eMedicine Specialties > Endocrinology > Metabolic Disorders

Scurvy

Author: Lynne Goebel, MD, Professor, Department of Internal Medicine, Marshall University Joan C Edwards School of Medicine
Coauthor(s): Henry Driscoll, MD, Professor, Department of Medicine, Section of Endocrinology, Marshall University School of Medicine
Contributor Information and Disclosures

Updated: Jun 25, 2009

Introduction

Background

Scurvy was first described in 1541 by a Dutch physician named Echthius working in Cologne, Germany. Mistakenly, he thought it was an infectious disease. In 1540, a French explorer named Jacques Cartier learned of a remedy for scurvy from the Native Americans of lower Canada, which was prepared by extracting the needles of pine trees with hot water. The first English reference to the disease occurred in the Oxford English Dictionary in 1565. (See image below and Image 1.)

In 1747, Lind, an officer in the British Royal Navy, conducted a study on 12 patients with scurvy. He divided the patients into 6 groups of 2 and gave each group a different remedy. Only the group given oranges and lemons recovered. It took Lind 41 years to convince the British Royal Navy to implement his recommendation. The British used lime juice instead of lemon or orange juice to prevent the disease, and the sailors became known as limeys.¹

Pathophysiology

Humans, other primates, and guinea pigs are unable to synthesize L-ascorbic acid (vitamin C); therefore, they require it in their diet.¹ The enzyme, L-gluconolactone oxidase, which usually would catalyze the conversion of L-gluconogammalactone to L-ascorbic acid, is defective due to a mutation or inborn error in carbohydrate metabolism.

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 necessary for the triple-helix formation of collagen. Deficiency of vitamin C leads to impaired collagen synthesis, causing capillary fragility, poor wound healing, and bony abnormalities in affected adults and children.

Although the clinical manifestations are unclear, vitamin C is a cofactor in the metabolism of tyrosine and cholesterol and the synthesis of carnitine, norepinephrine, peptide hormones, corticosteroids, and aldosterone.

It also enhances the absorption of iron from the small intestine. This may contribute to the anemia seen with vitamin C deficiency.

Frequency

United States

Data from the Third National Health and Nutrition Examination Survey (NHANES III) assessed the prevalence of vitamin C deficiency in the United States among a sample of 15,769 children and adults aged 12-74 years.² They found that 14% of males and 10% of females were vitamin C deficient.

International

A study of nonhospitalized patients in Paris found that 5% of women and 12% of men were deficient. In those older than 65 years, this proportion increased to 15% of women and 20% of men.³

In tests of plasma vitamin C levels in the low-income/materially deprived population of the United Kingdom, carried out between 2003 and 2005 (on 433 men and 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.⁴ 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.

Race

According to NHANES III, non-Hispanic black males had a slightly increased risk of vitamin C deficiency (OR = 1.2; 95% CI = 1.1,1.5) compared to white males.² Mexican American males and females had a lower risk of vitamin C deficiency compared to white males and females probably because the traditional Mexican diet is rich in chilies, tomatoes, and squashes, which are high in vitamin C.

Sex

Some studies show vitamin C deficiency to be more common among men, whereas others show equal distribution among men and women.

Age

• The incidence of scurvy peaks in children aged 6-12 months who are fed a diet deficient in citrus fruits or vegetables.
• Incidence also peaks in elderly populations, who sometimes have "tea-and-toast" diets deficient in vitamin C.

Clinical

History

• Early symptoms are malaise and lethargy.
• After 1-3 months, patients develop shortness of breath and bone pain. Myalgias may occur because of reduced carnitine production.
• Other symptoms include skin changes with roughness, easy bruising and petechiae, gum disease, loosening of teeth, poor wound healing, and emotional changes.
• Dry mouth and dry eyes similar to Sjögren syndrome may occur.
• In the late stages, jaundice, generalized edema, oliguria, neuropathy, fever, and convulsions can be seen.

Physical

• Vital signs: 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.
• Skin: Perifollicular hyperkeratotic papules, perifollicular hemorrhages, purpura, and ecchymoses are seen most commonly on the legs and buttocks where hydrostatic pressure is the greatest. Poor wound healing and breakdown of old scars may be seen.
• Nails: Splinter hemorrhages may occur.
• Head and neck: Gum swelling, friability, bleeding, and infection with loose teeth; mucosal petechiae; scleral icterus (late, probably secondary to hemolysis); and pale conjunctiva are seen. Conjunctival hemorrhage, flame-shaped hemorrhages, and cotton-wool spots may be seen. Bleeding into the periorbital area, eyelids, and retrobulbar space also can be seen. Alopecia may occur secondary to reduced disulfide bonding.
• Chest and cardiovascular: Scorbutic rosary (ie, sternum sinks inward) may occur in children. High-output heart failure due to anemia can be observed. Bleeding into the myocardium and pericardial space has been reported.
• Extremities: Fractures, dislocations, and tenderness of bones are common in children. Bleeding into muscles and joints may be seen. Edema may occur late in the disease.
• Gastrointestinal: Loss of weight secondary to anorexia is common. Upper endoscopy may show submucosal hemorrhage.

Causes

• Scurvy is caused by a dietary deficiency of vitamin C. The body's pool of vitamin C can be depleted in 1-3 months.
• Risk factors⁵ include the following:
  • Babies who are fed only cow's milk during the first year of life are at risk.
  • Alcoholism¹ and conforming to food fads are risk factors.
  • Elderly individuals who eat a tea-and-toast diet are at risk. Retired people who live alone and those who eat primarily at fast food restaurants face increased risk of deficiency.
  • Economically disadvantaged persons tend to not purchase foods high in vitamin C (eg, green vegetables, citrus fruits), which results in them being at high risk.⁴
  • More recently, vitamin C deficiency has been noted in refugees who are dependent on external suppliers for their food and have limited access to fresh fruits and vegetables.
  • Cigarette smokers require increased intake of vitamin C because of lower vitamin C absorption and increased catabolism.
  • Pregnant and lactating women and those with thyrotoxicosis require increased intake of vitamin C because of increased utilization.
  • People with anorexia nervosa or anorexia from other diseases such as AIDS or cancer are at increased risk of vitamin C deficiency.
  • People with type 1 diabetes have increased vitamin C requirements, as do those on hemodialysis and peritoneal dialysis.^6,7
  • Because vitamin C is absorbed in the small intestine, people with disease of the small intestine such as Crohn, Whipple, and celiac disease are at risk.
  • Iron overload disorders may lead to renal vitamin C wasting.

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