scholarly journals Digestive enzyme replacement relieves growth failure in preterm infants with poor exocrine pancreatic function: a retrospective case series

2021 ◽  
Author(s):  
Annette Münch ◽  
Christoph Bührer ◽  
Ann Carolin Longardt
Keyword(s):  
Weight Gain ◽  
Preterm Infants ◽  
Digestive Enzyme ◽  
Pancreatic Insufficiency ◽  
Growth Failure ◽  
Exocrine Pancreatic Function ◽  
Exocrine Pancreatic Insufficiency ◽  
Very Preterm Infants ◽  
Enzyme Replacement ◽  
Fecal Pancreatic Elastase

AbstractIn orally fed preterm infants, poor weight gain may be linked to low fecal pancreatic elastase-1 (FPE-1) activity, indicative of exocrine pancreatic insufficiency. The objective of this study was the retrospective assessment of the effect of exogenous digestive enzyme replacement by gavage in preterm infants with growth failure and low FPE-1 (<200 μg/g). We analyzed weight gain relative to baseline and caloric intake during 14-day periods before and after institution of digestive enzyme replacement containing 6000 U lipase and 240 U protease kg−1 d−1. Among 46 of 132 preterm infants < 1250g birth weight surviving to at least 14 days in whom FPE-1 was determined, 38 infants had low FPE-1 (< 200 μg/g), and 33 infants received exogenous digestive enzyme replacement. Average daily weight gain significantly increased from 14.4 [range 2.6–22.4] g kg−1 d−1 to 17.4 [8.4–29.0] g kg−1 d−1 (P = 0.001), as did weight gain per kcal, from 0.08 [0.02–0.13] g kcal−1 d−1 to 0.11 [0.05–0.18] g kcal−1 d−1.Conclusion: In preterm infants with signs and symptoms of exocrine pancreatic insufficiency, exogenous digestive enzyme replacement is associated with improved growth. What is Known:• Very preterm infants on full enteral nutrition may display growth failure linked to transient poor exocrine pancreatic function.• Porcine pancreatic enzymes covered with an acid-resistant coating are too large to pass the internal diameter of most gavage tubes used in very preterm infants.What is New:• Administration of a liquid formulation of acid-resistant microbial digestive enzymes in preterm infants with growth failure and low fecal pancreatic elastase-1 values was associated with improved weight gain.• Response to exogenous digestive enzyme replacement was associated with the prior extent of growth failure.

scholarly journals Causes of Exocrine Pancreatic Insufficiency Other Than Chronic Pancreatitis

2021 ◽  
Vol 10 (24) ◽  
pp. 5779
Author(s):  
Lumír Kunovský ◽  
Petr Dítě ◽  
Petr Jabandžiev ◽  
Michal Eid ◽  
Karolina Poredská ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Pancreatic Disease ◽  
Exocrine Pancreatic Function ◽  
Exocrine Pancreatic Insufficiency ◽  
Pancreatic Tumors ◽  
Enzyme Replacement ◽  
Pancreatic Enzyme Replacement Therapy ◽  
Exact Etiology

Exocrine pancreatic insufficiency (EPI), an important cause of maldigestion and malnutrition, results from primary pancreatic disease or is secondary to impaired exocrine pancreatic function. Although chronic pancreatitis is the most common cause of EPI, several additional causes exist. These include pancreatic tumors, pancreatic resection procedures, and cystic fibrosis. Other diseases and conditions, such as diabetes mellitus, celiac disease, inflammatory bowel disease, and advanced patient age, have also been shown to be associated with EPI, but the exact etiology of EPI has not been clearly elucidated in these cases. The causes of EPI can be divided into loss of pancreatic parenchyma, inhibition or inactivation of pancreatic secretion, and postcibal pancreatic asynchrony. Pancreatic enzyme replacement therapy (PERT) is indicated for the conditions described above presenting with clinically clear steatorrhea, weight loss, or symptoms related to maldigestion and malabsorption. This review summarizes the current literature concerning those etiologies of EPI less common than chronic pancreatitis, the pathophysiology of the mechanisms of EPI associated with each diagnosis, and treatment recommendations.

Aortic growth arrest after preterm birth: a lasting structural change of the vascular tree

2011 ◽  
Vol 2 (4) ◽  
pp. 218-225 ◽  
Author(s):  
U. Schubert ◽  
M. Müller ◽  
A.-K. Edstedt Bonamy ◽  
H. Abdul-Khaliq ◽  
M. Norman
Keyword(s):  
Preterm Birth ◽  
Carotid Artery ◽  
Preterm Infants ◽  
Growth Failure ◽  
Later Life ◽  
Postnatal Growth ◽  
Direct Result ◽  
Arterial Tree ◽  
Very Preterm Infants ◽  
Very Preterm

Young people who are born very preterm exhibit a narrower arterial tree as compared with people born at term. We hypothesized that such arterial narrowing occurs as a direct result of premature birth. The aim of this study was to compare aortic and carotid artery growth in infants born preterm and at term. Observational and longitudinal cohort study of 50 infants (21 born very preterm, all appropriate for gestational age, 29 controls born at term) was conducted. Diameters of the upper abdominal aorta and common carotid artery were measured with ultrasonography at three months before term, at term and three months after term-equivalent age. At the first assessment, the aortic end-diastolic diameter (aEDD) was slightly larger in very preterm infants as compared with fetal dimensions. Fetal aortic EDD increased by 2.6 mm during the third trimester, whereas very preterm infants exhibited 0.9 mm increase in aEDD during the same developmental period (P < 0.001 for group difference). During the following 3-month period, aortic growth continued unchanged (+0.9 mm) in very preterm infants, whereas postnatal growth in term controls slowed down to +1.3 mm (P < 0.001 v. fetal aortic growth). At the final examination, aEDD was 22% and carotid artery EDD was 14% narrower in infants born preterm compared with controls, also after adjusting for current weight (P < 0.01). Aortic and carotid artery growth is impaired after very preterm birth, resulting in arterial narrowing. Arterial growth failure may be a generalized vascular phenomenon after preterm birth, with implications for cardiovascular morbidity in later life.

scholarly journals Efficacy and Safety of a New Formulation of Pancrelipase (Ultrase MT20) in the Treatment of Malabsorption in Exocrine Pancreatic Insufficiency in Cystic Fibrosis

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Michael W. Konstan ◽  
Theodore G. Liou ◽  
Steven D. Strausbaugh ◽  
Richard Ahrens ◽  
Jamshed F. Kanga ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Gastrointestinal Symptoms ◽  
Signs And Symptoms ◽  
Exocrine Pancreatic Insufficiency ◽  
Efficacy And Safety ◽  
Protein Nitrogen ◽  
Enzyme Replacement ◽  
New Formulation

Background. Pancreatic enzyme replacement therapy is the standard of care for treatment of malabsorption in patients with cystic fibrosis (CF) and exocrine pancreatic insufficiency (PI).Aim. To evaluate efficacy and safety of a new formulation of pancrelipase (Ultrase MT20) in patients with CF and PI. Coefficients of fat absorption (CFA%) and nitrogen absorption (CNA%) were the main efficacy parameters. Safety was evaluated by monitoring laboratory analyses, adverse events (AEs), and overall signs and symptoms.Methods. Patients (n=31) were randomized in a crossover design comparing this pancrelipase with placebo during 2 inpatient evaluation periods (6-7 days each). Fat and protein/nitrogen ingestion and excretion were measured from food diaries and 72-hour stool collections. CFA% and CNA% were calculated for each period and compared.Results. Twenty-four patients provided analyzable data. This pancrelipase increased mean CFA% and CNA% (+34.7% and +25.7%, resp.,P<.0001for both), reduced stool frequency, and improved stool consistency compared with placebo. Placebo-treated patients reported more AEs, with gastrointestinal symptoms being the most frequently reported AE.Conclusions. This pancrelipase is a safe and effective treatment for malabsorption associated with exocrine PI in patients with CF.

Novel ciliate lipases for enzyme replacement during exocrine pancreatic insufficiency

2016 ◽  
Vol 28 (11) ◽  
pp. 1305-1312 ◽  
Author(s):  
Alexander Brock ◽  
Ingo Aldag ◽  
Stella Edskes ◽  
Marcus Hartmann ◽  
Torsten Herzog ◽  
...  
Keyword(s):  
Pancreatic Insufficiency ◽  
Exocrine Pancreatic Insufficiency ◽  
Enzyme Replacement

scholarly journals Evidence-based pancreatology 2018 (review of research results on diseases and exocrine pancreatic insufficiency)

2019 ◽  
Vol 43 (2) ◽  
pp. 4-14
Author(s):  
N. B. Gubergrits ◽  
N. V. Byelyayeva ◽  
A. Ye. Klochkov ◽  
G. M. Lukashevich ◽  
P. G. Fomenko ◽  
...  
Keyword(s):  
Enzyme Replacement Therapy ◽  
Replacement Therapy ◽  
Pancreatic Insufficiency ◽  
Bacterial Overgrowth ◽  
Exocrine Pancreatic Insufficiency ◽  
Pancreatic Tumors ◽  
Research Results ◽  
Enzyme Replacement ◽  
Pancreatic Pathology

The article presents a detailed review of the research results in the field of pancreatology published in 2018. Certain parts of the review are devoted to the pathogenesis, diagnostics, course of pancreatitis, its treatment, as well as autoimmune, hereditary pancreatitis, pancreatic pathology in children, as well as treatment. In studying the pathogenesis of pancreatitis, attention is paid to genetic markers of pancreatitis along with a role of bacterial overgrowth syndrome in the small intestine, both in terms of worsening of the course of pancreatitis and the lack of effectiveness of enzyme replacement therapy. The study of the role of alcohol abuse and smoking in the pathogenesis of pancreatic pathology is still in progress. Diagnostics is going on. Endosonography remains the most informative method. A number of studies have been devoted to the studying of exocrine and endocrine pancreatic insufficiency both upon pancreatitis, pancreatic tumors, and in functional dyspepsia and HIV infection. Autoimmune pancreatitis is increasingly being diagnosed, a number of studies are devoted to its diagnostics and treatment. Pancreatic diseases in children develop mainly on the background of genetic predisposition, while functional pancreatic insufficiency occurs in adult patients. The study of the peculiarities of the effect of enzyme replacement therapy continues. The immediate and remote results of the surgical treatment of pancreatic pathology are assessed.

scholarly journals A111 SEVERE FAT MALABSORPTION IN A PATIENT POST ILEAL POUCH ANAL ANASTAMOSIS: A RARE PRESENTATION OF MICROSCOPIC ENTERITIS

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 129-130
Author(s):  
M Ricci ◽  
M Ropeleski
Keyword(s):  
Weight Loss ◽  
Weight Gain ◽  
Small Bowel ◽  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Vitamin Deficiency ◽  
Vitamin Deficiencies ◽  
Enzyme Replacement ◽  
Fat Malabsorption ◽  
Subepithelial Layer

Abstract Background Microscopic enteritis (ME) is a rare enteropathy characterized by malabsorptive diarrhea and lymphocytic infiltration +/- collagen deposition in the subepithelial layer of the small bowel. Its etiology is unclear. Aims To elucidate a rare cause of fat malabsorption and vitamin deficiency in a patient with ulcerative colitis and an ileoanal pouch. Methods A 74 yo male with a prior IPAA was referred to Internal Medicine in August 2018 for a 36 kg weight loss over 18 months and &gt;16 bowel movements (BM) per day (baseline 6, no history of pouchitis). Celiac serology and infectious workup were negative. Medical management and nutritional supplements did not result in weight gain or improvement of diarrhea. He was admitted in June 2019 with ongoing weight loss, AKI, and signs of fat-soluble vitamin deficiency. A 72-hour fecal fat analysis showed an average fecal weight of 2100 g/d (ref &lt;250 g/d), and excretion of 70% of daily fat intake (ref &lt;7%). His fecal elastase (FE) was 147 µg/g, consistent with moderate pancreatic insufficiency (PI) with mild atrophy on CT. EGD and pouch endoscopy were macroscopically normal, with histological findings of intraepithelial lymphocytosis and mild villous blunting in the duodenum and afferent limb. CT enterography excluded small bowel abnormalities. He was started on pancreatic enzyme replacement and discharged. He returned with worsening diarrhea and AKI. He was treated with supportive care and sent home. In the ensuing 3 weeks, he had up to 24 BM per day and 4 kg of weight loss. He returned in August 2019 with AKI, lack of PO intake and worsened nutritional status. Re-examination of duodenal biopsies from June 2019 revealed an added finding of focal subepithelial collagen thickening. Budesonide was started. Results On budesonide, his symptoms improved within days. BMs decreased to baseline, and his ability to sustain PO intake improved. At his 4-week follow-up visit, BMs were stable with a 6 kg weight gain and no ensuing laboratory abnormalities. Conclusions ME is a rare enteropathy that presents with malabsorption. Fat-soluble vitamin deficiencies can develop with widespread physiological disruption of the mucosal surface. This patient was a diagnostic challenge. His steatorrhea and reduced FE levels led clinicians down a diagnostic pathway of PI. FE is the most common test used in the diagnosis of PI. Levels &lt;200 µg/g are abnormal. Specificity is highest in chronic pancreatitis; however, this decreases in the presence of mucosal atrophy (i.e. IBD and diffuse small bowel disease). Thus, FE could not delineate the cause of steatorrhea in our patient. We can surmise that he likely has diffuse disease that was underestimated on duodenal biopsy. This is supported by his response to budesonide. This case highlights the heterogeneity of clinical presentations of ME. Awareness can reduce patient morbidity. Funding Agencies None

scholarly journals State of the Art in Exocrine Pancreatic Insufficiency

Medicina ◽  
2020 ◽  
Vol 56 (10) ◽  
pp. 523
Author(s):  
Carmelo Diéguez-Castillo ◽  
Cristina Jiménez-Luna ◽  
Jose Prados ◽  
José Luis Martín-Ruiz ◽  
Octavio Caba
Keyword(s):  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Bacterial Overgrowth ◽  
Exocrine Pancreatic Insufficiency ◽  
Enzyme Replacement ◽  
Non Invasive ◽  
Invasive Test ◽  
Pancreatic Enzyme Replacement Therapy ◽  
Risk Patients

Exocrine pancreatic insufficiency (EPI) is defined as the maldigestion of foods due to inadequate pancreatic secretion, which can be caused by alterations in its stimulation, production, transport, or interaction with nutrients at duodenal level. The most frequent causes are chronic pancreatitis in adults and cystic fibrosis in children. The prevalence of EPI is high, varying according to its etiology, but it is considered to be underdiagnosed and undertreated. Its importance lies in the quality of life impairment that results from the malabsorption and malnutrition and in the increased morbidity and mortality, being associated with osteoporosis and cardiovascular events. The diagnosis is based on a set of symptoms, indicators of malnutrition, and an indirect non-invasive test in at-risk patients. The treatment of choice combines non-restrictive dietary measures with pancreatic enzyme replacement therapy to correct the associated symptoms and improve the nutritional status of patients. Non-responders require the adjustment of pancreatic enzyme therapy, the association of proton pump inhibitors, and/or the evaluation of alternative diagnoses such as bacterial overgrowth. This review offers an in-depth overview of EPI in order to support the proper management of this entity based on updated and integrated knowledge of its etiopathogenesis, prevalence, diagnosis, and treatment.

scholarly journals A Case of Chronic Pancreatic Insufficiency Due to Valproic Acid in a Child

2001 ◽  
Vol 15 (2) ◽  
pp. 127-130 ◽  
Author(s):  
Mary Anne Cooper ◽  
Aubrey Groll
Keyword(s):  
Valproic Acid ◽  
Weight Loss ◽  
Acute Pancreatitis ◽  
Abdominal Pain ◽  
Chronic Pancreatitis ◽  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Exocrine Pancreatic Insufficiency ◽  
Radiological Evaluation ◽  
Enzyme Replacement

A 14-year-old child treated with valproic acid over several years for a seizure disorder developed abdominal pain with radiological evidence of acute pancreatitis. The association with valproic acid was not recognized, and the child continued to take the drug. The patient eventually developed steatorrhea and weight loss that improved with pancreatic enzyme replacement. Radiological evaluation showed an atrophic pancreas. Without evidence of other etiological factors, valproic acid by itself appeared to be the cause of chronic pancreatitis with exocrine pancreatic insufficiency in this patient.

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