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Metabolism nutritional diseases

Osteoporosis is a metabolic bone disease characterized by low bone mass and micro-architectural deterioration of bone tissue. This will lead to bone fragility and consequent increase in bone fracture risk. Mean bone mineral density (BMD) is measured with dual X-ray absorptiometry (DEXA) and expressed in Tsc (Tscore). WHO standards are a Tsc that is 1 standard deviation (SD) below mean BMD is graded as normal bone, Tsc between 1 and 1.5 SD below mean BMD is graded as osteopenia and a Tsc of more than 2.5 SD below mean BMD is graded as osteoporosis. When the Tsc is below 1.5 SD mean BMD prevention of osteoporosis must be initiated. Primary osteoporosis is caused mainly by hormone deflciency in both women and men. Secondary osteoporosis may result from endocrine, metabolic, nutritional and autoimmune causes or from immobility because of trauma. Also the use of medicaments such as corticosteroids may be contributing. [Pg.668]

After persistent hypercalciuria, osteopenia can develop, causing metabolic bone disease, pathological fractures, and immobilization. Hypercalciuria can also lead to nephrolithiasis and nephrocalcinosis, factors that can impair renal function. Intravenous chlorothiazide has been successfully used for its hypocalciuric effect, with remarkable effect over a period of 6 months in a 13-year-old child who had received parenteral nutrition for 6 years. Calcium excretion and tubular reabsorption of phosphate returned to normal (48). What is not clear from this study is whether the drug actually has a positive long-term beneficial effect on metabolic bone disease. [Pg.2705]

Over the years, problems have arisen as a result of the presence of significant amounts of aluminium in parenteral nutrition solutions in particular they have been held responsible for hypercalciuria and its consequences (54). Parenterally administered aluminium bypasses the gastrointestinal tract, which normally serves as a protective barrier to aluminium entry into the blood. In the past, aluminium contamination of casein hydrolysate, which was used as a source of protein in parenteral nutrition solutions, was associated with low-turnover osteomalacia and with encephalopathy in uremic patients. Premature infants are still at risk of aluminium accumulation as a result of prolonged parenteral nutrition (as are patients receiving plasmapheresis with albumin contaminated in its preparation with aluminium). Metabolic bone disease can result (54). [Pg.2705]

Metabolic bone disease in children receiving parenteral nutrition manifests primarily as osteopenia and, on occasion, fractures (5). The etiology is multifactorial calcium and phosphate deficiency play a major role in the preterm infant but the part played by aluminium toxicity in this population is unknown. Lack of reference values of bone histomorphometry in the premature infant, as well as lack of reference data for biochemical markers of bone turnover in these patients, contributes to the uncertainty. Other factors that may play a role in the pathogenesis of bone disease associated with parenteral nutrition include lack of periodic enteral feeding underljdng intestinal disease, including malabsorption and inflammation the presence of neoplasms and drug-induced alterations in calcium and bone metabohsm. However, the true incidence and prevalence of parenteral nutrition-associated bone abnormalities in pediatric patients are unknown. [Pg.2713]

BQein GL. Metabolic bone disease of total parenteral nutrition. Nutrition 1998 14(l) 149-52. [Pg.2718]

Vargas JH, Klein GL, Ament ME, Ott SM, Sherrard DJ, Horst RL, Berquist WE, Alfrey AC, Slatopolsky E, Coburn JW. Metabolic bone disease of total parenteral nutrition course after changing from casein to amino acids in parenteral solutions with reduced aluminium content. Am J Clin Nutr 1988 48(4) 1070-8. [Pg.2720]

Cynober LA, ed. Amino acid metabolism in health St nutritional disease. Boca Raton CRC Press, 1995. [Pg.595]

Buchman AL, Moukarzel A. Metabolic bone disease associated with total parenteral nutrition. Clin Nutr 2000 19 217-231. [Pg.2613]

Jeejeebhoy KN. Metabolic bone disease and total parenteral nutrition A progress report. Am J Clin Nutr 1998 67 186-187. [Pg.2657]

Involutional (primary) osteoporosis is the manifestation of a metabolic bone disease in which the amount of normally mineralized bone matrix in affected patients has been reduced to a level below that of the normal population of the same age and sex. The disease is certainly of multifactorial origin, since genetic (Seeman etal. 1989), mechanical (e.g.. Frost 1988), nutritional (e.g., Hegsted 1986), and hormonal factors (e.g., Melton and Riggs 1988) can cause the severe impairment of the bone remodeling process (Eriksen etal. 1994) which underlies the observed reduction in bone mass and microarchitectural deterioration of bone tissue that lead to an increased risk of fractures at typical sites of the skeleton (for a definition, see Anonymous 1993)... [Pg.609]

The successful establishment of nondestructive NAA as an analytical technique for the study of the elemental composition of biological materials promoted the evaluation of its feasibility for determining some elements in living subjects by in vivo NAA (Anderson et al. 1964). From this first demonstration, the technique rapidly evolved (Ellis 1990). Currently, it is possible to measure total-body H, N, O, Na, P, Cl, K, and Ca and to determine most of the same elements in parts of the body, such as a limb or an organ. In special cases, additional important elements such as I (in thyroid), Cd (in kidney), as well as Mn, Fe, and Cu have been reported. The results of the measurements are used in clinical studies of mineral metabolism, nutrition, body physiology, and alterations in composition from clinical or enviromnental causes and diseases such as osteoporosis. [Pg.1567]

Editorial Nutrition and metabolic bone disease in the elderly. Nutr. Rev. 25, 71-72 (1967)... [Pg.361]

Some elements, for example calcium and molybdenum, may interfere with the absorption, transport, function, storage or excretion of other elements. There are many ways in which minerals may interact, but the three major ways involve the formation of unabsorbable compounds, competition for metabolic pathways and the induction of metal-binding proteins. The interaction of minerals with each other is an important factor in animal nutrition, and an imbalance of mineral elements -as distinct from a simple deficiency - is important in the aetiology of certain nutritional disorders of farm animals. The use of radioactive isotopes in recent years has advanced our knowledge of mineral nutrition, although there are many nutritional diseases associated with minerals whose exact causes are still unknown. [Pg.106]

Olsson, A.G., 2010b. HDL and LDL as therapeutic targets for cardiovascular disease prevention the possible role of niacin. Nutrition, Metabolism Cardiovascular Disease. 20 553-557. [Pg.687]

Christie (1987) discussed various functions of lipids as follow their involvement in disturbances of lipid metabolism associated with specific lipid disorders accumulation of various neutral, complex, and conjugated lipids in coronary artery and heart disease the role of lipids in nutrition, disease, and human welfare the importance of fats and oils as agricultural products and as major items in international trade the role of fats as a major dietary component and supplier of calories for humans in developed countries and the contribution that fats make to the taste and structure of foods. Ando and Saito (1987) contributed a review on TLC and HPTLC lipid analysis of normal and pathological tissues associated with specific lipidoses and gangliosidoses. [Pg.279]

Soli, F., Buccioni, A., Cesari, F., Gori, A.M., Minieri, S., Mannini, L., Casini, A., Gensini, G.F., Abbate, R., and Antongiovanni, M. 2010. Effects of a dairy product (pecorino cheese naturally rich in cis-9, trans-11 conjugated linoleic acid on lipid, inflammatory and haemorheological variables a dietary intervention study. Nutrition, Metabolism Cardiovascular Diseases 20, 117-124. [Pg.793]

Cynober LA. Amino Acid Metabolism and Therapy in Health and Nutritional Disease. Boca Raton, FL CRC Press, 1995, p. 361. [Pg.334]

One of the triumphs of the science of nutrition is the careful investigation that linked childhood rickets with vitamin D deficiency. This work, which led to methods for treating the disease, is too familiar to need repetition. A direct consequence of these efforts was the elucidation of the pivotal role played by vitamin D in calcium metabolism, as well as the structural studies that revealed that this compound (102) is in fact a steroid derivative. The past... [Pg.101]

For Further Reading J. J. R. Frausto da Silva and R. J. P. Williams, The Biological Chemistry of the Elements The Inorganic Chemistry of Life (Oxford Oxford University Press, 1991). M. F.. Wastney, W. A. House, R. M. Barnes, and K. N. S. Subramanian, "Kinetics of zinc metabolism variation with diet, genetics and disease, Journal of Nutrition, vol. 130, 2000, pp. 1355S-1359S. [Pg.789]

A knowledge of normal metabohsm is essential for an understanding of abnormalities underlying disease. Normal metabolism includes adaptation to periods of starvation, exercise, pregnancy, and lactation. Abnormal metabolism may result from nutritional deficiency, enzyme deficiency, abnormal secretion of hormones, or the actions of drugs and toxins. An important example of a metabolic disease is diabetes mellitus. [Pg.122]

Sequences of various bacterial genomes and other information.) Karolinska Institute Nutritional and Metabolic Diseases http // www.mic.ki.se/Diseases/cl8.html (Access to information on many nutritional and metabolic disorders.)... [Pg.639]

Most CF patients have an increased caloric need due to increased energy expenditure through increased work of breathing and increased basal metabolism. Prevention of malnutrition requires early nutritional intervention. In patients with mild lung disease and well-controlled absorption, required caloric intake is approximately 100% to 120% of the recommended daily allowance (RDA) for age.15 As lung disease progresses, caloric requirements increase. [Pg.249]

PBPK and classical pharmacokinetic models both have valid applications in lead risk assessment. Both approaches can incorporate capacity-limited or nonlinear kinetic behavior in parameter estimates. An advantage of classical pharmacokinetic models is that, because the kinetic characteristics of the compartments of which they are composed are not constrained, a best possible fit to empirical data can be arrived at by varying the values of the parameters (O Flaherty 1987). However, such models are not readily extrapolated to other species because the parameters do not have precise physiological correlates. Compartmental models developed to date also do not simulate changes in bone metabolism, tissue volumes, blood flow rates, and enzyme activities associated with pregnancy, adverse nutritional states, aging, or osteoporotic diseases. Therefore, extrapolation of classical compartmental model simulations... [Pg.233]

Protein requirements are based on age, nutrition status, disease state, and clinical condition. The usual recommended daily protein allowances are 0.8 g/kg for adults, 1.5 to 2 g/kg for patients with metabolic stress (e.g., infection, trauma, and surgery), and 2.5 to 3 g/kg for patients with burns. See Table 57-5 for recommendations for children. [Pg.666]


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