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)

Fat-soluble vitamin deficiency is known to result in various complications that may be prevented if the problem is recognized and managed appropriately. In infants and children with chronic cholestasis, replacement therapy of the fat-soluble vitamins, vitamins A, D, E, and K, may prove extremely difficult because low concentrations of intraluminal bile acids lead to malabsorption of these compounds and other fat-soluble substances. Recent progress in the use of a water-soluble form of vitamin E, d-alpha-tocopheryl polyethylene glycol-1000 succinate, has enabled correction of vitamin E-deficiency states in these patients. It has also allowed for the admixture and coadministration of other fat-soluble vitamins and compounds in d-alpha-tocopheryl polyethylene glycol-1000 succinate to enhance their absorption. For managing vitamin K deficiency, similar success has been achieved using a vitamin K compound solubilized in glycocholate and lecithin. Vitamin A deficiency has been implicated in the higher incidence of childhood mortality and morbidity in Third World countries. Increased risk of childhood cancer has recently been associated with intramuscular injection of vitamin K to newborns. Finally, it is worth noting that among the pediatric population, exclusively breastfed infants, in general, are at risk for hypovitaminosis D, and at even greater risk in the absence of adequate exposure to sunlight or when the maternal diet is not sufficient to provide for vitamin D requirements.
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PMID:Fat-soluble vitamin deficiency in infants and children. 828 79

Four infants with conjugated hyperbilirubinemia who were brought for treatment primarily because of a hemorrhage are reported. Underlying disorders included extrahepatic biliary atresia, choledochal cysts, and alpha 1-antitrypsin deficiency. Prodromal signs of disturbed coagulation and diminished bile excretion were not recognized. The increased bleeding tendency was probably caused by vitamin K deficiency, resulting from a combination of cholestasis-induced fat malabsorption, absence of vitamin K supplementation after birth, and low vitamin K intake as a result of breast feeding.
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PMID:Bleeding as presenting symptom of cholestasis. 841 Mar 91

Three unrelated infants presented with radiographic punctate calcifications, nasal hypoplasia, and abnormalities of the spine. Additional anomalies included cupped ears in 2 patients and one each with Dandy-Walker malformation with hydrocephaly, congenital cataracts, and peripheral pulmonary artery stenosis. The mothers of these 3 patients had chronic conditions associated with intestinal malabsorption requiring total parenteral nutrition for varying periods of time. The underlying causes of malabsorption were celiac disease, short bowel syndrome secondary to surgical resection, and jejuno-ileal bypass, respectively. Bleeding diathesis occurred in one mother requiring vitamin K supplementation during the second and third trimesters of pregnancy. We speculate that the chondrodysplasia punctata and other abnormalities in these children were caused by an acquired maternal vitamin K deficiency manifested during early pregnancy. However, the involvement of other vitamin deficiencies cannot be excluded. Thus, vitamin K deficiency of the embryo secondary to maternal malabsorption appears to be a third vitamin K-related mechanism leading to chondrodysplasia punctata in addition to warfarin embryopathy and epoxide reductase deficiency (pseudo-warfarin embryopathy).
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PMID:Vitamin K deficiency embryopathy: a phenocopy of the warfarin embryopathy due to a disorder of embryonic vitamin K metabolism. 938 32

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

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

Inflammatory bowel disease may manifest in various extra intestinal manifestations. Osteopenia and various arthropathies may be debilitating. These may be related to the disease itself, patient genetics, lifestyle, or disease treatment. Calcium and vitamin D malabsorption, vitamin K deficiency, malnutrition, corticosteroid and other immunosuppressive medications, smoking, lack of exercise and postmenopausal state may all play important roles. Treatment may be undertaken to correct nutrient deficiencies, inhibit bone resorption and increase bone formation.
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PMID:Bones and Crohn's: problems and solutions. 1045 78

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 severe nutritional deficiency status is described in a 22-year-old patient with Crohn's disease. The clinical picture on admission was dominated by an episode of gastrointestinal bleeding secondary to clotting disturbances (vitamin K deficiency) and severe cachexia due to a protein energy malnutrition. The mechanisms of severe nutritional disturbances in Crohn's disease are multifactorial. In this patient, lymphatic leakage into the intestinal lumen was a major contributing factor in the pathogenesis of protein-losing enteropathy, fat malabsorption, and lymphocytopenia. The authors were able to demonstrate this intestinal lymph loss by nuclear imaging.
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PMID:Lymph loss in the bowel and severe nutritional disturbances in Crohn's disease. 1050 57

Short bowel syndrome causes a complex of symptoms due to compromise of small intestinal nutrient absorption. A 60-year-old woman underwent major resection of the small intestine due to a road accident 3 years ago. The sole manifestation of short-bowel-syndrome was superficial skin necrosis due to vitamin K deficiency. She was asymptomatic for a long time, until treatment with antibiotics further intensified initially subclinical malabsorption. It is not clear why there had been no other symptoms and why the main impact was on the fibrinolytic system rather than the coagulation system, as is usually the case. It is recommended that patients after major resection of the small intestine be closely monitored for coagulation function if an oral antibiotic is prescribed.
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PMID:[Superficial skin necrosis--an uncommon manifestation of short bowel syndrome]. 1095 28

Vitamin K deficiency in infants can cause life-threatening haemorrhages. To prevent this, neonates in the Netherlands receive an oral dose of 1 mg vitamin K directly after birth. In addition, because breast milk contains little vitamin K, breast-fed infants receive a daily dose of 25 micrograms the first three months. Of three female infants aged 4 weeks, 5 months and 3 months, respectively, two developed an intracranial haemorrhage, which caused death in one. In two cases there were signs of a bleeding tendency, but no tests were done because the patients appeared healthy otherwise. The underlying resorptive disorders, cholestasis and fat malabsorption, caused few symptoms and were discovered only after a vitamin K deficiency bleeding had occurred. In an infant with a bleeding tendency, one should consider the possibility of vitamin K deficiency, even if adequate prophylaxis has been given.
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PMID:[Vitamin K deficiency bleeding in an infant despite adequate prophylaxis]. 1460 58


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