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Vitamin clinical presentation

Vitamin K is essential for the synthesis of coagulation factors II, VII, IX, X, and proteins C and S. About half of the daily requirement is synthesized by the gastrointestinal flora. Deficiency leads to an impairment in the coagulation cascade, clinically presenting as purpura, ecchymoses, and hemorrhage anywhere in the body.29 The recommended daily allowance is 90 fig for females and 120 fig for males.71... [Pg.384]

The majority of malformations of the spinal cord are the result of the failure of the caudal neuropore to properly close by the end of the fourth week of development. The defective closure of the caudal neuropore results in serious neural tube malformations known generally as spina bifida. There are many types of spina bifida, and the clinical presentation, including neurological deficits, can range from minor (e.g. spina bifida occulta) to severe (e.g. spina bifida with myeloschisis). Spina bifida cystica has been associated with exposure of the mother to large doses of retinoic acid, or vitamin A, via ingestion (Moore, 1988). [Pg.72]

Data are also available for MS patients, where supplementation with 25(OH)2D3 increased serum levels of antiinflammatory cytokine TGF-J3 after 6 months of treatment, whereas no or little effect was observed on TNF-a, IL-13, IFN-y and IL-2 [187]. No information was given on the clinical presentation of these patients after treatment. In type I diabetes, a long-term study proved dietary vitamin D supplementation was clinically beneficial in terms of reduced risk of the disease [165]. Heart transplant recipients that were treated with low-dose l,25(OH)2D3 aiming at reduction of bone loss required significantly less cyclosporin for prevention of organ rejection suggesting a potentially beneficial immunosuppressive role of l,25(OH)2D3 in transplantational medicine [188]. [Pg.345]

IV. Diagnosis is based on a history of exposure and clinical presentation (eg, evidence of asphyxia and an empty can or tank). It should also be considered in a patient with manifestations suggesting chronic vitamin B,2 deficiency but with normal vitamin B.,2 levels. [Pg.283]

The consumption of a mixture of phenolic compounds presented in apple or purple grape juice inhibited mammary carcinogenesis in 7,12-dimethylbenzo[a]anthracene (DMBA) treated rats (Liu and others 2005 Jung and others 2006). However, the individual antioxidants of these foods studied in clinical trials, including (3-carotene, vitamin C, and vitamin E, do not appear to have consistent preventive effects comparable to the observed health benefits of diets rich in fruits and vegetables, suggesting that natural phytochemicals in fresh fruits and vegetables could be more effective than a dietary supplement. [Pg.10]

At present, antioxidants are extensively studied as supplements for the treatment diabetic patients. Several clinical trials have been carried out with vitamin E. In 1991, Ceriello et al. [136] showed that supplementation of vitamin E to insulin-requiring diabetic patients reduced protein glycosylation without changing plasma glucose, probably due to the inhibition of the Maillard reaction. Then, Paolisso et al. [137] found that vitamin E decreased glucose level and improved insulin action in noninsulin-dependent diabetic patients. Recently, Jain et al. [138] showed that vitamin E supplementation increased glutathione level and diminished lipid peroxidation and HbAi level in erythrocytes of type 1 diabetic children. Similarly, Skyrme-Jones et al. [139] demonstrated that vitamin E supplementation improved endothelial vasodilator function in type 1 diabetic children supposedly due to the suppression of LDL oxidation. Devaraj et al. [140] used the urinary F2-isoprostane test for the estimate of LDL oxidation in type 2 diabetics. They also found that LDL oxidation decreased after vitamin E supplementation to patients. [Pg.925]

Clearly this patient has both clinical and haematological symptoms of severe anaemia. The cause is too few red cells low RBC count and PCV but the erythrocytes which are present contain a higher than usual concentration of haemoglobin (MCHC result). Iron deficiency and vitamin B12 deficiency can be ruled out by the high serum ferritin and normal MCV results respectively. The negative HbS screen rules out sickle cell anaemia which is fairly common in Africans. [Pg.167]

At present, antioxidants are extensively studied as supplements for the treatment diabetic patients. Several clinical trials have been carried out with vitamin E. In 1991, Ceriello et al. [Pg.926]

Cohall is present in vitamin Bi to Ihe extent of about 4ci-. Lack of cobalt in tlie soil and feedstuffs prevents tuniinants from synthesizing all of the vilamin B j for their needs. Thus, cobalt can be added to feedstuffs as the chloride, sulfate, oxide, nr carbonate. Excessive cobalt intakes are toxic, causing a reduction in feed intake and body weight, accompanied by emaciation, anemia, debility, and elevated levels of cobull in the liver. It is of interest to note that clinical coball tnxiciiy closely resembles clinical cobalt deficiency. [Pg.412]

Homocystinuria may result from one or several abnormalities in the mechanism whereby homocysteine is methylated to form methionine. About half of the patients respond to treatment with pyridoxine and it is thought that the vitamin overcomes a block at the homocysteine/cystathionine level by mass action (C23). However, Schuh et al. (S22) have recently described a patient who responded to vitamin B12. The infant presented with severe developmental delay, homocystinuria, and a megaloblastic anemia. Treatment with cyanocobalamin was without effect but treatment with hydroxocobalamin resulted in a rapid clinical improvement, and the homocystinuria disappeared. Methionine synthetase activity in cell extracts was normal, while cultured fibroblasts showed an absolute growth requirement for methionine. The defect appeared to be limited to methyleobalamin accumulation and an inability to transfer the methyl group from 5-methyltetrahydrofolate to homocysteine. [Pg.202]

The five articles comprising this volume were contributed by international scientists and edited by a Board of International Editors. A scan of the table of contents indicates the wide ranging subject matter presented. The fields of instrumentation analysis, metabolism, nutritional biochemistry, and immunology in its several phases have been presented. Two basic approaches for presentation have been used. The first approach is an in depth consideration of a specific subject, which is exemplified by the article on the clinical chemistry of vitamin B12. The second approach is an overview of an extensive field of active research as represented by the article on immune complexes. All of the articles comprising this volume reflect permutations on these approaches. [Pg.320]

Steatorrhea, the clinical result of insufficient intraluminal lipid hydrolysis, is the most important digestive malfunction in pancreatic exocrine insufficiency. As a rule, concomitant malabsorption of the lipid-soluble vitamins A, D, E, and K must be suspected in these patients. Naturally, potential differential diagnoses have to be considered in patients who present with steatorrhea (Table 26-1). The pivotal role of fat malabsorption in chronic pancreatitis is due to several interacting mechanisms ... [Pg.282]


See other pages where Vitamin clinical presentation is mentioned: [Pg.310]    [Pg.927]    [Pg.644]    [Pg.497]    [Pg.1294]    [Pg.268]    [Pg.337]    [Pg.780]    [Pg.920]    [Pg.134]    [Pg.1172]    [Pg.781]    [Pg.921]    [Pg.769]    [Pg.198]    [Pg.145]    [Pg.49]    [Pg.182]    [Pg.109]    [Pg.115]    [Pg.181]    [Pg.310]    [Pg.82]    [Pg.113]    [Pg.167]    [Pg.173]    [Pg.187]    [Pg.301]    [Pg.302]   
See also in sourсe #XX -- [ Pg.998 ]

See also in sourсe #XX -- [ Pg.365 ]

See also in sourсe #XX -- [ Pg.365 ]




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