Steatorrhea In Patients Research Articles

Dyslipidemia and its features in primary biliary cholangitis

Primary biliary cholangitis, previously known as primary biliary cirrhosis, is a rare autoimmune liver disease that mostly affects women. Disorder of biliary excretion and enterohepatic circulation of bile acids in patients with primary biliary cholangitis in the early stages of the disease leads to their insufficient flow into the intestine and ingestion of bile acids into the general bloodstream. Insufficient intake of bile acids into the duodenum contributes to malabsorption, energetic malnutrition, and a slowly progressing weight loss. Pathophysiological mechanisms of the development of weight loss are related to impaired emulsification of fats and decreased absorption of hydrolyzed products - fatty acids and monoglycerides, steatorrhea in patients with primary biliary cholangitis as well as to dysbiosis of intestinal microflora. Already in the early stages of the disease, this leads to accelerated ß-oxidation of fatty acids, which is aimed at compensating for the developing nutritional energy deficiency. Entry of bile acids into the general bloodstream in primary biliary cholangitis is accompanied by dyslipidemia. The mechanism of hyperlipidemia in patients with primary biliary cholangitis differs from that in other conditions because along with the increase in total cholesterol, there is an increase in high-density lipoproteins and the appearance of unusual lipoprotein X (Lp-X). The appearance of the latter is most likely a protective reaction of the body aimed at the inactivation of bile acids detergent action on membrane structures of blood-forming elements and vascular endotheliocytes. Exactly bile acids, but not the content of total cholesterol, correlates with the level of lipoprotein X and determine its formation. Concomitant hypercholesterolemia in patients with primary biliary cholangitis is also aimed at neutralizing the detergent action of bile acids that entered the general bloodstream and is most likely a compensatory reaction of the body. “Abnormal” hypercholesterolemia in primary biliary cholangitis can serve as a model system to search for and develop new ways of dyslipidemia treatment, as it proceeds without increasing the frequency of cardiovascular events.

Features of Lipid Metabolism Disorders in Primary Biliary Cholangitis.

Primary biliary cholangitis (PBC), previously known as primary biliary cirrhosis, is an autoimmune liver disease that mostly affects women. A progressive disorder in the processes of bile secretion and enterohepatic bile salts circulation in patients with PBC already in its early stages, leading to an insufficient release of bile acids into the bowel and their entry into the systemic circulation. Insufficient bile acids released into the duodenum contributes to the development of malabsorption, energy malnutrition, and slowly progressive weight loss. The pathophysiological mechanisms of weight loss and its slow progression are associated with the deterioration of the fat emulsification processes and with the reduced absorption of hydrolyzed products, such as fatty acids and monoglycerides, with steatorrhea in patients with PBC, as well as in those with gut dysbiosis. Just in the early stages of the disease, this results in accelerated fatty acid β-oxidation that is aimed at compensating for progressive energy malnutrition. The entry of bile acids into the systemic circulation in PBC is accompanied by dyslipidemia. The mechanism of hyperlipidemia in patients with PBC differs from that in other conditions because along with an increase in total cholesterol (TC), there are elevated high-density lipoprotein levels and the appearance of unusual lipoprotein X (Lp-X). The appearance of Lp-X is most likely to be the body's protective reaction to inactivate the detergent effect of bile acids on the membrane structures of blood corpuscles and vascular endothelial cells. It is bile acids, rather than TC levels, that correlate with the content of Lp-X and determine its formation. Concomitant hypercholesterolemia in patients with PBC is also aimed at neutralizing the detergent effect of bile acids that have entered the systemic circulation and is most likely a compensatory reaction of the body. "Anomalous" hypercholesterolemia in PBC can serve as a model system for the search and development of new methods for the treatment of dyslipidemia since it occurs without an increase in the incidence of cardiovascular events.

Exocrine pancreatic insufficiency after bariatric surgery

BackgroundExocrine pancreatic insufficiency (EPI) is a known complication of upper gastrointestinal surgery and has recently been associated with bariatric surgery. Our objectives were to determine the incidence of EPI in patients who underwent bariatric surgery and to identify the type of bariatric procedure most associated with EPI. MethodsThis retrospective cohort analysis included patients age ≥18 years who underwent bariatric surgery at Mayo Clinic between 2010 and 2020. Patients with a history of other gastrointestinal or hepatobiliary resection, revision of bariatric surgery, EPI prior to surgery, and surgery greater than >10 years earlier were excluded from the study. Characteristics were compared between two groups based on type of bariatric surgery including Roux-en-Y gastric bypass (RYGB) or gastric sleeve (GS). Characteristics were also analyzed between patients with RYGB who developed post-operative steatorrhea and those who did not. ResultsOf 150 patients, 126 underwent RYGB while 24 patients had GS. Thirty-one (20.6%) patients developed post-operative steatorrhea and 14 (9.3%) were diagnosed with EPI. Mean pancreatic elastase level was 287 ± 156 mcg/g and fecal fat level 31 ± 22 g/d. There was a significantly higher proportion of post-operative steatorrhea in patients who underwent RYGB compared to gastric sleeve surgery (p = 0.029). ConclusionThe incidence of EPI after bariatric surgery in our cohort was 9.3%. Overall, patients who underwent RYGB had higher rates of EPI (10.3%) than those who had GS (4.2%). Clinicians should be aware of EPI as a cause for steatorrhea in patients who underwent bariatric surgery and consider treatment with enzyme replacement therapy.

Deficiencies in specific nutrients and micronutrients in patients with exocrine pancreatic insufficiency

Exocrine pancreatic insufficiency (EPI) is a known complication of upper gastrointestinal surgery and has recently been associated with bariatric surgery. Our objectives were to determine the incidence of EPI in patients who underwent bariatric surgery and to identify the type of bariatric procedure most associated with EPI.This retrospective cohort analysis included patients age ≥18 years who underwent bariatric surgery at Mayo Clinic between 2010 and 2020. Patients with a history of other gastrointestinal or hepatobiliary resection, revision of bariatric surgery, EPI prior to surgery, and surgery greater than >10 years earlier were excluded from the study. Characteristics were compared between two groups based on type of bariatric surgery including Roux-en-Y gastric bypass (RYGB) or gastric sleeve (GS). Characteristics were also analyzed between patients with RYGB who developed post-operative steatorrhea and those who did not.Of 150 patients, 126 underwent RYGB while 24 patients had GS. Thirty-one (20.6%) patients developed post-operative steatorrhea and 14 (9.3%) were diagnosed with EPI. Mean pancreatic elastase level was 287 ± 156 mcg/g and fecal fat level 31 ± 22 g/d. There was a significantly higher proportion of post-operative steatorrhea in patients who underwent RYGB compared to gastric sleeve surgery (p = 0.029).The incidence of EPI after bariatric surgery in our cohort was 9.3%. Overall, patients who underwent RYGB had higher rates of EPI (10.3%) than those who had GS (4.2%). Clinicians should be aware of EPI as a cause for steatorrhea in patients who underwent bariatric surgery and consider treatment with enzyme replacement therapy.

SUN-P084: Fecal Elastase Fails to Detect Steatorrhea in Patients with Locally Advanced Pancreatic Cancer

SUN-P084: Fecal Elastase Fails to Detect Steatorrhea in Patients with Locally Advanced Pancreatic Cancer

Effect of colesevelam on faecal bile acids and bowel functions in diarrhoea-predominant irritable bowel syndrome.

About one-third of patients with IBS-diarrhoea (irritable bowel syndrome-D) have evidence of increased bile acid synthesis or excretion. To assess effects of the bile acid sequestrant, colesevelam, on faecal excretion of BAs, hepatic BA synthesis and diarrhoea in IBS-D; to appraise whether individual or random stool samples accurately reflect 48-h total faecal bile acid excretion and proportions of the main bile acids excreted and to study the faecal fat excretion in response to colesevelam. A single-centre, unblinded, single-dose trial of effects of colesevelam, 1875mg [3 tablets (625mg tablets)] orally, twice daily, for 10days on total 48-h faecal bile acid excretion and fasting serum C4 (7α-hydroxy-4-cholesten-3-one; surrogate of hepatic bile acid synthesis). Stool diaries documented bowel functions for 8days prior and 8days during colesevelam treatment. Stool 48-h samples and fasting serum were collected for faecal fat, faecal bile acid and serum C4. Colesevelam was associated with significantly increased faecal total bile acid excretion and deoxycholic acid excretion, increased serum C4 and more solid stool consistency. There was a significant inverse correlation between number of bowel movements per week and the total bile acid sequestered into stool during the last 48h of treatment. Random stool samples did not accurately reflect 48-h total or individual faecal bile acid excretion. Sequestration of bile acids by colesevelam did not increase faecal fat. Colesevelam increases delivery of bile acids to stool while improving stool consistency, and increases hepatic bile acid synthesis, avoiding steatorrhoea in patients with IBS-D. Overall effects are consistent with luminal bile acid sequestration by colesevelam.

Fecal elastase-1 is useful in the detection of steatorrhea in patients with pancreatic diseases but not after pancreatic resection

BackgroundFecal elastase-1(FE-1) has been suggested as an alternative to steatorrhea quantification to evaluate pancreatic insufficiency, but its diagnostic performance has not been compared with steatorrhea in chronic pancreatitis or after pancreatic resection. MethodsThe relationship between steatorrhea and FE-1 was studied in patients with chronic pancreatic disorders or pancreatic resection. Student's t test and ANOVA were used for statistical analysis, accepting 0.05 as limit for significance. ResultsEighty-two patients were studied (42 non-operated; 40 previously submitted to pancreatic resection). Fat output was higher in operated than non-operated patients (29.2 ± 3.1 vs 9.9 ± 2.2 g/day, p < 0.001) FE-1 was more severely reduced in operated patients (202 ± 32.3 μg/g in non operated vs 68.6 ± 18.2 in operated patients; p < 0.001). Steatorrhea was significantly more severe in operated patients across different levels of FE-1. The relationship between FE-1 and steatorrhea was described by a power regression model, with a regression line significantly different in operated and non-operated patients (p < 0.001). A steatorrhea of 7 g (upper limit of normal range) was calculated by this regression line when FE-1 is 15 μg/g in non-operated, but as high as 225 μg/g in operated patients. ConclusionFE-1 is useful to identify pancreatic insufficiency. Steatorrhea is anticipated in non-operated patients only when FE-1 is below the limit for a confident measurement of our assay. In operated patients, steatorrhea may be present even if FE-1 is only slightly reduced, that suggests a role for non pancreatic factors. FE1 is not useful to identify operated patients at risk of malabsorption.

M1387 Safety and Efficacy of Immediate-Release Pancrelipase, Viokase®16, With Proton Pump Inhibitor Therapy for Correction of Steatorrhea in Patients With Chronic Pancreatitis With Exocrine Pancreatic Insufficiency

M1387 Safety and Efficacy of Immediate-Release Pancrelipase, Viokase®16, With Proton Pump Inhibitor Therapy for Correction of Steatorrhea in Patients With Chronic Pancreatitis With Exocrine Pancreatic Insufficiency

An Enteric-Coated High-Buffered Pancrelipase Reduces Steatorrhea in Patients with Cystic Fibrosis: A Prospective, Randomized Study

Objective Enteric-coated (EC) high-buffered (2.5 mEq [2.5 mmol] bicarbonate per capsule) pancrelipase microsphere enzymes were compared to EC-nonbuffered pancreatic enzymes for efficacy in reducing steatorrhea in patients with cystic fibrosis. Design Prospective, randomized, controlled trial using a crossover design with each subject as his/her own control. Subjects/Setting Eighteen subjects with cystic fibrosis, who had pancreatic insufficiency and required large enzyme doses, were studied over two consecutive 7-day treatment periods. Intervention Each 7-day period consisted of 3 days at home followed by 4 days in a general clinical research center for careful control of diets, enzyme lipase doses (given at approximately 50% of the subject’s usual lipase dose), and carmine red-labeled stool collections for 72-hour fecal fat balance studies. Main Outcome Measure Fecal fat excretion. Statistical Analyses Performed Differences in fat excretion, when each subject received EC–high-buffered pancrelipase vs EC-nonbuffered enzymes, were compared using linear modeling. Results Mean fat excretion decreased significantly in each subject during periods when given EC–high-buffered pancrelipase compared with periods when given EC-nonbuffered enzymes (fat excretion 18.2% vs 24.9% or fat absorption 81.8% vs 75.1%, respectively; P=0.01). Thirteen of 18 subjects (72%) excreted less fat when receiving EC–high-buffered pancrelipase whereas 10 (56%) decreased fat excretion by more than 5%, and five subjects did not respond. Conclusions EC–high-buffered pancrelipase decreased fat excretion, symbolizing improved fat absorption, when compared with EC-nonbuffered pancreatic enzymes given at equivalent, reduced (approximately 50% of usual) lipase doses in nourished subjects with cystic fibrosis and mild pulmonary disease.

Etiology and Initial Management of Short Bowel Syndrome

o he normal human small intestine ranges between 3 and 8 m in length, depending on whether measureent is made by radiologic or surgical techniques or at utopsy when the intestine may be desicated.1–5 Short owel syndrome is defined in adults as 200 cm of small ntestine. Although usually acquired because of one or ore enterectomies, short bowel syndrome may also be ongenitally acquired. Nutrient, electrolyte, and fluid bsorption is proportional to the amount of residual ntestine. The degree of intestinal function is better escribed in terms of energy absorption/loss rather than ength of residual intestine.6 Intestinal failure may be efined as the inability to sustain adequate nutritional, lectrolyte, or hydrational status in the absence of speialized nutritional support. This requires an increase in ral intake because absorption is compromised. Clinially, nutrient assimilation is a function of intake and bsorption. As such, some patients with short bowel yndrome will not have sufficient loss of functional caacity as to develop intestinal failure. Significant indiidual variability in jejunal absorption efficiency may be ncountered.7 The patients with the greatest risk for development of ehydration, generalized protein-calorie malnutrition, nd multiple nutrient deficiencies are those with a duoenostomy or jejunoileal anastomosis and 35 cm of esidual small intestine; jejunocolic or ileocoloic anastoosis, and 60 cm of residual small intestine; or end ejunostomy with 115 cm of residual small intesine.6,8–11 Those patients with residual colon in continuty will have enhanced energy and fluid absorption. ence, such patients can tolerate greater loss of small ntestine and retain their nutritional autonomy.

Study on pancreatic steatorrhea in patients with chronic pancreatitis

Study on pancreatic steatorrhea in patients with chronic pancreatitis

What to Do when a Patient with Exocrine Pancreatic Insufficiency Does Not Respond to Pancreatic Enzyme Substitution

In the majority of patients, pancreatin microsphere preparations containing 25,000–40,000 FIP units of lipase will lead to a clinical improvement and reduction of steatorrhea in patients with exocrine pancreatic insufficiency. In patients failing to respond, the following stepwise procedure is recommended: increasing enzyme dosage; checking the patient’s compliance; reevaluating the diagnosis; and as a last resort to decrease fat intake or adding H₂-blockers or proton pump inhibitors. Although this stepwise procedure is time-consuming, it is necessary to prevent in patients not responding to pancreatic enzyme substitution the development of late complications of exocrine pancreatic insufficiency.

Prevalence and significance of steatorrhea in patients with active Graves’ disease

Objective: The aim of this study was to determine the prevalence of steatorrhea in patients with Graves’ disease and to assess its significance and correlation with changes in body mass index (BMI), coefficient of fat absorption (COFA), and pancreatic exocrine function in these patients. Methods: Daily dietary fat intake, 24 h fecal fat, COFA, fecal chymotrypsin activity (as an index of pancreatic exocrine function), and total T3, T4, and TSH levels were assessed in 28 patients with active Graves’ disease. In 24 patients, reassessment was done after attaining a euthyroid state with carbimazole therapy. Results: In the thyrotoxic state, 13 of 28 patients had steatorrhea, whereas 15 had normal (<6 g/day) fat excretion (11.4 ± 6.7 g vs 2.9 ± 0.8 g, p = 0.0007). Daily fat intake, basal BMI, and serum T3 and T4 levels were similar in the steatorrheic and nonsteatorrheic groups. The mean COFA of the steatorrheic group was significantly lower than that of nonsteatorrheic group (91.6% ± 4.8% vs 97.7% ± 0.9%, respectively; p = 0.0006). In the steatorrheic group, fat excretion and COFA normalized after attainment of euthyroidism (changes in fat excretion and COFA = 7.3% ± 6.3 g/day and 7.7% ± 5.4%, respectively). Fecal chymotrypsin levels were similar in the steatorrheic and nonsteatorrheic thyrotoxics and in 16 healthy control subjects. The levels did not show any significant changes following attainment of euthyroid status. Conclusion: Steatorrhea associated with a decrease in COFA can occur in a reversible manner in 46% of patients with Graves’ disease. However, steatorrhea in these patients is not linked with weight loss or with pancreatic exocrine dysfunction.

Prevalence and significance of steatorrhea in patients with active Graves' disease.

The aim of this study was to determine the prevalence of steatorrhea in patients with Graves' disease and to assess its significance and correlation with changes in body mass index (BMI), coefficient of fat absorption (COFA), and pancreatic exocrine function in these patients. Daily dietary fat intake, 24 h fecal fat, COFA, fecal chymotrypsin activity (as an index of pancreatic exocrine function), and total T3, T4, and TSH levels were assessed in 28 patients with active Graves' disease. In 24 patients, reassessment was done after attaining a euthyroid state with carbimazole therapy. In the thyrotoxic state, 13 of 28 patients had steatorrhea, whereas 15 had normal (<6 g/day) fat excretion (11.4 +/- 6.7 g vs 2.9 +/- 0.8 g, p = 0.0007). Daily fat intake, basal BMI, and serum T3 and T4 levels were similar in the steatorrheic and nonsteatorrheic groups. The mean COFA of the steatorrheic group was significantly lower than that of nonsteatorrheic group (91.6% +/- 4.8% vs 97.7% +/- 0.9%, respectively; p = 0.0006). In the steatorrheic group, fat excretion and COFA normalized after attainment of euthyroidism (changes in fat excretion and COFA = 7.3% +/- 6.3 g/day and 7.7% +/- 5.4%, respectively). Fecal chymotrypsin levels were similar in the steatorrheic and nonsteatorrheic thyrotoxics and in 16 healthy control subjects. The levels did not show any significant changes following attainment of euthyroid status. Steatorrhea associated with a decrease in COFA can occur in a reversible manner in 46% of patients with Graves' disease. However, steatorrhea in these patients is not linked with weight loss or with pancreatic exocrine dysfunction.

Efficacy of a pancreatic enzyme formulation in the treatment of steatorrhea in patients with chronic pancreatitis

The effect of an acid-protected pancreatic enzyme preparation was evaluated in 10 patients with chronic pancreatitis and steatorrhea. (Twelve patients were enrolled but two withdrew because of poor compliance.) Fecal fat excretion and stool weight were measured, a p-aminobenzoic acid (PABA) test was performed, and gastrointestinal symptoms were assessed before and after 4 weeks of treatment with a standardized dose of pancreatic enzymes (two capsules three times daily, each capsule containing 13,000 FU [Italian Official Pharmacopeia] units of lipase). After treatment, we observed a statistically significant reduction in fecal fat excretion and stool weight as well as improved PABA test results and symptoms. This study confirmed the efficacy of this pancreatic enzyme preparation in the treatment of patients with pancreatogenic steatorrhea.

Faecal triglycerides and fatty acids in the differential diagnosis of pancreatic insufficiency and intestinal malabsorption in patients with low fat intakes.

To investigate possible parameters for the differential diagnosis of steatorrhoea in patients with low fat intakes, faecal specimens were analysed from 15 patients with steatorrhoea due to chronic pancreatitis and seven patients with steatorrhoea due to intestinal malabsorption. The fat intakes of the patients ranged from 30.1 to 60 g, less than the average in American and European patients. The group with pancreatic steatorrhoea showed a significantly lower faecal output than the group with intestinal steatorrhoea but the two groups did not differ significantly in their total faecal fat excretion or concentration. The percentage triglycerides and the molecular ratio of triglycerides to fatty acids in the faeces were significantly higher (P < 0.01) in the group with pancreatic steatorrhoea than in those with intestinal steatorrhoea. The molecular percentage ratio of triglycerides to fatty acids was 6.8 +/- 2.2 for the chronic pancreatitis group and 2.4 +/- 1.0 for the intestinal malabsorption group; while the respective faecal hydroxy fatty acid contents were 3.1 +/- 3.6% and 10.1 +/- 3.3% (means +/- SDs). These latter two parameters appeared to be the most valuable for distinguishing the two forms of steatorrhoea.

Dietary fat in cystic fibrosis

Dietary fat in cystic fibrosis

Association of Primary Sclerosing Cholangitis and Celiac Disease: Fact or Fancy?

The association of primary sclerosing cholangitis and celiac disease was observed in three patients, an association not previously reported. All three patients were men who presented with chronic cholestatic liver disease at ages 32, 46, and 62 years, respectively. In each patient, endoscopic retrograde cholangiography showed the typical findings of primary sclerosing cholangitis. Histologic features of liver biopsy were compatible with the diagnosis. Two patients had associated chronic ulcerative colitis. All three patients complained of frequent loose stools and weight loss; subsequent testing showed severe steatorrhea (204 to 323 mmolfd of fecal fat on a 100 g fat diet). Total villous atrophy was found in all three patients on histologic examination of the small bowel. Celiac disease was diagnosed at the time of presentation in two patients who had primary sclerosing cholangitis and was diagnosed three years after the onset of primary sclerosing cholangitis in the third patient. The celiac disease responded to a gluten–free diet in each patient whereas the primary sclerosing cholangitis was not affected by dietary treatment. The possibility of a chance association of primary sclerosing cholangitis and celiac disease cannot be accurately assessed but seems unlikely given the rarity of both diseases. The relationship between the two diseases remains unknown, although an immunologic connection is suspected. Celiac disease should be considered in the differential diagnosis of severe steatorrhea in patients with primary sclerosing cholangitis.

Alterations in Digestive Function Caused by Pancreatic Disease

Pancreatic exocrine secretion is regulated by a complex interaction of meal-stimulated neurohormonal reflexes. Pancreatic enzyme output must be reduced to less than 10 per cent of normal before fat absorption is appreciably impaired, proving that the pancreas secretes a large surplus of enzymes. Surgical therapy does not improve pancreatic exocrine insufficiency, and partial pancreatic resection frequently precipitates steatorrhea in patients with chronic pancreatitis. Therefore, pancreatic resection should be undertaken cautiously in patients who do not yet have clinically evident exocrine insufficiency. In most patients, oral pancreatic enzymes will control diarrhea secondary to steatorrhea. In others, concurrent administration of an H2 blocker is required to reduce gastric acidity and prevent enzyme inactivation in the stomach. Formulations with an acid-resistant coating are also effective in some patients. However, complete normalization of fat absorption with restoration of body weight and nutritional well-being requires careful management of multiple dietary and behavioral factors, as well as long-term follow-up. Unfortunately, this appears to be an elusive goal, as many patients with chronic pancreatitis continue to die of malnutrition.

Duodenal instillation of pancreatin does not abolish steatorrhea in patients with pancreatic insufficiency.

Many believe that intragastric deactivation of lipase accounts for the frequent failure of orally ingested pancreatic enzymes to normalize fat absorption in patients with pancreatic insufficiency. To test this hypothesis, we measured fat absorption from a large test meal in six patients with pancreatic insufficiency after we had instilled Viokase directly into the postcibal duodenum in two doses, one to deliver lipase at about 10% of normal secretory rates and the other at four times this rate. Direct duodenal instillation of neither the low nor the high dose of Viokase, nor the low dose of Viokase plus sodium bicarbonate, normalized fat absorption from the test meal; none of these duodenal instillations significantly improved fat absorption over that after the test meal plus orally ingested Viokase. Despite these various treatments, the patients excreted an average of 25.5 g of dietary fat as opposed to 2.1 g excreted by six normal subjects after the same meal. We conclude that more than just intragastric destruction of lipase underlies the frequent failure of orally ingested pancreatin to normalize fat absorption in pancreatic insufficiency.