Anaemia scurvy

Deficiency symptoms In vitamin C deficiency scurvy develops. It is characterized by ecchymosis, petechiae, swollen and bleeding gums, subperiosteal haemorrhage, bones are painful to touch, impaired wound healing, anaemia, loosening of teeth and gingivitis. 

It is indicated for treatment of scurvy, for prophylaxis of vitamin C deficiency, to acidify urine, anaemia of vitamin C deficiency, as antioxidant to protect natural colour and flavour of many foods, dental caries and increased capillary fragility. 

Folic acid is itself inactive it is converted into the biologically active coenzyme, tetrahydrofolic acid, which is important in the biosynthesis of amino acids and DNA and therefore in cell division. The formyl derivative of tetrahydrofolic acid is folinic acid and this is used to bypass the block when the body fails to effect the conversion of folic acid (see Folic acid antagonists, p. 606). Ascorbic acid protects the active tetrahydrofolic acid from oxidation the anaemia of scurvy, although usually normoblastic, may be megaloblastic due to deficiency of tetrahydrofolic acid. 

Finally, what of anaemia This, too, is a symptom of scurvy, but is not a physiological failure in the sense of those discussed above. In this case, vitamin C acts on the inorganic iron in food in the stomach and intestines, converting it from the insoluble form usually found in food (Fe3+) to the soluble form (Fe2+) that we can absorb in our intestines. (This is the reverse of the reaction that took place on a huge scale in the Pre-cambrian oceans, leading to the precipitation of insoluble iron into banded iron formations, discussed in Chapter 3). Without adequate supplies of vitamin C, we cannot absorb enough iron to stock red blood cells with haemoglobin (which contains iron), and so we develop anaemia. 

What is this disease A textbook definition would be something like A disease which produces haemorrhaging into tissues, bleeding gums, loose teeth, anaemia and general weakness. However, contemporary descriptions of individual cases bring home to us the unpleasantness of scurvy. Thus Thomas Stevens wrote from a ship travelling from Lisbon to Goa in 1579 ... 

Anaemia is frequently associated with scurvy, and may be either macrocytic, indicative of folate deficiency (section 11.11.4), or hypochromic, indicative of iron deficiency (section 11.15.2.3). 

A disease resulting from a deficiency of one or more vitamins is hypovitaminosis (if vitamin is supplied in insufficient quantity) or avitaminosis (complete lack of vitamin manifested by some biochemical processes disorder). Deficiency of vitamins was formerly one of the main causes of many diseases and deaths. Pellagra (deficiency of some B-complex vitamins), scurvy (vitamin C), beriberi (thiamine), rickets (vitamin D), pernicious anaemia associated with reduced ability to absorb vitamin Bj2 (corrinoids) and xerophthalmia (vitamin A) are now well-known diseases caused by vitamin deficiency. Excessive intake of one or more vitamins (especially of lipophilic vitamins A and D) also causes an abnormal state resulting from disturbances of biochemical processes and can lead to severe diseases known as hypervitaminosis. 

A water soluble vitamin which cannot be synthesized by man and therefore has to be obtained from the diet. It is found extensively in vegetables and fruit, especially the citrus varieties. Since the vitamin is carried mainly in the leukocytes, its measurement in these cells gives some indication of the vitamin C status of the body. The ascorbic acid saturation test can also be used to assess the vitamin status. The biochemical role of the vitamin is obscure although it does seem to be required for collagen formation. Deficiency of the vitamin causes scurvy, the symptoms of which can be related to poor collagen formation. These include poor wound-healing, osteoporosis (due to bone matrix deficiency), a tendency to bleed (due to deficiences in the vascular walls) and anaemia. 

Effects of Vitamin C Deficiency.—(i.) Infantile Scurvy.—This condition is found in children fed exclusively on sterilised or artificial dietaries, or by mothers whose milk is deficient in ascorbic acid. After a period of anaemia and irregular growth, the characteristic syndrome appears sore gums, periosteal haemorrhages at the joints, subcutaneous haemorrhages and haematuria. 

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