Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with cystic fibrosis (CF) and pancreatic insufficiency usually have decreased linoleic and increased oleic, palmitoleic and eicosatrienoic (20:3 omega 9) acids compared to normal values of blood and tissue lipids. These changes are consistent with early essential fatty acid deficiency and are observed despite the regular use of exogenous pancreatic enzyme supplementation. As part of a study to determine the relative role of malabsorption as the etiology for the altered fatty acid status, the change in total plasma fatty acids and in area percent of plasma linoleic acid was determined in CF patients and control subjects following the ingestion of various lipid supplements, including two safflower oil preparations and two structured lipid preparations. Fasting subjects consumed 36 g of lipid in a milkshake containing 15 g of protein and 45 g of carbohydrate. Plasma samples obtained 0, 2, 4, 6 and 8 hr after the meal showed that the CF patients absorbed all preparations when administered with their regular dose of pancreatic enzyme supplement. Comparison of the patterns of increase for total plasma fatty acids and area percent of plasma linoleic acid following the administration of the different lipid supplements in CF patients and control subjects suggests that malabsorption alone is not the cause of the abnormal fatty acid composition in the lipids of CF patients and that increased caloric intake along with consumption of adequate amounts of linoleic acid should improve the linoleic acid status of CF patients; there may be selectively increased metabolism of certain fatty acids from the ingested lipids in the relatively malnourished CF patient compared to control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Absorption of safflower oil and structured lipid preparations in patients with cystic fibrosis. 361 73

Chronic pancreatic insufficiency (CPI) was induced in male Wistar rats by the injection of a zein-oleic acid-linoleic acid solution into their pancreaticobiliary ducts. Animals injected developed severe pancreatic atrophy with fibrosis and greater than 90% loss of pancreatic enzyme content. The animals also developed malabsorption of fat and bentiromide. Three weeks after the CPI lesion was induced, animals were randomized to receive cerulein 2 micrograms/kg twice daily subcutaneously or saline twice daily subcutaneously for 2 weeks. Cerulein significantly increased pancreatic trypsinogen (p less than 0.03), amylase (p less than 0.01), lipase (p less than 0.02), DNA (p less than 0.02), and RNA (p less than 0.01) content and improved fat and bentiromide malabsorption as compared to saline (p less than 0.05). We conclude that cerulein therapy can cause significant hyperplasia of pancreatic acinar parenchyma in an animal model of CPI and that this therapy can partially reverse malabsorption.
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PMID:Cerulein induces hyperplasia of the pancreas in a rat model of chronic pancreatic insufficiency. 362 23

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.
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PMID:Raised fecal fat concentration is not a valid indicator of pancreatic steatorrhea. 364 27

Pancreatic enzyme substitution may principally be used in few indications, whereof most of them are only relative. The most obvious indication is malabsorption in chronic pancreatic insufficiency, which is always associated with an advanced form of the disease. Only when the exocrine secretory capacity of the pancreas is 2% or less does the patient exhibit diarrhea with a daily excretion of 25 g of fat or more on a normal diet. There are also strong indications that pain can be controlled in some patients with chronic pancreatitis, and the mechanism for this can be given a plausible explanation. As the pancreatic enzymes (with a few interesting exceptions) are resistant to the hydrochloric acid of the stomach, the galenic preparation must be given attention, and means of reducing the amount of acid in the stomach can be considered. However, the patients' compliance is just as important; the dosage must be individualized. The enzyme preparations must be easy to handle and all patients on regular medication must be given full information of the goals of the therapy. The socio-psychological side effects of the chronic disease should also be considered to get an optimal effect of the enzyme substitution in pancreatic disease.
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PMID:Enzyme substitution in pancreatic disease. 365 Jan 82

Serum immunoreactive cationic trypsinogen levels were determined in 99 control subjects and 381 cystic fibrosis (CF) patients. To evaluate the status of the exocrine pancreas all CF patients had previously undergone fecal fat balance studies and/or pancreatic stimulation tests. Three hundred fourteen CF patients had fat malabsorption and/or had inadequate pancreatic enzyme secretion (pancreatic insufficiency) requiring oral pancreatic enzyme supplements with meals. Sixty-seven CF patients did not have fat malabsorption and/or had adequate enzyme secretion (pancreatic sufficiency) and were not receiving pancreatic enzyme supplements with meals. Mean serum trypsinogen in 99 control subjects was 31.4 +/- 14.8 micrograms/liter (+/- 2 SD) and levels did not vary with age or sex. In CF infants (less than 2 yr) with pancreatic insufficiency, mean serum trypsinogen was significantly above the non-CF values (p less than 0.001). Ninety-one percent of the CF infants had elevated levels. Serum trypsinogen values in the pancreatic insufficient group declined steeply up to 5 years, reaching subnormal values by age 6. An equation was developed which described these age-related changes very accurately. Only six CF patients with pancreatic insufficiency had serum trypsinogen levels above the 95% confidence limits of this equation. In contrast, there was no age related decline in serum trypsinogen among the CF group with pancreatic sufficiency. Under 7 yr, serum trypsinogen failed to distinguish the two groups. In those over 7 yr of age, however, serum trypsinogen was significantly higher than the CF group with pancreatic insufficiency (p less than 0.001), and 93% had values within or above the control range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Age-related alterations of immunoreactive pancreatic cationic trypsinogen in sera from cystic fibrosis patients with and without pancreatic insufficiency. 370 9

Twenty patients with exocrine pancreatic insufficiency secondary to alcohol abuse were studied for the presence of bile salt malabsorption. Fecal bile salts and fecal fat excretion were determined in 15 patients receiving pancreatic enzyme therapy, not receiving enzyme therapy, and on a regimen of pancreatic enzymes plus cimetidine. Serum bile salt levels were measured during fasting and postprandial conditions both during enzyme therapy and after it was stopped in 8 cases. In addition, 5 patients underwent [14C]cholylglycine breath testing during and after discontinuation of enzyme therapy. The fecal bile salt excretion varied between 610 and 3460 mg/day in the untreated patients. Treatment with pancreatic enzymes was associated with significant (p less than 0.05) reduction in fecal bile salt and fecal fat excretion. Cimetidine therapy in addition to enzyme therapy further reduced steatorrhea but failed to alter bile salt excretion significantly. Serum cholylglycine level showed significant (p less than 0.05) postprandial increase in patients receiving enzyme therapy, suggesting improved bile salt absorption. These data suggest a wide range of bile salt malabsorption in alcoholic patients with pancreatic insufficiency, which improves with pancreatic enzyme therapy.
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PMID:Bile salt malabsorption in pancreatic insufficiency secondary to alcoholic pancreatitis. 375 16

The absorption of 14C triolein in a standard fat meal was measured in 60 controls and 66 patients with gastrointestinal disorders by 14CO2 breath sampling. A reference range based upon cumulative eight hour values of the controls was independent of height, weight, and sex. The range was of log normal distribution and declined with age (p less than 0.05). Acceptable 'within-day' and 'between-day' reproducibility was found. All patients tested with untreated coeliac disease, pancreatic insufficiency and most with symptomatic small intestinal Crohn's disease had subnormal values. Twenty per cent of those with irritable bowel syndrome had subnormal values. Patients with ulcerative colitis were all normal. The reagents used and the breath samples after collection were stable. In our experience the 14C triolein test is simple, inexpensive, and helpful in the detection of diseases associated with fat malabsorption. It is of value in monitoring the response to treatment of individual patients with coeliac disease.
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PMID:14C triolein breath test: a routine test in the gastroenterology clinic? 379 16

21 patients with alcoholic cirrhosis were worked up for malabsorption. In three patients, the fecal weight was over 200 g/24 h; three had a steatorrhea over 6 g/24 h and in four the creatorrhea was over 2 g/24 h. The D-xylose test was abnormal 4 times out of 18, but these 4 patients presented an ascites. Alpha-1-antitrypsin clearance was increased in 1 out of 9 patients. The Lundh test demonstrated in 5 out of 8 cases an external pancreatic insufficiency, but without any relation with the fecal losses. The 4 patients with malabsorption showed signs of malnutrition (anthropometric criteria). In the course of an alcoholic cirrhosis, malabsorption seems therefore infrequent, dissociated, and only observed in patients with signs of malnutrition.
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PMID:[Malabsorption in alcoholic cirrhosis]. 381 79

Absorption of cobalamin free or bound to chicken serum was assessed in nine patients with pancreatic insufficiency. Simultaneously the in vitro effect of duodenal juice collected from six patients and seven controls was tested on labelled cobalamin complexed to chicken serum or to R salivary binder. Malabsorption of free cobalamin was observed in one of nine patients and in four of nine patients when cobalamin was administered bound to chicken serum. The in vitro effect of duodenal juice on cobalamin complexed to chicken serum or to R salivary binder was studied: the percentage of free cobalamin released was significantly decreased in pancreatic insufficiency compared with controls whatever the binder used; the degradation of R salivary binder was different in pancreatic insufficiency and in controls. Despite the in vitro abnormalities observed in pancreatic insufficiency, these did not correlate with the in vivo absorption of cobalamin which was often normal in our patients.
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PMID:In vitro effect of duodenal juice on R binders cobalamin complexes in subjects with pancreatic insufficiency: correlation with cobalamin absorption. 381 88

A 25-yr-old black man with cystic fibrosis and cirrhosis developed symptoms of osteomalacia and hypocalcemia, hypophosphatemia, secondary hyperparathyroidism, and low circulating 25-hydroxyvitamin D (25-OHD). Serum 1,25-dihydroxyvitamin D (1,25-[OH]2D) was within the normal range. Iliac crest bone biopsy confirmed the diagnosis of osteomalacia. Oral administration of 50,000 IU of vitamin D2 failed to relieve symptoms or raise serum 25-OHD levels to normal. Intramuscular vitamin D2, 10,000 IU every 8-12 week, improved symptoms, raised serum 25-OHD to normal, and increased circulating 1,25-[OH]2D to values five times normal. Over the next 10 mo circulating 1,25-[OH]2D remained elevated despite normalization of serum calcium, phosphorus, and parathyroid hormone. Repeat bone biopsy 1 yr after parenteral vitamin D showed healing of the osteomalacia. Malabsorption of vitamin D appears secondary to profound steatorrhea due to pancreatic insufficiency and secondary biliary cirrhosis. Although extensive hepatocellular disease was present, hepatic conversion of vitamin D to 25-OHD was intact. Both high and low circulating 1,25-[OH]2D levels during active osteomalacia have been reported; initially, the level was in the normal range and higher values in this patient occurred with repletion of 25-OHD substrate. This study shows that symptomatic osteomalacia may be a major manifestation of cystic fibrosis in those patients surviving into adulthood. Measurements of serum 25-OHD in cystic fibrosis patients may identify those who should receive supplemental vitamin D.
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PMID:Vitamin D metabolism and osteomalacia in cystic fibrosis. 387 14


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