Scurvy is caused by Vitamin C deficiency. Humans cannot synthesize Vitamin C endogenously, 1 so serum and tissue levels depend on dietary intake, metabolism and renal excretion. 1, 2

The Vitamin C pool in the body is usually depleted in 4-12 weeks if there is no intake of the vitamin. 3
Although far less common than in previous centuries, scurvy is still present even in the United States. In the National Health and Nutrition Examination Survey (NHANES) 2003-2004, serum concentrations of total Vitamin C were measured in 7,277 noninstitutionalized U.S. civilians. This cross-sectional, nationally representative survey found that the overall prevalence of Vitamin C deficiency was 7.1% ± 0.9%. 4

The prevalence of Vitamin C deficiency is higher than one would expect in other industrialized countries as well. In a study of 979 Canadians, aged 20-29 years, 14% of participants had deficient levels of serum ascorbic acid. 5 In a 2014 German study of 188 participants of a seminar on nutritional allergies and intolerance, the audience of which comprised individuals with higher levels of education who spend more time on nutrition and meal planning and consume more food supplements than the general population, 3.3% were found to have a potential scorbutogenic deficiency. 6

Other studies show that as many as 1/3 of critically ill patients and 40% of septic shock patients may have Vitamin C levels low enough to be scorbutic. 2, 7 These studies suggest that the prevalence of scurvy even in modern developed populations is more prevalent than is commonly assumed.

Click on Links Below to Access the Full Text Version of the Studies Cited Above:
Serum vitamin C and the prevalence of vitamin C deficiency in the United States: 2003–2004 National Health and Nutrition Examination Survey (NHANES) | The American Journal of Clinical Nutrition | Oxford Academic (oup.com)

Vitamin C Deficiency in a Population of Young Canadian Adults | American Journal of Epidemiology | Oxford Academic (oup.com)

Plasma concentrations of ascorbic acid in a cross section of the German population (nih.gov)

Total vitamin C, ascorbic acid, and dehydroascorbic acid concentrations in plasma of critically ill patients - PubMed (nih.gov)

Hypovitaminosis C and vitamin C deficiency in critically ill patients despite recommended enteral and parenteral intakes - PubMed (nih.gov)
Scurvy can be difficult to diagnose because early symptoms tend to be vague and nonspecific and can imitate a variety of more common disorders. 8 Scurvy as a clinical manifestation of extreme vitamin C deficiency is caused by the vital role ascorbic acid plays in collagen synthesis. Vitamin C is needed for hydroxylation and crosslinking of pro-collagen. Lack of Vitamin C decreases transcription of pro-collagen and inhibits the transcription of various types of collagen found in skin, blood vessels and tissue. The key feature of scurvy is hemorrhage, which can occur in any organ, and altered bone formation, which can cause bones to become brittle. 3

Initial symptoms:
  • Anorexia 3
  • Fatigue 1
  • Irritability 3
  • Lethargy 8
  • Malaise 1
  • Aching in the arms and/or legs 1
  • Inflammation of the gums 1
Advanced symptoms: 1
  • Impaired collagen synthesis
  • Weakened connective tissues
  • Petechiae
  • Ecchymoses
  • Purpura
  • Joint pain
  • Impaired wound healing
  • Hyperkeratosis
  • Corkscrew hairs
  • Depression
  • Swollen bleeding gums
  • Loosening or loss of teeth due to tissue and capillary fragility
  • Iron deficiency anemia due to increased bleeding and decreased nonheme iron absorption
  • Bone disease (in children)
It is important to treat scurvy because left untreated it is fatal. 1

Click on Links Below to Read Scurvy Case Studies:
Scurvy | The College of Family Physicians of Canada (cfp.ca)

Pediatric Scurvy: How an Old Disease Is Becoming a New Problem (nih.gov)
Scurvy can be caused by either insufficient dietary intake of Vitamin C or critical illness that is accompanied by inflammation and increased metabolic consumption of Vitamin C. The following groups may be at an increased risk for developing scurvy:

  • Alcoholics 1
  • Cancer patients 1
  • Critically ill patients 2, 7, 9, 10
  • People with Crohn's disease 8
  • People with Celiac disease 8
  • Children with autism spectrum disorder 11
  • Type I diabetics who have high Vitamin C requirements 3
  • Drug addicts 1
  • Elderly people or indigent people who prepare their own food 1
  • End-stage renal disease on chronic hemodialysis 1
  • Individuals with restrictive diets, including food faddists, 1 people with food allergies, 3 eating disorders 3 or oral aversion 11
  • Individuals with iron overload, which leads to wasting of Vitamin C by the kidneys 3
  • Mentally ill 1
  • People with severe intestinal malabsorption or cachexia 1
  • Pneumonia (Community-Acquired) 9
  • Smokers or people exposed to secondhand smoke 1
  • Septic patients 2, 7, 10
  1. National Institutes of Health Vitamin C Fact Sheet for Health Professionals, https://ods.od.nih.gov/factsheets/VitaminC-HealthProfessional/
  2. Carr A.C., Rosengrave P.C., Bayer S., et al. Hypovitaminosis C and vitamin C deficiency in critically ill patients despite recommended enteral and parenteral intakes. Crit Care. 2017; 21: 300. https://ccforum.biomedcentral.com/articles/10.1186/s13054-017-1891-y, last accessed February 24, 2021.
  3. Maxfield L, Crane JS. Vitamin C Deficiency (Scurvy). StatPearls Publishing; 2019. Vitamin C Deficiency - StatPearls - NCBI Bookshelf (nih.gov), last accessed February 24, 2021.
  4. Schleicher, RL,, Carroll MD, Ford, ES, Lacher DA. Serum vitamin C and the prevalence of vitamin C deficiency in the United States: 2003-2004 National Health and Nutrition Examination Survey (NHANES). Am. J. Clin. Nutr. 2009, 90, 1252-1263, https://academic.oup.com/ajcn/article/90/5/1252/4598114, last accessed February 24, 2021.
  5. Cahill, L., Corey, P., and El-Sohemy, A. Vitamin C Deficiency in a Population of Young Canadian Adults. Am J Epidemiol. 2009; 170:464-471, https://academic.oup.com/aje/article/170/4/464/89509, last accessed February 24, 2021.
  6. Hagel, H., Albrecht, H., Dauth, W., et al. Plasma concentrations of ascorbic acid in a cross section of the German population. Journal of International Medical Research. 2018; 46 (1): 168-174, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6011295, last accessed February 24, 2021.
  7. Schorah, C. et al. Total vitamin C, ascorbic acid, and dehydroascorbic acid concentrations in plasma of critically ill patients. Am J Clin Nutr.1996; 63:760-765. https://academic.oup.com/ajcn/article/63/5/760/4651444, last accessed February 24, 2021.
  8. Mutgi, K. et al. Perifollicular petechiae and easy brusing. The Journal of Family Practice 2016; 65 (12): 927-930, https://www.mdedge.com/familymedicine/article/118921/hepatology/perifollicular-petechiae-and-easy-bruising, last accessed March 17, 2021.
  9. Carr A.C., et al. Patients with Community-Acquired Pneumonia Exhibit Depleted Vitamin C Status and Elevated Oxidative Stress. Nutrients. 2020; 12: 1318.
  10. Borelli e, Roux-Lombard P, Grau GE, et al. Plasma concentrations of cytokines, their soluble receptors and antioxidant vitamins can predict the development of multiple organ failure in patients at risk. Crit Care Med. 1996; 24: 392-7.
  11. Fortenberry, M. et al. Pediatric Scurvy: How an Old Disease is Becoming a New Problem. J Pediatr Pharmacol Ther. 2020; 25 (8): 735-741, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7671015/, last accessed February 25, 2021.

Indication & Important Safety Information


ASCOR® is vitamin C indicated for the short term (up to 1 week) treatment of scurvy in adult and pediatric patients age 5 months and older for whom oral administration is not possible, insufficient or contraindicated.

Limitations of Use:
ASCOR® is not indicated for treatment of vitamin C deficiency that is not associated with signs and symptoms of scurvy.

Important Safety Information


Contraindications: None.

Administration site reactions include pain and swelling.

ASCOR® should not be rapidly administered. Rapid intravenous administration (>250 mg/minute) of ASCOR® may cause temporary faintness or nausea, lethargy, flushing, dizziness, and headache.

Acute and chronic oxalate nephropathy have occurred with prolonged administration of high doses of ascorbic acid. ASCOR® is not indicated for prolonged administration. The maximum recommended duration is one week.

In patients with glucose-6-phosphate dehydrogenase deficiency severe hemolysis has occurred.

Ascorbic acid may interfere with laboratory tests based on oxidation-reduction reactions, including blood and urine glucose testing, nitrite and bilirubin levels, and leucocyte count testing. If possible, laboratory tests based on oxidation-reduction reactions should be delayed until 24 hours after infusion of ASCOR®.

Please see accompanying Full Prescribing Information for ASCOR®.

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