digoxin and Pancreatitis

digoxin has been researched along with Pancreatitis* in 5 studies

Other Studies

5 other study(ies) available for digoxin and Pancreatitis

ArticleYear
Digoxin use may increase the relative risk of acute pancreatitis: A population-based case-control study in Taiwan.
    International journal of cardiology, 2015, Feb-15, Volume: 181

    The goal of this study was to evaluate the association between digoxin use and acute pancreatitis in Taiwan.. Utilizing the database of the Taiwan National Health Insurance Program, this case-control study consisted of 6116 subjects aged 20-84years with a first-attack of acute pancreatitis since 2000 to 2011 as the cases and 24,464 randomly selected subjects without acute pancreatitis as the controls. Both cases and controls were matched by sex, age and index year of diagnosing acute pancreatitis. The absence of digoxin prescription was defined as "never use". Active use of digoxin was defined as subjects who at least received 1 prescription for digoxin within 7days before the date of diagnosing acute pancreatitis. Non-active use of digoxin was defined as subjects who did not receive a prescription within 7days but at least received 1 prescription for digoxin ≥8days before the date of diagnosing acute pancreatitis. The odds ratio (OR) and 95% confidence interval (CI) were measured to evaluate the association between digoxin use and acute pancreatitis by a multivariable unconditional logistic regression model.. After adjusting for potential confounding factors, the adjusted OR of acute pancreatitis was 5.29 for subjects with active use of digoxin (95% CI 3.61, 7.73), when compared with subjects with never use of digoxin. The adjusted OR of acute pancreatitis decreased to 1.04 for subjects with non-active use of digoxin (95% CI 0.89, 1.21), but no statistical significance.. These data indicate that only persons actively using digoxin may have the high relative odds of acute pancreatitis. Further research or case report is warranted to evaluate the pathophysiological basis underlying the relationship between digoxin use and acute pancreatitis.

    Topics: Adult; Aged; Anti-Arrhythmia Agents; Case-Control Studies; Digoxin; Female; Humans; Male; Middle Aged; Pancreatitis; Population Surveillance; Risk Factors; Taiwan

2015
Digoxin and risk of acute pancreatitis.
    International journal of cardiology, 2015, May-06, Volume: 187

    Topics: Anti-Arrhythmia Agents; Digoxin; Female; Humans; Male; Pancreatitis; Population Surveillance

2015
Digoxin use may increase the relative risk of acute pancreatitis.
    International journal of cardiology, 2015, Jun-01, Volume: 188

    Topics: Anti-Arrhythmia Agents; Digoxin; Female; Humans; Male; Pancreatitis; Population Surveillance

2015
Author's reply to digoxin and risk of acute pancreatitis.
    International journal of cardiology, 2015, Jun-01, Volume: 188

    Topics: Anti-Arrhythmia Agents; Digoxin; Female; Humans; Male; Pancreatitis; Population Surveillance

2015
Inhibition of serum phospholipase-A2 in acute pancreatitis by pharmacological agents in vitro.
    Scandinavian journal of clinical and laboratory investigation, 1997, Volume: 57, Issue:5

    Phospholipase-A2 has been suggested as having a role in the pathophysiology of acute pancreatitis. The inhibition of phospholipase-A2 was studied in vitro using 17 pharmacological agents in the search for a specific therapy for acute pancreatitis. The inhibitory effect was tested using an isotopic assay system with 2-palmitoyl-(1-14C)-labelled dipalmitoyl phosphatidylcholine as a substrate and 10 microliters of serum from patients with acute necrotizing pancreatitis as an enzyme source. Among all agents tested, anti-inflammatory drugs inhibited enzyme activity most significantly: indomethacin (9.0 x 10(-3) mol l-1) decreased the phospholipase-A2 activity to one- tenth. The weak inhibitory effect could also be demonstrated using a lower concentration of 2 x 10(-5) mol l-1, which can be achieved after intravenous administration of 50 mg of this drug. The other drugs inhibited the enzyme activity at concentrations higher than those achieved after intravenous injections in clinical use. Diclofenac (3.1 x 10(-2) mol l-1) reduced the phospholipase-A2 activity by 93%, ketoprofen (2.0 x 10(-2) mol l-1) or chlorpromazine (1.4 x 10(-2) mol l-1) by 90%, tobramycin (1.7 x 10(-2) mol l-1) by 84%, doxycycline (9.0 x 10(-3) mol l-1) by 61%, dexamethasone (1.7 x 10(-3) mol l-1) by 62%, methylprednisolone (3.8 x 10(-2) mol l-1) by 50%, and pindolol (1.0 x 10(-4) mol l-1) by 59%. A weak inhibition of phospholipase-A2 activity was demonstrated by betamethasone, bupivacaine, digoxin, hydrocortisone, lidocaine, metoprolol, propranolol, and vancomycin. Indomethacin proved the most potent of the tested agents in inhibiting phospholipase-A2 activity in serum from patients with acute pancreatitis and should be further studied in vivo.

    Topics: Acute Disease; Adrenergic beta-Antagonists; Anti-Bacterial Agents; Anti-Inflammatory Agents, Non-Steroidal; Bupivacaine; Chlorpromazine; Digoxin; Enzyme Inhibitors; Glucocorticoids; Humans; Lidocaine; Pancreatitis; Phospholipases A; Phospholipases A2

1997