scurvy(redirected from Ascorbic acid deficiency)
Also found in: Dictionary, Thesaurus, Medical.
scurvy, deficiency disorder resulting from a lack of vitamin C (ascorbic acid) in the diet. Scurvy does not occur in most animals because they can synthesize their own vitamin C, but humans, other primates, guinea pigs, and a few other species lack an enzyme necessary for such synthesis and must obtain vitamin C through their diet. Vitamin C is widespread in plant tissues, with particularly high concentrations occurring in citrus fruits (oranges, lemons, limes, grapefruits); tomatoes, potatoes, cabbages, and green peppers are also good sources of this vitamin.
Scurvy results in the weakening of capillaries, which causes hemorrhages into the tissues, bleeding of the gums, loosening of the teeth, anemia, and general debility. In infants there is also interference with bone development. Severe phases of the disorder can result in death. Scurvy is treated with large doses of vitamin C. Modern methods of transporting and preserving foods have made a diet rich in vitamin C available everywhere throughout the year, and even infants' diets include orange juice. Vitamin C is also available in tablet or syrup form.
Scurvy was a serious problem in the past, when fresh fruits and vegetables were not available during the winter in many parts of the world. It was especially common among sailors in the days when only nonperishable foods could be stocked aboard ship. More than half the crew of Vasco da Gama died from scurvy on his first trip (1497–99) around the Cape of Good Hope. In 1747 the Scottish naval surgeon James Lind treated scurvy-ridden sailors with lemons and oranges and obtained dramatic cures. In 1795 the British navy began to distribute regular rations of lime juice during long sea voyages (hence the name limeys for British sailors), a measure that was largely successful in preventing scurvy. It was probably the first disease to be definitely associated with a dietary deficiency.
a disease of man caused by a deficiency of vitamin C (ascorbic acid) in the diet. Scurvy frequently occurred in members of expeditions to the North, among sailing crews during long journeys, and in the general population as a result of such social upheavals as war and famine. The connection between the incidence of scurvy and poor diet was theorized long ago. For example, 16th-century Russian land and sea travelers used popular antiscorbutic remedies, for example, eating fresh meat (especially deer meat) and drinking infusions and decoctions made from coniferous needles. Research on vitamins led to the discovery of the cause of the disease—a vitamin-C deficiency that results in very low blood and urine ascorbic-acid levels and in increased permeability of the vascular walls. The main sources of vitamin C are fresh vegetables, greens, and berries and other fruits; the vitamin is destroyed by prolonged storage or cooking. Scurvy usually occurs therefore in spring and early summer.
The early symptoms of scurvy are systemic, mostly nervous, disturbances, including loss of muscle strength, ready fatigability, drowsiness, and vertigo. Later symptoms are cyanosis of the ears, nose, lips, fingers, and nails; swelling and bleeding of the gums; and loosening and loss of teeth. A characteristic sign of scurvy is petechial hemorrhage in the hair follicles, resulting in a rash that is first bright red and then blue-black. The rash occurs mostly on the legs, thighs, and buttocks. Subcutaneous and intramuscular hemorrhages also occur in bruised regions and in places rubbed by clothing. Hemorrhages may also occur in organs and body cavities (usually the pleural). Hypochromic anemia and gastrointestinal disorders (low hydrochloric acid concentration in gastric juice and constipation followed by diarrhea and bloody stools) may also develop. Resistance to colds and other infectious diseases decreases sharply, and wounds and fractures heal slowly.
Treatment consists in the ingestion of 100 mg of ascorbic acid three to five times a day for 15 to 20 days or daily intramuscular or subcutaneous injection of 200–300 mg of ascorbic acid for ten to 15 days. General prophylactic measures include a diet balanced between animal proteins and vitamin C and, in the case of an unbalanced diet, the additional ingestion of 70–100 mg of ascorbic acid daily.
REFERENCESEfremov, V. V. Avitaminoz i gipovitaminoz C (tsinga). Moscow, 1942.
Vitaminy v pitanii i profilaktika vitaminnoi nedostatochnosti. Moscow, 1969.
Vitaminy. Moscow, 1974.
V. V. EFREMOV