Risk Of Pancreatic Insufficiency Research Articles

Pancreatic Dysfunction and Reduction in Quality of Life Is Common After Pancreaticoduodenectomy.

Improvements in survival after pancreaticoduodenectomy has increased the number of patients potentially at risk of pancreatic insufficiency. We studied long-term (> 1year) pancreatic functions (endocrine and exocrine) after pancreaticoduodenectomy and aimed to recognize the impact of various clinicopathological factors and postoperative complications on pancreatic functions. All patients who underwent pancreaticoduodenectomy at least 1year prior were recruited from July 2020 to December 2021. Endocrine function was assessed using HbA1c, fasting blood sugar and postprandial blood sugar levels. Pancreatic exocrine function was assessed clinically with history of steatorrhea and objectively with quantitative estimation of fecal elastase-1 levels in stool samples. Volume of remnant pancreas, parenchymal thickness and duct diameter were assessed by computed tomography. Quality of life assessment was done using SF-36 questionnaire. Of the 106 patients assessed, 64 patients met the inclusion criteria. Endocrine insufficiency was noted in 51.6%, and 34.3% had new onset diabetes mellitus. The incidence of pancreatic exocrine insufficiency was 87.5% and severe insufficiency was found in 62.5% of patients. Twenty-nine (45.3%) patients had both exocrine and endocrine insufficiency. Patients with CRPOPF had higher risk of severe exocrine insufficiency (5 vs. 2, OR 1.57(0.28-8.81) p = 0.6). The SF-36 scores were lower than general population especially in role limitation due to physical health, role limitation due to emotional problems, energy/fatigue, general health perception and health change domains. Post-pancreaticoduodenectomy patients have a high frequency of pancreatic insufficiency and should be screened for same. The post-operative pancreatic fistula increases the risk of pancreatic exocrine insufficiency.

Deficiency of folate and vitamin B12 increases oxidative stress in chronic pancreatitis patients.

Folate and vitamin B12 are involved in metabolic reactions for combating oxidative stress. We measured erythrocyte folate and plasma vitamin B12 and compared these with blood antioxidants - erythrocyte glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), and plasma vitamin C - and marker of lipid peroxidation, thiobarbituric acid reactive substance (TBARS), in chronic pancreatitis (CP) patients. One hundred and seventy-five CP patients (91 tropical, 84 alcoholic) and 113 healthy controls were recruited. Erythrocyte folate and plasma vitamin B12 were measured using microbiological assay, and antioxidant levels and erythrocyte TBARS by spectrophotometry. Erythrocyte folate and plasma vitamin B12 were significantly lower in CP patients than controls (225.4 ± 9.13 vs. 380.38 ± 17.29 nmol/L, p < 0.001 and 233.23 ± 10.4 vs. 338.84 ± 19.01 pmol/L, p < 0.001), and in diabetic- vs. non-diabetic CP patients. Blood antioxidant levels were significantly lower and TBARS was higher in CP patients as compared to controls. Low folate level correlated with low GSH levels (r = 0.314, p < 0.001). CP patients with low folate and vitamin B12 had low GSH and GPx levels as compared to patients with normal folate and vitamin B12 levels. Low vitamin B12 level was associated with 3.24 (95% CI 1.11-9.46, p < 0.05) fold increased risk of pancreatic insufficiency. Smoking was associated with 9.82 (95% confidence interval [CI] 3.3-29.22, p < 0.05) fold increased risk of having low folate levels. Low folate and vitamin B12 levels were associated with increased oxidative stress in CP patients.

Pancreatic Insufficiency Secondary to Tobacco Exposure: A Controlled Cross-Sectional Evaluation.

Tobacco exposure is an established risk factor for pancreatic cancer and chronic pancreatitis; however, its role in pancreatic insufficiency is not clear. This controlled, cross-sectional study examined smokers and nonsmokers with no history of pancreatic disease. Histories and validated inventories of alcohol and tobacco use were obtained, and pancreatic insufficiency was assessed using the fecal elastase-1 assay. Of 7854 patients approached, 226 were interviewed and 200 enrolled. The rates of pancreatic insufficiency [18% (18/100)] and severe pancreatic insufficiency [10% (10/100)] were significantly higher in smokers than in controls [6% (6/100), P = 0.009 and 1% (1/100), P = 0.010, respectively]. On multivariate logistic regression, the risk of pancreatic insufficiency in smokers was significantly increased [odds ratio, 4.34 (1.37-13.75); P = 0.012], controlling for alcohol use and relevant covariates. Tobacco exposure was associated with the highest odds ratio for pancreatic insufficiency. Alcohol consumption was strongly associated with tobacco exposure (P < 0.001), but not with pancreatic insufficiency by multivariate analysis (P = 0.792). This study suggests that tobacco exposure is independently associated with pancreatic exocrine insufficiency in patients without a prior diagnosis of pancreatic disease. Tobacco exposure seems to have greater detrimental effects on pancreatic function than alcohol in this population.

Cystic Fibrosis, Disease Severity, and a Macrophage Migration Inhibitory Factor Polymorphism

Macrophage migration inhibitory factor (MIF) is a key proinflammatory mediator. It contributes toward an exaggerated gram-negative inflammatory response via its ability to induce Toll-like receptor-4 expression. Studies have shown that MIF knockout mice have less aggressive Pseudomonas infection (compared with wild-type). To assess whether a novel functional MIF polymorphism was associated with clinical prognosis in a patient cohort with chronic gram-negative infection, namely cystic fibrosis (CF). Collected genomic DNA was analyzed via polymerase chain reaction amplification for the polymorphic region for the CATT repeat polymorphism. Individuals may have a 5-, 6-, 7-, or 8-CATT tetranucleotide repeat unit on each allele. The 5-CATT repeat allele exhibits the lowest MIF promoter activity. Patients with stable CF (n = 167) and a matched control group (n = 166) were enrolled. In patients with CF, the MIF5(+) group had a decreased incidence of Pseudomonas aeruginosa colonization (odds ratio, 0.25; 95% confidence interval, 0.09-0.65; p = 0.004) and a significant reduction in the risk of pancreatic insufficiency (odds ratio, 0.27; 95% confidence interval, 0.07-1.0; p = 0.05). A trend toward milder disease activity in the MIF5(+) group was seen with all other parameters. The results support the concept of a regulatory role for MIF in CF.