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IntroductionAfter bariatric surgery (BS), patients might suffer from nutrient maldigestion, malabsorption, and vitamin deficiencies. In this study, our aim was to assess pancreatic functions after BS using fecal elastase-1 assay (FE-1).Material and MethodsSixty patients (21M) undergoing BS and 20 (6M) healthy controls were included into the study. Stool samples were collected 1 year after surgery. Ten patients from one anastomosis gastric bypass (OAGB) and single anastomosis duodenal switch (SADS) groups with the lowest value of FE-1 and GIQLI scores were given pancreatic enzyme replacement therapy (PERT). After PERT, FE-1, excess weight loss (EWL), BMI, GIQLI scores, and vitamin D levels were measured.ResultsVitamin D levels were detected as 19.04 (9–46.5) pg/ml, 15.1 (8.4–23.6) pg/ml, 17.8 (5–30) pg/ml, and 21.79 (11–40.3) pg/ml after sleeve gastrectomy (SG), OAGB, SADS, and control groups, respectively (p = 0.04). GIQLI scores in the first year were found to have increased in all patients (p = 0.02). FE-1 levels were found as 642.35 (566.3–711.4) μg/g, 378.52 (183.5–561.1) μg/g, 458.88 (252.5–593, 5) μg/g, and 518.2 (351.6–691) μg/g for the SG, OAGB, SADS, and control groups, respectively. There was a strong inverse correlation between EWL and FE-1 levels at the end of the first year (Spearman’s rho = − 0.688, p = 0.003). After having performed PERT for patients with the lowest FE-1 levels, the levels increased to 683.39 (615.5–720) μg/g in the OAGB and 691.5 (643.1–720) μg/g in the SADS groups (p = 0.011).ConclusionFE-1 measurements demonstrated that many patients suffer from malabsorption after OAGB or SADS, whereas functions remain normal after SG. PERT corrects pancreatic functions without affecting weight loss and also contributes to the normal serum level of vitamin D.

Background: Carbohydrate antigen 19-9 (CA19-9) is used as a marker to predict recurrence and survival of patients with pancreatic ductal adenocarcinoma (PDAC). Recently, fecal elastase-1 (FE-1) has been shown to correlate with prognosis in patients with PDAC. Method: A total of 536 patients who underwent curative intent surgery between 2010 and 2019 were included in the study. The cutoff points of preoperative CA19-9 and FE-1 levels were extracted from the Youden index and previous studies. Cox proportional hazard models were used to investigate the association between preoperative tumor marker levels and survival after surgery. Results: Patients with CA19-9 ≥ 385 had more advanced T-/N-stages and lower survival rates compared to those with CA19-9 < 385. Multivariate Cox analyses demonstrated that combining preoperative tumor markers was associated with worse 3-year overall survival (both CA19-9 and FE-1 low, HR = 1.41, p = 0.044; both high, HR = 1.44, p = 0.047; CA19-9 high and FE-1 low, HR = 2.00, p < 0.001; and p for trend < 0.001). The same trend was confirmed in the analysis with recurrence-free survival. Conclusions: This study presents a new predictive strategy using combined CA19-9 and FE-1 levels to determine the treatment for resectable pancreatic cancer.

Several reports have indicated that fecal elastase-1 (EL-1) determination is a new, sensitive, and specific noninvasive pancreatic function test; however, very few patients with malabsorption due to small intestine diseases have been included in the previous studies. The aim of the study was to compare the diagnostic accuracy of fecal EL-1 and fecal chymotrypsin (FCT) in distinguishing between pancreatic maldigestion and intestinal malabsorption. Three groups of subjects were studied: group A included 49 patients with known cystic fibrosis (25 males, median age 5 years); group B included 43 subjects with various small intestine diseases (17 males, median age 6 years); and group C included 45 children without any history of gastrointestinal disease (22 males, median age 5 years). In all patients, stools were collected for 72 h on a standard diet and fecal EL-1, FCT, and steatocrit tests were performed. Both EL-1 and FCT were below normal limits in all CF patients with pancreatic maldigestion not treated with pancreatic enzyme (100% sensitivity for both assays); El-1, but not FCT, was also below normal in all the CF patients with pancreatic maldigestion treated with pancreatic extracts. Both EL-1 and FCT values in the CF group were significantly lower than in subjects with various small intestinal diseases and in children without any history of gastrointestinal disease (P < 0.0001). FCT, but not EL-1, values showed an inverse statistically significant correlation with steatocrit values in the whole CF group (P < 0.001); FCT was below normal in three of four CF patients with steatorrhea on pancreatic enzyme therapy. Both EL-1 and FCT had 100% specificity when calculated in children without any history of gastrointestinal disease; in contrast, specificity was 86% for EL-1 and 76% for FCT if we considered the control group with small intestinal diseases: low EL-1 was observed in two cases of intestinal giardiasis, two cases of short bowel syndrome, one case of celiac disease, and one case of intestinal pseudobstruction; FCT was abnormal in four cases of intestinal giardiasis, three cases of celiac disease, one case of short bowel syndrome, one case of Crohn's disease, and one case of intestinal pseudobstruction. Diagnostic accuracy was 92% for fecal EL-1 and 82% for FCT. Steatocrit values were over the normal limit in 11 patients with small intestine diseases; in 7/11 of these patients at least one of the pancreatic test results was below the normal limit. In conclusions, in patients with CF, fecal EL-1 determination is not more sensitive than FCT in identifying pancreatic maldigestion; however, fecal EL-1 assay is more specific than FCT determination in distinguishing pancreatic maldigestion from intestinal malabsorption.

The aim of this study was to compare the clinical characteristics of acute pancreatitis (AP) patients between those who developed pancreatic exocrine insufficiency (PEI) and those who did not, and to investigate the predictive factors of PEI. From October 1st 2019 to July 30th 2021, AP patients admitted at our center were included. The fecal elastase-1 assay was adopted for PEI diagnosis. The clinical characteristics, treatments, and outcomes between the patients with and without PEI were analyzed. In total, 63 males and 42 females were included. There were 27 patients with mild AP, 54 with moderately severe AP, and 24 with severe AP. The median modified computed tomography severity index (MCTSI) was 6.000(4.000, 8.000). During the follow-up, 38 patients developed PEI after AP. The univariate analysis showed that higher ASA grade (P = 0.006), more severe AP (P = 0.000), the presence of multiple organ dysfunction syndrome (P = 0.030), higher MCTSI (P = 0.000), the development of infected pancreatic necrosis (P = 0.002) and local complications (P = 0.000), higher levels of triacylglycerol (P = 0.022), video-assisted retroperitoneal debridement intervention (P = 0.015), and longer intensive care unit stay (P = 0.044) were correlated with PEI development. Furthermore, the logistic regression analyses showed that MCTSI during hospitalization is an independent risk factor for PEI development during the AP recovery period. ASA grade, severity of AP, multiple organ dysfunction syndrome, MCTSI, infected pancreatic necrosis, local complications, higher levels of triacylglycerol, video-assisted retroperitoneal debridement intervention, and longer intensive care unit stay were potentially associated with PEI development during the AP recovery period. High MCTSI was independently associated with the development of PEI during the AP recovery period, which may help alert to the possibility of PEI to help with its early detection and treatment.

Background Systemic sclerosis (SSc) has been suggested to cause exocrine pancreatic dysfunction. However, a case-control-based autopsy study failed to associate systemic sclerosis with any pancreatic histopathology. The primary objective of this study was to examine the exocrine pancreatic function in consecutive SSc patients in relation to an age- and sex-matched control group. A secondary objective was to relate exocrine pancreatic function to radiological, laboratory, and clinical SSc characteristics. Methods One hundred twelve consecutive patients fulfilling the 2013 American Congress of Rheumatology/European League Against Rheumatism criteria for SSc and 52 control subjects were matched for sex and age. Exocrine pancreatic function was assessed by ELISA-based measurement of fecal elastase, and levels ≤ 200 μg/g were considered pathological, i.e., representing exocrine pancreatic insufficiency. Patients were characterized regarding SSc manifestations including gastrointestinal and hepatobiliary function, by use of laboratory and clinical examinations. Pancreas parenchyma characteristics were evaluated by high-resolution computer tomography (HRCT). Results A similar proportion of subjects exhibited pathological levels of fecal elastase among SSc patients (6/112; 5.4%) and control subjects (3/52; 5.8%). Patients with fecal elastase ≤ 200 μg/g did not differ from other SSc patients with respect to laboratory and clinical characteristics, including malnutrition. SSc subjects with low levels of fecal elastase displayed significantly lower pancreas attenuation on HRCT examinations compared to the control subjects. Conclusions In this study encompassing 112 consecutive SSc patients and 52 matched control subjects, we were unable to associate systemic sclerosis with clinically significant exocrine pancreatic dysfunction.

Background: Diabetes mellitus (DM) is a chronic abnormal metabolic condition, which manifests elevated blood sugar level over a prolonged period. The pancreatic endocrine system generally gets affected during diabetes, but often abnormal exocrine functions are also manifested due to its proximity to the endocrine system. Fecal elastase-1 (FE-1) is found to be an ideal biomarker to reflect the exocrine insufficiency of the pancreas. Aim: The aim of this study was conducted to assess exocrine dysfunction of the pancreas in patients with type-2 DM (T2DM) by measuring FE levels and to associate the level of hyperglycemia with exocrine pancreatic dysfunction. Methodology: A prospective, cross-sectional comparative study was conducted on both T2DM patients and healthy nondiabetic volunteers. FE-1 levels were measured using a commercial kit (Human Pancreatic Elastase ELISA BS 86-01 from Bioserv Diagnostics). Data analysis was performed based on the important statistical parameters such as mean, standard deviation, standard error, t-test-independent samples, and Chi-square test/cross tabulation using SPSS for Windows version 20.0. Results: Statistically nonsignificant (P = 0.5051) relationship between FE-1 deficiency and age was obtained, which implied age as a noncontributing factor toward exocrine pancreatic insufficiency among diabetic patients. Statistically significant correlation (P = 0.003) between glycated hemoglobin and FE-1 levels was also noted. The association between retinopathy (P = 0.001) and peripheral pulses (P = 0.001) with FE-1 levels were found to be statistically significant. Conclusion: This study validates the benefit of FE-1 estimation, as a surrogate marker of exocrine pancreatic insufficiency, which remains unmanifest and subclinical.

Somatostatin-analogues (SSAs) are a first-line treatment of unresectable neuroendocrine tumours (NETs). However, SSAs inhibit pancreatic secretions, which could lead to pancreatic exocrine insufficiency (PEI). PEI is known to be detrimental to patient quality of life and nutritional status. This study aimed to evaluate the effect of SSAs on pancreatic exocrine function in patients with NETs, using the 13C-mixed triglyceride breath test (13C-MTGT). Exocrine function was assessed using the 13C-MTGT at baseline and after a third SSA injection (two months). A quotient of 13CO2/12CO2 was measured by mass spectrometry, and the cumulative percent dose recovered at 6 h (cPDR) is reported. The secondary endpoints investigated were change in weight, HbA1C, and vitamin D levels. Ten patients completed the study. Exocrine function reduced in all patients (n = 10) following SSA therapy (median reduction from baseline: −23.4% (range: −42.1–0.5%, p = 0.005)). vitamin D levels decreased in all but one patient (median decrease from baseline: −26.5%, (−44.7–10%; p = 0.038)), and median HbA1C levels increased by 8.0% (0–59.3%; p = 0.008). Change in weight was not significant (median decrease from baseline: −0.21% (−4.5–3.5%, p = 1.000)). SSA therapy has a consistent impact on exocrine function from early in the treatment course, but the long-term clinical effects of this remain to be defined. Further studies are required to determine the clinical relevance of this observation and optimise the management of PEI in this cohort.

Fecal elastase-1 concentration reflects exocrine pancreatic function. There have been some reports from Europe, but so far there has not been a report of fecal elastase-1 concentration in Indonesia, especially concerning infants. The aim of this study is to know the concentration of elastase-1 in feces of infants aged 1-120 days as a preliminary report of the study of the ontogeny of pancreatic elastase-1 in term and preterm infants. Fecal elastase-1 were measured from feces of 28 healthy preterm and 34 healthy term infants up to 120 days (4 month) of age. Elastase-1 concentration in infants less than 14 days of age fluctuated below 200 μg/gram feces. At the first day of life 80% preterm and 60% term infants had elastase-1 concentration less than 200 μg/gram feces, and by the age of 7 days 50% preterm and 33% term infants had elastase-1 concentration less than 200 μg/gram feces. After 14 days of age its concentration was more than 200 μg/gram feces, regardless of gestational age. This preliminary study corroborates supported the previous studies that the level of fecal elastase-1 reached normal level after 14 days. Future longitudinal study is needed to know elastase-1 concentration in infants less than 14 days. (Med J Indones 2003; 12: 69-72)