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Acute Necrotizing Pancreatitis: What Happens After the Thunderstorm?
Rafaela C. Gasparoto*1, Marcelo C. Racy3, Tercio De Campos2
1Gastroenterology, Santa Casa of São Paulo School of Medicine, São Paulo, Brazil; 2Emergency Unit, Santa Casa of São Paulo School of Medicine, São Paulo, Brazil; 3Radiology and Imaging, Santa Casa of São Paulo School of Medicine, São Paulo, Brazil

Introduction: Several researches have studied the long-term outcomes after recovery from acute pancreatitis, assessing whether there is damage in pancreatic function and morphology, associated with impairment in patients' quality of life (QoL). But yet the results are contradictory, with prevalences varying from 10 to 80% in literature. Moreover, there are few studies evaluating exclusively necrotizing pancreatitis cases. Objectives: The aims of this study are to evaluate exocrine and endocrine pancreatic function, pancreatic morphology and patients' QoL after a single episode of acute necrotizing pancreatitis.
Methods: Fourty-nine consecutive patients with acute necrotizing pancreatitis were identified, attended in our hospital from 2003 to 2012. Survivors (thirty-eight) were contacted to participate the study; thus, sixteen patients were included in the research. Pancreatic exocrine function was studied by qualitative fecal fat excretion. Endocrine function was evaluated by oral glucose tolerance test, C-Peptide and mathematical index HOMA-beta (Homeostasis Model Assessment-beta). Pancreatic morphology was examined by contrast-enhanced abdominal computed tomography. QoL was measured by 36-item Short-Form Health Survey questionnaire (SF-36). Tests were performed at least twelve months after the acute injury (average interval from diagnosis and the study was 2.9 years).
Results: The prevalence of pancreatic exocrine insufficiency was low (6.2%). Endocrine dysfunction was observed in half the cases, and no association with extension of necrosis was found (p>0.999). Morphological changes were common (62.5%) and more prevalent in those who experienced extensive necrosis, considered greater than 30% (p=0.011). Computed tomography findings were: glandular atrophy, dilatation of Wirsung's duct, pancreatic calcifications, pseudocysts and peripancreatic fat densification. Compared to general Brazilian population, QoL was considered good (preserved in seven of the eight domains assessed), whereas its impairment was found exclusively in mental health domain, particularly in patients who had alcoholic acute pancreatitis (p=0.028). There was no correlation between QoL and prognostic indicators, such as APACHE II, C - reactive protein and extension of necrosis.
Conclusions: All possible therapeutic measures for the treatment of acute necrotizing pancreatitis are justified, despite high costs and prolonged hospital stay, since patients exhibit good pancreatic exocrine function and QoL in long-term outcomes. Medical follow-up of these patients should be stimulated, given that late endocrine dysfunction and morphological abnormalities are frequent and may require specific therapy.


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