26-27/1/08 (12 CME) 3.3.2.1.17. 3 η εκπαιδευτική διημερίδα <<εξελίξεις στη γαστρεντερολογία και ηπατολογία>> ΕΛΙΓΑΣΤ 22-23/2/08 (8 CME) 3.3.2.1.18. Μετεκπαιδευτικά φροντιστηριακά μαθήματα (ΜΦΜ) ΕΓΕ 2007-2008 (6 ΜΟΡΙΑ CME-CPD) 3.3.2.1.19. Μετεκπαιδευτικό σεμινάριο ΕΓΕ 16/11/08 (3 CME) 3.3.2.1.20. 16 η Διεθνής Διημερίδα Ηπατίτιδας Β και C 31/1-1/2/09 Βιογραφικό σημείωμα 8 3.3.2.1.21. 4 η εκπαιδευτική διημερίδα <<εξελίξεις στη γαστρεντερολογία και ηπατολογία>> ΕΛΙΓΑΣΤ 20-21/2/09 (8 CME) 3.3.2.1.22. 14 ο Ελληνικό συνέδριο για το ελικοβακτηρίδιο του πυλωρού Ελληνική εταιρεία μελέτης του Hp (ΕΕΜHp) 6-7/3/09 (7 CME) 3.3.2.1.23. Νεότερες εξελίξεις στη Γαστρεντερολογία Αθήνα 3-5/4/09 (13 CME) 3.3.2.1.24. 11 ο Πανελλήνιο Ηπατολογικό συνέδριο Κέρκυρα 7-10/5/09 (13 CME).

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Fat digestion and exocrine pancreatic function in primary biliary cirrhosis

Cited by 46 publications

References 35 publications

Mechanisms of lipid malabsorption in Cystic Fibrosis: the impact of essential fatty acids deficiency

Mechanisms of lipid malabsorption in Cystic Fibrosis: the impact of essential fatty acids deficiency

Features of Lipid Metabolism Disorders in Primary Biliary Cholangitis

Παράγοντες Κινδύνου Για Θρόμβωση Σε Ασθενείς Με Πρωτοπαθή Χολική Κίρρωση Και Μη Αλκοολική Στεατοηπατίτιδα

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