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Background: Early-onset idiopathic chronic pancreatitis (EOICP) is a disease that affects young individuals. Data on pregnancy outcomes in EOICP are limited. Aim: To assess the pregnancy outcomes in patients with EOICP and the effect of pregnancy on the course of EOICP. Methods: Patients with EOICP with disease onset before their pregnancy were recruited. Data regarding demographic variables, disease duration, pregnancy outcomes, and course of illness were noted. Results: 50 patients were included in the study contributing to a total of 86 pregnancies. The mean age of onset of symptoms and at the time of delivery was 17.95 (5.71) and 23.44 (4.28) years, respectively. Gestational diabetes (GD) and gestational hypertension (GH) noted in one (1.5%) each. 3 (4.5%) pregnancies were preterm. 19 (22.1%) pregnancies did not have successful outcomes (7 (8.1%) were induced abortions). 12 (15.2%) pregnancies had spontaneous pregnancy losses. 8 (10.1%) were spontaneous abortions and 4 (5.1%) were stillbirths. Of 67 successful pregnancies, 33 (49.3%) pregnancies were delivered by LSCS. Compared to average rates of LSCS in India, this was significantly higher (21.5% vs 49.3%—p ≤ 0.001). The average birth weight was 2.87 (0.48) kg. There was one (1.5%) neonatal death. Compared to the published Indian data, there was no significant difference in the incidence of spontaneous pregnancy losses, GD, GH, preterm labor, and birth weight. Pancreatic pain was reported by 21 (42%) women in total 27 (31.4%) pregnancies. There was no difference in maternal or fetal outcomes between pregnancies with or without pancreatic pain. There were no pancreatitis-related complications reported during the pregnancies. Conclusion: The present study shows that mothers affected with EOICP have pregnancy outcomes similar to healthy women in India. [ABSTRACT FROM AUTHOR]

Background: Tobacco smoking is a known risk factor for progression of chronic pancreatitis (CP). Aim: We compare clinical outcomes of CP patients with current or former smoking with those who have never smoked. Methods: We reviewed all patients with followed at our Pancreas Center from 2016 to 2021, comparing the demographics, clinical features, comorbidities, outcomes, and resource utilization between smokers and non-smokers. Results: Of 439 CP patients, 283 were smokers (125 current, 158 former). Significantly more smokers were men (58.3% vs 40.4%), with alcoholic CP (45.5% vs 12.1%), chronic abdominal pain (77.7% vs 65.4%), anxiety and depression (22.6% vs 14.1% and 38.9% vs 23.1%), and with more local pancreatic complications [splanchnic vein thrombosis (15.7% vs 5.13%), pseudocyst (42.7% vs 23.7%), biliary obstruction (20.5% vs 5.88%)], exocrine pancreatic insufficiency (65.8% vs 46.2%), hospitalizations (2.59 vs 1.75 visits), and emergency department visits (8.96% vs 3.25%). Opioid and neuromodulator use were significantly higher (59.2% vs 30.3% and 58.4% vs 31.2%). Current smokers had worse outcomes than former smokers. Multivariate analysis controlling for multiple factors identified smoking as an independent predictor of chronic abdominal pain (OR 2.49, CI 1.23–5.04, p = 0.011), opioid (OR 2.36, CI 1.35–4.12, p = 0.002), neuromodulators (OR 2.55, CI 1.46–4.46, p = 0.001), and non-opioid-controlled medications (OR 2.28, CI 1.22–4.30, p = 0.01) use, as well as splanchnic vein thromboses (OR 2.65, CI 1.02–6.91, p = 0.045) and biliary obstruction (OR 4.12, CI 1.60–10.61, p = 0.003). Conclusion: CP patients who smoke or formerly smoked have greater morbidity and worse outcomes than non-smokers. [ABSTRACT FROM AUTHOR]

Background/Aims The prevalence and natural history of SPINK1, PRSS1, and CFTR mutations in idiopathic pancreatitis (ICP) are not well-documented. This study evaluates the prevalence, genetic and clinical characteristics, and long-term outcomes of gene-associated chronic pancreatitis (GCP) compared to alcoholic chronic pancreatitis (ACP). Methods From January 1997 to July 2023, a cohort of 711 ICP patients underwent DNA testing for SPINK1, PRSS1, and CFTR mutations. A propensity score-matched analysis was conducted to compare GCP to ACP patients at a 1:3 ratio. Results Gene mutations were identified in 23.2% of idiopathic pancreatitis patients, with SPINK1 being the most common mutation (70%). GCP patients experienced significantly more pancreatic pain (89.3% vs. 70.7%) and had a shorter median time to symptom onset (26.2 years vs. 42.6 years) compared to ACP patients. Pancreatic cancer was observed in 3.6% of GCP patients, with a cumulative risk reaching 16.7% by age 70, while the incidence was lower in ACP patients. Although GCP patients exhibited higher cumulative risks, the hazard ratio for gene mutation status was not statistically significant (HR: 1.53). However, a Cambridge classification grade ＞3 was a significant predictor of pancreatic cancer outcomes (HR: 4.58, p=0.034). Conclusion GCP patients exhibit distinct clinical characteristics and outcomes compared to ACP patients, necessitating individualized evaluation and management strategies. Given the significant cumulative risk of pancreatic cancer in GCP, early and regular surveillance is recommended, particularly for those with higher Cambridge classification grades. [ABSTRACT FROM AUTHOR]

Objectives: Steatorrhea, a sign of severe pancreatic exocrine insufficiency (PEI), is related to consequences caused by pancreatitis. This study aimed to identify predictors and to construct a nomogram for steatorrhea in idiopathic chronic pancreatitis (ICP). Methods: ICP patients admitted to our hospital from January 2000 to December 2013 were enrolled in this retrospective–prospective cohort study and randomly assigned to the training and validation cohorts. The cumulative rate of steatorrhea was calculated. A Cox proportional hazard regression model was used to identify predictors for steatorrhea and construct the nomogram. Internal and external validation of the nomogram was then performed. Results: There were 1633 ICP patients enrolled, with a median follow‐up duration of 9.8 years and 20.8% (339/1633) of patients developed steatorrhea following onset of ICP. Steatorrhea was observed in 93, 115, and 133 patients at 1, 3, and 5 years following diagnosis of CP, with a cumulative rate of 6.5% (95% confidence interval [CI] 5.1%–7.9%), 8.0% (95% CI 6.2%–9.8%), and 9.3% (95% CI 6.6%–12.0%), respectively. Male sex (hazard ratio [HR] 2.479, P < 0.001), diabetes mellitus at/before diagnosis of ICP (HR 2.274, P = 0.003), and aged less than 18 years at onset of ICP (HR 0.095, P < 0.001) were identified risk factors for steatorrhea. Initial manifestations were associated with development of steatorrhea. The nomogram was proven to have good concordance indexes. Conclusions: We identified predictors and developed a nomogram for predicting steatorrhea in ICP. It was recommended that high‐risk populations be followed up closely, which might contribute to the early diagnosis and treatment of PEI. [ABSTRACT FROM AUTHOR]

Tropical chronic pancreatitis (TCP) is a special variant of idiopathic chronic pancreatitis that is seen mainly in tropical countries. Although the prevalence of tropical pancreatitis is high in southern India, it is reported from most parts of India. It occurs usually in young people, involves the main pancreatic duct, and results in large ductal calculi with high incidence of diabetes and malignancy. Recent reports suggest that the presentation is changing. The age of onset is older and the disease course seems to be milder. The etiology is not known, but genetic mutations and environmental factors are likely causes. This article is a narrative review of the recent trends in the etiopathogenesis and management of tropical calcific pancreatitis (TCP). Extensive literature search was done from PubMed and Ovid. Article was prepared by reviewing full-text articles and abstracts related to chronic calcific pancreatitis (CCP) and TCP. [ABSTRACT FROM AUTHOR]

Certain cases of chronic pancreatitis (CP) occur without an apparent causative factor, diagnosed as idiopathic CP (ICP). Several studies have reported that ICP was associated with mutations in the SPINK1 and PRSS1 genes, but the studies were not conclusive as these polymorphisms can also occur in healthy individuals. In the present study, we aimed to study the genotypes of SPINK1 and PRSS1. Our study recruited nine ICP patients having no known risk factors. Symptoms relating to ICP were recorded. Genetic studies were performed in all ICP patients and 230 healthy controls. SPINK1 mutations in cases and controls were genotyped by genotyping assay. The entire PRSS1 gene was sequenced in all cases and controls to look for any mutations. Statistical analysis of genotypes and minor allele frequencies (MAF) was performed. All of the 9 ICP patients had SPINK1 mutations. The SPINK1 N34S heterozygous mutation (MAF 2.17%) was detected in 10 out of 230 controls, while the IVS3+2T>C mutation was not detected in any. PRSS1 mutations were detected in no cases or controls. In summary, SPINK1 mutations were associated with ICP. SPINK1 N34S carrier status was found in the general population with low prevalence, while IVS3+2T>C was rarely found in the controls. [ABSTRACT FROM AUTHOR]

Tropical chronic pancreatitis (TCP) is a special variant of idiopathic chronic pancreatitis that is seen mainly in tropical countries. Although the prevalence of tropical pancreatitis is high in southern India, it is reported from most parts of India. It occurs usually in young people, involves the main pancreatic duct, and results in large ductal calculi with high incidence of diabetes and malignancy. Recent reports suggest that the presentation is changing. The age of onset is older and the disease course seems to be milder. The etiology is not known, but genetic mutations and environmental factors are likely causes. This article is a narrative review of the recent trends in the etiopathogenesis and management of tropical calcific pancreatitis (TCP). Extensive literature search was done from PubMed and Ovid. Article was prepared by reviewing full-text articles and abstracts related to chronic calcific pancreatitis (CCP) and TCP. [ABSTRACT FROM AUTHOR]

Background and Aim: Diabetes mellitus (DM) is a common complication of idiopathic chronic pancreatitis (ICP), which impairs the quality of life for patients. This study aimed to identify risk factors and develop nomogram for DM in ICP to help early diagnosis. Methods: Idiopathic chronic pancreatitis patients admitted to our center from January 2000 to December 2013 were included. Cumulative rates of DM were calculated by Kaplan–Meier method. Patients were randomly assigned, in a 2:1 ratio, to the training and validation cohort. Based on training cohort, risk factors for DM were identified through Cox proportional hazards regression model, and nomogram was developed. Internal and external validations were performed based on the training and validation cohort, respectively. Results: Totally, 1633 patients with ICP were finally enrolled. The median follow‐up duration was 9.8 years. DM was found in 26.3% (430/1633) of patients after the onset of CP. Adult at onset of ICP, biliary stricture at/before diagnosis of CP, steatorrhea at/before diagnosis of CP, and complex pathologic changes in main pancreatic duct were identified risk factors for DM development. The nomogram achieved good concordance indexes in the training and validation cohorts, respectively, with well‐fitted calibration curves. Conclusions: Risk factors were identified, and nomogram was developed to determine the risk of DM in ICP patients. Patients with one or more of the risk factors including adult at onset of ICP, biliary stricture at/before diagnosis of CP, steatorrhea at/before diagnosis of CP, and complex pathologic changes in main pancreatic duct have higher incidence of DM. [ABSTRACT FROM AUTHOR]

Background: The main cause of chronic pancreatitis (CP) is excessive alcohol consumption. On the other hand, only 5-10% of heavy drinkers develop chronic pancreatitis. We have only limited information regarding the pathogenic mechanism by which alcohol leads to the disease. Mutations of the PRSS1 and SPINK 1 have been mostly implicated in hereditary and idiopathic CP, but their presence in other types of this disease have also been reported.Aims: The aim of the study was to determine the frequency of PRSS1 and SPINK1 mutations in patients with chronic alcoholic (ACP) and idiopathic pancreatitis (ICP) as well as to investigate their relation to the clinical course of the disease.Methods: The study included 33 ACP and 14 ICP patients as well 46 healthy subjects. The diagnosis of CP was based on clinical data, ultrasound, and computed tomography. After isolation of DNA from peripheral blood two trypsinogen mutations were detected N29I and R122H by allelo-specific amplification polymerase chain reaction (ASA-PCR) and by the PCR-restriction fragment length polymorphism (RFLP). Beside this N34S mutation of SPINK1 was analyzed by PCR restriction fragment length polymorphism (PCR-RFLP).Results: PRSS1 mutations have been detected in 11 (33%) patients with ACP. The frequency of the PRSS1 mutations was higher in patients with ACP than in controls (4.3%) (p < 0.001). The frequency of PRSS1 mutation was present in 21.4% of ICP patients, which was significantly higher (p < 0.05) than in controls. Overall, six (18%) SPINK1 mutations in ACP group have been detected. Among 14 patients with ICP, in four (28.6%) of them SPINK1 has been detected. The same mutations have also been found in three (6.5%) control subjects. The frequency of the N34S mutation was higher in patients with ICP than in the controls (p < 0.05), but the frequency of N34S mutation did not differ between ACP and the control group. No relations have been detected between PRSS1 and SPINK1 mutations presence and clinical course and complications of CP.Conclusions: Those preliminary data suggest the high prevalence of SPINK1 and PRSS1 mutations in the Polish population, generally, as well as in CP patients. It may be speculated that those mutations contribute to the development of chronic pancreatitis, especially in patients with alcohol overindulgence. [ABSTRACT FROM AUTHOR]

Mutations in cystic fibrosis transmembrane conductance regulator ( CFTR) gene have been reported in patients with chronic pancreatitis. The authors examine whether the mutations and haplotypes of CFTR will increase the risk of developing idiopathic chronic pancreatitis (ICP) in Chinese and their genotype and phenotype correlations. Seventy-eight patients with ICP and 200 geographically and ethnically matched controls in Taiwan were analyzed. The entire 27 coding and intronic regions of the CFTR gene were identified using heteroduplex analytical techniques and confirmed by sequencing analysis. The presence of 125G/C, 1001+10C>T, IVSTn(TG)m, 1540A>G, c2694T>G, and c4521G>A were determined by directing sequencing. Abnormal CFTR allele was found to be thrice as frequent in ICP patients as in controls (22/156 vs 19/400, p < 0.0001). T5 allele was associated with early onset of ICP. In six-loci haplotype analysis, 13 common haplotypes were assembled in the 278 individuals tested. The 125G/1001+11C/TG12/470M/2694T/4521G haplotype was associated with risk of ICP (odds ratio 11.3; 95% confidence interval 2.3–54.6, p = 0.008) in Chinese. The mutation spectrum is different from other ethnic groups. A population-specific panel of CFTR changes should be recommended for targeted populations including ICP in Chinese. It is important to design suitable screening programs for different populations. [ABSTRACT FROM AUTHOR]

Several genetic factors have been well known to predispose one to chronic pancreatitis (CP). However, little is known about the genetic factors that may provide a protective effect against the disease. Having found a nonsense mutation (c.111C > A; Y37X) and a splicing mutation (IVS2 + 1G > A) in the cationic trypsinogen gene (protease, serine, 1; PRSS1) in alcoholics without the development of CP, but not in alcoholics with CP and patients with hereditary or idiopathic CP, we propose that while “gain of function” mutations in the PRSS1 gene predispose one to pancreatitis, “loss of function” mutations in the gene may protect one against the disease. [Copyright &y& Elsevier]