Nutritional deficiency, manifestations

Cancer patients often develop symptoms from organs remote from the primary tumor. The symptoms are usually caused by metastasis or toxic effects of therapy and less often by such secondary factors as nutritional deficiency, metabolic disturbances, opportunistic infections, and effects of critical illness. Other systemic diseases such as diabetes or amyloid may become manifest or aggravated during the course of the cancer disease and cause symptoms from remote organs. Paraneoplastic neurological syndromes (PNS) are a rare cause of remote symptoms [1]. The PNS affect less than 1% of all cancer patients [2], Even in small cell lung cancer (SCLC), the tumor type most commonly associated with PNS, these disorders occur in less than 5% of the patients [3, 4],... 

Glusman M. The syndrome of burning feet (nutritional myalgia) as a manifestation of nutritional deficiency. Am J Med 1947 3 211-23. 

Isolated nutritional deficiencies. Iron, folate, or vitamin Bi2 deficiency may manifest as anemia, which may be mild vitamin K deficiency as a bleeding tendency and vitamin D deficiency as bone disease. They are reflected by a variety of signs and symptoms (glossitis, pallor, dermatitis, petechiae, bruising, hematuria, muscle or bone pain, or neurological abnormalities). 

Thiamine, also known as vitamin B, is fairly ubiquitous. Thiamine deficiency is uncommon except in alcoholics as a result of nutritional deficiencies and malabsorption. The classic clinical triad of dementia, ataxia (difficulty with walking), and eye findings may be seen, but more commonly, only forgetfulness is noted. Sometimes, thiamine deficiency can lead to vague symptoms such as leg numbness or tingling. Because thiamine is water soluble, it can be added to intravenous fluids and administered in that way. Other manifestations include beri beri, which is cardiac involvement leading to a high cardiac output, and vasodilation. Affected patients often feel warm and flushed, and they can have heart failure. 

Because biochemical changes may precede the development of any clinical manifestation of a nutritional deficiency, careful laboratory moniloring should be instituted. 

The effects of fat, protein, a variety of nutritional deficiencies, rate of growth, age of tissue, and sex of the animal on the many different functions of sex organs, muscle, liver, kidney, brain, and circulatory systems which may be manifested by either biochemical alterations or histological observations of tissue deterioration or pigmentation make for a staggering total of interplaying variables that would be beyond human capabilities of under-... 

To understand Marandn s meaning properly, it should be noted that he used the word cretinism as he was used to observe it, in sporadic congenital hypothyroidism, and that his reference to a pluriglandular lesion included short stature and dwarfism. It appears that it was conceptually difficult for him to accept that a nutritional deficiency could underly such complex and apparently unrelated manifestations, and he concluded that intermarriage, poverty, etc., were the most important etiological factors. This was most unfortunate, as Marandn was greatly respected, but his efforts in favour of iodine prophylaxis lacked complete conviction. 

A collective term for a group of nutritional deficiency diseases characterized by impaired absorption of nutrients from the small intestine, especially fats, glucose, and vitamins. Although all sprues exhibit the same general clinical manifestations of intestinal malabsorption and steatorrhea (fatty diarrhea), the following three etiologic classifications are presented in this book ... 

Magro C, Crowson NA, Mihm Jr, M (1997) Cutaneous manifestations of nutritional deficiency states and gastrointestinal disease. In D Elder et al (eds) Lever s Histopathology of the Skin, 8th ed. Lippincott-Raven, Philadelphia, 353-354... 

In the case of a nutrient there is a low-dose adverse effect due to nutritional inadequacy, but the nature of the adverse effect is completely different from that which becomes manifest as the region of high-dose toxicity is entered. Also, the very large risk associated with severe nutrient deficiency at doses near zero is not at all present in the case of hormesis. 

Hansen, A. E., Haggard, M. E., Borlsche, A. N., Adam, D.J.D. and Wiese, H. F. 1958. Essential fatty acid in infant nutrition. III. Clinical manifestations of linoleic acid deficiency. J. Nutr. 66, 565-576. 

Copper deficiency may present as hematological changes (anemia, leukopenia, and neutropenia) and skeletal demineralization. In severe cases, such as in Menkes syndrome, copper deficiency is further manifested as hypothermia, depigmentation of hair and skin, progressive mental deterioration, and growth retardation. Factors predisposing to copper deficiency include malabsorption states, protein-losing enteropathy, nephrotic syndrome, copper-free parenteral nutrition, and copper-deficient enteral nutrition. 

Zinc is a required mineral nutrient in the diet of animals and the signs and effects of a dietary deficiency have been described in several species ( ). Nutritional zinc deficiency has also been described in humans (2). Signs of nutritional zinc deficiency may be manifest even though the individual is consuming an amount of dietary zinc that exceeds the usually designated requirement (2). Thus, bloavailabillty of dietary zinc is a factor that must be evaluated in considering adequacy of dietary intake (jl). 

Hodges RE, Hood J, Canham JE, Sauberlich HE, and Baker EM (1971) Clinical manifestations of ascorbic acid deficiency in man. American Journal of Clinical Nutrition 24, 432-43. 

Animals and yeasts can synthesize nicotinamide from tryptophan via hydroxyanthranilic acid (52) and quinolinic acid (53, Fig. 6A) (31), but the biosynthetic capacity of humans is limited. On a diet that is low in tryptophan, the combined contributions of endogenous synthesis and nutritional supply of precursors, such as nicotinic acid, nicotinamide, and nicotinamide riboside, may be insufficient, which results in cutaneous manifestation of niacin deficiency under the clinical picture of pellagra. Exogenous supply of nicotinamide riboside was shown to promote NAD+-dependent Sir2-function and to extend life-span in yeast without calorie restriction (32). 

The EFAs LA and ALA are present in human diet in abundant amounts, and, hence, EFA deficiency is uncommon. In certain specific conditions, such as total parentaral nutrition (TPN) and severe malabsorption, occasionally EFA deficiency could be seen. The current TPN solutions contain adequate amounts of EFAs. The manifestations of an EFA deficiency include dry and scaly skin, hepatospleenomegaly, immunodeficiency, inappropriate water loss through the skin, dehydration, scalp dermatitis, alopecia, and depigmentation of hair (9, 10). EFAs are distributed widely in normal human diet. The main dietary sources of EFAs are as follows. 

The manifold relationships between the metabolic functions of the liver and the vitamins fulfil vital tasks in helping the organism to stay healthy. Nutrition low in vitamins or age-related reduction in intestinal vitamin resorption as well as chronic alcoholism may be responsible for the development of hypovitaminosis. Standard values of vitamins (including fat-soluble vitamins) in the serum do not exclude a deficit. Deficiency is often recognized for the first time owing to the manifestation of clinical symptoms, and now requires substitution. Substitution therapy may be recommended, even if no vitamin deficiencies have become manifest at this stage, (s. p. 47) (s. tab. 28.2 )... 

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. 

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