Diarrhoea vitamin

Oxidation of nicotine with chromic acid led to the isolation of pyridine-3-carboxylic acid, which was given the trivial name nicotinic acid. We now find that nicotinic acid derivatives, especially nicotinamide, are biochemically important. Nicotinic acid (niacin) is termed vitamin B3, though nicotinamide is also included under the umbrella term vitamin B3 and is the preferred material for dietary supplements. It is common practice to enrich many foodstuffs, including bread, flour, corn, and rice products. Deficiency in nicotinamide leads to pellagra, which manifests itself in diarrhoea, dermatitis, and dementia. 

Barreto, M. L., Santos, L. M., Assis, A. M., Araujo, M. P., Farenzena, G. G., Santos, P. A., and Fiaccone, R. L. (1994). Effect of vitamin A supplementation on diarrhoea and acute lower-respiratory-tract infections in young children in Brazil. Lancet 344, 228-231. 

The classical niacin deficiency disease is pellagra, which is characterized by symptoms including diarrhoea, dermatitis, dementia and eventually death. High-protein diets are rarely deficient in niacin since, in addition to the preformed vitamin, such diets supply sufficient tryptophan to meet dietary requirements. Large doses of niacin can cause the dilation of capillaries, resulting in a painful tingling sensation. 

Pantothenate deficiency is rare, occurring only in cases of severe malnutrition characteristic symptoms include vomiting, intestinal distress, insomnia, fatigue and occasional diarrhoea. Pantothenate is widespread in foods meat, fish, poulty, whole-grain cereals and legumes are particularly good sources. Although no RDA or RNI value has been established for panthothenate, safe and adequate intake of this vitamin for adults is estimated to be 3-7 mg day-1. Pantothenate is non-toxic at doses up to 10 g day-1. 

The main functions of the GI - digestion and absorption of nutrients, vitamins and cofactors as well as movements of ions and water - need a precise mechanisms of biochemical and physiological control to maintain barrier functions. The cells in the intestine are characterized by high enzymatic activity (lumen and wall), low permeability and typical resistance (between cells tight junctions are formed characterizing the very thight barriers in the organism), efflux pathways back into the gut lumen and first-pass metabolism. The barrier function of the gut is a crucial prerequisite for a normal function of intestine. Impairments lead to diarrhoea and other serious consequences. 

Adverse reactions. Heartburn, nausea and vomiting due to gastric irritation are common, and attempts to reduce this with milk or antacids impair absorption of tetracyclines (see below). Loose bowel movements occur, due to alteration of the bowel flora, and this sometimes develops into diarrhoea and opportunistic infection (antibiotic associated or pseudomembranous colitis) may supervene. Disorders of epithelial surfaces, perhaps due partly to vitamin B complex deficiency and partly due to mild opportunistic infection with yeasts and moulds, lead to sore mouth and throat, black hairy tongue, dysphagia and perianal soreness. Vitamin B preparations may prevent or arrest alimentary tract symptoms. 

Humans cannot synthesise vitamins in the body except some vitamin D in the skin and nicotinamide from tryptophan. Lack of a particular vitamin may lead to a specific deficiency syndrome. This may be primary (inadequate diet), or secondary, due to failure of absorption (intestinal abnormality or chronic diarrhoea), or to increased metabolic need (growth, pregnancy, lactation, hyperthyroidism). 

Biliary steatorrhoea is characterized by higher stool weight (>200 g) and increased excretion of fat (>7 g/ day). This condition correlates with the degree of severity of cholestasis. Stools are soft and smell unpleasant. Steatorrhoea is accompanied by additional diarrhoea. All these changes in the stools lead to a loss of liquid, electrolytes, fat-soluble vitamins and important trace elements. Intestinal bile deficiency causes the characteristic acholic stools, (s. tab. 12.6) (s. fig. 13.8)... 

In the case of Vitamin K-deficency owing to bile obstruction, which has lowered the value for prothrombin complex, vitamin K1 is administered intravenously. In moderate vitamin K-deficiency induced by therapy with antibiotics or diarrhoeas of long duration, oral vitamin K therapy is needed. Prophylactically vitamin K is used for treatment of haemorrhage in the newborn and therapeutically in cases of overdosage of warfarin-type anticoagulants. 

Since these drugs are not absorbed, side effects are confined to the intestine and include abdominal discomfort, diarrhoea or constipation. With long-term therapy, fat-soluble vitamin supplements are necessary. 

The vitamin has also been routinely prescribed in cases of threatened abortion, thyroxidosis, achlorhydia, diarrhoea, prickly heat, rheumatic fever, rheumatic arthritis, and in cases of spinal injury to reduce urine acidity. The physiological basis of these therapeutic applications is not entirely clear except in the cases of achlorhydia and diarrhoea where there is a risk of anaemia caused by a reduction in the intestinal absorption of non-haem iron which is enhanced by vitamin C. 

This patient needs magnesium supplements. As magnesium salts cause diarrhoea they need to be given parenterally, especially in this case where there is established diarrhoea and malabsorption. It is likely that once the patient is magnesium replete, her original Vitamin D and calcium supplements will be sufficient to maintain her in a normocalcaemic state. 

Substitutive drugs take the place of a missing substance the lack can be due to dietary reasons (vitamin deficiency) or to a physiological. disturbance (insulin in diabetes, estrogens in menopause). The substitutive treatment can cover a very short period (intravenous rehydration in case of haemorrhages and diarrhoea), or can last the whole life (hormonal treatment in Addison s disease). 

Standard AIO admixtures are used in most adults patients. However, the patients requirements regarding calories and electrolytes may vary. Dialysis patients require restricted administration of electrolytes, however patients with severe diarrhoea need a higher amount of electrolytes. Standard parenteral nutrition admixtures cannot be used in severely ill paediatric patients, neonates and premature newborns. These patients need individualised admixtures. In premature infants and newborns the all-in-two system is preferred [53]. The lipid emulsion is mixed with the vitamin combination in a separate container and either administered with the amino acid/glucose/electrolyte admixture in parallel (Y-site) or via a separate venous access. 

The vitamin is synthesised in the rumen and deficiencies in animals with functional rumens are unlikely to occur. However, riboflavin deficiencies have been demonstrated in young calves and lambs. Symptoms include loss of appetite, diarrhoea and lesions in the corners of the mouth. 

The classic condition in humans arising from a deficiency of vitamin C is scurvy, characterised by oedema, emaciation and diarrhoea. Failure in collagen formation results in structural defects in bone, teeth, cartilage, connective tissues and muscles. Resistance to infection is reduced. 

The inadequate intake of riboflavin seems to be the main cause for the deficiency of this vitamin, being common in populations whose diet lack dairy products and meat, and in anorexic individuals. Digestion and intestinal absorption disorders are other causes of disability, as observed in individuals with lactose intolerance, tropical sprue, coeliac disease and intestinal resection, as well as gastrointestinal and biliary obstruction. Other disorders such as diarrhoea, infectious enteritis and irritable bowel syndrome can cause poor absorption by increasing intestinal motility. Riboflavin deficiency also occurs in conditions such as chronic alcoholism, diabetes mellitus and inflammatory bowel diseases. 

Niacin is a water-soluble vitamin that has been available as a lipid-lowering medication and in prevention of atherosclerosis for half a century (Ganji et al. 2003 Olsson 2010). Numerous studies have documented its beneficial effects on reducing cardiovascular disease (CVD) (Olsson 2010). Clinically, the most well-known effect of niacin deficiency is pellagra which, as noted above, is manifested by dermatitis, diarrhoea and dementia (Bodor and Offermanns 2008 Ganji, et al. 2003). In this chapter we look at the effects of niacin on human physiology and its consequent effects on disease states. 

Pellagra A syndrome complex characterized by the three D s—dementia, dermatitis and diarrhoea—due to deficiency of vitamin B3 or niacin. 

If the rate of uptake of retinol from the intestine consistently exceeds the capacity of the liver to dispose of it, significant amounts of retinol, mainly in the form of retinyl palmitate, appear in the general circulation and may give rise to toxic effects. The effects of hypervitaminosis A are many and varied. They include increased intracranial pressure, severe headache, hyperirritability, vomiting, diarrhoea, bone decalcification and skin lesions. The condition can be fatal. It has in the past been caused by over-zealous administration of concentrated sources of the vitamin such as halibut liver oil. This may contain several hundred times as much vitamin A and 40 times as much vitamin D as cod liver oil. It has also occurred in people who have eaten polar bear or husky dog liver which contain massive amounts of vitamin A. 

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