Results from a dietary deficiency of vitamin C.
Symptoms related to impaired collagen synthesis.
A multisystem illness caused by vitamin C deficiency.
Scurvy signs can appear within 1 month of little or no vitamin C intake of below 10 mg/day: fatigue, malaise, and inflammation of the gums.
With progressive vitamin C deficiency, collagen synthesis becomes impaired and connective tissues become weakened, causing petechiae, ecchymoses, purpura, joint pain, poor wound healing, hyperkeratosis, and corkscrew hairs.
Vitamin C deficiency causes scurvy, in which defective collagen prevents the formation of strong connective tissue.
With scurvy gums deteriorate and bleed, with loss of teeth; skin discolors, and wounds do not heal.
Symptoms include bruisability, bleeding gums, petechial rash, hemarthrosis, corkscrew hairs, Sjogren-like symptoms, arthralgias, weakness, malaise, and depression.
Rarely encountered in the United States and other industrialized nations because of the widespread availability of fruits, vegetables, and fortified foods.
NHANESIII Found 5-17% of participants to have low vitamin C levels.
A rare disease resulting from a lack of vitamin C.
It is required to make the building blocks for collagen.
Early symptoms of deficiency include weakness, feeling tired, and sore arms and legs.
It takes at least a month of little to no vitamin C in the diet before symptoms occur.
Vitamin C must be completely absent from the diet for 60-to 90 days.
Early symptoms are malaise and lethargy.
Additional signs of scurvy include depression as well as swollen, bleeding gums and loosening or loss of teeth due to tissue and capillary fragility.
Iron deficiency anemia can also occur due to increased bleeding and decreased nonheme iron absorption secondary to low vitamin C intake.
Vitamin C facilitates the absorption of non-heme iron and may protect against oxidation of tetrahydrofolate and result in decreased folate levels.
Vitamin C deficiency can lead to iron and folate deficiencies.
Anemia in scurvy is caused by decreased erythrocytes production, hemolysis, and blood loss.
In children, bone disease can be present.
Vitamin C antioxidant properties are implicated in maintaining the red cells cytoskeleton proteins beta-spectrin, required for the structure and integrity of the cell.
The loss of beta-spectrin can contribute to hemolysis in patients with vitamin C deficiency.
Vitamin C functions as a moderator of neurotransmitter synthesis and release, it is suggested that psychiatric symptoms caused by scurvy precede the physical manifestations.
Scurvy is associated with mood disturbances, depression, cognitive impairment and delusions, which all quickly resolve with vitamin C therapy.
After one to three months, patients develop shortness of breath and bone pain.
Vitamin C is a co-factor for enzymes involved in the biosynthesis of carnitine, which plays in essential role in the release of energy through beta oxidation by facilitating the transport of fatty acids into mitochondria.
Impaired carnitine synthesis may account for the weakness, fatigue, and muscle cramping that occurs in patients with the scurvy.
Myalgias may occur because of reduced carnitine production.
Dry mouth and dry eyes may occur.
1/3 of patients have fatigue, related to impaired catecholamine synthesis, as well as anemia.
In the late stages, jaundice, generalised edema, oliguria, neuropathy, fever, convulsions, and eventual death are frequently seen.
Untreated scurvy is invariably fatal.
Risk factors:
Mental disorders, unusual eating habits, alcoholism, elderly living alone, intestinal malabsorption, and dialysis.
Treatment:Vitamin C supplements.
Scurvy occurs most commonly in people with mental disorders, unusual eating habits, alcoholism, and older people who live alone.
Occurs more often in the developing world in association with malnutrition.
Other risk factors include intestinal malabsorption and dialysis.
Diagnosis is based history, physical signs, X-rays, and improvement after treatment.
Treatment: vitamin C supplements taken by mouth.
Usually Improvement begins in a few days, with complete recovery in a few weeks.
Dietary sources include citrus fruit and a number of vegetables such as tomatoes and potatoes.
Cooking often decreases the vitamin C content in foods.
Rare occurrence in adults, although infants and elderly people are affected.
Virtually all commercially available baby formulas contain added vitamin C, preventing infantile scurvy.
Human breast milk contains sufficient vitamin C, if the mother has an adequate intake, but commercial milk is pasteurized, and that destroys the natural vitamin C content of the milk.
Ascorbic acid is needed for a variety of biosynthetic pathways.
Vitamin C accelerates hydroxylation and amidation reactions.
Ascorbic acid is required in the synthesis of collagen.
Ascorbic acid is a cofactor for prolyl hydroxylase and lysyl hydroxylase, enzymes are responsible for the hydroxylation of the proline and lysine amino acids in collagen.
Procollagen is modified by the addition of hydroxyl groups to the amino acids proline and lysine.
Its later glycosylation results in the formation of the triple helix structure of collagen.
The hydroxylase enzymes that perform these reactions require vitamin C as a cofactor, a long-term deficiency in this vitamin results in impaired collagen synthesis and scurvy.
Collagen the primary structural protein in the human body, that is necessary for healthy blood vessels, muscle, skin, bone, cartilage, and other connective tissues.
If defective, connective tissue can lead to fragile capillaries, resulting in abnormal bleeding, bruising, and internal hemorrhaging.
Cutaneous symptoms include follicular hyperkeratosis and perifollicular hemorrhage on the lower extremities, resembling vasculitis.
Bone formation is also affected, breaking more easily, and once-healed breaks may recur.
Defective collagen fibrillogenesis impairs wound healing.
Diagnosis is based history and physical signs, X-rays, and improvement after treatment.
Laboratory evaluation reveals anemia and 75% of patients with scurvy and values for inflammatory markers such as ESR may be elevated.
Diagnosis is often delayed and differential diagnosis includes osteomyelitis, septic arthritis, acute lymphoblastic leukemia, systemic lupus, Henoch-Schonlein purpura, DIC, imune thrombocytopenic purpura, leukocytoclastic vasculitis.
Symptoms of scurvy typically occur when plasma vitamin C levels are less than 0.2 mg/dL
A clinical diagnosis.
A leukocyte ascorbate level is the most accurate with determining tissue stores vitamin C, however the test is not readily available.
Foods and their Vitamin C content per 100 grams.
Amla 610.00
Urtica 333.00
Guava 228.30
Blackcurrant 181.00
Zespri sungold kiwifruit 161.30
Chili pepper 144.00
Parsley 133.00
Green kiwifruit 92.70
Broccoli 89.20
Brussels sprout 85.00
Bell pepper 80.40
Papaya 62.00
Strawberry 58.80
Orange 53.20
Lemon53.00
Cabbage 36.60
Spinach 28.00
Turnip 27.40
Potato 19.70
Scurvy can be prevented by a diet that includes vitamin C-rich foods.
Various nutritional supplements are available, which provide ascorbic acid well in excess of that required to prevent scurvy.
Some animal products, including liver, oysters, and parts of the central nervous system, including the adrenal medulla, brain, and spinal cord, contain large amounts of vitamin C, capable of treating scurvy.
Fresh meat from animals which make their own vitamin C contains enough vitamin C to prevent, and partly treat scurvy.
Scurvy will improve with doses of vitamin C as low as 10 mg per day.
Doses of around 100 mg per day of vitamin C are recommended.
Most people have a full recovery within 2 weeks of initiating treatment.
In a prison study, the first signs of scurvy about 4 weeks after starting the vitamin C-free diet.