Background: Propofol has been widely used as a sedative and an anesthetic. It sometimes causes side-effects such as hypotension, pain on injection and respiratory depression. In addition, it can, although rarely, produce acute pancreatitis.
Area of uncertainty: Several clinical and laboratory s...
Background: Propofol has been widely used as a sedative and an anesthetic. It sometimes causes side-effects such as hypotension, pain on injection and respiratory depression. In addition, it can, although rarely, produce acute pancreatitis.
Area of uncertainty: Several clinical and laboratory studies suggest that propofol increases triglycerides, cholesterol and lipase, but does not produce acute pancreatitis. However, several cases of propofol-induced acute pancreatitis have been reported. The underlying rationale of this discrepancy between clinical research and clinical case reports remains unknown. Thus, the goal of this study was to examine the confounding factors associated with this discrepancy, with a focus on the non-propofol related factors.
Data source: We searched “propofol and pancreatitis” in PubMed and Google Scholar. Sixteen case reports on propofol-induced acute pancreatitis involving 17 patients were retrieved. Components in each case report were analyzed and divided into propofol-related, and non-propofol-related factors.
Result: Other potential drugs, such as acetaminophen, hydrochlorothiazide, gadolinium, estradiol, methyldopa, hydrocortisone, enalapril, metronidazole, trimethoprim-sulfamethoxazole, losartan and omeprazole, which may produce pancreatitis, were co-administered with propofol in the reported propofol-induced acute pancreatitis cases. Propofol-induced acute pancreatitis occurred in patients with following underlying conditions: glycogen storage disease type 1A, sepsis, Cushing disease and severe burns. Median cumulative dose of propofol in the reported cases was 0.2 g. Ten out of the reported cases (total available data = 13) did not involve hypertriglyceridemia, but three did.
Conclusion: Non-propofol-related factors, which include other potential drugs that cause pancreatitis, and underlying diseases associated with pancreatitis, seem to contribute to propofol-induced acute pancreatitis rather than propofol alone. A well-controlled, randomized clinical study is needed to elucidate the underlying mechanism of propofol-induced acute pancreatitis.
Background: Propofol has been widely used as a sedative and an anesthetic. It sometimes causes side-effects such as hypotension, pain on injection and respiratory depression. In addition, it can, although rarely, produce acute pancreatitis.
Area of uncertainty: Several clinical and laboratory studies suggest that propofol increases triglycerides, cholesterol and lipase, but does not produce acute pancreatitis. However, several cases of propofol-induced acute pancreatitis have been reported. The underlying rationale of this discrepancy between clinical research and clinical case reports remains unknown. Thus, the goal of this study was to examine the confounding factors associated with this discrepancy, with a focus on the non-propofol related factors.
Data source: We searched “propofol and pancreatitis” in PubMed and Google Scholar. Sixteen case reports on propofol-induced acute pancreatitis involving 17 patients were retrieved. Components in each case report were analyzed and divided into propofol-related, and non-propofol-related factors.
Result: Other potential drugs, such as acetaminophen, hydrochlorothiazide, gadolinium, estradiol, methyldopa, hydrocortisone, enalapril, metronidazole, trimethoprim-sulfamethoxazole, losartan and omeprazole, which may produce pancreatitis, were co-administered with propofol in the reported propofol-induced acute pancreatitis cases. Propofol-induced acute pancreatitis occurred in patients with following underlying conditions: glycogen storage disease type 1A, sepsis, Cushing disease and severe burns. Median cumulative dose of propofol in the reported cases was 0.2 g. Ten out of the reported cases (total available data = 13) did not involve hypertriglyceridemia, but three did.
Conclusion: Non-propofol-related factors, which include other potential drugs that cause pancreatitis, and underlying diseases associated with pancreatitis, seem to contribute to propofol-induced acute pancreatitis rather than propofol alone. A well-controlled, randomized clinical study is needed to elucidate the underlying mechanism of propofol-induced acute pancreatitis.
주제어
#Drug-induced pancreatitis Propofol
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