Scurvy
A disease caused by prolonged severe dietary deficiency of ascorbic acid, in
which the breakdown of intercellular cement substances leads to capillary
haemorrhages and defective growth of fibroblasts, osteoblasts, and odontoblasts
results in impaired synthesis of collagen, osteoid, and dentine; it is characterized
by haemorrhagic gingivitis affecting especially the interdental papillae (in the
absence of teeth, the gums are normal), subperiosteal haemorrhages, bone lesions(including the corner fraction sign, a ground-glass appearance, and trabecularatrophy) seen on radiography, perifollicular haemorrhages, and frequently petechial haemorrhages (especially on the feet). Sudden death may occur as a result of cerebral or myocardial haemorrhage. Megaloblastic anaemia, usually due to concomitant iron and/or folate deficiency, is usual. The early manifestations include weakness, lethargy, myalgia, and arthralgia. In the infantile form (in which onset usually occurs in the second 6 months of life), gingival involvement is minimal and the infant assumes a ‘frog-like’ position and does not move its legs (owing to the intense pain of subperiosteal haemorrhages). In the adult form there are intraarticular and intramuscular haemorrhages, and osteoporosis may occur.The disorder may occur in infants born to mothers who are consuming large doses of ascorbic acid, and in adults following the abrupt discontinuation of large supplemental doses (despite relatively normal dietary intake of ascorbic acid).
Scurvy
Signs and symptoms
Classic scurvy
Vitamin C status follows the following stages (Hodges, 1980):
• The optimal stage with full saturation of the metabolic body pool.
• If the diet is less than optimal for some time, the metabolic body pool decreases in size, theperson remains clinically well, and plasma levels remain within the normal range.
• If a deficient diet is consumed for a long enough period, the body pool is substantially depleted and plasma levels decline to the lower ranges of normal but with no clinical signs.
• The continuation of a deficient diet results in further decreases in the body pool size of vitaminC to 300 mg or less, a reduction in the catabolic rate to 9 mg or less, and the whole blood vitamin C content to a level below 0.3 mg/100 ml. Clinical signs of scurvy appear. Manifest scurvy in adults is preceded by a period of latent scurvy whose early symptoms include lassitude, weakness and irritability; vague, dull aching pains in the muscles or joints of the legs and
feet; and weight loss. Shortness of breath may also occur and the skin can become dry and rough.
The principal signs and symptoms of manifest scurvy in adults consist of follicular hyperkeratosis,haemorrhagic manifestations, swollen joints, swollen bleeding gums, and peripheral oedema (Hodges et al., 1971). Anaemia of a variable degree occurs with scurvy in a certain percentage of adults and
infants, which is considered to be due in part to undernutrition and intercurrent infection. However,it is due chiefly to the effect of vitamin C on blood formation, folic acid metabolism, and bleeding.In children the syndrome is called Moeller-Barlow disease, and is seen in non-breast-fed infants
usually at about 5-6 months of age when maternally derived stores of vitamin C have been exhausted. No single symptom predominates, but the majority of infants with scurvy eventually show signs of irritability, tenderness of the legs, and pseudo paralysis, usually involving the lowerextremities. The “pithed-frog” position—legs flexed at the knees and hips partially flexed—is assumed by approximately half the sufferers. Involvement of the costochondral junctions is very common, and costochondral beading is found in 80% of infants with scurvy. Haemorrhage around erupting teeth is consistently present. Petechial haemorrhages in the skin may occur (10 -15% of infants with scurvy). Left untreated, scurvy in any age group can lead to death.