Diagnostic Value of the Fecal Chymotrypsin Test in Pancreatic Insufficiency, Particularly Chronic Pancreatitis: Correlation with the Pancreozymin-Secretin Test, Fecal Fat Excretion and Final Clinical Diagnosis

Digestion ◽  
1981 ◽  
Vol 21 (6) ◽  
pp. 281-289 ◽  
Author(s):  
R.W. Ammann ◽  
A. Akovbiantz ◽  
W. Häcki ◽  
F. Largiadèr ◽  
M. Schmid
Keyword(s):  
Chronic Pancreatitis ◽  
Clinical Diagnosis ◽  
Pancreatic Insufficiency ◽  
Diagnostic Value ◽  
Secretin Test ◽  
Fecal Fat ◽  
Fecal Chymotrypsin ◽  
Pancreozymin Secretin Test ◽  
Fat Excretion

scholarly journals Immunoreactive elastase I: clinical evaluation of a new noninvasive test of pancreatic function

1996 ◽  
Vol 42 (2) ◽  
pp. 222-226 ◽  
Author(s):  
J Stein ◽  
M Jung ◽  
A Sziegoleit ◽  
S Zeuzem ◽  
W F Caspary ◽  
...  
Keyword(s):  
Pancreatic Insufficiency ◽  
Pancreatic Enzyme ◽  
Correlation Coefficients ◽  
Diagnostic Value ◽  
Exocrine Pancreatic Insufficiency ◽  
Pancreatic Function ◽  
Noninvasive Test ◽  
Enzyme Replacement ◽  
Fecal Chymotrypsin ◽  
Immunoreactive Elastase

Abstract We have evaluated the diagnostic value of the fecal elastase test in comparison with the secretin-pancreozymin test in the diagnosis of exocrine pancreatic insufficiency. Pancreatic elastase was measured immunologically. Immunoreactive elastase activity in spot stools from controls ranged from 136 to 4440 microgram/g; 95% of all values were within 175 to 1500 microgram/g. The elastase assay CVs ranged from 3.3% to 6.3% (intraassay) and from 4.1% to 10.2% (interassay). The output of elastase correlated well with those of amylase, lipase, and trypsin, yielding respective correlation coefficients of 0.83, 0.82, and 0.84 in controls and 0.86, 0.91, and 0.91 in patients with impaired pancreatic function. In contrast to fecal chymotrypsin, the test results were unaffected by pancreatic enzyme replacement therapy. These results indicate that fecal immunoreactive elastase may be recommended as a new, noninvasive tubeless test of pancreatic function.

FECAL FAT AND NITROGEN IN HEALTHY CHILDREN AND IN CHILDREN WITH MALABSORPTION OR MALDIGESTION

PEDIATRICS ◽  
1970 ◽  
Vol 46 (5) ◽  
pp. 690-695
Author(s):  
D. H. Shmerling ◽  
J. C. W. Forrer ◽  
A. Prader
Keyword(s):  
Pancreatic Insufficiency ◽  
Diagnostic Value ◽  
Exocrine Pancreatic Insufficiency ◽  
Healthy Children ◽  
Older Children ◽  
Upper Limit ◽  
Fecal Fat ◽  
Daily Excretion ◽  
Total Fatty Acids ◽  
Untreated Celiac Disease

The daily excretion of total fatty acids and nitrogen in stool was assessed in 3 or 5 days' collection periods in 71 control patients and in 71 patients with different forms of malabsorption and maldigestion. Control infants have higher normal values for fecal fat (range 1.1 to 3.6 gm/day, upper limit, calculated as mean ± S.D. = 4.3 gm/day) than older children (range 0.2 to 2.2 gm/day, mean + 2 S.D. = 3.02 for children aged 1 to 4 years, and range 0.8 to 3.2 gm/day, mean + 2 S.D. = 3.11 gm/day for children aged 4 to 10 years). The upper limit of fecal nitrogen was found to be 1 gm in infants and 1.2 gm/day in children. Patients with exocrine pancreatic insufficiency excreted significantly higher amounts of both fat and nitrogen than those of camparable age with untreated Celiac disease. These findings can be of diagnostic value in this age group.

scholarly journals A276 TOTAL PANCREATIC LIPOMATOSIS AND EXOCRINE PANCREATIC INSUFFICIENCY IN A PATIENT WITH CELIAC DISEASE: AN UNUSUAL ENTITY

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 153-155
Author(s):  
S Nassiri ◽  
M Tomaszewski ◽  
G Ou
Keyword(s):  
Celiac Disease ◽  
Case Report ◽  
Chronic Pancreatitis ◽  
Small Bowel ◽  
Pancreatic Insufficiency ◽  
Exocrine Pancreatic Insufficiency ◽  
Pancreatic Parenchyma ◽  
Fecal Fat ◽  
Fatty Replacement ◽  
History Of

Abstract Background Exocrine pancreatic insufficiency (EPI) is characterized by maldigestion and malabsorption of nutrients and is most commonly caused by diseases of the pancreatic parenchyma including chronic pancreatitis and cystic fibrosis (CF). However, EPI is also observed in other conditions including celiac disease (CD). Aims We report a case of EPI in a patient with CD found to have total fatty replacement of the pancreas. Methods A case report and review of the literature were performed. Results Case Report: A 42-year-old man with CD on gluten-free diet (GFD) presented with a two-year history of increasing bowel frequency (4–6 times daily) and steatorrhea. Quantitative fecal fat over 72 hours confirmed fecal fat excretion of 101g/day; N < 7g) and total stool weight of 3761g. Nadir weight was 67.6 kg. There was a dramatic response to pancreatic enzyme replacement therapy (PERT) with marked improvement in bowel habits and weight gain to 74.8 kg over half a year. There is no history of pancreatitis, abdominal pain or alcohol abuse. He does not smoke but drinks 1–2 units of alcohol per week at most. Family history is negative for pancreatitis and pancreatic malignancy. On examination, following PERT, the patient appeared well-developed and nourished. He did not have clinical features or biochemical evidence of fat-soluble vitamin deficiency following PERT. Anti-tTG was equivocal (7.6 U/mL; N < 7 U/mL). IgG subclasses were normal. Chromogranin was mildly elevated (100mcg/L; N < 94mcg/L), but gastrin (15ng/L) and 24-hour urine for 5-hydroxyindoleacetate [5-HIAA] (23umol/d) were normal. Endoscopic evaluations including upper endoscopy, colonoscopy, and capsule endoscopy demonstrated intact duodenal villous architecture without inflammation, no microscopic colitis, and no small bowel mucosal disease, respectively. CT of the abdomen revealed total fatty replacement of the pancreas with no pancreatic parenchyma (Figure 1). Sweat sodium test was positive (67 mmol/L, N < 60 mmol/L) but CFTR gene sequencing was negative. There was no evidence of diabetes, hyperlipidemia, hyperferritinemia, Cushing’s syndrome, or hepatic disease on biochemical investigations. Literature Review: Total pancreatic lipomatosis (TPL), or fatty replacement of the pancreas, is a rare cause of EPI which leads to maldigestion, malabsorption, and malnutrition. The pathogenesis of TPL is poorly understood but predisposing factors include obesity, diabetes mellitus, hyperlipidemia, malnutrition, Cushing’s syndrome, hemochromatosis, chronic pancreatitis and CF. EPI can also manifest in patients with CD due to active small bowel inflammation or chronic pancreatitis. Last but not least, there appears to be higher prevalence of CD in CF patients. Conclusions Persistent steatorrhea with weight loss despite GFD in patients with CD should prompt other considerations of EPI and trial of PERT. Funding Agencies None

Evaluation of Pancreozymin-Secretin test for diagnosis of carcinoma of the pancreas and chronic pancreatitis

1970 ◽  
Vol 5 (4) ◽  
pp. 330-331
Author(s):  
T. Takeuchi ◽  
K. Ishii ◽  
K. Nakamura ◽  
G. Sato ◽  
H. Ozaki ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Secretin Test ◽  
Carcinoma Of The Pancreas ◽  
Pancreozymin Secretin Test

Fecal fat excretion. An analysis of four years' experience

1967 ◽  
Vol 119 (6) ◽  
pp. 573-576 ◽  
Author(s):  
E. C. Raffensperger
Keyword(s):  
Fecal Fat ◽  
Fat Excretion

Stimulation of fecal fat excretion and the disposal of protoporphyrin in a murine model for erythropoietic protoporphyria

2007 ◽  
Vol 293 (2) ◽  
pp. G510-G516
Author(s):  
Karin E. R. Gooijert ◽  
Rick Havinga ◽  
Alida R. Oosterloo-Duinkerken ◽  
Enge E. A. Venekamp-Hoolsema ◽  
Folkert Kuipers ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Fecal Excretion ◽  
High Fat ◽  
Erythropoietic Protoporphyria ◽  
Low Fat Diet ◽  
Fecal Fat ◽  
Sucrose Polyesters ◽  
Hydrophobic Compound ◽  
Fat Excretion ◽  
Stimulation Of

Erythropoietic protoporphyria (EPP) is characterized by toxic accumulation of the hydrophobic compound protoporphyrin (PP). Ferrochelatase-deficient ( fch/ fch) mice are an animal model for human EPP. Recently, we have demonstrated that the accumulation of another hydrophobic compound, unconjugated bilirubin, could effectively be treated by stimulation of fecal fat excretion. We investigated whether stimulation of fecal fat excretion enhanced the disposal of PP in fch/ fch mice. Fch/ fch mice were fed for 8 wk with a high-fat diet (16 wt% fat; control) or with the high-fat diet mixed with either a nonabsorbable fat (sucrose polyester) or the intestinal lipase inhibitor orlistat. The effects of the treatments on fecal excretion of fat and PP and on hepatic PP concentrations were compared with control diets. Fecal fat excretion in fch/ fch mice on a high-fat diet was higher than in mice on a low-fat diet (+149%, P < 0.05). Sucrose polyesters and orlistat increased fecal fat excretion even more, up to sixfold of control values. However, none of the different treatments affected fecal PP excretion or hepatic PP concentration. Treatment of fch/ fch mice with a high-fat diet, a nonabsorbable fat diet, or with orlistat increased the fecal excretion of fat but did not increase fecal PP excretion or decrease hepatic PP concentration. The present data indicate that accumulation of PP is not amenable to stimulation of fecal fat excretion.

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