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Cholesterol crystal embolization to liver, gallbladder, and pancreas
1Department of Internal Medicine, Wilhelmina Hospital, Assen, The Netherlands.
Insights
Cholesterol crystal embolization (CCE) can cause liver necrosis, cholecystitis, and pancreatitis, particularly in elderly males with atherosclerosis. This condition often arises after vascular procedures or anticoagulant therapy.
Area of Science:
- Pathology
- Vascular Medicine
- Gastroenterology
Background:
- Cholesterol crystal embolization (CCE) is a rare complication.
- Atherosclerotic vascular disease is a common comorbidity.
Purpose of the Study:
- To investigate the clinical features of CCE affecting the liver, biliary system, and pancreas.
- To identify patient demographics and risk factors associated with CCE.
Main Methods:
- Retrospective analysis of 44 patients diagnosed with CCE.
- Data collected from the Dutch National Pathology Information System (DNPIS) between 1973 and 1994.
Main Results:
- CCE was found in the liver, gallbladder, pancreas, or combinations thereof.
- Manifestations included liver cell necrosis, cholecystitis, and pancreatitis.
- A history of atherosclerosis was present in all patients; provoking factors were noted in half.
Conclusions:
- CCE can lead to significant hepatic, biliary, and pancreatic pathology.
- Elderly males with atherosclerosis are particularly susceptible.
- CCE should be considered in the differential diagnosis of unexplained organ injury in at-risk patients.
Abstract:
We retrospectively studied the clinical features of all 44 patients (35 men, 9 women, mean age 74.5 years) registered with a diagnosis of hepatic, biliary, and/or pancreatic cholesterol crystal embolization (CCE) in the Dutch National Pathology Information System (DNPIS) from 1973 through 1994. Liver CCE was found in 12 (11 autopsies and 1 biopsy), gallbladder CCE in 2 (resection specimens), pancreas CCE in 19 (18 autopsies and 1 biopsy), and both liver and pancreas CCE in 11 (all autopsies) patients. Five patients presented with focal liver cell necrosis, 1 with acalculous necrotizing cholecystitis, 1 with chronic cholecystitis, 10 with necrotizing pancreatitis, and 1 with chronic fibrosating pancreatitis. Four patients died of CCE-induced pancreatitis. Nineteen patients died as a consequence of other CCE sites. These were reported in 37 patients. All patients had a history of atherosclerotic vascular disease. In half the patients a possibly CCE provoking factor (vascular surgery and/or cannulation, anticoagulant treatment) was present. We conclude that liver cell necrosis, cholecystitis, and pancreatitis may be caused by CCE, particularly in elderly male patients with a history of atherosclerosis.