Infection vitamin

The first clues to the treatment of scurvy occurred in 1535—1536 when Jacques Cartier, on advice from Newfoundland Indians, fed his crew an extract from spmce tree needles to cure an epidemic. Various physicians were recommending the use of citms fmits to cure scurvy in the mid-sixteenth century. Two hundred years later, in 1753, it was proved by Dr. James Lind, in his famous clinical experiment, that scurvy was associated with diet and caused by lack of fresh vegetables. He also demonstrated that oranges and lemons were the most effective cure against this disease. In 1753, inM Treatise on the Scurvy[ Lind pubhshed his results and recommendations (7). Eorty-two years later, in 1795, the British Navy included lemon juice in seamen s diets, resulting in the familiar nickname "limeys" for British seamen. Evidence has shown that even with undefined scorbutic symptoms, vitamin C levels can be low, and can cause marked diminution in resistance to infections and slow healing of wounds. 

Vitamin C status is supposed to play a role in immune function and to influence the progression of some chronic degenerative diseases like atherosclerosis, cancer, cataracts, and osteoporosis. The role of vitamin C in immune function, especially during common cold and upper respiratory tract infection, is the subject of lively debate. The exact mechanisms of action have not yet been fully elucidated, but the results of several trials point to a reduced duration and intensity of infections in subjects consuming high amounts of vitamin C (200-1000 mg/d). However, the incidence of common cold was not influenced significantly (24). 

The classic example is that of Prontosil (Figure 2.12) in which the compound is active against bacterial infection in animals though inactive against the bacteria in pure culture. The toxicity in animals is the result of reduction to the sulfanilamide (4-aminobenzenesulfonamide) that competitively blocks the incorporation of 4-aminobenzoate into the vitamin folic acid. 

Connective tissue disease Substance abuse Stevens-Johnson syndrome Immunocompromised Atopic dermatitis Gonococcal infection Vitamin A deficiency... 

Cystic fibrosis is the most common lethal autosomal-recessive disease, in which oxidative stress takes place at the airway surface [274]. This disease is characterized by chronic infection and inflammation. Enhanced free radical formation in cystic fibrosis has been shown as early as 1989 [275] and was confirmed in many following studies (see references in Ref. [274]). Contemporary studies also confirm the importance of oxidative stress in the development of cystic fibrosis. Ciabattoni et al. [276] demonstrated the enhanced in vivo lipid peroxidation and platelet activation in this disease. These authors found that urinary excretion of the products of nonenzymatic lipid peroxidation PGF2 and TXB2 was significantly higher in cystic fibrotic patients than in control subjects. It is of importance that vitamin E supplementation resulted in the reduction of the levels of these products of peroxidation. Exhaled ethane, a noninvasive marker of oxidative stress, has also been shown to increase in cystic fibrosis patients [277]. 

A number of early in vitro studies demonstrated a considerable role of free radicals in liver injury (see, for example, Proceedings of International Meeting on Free Radicals in Liver Injury [341]). Later on, it was shown that chronic inflammation in the liver-induced oxidative DNA damage stimulated chronic active hepatitis and increased the risk of hepatocarcinogenesis [342,343]. Farinati et al. [344] showed that 8-OHdG content increased in circulating leukocytes of patients with chronic hepatitis C virus (HCV) infection. DNA oxidative damage is supposedly an early event of HCV-related hepatitis. The formation of isoprostanes in the liver of carbon tetrachloride-treated rats can be suppressed by the administration of vitamin E [345],... 

Other drugs can cause hypercalcaemia and increase the risk of forming kidney stones that can damage the kidneys and ureters and cause infections. Examples are cytostatic agents, sulphonamides, radiological contrast media, statins (through rhabdomyolysis), vitamin D and intake of calcium and antacids. 

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