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)

Fourteen cases of ASA induced hypoprothrombinemic bleeding, including three patients reported by the authors, are reviewed. Predisposing factors toward bleeding include malnutrition and malabsorption syndrome. Although the bleeding is usually benign, it may be serious on occasion. The importance of this rarely considered cause of ASA associated bleeding lies in the fact that it is readily corrected with Vitamin K.
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PMID:Bleeding, salicylates, and prolonged prothrombin time: three case reports and a review of the literature. 127 87

Vitamin K catalyzes the post-translational carboxylation of coagulation proteins C, S, and factors II, VII, XI, and X. Detection of the noncarboxylated forms allows an indirect and specific measure of the vitamin K deficiency found in early, classic, and late hemorrhagic disease of the newborn (HDN), malabsorption syndromes, and drug related (warfarin, anticonvulsants, and antibiotics) states. Idiopathic late HDN (CNS bleeding) occurs in exclusively breast-fed infants and is prevented by appropriate parenteral and oral vitamin K prophylaxis given at birth. All newborn infants and older infants with malabsorption syndromes should receive prophylactic vitamin K.
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PMID:New insights on vitamin K. 332 79

Two cats with intestinal malabsorption developed a hemorrhagic diathesis. Although unsubstantiated, the probable cause of bleeding was a chronic malabsorption of fat and the fat-soluble vitamin K. When treated with vitamin K1 per os, one cat's clotting times were only partially corrected. Since vitamin K1 is actively absorbed in the proximal small intestine, the incomplete response of this case to orally administered vitamin K1 was predictable. The infrequent occurrence of bleeding in animals with malabsorption is, in part, attributable to the ileal and colonic absorption of bacterially derived vitamin K2. For this reason, nonspecific use of antibiotics in these animals is contraindicated. Since long-chain, polyunsaturated fats impair vitamin K absorption, dietary fat given to animals with malabsorption should be restricted to medium- and short-chain, saturated fats. Vitamin K should be administered subcutaneously to these animals if prolonged clotting times or active bleeding is present, and routinely prior to surgery. Oral supplementation with vitamin K3, which is absorbed in the colon and less lipid soluble than vitamin K1, should be given to animals with malabsorption that are maintained as outpatients. Adequate dosage levels of vitamin K3, however, are yet to be established for the cat, and dose-dependent hemolytic anemia is a probable toxic manifestation.
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PMID:Probable vitamin K--deficient bleeding in two cats with malabsorption syndrome secondary to lymphocytic-plasmacytic enteritis. 350 99

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

Vitamin K is a cofactor for the synthesis of blood coagulation Factors II, VII, IX and X, and inhibitors such as Protein C and S and bone matrix protein. Its active form is a coenzyme in the glutamic acid carboxylation. Vitamin K-dependent factors form enzymatic complexes with calcium and membrane phospholipids. The insufficiency of gamma glutamic carboxylation impairs the hemostatic function. Hereditary deficiencies, antibiotics and oral anticoagulants, decrease the capacity of complex formation giving way to hemorrhage or thrombosis, or bone mass disturbances which are easily treated with administration of Vitamin K. The main causes of Vitamin K deficiency are lack of hepatic storage in newborns, liver insufficiency, malabsorption, dietetic deficiency, therapy with the antibiotics and coumarin administration. For the study of Vitamin K there are methods to measure the Vit K dependent proteins and as well methods to measure specifically the quinonas.
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PMID:[Vitamin K: biochemistry, function, and deficiency. Review]. 978 May 55

A major complication of cholestasis is fat malabsorption related to decreased intestinal bile acids, which leads to malnutrition and fat-soluble vitamin deficiency. The impaired excretion of bile acids leads to a low intraluminal micellar concentration that causes long-chain triglyceride lipolysis and absorption to be ineffective. Medium-chain triglycerides (MCTs) are more readily absorbed when there are low concentrations of bile acids and therefore are a good source of fat calories; MCTs can be administered as MCT-containing formulas. In those children who are unable to take sufficient calories by mouth, it is important to start nocturnal enteral feeding to improve nutritional status. In infants with cholestasis, the absorption of fat-soluble vitamins (A, D, E and K) that require bile acids is also impaired, and supplementation is mandatory. Vitamin K deficiency may be responsible for hypoprothrombinaemia, which may lead to bleeding diathesis, Vitamin K (phytomenadione) should therefore be promptly administered intravenously, at a dose of 1 mg. Chronic vitamin E (alpha-tocopherol) deficiency is associated with a progressive neuromuscular syndrome that can cause cerebellar ataxia, areflexia and peripheral neuropathy. Supplements are given orally in doses of 3-5 times the normal requirement if cholestasis is incomplete. In complete cholestasis, supplements must be given intramuscularly at monthly intervals. In infants who fail to thrive, dietary supplements of carbohydrate polymers and MCTs are required.
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PMID:Hepatitis and cholestasis in infancy: clinical and nutritional aspects. 1459 52

Coeliac disease is usually revealed by intestinal symptoms, but less frequently by deficiency symptoms. Early screening is very important to avoid with appropriate diet an intestinal lymphoma or epidermoid cancer. We report here the case of a 68-year old woman where coeliac disease was pointed out by very long Prothrombin Time (PT) and Activated Partial Thromboplastin Time (APTT). Clinical examination was strictly normal except for leanness, a small height, and several diarrhoea episodes 3 or 4 times a year. Other blood tests showed a macrocytic anemia, a fibrinogen level slightly above the upper limit, a decreased proteinaemia and albuminaemia, and a sideraemia at the lower normal limit. Liver tests pointed to a cytolysis. Vitamin K-dependent factors were decreased. A perfusion of vitamin-K allowed getting a normal PT. Duodenofiberscopy with biopsy allowed the diagnosis of coeliac disease. Neither lymphoma nor epidermoid cancer were detected. A gluten-free diet allowed the disappearing of digestive symptoms, weight rising and return to a normal PT. Searching for a coeliac disease is therefore relevant in aged patients even when very faint clinical or biological symptoms of malabsorption appear, particularly when PT is longer than the control with decreased vitamin-K dependant factors.
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PMID:[A case of celiac disease with late diagnosis by very long prothrombin and activated partial prothrombin times]. 1535 14

This study examined the prevalence of vitamin K deficiency in children pre-bone marrow transplantation (BMT). Vitamin K status was measured by the PIVKA-II assay and prothrombin times. Blood samples were obtained before vitamin-containing TPN was infused. Results indicated that eight of 26 patients (31%) were vitamin K deficient; four cases were attributed to drug antagonism (phenytoin) and four were due to inadequate vitamin K intake, synthesis or malabsorption. Only one patient had a prolonged prothrombin time. Prothrombin time, in our study, is shown to be an ineffective screening tool to determine vitamin K status. All patients receiving phenytoin and chemotherapy are at increased risk of vitamin K deficiency.
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PMID:Vitamin K deficiency in children pre-bone marrow transplantation. 1628 12

Vitamin K was discovered in the 1930s during cholesterol metabolism experiments in chickens. It is a fat-soluble vitamin which occurs naturally in plants as phylloquinone (vitamin K1) and is produced by gram-negative bacteria in the human gastrointestinal tract as menaquinone (vitamin K2). This vitamin was found to be essential for normal functioning of hemostasis. In addition, a number of clinical conditions in which vitamin K deficiency was found to be the underlying pathophysiologic problem were discovered. These conditions include hemorrhagic disease of the newborn, obstructive jaundice, and malabsorption syndromes. The importance of this vitamin has become more apparent with the discovery of the anticoagulant warfarin which is a vitamin K antagonist. There are millions of patients on this therapy for a variety of thrombogenic conditions such as atrial fibrillation, deep vein thrombosis, pulmonary embolism, and prosthetic cardiac valves. The wide use of this narrow therapeutic index drug has resulted in significant risk for major bleeding. Vitamin K serves as one of the major reversing agent for patients over-anticoagulated with warfarin. In the past few years, research has focused on new areas of vitamin K metabolism, which include bone and endovascular metabolism; cell growth, regulation, migration, and proliferation; cell survival, apoptosis, phagocytosis, and adhesion. These new areas of research highlight the significance of vitamin K but raise new clinical questions for patients who must be maintained on long-term warfarin therapy.
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PMID:Vitamin K and thrombosis. 1837 99

Vitamin K deficiency bleeding (VKDB) is a rare and potentially life-threatening bleeding disorder of early infancy. Vitamin K stores are low at birth; thereafter breast-fed infants are at risk because of low concentrations in human milk. Classical VKDB occurs in the first week of life, is related to delayed or inadequate feeding and is readily prevented by small doses of vitamin K at birth. Late VKDB peaks at 3-8 weeks, typically presents with intracranial haemorrhage often due to undiagnosed cholestasis with resultant malabsorption of vitamin K. Diagnosis can be difficult but PIVKA-II measurements can provide confirmation even several days post-treatment. Without vitamin K prophylaxis, the incidence of late VKDB in Europe is 4-7 cases per 10(5) births; it is higher in SE Asia where in rural, low-income areas some 0.1% of affected infants may suffer intracranial bleeding. Late VKDB is largely preventable with parenteral vitamin K providing the best protection. The efficacy of oral prophylaxis is related to the dose and frequency of administration. Most multi-dose oral regimens provide protection for all except a small reservoir of infants with undetected hepatobiliary disease. Targeted surveillance of high-risk groups (e.g. biliary atresia) offers a novel approach to assess efficacy of prophylaxis.
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PMID:Vitamin K deficiency bleeding (VKDB) in early infancy. 1880 3


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