Scurvy is a state of dietary deficiency of vitamin C (ascorbic acid). The human body lacks the ability to synthesize and make vitamin C and therefore depends on exogenous dietary sources to meet vitamin C needs.The body's pool of vitamin C can be depleted in 1-3 months. Ascorbic acid is prone to oxidation in vivo, and body stores are affected by environmental and lifestyle factors (eg, smoking), biological conditions (eg, inflammation, iron excess), and pathologic conditions (eg, malabsorption) that may alter its oxidation. Consumption of fruits and vegetables or diets fortified with vitamin C is essential to avoid ascorbic acid deficiency.[1, 2, 3, 4, 5, 6]
Although scurvy is uncommon, it still occurs and can affect adults and children who have chronic dietary vitamin C deficiency (see the image below).
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Anteroposterior radiograph of the lower extremities shows ground-glass osteopenia, a characteristic of scurvy.
See 21 Hidden Clues to Diagnosing Nutritional Deficiencies, a Critical Images slideshow, to help identify clues to conditions associated with malnutrition.
Signs and symptoms include fatigue, malaise, anemia, myalgia, bone pain, easy bruising, swelling, petechiae, gingivitis, perifollicular hemorrhages, corkscrew hairs, and poor wound healing. If left untreated, the disease can progress to jaundice, neuropathy, hemolysis, seizures, and death.
Plasma ascorbic acid level may help in establishing the diagnosis, but this level tends to reflect the recent dietary intake rather than the actual tissue levels of vitamin C. Signs of scurvy can occur with low-normal serum levels of vitamin C.
The only effective therapy for scurvy is vitamin C replacement. Thus, the goal of treatment is to saturate the body rapidly with ascorbic acid; at maximum doses, body stores become saturated in a few days. With proper treatment, bleeding stops within 24 hours, and perifollicular petechiae resolve in 2 weeks.
Humans, other primates, and guinea pigs are unable to synthesize L-ascorbic acid (vitamin C); therefore, they require it in their diet.[7] The enzyme L-gluconolactone oxidase, which would usually catalyze the conversion of L-gluconogammalactone to L-ascorbic acid, is defective due to a mutation or inborn error in carbohydrate metabolism.
The total body pool of vitamin C is approximately 1500 mg. The absorbed vitamin is found ubiquitously in body tissues, with the highest concentrations in glandular tissue and the lowest concentrations in muscle and stored fat. Ascorbic acid is metabolized in the liver by oxidation and sulfation. The renal threshold for excretion by the kidney in urine is approximately 1.4 mg/100 mL plasma. Excess amounts of ascorbic acid are excreted unchanged or as metabolites. When body tissue or plasma concentrations of vitamin C are low, excretion of the vitamin is decreased. Scurvy occurs after vitamin C has been eliminated from the diet for at least 3 months and when the body pool falls below 350 mg.
One study identified a genetic polymorphism of the human plasma protein haptoglobin, Hp 2, which may be an important non-nutritional modifying factor in the pathogenesis of vitamin C deficiency. The Hp 2-2 polymers are less efficient inhibitors of hemoglobin-driven oxidative stress, leading to ascorbic acid depletion. The Hp 2-2 phenotype is present in 35% of whites and 50% of South Asians and East Asians and may help identify patients who are more prone to develop clinically significant vitamin C deficiency.[1]
Vitamin C functionality
Vitamin C is required as a redox agent, reducing metal ions in many enzymes and removing free radicals. In this capacity, it protects DNA, protein, and vessel walls from damage caused by free radicals.
Vitamin C is functionally most relevant for the triple-helix formation of collagen; a vitamin C deficiency results in impaired collagen synthesis. The typical pathologic manifestations of vitamin C deficiency, including poor wound healing, are noted in collagen-containing tissues and in organs and tissues such as skin, cartilage, dentine, osteoid, and capillary blood vessels. Pathologic changes in affected children and adults are a function of the rate of growth of the affected tissues; hence, the bone changes are often observed only in infants during periods of rapid bone growth. Defective collagen synthesis leads to defective dentine formation, hemorrhaging into the gums, and loss of teeth. Hemorrhaging is a hallmark feature of scurvy and can occur in any organ. Hair follicles are one of the common sites of cutaneous bleeding.
The bony changes occur at the junction between the end of the diaphysis and growth cartilage. Osteoblasts fail to form osteoid (bone matrix), resulting in cessation of endochondral bone formation. Calcification of the growth cartilage at the end of the long bones continues, leading to the thickening of the growth plate. The typical invasion of the growth cartilage by the capillaries does not occur.
Preexisting bone becomes brittle and undergoes resorption at a normal rate, resulting in microscopic fractures of the spicules between the shaft and calcified cartilage. With these fractures, the periosteum becomes loosened, resulting in the classic subperiosteal hemorrhage at the ends of the long bones. Guidelines for the evaluation of fractures in infants and young children have been established.[8] Intra-articular hemorrhage is rare because the periosteal attachment to the growth plate is very firm.
Although the clinical manifestations are unclear, vitamin C is a cofactor in the metabolism of tyrosine and cholesterol and the synthesis of carnitine, neurotransmitters (eg, norepinephrine), peptide hormones, corticosteroids, and aldosterone.
Vitamin C also affects hematopoiesis by enhancing the absorption of iron from the small intestine by reducing dietary iron from the ferric form to the ferrous form. This may contribute to the anemia seen with vitamin C deficiency, in which the availability of intracellular iron is reduced. Vitamin C is also necessary to convert folic acid to its active metabolite, folinic acid.
Scurvy is caused by a prolonged dietary deficiency of vitamin C. Humans obtain 90% of their intake of vitamin C from fruits and vegetables, and cooking these sources decreases vitamin C content 20-40%. The National Health Institute (NIH), the Food and Nutrition Board of the National Academy of Sciences, and the National Research Council recommend a daily dietary allowance of vitamin C of 75 mg for women and 90 mg for men.
The body's pool of vitamin C can be depleted in 1-3 months. Ascorbic acid is prone to oxidation in vivo, and body stores are affected by environmental and lifestyle factors (eg, smoking), biological conditions (eg, inflammation, iron excess), and pathologic conditions (eg, malabsorption) that may alter its oxidation.
Risk factors for vitamin C deficiency include the following:[9]
Babies who are fed only cow's milk or plant-based beverages (almond milk)[10] during the first year of life
Alcoholic individuals[7] and those who conform to food fads
Elderly individuals who eat a tea-and-toast diet; retired people who live alone and those who eat primarily at fast food restaurants[2]
Economically disadvantaged persons, who tend to not purchase foods high in vitamin C (eg, green vegetables, citrus fruits)[11]
Refugees who are dependent on external suppliers for their food and have limited access to fresh fruits and vegetables
Cigarette smokers: These individuals require an increased intake of vitamin C because of lower vitamin C absorption and increased catabolism
Pregnant and lactating women and those with thyrotoxicosis: These individuals require an increased intake of vitamin C because of increased utilization
People with anorexia nervosa or anorexia from other diseases such as AIDS or cancer[12]
People with type 1 diabetes have increased vitamin C requirements, as do those on hemodialysis and peritoneal dialysis[13, 14]
People with disease of the small intestine such as Crohn, Whipple, and celiac disease, as well as after gastric bypass surgery,[15] because vitamin C is absorbed in the small intestine
Individuals with iron overload disorders - These may lead to renal vitamin C wasting
Other factors that may lead to vitamin C deficiency include ignorance (eg, boiling of fruit juices), restrictive diets imposed by food allergies, and neurodevelopmental disabilities associated with compromised oral intake of foods.[16, 3]
A case report of vitamin C deficiency in a patient on warfarin raises the possibility of risk in the vitamin K–restricted diet, since overlap exists in foods containing vitamin K and vitamin C.[17]
Studies have shown that iron is important in the absorption of vitamin C, and iron deficiency may lower the expression of the sodium-dependent vitamin C transporter in intestinal cells, leading to vitamin C deficiency.[18]
Besides poor diet and anorexia in cancer patients, another mechanism of vitamin C deficiency has been proposed. In a study of cancer patients with adequate daily intake but low serum vitamin C levels, authors proposed increased use of vitamin C possibly to scavenge lipid peroxides or vitamin C sequestration by tumor cells.[19]
Data from the National Health and Nutrition Examination Survey (NHANES 2003-2004) assessing the prevalence of vitamin C deficiency in the United States found that men aged 20-39 years and those older than 60 years had a higher prevalence of deficiency than similarly aged women. Overall, 8.2% of men and 6% of women (7.1% overall prevalence) were deficient in vitamin C, which is decreased from the NHANES 1994, which showed 14% of men and 10% of women deficient.[20] NHANES 2005-2006 showed a lower prevalence of 3.6% of vitamin C deficiency among men and women older than 6 years.[4]
Patients at risk include those who have chronic malnutrition, those who are elderly or alcoholic, those who subsist on diets devoid of fresh fruits and vegetables, and men who live alone (widower scurvy). Infants and children on restrictive diets because of medical, economic, or social reasons are at risk for scurvy. Occurrence of scurvy is uncommon in those younger than 7 months, although infants fed evaporated or condensed milk formulas may develop this disease. If a mother has an adequate diet, breast milk contains sufficient vitamin C for a baby's needs. Commercially available formulas and many prepared fruit juices are fortified with vitamin C.
Other reported cases include people with monotonous or peculiar diets, including patients undergoing dialysis; those with cognitive disorders,[21, 22] psychiatric illnesses,[23] malabsorption, inflammatory bowel disease, Whipple disease, or dyspepsia (those who avoid acidic foods); and those receiving cancer chemotherapy,
International statistics
Scurvy is a problem when general malnutrition exists, as in some impoverished, underdeveloped third-world countries. Scurvy also occurs in epidemic proportions in international refugee camps and in populations that subsist mainly on cereal grains.
A study of nonhospitalized patients in Paris found that 5% of women and 12% of men were deficient[24] ; in those older than 65 years, this proportion increased to 15% of women and 20% of men.
In a case series from Thailand that reviewed 28 cases of scurvy in infants and children (10 mo to 9 yr and 7 mo; median age, 29 mo) hospitalized over a 7-year period (1995-2002), investigators noted that prolonged consumption of heated milk (ultra-high temperature [UHT] milk) and inadequate intake of vegetables and fruits were the risk factors for the development of scurvy.[25]
In tests of plasma vitamin C levels in the low-income/materially deprived population of the United Kingdom, carried out between 2003 and 2005 (433 men; 876 women), the Low Income Diet and Nutrition Survey found evidence of vitamin C deficiency in an estimated 25% of men and 16% of women.[11] Another 20% of the study population had vitamin C levels in the depleted range. According to the report, predictors of plasma vitamin C levels at or below the depleted range include being male, having a low dietary intake of vitamin C, not taking vitamin supplements, and smoking.[11]
A study of healthy elderly (age 70-75 yr) persons living in Padua, Italy, took a baseline and 10-year follow-up dietary history and found vitamin C deficiency rose over the 10-year span, from 3% to 6% in men and from 2.3% to 4.5% in women, which led the authors to recommend multivitamin supplementation in healthy elderly persons.[26]
Race, sex, and age differences in incidence
According to NHANES 2004, non-Hispanic white men (11.8%) (had a slightly increased risk of vitamin C deficiency compared with non-Hispanic black men (8.9%) and Mexican American men (7.7%).[20] Similarly, the non-Hispanic white women (8.2%) had higher rates of vitamin C deficiency compared with non-Hispanic black women (5%) and Mexican American women (4.2%). Mexican American males and females had a lower risk of vitamin C deficiency probably because the traditional Mexican diet is rich in chilies, tomatoes, and squashes, which are high in vitamin C.[20]
Some studies show vitamin C deficiency to be more common among men, whereas others show equal distribution among men and women. NHANES 2004 shows slightly higher prevalence for men (8.2%) than for women (6%).
NHANES 2007-2008 data showed that among American males older than 20 years, the daily intake was 26 mg higher than for females. In fact, teenage females had the lowest intake, followed by preadolescent females and women in their 60s.[27]
Although scurvy can occur at any age, the incidence of scurvy peaks in children aged 6-12 months who are fed a diet deficient in citrus fruits or vegetables, as well as in elderly populations, who sometimes have "tea-and-toast" diets deficient in vitamin C. Scurvy is uncommon in the neonatal period.
Typically, scurvy carries an excellent prognosis if diagnosed and treated appropriately. Manifestations of scurvy, including the following, tend to dramatically improve, resolving within weeks, if adequate oral vitamin C is given in daily doses to recoup body stores:
Spontaneous bleeding stops within 1 day
Muscle and bone pain abate quickly
Bleeding and sore gums heal in 2-3 days
Ecchymoses heal within 12 days
In advanced scurvy, serum bilirubin normalizes in less than 1 week, and anemia is corrected in less than a month.
Complications
The predominant morbidity associated with this disease is a result of hemorrhage into various tissues and depends on the site of involvement. Subperiosteal hemorrhages cause pain and tenderness, resulting in pseudoparalysis. Loss of function at the site of the hemorrhage and anemia are typical sequelae of the hemorrhages observed in scurvy. Subperiosteal hemorrhage in the tibia and femur causes excruciating pain.
Laboratory data suggest that the neonatal brain is particularly susceptible to vitamin C deficiency and that this condition may adversely affect early brain development.[28]
Until minimal daily requirements of vitamin C were supplied, scurvy plagued prolonged naval voyages and military campaigns as personnel succumbed to its devastating effects. Lethargy, fatigue, and hemorrhagic manifestations of impaired collagen synthesis affecting oral, ophthalmic, musculoskeletal, cardiac, and gastrointestinal structures and functions incapacitated or killed more people than enemy action in many cases.
Symptoms and signs of scurvy may be remembered by the 4 Hs: hemorrhage, hyperkeratosis, hypochondriasis, and hematologic abnormalities.
The initial symptoms of scurvy are nonspecific and include the following:
Malaise
Lethargy
Loss of appetite
Peevishness (ill-tempered)
Poor weight gain
Diarrhea
Tachypnea
Fever
After 1-3 months of severe or total vitamin C deficiency, patients develop shortness of breath and bone pain. Myalgias may occur because of reduced carnitine production. Skin changes with roughness, easy bruising and petechiae, gum disease, loosening of teeth, poor wound healing, and emotional changes occur. Dry mouth and dry eyes similar to Sjögren syndrome may occur.
Other symptoms include the following:
Irritability
Pain and tenderness of the legs
Pseudoparalysis
Swelling over the long bones
Hemorrhage
In the late stages, jaundice, generalized edema, oliguria, neuropathy, fever, and convulsions can be seen. Left untreated, scurvy progresses, with potentially fatal complications, including cerebral hemorrhage or hemopericardium.[29]
Infantile scurvy is uncommon before age 7 months, and clinical and radiographic manifestations rarely occur in infants younger than 3 months. Early clinical manifestations consist of pallor, irritability, and poor weight gain.
In advanced infantile scurvy, the major clinical manifestation is extreme pain and tenderness of the arms and, particularly, the legs. The baby is miserable and tends to remain in a characteristic immobilized posture from subperiosteal pain, with semiflexion of the hips and the knees ("frog leg posture"), as described by Thomas Barlow in 1884.
The body is both wasted and edematous, and petechiae and ecchymoses are commonly present. Hyperkeratosis, corkscrew hair, and sicca syndrome are typically observed in adult scurvy but rarely occur in infantile scurvy. The case of an infant with diffuse, nonscarring alopecia of the scalp and radiologic features of scurvy was reported in India in 2008.[30] . Three cases of scurvy presenting as difficulty with walking have been reported in the United States, with only 1 out of 3 patients having classic gingival lesions at presentation.[31]
Circulatory system
Hypotension may be observed late in the disease. This may be due to an inability of the resistance vessels to constrict in response to adrenergic stimuli. Heart complications include cardiac enlargement, electrocardiographic (ECG) changes (reversible ST-segment and T-wave changes), hemopericardium, and sudden death. Bleeding into the myocardium and pericardial space has been reported. High-output heart failure due to anemia can be observed.
Two case reports of pulmonary hypertension in patients with vitamin C deficiency have been described, with complete reversal after vitamin C replacement.[32, 33]
Anemia develops in 75% of patients, resulting from blood loss into tissue, coexistent dietary deficiencies (folate deficiency), altered absorption and metabolism of iron and folate, gastrointestinal blood loss, and intravascular hemolysis. The anemia is most often characterized as normochromic and normocytic.
Nervous system
Ocular features include those of Sjögren syndrome, subconjunctival hemorrhage, and bleeding within the optic nerve sheath. Scleral icterus (late, probably secondary to hemolysis) and pale conjunctiva are seen. Funduscopic changes include flame-shaped hemorrhages, and cotton-wool spots may be seen. Bleeding into the periorbital area, eyelids, and retrobulbar space also can be seen. Proptosis of the eyeball secondary to orbital hemorrhage is a sign of scurvy.
Integumentary and skeletal system
Perifollicular hyperkeratotic papules, perifollicular hemorrhages, purpura, and ecchymoses are seen most commonly on the legs and buttocks where hydrostatic pressure is the greatest. The central hairs are twisted like corkscrews, and they may become fragmented.[34] Poor wound healing and breakdown of old scars may be seen. Capillary fragility can be checked by inflating a blood pressure cuff and looking for petechiae on the forearm. In the nails, splinter hemorrhages may occur.
Alopecia may occur secondary to reduced disulfide bonding.
In advanced cases, clinically detectable beading may be present at the costochondral junctions of the ribs. This finding is known as the scorbutic rosary (ie, sternum sinks inward) and may occur in children. The scorbutic rosary is distinguished from rickety rosary (which is knobby and nodular) by being more angular and having a step-off at the costochondral junction. Fractures, dislocations, and tenderness of bones are common in children.
Bleeding into the joints causes exquisitely painful hemarthroses. Subperiosteal hemorrhage may be palpable, especially along the distal portions of the femurs and the proximal parts of the tibias of infants. Bleeding into the femoral sheaths may cause femoral neuropathies, and bleeding into the muscles of the arms and the legs may cause woody edema.
A case of a 6-year-old boy with feeding difficulties and a monoarticular lesion of the distal femur mimicking a bone tumor was reported in India. After full assessment and investigation, he was found to have scurvy with significant improvement following vitamin C replacement.[35]
Gastrointestinal system
Gum hemorrhage occurs only if teeth have erupted and usually involve the tissue around the upper incisors. The gums have a bluish-purple hue and feel spongy. Gum swelling, friability, bleeding, and infection with loose teeth also occur, as do mucosal petechiae.
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Periodontal images of the patient taken before periodontal treatment. Extensive gingival overgrowth with severe periodontal inflammation was observed ....
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Treatment protocol for above patient with extensive gingival overgrowth with severe periodontal inflammation in the maxillary and mandibular arches. I....
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Periodontal images taken before and after ascorbic acid supplementation. (A) Recurrent gingival overgrowth observed after the second gingivectomy and ....
Loss of weight secondary to anorexia is common. Upper endoscopy may show submucosal hemorrhage. Rarely, hematuria, hematochezia, and melena are noted.
In both animal and human studies, vitamin C deficiency has been linked to possible pathogenesis of nonalcoholic fatty liver disease, given its anti-oxidant properties and inverse correlation with BMI.[36]
Laboratory tests are usually not helpful to ascertain a diagnosis of scurvy. Presentation of an infant with the typical clinical and radiologic picture of scurvy, along with a supportive history of dietary deficiency of vitamin C, is often sufficient to diagnose infantile scurvy.
Plasma ascorbic acid level may help in establishing the diagnosis, but this level tends to reflect the recent dietary intake rather than the actual tissue levels of vitamin C. Signs of scurvy can occur with low-normal serum levels of vitamin C.[29]
The best confirmation of the diagnosis of scurvy is its resolution following vitamin C administration.
Noninflammatory perivascular extravasation of red cells and deposition of hemosiderin near hair follicles with intrafollicular keratotic plugs and coiled hair may be seen in a skin biopsy specimen.
Obtaining a plasma or leukocyte vitamin C level can confirm clinical diagnosis.
Plasma levels
A fasting serum ascorbic acid level greater than 0.6 mg/dL rules out scurvy. Serum ascorbic acid levels of less than 0.2 mg/dL are deficient. levels of 0.2-0.29 mg/dL are low, and levels greater than 0.3 mg/dL are acceptable. Scurvy generally occurs at levels less than 0.1 mg/dL.[5]
Leukocyte levels
The level of vitamin C in leukocytes more accurately correlates to tissue stores compared with serum levels, because these cells are not affected acutely by circadian rhythm or dietary changes. A level of zero indicates latent scurvy; levels of 0-7 mg/dL reflect a state of deficiency; levels of 8-15 mg/dL are considered low; and levels greater than 15 mg/dL reflect a state of nutritional adequacy. A specific and reproducible reverse-phase, high-pressure liquid chromatographic method has been found to reliably measure vitamin C in lymphocytes.[38] This test is currently not clinically available, but it might be useful for screening.
Urinary levels
A more commonly used method is the ascorbic acid tolerance test, which quantitates urinary ascorbic acid over the 6 hours following an oral load of 1 g of ascorbic acid in water.
Radiographic findings in infantile scurvy are diagnostic and may show any of the following:
Subperiosteal elevation
Fractures and dislocation
Alveolar bone reabsorption
Ground-glass appearance of cortex, as in the image below.
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Anteroposterior radiograph of the lower extremities shows ground-glass osteopenia, a characteristic of scurvy.
The earliest radiologic manifestation of infantile scurvy is generally seen at the distal ends of the radii where fuzziness of the lateral aspects of the cortices is present with slight rarefaction of the neighboring cancellous bone. The characteristic radiologic changes occur at the growth cartilage-shaft junction of bones with rapid growth. The knee joint, wrist, and sternal ends of the ribs are typical sites of involvement.
As the disease progresses, radiographs demonstrate characteristic changes at the cartilage-shaft junctions of the long bones, especially at the distal ends of the femurs. Key imaging features show osteoporosis. The cortex becomes thin, and the trabecular structure of the medulla atrophies and develops a ground-glass appearance. The zone of provisional calcification becomes dense and widened, and this zone is referred to as the white line of Frankel. The epiphysis also shows cortical thinning and the ground-glass appearance.
Other features that may be noted are metaphyseal spurs or marginal fractures (Pelkan spur), a transverse band of radiolucency in the metaphysis (scurvy line or Trummerfeld zone), which is subjacent to the zone of provisional calcification; a ring of increased density surrounding the epiphysis (Wimberger ring); and periosteal elevation.
As scurvy becomes advanced, a zone of rarefaction occurs at the metaphysis under the white line. The zone of rarefaction typically involves the lateral aspects of the white line, resulting in triangular defects called the corner sign of Park. This area has multiple microscopic fractures and may collapse with impaction of the calcified cartilage onto the shaft. The lateral aspect of the calcified cartilage can project as a spur. Subperiosteal hemorrhages are not visualized in the active phase. With healing, they become calcified and are readily observed.
Because sudden death may occur in patients with scurvy, ensuring adequate vitamin C replenishment in patients with vitamin C deficiency is the hallmark of therapy. Restoration of body stores of vitamin C is essential to achieve complete resolution of symptoms. In most adult patients, provision of 250 mg of vitamin C 4 times a day for 1 week aids in achieving this goal.
Identifying and treating comorbid nutritional deficiencies (eg, iron deficiency anemia, folate deficiency, other vitamin deficiencies) are integral parts of management. Provision of a balanced and liberal diet to meet the nutritional needs of the patient aids in recovery.
Orange juice is an effective dietary remedy for curing infantile scurvy and was the standard treatment before the discovery of vitamin C. Upon instituting dietary or pharmacologic treatment, the clinical recovery is impressive. The appetite of the infant is recovered within 24-48 hours. The symptoms of irritability, fever, tenderness upon palpation, and hemorrhage generally resolve within 7 days.
Patients should take oral ascorbic acid at 100 mg 3-5 times a day until a total of 4 g is reached, and then they should decrease intake to 100 mg daily. Alternatively, ascorbic acid may be taken at 1 g/day for the first 3-5 days, followed by 300-500 mg/day for 1 week. Then, the recommended daily allowance is resumed.
Divided doses are given, because intestinal absorption is limited to 100 mg at one time. Parenteral doses are necessary in those with gastrointestinal malabsorption.
In October 2017, the Food and Drug Administration (FDA) approved Ascor (ascorbic acid) for the short-term (<1 wk) treatment of scurvy in adults and children aged 5 months or older for whom oral administration is not possible, is insufficient, or is contraindicated. The exact mechanism of action of ascorbic acid for the treatment of scurvy is unknown. It is believed that the administration restores the body pool of ascorbic acid.
The recommended adult dose is 200 mg IV daily, and treatment should not exceed 7 days. If there is no improvement in scorbutic symptoms, re-treat until resolution of scorbutic symptoms is observed.[39]
A diet adequate in vitamin C can prevent the development of scurvy. Foods high in vitamin C include citrus fruits, especially grapefruits and lemons; berries and cantaloupe; and vegetables, including broccoli, spinach, green peppers, tomatoes, potatoes, cauliflower, and cabbage.
The recommended daily allowance for vitamin C varies with the age of the individual. The current recommendation for adults is 120 mg daily, although a dose of 60 mg daily is all that is required to prevent scurvy. Some experts think the level should be as high as 200 mg daily to match the level present in 5 servings of fruits and vegetables daily, a diet shown to decrease cancer risk.
The Food and Nutrition Board of the National Academy of Sciences and the National Research Council have provided minimum recommended daily dietary allowances of vitamin C (see the table below)[6] :
Table.
View Table
See Table
Megadoses of vitamin C have not been shown in clinical trials to reduce viral illnesses such as colds. Large doses of vitamin C (ie, more than 1 g/day) may increase the risk of certain illnesses such as kidney stones, particularly oxalate stones.
The only effective therapy for scurvy is vitamin C replacement. Thus, the goal of treatment is to saturate the body rapidly with ascorbic acid; at maximum doses, body stores become saturated in a few days. With proper treatment, bleeding stops within 24 hours, and perifollicular petechiae resolve in 2 weeks.
Clinical Context:
Ascorbic acid (vitamin C) administered orally or parenterally effectively cures infantile and adult scurvy. This vitamin is used by the body for collagen synthesis and tissue repair.
Vitamins are organic substances required by the body in small amounts for various metabolic processes and are essential for normal DNA synthesis and cell function. Vitamins may be synthesized in small or insufficient amounts in the body or not synthesized at all, thus requiring supplementation. They are classified as either fat soluble or water soluble. Vitamins A, D, E, and K are fat soluble, whereas biotin, folic acid, niacin, pantothenic acid, the B vitamins (ie, B-1, B-2, B-6, B-12), and vitamin C are generally water soluble.
Vitamin deficiency may result from an inadequate diet, from increased requirements (eg, pregnancy, lactation), or secondary to disease or drugs. Vitamin supplements are used clinically for the prevention and treatment of specific vitamin-deficiency states.
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS, Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC
Disclosure: Nothing to disclose.
Chief Editor
George T Griffing, MD, Professor Emeritus of Medicine, St Louis University School of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Anne Elizabeth Laumann, MBChB, MRCP(UK), FAAD, Professor of Dermatology, Northwestern University, The Feinberg School of Medicine
Disclosure: Nothing to disclose.
Bradley S Buckler, MD, Fellow in Neonatal-Perinatal Medicine, Medical College of Georgia
Disclosure: Nothing to disclose.
Dirk M Elston, MD, Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine
Disclosure: Nothing to disclose.
Henry Driscoll, MD, Farrell Professor of Endocrinology, Chief, Department of Medicine, Section of Endocrinology, Joan C Edwards School of Medicine at Marshall University
Disclosure: Nothing to disclose.
Janet J Wong, MD, Consulting Dermatologist, Department of Dermatology, University of Connecticut School of Medicine
Disclosure: Nothing to disclose.
Julia Sanger Minocha, MD, Resident Physician, Department of Medicine, Northwestern University, The Feinberg School of Medicine
Disclosure: Nothing to disclose.
Kathryn Schwarzenberger, MD, Associate Professor of Medicine, Division of Dermatology, University of Vermont College of Medicine; Consulting Staff, Division of Dermatology, Fletcher Allen Health Care
Disclosure: Nothing to disclose.
Steven M Schwarz, MD, FAAP, FACN, AGAF, Professor of Pediatrics, Children's Hospital at Downstate, State University of New York Downstate Medical Center
Disclosure: Nothing to disclose.
Van Perry, MD, Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio
Disclosure: Nothing to disclose.
Acknowledgements
The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Anjali Parish, MD, Kumaravel Rajakumar, MD, and Tarita Thomas, PhD, MBA,to the development and writing of the source articles.
Centers for Disease Control and Prevention. NHANES 2005-2006. Available at http://www.cdc.gov/nchs/nhanes/nhanes2005-2006/lab05_06.htm. Accessed: September 14, 2012.
World Health Organization/NHD 99.11 Scurvy and its prevention and control in major emergencies. World Health Organization. Available at http://www.who.int/nutrition/publications/emergencies/WHO_NHD_99.11/en/. Accessed: July 28, 2011.
[Guideline] Dietary Reference Intakes from the Food and Nutrition Board, Institute of Medicine, National Academies. National Academies of Sciences, Engineering, Medicine. Available at http://nationalacademies.org/hmd/~/media/Files/Activity%20Files/Nutrition/DRI-Tables/1_%20EARs.pdf?la=en. 2012; Accessed: September 1, 2017.
Scheers NM, Sandberg AS. Iron regulates the uptake of scorbic acid and the expression of sodium-dependent vitamin C transporter1 (SVCT1) in human intestinal Caco-2 cells. Br J Nutr. 2011/03. 21:1-7.
USDA Agriculture Research Service. What we eat in America, NHANES 2007-2008. Available at http://www.ars.usda.gov/ba/bhnrc/fsrg. Accessed: September 14, 2012.
Ascor (ascorbic acid injection) [package insert]. Santa Ana, CA 92704: https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/209112s000lbl.pdf. 10/2017. Available at
Anteroposterior radiograph of the lower extremities shows ground-glass osteopenia, a characteristic of scurvy.
Periodontal images of the patient taken before periodontal treatment. Extensive gingival overgrowth with severe periodontal inflammation was observed in the maxillary and mandibular arches at the first visit (July, 2008). Image from open access article Omori K, Hanayama Y, Naruishi K, Akiyama K, Maeda H, Otsuka F, Takashiba S. Gingival overgrowth caused by vitamin C deficiency associated with metabolic syndrome and severe periodontal infection: a case report. Clin Case Rep. 2014 Dec; 2(6):286-95.
Treatment protocol for above patient with extensive gingival overgrowth with severe periodontal inflammation in the maxillary and mandibular arches. Image from open access article Omori K, Hanayama Y, Naruishi K, Akiyama K, Maeda H, Otsuka F, Takashiba S. Gingival overgrowth caused by vitamin C deficiency associated with metabolic syndrome and severe periodontal infection: a case report. Clin Case Rep. 2014 Dec; 2(6):286-95.
Periodontal images taken before and after ascorbic acid supplementation. (A) Recurrent gingival overgrowth observed after the second gingivectomy and before ascorbic acid supplementation (September, 2011), (B) images taken after 9 months of ascorbic acid supplementation (June, 2012). The white arrows indicate typical sites of recurrent gingival overgrowth. Image from open access article Omori K, Hanayama Y, Naruishi K, Akiyama K, Maeda H, Otsuka F, Takashiba S. Gingival overgrowth caused by vitamin C deficiency associated with metabolic syndrome and severe periodontal infection: a case report. Clin Case Rep. 2014 Dec; 2(6):286-95.
Anteroposterior radiograph of the lower extremities shows ground-glass osteopenia, a characteristic of scurvy.
Anteroposterior radiograph of the lower extremities shows ground-glass osteopenia, a characteristic of scurvy.
Perifollicular hemorrhage.
Periodontal images of the patient taken before periodontal treatment. Extensive gingival overgrowth with severe periodontal inflammation was observed in the maxillary and mandibular arches at the first visit (July, 2008). Image from open access article Omori K, Hanayama Y, Naruishi K, Akiyama K, Maeda H, Otsuka F, Takashiba S. Gingival overgrowth caused by vitamin C deficiency associated with metabolic syndrome and severe periodontal infection: a case report. Clin Case Rep. 2014 Dec; 2(6):286-95.
Treatment protocol for above patient with extensive gingival overgrowth with severe periodontal inflammation in the maxillary and mandibular arches. Image from open access article Omori K, Hanayama Y, Naruishi K, Akiyama K, Maeda H, Otsuka F, Takashiba S. Gingival overgrowth caused by vitamin C deficiency associated with metabolic syndrome and severe periodontal infection: a case report. Clin Case Rep. 2014 Dec; 2(6):286-95.
Periodontal images taken before and after ascorbic acid supplementation. (A) Recurrent gingival overgrowth observed after the second gingivectomy and before ascorbic acid supplementation (September, 2011), (B) images taken after 9 months of ascorbic acid supplementation (June, 2012). The white arrows indicate typical sites of recurrent gingival overgrowth. Image from open access article Omori K, Hanayama Y, Naruishi K, Akiyama K, Maeda H, Otsuka F, Takashiba S. Gingival overgrowth caused by vitamin C deficiency associated with metabolic syndrome and severe periodontal infection: a case report. Clin Case Rep. 2014 Dec; 2(6):286-95.
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