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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen patients with ileal dysfunction due to resection or bypass were encountered over an 18-month period. Symptoms had been present for a mean period of 1.8 years. Diarrhoea was a universal symptom, and varied from mild to incapacitating. Weight loss, due in part to malabsorption and in part to the patients' fear of eating, occurred in 10 of 14 patients. The chief metabolic abnormalities were steatorrhoea and hypokalaemia. Vitamin B12 deficiency, folate deficiency, anaemia, hypoalbuminaemia, hypocalcaemia, hypomagnesaemia, hyperoxaluria, and an abnormal prothrombin ratio were less frequently seen. Treatment with cholestyramine and/or long-chain fat restriction effectively reduced diarrhoea in every case, and this was supplemented by replacement of specific deficiencies. There was little added benefit from non-specific antidiarrhoeal agents. It was found that the major symptoms of ileal dysfunction are readily treated, but that attention should also be given to a number of nutritional deficiencies.
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PMID:Consequences of ileal dysfunction: an approach to management. 10 34

The relationship between dosage, prothrombin ratio, and steady-state plasma concentrations of warfarin and warfarin-alcohol, were determined in 43 patients regularly attending an anticoagulant clinic. The warfarin and warfarin-alcohol concentrations were determined by a gas chromatographic mass spectroscopic (GC/MS) method. A significant correlation was found between the dose and the plasma level of warfarin. There was no significant correlation between the prothrombin ratio and the dose of warfarin, the steady-state plasma levels of warfarin or warfarin-alcohol, or the sum of their plasma concentrations. Measurement of the plasma levels of warfarin and warfarin-alcohol is likely to be of little help clinically other than to detect failure of compliance or malabsorption.
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PMID:Warfarin and warfarin-alcohol levels in anticoagulated patients. 29 8

A patient congenitally deficient in factors II, VII, IX, and X has been further investigated after a follow-up of 15 yr. At birth, these factors, when determined by clotting assays, were undetectable. Following therapy with vitamin K1, the clotting activity of these factors rose but never exceeded 18% of normal. Immunologic assays revealed much higher levels of these factors than did clotting assays, thus suggesting that the vitamin-K-dependent factors were present in abnormal forms. Two-dimensional crossed immunoelectrophoresis showed that at least two forms of prothrombin were present in the patient's plasma. One form was similar to normal prothrombin; the other had the same mobility as acarboxyprothrombin. In addition, the majority of this fast-migrating peak was not adsorbable onto insoluble barium salts. These observations suggested that some molecules of the patient's prothrombin lacked the normal complement of gamma-carboxyglutamic acid residues. This observation was confirmed by a specific assay for gamma-carboxyglutamate. Since malabsorption of vitamin K, warfarin intoxication, and hepatic dysfunction were excluded as causes of this patient's syndrome, this rare congenital abnormality could represent either a defective gamma-carboxylation mechanism within the hepatocyte or faulty vitamin K transport.
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PMID:Congenital deficiency of blood clotting factors II, VII, IX, and X. 42 15

What will be our GI approach to a child with FTT syndrome? Detailed history and physical examination will give us the clue and often the probable diagnosis. Several laboratory tests are helpful in establishing the fact that there is malabsorption. Among them are a complete blood count with smear, quantitative stool fat excretion, serum protein and chemistry screen panel, prothrombin time, and oral tolerance and absorption--i.e., of glucose, iron, vitamin A, and xylose. Specialized procedures may be used to nail down the diagnosis: radiology, biopsy, duodenal intubation, etc. These should never be employed as routine screening tests, however. In outlining a comprehensive and successful therapy, the attending physician will find it helpful to consider the particular pathophysiologic mechanisms of a specific disease. Exact diagnosis makes the therapy both rational and effective.
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PMID:Pathophysiology of failure to thrive in gastrointestinal disorders. 74 Apr 23

The diagnosis of pancreatic disease is difficult. The first step is clinical suspicion, based on the symptoms and signs. If pancreatic disease is suspected, investigation is necessary to prove this diagnosis. Investigation aims to answer two questions: a) is there pancreatic disease and b) if so, what type? The first question may be answered by demonstrating abnormal pancreatic function, using pancreatic function tests, whereas the second is answered by using techniques to demonstrate structural (anatomical) abnormalities of the pancreas. a) The methods to establish abnormal pancreatic function consist of 1. tests to demonstrate abnormal digestive capability, 2. tests to study pancreatic exocrine secretion, and 3. tests to study endocrine secretion. The tests of group 1 are: chemical fat balance study before and during enzyme replacement therapy, faecal nitrogen balance study, and the demonstration of either the malabsorption of vitamins A, D and K or the sequelae of their malabsorption (low serum calcium, high alkaline phosphatase, prolonged prothrombin time, etc.). Abnormal vitamin B12 absorption also may be present. 2. The tests designed to study pancreatic exocrine secretion are determination of the presence or absence of proteolytic enzymes in the stool, the secretion test, the pancreozymin stimulation test and the Lundh test. The serum amylase and lipase values are of little help in assessment of pancreatic function. 3. The tests to study endocrine function are the glucose tolerances test (which frequently gives abnormal results in pancreatic disease), and radioimmunoassays for insulin and gastrointestinal hormones (which may be increased in patients with functioning tumours of the islet cells). b) The techniques used to establish structural abnormalities of the pancreas are: duodenal cytology (during secretin tests), radiological techniques (abdominal survey films, barium meal, hypotonic duodenography, roentgenography of the biliary tract, barium enema, and angiography,) gastroscopy, duodensocopy, endoscopy and retrograde pancreatography, echography, scan and laparotomy. The relative value of these tests is discussed.
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PMID:Diagnosis of chronic pancreatic disease. 127 46

Nutritional support via enteral feeding tubes may interfere with the response to medications by a number of mechanisms. A 31-year-old, white man was admitted after sustaining a gunshot wound to the chest and mandible. Subsequently, the patient developed pulmonary emboli documented by angiography. Attempts at anticoagulation with oral warfarin were unsuccessful while the patient was receiving 50-100 ml/hr of Osmolite through an Entriflex feeding tube and intermittent oral Ensure Plus supplements. Discontinuation of the Osmolite resulted in a prompt prolongation of the prothrombin time. The Ensure Plus was continued and adequate prothrombin times were achieved on 7.5 to 10 mg of warfarin daily. The total amount of vitamin K received from the enteral feedings ranged from 50 to 115 micrograms/day, which is less than the normal daily intake of 300 to 500 micrograms. Previous reports of warfarin resistance implicated older enteral feeding products with a much higher vitamin K content. Difficulty with anticoagulation may still be experienced with the newer formulations. It is unknown whether the vitamin K content or malabsorption of warfarin is the mechanism of resistance.
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PMID:Warfarin resistance and enteral feedings. 249 51

We studied intestinal absorption of vitamin E in 26 adults with primary biliary cirrhosis (PBC) and 6 control subjects. Seven (27%) PBC patients were vitamin E-deficient based on the ratio of serum vitamin E to serum total lipid concentrations. An oral vitamin E tolerance test was performed in all patients and control subjects using a loading dose of 2000 IU alpha-tocopheryl acetate with measurement of serial serum vitamin E concentrations over 24 h. Vitamin E absorption was expressed as the maximal rise in serum vitamin E above baseline, the area under the oral tolerance test curve, and these two values divided by the fasting total serum lipid concentration. Absorption of vitamin E was significantly impaired in all PBC patients vs. control subjects (p less than 0.01), in vitamin E-deficient vs. vitamin E-sufficient PBC patients (p less than 0.05 to p less than 0.01), and in PBC patients with serum vitamin E levels below 10 micrograms/ml vs. those with serum vitamin E levels above 10 micrograms/ml (p less than 0.01). Vitamin E absorption was inversely related to stage of PBC, serum cholylglycine, total bilirubin, cholesterol, alkaline phosphatase, aspartate aminotransferase, and prothrombin time. Patients with serum vitamin E below 10 micrograms/ml, serum total bilirubin above 3 mg/dl, serum cholylglycine above 600 micrograms/dl, or serum alkaline phosphatase above 1000 IU/L had severe malabsorption of vitamin E and would be at high risk for the development of vitamin E deficiency. Therefore, vitamin E supplementation should be considered not only in patients in whom overt vitamin E deficiency is present, but also in PBC patients meeting these criteria.
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PMID:Intestinal malabsorption of vitamin E in primary biliary cirrhosis. 291 Jul 63

A case of malabsorption of vitamin K, leading to a vitamin K-dependent clotting factor deficiency that developed during the eighth gestational month, is reported. Evaluation of the coagulopathy at term showed the cause to be an obstructive hepatobiliary disorder. Given the pathophysiologic relationship between the coagulation cascade and the hepatic and biliary systems, routine measurement of the prothrombin and partial thromboplastin times is advised for all patients with evidence of hepatobiliary dysfunction.
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PMID:Vitamin K-dependent clotting factor deficiency in pregnancy. 340 63

An outline has been given of the major abnormalities of coagulation which can occur secondary to diseases in previously normal individuals. First, the disorders due to deficiency of the vitamin K-dependent clotting factors are described. Vitamin K deficiency can occur in the newborn, or at later stages in life when there is intestinal malabsorption. The malabsorption disorders, such as coeliac disease, together with major abdominal surgery or prolonged use of broad-spectrum antibiotics can give rise to vitamin K deficiency. Additionally, in obstructive jaundice the lack of secretion of bile salts into the upper intestine causes vitamin K malabsorption. The use of oral anticoagulants is associated with haemorrhage in a small proportion of patients. These patients usually have an excessively prolonged prothrombin time, due to overdosage with anticoagulants, but occasionally haemorrhage can occur from a localized bleeding site, such as a duodenal ulcer, in patients under good anticoagulant control. The large number of drugs which can interact with anticoagulants are listed, from which it can be seen that careful monitoring of all patients on oral anticoagulants must be carried out. The haemostatic defects associated with liver disease are then tabulated. In this situation abnormalities may be due to deficient synthesis of coagulation factors in hepatocellular failure, by failure of vitamin K absorption, and also by disseminated intravascular coagulation (DIC). DIC occurs in hepatocellular failure, because the liver cells are normally responsible for clearing activated products of the coagulation and fibrinolytic enzyme systems. The presence of clinical haemorrhage and haemostatic breakdown in hepatic disease usually indicates a serious prognosis, but appropriate replacement therapy is indicated in this situation. Disseminated intravascular coagulation embraces a large number of clinical haemorrhagic syndromes, where intravascular activation of the coagulation system takes place accompanied by compensatory fibrinolytic activity. DIC can be initiated by intravascular release of procoagulant substances, such as tissue thromboplastin, or by damage to vascular endothelium and platelets. The main clinical conditions associated with DIC comprise the severe infections and septicaemias, obstetric accidents, shock and trauma, neoplasia and snake-bite envenoming. In all instances, the pathophysiological disorder of haemostasis is managed by treating the underlying disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acquired coagulation disorders. 389 41

Small bowel resection is often accompanied by malabsorption and nutritional deficiencies. Malabsorption of drugs may also occur; however, few reports have been published. We treated five patients with oral warfarin for thrombotic problems after substantial small bowel resection. All five had a documented hypoprothrombinemic response to the warfarin (patient prothrombin time: control greater than 1.5). Maintenance warfarin doses were up to 10 mg/day. Oral warfarin appears to be well absorbed after removal of the majority of the jejunum and ileum. This may indicate a proximal site of warfarin absorption.
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PMID:Warfarin absorption after massive small bowel resection. 397 8


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