Alcoholic Pancreatitis Patients Research Articles

Post-healing perceptions and experiences of alcohol withdrawal and life management in men with alcoholic pancreatitis: a qualitative study.

The aim of this study was to examine the perceptions and experiences of male patients with alcoholic pancreatitis after healing regarding alcohol withdrawal and life management. This study used a qualitative descriptive design, and participants were selected by purposive sampling from two tertiary care hospitals in Shandong Province, China. Semi-structured in-depth interviews were conducted with 18 male patients discharged from the gastroenterology department who had recovered from alcoholic pancreatitis. Colaizzi's method was used to analyze the interview data, and the findings were reported using COREQ criteria. By analyzing the interview data, we summarized five themes, (1) the dilemma of sobriety, (2) role change, (3) illness status, (4) family influence, and (5) life management. By profiling the perceptions and experiences of post-healing alcoholic pancreatitis patients' alcohol cessation and life management in men, it helps to grasp the details of alcohol cessation and health direction of patients' home management, which provides more directional guidance to help patients maintain positive and good lifestyle habits and active management awareness, followed by targeted personalized interventions to provide patients with knowledge of disease care and health management.

S105 The Quick Sepsis-Related Organ Failure Assessment Score Is Prognostic of Pancreatitis Severity in Patients With Alcohol-Induced Pancreatitis

Introduction: Multiple models already exist to prognosticate pancreatitis severity and mortality. However, most require invasive measurements and are cumbersome to use. The quick Sequential Organ Failure Assessment (SOFA) score (qSOFA) score is a bedside tool that may be useful in determining prognosis in patients with alcohol-induced acute pancreatitis (AAP). The goal of this study was to determine if the qSOFA and BISAP score assessed at admission is prognostic of severe clinical outcomes in AAP. Methods: This is a retrospective, single center, cohort review study of 147 patients admitted to a community academic hospital in Houston, Texas, USA with the diagnosis of AAP. IRB approval was granted by the University of Texas Health Science Center at Houston, Houston, Texas, USA. Patient records were obtained from an electronic medical record system between December 1st, 2014 to July 1st, 2020. Patients were included if they were >18 years of age, had a history of alcohol consumption and had acute pancreatitis based on the Atlanta criteria. Receiver operator characteristics (ROC) and area under the curve (AUC) analysis was used to assess the diagnostic accuracy of the qSOFA and BISAP score on admission. Logistic regression was used to assess the odds of developing severe pancreatitis based on the Atlanta criteria and need for ICU admission, intubation or vasopressors based on the BISAP and qSOFA scoring systems. Results: The qSOFA score ≥2 at admission to the hospital was found to be ≥94% specific and ≥33% sensitive while a BISAP score ≥3 at admission was found to be ≥96% specific and ≥20% sensitive for multiple clinical outcomes, including severe AAP and need for ICU admission, intubation or vasopressors. A qSOFA score ≥2 was prognostic of need for ICU admission by an adjusted odds ratio (aOR) of 48.5 (95% CI: 6.4-1,013.3; p< 0.001) and of severe AAP by an aOR of 35.3 (95% CI: 7.2-224.3; p< 0.001). A BISAP score ≥3 was prognostic of severe AAP by an aOR 7.1 (95% CI: 1.2-36.0; p< 0.05), need for ICU admission by an aOR 47.7 (95% CI: 6.9-487.1; p< 0.001), need for intubation by an aOR of 25.8 (95% CI: 3.5-238.4; p< 0.01) and need for vasopressors by an aOR of 14.2 (95% CI: 1.1-358.2; p< 0.05). Conclusion: At the time of admission, a BISAP score ≥3 or a qSOFA score ≥ 2 is highly specific and prognostic for multiple severe clinical outcomes of AAP. Since the qSOFA score has fewer variables than the BISAP score, it may be a more useful clinical tool to evaluate prognosis.Figure 1.: ROC-AUC curves showing the diagnostic accuracy of qSOFA score at admission (qSOFAADM) relative to the BISAP score at admission to diagnose clinical outcomes in alcoholic pancreatitis patients. (A) Overlayed ROC curves assessing severe pancreatitis. (B) Overlayed ROC curves assessing need for ICU admission. (C) Overlayed ROC curves assessing need for intubation. (D) Overlayed ROC curves assessing need for vasopressors.

Alcohol Reduction to Reduce Relapse in Acute Alcoholic Pancreatitis-Missed Opportunities.

AimResuming drinking is a main contributant to recurrence in alcoholic pancreatitis. We assessed current clinical practice in the Netherlands regarding alcohol in managing patients with a first episode of acute alcoholic pancreatitis.MethodsA survey was distributed to 35 hospitals affiliated with the Dutch Pancreatitis Study Group. We evaluated current support based on various components of brief interventions, the participation of psychosocial healthcare providers, the cooperation with the primary care physicians and the presence of a protocol and its implementation.ResultsThe response rate was 100% (n = 35). Psychoeducation is the most frequently performed intervention in current support treatment (97% of hospitals). In 17% of hospitals, healthcare providers with a psychosocial background routinely participate in current support treatment; 37% of hospitals create an individual treatment plan in which goals regarding alcohol cessation are specified and only 46% of hospitals provide the primary care physician with specific discharge information; 31% of hospitals indicate that the treatment is uniformly performed within their division of Gastroenterology. Protocols are available in 3% of the hospitals surveyed. Opportunities to involve the patient’s social network were not given sufficient priority.ConclusionAmong Dutch hospitals, there is no routine management strategy with regard to enhancing treatment for heavy alcohol use in alcoholic pancreatitis patients. There is a need to test a validated support program in randomized studies. Meanwhile, possible opportunities for effecting change are often missed.

S0077 Probable Association of Idiopathic Pancreatitis With Smoking of Tobacco

INTRODUCTION: Acute pancreatitis is a serious disease with high morbidity and mortality rates. Research shows that among the primary admissions for acute pancreatitis, 26.9% had gallstone pancreatitis, 25.1% had alcoholic pancreatitis and 36.5% had idiopathic pancreatitis. Idiopathic pancreatitis accounted for a higher mortality rate than both gallstone pancreatitis and alcoholic pancreatitis patients (Chen et al., 2013).1 Recent studies have shown that cigarette smoking can also be a risk factor of acute pancreatitis. The two main metabolites from cigarette smoke are nicotine and NNK, which cause histologic changes to the pancreas. There is also indirect evidence that nicotine and acrolein cause ductal secretion due to CFTR dysfunction. As mentioned above, this can be a direct cause of inducing an attack of acute pancreatitis (Barreto, 2016).2 METHODS: This study is a retrospective chart review of adult patients that would include all adults (age >18 years), both genders, of all ethnic backgrounds, adults presenting with symptoms consistent with acute pancreatitis. The rate of pancreatitis will be compared among tobacco smokers and non-tobacco smokers. The association between pancreatitis and tobacco use will be tested for significance at P < 0.05 with Chi-square analysis. The magnitude of the risk of use will be calculated using Odds Ratio. RESULTS: There was 301 total number of patients in the study. Mean age was 58.76 (SD: 14.13) years and predominantly male (n = 164, 54.5%). There is a 2.32 (odds ratio) higher risk of acute pancreatitis and a smoker. This study showed a significance of P-value <0.0001 between idiopathic pancreatitis and tobacco use. CONCLUSION: Tobacco use is a risk factor for chronic pancreatitis but has not been associated directly with acute pancreatitis previously. There were multiple case reports in the literature that reported tobacco use associated with acute pancreatitis. This study has shown a significant association between tobacco use and acute idiopathic pancreatitis.Table 1.: smoking_use * idiopathic_acute_pancreatitis CrosstabulationTable 2.: Chi-Square Tests

Serum lipase amylase ratio in predicting the etiology of acute pancreatitis

Background: Acute pancreatitis remains a major cause of significant morbidity and mortality. Alcoholism and biliary tract stone disease are the main causes in up to 80% of cases. The diagnosis of acute pancreatitis is based on the correlation of clinical, biochemical, and radiological criteria. Serum lipase and amylase have been used to diagnose acute pancreatitis with values greater than three times the upper limit of normal being diagnostic. Objective: The aim is to study the value of serum lipase: amylase ratio in predicting the etiology of acute pancreatitis. Materials and Methods: This prospective study was conducted in a tertiary care hospital in North-East India during a 2-year period. The serum lipase/amylase ratio has been evaluated in 52 patients (31 acute alcoholic pancreatitis, 19 acute gallstone pancreatitis, 2 idiopathic). Results: Analysis of data showed that patients with acute alcoholic pancreatitis had higher serum lipase levels (2722.5 ± 285.7, mean ± standard deviation) compared to acute gallstone pancreatitis (1565.21 ± 198.2). On the other hand, acute gallstone pancreatitis patients had higher serum amylase (862.3 ± 105.5) compared to acute alcoholic pancreatitis patients (683.03 ± 618.31). Determination of lipase: amylase ratio showed that out of 31 patients of acute alcoholic pancreatitis 22 patients (71%) had lipase: amylase ratio ≥3. Out of 19 patients of acute gallstone pancreatitis, 17 patients (89.5%) had lipase: amylase ratio Conclusion: Serum lipase: amylase ratio fixed at 3.0 can assist in differentiating acute biliary pancreatitis from acute alcoholic pancreatitis. The lipase: amylase ratio ≥3 is observed in alcoholic acute pancreatitis while biliary pancreatitis has ratio

Hospital contacts with alcohol problems prior to liver cirrhosis or pancreatitis diagnosis

AIMTo evaluate prior hospital contacts with alcohol problems in patients with alcoholic liver cirrhosis and pancreatitis.METHODSThis was a register-based study of all patients diagnosed with alcoholic liver cirrhosis or pancreatitis during 2008-2012 in Denmark. Hospital contacts with alcohol problems (intoxication, harmful use, or dependence) in the 10-year period preceding the diagnosis of alcoholic liver cirrhosis and pancreatitis were identified.RESULTSIn the 10 years prior to diagnosis, 40% of the 7719 alcoholic liver cirrhosis patients and 40% of the 1811 alcoholic pancreatitis patients had at least one prior hospital contact with alcohol problems. Every sixth patient (15%-16%) had more than five contacts. A similar pattern of prior hospital contacts was observed for alcoholic liver cirrhosis and pancreatitis. Around 30% were diagnosed with alcohol dependence and 10% with less severe alcohol diagnoses. For the majority, admission to somatic wards was the most common type of hospital care with alcohol problems. Most had their first contact with alcohol problems more than five years prior to diagnosis.CONCLUSIONThere may be opportunities to reach some of the patients who later develop alcoholic liver cirrhosis or pancreatitis with preventive interventions in the hospital setting.

Differences in Severity and Outcomes Between Hypertriglyceridemia and Alcohol-Induced Pancreatitis.

Background:Alcohol and hypertriglyceridemia (HTG) are among the most common causes of acute pancreatitis (AP) after gallstones. However, differences in severity at the time of presentation and outcomes have not been well-studied.Objective:The aim of this study is to assess the differences between severity at presentation and outcomes of AP of hypertriglyceridemic and alcoholic origins.Materials and Methods:A retrospective review of 177 patients who were discharged with diagnosis of AP was performed. Severity at presentation was identified by the presence of systemic inflammatory response syndrome, bedside index for severity in AP (BISAP) score, and Balthazar index. Outcomes were measured by the length of stay, intensive care unit care, surgical intervention, and mortality.Results:We found 147 patients with alcoholic pancreatitis and 30 patients with hypertriglyceridemic pancreatitis. A larger percentage of hypertriglyceridemic pancreatitis patients (23.33%) had a BISAP score of ≥2 compared to the alcoholic group (12.24%). Only 32.65% of the patients with alcoholic pancreatitis but 60% of the patients with hypertriglyceridemic pancreatitis had the presence of systemic inflammatory response syndrome (SIRS) at admission (P = 0.0067). There were 73.34% hypertriglyceridemic pancreatits patients and only 40.28% alcoholic pancreatitis patients with Balthazar index C or greater, suggesting a higher disease burden at admission for hypertriglyceridemic pancreatitis patients (P = 0.0047). There was a statistically significant difference in the relative number of hypertriglyceridemic and alcoholic pancreatitis patients receiving intensive care (P = 0.00030) and in receiving surgical interventions related to pancreatitis (P = 0.016).Conclusion:Our study found that patients with hypertriglyceridemic pancreatitis have a greater severity of disease and they experience less favorable outcomes than patients with alcoholic pancreatitis.

Morphological and Functional Evaluation of the Pancreatic Duct with Secretin-Stimulated Magnetic Resonance Cholangiopancreatography in Alcoholic Pancreatitis Patients

Morphological and Functional Evaluation of the Pancreatic Duct with Secretin-Stimulated Magnetic Resonance Cholangiopancreatography in Alcoholic Pancreatitis Patients

Morphological and Functional Evaluation of the Pancreatic Duct with Secretin-Stimulated Magnetic Resonance Cholangiopancreatography in Alcoholic Pancreatitis Patients

The aim of this investigation was to evaluate the pancreatographic findings and dynamics of pancreatic duct diameter, as determined by secretin-enhanced magnetic resonance cholangiopancreatography (S-MRCP), in patients with acute alcoholic pancreatitis or chronic alcoholic pancreatitis and in a control group. S-MRCP was performed in patients with acute alcoholic pancreatitis who did not manifest the functional and radiological (ultrasonography and computed tomography) criteria of chronic pancreatitis (n = 21), in patients with chronic alcoholic pancreatitis (n = 28) and in a control group (n = 16). The diameter of the main pancreatic duct (MPD) was monitored before secretin administration and at 3 and 10 min after secretin administration. Morphological features were also assessed before and after the administration of secretin. All ductal diameters were significantly larger in chronic alcoholic pancreatitis (P < 0.0001). There were no differences in MPD caliber between patients with acute alcoholic pancreatitis and the control group. The percentage of variation between basal MPD diameter and at 3 min post-secretin administration was lower in patients with chronic (35.5%) pancreatitis than in those with acute alcoholic pancreatitis (52.3%) and the control group (52.5%). There were no significant differences between patients with acute alcoholic pancreatitis and the control group in terms of the frequency of visualization of side branches, ductal narrowing, intraluminal filling defects, and ductal irregularity. One patient with acute alcoholic pancreatitis presented ductal criteria of chronic pancreatitis following the administration of secretin. The dynamics of MPD visualized on S-MRCP in patients with acute alcoholic pancreatitis is similar to that observed in the control group and different from that observed in patients with chronic alcoholic pancreatitis. There were no significant differences between patients with acute alcoholic pancreatitis and the control group in terms of morphological pancreatographic features.

Association analysis among polymorphisms of the various genes and chronic alcoholic pancreatitis

Chronic and excessive consumption of alcohol is an important factor responsible for the onset of pancreatitis. However, the incidence of chronic pancreatitis in heavy drinkers differs in individuals, suggesting that these individual differences may involve various genetic and environmental factors. In the present study, we investigated an association of alcoholic pancreatitis with polymorphisms of the various genes related to metabolism of the oxidative compounds. We analyzed polymorphisms of NADPH-quinone oxidoreductase 2 (NQO2), multidrug resistance 1 (MDR1), alcohol dehydrogenase 1B (ADH1B) and lipoprotein lipase (LPL). The subjects consisted of 53 patients with chronic alcoholic pancreatitis (AlCP), 54 alcoholic patients without pancreatic dysfunction (Alc), and 42 healthy individuals. DNA samples were prepared from the peripheral blood of all subjects, and the genetic mutations were analyzed by polymerase chain reaction and restriction fragment length polymorphism methods. The ADH1B gene frequencies were significantly different between healthy controls and Alc patients (P < 0.001), and also between AlCP and Alc patients (P < 0.05). However, no significant difference was found between healthy controls and AlCP patients. The gene frequencies of MDR1 (3435C > T) and MDR1 (2677G > A/T) of patients with AlCP or Alc were different when compared with healthy controls, although the difference was not significant. The NQO2 and LPL genes showed no relation with Alc and AlCP patients. The ADH1B*1 gene frequency in AlCP was significantly lower compared with Alc. We speculate that the ADH1B*1 gene may function by reducing vulnerability to the onset of alcoholic pancreatitis. Other genes analyzed in the present study lacked association with AlCP.

Clinical Impact of the Swollen Duodenal Papilla in Autoimmune Pancreatitis

Background: Although autoimmune pancreatitis (AIP) sometimes shows a swollen duodenal papilla, the significance of duodenal papilla of AIP has not been fully elucidated. Aim: To evaluate the clinical significance of the main duodenal papilla in AIP from the view point of endoscopic features and immunohistochemical findings. Patients and Methods: Sixteen patients (9 male, 7 female, age 54-76 years) were consecutively enrolled from April 2001 to October 2005. Patients with AIP that underwent ERCP as well as endoscopic biopsies were studied. AIP was diagnosed if all of the following criteria were met: a) irregular narrowing of the main pancreatic duct on ERCP, b) sausage-shaped pancreas on CT, c) histopathological findings of lymphoplasmacytic sclerosing pancreatitis, d) elevated serum immunoglobuline. Both the endoscopic features and the immunohistochemical findings of the duodenal papilla using IgG4 antibodies were retrospectively reviewed. These findings of the patients with AIP were compared to those of 13 patients with alcoholic pancreatitis. IgG4-positive plasma cell infiltration cell count of over 10 per high-power field was regarded as positive in all histopathological specimens. Results: Swollen main duodenal papilla was observed in 12 (85.7%) patients with AIP and 3 (18.8%) patients with alcoholic pancreatitis. Significant differences were found in the swelling of the main duodenal papilla between AIP and alcoholic pancreatitis (p < 0.05). The swollen main duodenal papilla in 12 (85.7%) patients with AIP improved in response to treatment with corticosteroids. In 4 patients without elevated serum IgG4, the swollen pancreas without swollen duodenal papilla improved spontaneously without corticosteroids. As for ERCP findings, the main pancreatic duct just proximal to the duodenal papilla (within 10 to 15 mm) had a normal caliber in 12 (85.7%) AIP patients with swollen duodenal papilla, but not in patients with alcoholic pancreatitis. Although in 14 of 16 AIP patients infiltration of IgG4-positive plasma cells was detected in the duodenal papilla as well in its pancreatic tissues, there was no infiltration of IgG4 in alcoholic pancreatitis patients. Significant differences were found in the IgG4 positive plasma cell in the duodenal papilla between AIP and alcoholic pancreatitis (p < 0.05). Conclusions: These results suggest that a swollen main duodenal papilla with IgG4 positive plasma cell infiltration and preserved segment of the main pancreatic duct just proximal to the duodenal papilla are characteristic findings in patients with AIP. We propose these novel findings are useful in the diagnosis of AIP as well as the choice for corticosteroids.

Pancreatic response to endotoxin after chronic alcohol exposure: switch from apoptosis to necrosis?

Chronic alcohol consumption is known to increase the susceptibility to acute and chronic pancreatitis, and it is likely that a cofactor is required to initiate the progression to alcoholic pancreatitis. The severity and complications of alcoholic and nonalcoholic acute pancreatitis may be influenced by a number of cofactors, including endotoxemia. To explore the effect of a possible cofactor, we used endotoxin [lipopolysaccharide (LPS)] as a tool to induce cellular injury in the alcoholic pancreas. Single, increasing doses of endotoxin were injected in rats fed an alcohol or control diet and killed 24 h after the injection. We examined the mechanism by which LPS exacerbates pancreatic injury in alcohol-fed rats and whether the injury is associated with apoptosis or necrosis. We showed that chronic alcohol exposure alone inhibits apoptosis through the intrinsic pathway and the downstream apoptosis executor caspase-3 compared with the controls. Pancreatic necrosis and inflammation increased after LPS injection in control and alcohol-fed rats in a dose-dependent fashion but with a significantly greater response in the alcohol-fed animals. Caspase activities and TdT-mediated dUTP nick-end labeling positivity were lower in the alcoholic pancreas injected with LPS, whereas the histopathology and inflammation were more severe compared with the control-fed animals. Assessment of a putative indicator of necrosis, the ratio of ADP to ATP, indicated that alcohol exposure accelerates pancreatic necrosis in response to endotoxin. These findings suggest that the pancreas exposed to alcohol is more sensitive to LPS-induced damage because of increased sensitivity to necrotic cell death rather than apoptotic cell death. Similar to the liver, the pancreas is capable of responding to LPS with a more severe response in alcohol-fed animals, favoring pancreatic necrosis rather than apoptosis. We speculate that this mechanism may occur in acute alcoholic pancreatitis patients.

Chinese alcoholic patients with esophageal cancer are genetically different from alcoholics with acute pancreatitis and liver cirrhosis

OBJECTIVE: It is a mystery why some alcoholic patients acquire certain organ-specific complications of alcoholism, whereas other alcoholic patients acquire different ones. The aim of this study was to investigate the differences among Chinese alcoholic patients with esophageal cancer, acute pancreatitis, and liver cirrhosis by studying the genetic polymorphisms of ADH2, ADH3, ALDH2, and P4502E1. METHODS: Liver alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and cytochrome P4502E1 (P4502E1) are polymorphic at the ADH2, ADH3, and ALDH2 loci and the 5′-flanking region of the P4502E1. Using the polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) method, we determined the polymorphism of the above-mentioned alcohol metabolizing genes in 59 alcoholics with carcinoma of the esophagus (alcoholic esophageal Ca), 87 acute alcoholic pancreatitis patients, 116 alcoholics with liver cirrhosis (alcoholic cirrhosis), 19 alcoholics with both liver cirrhosis and acute pancreatitis (alcoholic P plus C), and 241 nonalcoholic patients. RESULTS: The results showed that the allele frequency of ALDH2∗2 was significantly higher in the alcoholic esophageal Ca group than in the alcoholic pancreatitis and alcoholic cirrhosis groups. The allele frequency of ADH2∗1 was significantly higher in the alcoholic esophageal Ca patients than in nonalcoholic control groups. The ALDH2∗2 was significantly lower in alcoholic groups (except the alcoholic esophageal Ca group) than in nonalcoholic control groups. The allele frequencies of ADH2∗1 and ALDH2∗2 are higher in alcoholic patients with esophageal Ca than alcoholic patients without it. The genotype distribution of P4502E1, detected by RsaI and PstI, was not different among alcoholic patients with different organ diseases. CONCLUSIONS: The allele frequency of ADH2∗1 and ALDH2∗1 are different among subpopulations of alcoholics, suggesting that alcoholic patients with different specific types of organ damage are genetically different. The Chinese alcoholic patients with the ADH2∗1 and ALDH2∗2 allele are more susceptible to esophageal Ca.

Chinese alcoholic patients with esophageal cancer are genetically different from alcoholics with acute pancreatitis and liver cirrhosis.

It is a mystery why some alcoholic patients acquire certain organ-specific complications of alcoholism, whereas other alcoholic patients acquire different ones. The aim of this study was to investigate the differences among Chinese alcoholic patients with esophageal cancer, acute pancreatitis, and liver cirrhosis by studying the genetic polymorphisms of ADH2, ADH3, ALDH2, and P4502E1. Liver alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and cytochrome P4502E1 (P4502E1) are polymorphic at the ADH2, ADH3, and ALDH2 loci and the 5'-flanking region of the P4502E1. Using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, we determined the polymorphism of the above-mentioned alcohol metabolizing genes in 59 alcoholics with carcinoma of the esophagus (alcoholic esophageal Ca), 87 acute alcoholic pancreatitis patients, 116 alcoholics with liver cirrhosis (alcoholic cirrhosis), 19 alcoholics with both liver cirrhosis and acute pancreatitis (alcoholic P plus C), and 241 nonalcoholic patients. The results showed that the allele frequency of ALDH2*2 was significantly higher in the alcoholic esophageal Ca group than in the alcoholic pancreatitis and alcoholic cirrhosis groups. The allele frequency of ADH2*1 was significantly higher in the alcoholic esophageal Ca patients than in nonalcoholic control groups. The ALDH2*2 was significantly lower in alcoholic groups (except the alcoholic esophageal Ca group) than in nonalcoholic control groups. The allele frequencies of ADH2*1 and ALDH2*2 are higher in alcoholic patients with esophageal Ca than alcoholic patients without it. The genotype distribution of P4502E1, detected by RsaI and PstI, was not different among alcoholic patients with different organ diseases. The allele frequency of ADH2*1 and ALDH2*1 are different among subpopulations of alcoholics, suggesting that alcoholic patients with different specific types of organ damage are genetically different. The Chinese alcoholic patients with the ADH2*1 and ALDH2*2 allele are more susceptible to esophageal Ca.

Admission plasma cholecystokinin levels are low both in acute alcoholic and biliary pancreatitis

Background Recent studies have shown that cholecystokinin (CCK) agonist, cerulein can induce acute pancreatitis in animals. The role of CCK in the induction of acute pancreatitis in man is unclear. We investigated admission plasma CCK levels in alcoholic and biliary pancreatitis. Method Plasma CCK concentrations were determined by a specific and sensitive radioimmunoassey using CCK antiserum (Euro-Diagnostica, Malmti, Sweden) in 35 patients with acute alcoholic pancreatitis, in 27 patients with acute biliary pancreatitis, in 34 patients with non-pancreatic acute abdominal pain and in 43 healthy subjects. The mean time from the first symptoms to the plasma sample was 31 ( ± 3.7) hours in alcoholic pancreatitis patients and 25 ( ± 5.1) hours in biliary pancreatitis patients. Normal fasting level of CCK is _ 1.12 pmol/1) significantly more often in non-pancreatic acute abdominal pain patients than in alcoholic pancreatitis patients (12/34 vs 0/35, p=0.00006) or biliary pancreatitis patients (12/34 vs 1/27, p=0.002) and also significantly more often in healthy subjects than in alcoholic pancreatitis patients (17/43 vs 0/35, p=0.000007) or biliary pancreatitis patients (17/43 vs 1/27, p=0.0005). Conclusion Basal plasma CCK concentrations are significantly decreased in acute alcoholic and biliary pancreatitis early in the course of the disease.

Alcoholism and alcoholic organ damage and genetic polymorphisms of alcohol metabolizing enzymes in Chinese patients

It is still not clear why some alcoholic patients acquire certain organ-specific complications of alcoholism whereas other alcoholic patients acquire different ones. As we know the liver alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and cytochrome P4502E1 (P4502E1) are polymorphic at the ADH2, ADH3, and ALDH2 loci and the 5'-flanking region of the P4502E1. The aim of this study was to investigate the differences between Chinese alcoholic patients with cirrhosis and acute pancreatitis by studying the genetic polymorphisms of ADH2, ADH3, ALDH2, and P4502E1. Genotyping of ADH2, ADH3, ALDH2, and P4502E1 was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods on peripheral white blood cell DNA from 75 alcoholic cirrhotic patients, 48 acute alcoholic pancreatitis patients, 19 heavy drinkers without liver disease or pancreatitis, and 235 controls. The results showed that the frequencies of the alleles ADH2*1 and ALDH2*1 in the alcoholic cirrhotic patients were significantly higher than those in the nonalcoholic controls. In acute alcoholic pancreatitis patients, only the frequency of allele ALDH2*1, not ADH2*1 was significantly higher than in the nonalcoholic controls. The allele frequency of ADH2*1 in acute pancreatitis patients was significantly lower (P < .01) than in alcoholic cirrhotic patients. The daily amount of alcohol consumption was significantly lower in patients with acute pancreatitis than in patients with cirrhosis (P < .0005). The genotype distributions of P4502E1, detected by RsaI and PstI, were not different among alcoholic cirrhotic patients, alcoholic pancreatitis patients, heavy drinker, and nonalcoholic controls. In conclusion, ALDH2*1 is the most important alcohol metabolizing gene affecting predisposition to alcoholism whereas the ADH2*2 gene may influence susceptibility to acute alcoholic pancreatitis. The patients with alcohol-induced cirrhosis and with alcohol-induced acute pancreatitis are of two different subpopulations.(Hepatology 1997 Jan;25(1):112-7)

Alcoholism and alcoholic organ damage and genetic polymorphisms of alcohol metabolizing enzymes in Chinese patients.

It is still not clear why some alcoholic patients acquire certain organ-specific complications of alcoholism whereas other alcoholic patients acquire different ones. As we know the liver alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), and cytochrome P4502E1 (P4502E1) are polymorphic at the ADH2, ADH3, and ALDH2 loci and the 5'-flanking region of the P4502E1. The aim of this study was to investigate the differences between Chinese alcoholic patients with cirrhosis and acute pancreatitis by studying the genetic polymorphisms of ADH2, ADH3, ALDH2, and P4502E1. Genotyping of ADH2, ADH3, ALDH2, and P4502E1 was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methods on peripheral white blood cell DNA from 75 alcoholic cirrhotic patients, 48 acute alcoholic pancreatitis patients, 19 heavy drinkers without liver disease or pancreatitis, and 235 controls. The results showed that the frequencies of the alleles ADH2*1 and ALDH2*1 in the alcoholic cirrhotic patients were significantly higher than those in the nonalcoholic controls. In acute alcoholic pancreatitis patients, only the frequency of allele ALDH2*1, not ADH2*1 was significantly higher than in the nonalcoholic controls. The allele frequency of ADH2*1 in acute pancreatitis patients was significantly lower (P < .01) than in alcoholic cirrhotic patients. The daily amount of alcohol consumption was significantly lower in patients with acute pancreatitis than in patients with cirrhosis (P < .0005). The genotype distributions of P4502E1, detected by RsaI and PstI, were not different among alcoholic cirrhotic patients, alcoholic pancreatitis patients, heavy drinker, and nonalcoholic controls. In conclusion, ALDH2*1 is the most important alcohol metabolizing gene affecting predisposition to alcoholism whereas the ADH2*2 gene may influence susceptibility to acute alcoholic pancreatitis. The patients with alcohol-induced cirrhosis and with alcohol-induced acute pancreatitis are of two different subpopulations.

Genotypes of Alcohol‐Metabolizing Enzymes and the Risk for Alcoholic Chronic Pancreatitis in Japanese Alcoholics

Genetic predisposition to alcoholism and alcoholic liver disease has been reported. However, genetic susceptibility to alcoholic pancreatitis is still a matter of debate. To determine it, we examined genotype patterns of aldehyde dehydrogenase (ALDH2), alcohol dehydrogenase (ADH2 and ADH3), and cytochrome P-4502E1 (CYP2E1) in alcoholic pancreatitis patients. In 296 alcoholic patients, 52 cases showed findings of chronic pancreatitis by ultrasonography and x-ray computed tomography and/or had a history of pancreatitis (P+). The remaining 244 patients had neither abnormal findings of the image examinations nor a history of pancreatitis (P-). As for the ADH2 genotype, distribution of 2(1)/2(1), 2(1)/2(2), and 2(2)/2(2) was 22, 37, and 42% in P+ patients, whereas 34, 35, and 30% in P- patients, respectively. The frequency of ADH2(2)/2(2) genotype was significantly higher in P+ patients, compared with that in P- patients. There were no significant differences in the distribution of ADH3, ALDH2, and CYP2E1 genotypes between P+ and P- patients. In 14 alcoholic patients who showed low contents of fecal chymotrypsin, which suggests dysfunction of pancreatic exocrine, the rate of ADH2(2)/2(2) genotype also tended to be higher (50%) than in 74 controls who showed normal contents of the fecal chymotrypsin (28%). No differences were observed in genotypes of ADH3, ALDH2, and CYP2E1. Moreover, the frequency of ADH2(2)/2(2) genotype was significantly higher in autopsy cases with interlobular fibrosis in the pancreas, which suggests alcoholic pancreatic damage, than in cases with only intralobular pancreatic fibrosis. These data suggest that the risk of alcoholic pancreatitis seems to be associated with the presence of ADH2(2)/2(2) genotype.