Vitamin C deficiency: scurvy
The vitamin C deficiency disease scurvy was formerly a common problem at the end of winter, when there had been no fresh fruit and vegetables for many months.
Although there is no specific organ for storage of vitamin C in the body, signs of deficiency do not develop in previously adequately nourished subjects until they have been deprived of the vitamin for 4–6 months, by which time plasma and tissue concentra-tions have fallen considerably. The earliest signs of scurvy in volunteers maintained on a vitamin C-free diet are skin changes, beginning with plugging of hair follicles by horny material, followed by enlargement of the hyperkeratotic follicles, and petechial hemor-rhage with significant extravasation of red cells, pre-sumably as a result of the increased fragility of blood capillaries.
At a later stage there is also hemorrhage of the gums, beginning in the interdental papillae and pro-gressing to generalized sponginess and bleeding. This is frequently accompanied by secondary bacterial infection and considerable withdrawal of the gum from the necks of the teeth. As the condition pro-gresses, there is loss of dental cement, and the teeth become loose in the alveolar bone and may be lost.
Wounds show only superficial healing in scurvy, with little or no formation of (collagen-rich) scar tissue, so that healing is delayed and wounds can readily be reopened. The scorbutic scar tissue has only about half the tensile strength of that normally formed.
Advanced scurvy is accompanied by intense pain in the bones, which can be attributed to changes in bone mineralization as a result of abnormal collagen syn-thesis. Bone formation ceases and the existing bone becomes rarefied, so that the bones fracture with minimal trauma.
The name scurvy is derived from the Italian scor-butico, meaning an irritable, neurotic, discontented, whining, and cranky person. The disease is associated with listlessness and general malaise, and sometimes changes in personality and psychomotor performance and a lowering of the general level of arousal. These behavioral effects can be attributed to impaired syn-thesis of catecholamine neurotransmitters, as a result of low activity of dopamine β-hydroxylase.
Most of the other clinical signs of scurvy can be accounted for by the effects of ascorbate deficiency on collagen synthesis, as a result of impaired proline and lysine hydroxylase activity. Depletion of muscle car-nitine, due to impaired activity of trimethyllysine and γ-butyrobetaine hydroxylases, may account for the lassitude and fatigue that precede clinical signs of scurvy.
Anemia is frequently associated with scurvy, and may be either macrocytic, indicative of folate deficiency, or hypochromic, indicative of iron deficiency.
Folate deficiency may be epiphenomenal, since the major dietary sources of folate are the same as those of ascorbate. However, some patients with clear meg-aloblastic anemia respond to the administration of vitamin C alone, suggesting that there may be a role of ascorbate in the maintenance of normal pools of reduced folates, although there is no evidence that any of the reactions of folate is ascorbate dependent.
Iron deficiency in scurvy may well be secondary to reduced absorption of inorganic iron and impaired mobilization of tissue iron reserves . At the same time, the hemorrhages of advanced scurvy will cause a significant loss of blood.
There is also evidence that erythrocytes have a shorter half-life than normal in scurvy, possibly as a result of peroxidative damage to membrane lipids owing to impairment of the reduction of tocopher-oxyl radical by ascorbate.
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