Clinical Pearls & Morning Reports
Published September 1, 2021
Scurvy is a multisystem illness caused by vitamin C deficiency. Scurvy occurs infrequently in the United States. However, in the Third National Health and Nutrition Examination Survey in the United States, low vitamin C levels were identified in 5 to 17% of participants. Read the NEJM Clinical Problem-Solving Article here.
Q: Describe some of the manifestations of scurvy.
A: Scurvy often leads to periodontal degeneration, widespread bleeding, and generalized malaise. Orthostasis, lightheadedness, dyspnea, and leg pain can all arise from vitamin C deficiency or associated anemia. Scurvy is characterized by purpura, gum disease, corkscrew hairs, and perifollicular hemorrhages. Scurvy has been associated with mood disturbances, depression, cognitive impairment, and delusions.
Q: Who is at particular risk for scurvy?
A: Groups at risk for scurvy include persons with psychiatric illnesses who have eating disorders or selective eating habits, infants who consume only pasteurized milk, children with autism spectrum disorder, persons with alcohol use disorder, and isolated elderly persons with poor nutrition.
A: Nearly all tissues in the body require exogenous vitamin C as a cofactor for biosynthetic reactions that drive collagen synthesis and energy production. Vitamin C is required for hydroxylation of proline residues on procollagen molecules, which support the triple-helix structure of collagen that underpins the integrity of skin, vessels, mucous membranes, and bone. Disruption in collagen formation from vitamin C deficiency causes microfractures in bone, perifollicular hemorrhages, ecchymoses, hemarthroses, petechiae, and gingival bleeding. Vitamin C is also a cofactor for enzymes involved in the biosynthesis of carnitine, which plays an essential role in the release of energy through beta-oxidation by facilitating the transport of fatty acids into mitochondria. This impairment in carnitine synthesis may account for the weakness, fatigue, and muscle cramping that occur in patients with scurvy.
A: Anemia is commonly identified in patients with scurvy and is often caused by decreased erythrocyte production, hemolysis, and blood loss. Vitamin C facilitates the absorption of nonheme iron and may protect against oxidation of tetrahydrofolate and resultant decreased folate levels. Therefore, vitamin C deficiency can lead to iron and folate deficiencies (which compound the underlying deficiencies from malnutrition). In addition, the antioxidant property of vitamin C has been implicated in maintaining the red-cell cytoskeleton protein beta-spectrin, which is crucial to the structure and integrity of the cell. The pathophysiological mechanisms underlying the hematologic manifestations of scurvy are understood better than the mechanisms underlying the neuropsychiatric sequelae. Vitamin C functions as a modulator of neurotransmitter synthesis and release. Some studies have suggested that the psychiatric symptoms caused by scurvy precede the physical manifestations and can occur with less severe total body vitamin C deficits than those associated with the physical manifestations.