Effects of Deficiency of Vitamin C

Vitamin C is concerned fundamentally with the formation of intercellular substances including collagen of fibrous tissue structures, the matrices of bone, cartilage and dentine and all non-epithelial cement substances including that of vascular endothelium. The connective tissue has the highest concentration of vitamin C and after wounds it accumulates quickly in the scar tissue. An excessive intake of vitamin C is claimed to decrease the incidence of atherosclerosis and the common cold.

In the deficiency of vitamin C the disease called scurvy (scorbutus) results. Scurvy is liable to occur in artificially-fed infants. Breast-fed infants rarely suffer from scurvy. It should be noted that subclinical scurvy occurs much more frequently than frank scurvy. Scurvy has the following clinical picture:

1. Hemorrhages from the mucous membranes of the nose, mouth and gastrointestinal tract, skin, muscles, and in the subperiosteal tissues. The most frequent site of lesions is gums which show swelling, redness, ulceration etc which may lead to gangrene and loss of teeth. Capillaries show increased fragility.
   
   
2. Anemia, weakness and emaciation; there is a tendency to remain motionless.
   
   
3. Skin shows discoloration of perifollicular areas especially over back and thighs.
   
   
4. Since vitamin C is necessary for wound healing its deficiency results in delayed healing of wounds and fractures.
   
   
5. At the growing ends of long bones osteoblastic function is arrested but there is continued calcification of cartilage which leads to a piling up calcified matrix. This is brittle and commonly shows fragmentation while fracture may take place through the rarefield metaphysis immediately adjacent. In addition, a fibrous union is formed between the diaphysis and the epiphysis which be seen as an enlargement of the costochondral junctions. Characteristics hemorrhages occur beneath the periosteum of long bones; the hematomas may become calcified. There is pain in joints. Acute tenderness of the limbs causes the infant to cry with pain when limbs are touched. The legs are held in “the frog position’ in which the thighs are abducted and semi-flexed. X-rays shows the heavy ‘white line’ of calcified matrix at the ends of long bones, the rarefied zone adjacent to it and in severe cases a ground glass appearance of the long bones and epiphyses due to generalized rarefaction. Tooth development is impaired in the very young; this is due to non-formation of dentine by odontoblasts.

The diagnosis of scurvy is made from the patient’s history, physical findings and the following laboratory investigations:

1. Capillary fragility test or tourniquet test: A blood pressure cuff is maintained in place while it is inflated to a pressure between systolic and diastolic pressure for 5 to 15  minutes and the number of petechial hemorrhages in a 2.5 cm diameter circle on the upper forearms is recorded. A positive test (petechiae more than 10) is evidence of platelet or vascular defect. This test is however not specific for vitamin C deficiency.
   
   
2. Determination of Plasma ascorbic acid: Normal Plasma ascorbic acid level is 0.7 to 1.2 mg%; a level below 0.4mg% indicates severe deficiency.
   
   
3. The ascorbic acid level in the white cell-platelet (buffy coat) layer. This is more significant. A level below 4 mg per 100 ml is closely correlated with scurvy (normal=25 to 30 mg per 100 ml).
   
   
4. Saturation or load test: on giving standard does of ascorbic acid to the patient very little of it appears in the urine. This is because the tissues being deficient in ascorbic acid retain an excess of it. It is only when tissues become saturated with ascorbic acid that it starts appearing in urine in appreciable amounts.

The half life of ascorbic acid in main 16 days and it takes 3 to 4 months for scurvy to develop if a person is put on diet lacking vitamin C.