Scurvy is caused by prolonged dietary deficiency of vitamin C, the plasma 
concentration of which appears inversely related to mortality from all causes. 
Its clinical importance relates principally to its role as a cofactor in a 
number of enzyme reactions involved in collagen synthesis, dysfunction of which 
disrupts connective tissue integrity, resulting in impaired wound healing and 
capillary bleeding. In the UK, overt scurvy is diagnosed only rarely. However, 
subclinical vitamin C deficiency appears quite common, one study estimated that 
25% of men and 16% of women in the low income/materially deprived population had 
vitamin C deficiency, with smoking a strong predictor. Because many of the early 
symptoms of vitamin C deficiency (fatigue, malaise, depression and irritability) 
are non-specific, the diagnostic possibility of scurvy is usually delayed until 
haemorrhagic manifestations occur. The classical cutaneous features consist of 
perifollicular purpura, contorted (corkscrew) hairs and follicular 
hyperkeratosis, particularly affecting the legs. Large areas of purpura or 
ecchymosis may occur. Swelling and bleeding of the gums is an early mucosal 
symptom, and progressively severe gum disease causes loss of teeth. 
Subperiosteal haemorrhage, particularly in the femur and tibia, can present as 
pain, pseudoparalysis, swelling and discoloration of the legs. Haemorrhage into 
joints and muscle is very uncomfortable. Diagnosis is generally made on the 
basis of clinical features, corroborated by a history of dietary inadequacy, and 
the subsequent rapid resolution of symptoms with the restoration of an adequate 
vitamin C intake.