Elastase-1 Levels Research Articles

Pancreatic Enzyme Replacement Therapy in Children with Severe Acute Malnutrition: A Randomized Controlled Trial

To assess the benefits of pancreatic enzyme replacement therapy (PERT) in children with complicated severe acute malnutrition. We conducted a randomized, controlled trial in 90 children aged 6-60 months with complicated severe acute malnutrition at the Queen Elizabeth Central Hospital in Malawi. All children received standard care; the intervention group also received PERT for 28 days. Children treated with PERT for 28 days did not gain more weight than controls (13.7 ± 9.0% in controls vs 15.3 ± 11.3% in PERT; P = .56). Exocrine pancreatic insufficiency was present in 83.1% of patients on admission and fecal elastase-1 levels increased during hospitalization mostly seen in children with nonedematous severe acute malnutrition (P <.01). Although the study was not powered to detect differences in mortality, mortality was significantly lower in the intervention group treated with pancreatic enzymes (18.6% vs 37.8%; P < .05). Children who died had low fecal fatty acid split ratios at admission. Exocrine pancreatic insufficiency was not improved by PERT, but children receiving PERT were more likely to be discharged with every passing day (P = .02) compared with controls. PERT does not improve weight gain in severely malnourished children but does increase the rate of hospital discharge. Mortality was lower in patients on PERT, a finding that needs to be investigated in a larger cohort with stratification for edematous and nonedematous malnutrition. Mortality in severe acute malnutrition is associated with markers of poor digestive function. ISRCTN.com: 57423639.

Prediction of pancreatic fistula after pancreatoduodenectomy by preoperative dynamic CT and fecal elastase-1 levels.

ObjectiveTo validate preoperative dynamic CT and fecal elastase-1 level in predicting the development of pancreatic fistulae after pancreatoduodenectomy.Materials and methodsFor 146 consecutive patients, CT attenuation values of the nontumorous pancreatic parenchyma were retrospectively measured on precontrast, arterial and equilibrium phase images for calculation of enhancement ratios. CT enhancement ratios and preoperative fecal elastase-1 levels were correlated with the development of pancreatic fistulae using independent t-test, logistic regression models, ROC analysis, Youden method and tree analysis.ResultsThe mean value of enhancement ratio on equilibrium phase was significantly higher (p = 0.001) in the patients without pancreatic fistula (n = 107; 2.26±3.63) than in the patients with pancreatic fistula (n = 39; 1.04±0.51); in the logistic regression analyses, it was significant predictor for the development of pancreatic fistulae (odds ratio = 0.243, p = 0.002). The mean preoperative fecal elastase-1 levels were higher (odds ratio = 1.003, p = 0.034) in the pancreatic fistula patients than other patients, but there were no significant differences in the areas under the curve between the prediction values of CT enhancement ratios and fecal elastase-1 combined and those of CT enhancement ratios alone (P = 0.897, p = 0.917) on ROC curve analysis. Tree analysis revealed that the CT enhancement ratio was more powerful predictor of pancreatic fistula than fecal elastase-1 levels.ConclusionThe preoperative CT enhancement ratio of pancreas acquired at equilibrium phase regardless of combination with fecal elastase-1 levels might be a useful predictor of the risk of developing a pancreatic fistula following pancreatoduodenectomy.

Preoperative fecal elastase-1 is a useful prognostic marker following curative resection of pancreatic cancer

BackgroundThe clinical relevance of fibrosis with regard to tumor progression is supported by the correlation between fibrosis and poor outcomes. Fecal elastase-1 (FE-1) level has been used to assess exocrine dysfunction of the pancreas and to predict pancreas fibrosis. The aim of this study was to assess the impact of FE-1 on the survival of pancreatic cancer patients. MethodsBetween January 2006 and December 2014, 136 patients with pancreatic adenocarcinoma underwent R0 resection at Gangnam Severance Hospital, Korea. Preoperative FE-1 levels were available in 94 patients who were enrolled in the study. Patients were classified into two groups according to preoperative FE-1: “normal” (≥200 μg/g) or “reduced” (<200 μg/g). ResultsMedian preoperative FE-1 level was 130.1 μg/g (IQR 32.0; 238.3). 62 patients (66.0%) had reduced pancreatic function and 32 patients (34.0%) had normal pancreatic function. The two groups had significantly different disease-free survival (P < 0.001). On multivariate analysis, normal FE-1, no lymph node metastasis and completion of adjuvant chemotherapy were found to be independent prognostic factors for better DFS (P = 0.001, P = 0.017, P = 0.038, respectively). ConclusionFE-1 is a simple and non-invasive predictive clinical marker for prognosis of pancreatic cancer after attempted curative resection.

Enzyme replacement therapy for maldigestion syndrome: clinical surveillances

Maldigestion persists in most patients with chronic pancreatitis (CP) and celiac disease. The objective lipase and amylase insufficiency diagnosis is needed to achieve an adequate clinical response to oral pancreatic enzyme substitution therapy. The novel data are presented in the article on the role of 13C-mixed triglyceride and 13C-corn starch breath tests as tools for exocrine pancreatic insufficiency diagnostics, for evaluating fat and starch malabsorbtion in CP patients. 165 patients (135 with CP and 30 with CP + celiac disease) and 30 healthy volunteers were included in the investigation. Delayed results of enzyme replacement therapy for maldigestion were estimated in 1 and 2 year of surveillance. It has been shown that partial recovery of exocrine pancreatic function is possible, and replacement therapy leads to patients’ nutritional status improving. It has been shown that 13C-breath tests could be useful tools in clinical practice for CP diagnostics. They are well-correlated with fecal elastase-1 level, have high sensitivity and specificity for diagnostics of lipase and amylase deficiency. Tests make it possible to choose the initial pancreatic enzyme dosage and are beneficial during the treatment for pancreatic enzyme dose correction.

Pancreatic exocrine insufficiency in malnourished children and those with persistent diarrhoeae.

Persistent diarrhoea, a serious health problem, is closely related to malnutrition. Children with severe malnutrition have a 9-fold risk of death, and children with severe stunting have a 4-fold risk of death. Prolonged mucosal injury from diarrhoea causes reduced secretin and cholecystokinin secretion, which decreases stimulation to the pancreas, and is indicated by faecal elastase-1 levels. This further aggravates persistent diarrhoea and malnutrition because of the low levels of digestive enzyme production. This study evaluated the exocrine function of the pancreas in children with persistent diarrhoea and malnutrition. This study used a cross-sectional design to compare exocrine pancreatic function among children with persistent diarrhoea, children with malnutrition, and apparently healthy children as reference Children aged 6-60 months were selected from the inpatient and outpatient units of various general hospitals in Jakarta. Faecal elastase- 1 levels were used to determine exocrine pancreatic function. The median values of faecal elastase- 1 in children with persistent diarrhoea, children with malnutrition, and reference children were 743 (1-1503) mcg/g, 861 (17-2909) mcg/g, and 1210 (26-3000) mcg/g, respectively. A significant difference was observed in the faecal elastase-1 levels between reference children and those with persistent diarrhoea (p<0.001). However, no differences in the faecal elastase-1 levels were noted between malnourished and reference children (p>0.05). Children with both persistent diarrhoea and malnutrition showed mean FE-1 392.3±206.9 and median 419 (125- 593). Exocrine pancreatic insufficiency is found in children with persistent diarrhoea. Children with combined persistent diarrhoea and malnutrition have the lowest FE-1, to which persistent diarrhea has the most significant contribution.

Preoperative fecal elastase-1 is used as predictive prognostic marker of pancreatic adenocarcinoma

Introduction: The clinical relevance of the fibrosis regarding tumor progression is supported by the correlations seen between poor outcome. Pancreas cancer has a massive fibrotic stoma which contributes to the local inflammatory environment. Pancreatic fibrosis is thought to be responsible for occlusion of the pancreatic duct by a tumor, chronic inflammation of the tumor, or by chronic pancreatitis. Fecal elastase-1 level has been used to assess moderate to severe exocrine dysfunction of the pancreas and predict pancreas fibrosis. The aim of this study was to assess the impact of fecal elastase on the prognosis of pancreas cancer patients. Methods: Between January 2006 and December 2014, 134 patients with pancreatic adenocarcinoma underwent R0 resection at Gangnam Severance Hospital, Seoul, Korea. Patients were classified into two groups according to the preoperative Fecal elastase; “normal” (fecal elastase-1: ≥200 μg/g), “reduced” (fecal elastase-1: <200 μg/g). We evaluated disease free Survival (DFS) and overall survival (OS). Results: Median preoperative fecal elastase-1 level was 188.92 μg/g (5.5–753.00). 49 Patients had reduced pancreatic function, 29 patients had normal pancreatic function. Median Disease free survival (DFS) was 16.29 months (2–103). Two groups had significantly different DFS (p < 0.001). In the multivariate analysis, normal fecal elastase-1 level and early T stage was found to be an independent prognostic factor for DFS and OS (p < 0.01, p < 0.01 respectively). Conclusion: Pancreas fibrosis is a significant, unfavourable prognostic factor for pancreas cancer after curative resection. Fecal elastase-1 is simple and non invasive predictive clinical marker for prognosis of pancreatic cancer.

Zinc/copper ratio: a predictor of pancreatic function in chronic pancreatitis?

The role of trace elements in the maintenance of normal pancreatic function is unclear. To estimate trace elements (zinc and copper) in chronic pancreatitis (CP) patients and study their relationship with exocrine and endocrine insufficiency. Methods: The study involved 101 CP patients and 113 healthy controls. Disease characteristics and imaging features were recorded. Erythrocyte zinc (Zn) and copper (Cu) were estimated by flame atomic absorption spectrophotometry. Fecal pancreatic elastase1 was estimated by polyclonal antibody ELISA method as a marker of pancreatic exocrine function. The mean erythrocyte Zn level and Zn/Cu ratio were significantly lower whereas the copper level was significantly higher in CP patients than controls. The mean Zn level and Zn/Cu ratio was significantly lower in CP patients with diabetes and those with low elastase1 as compared to non-diabetics and those with normal elastase1 respectively. Erythrocyte Cu level was significantly higher in CP patients with diabetes and with low elastase1 than those without diabetes and with normal elastase1 levels respectively. There was a significant positive correlation between elastase1 and Zn/Cu ratio (r = 0.396, p < 0.001). Receiver operating characteristic curve (ROC) analysis was performed to predict the development of exocrine insufficiency and it indicated an area under curve (AUC) of 0.838 ± 0.047 (95% CI: 0.746-0.93). The optimal cutoff value was 9.03 (sensitivity 86.5%, specificity 73.5%). When the same was performed to predict the development of diabetes, the AUC was 0.710 ± 0.05 (95% CI: 0.607-0.812). The optimal cutoff value was 7.2 (sensitivity 69.1%, specificity 69.7%). Low erythrocyte Zn/Cu ratio was found to be associated with exocrine and endocrine insufficiency in CP patients.

Cardiovascular, renal and gastrointestinal effects of incretin-based therapies: an acute and 12-week randomised, double-blind, placebo-controlled, mechanistic intervention trial in type 2 diabetes

IntroductionIncretin-based therapies, that is, glucagon-like peptide (GLP)-1 receptor agonists and dipeptidyl peptidase (DPP)-4 inhibitors, are relatively novel antihyperglycaemic drugs that are frequently used in type 2 diabetes management. Apart from...

Gastrointestinal Pathology in Juvenile and Adult CFTR-Knockout Ferrets

Cystic fibrosis (CF) is a multiorgan disease caused by loss of a functional cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel in many epithelia of the body. Here we report the pathology observed in the gastrointestinal organs of juvenile to adult CFTR-knockout ferrets. CF gastrointestinal manifestations included gastric ulceration, intestinal bacterial overgrowth with villous atrophy, and rectal prolapse. Metagenomic phylogenetic analysis of fecal microbiota by deep sequencing revealed considerable genotype-independent microbial diversity between animals, with the majority of taxa overlapping between CF and non-CF pairs. CF hepatic manifestations were variable, but included steatosis, necrosis, biliary hyperplasia, and biliary fibrosis. Gallbladder cystic mucosal hyperplasia was commonly found in 67% of CF animals. The majority of CF animals (85%) had pancreatic abnormalities, including extensive fibrosis, loss of exocrine pancreas, and islet disorganization. Interestingly, 2 of 13 CF animals retained predominantly normal pancreatic histology (84% to 94%) at time of death. Fecal elastase-1 levels from these CF animals were similar to non-CF controls, whereas all other CF animals evaluated were pancreatic insufficient (<2 μg elastase-1 per gram of feces). These findings suggest that genetic factors likely influence the extent of exocrine pancreas disease in CF ferrets and have implications for the etiology of pancreatic sufficiency in CF patients. In summary, these studies demonstrate that the CF ferret model develops gastrointestinal pathology similar to CF patients.

Can We Predict Postoperative Pancreatic Leakage After Pancreaticoduodenectomy Using Preoperative Fecal Elastase‐1 Level?

The measurement of fecal elastas-1 in stools is a sensitive and relatively inexpensive noninvasive test. The aim of this study was to study fecal elastase levels in patients who develop pancreatic leakage after pancreaticoduodenectomy (PD) to determine if fecal elastase level can be used to predict patients at high risk for pancreatic leakage after PD. Pancreatic function was considered normal when fecal elastase-1 concentration exceeded 200 μg/g feces and moderately or severely insufficient when fecal elastas-1 concentration was less than 200 μg/g feces. Of 123 patients who underwent PD, 67 (54.5%) showed fecal elastase-1 levels less than 200 μg/g, indicating moderate or severe pancreatic insufficiency. Pancreas texture, pathology origin, and level of γ-glutamyl transferase (r-GT) were significantly correlated with fecal elastas-1 level. On univariate analysis, the incidence of pancreatic leakage was significantly greater in the group with normal fecal elastase-1 level (≥200 μg/g), pathologic origin (bile duct/ampulla/duodenum), and soft pancreas texture. In multivariate analysis, normal fecal elastase-1 level (≥200 μg/g) and soft pancreatic texture were identified as independent factors for pancreatic leakage. Fecal elastase-1 is the most simple and objective method for predicting pancreatic leakage after PD.

Early diagnosis of asparaginase-associated pancreatitis based on elevated serum elastase-1 levels: Case reports

L-asparaginase (L-asp) is a well-known anticancer agent used in the treatment of acute lymphoblastic leukemia (ALL) in children. However, it is also known to induce several acute complications, such as acute pancreatitis. This is a presentation of two pediatric acute lymphoblastic leukemia (ALL) cases of asparaginase-associated pancreatitis (AAP) diagnosed at an early stage based on elevated serum elastase-1 levels, in the presence of normal serum amylase levels. Early diagnosis and treatment of AAP, although imperative, is occasionally difficult if only standard diagnostic procedures are followed. Elastase-1 is a potentially useful marker for the early diagnosis of AAP. Therefore, the measurement of elastase-1 levels, in addition to amylase and lipase levels, is recommended in L-asp-treated patients.

Interferon Regulatory Factor-2 Regulates Exocytosis Mechanisms Mediated by SNAREs in Pancreatic Acinar Cells

Pancreatic acinar cells are used to study regulated exocytosis. We investigated the role of interferon regulatory factor-2 (IRF2) in exocytosis in pancreatic acinar cells. Pancreas tissues from Irf2⁺/⁺, Irf2⁺/⁻), and Irf2⁻/⁻ mice were examined by microscopy, immunohistochemical, and immunoblot analyses; amylase secretion was quantified. We also compared salivary glands and pancreatic islets of Irf2⁻/⁻ mice with those of Irf2⁺/⁻ mice. To examine the effects of increased signaling by type I interferons, we studied pancreatic acini from Irf2⁻/⁻Ifnar1⁻/⁻ mice. The effect of IRF2 on amylase secretion was studied using an acinar cell line and a retroviral system. We studied expression of IRF2 in wild-type mice with cerulein-induced pancreatitis and changes in pancreatic tissue of Irf2⁻/⁻ mice, compared with those of Irf2⁺/⁻ mice. Irf2⁻/⁻ pancreas was white and opaque; numerous and wide-spread zymogen granules were observed throughout the cytoplasm, along with lack of fusion between zymogen granules and the apical membrane, lack of secretagogue-stimulated amylase secretion, and low serum levels of amylase and elastase-1, indicating altered regulation of exocytosis. The expression pattern of soluble N-ethylmaleimide-sensitive factor attachment protein receptors changed significantly, specifically in pancreatic acini, and was not rescued by disruption of type I interferon signaling. Down-regulation of IRF2 decreased amylase secretion in an acinar cell line. In mice with pancreatitis, levels of IRF2 were reduced. Irf2⁻/⁻ acini were partially resistant to induction of pancreatitis. IRF2 regulates exocytosis in pancreatic acinar cells; defects in this process might be involved in the early phases of acute pancreatitis.

A prospective pilot study of the prevalence of pancreatic disease in patients with alcohol related liver disease using faecal elastase-1

IntroductionExcess alcohol intake is associated with liver disease and pancreatic disease, however, the majority of individuals appear to present with a single condition, for example, chronic liver disease. There is...

Fecal pancreatic elastase-1 levels in older individuals without known gastrointestinal diseases or diabetes mellitus

BackgroundStructural changes occur in the pancreas as a part of the natural aging process. With aging, also the incidence of maldigestive symptoms and malnutrition increases, raising the possibility that these might be caused at least in part by inadequate pancreatic enzyme secretion due to degenerative processes and damage of the gland. Fecal elastase-1 is a good marker of pancreatic exocrine secretion. The aim of this study was to investigate the fecal elastase-1 levels among over 60 years old Finnish and Polish healthy individuals without any special diet, known gastrointestinal disease, surgery or diabetes mellitus.MethodsA total of 159 patients participated in this cross-sectional study. 106 older individuals (aged 60-92 years) were recruited from outpatient clinics and elderly homes. They were divided to three age groups: 60-69 years old (n = 31); 70-79 years old (n = 38) and over 80 years old (n = 37). 53 young subjects (20-28 years old) were investigated as controls. Inclusion criteria were age over 60 years, normal status and competence. Exclusion criteria were any special diet, diabetes mellitus, any known gastrointestinal disease or prior gastrointestinal surgery. Fecal elastase-1 concentration was measured from stool samples with an ELISA that uses two monoclonal antibodies against different epitopes of human elastase-1.ResultsFecal elastase-1 concentrations correlated negatively with age (Pearson r = -0,3531, P < 0.001) and were significantly lower among subjects over 70 years old compared to controls (controls vs. 70-79 years old and controls vs. over 80 years old, both P < 0.001). Among the over 60 years old subjects, the fecal elastase-1 concentrations were below the cut off level of 200 μg/g in 23 of 106 (21.7%) individuals [mean 112 (86-138) μg/g] indicating pancreatic exocrine insufficiency. Of those, 9 subjects had fecal elastase-1 level below 100 μg/g as a marker of severe pancreatic insufficiency.ConclusionIn our study one fifth of healthy older individuals without any gastrointestinal disorder, surgery or diabetes mellitus suffer from pancreatic exocrine insufficiency and might benefit from enzyme supplementation therapy.

Normal levels of serum pancreatic enzymes in patients with progressive familial intrahepatic cholestasis type 2.

High prevalence of elevated serum pancreatic enzymes in children with cholestasis with normal fecal elastase-1 concentrations has been documented. However, this state is related predominantly to biliary atresia. Therefore, we aimed to assess pancreatic damage by measuring serum pancreatic enzymes in patients with progressive familial intrahepatic cholestasis type 2 (PFIC type 2). Twenty PFIC type 2 patients with normal serum bilirubin and bile acid concentrations were included in the study. Thirty pancreatic insufficient cystic fibrosis (PI-CF) patients, thirty patients with acute pancreatitis (AP) and thirty healthy subjects (HS) served for the purpose of comparison. In all subjects, serum lipase and elastase-1 levels were measured. In all but one PFIC type 2 patients and all HS normal lipase activities were found. Serum elastase-1 concentrations were normal in all PFIC type 2 patients and HS. The enzyme levels were very similar in both groups studied. Lipase activities in PFIC type 2 patients were significantly higher than in PI-CF patients (p < 0.00001) and lower than in patients with AP (p < 0.00001). Serum elastase-1 levels in PFIC type 2 patients were significantly lower than in patients with AP (p < 0.00001) and not different from those in PI-CF patients. In conclusion. serum pancreatic enzymes in patients with PFIC type 2 are normal. No pancreatic damage in these patients could be detected.

Management of pancreatic exocrine insufficiency: Australasian Pancreatic Club recommendations

Pancreatic exocrine insufficiency (PEI) occurs when the amounts of enzymes secreted into the duodenum in response to a meal are insufficient to maintain normal digestive processes. The main clinical consequence of PEI is fat maldigestion and malabsorption, resulting in steatorrhoea. Pancreatic exocrine function is commonly assessed by conducting a 3-day faecal fat test and by measuring levels of faecal elastase-1 and serum trypsinogen. Pancreatic enzyme replacement therapy is the mainstay of treatment for PEI. In adults, the initial recommended dose of pancreatic enzymes is 25,000 units of lipase per meal, titrating up to a maximum of 80,000 units of lipase per meal. In infants and children, the initial recommended dose of pancreatic enzymes is 500 units of lipase per gram of dietary fat; the maximum daily dose should not exceed 10,000 units of lipase per kilogram of bodyweight. Oral pancreatic enzymes should be taken with meals to ensure adequate mixing with the chyme. Adjunct therapy with acid-suppressing agents may be useful in patients who continue to experience symptoms of PEI despite high-dose enzyme therapy. A dietitian experienced in treating PEI should be involved in patient management. Dietary fat restriction is not recommended for patients with PEI. Patients with PEI should be encouraged to consume small, frequent meals and to abstain from alcohol. Medium-chain triglycerides do not provide any clear nutritional advantage over long-chain triglycerides, but can be trialled in patients who fail to gain or to maintain adequate bodyweight in order to increase energy intake.

Fecal elastase1 and acid steatocrit estimation in chronic pancreatitis

Measurement of pancreatic exocrine function and steatorrhea in chronic pancreatitis in the clinical setting has not received much attention. To assess pancreatic exocrine function and fecal fat excretion in a cohort of patients with chronic pancreatitis. Stool elastase1 levels were measured in 101 patients using polyclonal ELISA and acid steatocrit was measured in 86 chronic pancreatitis patients. Associations with etiology, clinical and radiological features, and diabetic status were examined. Low pancreatic stool elastase1 (<200 microg/g stool) was observed in two-thirds of chronic pancreatitis patients and correlated with ductal dilatation, pancreatic atrophy and calcification (p<0.05). Diabetes was more prevalent in chronic pancreatitis patients with low elastase1 (p=0.045). There was no difference in mean acid steatocrit between diabetics and non-diabetics (p=0.069). Elastase1 levels had a negative correlation with acid steatocrit (r=-0.606, p<0.001), and a positive correlation (r=0.412) with body mass index (p=0.013). Fifty-three percent of chronic pancreatitis patients with normal BMI had low elastase1. Fecal elastase1 levels correlated with fecal fat excretion and BMI. Fecal elastase1 estimation may be helpful in early detection of malabsorption in chronic pancreatitis.

Some Patients With Irritable Bowel Syndrome May Have Exocrine Pancreatic Insufficiency

Patients with irritable bowel syndrome (IBS) might have other underlying pathologies. Pancreatic disease can be elusive-especially in the early stages, and some symptoms overlap with those of IBS. We evaluated the prevalence of exocrine pancreatic insufficiency in diarrhea-predominant IBS (D-IBS) and assessed the effects of pancreatic enzyme supplementation. The study included patients who met the Rome II criteria for D-IBS, patients with chronic diarrhea, and subjects without diarrhea (controls). Subjects' baseline weight, stool frequency, stool consistency (using the Bristol score), and fecal elastase-1 (Fel-1) levels were determined. Patients were assessed using British Society of Gastroenterology IBS guidelines. Patients with Fel-1 levels less than 100 microg/g stool (indicating pancreatic exocrine insufficiency; group 1) were compared with age- and sex-matched patients with D-IBS and normal levels of Fel-1 (group 2), given pancreatic enzyme therapy, and reassessed at 12 weeks. Fel-1 levels were less than 100 microg/g in stool from 19 of 314 patients with D-IBS (6.1%; 95% confidence interval [CI], 3.7%-9.3%), none of the 105 patients with chronic diarrhea (95% CI, 0.0%-3.5%), and none of 95 controls (95% CI, 0.0-3.8%) (P < .001). After enzyme supplementation, improvements in stool frequency (P < .001), stool consistency (P < .001), and abdominal pain (P = .003) were observed in patients in group 1, but not in group 2. Pancreatic exocrine insufficiency was detected in 6.1% of patients who fulfilled the Rome II criteria for D-IBS. In these patients, pancreatic enzyme therapy might reduce diarrhea and abdominal pain. Pancreatic exocrine insufficiency should be considered in patients with D-IBS.

Chronic Hereditary Pancreatitis in a Girl With a Serine Protease Inhibitor Kazal Type I (SPINK-1) Gene Mutation and a Coxsackie Type B5 Infection

To the Editors: A 3-year-old girl presented with epigastric pain, vomiting, diarrhea, and anorexia. Blood results showed a serum lipase value of 10.784 U/L (normal 0–200 U/L), amylase 150 U/L (normal 0–85 U/L), alkaline phosphatase 218 U/L, ALT 23 U/L, AST 32 U/L, LD 695 U/L, and a total bilirubin of 3 μmol/L. Serologic tests showed a high antibody titer to Coxsackie virus type B5 (1:2048). IgM antibody for mumps, varicella zoster, rubella, measles, para-influenza, and cytomegalovirus were all undetectable. After a second episode of acute pancreatitis, a mutation in the serine protease inhibitor kazal type I (SPINK-1) was identified. Endoscopic ultrasonography (EUS) and retrograde cholangiopancreaticography (ERCP) showed a short distal stenosis in the pancreatic head. A 5 cm 7 Fr endoprosthesis was placed in the pancreatic duct. Exocrine pancreatic function remained undisturbed (elastase-1 levels >0.500). The child's mother also had a SPINK-1 mutation. SPINK-1 mutations are also found in 2% of patients without chronic pancreatitis.1,2 Therefore, the mutation by itself does not cause pancreatitis. Other factors (like in this case a Coxsackie type B5 infection3) must be present to cause pancreatitis. SPINK-1 mutation might predispose to chronic pancreatitis. Under normal conditions, SPINK-1 inhibits the transformation of trypsinogen in trypsin in the pancreas, by which auto-digestion is prevented. A SPINK-1 gene mutation leads to an increased trypsin activity in the pancreas, causing auto-digestion.2 In the case of a Coxsackie type B5 induced acute pancreatitis, screening for a SPINK-1 mutation is indicated if episodes of acute pancreatitis recur. Endoscopic ultrasonography is a useful diagnostic technique to visualize pancreatic duct abnormalities in children with chronic pancreatitis.4,5 Michael Groeneweg, MD, PhD Dept of Paediatrics, Sophia Children's Hospital Erasmus Medical Center Rotterdam Rotterdam, the Netherlands Dept of Paediatrics Maasstad Hospital Rotterdam, the Netherlands Jan W. Poley, MD, PhD Dept of Gastroenterology and Hepatology Erasmus Medical Center Rotterdam Rotterdam, the Netherlands Marlies Dansen, MD Dept of Paediatrics, Sophia Children's Hospital Erasmus Medical Center Rotterdam Rotterdam, the Netherlands Jan G. Brinkman, MD Dept of Paediatrics Maasstad Hospital Rotterdam, the Netherlands Johanna C. Escher, MD, PhD Edward E. S. Nieuwenhuis, MD, PhD Dept of Paediatrics, Sophia Children's Hospital Erasmus Medical Center Rotterdam Rotterdam, the Netherlands

Lack of Correlation Between Fecal Elastase‐1 Levels and Fecal Nitrogen Excretion in Preterm Infants

We measured fecal elastase-1 (FE1) levels in 34 preterm newborns (15 small-for-gestational-age and 19 appropriate-for-gestational-age) during the first 2 months of life and evaluated whether they were correlated with nitrogen loss in stools. FE1 increased over time, and values were similar in both groups of newborns. Fecal nitrogen was significantly higher in small-for-gestational-age infants. There was no correlation between FE1 levels and fecal nitrogen excretion. Pancreatic proteolytic function was efficient at an early stage in enterally fed preterm newborns. Despite the similar FE1 values, fecal nitrogen loss was significantly higher in small-for-gestational-age preterm infants than in appropriate-for-gestational-age preterm infants.