Vitamin pathophysiology

Dietary deficiency of thiamine (vitamin 6,j results In an Inability to synthesize thiamine pyrophosphate, and the pathophysiology arises from Impaired glucose utilization, especially manifested In the nervous system. 

Pathophysiologically, there is a macrocytic anaemia with megaloblastic haematopoiesis that occurs in the face of normal folate and vitamin B12 and is refractory to therapeutic trials of these two nutrients. Patients are characterized as having a preleukaemic syndrome, which is currently regarded by many as a neoplastic process arising in the haematopoietic stem cells that is analogous to early acute myeloblas-tic leukaemia. 

Pathophysiologically, this arises in three ways. First, output may be ineffective as occurs with deficiencies of folate and vitamin B12, or in the myelodys-plastic syndromes. Second, extensive infiltration by malignant disease or fibrous is to blame. Third, the blood-forming tissue is deleted - usually reversible... 

Disease Hypoparathyroidism Pathophysiology Decreased parathyroid hormone secretion leads to impaired bone resorption and hypocalcemia Primary Drug Treatment Calcium supplements, vitamin D... 

High-dose pretreatment with vitamin E (1000IU p.o. once daily for 5 days) has been shown to promote the chronic recovery of spinal-cord injured cats [45]. This is consistent with its ability to prevent post-traumatic spinal-cord hypoperfusion [29] and lipid peroxidation [8] and with the hypothesis that oxygen-radical generation and lipid peroxidation are important mediators of post-traumatic spinal-cord pathophysiology and degeneration. 

Audran M. The physiology and pathophysiology of vitamin D. Mayo Clin Proc 1985 60 851-66. 

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. 

Jurutka, P. W. et al. 2007. Vitamin D receptor Key roles in bone mineral pathophysiology, molecular mechanism of action, and novel nutritional ligands. Journal of Bone and Mineral Research 22 (Suppl. 2) V2-10. 

Most, if not all, of the tissues and organs in the body are adversely affected by chronic ingestion of excessive amounts of alcohol, including the liver, pancreas, heart, reproductive organs, central nervous system, and the fetus. Some of the effects of alcohol ingestion, such as the psychotropic effects on the brain or inhibition of vitamin transport, are direct effects caused by ethanol itself. However, many of the acute and chronic pathophysiologic effects of alcohol relate to the pathways of ethanol metabolism (see Chapter 25). 

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