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)

A patient underwent end-to-side jejunoileostomy for morbid obesity, and 3 years later an end-to-end jejunoileostomy with ileotransversostomy was performed. Nine years later she presented with night blindness, severe diarrhea and mild jaundice and was found to have malabsorption with vitamin A and K deficiencies as well as asymptomatic liver cirrhosis. Her shunt was removed, and a gastric partition was performed. The night blindness and abnormal prothrombin time were corrected by the administration of vitamins A and K. This case demonstrates that complications may appear many years after jejunoileal bypass surgery, and therefore, the patients should remain under strict medical supervision indefinitely.
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PMID:Night blindness and liver cirrhosis as late complications of jejunoileal bypass surgery for morbid obesity. 633 98

Therapy of the malabsorption syndrome centers on adequate diagnosis of the underlying pathology, with vigorous therapeutic efforts directed at correcting this and thereby preventing ongoing losses of nutrients. Dietary therapy includes a high-protein, high-calorie, low-fat diet often supplemented with MCTs in an effort to minimize steatorrhea. Water-soluble vitamin deficiency is rare, but supplementation with small daily doses is innocuous and probably should be prescribed. Significant fat-soluble vitamin deficiencies are seen more commonly and can be monitored by physical examination and the prothrombin time. Calcium, magnesium, and vitamin D deficiencies are more common than originally suspected. Adequate therapy requires monitoring of the serum calcium, magnesium, parathyroid hormone levels, and, optimally, 24-hour urinary collections for calcium. Supplementation of these mineral deficiencies requires ongoing close observation to prevent hypercalcemia. Iron deficiency can be easily diagnosed by available serum iron determination, and replacement with oral supplements is curative. Trace metal deficiencies occur, but our capabilities of detecting and treating them is still in its infancy. Figure 3 outlines our approach to the evaluation and treatment of the patients suspected of having the malabsorption syndrome.
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PMID:Nutritional aspects of malabsorption syndromes. 641 33

A 15-month-old girl from Coimbra (Portugal) had a history of numerous hemorrhagic episodes with multiple bruises, hematomas but not hemarthroses. On serial testing she showed deficiency of factors II, VII, IX, X and protein C. Malabsorption-induced vitamin K deficiency, liver disease or ingestion of a coumarin compound were excluded. An absence of detectable abnormalities was found among her relatives. Consanguinity was not present. The immunologic assay, immunoelectrophoresis or antibody neutralization, revealed much higher levels of these factors than the clotting assay. The non-physiological activator (Echis carinatus venom) produced higher levels of prothrombin activation than those detected by physiological activation. Two-dimensional immunoelectrophoresis of the patient's plasma in calcium showed that prothrombin had the same mobility as acarboxyprothrombin. No significant response to large doses of intravenous vitamin K3 (6 mg) was observed. Transfusion of 120 ml of frozen fresh plasma led to an immediate increase in the procoagulant activities of vitamin K dependent protein, similar to that found after perfusion of plasma plus vitamin K3. The results obtained from this patient suggest a defect in the gammacarboxylation mechanism inside the hepatocyte.
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PMID:Congenital deficiency of vitamin K-dependent coagulation factors and protein C. 654 83

An 18-month-old child, who had no evidence of liver disease, malabsorption, or chronic ingestion of coumarin compounds, was found to have plasma deficiencies of factors II, VII, IX and X. Assays for factor II and X by immunological techniques (antibody neutralization and immunoelectrophoresis) revealed normal or elevated antigenic activity of these factors, suggesting the presence of abnormal protein variants in the patient's plasma. On two-dimensional immunoelectrophoresis of the patient's plasma in calcium, a normal and an abnormal population of prothrombin were seen. The abnormal prothrombin had a mobility more anodal than that of normal prothrombin, but less anodal than that of acarboxyprothrombin. The abnormal prothrombin, in contrast to acarboxyprothrombin, adsorbed readily to both aluminum hydroxide and barium citrate, and could be identified by two-dimensional immunoelectrophoresis of a barium citrate eluate. We suspect that the abnormal variant represents a partially carboxylated prothrombin.
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PMID:Characterization of a variant prothrombin in a patient congenitally deficient in factors II, VII, IX and X. 737 10

Vitamin K (phylloquinone, K1; menaquinone, K2) functions as an essential cofactor for the synthesis of the coagulation protein factors II, VII, IX, X and protein C and S by promoting a unique post-translational modification of specific glutamic acid residues to gamma-carboxylglutamic acid, thus mediating calcium binding to phospholipid surfaces. Vitamin K deficiency results in a depletion of liver stores of phylloquinone, decreased plasma levels of vitamin K1, increased levels of K1 epoxide, appearance of noncarboxylated protein (PIVKA), decreased levels of functioning vitamin K-dependent clotting factors and prolongation of the APTT, PT and thrombotest. When the progression of deficiency leads to abnormal clotting tests a generalized bleeding tendency occurs. Noncarboxylated prothrombin (PIVKA-II) determinations are a sensitive indicator of vitamin K deficiency. Although Vitamin K deficiency can occur at any age (warfarin, fasting, antibiotic therapy, malabsorption syndromes) the major public health problem is related to prevention of early, classic and late hemorrhagic disease of the newborn (HDN). A single dose of oral or parenteral vitamin K prevents classic HDN but the most effective way to prevent early HDN is by giving large doses to the mother prior to delivery (2 weeks). Late HDN in breastfed infant occurs with a prevalence of about 20 per 100,000 live births when no neonatal prophylaxis is given. Parenteral (1 mg) K1 prevents late HDN and single or repeated doses of oral vitamin K reduces the incidence but does not eliminate all late HDN. The optimal (cost, feasibility, effective) mode of neonatal prophylaxis remains to be determined.
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PMID:Vitamin K deficiency. 788 7

Patients with burn injuries exhibit multiple risk factors for the development of vitamin K deficiency, including malabsorption, limited enteral intake, antibiotic therapy, and multiple surgical procedures. A prospective evaluation of 48 children was conducted to evaluate serum vitamin K values during the first 4 postburn weeks. Serum levels were analyzed in relation to clinical course. Days of antibiotic (p < 0.02) and albumin therapy (p < 0.003), percentage body surface area excised (p < 0.006), and the administration of blood products (p < 0.05) were significantly correlated with serum vitamin K levels, and days of diarrhea approached statistical significance (p < 0.06). No relationship was found between serum values and prothrombin time, activated partial thromboplastin time, or serum albumin. Ninety-one percent of the children demonstrated serum values below expected norms. These data suggest a relationship between coagulopathy and an intact functioning gastrointestinal tract. However, the relative importance of dietary versus endogenous vitamin K produced by intestinal bacteria remains to be elucidated.
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PMID:A prospective analysis of serum vitamin K in severely burned pediatric patients. 950 29

Long-chain polyunsaturated fatty acids are important for the growth and early development of the central nervous system. Cholestatic infants suffer from fat malabsorption and disturbed lipid metabolism and therefore may be at risk of developing polyunsaturated fatty acid depletion. The aims of this study were to determine essential fatty acid status in cholestatic infants and to study the relationship to disease severity, degree of undernutrition, antioxidant status and mode of feeding. Twenty-four-hour dietary records were obtained in 34 cholestatic infants, and measurements were taken of skin fold thicknesses, bilirubin levels, activities of serum alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, prothrombin time, serum concentrations of albumin, bile acids, total lipids, phospholipids, cholesterol, vitamins A and E, the fatty acid composition of plasma phospholipids and plasma lipid peroxides expressed as thiobarbiturate reactive substance (TBARS). Plasma phospholipid fatty acids and TBARS were also determined in 12 age-matched healthy control infants. The cholestatic patients had very low percentage values of phospholipid essential fatty acids, particularly linoleic acid ( 18:2omega-6, median 14.74% vs 20.76% in controls, p < 0.001) and its major metabolite arachidonic acid (20:4omega-6, 6.80 vs 7.87%, p=0.04). The patients' essential fatty acid depletion was reflected by increased levels of the non-essential fatty acids, Mead acid (20:3omega-9, 0.74 vs 0.21%, p < 0.001) and palmitoleic acid (16:1omega-7, 2.20 vs 0.43%, p < 0.001). Polyunsaturated fatty acid profiles did not differ between infants with biliary atresia (n=13) and those with intrahepatic cholestasis (n=21), or between 17 infants with severe malnutrition (all skin folds < 10th percentile) and mild malnutrition (at least two skin folds > 10th percentile). TBARS were significantly higher in cholestatic patients than in controls (2.74 vs 0.85 nmol ml(-1), p < 0.001) and correlated with direct (r=0.41, p=0.02) and total bilirubin. The daily dietary intake of linoleic acid (per 100 kcal) correlated with plasma phospholipid linoleic acid (r=0.38,p=0.037) and total omega-6 fatty acids (r=0.38,p=0.036). Breastfed cholestatic infants (n=6) had higher values of the omega-3 long-chain polyunsaturated fatty acids docosapentanoic acid (22:5omega-3, 0.47 vs 0.28%, p=0.0006) and docosahexanoic acid (22:6omega-3, 2.39 vs 1.73%, p=0.01) than formula-fed infants, while disease severity was similar in the two groups. In conclusion, cholestatic infants are at high risk of essential fatty acid depletion, which appears to be related to fat malabsorption, hepatic essential fatty metabolism, enhanced lipid peroxidation and dietary intake.
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PMID:Essential fatty acid metabolism in infants with cholestasis. 956 34

A 47 year old patient was admitted because of 20 kg weight loss and microcytic anaemia. There wasn't any important disease in his medical history. During examinations it has been found microcytic anaemia, hypoproteinaemia, low serum potassium, elevated prothrombin INR value, malabsorption and mild hepatosplenomegaly. After precluding the possibility of malignant disorders and any other chronic diseases, examinations have cleared Whipple-disease.
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PMID:[An unusual case of morbid weight loss]. 957 3

A major hemorrhagic insult may require massive transfusions to maintain oxygen transport and hemostasis. Thus an adequate transfusion budget must consider losses, patient's blood volume, critical levels of laboratory parameters, replacement rates of coagulation factors from the extravascular space, and the efficacy of blood products. The substitution of large quantities of blood or red cell concentrates can induce and aggravate a complex haemostatic disorder. Some patients develop generalized microvascular bleeding. A transfusion regimen is described, which in our hands can reduce complications of massive transfusion. For hemostatic support, platelet concentrates and fresh frozen plasma are the treatment of choice. Localization and persistence of bleeding, hepatic disease, and vitamin K deficiency due to medication or intestinal malabsorption may require the supplementary use of prothrombin complex concentrates. Furthermore, antithrombin and fibrinogen concentrates may be indispensable.
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PMID:Indications for prothrombin complex concentrates in massive transfusions. 1049 11

A 46-year old nurse complaining of multiple hematomas including bleeding into the tongue was referred for hemostasis evaluation. A very low Quick percentage value, i.e. a severely prolonged prothrombin time with severely depressed vitamin K-dependent coagulation factors (FII:C, FVII:C, FX:C) and normal FV:C and fibrinogen level was found. In the absence of cholestasis, malabsorption and broad-spectrum antibiotic therapy, ingestion of vitamin K antagonists was suspected. Three years previously, she had been on oral anticoagulant treatment with phenprocoumon (Marcoumar) for postoperative pulmonary embolism. She denied having voluntarily ingested anticoagulant drugs. A high plasma level of coumarins was found. To exclude accidental ingestion, the patient's son living in the same household was tested as well. Surprisingly, a low level of coumarin was found also in his plasma. We suspect that the patient voluntarily intoxicated herself and gave a low dose of coumarin anticoagulant to her son as well.
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PMID:[46-year-old woman with multiple hematomas and bleeding of the base of the tongue: phenprocoumon poisoning]. 1051 30


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