7Alcohol-induced pancreatic injury
Section snippets
Natural history and clinical features
The traditionally accepted view of alcoholic pancreatitis was that it was a form of chronic pancreatitis from the beginning, punctuated during its course by acute exacerbations.6., 7. This notion was based on studies showing that histological and radiological evidence of chronic pancreatitis (atrophy, fibrosis and calcification) could be found in the pancreas of many alcoholics at the time of their first clinical attack of pancreatitis.8., 9. Furthermore, an autopsy study demonstrated evidence
Diagnosis
A clinical diagnosis of acute pancreatitis is usually made on the basis of an attack of severe abdominal pain and tenderness, accompanied by a rise in the levels of amylase and lipase (pancreatic digestive enzymes) in the blood to more than three times the upper limit of normal. In recent years, there has been increasing use of serum lipase levels in the diagnosis of acute pancreatitis. Serum lipase is more specific for a pancreatic origin and levels remain elevated for a longer period than
Pathology
Most of the morphological and histological changes observed in alcoholic pancreatitis have been reported in pancreatic tissue obtained at autopsies or during surgical resection. It is possible therefore that the advanced forms of pancreatitis are over represented in such reports. In mild acute pancreatitis, the only gross change may be oedema of the gland, while in severe acute pancreatitis overt necrosis, haemorrhage, abscess formation and fluid collections may be evident. The gland of chronic
Treatment
The mainstays of treatment of an acute attack of alcoholic pancreatitis are bed rest, analgesia, fasting, nasogastric suction (if nausea and vomiting are problematical) and intravenous fluids.60 Most patients with mild pancreatitis recover quickly and do not require any additional support. In severe pancreatitis, nutritional support is required; this is usually provided via the intravenous route (parenteral nutrition). The enteral route had not been commonly used for nutritional support in
Pathogenesis
An understanding of the mechanism(s) responsible for the injurious effects of alcohol on the pancreas is an essential step towards the development of novel therapeutic strategies to prevent alcoholic pancreatitis or improve its outcome. Studies on the pathogenesis of alcoholic pancreatitis have often been hampered by the lack of suitable animal models of the disease and the difficulty in obtaining human pancreatic tissue for analysis. Nevertheless, significant advances have been made in recent
Current concept of the pathogenesis of alcoholic pancreatitis
The clinical and experimental evidence of alcohol-related pancreatic injury available in the literature has led us to propose the concept of the Drinker's Pancreas (Figure 2).
We postulate that the effects of alcohol, its metabolites (generated via both oxidative and non-oxidative pathways within the acinar cell) and its metabolic by-products (reactive oxygen species) lead to: (i) increased content of digestive and lysosomal enzymes (via increased synthesis and possibly decreased secretion in
Summary
Alcoholic pancreatitis is thought to begin as an acute necroinflammatory/autodigestive process in a susceptible individual and to progress with repeated episodes. The clinical spectrum of the disease includes acute pancreatitis (acute abdominal pain and raised serum levels of pancreatic enzymes) and chronic pancreatitis (abdominal pain, maldigestion, diabetes). Acute and chronic features can coincide.
Treatment of acute episodes is as for acute pancreatitis of other aetiologies and includes bed
References (140)
- et al.
Revised classification of pancreatitis. Report of the Second International Symposium on the Classification of Pancreatitis in Marseille, France, March 28–30, 1984
Gastroenterology
(1985) - et al.
The different courses of early- and late-onset idiopathic and alcoholic chronic pancreatitis
Gastroenterology
(1994) - et al.
Reversibility of exocrine pancreatic failure in chronic pancreatitis
Gastroenterology
(1986) - et al.
Effect of cessation of alcohol use on the course of pancreatic dysfunction in alcoholic pancreatitis
Gastroenterology
(1988) - et al.
Mortality factors associated with chronic pancreatitis
Gastroenterology
(1989) - et al.
Starch digestion in normal subjects and patients with pancreatic disease, using a 13co2 breath test
Gastroenterology
(1989) - et al.
How useful is fecal pancreatic elastase 1 as a marker of exocrine pancreatic disease?
Journal of Pediatrics
(2002) - et al.
Steatorrhoea: you cannot trust your eyes when it comes to diagnosis
Lancet
(1996) - et al.
Fecal fat concentration in patients with steatorrhea
Gastroenterology
(1984) - et al.
Rapid method for the determination of fat in feces
Journal of Biological Chemistry
(1949)
A rapid reliable procedure for the determination of total fecal lipids with observation of the lipids excreted by human subjects in normal and pathological states
Clinica Chimica Acta
Improved recovery of fatty acid through direct transesterification without prior extraction or purification
Journal of Lipid Research
Separation and quantitation of fatty acids, sterols and bile acids in feces by gas chromatography as the butyl ester-acetate derivatives
Journal of Chromatography
Cholesteryl octanoate breath test. Preliminary studies on a new noninvasive test of human pancreatic exocrine function
Gastroenterology
Mixed triglyceride breath test: a noninvasive test of pancreatic lipase activity in the duodenum
Gastroenterology
Intrajejunal administration of an elemental diet at neutral ph avoids pancreatic stimulation. Studies in dog and man
American Journal of Surgery
Effect of enteral nutrition on exocrine pancreatic function
American Journal of Surgery
Endoscopic stenting for pain relief in chronic pancreatitis: results of a standardized protocol
Gastrointestinal Endoscopy
Long-term results of pancreatic stents in chronic pancreatitis
Gastrointestinal Endoscopy
Pancreas divisum: results of minor papilla sphincterotomy
Gastrointestinal Endoscopy
Enzymatic therapy in patients with chronic pancreatitis
Gastroenterology Clinics of North America
Disease of the pancreas
Alcohol-induced pancreatic injury (part i). Unexplained features and ductular theories of pathogenesis
International Journal of Pancreatology
Acute pancreatitis
New England Journal of Medicine
The natural history of alcoholic pancreatitis: update 1985
Mount Sinai Journal of Medicine
Chronic pancreatitis
Classification of pancreatitis
Gut
The etiology of pancreatitis. A review of clinical experience
Annals of Surgery
Chronic pancreatitis
Annals of Internal Medicine
Pancreatic fibrosis in chronic alcoholics and nonalcoholics without clinical pancreatitis
American Journal of Gastroenterology
Chronic relapsing pancreatitis: a study of 29 cases without associated disease of the biliary or gastrointestinal tract
Gastroenterology
Progression of alcoholic acute to chronic pancreatitis
Gut
Development of chronic pancreatitis from acute pancreatitis: a pathogenetic concept
Zentralblatt fur Chirurgie
Death due to acute pancreatitis
Digestive Diseases and Sciences
Repetitive cerulein-induced pancreatitis and pancreatic fibrosis in the rat
Pancreas
Repetitive self-limited acute pancreatitis induces pancreatic fibrogenesis in the mouse
Digestive Diseases and Sciences
Is tobacco a risk factor for chronic pancreatitis and alcoholic cirrhosis?
Gut
Multicenter survey of the etiology of pancreatic diseases. Relationship between the relative risk of developing chronic pancreatitis and alcohol, protein and lipid composition
Digestion
Course and outcome of chronic pancreatitis. Longitudinal study of a mixed medical-surgical series of 245 patients
Gastroenterology
The course of pain is the same in alcohol- and nonalcohol-induced chronic pancreatitis
Pancreas
Follow-up study of chronic pancreatitis
Gastroenterology Japan
Clinical course and prognosis of chronic pancreatitis
Pancreas
Alcohol abuse and chronic pancreatitis
Surgery
Natural course in chronic pancreatitis. Pain, exocrine and endocrine pancreatic insufficiency and prognosis of the disease
Digestion
Epidemiology and risk factors in pancreatic cancer
Seminars in Oncology
Alcohol and pancreatic cancer: insufficient epidemiologic evidence for a causal relationship
Epidemiologic Reviews
Etiologic links between chronic pancreatitis and pancreatic cancer
Scandinavian Journal of Gastroenterology
Pancreatitis in a native American Indian population
Pancreas
Comparison of serum amylase, pancreatic isoamylase and lipase in patients with hyperamylasemia
Digestive Diseases and Sciences
Prevalence of normal serum amylase levels in patients with acute alcoholic pancreatitis
Digestive Diseases and Sciences
Cited by (79)
Isolation and characterization of human islet stellate cells
2016, Experimental Cell ResearchCitation Excerpt :However PSCs can be activated in response to pancreatic injury and inflammation, or by exposure to inflammatory cytokines or oxidant stress [14–17], which induces increased proliferation; morphological changes into myofibroblast-like cells; up-regulation of the expression of α-smooth muscle actin (α-SMA); and increased synthesis and secretion of extracellular matrix (ECM) components [18]. Numerous in vivo and in vitro studies have demonstrated a central role for PSCs in the pancreatic fibrogenesis associated with chronic pancreatitis and pancreatic cancer [17–24], but much less is known about the role(s) in the endocrine pancreas of islet-specific stellate cells. We have previously reported the use of standard explant techniques to isolate and characterize a population of islet stellate cells (ISC) from rat pancreatic islets [25].
Chapter 16 - Pancreatic Stellate Cells
2015, Stellate Cells in Health and DiseaseAlcohol-drinking patterns and metabolic syndrome risk: The 2007 Korean National Health and Nutrition Examination Survey
2011, AlcoholCitation Excerpt :In fact, the prevalence of type 2 diabetes among current drinkers was substantially high (27.5% in men and 16.7% of women) in the present study. Excessive alcohol consumption might also cause hypertension, hyperlipidemia, and hyperglycemia via mechanisms that are apparently independent from obesity (Apte and Wilson, 2003; Miller et al., 2005). Although the reason for discrepancies by gender in the association of drinking patterns with MS prevalence is unclear, we may suggest some explanations.
Ethanol inhibits pancreatic acinar cell autophagy through upregulation of ATG4B, mediating pathological responses of alcoholic pancreatitis
2023, American Journal of Physiology - Gastrointestinal and Liver PhysiologyIncreased mortality in patients with alcohol-induced pancreatitis during the COVID-19 pandemic
2023, Annals of Gastroenterology