Recurrent acute pancreatitis (RAP) is a complex syndrome that presents variably, with many cases remaining idiopathic after thorough diagnostics. For evaluating structural etiologies, endoscopic ultrasound and MR cholangiopancreatography are preferred over endoscopic retrograde cholangiopancreatography (ERCP) given their more favorable risk profile and sensitivity. The diagnostic work-up remains paramount since treatment should focus on addressing underlying causes such as early cholecystectomy for gallstone pancreatitis. As more etiologic factors are uncovered, such as genetic susceptibility, causality becomes more nuanced. Earlier enthusiasm for endoscopic sphincterotomy as a treatment for idiopathic RAP has been tempered by less favorable studies in recent years.

Chronic pancreatitis is a fibroinflammatory disease of the pancreas with heterogeneous clinical features and a significant socioeconomic burden. Assessing its aetiology and early diagnosis of associated complications remain challenging. Personalized therapy necessitates precise knowledge of the genetic, biological, and clinical differences within a patient population. In this context, the identification of the underlying aetiology represents an essential cornerstone. This review elucidates current standards for identifying underlying aetiologies and the diagnostic work-up for idiopathic cases. It provides an overview of general therapeutic approaches and highlights individual treatment options. Additionally, the follow-up management of pancreatitis-associated complications, namely exocrine pancreatic insufficiency, post-pancreatitis diabetes mellitus, pain management, pancreatic fluid collections, and pancreatic cancer risk, is summarized.

Patients with chronic illnesses are susceptible to the financial burden of disease-related treatment costs. Financial toxicity is well researched in cancer and several chronic diseases. This review explores the financial challenges faced by patients with chronic pancreatitis and the impact of financial hardship on their well-being.

We performed a review of the published literature to summarize the body of existing research and to identify knowledge gaps related to the financial burden experienced by patients with chronic pancreatitis.

Research on financial burden, cost-coping behaviors, cost-related nonadherence to prescribed medications, and social vulnerabilities in people with chronic pancreatitis is sparse. No studies have assessed the suitability and validity of instruments measuring subjective financial toxicity in a patient population with chronic pancreatitis.

There is a critical need for further studies of financial toxicity in the patient population with chronic pancreatitis, considering that if the sources of financial burden can be identified, opportunities emerge to dampen or mitigate their impact on patients with chronic pancreatitis.

Alcohol and nicotine are the two most important risk factors of chronic pancreatitis, and they often occur together. It is still unclear how much they influence the severity of the disease and which of the two addictions should be treated with priority.

We performed a single-center, retrospective, cross-sectional study in a mixed medicosurgical cohort of 870 patients diagnosed with chronic pancreatitis (CP). We analyzed the impact of the drinking pattern and abstinence for alcohol and nicotine on the course of the disease. Patients with alcoholic CP were subdivided into 1) patients with "life-time drinking history" (LTDH), 2) "current drinkers" with current alcohol abuse without signs of LTDH, and 3) "former drinkers" who stopped or reduced alcohol intake dramatically.

Compared to patients with LTDH, "former drinkers" had a lower rate of exocrine insufficiency (29% vs. 59%) and pseudocysts (33% vs. 49%), were more often relapse-free (37% vs. 5%), and had less abdominal pain. There was no correlation detected between the quantity of alcohol consumption and the severity or progression of the disease. Regarding nicotine, 29 pack-years are the threshold for developing the early stage of CP. Under nicotine abstinence, only slightly more patients were relapse-free (37% vs. 22%). In contrast, the cumulative amount of nicotine consumed correlated with overall disease severity and the development of pseudocysts. The need for surgery was increased, with odds ratios of 1.8, for both alcohol and nicotine abuse.

Alcohol cessation in chronic pancreatitis reduces exocrine insufficiency, abdominal pain, and local complications. The effect of nicotine cessation is less pronounced in our cohort. However, nicotine abuse represents an important factor for the development of the disease.

Chronic pancreatitis (CP) is a progressive inflammatory disorder associated with marked morbidity and mortality and frequently requires hospitalization. This study aimed to investigate the time trends and geographical distribution of hospital admissions, the lethality rate of CP across Brazil, and the potential relationship with social indicators and associated risk factors.

Data were retrospectively obtained from the Brazilian Public Health System Registry between January 2009 and December 2019. The prevalence and lethality rates of CP per 100,000 inhabitants in each municipality were estimated from hospitalizations to in-hospital deaths and classified by age, sex, and demographic features.

During the study period, 64,609 admissions were retrieved, and most of the patients were males (63.54%). Hospitalization decreased by nearly half (-54.68%) in both sexes. CP rates in males were higher in all age groups. The greatest reduction in admissions (- 64%) was also noted in patients ≥ 70y. CP In-hospital lethality remained stable (5-6%) and similar for males and females. Patients ≥ 70y showed the highest lethality. The greatest increase in CP lethality rates (+ 10%) was observed in municipalities integrated into metropolises, which was mainly driven by small-sized municipalities (+ 124%).

CP hospitalizations decrease in both urban and rural areas, particularly in the North, Northeast, and Central-West regions, and in those above 70 years of age, but are not correlated with lethality rates in the South. This suggests ongoing changes in the environmental and socioeconomic factors in Brazil.

Pain in chronic pancreatitis (CP) is difficult to manage. Many patients suffer from inadequate pain relief, completely incapacitating them in their daily activities. Historically, despite their well-known adverse effects, opioids have been the pillar of treatment regimens in painful CP. The management is now gradually evolving with a better understanding of the underlying pathophysiology of CP-related pain. Clinicians should follow a holistic approach to the management of CP-associated pain, which must involve lifestyle changes that are coupled with analgesic medications and other pain-relieving interventions. Furthermore, there is no easy cure for vanquishing CP-associated pain. Each patient must be evaluated on a case-by-case basis by a multidisciplinary team to decide which treatment option is best suited for that individual.

Pain is the primary symptom of chronic pancreatitis (CP) and has been associated with abnormal pain processing and psychologic distress. Little is known about these phenomena in patients with painless disease. The aim of this study was to characterize patterns of pain processing and psychologic distress in patients with primary painless vs painful CP.

This was a cross-sectional multicenter study of 235 patients with definitive CP. Patients were categorized based on current and past pain history; current pain (79%), no current (but prior) pain (11%), and painless CP (10%). Demographic information and clinical data including symptoms of anxiety and depression using the Hospital Anxiety and Depression Scale were collected. All patients underwent quantitative sensory testing to assess patterns of pain processing.

A total of 235 patients (57% males, mean age 53.9 ± 14.0 years, 41% alcohol etiology) were included. Compared to patients with painless CP, enhanced pain sensitivity was observed in both patients with current pain (odds ratio [OR] 3.29; 95% confidence interval [CI] [1.11-9.77], P = .032) and no current pain (OR 4.07; 95% CI [1.10-15.03], P = .035). Patients with current pain also had increased depression prevalence compared to patients with painless CP (OR 6.15; 95% CI [1.28-29.41], P = .023), while no difference was seen for patients with no current pain (OR 1.24; 95% CI [0.19-8.26], P = .824).

Total absence of pain in CP is associated with normal pain processing and low prevalence of psychologic distress, whereas patients with prior pain experience appear to have persistent and enhanced pain sensitivity even in the absence of clinical pain and psychologic distress.

The aim of the present study is to assess the impact of smoking dose and duration on the distribution of risk factor(s) in patients with RAP and CP, and the impact of genetic testing on the distribution of risk factor(s) in patients with idiopathic RAP and CP.

All adult patients with RAP and CP referred to a multidisciplinary pancreatitis clinic between 2010 and 2017 were evaluated. Risk factors included alcohol and smoking, hypertriglyceridemia, biliary, and other etiologies. Genetic testing was only pursued in patients with idiopathic RAP or CP.

Among the 1770 patients evaluated, 167 had RAP and 303 had CP. After genetic testing and smoking, the most common risk factors for RAP and CP were pathogenic variant(s) (23%) and the combination of alcohol and smoking (23%), respectively. Genetic testing and smoking assessment decreased the proportion of patients with alcoholic RAP from 17% to 5%, alcoholic CP from 33% to 10%, idiopathic RAP from 49% to 12%, and idiopathic CP from 54% to 14%. Pathogenic CFTR variants were the most common variant in patients with RAP (51%) and CP (43%). Among the 68 patients with pancreas divisum, other risk factor(s) were identified in 72%.

Genetic testing and a detailed assessment of smoking dose and duration reduce the proportion of patients with alcoholic and idiopathic pancreatitis. Other risk factor(s) for pancreatitis are found in the majority of patients with pancreas divisum further questioning its role as an independent risk factor.1. What is the current knowledge?Approximately 30% of patients with pancreatitis have no clear risk factor(s) and are categorized as having an idiopathic etiology.Pathogenic variant(s) as well as smoking dose and duration are well-established risk factors for recurrent acute and chronic pancreatitis but are not widely recognized or incorporated into clinical practice.2. What is new here?Genetic testing and a detailed assessment of smoking dose and duration reduced the proportion of patients with alcoholic and idiopathic acute recurrent and chronic pancreatitis.Approximately three-fourths of patients with pancreas divisum have a risk factor for pancreatitis.

Throughout the past decades, considerable progress has been made in the (early) diagnosis and treatment of gastrointestinal cancers. However, the prognosis for advanced stages of gastrointestinal tumors remains limited for many patients and approximately one third of all tumor patients die as a result of gastrointestinal tumors. The prevention and early detection of gastrointestinal tumors is therefore of great importance.For this reason, we summarize the current state of knowledge and recommendations for the primary, secondary and tertiary prevention of esophageal, stomach, pancreas, liver and colorectal cancer in the following.

Smoking and alcohol use are risk factors for acute and chronic pancreatitis, and their role on anxiety, depression, and opioid use in patients who undergo total pancreatectomy and islet autotransplantation (TPIAT) is unknown.

We included adults enrolled in the Prospective Observational Study of TPIAT (POST). Measured variables included smoking (never, former, current) and alcohol abuse or dependency history (yes vs no). Using univariable and multivariable analyses, we investigated the association of smoking and alcohol dependency history with anxiety and depression, opioid use, and postsurgical outcomes.

Of 195 adults studied, 25 were current smokers and 77 former smokers, whereas 18 had a history of alcohol dependency (of whom 10 were current smokers). A diagnosis of anxiety was associated with current smoking (P = 0.005), and depression was associated with history of alcohol abuse/dependency (P = 0.0001). However, active symptoms of anxiety and depression at the time of TPIAT were not associated with smoking or alcohol status. Opioid use in the past 14 days was associated with being a former smoker (P = 0.005).

Active smoking and alcohol abuse history were associated with a diagnosis of anxiety and depression, respectively; however, at the time of TPIAT, symptom scores suggested that they were being addressed.

Smoking prevalence in patients with chronic pancreatitis [CP] is high. We aimed to understand lifetime history of smoking and cohort trends in CP patients to inform effective strategies for smoking cessation.

Data on 317 CP patients from the North American Pancreatitis Study 2 [NAPS2] Continuation and Validation Study and the NAPS2 Ancillary Study were analyzed. Smoking history was assessed for each phase of life from the onset of smoking to study enrollment. Data on second-hand smoke and drinking history were also collected. We compared demographic factors, drinking history, pain level and pancreas morphology by smoking status at age 25 (non-smoking, <1 pack per day [PPD], ≥1 PPD). We compared smoking prevalence by birth cohorts: 1930-1949, 1950-1969, 1970-1989.

Fifty-one percent of CP patients reported smoking at the time of enrollment. Those who smoked ≥1 PPD at age 25 smoked a cumulative total of 30.3 pack-years of cigarettes over a lifetime. Smoking at age 25 was associated with greater lifetime drinking and greater exposure to second-hand smoke at home and at workplace. Pancreatic atrophy and pseudocysts were more common among smokers. Pancreatic pain was more severe among smokers, and 12-13% of smokers reported smoking to alleviate pain. Male CP patients born in 1950-1969 reported the highest peak prevalence of smoking, and female CP patients born in 1970-1989 reported highest peak prevalence of smoking.

CP patients exhibit intense and sustained smoking behavior once established in the 20s. Regardless, cohort analyses demonstrate that the behaviors could potentially be altered by policy changes.

Pain is the most distressing and disruptive feature of recurrent acute pancreatitis (RAP) and chronic pancreatitis (CP) resulting in low quality of life (QOL) and disabilities. There is no single, characteristic pain pattern in patients with RAP and CP. Abdominal imaging features of CP accurately reflect morphologic features but they do not correlate with pain. Pain is the major driver of poor quality of life (QOL) and it is the constant pain, rather than intermittent pain that drives poor QOL. Furthermore, the most severe constant pain experience in CP is also a complex condition. The ability to target the etiopathogenesis of severe pain requires new methods to detect the exact pain mechanisms in an individual at cellular, tissue, system and psychiatric levels. In patients with complex and severe disease, it is likely that multiple overlapping mechanisms are simultaneously driving pain, anxiety and depression. Quantitative sensory testing (QST) shows promise in detecting alterations in central processing of pain signals and to classify patients for mechanistic and therapeutic studies. New genetic research suggests that genetic loci for severe pain in CP overlap with genetic loci for depression and other psychiatric disorders, providing additional insights and therapeutic targets for individual patients with severe CP pain. Well-designed clinical trials that integrate clinical features, QST, genetics and psychological assessments with targeted treatment and assessment of responses are required for a quantum leap forward. A better understanding of the context and mechanisms contributing to severe pain experiences in individual patients is predicted to lead to better therapies and quality of life.

/Objectives: Alcohol and smoking cessation are recommended in chronic pancreatitis. The aim of this study is to measure the rates of alcohol and smoking cessation counselling among providers and adherence to recommendations.

Retrospective cohort study of chronic pancreatitis patients at a tertiary hospital. Provider types were defined as primary care (PCP), gastroenterologist, or pancreas specialist. Pairwise comparisons and multivariable analysis were conducted to assess the relation between provider type and smoking/alcohol cessation.

Of 256 patients with chronic pancreatitis, 142 (55.5%) consumed alcohol and 130 (91.5%) were advised to stop. Alcohol cessation was advised to 88.9, 96.0 and 92.5% of patients followed by PCP, gastroenterologists and pancreas specialists, respectively. Sixty-one patients (46.9%) were compliant with the recommendation: 31.3, 44.0 and 54.1% of patients followed by PCP, gastroenterologists and pancreas specialists, respectively (Pairwise comparisons PCP vs Pancreas: p = 0.03, others nonsignificant). In multivariable analysis, patients followed by pancreas specialists were more likely to adhere to alcohol cessation recommendation compared to those followed by PCP (OR = 4.31, CI 1.52-12.20, p = 0.006). Smoking cessation was advised to all the 127 current smokers (100%). Fifty-six (44.1%) were compliant with the recommendation: 24.1, 58.3 and 47.3% of patients followed by PCP, gastroenterologists and pancreas specialists, respectively (Pairwise comparisons PCP vs Pancreas: p = 0.03, PCP vs. Gastroenterologist: p = 0.01, others nonsignificant). Multivariable analysis did not confirm this finding.

The majority of providers counsel for alcohol/smoking cessation. Less than half the patients follow the recommendations. Patients followed by pancreas specialists were more likely to adhere to alcohol cessation recommendation.

Abdominal pain, frequent in patients with chronic pancreatitis (CP), has a negative impact on quality of life (QOL). Psychiatric comorbidities including anxiety and depression are associated with pain, but their prevalence and effects on QOL in CP have not been quantified. We studied the prevalence of anxiety and depression in patients with CP and their associated patient and disease characteristics and impact on QOL.

This was a cross-sectional, multicenter prospective study. Patients were screened with the Hospital Anxiety and Depression Scale questionnaire. A Hospital Anxiety and Depression Scale score >7 on the respective anxiety or depression subscales indicated the presence of anxiety or depression and was used as a surrogate for the diagnosis of psychiatric comorbidities. Patient demographics, disease characteristics, QOL (EORTC-QLQ-C30), and pain symptoms (Brief Pain Inventory Short Form) were compared between patients with and without psychiatric comorbidities.

One hundred seventy-one patients with CP (mean age 53.8 ± 13.7 years, 60% men) were included. Anxiety and depression were present in 80 (46.8%) and 66 (38.6%) patients, with overlap in 50 (29%). Patients with anxiety or depression reported higher pain prevalence, pain severity, and pain interference scores (all P < 0.001). Psychiatric comorbidities also associated with reduced global health scores and functional subscales (all P < 0.001) and higher symptom burden (P ≤ 0.03). An independent association was noted between global health status and depression (P < 0.001).

Psychiatric comorbidities are prevalent in patients with CP and associated with pain and QOL. Where the effect of anxiety on QOL may be mediated via pain, depression is independently related to QOL. These findings warrant consideration in the management of patients with CP.

Chronic pancreatitis (CP) is a debilitating fibro-inflammatory disease with a profound impact on patients' quality of life (QOL). We investigated determinants of QOL in a large cohort of CP patients.

This was a multicentre study including 517 patients with CP. All patients fulfilled the EORTC QLQ-C30 questionnaire. Questionnaire responses were compared to results obtained from a general reference population (n = 11,343). Demographic characteristics, risk factors (smoking and alcohol consumption), pain symptoms, disease phenotype (complications) and treatments were recorded. A multivariable regression model was used to identify factors independently associated with QOL scores.

Included patients had a mean age of 56.3 ± 12.8 years, 355 (69%) were men and 309 (60%) had alcohol aetiology. Compared to the reference population, patients with CP had lower global health status (50.5 vs. 66.1; p < 0.001) as well as reduced scores for all functional scales (all p < 0.001). Additionally, CP patients reported a higher burden for all symptom items, with pain being the most prominent complaint (all p < 0.001). Constant pain (coefficient -11.3; p = 0.02), opioid based pain treatment (coefficient -19.7; p < 0.001) and alcoholic aetiology (coefficient -5.1; p = 0.03) were independently associated with lowered global health status. The final multivariable model explained 18% of the variance in global health status.

Patients with CP have significantly lower QOL compared to a population-based reference population. Factors independently associated with a lowered QOL are constant pain, opioid based pain treatment and alcohol aetiology. However, these factors only explain a fraction of QOL and additional factors need identification.

Chronic pancreatitis (CP) is historically defined as an irreversible inflammatory condition of the pancreas leading to varying degrees of exocrine and endocrine dysfunction. Recently however, the paradigm for the diagnosis has changed in that it breaks with the traditional clinicopathologic-based definition of disease, focusing instead on diagnosing the underlying pathologic process early in the disease course and managing the syndrome more holistically to change the natural course of disease and minimize adverse disease effects. Currently, the most accepted mechanistically derived definition of CP is a pathologic fibroinflammatory syndrome of the pancreas in individuals with genetic, environmental, and/or other risk factors who develop persistent pathologic responses to parenchymal injury or stress. The most common symptom of CP is abdominal pain, with other symptoms such as exocrine pancreatic insufficiency and diabetes developing at highly variable rates. CP is most commonly caused by toxins such as alcohol or tobacco use, genetic polymorphisms, and recurrent attacks of acute pancreatitis, although no history of acute pancreatitis is seen in many patients. Diagnosis is made usually on cross-sectional imaging, with modalities such as endoscopic ultrasonography and pancreatic function tests playing a secondary role. Total pancreatectomy represents the only known cure for CP, although difficulty in patient selection and the complications inherent to this intervention make it usually an unattractive option. This guideline will provide an evidence-based practical approach to the diagnosis and management of CP for the general gastroenterologist.

We have previously reported that physicians under-recognize smoking as a chronic pancreatitis (CP) risk factor. We hypothesized that availability of empiric data will influence physician recognition of this relationship.

We analyzed data from 508 CP patients prospectively enrolled in the North American Pancreatitis Study-2 Continuation and Validation (NAPS2-CV) or NAPS2-Ancillary (AS) studies (2008-2014) from 26 US centers who self-reported ever-smoking. Information on smoking status, physician-defined etiology and identification of smoking as a CP risk factor was obtained from structured patient and physician questionnaires. We compared how often physician identified smoking as a CP risk factor in NAPS2-CV/NAPS2-AS studies with NAPS2-original study (2000-2006).

Enrolling physician identified smoking as a risk factor in significantly (all p < 0.001) greater proportion of patients in NAPS2-CV/AS studies when compared with NAPS2-original study among ever (80.7 vs. 45.3%), current (91.3 vs. 53%), past (60.3 vs. 30.2%) smokers, in those who smoked ≤1 pack/day (79.3 vs. 39.5%) or ≥1 packs/day (83 vs. 49.8%). In multivariable analyses, the enrolling physician was 3.32-8.49 times more likely to cite smoking as a CP risk factor in the NAPS2-CV/NAPS2-AS studies based on smoking status and amount after controlling for age, sex, race and alcohol etiology. The effect was independent of enrolling site in a sub-analysis limited to sites participating in both phases of enrollment.

Availability of empiric data likely enhanced physician recognition of the association between smoking and CP. Wide-spread dissemination of this information could potentially curtail smoking rates in subjects with and those at risk of CP.

Alcohol and smoking play an important role in pancreatitis. The present review will address the myths and evidences about alcohol and smoking with pancreatitis to help improve the approach of healthcare professionals when managing of these patients.

There is a growing recognition that chronic pancreatitis is a multifactorial disease. Eliciting an accurate history of alcohol consumption and smoking from patients, and if necessary, family members, can help determine their contribution to the patient's disease. In the absence of a convincing history, physicians should be open to consideration of other etiologies. The amount and duration of alcohol consumption is the most important determinant in increasing pancreatitis risk. Alcohol sensitizes the pancreas to other insults or injury and promotes disease progression. Smoking is an independent risk factor or chronic pancreatitis and has synergistic pathogenic effects with alcohol. The natural history of chronic pancreatitis is highly variable. A patient with alcoholic pancreatitis can have symptoms, recurrences or exacerbations from disease-related complications or nonpancreatic causes. Novel strategies are needed to enable patients quit smoking.

Obtaining accurate history, appropriate evaluation and management can help to achieve meaningful improvement in symptoms in patients with chronic pancreatitis. Abstinence from alcohol and smoking cessation, when applicable, should be recommended in all patients to prevent disease recurrences and progression.

The aim of this study was to evaluate the impact of smoking on quality of life in patients with chronic pancreatitis.

This is a cross-sectional study of chronic pancreatitis patients followed at a single institution comparing smokers with non-smokers. The primary outcome was quality of life and secondary outcomes included demographics, drug and alcohol use, anxiety and depression, pain level, nutritional status, and metabolic factors.

48 smokers and 45 non-smokers participated in this study. Smokers had a worse overall quality of life and higher rates of opioid addiction and depression than non-smokers. Smokers also had less racial diversity, lower education levels, and higher amounts of narcotic use than non-smokers. Furthermore, smokers had a lower BMI and a higher proportional use of pancreatic enzyme replacement therapy. Smoking was found to be independently associated with worse quality of life on multivariable regression.

The worse overall quality of life and higher rates of depression and anxiety create cause for concern in chronic pancreatitis patients who smoke. Smoking cessation should be an important target in chronic pancreatitis patients. Multicenter, multiethnic studies are needed to further elucidate this relationship.

This report reviews recent aspects of pancreatitis immunology and environmental factors that link to development and progression of disease.

Limited human and animal model studies have recently attempted to understand immune mechanisms that lead to the pathogenesis of acute and chronic pancreatitis. Based on these studies innate immune responses emerge as critical elements in disease pathogenesis and severity of inflammation. The immune basis for environmental factors such as smoking, which are highly associated with disease progression highlight novel cross talk mechanisms between immune and nonimmune pancreatic cells such as the pancreatic stellate cells.

Better understanding of immune responses and signaling pathways are emerging as important contributors in pancreatitis development and progression. Such mechanisms are likely to offer future targetable therapies that can either halt or reverse disease progression.

The medical management of pain in chronic pancreatitis continues to pose significant challenges for clinicians caring for these patients. There are increasing data, suggesting that pain in chronic pancreatitis is largely due to peripheral and central sensitization that evolves, over time, as a result of nociceptive afferent associated with chronic inflammation and fibrosis of the pancreas. In many instances, patients rapidly progress to requiring opioid analgesics for the adequate treatment of pain despite the unequivocal risks associated with the long-term use of these drugs. Centrally acting drugs, such as gabapentinoids, appear to be effective means of treating pain due to their inhibition of neurotransmitters involved in central sensitization, but side effects limit their use. The present review explores the evidence for various non-pharmacologic and pharmacologic treatments for pain in chronic pancreatitis.

Chronic pancreatitis (CP) has a profound independent effect on quality of life (QOL). Our aim was to identify factors that impact the QOL in CP patients.

We used data on 1,024 CP patients enrolled in the three NAPS2 studies. Information on demographics, risk factors, co-morbidities, disease phenotype, and treatments was obtained from responses to structured questionnaires. Physical and mental component summary (PCS and MCS, respectively) scores generated using responses to the Short Form-12 (SF-12) survey were used to assess QOL at enrollment. Multivariable linear regression models determined independent predictors of QOL.

Mean PCS and MCS scores were 36.7±11.7 and 42.4±12.2, respectively. Significant (P<0.05) negative impact on PCS scores in multivariable analyses was noted owing to constant mild-moderate pain with episodes of severe pain or constant severe pain (10 points), constant mild-moderate pain (5.2), pain-related disability/unemployment (5.1), current smoking (2.9 points), and medical co-morbidities. Significant (P<0.05) negative impact on MCS scores was related to constant pain irrespective of severity (6.8-6.9 points), current smoking (3.9 points), and pain-related disability/unemployment (2.4 points). In women, disability/unemployment resulted in an additional 3.7 point reduction in MCS score. Final multivariable models explained 27% and 18% of the variance in PCS and MCS scores, respectively. Etiology, disease duration, pancreatic morphology, diabetes, exocrine insufficiency, and prior endotherapy/pancreatic surgery had no significant independent effect on QOL.

Constant pain, pain-related disability/unemployment, current smoking, and concurrent co-morbidities significantly affect the QOL in CP. Further research is needed to identify factors impacting QOL not explained by our analyses.