Acute pancreatitis during interferon-alpha and ribavirin treatment for hepatitis C

Silva, Jane da; Giroldi, Simone Batisti; Basso, Franciani de Oliveira; Antunes, Georgia Nunes; Borba, Luis Augusto; Lima, Cássio Renato Montenegro de

doi:10.1136/bcr.09.2008.0998

Cited by 11 publications

(10 citation statements)

References 10 publications

(8 reference statements)

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“…Some questions in the Naranjo scale could not be considered (e.g. it is not ethical to increase the dose or to repeat the administration of the drug) and, for this reason, a higher score is difficult to achieve [50].…”

Section: Discussionmentioning

confidence: 99%

Acute pancreatitis associated with intravenous administration of propofol: evaluation of causality in a systematic review of the literature

Haffar¹,

Kaur

Garg

et al. 2018

Gastroenterology Report

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Acute pancreatitis (AP) associated with intravenous administration of propofol has been described with unknown causal relation. We therefore assessed this causality in a systematic review. Multiple databases were searched on 16 August 2017; studies were appraised and selected by two reviewers based on a priori criteria. Propofol causality was evaluated with the Naranjo scale and Badalov classification.We identified 18 studies from 11 countries with a total of 21 patients, and the majority had adequate methodological quality. The median age was 35 years (range, 4–77) and 10 (48%) were males. Overall, propofol was administrated in 8 patients as sedative along with induction/maintenance of anesthesia in 13 patients; median dose was 200 mg, with intermediate latency (1–30 days) in 14 (67%). Serum triglycerides were >1000 mg/dL in four patients. Severe AP was observed in four patients (19%). AP recurrence occurred in one out of two patients who underwent rechallenge. Mortality related to AP was 3/21(14%). Propofol was the probable cause of AP according to the Naranjo scale in 19 patients (89%).Propofol-induced AP has a probable causal relation and evidence supports Badalov class Ib. Hypertriglyceridemia is not the only mechanism by which propofol illicit AP. Propofol-induced AP was severe in 19% of patients with a mortality rate related to AP of 14%. Future research is needed to delineate whether this risk is higher if combined with other procedures that portend inherent risk of pancreatitis such as endoscopic retrograde cholangiopancreatography.

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Section: Discussionmentioning

confidence: 99%

Acute pancreatitis associated with intravenous administration of propofol: evaluation of causality in a systematic review of the literature

Haffar¹,

Kaur

Garg

et al. 2018

Gastroenterology Report

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“…Interestingly, blood or tissue levels of these cytokines are increased in patients with chronic or acute pancreatitis and pancreatic adenocarcinoma 26 - 29 . Furthermore, IFNγ administration aggravates autoimmune pancreatitis in mice 30 and case reports describe induction of pancreatitis by anti-viral interferon-based therapy in human patients 26 . Nevertheless, the involvement of proinflammatory cytokines in disruption of the pancreatic ductal barrier has not been previously addressed.…”

Section: Introductionmentioning

confidence: 99%

Novel mechanism of cytokine-induced disruption of epithelial barriers

et al. 2013

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The ductal epithelium plays a key role in physiological secretion of pancreatic enzymes into the digestive system. Loss of barrier properties of the pancreatic duct may contribute to the development of pancreatitis and metastatic dissemination of pancreatic tumors. Proinflammatory cytokines are essential mediators of pancreatic inflammation and tumor progression; however, their effects on the integrity and barrier properties of the ductal epithelium have not been previously addressed. In the present study, we investigate mechanisms of cytokine-induced disassembly of tight junctions (TJs) and adherens junctions (AJs) in a model pancreatic epithelium. Exposure of HPAF-II human pancreatic epithelial cell monolayers to interferon (IFN)γ disrupted integrity and function of apical junctions as manifested by increased epithelial permeability and cytosolic translocation of AJ and TJ proteins. Tumor necrosis factor (TNF)α potentiated the effects of IFNγ on pancreatic epithelial junctions. The cytokine-induced increase in epithelial permeability and AJ/TJ disassembly was attenuated by pharmacological inhibition of Janus kinase (JAK) and protein kinase D (PKD). Loss of apical junctions in IFNγ/TNFα-treated HPAF-II cells was accompanied by JAK and PKD dependent decrease in expression of AJ (E-cadherin, p120 catenin) and TJ (occludin, ZO-1) proteins. Depletion of E-cadherin or p120 catenin recapitulated the effects of cytokines on HPAF-II cell permeability and junctions. Our data suggests that proinflammatory cytokines disrupt pancreatic epithelial barrier via expressional downregulation of key structural components of AJs and TJs. This mechanism is likely to be important for pancreatic inflammatory injury and tumorigenesis.

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“…The Naranjo adverse drug reaction probability scale (table 1) is commonly used in clinical practice 5. Implementation of this probability scale yielded a score of 5, which correlates to a probable adverse drug reaction association.…”

Section: Discussionmentioning

confidence: 99%

Acute pancreatitis following paracetamol overdose

Fernandes

2009

Case Reports

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A 17-year-old woman presented with acute abdominal pain and vomiting 3 h after she attempted to commit suicide by ingesting 30×500 mg paracetamol tablets. The woman was found to have a raised amylase level, and a CT scan confirmed the diagnosis of acute pancreatitis. According to the Naranjo adverse drug reaction probability scale, it is likely that the pancreatitis was induced by the paracetamol ingestion. A literature search reported 36 cases of pancreatitis following excessive doses of paracetamol, however this possible drug reaction is not widely recognised and not documented in the British National Formulary (BNF) list of possible adverse reactions from paracetamol. Being aware of the possibility that abdominal pain following paracetamol overdose may be a manifestation of pancreatitis can help the early detection and initiation of treatment for pancreatitis.

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Acute pancreatitis during interferon-alpha and ribavirin treatment for hepatitis C

Cited by 11 publications

References 10 publications

Acute pancreatitis associated with intravenous administration of propofol: evaluation of causality in a systematic review of the literature

Acute pancreatitis associated with intravenous administration of propofol: evaluation of causality in a systematic review of the literature

Novel mechanism of cytokine-induced disruption of epithelial barriers

Acute pancreatitis following paracetamol overdose

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