Prognosis of Chronic Pancreatitis: An International Multicenter Study

Objectives: Tbe aim of this study was to determine which factors predict mortality in a cobort of patients with cbronic alcoholic and nonalcoholic pancreatitis. Patients with chronic pancreatitis are known to have a reduced life expectancy, but the quantitative relationship between various clinical features and survival is unclear. Methods: We evaluated survival among 2015 subjects with chronic pancreatitis treated at seven centers located in six countries. Results: Mean age at diagnosis was 46 ± 13 yr and mean duration of follow-up was 7.4 ± 6.2 yr. Overall survival at 10 yr was 70% (95% confidence interval (CI), 68–73%) and at 20 yr was 45% (95% CI, 41–49%). Survival was significantly less than in the background population. There were 559 deaths observed among those with chronic pancreatitis compared with an expected number of 157.4, yielding a standardized mortality ratio (SMR) of 3.6 (95% CI, 3.3–3.9). Older subjects and those with alcoholic pancreatitis had a significant reduction in survival. In a mul-tivariate analysis, mortality of middle-aged and older subjects was 2.3 (95% CI, 1.8–2.8) and 6.3 (95% CI, 4.7–8.3) times greater than subjects less than 40 yr at diagnosis. Smoking (hazard ratio, 1.4; 95% CI, 1.0–1.9), drinking (hazard ratio, 1.6; 95% CI, 1.2–2.2), or development of cirrhosis (hazard ratio, 2.5; 95% CI, 2.0–3.2) increased the risk of death during the observation period, but we observed no survival difference in operated vs . nonoperated patients. Conclusions: Age at diagnosis, smoking, and drinking are major predictors of mortality in patients with chronic pancreatitis.     

135例慢性胰腺炎临床病例分析

探讨慢性胰腺炎的不同病因和临床表现特点。回顾性分析本院135例慢性胰腺炎的住院患者的主要病因包括胆道系统疾病(31．85％)和酒精中毒(35．56％),其他病因包括特发性、自身免疫性疾病、外伤或遗传等。酒精性CP临床症状发生的比例较胆源性高,特别是腹痛、腹泻、糖尿病的发生率明显高于胆源性CP。酒精性与非酒精性CP组、对照组相比,TG、HDL-C、G／HDL-C差别显著。胆道系统疾病和酒精中毒为CP主要病因,近年来酒精性因素呈上升趋势。临床表现上,酒精性较胆源性CP的发生率高。TG／HDL-C比值可能有助于鉴别酒精性和非酒精性胰腺炎。     

Latent portasystemic encephalopathy

Forty patients with chronic liver disease and portal hypertension but without clinical signs of portasystemic encephalopathy (15 patients with nonalcoholic cirrhosis, 15 patients with alcoholic cirrhosis, and 10 patients with minimal EEG changes) and a control group of 12 patients with chronic alcoholic pancreatitis were studied using an extensive psychometric program, which, in the same form, is used for expert reports on driving capacity. Of the cirrhotic patients, 60% were considered unfit to drive; in 25% driving capacity was questionable, 15% (only nonalcoholic cirrhotics) were considered fit to drive. In contrast 75% of the patients with alcoholic pancreatitis were considered fit to drive. Major defects were found only in three heavy alcoholics. Patients with alcoholic cirrhosis scored lower than patients with nonalcoholic cirrhosis. This was due, to differences in liver function rather than to the effect of alcohol consumption. Patients with minimal EEG changes were practically all considered unfit to drive.     

Modifications of pure human pancreatic juice induced by chronic alcohol consumption

Pure pancreatic juice has been collected from 25 humans by endoscopic retrograde catheterization of the papilla. Nine did not present with digestive diseases and their mean daily alcohol consumption had never exceeded 40 g (nonalcoholic controls). Sixteen drank more than 100 g alcohol per day for at least 5 years previously (alcoholic patients). Five of those presented with chronic pancreatitis and 11 were apparently normal (alcoholic controls). Juice was collected in 1-min fractions for 20 min. 0.5 CU/kg secretin was injected at the beginning and 3 CHR U/kg cholecystokinin-pancreozymin at the 10th min. Protein concentration was significantly greater in alcoholic patients than in nonalcoholic controls in the samples following both secretin and cholecystokinin-pancreozymin injections, and the highest observed protein concentration was significantly greater in alcoholic controls than in nonalcoholic controls. When it had returned to resting values after hormonal injections, protein concentration was significantly higher in alcoholic chronic pancreatitis patients than in alcoholic controls in six samples, and in two similar samples it was higher in alcoholic chronic pancreatitis patients than in nonalcoholic controls. Protein output was not significantly different in alcoholic controls than in nonalcoholic controls. Bicarbonate concentration was significantly lower in alcoholic patients than in nonalcoholic controls in two samples following secretin injection. Volume was similar in alcoholic controls and nonalcoholic controls, but lower in alcoholic chronic pancreatitis patients than in alcoholic controls in three samples. These results substantiate the assumption already put forward of a hypersecretion of protein not compensated for by a hypersecretion of water and bicarbonate as the origin of alcoholic pancreatitis.     

Alcohol intake, cigarette smoking, and body mass index in patients with alcohol-associated pancreatitis

The differential diagnosis between acute and chronic alcohol-associated pancreatitis is often difficult or impossible at onset of the disease. A study was conducted to determine possible relationships between patients suffering from a first episode of acute alcoholic pancreatitis and patients with unequivocal chronic alcoholic pancreatitis, comparing age, drinking and smoking habits, and body mass index (BMI). Two groups of men were considered. The first group consisted of 67 patients with a diagnosis of acute alcohol-associated pancreatitis in the absence of other potential pathogenic factors; in this group, 48 of the 56 patients surviving the acute attack were submitted to imaging studies for a median period of 9 years. The second group consisted of 396 patients with chronic alcoholic pancreatitis with a median follow-up period of 12 years. The variables that differed significantly in the two groups were BMI (p < 0.009) and number of smokers (p < 0.001). Logistic regression analysis selected only BMI with an odds ratio of 1.19 (95% CI, 1.07-1.33; p < 0.00015) in favor of acute alcoholic pancreatitis. In male patients, from an epidemiologic standpoint, only smoking habits and BMI are significant differences at clinical onset between the two types of pancreatitis.     

Serum amylase and lipase concentrations and lipase/amylase ratio in assessment of etiology and severity of acute pancreatitis

We studied the behavior of serum amylase and lipase in 66 consecutive patients with acute pancreatitis in order to assess the ability of these tests and of the serum lipase-amylase ratio to establish the etiology and predict the severity of acute pancreatitis. Forty-two patients had biliary acute pancreatitis, 14 had alcoholic acute pancreatitis, and the remaining 10 nonbiliary, nonalcoholic (NBNA) acute pancreatitis. Serum amylase and lipase were abnormally high in all patients. The elevations of both serum amylase and lipase were significantly lower in patients with alcoholic pancreatitis than in those with biliary pancreatitis, although a considerable overlap was observed between the two groups. No statistically significant differences were found between NBNA patients and those with either biliary or alcoholic forms of the disease. The serum lipase-amylase ratios in patients with alcoholic pancreatitis ranged from 0.2 to 5.6, in those with biliary pancreatitis from 0.1 to 7.9, and in those with NBNA pancreatitis from 0.1 to 4.4. These differences were not statistically significant. No differences in serum enzyme levels were observed among patients without apparent imaging signs of acute pancreatitis (N=20), those with signs of Pancreatic edema (N=36), and those with necrotizing pancreatitis (N=10). The results indicate that serum amylase and lipase concentrations are not able to establish either the etiology or to predict the severity of acute pancreatitis as assessed by imaging techniques. Furthermore, the serum lipase-amylase ratio is not useful in distinguishing acute episodes of alcoholic from nonalcoholic acute pancreatitis.     

Exocrine Pancreatic Function in Chronic Liver Diseases

To confirm the respective influence of chronic alcoholism and liver disease on exocrine pancreatic function in cholecystokinin secretin (CS), tests were performed on patients with chronic liver cirrhosis (LC) and non-cirrhotic (nLC) disease of alcoholic (A) and nonalcoholic (nA) etiology. Results were compared in four subgroups (ALC, N = 26; AnLC, N = 45; nALC, N = 18; and nAnLC, N = 43). Volume of duodenal juice and bicarbonate output (BO) were increased and maximal bicarbonate concentration was decreased in ALC, compared with those in normal controls. Comparison of LC and nLC indicated that the volume, BO, and amylase output (AO) were greater in LC than in nLC of alcoholic etiology, but not in those of nonalcoholic etiology. The initial disappearance rate (KICG) of indocyanine green (ICG) excretion correlated with a parameter of CS test in alcoholic liver disease (vs. volume: r = -0.51, p less than 0.01 vs BO: r = -0.40, p less than 0.01), but not in nonalcoholic liver disease. Concurrent chronic pancreatitis with pain and definite exocrine insufficiency was observed in only one ALC patient and in four AnLC patients, but in none of the nonalcoholics. In alcoholic liver disease, exocrine pancreatic secretion tends to increase with severity of liver damage, but concurrence of definite chronic pancreatitis is not correlated with the severity.     

The Admission Serum Lipase:Amylase Ratio Differentiates Alcoholic from Nonalcoholic Acute Pancreatitis

To determine whether the lipase:amylase ratio differentiates alcoholic from nonalcoholic pancreatitis, we conducted a retrospective review of charts with the diagnosis of acute pancreatitis at the George Washington University Medical Center between January 1988 and July 1990. A total of 446 charts were reviewed. For a patient to be included in the subsequent analysis, the following criteria were met: 1) the patient had typical symptoms of pancreatitis, 2) serum amylase and lipase were analyzed on admission, and 3) a computerized tomographic (CT) scan or ultrasound of the abdomen was obtained within 72 h of admission. Forty-seven charts satisfied the requirements for inclusion in the study. Data collected from the charts included history of alcohol consumption, age, sex, race, admission serum amylase and serum lipase (from this the amylase:lipase ratio was calculated), peak serum amylase and serum lipase, and number of days of abdominal pain before admission. Patients with alcoholic pancreatitis had significantly lower serum amylase levels and significantly higher lipase:amylase ratios than those with nonalcoholic pancreatitis (p < 0.01). There was no difference in the serum lipase between the groups. The higher the lipase:amylase ratio, the greater the specificity of alcohol as the etiology of acute pancreatitis. Only patients with alcoholic acute pancreatitis had lipase:amylase ratios > 5.0 (sensitivity 31%, specificity 100%). Our data point to the clinical utility of the lipase:amylase ratio in differentiating alcoholic from nonalcoholic acute pancreatitis. Prospective studies will be needed to confirm the clinical utility of this ratio.     

Pancreas divisum does not modify the natural course of chronic pancreatitis

Background Pancreas divisum is the most common congenital variant of the pancreas; however, its clinical significance remains controversial. The purpose of our study was to determine the role of pancreas divisum in the development of chronic pancreatitis. Methods We compared the clinical presentation, morphological findings, and course of disease of 30 patients with chronic pancreatitis associated with pancreas divisum (there was coexisting chronic alcohol abuse in 18 cases) to those of 57 patients with chronic pancreatitis and no evidence of pancreas divisum (15 with nonalcoholic pancreatitis and 42 with alcoholic pancreatitis). Results Sex distribution, age at onset of disease, clinical presentation, course of disease, and frequency of complications were not affected by the presence of pancreas divisum. Although the etiology of pancreatitis in patients with pancreas divisum may be attributed to impaired drainage of the majority of the gland through the minor papilla, we observed a relatively low frequency of isolated dorsal duct involvement in our patients irrespective of alcohol use (25% and 28% in patients with and without a history of alcohol abuse, respectively). However, involvement of the ventral duct was commonly observed (75% and 72%, respectively). Conclusions The presence of pancreas divisum in our study did not modify the natural course of chronic nonalcoholic or alcoholic pancreatitis. Pancreas divisum is not likely to play a dominant role in the etiopathogenesis of chronic pancreatitis.     

The Lipase to Amylase Ratio in Acute Pancreatitis

Objectives : The ratio of serum lipase to serum amylase has been proposed to distinguish acute episodes of alcoholic from nonalcoholic pancreatitis. We evaluated the efficacy of this test in a community hospital setting. Methods : Charts of all patients discharged with a diagnosis of acute pancreatitis over 19 months were retrospectively reviewed. Patients were excluded if their cre-atinine was greater than 3.0 mg/dl, if the amylase and lipase were not measured within 72 h of the onset of symptoms, or if the cause of pancreatitis was not known by the time of discharge. Results : Of the 56 patients, 31 had alcoholic pancreatitis. The lipase to amylase ratio did not differ significantly between patients with alcoholic and nonalcoholic pancreatitis. Median amylase and lipase were significantly higher in nonalcoholic pancreatitis; however, the wide ranges of both meant that neither amylase nor lipase accurately determined the cause of pancreatitis. Conclusion : The lipase to amylase ratio does not appear to be sufficiently sensitive or specific to distinguish alcoholic from nonalcoholic acute pancreatitis.     

Diagnosis and management of chronic pancreatitis: current knowledge

This paper reviews the current literature on chronic pancreatitis (CP). Despite marked progress in diagnostic tools, predominately imaging methods, no consensus has been reached on the nomenclature of CP, ie diagnosis, classification, staging, pathomechanisms of pain and its optimal treatment. A major problem is that no single reliable diagnostic test exists for early-stage CP except histopathology (rarely available). This stage is characterised typically by recurrent acute pancreatitis +/- necrosis (eg pseudocysts). Acute pancreatitis is a well-defined condition caused in 80% of cases by gallstones or alcohol abuse. Alcoholic pancreatitis, in contrast to biliary pancreatitis, progresses to CP in the majority of patients. However, a definite CP-diagnosis is often delayed because progressive dysfunction and/or calcification, the clinical markers of CP, develop on average 5 years from disease onset. The progression rate is variable and depends on several factors eg aetiology, smoking, continued alcohol abuse. Repeated function testing eg by the faecal elastase test, is the best alternative for histology to monitor progression (or non-progression) of suspected (probable) to definite CP. The pathomechanism of pain in CP is multifactorial and data from different series are hardly comparable mainly because insufficient data of the various variables ie diagnosis, classification, staging of CP, pain pattern and presumptive pain cause, are provided. Pain in CP is rarely intractable except in the presence of cancer, opiate addiction or extra-pancreatic pain causes. Local complications like pseudocysts or obstructive cholestasis are the most common causes of severe persistent pain which can be relieved promptly by an appropriate drainage procedure. Notably, partial to complete pain relief is a common feature in 50-80% of patients with late-stage CP irrespective of surgery and about 50% of CP-patients never need surgery (or endoscopic intervention). The spontaneous "burn-out" thesis of CP is in accordance with this observation although precise data of this phenomenon are scarce. Recent observations indicate that the progression to late-stage CP is markedly delayed in non-alcoholic compared to alcoholic CP. Therefore, spontaneous pain relief is also delayed but it occurs in close association with severe exocrine insufficiency suggesting that aetiology has a major impact on the duration of early-stage CP and that the "burn-out" thesis appears valid both in uncomplicated alcoholic and nonalcoholic late-stage CP. For treatment of steatorrhea and diabetes the reader is referred to recent reviews. Mortality and survival are closely related to aetiology with an increased death rate of about 50% within 20 years from onset in alcoholic CP compared to a markedly better prognosis in hereditary and idiopathic "juvenile" CP. The risk of pancreatic cancer is increased particularly in nonalcoholic CP based on the longer survival, whereas the risk of extra-pancreatic (smoking-related) cancer is about 12-fold higher in alcoholic CP.     

Analytical studies of both initial symptoms and clinical symptoms and signs of different etiologies of chronic pancreatitis: an approach by using odds ratios]

We conducted the statistical analysis of both initial symptoms and clinical symptoms and signs of different etiologies of chronic pancreatitis by using odds ratios which was one of the techniques of evidence-based medicine. The official report published by The Research Group of Intractable Pancreatic Diseases sponsored by the Welfare Ministry of Japan in 1986 was available as the data source of the present study. Nine items of initial symptoms and 25 items of 28 clinical symptoms and signs were compared in 4 different etiologies of the disease which were alcoholic, biliary, idiopatic and nonalcoholic (both biliary and idiopatic). In initial symptoms, 1.5 items were significantly more observed in alcoholic pancreatitis than in nonalcoholic, biliary and idioatic pancreatitis, 4 of which (abdominal pain, back pain, poor appetite and loss of body weight) were common items as might be related closely to the alcohol intake, 2. only one item of jaundice was significantly more observed in biliary pancreatitis than in alcoholic and idiopatic pancreatitis, 3.3 items of poor appetite, diarrhea and abdominal mass were more frequently observed in idiopatic pancreatitis than in biliary pancreatitis. In clinical symptoms and signs, 1. almost all items (21 to 24) were significantly more observed in alcoholic pancreatitis than in the other etiologies of the disease, and seemed to be related directly or indirectly to alcohol intake, 2.3 or 4 items which were related closely to gallstone and acute cholecystitis were significantly more observed in biliary pancreatitis than the other two etiologies of the disease, and 3.4 items consisting of diarrhea, loss of body weight, and pancreatic swelling were more frequently observed in idiopathic pancreatitis than in biliary pancreatitis.     

Maximizing scarce service resources in a rural mental health clinic: should alcoholics be treated in separate programs?

One hundred nineteen patients at rural community mental health centers were divided into three diagnostic groups and compared to determine if alcoholic and nonalcoholic patients differ significantly in terms of psychopathology. The three diagnostic groups were primary diagnosis of alcoholism (N = 34), primary diagnosis of emotional disturbance (N = 39), and "other" diagnoses (N = 46). These groups were compared with respect to demographic variables, alcohol drinking patterns, psychopathology, and attitude toward treatment. The alcoholic patient group tended to be single, male, and inpatients; while the nonalcoholic group tended to be married, female, and outpatients. These groups differed significantly with respect to alcohol consumption and drinking patterns and effects, but did not differ significantly with respect to their attitudes toward mental illness or their MMPI profiles. The results of the "other" diagnostic group generally fell between those of the alcoholic and nonalcoholic groups, suggesting that it was a heterogeneous group of subjects. The total subject population evidenced elevated MMPI profiles, indicating the presence of a high level of psychopathology, but there was no clear distinction between the alcoholics and the other groups in terms of type or degree of psychopathology. Implications for treatment are discussed.     

Chronic pancreatitis progressing from segmental lesions

BACKGROUND/AIMS: Chronic pancreatitis is histologically and functionally a progressive disease. To examine the natural history of chronic pancreatitis, we evaluated serial pancreatography in cases of chronic pancreatitis, focusing on the progression of diffuse-type chronic pancreatitis from the segmental type. METHODOLOGY: We reviewed 57 patients with chronic pancreatitis who had undergone endoscopic retrograde pancreatography on more than 2 occasions at intervals of at least 1 year. Cases of chronic pancreatitis were categorized as diffuse (n=37) and segmental (n=20) on the findings of initial endoscopic retrograde pancreatography. RESULTS: Twenty-three cases of diffuse-type chronic pancreatitis showed progression of pancreatic duct abnormalities. Segmental abnormalities of the main pancreatic duct at the body or tail of the pancreas spread to the head of the pancreas in 8 cases. Etiologies of these cases of chronic pancreatitis were alcoholic, in which patients continued drinking after initial endoscopic retrograde pancreatography. In 2 patients who underwent distal pancreatectomy, although segmental lesions showed typical histological findings of alcoholic chronic pancreatitis, appearances near the margin of these lesions were almost normal or indicated slight interlobular fibrosis. CONCLUSIONS: The pancreatic tail might represent the site of the initial lesion in some cases of alcoholic pancreatitis.     

Hepatic Circulation and Hepatic Oxygen Consumption in Alcoholic and Nonalcoholic Fatty Liver

The purpose of this study was to determine the differences in hepatic circulation and oxygen consumption in two groups: those with nonalcoholic obesity-related fatty live and those with alcoholic fatty liver. Although the histological degree of fatty infiltration was equal in the two groups, the delta Er569-650, as an index of the regional liver blood flow estimated by spectrophotometric method, was significantly lower in alcoholic fatty liver than in nonalcoholic fatty liver, and the in vivo hepatic oxygen consumption (VO2), also determined by hepatic reflectance spectrophotometry during peritoneoscopy, tended to be lower in alcoholic fatty liver than in nonalcoholic fatty liver. The oxygen saturation of hemoglobin in local liver blood (SO2) was, however, significantly higher in alcoholic fatty liver than in nonalcoholic fatty liver. These results suggest that an increase in oxygen extraction to maintain oxygen consumption, which was indicated by the lowering of the SO2, was not found in alcoholic fatty liver, in spite of a reduction of oxygen supply to the liver. It is concluded that the impairment of hepatic circulation and hepatic oxygen consumption was more serious in alcoholic fatty liver than in nonalcoholic fatty liver, possibly contributing to a different prognosis for the two forms of fatty liver.     

Venous thromboembolism with chronic liver disease

Background

Patients with chronic liver disease have both antithrombotic and prothrombotic coagulation abnormalities. Published data conflict on whether patients with chronic liver disease have a high or low prevalence of venous thromboembolism.

Methods

The number of patients discharged from hospitals throughout the US with a diagnostic code for chronic alcoholic and chronic nonalcoholic liver disease from 1979 through 2006 was obtained from the National Hospital Discharge Survey. We compared prevalences of venous thromboembolism among patients with chronic alcoholic liver disease and chronic nonalcoholic liver disease.

Results

Among 4,927,000 hospitalized patients with chronic alcoholic liver disease from 1979-2006, the prevalence of venous thromboembolism was 0.6%, compared with 0.9% among 4,565,000 hospitalized patients with chronic nonalcoholic liver disease.

Conclusion

The prevalence of venous thromboembolism in hospitalized patients with chronic liver disease, both alcoholic and nonalcoholic, was low. The prevalence of venous thromboembolism was higher in those with chronic non-alcoholic liver disease, but the difference was small and of no clinical consequence. Based on the literature, both showed a lower prevalence of venous thromboembolism than in hospitalized patients with most other medical diseases. It may be that both chronic alcoholic liver disease and chronic nonalcoholic liver disease have protective antithrombotic mechanisms, although the mechanisms differ.     

Usefulness of carbohydrate-deficient transferrin and trypsin activity in the diagnosis of acute alcoholic pancreatitis

OBJECTIVE: The aim of this study was to assess if carbohydrate-deficient transferrin (CDT) and trypsin activity differentiate acute alcoholic pancreatitis from nonalcohol-related pancreatitis, and as a secondary goal to evaluate its use in comparison to healthy controls. METHODS: Serum levels of CDT and trypsin activity were measured in frozen sera from 70 nonconsecutive patients with acute pancreatitis and in 16 healthy controls. RESULTS: Causes of pancreatitis were gallstones in 51%, chronic alcoholism in 23%, and other or unknown causes in 26% of the patients. Serum CDT was significantly higher in alcoholic pancreatitis than in the nonalcoholic disease (p < 0.0001) with a median (interquartile range) of 30.8 U/L (23.6-41.7 U/L) in chronic alcoholism, 16.7 U/L (13.05-21.1 U/L) in gallstones, 17.5 U/L (15.9-21.6 U/L) in unknown cause, 19.3 U/L (15.1-27.7 U/L) in other etiologies, and 16.1 U/L (12.1-18.8 U/L) in controls. At a cutoff over 22.5 U/L, CDT showed a sensitivity of 87.5% and a specificity of 85.2%. Serum levels of trypsin activity were significantly higher (p = 0.0007) in alcoholic pancreatitis, median 165 U/L (76-405 U/L) than in nonalcoholic pancreatitis, median 73 U/L (46.5-100.5 U/L). At a cutoff value over 152 U/L, the sensitivity of trypsin activity was 60% with a specificity of 100%. In the multivariate analysis, patient's age (< or = 44 yr), CDT (>22.5 U/L), and trypsin activity (>152 U/L) enabled correct prediction of acute alcoholic pancreatitis in 98% of the cases. CONCLUSION: Serum CDT and trypsin activity are of clinical utility in differentiating alcoholic from nonalcoholic acute pancreatitis.     

Pancreatitis in a native American Indian population

We have studied pancreatitis in a population of Southwestern American Indians where gallstones are frequent, alcohol consumption is presumably high, but where smoking is an uncommon habit. Over a 5-year period, 131 cases of pancreatitis (65 males, 66 females) were observed: 66 (50%) were thought to be biliary pancreatitis, 54 cases (41%) alcoholic pancreatitis, and 5 cases (4%) were caused by injuries. In 6 cases (5%) no definite cause was found. Smoking appeared to be increased in male subjects with alcoholic pancreatitis when compared to subjects with alcoholic liver cirrhosis--a group with similar drinking habits. (Adjusted odds ratio = 12.5, p = 0.008). No such relationship was observed for females. Our findings suggest that in this population smoking may be an additional important risk factor for male subjects with alcoholic pancreatitis.     

Increased Risk of Esophageal Varices,Liver Cancer,and Death in Patients With Alcoholic Liver Disease

Background and Aims: During the last decades, a multitude of different treatments for chronic liver disease have been introduced. New surveillance programs have been established to detect esophageal varices and liver cancer. The aims of our study were to assess whether the prognosis for patients hospitalized with liver diseases between 1969 and 2006 had improved and to study the differences in mortality and complications between patients with alcoholic liver disease and nonalcoholic liver diseases. Methods: We used the Swedish Hospital Discharge Register and Cause of Death Register at the National Board of Health and Welfare in Sweden between 1969 and 2006 to identify and follow‐up a cohort of patients with liver disease according to the International Classification of Diseases‐8, ‐9, and ‐10. Results: There were 36,462 patients hospitalized with alcoholic and 95,842 with nonalcoholic liver diseases. The main finding was that patients hospitalized with alcoholic liver disease had an increased mortality risk, compared to patient with nonalcoholic liver disease, 1.89 (1.85 to 1.92). In addition, the patients with alcoholic liver disease had an increased risk for esophageal varices and liver cancer. There was a reduced risk for hospitalization with esophageal varices for patients with nonalcoholic liver disease up to 1998. Conclusions: We found that the prognosis for patients hospitalized with chronic liver diseases had not improved. Patients with alcoholic liver disease have an increased risk of complications, which suggest that the disease is more aggressive and are in need of closer follow‐up than other chronic liver diseases.     

Nutritional data and etiology of chronic pancreatitis in Mexico

Alcoholism and malnutrition have been implicated commonly in the etiology of chronic pancreatitis (CP). The geographical distribution and clinical and nutritional features differ between the alcoholic and tropical forms of CP. This work presents the etiology and nutritional characteristics of CP in Mexico, a country in which both alcoholism and childhood malnutrition are common. Two well-defined groups of patients have been identified: an alcoholic group composed mainly of males with a mean age at clinical onset of 41 years and a high dietary intake of fat, protein, carbohydrates, and calories; and a nonalcoholic group with a female preponderance, a mean age at onset of 23 years, and a higher intake of protein than controls. We conclude that alcoholic chronic pancreatitis in Mexico is similar to that reported in other temperate countries. Although the nonalcoholic group resembles that observed in tropical countries in many ways, our patients are not malnourished, further questioning the role of childhood malnutrition in the pathogenesis of this type of chronic pancreatitis.