[Pancreatic steatorrhea; pancreatic diabetes and the repercussions of pancreatic steatorrhea for the organism].
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Disease↗
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[Neomycin cure of steatorrhea associated with Proteus hauseri enteritis; relation of infectious steatorrhea to sprue nostras].
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Celiac Disease↗
[Steatorrheas. Methodological study. Applications to pancreatic steatorrheas].
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Celiac Disease↗
Increased risk of nephrolithiasis in patients with steatorrhea.
Patients with ileal disease have increased absorption of dietary oxalate, hyperoxaluria, and an increased incidence of nephrolithiasis. Patients with steatorrhea of varying etiologies also have hyperoxaluria. To determine whether steatorrhea per se is associated with nephrolithiasis, we reviewed the charts of all adult patients who had a 72-hr fecal fat analysis from 1968 to 1978. The 159 patients with steatorrhea were compared to 162 patients without steatorrhea. The two groups were comparable in age, sex, urine specific gravity, and serum uric acid and phosphorus; serum calcium was slightly less in the steatorrhea group (8.7 +/- 0.1 vs 9.0 +/- 0.1, P less than 0.02). Although 19 patients with steatorrhea had nephrolithiasis compared to 7 control patients (P = 0.01), 15 of these 19 patients had ileal disease and only 4 of the 118 patients with steatorrhea but without ileal disease had stones. Categorical data analysis revealed that steatorrhea, diarrhea (stool weight greater than 225 g/day), male sex, and ileal disease were significantly associated with nephrolithiasis with a relative risk of 3.0, 2.7, 3.1, and 8.0, respectively. When patients without ileal disease were analyzed separately, however, steatorrhea, diarrhea, and sex were no longer risk factors. In contrast, in patients with ileal disease the incidence of nephrolithiasis increased with the severity of steatorrhea. The relative risk of nephrolithiasis in male patients with ileal disease and fecal fat greater than 20 g/day was 26.3 (P less than 0.01). Thus, the presence of both ileal disease and steatorrhea greatly increases the risk of nephrolithiasis; however, neither steatorrhea alone nor ileal disease alone are risk factors for nephrolithiasis.
Celiac Disease↗
Raised fecal fat concentration is not a valid indicator of pancreatic steatorrhea.
The hypothesis that fecal fat concentration (FFC; g fat/100 g wet stool weight) should be higher in pancreatic steatorrhea than in steatorrhea due to gastrointestinal disease was investigated. Fecal weight and fat excretion were measured in 59 patients with pancreatic steatorrhea and in 53 patients with nonpancreatic steatorrhea. A further 42 patients were studied who had normal fecal fat excretion but exocrine pancreatic insufficiency proven by a secretin-pancreozymin test along with 31 patients with well-defined gastrointestinal disease but without steatorrhea. The control group consisted of 184 subjects without evidence for malabsorption. FFC was significantly higher in patients with pancreatic compared to those with nonpancreatic steatorrhea. However, because of the almost identical concentrations in patients with steatorrhea due to celiac sprue (FFC 10.5 +/- 4.3%, mean +/- SD) and those with pancreatic steatorrhea (FFC 11.5 +/- 4.7%), FFC was of no value for the differential diagnosis between pancreatic and nonpancreatic steatorrhea.
Celiac Disease↗
Steatorrhea in Japanese patients with chronic pancreatitis.
Fecal fat excretion, fecal mass, fecal fat concentration, and the coefficient of fat absorption were evaluated in 31 normal Japanese subjects with a mean fat consumption of 61.8 g and compared with the values in 43 Japanese patients with chronic pancreatitis (CP) with a fat consumption of 40.2 g. Fecal fatty acids were analyzed by the gas chromatographic method. Fecal fat excretion by normal individuals was 1.7 +/- 1.0 (Mean +/- SD) g/day (range, 0.4-4.9 g/day). Steatorrhea was therefore defined as fecal fat excretion that exceeded 5.0 g/day. The patients with CP were divided into three groups: non-steatorrhea (fecal fat < 5.0 g/day), chemical steatorrhea (fecal fat > or = 5 g/day and no appearance of fatty stool), and manifest steatorrhea (evaluated from the appearance of fatty stool). In addition, we investigated the correlation between fecal fat excretion and pancreatic exocrine function, obtained by the pancreozymin-secretin (or secretin) test in 24 controls and 30 CP patients. Fecal fat excretion by CP patients was 9.1 +/- 8.8 g/day, which was significantly higher (P < 0.01) than that of controls. There were 28 (65%) CP patients with steatorrhea. Of these, 15 (35%) showed chemical steatorrhea and 13 (30%) manifest steatorrhea. In CP patients, the fecal mass (250.5 +/- 133.6 g vs control, 125.6 +/- 52.5 g), fecal fat concentration (3.40 +/- 2.16 g% vs control, 1.48 +/- 0.89 g%), and coefficient of fat absorption (77.3 +/- 20.2% vs control, 97.2 +/- 1.7%) all showed significant differences from the controls.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Bacterial lipase and high-fat diets in canine exocrine pancreatic insufficiency: a new therapy of steatorrhea?
BACKGROUND & AIMS: Nutrients and properties of lipases affect survival of lipolytic activity during aboral gastrointestinal transit. Whether different doses and formulations of bacterial lipase and diets affect steatorrhea was tested in pancreatic-insufficient dogs. METHODS: A dose of 0-600,000 IU of powdered and 135,000 and 300,000 IU of liquid bacterial lipase was given with a standard meal to 5 dogs with ligated pancreatic ducts. In 4 dogs, 0 or 300,000 IU (normal 6-hour postprandial amount) of powder bacterial lipase was also given with five meals containing 850 kcal with different nutrient caloric densities (mixture design). Coefficients of fat absorption during 72-hour fecal balance studies were used to assess treatments. RESULTS: With the standard meal, powder bacterial lipase reduced steatorrhea in a dose-dependent manner (P = 0.03), and 135,000 and 300,000 IU of the liquid form decreased steatorrhea more than powder bacterial lipase (P = 0.017 and 0.057, respectively). Coefficients of fat absorption with 300,000 IU of powder bacterial lipase correlated (r2 = 0.79; P < 0.001) with increasing proportions of fat calories in diets. CONCLUSIONS: Liquid bacterial lipase decreases steatorrhea more than powder, and 300,000 IU of powder bacterial lipase ingested with high-fat meals corrects canine pancreatic steatorrhea. The combination of adequate mixing of small amounts (milligrams) of bacterial lipase and high-fat meals abolishes canine steatorrhea and may abolish human pancreatic steatorrhea.
Animals↗
Role of fat maldigestion in pathogenesis of steatorrhea in ileal resection. Fat digestion after two sequential test meals with and without cholestyramine.
To clarify the role of fat maldigestion in the pathogenesis of steatorrhea in patients with ileal resection the total and aqueous phase concentrations of bile acid and fatty acid were characterized in 8 such patients (5 patients with small ileal resection, bile acid diarrhea, and steatorrhea less than 20 g per day; 3 patients with large ileal resection, fatty acid diarrhea, and steatorrhea greater than 20 g per day) as well as 4 healthy control subjects after a morning and an afternoon liquid test meal. The study was then repeated with cholestyramine, 4 g being administered before each meal to induce fat maldigestion. After a conventional test meal, patients with large resections and severe steatorrhea had significantly lower aqueous phase concentrations of bile acids (and fatty acids) than patients with smaller resections or control subjects, explained in part by intraluminal precipitation of about one-half of the bile acids during digestion. When cholestyramine was administered before the meal, aqueous phase bile acid concentrations decreased in all patients, including the normal control subjects; the degree of fat maldigestion induced in the patients with small resections (and the control subjects) became similar to that present after the conventional test meal in the patients with large resections. Because steatorrhea increased little in the patients with small resections when cholestyramine was administered continuously, the data suggest that fat maldigestion per se does not induce severe fat malabsorption in patients with sufficient anatomical reserve, because such patients can absorb fat efficiently by utilizing the distal small intestine. In patients with large ileal resections, severe steatorrhea is explained in part by the combination of fat maldigestion and decreased surface area. It is also speculated that the steatorrhea occurring in patients with small resections and relatively normal fat digestion during two test meals may be explained by impaired fat digestion which occurs during the final meal of the day, which is often the largest meal.
Adult↗
[Endogenous steatorrhea during total parenteral nutrition. Study of 22 patients with gastrointestinal diseases].
Endogenous steatorrhea has only been evaluated in patients with non-pathological digestive tract. We decided, therefore, to study this parameter in 22 consecutive patients submitted to total parenteral nutrition for severe gastrointestinal diseases. The determination of steatorrhea, creatorrhea, and fecal clearance of alpha 1-antitrypsin was performed by three days stool collections. After 10 days of parenteral nutrition, 13 of the 22 patients still had measurable stool losses and 106 fecal collections were done. In these 13 patients, fecal weight was 610 +/- 130 g.d-1, (mean +/- SEM), steatorrhea was: 3.1 +/- 0.4 g.d-1, creatorrhea was: 1.7 +/- 0.6 g.d-1, alpha 1-antitrypsin clearance was: 58 +/- 13 ml.d-1 (N less than 10 ml.d-1). The mean endogenous steatorrhea was therefore 5 fold larger than normal and creatorrhea 1.8 fold larger than normal. This discrepancy could be due to metabolism of nutrients by colonic bacterial flora. The comparison of patients with and without increased endogenous losses showed significant differences in the mean number of intestinal lesions (1.4 +/- 0.3 versus 0.5 +/- 0.2) and in the presence or absence of ileal involvement (p less than 0.05). A positive correlation was found between steatorrhea and stool weight but not between steatorrhea and creatorrhea or fecal clearance of alpha 1-antitrypsin. This first study of pathological endogenous steatorrhea does not suggest a relationship of this parameter with protein losing enteropathy. The main contribution to increased endogenous losses may be related to increased epithelial cell renewal of the intestine associated with malabsorption. The role of bacterial overgrowth in the gut cannot be ruled out by the present data.
Celiac Disease↗
Fecal fat concentration in patients with steatorrhea.
We predicted that fecal fat concentration (grams of fat per gram of stool wet weight) would be higher in patients with pancreatic steatorrhea than in those with steatorrhea due to gastrointestinal disease. To evaluate this hypothesis, we examined fecal weight, fecal fat excretion, and fecal fat concentration in 19 patients with steatorrhea due to pancreatic insufficiency and in 31 patients whose steatorrhea was due to various gastrointestinal diseases. There was no consistent difference in the severity of steatorrhea or diarrhea between the two groups of patients. Fecal fat concentration, however, was usually higher in patients with pancreatic insufficiency. Fecal fat concentration may be a useful clue in distinguishing pancreatic steatorrhea from steatorrhea due to gastrointestinal disease.
Celiac Disease↗
Acid steatocrit: a simple, rapid gravimetric method to determine steatorrhea.
OBJECTIVES: The detection and evaluation of steatorrhea in a rapid, quantitative fashion are clinically needed in patients with suspected steatorrhea. Our aim was to evaluate the acid steatocrit method, on random spot stools in adults with and without steatorrhea, relative to the qualitative (microscopic) and quantitative assessments for fecal fat. METHODS: Stool samples were collected 72 h after a diet of 100 g of fat per day and randomly from 15 healthy controls, 14 patients with chronic pancreatitis, and seven patients with small bowel disease. All stools had quantitative, qualitative, and acid steatocrit analyses performed for fecal fat. RESULTS: The sensitivity and specificity for the detection of steatorrhea by the spot stool qualitative fecal fat were 78 and 70%, respectively. The spot stool acid steatocrit correlated linearly with the 72-h stool quantitative fecal fat (g/24 h), r = 0.761 and p < 0.001. The acid steatocrit on random spot stools, compared with the 72-h stool quantitative fecal fat, revealed a sensitivity of 100%, a specificity of 95%, and a positive predictive value of 90% for the detection of steatorrhea. It also estimated the quantitative fecal fat. CONCLUSIONS: The acid steatocrit can be performed accurately on random spot stools and can be used to detect the presence of steatorrhea and estimate the quantitative fecal fat. This assay can be done with readily available equipment for rapid evaluation. Use of a spot stool sample simplifies the acid steatocrit, further improving on the practicality of this test. This study also confirms the clinical usefulness of this simplified method to detect steatorrhea.
Adult↗
Can pancreatic steatorrhea be diagnosed without chemical analysis?
CONCLUSION: Visual observation of feces, considering fecal output, is considered to be an excellent method of detection of steatorrhea when judged by experienced doctors. METHODS: Feces from 192 patients with untreated chronic pancreatitis or under pancreatic enzyme therapy were investigated. Feces were collected for three consecutive days and homogenized with water. Fecal samples were freeze-dried and analyzed for fatty acids by gas chromatography (GLC). The quantity of fat was calculated from the amount of fatty acid to obtain daily fecal fat excretion. Comparison of GLC method with van de Kamer method gave a significant (p < 0.01) positive correlation with correlation coefficient of 0.916 (n = 38). Steatorrhea was defined as fecal fat excretion exceeding 5 g/d. Mild steatorrhea was defined as 5-10 g/d, and severe steatorrhea as more than 10 g/d. RESULTS: Three visual identification items were used to consider fecal output exceeding 200 g/d: fecal fat concentration exceeding 4%, appearance, and odor. The results were compared with the results from GLC method. Detection of steatorrhea by means of visual properties was the most accurate, and correlation coefficient was 0.843 (p < 0.01) by Spearman's rank correlation test. This detection method was also significantly effective for differentiation of normal stool from mild and severe steatorrhea. The sensitivity and specificity were 89.3 and 91.1%, respectively, indicating a favorable result.
Celiac Disease↗
Esophageal impairment in adult celiac disease with steatorrhea.
OBJECTIVE: A high prevalence of reflux esophagitis in celiac children and gut motor disorders in adult patients have been described. The aim of this study is to investigate the prevalence of esophageal symptoms and the esophageal motility pattern in adult celiac patients before and after gluten-free diet. METHODS: In 22 consecutive adult celiac patients, before and after gluten-free diet, and in controls we calculated an esophageal symptom score regarding heartburn, regurgitation, dysphagia, and chest pain, and performed esophageal manometry using a constantly perfused multilumen catheter. RESULTS: Patients were divided into two groups: with and without steatorrhea. Before gluten-free diet, the prevalence of esophageal symptoms was 45.5 % in all patients, but was significantly higher in patients with steatorrhea than in those without and in 44 control subjects (80% vs 16.7% and 27%, p < 0.05). Lower esophageal sphincter pressure was 17.5+/-5.3 in all patients, but was significantly lower in patients with steatorrhea than in patients without steatorrhea and 11 controls subjects (13.1+/-4.1 vs 21.0+/-2.9 and 20.7+/-3.7 mm Hg (mean+/-SD, p < 0.05). After the diet, the prevalence of esophageal symptoms diminished in all patients (9% vs 45.4%, p < 0.05) and lower esophageal sphincter pressure, measured in 13 patients, increased (19.0+/-3.7 vs 15.7+/-5.3 mm Hg, p < 0.05). CONCLUSION: Adult celiac patients with steatorrhea present a higher prevalence of esophageal symptoms and a lowered lower esophageal sphincter pressure compared with celiac patients without steatorrhea and control subjects, but these phenomena can be reverted to control levels by gluten-free diet.
Adolescent↗
Serum cathodic trypsin-like immunoreactivity, pancreatic lipase, and pancreatic isoamylase as diagnostic tests of chronic pancreatitis or pancreatic steatorrhea.
We compared serum concentrations of cathodic trypsin-like immunoreactivity, pancreatic lipase, and pancreatic isoamylase as diagnostic tests of chronic pancreatitis (and of pancreatic steatorrhea in the 41 patients with steatorrhea) in 105 patients (57 men, 48 women) consecutively investigated because of clinical suspicion of chronic pancreatitis. Chronic pancreatitis (36 patients), pancreatic steatorrhea (24 patients), and other diseases were diagnosed without knowledge of the serum levels of the three enzymes. When evaluated by means of receiver operating characteristic curves, no differences were found in diagnostic performance of the enzymes with regard to chronic pancreatitis or pancreatic steatorrhea. The sensitivity and specificity for recognition of chronic pancreatitis ranged from 0.306 to 0.444 and from 0.942 to 0.986 when the discrimination values were chosen to give highest efficiencies. The similar ranges for pancreatic steatorrhea were 0.500-0.708 and 0.882-0.941. In conclusion, none of the three enzymes had any advantage over the others as diagnostic tests of chronic pancreatitis or of pancreatic steatorrhea. Only positive test results have clinical importance because of the low sensitivities of the three enzymes.
Adult↗
Fecal fat concentration in the differential diagnosis of steatorrhea.
Many approaches have been proposed to differentiate between steatorrhea due to pancreatic insufficiency and intestinal disease. Bo-Linn and Fordtran recently suggested that fecal fat concentration (FFC) is a useful screening test for this distinction. Our aim was to validate their result in a large group of patients. Fecal fat concentrations were calculated for 613 fecal fat tests in 538 patients. Included were 88 patients with pancreatic steatorrhea (13 pancreatic carcinoma, 6 cystic fibrosis, and 69 chronic pancreatitis) and 525 with nonpancreatic steatorrhea. The mean FFC of patients with pancreatic disease (15.0 +/- 1.9 g%, mean +/- SEM) was significantly higher than that of patients with other diseases causing malabsorption (8.9 +/- 0.3 g%, p less than 0.001). Forty-two percent of patients with pancreatic steatorrhea had an FFC below 10 g%. The overlapping of the FFC of steatorrhea due to pancreatic disease and that produced by celiac disease, gastric resection, and other conditions suggests that this approach does not differentiate between pancreatic and intestinal steatorrhea.
Celiac Disease↗
Association between steatorrhea, growth, and immunologic status in children with perinatally acquired HIV infection.
OBJECTIVE: To examine the prevalence of steatorrhea and exocrine pancreatic insufficiency (EPI) and their association with growth and immune status variables in children with perinatally acquired human immunodeficiency virus (HIV) infection. DESIGN: Cross-sectional study. SETTING: Tertiary care HIV subspecialty practice. PARTICIPANTS: Children with perinatally acquired HIV infection. Exclusion criteria included being younger than 1 year and receiving mineral oil as a medication. METHODS: Weight, height, and upper arm anthropometric variables were measured. Spot stool samples were analyzed for steatorrhea using the Sudan III qualitative test and for EPI using fecal elastase-1 enzyme assay. Hormone-stimulated pancreatic function testing and 72-hour stool and dietary fat sample collection were performed when fecal elastase-1 enzyme was in the range of EPI, defined as less than 200 microgram/g. HIV RNA viral load, CD4 status, type of antiretroviral therapy, and biochemical evidence of hepatobiliary disease were measured within 3 months of stool sample collection. z Scores were computed for height, weight, triceps skinfold, and upper arm muscle area. RESULTS: We enrolled 44 patients (23 girls [52%]) with a mean +/- SD age of 7.4 +/- 3.1 years. None had hepatobiliary disease. The prevalence of steatorrhea was 39% (95% confidence interval, 23%-56%). The prevalence of EPI was 0% (95% confidence interval, 0%-9%). There were no associations between steatorrhea and EPI, growth, HIV RNA viral load, CD4 status, or type of antiretroviral therapy. Older children had decreased z scores for height (r = -0.42; P =.006). CONCLUSIONS: The clinical significance of steatorrhea in children with HIV infection is unclear. Furthermore, its evaluation should focus on nonpancreas-based conditions. Continual close monitoring of growth is essential in children with HIV infection.
Celiac Disease↗
Steatorrhea, a simple and rapid method of diagnosis.
A simple and rapid method for the diagnosis of steatorrhea is described. The method is based on the assessment of the difference of specific gravity and lipophilic property between a normal stool and that in steatorrhea, using a benzene-NaBr system. The stool samples are dried, pulverized, and then investigated. Steatorrhea is defined either as a fat or more in a 24-hour sample. Stool samples of 71 infants and children were examined. Among these were 23 healthy subjects, 10 with upper respiratory tract infections, and 6 with pneumonia. A further 31 children had celiac disease, 9 of them were on a gluten-free diet, and one child had cystic fibrosis. The procedure described renders single stool samples suitable for the assessment of steatorrhea. As a screening test the method proved to be rapid and accurate in the diagnosis of steatorrhea.
Adolescent↗
Intestinal lymphangiectasia in a patient with autoimmune polyglandular disease type I and steatorrhea.
Steatorrhea is seen in 18-24% of patients with autoimmune polyglandular disease (APD) type 1. The etiology and pathophysiology of the steatorrhea in this disease are unknown. We present a patient with APD type 1 and steatorrhea in whom biopsies revealed intestinal lymphangiectasia. This association has not been previously described. Intestinal lymphangiectasia may explain the steatorrhea in some patients with ADP type 1. As blind intestinal biopsies may miss areas of intestinal lymphangiectasia, endoscopically directed intestinal biopsies should be included in the evaluation of steatorrhea in APD type 1.
Celiac Disease↗