Vitamin disease/disorder effects

Enhanced anticoagulant effects Endogenous factors that may be responsible for increased PT/INR response include the following Blood dyscrasias cancer collagen vascular disease CHF diarrhea elevated temperature hepatic disorders (eg, infectious hepatitis, jaundice) hyperthyroidism poor nutritional state steatorrhea vitamin K deficiency. 

United States Congress passes Dietary Supplement Health and Education Act, which expressly defines a dietary supplement as a vitamin, a mineral, an herb or other botanical, an amino acid, or any other dietary substance. This law prohibits claims that herbs can treat diseases or disorders, but it allows more general health claims about the effect of herbs on the structure or function of the body or about the well-being they induce. Under this law, the FDA bears the burden of having to prove an herbal is unsafe before restricting its use. This law also establishes the Office of Dietary Supplements within the National Institutes of Health to promote and compile research on dietary supplements. 

The scientific community has been discussing for quite some time now the relationship between oxidative stress, defined as the imbalance between oxidant and antioxidants [45], and the health-disease status. An impressive amount of information available in the literature deals with the effects of the classic antioxidants, ascorbic acid, a-tocopherol, and jS-carotene in a huge series of pathophysiological situations in experimental animals and humans. Concerning the effects of the classic antioxidants on mitochondrial function in situations of oxidative stress, the information is not so vast and most of the time it is not conclusive. However, substantial progress has been made in the description of the mitochondrial alterations in neurodegenerative diseases and in the a-tocopherol effects,both as prevention and as treatment [46]. We will briefly review some reports related to vitamin E and mitochondrial dysfunction in oxidative metaboHc disorders and in the neurodegenerative Alzheimer s and Parkinson s diseases. 

A multiphcity of metabolic disorders in patients with CKD contributes to worsening sHPT and the consequences associated with elevated PTH (Fig. 44-4). The continuous production of PTH by the parathyroid glands leads to parathyroid hyperplasia (nodular or diffuse). Nodular tissue demonstrates more rapid growth potential and appears to be associated with fewer vitamin D and calcium-sensing receptors, which results in resistance to the effects of calcium and vitamin D therapy and subsequent development of ROD. Bone loss can be detected in patients with early stages of kidney disease and multiple types of bone lesions have been identified from bone biopsies of patients on dialysis. The skeletal complications associated with ROD... 

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