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Vitasearch
http://www.clinicalpearls.com/

My Name
Search terms: Crohn's disease, pancreas
Type of study: human intervention study
Keywords: CROHN'S DISEASE - Gastric Acid, Pancreatic Enzyme
Reference: "Impaired Gastric Acid and Pancreatic Enzyme Secretion in Patients With Crohn's Disease May Be a Consequence of a Poor Nutritional State," Winter TA, O'Keefe SJD, et al, Inflamm Bowel Dis, September 2004;10(5):618-625. (Address: Trevor A. Winter, MD, PhD, E-mail: winter@uky.edu)

This study was an attempt to discover why Crohn's patients have impaired pancreatic function. A group of 9 severely undernourished patients were evaluated for digestive function, and found to have hypochlorhydria and low pancreatic exocrine function relative to a control group of healthy volunteers. The theory was that the patients were unable to synthesize proteins including enzymes due to malnutrition, which then exacerbated their malnutrition. A number of other measures of digestive function were compared including urinary xylose excretion (was increased in pts indicating leaky gut), fecal fat excretion (elevated dt low lipase), serum albumin, fasting blood glucose and mean stool frequency (which was elevated pre-tx). After measuring enzyme synthesis the researchers then were able to tempt six malnourished Crohn's patients to inpatient nutritional care via nasogastric tube. After three weeks of nutritional support, they measured gastric acid and pancreatic enyzme outputs and found them significantly increased. The conclusion of the study was that malnutrition contributes to the poor digestive function in Crohn's patients by interfering with protein synthesis.

The intervention involved inpatient "re-feeding" of the malnourished Crohn's patients with "polymeric feeding formulations" and "a normal ward diet" administered through a nasogastric tube. It sounds as if the formulation was hydrolyzed or "predigested", and the food substance was described as "semi-elemental". It appears that the nutritional support period was 3 weeks in duration. It also appears that there was no blinding or placebos used, as they are not mentioned. It is doubtful that "healthy volunteers" would consent to 3 weeks of refeeding through a nasogastric tube unless handsomely rewarded. There was no randomization. There is also no report on the 3 (of the original 9 pts) who did not consent to the refeeding.

This study could be replicated on a larger population only if a substantial number emaciated Crohn's patients were available and would consent to being fed via nose tube in a hospital for 3 weeks. In other words, this study is highly unlikely to be replicated on a large scale.

The conclusion, that adequate nutrition is needed for adequate pancreatic function, may seem rather obvious. However for doctors who hope to find and treat the cause, the chicken and the egg question is always there. This study brings that question clearly into function. Is the poor nutrition due to malabsorption, or is the malabsorption due to malnutrition? Perhaps both. Having clarity about the complexity of the questions will help us to be more sensitive and hopefully effective in treating complex disorders such as Crohn's.

In conclusion I am unimpressed with vitasearch. I looked up the study on pub med and got a different impression of it from the abstract. I will not trust vitasearch to summarize the research cohesively, and will go to the source whenever possible so that I may draw my own conclusions.

FROM VITASEARCH:
Summary# 42531
Keywords: CROHN'S DISEASE - Gastric Acid, Pancreatic Enzyme
Reference: "Impaired Gastric Acid and Pancreatic Enzyme Secretion in Patients With Crohn's Disease May Be a Consequence of a Poor Nutritional State," Winter TA, O'Keefe SJD, et al, Inflamm Bowel Dis, September 2004;10(5):618-625. (Address: Trevor A. Winter, MD, PhD, E-mail: winter@uky.edu)
Summary: In a study of 8 severely undernourished patients with Crohn's disease whose body mass indices were <17 kg/m2, a variety of gut absorption studies were done, which included urinary xylose excretion following a 5-g oral dose, and fecal fat excretion while on a standard diet containing 100 g/day of fat for a period of 3 days. Stimulation of gastric acid secretion was caused by a 1-hour intravenous infusion of pentagastrin at 6 mcg/kg. Pancreatic exocrine secretion was stimulated by a continuous infusion of cholecystokinin in the form of the octapeptide, CCK-8, at a rate of 40 ng/kg/hour. Measurement of gastric acid output was done by titrametric analysis of the gastric juice, while pancreatic enzyme activities in the duodenal juice were assessed on the day of the study using standard laboratory techniques. Amylase and trypsin activity were also evaluated. Following the initial assessments, the malnourished Crohn's disease subjects received intensive nutritional support as inpatients, with a goal of providing 30 kcal/kg/day of energy and 1.5 g/kg/day of protein. On admission to the study, the mean body mass index of the Crohn's disease subjects was 14.14 versus 23.36 kg/m2 in the control subjects. The mean serum albumin of the Crohn's disease patients was 27.88 g/l; and a mean fasting blood glucose was 5.26 mmol/l. The mean stool frequency was 4.71/day with a fecal fat excretion of 25.86 mmol/day, with the normal level being <18 mmol/day. Urinary xylose excretion following a 5-g oral load was 0.99 g/5 hours, with the normal being >1.2 g/5 hours. Six of the subjects gave consent for intestinal absorption, gastropancreatic secretion and protein synthesis studies to be performed following the period of nutritional support. Following the period of intensive nutritional support from 3 weeks to 3 months, the mean body mass index of the patients increased to 16.80 kg/m2 and the albumin to 37.50 g/l. The mean stool frequency was significantly reduced to 1.50/day, and the daily fecal fat excretion was 14.50 mmol/day. The Crohn's disease patients were hypochlorhydric, with a mean basal acid output of 0.64 mEq/hour compared with 3.85 mEq/hour in the control subjects, with a maximal acid output of 7.36 mEq/hour compared with 25.53 mEq/hour in the controls. After the nutritional support the basal acid output improved from 0.64 to 2.12 mEq/hour and the maximal acid output increased from 7.36 to 12.76 mEq/hour. The output of the pancreatic enzymes amylase, lipase and trypsin were significantly impaired in the Crohn's disease patients compared with the control subjects, with amylase at 759.6 versus 2,305 U/hour; lipase at 33.01 versus 118.6 U/hour; and trypsin at 97.43 versus 341.4 U/hour, respectively. Following intensive nutritional support, there was an improvement in the enzyme output, with amylase increasing from 759.6 to 2,758 U/hour; lipase increasing from 33.01 to 104.4 U/hour; and trypsin increasing from 97.43 to 256.2 U/hour, which was not significantly different from the controls. In this study, malnourished Crohn's disease patients had significantly impaired gastric as well as pancreatic secretory function. Exocrine pancreatic insufficiency is present in malnourished Crohn's disease patients, which may be due to both a mucosal abnormality, as evidenced by the impaired xylose absorption, as well as pancreatic insufficiency. Refeeding may necessitate a hydrolyzed or pre-digested "semi-elemental" formulation administered through a nasogastric tube. When polymeric feeding formulations are introduced and ultimately a normal ward diet, these data show that protein synthesis, the secretion of pancreatic enzymes and mucosal absorption return rapidly.

AND FROM PUB MED:
1: Inflamm Bowel Dis. 2004 Sep;10(5):618-25.Links
Impaired gastric acid and pancreatic enzyme secretion in patients with Crohn's disease may be a consequence of a poor nutritional state.
Winter TA, O'keefe SJ, Callanan M, Marks T.

Gastrointestinal Clinic, Department of Medicine, University of Cape Town, Groote Schuur hospital, Observatory, Cape Town, 7925, South Africa. winter@uky.edu

INTRODUCTION: Impaired pancreatic function has been reported in Crohn's disease, the cause of which is uncertain. This study investigated the effect of malnutrition, and subsequent re-feeding, on digestive function and protein synthesis in Crohn's disease patients. METHODS: Gastric acid and pancreatic secretion studies were performed on malnourished Crohn's patients before, and after a period of intensive nutritional support. Whole body, as well as pancreatic enzyme protein synthesis was investigated by [14C]leucine isotope incorporation studies. Results were evaluated in comparison to normal healthy volunteers. RESULTS: The mean body mass index (BMI) of the Crohn's patients was 14.14 kg/m2. The Crohn's patients had reduction in the secretion of gastric acid (7.36 versus 25.53 mEq/h; P < 0.01), and the pancreatic enzymes, amylase (759.6 versus 2305 U/h; P < 0.01), lipase (33.01 versus 118.6 U/h; P < 0.01) and trypsin (97.43 versus 341.4 U/h; P < 0.01). Resting energy expenditure (REE), expressed in relation to body mass, was greater in the malnourished Crohn's disease patients (38.25 versus 25.36 kcal/kg/d; P = 0.01). Total body protein synthesis was reduced (2.82 versus 4.39 g protein/kg/d; P < 0.05), with significant impairment in the synthesis of pancreatic enzymes, and reduction of zymogen stores. Following re-feeding, the BMI of the Crohn's patients improved to 16.80 +/- 0.66 kg/m2. Pancreatic enzyme synthesis improved, with significant increase in pancreatic enzyme stores and secretion, to levels similar to control values. Gastric acid secretion also improved, although still lower than the control value. CONCLUSION: Malnutrition may play a significant role in the impairment of gastric acid and pancreatic secretion in Crohn's disease patients. Copyright 2004 Lippincott Williams & Wilkins
PMID: 15472524 [PubMed - indexed for MEDLINE


MY NOTES
--looking for the cause of impaired pancreatic fx in Crohn's
--theory: could it be due to malnutrition?
--study looked at effect of "re-feeding" on digestive fx and prot syn
--pancreatic enzyme protein synthesis was investigated by 14C leucine isotope incorporation studies
--controls were healthy volunteers
--resting energy expenditure (REE), expressed in relation to body mass, was greater in the malnourished Crohn's disease patients (38.25 versus 25.36 kcal/kg/d; P = 0.01)
--total body protein synthesis was reduced (2.82 versus 4.39 g protein/kg/d; P < 0.05), with significant impairment in the synthesis of pancreatic enzymes, and reduction of zymogen stores
--following re-feeding BMI increased and pancreatic enzyme sythesis improved to levels similar to controls
--gastric acid secretion improved but was still lower than controls
--conclusion: "Malnutrition may play a significant role in the impairment of gastric acid and pancreatic secretion in Crohn's disease patients."
--malnourished Crohn's disease patients had sig. impaired gastric & pancreatic secretory function
--impaired Gastric Acid and Pancreatic Enzyme Secretion in Patients With Crohn's Disease
--mbdt poor nutritional state
--n=8 severely undernourished pts with BMI's under 17 kg/m2
--mean body mass of dz subjects was 14.14, control subjects were 23.36 kg/m2
--studied gut absorption:
----urinary xylose excretion after 5g oral dose
----fecal fat excretion while on standard diet with 100g/day of fat for 3 days
--mean serum albumin of dz pts was 27.88 g/l
--mean fasting blood glucose was 5.26 mmol/l
--mean stool frequency was 4.71/day
--fecal fat excretion was 25.86 mmol/day normal is <18 mmol/day)
--urinary xylose excretion following a 5-g oral load was 0.99 g/5 hours (normal is >1.2 g/5 hours)

GASTRIC ACID
----1-hour intravenous infusion of pentagastrin at 6mcg/kg to measure gastric acid secretion
----continuous infusion of cholecystokinin (in form of octapeptide CCK-8) at rate of 40ng/kg/hr to test pancreatic exocrine secretion
--gastric acid output measured by titrametric analysis of gastric juice (they were hypochlorhydric)
----mean basal acid output of 0.64 mEq/hour compared with 3.85 mEq/hour in the controls
----maximal acid output of 7.36 mEq/hour compared with 25.53 mEq/hour in the controls

PANCREATIC ENZYMES
--pancreatic enyzmes assessed in duodenal juice
--amylase and trypsin activity evaluated
--amylase, lipase and trypsin outputs were significantly impaired in the Crohn's disease patients
----amylase at 759.6 versus 2,305 U/hour in controls
----lipase at 33.01 versus 118.6 U/hour
----trypsin at 97.43 versus 341.4 U/hour

AFTER NUTRITIONAL SUPPORT
--after initial assessments subjects given inpatient nutrition support:
--goal of 30 kcal/kg/day energy and 1.5 g/kg/day protein
--6 pts agreed to intestinal absorption, gastropancreatic secretion and prot synthesis studies after nutritional support period (from 3 weeks to 3 months)
--refeeding of hydrolyzed/pre-digested formulation via nasogastric tube
--polymeric feeding formulations are introduced and a "normal ward diet"
--during this period in the 6 the mean body mass index increased to 16.80 kg/m2, albumin to 37.50 g/l
--mean stool frequency reduced to 1.50/day
--daily fecal fat excretion was 14.50 mmol/day
--hypochlorhydria was reduced: basal acid output improved from 0.64 to 2.12 mEq/hour
----maximal acid output increased from 7.36 to 12.76 mEq/hour
--pancreatic enzyme output increased
----amylase increasing from 759.6 to 2,758 U/hour
----lipase increasing from 33.01 to 104.4 U/hour
----trypsin increasing from 97.43 to 256.2 U/hour (not significant relative to controls)
--absorptive insuff mbdt mucosal abnormality (impaired xylose absorption) AND pancreatic insufficiency
--after TX: protein synthesis, the secretion of pancreatic enzymes and mucosal absorption return rapidly

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